lOTES 01 PATHOLOGY 
For Students’ Use. 
BY 
W. A. EVANS. B. SC., M. 1). 
PROFESSOR OF PATHOLOGY MEDICAL SCHOOL OF THE UNIVERSITY 
OF ILLINOIS*. PROFESSOR OF PATHOLOGY MILWAUKEE 
MEDICAL COLLEGE; PATHOLOGIST COLUMBUS 
MEDICAL LABORATORY, ETC. 1, 
CHICAGO MEDICAL BOOK CO., 
35-37 Randolph Street, 
CHICAGO: 
1898. Copyright, 1897 PREFACE 
This has been written by a teacher for stu- 
dents, It does not pretend to originality. 
Green, Hamilton, Zeigler, Orth, Woodhead, 
Cabot have been freely consulted. My thanks 
are due Drs. L. J. Mitchell and C. C. O’Byrne. 
W. A. Evans. TABLE OF CONTENTS. 
PAGE 
Blood and Blood Organs, Diseases of 398 
Circulatory System, Diseases of 156 
Definitions 2 
Degenerations 20 
Female Genitals, Diseases of 342 
Gastro-Intestinal Tract, Diseases of 234 
Infiltrations ■ 23 
Inflammations 2 
Kidney, Diseases of 288 
Liver, Diseases of 248 
Male Genitals, Diseases of 322 
Mouth, Diseases of 458 
Nervous System, Diseases of 370 
Respiratory Apparatus, Diseases of 90 
Teeth, Diseases of 430 
Transudation? 8 
Tumors 50 
Zounds, Healing of 46 NOTES ON PATHOLOGY. 
Pathology is the science of the lesions found 
in tissues, both as a cause of, and as a result of 
disease. 
Pathological anatomy is the science of the 
lesions recognizable by the unaided eye. 
Pathological histology is the science of the 
lesions recognizable by the microscope. 
Pathological processes divide themselves 
into: 
1. Inflammations. 
2. Degenerations. 
3. Tumor growths. 
INFLAMMATIONS. 
Inflammations are pathological exaggera- 
tions of the normal processes of repair. Every 
inflammation depends upon irritation. In 
every irritation there are two factors: (1) the 
irritant, and (2) the cell irritated. 
The Cell Irritated. As a rule, the more 
highy differentiated a cell, the greater its ir- 
ritability. 4 
Inflammations. 
All cells spring originally from the ovum; 
they arrange themselves into three layers, and 
these further develop into tissues and organs. 
The faet that the cells of a certain organ do 
a certain work is proof that the demand for 
that work is an irritant to those cells; e.g., the 
fact that the kidney epithelium secretes urine 
is proof that these epithelial cells are irritated 
by the antecedents of urine. Urea is, then, a 
special irritant to kidney epithelium, and only 
a general irritant to the other tissues of the 
body. 
The parenchyma is the working part of an 
organ. It is immaterial from what blastic 
layer it is derived; it is the most easily irritated 
of the tissues of that organ. 
Irritants are general and special: A gen- 
eral irritant is one that is irritating in pro- 
portion to the irritability of the cells. Special 
irritants are those that only irritate certain 
cells; e.g., the irritant causing destruction of 
liver epithelium in acute yellow atrophy. 
Inflammations are divisible into two great 
classes: 
i. Productive. 
2. Destructive. 
Physiological irritation is responsible for 
function. Moderate pathological irritation 6 
Inflammations. 
gives productive inflamrtiation; this, carried 
one step further, gives destructive inflamma- 
tion. 
Productive inflammations are divisible into; 
i. Non-exudative. 
2. Exudative. 
The elements that make up a tissue can, 
then, be divided for our purposes into: 
i. The local cells. 
2. The vessels. 
If an irritant affect the first only, we have a 
non-uxudative productive inflammation.' If it 
affect the first and second, we have an exuda- 
tive productive inflammation. If it involve 
the second only, we have an angio-neurotic 
oedema (urticaria), a condition scarcely con- 
sequential enough to be considered in this 
connection. 
When cells are irritated beyond the usual 
limits, and yet short of destruction, partial or 
complete, they divide by: 
i. Direct division, in which the nucleus 
and the cell protoplasm divide simultaneously; 
this is unusual. Or by: 
2. Indirect division, called also mitosis and 
karyokinesis. In this the nucleus first divides, 
then the cell protoplasm. The nucleus is 
made up of a threadwork and a delicate semi- 8 
Inflammations. 
fluid interfibrillar substance. This skeinwork 
first arranges itself regularly, then unravels, 
and the two stars assume opposite poles of the 
nucleus; then the spongioplasm divides, then 
the cell protoplasm cleaves. The new skein 
in the new nucleus assumes then its irregular 
resting stage. This is the usual method of 
dividing. 
A transudation is constantly taking place 
from the vessels. So long as the capillaries 
and lymphatics bear off the transudate as fast 
as it pours out, no accumulation takes place. 
This is physiological transudation, and is the 
means of much of nutrition. 
TRANSUDATIONS. 
Pathological transudates arc divisible into 
(i) active and (2) passive. 
Passive transudation is due to mechanical 
disturbance of the relation between heart force 
and the opposing forces. Examples: oedema, 
ascites. 
Active transudations, called exudations, are 
clue to exaggerated permeability of the capil- 
lary wall as a result of inflammation. A vaso- 
motor nerve irritated causes the circular mus- 
cular fiber of the vessel to contract, the lumen 
is lessened, the current rapidity is increased 
If the irritation is increased or continued, the 
nerve is paralyzed, the fiber relaxes, the 10 
Inflammations. 
lumen is increased; the normal blood current 
arrangement (from center out—red cells, red 
cells and whites, plasma, wall) is lost; leu- 
cocytes gather along the wall; the irritated 
endothelial cells contract and become cubi- 
cal, and stomata opened at the points of junc- 
ture with other cells; through these openings 
the exudate passes. In ordinary transudation 
the larger part of the plasma passes through 
the endothelial cells and is changed thereby ; 
the process is akin to a secretion or a selec- 
tive action.—Plasma goes through with 
greatest readiness, therefore, in mild vaso- 
motor irritation the exudate consists of 
plasma only; more violent irritation gives 
plasma and leucocytes, and if still more vio- 
lent gives plasma, leucocytes and red cells. 
NON-EXUDATIVE PRODUCTIVE INFLAM- 
MATION. 
This variety of inflammation is of no great 
significance unless there is an appreciable 
accumulation of tissue elements; therefore, it 
demands a mild irritation, long continued. It 
can involve highly differentiated cells alone, 
in which event the more lowly differentiated 
connective tissue is unaffected. Generally it in- 
volves the more lowly differentiated connect- 
ive tissue. In this event the more highly dif- 12 
Inflammations. 
fercntiated forces are sometimes unaffected, 
sometimes proliferating, and sometimes 
undergoing some of the varieties of destruc- 
tive inflammation, dependent upon whether 
the irritant is very irritating to them or not. 
Usually the state is that of cloudy swelling. 
The irritant must be mild, else it will involve 
the vaso-motor apparatus. It must be long 
continued in order that production may be 
appreciable. The irritant, again, must be 
mild in order to be long continued, for more 
violent irritation set in motion processes that 
limit or annul them. 
For this reason, non-exudative productive 
inflammations are usually due to alcohols, leu- 
comaines, and the milder toxalbumins. There 
is a marked production of new connective 
tissue; this starts as young round cells, which 
develop into spindles, and then into fibril- 
lated fibers. Bear in mind the tendency of 
this new pathological connective tissue to 
contract and pucker. This contraction is re- 
sponsible for pressure atrophy in the included 
tissues. This process is not an even one; it 
is usually in bands or wedges, dependent on 
vessel arrangement. 
The lessons to learn are: 
i. Pathological connective tissue con- 
tracts as it matures. 14 
Inflammations. 
2. That while the lowly differentiated cells 
are dividing—actively increasing—the same 
irritation may cause the highly differentiated 
cells to proliferate or to break down. 
EXUDATIVE PRODUCTIVE INFLAMMA- 
TIONS. 
The irritant affects the vaso-motor appara- 
tus and the local cells. The highly differen- 
tiated may be proliferating, but are usually 
undergoing some form of destructive inflam- 
mation, such as cloudy swelling. The lowly 
differentiated cells proliferate very actively, 
especially in the vicinity of the poison. The 
vessels are exuding plasma, leucocytes and 
red cells, all or either. This exudate over- 
shadows the new cells born of the local cells. 
These inflammations are generally more 
violent and always shorter lived. In this 
variety are found the classical symptoms of 
inflammation: 
Pain, from pressure on nerve endings; 
Heat, from increased metabolism; 
Redness, from the presence of blood; 
Swelling, from the accumulation of exudate 
and blood in the part; 
Impairment of function, by reason (i) swell- 
ing, and (2) inflammatory changes in the 
functioning elements. 16 
Inflammations. 
These inflammations lend themselves easily 
to supperative processes. The irritant sub- 
siding, the vessel tone returns; the unim- 
paired leucocytes get back into the circula- 
tion; the new cells and the impaired leuco- 
cytes undergo granular degeneration and ab- 
sorption by leucocytes. 
DESTRUCTIVE INFLAMMATIONS. 
i. Cloudy Swelling—a form of inflamma- 
tory degeneration in which granules precipi- 
tate in the substance of the semi-liquid pro- 
toplasm. 
2. Fatty Degeneration—an inflammatory 
degeneration following the first mentioned, 
in which portions of the albuminous proto- 
plasm is converted into fat. 
3. Granular Degeneration—necrosis a 
breaking down of the albuminous cells, a loss 
of organic form. The nucleus persists for a 
while, but it, too, breaks down. In some 
areas such a pultaceous mass is called ather- 
oma. 
4. Caseation—the liquids absorb and leave 
the granules behind. 
5. Liquefaction—due to digestion of the 
dead masses. 
6. Calcification.—ln the process of break.- 18 
Inflammations. 
ing down, organic acids result. These com- 
bine with the calcium of the plasma and tis- 
sue juices to form calcium salts. Calcifica- 
tion is secondary to necrosis. 
y. Suppuration.—Death and partial diges- 
tion by the poison of, not only the fixed cells 
and their offspring, but of wandering cells at- 
tracted to the focus of poison—chemotaxis. 
Chemical irritants disassociated from bacte- 
ria can produce suppuration; but practically 
the only suppurations are those of bacterial 
origin. In killing and digesting the leucocyte 
and inflammatory connective tissue cell, much 
of the poison is destroyed, and new poison re- 
quires the presence of secreting organisms.— 
If these phagocytes destroy the cocci, the 
process terminates. If the local tissues be- 
come habituated to the poison, the process 
ends. If the cocci become attenuated from 
soaking in their own poisons, the process 
ends. 
Suppuration on a surface is called an ulcer; 
below a surface it is called an abscess. 
The irritation having subsided, the amount 
of dead and functionally inactive tissue is so 
small that the phagocytes can assimilate or 
transport it. 
RESOLUTION. Degenerations and Infiltrations. 
20 
DEGENERATIONS AND INFILTRATIONS. 
A degeneration is the substitution for a 
higher protoplasm of a substance lower in 
the chemical scale. It is, therefore, a molec- 
ular transformation, and does not apply to 
the substitution of one class of cells by an- 
other. 
An infiltration is the addition to a higher 
protoplasm of a substance lower in the scale 
without any change in the higher protoplasm. 
The line between these processes is diffi- 
cult to draw. 
The degenerations are; 
1. Cloudy swelling. 
2. Fatty degeneration. 
3. Necrosis. 
4. Coagulation necrosis. 
5. Caseation. 
6. Gangrene. 
The infiltrations are: 
1. Fatty. 
2. Glycogenic. 
3. Serous. 22 
Degenerations and Infiltrations. 
The mixed degenerations and infiltrations 
are those in which there is some preliminary 
change in the cell protoplasm, but in which 
the amount of infikered substance overshad- 
ows the primary change. These are; 
i. Amyloid. 
2. Mucoid. 
3. Colloid. 
Degenerations are due to faults of nutri- 
tion as to (a) quantity, and (b) quality. A 
degeneration may accompany inflammation, 
in which event the quality of the pabulum is 
at fault, as in cloudy swelling due to irritant 
poisons. The degenerations that may be in- 
flammatory are cloudy swelling, fatty degen- 
eration and all forms of necrosis. 
4. Hyaline. 
Or, it may not be connected with inflam- 
mation, in which event the quantity of nutri- 
tion is less than the cell requires for its pun- 
pose. 
The degenerations that may be non-inflam- 
matory are fatty, amyloid, mucoid, colloid, 
serous. 
The inflammatory infiltrations are serous. 
The non-inflammatory infiltrations are fatty, 
glycogenous and serous. 
It is to be borne in mind that certain of the 24 
Degenerations and Infiltrations. 
degenerations and infiltrations are under cer- 
tain circumstances entirely physiological 
For example, milk is a composite of a watery 
exudate and the epithelial cells of the mam- 
mary gland in a state of fatty degeneration. 
The sebaceous secretion of the skin is of the 
same nature. 
ALBUMINOUS DEGENERATION. 
Synonym: Gloudy swelling. 
Causes: Nutrition minus—deficiency in 
quality; nutritive fluids contain a poison. 
Nature: An inflammatory degeneration 
Results histologically: Return to normal, 
fatty degeneration, or, if process is more vio- 
lent, necrosis. 
Effects physiologically: Loss of function. 
Gross appearance: Organ is swollen, paler 
than normal. 
Microscopic appearance: Nucleus is ob- 
scured in varying degree; may not be appar- 
ent, may be incapable of taking stain, may 
have disappeared; cell usually swollen, gran- 
ular; granules small, not highly refractile. 
Chemically, cell stains poorly, granules sol- 
uble in acetic acid. Method: Place a few 
teased cells on a slide in physiological salt 
solution; cover; run under cover a drop of I 2G 
Degenerations and Infiltrations. 
per cent, solution of acetic acid; granules dis- 
appear. 
Nature of process: The increase in size is 
due to absorption of water. The granules 
consist of albuminous or albuminoid material, 
lower in the chemical scale than the normal 
protoplasm. 
FATTY DEGENERATION. 
Synonyms: None. 
Causes: Nutrition minus, either lack of 
food supply or toxaemia. 
Origin: May be inflammatory, in which 
event it is preceded by albuminous degenera- 
tion, or it may be non-inflammatory. 
Results histologically: Return to normal; 
nearosis and the resulting possibilities of an 
area of necrosis. 
Effects; Loss of function, partial or com- 
plete. 
size. 
Anatomy; Organ pale, not much altered in 
Microscopic appearance: (Comparison with 
albuminous degeneration.) Nucleus much 
less obscured; granules larger, may be glob- 
ules; granules refract light more. 
Chemically: Teased elements show gran- 
ules or globules of fat; replace salt solution 28 
Degenerations and Infiltrations. 
by ether; the grannies are dissolved; stain 
with a one-fifth of I per cent, solution of 
osmic acid, grannies become black. Into 
teased specimen run I per cent, acetic acid, 
no change is observed; specimens fixed, 
hardened, embedded, stained and mounted 
show clear vesicles where the fat originally 
was. 
Nature of process: This represents a re- 
trograde process wherein the higher proto- 
plasm is replaced by fat; This fat is at first 
in small granules and these coalesce to form 
globules, though the globules are never as 
prominent as they are in fatty infiltration. It 
represents a more violent or a more pro- 
longed nutrition minus or toxaemia than al- 
buminous degeneration, therefore cells so 
affected less readily return to the normal. 
FATTY INFILTRATION. 
Synonym: Lipomatosis. 
Nature: Generally physiological, witness 
adipose tissue; usually physiological in liver. 
Causes; Too much fat ingestion; too much 
ingestion of easily oxidizable substances, such 
as alcohol. The alcohol is burned and the 
other food elements are stored up as fat. This 
includes albumen and carbo-hydrates, which Degenerations and Infiltrations. 
are converted into fats and stored. Fatty in- 
filtration is a storing up of fat within the cells 
without any decrease in the amount of albu- 
men in the cell. It may represent the storing 
of fat brought to the cell as fat, or it may 
represent fat manufactured by the cell out of 
albumens and carbo-hydrates. Note differ- 
ences here from fatty degeneration. 
Results histologically: Return to normal; 
fatty degeneration frequently ensues. 
Effects physiologically: Much less than it 
would seem possible; it interferes but little 
with the chemistry or the physics of the cells. 
Anatomy: Organ markedly increased in 
size and consistency; edges rounded; very 
pale; greasy feel. 
Microscopic appearance: Signet ring, a 
central mass of fat that in specimens, as ordi- 
narily prepared, has dissolved away, leaving 
a clear zone; around this is a rim of com- 
pressed protoplasm, and at one side is the 
nucleus—the signet; protoplasm and nucleus 
are clear and distinct, unless secondary de- 
-generations have taken place. 
Chemistry: See fatty degeneration. 32 
Degenerations and Infiltrations. 
AMYLOID DEGENERATION. 
Synonyms: Waxy; lardaceous. 
Causes: Prolonged suppuration; syphilis; 
tuberculosis; leukaemia. It is due to nutri- 
tion minus; the elements lacking are not un- 
derstood. 
Results histologically: We do not know 
that it leads to necrosis; nor do we know that 
it may disappear and the fibers return to 
normal; yet there are good reasons for think- 
ing that the latter occurs. 
Effects: Impairment of function. 
Site; Connective tissues and especially ves- 
sel walls; where disease is just beginning, it is 
to be found in the middle coat of the arteries 
of small size. 
Anatomy: Organ very large with rounded 
edges; firm; pale; surface glistens. Thin sec- 
tions made with a parallel bladed knife may 
show the waxy material. Stain such a sec- 
tion with a mixture of iodine i, potassium 
iodine 10, water 100. The waxy areas be- 
come mahogany brown, the others a straw 
yellow. 
Microscopic appearance: In the middle coat 
of the vessel between the muscle fibers; here 
there is a deposit of this albuminoid substance 
as a result of a reaction between the cells here Degenerations and Infiltrations. 
and the plasma; walls thickened; homogene- 
ous, glistening, muscle fibers atrophying; 
connective tissue cells enclosed by this ma- 
terial are atrophying; epithelial cells not af- 
fected by the amyloid process, though it may 
undergo fatty or other degeneration. 
Chemically: Stain sections for five min- 
utes in methyl violet, then for one minute in 
a saturated watery solution of oxalic acid; 
wash in water thoroughly, then mount in Far- 
rant’s solution. The tissue cells will be 
stained blue; amyloid will be red. It resists 
acids and alkalies, is not soluble in alcohol 
nor water, nor does gastric juice digest it. 
Nature of the process: The material is not 
a starch. It contains nitrogen in about the 
same proportion as albumens, yet it is not 
acted upon by acids, alkalies or the gastric 
juice. It is a mixed infiltration and degen- 
eration; the appearances and all the charac- 
teristics are those of an infiltration, but there 
must be a primary change in both the fibers 
and in the chemistry of the plasma. 
Usual sites: Glomeruli of kidney, capilla- 
ries of liver, corpuscles of spleen. Degenerations and Infiltrations. 
Synonym: Vitreous degeneration. 
HYALINE DEGENERATION. 
Causes: Nutrition minus. 
Locations: In muscles that have been rup- 
tured or overstrained there is always hyaline 
degeneration in the affected areas. This is 
especially true after prolonged toxaemias, such 
as typhoid fever; found here in rectus abdo- 
minalis, because of the strain to which it is 
subjected in changing posture. Found in 
blood clots shielded from-infection; therefore 
frequent in the ovary and in thrombi. Found 
in tumors, especially in those of the abdomen; 
in the thyroid gland in goiter. 
Effects physiologically: Loss of function. 
Microscopic appearance; Intrinsically it 
cannot be differentiated from mucoid and from 
amyloid; all three are hyaline degenerations. 
Chemistry: Stains markedly with acid 
stains, especially oesin. 
MUCOID AND COLLOID DEGENERA- 
TIONS. 
Location: Found in carcinoma in which 
the epithelium springs from mucus secreting 
epithelium. In chondromata, lipomata, myx- 
omata, myomata, gliomata and sarcomata; in 
the walls of glands, such as in the secreting 38 
Degenerations and Infiltrations. 
structure of the stomach; secondarily it in- 
volves the fibrous stroma of such structures. 
Effects histologically: In the protoplasm of 
the cell a globule of hyaline material appears. 
This increases in size until the cell is dis- 
tended, much as the cell is distended in fatty 
infiltration. The cell ruptures and the mass 
becomes an even lake of mucoid material, in- 
tersected by fibrous tissue walls. 
Microchemistry: It is precipitated as a 
granular material by acetic acid. It is less 
firm than is colloid. 
GLYCOGEN INFILTRATION. 
Synonyms: None 
Nature: Occurs in the liver and many other 
localities when too much carbo-hydrates are 
taken; found especially in diabetes, in which 
some step in the destruction of carbo-hydrates 
is interfered with. 
Cause: Nutrition plus. 
Effects physiologically: Cells and fibers 
are swollen by a clear and homogeneous mass, 
or by a granular substance arranged in glob- 
ules. 
Microchemistry: Soluble in water; gives 
the amyloid reaction with iodine, but does 
not stain blue with sulphuric acid. This in- 40 
Degenerations and Infiltrations. 
filtrate being soluble in water, the section 
must at no time come in contact with water. 
Fix, harden, embed, cut, wash in benzine. 
Alcohol. A mixture of I part tr. iodine and 
4 parts of absolute alcohol; oil origanum; 
balsam. , 
An infiltration may represent nutrition 
plus. The normal individual cell if in a state 
of nutrition plus works extra hard and begets 
its kind. In the infiltrations of nutrition plus 
the protoplasm of the individual cells is un- 
affected or even in nutrition minus. It is the 
general system which is nutrition plus, not the 
infiltrated cell. 
In the degenerations, which all represent 
nutrition minus, there is a class of affections 
in which nutrition is entirely at an end. These 
are called the necroses, and take several 
names, dependent upon what happens after 
the cells are dead. 
Necrosis in a general way is first to be 
described. Due to entire cessation of nutri- 
tion, because either no food is furnished, or 
else the protoplasm of the cell is so altered 
that it is incapable of appropriating food. 
Therefore frequent causes are: 
i.—Thrombus and embolus. 
Angio-sclerosis. 
Pressure.  Degenerations and Infiltrations. 
2>.—Burns, scalds, freezing. 
Ergot. 
Infections. 
Nerve lesions. 
Effects physiologically: Loss of function. 
Microscopical appearance: The nucleus 
disappears, the protoplasm becomes granular, 
the cell outlines are lost, a mass of granular 
material is the sole representative of the tis- 
sue. 
Chemical reaction; Elements stain with 
great difficulty. 
The area of necrosis is frequently the seat 
of infection with pus germs; result—suppura- 
tion. It frequently is the seat of a deposit of 
lime salts—calcareous degeneration. 
Calcareous degeneration. Microscopical 
appearance: Opaque; granules and plates. 
If to a section under the microscope a drop 
of a mineral acid be added, the granules dis- 
appear and bubbles of carbon dioxide accum- 
ulate under the cover. 
Nature; A combination of fatty acids and 
acids derived therefrom, with lime basis of the 
blood and tissue juices. 
Most frequent locations; Atheromatous 
patches in arteris, tumors, old suppurations, 
such as pleurisies. 44 
Degenerations and Infiltrations. 
Caseation: If from an area of necrosis the 
fluids absorb, the resulting relatively dry mass 
is an area of caseation. 
Liquefaction; Such a necrosed area or a 
living area may be acted on by digestive fer- 
ments secreted by bacilli, leucocytes, or from 
other sources so that the protoplasm of the 
cells and intercellular substance is dissolved 
in the fluids of the part. 
Coagulation necrosis; Necrosis plus coag- 
ulation; death in the cells accompanied or fol- 
lowed by coagulation in its protoplasm. 
Most frequent site; the pharynx in diph- 
theria. 
Gangrene: Necrosis of a considerable area, 
with primary or secondary infection. 
Causes: Those of necrosis (see above), cold, 
pressure, arteriosclerosis, or better angioscler- 
osis, for the sclerosis may be in vessels other 
than the arteries; nervous diseases; ergot. In- 
fection; several organisms; most frequent 
bacillus of malignant oedema, bacillus coli 
communis. 
Gross appearance: Organ black, greenish 
(from decomposing blood) with raised blebs 
filled with reddish to greenish fluid. Odor 
may be foul, dependent on infecting germ. Degenerations and Infiltrations. 
HEALING OF WOUNDS. 
In this I will describe the process by 
which an incised wound in a soft part heals. 
The incision severs capillaries, lymphatics, 
nerve filaments and both epithelial and con- 
nective tissue cells. 
i. The plasma and blood flow into the 
rent and coagulate, binding together the two 
sides of the incision. 
2. The portions of the cells cut away from 
their nuclei die and are absorbed by the ex- 
uded leucocytes. 
3. The cells irritated, by (a) the direct 
stimulus of the cut, and (b) the indirect stimu- 
lus through the nerves that are hurt—divide 
by indirect division: 
4. These cells and leucocytes wander into 
the clot. 
5. Capillary loops, springing from the cap- 
illaries, developing step by step with the 
cell development, extend into the clot. 
6. The gap, being filled to the skin level, 
the epithelial cells grow over the surface. 
Note. The irritation causing the epithelium 
to proliferate is supplied, as in the case of the 
underlying tissue, by (1) the direct stimulus 
of the cut and (2) by the indirect stimulus 
through the hurt nerves. New cells were being 48 
Degenerations and Infiltrations. 
formed from the beginning. They do not 
stick until the skin level is reached. 
7. The leucocytes carry off any tissue not 
needed for permanent structure. 
8. The connective tissue cells certainly, 
and the leucocytes possibly, mature into con- 
nective tissues. 
9. The blood capillaries disappear by (1) 
contraction of maturing fibers, (2) by endar- 
teritis obliterans. 
The above is called healing by first inten- 
tion. If the plasma does not glue together 
the surfaces, and if a larger space is to be 
filled in, the histologic granulations become 
anatomic, and we term the process healing by 
second intention. The only difference is in 
degree. 
Healthy granulations are those in which 
there is a pari passu growth between em- 
bryonal blood vessels and young tissue cells. 
Foul graulations are those in which there 
is a loss of relation between growth of em- 
bryonal blood vessels and young tissue cells. 
The necessity for healing by second inten- 
tion arises most frequently from infection. 50 
Tumors. 
TUMORS. 
A tumor is a cystic or solid new growth 
They are divided into: 
1. Connective tissue tumors, 
2. Epithelial tumors. 
3. Dermoids. 
4. Teratomata. 
5. Cysts. 
The connective tissue tumors are: 
A. Benign— 
Fibromata. 
Lipomata. 
Myxomata. 
Chondromata. 
Osteomata. 
Odontomata. 
Gliomata. 
Myomata. 
Angiomata. 
Lymphangiomata. 
tions of some of these. 
B. Malignant— 
And a few less important modifica 
Sarcomata. 52 
T nmors. 
The epithelial tumors are: 
A. Benign— 
Papillomata. 
Adenomata. 
Neuromata. 
B. Malignant— 
Epitheliomata. 
Carcinomata. 
A dermoid is a tumor composed of hair, 
teeth, etc., developed from an inclusion of 
some blastic structure in an area abnormal 
to it. This inclusion is characterized by a 
tendency to make mature tissues. 
A teratoma is developed from a second 
ovum, acting as a parasite on the host; e.g., 
a four-legged man or a double-headed calf. 
A cyst is a pathological mass of fluid con- 
stituents surrounded by a wall. 
CAUSE OF TUMORS. 
There are two principal theories, neither of 
of which has been demonstrated. 
(i) That tumors, and especially malignant 
tumors, are due to organisms. These organ- 
isms are held to belong to the protozoa or to 
the yeasts. 
(2J That tumors are remnants of foetal 
structures or inclusions of post-natal struc- 
tures that in later life develop. 54 
Tumors. 
FIBROMATA. 
These can be taken as the basis of connect- 
ive tissue tumors, both benign and malignant 
—a tumor composed of white fibrous con- 
nective tissue. 
Location: Anywhere in the body. 
Varieties; Simple fibroma, molluscum 
fibrosum, keloid, false neuroma endothelioma. 
Anatomy: These tumors are generally mul- 
tiple; they are always incapsulated and be- 
nign. They are generally hard, dense, and 
on cut section are found to be composed of 
bands of fibers running in various directions. 
Histology: The tumor is composed of fibril- 
lated connective tissues, running in various 
directions, generally in dense bundles; 
amongst the fibers there are a few spindle- 
shaped nuclei; there is a comparatively small 
number of blood vessels, and these have fully 
matured walls. 
Degenerations: Serous, mucoid, fatty—cal- 
cification—cyst formation. These tumors are 
liable to inflammations. 
LIPOMATA. 
Location: Found anywhere in the body, 
but more abundant in the subcutaneous tis- 
sues; may be multiple, when they are gener- 56 
Tumors. 
ally small, or there may be a single large 
tumor. 
Anatomy: The tumors move freely on the 
underlying structures; generally the skin slips 
easily over them, though sometimes they are 
attached to this structure. They are rounded, 
lobulated, encapsulated, and show as masses 
of yellow fat with trabeculae of white fibrous 
connective tissue. 
Histology: That of adipose tissue; con- 
nective tissue cells are filled with globules of 
fat, the protoplasm showing as a ring around 
the globules; nucleus found as an enlarge- 
ment at one point of this ring. 
Degenerations: Molecular softening, a star- 
vation necrosis, in which the tumor elements 
break down into granular debris and fatty 
crystals; calcareous infiltrations subsequent to 
the first variety of degenerations mentioned. 
They are subject to inflammation and ulcera- 
tion. 
Lipomata can be considered as bearing the 
same relation to fibromata that adipose tis- 
sue does to' ordinary white fibrous t issue. 
MYXOMATA. 
Tumors made up of branching connective 
tissue cells, infiltrated with mucoid material. 58 
Tumors. 
Location: Found in any part of the body, 
but more frequently in the nose and in the 
subcutaneous connective tissue. 
Anatomy: These tumors grow slowly; lob- 
ulated, encapsulated. From this capsule tra- 
beculae run into the tumor mass. The spaces 
between the trabeculae are filled by a mass of 
clear, gelatinous material, resembling boiled 
tapioca. If a small portion of this tumor be 
immersed in dilute acetic acid, the clear, gel- 
atinous areas become slightly opaque, losing 
their luster. 
Histology: There are bands of fibrous tis- 
sue, composed of fibers with a small number 
of cells. In these bands are matured blood 
vessels; between the bands are zones, con- 
sisting of a comparatively delicate connective 
tissue reticulum, with spaces filled in with 
mucin. The individual cells of this reticulum 
are branched. 
Degenerations; Hemorrhage, from rupture 
of the vessels; ulcerative inflammation. 
A myxoma may be said to be a fibroma in- 
filtrated with mucoid substance. 
Location: Periosteum of bones; in the pa- 
rotid and salivary glands, testicle, skin, mam- 
ma. 
■CHONDROMATA. 60 
Tumors. 
Anatomy: The growths are not infrequent- 
ly multiple. They are firm, elastic, rounded, 
tabulated, with distinct fibrous capsule, tra- 
beculae running in therefrom. The tumor cuts 
with a creaky, cartilaginous feeling. 
Histology; Between the bands of fibrous 
tissue there are areas of hyaline matrix, in 
which are the usual cartilage cells placed in 
a cartilage cell space. In some of these spaces 
there are two nuclei. 
Degenerations; They are subject to myx- 
omatous or mucoid infiltration; to bone for- 
mation; to calcification; to ulcerative inflam- 
mation. 
OSTEOMATA. 
Location: They grow chiefly at points of 
junction between a bone and cartilage. 
Varieties; Eburnated, compact, spongy. 
Eburnated osteomata are found always in 
the vicinity of bone or on the surface of bone. 
They consist of dense 2 bone, laminated in 
structure, the layers parallel with the free sur- 
face; no Haversian systems. 
The compact osteomata are found in bone, 
and in a good many connective tissue areas 
entirely separated from bone. The structure 
is that of normal bone. There is a periosteal 
covering, and the bone is around Haversian 
systems. 62 
Tumors. 
The spongy osteomata are those in which 
the Haversian canals are very wide, and com- 
paratively few layers of bone have been de- 
posited by the osteoblasts. 
It is doubtful if these should be classed 
among the connective tissue tumors, since 
many histologists hold that the neuroglia 
cells are derived from the epiblast. They are 
tumors, composed of neuroglia cells. 
GLYOMATA. 
Anatomy; They are found in the central 
nervous system; are usually single, sometimes 
multiple. Encapsulated, gray to reddish in 
color; frequently distinguished from the brain 
substance with great difficulty. Sometimes 
raises the brain substance so as to give the 
appearance of an hypertrophy of the convolu- 
tions. In processes of hardening the tumor 
structure shrinks from the brain substance, so 
that it stands out more prominently. 
Histology: There is a recticulum of deli- 
cate fibers. These fibers are protoplasmic 
prolongations of small cells characterized by 
these branching processes. The cells have 
one or more deeply stained nuclei, and seem 
to stud the mass of fibrous recticulum. The 
number of blood vessels is very considerable; 64 
Tumors. 
some are young with thin walls; some are old 
with thick walls; there are usually considerable 
numbers of large cells thickly studded with 
golden-brown pigment. 
Degenerations: Haemorrhagic infiltration, 
from rupture of the vessels; fatty degenera- 
tion; starvation necrosis. 
MYOMATA 
Two varieties: 
(i.) Leiomyomata, composed of non-stri 
ated muscle; and 
(2.) Rhabdomyomata, composed of stri- 
ated muscle. 
LEIOMYOMATA. 
They are by far the more frequent of the 
two. 
Location: Uterus; broad ligament; ovary; 
gastro-intestinal tract; prostrate gland. 
Anatomy: They are generally encapsu- 
lated; firm; multiple. Cut section has a banded 
appearance, bands running in every direc- 
tion. They vary very greatly in the number 
of blood vessels; not infrequently they con- 
tain so large a number of blood vessels that 
they give the appearance of angioma. 
Histology: The tumor consists of inter- 
lacing bundles of involuntary muscle, with 66 
Tumors. 
large, rather rounded nuclei. It is difficult 
to tell this tumor from fibroma when the tu- 
mor is matured. 
Degenerations: Mucoid; fatty; necrosis, 
followed by calcification; cyst formation; in- 
fection. 
ANGIOMATA AND LYMPHANGIOMATA. 
Angiomata are tumors composed of blood 
vessels. Lymphangiomata are tumors com- 
posed of lymph vessels. 
ANGIOMATA. 
Are divided into (i) simple angiomata, in 
which the blood vessels are of moderate di- 
ameter; and (2) cavernous angiomata, in which 
the bloocl vessels are widely dilated. 
Synonyms: Nsevus, birth marks. 
Location: In the subcutaneous tissue, es- 
pecially of the face, in the tongue, in the 
liver. 
Anatomy; An angiomata shows as a plaque 
—red in color if the blood is arterial, dark if 
venous; very slightly elevated above the sur- 
face. 
Histology: The tumors are found to be 
composed of blood vessels, embedded in 
areolar tissue. These blood vessels are of 68 
Tumors. 
normal size in simple angioma; in cavernous 
angioma they consist of lakes, bounded by 
comparatively thin fibrous tissue walls. 
LYMPHANGIOMATA. 
Location: In the tongue; in the subcuta- 
neous tissue; in the mucous membrane of the 
lips. 
Anatomy: A pale, pinkish patch, very 
slightly raised above the surrounding surface. 
Macroglossia is lymphangioma of the 
tongue. 
Histology: The tumor is composed of 
lymph tubes. 
Varieties: Round celled, small and large; 
spindle celled, small and large; myeloid sar- 
coma; melano sarcoma. We seldom find a 
isarcoma composed of one variety of cells 
alone. The tumor generally bears the name 
of that variety of cell which predominates. 
SARCOMATA. 
Location; In any organ of the body. 
Nature: Malignant, malignancy being in 
the following order: Melano sarcoma, round 
celled, spindle celled, fibro sarcoma. 
Etiology: Not known. They present a 
perfect picture of connective tissue reaction 70 
Tumors. 
to irritation. There exists but little doubt 
but that they are parasitic in origin. 
General characteristics; They have no cap- 
sule, except where they have developed in an 
organ with a capsule, in which event the cap- 
sule is not theirs, but is the capsule of the 
organ. They are more frequent in young 
people. They are richly supplied with ves- 
sels, the vessels being in the same state of 
immaturity as the cell. They grow rapidly, 
infiltrate the surrounding structures, causing 
degeneration and absorption of the elements 
of the part invaded. They spread by blood 
vessels, and in consequence metastases are 
found in the first set of capillaries through 
which the blood passes after leaving the tu- 
mor. They are composed of connective tissue 
cells, which begin as round cells, with an 
inherent tendency to form fibers. They are 
malignant just in the same proportion as this 
tendency is interfered with; not that the round 
cell is in itself more malignant than the spindle 
cell or the fiber, but that the cause which 
produces them in so great rapidity and with 
such abnormality that they do not have time 
or disposition to proceed beyond round cells, 
would be violently injurious to other centers, 72 
Tumors. 
for but a small part of the effects of sarcoma 
are local, the larger part are constitutional. 
ROUND CELLED SARCOMATA. 
Anatomy: The tumor is very soft, gener- 
ally rounded, but without a capsule. On sec- 
tion it has an even pink appearance, with 
small red or brown haemorrhagic patches. 
Histology: The tumor is composed of 
round cells, usually small, sometimes large, 
with a single nucleus, and with a minimum 
amount of intercellular substance. In the 
midst of the round cells are blood vessels 
whose only wall consists of a single layer of 
elongated cells. 
MELANO SARCOMA. 
Anatomy: These tumors are small, rarely 
larger than one inch in diameter. They are 
dark in color, frequently almost black; the 
color is comparatively uniform. They are 
soft in consistency, have no capsule; they form 
metastases while yet the tumor is almost mi- 
croscopic in size. 
Histology: The cells are round cells, gen- 
erally larger than in the small round celled 
sarcomata. There are many spindles. They 
are fdled with rather coarse pigment granules; 74 
Tumors. 
but these pigment grannies do not give the 
color reactions of melanin. 
Location; Choroid coat of the eye; the 
skin; the suprarenal capsules; they very fre- 
quently form a secondary growth in the liver. 
SPINDLE CELLED SARCOMATA. 
Location: In any connective tissue struc- 
tures; metastases are not so frequent as in 
round celled sarcomata—the lung is the most 
frequent seat of secondary growth, liver sec- 
ond in frequency. 
Malignancy: Less malignant than round 
celled sarcomata. 
Anatomy; May have reached considerable 
size. There may be some external condensa- 
tion of fibers, resembling a capsule. On cut 
section the tumor is moderately firm and 
fleshy in appearance. 
Histology: There is an abundance of 
spindle cells, either small or large; among 
these spindle cells are large numbers of blood 
vessels with embryonal walls, that is, walls 
composed of a single layer of spindle cells ar- 
ranged end to end. 76 
Tumors. 
Synonym: Myeloid sarcomata; epulis. 
GIANT CELLED SARCOMATA. 
Location: Found especially in connection 
with bone and periosteum. 
Anatomy: The tumor grows with only 
moderate rapidity; it very frequently has an 
apparent capsule; it is moderately firm and 
elastic, pinkish in color; it is irregular both in 
color and in consistency. Not infrequently 
islands of bone are found in its midst. 
Histology; There is a great abundance of 
round and spindle cells and embryonal blood 
vessels, and among these are large, irregular 
masses of protoplasm, with multiple nuclei. 
These cells resemble osteoclasts, and give the 
appearance of cells set in nests. 
This tumor in malignancy vaiies within 
wide limits. 78 
Epithelial Tumors. 
EPITHELIAL TUMORS. 
BENIGN EPITHELIAL GROWTHS. 
Varieties: Corns, warts, vegetations, horns. 
PAPILLOMATA. 
General characteristics: There is a cen- 
tral stalk of fibrous tissue covered by epi- 
thelium. This epithelium may be piled up 
in an, indefinite number of layers, but its 
basement membrane is unbroken, and the 
lower germinating layers of epithelium show 
no tendency to grow into the underlying 
structures. 
These are new developments of glands in 
which the epithelium arranges itself in a nor- 
mal fashion. The glands are always func- 
tionally inactive. The epithelium is set on a 
basement membrane, and shows no disposi- 
tion to invade this basement membrane. 
These tumors are on the border line of malig- 
nancy, and no hard and fast line of benign- 
ancy can be drawn. 
ADENOMA. 80 
Epithelial Tumors. 
NEUROMATA. 
Two varieties: (i) Composed of nerve 
fibrils, and (2) composed of ganglion cells. 
These tumors are rare. 
Varieties; Springing from squamous cov- 
ering epithelium, called epitheliomata; and 
growing from glandular epithelium, called car- 
cinomata. 
MALIGNANT EPITHELIAL GROWTHS. 
General considerations: Carcinomata are 
rare except in points where mechanical irri- 
tation is frequent. They are more frequent 
in maturer life. They spread by lymphatics 
alone, except late in their history, when gen- 
eral carcinosis is possible. Generally speak- 
ing, they are more malignant than sarcomata, 
and the hypoblastic carcinomata are more 
malignant than those of epiblastic origin. 
Malignant adenomata, called carcinomata, 
differ from benign adenomata in that they 
are never encapsulated, properly speaking. 
They are never polypoid or pedunculated: and 
the epithelium not only fills the glandular 
acini, but it breaks through the basement 
membrane, and extends, as more or less regu- 
lar gland tubes, into the surrounding struc- 
tures. 82 
Epithelial Tumors. 
EPITH ELIO MATA. 
Location: The lips, the tongue, the anus, 
the penis, the vagina and cervix of the uterus, 
the skin and the subcutaneous tissues. 
Method of spreading: These tumors stick 
to the lymphatic channels very much more 
closely and invade the blood channels with 
much more reluctancy than any of the other 
malignant growths. 
Anatomy: They may present either one of 
two forms. 
i. Fungus, in which there are rich vegeta- 
tions projecting above the surface. These 
vegetations bleed readily, and are the seat of 
a foul, sanious discharge. 
2. Flat ulcerating form in which the tumor 
level is below that of the surrounding tissues. 
Histology: At the margin of the malig- 
nant area, the normal epithelium of the sur- 
face can be seen growing into the underlying- 
tissue, in bands or fingers, or columns of epi- 
thelial cells. These’cells are dividing active- 
ly. The finger shape is given by the shape 
of the lymph tube in which they are con- 
tained. In places, in which there is less re- 
sistance on the part of the invaded tissue, the 
cells are gathered together in nests. The cells 
in these nests are generally concentrically af-  Epithelial Tumors. 
ranged. The connective tissue between the 
lymph tubes, sometimes called the alveolar 
walls, may be normal, or they may be the seat 
of a simple inflammation ; inflammatory cells, 
and sometimes giant cells, are found in the 
midst of the epithelial cell masses. The blood 
vessels are in the connective tissue walls. 
Degenerations: (i) pearls; the cells of 
which these tumors are formed are subject to 
keratin degeneration; and, therefore, in their 
new locations, as they become old, or are sub- 
jected to pressure, they form nests of keratin, 
called epithelial pearls. Pearls are not found 
except in cells derived from areas that are 
prone to keratin transformation. (2) Second- 
ary infection and round cell inflammation. 
Infection: Neighboring lymph glands. 
CARCINOMATA. 
The shape of the epithelial cells and their 
arrangement within the alveoli, depends (1) 
upon the epithelium and arrangement in the 
structure from which the carcinoma grew, 
and, (2) upon the tissues into which it grows; 
for example, a carcinoma springing from col- 
umnar epithelium arranged in a glandular ar- 
rangement is very prone to retain both the 
shape of the epithelial cell and its arrange- 86 
Epithelial Tumors. 
ment. Such a carcinoma, growing from the 
mucous membrane of the stomach in the sub- 
mucosa, will be distinctly glandular; but, 
tiaversing the muscular coats, we will see col- 
umns of epithelial cells. These take the 
glandular arrangement upon reaching the 
serous surface. These tumors, growing from 
epithelium which normally has a tendency to 
dip into the underlying structures, more 
easily invade those structures than do the 
epitheliomata. They are, therefore, more 
malignant. 
Anatomy: The tumors have no capsule 
and no pedicle; they are closely attached to 
the surrounding tissues. On cut section they 
are generally soft, pink, with trabeculje of 
fibrous tissue mapping them off into areas. 
There may be ulceration. 
Histology: The walls, called alveoli, are 
composed of fibrous tissue, that may or not 
be filled with roud cells of inflammation. In 
this fibrous tissue stroma are the blood ves- 
sels of the cancer. The epithelial cells may 
be arranged as fairly regular columnar epi- 
thelial gland tubes, or they may be nests of 
epithelial cells of any shape or size. 
Degenerations: They are subject to the 
same degenerations as the epithelium in the 88 
Epithelial Tumors. 
locality from which the tumor sprung; e.g., 
(1) carcinomata springing from the gastro- 
intestinal tract, therefore areas of mucus-se- 
creting cells, are prone to colloid degeneration; 
(2) infections; (3) ulcerations. 
DERMOIDS. 
Location: In the ovary; testicle, subcu- 
taneous tissue, especially of the median line: 
along the lines of foetal union; e.g., around the 
branchial clefts. They are generally cysts, 
containing sebaceous matter, skin, hair, nails, 
teeth, mucous membrane. 
CYSTS. 
1. Retention cysts; cysts formed in a gland 
duct in which the lumen of the duct has be- 
come occluded; e.g., ranulse, ovules of Na- 
both. 
These are divided into: 
2. Secretion cysts, those taking place in 
ductless gland structures as a result of loss 
of relation between secretion and absorption, 
e.g., cysts of the thyroid gland; bursae. 
3. Degeneration cysts, ensuing by degen- 
eration and liquefaction, e.g., around bullets 
and other foreign bodies, an area of infarct; 
cold abscesses. 90 
The Respiratory Apparatus. 
THE RESPIRATORY APPARATUS. 
SOME POINTS IN HISTOLOGY. 
Nose; portions of the pharynx; larynx; 
trachea; bronchial tubes, lung substance and 
the pleura. All, with the exception of the 
pleura, are tubes, certain parts that do special 
work have a special arrangement. The tube 
consists of an intima, a media, and an adven- 
titia. The intima is especially well developed, 
and is imperfectly divided into a mucosa and 
submucosa. The media is divided into a 
longitudinal and a circular layer. The adven- 
titia in some places contains cartilage plates. 
i. A single layer of ciliated epithelial cells, 
columnar in type. 
From within out, the layers are: 
2. A basement membrane. 
3. A mucosa. 
4. A muscularis mucosa. 
Mucosa. 
5. A submucosa. 
6. Inner longitudinal muscle. 
7. Outer circular muscle. 
j. 
8. A fibrous tissue coat.—Adventitia. 92 
The Respiratory Apparatus. 
In the foetus there is nothing to the lungs 
but these tubes. When at birth, air is for- 
cibly inhaled, the tubes are stretched into 
sacs, called air spaces and foyers, called in- 
fnndibnli. 
In the air sacs the necessities are for a free 
interchange of gases between the air spaces 
and the blood in the capillaries. 
The walls of air vesicle then are: 
i. Stretched, thin, epithelial scales. 
2. Connective tissue, white fibrous and 
yellow elastic. 
3. A connective tissue blood vessel wall. 
4. A layer of endothelial cells. 
These are the four layers, all thin and 
delicate, which gases have to traverse. The 
bronchial tubes break into tubes of con- 
stantly diminishing size. 
As the force of suction is applied to the 
air cells and as one bronchial tube stipplies 
numberless air cells, it is very necessary that 
the bronchial tubes should not collapse, so 
that cartilage plates are located in their 
fibrous coats. 
Bronchi less than 1 mm.—terminal bronchi 
structure. 
1. Single layer of ciliated columnar epithe- 
lial cells. 94 
The Respiratory Apparatus. 
2. Mucosa, elastic fibers, a few muscle 
fibers, and lymphoid tissue. 
A terminal bronchiole and its vesicles is 
termed a lobule. 
The ligaments of the lungs—bands of white 
fibrous and yellow elastic tissue, run from the 
root of the lung to the pleura. 
There is a double set of arteries: 
i. Pulmonary arteries. 
Lymphatic tissue is very abundant. Most 
of the channels begin in the air cell walls, fol- 
low the walls of the bronchial tubes and filter 
through the bronchial glands at the root of 
the lung. Others (i) run in the septa, (2) a 
few near the pleura drain to that membrane. 
2. Bronchial arteries. 
Pleura: 
1. A layer of large flat endothelial cells with 
stomata between. 
2. White fibrous tissue, yellow elastic tis- 
sue, and some nonstriated muscle. 
This connective tissue, its vessels and its 
lymphatics, communicate slightly with the 
underlying lung. The amount of communi- 
cation is in the order in which the tissues are 
named. 
PNEUMONIAS. 
The term pneumonia is used in lieu of 
pneumonitis, to indicate inflammation of the The Respiratory Apparatus. 
lung. It includes all of the inflammatory proc- 
esses, acute and chronic, in the interstitial 
tissue and air vesicles. It does not apply to 
inflammation of the pleura or bronchi. 
As the lungs have no chemistry aside from 
the chemistry of their own nutrition they are 
not prone to degenerations. They are lowly 
organized, being simply a tryst for the gases 
borne in the air current on the one hand, and 
in the blood current on the other. These in- 
flammations are therefore nearly always germ 
inflammations. 
Acute pneumonias: 
Lobar, exudative in type. 
Lobular, productive in type. (Exudation 
less prominent.) 
Abscess, destructive in type. 
Gangrene, destructive in type with a sec- 
ondary infection with saprophytes. 
Hypostatic, mildly exudative. 
Chronic pneumonias; 
Interstitial, productive in type. 
A group due to physical irritation, as an- 
thracosis in coal miners; silicosis in 
sand workers; siderosis in metal work- 
ers. 
Tubercular. 
Syphilitic. 
Heart disease. 98 
A cute Infta mm at ions. 
(A) ACUTE INFLAMMATIONS 
Synonyms: Croupous, pneumonia; lung 
fever. 
LOBAR PNEUMONIA. 
Cause: In order of frequency—diplococ- 
cus of Fraenkel, bacillus of Friedlander, strep- 
tococcus, staphylococcus; always microbic 
in origin. 
Nature of process: Exudative, productive 
inflammation, spending its force on the vaso- 
motor apparatus; a type of exudative inflam- 
mation. 
Anatomy: Usually involves the lower lobe 
of one lung; may involve a middle or upper 
lobe, usually most marked on lower and more 
dependent surface. Lung swollen and shows 
imprint of ribs; injection of overlying pleura 
with effusion of some fluid, which may or may 
not be coagulated. . Lung bright red, dark 
red, mottled gray and red, or gray, according 
to the stage of the process. If all alveoli are 
filled, it sinks in water. In any event it floats 
deep in the water. Heavy “cuts” resistant. 
Pressure causes a bloody froth to exude from 100 
A cute Inflammations. 
the cut bronchioles. The consistency is 
about even everywhere in the affected lobe. 
The bronchial and mediastinal glands are 
swollen. 
Philosophy of the process; Pneumococcus 
secretes its toxine, which irritates vasomotor 
nerves'; vessels dilate, fluids exude, white and 
red cells go out freely. The foreign material 
goes into the alveoli as the areas of least re- 
sistance. The epithelial plates of the air 
cells are washed away, the connective tissue 
cells proliferate. The white and red cell 
producers are stimulated into compensatory 
activity. The absorbed toxine acts on the 
heat centers, causing fever; on the sensory 
centers, causing malaise, headaches, etc.; on 
the heart centers, causing fast pulse; on the 
respiratory centers, causing hastened respira- 
tion; on the liver and kidney cells it acts as a 
stimulant to function, or, the irritation be- 
coming more violent, inflammatory degenera- 
tion ensues with lessening of function. 
Congestion and exudation: Until the plas- 
ma coagulates, the stage is called congestion 
and exudation. 
In this stage from the cut surface the exu- 
date can be squeezed until the lung collapses 
completely. 102 
A cute In flammations. 
Reel hepatization: When the exudate has 
coagulated, the stage is called hepatization, 
and its first snbstage is red hepatization; 
red because of the red cells in the exudate; 
hepatization, because the filled lobule looks 
like the liver lobule. The air vesicles are in 
varying degree filled with a skein of delicate 
fibrin filaments, holding in its meshes red 
cells, white cells, inflammatory cells, and epi- 
thelial cells. The packing is close, and the 
alveolar wall is made out with dfficulty. The 
vessels of the alveolar wall can be seen filled 
with blood, and its connective tissue is filled 
with proliferating cells. 
Gray hepatization: The next substage is 
called gray hepatization. It is the first step 
toward liquefaction. The appearance starts 
as an irregular distributed marking, which 
gradually diffuse from multiple foci, until 
there is a moderately even color. The gray 
is due to the dark reduced haemoglobin and 
the whiter fibrin, leucocytes, and inflamma- 
tory cells. The serum has either been 
coughed up, or has been absorbed through 
the vessels and lymphatics. The fibrin is 
beginning to liquefy from the ferment of the 
germs and of the leucocytes. The air vesi- 
cles are not so full; a thin, clear area begins 104 
Acute Inflammations. 
to bound the exudate, the wall shows plainer, 
and its vessels are more full. When the 
process of licpiefaction has been completed 
and the exudate is again fluid, as it was in the 
stage called exudation, we call it resolution. 
Resolution: The fibrin is liquid, the cells 
(red, white and inflammatory) have under- 
gone fatty degeneration and liquefaction. 
The vessels are approaching their regular 
size, the cells are ceasing their division. The 
lymphatics are filled with debris; pigment is 
abundant. This result has been brought 
about by an anti-pneumotoxine. 
Sequelae: This is the type of result in the 
cases which recover. Remember it is a vio- 
lent toxaemia, and not a local affection; that 
it is caused by a germ that is just short of 
sufficient virulence to cause necrosis in this 
lowly organized tissue. It may on the one 
hand cause necrosis, abscess or gangrene; 
on the other hand, it may be less irritating 
than usual, when the reactionary processes 
are not operative to the same degree, lique- 
faction does not ensue, but into the clot 
within the alveoli connective tissue grows 
from the walls, giving a nonresolving, chronic 
interstitial pneumonia. These lungs arc 
prone to tubercular infection. 106 
A cute InHammations. 
Synonyms: Lobular pneumonia, catarrhal 
pneumonia, pneumonia of childhood, capil- 
lary bronchitis. 
BRONCHO PNEUMONIA. 
Causes: An irritant, milder in type than 
those causing lobular pneumonia. Generally 
the streptococcus and staphylococcus, per- 
haps also the organism of pertussis, measles 
and scarlet fever. The number of organisms 
which may be pathogenic here is large. The 
irritant enters by the bronchial tube. 
Nature of the process; A bronchitis is 
usually the starting point. The cause of this 
bronchitis either gets into the deeper layers 
of the bronchi, from which it extends by 
lymphatic continuity to the alevolar walls 
surrounding, or else it extends to the air 
vesicle by force of the air current. This 
last is not as considerable a factor as it would 
seem, as in the smaller tubes exchange of 
gases is not by currents. The flow of lymph 
and blood is from the alveolar to the bron- 
chial wall, so we expect very few of the cases 
of bronchitis to cause broncho-pneumonia. 
Histology; It involves a lobule, and has a 
bronchiole as its center. In this tube the 
epithelium is degenerating; the mucosa and 
submucosa are infiltrated with inflammatory 108 
Acute Inflammations. 
cells, which are piling over the bronchial 
glands and destroying the regularity of the 
individual layers. The alveoli contiguous 
are filled with the products of exudative and 
proliferative inflammations, fibrin, white, red 
and connective tissue cells; the alveolar walls 
are filled with inflammatory cells. In the 
outer zone the poisoning is less severe, and 
the alveoli are filled with epithelial and con- 
nective tissue cells; the alveolar walls are 
thickened by connective tissue inflammatory 
cells—a productive inflammation. 
Such an inflammation has a lessened ten- 
dency toward resolution as compared with 
lobar pneumonia, because (i) the less severe 
infection does not produce as large an amount 
of a curative product, and (2) there is more 
connective tissue proliferation in the alveolar 
walls and in the deeper layers of the bron- 
chial tube. 
Anatomy: The lung is usually irregularly 
mottled. It is diffusely oedematous, with 
here and there wedges of denser lobules that 
are solid. If it is a surface lobule, it projects 
above the surface, thus being distinguished 
from atelectasis, in which the solid area is 
sunken. From the tubes muco - purulent 
material is squeezed. An extensive bronchi- Acute Inflammations. 
tis may eventuate in an extensive pneumonia, 
when you get a lung much resembling lobar 
pneumonia. Look closely, especially near 
the periphery of the lobe, for evidences of 
lobulation. 
Complicating pneumonias are generally 
lobular in type; they may be lobar. 
HYPOSTATIC PNEUMONIA. 
Etiology: Two elements. 
i. Loss of relation between the power ex- 
erted by the right ventricle on the one hand, 
and friction, gravity and other forces to be 
overcome by this power on the other. This 
element causes venous congestion and an ex- 
udate, consisting of much water and salts, 
little plasma, few leucocytes, fewer red cells. 
2. Infection of the area of poor nutrition. 
The factors in the first are weakening of 
the power of the heart, or impediment to the 
return of blood. So the question rapidly gets 
back to the universal question of lowered re- 
sistance and consequent infection. The 
germs are of about the same limitations as 
broncho-pneumonia. The channels of in- 
vasion are the bronchial tubes and the vascu- 
lar channels, carrying infection from the 
original site, e.g., pus germs from the ty- 
phoid ulcer. 112 
Acute Inflammations. 
Anatomy; The dependent part of the lung 
is dark, full of blood, oedematous, with scat- 
tered patches of broncho-pneumonia. On 
cut section the bloody froth squeezes out 
until the lung is collapsed, except in the 
islands of inflammation. As there are these 
several factors, the variations in appearance 
are almost limitless. 
(i) Pysemic. 
ABSCESS. 
(2) Secondary to lobar or broncho-pneu- 
monia. 
Pyaemic: Usually multiple, small, widely 
distributed, but generally near the surface. 
Secondary: Larger, single, or few in num- 
ber. May be anywhere, but more frequent 
in the upper lobe. They may not, though 
they generally do, communicate with a bron- 
chial tube. 
Routes of infection: (1) Blood current, 
(2) bronchi. 
Cause: Any organism that either is usually 
or could under these circumstances become 
pus producing. 
Histology; In each the same; a central 
zone of pus; next a layer of degenerated cells 
that do not take any. stain, mixed with deeply 114 
Acute Inflammations. 
stained leucocytes; next a layer of granula- 
tion tissue, water soaked, consisting of embry- 
onal vessels, leucocytes, and connective tis- 
sue cells; next an older layer of cells varying 
from round to matured connective tissue, ac- 
cording to the age of the process. Partial 
obliteration of the air vesicles, general thick- 
ening of the alveolar walls. The lymphatics 
carry an excessive amount of pigment; swell- 
ing of the glands. 
Cure takes place by (i) destruction of the 
organisms, or habituation of the tissues to 
them so that their toxine is no longer irritat- 
ing; and (2) growth of tissue from the walls 
until the cavity is obliterated. 
GANGRENE. 
Cause; Infection with a gas producing 
saprophyte. 
Nutrition is usually cut off from the lung 
by thrombus, embolus or aneurism; this, 
however, is not necessary. 
Recognized by the unaided senses by (1) 
odor, (2) color; bacteriologically by organism 
isolated; microscopically the findings are 
those of necrosis. 116 
C hro nic In Hamm a tions. 
(B) CHRONIC INFLAMMATIONS. 
Synonyms; Substantial emphysema; Cor- 
rigan’s lung; cirrhotic lung. 
CHRONIC INTERSTITIAL PNEUMONIA. 
Definition; A chronic inflammation of in- 
terstitial tissue of the lung, that is not due to 
disease of the heart, the tubercle bacillus, the 
syphilis bacillus, actinomycosis hominis, or 
the mechanical irritants as coal dust, stone 
dust, or what not. 
Etiology: It is due to a mild irritation 
long continued. It is caused in frequency in 
the following order; Asthma, broncho-pneu- 
monia, lobar pneumonia, pleurisy, collapse. 
Philosophy of the process: There is a new 
growth of connective tissue, most of which is 
at any given time fully matured. There is 
always thickening of the pleura and of 
the bronchial wall, and one or the other of 
them assumes unusual prominence, according 
to the area of origin of the disease. All in- 
terstitial processes are uneven processes— 
that is to say, the amount of aveolar thicken- 118 
Chronic Inflammations. 
ing will be greater in some zones than in 
others. The tendency of inflammatory con- 
nective tissue to contract is to be borne in 
mind. Therefore some of the tubes and the 
air vesicles will be obliterated, or nearly so, 
by the connective tissue overgrowth and con- 
traction, and others will be dilated even to 
cyst formation. The epithelium of the ves- 
icles springs from cubical epithelium; so un- 
der the disturbed conditions it again becomes 
cubical. 
Disturbances in circulation result in ex- 
travasations of blood; disturbed nutrition re- 
sults in loss of cilia from epithelium, so that 
pigmentation is usually more marked than it 
is in health. 
Anatomy: The lung is small, pale, firm, 
with a very thick pleura. If it is collapsed it 
is found next the vertebrse, reaching to or 
almost to, the diaphragm on its posterior sur- 
face. On section it is pale, tough, resistant, 
sometimes gritty. 
Histology: Microscopically we find con- 
nective tissue bands with spindle shaped nu- 
clei scattered here and there. These bands 
surround openings of irregular size and shape. 
The smallest of these are occupied by small 
masses of round epithelial cells, apparently 120 
Chronic Inflammations. 
lying- loose in the space, but in a good state 
of nutrition, as evidenced by the clearness of 
detail and the vividness of the staining. 
Other openings are much more readily rec- 
ognized as alveoli. These are lined by a sin- 
gle layer of cubical epithelial cells, generally 
very regularly arranged. In still other areas 
the only change is in a thickening of the alve- 
olar wall to about twice its regular diameter, 
together with some tendency to a cuboid 
shape in the epithelium. The greatest thick- 
ening of the connective tissue is in those 
areas where the conditions are most inviting, 
and this is near those broad connective tissue 
bands that radiate from the root of the lung 
to the pleura, and are sometimes called the 
ligaments of the lungs. The next greatest 
overgrowth is beneath the pleura. 
Ultimate effects: Eventually the lung will 
almost entirely lose its capacity as a sac. At 
this time it is largely indifferent to all forms 
of infection. 
PNEUMONIA OF HEART DISEASE. 
Synonyms: Brown induration of the lungs; 
mechanical hypersemia; brown oedema. 
Cause; Long continued disease in the 
mitral and aortic valves. 122 
Chronic Inflammations, 
Philosophy of the process: The leak in 
the heart valves increases the pressure in the 
pulmonary veins. This is compensated for 
in a measure by the yellow elastic tissue in 
the walls of the veins, but here the elastic 
fibers are far fewer than in the arteries; the 
increased pressure extends to the capillaries; 
the capillaries are tortuous and loosely sur- 
rounded, They dilate both in diameter and 
in length—cirsoid aneurism. This causes 
them to project, knob-like, into the air vesi- 
cles; the obstruction from above causes a 
slowing of the current. This means decreased 
nutrition and a prolonged bathing, both in 
their own leucomaines and in the leucomaines 
from the other tissues of the body. . The re- 
sult of this mild irritation long continued is 
an overgrowth of connective tissue—alveolar. 
The epithelium becomes cubical or round and 
proliferates. These make haemorrhage by 
rhexis and diapedesis easy, and so there is an 
excess of pigment. 
Anatomy; The lung is brown, somewhat 
small, heavy; “cuts” with difficulty; much 
dark blood exudes. It may be, and fre- 
quently is, oedematous. 
Histology: There is. a moderate increase 
in connective tissue, which is moderately 124 
Chronic Inflammatioiis. 
well matured, though not as fully as in other 
forms of interstitial inflammation. The ves- 
sels are seen projecting as globular knobs on 
each side of the alveolar walls; many of the 
alveoli are filled with large round epithelial 
cells containing reddish brown pigment. 
Synonyms; Coal miners’ phthisis; scissors- 
grinders’ phthisis; stonemasons’ phthisis; 
lithicosis; chalicosis. 
ANTHRACOSIS, SIDEROSIS, SILICOSIS. 
Etiology: Chemically inert, but physically 
irritating particles of coal, metal, stone or 
what not are deposited on the bronchial walls 
beyond the zone of cilia, and in the air ves- 
icles themselves. Nature wisely provides 
that no air currents shall go beyond the lati- 
tude of cilia, but nevertheless some particles 
fall in the forbidden territory. They admira- 
bly fill the rec|iurements of a mild irritation 
long continued. 
Philosophy of the process: The irritating 
particles are carried into the lymph channels 
to the alveolar walls, and from there to those 
of the septa. They set up productive inflam- 
mation; as most of the lymph channels are 
perivascular, changes rapidly involve the ves- 
sels; this connective tissue contracts; nutri- 126 
Chronic Inflammations. 
tion is shut off and necrosis from starvation 
ensues. 
Anatomy; The pleura is thickened, and 
there are adhesions of varying toughness. 
The lung is very black when the irritant is 
coal dust, less so when it is otherwise. There 
is increase in weight and in resistance. It 
“cuts” tough and often gritty. Here and 
there are nodules reaching considerable size. 
On cut section the center is yellow detritus; 
this may be calcified: The periphery is 
dense, laminated; it merges into the surround- 
ing tissues. The glands are large and black, 
not only the glands of the root, but those 
throughout the septa. The septa are more 
than usually prominent. 
Histology: In the center of these nodules 
is a mass of tissue detritus mingled with 
some mineral material. Around this is a zone 
of denser connective tissue; outside this a 
zone of newly proliferating connective tissue 
with an abundance of nuclei and round cells. 
In these zones there is evidence of diffuse 
arteritis, thickening of the adventitia and 
media, and active proliferation of the cells of 
the intima. All of the alveolar walls are 128 
Chronic Inflammations. 
thickened. Some of the alveolar epithelium 
is normal in position and in shape; some is 
cubical or flat; some is loose in the vesicle; 
some of the cells contain pigment. Tnhcrculosis and Phthisis. 
TUBERCULOSIS AND PHTHISIS. 
Under the head of tuberculosis we will 
treat those affections in which the tubercle 
bacillus is alone operative; under phthisis 
those cases in which there is engrafted on 
the lungs a second infection. 
Then tuberculosis is an interstitial inflam- 
mation with a strong tendency to become 
localized; a nodular interstitial pneumonia 
due to the tubercle bacillus. Phthisis is tu- 
berculosis plus pneumonia. 
TUBERCULOSIS. 
Varieties: Subacute and chronic. 
Etiology: Tubercle bacillus. 
Channel of infection: Blood current. 
Philosophy of the process; The tubercle 
bacillus lodges in a capillary. It secretes its 
toxin. This toxin is a mild irritant. The 
local tissues are stimulated into activity; leu- 
cocytes rapidly wander to the local area. If 
the irritant is rather severe, the central cells 
immediately surrounding the bacillus die; 
those further away develop into fibers; some 132 
Tuberculosis and Phthisis. 
form giant cells, if the process is not too 
acute. This intermingled developed and de- 
veloping mass of cells, leucocytes and con- 
nective tissue cells give the reticulated ap- 
pearance that is so suggestive of tuberculosis. 
If the bacilli are not very virulent, they are 
either circumscribed by connective tissue ci- 
catrices, or else they are destroyed by phago- 
cytes and the tubercular process is at an end. 
The mass of inflammatory tissue may be ab- 
sorbed entirely, though this is unusual. It 
may become calcified. It usually remains as 
an old cicatricial mass with rarely caseated 
foci. The inflammatory masses necessarily 
involve nerve endings. This irritation, which 
in nerves of sensation would be intrepreted 
by pain, in nerves of sight by a light picture, 
is in this locality interpreted by cough; cough 
means some mechanical injury to the bron- 
chial tubes. So a light bronchitis may com- 
plicate the tubercular process. 
Anatomy: Such a lung is usually moder- 
ately congested and mildly oedem.atous. Here 
and there are multiple small nodules, rather 
more frequently found in the lower lobe than 
in the upper. They vary from a size too small 
to be seen with the naked eye, to the size of 
a pea. In color they are gray to pearly gray, Tuberculosis and Phthisis 
when growing; yellowish, when breaking 
down. 
i. Miliary tubercles, typical in character 
In the center is a giant cell, about ten times 
the diameter of the ordinary cell, with as 
many as twenty nuclei arranged around the 
periphery of the protoplasm. This protoplasm 
may be quite granular. Tubercle bacilli can 
frequently be stained within them, though 
when they pick up the bacillus, the bacillus 
very promptly loses its power to take up a 
stain. Frequently the border of the giant 
cell seems to shade into the surrounding in- 
tercellular substance; frequently from it pro- 
longations seem to run to the contiguous 
fibrillse. Around this will be a zone of mixed 
leucocytes, connective tissue cells and fibers. 
The contiguous blood vessels show some in- 
flammation of the endarterium, but much 
more inflammation of the adventitia. The 
variations from this type usually consist in the 
following; 
Histology; We may have: 
2. The tubercle is made up of round cells 
and leucocytes alone. 
i. The center is caseated. 
In addition to the tubercle, in its vicinity 
there will be seen a somewhat even thicken- 
ing of the alveolar walls. Tuberculosis and Phthisis. 
PHTHISIS. 
Phthisis is tuberculosis plus pneumonia. 
If one or the other or both conjointly are vio- 
lent processes, the lesion rapidly ends life, 
and is known as acute phthisis. If these fac- 
tors are less violent and the reaction thereto 
is less forceful, the result is common chronic 
phthisis or ulcerative phthisis. If these fac- 
tors are still less forceful, destruction of tis- 
sue is less prominent, maturing of tissue is 
more prominent, and fibroid phthisis is the 
result. Between these three there are no lines 
of demarkation, and there are cases that are 
placed in different categories according to the 
individuality of the observer. 
ACUTE PHTHISIS, 
Etiology: The tubercle bacillus and any of 
the other organisms. The most frequent are 
staphylococcus, streptococcus, pyocyaneus, 
bacilluscoli communis, pneumococcus. For 
be it known that the lesions of the tubercle 
bacillus are productive; they are but mildly 
destructive, but they render infection with 
other organisms very easy. 
Philosophy of the process: The tubercular 
lesion is produced as in the other case. 
Owing to the lack of time giant cell systems 138 
Tuberculosis and Phthisis. 
are not prominent. Owing to the complicat- 
ing organisms, destructive processes are 
more prominent. The channel of infection 
is through the air routes and the lymphatics; 
the route of the secondary infection is 
through the bronchial tube. As the elements 
that enter into the causation are multiple, the 
variations from the type become more promi- 
nent. For intsance, the accidental placing 
near to or far away from a bronchial tube 
makes a great difference in the time of sec- 
ondary infection, and therefore in the promi- 
nence of destruction. 
Anatomy: The pleura is usually thickened; 
there are fresh adhesions, especially at the 
apex; the lung is solid, perhaps entirely, per- 
haps in a lobe. It is red and heavy. Here 
and there are yellow patches; these are more 
prominent at the apex. Cut sections may 
show within their patches a cavity communi- 
cating with a bronchial tube, and containing 
some pus, or it may be merely a mass of 
cheesy material with a less distinct wall than 
in the first instance. The near neighborhood 
of the cavity will be solid; as we go farther 
away, it becomes progressively more open. 
From the tubes, pus and mucus exude on 
pressure. 140 
Tuberculosis and Phthisis. 
Histology: The center of the nodule shows 
only amorphous material. In a single micro- 
scopical section we may find multiple foci of 
degeneration. Around the patch of breaking 
down is an area of round cells, leucocytes 
and fibrous tissue mesh; vessels can be made 
out with difficulty here. Further out the con- 
dition merges into a simple alveolar thicken- 
ing. Here the vessels show plainly. Here 
the air vesicles are filled, not by overgrowth 
of the connective tissue of the alveolar wall 
as is the case in the tubercular area, but by 
pneumonic products, fibrin filaments, white 
cells, red cells, connective tissue and epithe- 
lial cells. 
COMMON CHRONIC PHTHISIS. 
Synonyms: Consumption; ulcerative 
phthisis. 
Cause: Tubercle bacillus plus other organ- 
isms. 
Channel of infection: Bronchi and lymph 
vessels. 
Philosophy of the process: Same as in 
acute phthisis, except that the processes have 
more time to develop. The vessels are bet- 
ter spared than in any of the other inflam- 
mations of this group (syphilis, sarcoma, 142 
Tuberculosis and Phthisis. 
actinomycosis); the lesions are usually peri- 
arteritis. Endarteritis is less marked. 
Anatomy: The process is usually most 
marked at the apex of one lung, though both 
may be involved. The pleura is thickened, 
and tubercles are the rule rather than the ex- 
ception. There are old adhesions over the 
zone of inflammation and sometimes else- 
where. The cavity may be obliterated; 
effusion, clear or bloody or purulent, may be 
present. The lung shows hard nodules, 
wedge-shaped, separated by patches of the 
consistency of simple inflammation. Lymph 
glands and septa are involved. On section 
multiple, ragged walled cavities are seen. 
These are in a measure filled with pus that 
may be colored and odored, dependent upon 
the germs growing there. Connective tissue 
bands and blood vessels may stretch across, 
unsupported; around the cavities, in the walls, 
and further away are fibrous nodules, some of 
which are yellow and caseated, others gray 
shading off to pink. Between these nodules 
are zones presenting the appearance either of 
lobar or broncho pneumonia. 
Histology: A caseous area, surrounded by 
mingled cells and fibers; giant cell systems 
are here more prominent than in any other 
form of tuberculosis. There is a large quan- 144 
Tuberculosis and Phthisis. 
tity of old matured dense connective tissue. 
In this tissue is an abundance of pigment in 
tracts that were once lymphatic channels. 
Blood vessels of small size can be demon- 
strated with difficulty. Those of larger size 
have their adventitia swollen and thickened, 
or ulcerated if secondary infection is operat- 
ing on them. The walls of the bronchi are 
the seat of tubercular nodules that extend 
into the lumen, or ulcerate and leave cavities 
communicating with the tube. The old scar 
tissue contracting in many places destroys 
the relations of the parts. The alveolar walls 
in the vicinity of the nodules are thickened to 
twice the normal size. The alveoli are filled 
with fibrin, white and red cells, detritus, 
epithelial cells. 
Cure takes place from (i) defeat of the 
bacillus and its companions by (a) discharge, 
(b) phagocytic action, (c) exclusion from 
maturing connective tissues. 
1 )eath ensues from toxaemia. 
Synonym: Lues. 
SYPHILIS. 
Etiology: Possibly the syphilis bacillus of 
Lustgarten. 
Philosophy of the process; A leucocyte and 146 
Tuberculosis and Phthisis 
connective tissue resistance to the toxins of 
the germ. 
The disease is rare in the lungs. It gives 
a lesion which is similar to tuberculosis, ex- 
cept that endarteritis is much more promi- 
nent. The channel of infection here is the 
blood vessel, and this in part accounts for the 
prominence of the lesion of the intima. 
The other inflammations of this character 
to which the lungs are subject are; 
Actinomycocsis, due to the actinomvces 
hominis, and giving small millet-seed-yel- 
low masses in the midst of the inflammation 
and in the pus. 
Glanders, due to the bacillus mallei. Giv- 
ing small nodules, miliary and multiple if the 
infection be from the blood, and frequently 
single and ulcerated if from the air passages. 
When miliary and degenerated they may be 
yellow, or stained the color of any pigment 
that happens to be present. 
TUMORS OF THE LUNGS. 
The primary tumors found in the lungs are 
lipoma, osteoma, fibroma, chondroma, cylin- 
drical celled carcinoma, sarcoma. 
The secondary tumors are much the more 
frequent, because the lungs present the first 
set of capillaries that a malignant fragment 148 
Tuberculosis and Phthisis. 
would encounter after leaving its site of 
origin. As sarcoma contains so many wall- 
less vessels, and as they frequently spring 
from the intima of veins, they constitute the 
bulk of secondary tumors. 
All of the vegetable parasites that can be 
carried by the air or by the blood current. 
PARASITES OF THE LUNGS. 
Amongst the animal parasites: The 
amoeba coli, hydatids, filaria bronchialis and 
cysticercus cellulosse. 
ACUTE BRONCHITIS. 
Etiology: First, bacterial, influenza bacil- 
lus, pus cocci, pneumococci, the germ of 
measles, smallpox, scarlet fever. Second, in- 
halation of gases, powders, steam. 
Nature of the process; An acute exuda- 
tive, productive inflammation. It is much 
more liable to involve the smaller bronchi and 
the lung substance in children than in adults. 
Anatomy; The lung is congested and 
ocdematous. On squeezing a section serum 
oozes from the substance and muco-puru- 
lent material comes from the bronchi. On 
laying open a bronchus its wall is seen to be 
thickened. The mucosa is especially thick- 
ened. It is covered by tenacious muco-pus. 150 
Tuberculosis and Phthisis. 
When this is removed the membrane has lost 
its luster. It is red and uneven. 
Histology: Epithelial surface. The epi- 
thelial cells are irregular in shape; in many 
places they have fallen away entirely. Many 
are in a state of cloudy swelling. Among the 
epithelial cells are leucocytes, red cells and 
round cells of inflammation. The fibers of 
the basement membrane are separated by 
new cells and leucocytes. The inner fibrous, 
muscular and outer fibrous coat are closely 
packed with round cells. The intensity of 
the process is less as we go outward. At the 
periphery it extends along the lymphatics. 
Sequelae: It may undergo resolution. It 
may go on to the chronic disorder. It may 
eventuate in broncho pneumonia. 
Atelectasis; Collapse of the lung. Due 
to (i) imperfect expansion immediately after 
birth. (2) Penetrating wounds of the pleura 
and chest walls. (3) Plugging as in bron- 
chitis. 
Bronchiectasis; Dilatation of bronchial wall, 
from any cause, either within the wall or 
within the fibrous structures attached to it. 
Emphysema: Overdilation of the air 
vesicles. Found in old people in heart dis- 
ease, asthma, whooping cough, chronic inter- 
stitial pneumonia, pleurisy of the other side. 152 
Tuberculosis and Phthisis. 
It is not infrequently compensatory, that is 
to say, that when the respiratory capacity of 
one lung is decreased the other increases 
pari passu. The term emphysema is also ap- 
plied to that condition in which from rupture 
of vesicle or bronchial wall air is loose in the 
midst of the tissues. 
Synonyms: Pleurisy, empyema. 
PLEURITIS. 
Varieties: Dry pleurisy, pleurisy with 
effusion, pleurisy with adhesions, pleurisy 
with formation of fibrin, suppurating pleurisy, 
tubercular pleurisy: 
Nature of the process: Pleurisy is always 
an exudative, productive inflammation. The 
fluid seeks the cavity as the area of least re- 
sistance. The pleura has large capacity for 
absorption. If the amount of exudation is 
within the capacity of the pleura for absorp- 
tion, no fluids accumulate, the inflammatory 
cells develop into fibers; the pleura is thick- 
ened—dry pleurisy. 
If the amount of effusion is large, it accu- 
mulates as a straw colored fluid in the de- 
pendent parts of the pleura; proliferation of 
the inflamed area causes thickening; pleu- 
risy with effusion. If coagulation occurs 
in the exudation, we have pleurisy with the 154 
Tuberculosis and Phthisis. 
formation of fibrin. If this fibrin glues to- 
gether adjacent parts of the pleura, then con- 
nective tissues and capillary blood vessels 
grow into the coagulated fibrin. This con- 
tinues until a band of fibrous tissue unites 
the “glued” parts—pleurisy with adhesions. 
If infection of the pleura has been with 
pus germs the process becomes suppurative; 
the pleural cavity becomes a true abscess 
cavity—empyema. Tubercular pleurisy does 
not differ from tuberculosis elsewhere. 
Basic histology of pleurisy: The epithe- 
lial cells that cover the inflamed area swell 
and fall off. Inflammatory cells are massed 
among the connective tissue fibers. These 
cells pile up on the surface. Capillary blood 
vessels grow from older vessels, tunneling 
their way among the new cells. The process 
ends by the new cells maturing into fibers, 
which fibers contract. The new vessels dis- 
appear by (i) contraction of fiber, (2) endar- 
teritis obliterans. The area is covered by 
(1) epithelial cells growing from the neighbor- 
ing epithelium, or (2) the cavity is obliter- 
ated by union of its parietal and visceral 
layers, or (3) the superficial connective tissue 
cells are condensed and flattened as in large 
scars in other localities. 156 
Ci rc til at ory Systcn i. 
CIRCULATORY SYSTEM. 
HEART. ARTERIES, CAPILLARIES, VEINS, 
LYMPHATICS. 
The whole contents of the blood current 
have not made the double circuit until the 
lymphatics have emptied their contents. The 
whole constitutes a tube. This tube has three 
coats, an intima, a media and an adventitia. 
There is one part of the tube that has to 
do much muscular work; its muscularis is 
well developed; we call this muscularis the 
myocardium. There is another part of the 
tube that must permit of no leaking, and must 
receive the intermittent force and convert it 
into an even force; it is’ the aorta; hence 
it is dense, little muscular, but very elastic 
from an abundance of yellow elastic tissue. 
There is another part that must permit an in- 
terchange of gasses and liquids between, within 
and without; its wall must be thin; it is the 
capillary, with a wall consisting of a single 
layer of endothelial cells and a little loose 
connective tissue. There is another part that 
must change its size in order to regulate pres- 158 
Circulatory System. 
sure and nutrition; this is the arteriole with 
prominent circular muscular fibers. There is 
another part which must not leak, nor stretch 
much, nor permit the blood to flow back; 
this is the vein, with the intima loose and 
picked up into folds—valves. In all of them 
no blood soaks in further than the intima, so 
a separate set of vessels is provided to nour- 
ish the other coats; those in the heart are 
called coronary arteries, in the vessels the 
vasa vasormn. 
The heart is inclosed in a sac similar in its 
anatomy and in its histology to the pleura. 
This sac is called the pericardium. Under- 
neath this is a layer of loose connective tis- 
sue that usually contains fat. This is the epi- 
cardium or adventitia. Under this is a mass 
of muscle fibers, running in every direction, 
separated by bands of fibrous tissue continu- 
ous with the fibrous tissue of the epicar- 
dium. These fibers are involuntary, striated, 
branched. In the embryonal state, and in 
certain of the lower animals, the protoplasm 
is granular and there are no strise; striation 
begins at the poles and in different animals 
approaches the center in varying degree—in 
man according to the degree of disturbance 
of normal processes of repair. The cor- Circulatory System. 
onary arteries and their capillaries radiate in 
the epicardinm and myocardium, and in a 
small measure in the endocardium. The inner 
layer consists of white fibrous and yellow elas- 
tic tissue, covered by a single layer of endo- 
thelial cells, just as in a serous membrane. 
Valves are made by a picking up of this endo- 
cardium. 
Arteries: A loose adventitia of white fibrous 
and yellow elastic connective tissue; in this 
are the larger branches of the vasa vasorum. 
Next comes the media, mostly muscle fibers 
—nonstriated, arranged circularly, some 
longitudinally—and some yellow elastic and 
some white fibrous connective tissue, in which 
are the smaller branches of the vasa vasorum. 
Internally the intima with a thin layer of yel- 
low elastic tissue, called the inner elastic 
lamina, forming its outer border ; then a mix- 
ture of white fibrous and yellow elastic tissue, 
covered or lined by a single layer of endothe- 
lial cells. 
The parenchyma of the heart is its muscle 
fibers; muscle work is the physical expression 
of chemical equation; therefore the heart is 
a highly differentiated organ. It is prone to 
inflammatory changes. In its physiological 
nutritional changes, such as hypertrophy and 162 
Circulatory System. 
atrophy, are prominent. It is subject to 
many of the degenerations and to various 
tumor growths, both secondary and primary. 
Systemic infection is prone to attack its lining 
coat, though its other layers are very free 
from them, as the coronary arteries are given 
off at right angles to the direction of the main 
current and solid particles, such as bacteria, 
travel with the main direction of the current. 
The degenerations to which the heart is 
subject are; cloudy swelling, fatty and hy- 
aline degenerations, myomalacia, and those 
which are common to every tissue and present 
no structural peculiarities, necrosis and cal- 
cification. 
CLOUDY SWELLING. 
Synonyms: Albuminous degeneration,, 
acute parenchymatous degeneration. 
Cause: Toxaemias from organic poisons, 
e.g., typhoid fever, pneumonia, diphtheria, 
septicaemia, burns; inorganic poisons, e.g., 
phosphorus, iodoform. 
Philosophy of the process: The proto- 
plasm of the muscle fiber is a delicate semi- 
solid. These poisons change its chemistry 
so that certain elements precipitate as solid 
granules and the protoplasm takes up water 164 
Circulatory System. 
from the intercellular substance. In the same 
line of chemical change is fatty degeneration, 
and if the process proceeds slowly, fatty 
change soon ensues. If the process is more 
rapid, there ensues a granular degeneration, 
called in this area myomalacia. 
Anatomy; The muscular wall is soft and 
friable. The deep red flesh color is lost, 
and a dirty gray, boiled appearance is substi- 
tuted. 
Histology; The fibers are swollen, finely 
granular; the striae obscure or absent; nuclei 
obscured or cannot be seen. Fresh unstained 
specimens mounted in salt solution, or acetic 
acid run under the cover, will show fibers 
normal in appearance. Ether and osmic acid 
will not affect the granules. 
Cause: Organic poisons longer continued 
as those of phthisis, pernicious anaemia, 
leucocythaefmia, Addison’s disease, septicae- 
mia; inorganic poisons longer continued, as 
phosphorus, arsenic, alcohol; nutrition minus, 
slowly progressing, as in sclerosis of the 
coronary arteries. 
FATTY DEGENERATION. 
Philosophy of the process: The precipi- 
tated albumen granules, having lost their 166 
Circulatory System. 
chemical relations to the balance of the pro- 
toplasm, enter the next stage of slow death, 
fatty metamorphosis. In sclerosis, nutrition 
minus destroys the balance between waste 
and repair, and the lower protoplasm (fat) 
is substituted for the higher. It is impossible 
to explain why the process should be an un- 
even one. 
Anatomy: The heart is flabby and friable. 
The cavities are dilated. The fatty changes 
show as white, creamy, smooth patches, 
usually beginning under endocardium, and 
especially in the musculi papillares and col- 
umnae carnese. A thrush-breast, or streak of 
lean and streak of fat appearance here, is 
characteristic of the earlier stages. 
Histology: There may be slight increase 
in the number of round cells in the connec- 
tive tissue, especially around the blood ves- 
sels. This, however, is not prominent. The 
muscle fibers are swollen slightly. Their 
striae are absent or indistinct, especially 
around the center of the fiber. The nucleus 
is obscured or unseen. The globules are 
larger and more refractile than in cloudy 
swelling. If under cover of a piece mounted 
unstained you run ether, the granules disap- 
pear, contrary to what you find in cloudy 168 
Circulatory System. 
swelling. Acetic acid, run under cover, has 
no effect. Osmic acid stains the globules jet 
black and renders them brittle. 
Finale. The condition may be cleared up 
and return to the normal if the cause is re- 
moved; or, it may result in myomalacia, 
aneurism, rupture, or interstitial myocarditis. 
FATTY INFILTRATION. 
This condition does not belong in the same 
category as fatty degeneration, yet it will be 
treated here. 
Synonyms: Fatty overgrowth of the heart; 
lipomatosis; adipose heart. 
Philosophy of the process: From surcharg- 
ing the blood with hydrocarbons and carbo- 
hydrates, some fat is stored in many connec- 
tive tissufe cells for future use. One of the 
most constant sites is the loose tissue over 
the myocardium. So long as it is limited to 
this area, it is of little consequence; but 
when it begins to be deposited in the connec- 
tive tissue septa that run down into the 
myocardium, it, on the one hand, places the 
muscle fibers at a disadvantage, and, on the 
other, causes fatty degeneration. 
Cause; General obesity; alcohol. 
Anatomy: The heart is large, covered by 170 
Cire ulato ry Systcrll. 
a heavy layer of fat. Lines of pale fat ex- 
tend down into the myocardium. The ven- 
tricles are apt to be dilated, and the muscle 
flabby for the same reason that every muscle 
in such a subject is flabby. Such subjects 
are prone to the arterio-sderosis and athe- 
romas. 
Histology; In the connective tissue are 
the typical appearances of adipose tissue. 
In specimens hardened in alcohol, you see 
large clear circles, signet ring shaped, being 
a ring of protoplasm and the nucleus crowded 
to one corner. If the specimen was hardened 
with osmic acid, these globules are black and 
opaque. In advanced cases these globules 
are found in the septa and in the connective 
tissue bundles between the muscle fibers. 
Causes: Prolonged toxaemias of typhoid. 
Philosophy of the process: The change is 
in the muscle fiber. The supposition is that 
by reason of some strain, when the fiber is 
weak, as in cloudy swelling, it ruptures, 
whereupon the protoplasm undergoes this 
change into hyaline material. 
HYALINE DEGENERATION. 
Histology; The affected fibers have lost 
their striated appearance, are homogeneous, 
refractile and shiny. They stain with eosin. 172 
Circulate ry S ystern. 
Nature of process: A form of necrosis. 
MYOMALACIA. 
This lesion is an accompaniment of endo- 
carditis and pericarditis. It is limited to a 
zone near the one of these in which it starts. 
To illustrate: Beneath the endocardium is a 
small area in which there is cloudy swelling 
of the muscle fibers and round cell prolifera- 
tion in the connective tissue with some dila- 
tation of the vessels, stasis and exudation. 
PRODUCTIVE MYOCARDITIS. 
Inflammations of the myocardium are pro- 
ductive and suppurative; neither is promi- 
nent. 
The route of infection is the blood vessels. 
As the coronaries come off at right angles, it 
is rare. It may be quite diffused, or localized, 
forming abscess. 
SUPPURATIVE. 
CHRONIC MYOCARDITIS. 
Cause; In the great majority of instances, 
sclerosis of the coronary arteries. 
Philosophy of the process: Nutrition 
minus, and overgrowth of connective tissue. 
Anatomy: There is usually marked evi- 
dence of endocarditis and endarteritis. The 174 
Circulatory System. 
coronary arteries have thickened walls; they 
are stiff, patulous, and often atheromatous; 
many of their branches are obliterated. There 
are usually present milk-white fatty patches 
underneath the endocardium, especially near 
the columnge carneae. Here and there, gener- 
ally in the left ventricular wall other than the 
septum, there is a white and brown streaking. 
These areas are firmer than normal, though 
the heart wall as a whole is apt to be fatty. 
Histology; There is a marked increase in 
the connective tissue. This tissue is usually 
old, fibrillated; It is most marked around 
the vessels and lymphatics and in the con- 
nective tissue septa. At its margin the tis- 
sue is younger, and in its loops are seen mus- 
cle fibers—some degenerating, some in a 
good state of preservation. Thickening of 
the arterial walls is much in evidence. 
ENDOCARDITIS. 
(i) Acute; (2) simple, and (3) ulcerative. 
The only difference between these processes 
is a difference of degree. If the process pro- 
duces tissue, which dies only from nutrition 
minus, we call it simple endocarditis; if death 
of the produced tissue, and of some old tissue 
as well, is due to active enzymes, we call it 
ulcerative. 176 
Circulatory System. 
Cause: The most frequent cause of the 
first and second is rheumatism, gout, scarla- 
tina; the third is due to organisms that locate 
on the endocardium. The more frequent of 
these are the streptococci, staphylococci, 
gonococci and pyocyanei. It seems probable 
that most any pathogenic germ can induce 
the trouble. 
Philosophy of the process: As a result of 
irritation from toxines, connective tissue pro- 
liferates. The process is a productive in- 
flammation, and as the endocardium is free 
from vessels, it is an excellent illustration of 
productive inflammation. As a result of pro- 
liferation, an endocardial mass is formed, 
which projects into the lumen. The histol- 
ogy and the chemistry of the endothelium 
are both changed; behind the eminence there 
is a slowing of the current; a coagulum forms; 
into this connective tissue may grow from 
the endocardium, and it is then known as a 
vegetation. Some of these vegetations frac- 
ture, and the remnants are swept away to be 
stopped, and known as emboli. The tissue is 
not well nourished, for its food must Come 
by omosis; therefore it dies—necrosis. Lime 
salts from the blood are deposited in the 
masses of detritus—calcification. The pul- Circulatory System. 
taceous mass is known as atheroma. Some 
of these patches empty into the blood cur- 
rent, leaving an ulcer. If the process is ulcer- 
ative, clotting is earlier. The germs multiply 
on the clot; they liquefy it; it fractures easily. 
The remnants, full of germs, are swept away, 
to set up the process in new areas. Ulcera- 
tion is much more prominent. 
Anatomy: The endocardium may be some 
what more succulent than normal; this is 
more liable to be appreciable over the valves. 
Near the free margins of the mitral and aortic 
valves will be seen a row of small, semi-trans- 
parent, friable warts. Some of these may 
have broken off, leaving ragged ulcers be- 
hind. In the ulcerative form the vegetations 
will be softer, will pull away easier, and more 
patches of ulceration will be seen. 
Histology: In the coagulum we find leu- 
cocytes, some red cells, and fibrin in layers 
that show some tendency to be alternate. In 
the clot next the endocardium, connective 
tissue round cells are appearing. Deeper 
down we have a mass of inflammatory con- 
nective tissue and leucocytes, spindle and 
round cells. Here embryonal vessels, de- 
rived from the myocardium, can sometimes be 
made out. In patches there is evidence of 180 
Circulatory System. 
granular degeneration, necrosis, or ulcera- 
tion. 
Causes: Rheumatism; gout; acute endo- 
carditis. 
CHRONIC ENDOCARDITIS. 
Philosophy of the process: The difference 
between this and the acute process is the 
change that time makes in inflammatory con- 
nective tissue. 
Anatomy: The heart is apt to be fatty and 
sclerotic. The walls are nearly always either 
dilated or hypertrophied, or both dilated and 
hypertrophied. The process is usually in 
evidence in the aorta, and not infrequently 
in the coronaries. The vegetations are on 
the side of contact; that is, on the ventricular 
side of the aorta, and on the auricular side of 
the mitral. The vegetations are firmer and 
more adherent; the valves are sometimes glu- 
tinated at their edges; sometimes they are 
scarred, thickened, and so retracted that they 
cannot close the orifice. They may be the 
seat of calcareous plaques, and these plaques 
are frequently covered by endothelium, and 
frequently are bare. There are erosions and 
curdy masses here and there. 
Histology: The histology is that of chronic 182 
Circulatory System. 
productive inflammation, with marked ten- 
dency to necrosis and calcifications. 
Effects: Stenosis, or leaking; embolus; an- 
gina; hypertrophy and dilatation; connective 
tissue overgrowth in the liver and lungs. 
BROWN ATROPHY OF THE HEART. 
Synonym; Pigmentary degeneration. 
Cause: Old age; phthisis; anaemia; Addi- 
son’s disease. 
Philosophy of the process: In the foetus, 
and in certain of the lower animals, the heart 
protoplasm is a granular mass without 
transverse striations, or with striation only 
apparent at the extremities of the fibers. Un- 
der these conditions of perturbed nutrition, 
there is this exhibition of embryonal return. 
The pigment is not from the blood; it is from 
the fiber. 
Anatomy: The heart is small, flabby, dark 
brown in color. Held on the tips of the fin- 
gers, it falls over the hand. It may be changed 
somewhat by associated fatty changes. 
Histology: The ends of the heart fiber are 
normal. Around the nucleus, in the area 
called “Schultze’s corpuscle,” there is marked 
granularity and pigmentation. The pigment 
is golden yellow. The area is far in excess 184 
Circulatory System. 
of the size of that found in the normal heart. 
Between the muscle fibers there is an over- 
growth of connective tissue. 
HYPERTROPHY OF THE HEART. 
Cause: When from any cause there is in- 
crease in the work demanded of the heart, it 
hypertrophies. 
A true hypertrophy is an increase in the 
size of each fiber. A false hypertrophy is an 
increase in the number of fibers. The in- 
creased work causes increase in both the size 
and the number of fibers. It is prone to be 
followed by atrophy, when dilatation ensues; 
or, hypertrophy and atrophy may be associa- 
ted, as when the heart increases in size and 
pari passu with the increase in size and num- 
ber of the corpuscles, there is atrophy of cer- 
tain fibers next to the cavity of the ventricle. 
Hypertrophies are (i) true, and (2) false. 
SCLEROSIS OF THE CORONARY ARTER- 
IES. 
The coronary arteries are prone to both en- 
darteritis deformans and obliterans. These 
processes present no peculiarities in this 
locality. But there are certain effects on the 
heart muscle, and its contained nerves, that 
are worthy of note. 186 
Circulatory System. 
Effects: Angina pectoris; neuralgia from 
nutrition minus; fatty degeneration; scler- 
osis; interstitial myocarditis; abscess from in- 
fection of a branch with pus germs. 
Myomalacia—nutrition rapidly minus. 
Aneurism—nutrition minus over a limited 
area. 
Rupture—nutrition minus over a limited 
area, muscular power retained in other areas, 
and an extraordinary compressing of the con- 
tained blood. 
INFLAMMATIONS IN ARTERIES. 
We have inflammations of the coats of 
arteries—periarteritis, mesarteritis and en- 
darteritis. The inflammations that are of 
greatest practical interest are the forms of 
endarteritis. These are endarteritis defor- 
mans and obliterans, the difference between 
them being that endarteritis obliterans is a 
diffuse endarteritis, and the other is in 
plaques. Obliterans has a growth of capil- 
laries into the new tissue of the intima from 
the media; deformans has none. For this 
reason, deformans is much more subject to 
regressive phenomena, atheroma, calcifica- 
tion. 
Inflammation of the intima is very prone to 
involve the media as well. Circulatory System. 
ENDARTERITIS OBLITERANS. 
Process by which obliteration of the in- 
flamed capillaries takes place. 
Cause: Continuation of a mild irritation, 
as syphilis, alcohol. 
This is the condition found in arterio-scle- 
rosis. It is a precursor of, or associated with 
sclerosis in the kidneys, liver, cord, brain, 
etc. 
Philosophy of the process: The entire 
vessel is mildly irritated. There is a produc- 
tive inflammation of the connective tissue of 
the intima and inner layers of the media. 
The capillaries of the vasa-vasorum send oft 
shoots into the intima, which proliferate in- 
definitely, or until the space is occupied, the 
lumen is obliterated. 
Anatomy; The vessel wall is thickened 
evenly; there are seldom any patches of 
atheroma; the intima is usually preserved. 
Histology: There is a layer of young, 
flattened cells next the intima; outside of 
this a region of young connective tissue cells, 
in which young capillaries are appearing. 
The inner elastic lamina is considerably 
broken up by the new connective tissue and 
vessel proliferation. The media may be 
thinned; connective tissue is proliferating 190 
Circulatory System. 
here. There is usually some inflammation in 
the adventitia. 
Synonym; Atheroma. 
ENDARTERITIS DEFORMANS. 
Cause: Found especially in the vessels of 
old people. It is a nutritional disease. It is 
most frequent due to leucomaines or 
ptomaines that are very mild in their capacity 
for irritation. 
Philosophy of the process; The irritation 
is applied to scattered spots, so it is an in- 
flammation in plaques. As it is a pure con- 
nective tissue proliferation without any 
growth of vessels, it is much more prone to 
degeneration, called atheroma. As the nu- 
trition of the intima comes largely from the 
blood current, it is the layers next the inner 
elastic lamina that first begin to die. The 
intima is preserved for a considerable time, 
and this is a very wise provision. 
Anatomy: There are patches placed ir- 
regularly along the walls of the vessel, some- 
times on one side and sometimes on the 
other. They are pink or pearly when young, 
but soon become curdy, then yellowish. 
They are at first resistant to the knife, then 
become gritty. The patches are by prefer- 192 
Circulatory System. 
ence located at the points of greatest friction, 
and especially around the orifices of 
branches. It is a disease to which the aorta, 
the coronaries and the cerebral arteries are 
very prone. Owing to the irregular location 
of the plaques, the blood current runs from 
side to side, first near one bank and then 
near the other. At first over the plaques 
can be seen the shining endothelium; later 
this is lost. The calcareous mass may be 
covered by blood clot. Sometimes the mass 
of degenerated tissue has dropped out, and a 
ragged, denuded patch, called an atheroma- 
tous ulcer, is left. 
Histology: There -is a proliferation of con- 
nective tissue, especially in the intima, so 
that this layer is many times its normal 
thickness. Its inner layer, which was con- 
cave, may now be convex. Under the endo- 
thelium there appear between the laminae of 
fibers layers of cells. This process continues 
indefinitely. The landmark of this area, the 
wavy elastic lamina, is seen to separate the 
media from the connective tissue prolifera- 
tion. In these streaks of cells, and especially 
in those next the inner elastic lamina, granu- 
lar and fatty degeneration begins to appear; 
then the fibers become granular and fatty. 194 
Circulatory System. 
These areas become dark and translucent if 
they have been brought to the microscope 
without change. If hydrochloric acid is run 
under the cover the granules disappear and 
bubbles of carbon dioxide appear. 
Effects: Thrombosis, embolism, a slight 
tendency to aneurism and varicosities, rup- 
ture. 
MESARTERIUM. 
The middle coat of the artery is subject to 
chronic inflammation, to inflammatory degen- 
eration, to fatty degeneration, to calcification, 
and to waxy degeneration. 
In old people the media of the middle 
sized arteries become so calcified as to give 
a lime tube. This especially is true of the 
arteries of the brain. 
As the media is the strong coat, to inflam- 
matory or degenerative changes in it are due 
most of the forms of aneurism. 
The media of small vessels, and the rem- 
nant of the media and adventitia of still 
smaller vessels, is the seat of waxy degenera- 
tion. There is a prior change in the muscle 
fiber that makes possible the soaking with 
modified plasma. 
In such a vessel the lumen is encroached 
upon, but the chief expansion seems to be 196 
Circulatory System. 
outward. Microscopically we see a broad, 
shiny, waxy band, interspersed with spindle 
shaped connective tissue and rod shaped 
muscle nuclei. The percentage of nuclei is 
small. (For staining see chapter on degen- 
erations.) 
The adventitia also inflames, but its in- 
flammations are peculiar to, and connected 
with, the surrounding connective tissue rather 
than with the structures of the deeper layers. 
It is a very wise provision that in no location 
in the body is it as nearly possible for patho- 
logical processes, in structures so close to- 
gether, to be so dissociated. 
Aneurisms; Aneurisms are divided into 
two classes, true and false. 
True aneurisms are localized dilatations of 
the vessel wall, the dilated area being made 
up of at least one coat of the vessel. 
False aneurisms are simply accessory to 
the vessels, and have as their walls the sur- 
rounding tissue or inflammatory new tissue. 
i. Sacculated—in which there has been a 
localized weakening of the vessel wall; this 
is usually in the media, sometimes in the 
adventitia. The point dilates; the more it 
dilates the greater the pressure in its direc- 
The true aneurisms are divided into; 198 
Circulatory System. 
tion. Its walls from without in are adventitia 
(media usually absent), intima, layers of fibrin 
in process of organization, layers of fresh 
fibrin, and blood cells. 
2. Cylindrical and fusiform—in which the 
entire periphery bulges out. The walls are 
made up of intima and adventitia; clotting is 
much rarer. It is given one or the other 
name, dependent on its shape. 
3. Dissecting—in which there is a rupture 
in the intima, and the blood dissects its way 
between the layers of the vessel wall. 
4. Miliary—are usually found on the cere- 
bral vessels. They are sacculated, and their 
name comes from their size. They are gen- 
erally multiple, and frequently are found in 
enormous numbers. 
5. Cirsoid—in which there is an increase 
in the breadth and length of the arteries; 
they become tortuous;- the condition ap- 
proaches closely to angioma. In the veins it 
finds a similar condition in varicose veins. 
False aneurisms: In these there is a rup- 
ture, or several ruptures, of the vessel walls; 
these ruptures become permanent. The 
blood forces its way until the surrounding 
tissues are resistant enough to circumscribe 
it. If the blood clots, it forms a hsematoma. 200 
Circulatory System. 
Varicose aneurisms—are true or false an- 
eurisms, opening directly into a vein. The 
vein here markedly dilates, because its walls 
are not arranged with a view to resist direct 
arterial pressure. 
The veins are subject to all inflammations 
and tumor growths that affect the arteries. 
They are not nearly so subject to intima 
changes, etc. The tendency to sarcoma- 
growth in their walls is the most striking ten- 
dency in the tumor line. Their tendency to 
inflame in infectious conditions (typhoid 
fever, puerperal fever, septicaemia, milk leg 
with the attendant clotting) is always to be 
borne in mind. 
VEINS. 
Synonym: Varix. 
VARICOSE VEINS. 
Philosophy of the process: The condition 
is found only in those regions in which the 
veins that are habitually under heavy gravity 
pressure are unsupported by the surrounding- 
tissues. Such veins are those of the rectum 
(piles), the spermatic vein (varicocele), and 
the leg. 
Anatomy: They are tortuous, firm, with 202 
Circulatory System. 
irregular dilatations, and frequently patches 
of calcification. The normal valves are gen- 
erally not in evidence. 
Histology; There is a new growth of con- 
nective tissue in every coat of the vein. The 
muscle fibers, especially in the stretched, 
areas, are not in evidence. There is usually 
some necrosis and calcification, especially in 
those layers of the intima that are next the 
media. 204 
The Gastro-Iniestinal Traci. 
SOME POINTS IN THE HISTOLOGY OF 
THE GASTROINTESTINAL TRACT. 
* 
This tract is a tube. The stomach is a 
dilatation in the tube. Its intima is divided 
into two layers, the mucosa and the submu- 
cosa, and the separation, which is somewhat 
indistinct, is by the muscularis muscosa. The 
intima is thrown into longitudinal folds by 
muscular contraction. In addition to the 
folds, which embrace both layers of the in- 
tima, the epithelium dips in to form two sets 
of glands. The epithelium is columnar. The 
peptic glands, most abundant near the fun- 
dus, are straight tubes with two sets of cells, 
one columnar, lining the lumen; and another, 
large, round, outside of the columnar layer. 
The pyloric glands are compound, wavy, and 
show a disposition to go below the muscu- 
laris. The mucosa and the submucosa are 
connective tissue structures, with many blood 
vessels, and a large amount of lymph tissue. 
The most important of the stomach’s func- 
tions is its motor function; so its muscle 
layer is most prominent. It is in three lay- 206 
The Gastro-Intcstinal Tract. 
ers, circular, longitudinal and oblique. The 
adventitia is of little importance. 
DISEASES OF THE STOMACH. 
I. Acute gastritis. 
2. Subacute gastritis. 
3. Chronic gastritis—atrophic gastritis. 
4. Round ulcer. 
5. Cancer. 
In discussing stomach conditions it is to be 
borne in mind that the stomach remains in 
contact with the gastric juice after death, and 
that therefore punctures, holes, loss of mu- 
cosa etc., may be present, independently of 
pathological processes. The stomach is a 
large viscus in which substances remain for 
some hours, therefore violent irritants show 
their effects markedly here. It is not distinct- 
ively an absorptive organ unless the sub- 
stance is very volatile. The tissues by which 
poisons are destroyed or by which they leave 
the body will be more affected by them than 
will be organs by which they enter, other 
things being equal. 
ACUTE GASTRITIS 
Cause: Violent irritants of any kind: or- 
ganic, as ptomaines, tyrotoxicon, decayed 208 
The Gastro-intestinal Traci. 
meats; inorganic, as mineral acids, arsenic, 
phosphorus, etc. 
Philosophy of the process: Similar to acute 
bronchitis, except that there is greater irrita- 
tion, therefore greater haemorrhage and stasis 
of blood. 
Anatomy: The mucous surface is covered 
by mucus, or shreds of mucous membrane if 
the process is violent, as in poisoning by min- 
eral acids. The mucosa is swollen and irreg- 
ular. Twigs of injected vessels stand out 
prominently. The injection on the peritoneal 
surface is apparent. 
Histology: There is abundant small, round 
cell infiltration of the mucosa, submucosa and 
of the connective tissue between the muscle 
fibers. The blood vessels are distended and 
around them the inflammatory connective tis- 
sue proliferation is most marked. The epi- 
thelium of the surface and of the glands is 
swollen, granular and shows either fatty or 
mucous granules. In places it is falling away. 
SUBACUTE GASTRITIS. 
Synonyms: Adenomatous gastritis; gas- 
tritis glandularis. 
Cause: An irritation milder than the one 
just mentioned, e.g., alcohol. 210 
The Gastro-Intestinal Tract. 
Philosophy of the process: The position of 
the process is not well determined. There is 
an overgrowth of lymphoid tissue and of 
gland tubes, very similar to that found in en- 
dometritis. The gland tubes are lined by epi- 
thelium that rapidly becomes mucus secret- 
ing. Either as a cause or an effect the mus- 
cular coat atrophies. Dilatation takes place 
and the process is indefinitely continued. 
More dilatation, more fermentation; therefore 
more irritation and more adenomatous 
growth. 
Anatomy; The stomach is dilated. The 
mucosa is greatly thickened; in places it is 
polypoid; in places it is apparently ulcerated. 
The muscularis is thickened. 
Histology: The mucosa is made up of a 
mass of round cells, actively proliferating; 
among the round cells are very irregular 
gland tubes, the epithelium of which is swol- 
len, granular and oftentimes lying loose in the 
tubes. The muscularis mucosa is not ap- 
parent. The mucous overgrowth impinges 
on the muscular layers; the muscle layers 
show some degenerating fibers. 
Effects: The effect is a continued secretion 
of mucus, continued fermentation, growing 
dilatation, fatty and cirrhotic liver. 212 
The Castro-Intestinal Tract. 
ATROPHIC GASTRITIS. 
Synonym: Cirrhosis of the stomach. 
Philosophy of the process: The inflamma- 
tory cells mature; the matured connective 
tissue contracts, and so obliterates the gas- 
tric tubules; it in places causes degeneration 
of the muscularis. 
Anatomy: The stomach is thin-walled and 
dilated, and may contain a large quantity of 
clear water or watery secretion, containing 
some mucus. The mucous surface is irregu- 
lar; in places it is wholly fibrous, in others 
polypoid. This tendency to polypoid arrange- 
ment is very prominent in any mucous mem- 
brane that is bathed in moisture and continu- 
ously irritated. < 
Histology; There is an abundance of dense, 
laminated connective tissue in the mucosa 
and submucosa. The epithelium is either 
rounded, irregular in shape or absent. The 
glands are small in size, and with fairly regu- 
lar epithelial cells, or else they are cystic, in 
which event the epithelium is very irregular. 
This sclerosis extends into the space between 
the muscular fibers, so they are undergoing 
pressure atrophy also. The Gastro-intestinal Tract. 
Synonyms: Solitary nicer; perforating ni- 
cer; nlcns ventricnli. 
ROUND ULCER OF THE STOMACH. 
Philosophy of the process: The theory is, 
there is an embolus, or else an arteritis block- 
ing a branch of the gastric artery. This area, 
deprived of its nourishment, is digested by 
the gastric juice. There is a minimum amount 
of inflammatory reaction in the vicinity of 
the ulceration; therefore, the particular area 
must either be subjected to peculiar irritation, 
or else the tissues must have lost their ca- 
pacity for resistance in a peculiar way. 
Causes: Unknown. 
Anatomy: The stomach, as a whole, looks 
very natural. In the great majority of cases 
the ulcer is found on the posterior surface, or 
the lesser curvature; the fundus and the car- 
diac end are nearly always spared. It occurs 
in women more frequently than in men, and 
in young people more frequently than in old. 
It frequently heals. The ulcer has a punched- 
out appearance. There is little elevation of 
its edges. Its mucous extremity is the larger 
extremity. Sometimes it “shelves” as it 
passes through successive layers of stomach 
wall. On the peritoneal surface there is often 
evidence of local peritonitis, and sometimes 216 
The Gcistro-Intestinal Tract. 
the liver, diaphragm, or any adjacent struc- 
ture, is so closely bound to the stomach as to 
form a bottom for the ulcer. 
Histology; There is little to be seen. In 
the vicinity of the punched-out area there is 
a small amount of round cell proliferation. 
Its striking peculiarity is this negativeness. 
DEGENERATIONS. 
The stomach is subject to few degenera- 
tions beyond the degeneration of the glandu- 
lar structures into mucous glands. 
TUMOR GROWTHS. 
The most important of the tumors of the 
stomach are carcinomata. Carcinoma of 
the stomach is usually primary in that organ. 
It is located by preference near the pyloric 
extremity. 
Anatomy; The new growth may present 
one of two peculiarities; it may be diffused 
throughout the stomach wall without nodules, 
or it may produce nodular growths that pro- 
ject into the lumen of the stomach. The first 
variety has much less tendency to ulceration 
than has the second. The stomach is usually 
dilated. The pylorus is contracted, or it may 
be widely patulous. There is considerable 218 
The Gastro-intestinal Tract. 
secondary gastritis. There is evidence of ex- 
tension to the liver, to the diaphragm, to the 
omentum, mesenteric glands. 
Histology: The carcinoma is always of the 
columnar celled type. There is extension of 
the epithelium through the basement mem- 
brane. In the mucosa and submucosa the 
epithelial cells attempt to arrange themselves 
in glands; some of these are easily recogniz- 
able as such ; some as simple alveoli. While 
the glands are derived from glandular epithe- 
lium, many of them lose their shape, and 
become simple indifferent epithelium. This 
epithelium is growing actively. In the mus- 
cular layers the epithelium is seen to extend 
as long, narrow ribbons, one or two cells in 
width. These are lymph channels, filled. On 
the peritoneal surface, the epithelium again 
breaks out into greater activity. There is 
usually considerable round cell proliferation, 
and leucocyte invasion in the connective tis- 
sue of carcinoma of the stomach. 
SMALL INTESTINES. 
The small intestine consists of three layers. 
The most important is the intima. It consists 
of a mucosa and a submucosa, separated by a 
muscularis mucosa. The mucosa is thrown 220 
The Gastro-intestinal Tract. 
into transverse folds, called valvnlse conni- 
ventes. In addition it has normal polypoid 
growths, called villi. The epithelium is col- 
umnar. The glands are simple tubular glands, 
except in the region of the duodenum, where 
there is an additional set of duodenal glands 
that run into the submucosa. The lymphoid 
tissue is abundant everywhere. It is gathered 
together in solitary follicles throughout the 
entire tract. In places, especially in the ileum, 
there are aggregations of these follicles, 
called Peyer’s patches. 
The media is divided into two considerable 
muscle layers, the inner circular and outer 
longitudinal layer. 
The adventitia is of minor importance. 
The peculiarities of the smaller intestine, as 
distinguished from the stomach, are: 
Its transverse folds. 
Its villi. 
The absence of glands with marginal cells 
(peptic). 
The lesser prominence of the muscle. 
The greater prominence of the lymphoid 
structures. 
Anatomy; The intestine is intensely in- 
jected, especially on the mucous surface. The 
ACUTE ENTERITIS. The Gastro-intestinal Tract. 
color is red, dark red, or brown. There may 
be injection of the overlying peritoneum. The 
mucosa is swollen, soft, and covered by 
thick mucus. This appearance is to be dis- 
tinguished from post-mortem appearances. 
There may be some swelling of the adjacent 
mesenteric glands. 
Histology: There is great piling up of the 
round cells of the mucosa and submucosa. 
The muscularis mucosa is overrun by these 
cells. ■ Here and there are scattered glands. 
There is no epithelium on the surface, or only 
a few scattered cells. Amongst the cells are 
some islands of extravasated blood. There may 
be round cell proliferation between the bands 
of muscle fibers of the muscular layers. 
TYPHOID INTESTINE. 
Synonyms: Enteric fever; dothienteric 
fever. 
Cause; The bacillus typhosus. 
Philosophy of the process: The bacillus en- 
ters the lymphatics of the intestine, and is 
carried to the lymph glands, solitary and ag- 
minated. Its toxin produces an inflamma- 
tion. The irritated tissue is destroyed. The 
bacillus, multiplying in the deeper structures, 
the inflammatory and destructive process 224 
The Gastro-hitcstinal Tract. 
continues. The gland being destroyed, the 
poison travels through the muscular coat into 
the peritoneal, and up to the lymphatic 
glands. The intestine is in direct continuity 
with the outside world; therefore the intes- 
tine is constantly loaded with germs, patho- 
genic and otherwise. Through this abraded 
surface these organisms secure entrance, giv- 
ing rise to secondary infections of various 
kinds. To the toxsemise are due the cloudy 
swelling of the liver, kidney and heart, the 
fever, the rapid pulse and respiration, and 
the other neuralgias. Perforation is frequently 
prevented by localized peritonitis. Haemor- 
rhage is due to ulceration into a vessel in the 
submucosa or on the peritoneal surface. 
Anatomy: The intestine is the seat of an 
enteritis, which is usually rather mild and 
diffuse. In the early stages the solitary 
glands and Peyer’s patches are swollen and 
stand out above the intestinal surface. Later 
these present themselves as oval ulcers, gen- 
erally on the side away from the mesenteric 
attachment. These ulcers have ragged, over- 
hanging edges. There is thickening of the 
edges in the vicinity of the ulcer. Over the 
outside there is some local peritonitis. Lym- 
phatic bands, indurated, can be traced to 226 
The Gastro-intestinal Tract. 
the neighboring swollen glands. Later 
those of the patches that did not ulcerate 
show as shaven beard areas, a streaking of 
white around small islands of black. The 
name is descriptive. The glands that ulcer- 
ated show as smooth, grayish scars. 
Histology; The surrounding tissue shows 
typical, violent inflammation; round cells pile 
up over small remnants of epithelial glands; 
farther away the inflammatory process can be 
seen extending along lymphatics and in peri- 
vascular areas. 
TUBERCULOSIS OF THE INTESTINE. 
We may have a tubercular peritonitis, in 
which the tubercles are over the intestinal 
wall. We have tuberculosis beginning in tbe 
mucosa, and this process infecting the peri- 
toneum. When the peritoneum has been in- 
fected, either from the blood current or the 
sexual apparatus, that is, when the infection 
is from a source other than the intestine, it 
does not usually ulcerate into the intestine, 
though it may be productive of diarrhoea. The 
nerves of the intestine pressed on are apt to 
give interpretation to irritation in this way. 
TUBERCULAR ULCER. 
Cause: The tubercle bacillus. 228 
The Gastro-intestinal Tract. 
Philosophy of the process: Location gen- 
erally takes place in the glands; irritation, 
proliferation. Around each cluster of bacilli 
there is a nodule of tuberculosis. These 
necrose, become infected, ulcerate; the ul- 
ceration extends irregularly from one nodule 
to another. The ulceration seldom perforates 
but the gland being* destroyed, tubercle bacilli 
can spread to the peritoneal surface and 
thence to the mesenteric glands. 
Anatomy: The ulcer is worm-eaten; in its 
walls tubercular nodules may be apparent; in 
its bottom tubercular nodules can be felt; 
over its peritoneal surface there appear tuber- 
cular nodules, and the lymphatics can be 
plainly seen and felt as solid cords. 
Histology; There is thickening of the mu- 
cosa and submucosa that make up the ulcer 
wall. They are fairly well covered with epithe- 
lium; here are seen tubercular nodules and 
some show giant cells. 
LARGE INTESTINE. 
Histology: The large intestine differs from 
the small in that 
i. It has no villi—-the fecal contents are 
becoming solid. The Gastro-intestinal Tract. 
2. It has no Fever’s patches; the solitary 
follicles are larger. 
8. Its longitudinal muscular fibers are not 
continuous over the circumference, but are 
gathered together in bands. It is to tins that 
is due the puckering of the large intestine. 
4. More of the glands are mucous glands. 
Acute proctitis does not differ in any par- 
ticular from acute disease elsewhere in the 
intestine. The gross anatomy and the minute 
anatomy are the same. It is the seat of a 
croupous inflammation in which the exuded 
plasma coagulates on the surface and in the 
substance of the mneosa and fibrinous casts 
of the bowels are evacuated. The histology 
is the same as that of diphtheria in the 
pharynx or larynx. 
ACUTE PROCTITIS. 
Synonyms: Dysentery; bloody flux 
Etiology: All kinds of organisms. 
Nature of the process: The nature of the 
diseased process is dependent upon the nature 
of the infection. It may be what is termed 
catarrhal, when we have the surface covered 
by mucus and serous exudate, the epithelial 
cells, some proliferating and some undergoing 
mucous degeneration. The blood vessels are The Gastro-intestinal Tract. 
moderately injected, and the mucosa and sub- 
mucosa contain a few round cells. 
In more violent cases, the epithelium is de- 
generating and falling away, the mucosa and 
submucosa violently filled with inflammatory 
cells and exudation products. 
In most cases extravasation of red cells is 
a very prominent feature. In some cases both 
the mucosa and submucosa may be black 
and gangrenous. 
AMOEBIC COLITIS. 
Etiology; The amoeba coli. 
Nature of the process: The disease is gen- 
erally subacute. The amoeba coli is found 
most abundant in the submucosa. Here it 
causes a destructive inflammation. Therefore 
the markedly overhanging edges of the ulcers. 
From the colon it is sometimes transported 
to the liver, where it causes solitary abscess. 
Anatomy: The mucosa is swollen, red. 
There are irregular ulcers in its surface. 
These have ragged, overhanging edges. 
Sometimes considerable areas of mucosa can 
be lifted from its deeper attachments. 
Histology; There is moderate increase in 
the subepithelial mucosa. In places the mu- 234 
The Gastro-Intcstinal Tract. 
cosa is ulcerated away. There is found vio- 
lent round cell inflammation in the submu- 
cosa. The organism, larger than an epithelial 
cell, can be seen in the mucosa, but it is far 
more prominent and abundant in the lymph 
spaces of the submucosa. There may be 
moderate inflammation in the muscularis and 
the serosa. 
CHRONIC COLITIS. 
Other forms of chronic colitis are mucous 
colitis, follicular colitis. 
Mucous colitis: A very moderate inflam- 
matory degeneration, mucous in type, limited 
to the epithelial structures of the colon. It is 
characterized by the presence in the stools of 
mucous casts of the bowel. These casts are 
molds of the bowel and consist of masses of 
epithelial cells in a state of marked mucous 
degeneration. The cells remaining attached 
to the basement membrane are dividing. 
FOLLICULAR COLITIS. 
Anatomy; The mucosa is generally not 
markedly injected. Here and there over its 
surface are enlarged solitary follicles that pro- 
ject into the lumen of the colon like a tick. 
They are sometimes covered by unimpaired 236 
The Gastro-Intestinal Tract. 
epithelium; sometimes the center is excavated, 
giving' an umbilicated appearance. Some of 
them have ulcerated, giving a follicular ulcer. 
The muscular coat is sometimes greatly thick- 
ened as a result of the muscular work of fre- 
quent bowel movement. Sometimes it is at- 
rophied. 
Histology: The covering of epithelium on 
the mucosa is imperfect; where it is present 
the cells are indifferent in shape. The mu- 
cosa is moderately inflamed, partially filled 
with round .cells and the relations of the 
glands are abnormal. The glands, which 
ordinarily lie just on the border line between 
the mucosa and submucosa, are filled with 
round cells, and the center may be caseating. 
If the form is ulcerating the follicular locations 
represent depressions with follicular walls. 
THE APPENDIX. 
This has a histology identical with that of 
the large intestine. It is subject to exactly 
the same processes, but by reason of the 
smallness of its lumen, frequently conditions 
arise which prevent the draining of both 
pathological and normal products. The in- 
testine is prone to suppurative process, but 
its mean of exit is never stopped. As a re- The Gastro-intestinal Tract. 
suit of ulceration involving the circumference 
a stricture is formed, and contraction of the 
inflammatory connective tissue in the submu- 
cosa shuts ofif the lower part of the appendix, 
or the appendix may be stopped by a foreign 
body; or it may fail to empty itself from mus- 
cular atrophy, for it must work against grav- 
ity; or it becomes twisted or turned so as to 
obliterate the lumen. In the event that a 
suppurating process is then going on, the pus 
can not drain away, and the organisms are 
carried by the lymphatics into the surround- 
ing connective tissue or peritoneum. In the 
event that infection has not taken place the 
glandular secretions accumulate until the ap- 
pendix becomes cystic. This sets up a me- 
chanical irritation, which invites infection of 
the contained fluids. 
SUPPURATIVE APPENDICITIS 
Etiology: Any of the pus germs, e.g., 
bacillus coli communis, streptococcus, staphy- 
lococcus, may be the direct agents; foreign 
bodies may be contributing agents. 
Philosophy of the process: In the more 
violent forms, an acute destructive inflamma- 
tion. Destruction is more violent in the areas 
in which the germs are most abundant. In 240 
The Gastro-Intestinal Tract. 
infection with bacillus coli communis the mu- 
cosa is apt to show comparatively evenly black 
and sloughing. 
In staphylococcus infection there is not in- 
frequently large accumulation of pus in the 
neighborhood of the appendix. 
In streptococcus infection there is more apt 
to be diffuse peritonitis without large accumu- 
lation of pus. 
Anatomy: The mucosa is dark red or black, 
sloughing away in places. The entire wall is 
swollen. When the appendix is split longi- 
tudinally the mucosa rolls out and the con- 
cavity becomes the convexity. The odor of 
gangrene is often apparent. 
Histology: There is loss of epithelial cover- 
ing; the mucosa and submucosa are markedly 
filled with round cells, with islands of blood 
here and there. Patches of necrosis are pres- 
ent. The muscular bands are separated by 
inflammatory cells, The adventitia is acutely 
and violently inflamed. 
In cases of recurring appendicitis there is 
generally stricture formation at the proximal 
end causing cyst formation. At the stricture, 
we find an absence of epithelial covering, or 
else a few scattered indifferent epithelial cells; 
underneath this is a mass of laminated ma- 242 
The Gastro-intestinal Tract. 
tured fibrous tissue, running around the lumen 
of the tube and parallel with the mucous sur- 
face. If this is at the distal end of the tube, 
there is no cystic accumulation, of course. 
The media of the intestine is subject to waxy 
degeneration. 
The tumors to which tlie intestines are sub- 
ject are: Lipoma; fibroma; myoma; lymphan- 
gioma; angioma; papilloma; simple adenoma; 
sarcoma; lympho-sarcoma; epithelioma (near 
the anus); alveolar carcinoma; columnar car- 
cinoma. The tendency of carcinoma in this 
locality is to become colloid, because the cells 
from which it begins are mucus-forming cells, 
or else they readily become mucus-forming 
cells. 
There are certain adventitious diseases, 
aside from these already spoken of, that affect 
the intestine. 
Invagination is where a slip of intestine 
from above glides into a slip from below. 
The condition is more or less physiological; 
but if it interferes with nutrition, and if mus- 
cular effort on the part of the longitudinal 
fibers does not reduce it, we have sloughing, 
necrosis, gangrene, intussusception. 
Kinking, twisting, turning, incarceration, 
either in an inclosed hole, as that into the 244 
The Castro-Intestinal Tract. 
scrotum in hernia, or else behind a band of 
adhesion, produces pathological processes on 
the same principle of nutrition “nil.” 
PERITONEUM. 
This has the same histology as the pleura 
and the pericardium. It is of greater patho- 
logical interest, because it is larger, more 
loose, and between its folds it has a richness 
in lymphatics and blood vessels that the pleura 
has not. It is subject to all the infections. 
By reason of the number of its vessels, and 
the looseness of the tissue which surrounds 
them, it is a favorite seat of the noninflam- 
matory transudations from loss of relation (i) 
between the forces of gravity and heart pres- 
sure and (2) between the blood plasma and 
the connective tissue of the wall. 
It has the same varieties of inflammation 
as the pleura. 
Cellular: Dry peritonitis: Productive in- 
flammation with presence of, though not 
prominence of, exudation. 
Serum. 
Blood. 
Pus. 
Adhesions, 
Exudative. The Gostro-Intestinal Tract. 
The infective granulomata are found in the 
peritoneum frequently. 
Tuberculosis: The process shows beauti- 
fully as small pearly nodules with radiating 
lymphatics. 
Histology: Along the course of the small 
arteries, and the lymphatics, are little 
nodules, which start as end or periarteritis. 
The masses are composed of proliferating 
endothelial, cells. If the process is slower, 
giant cell systems are formed. The histology 
is the same as tubercle elsewhere. 
Carcinoma, adenoma, cystadenoma, papil- 
lary cystadenoma, sarcoma, are perhaps the 
most frequent varieties of tumors of the 
peritoneum. They are usually secondary. 
The carcinoma is colloid. 248 
The Liver. 
POINTS IN HISTOLOGY. 
LIVER. 
The liver has both duct and ductless gland 
functions. To the former system belongs the 
bile apparatus; to the latter the arrangement 
of the epithelium into cords radiating from 
the center to the periphery of the lobule. 
The liver springs as a bud of the intestinal 
tract, and in consequence its earliest arrange- 
ment is that of. a racemose gland. Soon, 
however, the perivascular arrangement into 
cords overshadows everything else. The por- 
tal branches, known as the peripheral veins, 
divide into the capillaries of the lobule, and 
these in turn empty into the central vein; the 
branches from the portal vein mingle with the 
branches of the hepatic artery in the lobule. 
The lobule is the liver unit; for convenience 
we arbitrarily divide it into three zones, the 
central zone, the middle zone, and the pe- 
ripheral zone. 
The capsule of the liver is dense and closely 
acuierent 250 
The Liver. 
ACUTE PARENCHYMATOUS HEPATITIS. 
Synonym: Cloudy swelling. 
Etiology: It is due to poisons brought to 
the liver by the blood vessels; organic 
poisons, e.g., those of typhoid fever, scarlet 
fever, pernicious anaemia, the infectious fe- 
vers, septicaemia, pyaemia, etc.; the inorganic 
poisons, e.g., iodoform, iodol, phosphorus, 
arsenic. 
Philosophy of the process: The process is 
an inflammatory degeneration, the irritation 
being just within the limits for the epithelial 
cell and without the limits for the connective 
tissue cell. The irritation ending, the albu- 
minous granules in some of the cells go into 
solution, in others they undergo fatty degen- 
eration, in others the cells undergo some form 
of death, followed by absorption. 
Anatomy: The liver is enlarged and pale; 
capsule tense; the central vein shows more 
distinctly than normal. 
Histology: The liver cells are swollen, 
granular, and rounded. The cells stain poorly. 
The capillary spaces are markedly dimin- 
ished in size. In this stage the granules are 
soluble in acetic acid. Later the nucleus be- 
gins to lose its staining capacity, and still later 
all cell outlines are lost. 252 
The Liver. 
Sequelae: Fatty degeneration. 
ACUTE DIFFUSE HEPATITIS. 
Etiology: An irritation a shade more vio- 
lent than the preceding, affecting the connec- 
tive tissues as well as the parenchyma; or- 
ganic poisons, e.g., severer cases of smallpox, 
scarlet fever, diphtheria, typhoid. 
Philosophy of the process: Cloudy swell- 
ing of the highly differentiated parenchyma, 
non-exudative, productive inflammation of the 
lowly differentiated tissues. This condition 
is closely akin to, and merges imperceptibly 
into, hypertrophic cirrhosis, but differ radi- 
cally from atrophic cirrhosis. Under the 
microscope it differs only in degree from mili- 
ary abscess. In diffuse hepatitis the fountain 
of the poison is located outside the liver; in 
abscess it is in situ. The process is the same 
in character up to the point where in abscess 
breaking down becomes prominent. 
Anatomy: The liver is enlarged, pale. 
The capsule is tense. More than the usual 
amount of blood is found in the portal spaces; 
there are points of red or gelatinous appear- 
ance in the portal space. If these places are 
small, the liver cannot be told from cloudy 
swelling; if large, from miliary abscess. 254 
The Liver. 
Histology: There is the cloudy swelling 
oi the epithelial cells perviously described. 
In the connective tissues are islands of round 
cells; these patches are sometimes rounded 
and sometimes in bands extending along the 
capillary walls. 
ABSCESS. 
The liver is a filter for the portal area. This 
area is in direct ■ contact with the external 
world. It is moist and warm; therefore it is 
always infected. Contrary to the arrange- 
ment of the skin and bronchial tube lining, 
there is no protection against absorption, but 
there is rather arrangement for absorption. 
A very small percentage of the poisonous 
chemicals absorbed into the portal veins 
reach the hepatic vein. This is probably 
true also of the germs that secure entrance. 
The abscesses of the liver are of two 
kinds: (i) multiple and (2) single. The dif- 
ference between them lies more in the infect- 
ing material than in anything else, as the chan- 
nel of infection is the same in both varieties. 
MULTIPLE ABSCESS. 
Synonyms: Pysemic abscess; bacterial ne- 
crosis; infection. 
Etiology: Some of the forms of pus germs. 256 
The Liver. 
Under this head we include infections with 
organisms that are not usually pyogenic, e.g., 
the typhoid and diphtheria bacilli. 
Philosophy of the process; The liver is 
much less frequently the seat of abscess in 
pyaemia than are the other organs, because 
the portal blood has already passed through 
one set of capillaries and the hepatic arteries 
are relatively small in size. Most frequently 
the source of infection is in the gastrointes- 
tinal tract. Those abscesses due to pus 
germs give the phenomenon of abscess for- 
mation elsewhere, except for the general rule 
that all dead tissue in the liver becomes bile 
stained. Those abscesses due to other 
germs, e.g., the typhoid bacillus, give areas 
of necrosis with a limited amount of leuco- 
cytic reaction. 
Anatomy; The liver is pale and in a state 
of cloudy swelling. On cut section, multiple 
abscesses, ranging from a pin point to bean 
size; they may be bile stained (green or yel- 
low), or red and gelatinous. Pus may flow. 
They may be cheesy or calcareous. If they 
make cavities, these cavities are wall-less. 
When the organism is the bacillus typhosus, 
pus is unusual. 
Plistology: The histology is the same as 258 
The Liver. 
that of ordinary abscess. In the beginning 
the arrangement is, an infected thrombus in 
the center; around this degenerating liver 
cells and leucocytes; some free nuclei; much 
tissue detritus; around this, granular epithe- 
lium; breaking down and massing of leuco- 
cytes; further out leucocytic massing, dilated 
congested vessels, liver epithelium, shows 
cloudy swelling. 
SOLITARY ABSCESS. 
Synonyms: Tropical abscess; amoebic ab- 
scess. 
Etiology: Infection with amoeba coli in 
the majority of instances. In these cases 
there is oftentimes a primary colonic infec- 
tion. 
Philosophy of the process; The cause of 
this process is destructive to the liver cells 
and at the same time is very slightly irritating 
to other tissues. Special irritation. 
Anatomy: The abscess is usually single. 
It may project above the surface; peritoneal 
adhesions bind it to the diaphragm, or to any 
of the neighboring viscera. The cavity some- 
times opens through the diaphragm into the 
pleura or into a bronchial tube. It may open 
into the stomach, or intestine, or abdominal 260 
The Liver. 
wall, or into the peritoneum. The cavity has 
a ragged, uneven wall. The pus is reddish, 
somewhat like prune-juice. 
Histology: There is little connective tissue 
in the abscess wall. 
We will study first that interstitial lesion 
in the liver which is most marked and pre- 
sents the most salient points. 
CHRONIC INFLAMMATIONS. 
Synonyms: Common cirrhosis; alcoholic 
cirrhosis; sclerosis of the liver; gin drinker’s 
liver; granular liver; hob-nail liver. 
ATROPHIC CIRRHOSIS. 
Etiology: A mild irritation long continued, 
an irritant affecting the connective tissues 
only, and borne to the liver, in greatest part, 
by the portal veins. Such an irritation is pro- 
duced by alcohol or ether, taken into the gas- 
tro-intestinal tract, or manufactured by fer- 
mentation processes therein. 
Philosophy of the process: The poison is 
carried to the liver by the portal vein. In 
consequence it is in the vicinity of the portal 
structures—the interlobular spaces—that the 
lesion first manifests itself. It is a blood- 
vessel-wall disease, and all the effects, and 
therefore all the symptoms, are due, not to 262 
The Liver. 
the inflammatory process, for the structures 
inflamed are of minor importance, but to the 
thickening of the vascular walls and to the 
secondary contraction that characterizes all 
inflammatory connective tissue. 
Associated with cirrhosis is always marked 
fatty change, for two reasons. In the first 
place, there cannot be a proper liver work 
through thick-walled capillaries; in the sec- 
ond place, the alcoholics, in whom cirrhosis 
is found, are prone to obesity. 
Anatomy: The liver is diminished in size. 
No other affection, except acute yellow 
atrophy, gives a small liver. The capsule is 
thickened and firmly adherent. To the 
touch the liver is hard. The scarring is the 
most striking feature. The surface is cov- 
ered in whole or in part by small elevations 
about the size of a hob-nail, or shoe nail 
head. Some of the eminences may be of large 
size. The fissures that mark the eminences 
arc hard and paler. On cut section the liver 
is usually yellow. It may be pale and per- 
ceptibly fatty. The capsule can be seen 
sending trabeculae into the substance. The 
section cuts and feels firm. The intertrabec- 
ular tissue is softer; the trabeculae are firm, 
grayish. The Liver. 
Histology; With the low power it will be 
easily seen that the portal trabeculae are 
markedly increased in size. The inner layers 
will be old; the layers next the lobules will 
be more nucleated; at the periphery of the 
lobule it will be apparent that the connective 
tissue is “shaving off’ the epithelial cells. 
Some of the lobules will be nothing but small 
islands. 
With the high power the increase in con- 
nective tissue at the edge of the trabeculae 
will be evident. In some foci this tissue will 
be round cell tissue. The bulk of it will be 
fibrillated connective tissue, but with a con- 
siderable number of spindle nuclei. In its 
meshes are ribbons of epithelial cells, usually 
compressed. These cells resist degenerations 
longer than the cells of the remainder of the 
lobule; they are recognizable as liver epithe- 
lium until compression is very advanced. Be- 
yond this zone there is proliferation of the 
connective tissue between the liver cells. 
While the process is more marked in the pe- 
riphery of the lobule, it can in some lobules be 
seen to reach to the center; but near the center 
the cells are round or spindles or young fibers. 
The epithelial cells are usually very fatty. In 
some the fat is in granules, but usually it is 266 
The Liver. 
in globules. Signet ring cells are the rule. 
The new development of bile capillaries among 
the liver cells is not prominent. In fact the 
epithelium is undergoing very little inflam- 
matory reaction. In the hands of the con- 
nective tissue there are found considerable 
numbers of bile capillaries, and occasionally 
these are seen extending into the liver cell 
areas; but as a general thing the liver cells 
are fatty and nothing more. 
Effects: Venous congestion effects in the 
abdominal area, e.g., ascites, haemorrhage into 
the stomach and intestines, haemorrhoids; loss 
of liver function, deficient urea. 
Tendency: It is progressive; usually pro- 
gressive by invasion by inflammatory connect- 
ive tissue, but always progressive by con- 
traction of inflammatory connective tissue. 
Synonyms: Biliary cirrhosis; monolobular 
cirrhosis. 
HYPERTROPHIC CIRRHOSIS. 
Etiology: A mild irritation long continued. 
The irritant affects both the connective tissue 
and the epithelial cell. 
Philosophy of the process; We have a pro- 
ductive inflammation in both the parenchyma 
of the organ and in its interstitial tissue. The 268 
The Liver. 
effects are spread throughout the lobule much 
more evenly. Tying the bile duct in lower 
animals has produced this form of cirrhosis. 
The liver epithelium in its embryonal form 
was a columnar epithelium lining a duct; 
when it is irritated, as in this affection, it has 
a tendency to arrange itself in tubular form 
and assume columnar shape. As the epi- 
thelium is affected liver function is rapidly in- 
terfered with, and death comes before time is 
had for atrophic changes. 
Anatomy: The liver is greatly enlarged at 
times. The capsule is but little thickened. 
The surface is irregular, but the elevations 
are very uniform in size. The liver “cuts” 
tough; cut section looks granular and bile 
stained. 
Histology: The round and spindle cells 
are found throughout the lobule, although not 
as abundant in the center as at the periphery. 
There is not the same massing of large quan- 
tities of connective tissue as seen in the 
atrophic form. Some of the liver cells are 
swollen and granular; some are dividing. In 
the connective tissue there is an unusually 
large number of bile capillaries; at the mar- 
gins of the connective tissue, the liver cells, 
cubical in shape, are arranging themselves as 
double columns—bile capillaries. 270 
The Liver. 
CHRONIC VENOUS CONGESTION. 
Synonyms; Nutmeg liver; liver of heart 
disease; cyanotic atrophy. 
Etiology; This form of chronic interstitial 
hepatitis is clue to long continued venous 
stasis from obstruction to the return of blood 
to the heart; e.g., valvular lesions of the 
heart, long continued; pleurisy with effusion; 
tumors of the lung; emphysema. 
Philosophy of the process: The damming 
of blood causes stasis in the central vein of 
lobule, and thence in the capillaries running 
into it. The vessels then are chronically di- 
lated and the liver effects are due to (i) 
pressure, (2) nutrition minus, (3) prolonged 
contact with the leucomaines representing 
tissue waste. Here, as well as in all venous 
congestions, there is a minus condition of the 
highly differentiated parenchyma, and a 
plus condition of the lowly differentiated con- 
nective tissue. 
Anatomy; Capsule tense, thin. On cut 
section the liver lobule shows very plainly. 
The central zone is dark red; the middle and 
outer zone is pale and fatty. Later we find 
irregular patches of connective tissue, and the 
contraction effects of such bands. 
Histology: Thei central veins and the The Liver. 
radiating capillaries are distended. The en- 
closed cells are shrunken and pigmented. 
This inner zone is called the zone of nutmeg 
changes. Later there is an overgrowth of 
connective tissue, attended by further com- 
pression of the liver cells. The middle and 
outer zones are fatty. 
TUBERCULOSIS OF THE LIVER. 
Etiology; Tubercle bacillus. 
Philosophy of the process; Tuberculosis 
presents no peculiarities here. It very fre- 
quently makes giant cells. It is stained green 
or yellow from bile while still small. 
Anatomy: The liver may show cloudy 
swelling; scattered throughout, but more 
abundant near the capsule and in the portal 
spaces, are small nodules, gray at first, later 
green. 
Histology: In or near the center is a giant 
cell with multiple nuclei; from some portion 
of its periphery, trabeculje run out among 
the surrounding cells. Outside this is a 
massing of round cells with some reticulum. 
At the margin these connective tissue cells 
and leucocytes can be seen growing among 
the liver cells, while liver cells are showing 
evidence of degeneration. The tubercular 274 
The Liver. 
nodules are found toward the periphery of 
the liver lobule. 
Syphilis of the liver begins as a diffuse 
sclerosis with marked increase in the con- 
nective tissue—the portal areas. There are 
the usual contraction effects in the paren- 
chyma. It spends much of its force on blood 
vessels, so that there is abundant making of 
capillary loops. This same irritation of ves- 
sel walls causes thickening of the vessel wall 
as it grows older, and finally an obliteration 
by endarteritis obliterans. With this the stage 
of gumma is reached. 
SYPHILIS. 
GUMMATA. 
Anatomy: The tumor may reach consider- 
able size. It may be multiple, but it frequently 
is single. It is most frequently on the 
surface, and often near the suspensory liga- 
ment. Early it is rose gray; later it is green. 
It has a capsule, which capsule is intimately 
connected with the surrounding tissue. This 
is always marked in syphilitic capsules. The 
contents are apt to be grumous. 276 
Degenerations of the Liver. 
DEGENERATIONS OF THE LIVER 
CLOUDY SWELLING. 
Treated under acute parenchymatous in- 
flammation. 
FATTY DEGENERATION. 
Etiology: It is found as a later stage of 
cloudy swelling, and therefore due to the 
same causes; organic poisons—toxins of 
continued fevers, Addison’s disease, perni- 
cious anaemia, phthisis, cancer, etc.; inorganic 
poisons—phosporus, arsenic, iodoform, anti- 
mony, alcohol, ether. 
Philosophy of the process: It is a degen- 
eration, conforming to the general laws of 
fatty degeneration. The liver is a favorite 
seat because of its position with relation to 
the intestines, and also because the liver is 
the great toxin destroyer of the body. It 
represents faulty internal oxidation. 
Anatomy; The liver is somewhat decreased 
in size, in weight and in specific gravity. On 
section it is pale. 
Histology: The liver cells are shrunken, 278 
Degenerations of the Liver. 
angular, and contain granules of fat. These 
dissolve in ether, stain black with osmic acid. 
In specimens prepared in the ordinary way, 
the areas of former fat shows as small clear 
points, or vesicles. 
Note.—To get the ether and osmic reac- 
tions the specimens must be taken fresh and 
treated with these agents as the first step in 
handling. 
FATTY INFILTRATION. 
Far the more frequent of the fatty proc- 
esses. It is always pathological, but not 
necessarily symptomatically so, nor even usu- 
ally symptomically so. 
Synonyms: Lipomatosis; adiposis. 
Etiology: Alcohol; fatty or starchy diet; 
maltose; sugars. 
Philosophy of the process: It is due to 
external error; that is to say, the liver proto- 
plasm itself is not changed into fat. Fatty 
liver, presenting all the characteristics of 
fatty infiltration, is found in many diseases 
accompanied by great emaciation. It is regu- 
larly found when there is a lack of relation 
between food taken and exercise. This is 
true not only of carbonaceous foods, but also 
of nitrogenous diet. 280 
Degenerations of the Liver. 
Anatomy: The liver is large, firm. It pits 
on pressure and these pits remain. It is in- 
creased in weight and decreased in specific 
gravity. The organ is pale yellow in color. 
It is greasy, and scrapings will float as grease 
on the surface of the water. 
Histology: In specimens prepared in alco- 
hol, etc., the liver lobule shows as a mesh- 
work enclosing holes of various sizes, up to 
somewhat larger than a liver cell. Close ex- 
amination shows the liver protoplasm pushed 
as a delicate ring around this clear zone; at 
one point the nucleus is seen as a projecting 
mass. In the later stages the lobule is about 
evenly affected. Frequently the process be- 
gins in the external third of the liver lobule, 
so this is called the zone of fatty infiltration. 
This distribution is by no means constant. 
Effects: Slight; life piocesses are but little 
interfered with. A certain degree of fatty in- 
filtration is entirely physiological. 
WAXY LIVER. 
Synonyms: Waxlike liver; amyloid, lar- 
daceous, bacony liver. 
Etiology; Long continued suppuration; 
phthisis, empyema, leucocythsemia, dysentery, 
syphilis. 282 
Degenerations of the Liver. 
Philosophy of the process: An infiltration 
of the connective tissue, and especially of the 
capillary wall, with a modified albumin. The 
only effects on the liver cells are (i) nutrition 
effects from the relatively impermeable vessel 
wall, and (2) pressure effects. 
Anatomy: The liver is very large—some- 
times twice its normal size. It is heavy and 
increased in specific gravity. The contour is 
rounded. The capsule thin and tense. It pits 
on pressure, but the pits are soon lost. Cut 
surface is pale, shiny, waxlike, or dull pink. 
The lobules are indistinct. Thin sections with 
a double-bladed knife show waxy areas. . These 
stain brown with iodine. 
Histology: The capillary walls are widely 
distended with a homogeneous substance; no 
tissue except the nuclei show in the areas, but 
the nuclei show very distinctly. The liver 
cells may be compressed into apparent solid 
cords. The process begins in the capillaries 
of the middle third of the lobule; this is, there- 
fore, called the zone of waxy infiltration. 
ACUTE YELLOW 'ATROPHY. 
Synonyms: Icterus gravus. 
Etiology: Not known; found most fre- 
quently in young pregnant women. 284 
Degenerations of the Liver. 
Philosophy of the process. There is a sub- 
stance which is violently toxic to the liver 
epithelium, and is nonirritating to the con- 
nective tissue. 
Anatomy: The liver is markedly decreased 
in size, weighing about thirty-five ounces. Its 
capsule is wrinkled. It “cuts” tough, and 
cut section is ochre yellow with islands of 
deep bile staining. 
Histology: The network of connective tis- 
sue stands out very plainly. But slight evi- 
dence of proliferation is found in this. The 
liver cells are indistinct in outline, most of 
them simply being masses of granular debris. 
The cells and their nuclei stain very poorly; 
crystals of leucin and tyrosin can sometimes 
be found. 
TUMORS OF THE LIVER 
The liver is the seat of multiple (i) con- 
genital cysts, (2) retention cysts, (3) ecchino- 
coccus cysts. It is a favorite site of both an- 
gioma telangiectoides and angioma cavernosa. 
SARCOMATA. 
When primary anywhere in the intestinal 
tract, they are very apt to give secondary 
growths in the liver. These are frequently 286 
Degenerations of the Liver. 
melanotic. The tumors are generally nodu- 
lar, multiple, soft, not unbilicated, and cut 
section shows islands of haemorrhages. 
CARCINOMATA. 
This is a frequent secondary tumor in the 
liver. It may be carried from almost any 
locality by lymphatics, by blood vessels, and 
along bile channels. The more frequent 
point of origin is the stomach, lower end of 
oesophagus, and upper end of the duodenum. 
The nodules are usually large, unbilicated. 
Around the nodules, and sometimes in areas 
some distance removed from the nodules, the 
liver is honeycombed; that is, the liver cells 
are broken down, as in acute yellow atrophy, 
and the connective tissue stands out more 
prominently. The carcinoma tends to assume 
the same arrangement of epithelium as in the 
areas from which it sprung. 
ADENOMATA. 
Are sometimes found in the lower animals; 
coccidium oviforme produces a typical ade- 
noma. 
Angiomata find here one of their most fre- 
quent sites. 288 
The Kidney. 
THE KIDNEY. 
The kidney is a tubular gland in which the 
tube begins at the Malpighian corpuscle and 
ends at the apex of the pyramid. In the cor- 
tex are found all the convoluted tubules and 
some of the straight tubules. In the medulla 
are found most of the straight tubules. The 
blood supply of the kidney is remarkably rich. 
The space between the tubules is filled with 
blood vessels and a small amount of connect- 
ive tissue. The tubes are lined by epithelial 
cells. The kidneys are derived from the 
Wolfiian bodies, and these in turn from the 
mesoblast. The markings are due to the al- 
ternating blood vessels and uriniferous 
tubules. 
The lesions of the kidney are due to inflam- 
mations, degenerations, tumors and develop- 
mental errors. 
Inflammations. 
Acute. 
(i) Cloudy swelling. 
Synonyms: Acute parenchymatous, nephri- 290 
The Kidney. 
tis, acute parenchymatous degeneration, acute 
Bright’s disease, molecular degeneration. 
Etiology: Toxaemias, especially those in 
which the poison is eliminated by the kidney. 
All acute febrile conditions, severe in type, 
e.g., septicaemia, scarlet fever, measles, small- 
pox, yellow fever; inorganic poisons, e.g., 
phosphorus, arsenic, carbolic acid, iodoform, 
chloroform and ether. 
Philosophy of the process: The same as 
cloudy swelling elsewehere. It is an inflam- 
matory degeneration and may return to nor- 
mal or progress to fatty degeneration or ne- 
crosis, resulting in granular debris. It is 
to be borne in mind that it is the channel by 
which the poison leaves a body that is most 
affected by it, for its excretion means a spe- 
cial irritability on the part of that cell toward 
that particular poison. This physiological 
irritability increased gives pathological irrita- 
bility. 
Anatomy: The kidney is enlarged and pale. 
Its capsule strips off easily; the stellate veins 
show distinctly. On cut section the thicken- 
ing is seen to be in the cortex. The mark- 
ings show plainly; the Malpighian corpuscles, 
being filled with blood, are accentuated. 
The medulla is not markedly affected. 292 
The Kidney. 
Histology: The tubes, especially the convo- 
luted tubes, are widely dilated. The epithe- 
lium is so swollen as to obliterate the lumen 
in many tubules—to decrease it in all. The 
outline of the individual cell cannot be made 
out. The nucleus stains well with a nuclear 
stain, such as haematoxylon. Casts are seen 
in many of the tubes. The connective tissue 
is unaffected. 
Vessels: The Malpighian tuft fills the cap- 
sule. In some cases, merging into the next 
form, there is marked dilation of the ves- 
sels and exudation of red cells into the con- 
nective tissue and into the surrounding tubes. 
Sequelae: This form of nephritis gives 
scanty urine, containing albumin, casts and 
epithelial cells. It never proceeds to chronic 
inflammations. 
ACUTE DIFFUSE NEPHRITIS. 
Synonyms: Acute exudative nephritis; 
acute Bright’s disease; acute desquamative 
nephritis. 
Etiology: Toxaemias a shade more violent 
than those of cloudy swelling, e.g., scarlet 
fever, diphtheria, etc.; turpentine, etc. 
Philosophy of the process; The principle 
involved is that of general irritability. As a  The Kidney. 
rule the more highly specialized chemically- 
functioning epithelium is breaking down- 
destructive inflammation—whilst the more 
lowly differentiated connective tissue is in a 
state of productive inflammation. Being a 
productive inflammation, it is much more 
liable to produce chronic disorder than is par- 
enchymatous nephritis. 
Anatomy: Capsule tense, peels off easily, 
kidney swollen, redder than in acute paren- 
chymatous; moist. Red patches are seen here 
and there. Glomeruli distinct, markings dis- 
tinct. Stellate veins stand out prominently; 
cortex thickened; markings distinct; show 
glomeruli and islands of haemorrhage, as pink- 
ish points. Mucous membrane of the pelvis 
injected. It is difficult with the naked eye to 
distinguish this kidney from its predecessor, 
because they merge imperceptibly into each 
other. 
Histology: (a) Epithelium: The epithe- 
lium is in about the same condition as in 
parenchymatous nephritis, swollen, granular, 
filling the tube, falling away from the base- 
ment membrane. In the tubes are casts, 
hyalin, granular, epithelial and blood. 
Vessels and connective tissue: A Malpi- 
ghian tuft fills the capsule, there may be an in- The Kidney. 
crease in the tuft cells. Islands of extravasated 
blood can be seen sometimes among the capil- 
laries of the tuft. The capsule is thickened 
by round cell proliferation, and this extends 
into the adjoining connective tissue. 
(b) Interlobular vessels: In formalin pre- 
pared specimens the arteries are dilated; is- 
lands of extravasated blood are found in the 
connective tissue and in the tubes. The walls 
and other connective tissue are thickened by 
round cells, leucocytes and connective tissue 
cells. The exuded plasma may be coagulated 
in the connective tissue, in which event the 
tissues give the homogeneous appearance of 
amyloid. The staining reactions differentiate 
them. 
Variations; If the process is violent there 
is a large exudatoin of red cells and the pro- 
cess is called haemorrhagic nephritis. 
In scarlet fever the poison spends its great- 
est force on the glomerulus and the disease 
is known as glomerular nephritis. The other 
tissues are involved as in diffuse nephritis. 
The maximum of intensity is found in the 
glomerulus. This variety is very prone to 
eventuate in chronic interstitial nephritis. 298 
Suppurative Nephritis. 
SUPPURATIVE NEPHRITIS. 
Two forms. Pysemic and pyelonephritic. 
PYvEMIC KIDNEY. 
Synonyms: Multiple abscess of the kidney; 
embolic abscess; miliary abscess. 
Etiology: Infection with some of the or- 
ganisms that produce pus, or that can produce 
pus in this locality, either as usually existing 
or as modified by circumstances. These in- 
clude streptococcus, staphylococcus, pneu- 
mococcus, bacillus coli communis, bacillus ty- 
phosus. 
Philosophy of the process: The route of 
infection is the blood current. The process 
is the destructive inflammation usual in ab- 
scess formation. In the area more remote, 
where the poison is dilute, we may have pro- 
ductive inflammation or cloudy swelling. The 
kidney is a frequent site because of its large 
blood supply, its double set of capillaries, and 
the tortuosity of the capillaries in the tuft. 
Not all abscesses are symptomatic, nor ne- 
cessarily fatal. 300 
.S'uppurativc Nephritis. 
Anatomy; The kidney is usually enlarged, 
pale and moist. The capsule strips easily. 
On cut section there is a varying pallor, in- 
terspread with multiple millet seed foci, red 
or white or yellow in color, and purulent. 
These are seldom larger than 2 mm. across. 
While they are sometimes round, they have a 
tendency to be elongated. They are located 
in the cortex. Some of these foci are recog- 
nizable as abscesses filled with pus. 
Histology: The foci show a central mass 
of pus corpuscles and around this a typical 
inflammation, some gradually merging into 
the surrounding tissue. In these areas the 
fixed elements, epithelium, connective tissue, 
etc., are degenerating, granular, fragmenting 
nuclei, etc. The areas of usual involvement 
are the tufts and the intertubular vessels. 
The tubules away from the zone of pus show 
pus casts and organisms. The cortical tubes 
show cloudy swelling. 
SUPPURATIVE PYELONEPHRITIS. 
Synonyms; Surgical kidney; pyelonephro- 
Etiology: Pus germs traveling from the 
urethra, bladder or ureter to the pelvis of the 
kidney, thence along the lymph spaces be- Sup par at ive Neph rit is. 
tween the uriniferous tubules to medulla, later 
to the cortex, rarely to the perinephritic tis- 
sue. 
Philosophy of the process: This is much 
the more frequent and the more important 
form of nephritis. The kidney may be con- 
verted into multilocular cysts, or by liquefac- 
tion of the capsule, extension externally may 
be produced. Pus germs can only travel 
through the capsule by liquefaction. The 
putrefaction in the urine causes deposits in 
the pelvis or ureter, and these calculi cause 
a persistence of the infection which other- 
wise the leucocytes might overcome. 
Anatomy; The kidney is large, red, moist, 
friable. It may be cystic. The capsule usu- 
ally strips off easily. On cut section strise 
and foci of abscess formation can be seen in 
the medulla extending sometimes to the cor- 
tex. The pelvis is dilated, with thick walls. 
The cavity is filled with pus. Calculi are not 
infrequent. The ureters are widely dilated, 
and with irregularly thickened walls. 
Histology; That of abscess formation; 
granulation tissue, and destruction of local 
tissues. Bands of extension can be seen be- 
tween the collecting tubes of the medullary 
pyramids. Chronic Nephritis. 
Chronic inflammation of the kidneys. We 
will study first the extreme type. 
CHRONIC INTERSTITIAL NEPHRITIS. 
Synonyms: Granular contracted kidney; 
cirrhosis of the kidney; sclerosis; small red 
kidney; gouty kidney; chronic indurative 
nephritis; arterio sclerotic kidney. 
Etiology: A mild irritation long continued, 
borne to the kidney by the vessels, and affect- 
ing the vessel wall and the perivascular con- 
nective tissue; chronic alcoholism, gout. 
Philosophy of the process: The process is 
the same as in cirrhosis of various other or- 
gans, e.g., liver, brain, cord. It is due to 
mild irritation from leucomaines or substances 
similar in the scale of toxicity. To the same 
class belong the lesions of age. In old age 
there is frequently more obliterating endar- 
teritis. Like cirrhosis elsewhere, the process 
is uneven in wedge-shaped masses in the kid- 
ney, in irregular bands in the liver, in dis- 
seminated plaques in multiple sclerosis of the 
cord or brain. The epithelium in the patches 
of sclerosis is compressed and angular and 
disappears from many tubules so as to show 
as an obliterated tube, but when examined 
microscopically is is found as much the Chronic Nephritis. 
healthiest epithelium in the kidney. Death 
in all cases ensues from some form of ter- 
minal infection, giving cloudy swelling of the 
epithelium between the tubes. The affection 
is of the vessel wall, and in consequence kid- 
ney functions are imperfectly performed. For 
this same reason the irritant that causes cloudy 
swelling of the epithelium of the normal tubes 
does not affect that of the compressed tube. 
Secondary atrophy of tubules after affec- 
tions of glomeruli. 
Anatomy: The kidney is very small, weigh- 
ing from one and a half to three ounces. The 
capsule is thick and laminated. The surface 
is very granular, leathery in appearance. In 
the aged this roughing is more irregular. 
When the capsule is torn off, it may split in 
layers, leaving a smooth surface behind, or 
else it tears off with difficulty, bringing with 
it pieces of kidney. On cut section multiple 
cortical cysts are seen, varying in size from a 
millet seed to a marble. The cyst walls are 
smooth. The contents are either clear water 
or colloid. The kidney “cuts” tough. The 
cortex is markedly thinned. The striations 
are obscured or not apparent. The arteries 
have thick, rigid walls.  Chronic Nephritis. 
308 
Histology: There wedge-shaped masses 
of fibrillated connective tissue, denser and less 
nucleated in the center than at the periphery. 
There are pin point holes, remnants of kidney 
tubes; other tubes that are larger contain sev- 
eral cells, showing multiple nuclei that are 
distinct, but in which the cell outlines cannot 
be differentiated. Others, and these comprise 
the bulk of the tubules, show a ring of epithe- 
lial cells staining distinctly. Some of the 
glomeruli are converted into a solid mass of 
connective tissue, and others show only a 
capsular thickening. The vessels in these 
central areas show as irregular clefts whose 
walls merge intimately into the surrounding 
connective tissue. At the periphery of these 
wedges there are embryonal cells, round and 
spindle. These areas, and especially the 
glomeruli, are frequently infiltrated with co- 
agulated plasma, giving the appearance of 
amyloid; this to be differentiated by special 
staining. Between these wedges the tubules 
are widely dilated, and the epithelium is in a 
state of cloudy swelling. In this area we not 
infrequently find foci of acute round cell infil- 
tration. Here the terminal infection has been 
with a pus germ. 
Variations. 310 
Chr aide Nephrit is. 
The large white kiclnev of chronic inflam- 
ination. 
It is difficult to write clearly of this sympo- 
sium of lesions, because there is no clear-cut 
line by which it can be subdivided, and it 
thus stretches by easy gradations from acute 
nephritis with increase in bulk, to the matur- 
ing lesions of chronic nephritis with a small 
kidney. 
Synonyms: Fatty kidney; chronic paren- 
chymatous nephritis; subacute Bright’s dis- 
ease; large mottled kidney. 
Etiology: Mild irritations, long continued, 
in which the epithelium is pathologically irri- 
tated. It may follow acute diffuse forms or 
glomerular nephritis. Generally it is found 
existent without any history of a beginning. 
Philosophy: Beginning as a diffuse nephri- 
tis, caused by an irritant that is pathological 
to kidney epithelium, it cannot, and does not, 
last long enough for the connective tissue to 
mature and develop either pressure effects or 
sufficient density to wholly prevent inter- 
change of nutrition elements. Much of its 
pathology is dependent upon the principle 
that a breaking down of highly differentiated 
elements is followed by an overgrowth of 
lowly differentiated connective tissue. Chronic Nephritis. 
Anatomy: Early stages—Kidney large, 
sometimes double the normal size. It is 
smooth; capsule slightly thickened and mod- 
erately adherent. The surface is pale and 
mottled with distinct stellate veins. Cut sur- 
face shows a thickened, pale, yellowish or 
reddish yellow cortex, mottled with islands 
of haemorrhage. 
Late stages-—The kidney is normal in size 
or mildly decreased. The capsule thickened 
and moderately adherent. The surface is 
mottled and irregular. There are depres- 
sions and elevations, but the granular appear- 
ance is nothing like so typical as in the 
variety called chronic interstitial nephritis. 
The kidney cuts tough; a few cortical cysts 
are found. The cortex is thinned; the mark- 
ings indistinct. 
Histology: a Epithelium; The epithelum 
is in a state of cloudy swelling, or loose in the 
tubules. In many of the tubes the epithelium 
is entirely gone. Casts of all kinds are found 
in the tubes. 
Vessels and connective tissue: In the 
glomeruli, and in the vessels making up the 
tube walls, there is an increase of connective 
tissue in spindles and fibers. It differs from 
the other variety, in that there is not the 314 
Tuberclllons Nephritis. 
same extensive blocking of everything by 
connective tissue and in the greater abun- 
dance of young connective tissue elements. 
TUBERCULOSIS OF THE KIDNEY. 
Two kinds: Miliary and tubercular pyelone- 
phritis. 
MILIARY TUBERCULOSIS. 
Philosophy of the process: That of miliary 
tubercle elsewhere. In this form of kidney 
tuberculosis there is a general miliary tuber- 
culosis, and in consequence the kidney shows 
cloudy swelling. Again, the patient does not 
long survive; hence the lesions are usually 
found in the round cell stage. 
Route of infection; Blood vessels. 
Anatomy: The kidney may be slightly in- 
creased in size and pale. Underneath the 
capsule and generally in the cortex or multi- 
ple millet seed, gray, gelatinous or yellow 
tubercles. 
Histology; The histology is that of a small 
tubercle in its round cell stage. Exception- 
ally there are giant cell systems. The tuber- 
cles are found along the interlobular arteries. 
Route of infection: Up the lymphatics of 
the lower urinary apparatus. 
TUBERCULAR PYELONEPHRITIS.  Tuberculous Nephritis. 
Philosophy: Attention is directed to the 
similarity in tuberculosis to infection with pus 
microbes. In this form of tuberculosis we 
find even distribution of the lesions rather 
than the nodular arrangement of the miliary 
tubercle. A similar appearance is seen in 
some cases of tubercular bronchitis. It is 
due to the attending pus infection. The 
nodules are joined together by masses of 
streptococcus, staphylococcus, or other germ 
inflammation. They then belong in the same 
category as phthisis, as distinguished from 
lung tuberculosis. 
Anatomy: Both kidneys are usually af- 
fected. The ureters are usually widely dilated 
and have thick walls. The pelvis of the kid- 
ney is dilated. We are apt to find pus in the 
pelvis. The kidney may be converted into 
one or multiple cysts. The pelvic mucosa is 
rather evenly thickened and whitish, or yel- 
lowish and dirty There are tubercular 
nodules, most prominent in the medulla, but 
found also in the cortex; calculi are found. 
Plistology: We find tubercular nodules in 
the pyramids between the tubules. There 
are giant cell systems more frequently than 
in miliary tubercle. The mucosa of the pel- 
vis is covered by lime deposits. Underneath 318 
Waxy Kidney. 
this are tubercular nodules and surrounding 
these diffuse, round cell infiltration. The 
epithelial covering cannot be demonstrated. 
Syphilis: The syphilitic granuloma shows 
a marked tendency to develop into gummata. 
WAXY KIDNEY. 
Synonyms: Amyloid; lardaceous. 
Etiology: Prolonged suppuration; phthisis 
with cavities; empyema; syphilis; leucocy-- 
thaemia; Addison's disease. 
Philosophy of the process: As elsewhere, 
it is an infiltration of the vessel walls with 
lardacein, which albumin coagulates there. 
If the albumin goes through into the tube and 
remains in solution, it reacts as albumin in 
the urine; that which coagulates in the tube 
gives a cast, that which coagulates in the 
tissue gives the lesion now described. 
Anatomy: The kidney is very much en- 
larged, up to twice its normal size. The 
capsule strips easily, leaving a smooth, 
brownish yellow surface, mottled with lighter 
areas. On section the cortex is thickened, 
and the glomeruli stand out as glistening 
masses. Thin sections cut with a Valentine 
knife show intertubular bands and glomeruli 
of translucent material. This, stained with 320 
Waxy Kidney. 
iodine, shows brown. The papillae are very 
pale. The boundary zone is deeper in color. 
Histology: Epithelium unaffected. 
Vessels and connective tissue: In the tufts 
in which the process is just beginning one or 
two of the capillary loops show as thick 
homogeneous bands, the nuclei showing dis- 
tinctly. In others the tuft is a mass of homo- 
geneous material, showing no structure but 
the nuclei. The capsule is infiltrated. The 
epithelium of the tubes rests on a thickened 
basement membrane. This epithelium is 
granular and falls away. The change is very 
marked in the arteriae rectae near the tip of 
the pyramid. Staining reaction with iodine 
and sulphuric acid; with methylanilin violet 
and oxalic acid. 
Pyonephrosis. In this condition there is 
suppuration of the pelvis with dilatation. 
Plydronephrosis. This is a dilatation of 
the pelvis with urine. 
Cystic Kidney. This is a congenital affec- 
tion in which the kidney (usually both) is 
converted into a mass of cysts of compara- 
tively uniform size. No stoppage of the 
ureter is discoverable. It is sometimes diffi- 
cult to diagnose any kidney stroma with the 322 
Cystic Kidney. 
unaided eye. Microscopically we find the 
septa composed of kidney stroma. 
Cysts of the kidney and hydronephrosis are 
due to obstruction somewhere between the 
glomerulus and the glans penis. The more 
frequent causes are stricture of the urethra, 
calculus, enlarged prostate, cystitis, malfor- 
mations of the bladder, pelvic tumors, stric- 
ture of the ureter, organic, or due to bending 
or kinking, tumors, chronic interstitial ne- 
phritis, suppuration of the pelvis. The kidney 
may be converted into one large somewhat 
kidney shaped cyst, or into any number ot 
smaller cysts. 
Movable kidney is frequently movable be- 
hind the peritoneum. A floating kidney has 
grown into the peritoneum, gaining a mesen- 
tery. 
Tumors: The kidney is the seat of malig- 
nant growths much more frequently than it is 
of nonmalignant growths. It can be assumed 
that any tumor of appreciable size is malig- 
nant. It is subject to both sarcomata and 
carcinomata. 
GONORRHCEAL URETHRITIS. 
Etiology: Gonococcus, not infrequently 
associated with other pus cocci. Stricture. 
Philosophy of the process: This organism 
is essentially an epithelial organism. Its 
toxin absorbs, producing some inflammatory 
reaction in the lymph channels in which it 
travels, and also general toxaemia. When 
strictures result, there is probably secondary 
infection of the submucosa with other germs. 
It is prone to wander into the crypts of 
glands, and there lose its virulency, some- 
times to regain it on proper occasion, some- 
times never. 
Anatomy: The membrane is covered by 
yellow pus; it is red, moist, swollen. There 
is some injection of the corpora and of the 
glans. 
Histology; The surface layers of epithe- 
lium are irregular in shape, falling away. The 
deep layers are actively dividing. Along the 
lymphatics and capillaries of the submucosa.. 
there is mild round cell infiltration. 
STRICTURE. 
Philosophy of the process: Maturing in- 
flammatory connective tissue in the sub- 
mucosa. 
Etiology: Gonorrhoea; trauma. 
Histology: Bands of fibrillated connective 
tissue encircle the lumen, decreasing it. The 326 
Syphilis. 
epithelial covering may be normal; it may be 
thickened with irregular cells; it may be ab- 
sent. 
Epispadias: A malformation in which the 
urethra opens on the top of the penis, back 
of the glans. 
Hypospadias: A malformation in which 
the urethra opens under the penis, back of 
the glans. 
SYPHILIS. 
The lesions of syphilis are divided into 
three groups; 
I. Primary—chancres, mucous patches. 
2. Secondary—the roseola, skin eruption. 
3. Tertiary—granulomata, similar to tuber- 
culosis, actinomycosis and sarcoma. 
CHANCRE. 
I. Primary. 
Synonyms: Chancre, mucous patches. 
Etiology: A specific organism, not yet de- 
termined; the Lustgarten bacillus is not ac- 
cepted. 
Philosophy of the process; It is a granu- 
loma, a productive inflammation, nonexuda- 
tive in character. Destruction and ulceration 
is secondary. 
. Anatomy: The sore is indurated with a 328 
Syphilis. 
hard, raised edge. It is “punched out;” is 
pyramidal in shape with its base at the skin 
surface. 
Histology; The more superficial layers of 
the corium are proliferating actively. The 
blood vessels are moderately distended with 
blood. There is inflammation in the vessel 
wall. 
2. Secondary. 
The erythemas— 
Philosophy of the process: The lesions arc 
those of toxaemia, and give the same anatomy 
and histology, varying in degree only, as 
other toxaemias, such as fish poisoning, 
measles, scarlet fever. 
3. Tertiary. 
Philosophy of the process; A granuloma 
as in tubercle, sarcoma, actinomycosis. The 
spindle cells have little tendency to mature 
into fibers. There is a great tendency to 
some of the forms of death, simple necrosis, 
formation of fat, caseation. There is less dis- 
position to secondary infection with pus 
germs than in tuberculosis. There is a 
greater prominence of arteritis. This in some 
measure accounts for the prominence of the 
various forms of death. Diseases of the Bladder. 
DISEASES OF THE BLADDER. 
ACUTE CYSTITIS. 
Etiology: Due to pus germs, to gonococ- 
cus, or to milder irritants. Presents no 
points of peculiarity marking it from other 
acute inflammations of mucous structures. 
Hypertrophy follows dilatation of the 
bladder. 
CHRONIC CYSTITIS. 
Differs in no particular from chronic in- 
flammations in other mucous membranes. In 
this connection see inflammation of the 
stomach. 
There is the great tendency to irregularity 
of the mucosa in places resulting in polypoid 
growths, always the tendency in a mucosa 
which is bathed in moisture, and is chronic- 
ally inflamed. The urine is acid until after 
infection with the micrococcus urese takes 
place, when ammonia is produced. This con- 
tinues the irritation in two ways. In the first 
place it is in itself an irritant; in the second 
place it causes a deposit of triple phosphates. 
The most frequent cause is infection through 
the urethra; the second, enlarged prostate. Diseases of the Bladder. 
The bladder is found dilated, sometimes 
with thin walls, but generally with walls im- 
mensely thickened. 
All suppurative inflammation back of com- 
pressor urethrae drains into the bladder. 
TUBERCULOSIS IN THE BLADDER. 
May be a result of infection from the kid- 
ney. It generally involves the base. Very 
frequently the seminal vesicles are involved. 
Early involvement of the epididymis and tes- 
ticle may ensue. The sequence of involve- 
ment may be reversed. The lesion is mixed; 
the tubercular nodules are imbedded in a 
mass of diffuse granulation tissue, due to the 
other germs. Ulceration is early and marked. 
In this it shows resemblance to tubercular 
pyelo-nephritis, bronchitis and phthisis pul- 
monalis. 
TESTICLE. 
The testicle is subject to malformation, 
malposition, errors in development of the in- 
vesting membrane, acute and chronic inflam- 
mations and tumors. 
ACUTE INFLAMMATIONS. 
Acute orchitis may exist without epididy- 
mitis, epididymitis without orchitis, or they 
may exist conjointly. 334 
Diseases of the Bladder. 
Etiology: Gonorrhoea, smallpox, mumps, 
trauma. 
Philosophy of the process: Gonorrhoeal in- 
flammation tends to limit itself to the epithe- 
lium of the tubule. In consequence there is 
parenchymatous orchitis and subsidence of 
the disease without permanent pathology. 
The orchitis of smallpox and of mumps in- 
volves the interstitial tissue, and there is far 
greater tendency to interstitial overgrowth 
and consequent atrophy. In trauma there are 
all grades of injury and all shades of re- 
sults; abscess formation is due to pus germs 
and is rather unusual except in severe trauma 
with infection, and in tuberculosis. 
Anatomy; The testicle is enlarged, the 
tunica tense. On section the parenchyma 
rolls out of its envelope and the tunic side 
becomes concave. The vessels of the vagi- 
nalis are congested; the membrane oedema- 
tons. 
Histology: The tube is filled with swollen 
granular epithelial cells. In some cases the 
interstitial tissue is filled with round cells 
also. Blood vessels dilated; much oedema of 
interstitial tissue. 
'Sequelae: Gonorrhoeal, usually none. 
Many cases of mumps, and some cases of Diseases of the Testicle 
trauma and gonorrhoea are followed by 
atrophy. 
TUBERCULAR TESTICLE. 
Route of infection: Generally along the 
spermatic cord and down the tubes; rarely 
by way of the vessels. 
Anatomy: The testicle is enlarged; the 
epididymis generally participates in the proc- 
ess; most frequently one testicle is involved. 
On section, scattered tubercular nodules in 
varying stages, abscess cavities, cheesy zones, 
yellow nodes, small gray gelatinous miliary 
points. 
Histology: That of tubercle with a large 
amount of simple inflammation diffusely scat- 
tered. 
Sequelae: The abscesses are liable to per- 
forate both albuginea and vaginalis, and, in- 
fecting the scrotum, make a persistent sinus. 
It is very liable to cause a general tubercular 
infection. 
SYPHILIS. 
Origin: The disease may be acquired or 
inherited. In acquired syphilis gummata 
and necrosis forms are more prominent. 
In inherited syphilis diffuse sclerosis and 
atrophic phenomena predominate. Diseases of the Testicle. 
Anatomy: The scrotum is frequently joined 
to the testicle by close connective tissue in- 
vestment. Both albuginea and vaginalis are 
greatly thickened. Some degree of hydro- 
cele is the rule. The mediastinal bands are 
thickened; there are usually multiple gum- 
mata. These grow by preference from the pe- 
riphery into the interior. The larger masses 
are cheesy or purulent; they may open ex- 
ternally. 
Histology: Bands of connective tissue, 
old and fibrillated, enclose tubules. Some of 
these tubules are of small caliber and free 
from epithelium. The vessels have thick- 
ened walls. The gumma is a mass of round 
and spindle cell granulation tissue. This is 
oftentimes a mass of granular debris 
TUMORS. 
Sarcoma: Generally round and spindle 
cells, and markedly malignant. Cysto-sar- 
coma are frequent. 
Carcinoma: A great preponderance of 
medullary carcinoma. This may in part be 
accounted for by the fact that the testicle is 
almost a purely epithelial structure. Its con- 
nective tissue is normally inconsiderable in 
amount. 340 
Diseases of the Testicle 
Chondroma, fibroma, cysts, retention cysts, 
dermoid cysts are found. 
Hydrocele, or water in the tunica, is fre- 
quent. It is of three varieties: 
i. Congenital hydrocele, in which the con- 
nection between the tunica vaginalis and the 
peritoneal cavity remains patulous and the 
cavity fills up with peritoneal fluid. 
2. Hydrocele proper, in which the connec- 
tion is obliterated and there is an exudation 
cyst in the vaginalis proper. It is situated 
anterior to the testicle. 
3. Hydrocele of the cord, in which an 
island of the peritoneum remains at some 
point along the vas deferens. The connec- 
tion with the peritoneum is obliterated, also 
that with the tunica vaginalis. It is above 
the testicle. 
Varicocele. Cirsoid aneurism of the sper 
matic veins. It exists by reason of two fac 
tors: 
1. Frequent congestion of the testicle. 
2. The unsupported condition of the veins. 342 
Diseases of' the Female Genital Organs. 
DISEASES OF THE FEMALE GENITAL 
ORGANS. 
POINTS IN HISTOLOGY AND DEVELOP- 
MENT. 
From the uro-genital eminence develops 
the ovary proper. In the vicinity of this 
develops the Wolffian body. In the Wolffian 
body the Wolffian duct and Mueller's duct 
develop as parallel tubes. The Wolffian 
body develops into the broad ligaments; the 
Wolffian ducts develop into Gartner’s duct, 
Rosenmueller s ducts and Kobelt’s tubes. 
Mueller’s ducts develop into the vagina, the 
uterus, the Fallopian tubes. The lower end 
of the Wolffian ducts and Mueller’s ducts 
empty into the allantois. As this hind gut 
grows toward the surface, the epiblast begins 
to dent in. Then the two blind sacs coalesce, 
septa grow down, making separate openings, 
and the urethra, vagina and rectum are at 
hand. 
Malformations: By reason of failure of 
some of these steps, we sometimes have im- 
perforate vagina, vesico-vaginal fistula, recto- 344 
Diseases of the Female Genital Organs. 
vaginal fistula, vesicocele, rectocele, double 
vagina, double uterus, single Fallopian tube. 
Histology: The vulva, vagina and cervix 
uteri are musculo-fibrous tubes, covered by 
squamous epithelium. The vulva has race- 
mose glands. The uterus has a very well 
developed muscular coat, a lymphoid mucosa 
without submucosa or muscularis mucosa, 
and long cylindrical glands. The mucosa of 
the Fallopian tube is thrown into branching- 
folds, covered by cylindrical epithelium. The 
Fallopian tube opens into the peritoneal cav- 
ity at its outer end. 
The lesions of the uterus are, the deform- 
ities already mentioned, inflammations, de- 
generations and tumor growths. We some- 
times have inflammation limited to the 
mucous layer, endometritis; inflammation of 
the several layers, metritis; inflammation of 
the peritoneal covering, perimetritis; inflam- 
mation of the connective tissues adjoining 
the uterus other than the peritoneum, para- 
metritis. 
ACUTE METRITIS. 
Synonyms; Puerperal fever; gangrenous 
endometritis. 
Etiology: Some of the pus germs infecting Diseases of the Female Genital Organs. 
the uterus, either through tears in the cervix 
or elsewhere, or at the placental site. 
Philosophy of the process: We can have 
infection through perineal tears; the route of 
infection here is through the inguinal lym- 
phatics, for the vulva and the lower third of 
the vagina drain through the inguinal glands. 
Infection of the body through uterine tears 
spreads by the lymphatics, by the veins, and 
along the Fallopian tubes; the lymphatics of 
the vagina and the cervix drain to the hypo- 
gastric glands; the body of the uterus drains 
to the lumbar glands. Death may ensue 
from acute toxaemia without any lesion in 
other organs. We may have a slowly ex- 
tending thrombus, giving phlegmasia alba 
dolens. We may have suppurative peritoni- 
tis, or pyaemia with multiple abscesses. 
Anatomy: The uterus is enlarged, swollen, 
red, moist. The mucosa is thickened and 
injected. At the points infected there are 
large irregular ulcers, with ragged edges and 
yellow or black bottoms. Sometimes the 
veins leading from the uterus are thrombosed. 
Histology: That of acute suppurative in- 
flammation. The venous channels are filled 
with thrombi, and around these thrombi are 
the aggregations of round cells. The highly  Diseases of the Female Genital Organs. 
specialized elements are in cloudy swelling 
and mucous degeneration. 
Synonyms: Uterine catarrh; leucorrhoea; 
ulceration; erosion of the cervix; fungus en- 
dometritis; adenomatous endometritis; be- 
nign adenoma. 
CHRONIC ENDOMETRITIS. 
Etiology; There are two factors in the 
etiology of this affection, and the differences 
in these two factors are responsible for the 
wide variances in the disease. The first of 
these are infecting organisms; the second— 
changes in the host, by reason of which these 
infections become possible. 
First factor: Gonococcus, streptococcus, 
staphylococcus, saprophytes, tubercle bacil- 
lus. These organisms either are in them- 
selves milder than in the acute variety, or 
else there is a certain amount of acquired im- 
munity. 
Second factor; Subinvolution; ovarian dis- 
ease; marked flexions; foetal remains. 
Philosophy of the process: It is never an 
endometritis, properly speaking, because 
there is no muscularis mucosa separating the 
mucosa from the uterine muscle. The veins, 
capillaries and lymphatics are continuous be- 350 
Diseases of the Female Genital Organs. 
tween the layers. The endometrium is simply 
the seat of most marked inflammatory re- 
action. There is the usual piling up of lymph 
tissue. The irritated glands may do one of 
several things—some may undergo degenera- 
tion, and their epithelium becomes typical, 
mucus secreting epithelium; some become 
occluded and form cysts—such are the ovules 
of Naboth ; some of the irrigated glands make 
new granular tissue. This process is the same 
as the formation of new tubes in cirrhosis of 
the liver, in ordinary adenoma, or in the ade- 
noma due to coccidia; to this class belong 
endometritis fungosa, hyperplastic endome- 
tritis, adenomatous endometritis. Coincident 
with this development of tissue, there is nec- 
essarily a development of thin capillary ves- 
sels. There is the usual tendency of chron- 
ically inflamed mucous membrane, kept moist 
to form polypi. 
Anatomy: The uterus is enlarged, red, gen- 
erally moist, and soft. Patches of red extend 
from the cervix over the vaginal aspect. From 
the cervix pours glairy muco-pus. On cut 
surface the mucous membrane is greatly and 
irregularly thickened and injected. The 
mouths of the glands can be seen. In the 
mucosa, and in the deeper structures, some 352 
Diseases of the Female Genital Organs. 
of these glands show as cysts as large as a 
pea, filled with thick mucus. 
Histology: The apparent ulcers on the 
surface are wavy papillae of spindle cells, 
covered by a single layer of columnar epithe- 
lial cells. The mucosa consists of round cells, 
imbedded in which are glands—some dilated, 
some normal in size. In older cases, between 
the gland tubes there are bands of old con- 
nective tissue. The findings vary so much in 
different sets of cases that an accurate de- 
scription cannot be made to fit any number of 
consecutive cases. 
TUBERCULOSIS. 
The usual route of infection is via the 
vagina. It may come from fistula in ano, 
tubercular in origin. 
Anatomy; The tubercles are found more 
frequently in the body of the uterus than in 
the cervix. The tubercles are along lymph 
channels in the deeper layers of the mucosa 
and in the muscular walls, the latter being 
the more frequent site. They ulcerate and 
discharge on the surface, giving irregular 
tubercular ulcers. They spread easily to the 
Fallopian tubes, ovaries, bladder, peritoneum, 
and later may become general.  Diseases of the Female Genital Organs. 
SUBINVOLUTION. 
Incomplete degeneration of the added ele- 
ments of the uterus, after pregnancy and 
menstruation. It is accompanied by a growth 
of connective tissue and a chronic venous 
congestion. 
Polypus: A growth consisting of mucosa, 
uterine glands and blood vessels and covered 
by cylindrical epithelium. It springs from the 
mucosa exclusively. It is irsually water 
soaked. It is usually pedunculated. It may 
be smooth or eroded or villous. It generally 
springs from near the cervix. 
TUMORS. 
ITBROMYOMA. 
Three varieties—according to location: 
(i) Submucous, usually single, nonpedun- 
culated, covered by areas of chronic endome- 
tritis. 
(2) Intramural, imbedded in the uterine 
wall. 
(3) Subperitoneal, usually multiple, globu- 
lar, pedunculated. They sometimes become 
separated from the uterus. 
These tumors grow to enormous size, or 
are present in large number. 
Histology: There are bands of nonstriated 
muscle, and fibrous tissue, running in every 356 
Diseases of the Female Genital Organs. 
direction. They contain vessels with thick, 
rigid walls. 
Degenerations: They are prone to cystic 
degeneration, when they may be converted 
into a single irregular large cyst; to calcare- 
ous degeneration; to infection, giving suppu- 
ration and sloughing; to ulceration, giving 
abundant haemorrhage. 
CARCINOMA 
May be of two varieties: (i) Carcinoma 
of the body, belonging to the class of cylin- 
drical celled carcinomas. It rapidly passes to 
the Fallopian tube, or lumbar glands, or be- 
comes general. (2) Of the cervix. This is 
squamous. The cervix may be hard and ul- 
cerated, or it may be covered by fungous vil- 
losities. It is enlarged and hard and injected. 
The growth spreads to the vagina, the hypo- 
gastric glands, the uterine body, the neigh- 
boring organs. 
SARCOMA. 
Sarcoma of th£ vaginal portion gives a 
uterus that is enlarged and covered with a 
warty, villous growth. Microscopically, these 
villi are seen to be composed of spindle cells, 
covered by a single regular layer of epithelial 358 
Diseases of the Female Genital Organs. 
cells, columnar in type. In the body the sar- 
coma again has a tendency to a papillary sur- 
face structure. It is generally round celled 
in type. The cells grow from the mucosa and 
from fibrous tissue and from the muscle fibers 
of the uterine body. 
A form of sarcoma, called deciduoma ma- 
lignum, is found. In this the point of infec- 
tion is the placental site. It occurs soon after 
labor when the uterus is still under the influ- 
ences of the parturient state. There are pres- 
ent large decidual cells. 
FALLOPIAN TUBES. 
The arrangement of the epithelium of the 
tube gives a large amount of epithelial sur- 
face in a very small lumen. In consequence, 
there is frequent organic stricturing. Again, 
this long, delicate tube develops from one 
center, while- its peritoneal covering develops 
from another. In consequence, the tube fre- 
quently kinks so as to form an occlusion of 
the tube. Again, this peritoneal covering is 
prone to adhesions, which furnish another 
source of stricturing. 
SALPINGITIS. 
Etiology: Streptococcus, gonococcus, sta- 
phylococcus, and other pus germs. These 360 
Diseases of the Female Genital Organs. 
germs spread from the uterus along the 
mucosa to the tubal mucosa (usual with gon- 
ococcus), or along the lymphatics from the 
lower regions. Stricturing with cystic 
mulations forms a focus, inviting infection; 
abortion and miscarriage are the most fre- 
quent causes of infection. 
Anatomy: There is considerable variation 
in the appearance of the tube, dependent upon 
the dififering conditions bringing them about. 
It is tortuous; sometimes widely dilated, 
pear shaped and bound by surrounding ad- 
hesions. On cutting, sometimes clear water 
is found, sometimes pus, sometimes bloody 
water; sometimes the lumen is obliterated 
by a thick fibrous stricture; sometimes on 
straightening the tube, pus or serum can be 
squeezed into the uterus. The fimbriated 
end is almost always occluded. The wall is 
sometimes greatly thickened. This is due to 
an enormous overgrowth of circularly ar- 
ranged, dense connective tissue. Sometimes 
the tubes are two inches in diameter. The 
thickening of fibrous tissue may be nodular. 
Pyosalpinx is where the tubes are dilated 
by pus. 
Hydrosalpinx is where the tubes are filled 
with albuminous water, derived either from 
the epithelium, or degenerated blood. 362 
Diseases of the Female Genital Organs. 
Infection of the peritoneum from suppu- 
rating tubes is habitual, until inflammation 
closes the fimbriated extremity. 
Tuberculosis is frequent in the tube. It is 
found usually at the outer end as rather dif- 
fused tuberculosis of the submucous and 
muscular coats and neighboring broad liga- 
ment. It quickly infects the uterus, ovaries, 
and peritoneum. 
The hydatid of Morgagni is a small reten- 
tion cyst, hanging by a pedicle to the fim- 
briated extremity of the tube. 
OVARIES. 
Abscess of the ovary. 
Acute inflammation of the ovary, other than 
suppurative in character, is seldom se£n. The 
route of infection is along the tubes, either 
by the lymph channels, or by the mucous 
surface. 
Synonyms: Chronic interstitial oophoritis; 
cystic ovary. 
CIRRHOSIS OF THE OVARY. 
Anatomy: The surface of the ovary is very 
irregular. It is sometimes somewhat en- 
larged, sometimes it is small and corrugated. 
Multiple small cysts project from the surface.  Diseases of the Female Genital Organs. 
It “cuts” tough. There are variously arranged 
bauds of fibrous tissue, running in every di- 
rection. These enclose ovarian stroma, and 
in this stroma are cysts filled with clear fluid. 
These cysts are dilated or dropsical Graafian 
follicles. 
Histology: There is little to be seen, save 
dense bands of fibrous tissue. Some of the 
follicles are cystic, while others are com- 
pressed and undergoing pressure atrophy. 
TUMORS. 
Cysts: The simplest cyst of the ovary is 
the dropsy of the follicles already mentioned. 
These are small and multiple. 
OVARIAN CYSTS. 
These are secretion cysts. The secretion 
is into the lumen of a previously formed 
adenoma. The cysts are always multiple to 
begin with. As they grow usually one cyst 
overshadows the others, so that we have an 
unilocular cyst. They attain very large size. 
The fluid may be mucus, serum, blood, etc. 
Histology: Wall; young cyst, there is a 
fibrous tissue coat lined by columnar epithe- 
lium. Wall; old cyst, there is a fibrous tis- 
sue wall, in places thin, in places thickened. 
There is a varying amount of deposit of 366 
Diseases of the Female Genital Organs. 
fibrin on the inner surface of the wall. The 
epithelium is irregular in shape or amount or 
absent entirely. 
PAPILLARY CYST ADENOMA. 
A secretion cyst, developing in a previously 
developed adenoma. In this type there is a 
villous growth from the wall into the cyst 
cavity. After this arborization, covered by 
epithelium, has filled the cavity, it pushes its 
way through the wall opposite to that from 
which it springs, and appears on the surface 
of the ovary as irregular warts. These are 
easily detached. On whatever structure they 
fall they are prone to locate, and grow, giving- 
villous tumors. They spring usually, though 
not always, from the hilum of the ovary, the 
epoophoron, and grow into the ovarian struc- 
ture. 
Secondarily—These tumors cover the peri- 
toneum, omentum, liver. 
Fibroma, myoma, chondroma, carcinoma 
and sarcoma are found in the ovary. 
The ovary is a favorite site of dermoids. 
CYSTS OF THE BROAD LIGAMENT. 
(Refer to embryology notes.) 
Synonym: Parovarian cysts. 368 
Diseases of the Female Genital Organs. 
Philosophy of the process: There may be 
a retention cyst in Gartner’s duct. This may 
show in the walls of the vagina or uterus. The 
usual broad ligament cyst is in one of Rosen- 
mueller’s tubes. These run from the hilum 
of the ovary to Gartner’s duct. These cysts 
may be multiple or single, and occasionally 
are of large size. They have no pedicle. They 
are filled with a clear fluid. There are a few 
small tubes tributary to Gartner's ducts that 
do not run toward the ovarian hilum. These 
are Kobelt’s tubes. They are the seat of small 
retention cysts, with long pedicles. 370 
The Nervous System. 
THE NERVOUS SYSTEM. 
POINTS IN HISTOLOGY. 
The unit of the nervous system is the 
neuron. A neuron is a nerve cell with all its 
prolongations, both its axis cylinder and its 
shorter protoplasmic prolongations. The 
nerve fiber does not run direct into a second 
nerve cell, but encloses it in a basketwork of 
fine filaments. 
The dura is a dense connective tissue layer. 
While it encloses large vessels it contains 
few vessels and few lymphatics. The pia is 
rich in blood vessels and in lymph spaces. 
Its vessels, lymphatics and connective tissue 
filaments run into the substance of the nerv- 
ous tissues. 
The vessels supplying the cortex are small 
in size and anastomose freely. The basal ves- 
sels are larger and do not have arterial anas- 
tomosis beyond the circle of Willis. It is well 
to bear in mind also that the basal areas be- 
long to two classes, first, commissual, second, 
ganglionic presiding over coordination and 
the vital processes. 372 
The Nervous System. 
The meninges are subject to acute and 
chronic inflammation and tumor growths. 
By reason of the different blood and lymph 
connections we have inflammations of the 
dura without pial involvement and vice versa. 
Acute pachymeningitis. 
Etiology: Sepsis, originating from injury 
to the scalp or skull, disease of the middle ear, 
infection from the venous sinuses. 
Philosophy: There is more or less lymph 
connection with the cranial bones and through 
them into the neighboring cavities. It is pos- 
sible to have an infection of the outer side of 
the dura without extension to its inner sur- 
face. 
Anatomy: That of acute suppurative in- 
flammation in the pleura, pericardium, etc., 
except that extravasation of blood is more 
prominent. 
Pachymeningitis interna hsemorrhagica is 
a chronic inflammation with an abundant 
formation of granulation tissue. It corre- 
sponds to chronic pleurisy. 
Leptomeningitis: Inflammation of the pia 
and arachnoid. 
Varieties: Epidemic cerebro-spinal men- 
ingitis; suppurative meningitis. 
Suppurative leptomeningitis. 374 
The Nervous System. 
Philosophy: The acute inflammations of 
the pia are productive, exudative in type, and 
are usually suppurative. There is a lack of 
relation between the post-mortem findings 
and the symptoms that is more marked in 
meningitis than in any other affection. This 
for two reasons: Firstly, the classical symp- 
toms of meningitis are the results of cere- 
britis. Secondly, the toxins are found fresh 
and concentrated in the areas presiding over 
vital phenomena. 
Etiology: Suppuration, i. Neighboring, 
the middle ear, orbit, nose, scalp. 2. Dis- 
tant, e.g., empyema. In the epidemic variety 
the pneumococcus has been found most fre- 
quently. 
Anatomy; The effusion is more frecpient at 
the base, where it tends to accumulate under 
the cerebellum around the pons in front to 
the longitudinal sinus and laterally into the 
Sylvian fissures. The ventricles may be filled. 
The effusion into the ventricles frequently 
exists without involvement of the base and 
vice versa. There is the same lack of con- 
nection with the convexity. The remaining 
anatomy and the histology are the same as in 
typical suppurative inflammation in serous 
structures. 376 
The Nervous System. 
Philosophy: This is a disease of child' 
hood. It is nearly always located in the pia. 
It is a blood vessel infection. It is found 
nearly always at the base. Along the Syl- 
vian artery and its branches, the surface of 
pons and bottom of the cerebellum are the 
areas of selection. Dural tuberculosis and 
occasionally pial tuberculosis may arise from 
bacilli in the skin, nose or eye, being trans- 
ported by lymphatics. 
Tubercular meningitis. 
Anatomy: The distribution of the nodules 
along the arterioles and venules of the base 
has already been outlined. There is exten- 
sive effusion into the great lymph space of 
the base and into the ventricles. This is 
largely a passive transudation due to oblit- 
erating lesions in vessels. This is sometimes 
so considerable as to be termed acute hydro- 
cephalus. The possibility of secondary infec- 
tion and its changes are to be remembered. 
Histology: The lesions are generally of the 
round cell type. Reticular tissue and giant 
cell formation is exceptional. The small 
nodules of endothelial cells may be due to 
proliferation of the cells of the intima, of the 
adventitia or of all the coats. 
Syphilis. 378 
The Nervous System. 
Philosophy: It is usually a dural disease. 
It is most frequently in the shape of a solitary 
gumma. From pressure the cranial bones 
become porous and disappear in the areas of 
pressure. If the syphilitic lesion begins on 
the inner surface of the dura, it projects into 
the brain area, flattening the substance. A 
gumma primary in the brain substance is 
rare. 
The histology of gumma has already been 
studied. 
Hydrocephalus: May be congenital or ac- 
quired. 
Congenital hydrocephalus. 
Anatomy; The ventricles are widely di- 
lated and filled with clear fluid. The brain 
substance is thin, compressed and with only 
rudimentary convolutions. The cranial bones 
of the vertex are thin. The sutures and 
fontanelles are so wide that the cranium 
bulges, giving the appearance of overhanging 
the face and neck. 
THE CEREBRUM. 
It is well to study the cerebrum as com- 
posed of parenchyma (the brain cells and 
those portions of the cells called fibers) and 
interstitial tissue. 380 
The Nervous System. 
The Parenchyma: Our known technical 
methods are of very little service in showing 
affections of the cells of the nervous system. 
We know of fatty degeneration, and vacuola- 
tion of the nucleus. We are not able to sat- 
isfactorily distinguish cloudy swelling or the 
phenomena of productive inflammation in the 
parenchyma. That they exist is beyond 
doubt. A perverted chemistry in a nerve 
cell will give expression to a symptom far 
more promptly than in any other structures. 
ACUTE DIFFUSE INFLAMMATORY PHE- 
NOMENA. 
Histology: The nerve cells are rounded in 
shape. Their nuclei may be vacuolated; 
there is a diminution in the number of pro- 
toplasmic processes which can be demon- 
strated; the fibrous prolongations are swollen, 
making globular colloid looking bodies. The 
neuroglia and pial connective tissues are pro- 
liferating. 
Abscess of the brain 
Two Varieties. 
i. Pysemic abscess. 
Etiology: Infection with some of the pus 
germs through the circulation. 
Anatomy: These abscesses are multiple, 382 
The Nervous System. 
of small size, and death ensues before there 
is evidence of more than slight pus formation. 
Second Variety: In this the infection is 
from without through lymph connections or 
lymph connections in greatest part. 
Etiology: The most frequent cause is 
suppuration of the middle ear; then in about 
the following order, trauma, suppuration in 
the nose, orbit, scalp—unknown. 
Anatomy; Generally speaking, there is a 
single large abscess with green or gray pus 
and a ragged soft wall in the vicinity of the 
point of infection. In cases of trauma with- 
out fracture, and in some cases of otitis media 
the abscess is some distance away from the 
surface and the point of infection and no 
route of infection can be demonstrated. 
INTERSTITIAL TISSUE. 
The interstitial tissue is of two types. The 
neuroglia tissue derived from the epiblast, the 
ordinary connective tissue derived through 
the pia from the mesoblast. This includes 
the vascular and lymph vessel supply. 
Scleroses. 
Varieties: Diffuse; multiple. 
Diffuse. In old people there is an over- 
growth of connective tissue that is diffused 384 
The Nervous System. 
throughout. The convolutions are flattened; 
the membranes are thickened. The attach- 
ment of the dura to the calvarium is more 
close than normal. There are isolated cases 
in people other than the aged. 
Multiple Sclerosis: 
Philosophy: The process is the same as 
sclerosis in other organs. What determines 
the location other than its arrangement with 
regard to blood vessels is as unknown here as 
elsewhere. It is subject to the same serous 
infiltration and to colloid or mucoid degener- 
ation. 
Anatomy: Irregularly placed in the brain 
and cord are irregularly shaped patches that 
are gray in color. They are sometimes hard 
and sometimes soft, waxy and translucent. 
They blend insensibly into the surrounding 
tissue. They are not raised above the sur- 
face, but rather depressed. 
Histology: That of cirrhosis. Bands of 
fibrous tissue enclosing atrophying, degen- 
erating nerve elements. 
Disease of the vessels. 
Apoplexy: Haemorrhage into the brain as 
a result of rupture of a vessel. 
Etiology: There is always disease of the 
arteries; atheroma or miliary aneurism. 
Philosophy: The effects are divided into 386 
The Nervous System. 
primary and secondary. Both depend in 
great measure upon the areas into which the 
effusion takes place. The secondary effects 
depend upon the fact that the nerve fiber is a 
part of the nerve cell, and any part of a cell 
separated from its nucleus dies. If the cell 
is in the cortex the areas of secondary death 
are below the injury. If the cells are in the 
medulla or pons, etc., the areas of secondary 
death are above. These are called respect- 
ively descending degeneration and ascending 
degeneration. 
The fifst effect is an outpouring of blood 
proceeding until clotting stops the vessel, or 
until external pressure equals internal. The 
area of haemorrhage breaks down into granu- 
lar debris. At the periphery, where there is 
blood supply intact, there is reactive inflam- 
mation. This may build up a cyst wall and 
liquefaction proceeding in the center a cyst 
may result. The surrounding fibrous tissue 
and vessels may grow into the clot organiz- 
ing it and giving an area of sclerosis. The 
waters of the area may absorb and leave a 
caseated mass behind. 
Descending degeneration: When the nerve 
fiber is separated from its nucleus it dies 
throughout its length. To illustrate: A The Nervous System. 
haemorrhage into the internal capsule would 
give degeneration of the crusta of the crura, 
anterior pyramids of the pons and the 
medulla, the direct and crossed pyramidal 
tracts in the cord, to the anterior horns. Here 
they form a plexus around the motor cells and 
end. Therefore degeneration ends. 
The histological phenomena are; Forma- 
tion of colloid masses in the axis cylinder 
processes, globular aggregations of fats in 
the white substance of Schwann, overgrowth 
of connective tissue, converting the area into 
a fibrous patch. 
Thrombus: A clot in situ. This forms 
more frequently in the carotid artery. 
Embolus. 
Etiology; A clot or vegetation from some 
larger vessel. It may be composed of fat 
in lipsemia, or of other foreign matter. It 
may be infected. 
Philosophy: The vessel generally occluded 
is the middle cerebral, because it gives a 
nearly straight course from the heart. As 
this vessel is a terminal artery, the area sup- 
plied by it undergoes starvation necrosis. 
Whether the area is to be pale or red depends 
upon principles already discussed. Its anat- 
omy, histology and secondary degenerations 
are similar to those of apoplexy. 390 
The Nervous System. 
THE SPINAL CORD. 
The inflammations of the chord are acute 
and chronic. 
The acute inflammations termed myelitis 
are somewhat better known than those of the 
brain, because the cord is much more accu- 
rately mapped out. 
Myelitis shows the same phenomena al- 
ready described in cerebritis. There is con- 
gestion of the vessels, both of the pia and of 
the cord substance. The cells are rounded, 
granular,*poleless. There is breaking down 
of the protoplasmic processes. There is pro- 
duction of round cells by the connective tis- 
sue and exudation from the vessels. In trans- 
verse myelitis the process affects a transverse 
section of the cord. There is secondary as- 
cending and descending degeneration in the 
cord. 
Anterior poliomyelitis: Synonyms. In- 
fantile paralysis. Acute atrophic paralysis. 
Etiology: Intoxication, sometimes from 
absorption from the intestinal tract, some- 
times of unrecognized origin. Exposure to 
cold. This last probably acts by locating an 
irritant already absorbed or causing the ab- 
sorption of an irritant already produced. 
Philosophy: The process nearly always The Nervous System. 
begins as an acute infection accompanied by 
the phenomena of acute toxaemia. During 
this stage the lesions are those of myelitis, 
limited to the anterior horns. With the sub- 
sidence of the intoxication the disease is, 
properly speaking, at an end. Such of the 
cells as are not irretrievably injured return to 
the normal. Those that are injured beyond 
repair are absorbed by the leucocytes. The 
protoplasmic processes of those cells degener- 
ate. There is an overgrowth of connective 
tissue. The degeneration involves the anterior 
roots of the nerves and the nerves themselves. 
The muscle fibers supplied by the cord at 
that level atrophy, not only from disuse, but 
also from having- their trophic center de- 
stroyed, it being in the anterior horn of gray 
matter. The muscles are the seat of fibrous 
tissue overgrowth. 
Anatomy: A cord, years after primary 
lesion. The gray matter of the affected half 
of the cord, when it is a hemiplegic lesion, is 
markedly decreased in size. This gray mat- 
ter is translucent. The changes are not in 
continuous areas, but in disconnected foci. 
The half of the cord is decreased markedly in 
size. 
Histology; In acute stage the histology is 394 
The Nervous System. 
that of acute myelitis limited to the anterior 
horns and to the protoplasmic prolongations 
of their nerves. In the wake of the disease 
we find connective tissue overgrowth and 
atrophy of the parenchyma elements, both 
from pressure and from inflammation. 
Chronic interstitial myelitis: According to 
the location in the chord of this cirrhosis we 
may have multiple sclerosis, antero-lateral 
sclerosis, amyotrophic lateral sclerosis, or lo- 
comotor ataxia, glosso-labial paralysis. 
We will study locomotor ataxia. 
LOCOMOTOR ATAXIA. 
Synonyms: Tabes dorsalis, posterior spinal 
sclerosis. 
Etiology: Obscure; syphilis, lead poison- 
ing, sexual excess. 
Philosophy of the process; The cells of the 
posterior columns are located either periph- 
erally or on the ganglia of the posterior roots. 
Perhaps there is sometimes primary disease 
in these ganglion cells, and perhaps the dis- 
ease is an inflammation of the meninges at the 
point of entrance of the posterior roots, but 
at any rate the lesions of tabes are those of 
degeneration in nerve fibers separated from 
their nuclei. The degeneration enters the cord 396 
The Nervous System. 
by the posterior root zone, travels from there 
to Goll and Burdach, thence across the pos- 
terior horn, where some of them surround 
cells and end; others run to the direct cere- 
bellar tract, the ascending, lateral and mixed 
lateral columns and anterior horns. 
Anatomy; The meninges are thickened and 
adherent, especially in its posterior segment. 
The posterior portions of the cord, especially 
in the lumbar region, are flattened. Cross sec- 
tions show the posterior columns, the seat of 
grayish, gelatinous looking, fibrous tissue. 
Less well marked areas are seen in the lateral 
columns. The extent of the lesion becomes 
less as we proceed toward the medulla. 
Histology: That of degeneration of paren- 
chyma and overgrowth of connective tissue. 
Tumors of the brain and cord. 
Fibroma, endothelioma, glioma, sarcoma, 
carcinoma, cysticercus, echinococcus, chole- 
steatoma. Some claim all gliomata to be sar- 
comata. 
In spina bifida there is an imperfect closure 
of the vertebral bones posteriorly and gener- 
ally at the base of the cord. Through the 
opening the cord prolapses. It may hang in- 
tact, but usually there is varying degree of 
deformity. 398 
Diseases of the Blood. 
DISEASES OF THE BLOOD. 
Points in Histology; The blood is a meso- 
blastic tissue. It differs from other tissues 
in that there is more intercellular substance 
than usual, and this intercellular substance 
contains more than the usual quantity of 
water. The cells are the red cell, the white 
cell and the third corpuscle. The red cell is 
a non-nucleated mass of protoplasm contain- 
ing haemoglobin. Its sole capacity is that of 
a gas transporter. The white cell contains 
no haemoglobin. In the mature state it has 
a nucleus surrounded by granular protoplasm. 
Each cubic millimeter of blood contains 
5,000,000 red cells and 5,000 to 10,000 leu- 
cocytes and enough plasma to make up the 
volume. 
The organs to be studied in connection 
with the blood are the spleen, the bone mar- 
row, the lymph tubes, and probably also the 
endothelium of the vessel. 
The spleen: The spleen consists of a con- 
nective tissue framework and of spleen cells. 
These spleen cells are in two groups. First, 400 
Diseases of the Blood. 
Malpighian corpuscles. Second, the spleen 
pulp. The smaller arteries are surrounded 
by Malpighian corpuscles, then the blood 
flows among the spleen cells, then being 
gathered up into venous radicles, then veins. 
In the spleen pulp the blood is free among 
the spleen cells. The area between the arte- 
rial and the venous radicle is a pulp space. 
ACUTE SPLENIC TUMOR. 
Synonyms; Active hypersemia of the spleen; 
acute splenitis. 
Etiology: All toxaemias, e.g., malaria, ty- 
phoid, typhus, scarlet fever, smallpox, pyae- 
mia and septicaemia. 
Philosophy of the process; The spleen be- 
ing both a chemical filter and a source of leu- 
cocytes, it rapidly responds to the irritation 
of the poisons on which it acts, for the fact 
that it acts on those poisons is proof that it is 
susceptible to them. 
Anatomy: The spleen increases to as much 
as four times the normal size. The capsule 
is tense. The substance is soft, diffluent, 
chocolate brown in color, and rapidly oxidizes 
to a brighter red. It may seem creamy, al- 
most pus-like. 402 
Diseases of the Blood. 
CHRONIC INTERSTITIAL SPLENITIS. 
Philosophy of the process: That of cirrhotic 
lesions elsewhere. The spleen is the chief 
source of destruction of the malarial organ- 
ism. This is accomplished by the endothelial 
cells of the trabeculae and lymph spaces. 
This mild irritation, when continued, results 
in cirrhosis; at the same time there is accumu- 
lation of pigment granules, derived from the 
blood. 
Etiology: Malaria; rickets; syphilis. 
Anatomy: The spleen is enlarged, firm. 
The capsule thick. It cuts firm. The color 
is pale except in the malarial, when there is 
pigmentation. 
Histology: The trabeculae are increased in 
thickness. The blood vessels have thickened 
walls. The pulp spaces are decreased in size 
and the connective tissue wall is thickened. 
In this wall contained within cells are gran- 
ules of golden brown pigment. 
Synonym: Sago spleen. 
WAXY SPLEEN. 
Etiology: Same as waxy disease elsewhere. 
Philosophy: As the spleen is a blood 
structure it is a very frequent Seat of waxy 
infiltration. The deposit may be principally 404 
Diseases of the Blood. 
in the corpuscle, in which event the sago 
appearance is most marked, or else it may be 
in the walls of the pulp spaces, when the ap- 
pearance is somewhat different. 
Anatomy: The spleen is enlarged, firm, 
elastic, with rounded edges. On section the 
corpuscles look like grains of boiled sago. 
The spleen pulp is pale, gelatinous. lodine 
stains the amyloid brown; the other areas 
yellow. 
Histology: The waxy homogeneous areas 
map out the trabeculae and the blood vessel 
wall. The staining reactions are the same as 
waxy degeneration elsewhere. 
THE PLASMA. 
The plasma is at once the source of nutri- 
tion and the sewer channel for the body. 
Therefore it will not be inappropriate to 
describe the post-mortem findings in cer- 
tain diseases that are purely toxaemias, in 
which the organism may be in the plasma, 
in which, certainly, the toxin is in the 
plasma, and in which death ensues without 
production of special lesion in any organ. To 
this class would belong septicaemia, typhus, 
yellow fever, cholera. 
Post-mortem findings; Cadaveric rigidity 406 
Diseases of the Blood. 
is early and well marked. Putrefaction be- 
gins early. The blood is dark and fluid. 
There is much evidence of staining of the 
vessels and surrounding tissue with blood. 
The lungs are congested. The same is true 
of the meninges. There may be fluid in the 
ventricles. There are usually small pete- 
chise in the gastro-intestinal and bronchial 
mucosae and in the serous membranes, the 
meninges, pericardium, pleura, etc. There 
is swelling of the glands of the ileum and of 
the mesenteric glands. 
Scurvy; Purpura haemorrhagica; haemo- 
philia. 
Scurvy is a nutritional disease in which 
some of the organic salts of the plasma are 
deficient. It seems probable that potassium 
enters into this combination. It is character- 
ized by a diminution of the tendency to coag- 
ulation, but less marked than in the next two 
members of the group. 
Purpura haemorrhagica: This condition is 
merely symptomatic. It is found in many of 
the prolonged toxaemias. There is a dimin- 
ished tendency to coagulation. 
Haemophilia: This disease may be con- 
genital or acquired. Its subjects are recog- 
nized as “bleeders.” The blood has lost all 408 
Diseases of the Blood. 
tendency to coagulate. The plasma is en- 
tirely free from calcium salts. The assimila- 
tion of calcium is curative. With the return 
of calcium to the plasma the capacity to co- 
agulate is regained. 
Diabetes: In diabetes mellitus the percent- 
age of sugar in the plasma rises from one- 
tenth of one per cent to six-tenths of one per 
cent. This causes an absorption of water 
from the tissues and the blood becomes hy- 
drsemic. In turn the kidneys secrete an ex- 
cess of urine and the specific gravity of plas- 
ma arises. In diabetes sometimes the amount 
of suspended fat so increases as to give the 
condition known as lipsemia. 
THE RED CELL. 
Each cubic millimeter contains 5,000,000 
red cells. This we term 100 per cent. A 
certain shade of color, as determined by a 
scale of comparison, we term 10a per cent 
of haemoglobin. Now, then, if 100 per cent 
of red cells carry 100 per cent haemoglobin, 
each corpuscle carries its normal load or 100 
per cent. This is called the corpuscle index. 
The red blood cell in adidt life is manu- 
factured in the bone marrow almost exclu- 
sively. An ordinary nucleated connective tis- 410 
Diseases of the Blood. 
sue cell containing no haemoglobin divides 
and produces a new cell, which has the ca- 
pacity of taking up haemoglobin. This cell is 
large and nucleated. This divides and forms 
a small cell seven mikrons in diameter, con- 
taining a nucleus and charged with haemoglo- 
bin. This in turn loses its nucleus and as- 
sumes the shape of the red cell. It is the 
red cell. Normally no red cells appear in the 
blood stream except the completed product. 
In times of emergency all or any of these ele- 
ments may be rushed into the blood current. 
Anaemias divide themselves along lines of 
etiology into those that are haemogenic, and 
those that are haemolytic. To the former 
type belongs chlorosis. To the latter per- 
nicious anaemia. 
Number of red 
cells per ctm. 
Percentage. 
Percentage of 
haemoglobin. 
Corpuscle 
index. 
Immediately after 10 per 
cent haemorrhage 
5,000,000 
IOO 
* IOO 
IOO 
One day after 10 per cent 
haemorrhage 
4,000,000 
90 
90 
IOO 
Chlorosis 
4,000.000 
SO 
■ 4° 
50 
Pernicious anaemia 
i, 250,000 
25 
30 
120 
Normal blood 
5,000,000 
IOO 
IOO 
IOO 412 
Diseases of the Blood. 
The above is an illustrative table. The loss 
from haemorrhage is purposely made large. 
These figures in chlorosis and pernicious anae- 
mia are very frequently found. 
Anaemia after haemorrhage: As plasma, 
red and white cells are lost in the same pro- 
portion, each cubic millimeter of blood con- 
tains the same relative amount of plasma, 
red cells and haemoglobin and leucocytes as 
in health. Immediately fluids begin to soak 
in from the tissues. In consequence each 
cubic millimeter contains a large quantity of 
plasma and a small quantity of red cells and 
white cells. The white cells are formed with 
great rapidity, so that within a few hours 
there is a post-haemorrhagic leucocytosis. 
The low specific gravity and the changed 
chemistry of the plasma causes a destruction 
of some of the red cells and a loss of haemo- 
globin that is still more marked. Next the 
marrow supplies new red cells, generally non- 
nucleated, but some nucleated, and all defi- 
cient in haemoglobin. So that the percent- 
age of haemoglobin falls below the percentage 
of red cells. We have a low corpuscle index. 
This is not to be confounded with chlorosis. 
Later the haemoglobin rises to the normal. 
The small nucleated cell present is called a 414 
Diseases of the Blood. 
normoblast. The large nucleated cell, rarely 
present, is called a gigantoblast or megalo- 
blast. The bone marrow normally yellow be- 
comes red. 
Chlorosis: If the percentage of red cells 
stays above 80 the disease is termed chlorosis. 
If it falls below 80 it is termed chloro- 
anaemia. 
Etiology: Absorption of ptomaines from 
the gastro-intestinal tract. It is especially a 
disease of constipated women, breathing bad 
air and removed from the effects of sunlight. 
Philosophy: It is a hsemogenic disease. 
The urine is pale, indicating that the amount 
of coloring matter manufactured from the 
blood is not in excess of the normal. 
Examination of the blood: The blood 
count shows a high corpuscle percentage, a 
low haemoglobin percentage, a low corpuscle 
index. Examination shows pale corpuscles, 
irregular in size and in elasticity; a very few 
normoblasts. The specific gravity is low; 
!,035-38 is about an average. Leucocytosis 
is absent 
PERNICIOUS AN3EMIA. 
This is only a symptomatic disease. The 
primary disease is chemical and is located 416 
Diseases of the Blood. 
somewhere in the portal circuit, the area of 
both normal and pathological haemolyses. 
Etiology: Ptomaines absorbed from the 
gastro-intestinal tract. Whether there is a 
special germ manufacturing a special pto- 
maine, or whether there is change in the 
alimentary tube by which an ordinary germ is 
provided with a medium from which it can 
manufacture a special ptomaine, or whether 
the absorptive apparatus is so changed that it 
takes up a ptomaine usually rejected, or 
whether the liver fails to destroy a ptomaine 
that is normally destroyed, we do not know. 
Philosophy of the process: It is a haemo- 
lytic disease. The urine is highly colored, 
indicating that there is increased destruction 
of haemoglobin. We are to bear in mind that 
20 per cent haemoglobin should mean one- 
fifth the normal coloring matter in the urine. 
The urine contains an increase of aromatic 
sulphates and is rich in pathological urobilin. 
The blood gives every evidence that haemo- 
genesis is making a gigantic effort to com- 
pensate. 
Blood Examination: The blood shows a 
small percentage of red cells, a small percent- 
age of haemoglobin, a high corpuscle index. 
Note this. The index ranges very close to 418 
Diseases of the Blood. 
ioo, and it may go considerably over it. The 
red cells are variable in size, shape and elas- 
ticity. Large cells called macrocytes pre- 
dominate. Normoblasts and megaloblasts 
are both present. No lencocytosis. In ex- 
treme cases there may be an apparent, though 
there is no real lencocytosis. Fibrin forma- 
tion takes places more rapidly than normal. 
The White Cell: The white cell is certainly 
manufactured by the lymph tubes and glands 
and probably also by the spleen, and, possibly, 
by the endothelium of the vessels. It is a 
mesoblastic cell that wanders in and out of 
the blood current with so much of facility 
and is so closely related to other mesoblastic 
cells that likewise wander, that it is easy of 
study, but difficult for satisfactory conclu- 
sions. It begins by fission of mesoblastic 
cells outside the blood current. In the blood 
current it does not divide. The new cell is 
small, about 8 , consisting of a central nu- 
cleus and a very faint small rim of non-gran- 
ular protoplasm surrounding. This acquires 
protoplasm, making a larger cell about io 
in size. This protoplasm becomes filled with 
fine granules that stain with neutral stains, 
and at the same time the nucleus twists into 420 
Diseases of the Blood. 
an irregularity of design, giving the idea of 
multiple nuclei. These so-called polynuclear 
neutrophiles make up 60 per cent of the 
whole number. The small lymphocyte makes 
up 30 per cent, and the other 10 per cent is 
furnished by the intermediate stage by eosin- 
ophiles and basophiles. The eosinophile is 
a large cell with a simpler or twisted nucleus 
and filled with large granules resembling ves- 
icles that stain with an acid stain, e.g., eosin. 
Rarely we find a cell with granules staining 
with a basic stain such as methylin blue. 
These are basophiles and are closely akin at 
least to the “mast” cells of the tissues, and 
especially of the gastro-intestinal tract. The 
fact that the number of corpuscles can mul- 
tiply several fold in a few hours would indi- 
cate that any percentage here is rather hap- 
hazard. 
In addition to the above there is a cell of 
great diagnostic, though not pathognomonic, 
significance. It is called the myelocyte. It 
is the largest of all the cells, averaging 15.7 
The large twisted nucleus neutrophiles aver- 
age 13-5 /*• The myelocyte has a single large 
oval nucleus, generally eccentrically placed. 
The nucleus stains evenly. The cell proto- 
plasm is granular. The granules are, gener- 422 
Diseases of the Blood. 
ally speaking, fine. They are neutrophiles, 
that is, the grannies stain with a combination 
of an acid and a basic stain. 
Lencocytosis: A temporary increase in the 
number of leucocytes. It is purely sympto- 
matic. The term can be applied to either an 
increase in the whole number of leucocytes, 
or to an increase of some special variety or 
stage. 
Physiological leucocytoses: 
1. Lencocytosis of the newborn. 
2. Lencocytosis of digestion. 
3. Lencocytosis of pregnancy. 
4. Lencocytosis of puerperal state. 
5. Leucocytosis after violent exercise, mas- 
sage and cold baths. 
6. Leucocytosis of the moribund state. 
Pathological leucocytoses: 
1. Post-hamiorrhagic leucocytosis. 
2. Inflammatory leucocytosis. 
3. Toxic leucocytosis. 
4. Leucocytosis in malignant disease. 
5. Other leucocytoses. 
Post-haemorrhagic leucocytosis. Within 
an hour after haemorrhage the number of leu- 
cocytes may rise to 18,000 per cm. This, 
though the haemorrhage be inconsiderable. 
Inflammatory leucocytoses: 424 
Diseases of the Blood. 
i. Infection mild; resistance good; small 
leucocytosis. 
2. Infection less mild; resistance less good; 
moderate leucocytosis. 
3. Infection severe; resistance good; 
marked leucocytosis. 
4. Infection severe; resistance poor; no 
leucocytosis. 
Infectious disease giving leucocytosis: 
Asiatic cholera, relapsing fever, typhus, scar- 
let fever, diphtheria, follicular tonsilitis, syph- 
ilis (secondary stage), erysipelas, bubonic 
plague, pneumonia, smallpox, pyaemia and 
septicaemia, actinomycosis, trichinosis, glan- 
ders, acute multiple neuritis, beriberi, acute 
articular rheumatism, cerebro-spinal menin- 
gitis empyema of the gall bladder, acute 
pancreatitis, endometritis, cystitis, gonor- 
rhoea, abscesses of all kinds, including appen- 
dicitis, pyonephrosis, osteomyelitis, psoas 
and hip abscess, salpingitis. Inflammations 
of the serous membranes, gangrenous inflam- 
mations. Many inflammatory dermatites, 
pemphigus, herpes zoster, prurigo, and some 
cases of universal eczema. 
Toxic Leucocytosis. 
Causes: Illuminating gas, quinine, rick- 
ets, gout, acute yellow atrophy, advanced 426 
Diseases of the Blood. 
cirrhosis, acute gastro-enteritis, acute nephri- 
tis, hydronephrosis, tubercular and thyroid 
extract injections, after injection of normal 
salt solution, salicylates, ether. 
Diseases in which there is absence of leu- 
cocytosis: Typhoid fever, malaria, grippe, 
measles, rotheln, all forms of tuberculosis. 
LEUKyEMIA. 
Etiology: Not known. 
Varieties: Lymphatic; spleno-myelogenic. 
Blood; The percentage of red cells is about 
50, and that of haemoglobin somewhat lower. 
There are nucleated reds, both normoblasts 
and megaloblasts present, though they are 
not prominent. 
i. Lymphatic leukaemia. 
White cells: The average number of whites 
is about 150,000 per cm.; about 90 per cent 
of the white cells are small lymphocytes un- 
der 10 m. in size. Myelocytes are rare. Plasma 
coagulation delayed. 
Body: The lymph glands are diffusely en- 
larged. The enlargement is due to true lymph 
gland overgrowth. There is but slight en- 
largement in the spleen. 
2. Spleno-myelogenic leukaemia. 
Blood: Red cells. The red cells average 428 
Diseases of the Blood. 
about 60 per cent, and the contained haemo- 
globin somewhat less. These will depend 
very much upon the amount of haemorrhage. 
Haemorrhage is prominent in this affection. 
There is a great increase in nucleated reds, 
especially the normoblast. 
White cells; The number of white cells is 
increased to from 100,000 to 1,000,000 per 
cm. The increase is principally in the so- 
called polynuclear form and in the myelocyte. 
These average as high as 30 per cent of all 
the forms. The small lymphocyte is relatively 
diminished. 
The plasma is very slow to coagulate. 
Body: The spleen is enormously over- 
grown. While there is a moderate increase 
in the connective tissue, the main increase is 
in the lymph elements, especially those filling 
the pulp spaces. The bone marrow is red. 
Petechiae and punctate haemorrhages are fre- 
quent. 
The parasites of the blood are: 
1. Animal: Malaria (the red cell); filaria 
sanguinis hominis; distoma haematobium. 
2. Vegetable: Spirochaete of Obermeyer; 
anthrax; pus germs, etc. 430 
Anatomy and Histology of the Teeth. 
POINTS IN ANATOMY AND HISTOLOGY 
OF THE TEETH. 
The roots of the teeth are in sockets in the 
alveolar processes. These alveolar processes 
are merely ridges on the maxillary bones. 
Binding the teeth to the bone is a peridental 
membrane composed of white fibrous con- 
nective tissue, many lymphatic glands and 
many blood vessels. The tooth proper is 
composed of an enamel which is epiblastic in 
origin, a dentine which is mesoblastic in 
origin, a cementum which is due to ossifica- 
tion of those portions of the peridental mem- 
brane next the dentine. Therefore the centers 
of development of a tooth are enamel, epi- 
blast, dentine, mesoblast, cementum meso- 
blast through peridental membrane. Centers 
of ossification of the alveolar processes of 
the maxillary bones. Upper incisor for the 
four incisor teeth; palatal for the remainder 
of the teeth. This would mean four centers 
in all. Lower, one for each side, two in all. 
The pulp is made up of connective tissue, Anatomy and Histology of the Teeth. 
blood vessels and nerves. Both of these 
leave the bone at the apex of the socket, 
give off lateral branches to the peridental 
membrane, then enter the tooth at the apex 
of the root. Neither runs into the dentinal 
tubules. 
FORMATION AND ERUPTION OF TEETH. 
Calcification of the deciduous teeth begins 
with the crown of the central incisors during 
the seventeenth week of foetal life, and ends 
with the second molar and canine of twenty- 
two months after birth. During this time 
any severe constitutional strain will show it- 
self in abnormalities in these teeth. Calci- 
fication of the permanent teeth begins during 
the twenty-fifth week of foetal life and ends 
at the twelfth year of post-foetal life. These 
teeth are subject to the same laws of nutrition 
as their predecessors. 
Eruption of the deciduous teeth is hastened 
by nutritional diseases and especially by 
rickets. 
Eruption is delayed by grave systemic dis- 
ease or by a lack of vitality. As a general 
proposition delayed dentition is not as sig- 
nificant as premature dentition. Diseases of the Teeth. 
TARTAR. 
By this is meant the deposits on the teeth 
above the gingival border. 
It is composed of the solid ingredients of 
the saliva combined with food remnants and 
a rich growth of bacteria. It accumulates on 
the teeth because they are subject to less 
irrigation and friction than the balance of the 
mouth. It is, generally speaking, most abun- 
dant on those teeth placed near the outlets of 
salivary ducts—e.g., the second molars of 
the upper jaw; the central incisors of the 
lower jaw. 
Fresh tartar is soft, moist, yellowish white, 
and offensive in odor. 
Microscopically: It is composed of granu- 
lar debris, epithelial cells and bacteria of vari- 
ous kinds. 
Old tartar; Is firmly adherent to the 
enamel; so much so that considerable force 
is necessary to remove it. It is black or dark 
brown in color. It may extend below the 
line of gum attachment. This is not the rule. 
Microscopically: It is composed of lime 
salts and bacteria. Tartar is only of impor- 
tance in that it is generally though to predis- 
pose to decay. When the accumulation of Diseases of the Teeth. 
tartar becomes large the condition is known 
as salivary calculi. Cases are not exceed- 
ingly rare in which masses fill the roof of the 
mouth, completely hiding the teeth. The 
masses are bone-like in appearance. Chemi- 
cally they are composed of sodium carbonate 
potassium sulpho-cyanide, calcium salts, pty- 
alin and occasionally uric acid. 
DECAY. 
There are many points in dental caries that 
are not yet solved, and that will not be solved 
soon. Many of these questions hinge on (i) 
why infection takes place, and (2) the rela- 
tion of germs to germs. Both questions are 
difficult of solution. As the enamel is by all 
conceded to be relatively passive, by nearly 
all to be absolutely passive, the question re- 
solves itself into three suppositions. First, 
that the proper germs do not happen in the 
mouth until a certain time. This is im- 
probable. Second, that certain resident 
germs that combat the germs of decay fail to 
do their work. Third, that there is some 
change in the chemistry of the secretions of 
(1) the mouth, (2) the enamel plate, or (3) 
the intercellular substance, so that they fur- 
Synonym; Caries. Diseases of the Teeth. 
rush a feeding-place for the germs of decay. 
This is probable. 
i. Immediate. Two varieties of germs are 
needed, one living largely on starches and 
sugars secretes lactic acid, which dissolves the 
lime salts in all the structures of the tooth; 
a second living on albuminous foods, and fol- 
lowing in the territory previously prepared 
by the first. It secretes a ferment which di- 
gests the epithelium of the enamel plates and 
Etiology: Two sets of causes. 
the connective tissue of the dentine and ce- 
mentum. 
2. Remote. Illy formed teeth. Illustra- 
tions. Fissures and depressions in teeth so 
placed as to be protected from friction; badly 
placed teeth by making cleansing difficult; 
recession of the gums. Diseases—rheuma- 
tism, gout, diabetes, dyspepsia, cancer of the 
stomach, rickets, scrofula, tuberculosis, syph- 
ilis. Occupations—bakers, confectioners. The 
carbohydrates furnish food for the growth of 
the lactic acid germ. 
Location: The most frequent point of be- 
ginning is in a fissure or depression on the 
grinding surface. Next in frequency comes 
the spaces between the teeth, then the labial, 
lastly the lingual surface. Caries beginning 440 
Diseases of the Teeth. 
in the cementum covering the root is rare, 
even in cases of marked recession. 
Nature of the process: The area to be af- 
fected is covered by a layer of germs se- 
creting acids. These decalcify the enamel, 
and the germs grow into the enamel area as 
slender rows parallel with the long diameter 
of the enamel plates. These rows extend un- 
til the dentine is reached, when the germs 
get into the dentinal tubules. In these 
tubes they grow with greater rapidity. Fol- 
lowing close behind this advanced guard is 
an organism or a set of organisms secreting 
a substance which digests the organic parts 
of the structure. In the dentine both of 
these processes extend more rapidly than in 
the enamel. In consequence the enamel is 
undermined, and crumbles off. In the cavity 
thus formed many kinds of germs multiply. 
Some are chromogenic, giving the black 
color ; some secrete odoriferous gases, giving 
the odors of decomposition; some are ac- 
tively pyogenic. When these last secure 
entrance to the pulp chamber or to the peri- 
dental membrane, there is pus formation; 
abscess. Sometimes the pyogenic germs are 
either gas producers, or are associated with 
saprophytic germs producing gases; the ab- 442 
Diseases of the Teeth. 
scess contains both pns and gas. Infection 
may extend to the bone, causing necrosis that 
may be extensive. 
Anatomy: In the very beginning the 
enamel has lost its polish; it is whiter than 
its surrounding. It is slightly roughened. 
Later a cavity is formed. This cavity is 
globular in shape, being larger below than 
on the surface. The wall is rough.' It is 
some dark shade of color. 
Histology: Enamel. Rows of some form 
of bacillus or coccus are seen extending be- 
tween the enamel plates. The plates are gran- 
ular, disintegrating and falling loose from 
their fellows and from the basement mem- 
brane underneath. 
Dentine: Masses of organisms are seen 
especially in the dentinal tubules, and less 
frequently in the interglobular spaces. The 
areas deprived of lime salts show anatomi- 
cally as softened gelatinous areas. Histo- 
logically there is slight change in appearance. 
Later the dentinal structure begins to break 
down into granular debris, some of it passing 
through the stages of cloudy swelling and 
fatty degeneration. In the vicinity of the 
breaking down process the dentinal tubules 
are filled with proliferated osteoblasts or with 
secondary dentine produced thereby. Diseases of the Teeth. 
Pulp: When the germs reach the pulp cav- 
ity we may have chronic pulpititis with form- 
ation of secondary denture and lessening of 
the cavity, or suppuration, or suppuration 
with formation of gases, all of these being 
dependent upon the infecting germ. 
EROSION. 
This is a condition in which on surfaces 
not exposed to wear depressions, generally 
angular and clear cut, appear. The term is 
not applied to the wear resulting from use. 
Etiology: Unknown. It is found in people 
subjected to severe, long continued illness or 
great mental strain. It is not a common 
effect of these conditions, but is seldom found 
unassociated with them. 
Anatomy: On the labial surface, most fre- 
quently in the enamel, but sometimes on the 
root there appears a depression giving every 
appearance of an area of wear. The loss is 
usually about one-third the diameter of the 
tooth. The bottom is smooth, polished, firm. 
Histology: Except for a thickening of the 
dentine and a lessening of the pulp cham- 
ber, I have been unable to find any changes 
in the few cases that I have examined. Diseases of the Teeth. 
TEETH OF SYPHILIS. 
Hutchinson’s teeth. In the permanent teeth 
of the subjects of inherited syphilis the grind- 
ing surfaces have a large single crescentic 
notch. 
Teeth of rickets: In either set of teeth, but 
especially in the milk teeth, there are changes 
due to rickets. The teeth are yellow, soft 
and porous. They begin to decay very early 
and decay with great rapidity. 
Any severe disease causing profound dis- 
order of nutrition affects the teeth as to their 
time of eruption, their placing, the develop- 
ment of the dentine and of the enamel. The 
teeth are most subject to these changes dur- 
ing their formative period. The milk teeth 
would be most affected by intrauterine con- 
ditions and affections during the first year. 
The permanent teeth by affections during 
the first and second and up to the tenth year 
of life. 
Diseases of the pulp cavity: The pulp 
chamber is, properly speaking, nothing more 
than that portion of the tooth organ which 
has not been converted into dentine by the 
odontoblasts. Any irritation that is mild is 
liable to cause proliferation of odontoblasts 
and the formation of new dentine. This may 448 
Diseases of the Teeth. 
proceed until the pulp chamber is obliterated, 
either at some point or throughout. As a 
matter of fact, the size of the pulp chamber 
varies greatly at different periods of life. Such 
a production of dentine can clearly be classed 
as a chronic productive inflammation of the 
pulp; a chronic interstitial pulpitis. In the 
same area are large cells called odontoblasts 
that cause absorption of dentine and a conse- 
quent increase in the size of the pulp cavity. 
Infection of the pulp chamber: Route of 
infection. Through decay in the enamel and 
dentine. 
Etiology: Some of the pyogenic germs fre- 
quently associated with gas producers. 
Nature of the process; Pulp cavity is in- 
tensely inflamed. The inflammation extends 
to the apical foramen. The pus germs may 
cause liquefaction of the peridental mem- 
brane, when the pus will appear at the side 
of the tooth, or it may remain at the apex 
liquefying the bone. Infection of the lymph 
spaces of the bone may ensue, causing ne- 
crosis of considerable areas. General infec- 
tion may result. The production of gases is 
the rule. 
Histology: The pulp is filled with round 
cells of inflammation. Among these are large 450 
Diseases of the Teeth. 
giant cells called odontoclasts that are lique- 
fying the dentine. Around the apex and the 
lymph spaces leading therefrom are masses 
of inflammatory cells. 
Sequelae: An apical abscess may terminate 
by phagocytes overcoming the infecting 
germs. It may infect the peridental mem- 
brane, giving pyorrhoea alveolaris, beginning 
at the apex of the root. 
Sometimes tumors are found in the pulp. 
These may be fibromata, or they may be de- 
posits of lime salts—odontoliths. 
Diseases of the peridental membrane; The 
blood and lymph supply of the peridental 
membrane is from two principal sources. 
First, branches of the vessels to the tooth at 
the apex; second, branches from the gingival 
border. 
Synonym: Rigg’s disease. 
PYORRHCEA ALVEOLARIS. 
Definition; A chronic inflammatory proc- 
ess located in the peridental membrane, re- 
sulting in disintegration of those fibers run- 
ning into the cementum. 
Etiology: Anything causing mild, chronic 
irritation, such as deposit of inorganic salts, 
continued irritation of the gums, lead and mer- 452 
Diseases of the Teeth. 
cury poisoning, scurvy. If this area becomes 
infected with pus germs either down the gin- 
gival border, or at the apex through the pulp, 
the process is greatly hastened. Decay plays 
very small part in the process. 
Anatomy: The teeth are usually sound. 
The loosening usually takes place from the 
neck toward the apex. This shows as a rough- 
ened area. This area may be broad, or it may 
be in strke running lengthwise of the root. 
There are generally deposits of mineral matter 
in this area. Beyond the zone of loosening 
there may be deposits, but this is exceptional. 
Histology; The peridental membrane is 
filled with round cells. In some cases this 
round cell infiltration and proliferation are 
evenly distributed throughout. In other cases 
it is collected in multiple foci. In many of 
these foci there is granular degeneration of 
the inflammatory cells (atheroma) with 
secondary deposit of lime salts (calcifica- 
tion). The process is very similar to that in 
periostitis and in arteritis. In this connec- 
tion study those conditions carefully. To this 
class belong “seminal calculi.” Beyond a 
slight amount of mechanical injury the calculi 
do no harm. 454 
Diseases of the Teeth. 
MERCURY POISONING. 
In poisoning by mercury there is an acute 
inflammation of the peridental membrane 
followed generally by pus infection. 
Etiology; Certainly some part of the mer- 
cury in the system is eliminated by the sali- 
vary glands and other structures of the 
mouth. This fact means special irritability. 
The infection follows because the inflamed 
area is one of lowered resistance. 
Anatomy: The gums are swollen, soft, red 
oedematous. The tooth is partially loosened. 
Frequently pus exudes. 
Histology: The peridental membrane is 
the seat of acute productive exudative in- 
flammation. Its meshes are filled with round 
cells. Sometimes foci of pus are to be seen. 
LEAD POISONING. 
Poisoning with lead gives about the same 
anatomical and histological findings. Gen- 
erally speaking, the' process is less virulent 
and less acute than that of mercury. 
In scurvy much the same findings are seen. 
DISEASES OF THE GUMS. 
The gums consist of stratified squamous 
epithelium arranged over papillae. They 456 
Diseases of the Teeth. 
covei the peridental membrane. Around the 
neck of the tooth the cells take on a some- 
what glandular arrangement. These cells re- 
semble those of sebaceous glands. It is this 
collection of cells called the glands of Serres 
that is most sensitive to mercury, potassium 
iodide, lead and scurvy, and therefore they 
are the starting point of the disease in the 
underlying structure. The gums cannot be 
treated apart from the peridental membrane, 
because the capillaries, blood vessels and 
nerves are continuous between the two. The 
gums are the more subject to pathologi- 
cal processes, because 
i. Epithelium is the more irritable tissue. 
2. Its position subjects it to mechanical, 
chemical and bacterial irritations. From the 
gums start the larger number of cases of 
pyorrhoea alveolaris. 458 
The Mouth. 
THE MOUTH. 
The more important inflammations of the 
mouth are aphthous stomatitis, thrush, ulcera- 
tive stomatitis, gangrenous stomatitis, diph- 
theria, follicular tonsillitis, syphilis. 
Aphthous stomatitis: Etiology not known. 
Several germs have been cultivated from these 
“ulcers,” but the probability is that the main 
cause lies in some change in the general econ- 
omy through which these cells become sub- 
ject to infection with germs omnipresent. 
Philosophy of the process: A mild inflam- 
mation causing destruction of superficial cells, 
proliferation of deeper cells, but limited to 
the epithelial structures and the connective 
tissue immediately underneath. 
Anatomy: Generally the ulcers are pea 
size, white, rough, with a red setting. 
Histology: Proliferation of granular layer 
of epithelial cells, with mild infiltration of 
underlying connective tissue with inflamma- 
tory cells. 
Thrush; A form of superficial stomatitis 
affecting bottle-fed babies especially. 460 
The Mouth. 
Etiology: Oidium albicans, a mold feed- 
ing especially on sugars and starches and 
mycoderma vini, a yeast. 
Philosophy of the process; A mild irritant 
causing inflammation limited to the epithelial 
structures. If the irritation be more severe, 
it may involve the mucosa underneath tlie 
epithelium. 
Anatomy: The mucous membrane is in- 
jected. On this red base is a white membrane 
which scrapes off easily, leaving a slightly 
roughened surface. 
Histology: Among the loosened and the 
proliferating epithelial cells are cells and 
branching threads of the yeast or mold. 
ULCERATIVE STOMATITIS. 
Synonym; Cancrum oris. 
Etiology: Pus infection, due to poor hy- 
gienic surroundings. 
Anatomy; The lesion begins in the gums. 
From around the teeth pus oozes; the teeth 
are loose; parts of the bone may necrose and 
come away. The mucous membrane of the 
gums and cheeks sloughs away. An exudate 
of plasma and leucocytes mixed with tissue 
debris partly covers the raw surface. 
Histology: That of suppurative inflamma- 
tion in mucous membranes. 462 
The Mouth. 
In gangrene of the month, called noma, the 
process is the same, except that the infecting 
germ is one of those causing gangrene. 
DIPHTHERIA. 
Synonym: Membranous croup. 
Philosophy of the process: This bacillus, 
more than any other, causes exudation of 
plasma. It is then violently irritative to the 
vaso-motor apparatus. In addition, it has 
capacity to coagulate albumins in a much 
more marked degree than have the toxins of 
most germs. 
Etiology; The diphtheria bacillus. 
The lesions of diphtheria are of three 
classes. 
i. Local: An exudative inflammation with 
coagulation not only of the exudate, but also 
of every tissue cell in close proximity to the 
toxin. 
2. General; Due to the absorbed toxin. 
3. Secondary infections—e.g., pneumonia. 
Point of infection: Area of selection, the 
tonsils. It may begin in, or it may spread to 
the nose, the pharynx, larynx, trachea, oesoph- 
agus, eyes, skin, rectum, vagina, anus. 
Anatomy: The mucous membrane is red 
and swollen. The diphtheritic membrane is 464 
The Mouth. 
white to gray in color. It is closely adher- 
ent. A bleeding surface is left when it is re- 
moved. It is usually on the tonsil, but it 
grows out over the surrounding mucosa. 
Histology: The superficial layers consist 
of fibrin, coagulated cells and bacilli. The 
deeper layers show cells separated by bands 
of coagulated fibrin. Deeper there is violent 
round cell inflammation. 
Constitutional lesions: As a rule, the ba- 
cillus does not go beyond the area of infec- 
tion. Its toxin absorbs, causing cloudy 
swelling of the kidney, cloudy swelling of the 
liver, cloudy swelling of the heart, neuritis. 
Complicating lesions: The paralyses are 
due to the toxaemia. The diphtheritic throat 
is a good growing area for other germs, and 
these inspired are apt to cause either broncho 
or lobar pneumonia. 
FOLLICULAR TONSILLITIS. 
Ulcerations of the throat. 
Etiology: The pus cocci. 
Philosophy: In the crypts of the tonsils 
one or more of these germs grow in rich pro- 
fusion, secreting toxine, which is absorbed, 
causing the symptoms. 
Anatomy: The white masses, generally 466 
The Mouth. 
speaking, grow as islands and are limited to 
the tonsil. They are easily scraped off. The 
mucous membrane is red and swollen. 
SYPHILIS. 
We may have a primary chancre, a mucous 
patch or a gumma. Syphilitic teeth have al- 
ready been referred to. The lesion of syph- 
ilis is an overgrowth of fibrous tissue in the 
submucosa. There may or may not be ne- 
crosis, ulceration. 
As we consider the lesions of the mouth, 
remember that the mucous membrane of the 
mouth is continuous with that of the nose, 
pharynx, larynx, oesophagus, Eustachian tube 
and ear, eye, frontal sinus and antrum of 
Highmore. Into this last occasionally the 
roots of the first and second molars penetrate. 
The bones: The alveolar portion of the 
superior maxillary bone developing from two 
centers for each half, and the inferior maxil- 
lary from one for each side, the upper teeth 
are more subject to irregularity than are the 
lower. 
Abnormal forms of arch. U-shaped, in 
which the arch is too broad. V-shaped, in 
which the two sides form a V with the angle 
in the center. Saddle-shaped arch, in which 468 
The Mouth. 
there is an angle pointing inward just ex- 
ternal to the lateral incisors. Irregular plac- 
ing or spacing is found in all of these. 
Frequently the alveolar process is not long 
enough to hold all the teeth, when crowding 
and irregularity ensue. 470 
Tumors of the Mouth, Jazvs and Teeth. 
TUMORS OF THE MOUTH, JAWS AND 
TEETH. 
Cysts: Retention cysts are not unusual in 
the glands accessory to the mouth. Dermoid 
cysts are not infrequent in the face and 
mouth. Sites—angles of the orbit, upper 
eyelid, along the nose, chin, angle of the 
mouth, tongue. Branchial cysts, due to im- 
perfect closure of the branchial clefts. Sites 
—the ear, and in the neck along the anterior 
border of the sterno-mastoid muscle. 
Epithelioma: The carcinomas of the 
mouth are epitheliomata. In the tongue they 
are virulent; in the lips they are but mildly 
malignant; in the gums they occupy middle 
ground. 
Epulis; Most of the tumors of the maxil- 
lary bones that were formerly called epulis 
belong to two classes: 
i. Giant celled sarcoma. This springs 
from the peridental membrane or the alveo- 
lar process. It has been described under 
tumors. 
2. Cysts developing as a perversion in a 
tooth organ. These develop around perma- 472 
Tumors of the Mouth, Jaws and Teeth. 
nent teeth. Less frequently from undeveloped 
teeth. 
Anatomy; There is a thin envelope of os- 
teosclerotic bone around the cyst. This is 
globular in shape. Within this is a thin con- 
nective tissue wall, and within this clear fluid. 
In the cyst is found some part of a tooth. 
Bone is subject to (i) necrosis or simulta- 
neous death of a considerable mass of bone. 
(2) Caries: Ulceration of bone. Solu- 
tion of lime salts liquefaction of the connective 
tissue framework. The irritant of the latter 
is the more violent. 
Osteosclerosis is that condition in which 
osteoblasts form a greater quantity of bone 
than normal or fill up the Haversian spaces 
more completely than normal. 
Osteoporosis is that condition in which the 
phagocytic cells called osteoclasts have ab- 
sorbed some bone either in the central canal 
at the periphery, or in the Haversian spaces. 
Generally speaking, when in an area of con- 
centrated irritation osteoclasts are causing ab- 
sorption in surrounding areas of lesser irrita- 
tion; osteoblasts are laying down new dense 
bone.