Chapter 2

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Chapter 2 Cell and Tissue Injury and Adaptation
AIMS
1. To grasp concepts of atrophy, hypertrophy, hyperplasia, metaplasia, and to be
familiar with morphologic characteristics of atrophy, hypertrophy and
metaplasia.
2. To grasp morphologic changes of common types of degeneration and their
favorite tissue or organ.
3. To grasp pathological changes and types of necrosis, and morphologic
character of each type.
4. To grasp concept and morphologic characteristics of apoptosis.
CONTENTS
Atrophy
Gross specimen
Tissue section
Pressure atrophy of the kidney
Brown atrophy of the myocardium
Pressure atrophy of the brain
Granular atrophy of the kidney
Brown atrophy of the myocardium
Hypertrophy
Hypertrophy of the myocardium
Hypertrophy of the myocardium
Squamous metaplasia
Metaplasia
Intestinal metaplasia
Cellular degeneration and intracellular and extra cellular accumulations
Cellular swelling
Fatty degeneration
Cellular swelling of the kidney
Cellular swelling of the kidney
Cellular swelling of the liver
Cellular swelling of the liver
Fatty degeneration of the liver
Fatty degeneration of the liver
Fatty degeneration of the
Fatty degeneration of the
myocardium
Hyaline degeneration
Hyaline degeneration of the pleura
myocardium
Hyaline degeneration of the
connective tissue
Hyaline degeneration of the
splenic capsule
Hyaline degeneration of the central
artery of the spleen
Intracellular hyaline degeneration of
the liver
Hemosiderosis
Hemosiderosis of the lung
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Hemosiderosis of the lung
Calcification
Calcification of the pulmonary
Calcification of the atheromatous
tuberculosis
plaque
Necrosis and apoptosis
Coagulative necrosis
Coagulative necrosis of the spleen
Coagulative necrosis of the spleen
Liquefactive necrosis
Abscess of the cerebra
Epidemic encephalitis B
Encephalomalacia
Intestinal amoebiasis
Amoebic liver abscess
Caseous necrosis
Tuberculosis of the kidney
Tuberculosis of the lymph node
Tuberculosis of the lymph node
Gangrene
Dry gangrene of the foot
Wet gangrene of the small intestine
Fibrinoid necrosis
Fibrinoid necrosis of the vessel
wall
Reaction to necrosis
Cavity
Ulcer
Calcification
Apoptosis
Apoptosis of hepatocyte
KEY POINTS OF SPECIMEN OBSERVATION
1. Atrophy
Basic pathologic changes
(1) Gross morphology
◆
Decrease in size or shrinkage of an organ; the color is darker than normal; the
texture becomes hard or firm; the edge of the organ is thinned.
◆
The arteries on the surface of organs may be tortuous.
(2) Histopathology
◆
Reduction in cell size and/or decrease in cell number; usually parenchyma cell.
◆
Proliferation of the connective tissue and the adipose tissue or not.
◆
Pigment deposition can be seen in the cytoplasm of the parenchyma cells.
Specimen observation
(ⅰ) Pressure atrophy of the kidney
Case abstract: The 20-year-old man, complained of a 8-year intermittent abdominal
angina in the right lower abdomen. The X-ray shows there was a nephrolith in the
right ureter and an increase of the size of the kidney as the result of hydronephrosis.
Gross specimen: (Fig. 2-01) The kidney is enlarged with scraggy and tuberculous
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surface. On the cut surface, there is significant dilatation of the renal pelvis. The renal
cortex is shrunken (normal 2cm~2.5cm). It is hard to distinguish the corticomedullary
junction. The medullary pyramid is disappeared.
Question: Why is the kidney still called atrophy in spite of the enlargement of its
size?
(ⅱ) Granular atrophy of the kidney
Case abstract: The 55-year-old man complained of hematuria, albuminuria and
hypertension for ten years. He died of kidney failure.
Gross specimen: (Fig. 2-02a) The kidney is contracted. There are fine granules
diffusely scattered over the surface of the kidney. On the cut surface (Fig. 2-02b), the
cortex is thinned (normal 2cm~2.5cm). It is hard to distinguish the corticomedullary
junction. There is an increase in the pararenal fat.
Question: What is the reason of the atrophy? How about its influence upon human
body?
(ⅲ) Brown atrophy of the myocardium
Gross specimen: (Fig. 2-03) The heart is smaller than normal. On the surface the
coronary arteries are tortuous. The cut surface is brown.
Tissue section: (Fig. 2-04) ①The myocardium reduces in size; ②Yellow-brown
lipofuscin pigment can be seen in the cytoplasm. This pigment is deposited primarily
in the vincinity of the nucleus.
(ⅳ) Pressure atrophy of the brain
Gross specimen: (Fig. 2-05) Please observe and describe by yourself.
2. Hypertrophy
Basic pathologic changes
(1) Gross morphology
◆
In hypertrophy of the organs there is an increase in the size, and the arteries on the
surface are straight.
◆
The parenchyma becomes thicken on the cut surface.
(2) Histopathology
23
◆
Increase in parenchyma cell size, the nuclei of the parenchyma cells are enlarged
and become darker than normal.
◆
The connective tissue is decreased correspondingly.
Specimen observation
Hypertrophy of the myocardium
Case abstract: The 58-year-old woman had felt dizziness and headache for more than
ten years, accompanying with dyspnea and edema of the lower limbs for half a month.
She died of pulmonary infection.
Gross specimen: (Fig. 2-06) The size of the heart is as large as a normal heart, but the
weight is increased. On the cut surface, the musculature of the left ventricle and
interventricular septum, thicken apparently, measuring 2cm in thickness (normal
0.8cm~1.2cm). The papillary muscles and trabeculae carneae are thickened without
dilatation of the left ventricle, concentric hypertrophy results.
Tissue section: (Fig. 2-07) ①The myocardial fibers are thickened. The connective
tissue is decreased correspondingly; ②The size of the myocardial cells is increased,
and the nuclei are enlarged.
Question:
How many types of hypertrophy are there? Which type does this
specimen belong to?
3. Metaplasia
Specimen observation
(ⅰ) Squamous metaplasia of bronchus
Case abstract: The 50-year-old man complained of a cough accompanied by purulent
sputum for more than 15 years. The diagnosis was chronic bronchitis accompanying
with bronchiectasis.
Tissue section: (Fig. 2-08) ① The bronchiole dilates; ② The normal columnar
ciliated epithelial cells of the bronchi are replaced focally by stratified squamous
epithelium.
Question: What is the influence of squamous metaplasia of bronchus upon human
body?
(ⅱ) Intestinal metaplasia of gastric gland
Case abstract: The female patient complained of a 6-year intermittent abdominal
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pain. The diagnosis was chronic atrophic gastritis.
Tissue section: (Fig. 2-09a,b) ①The mucosa becomes thin. The size and the number
of the gastric gland are reduced with inflammation of the lamina propria involving
lymphocytes and plasma cells. ②The gastric mucosal epithelia are replaced by goblet
cells and some Paneth’s cells
4. Cellular degeneration and intracellular and extra cellular accumulations
(ⅰ) Cellular swelling (Hydropic degeneration)
Basic pathologic changes
(1) Gross morphology
◆
The organs or tissues are swollen in various degrees.
◆
The color becomes pale and cloudy.
◆The
capsule is tense.
(2) Histopathology
◆
The parenchyma cells are swollen in various degrees and crowded together.
◆
The cytoplasm is translucent and lightly stained. The nucleus usually locates in the
center.
Specimen observation
1) Cellular swelling of the kidney
Case abstract: The 1-year-old boy was brought to the hospital for fever and cough
associated with dyspnea for three days. The diagnosis was lobular pneumonia. The
patient died of failure of respiration.
Gross specimen: (Fig. 2-10) The kidney is enlarged with obtunded edges, tense
capsule and pale in color.
Tissue section: (Fig. 2-11a,b) ① The pathological changes are located in the
proximal tubules in the cortex. The proximal tubule epithelium takes the form of
swelling and protrudes into the lumen, as a result, the lumen of the proximal tubules
becomes narrow and asteroid; ②The epithelium is swollen and the cytoplasm is
translucent, lightly stained and filled with fine eosinophilic granule. There is no
obvious pathological change on the nuclei.
Question: What will the gross morphology of the kidney be like according to its
pathological changes in tissue section?
2) Cellular swelling of the liver
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Case abstract: 35-year-old man complained of a pain in the right upper abdomen
along with poor appetite, nausea and vomiting for three weeks. Physical examination
shows the liver is palpable 2cm below the costal margin. The ALT lever is higher.
Needle biopsy of the liver is made and the diagnosis of viral hepatitis is certified.
Gross specimen:(Fig. 2-12) The liver is swollen with obtunded edges, tense capsule
and pale color.
Tissue section: (Fig. 2-13a,b,c) ①The liver lose normal lobular architecture. The
liver cell cords are crowded together. The hepatocytes are diffuse swelling, and the
sinusoid is narrow, distorted and obliterated; ②The cytoplasm looks empty or
vacuolated and contains only scattered wisps of cytoplasmic remnauts, that is,
ballooning degeneration of hepatocyte.
(ⅱ) Fatty degeneration
Basic pathologic changes
(1) Gross morphology
◆
An increase in the size.
◆
The capsule is tense; the edges are obtunded.
◆
The surface and the cut surface are bright yellow, soft, and greasy.
(2) Histopathology
◆
In fatty degeneration of the cells, there is an increase of the size at various
degrees.
◆
There are many small vacuoles in the cytoplasm around the nucleus, or coalesce to
form one large vacuole filling the cell and/or displace the nucleus to the periphery
of the cell.
Specimen observation
1) Fatty degeneration of the liver
Case abstract: The 8-year-old boy was hospitalized for diarrhoea and emaciation for
one year. The diagnosis of diarrhoea and malnutrition grade Ⅲ (severe) is certified.
The patient died although an emergency treatment had been given.
Gross specimen: (Fig. 2-14a,b) The liver is enlarged with obtunded edges, tense
capsule, and is bright yellow, soft and greasy, and is also called fatty liver. (Fig. 2-14c)
The liver can be stained red by Sudan-Ⅲ.
Tissue section: (Fig. 2-15a,b,c) ①The lobular architecture is intact. Most of the liver
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cells are enlarged and crowded together; ②Most of the liver cells are filled with
drops of fat. The fat droplets appear as round vacuole with clear edge and vary in size.
Some large vacuoles fill the cell and displace the nucleus; ③(Fig. 2-15d.) Fat
droplets in cytoplasm of liver cells are stained into orange (Sudan III staining).
Question: How to certify that the droplets in the cytoplasm of the liver cells are fat
droplets?
2) Fatty degeneration of the myocardium (Severe anemia)
Gross specimen: (Fig. 2-16) In the myocardium of the left ventricle, particularly
around the papillary muscles, apparent bands of yellowed myocardium anastomose
with each other and alternate with bands of darker reddish-brown uninvolved
myocardium, resulting a tigered effect.
Tissue section: (Fig. 2-17) Lipid droplets in cytoplasm of heart cells are stained into
orange (Sudan-Ⅲ).
(ⅲ) Hyaline degeneration
Basic pahological changes
(1) Gross morphology
◆
The tissue hyaline degeneration appears to be gray, homogenous and translucent,
and the texture is firm.
(2) Histopathology
◆
Hyaline degeneration of cells or tissues appears to be homogenous, eosinophilic
and glassy.
Specimen observation
1) Hyaline degeneration of the connective tissue
Gross specimen: (Fig. 2-18a, b) The splenic capsule and pleura are thickened, gray
white and translucent.
Tissue section: (Fig2-19a) Hyaline degeneration of the fibrous cap of atheromatous
plaque; (Fig2-19b) It is a scar tissue. ①Collagen fibrils distribute in parallel or cross
mode. Fibrocytes and small vessels are scare; ②Dense collagenous fibrils assume a
homogeneous pink hyaline appearance.
2) Hyaline degeneration of the central artery of the spleen (Spleen of hypertensive
disease)
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Tissue section: (Figs. 2-20a,b,c) ①First, identify the splenic corpuscula and the
central artery; ②Numerous homogenous pink materials deposit under the intima,
resulting in thickening of the walls of the central artery as well as narrowing of the
lumen.
3) Intracellular hyaline degeneration of the liver (Alcoholic hepatitis).
Tissue section: (Fig. 2-21) ①The hepatocytes enlarge with irregular shape and
different size; ②In the cytoplasm of the hepatocytes there are thick, eosinophilic
granules- Mallory bodies, different in size.
(ⅳ) Hemosiderosis
Basic pathologic changes
(1) Gross morphology
◆
Organ or tissue shows brown color with a firm texture.
(2) Histopathology
◆
Intercellular or intracellular brown, finely granular hemosiderin pigment can be
seen.
Specimen observation
Hemosiderosis of the lung (Chronic congestion of the lung)
Gross specimen: (Fig. 2-22) The size of the lung is increased and the capsule is tense.
The cut surface is brown. It has a firm consistency.
Tissue section: (Fig.2-23a,b) ① The alveolar walls are thickened. There is
proliferation of the connective tissue; ②Macrophages are seen in the lumen of the
alveoli, some of them contain golden-brown, finely granular hemosiderin pigment.
Question: How to certify that the brown granule is hemosiderin? How does it form?
What is its clinical significance?
(ⅴ) Pathologic calcification
Basic pathologic changes
(1) Gross morphology
◆
The calcium deposits appear as calcareousness with hard consistency.
(2) Histopathology
◆
In the tissue that does not contain solid calcium salt, the hematoxylin-Eosin (HE)
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stain shows the calcium deposits appear as bluish granules or masses.
Specimen observation
1) Calcification of the pulmonary tuberculosis
Gross specimen: (Fig. 2-24) There are three focuses with clear margin and in
different size on the cut surface of the lung, appearing as fine, white granules, feel as
gritty deposits.
2) Calcification of atheromatous plaque
Tissue section: (Fig. 2-25) There are basophilic, amorphous granular deposit in the
necrotic area of the atheromatous plaque in the aorta.
5. Necrosis
Basic pathologic changes
(1) Gross morphology: The necrotic presents a variety of morphologic appearances
according to different types of necrosis.
◆
Coagulative necrosis: The tissue is grayish-white or yellowish-white, and
exhibit a firm texture, losing the normal structure.
◆
Liquefactive necrosis: The necrotic tissue liquefies and heals by cyst formation.
◆
Caseous necrosis: The necrotic tissue is yellow-white, and cheesy due to
lipoids.
◆
Gangrene: Large areas of necrosis with putrefaction of the tissues. The affected
tissues appear black, dark green.
(2) Histopathology
◆
The necrotic cell presents pyknosis, karyorrhexis and karyolysis, showing a
solid, shrunken basophilic mass, or breaking into pieces, or totally disappearing.
◆
The necrotic cell may have a more glassy homogeneous appearance than that of
normal cell. The cytoplasm shows increased eosinophilia, the plasma is
disrupted, and the normal structure is blurred or disappeared.
◆
Coagulative necrosis: The general tissue architecture of affected tissue is
preserved. Liquefactive necrosis: The affected tissues are transformed into a
liquid viscous mass. Caseous necrosis: The affected tissues appear as
amorphous, eosinophilic granular debris, the tissue architecture is completely
obliterated.
◆
The tissues surrounding the necrotic area are frequently accompanied by
29
hyperemia (vascular dilatation) and inflammatory cell infiltration. If not
detached or completely absorbed granulation tissue could grow into it.
Specimen observation
(ⅰ) Coagulative necrosis of the spleen
Case abstract:A 30-year-old female patient died of myocardial infarction.
Gross specimen: (Fig. 2-26) It is thus evident that there is a grayish-white or
grayish–yellow, irregular area on the surface of the spleen。The infarct is roughly
wedge-shaped and sharply demarcated, with the top toward the hilum of the organ,
and the base is a serosal surface. The texture is pale and firm with a red hyperemic
rim.
Tissue section: (Fig. 2-27a,b,c,d) ①Gross observation of this section shows that it is
a bright red, dense tissue. There is a pink and wedge area in it; ②Under low
magnification, the normal splenic structure is lost in pink-stained zone, where is just
the necrosis. It is surrounded by irregular, dark red band (hemorrhagic margin); ③
Under high magnification, the tissues in the necrotic area preserve basic contour of
the spleen, strongly eosinophilic. All forms of necrosis decline can be seen: pyknosis,
karyorrhexis and karyolysis.
(ⅱ) Liquefactive necrosis
1) Abscess of the cerebra
Case abstract: A 15-year-old male patient was hospitalized for headache and
vomiting for five days. He had a chronic purulent tympanitis history. The patient died
of respiratory failure.
Gross specimen: (Fig. 2-28) It is a coronal cut surface of the cerebral tissue. The
surface presents hemangiectasis, and the gyruses are wider. On the cut surface of the
brain, several oval, regular cysts are located just below the surface. The inter wall of
such cyst is covered with white-yellowish necrotic tissue. There is till pus in the
cavums.
2) Encephalomalacia (Cerebral infarct)
Gross specimen: (Fig. 2-29) On the coronal cut surface of the brain, a round and
irregular cyst is located just below the surface, the content of the cyst have run off.
Surrounding cerebral tissues show loose griddle form.
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3) Liquefactive necrosis of the brain (Epidemic encephalitis B)
Tissue section: (Fig. 2-30a,b) ①Gross observation of this section shows that it is a
red, dense tissue; there are some light stained foci in it. ②Under low magnification,
the scattered liquefactive multiple foci are encephalomalacia focuses, which are
necrosis of the brain tissue, loose and light stained, usually presents oval shape. ③
High magnification shows debris of necrotic cells in the encephalomalacia focuses.
Surrounding the focuses, the degeneration and necrosis of the nerve or the
neuronophagia and satellitism can be seen.
Question: Why is it easy for the brain to occur with liquefactive necrosis?
4) Liquefactive necrosis of the liver (Amoebic liver abscess)
Case abstract: A 40-year-old female patient complained of a 3-month pain in the
right upper abdomen. She has had a cough and asthma for two months. Physical
Examination: The right upper abdomen was distended, and the lower border of the
liver had moved down to 5cm below the right costal margin.
Gross specimen: (Fig. 2-31) The liver is enlarged, it shows an irregular, nodular
surface. On the cut surface, a large capsule can be seen. The content of the capsule
have run off, left incompletely liquefied fluffy materials inside. The inter wall of the
capsule is coarse.
(ⅲ) Caseous necrosis
1) Caseous necrosis of the kidney
Case abstract: A 50-year-old male patient gained admission to the hospital for
urgency and frequency of urination for 30 days and emaciated for one year. But no
any chronic cough and haemoptysis were complained. Physical examination: Lungs
are normal. Urine culture: Tubercle bacillus was isolated.
Gross specimen: (Fig. 2-32) A tuberculous kidney with different size, multiple foci of
caseous necrosis. The necrosis is yellow-white and cheesy. There are cavitations in
some foci attach with caseous material on the wall.
2) Caseous necrosis of the lymph node (Caseating lymph node tuberculosis of the
hilum of the lung)
Gross specimen: (Fig. 2-33) On the cut surface, the necrotic areas foci are
yellow-white and cheesy, different in size. Some necrotic foci are confluent.
Tissue section: (Fig. 2-34) Normal structure of lymph node is devastated, which is
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substituted by pink amorphous granular debris enclosed by tuberculous granuloma.
Question: Which diseases can frequently occur with coagulation necrosis?
(ⅳ) Gangrene
1) Dry gangrene of the foot
Case abstract: A 43-year-old male patient felt a pain in the great toe of the left foot
about two years ago. In the last six months, the great toe has gradually changed the
color into black, following this change expanded to the whole left foot quickly.
Physical Examination: The dorsal artery of left foot was pulseless.
Gross specimen: (Fig.2-35) The skin of lesion is shrinkage, dry, and brown-black.
The necrotic area is fairly well demarcated from the healthy tissue.
Question: Which organs can occur easily with dry gangrene?
2) Moist gangrene of the small intestine
Case abstract: A 27-year-old male patient complained of a intense pain in the
abdomen accompanied with nausea for one day. Physical Examination: Marked
tenderness present in the abdomen. Abdomen x-ray showed intestinal obstruction.
Gross specimen: (Fig. 2-36) It is a portion of the small intestine. The intestinal wall
is thickened. It loses its normal sheen and turn to a gray black color. The surface of
local serosal membrane is rude due to exudates on it. The necrotic area isn’t fairly
demarcated from healthy tissue.
(ⅴ) Fibrinoid necrosis of the vessel wall
Case abstract:A 11-year-old female patient had a fever accompanied by palpitation
for 15 days. She was diagnosed as rheumatism.
Tissue section: (Fig. 2-37) A cross section of vessel shows irregular thickening of the
wall, the lumen is stenosis. The thickening vessel wall shows a sharply demarcated,
homogeneous, deeply eosinophilic zone of necrosis.
(ⅵ) Reaction to necrosis
1) Cavity (Pulmonary tuberculosis)
Case abstract: A 45-year-old male patient has had pulmonary tuberculosis for about
25 years. He complained of massive hemoptysis many times last years.
Gross specimen: (Fig. 2-36) The cavities are located in the lesion lung, multiple and
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irregular. The wall of the cavity is covered with caseous material. The peripheral
tissue is fibrotic and grayish-white.
Question: How did the cavity form?
2) Ulcer (Ulcer of the stomach)
Case abstract: A 36-year-old male patient, he has epigastric pain usually after meals
for six years. The pain has got worse in the last three days.
Gross specimen: (Fig. 2-39) A portion of stomach has been opened along the greater
curvature of stomach. There is an oval deep defect in the mucosa of the lesser
curvature. The ulcer penetrates deeply down to muscular layer, and it is about 1.5cm
in diameter. The mucosal folds surrounding the ulcer converge in a star-shaped
pattern toward the ulcer.
Question: Where dose the ulcer often occur in the stomach?
3) Calcification (Calcification of the lung tuberculosis)
Case abstract: A 50-year-old man had pulmonary tuberculosis during childhood. In
this health examination, chest x-ray showed several dense and round shadows in the
right upper lobe of lung.
Gross specimen: (Fig. 2-24) It is a cut surface of the lesion lung. There are several
grayish-white, gritty-like granules on the cut face of the lung, fairly well demarcated
from surrounding tissue, and the sizes are different. They are just calcified material.
Question: What kind of pathologic calcification do this calcification belong to?
(ⅶ) Apoptosis
Basic pathologic changes
◆The
affected cell shrinks.
◆
The cytoplasm is intensely eosinophilic.
◆
The nucleus is small and dense or disappeared.
◆
Apoptotic body: A round or oval mass of intensely eosinophilic cytoplasm..
Specimen observation
Apoptosis of hepatocyte
Tissue section: (Fig. 2-40a,b,c) ①It presents diffuse hydrophic degeneration of
many hepatocytes. The single apoptotic hepatocyte is visible in the hepatic cord with
dense eosinophilic cytoplasm; ②The apoptotic cell is small in size, and the nucleus is
small, deep stained or even disappeared.
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Question: What is the difference between apoptosis and necrosis?
CASE DISCUSSION
Autopsy case
Case abstract. The 50-year-old man, with hypertension for over 20 years, had frequent
dizziness and headache. His B.P. fluctuated between 33kPa/14.5kPa and 26kPa/13kPa.
About two years ago, he had felt palpitation, panting and fatigued decrement upon
physical exertion. In the last one year, his condition had become aggravated by
dyspnea, oliguria and edema of both lower extremities and he had been thus unable to
lie down flat. Cough with frothy sputum presented at the same time. Half a year ago,
his lower extremities had been cool and numbed. He had felt apparent legs pain while
walking, and the symptoms mentioned above had also intensified. In the last several
days, he had felt sharp pain in the right foot, and the dorsal artery of right foot had
been pulseless. The skin of the foot had gradually changed the color into black.
Finally, the foot didn’t act completely. The patient died of heart failure at last.
Autopsy records.
1. Cardiac hypertrophy, there is a sheet of grayish-white scar on the wall of left
ventricle.
2. Aorta atheromatosis and coronary atheromatosis.
3. Chronic congestion of the lungs.
4. Chronic congestion and fatty degeneration of the liver.
5. Congestion and hydropic degeneration of the kidneys, hyaline degeneration of
afferent glomerular arterioles.
6. Hyaline degeneration of the arteriole and congestion of the spleen.
7. Thrombosis in the anterior tibial artery of the right foot.
8. Gangrene of the right foot.
Discussion
1. What are the causes of the cardiac lesion?
2. How to explain these symptoms: dyspnea, cough with frothy sputum, oliguria,
and edema of both lower extremities?
3. What are the causes of fatty degeneration of the liver and hydropic
degeneration of the kidney?
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4. Why does thrombosis occur in the anterior tibial artery of the right foot?
5. Why dose the right foot take place gangrene? What kind of gangrene does it
belong to?
PRACTICE REPORT
1. Illustrate the histological morphology of ①fatty degeneration of the liver;
②hydropic degeneration of the renal tubular epithelial cell.
2. Describe the gross morphology of ①pressure atrophy of the kidney; ②
coagulation necrosis of the spleen.
3. To compare dry gangrene with wet gangrene.
QUESTIONS FOR REVIEW
1. What are the differences between degeneration and necrosis?
2. What are the differences in the vacuoles of the parenchymal cell between
hydropic degeneration and fatty degeneration?
3. What are the pathological diagnostic criteria for necrosis?
4. What kind of necrosis does caseous necrosis belong to?
5. To grasp concept of terms listed below: atrophy,metaplasia,degeneration,
tiger skin-like heart, necrosis,gangrene, organization, ulcer, cavum, sinus tract,
fistula cannulas and apoptosis.
(Kunming Medical University Cui Jin, Hua Hairong, Zhou Yingying)
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