1. A pathologic reaction is:
1. Reaction of the organism to extraordinary irritants
2. Prolonged inadequate reaction of the organism
3. Short-lasting inadequate reaction of the organism
4. Short-lasting, adequate response
5. Specific response to endogenous noxae
2. From the point of view of a disease the pathologic process is:
1. Generalized reaction of the organism
2. Local manifestation of the disease
3. Consequence of every disease
4. An example of pathologic reactivity
5. A parallel pathologic phenomenon
3. A pathologic process is:
1. Stable chain of pathologic connections
2. Integral network of pathologic phenomena
3. A complex of pathologic and defensive-adaptive reactions
4. Unity of diverse reactions
5. A complex of reactions non-typical of the organism
4. A pathologic condition is:
1. A pathologic process that engages the attention
2. Slow developing pathologic process
3. A consequence of a pathologic process
4. A vicious circle in action
5. 2, 3
6. 1,3,4
5. A disease is disturbed living activity of the organism and its characteristics are:
1. Causal dependency. Determination
2. Disturbed correlations and regulations
3. Lowered adaptability
4. Lowered (to missing) working capacity
5. A new condition – denial of life sustainability
6. All of the above
6. The period when the pathogenic agent has impact on the organism but any signs of disease are missing is called:
1. Prodromal
2. Manifest
3. Latent
4. Passive
5. Non-reactive
Latent
7. The most important characteristics of the period of full development of a disease is:
1. The presence of non-specific symptoms
2. The development of specific for a certain disease signs
3. Distorted, inadequate reactions of the organism
4. The transition from hyper- to hypergic reactivity
5. Development of specific immunity
8. The end of a disease could be:
1. Full recovery
2. A pathologic condition
3. Death 4. Remission
5. All of the above
al of the above
9. Full recovery means:
1. Returning to health status before the disease started
2. Formation of a new, “modulated” health
3. Post disease reprogramming
4. Activated health motivation
5. Stabilizing of the genetically encoded program of life
10. Which mechanisms take part in the genesis of every disease:
1. Cortico-visceral and viscero-visceral
2. Allergic, reproductive and dismetabolic
3. Autoimmune and cell-inductive
4. Reflex, hormonal-humoral and the mechanism regarding cells and tissues
5. Hypo-, Hyper-, and disbiotic
11. Typical for the defensive reactions of the organism is:
1. Do not allow or remove the pathogenic agent
2. Replace lost physiologic reactions
3. Directly increase the anti-stress resistance
4. Activate the non-specific adaptability of the organism
5. Compensate lost specific functions
12. Etiology is a science about:
1. The mechanisms – generating a disease
2. The reasons and conditions for developing of a disease
3. Types of pathologic processes 4. Genetic predisposition to damaging factors
5. Complications in the course of a disease
13. A compensation is:
1. A reaction of the organism to extraordinary irritant
2. A defensive barrier against damage
3. A terminal answer towards damaging irritants
4. An adaptive replacement of lost functions and structures
5. An adaptive replacement of certain functions with others
14. The “vicar” compensation is characteristic of:
1. The skin and mucous membranes
2. The liver and spleen
3. The gastrointestinal tract
4. The sympathetic and parasympathetic division of the autonomic nervous system
5. The kidneys and lungs
15. Pathogenesis is a science of:
1. The reasons for a disease
2. The complications of a disease
3. Prophylaxis of diseases
4. The dangerous effects of the environment
5. The mechanisms of origin, course and end of a disease
5
16. Pathogenesis deals with all listed EXCEPT:
1. Urbanization, application of chemicals and industrialization of society
2. The role of the etiologic factor in pathogenesis
3. Basic mechanisms for disease onset 4. Cause-effect relationships in disease
5. Relationships between function and structure, local and general, specific and nonspecific
1
17. The most important process of the pathogenesis is that which:
1. Counteracts the etiological factor
2. Precedes and causes the others
3. Takes part from the beginning to the end of the disease
4. Is a universal process for all diseases
6. 1, 2, 4
18. What are the relationships between the “local” and the “general” in pathogenesis
1. The “general” always determines the “local”
2. The “”local” is autonomic and independent of the “general”
3. The “general” equals the “local”
4. The “local” and the “general” are tightly connected and always interact
5. The “local” always determines the “general”
4
19. For a disease to appear the reasons are:
1. Obligatory factors
2. Accidental noxae
3. Parallel phenomena
4. Consequences
5. Side effects
20. We could speak about “etiopathogenesis” of a disease if the role of the etiologic factor is:
1. Triggering 2. Variable
3. Constant from the beginning to the end of the disease
4. Variable in the course of the disease
5. Unknown
3
21. What determines the reason for a disease:
1. The particular, the specific
2. The non-characteristic
3. The accidental
4. The exogenous
5. The non-specific
22. The localization of a disease (the “local”) depends on:
1. The “entering door” for the etiologic factor
2. The routes of dissemination in the organism
3. The local reactivity
4. The nature of the tissue/organ
5. 1, 2, 3, 4
23. Pathogenesis is:
1. A complex of non-connected processes
2. An integral network of risk factors
3. A response reaction towards a harmless factor
4. A complex network of cause-effect relationships
5. A complex network of endogenous and exogenous factors
24. For a vicious circle to be triggered it is necessary:
1. Formation of a self-amplified closed pathogenetic chain 2. The presence of a branched pathogenetic chain
3. Formation of a hyperbolic dependency
4. The presence of a linear pathogenetic chain
5. The formation of an intermediate pathogenetic chain
25. The leading pathogenetic factors are:
1. Specific for a disease
2. Primarily independent
3. Consequences and not always with a decisive role
4. In general, common for a lot of diseases
5. 3, 4
26. To the reflex mechanism of a disease DOES NOT belong:
1. The pathologic reflex
2. Necrotic and apoptotic cellular death
3. The pathologic dominant
4. The cortico-visceral mechanism
5. The viscero-visceral mechanism
2
27. The risk factors are closest to:
1. Provoking factors
2. The conditions of a disease
3. Human general instincts
4. The reasons for a disease
5. Pathologic reactions
28. Every damage of cells and tissues is characterized by: 1. Specific activation of the cells
2. Permanent apoptosis
3. Releasing of mediators – signals of the damage
4. The emerging of new, more durable cells
5. Evolutionary re-development of the cells
29. For the damage of cells and tissues it is NOT typical the presence of:
1. Denaturation of the membrane proteins
2. Releasing of the lysosomal enzymes
3. Accumulating of high-active free radicals
4. Deficit of anti-stress cellular proteins
5. Accelerated development and differentiation of the cells
1. Resistance is:
1.The ability of the living system to respond precisely to irritants.
2. The ability of the living system not to respond to irritants.
3. The ability of the living system to oppose irritants.
4. The ability of the living system of self – improvement.
5. 1, 4.
2. The most precise definition of reactivity is:
1. The ability of the living system to adapt.
2. The response of the living system to irritants.
3. The combination of reactions of the living system.
4. The ability of the living system to change its living activity
5. The continuous adaptive alterability of the organisms.
3. The external factors, influencing reactivity and resistance are:
1. Environment.
2. Ecology.
3. Nutrition.
4. Gender and age.
5. 1, 2, 3.
6. 1, 3, 4.
4. The internal factors, influencing reactivity and resistance are:
1. Social conflicts.
2. Psychological factors.
3. Climate and geographic influence.
4. Heredity, gender and age.
5. Lifestyle of the individual.
5. According to the reaction magnitude, reactivity is classified as:
1. Normergic, hyperergic, hypergic, super-allergic.
2. Normergic, hyperergic, hypergic, anergic.
3. Local, segment, diffuse, generalized.
4. Organelle, cellular, organ, organism.
5. Paralytic, kinetic, tonic.
6. Natural resistance is:
1. Acquired.
2. Postnatal.
3. Adaptively developed.
4. Neurogenic developed.
5.Genetically pre-programmed.
7. What type of resistance is acquired by vaccination:
1. Natural, absolute, active.
2. Natural, relative, passive.
3. Acquired, artificial, active.
4. Acquired, artificial, passive.
5. Acquired, natural, active.
6. Acquired, natural, passive.
8. The type of resistance, acquired by hyperimmune serum therapy:
1. Acquired, artificial, active.
2. Acquired, artificial, passive.
3. Natural, absolute, passive.
4. Natural, relative, active.
9. What type of resistance is acquired following an infectious disease:
3. Natural, absolute.
4. Acquired, natural, active.
5. Acquired, natural, passive.
10. Allergy is developed by the following mechanisms:
1. Non-immunological mechanisms.
2. Mechanisms of direct injury.
3. Mechanisms of disturbed reflex arc.
4. Immunological mechanisms .
5. 1, 2.
11. Allergy is:
1. Normergic immunological reactivity.
2. Hyperergic immunological reactivity.
3. Reaction of idiosyncrasy.
4. Explosive cellular – tissue distress.
5. Non – specific hypersensitivity.
12. The main types of allergic reactions are:
1. Of humoral type.
2. Of neuro – reflex type.
3. Of cellular type.
4. Of neuroendocrine type.
5. 1, 3.
6. 2, 4.
13. The main types of disturbed immune response are:
1. Immune hypersensitivity.
2. Immune idiosyncrasy.
3. Disturbed auto - tolerance.
4. Immune insufficiency.
5. 1, 3, 4.
6. 1, 2, 3, 4.
14. Humoral immunity deficiency is characterized:
1. Failure to recognise foreign antigens.
2. Lack of activation of T-helpers.
3. Suppressed proliferation and differentiation of B – Lymphocytes.
4. Disturbed synthesis of specific immunoglobulines.
5. 3, 4.
15. The alteration of which mechanisms does not disturb the immune response:
1. Phagocytosis, processing and presentation of the antigen.
2. Activation of T – helper Lymphocytes.
3. Activation of cytotoxic T – cells and B – Lymphocytes.
4. Reflex activation of the HPA axis ( hypothalamus – pituitary – adrenal)
5. Binding and clearance of antigens.
16. Type I hypersensitivity (anaphylaxis) is related to the presence of:
1. Plasma IgG and/or IgM .
2. Cytotoxic Т-Ly.
3. Mast cell / basophil – bound IgE.
4. Epithelium – bound IgA2.
5. Circulating free IgE.
17. Atopy is:
1. IgE mediated hypersensitivity.
2. IgM mediated hypersensitivity.
3. IgA secretory hypersensitivity.
4. Non-specific hyperreactivity.
5. IgG mediated idiosyncrasy.
18. In the mechanism of cell-dependent cytotoxicity in allergy are NOT involved:
1. NK- cells.
2. Т-helper lymphocytes.
3. Macrophages.
4. Т- killer lymphocytes.
5. All of the above–mentioned are involved.
19. Cell-mediated allergic reactions of delayed type are a manifestation of the interactions between:
1. Macrophages and Т-helper lymphocytes.
2. Memory lymphocytes and idiotype antibodies.
3. Null lymphocytes, complement and antigens.
4. B-sensitized lymphocytes and antigens. В
5. T-sensitized lymphocytes and antigens
6. Activated segments cells.
20. The Arthus reaction (e.g. Farmer’s Lung) is:
1. Cytotoxic immune reaction.
2. Immunocomplex hypersensitivity with excess of antigens.
3. Granulomatous type of hypersensitivity.
4. Immunocomplex hypersensitivity with excess of antibodies.
5. Atopic allergic effect.
21. Which of the mechanisms of antigen elimination always has clinical manifestations:
1. Steric antigen elimination.
2. Immune inflammation.
3. Opsonization and phagocytosis.
4. Immune-dependent apoptosis.
5. Macrophageal antigen adhesion.
22. The disturbed immune memory disrupts:
1. The specificity of the immune response to the antigen.
2. The magnitude and speed of the consequent immune reaction.
3. The combination of humoral and cellular immune responses.
4. The transition of immunological stress into distress.
5. The interaction between immune and neuronal memory.
23. Autoimmune reaction is:
1. The interrupted tolerance towards own antigens.
2. Embryonic genetic autointolerance.
3. A synonym of autoimmune disease.
4. An attempt for immune-mediated species self-isolation of the individual
5. A component of the immune autoregulation that cannot be omitted.
24. Lost autotolerance is a manifestation of :
1. Unveiling sequestered, hidden autoantigens.
2. HPA-axis (hypothalamus-pituitary-adrenal) activation.
3. T–suppressors insufficiency.
4. T-helpers mistake and/or T-effectors or B-lymphocyte direct activation.
5. 1, 2, 3, 4.
6
25. Which of the following mechanisms prevents the occurrence of autoimmune reaction:
1. Unveiling sequestered antigens.
2. Autoreactive T-helpers deficiency.
3. Autoreactive T-suppressors activation.
4. Modulation of own antigens – “self plus X”.
5. Direct stimulation of cytotoxic autoreactive cells.
26. Which of the mechanisms of disturbed autotolerance switches-off T-helper involvement:
1. Flaws in the process of antigen recognition.
2. Contact of sequestered antigens with competent T- and B-cells.
3. Direct activation of the autoreactive T-effectors and/or B-cells.
4. Suppressed T-suppressor activity.
5. Inadequate presentation of own antigens by APC.
27. Immunodeficient states are a representation of:
1. Specific enzymopathy.
2. Antigen deficiency.
3. Inadequate immune reaction.
4. Hypo-, anergic immune response.
5. Hyperergic immune reaction.
28. The most common consequences of immunodeficiencies are:
1. Susceptibility to hemorrhagic diathesis.
2. Facilitated development of hypoxia.
3. Increased susceptibility to infections.
4. Starvation (cachexia).
5. Facilitated cancerogenesis.
29. Non-specific inborn immunodeficit state is present in:
1. Genetic defects of the immunoglobulin synthesis.
2. Thymus embryogenesis disturbances.
3. Genetically determined phagocyte hypofunction.
4. Genetic abnormalities in the complement.
6. 3, 4.
30. AIDS-related immune deficiency is associated predominantly with the damage of:
1. All types of lymphocytes.
3. B- lymphocytes.
4. Т-suppressor lymphocytes.
5. Null lymphocytes.
1. Arterial hyperemia is:
1. Increased incoming amount of blood to a certain organ with decreased outflow.
2. Increased incoming amount of blood to a certain organ with normal outflow.
3. Decreased incoming amount of blood with normal outflow.
4. Decreased or blocked incoming of blood.
5. Disturbed perfusion of a tissue.
2. Venous hyperemia is:
1. Localized increase of blood amount due to impaired outflow.
2. Slowing or blocking of the blood flow in capillaries, small arteries and veins.
3. Increased incoming blood flow and more rapid outflow.
4. Redistribution of the blood flow.
5. Increased tissue perfusion due to larger amount of blood coming.
3. From functional point of view, the arterial hyperemia is a sign of:
1. Filling of blood with storing it.
2. Hyperperfusion of the area.
3. Compensatory shunting of the blood flow.
4. Edema formation. 5. Lymph production.
4. Arterial hyperemia could be a result of:
1. Increased function of an organ.
2. Inflammation, fever.
3. The action of thermal, chemical irritants, etc.
4. Thrombosis and embolism of the vessel.
6. 2, 3, 4.
5. The mechanisms taking part in arterial hyperemia are:
1. Neurogenous.
2. Humoral.
3. Cellular-inductive.
4. Immunogenous.
6. Neurotonic arterial hyperemia is mainly the result of:
1. Increased tone of the vasodilatatory nerves.
2. Increased tone of the vasoconstrictive nerves.
3. Periodic change of the tone of n. vagus.
4. Decreased vasoconstrictive tone.
5. 1, 4
7. Which of the following factors take place in the mechanism of arterial hyperemia:
1. Bioactive substances /histamine, bradykinin, etc./
2. Metabolites /lactic acid, adenosine, СО2 etc./
3. Changes in pH (acidosis).
4. 1, 2.
8. In case of rapid evacuation of a liquid out of the abdominal or pleural cavity the result could be:
1. Reflex decompression hyperemia.
2. venous hyperemia.
3. Ischemia.
4. Working hyperemia.
5. None of the above.
9. Point out the clinical and functional signs of arterial hyperemia:
1 Redness and increase of temperature.
2. Cyanosis and decrease of temperature.
3. Edema.
4. Increased turgor.
10. The changes in blood flow in a prominent constriction of the veins are:
1. Increased incoming blood, normal outflow.
2. Decreased incoming amount of blood, disturbed outflow.
3. Normal incoming amount of blood, disturbed outflow.
4. Decreased collateral circulation.
5. Compensatory shunting of the blood flow.
11. Reasons for observing venous hyperemia could be:
1. Blocked vessel.
2. Compressed vessel.
3. Constitutional weakness of the venous apparatus.
12. From microscopic point of view arterial hyperemia is characterized by:
1. Increased diameter of the vessels and more rapid blood flow.
2. Increased diameter of the vessels and slowed down blood flow.
3. Normal diameter of the vessels and slowed down blood flow.
4. Reduced vascular network.
13. From microscopic point of view venous hyperemia is characterized by:
1. Increased diameter of the vessels and more rapid blood flow. 2. Increased diameter of the vessels and slowed down blood flow, sludge
phenomenon, diapedesis of RBC.
3. Reduced vascular diameter, slowed down blood flow.
4. Increased vascular network.
5. Reduced vascular network, “steal phenomenon”.
14. In what type of hyperemia hypoxia, disturbed metabolism, metabolic acidosis and dystrophy are present:
1. Arterial hyperemia.
2. Venous hyperemia.
3. Reactive hyperemia.
15. Define blood stasis:
1. Normal incoming of blood with disturbed outflow.
2. Increased incoming blood with normal outflow.
3. Decrease to full blocking of the blood flow to a certain area.
4. Blocking of the blood flow in capillaries, small arteries and veins.
5. Redistribution of the blood flow in a certain area.
16. Ischemia is a state of:
1. Decreased or completely missing arterial blood supply.
2. Normal amount of incoming blood with disturbed outflow.
3. Increased arterial blood flow with normal outflow. 4. Increased “pumping out” of the blood from an area.
5. Centralisation of the blood flow.
17. Depending on the causing factor, microcirculatory ischemia could be:
1. Due to compression.
2. Due to obturation.
3. Angiospastic.
4. Due to redistribution.
18. The most common reason for infarction is:
1. A sudden, critical reduction of the blood flow.
2. Venous obstruction.
3. Capillary blood stasis.
4. Arterial hyperemia.
5. Collateral hypocirculation.
19. Thrombosis is a process of:
1. Formation of a blood clot in a vessel of a living organism.
2. Formation of a blood clot in the tissues of a living organism.
3. Formation of blood clots “post mortem” or “in vitro”.
4. Formation of posttraumatic hematoma.
5. Spontaneous hemoconcentration.
20. The main factors leading to blood clotting (the so called Virchow’s triad) are:
1. Changes in the endothelium.
2. Changes in the diameter of the vessel.
3. Disturbance in the blood flow (speed, character).
4. Changes in the composition of the blood.
6. 1, 2, 3.
21. The triggering factor for a thrombus formation is usually:
1. Activation of the platelets.
2. Damage to the endothelium.
3. Changes in the velocity or characteristics of the blood flow.
4. Primarily activated fibrinolysis.
5. Obligatory activated leucocytes.
22. Which factors determine the antithrombogenic qualities of the endothelium:
1. Prostacyclin, adenosine, nitric oxide.
2. Heparin, protein С, АТ-III.
3. Endocapillary glycocalyx.
23. Aggregation of platelets is stimulated by: 1. Increased level of heparin.
2. Increased ratio ТхА2 / PG-I2.
3. Equal deficiency of ТхА2 and PG-I2.
4. Decreased ratio ТхА2 / PG-I2.
5. Calcium deconjugation.
24. Embolism is a process of:
1. Blocking of a vessel by abnormal matter, travelling with the blood flow.
2. Disturbing the rheological characteristics of the blood.
3. Formation of a blood clot due to overactivation of the coagulation system in a living organism.
4. Local formation of a blood clot.
5. Premature activation of fibrinolysis.
25. Which of the following could be attributed to endogenous embolism:
1. Thromboembolism.
2. Air / fat / bacterial embolism.
3. Gas / parasitic embolism.
4. Gas / fat / hard foreign bodies embolism.
26. Thromboembolism could be observed in:
1. Anaerobic gas gangrene, caisson disease.
2. Rupture of subcutaneous fat tissue, fracture of long bones. 3. Entering of amniotic fluid into the uterine arteries.
4. Trauma to the lungs, artificial pneumothorax.
5. Detachment of parts of the thrombus or its aseptic / putrid decomposition.
27. Gas embolism could be observed in:
1. Injury of big vessels and air entering inside them.
2. Artificial pneumothorax.
3. Caisson disease, gas gangrene.
4. Thrombophlebitis.
5. Fracture of a long bone
28. The most common reason for air embolism is:
1. Laceration wounds in the region of v. jugularis and the venae cavae.
3. A breach in the hermetization of an aircraft.
4. Caisson disease.
6. 1, 2.
29. When a long bone fracture is present in an adult, there is a risk of:
2. Bacterial embolism.
3. Gas embolism.
4. Air embolism. 5. Fat ebmolism
30. Embolism in the small circulatory system emerges as a result of:
1. Left ventricle aunerysm.
2. Blocking of а. pulmonalis by a thromboembolism.
3. Blocking of art. carotis by a thromboembolism.
4. Acute left ventricle insufficiency.
5. Progressive mitral stenosis.
1. Alimentary chylomicronemia is sustained in:
1. Lipoprotein lipase deficiency.
2. Inhibited lipoprotein lipase.
3. Hypoalbuminemia.
4. Hyperalbuminemia.
6. 1, 2, 4.
2. Direct source of LDL are:
1. VLDL.
2. IDL.
3. HDL.
4. VLDL and HDL.
5. Chylomicrones.
3. The main pathogenic factor for atherosclerosis is:
1. Blood hyper-LDL.
2. Blood hyper-VLDL.
3. Blood hypo-HDL.
4.Hyperproteinemia.
5. Hypercoagulation.
4. The main reason for the atherogenic effects of LDL is:
1. Their cholesterol ester content
2. Their TriAcylGlycerols (TAGs) content.
3. Their oxidized form(oxy-LDL)
4. Their protein component.
5. Their phospholipids content.
5. The main reason for the atherogenic effects of oxy-LDL is their ability to:
1. Form interplatelet bounds.
2. Damage the endothelial membrane.
3. Stimulate macrophagephagocytosis in subendothelium.
4. Induce dysproteinemia.
5. 2, 3.
6. Macrophages are capable of phagocyting oxy-LDL due to:
1. Chemotactic factors
2. Lipid peroxides produced subendothelially by the arterial wall intimal layer.
3. Specific receptors for oxy-LDLdetection
4. Cytokines produced by the arterial wall intima. 5. 1, 2, 4.
7. “Foam cells” are:
1.Specialized cleaning LDL-macrophages.
2. Transformed endothelial cells .
3. Fixed multinucleate cells.
4. Activated multipotent cells.
5. Modified platelets.
8. Where does atherosclerotic plaque develop?
1. In the subendothelial space of the arterial wall.
2. In the medial layer of the arterial wall.
3. Bellow the medial layer of the arterial wall.
4. Bellow the adventitious layer of the arterial wall
5. In the adventitious layer of the arterial wall.
9. Reversibility of theatheroscleroticplaqueis determined mainly by:
1. The presence of “Foam cells”
2. The presence of smooth muscle cells.
3. The presence of extracellular collagen
4. Platelet adhesion.
5. Plaque capillarization.
10. Conditions for ketonemia are:
1Increased mobilizationof the free fatty acids (FFA) from fat depots.
2. Depressed beta-oxidation in the muscles
3. Krebs cycle activation in the liver.
4. β-hydroxy-β-methylglutaryl CoAcycle activationin the liver.
11. Which plasma lipid constellation represents the highest atherogenic risk?
1. Hyperchylomicronemiaand hypoHDL-lipoproteinemia.
2. HyperLDL and hyperHDL lipoproteinemia.
3. Hyper VLDL, LDL andHDL lipoproteinemia.
4. HyperLDL and hypo HDL lipoproteinemia
5. HypoHDL and hypoLDL lipoproteinemia.
12. In pathophysiologic aspect obesity is divided into:
1. Hypertrophicandatrophic obesity
2. Aplastic, hypoplasticandhyperplastic obesity
3. Obesity with increased volume of fat, decreased volume of fat and with disturbed fat distribution.
4. Alimentary, regulatory andmetabolic obesity.
5. Alimentary obesity, obesity due to decreased physical activity, hereditary obesity.
13. Hyperinsulinemia leads to obesity by:
1. Stimulatingthe production ofglycerol-3-phosphate.
2. Pentosecycle (NADPH2 ) activation.
3. IncreasedacetylCoA synthesis.
4. Inhibiting the activityofhormone-sensitive lipase.
5. 1, 2, 4.
14. Blocked VLDL fromation in the liver leads to:
1. Cirrhosis
2. Lipid dystrophy
3. Hemochromatosis
4. Hepatocytic regeneration.
5. Hepatocytic apoptosis.
15. VLDLsynthesis in the hepatocytes is impaired in:
1. Suppressed apoprotein synthesis.
2. Lipid/apoprotein decomposition.
3. Impaired VLDL- secretion.
4. Lipid(TG, PhL, Cholesterol)synthesis dissociation in hepatocytes.
16. Which hormone ratio determines liver ketogenic potential:
1Glucocorticosteroids/thyroxine.
2. Glucagon/insulin.
3. Tropichormones/somatomedin.
4. Catecholamines/glucocorticosteroids.
5. Renin/plasmin.
17. Ketonemiais a manifestation of:
1. Increasedketogenesisin the liver.
2. Keto-production from adipocytes.
3. Suppressedextrahepaticketolysis.
4. Blockedhepaticketolysis.
18. Receptor-independent pathway of eliminationof plasmaLDLismainly presentedin:
1.Adipocytes.
2. Fibrocytes.
3. Mononuclear phagocyte system.
4. Myofibers.
5. Epithelium.
19. Which are the mechanisms that protect cells from accumulating cholesterol?
1. Own cholesterolsynthesis(HMG-CoA reductase) inhibition. 2. Increasedesterificationof freecholesterol (AHA).
3. Hiding(decomposition) of LDL-receptors anddecreased synthesis
4. Increasedcholesterolexport – contact with HDL3
6. 1, 3, 4
20. The antiatherogenic effect of HDL is associated with:
1. Adsorption, esterification and transport of cell cholesterol to the liver.
2. Inhibition of LDL oxidation.
3. Prolongation and enhancing the effects of prostacyclin.
4. Binding and inhibition of bacterial lipopolysaccharides
21. Mandatorytriggerofatherogenicvascular damageis:
1. Endothelialdysfunction.
2. Hyperlipoproteinemia.
3. Hyperuricemia.
4. Structuralvascular" injury” - lesion.
5. Pericytes remodeling.
22. Atherogenicendothelial dysfunctionis associated with:
1. Increasedendothelialpermeability.
2. Reducedplateletresistance.
3. Increasedadhesionof blood cells.
23. Endothelial dysfunction (caused by hyperlipoproteinemia) is a result of:
1. Increased endothelial membrane cholesterol.
2. Increasedrigidityof theendothelial cells.
3. Endothelialseparation andrestriction.
4. Increasedendothelialpermeability.
24. Exogenoushyperlipidemiais:
1. Hyper HDL – lipoproteinemia.
2. Hyperchylomicronemia.
3. Hyper LDL – lipoproteinemia.
4. Hyper VLDL – lipoproteinemia.
5. Hyper IDL – lipoproteinemia
25. Regarding the lipoprotein-lipase NaCl acts as a:
1. Cofactor.
2. Inhibitor.
3. Activator.
4. Signal modulator.
5. NaCl does not affect the activity of LPL.
26. How does hypoalbuminemia lead to hyperlipidemia?
1. Impaired LPL secretion.
2. Enhanced LPL.
3. Incompleteacceptanceof the releasedFFA (free fat acids).
4. Impaired LPL binding to lipoproteins
5. Stabilizingthe structure ofchylomicrones.
27 . Which is the inhibitor of LPL during cholestasis?
1. Bilirubin.
2. Bile salts.
3. ALP(alkaline phosphatase).
4. ASAT and ALAT.
5. Cholesterol
28. Inadequateand /or delayedleptin secretionleads to:
1. Redistribution oftriglyceridesbetweenadipocytes.
2. Lossof triglyceridesfromadipocytes.
3. Appetite suppression.
4. Accumulation of triglyceridesin adipocytes.
5. Activationof thesatietycenter.
29. Secretion of leptin leads to:
1. Enhancedlipogenesis.
2. Directstimulation of lipolysis.
3. Regulation ofthe relationship betweenlipolysisandlipogenesis.
4. Activation ofhormone-sensitive lipase.
5. Stimulattion ofcatecholaminebeta-receptors.
30. The amountof leptinin the circulationcorrelateswith:
1. Physical capacity.
2. Adipose tissue volume.
3. Visceralorgans size.
4. Pituitarytropichormones.
5. Lipoproteins concentration.
31. What is the most characteristic behavior for Homo sapiens regarding obesity?
1. To controlhis foodbiorhythms.
2. To regulatesatiety.
3. To eatwithout beinghungry.
4. To eatwithoutchewing.
5. To stimulatehis sense ofhunger.
1. Blood glucose cannot be sensed by the β-cells of the Langerhans islets when there is impairment of:
1. GLUT-4.
2. GLUT -2.
3. GLUT -1.
4. GLUT -3.
5. GLUT -9
2. Important pathogenetic stages of DM type I are:
1. Genetic predisposition to damaging the β-cells.
2. Viral infections.
3. Autoimmune mechanism.
4. Insulin resistance.
3. In DM type I there could be damages in the following chromosomes:
1. 9, 22.
2. 6, 11.
3. 7, 12. 4. 2, 8.
5. Х, У.
4. Important risk factors for development of DM type II are:
1. Obesity, family predisposition.
2. Hyperkinetic lifestyle, normosomnia.
3. Hypouricemia, cachexia, family predisposition.
4. Smoking.
5. Often viral infections.
5. In DM the plasma levels of FFA are elevated because of:
1. Activation of the hormone-sensitive triacylglycerol-lipase.
2. Inhibition of the resynthesis of the triacylglycerols.
3. Activation of cholesterol synthesis.
6. The hypertriacylglycerolemia in diabetic patients is mostly due to:
1. Increased synthesis of VLDL in the liver.
2. Inhibition of the lipoprotein lipase.
3. Hyperchylomicronemia.
4. 1, 2, 3.
7. The activated gluconeogenesis in DM is mainly regarding the amino acid: 1. Alanine.
2. Valine.
3. Leucine.
4. Isoleucin.
5. Glutamine.
8. The high level of cholesterol in DM is due to:
1. Activated synthesis.
2. Inhibited degradation.
3. Disturbed utilization.
4. Unknown reason.
9. Major pathogenetic stages in the vicious circle of diabetic ketoacidotic coma:
1. Hyperketonemia hypovolemia.
2. Adynamia, hypothermia.
3. Glucosuria, polydipsia.
4. Tachycardia, somnolence.
5. All of the above.
10. Peripheral neuropathy in DM is due to:
1. Accumulation of sorbitol and fructose.
2. Myoinositol deficiency.
3. Elevated plasma concentration of FFAs. 4. 1, 2.
11. Which regulatory constellation leads to hypoglycemia:
1. Hyperinsulinism and hypercontrainsulinism.
2. Hypoinsulinism and hypercontrainsulinism.
3. Hypoinsulinism and hypocontrainsulinism.
4. Hyperinsulinism and hypocontrainsulinism.
6. 2, 3.
12. Hypoglycemia could be a result of:
1. Suppressed intestinal glucose absorption.
2. Suppressed glycogenolysis in the liver.
3. Decreased gluconeogenesis.
4. Increased glucose uptake in the insulin-dependent tissues.
13. Which HLA haplotypes present a high risk for developing DM type I:
1. DR1 and DR2.
2. DR3 and DR4.
3. DR5 and DR6.
4. DR7 and DR8.
5. DR9 and DR10.
14. Which mechanism lies at the basis of developing DM type I:
1. Increased destruction of insulin in the liver.
2. Autoimmune-provoked destruction of the β-cells.
3. Production of abnormal insulin.
4. Paralysis of the β-cells with insulin-dependent destruction.
5. Ischemic destruction of the β-cells.
15. Select the mechanisms that lead to insulin resistance:
1. Abnormal (count, structure) insulin receptors.
2. Inefficient glucose-stimulated insulin secretion.
3. Post-receptor suppression of the insulin signal.
4. Increased extraction and secretion of insulin from the tissues.
16. The “vulnerability” of the β-cells in genetic predisposition to DM is presented as:
1. Unmotivated β-cell apoptosis.
2. Increased sensitivity to external provocateurs (viruses, toxins).
3. Autochthonic autoimmune β-cellular rejection.
4. Hypoxic β-cellular hypersensitivity.
5. Normoglycemic β-cellular vulnerability.
17. The insulin resistance in DM type II is: 1. Genetically determined lack of insulin action.
2. Lowered insulin action.
3. Distorted cellular effect of insulin.
4. New, unexpected insulin effect.
5. Toxic-dependent universal loss of insulin sensitivity.
18. Major pathogenetic stage of the disturbed carbohydrate metabolism in DM is:
1. β-cellular vulnerability.
2. Variations in plasma glucose levels.
3. Stable hyperglucosemia.
4. The peak of intercurrent hyperglucosemia.
5. The levels of non-glucose carbohydrates.
6. Insulinemia.
19. What are the metabolic defects typical for DM type II:
1. Formation of insulin resistance.
2. Increased engagement of glucose as a source of energy.
3. Disturbed insulin secretion after glucose loading.
4. More easily facilitated intestinal absorption and tubular reabsorption of glucose.
20. DM with normo- or hyperinsulinemia is an indication of:
1. Compensated DM. 2. Neurovegetative hyperglycemia.
3. Elongated half-life of insulin.
4. Insulin resistance that is present.
5. Development of non-insulin-dependent glucose metabolism.
6. 1, 3.
21. It is pathognomonic for a patient with DM to have:
1. Absolute or relative insulin deficiency.
2. Obligatory hypercontrainsulinemia.
4. Obesity.
22. Which is the major pathogenetic element that is common for the different types of DM:
1. Hypoinsulinemia.
2. Hyperglucagonemia.
3. Hyposomatostatinism.
4. Hypercontrainsulinism.
5. Hypercontrainsulinemia.
6. Hypoinsulinism.
23. Stable diabetic hyperglycemia is a result of:
1. Overproduction of glucose in the liver. 2. Increased muscular glycogenolysis.
3. Difficulties in glucose utilization in the tissues.
4. Increased glucose consumption and absorption.
24. What mechanisms are involved in hyperglycemic toxicity:
1. Non-enzymatic glycosylation of proteins.
2. Activation of the polyol pathway of glucose degradation.
3. Hyperglycemic stimulation of glycolysis.
4. Domination of the hexose monophosphate shunt.
25. The major (most important) mechanism for hyperketonemia in DM is:
1. Increased ketogenesis in the liver.
2. Decreased utilization of ketons in the muscles.
3. Redistribution of ketons from the liver to the tissues.
4. Development of abnormal ketogenesis outside the liver.
5. Impossible degradation of ketons in the liver.
26. Ketogenesis in the liver in absolute insulin deficiency is activated because of:
1. Elevated levels of FFAs in the plasma and in the hepatocytes.
2. Activated gluconeogenesis. 3. Increase of the levels of the free carnitine in the hepatocytes.
4. Stimulated acylcarnitinetransferase.
6. 1,2,4.
27. Hyperosmolar non-ketogenic coma is a complication of:
1. Insulin-dependent DM type I.
2. Renal diabetes.
3. Symptomatic (secondary) diabetes.
4. Non-insulin-dependent DM type II.
5. Drug-induced DM.
28. Which is the most dangerous complication of DM type I:
1. Ketoacidotic coma.
2. Ischemic cerebral infarction (stroke).
3. Acute myocardial infarction.
4. Acute peripheral vascular occlusion.
5. Hyperosmolar coma.
6. Acute pulmonary edema.
29. Which complication in DM is a representation of carbohydrate “starving”:
1. Polyneuropathy.
2. Adynamia.
3. Cataract.
4. Retinopathy. 5. Itching.
30. Which complication is a direct consequence of hyperglycemic toxicity:
1. Microangiopathy.
2. Impotence
3. Cachexia.
4. Diabetic foot.
5. Hypercholesterolemia.
1. The degradation of proteins is selectively disturbed when there is deficit of (pick the most complete answer):
1. Saliva, amylase, lipase, carboxypeptidases.
2. Pepsin, trypsin, elastase, amino- and carboxypeptidases.
3. Bile salts, pepsinogen, amylase, trypsinogen.
4. Pepsinogen, amylase, lipase, hydrochloric acid.
5. Hydrochloric acid in the stomach and bicarbonates in the duodenum.
2. Impaired degradation and absorption of proteins is not present in:
1. Diseases of the stomach.
2. Diseases of the pancreas.
3. Disturbance in the endocrine function of the pancreas.
4. Disturbed motion of the gastro-intestinal tract.
5. Malnutrition with essential amino acids.
3. In patients with coeliac disease is present:
1. Deficiency of Vit.B6 and of active transporters of amino acids.
2. Inability to degrade the gliadin component of gluten in cereals.
3. Pepsin and trypsinogen deficiency.
4. Carboxypeptidase А and chymotrypsin deficiency.
4. What are the consequences of disturbed degradation and absorption of proteins in the GIT:
1. Hypoproteinemia, hypoalbuminemia, edemas.
2. Hypoproteinemia, hyperferritinemia, anemia.
3. Dysproteinemia with hypervolemia.
4. Elevated level of glycosylated Hb.
5. Micromolecular paraproteinemia.
5. Under the influence of the intestinal bacteria the undegraded and unabsorbed proteins are subjected to:
1. Fermentation.
2. Decay.
3. Steatorrhea.
4. Halytosis.
5. Steatosis.
6. What is not a consequence of plasma protein levels distrubance:
1. The colloid osmotic pressure of blood.
2. The transport of lipids, hormones, iron, calcium, bilirubin etc.
3. Proton buffering.
4. The defensive function of blood.
5. Coagulation process.
6. Glucose transport.
7. Hypoproteinemia is usualy due to:
1. Decreased albumins.
2. Decreased fibrinogen. 3. Decreased α-globulins.
4. Decreased α- and β- globulins.
5. Decreased glycoproteins.
8. Which of the following is not accompanied by hypoproteinemia:
1. Protein malnutrition, disturbed degradation and absorption.
2. Liver diseases.
3. Increased degradation of proteins in the organism.
4. Increased protein loss through the kidneys and the GIT.
5. Dehydration.
9. Hyperproteinemia is most often due to:
1. α1 - globulins.
2. Fibrinogen.
3. Albumins.
4. γ-globulins or paraproteins.
5. α1 –antitrypsin
10. Dysproteinemia as a clinical finding means:
1. Low proteins.
2. High albumins.
3. Altered ratio between the different fractions of plasma proteins.
4. The presence of pathologic proteins.
5. “Debut” of inflammatory proteins.
11. In hyperamonnemia most active in the detoxication of ammonia are:
1. The lungs.
2. The skin.
3. The bones.
4. The striated muscles.
5. The cartilages.
12. The striated muscles detoxify ammonia through:
1. Aromatic amino acids.
2. Ketogenesis.
3. Lactic acid in the muscle cells.
4. Branched chain amino acids.
5. Ornithin cycle.
13. After the full detoxificating capacity of ammonia in the muscles is reached pathogenetically important is the detoxification in:
1. The brain.
2. Белите дробове.
3. The skin.
4. The bones.
14. The theory about the “energy depletion” in the brain in hyperammonemia is related to:
1. Transformation of valine, isoleucine and leucine into α-keto acids.
2. Transformation of α-ketoglutarate into glutamate and glutamine.
3. Transformation of phenylalanine into phenylpyruvic acid. 4. Compulsory oversynthesis of acetylcholine.
5. Glutamate and aspartate deficiency.
15. The toxic effect of hyperammonemia to CNS is related mostly to:
1. Stable blockage of the N-type voltage dependent Са 2+ channels.
2. Inactivation of the mechanism to excrete Cl from the neurons.
3. Suppression of the К+/Na+ pump.
4. Suppressed presynaptic captation of neurotransmitters.
5. Increased K+ excretion from the neurons.
16. When there are eleveted levels of nitrogen in the blood, what is actually eleveted:
1. Nitrogen contained in proteins.
2. Nucleoproteins.
3. Nitrogen not contained in proteins.
4. Amino acids.
5. Biogenic amines.
17. The different types of elevated nitrogen levels in blood are:
1. Productive.
2. Due ot inactivation.
3. Retentive.
4. Mixed.
18. Productive hypernitrogenemia is not characteristic for:
1. Liver failure.
2. Neoplasms.
3. Haemolytic anemias.
4. Chronic renal failure.
5. Tissue degradation.
19. A key pathogenetic factor in gout is:
1. Hyperammonemia.
2. Huyperuricemia.
3. Hyperglycemia.
4. Hypercalcemia.
5. Hypercapnia.
20. Gout is a disease related to:
1. Disturbance in the metabolism of hemoglobin.
2. Disturbance in the metabolism of lipoproteins.
3. Disturbance in the metabolism of tyrosine.
4. Disturbance in the metabolism of purines.
5. Disturbance in the metabolism of long chain fatty acids.
21. Increased production of uric acid is due to:
1. Defect in the enzyme hypoxanthine-guanine phosphoribosyltransferase.
2. Decreased inhibition of glutamine phosphoribosylpyrophosphate amidotransferase.
3. Defect in glucose-6-phosphatedehydrogenase. 4. 1, 2.
22. Secondary gout develops when there is:
1. Increased production of nucleic acids.
2. Decreased excretion of nucleic acids through the kidneys.
3. Increased production of aromatic amino acids.
4. Increased production of branch chain amino acids.
23. In the basis of the gout exacerbation lies:
1. A distrophic process.
2. An inflammatory process.
3. A necrotic process.
4. An atrophic process.
5. A hypertrophic process.
24. Disturbance in the middle stages of protein metabolism is present when there is a problem in:
1. Oxidative desamination.
2. Decarboxylation and transamination.
3. β–hydroxy - β-methylglutaryl CоА-cycle in the liver.
25. Phenylketonuria is a result of disturbed function of:
1. Glucose-6-phosphatedehydrogenase.
2. Phosphoribosyltransferase.
3. Glutamatedehydrogenase.
4. Pyruvatkinase.
5. Phenylalaninehydroxylas
26. Phenylketonuria is a reason for:
1. Severe damage of CNS.
2. Albinism.
3. Myxedema.
4. Pituitary nanism.
5. Lung emphysema.
27. Disturbed metabolism of tyrosine leads to:
1. Alkaptonuria.
2. Tyrosinuria.
3. Glucosuria.
4. Myoglobinuria.
28. Hyperaminoaciduria is a consequence of:
1. A transport defect in the renal tubules
2. Tubular oversecretion of amino acids. 3. Hyperaminoacidemia over the threshold.
4. Increased postnephronal diffusion of amino acids.
6. 2, 3, 4
1. Overhydrated is this organism in which the water content is more than:
1. 20% of the body weight.
2. 45% of the body weight.
3. 65% of the body weight.
4. 80% of the body weight.
5. 95% of the body weight.
2. An adult organism with a normal BMI is dehydrated when the water content is:
1. 90% of the body weight.
2. 80% of the body weight.
3. 70% of the body weight.
4. 60% of the body weight.
5. 40% of the body weight.
3. “Blocked” osmotic transfer of water between cellular and intracellular space is observed in case of:
1. Lower osmotic pressure in the extracellular space.
2. Higher osmotic pressure in the cells.
3. Higher osmotic pressure in the extracellular space.
4. Lower intracellular osmotic pressure.
5. Cellular and extracellular osmotic pressure without changing.
4. Water goes in the cells and damages them under what circumstances:
1. Lower intracellular osmotic pressure.
2. Lower exracellular osmotic pressure.
3. Higher exracellular osmotic pressure.
4. Higher intracellular osmotic pressure.
5. The extracellular osmotic pressure could be disturbed in:
1. Activated or suppressed renin-angiotensin-aldosterone system.
2. Disturbance in the prostacyclin / thromboxane А2 system.
3. Hypo- or hypersensitivity of the center of thirst.
4. A-, hypo-, or hyperbulia.
6. Hypotonic dehydration is observed when there is:
1. Parallel loss of water and electrolytes.
2. Greater loss of electrolytes.
3. Greater loss of water.
4. Hypotonic osmotic extracellular reset.
5. 2, 4.
7. The Darrow-Yannet mechanism does not take place in:
1.Hypotonic dehydration.
2. Hypertonic dehydration.
3. Isotonic dehydration.
4. Intracellular dehydration.
5. Intracellular hyperhydration.
8. There is no thirst in case of:
1. Decreased volume of extracellular fluid.
2. Hyperfunction of the renin-angiotensin-aldosterone system.
3. Hypothalamic lesion of osmotic receptors.
4. Hypersecretion of renal prostaglandins.
5. Hypertonic dehydration.
9. The volume of interstitial fluid is increased in:
1. Hypoproteinemia
2. Overinfusion.
3. Venous stasis.
4. Disturbed lymphatic flow.
10. In what conditions there is an isotonic dehydration:
1. Parallel loss of water and electrolytes. 2. Greater loss of electrolytes.
3. Greater loss of water
4. Unsatisfied thirst.
5. A diet lacking salt.
11. The infusion of normal saline to patients with disturbed renal function leads to:
1. Isotonic hyperhydration.
2. Hypertonic hyperhydration.
3. Hypotonic hyperhydration.
4. Hypotonic normovolemia.
12. The patients feel extreme thirst (or they get the so called “thirsty” edema) in:
1. Hypertonic hyperhydration.
2. Hypotonic hyperhydration.
3. Hypertonic dehydration.
4. Hypotonic dehydration.
13. Edema is defined as a condition of positive water balance with:
1. Elevated amount of liquid in the interstitial space and body cavities. 2. Cellular expansion.
3. Adaptive water-salt replacement of damaged tissues.
4. Intravascular hypervolemia.
5. Hemo- or lymphodilution.
14. Which is the major pathogenetic factor in the genesis of generalized cardiac edemas:
1. Disturbed Starling equilibrium.
2. Renal sodium and water retention.
3. Insufficient lymph drainage.
4. Increased affinity of the tissues to water and sodium.
5. Subatmospheric pressure of the free interstitial liquid.
15. Conditions for edema are present when:
1. Domination of the filtration force over the absorption force.
2. Filtration force equal to the absorption force.
3. Domination of the absorption force.
4. Exceeded lymph drainage.
16. The decrease in osmotic pressure due to increased membrane permeability always includes:
1. Elevated colloid osmotic pressure in the plasma. 2. Decreased colloid osmotic pressure in the interstitial space.
3. Increased vascular permeability.
4. Increased permeability of the cellular membrane.
5. Decreased colloid osmotic pressure in the lymph.
17. The colloid osmotic pressure in the interstitial space could be elevated when there is:
1. Decreased lymph drainage.
2. Functional tissue hypoperfusion.
3. Increased permeability of the vascular wall.
4. Tissue remodelling.
18. It is easy to exceed the capacity of the lymph drainage when there is:
1. Inhibition of the “suction pump”.
2. Hypofunction of the central lymph drainage.
3. Variations in the blood pressure.
4. Hyperfunction of the lymph valves.
19. Which of the following factors leads to water-salt retention and edema formation: 1. Increased dietary sodium intake.
2. Increased secretion of natriuretic factors.
3. Reduced renal perfusion.
4. Hyperactivity of the renin-angiotensin-aldosterone system.
5. Increased secretion of antidiuretic hormone.
20. Neurotrophic edemas (hemiplegia, paralysis of n. facialis) are due mainly to:
1. Increased intravascular hydrostatic pressure.
2. Decreased colloid osmotic pressure in the vessels.
3. Disturbed lymphatic drainage.
4. Increased permeability of the vascular wall.
5. Local production of sodium retentive cytokines.
21. Point out the key pathogenetic reason(s) for ascites when accompanying liver cirrhosis:
1. Hypoalbuminemia.
2. Portal hypertension.
22. The major reason for the edema in right heart failure is:
1. Increased hydrostatic pressure in the venous part of the capillaries. 2. Increased hydrostatic pressure in the arterial part of the capillaries.
3. Decreased colloid osmotic pressure in the plasma.
4. Decreased osmotic pressure due to increased permeability.
5. Increased vascular permeability.
23. The key pathogenetic factor in cachectic edema is:
1. Increased lymphatic drainage.
2. Decreased colloid osmotic pressure.
3. Sodium retention.
4. Capillary hyperpermeability.
5. Fibrin blockage.
24. Key pathogenetic factor(s) in nephritic edema is/are:
1. Decreased oncotic pressure.
2. Glomerular water-salt retention.
3. Capillary hyperpermeability.
4. Obligatory hyperaldosteronism.
25. Increased risk of diastolic asystolia:
1. Low potassium levels.
2. High sodium levels.
3. Low calcium levels. 4. High potassium levels.
5. High calcium levels.
6. High phosphate levels.
26. In intensive tissue degradation there is a risk of:
1. Elevation of calcium and sodium levels.
2. Elevation of potassium and phosphate levels.
3. Decrease in magnesium and increase of sulfate levels.
4. Decrease in sodium and increase in bicarbonate levels.
5. Decrease in the levels of potassium and sulfate.
27. Which is the key pathogenetic factor in the disturbances of the cardiac function related to abnormally low or abnormally high levels of potassium ?
1. Disturbed depolarization.
2. Altered genomic cardiofunction.
3. Disturbed repolarization.
4. Blockage of the Na/K pump.
5. Mitochondrial lysis.
1. What is the most common reason for hypercalcemia:
1. Excessive intestinal Ca++ absorption.
2. Excessive oral calcium intake.
3. Excessive production of parathormone (PTH).
4. Excessive amounts of calcitonin.
5. Calcium deficiency in the urine.
2. Vitamin D 3 deficiency leads to:
1. Impaired intestinal calcium absorption.
2. Hypoparathyroidism.
3. Impaired calcitonin production.
4. More effective bone remodelling.
5. A block of the alkaline phosphatase of the osteoblasts.
3. Which condition corresponds to osteomalacia:
1. Hypothyroidism. 2. Osteoporosis.
3. Hypoparathyroidism.
4. Rickets.
5. Hypervitaminosis D.
4. Impaired bone mineralisation leads to:
1. Osteoporosis.
2. Osteopetrosis.
3. Osteodystrophy.
4. Osteomalacia.
5. Osteolysis.
5. The most common reason for primary hyperparathyroidism is:
1. Adenoma of the parathyroid glands.
2. Hypophosphatemia.
3. Hypervitaminosis D
4. Cellular hyperplasia of the thyroid gland.
5. Parathyroid carcinoma
6. What is the effect of alkalosis on the ionized calcium: 1. No effect.
2. Elevates it.
3. Decreases it.
4. Increases ionized calcium activity.
5. Different effects, depending on the ammount of ionized calcium.
7. All the following are consequences of hypocalcemia except one. Point it out:
1. Osteopenia.
3. Senile osteoporosis.
5. Osteodystrophy.
8. Hypocalcemia could be present in all of the following conditions except one, which is it:
1. Hypovitaminosis D3 .
3. Malabsorption syndrome.
4. Rickets. 5. Adenoma of the parathyroid glands.
9. The main reason for postmenopausal osteoporosis is:
1. Estrogen deficiency with insufficient calcium intake.
2. Reduced physical activity.
3. Postmenopausal obesity.
4. Polypragmasia after menopause.
5. Disturbed libido.
10. Hypercalcemia DOES NOT lead to:
1. Calcinosis.
3. Peptic ulcers in the digestive system.
4. Tetania.
5. Depression and reduced labour capacity.
11. Secondary hyperparathyroidism is present in:
1. Hypercalcemia.
2. Hypervitaminosis D.
3. Milk alkali syndrome. 4. Graves’ disease.
5. Long-lasting hypocalcemia.
12. Hypercalcemia is a prerequisite for:
1. Urolithiasis.
2. Nephrocalcinosis.
3. Renal cyst formation.
4. Hyperparathyroidism.
13. Which one is NOT affected by calcium dysbalance:
1. Hemostasis.
2. Neuro-muscular excitability.
3. Bone metabolism.
4. Cellular signal transmission.
5. Parathormone secretion.
6. Hypoxic stimulation of erythropoietin.
1. Metabolic acidosisis a process of:
1. Accumulation and/or excess ofnon-respiratoryH+ .
2. Deficiency of non-respiratory H+ .
3. DecresedCO 2 partial pressure.
4. Increased CO 2 partial pressure.
5. Increased bicarbonate concentration.
2. Main pathogenetic mechanism for metabolic acidosis development is:
1. Excess production of H + in the body.
2. Decreased H + excretion by kidneys.
3. Increased bicarbonate production by kidneys.
4. Activated Darrow– Kotlov mechanism
3. Which process is characterized with accumulation of metabolic H+ ?
1. Respiratory center depression.
2. Diminished endogenous production of H + donors.
3. Exogenous intake of acid products.
4. Reduced buffer capacity of extracellular space.
5. Disturbed Starling equation.
6. 3, 4
4. In which case the metabolic acidosis is NOT caused by increased production of H+ ?
1. Diabetes mellitus.
2. Prolonged fasting.
3. Renal failure.
4. Acute intoxication.
5. Shock.
6. Severe hypoxia
5. Hypoxic type lactic acidosis occurs when tissue pO2 falls:
1. Under 70 mmHg.
2. Under 60 mmHg.
3. Under 40 mmHg.
4. Under 20 mmHg.
5. Under 10 mmHg. 6. pO2 is not essential for lactic acidosis
6. Not-hypoxic lactic acidosis is most commonly observed in:
1. Physical exercise.
2. Enzyme defects in lactate metabolism.
3. Hyperoxia.
4. Respiratory acidosis.
7. Main pathogenetic unit in hypoalkaline metabolic acidosis is:
1. Increased bicarbonate loss from extracellular space.
2. Increased intracellular bicarbonates.
3. Protein buffers deficiency.
4. Disturbance in hemoglobin buffer system.
5. Bicarbonates transfer into the cells.
8. Retention type metabolic acidosisis a result of:
1. Retention of acid products.
2. Impaired H + secretory capacityof the kidney.
3. Increased absorption of H + ions.
4. Development of renal H + generator.
9. Metabolic alkalosis is a process of:
1. Accumulation and/or excess of non-respiratory H+
2. H + reduction and/or non-respiratory H + deficiency .
3. Cells and tissues H + imbalance.
4. Organic anions accumulation.
5. Impaired hemoglobin buffering.
10. Main pathogenetic unit for metabolic alkalosis development is:
1. Decreased bicarbonate concentration in extracellular space.
2. Increased bicarbonate concentration in extracellular space.
3. Bicarbonate transfer between cells and extracellular space.
4. Decreased CO 2 partial pressure.
5. Increased CO 2 partial pressure.
11. Main pathogenetic mechanism for metabolic alkalosis development is:
1. Suppressed renal bicarbonate generation.
2. Activated renal bicarbonate generation. 3. Acids loss with subsequent chlor deficiency.
12. Trigger for metabolic alkalosis is:
1.Synthesis or intake of bicarbonate.
2. Increased renal bicarbonate affinity.
3. Increased plasma-erythrocyte HCO 3 translocation.
13. How can metabolic alkalosis be stabilized?
1. Hypocapnia development.
2. Compensatory glutamin lysis.
3. Urea synthesis stimulation.
4. Increased renal bicarbonate retention.
5. Increased bicarbonate synthesis from monocyte-macrophage system.
14. How can metabolic alkalosis be divided?
1. Hypoxic and non-hypoxic.
2. Congenital and acquired.
3. Calcium dependent andcalcium independent.
4. Chlor dependent and chlor independent.
5. Normo-, hypo- and hyperosmotic.
15. Which is the clinical breathing manifestations in metabolic alkalosis?
1. Loud and deep breathing – Kussmaul’s respiration.
2. Agonal breathing.
3. Slow and/ or shallow breathing.
4. Biot’s respiration.
5. Breathing is not changed.
16. What is the characteristic of respiratory acidosis?
1. Decreased рСО2 .
2. Increased рСО2 . 3. Increased рО2 .
4. Decreased рО2 .
5. Decreased НbСО.
17. Main pathogenetic mechanism for respiratory acidosis development is:
1. Alveolar hyperventilation.
2. Alveolar hypoventilation.
3. Disturbed gases diffusion in lungs.
4. Isolated increase of CO 2 production.
18. Which of the followed does NOT lead to development of primary respiratory acidosis?:
1. Supressed respiratory center.
2. Mechanical asphyxia.
3. Inadequate dosed oxygen therapy.
4. Airways spasm.
5. Psycho-emotional excitement
19.What is the compensation of respiratory acidosis?
1. Tubular bicarbonate excretion.
2. Activated tubular acid- and ammonia genesis.
3. Activated ketone synthesis.
4. Suppressed ornithine cycle.
5. Activated pentosephosphate cycle.
20. What is the characteristic of primary respiratory alkalosis?
1. Increased bicarbonate level.
2. Decreased bicarbonate level.
3. Increased CO 2 partial pressure.
5. Mandatory presence of HbCO.
21. Main pathogenetic mechanism for respiratory alkalosis development is:
1. Collateral alveolar ventilation.
2. Alveolar hyperventilation.
3. Alveolar hypoventilation.
4. Decreased ventilation/perfussion ratio.
5. Increased alveolar CO2 export.
22. What is the compensation of primary respiratory alkalosis?
1. Hypercapnia development.
2. Hypocapnia development.
3. Chlorid deficiency development.
4. Increased plasma bicarbonates.
5. Decreased plasma bicarbonates.
23. What is the renal compensation of primary respiratory alkalosis?
1. Decreased tubular H + secretion.
2. Increased tubular H + secretion.
3. Increased amino acid clearance.
4. Activated renin-angiotensin system.
5. Increased aldosteron effects.
24. Decreased plasma bicarbonate level in respiratory alkalosisis a result of:
1. Supressed acido- and amonnia genesis.
2. Hamburger’s effect.
3. Increased cellular lactate productionandsecretion.
25. Symptoms of " dizziness" and muscles tremor in respiratory alkalosis are associated with:
1. Increased sodium level.
2. Increased calcium level.
3. Decreased sodium level.
4. Decreased calcium level.
5. Increased urea level.
26. The inadequacy in which processes leads to acid-base balance distublance?
1. Production, transport and excretion of organic anions.
2. Production, transport and excretion of lactate.
3. Production, transport and excretion of electrolytes.
4. Production, transport and excretion of CO2 .
5. Production, transport and excretion of H+ .
27. The term “Hypoprotonemia”describes the presence of:
1. Alkalosis.
2. Bicarbonatemia.
3. Alkalemia 4. Hyposmia.
28. Which of the following is NOT a classification of acid-base disorders?
1. Compensated, subcompensated and uncompensated.
2. Mild, moderate, severe, life-threatening.
3. Respiratory, metabolic, mixed.
4. Local and general.
5. Hereditary, congenital, acquired.
29. Neutralization of H + excess/ or deficiency / in the extracellular space is achieved by:
1. Extracellular buffering
2. Ion exchange in renal tubules.
3. Metabolic transformations.
4. Alterations of pulmonary ventilation.
30. When an acid-base balanace disturbance can be definied as compensated?
1. pH is in the references, but the other indexes are out if it.
2. pH is out of the references, but the other indexes are normal.
3. All the indexes are in the references.
4. All the indexes are out of the references.
5. All mentioned, but monitored in a timely manner.
1. The state of impaired oxygen regimeis defined as:
1. Anoxia.
2. Hyperoxia.
3. Hypoxemia.
4. Hypoxia.
5. Hypoxidosis.
2.What is “hypoxidation”?
1. Reduced PO 2 in arterial blood.
2. Reduced oxygen content in arterial blood
3.Reduced oxygen demand that is not due to hypoxia.
4. Reduced amount of oxyhaemoglobin.
5. State of impaired oxygen regime.
3. What is “hypoxia”?
1. Disrupted oxygen exchange.
2. Oxygen toxicity.
3. Oxygen deficiency.
4. Reduced oxygen needs.
5. Limited aerobic capacity.
4. What is the main functional aspect of hypoxia?
1. Decreased oxygen reserves in the body.
2. Adequate oxygen deficiency.
3. Oxygen hyporesponsiveness.
4. Hyperadaptation to oxygen insufficiency.
5. Inadequate oxygen supply/oxygen demand.
5. Which is NOT a cause for the development of local hypoxia?
1. Arterial spasm.
2. Arterial hyperemia.
3. Arterial compression.
4. Arterial obstruction.
5. Arterial occlusion.
6. What is the pathophysiological classification of hypoxia:
1.Hypoxic, hemic, circulatory,O 2 utilization, mixed.
2. Compensated, uncompensated,subcompensated, overcompensated. 3. Fulminant, acute, subacute, chronic.
4. Local, organic, systemic, generalized.
5. Pulmonary, cardiovascular, blood, mixed.
7. What could cause hypoxic hypoxia?
1. Acute haemoglobin deficiency.
2. Blocked cytochrome oxidase.
3. Increased oxygen export by the lungs.
4. Increased CO 2 production.
5. Insufficient pulmonary oxygen transfer.
8. Exogenic hypoxic hypoxia is a result of:
1. Disturbance in respiratory lung function.
2. Decreased pO 2 in the inhaled air.
3. Damaged respiratory center.
4. Increased pO 2 in the exhaled air.
5. Disorders of the respiratory muscles.
9 . Which index is primary decreased in exogenous hypoxic hypoxia?
1. Alveolar pO2 .
2. Inspiratory pO2 .
3. Arterial pO2 .
4. Oxyhemoglobin saturation.
5. Alveolar oxygen transfer.
10. Which statement refers to exogenous hypoxic hypoxia?:
1. Respiratory system is seriously compromised.
2. Respiratory system is intact.
3. Must be accompanied by hypercapnia.
4. Dramatically reduction of hemoglobin amount.
5. There is a risk for atelectasis.
11. The main pathogenetic unit of hypoxic hypoxia is:
1. Arterial hypoxemia.
2. Arterial hypercapnia.
3. Arterial hypoxia.
4. Arerial hyperoxia
5. Arterial disoxia.
12. Main mechanisms disturbing oxygen intake in endogenous hypoxic hypoxia are:
1. General alveolar hypoventilation.
2. Decreased ventilation/perfusion ratio.
3. Impaired oxygen diffusion.
4. Oxygen insufficiency in the inhaled air.
13. Hemic (blood) hypoxia is generally devided into:
1. Exogenous and endogenous.
3. Compensated and decompensated.
4. Anemic and inactivity.
5. Hypo- and hyperoxic.
14. Hemic (blood) hypoxia is characterized with:
1. Arterial hypoxia.
2. Reduced oxygen transporting capacity of the blood.
3. Arterial hypercapnia.
4. Impaired oxygen utilization from cells.
5. Independently reduced tissue pO2.
15. Carboxyhemoglobinemia develops as a result of:
1. CO poisoning.
2. KCN poisoning.
3. vit B12 deficiency .
4. Sulfonamides overdose.
5. NO deficiency
16. Which of the following characteristics is not typical for CO?:
1. High haemoglobin affinity.
2. Cytochromes inhibitionin tissues.
3. Strong pyrogenic effect.
4. Shifting oxyhaemoglobin dissociationcurveto the left.
5. Carboxyhemoglobin formation.
17. Which statement refers to methemoglobin:
1. It is irreversible compound.
2. Iron is a third valence.
3. It is formed in the presence ofCO. 4. Congenital form is hemoglobinF.
5. Physiologic methemoglobinemi ais not significant for the body.
18. The main pathogenetic unito f hemic hypoxia is:
1. Decreased pO2 inarterial blood.
2. Decreased blood volume.
3. Decreased oxygen capacity of blood.
4. Reduced erythrocytes life.
19. What is the general effect from the development of circulatory hypoxia?
1. Methemoglobin reductase block.
3. Effective hemoglobin deficiency.
4. Direct mitochondrial decoupling.
5. Tissue hypoperfusion.
20.Which of the following is NOT a cause for circulatory hypoxia development?
2. Arterial spasm.
3. Decreased blood flow to tissues in Right-Sided Heart Failure (RSHF).
4. Blockage of arterial vessel by thrombus.
5. Thromboembolic development.
21. Which statement refers to ischemic type circulatory hypoxia?
1. There is oxygen substrate deficiency.
2. Shortened blood/tissue contact time.
3. Reduced cellular O 2 utilization.
4. Generalized edema development.
5. General indicator is venous hyperoxia.
22. The main pathogenetic unit of circulatory hypoxia is:
1. Reduced effective hemoglobin.
2. Systolic cardiac dysfunction.
3. Reduced effective circulatory volume.
4. Decreased hematocrit.
5. Blood depots depletion.
23. In which hypoxia type the processes of O 2 intake, transport and deliveryto the cells are not disturbed?:
1. Circulatory hypoxia.
2. Hypoxic hypoxia.
3. Hemic hypoxia of anemic type.
4. O2 utilization hypoxia.
5. Hemic hypoxia of inactivity type.
24. Basic mechanisms for development of O2 utilization hypoxia are:
1. Increased mitochondrial oxygen reduction.
2. Decreased mitochondrial oxygen reduction.
3. Reduced efficiency of the oxygen energy production.
4. Insufficient functional energy provision.
25. Toxic suppression of transelectronases leads to:
1. Decoupling of oxidative phosphorylation.
2. Mitochondrial lysis.
3. Non-utilization of the delivered oxygen.
4. Tissue oxygen redistribution.
5. Reverse oxygen transport.
26. Tissue hypoxia is the final result of:
1. Reduced physical activity.
2. Absolute starvation.
3. Each metabolic abnormality.
4. Severe and/ or progressive systemic hypoxia
5. Progressive,oxygen-dependent enzyme dysfunctions.
27. Which of the following pulmonary reactions has no adaptive function?:
2. Increased oxygen diffusion through the alveolar-capillary membrane.
3. Increased pulmonary perfusion.
4. Pulmonary atelectasis development.
5. Euler-Liljestrand reflex.
28. What is the aim of lung adaptations?
1. Easier CO 2 export.
2. Increasing pCO 2 above 44 mmHg. 3. Increasing arterial pO2
4. Increasing pulmonary arteries pressure.
5. Increased converting enzyme formation.
29. What is the aim of cardio-circulatory adaptations:
1. Increasing alveolar ventilation.
2. Improved tissue perfusion.
3. Increased oxygen transporting capacity of the blood.
4. Alteration in tissue enzymes activity.
5. They are not essential.
30. Increased oxygen transporting capacity of the blood is a result of:
1. Increased blood pressure.
2. Increased tissues vascularization.
3. Compensatory heart hypertrophy.
4. Compensatory diminished erithrolysis.
5. Compensatory erythropoesis.
31.Which are tissue-cellular adaptations caused by reduced oxygen delivery to cells?
1. Increasing oxygen transport.
2. Improvement of tissue perfusion.
3. Increasing utilization of supplied oxygen.
4. Improving oxygen delivery to vital organs.
5. Inhibition of key cell enzymes
1. What is inflammation:
1. Selective anti-infective pathological reaction.
2. Pathological process, typical for vascularized tissues.
3. Self-sustained pathological condition.
4. Disease with unknown etiology.
2. Inflammation is a unity between:
1. Alteration, exudation, proliferation.
2. Functional and structural disorders.
3. Local and general manifestations.
4. Adaptive and pathological reactions.
3. Exogenous causes of inflammation are:
1. Bacteria, viruses, fungi, parasites, insects
2. Acids, bases, salts, drugs, toxins.
3. Trauma, foreign bodies, thermal factors, ionizing radiation, electricity.
4. Deposition of uric acid, urea, bile and other tissue.
4. Endogenous causes of inflammation are:
1. Deposition of bile, urea, uric acid, of, calcium salts and more.
2. Products of tissue decay, hemorrhage, thrombosis, embolism, heart attacks.
3. Deposition of immune complexes.
4. Viruses, bacteria, thermal factors.
5. Which are the main phases of inflammation in their " sequence" :
1. Initiation, promotion, progression. 2. Alteration, exudation, proliferation.
3. Alteration, promotion, progression.
4. Initiation, exudation, progression.
5. Alteration, progression, proliferation.
6. Inflammatory alteration is :
1. Programmed irreversible cell and tissue damage.
2. Reversible cellular lesion.
3. Spontaneous genome mutation.
4. Irreversible cell and tissue damage.
7. Alteration is a process of:
1. Rearrangement of cells and extramedullar matrix.
2. Formation of exudate.
3. Cell matrix and plasma proteins damage.
4. Progressive cell proliferation.
5. Cells infiltratio
8. Primary alteration occurs as a result of:
1. Mediators released.
2. The damaging action of the pathogen.
3. Lysosomal hydrolytic enzymes.
4. Activated platelets.
5. Activated white blood cells.
9. The bioactive substances released during alteration are called:
1. Mediators.
2. Synchronizing factors.
3. Statins.
4. Agglutinins.
5. Inhibitors.
10. Which of the following statements is true about mediators?
1. They cause the reactions in the inflammatory process.
2. They modulate (positively of negatively) the inflammatory process.
3. They inhibit the exudative phase.
4. They co-stimulate the development of the inflammatory process.
5. They reprogram the genome of macrophages.
11. Important for the occurrence of cell alteration is:
1. The lost ability for contact inhibition.
2. Alteration of the cell membrane.
3. Stabilization of lysosome membranes.
4. Decreased mechanical resistance of cells.
5. Obligatory opsonization of cells.
12. Of great importance for the alteration is:
1. Decreased levels of cyclooxygenase products
2. Hydrolytic enzymes, released by the damaged lysosomes.
3. The limited activity of the enzymes of the electron transport chains in the mitochondria.
4. Structural alterations of cell receptors.
5. Blocked activity of free radicals.
13. Which of the following biologically active substances may also act as modulators:
1. Serotonin, histamine.
2. Reactive oxygen species.
3. Prostaglandins and сАМР .
4. Tumor – necrosis factor, bradykinin.
5. The complement system, neutrophil chemotaxis factor.
14. Point out the role of the modulators in the process of inflammation:
1. They inhibit the metabolites of the arachidonic acid.
2. They block the kinin and the complement systems.
3. They stimulate the secretion of growth factors and the proliferation phase. 4. Enhance or inhibit the mediator-initiated inflammatory process.
5. They are not involved in inflammation.
15. The released lysosome enzymes mainly:
1. Stimulate the phase of proliferation.
2. Increase capillary permeability and destroy cells.
3. Play the role of intercellular regulators.
4. Block the kinin system.
5. Provoke autoimmune progression.
16. The hemodynamic vascular changes in inflammation in chronological order are:
1. Arterial hyperemia, spasm of the arterioles, stasis.
2. Stasis, arterial hyperaemia, venous hyperaemia.
3. Ischemia, thrombosis, arterial hyperemia.
4. Spasm, reversible ischemia, venous hyperemia.
5. Spasm, arterial hyperaemia, venous hyperaemia, stasis.
17. Permeability disturbances in inflammation are a result of:
1. Hemodynamic changes in blood vessels.
2. Structural changes in blood vessel walls.
3. Disturbed speed of blood flow.
4. Smooth-muscle hypertrophy.
5. Alteration in receptor structure
18. Exudation is:
1. The effusion of plasmatic fluid and proteins from the microcirculation
to the inflammatory focus.
2. Accumulation of fluid and proteins in the inflammatory focus, independent of microcirculation.
3. A process of rearrangement of interstitial fluid in the inflammatory focus.
4. Movement and congestion of cellular fluid in the inflammatory focus.
5. А process of decreased lymph drainage.
19. A main pathogenic factor for exudate formation is:
1. Impeded blood drainage.
2. Increased vascular permeability.
3. Primarily increased oncotic pressure in the inflammatory focus.
4. Sodium metabolism disturbances.
5. Hormonal disturbances /aldosterone and ADH/.
20. The early cell migration during the acute inflammation is associated with:
1. Fibroblast proliferation.
2. Accumulation of neutrophils.
3. Active diapedesis of erythrocytes.
4. Proliferation of angioblasts.
5. Eosinophils and basophils.
21. Which of the processes is affected to the highest extent by adhesion molecules deficit:
1. Proliferation
2. Alteration.
3. Emigration.
4. Regeneration.
5. Exudation.
22. The leucocytes that have migrated into the inflammatory focus:
1. Execute opsonization of the pathogenic agent.
2. Phagocyte bacteria and dead cells.
3. Participate in the “cleaning” phase.
4. Act as matrix for proliferation.
23. Suppressed phagocytosis complements to the inflammation:
1. More effective development.
2. Definitely pathological character.
3. More adaptive course.
4. Ability of unusual development.
5. Obligatory chronification.
24. The phase of proliferation includes:
1. Alteration of cells and intercellular matter by the pathological agent.
2. Growing of connective tissue and capillaries.
3. Formation of inflammatory oedema.
4. Hemodynamic vessel changes.
25. Which of the local signs of inflammation is related to the increased vessel permeability:
1. Redness.
2. Swelling.
3. Pain.
4. Increased temperature (heat).
5. Disturbed function.
26. According to the prevailing pathological processes, the inflammation could be:
1. Alterative, exudative, proliferative.
2. Hypo-, normo-, hyperergic.
3. Specific, non-specific.
4. Viral, bacterial, immunologic.
5. Typical, atypical.
6. 1, 3, 5.
27. An inflammation could be accepted as chronic when its duration is over:
1. 6 hours.
2. 6 days.
3. 6 weeks.
4. 6 months.
5. 6 years.
6. It is not related to duration, but to the nature of the cellular alteration.
28. Chronic inflammation is characterized with a more pronounced infiltration with:
1. Adipocytes and segmented leukocytes.
2. Tissue degradation products.
3. Platelets and B-lymphocytes.
4. Mast cells and erythrocytes.
5. Lymphocytes and macrophages.
1. Heat production is increased in:
1. Decreased ambient temperature.
2. Uncoupling of oxidative phosphorylation.
3. Exercise
4. Increased ambient temperature.
5. 1, 2. 3.
2. Physical heat dissipation is increased in:
1. Increased ambient temperature.
2. Acute intoxication.
3. Reduced ambient temperature.
4. Starvation.
3. Environmental factors for ineffective heat dissipation are:
1. Low temperature and low humidity.
2. High temperature and low humidity.
3. High temperature and high humidity.
4. Low temperatures and high humidity.
5. Normal temperature and low humidity.
4. The peak stage (stadium fastigii) of fever is characterized by:
1. Deficiency of heat production.
2. New set point of the heat production/heat dissipation balance.
3. Limited heat dissipation.
4. Enhanced heat production.
5. Change in the heat production/heat dissipation ratio.
5. Which areas of the thermoregulatory center are responsible for fever onset:
1 .Sympathetic neurons.
2. Tonic motoneurons.
3. Thermo effector neuronal pathways.
4.Set-point neurons.
5. Thermostatic neurons.
6. Fever is a pathologic process that develops due to the action of:
1. Carcinogens.
2. Mutagens.
3. Pyrogens.
4. Stimulants.
5. Thymosins.
7. Fever is a process in which:
1. Thermoregulation is unchanged.
2. Thermoregulation takes place at a higher level.
3. Heat dissipation increases.
4. There is a close correlation between external and internal temperature.
5. Thermoregulation is disturbed.
8. Adjustment of the set point of temperature homeostasis in fever depends on:
1. The nature of pyrogens and their amount.
2. The functional state of the thermoregulatory center.
3. The reactivity of the organism.
4. Age.
9. What is the common feature between fever and hyperthermic conditions?
1. Increase of the body temperature.
2. Unchanged thermoregulation.
3. Constantly increased heat production.
4. Direct link between external/internal temperature.
5. Different developmental stages.
10. Exogenous bacterial pyrogens are mainly:
1. Proteins.
2. Lipoproteins.
3. Steroids.
4. Endorphins.
5. Lipopolysaccharides.
11. Which microorganisms have strong pyrogenic features?
1. Gram negative organisms.
2. Gram positive bacteria.
3. Rickettsiae.
4. Viruses.
5. Spirochetes.
12. Endogenous pyrogens are:
1. Substances of cell or tissue origin.
2. Substances produced by " activated" leukocytes.
3. Substances stored in leukocytes.
13. Which mediators have pyrogenic influence at the level of the set-point neurons?
1. Norepinephrine, serotonin.
2. Acetylcholine, prostaglandins E1 and E2.
3. Cortisol.
4. Тhyroxine
5. ACTH.
14. What plays a key role in fever development when caused by viral infections?
1. α-interferon.
2. TNF.
3. IL-4, IL-1.
4. β-endorphins.
5. Cachectin
15. Increasing body temperature (stadium incrementi) in fever, is mainly a result of:
1. Increased heat production.
2. Increased heat production and decreased heat dissipation.
3. Reduced heat dissipation.
4. Initiated mechanism of tissue conductivity.
16. Which factor determines the pattern of temperature decrease?
1.Speed and nature of the pyrogen’s action suspension.
2. Functional state of the thermoregulatory center.
3. Ambient temperature.
4. Fluids intake.
17. Critical drop in temperature in stadium decrementi of fever may lead to acute circulatory failure due to:
1. Sympathetic stimulation.
2. Cardiac arrest.
3. Vasodilation, hypotension and reduced MCO (minute cardiac output).
4. Depressed vasomotor center.
5. Any of the foregoing.
18. Negative nitrogen balance in fever is due to:
1. Enhanced protein degradation.
2. Decreased absorption and synthesis.
3. Increased removal from the body.
4. Increased use of proteins for heat production.
19. What contributes to the intoxication during fever:
1. Reduction of gastric secretion.
2. Delayed gastrointestinal motility.
3. Absorption of toxic products.
4. 2, 3.
20. Fever has a favourable impact on:
1. B-lymphocyte activity.
2. T-cell proliferation.
3. Phagocytic activity.
4. Activation of pituitary-adrenal system.
1. Point out the correct sequence of the stages in malignant neoplasm:
1 Promotion, initiation, dissemination, progression.
2. Progression, promotion, initiation, dissemination.
3. Initiation, promotion, progression, dissemination.
4. Initiation, dissemination, promotion, progression.
5. Dissemination, progression, promotion, initiation.
2. True carcinogens determine the stage of:
1. Promotion.
2. Initiation.
3. Progression.
4. Angiogenesis.
5. Metastasis.
3. What do carcinogens have in common?
1. Physical and chemical structure.
2. Lethal and irreversible disturbance of the genome.
3. Their mitogenic effect.
4. Irreversible, non-lethal and inherited disturbance of the cellular genome.
5. The similar mechanism of causing impact on the genome.
4. Neoplasms are characterized by:
1. Monoclonal cell reproduction.
2. Autonomic reproduction, non-subjected to organism’s regulation.
3. Parasitic and toxic behaviour.
4. The individual gets ontogenetically younger.
5. Initiation leads to:
1. Activation of oncogenes.
2. Inhibition of oncogenes.
3. Changes in the activity of apoptotic genes.
4. Stable activation of functionally specific genes.
6. How do the promotors affect the cellular genome:
1. In a cumulative manner with long term effect.
2. To a certain threshold, with no long term effect.
3. Interfering with or without a long term effect.
4. To a certain threshold with an intermittent after effect.
5. They do not affect the cell genome.
7. What kind of effect is caused by the procarcinogenes? 1. Direct carcinogenic.
2. Mitogenic.
3. Stimulating.
4. Indirect carcinogenic.
5. Antimitogenic.
8. What is the common feature of chemical carcinogenes?
1. The cyclopentanoperhydrophenanthrene ring.
2. The electrophilic parts of their molecules.
3. Acetylation of the molecule.
4. They are all polymers.
5. The presence of an organic compound.
9. What mechanism is involved in chemical carcinogenesis?
1. Rupture mutagenesis.
2. Genomic deletion.
3. Spontaneous mutation.
4. DNA adduction mutagenesis.
5. Blocked vital procesess.
10. Once the neoplasm is formed it grows at the account of:
1. Transforming all the surrounding cells into neoplastic.
2. Proliferation and divergent development of a newly formed cellular line.
3. Increased proliferation of pluripotent stem cells. 4. Independent hyperproduction of extracellular matrix.
5. Adaptive polyclonal cellular proliferation.
11. Which of the following are chemical carcinogenes?
1. Heterocyclic and polycyclic hydrocarbons.
2. Aromatic amines and nitrozamines.
3. Alkylating and acetylating agents.
4. Antracyclic antibiotics.
12. What mechanism is involved in radiation carcinogenesis?
1. Radiation dose incorporated in the genome.
2. Effect of DNA adduct into the genome.
3. Mutagenesis due to rupture and deletion.
4. Apoptotic mutagenesis.
13. UV rays have a carcinogenic effect on the genome through what mechanism?
1. Formation of thymine dimers.
2. De novo synthesis of DNA
3. DNA adduct.
4. Transversion of purines into pyrimidines.
5. Selective telomerase effect.
14. Fast transforming RNA viruses have:
1. Blockers of oncogenes.
2. Apoptotic modulators.
3. Virus-modified cellular oncogenes.
4. Antioncogenic moderators.
5. Apoptotic inductors.
15. What mechanism is involved in hormonal carcinogenesis?
1. Permament activation / inactivation of regulatory genes.
2. Transposition of genetic material.
3. Genomic “sensibilization” to other carcinogenes (cocarcinogenesis).
4. Obligatory preceding cellular disproduction of hormones.
16. The term “malignant potential” is related most often with:
1. Greater number of non-aggressive tumor cells
2. Rapid increase in the number of tumor cells.
3. Increase in the number and activity of the tumor cells
4. Aggressive behaviour of a constant number of tumor cells
5. The time required for double increase the number of tumor cells.
17. What is characteristic for the neoplastic transformation of the genome?
1. Uncontrolled and unnecessary for the organism cellular proliferation. 2. Accelerated cellular proliferation.
3. Non-typical cellular proliferation.
4. More precise and energy sparing cellular proliferation.
5. Biologically defective cellular proliferation.
18. What is the most common mechanism involved in retroviral oncogenesis?
1. Deletion of genetic material.
2. Mutagenesis due to a rupture.
3.Translocation of gene parts.
4. Transversion purines / pyrimidines.
5. Insertional mutagenesis
19. What determines the growth of neoplasms?
1. The time cells need to divide.
2. The percentage of cells currently dividing (proliferating fraction).
3. The number of differentiating tumor cells.
4. The percentage of cells currently dying (dying fraction).
20. Which factor is absolutely necessary for tumor development?
1. Toxic substances secreted by the tumor.
2. The formation of the tumor stroma with adequate vascularization.
3. The need of collaterals. 4. Generating of anticancer immunity.
5. Constant intake of carcinogenes.
21. The term “anaplasia” introduced by Hansemann describes:
1. The nature of the neo - transformation
2. The presence of a cellular program that is not fulfilled
3. Biological cellular disbalance
4. The observed differences between cancer cells and normal cells.
5. Interspecies cellular symbiosis
22. Which is the earliest pathognomonic functional criterion for neoplastic transformation?
1. Ectopic hormone secretion.
2. Obligatory phagocytic activity of tumor cells.
3. Hyperergy of the cell.
4. The lost of contact inhibition of cellular division.
5. “Outsmarting” the adjacent cells.
23. The energy for most neoplastic cells is created by:
1. Oxidative phosphorylation.
2. Isolated anaerobic glycolysis.
3. Aerobic glycolysis.
4. Substrate phosphorylation.
5. Electrochemical transformation.
24. Biochemical analplasia in neoplasms most often refers to:
1. Increased ratio between essential / facultative cellular metabolism.
2. Increased aerobic glycolysis with increased substrate utilisation.
3. Increased metabolism of purines and pyrimidines.
4. Inhibited catabolism of proteins and aminoacids.
25. The biological advantages of neoplastic cells are a result of:
1. More effective substrate utilisation.
2. Distorted hypersensitivity to cellular signals.
3. Their ability to go into mitosis with damaged DNA.
4. Their lack of homotypic cell adhesion molecules.
26. What plays a role in the natural anti-tumor defence?
1. Activated NK-cells and cytotoxic macrophages.
2. Increased secretion of PG Е 1 and PG Е2 .
3. Increased liver detoxicating function.
4. The paratumor breaking down of secreted neo-metabolites.
5. 2, 3, 4.
27. Which mechanism directly protects the tumor cells from the killer cells of the organism?
1. Non-specific lysis of the attacking cells. 2. Surrounding of the neoplastic cells by blocking antibodies.
3. Secretion of tumor cell inhibitors.
4. Prostaglandine secretion.
5. The coating of the neoplastic cells with an impervious extracellular matrix.
28. What exists as a hypothesis for the inability of the organism to deal with the tumor?
1. Failure of their genes and reduced intensity of the immune reaction.
2. Insufficient number or insufficient activity of the NK-cells (cytotoxic macrophages respectively).
3. Weak antigen immunnogenicity of the neo-antigens.
4. Defect contacts between the tumor cells and antitumor antibodies.
29. What is the concept of the hypothesis explaining that the organism could not deal with the tumor because of too delayed immune response?
1. Higher growth potential of the neo-cells.
2. Increased division cycle of the immunoblasts.
3. Everlasting modulation of the tumor surface antigens.
4. Т2 -helper activity.
5. 1, 3
30. The effects of the neoplasms on the organism are determined by:
1. Number of tumor cells. 2. Malignant potential of the neoplasm.
3. Localisation of the tumor.
4. Tumor blood supply.
1. The hypoxic-hyperoxic lesion of alveolocytes type II leads to:
1. Mucus hypersecretion.
2. Disturbed synthesis of antiprotease inhibitor.
3. Ig A hyposecretion.
4. Secretion of specific enzymes.
5. Insufficient surfactant production.
2. Surfactant deficiency in the alveoles leads to:
1. Lyophilization of the alveolar membrane.
2. Expiratory collapse of the alveoles.
3. Substrate deficit in the alveoles.
4. Sudden stop of breathing.
5. Abrupt decrease of alveolar pressure.
3. Which respiratory stimulator best reflects the level of damage to the respiratory center?
1. Decreased рО2.
2. Increased рСО2.
3. Decreased рН.
4. Apomorphine.
5. Hyperprogesteronemia.
4. When the pleural cavity is filled with fluid this leads to:
1. Lung collapse and atelectasis.
2. Inhibited stimulation of the respiratory center.
3. Lung immune deficiency.
4. Increased proliferation of alveolar macrophages.
5. Increased lung compliance.
5. Which defense mechanism of the respiratory system has a reflex character?
1. Cough.
2. Alveolar macrophage system.
3. Mucocilliary escalator.
4. Antioxidant systems.
5. Nasopharyngeal filter.
6. Which of the following should be decreased for the patient to have oligopnea?
1. Dead space.
2. Tidal volume.
3. Respiratory rate.
4. Ventilation.
5. Diffusion.
7. Hyperpnea is breathing with:
1. Increased respiratory rate.
2. Increased tidal volume. 3. Increased ventilation.
4. Inadequately high effort.
5. Periodical apneic pauses.
8. The most important outcome of alveolar hypoventilation is:
1. Cyanosis.
2. Increased airway resistance.
3. Dyspnea.
4. Orthopnea.
5. Respiratory acidosis.
9. Which pathologic type of breathing represents with lung hyperventilation and alveolar hypoventilation at the same time?
1. Bradypnea with hyperpnea.
2. Tachypnea with hypopnea.
3. Tachypnea with hyperpnea.
4. Bradypnea with hypopnea.
5. Kussmaul’s breathing.
10. What does ventilation/perfusion mismatch mean?
1. Absolutely increased or decreased ventilation and bloodflow in the lungs.
2. Inadequately distributed bloodflow in the lungs.
3. Limited capillary bloodflow during maximal inspiration.
4. Mismatch between the airflow in the lungs and capillary bloodflow. 5. Discrepancy between the ventilation and perfusion in the different parts of the lung.
11. What is true for a part of the lung with a ventilation/perfusion ratio = 10?
1. There is low alveolar рО2.
2. There is high alveolar рСО2.
3. There is increased physiological dead space.
4. There is a local hyperbaric effect.
5. Presents a risk for gas embolia.
12. What is increased when the respiratory rate >35/min ?
1. Absolute dead space in the lungs.
2. The impact of venous blood in the arteries.
3. The ventilatory effect of the dead space.
4. The right-left transpulmonary shunt.
5. The overall effect of bronchial resistance.
13. What is the common finding in the arterial blood of patients with ventilation/perfusion mismatch?
1. Hypocapnia.
2. Hypoxia.
3. Hypercapnia.
4. Hyperoxia.
5. Normocapnia.
14. The diffusion capacity of the lungs decreases in all of the following, except one: 1. Anemia.
2. Interstitial fibrosis.
3. Bullous emphysema.
4. Pulmonary edema.
5. Increased cardiac output.
15. Each of the following could reduce bronchial conductivity except for one:
1. Bronchospasm.
2. Altered sensitivity of the respiratory center.
3. Weakness of the respiratory muscles.
4. Increased residual volume
5. Edema and hypersecretion of the bronchial mucosa.
16. Hypercapnia could be due to:
1. Hyperventilation.
2. State of anxiety and excitement.
3. Hypoxic stimuli.
4. Drugs suppressing the respiratory center.
5. Increased physical activity.
17. Cyanosis in respiratory failure is mostly due to:
1. Polycythemia.
2. Hypercapnia.
3. Increased fraction of reduced hemoglobin. 4. Peripheral vascular spasm.
5. Decreased dyshemoglobin.
18. Which disease is typically accompanied by chest pain while breathing:
1. Pulmonary emphysema.
2. Bronchial asthma.
3. Tuberculosis.
4. Pleural impairment.
5. Pulmonary edema.
19. One of the most common symptoms in pulmonary diseases is:
1. Chest pain.
2. Orthopnea.
3. Muscle weakness.
4. Dyspnea.
5. Headache.
20. What is characteristic for obstructive pulmonary diseases?
2. Decreased bronchial conductivity.
3. Increased bronchial resistance.
4. Decreased static lung volumes.
5. Decreased dynamic lung volumes.
6. 2, 3, 5.
21. What is characteristic for the bronchial obstruction in asthma?
1. Progressive and irreversible.
2. Progressive and reversible.
3. Remittent irreversibility.
4. Relapsing nature and irreversibility.
5. Sudden and non-repeated attacks.
22. The pathologic characteristics of bronchial asthma includes:
1. Bronchospasm, bronchial edema, viscous mucus.
2. Peribronchial and interstitial infiltrate.
3. Alveolar and peribronchial destruction.
4. Recurrent bronchial epithelial necrosis.
5. Alveolar-capillary destruction.
23. Which of the functional tests is a “conditio sine qua non” for diagnosing an obstructive pulmonary disease:
1. Diffusion testing.
2. Blood gas analysis.
3. Measurement of the static lung volumes.
4. Forced expiration.
5. Measurement of the lung compliance.
24. Tobacco smoking and poluted air lead to COPD by having a negative impact on: 1. Pulmonary immune reactivity.
2. The ratios between proteases/antiproteases and oxidants/antioxidants.
3. Laryngospasm and bronchospasm reflexes.
4. The ratio between alveolar cells type I and II.
5. Stress induced non-specific pulmonary resistance.
25. In manifested pulmonary failure the observed polycythemia is due to:
1. Decreased lysis of red blood cells.
2. Increased red blood cell life.
3. Hypoxia-induced erythropoesis.
4. Dehydration and hemoconcentration.
5. Hypercapnia-dependent increased size of the red blood cells.
26. What is a common complication in the advanced stages of COPD?
1. Cor pulmonale chronicum.
2. Hypocapnia.
3. Anemic syndrome.
4. Pulmonary thromboembolism.
27. Restrictive ventilatory disturbance leads to:
1. Cheyne-Stokes breathing.
2. Inhomogenous alveolar ventilation.
3. Decrease in the lung volumes. 4. Incomplete functional shunt.
5. Increase of the functional residual capacity.
28. In what case should you observe acute restriction?
1. Asthma attack.
2. Pulmonary edema. Pneumothorax
3. Chronic obstructive bronchitis.
4. Pulmonary emphysema.
5. Tracheobronchitis.
29. What is the key pathogenetic unit of pneumothorax?
1. Presence of air in the mediastinum.
2. Collapse of the alveoli.
3. Increased pleural resistance.
4. Presence of air in the pleural cavity.
30. Which are the direct consequences of air entering the pleural cavity?
1. Collapse of the alveoli.
2. Disturbed to imposible breathing.
3. Suppressed respiratory center.
4. Disturbed venous flow (into the heart).
31. Pulmonary hypertension could be due to:
1. Chronic respiratory acidosis and hypoxia.
2. Chronic respiratory alkalosis and hypovolemia.
3. Loss of pulmonary capillaries.
4. Multiple pulmonary thromboembolism.
32. What is necessary for the development of cor pulmonale chronicum?
1. Pulmonary hypertension.
2. Systemic hypertension.
3. Presence of pathologic breathing.
4. Increased respiratory workload.
5. Thoracopulmonary malformation.
33. What is the most important and definitive sign of respiratory failure:
1. Hypercapnia.
2. Arterial hypoxia.
3. Arterial hypoxemia.
5. Persisting cough with expectoration.
34. What is the basic pathogenic mechanism for hypercapnic respiratory failure: 1. Pulmonary edema.
2. Pulmonary thrombembolism.
3. Reduced pulmonary perfusion.
4. Alveolar hypoventilation.
5. Impaired diffusion of СО2.
35. What could be the reason for arterial hypoxia in respiratory failure:
1. Anemia.
3. Ventilation/perfusion mismatch.
4. Right-left shunt.
5. Alveolar hyperventilation.
36. What is the basic pathogenetic unit in the respiratory distress syndrome of the newborn:
1. Immaturity of the surfactant.
2. Bronchiolar constriction.
3. Pleural fibrosis.
4. Alveolar edema.
5. Narrow airways.
37. What is the key pathogenetic factor in the respiratory distress syndrome in adults?
1. Bronchospasm and laryngospasm.
2. Alveolar hyperventilation. 3. Increased permeability of the alveolocapillary membrane.
4. Pulmonary hypertension.
5. Systemic hypertension.
38. Which factors could lead to decompensation of chronic respiratory failure?
1. Pulmonary infection and bronchospasm.
2. Fever, physical exercise.
3. Disturbed drainage of secretions.
4. Suppression of the respiratory center.
39. What is a pathognomonic symptom for sleep apnea syndrome?
1. Daytime sleepiness.
2. Stop of breathing during sleep.
3. Snoring.
4. Cardio-vascular disorders.
5. Anemic syndrome.
40. What is the key pathogenetic unit in obstructive sleep apnea?
1. Collapse in the region of the pharynx.
2. Disorder in the respiratory center.
3. Bronchial obstruction.
4. Overweight.
5. Thoracic cage disorders.
41. All of the following could lead to acute respiratory failure, except for one:
1. Respiratory muscles paralysis.
2. Acute obstruction of the airways.
3. Respiratory center suppression.
4. Anemia and polycythemia.
5. Thoracic cage damages.
42. All of the following are diseases with impaired respiratory control, except for one:
1. Hyperventilation syndrome.
2. Cystic fibrosis.
3. Sudden infant death syndrome. / SIDS/
4. Sleep apnea syndrome.
5. Pickwick syndrome.
43. Which of the following statements, regarding the alveolocapillary destruction is FALSE:
1. Leads to reduced compliance of the lungs.
2. Has a key role for the development of pulmonary emphysema.
3. Decreases the diffusion capacity of the lungs.
4. Leads to airflow obstruction.
5. Leads to decrease of the lung total capacity.
44. In terms of tissue metabolism what does disturbed breathing mean?
1. Insufficient inhalation/exhalation. 2. Wasted ventilation.
3. Disturbed oxygen consumption and CO2 production.
4. Disturbed gas transport in the blood.
5. Block of diffusion between blood and tissues.
45. The terminal vicious circle that leads to death in chronic obstructive respiratory failure includes:
1. Hyposensitivity of the respiratory center to СО2.
2. Respiratory muscle fatigue.
3. Cough, wheezing, expectorations, dyspnea.
4. Hyperinflation and forcefully decreased respiratory volume.
6. 1, 2, 3, 4
46. What is dyspnea?
1. Spontaneously occuring respiratory feeling.
2. A neural reflection of the metabolic activity.
3. Subconscious perception of gas exchange.
4. Unpleasant respiratory effort that engages the central nervous system.
5. Dyscrepancy between breathing and metabolism.
6. Voluntary breathing that supports physical effort.
1. Myocardia lischemia is mainly a result of:
1.Coronary hypoxemia.
2. Coronary artery disease (CAD).
3. Acute coronaritis.
4. Coronary anemia.
5. Heart remodelling.
2. The essence of myocardial ischemia is:
1.Mismatch between import and export ofoxygen in the myocardium.
2. Inadequacy between arterial and venous circulation of the heart
3. Mismatch between coronary blood flow and myocardial demands.
4. Inactivated myocardial oxygen.
5. Circadian oxyge nimbalance in themyocardium.
3. Which of the following causes refer to the " risk factors" for CAD (coronary artery disease):
1. Atherogenic dyslipoproteinemia, smoking.
2. Arterial hypertension, diabetes.
3. Fasting and increased physical activity.
4. Obesity, decrease physical activity.
4. The main cause of CAD (coronary artery disease)is:
1.Coronary atherosclerosis.
2. Platelet aggregation in the coronary vessels.
3. Impaired oxygen transport function of the blood.
4. Coronary spasm induced by gastro-coronary reflex.
5. Variations in oxygen demands of the myocardium.
5. For which forms of CAD coronary artery spasm is the major pathogenetic mechanism:
1.Myocardial sclerosis.
2. Sudden cardiac death.
3. Prinzmetal’s angina pectoris.
4. Myocardial infarction.
5. Stable angina pectoris.
6. What is angina?:
1.Respiratory-related chest pain.
2. Transient ischemic chest pain.
3. Neuralgic chest pain. 4. Chest pain which depends on the position of the body.
5. Neuralgic pain in a fixed location.
7. The clinical manifestation of stable angina is provoked by:
1.Physical effort.
2. Mental stress.
3. Arterial hypertension.
4. Prolonged sleep.
8. The main pathogenetic mechanism of stable angina pectorisis:
1.Increased oxygen requirements of the myocardium.
2. Rapidly progressive coronary stenosis.
3. Coronary thrombosis.
4. Coronary dissection.
5. Acute coronaritis.
9. The main pathogenetic mechanism of unstable angina pectoris is:
1.Intramural myocardial coronary compression.
2. Fixed coronary stenosis with primary arterial hypotension.
3. Rapid onset and /or progressive narrowing of the coronary vessel.
4. Hormonal oxidative phosphorylation explosion in myocardium.
5. Exacerbated coronaritis.
10. Increased oxygen requirements of the myocardium, can be satisfied primarily by:
1.Increasing oxygen capacity.
2. Facilitated hemoglobin oxygen release.
3. Internal reallocation of the coronary blood flow.
4. Adequately increased coronary blood flow.
5. Compensatory polycythemia.
11. Each coronary stenosis (at any time and/or degree) leads to decrease of:
1.Myocardial oxygen demands.
2. Deposited myocardium oxygen.
3. Oxygen content in the coronary sinus.
4. Collateral coronary blood flow.
5. Coronary heart reserve.
12. What is acute myocardial infarction?:
1.Myocardial dystrophy.
2. Ischemic necrosis of the myocardium.
3. Myocardial fibrosis.
4. Acute inflammatory process.
5. Spontaneous apoptosis of myocardiocytes.
13. What is the main pathogenetic unit in myocardial infarction formation?:
1.Fixed coronary stenosis.
2. Turbulence in the coronary blood flow.
3. Acute ventricle-coronary reflux.
4. Coronary thrombosis.
5. Hyperemic coronary shunt.
14. Which pathogenetic mechanisms in the cell lead to irreversible ischemic necrosis?
1.Lack of ATP.
2. Lactic acidosis and cytosolic Ca 2+ accumulation.
3. Direct ischemic genomic paralysis.
4. Rapid accumulation of free radicals.
15. The most severe complication of acute myocardial infarction is:
1.Pulmonary embolism.
2. Cardiogenic shock.
3. Acute aneurysm.
4. Pericardial effusion.
5. Ventrical thrombosis.
16. The most common complications of acute myocardial infarction are:
1.Thromboembolism of cerebral vessels.
2. Chronic left-sided heart failure.
3. Heart aneurysm.
4. Rhythm and conduction disorders.
5. Acute pericarditis
17. Which of the following are complications in chronic phase of myocardial infarction:
1. Heart aneurysm.
2. Chronic heart failure.
3. Cardiogenic shock.
18. Which clinical type of CAD is associated with apoptosis and loss of myocardial cells?:
1.Acute myocardial infarction.
2. Atherosclerotic myocardiosclerosis.
3. Stable angina. 4. Ischemic sudden cardiac death.
5. Progressive unstable angina.
19. What is the main cause of atherosclerotic myocardiosclerosis?
1.Acute myocardial ischemia.
2. Postischemic immune response against the heart cells.
3. Steady chronic myocardial hypoperfusion.
4. Progressive inflammatory process in the myocardium.
5. Continuous spasm of the coronary vessels.
20. Which is the most common mechanism of sudden cardiac death?
1.Ventricular fibrilation.
2. Ventricular rupture.
3. Cardiac tamponade.
3. Electromechanical ventricular dissociation.
5. Sudden block in ventrical contractions.
21. The lack of pain during myocardial ischemia could be caused by:
1. Decreased pain sensitivity.
2. Ischemic generation of high-frequency pain impulses.
3. Mild ischemia, that does not reach the pain threshold.
4. Ischemic block of the pain impulses conduction.
22. Main pathogenetic factor for the diastolic dysfunction in pericardial disorders is:
1.Pericardial-myocardial pathological reflex.
2. Presence of fluid in the pericardium.
3. Increased intrapericardial pressure.
4. Reduced pericardial-epicardial contact.
5. Dysfunction between the left and right side of the heart.
23. Main pathogenetic mechanism in cardiac tamponade is:
1.Reduced myocardial contractility.
2. Impaired diastolic filling of the heart.
3. Reflex tachycardia.
4. Increased afterload.
5. Increased blood accumulation in the heart chambers.
24. Pathophysiological manifestations of pericardial effusions are:
1. Diastolic dysfunction and central venous stasis.
2. Systolic dysfunction and central venous stasis.
3. Diastolic dysfunction with empty central circulation.
4. Diastolic dysfunction with arterial hypertension.
5. Decompensated ventricular diastolic dysfunction.
25. Main pathogenetic mechanisms imparing contractility of cardiomyocytes are:
1.Reduced capacity of ion-transport mechanisms.
2. Reduced effectiveness of cardiac adrenergic regulation.
3. Damage to cell membranes and cardiomyocyte enzymes.
4. Genomic blocking of myocyte hypertrophy.
26. What kind of changes are induced by the mechanism of Frank-Starling?
1.Increasing the strength, speed and amplitude of contraction.
2. Increasing the primary length of myofibres and thediastolic volume.
3. Increasing the contact area actin/myosin (S/N) and the number of A-N bridges.
4. Increasing the amount of Ca 2+ in cardiomyocytes.
27. Conditions leading to activation of the Frank-Starling mechanism are::
1. Increased afterload.
2. Increased preload.
3. Sinus tachycardia.
4. Physical exercise.
5. Increased myocardium contractility.
28. Compensatory character of myocardial hypertrophy depends on:
1.Increased number of sarcomeres.
2. Increasing the amount and size of the sarcomeres.
3. Adaptive reordering of the sarcomeres.
4. Hyperplasia of the myocardiocytes, not associated with the sarcomeres.
29. Pathological hypertrophy is characterized by:
1.Excessive hypertrophy of organelles, cells and capillaries.
2. Hyperplasia of cardiomyocytes.
3. Cardiomyocyte polyploidy.
4. Multiplication of cardiac connective tissue elements.
5. Мassive intramyocardial hemorrhage.
30. What is the main purpose of hypertrophy?
1.To progressively increase hyperfunction.
2. Attempt to reduce hyperfunction.
3. To relatively stabilize the hyperfunction. 4. To compensate hyperfunction.
5. To provide better functional status of the heart.
31. Power and rate of contraction and relaxation are compensatory increased via massive Ca2+ release in :
1.Increased length of cardiomyocytes.
2. Simpathetic adrenal stimulation of the heart.
3. Increased force of contraction with unchanged length of cardiomyocytes.
4. Increased volume of cardiomyocytes.
5. Vagal stimulatio
32. Prolonged tachycardia has negative effects on the heart due to:
1.Shorten diastolic filling.
2. Increased oxygen consumption of the myocardium.
3. Impaired synchronization between the left and right ventricle.
4. Dysfunctionof the valve apparatus.
33. Pathological consequences of long-standing myocardial hypertrophy are:
1. Reduced ventricular compliance.
2. Completely suppressed mechanism of Frank-Starling.
3. Decreased myocardial contractility.
4. Cardiac chronotropic hypersensitivity.
34. The most important non-cardiac compensations in heart failure are related to:
1.Stimulation of the renin-angiotensin-aldosterone system.
2. Increased secretion of ADH.
3. Increasing the concentration of 2,3-DPG in erythrocytes.
4. Increased oxygen affinity of hemoglobin.
35. Heart failure is a clinical manifestation of:
1.Ventricular contractile dysfunction.
2. Pumping heart failure.
3. Electrical instabilityof the heart.
4. Decentralization of circulation.
5. Inappropriate centralization of blood flow.
36. Which are the main causes for development of cardiogenic pump deficiency?
1.Impaired, reduced and limited ventricular filling.
2. Excessively increased resistance in systole. 3. Critically lowered blood volume.
4. Functionally inefficient cardiac contractions.
37. Which are the main causes for development of hemodynamic heart failure (HF)?
1. Aortic and pulmonary stenosis.
2. Pulmonary and systemic hypertension.
3. Insufficient valvular defects.
4. Myocardial ischemia, myocarditis, cardiomyopathy.
38. Energetic type heart failure develops in:
1. Coronary artery disease, myocarditis,myocardiodystrophy.
2. Stenotic valvular defects.
3. Systemic and pulmonary arterial hypertension.
4. Congenital valvular defects without cyanosis.
5. Prolonged exercise.
39. What is the main pathogenetic unit of cardiogenic pulmonary edema?:
1.Decreased pulmonary lymphatic drainage.
2. Increased hydrostatic pressure in pulmonary capillaries.
3. Low counter pressure in pulmonary interstitium.
4. Increased permeability of the alveoli-capillary barrier.
5. Reduced plasma concentration.
40. Which is the most common cause of right-sided heart failure development?:
1. Chronic obstructive pulmonary disease (COPD).
2. Arterial hypertension.
3. Congenital and acquired defects of the mitral valve.
41. What is the main pathogenetic factor of “cor pulmonale” development:
1.Arterial hypertension.
2. Pulmonary hypotension.
3. Pulmonary hypertension.
4. Stagnant bloodflow in the pulmonary circulation due to weakness of the left ventricle.
5. Arterial hypercapnia.
42. Which of the following could be a cause of rhythm and conduction heart disorders?
1.Intoxication.
2. Metabolic disorders.
3. Emotional stress. 4. Electrolyte imbalance.
5. Excessive physical exercise.
6. All stated.
43. What are the basic mechanisms for arrhythmias development?
1.Increased automaticityof the heart.
2. Occurrence of re-entry mechanism.
3. Occurrence of ectopic excitatory pulse.
4. Ventricular hypo- and akinesia.
6. 1, 2, 3
44. Pathogenesis of reumocarditis is based on:
1. Streptococcal induced myocardial intoxication.
2. Crossed (streptococcus A / cardiomyocytes) immunological reactivity.
3. Autoimmune reaction against cardiac immunologically privileged antigens.
4. Generalized immune deficiency.
5. Genetic defects in myocardium.
45. Etiology is still unclear in:
1.Acute bacterial myocarditis.
2. Ischemic myocardial damage.
3. Cardiomyopathy.
4. Myocardiodystrophy.
5. Tezaurismozes of the myocardium.
46. Hemodynamic disorders in acute myocarditis are closest to those of:
2. Dilated cardiomyopathy.
3. Acute pericardial injury.
4. Chronic atherosclerotic cardiomyopathy.
5. Obstructive-restrictive cardiomyopathy.
1. Systolic blood pressure is elevated when it is over:
1. 120mmHg.
2. 130mmHg.
3. 160mmHg.
4. 140mmHg.
5. 150mmHg.
2. Diastolic blood pressure is elevated when it is over:
1. 80mmHg.
2. 90mmHg.
3. 95mmHg.
4. 100mmHg.
5. 110mmHg.
3. Which factors are able to increase systemic blood pressure?:
1. Stroke volume of the heart.
2. Cardiac output.
3. Total peripheral vascular resistance (TPR).
4. Blood pressure is increased when there is:
1. Prevalence of pressor mechanisms.
2. Activation of pressor and depressor factors.
3. Insuffiecient depressor factors.
4. Pressor-depressor dissociation.
5. Arterial hypertension is acondition of:
1.Elevated blood pressure adequate to metabolic needs.
2. Form of adaptation to generalized hyperperfusion.
3. Functionally inadequate elevated blood pressure.
4. Form of maintaining blood flow in vital organs.
5. Circulatory overcompensation.
6. What is the pathogenetic classification of arterial hypertension?
1. Congenital and acquired.
2. Uncompensated and overcompensated.
3. Infectious and non-infectious.
4. Essential and symptomatic. 5. Localized and generalized.
6. According to age and gender.
7. Which factors play an important role in the genesis of essential hypertension?
1. Acute infections.
2. Psychological traumas.
3. Genetic predisposition.
4. Kidney diseases.
8. Which pathogenic units are involved in the pathogenesis of essential hypertension?
1.Vessels.
2. Renal.
3. Autoimmune.
4. Metabolic-perfusion.
9. Retention of sodium and water in patients with essential hypertension is associated with:
1. Decreased excretion of sodium and water.
2. Lost potential of sodium and water excretion.
3. Neuro-dependent retention of sodium and water.
4. Renoprival retention of sodium and water.
5. Vasopressin-dependent sodium and water retention.
10. Renin is:
1. Hormone produced by the kidneys
2. Hormone that stimulates the function of the adrenal glands
3. Enzyme produced by the kidneys
4. Enzyme that catalyzes ATI-->ATII conversion
5. 1,2
6. 3,4
11. What is the classification of essential hypertension accoding to the dominant pathogenetic mechanism?
1. Hyper-, normo- and hypoperfussion.
2. Hyperkinetic, volume and vasoconstrictory.
3. High, normal and low-flow.
4. Hyper-, normo- and hyporeactive.
5. Stretch- and chemoreceptor dependent.
12. Vasoconstriction elevates blood pressure by:
1. Increasing heart rate.
2. Increasing cardiac output. 3. Increased afterload.
4. Increased total peripheral resistance.
5. Generalized tissue hypoperfusion.
13. How the hyperkinetic mechanism increases blood pressure?
1. Venoconstriction increases central blood flow.
2. Primary hypervolemia.
3. Positive chornotropic and inotropic effects.
4. Generalized arterio-venous shunting of blood.
14. The main pathogenetic unit of volume-dependent arterial hypertension is:
1. Decreased renal excretion of sodium and water.
2. Increased sympathetic tone.
3. Lost baroreceptor depressor mechanism.
4. Genetically, higher extracellular volume.
5. Ineffective Darrow-Yannet mechanism.
15. Mandatory factor for stabilization of high blood pressure is:
1.Sustainable increase in extracellular fluid volume.
2. Increased peripheral vascular resistance inadequate to the actual blood volume.
3. Inadequately elevated hematocrit.
4. Shortened circulating time.
16. Which renal prostaglandin has depressor activity?
1. PgF2α .
2. PgE 2 and A2 .
3. PgD and H.
4. PgA 2 and B2 .
5. Endoperoxide.
17. Which are the pathogenic forms of renal hypertension?
1. Acute and chronic.
2. Latent and manifested.
3. Renal-parenchymal and renal-vascular.
4. Compensated and decompensated.
18. Renal-parenchymal hypertension develops in cases of:
1. Glomerulonephritis, chronic pyelonephritis.
2. Surgical removalof the kidney.
3. Fibromuscular hyperplasia of a. renalis. 4. Embolism of a. renalis.
5. Presence of an aberrant vessel.
19. The main pathogenetic mechanism in renal-parenchymal hypertension is:
1.Relatively increased renin activity.
2. Decreased ability of the kidneys to excrete sodium and water.
3. Increased level of renal prostaglandins and kinins.
4. 1, 3.
20. Renal-vascular hypertension develops in:
1. Reduction of the renal parenchyma.
2. Stenosis of a.renalis.
3. Bilateral nephrectomy.
4. Polycystic kidney disease.
5. Acute pyelonephritis.
21. Which is the main pathogenetic mechanism for development of renal-vascular hypertension?
1. Decreased ability of the kidneys to excrete Na+ and water.
2. Increased concentration of Na + in the blood vessel wall.
3. Activation of the renin-angiotensin-aldosterone system.
4. Stimulation of the depressor part of the vasomotor center.
5. Reduced sensitivity of the renal receptors for ADH.
22. Arterial hypertension in atherosclerosis is a result of:
1.Increased Na+ concentration in the blood.
2. Increased release of pressor factors.
3. Reduced elasticity of the large arterial vessels.
4. Increased pressor effect of the vasomotorcenter.
23. Arterial hypertension in thyrotoxicosis is:
1. Diastolic type.
2. Systolic /hyperkinetic/ type.
3. Volume type.
4. Blood pressure is not affected in thyrotoxicosis.
5. Systolic-diastolic type.
24. The main hypertensive mechanism in hyperaldosteronism is:
1. Spasm of the peripheral blood vessels.
2. Increased Na + and water retention in the body.
3. Sensitization of the vascular wall to pressor factors. 4. Hypertrophy of the vascular wall.
5. Stimulation of the renin-angiotensin system
25. The main hypertensive mechanism in hyperglucocorticism is:
1. Peripheral blood vessels spasm.
2. Increased Na+ and water retention in the body.
3. Sensitization of the vascular wall to pressor factors.
4. Hypertrophy of the vascular wall.
5. Altered sensitivity of stretch- and chemoreceptors.
26. Endocrine hypertension in pheochromocytoma is determined by:
1. Increased peripheral vascular resistance.
2. Tachycardia with increased cardiac output.
3. Increased Na+ and water retention in the body.
4. 1.2, 3.
1. How do we call blood pressure values below the reference range?
1.Hypovolemia.
2. Hypothermia.
3. Hypooncia.
4. Hypoosmia.
5. Hypotension.
2. What is acute circulatory failure?:
1.Massive erythrolysis.
2. Acute thrombocytopenia.
3. Haemodynamic collapse.
4. Acute venous stasis in the lower limbs.
5. Acute inflammation of the vessels.
3. Which are the main forms of acute circulatory failure?:
1.Acute pulmonary edema,cardiac asthma.
2. Syncope, collapse and shock.
3. Angina, myocardial infarction, myocardiosclerosis.
4. Primary and secondary hypotension.
4. What is syncope?:
1.Respiratory and cardiac arrest.
2. Sudden increase in blood pressure with hallucinations.
3. Sudden, transient disturbance of consciousness due to brain hypoperfusion.
4. Sudden, severe and prolonged circulatory failure.
5. Chronic brain hypoperfusion.
5. The mechanisms responsible for development of syncope are:
1.Sudden decrease in peripheral vascular resistance.
2. Impaired autonomic regulation of vascular tone.
3. Sympathetic overstimulation.
4. Suppressing pacemaker activity of the sinus node.
6. What is the type of syncope that you get when standing up quickly?:
1.Reflex.
2. Vasodepressive.
3. Situational.
4. Orthostatic.
5. Primary cerebral ischemic.
7. Prolonged cough attack or rapid evacuation of ascites fluid could lead to:
1.Acute circulatory failure.
2. Situational syncope.
3. Suppression of vasomotor center.
4. Orthostatic collapse.
5. Transitional AV-block.
6. Hypertensive crisis.
8. Syncope in cerebrovascular disease is mostly a result of:
1.Atherosclerosis of large cerebral arteries.
2. Atherosclerosis of the coronary vessels.
3. Atherosclerosis of the aorta.
4. Spasm of the carotid arteries.
5. Thrombosis of major cerebral arteries.
9. What ist he definition of shock?:
1. Brief loss of consciousness.
2. Locally disturbed blood flow in one or more organs.
3. Acute systemic circulatory insufficiency with hypoperfusion of vital organs.
4. Health disorder induced by stress.
5. Temporary disturbance in hemodynamic with normal tissue perfusion.
10. Which of the following is/are included in the pathogenetic classification of the shock?:
1. Hypovolemic.
2. Hypervolemic.
3. Cardiogenic.
4. Distributive.
11. Which could be a cause of hypovolemic shock?:
1.Significant and rapid loss of blood.
2. Dehydration, acute loss of plasma.
3. Massive and severe myocardial infarction.
4. Heavy mechanical trauma.
12. Which could be a cause of cardiogenic shock?:
1. Acute myocarditis.
2. Severe hypovolemia.
4. Massive pulmonary embolism.
13. Distributive shock occurs when there is:
1.Endotoxinemia.
2. Pulmonary embolism.
3. Posthaemorrhagic incompatible blood transfusion.
4. Antigen/antibody reaction.
14. Which is the main pathogenetic unit in the development of hypovolemic shock?
1.Blood loss.
2. Intoxication.
4. Hypovolemia.
5. Impaired cardiac function.
15. Which is the main pathogenetic unit in the developmentof cardiogenic shock?:
1. Blood loss.
2. Chest pain.
3. Reduced cardiac output.
4. Reduced venous inflow to the heart.
5. Sudden collapse of blood pressure.
16. Which is the main pathogenic unit in the development of distributive shocks?:
1. Intoxication.
2. Pain. 3. Reduced cardiac output.
4. Reduced venous inflow to the right heart.
5. 1, 2
17. What is the amount of blood loss needed for the development of haemorrhagic shock?:
1.Less than 5% of the total blood volume.
2. Over 10% of the total blood volume.
3. More than 20% of the total blood volume.
4. Less than 4% of the total blood volume.
5. More than 30% of the total blood volume.
18. Erectile phase of traumatic shock is caused by:
2. Sympathetic overactivation.
3. Loss of plasma.
4. Centralization of the circulation.
5. Kinin–kallikrein system activation.
19. What is the main pathogenic unit in the development of traumatic shock?:
1. Pain.
3. Blood loss.
5. Hypovolemia.
20. Venous dilation in septic shock is mostly due to:
2. Vagotonia.
3. Vegetative dystonia.
4. Fever.
5. Hypometabolism.
21. Which are the phases in the development of septic shock?:
1.Excitatory and inhibitory.
2. Active and passive.
3. Specific and nonspecific.
4. Hyperdynamic and hypodynamic.
5. Hyperpyretic and hypopyretic
22. The hyperdynamic phase of septic shock is characterized by:
1.Reduced cardiac output and increased peripheral vascular resistance.
2. Increased cardiac output and decreased peripheral vascular resistance.
3. Unchanged cardiac output and peripheral vascular resistance.
4. Reduced cardiac output and decreased peripheral vascularresistance.
5. Increased cardiac output and increased peripheral vascular resistance.
23. Peripheral venous vasodilation in allergic shock is a result of:
1.Sensitization of the organism to foreign antigens.
2. Overproduction of vasodilators.
3. Altered T-helper/T-suppressor ratio.
4. Primary depressed sympathetic tone.
5. Spontaneously activated parasympathetic tone.
24. What is the cause of vasodilation in spinal shock?:
1.Production of biologically active substances.
2. Impaired vascular innervation.
3. Sudden blockage of efferent sympathetic innervation.
4. Neuromuscular paralysis of the vascular walls.
1. Anemia is defined as:
1. Reduced count of erythrocytes, leukocytes, reticulocytes in given amount of blood
2. Reduced count of erythrocytes, trombocytes, leukocytes in given amount of blood
3. Reduced count of erythrocytes, haemoglobin in given amount of blood
4. Reduced count of erythrocytes, haemoglobin and hypovolemia
5. Olygocythemic hypervolemia
2. Main pathogenetic factor in all anemic syndromes is:
1. Reduced oxygen partial pressure in arterial blood
2. Reduced oxygen concentration in blood
3. Impaired oxygen metabolism in the tissues
4. Non-hypoxically decreased oxygen demand
5. Increased oxygen consumption, resulting from genetic abnormality
3. Anemia is:
1. Reduced oxygen transporting capacity of the blood
2. Reduced oxygen transporting capacity of the blood
3. Haemotoxic hypoxia of any kind
4. 1,2
5. 1,2,3
4. The pathogenetic classification of anemias includes:
1. Acute and chronic haemorrhagic anemias, acute and chronic haemolytic anemias
2. Haemorrhagic anemias, anemias due to impaired erythropoesis and
haemolytic anemias
3. Hypo- and Aplastic anemias, sideroachrestic anemias
4. Hyper-and hyporegenerative anemias
5. 1,3,4
5. In the first hours after haemorrhage usually there is: 1. No laboratory data, indicating anemia are present
2. Significantly decreasedlevelsof erythrocytes and haemoglobin
3. Marked reticulocytosis
4. Compensatory polyglobulia
5. Increased megalocyte number
6. At the 4th-5th day after significant haemorrhage the following findings may be observed:
1. Olygocythaemic normovolemia
2. Normocytic hypovolemia
3. Normocytic normovolemia
4. Compensatory hypervolemia
5. Compensatory polyglobulia
7. Which of the following anemias are due to impaired erythropoesis:
1. Iron-deficient anemia, B12-folic acid-deficient anemia
2. Hypo- and aplastic anemias, achrestic anemias
3. Chronic anemiasdue to enzyme deficiency
8. Anemias, due to impaired erythropoesis may be associated with deficiency in:
1. Iron, Vit B12, Folic acid
2. Spectrin, glutamine
3. Erythropoietin, microelements
4. 1,3
9. Iron deficiency in anemia is a results of:
1. Reduced alimentary intake
2. Impaired ionization and resorption in gastro-intestinal tract
3. Impaired transport to the liver and the bone marrow
4. Impaired utilization in the bone marrow
5. Increased demands or increased loss
10. The main pathogenetic factor in iron-deficient anemia is:
1. Impaired haemoglobin synthesis 2. Reduced stimulus for erythropoesis
3. Impaired maturation of the erythroblasts
4. Reduced protoporfirin levels
5. Genetic transferin deficiency
11. The mechanism of action of Vit B12 is:
1. Transforms folic acid into folinic; activates nucliec acids synthesis
2. Stimulates the M-phase during mitosis in erythrocytes
3. Stimulates transformation of protoporfirin into haemoglobin
4. Stimulates the accumulation of haemosiderin and development of haemosiderosis
5. Stabilizes the haemoglobin molecule
12. The pathogenesis of pernicious anaemia is due to:
1. Genetically determined insufficiency of the haemopoesis
2. Production of autoantibodies against gastric parietal cells and/or
gastromucoprotein
3. Structural alterations in the erythrocytic membrane
4. Intestinal parasites (Diphylobotrium latum)
5. Insufficient secretion of Hydrochloricacid and pepsin
13. Pathognomonic sign of pernicious anaemia is:
1. Hunter’s glossitis
2. Funicular myelosis
3. Shunt hyperbilirubinemia
4. Megaloblasts in the bone marrow and megalocytes in the peripheral blood
5. Nocturnal haemoglobinuria
14. Causes for haemolytic anaemias are:
1. Exogenous factors in primarily intact erythrocytes
2. Endogenous extra-erythrocyte factors in primarily intact erythrocytes
3. Intraerythrocyte factors
4. Combined effect of intra- and extraerythrocyte factors
6. 1,2,3,4
15. Which of the following exogenous extraerythrocytic factors are causes for haemolysis: 1. Serpent and fungal poisons, drugs
2. Aniline-containing paints, x-ray radiation
3. Thermogenic and cryogenic antibodies
16. Haemolytic anaemias due to intraerythrocytic factors are:
1. Hereditary shperocytic anaemia of Minkowski-Chauffard
2. Hereditary non-spherocytic enzyme-deficient anaemias
3. Haemoglobinopathies
4. Haemolytic anaemias in malaria and kala-azar
17. Haemolytic disease of the newborn is a consequence of:
1. Increased HbF levels
2. Increased number of enzyme deficient erythrocytes
3. Increaed levels of maternal Rh antibodies in the blood of Rh-negative fetus
4. Incompatible (ABO) haemotransfusion to the mother during delivery
5. Spontaneous activation of cryogenic antibodies during delivery
18. Haemoglobinopathies are hereditary diseases, resulting from:
1. Enzyme defect in the glicolytic cycle
2. Glucose-6-phosphatedehydrogenase deficiency in erythrocytes
3. Reduced gluthatione deficiency in erythrocytes
4. Genetically determined defect in the globin synthesis of haemoglobin
5. Genetically determined defect in the protoporphyrin ring synthesis
19. Microshperocytic anaemia of Minkowski-Chauffard is a result of:
1. Defect in the synthesis of haemoglobin beta chains
2. Genetic defect in the protein structure of the erythrocyte membrane
3. Inactivated glucose-6-phosphate-dehydrogenase and presence of cryogenic autoantibodies
4. Hexokinase inactivation
5. Methaemoglobin reductase deficiency
20. Glucose-6-phosphate-dehydrogenase deficiency in erythrocytes leads to: 1. Glycolytic chain disturbance with consequent energetic deficiency
2. Impaired glutathione reduction with decreased erythrocyte resistance
3. Increased tendency to polymerisation of haemoglobin
4. Impaired synthesis of globin beta-chain
5. Disturbances in the tricarbonic acids cycle
21. Cooley’s anemia (Thalassemia major) is a result of:
1. Genetic deffect in the synthesis of haemoglobin beta-chain
2. Genetic deffect in the synthesis of haemoglobin alpha-chain
3. Deficiency of glucose-6-phosphate-dehydrogenase and reduced gluthatione
4. Replacement of glutamine with valine at 6th place in the beta-chain
5. A complication of haemorrhagic disease of the newborn
22. The basic mechanisms for quantitative changes in leukocytes are:
1. Stimulated or suppressed leukopoesis
2. Recruitment of reserve leukocytes from haemopoetic organs
3. Re-distribution of leukocytes in the vascular system
4. ncreased leukocyte destruction in peripheral tissues
23. Distributive (peripheral) leukocytosis is observed in:
1. Strenuous physical work
2. Infectious diseases
3. Inflammatory and necrotic processes
4. Stress conditions
5. 1,4
24. Causes for leukopenia are all of the stated, except for:
1. Severe and continuous intoxication
2. Treatment with cytostatic drugs
3. Hypersplenism
4. Increased sympathetic tone
5. Decreased vagal tone
25. The clinical manifestation of leukopenia is related to: 1. Impaired defensive reactions of the organism
2. Development of oedematous syndrome
3. Disturbed control of anabolic processes
4. Postponed regenerative ability of the bone marrow
5. Thromboembolic diatheses
26. Leukosis is characterized by:
1. Isolated bone marrow hypoplasia
2. Inflammatory-toxic leukoproliferation
3. Hyperplasia, metaplasia and dedifferentiation of haemopoetic cells
4. Metaplasia of hemopoeticcells into non-hemopoetic
5. 1,2,4
27. Leukemoid reactions are considered as:
1. Premorbid conditions, potentially progressing into leukosis
2. Reactive alterations in haemopoesis, similar to leukoses
3. Post-leukotic pathological conditions
4. Antigene-provoked response of the haemopoesis
5. A form of leukosis remission
28. The ethiologyof leukoses is related to:
1. Ionizing radiation
2. RNA-viruses
3. Chromozome anomalies
4. Exogenous and endogenouscancerogenic substances
29. Haemorrhagic diatheses are characterized by:
1. Increased propensity tohaemorrhages
2. Increased propensity to haemoconcentration
3. Decreased fibrinolytic activity
4. Potential for embolism development
30. Disturbances in haemostasis are classified as:
1. Coagulopathies 2. Thrombocytopathies
3. Vasopathies
4. Fibrilopathies
31. Coagulopathies develop as a result of:
1. Quantitative and qualitative alterations in thrombocytes
2. Alterations in the permeability of the vessel wall
3. Quantitative and qualitative alterations in plasma factors
4. Quantitative and qualitative alterations in erythrocytes
5. Spontaneous haemodilution
32. Which are the alterations in plasma factors thatparticipate in coagulation?:
1. Congenital, related to genetic defect
2. Acquired, resulting from liver and renal disease
3. Manifestation of disturbed Vit K metabolism
4. Consequences of uncontrolled anticoagulant application
33. The genetically caused deficiency of factor VIII is a main pathogeneticunit in:
1. Haemolytic disease of the newborn
2. Haemophilia A
3. Haemolytic anemia of Minkowski-Chauffard
4. Haemoglobinopathies
5. Thrombasthenias
34. Which phase of coagulationis affected in haemophilias?:
1. Fibrinolysis 2. Fibrinogenesis
3. Blood clot retraction
4. Thromboplastin synthesis
5. Transformation of prothrombin into thrombin
35. Which are the pathogenetic mechanisms in the development of thrombocytopenia?:
1. Suppressed thrombogenesis
2. Increased platelets destruction in the periphery
3. Suppressed thrombin synthesis
5. 1,3
36. Haemorrhagic syndrome in thrombasthenia is a result of:
1. Significant thrombocytopenia
2. Acquired or genetically determined functional insufficiency of platelets
3. Disturbed thrombin synthesis
4. Disturbed thromboplastinsynthesis
5. Increased blood clot retraction
37. The main pathogeneticunit in capillaropathies is:
1. Insufficient platelets adhesion
2. Procoagulant deficit
3. Affected endothelial barrier and capillary permeability
4. Anticoagulant surplus
5. 2,3
1. Which are the most common causes of chronic gastritis?
1. Toxic substances
2. Chronic stress
3. Alimentary factors
4. Endogenous noxious stimuli
5. Genetic factors
2. Chronic atrophic gastritis is a prerequisite for:
1. Ulcer disease and gastric carcinoma
2. Pyloric stenosis.
3. B12 / folic acid / Fe-deficient anemias
4. Perforation of the stomach.
3. Pathogenetic factors for chronic atrophic gastritis are:
1. The genetic inferiority of the gastric mucosa.
2. Autoimmune destruction of the epithelium.
3. Infectious and hypoxic lesions of the gastric mucosa
4. Neural reflex / stress influences.
4. Duodenal reflux primarily leads to:
1. Total gastritis
2. Fundus gastritis
3. Prepiloric and antral gastritis
4. Diffuse mucosal hyperplasia
5. Gastric carcinoma.
5. Which component of the duodenal contents entering the stomach causes the most severe changes to gastric mucosa:
1. Pancreatic enzymes
2. The bicarbonates of the pancreas.
3. Bile salts and acids.
4. Lysolecithin
6. The late development of the vitamin B12 / folic acid deficiency anemia in chronic atrophic gastritis is associated with:
1. Achlorhydria.
2. Preserved synthesis of vit. B12 by the chief cells
3. Persistent protection of vit. B12.
4. Significant hepatic reserve of vit. B12.
5. Slow metabolism of vit. B12 in the body
7. The main pathogenic unit for the formation of ulcer defect is:
1. Impaired gastric motility.
2. Recurrent duodenal refluxes.
3. Mandatory bacterial presence in the gastric juice.
4. Dominant peptic activity of the gastric juice.
5. Existing imbalance in gastrin / hydrochloric acid relationship
8. The most significant pathogenetic unit in duodenal ulcer is:
1. Increased acid/peptic activity of gastric juice.
2. Impaired secretion/evacuation kinetics of the stomach
3. Reduced resistance of duodenal mucosa
4. Delayed intestinal peristalsis.
5. Deficiency of gastro-duodenal hormones
9. Which bacterial colonization proven in the stomach is essential for the emergence of gastritis and peptic ulcer:
1. Staphylococcus aureus.
2. Escherichia Coli.
3. Streptococcus pyogenes
4. Helicobacter pylori.
5. Rickettsia conori
10. What is the central unit in the pathogenesis of ulcer on the body of the stomach:
1. Hyperfunction of the parietal cells of the stomach.
2. Duodenal reflux.
3. Reduced resistance of the gastric mucosa
4. Presence in the mucosa of Staphylococcus aureus
5. Lost neuro-humoral regulation of secretion.
11. Which of the mechanisms participate in the pathogenesis of duodenal ulcer:
2. Impaired secretory-evacuation kinetics of the stomach 3. Helicobacter pylori.
4. The reduced resistance of the duodenal mucosa.
12. Main stimuli for increased acid-peptic activity of the gastric juice are:
1. Increased tone of the vagal nerve
2. Hypergastrinaemia.
3. Increased histamine secretion
4. Increased pepsinogen secretion
13. Which factor does not take part in the alkalization of gastric contents:
1. Bicarbonates in the pancreatic juice.
2. Swallowed saliva
3. Acid-stimulated duodenal motility
4. Duodenal and biliary secretion.
5. Diffusion of H + ions across the intestinal wall
14. Mucus protects duodenal mucosa by:
1. Its gel-form creating mechanical barrier
2. Alkalizing effect.
3. Presence of glycoproteins A and B
4. Presence of pepsinogen
15. The resistance of duodenal mucosa is primarily due to:
1. Mucus.
2. Glycoproteins A and B.
3. Enzyme inhibitors
4. Prostaglandins of group E.
5. Helicobacter pylori.
16. The ulcer of the body of the stomach occurs with:
1. Hyperchlorhydria.
2. Hypo- or normochlorhydria. 3. Low basal secretion
4. Low maximum secretion.
17. Duodenal ulcer occurs with:
2. Increased basal and maximal secretion.
3. Hipochlorhydria.
18. The development of acute pancreatitis is a result of:
1. Spontaneous apoptosis of acinar cells
2. Chronic dystrophic process
3. The process of self-digestion of the gland
4. Mandatory bacterial infection
5. Complication due to damage of the endocrine function of the pancreas
19. Important factors for the development of pancreatitis are:
1. Alcohol abuse.
2. Deficiency of antiproteases.
3. Gallstones.
4. Carbohydrate overload
20. The edematous phase of acute pancreatitis is associated with increased blood level of:
1. Pancreatic amylase.
2. Salivary amylase
3. Lipase
4. Carboxypeptidase
5. Elastase
21. Alcohol triggers the pathogenetic chain of events leading to acute pancreatitis by:
1. Stimulation of exogenous secretion of the pancreas.
2. Spasm of the sphincter of Oddi.
3. Direct activation of the pancreatic lipase. 4. Blocking the activity α1-antitrypsin, and α2-macroglobulins.
22. Obstructive ileus is usually due to:
1. Complication after abdominal surgery.
2. Severe contusion to the abdominal wall.
3. Spasm of the intestinal musculature.
4. Tumors of the colon.
5. Mesenteric thrombosis.
23. In case of high intestinal obstruction the following signs dominate:
1. Water and electrolyte disturbances.
3. Disorders in fat metabolism
4. Arterial hypertension
5. Chronic constipation.
24. The classification of intestinal obstruction does not include:
1. Mechanical ileus
2. Dynamic ileus
3. Restrictive ileus
4. Paralytic ileus
5. Strangulation ileus
1. Hepatic encephalopathy is a result of:
1. Liver damage.
2. Terminal liver failure.
3. Alcoholic fatty liver dystrophy.
4. Diabetic steatosis.
5. Thrombosis of the hepatic veins.
2. In hepatic encephalopathy the hyperammoniemia is mainly a result of:
1.Increased desamination of aminoacids.
2. Impaired renal ammoniogenesis.
3. Suppresion of the ornithine cycle in the liver.
4. Entering of ammonia in the organs is slowed down.
5. Hyperglutaminemia.
3. The increased levels of fatty acids with short and middle sized chains in hepatic encephalopathy is due to:
1. Increased production in the colon and fat tissue.
2. Disturbed esterification in the liver and insufficient extraction from the blood.
3. Increased mobilisation from the fat tissue.
4. Increased fatty acid synthesis from carbohydrate sources.
5. Primarily increased renal retention
4. Increased GABA level in the blood in hepatic encephalopathy is due to:
1. Increased production in the colon.
2. Disturbed receptor binding and exiting the nervous system.
3. Decreased metabolisation in extrahepatic structures.
4. Disturbed esterification in the liver and insufficient extraction from the blood.
5. Spontaneously increased production.
5. How does the “hyperammoniemic theory” explain the pathogenesis of hepatic encephalopathy:
1. Decreased energy in the brain.
2. Direct toxic effect.
3. Synthesis of false neurotransmitters.
4. Neuronal mutagenic effect.
5. Disturbed interaction between neurons and glial cells.
6. The accumulation of the false neurotransmitter octopamine in the CNS is a direct effect of:
1. Increased transportation of aromatic aminoacids from the blood to the brain.
2. Large ammounts of phenylalanine in the brain.
3. Accumulation of tyrosine in the brain cells.
4. Disturbed transformation of DOPA into dopamine.
5. Disturbed transormation of dopamine into catecholamines.
7. Why does tyrosine accumulate in the brain during hepatic encephalopathy?
1. Inhibition of tyrosine hydroxylase.
2. Increased concentration of phenylalanine in the brain.
3. Activation of phenylalanine hydroxylase.
4. Blocked transformation of noradrenaline into adrenaline.
5. Increased levels of octopamine in the brain cells.
8. What is the role of octopamine in the pathogenesis of hepatic encephalopathy?
1. Blocks the synthesis of catecholamines in the brain.
2. Competitively displaces dopamine and noradrenaline in the respective synaptosomes.
3. Has a direct toxic effect on the CNS.
4. Takes the role of a real mediator in the brain.
9. If bilirubin cannot enter the hepatocytes the result would be what type of jaundice? 1. Prehepatic unconjugated.
2. Posthepatic conjugated.
3. Hepatic unconjugated.
4. Hepatic conjugated.
5. Posthepatic unconjugated.
10. Prehepatic jaundice is present in which of the following?
1. Massive hemolysis.
2. Liver disease.
3. Obstructed bile ducts.
4. Intrahepatic cholestasis.
11. In what condition bilirubin cannot enter the hepatocyte?
1. Deficiency of the proteins Z and Y.
2. Deficiency of a special membrane-linked protein.
3. High levels od the complex albumin-bilirubin.
4. Deficiency of glucuronic acid.
5. Inhibited UDPGT
12. The conjugation of bilirubin in the hepatocytes is mainly disturbed in what condition?
1. Low levels of the proteins Z and Y.
3. Inhibited UDPGT.
5. Massive hemolysis.
13. Dubin-Johnson syndrome is due to:
1. Impaired conjugation of bilirubin in the hepatocytes.
2. Deficiency of a special membrane-linked protein. 3. Deficiency of the transport proteins Z and Y.
4. Defective excretion of the conjugated bilirubin.
5. Obstructed bile ducts.
14. Cholestatic jaundice is due to:
1. Disturbed captation of bilirubin.
2. Disturbed bile transport.
3. Disturbed bilirubin conjugation.
4. Defective excretion of the conjugated bilirubin out of the hepatocyte.
15. What mechanisms are involved in the pathogenesis of drug hepatotoxicity?
1. Direct suppression of protein synthesis.
2. Binding to proteins and forming antigens.
3. Prominent chromozome anomalies.
4. Mitotic burst.
16. Which of the following is the most common etiological factor damaging the liver?
1. Heart failure.
2. Hepatotropic viruses.
3. Bacteria.
4. Parasites.
5. Snake poisoning.
17. What mechanisms are involved in alcoholic liver damage?
1. NADH-2 – dependant liver lipogenesis.
2. Changes in the phenotype of the hepatocytes. 3. Impaired VLDL secretion.
4. Membrane damage of the hepatocytes.
18. What are the possible outcomes from an acute hepatitis?
1. Developing of cirrhosis.
2. Recovery or chronification.
3. Acute liver failure.
4. Malignisation.
19. What is the leading cause of hepatitis chronification?
1. Provocation of a genetically-determined liver remodelling.
2. Immune-dependant liver damage.
3. Direct viral lesion of the hepatocytes.
4. Systemic reaction of mono- and phagocytes.
20. Which cells are mostly responsible for the fibrosis in cirrhosis?
1. Endothelial cells of the sinusoids.
2. Kupffer cells.
3. Immobilised monocytes.
4. Pseudolobated hepatocytes.
5. Ito cells - lipocytes.
21. Prominent portal hypertension is present in portal pressure above:
1. 5 cm Н2О. 2. 10 cm Н2О.
3. 20 cm Н2О.
4. 50 cm Н2О.
5. 100 cm Н2О.
22. What is the most common mechanism of portal hypertension in liver cirrhosis?
1. Intrahepatic presinusoidal block.
2. Posthepatic compressive block.
3. Prehepatic obstructive block.
4. Intrahepatic postsinusoidal block.
5. Combined pre- and posthepatic block
23. What is the most important pathogenetic unit for ascites development in liver cirrhosis?
1. Portal hypertension.
2. Hypoalbuminemia.
3. Impaired lymphatic drainage.
4. Increased capillary permeability.
5. Inhibited secretion of natriuretic factors.
24. Which is the second most important factor for ascites development and directly participates in the stabilisation of the condition?
1. Increased membrane permeability.
2. Low oncotic pressure.
4. Lowered peritoneal antipressure.
5. Renal retention of water and salts.
1. The most common route of renal interstitial infections is:
1. Via adjacent tissues
2. Haematogenic
3. Lymphogenic
4. Ascending (through the urinary tract)
5. Descending from the glomeruli
6. Always a combination of at least two of the above.
2. The chronification and progression of pyelonephritis is associated with:
1. The impeded activity of macrophages in a hyperosmotic environment
2. The formation of highly resistant protoplast (L) forms of bacteria
3. Primary immunodeficiency
4. 1, 2
3. Pyelonephritis is best defined as:
1. Diffuse renoparenchimal dystrophy
2. Non-specific tubulointerstitial bacterial inflammation
3. Tubulo-renal virus lesion
4. Reno-interstitial immune conflict
5. Specific reno-parenchymal process
4. The urinary tract reflux is a mechanism, associated with the pathogenesis of:
1. Polycystic kidney disease
2. Nephrolithiasis
3. Glomerulonephritis
4. Wilms‘ Tumor
5. Pyelonephritis
5. Gram-negative bacteria are the most common etiology of pyelonephritis:
1. They predominate in the urinary tract
2. They bind easier to the epithelium of the urinary tract
3. They easily reproduce in the primary urine
6.The main pathogenetic unit for the development of diffuse glomerulonephritis is:
1. Acute intoxication
2. Idiopathic sclerosis 3. Immune inflammation
4. Glomerular capillary thrombosis
5. Virus inflammation
7.Which of the following bacterial antigens are markedly nephritogenic:
1. Haemophilus influenzae
2. Beta-haemolytic streptococcus group A
3. Pneumococcus
4. Escherichia coli
5. Proteus
8.The immune lesion in immune complex glomerulonephritis is a result of:
1. Degranulation of mast cells and basophiles
2. Isolated T-killer cells activity
3. Single NK-cell stimulation
4. Antibody-dependent cell mediated and/or complement dependent cell
mediated cytotoxicity
5. Thrombocyte adhesion
9. In glomerulonephritis the immunologic conflict is a result of:
1. In-situ formed immune complexes in the glomeruli
2. Deposition of soluble circulating immune complexes in the glomerulus
3. Renal type of Arthus phenomenon
10. Point out the representation of renal tubular dysfunction:
1. Disturbed mechanisms of urinary concentration and dilution
2. Hyperazotemia due to retention
3. Renal hypertension and/or anemia
4. Renal polyuria and tubular acidosis
11. The pathogenesis of nephritic edemas in the acute phase is:
2. Increased permeability (membranogenic)
3. Lymphostasis and/or primary hyperaldosteronism
4. Primary (glomerular) hypervolemia
5. 2, 4
12. The main pathogenetic unit of nephrotic edema is:
1. Increased capillary permeability 2. Decreased plasma oncotic pressure
3. A block in the lymph drainage
4. Increased capillary hydrostatic pressure
5. Primary NaCl retention
13. Point out the specific pathophysiological representation of the nephrotic syndrome:
1. Massive proteinuria, hyperlipidemia, hypoproteinemia and edema
2. Arterial hypertension, hematuria, oligo- and anuria
3. Hyperlipidemia, hypoproteinemia, hematuria
4. Microhematuria, pyuria, cristaluria
5. Pollakiuria, hyperproteinuria, arterial hypotension
14. The supression in erythropoesis in renal failure is mainly due to:
1. Decreased secretion of renal erythropoetic factor
2. Microangiopathic hemolysis
3. Decreased activity of erythropoetin in the bone marrow
4. Relative deficit and decreased utilization of iron
5. Accumulation of erythropoesis inhibitors
15. Which changes in the urine are indicative for chronic renal failure:
1. Disuria and pollakiuria
2. Oliguria and hypersthenuria
3. Hematuria
4. Varying massive proteinuria
5. Polyuria and isosthenuria
16. Uremic intoxication leads to:
1. Increased permeability of barriers
2. Cellular membrane functional lesions with ion asymetry
3. Sepsis
5. 1, 2, 3
17. The most important pathophysiological representation of uremic intoxication is:
1. Encephalopathy
2. Hemorrhagic diathesis
3. Normocytic anemia
4. Peripheral neuropathy
5. The disappearance of polyuria
18. Uremic encephalopathy is associated with:
1. Increased permeability of the hematoencephalic barrier
2. Continuous activation of the reticular formation
3. Deficit of neurotransmitters 4. Neuronal bioelectric destabilization
19. In chronic renal faiure the remaining glomeruli compensate decreased glomerular filtration by:
1. Increased glomerular filtrartion per single
functional
glomerulus
2. Generation of new glomeruli
3. Supression of periglomerular lymph drainage
4. Severe increase of glomerular membrane permeability
5. Phenomenon of podocyte injury
20. In chronic kidney failure the tubules of the intact nephrons compensate the nephrone deficit by:
1. Increased number of cells in the tubule
2. A connection of several tubules with one glomerulus
3. Increase of the reabsorption and secretion capabilities of the single tubule cell
4. 2, 3
21. The main pathophysiologic presentation of oligoanuric stage in acute renal failure is:
1. Progressive azotemia, hyperhydration
2. Movement of intracellular ions into the circulation and of extracellular into the cells
3. Blockage of the albumin synthesis in the liver
4. Fatigue of the sympathetic-adrenal system
22. Which is the most characteristic (pathognomonic) stage of acute renal failure:
1. Shock, septic, toxic
2. Oliguanuric
3. Polyuric
4. Isostenuria
5. Dehydratation
23. Which of the following has a leading role for the development of renal failure:
1. Overall disturbance of vital functions
2. Severe deficit of nephrons
3. The urinary syndrome
4. Nitrogen retention
24. Acute renal failure is a presentation of:
1. Destroyed nephrons 2. Ineffective nephrons
3. Functionally switched-off nephrons
4. Genetically insufficient nephrones
5. Chronic hypoperfusion of nephrones
25. Which are the pre-renal causes for the development of acute renal failure:
1. Shock, hemolysis, dehydration
2. Intoxications with heavy metal salts
3. Urinary tract obstruction
4. Ureteral stricture
5. Acute pyelonephritis
26. Which are the renal causes, leading to acute renal failure:
1. Ileus, acute pancreatitis, peritonitis
2. Acute glomerulonephritis and pyelonrphritis
3. Acute abnormalities in the acid-base balance
4. Prostate hypertrophy
5. Burns
27. Glomerular mechanisms of acute renal failure are:
1. Renal interstitial edema
2. Afferent arteriolar spasm
3. Efferent arteriolar dilation
4. Decreased permeability of glomerular basal membrane
28. Osmotically dependent renal polyuria develops in cases of:
1. Supressed reabsorption of Na+ /Cl-
2. Decreased levels and/ or activity of ADH
3. Genetic deficit of aquaphores
4. Increased excretion of glucose, urea, etc.
29. The main mechanism, disturbing urinary concentration and dilution in the course of acute renal failure is:
1. Inability to establish a corticomedullary osmotic gradient
2. Inability to utilize the gradient
3. Augmented „wash-out“ of the gradient
4. Decreased secretion of ADH
5. 1, 2, 3 6. 1, 2, 3, 4
30. During the polyuric stage of acute renal failure there is a risk for:
1. Disturbed metabolism, due to the fast nitrogen clearance of the organism
2. Hypokalemia, hyponatremia and dehydration
3. Hypervolemia, heart failure
4. Tubular necrosis and rrhexis
5. Nonselective proteinuria, hypoproteinemia
31. The uremic stage of the chronic renal failure develops when :
1. 90% of nephrones are not functioning
2. 80% of nephrones are not functioning
3. 75% of nephrones are not functioning
4. 70% of nephrones are not functioning
5. 100% of nephrones are not functioning
32. The main pathogenetic unit for the development of proteinuria is:
1. A primary supression of proximal reabsorption of proteins
2. Increased secretion of proteins in the tubules
3. Decreased excretion of proteins with lymphatic drainage
4. Increased permeability of glomeruli for proteins
5. Decreased mesangial phagocyte activit
1. How can endocrine disorders be classified?
1. Hereditary, acquired
2. Active, passive
3. Uncompensated, overcompensated
4. Primary, secondary
5.1, 4
6.1, 2, 3, 4.
2. Which is the MAIN pathogenic unit in endocrine disorders?
1. Changed level of a certain hormone
2. Disbalance between hormones and receptors
3. Uncontrolled hormone function
4. Increased or decreased “life” of a certain hormone
5. Changes in the hormonal sensitivity
3. Which endocrine disorder is defined as secondary/tertiary?
1. Pathological process in a certain endocrine gland
2. It is a result of an increased releasing factors level
3. It is a result of an impaired tropic hormones regulation
4. It is a result of genetic defect in the gland
5. 2. 3
4. The increased metabolism in hyperthyroidism is a result of:
1. High iodine plasma levels
2. Stimulation of the oxygen consumption
3. Suppressed oxygen consumption
4. Impaired extramitochondrial oxygen use
5. Decreased oxygen diffusion through the cellular membrane
5. Hyperthermia in hyperthyroidism is a result of:
1. Activate the Krebs cycle
2. Activate the Pentose phosphate pathway
3. Decoupling of oxidative phosphorylation
4. Increased mitochondrial redox-potential
5. Primary mitochondrial hyperplasia.
6. Which of the following factors is NOT associated with thyrotoxicosis development?
1. Genetic predisposition
2. Obesity
3. Psychic trauma
4. Hormonal disbalance
5. Increased levels of TSH
7. The pathogenesis of Graves-Basedow disease is associated with:
1. Autoimmune stimulation of the gland.
2. Toxic-dystrophic stimulation of the gland
3. Increased affinity of the gland to iodine ions
4. Primary hypersensitivity of the gland to catecholamine hormones
8. What is the TSH level in primary hyperthyroidism?
1. Constantly increased
2. Decreased
3. Unchanged
4. With circadian fluctuations
5. It does not concern the thyroid gland function
9. Tachycardia in hyperthyroidism is a result of:
1. Blocked parasympathetic activation
2. Increased cardiac afterload
3. Decreased cardiac preload
4. Increased sympathetic activation
5. Malignant hyperthermia
10. Hypofunction of the thyroid gland could be a result of:
1. Decreased TSH levels
2. Insufficient iodine consumption
3. Increased levels of thyroid-stimulating antibodies
4. Long-term anti-thyroid function treatment
11. Hypothyroidism in children and adults leads to different pathologies. Which are they?
1. Cretinism/Myxedema
2. Gigantism/Acromegaly
3. Dwarfism/Hypopituitarism
4. Turner’s syndrome/Adipose-genetalia dystrophy
5. Diabetes insipidus/Addison's disease
12. Which is NOT part of myxedema symptoms?
1. Decreased metabolism
2. Decreased psychic activity
3. Tachycardia
4. Inclination to hypothermia
5. Obesity
13. In primary hypothyroidism:
1. TSH is increased
2. TSH is decreased
3. Thyreotoxin is increased
4. Iodine accumulation in the gland is increased
5. Thyreoglobulin levels are increased
14. Which is NOT a cause for primary hypothyroidism?
1. Congenital gland hypoplasia
2. Thyroid stimulating growth factors
3. Congenital defects in hormone synthesis
4. TSH receptors resistance
5. Long-term X-ray radiation
15. The pathogenesis of chronic hypocorticism is associated with decreased levels of:
1. GCS
2. MCS
3. Suprarenal sex hormones
4. Catecholamines
16. Inclination to hypoglycemia in Addison disease is a result of:
1. Increased insulin secretion
2. Renal diabetes
3. Decreased gluconeogenesis and glycogenosynthesis
4. Pathological glycogen synthesis in the liver
5. Increased glycogen synthesis in the muscles
17. Arterial hypotension in Addison disease is associated with:
1. Decreased catecholamine levels
2. Impaired sensitivity of the arterial baroreceptors
3. Decreased levels of GCS and hypovolemia
4. Genetic predisposition
5. Decreased central stimulation
18. Skin hyperpigmentation in chronic hypocorticism is a result of:
1. Increased sun sensitivity
2. Increased levels of ACTH and MSH
3. Increased vitamin D synthesis in the skin
4. Hereditary increased melanocytes
5. Secondary siderosis
19. Which are the water-electrolyte disorders in hypocorticism:
1. Hypernatremia, hyperkalemia, normovolemia
2. Hyponatremia, hyperkalemia, hypervolemia 3. There are no changes in the electrolytes
4. Hypertonic hydration, cellular edema
5. Hyponatremia, hyperkalemia, dehydration.
20. Which of the following is typical for secondary chronic hypocorticism?
1. Arterial hypertension
2. No skin pigmentation
3. Diabetes mellitus type II
4. Fat tissue redistribution
5. Malignant hypothermia
21. Primary hypercorticism could be a result of:
1. Pathological process in the hypothalamus
2. Eosinophilic adenoma of the adenohypophysis
3. Cortex hyperplasia of the adrenal gland
4. Long-term Cortison treatment
5. Hyperplasia of the adrenal medulla
22. Secondary hypeglucocorticism could be a result of:
1. Increased levels of ACTH
2. Autoimmune lesions in zona glomerulosa
3. Basophilic adenoma of the adenohypophisis
4. Benign tumor of the adrenal cortex
23. The pathogenesis of hypercorticism is mainly associated with increased levels of:
3. Catecholamines
4. Dopamine
5. Suprarenal sex hormones
24. Protein metabolism disturbances in hypercorticism are associated with:
1. Delayed transport of aminoacids in the cells
2. Augmented catabolic processes
3. Change in the primary polypeptides structure
4. Locally increased anabolism in the limbs
5. Redistribution of the muscle tissue
25. In primary hyperaldosteronism:
1. Aldosterone does not affect renin secretion
2. There is increased level of aldosterone and increased level of renin
3. There is decreased level of aldosterone and decreased level of renin
4. There is increased level of aldosterone and decreased level of renin
5. Aldosterone augments the circadian rhythm of renin secretion
26. What are the disturbances in water-electrolyte balance in primary hyperaldosteronism?
1. Hypernatremia, hyperkalemia, hypovolemia
2. Hyponatremia, hypokalemia, hypovolemia
3. Hypernatremia, hypokalemia, hypervolemia
4. Hypernatremia, hyperkalemia, hypervolemia
5. Hypercalcemia, hypokalemia, hypervolemia
27. Which of the following is a common cause for adrenal medulla hyperfunction?
1. Increased stimulation of the adenohypophysis
2. Pheochromocytoma
3. Increased activity of RAAS
4. Electrolyte stimuli – hyponatremia, hyperkalemia
28. Pheochromocytoma leads to:
1. Elevated catecholamines
2. Elevated aldosterone
3. Increased level of tropic hormones
4. Decreased level of catecholamines
5. Overactivated parasympathetic nervous system
29. The biological effects of STH could be diminished in a deficiency of:
1. Somatostatins
2. Somatoliberins
3. Somatomedins
4. Prostaglandins
5. Leukotriens
30. The growing effect of STH is associated with:
1. Increased activity of peptide hydrolases
2. Positive nitric and phosphorous balance
3. Decreased catabolic processes
4. Stimulated lipogenesis
5. Increased appetite
31. Which factor plays a major role in the pathogenesis of pituitary dwarfism?
1. Decreased production of TSH
2. Decreased production of ACTH
3. Decreased production of FSH
5. Decreased secretion of STH
32. Panhypopituitarism is a result of damaged:
1. Adenohypophysis 2. Supraoptic nucleus of the hypothalamus
3. Neurohypophysis
4. Epiphysis
33. Which are the causes of panhypopituitarism?
1. Pituitary gland damage during pregnancy
2. Tumor or inflammation that affects the pituitary gland
3. Craniocerebral trauma, massive hemorrhage
4. 1, 3
34. The pathogenesis of panhypopituitarism is associated with decreased levels of:
1. GTH, TSH, ACTH
2. ADH, oxytocin
3. MSH, GCS, catecholamines
4. Somatomedins, melatonin
5. Thymosins, substance P
35. What is the cause of primary diabetes insipidus?
1. Damage in the hypothalamus and hypophysis
2. Hereditary defect of the ADH receptors in the renal tubules
3. Acquired defect of the ADH receptors in the renal tubules
4. Hyperplasia of the epiphysis
5. Atrophy in substantia nigra
The definition of pain, according to the World Health Organization is:
1. Intensive sensation, obsessing attention
2. An alarm reaction of the organism (reflecting abnormality)
3. Unpleasant sensory or emotional experience associated with actual or potential
tissue damage.
4. Defensive sensation, alarming for an iminent danger.
5. Physiological reaction of the CNS to unpleasant external or internal influences.
What is nociception?
1. Subjective stress sensation
2. Recieving, transmitting and processing of information for tissue damage.
3. A type of vegetative dystonia.
4. A teaching for the mechanisms of cellular and tissue damage.
5. A teaching for sanogenesis.
The (presence of) pain is:
1. A mandatory symptom of every disease.
2. A subconscious neuroemotional reaction.
3. Unpleasant psychic self-detachment from reality.
4. A somatic-independent psychoemotional affect.
5. A signal for actual or potential tissue damage.
From a physiological perspective pain is:
1. A sensory modality, characterizing the negative effect of the noxious factor,
rather than its characteristics.
2. Multilevel complex reaction of the CNS
3. Alteration in consciousness.
4. Sensation, characterizing precisely the qualities of the noxious stimulus.
The pathogenesis of pain comprise the following mechanisms:
1. Noxious stimulus and reception
2. Transmission and modulation of pain impulses
3. Comprehension - sensation and emotion.
4. Reaction (anti-pain behaviour).
Which of the following are nociceptors:
1. Pacini bodies.
2. Golgi tendon organs. 3. Ergoreceptors.
4. Free nerve endings.
5. Ruffini-Crause receptors.
Nociceptors are characterized by:
1. High sensitive threshold.
2. Post-stimulus sensitization.
3. Adaptation (to the noxious stimulus).
Regarding the mechanism of excitation, nociceptors are classified as:
1. Mono- and poly-modal.
2. Mechano- and chemo-nociceptors.
3. Extero-, proprio- and entero-nociceptors.
4. Stable and unstable.
5. Hypo- and hyperalgic.
Which of the following neurotransmitters and neuromodulators are noxious stimuli?
1. Dinorphins, enkephalins, endorphins.
2. Urea, creatinin, xanthoproteins.
3. Glycin, GABA.
4. Bradykinin, histamin, substance P.
5. Glucose, non-esterified fatty acids.
Nociceptive pain is characterized by:
1. Results from irritation of superficial nociceptors.
2. Is transmitted via Aδ fibers and the neospinothalamic tract.
3. Is felt as a localized sensation.
4. Is accompanied by distinct emotional component and sadness or fury.
Which of the following (metabolites) are noxious stimuli:
1. Urea, creatinin, uric acid.
2. Lactate, K+ , H+ .
3. Branched-chain amino acids.
4. Short and medium-chain fatty acids.
Neuropathic pain is characterized by:
1. Engagement of polymodal visceral nociceptors.
2. Transmission via non-myelinated C fibers and the paleospinorethiculothalamic tract.
3. Diffuse character and emotional and vegetative reactions. 4. Is a protective mechanism
The CNS interneurons with analgetic effect release:
1. Acetylcholine, substance P.
2. Opioid endogenic peptides - endorphins, enkephalins.
3. Adrenalin, noradrenalin, dopamin.
4. Serotonin, calcitonin, somatostatin.
5. Glutamate, aspartate, adenosine.
Causalgia is:
1. Severe torturing neuropathic pain in the dermatome area of a certain nerve.
2. A consequence of nerve damage (contusion, severance).
3. Axon-reflex associated with vegetative skin signs - atrophy, pigmentation, hyperemia.
4. Pain, always accompanied by local seizures.
The opioid neuropeptides exert their analgetic effect in the CNS via:
1. α1 and α2 receptors.
2. A1 and A2 receptors.
3. µ, κ- and δ- receptors.
4. β1 and β2 receptors
5. M and H cholinergic receptors.
Hyperalgesia is:
1. Comprehension of non-noxous stimuli as noxious.
2. Increased nociceptive sensitivity to noxious stimuli.
3. Faster conduction of noxious stimuli to the CNS.
4. Explosive generation of tissue noxious stimuli.
5. Decreased conductivity of the noxious impulses to the CNS.
Pain comprehension includes:
1. Localization and characterizing of the pain sensation.
2. Assessment of the positive and negative effects of pain.
3. The necessity of targeted and adequate behaviour.
The "pain gate" in the posterior horns of the spinal cord "opens" in response to:
1. Afferent signals from A(α) and A(β) fibres.
2. Descending serotoninergic impulses.
3. Stable nociceptive afferent stimulation from A(δ) or C fibers. 4. T-neuron positive feedback mechanism.
5. Afferent signals from µ- and κ- receptors.
Reflected pain is related to:
1. The dermatome rule - the skin-visceral branches of the afferent nerve.
2. γ-slef-control of the afferent activity.
3. Cortico-visceral reflex mechanism.
4. Skin- visceral convergation of impulses on a single neuron.
The pain present with damaged tracts for transmission of the nociceptive information is classified as:
1. Nociceptive.
2. Psychogenic.
3. Neuropathic.
4. Idiopatic.
5. Alodynic.
1. What is the common finding in the arterial blood of patients with ventilation/perfusion mismatch?
2. Which respiratory stimulator best reflects the level of damage to the respiratory center?
1. Decreased рО2 .
2. Increased рСО2 .
3. The most important outcome of alveolar hypoventilation is:
4. Tobacco smoking and poluted air lead to COPD by having a negative impact on:
1. Pulmonary immune reactivity.
5. What is a common complication in the advanced stages of COPD?
6. What is necessary for the development of cor pulmonale chronicum?
7. What model of dyspnea is observed in emphysema of lungs?
1. Inspiratory.
2. Expiratory.
8. What pathologies cause perfusion respiratory insufficiency?
1. Chronic bronchitis.
3. Pulmonary embolism
10. Anemia is defined as:
1. Reduced count of erythrocytes, leukocytes, reticulocytes in given amount of blood.
2. Reduced count of erythrocytes, trombocytes, leukocytes in given amount of blood.
3. Reduced count of erythrocytes, haemoglobin in given amount of blood.
4. Reduced count of erythrocytes.
11. The pathogenetic classification of anemias includes:
1. Acute and chronic haemorrhagic anemias, acute and chronic haemolytic anemias.
haemolytic anemias.
3. Hypo- and aplastic anemias, sideroachrestic anemias.
4. Hyper-and hyporegenerative anemias.
12. The main pathogenetic factor in iron-deficient anemia is:
1. Impaired haemoglobin synthesis.
2. Reduced stimulus for erythropoesis.
3. Impaired maturation of the erythroblasts.
4. Reduced protoporfirin levels.
5. Genetic transferin deficiency.
1. Hunter’s glossitis.
2. Funicular myelosis.
3. Shunt hyperbilirubinemia.
4. Megaloblasts in the bone marrow and megalocytes in the peripheral blood.
5. Nocturnal haemoglobinuria.
14. Cooley’s anemia (Thalassemia major) is a result of:
1. Genetic deffect in the synthesis of haemoglobin beta-chain.
2. Genetic deffect in the synthesis of haemoglobin alpha-chain.
3. Deficiency of glucose-6-phosphate-dehydrogenase and reduced gluthatione.
4. Replacement of glutamine with valine at 6th place in the beta-chain.
15. In what anemia RBCs contain abnormal hemoglobin:
1. Thalassemia.
2. Iron deficiency anemia.
3. Folic acid deficiency anemia.
16. Syntesis of hemoglobin S is representative for:
2. Sickle-cell anemia.
3. Ellyptocytosis.
17. In what anemia the count of reticulocytes is reduced?
1. Acute posthemorrhagic anemia.
2. Hemolytic anemia.
3. Aplastic anemia.
19. Acute purulent inflammatory processes lead to:
1. Eosinophilia.
2. Lymphocytosis.
3. Neutrophilic leukocytosis.
20. Leukocyte formula is:
1. Percentage of the different types of the leukocytes
2. Absolute leukocytes count.
.
3. Relation of nonmature forms of leucocutes to mature ones.
4. Relation of granulocytes and nongranulocytes.
21. The ethiology of leukoses is related to:
1. Ionizing radiation.
2. RNA-viruses.
3. Chromozome anomalies.
4. Exogenous and endogenouscancerogenic substances.
22. What form of heart insufficiency causes blood congestion in the lungs?
1. Left ventricle insufficiency.
2. Right ventricle insufficiency.
23. Systemic circulation congestion is observed in insufficiency of:
1. Left ventricle.
2. Right ventricle.
25. In what kind of cardial insufficiency Frank-Starling mechanism plays the important role?
1. In volume overload.
2. In pressure overload.
26. The essence of myocardial ischemia is:
1. Mismatch between import and export ofoxygen in the myocardium.
2. Inadequacy between arterial and venous circulation of the heart.
28. The main pathogenetic mechanism of stable angina pectorisis is:
1. Increased oxygen requirements of the myocardium.
29. What is acute myocardial infarction?
1. Myocardial dystrophy.
30. What is the main pathogenetic unit in myocardial infarction formation?
1. Fixed coronary stenosis.
31. The most severe complication of acute myocardial infarction is:
1. Pulmonary embolism.
32. Main pathogenetic mechanism in cardiac tamponade is:
1. Reduced myocardial contractility.
33. Pathophysiological manifestations of pericardial effusions are:
34. Which are the main causes for development of hemodynamic heart failure?
36. Systolic blood pressure is elevated when it is over:
1. 130 mmHg.
2. 140 mmHg.
3. 150 mmHg. 4. 160 mmHg.
37. Which factors are able to increase systemic blood pressure?
38. What is the pathogenetic classification of arterial hypertension?
4. Essential and symptomatic.
5. Localized and generalized.
39. Endocrine hypertension in pheochromocytoma is determined by:
3. Increased Na + and water retention in the body.
1. Etiology is a science about:
1. The mechanisms generating a disease.
2. The reasons and conditions for developing of a disease.
3. Types of pathologic processes.
4. Genetic predisposition to damaging factors.
2. Pathogenesis is a science of:
1. The reasons for a disease.
2. The complications of a disease.
3. Prophylaxis of diseases.
4. The dangerous effects of the environment.
5. The mechanisms of origin, course and end of a disease.
3. Which mechanism lies at the basis of developing DM type I:
4. Ischemic destruction of the β-cells.
5. The major (most important) mechanism for hyperketonemia in DM is:
1 2. Decreased utilization of ketons in the muscles.
6. Hyperosmolar non-ketogenic coma is a complication of:
2. Decreased fibrinogen.
3. Decreased α-globulins.
4. Decreased α- and β-globulins.
8. Conditions for edema are present when:
10. Vitamin D 3 deficiency leads to:
11. What is the characteristic of respiratory acidosis?
1. Decreased РСО2 .
2. Increased РСО2 .
3. Increased РО2 .
4. Decreased РО2 .
5. Decreased НbСО
12. What is the pathophysiological classification of hypoxia:
1.Hypoxic, hemic, circulatory, O 2 utilization, mixed.
2. Compensated, uncompensated,subcompensated, overcompensated.
3. Fulminant, acute, subacute, chronic.
5. Pulmonary, cardiovascular, blood, mixed
13. The main factors leading to blood clotting are:
14. The triggering factor for a thrombus formation is usually:
16. Embolism is a process of:
17. The most important outcome of alveolar hypoventilation is:
18. What is a common complication in the advanced stages of COPD?
19. What is necessary for the development of cor pulmonale chronicum?
20. Anemia is defined as:
21. The pathogenetic classification of anemias includes:
2. Haemorrhagic anemias, anemias due to impaired erythropoesis and haemolytic anemias.
22. The main pathogenetic factor in iron-deficient anemia is:
23. Pathognomonic sign of pernicious anaemia is:
24. Cooley’s anemia (Thalassemia major) is a result of:
5. A complication of haemorrhagic disease of the newborn.
26. The ethiology of leukoses is related to:
27. The essence of myocardial ischemia is:
29. The main pathogenetic mechanism of stable angina pectorisis:
30. What is acute myocardial infarction?
31. What is the main pathogenetic unit in myocardial infarction formation?
32. The most severe complication of acute myocardial infarction is:
33. Main pathogenetic mechanism in cardiac tamponade is:
34. Pathophysiological manifestations of pericardial effusions are:
36. In hypertension, systolic blood pressure is elevated when it is over:
1. 120 mmHg.
2. 130 mmHg.
3. 160 mmHg.
4. 140 mmHg.
5. 150 mmHg.
37. In hypertension, diastolic blood pressure is elevated when it is over:
1. 80 mmHg.
2. 90 mmHg.
3. 95 mmHg.
4. 100 mmHg.
5. 110 mmHg.
38. Which factors are able to increase systemic blood pressure?
6 3. Total peripheral vascular resistance (TPR).
39. What is the pathogenetic classification of arterial hypertension?
40. Endocrine hypertension in pheochromocytoma is determined by:
1. What is the term that is used to identify a factor that triggers an acute episode?
A. Precipitating factor
B. Stress-inducing factor
C. Contributing factor
D. Determining factor
E. Causal factor
e
2. A disease that arises from the activity (treatment, procedures or errors) of a physician is known as:
A. Adverse event
B. Idiopathic
C. Iatrogenic
D. Malpractice
E. Psychogenic
c
3. Which is not a cardinal sign of inflammation?
A. Rubor
B. Calor
C. Tumor
D. Functio laesa
E. Amaurosis fugax
7. The following are all characteristics of metabolic syndrome:
A. Hypertension, hypoglycemia, and high HDL
B. Intra-abdominal obesity, hypertension, and low HDL
C. Dyslipidemia, intra-abdominal obesity, and insulin insensitivity
D. Intra-abdominal obesity, hypotension, and low LDLs
8. Which of the following clinical manifestations differentiate myocardial infarction from angina pectoris?
A. Chest pain affected by breathing and relieved by nitroglycerin administration
B. Chest pain initiated by exercise or stress and diaphoresis
C. Radiating chest pain, ST-segment changes on the ECG, and elevated serum levels of
troponin
D. Chest pain aggravated by coughing and deep breathing
9. In a patient with mitral stenosis, cardiac catheterization findings would indicate:
A. Increased pressure in the right ventricle
B. Increased pressure in the left atria
C. Increased pressure in the left ventricle
D. Increased pressure in the right atria
b
10. What is the pathophysiologic phenomenon underlying disseminated intravascular coagulation (DIC)?
A. Clotting that leads to bleeding
B. Elevated platelet and fibrinogen levels
C. Inadequate cardiac output
D. Mast cell degranulation
a
11. Uncontrolled massive bleeding causes which of the following types of shock?
A. Cardiogenic
B. Neurogenic
C. Hypovolemic
D. Septic
12. What occurs with hypoventilation?
A. The amount of air entering the alveoli increases.
B. The PaCO 2 exceeds 45 mmHg
C. It is a normal response to high altitude
D. Hypocapnia occur
13. Areas of the lung that have little ventilation and thus little oxygen will cause the blood vessels of that area to ______________.
A. vasoconstrict
B. vasodilate
C. remain the same
D. clot off
14. Carbon dioxide diffuses faster than oxygen; therefore problems with diffusion often affect the levels of ______________ first.
A. oxygen
B. carbon dioxide
C. nitrogen
D. none of these
15. A 24-year-old male presents with emphysema. He has never smoked and does not get much exposure to secondhand smoke. What is the name of the hereditary disease that may be responsible for his emphysema?
A. Intrinsic asthma
B. 1-Antitrypsin deficiency
C. Duchenne muscular
16. Accumulation of fluid in the pericardial cavity is referred to as which of the following terms?
A. Pericarditis
B. Pericardial effusion
C. Pericardial rub
17. Which of the following conditions occurs when blood cannot flow forward due to the orifice being constricted and narrowed, causing the pressure in the chamber to rise and the myocardium to work harder and eventually hypertrophy?
A. Valvular dysfunction
B. Valvular stenosis
C. Valvular regurgitation
18. Orthopnea can be described as:
A. Difficulty breathing during exercise
B. Difficulty breaking while lying flat
C. Coughing and wheezing
D. Nasal congestion
19. Stools contain excess fat:
A. Fistulas
B. Zollinger-Ellison syndrome
C. Amebiasis
D. Osmotic diarrhea
E. Hypergastrinemia
F. Steatorrheic
f
20. Which cause of hypertension is the most common in acute renal failure?
A. Pulmonary edema
B. Hypervolemia
C. Hypovolemia
D. Anemia
21. What change indicates recovery in a patient with nephrotic syndrome?
A. Disappearance of protein from the urine
B. Decrease in blood pressure to normal
C. Increase in serum lipid levels
D. Gain in body weight
22. Which of the following diagnostic findings are most likely for a client with aplastic anemia?
A. Decreased production of T-helper cells
B. Decreased levels of white blood cells, red blood cells, and platelets
C. Increased levels of WBCs, RBCs, and platelets
D. Reed-Sternberg cells and lymph node enlargement
23. Pulmonary embolism is most closely related to:
A. Deep vein thrombosis
B. A collapsed lung
C. Hemophilia
D. Bronchitis
24. You expect a patient in the oliguric phase of renal failure to have a 24-hour urine output less than:
A. 200 ml
B. 400 ml
C. 800 ml
D. 1000 ml
27. Which one of the following is NOT a symptom of hypoxia?
A. Pain
B. Headache
C. Fatigue
D. Increased energy
d
28. Which of the following disorders results from a deficiency of factor VIII?
A. Sickle cell disease
B. Christmas disease
C. Hemophilia A
D. Hemophilia B
29. A predominantly conjugated hyperbilirubinemia is present in all of the following causes of jaundice, except:
A. Hemolysis
B. Bile duct obstruction
C. Primary biliary cirrhosis
D. Biliary atresia
30. What important functions are affected by severe, acute, or chronic liver disease?
A. Blood clotting
B. Elimination of water, salt, drugs, and toxins from the body
C. Manufacture of blood proteins
D. All of the above
31. Pigment gall bladder stones are commonly seen in all except:
A. Gilbert’s syndrome
B. Ileal resection
D. Pernicious anemia.
32. If insufficient PTH is produced, the blood calcium level drops, resulting in:
A. Reduced growth in childhood or parathyroid dwarfism
B. Tetany, where the body shakes from continuous muscle contraction
C. Osteoporosis
D. Blood clotting
E. Exophthalmic goiter
33. Iodine deficiency may result in:
A. Nervousness
B. Weight loss
C. Increased sweating
D. Increased synthesis of thyroglobulin
34. Which of the following is an auto-immune condition of the thyroid?
A. Hashimoto thyroiditis
B. Myxedema
C. Cretinism
D. Graves dis
35. A patient with a pituitary tumor that secretes a large amount of TSH would have which of the following features:
A. Normal plasma T3
B. Exopthalmos
C. Normal plasma T4
D. Goiter
36. A person with Addison disease:
A. Is unable to replenish blood glucose levels under stressful conditions
B. Develops dramatically more male features
C. Develops a rounded face and edema
D. Has overgrowth of hands and face
E. All of the above
37. Excess cortisol is represented by which condition?
A. Addison’s disease
B. Cushing’s syndrome
C. Diabetes insipidus
D. Hyperthyroidism
38. You are experiencing constipation, dry skin, weight gain, and cold intolerance. Which condition are you most likely experiencing?
A. Hyperthyroidism
B. Addison’s disease
C. Cushing’s syndrome
D. Hypothyroidism
39. Diabetes insipidus, if left untreated, will rapidly develop into:
A. Malignant hypertension
B. Diabetic coma
C. Dehydration
D. Metabolic alkalosis
1. The main component of the immune system in allergy reaction type I is:
1. Immunoglobulin Е.
2. Immunoglobulins М and G.
3. Sensibilizated Т-lymphocyte
2. What cells have receptors with high affinity to Ig E?
1. Macrophages.
2. Mast cells.
3. Lymphocytes.
3. Anaphylactic shock is the allergy of:
1. Type I.
2. Type II.
3. Type III.
4. Type IV.
4. The example of type I allergic reaction is:
1. Hives.
2. Autoimmune hemolytic anemia.
3. Autoimmune glomerulonephritis.
5. The main component of the immune system in allergy reaction type II is :
3. Sensibilizated Т-lymphocytes.
6. What type of allergy is the leader in serum sickness?
7. The main component of the immune system in allergy reaction type IV is:
4. Sensibilizated Т-lymphocytes.
8. What of the listed is the most important sign of respiratory failure:
3. Persisting cough.
9. Hypoxemia is a reduction of:
1. Oxygen in the tissues.
2. Oxygen in the blood.
3. Alveolar ventilation.
10 Hypercapnia is:
1. Increase of PaCO2 more than 44 mmHg.
2. Decrease of PaCO2 less than 40 mmHg
11. Hypocapnia is:
1. Increase of PaCO2 more than 40 mmHg.
2. Decrease of PaCO2 less than 36 mmHg.
12. Arterial blood oxyhemoglobin content is:
1. 96 %.
2. 80 %.
3. 65-70 %.
13. Cyanosis occurs when there is an increase in the blood of:
2. Oxyhemoglobin.
3. Reduced hemoglobin.
15. What is the hypersensitivity type in the allergic form of bronchial asthma?
3. Type IV.
20. Chejn-Stokes breath is characterized by:
1. Apnoea alternates with respiratory movement of increasing, and then decreasing depth.
2. Apnoea alternates with respiratory movement of identical depth.
3. Bradypnoea with the enhanced inhale and exhale.
4. Deep and noisy breath.
29. What are the normal values of leukocytes in the blood?
1. 4,5 - 15,5.109 /l.
2. 3,5 - 10,5.109 /l.
3.
2,5 — 3,5.109/l.
34. In leukemias are observed:
1. Hyperplasia of the hematopoietic organs.
2. Metaplasia in medullary and extamedullary foci.
3. Stopping cell differentiation.
35. What does the term “hiatus leucaemicus” mean?
1. Lack of intermediate cell forms in the peripheral blood.
2. Lack of blast cells in the peripheral blood.
3. Presence in the blood of all cells characteristic of the bone marrow.
36. Heart failure is a clinical manifestation of:
1. Systolic and/or diastolic myocardial dysfunction.
2. Electrical instability of the heart.
39. Which of the following is not a compensatory mechanism in heart failure?
1. Frank-Starling mechanism.
2. Sympathetic nervous system activation.
3. Renin-angiotensin-aldosterone system activation.
4. Myocardial fibrosis
5. Myocardial hypertrophy.
40. The Frank-Starling mechanism is activated in one of the following states:
3. Increased myocardial contractility.
42. Myocarditis is a disease that is characterized by:
1. Inflammation of the heart muscle.
2. Reducing heart's ability to pump.
4. Arrhythmias.
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