Pathanatomy Unit 1 -6

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) Virchovs triad : Endothelial injury Disturbance of blood flow Blood component alteration (blood hypercoagulability) 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. cadaver after 24 hrs in warm room has a 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( fistula ) - PostIschemic 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 abdominal wall, 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 - Cardiomyotitis - Cardiomyopathy - 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 decompensation? (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 gastric jus 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 =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 clot. 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 vessel wall by plasma protein 55. Give definition of thrombosis. p=3 - Blood clotting within the vascular system or cardiac chambers - Thrombus is the product of thrombosis 56. Identify of thrombi according to their composition. p=4

White Red Mixed Hyaline

57. Specify macroscopic parts of the thrombus. - 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) - Splenic 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.

- Petechiae over upper half of body, conjunctiva, oral mucosa and retina 77. What is shock? (p=4)

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? 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. - 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. - 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? - 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 membranes destruction? - 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

shock systemic hypoperfusion due

to reduction in 1.) cardiac output 2.) effective circulating blood volumecoz hypotension impaired tissue perfusion and cellular hypoxia.

Thromboembolism Fatty Bubble of air Nitrogen Tissue embolism Foreign bodies Microbial (bacterial)

78. Give the definition of DICsyndrome.(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 pulmocoronary 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

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 and with fragments 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 - Pulmo-bronchial 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 meningitis

- 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. - 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 Infectious agent Ischemic

110. Specify nucleus changes of necrosis. (p=3) -Karyopyknosis (nuclear shrinkage & basophilia ) -Karyorrhexis (nucleus fragmentation ) -Karyolysis (nucleus fade away & dissolving) 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. - 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 patients 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 lipids revealed in fatty changes? (p=3) - Neutral fat - Cholesterin - Phosphotide 134. What is decomposition? What is another term for it? P=3 - Its a catabolism as disintegration of intracellular organelles and extracellular matrix with accumulation of abnormal metabolic substances. Its 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? - 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 reversible disorganization of connective tissues(protein ) 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

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 ( in dead/dying tissues ) Metastatic (normal tissues ) Tumoral 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. 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. 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 2 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 B-lymphocyte proliferation plasma cells Ig light chains AL protein.

202. Pathogenetic chains AAamyloid form. (p=5)

Chronic inflammation Macrophage

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. 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). 148. Name jaundice types according to mechanisms of development. (p=3) - Hemolytic (supra hepatic), parenchymal (hepatic) & mechanical (obstructive, sub hepatic) 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. 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. 152. Name melanin-producing cell. (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

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 amyloidosis? (p=2) - Thyroid gland - Islet of Langerhans (pancreas) 207. Amyloidosis forms in which AA-amyloid takes part. (p=2) - Secondary amyloidosis complicates chronic inflammatory disease - Hereditary form 208. Types of systemic (p=1) & local (p=1) amyloidosis in genesis of which ATTR-form takes part [amyloid is transported by thyroxin and retine]. (p=2) - Systemic (familial amyloidotic polyneuropathies, senile systemic amyloidosis) [hereditary] - Local (senile amyloidosis of heart and vessels) 209. Possible causes of death for patients with 2 amyloidosis. (p=2) - Cardiac (fatal) Arrhythmias - Uremia (renal failure) 210. Patient with bronchiectatic disease had renal and extra-renal symptoms. Then the patient died. In postmortem examination, enlarged lard kidneys were observed. What was the complication of the disease? What substance was deposited in the kidney structures? What structures of the kidney was the substance found in? (p=5) - Disease: Secondary Amyloidosis of the kidney (reactive systemic) - Complication: Amyloid Nephrosis (renal failure) - Substance deposited: Amyloid - Found in: basal membrane of ducts, glomeruli, mesangial wall, stroma, vessels wall

Additional Questions

1. Sign of bone with hyperparathyroidism (p=6) - 1st lacuna form osteoclast activated work to clear old osteoclast work to form new bone tissue 2. Kind of renal stone according to its content (p=5) - Calcium oxalate - Urates - Phosphates - Cystines - Xanthines 3. Kind of gall stone according to its content - Cholesterol - Pigment - Mixed 4. Four major causes of hypercalcemia (p=4) - Increased secretion of parathyroid hormone - Destruction of bones - Vit D related disorders - Renal failure 5. Causes of Addisons syndrome (p=6) - Tuberculosis, - Metastases of carcinoma, - Amyloidosis - Immune disorder of adrenals, - AIDS, - Hemachromatosis 6. Causes of hemolytic jaundice - Hemolytic anemia, resorption of blood from internal hemorrhage, ineffective erythropoeisis syndromes 7. Normal and abnormal hemoglobinous derived pigments (p=6) - Hemosiderin - Hemotoidin - Hematins - Ferritin - Billirubin - Poryphyrins 8. Examples of hyperpigmenation (p=2) - Pigmented nervus - Melanoma 9. What is lipofuschin (p=5) - Lpf is an endogenous lipidogenic brownish yellow granular pigment accumulated intracellular as a function of age or atrophy 10. Most common exogenous pigment - Carbon 11. Lipidogenous derived pigments (p=3) - Lipofuscin - Lipochrom - Carotene 12. Feature of bone with osteomalacia (p=2) - Weakness of bone - Ease in fracture of bone 13. Normal haemogoblin derived pigments (p=3) - Billirubin

- Hemosiderin - Ferritin 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