Pathology Anatomy Colloquium 1
cadaver after 24 hrs in warm room has a
1. Specify tasks of pathological anatomy (p=4)
- Establish cause of death, pathogenesis,
diagnosis, scientific research work
2. Define principal services of R Virchov in
the development of Path Anatomy (p=3)
3. Define general lines of IV Davidovsky
scientific effort (p=5)
4. Specify levels due to study of disease
structural basis (p=7)
5. What is autopsy? (p=2)
- Known as post-mortem examination
necropsy, or abduc. Is a medical procedure that
consists of a thorough examination of corpse to
determine cause, manner of death, evaluate
any disease or injury.
6. What is biopsy? (p=2)
- A medical test involving removal of cells,
tissues for examination
7. Name types of death according to etiology
(p=3)
- Fatal trauma
- Diseased death
- Violent death
8. Specify causes of violent death (p=3)
- Murder
- Suicide
- Trauma
9. Name signs of death discovered in external
examination (p=6)
- Absence of breathing and asystole
- Absence of pulsation
- Clouding of cornea
- Brown macular cornea
- Decreased rectal temperature
- Stiff cadaver
- Cadaver staining
- Cadaver putrefaction
10. What are cadaver stains? (2)
- Postmorten hypostasis of blood with
hemolysis and redistribution of blood.
11. What are cadaver hypostases? (p=1)
- Flowing down of blood under the influence
of gravity, without heart intervention
12. What is cadaver inhibition? (1)
- Postmortem saturation of tissue with products
of Hb disintegration
13.
gray and green belly skin, its soft tissues have
crepitas with palpation, contains gas bubbles.
What is the name of these cadaver changes and
what is their etiology? (4)
- Name of cadaver: Cadaver emphysema
- Etiology: Autolysis and putrefaction
14. What is hyperemia? (p=1)
- Blood volume increase in the organ or tissue.
15. Specify types of local hyperemia. (p=6)
- Collateral - Angioneurotic
- Vocational - Inflammatory
- AV- Shunt - Post- Ischemic
16. Give the definition of vocational
hyperemia. (p=6)
- Type of hyperemia characterized by a sudden
decrease in local barometric pressure
17. What is collateral hyperemia? What is the
significance of the process? (p=3)
- Dilation of collateral vessels, filled with
blood due to obstruction of its main vessel (eg
stenosis and thrombosis)
18. What is Medusa head? What is the type of
hemodynamic disorder? (p=4)
- It is a type of collateral hyperemia
- It happens during liver cirrhosis
- Portal hypertension causes congestion of
collateral veins
- Prominent dilation of subcutaneous veins of
the anterior abdominalwall, especially the vena
paraumbilicus and vena epigastricus which
forms a peculiar shape.
19. Specify basic ways of collateral blood flow
with hepatic cirrhosis. (p=3)
- Portal – Esophageal anastomoses
- Portal – Abdominal anastomoses
- Portal – Rectal anastomoses
20. During postmortem examination, a
network of enlarged hypodermic veins and
hemorrhage from enlarged esophageal veins
were found. Name the process. What is the
basic vessel with blood stream disorders?
What is the significance of designated vein
alterations? (p=3)
- Portal vein is the basic disorderly vessel
- Portal hypertension causes collateral
hyperemia of vena gastricus, esophageal vein
which have adaptive compensatory process for
general blood stream disorder
- Collateral hyperemia of esophageal vein can
result in vertical rupture and produce massive
hemorrhage.
21. What are cells of heart valvular diseases?
Where are they detected during medical
examination? What happens in the lungs?
(p=4)
- Siderophage cells (macrophages laden with
hemosiderin)
- They are detected in rusty phlegm
- The lungs undergo brown induration and
chronic pulmonary congestion
22. In patients with mitral valvular diseases,
cough and ‘rusty phlegm’; explain rusty colour
of the phlegm. Give the characteristics of left
heart functional condition and the
hemodynamic changes in the lung. (p=4)
- It is rusty coloured due to siderophages
(hemosiderin laden mphs)
- There is left heart failure due to mitral
prolapse and pulmonary congestion with
dilated capillaries and diapedic blood flow into
alveolar spaces.
- This leads to an increase in siderophages,
which in turn causes brown induration of the
lung
23. Specify processes which take place with
brown induration of the lung.
- Venous hyperemia.
- Per diapedic blood flow into the alveoli
- Siderophage activity
- Pneumosclerosis
24. Name basic macroscopic sign of chronic
venous hyperemia within organs and tissues.
- Red-blue colour
- Surrounded by a zone of uncongested
substance
- Enlarged and firm with a smooth surface
25. Figurative name of the liver in chronic
venous hyperemia.
- Nutmeg liver
26. What local processes does
phlebothrombosis lead to? (p=1)
-Local venous hyperemia and stasis
27. What terms are hemodynamic disorders
designated, which are caused by heart
disturbance? (p=2)
- Hyperemia, Thrombosis, Oedema,
Aneurysm.
28. Name cardial pathology associated with
heart failure. (p=5)
- Phlebothrombosis of endocardium
- Myocardial Infarction
- Cardiomyotis
- Cardiomyopathia
- Valvular defects
29. What organs and systems which pathology
due to development of heart failure? (p=5)
- Heart, Brain, Liver, Kidney, Spleen
30. What does left sided heart failure prove?
(p=3)
- Systemic hypertension, mitral or aortic valve
disease, ischemic heart disease and primary
disease of the myocardium
32. Name the most severe degree of heart
decompensation. (p=3)
- 3rd stage; change in internal organ, sclerosis,
atrophy, wrinkled kidney, oedema of
extremities, accumulation of fluid in body
cavity
33. What do morphological change originate in
tissues and organs from right sided heart
decompensayion? (p=3)
- Liver; nutmeg liver
- Kidney; cyanotic induration
- Spleen; cyanotic induration, splenomegaly
- Serous cavities; dropsy (oedema)
34. In deceased patient, was found chronic
venous hyperemia in internal organs and
dropsy of cavities. Name the cause of death.
(p=3)
- Heart insufficiency (heart failure)
- Decompensation of heart
35. A patient died of heart failure, during post-
mortem examination, you see an enlarged firm
spleen with a smooth capsule; the cut surface
resembles a meaty appearance without scrapes;
dark cherry coloured with cyanotic hues. Name
the changes of spleen.
- Cyanotic induration of the spleen.
36. What are necrosis foci termed within
organs in heart failure? (p=1)
- Marantic necrosis thrombosis
37. Specify marantic necrosis of organs in
patients with heart failure. (p=6)
- Liver, kidney, lung, spleen, brain, colon
38. Name the Greek term for ‘blood volume
losses’. (p=1)
- Ischemia
39. After rapid exhaustion of ascites fluid, the
patient loses his consciousness. Designate
mechanisms of the phenomenon. (p=2)
- Vocational hyperemia of vessel of abdomen
after rapid removal of pressure of abdominal
cavity
- Sudden decrease in blood volume causes
hypovolumic shock
40. What is stasis? (p=3)
- Cessation of natural flow of physiological
fluid in an organism…
- …characterized by the slowing down of
circulation and increased microvascular
permeability and…
- …and increased concentration of RBC and
dilation of small vessels
41. What is hemorrhagia? (p=2)
- Blood outcome from vessels or the heart.
42. Specify and give Latin terms of
hemorrhagia mechanisms. (p=6)
- Per Rhexin: Rupture of vessels
- Per Diabroxin: Erosion of vessels
- Per Diapedesin: Hypermobility of small
vessels
43. Give classification of hemorrhagia
according to source. (p=5)
- Arterial, Venous, Capillaries, Parenchymal,
Cardiac.
44. Specify in English and Latin terms of
external hemorrhage types. P=14
- Nasal (Epistaxis)
- Blood Vomiting (Haematemesis)
- Irregular uteral bleeding (Metrorrhagia)
- Regular uteral bleeding (Menorrhagia)
- Presence of blood in urine (Hematuria)
- Tarry stool as sign of bleeding in GIT
(Melena)
- Blood in the phlegm (hemoptysis)
45. Mechanisms of hemorrhage from gastric
ulcer. (p=2)
- Per diabroxin: Hemorrhage due to erosion of
the vessel wall by pus and enzyme
46. Explain the melena of a patient with gastric
carcinoma. (p=3)
- Stool is black due to infiltration of blood by
per diabroxin bleeding of the erosion of the
vessel wall by malignant tumour enzymes in
peptic ulcer disease
47. Explain the hemaptoe of patient with lung
carcinoma. (p=2)
- Per diabroxin erosion of the capillaries
- Usually by tumour enzymes
- Results in fucking blood in the phlegm
48. What is extravasation? (p=2)
- Exudation of fluid from vessels into the
surrounding tissues.
- Fluids can be blood, lymph or urine.
49. Name basic hemorrhage types. (p=3)
- Internal: Hematoma, purpura, petechii,
ecchymsi, hemorrhagic infiltration.
- External: Epistaxis, hemaptoe, melena
50. What is hematoma? (p=2)
Hematoma is a type of hemorrhage when the
blood is trapped within the tissue, forming a
cavity of blood.
51. What is hemorrhagic infiltration? (p=2)
- Blood saturation of the tissues.
- Blood saturates within tissue without its
destruction
52. Specify and give Latin terms of
hemorrhage types when blood accumulates in
the body cavities. (p=6)
- Hemothorax (blood in the pleural cavity)
- Hemarthrosis (blood in the synovial cavity)
- Hemopericardium (blood in the pericardial
cavity)
- Hemoperitoneum (blood in the peritoneal
cavity)
53. Give names of frequent causes of
hemopericardium. (p=2)
- Acute hemorrhage in heart aneurysm
- Myocardial infarction
54. What is plasmorrhagia? (p=2)
- Saturation of vesselwall by plasma protein
55. Give definition of thrombosis. p=3
- Blood clotting within the vascular system or
cardiac chambers
- Product of thrombosis
56. Identify of thrombi according to their
composition. p=4
- White
- Red
- Mixed
- Hyaline
57. Specify macroscopic parts of the thrombus.
(p=3)
- Head, Body , and Tail.
58. Specify microscopic particles (the
composition) of the mixed thrombus. p=4
- Platelets
- Erythrocytes
- Leukocytes
- Fibrin
59. What is the name of the thrombus to
occlude vessel lumen?
- Obturative thrombus
60. Specify the most frequent arterial
thrombosis.(p=8)
- aorta, cerebral, coronary a, renal, popliteal a,
femoral a.
61. Specify the most frequent venous
thrombosis.(p=6)
- Deep veins of leg
- Right atrial auricle
- Right ventrical
- Veins of small pelvis
- Inferior vena cava
62. Name three localizations of thrombi in the
system of the portal vein.(p=3)
- Splenc vein
- Hepatic vein
- Umbilical vein
63. Specify possible consequences of the
thrombus.(p=6)
- organization
- canalization
- calcification (phleboliths)
- septic dissolution
- embolism
- aseptic dissolution
64. During postmortem examination elastic,
wet plagues of blood with smooth surfaces are
found. They are extracted from vessels easily.
What is their name? What are they
differentiated with? (p=2)
-They are postmortem blood clots
-Differentiated with thrombus
65. Mitral valve leaflets are grown together
with stenosis. There is free spherical large
thrombus with smooth surface into left.
Explain the formation. (p=3)
-Part of the thrombus from the mitral valve
comes out to the left atrium, and is surrounded
by blood, making the surface smooth and
spherical
66. Give the definition of embolism. (p=3)
-Circulation of foreign mass with blood or
lymph which may come to rest anywhere
within the cardiovascular and lymph system
67. Specify types of embolism according to the
direction of embolus pathways. (p=3)
-direct
-indirect/retrograde
-Paradoxical
68. What is retrograde embolism? (p=2)
-It is an embolism which moves in the opposite
direction of blood flow due to the influence of
gravity
69. Identify emboli according to their
composition.
a. thromboembolism
b. fatty
c. bubble of air
d. nitrogen
e. tissue embolism
f. foreign bodies
g. microbial (bacterial)
70. Give the definition of tissue embolism.
- Outcome in metastasis of the malignant cells,
metastasis shows development of secondary
implants discontinued in primary tumours,
possibly in distant tissues
- 3 types: with malignant cells, with amniotic
fluid or with segments of traumatic tissues
71. What is metastasis?
-Appearance of secondary purulent foci away
from the primary foci OR
-Spreading of pathological malignant tissue
72. Specify basic sources of thromboemboli of
pulmonary arteries(p=5)
-deep leg vein thrombi above the level of the
knee joint.
-eg., popliteal ,femoral & iliac veins.
73. What are mechanisms of the death with
pulmonary thromboembolism?
-Pulmo-coronary reflex: causing spasm of
coronary artery and acute left sided heart
failure
- Pulmobronchial reflex: spasm of pulmonary
artery and musculature of bronchial tree
- Acute right sided heart failure
74. Specify contributory conditions for the
development of fatty embolism. (p=4)
-Trauma to subcutaneous fatty tissue
-Trauma to (fatty) bone marrow
-Faulty administration of oil-based injections
-amniotic fluid in newborns during pregnancy
75. Specify possible consequences of fatty
embolism. (p=3)
-respiratory insufficiency
-stroke
-resolution by macrophages
76. What are cases with fatty embolism due to
death? (p=3)
- Respiratory failure
- Cerebral dysfunction with hypoxia and
meningitides
- Petechiae over upper half of body,
conjunctiva, oral mucosa and retina
77. What is shock? (p=4)
-shock systemic hypoperfusion due to 
reduction in 1.) cardiac output 2.) effective
circulating blood volume. -coz hypotension 
impaired tissue perfusion and cellular hypoxia.
78. Give the definition of DIC-syndrome.(p=4)
-Disseminated intravascular coagulation (DIC)
is a complex systemic thrombohemorrhagic
disorder.
-activation of coagulation sequence, leading to
formation of thrombi throughout the
microcirculation.
-coz consumption of coagulants and platelets.
-and secondarily, activation of fibrinolysis.
79. Identify four synonyms of DIC syndrome.
(p=4)
- Consumptive thrombohemorrhagic disorder
- Consumptive coagulopathy
- Defribination syndrome
- Hypocoagulation
80. Patient with phlebothrombosis of leg has a
long bed regime. He suddenly dies with
asphyxia and acute heart failure after he gets
up. Specify cause of death. Give your reasoned
arguments of acute clinic symptoms.
-Cause of death: massive pulmonary embolism
of trunkus pulmonalis and the main pulmonary
artery
-Acute heart failure due to pulmo-coronary
reflex with spasm of coronary artery
-Asphyxia due to pulmo-bronchial reflex due
to spasm of pulmonary artery and musculature
of the bronchial tree
81. In deceased patient with purulent wound of
thigh and regional thrombophile bitis,
multitudinous abscesses are found in the
internal organs. What is the name of the
process spread? What are the mechanisms in
its basis?
-Process: generalisation of septicopyemia
-Mechanism: metastasis of bacterial emboli
82. Give the definition of autolysis. (p=4)
- Enzymatic digestion of cell after its death by
own lysosome enzymes.
83. Give the definition of apoptosis. (p=4)
- Only seen in the cellular level
- a mode of cell death in the living organism as
the genetic programmed cell death
- a pathway of cellular “suicide”.
- Formation of apoptotic bodies.
84. Name basic groups of complications
developing in patients after measures. (p=3)
- Hyperemia, Oedema, Stasis
85. Name clinical anatomic variants
(syndromes) of post-resuscitation disease
(according to V.A. negovsky) (p=5)
86. Which changes of the brain can develop in
patients with long artificial lung ventilation?
(p=4)
87. Which hemodynamic disorders develop
irreversible changes in late reperfusion? (p=3)
88. Name target organs to develop irreversible
changes in late reperfusion. (p=5)
89. Give names of successive stages of cellular
injury in continuous action of pathogenic
factor.（p=4）
- Adaptive changes
- Reversible cell injury
- Irreversible cell injury
- Death of cell
90. Specify time interval of irreversible
ischemic injury of cardiomyocytes and their
diagnose possibilities by routine light
microscopy. (p=2)
- In 30-60 minutes (irreversible ischemic
injury)
- In 10-12 hours (microscopic diagnosis)
91. Explain, why morphologic signs of cellular
death can be diagnosed as a rule, only after
certain
time for each tissue due to cellular death.
(p=5)
- Signs of cellular death are diagnosed reliably
with nucleus changes (karyopyknosis,
karyorrhexis, karyolysis)
- they arise a certain time after death followed
by autolytic processes.
92. Why does suppression oxidative
phosphorylation in the cell lead to cell
swelling? (p=4)
- Loss of ATP production leads to
- depression of Na pumping, accumulation of
water, sodium and calcium in cytoplasm.
93. Why does swelling of cells and organelles
arise after cellular membrane’s destruction?
(p=3)
- Cellular membrane destruction will lead to
disturbances of ionic and osmotic homeostasis
of the cells organelles causing accumulation of
H20. Swelling of cells and organelles.
94. What do morphologic signs of cellular
reaction of pathogenic factor depend on? (p=4)
- They depend on peculiarities of pathogenic
factor (type, duration, severity)
- And cellular condition (adaptive capability)
95. Give examples of cells having high,
moderate and low sensibility in relation to
ischemic (hypoxic)
factor. (p=7)
- High sensibility: neurons
- Moderate sensibility: cardiomyocytes,
hepatocytes, nephrocytes
- Low sensibility: cells of skeletal muscles,
fibroblasts, epidermocytes.
96. Explain essential importance of oxygen in
the progress of cellular injury. (p=5)
- Ischemia – reducing cellular oxygen supplies,
causing cell injury
- Other stimuli such as radiation,
inflammation, chemical, oxygen toxins, aging,
reperfusion injury, lipid peroxidation
97. Name morphologic signs of reversible
cellular injury. P=11
- Cell and its organelles are swelling.
- Early aggregation of nucleus chromatin.
- Reduction of granules amount of glycogen.
- Enlargement of ER.
- Detachment of ribosomes from membranes
of rER.
- Dissociation of polysomes into monosomes.
- Blebs may form at the cell surface.
- Loss of cell microvilli.
- “Myelin figures”
- Autophagosomes
- Light floccular deposits in mitochondrions.
98. Name morphologic signs of irreversible
cellular injury. (p=13)
- There are defects in cell membrane.
- Progressive destruction in cell membrane.
- Mitochondrial swelling with large calcium
containing deposits.
- Lysis of ER.
- Myelin figures and lysosome ruptures.
- Autolysis and changes of nucleus (pyknosis,
rhexis, lysis).
99. Name two basic pathogenic factors
defined, so called, “point of no return” in
cellular injury. (p=2)
- The inability to restore mitochondrial
function because of full exhaustion of
structural providing ATP synthesis.
- Profound disturbance in cell membranes.
100. Name and explain basic mechanisms of
cell membrane damages. (p=9)
- Progressive loss of phospholipases due to
increased phospholipids degradation (the
activation of phospholipases in condtions of
increased calcium concentration.)
- Decreased novo synthesis of phospholipids
(because of ATP decreasing)
- Cytoskeletal abnormalities caused by
protease activation, the detachment of cell
membrane from the cytoskeleton by physical
acting from the cell swelling.
- Abnormalities caused by acting oxygen free
radicals (activation of lipid peroxidation)
- Abnormalities caused by the influence of
lipid waste products (free fatty acids, acyl
carnitine, lysophospholipids)
101. Give examples of cell injury followed by
free radicals activity. (p=5)
- The effect of chemical and drug factors.
- Inflammation.
- Radiation destruction.
- Toxic action of oxygen.
- Agiry.
102. Name two basic mechanisms of viral cell
damage. (p=2)
- Direct cytopathic effect.
- Induction of immune response
103. Name basic morphologic signs in viral
cell damage. (p=4)
- Cell lysis
- Cytoskeletal damage
- Intracellular viral accumulations
- Formation of polynuclear cells
104. Name three basic groups of intracellular
accumulations into non-neoplastic cells
according to mechanisms of their formation
and give an example of each group. (p=12)
- Normal or abnormal endogenous substances
accumulate into cell because they can not be
utilized due to genetic enzyme defect; e.g.
lysosomal storage diseases.
- Normal endogenous substances are produced
at normal or increased rate but the rate of
metabolism is inadequate for consumption;
e.g. fatty liver.
- Exogenous substances accumulate into cells
because cells have neither the enzyme
machinery nor their utilization or the capability
for transportation and release of the organism;
e.g. anthracosis
105. Specify morphologic peculiarities of
cardiomyocytes damage in moderate and
profound hypoxia. (p=2)
- Moderate hypoxia causes the so called ‘tiger
heart’.
- Profound hypoxia causes diffuse changes.
106. Disclose two basic mechanisms of
appearance of fatty droplets in cardiomyocytes
in hypoxia. (p=6)
- Fatty infiltration because of oxygenous
abnormality of fatty acids in conditions of
decreased aerobic metabolism.
- Decomposition of cell membranes followed
by phospholipases activation in conditions of
increased calcium concentration in
sarcoplasma.
107. Explain mechanisms of cardiomyoctes
damage in diphtheria. (p=3)
- Abnormal oxidation of fatty acids
- followed by direct toxic action of diphtheric
exotoxin in mitochondrial membrane
- leading to abnormal carnitine metabolism.
108. Give the definition of necrosis. (p=2)
- one of morphological patterns of death.
- the death of cell or tissue parts or organ parts
in a living organism.
109. Name types of necrosis according to
etiology. (p=5)
- Traumatic
- Toxic
- Allergic
- Trophonecrotic
- Ischemic
110. Specify nucleus changes of necrosis.
(p=3)
-Karyopyknosis
-Karyorrhexis
-Karyolysis
111. Specify cytoplasm changes of necrosis.
(p=3)
-Cytolysis (plasmolysis)
- Cytorrhexis (plasmorhexis)
- Denaturation (coagulation of plasma
proteins)
112. What is tissue detritus? (p=2)
-It is the product of dead cellular autolysis and
heterolysis.
113. Name possible consequences of necrosis.
(p=6)
- Organization
- Encapsulation
- Petrification
- Ossification
- Cyst formation
- Suppurative inflammation
114. What is mutilation? (p=3)
- The spontaneous extraction of necrotic part
of an organ or tissue from its necrotic site
- Possible outcome of necrosis.
115. What is demarcating inflammation? (p=1)
- Inflammation which is surrounded by area
with necrosis. Border between necrotic and
healthy tissues
116. Name clinical-morphological forms of
necrosis. (p=5)
- Coagulative
- Liquefactive
- Gangrenous
- Infarction
- Sequestra
- Fatty
117. What is infarct? Name specific causes of
its onset. (p=5)
- Infarct is an area of ischemic necrosis within
tissue or organ due to obstruction of its arterial
supply or its venous drainage.
-Causes: -Thrombosis
-Embolism
-Stenotic atherosclerosis
-Prolonged spasm of artery
118. Name morphologic types of infarction.
(p=3)
- Hemorrhagic(red) infarction
- Ischemic(white) infarction
- Ischemic infarction with hemorrhagic border
119. Specify conditions that lead to
hemorrhagic infarction of the lung. Describe
its typical clinic symptoms. (p=4)
- Condition: obstruction of double blood
supply to the lung (bronchial and pulmonary
artery).
- Clinical symptoms: Chest pain
Dyspnea
Hemaptysis
Pleural friction rubbing
120. What is gangrene? (p=2)
- Necrosis of tissue with contact with external
environment
121. Specify types of wet gangrene. (p=3)
- Bedsore
- Noma
122. Patient suddenly died. In postmortem
examination were found lumen of the left
middle cerebral artery closed with thrombus;
temporal and parietal lobes of left hemisphere
had disturbance correlation of gray and white
substances: there was an extensive source of
gelatinous and friable gray tissue. Give the
name of this process. (p=2)
-White infarction of the brain.
123. The deceased with heart failure has dark
red airless, triangular sites of the lung under
the pleural. The lumen of vessels is closed by
dark red, solid clots, not extracted at a short
distance from vessels. Give the name of these
changes and explain the cause of blood
disturbances in vessels of the deceased. (p=3)
- Name: Hemorrhagic(red) infarction of the
lung
- Cause: Thromboembolism of pulmonary
arteries. Marantic thrombosis of pulmonary
artery.
124. The male of 78 years old, has the leg with
swell, edema, of black and green colours, with
stinking smell. Give the names of process and
its variety. Name more frequent disease (taking
into account patient’s age) and its complication
leading the above mentioned changes. (p=4)
- Name of process: wet gangrenous necrosis
- Variety: dry and wet (wet is divided into
bedsore and noma)
- Disease: stenotic atherosclerosis
- Complications: thrombosis,
thromboembolism
125. During special operation in connection
with the infringement of herniated small
intestine loop, after cutting the gate, a surgeon
can see dark purple, acute edema of small
intestine loop. This loop needs cutting. Give
process name in the small intestine loop and
explain necessity of the loop removal. (p=3)
- Name: Gangrenous necrosis of intestinal
loop.
- It must be removed because it may cause
death due to peritonitis and intoxication.
126. The female, 69 years old, died of brain
softening in the subcortical nuclei region.
There were big ulcer tissue disintegration
of gray-purple color, on the skin of buttocks
and sacrum and with the bareness of
the sacrum bone with rotting smell.
Give names of the process, its types and
explain its origin. (p=4)
- Name: Wet gangrenous necrosis
- Type: bedsore
- Origin: Trophoneurotic necrosis of skin and
soft tissue due to prolonged pressure by their
own body weight.
127. Specify parenchymal dysproteinoses.
(p=5)
- Intracellular accumulation of protein
substance
- Swelling of cytoplasm resulting fr disorder of
Na K pump
- Necrosis as a result of dystrophic change
128. What is a hydropic change or vacuolar
degeneration? (p=4)
- It is a type of parenchymal dysproteinosis
with cellular swelling and appearance of clear
vacuoles within the cytoplasm.
- Because the cell is incapable of maintaining
its fluid-ionic balance.
129. Specify organs with very clear
manifestation of cells injury connected with
dysproteinosis (p=3)
- Heart
- Kidney
- Liver
130. What is fatty change? (p=2)
- It is a type of parenchymal lipidosis due to
disturbance of fat exchange
- Resulting in accumulation of TG in
parenchymal cells and characterized by
appearance of lipid vacuoles in the cytoplasm.
131. What is a fatty infiltration? What are its
mechanisms? (p=4)
- Fatty infiltration is the deposit of fat in the
cytoplasm which is brought in by lymph and
blood.
- Mechanism: Insufficiency of enzymatic
system and fat metabolism.
132. Specify basic mechanism of fatty liver
irritation. (p=6)
- Extensive entry of fatty acid into liver
- Increase synthesis of fatty acid
- Decrease oxidation of fatty acid
- Increased esterification of fatty acid to
triglycerides
- Decreased synthesis of apoprotein
133. What are lipids revealed in fatty changes?
(p=3)
- Neutral fat
- Cholesterin
- Phosphotide
134. What is decomposition? What is another
term for it? P=3
- It’s a catabolism as disintegration of
intracellular organelles and extracellular matrix
with accumulation of abnormal metabolic
substances. It’s also called phanyrosis.
135. What is the cause of “tiger heart” with
fatty degeneration? (p=3)
- Local parenchymal fat dystrophy on
myocardium localized near venule part of
capillary
- In case not involve myocardium it may be
diffuse change.
136. What is the structure of the myocardium
with fat accumulation in fatty degeneration?
(p=1)
- Cytoplasm of cardiomyocytes.
Definition of Ichtyosis: Type of
hyperkeratinosis characterized by
hyperproduction of keratin by squamous
epithelium with keratinization. Hereditary
disease.
137. Mucoid swelling? (p=5)
- Stromal dysproteinosis with
- Superficial disorganization of protein in
connective tissues with
- Accumulation of basic substance
glycoaminoglycan &
- Their redistribution which cause the
increasing of vessels permeability.
- Characterized by metachromasia.
138. Fibrinoid swelling? (p=5)
- Stromal vascular dystrophy defined by
- Destruction of collagen fibers &
- Basic substances with plasmorrhagia &
- Formation of protein & polysaccharide
complexes on fibrinoid substance.
- Increased permeability of vascular causing
exudation
139. Tissues & organs in which fibrinoid
swelling usually develops. (p=5)
- Myocardial stroma
- Skin
- Synovium
- Valves of the heart
- Vessels wall
140. Hyalinosis? (p=3)
- Stromal vascular dysproteinosis defined by
- Alteration in the extracellular matrix which
- Becomes homogenous, glassy, pink
appearance in section stained by H&E.
141. Processes with hyalinosis as consequence.
(p=3)
- Lipidosis
- Lysis by macrophages
- Necrosis, Sclerosis with Petrification
- Fibrinoid Swelling
- Mucous production
142. ‘Icing spleen’? (p=1)
- Hyalinosis of splenic capsule
143. Metabolic neutral fatty disease developed
by? (p=3)
- Local obesity
- Cacchexia
- Obesity
144. Forms of obesity according to etiology
and pathogenic factors. (p=3)
- Alimentary disturbance - Genetic
- Cerebral disease - Environmental
- Endocrine disorder -
Psychologic
145. Name localization sites of fatty deposits
in obesity. (p=5)
- Heart: stroma and epicardium
- Omentum, Caul
- Pararenal fatty tissue
- Retroperitoneal fatty tissue
- Subcutaneous fatty tissue
146.) Name characteristic properties of
hemosiderin. (p=5)
a) amorphous b) brown c) intra cellular d) yes,
it contents iron e) about 24-48 hr. p=5
147.) What is jaundice? What types of the
jaundice are observed with cirrhosis of liver?
(p=5)
Jaundice is yellow pigmentation of the skin,
sclera, mucous membranes & organ
parenchyma with hyperbilirubinemia.
Parenchymal (hepatic) & mechanical (sub
hepatic). p=5
148.) Name jaundice types according to
mechanisms of development. (p=3)
Hemolytic (supra hepatic), parenchymal
(hepatic) & mechanical (obstructive, sub
hepatic) p=3
149.) Specify diseases and conditions with
typical syndrome of mechanical jaundice.
(p=4)
. Gallstone obstructive of common hepatic or
common bile duct, carcinoma of pancreatic
head, primary sclerosing cholangitis, gallstone
obstructive or carcinoma of Vater ampula. p=4
150.) What bile ducts embolism does with
calculous cholecystitis lead to the progress of
mechanic jaundice? (p=2)
Common hepatic or common bile duct.
151.) What is leukoderma? (p=3)
Leukoderma is local depigmentation of the
skin. p=3
152.) Name calls producing melanin. (p=1)
- Melanocytes
153.) What is the term for hereditary failure of
melanin production? (p=1)
- Albinism
154.) The hemorrhage and forming cyst are
found in brain during the section. The cyst is
filled with yellow and brown substances.
Name pigments in source of hemorrhage and
substantiate your arguments of the hemorrhage
duration. (p=4)
- Name of pigments: Hemosiderin and
hemotoidin
- Duration: 7 days because the yellow colour
explains the presence of hemotoidin which is
disclosed after 7 days
155.) In postmortem examination gray aspic
color of spleen and liver is observed. What is
the colour explained? What is the disease
suspected? (p=3)
Pigment is termed hemomelanin (hematin).
Malaria
156.) The deceased is on the section table. He
is very exhausted male. He has
hyperpigmentation of skin and his both
adrenals are destroyed by tubercular process.
What is the syndrome described above? (p=1)
- Addison syndrome
157.) Name types of calcification. (p=3)
- Dystrophic metastatic and tumoral
calcification p=2
158.) What is dystrophic calcification? What
are tissue changes observed? (p=3)
- Dystrophic calcification is the abnormal
deposition of calcium salts occurring in dead
or dying tissues without hypercalcemia. p=5
159.) Present examples of dystrophic
limestone with necrosis and the inflammation
(p=6)
- Focal caseous necrosis
- focal Chronic inflammation
- gumma
- infarct
- deep parasite
- lithopedion
160.) Give definition of the concept of ‘lime
metastases’ and give explanation of their
selective localisation (p=4)
“Lime metatasis” is the deposition of calcium
salts in normal tissues as a reflects some
derangement in calcium metabolism with
hypercalcemia. p=4
161.) Name most frequent localization with
deposits of calcium salts according to type of
‘lime metastases’. (p=5)
The vasculature, heart, lungs, kidneys, gastric
mucosa.
198. Amyloidosis? (p=4)
- Pathological process characterized by
- Stromal vascular dysproteinosis with an
- Abnormal protein deposition called Amyloid.
- Amyloid is a proteinaceous substance
- Deposited between cells of various tissues &
organs.
199. Dyes used for microscopic assessment of
amyloid. (p=3)
- Congo red
- Methylene violet
- Luminescence with Thioflavin
200. Diseases complicated by 2º amyloidosis.
(p=4)
- Bronchiectasis
- COPD (Chronic Obstructive Pulmonary
Disease)
- Pyogenic Osteomyelitis
- Rheumatic Fever
- Tuberculosis (of lung & bones)
201. Pathogenesis of AL-amyloid. (p=4)
Product of abnormal amount of protein –
Monoclonal Blymphocyte proliferation –
plasma cells – Ig light chains – AL protein.
202. Pathogenetic chains AA-amyloid form.
(p=5)
- Chronic inflammation – Macrophage
activation – IL1,6 – Liver cells – SAA protein
– AA protein (must be in order)
203. Types of systemic [general] amyloidosis.
(p=4)
- Primary (idiopathic)
- Secondary
- Senile
- Hereditary
204. Name types of hereditary amyloidosis.
(p=2)
- Familial Mediterranean Fever,
- Familial Amyloidotic Neuropathy
205. Name types of localized amyloidosis.
(p=4)
- Cardiopathic
- Endocrinepathic
- Epinephropathic
- Neuropathic
206. Organs mainly involved in endocrine - Cholesterol
amyloidosis? (p=2) - Pigment
- Thyroid gland - Mixed
- Islet of Langerhans (pancreas)
4. Four major causes of hypercalcemia (p=4)
207. Amyloidosis forms in which AA-amyloid - Increased secretion of parathyroid hormone
takes part. (p=2) - Destruction of bones
- Secondary amyloidosis – complicates chronic - Vit D related disorders
inflammatory disease - Renal failure
- Hereditary form
5. Causes of Addison’s syndrome (p=6)
208. Types of systemic (p=1) & local (p=1) - Tuberculosis,
amyloidosis in genesis of which ATTR-form - Metastases of carcinoma,
takes part [amyloid is transported by thyroxin - Amyloidosis
and retine]. (p=2) - Immune disorder of adrenals,
- Systemic (familial amyloidotic - AIDS,
polyneuropathies, senile systemic amyloidosis) - Hemachromatosis
[hereditary]
- Local (senile amyloidosis of heart and 6. Causes of hemolytic jaundice
vessels) - Hemolytic anemia, resorption of blood from
internal hemorrhage, ineffective erythropoeisis
209. Possible causes of death for patients with syndromes
2º amyloidosis. (p=2)
- Cardiac (fatal) Arrhythmias 7. Normal and abnormal hemoglobinous
- Uremia (renal failure) derived pigments (p=6)
- Hemosiderin
210. Patient with bronchiectatic disease had - Hemotoidin
renal and extra-renal symptoms. Then the - Hematins
patient died. In postmortem examination, - Ferritin
enlarged lard kidneys were observed. What - Billirubin
was the complication of the disease? What - Poryphyrins
substance was deposited in the kidney
structures? What structures of the kidney was 8. Examples of hyperpigmenation (p=2)
the substance found in? (p=5) - Pigmented nervus
- Disease: Secondary Amyloidosis of the - Melanoma
kidney (reactive systemic)
- Complication: Amyloid Nephrosis (renal 9. What is lipofuschin (p=5)
failure) - Lpf is an endogenous lipidogenic brownish
- Substance deposited: Amyloid yellow granular pigment accumulated
- Found in: basal membrane of ducts, intracellular as a function of age or atrophy
glomeruli, mesangial wall, stroma, vessels wall
10. Most common exogenous pigment
Additional Questions - Carbon

1. Sign of bone with hyperparathyroidism 11. Lipidogenous derived pigments (p=3)

(p=6) - Lipofuscin
- 1st lacuna form – osteoclast activated work to - Lipochrom
clear old osteoclast work to form new bone - Carotene
tissue
12. Feature of bone with osteomalacia (p=2)
2. Kind of renal stone according to its content - Weakness of bone
(p=5) - Ease in fracture of bone
- Calcium oxalate
- Urates 13. Normal haemogoblin derived pigments
- Phosphates (p=3)
- Cystines - Billirubin
- Xanthines - Hemosiderin
- Ferritin
3. Kind of gall stone according to its content
(three fucking marks)
14. Name the characteristic properties of
hematoidin (p=5)
- Crystal physical state
- Yellow colour
- Located extracellularly
- Does not contain iron
- Formation time is 7 days