Tver State Medical Academy
The Department Of Anatomic Pathology
Examination materials for Foreign Students
with Instruction Conducted in English
«ANATOMIC PATHOLOGY»
Tver 2014
1
Составители:
Гуськова О.Н. – зав. кафедрой, к.м.н., доцент
Евсеев И.В. – к.м.н., доцент
Серова Н.Е. – к.м.н., доцент
Гладкова Н.Н. – к.м.н., ст. преподаватель
Лаврентьева И.А. - к.м.н., ст. преподаватель
Скарякина О.Н. - ассистент
CONTENTS
1. INRODUCTION …………………………………………………………………….............…………. 3
2. INTRACELLULAR ACCUMULATION ………………………………..............................…………. 7
3. HEMODINAMIC DISORDERS ………………………………………………………….………….. 20
4. CELL DEATH …………………………………………………………………………….………….. 30
5. INFLAMMATION & IMMUNE SYSTEM PATHOLOGY …………………………….………...… 37
6. ADAPTATION ……….................................................................................................................……. 48
7. NEOPLASIA ……………………………………………………………………………….………… 51
8. CARDIO-VASCULAR DISEASES ………………………..........................................…..………….. 56
9. PULMONARY DISEASES ……………..................................................................................………. 64
10. GIT DISEASES …………………..................................................................................................…. 72
11. LIVER PATHOLOGY …………………...............................................................................………. 80
12. KIDNEYS PATHOLOGY ………………………………………………………………...………… 88
13. ENDOCRINOLOGY ………………………..............................................................................……. 95
14. FEMALE GENITAL TRACT PATHOLOGY. PREGNANCY PATHOLOGY ………......…….. 101
15. VIRAL & CHILDREN DISEASES ……….............................................................................……. 107
16. BACTERIAL INFECTIONS …………………………………………………………………….… 113
17. TUBERCULOSIS. SYPHILIS …………………………………………………………………..… 114
18. SEPSIS …………………………………………………………………………………………...… 120
EXAMINATIONAL TASKS FOR FOREIGN STUDENTS .................................................................. 125
MACROPREPARATES ………………………………………………………………………..……… 134
MICROPREPARATES ……….................................................................................................……….. 136
ELECTRONOGRAMMS …………...................................................................................................…. 138
ANSWERS ON TASKS ……………………………………………………………………….………. 138
ANSWERS ON TESTS ……………………………………………………………………………...… 147
2
1. INTRODUCTION
1. THE TERM "ETHIOLOGY" IN RELATION TO DISEAS MEANS:
1. Complications
2. Variability
3. The mechanism of death
4. The reason of development
5. The mechanism of development
2. THE MICROSECTION IN THE LIGHT MICROSCOPE IS STUDIED BY INTEGUMENTARY
GLASS TURNED:
1. Downwards
2. Upwards
3. Without it
4. All true
3. THE SPECIAL STAIN FOR GLYCOGEN AND GAG IS:
1. Sudan III
2. Picrofuchsin by von Giesone
3. PAS-reaction
4. Perl's reaction
5. By Ziehl-Nielsen
4. THE TERM " PATHOGENESIS" IN RELATION TO DISEASE MEANS:
1. Complications
2. Variability
3. The mechanism of death
4. The reason of development
5. The mechanism of development
5. STUDY OF MICROSECTION IN THE LIGHT MICROSCOPE BEGINS:
1. Under immersion oil
2. In polarized light
3. Under small magnification
4. Under the large magnification
6. POPULARITY OF IMMUNOHYSTOCHEMICAL METHOD DETERMINES BY:
1. Simplicity
2. High sensitivity
3. High specificity
4. Availability
5. All true
7. THE TERM " THANATOGENESIS" IN RELATION TO DISEASE MEANS:
1. Complications
2. Variability
3. The mechanism of death
4. The reason of development
5. The mechanism of development
8. THE SUBJECT OF CYTOLOGY RESEARCH ARE ALL, EXCEPT:
1. Aspirate
3
2. Biopsy material
3. Smears
4. Biological fluids and feces
5. Scrape from the surface
9. THE OBJECTS INVESTIGATED BY PATHOLOGIST ARE:
1. Experimental material
2. Postmortem and surgical material
3. Alive patients
4. The data of sociological interrogations
5. Biological liquids and feces
10. THE TERM " PATHOMORPHOSIS" IN RELATION TO DISEAS MEANS:
1. Complications
2. Variability
3. The mechanism of death
4. The reason of development
5. The mechanism of development
11. IMMUNOHISTOCHEMICAL RESEARCH IS USED FOR REVEALING OF:
1. Аutoantygenes
2. Tumorous histogenesis
3. Genetic diseases
4. A kind of infection
5. Autoantybodies
12. THE BASIC PURPOSES OF AUTOPSY IS:
1. To define correctness of treatment
2. To reveal the reason of death of the patient
3. To establish the final diagnosis
4. To establish biological age of patient
5. To investigate internal organs
13. THE FOUNDER OF MODERN ANATOMIC PATHOLOGY IS:
1. R.Brhait
2. R.Virchov
3. A.I.Over
4. E.O.Mukhin
5. K.Rokitansky
14. THE MAIN METHOD OF BIOPSY EXAMINATION IS:
1. Biochemical
2. Radiological
3. Microbiological
4. Histological
5. Ultrasonic
15. THE MAIN LEVEL OF PATHOLOGICAL PROCESS STUDY IS:
1. Subcellular
2. Tissue
3. Cellular
4. Systemic
4
5. Organic
16. PICROFUCHSIN BY VON GIESONE SELECTIVELY REVEALS:
1. Nervous fibers
2. Smooth muscle cells
3. Epithelial cells
4. Connective tissue and collagen fibers
5. Fat
17. THE TERM "ETHIOLOGY" IN RELATION TO DISEASE MEANS:
1. Complications
2. Variability
3. The mechanism of death
4. The reason of development
5. The mechanism of development
18. AUTOPSY IS PERFOMED IN CASE OF DEATH FROM:
1. Gunshot wound
2. Hangings
3. Poisonings
4. Diseases
5. Not clear reasons
19. THE SYNONYM OF THE TERM "POSTMORTEM EXAMINATION" IS:
1. Section
2. Biopsy
3. Autopsy
4. Necrosy
5. Vivisection
20. THE MOST WIDESPREAD LEVEL OF BIOPSY MATERIAL EXAMINATION IS:
1. Subcellular (ultrastructural)
2. Macroscopical (anatomic)
3. Microscopic (histologic)
4. Chemical (laboratoric)
5. Surgical
21. SPECIAL STAIN FOR IRON -CONTAINED SUBSTANCES DETECTION IS:
1. Sudan III
2. Picrofuchsin by von Giesone
3. PAS-reaction
4. Perl's reaction
5. By Ziehl-Nielsen
22. TOLUIDINE BLUE IS STAIN FOR DETECTION OF:
1. Neural tissue
2. Cellular nucleus
3. Basophilic structures
4. Metachromatic substances
5. All true
23. SPECIAL COURSE OF ANATOMIC PATHOLOGY STUDIES:
5
1. Diseases of kidneys
2. Structure of the diagnosis
3. Processes of adaptation
4. Changers at single diseases
5. All true
24. INVESTIGATION OF THE SLICE OF ALIFE PATIENT TISSUE WITH THE DIAGNOSTIC
PURPOSE IS:
1. Section
2. Biopsy
3. Autopsy
4. Necropsy
5. Vivisection
25. SPECIAL STAIN FOR LIPIDS DETECTION IS:
1. Sudan III
2. Picrofuchsin by von Giesone
3. PAS- reaction
4. Perl's reaction
5. By Ziehl-Nielsen
26. THE STAIN WHICH USUALLY USED FOR PRIMARY HISTOLOGIC EXAMINATION IS:
1. Sudan III
2. Hematoxyline and eosin
3. Picrofuchsin by von Giesone
4. Alcian blue
5. Congo red
27. THE AUTOPSY IS REVEALED:
1. Efficiency of treatment
2. The reason of death of the patient
3. Metabolism in an organism
4. Correctness of the clinical diagnosis
5. All true
28. THE STAIN USUALLY USED FOR DETECTION OF AMYLOID IS:
1. Sudan III
2. Hematoxyline and eosin
3. Picrofuchsin by von Giesone
4. Alcian blue
5. Congo red
29. REACTIONS OF METHACHROMASIA PREDISPOSE:
1. Change of size
2. Change of density
3. Change of brightness
4. Change of color
5. Decreasing of object
30. STAIN FOR DETECTION OF ACID GLYCOSAMINOGLYCANS IS:
1. Hematoxyline and eosine
2. Sudan-III
6
3. Alcian blue
4. Congo red
5. Sudan-IV
31. « CONGO RED » IS USED FOR DETECTION OF:
1. Glycogen
2. DNA
3. Fat
4. Amyloid
5. Melanin
32. STAINING IN FOCI OF MUCOID DEGENERATION REFERS TO PHENOMENON:
1. Fluorescence
2. Birefringence
3. Yellow or green metachromasia
4. Orange or red metachromasia
5. Pink or violet metachromasia
33. THE STAIN FOR REVEALING OF LIPID INCLUSIONS IS:
1. Eosin
2. Sudan III
3. Congo red
4. Picrofuchsin
5. Hematoxyline
34. WHAT STAIN IS SPECIFIC FOR IRON:
1. Hematoxylin and eosin
2. Sudan III
3. Perl’s reaction
4. Congo red
5. PAS-reaction
35. RESULT OF PERLS’ REACTION IS:
1. Nil’s blue
2. Prussian blue
3. Congo red
4. Sudan III
5. Cancer pearls
2. INTRACELLULAR ACCUMULATION
1. STEATOSIS OF LIVER IS OBSERVED AT:
1. Anemia
2. Adiposity
3. Alcoholism
4. Thyrotoxicosis
5. All true
2. INTRACELLULAR ACCUMULATION OF GLYCOGEN ARE MARKED AT:
1. Anemia
2. Adiposity
3. Alcoholisms
7
4. Tesaurismoses
5. Diabetes
3. THE MECHANISM OF FATTY DYSTROPHY DEVELOPMENT ON THE PERIPHERY OF
HEPATIC LOBULE IS:
1. Infiltration
2. Decomposition
3. Plasmorrhagia
4. Transformation
5. Perverted synthesis
4. PARENCHIMATOUSE DYSTROPHIES MAY BE:
1. Water-mineral
2. Nucleoproteins
3. Chromoproteinous
4. Carbohydrate
5. All true
5. THE TRIVIAL NAME OF HEART AT THE FATTY DYSTROPHY IS:
1. "Bull"
2. "Goose"
3. "Hairy"
4. "Tiger"
5. "Porphyry"
6. TYPICAL OUTCOME OF BALOON DYSTROPHY OF CELL IS:
1. Apoptosis
2. Swelling of cell
3. Coagulative necrosis
4. Colliquative necrosis
5. Crush of cell
7. ACCUMULATION OF LIPIDS IN PARENCHYMATOUS CELLS IS TERMED AS:
1. Steatosis
2. Sclerosis
3. Melanosis
4. Hyalinosis
5. Lipomatosis
8. HEREDITARY DISEASES OF INTRACELLULAR ACCUMULATION ARE KNOWN AS:
1. System
2. Tesauresmoses
3. Autoimmune
4. Cerebrovascular
5. Immuncomplexis
9. THE CONSISTENCE OF THE LIVER AT STEATOSIS:
1. Flabby
2. Dense
3. Not changed
4. Soft-elastic
5. Stone-like
8
10. PROTEINURIA REFLECTS PRESENCE OF ALBUMINOUS DYSTROPHY IN:
1. Kidney
2. Liver
3. Urethra
4. Urinary bladder
5. Intestine
11. THE SURFACE OF THE LIVER AT STEATOSIS IS:
1. Smooth
2. Rough
3. Glaze
4. Granulated
5. Wrinkled
12. HYDROPIC DYSTROPHY OF HEPATOCYTES IS CHARACTERISTIC FOR:
1. Steatosis
2. Hepatitis
3. Fibrosis
4. Diabetes
5. Hemochromatosis
13. THE REASONS OF FATTY DYSTROPHY IN MYOCARDIUM ARE:
1. Hypoxia, intoxication
2. Arterial hypertension
3. Hypercholesterinemia, hypoxia
4. Albuminous insufficiency, intoxication
5. Hyperglycemia, hypercholesterinemia
14. THE SIZE OF THE LIVER AT STEATOSIS:
1. Increased
2. Reduced
3. Not changed
4. All true
15. STEATOSIS AS A CONSEQUENCE OF ALBUMINOUS INSUFFICIENCY DEVELOPS IN:
1. Heart
2. Kidneys
3. Liver
4. Spleen
5. Brain
16. THE FEATURES OF FATTY DYSTROPHY IN MYOCARDIUM ARE:
1. Focal character of lipids deposition
2. Diffuse character of lipids deposition
3. Pulverized accumulation of lipids
4. Accumulation of lipids on pathway of fine veins
5. Decrease of myocardium contract abilities
17. THE TRIVIAL NAME OF THE LIVER AT STEATOSIS IS:
1. "Sago liver"
2. "Beckon"
9
3. "Goose"
4. "Tiger"
5. "Icing"
18. HYDROPIC DYSTROPHY OF RENAL TUBULES IS CHARACTERISTIC FOR:
1. Steatosis
2. Inflammation
3. Fibrosis
4. Diabetes
5. Alcoholisms
19. PARENCHIMATOUSE DYSTROPHIES MAY BE:
1. Albuminous
2. Water-mineral
3. Nucleoproteins
4. Chromoproteins
5. All true
20. MORPHOGENETIC MECHANISM OF DYSTROPHY DEVELOPMENT IS:
1. Plasmorrhagia
2. Destruction
3. Infiltration
4. Transmission
5. Resolution
21. STEATOSIS CAN DEVELOP IN:
1. Liver
2. Lungs
3. Spleen
4. Vessels
5. Intestine
22. THE NEPHROTIC SYNDROME IS CHARACTERIZED BY ALL, EXCEPT:
1. Massive proteinuria
2. Hypoalbuminemia
3. Generalized edema
4. Hyperproteinemia
5. Hypertension
23. THE MECHANISM OF FATTY DYSTROPHY DEVELOPMENT IN THE CENTER OF HEPATIC
LOBULE:
1. Infiltration
2. Decomposition
3. Plasmorrhagia
4. Transformation
5. Perverted synthesis
24. SEVERE FORM OF FATTY DYSTROPHY IN MYOCARDIUM IS CHARACTERIZED BY:
1. Expansion of chambers of heart
2. Flabby consistence of heart
3. Focal character
4. Pulverized accumulation of lipids
10
5. All true
25. ALL OF THE FOLLOWING FACTORS MAY RESULT BY THE INTRACELLULAR
ACCUMULATION OF FAT EXCEPT
1. Increased transport of precursor substances to cells.
2. Overproduction of accumulated material by cells.
3. Decreased mobilization of accumulated material.
4. Decreased amount of fat nutrition.
5. Irreversible damage to mitochondria.
26. WHAT KIND OF DYSTROPHY IS CHARACTERISTIC FOR “TIGER HEART”:
1. Albuminous
2. Balloon
3. Hydropic
4. Fatty
5. Carbohydrate
27. MORPHOGENETIC MECHANISM OF FATTY DYSTROPHY IN HEPATOCYTES IS:
1. Infiltration
2. Decomposition
3. Plasmorrhagia
4. Transformations
5. The perverted synthesis
28. THE PATHOLOGIC PROTEINACEOUS SUBSTANCE ACCUMULATING ONLY BETWEEN
CELLS IN VARIOUS TISSUE AND ORGANS IS:
1. Glycogen
2. Hyaline
3. Water
4. Amyloid
5. Lipids
29. THE STROMA-VASCULAR DYSTROPHY IS:
1. Lethal damage of cells
2. Overgrowth of collagen in stroma
3. Infringement of parenchymatouse organs function
4. Convertible damage of connective tissue
5. The kind of damage by extracellular accumulation of abnormal quantities of various substances
30. THE SUBSTANCE WHICH HAS RED COLOR AFTER CONGO RED STAINING IS:
1. Lipid
2. Hyaline
3. Water
4. Amyloid
5. Glycogen
31. DUE TO LONG-TERM HYPERTENSION AND DIABETES MELLITUS THE WALLS OF
ARTERIOLS, ESPECIALLY IN KIDNEY, BECOME:
1. Serous
2. Thinned
3. Hyalinized
4. Ulcereted
11
5. Pigmented
32. THE CHARACTERISTIC OF AMYLOID FIBRILS INCLUDE ALL, EXCEPT:
1. Composed of paired filaments
2. No branching
3. With an indefinite diameter
4. With indefinite length
5. With definite length
33. REVERSABLE AMONG THE FOLLOWING PATHOLOGICAL PROCESES IS:
1. Mucoid swelling
2. Fibrinoid degeneration
3. Amyloidosis
4. Apoptosis
5. Necrosis
34. THE ORGAN AFFECTED IN BOTH PRIMARY AND SECONDARY AMYLOIDOSIS IS:
1. Kidneys
2. Stomach
3. Uterus
4. Brain
5. Lungs
35. THE CELLS ACCUMULATING FAT IN ATHEROSCLEROTIC PLAQUE ARE:
1. Fibroblasts
2. Epithelial cells
3. Foam cells
4. Lymphocytes
5. Leukocyte
36. THE DEPOSITIONS OF AMYLOID IS NOT REVEALED IN:
1. Mesangium
2. Basement membranes of blood vessels
3. Tubular basement membranes
4. Epithelium of proximal renal tubules
5. Interstitium of the kidneys
37. AT ATHEROSCLEROSIS UNDER INTIMA OF AORTA ACCUMULATE:
1. Apolipids
2. Cholesterol
3. Fatty acids
4. Cholesterol and its ethers
5. Thriglycerids
38. THE IRREVESIBLE PROCESS OF HIGH WEIGHT MOLECULAR PROTEINS
ACCUMULATION IN EXTRCELLULAR MATRIX IS:
1. Hemosiderosis
2. Glycogenoses
3. Melanosis
4. Mucoid changes
5. Fibrinoid changes
12
39. INTRACELLULAR ACCUMALATIONS ARE CHARACTERIZED BY DEPOSITION IN CELL
OF:
1. Exogenous substances
2. Organic acids
3. Nucleic acids
4. Lipids, albumins, carbohydrates, pigments
5. Products of metabolism
40. ACCUMULATION OF ETHERS OF CHOLESTEROL IN MACROPHAGES AT THE CHRONIC
CHOLECYSTITIS REFERS TO:
1. Steatosis
2. Lipidosis
3. Cholesterolosis
4. Xantomatosis
5. Apoptosis
41. CHOLESTEROL ACCUMULATION IN CELLS IS NOT OCCUR IN:
1. Atherosclerosis
2. Xanthomatosis
3. Apoptosis
4. Inflammation and necrosis
5. Cholesterolosis
42. CELLS WHICH ACCUMULATED CHOLESTEROL AND ITS ESTERS IN
ATHEROSCLEROTIC PLAQUE ARE:
1. Macrophages and smooth muscle cells
2. Leukocytes and fibroblasts
3. Lymphocytes and erythrocytes
4. Fibroblasts and leukocytes
5. Erythrocytes and lymphocytes
43. ACCUMULATION OF AMYLOID IN RENAL TISSUE CAN’T BE OBSERVED IN:
1. Arterioles walls
2. Cytoplasm of tubules epithelium
3. Glomerules
4. Basement membrane of tubules epithelium
5. Stroma
44. THE STROMA-VASCULAR DYSTROPHY IS:
1. Lethal damage of cells
2. Overgrowth of collagen in stroma
3. Infringement of parenchymatous organs function
4. Reversible damage of connective tissue
5. The kind of damage by extracellular congestions of abnormal quantities of various substances
45. THE ORGAN, WHICH ISN’T AFFECTED IN PRIMARY AMYLOIDOSIS:
1. Heart
2. Kidneys
3. Liver
4. Striated muscles
5. Lungs
13
46. REACTIVE SYSTEMIC AMYLOIDOSIS MAY OCCUR IN ASSOCIATION WITH ALL
DISEASES, EXCEPT:
1. Rheumatoid arthritis
2. Ankylosing spondylitis
3. Chronic appendicitis
4. Myeloma
5. Tuberculosis
47. THE STAINS FOR DETECTION OF AMYLOID ARE ALL, EXCEPT:
1. Congo red
2. Iodine green
3. Methyl violet
4. Sudan III
5. Gentian violet
48. LIPIDS CAN COLLECT IN VESSEL WALL AS:
1. Phospholipids
2. Triglycerides
3. Cholesterol ethers
4. Threglycerids ethers
5. Phospholipids ethers
49. THE SUBSTANCE WITH FIBRILLAR STRUCTURE THAT FORMS IN PATHOLOGICAL
CONDITIONS IS:
1. Reabsorption droplets
2. Russell bodies
3. Lipids
4. Amyloid
5. Calcificates
50. CHOLESTEROL ACCUMULATION IN CELL OCCURS IN:
1. Hypertension
2. Atherosclerosis
3. Apoptosis
4. Inflammation
5. Necrosis
51. PRIMARY ADIPOSITY BY ETHYOLIGY MAY BE ALL, EXCEPT:
1. Alimentary
2. Cerebral
3. Cardio-vascular
4. Hereditary
5. Endocrinal
52. MACROSCOPICALLY, ORGANS AFFECTED BY AMYLOIDOSIS ARE:
1. Enlarged, firm, waxy
2. Diminished, firm, waxy
3. Enlarged, soft, smooth
4. Diminished, soft, smooth
5. Rough, enlarged, firm
53. FOCAL ACCUMULATION OF LIPIDS AT STROMA-VASCULAR DISRTOPHY IS:
1. Steatosis
14
2. Sclerosis
3. Melanosis
4. Hyalinosis
5. Lipomatosis
54. THE COMMON CAUSE OF DEATH FROM SECONDARY AMYLOIDOSIS IS INSUFFICIENCY
OF:
1. Kidneys
2. Heart
3. Liver
4. Lungs
5. Adrenals
55. HYALINOSIS MEETS IN OUTCOME OF:
1. Fatty dystrophy
2. Collicvation necrosis
3. Mucoid and fibrinoid degeneration
4. Vacuolar dystrophy
5. Leucocytes infiltration
56. CHOOSE WHICH OF THE FOLLOWING IS NOT A KIND OF STROMA-VASCULAR
DYSTROPHIES:
1. Mucoid degeneration
2. Fibrinoid degeneration
3. Fatty change
4. Amyloidosis
5. Hyalinosis
57. THREE KINDS OF DYSPROTEINOSIS CAN PASS ONE INTO ANOTHER EXCEPT:
1. Hyalinosis
2. Amyloidosis
3. Mucoid degeneration
4. Fibrinoid degeneration
58. AMYLOIDOSIS CAN BE COMPLICATION OF:
1. Essential hypertension
2. Atherosclerosis
3. IHD
4. Cirrhosis of liver
5. Chronic fibrous-cavernous tuberculosis
59. AMYLOIDOSIS CAN BE COMPLICATION OF:
1. Hypertonic disease
2. Atherosclerosis
3. Cirrhosis of liver
4. Chronic pulmonary abscess
5. Ischemic heart disease
60. WHAT OF THE FOLLOWING ABNORMAL CLINICAL MANIFESTATIONS IS CORRECTLY
PAIRED WITH THE APPROPRIATE PIGMENT DEPOSITIONS?
1. Poisoning - fat
2. Hemolytic anemia - lipofuscin
15
3. Idiopathic hemosiderosis - hematin
4. Addison’s disease - melanin
5. Atrophy of hepatic cells – enterochromophinic pigment
61. HEMOSIDERIN IN LUNG IS ACCUMULATED IN:
1. Leukocytes
2. Lymphocytes
3. Macrophages
4. Fibroblasts
5. Erythrocytes
62. HEMOSIDERIN HAS ALL OF THE FOLLOWING FEATURES, EXCEPT:
1. Hemoglobin-derived
2. Golden yellow-to-brown
3. Granular or crystalline
4. Synthesized by ensyme tyrosinase
5. Aggregate of ferritin
63. HEART AND LIVER OF PATIENT WITH CACHEXIA ARE MACROSCOPICALLY SEEN AS:
1. Diminished and brown
2. Diminished and yellow
3. Enlarged and brown
4. Enlarged and yellow
5. Unchanged
64. INCREASED AMOUNT OF MELANIN IS KNOWN AS:
1. Vacuolization
2. Vitiligo
3. Melanosis
4. Albinism
5. Hypomelanosis
65. MELANIN HAS ALL OF THE FOLLOWING FEATURES, EXCEPT:
1. Localized endogenously
2. Forms from ferritin
3. Non-hemoglobin-derived
4. Black-brown
5. Forms in melanocytes
66. LIPOFUSCIN HAS ALL OF THE FOLLOWING FEATURES, EXCEPT:
1. Aging pigment
2. Most often seen in kidney
3. Yellow-brown
4. Noninjurious to the cells or their function
5. Endogenous pigment
67. LIPOFUSCIN PIGMENT ACCUMULATION IN CELLS IS THE RESULT OF:
1. Hemosiderosis
2. Protein accumulation in cytoplasm
3. Lipid accumulation in cytoplasm
4. Cellular swelling
5. Intracellular lipid peroxidation
16
68. THE LUNGS IN PULMONARY HEMOSIDEROSIS ARE CHARACTERIZED BY:
1. Only enlarged in size
2. Increased in weight with red-brown areas
3. Diminished with areas of red-brown consolidation
4. Diminished with fluid exuding from cut surface
5. Unchanged
69. JAUNDICE OCCURS IN THE FOLLOWING PATHOLOGICAL PROCESSE:
1. Increased hepatocellular excretion
2. Reduced production of bilirubin
3. Increased hepatocyte uptake
4. Impaired conjugation of bilirubin
5. Increased bile flow
70. LOCAL DECREASED AMOUNT OF MELANIN IS KNOWN AS:
1. Vacuolization
2. Vitiligo
3. Hyperpigmentation (melanosis)
4. Albinism
5. Hyperkeratosis
71. LIPOFUSCIN GRANULES IN CELLS ARE SEEN IN:
1. Necrosis
2. Denervation
3. Brown atrophy
4. Atrophy from pressure
5. Apoptosis
72. UNCONJUGATED HYPERBILIRUBINEMIA OCCURS IN:
1. Obstruction of bile duct
2. Increased hepatocyte uptake
3. Increased hepatocellular excretion
4. Increased conjugation
5. Hepatocyte injury in hepatitis В
73. EXOGENIOUS PIGMENT IS:
1. Lipofuscin
2. Hemosiderin
3. Carmin
4. Ferritin
5. Hematin
74. LIPOFUCSIN IN THE LIVER MAY BE FOUND IN:
1. Unchanged cells
2. Cells with ballooning degeneration
3. Cells with hyaline droplets
4. Cells with regressive changes
5. Necrotic cells
75. BILIARY DUCTS' OBSTRUCTION MAY LEAD TO:
1. Liver hemosiderosis
17
2. Liver steatosis
3. Ballooning degeneration of hepatocytes
4. Cholestasis and jaundice
5. Hemochromatosis
76. LOCAL HEMOSIDEROSIS IS SEEN IN:
1. Diabetes mellitus
2. Hereditary increased absorption of dietary iron
3. Focus of hemorrhage
4. Hemolytic anemia
5. Impaired uptake of iron
77. BILIRUBIN HAS ALL OF THE FOLLOWING FEATURES, EXCEPT:
1. The end product of hem degradation
2. Derived from destroyed erythrocytes
3. Brilliant-yellow color
4. Blue-black color with Perls’ reaction
5. Conjugated and unconjugated form
78. WIDESPREAD DECREASED AMOUNT OF MELANIN IS KNOWN AS:
1. Vacuolization
2. Vitiligo
3. Hyperpigmentation (melanosis)
4. Albinism
5. Hyperkeratosis
79. IRON CONTENTED SUBSTANCE AMONG PIGMENTS IS:
1. Bilirubin
2. Hematoidin
3. Lipofuscin
4. Hematin
5. Ceroid
80. MORPHOLOGIC CHANGES IN GENETIC HEMOCHROMATOSIS ARE CHARACTERIZED BY
ALL, EXCEPT:
1. Deposition of melanin in skin
2. Deposition of hemosiderin in many organs
3. Deposition of hemosiderin in the skin
4. Liver cirrhosis
5. Pancreatic hemosiderosis
81. TO LIPIDOGENIUS PIGMENTS REFER:
1. Hemosiderin
2. Ceroid
3. Pigment of entherochromophinic cells
4. Hemin
5. Adrenochrom
82. IRON ISN’T PRESENT IN STRUCTURE OF PIGMENT:
1. Hematoidin
2. Hemin
3. Formalized hematin
18
4. Hemomelanin
5. Ferritin
83. TO TYROSINOGENIOUS PIGMENTS REFER:
1. Hemosiderin
2. Ceroid
3. Pigment of vitamin E deficiency
4. Hemin
5. Adrenochrom
84. SUPRAHEPATIC JAUNDICE DEVELOPS AS RESULT OF:
1. Billiary obstruction
2. Brown atrophy of the liver
3. Hepatitis B
4. Intestinal obstruction
5. Hemolytic anemia
85. WHICH OF THE FOLLOWING SITES IS AN EXAMPLE OF LOCAL HEMOSIDEROSIS?
1. Mitral valvе in mitral stenosis of reumatic origin
2. Left anterior ascending coronary artery involved by ateromatous plaques
3. Brain with pigmented cyst in the place of hemorrhage
4. Lung in areas of old tuberculosis infection
86. STAIN, WHICH USED FOR DETECTION OF HEMOSIDERIN, IS:
1. Hematoxyline and eosine
2. Prussian blue
3. Congo-red
3. Sudan-III
4. Picrofuschin
87. WIDESPREAD MELANOSIS DEVELOPS AT:
1. Albinism
2. Melanoma
3. Addison’s disease
4. Pigmentary nevus
5. Glomerulopathy
88. AN EXAMPLE OF METASTATIC CALCIFICATION IS:
1. The kidney in nephrocalcynosis
2. The mitral valve in mitral stenosis of rheumatic origin
3. The left anterior ascending coronary artery involved by atheromatous plaques
4. The lung in areas of old tuberculosis infection
5. Epidermoid cyst
89. WHAT OF THE FOLLOWING CONCRETIONS (STONES) IS NOT FORMED IN KIDNEYS:
1. Urates
2. Oxalates
3. Pigmentary
4. Phosphates
5. All true
90. BILIARY DUCTS' OBSTRUCTION BY GALLSTONES MAY LEAD TO:
19
1. Liver hemosiderosis
2. Liver steatosis
3. Ballooning degeneration of hepatocytes
4. Cholestasis and jaundice
5. Hemochromatosis
91. METASTATIC CALCIFICATION OCCURS IN WHICH OF THE FOLLOWING DISEASES:
1. Parathyroid adenoma
2. Rheumatic heart disease
3. Atherosclerosis
4. Phlebothrombosis
5. Tuberculosis
92. THE KIND OF CALCIFICATION IS:
1. Necrotic
2. Dystrophic
3. Hypertrophic
4. Atrophic
5. Proliferative
93. DISEASE WHICH NOT CAUSE METASTATIC CALCIFICATION IS:
1. Diabetes mellitus
2. Increased secretion of parathyroid hormone
3. Destruction of bone tissue
4. Vitamin D-related disorders
5. Renal failure
94. IN WHICH ORGAN METASTATIC CALCIFICATION NEVER OCCURS:
1. Stomach (gastric mucosa)
2. Kidneys
3. Lungs
4. Liver
5. Heart, systemic arteries and pulmonary veins
95. DEFICIENCY OF VITAMIN D TENDS TO CAUSE WHICH OF THE FOLLOWING:
1. Hypercalcemia
2. Hypocalcemia
3. Hyperpigmentation
4. Hypopigmentation
5. Calcification
3. HEMODINAMIC DISORDERS
1. “АNASARCA” IS THE NAME OF:
1. Limphedema
2. Local swelling
3. General edema
4. Subcutaneous haemorrhage
5. Puffiness
2. METAPHORICALLY THE NAME OF LIVER AT CHRONIC VENOUS CONGESTION IS:
1. "Porphyry"
2. "Sago"
20
3. "Grease"
4. "Nutmeg"
5. "Backon"
3. MECHANISM OF BLEEDING IS:
1. Diathesis
2. Plasmorrhagia
3. Hemorrhagia
4. Diapedesis
5. Myolysis
4. THE EDEMA IS:
1. Increased volume of blood
2. Increase in volume of lymph
3. Accumulation of interstitial fluid
4. Accumulation of fluid in abdominal cavity
5. Accumulation of fluid between testis’ environments
5. ACCUMULATION OF BLOOD IN THE PLEURAL CAVITY IS:
1. Hematoma
2. Hematuria
3. Hemathemesis
4. Hemathorax
5. Hemangioma
6. AT ACUTE VENOUS CONGESTION IN NEPHROCYTES DEVELOPS:
1. Dystrophy and necrosis
2. Hyalinosis and sclerosis
3. Sclerosis
4. Amyloidosis
5. Hemosiderosis
7. COLOR OF LUNG AT CHRONIC VENOUS CONGESTION DETERMINATES BY PIGMENT
PRESENCE:
1. Hematin
2. Bilirubin
3. Hemosiderin
4. Hematoidin
5. Lipofuscin
8. THE NAME OF EDEMATOUS FLUID ACCUMULATION IN ABDOMINAL CAVITY IS:
1. Ascites
2. Anasarca
3. Hydrocele
4. Hydrothorax
5. Hydronephrosis
9. CHRONIC VENOUS CONGESTION IN SPLEEN LEADS TO:
1. Brown atrophy
2. Brown induration
3. Cyanotic induration
4. Hemochromatosis
21
5. Amyloidosis
10. THE NAME OF FLUID ACCUMULATING IN CAVITIES DUE TO CONGESTION IS:
1. Lymphorrhea
2. Exudate
3. Transudate
4. Hydrops
5. Anasarca
11. THE NAME OF CHRONIC VENOUS CONGESTION IN KIDNEY IS:
1. Brown atrophy
2. Hydronephrosis
3. Brown induration
4. Cyanotic induration
5. Nephrochirrosis
12. THE STOMACH BLEEDING AS COMPLICATION IS FREQUENTLY MEETS AT:
1. Gastritis
2. Stomach ulcer
3. Tesaurismoses
4. Colitis
5. Pancreatitis
13. MICROSCOPICALLY, ACUTE PULMONARY CONGESTION IS CHARACTERIZED BY ALL
OF THE FOLLOWING, EXCEPT:
1. Engorged alveolar capillaries
2. Thickened and fibrotic alveolar septa
3. Edema fluid in alveoli
4. Focal intra-alveolar hemorrhage
5. Foci of atelectasis
14. MICROSCOPICALLY, CHRONIC PULMONARY CONGESTION IS CHARACTERIZED BY
ALL OF THE FOLLOWING, EXCEPT:
1. Engorged alveolar capillaries
2. Thickened and fibrotic alveolar septa
3. Focal intra-alveolar hemorrhage
4. Hemosiderosis
5. Abscesses in lung tissue
15. CHRONIC VENOUS CONGESTION RESULTS IN DEVELOPING IN LUNG:
1. Muddy swelling
2. Lipofuscinosis
3. Brown induration
4. Mucoid swelling
5. Fibrinoid swelling
16. STASIS DEVELOPMENT IS CHARACTERIZED BY:
1. Loss of fibrin
2. Damage of vascular wall
3. Agglutination of erythrocytes
4. Leucodiapedesis
5. Pinocytosis
22
17. MICROSCOPICALLY, CHRONIC PASSIVE CONGESTION OF THE LIVER IS
CHARACTERIZED BY ALL OF THE FOLLOWING, EXCEPT:
1. Centrolobular necrosis of hepatocytes
2. Centrolobular hemorrhages
3. Engorged periportal sinusoids
4. Capillarisation of sinusoids
5. Fatty changes of periportal hepatocytes
18. ORGANS AT CHRONIC VENOUS CONGESTION:
1. Are reduced in sizes
2. Have a flabby consistence
3. Have a dense consistence
4. Yellow color
5. Mucous degeneration
19. PRINCIPAL CAUSE OF VENOUS HYPEREMIA IS:
1. Reduction of blood inflow
2. Increase of blood inflow
3. Difficulty of blood outflow
4. Increase of blood outflow
5. Stasis
20. HEMORRHAGE ENCLOSED WITHIN A TISSUE CAUSING ITS DESTRUCTION IS TERMED AS:
1. Hematoma
2. Petechia
3. Purpura
4. Ecchymosis
5. Hemothorax
21. MINUTE (1- TO 2-MM) HEMORRHAGES INTO SKIN, MUCOUS MEMBRANES OR SEROSAL
SURFACES ARE CALLED:
1. Hematomas
2. Petechiae
3. Purpura
4. Ecchymoses
5. Hemothorax
22. MACROSCOPICALLY, CHRONIC PASSIVE CONGESTION OF THE LIVER IS
CHARACTERIZED BY ALL OF THE FOLLOWING, EXCEPT:
1. Enlargement of the liver
2. Red-brown central areas of the hepatic lobules
3. Decreasing in sizes
4. Tan periportal areas (fatty changes)
5. Nutmeg liver
23. THE FIGURATIVE NAME OF LIVER AT CHRONIC VENOUS CONGESTION IS:
1. Grease
2. Sago
3. Brown
4. Nutmeg
5. Icing
23
24. GENERAL VENOUS CONGESTION DEVELOPS AT:
1. Compression of superior cava vein
2. Thrombosis of portal vein
3. Compression of renal vein by tumor
4. Polycythemia
5. Heart diseases
25. «NUTMEG LIVER» CAN BE CAUSED BY:
1. Brain hyperemia
2. Spleen hyperemia
3.Cyanotic induration of kidneys
4. Mitral valve stenosis
5. Acute coronary insufficiency
26. EMBOLISM UNDERLIES DISSEMINATION OF TUMOR (METASTASIS) IS:
1. Fatty
2. Bacterial
3. Cellular
4. Thrombus
5. Purulent
27. THE THROMBOSIS IS NOT DEVELOPING DUE TO:
1. Change of blood quality
2. Hereditary trombastenia
3. Change of blood flow direction
4. Damage of vascular endothelium
5. Slow blood flow
28. THE SYNONYM OF THE DIС-SYNDROME:
1. Hemorrhagic diathesis
2. Coagulopathy of consumption
3. Thrombohemorhagic syndrome
4. Trombocytopenian syndrome
5. Antycoagulative syndrome
29. CHARACTERISTIC OF THE NON-PROGRESSIVE STAGE OF SHOCK IS:
1. Decreasing of heart outcome
2. Decreasing of organs’ blood supply
3. Damages of endothelium, cells membranes
4. Compensated decreasing of blood pressure
5. Insufficiency of microcirculatory blood supply
30. SYNDROME FREQUENTLY ASSOCIATED WITH SHOCK IS:
1. Pulmono-coronary
2. Nephrotic
3. Thrombohemorrhagic
4. Thromboembolic
5. DIС
31. THE PROGRESSIVE STAGE OF SHOCK IS CHARACTERISED BY:
1. Increasing of heart outcome
24
2. Increasing of organs’ blood supply
3. Beginning of metabolic and discirculatory changes in organs
4. Compensated decreasing of blood pressure
5. Necrotic changes in parenchymatous organs
32. THROMBUS IN HEART CHAMBERS MAY BE:
1. Ball-shaped
2. Occlusive
3. Circular
4. Parietal
5. Progressive
33. HEMORRHAGE ENCLOSED WITHIN A TISSUE CAUSING ITS DESTRUCTION IS TERMED AS:
1. Hemothorax
2. Petechia
3. Purpura
4. Ecchymosis
5. Hematoma
34. THE IRREVERSIBLE STAGE OF SHOCK IS CHARACTERIZED BY:
1. Decentralization of blood flow
2. Severe metabolic changers in organs
3. Inflammation of endothelium
4. Compensated decreasing of blood pressure
5. Hypertrophy of heart
35. AT DIС-SYNDROME IN BRAIN MAY BE REVEALED:
1. Necrosis of epithelium
2. Centers of caseous necrosis
3. Ischemia and focal necrosis
4. Serous-hemorrhagic exudates
5. Microthrombi
36. THE BODY OF THE MIXED THROMBUS ACCORDING TO STRUCTURE AND
APPEARANCE IS:
1. White
2. Red
3. Mixed
4. Hyaloid
5. Fibrinous
37. ONE OF THE BASIC TYPES OF SHOCK IS:
1. Septic
2. Anaphylactic
3. Cardiogenic
4. Humoral
5. Traumatic
38. THE HEAD OF THE MIXED THROMBUS ACCORDING TO STRUCTURE AND
APPEARANCE IS:
1. White
2. Red
25
3. Mixed
4. Hyaloid
5. Fibrinous
39. SEPTIC SHOCK IS USUALLY CAUSED BY:
1. Viruses
2. Parasites
3. Foreign bodies
4. Bacteriemia
5. Micoplasma
40. ONE OF THE STAGES OF DIС-SYNDROME DEVELOPMENT IS:
1. Aggregation of cells
2. Inflammation
3. Coagulopathy of consumption
4. Activation of coagulation
5. Reconvalescention
41. THE TAIL OF THE MIXED THROMBUS ACCORDING TO STRUCTURE AND APPEARANCE
IS:
1. White
2. Red
3. Mixed
4. Hyaloid
5. Fibrinous
42. INCREASED COAGULABILITY OF BLOOD IS OBSERVED AT:
1. Nephrotic syndrome
2. Willebrandt disease
3. Thrombocytopenian purpura
4. Last term of pregnancy
5. Disseminative canceromatous
43. THROMBUS IS DIFFERED FROM BLOOD CLOTS BY:
1. Postmortem appearance
2. Attachment to vessel wall
3. Smooth surface
4. Soft consistence
5. Amorphous
44. THE RESULT OF MASSIVE FATTY EMBOLISM IS ACUTE INSUFFICIENCY OF:
1. Kidneys
2. Polyorganic
3. Lungs
4. Heart and vessels
5. Liver
45. BY DIС-SYNDROME CAN COMPLICATE:
1. Essential hypertension
2. Obstetrics sepsis
3. Gout
4. Fatty dystrophy of liver
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5. Adiposity
46. FAVORABLE OUTCOME OF THROMBOSIS IS:
1. Organization
2. Putrefaction
3. Destruction
4. Septic fusion
5. Retraction
47. THROMBI FORMED AT DIС-SYNDROME MOSTLY ARE:
1. White
2. Mixed
3. Red
4. Hyaloid
5. Fibrinous
48. AT FATTY PULMONARY EMBOLISM FATTY DROPS ARE FOUND OUT IN:
1. Veins
2. Alveolar spaces
3. Segmental bronchus
4. Capillaries of alveolar septum
5. Pulmonary trunk
49. THE SECOND STAGE OF THE SHOCK IS:
1. Non- progressive
2. Progressive
3. Irreversible
4. Reversible
5. Clinical
50. THE REASON OF FATTY EMBOLISM IS:
1. Fracture of long tubular bones
2. Fatty dystrophy of myocardium and liver
3. Subcutaneous injections of oil
4. Intramuscular injections of oil
5. Proliferation of bone marrow
51. THE STANE USED FOR DIAGNOSTICS FATTY PULMONARY EMBOLISM IS:
1. Perls’ reaction
2. Sudan III
3. Picrofuchsin by van Gesoune
4. Toluidin blue
5. Congo red
52. THE FIRST STAGE OF THE SHOCK IS:
1. Non- progressive
2. Progressive
3. Irreversible
4. Reversible
5. Preclinical
53. UNFAVOURABLE OUTCOME OF THROMBOSIS IS:
27
1. Organization
2. Detoughchment of thrombus
3. Recanalization
4. Vascularization
5. Aseptic ressolution
54. IN LUNGS AT DIС-SYNDROME MAY BE REVEALED:
1. Necrosis of epithelium
2. Centers of caseous necrosis
3. Ischemia and focal necrosis
4. Serous-hemorrhagic exudates
5. Microthrombi in capillary vessels
55. STAGES OF THROMBI MORPHOGENESIS ARE ALL, EXCEPT:
1. Coagulation of fibrinogen
2. Agglutination of thrombocytes
3. Agglutination of erythrocytes
4. Precipitation of plasma proteins
5. Coagulopathy of consumption
56. WHITE THROMBI ARE FORMED IN:
1. Veins
2. Arteries
3. Cavities aneurysms
4. Microcirculatory vessels
5. Heart cavities
57. RESTORATION OF BLOOD FLOW IN VESSEL AFTER THROMBOSIS IS:
1. Organization
2. Petrifaction
3. Occlusion
4. Vascularization
5. Recanalization
58. THE PULMONOCORONARY REFLEX INCLUDES SPASM OF:
1. Pulmonary veins, Bronchial tree, Coronary arteries of heart
2. Carotids, Branches of pulmonary arteries
3. Pulmonary veins
4. Carotids, Branches of pulmonary arteries, Coronary arteries of heart
5. All true
59. RED THROMBI ARE FORMED IN:
1. Veins
2. Arteries
3. Cavities aneurysms
4. Microcirculatory vessels
5. Heart cavities
60. THE MIXED THROMBI ARE FORMED IN:
1. Veins
2. Arteries
3. Cavities aneurysms
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4. Microcirculatory vessels
5. Lymph vessels
61. OCCLUSIVE THROMBI IN ARTERIES CAN LEAD TO DEVELOPMENT OF:
1. Lymphostasis
2. Infarction and gangrene
3. Thromboembolism of pulmonary arteries
4. Dystrophies of parenchimatous organs
5. Thrombophlebitis
62. AIR EMBOLISM CAN DEVELOP DUE TO:
1. Childbirths and abortions
2. Wounds of abdominal cavity
3. Fracture of bones
4. Gangrene of lung
5. Tamponade of heart
63. MIXED THROMBUS CONSISTS OF:
1. Fibrin, hyaline
2. Thrombocytes, fibrin, some erythrocytes
3. Thrombocytes, fibrin, leukocytes
4. Thrombocytes, fibrin, leukocytes, erythrocytes
5. Thrombocytes, fibrin, leukocytes, erythrocytes, hyaline
64. LOW EXTRIMITIES PHLEBOTHROMBOSIS CAN LEAD TO DEVELOPMENT OF:
1. Neoplasia
2. Infarctions and gangrene
3. Massive pulmonary thromboembolism
4. Dystrophies of parenchimatous organs
5. Rupture of heart
65. REFLEX CONNECTED WITH ТHАNATOGENESIS OF MASSIVE PULMONARY
TROMBOEMBOLISM IS:
1. Somatic
2. Pulmono-coronary
3. Viscera-visceral
4. Adaptive
5. Basilar
66. PULMONARY THROMBOEMBOLUS MAY ORIGINATE FROM:
1. Deep leg veins
2. Superior vena cava
3. Pelvic arteries
4. Portal vein
5. Microcirculation net
67. EMBOLISM CAN BE:
1. Hemolytic
2. Septic
3. Mechanical
4. Parenchimatous
5. Fatty
29
68. OPTIMUM OUTCOME OF THROMBOSIS IS:
1. Thrombus taking off
2. Septic lyses
3. Aseptic lyses
4. Organization
5. Petrifaction
69. THE POSSIBLE COMPONENTS OF EMBOLI ARE ALL OF THE FOLLOWING, EXCEPT:
1. Thrombotic masses
2. Fat droplets
3. Air bubbles
4. Amyloid masses
5. Microorganisms
70. FATTY EMBOLISM DIAGNOSIS IS VERIFICATED BY:
1. Macroscopically
2. Endoscopically
3. Microscopically
4. Visually
5. Ultramicroscopically
71. THE GREATEST VALUE AT FATTY EMBOLISM HAS CAPILLARIES OBTURATION OF:
1. Kidneys and liver
2. Lung and brain
3. Liver and spleen
4. Heart
5. Brain and bone marrow
4. CELL DEATH
1. DIGESTION OF THE CELL BY LYSOSOME ENZYMES OF IMMIGRANT LEUKOCYTES IS
TERMED AS WHICH OF THE FOLLOWING:
1. Apoptosis
2. Autolysis
3. Heterolysis
4. Inflammation
5. Metaplasia
2. CASEOUS NECROSIS IS CHARACTERISTIC FOR:
1. Gas gangrene
2. Frostbite
3. Myocardial infarction
4. Tuberculosis
5. Typhoid fever
3. THE FOLLOWING VARIANT OF NECROSIS CAN BE FOUND IN TUBERCULOSIS
1. Caseous
2. Gangrenous
3. Liquefactive
4. Enzymatic fat
5. Fibrinoid
30
4. CASEOUS NECROSIS MEETS AT:
1. Diphtheria
2. Gas gangrene
3. Tuberculosis
4. Infarction of kidney
5. Myocardial infarction
5. DEPENDING ON MECANISM OF NECROSIS, INFARCTION IS:
1. Direct
2. Ischemic
3. Traumatic
4. Toxic
5. Allergic
6. POSSIBLE OUTCOME OF LIQUEFACTIVE NECROSIS CAN BE:
1. Petrifaction
2. Ossification
3. Cyst-formation
4. Scarring
5. Mummification
7. WHICH OF THE FOLLOWING VARIANTS OF NECROSIS CAN BE FOUND IN CEREBRAL
INFARCT?
1. Coagulative
2. Liquefactive
3. Caseous
4. Gangrenous
5. Enzymatic fat
8. ALL OF THE FOLLOWING FEATURES DISTINGUISH APOPTOSIS FROM NECROSIS,
EXCEPT:
1. Programmed cell death
2. Fragmentation of nuclear chromatin only
3. Formation of apoptotic bodies
4. Affection of the separate cells or clusters of the cells
5. Presence of inflammation nearby the injured cells
9. THE CAUSES OF INFARCT INCLUDE ALL PATHOLOGIC CONDITIONS, EXCEPT:
1. Thrombotic events
2. Embolic events
3. Arterial occlusion
4. Local vasospasm
5. Hemophilia
10. WHITE INFARCT RESULTS FROM:
1. Venous occlusion
2. Arterial occlusion
3. Loose tissues
4. Tissues with dual circulation
5. Congested tissues
31
11. UNFAVORABLE OUTCOME OF NECROSIS IS:
1. Organization
2. Encapsulation
3. Petrifaction
4. Purulent putrefaction
5. Cyst formation
12. MORPHOLOGICAL CHANGES OF APOPTOSIS INCLUDE:
1. Membrane blebs
2. Inflammation
3. Nuclear fragmentation
4. Cell swelling
13. STARTING POINT OF APOPTOSIS FOR PROGRAMM CELL DEATH IS:
1. Activation of endonuclease
2. Release of enzyme
3. Accumulation of calcium
4. Destruction by macrophages
14. ONE OF THE FOLLOWING IS AN APOPTOSIS INHIBITOR GENE:
1. p53
2. Bcl-2
3. Rb
4. c-Myc
15. THE FOLLOWING ARE EXAMPLE OF APOPTOSIS, EXCEPT:
1. Graft versus host disease
2. Menstrual cycle
3. Pathological atrophy following duct obstruction
4. Tumour necrosis
5. None of the above
16. MOST COMMON TYPE OF CELL DEATH DUE TO SUDDEN OCCLUSION OF BLOOD
SUPPLY IS:
1. Coagulation necrosis
2. Caseous necrosis
3. Liquifactive necrosis
4. Gangrene
17. CLOUDY SWELLING IS DUE TO:
1. Accumulation of water intracellularly
2. Fat accumulation intracellular
3. Lysozyme degeneration
4. Glycogen accumulation intracellularly
18. LIQUAFACTION NECROSIS OCCURS IN:
1. Brain
2. Heart
3. Liver
4. Kidney
19. FAT NECROSIS IS COMMON IN:
32
1. Omentum
2. Breast
3. Retroperitoneal fat
4. All of the above
20. THE CELL MOST SENSITIVE TO ISCHEMIA IS:
1. Myocardial fibres
2. Glial cells of brain
3. Renal tubular epithelium
4. Cortical neurone
21. CELLS MOST SENSITIVE TO HYPOXIA ARE:
1. Myocardial cells
2. Neurones
3. Hepatocytes
4. Renal tubular epithelial cells
22. RED INFARCTION IS SEEN IN:
1. Kidney
2. Spleen
3. Small instestine
4. Heart
23. PALE INFARCTION IS NOT SEEN IN:
1. Lung
2. Kidney
3. Spleen
4. Heart
24. THE FIRST EFFECT OF ENDOTOXIN IS:
1. Endothelial damage
2. Perivascular necrosis
3. DIC
4. All true
5. None true
25. MICROSCOPICAL FEATURES OF NUCLEAR NECROSIS ARE:
1. Karyopicnosis, karyorrhexis, plasmolysis
2. Karyopicnosis, karyorrhexis, karyolysis
3. Plasmorrhexis, plasmolysis, karyorrhexis
4. Karyopicnosis, plasmorrhexis, karyorlysis
5. None true
26. ON VISCERAL SURFACE OF SEROUS MEMBRANE IN PLACE OF NECROSISI DEVELOPS:
1. Edema
2. Hyalinosis
3. Gangrene
4. Catarrhal inflammation
5. Fibrinous inflammation
27. FAVOURABLE OUTCOMES OF NECROSIS ARE:
1. Cyst formation, encapsulation
33
2. Organisation, ossification
3. Petrification, scarring
4. True 1&3
5. All true
28. MACROSCOPICAL CHARACTERISTIC OF SPLEEN INFARCTION IS:
1. Triangular, whitish-grey, dense
2. Triangular, whitish-grey, soft
3. Irregular, whitish-grey, dense
4. Irregular, whitish-grey, soft
5. Triangular, red, dense
29. AT ISCHEMIA IN MYOCARDIOCYTES DISSAPPEARE:
1. Lipid droplets
2. Glucose granules
3. Glycogen granules
4. Lipofuscine granules
5. Cholesteryne crystals
30. THE REASON OF INFARCTION IS:
1. Thrombosis
2. Embolism
3. Functional intention of organ in conditions of hemodynamic dysorders
4. Insufficiency of anastomoses and collateral blood supply
5. All true
31. NECROSIS DEPENDING ON REASON CAN BE:
1. Traumatic
2. Toxic
3. Allergic
4. Vascular
5. All true
32. THE MOST TYPICAL REASON OF ISCHAMIC BRAIN INFARCTION IS:
1. Tromboembolism
2. Thrombosis
3. Long-durating spasm
4. Functional intention of organ
5. All true
33. MICROSCOPICAL FEATURES OF NECROSIS IN CYTOPLASMA ARE:
1. Proteins denaturation
2. Coagulation of plasma protins
3. Plasmorrhexis, plasmolysis
4. True 1&3
5. All true
34. BLACK COLOR OF TISSUE AT GANGRENE IS DETERMINATED BY:
1. Hematin deposition
2. Presence of magnesium
3. Presence of iron sulfatis
4. Calcification
34
5. Presence of lipofuscine
35. THE SHAPE OF MYOCARDIAL INFARCTION IS:
1. Round
2. Oval
3. Triangular
4. Irregular
36. THE REASON OF RED INFARCTION DEVELOPMENT IS:
1. Thrombosis of upper mesenterial artery
2. Portal vein thrombosis
3. Minor pulmonary embolism
4. True 1&3
5. All true
37. STAGES OF NECROSIS LIKE PROCESS ARE:
1. Autolysis
2. Necrobiosis
3. Paranecrosis
4. Cell death
5. All true
38. CELLS PHAGOCYTING APOPTOTIC BODIES ARE:
1. Macrophages
2. Stromal
3. Parenchimatous
4. All true
39. SEQUESTER IS:
1. Organizated thrombus
2. Non-resolved part of dead tissue
3. Vascular necrosis
4. Necrosis of tissue connected with environment
5. Fusion of tissue
40. NOMA IS:
1. Organizated thrombus
2. Non-resolved part of dead tissue
3. Vascular necrosis
4. Necrosis of tissue connected with environment
5. Wet gangrene of soft tissue
41. GANGRENE IS:
1. Organizated thrombus
2. Non-resolved part of dead tissue
3. Vascular necrosis
4. Necrosis of tissue connected with environment
5. Fusion of tissue
42. INFARCTION IS:
1. Organizated thrombus
2. Non-resolved part of dead tissue
35
3. Vascular necrosis
4. Necrosis of tissue connected with environment
5. Fusion of tissue
43. NECROSIS IS:
1. Program cell death
2. Death of cells in living organism
3. Stopping of functions in living organism
4. Cell injury
5. All true
44. APOPTOSIS IS:
1. Program cell death
2. Death of cells in living organism
3. Stopping of functions in living organism
4. Cell injury
5. All true
45. THE TYPE OF CELL DEATH IS:
1. Fragmentation
2. Hydrolysis
3. Apoptosis
4. Mummification
5. Swelling
46. THE TYPE OF CELL DEATH IS:
1. Fragmentation
2. Hydrolysis
3. Necrosis
4. Mummification
5. Swelling
47. MACROSCOPICAL CHARACTERISTIC OF BRAIN INFARCTION IS:
1. Soft consistence
2. Triangular shape
3. Basis turned to cortex
4. Dark red areole
5. All true
48. TYPE OF GANGRENE:
1. Dry
2. Bedsore
3. Gas
4. True 1&2
5. All true
49. MAIN MORPHOLOGICAL FEATURES OF APOPTOSIS ARE:
1. Condensation of nuclear chromatin
2. Reduction of cell
3. Saving of organelles
4. True 1&2
5. All true
36
50. THE SYNONIM OF WHITE INFARCTION IS:
1. Coagulative
2. Colliquattive
3. Hemorrhagic
4. Ischemic
5. Gangrene
5. INFLAMMATION & IMMUNE SYSTEM PATHOLOGY
1. FLUID THAT COLLECTS DURING ACUTE INFLAMMATION AND THAT HAS A PROTEIN
CONTENT EXCEEDING 3 G/DL AND A SPECIFIC GRAVITY EXCEEDING 1.015 IS REFERRED
TO AS:
1. Edema
2. Effusion
3. Transudate
4. Serum
5. Exudate
2. PHASE OF ALTERATION AT INFLAMMATION IS CHARACTERIZED:
1. Suppuration
2. Chemotaxis
3. Pinocytosis
4. Dystrophy
5. Thixotropy
3. PHASE OF PROLIFERATION AT INFLAMMATION IS CHARACTERIZED BY:
1. Damage of tissue
2. Infringement of blood circulation
3. Duplication of cells
4. Phagocytosis
5. Exudates formation
4. POSITIVE OUTCOME OF INFLAMMATION IS:
1. Incomplete regeneration
2. Elimination of microbes and toxins
3. Sclerosis and strictures formation
4. Reaction of hypersensitivity to toxins and medicines
5. Massive replacement by connective tissue
5. FIBRINOUS INFLAMMATION IS LOCALIZATED ON:
1. Kidney
2. Brain
3. Liver
4. Serous membranes
5. Endocardium
6. CHRONIC ABSCESS DIFFERS FROM ACUTE BY:
1. Shape
2. Size
3. Contents
4. Structure of walls
5. Localization
37
7. NEGATIVE OUTCOMES OF INFLAMMATION ARE ALL, EXCEPT:
1. Incomplete regeneration
2. Sclerosis and stricture formation
3. Elimination of necrozed cells
4. Reaction of hypersensitivity to toxins and medicines
5. Massive replacement by connective tissue
8. CROUPOUS INFLAMMATION DEVELOPS ON THE MEMBRANES COVERED BY:
1. Mesothelium
2. Cylindrical epithelium
3. Skin
4. Squamous keratinizing epithelium
5. Squamous no keratinizing epithelium
9. INFLAMMATION IS:
1. Hyperplasia of cells ultrastructures
2. Restoration of the lost structures
3. Impetuous growth of cellular elements
4. Exudative-proliferative reaction to damage
5. Cellular infiltration in stroma of organs
10. PURULENT INFLAMMATION IN PLEURAL CAVITY IS TERMED AS:
1. Abscess
2. Apostema
3. Furuncle
4. Empyema
5. Carbuncle
11. PHASE OF EXUDATION IS BASED ON:
1. Alteration
2. Proliferation of cells
3. Change of a blood-flow
4. Emigration of cells and phagocytosis
5. Formation of an inflammatory edema
12. AS RESPONSE TO DAMAGE OF TISSUE IN ORGANISM DEVELOPS:
1. Amyloidosis
2. Inflammation
3. Regeneration
4. Granuloma formation
5. Hyperplasia of cells ultrastructures
13. AT THE DIPHTHERITIC INFLAMMATION ON TONSILS CAN BE FOUND:
1. Pus
2. Slime (mucus)
3. Cells elements proliferation
4. Fibrinous pellicle
5. Hematoma
14. STARTING MECHANISM OF INFLAMMATORY REACTION IS:
1. Exudation
2. Mediation
3. Emigration
38
4. Phagocytosis
5. Regeneration
15. LOCALIZATION OF THE CATARRHAL INFLAMMATION:
1. Brain
2. Serous membranes
3. Kidney
4. Mucous membranes
5. Liver
16. CHARACTERISTICS OF LEUCODIAPEDESIS ARE ALL, EXCEPT:
1. Formation of pseudopodiums at leukocytes
2. Intraendotelial migration of leukocytes
3. Emigration with the help of pinocytosis
4. Basal membrane is overcome with the help of tixothropy
5. Phagocytosis
17. TYPE OF INFLAMMATION (DEPENDING ON DURATION) IS:
1. Acute
2. Simple
3. Recurrent
4. Repeated
5. Complicated
18. THE TYPE OF INFLAMMATION WHICH CAN NOT RESULT WITH COMPLETE RESTORATION
OF ORGANS’ STRUCTURE IS:
1. Serous
2. Catarrhal
3. Croupous
4. Diphtheritic
5. Proliferative
19. TYPE OF EXUDATIVE INFLAMMATION (DEPENDING ON EXUDATE) IS:
1. Acute
2. Purulent
3. Chronic
4. Granulematous
5. Interstitial
20. THE TRIVIAL NAME OF HEART FIBRINOUS INFLAMMATION IS:
1. "Bull"
2. "Tiger"
3. "Goose"
4. "Drop-like"
5. "Hairy"
21. TYPICAL FOR CATARRHAL INFLAMMATION IS:
1. Lysis of pellicle
2. Presence of mucus in exudates
3. Proliferation of cell elements
4. Formation of pellicle on mucous membrane
5. Putrefaction
39
22. THE PHASE OF INFLAMMATORY REACTION IS:
1. Pinocytosis
2. Proliferation
3. Thixotropy
4. Phagocytosis
5. Leucodiapedesis
23. OUTCOMES OF ACUTE INFLAMMATION MAY BE ALL, EXCEPT:
1. Complete regeneration
2. Development of malignant tumor
3. Formation of chronic abscess
4. Healing by replacement by connective tissue
5. Progressing in various forms of chronic inflammation
24. INFLAMMATION OF SMALL INTESTIN IS TERMED AS:
1. Intestinitis
2. Colitis
3. Duadenitis
4. Enteritis
5. Proctitis
25. THE TYPE OF PURULENT INFLAMMATION IS:
1. Croupous
2. Phlegmonous
3. Catarrhal
4. Granulomatous
5. Diphtheritic
26. FLUID THAT COLLECTS IN CAVETIES AT ACUTE INFLAMMATION IS:
1. Edema
2. Effusion
3. Transudate
4. Serum
5. Exudate
27. TYPE OF FIBRINOUS INFLAMMATION IS:
1. Interstitial
2. Diphtheric
3. Catarrhal
4. Phlegmonous
5. Granulomatous
28. THE INFLAMMATORY RESPONSE LEADS TO ALL, EXCEPT:
1. Isolation of infective tissue
2. Inactivation of injury factor
3. Neutralization of toxins
4. Removing of necrotic tissue
5. Dysregeneration
29. INFLAMMATORY PHASE OF PROLIFERATION IS CHARACTERIZED BY:
1. Damage of tissue
40
2.
3.
4.
5.
Infringement of blood circulation
Division of cells
Phagocytosis
Exudates formation
30. FIBRINOUS INFLAMMATION CAN LOCALIZE IN ALL, EXCEPT:
1. Kidney
2. Pericardium
3. Lung
4. Serous membranes
5. Mucous membranes
31. THE KINDS OF THE PURULENT INFLAMMATION ARE ALL, EXCEPT:
1. Abscess
2. Furuncule
3. Phlegmonous
4. Catarrhal
5. Empyema
32. TYPE OF INFLAMMATION AT CROUPOUS PNEUMONIA IS:
1. Purulent
2. Fibrinous
3. Serous
4. Catarrhal
5. Granulomatous
33. THE ADHESION OF LEUCOCYTES TO VESSEL WALL BEFORE EMIGRATION IS:
1. Margination
2. Diapedesis
3. Clotting
4. Congestion
5. Proliferation
34. OF FIBRINOUS PERICARDITIS IS CHARACTERIZED BY ALL, EXCEPT:
1. Develops at uremia
2. Diphteric type of inflammation
3. Figuratively refers to «hairy heart»
4. Accompanied by auscultative symptoms
5. Meet at myocardial infarction
35. MORPHOLOGICAL MANIFESTATION OF ALTERATION:
1. Necrosis
2. Proliferation
3. Atrophy
4. Lipofuscinosis
5. Apoptosis
36. THE MOST TYPICAL OUTCOME OF PRODUCTIVE INFLAMMATION IS:
1. Sclerosis
2. Fusion
3. Petrification
4. Ulceration
41
5. Methaplasia
37. PURULENT INFLAMMATION IS CHARACTERIZED BY:
1. Neutrophils infiltration with tissue lysis
2. Fibrin deposition
3. Mucus production
4. Lymphocyte infiltration
5. Erythrocyte infiltration
38. TYPE OF INFLAMMATION IS FOUND IN LOBAR PNEUMONIA:
1. Purulent
2. Fibrinous
3. Serous
4. Catarrhal
5. Granulomatous
39. KIND OF PRODUCTIVE INFLAMMATION IS:
1. Serous
2.Catarrhal
3.Croupous
4.Granulomatous
5. Diphtheric
40. A LARGE AGGREGATE OF EPITHELIOID CELLS IS SEEN IN:
1. Granulation tissue
2. Pyogenic granuloma
3. Granulosa cell tumor
4. Granulocytosis
5. Granuloma
41. GRANULOMA IS:
1. Focal accumulation of leukocytes
2. Focal accumulation of slime
3. Focal accumulation of fibrin
4. Focal productive inflammatory reaction
5. Focal hemorrhagic infiltration
42. THE GRANULOMATOUS INFILTRATE IN TERTIARY SYPHILIS IS COMPOSED
PREDOMINANTLY OF:
1. Neutrophils
2. Monocytes/macrophages
3. Plasma cells
4. Eosinophiles
5. Lymphocytes
43. MILIARY LUNG TUBERCULOSIS IS CHARACTERIZED BY INFLAMMATION:
1. Granulomatous
2. Serous
3. Fibrinous
4. Suppurative
5. Hemorrhagic
42
44. TYPE OF NECROSIS CAN BE FOUND IN TUBERCULAR GRANULOMA IS:
1. Coagulative
2. Liquefactive
3. Caseous
4. Enzymatic fat
5. Fibrinoid
45. KIND OF FIBRINOUS INFLAMMATION DEVELOPED ON MUCOUS MEMBRANE OF
ORAL CAVITY IS:
1. Phlegmonous
2. Interstitial
3. Hemorrhagic
4. Putrefactive
5. Diphteric
46. ALL OF THE FOLLOWING CELLS ARE INVOLVED IN IMMUNE RESPONSE, EXCEPT:
1. Erythrocytes
2. Macrophages
3. Natural killer cells
4. Т lymphocytes
5. В lymphocytes
47. LARGE AGGREGATE OF EPITHELIOID CELLS IN MICROSCOPIC SECTION OF AN OVARY
CHARACTERISTIC FOR:
1. Granulation tissue
2. Pyogenic granuloma
3. Granulosa cell tumor
4. Granulocytosis
5. Granulomatous inflammation
48. MILIARY LUNG TUBERCULOSIS IS CHARACTERIZED BY TYPE OF INFLAMMATORY
REACTION:
1. Granulomatous
2. Serous
3. Fibrinous
4. Suppurative
5. Hemorrhagic
49.
1.
2.
3.
4.
5.
THE MOST IMPORTANT ROLE IN CHRONIC TUBERCULOUS INFLAMMATION PLAY:
Macrophages
Leukocytes
Eosinophiles
Erythrocytes
Plasma cells
50. TYPICAL SYPHILITIC GRANULOMA IS CHARACTERIZED BY ALL OF THE
FOLLOWING FEATURES, EXCEPT:
1. Area of central necrosis
2. Plasma cell infiltrate
3. Lymphocyte infiltrate
4. Productive vasculitis
5. Platelet infiltrate
43
51. A MICROSCOPIC AGGREGATION OF THE EPITHELIOID CELLS USUALLY
SURROUNDED BY A COLLAR OF LYMPHOCYTES IS REFERRED TO AS:
1. Papilloma
2. Condyloma
3. Melanoma
4. Lipoma
5. Granuloma
52. GRANULOMATOUS INFLAMMATION DEVELOPS IN ALL OF THE FOLLOWING DISEASES,
EXCEPT:
1. Tuberculosis
2. Leprosy
3. Syphilis
4. Cat-scratch disease
5. Bronchial asthma
53. TYPICAL TUBERCULAR GRANULOMA IS CHARACTERIZED BY ALL OF THE FOLLOWING
FEATURES, EXCEPT:
1. Leucocytes
2. Central caseous necrosis
3. Epithelioid cells
4. Langhans' giant cells
5. Lymphocytes
54. AS «LEPRA CELLS» IN LEPROMATOUS LEPROSY ARE KNOWN THE FOLLOWING
CELLS:
1. Foam cells filled with lipid droplets
2. Macrophages filled with masses of acid-fast bacilli
3. Epitheliod cells
4. Langhans' giant cells
5. Schwann cells
55. PATHOGENESIS OF “HASHIMOTO’S THYROIDITIS” IS ASSOCIATED WITH WHICH OF
THE FOLLOWING FACTORS:
1. Alloantibody
2. Alloantigens
3. Autoantigens
4. Heteroantibody
5. Heteroantigens
56. MACROPHAGES IN GRANULOMATOUS INFLAMMATION MAY TRANSFORM INTO
WHICH OF THE FOLLOWING CELLS:
1. Monocytes
2. Epithelial cells
3. Epithelioid cells
4. Plasma cells
5. Lymphocytes
57. HYDATID CYST OF THE LIVER IS AN EXAMPLE OF WHICH OF THE FOLLOWING TYPES
OF INFLAMMATION:
1. Purulent
44
2. Interstitial
3. Serous
4. Catarrhal
5. Productive
58. THE MOST COMMON CAUSE OF THE HIVES (ACUTE ALLERGIC RHINITHIS) IS WHICH
OF THE FOLLOWING:
1. Local anaphylaxis
2. Immune complex injury
3. Immunologic tolerance
4. Genetic deficiency of the monocyte/macrophage system
5. Genetic deficiency of the complement system
59. DISORDERS OF THE IMMUNE SYSTEM INCLUDE ALL OF THE FOLLOWING, EXCEPT:
1.Hyalinosis
2.Hypersensitivity reactions
3.Autoimmune diseases
4.Immunologic deficiency syndromes
5.Accidental involution of thymus gland
60. CHARACTERISTICS OR PHENOMENA ASSOCIATED WITH ACUTE REJECTION AFTER
RENAL TRANSPLANTATION INCLUDE ALL OF THE FOLLOWING, EXCEPT:
1. Occurs days to months after transplantation
2. Antibody-mediated or cell- mediated
3. Localized Arthus reaction
4. Mononuclear infiltrates
5. Arteritis with thrombosis
61. ALL OF THE FOLLOWING DISEASES RESULT FROM TYPE Ш HYPERSENSITIVITY
(IMMUNE COMPLEX DISORDERS), EXCEPT:
1. Glomerulonephritis
2. Farmer's lung
3. Myocardial infarction
4. Hemolytic anemia
5. Systemic lupus erythematosus
62. TYPE I HYPERSENSITIVITY (ANAPHYLACTIC TYPE) IS CHARACTERIZED BY ALL OF
THE FOLLOWING FEATURES, EXCEPT:
1. Occurs in humans previously sensitized to the antigen
2. Develops rapidly (within minutes)
3. Mediates by Ig E antibodies in humans
4. Develops slowly (within days)
5. Induced by mast cell or basophil degranulation
63. CELLS WHICH COMPOSE THE GRANULOMA IN TYPE IV HYPERSENSITIVITY
REACTION ARE ALL OF THE FOLLOWING, EXCEPT:
1. Lymphocytes
2. Erythrocytes
3. Macrophages
4. Epithelioid cells
5. Giant cells
45
64. DISORDERS OF THE IMMUNE SYSTEM INCLUDE ALL OF THE FOLLOWING:
1. Hypersensitivity reactions
2. Autoimmune diseases
3. Hyalinosis
4. True 1&2
5. All true
65. IMMUMOPATHOLOGICAL PROCESS IS:
1. Hyperplasia
2. Hyperkeratosis
3. Hypersensitivity of delayed type
4. Hypertrophy
5. Hypercoagulation
66. THE MOST TYPICAL PATHOLOGY OF AIDS PULMONARY SYNDROME IS:
1. Cachexia
2. Hepatitis
3. Lymphoadenopathy
4. Pneumocystic pneumonia
5. Enterocolitis
67. TYPICAL OPPORTUNISTIC TUMOR AT CLINICAL PICTURE OF THE HIV- INFECTION
IS:
1. Sinovial ssarcoma
2. Osteosarcoma
3. Juing’s sarcoma
4. Caposhy’s sarcoma
5. Leiomyosarcoma
68. CHANGES OF IMMUNE SYSTEM ORGANS AT AIDS ARE:
1. Hyperplasia
2. Necrosis
3. Atrophy
4. Sclerosis
5. Plethora
69. THE SUBTYPE OF PRODUCTIVE INFLAMMATION IS:
1. Interstitial
2. Serous
3. Fibrinouse
4. Purulent
4. Proliferative
70. THE REASON OF CHRONIC INFLAMMATION IS:
1. Acute infection
2. Facultative infection
3. Persisted infection
4. Virus
5. Exogenic toxins
71. CHRONIC INFLAMMATION IS CHARACTERIZED BY ALL, EXCEPT:
1. Deposition of amyloid
46
2. Mononuclear infiltration
3. Fibrosis of damage tissue
4. Polyps formation
5. Persisted destruction of connective tissue
72. THE CHARACTERISTIC OUTCOME OF INTERSTITIAL INFLAMMATION IS:
1. Edema
2. Sclerosis
3. Necrosis
4. Petrification
5. Fusion by pus
73. THE OUTCOMES OF INFLAMMATION AROUND PARASITES ARE ALL, EXCEPT:
1. Petrification
2. Encapsulation
3. Putrefaction
4. Necrosis of tissue
5. Secondary amyloidosis
74. TISSUE REACTION AT GRANULEMATOUS INFLAMMATION IS:
1. Alterative
2. Exudative
3. Proliferative
4. Necrotic
5. Dystrophic
75. THE CELLS PARTICIPATING IN PHAGOCYTOSIS ARE ALL, EXCEPT:
1. Macrophages
2. Erythrocytes
3. Lymphocytes
4. Epithelioid cells
5. Plasmacytes
76. CLINICAL CURRENT OF DISEASES BASED ON PROLIPHERATIVE INFLAMMATION IS:
1. Acute
2. Fulminant
3. Subacute
4. Chronic
5. Acutest
77. THE TYPE OF GRANULOMAS DEPENDING ON CELLULAR STRUCTURE IS:
1. Macrophage cellular
2. Plasma cellular
3. Lymphocytic
4. Erythrocytic
5. Leucocytic
78. THE TYPE OF GRANULOMAS DEPENDING ON CELLULAR STRUCTURE IS:
1. Lymphocytic
2. Plasma cellular
3. Epithelioid cellular
4. Erythrocytic
47
5. Leucocytic
79. NON INFECTIOUS GRANULOMA IS MAET AT:
1. Typhoid fiver
2. Syphilis
3. Tuberculosis
4. Silicosis
5. Lepra
80. INFECTIOUS GRANULOMA IS MAET AT:
1. Anthracosis
2. Disease of cat’s scratch
3. Silicosis
4. Around of surgical sutures
5. Foreign body
6. ADAPTATION
1. REVERSIBLE DISORDER IN MATURATION OF CELLS WITH VARIABILITY IN SIZE,
SHAPE AND POLARITY:
1. Metaplasia
2. Dysplasia
3. Anaplasia
4. Hyperplasia
5. Desmoplasia
2.
REGENERATION IS:
1. Transformation of one kind of tissue into another
2. Restoration of tissue instead of lost
3. Increasing of organ in mass
4. Reaction, directed on restoration of structure and function
5. Process, directed on preservation of kind
3. CAUSES OF PATHOLOGIC ATROPHY ARE ALL, EXCEPT:
1. Loss of endocrine stimulation
2. Intracellular fat accumulation
3. Pressure
4. Inadequate nutrition
5. Denervation
4. HYPERTROPHY IS:
1. Restoration of tissue instead of lost
2. Increase in volume of cells, tissue, organs
3. Reduction of cells, tissue, organ in volume
4. Transition of one kind of tissue into another
5. Replacement by connective tissue
5. COMPENSATARY ENLARGEMENT OF HEART IS TERMED AS:
1. Dilative
2. Myogenic
3. Excentric
48
4. Concentric
2. Decompensative
6. DYSPLASIA CAN RESULT BY:
1. Aplasia
2. Hypoplasia
3. Hyperpigmentation
4. Calcification
5. Neoplasia
7. HYPERPLASIA IS CHARACTERIZED BY:
1. Increase in the size of cells
2. Increase in the number of cells
3. Increase in the number of nuclei
4. Shrinkage of cells
5. Atypia of cells
8. HYPOPLASIA IS CHARACTERIZED BY ALL, EXCEPT:
1. Incomplete development of an organ
2. Decreased number of cells
3. Increased number of cells
4. Underdevelopment of an organ
5. Decreased function of an organ
9. PROLIFERATION OF ENDOMETRIUM DURING PREGNANCY IS WHICH OF VARIANTS
IN ADAPTATION:
1. Compensatory hyperplasia
2. Pathologic hyperplasia
3. Hormonal hyperplasia
4. Compensatory hypertrophy
5. Hormonal hypertrophy
10. TYPE OF METAPLASIA THAT OCCURS IN RESPIRATORY TRACT OF A HABITUAL
CIGARETTE SMOKER IS:
1. Squamous to columnar epithelial metaplasia
2. Metaplasia to undifferentiated mesenchymal cells
3. Squamous to cuboidal epithelial metaplasia
4. Columnar to squamous epithelial metaplasia
5. Intestinal metaplasia
11. COMPENSATION IS:
1. Transition of one kind of tissue into another
2. Restoration of tissue instead of lost
3. Process, directed on preservation of kind in changed conditions
4. Proliferation of cells
5. Reaction, directed on restoration of structure and function
12. HYPERTROPHY AS A PROCESS IS CHARACTERIZED BY:
1. Increase of cell and organ in size
2. Shrinkage of cell and organ
3. Increase in number of cells
4. Abnormal organization of cells
49
5. Variation of cells in size and shape
13. SIMPLE ENDOMETRIAL HYPERPLASIA IS CHARACTERIZED BY ALL, EXCEPT:
1. Increase in the number and size of endometrial glands
2. Atypia of gland cells
3. Glands' crowding
4. Increase in gland-to-stroma ratio
5. Dilated endometrial glands
14. IN THE CYTOPLASM OF HEART MUSCLE CELLS DUE TO SENILE ATROPH Y CAN BE
FOUND PIGMENT:
1. Lipofuscin
2. Melanin
3. Hemosiderin
4. Bilirubin
5. Ferritin
15. ORGANIZATION IS:
1. Transition of one kind of tissue into another
2. Restoration of tissue instead of lost
3. Replacement by connective tissue
4. Increasing of organ in mass
5. Reduction of cells, tissue, organ in volume
16. ALL ARE EXAMPLES OF ADAPTIVE RESPONSE, EXCEPT:
1. Hypertrophy of breast during lactation
2. Hypertrophy of skeletal muscles cells in a body-builder
3. Hypertrophy of uterus during pregnancy
4. Hypertrophy of skeletal muscle cells of the patient with immobilized of fracture
5. Hypertrophy of the urinary bladder due to hyperplasia of prostate gland
17. HYPOPLASIA IS:
1. Restoration of tissue instead of lost
2. Increase in volume of cells, tissue, organs .
3. Reduction of cells, tissues, organs in volume
4. Underdevelopment of organ
5. Replacement by connective tissue
18. TYPE OF CONGENITAL ATROPHY IS:
1. Aplasia
2. Agenesia
3. Hypoplasia
4. Hypogenesia
5. Cirrhosis
19. SYSTEMIC FACTORS THAT INFLUENCE WOUND HEALING ARE ALL OF THE
FOLLOWING, EXCEPT:
1. Nutrition
2. Metabolic status
3. Blood group
4. Circulatory status
5. Hormones (glucocorticoids)
50
20. LOCAL FACTORS THAT INFLUENCE WOUND HEALING ARE ALL OF THE
FOLLOWING, EXCEPT:
1. Wound infection
2. Abnormal blood supply
3. Foreign bodies
4. Hormones (glucocorticoids)
5. Size, localization and type of the wound
21. TYPE OF WOUND HEALING WHICH TERMED AS «KELOID» IS:
1. Atrophic scar
2. Scar with dysplasia
3. Abnormal organization of cells
4. Hypotrophic scar
5. Hypertrophic scar
22. ALL OF THE FOLLOWING ARE EXAMPLES OF ORGANIZATION, EXCEPT:
1. Healing of productive inflammation by scar formation
2. Replacement of necrosis focus by connective tissue
3. Replacement of thrombus by connective tissue
4. Encapsulation of caseous necrosis
5. Deposits of calcium salts in the collagen and caseous material
23. HYDRONEPHROSIS IS CHARACTERIZED BY ALL OF THE FOLLOWING, EXCEPT:
1. Thickening of the renal parenchyma
2. Enlargement of the kidney
3. Dilatation of the renal pelvis
4. Dilatation of the renal calyces
5. Progressive atrophy of the kidney
24.
VOLUME-OVERLOADED
(ECCENTRIC)
CARDIAC
CHARACTERIZED BY ALL OF THE FOLLOWING, EXCEPT:
1. Papillary muscle hypertrophy
2. Dilated left cavity diameter
3. Trabecular muscle hypertrophy
4. Diminished left wall thickness
5. Reduced left cavity diameter
HYPERTROPHY
IS
25. METAPLASIA IS CHARACTERIZED BY:
1. Reversible increase in the size of cells
2. Irreversible changes in which one adult cell type is replaced by another adult cell type
3. Reversible changes in which one adult cell type is replaced by another adult cell type
4. Reversible abnormal organization of atypical cells
5. Irreversible abnormal organization of atypical cells
7. NEOPLASIA
1. THE TERM OF A BENIGN MESENCHYMAL TUMOR IS CONSTRUCTED BY COMBINING
THE WORD DESIGNATING THE TUMOR CELL ORIGIN PLUS ENDING:
1. -sarcoma
2. -carcinoma
51
3. -oma
4. -itis
5. -osis (-asis)
2. BENIGN TUMOR ARISING FROM FIBROBLASTIC CELLS IS CALLED:
1. Chondroma
2. Adenoma
3. Osteoma
4. Fibroma
5. Papilloma
3.
HOW DO YOU DIFFERENTIATE CANCER IN SITU FROM INVASIVE CANCER
1. Penetration of Basement membrane
2. Number of mitotic cells
3. Metastasis
4. Nuclear plemorphism
5. All the above
4. MALIGNANT TUMORS ARISING FROM THE MESENCHIMAL TISSUE ARE:
1. Sarcomas
2. Adenocarcinomas
3. Papillomas
4. Cystadenomas
5. Polyps
5. PAPILLOMA OF SKIN IS:
1. A senile wart
2. Epithelial benign tumor
3. Epithelial malignant tumor
4. Vascular benign tumor
5. Inflammatory growth of skin
6. CANCER IS MALIGNANT TUMOUR DEVELOPING FROM:
1. Mesenchimal tissue
2. Muscular tissue
3. Epithelial tissue
4. Nervous tissue
5. Vascular tissue
7. HISTOLOGICAL ATTRIBUTE OF CANCER IN SITU (CARCINOMA IN SITU) IS:
1. Invasive growth
2. Metastasises
3. Intraepithelial malignant growth
4. Haemorrhages in tumor tissue
5. Focus of necrosis in tumor
8. FOLLICULAR CANCER OF THYROID GLAND DEVELOPS FROM:
1. A-cells
2. B-cells
3. C-cells
4. Mast cells
5. Reticular cells
52
9. SARCOMA IS:
1. Tumor-like formation
2. Benign tumor from mesenchimal tissue
3. Malignant tumor from mesenchimal tissue
4. Focal hyperplasia of epithelium
5. Malignant tumor from epithelial tissue
10. THE FIRST HEMATOGENIOUS METASTASES OF FEMUR SARCOMA APPEAR IN:
1. Liver
2. Kidneys
3. Spleen
4. Lungs
5. Organs of pelvis
11. THE EARLIEST KIND OF CANCER METASTATIC SPREADING IS:
1. Hematogenic
2. Lymphogenic
3. Perineural
4. Periductal
5. Mixed
12. THE CRITERIA BY WHICH BENIGN TUMORS CAN BE DIFFERENTIATED FROM THE
MALIGNANT ONES ARE ALL OF THE FOLLOWING, EXCEPT:
1. Maturity
2. Rate and character of the growth
3. Localization
4. Anaplasia
5. Metastases
13. MULTIPLE MYELOMA IS CHARACTERIZED BY THE SECONDARY ACCUMULATION
IN TISSUES OF:
1. Hyaline
2. Lipofuscin
3. Amyloid
4. Hemosiderin
5. Melanin
14. IRON-DEFICIENCY ANEMIA IS COMMONLY ASSOCIATED WITH ALL OF THE
FOLLOWING FACTORS, EXCEPT:
1. Colon cancer
2. Polycythemia
3. Gastrectomy
4. Normal menses
5. Pregnancy
15. DIAGNOSTIC CELLS FOR HODGKIN'S DISEASE ARE:
1. Eosinophils
2. Epithelioid cells
3. Reed - Berezovsky-Shternberg’s cells
4. Reticular cells
5. Virchov’s "spheres"
53
16. FILADELFIAL CHROMOSOME IS CHARACTERISTIC FOR:
1. Myeloma disease
2. Lymphogranulomatosis
3. Berkytt’s lymphoma
4. Myeloleucosis
5. Lympholeucosis
17. LEUCEMIC INFILTRATION IS:
1. The center of inflammation
2. The center of leucemic cells growth
3. The center of extramedullar hematopoesis
4. The center of inflammatory proliferation
5. The center of leucocitic infiltration
18. PROGENITOR CELL OF HEMOPOETIC TISSUE IS:
1. Reticular cell
2. Stem cell
3. Lymphoblast
4. Myeloblast
5. Erythroblast
19. HISTOLOGICAL SUBTYPE OF HODGKIN'S DISEASE IS:
1.Nodular sclerosis
2. Nodular necrosis
3.Leucocyte predominance
4.Nodular amyloidosis
5. Leucocytes depletion
20. HISTOLOGICAL SUBTYPE OF HODGKIN'S DISEASE IS:
1.Nodular necrosis
2. Leucocyte predominance
3.Lymphocyte predominance
4.Nodular amyloidosis
5. Aleucemic
21. PRIMARY TUMOR DAMAGE OF BONE MARROW IS NAMED AS:
1. Leucemic reaction
2. Leucemoid reaction
3. Lymphomatosis
4. Leucemia
5. Metastatic
22. PATHOHISTOLOGICAL TYPE OF LYMPHOGRANULEMATOSIS IS:
1. With prevalence of leucocytes
2. With leucopenia
3. Mixed cellular
4. Round cellular
5. Necrotic
23. REASON OF HEMOLYTIC ANEMIA (INTRAVASCULAR HEMOLYSIS):
1. Burns disease
54
2.
3.
4.
5.
Myocarditis
Insult
Trauma
Lung diseases
24. TYPES OF LEUKEMIA DEPENDING
DIFFERENTIATION OF TUMOR CELLS ARE:
1. Acute, chronic
2. Acute, subacute, chronic
3. Acute, relapsing
4. Acute, recurrent
ON
CURRENT
AND
DEGREE
OF
25. ONE OF TYPES OF LYMPHOMAS NAMED AS:
1. Franclin’s disease
2. Valdenstrem’s disease
3. Mieloma disease
4. Hodgkin’s disease
5. Addisson’ disease
26. ANEMIA IS CHARACTERIZED BY:
1. Local ischemia
2. Type of systemic hemoblastoses
3. General ischemia
4. Type of regional hemoblastoses
5. General hyperemia
27. SIGNIFICANT ENLARGEMENT OF ORGANS AT LEUCEMIAS DETERMINATES BY:
1. Hyperemia
2. Sclerosis
3. Necrosis
4. Leucemic infiltration
5. Inflammation
28. “PORPHYRY” SPLEEN IS MAT AT:
1. Anemia
2. Sepsis
3. Hodgkin’s disease
4. Reticulosarcoma
5. Hypertension
29. BONE MARROW AT ACUTE MYELOBLASTIC LEUKEMIA IS CHARACTERIZED BY:
1. Greenish-grey color
2. Like “current-jelly”
3. Bright-red
4. Focuses of necrosis
5. Brown
30.
THE
MAIN
DIFFERENCE
HYPOREGENERATIVE IS:
1. Different amount of reticulocytes
2. Atrophy of bone marrow
3. Blast proliferation in bone marrow
BETWEEN
HYPOPLASTIC
ANEMIA
FROM
55
4.
5.
Megacariocytic dysplasia
Hemosiderosis
8. CARDIO-VASCULAR DISEASES
1. GENERAL PATHOLOGICAL PROCESS IN MYOCARDIOCYTES AT DECOMPENSATE
HEART DEFECTS IS:
1. Atrophy
2. Fatty dystrophy
3. Calcification
4. Hemosiderosis
5. Necrosis
2. NONBACTERIAL ACUTE WARTY ENDOCARDITIS IS CHARACTERIZED BY ALL OF THE
FOLLOWING FEATURES, EXCEPT:
1. Mitral and/or aortic valve involvement
2. Tricuspid valve involvement
3. Small (1 to 5 mm), sterile verrucae
4. Verrucae along the line of valve closure
5. Disorganization of connective tissue
3. COMPLICATION OF ACUTE WARTY ENDOCARDITIS OF MITRAL VALVE CAN BE:
1. Infarction of lung
2. Thromboembolism of lung arteries
3. Abscess of brain
4. Infarction of kidney
5. Embolic nephritis
4. CHRONIC RHEUMATIC HEART DISEASE IS CHARACTERIZED BY ALL CHANGES OF
MITRAL VALVE, EXCEPT:
1. Thickened and deformed valve leaflets
2. Valvular calcification
3. Thickened and shortened chordae tendineae
4. «Fish mouth» appearance of the mitral valve
5. Abscess formation
5. MATERIAL WHICH DEPOSITED
HYPERTENSION IS:
1. Amyloid
2. Glycogen
3. Cholesterol or cholesterolesters
4. Lipoprotein
5. Hyaline
IN
ARTERIOLAR
WALLS
IN
SYSTEMIC
6. CHANGES IN KIDNEY DEVELOPING AT BENIGN FORM OF HYPERTONIC DISEASE
HAVE THE NAME:
1. Secondary - wrinkled kidney
2. Primarily - wrinkled kidney
3. Far’s nephrosclerosis
4. Kimmelstyl-Wilson's syndrome
5. Polycistosis
56
7. RISK FACTORS FOR ENDOTHELIAL INJURY IN ATHEROSCLEROSIS MAY BE ALL,
EXCEPT:
1. Hyperlipidemia
2. Hypertension
3. Smoking
4. Genetic defects
5. Immune reactions
8. THE COMPLICATION OF ATHEROMATOUS PLAQUE FORMATION IS:
1. Thrombus formation
2. Stone formation
3. Plaque malformation
4. Inflammation
5. Metastatic calcification
9. BROWN ATROPHY OF THE MYOCARDIUM CHARACTERIZED BY ALL, EXCEPT:
1. Decreased left ventricular cavity size
2. Twisting of epicardial coronary artery
3. Decreased subepicardial fat
4. Flabby brown-colored myocardium
5. Increased number of inflammatory cells in the myocardium
10. LEFT-SIDED HEART FAILURE IS MOST OFTEN CAUSED BY:
1. Ischemic heart disease
2. Brown atrophy of the myocardium
3. Pulmonary edema
4. Hepatitis
5. Anasarca
11. TERM OF MYOCARDIAL INFARCTION FULL ORGANIZATION PUT BY THE CART
EXPERTS IS:
1. 2 weeks
2. 1 month
3. 1,5 months
4. 2 months
5. 3 months
12. THE MORPHOLOGICAL AND CLINICAL EFFECTS OF PURE (ISOLATED) RIGHT-SIDED
HEART FAILURE ARE ALL, EXCEPT:
1. Cerebral hematoma
2. Congestive hepatomegaly
3. Ascites
4. Pleural and pericardial effusions
5. Anasarca
13. ACUTE RHEUMATIC CARDITIS IS CHARACTERIZED BY:
1. Brown atrophy of heart
2. Aschoff bodies in the myocardium
3. Goose liver
4. Cardiosclerosis
5. Tiger heart
57
14. ETIOLOGY AND PATHOGENESIS OF RHEUMATIC FEVER AND RHEUMATIC HEART
DISEASE ARE CHARACTERIZED BY ALL, EXCEPT:
1. Initial attack of disease some weeks after streptococcal infection
2. Elevated serum titers of antibodies to streptolysin and hyaluronidase
3. Sterile tissue lesions
4. Recurrent acute illness following the streptococcal infection
5. Decreased serum protein levels
15. HEART LESIONS IN ACUTE RHEUMATIC FEVER ARE CALLED:
1. Tuberculoma
2. Aschoff bodies
3. Foreign bodies
4. Gumma
5. Mitral stenosis
16. MICROSCOPICALLY, CHRONIC RHEUMATIC HEART DISEASE IS CHARACTERIZED
BY ALL, EXCEPT:
1. Diffuse fibrosis of leaflets
2. Neovascularization of leaflets
3. Acute purulent inflammation
4. Destruction of original leaflet architecture
5. Aschoff bodies in perivascular connective tissue
17. POSSIBLE OUTCOME OF RHEUMATIC MYOCARDITIS IS:
1. Heart defect
2. Cardiosclerosis
3. Brown atrophy of heart
4. Obliteration of pericardium cavity
5. Adiposity of heart
18. THE "FIGURATIVE" NAME OF HEART AT RHEUMATIC PERICARDITIS IS:
1. Pulmonary heart
2. "Bull" heart
3. "Tiger" heart
4. "Hairy" heart
5. Stone heart
19. ENDOCARDITIS AT RHEUMATISM OCCURS AS:
1. Polipous-ulcer
2. Diffuse [Talalaev's] valvulitis
3. Acute ulcer
4. Calcification
5. Dystrophic
20. CHARACTERISTIC MORPHOLOGICAL CHANGE AT NODULAR PERIARTERITIS IS:
1. Arteriolosclerosis
2. Atherosclerosis
3. Fibrinoid necrosis
4. Destructive – proliferative vasculitis
5. Amyloidosis
58
21. AT ATHEROSCLEROSIS PREDOMINANTLY SUFFERED:
1. Veins
2. Arteries
3. Arteriols
4. Large and middle arteries
5. All true
22. THE DIAGNOSIS OF ESSENTIAL HYPERTENSION IS GIVEN ONLY AT:
1. Presence of risk factors
2. Presence of arteriolosclerotic nephrosirrhosis
3. Absence of organic diseases, explained hypertension
4. Presence of true features of connection with psychoemoutional stress
5. Coronary insufficiency development
23. DECOMPENSATION OF HYPERTROPHIED HEART IS APPEARED AS:
1. Myogenic dilation of cavities
2. Tonogenic dilation of cavities
3. Rheumatic myocarditis
4. Fibrinouse pericarditis
5. Acute warty endocarditis
24. THE ESSENTIAL HYPERTENSION IS CHARACTERIZED AS:
1. Hypertension – primary appearance of disease
2. Hypertension – complication of other disease
3. Hypertension – secondary appearency of other disease
4. Hypertension on background of atherosclerosis
5. Hypertension on background of heart defect
25. COMPLICATION OF BRAIN INFARCTION CAN BE:
1. Pneumonia
2. Edema and dislocation of brain
3. Pulmonary thromboembolism
4. True 1 & 2
5. All true
26. THE CHRONIC ISCHEMIA OF RENAL TISSUE DUE TO ATHEROSCLEROSIS IS LEADING
TO:
1. Atrophy of parenchyma
2. Sclerosis of stroma
3. Infarction
4. Gangrene
5. True 1 & 2
27. CHANGES IN ARTERIOLS DUE TO ESSENTIAL HYPERTENSION ARE:
1. amyloidosis
2. liposclerosis, calcynosis
3. atheromatosis, ulceration
4. atherosclerosis, elastofibrosis
5. infiltration by plasma, hyalinosis
28. THE MOST OFTEN OUTCOME OF ISCHEMIC INFARCTION IN BRAIN IS:
1. Complete regeneration
59
2. Scarring
3. Cyst formation
4. Hydrocephalus
5. Purulent leptomeningitis
29. ATHEROSCLEROSIS OF RENAL ARTERIES CAN FOLLOW WITH:
1. Infarctions
2. Amyloidosis
3. Embolic purulent nephritis
4. Hydronephrosis
5. Calcinosis
30. MORPHOLOGICAL CHANGES OF ARTERIOLS AT HYPERTENSION STROKE ARE:
1. Liposclerosis
2. Elastofibrosis
3. Plasmatic infiltration, fibrinoid necrosis
4. Hyalinosis, sclerosis
5. Atherosclerosis, calcinosis
31. THE IMMEDIATE CAUSE OF ATHEROSCLEROTIC LOW EXTREMITY GANGRENE IS:
1. Limphostasis
2. Thrombosis of arteries
3. Thrombosis of deep veins
4. Rupture of varecious-expended veins
5. Endarteriitis
32. IN ABDOMINAL PART OF AORTA AT ATHEROSCLEROSIS CAN BE SEEN:
1. Fatty stains and strips, fibrous plaques
2. Complicated damages (ulcerations, thrombosis), calcinosis
3. Amyloidosis
4. True 1 & 2
5. All true
33. IN BRAIN TISSUE DUE TO HYPERTENSION STROKE CAN BE SEEN:
1. Cyst
2. Glial scar
3. Atrophy of cortex
4. Diapedetic hemorrhages
5. All true
34. CLINICAL-MORPHOLOGICAL TYPES OF ESSENTIAL HYPERTENSION BY CURRENT:
1. Cardiac, brain
2. Mesenterial, pulmonary
3. Hepatic, aortal
4. Low extremity
5. Benign, malignant
35. CEREBRAL FORM OF ESSENTIAL HYPERTENSION IS CHARACTERIZED BY:
1. Atrophy of cortex
2. Hydrocephalus
3. Encephalitis
4. Brain hemorrhage
60
5. Meningitis
36. ATHEROSCLEROSIS IS CHARACTERIZED BY:
1. Progressive desorganisation of connective tissue
2. Hyalinosis of vessels
3. Damage of microcirculative blood supply
4. Adge-prowided sclerosis of vessels walls
5. Damage of elastic and muscle-elastic type arteries as a result of fat and protein metabolism
infringements
37.
RENAL FORM OF ESSENTIAL
CHARACTERIZED BY:
1. Primary reduced kidney
2. Amyloido-reduced kidney
3. Secondary reduced kidney
4. Hydronephrosis
5. Glomerulonephritis
HYPERTENSION
MORPHOLOGICALLY
38.
1.
2.
3.
4.
5.
DURATION OF PRENECROTIC STAGE OF MYOCARDIAL INFARCTION IS:
Till two hours
Till 1 month
Till 10 days
Till 2 days
Till 18 hours
IS
39. ONE OF THE STAGES OF MYOCARDIAL INFARCTION DEVELOPMENT IS:
1. Dyscirculational
2. Transitional
3. Dystrophyc
4. Necrotic
5. Reconvalescentional
40. TRANSMURAL MYOCARDIAL INFARCTION MAY FOLLOW WITH:
1. Fibrinous pericarditis
2. Acute aneurysm
3. Thrombosis in left ventricle
4. All true
5. All wrong
41. THE MOST FREQUENT REASON OF SUBARACHNOID HEMORRHAGE IS:
1. Rupture of brain artery aneurism
2. Rupture of atherosclerotic plaque
3. Closed cranio-cerebral trauma
4. Blood disease
5. Vasculitis
42. THE RISK FACTORS OF IHD DEVELOPMENT ARE:
1. Arterial hypertension and hyperlipidemia
2. Smoking and atherosclerosis
3. Diabetes
4. Adiposity
5. All true
61
43. CHRONIC ISCHEMIC HEART DISEASE RESULTS BY:
1. Cardiosclerosis
2. Myocardial infarction
3. Tamponade of heart
4. True 1& 2
5. All true
44. THE MAIN REASON OF DEATH AT SUBARACHNOID HEMORRHAGES IS:
1. Dislocation of brain
2. Destruction of vegetative centers of regulation
3. Destruction of sensomotoric centers
4. Hypothalamic-pituitary disorders
5. Anemia and shock
45. EXCEPT HEART DAMAGE RHEUMATISM IS CHARACTERIZED BY:
1. Damage of big joints
2. Caseouse erythema
3. Pancreatitis
4. Pyelonephritis
5. Gettington’s choreya
46. THE MOST OFTEN CONGENITAL HEART DEFECT IS:
1. The common arterial trunk
2. Three-chambered heart
3. Coarctation of aorta
4. Luthambasher’s disease
5. Phallot’s tetrad
47. RHEUMATISM MOST COMMONLY AFFECTS:
1. Aortal valve
2. Mitral valve
3. Tricuspid valve
4. Pulmonary artery valve
48. ENDOCARDITIS AT SYSTEMIC LUPUS ERYTHEMATOSUS IS:
1. Relapsing warty endocarditis
2. Diffuse
3. Fibroplastic
4. Abacterial warty
5. Polypous-ulceral
49. AORTAL VALVE STENOSIS FOLLOWING WITH:
1. Small circle bloodcerculation hypertension
2. Hypertrophy of left ventricle
3. Hypertrophy of right ventricle
4. Myocardial infarction
5. Heart aneurysm
50. RHEUMATICС DAMAGE OF JOINTS CHARACTERIZED BY:
1. Acute serous-fibrinouse synovitis
2. Productive nonpurulent synovitis
62
3. Purulent destructive arthritis
4. Ankylosis
5. All true
51. THE CHARACTERISTIC FEATURE OF RELAPSING-WARTY ENDOCARDITIS IS :
1. Sclerosis of shutters and there ulceration
2. Perivascular cardiosclerosis
3. Sclerosis of shutters with thrombotic depositions
4. Petrifaction and hyalinosis of shutters
5. Perforation of shutters
52. AT RHEUMATOID ARTHRITIS IN JOINTS DEVELOPS:
1. Acute serous-fibrinouse sinoviitis
2. Productive non-purulent synovitis
3. Purulent destructive arthritis
4. Amyloidosis
5. All true
53. SKIN CHANGES DUE TO SYSTEMIC SCLERODERMA ARE CHARACTERIZED BY:
1. Hyalinosis
2. Petrifaction
3. Dermatitis
4. Suppuration
5. Coagulation
54. THE MOST CHARACTERISTIC
ERYTHEMATOSUS IS:
1. Amyloidosis
2. Nephrolitiasis
3. Pyelonephritis
4. Glomerulonephritis
5. Papillary necrosis
RENAL
DAMAGE
AT
SYSTEMIC
LUPUS
55. THE DEVELOPMENT OF RHEUMATISM IS PROVIDED BY:
1. Staphylococcus Aureus
2. -Hemolytic Streptococcus
3. Streptococcus Type B
4. Esherichia Colli
5. Clostridia Perphringens
56. RHEUMATOID ARTHRITIS USUALLY RESULTS BY:
1. Idiopathic primary amyloidosis
2. Chronic gastric ulcer
3. Reiter’s syndrome
4. Anchylosis
5. Obliterative thrombangitis
57. TO COLLAGENOSES REFERS:
1. Tuberculosis
2. Scleroderma
3. Atherosclerosis
4. Amyloidosis
63
5. Arthrosis
58. THE DIFFERENTIAL FEATURE OF ACUTE WARTY ENDOCARDITIS FROM RELAPSING
WARTY IS:
1. Presence of endothelial damage
2. Degree of connective tissue disorganization
3. Fibrosis of valve
4. Progression
5. All true
59. POSSIBLE COMPLICATION OF RELAPSING WARTY ENDOCARDITIS IS:
1. Purulent meningitis
2. Mediastinitis
3. Infarction of spleen
4. Thrombosis of veins
5. Pulmonary infarction
60. THE FEATURE OF ACTIVITY OF RHEUMATIC PROCESS IS:
1. Aortal valve insufficiency
2. Aortal valve stenosis
3. Ashoff- Thalalaev’s granuloma
4. Shorting and thickening of chords
5. Perivascular cardiosclerosis
61. THE OUTCOME OF VALVULAR ENDOCARDITIS IS:
1. Mccallum’s plaques
2. Diffuse cardiosclerosis
3. Constrictive perycarditis
4. Heart defect
5. Macrofocal cardiosclerosis
62. THE COMPLICATION OF RELAPSING-WARTY ENDOCARDITIS IS:
1. Infarctions in organs of systemic circulation
2. Cachexia
3. Abscess of brain
4. Pericarditis
5. Pulmonary thromboembolism
9. PULMONARY DISEASES
1. HEART INJURY AT PULMONARY FIBROSIS AND EMPHYSEMA OF LUNGS
RESULTS IN:
1. Atrophy of myocardium
2. Adiposity
3. Hypertrophy of left ventricle
4. Hypertrophy of right ventricle
5. Infarction of myocardium
2. ONE OF POSSIBLE COMPLICATIONS OF BRONCHOPNEUMONIA IS:
1. Lung infarction
2. Pneumothorax
64
3. Milliary tuberculosis
4. Abscess formation
5. Renal failure
3. ALL OF THE FOLLOWING FACTORS COMMONLY PREDISPOSE TO BACTERIAL
PNEUMONIAS, EXCEPT:
1. Viral respiratory tract infections
2. Cigarette smoking
3. Congestive heart failure
4. Bacterial urinary tract infection
5. Narcosis
4. THE ABNORMAL DILATION OF BRONCHI AND BRONCHIAL TUBES IS THE
CHARACTERISTIC FEATURE OF:
1. Emphysema
2. Lung abscess
3. Bronchiectasis
4. Bronchial asthma
5. Pneumonia
5. CARNIFICATION OF LUNG FOR CROUPOUSE PNEUMONIA IS:
1. Outcome
2. Complication
3. Appearance
4. Reason
5. Background
6. NAME TYPES OF BRONCHOECTASES:
1. Pneomoniogenic
2. Obstructive
3. Saccular
4. Infection
5. Dystrophic
7. THE MOST OFTEN TYPE OF ACUTE BRONCHITIS IS:
1. Obstructive
2. Deformative
3. Catarrhal
4. Polipouse
5. Fibrinouse
8. THE MOST COMMON REASON OF LUNG EMPHYSEMA IS:
1. Lung abscess
2. Chronic bronchitis
3. Focal pneumonia
4. Tracheitis
9. ONE POSSIBLE OF PULMONARY COMPLICATIONS OF CROUPOUSE PNEUMONIA IS:
1. Lung abscess
2. Mediastenitis
3. Lung cancer
4. Chronic bronchitis
65
5.
caverns formation
10. ACUTE ABSCESS BECOMES CHRONIC AFTER:
1. 2 weeks
2. 2 month
3. 2 years
4. 8 month
5. 2 hours
11. BROWN INDURATION OF LUNG IS RESULT OF:
1. Inflammation
2. Athelectasis
3. Necrosis
4. Congestion
5. Bronchoectasis
12. THE CHARACTER OF INFLAMMATION AT BRONCHOPNEUMONIA DETERMINATES
BY:
1. Volume of destruction
2. Age of patient
3. Type of pathogenic agent
4. Mechanism of inflammation
5. Localization of process
13.
EXTRAPULMONARY COMPLICATION OF CHRONIC PURULENT PROCESSES IN
LUNGS IS:
1. Amyloidosis
2. Hyalinosis
3. Lipidosis
4. Hyperglycemia
5. Cirrhosis
14. AT PNEUMOFIBROSIS AND EMPHYSEMA OF LUNGS IN THE HEART DEVELOPS:
1. Atrophy of myocardium
2. Adiposity
3. Hypertrophy of left ventricle wall
4. Hypertrophy of right ventricle wall
5. Myocardial infarction
15. EXUDATES IN STAGE OF GREY HEPATISATION IN CROUPOUS PNEUMONIA
CONSISTS OF:
1. Edematous fluid and bacteria
2. Erythrocytes and fibrin
3. Leucocytes and fibrin
4. Granulation tissue
5. Lymphocytes
16. AT WHICH STAGES OF CROUPOUSE PNEUMONIA LUNG ABSCESS MORE OFTEN
MEETS:
1. Inflow
2. Red hepatization
3. Grey hepatization
66
4. Resolution
5. 2&3 true
17. IN CROUPOUS PNEUMONIA STAGE OF INFLOW LASTS:
1. 5 day
2. 1-2 day
3. 4-6 day
4. 9-11 day
5. All answers wrong
18. WHAT DISEASE IS LEAD TO CHRONIC OBSTRUCTIVE LUNG EMPHYSEMA
DEVELOPMENT:
1. Chronic bronchitis
2. Tracheitis
3. Focal pneumonia
4. Lung abscess
5. Lung cancer
19. THE SYNONYM OF FOCAL PNEUMONIA IS:
1. Croupouse pneumonia
2. Pleuropneumonia
3. Bronchopneumonia
4. Interstitial pneumonia
5. Caseous pneumonia
20. MINOR PULMONARY THROMBOEMBOLISM RESULTS IN:
1. Sudden death from pulmonocoronary reflex
2. Myocardial infarction
3. Shock
4. Hemorrhagic pulmonary infarction
5. DIC
21. THE SYNONYM OF CROUPOUSE PNEUMONIA IS:
1. Lobar
2. Lobular
3. Hemorrhagic
4. Focal
5. Purulent
22. CARNIFICATION OF LUNGS IS:
1. Inflammatory infiltration of interstitial tissue
2. Persistention of pulmonary exudates in alveoli
3. Deposition of pigment in intraalveolar septs
4. formation of hyalinic membranes on alveolar walls
5. Organization of nonresolated exudates
23. THE CHARACTER OF PLEURISY AT CROUPOUSE PNEUMONIA IS:
1. Serous
2. Purulent
3. Granulematous
4. Fibrinous
5. Hemorrhagic
67
24. THE MOST COMMON ETHYOLOGICAL FACTORS OF BRONCHOPNEUMONIA ARE:
1. Bacterii, viral-bacterial association
2. Mycoplasma, chlamidii
3. Viri
4. Fungi
5. Riccetsii
25. PULMONARY COMPLICATIONS OF CROUPOUS PNEUMONIA ARE:
1. Abscess, carnification
2. Chronic bronchitis, emphisema
3. Bronchoectases development
4. Pneumothorax, empyema
5. Abscess of brain
26. MORPHOLOGICAL CHANGES IN LUNGS DUE TO CHRONIC VENOUS CONGESTION
ARE:
1. Hemorrhagic infarction and petrifaction
2. Acute edema
3. Antracosis and necrosis
4. Hemosiderosis and diffuse pneumosclerosis
5. Carnification
27. MORPHOLOGICAL CHANGES IN LUNGS DUE TO ASPIRATION PNEUMONIA ARE:
1. Infarction and petrifaction
2. Hemorrhage
3. Necrosis and suppuration
4. Serous inflammation
5. Edema
28. FOCAL PNEUMONIA DEPENDING ON SPREADING OF PATHOLOGICAL PROCESS CAN
BE:
1. Hypostatic, viral
2. Pneumococcal
3. Aspiration, lobar
4. Lobular, segmentary
5. Interstitial, bronchopneumonia
29. MACROSCOPICALLY AT PULMONARY EMPHYSEMA THE LUNGS ARE:
1. Increased size, dense consistence, pail
2. Increased size, soft consistence, pail
3. Increased size, soft consistence, hyperemia
4. Decreased size, soft consistence, honeycomb appearance
30. MASSIVE PULMONARY THROMBOEMBOLISM RESULTS IN:
1. Sudden death from pulmonocoronary reflex
2. Myocardial infarction
3. Shock
4. Hemorrhagic pulmonary infarction
5. DIC
31. STAPHYLOCOCCAL BRONCHOPNEUMONIA IS CHARACTERIZED BY:
68
1.
2.
3.
4.
5.
Fibrinous exudates
Hemorrhagic exudates
Purulent exudates, necrosis
Lymphoid infiltrations
Granulomatous inflammation
32. AT ACUE RESPIRATORY DISTRESS SINDROM HYALINE MEMBRANE IN THE LUNG
CONSISTS OF:
1. Albumin and complement
2. Fibrin
3. Precipitated surfactant
4. Mucus
33. IN THE STAGE OF GREY HEPATIZATION:
1. White Blood cells fill the alveoli
2. Red Blood cells fill the alveoli
3. Organisms fill the alveoli.
4. Accumulation of fibrin
34. GOOD PASTURE'S SYNDROME IS CHARACTERISED BY:
1. Necrotisting hemorrhagic interstitial pneumonitis
2. Alveolitis
3. Patchy consolidation
4. Pulmonary edema
35. THE COMMONEST OUTCOME OF LOBAR PNEUMONIA IS:
1. Consolidation
2. Resolution
3. Abscess formation
4. Empyema
36. BROWN INDURATION OF LUNG IS SEEN IN:
1. Silicosis
2. Siderosis
3. Asbestosis
4. Bagassosis
5. None of the above
37. ALPHA I ANTITRYPSIN DEFICIENCY OCCURS IN:
1. Emphysema
2. Bronchiectasis
3. Empyema
4. Bronchogenic carcinoma
38. COMMONEST TYPE OF EMPHYSEMA IS:
1. Centriacinar
2. Obstructed
3. Irregular
4. Panacinar
39. THE ALVEOLI ARE FILLED WITH EXUDATES THE AIR IS DISPLACED CONVERTING
THE LUNG INTO A SOLID ORGAN. THIS DESCRIPTION SUGGESTS:
69
1.
2.
3.
4.
5.
Chronic bronchitis
Bronchial asthma
Bronchiectasis
Lobar pneumonia
Pneumonitis
40. ABOUT PULMONARY INFARCT ALL ARE TRUE EXCEPT:
1. Occurs commonly with fat embolism
2. Mostly red infarct with haemorrhagic exudate
3. Haemorrhagic effusion may occur
4. Often from deep veins of legs or pelvis
5. Triangular shaped
41. SPUTUM FROM AN ASTHMA PATIENT MAY SHOW:
1. Numerous eosinophils
2. Curschmann's spirals
3. Charcot-Leyden crystals
4. All of the above
5. None of the above
42. MOST COMMON LUNG MALFORMATION:
1. Hypoplasia of lung
2. Congenital cyst
3. Vascular anomalies
4. Lobar sequestration
43. THE MOST COMMON SITE FOR METASTASIS OF SMALL CELL CARCINOMA OF LUNG
IS:
1. Brain
2. Adrenal
3. Liver
4. Bones
44. CHARACTERISTIC FEATURE OF VIRAL PNEUMONIAS IS:
1. Interstitial mononuclear infiltration
2. Intra-alveolar proteinaceous exudate
3. Hyaline membrane lining alveoli
4. Fibrotic septa
5. Fibrinous exudate
45. EMPHYSEMA PATHOLOGICALLY INVOLVES BEYOND THE:
1. Bronchi
2. Terminal bronchiole
3. Respiratory bronchiole
4. Alveolar Sac
46. COMMONEST TYPE OF LUNG CANCER IN NON-SMOKER IS:
1. Squamous cell carcinoma
2. Adenocarcinoma
3. Small cell carcinoma
4. Large cell carcinoma
5. Chorioepithelioma
70
47. COMPLICATION OF BRONCHIECTASIS ARE ALL EXCEPT:
1. Amyloidosis
2. Carcinoma of bronchus
3. Lung abscess
4. Cor pulmonale
5. Obstructive emphysema
48. CLASSICAL FIBRINOUS INFLAMMATION IS SEEN IN WHICH ONE OF THE
FOLLOWING STAGES OF LOBAR PNEUMONIA:
1. Hyperemia
2. Red hepaization
3. Grey hepatization
4. Resolution
49. IN PRIMARY ATYPICAL PNEUMONIA INFLAMMATORY CELLS ACCUMULATE IN:
1. Alveolar lumen
2. Bronchioles
3. Alveolar wall
4. Pleural space
50. REID'S INDEX IS USED IN DIAGNOSIS OF:
1. Chronic bronchitis
2. Bronchiectasis
3. Bronchial asthma
4. Pneumonia
51. SMOKING CAUSES ALL EXCEPT
1. Chronic bronchitis
2. Bronchiectasis
3. Emphysema
4. Bronchogenic cancer
5. Antracosis
52. HYALINE MEMBRANES IN THE LUNG IS SEEN IN:
1. Respiratory distress syndrome
2. Pulmonary edema
3. Pneumococcal Pneumonia
4. Acute viral hepatitis
5. None of the above
53. LONG TERM COMPLICATION OF BRONCHOPULMONARY DYSPLASIA ARE ALL
EXCEPT:
1. Decreased functional residual capacity
2. Small airway disease
3. Large airway disease
4. Interstitial lung disease
54. MYCOPLASMA INFECTION SIMULATES:
1. Pneumococcal pneumonia
2. Viral pneumonia
3. Hypersensitivity pneumonia
71
4. Aspiration pneumonia
55. NORMAL AMOUNT OF PLEURAL FLUID IS APPROXIMATELY:
1. 5 ml
2. 15 ml
3. 50ml
4. 100ml
56. PREDISPOSING FACTORS OF LUNG ABSCESS ARE ALL EXCEPT:
1. Altered sensorium
2. Dental sepsis
3. Aggressive treatment of pneumonia
4. Subpulmonic effusion
5. Endobronchial obstruction
57. WHICH IS NOT AN INFLAMMATORY STAGE IN PNEUMONIA?
1. Organisation
2. Congestion
3. Resolution
4. Hepatisation
58. LUNG CANCER COMMONLY METASTASISES TO ALL SITES, EXCEPT:
1. Brain
2. Liver
3. Bone
4. Kidney
5. Adrenals
59. FOCAL PNEUMONIA IS CHARACTERIZED BY:
1. Damage of lung lobe
2. Involving of pleura in process
3. Presence of bronchitis, bronchiolitis
4. Caseouse necrosis of exudates
5. Pulmonary tissue necrosis
10. GIT DISEASES
1. MICROSCOPICAL FEATURES OF ACUTE APPENDICITIS ARE ALL, EXCEPT:
1. Epithelioid cell infiltration
2. Diffuse neutrophil infiltration
3. Abscesses
4. Ulceration of the mucosa
5. Foci of hemorrhages
2. THE CELL TYPES IN THE CORPUS GASTRIC GLANDS ARE ALL OF THE FOLLOWING,
EXCEPT:
1. Mucous
2. Parietal
3. Chief
4. Hurtle
5. Endocrine
72
3. CHRONIC INFECTION OF THE GASTRIC MUCOSA IS ASSOCIATED WITH WHICH OF
THE FOLLOWING BACTERIA:
1. Escherichia coli
2. Helicobacter pylori
3. Campilobacter jejuni
4. Enterococcus falcium
5. Escherichia aurescens
4. ACUTE GASTRITIS IS COMMONLY ASSOCIATED WITH ALL OF THE FOLLOWING
FACTORS, EXCEPT:
1. Uremia
2. Severe stress
3. Systemic infections
4. Delayed gastric emptying
5. Ischemia and shock
5. THE MOST TYPICAL CHANGES OF VESSELS AT STAGE OF CHRONIC ULCER
REMISSION ARE:
1. Sclerosis of walls
2. Plethora
3. Anemia
4. Large thin-walled sinusoidal vessels
5. Lipoidosis
6. THE APPENDIX IN ACUTE APPENDICITIS IS GROSSLY CHARACTERIZED BY ALL OF
THE FOLLOWING FEATURES, EXCEPT:
1. Enlarged with thickened walls
2. Firm and indurate
3. Swollen
4. Hyperemic with engorged vessels
5. Fibrin covered serosa
7. MORE OFTEN PRIMARY MALIGNANT TUMOR OF ESOPHAGUS IS:
1. Adenocarcinoma
2. Squamous cancer
3. Not differentiated cancer
4. Malignant melanoma
5. Leiomyosarcoma
8. LARGE ULCER WITH DIRTY YELLOW-GREEN BOTTOM AND ROUGH EDGES IS
FOUND OUT ON MUCOUS MEMBRANE OF RECTUM AT AUTOPSY. THIS SPECIFIED
PICTURE IS CHARACTERISTIC FOR:
1. Cancer of rectum
2. Amebiasis
3. Cholera
4. Iersiniosis
5. Salmonellosis
9. KRUKENBERG'S TUMOR IS:
1. Teratoblastoma of ovary
2. Bilateral ovary cancer with solid structure
3. Metastasis of stomach cancer to ovary
73
4. Metastasis of stomach cancer to supraclavicular lymph node
5. Tumour of kidney
10. IN STOMACH PRECANCEROUS CONDITION IS:
1. Melory-Vayss’s syndrome
2. Fibrous gastritis
3. Squamous methaplasia of epithelium
4. Chronic atrophic gastritis with dysplasia
5. Erosive gastritis
11. THE PIGMENT FORMATING IN THE BOTTOM OF ULCER IS:
1. Hemomelanin
2. Hemosiderin
3. Hydrochlorid hematin
4. Porphyrin
5. Hemochromatin
12. GENERAL FACTORS OF ULCERAL DISEASE PATHOGENESIS ARE:
1. Vascular, necrotic
2. Neural, humoral
3. Toxic, traumatic
4. Chemical, physical
5. Exogenic, endogenic
13. STOMAC CANCER MORE OFTEN GIVES HEMATOGENIOUS METASTASES IN:
1. Liver
2. Ovary
3. Adrenals
4. Regional lymph nods
5. Pararectal adiposal tissue
14. THE DESTRUCTIVE TYPE OF APPENDICITIS IS:
1. Simple
2. Superficial
3. Phlegmanous
4. Catarrhal
5. Serous
15. THE MOST OFTEN LOCALISATION OF LARGE INTESTINE CANCER IS:
1. Caecum
2. Ascending
3. Recto-sigmoid
4. Colon
5. All true
16. CHANGES IN MUSCLE LAYER OF STOMACH WALL AT CHRONIC ULCER IS:
1. Replacement by connective tissue
2. Dystrophy
3. Atrophy
4. Inflammation
5. Petrifaction
74
17. POSSIBLE COMPLICATION OF ULCERAL DISEASE OF STOMACH IS:
1. Duodenitis
2. Antral stenosis
3. Hepatitis
4. Sepsis
5. Meningitis
18. “VIRCHOV’S METASTASIES” OF STOMACH CANCER IS:
1. Lymph nods of curvature minor
2. Supraclavicular lymph nods
3. Ovary
4. Pararectal lymph nods
5. Mesenterical lymph nods
19. THE MOST COMON HYSTOLOGICAL TYPE OF STOMACH CANCER NIS:
1. Adenocarcinoma
2. Signet ring cell carcinoma
3. Squamouse cellular carcinoma
4. Non differenciated cancer
5. Scirr (fibrous cancer)
20. POSSIBLE COMPLICATIONS OF DESTRUCTIVE APPENDICITIS ARE:
1. Perforation and peritonitis
2. Self-amputation of appendix
3. Empyema of appendix and periappendicitis
4. All true
5. True 1&3
21. ETIOLOGICAL FACTORS OF ESOPHAGITIS ARE ALL, EXCEPT:
1. REFLUX-GASTRITIS
2. Chronic gastritis
3. Chemical burn
4. Stenosis of esophagus
5. Uremia
22. DELATION OF APPENDIX LUMEN DUE TO ACCUMULATION OF MUCOSAL SECRET IS
TERMED AS:
1. Cyst
2. Hydrocele
3. Mucocele
4. Pneumocele
5. Varicocele
23. THE DIFFERENCE BETWEEN EROSION AND ACUTE ULCER OF STOMACH IS:
1. Bottom sclerosis
2. Deepness of necrosis
3. Inflammatory reaction
4. Hyperplasia of glands in margins
5. Epithelial metaplasia
24. THE COMPLICATION DEVELOPING AT ACUTION OF CHRONIC STOMACH ULCER IS:
1. Deformation of stomach
75
2. Pylorostenosis
3. Malignesation
4. Hemorrhage
5. Polyp formation
25. THE ENTEROLISATION OF STOMACH MUCOSA IS:
1. Hyperplasia of epithelium
2. Aplasia of epithelium
3. Metaplasia of epithelium
4. Hypertrophy of epithelium
5. Atrophy of epithelium
26. THE ULCERAL-DESTRUCTIVE COMPLICATION OF ULCERAL DISEASE OF STOMACH
IS:
1. Gastritis
2. Stenosis of lumen
3. Perforation
4. Malignesation
5. Penetration
27. FACTORS PROVIDED APPENDICITIS DEVELOPMENT ARE ALL, EXCEPT:
1. Thrombosis of mesenteric arteries
2. Occlusion by coprolythies
3. Occlusion by foreign bodies
4. Hemodynamic disorders of appendix wall
5. Enterogenic autoinfection
28. “SHNIZLER’S METASTASIES” OF STOMACH CANCER ARE FOUND OUT IN:
1. Lymph nods of curvature minor
2. Ovary
3. Supraclavicular lymph nodes
4. Pararectal lymph nodes
5. Parabronchial lymph nodes
29. THE TYPES OF ESOPHAGEAL DIVERTICULI ARE:
1. True, false
2. Exophitic, endophitic
3. True, muscle
4. Cylindrical, saccular
5. Tonogenic, myogenic
30. PRECANCEROUS DISEASES OF RECTUM ARE ALL, EXCEPT:
1. Chronic ulceral colitis
2. Adenomatous polips
3. Chronic fistules of rectum
4. Hemorrhoyhaemorrhoids
5. Black akantosis
31. COLORECTAL CARCINOMA IS ASSOCIATED WITH:
1. High fibre intake
2. High fibre intake
3. Low fibre & high fat intake
76
4. Smoked fish
32. PREMALIGNANT CONDITIONS OF THE GIT ARE ALL OF THE FOLLOWING EXCEPT:
1. Iliocecal Tuberculosis
2. Familial polyposis
3. Villous adenomas
4. Ulcerative colitis
33. COMMONEST VARIETY OF STOMACH CARCINOMA IS:
1. Squamous carcinoma
2. Adenocarcinoma
3. Colloid carcinoma
4. None
34. GREATER RISK OF STOMACH CARCINOMA IS ASSOCIATED WITH:
1. Old age
2. Intestinal metaplasia
3. Cardiac end ulcer
4. Prepyloric ulcer
35. FALSE ABOUT THE MALIGNANT ULCER OF STOMACH IS:
1. The mucosal folds do not reach the edge of the ulcer
2. Mucosal folds are thickened and fused
3. Ulcer crator is eccentric
4. Margins of the ulcer are overhanging
36. INTESTINAL EPITHELIUM IS RICH IN WHICH OF THE FOLLOWING:
1. T-cells
2. B-cells
3. Plasma cells
4. Macrophages
37. CHRONIC GASTIRITIS IS CAUSED BY ALL EXCEPT:
1. H. Pylori
2. Pernicious anaemia
3. Alcohol
4. Overuse of salicylates
38. LORDACEOUS SPLEEN IS SEEN IN:
1. Alcoholic hepatitis
2. Chronic active hepatitis
3. Focal amyloidosis
4. Diffuse amyloidosis
39. PEPTIC ULCERATION OCCURS AT ALL THE FOLLOWING SITES EXCEPT:
1. Lesser cuvature
2. First part of duodenum
3. Lower end of esophagus
4. Stoma of gastric portion of gastrojejunostomy
40. MOST COMMON TYPE OF GASTRIC POLYP IS:
1. Hyperplastic polyp
77
2. Hamartomatous polyp
3. Malignant polyp
4. Familial polyposis
41. ONE OF THE FOLLOWING POLYPS IN THE STOMACH DOES NOT BECOME
MALIGANT:
1. Tubular adenoma
2. Villous adenoma
3. Multiple polyposis
4. Hyperplastic polyps
42. SECRETORY DIARRHEA IS CAUSED BY ALL EXCEPT:
1. Gastrinoma
2. After bowel resection
3. Pancreatic exocrine deficiency
4. Vipoma
43. PATHOGENETIC TYPES OF CHRONIC GASTRITIS:
1. Primary, secondary
2. Exogenic, endogenic
3. Deep, superficial
4. Type A, type B, reflux-gastritis
44. CHRONIC INFECTION OF THE GASTRIC MUCOSA IS ASSOCIATED WITH WHICH
BACTERIA:
1. Escherichia coli
2. Helicobacter pylori
3. Campilobacter jejuni
4. Enterococcus falcium
5. Escherichia aurescens
45. CHRONIC GASTRITIS MAY BE CHARACTERIZE BY ALL, EXCEPT:
1. Suppurative inflammation
2. Lymphocyte infiltration
3. Plasma cell infiltration
4. Intestinal metaplasia
5. Atrophy
46. ACUTE CATARRHAL GASTRITIS IS MORPHOLOGICALLY CHARACTERIZED BY ALL
FEATURES, EXCEPT:
1. Moderate edema of the lamina propria
2. Vascular congestion of the lamina propria
3. Atrophy of the mucosa
4. Neutrophil infiltration
5. Abundant mucus on the gastric epithelium
47. THE MAJOR ETIOLOGIC ASSOCIATIONS OF CHRONIC GASTRITIS ARE ALL , EXCEPT:
1. Chronic Heficobacter pylori mfectioe
2. Ischemia and shock
3. Autoimmune factors
4. Toxic factors
5. Bile reflux
78
48. SPECIAL FORMS OF GASTRITIS ARE ALL, EXCEPT:
1. Eosinophffic gastritis
2. Collagenouse gastritis
3. Lymphocytic gastritis
4. Granulomatous gastritis
5. Interstitial gastritis
49. CLINICAL SYNDROME ASSOCIATED WITH GASTRIC, DUODENAL AND JEJUNAL
PEPTIC GASTRIN-INDUCED ULCERS IS WHICH OF THE FOLLOWING:
1. Horner's
2. Nephrotic
3. DIC
4. Zollinger-Ellison
5. Malabsorption
50. PREDISPOSING CONDITIONS FOR ISCHEMIC BOWEL DISEASE ARE ALL, EXCEPT:
1. Arteriolar thrombosis
2. Arteriolar embolism
3. Venous thrombosis
4. Helicobacter pylori infection
5. Portal hypertension syndrome
51. GIANT CEREBRIFORM ENLARGEMENT OF THE GASTRIC MUCOSA IN MENETRIER
DISEASE IS CAUSED BY WHICH PATHOLOGIC PROCESSES:
1. Inflammation
2. Hyperplasia of the mucosal epithelial cells
3. Atrophy of the mucosa
4. Interstitial metaplasia
5. Fibrosis
52. COMPLICATIONS OF DUODENAL PEPTIC ULCER INCLUDE ALL OF THE
FOLLOWING, EXCEPT:
1. Malabsorption
2. Bleeding
3. Perforation
4. Penetration
5. Obstruction by edema or scarring
53. THE MOST COMMON LOCALIZATION OF GASTRIC PEPTIC ULCER IS WHICH OF THE
FOLLOWING:
1. Greater curvature2. Lesser curvature
3. Duodenal pyloric ring
4. Anterior wall of the gastric corpus
5. Posterior wall of the gastric corpus
54. CLASSICAL PEPTIC ULCER IS GROSSLY CHARACTERIZED BY ALL FEATURES,
EXCEPT:
1. Round-to-oval
2. Sharply defined
3. Punched-out defect
79
4. Elevated margins
5. Superficial defect
55. THE MOST COMMON PATHOLOGIC CHANGE OF THE GASTRIC MUCOSA ADJACENT
TO PEPTIC ULCER IS:
1. Cancerous ulcer
2. Hypertrophic gastropathy
3. Gastric dilatation
4. Menetrier disease
5. Chronic gastritis
56. ALL OF THE FOLLOWING COMPLICATIONS
ULCER, EXCEPT:
1. Caseation
2. Perforation
3. Bleeding
4. Malignization
5. Penetration
MAY BE FOUND IN CHRONIC PEPTIC
11. LIVER PATHOLOGY
1. AN OUTCOME OF ACUTE VIRAL HEPATITIS A:
1. Postnecrotic cirrhosis of the liver
2. Carrier state formation
3. Portal cirrhosis
4. Chronic hepatitis
5. Recovery
2. DUE TO CHRONIC CHOLESTASIS COLOR OF THE LIVER IS:
1. Grayish
2. Yellowish
3. Greenish
4. Brown
5. All true
3. THE TOXIC DYSTROPHY OF THE LIVER CAN DEVELOP AT:
1. Leukemia
2. Gestational toxicosis
3. Dysentery
4. Cardiac insufficiency
5. Typhoid fever
4.
FORM OF VIRAL HEPATITIS THAT CAN FOLLOW WITH POSTNECROTIC CIRRHOSIS
OF THE LIVER IS:
1. Anicteric
2. Acute cyclic
3. Chronic
4. Cholestatic
5. Fulminant
5.
THE CLINICAL-MORPHOLOGICAL FORMS OF ACUTE VIRAL HEPATITIS ARE:
80
1.
2.
3.
4.
5.
6.
Hepatomegalic
Cyclic icteric, anicteric
Dystrophic, splenomegalyс
Hypoproteinemic
Obstructive, hydropic
FATTY HEPATOSIS MOST COMMONLY IS A RESULT OF:
1. Glycogenosis
2. Viral hepatitis
3. Essential hypertension
4. Lung cancer
5. Chronic alcoholism
7. IN STAGE OF YELLOW DYSTROPHY THE LIVER IS:
1. Red, reduced
2. Brightly yellow, increased
3. Red, increased
4. Dense, sclerozed
5. Diffuse hemorrhages in liver tissue
8. MACROSCOPICAL ATTRIBUTE CHARACTERISTIC FOR ALCOHOLIC (PORTAL)
CIRRHOSIS OF THE LIVER IS:
1. Macronodular surface of liver
2. Micronodular surface of liver
3. Expansion of bilious channels
4. Wide fibrous fields between lobules
5. All true
9. HISTOLOGICAL STAIN FOR REVEALING OF LIVER CIRRHOSIS IS:
1. Sudan III
2. Picrofuchsin by von Giesone
3. PAS-reaction
4. Perl's reaction
5. By Ziehl-Nielsen
10. POSSIBLE OUTCOME OF ACUTE VIRAL HEPATITIS IS:
1. Nutmeg liver
2. Brown atrophy of liver
3. Glycogenosis of liver
4. Cirrhosis of liver
5. Hemosiderosis of liver
11. THE SYNDROME OF PORTAL HYPERTENSION IS CHARACTERIZED BY:
1.
Pulmonary embolism
2.
Syndrome of compression of superior vena cava
3.
Ascites, expansion of esophagus veins, splenomegaly
4.
Ischemia of mesenteric vessels
5.
Thrombosis of mesenteric vessels
12. THE FIGURATIVE NAME OF LIVER AT STEATOSIS IS:
1. "Goose"
2. "Tiger"
81
3. "Grease"
4. "Sago"
5. Nutmeg
13. OCCURRENCE OF INFLAMMATORY INFILTRATE IN THE LIVER MEANS:
1. Regeneration
2. Cirrhosis
3. Hematoma
4. Dystrophy
5. Hepatitis
14. THE MOST OFTEN REASON OF TOXIC DYSTROPHY OF THE LIVER:
1. Haemorrhage in brain
2. Poisoning by hepatotropic poisons
3. Stomach ulcer
4. Diabetes
5. Hypertension
15. CHARACTERISTIC MICROSCOPIC FEATURES OF POSTNECROTIC LIVER CIRRHOSIS
ARE:
1. Contiguity of triads, wide fibrous layers
2. Hemosiderosis
3. Amyloidisis
4. Hyalinosis
5. Diffuse hemorrhages in liver tissue
16. VIRAL HEPATITIS A IS CHARACTERIZED BY ALL, EXCEPT:
1. Benign cyclic current;
2. Faecal -oral pathway of transmission
3. Low mortality
4. Development of cirrhosis of liver
5. Lifelong immunity
17. NUTMEG LIVER DEVELOPS AT:
1. Chronic alcoholism
2. Hepatitis;
3. Cancer of liver
4. The general venous congestion
5. Hydatid cyst
18. VIRAL HEPATITIS B IS CHARACTERIZED BY ALL, EXCEPT:
1. Transplacental pathway of transmission
2. The fine sizes of virus with defective RNA
3. Long persistence virus in host organism
4. Carrier state formation
5. Parenteral pathway of transmission
19. FATTY HEPATOSIS DEVELOPS AT:
1. Appendicitis
2. Diabetes
3. Cholangitis
4. Hypertension
82
5. Chronic pyelonephritis
20. THE MOST OFTEN REASON OF DEATH OF PATIENTS SUFFERING CIRRHOSIS OF
LIVER IS:
1. Acute cardiac insufficiency
2. Bleeding from esophagus veins
3. Pneumonia
4. Respiratory-cardiac insufficiency
5. Cachexy
21. VIRAL HEPATITIS C IS CHARACTERIZED BY ALL, EXCEPT:
1. Parenteral pathway of transmission
2. Absence of effective immunity
3. Low frequency of development of liver cirrhosis
4. High frequency of progressing to chronic
5. Not heavy clinical current
22. THE MASSIVE BLEEDING IS OBSERVED AT:
1. Viral hepatitis
2. Billiary cirrhosis
3. Nutmeg cirrhosis
4. Gallstones
5. Abscess of liver
23. IN AN OUTCOME OF PROGRESSING MASSIVE LIVER NECROSIS DEVELOPS:
1. Postnecrotic cirrhosis
2. Portal cirrhosis
3. Mixed cirrhosis
4. Biliary cirrhosis
5. Nutmeg cirrhosis
24. VIRAL HEPATITIS D IS CHARACTERIZED BY ALL, EXCEPT:
1. Low frequency of progressing to chronic
2. Meets at homosexuals
3. Transforms hepatitis B in fulminant form
4. Meets at patients with a hemophilia;
5. Following with hepato-cellular carcinoma
25. COLOR CHANGE OF SKIN, SCLERA, SEROUS AND MUCOUS MEMBRANES AS A
RESULT OF INCREASED LEVEL OF BILIRUBIN IN BLOOD IS:
1. Melanosis
2. Vitiligo
3. Jaundice
4. Cyanosis
5. Nevus
26. PERIPHERAL EDEMATA ARE OBSERVED AT:
1. Portal cirrhosis of liver
2. Postnecrotic cirrhosis of liver
3. Biliary cirrhosis of liver
4. Nutmeg cirrhosis of liver
5. All true
83
27. IN CIRRHOSIS LIVER ALL ARE SEEN EXCEPT –
1. Loss of normal architecture
2. Fatty infiltration
3. Degeneration of hepatocytes
4. Loss of inter cellular connective tissue matrix
28. POSTNECROTIC LIVER CIRRHOSIS IS A RESULT OF:
1. Toxic dystrophy of liver
2. Chronic persistent hepatitis
3. Bilious - stone illness
4. The cyclic form of viral hepatitis
5. Anicteric forms of viral hepatitis
29. SECONDARY BILIARY CIRRHOSIS OF LIVER DEVELOPS IN OUTCOME OF:
1. Cholelithiasis with chronic cholestasis
2. Toxic dystrophy of liver
3. Non purulent cholangitis
4. Acute viral hepatitis A
5. Chronic persistent hepatitis
30. CHARACTERISTIC MACROSCOPICAL FEATURE VIRAL (POSTNECROTIC) CIRRHOSIS
OF LIVER IS:
1. Macronodular surface of liver
2. Micronodular surface of liver
3. Narrow fibrous band between lobules
4. Nutmeg liver
5. Smooth surface of a liver
31. THE FORM OF LIVER CIRRHOSIS WITH ESPECIALLY HIGH RISK OF HEPATOCELLULAR CARCINOMA DEVELOPMENT IS:
1. Alcoholic
2. After hepatitis C
3. Primary biliary
4. Secondary biliary
5. Dyscirculatory
32. A SINGLE LARGE LIPID DROPLET (MACROVESICULAR STEATOSIS) THAT
DISPLACES THE NUCLEUS MAY BE SEEN IN ALL OF THE FOLLOWING PATHOLOGIC
CONDITIONS, EXCEPT:
1. Hepatitis С
2. Alcohol abuse
3. Obesity
4. Hepatitis В
5. Diabetes mellitus
33. CIRRHOSIS OF LIVER IS CHARACTERIZED BY ALL ATTRIBUTES, EXEPT:
1. Fibrous band between lobules
2. Necrosis of hepatocytes
3. False lobules
4. Disorder of liver tissue architecture
5. Cellular atypia
84
34. HISTOLOGICAL ATTRIBUTE OF VIRAL HEPATITIS B IS:
1. Steatosis of hepatocytes
2. Plethora of the central veins
3. Matte – glassy hepatocytes
4. Huge multinuclear hepatocytes
5. Light Kraevsky’s cells
35. ONE OF THE BASIC HISTOLOGICAL ATTRIBUTES OF VIRAL HEPATITIS IS:
1. Caunsilman’s corpuscles
2. Giant mitochondrion
3. Granulomatous inflammation
4. Pericellular fibrous
5. Sclerosis
36. LIVER CIRRHOSIS IS CHARACTERIZED
MORPHOLOGICAL FEATURES, EXCEPT:
1. Bridging fibrous septae
2. Hemosiderin granules in liver cells
3. Parenchymal nodular architecture
4. Reorganized vascular architecture
5. Disrupted liver architecture
BY
ALL
OF
THE
FOLLOWING
37. MICRONODULAR CIRRHOSIS IS SEEN IN 1. Alcoholic cirrhosis
2. Wilson’s disease
3. Budd chiari syndrome
4. Post necrotic cirrhosis
5. None
38. PATHOLOGICAL CHANGE OF LIVER CELLS IN ACUTE VIRAL HEPATITIS ARE ALL,
EXCEPT1. Ballooning degeneration
2. Ground glass hepatocytes
3. Piece meal necrosis
4. Fatty change
39. GALL STONES IN HEMOLYTIC ANAEMIA ARE:
1. Pigment
2. Mixed
3. Cholesterol
4. Any type
40. A PERSON IS LABELLED AS HEPATITIS CARRIER IF HBS AG IS POSITIVE AFTER:
1. 2 weeks
2. 2 months
3. 4 months
4. 6 months
41. IN INDIA ACUTE HEPATITIS A MOSTLY AFFECTS:
1. Elderly diabetics
2. Children between ages 3 and 12 years
3. Pregnant women in 3rd trimester
85
4. New born infants
42. MALLORY HYALINE IS NOT FOUND IN:
1. Alcoholic cirrhosis
2. Indian childhood cirrhosis
3. Wilson's disease
4. Chronic active hepatitis
43. MALLORY HYALINE BODIES ARE PRESENT IN ALL EXCEPT:
1. Alocholic cirrhosis
2. Indian childhood cirrhosis
3. Primary biliary cirrhosis
4. Secondary biliary cirrhosis
44. LARGE GIANT CELLS ARE FOUND IN:
1. Alcoholic hepatitis
2. Neonatal hepatitis
3. Serum hepatitis
4. Amoebic hepatitis
45. MACRONODULAR CIRRHOSIS OCCURS IN:
1. Postnecrotic
2. Willsons disease
3. Cryptogenic
4. Billiary
46. PERIPORTAL FATTY INFILTRATION OF LIVER IS SEEN WITH:
1. Alcoholism
2. Viral hepatitis
3. Malnutrition
4. Tetracycline
47. IN CIRRHOSIS LIVER ALL ARE SEEN EXCEPT –
1. Loss of normal architecture
2. Degeneration of hepatocytes
3. Fatty infiltration
4. Loss of inter cellular connective tissue matrix
48. HBV IS NOT ASSOCIATED WITH
1. Chronic active hepatitis
2. Chronic persistent hepatitis
3. Post necrotic cirrhosis
4. Cholangio carcinoma
49. THE FOLLOWING IS FECAL-ORALLY TRANSMITTED:
1. Hepatitis A
2. Hepatitis B
3. Hepatitis C
4. Hepatitis D
50. NUTMEG LIVER IS GROSS APPEARANCE OF LIVER IN ONE OF THE FOLLOWING:
1. Cirrhosis of liver
86
2. Hepatoma
3. Secondary carcinomatous deposit in liver
4. Chronic passive congestion in liver
51. HEPATITIS ENCEPHALOPATHY OF PREGNANT LADY CAN CAUSE BY:
1. HEV
2. Acute fatty liver of pregnancy
3. HBV
4. HAV
52. HYPOGONADISM IN CIRRHOSIS IS DUE TO ALL EXCEPT:
1. Direct effect of alcohol on testes
2. Increased estrogen due to decreased catabolism
3. Increased peripheral conversion of androgens into estrogen
4. Increased testosterone
53. HISTOPATHOLOGIC FEATURES OF BILE DUCT OBSTRUCTION ARE:
1. Proliferation of bile duct
2. Bile lakes
3. Portal fibrosis
4. Cholestasis
5. All the above
54. IN ANOXIA OF LIVER, NECROSIS IS SEEN IN:
1. Centrilobular
2. Around the periphery
3. Around the central vein
4. Around the bile duct
55. FEATURE OF ALCOHOLIC LIVER DISEASE:
1. Fatty changes
2. Pericellular fibrosis
3. Mallory bodies seen
4. Microvesicular fatty deposits
5. All
56. INCREASED LIVER ATTENUATION WITH INTRACELLULAR INFILTRATION IS SEEN
IN:
1. Fatty liver
2. Amyloidosis
3. Hemochromatosis
4. All
57. MACRONUDULAR CIRRHOSIS IS CONSIDERED ONCE NODULE DIAMETER IS
GREATER THAN:
1. 1 m.m
2. 2 m.m
3. 3 m.m
4. 4 m.m
87
12. KIDNEYS PATHOLOGY
1. MICROSCOPICAL CHANGES CHARACTERISTIC FOR ACUTE POSTSTREPTOCOCCAL
GLOMERULONEPHRITIS:
1. Losing of small podocytes processes
2. Membranous transformation
3. Extracapillary productive glomerulonephritis (semi-loons formation)
4. Intracapillary productive glomerulonephritis
5. All true
2. CHRONIC PYELONEPHRITIS CAN CAUSED BY:
1. Transfusion of incompatible blood
2. Poisoning by quicksilver
3. Smoking
4. Stone in renal pelvis
5. All true
3. MICROSCOPICAL FEATURE FOR DIFFERENTIATION CHRONIC PYELONEPHRITIS
FROM INTERSTITIAL NEPHRITIS IS:
1. Presence a lot of macrophages in infiltrate
2. Line-radial scarring
3. Fibrosis of intersticium
4. “Thyrioidisation” of kidney
5. Sclerosis and mononuclear infiltration of pelvis and calices
4. THE COMPLICATION OF ACUTE PYELONEPHRITIS IS:
1. Papillonecrosis
2. Glomerulosclerosis
3. Hemosiderosis of kidney
4. Cyanotic induration
5. Ischemic infarction
5. TO TUBULOPATHIES IS REFEREED:
1. Acute renal failure
2. Pyelonephritis
3. Glomerulonephritis
4. Chronic renal failure
5. Berge disease
6. THE OUTCOME OF CHRONIC LONG-DURATING GLOMERULOPATHIES IS:
1. Arteriolosclerosis
2. Dilatation and obstruction of tubules
3. Nephrosclerosis
4. Hydronephrosis
7. THE MAIN CONDITION OF EPITHELIUM COMPLETE REGENERATION AT NECROTIC
NEPHROSIS IS:
1. Saving of single glomuli
2. Undamaged of basal membrane
3. Evident lympho- plasmocytic infiltration
4. Presence of fibroblasts in stroma
5. Medium edema of stroma
88
8. ACUTE RENAL FAILURE CAN DEVELOP AT:
1. Shock
2. Intravascular hemolysis
3. Obstruction of urinary tract
4. All true
5. True 1&2
9. GLOMERULONEPHRITIS IS DEFINED AS:
1. Infectious-allergic inflammation of renal glomerules
2. Infectious inflammation of interstitial tissue, pelvis and calicis of kidneys
3. Congenital defect with prevalence of canalicular epithelium damage
4. Dystrophy and necrosis of tubular epithelium
10. MACROSCOPICAL APPEARANCE OF KIDNEYS AT ACUTE GLOMERULONEPHRITIS IS:
1. Primary reduced kidney
2. Big bacon kidney
3. Big white kidney
4. Big motley kidney
11. THE OUTCOME OF CHRONIC LONG-DURATING STROMAL DISEASES OF KIDNEY IS:
1. Arteriolosclerosis
2. Amyloidosis
3. Hydronephrosis
4. Nephrosclerosis
5. Pyonephrosis
12. THE MAIN MORPHOLOGICAL FEATURE OF ACUTE GLOMERULONEPHRITIS IS:
1. Interstitial infiltration by leucocytes
2. Dystrophic changes of tubular epithelium
3. Hyperemia of juxtamedullary area of kidney
4. Protein cylinders in tubules
5. All true
13. SECONDARY-REDUCED KIDNEY IS DEVELOPED IN OUTCOME OF:
1. Essential hypertension
2. Chronic glomerulonephritis
3. Diabetes mellitus
4. Chronic pyelonephritis
5. Acute glomerulonephritis
14. ACUTE GLOMERULONEPHRITIS IS APPEARED AS:
1. Intracapillary productive
2. Mesangial
3. Mesangial proliferative
4. Extracapillary productive
15. THE MOST OFTEN VARIANT OF KIDNEY’S AMYLOIDOSIS IS:
1. Primary
2. Senile
3. Secondary
4. Local
89
16. EXTRACAPILLARY TYPE OF GLOMERULONEPHRITIS IS CHARACTERIZED:
1. Inflammation of vessel loops and mesangium
2. Isolated inflammation of glomerular capsule
3. Inflammation of glomerular capsule and glomuli
4. Inflammation of vessel loops with spreading on glomerular capsule
5. Tubular necrosis
17. THE OUTCOME OF ACUTE GLOMERULONEPHRITIS IS:
1. Progressing to chronic
2. Chronic renal failure
3. Secondary-reduced kidney
4. Convalescence
5. True 1&4
18. THE ACUTE DIFFUSE GLOMERULONEPHRITIS DEVELOPS ON BACKGROUND OF:
1. Streptococcal infection
2. Staphylococcal infection
3. Viral infection
4. Pneumococcal infection
19. THE MORPHOLOGICAL SUBSTRATE OF
GLOMERULONEPHRITIS IS:
1. Timorous growth
2. Proliferation of vascular endothelium
3. Deposition of amyloid in glomerules
4. Formation of fibroepithelial “demilunes” in glomerules
5. Accumulation of purulent exudates in glomerules
SUBACUTE
EXTRACAPILLARY
20. AT ACUTE RENAL FAILURE IS MARKED:
1. Plethora of cortex
2. Ischemia of cortex
3. Ischemia of medullary layer
4. Plethora of medullary layer
5. All true
21. SUBACUTE GLOMERULONEPHRITIS IS APPEARED AS:
1. Intracapillary productive
2. Mesangiocapillary
3. Mesangioproliferative
4. Extracapillary productive
22. THE MAIN MORPHOLOGICAL CHANGES AT ACUTE RENAL FAILURE ARE SEEN IN:
1. Glomerule
2. Tubules
3. Vessels
4. Stroma
23. PROGRESSION OF ENDO- AND EXTRACAPILLARY CHRONIC GLOMERULONEPHRITIS
IS CONNECTED WITH:
1. Acute inflammatory process in glomerules
2. Progressive sclerosis due to deposition of plasma proteins
90
3. Coagulopathic changers in microcirculation
4. Increased proliferationof endothelial cells and mesangium
5. True2&3
24. THE STAGE OF NECROTIC NEPHROSIS IS:
1. Latent
2. Oligoanuric
3. Proteinuric
4. Edematous-hypotonic
5. Clinical appearance
25. THE MAIN MORPHOLOGICAL FEATURE OF ACUTE PYELONEPHRITIS IS:
1. Interstitial infiltration by leucocytes
2. Dystrophic changes of tubular epithelium
3. Hyperemia of juxtemedullary area of kidney
4. Hyalinosis of glomerules
26. THE MOST CHARACTERISTIC MORPHOLOGICAL
GLOMERULONEPHRITIS IS:
1. Proliferation of glomerular cells
2. Fibrinoid necrosis
3. Evident thickness of capillary basal membrane
4. Necrosis of capillary loops
FEATURE
OF
ACUTE
27. PRIMARY-REDUCED KIDNEY DEVELOPS IN OUTCOME OF:
1. Essential hypertension
2. Chronic glomerulonephritis
3. Diabetes mellitus
4. Chronic pielonephritis
5. Acute glomerulonephritis
28. WHAT OUTCOME IS CHARACTERISTIC FOR AMYLOIDOSIS:
1. Reconvalescention
2. Chronic renal failure
3. Malignisation
4. Formation of chronic pulmonary heart
5. Acute renal failure
29. EXTRACAPILLARY GLOMERULONEPHRITIS DEPENDING ON CHARACTER OF
EXUDATES CAN BE:
1. Putrefactive
2. Purulent
3. Hemorrhagic
4. Mucinouse
5. Catarrhal
30. THE TYPE OF GLOMERULONEPHRITIS DEPENDING ON DURATION IS:
1. Active
2. Persistent
3. Subacute
4. True 1&2
91
31. THE MAIN COMPLICATIONS OF ACUTE PYELONEPHRITIS ARE ALL, EXCEPT:
1. Pyonephrosis
2. Papillary necrosis
3. Carbuncle of kidney
4. Perinephritic abscess
5. Pylephlebitic abscess of liver
32. BIG BACON KIDNEY IS RESULT OF:
1. Necrosis of tubular epithelium
2. Proliferation of mesangium
3. Deposition of amyloid
4. Proliferation of podocytes and nephrothelium
5. Subendothelial deposition of electron-dense sediments
33. AT NEPHRITIC SYNDROME IS ABSENT:
1. Proteinuria
2. Hypoproteinemia
3. Dehydratation
4. Hyperlipidemia
34. GLOMERULAR INJURY CAUSED BY CIRCULATING IMMUNE COMPLEXES OCCURS IN
ALL OF THE FOLLOWING DISORDERS, EXCEPT:
1. Syphilis
2. Goodpasture's syndrome
3. Hepatitis В
4. Systemic lupus erythematosus
5. Lung cancer
35. HYALINOSIS OF GLOMERULAR APPARATUS USUALLY DOES NOT REVEALS AT:
1. Acute glomerulonephritis
2. Chronic glomerulonephritis
3. Chronic pyelonephritis
4. Arteriolonephrosclerosis
5. All listed diseases
36. GLOMERULONEPHRITIS IS DUE TO:
1. Type I hypersensitivity reaction
2. Type IV hypersensitivity reation
3. Immune complex deposition
4. Type V hypersensitivity reaction
37. WHICH IS NOT A FEATURE OF BENIGN HYPERTENSION IN KIDNEY?
1. Hyaline arteriosclerosis
2. Interstitial lobular fibrosis
3. Medial hypertrophy of small vessels
4. Fibrinoid necrosis
38. THE WORST PROGNOSIS FOR RENAL CELL CARCINOMA IS CONNECTED WITH:
1. Vascular invasion
2. Associated with hypercalcemia
3. Presence of Hematuria
4. Size more than 5 cm.
92
39. BILATERAL SYMMETRICAL CONTRACTED SCARRED KIDNEY IS SEEN IN:
1. Nephrosclerosis due to atherosclerosis of renal arteries
2. Chronic glomerulonephritis
3. End stage of renal disease
4. Chronic pyelonephritis
40. CYLINDRICAL DILATATION OF RENAL TUBULES IS SEEN IN:
1. Polycystic disease of kidney
2. Medullary cystic disease
3. Wilms tumour
4. Lipoid nephrosis
41. LIPID CAST ARE SEEN IN:
1. Acute tubular necrosis
2. Nephrotic syndrome
3. Cytomegalic inclusion disease
4. None
42. BENIGN HYPERTENSION IS ASSOCIATED WITH:
1. Hyaline arteriolosclerosis
2. Fibrinoid necrosis
3. Basal ganglia
4. Periventricle
43. THICKENING OF BASEMENT MEMBRANE OF GLOMERULI IS SEEN IN:
1. IgA nephropathy
2. Membranous proliferative glomerulonephritis
3. Lipoid nephrosis
4. Post streptococcal glomerulonephrities
44. SUB-EPITHELIAL HUMPS ARE CHARACTERISTIC OF:
1. Minimal change glomerulonephritis
2. Membranous glomerulonephritis
3. Membranoproliferative glomerulonephritis
4. Post-steptococcal glomerulonephritis
45. FOCAL GLOMERULONEPHRITIS IS CAUSED BY ALL EXCEPT
1. IgA nephropathy
2. Post streptococcal
3. Infective endocarditis
4. None
46. UREMIA OCCURS WHEN TOTAL RENAL GLOMERULAR FILTER IS REDUCED BY:
1. 25%
2. 50%
3. 60%
4. 80%
47. CLINICAL FEATURE OF CHRONIC RENAL FAILURE APPEAR WHEN RENAL
FUNCTION IS REDUCE TO:
1. 70%
93
2.50%
3. 30%
4. 20% of normal
48. ALL OF THE FOLLOWING MAY BE ASSOCIATED WITH MASSIVE PROTEINURIA
EXCEPT:
1. Amyloidosis
2. Renal vein thrombosis
3. Polycystic kidneys
4. None
49. IN AN ADULT UNILATERAL
HYPERTENSION IS SEEN IN:
1. Stenosis of renal artery
2. Chronic glomerulonephritis
3. Renal cell carcinoma
4. Pyelonephritis
SMOOTH
CONTRACTED
KIDNEY
WITH
50. CRESCENTS ARE DERIVED FROM:
1. Epithelial cells + fibrin + macrophage
2. Mesangium + fibrin + macrophage
3. Tubule + mesangiaum + fibrin
4. Mesangiaum + fibrin
51. DISEASE THAT RECURS AFTER TRANSPLANTATION OF KIDNEY IS:
1. Pyelonephritis
2. Memraneous proliferative GN
3. SLE
4. Mesangial
52. CAUSES OF NEPHROCALCINOSIS ARE ALL EXCEPT:
1. Hyperparathyroidism
2. Tuberculosis of kidney
3. Hypercalcemia
4. Glomerulonephritis
53. BILATERALLY ENLARGED KIDNEYS ARE SEEN IN1. Chronic glomerulonephritis
2. Chronic pyelonephritis
3. Benign nephrosclerosis
4. Amyloidosis
54. NEPHROTIC SYNDROME IS CHARACTERIZED BY ALL, EXCEPT:
1. Proteinuria
2. Hyperlipidemia
3. Oedema
4. Haematuria
5. Lipiduria
55. THE FACTOR LEAST LIKELY TO CAUSE ACUTE PYELONEPHRITIS IS:
1. Pregnancy
2. Nephrolithiasis
94
3. Catheterization of the bladder
4. Prostatic hypertrophy
5. Septicemia
13. ENDOCRINOLOGY
1. THE COMMON REASON OF ADDISON’S DISEASE AT DAMAGE OF ADRENALS IS:
1. Amyloidosis
2. Tuberculosis
3. Hypoplasia
4. Hyperplasia
5. Tumor
2. GOITER IS:
1. Increasing of thyroid gland
2. Increasing of parathyroid glands
3. Decreasing of thyroid gland
4. Increasing of tymus
3. LOOSING OF TEETH MEANES AVITAMINOSIS:
1. A
2. B1
3. B6
4. C
5. D
4. THE PATIENTS WITH DIFFUSE TOXIC GOITER CAN DIED FROM:
1. Heart failure
2. Acute adrenal failure
3. Liver failure
4. Adiposity
5. ITCENCO-KUSHING’S DISEASE IS CHARACTERIZED BY:
1. Diffuse adiposity
2. Hyperplasia of adrenal’s cortex
3. Hypoplasia of adrenal’s cortex
4. Hypotonia
5. Hyperfunction of ovary
6. HYPOVITAMINOSIS PP IS CHARACTERIZED BY:
1. Blood coagulation disorder
2. Hyperkeratosis and atrophy of skin
3. Loosing of teeth
4. Osteoporosis
5. Hemeralopia
7. THE TYPES OF THYROIDITIS DEPENDING ON CURRENT ARE:
1. Acute, chronic
2. Primary, secondary
3. Acute, relapsing
4. Acute, subacute, chronic
95
5. Simple, progressive, regressive
8. DUE TO NECROTIC FOCI IN HYPOPHYSIS DEVELOPS:
1. Acromegaly
2. Cerebro-hypophisal cachexia (Simmond’s disease)
3. Gigantism
4. Nannism
5. Adipose-genital dystrophy
9. THE MORPHOLOGICAL APPEARANCE OF DIABETIC MICROANGIOPATHY IS:
1. Atherosclerosis
2. Lipoidosis
3. Hyalinosis
4. Thrombosis
10. THE CHARACTERISTIC CHANGES IN PANCREAS AT DIABETES ARE:
1. Lipomatosis and sclerosis
2. Pancreonecrosis
3. Hyalinosis of stroma and fibrosis
4. Fusion by pus
5. Amyloidosis
11. THE THYROID GLAND FUNCTION AT THYROTOXIC GOITER IS:
1. Increased
2. Not changed
3. Decreased
4. True 1 & 2
12. ADULTS WITH ADENOMA FROM EOSYNOPHILIC CELLS OF FRONT HYPOPHISAL
PART ARE SUFFERED FROM:
1. Gigantism
2. Diabetes incipit
3. Acromegaly
4. Nanism
5. All true
13. THE POSSIBLE REASON OF DEATH AT DIABETES MELLITUS IS:
1. Sepsis
2. Uremia
3. Cancer of lung
4. True 1& 2
5. True 2 & 3
14. ADENOMA FROM BASOPHILIC CELLS OF FRONT HYPOPHISAL PART IS
ACCOMPANIES WITH:
1. Itcenko-Kushing disease
2. Diabetes incipit
3. Acromegaly
4. Adipose-genital dystrophy
15. CHILDREN WITH GOITER ARE SUFFERED FROM:
1. Gigantism
96
2. Cretinism
3. Acromegaly
4. Nannism
5. All true
16. THE REASON OF ENDEMIC GOITER DEVELOPMENT IS:
1. Iodine deficiency
2. Iodine prevalence
3. Potassium prevalence
4. True 1& 2
17. AT DIABETES MELLITUS THE CHANGES IN KIDNEY GLOMERULES ARE:
1. Hyalinosis and Sclerosis
2. Dystrophy and necrosis
3. Atrophy
4. Hypertrophy
18. The main biochemical appearance of hyperparathyroidism is:
1. Hypercalciuria and hyperphosphaturia
2. Increased level of sialic acid
3. Increased amount of proteins in urine
4. All true
5. Non true
19. DUE TO NECROTIC FOCI IN HYPOPHYSIS OF CHILDREN DEVELOPS:
1. Acromegaly
2. Cerebro-hypophisal (Simmond’s disease)
3. Gigantism
4. Nanism
5. Addison’s disease
20. THE DIABETES MELLITUS DEVELOPMENT IS CONNECTED WITH FUNCTIONAL
DISORDER OF:
1. Α–cells
2. Β-cells
3. D-cells
4. E-cells
5. All true
21. DEPENDING ON FUNCTION OF THYROID GLAND THE GOITER CLASSIFIED ON:
1. Euthyroid
2. Hyperthyroid
3. Hypothyroid
4. True 2 & 3
5. All true
22. THE TYPES OF GOITER BY APPEARANCE IS:
1. Nodular
2. Diffuse
3. Follicular
4. All true
5. Only 1& 2
97
23. THE MORPHOLOGICAL APPEARANCE OF DIABETIC MACROANGYOPATHY IS:
1. Plasmorrhagia
2. Atherosclerosis
3. Vasculitis
4. Calcinosis
24. THE CRANIOTABES DEVELOPMENT IS CHARACTERISTIC FOR DEFICIENCY OF
VITAMIN:
1. A
2. B1
3. B6
4. C
5. D
25. THE REASON OF SPORADIC GOITER IS:
1. Iodine deficiency
2. Iodine prevalence
3. Potassium prevalence
4. All true
5. Action of goitrogenic factors
26. THE MORPHOLOGICAL APPEARANCE OF DIABETIC MICROANGIOPATHY IS:
1. Plasmorrhagia
2. Atherosclerosis
3. Vasculitis
4. Calcinosis
5. Necrosis
27. THE REASON OF PARATHYROIDISM IS:
1. Endocrine glands disfunction
2. Adenoma of parathyroid gland
3. Hypoplasia of parathyroid apparatus
4. All true
28. HYPOVITAMINOSIS D IS CHARACTERIZED BY:
1. Hemorrhagic syndrome
2. Rickets
3. Keratomalacia
4. Disorder of hemopoiesis
5. Hyperkeratosis
29. HYPOVITAMINOSIS B12 and folic acid IS CHARACTERIZED BY:
1. Hemorrhagic syndrome
2. Rickets
3. Keratomalacia
4. Disorder of hemopoiesis and hemosiderosis
5. Hyperkeratosis and melanosis
30. HYPOVITAMINOSIS A IS CHARACTERIZED BY:
1. Hemorrhagic syndrome
2. Rickets
98
3. Keratomalacia
4. Disorder of hemopoiesis
5. Hemeralopia (day-blindness)
31. PHEOCHROMOCYTOMA DOES NOT ARISE FROM WHICH OF THE FOLLOWING1. Adrenal medulla
2. Adrenal cortex
3. Extra adrenal sites
4. Sympathetic chain
32. COMMONEST CAUSE OF RAISED SERUM CALCIUM IS —
1. Ectopic secretion
2. Parathyroid hyperplasia
3. Parathyroid adenoma
4. Parathyroid carcinoma
33. IN HASHIMOTO'S DISEASE SERUM ANTIBODIES ARE MAINLY AGAINST1. Thyroid follicles
2. Thyroxine
3. Thyroglobulins
4. Iodine
34. MEDULLARY CARCINOMA OF THYROID IS ASSOCIATED WITH INCREASE IN 1. Calcitonin
2. Thyroglobulin
3. T3
4. T4
5. true 3&4
35. DIABETES MELLITUS IS ASSOCIATED WITH ALL OF THE FOLLOWING RENAL
DISORDERS, EXCEPT:
1. Diffuse glomerulosclerosis
2. Nodular glomerulosclerosis
3. Benign nephrosclerosis
4. Urate nephropathy
5. Acute pyelonephritis
36. ALL OF THE FOLLOWING CONDITIONS PREDISPOSE TO UROLITHIASIS, EXCEPT:
1. Sickle cell nephropathy
2. Hyperparathyroidism
3. Gout
4. Proteus pyelonephritis
5. Enteric hyperoxaluria
37. THE MOST OFTEN CHANGES OF PANCREAS AT DIABETES:
1. Atrophy and sclerosis
2. Hypertrophy
3. Hyperplasia
4. Purulent inflammation
5. Necrosis
99
38. CLINICALLY, INSULIN-DEPENDENT DIABETES MELLITUS IS CHARACTERIZED BY
ALL OF THE FOLLOWING FEATURES, EXCEPT:
1. Normal or increased blood insulin level
2. Normal weight
3. Anti-islet cell antibodies in the serum
4. Ketoacidosis
5. Decreased blood insulin level
39. THE CAUSES OF MORBIDITY AND DEATH FROM DIABETES ARE THE LONG-TERM
COMPLICATIONS DEVELOPING IN ALL OF THE FOLLOWING ORGANS AND TISSUES,
EXCEPT:
1. Blood vessels
2. Kidneys
3. Liver
4. Retina
5. Nerves
40. DIABETIC NEPHROPATHY CAN LEAD TO ALL OF THE FOLLOWING PATHOLOGIC
PROCESSES, EXCEPT:
1. Nephrosclerosis
2. Hydronephrosis
3. Glomerulosclerosis
4. Tubulopathy
5. Pyelonephritis
41. DEVELOPMENT OF DIABETES IS CONNECTED WITH INFRINGEMENT OF
FOLLOWING CELLS FUNCTION:
1. Alpha
2. Betta
3. Sigma
4. Gamma
5. Delta
42. THE CLINICAL MANIFESTATIONS OF HYPERTHYROIDISM INCLUDE ALL OF THE
FOLLOWING SYMPTOMS, EXCEPT:
1. Skin striae
2. Tremor
3. Exophthalmos
4. Tachycardia
5. Hypertrophy of myocardium
43. FUNCTION OF THYROID GLAND AT THYROTOXIC GOITER:
1. Increased
2. Didn’t change
3. Decreased
4. Absent
5. Perverted
44. LONG EXISTENCE OF ENDEMIC GOITER AT ADULTS RESULTS IN:
1. Basedowism
2. Carcinoma
3. Cushing’s syndrome
100
4. Simond’s disease
5. Addison’s disease
45. BACK LOBE OF HYPOPHYSIS INJURY RESULTS IN:
1. Itcenco-Kushing’s disease
2. Diabetes insipidus
3. Acromegalia
4. Mixedema
5. Adiposogenital dystrophy
46. SECONDARY HYPERTENSION IS FOUND IN ALL OF THE FOLLOWING ENDOCRINE
DISORDERS, EXCEPT:
1. Cushing's syndrome
2. Pheochromocytoma
3. Adrenal medullary hyperplasia
4. Addison's disease
5. Conn's syndrome
47. THE SKIN PIGMENTATION IN BRONZE DIABETES IS DUE TO1. Hemosiderin
2. Lipofuscin
3. Melanin
4. Both melanine & hemosiderin
14. FEMALE GENITAL TRACT PATHOLOGY. PREGNANCY PATHOLOGY.
1. MACROSCOPICAL CHARACTERISTIC OF UTERUS AT SEPTIC ENDOMETRITIS IS:
1. Increased in sizes, flabby
2. Endometrium is impregnated with pus
3. Depositions of fibrin on serous environment
4. Endometrial veins occluded by thrombi
5. True 1&3
2. THE MOST PROBABLE REASON OF SPONTANEOUS ABORTIONS IS:
1. Cyst of corpus luteum in ovary
2. Aplasia of ovary
3. Transferred earlier acute purulent endometritis
4. Impassability of fallopian tubs
5. All true
3. BIOLOGICAL FACTOR WITH GREATEST TERATOGENIOUS EFFECT IS:
1. Bacteria
2. Viruses
3. Parasites
4. Fungi
5. Rikketsia
4. AT UTEROGENOUS SEPSIS PRIMARY METASTATIC ABSCESSES APPEAR IN:
1. Liver
101
2.
3.
4.
5.
Lung
Ovary
Brain
Kidney
5. CONDITIONS FOR ECTOPIC PREGNANCY DEVELOPMENT ARE:
1. Hypoplasia of tubs
2. Tumors of tube
3. Salpingooforitis
4. All is true
5. True 2 and 3
6.
HISTOLOGICALLY
GLANDULAR
ENDOMETRIAL
HYPERPLASIA
CHARACTERIZED BY:
1. Distinct division of endometrium on compact and spongious layers
2. The expressed polymorphism of endometrial glandular epithelium
3. Hyperplastic condition of uterus mucous membrane with attributes of glandular
epithelium hyperactivity
4. Papillary proliferation of glandular epithelium
5. Impregnation of endometrium by pus
IS
7. THE DIAGNOSIS OF ATYPICAL ENDOMETRIAL HYPERPLASIA IS BASED ON:
1. Expressed atrophy of glands in combination with increased proliferative activity of glandular
epithelium in parts of glands
2. Expressed proliferation of glands with change of their figure (" gland-into-gland ") and
occurrence of papillary structures
3. Tumoral polymorphism in single epithelial cells
4. Hormonal proliferation of glandular epithelium with thickness of endometrium
5. All true
8. DEVELOPMENT OF LACTATION MASTITIS IS PROMOTED BY:
1. Lactostasis
2. Cracks of
3. Decreasing of immune protection of organism
4. All true
5. All wrong
9. CAMBIAL FUNCTION IN CERVICAL PART UTERUS CERVIX IS CARRIED OUT BY:
1. Stromal cells
2. Epithelial cells
3. Reserve cells
4. Lymphocytes
5. All true
10. HYDATID (VESICULAR) MOLE IS THE FORM OF:
1. Toxicosis of pregnancy
2. Throphoblastic diseases
3. Noncarrying pregnancy syndrome
4. Ectopic pregnancy
5. All true
102
11. DISORDERS OF ESTROGENIC HORMONES SECRETION
ENDOMETRIUM:
1. Secretory transformations of glandular epithelium
2. Focal plasma cellular perivascular infiltration
3. Structure of endometrium according to proliferative phase
4. Atrophy of endometrium
5. All true
CAUSE
IN
12. MACROSCOPICALLY UTERUS BODY CANCER CAN LOOK LIKE:
1. "Cauliflower"
2. Exophytic growth
3. Polyp on the wide basis
4. Endophytic growth
5. All true
13. CURETTAGE OF UTERINE CAVITY AT ECTOPIC PREGNANCY IS CHARACTERIZED
BY PRESENCE OF:
1. Normal endomertium in proliferative phase
2. Decidual tissue and chorionic villes
3. Decidual tissue and absence of chorionic villes
4. Normal endomertium in secretion phase
5. All true
14. MOST FREQUENTLY ENDOMETRIOSIS OF UTERUS CERVIX MEETS AFTER:
1. Abortions
2. Diathermic coagulation of uterus cervix
3. Gysterosalpingographia
4. True 1 &3
5. All true
15. VARIANT OF LEIOMYOMA DEPENDING ON LOCALIZATION IN UTERUS WALL IS:
1. Nodular
2. Subtotal
3. Submucosal
4. Transmural
5. Diffuse
16. SOURCE OF INFECTION AT POSTNATAL MASTITIS IS:
1. Microbial flora from pharynx and nose of newborn
2. Focus of infection in mother organism
3. Infringement of sanitary-and-epidemiologic order
4. True 2 & 3
5. All true
17. TRUE EROSION OF UTERUS CERVIX IS CHARACTERIZED AS:
1. Increasing of cellular elements differentiation with the tendency to keratinization of
squamous epithelium
2. Destruction of epithelium with inflammatory infiltration of subjunctive tissue
3. Proliferation of reserve cells
4. Presence of endometrial glands in ectocervix
5. All true
103
18. THE KRUKENBERG’S TUMOR REPRESENTS:
1. Tumor from stroma of sexual band
2. Metastasis of stomach cancer in ovary
3. Metastasis of uterus cancer in ovary
4. Metastasis of lung cancer
5. Metastasis of stomach cancer in the liver
19. MORPHOLOGICAL FEATURES OF VULVA CONDILOMA ARE:
1. Papillomatosis, acantosis and hyperkeraosis
2. Papillomatosis, acantosis, pararkeratosis and inflammation of stroma
3. Dysplasia of epithelium with hyperkeratosis
4. All true
5. All wrong
20. THE MOST COMMON MORPHOLOGICAL VARIANT OF BREAST CANCER IS:
1. Invasive canalicular cancer
2. Invasive lobular cancer
3. Medullary cancer
4. Colloid cancer
5. Noninvasive canalicular cancer
21. MAJORITY OF ECTOPIC PREGNANCY CASES ARE:
1. Ovarial
2. Cervical
3. Tubal
4. Abdominal
5. Thoracic
22. THE MOST COMMON HISTOLOGICAL VARIANT OF ENDOMETRIAL CANCER IS:
1. Adenocarcinoma
2. Squamous cancer
3. Transition-cellular cancer
4. Light-cellular cancer
5. Choriocarcinoma
23. ENDOMETRIOSIS IS:
1. Dishormonal hyperplasia of ectopic endometrium
2. Presence of endometrial glands or stroma in abnormal location outside of uterus
3. Benign growth of tissue morphologically and functionally similar to
endometrium
4. Inflammation of endometrium
5. All true
24. CHANGES IN ENDOMETRIUM, WHICH CAN BE REFEREED TO PROGESTIN PHASE OF
MENSTRUAL CYCLE, ARE:
1. Acinar glands from light secretional epithelium
2. Glands from dark non-secretional epithelium with hyperchromic extended many-layer
located nucleus
3. Decidual-like transformation of stromal cells
4. All true
5. True 1 and 3
104
25. CHORIONEPITHELIOMA CAN BE SUSPECTED IF IN CURETTAGE OF UTERINE
CAVITY BECOME EVIDENT:
1. Presence of chorionic villi and growth of throphoblast
2. Absence of chorionic villi and growth of throphoblast
3. Presence of Aryas-Stell’s reaction in endometrial glands
4. Absence of endometrial decidual reaction
5. All true
26. FIBROCYSTIC DISEASE OF BREAST IS:
1. Sclerosing adenosis
2. Intracanalicular fibroadenoma
3. Pericanalicular fibroadenoma
4. Peget disease
5. Cystadenoma of breast
27. CHARACTERISTIC OF ESTROGENIC PHASE CHANGES IN ENDOMETRIUM IS:
1. Presence of tubular glands from dark non-secretional epithelium
2. Presence of spiral vessels balls
3. Edema of cellular stroma
4. True 1and 2
5. True 1and 3
28. MACROSCOPICALLY VESICULAR MOLE LOOKS AS:
1. Cyst cavity
2. Dense polycystic node
3. Grapes-like congestions of numerous babbles
4. Spongy structure formation
5. All true
29. DYSPLASIA OF UTERUS CERVIX MUCOUS IS:
1. Presence of glandular structures in ectocervix
2. Increased proliferation of ectocervix cellular elements without their tendencies to maturation
3. Increased differentiation of cellular elements with tendency to keratinization of squamous cells
epithelium
4. Replacement of squamoused epithelium on cylindrical
5. All true
30. MACROSCOPICALLY CANCER OF UTERUS CERVIX LOOKS LIKE AS:
1. "Cauliflower"
2. Exsophytic growth
3. Polyp on wide basis
4. Dark-red colored spongy tissue
5. True 1and 2
31. ATTRIBUTE OF UTERINE PREGNANCY IN CURETTAGE FROM
UTERINE CAVITY IS:
1. Division of endometrium on compact and spongy layers
2. Presence of great number of vessels
3. Presence of throphoblast
4. Absence chorionic villi
5. All true
105
32. INFLAMMATORY DISEASE OF UTERUS MUCOUS MEMBRANE IS TERMED AS:
1. Ectropion
2. Endometritis
3. Salpingoophoritis
4. Glandular hyperplasia of endometrium
5. Fibroadenoma
33. DISHORMONAL CONDITIONS OF UTERUS MUCOUS MEMBRANE ARE
CHARACTERIZED BY:
1. Presence of structures from one of menstrual cycle phases according to must observed in
norm
2. Attributes of atrophy and cystical changes of endometrial glands
3. Massive round-cellular infiltration of stroma
4. True 1&2
5. All true
34. THE MOST OFTEN REASON OF ENDOMETRITIS DEVELOPMENT IS:
1. Infringement of blood circulation in uterus
2. Hormonal disorders
3. Disregeneration
4. Tumor growth
5. Entry of infection in uterine cavity
35. FOR SIMPLE GLANDULAR ENDOMETRIAL HYPERPLASIA IS CHARACTERISTIC:
1. Division of endometrium on compact and spongiest layers
2. Expressed polymorphism of glandular epithelium
3. Uterus mucous membrane hyperplasia with corkscrew- twisted glands
4. Presence of papillary proliferation in glandular epithelium
5. Presence of decidual tissue
36. VESICULAR MOLE IS CHARACTERIZED BY MORPHOLOGICAL ATTRIBUTES:
1. Presence of large vessels less villes
2. Absence of chorion villes
3. Proliferation of endometrial basal layer
4. Hyperplasia of endometrial glands
5. Atrophy of uterus mucous
37. SIMPLE LEUCOPLACIA OF UTERUS CERVIX IS CHARACTERIZED BY:
1. Presence of immature forms of epithelium
2. The tendency of epithelium to keratization
3. Presence of glandular structures
4. Presence of papillary structures
5. Presence ofcysts filled with slime
38. CONDITIONS LEADING TO ENDOMETRIAL HYPERPLASIA INCLUDE ALL, EXCEPT:
1. Polycystic ovarian disease
2. Functioning granulosa cell tumors of the ovary
1. Excessive ovarian cortical function (cortical stroma hyperplasia)
4. Endometriosis
5. Estrogens replacement therapy
39. ALL STATEMENTS CONCERNING LEIOMYOMAS ARE TRUE, EXCEPT:
106
1.
2.
3.
4.
5.
They regress or calcify after castration or menopause
They do not responds to estrogens
They may undergo rapid increase in size during pregnancy
Their cause is unknown
They are found in 25% of reproductive women
40. ATTRIBUTES OF UTERINE PREGNANCY IN SCRAPE FROM UTERINE CAVITY:
1. Decidual reaction
2. Presence a lot of vessels
3. Presence invasive trophoblast
4. Absence of chorion villous
5. Hyperplasia of endometrial basal layer
15. VIRAL & CHILDREN DISEASES
1. TO THE GROUP OF ARVI IS REFEREED:
1. Chicken pox
2. Meningococcal infection
3. Shigellosis
4. Flue
5. Measles
2. MORPHOLOGICAL CHANGES IN LUNGS AT HEAVY TOXIC TYPES OF FLUE IS:
1. Foci of caseouse necrosis
2. Foci of purulent inflammation and panbronchitis
3. Massive diapedetic hemorrhages
4. Vasculitis
5. Granulomatouse inflammation
3. RESPIRATORY SYNCYTIAL INFECTION AFFECTING:
1. Upper respiratory tract
2. Low respiratory tract
3. Urinary tract
4. Gastro-intestinal tract
4. THE MACROSCOPICAL DAMAGE OF BRAIN AT VIRAL INFECTIONS IS:
1. Edema, swelling and hemorrhages
2. Cyst with rusty walls
3. Hydrocephalus
4. Dystrophy and necrosis
5. Purulent infiltration of meningei
5. THE MICROSCOPICAL CHANGES IN LUNGS AT CROUPOUS PNEUMONIA ARE:
1. Serous exudates in lumens of alveoli
2. Purulent exudates with formation of micro-abscesses
3. Athelectases
4. Carnification
5. Fibrinous-purulent exudates in alveolar space
6. THE MAIN PATHWAY OF FLUE TRANSMISSION IS:
107
1. Alimentary
2. Parenteral
3. Aero-droplet
4. Genital
5. All
7. THE VARIANT OF HERPES INFECTION OF CNS IS:
1. Diffuse purulent meningitis
2. Purulent meningitis
3. Acute necrotizating encephalitis
4. Fibrinous encephalitis
5. Purulent encephalitis
8. THE SYNONYM OF ACUTE INTERSTITIAL PNEUMONIA IS:
1. Desquamational pneumonia
2. Acute bronchiolitis
3. Acute fibrosating alveolitis
4. Obstructive bronhiolitis with carnificative pneumonia
5. Respiratory distress-syndrome of adults
9. THE PNEUMONIA CAUSED BY STAPHILLOCOCCUS AS A RULE IS:
1. Catarrhal
2. Croupouse
3. Serous-hemorrhagic
4. Purulent
5. Interstitial
10. MODERATE TYPE OF FLUE IS CHARACTERIZED BY INFLAMMATION IN TRACHEA
AND BRONCHI:
1. Catarrhal
2. Serouse-hemorrhagic
3. Purulent-hemorrhagic
4. Croupouse
5. Diphteric
11. THE HEAVY TYPE OF FLUE WITH PULMONARY COMPLICATIONS DEVELOPMENT
IS CONNECTED WITH:
1. Specific pneumotropism of virus
2. Connection of bacterial flora
3. Evident vasoparalitic action of virus
4. Athelectasis and respiratory insufficiency
5. Bronchial obstruction
12. THE MOST CHARACTERISTIC APPEARANCE OF TYPHUS FEVER IS:
1. Enteritis
2. Colitis
3. Myositis
4. Vasculitis
13. ONE OF THE VARIANTS OF HEAVY TYPE OF FLUE IS:
1. Toxic
2. Neuropathic
108
3. With complications on heart
4. Hyperergic
5. Nephropathic
14. THE FAVORITE LOCALIZATION OF TYPHUS FEVER GRANULOMAS IS:
1. Liver
2. Spleen
3. CNS
4. Bone marrow
15. IT IS CHARACTERISTIC FOR SLIGHT TYPE OF FLU:
1. Serous laringo-tracheitis
2. Serous-hemorrhagic pneumonia
3. Purulent panbronchitis
4. Productive pneumonitis
5. Serous nasopharingitis
16. THE FAVORABLE PATHWAY OF VIRAL HEPATITIS B TRANSMISSION IS:
1. Alimentary
2. Parenteral
3. Aerogenic
4. Genital
5. All
17. TRANSMISSION OF TYPHUS IS PROVIDING BY:
1. Ticks bite
2. Louse feces
3. Mosquitoes bite
4. Fly bite
5. Animal’s bite
18. THE SEVERE TOXIC TYPE OF FLUE IS CHARACTERIZED BY DEVELOPMENT OF:
1. Pneumosclerosis
2. Plural hemorrhages
3. Brain abscess
4. Spleen infarction
5. Fibrinouse pericarditis
19. TO GROUP OF ACUTE RESPIRATORY VIRAL INFECTIONS IS NOT REFEREED:
1. Paraflue
2. Adeno-viral infection
3. Rubeola
4. Flue
5. Respiratory-syncytial infection
20. THE MODERATE FORM OF FLUE IS CHARACTERIZED BY INFLAMMATION IN
TRACHEA:
1. Catarrhal
2. Serous-hemorrhagic
3. Purulent-hemorrhagic
4. Croupouse
5. Diphteric
109
21. HIV HAS TROPISM TO THE NEXT CELLS:
1. Cd8+t-cells
2. Cd4+t-cells
3. Nk-cells
4. Dendritic cells
5. Granulocytes
22. TYFUS GRANULOMA BY AUTHOR IS NAMED AS:
1. Virchov’s
2. Miculitch
3. Berezovsky
4. Popov’s
5. Pirogov’s
23. THE TRANSMISSION PATHWAY OF HAV-INFECTION IS:
1. Alimentary
2. Parenteral
3. Aerogenic
4. Genital
5. Insect bite
24. SECONDARY BACTERIAL SUPERINFECTION AT FLU IS LEAD TO:
1. Inflammation become hemorrhagic
2. Development of extrapulmonary complications
3. Development of purulent meningitis and encephalitis
4. Inflammation becomes purulent with massive destruction of pulmonary tissue
5. Development of hemorrhages and hemorrhagic infarctions
25. PROBABLE DIAGNOSIS AT
PNEUMOCYSTIC PNEUMONIA:
1. Sogren diseas
2. Heavy combined immunodefficiency
3. Gudpascher syndrome
4. Isolated deficiency ig a
5. AIDS
THE
PATIENT
WITH
LYMPHOPENIA
AND
26. TO DNA-VIRUS REFEREES HEPATITIS VIRUS:
1. A
2. B
3. C
4. D
5. E
27. HIV IS NOT ASSOSIATED WITH:
1. Pneumocystic oneumonia
2. Kuru
3. T-cell leukemia
4. Kaposi's sarcoma
28. BIG MOTLEY LUNG IS TYPICAL FOR:
1. Viral hepatitis
110
2. Grippe
3. Herpes
4. Viral parotitis
5. Viral papillomatosis
29. THE MOST TYPICAL CHANGES IN TRACHEA AND LARGE BRONCHIAL TUBES AT
TOXIC FORM OF FLU IS:
1. Serous-hemorrhagic inflammation
2. Necrotic process
3. Granulematous inflammation
4. Purulent inflammation
5. Fibrinous inflammation
30. THE TRANSMISSION PATHWAY OF RABIES IS:
1. Alimentary
2. Sec animal bite
3. Aerogenic
4. Genital
5. Insect bite
31. INFLAMMATION OF RESPIRATORY TRACT MUCOUS MEMBRANE AT NOT
COMPLICATED MEASLES HAS CHARACTER:
1. Purulent
2. Necrotic
3. Fibrinous
4. Catarrhal
5. Hemorrhegic
32. MEASLES EXANTEMA IS FINISHED BY:
1. Macrolamellar peeling
2. Scaly peeling
3. Focal hyperpigmentation
4. Focal leicoderma
5. Complete disappearance
33. USUAL WAY OF INFECTION AT MEASLES IS:
1. Alimentary
2. Parenteral
3. Air - drop
4. Hematogenic
5. Transmissive
34. BELSKY -KOPLIC-FYLATOV’S MACULES ARE FOUND OUT AT MEASLES ON:
1. Palms and stops
2. Extensor surfaces of forearm
3. Tongue
4. Internal surface of cheeks
5. Head
35. BRONCHIAL INFLAMMATION AT COMPLICATED MEASLES HAS CHARACTER:
1. Granulematous
2. Purulent-necroyic
111
3. Catarrhal
4. Serous
5. hemorrhagic
36. CHARACTER OF EXUDATES AT MENINGOCOCCAL MENINGITIS IS:
1. Putrefactive
2. Hemorrhagic
3. fibrinous
4. Purulent
5. Fibrinous-hemorrhagic
37. USUAL COMPLICATION OF MENINGOCOCCAL MENINGITIS IS:
1. Cyst of brain
2. Tumor of brain
3. Hemorrhagic infarction of brain
4. Hydrocephalus
5. Glial scar
38. AT MENINGOCOCCAL MENINDITIS TYPICAL INFLAMMATION IS:
1. Hemorrhagic
2. Catarrhal
3. Productive
4. Purulent
5. Granulomatous
39. IN ENTRY OF DIPHTHERIA INFECTION INFLAMMATION HAS CHARACTER:
1. Purulent
2. Fibrinous
3. Productive
4. Hemarrhagic
5. Putrefactive
40. THE MOST SENSITIVE TO DIPHTERITIC TOXIN ARE:
1. Adrenal glands
2. Lungs
3. Liver
4. Spleen
5. Intestines
41. RASH AT SCARLET FEVER IS:
1. Macromacular
2. Punctate
3. Roseola-papular
4. Vesicular
5. Hemorrhagic
42. TYPICAL LOCALIZATION OF LOCAL CHANGES AT SCARLET FEVER IS:
1. Mucous of oral cavity
2. Skin
3. Conjunctive of an eye
4. Mucous of genital tracts
5. Mucous of esophagus
112
43. SCARLET FEVER IS CAUSED BY:
1. Diplococcus
2. Escherichia coli
3. Streptococcus of type A
4. Alpha- hemolytic streptococcus
5. Staphilococcus
44. IN REGIONAL LYMPHATIC NODES AT SCARLET FEVER DEVELOPS:
1. Necrosis
2. Anemia
3. Sclerosis
4. Hypoplasia
5. Atrophy
16. BACTERIAL INFECTIONS
1. FOR TYPHOID FEVER THE MOST TYPICAL IS:
1. Fibrinous colitis
2. Diphteric inflammation of intestine
3. Ulceral colitis
4. Medullary swelling of Peyer’s patches with ulceration in ileum
5. Catarrhal enterocolitis1
2. THE TERM “DYSENTERY” REFERS TO DIARRHEA ASSOCIATED WITH ALL OF THE
FOLLOWING SYMPTOMS, EXCEPT:
1. Abdominal cramping
2. Tenesmus
3. Stools containing blood
4. “Rice-water” stools
5. Stools containing pus and mucus
3. SHIGELLAE CAUSE ALL OF THE PATHOLOGIC PROCESS, EXCEPT:
1. Hemorrhagic colitis
2. Hemolitic-uremic syndrome
3. Damage of endothelial cells in the colon microvasculature
4. Acute tubular necrosis
5. Stools containing blood, pus and mucus
4. THE INVASIVE PROPERTIES OF BACTERIA IN INTESTINAL INFECTION INCLUDE
THE ABILITY TO DO ALL OF THE FOLLOWING, EXCEPT:
1.Adhere to the mucosal epithelial cells
2.Replicate in the mucosal epithelial cells
3.Synthesize serotonin
4.Elaborate enterotoxins
5.Invade mucosal epithelial cells
5. CHARACTERISTIC MORPHOLOGICAL ATTRIBUTE OF CHOLERA IS:
1. Follicular colitis
2. Medullary swelling of ileum group follicles
3. Serous-hemorrhagic enteritis, gastritis
4. Fibrinous colitis
113
5. Ulceral colitis with purulent exudates
6. THE COMPLICATIONS OF SEVERE BACTERIAL ENTEROCOLITIS ARE ALL OF THE
FOLLOWING, EXCEPT:
1. Massive fluid loss (dehydration)
2. Destruction of the intestinal mucosal barrier
3. Perforation of the intestinal wall
4. Generalization of infection (sepsis)
5. Intestinal stenosis
7. TYPHOID ULCER IS:
1. Ulceration of the Peyer's pathch
2. Longitudinal ulcer
3. May perforate
4. Stricture is rare
5. All of the above
8. ULCERATION OF PEYER'S PATCHES OCCUR IN WHICH INFECTION:
1. Amoebiasis
2. Crohn's
3. Salmonella
4. Clostridium
9. POSSIBLE REASON OF DEATH OF PATIENTS AT FLU WITH SEVERE INTOXICATION
IS:
1. Asphyxia
2. Liver failure
3. Acute liver failure
4. Uremia
5. Hemorrhages in brain vital centers
10. CHANGES IN PEYER'S PATCHES OF SMALL INTESTINE AT TYPHOID FEVER ARE:
1. Fibrinous enteritis
2. Mucoid degeneration
3. Medullary swelling
4. Murder swelling
5. Ulceral enteritis
17. TUBERCULOSIS. SYPHILIS.
1. MORPHOLOGICAL APPEARANCE OF PRIMARY TUBERCULOSIS:
1. Caseous pneumonia
2. Primary tuberculous complex
3. Caseouse lymphadenitis
4. Primary cavern
5. Primary affect
2. HUTCHINSON’S TRIAD IS CHARACTERISTIC FOR:
1. Sepsis
2. Scarlet fevers
3. Syphilis
114
4. Typhus
5. AIDS
3. INFECTION AGENT OF SYPHILIS IS:
1. Shigella
2. Lamblia
3. Listeria
4. Corynobacterium
5. Threponema Pallidum
4. THE BASIC COMPONENT OF PRIMARY INFECTIOUS COMPLEX AT SYPHILIS IS:
1. Bubo
2. Chancre
3. Vesicles
4. Carbuncul
5. Phlyctena
5. THE MOST OFTEN COMPLICATION OF SYPHILITIC MESAORTITIS IS:
1. Ulceration
2. Sclerosis
3. Aneurysm
4. Petrification
5. Plasmorrhagia
6. SYPHILITIC MESAORTITIS DEVELOPS AT:
1. Primary syphilis
2. Secondary
3. Tertiary
4. Early congenital
5. Late congenital
7. GHONS’ FOCUS IS:
1. The center of fibrosis
2. The center of caseous
3. The center of haemorrhage
4. The center of primary affect calcification
5. The center of incapsulated pneumonia
8. PRIMARY TUBERCULOSIS IS A RESULT OF:
1. Infection
2. Reinfection
3. Hematogenic dissemination
4. Food intoxication
5. Chronic bronchitis
9. ТUBERCULOMA IS CHARACTERISTIC FOR:
1. Primary pulmonary tuberculosis
2. Primary with hematogenic dissimination
3. Hematogenic pulmonary tuberculosis
4. Hematogenic tuberculosis of bones and joints
5. Secondary pulmonary tuberculosis
115
10. TUBERCULOSIS OF LUNGS IS CAUSED BY:
1. Pneumococcus
2. Carynobacterium
3. Mycobacterium
4. Blue pus bacillus
5. Streptococcus
11. THE CONDITION IN WHICH THE LUNG HAS MULTIPLE TUBERCULOUS
GRANULOMAS IS CALLED AS:
1. Tuberculous pneumonia
2. Brown induration of the lungs
3. Miliary tuberculosis
4. Cavitary fibrocaseous tuberculosis
5. Tuberculoma
12. TUBERCULIN TEST POSITIVISM INDICATES 1. Good humoral immunity
2. Infection with mycobacterium
3. Good cell mediated immunity
4. None
5. True 1&3
13. ROUTE OF INFECTION IN TUBERCULAR PYELONEPHRITIS 1. Ascending
2. Descending
3. Haemotogenous
4. Airborn
5. Intracanalicular
14. MICROORGANISMS CAN ESCAPE THE IMMUNE SYSTEM BY ALL OF THE
FOLLOWING WAYS, EXCEPT:
1. Immune tolerance
2. Resistance to complement-mediated lysis and phagocytosis
3. Variation or shedding of antigens
4. Increasing vascular permeability
5. Immunosuppression
15. PRIMARY COMPLEX AT TUBERCULOSIS MAY DIRECTLY TRANSFORM INTO ALL
PATHOLOGIC CONDITIONS, EXCEPT:
1. Fibrocalcific scars
2. Latent pulmonary lesions
3. Miliary tuberculosis
4. Latent extrapulmonary lesions
5. Progressive primary tuberculosis
16. FAVORED TARGETS FOR MILIARY
TUBERCULOSIS ARE ALL ORGANS, EXCEPT:
1. Bone marrow
2. Kidneys
3. Liver
4. Uterus
5. Spleen
EXTRAPULMONARY
SEEDING
AT
116
17.
A CALCIFIED FOCUS (FIBROCALCIFIC SCAR) FORMING IN THE LUNG
PARENCHYMA AFTER SECONDARY TUBERCULOSIS INFECTION IS REFERRED TO AS:
1. Keloid
2. Granuloma
3. Ghon focus
4. Aschoff-Pule focus
5. Simon focus
18. THE MOST COMMON SITES OF SKELETAL TUBERCULOSIS INVOLVEMENT ARE
ALL OF THE FOLLOWING, EXCEPT:
1. Skull bones
2. Thoracic vertebrae
3. Lumbar vertebrae
4. Knees
5. Hips
19. THE INTESTINE MAY BE AFFECTED AT WHICH OF THE FOLLOWING FORMS OF
TUBERCULOSIS:
1. Secondary
2. Cavitary flbrocaseous
3. Dormant
4. Primary complex
5. Miliary
20. PATHOLOGIC CHANGES OF VASA VASORUM AT SYPHILITIC MESAORTITIS
ARE CALLED:
1. Migratory thrombophlebitis
2. Productive vasculitis (obliterative endarteritis)
3. Thromboangitis obliterance
4. Necrotising arteriolitis
5. Thrombotic microangiophathy
21. THE TYPE OF IMMUNE RESPONSE INITIATED AT TUBERCULOSIS IS:
1. Direct cell cytotoxicity reaction mediated by CD4+ T cells
2. Delayed-type hypersensitivity reaction mediated by CD4+T cells
3. Complement-dependent reaction
4. Antibody-mediated cellular dysfunction
5. Antibody-dependent cell-mediated cytotoxicity
22. THE TYPE OF NECROSIS THAT CAN BE FOUND IN TUBERCULOUS GRANULOMA
IS:
1.Coagulative
2. Liquefactive
3. Caseous
4. Enzymatic fat
5. Fibrinoid
23. MILIARY TUBERCULOSIS IS ASSOCIATED WITH:
1. Reinfection
2. Lung caseation
3. Lymph node caseation
117
4. Primary infection
5. Hematogenous tuberculosis
24. SECONDARY TUBERCULOSIS IS CHARACTERIZED BY ALL FEATURES, EXCEPT:
1. Caseous necrosis and cavities in lungs
2. Primary focus in the lung
3. Reinfection focus
4. Reactivation of dormant disease
5. Dystrophic calcified foci
25. TUBERCULOUS SPONDILITIS WITH INVOLVEMENT OF INTERVERTEBRAL DISCS
AND SOFT TISSUES WITH COLD ABSCESSES FORMATION IS REFERRED TO AS:
1. Paget's disease
2. Pott disease
3. Gohn complex
4. Reinfection focus
5. Dormant disease
26. CASEATING DESTRUCTIVE SECONDARY TUBERCULOSIS INCLUDES ALL,
EXCEPT:
1. Lung caseation
2. Lung cavities
3. Lung lymph node caseation
4. Miliary extrapulmonary lesions
5. Extrapulmonary caseation
27. SYPHILITIC GRANULOMA IS ALSO CALLED:
1. Fibroma
2. Gumma
3. Tuberculoma
4. Leproma
5. Hepatoma
28. MEDIAL DESTRUCTION OF AORTA AT TERTIARY SYPHILIS MAY LEAD TO THE
FOLLOWING COMPLICATION:
1. Aneurismal dilation of aorta
2. Marfan's syndrome
3. Atherosclerotic aneurism
4. Takayasu artritis
5. Giant cell arteritis
29. MYCOBACTERIUM TUBERCULOSIS IS CHARACTERIZED BY ALL FEATURES,
EXCEPT:
1. Pili-forming
2. Aerobic
3. Non-spore-forming
4. Nonmotile
5. Red colored in acid-fast staining
30. THE CAVITY AT CAVITARY FIBROCASEOUS TUBERCULOSIS IS CHARACTERIZED
BY ALL FEATURES, EXCEPT:
1. Localized in the apex of the lung
118
2.
3.
4.
5.
Lined by yellow-grey caseous material
Walled by fibrous tissue
Drained by bronchus
Filled with suppurative exudate
31. THE LIVER MAY BE AFFECTED IN WHICH FORM OF TUBERCULOSIS:
1. Secondary
2. Cavitary fibrocaseous
3. Dormant
4. Primary complex
5. Miliary
32. THE POSSIBLE CAUSES OF CHRONICITY OF INFLAMMATION AT TUBERCULOSIS
ARE ALL OF THE FOLLOWING, EXCEPT:
1. Persistence of certain microorganisms
2. Prolonged exposure to toxic agents
3. Incomplete phagocytosis
4. Complete phagocytosis
5. Resistance of etiologic agent
33. On gross inspection, syphilitic gumma is characterized by all features, EXCEPT:
1. Sharply defined
2. Rubbery
3. Solitary
4. Red-brown
5. Tumor-like
34. MILIARY LUNG
INFLAMMATION:
1. Hemorrhagic
2. Fibrinous
3. Granulomatous
4. Serous
5. Suppurative
TUBERCULOSIS
IS
CHARACTERIZED
BY
TYPE
OF
35. SEVERE DESTRUCTION OF VERTEBRAE AT TUBERCULOUS SPONDILITIS MAY
RESULT IN ALL PATHOLOGICCONDITIONS, EXCEPT:
1. Permanent compression fractures
2. Scoliotic deformities
3. Drainage tract (sequestrum) formation
4. Kyphotic deformities
5. Neurologic defects
36. TUBERCULOMA IS MACROSCOPICALLY CHARACTERIZED BY ALL FEATURES,
EXCEPT:
1. Intraparenchymal single mass
2. Greyish-white
3. Well-circumscribed
4. Several centimeters in diameter
5. Several millimeters in diameter
37. TYPICAL SYPHILIS GRANULOMA IS CHARACTERIZED BY ALL FEATURES, EXCEPT:
119
1.
2.
3.
4.
5.
Area of central necrosis
Plasma cell infiltrate
Lymphocyte infiltrate
Productive vasculitis
Platelet infiltrate
38. Healed lesions in primary tuberculosis include all EXCEPT:
1. Fibrous incapsulation
2. Assmann's focus
3. Fibrocalcific scar
4. Foci of ossification
5. Focal pleural adhesions
39. FAVORED PATHOLOGIC CONDITIONS FOR GROWTH AND MULTIPLICATION OF
THE TUBERCULOUSE BACILLI AT CAVITARY FIBROCASEOUS TUBERCULOSIS ARE:
1. Lymphatic drainage obstruction
2. Progressive hypoxia
3. Increased perfusion
4. Increased oxygen tension
5. Sludging of blood in alveolar capillaries
40. COMPLICATIONS OF TUBERCULOUS OSTEOMYELITIS ARE ALL, EXCEPT:
1. Tuberculous arthritis
2. Sinus tract formation
3. Cold abscess formation
4. Caseation in the lung
5. Amyloidosis
41. TUBERCULOUS SALPINGITIS CAN BE FOUND IN WHICH OF THE FOLLOWING
FORMS OF TUBERCULOSIS:
1. Secondary
2. Cavitary fibrocaseous
3. Dormant disease
4. Miliary
5. Primary
42. GUMMOUS INFILTRATE AT TERTIARY SYPHILIS CAN BE FOUND IN:
1. Aorta
2. Testes
3. Liver
4. Bones and joints
5. Skin and subcutaneous tissue
18. SEPSIS
1. TYPE OF SEPSIS THAT CHARACTERIZED BY ABSCESS DEVELOPMENT IS:
1. Septicemia
2. Septicopiemia
3. Chroniosepsis
4. Septic endocarditis
5. Cryptogenic sepsis
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2. EMBOLIC PYOGENIC NEPHRITIS IS MOST COMMONLY CAUSED BY WHICH OF THE
FOLLOWING FACTORS:
1. Thromboembolism
3. Viral embolism
4. Acute tubular necrosis
5. Bacterial embolism
3. COMMON HISTOLOGICAL FINDINGS IN PYOGENIC LEPTOMENINGITIS INCLUDE
ALL, EXCEPT:
1. Neutrophil infiltration of the leptomeninges
2. Neutrophii deposition in the subarachnoidal space
3. Engorged blood vessels
4. Pyemic abscesses in the cerebral tissue
5. Edema of the cerebral tissue
4. FORM OF SEPSIS THAT CAN BE FOLLOW WITH AMYLOIDOSIS IS:
1. Septicemia
2. Septicopyemia
3. Chronic sepsis
4. Bacterial endocarditis
5. Infective nonbacterial thrombotic endocarditis
5. SEPTICOPYEMIA IS CHARACTERIZED BY THE PRESENCE OF WHICHTYPE OF
INFLAMMATION IN THE ORGANS AND TISSUES:
1. Purulent
2. Fibrinous
3. Granulomatous
4. Serous
5. Catarrhal
6. SEPSIS DIFFERS FROM OTHER INFECTIONS BY:
1. Proof immunity
2. Infectivity
3. Cyclicity
4. Specificity of infection agent
5. Polyetiologity
7. PLURAL ABSCESSES IN ORGANS ARE FOUND OUT AT AUTOPSY
ACCOMPANYING WITH SUPPURATING WOUND OF FEMUR AND REGIONAL
THROMBOPHLEBITIS. WHAT COMPLICATION DEVELOPED AT THE PATIENT?
1. An abscess
2. Phlegmon
3. Purulent leakage
4. Septicemia
5. Septicopyemia
8. CLINICAL-MORPHOLOGICAL FORM OF SEPSIS IS:
1. Therapeutic
2. Surgical
3. Fungoid
4. Chroniosepsis
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5. Viral
9. ALL OF THE FOLLOWING MICROORGANISMS CAN CAUSE SEPSIS, EXCEPT:
1. Bacteria
2. Viruses
3. Fungi
4. Protozoa
5. Chlamydeous
10. RING ABSCESSES IN THE MYOCARDIUM ARE THE CHARACTERISTIC FEATURES
OF WHICH DISEASE:
1. Bacterial endocarditis
2. Nonbacterial thrombotic endocarditis
3. Libman-Sacks endocarditis
4. Rheumatic endocarditis
5. Syphilis
11. THE MOST COMMON CAUSE OF DEATH AT PATIENTS WITH SUBACUTE SEPTIC
ENDOCARDITIS IS:
1. Amyloidosis
2. Chronic heart failure
3. Brown atrophy of the myocardium
4. Infarct of the kidney
5. Cachexia
12. SEPTIC SHOCK IS CAUSED BY ALL OF THE FOLLOWING MICROORGANISMS,
EXCEPT:
1. Gram-positive
2. Gram-negative
3. Viral
4. Fungal
5. Chlamydiae
13. GRAYISH-WHITE ROUND AREAS IN THE CORTICAL SURFACE, CORTEX AND
MEDULLA OF THE KIDNEY AT EMBOLIC PYOGENIC NEPHRITIS ARE REFERRED TO
AS:
1. Pyemic abscesses
2. Hemorrhages
3. Fat droplets
4. Thromboembolism
5. Focal atrophy
14. PYOGENIC LEPTOMENIGITIS CAN BE FOUND AT THE FOLLOWING FORM OF
SEPSIS:
1. Septicemia
2. Septicopyemia
3. Chronic sepsis
4. Bacterial endocarditis
5. Infective nonbacterial thrombotic endocarditis
15. SEPTICOPYEMIA IS CHARACTERIZED BY THE PRESENCE OF THE FOLLOWING
TYPE OF INFLAMMATION IN THE ORGANS AND TISSUES:
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1.
2.
3.
4.
5.
Purulent
Fibrinous
Granulomatous
Serous
Catarrhal
16. ON GROSS EXAMINATION, THE KIDNEY AT EMBOLIC PYOGENIC NEPHRITIS
HAS FOLLOWING APPEARANCES:
1. Enlarged and soft
2. Enlarged and firm
3. Diminished and firm
4. Diminished and soft
5. Diminished with granular surface
17. CARDIAC COMPLICATIONS IN PATIENTS WITH BACTERIAL ENDOCARDITIS
INCLUDE ALL OF THE FOLLOWING, EXCEPT:
1. Valvular insufficiency
2. Valvular stenosis
3. Myocardial ring abscess
4. Brown atrophy of the heart
5. Fibrinous pericarditis
18. THE PATHOLOGICAL PROCESS IN THE MYOCARDIUM THAT CAN BE FOUND AT
PATIENTS WITH CHRONIC SEPTIC ENDOCARDITIS IS:
1. Brown atrophy
2. Heart amyloidosis
3. Hemosiderosis
4. Left-sided heart hypertrophy
5. Right-sided heart hypertrophy
19. THE PATHOLOGICAL PROCESS THAT CAN BE FOUND IN LYMPHOID ORGANS
AT SEPTICEMIA IS:
1. Hypoplasia
2. Hyperplasia
3. Infarct
4. Acute inflammation
5. Hemosiderosis
20. FIRST PYEMIC METASTASES AT SEPTICOPYEMIA CAN BE FOUND IN:
1. Lymph nodes
2. Spleen
3. Lungs
4. Heart
5. Skin
21. RENAL PATHOLOGY THAT CAN BE FOUND AT PATIENTS WITH SUBACUTE
SEPTIC ENDOCARDITIS IS:
1. Glomerulonephritis
2. Kidney amyloidosis
3. Pyelonephritis
4. Hemosiderosis
5. Lipoid nephrosis
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22. THE PATHOLOGICAL PROCESS DEVELOPING IN PARENCHYMA OF THE
ORGANS DUE TO CHRONIC SEPSIS IS:
1. HYALINOSIS
2. Hypertrophy
3. Calcinosis
4. Hemosiderosis
5. Atrophy
23. THE PATHOLOGICAL PROCESS THAT CAN BE FOUND IN STROMA OF ORGANS AT
SEPTICEMIA IS:
1. Interstitial inflammation
2. Hyalinosis
3. Necrosis
4. Apoptosis
5. Hyperplasia
24. PYEMIC ABSCESSES AT EMBOLIC PYOGENIC NEPHRITIS ON HISTOLOGIC
EXAMINATION CONTAINS CELLS:
1. Macrophages
2. Lymphocytes
3. Neutrophils
4. Plasma cells
5. Erythrocytes
25. WHAT PATHOLOGICAL PROCESS CAN BE FOUND IN BLOOD VESSELS AT
INFECTIVE SEPTIC ENDOCARDITIS:
1. Hemosiderosis
2. Vasculitis
3. Hyalinosis
4. Sclerosis
5. Amyloidosis
26. THE PATHOLOGICAL PROCESS THAT CAN BE FOUND IN SPLEEN AT CHRONIC
SEPSIS IS:
1. Hemochromatosis
2. Infarct
3. Hyperplasia
4. Cyanotic induration
5. Atrophy
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EXAMINATIONAL TASKS FOR FOREIGN STUDENTS
Task 1. A child was admitted to the hospital with weakness, fever and nasal hemorrhage. The
examinations revealed: sharp elevation of lymphocytes (about several tens of thousands) and
numerous lymphoblasts; enlarged lymph nodes of mediastinum; hepatosplenomegaly.
1. What disease had this patient?
2. Name the morphological subtype of the disease.
3. Name the typical complications of the disease.
4. Explain pathogenesis of hepatospleno-megaly.
5. What histological changes in the liver and spleen tissue must be revealing?
Task 2. 50 years old patient has noted augmentation of lymph nodes. He com-plains of weakness,
periodical fever. In peripheral blood test excess amount of myelo-cytes and promyelocytes was
revealed. Physical examination revealed enlargement of spleen and liver.
1. Name the disease.
2. What morphological variant of the dis-ease depending on histogenesis?
3. Explain pathogenesis of enlargement of spleen and liver.
4. How excess enlargement of spleen and liver is termed?
5. What outcome of the disease is possible in this case?
Task 3. 50 years old patient has noted augmentation of lymph nodes group at the left of neck. He
complains of weakness, loss of body weight, dermal itch, fever. In peripheral blood test: ESR - 40
mm/hour, there are no changes in the leukocytes. The biopsy of lymph node revealed proliferation
of atypical reticular cells among lymphoid elements, huge multinuclear cells (diagnostic cells of
Berezovsky-Shternberg-Rid) and foci of necrosis and sclerosis.
1. Name the disease.
2. What is the morphological variant of the disease basing on results of histological research?
3. What morphological features are the hallmarks the disease?
4. How does the spleen look like at this disease?
5. Give its name.
Task 4. The patient suffering from stomach ulcer died suddenly. In autopsy his skin was pale, in
the lumen of stomach and intestine 3,5 liters of blood were revealed.
1. What complication of the stomach ulcer took place in the case?
2. What general pathological process did develop in its result?
3. Name its kind depending on pathogenesis.
4. Describe gross changes of inner organs (size, color, density).
5. What general acute hemodinamic disorder caused the death of the patient?
Task 5. The man of 32 years after sharp supercooling felt weakness, dyspnea, and pains in the right
half of thorax at a brith; body temperature is 39C. Blunted sound, absence of breath in low part of
right lung, pleural murmur was revealed at examination. Treatment was without effect; patient died
a week later after beginning of disease from pulmonary-coronary insufficiency. Autopsy revealed:
enlarged heavy dense low lobe of right lung with imposing of fibrin on pleura, on cut section the
whole lobe is air-less and grey; there is round cavity filled with pus at 9-10 segments.
1. What disease developed at the patient?
2. What pleural murmur was connected with?
3. What stage of disease took place on section?
4. What microscopical changes are characteristic for this disease?
5. What pulmonary complication developed at the patient?
Task 6. The man of 51 years arrived in clinic with complaints to dispnea, cough with plentiful
125
sputum. Disease began 30 years ago, all this time he smoked much. X-ray examination of lung is
found out: emphysema, saccular and cylindrical bronchial expansions; borders of heart are
expanded due to right ventricle; fingers look like “drum-type sticks”. Symptoms of increasing renal
failure appeared in hospital and patient died from uremia.
1. What pulmonary disease took place at the patient?
2. To what group of pulmonary diseases it refer?
3. What figurative name of lung with this pathology?
4. What changes of heart are revealed on section?
5. What pathological process complicated pulmonary disease and was the reason of renal failure?
Task 7. The patient has arrived in clinic with sharp pains in abdomen, weakness. He lost
consciousness in few minutes after hospitalization, pulse is threadlike. Approximately 1500 ml of
blood revealed in abdominal cavity during operation, abdominal part of aorta protruded, its wall in
this place was thinned.
1. Name abnormal dilation of aorta.
2. What dangerous complication of it occurred?
3. What disease predisposed to such changes in aorta wall?
4. Give the definition of this disease.
5. What other local complication of the disease can take place in aorta?
Task 8. The patient with severe pains in abdomen died suddenly. Autopsy revealed expanded loops
of small intestine with dark red to black wall. The mesenteric vessels are rigid, thickened, occluded
by dark red solid masses.
1. What general pathological process developed in intestinal wall?
2. What vascular disease predisposed to it?
3. Name the clinico-morphological form of this disease.
4. What local hemodynamic complication was immediate reason of changes in intestinal wall?
5. What type of shock caused the death of the patient?
Task 9. The patient suffered from essential hypertension with manifestation of chronic renal failure
has died. The autopsy revealed reduced kidneys with fine-granular surface. At microscopic
examination in many organs the changes of arterioles are found: walls are thickened, lumen is
narrowed, intima infiltrated with homogeneous pink masses.
1. Name the clinico-morphological form of the disease.
2. What stages of it?
3 What dystrophy developed in vessels walls?
4. Name the general pathological process developed in the kidneys.
5. What pathological changes in other parenchimal organs are possible in this stage?
Task 10. The 70-years old patient complained of pain in right foot. The soft tissues of the 1-st
finger became black, mummified, shrinkages.
1. What general pathologic process developed in the low extremity?
2. What clinico-morphological pattern of it?
3. What vascular disease caused these changes?
4. Name its clinico-morphological form.
5. What complications are possible in this case?
Task 11. Patient with severe form of atherosclerosis of coronary arteries died in two days after
onset of retrosternal pain attack. Myocardial infarction is diagnosed at ECG recording.
1. What stage of myocardial infarction was diagnosed?
2. Give the definition of myocardial infarction.
3. What is the reason of death at this stage infarction of?
126
4. What immediate cause of myocardial infarction is possible?
5. Describe macroscopical changes in myocardium.
Task 12. Unconsciousness patient of 70 years old with stroke and left-side paralysis was admitted
in clinic. Dyscirculatory ischemic infringements of brain and severe atherosclerosis are in
anamnesis.
1. What changes can be found out in brain tissue on section?
2. What disease was the cause of these changes?
3. Explain the mining of term “stroke”
4. List two types of it: a), b).
Task 13. A 69-year-old man died from the chronic heart failure. 15 years ago he had myocardial
infarction.
1. What general hemodynamic process developed in his organs and tissues due to chronic heart
failure?
2. Describe the liver on gross inspection.
3. How this is liver called?
4. Name the form of chronic ischemic heart disease at that patient.
5. What morphological changes are characteristic for it?
Task 14. A 66-year-old woman suffering from hypertensive vascular disease (HVD) about 10 years
died from intracerebral hemorrhage.
1. What clinico-morphological form of HVD took place in this case?
2. Describe the brain on gross inspection.
3. What is the possible cause of death?
4. What material is deposited in arteriolar walls in the systemic hypertension?
5. What pathological process can be found in the kidneys in this disease?
Task 15. A 70-year-old man with left-sided heart failure and severe pulmonary hypertension died
from chronic cardiac and lung insufficiency.
1. Describe the lung on gross inspection.
2. How is this lung termed?
3. Explain the mechanism of the development of the changes.
4. What changes can be found in different body cavities and in subcutaneous tissue?
5. Give definition of chronic ischemic heart disease
Task 16. The 50 years old man suffered from rheumatism since the childhood, has arrived to clinic
with disorder of blood circulation. He died at the background of progressing heart failure. Autopsy
investigation revealed mitral valve damage: the atrium-ventricular foramen narrowed to 1 cm,
shutters are thickened; sclerosed, warty-like thrombotic masses are displaced on shutters closing
edges.
1. What diagnosis is probable?
2. What its kind has developed at the patient as a result of rheumatism according to character of
pathological process?
3. Give the definition of rheumatism
4. What microscopical changes can be revealed in the valve endocardium?
5. How termed irreversible stenosis of the valve in this case?
Task 17. The girl of 12 years died from quickly progressing rheumatism with the expressed allergic
reactions. Streptococcal tonsilitis is in anamnesis 2 month ago. Histological examination of autopsy
material revealed diffuse inflammatory infiltration of whole heart wall.
1. What clinico-morphological form of rheumatism took place?
127
2. Explain pathogenesis of the disease.
3. How the inflammation of heart in this case need termed?
4. Describe the heart at opening of pericardium cavity?
5. What is the possible cause of death in this case?
Task 18. The patient had transmural myocardial infarction some years ago. Chronic heart aneurysm
with chronic heart failure followed.
1. Explain the pathogenesis of heart aneurysm.
2. Is it true or false?
3. What hemodynamic disorders can complicate the heart aneurysm: a), b) ?
4. What pigment accumulation is the hallmark of chronic heart failure?
Task 19. The patient after aortal-coronary shunting surgery suffered with progressing chronic heart
failure. Autopsy revealed enlargement of heart. Pericardial cavity obliterated completely,
myocardium is flabby, yellowish brown.
1. What is the probable diagnosis?
2. What is the figurative name of heart at this pathology?
3. Explain pathogenesis of deposition of calcium salts.
4. What general pathological process in myocardium followed?
5. What special stain needs to use for detection of such change?
Task 20. The patient suffered from chronic stomach ulcer. Sudden severe pain in epigastrium
occurred with irradiation in shoulder. Cold sweat and paleness of skin appeared. Sharp intention of
abdominal wall muscles is marked at palpation.
1. What complication of stomach ulcer developed at the patient?
2. Explain the pathogenesis of sharp intention of abdominal wall muscles?
3. What period of the disease took place (acute attack or remission)?
4. What histological findings can be seen in the bottom of ulcer in this period?
5. Name ulceral-neoplastic complication of chronic stomach ulcer?
Task 21. During investigation of gastroscopy biopsy material in mucous and submucosal layers of
stomach wall invasive growth of atypical epithelial cells was revealed. Some large cells with pale
pink cytoplasm and constricted nucleus (signet ring cells) were reveled between tumor cells.
1. What tumor was diagnosed?
2. Where can be found first limphogenous metastases of stomach cancer?
3. What is Krukenberg’s tumor?
4. What is Virchov’s metastasis?
5. What complication of stomach cancer can cause by secondary necrotic changes in the tumor?
Task 22. Pains in right iliac area, nausea, vomiting suddenly appeared at the patient. Pains in right
area under ribs body temperature of 39 degrees joined for the second day. Operation was done.
Enlarged and thickened appendix with plethoric serous membrane covered by fibrinous-purulent
sedimentation was removed during operation.
1. What morphological type of acute appendicitis took place?
2. List microscopic changes of appendix.
3. What are possible complications of acute destructive appendicitis? a), b)
4. What are the two main reasons of appendicitis?
Task 23. During microscopical investigation of removed appendix was reveled infiltration of all
layers of its wall by leucocytes with superficial and deep mucosal defects.
1. What type of acute appendicitis took place?
2. How did this appendix look like?
128
3. What complication of this type of appendicitis is lead to peritonitis development?
4. What complication can develop if inflammation will spread to branches of portal vein?
5. To development of what complications is lead spreading of purulent process on surrounding
tissue and caecum?
Task 24. A 67-years man complained on intermitted abdominal pain, weight loss and melena. He had
died 1,5 month later. Whitish-grey dense tumor with mixed (exso-endophitic) growth was reveled in
colon on autopsy.
1. Give the diagnosis.
2. What histological type of tumor can be suspected at this patient?
3. Where first hematogenous metastases can be found?
4. What local complication of tumor had developed at this patient?
5. What general complication occurred at this patient?
Task 25. The symptoms of acute liver failure had been developed at the 25-year woman after
poisoning by mushrooms. Investigation revealed progressive decreasing of liver.
1. What general pathological process had developed in patient’s liver?
2. What diagnosis can be at this case?
3. What is the stage of this disease?
4. What can be reveled in liver tissue during histological investigation?
5. What possible outcomes of this disease?
Task 26. Cirrhosis of liver was diagnosed at the patient in gastroenterologic department. It is
known from anamnesis, that five years ago he had transferred the heavy form of viral hepatitis B.
Laparoscopy reviled reduction of liver in sizes its surface is irregularly nodular, character of surface
is caused by presence of nodes with 5cm in diameter.
1. What morphological (macroscopical) variant of liver cirrhosis found out at the patient?
2. What morphogenetic type of cirrhosis?
3. What microscopic features of this cirrhosis?
4. What special stain needs to use for detection of cirrosis?
5. Name the possible reasons of death at cirrhosis of liver.
Task 27. 64-years woman during last 6 month felled weakness, losing of weight on10 kg. Large
dense rough liver with multiple nodes, iron-deficiency anemia was reveled at examination. In the
colon was found dense large tumor circularly grows in wall with ulceration in center.
1. What tumor was at this patient?
2. Is it benign or malignant?
3. Explain the pathogenesis of changes in the liver?
4. What pigment can deposit in the liver cells due to progressing of tumor and cachexia?
5. Give the definition of cachexia.
Task 28. The patient, suffering from gallstones, had pains in right below the ribs, the jaundice was
developed.
1. Explain the pathogenesis of jaundice?
2. Name morphologic kind of jaundice?
3. What is the chemical composition of gallstones?
4. Name the most common complication of gallstones.
5. List etiological factors of gallstones.
Task 29. The patient was ill acutely after overcooling. Hypertension, hematuria, edema of face and
phenomena of renal failure are marked. Patient died 6 month later the beginning of the disease. On
section: kidneys are increased in size, flabby; cortical layer yellow - grey with red mottled,
129
pyramids are dark red on cut surface.
1. What disease was at the patient?
2. Give the name to found out macroscopic changes in kidneys?
3. What changes in kidneys were found out at microscopic investigation?
4. Name the histological pattern of this disease.
5. What direct reason of patient death?
Task 30. Following changes were revealed on section of the patient, suffering from chronic
glomerulonephritis during 12 years: kidneys are sharply reduced in sizes, dense, their surface finegrained; fibrinous inflammation of serous and mucous membranes; dystrophic changes in
myocardium and liver, edema of brain.
1. Name the found out macroscopic changes of kidneys.
2. Give the microscopic characteristic of these changes.
3. What complication occurred in the end of disease?
4. Explain pathogenesis of fibrinous inflammation in mucous and serous membranes.
5. Name other, most often diseases of kidneys with same complication.
Task 31. Increasing of thyroid gland at the patient living in mountain area leaded to breathing
disorders, difficult gulp, and expansion of subcutaneous veins of neck frontal surface. Thyroid
hormone amount did not change.
1. What disease of thyroid gland developed at the patient?
2. Name its pattern depending on functionof thyroid.
3. What the reason and pathogenesis of this diseases?
4. What macroscopic changes of thyroid gland are characteristic for this disease?
5. What changes of glands are found out at microscopic investigation?
Task 32. The patient complains of increased appetite, thirst, poliuria, dryness and itch of
integuments, often-purulent diseases. Hyperglycemia and glycosuria is marked.
1. Name this disease.
2. What endocrine gland is damaged by pathological process?
3. What macroscopic changes developed in it?
4. What microscopic changes are in it?
5. What changes take place in kidneys?
Task 33. 70-yars woman suffered from decompensate diabetes mellitus II type had died from
ischemic infarction of brain. In anamnesis periodic hyperglycemia and glucosuria was. Obesity is
45%. Autopsy revealed severe metabolic changes in the vessels, heart, liver and kidneys.
1. Is this type of diabetes insulin dependent?
2. Pathology of which organ is this disease connected with?
3. Name complication of the disease in the vascular walls.
4. What general pathological process was reveled in the liver?
5. What is the main morphogenetic mechanism of its development?
Task 34. A 41-year-old woman with repeated metrorrhagia was admitted to the hospital for a
routine hysterectomy, which revealed enlarged irregular uterus. Macroscopic examination of
surgical material showed multiple, round-shaped, dense-elastic, pale-pink tumors with fibrous
structure and well defined borders in the myometrium. Histological examination revealed well
differentiated tumor tissue consisting fascicles of collagen fibers.
1. What is probable diagnosis?
2. Is it benign or malignant neoplasm?
3. Name two histological variants of this tumor depending on predominance of cells or fibers.
4. What are possible sites of its localization in the uterine wall? - a), b), c).
130
5. What special stain must be used for detection of its origin?
Task 35. A 30-year-old woman was admitted to the hospital in three years after delivery. On
examination of cervix irregular-shaped focus of bright red color was found out on a background of a
pale mucous membrane. On histologic examination a growth of cylindrical epithelium was founded.
1. What pathological process (disease) takes place?
2. What is the disease depending on pathogenesis?
3. Is it reversible?
4. What general pathologic process underlies such changes of epithelium?
5. What disease can develop on its background?
Task 36. Pulmonary bleeding occurred in the young woman. Abortion is in anamnesis 6 month
ago. X-ray examination revealed multiple tumor-like centers of consolidation in the lungs.
Overgrowth of atypical cells cyto- and sincytiotrophoblast are found at histological examination of
diagnostic scrape from uterus cavity.
1. Name this tumor?
2. Is it benign or malignant?
3. Is it organ specific?
4. Describe macroscopic changes in uterus cavity.
5. How were connected changes in lung with this tumor?
Task 37. A focus consolidation occurred in the left breast of 38-years old woman. The sectoral
resection of breast was made. Surgical material examination revealed dense-elastic tumor node 3 cm
in diameter surrounded with capsule. On cut section tumor tissue is whitish-gray with dilated lumens
of ducts. Histological investigation revealed slit-like glandular and tubular structures, compressed
by overgrowth of connective tissue predominated above parenchyma.
1. What is the probable diagnosis?
2. Give the morphological variant of this tumor depending on connective tissue overgrowth?
3. Is it benign or malignant?
4. Is this tumor organospecific?
5. What category of breast diseases is it refereed to?
Task 38. Patient complained on fever, temperature up to 40C, headache, cough, and expressed
dyspnea arrived in clinic during flu epidemic. Moist wheeze were listened in lungs. In spite of
treatment, patient died at phenomena of pulmonary-cardiac insufficiency three days later.
1. What disease was the reason of patient’s death?
2. What form of disease?
3. What kind of inflammation was found out at autopsy in trachea?
4. Describe appearance of lungs?
5. How named the lung with such appearance figuratively?
Task 39. The child attending kinder garden had high temperature up to 38,5C, cold, conjunctivitis
and cough. There is macular rash on skin, whitish branny appearance on mucous membrane of
cheeks in oral cavity. Dyspnea and moist wheeze in lungs developed on the fourth day. The
difficulty of breath has suddenly appeared. The child died from phenomena of asphyxia.
1. Give the name of the disease.
2. What is its etiology?
3. Name the appearances on mucous membrane of cheeks?
4. What process in lungs was complicated this disease?
5. What complication was the reason of child death?
131
Task 40. A 26-year-old man complained of massive diarrhea about liters of dilute “rice-water” stool
containing flecks of mucus.
1. What disease did the patient suffer from?
2. What are the mechanisms and cause of the disease?
3. Name the stages of the disease.
4. Describe the intestine on gross inspection.
5. Name the possible complications of the disease.
Task 41. Typhoid fever was diagnosed in 56-year-old man.
1. What is the cause of the disease?
2. What type of interaction between microorganism and epithelium of intestine in this disease?
3. What department of intestine is commonly affected?
4. Name the gross changes in the intestine in the 1-st stage of the disease.
5. Name the possible complications of the disease in second week from the onset.
Task 42. A 30-year-old man was diagnosed to have acute infection with bloody diarrhea, tenesmus, and
fever. The phenomena of paraproctitis are found out. Later the pains in a waist show up, pyuria, has
appeared, the body temperature has sharply increased.
1. What bacterial infection occurred in the patient?
2. Where is entry of infection?
3. What form of colitis took place?
4. What is cause of the paraproctitis?
5. What type of interaction between microorganism and epithelium of intestine in this disease?
Task 43. A 41-year-old man was admitted to the hospital with symptoms of acute infectious disease.
The physical examination revealed dirty-white films on the tonsils and larynx.
1. What is the most likely diagnosis in this case?
2. What etiology of the disease?
3. What general pathologic process can be found in the trachea?
4. Describe gross appearance of the tonsils.
5. What fatal complication is possible in this disease?
Task 44. A 5-year-old child was admitted to the hospital with symptoms of acute infectious disease
and dot erythematous skin rash over the trunk and face. The examination revealed severe necrotic
tonsillitis.
1. What is the diagnosis?
2. What is its etiology?
3. Name the variant of this disease depending severity of course.
4. Describe the tonsils on gross inspection.
5. List possible local complications of necrotic tonsillitis.
Task 45. Increasing of the temperature up to 40C, cloudiness of consciousness, presence of plural
haemorrhages on skin is marked at the patient three days after criminal abortion. She died insecond
day after occurrence of these symptoms.
1. What did clinical-morphological form of sepsis take place?
2. What was a kind of sepsis depending on character of entry of infection?
3. Characterize morphology of local changes.
4. What general pathologic process can be found out: in parenchyma of organs?
5. What general pathologic process can be found out n hemopoeitic and lymph tissues?
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Task 46. The patient arrived in clinic for draining of abscess on buttock which is formed after
intramuscular injection. The temperature remained 39C, dyspnea and cloudiness of consciousness
appeared after draining of abscess. The patient died at phenomena of acute heart failure.
1. What did clinical-morphological form of sepsis develop at the patient?
2. What was a kind of sepsis depending on character of entry of infection agent?
3. What macroscopical changes in connection with widespread of infection can be found in lungs,
heart, brain?
4. What general pathologic process must be in spleen?
5. How termed the spleen with such changes?
Task 47. A 5 years-old child after transferred measles had marked weakness, hyperhidrosis, and
high temperature. The skin is pale. Tuberculin test is sharply positive. X-ray examination of thorax
revealed the round-shaped consolidations in IХ segment of right lung under the pleura and near root
of lung. The primary lung tuberculosis had diagnosed.
1. What morphological manifestation of primary tuberculous complex in the lungs.
2. Name its elements.
3. What tissue reaction prevails?
4. Name favorable outcome of primary tuberculosis.
5. What the pathways of primary tuberculosis spreading?
Task 48. A 25 years-old man who had transferred primary tuberculosis in the childhood, the signs
of thoracic vertebrae deformation have appeared and began to accrue. The tuberculous spondylitis
has diagnosed. Later 4 years a hunch is developed.
1. Name the clinico-morphologic form of tuberculosis?
2. Explain pathogenesis of spondylitis?
3. Describe gross changes in the vertebrae characteristic for tubercular infection.
4. Where the primary lesion settles down: in marrow, in a bone tissue or in the bones and joints?
5. What pathologic changes must be revealed in the entry of infection?
Task 49. A 32-year-old woman was admitted to the hospital because of the productive cough with
high temperature. A peripheral round shaped subpleural shadow was found on radiological
examination. Following further examination, mycobacterium tuberculosis was cultured. The miliary
tuberculosis was diagnosed.
1. What are the histological findings in the lungs of the patient?
2. What is the pathogenesis of tuberculous granuloma?
3. What cell transformations can be found in tuberculous granuloma?
4. What are the causes of caseous necrosis in tuberculous granuloma?
5. What favorable outcome of the disease is possible?
Task 50. A 53 years-old man suffered from cavitary fibrocaseous tuberculosis complicated by
pleura empyema. Later 6 years the progressing renal insufficiency is associated oneself with lung
process. The patient died at the phenomena of uremia.
1. What kind of tuberculosis is it: primary, hematogenous or secondary?
2. Describe the changes in the lungs characteristic for this stage of tuberculosis.
3. What special stain needs to use for detection of etiologic agent in microsections?
4. What process had developed in the kidneys?
5. What complication determined the development of uremia?
Task 51. A 30 years-old man had transferred primary syphilis 7 years ago. He had marked
retrosternal pains as stenocardia. Acute infringement of coronary blood was diagnosed.
1. What period of syphilitic process is it?
2. What is the clinic-morphologic form of it?
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3. What tissue reaction is typical for this period?
4. Where is localized inflammatory process?
5. What is its morphological picture?
Task 52. The liver biopsy of the 25-year-old man revealed multiple gummous granulomas.
1. What disease had this patient?
2. What stage of it?
3. What is the cause of the disease?
4. What type of inflammation is characteristic for it?
5. Describe gross appearance of the liver.
MACROPREPARATES
1. 1 «Acute warty endocarditis of mitral valve»
2. 6 «Polipous-ulcerosal endocarditis of aortal valves»
3. 9 «Fibroplastic endocarditis, mitral valve stenosis»
4. 16 «Chronic aneurysm of heart»
5. 18 «Fibrinous pericarditis»
6. 21 «Hypertrophy of the heart»
7. 26 «Brown atrophy of myocardium»
8. 28 «Gangrene of the small intestine»
9. 31 «Aneurysm of the arch of aorta at syphilis»
10. 32 « Pulmonary thromboembolism»
11. 35 «Aneurysm of aorta with thrombosis »
12. 48 «Subarachnoid hemorrhage»
13. 50 «White (ischemic) infarcts of spleen»
14. 53 «Red (hemorrhagic) pulmonary infarct»
15. 70 «Bullous emphysema of lung»
16. 74 «Repeated myocardial infarction»
17. 84 «Compound congenital heart disease»
18. 90 «Hypertrophic gastritis»
19. 97 «Phlegmonous appendicitis»
20. 98 «Chronic stomach ulcer»
21. 104 «Fatty dystrophy of liver»
22. 110 «Nutmeg liver»
23. 115 «Сirrhosis of the liver»
24. 116 “Uterus cancer “
25. 118 «An esophageal varices with rupture of the vessels wall»
134
26. 125 «Tubal pregnancy»
27. 131 “Saucer-like stomach cancer”
28. 154 «Leiomyoma of the uterus»
29. 165 «Urinary bladder papilloma»
30. 172 «Lipoma»
31. 175 «Osteogenic sarcoma of a femur»
32. 178 “Lung cancer”
33. 179 “Colon cancer”
34. 191 «Embolic purulent interstitial nephritis»
35. 199 «Nephrocirrhosis»
36. 207 «Nephrolithiasis»
37. 208 «Vicarious hypertrophy and hypoplasia of kidneys»
38. 223 «Subacute glomerulonephritis»
39. 232 «Colitis at the dysentery»
40. 236 «Medullary swelling and necrosis of Peyer’s patches in typhoid fever»
41. 237 “Ulceral-necrotic tonsillitis”
42. 238 «Purulent leptomeningitis»
43. 240 «Hyperplasia of spleen at sepsis»
44. 242 “Primary pulmonary tubercular complex with miliary generalization”
45. 245 «Caseous necrosis of lymph node at the tuberculosis»
46. 248 “Adrenals adenoma”
47. 252 “Caseous pneumonia”
48. 254 “Fibrous-cavernous tuberculosis of lungs”
49. 259 «Hydatid cyst of the liver»
50. 269 «Diffuse goiter»
51. 280 «Hydrocephalus»
52. 282 «Splenomegalia at chronic myeloleukemia»
53. 289 “Tuberculosis of a kidney”
54. 294 «Bile-cystolithiasis»
55. 306 «Lymph nodes in chronic lymphocytic leukemia»
56. 311 «Big motley lung at flu»
57. 313 “Chorionepithelioma”
58. 319 «Gangrene of foot fingers»
59. 350 «Varicose veins with phlebothrombosis»
60. 363 «Hydatidiform mole»
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61. 364 «Hyaline change of spleen capsule» («icing spleen»)
62. 372 «Amyloidosis of kidney» («big bacon kidney»)
63. 378 «Teratoma»
64. 418 “True croup at diphtheria”
65. 420 «Croupous pneumonia»
66. 421 «Chronic lung abscess»
67. 422 «Recurrent myocardial infarction with acute aneurism and its thrombosis»
68. 439 “Spleen at lymphogranulomatosis”
69. 457 «Ascending pyelonephritis»
70. 500 «Measles rash», «Rash at scarlet fever»
71. 520 «Pigmented cyst of brain»
MICROPREPARATES
1.
2. «Croupous pneumonia» (hematoxylin and eosin)
2.
8. «Chronic stomach ulcer» (hematoxylin and eosin)
3.
9. «Mucous cancer» (hematoxylin and eosine)
4.
14. «Fatty dystrophy of liver» (Sudan - III)
5.
15. «Amyloidosis of kidney» (Congo - red)
6.
16. «Caseous necrosis of lymph node at the tuberculosis» (hematoxylin and eosin)
7.
18. «Septic myocarditis» (hematoxylin and eosin)
8.
20. «Granulation tissue» (hematoxylin and eosin)
9.
23. «Hemosiderin in the locus of hemorrhage» (reaction of Perls)
10. 25. “Squamous skin cancer” (hematoxylin and eosin),
11. 27. “Stomach adenocarcinoma”( hematoxylin and eosin),
12. 35. «Abscesses of kidney at septicopiemia» (hematoxylin and eosin)
13. 36. “Syphilitic mesaortitis” (hematoxylin and eosin)
14. 38. «Hypertrophy of the myocardium» (hematoxylin and eosin)
15. 39. «Purulent leptomeningitis» (hematoxylin and eosin)
16. 58. «Leiomyoma» (picrofuscin by Von Hyzone)
17. 61. «Ischemic renal infarct» (hematoxylin and eosin)
18. 62. «Hemorrhagic pulmonary infarct» (hematoxylin and eosin)
19. 71. «Intracerebral hematoma» (hematoxylin and eosin)
20. 75. «Fat embolism of the lung» (Sudan - III)
21. 80. «Glandular hyperplasia of the endometrium» (hematoxylin and eosin)
136
22. 81. “Lymphatic node at lymphogranulomatosis” (hematoxylin and eosin)
23. 87. “Papillary thyroid cancer “ (hematoxylin and eosin)
24. 88. «Actinomycosis» (hematoxylin and eosin)
25. 89. «Сardiosclerosis» (picrofuscin by Von Hyzone)
26. 90. «Kidney in acute myeloblastic leukemia» (hematoxylin and eosin)
27. 94. «Acute myocardial infarction» (hematoxyline and eosin)
28. 97. «Brown induration of the lungs» (Prussian blue)
29. 100. «Multilobular cirrhosis of liver» (picrofucsin on van Hyson)
30. 103. «Nutmeg liver» (stained by hematoxylin and eosin)
31. 109. «Focal influenzal pneumonia» (hematoxylin and eosin)
32. 110. «Mixed thrombus in vein» (hematoxylin and eosin)
33. 113. «Miliary tuberculosis of lung» (hematoxylin and eosin)
34. 117. «Colloid goiter» (hematoxylin and eosin)
35. 126. «Melanoma of skin» (hematoxylin and eosine)
36. 127. "Bronchopneumonia" (hematoxylin and eosin)
37. 133. «Lung emphysema» (hematoxylin and eosin)
38. 135. «Hyaline changes of pleura» (hematoxylin and eosine)
39. 136. «Petrifications in lung (Ghon focus)» (hematoxylin and eosine)
40. 141. “Papilloma of skin “(hematoxylin and eosin)
41. 150. «Hydatidiform mole» (hematoxylin and eosin)
42. 153. «Atherosclerosis of arteria» (Sudan - III)
43. 159. «Tubal pregnancy» (hematoxylin and eosin)
44. 163. “Mammary gland fibroadenoma”(hematoxylin and eosin)
45. 165. «Fibrinous pericarditis» (hematoxylin and eosin)
46. 178. «Cavernous hemangioma of the liver» (hematoxylin and eosin)
47. 182. «Ulceral enteritis in salmonellosis» (hematoxylin and eosin)
48. 183. “Chorionepithelioma” (hematoxylin and eosin)
49. 187. «Atrophy of pancreas at diabetes» (hematoxylin and eosin)
50. 198. «Phlegmonous appendicitis» (hematoxylin and eosin)
51. 203. «Extracapillary serous glomerulonephritis» (hematoxylin and eosin)
52. 205. «Septic polypous-ulcerous endocarditis» (hematoxylin and eosin)
137
ELECTRONOGRAMMS
1. Baloon dystrophy of hepatocyte (atlas fig. 8)
2. Fibrinoid degeneration of collagenic fibers (fig. 25)
3. Amyloidosis of glomerulus (fig. 38)
4. Ischemic myocardium (fig. 74)
5. Inflammation, emigration of segmentonuclear leukocytes (fig. 98)
6. Hypertrophy of the myocardium (the stage of compensation) (fig. 166)
7. Hypertrophy of the myocardium (the stage of decompensation) (fig. 166)
8. Ultrastructural atypia of tumor cell (fig. 175)
9. Membranous glomerulonephritis (fig. 320)
10. Croupous pneumonia, fibrin resorbtion (fig. 280)
ANSWERS ON TASKS
Task №1
1. Acute leukemia.
2. Lymphoblast leukemia.
3. Septic complications.
4. Unchecked increasing of neoplastic cells in hematopoietic organs, there hematogenic spreading
in other organs with infiltration of them.
5. Infiltration of tissue by lymphoblasts, diapedetic hemorrhgias, venous congestion.
Task №2
1. Chronic leukemia.
2. Myelocytic leukemia.
3. Unchecked increasing of neoplastic cells in hematopoietic organs, there hematogenic spreading
in other organs with infiltration of them, what resulted in edema, infarctions and congestion.
4. Hepato-, splenomegalia.
5. Slow progression with blast crisis, transformation in acute leukemia.
Task №3
1. Lymphogranulematosis.
2. Mixed-cellular variant.
3. Diagnostic giant multinuclear cells of Berezovsky-Shtermberg-Rid.
4. Spleen is enlarget, consistence is dense, change of foci: dark red, grey and whitish-yellow,
reminds porphyry.
5. Porphyric spleen, diffuse waxy spleen.
Task №4
1. Bleeding.
2. Anaemia.
3. Posthemorrhagic.
4. Size-diminished, color-pail, density-flabby.
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5. Hemorrhagic shock.
Task №5
1. Croupouse (fibrinouse) pneumonia.
2. Fibrinouse pleuritis.
3. III stage, grey hepatisation.
4. Diffuse loading of alveoli with fibrinose exudates (croupouse inflammation), Konn’s bridges.
5. Abscess of lung.
Task №6
1. Bronchoectatic disease.
2. Chronic Non-specific pulmonary diseases (CNPD).
3. Honey-comb lung.
4. Hypertrophy of heart (cor bovinum).
5. Amyloidosis.
Task №7
1. Aneurism.
2. Rupture of aneurism.
3. Atherosclerosis.
4. Atherosclerosis is the chronic disease arising as a result of fatty and protein methabolism
abnormality, characterized by injury of muscle and muscle-elastic types arteries as focal deposition
of lipids, proteins and reactive overgrowth of connective tissue in its intima.
5. Thrombosis.
Task №8
1. Necrosis.
2. Atherosclerosis.
3. Atherosclerosis of mesenteric vessels.
4. Thrombosis.
5. Pain shock.
Task №9
1. Renal type.
2. III stage, changes of organs in connection with arterieschanges and intraorganic blood circulation
disorder.
3. Hylinosis.
4. Cirrhosis.
5. Infarctions, gangrene, hemorrhages, hematoms, cyst formation.
Task №10
1. Gangrene.
2. Wet gangrene.
3. Atherosclerosis.
4. Atherosclerosis of low extrimity.
5. Mutilation (selfamputation).
Task №11
1. II stage (necrosis).
2. Coronary disease of heart is caused by acute absolute or relative insufficiency of coronary blood
supply.
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3. Caused by early complications:acute cardiac failure, cardiogenic shock, asystoly, ventricular
fibrillation, rupture of heart.
4. Occlusion of coronary arteryby atherosclerotic plaque.
5. Yellowis irregular flabby focus of necrosis.
Task №12
1. Intracerebral hemorrhage.
2. Atherosclerosis of brain arteries.
3. Insult (formation of brain hematoma).
4. a) ischemic,
b) hemorrhagic.
Task №13
1. General venouse congestion.
2. On cut cection liver has motly painting: small black points(hemorrhages) on yellow background
(fatty dystrophy).
3. Nutmeg liver.
4. Macrofocal cardiosclerosis.
5. Organisation of necrosis, replacement of myocardium on connective tissue.
Task №14
1. Cerebral form.
2. Intracerebral hematoma in place of ganglions.
3. Distruction of vital centers.
4. Hyaline.
5. Nephrocirrhosis.
Task №15
1. Lung is enlarged, consistence is dense, color - brown.
2. Brown induration of lung.
3. Increased pressure in small circle of blood supply (pulmonary hypertension) causes increasing of
vessel wall permeability and exudation of blood.
4. Anasarca and accumulation of fluid (edema) in all cavities of body (hydrothorax,
hydropericardium, ascitis,hydrocele).
5. Chronic IHD is disease caused by absolute or relative chronic coronary insufficiency.
Task №16
1. Rheumacarditis.
2. Relapsing warty endocarditis of mitral valve with atrioventricular stenosis.
3. Rheumatism is the group of diseases characterized by connective tissue injury, caused by
infringement of an organism immune homeostasis.
4. Shutters of valve are thickened, submitted by hyalinizated tissue. Fresh centers of connective
tissue disorganization (mucoid swelling and fibrinoid degeneration) are visible on background of
sclerosis. Covering endothelium is destroyed with warty-like fresh thrombotic mass
imposing.Endocardium diffusely infiltrated by lymphocytes and macrophages.
5. Acquired heart defect, stenosis – “fish mouth”.
Task №17
1. Cardiovascular form (rheumatic carditis).
2. Reaction of hypersensitivity III type (immune-complex), autoimmunization with damage of
vessels walls and systemic progression of disorganization of connective tissue in certain organs.
3. Pancarditis.
140
4. “Hairy heart”(fibrinouse pericarditis), strings of fibrin can be seen on surface of pericardium.
5. Acute coronary insufficiency.
Task №18
1. Protrusion of heart wall on the background of macrofocal cardiosclerosis.
2. True.
3. a) Rupture of aneurism,
b) thrombosis.
4. Lipofuscine.
Task №19
1. Pancarditis with fibrinouse pericarditis (Hairy heart) complicated by adhesive pericarditis and
cavity obliteration.
2. “Stone heart”.
3. Surface of pericardium become rough due to fibrinouse exudates imposing and fibrin strings are
the matrix for calcium salts deposition (dystrophic calcification) and cavity obliteration.
4. Diffuse microfocal cardiosclerosis (in outcome of interstitial inflammation).
5. Picrofuchsine ( by von Giesone).
Task №20
1. Perforation of stomach wall with ulceral bleeding.
2. Outcome of blod in abdominal cavity with peritonitis development.
3. Acute attack.
4. Ulceral defect extends on mucosa and muscle layers with destruction of muscle fibers. Four layer
can be seen in the bottom of ulcer: fibrinous-purulent exudates, fibrinoid necrosis, granulation
tissue and cicatricle tissue.
5. Malignesation, transformation of chronic ulcer in ulcer-cancer (malignant neoplasm).
Task №21
1. Ring-cell carcinoma of stomach.
2. In mesenteric lymph nods and omentum (regional lymph nods).
3. Metastasis of stomach cancer in ovary.
4. Retrograde lymphogenic metastases of stomach cancer in supra-clavicles lymph nods.
5. Erosive bleeding.
Task №22
1. Phlegmanouse appendicitis.
2. The wall of appendix is thickened, all layers are diffusely infiltrated by polymorphonuclear
leucocytes, serous membrane covered by fibrinous exudates (reactive inflammation).
3. a) perforation→peritonitis; b) gangrene of appendix→mutilation.
4. Development of sclerosis, atrophic changers and immune difficiency..
Task №23
1. Ulceral-phlegmanouse appendicitis.
2. Appendix is increased in size, serouse membrane is dim, red (due to plethora), covered by
fibrinouse exudate.
3. Perforation in place of ulceral defect.
4. Pilephlebitic liver abscess.
5. Typhlitis and perityphlitis.
Task №24
1. Colon cancer.
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2. Adenocarcinoma.
3. First hematogenous metastases can be found in liver.
4. Necrosos and ulceration of tumor.
5. Erosive bleeding.
Task №25
1. Acute hepatosis of liver.
2.Toxic dystrophy of liver .
3. The stage of “red atrophy”.
4. Various (from dusty to lager) droplets of fat colored by Sudan III in orange.
5. Progressive massive necrosis of liver→hepato-rhenal insufficiency, cirrhosis of liver.
Task №26
1. Macronodular cirrhosis of liver.
2. Postnecrotic cirrhosis.
3. Parenchima of liver is submitted by various oval false lobules, where central vein is absent,
hepatic beams are destroyed, pulled together hepatic triads are visible among wide areas of
connective tissue .
4. Picrofuchsin by von Giesone.
5. Hepatic coma, hepato-renal insufficiency.
Task №27
1. Circular colon cancer.
2. Malignant.
3. Cirrhosis of liver due to cancerous cachexia connect with intoxication and anemia.
4. Lipofuscin.
5. Cachexia is the general atrtophy (diffuse reduction of organs in size in alive organism).
Task №28
1. Mechanical jaundice (obturative) due to occlusion of bile tract by concrement.
2. Subhepatic.
3. Phosphates, cholesteric, pigmentary and mixed.
4. Obturation of common bile duct.
5. General (disbalance between buffer systems, alkaline ph) and local (inflammation, narrowing of
lumen, scarring, infringement of passage, high viscosity of secret and etc.).
Task №29
1. Acute glomerulonephritis.
2. Big motley kidney.
3. Observed marked capillary hyperemia, lumens of glomulei are increased, filled with serous
exudates looking like semy-lunes.
4. Exudative exstracapillary glomerulonephritis.
5. Acute renal failure.
Task №30
1. Secondary reduced kidney (arteriolosclerotic nephrocirrhosis).
2. Overgrowth of connective tissue is seen on background of renal tissue.
3. Acute renal failure.
4. Uremia.
5. Renal form of hypertensive disease, nephropathy at diabetes.
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Task №31
1. Goiter.
2. Euthyroid.
3. Iodine deficiency in water and food (endemia – natural absence of iodine in mountain area).
4. Thyroid gland is diffusely increased in size in all anatomical parts, homogeneous. Morphological
features of structure are determined at histological investigation.
5. Follicles of thyroid gland are enlarged in size, overloading with dense colloid, some of them
ruptured forming cysts. There walls are thinned, covered by atrophic and flat epithelium (atrophy
from hydrostatic pressure). Interlobular overgrowth of connective tissue is observed.
Task №32
1. Diabetes.
2. Pancreas.
3. Gland is reduced in size, dense, overgrowth of adiposal and fibrosal tissue (lipomatosis and
sclerosis) is marked in it.
4. Langergans’s isles are reduced in size (atrophy), some of them vicariously hypertrophied,
overgrowth of adiposal (lipomatosis) and connective tissue (sclerosis) is marked, vessels walls are
hyalinizated.
5. Nephropathy →nephrocirrhosis (primary reduced kidney.
Task №33
1. No (insulinindependent).
2. Pancreas.
3. Hyalinosis of vessels (stroma-vascular protein distrophy.
4. Fatty dystrophy of liver (“Goose liver”).
5. Transformation, decomposition (infiltration).
Task №34
1. Fibromyoma of uterus.
2. Benign.
3. Fibromyoma (hard, predominance of collagen fibers), myofibroma (soft, predominance of muscle
fibers).
4. a) submucosal, b) intramural, c) subserosal.
5. Picrofuchsin.
Task №35
1. Endocervicosis (pseudoerosion (false erosion) of uterus cervix).
2. Dishormonal disease.
3. Yes (after adequate treatment).
4. Metaplasia of epithelium.
5. Uterus cervix cancer.
Task №36
1. Chorionepithelioma (chorioncarcinoma).
2. Malignant.
3. Yes (organospecific).
4. Uterus cavity contains dark red tumoral node with rough surface and spongiform structure which
ingrowths in myometrium. Plural foci of hemorrhage are visible in it.
5. Tumor has given metastases in lungs.
Task №37
1. Fibroadenoma of brest .
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2. Intracanalicular variant.
3. Benign.
4. Yes, organospecific.
5. Dishormonal diseases.
Task №38
1. Pneumonia at flue.
2. Severe toxic form.
3. Necrotic tracheitis.
4. Lung is enlarged in size. Plural centers of acinary or lobulary pneumonia with ability to abscess
formation (whitish yellow) and centers of hemorrhages (dark red) are visible in pulmonary tissue.
5. “Big motley lung”.
Task №39
1. Measels.
2. Viral diseas.
3. Enanthema (Belsky-Copplik-Filatov’s spot).
4. Viral pneumonia.
5. False croup.
Task №40
1. Cholera.
2. Vibrio cholerae, vibrio El-Tor.
3. 1) Cholera enteritis, 2) Cholera gastroenteritis, 3) Algid period.
4. Loops of small intestine are swollen, serous membrane is dry with necrosis of enterocytes, lumen
contains colorless liquor looking like “rice-water”.
5. Exicosis (dryness of the body), reduction of spleen, necrotic and necrobiotic changes in liver,
brain, myocardium, acute renal failure (necrosis of renal tubular epithelium).
Task №41
1. Salmonella typhi, Salmonella paratyphi.
2. Transenterocytary relation.
3. Large intestinum.
4. In stage of medullary swelling Peyer’s patches are increased, jut out above mucosa, forming
convolutions and bulgings similar to surface of brain.
5. Stage of necrosis of Peyer’s patches can complicated by perforation with peritonitis development,
severe intoxication, sepsis, intestinal bleeding.
Task №42
1. Dysentery (shigellosis).
2. Oral cavity (fecaly-oral way).
3. Purulent colitis.
4. Spreading of infection on surrounded tissue.
5. Intraenterocytary.
Task №43
1. Diphtheria.
2. Bacterial infection, corynebacteria diphtheriae (Leffler’s bacillus).
3. Fibrinous inflammation (croupous and diphtheritic).
4. Tonsils are enlarged in size, red, soft, edematic, covered by thick whitish-grey pellicle which is
closely related to the surface of epithelium, difficultly removed with deep ulceral defects after
removing.
144
5. True croup (mechanical asphyxia, occlusion of trachea by diphtheria pellicle).
Task №44
1. Scarlet fever.
2. Bacterial infection, ß-hemolitic streptococcus group A (Streptococcus pyogenes).
3. Toxic-allergic.
4. Tonsills are enlarged in size, swollen, dark red. There are ulceral defects with necrotic masses
inside on there surface.
5. Gangrene of tonsils, retrotonsilar abscess, phlegmone of neck, otitis, antritis.
Task №45
1. Septicemia (acutest, fulminant form).
2. Obstetrical (uterogenic).
3. Uterus enlarged in size, swelled, edematic, dark red with plural petechial hemorrhages.
4. Dystrophic changers.
5. Hyperplasia.
Task №46
1. Septicopiemia (acute form).
2. Surgical sepsis.
3. Organs enlarged in size, flabby, edematic with plural foci of purulent inflammation.
4. Hyperplasia and hypertrophy.
5. Splenomegalia.
Task №47
1. Tuberculous granulema.
2. Primary affect (Ghon’s focus), lymphangitis, lymphadenitis.
3. Productive-necrotic.
4. Intention of primary affect, encapsulation, fibrosis (scar formation), petrification, ossification.
5. Growth of primary affect, lymphogenic, hematogenic, mixed.
Task №48
1. Extrapulmonary tuberculosis of bones (primary tuberculous spondilitis).
2. Lymphogenic spreading of infection from primary affect.
3. Plural foci of caseous necrosis with destruction of bodies in vertebral bones.
4. In bone marrow.
5. Primary tuberculous complex.
Task №49
1. Lungs are enlarged with numerous whitish-yellow foci 1-2 mm with dense necrotic masses
looking like cottage cheese (casious necrosis) in all fields of lungs.
2. Productive tissue reaction, hematogenic spreading from primary affect.
3. Transformations of macrophages in large cells: mononuclear epithelioid cells and giant PirogovLanghans’s cells.
4. destruction of tissue by productive inflammation (fibrinoid necrosis).
5. Scarring of granulemas.
Task №50
1. Secondary.
2. Extensive irregular shaped cavities with thick and dense walls are seen in tissue of lung. Cavities
contain yellowish-grey breaking caseous mass. Large bronchi are open in the cavities. Peribronchial
and privascular sclerosis are visible on the background of emphysema.
145
3. Ziehl-Nielsen.
4. Amyloidosis of kidney.
5. Acute renal failure.
Task №51
1. Tertiary syphilis.
2. Cardiovascular syphilis.
3. Productive-necrotic reaction.
4. In ascending aorta, thoracic aorta, aortal valves, coronary arteries. (Fibrosis of aortal and arterial
walls →aneurisms formation, narrowing of lumens.)
5. Cellular infiltrates represented by lymphocytes, plasma-cells, fibroblasts and singular Langhan’s
giant cells are observed in mesangium by pathway of vasa vasorum.
Task №52
1. Syphilis.
2. Tertiary gummous syphilis.
3. Treponema pallidum.
4. Productive inflammation.
5. Liver is enlarged in size, with single whitish-grey foci of gummous (liquafactive) necrosis and
sclerosis on background of fatty dystrophy.
146
ANSWERS ON TESTS
1. INRODUCTION
4
2
3
5
3
3
3
2
2
2
1
2
3
4
5
6
7
8
9
10
2
3
2
4
2
4
4
4
3
3
11
12
13
14
15
16
17
18
19
20
4
4
2
2
1
2
2
5
4
3
21
22
23
24
25
26
27
28
29
30
4
5
2
3
2
31
32
33
34
35
2. INTRACELLULAR ACCUMULATION
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
5
4
1
4
4
4
1
2
1
1
1
2
1
1
3
3
3
2
1
3
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
40
1
4
2
5
4
4
2
4
5
4
3
5
1
1
3
4
4
5
4
3
41
42
43
44
45
46
47
48
49
50
51
52
53
54
55
56
57
58
59
60
3
1
2
5
5
3
4
3
4
2
3
1
5
1
3
3
2
5
4
4
61
62
63
64
65
66
67
68
69
70
71
72
73
74
75
76
77
78
79
80
3
4
1
3
2
2
5
2
4
2
3
5
3
4
4
3
4
4
4
3
81
82
83
84
85
86
87
88
89
90
91
92
93
94
95
2
1
5
5
3
2
3
1
3
4
1
2
1
4
2
147
3. HEMODINAMIC DISORDERS
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
3
4
4
3
4
1
3
1
3
3
4
2
2
5
3
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
3
4
3
3
1
2
3
4
5
4
3
2
2
4
5
31
32
33
34
35
36
37
38
39
40
41
42
43
44
45
3
1
5
2
5
3
4
1
4
3
2
4
2
3
2
46
47
48
49
50
51
52
53
54
55
56
57
58
59
60
1
4
4
2
1
2
1
2
5
5
2
5
1
1
3
61
62
63
64
65
66
67
68
69
70
71
2
1
4
3
2
1
5
3
4
3
2
31
32
33
34
35
36
37
38
39
40
5
2
5
3
4
5
5
4
2
5
41
42
43
44
45
46
47
48
49
50
4
3
2
1
3
3
1
4
5
4
65
66
67
68
69
70
71
72
73
74
75
76
77
78
79
80
3
4
4
3
1
3
1
2
5
3
2
4
1
3
4
2
4. CELL DEATH
1
2
3
4
5
6
7
8
9
10
3
4
1
3
2
3
2
5
5
2
11
12
13
14
15
16
17
18
19
20
4
1
1
2
5
1
1
1
4
4
21
22
23
24
25
26
27
28
29
30
2
3
1
1
2
5
5
1
3
5
5. INFLAMMATION & IMMUNE SYSTEM PATHOLOGY
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
5
4
3
2
4
4
3
2
4
4
4
2
4
2
4
5
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
1
5
2
5
2
2
2
4
2
5
2
5
3
1
4
2
33
34
35
36
37
38
39
40
41
42
43
44
45
46
47
48
1
2
1
1
1
2
4
5
4
3
1
3
5
1
5
1
49
50
51
52
53
54
55
56
57
58
59
60
61
62
63
64
1
5
5
5
1
2
3
3
5
1
1
3
3
4
2
4
148
6. ADAPTATION
1
2
3
4
5
2
4
2
2
4
6
7
8
9
10
5
2
3
3
4
11
12
13
14
15
3
1
2
1
3
16
17
18
19
20
4
4
3
3
4
21
22
23
24
25
5
5
1
5
2
19
20
21
22
23
24
1
3
4
3
1
1
25
26
27
28
29
30
4
3
4
3
1
2
4
1
5
1
1
1
5
2
4
2
1
3
2
53
54
55
56
57
58
59
60
61
62
1
4
2
4
2
3
3
5
4
1
1
4
2
2
1
2
2
2
3
3
1
2
1
53
54
55
56
57
58
59
3
2
2
3
1
4
3
7. NEOPLASIA
1
2
3
4
5
6
3
4
1
1
2
3
7
8
9
10
11
12
3
1
3
4
2
3
13
14
15
16
17
18
3
2
3
4
2
2
8. CARDIO-VASCULAR DISEASES
1
2
3
4
5
6
7
8
9
10
11
12
13
2
2
4
5
5
2
5
1
5
1
4
1
2
14
15
16
17
18
19
20
21
22
23
24
25
26
5
2
3
2
4
2
4
4
3
1
1
2
5
27
28
29
30
31
32
33
34
35
36
37
38
39
5
3
1
3
2
4
4
5
4
5
1
5
4
40
41
42
43
44
45
46
47
48
49
50
51
52
9. PULMONARY DISEASES
1
2
3
4
5
6
7
8
9
10
11
12
13
4
4
4
3
2
3
3
2
1
2
4
4
1
14
15
16
17
18
19
20
21
22
23
24
25
26
4
3
4
2
1
3
4
1
5
4
1
1
4
27
28
29
30
31
32
33
34
35
36
37
38
39
3
4
2
1
3
2
4
1
2
5
1
1
4
40
41
42
43
44
45
46
47
48
49
50
51
52
149
10. GIT DISEASES
1
2
3
4
5
6
7
8
9
10
11
12
13
1
4
2
4
1
2
2
1
3
4
3
2
1
14
15
16
17
18
19
20
21
22
23
24
25
26
3
3
1
2
2
1
4
2
3
2
4
3
2
27
28
29
30
31
32
33
34
35
36
37
38
39
1
4
1
4
3
1
2
2
2
1
4
4
4
40
41
42
43
44
45
46
47
48
49
50
51
52
1
4
3
4
2
1
3
2
5
4
4
3
1
53
54
55
56
2
5
5
1
4
2
4
4
2
1
3
3
4
1
4
1
4
53
54
55
56
57
5
1
5
1
3
1
2
1
2
4
2
1
4
3
1
1
2
4
53
54
55
4
4
5
11. LIVER PATHOLOGY
1
2
3
4
5
6
7
8
9
10
11
12
13
5
3
2
5
2
5
2
2
2
4
3
1
5
14
15
16
17
18
19
20
21
22
23
24
25
26
2
1
4
4
2
2
2
3
3
1
5
3
4
27
28
29
30
31
32
33
34
35
36
37
38
39
2
1
1
1
2
4
5
3
1
2
1
3
1
40
41
42
43
44
45
46
47
48
49
50
51
52
12. KIDNEYS PATHOLOGY
1
2
3
4
5
6
7
8
9
10
11
12
13
5
4
5
1
1
3
2
4
1
4
4
1
2
14
15
16
17
18
19
20
21
22
23
24
25
26
1
3
4
5
1
4
2
4
2
5
2
1
1
27
28
29
30
31
32
33
34
35
36
37
38
39
1
2
3
3
5
3
3
5
3
3
4
1
2
40
41
42
43
44
45
46
47
48
49
50
51
52
150
13. ENDOCRINOLOGY
5
1
4
1
2
2
4
2
3
1
1
2
3
4
5
6
7
8
9
10
1
3
4
1
2
1
1
1
4
2
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
5
5
2
5
5
1
2
2
4
3
2
3
3
1
4
1
1
1
3
2
31
32
33
34
35
36
37
38
39
40
2
1
1
2
2
4
4
41
42
43
44
45
46
47
14. FEMALE GENITAL TRACT PATHOLOGY. PREGNANCY PATHOLOGY.
5
3
2
2
4
3
2
4
3
2
1
2
3
4
5
6
7
8
9
10
3
5
3
1
3
4
2
2
2
1
11
12
13
14
15
16
17
18
19
20
3
1
2
5
2
1
5
3
2
5
21
22
23
24
25
26
27
28
29
30
3
2
5
5
3
1
2
4
2
1
31
32
33
34
35
36
37
38
39
40
15. VIRAL & CHILDREN DISEASES
1
2
3
4
5
6
7
8
9
10
4
3
1
1
5
3
3
3
4
2
11
12
13
14
15
16
17
18
19
20
2
4
1
3
1
2
2
2
3
2
21
22
23
24
25
26
27
28
29
30
2
4
1
4
5
2
2
2
1
2
31
32
33
34
35
36
37
38
39
40
4
2
3
4
2
4
4
4
2
1
41
42
43
44
2
1
3
1
5
3
9
10
5
3
16. BACTERIAL INFECTIONS
1
2
4
4
3
4
4
3
5
6
3
5
7
8
151
17. TUBERCULOSIS. SYPHILIS.
1
2
3
4
5
6
7
8
9
10
2
3
5
2
3
3
4
1
5
3
11
12
13
14
15
16
17
18
19
20
3
3
3
4
3
4
5
1
4
2
21
22
23
24
25
26
27
28
29
30
2
3
5
2
2
4
2
1
1
5
31
32
33
34
35
36
37
38
39
40
5
4
4
3
3
5
5
2
4
2
41
42
4
3
19
20
21
22
23
24
2
3
1
5
1
3
25
26
2
5
18. SEPSIS
1
2
3
4
5
6
2
5
4
3
1
5
7
8
9
10
11
12
5
4
2
1
2
3
13
14
15
16
17
18
1
2
1
1
4
4
152