Chapter 4 Hemodynamic Disorders
AIMS
1.To grasp the pathological characters and influences of congestion, thrombus and
infarction.
2. To be familiar with the classification of thrombus and hemorrhage, and influences
of embolism and the conditions of thrombosis.
CONTENTS
Congestion
Gross specimen
Tissue section
Chronic congestion of the lung
Chronic congestion of the lung
Chronic congestion of the liver
Chronic congestion of the liver
Chronic congestion of the kidney
Chronic congestion of the kidney
Congestive cirrhosis of the liver
Congestive splenomegaly
Congestive edema of the intestine
Thrombosis
Embolism
Valvular thrombus
Pale thrombus
Ventricular mural thrombus
Mixed thrombus
Thrombus in iliac artery
Red thrombus
Thrombus in coronary
Hyaline thrombus
Thrombus in femoral vein
Thromboembolism of pulmonary artery
Organization and recanalization of
thrombus
Thromboembolism
Fat embolism of brain
Fat embolism
Cholesterol embolism
Cholesterol embolism
Tumor cell embolism
Infarct
Anemic infarct of the kidney
Anemic infarct of the kidney
Anemic infarct of the spleen
Anemic infarct of the spleen
Anemic infarct of the liver
Myocardial infarct
Myocardial infarct
Cerebral infarct
Cerebral infarct
Hemorrhagic infarct of the lung
Hemorrhagic infarct of the lung
Hemorrhagic infarct of the intestine
Hemorrhage
Cerebral hemorrhage
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Edema
Pulmonary edema
Pulmonary edema
Cerebral edema
KEY POINTS OF SPECIMEN OBSERVATION
1. Congestion
Basic pathologic changes
(1) Gross morphology
◆
Congested organ often represents enlargement with tunica tensed;
◆
Both surface and cut surface of congested organ are dark-red;
◆
Dilated and darkened capillaries and minimal blood vessfdfels can be seen on the
surface of congested organ;
◆
Long-standing congestion can cause consolidation of affected organ with
red-brown micro-nodular appearance.
(2) Histopathology
◆
Capillaries and minimal blood vessels inside the congested tissue are dilated with
engorgement of RBC;
◆
Pink edematous fluid, RBC and hemosiderin-laden macrophage can be seen;.
◆
Atrophy or necrosis of parenchyma cells can be seen after a long-standing
congestion, along with the proliferation of mesenchyma.
Specimen observation
(ⅰ)Chronic congestion of the lung
Case abstract: A 45-year-old female was complaint of palpitation, short breath and
cough for 6 years with dyspnea and edematous lower extremities for half a year.
Frequent pharyngodynia and mobile arthragia had presented 20 years before. The
symptom of palpitation, dyspnea and edema worsened recently and she was unable to
lie horizontally on active position. Physical examination showed cyanosis and
precordium rales. She was invalidation to the medical treatment and died.
Gross specimen: (Fig.4-01a,b) The congested lung appears enlargement, overweight,
with tunica tensed. The cut surface is red-brown and consolidated, without normally
honeycomb –like structure. Flowing of pink frothy edema fluid may be seen in fresh
specimen.
Tissue section: (Fig.4-02a,b,c) ①Uniformly diffuse consolidation of lung tissue can
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be seen. ②The capillaries in the alveolar septa are dilated and engorged with RBC,
the alveolar septa appear thickened (normally, there are 1 to 2 RBC inside the
capillary on cross section).③The alveolar spaces contain pink edema fluid, RBC and
hemosiderin-laden macrophages (so-called heart failure cell).
Question: What is heart failure cell referred to? Are the hemosiderin-phagocytized
macrophages seen in the pulmonary tissue all heart failure cells?
(ⅱ) Chronic congestion of the liver
Case abstract: A 62-year-old female with a history of chronic bronchitis and
emphysema for more than 20 years was admitted due to palpitation, short breath and
edema
in
lower
extremities.
Abdominal
turgor,
mobile
dullness
and
hepatosplenomegaly were noticed during physical examination. She died after active
medical treatment.
Gross specimen: (Fig.4-03a,b,c) The affected liver appears enlargement, overweight,
with tensed tunica and blunt edge. The cut surface is protruded and cut-edge is
eversion. The surface and cut surface of liver appear regular interval with red zone
and yellow zone, which just looks like the cut surface of nutmeg. So it is also called
‘nutmeg liver’.
Tissue section: (Fig.4-04a,b) ①Normal lobular structure of liver exists and numerous
RBC are aggregating in the centrolobular region. ②The central veins and surrounding
hepatic sinus become intensely congested, and the hepatocytes are atrophy or
disappear in the central zone. ③The periportal hepatocytes undergo various degree of
fatty change, and fatty vacuoles in different size can be seen in the cytoplasm around
the nucleus.
(ⅲ) Chronic congestion of the kidney
Gross specimen: (Fig.4-05) The congested kidney is enlarged with dark-red color.
And blood is pooled in the medulla.
Tissue section: (Fig.4-06) The engorged vessels and hyperemic glomeruli is noted.
Normally, only a few RBCs in the capilllary loops of the glomerulus can be seen.
(ⅳ) Congestive cirrhosis of the liver
Case abstract: A 70-year-old female who was diagnosed as chronic cor pulmonale 10
years ago was dead as a result of her recently worsen physical status.
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Gross specimen: (Fig.4-07) The liver is volume-decreased, lighten and harden,
alternate with red and yellow. There are uniform, numerous micro-nodules on the
surface and cut surface of it.
Tissue section: (Fig.4-08) The congestive region of liver tissue is divided and
substituted by fibrous mesenchyma so as to form pseudolobular.
(ⅴ) Congestive splenomegaly
Case abstract: A 68-year-male was complicated with liver cirrhosis for 8 years after
being diagnosed as chronic virus hepatitis 15 years ago. Recently, his ascites
increased and coma presented. As a result of ineffectiveness to the medical treatment,
he died.
Gross specimen: (Fig.4-09a,b) The volume of spleen is increased and the organ
appears swollen, red-brown. Irregular tan-white fibrous plaques can be seen over the
purple surface.
(ⅵ) Congestive edema of the intestine
Gross specimen: (Fig.4-10) The colonic mucosa appears edematous thicker, and the
mucosa folds are broadening and the color turns white.
2. Thrombosis
Basic pathologic changes
(1) Gross Morphology
◆
Location of thrombus: cardiac chamber, valve or vascular lumen;
◆
Color of thrombus: gray (pale thrombus); red and gray (mixed thrombus); red or
dark (red thrombus);
◆
If the thrombus is intensely adherent to the vessel wall.
(2) Histopathology
◆
Pale thrombus is composed of pink granular platelet and red string-like fibrin;
◆
Mixed thrombus is mainly composed of trabecular platelet, fibrin network, RBC
and WBC. A small number of WBC can be seen attaching to the trabecular
platelet;
◆
Red thrombus is composed of fibrin network, a large amount of RBC and a small
number of WBC;
◆
Hyaline thrombus is composed of fibrin.
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Specimen observation
(ⅰ) Pale thrombus
Valvular thrombus (Acute rheumatic endocarditis)
Gross specimen: (Fig.4-11) The small verrucous vegetations seen along the closure
line of atrial surface of the mitral valve are tightly adherent to the mitral valve. These
warty vegetations average only a few millimeters, 1 to 2 mm in diameter.
Tissue section: (Fig.4-12a,b) The thrombus seen along the surface of the affected
valve is composed of pink granular platelet and red string-like fibrin.
(ⅱ) Mixed thrombus
1) Ventricular mural thrombus
Case abstract: A 56-year-old male who was diagnosed as myocardial infarction half
a year before was dead because of left-side paralysis with coma and ineffectiveness to
treatment.
Gross specimen: (Fig.4-13) Two pieces of large, irregular, gray white thrombus are
visible attaching to both the anterior free wall and the septa of the left ventricle
intensely, where dark-red intima is presented, so called subendocardial infarct.
Question: What are the causes of this thrombus? What consequences can be incurred
when the thrombus is detached from the ventricular wall?
2) Thrombus in iliac artery
Gross specimen: (Fig.4-14) A pupa-like thrombus can be seen at the branching site
of abdominal aorta and iliac artery with a coarse, crisp, gray-and-dark color
appearance, and intensely adheres to the intima. The yellow-white sclerosing plaques
can also be seen along the intima of artery.
Question: What are the causes of this thrombus? What consequences can be incurred
when the thrombus is detached from the venous wall?
3) Intravenous thrombus
Tissue section: (Fig.4-15) The venous lumen is occluded by a thrombus and the
thrombus is mainly composed of pink, trabecular platelet, dark-red fibrin network, a
large amount of RBC and a few WBC.
(ⅲ) Red thrombus
1) Thrombus in femur vein
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Case abstract: A 24-year-old male suffered from infective pyogenesis because of
being stabbed by a nail in his left foot half a year ago. After internal medication, he
recovered. From then on, recurrently pain and swelling in his left leg began. Today he
was suddenly fallen down during ambulation and died after emergency treatment.
Gross specimen: (Fig.4-16) A dark-red crosslinked thrombus can be seen inside the
femur vein. The thrombus attaches intensely to the venous wall and makes the vein
occluded.
Question: Where can be the destination of this thrombus after detaching?
Tissue section: (Fig.4-17) A newly formed thrombus which consists of fibrin network
together with RBC and WBC is noted.
2) Thrombus in coronary artery
Case abstract: A 45-year- old male died on the way to hospital as a result of sudden
awful precordium pain, which ejected to the shoulder, upper extremities and was
unresponsive to Nitmglysertdn, complicated by the symptoms of chest distress and
short breath.
Gross specimen: (Fig.4-18a,b,c,d) The anterior surface of the heart demonstrates an
opened left anterior descending coronary artery. In the lumen of the coronary artery a
dark red recent coronary thrombus is visible. The dull red color to the myocardium as
seen below the glistening epicardium to the lower right of the thrombus is consistent
with underlying myocardial infarction.
(ⅳ) Organization and recanalization of thrombus
Tissue section: (Fig.4-19a,b,c) The formation of new small vessels and the
proliferation of fibroblast can be seen as a sign of thrombus organization, and newly
formed vessels regain blood flow.
(ⅴ) Hyaline thrombus (DIC)
Case abstract: A 25-year-old female who suffered a large scale of burn died during
emergency medication because of subcutaneous and multiple organs hemorrhage and
shock, with a diagnosis of DIC.
Tissue section: (Fig.4-20) Fibrinous thrombus is visible within the pulmonary small
vessels.
3. Embolism
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Basic pathologic changes
(1) Gross morphology
◆
The lumen of either pulmonary or systemic artery is occluded by thrombus or
other foreign substance;
◆
The foreign substance stuck inside the vessel is not tightly adherent to the wall.
(2) Histopathology
◆
Ischemia or congestion can be seen in the affected organ or tissue;.
◆
Histological types of embolus include thromboembolus, amniotic embolus, fat
embolus, bacterial embolus and tumor cell embolus, and etc.
Specimen observation
(ⅰ) Thromboembolism of pulmonary artery
Gross specimen: (Fig.4-21a,b,c,d) The main pulmonary artery is occluded by a large
dark-red mass, which is not adherent to the vessel wall. Such thromboemboli typically
originate from the veins of lower extremity.
Tissue section: (Fig.4-22a,b) The thromboembolus is seen in the main branch of
pulmonary artery occluding the lumen. The embolus is composed of pink trabecular
platelet and fibrin, and it shows no adherent to the vessel wall.
(ⅱ) Fat embolism
Case abstract: A 35-year- old male who underwent both tibia and fibula fracture and
soft tissue bruise caused by a traffic accident died during medication after a sudden
burst of dyspnea, headache and blood pressure decreased.
Tissue section: (Fig.4-23a,b) The pulmonary vessel is plugged up by fatty materials.
The bone marrow component (marrow fat) inside the small pulmonary artery is noted
at high magnification.
(ⅲ) Cholesterol embolism
Tissue section: (Fig.4-24a,b) A cholesterol embolus in an artery near the pancreas is
seen. The thin, clear spaces, which represent cholesterol crystals, are noted. In severe
atherosclerosis, plaques will occasionally break off and embolize throughout the
arterial system.
(ⅳ) Tumor cell embolism
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Tissue section: (Fig.4-25a,b) A group of tumor cells can be seen uniformly in the
small vessel of brain and the tumor cells are polyangular with diversity of sizes,
enlarged nuclear, prominent nucleoli and show obvious atypia.
4. Infarct
Basic pathologic changes
(1) Gross morphology
Infarct is commonly seen in kidney, spleen, lung, intestine, heart, brain and etc,
◆
and usually located beneath the tunica of the organ.
◆
Color of infarct
White infarct: anemic infarct, mainly involve solid organs such as liver, spleen
kidney, myocardium and so on;
Red infarct: hemorrhagic infarct, mainly involve loose tissues and tissues with
dual circulations such as lung, intestine and so on.
◆
Shape of infarct
Wedge-shape: infarct of liver, spleen, kidney, lung;
Map-like shape: myocardial infarct;
Segmental shape: intestinal infarct.
◆
At early stage, all infarcts are poorly defined. The margins of both types of infarcts
tend to become better defined with time by a narrow rim of hyperemia and/or
hemorrhage attributable to inflammation at the edge of infarct.
(2) Histopathology
◆
The essence of infarct
Coagulative necrosis: liver, spleen, kidney, myocardium, lung and so on;
Liquefactive necrosis: brain, pancreas and so on;
◆
The infarct is a kind of tissue necrosis among which pyknosis, karyorrhexis and
karyolysis can be seen. The outline of original tissue can be discerned despite that
the cells are dead.
◆
Anemic infarct contains few RBC; while hemorrhagic infarct has engorgement
and hemorrhage;
◆
The pathological changes secondary to infarct such as hyperemia, hemorrhage,
inflammation, organization and so on.
Specimen observation
(ⅰ) Anemic infarct
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1) Anemic infarct of the kidney
Gross specimen: (Fig.4-26a,b) Infarcts in the kidney are wedge-shaped, the bottom
based on the tunica and the apical point to the hilum. They have a gray or yellow
bulged appearance, well demarcated, and with a hyperemic and hemorrhagic margin.
Tissue section: (Fig.4-27a,b) At the right is normal kidney, then to the left of that is
pale pink infarcted kidney in which both tubules and glomeruli are dead. The outline
of glomeroli and tubule of kidney is reserved .The zone of hyperemia and hemorrhage
where the dilated vessels and hemorrhage can be seen, locates between the normal
and infarcted kidney.
2) Anemic infarct of the spleen
Gross specimen: (Fig.4-28a,b) ①Please pay attention to observe the shape and the
color of the lesion. ②Please notice the margin of the lesion.
Tissue section: (Fig.2-27) ①Firstly, discern the infarction and the non-infarction
regions please. ②Compared with the non-infarction, please notice the pathological
characters of infarction. ③To observe the adjacency between the infarction and
non-infarction.
3) Anemic infarct of the liver
Gross specimen: (Fig.4-29a,b) Infarct is seen on the cut surface of the liver. The
infarct is yellow, with geographic borders and surrounding hyperemia.
4) Myocardial infarct
Case abstract: A 58-year-old female had a 10-year-history of hypertension and
hypercholesteremia. 3 days ago she felt precordium pain with a ejection to left
shoulder and this symptom worsened gradually with coma. She died soon though
emergency treatment was adopted. At autopsy, coronary atherosclerosis with
secondary thrombus was revealed.
Gross specimen: The cross section of the heart demonstrates the left ventricle on the
left. (Fig.4-30a,b,c) (a) Circumferential infarction of left ventricle. The infarct is
confined to the sub-endocardial zone of the entire left ventricle. Locally thick wall MI
is presented. (b) Acute myocardial infarct involving the posterior wall of left ventricle.
The zone of infarct is mottled with yellow-tan center, and surrounded by hyperemic
border, extending through the full thickness of the wall, called "transmural" infarct.
(c) The myocardial infarct scar in anterior wall of left ventricle and anterior 1/3
portion of ventricular septum.
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Tissue section: (Fig.4-31a,b,c) (a) Early stage of acute myocardial infarct. The
myocardial fibers lose cross striations and the nuclei are not clearly visible in most of
the cells seen here. Note the many irregular darker pink wavy contraction bands
extending across the fibers. (b, c) This myocardial infarction is about 3 to 4 days
duration. There is an extensive acute inflammatory cell infiltrate and the myocardial
fibers are so necrotic that the outlines of them are only barely visible.
5) Cerebral infarct
Gross specimen: (Fig.4-32) It is the same appearance as the liquefactive necrosis of
brain, please describe the pathological change by yourself.
Tissue section: (Fig.4-33a,b,c) It is the same appearance as the liquefactive necrosis
of brain, please describe the pathological change by yourself.
Question: Does the resolution of an infarct in the brain produce a fibrous scar, as
occurs in other body tissues? Notice the tissue at the edges of the infarct. Is the
number of astrocytes normal? What is the role of the astrocytes in this setting?
(ⅱ) Hemorrhagic infarct
1) Hemorrhagic infarct of the lung
Case abstract: A 65-year-old female had a history of mitral stenosis and insufficiency
for 10 years as a result of rheumatic heart disease. Recently, her dyspnea worsened,
pink foamy sputum and hemoptysis were produced. Hepatosplenomegaly, pleural
effusion, ascites, and systemic edema were noticed and she died after active treatment.
Gross specimen: (Fig.4-34a,b,c) The seen dark-red infarcts in the lung is
well-demarcated, wedge-shaped, the bottom based on the tunica and the apical point
to the hilum.
Tissue section: (Fig.4-35a,b,c) ① A wedge-shaped lesion can be seen in the lung; ②
Diffused hemorrhage and large scale of necrosis can be seen in the affected
pulmonary tissue; ③ The outline of alveoli and septum can be discerned in the
pulmonary infarct; ④ Congestion is noted in non-infarcted pulmonary tissue.
2) Hemorrhagic infarct of the intestine
Gross specimen: (Fig.4-36a,b) The hemorrhagic infarct of intestine is segmental,
dark-red with unclear borderline and obvious edema.
5. Hemorrhage
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Basic pathologic changes
(1) Gross morphology
◆
The pathological changes differ as the result of different location or different
amount of bleed. For instance, it can manifest as petechia, hematoma , blood
effusion and etc.
◆The
red color of lesion means a recent hemorrhage and the red-dark blood clot
indicate a dated hemorrhage.
(2) Histopathology
◆
A various amount of blood element can be seen in the tissue (outside the vessel).
Specimen observation
Cerebral hemorrhage
Case abstract: A 65-year-old male had a more than 20-year-history of hypertension
with an average blood pressure 27.5/13.6KPa. He felt dizziness, headache and nausea.
After once falling down, he was disabled with coma and finally died.
Gross specimen: (Fig.4-37) A large scope of dark-red bleed can be seen near the
capsula interna of brain from coronary or horizontal cut. The cerebral tissues there are
destroyed.
6. Edema
Basic pathologic changes
(1) Gross morphology
◆
The organ or tissue which endure edema usually appear enlargement, soft,
overweight with tunica tensed and color tinged.
◆
The edematous fluid inside the body cavity is referred as edematous effusion.
(2) Histopathology
◆
The edematous fluid scatters inside the cell, tissue or body cavity.
◆
Various amount of proteinaceous edema fluid can be seen in the involved tissue
and the cells are swollen, round and tinged.
Specimen observation
(ⅰ) Pulmonary edema
Case abstract: A 19-year-old male died from anaphylactic shock after injection of
penicillin, which was to cure his influenza and fever.
Gross specimen: (Fig.4-38) The smooth, glistening pleural surface of a lung is shown,
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and the lung lobules are outlined in white.
Tissue section: (Fig.4-39a,b) Septal capillaries are congested and the alveoli are filled
with pink-staining proteinaceous edema fluid.
(ⅱ) Cerebral edema
Case abstract: A 58-year-old male had a 15-year-history of hypertension died of
suddenly awful headache, vomiting, convulsion and coma though emergency
treatment was induced.
Gross specimen: (Fig.4-40) The herniation into the foramen magnum caused by
cerebral edema is shown here.
CASE DISCUSSION
Clinical case
Case abstract. Female, 30 years old, farmer.
Chief complaint. Intermittent palpitation and short breathe for 1 year; lower
extremities edema and oligouria for 1month.
Current medical history. Since last year, she felt palpitation and short breath after
laboring, and these symptoms were relieved when relaxation. She caught a cold, and
presented fever, pharyngodynia, worsen palpitation and short breath one month before.
Simultaneously, lower extremities edema, oligouria, and right-upper abdominal turgor
began and her appetite decreased, especially she was unable to lie horizontally. She
was admitted to hospital because the general medical treatment was ineffective to her.
Past medical history. Frequent pharyngodynia and arthralgia 10 years before was
mentioned.
Physical examination. She was semireclining position, chronic sickly complexion
with terminal and lips cyanosis. Jugular vein dilated, and mild-moderate rales in the
dorsal of both lungs were noticed. Fremitus during diastolic phase was palpated in
precordium region. The cardiac border was enlarged bilaterally. HR 110/min, BP:
110/70 mmHg. Arrythmia, thunder-like murmur during diastolic phase and blowing
murmur during systolic phase was ausculatated. The liver was 3 cm beneath the rib
and 5 cm beneath the xiphoid process, tough and mild tenderness. Hepato-jugular
veins regurgitation sign was positive and the lower extremities was depressive edema.
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Lab examination. Urine: protein (+), RBC 1-2/HP, hyaline cast 1-2/HP.
X-ray. The heart was bilaterally enlarged and the texture of both lungs increased.
Clinical diagnosis:
(1) Rheumatic heart disease;
(2) Mitral stenosis and insufficiency;
(3) Pan-heart failure.
Questions
1. What evidences can be based on to make the clinical diagnosis of pan-heart
failure?
2. What kinds of pathological changes exist in this patient on the basis of her
clinical feature?
3. What medication should be taken to treat this patient?
Autopsy case
Case abstract. Male, 24 years old, worker
Current medical history. The patient was stabbed by a nail in his left foot during
working half a year ago. Locally infective pyogenesis, lower extremity reddish and
swelling presented and recovered gradually 2 weeks later. Ever since then, several
times of pain and swelling in his left shank were mentioned. The pain and swelling
extended to the ambient of knee joint 2 months before and was relieved by the
mediation in hospital. 4 days before, the mentioned pain and swelling became
worsened, accompanied by fever. He was cough, expectoration since yesterday and
this morning a small amount of hemoptysis without chest pain was found. Physical
examination: unremarkable except edematous left lower extremity. This afternoon at
2:15 the patient suddenly fell down after a cry-out on the way from toilet to ward. The
patient was seen spasm, facial cyanosis, pupil enlarged with white froth out from his
mouth when the medical staff came. Finally, he died at 2:50 after emergency
treatment, which was ineffective to him.
Clinical diagnosis. Sudden death with unknown etiology
Autopsy records.
Gross specimen examination: the left leg was edematous which was dominant below
the knee joint. A post-trauma scar was seen on his left foot. After being incised, the
femoral artery and its branches was shown no remarkable change (Fig. 4-41). A large
portion of the left femoral vein was thicken and harden. The segment between fossa
and oval foramen was obstructed by a clot-like mass, which was 40 cm long, dark-red,
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coarse, crisp and was not tightly adherent to the venous wall. Some portion of it was
gray and adhered to the wall (Fig.4-42). The main pulmonary artery, two branches of
it and the small arteries were also blocked by the dark-red, coarse, crisp clot-like mass,
which were not adherents to the vessel wall.
Microscopic examination. The mass inside the left femoral vein was mainly red
thrombus (a large amount of RBC filling in the fibrinous network) and a small portion
of mixed thrombus(trabecular platelet being seen). Granulation tissue was seen
growing into the thrombus at the edge of venous wall. The mass inside the main
pulmonary artery, the two branches of it and the small arteries were dominantly red
thrombus, within which granulation tissue could also be seen (Fig.4-43).
Question
1. What was the lesion inside the femoral vein? How did his lesion form? Why this
kind of lesion was not seen in femoral artery?
2. What was the lesion inside the femoral artery? Why?
3. What could be inferred from the evidence that granulation tissue had grown into
the clot-like mass in the small pulmonary artery? Why the according pulmonary
infarction was not induced?
4. Please say the correlation between the lesions mentioned above?
5. What was the cause of his death? Why?
PRACTICE REPORT
1. Illustrate the histological morphology of ①chronic congestion of lung; ②mixed
thrombus
2. Describe ①the microscopic appearance of valvular thrombus and pulmonary
hemorrhagic infarct; ②the gross specimen of splenic anemic infarct.
3. Please illustrate all the hemodynamic disorders with arrow and mark the causes of
each disorder.
4. To write the discussion epitome of each case.
QUESTIONS FOR REVIEW
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1. Which organs should be paid special attention during autopsy to a patient who died
of right heart failure? What are the probable lesions in these organs and how can
these lesions correlate with heart failure?
2. Why motionless patient who has underwent operation and stayed in bed for a long
time is prone to venous thrombosis? Under what circumstance that the venous
thrombus is easy to break off and what consequence can be brought about? How to
prevent it from happening?
(China Medical University Li Qingchang, Lin Dong, Zhao Yue)
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