Pathology Anatomy Colloquium 1
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
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 - 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 \u2013 Esophageal anastomoses - Portal \u2013 Abdominal anastomoses - Portal \u2013 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 10. What are cadaver stains? (2) basic vessel with blood stream disorders? - Postmorten hypostasis of blood with What is the significance of designated vein hemolysis and redistribution of blood. alterations? (p=3) - Portal vein is the basic disorderly vessel 11. What are cadaver hypostases? (p=1) - Portal hypertension causes collateral - Flowing down of blood under the influence hyperemia of vena gastricus, esophageal vein of gravity, without heart intervention which have adaptive compensatory process for general blood stream disorder 12. What is cadaver inhibition? (1) - Collateral hyperemia of esophageal vein can - Postmortem saturation of tissue with products result in vertical rupture and produce massive of Hb disintegration 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
- 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
22. In patients with mitral valvular diseases, 32. Name cough and \u2018rusty phlegm\u2019; explain rusty colourthe most severe degree of heart decompensation. (p=3) of the phlegm. Give the characteristics of left - 3rd stage; change in internal organ, sclerosis, heart functional condition and the atrophy, wrinkled kidney, oedema of hemodynamic changes in the lung. (p=4) extremities, accumulation of fluid in body - It is rusty coloured due to siderophages cavity (hemosiderin laden mphs) - There is left heart failure due to mitral 33. What do morphological change originate in prolapse and pulmonary congestion with dilated capillaries and diapedic blood flow into tissues and organs from right sided heart decompensayion? (p=3) alveolar spaces. - Liver; nutmeg liver - This leads to an increase in siderophages, - Kidney; cyanotic induration which in turn causes brown induration of the - Spleen; cyanotic induration, splenomegaly lung - Serous cavities; dropsy (oedema) 23. Specify processes which take place with brown induration of the lung. 34. In deceased patient, was found chronic - Venous hyperemia. venous hyperemia in internal organs and - Per diapedic blood flow into the alveoli dropsy of cavities. Name the cause of death. - Siderophage activity (p=3) - Pneumosclerosis - Heart insufficiency (heart failure) - Decompensation of heart 24. Name basic macroscopic sign of chronic 35. A patient died of heart failure, during postvenous hyperemia within organs and tissues. mortem examination, you see an enlarged firm - Red-blue colour spleen with a smooth capsule; the cut surface - Surrounded by a zone of uncongested resembles a meaty appearance without scrapes; substance dark cherry coloured with cyanotic hues. Name - Enlarged and firm with a smooth surface the changes of spleen. 25. Figurative name of the liver in chronic - Cyanotic induration of the spleen. venous hyperemia. 36. What are necrosis foci termed within - Nutmeg liver organs in heart failure? (p=1) 26. What local processes does - Marantic necrosis thrombosis phlebothrombosis lead to? (p=1) -Local venous hyperemia and stasis 37. Specify marantic necrosis of organs in patients with heart failure. (p=6) 27. What terms are hemodynamic disorders - Liver, kidney, lung, spleen, brain, colon designated, which are caused by heart disturbance? (p=2) 38. Name the Greek term for \u2018blood volume - Hyperemia, Thrombosis, Oedema, losses\u2019. (p=1) Aneurysm. - Ischemia 28. Name cardial pathology associated with heart failure. (p=5) - Phlebothrombosis of endocardium - Myocardial Infarction - Cardiomyotis
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
- 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
40. What is stasis? (p=3) - Cessation of natural flow of physiological fluid in an organism\u2026 50. What is hematoma? (p=2) - \u2026characterized by the slowing down of Hematoma is a type of hemorrhage when the circulation and increased microvascular blood is trapped within the tissue, forming a permeability and\u2026 - \u2026and increased concentration of RBC and cavity of blood. dilation of small vessels 51. What is hemorrhagic infiltration? (p=2) 41. What is hemorrhagia? (p=2) - Blood saturation of the tissues. - Blood outcome from vessels or the heart. - Blood saturates within tissue without its destruction 42. Specify and give Latin terms of 52. Specify and give Latin terms of hemorrhagia mechanisms. (p=6) hemorrhage types when blood accumulates in - Per Rhexin: Rupture of vessels the body cavities. (p=6) - Per Diabroxin: Erosion of vessels - Hemothorax (blood in the pleural cavity) - Per Diapedesin: Hypermobility of small - Hemarthrosis (blood in the synovial cavity) vessels - Hemopericardium (blood in the pericardial 43. Give classification of hemorrhagia cavity) according to source. (p=5) - Hemoperitoneum (blood in the peritoneal - Arterial, Venous, Capillaries, Parenchymal, cavity) Cardiac. 53. Give names of frequent causes of 44. Specify in English and Latin terms of hemopericardium. (p=2) external hemorrhage types. P=14 - Acute hemorrhage in heart aneurysm - Nasal (Epistaxis) - Myocardial infarction - Blood Vomiting (Haematemesis) 54. What is plasmorrhagia? (p=2) - Irregular uteral bleeding (Metrorrhagia) - Saturation of vesselwall by plasma protein - Regular uteral bleeding (Menorrhagia) - Presence of blood in urine (Hematuria) 55. Give definition of thrombosis. p=3 - Tarry stool as sign of bleeding in GIT - Blood clotting within the vascular system or (Melena) cardiac chambers - Blood in the phlegm (hemoptysis) - Product of thrombosis 45. Mechanisms of hemorrhage from gastric ulcer. (p=2) 56. Identify of thrombi according to their - Per diabroxin: Hemorrhage due to erosion of composition. p=4 the vessel wall by pus and enzyme - White - Red 46. Explain the melena of a patient with gastric - Mixed carcinoma. (p=3) - Hyaline - Stool is black due to infiltration of blood by 57. Specify macroscopic parts of the thrombus. per diabroxin bleeding of the erosion of the (p=3) vessel wall by malignant tumour enzymes in - Head, Body , and Tail. 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)
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
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
60. Specify the most frequent arterial thrombosis.(p=8) - aorta, cerebral, coronary a, renal, popliteal a, 69. Identify emboli according to their composition. femoral a. a. thromboembolism 61. Specify the most frequent venous b. fatty thrombosis.(p=6) c. bubble of air - Deep veins of leg d. nitrogen - Right atrial auricle e. tissue embolism - Right ventrical f. foreign bodies - Veins of small pelvis g. microbial (bacterial) - Inferior vena cava 70. Give the definition of tissue embolism. 62. Name three localizations of thrombi in the - Outcome in metastasis of the malignant cells, system of the portal vein.(p=3) metastasis shows development of secondary - Splenc vein implants discontinued in primary tumours, - Hepatic vein possibly in distant tissues - Umbilical vein - 3 types: with malignant cells, with amniotic fluid or with segments of traumatic tissues 63. Specify possible consequences of the thrombus.(p=6) 71. What is metastasis? - organization -Appearance of secondary purulent foci away - canalization from the primary foci OR - calcification (phleboliths) -Spreading of pathological malignant tissue - septic dissolution 72. Specify basic sources of thromboemboli of - embolism pulmonary arteries(p=5) - aseptic dissolution -deep leg vein thrombi above the level of the knee joint. 64. During postmortem examination elastic, wet plagues of blood with smooth surfaces are -eg., popliteal ,femoral & iliac veins. found. They are extracted from vessels easily. 73. What are mechanisms of the death with What is their name? What are they pulmonary thromboembolism? differentiated with? (p=2) -Pulmo-coronary reflex: causing spasm of -They are postmortem blood clots coronary artery and acute left sided heart -Differentiated with thrombus failure - Pulmobronchial reflex: spasm of pulmonary 65. Mitral valve leaflets are grown together artery and musculature of bronchial tree with stenosis. There is free spherical large - Acute right sided heart failure thrombus with smooth surface into left. Explain the formation. (p=3) 74. Specify contributory conditions for the -Part of the thrombus from the mitral valve development of fatty embolism. (p=4) comes out to the left atrium, and is surrounded -Trauma to subcutaneous fatty tissue by blood, making the surface smooth and -Trauma to (fatty) bone marrow spherical -Faulty administration of oil-based injections -amniotic fluid in newborns during pregnancy 66. Give the definition of embolism. (p=3) 75. Specify possible consequences of fatty -Circulation of foreign mass with blood or embolism. (p=3) lymph which may come to rest anywhere -respiratory insufficiency within the cardiovascular and lymph system -stroke 67. Specify types of embolism according to the -resolution by macrophages direction of embolus pathways. (p=3) -direct 76. What are cases with fatty embolism due to -indirect/retrograde death? (p=3) -Paradoxical - Respiratory failure
- Cerebral dysfunction with hypoxia and meningitides - Petechiae over upper half of body, conjunctiva, oral mucosa and retina
- Formation of apoptotic bodies. 84. Name basic groups of complications developing in patients after measures. (p=3) - Hyperemia, Oedema, Stasis
77. What is shock? (p=4) 85. Name clinical anatomic variants -shock systemic hypoperfusion due to (syndromes) of post-resuscitation disease reduction in 1.) cardiac output 2.) effective (according to V.A. negovsky) (p=5) circulating blood volume. -coz hypotension impaired tissue perfusion and cellular hypoxia. 86. Which changes of the brain can develop in 78. Give the definition of DIC-syndrome.(p=4) patients with long artificial lung ventilation? -Disseminated intravascular coagulation (DIC) (p=4) is a complex systemic thrombohemorrhagic 87. Which hemodynamic disorders develop disorder. -activation of coagulation sequence, leading to irreversible changes in late reperfusion? (p=3) formation of thrombi throughout the 88. Name target organs to develop irreversible microcirculation. changes in late reperfusion. (p=5) -coz consumption of coagulants and platelets. -and secondarily, activation of fibrinolysis. 89. Give names of successive stages of cellular injury in continuous action of pathogenic 79. Identify four synonyms of DIC syndrome. factor. p=4 (p=4) - Adaptive changes - Consumptive thrombohemorrhagic disorder - Reversible cell injury - Consumptive coagulopathy - Irreversible cell injury - Defribination syndrome - Death of cell - 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
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 81. In deceased patient with purulent wound of with nucleus changes (karyopyknosis, karyorrhexis, karyolysis) thigh and regional thrombophile bitis, - they arise a certain time after death followed multitudinous abscesses are found in the by autolytic processes. internal organs. What is the name of the process spread? What are the mechanisms in 92. Why does suppression oxidative its basis? phosphorylation in the cell lead to cell -Process: generalisation of septicopyemia swelling? (p=4) -Mechanism: metastasis of bacterial emboli - Loss of ATP production leads to - depression of Na pumping, accumulation of 82. Give the definition of autolysis. (p=4) - Enzymatic digestion of cell after its death by water, sodium and calcium in cytoplasm. own lysosome enzymes. 93. Why does swelling of cells and organelles arise after cellular membrane’s destruction? 83. Give the definition of apoptosis. (p=4) (p=3) - Only seen in the cellular level - a mode of cell death in the living organism as - Cellular membrane destruction will lead to disturbances of ionic and osmotic homeostasis the genetic programmed cell death - a pathway of cellular “suicide”.
of the cells organelles causing accumulation of 100. Name and explain basic mechanisms of H20. Swelling of cells and organelles. cell membrane damages. (p=9) - Progressive loss of phospholipases due to 94. What do morphologic signs of cellular reaction of pathogenic factor depend on? (p=4) increased phospholipids degradation (the activation of phospholipases in condtions of - They depend on peculiarities of pathogenic increased calcium concentration.) factor (type, duration, severity) - Decreased novo synthesis of phospholipids - And cellular condition (adaptive capability) (because of ATP decreasing) 95. Give examples of cells having high, - Cytoskeletal abnormalities caused by moderate and low sensibility in relation to protease activation, the detachment of cell ischemic (hypoxic) membrane from the cytoskeleton by physical factor. (p=7) acting from the cell swelling. - High sensibility: neurons - Abnormalities caused by acting oxygen free - Moderate sensibility: cardiomyocytes, radicals (activation of lipid peroxidation) hepatocytes, nephrocytes - Abnormalities caused by the influence of - Low sensibility: cells of skeletal muscles, lipid waste products (free fatty acids, acyl fibroblasts, epidermocytes. carnitine, lysophospholipids) 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
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.
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.
102. Name two basic mechanisms of viral cell damage. (p=2) - Direct cytopathic effect. - Induction of immune response
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.
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.
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) 108. Give the definition of necrosis. (p=2) - Infarct is an area of ischemic necrosis within tissue or organ due to obstruction of its arterial - one of morphological patterns of death. - the death of cell or tissue parts or organ parts supply or its venous drainage. -Causes: -Thrombosis in a living organism. -Embolism 109. Name types of necrosis according to -Stenotic atherosclerosis etiology. (p=5) -Prolonged spasm of artery - Traumatic - Toxic 118. Name morphologic types of infarction. - Allergic (p=3) - Trophonecrotic - Hemorrhagic(red) infarction - Ischemic - Ischemic(white) infarction - Ischemic infarction with hemorrhagic border 110. Specify nucleus changes of necrosis. (p=3) 119. Specify conditions that lead to -Karyopyknosis hemorrhagic infarction of the lung. Describe -Karyorrhexis its typical clinic symptoms. (p=4) -Karyolysis - Condition: obstruction of double blood supply to the lung (bronchial and pulmonary 111. Specify cytoplasm changes of necrosis. artery). (p=3) - Clinical symptoms: Chest pain -Cytolysis (plasmolysis) Dyspnea - Cytorrhexis (plasmorhexis) Hemaptysis - Denaturation (coagulation of plasma Pleural friction rubbing proteins) 120. What is gangrene? (p=2) 112. What is tissue detritus? (p=2) - Necrosis of tissue with contact with external -It is the product of dead cellular autolysis and environment heterolysis. 121. Specify types of wet gangrene. (p=3) 113. Name possible consequences of necrosis. - Bedsore - Noma (p=6) - Organization 122. Patient suddenly died. In postmortem - Encapsulation examination were found lumen of the left - Petrification middle cerebral artery closed with thrombus; - Ossification temporal and parietal lobes of left hemisphere - Cyst formation had disturbance correlation of gray and white - Suppurative inflammation
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
- 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 125. During special operation in connection cytoplasm which is brought in by lymph and with the infringement of herniated small blood. intestine loop, after cutting the gate, a surgeon - Mechanism: Insufficiency of enzymatic can see dark purple, acute edema of small system and fat metabolism. intestine loop. This loop needs cutting. Give process name in the small intestine loop and 132. Specify basic mechanism of fatty liver explain necessity of the loop removal. (p=3) irritation. (p=6) - Name: Gangrenous necrosis of intestinal - Extensive entry of fatty acid into liver loop. - Increase synthesis of fatty acid - It must be removed because it may cause - Decrease oxidation of fatty acid death due to peritonitis and intoxication. - Increased esterification of fatty acid to triglycerides 126. The female, 69 years old, died of brain - Decreased synthesis of apoprotein softening in the subcortical nuclei region. There were big ulcer tissue disintegration 133. What are lipids revealed in fatty changes? of gray-purple color, on the skin of buttocks (p=3) and sacrum and with the bareness of - Neutral fat - Cholesterin the sacrum bone with rotting smell. - Phosphotide Give names of the process, its types and explain its origin. (p=4) 134. What is decomposition? What is another - Name: Wet gangrenous necrosis term for it? P=3 - Type: bedsore - It’s a catabolism as disintegration of - Origin: Trophoneurotic necrosis of skin and intracellular organelles and extracellular matrix soft tissue due to prolonged pressure by their with accumulation of abnormal metabolic own body weight. substances. It’s also called phanyrosis. 127. Specify parenchymal dysproteinoses. (p=5) 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 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 2º 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
- 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 Addison’s 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
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 - Ease in fracture of bone (p=5) - Calcium oxalate 13. Normal haemogoblin derived pigments - Urates (p=3) - Phosphates - Billirubin - Cystines - Hemosiderin - Xanthines - 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
