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Questions to prepare for examination 2015-16
1. The notion of "nosology", parts nosology.
2. The notions of "pathologic process", pathologic state", "pathologic reactions", "typical
pathologic processes", "remission", “recurrence","complication".
3. Disease, definition. Principles used in classification of diseases. Stages of disease.
4. Etiology, definition. The nature and characteristics of pathogenic factors. Factors of
diseases: environmental, genetic, social. The relation between causes and conditions in the
development of diseases.
6. The notions of "pathogenesis", "vicious circles".
7. Reactivity of the body and its role in the development of disease. Forms and types of
reactivity.
8. Arterial hyperemia: definition, causes, types (physiologic and pathologic), mechanisms
(neurogenous, neuromyoparalytic and humoral) and consequences. Reactive hyperemia.
Manifestations of arterial hyperemia and its mechanisms.
9. Venous hyperemia: definition, causes and consequences. Manifestations of venous
hyperemia and their mechanisms.
10. Ischemia: definition, causes and consequences. Manifestations of ischemia and their
mechanisms, factors that influence on the consequences of ischemia.
11 Stasis: types and causes.
12. Sludge syndrome: types, causes, and mechanisms.
13.Definition and significance of inflammation. Causes of inflammation.
14. Primary and secondary alteration in the focus of acute inflammation: causes, mechanisms
of development, manifestation. Physico-chemical changes in the focus of inflammation.
15. Exudation. Definitions of an exudate and transudate. Sequence and mechanisms of
vascular changes in acute inflammation.
16. Inflammatory mediators that influence on these processes.
17. Phagocytosis: stages.
18. Local and systemic signs of inflammation.
19. Nature and effects of inflammatory mediators: vasoactive amines, complement, kinin,
and clotting systems, arachidonic acid metabolites, platelet-derived factor, cytokines and
chemokines, nitric oxide, lysosomal constituents
20.General features of acute and chronic inflammation.
21. Typical forms of disordered immunologic reactivity. Principles of classification of
immunodeficiency states.
22. Primary immunodeficiencies: classification and clinical manifestations.
Forms of primary immunodeficiency (causes, mechanisms, clinical manifestations):
a) B system-dependent:
b) T system-dependent:
с) combined.
23. Secondary (acquired) immunodeficiency states. AIDS
24. The notion of the "allergy". Types of allergens. Exogenous and endogenous allergens.
25. Stages of allergy.
a) Immunologic stage.
b) Pathochemical stage.
c) Pathophysiological stage
26. Anaphylactic (I) type of allergy. The nature of allergen and antibody. Mediators of the
anaphylactic reaction.
27. Type II hypersensitivity. The nature of allergen and antibody. Mechanisms and clinical
examples of type II allergies.
28. Type III hypersensitivity. The nature of allergen and antibody.
Mechanisms and clinical examples of type III allergies. Systemic and local immune complex
disease.
29. Type IV hypersensitivity. The nature of allergen and antibody.
30. Definition of fever. Differences between fever and hyperthermia. Types of pyrogens. The
biological significance of fever
31. Pathogenesis of fever. Features of thermoregulation at different stages of fever.
32. Types of fever:
- based on the extent of temperature rise;
- based on the circadian temperature fluctuations.
33. Exertional hyperthermia: causes, mechanisms
34. Definition of hypoxia and its classification
35. Exogenous hypoxia: causes, types and typical changes
36. Respiratory hypoxia: causes, types and typical changes in the given type of hypoxia
37. Anemic hypoxia: causes, types and typical changes
38. Circulatory hypoxia: causes, types and typical changes
39. Histotoxic and substrate types of hypoxia: causes, types and typical changes
40. Adaptive reactions in acute hypoxia.
41. Mechanisms of long-term adaptation to hypoxia.
42. Hypoglycemia: сauses and mechanisms. Hypoglycemic coma.
43. Hyperglycemia: causes and mechanisms.
44. Diabetes mellitus: characteristic features, classification, pathogenesis of type I and type II
forms.
45. Metabolic disorders (carohydrate, protein, lipid) in diabetes mellitus.
46. Complications of diabetes mellitus (chronic and acute). Ketoacidotic coma.
47. The main classes of lipoproteins and their functions. Atherogenic and antiatherogenic
lipoproteins. Mechanisms of hyperlipidemia.
48. Obesity: definition, diagnostic approaches, pathological significance. Types and
pathogenesis of obesity.
49. Atherosclerosis: description and pathological features. Risk factors of atherosclerosis.
Stages of atherogenesis:
- initiation;
- formation and evolution of atheroma;
- complications.
50. Hypohydration: causes, types, mechanisms
consequences, and pronciples of treatment.
of
development,
manifestations,
51. Overhydration: causes, types, mechanisms
consequences, and pronciples of treatment.
of
development,
manifestations,
52. Edema: definition, types, the main factors of development, principles of treatment.
53. Edema during cradiac failure: etiology, pathogenesis, and manifestations.
54. Renal edema: etiology, pathogenesis, manifestations, and consequences.
55. Shock: characteristics, types, etiology, pathogenesis, manifestations, principles of
treatment.
56. Coma: characteristics, types, etiology, general pathogenesis, manifestations, principles of
treatment.
57. Definition of anemia and its classification.
58. Anemias of blood loss: types, causes, hematological signs.
59. Hemolytic anemias: types, common causes, manifestations, hematological signs.
Hereditary spherocytosis: pathogenesis, manifestations, hematological signs. Sickle cell
disease: pathogenesis, manifestations, hematological signs. Thalassemia syndromes: types,
pathogenesis, manifestations, hematological signs.
60.B12 (Megaloblastic) anemia: causes, pathogenesis, manifestations, hematological signs.
61. Iron deficiency anemia: causes, pathogenesis, manifestations, hematological signs.
62. Aplastic anemia: causes and pathogenesis, hematological signs.
63. Erythrocytosis: causes and mechanisms
64. Leukopenia: definition and causes. General mechanisms of leukopenia. Patterns of shift
to the right.
65. Leukocytosis: causes and mechanisms. Types of leukocytosis; patterns of shift to the left.
66. Leukemoid reactions: typical features, causes, mechanisms of development, physiologic
significance.
67. The system of hemostasis: components and their function. Typical forms of pathology of
the hemostatic system.
68. Thrombotic syndrome: its main causes, mechanisms of development, manifestations and
consequences.
69. Hemorrhagic syndrome: causes, mechanisms of development, manifestations and
consequences.
70. Causes and mechanisms of thrombocytopenia and thrombocytopathia.
71. Abnormalities in clotting factors. Hemophylias.
72. The syndrome of disseminated intravascular coagulation: stages, mechanisms of
development, manifestations and consequences.
73. Definition of coronary insufficiency. The main cuases of coronary insufficiency.
Adaptive mechanisms developing during acute and chronic coronary insufficiency.
74. The syndromes of coronary insufficiency: angina pectoris, myocardial infarction, chronic
ischemic heart disease, sudden coronary death.
75. Definition, general causes and classification of heart failure. Myocardial and
nonmyocardial cardiac insufficiency.
76. Adaptive reactions during acute and chronic heart failure: Frank-Starling mechanism,
myocardial hypertrophy, redistribution of cardiac output, salt and water retention, activation
of the sympathetic system.
77. Pathogenesis of the myocardium decompensation during hypertrophy. 78.Hemodynamic
abnormalities in heart failure. Clinical features of heart failure: the syndromes of cardiac
edema and cachexia.
79. Definition and principles of classification of arterial hypertension.
80. Renal arterial hypertension: pathogenesis of renovascular, renoprival, renal parenchymal
hypertension.
81. Pathogenesis of endocrinogenic arterial hypertension.
82. Essential hypertension: etiology and pathogenesis.
83. Alveolar hyper- and hypoventilation: causes, mechanisms of development, consequences,
and typical changes in breathing volumes.
84. Disorders of the neurogenic control of breathing. Pathological forms of breathing.
85. Types and consequences of perfusion disorders: pulmonary arterial hyper- and
hypotension.
86. Types and mechanisms of ventilation-perfusion mismatch.
87. Abnormal diffusive capacity of the alveolar-capillary barrier.
88. Typical forms of functional pathology of the digestive tract: general etiology.
89. Disorders of appetite, taste, and initial treatment of food in the oral cavity.
90. Disorders of swallowing: dysphagia, achalasia, diffuse esophageal spasm.
91. Disorders of digestion in the stomach: disturbance of secretory and motor function.
92. Disorders of digestion in the intestine: disturbance of secretion, motor function, and
absorption.
93. The syndrome of malabsorption: etiopathogenesis, manifestations and consequences.
94. Typical disorders of cavity digestion: causes, manifestations.
95. Typical disorders of parietal digestion: causes, manifestations.
96. Pathogenesis of peptic ulcer of the stomach and duodenum.
97. General causes of liver dysfunction. The syndrome of hepatic insufficiency Causes,
types and pathogenesis of hepatic coma.
98. The syndrome of hepatic insufficiency. Typical disorders of carbohydrate, aminoacid,
protein, and lipid metabolism in hepatic insufficiency; failure of detoxification function.
99. Hemolytic jaundice: causes, mechanisms, clinical and laboratory manifestations.
100. Obstructive jaundice: types, causes, mechanisms, clinical and laboratory manifestations,
consequences.
101. Hepatocellular jaundice: causes, mechanisms, stages, clinical and laboratory
manifestations.
102. General causes and mechanisms of kidneys dysfunction. Disorders of filtration, tubular
reabsorption and excretion.
103. Syndromes of acute renal insufficiency: typical features, causes and manifestations
104. Syndromes of chronic renal insufficiency: typical features, causes and manifestations.
Uremic coma.
105. Nephrotic and nefritic syndromes: typical features, causes and manifestations.
106. Pyelonephritis: characteristic features, causes and pathogenesis.
107. Nephrolitiasis: causes, mechanisms of development, consequences.
108. General etiology and pathogenesis of endocrine disorders. Typical forms of functional
pathology of adenopituitary. Hypopituitarism: types, causes, mechanisms of development
and manifestations
108. Hyperpituitarism: types, causes, mechanisms of development and manifestations.
Acromegaly and gigantism. Typical forms of disorders of neurohypophysis. Diabetes
insipidus
109. Typical forms of adrenals’ dysfunstion. Hypercortisolism: types, pathogenesis and
manifestations. Cushing’s disease and syndrome, hyperaldosteronism.
110. Hypocortisolism: types, pathogenesis and manifestations. Acute adrenal failure and
Addison’s disease, hypoaldosteronism, syndromes of adrenal androgen excess.
111. Disorders of adrenal’s medulla. Manifestations and consequences of
phyochromocytoma.
112. Hypothyroidism: types, causes, mechanisms of development and clinical
manifestations. Common hypothyroid states: myxedema, cretinism, endemic goiter.
113. Hyperthyroidism: types, causes, mechanisms of development and clinical
manifestations. Pathogenesis and manifestations of Grave’s disease, Hashimoto’s thyroiditis.
114. General etiology, pathogenesis, and typical forms of pathology of the nervous system.
115. Disorders of locomotion: manifestations of the upper (central) and lower (peripheral)
motor neuron damage.
116. Hypokinetic and hyperkinetic movement disorders: types, etiology and pathogenesis.
117. Disorders of sensation: general etiology and classification.Hypo- and hypersthesia,
dysesthesia: types and mechanisms of disorders.
HYPOXIA
3. Urgent compensatory reaction at acute hypoxia (reduced pO2 in air):
tachypnoe
stimulation of erythropoesis
redistribution of blood
tachycardia
increase blood supply in liver
spasm vessels into internal organs
4. Choose the reasons of hypoxie hypoxia:
mountain sickness
increased pO2 in air
emphysema
reduced pO2 in air
poisoning by aniline
5. Choose the reasons of blood type hypoxia:
poisoning by charcoal gaze
mountain sickness
reduced pO2 in air
anemia
poisoning by methemoglobin-complexes
presence into closed space
6.Which changes in cells яге adaptive in the case of hypoxia?
inhibition of glycolysis
r e d u c e d act ivity of Na/K t and Ca2+ ATP-enzymes
activation of' glycolysis
mobilization of kreatinphosphate
mobilization of glycogen from depot
activation of peroxidative oxidation of lipids
increased concentration of Sodium into cells
7. Which factor can promote oxygenic capacity of blood at hypoxia?
tachypnoe
mobilization of blood from depot
tachycardia
stimulation of erythropoesis into bone marrow
activation of erythropoietins
increased cardiac output
8. Choose clinical signs of long-time adaptation to hypoxia:
hypertrophy of lungs
tachypnoe
hypertrophy of myocardium
tachycardia
increased number of mitochondria into cells
stimulation of erythropoesis
mobilization of blood from depot
9. Choose the reason of blood type hypoxia:
poisoning by CO (charcoal gaze)
vit. D deficiency
vit. В12 deficiency
shperocytosis
gaseous embolism
10. Choose the reason of blood type hypoxia:
hemoglobinosis S
reduced activity of respiratory enzymes in tissues
poisoning by cyanides
poisoning by nitrates
chronic blood loss
11. Choose the reasons of tissue type hypoxia:
vit. A deficiency
poisoning by methemoglobin-complexes
poisoning by cyanides
acute blood loss
increased formation of prostaglandins E1
12. Choose cases when hemoglobin affinity to oxygen is reduced?
metabolic acidosis
sickle-cells disease
metabolic alkalosis
reduced activity 2,3-diphosphoglycerate in red blood cells
reduced body temperature
increased body temperature
hypocapnia
13. Choose cases when hemoglobin affinity to oxygen is increased?
metabolic acidosis
sickle-cells disease
metabolic alkalosis
reduced activity 2,3-diphosphoglycerate in red blood cells
reduced body temperature
increased body temperature
hypocapnia
14. Choose changes in human body at long presence in mountains:
increased activity 2,3-diphosphoglycerate in red blood cells
increased hematocrit
hypertrophy of myocardium
hypoventilation in lungs
reduced activity of respiratory enzymes in cells
inhibition of nucleonic acids' synthesis
increased concentration of endogenous opiates
increased vascularisation in peripheral organs and tissues
increased basal metabolism
15. Choose the reasons of respiratory hypoxia:
anemia
pneumonia
poisoning by nitrates
lung's collapse
poisoning by charcoal gaze
pneumothorax
17.Choose the reasons of tissue type hypoxia:
poisoning by charcoal gaze
poisoning by cyanides
poisoning by aniline
poisoning by monoiodineacetate
poisoning by barbiturates
18. Choose the signs of circulatory hypoxia:
increased arterio-venous difference of oxygen
reduction of linear blood velocity
respiratory acidosis -hypertension
braducardia
reduction of volumetric blood velocity into capillaries
reduced arterio-venous difference of oxygen.
19.Choose the mechanisms of long-time adaptation to hypoxia:
mobilization of blood from depot
increased number of capillaries
increased number of mitochondria
dyspnea
hyperplasia of bone marrow
tachycardia
hypertrophy of myocardium
20.
Choose the mechanisms of circulatory hypoxia:
reduction of oxygen transport to tissues
reduction of oxygen utilization in tissues
reduced activity of respiratory enzymes in tissues
chronic heart insufficiency
increased consumption of oxygen at physical loading
21. Choose the reasons of respiratory hypoxia:
emphysema
pneumonia
collapse
lung's collapse
chronic heart insufficiency
pneumothorax
reduction of blood volume
22. Choose clinical signs for circulatory hypoxia:
hypotension
decreased arterio-venous difference of oxygen
reduced concentration of oxygen into arterial blood
reduction of volumetric blood velocity into capillaries
tachycardia
23. Choose reaction in organism at hyperoxia:
inhibition of chemo-receptors into vessels
dyspnea
suppression of heart rate and rhythm of respiration
activation of chemo-receptors into vessels
reduced cardiac output
tachycardia
DISORDERS OF MICROCIRCULATIOIN
1. Give types of venous hyperemia due to pathogenesis:
myoparalytic
obstructive
cardiogenic (at heart failure)
compressive
neuroparalytic
2. Which factors can increase permeability of vascular wall?
increased blood velocity in capillaries
increased viscosity of blood
products of must cells degranulation
acidosis
leucopenia
activation of hydroiyzes in interstitial liquid
3. Give types of arterial hyperemia due to pathogenesis:
neurotonic
obstructive
neuroparalytic
myoparalytic
comprcssive
4. Which changes of microcirculation are characteristic for ischemia?
increased arlerio-venous difference into vessels
reduction of hydrostatic pressure in arterioles and pre-capillaries
incretled linear blood velocity
increased reabsorption of liquid from tissues into capillaries
reduced number of capillaries with blood
5. Which factors can promote development of thrombosis?
reduction of blood velocity
increased blood velocity
reduced number of platelets
aggregation of platelets
exudation
atherosclerosis
6. "Sludge" phenomenon is:
the first stage of cloth formation
vital aggregation of red blood cells into microcirculatory vessels at increased blood viscosity and separation of
blood
formation of thrombo-leucocytic aggregates on the vessel's wall
separation of btood on cells and plasma
coagulation of blood
7. "Sludge" phenomenon can develop at the next types pathology:
acute heart failure
massive burn
shock
massive blood loss
hypervolemia (increased blood volume)
hyperhydratation
8. Which factors can promote development of thrombosis?
damages of vascular wall
decreased blood velocity
activation of coagulation
increased blood viscosity
activation of anti-coagulant system
vit. К deficiency
excess of epinephrine in blood
9. Choose the normal level of hydrostatic pressure into arterial part of capillaries:
15 mm of Mercury
25 mm of Mercury
35 mm of Mercury
55 mm of Mercury
10. Which changes can develop in the focus of ischemia?
necrosis
acidosis
hypofunction
hyperfunction
excess of K+ into cells
deficiency of Na+ into cells
excess of Си++ into cells
11. Stasis is:
complete stop of blood circulation into vessels
increased blood supply in organs or tissues due to dilatation of arterioles
decreased blood supply in organs or tissues due to spasm of arterioles
12. True stasis is:
increased blood supply in organs or tissue due to reduced blood outflow
local spot of blood circulation due to increased blood viscosity
13. Choose pathogenic factors of neuroparalytie arterial hyperemia:
activation of parasympathetic system
irritation of cholinergic system
blockade of adrenergic system
activation of histamine and serotonin system
activation of vegetative system
14. Heat in the focus of arterial hyperemia can be explained by:
increased inflow of arterial blood
activation of oxidative processes
excessive formation of lymph
increased number of capillaries with blood
15. Choose the reasons of true (capillary) stasis:
compression of arteries by scar-tissue
direct action temperature on vascular wall
damages of tissues by acid and alkaline
thromboembolism
spasm of peripheral vessels
actions of toxins on organism
16. Rheological state of blood depends on:
cardiac output
concentration of proteins in plasma
ratio between blood cells and plasma
deformation's properties of red blood cells
functions of collateral vessels
17. Which changes of microcirculation are characteristic for arterial hyperemia?
increased number of capillaries with blood
reduction of hydrostatic pressure in capillaries
increased blood velocity in capillaries
increased outflow of lymph
increased filtration of liquid from vessels into tissues
18. Choose the sequences of venous hyperemia:
infarction
embolism
atrophy
hemorrhage into tissues
thrombosis
stasis
sclerosis
19. Choose the sequences of venous hyperemia:
growth of connective tissue
increased function of organs
dystrophy of tissues
hemorrhage into tissues
20. Which changes of microcirculation are characteristic for venous hyperemia?
decreased blood velocity in small arteries, capillaries and veins
pendulum-like circulation
increased outflow of lymph
reduced number of capillaries with blood
21. Filtrative pressure is:
difference between oncotic pressure in blood and in tissues
difference between hydrostatic arterial and hydrostatic venous pressure
difference between hydrostatic presuure and oncotic pressure in blood
oncotic pressure and osmotic pressure in blood
22. Venous hyperemia can localize focus of inflammation:
yes
no
23. Physiologic arterial hyperemia is:
arterial hyperemia in the focus if inflammation
post-ischemic arterial hyperemia
activation of thyroid gland function
action of turpentine on skin
Choose the types of endogenous embolism:
fatty
air
tissue
gaze
thromboembolism
embolism by foreign bodies
embolism by amniotic water
parasite
25. Give characteristics of microcirculation for arterial hyperemia:
increased hydrostatic pressure in capillaries
reduced number of capillaries with blood
increased number of capillaries with blood
increased reapsorption of liquid from tissues into capillaries
decreased linear and volumetric blood velocity
increased linear and volumetric blood velocity
reduced outflow of lymph
26. Choose correct sentences:
thrombus, foreign bodies, tissues, fat, bubbles of air, parasites can be embolus
arterial embolus can stay in lung's vessels, but venous embolus can stay in any organ
embolus of pulmonary vessels, coronary vessels and cerebral vessels are dangerous
27
Choose я possible reasons of gaseous embolism:
rapid increasing of barometric pressure
wounding of big veins
rapid change of barometric pressure from increased level to normal level
inspiration of inert gazes
sudden change of barometric pressure from normal level to reduced level
28
Which substances can cause arterial hyperemia?
acetylcholine
epinephrine
histamine
bradykinin
thromboxane A2
29 Which pathogenic factors can cause arterial hyperemia?
cutting of peripheral nerves
mechanical irritation of tissues and organs.
remove of ligature
occlusion of arteries by cloth
action of mustard plaster on skin
compression of veins by tumor V
30 Which substances can cause ischemia?
histamine
epinephrine
acetylcholine
bradykinin
thromboxane A2
31. Which pathogenic factors can cause venous hyperemia?
cutting of peripheral nerves
increased pressure into big veins
thrombosis of veins at insufficient collaterals
compression of veins at pregnancy
increased concentration of epinephrine in blood
mechanical irritation of organs
32. Aggregation of erythrocytes can be promoted by:
increased concentration of globulins in blood
decreased concentration of fibrinogen in blood
change of electrical charge in red blood cells
damages of small vessels
reduction of arterial pressure
extra-cellular dehydration
33. Choose the types of stasis:
hyperemia
congestive
ischemic
true
34. Give characteristics of microcirculation for ischemia:
primary dilatation of arteries and secondary dilatation of veins and capillaries
spasm capillaries and veins after occlusion in arteries
increased linear and volumetric blood velocity
decreased linear and volumetric blood velocity
increased temperature of organs and tissues
decreased temperature of organs and tissues
35. "Sludge-phenomenon" is a main mechanism of:
arterial hyperemia
venous hyperemia
thrombosis
stasis
ischemia
36. Choose clinical symptoms of venous hyperemia:
redness of organs and tissues
paleness
cyanosis
edema
increased turgor
increased temperature of organ or tissue
3. INFLAMMATION
1. Mechanisms of glucocorticoids effects at inflammation:
increase permeability of vascular wall
decrease permeability of vascular wall
inhibit of kinins production
stabilizeof lysosomal membranes
inhibit growth of connective tissue
2. Intra-vascular factors of exudation:
ncreased viscosity of blood
hyperosmia in the focus of inflammation
hyperoncm of tissues in the focus of inflammation
margination of leucocytes
3. Choose properties of activated components of complement system:
provide lyses of foreign cells
play role of chemo-attractive substances for neutrophiles and monocytes
can activate phagocytosis
can cause degranulation of must cells
can reduce permeability of vascular wall
4. Choose characteristics of neutrophiles:
can recognize and neutralize host dead cells
participate in acute inflammation
can produce mediators of inflammation
can form giant multi-nuclear cells in the focus of inflammation
present in the focus of inflammation about 1-2 days
5. Which pathogenic factors can promote
transformation arterial hyperemia into venous
hyperemia in the focus of acute inflammation?
increased permeability of vascular wall
increased blood viscosity
increased adhesion of endothelium and blood cells
6.
Which
biological
active
neutrophiles?
C3a-component of complement
C5a- component of complement
substances
play
role
of chemo-attractive substances for
eukotriens B4
prostaglandins E2
7
Enzyme systems of macrophages which have direct bacteriostatic and bacteriolytic effects?
katalaze
neutral proteazes
myeloperoxidaze
katepsines
8. Which from listed substances are contained in neutrophiles?
lyoscim
myeloperoxidaze
serotonin
prostaglandins
9. Which mediators are produced from phospholipids of cellular membranes?
prostaglandins
leucotriens
factor of platelet's activation
bradykinin
10. Which cells play main role in chronic inflammation?
micro-phages
tissue macrophages
macrophages (monocytes)
11. Inflammation is a specific response of organism on injury:
yes
no
12. Which substance will be loss at cell's destruction:
Potassium
Sodium
Calcium
13. Permeability of vascular wall at alteration is:
reduced
not changed
ncreased
14. Inflammation is developed in three stages:
yes
no
.
15. Which physical-chemical changes in tissues are characteristic for acute inflammation?
H+-hyperionia
hyperoncia
K+-hyperionia
hypooncia
hyperosmia
hypoosmia
16. Which from listed substances are contained in granules of neutrophiles?
bradykinin
prostaglandins
lactoferrin
kationic proteins
17. Mediators (stimulators) of proliferation:
histamin
serotonin
polyamines
keylones
platelet's growth factor
18. Which biological active substances have chemo-attractive properties for neutrophiles?
kallidin
rkujlicrein
histamin
Cl-component of complement
19. Which substances can cause pain at inflammation?
histamine
Sodium ions
epinephrine
Potassium ions
bradykinin
prostaglandins
20. Which pathogenic factors can promote transformation of arterial hyperemia into venous
hyperemia?
dilatation of venules
exudation
margination of leucocytes
aggregation of platelets V
21. Effects of glucocorticoids on inflammation:
stimulate proliferation of connective tissue
activate histaminaze
inhibit of antibodies production
cause edemas
22. Primary mediators of inflammation:
complement system (C)
biogenic amines
elasthaze
bradykinin
serotonin
23. Choose effects of kinins:
fibrinolysis
activation of all components in guard system of blood
pain
alteration of cellular membranes
spasin of smooth muscles
hemostasis
chemotaxis of leucocytes
24. Mediators of late (steadfast) exudation:
serotonin
leucotriens
histamine
factor of platelet's activation
bradykinin
25. Local reactions at inflammation:
heat
fever
redness
edema
general adaptive syndrome
increased RSE
26. Choose cellular mediators of inflammation:
kinins
ysosomal enzymes
vaso-active amines
components of complement (C)
lymphokins
27. Choose mediators - inhibitors of proliferation:
monokins
keylones
immunoglobulins
endothelial factor of chemotaxis
prostaglandins
filldin
28. Factors of exudation are linked with intra-vascular changes in the focus of inflammation:
aggregation of fed blood cells
increased hydrostatic pressure into vessels
increased viscosity of blood
inter-cellular edema of endolhelium
destruction of desmosomes
29. Enervation of tissues at inflammation can cause the next effects:
activation of energy metabolism
inhibition of energy metabolism
immune depression
immune stimulation
activation of proliferation
inhibition of proliferation
30. Choose hormones which have anti-inflammatory effects:
mineralocotricoids
giucocorticoids
thyroxin
epinephrine
ACTH
TSH
31. Effects of activated components in complements system:
stimulation of histamine's releasing from must cells
destruction of attacked cells
activation of leucocytes
activation of pain terminals
32. Which processes can cause adhesion of leucocytes on the surface of endothelial cells at acute
inflammation?
neutralization of negative charge in leucocytes and endothelium by positive ions and kationinc proteins
reduction of blood supply in venous vessels
exposition of P-selectines on the surface of endothelium
arterial hyperemia
ischemia
33. Acute inflammatory response is characterized by:
formation of inflammatory granules
increased permeability in micro-circulatory vessels
accumulation of giant poly-nuclear cells
accumulation of neutrophiles in the focus of inflammation
34. Which processes can be stimulated by neutrophiles at inflammation:
chemotaxis of monocytes
degranulation of must cells
reduced permeability of vascular wall
destruction of cells
35. Choose effects of bradykinin:
increased arterial pressure in aorta
spasm of smooth muscles in organs
increase permeability of vascular wall
irritate pain terminals
reduce permeability of vascular wall
36. Adhesion of leucocytes to endothelium primary develops in:
arterioles
capillaries
post-capillary venules
37. Choose characteristics for histamine:
belongs to preformed mediators of inflammation
can cause dilatation of micro-circulatory vessels
can cause late vascular permeability at acute inflammation
irritate pain terminals
38. Which types of exudates are more often at pericarditis?
purulent
serous
hemorrhagic
fibrinous
39. Choose obligate (professional) phagocytes:
neutrophiles
monocytes
lymphocytes
eosinophiles
40. Which cells can produce mediators at inflammation?
basophiles
platelets
smooth muscles
endothelium
41. Choose characteristics for histamine:
belong to a new-formed mediators of inflammation
can cause immediate permeability of vascular wall at acute inflammation
can cause degranulation of must cells
product of histidin decarboxilation
42. Choose characteristics for neutrophiles:
belong to obligate (professional) phagocytes
can produce free radicals
have myeloperoxidaze activity
contain azurophilic granules
can differentiate into focus of inflammation
43. Which substances can activate phagocytosis?
IgG
IgE
prostagiandins E2
fragment C3b of complement system
44. Aspirin inhibits cyclic-oxygenize and suppress the next mediators of inflammation:
prostaglandin E2
factor of platelet's aggregation *prostaglandin D2
thromboxane A2
45. Which cells participate in chronic inflammation?
macrophages
lymphocytes
epithelial cells
must cells
46. Which factors promote exudates formation at acute inflammation?
difficulties of venous outflow
reduction of hydrostatic pressure into micro-circulatory vessels
retraction of endothelial cells in post-capillary venules
destruction of basal membrane in micro-circulatory vessels by enzymes of leucocytes
47. Which cells can produce mediators of inflammation?
must cells
red blood cells
monocytes
lymphocytes
48. Choose mechanisms of anti-inflammatory effects of glucocorticoids:
inhibit activity of phospholipaze A2
reduce permeability in vessels
inhibit of interleukins
inhibit of complement system
49. Choose effects of complement system at inflammation:
chernotaxis
increase permeability in vessels
dilatation of vessels
50. Choose correct sequence of leucocyte's emigration in the focus of acute inflammation:
1 .monocytes
2.lymphocytes
3.neutrophiles
3-1-2
1-2-3
2-3-1
4. PATHOPHYSIOLOGY OF THERMOREGULATION. FEVER
1. Choose negative sequences of fever:
renal failure
vascular failure
heart failure
hyperthermia
damages of liver
2. Effects of endogenous pyrogens on center of thermoregulation:
increased production of 1L-1
increased activity of cold-sensitive receptors
increased activity of warm-sensitive receptors
decreased production of prostaglandins E
increased production of prostaglandins E
3. Heat-stroke can develop at the next body temperature:
39°C
40°C
41°C
42°C
4. Which changes of metabolism cam develop at fever?
hypoglycemia
positive nitrogen balance
metabolic acidosis
activation of lipolysis
inhibition of glycolysis
5. Adaptive reactions of organism to cold temperature:
shivering
hypertonus of muscles
increased sweating
decreased excitability of cold-sensitive receptors
reduction of respiratory rhythm
increased affinity receptors to epinephrine
hyperglycemia
dilatation of peripheral vessels
6. Choose substances with pyrogenic activity:
histamine
prostaglandins E
lypopolysachrids
1L-1
IL-2
1L-6
kinins
factor of platelet's aggregation .
7. Exogenous pyrogens can influence on:
cerebral cortex
hypothalamus
peripheral thermoreceptors
neutrophiles
monocytes
B-lymphocytes
red blood cells V
8. Adaptive reactions of organism to cold temperature:
increased activity of metabolic processes
«muscular shivering»
hyperventilation +hypoventilation
reduction of basal metabolism
spasm of peripheral vessels
dilatation of peripheral vessels
reduction of sweating
increased sweating
9. Choose mechanisms of physical thermoregulation:
production of primary heat
production of secondary heat («muscular shivering»)
increased circulation into superficial tissues
spasm of peripheral vessels
sweating
convection V
10. Choose symptoms of the 1Ststage of fever:
shivering
heat
intensive perspiration
spasm of peripheral vessels
hyperemia into superficial tissues
prevalence heat-loss over heat-production
prevalence heat-production over heat-loss
11. Choose signs of overheating:
activity of termoregulative center is saved
depends on environmental temperature
absence of shivering
anti-pyretic therapy is effective
12. Choose signs of overheating:
is caused by pyrogens
disorders of thermoregulation
active regulation of body temperature
13. Choose mediators with pyrogenic activity:
L-1
IL-2
IL-6
G-colony-stimulating factor
*factor of tumor necrosis alpha (TNF)
IL-8
14. Defense-adaptive reaction at exogenous hyperthermia:
shivering
intensive perspiration
dryness of skin
paleness of skin
hyperemia of skin
dyspnea
15. Mechanisms of urgent adaptation to cold:
spasm of peripheral vessels
stimulation of fatty tissues
«muscular shivering»
morphologic-functional changes into muscles
increased activity of metabolic processes
increased sensitivity of receptors to epinephrine
16. Which action on CNS can promote fever:
injection of psychostimulators (phenamin, caffeine)
deep narcosis
bilateral decortication
injection of sedative and neuroleptics (bromides, aminazin)
17. Choose inductors of IL-1:
bacterial lipopolysacharides
IL-2
IL-1
IL-6
factor of tumor necrosis alpha (TNF)
G-colony-stimulating factor
18. Choose effects of IL-6:
induction of IL-1 synthesis
induction of TNF synthesis
fever
neurtophilia
induction of stress-reaction
19. Choose clinical symptoms of compensatory stage in the case of hyperthermia:
tachycardia
bradycardia
dyspnea
suppression of respiration
dilatation of peripheral vessels
dilatation of vessels in internal organs
hemodilution
hemoconcentration
20. Choose clinical symptoms of non-compensatory stage in the case of hyperthermia:
tachycardia
bradycardia
dyspnea
dilatation of peripheral vessels
dilatation of vessels in internal organs + suppression of respiration * hemodilution
hemoconcentration
21. Successful reanimation is possible at the next body
temperature:
24°C
25°C
26°С
27°С
28°С
22. Which protein's concentration is increased at response of acute phase?
C-reactive protein
transferrin
fibrinogen
alpha-2-macroglobu 1 in
serum amyloid A
23. Neurtophilia at response of acute phase is caused by:
IL-1
IL-6
IL-2
TNF alpha
IL-8
24 Which proteins of acute phase have anti-inflammatory effects:
C-reactive protein
alpha-2-macroglobulin
alpha-1 -antitripsin
cerulloplasmin
fibrinogen
crotisol
alpha-1 -chemotripsin
25. Choose effects of IL-6:
fever
activation of T-lymphocytes
activation of B-lymphocytes
stimulation of immunoglobulins synthesis
synthesis of proteins acute phase in liver
anorexia
activation of endothelial cells
26. Which cytokine can cause synthesis of proteins acute phase in liver?
IL-1
TNF alpha
11-6
26
27. Choose urgent adaptive reactions at hypothermia:
spasm of peripheral vessels
dilatation of peripheral vessels
reduction of metabolism
activation of glycogenolysis into liver and muscles
increased perspiration
muscular shivering
dyspnea
28. Choose clinical symptoms for non-compensatory stage of hypothermia:
reduction of basal metabolism
activation of basal metabolism
spasm of peripheral vessels
dilatation of peripheral vessels
arterial hypotension
arterial hypertension
tachycardia
bradycardia
29. Choose the main mechanism of sun-stroke:
hyperemia of skin covers
dilatation of cerebral vessels
dyspnea
increasing of arterial pressure
reduction of inter-cerebral pressure
30. Endogenous hyperthermia is caused by endogenous pyrogens:
yes
no
31. Choose correct sentences:
pyrogenic activity of microbes is not equal their pathogenic properties
only endotoxins have pyrogenic activity
components of bacterial membranes have pyrogenic activity
nucleonic acids of phagocytes have direct pyrogenic activity
5. ALLERGY
1. Give definition of "hypoergia":
State of organism with abnormal (deviated) reactivity and resistance
State of organism with reduced non-specific reactivity and resistance
State of organism with increased specific reactivity and reduced resistance
2. Give characteristics for phase sensibilization of delayed type allergy:
antigen presentation by macrophages
reduced number of T-helpers
increased number of T-helpers
production of 1L-2
increased number of T-suppressors
activation of B-lymphocytes
formation of sensibilizeted T-lymphocytes
synthesis of antibodies by B-lymphocytes (Ig)
3. Target-cells of the 1st order at reaginic type of allergy:
monocytes
must cells
eosinophiles
neutrophiles
lymphocytes
basophiles
smooth muscles
4. Choose clinical manifestation of Arthus' phenomenon:
periodical edema and blisters into skin, mucous membranes, itch, fever
periodical conjunctivitis, rhinitis caused by pollen
ocal inflammatory-necrotic reaction in skin and subcutaneous tissue caused by multiply injection of alien
proteins
5. Is it correct that medicinal allergy can develop due to the II and the IV types of allergic reactions?
yes
no
6. Choose allergic reaction of III type:
Arthus' phenomenon
pollen allergy
medicinal agranulocytosis (leucopenia)
allergic orhitis
acute glomerulonephritis
Hashimoto' thyroiditis
rhesus-conflict between mother and fetus
7. Choose allergic reactions of the III type:
anaphylactic shock
reaction of transplantation rejection
serum sickness
bronchial asthma
urticaria
contact dermatitis
8. Is it possible to release mediators from must cells without complement participation?
yes
no
9. Choose allergic reaction of the IV type:
Arthus' phenomenon
pollen allergy
medicinal agranulocytosis (leucopenia)
allergic orhitis
acute glomerulonephritis
Hashimoto' thyroiditis
rhesus-conflict between mother and fetus
10. Choose allergic reactions of the IV type:
anaphylactic shock
reaction of transplantation rejection
serum sickness
bronchial asthma
urticaria
contact dermatitis
11. Mechanism of tissue injury at reaginic type of allergy:
excess formation super-oxide anion-radicals
activation of complement-depended cytotoxity
activation of antibody-depended cytotoxity
degranulation of must cells and releasing of mediators
12. Mechanism of tissue injury at reaginic type of allergy:
releasing of mediators from eosinophiles, platelets, neutrophiles
releasing of lymphokins
activation of complement fragments C3, C5, C8, C9
activation of к in in system
activation of phagocytes and effects of lysosomal enzymes
13. Methods of desinsibilizaton at delayed type allergy:
injection of anti-histamine medicine
injection of glucocorticoids
gradual injection of allergens
blockade of kinin system
activation of adenylatecyclaze
inhibition of phosphodiesthraze
inhibition of lymphokins
inhibition of 1L-2
14. Primary mediators of anaphylaxia:
serotonin
interleucins
factor causing stimulation of neutropiles migration
histamine
prostaglandins E, F
factor causing inhibition of macrophage's migration
15. Primary mediators of anaphylaxia:
kinins
heparin
histamin
interferon
eosiniphilic factor of chemotaxis
lysosomal enzymes
16. Is it correct sentence "specific degranulation of must cells is accompanied by their destruction"?
yes
no
17. Red blood cells destruction at autoimmune hemolytic anemia is a result interaction between allergen
and fixed on their surface antibodies:
yes
no
18. Main role in pathogenesis of the IV type allergy belongs to mediators released from must cells:
yes
no
19. Can allergic diseases develop due to different mechanism of tissue injury?
yes
no
20. Is specific hyposensibilization effective at atopias?
yes
no
21. Is specific hyposensibilization effective at the IV type of allergy?
yes
no
22. Choose characteristics of complete antigen:
molecular mass less than 1000 Dalton
molecular.mass more than 50000 Dalton
has 1-2 antigenic determinants
has more than 5-10 antigenic determinants
can induce formation of specific antibodies and sensibilizated lymphocytes directly
receives immunogenic properties after combination with host proteins
can interact with antibodies and sensibilizated lymphocytes
23. Production which factors can reduce tissue injury at allergy:
factor of platelets activation
histamin
arylsulfataze
histaminaze
hosphodiesthraze cGMP
leucotriens
24. Choose allergic reaction of immediate type:
Quinke edema
Hashimoto's thyroiditis
urticaria
bronchial asthma
rheumatic myocarditis
acute glomerulonephritis
25. Choose allergic reaction of immediate type:
anaphylaxia
serum sickness
tuberculin test
contact dermatitis
pollen allergy
medicinal allergy
26. Which from listed allergens can cause atopies?
domestic dust
bacterial toxins
viruses
bacteria
micro-anthraces
epidermal allergens
pollen
spores
cow' milk
27. Which from listed allergens can cause pollen allergy?
domestic dust
cereal's pollen
micro-anthraces
tree's pollen
flower's pollen
antibiotics
spores
28. Choose allergic disease of the I type immune injury:
urticaria
myasthenia gravis
«pollen» bronchial asthma
anaphylactic shock
Qunke's edema
serum sickness
pollen allergy
insect allergy
29. Which from listed diseases are atopies?
pollen allergy
urticaria
Qunke's edema
serum sickness
30. Choose allergic reactions of the II type immune injury:
serum sickness
immune agranulocytosis
autoimmune hemolytic allergy
31. Choose allergic reactions of the I II type immune injury:
serum sickness
local reactions (Arthus' phenomenon)
immune agranulocytosis
allergic alveolitis
acute glomerulonephritis
autoimmune hemolytic anemia
32. Choose allergic reactions of the IV type immune injury:
contact dermatitis
Arthus' phenomenon
bacterial allergy
food allergy
transplantation rejection
Hashimoto's thyroiditis
33. Choose autoimmune diseases:
Hashimoto's thyroiditis
Arthus' phenomenon
rheumatoid arthritis
myasthenia gravis
immune agranulocytosis
lupus erythrematous
autoimmune-hemolytic anemia
34. Choose allergic reactions of the II type immune injury:
thyroiditis
tuberculin test
contact dermatitis
acute glomerulonephritis
autoimmune hemolytic anemia
35.Which allergic diseases have been need for diagnostics of skin test with allergen?
allergic rhinitis
medicinal allergy
bronchial asthma
pollen allergy
immune agranulocytosis
tuberculosis of lung
brucellosis
36. Choose characteristics for the I (reaginic) type immune injury:
main role in pathogenesis play Ig E
clinical manifestations develop in a 15-20 minutes after repeated contact with allergen
clinical manifestations develop in a 6-8 hrs after repeated contact with allergen
histamine, kinins, leucotriens, factor of platelet's aggregation participate in this type immune injury
lymphokins play main role in this type immune tissue injury
37. Choose time of appearance clinical manifestation of the 1 type immune tissue injury after repeated
injection allergen:
15-30 minutes
6-8 hrs
24-48 hrs
10-14 days
38. Choose types of Ig which participate in the I type allergic reactions:
IgGl
IgO4
IgE
IgA
IgM
39. Choose correct sentences:
the 1st stage of allergic reaction starts after primary contact with allergen
the 1st stage of allergic reaction starts after secondary contact with allergen
specific antibodies or sensibilizated lymphocytes are produced during the 1st stage of allergic reaction
mediators are produced during the 2nd stage of allergic reaction
the 3rd stage of allergic reaction is characterized by clinical manifestations
40. Choose events for the 1st stage allergic reaction reaginic type:
cooperation of T-, B-lymphocytes and macrophages
cooperation of must cells, neutrophiles and eosinophiles
formation of plasmatic cells clone
formation of specific T-effectors clone
synthesis and accumulation of antibodies
activation of must cells
41. Choose cells which play main role in the I type of immune tissue injury:
B-lymphocytes
T-lymphocytes
macrophages
eosinophiles
neutrophiles
must cells
plasmatic cells
42. Choose processes which play main role in the II type of immune tissue injury:
interaction circulated antibodies (igG, IgM) with antigen fixed on the surface target-cells a.t participation
complement, phagocytes and NIC-cells
interaction circulated antibodies (IgG, IgM) with antigen at formation soluble immune
complexes with
complement participation
interaction sensibilizated lymphocytes with antigen
interaction antibodies fixed on the surface target-cells (IgG, IgM) with antigen without complement
participation
43. Choose processes which play main, role in the IV type of immune tissue injury:
interaction
circulated
antibodies
(IgG,
IgM)
with
antigen
fixed
on
the
surface target-cells at participation complement, phagocytes and NK-cells;
interaction circulated antibodies (IgG, IgM) with antigen at formation
soluble immune complexes with complement participation;
interaction sensibilizated lymphocytes with antigen
interaction
antibodies
fixed
on
the
surface
target-cells
antigen without complement participation;
44. Which mediators and enzymes can produced by activated must cells?
histamine
eucotrins C4, D4
prostaglandins
(IgG,
IgM)
with
arylsulfateze
histaminaze
oxidants
lysosomal enzymes
factor of platelet's activation
45. Can Iodine, Gold, Platinum, Cobalt cause state of sensibjlization?
yes
no
46. Which from listed allergens can be more frequent reason of atopies?
domestic dust
bacterial toxins
viruses
microbes
micro-anth races
epidermal allergens
pollen
mycosis spores
47. Choose correct sentences:
reagines and skin-sensibilizating antibodies are produced at atopia
IgG] and IgG2 are produced at atopia
antibodies have cellular affinity at atopia
reagines can cause cell's destruction after fixation on the surface of target-cells;
main role in pathogenesis of atopia play oxidants, anaphylotoxins and lysosomal enzymes;
48. Which events develop in the 1 s t stage of rcaginic type?
formation of complexes Ag+Ab
cooperation of T-,B-lymphocytes and macrophages
cooperation of must cells,neutrophiles and eosinophiles
contact of antigen (allergen) with specific antibodies
activation of must cells
47. Can serum sickness develop:
at primary injection of small dozes alien serum
at primary injection of large dozes alien serum
at repeated injection of large dozes alien serum
48. Can complement participates in the IV type allergy:
yes
no
49. Main role in pathogenesis of the I type of allergy belongs to Jg E:
yes
no
50. Main role in pathogenesis of the I type of allergy belongs to Jg M:
yes
no
51. Fixed antigens present:
1 type
П type
Ш type
IV type
52. Activation of complement system (C) due to classic way is caused by:
super-oxide anion-radical
immune complex
bacterial lipopolysacharides
endogenous enzymes (plasmin, trypsin, kallikrein)
53. Alternative way activation of complement system (C):
activation of fragments C5-C9
activation of C1
activation of C3
54. Activation of complement system (c) is accompanied by:
lysis of target-cells
reduction of vascular permeability
destruction of cellular membranes and releasing of lysosomal enzymes
stabilization of cellular membranes and inhibition of lysosomal enzymes
activation of kinin system
inhibition of chemotaxis
activation of chemotaxis
55. Choose correct sentences:
allergy and immune response can be caused by the same antigens
allergy and immune response can't be caused by the same antigens
allergy unlike immune response can't be caused by physical factors
immune response unlike allergy can't be caused by chemical factors
allergy is reduction, but immune response is activation resistance to antigen
allergy is increasing, but immune response is reduction of resistance to antigen
56. Reactivity is:
state of organism which characterized by resistance to different pathogenic factors;
state of organism which characterized by inadequate reactions on ordinary factors and predisposition to action
of pathogenic factors;
ability of organism to response on environmental actions
57. Types of reactivity:
biological (primary)
individual
pathological
age
sexual
58. Primary mechanisms of tissue injury at allergic reactions of the IV type:
complex AB+AG which can activate complement (C)
sesibilizated T-lymphocytes (effectors)
lymphokins
lysomal enzymes of macrophages
lysosomal enzymes of neutrophiles
mediators which released after formation complex (AG+lgE) on the surface of cells
59. Which cells can produce iminunoglobulins:
B-lymphocytes
macrophages
plasmatic cells
T-helpers
T-inductors
60. Mechanisms of ig E-depended allergic reactions:
action of 1L-4
presentation of antigen by B-lymphocytes
deficiency of T-helpers
excess of T-helpers
excess of cytotoxic T-effectors
prevalence of T-helpers
61. Choose tissues isolated from immune system during embryogenesis (primary endogenous
allergens):
heart
kidney
lens of eye
adrenal glands
thyroid gland
testicules
myelin of neurons
liver
62. Clinical-physiological manifestation of sensibilization:
reduction of arterial pressure
urticaria
leukocytosis
absence of clinical symptoms
fever
local edemas
increased concentration of specific Ig
increased number of T-lymphocytes
6. PATHOPHYSIOLOGY OF TISSUE'S GROWTH. TUMORS
1. Choose endogenous cancerogenes:
a) estrogens,
b) aniline,
c)cholic acid,
d) litocholic acid,
e)methylcholantren,
Oderivates of triptophane
a, b, с
b, c, d
c, d, e
a, d, f
2. Choose functions of oncoproteins:
stimulate of neoplastic progression
stimulate of tissue respiration
inhibit of glycolysis
stimulate of neoplastic transformation
3. Which cells can produce TNF (tumor necrotic factor)?
neutrophiles
eosinophiles
monocytes
platelets
red blood cells
tissue macrophages
4. Give the mechanisms of growth and differentiation at neoplastic transformation:
excessive activity of cGMP
excessive activity of с AMP
reduced activity of tyrosine-dependent proteinkinazes
increased activity of tyrosine-dependent proteinkinazes
hyper-activity of Ca- dependent proteinkinazes
presence of proteins which phosphorilated by tyrosine
increased concentration of phosphotirosines
5. which "host" factors can kill the tumors?
T-kiIlers
blocking antibodies
allogenic inhibition
NK. (natural kiilers)
phagocytosis
antigenic simplification
masking of antigenic structures
6. Which metabolites can be endogenous cancerogenes
cholesterol
galactose
cholic acid
tryptophane
estradiol
acorbinic acid (vit. C)
7. Which effects belong to morphologic atypism?
a) negative Pasteur's effect, b) reduced number of nexuses, c) reduced number of mitochondria, d) defective
receptors, e) increased synthesis of P-proteins
a, b, с
a, c, d
b, c, d
b, d, e
8. Choose the possible reasons of tumor's return:
suppression of local immunity
reduced activity of anti-cellular mechanisms anti-tumor resistance
surviving of tumor's cells after their extraction or destruction
insert of DNA tumor cells into genome of normal cells
9. Which effects belong to functional atypism?
loss of specific functions
aerobic glycolysis
reduced number of nexuses
infiltrative growth
utilization of substrates at low concentration
reduced number of mitochondria
antigenic transformation
metastasis
10. Choose oncogenes of initiation stage at tumor process:
a) c-rnyc, b) c-fos, c) c-sis, d)c-jin, e)c-erb
a, b, d
a, c, d
c, d
b, d, e
11. Choose typical forms of pathology in tissue growth:
necrosis
pathologic hypertrophy
pathologic hyperplasia
sarcoma
hyperplasia of mitochondria
dysplasia
carcinoma
12. Choose functions of oncoproteins:
inductors of oxidative phosphorilation
inductors of protein's phosphorilation by tyrosine
inductors of cGMP
inductors of cAMP
hormones - growth factors
receptors to growth factors
receptors to steroid hormones
homologies to growth factors
13. Choose features of carbohydrate metabolism in tumors:
ability to utilize glucose in low concentration
excessive activity of oxidative phosphorilation
excessive activity of glycolysis
positive Pasteur's effect
negative Pasteur's effect
14. Which metabolites can be endogenous cancerogenes:
thyroxin fcorticosterone
estradiole
epinephrine
growth hormone
insulin
15. Choose the signs of benign tumors:
metastasis
expansive growth
return (relapse)
formation of blocking antibodies
high level of neoplastic progression
absence of contact breaking
infiltrative growth
high level of proliferation
block of cellular maturation
16. Absence of Haiflik's limit presence at:
normal regeneration of tissue
low regeneration of tissue
high regeneration of tissue
stage of "initiation"
stage of "transformation"
equilibrium between growth and differentiation in tissues
17. Choose correct definition for "pathological hypertrophy of tissue":
increase mass and size of structural elements in tissue
increase mass and size of structural elements after excessive physical load
increasing mass and size of structural elements in tissue inadequate to their function
18. Choose the main mechanism of dysplasia:
disorders in mitosis
disorders in meiosis
disorders of metabolic regulation
extra-cellular acidosis
disorders in cellular differentiation
acute hypoglycemia
disorders in genetic program of cells
19. Choose factors which can cause cell's division:
cAMP
keylones
reduction of superficial stretching
growth factors
cGMP V
20. Malignant tumors after ionizing radiation develop more in the next organs:
lungs
breast
stomach
bone marrow
skin
hemopoetic tissue
21. Choose states with increased risk of tumor's development:
acute inflammation
chronic inflammation
old age
onizing radiation
immune deficiency
vaccination
22. Choose the signs of malignant tumors:
absence of contact breaking in tissue
increased concentration of keylones
ctivation of anaerobic glycolysis
inhibition of protein's phosphorilation by tyrosine
presence of factors which stimulate angiogenesis in tissues
nhibition of cell's differentiation
23. Which cellular structure is target for chemical cancerogenes?
cytoplasmatic membranes
lysosomes
sarcoplasmatic reticulum
inter-cellular matrix
mitochondria
DNA
24. Choose the signs of neoplastic progression:
anaplasia
loss of autonomy
invasive growth
infiltrative growth
terminal differentiation is saved
antigenic stimulation of organism by tumors
inability to metastasis
25. Choose effects of TNF (tumor necrotic factor):
cahexia
activation of cytotoxic function of macrophages
nduction of terminal differentiation in tumor cells
reduce antigenic abilities in tumor cells
activation of natural killers
increase activity of lipoproteinlipaze in tissues
26. Choose virues which contain DNA:
virus of Raus's sarcoma
Epstein-Barr's virus
вирус папилломы шейки матки
virus of adult T-leukemia
virus of Showp's papiloma
virus of mouse leukemia
Brittner's virus
1. PATHOPHYSIOLOGY OF RED BLOOD
1.Picture of blood at B12-folic deficiency anemia:
anisocytosis
anulocytosis
poikilocytose
microcytosis
target-cell
macrocytosis
megalocytes with Jolly's bodies
megalocytes with Kebot's rings
2.Reasons of inherited hemolytic anemias:
action of biological poisons
transfusion of incompatible blood group
enzyme's deficiency (glucose-6-phsphate dehydrogenaze)
ATP deficiency in erythrocytes
action of drugs
abnormal hemoglobin presence
3.Reasons of congenital hemolytic anemia:
action of biological poisons
transfusion of incompatible blood group
enzyme's deficiency (glucose-6-phsphate dehydrogenaze)
ATP deficiency in erythrocytes
action of drugs
abnormal hemoglobin presence
4.Erythrocytosis is observer at:
mountain sickness
poisoning with charcoal gas
inborn defect of heart
hemoglobinopathy
5.Reasons autoimmune hemolytic anemias are:
transfusion of incompatible blood group
systemic diseases of connective tissue
hemoglobinuria due to decreased temperature action
hemoglobinopathy
action of drugs
7.Signs of aplastic anemia:
blood volume is increased (hypervolemia)
reticulocytes are decreased
secondary infection
erythropoetins are increased
megaloblastosis
8.Etiology of aplastic anemia:
ionizing radiation
vitamin's deficiency
drugs (cytostatic)
protein's deficiency
9. lmportant role in pathogenesis B12-deficiency anemia play next factors:
insufficient erythrocyte saturation by hemoglobin
disorders of DNA synthesis in nucleus of erythroblasts
period of erythrocyte's life is decreased
10.Common sings of anemia:
pain
tachycardia
dyspnea
hypertension
paleness
11.What reasons can cause hypo-aplastic anemia:
stomach resection
ionizing radiation
chronic kidney failure
toxic mania
vitamin B12 deficiency
12.Syroptoms B12-folic acid deficiency anemia are:
jaundice
polyneuritis
normoblastosis
megaloblastosis
airophy of mucous in stomach
splenomegaly
13.Erythrocyte's shape at thalassemia:
target-liked cells
sickle-liked cells
microspherocytes
14.Bilirubinemia presence at:
sideroachristic anemia
hemoglobinopathy
hemolytic disease at newborns
aplastic anemia
15.Reasons of iron deficiency anemia:
hypoacidic gastritis
tumor
acute hemorrhage
chronic hemorrhage
16.Urgent compensative mechanisms at hemorrhage:
spasm peripheral vessels
tachycardia
hyperpnoea
increased blood coagulation
increased hemopoesis (increased hemopoetic activity of bone marrow)
increased protein's synthesis in liver
intratissue liquid comes in vessels
17.Factors can cause iron-deficiency anemia:
deficiency intrinsic Castle's factor
non-compensated loss of iron
suppression HCL secretion in stomach
disorders of folic acid activation
vitamin В12 deficiency
decreased erythropoetin's production
increased expenditure of iron
exhaustion of iron's depot
18.Choose factors which can cause megaloblastic anemia:
hypoxia of myeloid tissue
chronic iron deficiency
vitamin В12 deficiency in food
disorders of folic acid activation
deficiency of intrinsic Castle's factor
inherited disorders of hemoglobin's synthesis
competitive consumption of vitamin В12
disorders of vitamin В12 utilization in bone marrow
19. At what case iron deficiency anemia can develop?
chronic blood loss
rhesus conflict
folic acid deficiency
stomach resection
acute blood loss
chronic enteritis
20. At what case hemolytic anemia can develop?
hemophilia
rhesus conflict
protein starvation
gastromucoprotein's deficiency
hemoglobinopathy
malaria
21.Hematoiogicai signs of hypoplastic anemia are:
hypochromia of red cells
neutrophilia
normochromia of red cells
relative lymphocytosis
neutrophile's number is decreased in peripheral blood
latent ability of iron's consumption is decreased in blood
22.Hematoiogicai signs of hypo-aplastic anemia are:
non-effective erythropoesis is increased
period of erythrocyte's life is decreased
neutrophile's number is decreased in peripheral blood
hyperchromia of red cells
norm-megaloblastic type of hemopoesis
latent ability of iron's consumption is increased in blood
23.Моге often reasons of iron deficiency anemia are:
chronic blood loss
inborn deficiency of Castle's factor
ionizing radiation
folic acid's deficiency in meal
chronic enteritis
hypo-acidic gastritis
24.Hematological signs of chronic post hemorrhage anemia are:
iron's level is increased in blood
iron's level is decreased in blood
coefficient of transferrin' saturation is increased
coefficient of transferrin' saturation is decreased
sideroblast's number is increased in bone marrow
sideroblast's number is decreased in bone marrow
25.Choose anemias with megaloblastic type of hemopoesis:
post hemorrhage anemia
anemia at folic acid's deficiency
inherited hemolytic anemia
anemia at worm invasion
Addison-Birmer's anemia
26.Reasons of hypo-aplastic anemia:
stomach' resection
leukemia
ionizingradiation
toxin'and poison'action
vitamin В12 deficiency in meal
27.Factors, which can cause iron deficiency anemia more often:
acute blood loss
immunodepressants
chronic blood loss
chronic enteritis
tiredness at training
hypoacidic gastritis
folic acid's deficiency
28.Choose more often reasons of iron deficiency anemia:
iron' deficiency in meal
inherited deficiency of transferrin
chronic blood loss
kidney diseases
pregnancy and lactation
disease of gastro-intestinal tract
2.
PATHOPHYSIOLOGY OF WHITE BLOOD
1.Which changes in peripheral blood are characteristic for neutrophilic leukocytosis:
percentage concentration of lymphocytes is decreased
leukocyte's number is increased
presence of myeloblasts
percentage concentration of stabs neutrophiles is increased
percentage concentration of juvenile neutrophiles is increased
percentage concentration of eosinophiles and basophiles is increased
2.Which changes in peripheral blood are characteristic for chronic myeloleukemia at flare:
percentage concentration of lymphocytes is decreased
leukocyte's number is increased
presence of myeloblasts
percentage concentration of stabs neutrophiles is increased
percentage concentration of juvenile neutrophiles is increased
percentage concentration of eosinophiles and basophiles is increased
3.Which leukemia is accompanied acute disorders of maturation ("leukemic gap"): myeloblasts leukemia
erythremia
lympholeukemia
monocytic leukemia
myeloleukemia
monoblastic leukemia
lymphoblastic leukemia
4.More possible reasons of agranulocytosis:
vitamin В12 deficiency
viral infection
lupus erythematosus
acute infection
fungal intoxication
5.More possible reason of patient's death with agranulocytosis is:
uremia
secondary infection
acute heart failure
hypoxia
acidosis
6.More possible reason of patient's death at leukemia:
hypoglycemia
hemorrhage in brain
acute heart failure
hypoxia
edema of brain
7.Which changes in peripheral blood are characteristic for acute myeloblasts leukemia?
all type myeloid cell presence in peripheral blood (from myeloblasts to granulocytes)
"leukemic gap" absence of pre-matured cells
anemia
thrombocytopenia
8.Which changes in peripheral blood are characteristic for chronic myeloleukemia: presence of all cell's
types (from myeloblasts up to granulocytes)
absence of pre-matured cells - "leukemic gap"
anemia
thrombocytopenia
9.Clinical symptoms arc characteristic for leukemia:
anemia, leukocytosis, jaundice
hemolytic anemia, splenomegaly, jaundice
megaloblastic anemia, polyneropathy, atrophy of stomach' mucosa
metaplastic anemia, secondary infections, thrombocytopenia
aplastic anemia, leucopenia, thrombocytopenia
10.Which reasons can cause physiological leukocytosis:
glucocorticoid's abuse
infarction of myocardium
infection
newborn state+meal loading
11.Which reasons can cause "pathological" leukocytosis:
glucocorticoid's abuse
infection
infarction of myocardium
newborn state
meal loading
physical loading
mental loading
12.Which disorders of hemostasis accompany chronic leukemia?
bleeding due lo fibrinogen's deficiency
bleeding due to thrombocyte's deficiency
bleeding due to vitamin С deficiency
physical loading+mental loading
bleeding due to vitamin К deficiency
3.
PATHOPHYSIOLOGV OF HEMOSTASIS
1.Which diseases are coagulopathy?
Shonlein-Henoch disease
afibrinogenemia
hemophilia
vitamin С deficiency
vitamin К deficiency
2.Which mechanisms are thrombocyte's factor of hemostasis:
thrombocyte's adhesion
cloth's retraction
active thromboplastin's formation
adhesive molecule's formation
vessel's spasm
white agglutinative thrombus's formation
thrombin's formation
contact factor's activation
3.Which mechanisms are vascular factors of hemostasis:
thrombocyte's adhesion
cloth's retraction
active thromboplastin's formation
adhesive molecule's formation
vessel's spasm
white agglutinative thrombus's formation
thrombin's formation
contact factor's activation
4.Which mechanisms are coagulative factors of hemostasis:
thrombocyte's adhesion
cloth's retraction
active thromboplastin's formation
adhesive molecule's formation
vessel's spasm
white agglutinative thrombus's formation
thrombin's formation
contact factor's activation
5.Factors of coagulation system:
heparin
antithromboplastin
antithrombin
tissue thromboplastin
fibrinogen
plasmin
6.Factors of anti-coagulation system:
heparin
antithromboplaslin
antithrombin
tissue thromboplastin
fibrinogen
plasmin
7.Hemorrhagic diathesis linked with vascular disorders:
vitamin С deficiency
Shonlein-Henoch disease
hemophilia
Werlgoff disease
Rendu-Osler disease (angiotelectasia)
afibrinogenemia
8.Which mechanisms can cause activation of coagulation at DIC-syndrome?
decreased blood viscosity
increased tissue thromboplastin in blood
disseminated damages of vessel's wall
decreased thrombocyte's number
increased blood viscosity
intensive inter-vascular aggregation of blood cells
9.Reasons of coagulopathies:
absence of anti-hemophilic globulins
thrombocytopenia
vitamin С deficiency
obturative jaundice
vitamin К deficiency
afibrinogenemia
10.Which plasma factor is absence at hemophilia A?
Hagemann' factor
anti-hemophilic globulin С (Rosental' factor)
anti-hemophilic globulin В (Christmas' factor)
VIII factor
11.Reasons of DIC-syndrome:
sepsis
lupus erythrematosis
hey fever
bronchial asthma
vitamin С deficiency
cardiogenic shock
trauma with tissue damages
12.Factors promoted of thrombus formation:
reduced thrombocyte's number
vessel's wall damages
decreased blood velocity
change of endothelium's charge from negative on positive
decreased coagulants activity
13.Thrombocylopathy is:
changes of physiological function of thrombocytes independently from their number
changes of physiological function of thrombocytes obligatory combined with changed thrombocyte's number
changes of physiological function of thrombocytes obligatory combined with decreased thrombocyte's
number
14.Reasons of DIC-syndrome:
sepsis
shock
damages of placenta
acute leukemia
15.Vascular-thrombocytic hemostasis is changed at:
decreased of thrombocyte's number
disorders of thrombocyte's function
inherited angiopathy
deficiency VIII factor
deficiency of Willebrand's factor
expression on the surface of thrombocytes receptors to fibrinogen
absence on the surface of thrombocytes receptors to Willebrand's factor
16.Hemorrhagic syndrome is result:
increased vessel's permeability
decreased activity of plasminogen system
deficiency of procoagulants
functional disorders of thrombocytes
increased activity of plasmin system
decreased of thrombocyte's number
increased concentration of fibrinolysis's inhibitors
17.Choose clinical signs characteristic for thrombocytopenic purpura (Werlgoff's disease):
increased of thrombopoetin's production
disorders of vessel's wall
short time of capillary bleeding
short time of thrombocyte's life
disorders of cloth's retraction
+petechial type of bleeding
hematomic type of bleeding
increased of anti-thrombocytic antibodies in plasma (IgG3)
18.Choose changes characteristic for hemophilia:
long time of capillary bleeding
decreased procoagulant activity of VIII factor
long time of coagulation
disorders in synthesis of VIII factor
positive ligature test
deficiency of Willebrand's factor
19.Choose disorders characteristic for thrombocytopathy:
decreased synthesis of thromboxan A2
deficiency of thrombostenin in thrombocytes
absence of thrombocyte's aggregation
defreased releasing from thrombocytes ADP and serotonin
+decreased cloth's retraction
20.Choose factors which can cause thrombocytopenia:
suppression of megacariocyte's proliferation
suppression of megacariocyte's locus by tumor cells at leukemia
activation of Leukocytic locus in bone marrow at inflammation
increased "consumption" of thrombocytes at thrombopoesis
immune damages of thrombocytes
large doze of ionizing radiation
leukolysis
21.Reasons of long-time coagulation:
excess of anticoagulants
activation of fibrinolytic system
inhibition of fibrinolysis
deficiency of procoagulants
decreased activity of natural coagulants
increased concentration of procoagulants in blood
4.
PATHOPHYSIOLOGY OF CARDIO-VASCULAR SYSTHEM
1.Clinical manifestation of right-ventricular cardiac insufficiency:
portal hypertension
tachycardia
lung's edema
circulatory hypoxia-gaseous acidosis
cyanosis
ascites
2.Which from listed mechanisms is initial for cardiac edema:
decreased of sodium and water reabsorption in kidney
increased vessel's permeability
venous congestion
decreased oncotic pressure in blood
decreased cardiac output
3.Mixed hyperfunction of myocardium develops at next diseases:
essential hypertension
thyreotoxicosis
emphysema of lungs
infarction of myocardium
combined aortal defect
mitral stenosis
4.Inter-cardiac reasons of cardiac insufficiency:
stenosis of aorta
lung's emphysema
essential hypertension
renal hypertension
myocarditis
5.Extra-cardiac reasons of cardiac insufficiency:
myocarditis
thyreotoxicosis
myocardiodystrophy
renal hypertension
endocarditis
6.Which diseases can cause isometric hyperfunction of myocardium:
defect of inter-atrial septum
caorctation (narrowing) of aorta
essential hypertension
infarction of myocardium
7.Choose inter-cardiac reasons of cardiac insufficiency:
thyreotoxicosis
pericarditis
myocarditis
ischemic disease of heat
essential hypertension
endocarditis
8.Choose possible reasons of right ventricle cardiac insufficiency:
infarction of forward wall left ventricle
thyreotoxicosis
exudative pericarditis
lung's emphysema
essential hypertension
9.How blood velocity change in coronary vessels at chronic coronary insufficiency:
doesn't change
is decreased non-significantly
is decreased significantly
is increased
10.Which states can cause myocardium's over-loading by pressure:
anemia
insufficiency of aortal valve
general atherosclerosis
insufficiency of mitral valve
arterial hypertension
aortal stenosis
11.Choose reasons can cause myocardium's overloading by volume:
aortal valve insufficiency
diabetes mellitus
excessive production of norepinephrine
arterial hypertension
stenosis of left atrio-ventricular foramen
mitral valve insufficiency
12.Clinical manifestation at left ventricular cardiac insufficiency:
edema on legs
decreased cardiac output
dyspnea
hepatomegaly
tachycardia
bubbly sounds in basal fields of lungs
angiotelectasis
13.Coronary insufficiency is result of:
paroxysmal tachycardia
endocarditis
spasm of coronary arteries
hypercapnia
adenosine cumulation in myocardium
stenotic coronarosclerosis
14.Choose events and factors at increased epinephrine's concentration causing myocardium's damages:
oxygen's consumption by myocardium is decreased
oxygen's transport to myocardium is decreased absolutely
oxygen's transport to myocardium is decreased relatively
phosphorilation and aerobic oxidation in cardiomyocytes are decreased
phosphorilation and aerobic oxidation in cardiomyocytes are increased
glycogen's storage is decreased in cardiomyocytes
15.Which diseases can cause right-ventricular cardiac insufficiency:
lung's emphysema
defect of inter-ventricular septum
thyreotoxicosis
caorctation (narrowing) of aorta
acute myocarditis
16.What events are characteristic for renin-depended hypertension:
increased tonus of peripheral vessels at the expense of adrenoreceptor's sensitivity
increased tonus peripheral vessel is result activation RAAS
significant increasing of blood volume
increased excretion Na+ and water by kidney
decreased excretion Na+ and water by kidney
activation of JGZ
17.Mechanism of arterial hypertension:
cardiac work is decreased
blood volume is decreased
blood volume is increased
vessel's tonus is decreased
18.Choose secondary (symptomatic) arterial hypertension:
hypovolemic (blood volume is decreased)
pituitary
renal
reflexogenic
thyroid
adrenal
essential
portal
19.Choose main differences between essential hypertension and secondary hypertension:
increased arterial pressure develops without organic damages internal organs
develops as result primary renal disorders
inherited predisposition has important role
develops as result adrenal glands disorders
develops as result primary damages of aortal receptors
important role have hypothalamic disorders (vaso-motor center)
20.Risk factors at hypertension:
obesity
decreased activity of sympathetic system
weight loss
increased activity of sympathetic system
diabetes mellitus
hyperthyroidism
21.Mechanisms of reno-vascular hypertension is:
activation of RAAS
insufficiency of prostaglandin and kinin system in kidney
insufficiency of RAAS
22.Which substances produced in kidney can cause direct vasodilatation:
renin
prostaglandin F2alpha
bradikinin
callidin
prostaglandins A, E
23.Endocrine hypertensions develop at:
total hypofunction of adrenal cortex
hyperfunction of adrenal cortex (zone glomeruloza)
hyperfunction of adrenal medulla
hypophyseal cachexia
hypofunction of thyroid gland
thyreotoxicosis
24.Complications at hypertonic disease:
acute renal failure
extrasystoles
chronic renal failure
lung's edema
cardiac asthma
atrio-ventricular block 1st degree
fibrillar palpitation
25.Which disorders can develop at acute arterial hypotension:
blood type of hypoxia
disorders of microcirculation
circulatory hypoxia
cardiac insufficiency
coronary insufficiency
syncope
anuria
PATHOPHYSIOLOGY OF LIVER
1.Which signs characteristic for physiological jaundice of newborns:
increased concentration of indirect bilirubin in blood
increased concentration of direct bilirubin in blood
yellow color of skin and mucous
feces is normal color
feces is black color
presence of biliary pigments in urine
2.Which symptoms characteristic for aholia:
increased arterial pressure
diarrhea
steatorrhea
constipation
disorders of vitamin resorption
disorders of intestinal digestion
bleeding
meteorism
tachycardia
3.What variant of symptom complex characteristic for mechanical jaundice:
result of hepatocyte's damages at infections or intoxication, direct and indirect bilirubin in blood, decreased
urobilin in urine, biliary acids and pigments, decreased stercobilin in feces
result of hemolysis, increased indirect bilirubin in blood, negative urobilin in urine, absence of biliary acids,
increased stercobilin in feces
result of bile congestion, direct and indirect bilirubin in blood, decreased urobilin in urine, positive biliary
acids and pigments, decreased stercobilin in feces
4.CIinical signs characteristic for mechanical jaundice:
cholemia
increased concentration indirect and direct bilirubin in blood
increased concentration indirect bilirubin in blood
acholia
hypercholia
bradycardia
yellow color skin, mucous and while of the eye
itch
5.At what types of jaundice indirect bilirubin is in urine?
mechanical
with one of listed
hemolytic
parenchial
6.Mechanism of bradycardia at cholemia:
increased of n. vagus activity
direct action of bile acids on sinus nodes
decreased activity of adrenoreceptors
7.Which from listed signs are characteristic for total hepatic failure?
hyperglycemia without meal loading
bilirubin in blood
hypoglycemia without meal loading
decreased oncotic pressure of blood
increased oncotic pressure of blood
8.Which from listed signs are characteristic for cholemia?
tachycardia
skin itch
bradycardia
hyporeflexia
arterial hypertension
hyperrreflexia
arterial hypotension
9.Choose signs characteristic for pre-hepatic (hemolytic) jaundice:
increased non-conjugated bilirubin in blood
increased reticulocyte's number in blood
increased conjugated bilirubin in blood
foamy urine
bilirubin in urine
hypoxia
urobilin in urine
decreased arterial pressure
tachycardia
10.Syndrome cholestasis is characteristic for next jaundice :
pre-hepatic (hemolytic)
hepatic (parenhial)
post-hepatic (mechanical)
11.Reasons of hepatic (parenhial) jaundice:
viral hepatitis
hypoxia
hemolytic anemia
rheumatism
toxic hepatitis
intoxication of hemolytic poisons
cirrhosis of liver
cancer of liver
sepsis
pneumonia
GASTROINTESTINAL TRACKT PATHOPHYSIOLOGY
1.Achilia:
deficiency of bile
absence of pepsin in stomach juice
absence of HC1 and pepsin in stomach juice absence of tripsin in intestine juice
absence of HC1 in stomach juice
2.Disorders of digestion can cause:
starvation
auto-allergic diseases
autointoxication
psycho-emotional stress
chronic cardiac failure
dyspeptic disorders
chronic renal insufficiency
3.Which states can cause functional disorders of parietal digestion?
stress
cholera
changes in composition and structure of enzymes in surface of intestine
spry
ionizing radiation
action of antibiotics
4.Complications of ulcer disease:
decreased of blood supply in coronary vessels
chronic adrenal cortex insufficiency
hyperchromic anemia
penetration
cancer (malignant tumor)
peritonitis
decreased blood volume
5.Choose possible mechanisms of hyposecretion in stomach:
excessive parasympathetic stimulation of stomach
excessive sympathetic stimulation of stomach
decreased production and secretion of histamine
decreased production and secretion of secretin
increased formation of enterogastron
decreased secretion of cholecystokinin
6.Which factors play role in ulcers development of stomach and duodenum?
infection
excessive glucocorticoid's production
increased mucosa production
increased parasympathetic stimulation
increased sympathetic stimulation
duodenal reflex
7.Mechanisms resistance of Helicobacter pylori to bactericide action of stomach juice:
adaptation to inhabit under mucosa of stomach
ability to decompose of urea
adaptation to inhabit in mucosa of stomach
decreased catalyze activity
8.Factors play role in pathogenesis of "aspirin" ulcers in stomach:
decreased synthesis of prostaglandins E
decreasing inverse diffusion H+ in mucous of stomach
increased synthesis of prostaglandins E
increasing inverse diffusion H+ in mucous of stomach
increased production of mucus
decreased production of mucus
9.Choose characteristic signs for increased secretion of stomach juice:
rapid evacuation meal from stomach
slow evacuation meal from stomach
increased secretion of stomach juice before meal
absence of pepsin activity
long-time spasm of pylorus
heartburn
decreased production of pancreatic juice
increased motility of intestine, diarrhea
10.Which diseases can cause disorders of parietal digestion?
mechanical jaundice
lactaze insufficiency
chronic pancreatitis
duodenitis
11.Choose sequences of acholia:
bile absence in duodenum
increased rotting in intestine
decreased pH in duodenum
fatty diarrhea
absence of lipase
disorders of fatty acids absorption
decreased lipaze activity
absence of lipids decomposition
disorders of lipids emulgation
12.Symptoms at malabsorption:
meteorism
vitamin В12 deficiency
diarrhea
vitamins A, D, E, K deficiency
constipation
fatty diarrhea
weight loss
decreased ammonia in blood
decreased oncotic pressure of blood
13.Choose reasons of decreased intestinal absorption:
inflammation caused by infection
inflammation caused by toxins action (diabetes, uremia)
resection 25% of small intestine
resection 50% of small intestine
resection 75% of small intestine
atrophy of mucous in small intestine
RESPIRATORY SYSTHEM PATHOPHYSIOLOGY
1.What type of respiration is characteristic for pneumonia?
frequent deep respiration (hyperpnoe) Kussmaul' respiration
deep редкое respiration
frequent superficial respiration (polipnoe)
Biot' respiration
2.What types of respiration can develop at suppression of respiratory center?
polipnoe
hyperpnoe
Chain-Stocks' respiration
Kussmaul' respiration
Biot' respiration
oligopnoe
3.Kussmaul' respiration takes place at patients with:
respiratory alkalosis
metabolic acidosis
metabolic alkalosis
respiratory acidosis
4.Inspiratory dyspnea develops at next diseases:
1st stage of asphyxia
closed pneumothorax
pulmonary emphysema
trachea stenosis
lагуnх edema
attack of bronchial asthma
5.Chose possible reasons of respiratory insufficiency obstructive type:
spasm of bronchus
pleuritis
pneumothorax
collapse of bronchioles
increased intrapulmonary pressure
decreased surfactant production
bronchial asthma
6.Chose possible reasons of respiratory insufficiency restrictive type:
inflammatory damage of bronchioles
pneumofibrosis
diffuse fibrous alveolitis
spasm of bronchioles
massive pulmonary inflammation
collapse of lung
7.Disorders of diffusion in alveolar-capillary membrane plays main role in development of respiratory
insufficiency at:
bronchial asthma
decreased surfactant production
larynx edema
silicosis
interstitial edema of lungs
8.Disorder of perfusion plays main role in development of respiratory insufficiency at next pathological
states:
bronchial asthma
Fallow' tetrad
larynx edema
left-ventricular cardiac insufficiency
tuberculosis
blood loss
myasthenia
hysteria
9.Which from listed diseases and pathological states can cause development of respiratory insufficiency?
bronchial asthma
emphysema
asphyxia
acute renal failure
anemia
10.Mechanisms disorders of gases exchange at emphysema:
increased air in pulmonary tissue
decreased respiratory surface
decreased oxygen in alveolar air
increased perfusion in pulmonary vessels
11.Which from listed diseases develop due to disorders of perfusion?
emphysema
pulmonary collapse
embolism of pulmonary vessels
pneumothorax
12.Which reasons can cause pulmonary collapse?
cardiac insufficiency
chronic bronchitis
chronic renal insufficiency
pneumofibrosis
surfactant insufficiency
13.Respiratory insufficiency is characterized by:
dyspnea
hypoxia
tachycardia
cyanosis
changes of 02 and CO2 levels in blood
anemia
changes of acid-base balance
14.Reasons of restrictive disorders of ventilation:
chronic bronchitis
intercostals myositis
closed pneumothorax
15.Internal respiration is process of gases exchange between:
environmental air and tissue
blood and tissue
alveolar air and blood
16.Dyspnea is:
increased frequency and deepness of respiration, accompanied with sensation of air deficiency
increased frequency and deepness of respiration
sensation of air deficiency
Pathophysiology of endocrine system
1.Diseases are accompanied with disorders of ADH (antidiuretic hormone) production:
-diabetes insipidus
- acromegaly
- somatomegaly (gigantism)
- Cushng's disease
- pituitary dwarfism
- hypothyroidism
2.Diseases are accompanied with disorders of GH (growth hormone):
- diabetes insipidus
- acromegaly
- eunuchoidism
- somatomegaly (gigantism)
- Cushng's disease
- hyperthyroidism
- early (premature) sexual development
-pituitary dwarfism
3.At what disorders of adrenal cortex can develop next syndromes and diseases:
- Conn's syndrome
-Addison's disease
- Cushing's syndrome
- adreno-genital syndrome
- Simmond's disease
- pheohromocytoma
4.Choose main effects of thyroid hormones:
-increase of protein anabolism (in physiological concentration)
- permissive action on catecholamines
- increase of oxygen's consumption by tissues
- mobilization of lipids from depot
- activation of lipogenesis
- activation of glycogenosis
- bradycardia
- activation heat-production
5.Signs, characteristic for Cushing's syndrome:
-hypotension
-hypertension
-local obesity
-dehydration
-increase of sodium's concentration in blood
-decrease of sodium's concentration in blood
-hyperglycemia
-hypoglycemia
-secondary infection
6.Manifestation of hyperthyroidism, causing by direct action of TTH:
-increase of base metabolism
-exophthalmos
-tachycardia
-goiter
-tremor
-increase of body's temperature
-increase of protein's decomposition
7.Pathological states, appear at excessive production ACTH:
- adrenogenital syndrome
- gigantism
- Cushing's disease
- hyperthyroidism
- acromegaly
8.Manifestation of primary aldosteronism:
-increase of potassium in blood
-normal level of potassium in blood
-increase of sodium in blood
-normal level of sodium in blood
-polyuria
-edema
-increase of renin secretion
-decrease of renin secretion
9.Manifestation of increased function of adrenal cortex:
- increase of ACTH production
- decrease of ACTH production
- hypoglycemia
- decrease of sodium in blood
- hyperglycemia
- increase of sodium in blood
- hypotension
- hypertension
- increase of MSH production
- increase of calcium in blood
10.Which changes characteristic for Addison's disease?
- decrease blood volume and dehydration
- decreased arterial pressure
- muscular weakness
- edema
- cumulation of Na+ and loss of K+
- hypoglycemia
- tachycardia
III.
Pathophysiology of carbohydrate metabolism
1.Which form listed states are complication of diabetes mellitus:
-ascites
-neuropathy
-retinopathy
-cellular jaundice
-hypertension
-mixedema
-nephropathy
2.Reasons can cause functional hyperglycemia:
-emotional stress
-the 1st period complete starvation
-gigantism
-Cushing's syndrome
-meal loading
-hyperthyroidism
3.Which from listed states are accompanied with increased base metabolism: -hyperthyroidism
-Cushing's syndrome
-Addison's disease
-physical loading
-heart insufficiency
-iron-deficiency anemia
-emotional stress
-the 2nd period of complete starvation
4.Which from listed states are accompanied with alimentary hyperglycemia (hyperglycemia after
meal):
-atherosclerosis
-diabetes mellitus
-spleen extraction
-starvation
-pheochromocytoma
-decrease of heparin production
5.Which states lead to relative insufficiency of insulin:
-pancreatitis
-increase of glucocorticoids production
-increase of insulinaze activity
-cumulation of anti-bodies to insulin
-decrease of receptors number on target-cells
-multicystosis of pancreas
6.Which mechanisms are main in pathogenesis of diabetic coma:
-disorders of carbohydrate metabolism, lipid metabolism, protein
metabolism lead to disorders of energy metabolism in brain and other
tissues, water-electrolyte disorders and intoxication
-disorders of water-electrolyte balance causing increased osmotic pressure
in blood, intra-cellular hypohydration
- disorders of carbohydrate metabolism, lipid metabolism, protein
metabolism lead to disorders of energy metabolism in central nervous
system causing substrate and oxygen starvation of brain
7.Which symptoms are characteristic for diabetic coma:
-acute beginning
-giddiness, entangled consciousness, feeling of hunger
-periodical respiration type Kussmaul
-decrease of arterial pressure
-smell of acetone
-cramps
-hyperemia of skin
-eyeballs are firm at palpation
8.Which hormones excess can cause hyperglycemia?
-epinephrine
-thyroid hormones (ТЗ, Т4)
-glucocorticoids
-growth hormone
-insulin
-vasopressin
-ADH
-glucagone
9.Which type of lipids excess plays atherogenic role?
-cholesterol
-lipoproteins high density
-lipoproteins very low density
-lipoproteins low density
-phosphoproteins
10Development of atherosclerosis is promoted:
-decreased activity of lipoproteinlipaze
-deficiency of receptors to lipoproteins low density
-excess of receptors to lipoproteins low density
-increased heparin concentration in blood
11.Choose the risk factors for atherosclerosis:
-decreased insulin concentration
-hyperlipidemia
-obesity
-local infiltrative sclerosis of arterioles
-fibromucular hypertrophy of vessels wall
-endarteritis
-phlebitis
12.Which factors promote atherosclerosis development at obesity?
-arterial hypertension
-hypercholesterolemia
-hyperglycemia
-polyuria
-polydipsia
-hypertriglycerolemia
-dyslipoproteinemia
^
13.More frequent complications of atherosclerosis:
-aneurysm of aorta and/or other big arteries
-hemophilia A
-hemophilia В
-insult of brain
-thrombosis of arteries
-thrombosis, of veins
-thromboembolism
-schemia of myocardium
14.Choose factors promote development of diabetic angiopathy:
-excessive glycosy lation of proteins
-hyperlipoproteinemia
-dyslipoproteinemia
-sorbite formation
-activation of gluconeogenesis
15.Choose the complications of diabetes mellitus:
-immunodeficiency states
-rapid development or atherosclerosis
-decreased resistance to infection
-decreased anti-tumor resistance
-hypothyroidism
-nephropathy
-arterial hypotension
Pathophysiology of kidney
1.Exogenous reasons of nephrolitiasis are:
-inherited diseases of aminoacids metabolism
-hypercalciuria
-work in metallurgical factory
-infection of urinary tract
-disorders in mechanisms of urine elimination
2.Endogenous reasons of nephrolitiasis are:
-disorders of aminoacids reabsorption
-vitamin В deficiency
-drinking water saturated with calcium
-endocrine disorders (hyperparathyroidsm)
-diseases of metabolism
3.Uremic stage chronic renal insufficiency is characterized by:
-pleuritis and pericarditis
-eliminative acidosis
-delay of sodium in organism
-decreasing of creatinine's clearance
-metabolic alkalosis
-gastroenteritis
-nitrogenemia
-disorders of parathyroid glands function
4.Which symptoms are characteristic for decompensative stage of chronic
renal insufficiency:
-oligouria
-acidosis
-hypercalciumemia
-polyuria
-hypersodiumemia
-hypocaiciumemia
-increasing of nitrogen in urine
-pericarditis, pleuritis, gastroenteritis
-decreasing of creatinine's clearance
5.Which from listed states characterize functional proteinuria:
-nephrotic syndrome
-glomerulonephritis
-proteinuria at physical loading
-pyelonephritis
-dehydration
-proteinuria after meal loading
-ortostatic proteinuria
6.Which reasons can cause primary nephrotic syndrome:
-poisoning with heavy metals
-rejection of kidney transplantant
-disorders of blood supply in kidney
-inherited diseases of lipid metabolism
-penetration specific antibodies to kidney through placenta
-glomerulonephritis
-serum sickness
7.Which reasons of acute renal failure are included in group post-renal:
-shock
-collapse
-dehydration
-acute glomerulonephritis
-sepsis
-pyelonephritis
-toxicosis at pregnancy
-tumor in urinary tract
-thrombus in renal vessels
-nephrolithiasis
8.Choose main mechanism promote renal hypertension
-activation of rennin-angiotensin-aldosterone system
-activation of kallikrein-kinin system
- activation of symphato-adrenal system
-delay of sodium in organism
-rennin synthesis is decreased
-synthesis of kidney Prostaglandines is decreased
9.Which from listed symptoms and syndromes can develop in oligo-anuric
stage of acute renal failure?
-immunodeficient state
-hypervolumia (increased blood volume)
-dehydration of organism
-edema of brain
-acidotic coma
10.Mechanisms can cause increased glomerular filtration:
-increased tonus afferent arteria
-decreased tonus afferent arteria
-increased tonus efferent arteria
-increased oncotic pressure of blood
-decreased oncotic pressure of blood
-increased intra-renal pressure
-decreased intra-renal pressure
11.Choose pathological components of urine renal nature:
-urobilin
-bilirubin
-stercobilin
-keton bodies
-erythrocytes (changed)
-protein
-cylinders
-bile acids