GENERAL PATHOPHYSIOLOGY
DISORDERS OF PERIPHERAL CIRCULATION
Tests:
1. Arterial hyperemia is:
a)
organ augmented blood flow due to increase of blood supply from the
arterial vessels
b)
organ augmented blood flow as a result of impaired venous return from a
tissue
c)
increased amount of blood in the organism
d)
hematocrit increase
2. Clinical signs of arterial hyperemia are:
a)
redness
b)
cyanosis
c)
skin temperature increase
d)
skin temperature decrease
3. Types of physiological arterial hyperemia are:
a)
functional
b)
inflammatory
c)
postischemic
d)
after action of some physical and chemical factors (mustard plaster, heat)
e)
conditioned by reflex reaction (shame blush)
4. The causes of pathological arterial hyperemia are:
a)
inflammation
b)
organ reperfusion
c)
action of vacuum
d)
exercises
e)
elimination of vessels sympathetic innervation influence
5. Postischemic hyperemia occurs due to:
a)
organ reperfusion
b)
quick removing of ascetic fluid
c)
paralysis of vasoconstrictive nerves or their centers
6. The causes of neuroparalytic arterial hyperemia are:
a)
transection of vasoconstrictive vegetative nerves
b)
temporal stagnation of the circulation
c)
action of vacuum
7. How does microcirculation change in arterial hyperemia?
a)
dilation of arterioles
b)
constriction of venes
c)
opening of nonoperation capillaries
8. The mechanisms of increased temperature in arterial hyperemia are:
a)
increased warmth of arterial flow
b)
intensification of oxidative processes
c)
inhibition of respiratory enzymes activity
d)
decreased heat emission
9.
a)
b)
c)
The causes of pathological arterial hyperemia are:
action of pathogenic factors
in physical work
injury of soft tissues
10. The causes of venous hyperemia are:
a)
increased arterial flow
b)
impediment outflow of venous blood
c)
thrombosis of abdominal veins
11. The causes of venous hyperemia are:
a)
thrombosis of veins
b)
exercise stress
c)
compression of veins by tumor
d)
heart failure
12. The causes of venous hyperemia in organs of abdominal cavity are:
a)
thrombosis of the portal vein
b)
thrombosis of mesenteric arteries
c)
left-sided heart failure
d)
right-sided cardiac failure
e)
hepatic cirrhosis
13. Clinical signs of venous hyperemia are:
a)
cyanosis
b)
redness
c)
reduced organ temperature
d)
increased organ temperature
e)
organ reduction
14. The causes of reduction of the skin temperature in venous hyperemia are:
a)
intensification of heat loss
b)
disconnection of oxidation and phosphorilation in mitochondria
c)
heat production decrease
d)
feebleness circulation
15. The causes of stasis are:
a)
impediment blood outflow in veins
b)
increased blood flow
c)
decreased blood flow
d)
increased blood outflow from organs
e)
increased blood viscosity
16. The causes of capillary stasis are:
a)
erythrocyte aggregation (sludge)
b)
venous thrombosis
c)
reduced blood flow to capillaries
d)
decreased hematocrit
17. Ischemia is the decreasing of blood flow due to:
a)
decreasing blood flow in arteries
b)
anemia
c)
low count of erythrocytes in blood
d)
decreased hematocrit
18. The clinical signs of ischemia are:
a)
skin paleness
b)
cyanosis
c)
redness
d)
decreased temperature of the organ
e)
increased temperature of the organ
19. Peculiarities of microcirculation in ischemia are:
a)
feebleness circularity
b)
increased blood flow
c)
reduction of capillaries diameter
d)
extension of capillaries diameter
20. The organs with functionally absolute sufficient collaterals are:
a)
distal part of lower extremities
b)
c)
d)
brain
heart
upper extremities
21. Following vasodilators are synthesized in endothelium:
a)
prostacyclin
b)
prostaglandin F2α
c)
NO
d)
acetylcholine
e)
endothelin
22. Following vasoconstictors are synthesized in endothelium:
a)
prostacyclin
b)
prostaglandin F2α
c)
NO
d)
acetylcholine
e)
endothelin
23. What form of NO-synthase takes part in vasodilatation:
a)
cerebral
b)
endothelial
c)
induced (macrophage)
24. Glutamate toxicity participates in:
a)
neuroparalitic arterial hyperemia
b)
brain ischemia
c)
portal hypertension
d)
true capillary stasis in the heart
25. Reperfusion syndrome occurs due to:
a)
resuscitation
b)
intra-arterial infusion of blood
c)
removing of ascetic fluid from the abdominal cavity
d)
thrombolysis in arteries
e)
intravenous infusion of plasma substitutes
26. The main pathogenic mechanism of reperfusion syndrome is:
a)
development of edema
b)
c)
d)
oxidative stress
deficiency of energy
action of lysosomal enzymes
Answers:
1a, 2ac, 3ade, 4abce, 5ab, 6a, 7aс, 8ab, 9ac, 10bc, 11acd, 12ade, 13ac, 14acd,
15aсe, 16a, 17a, 18ad, 19ac, 20ad, 21ac, 22be, 23b, 24b, 25 асd, 26b.
INFLAMMATION. ALTERATION AND EXUDATION
Tests:
1. The рН in the focus of inflammation:
a)
reduces
b)
increases
c)
is unaffected
2. Osmotic pressure in the focus of inflammation is:
a)
reduced
b)
increased
c)
unaffected
3. Disturbances of microcirculation in the focus of inflammation have following
succession:
a)
arterial hyperemia, ischemia, venous hyperemia, stasis
b)
ischemia, arterial hyperemia, venous hyperemia, stasis
c)
venous hyperemia, arterial hyperemia, stasis, ischemia
4. Kinine system in the focus of inflammation causes:
a)
increased arterioles tone
b)
decreased arterioles tone
c)
no changes with arterioles tone
5. Prostaglandin E and prostacyclin in the focus of inflammation causes:
a)
arteriolar constriction
b)
arteriolar dilation
c)
no changes with arterioles tone
6. Vascular permeability under the action of histamine and serotonine in the
focus of inflammation is:
a)
increased
b)
reduced
c)
unaffected
7. Vascular permeability under the action of bradykinine in the focus of
inflammation is
a)
increased
b)
reduced
c)
unaffeated
8. The chemical structure of prostaglandins derived from the metabolism of:
a)
amino acids
b)
peptides
c)
arachidonic acid by cyclooxygenase pathway
d)
of arachidonic acid by lipoxygenase pathway
9. The chemical structure of leukotrienes derived from the metabolism of:
a)
amino acids
b)
peptides
c)
arachidonic acid by cyclooxygenase pathway
d)
arachidonic acid by lipoxygenase pathway
10.Diphtheria is characterized by:
a)
serous exudate
b)
catarrhal exudate
c)
fibrinogenous exudate
d)
purulent exudate
11.What substances inhibit scar formation after operation?
a)
heparin
b)
IL-1
c)
γ-interferon
d)
thrombin
12.Emigration of leukocytes occurs in:
a)
arteriole
b)
arteriolar end of capillary
c)
venous end of the capillary
d)
postcapillary venule
13.How does the concentration of C-reactive protein change in inflammation?
a)
it is increased
b)
it is reduced
c)
it is unaffected
14.The most important mediator of the acute-phase reaction (fever) is:
a)
histamine
b)
IL-1
c)
bradykinine
d)
serotonine
15. The cause of inflammation is:
a)
b)
local action of damage factor
apoptosis
16. Inflammation is the process intended to:
a)
damage
b)
destruction of damage factor
c)
restoration of injury
17. What processes occur in inflammation?
a)
alteration
b)
transudation
c)
fibrosis
d)
embolism
18. Emigration of leukocytes is the process of:
a)
b)
c)
leucocytes transit from the intravascular space to the focus of inflammation
leucocytes transit from the tissue to the blood
spreading of leukocytes in blood
19. The causes of primary alteration are:
a)
b)
c)
d)
e)
active forms of oxygen
disturbance of microcirculation
microorganisms
mediators of inflammation
circulating immune complexes
20. The causes of secondary alteration are the action of:
a)
active forms of oxygen
b)
disturbance of microcirculation
c)
microorganisms
d)
mediators of inflammation
e)
circulating immune complexes
21. Local signs of acute inflammation are:
a)
b)
c)
d)
e)
redness
swelling
pain
heat in the focus of inflammation
leucocytosis
22. Systemic signs of acute inflammation are:
a)
b)
c)
d)
e)
redness
swelling
pain
fever
leukocytosis
23. Physicochemical changes in the focus of alteration are:
a)
b)
c)
d)
e)
increased anaerobic glycolysis
increased hydrolysis
hyperoncia
hyperosmia
acidosis
24. Metabolic changes in the focus of alteration are:
a)
b)
c)
d)
e)
hyperoncia
increased anaerobic glycolysis
increased hydrolysis
hyperosmia
activation of peroxidation
25.
Cellular mediators are:
a)
b)
c)
d)
e)
histamine
kinins
complement
serotonine
thromboxane
26.
Plasma-derived mediators are:
a)
b)
c)
d)
e)
histamine
kinins
the complement system
serotonine
thromboxane
27. Primary alteration occurs:
a)
b)
under the influence of disturbing factor
during inflammatory process itself
28. Secondary alteration occurs:
a)
b)
under the influence of disturbing factor
during inflammatory process itself
29. Exudation is characterized by:
a)
b)
c)
d)
amount of protein more than 3%
amount of protein content less than 3%
the content of the cells more than 3000/mm3
the content of the cells less than 3000/mm3
30. Exudation is characterized by:
a)
b)
c)
d)
specific gravity is above 1018
specific gravity is below 1018
high concentration of hydrogen ions
low concentration of hydrogen ions
31. Transudation is characterized by:
a)
b)
c)
d)
amount of protein more than 3%
amount of protein less than 3%
the content of the cells more than 3000/mm3
the content of the cells less than 3000/mm3
32. Transudation is characterized by:
a)
b)
c)
d)
specific gravity is above 1018
specific gravity is below 1018
high concentration of hydrogen ions
low concentration of hydrogen ions
33. Positive role of exudation consists in:
a)
decreased concentration of microbes, their toxins and biological active
substances
b)
exacerbate of alteration
c)
it causes pain
d)
it prevents the spread of microbes and toxins throughout the organism
34. Negative role of exudation consists in:
a)
decreased concentration of microbes, their toxins and biological active
substances
b)
exacerbate of alteration
c)
it causes pain
d)
it prevents the spread of microbes and toxins throughout the organism
e)
worsening of blood supply
35. Oxygen-dependent bactericidal system of leucocytes includes:
a)
b)
c)
d)
e)
lactoferrin
nonenzymatic cation proteins
hypochlorid
superoxide
lysozyme
36. Oxygen-independent bactericidal system of leucocytes includes:
a)
lactoferrin
b)
nonenzymatic cation proteins
c)
hypochloride
d)
superoxide
37. Composition of the pus:
a)
purulent corpuscules
b)
c)
d)
e)
fibrin
collagen fibers
microorganisms
platelets
38. Abscess is a suppurative inflammation:
a)
b)
c)
limited
diffused
in cavities and hollow organs
39. Phlegmon is a suppurative inflammation:
a)
b)
c)
limited
diffused
in cavities and hollow organs
40. Empyema is a suppurative inflammation:
a)
b)
c)
limited
diffused
in cavities and hollow organs
41. What pathogenic factors lead to edema in inflammation?
a)
b)
c)
d)
the high hydrostatic pressure at the arteriolar end of capillaries
reduced hydrostatic pressure at the arteriolar end of capillaries
decreased vascular permeability
increased vascular permeability
42. What pathogenic factors lead to edema in inflammation?
a)
b)
c)
d)
decreasing of colloid-osmotic pressure in the focus of inflammation
increasing of oncotic pressure in blood
increasing of colloid-osmotic pressure in the focus of inflammation
decreased of the lymph outflow
43. Acute purulent inflammation is characterized by prevalence in infiltrate of:
a)
b)
neutrophills
lymphocytes
c)
d)
epithelial cells
plasmatic cells
44. Alterative inflammation is characterized by:
a)
prevalence of dystrophic, necrotic and necrobiotic processes
b)
migration of eosinophills in focus of alteration
c)
accumulation of water in focus of alteration
45. Next components take part in phagocytosit:
a)
mitochondrions
b)
lysosomes
c)
ribosomes
d)
Golgi complex
46. Vascular response in inflammation occurs under the influence of:
a)
increased osmotic pressure in the focus of inflammation
b)
increased count of leucocytes
c)
action of mediators
d)
activation of phagocytosis
47. High level of lymphocytes, histiocytes, plasmatic cells, macrophages in
thepunctate occurs in:
a)
acute allergic inflammation
b)
acute exudative inflammation
c)
chronic inflammation
d)
aseptic inflammation
48. High level of erythrocytes, macrophages, lymphocytes, neutrophills in the
punctate occurs in:
a)
cataral inflammation
b)
putrid inflammation
c)
hemorrhagic inflammation
d)
purulent inflammation
Answers:
1а, 2b, 3b, 4b, 5b, 6a, 7a, 8c, 9d, 10c, 11ac, 12d, 13a, 14b, 15а, 16bc, 17ас, 18а,
19ce, 20abd, 21abcd, 22de, 23cde, 24bce, 25ade, 26bc, 27a, 28b, 29ac, 30ac, 31bd,
32bd, 33ad, 34bce, 35сd, 36ab, 37acd, 38a, 39b, 40c, 41ad, 42cd, 43a, 44a, 45b,
46c, 47c, 48с.
THERMAL REGULATORY DYSFUNCTION. FEVER. HYPERTHERMIA.
HYPOTHERMIA
Tests:
1.
a)
b)
c)
d)
The causes of noninfectious fever are:
aseptic injury of tissues
protein injection
bacteria synthesized products
immune complexes
2.
a)
b)
c)
Exogenous pyrogenes are:
gram-negative bacteria endotoxins
leucocyte synthesized substances
glucose
3.
a)
b)
c)
Endogenous pyrogenes are:
bacterial lipopolysaccharides
bacteria exotoxins
leucocyte synthesized substances (IL-1)
4.
a)
b)
c)
d)
Endopyrogenes are:
histamin
IL-1
bradykinin
platelet-activating factor, PAF
5.
a)
b)
c)
d)
Exopyrogenes stimulate synthesis of:
IL-1
thromboxan А2
prostacyclin
TNF
6.
a)
b)
c)
d)
Endopyrogenes stimulate synthesis of:
IL-1
thromboxan А2
prostacyclin
prostaglandin Е2
7.
a)
b)
c)
d)
What cells are the sources of endogenous pyrogens?
lymphocytes
macrophages
eosinophills
endoteliocytes
8.
a)
b)
c)
d)
Pyrogenic effect due to gram-negative bacterias is determined by:
lipoid А
peptides
nucleic acids
polysaccharides
9. What mechanisms promote increasing of temperature in the first stage of
fever?
a)
muscular quiver
b)
increased heat emission
c)
reduction of heat emission
d)
skin vessels dilation
10. The mechanisms of increasing temperature in the first stage of fever are:
a)
vasoconstriction
b)
reduced perspiration
c)
vasodilation
d)
increased perspiration
11. Heat regulation in the first stage of fever in infants is characterized by:
a)
increased heat production
b)
reduction of heat emission
c)
absence of muscular quiver
12. The mechanisms of temperature decrease at the third stage of fever are:
a)
increase of perspiration
b)
reduction of perspiration
c)
decrease of diuresis
d)
increase of diuresis
13. The heat regulation at the third stage of fever:
a)
is unaffected
b)
is characterized by decreased of heat production
c)
remains at higher level
d)
is characterized by intensification of heat emission
14. The third stage of fever is characterized by:
a)
increased perspiration
b)
dilatation of skin blood vessels
c)
increased synthesis of aldosterone
d)
increased blood volume
15. Temperature homeostsasis point in the third stage of fever:
a)
does not change
b)
stays at a higher heat regulation level
c)
returns to starting position
16. What is critical decrease of temperature?
a)
rapid reduction of temperature
b)
gradual reduction of temperature
17. What lytic decrease of temperature means?
a)
reduction of temperature in few hours
b)
gradual reduction of temperature
18. What type of temperature decrease is more dangerous?
a)
critical
b)
lytic
19. How does the function of respiratory system change in fever?
a)
tachypnoe with reduced respiration depth
b)
bradipnoe with increased respiration depth
20. How does the secretory and motoric function of gastrointestinal system
change in fever?
a)
inhibits
b)
intensifies
21. Nitrogen balance in fever is:
a)
negative
b)
positive
22. Diuresis in stadium fastigii is:
a)
decreased
b)
increased
23. Diuresis in stadium decrementi is:
a)
decreased
b)
increased
24. What is the mechanism of collapse during fever?
a)
reduction of cardiac work
b)
vasodilation
25. In what stage of fever does heat production exeeds heat emission?
a)
st. incrementi
b)
st. fastigii
c)
st. decrementi
26. Subfebrile fever is characterized by:
a)
rise of temperature to 38 0С
b)
rise of temperature to 38-39 0С
c)
rise of temperature to 39-41 0С
27. Moderate fever is characterized by:
a)
rise of temperature to 380С
b)
rise of temperature to 38-390С
c)
rise of temperature to 39-410С
d)
rise of temperature to 41-420С
28. High fever is characterized by:
a)
rise of temperature to 380С
b)
rise of temperature to 38-390С
c)
rise of temperature to 39-410С
d)
rise of temperature to 41-420С
29. Hyperpyretic fever is characterizes by:
a)
b)
c)
d)
Rise of temperature to 380С
Rise of temperature to 38-390С
Rise of temperature to 39-410С
Rise of temperature to 41-420С
30. MPD is:
a)
b)
c)
maximal pyrogenic dose
minimal purulentic dose
minimal pyrogenic dose
31. Properties of exogenous pyrogens are:
a)
b)
c)
d)
e)
thermostable
carbohydrate
peptide
thermolabile
lypopolysaccharide
32. Endogenous pyrogens are characterized by:
a)
b)
c)
d)
e)
thermostable
carbohydrate
peptide
thermolabile
lypopolysaccharide
33. Metabolism in the first stage of fever is characterizes by:
a)
decrease of glycogenolysis
b)
decrease of anaerobic glycolysis
c)
increase of glycogenolysis
d)
increase of anaerobic glycolysis
34. Hyperthermia is the type of heat regulation disturbance characterized by:
a)
b)
c)
progressing temperature increase
unaffected mechanisms of heat regulation
affected mechanisms of heat regulation
35. The causes of hyperthermia are:
a)
insufficient heat inflow in organism
b)
c)
d)
increased heat production
reduced heat production
insufficient emission of heat
Answers:
1abd, 2a, 3c, 4b, 5ad, 6d, 7bd, 8a, 9ac, 10ab, 11ac, 12ad, 13bd, 14ab, 15c, 16a,
17b, 18a, 19a, 20a, 21a, 22a, 23b, 24b, 25b, 26a, 27b, 28c, 29d, 30c, 31ae, 32cd,
33cd, 34ac, 35bd.
IMMUNOLOGICAL DISORDERS. AIDS
Tests
1. Nonspecific mechanisms of the immune defense:
a)
system of the phagocytic cells
b)
antibodies (Ig A, G, M, E, D)
c)
cytotoxic lymphocytes-killers
d)
complement system
2. Nonspecific mechanisms of the immune defense:
a)
system of the phagocytic cells
b)
antibodies (Ig A, G, M, E, D)
c)
cytotoxic lymphocytes-killers
d)
complement system
3. Immunodeficiency – is the condition of:
a)
b)
c)
insufficiency of the immune system
insufficiency of the all forms of reactivity
antigen overload
4. During immunodeficiency suffers:
a)
b)
c)
resistance to infectious
resistance to noninfectious agents
resistance to stressors
5. Causes of the acquired immunodeficiency states:
a)
b)
c)
d)
lack of the gene, which is necessary for immunoglobulin syntesis
genetic defect in blood stem cell maturation
poor nutrition
contomination by human immunodeficiency virus
6. The humoral immunity realizes defense against:
a)
b)
c)
bacterias
fungies
viruses
d)
protozoas
7. Cell immunity realizes defense against:
a)
b)
c)
d)
bacterias
fungies
viruses
protozoas
8. Sighns of insufficiency of the humoral immunity are:
a)
b)
c)
d)
decreased B-lymphocytes level
presnce of antivirus immunity
development of the virus infections
development of the pneumocystosis
9. Sighns of insufficiency of the humoral immunity are:
a)
b)
c)
d)
presence of antivirus immunity
decreased resistance to fungies
tumor development
decreased resistance to pneumocystosis
10. Signs of humoral immunity imsufficiency are:
a)
b)
c)
d)
disturbances in the specific antibodies production
absence of the lymph nodes reaction
decrease of the antitransplantat immunity
fungies induced infections
11. Signs of cellular immunity insufficiency are:
a)
b)
c)
d)
disturbances in specific antibodies production
absence of the lymph nodes reaction
normal antivirus immunity
absesnce of innune reaction against transplantat
12. Two signs of cellular immunity imsufficiency are:
a)
b)
disturbances in specific antibodies production
absence of the lymph nodes reaction
c)
d)
normal antivirus immunity
tumors development
13. Syndroms of cellular immunity imsufficiency are:
a)
b)
c)
d)
e)
Bruton syndrom
selective IgA immunodeficite
di George syndrom
Chediak-Chigashi syndrom
Nezelof syndrom
14. Syndroms of humoral immunity insufficiency are:
a)
b)
c)
d)
e)
Bruton syndrom
selective IgA immunodeficite
Chediak-Chigashi syndrom
Nezelof syndrom
dysgammaglobulinemia
15. Syndroms of phagocytosis insufficiency are:
a)
b)
c)
d)
e)
Bruton syndrom
selective IgA immunodeficite
DiGeorge syndrom
Chediak-Chigashi syndrom
Nezelof syndrom
16. Syndroms of complement system insufficiency are:
a)
b)
c)
d)
e)
Bruton disease
immunocomplex pathology
Chediak-Chigashi syndrome
angionevrotic oedema
dysgammaglobulinemia
17. Which part of the immune system is affected in Di George syndrome?
a)
b)
c)
d)
disturbances in the cellular and humoral immunity
disturbances in the humoral immunity
disturbances in the cellular immunity
phagocytosis disturbances
18. What mechanism determines disturbances in the organism defence in
Bruton syndrome?
a)
b)
c)
d)
disturbances in the cellular immunity
disturbances in the humoral immunity
disturbances in the cellular and humoral immunity
phagocytosis disturbances
19. Which biological fluids can contaminate organism by AIDS?
a)
b)
c)
d)
e)
blood
sperm
sweat
breast milk
saliva
20. What are the target cells for human immunodeficiency virus?
a)
b)
c)
d)
e)
nerouns
macrophags
t-killers
t-helpers
t-supressors
21. What signs present at AIDS ?
a)
b)
c)
d)
e)
Kaposhi sarcoma
memory decreasing
icheterus
lymphoma
pneumocystic pneumonia
Answers:
1ad, 2bc, 3ac, 4ab, 5cd, 6a, 7bcd, 8ab, 9a, 10ab, 11bd, 12bd, 13ce, 14abe, 15d,
16bd, 17a, 18b, 19abd, 20abd, 21abde.
ALLERGY
Tests:
1.
a)
b)
c)
2.
a)
b)
c)
The first stage of allergy is:
pathochemical
immunological
pathophysiological
The second stage of allergy is:
pathochemical
immunological
pathophysiological
3.
a)
b)
c)
The third stage of allergy is:
pathochemical
immunological
pathophysiological
4.
a)
b)
c)
The main component of the immune system in allergy reaction 1 type is:
immunoglobulin Е
immunoglobulins М, G
sensibilizated Т-lymphocyte
5. The main component of the immune system in allergy reaction II type
(cytotoxic) is:
a)
immunoglobulin Е
b)
immunoglobulins М, G
c)
sensibilizated Т-lymphocytes
d)
complement
6.
a)
b)
c)
d)
e)
The main component of the immune system in allergy reaction III type is:
immunoglobulin Е
immunoglobulins М, G
sensibilizated Т-lymphocytes
complement
phagocytes
7.
a)
The main component of the immune system in allergy reaction IV type is:
immunoglobulin Е
b)
c)
d)
immunoglobulin М
sensibilizated Т-lymphocytes
complement
8.
a)
b)
c)
d)
What cells have receptors with high affinity to Ig E?
macrophages
eosinophils
mast cells
platelets
9.
a)
b)
c)
d)
e)
Primary mediators of allergic reaction 1 type are:
noradrenaline
histamine
thromboxane
prostacycline
serotonine
10. Secondary mediators of allergic reaction 1 type are:
a)
noradrenaline
b)
histamine
c)
heparin
d)
neutrophylls chemotaxic factor
e)
leucotriene D
11. What cells can release factors for inactivation of allergic mediators?
a)
neutrophils
b)
lymphocytes
c)
eosinophils
d)
macrophages
12. The role of eosinophils in allergy is:
a)
activation of histamine synthesis
b)
activation of histamine excretion
c)
intensification of histamine biological action
d)
inactivation of histamine
13. Anaphylactic shock is the allergy of:
a)
type I
b)
type II
c)
type III
d)
type IV
14. Anaphylactic shock leads to:
a)
b)
c)
d)
pneumonia
lung oedema
bronchoconstriction
lung atelectasis
15. How does the tonus of arterioles change in anaphylactic shock?
a)
it is raised
b)
it is reduced
c)
it is unaffected
16. The examples of the I type of allergic reaction are:
a)
hives
b)
autoimmune anemia
c)
autoimmune glomerulonephritis
d)
reaction against transplant
17. The examples of the II type of allergic reaction are:
a)
hives
b)
autoimmune anemia
c)
autoimmune glomerulonephritis
d)
reaction against transplant
18. The examples of the III type of allergic reaction are:
a)
hives
b)
autoimmune anemia
c)
autoimmune glomerulonephritis
d)
reaction against transplant
19. The examples of the IV type of allergic reaction are:
a)
hives
b)
autoimmune anemia
c)
autoimmune glomerulonephritis
d)
reaction against transplant
20. What mediator of allergy leads to bronchospasm?
a)
heparin
b)
chymase
c)
leukotrien С
d)
triptase
21. The release of histamine occurs in:
a)
immunological stage of allergy
b)
c)
biochemical stage of allergy
pathophysiological stage of allergy
22. What type of allergy is the leader in non-infectious bronchial asthma?
a)
I
b)
II
c)
III
d)
IV
23. What type of allergy is the leader in angioneurotic edema?
a)
I
b)
II
c)
III
d)
IV
24. What type of allergy is the leader in allergic rhinitis?
a)
I
b)
II
c)
III
d)
IV
25. What type of allergy is the hives (urticaria)?
a)
I
b)
II
c)
III
d)
IV
26. What type of allergic reaction is complement-dependent?
a)
I
b)
II
c)
III
d)
IV
27. What type of allergic reaction is dependent on antibodies and is caused by
immune complexes?
a)
I
b)
II
c)
III
d)
IV
28. What elements of the blood prevent adjournment of immune complexes in a
vascular wall?
a)
neutrophils
b)
eosinophils
c)
erythrocytes
d)
basophils
29. What cells phagocyted immune complexes?
a)
neutrophils
b)
eosinophils
c)
macrophages
d)
basophils
30. What type of allergy is the leader in serum sickness?
a)
I
b)
II
c)
III
d)
IV
31. What type of allergy is Arstus-Sacharov phenomeon?
a)
I
b)
II
c)
III
d)
IV
32. What cells mediate the IV type of allergy?
a)
T-lymphocytes-killers
b)
T- lymphocytes-supressors
c)
B-lymphocyte
d)
NK- cells
33. The cause of pollinosis is:
a)
pollen of plants
b)
house dust
c)
street dust
d)
library dust
e)
wool of animals
Ansews:
1b, 2a, 3c, 4a, 5bd, 6bde, 7c, 8c, 9be, 10e, 11c, 12d, 13a, 14c, 15b, 16a, 17b, 18c,
19d, 20c, 21b, 22aс, 23a, 24a, 25a, 26b, 27c, 28b, 29c, 30c, 31c, 32a, 33a.
DISORDERS OF CARBOHYDRATE METABOLISM
Tests
1. The most difficult consequences for organism are:
a)
b)
c)
d)
carbohydrate starvation
proteinic starvation
fat starvation
vitamin starvation
2. Which carbohydrate absorbs in the intestine?
a)
b)
c)
d)
mucopolysaccharide
fructose
glycogen
starch
3. Which enzyme hereditary deficiency leads to von Gierke disease?
a)
b)
c)
d)
hexokinase
glucose-6-phosphatase
acid α-1,4-glucosidase
amylo-1,6-glucosidase
4. In children very often occurs deficiency of:
a)
maltase
b)
amylase
c)
isomaltase
d)
lactase
e)
saccharase
5. In what diabetes is high risk of ketoacidosis development?
a)
b)
type 1
type 2
6. Insulin stimulates:
a)
synthesis of lipid
b)
c)
d)
e)
lipolysis
synthesis of ketone bodies
synthesis of cholesterol
synthesis of lactic acid
7. Insulin inhibits:
a)
b)
c)
d)
synthesis of lipids
lipolysis
synthesis of ketone bodies
synthesis of cholesterol
8. Consequences of carbohydrate starvation is increasing in blood level of:
a)
b)
c)
acetone oxaloacetic acid
pyruvic acid
glucose
9. Reasons of increased level of glucosae in blood after its intake are:
a)
b)
c)
suction in intestine
increased glycogenolysis
activation of gluconeogenesis
10 The causes of hyperglycemia are the increased blood level of:
a)
b)
c)
d)
insulin
glucagon
glucocorticoid
adrenaline
11. The causes of hyperglycemia are the decreased blood level of:
a)
b)
c)
d)
glucagon
glucocorticoid
adrenaline
insulin
12. Reasons of increased sensitivity of nerve cells to deficiency of glucosae are:
a)
absence of reserve of glicogen
b)
c)
insulin-dependent tissue
impossibility usage of fatty acids as source of energy
13. The causes of diabetes mellitus type 2 are:
a)
b)
c)
insufficient synthesis of proinsulin
raised catabolism of insulin
lack of receptors to insulin on target organs
14. Clinical onset of mild hypoglycemia is:
a)
b)
c)
d)
disturbances coordination of movements
convulsions
movement exitement
rise of appetite
15. Risk factors of diabetes mellitus are overconsumption of:
a)
b)
c)
d)
sugar
alcohol
proteins
unsaturated fat acids
16. Hypoglicemic coma can occur in:
a)
b)
c)
thyrotoxicosis
deficiency in insulin
insuloma
17. Diabetes mellitus is characterized by the increased blood level of:
a)
b)
c)
d)
glucose
maltose
saccharose
urea
18. Deficiency of what enzyme leads to disturbance digestion of carbohydrate in
the intestine?
a)
b)
hexokinase
alkaline phosphatase
c)
d)
amylase
phospholipase
19. Clinical onset of ketoacidic coma expresses in:
a)
b)
c)
d)
soft eye-bulbes
muscular trembling
hunger
aceton-like smell
20. Reactions of intermediatory carbohydrate metabolism are:
a)
transamination
b)
gluconeogenesis
c)
β-oxydation
d)
anaerobic glycolysis
21. Clinical onset of lactacidic coma expresses in:
a)
b)
c)
d)
muscular trembling
hunger
aceton-like smell
decrease of blood рН
22. Causes of hyperglycemia in diabetes mellitus are:
a)
b)
c)
d)
inadequate synthesis of glycogen
increased synthesis of glycogen
disorders in utilization of glucosae by cells
increased suction of glucosae in the intestine
23. Normal level of glucosae in blood is:
a)
b)
c)
d)
2,2-3,3 mM
3,3-5,5 mM
5,1-6,4 mM
2,7-3,6 mM
24. Easily absorbted carbohydrate is:
a)
b)
mucopolysaccharide
glucose
c)
d)
glycogen
starch
25. Causes of intermediatory carbohydrate metabolism disorder are:
a)
b)
c)
d)
lack of insulin
hypoxia
deficiency in bile
hypercholesterolemia
26. Reason of glucose malabsorption is hereditary deficiency of:
a)
b)
c)
d)
hexokinase
glucose-6-phosphatase
acid α-1,4-glucosidase
amylo-1,6-glucosidase
27. Causes of Pompe’s disease are hereditary deficiency of:
a)
b)
c)
d)
hexokinase
glucose 6-phosphatase
acid α-1,4-glucosidase
amylo-1,6-glucosidase
28. Insulin stimulates:
a)
b)
c)
d)
aerobic glycolysis
proteolysis
Krebs cycle
gluconeogenesis
29. What kind of coma in diabetes mellitus is characterized by very high level of
glucosae?
a)
b)
c)
d)
ketoacidotic
hyperosmolarity
lactatic
hypoglycemic
30. Insulin inhibits:
a)
b)
c)
d)
aerobic glycolysis
lipolysis
gluconeogenesis
glycogenolysis
31. Deficiency of insulin is characterized by increased blood level of:
a)
b)
c)
d)
glucose
phospholipids
ketone bodies
urea
32. Gierke disease is characterized by accumulation of:
a)
b)
c)
d)
sphingomyelin
triglyceride
proteins
glycogen
33. The kidney barier for glucosae is the level of glucosae:
a)
b)
c)
in blood in which glucosae appear in primary urine
in primary urine, which enters to secondary urine
in blood, in which glucose can’t be fully absorbed
34. Hypoglycemia is caused by increased level of:
a)
b)
c)
d)
insulin
glucagon
glycocorticoid
adrenalin
35. The causes of diabetes mellitus type 1 are:
a)
b)
c)
insuffitient synthesis of proinsulin
heightened catabolism of insulin
lack of receptors to insulin on target tissures
36. Insulin promotes glucose uptake by:
a)
fatty tissue
b)
c)
d)
liver
blood cells
brain
37. The clinical features of severe hypoglycemic coma are:
a)
b)
c)
d)
disorder of coordination of movement
convulsions
acetone-like smell
loss of consciousness
38. The clinical onset of diabetes mellitus type 1 expresses in:
a)
b)
c)
d)
thirst
oliguria
weight loss
obesity
39. Acetone-like smell is the clinical feature of:
a)
b)
c)
d)
hypoglycemic coma
renal diabetes
ketoacidosis
hyperosmolar coma
40. The complications of diabetes mellitus are:
a)
b)
c)
d)
hypoglycemic coma
hyperosmolar coma
nephropathy
gangrene
41. The complications of diabetes mellitus are:
a)
b)
c)
d)
anemia
retinopathy
thirst
hyperglycemia
42. In diabetes mellitus urine analysis detects:
a)
b)
c)
d)
erythrocytes
bilirubin
glucose
ketone bodies
43. Carbohydrate starvation leads to:
a)
b)
c)
d)
increased synthesis of ketone bodies
weight loss
increase synthesis of proteins
no consequences
44. Diabetus mellitus leads to disorder:
a)
only of protein metabolism
b)
only of lipid metabolism
c)
of all metabolism kinds
d)
only of carbohydrate metabolism
e)
only of water-salt metabolism
45. The causes of intermediatjry carbohydrate metabolism disorder are:
a)
b)
c)
d)
В1 hypovitaminosis
hypoxia
deficiency in bile
hypercholesterolemia
46. Clinical manifestations of hypoglycemic coma are:
a)
b)
c)
d)
acetone in urine
Kussmaul’s respiration
soft eye-bulbes
decreased level of glucose in blood
Answers:
1bd, 2b, 3b, 4d, 5a, 6a, 7bcd, 8aс, 9a, 10bcd, 11d, 12ac, 13bc, 14сd, 15ab, 16c,
17ad, 18c, 19ad, 20bd, 21d, 22ac, 23b, 24b, 25ab, 26a, 27c, 28ac, 29b, 30bcd,
31acd, 32d, 33c, 34a, 35a, 36ab, 37bd, 38ac, 39с, 40bcd, 41b, 42cd, 43аb, 44с,
45ab, 46d.
DISORDERS OF LIPID METABOLISM
Tests
1. Unsaturated fatty acid is also called vitamin:
a)
F
b)
E
c)
U
d)
A
e)
B
2. Leptin is hormone of:
a)
b)
c)
d)
hypothalamus
hypophysis
gastrointestinal tract
adipocytes
3. Emulsification of lipids is:
a)
b)
c)
splitting of triglyceride into glycerine and fatty acid
dividing of big lipid drops to small by bile acids
synthesis of chylomicrons
4. What factors lead to development of cholelithiasis?
a)
b)
c)
d)
lack of low density lipoproteins (LDL)
lack of high density lipoproteins (HDL)
deficiency of apoprotein А
excess of apoprotein C-II
5. What factors lead to development of obesity?
a)
b)
c)
d)
inhibition of sympathetic nervous system
activation of sympathetic nervous system
increased level of insulin
increased level of glucocorticoids
6. Obesity leads to:
a)
b)
elevated blood pressure
decreased blood pressure
c)
d)
increased blood coagulation
reduction of blood coagulation
7. What lipoproteins carry cholesterol to the cells?
a)
b)
c)
d)
chylomicrons
LDL
HDL
very low density lipoprotein (VLDL)
8. What substances are nessesery for digestion of triglycerides in the intestine?
a)
b)
c)
d)
hydrochloric acid
amylasa
apoprotein С
bile
9. Main transport form of exogenous fat is:
a)
LDL
b)
VLDL
c)
HDL
d)
chylomicrons
10. The consequences of lipid starvation are:
a)
b)
c)
d)
absent
increased protheolysis
deficiency of all vitamins
deficiency of fatsolubile vitamins
11. Unsaturated fatty acids are:
a)
b)
c)
d)
butyric acid
palmitinic acid
stearic acid
arachidonic acid
12. The atherogenic lipoproteins are:
a)
b)
HDL
LDL
c)
d)
IDL
chylomicrons
13. Antiatherogenic propeties of HDL are determined by:
a)
b)
c)
d)
acetilcholesterolaciltransferase
endothelial lipoprotein lipase
hepatic lipoprotein lipase
ornithincarbamailtransferase
14. Lipopectic function in lungs is realized by:
a)
b)
c)
d)
acetilcholesterolaciltransferase
endothelial lipoprotein lipase
hepatic lipoprotein lipase
lipokain
15. Disorder of lipid metabolism leads to:
a)
b)
c)
d)
ischaemic heart disease
diabetes insipidus
kwashiorkor
stroke
16. The causes of hyperchylomicronemia are:
a)
b)
c)
d)
the absence of receptors to apoprotein В
lack of lipoprotein lipase
deficiency in apoprotein С-II
synthesis of abnormal VLDL
17. Arachidonic acid is the precursor of:
a)
b)
c)
d)
leukotrienes
prostaglandins
bradykinins
thromboxane А2
18. Triglycerides are digested in the intestin to:
a)
valine
b)
c)
d)
chylomicrons
fatty acids
ketone bodies
19. Lipotropic factors are:
a)
b)
c)
d)
methionine
lipokain
leptin
phospholipids
20. Deficiency of unsaturated fatty acids leads to:
a)
b)
c)
d)
disturbance of spermatogenesis
dermatitis
obesity
fatty degeneration of liver
21. Disturbances in lipid digestion and absorption are caused by deficiency of:
a)
b)
c)
d)
lactase
leptine
lipase
aminopeptidase
22. Increased level of ketone bodies is not specific for:
a)
b)
c)
d)
hypoglycemic coma
ketoacidic coma
heperosmolar coma
lactacidic coma
23. What factors prevent obesity?
a)
increased level of androgens hormones
b)
increased level of thyroxine
c)
activation sympathetic nervous system
d)
inhibition sympathetic nervous system
24. Biliary obstruction leads to:
a)
b)
hyperchylomicronemia
steatorrhea
c)
d)
polyuria
deficiency of vit D
25. The lipid mobilization hormones are:
a)
insuline
b)
thyroxine
c)
aldosterone
d)
oxytocin
26. Saturated fatty acids are:
a)
b)
c)
d)
docosahexaenoic
arachic
palmitic
arachidonic
27. Reaction of intermediatiry lipid methabolism is:
a)
b)
c)
d)
transamination
β-oxidation
decarboxylation
synthesis of ketone bodies
28. Normal cholesterol level in blood is:
a)
b)
c)
d)
3,9-6,2 mM
2,2-3,8 mM
2,8-4,7 mM
6,3-9,5 mM
29. What substances are needed for digestion of triglicerides in the intestine?
a)
b)
c)
d)
hydrochloric acid
amylase
lipase
bile
30. Antiatherogenic lipoproteins are:
a)
b)
HDL
LDL
c)
d)
chylomicrones
VLDL
31. Transport form of endogenous fat is:
a)
b)
c)
d)
HDL
LDL
chylomicrones
VLDL
32. Cholesterol mobilization from tissue realizes by:
a)
b)
c)
d)
LDL
chylomicrones
HDL
VLDL
33. What factors are promoted formation of stones during holelithiasis?
a)
b)
c)
d)
increased level of cholesterol in bile
increased level of bile acids in bile
decreased level of bile acids in bile
increased etherification of cholesterol
34. What activate endothelial lipoproteine lipase?
a)
b)
c)
d)
apoprotheine C-I
apoprotheine C-II
apoprotheine C-III
apoprotheine A-I
35. The reasons of dys-β «floating» hyperlipoprotheinemia are:
a)
b)
c)
d)
absence of receptors to apoprothein В
lack of lipoprotheine lipase
deficit of apoprotheine С-II
synthesis of abnormal VLDL
36. The amount of adipocytes after puberty is:
a)
increased
b)
c)
decreased
don’t change
37. The causes of adipose infiltration of liver are lack of:
a)
b)
c)
d)
tryptophan
arginine
methionine
valine
38. Lack of what substances lead to fatty degeneration of liver?
a)
b)
c)
d)
histidine
glutamine
lipokaine
taurine
39. What factors lead to atherosclerosis?
a)
b)
c)
d)
40.
a)
b)
c)
d)
increased cholesterol level in blood
obesity
damage of endothelium
increased synthesis of prostacycline
What factors lead to atherosclerosis?
decreased synthesis of nitric oxide (NO) in endothelium
increased level of chylomicrones in blood
increased level of cholesterol in blood
increased synthesis of NO in endothelium
41.
a)
b)
c)
What blood cells take part in pathogenesis of atherosclerosis?
basophils
eosinophils
monocytes
42.
a)
b)
c)
d)
What vascular cells turn into foam cells during atherosclerosis?
endothelials
smooth muscle
fibroblasts
macrophages
Ansews:
1a, 2d, 3b, 4bc, 5acd, 6ac, 7b, 8d, 9d, 10d, 11d, 12b, 13a, 14b, 15ad, 16bc, 17abd,
18c, 19abd, 20abd, 21c, 22acd, 23abc, 24bd, 25b, 26bc, 27bd, 28a, 29cd, 30a, 31d,
32c, 33ac, 34b, 35d, 36c, 37c, 38c, 39abc, 40ac, 41c, 42bcd.
Topic: DISORDERS OF PROTEIN METABOLISM. GOUT
Tests
1. Disorder of tyrosine methabolism leads to:
a)
b)
c)
d)
tyrosinosis
alkaptonuria
albinism
phenylketonuria
2. The causes of positive nitrogen balance are:
a)
b)
c)
d)
growth
pregnancy
fever
burn
3. What substances are inhibitory transmitters?
a)
b)
c)
d)
aspartate
glutamate
glycine
Gamma-aminobutiric acid (GABA)
4. What substances are excitatory neurotransmitters?
a)
b)
c)
d)
aspartate
glutamate
glycine
gamma-aminobutiric acid (GABA)
5. Increased basal metabolic rate is the result of increased level of:
a)
b)
c)
d)
adrenocorticotropic hormone (ACTH)
insuline
parathormone
thyroxine
6. Which protein fraction prevails in blood?
a)
b)
c)
d)
α1-globuline
β-globuline
albumen
α2-globuline
7. Which protein fraction acts as an antibody?
a)
b)
c)
α1-globuline
γ-globulins
α2-globuline
8. Phenilketonuria is characterized by increased synthesis of:
a)
b)
c)
d)
homogentisic acid
dioxyphenylalanine
melanin
phenylpyruvic acid
9. The cause of positive nitrogen balance is the increased synthesis of:
a)
b)
c)
d)
somatotropic hormone
insuline
glucocorticoid
thyroxine
10. The causes of positive nitrogen balance are:
a)
b)
c)
d)
lack of androgens
lack of insuline
pregnancy
childhood
11. Positive nitrogen balance can be observed in:
a)
b)
c)
d)
fever
starvation
recovery
hyperthyreosis
12. The reason of lipokaine synthesis deficiency is deficit of:
a)
b)
c)
d)
histidine
glutamin
methionine
taurine
13. The precursors of catecholamines are:
a)
b)
c)
d)
arginine
phenylalanine
tyrosine
lysine
14. The precursor of nitric oxide:
a)
b)
c)
d)
asparagine
glutamine
L-arginine
alanin
15. The types of hyperazotemia are:
a)
b)
c)
d)
lactacidic
ketoacidic
hypochloremic
hyperglycemic
16. What process leads to synthesis of new aminoacids?
a)
b)
c)
transamination
deamination
decarboxylation
17. What enzymes digest the proteins in stomach?
a)
b)
c)
d)
pepsin
chemotrypsin
rennin
phospholipase
18. Celiac disease is a disease which is characterized by deficiency in digestion
of:
a)
b)
c)
d)
meat proteins
lipids
saccharose
protein from cereals
19. The result of deamination is synthesis of:
a)
b)
c)
d)
ammonia
uric acid
histamine
urea
20. Lack of vit B6 leads to disorder of:
a)
b)
c)
deamination
decarboxylation
transamination
21. Decreased nonessential amino acid synthesis is caused by:
a)
b)
c)
disorder of deamination
disorder of decarboxylation
disorder of transamination
22. The components of the residual nitrogen are:
a)
b)
c)
d)
proteins
peptides
amino acids
ammonia
23. The types of hyperazotemia are:
a)
b)
c)
d)
retentive
hypochloremic
hyperchloremic
hypoammonia
24. The causes of retentive azotemia are:
a)
b)
c)
d)
nephropathy
shock
thrombosis of venae porta
fever
25. What type of hyperazotemia leads to disorder in urea synthesis?
a)
b)
c)
retentive
hypochloremic
hyperammonia
26. The cause of gout is breakup of:
a)
b)
c)
d)
guanine
uracil
thymidine
adenine
27. Hyperammaniemia is the result of decreasing action of:
a)
b)
c)
d)
ornithine-carbomailtransferase
phosphodiesterase
acetylcholinesterase
carbonic anhydrase
28. Final product of breakup of protein is:
a)
b)
c)
d)
lactic acid
glutamic acid
ammonia
pyruvic acid
29. What biologically active substances are synthesized in decarboxylation?
a)
b)
c)
d)
Thyroid hormones
melanin
histamin
serotonin
30. Phenylketonuria is the disease which is characrerized by metabolism
disorder of:
a)
b)
c)
tyrosine
phenylalanine
homogentisic acid
31. What enzymes digest proteins in the intestine?
a)
b)
c)
d)
pepsin
chemotrypsin
renin
dipeptidase
32. Abnormality proteins are:
a)
albumens
b)
γ-globulins
c)
cryoglobulins
d)
α-globulins
33. The type of hyperazotemia is:
a)
b)
c)
d)
hyperosmolaric
ketoacidic
retentive
hypoglycemic
34. Reactions of intermediary amino acid’s metabolism are:
a)
b)
c)
d)
transamination
deamination
gluconeogenesis
β-oxydation
35. The reasons of increasing deamination are:
a)
b)
c)
d)
starvation
increased consumption of amino acids
lack of vit PP
lack of vit В6
36. Consequences of decreased deamination are:
a)
b)
c)
decreased synthesis of proteins
decreased synthesis of nonessential amino acids
increased level of ammonia
37. What reaction leads to synthesis of histamine?
a)
b)
c)
deamination
decarboxylation
trancamination
38. The main component of residual plasma nitrogen level is/are:
a)
b)
c)
d)
amino acids
ammonia
ammonia ions
urea
39. Predisposing factors for gout are:
a)
b)
c)
d)
meat
male sex
femail sex
acidosis
40. The productive hyperazothemia is characterized by increasd plasma level of:
a)
b)
c)
d)
ammonia
protein
amino acids
creatinine
41. Gout is the disease which is characterized by disorder in metabolism of:
a)
b)
c)
d)
protamines
histone
urea
purine bases
42. Gout is the disease which is characterized by involvement of:
a)
b)
c)
d)
bones
cartilages
rens
cor
43. The causes of negative nitrogen balance are:
a)
b)
c)
d)
obesity
emaciation
excess of insuline
hemorrhage
44. Most common reasons of hereditary enzymopathies are disordes in
metabolism of:
a)
b)
c)
d)
valine
phenylalanine
isoleucine
leucine
Answers:
1abc, 2ab, 3cd, 4ab, 5d, 6c, 7b, 8d, 9ab, 10ab, 11c, 12c, 13bc, 14c, 15c, 16a, 17ac,
18d, 19a, 20bc, 21ac, 22bcd, 23ab, 24ab, 25c, 26ad, 27a, 28c, 29cd, 30b, 31bd,
32c, 33c, 34ab, 35ab, 36ab, 37b, 38d, 39abd, 40c, 41d, 42bc, 43bd, 44b.
STARVATION
1.
a)
b)
c)
In the 1st period of complete starvation respiratory coefficient is?
0,7
0,8
1,0
2.
a)
b)
c)
In the 2nd period of complete starvation respiratory coefficient is:
0,7
0,8
1,0
3.
a)
b)
In the 3d period of complete starvation respiratory coefficient is:
0,7
0,8
c)
1,0
4.
a)
b)
c)
The first period of complete starvation is characterized by disturbances of:
proteins
glicogene
triglycerides
5.
of:
a)
b)
c)
d)
e)
The second period of complete starvation is characterized by disturbances
proteins
starch
glicogene
triglycerides
nucleoproteins
6.
What period of complete starvation is most prolonged?
a)
the first
b)
the second
c)
the third
7.
Which two organs (tissue) loose mass less than others in complete
starvation?
a)
liver
b)
cor
c)
fatty tissue
d)
muscles
e)
nervous tissue
8.
a)
b)
c)
d)
e)
What organ (tissue) looses mass more than others in complete starvation?
liver
cor
lung
fatty tissue
nervous tissue
9.
What nutrients are not used by an organism in the first period of the full
starvation?
a)
proteins
b)
lipids
c)
carbohydrates
10.
a)
b)
c)
The 2nd period of complete starvation is characterized by disturbance of:
proteins
lipids
carbohydrates
11.
a)
b)
c)
The 3d period of complete starvation is characterized by disturbance of:
proteins
lipids
carbohydrates
12.
a)
b)
c)
13.
a)
b)
c)
Basal metabolism in the 1st period of complete starvation:
rises
reduces
doesn’t change
Basal metabolism in the 2nd period of complete starvation:
rises
reduces
doesn’t change
14.
a)
b)
c)
Glycogen reserve at starvation:
increases
doesn’t change
decreases
15.
a)
b)
c)
d)
The cause of increased synthesis of ketone bodies in starvation is:
Disorder of mineral metabolism
increased splitting of lipids
Disorder in function of rens
Deficit of substrates of Krebs cycle
16.
a)
b)
c)
d)
In what diseases fast therapy is prescribed:
allergy
obesity
cachexia
neuropsychic disease
17. What tissues lose mass more than others in starvation?
a)
b)
fatty tissue
muscles
c)
d)
bones
nervous tissue
Answers:
1c, 2a, 3b, 4b, 5d, 6b, 7be, 8d, 9ab, 10b, 11a, 12a, 13b, 14c, 15bd, 16 ab, 17ab.
DISORDERS OF WATER-ELECTROLITE METABOLISM
Tests
1.
a)
b)
c)
d)
Which water compartment is the biggest one?
intracellular
interstitial
plasma
transcellular
2.
a)
b)
c)
d)
The highest quantity of the water lost from the human body by:
evaporation
ventilation
excrement
urinary excretion
3. The smallest amoughnt of the water is in the:
a)
b)
c)
d)
fat
nervous tissue
bones
teeth
4. The largest amount of the water is in the:
a)
b)
c)
d)
e)
lung
liver
fat
nervous tissue
bones
5. Hormone that increases sodium reabsorption in kidhey is:
a)
b)
c)
d)
aldosterone
antidiuretic hormone
corticosterone
natriuretic hormone
6. Hormone that increases sodium excretion by kidney is:
a)
b)
c)
d)
aldosterone
antidiuretic hormone
corticosterone
natriuretic hormone
7. Which transfusion can lead to water poisoning?
a)
b)
c)
3,0 % NaCl
0,4 % NaCl
0,9 % NaCl
8. Which changing in plasma can lead to increased water accamulation in
vessels?
a)
b)
c)
d)
increased osmotic preassure
decreased osmotic preassure
increased oncotic preassure
decreased of oncotic preassure
9. Which changing in plasma can lead to increased water accamulation in
tissues?
a)
b)
c)
d)
increased osmotic preassure
decreased osmotic preassure
increased oncotic preassure
decreased oncotic preassure
10. The reasons of increased synthesis of vasopressin are:
a)
b)
c)
d)
increased content of water in the organism
reduced osmotic preassure in plasma
reduced of oncotic preassure in plasma
increased osmotic preassure in plasma
11. Clinical onset of hyperhydration includes:
a)
b)
c)
d)
increased blood pressure
decreased blood pressure
increased size of heart
decreased size of heart
12. Diabetes insipidus is characrerized by:
a)
hyperosmolar hyperhydration
b)
hypoosmolar hyperhydration
c)
isosmolar hyperhydration
d)
hyperosmolar hypohydration
13. What kind of urine osmolarity is often observed in diabetes insipidus?
a)
b)
c)
hypertonic
hypotonic
isotonic
14. The symptoms of hypotonic (hypoosmolaric) overhydration are:
a)
b)
c)
d)
vomiting
thirst
dryness of skin
convulsions
15. The signs of hypotonic (hypoosmolaric) dehydration are:
a)
b)
c)
d)
vomiting
thirst
increase blood pressure
decrease diuresis
16. Which medicine should be used for treatment of hypotonic dehydration?
a)
b)
c)
d)
0,9 % NaCl
2 % NaCl
5 % glucosae
10 % albumen
17. The symptoms of hypertonic overhydration are:
a)
b)
c)
d)
vomiting
thirst
convulsion
increase diuresis
18. Hypertonic overhydration is the increased concentration of electrolytes in:
a)
cells
b)
plasma
c)
intercellular sector
d)
all water sectors
19. Hypotonic overhydration – is decreased concentration of electrolytes in:
a)
b)
c)
d)
plasma
cells
intercellular sector
all water sectors
20. Which medicine should be used for treatment of isotonic dehydration?
a)
b)
c)
d)
0,9 % NaCl
plasma
3 % NaCl
10 % albumen
21. Which medicine should be used for treatment of hyperosmolar dehydration?
a)
b)
c)
d)
e)
0,9% NaCl
plasma
2 % NaCl
5 % glucosae
10 % albumen
22. Lack of aldosterone leads to:
a)
b)
c)
d)
increas of potassium concentration in blood
increas of sodium concentration in blood
decrease of potassium concentration in blood
decrease of sodium concentration in blood
23. How is water conent changed during hypoaldosteronism?
a)
b)
c)
it is increased
it is decreased
it isn’t changed
24. How is water conent changed during increased synthesis of vasopressin?
a)
it is increased
b)
it is decreased
c)
it isn’t changed
25. What disorders are characterized by tetany?
a)
b)
c)
hypomagnesemia
hypercalcemia
hypocalcemia
26. What influence does parathormone perform on the calcium and phosphorus
contentin in the blood?
a)
b)
c)
d)
calcium increasing
phosphorus increasing
calcium decreasing
phosphorus decreasing
27. Excess of aldosterone leads to:
a)
b)
c)
d)
hyperpotassemia
hypopotassemia
hypernatremia
hyponatremia
28. Natriuretic hormone promotes:
a)
b)
c)
dehydration
excretion of sodium and water
lowering of blood pressure
29. Which hormones can regulate water-electrolyte metabolism in organism?
a)
b)
c)
d)
aldosterone
vasopressin
tymaline
natriuretic hormone
30. Which hormones can save electrolytes in organism?
a)
b)
c)
d)
aldosterone
antidiuretic hormone
natriuretic hormone
desoxicorticosteron
31. Which hormones can save water in organism?
a)
b)
c)
d)
testosterone
antidiuretic hormone
corticosterone
natriuretic hormone
32. Water poisoning – is a consequence of:
a)
b)
c)
hyperosmolar overhydration
hypoosmolar overhydration
isoosmolar overhydration
33. What reasons can lead to increased synthesis of aldosterone?
a)
b)
c)
d)
increased blood pressure
increased synthesis of angiothensine
increased osmolar pressure in blood
decreased blood pressure
34. Diabetes mellitus leads to:
a)
b)
c)
d)
hyperosmic overhydration
hypoosmic overhydration
isoosmic overhydration
hyperosmic dehydration
35. The causes of diabetes insipidus are:
a)
b)
c)
d)
low level of sugar in blood
lack of vasopressin
lack of insuline
excess of insuline
36. What osmolarity in urine is generally observed during diabetes mellitus?
a)
b)
c)
hypertonic
hypotonic
isotonic
37. What factors lead to oedema?
a)
increased oncotic pressure in blood
b)
increased vascular permeability
c)
increased hydrostatic pressure in capillaries
d)
increased outflow of limph
38. The water content in organism during hyperaldosteronism is:
a)
b)
c)
increased
decreased
nto changed
39. In diabetes insipidus the concentration of electrolytes is:
a)
b)
c)
increased
decreased
not changed
40. Thirst is a symptom of:
a)
b)
c)
d)
hyperosmic overhydration
hypoosmic overhydration
hyperosmic dehydration
hypoosmic dehydration
41. What disorders lead to muscular hypotonia?
a)
b)
c)
d)
hypernatremia
hyponatremia
hypercalcemia
hypocalcemia
Answers:
1a, 2d, 3e, 4d, 5a, 6d, 7b, 8ac, 9bd, 10d, 11ac, 12d, 13b, 14ad, 15ad, 16bd, 17bd,
18bc, 19aс, 20ab, 21d, 22ad, 23b, 24a, 25aс, 26ad, 27bc, 28bc, 29abd, 30ad, 31ab,
32b, 33bd, 34d, 35b, 36a, 37bc, 38a, 39a, 40ac, 41bc.
DISORDERS OF ACID-BASE BALANCE
Tests
1. The normal рН range of venous blood is:
a)
b)
c)
d)
7,32 – 7,42
7,0 – 7,45
7,35 – 7,7
6,9 – 7,35
2. Acid-base balance is regulated by:
a)
b)
c)
d)
e)
buffer systems
kidneys function
lungs function
heart function
brain function
3. Buffer system consists of:
a)
b)
c)
weak acid and weak base
weak acid and strong base
weak acid and salt that synthesized by this acid and strong base
4. What buffer takes part in acidogenesis?
a)
b)
c)
d)
protein
phosphate
hemoglobine
acetate
5. In increased [H+] in blood lungs regulate acid base balance by:
a)
b)
c)
hyperventilation
hypoventilation
irregular ventilation
6. Increased pСO2 in the blood is the cause of:
a)
b)
c)
d)
respiratory acidosis
respiratory alkalosis
metabolic acidosis
metabolic alkalosis
7. Decreased pСO2 in the blood is the cause of:
a)
b)
c)
d)
respiratory acidosis
respiratory alkalosis
metabolic acidosis
metabolic alkalosis
8. Decreased buffer base (BB) is the cause of:
a)
b)
c)
d)
respiratory acidosis
respiratory alkalosis
metabolic acidosis
metabolic alkalosis
9. BB and base excess (BE) have no changes in:
a)
b)
c)
d)
respiratory acidosis
respiratory alkalosis
metabolic acidosis
metabolic alkalosis
10. The causes of respiratory acidosis are:
a)
b)
c)
d)
hypoventilation
hyperventilation
expansion of dead space
increased concentration of СО2 in air
11. The causes of metabolic acidosis are:
a)
b)
c)
d)
e)
hypoventilation
hyperventilation
expansion of dead space
vomiting
diarrhoea
12. The causes of metabolic acidosis are:
a)
b)
c)
d)
diabetes mellitus
hypoxia
diabetes insipidus
administration of chlorides
13. The causes of absolute metabolic alkalosis are:
a)
b)
c)
d)
diabetes insipidus
vomiting
intake of bacing soda
intravenous administration of sodium bicarbonate
14. Excess of aldosterone results in:
a)
b)
c)
d)
respiratory acidosis
respiratory alkalosis
metabolic acidosis
metabolic alkalosis
15. Lack of aldosterone leads to:
a)
b)
c)
d)
respiratory acidosis
respiratory alkalosis
metabolic acidosis
metabolic alkolosis
16. What disorder of actual buffer base (ABB) is characterized by tetany due to
decreased level of Ca++ in blood:
a)
b)
c)
d)
respiratory acidosis
respiratory alkalosis
metabolic acidosis
metabolic alkalosis
17. Acidosis is lowering of venous blood рН below:
a)
b)
7,05
7,15
c)
d)
7,25
7,32
18. Phosphate buffer consists of:
a)
b)
c)
d)
e)
carbonic acid
carbonic gas
acetic acid
monosubstituted sodium phosphate
twice-substituted sodium phosphate
19. Enzyme carbonic anhydrase is necessary in kidneys for:
a)
b)
c)
d)
acidogenesis
ammoniagenesis
reabsorption of bicarbonate
reapsorption of glucosae
20. Main mechanisms in ABB regulation in kidneys are:
a)
b)
c)
d)
e)
acidogenesis
reabsorption of bicarbonate
reabsorption of chlorides
excretion of bicarbonate
ammoniagenesis
21. Reaction of deamination of amino acids takes part in:
a)
b)
c)
acidogenesis
ammoniagenesis
reabsorption of bicarbonate
22. The increase of pСO2 is a compensation of:
a)
b)
c)
d)
respiratory acidosis
respiratory alkalosis
metabolic acidosis
metabolic alkalosis
23. Decreased pСO2 is a compensation of:
a)
b)
c)
d)
respiratory acidosis
respiratory alkalosis
metabolic acidosis
metabolic alkalosis
24. Increased level of BB is the sign of:
a)
b)
c)
d)
respiratory acidosis
respiratory alkalosis
metabolic acidosis
metabolic alkalosis
25. The cause of respiratory alkalosis is:
a)
b)
c)
d)
hypoventilation
hyperventilation
extension of dead space
increased level of СО2 in air
26. The causes of metabolic alkalosis are:
a)
b)
c)
d)
hyperventilation
vomiting
diarrhoea
intake baking soda
27. The causes of metabolic acidosis are:
a)
b)
c)
d)
diarrhoea
diabetes insipidus
hypoxia
vomiting
28. The causes of relative metabolic alkalosis are:
a)
b)
c)
d)
diarrhoea
diabetes mellitus
excess intake of baking soda
vomiting
29. Metabolic disorders of ABB result in the changing of:
a)
b)
c)
d)
pСО2
aсtual bicarbonate
BB
BE, BD
Answers:
1a, 2abc, 3c, 4b, 5a, 6a, 7b, 8c, 9ab, 10acd, 11e, 12abd, 13cd, 14d, 15c, 16bd, 17d,
18de, 19abc, 20abe, 21b, 22d, 23c, 24d, 25b, 26bd, 27ac, 28d, 29сd.
PATHOLOGY OF VITAMINES METHABOLISM
Tests
1.
a)
b)
c)
d)
What vitamins are water-soluble ones?
В1
В2
А
D
2.
a)
b)
c)
d)
e)
What vitamins are fat-soluble ones?
А
В6
В12
D
Е
3.
a)
b)
c)
d)
e)
Vitamines with antioxidative properties are:
В1
В12
А
Е
С
4.
a)
b)
c)
d)
e)
The reason of disease beriberi is deficiency of vitamin:
А
D
В1
В5
В6
5.
a)
b)
c)
d)
e)
The cause of pellagra is deficiency of vitamin:
А
D
В1
В5
РР
6.
a)
b)
c)
d)
e)
Lack of what vitamin leads to megaloblastic anemia?
А
D
В1
С
В12
7.
a)
b)
c)
d)
e)
The cause of rachitis is deficiency of vitamin:
А
D
В1
С
В12
8.
a)
b)
c)
d)
e)
The reason of haemorrhagic syndrome is deficit of vitamin:
В1
В6
Е
С
К
9.
a)
b)
c)
d)
e)
The cause of scorbutus is deficiency of vitamin:
А
С
В1
В6
Е
10. The signs of scorbutus are:
a)
bruise
b)
trombosis
c)
infectious disease
d)
hyperglycemia
e)
hyperazotemia
11. The signs of disease beriberi are:
a)
neuritis
b)
trombosis
c)
cardiac failure
d)
hyperglicemia
e)
hyperazotemia
12. Deficiency of vitamin B2 is characterized by:
a)
angular stomatitis
b)
trombosis
c)
cardiac failure
d)
conjunctivitis
e)
hyperazotemia
13. Clinical manifestations of deficiency of vitamin B6 are:
a)
dermatitis
b)
c)
d)
deficit of nicotinic acid
cardiac failure
conjunctivitis
14. Deficiency of vitamin B6 is characterized by the disorder of:
a)
transamination
b)
decarboxylation
c)
formation of prothrombinase
d)
fibrinolysis
e)
glicogenesis
15. Clinical manifestations of vitamin B12 deficit are:
a)
anemia
b)
cholelythiasis
c)
disorder movements coordination
d)
involvement of gastrointestinal tract
e)
icterus
16. Coenzyme forms of vitamin B12 are:
a)
methylcobalamin
b)
adenosilcobalamin
c)
tetrahydrobiopterin
17. The reason of nervous system disorder in vitamin B12 deficiency is the deficit
of:
a)
methylcobalamin
b)
adenosilcobalamin
c)
tetrahydrobiopterin
18. The cause of anemia in vitamin B12 deficiency is the deficit of:
a)
methylcobalamin
b)
adenosilcobalamin
c)
tetrahydrobiopterin
19. The reason of gastrointestinal tract disturbance in vitamin B12 deficiency is
the deficit of:
a)
methylcobalamin
b)
adenosilcobalamin
c)
tetrahydrobiopterin
20. The signs of folic acid insufficiency are:
a)
anemia
b)
f)
c)
d)
cholelythiasis
disorder movements coordination
involvement of gastrointestinal tract
icterus
21. Nicotinic acid deficiency leads to:
a)
pellagra
b)
anemia
c)
scorbutus
d)
beriberi
e)
homocysteinemia
22. Signs of pellagra are (3):
a)
icterus
b)
diarrhea
c)
dermatitis
d)
steatorrhea
e)
dementia
23. Coenzyme form of nicotinic acid is:
a)
nicotinamide adenine dinucleotide
b)
coenzyme А
c)
methylcobalamin
24. Coenzyme form of pantothenic acid is:
a)
nicotinamide adenine dinucleotide
b)
coenzyme А
c)
methylcobalamin
25. Lack of vitamin D leads to:
a)
pellagra
b)
rachitis
c)
scorbutus
d)
beriberi
e)
homocysteinemia
26. Deficit of vitamin А leads to:
a)
pellagra
b)
hyperkeratosis
c)
visual impairment
d)
beriberi
e)
homocysteinemia
27. Where does the synthesis of the most active metabolite of vitamin D3 occur:
a)
liver
b)
c)
kidney
scin
28. The signs of rachitis are:
a)
muscular hypotonia
b)
muscular hypertonia
c)
osteomalacia
d)
bones fragility
29. Clinical onset of vitamin E deficit is:
a)
icterus
b)
ketonemia
c)
abnormalities of spermatigenesis
d)
spontaneous abortions
e)
haemorrhagic disease of newborn
30. Signs of vitamin К deficiency are:
a)
icterus
b)
haemolytic disease of newborn
c)
sterility
d)
haemorrhagic disease of newborn
Ansews:
1ab, 2ade, 3сde, 4c, 5e, 6e, 7b, 8de, 9b, 10ac, 11ac, 12ad, 13ab, 14 ab, 15 acd,
16ab, 17b, 18a, 19a, 20ad, 21a, 22bce, 23a, 24b, 25b, 26bc, 27b, 28ac, 29сd, 30d.
CELL PATHOLOGY
Tests:
1. Shortage of cytochromes c is the cause of:
a)
b)
c)
d)
e)
Damages in genetic system of a cell
Disturbances of implementation of genetic program in a cell
Abnormalities of ATP synthesis
Disorder of ATP transport
Disorder of ATP consumption
2. The cause of abnormalities in supply of energy is damage of:
a)
b)
c)
d)
e)
mitochondrione
lysosome
peroxisome
rough endoplasmatic reticulum (ER)
agranular endoplasmatic reticulum ER
3. The deficit of kreatine leads to:
a)
b)
c)
damage of ATP synthesis
damage of ATP transport
disorder of consumption ATP
4. Shortage of carnitine leads to:
d)
e)
f)
damages of ATP synthesis
damages of ATP transport
disorder of consumption ATP
5. The causes of insufficiency in synthesis of ATP are lack of:
a)
b)
c)
d)
oxygen
kreatine
glucosae
G protein
6. The causes of insufficiency in ATP transport are lack of:
a)
b)
c)
d)
oxygen
kreatine
carnitine
G protein
7. Damage of mitochondrions leads to:
a)
b)
c)
d)
disturbances of energy synthesis
disturbances of the mechanisms of genetic programme realization
transcription abnormalities
translation abnormalities
8. Inhibition of oxidative phosphorylation leads to disorder of:
a)
b)
c)
synthesis of energy
storage of genetic information
cellular interaction
9. Injury of mitochondria leads to:
a)
b)
c)
d)
activation of apoptosis
disturbances of the mechanisms of the realization of the genetic program
abnormalities of replication
disorder of cellular interaction
10. Injury of cell membrane leads to:
a)
b)
c)
d)
e)
disturbances of energy synthesis
activation of apoptosis
imbalance of ion and water in the cell
disturbances of the mechanisms of genetic program realization
disturbances of signals translation
11. The cause of disturbance of genetic program of the cell is damage of:
a)
b)
c)
d)
e)
nuclei
lysosomes
peroxysome
rough ER
agranular ER
12. The cause of water and ions imbalance in the cell is injury of:
a)
b)
c)
d)
e)
nuclei
ribosome
peroxysome
cell membrane
agranular ER
13. The cause of abnormalities reception is damage of:
a)
b)
c)
d)
e)
mitochondrion
lysosome
peroxysome
cell membrane
agranular ER
14. The cause of oxydative stress is prevalence of:
a)
b)
oxydantes in antioxydantes
antioxydantes in oxydantes
15. Oxydative strees leads to:
a)
b)
c)
disorder of replication
increasing antioxidant protection in the cell
increase of cell permeability
16. Damage of DNA leads to:
a)
b)
c)
d)
edema of the cells
abnormalities reception
genetic apparatus of the cell
realization of genetic program
17. The cause of intracellular edema is:
a)
b)
c)
d)
activation of apoptosis
disturbances of the mechanisms of the realization of the genetic programme
disorder of replication
damage of ion channel
18. Injury of rough ER leads to:
a)
b)
c)
d)
decreased synthesis of protein
decaresed synthesis of lipids
disturbances of fluid balance of the cell
decreased carbohydrate synthesis
19. Injury of rough ER leads to:
a)
b)
c)
abnormalities level of calcium in the cytosole
water imbalance in the cell
reduction of antioxidant protection in the cell
20. Damage of the agranular ER leads to:
a)
b)
c)
disturbances of the calcium level in the cytosol
decreasing of the detoxication processes
water imbalance in the cell
21. Injury of the agranular ER leads to:
a)
b)
c)
decrease of protein synthesis
water imbalance in the cell
decarese of carbohydrate synthesis
22. Conciquences of the damage of Golgi complex are:
a)
b)
c)
abnormalities of synthesis
disorder of transport of substances
disorder of detoxication
23. «Storage diseases» is the result of injury of the:
a)
b)
c)
d)
e)
nuclei
lysosome
peroxysome
cell membrane
agranular ER
24. Decreased activity of katalase is the result of injury of the:
a)
nuclei
b)
c)
d)
e)
lysosome
peroxysome
cell membrane
agranular ER
25. Zellweger syndrom is the result of damage of:
a)
b)
c)
d)
e)
nuclei
lysosome
peroxysome
cell membrane
agranular ER
26. The cause of chronic inflammation of respiratory tracts is the damage of:
a)
b)
c)
d)
e)
nuclei
microtubule
peroxysome
cell membrane
agranular ER
27. The cause of non-insulin-dependent diabetes mellitus is abnormalities of:
a)
b)
c)
d)
processes of cellular signalling
synthesis of insuline
cellular distribution of water and ions
cell receptors
28. The cause of disturbances of realization of postreceptors mechanisms is
imbalance of:
a)
b)
c)
d)
calcium ions
diacylglycerol
interferone
epidermal growth factor
29. The main effector molecules in apoptosis are:
a)
b)
c)
d)
cytochrome с
domain of death
caspase
endonuclease
30. Insufficiency of apoptosis leads to:
a)
b)
c)
d)
tumors
AIDS
alzheimer's disease
autoimmune disease
31. The excess of apoptosis leads to:
a)
b)
c)
d)
tumors
AIDS
alzheimer s disease
autoimmune disease
Answers:
1c, 2a, 3b, 4a, 5ac, 6b, 7a, 8a, 9a, 10ce, 11a, 12d, 13d, 14a, 15aс, 16cd, 17d, 18a,
19a, 20b, 21с, 22ab, 23b, 24c, 25с, 26bc, 27ad, 28ab, 29cd, 30a, 31bcd.
HYPOXIA. HYPEROXIA
Tests:
1.
Hypoxia is a condition, in which tissues:
a) receive insufficient amount of oxygen
b) do not receive oxygen at all
c) receive increased amount of oxygen
2.
Hypoxemia – is a reduction:
a) of oxygen in tissues
b) PaO2 in blood
c) alveolar ventilation
3.
Blood oxygen capacity is:
a) maximal amount of oxygen, which can connect 100 ml of blood in oxygen
complete Hb saturation
b) contained in blood oxygen amount
c) dissolved in plasma oxygen amount
4.
Arterial blood oxygen capacity is:
a) 19-20 vol.%
b) 15-17 vol.%
c) 25-30 vol.%
5.
in:
а)
b)
с)
To determinate blood oxygen capacity we have Hb amount in g% multiply
1,34
2,34
3,4
6.
Healthy man arterio-venous difference in oxygen is:
a) 5 – 6 vol.%
b) 8 – 10 vol.%
c) 10 – 12 vol.%
d) 2 – 4 vol.%
7.
a)
b)
c)
Arterial blood oxyhemoglobin content is:
96 %
65-70 %
80 %
8.
Venous blood oxyhemoglobin content is
a) 96 %
b) 65-70 %
c) 80 %
9.
Blood oxygen capacity value depends on:
a) Hb quantity and quality
b) red blood cells amount
c) alveolar air oxygen content
10. Oxygen sufficiency of organism is characterized by:
a) O2 amount absorbed during period of unit time
b) partial pressure of O2 in arterial blood
c) partial pressure of O2 in venous blood
11. Arterial blood oxygen content is:
a) 18-20 vol.%
b)
10-14 vol.%
c) 25-30 vol.%
12. Venous blood oxygen content is:
a) 19 vol.%
b) 14 vol. %
c) 25 vol. %
13. Cyanosis appears in arterial blood when content of oxygen is:
a) 10 vol.%
b) 12 – 13 vol.%
c) 18 – 20 vol.%
14. Cyanosis appears in blood increase of:
a)
b)
c)
d)
reduction of Hb
methemoglobin
oxyhemoglobin
carboxihemoglobin
15. Hypercapnia – is:
a) increase of paCO2 more than 44 mmHg
b) decrease of paCO2 less than 40 mmHg
c) increase of pvCO2 more than 42 mmHg
16. Hypocapnia – is:
a)
increase of paCO2 more than 40 mmHg
b)
decrease of paCO2 less than 36 mmHg
c)
decrease of pvCO2 less than 44 mmHg
17.
a)
b)
c)
d)
Standart arterial blood pСО2 is:
40 mmHg
90 mmHg
50 mmHg
60 mmHg
18. What kind of hypoxia caused by pulmonary gas exchange disturbance:
a)
exogenic
b) respiratory
c)
hemic
d) tissue
19.
a)
b)
c)
d)
What pathogenic factor leads to exogenous hypoxia?
decreased paO2 in inspiratory air
respiratory failure
poisoning of carbon monoxide
cyanide poisoning
20. Circulatory hypoxia reasons are:
a) heart failure
b) circulatory collapse
c)
d)
respiratory failure
cyanide poisoning
21.
a)
b)
c)
The mechanism of circulatory hypoxia is:
decreased blood velocity
blood oxygen capacity decrease
inspiratory air oxygen partial pressure decrease
22.
a)
b)
c)
d)
e)
The reasons of hemic hypoxia:
decreased blood velocity
blood oxygen capacity decrease
inspiratory air oxygen partial pressure decrease
hemorrhage
nitrits poisoning
23. The reason of primary tissue hypoxia is decrease of:
a)
blood oxygen capacity
b)
inspiratory air oxygen partial pressure
c)
respiratory enzymes activity
24. Oxygen arterio-venous difference in primary tissue hypoxia is:
a) unchanged
b) increased
c) decreased
25. Dissociation of HbO2 in right-side shift of dissociation curve is:
a)
increased
b)
decreased
c)
unchanged
26. Dissociation of HbO2 in left-side shift of dissociation curve is:
a)
increased
b)
decreased
c)
unchanged
27. Factors of right-side shift of dissociation curve are:
a)
temperature decrease
b)
c)
d)
e)
alkalosis
temperature increase
acidosis
hypercapnia
28. Factors of left-side shift of dissociation curve are:
a)
temperature decrease
b)
hypocapnia
c)
temperature increase
d)
acidosis
29. Frequent mechanisms of hypoxia compensation are:
a)
hyperventilation
b)
tachycardia
c)
blood coming out from depo
d)
hemopoiesis intensification
30. What kind of breathlessness occurs during bronchial asthma?
a) expiratory
b) inspiratory
31. Hypobaric hypoxic hypoxia is characterized by:
a)
decrease of general atmospheric pressure
b)
decrease of partial pressure of oxygen in closed rooms
32. Hypoxia development mechanism in CO poisoning:
a)
methemoglobin formation
b)
carboxyhemoglobin formation
c)
cytochrome oxidase inhibition
33. Hypoxia development mechanism at nitrite/nitrate poisoning:
a)
methemoglobin formation
b)
carboxyhemoglobin formation
c)
cytochrome oxidase inhibition
34. Hypoxia development mechanism at cyanide poisoning:
a)
methemoglobin formation
b)
carboxyhemoglobin formation
c)
cytochrome oxidase inhibition
35. Hypoxia type at cyanide poisoning is:
a)
respiratory
b)
hemic
c)
tissuer
d)
hypoxic
36. Hypoxia type at CO poisoning is:
a)
respiratory
b)
hemic
c)
tissue
d)
circulatory
37. During adaptation to hypoxic hypoxia the breathing is:
a)
deep and frequent
b)
deep and rare
c)
superficial and frequent
d)
superficial and rare
38. During adaptation to hypoxia haemodynamic changes are:
a)
tachycardia
b)
increased cardiac output
c)
decreased cardiac output
d)
bradycardia
39. Long term mechanisms of adaptation to hypoxic hypoxia include:
a)
increased hemoglobin oxygen affinity
b)
decreased hemoglobin oxygen affinity
c)
intensification of hemopoiesis
d)
suppression of hemopoiesis
40. Which hypoxia is characterizied by increased oxygen arterio-venous
difference?
a)
hemic
b)
circulatory
c)
respiratory
d)
tissue
41. What kind of hypoxia is characterized by essentially decreased arteriovenous difference by oxygen?
a)
b)
hemic (blood-depended)
circulatory
c)
d)
respiratory
tissue
42. What disturbance of acid-base balance occurs in initial phase of mountain
illness?
a)
b)
c)
d)
respiratory acidosis
respiratory alkalosis
metabolic acidosis
metabolic alkalosis
43 Formation of what substance is faster?
a)
b)
oxyhemoglobin
carboxyhemoglobin
44. Which gas is used in gas mixture with oxygen for prevention of kessone
disease?
a)
carbon monoxide
b)
helium
c)
carbon dioxide
d)
nitrogen
45. What happens during kessone disease (decompression)?
a)
b)
c)
d)
cytochrome oxidase inhibition
formation of nitrogen bubbles in the vessels
formation of carboxyhemoglobin
methemoglobin formation
46.
How is the blood oxygen capacity changed during chronic
exogenous hypoxia?
a)
it is decreased
b)
it is unchanged
c)
it is increased
47.
a)
b)
c)
How is called hypoxia caused by blood circulation disturbances?
circulatory hypoxia
hemic hypoxia
respiratory hypoxia
ROLE OF HEREDITY IN PATHOLOGY
Tests:
1.
a)
b)
c)
Karyotype is:
complex of all genes in the organism
full number of chromosomes in somatic cells
complex of all signs in the organism
2.
a)
b)
c)
d)
Factors causing heredity diseases are called:
teratogens
mutagens
carcinogens
flogogens
3.
a)
b)
c)
d)
e)
Biological mutagens are:
viruses
microorganisms
food supplements
oil products
organic solvent
4.
a)
b)
c)
d)
e)
Chemical mutagens are:
microorganisms
pesticides
nitrites, nitrates
radioactive elements
ultraviolet radiation
5.
a)
b)
c)
6.
a)
b)
c)
d)
Genomic mutations are characterized by:
numeric abnormalities of chromosome
changing of chromosome structure
changing of structure of gens
Genomic mutations lead to:
duplication of chromosome number
appearance of additional chromosomes in genotype
duplication of the chromosome segment
deletion of the chromosome segment
7.
a)
b)
c)
d)
Consequences of gens mutations are:
abnormal protein synthesis
malformation of heart
disorder of the structure of erythrocyte membrane
decreasing of chromosome number
8.
a)
b)
Mutations that lead to mosaicism occur in:
somatic cells
gametes
9.
a)
b)
c)
What mutations lead to chromosomal diseases?
gene
chromosomal
genomic
10.
a)
b)
c)
What mutations lead to gene diseases?
gene
chromosomal
genomic
11.
a)
b)
c)
d)
Chromosome mutations are:
deletion
polyploidy
trisomy
translocation
12.
a)
b)
c)
d)
Autosomal dominant disorders are:
phenylketonuria
Marfan syndrome
haemophilia А
Huntington chorea
13.
a)
b)
c)
d)
Autosomal dominant disorders are characterized by:
the fact that every child has one chance per two to have the disease
presence of affected children in every generation
the fact that affected are only females
the fact that the recurrence risk is 25% for each birth
14. Autosomal recessive disorders are:
a)
b)
c)
d)
alkaptonuria
hemophilia А
Marfan syndrome
daltonism
15.
a)
b)
c)
d)
Autosomal recessive disorders are characterized by:
the fact that the recurrence risk is 100% for each birth
phenotypically healthy parents
the fact that siblings have one chance per four to be affected
the fact that affected are only females
16.
a)
b)
c)
d)
X-linked recessive disorders are:
daltonism
alkaptonuria
tyrosinosis
hemophilia А
17. X-linked recessive disorders are characterized by:
a)
the fact that both males and females are affected
b)
healthy parents
c)
Ill parents
d)
the fact that affected are only females
18.
a)
b)
c)
d)
Codominant disorders are:
hemophilia В
tyrosinosis
lactase deficiency
sickle-cell anemia
19.
a)
b)
c)
Y-linked disorders are characterized by:
transmission of the disease to sons
transmission of the disease to daughters
the fact that both males and females are affected
20.
a)
b)
c)
Sex-linked disorders are:
hemophilia В
galactosemia
six-fingered
d)
hypertrichosis of ears
21.
a)
b)
c)
d)
Diseases caused by mutation in mitochondrial genes are characterized by:
the fact that both males and females are affected
the fact that only mothers transmit the mitochondrial genes
the fact that only fathers transmit the mitochondrial genes
the fact that the mutation is transmited only to daughters
22.
a)
b)
c)
d)
Karyotype 45, ХО is:
Down syndrome
Turner syndrome
cri du cat syndrome
Patau syndrome
23.
a)
b)
c)
d)
e)
Karyotype 48, ХХХY is:
Patau syndrome
Edwards syndrome
Down syndrome
Klinfelter syndrome
Turner syndrome
24.
a)
b)
c)
d)
e)
Karyotype 47, ХХХ characterized by:
male phenotype
female phenotype
mental retardation
normal mentation
sexual retardation
25.
a)
b)
c)
d)
The karyotype of Down syndrome is:
47, ХХ (13)
47, ХY (18)
45, ХО
47, ХY (21)
26.
a)
b)
c)
d)
The karyotype for Patau syndrome is:
47, ХХ (13)
47, ХY (18)
45, ХО
47, ХY (21)
27.
a)
b)
c)
d)
The karyotype for Edwards syndrome is:
47, ХХ (13)
47, ХY (18)
45, ХО
47, ХY (21)
28.
a)
b)
c)
d)
Down syndrome is characterized by:
the fact that only males are affected
mental retardation
tall stature
pterygium colli
29.
a)
b)
c)
d)
Patau syndrome is characterized by:
tall stature
internal malformations
the fact that patients die before the age of 1
increased level of phenyl pyruvate in the blood
30.
a)
b)
c)
d)
Turner syndrome is characterized by:
pterygium colli
short stature
male phenotype
simian crease in palm
31.
a)
b)
c)
d)
Klinefelter syndrome is characterized by:
pterygium colli
tall stature
male phenotype
gonadal dysgenesis
32.
a)
b)
c)
d)
Klinefelter syndrome is characterized by:
congenital heart defects
short stature
gynecomastia
low posterior hairline
33.
a)
b)
c)
Down syndrome results due to:
gen mutation
nondisjunction of sex chromosomes during meiosis
nondisjunction of 21 pair of chromosome during meiosis
d)
polyploidy
34.
a)
b)
c)
d)
Turner syndrome results from:
gen mutation
nondisjunction of sex chromosomes during meiosis
nondisjunction of 21 pair of chromosome during meiosis
polyploidy
Answers:
1b, 2b, 3ab, 4bc, 5a, 6ab, 7ac, 8a, 9bc, 10a, 11ad, 12bd, 13ab, 14a, 15bc, 16ad,
17b, 18d, 19a, 20ad, 21ab, 22b, 23d, 24be, 25d, 26a, 27b, 28b, 29bc, 30ab, 31bc,
32c, 33c, 34b.
EXTREME CONDITIONS. STRESS. SHOCK. COMA. COLLAPSE
Tests:
1. What conditions pertain to extremal state?
a)
b)
c)
d)
collapse
paralysis
coma
shock
2
a)
b)
c)
d)
What changes characterize hypovolemic shock?
increased blood volume
decreased blood volume
decreased cardiac output
increased vascular resistance
3. What changes characterize cardiogenic shock?
a)
b)
c)
d)
rapid, weak pulse
decrease of cardiac output
increase of vascular resistance
decrease of vascular resistance
4. Torpid phase of shock is characterized by:
a)
b)
c)
d)
fall down of arterial blood pressure
increased diuresis
loss of consciousness
crackles in the lungs
5. Burn shock is characterized by:
a)
b)
c)
d)
sharp pain reaction
intoxication by waste products
reduced arterial blood pressure
polyuria
6. What disturbances can be registered in anaphylactic shock?
a)
b)
c)
d)
expiratory dyspnea
reduced of blood pressure
increased blood pressure
inspiratory dyspnea
7. How does aggregation of erythrocytes change in shock?
a)
b)
c)
decreased
increased
unaffected
8. How does circulation time change in microvessels during shock?
a)
b)
c)
it is reduced
it is increased
it is unaffected
9. How is quantity of functional arteriovenous shunts changed in shock?
a)
b)
c)
it is decreased
it is increased
it is unaffected
10. The permeability of vessels in shock is:
a)
b)
c)
decreased
increased
unaffected
11. The blood supply of kidneys, intestines, muscles due to centralization of
blood is:
a)
b)
c)
reduced
increased
unaffected
12. Centralization of circulation during shock helps to:
a)
b)
c)
d)
reduce brain damage
prevent from ischemia skin and muscles
reduce liver damage
reduce heart damage
13. The negative consequences of centralization of blood circulation are:
a)
b)
c)
cerebral edema
increased overloading of heart
oliguria
14. What type of acid-base disturbances occur in torpid phase of shock?
a)
b)
c)
d)
metabolic acidosis
respiratory acidosis
metabolic alkalosis
respiratory alkalosis
15. What terminal condition is characterized by temporary cessation of
breathing?
a)
preagony
b)
terminal pause
c)
agony
16. Clinical death is characterized by:
a)
b)
c)
d)
absence of breathing
reversible changing in neurons of brain
irreversible changing in neurons of brain
shallow breathing
17. Clinical death is characterized by:
a)
b)
c)
d)
irreversible changing of neurons of brain
shallow breathing
fibrillation of heart
cessation of heartbeat
18. Biological death is characterized by:
a)
b)
c)
presence of breathing
presence of heart rate
irreversible changing of neurons of brain
19. Biological death is characterized by:
a)
b)
c)
d)
absence of heart beats
reversible changing of neurons of brain
absence of breathing
irreversible changing of neurons of brain
20. The succession of terminal condition are:
a)
b)
c)
predagony, terminal pause, agony
terminal pause, predagony, agony
predagony, agony, terminal pause
21. Phases of shock are:
a)
b)
c)
d)
erectile
latent
prodromal
torpid
22. Erectile phase of shock is characterized by:
a)
b)
c)
d)
centralization of blood circulation
decreased vascular tone
blood storage in depo
activation of central nervous system
23. Torpid phase of shoke is characterized by:
a)
b)
c)
d)
centralization of blood circulation
decreased vascular tone
loss of consciousness
activation of central nerouse system
24. Volume of blood circulation in torpid phase in traumatic shock is:
a)
b)
reduced
increased
25. Blood pressure in erectile phase in traumatic shock is:
a)
b)
reduced
increased
26. Collapse is characterized by:
a)
b)
c)
decreased vascular tone
centralization of blood circulation
reduced blood pressure
27. Coma is characterized by:
a)
b)
c)
loss of consciousness
presence of reflex to external irritants
normal vital functions of organism
28. Coma is characterized by:
a)
b)
c)
normal consciousness
absence of reflex to external irritants
disturbances of vital functions of organism
29. Ammonia has an important role in the development of:
a)
b)
c)
d)
ketoacidic coma
hypoglycemic coma
hepatic coma
hyperosmolar coma
30. High glucose level has pathogenic role in the development of:
a)
b)
c)
hyperosmolar coma
hypoglycemic coma
hepatic coma
Answers:
1аbd, 2bcd, 3abc, 4acd, 5abc, 6ab, 7b, 8b, 9b, 10b, 11a, 12ad, 13c, 14a, 15b, 16ab,
17d, 18c, 19асd, 20а, 21аd, 22аd, 23bс, 24а, 25а, 26аc, 27а, 28bс, 29с, 30а.
TUMOR GROWING
Tests
1.
a)
b)
c)
“Anaplasia" – is:
increase of tumor mass
high speed of proliferation of tumor cells
disorder in maturation of tumor cells
2.
a)
b)
c)
Glycolysis in tumor cells is:
increased
decreased
unchanged
3.
a)
b)
c)
Biosynthesis of nucleoacids in tumor cells is:
increased
decreased
unchanged
4.
a)
b)
c)
The type of regulation of tumor cell proliferation is:
endocrine
autocrine
paracrine
5.
a)
b)
c)
d)
Proliferation of tumor cells is caused by:
activation of onco-genes
activation of apoptosis
inactivation of suppressor-genes
disturbances in apoptosis
6.
a)
b)
c)
d)
The carbohydrate metabolism in tumor cells is characterized by:
activated glycogen syntesis
decreased glycolysis
increased glycolysis
increased glyconeogenesis
7.
a)
Lipid metabolism in tumor cells is characterized by:
increased lipolysis
b)
c)
increased phospholipid synthesis
decreased synthesis of fatty acids
8.
a)
b)
c)
d)
During kidney sarcoma the metastasis first of all occurs in:
liver
uterus
intestine
lungs
9.
a)
b)
c)
Antigens of tumor cells are characterized by:
normal structure
embryonic structure
specific structure
10.Malignant tumors are characterized by:
a) slow growth
b) absence of metastasis
c) autonomous growth
d) atypical cells
11.Benign tumors are characterized by:
a) slow growth
b) absence of metastases
c) presence of metastases
d) atypical cells
12. The stages of tumor growth are:
a)
b)
c)
d)
promotion
progression
translocation
inversion
13. The local effects of tumors are:
a)
b)
c)
d)
e)
bleeding
ileus
anemia
anorexia
endocrine changes
14. The common effects of tumors are:
a)
b)
c)
d)
e)
bleeding
ileus
anemia
anorexia
endocrine changes
15. Anticancerogenic factors are:
a)
b)
c)
d)
antioxidants
lymphocytes
glucose
ammonia
16. The mechanisms of anticancerogenic defense are:
a)
b)
c)
anti-cellular
anti-mutagenic
antibacterial
Answers:
1c, 2a, 3a, 4c, 5acd, 6c, 7b, 8d, 9b, 10ab, 11cd, 12ab, 13ab, 14cde, 15ab, 16ab.
RADIATION SICKNESS
Tests
1.
a)
b)
c)
What radiance possesses the greatest ionising ability?
α-irradiation
β-irradiation
γ-irradiation
2.
a)
b)
c)
Which of radiances possesses the greatest making through ability?
α-irradiation
β-irradiation
γ-irradiation
3.
a)
b)
c)
Which of radiances possesses the least ionising ability?
α-irradiation
β-irradiation
γ-irradiation
4.
a)
b)
c)
Which of radiances possesses the least making through ability?
α-irradiation
β-irradiation
γ-irradiation
5.
a)
b)
c)
d)
What blood cells are most sensitive to ionising radiation action?:
erythrocytes
neutrophils
basophils
lymphocytes
6.
What form of acute radiation sickness arises at irradiating of a person in
doses of 1-10 Gr?
a)
the marrowy
b)
the intestinal
c)
toxemic
d)
the cerebral
7.
What form of acute radiation sickness arises at irradiating of a person in
doses 10-20 Gr?
a)
the marrowy
b)
the intestinal
c)
toxemic
d)
the cerebral
8.
What form of acute radiation sickness arises at irradiating of a person in
doses 20-50 Gr
a)
the marrowy
b)
the intestinal
c)
toxemic
d)
the cerebral
9.
What form of acute radiation sickness arises at irradiating of a person in
doses more than 80 Gr?
a)
the marrowy
b)
the intestinal
c)
toxemic
d)
the cerebral
10. What changes of blood are characteristic of the marrowy form of sharp
radiation sickness in clinically expressed signs?
a)
reduction of quantity of leucocytes
b)
augmentation of quantity of leucocytes
c)
reduction of quantity of erythrocytes
11. What changes of blood are characteristic of the marrowy form of sharp
radiation sickness in clinically expressed signs?
a)
b)
c)
augmentation of the maintenance of erythrocytes
augmentation of the maintenance of thrombocytes
reduction of quantity of thrombocytes
12.
a)
b)
What organism is more sensitive to ionising radiation action?
the young
the mature
13. In what case action of a radioactive irradiating will be more pathogenic?
a)
b)
at the single exposition equal 400 rentgens
at the fractional irradiation, integrally compounding 400 rentgens
14. What cells are most affected in ionising radiation action?
a)
b)
c)
the mature
embrionic
not differentiated
15. In what case a cell radiosensitiveness of above?
a)
b)
at intensively going metabolism processes
at low intensity of a cellular metabolism
16. What part of a cell is more sensitive to radiation?
a)
a nucleus
b)
cytoplasm
17. Specify mechanisms of direct action of radiation in the irradiated medium:
a)
b)
c)
d)
ionisation of moleculas
damage by free radicals of chemical bonds
change of chemical constitution of DNA
formation lipids and chinone radio toxines
18. Specify mechanisms of the indirect (mediated) action of radiation in the
irradiated medium:
a)
b)
c)
d)
ionisation of moleculas
damage of chemical bonds by active forms of oxygen
change of chemical constitution of DNA
formation of lipids and chinone radio toxines
19. Specify the tissuers possessing high radio damage ability (3 answers):
a)
b)
c)
d)
e)
the lymphoid
the osteal
hemopoetic
the epithelial
nervous
20. Specify the tissuers possessing low radiodamage ability:
a)
b)
c)
d)
e)
the lymphoid
the osteal
hemopoetic
the epithelial
nervous
21. What is characteristic of the 1st period of acute radiation sickness?
a)
b)
c)
d)
a headache
a nausea, vomiting
hemorrhages in an internal organs
absence of visible clinical exhibitings of disease
22. What is characteristic of the 2nd period of acute radiation sickness?
a)
b)
c)
d)
hemopoiesis oppression
hemorrhages
absence of visible clinical exhibitings of disease
infectious diseases
23. What is characteristic of the 3rd period of acute radiation sickness?
a)
b)
c)
d)
infringement of liver function
hemorrhages in an internal
infringement of function of the excitatory nervous tissue
anaemia
24. Changes in blood in 1 period of acute radiation sickness
a)
b)
c)
d)
neutrophilic leukocytosis
agranulocytosis
a lymphopenia
a lymphocytosis
25. Changes in blood in 2 period of acute radiation sickness:
a)
b)
c)
leukocytosis
leucopenia
a lymphocytosis
26. Changes in blood in 3 period of acute radiation sickness:
a)
b)
c)
d)
leukocytosis
agranulocytosis
an anaemia
a thrombocytopenia
27. Manifestations of the 3rd period of acute radiation sickness
a)
b)
c)
d)
infectious complications
CNS excitation
bleedings
thrombosis
28. The haemorragic syndrome in acute radiation sickness is caused:
a)
b)
c)
d)
e)
decrease in quantity of thrombocytes
increase in quantity of thrombocytes
plasmin system activation
increase in ability of thrombocytes to aggregation
increase in permeability of vascular wall
29. Non-ionising radiances concern:
a)
b)
c)
d)
γ-beams
an invisible heat
β-particles
a visible part of a spectrum
30. Ionising radiation concerns:
a)
b)
c)
d)
β-particles
X-rays
an ultraviolet radiation
an infrared rays
31. What biological effects of an ultraviolet radiation are used with the medical
purpose?
a)
b)
c)
erythema
thermal action
bactericidal effect
d)
blastomogenic action
32. Manifestations of pathogenic action of UV radiation on organism.
a)
b)
c)
d)
a thermal shock
bactericidal effect
cancerogenic effect
mutagen action
Answers:
1a, 2c, 3c, 4a, 5d, 6a, 7b, 8c, 9d, 10ac, 11с, 12a, 13a, 14b, 15a, 16a, 17ac, 18bd,
19аcd, 20be, 21аb, 22аc, 23bd, 24аc, 25b, 26bсd, 27ac, 28ace, 29bd, 30ab, 31bd,
32ad.
SYSTEMIC PATHOPHYSIOLOGY
PATHOLOGY OF CIRCULATING BLOOD VOLUME. BLEEDING.
Tests:
1. Hematocrit in oligocythemic normovolemia:
a)
increases
b)
decreases
c)
is normal
2. Hematocrit in polycythemic normovolemia:
a) increases
b) decreases
c) is normal
3. Hematocrite in simple normovolemia:
a) increases
b) decreases
c) is normal
4. What kind of normovolemia leads to the increase of blood viscosity,
susceptibility to thrombosis?
a) simple
b) polycythemic
c) oligocythemic
5. In what normovolemia appeares anemia and hypoxia?
a) simple
b) olygocythemic
c) polycythemic
6. How is hematocrit changed in simple normovolemia?
a) it is increased
b) it is decreased
c) it has no changes
7. How is hematocrit changed in olygocytemic hypovolemia?
a) it is increased
a) it is decreased
b) it has no changes
8. How is hematocrit changed in simple hypovolemia?
a) it is increased
b) it is decreased
c) it has no changes
9. How is hematocrit changed in polycythemic hypovolemia?
a) it is increased
b) it is decreased
c) it has no changes
10. How is hematocrit changed in olygocytemic hypovolemia?
a) it is increased
b) it is decreased
c) it has no changes
11. Dehydration leds to:
a) olygocythemic hypovolemia
b) polycythemic hypovolemia
c) olygocythemic normovolemia
12. Excess entrance of water leads to
a) polycythemic normovolemia
b) olygocythemic hypervolemia
c) polycythemic hypovolemia
13.Chronic hypoxia results in:
a) olygocytemic hypervolemia
b) polycythemic normovolemia
c) polycythemic hypovolemia
14. Depression of the erythropoiesis leads to:
a) polycythemic normovolemia
b) polycythemic hypovolemia
c) olygocythemic normovolemia
15. Massive haemolysis of erythrocytes results in:
a) olygocythemic hypervolemia
b) polycythemic hypovolemia
c) olygocythemic normovolemia
16. Massive hemotransfusion leads to:
a) simple hypervolemia
b) olygocythemic hypervolemia
c) olygocythemic normovolemia
17. The causes of simple hypovolemia are:
a)
b)
c)
d)
e)
dehydration
hemorrhage (immediately after it)
erythremia
hemorrhage (in a few days)
massive introduction of plasma substitutes
18. The causes of polycythemic hypovolemia are:
a)
b)
c)
d)
e)
dehydration
massive haemolysis of erythrocytes
erythremia
anemia
hemorrhage
19. The causes of olygocythemic normovolemia are:
a) dehydration
b) tissue hypoxia
c) renal insufficiency
d) erythremia
e) haemolysis of erythrocytes
20. Polycythemic hypervolemia results from:
a)
b)
c)
d)
erythremia
dehydration
anemia
haemorrhage
21. Massive introduction of the isotonic solutions leads to:
a)
b)
c)
d)
e)
simple hypervolemia
polycythemic hypervolemia
olygocythemic hypervolemia
polycythemic hypovolemia
olygocytemic hypovolemia
22. The causes of simple hypovolemia are:
a) acute haemorrhage (in 30-40 minutes)
b) moderate haemorrhage (in 24 hours)
c) haemolysis of erythrocytes
23. What conditions lead to polycythemic hypovolemia?
a)
b)
c)
d)
extensive burns
overheating
water intoxication
erythremia
24. The causes of simple hypervolemia are:
a)
b)
c)
d)
massive blood transfusion
nephrotic disease
erythremia
intravenous introduction of salt solution
25. The causes of olygocythemic normovolemia are:
а) massive infusion of plasma substitute
b) moderate hemolysis of RBC
c) massive hemolysis of RBC
26. Hydremic phase of acute haemorrhage is characterized by:
а) simple hypovolemia
b) olygocytemic hypovolemia
c) olygocytemic normovolemia
d) simple hypervolemia
27. Reflectory phase of acute haemorrhage is characterized by:
а) simple hypovolemia
b) olygocythemic hypovolemia
c) olygocythemic normovolemia
d) simple hypervolemia
28. The reasons of polycythemic normovolemia are:
а) living in the hills
b) dehydration
c) decreased synthesis of erytropoethine
29. The reasons of simple hypervolemia are:
а) infusion of plasma substitute
b) blood transfusion
c) packed red cell transfusion
d) reduction of excretory function of the kidneys
30. The reasons of polycythemic hypervolemia are:
а) haemotransfusion
b) packed red cell transfusion
c) erythremia
d) infusion of polyglucine
31. The causes of olygocythemic hypervolemia are:
а) packed red cell transfusion
b) reduction of excretory function of the kidneys
c) haemotransfusion
d) excess of vasopressin
32. What phase of acute haemorrhage leads to simple hypovolemia?
а) reflex
b) hydremic
c) bone-marrow
33. The reasons of simple hypovolemia are:
а) lack of erythropoetin
b) haemorrhage
c) erythremia
34. The causes of polycythemic hypovolemia are:
а) erythremia
b) lack of vasopressine
c) packed red cell transfusion
35. The reasons of olygocythemic hypovolemia are:
а) diarrhea
b) aplasia of bone marrow
c) intravenous introduction of salt solution
36. The causes of olygocythemic hypovolemia are:
а) polyuria
b) living in the hills
c) lack of synthesis of erythropoetine
37. The first hours after acute haemorrhage are characterized by:
a) polycythemic hypovolemia
b) simple hypovolemia
c) olygocythemic hypovolemia
38. The second day after acute haemorrhage is characterized by:
a) polycythemic hypovolemia
b) olygocytemic (normovolemia) hypovolemia
c) olygocythemic hypervolemia
39. What is the reason of compensation in reflex phase of haemorrhage?
а) stimulation of baroceptor reflexogen regione
b) activation of sympathoadrenal system
с) decreased stroke volume
d) decreased peripheral resistance
40. What is the reason of adjustment of blood volume in haemorrhage?
а) spasm of the peripheral vessels
b) activation of blood coagulation system
c) decreased diuresis
d) redistribution of the water between sectors
41. What is the reason of normalization of blood preassure in reflectory
phase of haemorrhage?
а) output of blood from store
b) increased sympathetic influence of cor
c) stimulation of baroceptor reflexogen regione
d) activation of renin-aldosterone- angiothensin system
42. What is the reason of normalization of blood pressure at hydremic phase
of haemorrhage ?
а) activation of renin-aldosterone- angiothensin system
b) increased output of vasopressine
c) entrance water from intersticium to the vessels
d) centralization of blood circulation
43. The main links of pathogenesis of middle degree of haemorrhage are:
а) cells dehydration
b) disorder of microcirculation
c) disorder of oxygen transport function of hemoglobine
44. The reflex phase of acute haemorrhage is characterized by:
а) hyperventilation
b) bradycardia
c) appearance of young red blood cells in blood
d) tachycardia
45. The reflectory phase of acute haemorrhage is characterized by:
а) increased of the peripheral resistance
b) increased synthesis of angiotensine
c) increased synthesis of prothein
46. In what time after acute haemorrhage reticulocytosis will occur?
a)
b)
c)
d)
in 5-6 hours
in 4-5 days
in 24-48 hours
immediately after haemorrhage
47. Adaptive response in acute haemorrhage in few hours is:
a)
b)
c)
d)
decreased venous return
centralization of blood circulation
tissue hypoperfusion
hyperventilation
48. Factors of the severe consequences of the bleeding are:
a) female sex
b) newborn period
c) old age
d) slow velocity of the bleeding
49. Normal count of reticulocytes is:
a) 0-1 ‰
b) 2-12 ‰
c) 20-25 ‰
d) 25-50 ‰
50. Compensated hemorrhagic shock will occur in loss of:
а) 20-30 % blood volume
b) 30-40 % blood volume
c) > 40 % blood volume
51. Decompensated reversible hemorrhagic shock will occur in loss of:
а) 20-30 % blood volume
b) 30-40 % blood volume
c) > 40 % blood volume
52. The reason of hemorrhagic shock is loss of blood:
а) more than 10% blood volume
b) more than 30% blood volume
c) more than 20% blood volume
53. The torpid phase of hemorrhagic shock is characterized by:
а) unconscious
b) decreased blood preassure
c) excitement
d) increased cardiac output
e) multiple organ failure
54. The pathogenic factors of hemorrhagic shock are:
а) decreased blood pressure
b) decreased coronary circulation
c) increased venous return
d) increased blood viscosity
Answers:
1b, 2a, 3c, 4b, 5b, 6c, 7b, 8c, 9a, 10b, 11b, 12b, 13b, 14c, 15c, 16a, 17b, 18a,
19e, 20a, 21c, 22a, 23ab, 24a, 25b, 26bc, 27a, 28a, 29b, 30bc, 31bd, 32a, 33b, 34b,
35b, 36c, 37b, 38b, 39ab, 40cd, 41abc, 42abc, 43b, 44ad, 45ab, 46b, 47bd, 48bc,
49b, 50a, 51b, 52b, 53abe, 54abd.
ANEMIAS
Tests:
1. Content of reticulocytes in hemolytic anemia is:
a) 0-1 ‰
b) 2-12 ‰
c) 20-25 ‰
2. Sideropenic syndrome is the result of lack of:
a) copper
b) iron
c) vitamin B12
d) folic acid
3. Sideroachrestic anemia is the result of:
a) deficiency of copper
b) deficiency of iron
c) disturbance utilization of iron by cells
d) deficiency of folic acid
4. Mean corpuscular hemoglobin (МСН) in erythrocytes is:
a) 15,2-20,4 pg
b) 25,4-34,6 pg
c) 35,5-43,2 pg
5. Mean corpuscular hemoglobin (MCH) in iron deficiency anemia is:
a) 15,2-20,4 pg
b) 25,4-34,6 pg
c) 35,5-43,2 pg
6. Mean corpuscular hemoglobin (MCH) in vitamin B12 deficiency anemia is:
a) 15,2-20,4 pg
b) 25,4-34,6 pg
c) 35,5-43,2 pg
7. Destruction of erythrocytes in spleen is called:
a) erythropoiesis
b) erythrodiapedesis
c) erythrodieresis
8. The term «poikilocytosis» means:
a) RBCs with a normal content of hemoglobin;
b) abnormally shaped RBCs;
c) RBCs that are irregular in size.
9. Anisocytosis is the changing of:
a) shape of RBCs
b) size of RBCs
c) content of hemoglobin in RBCs
10. Anisochromia – is:
a) changing of erythrocyte's shape
b) changing of erythrocyte's size
c) different intensity of erythrocyte stain
11. In what anemia the color index is increased?
a) acute posthemorrhagic anemia
b) vitamin B12 deficiency anemia
c) chronic posthemorrhagic anemia
12. In what anemia the count of reticulocytes is reduced?
a) acute posthemorrhagic anemia
b) hemolytic anemia
c) aplastic anemia
13. In what anemia the count of reticulocytes is increased?
a) acute posthemorrhagic anemia
b) vitamin B12 deficiency anemia
c) aplastic anemia
14. Megaloblastic anemia is:
a) chronic posthemorrhagic anemia
b) folic acid deficiency anemia
c) aplastic anemia
d) hemolytic anemia
15. In what anemia RBCs contain abnormal hemoglobin:
a) thalassemia
b) iron deficiency anemia
c) folic acid deficiency anemia
16. Syntesis of hemoglobin S is representative for:
a) thalassemia
b) sickle-cell anemia
c) ellyptocytosis
17. Decreasing activity of what enzyme of RBCs leads to hemolytic anemia
due to deficiency of ATP?
a) dehydrogenase glucose 6-phosphate
b) sodium-potassium ATPase
c) pyruvate kinase
18. Decreasing activity of what enzyme of RBCs leads to hemolytic anemia due to
oxidative stress?
a) dehydrogenase glucose 6-phosphate
b) pyruvate kinase
c) hexokinase
19. Abnormality synthesis of what substance lead to microspherocytosis?
a) hemoglobin A
b) 2,3-biphosphoglyceric acid
c) spectrin
20. Abnormality syntesis of what substance lead to elliptocytosis?
a) hemoglobin А
b) 2,3-biphosphoglyceric acid
c) spectrin
21. What kind of anemia is the result of action of ionizing radiation?
a) aplastic anemia
b) iron deficiency anemia
c) hemolytic anemia
22. What kind of anemia is the result of disturbance of synthesis in stomach
parietal cells intrinsic Castl's factor?
a) hemolytic anemia
b) iron deficiency anemia
c) vitamin В12-deficiency anemia
23. What disturbance leads to anemia in deficiency of vitamin B12 and folic
acid?
a) decrease of syntesis of nucleic acids
b) intensification peroxidation
c) deranged glycolysis
24. What kind of anemia is characterized by megaloblastic type of
hemapoiesis?
a) hemolytic anemia
b) chronic posthemorrhagic anemia
c) vitamin В12-deficiency anemia
25. What kind of anemia is characterized by decreasing syntesis of heme?
a) iron deficiency anemia
b) sickle-cell anemia
c) thalassemia
Anwers:
1bc, 2b, 3c, 4b, 5a, 6c, 7c, 8a, 9b, 10c, 11b, 12c, 13a, 14b, 15a, 16b, 17с,
18a, 19c, 20c, 21a, 22c, 23a, 24c, 25a
QUANTITATIVE DISORDERS OF NEUTROPHILS. LEUKOCYTOSIS
AND LEUKOPENIA
Tests
1. One of the developmental stages of neutrophylic leukocyte is:
a) myeloblast
b) prolymphocyte
c) promonocyte
d) monoblast
2. One of the developmental stages of lymphocyte is:
a) myeloblast
b) lymphoblast
c) promonocyte
d) monoblast
3. Stages of development of monocyte are:
a) myeloblast
b) prolymphocyte
c) promonocyte
d) monoblast
4. Morphologically recognized granulocytic cell is:
a) lymphoblast
b) myeloblast
c) monoblast
d) erythroblast
5. Granulocytes synthesize in:
a) spleen
b) bone marrow
c) liver
d) nodi lymphatici
6. What cells are mononuclear leukocytes?
a) eosinophil
b) monocyte
c) neutrophil
d) basophil
7. The functions of neutrophils are:
a) synthesis of antibodies
b) phagocytosis
c) secretion of enzymes and bactericide agents
d) secretion of histamine and heparin
8. The calculation of leucocytes count occurs in:
a) blood smear
b) Goryave camera
c) special tube
d) photocolorimetric determination
9. The calculation of leucocyte formula occurs in:
a) blood smear
b) Goryaev camera
c) special tube
d) photocolorimetric determination
10. Leukocyte formula is:
a) percentage of the different types of the leukocytes
b) absolute leukocytes count
c) relation of nonmature forms of leucocutes to mature ones
d) relation of granulocytes and nongranulocytes
11. Children have the following peculiarities of leukocyte formula:
a) lymphocytes predominate at birth
b) neutrophils predominate on the 5th year
c) leukocyte formula is the same as in adults on the 5th day of life
d) lymphocytes predominate at 2 years old
12. Physiologic leukocytosis occurs:
a) in administration of glucocorticoids
b) after food intake
c) in physical activity
d) in sleep
13. The causes of relative leukocytosis are:
a) pregnancy
b) hemorrhage
c) fever
d) food intake
14. Acute purulent inflammatory processes lead to:
a) eosinophilia
b) lymphocytosis
c) neutrophilic leukocytosis
15. What type of leukocytes increase in allergic reactions more often?
a) eosinophils
b) neutrophils
c) lymphocytes
16. What type of leukocytosis appears in chronic inflammatory processes
very often?
a) eosinophilic
b) basophilic
c) neutrophilic
d) monocytic
17. Index of the nuclear shift is relation:
a) of the count of inmature forms of neutrophyls to mature ones;
b) of granulocytes and nongranilocytes;
c) of the count of granulocytes to band forms;
d) of myeloblasts to myelocytes.
18. The types of nuclear shift to the left are:
a) myelocytic
b) degenerative
c) monocytic
d) leukemoid
19. The nuclear shift to the right is the increase of the:
a) common count of leukocytes
b) percent of the mature neutrophils
c) percent of the lymphocytes
d) count of granular leukocytes
20. The nuclear shift to the left is:
a) decrease the mature leucocytes from common count of leucocytes
b) increase the count of immature neutrophils
c) increase percent of the lymphocytes
d) decrease the count of granular leukocytes
21. Nuclear shift shows:
a) type of leukocytosis
b) severity of inflammation
c) type of leukopenia
d) stage of inflammation
22. What index is used for assessment of degree of the nuclear shift in
leukogramm?
a) Bobrov's
b) Tiffno
c) nucleocytoplasmic
23. When does eosinophil leukocytosis occur?
a) in viral diseases
b) in autoimmune processes
c) in bacterial infection in recovery
24. What diseases can lead to eosinophilia?
a) croupous pneumonia
b) tuberculosis
c) helminthic invasion
d) cardiac infarction
e) viral hepatitis
25. Pathologic leukocytosis can occur:
a) after a hot bath
b) at pregnancy
c) at administration of glucocorticoids
d) at helminthiasis
26. What type of leukocytes increase in viral infection more often?
a) eosinophils
b) neutrophils
c) monocytes
d) lymphocytes
27. Administration of cytostatics leads to:
a) neutrophilia
b) monocytosis
c) thrombocytosis
d) agranulocytosis
28. Mycosis leads to:
a) eosinophilia
b) lymphocytosis
c) monocytopenia
29. We should differentiate leukemoid reaction of neutrophils type with:
a) chronic lymphatic leukemia
b) chronic myeloid leukemia
c) acute myeloblastic leukemia
d) acute lymphoblastic leukemia
30. The criteria of agranulocytosis is:
a) count of leukocytes below 2,5 х 109 /l
b) count of leukocytes below 1 х 109 /l
c) absence of agranular leukocytes
d) increasing count of agranular leukocytes
31. The term “agranulocytosis”denotes:
a) increased count of agranulocytes in blood
b) abrupt decreased count of granulocytes in blood
c) disappearance of specific granulosity in cells
Answers:
1a, 2b, 3сd, 4b, 5b, 6b, 7bc, 8b, 9a, 10a, 11d, 12bc, 13ad, 14c, 15a, 16d, 17a,
18bd, 19b, 20b, 21b, 22a, 23bc, 24c, 25cd, 26d, 27d, 28b, 29b, 30b, 31b
LEUKEMIAS
Tests
1. The term "anaplasia" means:
b) increase of tumor mass
c) accelerated tumor cells division
d) differentiation disorders of the tumor cells
2. Itensity of glycolisis in the tumor cells:
d) rises
e) diminishes
f) is unchanged
1.
Synthesis of nucleic acids in the malignant cells:
d) rises
e) diminishes
f) has no change
2. The type of regulation of tumor cells growth is:
d) endocrine
e) autocrine
f) paracrine
3. Proliferation of the malignant cells is conditioned by:
e) activation of the oncogenes
f) intensification of apoptosis
g) inactivation of the suppressor genes
h) derangement of apoptosis
4. Carbohydrate metabolism in tumor is characterized by:
e) increase of the glycogen synthesis
f) intensification of glycogenesis
g) activation of glycolysis
h) intensification of glycogenolysis
5. Lipid metabolism in tumor is characterized by:
d) intensification of lipolysis
e) intensification of lipogenesis
f) decrease of the fatty acids synthesis
6. First of all ren sarcoma metastasize into:
e) liver
f) organs of pelvis minor
g) intestine
h) lung
7. Antigenic complex in malignant cells is characterized by:
d) increase of normal gens synthesis
e) appearance of the carcinoembryonic antigens
f) appearance of the specific antigens
8. Malignant tumor is characterized by:
e) expansive growth
f) the absence of metastases
g) autonomy, self-regulation of growth
h) cellular atypism
9. Bening tumor is characterized by:
e) expansive growth
f) the absence of metastases
g) metastases
h) cellular atypism
12. Stages of the tumor development are:
e) promotion
f) progression
g) translocation
h) inversion
13. The local effects of the tumor include:
f) bleeding
g) bowel obstruction
h) anemia
i) anorexia
j) endocrine syndromes
14. Common systemic effects of the tumor include:
f) bleeding
g) bowel obstruction
h) anemia
i) anorexia
j) endocrine syndromes
15. Anticancerogenic protection includes:
e) antioxidants
f) lymphocytes
g) glucose
h) ammonia
16. The mechanisms of anticancerogenic protection are:
d) atnicellular
e) antimutative
f) antimicrobial
17. In aleucaemic type of leucaemias:
a) amount of leukocytes increases in blood
b) amount of leukocytes decreases in blood
c) normal count of leukocytes in blood
d) blasts are absent
18. Chronic myeloleucaemia may be associated with:
a) increasing blast count
b) decreasing blast count
c) increasing amount of basophils and eosinophils
d) absent hiatus leucaemicus
19. Following changes are observed in peripheral blood in acute
myeloblastic leucaemia:
a) elevated peripheral blood myeloblast count
b) low peripheral blood myeloblast count
c) the presence of Botkin-Gumbrecht bodies
d) the presence of hiatus leukemicus
20. Following changes are observed in the peripheral blood in chronic
lymphoblastic laeucaemia:
a) decreased count of lymphoblasts
b) increased count of myeloblasts
c) the presence of Botkin-Gumbrecht bodies
d) increased amount of eosinophils and basophils
21. Following changes are observed in the peripheral blood in acute
lymphoblastic leucaemia:
a) small count of lymphoblasts
b) increased count of megaloblasts
c) increased count of lymphoblasts
d) the presence of Botkin-Gumbrecht bodies
22. Hiatus leukemicus is the absence of:
a) immature cells
b) morphologically don’t differentiation cells
c) mature cells
23. Increased count of eosinophils and basophils can be observed in:
a) chronic lympholeukosis
b) chronic myeloleukosis
c) acute lympholeukosis
d) acute myelogenus leukosis
24. Leucaemia is:
a) benign tumor of hematopoietic tissue
b) sign of the inflammation
c) malignant tumor of hematopoietic tissue
d) sign of the allergy
25. Acute leucaemia differs from chronic one by:
a) the presence of anemia
b) the absence of hiatus leukemicus
c) the presence of hiatus leukemicus
d) small blast count in peripheral blood
26. Chronic leucaemia differs from acute leukosis by:
a) the absence of hiatus leukemicus
b) the presence of hiatus leukemicus
c) small blast count in peripheral blood
d) increase of blast count in peripheral blood
27. The main change in a hemogram in acute laeucamias is:
a) low percent of the blasts
b) the presence of the cells of 5 class of maturation
c) the presence of hiatus leucaemicus
d) high percent of the blast cells
28. The main change in a hemogram at chronic laeucamias is:
a) low percent of the blasts
b) the presence of the cells of 5 class of maturation
c) the presence of hiatus leukemicus
d) high percent of the blast cells
e) the absence of the blasts
29. In acute laecaemia:
a) cellular differentiation fully stops on the 2-4 class level
b) cellular differentiation don’t fully stops on the 2-4 class level
Answers:
1c, 2a, 3а, 4b, 5асd, 6cd, 7а, 8d, 9bc, 10сd, 11ab, 12ab, 13ab, 14cde, 15ab,
16ab, 17cd, 18bcd, 19ad, 20a, 21ac, 22a, 23b, 24c, 25c, 26ac, 27cd, 28ab, 29a.
DISORDERS OF HEMOSTASIS. THROMBOPHILIC DISORDERS OF
HEMOSTASIS. THROMBOSIS AND EMBOLISM
Tests
1. The functions of platelets in hemostasis are:
a) angiotrophic
b) adhesive
c) coagulative
d) bactericidic
2. Platelet precursor is:
a) plasmacytoblast
b) myeloblast
c) megacaryoblast
d) lymphoblast
3. Which factor can initiate blood coagulation?
a) factor I
b) factor Х
c) factor ХII
d) prothrombin
4. What platelet factor takes part in the prothrombinase synthesis?
a) 3
b) 4
c) actomyosin
d) thromboxane
5. Inducer of platelets aggregation is:
a) aspirin
b) ADP
c) urea
d) thrombin
6. Antiaggregant for thrombocytes is:
a) thrombin
b) ADP
c) collagen
d) aspirin
7. Extrinsic coagulation pathway of hemostasis includes activation of:
a) factor VII
b) factor VIII
c) factor IX
d) factor XII
8. The factor which converts the prothrombin to thrombin:
a) factor I
b) factor VII
c) factor IХа
d) factor Ха
e) factor ХIII
9. The platelet-vascular hemostasis is nessesary for:
a) white trombus formation
b) red thrombus formation
c) the postcagulative changing of the thrombus
10. The anticoagulants are:
a) fibrinogen and fibrin-split products
b) antithrombin III
c) heparin
d) ADP
11. Fibrin-split products stimulate:
a) synthesis of factor III
b) destruction of fibrin
c) activation of factor XII
12. The clot retracts by:
a) fibrin-stabilizing factor
b) thrombocytes factors
c) kinins system
13. The synthesis of thrombin is blocked by:
a) calcium ions
b) collagen
c) von Willebrand factor
d) anticoagulants
14. The endothelial cells of intact vessels prevent blood coagulation by secretion
of:
a) prostacyclin
b) thromboxane
c) factor IX
d) vitamin К
15. Antithrombogenic property of the endothelium is caused by production of:
a) prostacyclin
b) protein C
c) NO
d) angiotensin II
16. Procoagulant activity of the endothelium is caused by the production of:
a) prostaglandin I2
b) NO
c) angiotensin II
d) endothelin
17. Anticoagulant system is aimed at:
a) depression of blood coagulation
b) thrombolysis
18. Plasmin system is aimed at:
a) depression of blood coagulation
b) thrombolysis
19. What thrombus forms the first phase of blood clot formation?
a) white
b) red
20. The distinctive signs of a clot are:
a) has white head that fixed to the vessels
b) synthesis intravital
c) doesn’t fixed to the vessels
d) synthesis posthumously
21. The major constituent of red thrombus is:
a) fibrin
b) RBC
c) WBC
d) albumens
e) platelets
22. The major constituent of white thrombus is:
a) fibrin
b) RBC
c) WBC
d) albumens
e) platelets
23. Types of endogenous embolism are:
a) thromboembolism
b) gas embolism
c) air embolism
d) embolism by foreign bodies
e) cellular embolism
24. Types of exogenous embolism are:
a) gas embolism
b) thromboembolism
c) air embolism
f) embolism by foreign bodies
d) embolism by bacteria
25. What is the localization of the thrombus in embolism of the pulmonary vessels?
a)
b)
c)
d)
e)
in the veins of the greater circulation
in the right part of the heart
in the left part of the heart
in arteries of the greater circulation
in portal veins system
28. What is the localization of thrombus in embolism of arterial vessels of greater
circulation?
a)
b)
c)
d)
e)
in the veins of the greater circulation
in the right part of the heart
in the left part of the heart
in arteries of the greater circulation
in portal veins system
Answers:
1abc, 2c, 3c, 4a, 5bd, 6d, 7a, 8d, 9ac, 10abc, 11b, 12ab, 13d, 14ab, 15abc, 16cd,
17a, 18b, 19a, 20ab, 21cd, 22a, 23e, 24abe, 25cde, 26ab, 27cd.
DISORDERS OF HEMOSTASIS. HEMORRHAGIC DISORDERS OF
HEMOSTASIS
Tests:
1. Disturbances of blood coagulation lead to:
a)
b)
c)
d)
disease of hemostasis
disease of homeostasis
metabolism disorder
inflammation
2. Hemosthasiopathia is the disturbance of:
a)
b)
c)
d)
e)
the whole haemostasis system
blood coagulation
anticoagulation system
plattelets
vessel wall
3. Hemorragic hemostasiopathia is a kind of hemostasis disorder
connected with:
a)
increased coagulability of blood
b)
increased bleeding
c)
increased thrombocytopoiesis
d)
simultaneous thrombosis and bleeding
4. Trombophilic hemostasiopathias is a kind of hemostasis disorder
connected with:
a)
increased coagulability of blood
b)
increased bleeding
c)
increased thrombocytopoiesis
d)
simultaneous thrombosis and bleeding
5. Trombohemorrhagic hemostasiopathias is a kind of pathology with:
a) increased bleeding
b) increased trombocytopoiesis
c) simultaneous thrombosis and bleeding
6.What concerns to hemorrhagic hemostasiopathias?
a)
b)
c)
d)
e)
DIC
thrombosis
angiopathies
coagulation disorders
thrombocytopenia
7. The count of platelets in hemorrhagic syndrome is less than:
a)
b)
c)
d)
150 х 109 /l
320 х 109 /l
50 х 109 /l
400 х 109 /l
8. The causes of thrombocytopenia are:
a)
b)
c)
d)
malignant tumor
radiation
acute hemorrhage
icterus
9. Idiopathic thrombocytopenic purpura is a:
a)
b)
c)
d)
coagulation disorder
thrombocytopenia
angiopathy
thrombophilia
10. The causes of angiopathy are:
a)
b)
c)
d)
infectious disease
allergy
diabetes mellitus
hypovitaminosis Р and С
11. Scorbutus is a:
a)
b)
c)
d)
coagulation disorder
thrombocytopenia
angiopathy
trombohemorrhagic hemostasiopathias
12. Henoch-Schonlein purpura is:
a)
b)
c)
d)
coagulation disorder
thrombocytopenia
angiopathy
trombohemorrhagic hemostasiopathias
13. The mechanism of increased hemorrhage in immune
thrombocytopenic purpura is:
a)
b)
c)
d)
decreased platelet adhesion
decreased platelet aggregation
lack of nutrition function of the platelets
disorder of vasoactive function of platelets
14. Glanzmann thrombasthenia is:
a)
b)
a)
b)
angiopathy
qualitative disorder of platelets
coagulation disorder
disorder of plasmin system
15. Hemorrhagic hemostasiopathies are:
a)
b)
c)
qualitative disorders of platelets
angiopathy
posthemorrhagic anemia
d)
leukemoid response
16. Following tests are used for assessment of aggregation properties of
trombocyte hemostasis component:
a)
b)
c)
d)
pinch test
Nesterovs test
tromboelastography
aggregatogram
17. Anticoagulative system is:
a)
b)
c)
d)
antithrombin III
antihemophilic globulin
angiotensin
plasmin
18. Anticoagulants are:
a)
b)
c)
d)
antithrombin III
antihemophylic globulin
heparin
plasmin
19. Fibrinolytics are:
a)
b)
c)
d)
antithrombin III
antihemophylic globulin
heparin
plasmin
20. Anticoagulative effect of heparin is inhibition of:
a)
b)
c)
d)
prothrombinase synthesis
the synthesis of thrombin
fibrin synthesis
all the phases of blood coagulation
21. The anticoagulative effect of plasmin is:
a)
inhibition of prothrombinase formation
b)
c)
d)
inhibition of thrombin formation
inhibition of fibrinogenesis
activation of fibrinolysis
22. Coagulation disorders are:
a)
b)
c)
d)
scorbut
Henoch-Schonlein purpura
idiopapthic thrombocytopenic purpura
haemophilia
23. The coagulation disorders are:
a)
b)
c)
d)
hemorrhagic newborn disease
Henoch-Schonlein purpura
idiopathic thrombocytopenic purpura
hemophylia
24. Coagulation disorder of the first phase of blood coagulation is:
a)
b)
c)
d)
hemorrhagic newborn disease
lack of Fitzgerald factor
idiopathic thrombocytopenic purpura
hemophylia
25. The cause of the coagulation disorders with disturbance of the first
phase of blood coagulation is the deficiency of:
a)
b)
c)
d)
vitamin K
Fletcher's factor
Hageman's factor
fibrinogen
26. Deficiency of what factor leads to hemophilia A?
a)
b)
c)
VIII
IX
XI
27. Deficiency of what factor leads to hemophilia B?
a)
b)
c)
VIII
IX
XI
28. Deficiency of fibrinogen leads to disorder of:
a)
b)
c)
d)
synthesis of prothrombinase
thrombinogenesis
fibrinogenesis
retraction and fibrinolysis
29. Lack of plasmin leads to disorder of:
a)
b)
c)
d)
prothrombinogenesis
trombinogenesis
fibrinogenesis
retraction and fibrinolysis
30. Deficiency of prothrombin leads to disorder of:
a)
b)
c)
d)
prothrombinogenesis
trombinogenesis
fibrinogenesis
retraction and fibrinolysis
31. Defficiency of retractozim leads to disturbance of:
a)
b)
c)
d)
synthesis of prothrombinase
synthesis of thrombin
synthesis of fibrin
retraction and fibrinolysis
32. Deficit of calcium leads to disturbance of:
a)
b)
c)
d)
synthesis of prothrombinase
synthesis of thrombin
synthesis of fibrin
all phases of secondary hemostasis
33. Lack of calcium leads to:
a)
b)
c)
d)
increasing haemorrage
Thrombosis
DIC
Excess of thrombus retraction
34. The coagulation disorder with disturbance of the 2nd stage of blood
coagulation is:
a)
b)
c)
d)
hemorrhagic newborn disease
lack of fibrinogen
idiopathic thrombocytopenic purpura
excess use of coumarin drugs
35. The coagulation disorder with disturbance of the 3d stage of blood
coagulation are:
a)
b)
c)
d)
hemorrhagic newborn disease
lack of kininogen
idiopathic thrombocytopenic purpura
lack of fibrinogen
36. Lack of vitamin K leads to:
a)
b)
c)
d)
coagulation disorder
DIC
thrombocytopenia
angiopathy
37. Hemophilia is a:
a)
b)
c)
d)
coagulation disoder
thrombocytopenia
angiopathy
thrombohemorrhagic hemostaiopathias
38.Von Willebrand disease is:
a)
b)
c)
d)
angiopathy
thrombocytopenia
coagulation disorder
admixed hemorrhagic hemostasiopathias
39. DIC concerns to hemostasiopathias:
a)
b)
c)
thrombophilic
hemorrhagic
thrombohemorrhagic
40. The causes of DIC are:
a)
b)
c)
d)
malignant tumor
acute radiation sickness
acute bleeding
cardiac insufficiency
Answers:
1a, 2a, 3b, 4ac, 5с, 6cde, 7c, 8ab, 9b, 10d, 11c, 12c, 13c, 14b, 15ab, 16d,
17ad, 18ac, 19d, 20d, 21d, 22d, 23ad, 24bd, 25bd, 26a, 27b, 28c, 29d, 30b, 31d,
32d, 33a, 34ad, 35d, 36a, 37a, 38d, 39c, 40ab.
PATHOPHYSIOLOGY OF NERVOUS SYSTEM
1.
a)
b)
c)
d)
Tests:
What is the consequence of corticospinal path integrity infringement?
hyperkinesia
central paralysis
peripheric paralysis
ataxia
2.
a)
b)
c)
d)
What is the consequence of damage of peripheral motoneurons?
hyperkinesia
central paralysis
peripheric paralysis
ataxia
3.
a)
b)
c)
d)
What signs are characteristic of the central paralysis?
Intensifying of reflex movements
Absence of autokinesias
Absence of reflex movements
Intensifying of autokinesias
4.
a)
b)
c)
d)
What signs are characteristic of a peripheral paralysis?
Absence of autokinesias
Absence of reflex movements
Intensifying of reflex movements
Intensifying of autokinesias
5.
a)
b)
Central paralysis is characterized by:
Muscle tone increase
Muscle tone decrease
6.
a)
b)
Peripheral paralysis is characterized by:
Muscle tone increase
Muscle tone decrease
7.
What sensitivity is changed due to damage of Gaulle and Burdach’s
fascicles of the spinal cord?
Absence of the proprioceptive sensitivities on the damaged side
Absence of the proprioceptive sensitivities on the opposite side
Absence of temperature and pain sensitivity on the damaged side
Absence of temperature and pain sensitivity on the opposite side
a)
b)
c)
d)
8.
a)
b)
c)
d)
9.
a)
b)
c)
d)
e)
10.
What sensitivity is changed due to damage of lateral spinothalamic tract of
the spinal cord?
Absence of the proprioceptive sensitivities on the damaged side
Absence of the proprioceptive sensitivities on the opposite side
Absence of temperature sensitivity on the damaged side
Absence of temperature sensitivity on the opposite side
What sensitivity is changed due to damage of posterior horns of the spinal
cord?
Absence of the proprioceptive sensitivities on the damaged side
Absence of the proprioceptive sensitivities on the opposite side
Absence of temperature sensitivity on the damaged side
Absence of pain sensitivity on the damaged side
Absence of temperature sensitivity on the opposite side
a)
b)
c)
d)
What change of motor function occurs due to damage of Gaulle and
Burdach’s fascicles of the spinal cord?
central paralysis
Peripheric paralysis
Hyperkinesia
Sensitive ataxy
11.
a)
b)
c)
d)
The cause of coordination locomotion infringement is the damage of:
Cerebellum
anterior horns of the spinal cord
posterior horns of the spinal cord
Lateral horns of a spinal cord
12.
a)
b)
c)
What is the reason of Broun-Sekar syndrome?
full transection of the spinal cord
half longitudinal transaction of the spinal cord
half cross transaction of the spinal cord
13.
a)
b)
c)
d)
The cause of spasms in tetanus is infringement of:
mediator synthesis
axon mediator transport
mediator secretions in a synaptic gap
interactions of a mediator with a receptor
14.
a)
The cause of spasms in strychnine poisoning is infringement of:
mediator synthesis
b)
c)
d)
axon mediator transport
mediator secretions in a synaptic gap
interactions of a mediator with a receptor
15.
a)
b)
c)
d)
Lack of which mediator leads to a convulsive syndrome?
opioid peptides
dofamin
GABA
neurotensin
16.
a)
b)
c)
d)
Botulism toxine blocks transport of … in a synaptic gap:
Noradrenaline
Glycine
Acetylcholine
Serotonin
17. What is characteristic of a critial pain?
a)
b)
c)
d)
e)
distinct localisation
indistinct localisation
it is brief
it is prolonged
it is weak
Answers:
1b, 2c, 3ab, 4ab, 5a, 6b, 7a, 8d, 9сd, 10d, 11ac, 12c, 13c, 14d, 15c, 16c, 17ace.
Tests:
1. Following substances are concerned to narcotics:
a)
b)
c)
d)
e)
Nicotine
Cannabis drugs
Cocaine
dichlorvos
Hallucinogens
2. Choose true statements:
a)
b)
c)
d)
Alcohol is not produced by human organism
Alcohol is endogenous metabolite
Nicotine is not formed in human organism
Nicotine is endogenous metabolite
3. The euphoric effect of alcohol on CNS is connected, first of all, with:
a)
b)
c)
Activation of processes of excitation in the cortex of the hemispheres
Weakening of processes of inhibition in the cortex of the hemispheres
Oppression of the subcortical centres
4. Specify changes in cell membranes in acute alcohol intoxication:
a)
b)
c)
increased fluidity of lipidic bilayer
decreased fluidity of lipidic bilayer
increased cholesterol level
5. Specify metabolism changes in acute alcohol intoxication:
a)
b)
c)
Oppression of oxidative phosphorylation
Decrease in synthesis of protein
Increase in synthesis of protein
6. Death in acute alcoholic poisoning can come from:
a)
b)
c)
d)
emetic masses aspiration
Respiratory centre oppressions
Fibrillations of heart ventricles
hypoglycemic comas
7. Defence reaction in chronic alcohol abuse is:
a)
b)
c)
d)
Increase of cell permeability to alcohol
Decrease in cell permeability to alcohol
Increase of suction of ethanol in a gastrointestinal path
Weakening of oxidation of ethanol and acetic aldehyde
8. Alcoholism developes faster:
a)
At young age
b)
c)
d)
At mature age
At all age-grades equally
In people with hereditary predisposition
9. Ferment participating in oxidation of ethanol is:
a)
b)
c)
d)
insulinase
alcohol dehydrogenase
Peptase
Lactase
10. Specify stages of alcoholism (narcotisms):
a)
b)
c)
d)
drug addiction stage
encephalopathic stage
euphoric stage
narcotic stage
11. What stage of alcoholism is characterised by the maximum tolerance to
ethanol?
a)
b)
c)
neurotic stage
drug addiction
encephalopathy
12. What stage of alcoholism is characterised by organ and system
decompensation?
a)
b)
c)
neurotic stage
drug addiction
encephalopathy
13. In alcoholism abstinence stage next symptoms take place:
a)
b)
c)
d)
neuromediator exchange infringements
tissue hypoxia deveopment
alchohol dehydrogenase activation
organism functions normalisation
14. The neurotic stage of alcoholism is characterised by:
a)
b)
c)
increase of tolerance to alcohol
maximal tolerance to alcohol
low tolerance to alcohol
15. The drug addiction stage of alcoholism is characterised by:
a)
b)
c)
maximal tolerance to alcohol
Low tolerance to alcohol
abstinence syndrome presence
16. The encephalopathy stage of alcoholism is characterised by:
a)
b)
c)
maximal tolerance to alcohol
Low tolerance to alcohol
polyorganic insufficiency
17. Specify manifestations of experimental neuroses:
a)
b)
c)
phase states development
Simplification of development of conditioned reflexes
vegetative functions distress
18. Manifestations of experimental neuroses are:
a)
b)
c)
Simplification of development of conditioned reflexes
Impossibility of development of new conditioned reflexes
hypo- and hyperkinesias, sensitivity distresses
19. How is paradoxical phase manifested?
a)
b)
c)
Strong reaction to a weak conditioned stimulus and vice versa
Identical responses of nervous structure to influences of different intensity
Development of negative reactions in response to positive stimuli, and vice
versa
20. The ultraparadoxal phase state is characterized by:
a)
d)
Strong reaction to weak conditioned stimulus and vice versa
Development of negative reactions in response to positive stimuli, and vice
versa
21. The equalizing phase is characterized by:
a)
b)
Identical responses of nervous structure to influences of different intensity
Development of negative reactions in response to positive stimuli, and vice
versa
22. The obstacle phase is characterised by:
a)
b)
Absence of reactions to weak and strong stimuli
Development of negative reactions in response to positive stimuli, and vice
versa
23. The overstrain of excitatory process can be provoked by:
a)
b)
Prolonged action of strong conditioned stimuli
Necessity of development of subtle and complex differentiations
24. The overstrain of excitatory process can be provoked by:
a)
b)
A considerable quantity of conditioned excitators
Alteration of alarm value of conditioned excitators
25. The overstrain of inhibitory process can be provoked by:
a)
b)
c)
d)
prolonged action of strong conditioned excitators
Great number of conditioned excitators
Necessity of development of subtle and complex differentiations
Alteration of signal value of conditioned stimuli
26. The overstrain of mobility of the excitatory processes can be provoked by:
a)
b)
c)
d)
prolonged action of strong conditioned stimuli
A considerable quantity of conditioned stimuli
Necessity of development of subtle and complex differentiations
Alteration of signal value of conditioned stimuli
27. Which neurosis can be modeled by overstrain of inhibitory process:
a)
b)
neurosis with prevalence of excitation
neurosis with prevalence of inhibition
c)
neurosis with pathological mobility of the excitatory processes
28. An overstrain of exciting process it is possible to model a neurosis:
a)
b)
c)
With prevalence of inhibition
With pathological mobility of the excitatory processes
With prevalence of excitation
29. Neurosis with prevalence of excitation process in animals is manifested by:
a)
b)
c)
d)
Inadequate excitement
Aggressiveness and malignancy
Drowsiness
slow response
30. Neurosis with prevalence of inhibition process in animals is manifested by:
a)
b)
c)
d)
Inadequate excitement
Aggressiveness and malignancy
Drowsiness
Fussiness
31. Neurosis with pathological mobility in animals is manifested by:
a)
b)
c)
d)
Inadequate excitement
Aggressiveness and malignancy
Drowsiness
Fussiness
32. Following states concern to neuroses:
a)
b)
c)
d)
e)
Neurasthenia
Schizophrenia
Hysteria
maniacal-depressive psychosis
obsessive neurosis
33. What temperament is most often subject to neurotic distresses:
a)
b)
a melancholic person
a phlegmatic person
c)
d)
a choleric person
a sanguine person
34. An information triad as the condition of neuroses occurrence includes:
a)
b)
c)
d)
e)
Limitation of time
High level of motivations
Low level of motivations
Personal features
Great volume of the information which is necessary to adopt
35. Characteristic features of neurasthenia are:
a)
b)
c)
d)
Hypererethism and irritability in combination with fast fatigability
Phobias
reduced working capacity, flaccidity
increased suggestibility
36. Characteristic features of obsessive neurosis:
a)
b)
c)
d)
Hypererethism and irritability in combination with fast fatigability
Phobias
Delirium, hallucinations
increased suggestibility
37. Characteristic features of hysteria:
a)
b)
c)
d)
Hypererethism and irritability in combination with fast fatigability
Phobias
Deafness, dumbness
paresis, paralyses
38. The amnesia can be observed in:
a)
b)
c)
d)
Neuroses
maniacal-depressive syndrome
Korsakov syndrome
Alzheimer's diseases
39. Oligophrenia is a syndrome in:
a)
b)
c)
d)
Diabetes
Down`s syndrom
phenylketonuria
Cerebral circulation infringement
40. Depression can arise in following brain disorders:
a)
b)
c)
d)
endorphins level increase
endorphins level decrease
serotonin level decrease
serotonin level increase
Answers:
1bce, 2bc, 3b, 4a, 5ab, 6abc, 7b, 8ad, 9b, 10ab, 11b, 12c, 13ab, 14a, 15ac, 16bc,
17ac, 18bc, 19a, 20b, 21а, 22а, 23a, 24a, 25c, 26d, 27a, 28a, 29ab, 30c, 31d, 32ace,
33a, 34abe, 35ac, 36b, 37cd, 38cd, 39bc, 40bc.
PATHOPHYSIOLOGY OF ENDOCRINE SYSTEM. PITUITARY GLAND
AND ADRENAL GLAND FUNCTIONS DISORDERS
1.
Tests:
What hormones formation infringement takes place in pituitary gigantism?
a) gonadotropin
b) somatotropinum
c) prolactin
d) melanocyte-stimulating hormone
2.
What infringements are characteristic of pituitary nanism?
a) augmentation of protein synthesis
b) reduction of protein synthesis
c) tissue differentiation infringement
d) tissue differentiation is not variated
3.
What hormones formation infringement in Simmonds disease takes place?
a) gonadotropin
b) somatotropin
c) thyrotropin
d) anterior pituitary hormones
4.
What hormones formation infringement in Shihen disease takes place?
a) gonadotropin
b) somatotropinum
c) corticotropin (ACTH)
d) anterior pituitary hormones
5.
What metabolic infringements are
hyperproduction?
a)augmentation of synthesis of protein
b) lipolysis augmentation
c)reduction of synthesis of protein
d) lipogenesis augmentation
6.
What hormones formation infringement in Itsenko-Cushing disease
occurence probably takes place?
a) somatoliberin
b) corticoliberin
c) somatostatin
d) thyroliberin
characteristic
of
Somatotropin
7.
To what hormone formation decrease acromegaly is related?
a) somatoliberin
b) coticoliberin
c) somatostatin
d) thyroliberin
8.
What change of protein metabolism characterises Itsenko-Cushing disease?
a) augmentation of synthesis of protein
b) augmentation of a katabolism of protein
9.
What change of fat metabolism characterises Itsenko-Cushing disease?
a) lipolysis augmentation
b) lipogenesis augmentation
10.
What changes of metabolism characterises Itsenko-Cushing disease?
a) glyconeogenesis intensifying
b) augmentation of fat synthesis
c) glyconeogenesis reduction
d) protein synthesis augmentation
e) protein katabolism augmentation
11.
What change of blood arterial pressure is characteristic of Itsenko-Cushing
disease?
a) it increases
b) it decreases
c) it is normal
12.
What state of immune system is characteristic of Itsenko-Cushing disease?
a) occurrence autoimmune processes
b) activity decrease
c) it is not broken
13.
What mechanism takes place in immune system activity decrease in ItsenkoCushing disease?
a) intensifying of protein katabolism
b) increase of intensity of protein synthesis
c) lipogenesis augmentation
d) lipolysis intensification
14.
What endocrine function changes lead to diabetes insipidus?
a) vasopressinum increase
b) vasopressinum reduction
c) electrocortin increase
d) insulin lack
15.
What changes are characteristic of diabetes insipidus?
a) polyuria
b) polydipsia
c) dehydration
d) oliguria
e) hyperhydration
16.
What changes are characteristic of vasopressinum surplus?
a) polyuria
b) polydipsia
c) dehydration
d) oliguria
e) hyperhydration
17.
What symptoms are characteristic of Itsenko-Cushing disease?
a) the round-shaped face
b) attrition
c) low blood pressure
d) high blood pressure
18.
What change is observed in diabetes insipidus?
a) increased water reabsorption
b) reduction of water reabsorption
c) glomerular filtration increase
d) glomerular filtration reduction
19.
What mechanism participates in diuresis change in Parhon syndrome
(surplus of vasopressinum)?
a) increased water reabsorption
b) reduction of water reabsorption
c) glomerular filtration increase
d) glomerular filtration reduction
20.
What changes of electrolytic exchange in kidney are characteristic of
adrenal gland failure?
a) increased sodium reabsorption
b) reduction of sodium reabsorption
c) increased secretion of potassium
d) reduction of secretion of potassium
21.
What endocrine function causes steroid diabetes?
a) increase of mineralocorticoids
b) reduction of glucocorticoids
c) surplus of glucocorticoids
22.
What changes in nephrons are observed in primary hyperaldosteronism?
a) augmentation of sodium reabsorption
b) augmentation of potassium secretion
c) reduction of sodium reabsorption
d) reduction of potassium secretion
23.
What changes in nephrons are characteristic of hypoaldosteronism?
a) augmentation of sodium reabsorption
b) augmentation of potassium secretion
c) reduction of sodium reabsorption
d) reduction of potassium secretion
24.
What changes of cell electrolite composition are characteristic of primary
hyperaldosteronism?
a) augmentation of potassium maintenance
b) reduction of sodium maintenance, water
c) reduction of potassium maintenance
d) augmentation of sodium maintenance, water
25.
What changes of blood electrolite composition are characteristic of
hypoaldosteronism?
a) augmentation of potassium maintenance
b) reduction of sodium maintenance
c) reduction of potassium maintenance
d) augmentation of sodium maintenance
26.
How does arterial pressure variate in hypoaldosteronism?
a) increases
b) decreases
c) does not variate essentially
27.
How does the arterial blood pressure variate in total hypoactivity of adrenal
cortex?
a) increases
b) decreases
d) does not variate essentially
28.
What changes of carbohydrate metabolism are characteristic of total
hypoactivity of adrenal cortex?
a) glyconeogenesis intensity augmentation
b) glyconeogenesis intensity decrease
c) maintenance augmentation of blood glucose
d) maintenance decrease of blood glucose
29.
What hormones formation infringement in secondary hypergonadism takes
place?
a) gonadotropin
b) somatotropin
c) chromatophorotropic hormone
d) corticotropin (ACTH)
30.
What hormones formation infringement in persistent lactorrhea syndrom
takes place?
a) gonadotropin
b) somatotropin
c) prolactin
d) chromatophorotropic hormone
31.
What hormones formation infringement in skin pigmentation augmentation
takes place?
a) gonadotropin
b) somatotropin
c) prolactin
d) chromatophoroptropic hormone
32.
Synthesis of which biologically active substances cause pituatary nanism?
a) gonadotropin
b) somatotropin
c) corticotropin (ACTH)
d) thyrotropin
e) somatomedins
33.
What hormones formation infringement in adrenal cortex secondary
hypoactivity takes place?
a) gonadotropin
b) somatotropin
c) corticotropin (ACTH)
d) thyrotropin
34.
What hormones formation infringement in adrenal cortex secondary
hypoactivity development probably takes place?
a) somatoliberin
b) corticoliberin
c) somatostatin
d) thyroliberin
35.
A congenital adrenogenital syndrome is characterized by:
a) hydrocortisone augmentation
b) adrenocorticotropic hormone (ACTH) reduction
c) androgenic hormones augmentation
d) hydrocortisone reduction
Answers:
1b, 2bc, 3d, 4d, 5ab, 6b, 7c, 8b, 9b, 10abe, 11a, 12b, 13a, 14b, 15abc, 16de, 17ad,
18b, 19a, 20bd, 21c, 22ab, 23cd, 24cd, 25ab, 26b, 27b, 28bd, 29a, 30c, 31d, 32be,
33c, 34b, 35cd
PATHOPHYSIOLOGY OF ENDOCRINE SYSTEM. PATOLOGY OF
THYROID, PARATHYROID AND SEX GLANDS
Tests:
1. Insufficiency of iodine in nutrition causes:
a) autoimmune thyroidithis
b) hyperthyrosis
c) hypoparathyroidism
d) endemial struma
e) diffuse toxic struma
2. In severe hypotyroidism in adults leads to:
a)
b)
c)
d)
e)
cretinism
myxedema
eunuchoidism
nanism
hypergonadism
3. Surplus of hormones of the thyroid gland occurs in:
a) myxedema
b) diffuse toxic struma
c) endemial cretinism
d) acromegaly
e) insulinoma
4. Surplus of which hormones is characteristic of hyperthyroidism:
a)
b)
c)
d)
triiodthyronine and thyroxine
prolactin
hydrocortisone
insulin
5. The thyrotropic hormone blood concentration augmentation in hypothyroidism
testifies localisation of pathological process in:
a)
b)
c)
d)
pituitary body
thyroid gland
parathyroid gland
hypothalamus
e) thymus
6. Hypothyroidism is characterised by:
a) metabolism augmentation
b) lipolysis increase
c) metabolism decrease
d) lipolysis decrease
7Hyperthyroidism is characterised by:
a) metabolism augmentation
b) protein katabolism intensifying
c) lipolysis increase
d) metabolism decrease
8. What is typical for hypothyroidism:
a) increased irritability
b) thinking sluggishness
c) drowsiness
d) decrease of intellectual and physical effeciency
e) tremor
9.
What is typical for hyperthyroidism:
a) increased irritability
b) drowsiness
c) tremor of dactyls of hands
d) memory weakening
10.
How does phosphorus reabsorption in nephrons tubules variate in
parathyroid glands hypoactivity?
a) increases
b) decreases
11. How does phosphorus reabsorption in nephrons tubules variate in
parathyroid glands hyperfunction?
a) decreases
b) increases
12.
How does calcium and phosphorus maintenance in blood variates in
hypoparathyroidism?
a) calcium maintenance increases
b) phosphorus maintenance increases
c) calcium maintenance decreases
d) phosphorus maintenance decreases
13.
What hormones formation infringement in thyroid gland hypoactivity takes
place?
a) gonadotropin
b) somatotropinum
c) corticotropin (ACTH)
d) thyrotropin
Answers:
1d, 2b, 3b, 4a, 5b, 6d, 7cd, 8abc, 9bcd, 10ac, 11a, 12a, 13bc, 14d
INSUFFICIENCY OF BLOOD CIRCULATION.
MYOCARDIAL INFARCTION
Tests:
1.What pathology refers to coronarogenous myocardial blood circulation
insufficiency?
a) ischemic heart disease
b) the valve insufficiency
c) valvular stenosis
2. What pathology leads to noncoronary myocardial blood circulation
insufficiency?
a)
b)
ischemic heart disease
the valve insufficiency
c) valvular stenosis
d) hypercalcemia
3.What pathology leads to myocardial blood circulation insufficiency?
a) myocardithis
b) the valve insufficiency
c) valvular stenosis
d) hearts tamponade
a)
b)
c)
d)
4. What factor is the reason of cardiac insufficiency due to its overload by
blood pressure?
ischemic heart disease
myocardithis
mitral valve insufficiency
aortic stenosis
a)
b)
c)
d)
5.What factor is the cause of heart insufficiency as a result of its volume
overload?
ischemic heart disease
myocardithis
aortal valve insufficiency
aortic stenosis
6.What factor leads to heart insufficiency as a result of its volume overload?
a)
b)
c)
d)
ischemic heart trouble
myocardithis
valving foramen stenosis
tricuspid valve insufficiency
7.What factor leads to heart pressure overload?
a)
b)
c)
d)
ischemic heart trouble
myocardithis
mitral foramen stenosis
tricuspid insufficiency
8.What changes of hemodynamics occur in heart insufficiency?
a)
b)
c)
reduction of systolic outcome
reduction of minute volume of blood
reduction of residual volume of blood
9.What change of hemodynamics verifies heart insufficiency?
a)
b)
c)
augmentation of residual volume of blood
augmentation of minute volume of blood
augmentation of systolic outcome
10.In what kind of cardial insufficiency Frank-Starling mechanism plays the
important role?
a) in volume overload
b) in pressure overload
11.What is characteristic of decompensated heart insufficiency induced by
volume overload?
a) increase of diastolic filling
b) reduction of systolic outcome
c) increase of isometric strain of myocardium
12.The heart insufficiency with pressure overload is characterized by:
a) increase of diastolic filling
b) increase of isometric strain of myocardium
c) fast decompensation
13. The heart hypertrophy is characterized by:
a)
b)
c)
d)
the conductive system of heart lags from increase of myocardium mass
the conductive system of heart advances from increase of myocardium mass
growth of vessels is behind the increase of cardiomyocytes mass
growth of vessels leaves behind the increase cardiomyocytes mass
14. The heart hypertrophy in stage 2 is characterized by:
a)
b)
c)
the increase of myofibrill mass leaves behind the mitochondrium mass
increase
the increase mitochondrium mass leaves behind the myofibril mass increase
the myofibril mass and mitochondrium mass increase equally
15. The heterometrical mechanism of the compensation arises in heart overload
by:
a)
b)
volume
resistance (pressure)
16. The gomeometrical mechanism of the compensation arises in heart overload
by:
a)
b)
volume
resistance (pressure)
17. In the first (emergency) stage compensatory hyperfunction of heart the
synthesis of nucleic acids and proteins:
a)
b)
c)
increases
decreases
it is close to normal
18. What form of heart insufficiency causes blood congestion in the lungs?
a) left ventricle insufficiency
b) right ventricle insufficiency
19. Systemic circulation congestion is observed in insufficiency of:
a) left ventricle
b) right ventricle
20. Intracardiac compensation mechanisms in acute heart insufficiency are:
a) tachycardia
b) bradycardia
c)
d)
e)
decrease of vascular tone
increase of vascular tone
blood volume increase
21. Extracardiac compensation mechanisms in acute heart insufficiency are:
a) tachycardia
b) bradycardia
c) decrease of vascular tone
d) increase of vascular tone
e) blood volume increase
22. A major factor in hypostasis development in heart insufficiency is:
a)
b)
c)
d)
oncotic pressure decrease
vascular permeability increase
increase of osmotic pressure in kidneys
hydrostatic pressure increase in veins
Answers:
1а, 2d, 3a, 4d, 5c, 6d, 7c, 8ab, 9a, 10a, 11ab, 12bc, 13aс, 14a, 15a, 16b, 17a, 18a,
19b, 20a, 21de, 22d.
PATHOLOGY OF HEART RATE. ARTERIAL HYPERTENSION
Tests:
1.
a)
b)
c)
d)
e)
2.
a)
b)
c)
d)
What excess of systolic pressure value in the pulmonary artery leads to
pulmonary hypertensia?
100 mm Hg
50 mm Hg
40 mm Hg
30 mm Hg
20 mm Hg
What excess of systolic pressure value of blood in the greater circulation
leads to hypertensia development?
120 mm Hg
130 mm Hg
140 mm Hg
160 mm Hg
3. What excess of diastolic pressure value leads to hypertensia development?
a) 80 mm Hg
b) 85 mm Hg
c) 90 mm Hg
d) 100 mm Hg
4. What pathology is risk factor of arterial hypertensia?
a) diabetes
b) diabetes insipidus
c) allergy
5. The least duration of myocardium ischemia which leads to cardyomyocytes
irreciprocal damage is?
a) 10 min
b) 20 min
c) 30 min
d) 40 min
e) 50 min
6. What is the basic energy source in the heart?
a)
b)
c)
d)
noneterificite fatty acids
glucose
amino acids
ketone bodies
7. The atrioventricular block of I degree is characterized by:
a)
b)
c)
d)
elongation of Р-Q interval
occurrence of the Venkebah-Samojlov periods
missed ventricular contractions
contraction of auricles independent from each other and ventricles
8. What is characteristic of the atrioventricular block of I degree (type of I
Mobits)?
a)
b)
c)
d)
elongation of Р-Q interval
occurrence of the Venkebah-Samojlov periods
fallout of some ventricle contractions
contraction of auricles independent from each other and ventricles
9. The full atrioventricular block is characterized by:
a)
b)
c)
d)
elongation of Р-Q interval
occurrence of the Venkebah-Samojlov periods
fallout of some ventricle contractions
contraction of auricles independent from each other and ventricles
10. In what type of blockage Morgani-Adams-Stoke attacks are most common?
a)
b)
c)
d)
e)
sinoatrium
intraatrial
atrioventricular of the I degree
atrioventricular of the II degree (type of I Mobits)
full atrioventricular block
11. At what extrasystole does full compensatory pause take place?
a)
b)
c)
atrial
atrioventricular
ventricular
12. Fibrillation is characterized by:
a)
b)
chaotic excitation and contraction of cardiomyocytes
paroxismal significant increase of heart contractions
c) alternating of the periods of normal rhythm with tahy- and a bradycardia
d) high frequency of correct rhythm contractions (more than 400 per minute)
13. Trembling of auricles or ventricles is characterized by
a)
b)
c)
d)
chaotic excitation and contraction of cardiomyocytes
paroxismal significant increase of heart contractions
alternating of the perods of normal rhythm with tahy- and a bradycardia
high frequency of contractions (more than 200 per minute)
14.Paroxismal tachycardia is characterized by
a)
b)
c)
d)
chaotic excitation and contraction of some cardiomyocytes
paroxismal significant increase of heart contractions
alternating of the periods of normal rhythm, tahy- and bradycardia
high frequency of correct rhythm contractions (more than 200 per minute)
15. Sinus arrhythmia is characterized by:
a)
b)
c)
e)
chaotic excitation and contraction of some cardiomyocytes
paroxismal significant increase of heart contractions
alternating of the periods of normal rhythm with tahy- and a bradycardia
high frequency of correct rhythm contractions (more than 200 per minute)
Answers:
1d, 2c, 3c, 4a, 5d, 6a, 7a, 8abc, 9d, 10e, 11c, 12a, 13d, 14b, 15c.
PATHOLOGY OF RESPIRATORY SYSTEM
Tests:
1.
What infringements can lead to external breath insufficiency?
a) alveolar ventilation
b) diffusion of gases through alveolo-capillary membrane
c) transport of oxygen blood from lungs to tissues
d) tissue oxigenation
2.
What systems participate in external breath?
a) respiratory
b) blood circulation
c) blood
d) central nervous system
e) excretion
3.
Give causes of alveolar ventilation disturbances:
a) reduction of respiratory surface of lungs
b) constriction of respiratory tract
4.
What is the mechanism of obstructive infringements of alveolar ventilation?
а) reduction of respiratory surface of lungs
b) infringement of passableness of respiratory tracts
5.
Restrictive infringement of pulmonary ventilation are observed at:
a) pneumonia
b) pleurisy
c) retropharyngeal abscess
d) bronchial asthma
6.
Obstructive infringements of pulmonary ventilation are observed in:
a) bronchial asthma
b) emphysema of lungs
c) pneumonia
d) tuberculosis
e) pleurisy
1.
How is the residual volume changed in obstructive type of pulmonary
insufficiency?
a) no change
b) increased
c) decreased
2. How is the residual volume changed in restrictive type of pulmonary
insufficiency?
a) no change
b) increased
c) decreased
9.
The vital capacity of lungs is volume of air which can be exhaled after?
a) the maximum breath
b) usual exhalation
c) usual breath
10. How is the vital capacity of lungs changed in obstructive type of pulmonary
insufficiency?
a) no change
b) decreased
c) increased
11. How is the vital capacity of lungs changed in restrictive type of pulmonary
insufficiency?
a) decreased
b) no change
c) increased
12. What is the Tiffno index?
a) the attitude of the forced vital capacity of lungs to the first second of vital
capacity (VC), expressed in percentage
b) ratio of VC to respiratory volume
c) ratio of VC to reserve volume of an expiration
13. How the Tiffno index variates in obstructive model of respiratory
insufficiency?
a) isn’t changed
b) decreases
c) increases
14. How the Tiffno index variates in restrictive model of respiratory insufficiency?
a) decreases
b) isn’t changed
c) increases
15. The perfusion respiratory insufficiency is caused by?
a) reduction of blood-groove through lungs
b) reduction of lungs ventilation
c) augmentation of blood-groove through lungs
16. What pathologies cause perfusion respiratory insufficiency?
a) chronic bronchitis
b) bronchial asthma
c) pulmonary embolism
d) congenital heart diseases with the shunt from right to left
17.
What factors cause respiratory insufficiency of obstructive model?
a) bronchospasm
b) foreign bodys in respiratory paths
c) pneumothorax
e) thyroid gland enlargement
18. What index variates in obstructive model of respiratory insufficiency?
a) minute volume of breath
b) index Tiffno
c) vital capacity of lungs
19. What pathology appears at reduction of surfactant synthesis in lungs?
a) pneumonia
b) hypostasis of lungs
c) pneumofibrosis
d) pulmonary collapse
20. What pathology leads to occurrence of restrictive model of respiratory
insufficiency?
a) bronchial asthma
b) bronchitis
c) pneumofibrosis
21. What kind of infringement of alveolar ventilation occurs in secund
pneumothorax?
a) the obstructive
b) restrictive
22. The restrictive infringement model is characterized by:
a) lungs straight
b) patency of upper airways
c) patency of lower airways
23. What type of dyspnoe occurs in restrictive model of alveolar ventilation
disturbance?
a) inspiratory
b) expiratory
24. What type of dyspnoe is observed in bronchiolospasm?
a) inspiratory
b) admixed
c) expiratory
25. What type of dyspnoe is observed in stricture formation in tracheas and
larynx?
a) inspiratory
b) expiratory
c) admixed
26. What character of respiration is observed in upper respiratory paths stenosis?
a) frequent and superficial
b) frequent and penetrating
c) infrequent and superficial
d) infrequent and penetrating
27. What character of breath is observed in the first period of asphyxia?
a) frequent and penetrating
b) frequent and superficial
c) infrequent and superficial
28. What character of breath is observed in the second period of asphyxia?
a) frequent and penetrating
b) frequent and superficial
c) infrequent and penetrating
d) infrequent and superficial
29. What character of breath is observed in the third period of asphyxia?
a) penetrating and frequent
b) infrequent and superficial
c) apnoea
d) infrequent and penetrating
30. Hemodynamics in the first period of asphyxia is characterised by:
a) increase of minute volume of blood
b) increase of arterial blood pressure
c) reduction of minute volume of blood
d) reduction of arterial blood pressure
e) asystolia
31. Hemodynamics in the second period of asphyxia is characterised by:
a) increase of minute volume of blood
b) increase of arterial blood pressure
c) reduction of minute volume of blood
d) reduction of arterial blood pressure
e) asystolia
32. What model of dyspnea is observed in emphysema of lungs?
a) inspiratory
b) expiratory
33. Chejn-Stokes breath is characterized by:
a) apnoea alternates with respiratory locomotions of increasing, and then
decreasing depth
b) apnoea alternates with respiratory locomotions of identical depth
c) bradypnoea with the enhanced inhale and exhale
d) deep and noisy breath
34. Biot breath is characterised by:
a) apnoea alternates with respiratory locomotions of increasing, and then
decreasing depth
b) apnoea alternates with respiratory locomotions of identical depth
c) bradypnoea with the enhanced inhale and exhale
d) deep and noisy breath
35. Cussmaul breath is characterised by:
a) apnoea alternates with respiratory locomotions of increasing, and then
decreasing depth
b) apnoea alternates with respiratory locomotions of identical depth
c) bradypnoea with the enhanced inhale and exhale
d) deep and noisy breath
Answers:
1аb, 2abcd, 3a, 4b, 5ab, 6ab, 7b, 8c, 9a, 10a, 11a, 12a, 13b, 14b, 15a, 16cd, 17abd,
18b, 19d, 20c, 21b, 22a, 23a, 24c, 25c, 26d, 27a, 28b, 29b, 30ab, 31cd, 32b, 33a,
34b, 35d.
KIDNEY PATHOLOGY
Tests:
1.
The factors promoting increase of glomerular filtration:
a) hydrostatic pressure augmentation in capillars
b) hydrostatic pressure reduction in capillars
c) augmentation of oncotic pressure in capillars
d) reduction of oncotic pressure in capillars
e) augmentation of intrarenal pressure
2.
The factors causing decrease of glomerular filtration:
a) decrease in a tone of efferent arteriole
b) decrease of oncotic pressure in capillars
c) iincrease of oncotic pressure in capillars
d) decrease in intrarenal pressure
e) increase of intrarenal pressure
3.
The materials which are exposed to reabsorption in proximal departments of
renal tubule:
a) glucose
b) amino acids
c) Nа
d) inulin
4.
The factors disturbing reabsorption of substances in proximal departments
of renal tubule:
a) depressing of activity of ferments in renal tubule epithelium
b) increaseв activity of ferments in renal tubule epithelium
c) surplus of reapsorption materials in primary urine
d) tubule damage
5.
The water reabsorption in proximal department of renal tubule is caused:
a) active transport Nа+
b) glucose reabsorption
c) reabsorption K+
d) vasopressinum action
6.
Factors of water reabsorption decrease in proximal kidney tubule
nephroses:
a) primary urine osmolar depressing
b) glucose level increase above 10,0 mmol/l in blood
c) electrocortin introduction
d) furosemide Introduction
7.
The water reabsorption in distal department of renal tubule is controlled by:
a) vasopressinum
b) electrocortin
c) atrial natriuretic factor
d) insulin
8.
Hyposthenuria is:
a) depressing of relative density of urine
b) depressing of diurnal diuresis
c) decresed urination frequency
9.
Hyposthenuria is caused by:
a) tubular nephron device damage
b) Shumljansky-Boumen sheath damage
c) acute glomerulonethrithis
d) chronic glomerulonethrithis
10.
Hypersthenuria is:
a) increase of urination frequency
b) increase of relative density of urine
c) prevalence of a night diuresis over a diurnal diuresis
11.
Hypersthenuria is caused by:
a) tubular nephron device damage
b) acute glomerulonethritis
c) chronic glomerulonethritis
12.
Polyuria is augmentation:
a) diurnal quantity of urine more than 2: l
b) urination frequency
c) portions of urine
13.
Oliguria is:
a) hematocrite index decrease
b) diurnal quantity of urine reduction less than 0,5/l
c) circulating blood volume reduction
d) decresed urination frequency
14.
Anuria is:
a) augmentation of diurnal quantity of urine (it is more 1,5)
b) reduction of diurnal quantity of urine (less than 0,5)
c) reduction of diurnal quantity of urine (less than 100 ml)
15.
The renal clearance is:
a) volume of plasma which refines from the yielded material nephroses at
one minute
b) minute diuresis
c) the volume of urine formed in one minute
16.
c)
To detect the volume glomerular filtration substances which... are used:
a) precipitate out by a filtration in renal glomuluses
b) are not exposed to an anatropic reabsorption
are exposed to an anatropic reabsorption
17.
a)
b)
c)
d)
To detect glomerular volume filtration following substances are used:
inulin
endogenous kreatinine
glucose
protein
18.
a)
b)
c)
d)
Normal protein level in urine of the adults comprises:
less than 0,033 g/l
0,33 g/l
0,66 g/l
1 g/l
19.
a)
b)
c)
The proteinuria ekstrarenal causes are:
paraproteinemia
tubular epithelium damage
chronic renal insufficiency
d) diabetes insipidus
e) inflammatory processes in urinary paths
20.
The polyuria renal causes are:
a) diabetes
b) renal insufficiency
c) chronic glomerulonethrithis
d) inflammatory processes in urinary paths
21.
Basic pathogenesis links of acute diffusive glomerulonephrirthis are:
a) decrease in a circulation of blood in nephroses
b) infringement of tubules secretory function
c) occurrence of antibodies against streptococcus antigens
d) lack of liposoluble vitamins
22.
Nethrotic syndrome symptoms are:
a) decrease in quantity of lipids in blood
b) proteinuria
c) high blood pressure
d) hypoproteinemia
e) hypercholesterinemia
23.
The mechanism of filtration decrease in hypovolemic shock:
a) decrease in effective filtration pressure
b) area reduction of the glomerular filter
c) decrease in permeability of membranes of glomuluses
24.
The mechanism of glomerular filtration decrease in urinary retention is
following:
a) decrease in effective filtration pressure
b) area reduction of the glomerular filter
c) decrease in permeability of membranes of glomuluses
25.
The mechanism of glomerular filtrations decrease the at chronic
glomerulonephrithis:
a) decrease in effective filtration pressure
b) area reduction of the glomerular filter
c) blood oncotic pressure increase
26.
The glucose reabsorption reduces in damage of epithelium of:
a) proximal tubules
b) distal tubules
c) the collective tubules
d) Henle's loops
27.
The reabsorption of amino acids reduces in damage of epithelium of:
a) proximal tubules
b) distal tubules
c) the collective tubules
d) Henle's loops
28.
Albumin-globulin factor in nephrosis:
a) is not variated
b) increases
c) decreases
29.
The protein reabsorption is disturbed in damage of epithelium of:
a) proximal tubules
b) distal tubules
c) the collective tubes
d) henle's loops
30.The main symptom in the development of edemas in nephrotic syndrome is:
a) increase of permeability of pots
b) augmentation of production of electrocortin
c) hypoproteinemia
d) augmentation of production of vasopressinum
31.
Combined increase of glomerular filtration and reduction of tubular fluid
reabsorption leads to:
a) polyuria
b) oliguria
c) anuria
32.
Combined decrease of glomerular filtration and increase of tubular fluid
reabsorption leads to:
a) polyuria
b) oliguria
c) anuria
33.
Increased glomerular filtration accompanied by normal tubular fluid
reabsorption leads to:
a) polyuria
b) oliguria
c) anuria
34.
The reduction of glomerular filtration accompanied by normal tubular fluid
reabsorption leads to:
a) polyuria
b) oliguria
35.
The main pathogeny link of acute renal insufficiency is:
a) glomerular filtration decrease
b) glomerular filtration increase
c) tubular reabsorption decrease
36.
The main pathogeny link of chronic renal insufficiency:
a) renal concentration ability decrease
b) renal concentration ability increase
c) tubular reabsorbtion increase
d) glomerular filtration augmentation
37.
What is observed in the first stage of acute renal insufficiency:
a) oliguria
b) pollakiuria (frequent urination)
c) polyuria
d) nycturia
38.
Mechanisms of metabolic acidosis in renal function disturbances:
a) renal tubules carbonic anhydrase deficiency
b) infringement of process of deamination
c) renal tubules transamination infringement
d) glomerular filtration increase
39.
Azotemia mechanism in renal insufficiency is:
a) glomerular filtration decrease
b) reduction of tubular reabsorption
c) reduction of tubular secretions
40.
Anaemia mechanism in chronic renal insufficiency is:
a) metabolism products excretion infringement
b) organism intoxication
c) erythropoietin insufficiency
d) hemolysis of erythrocytes in renal tubules
Answers:
1аd, 2ace, 3abc, 4aсd, 5ab, 6abd, 7a, 8a, 9ad, 10b, 11b, 12a, 13b, 14c, 15a, 16ab,
17ab, 18a, 19ae, 20bc, 21ac, 22bde, 23a, 24a, 25b, 26a, 27a, 28c, 29a, 30c, 31a,
32b, 33a, 34b, 35a, 36a, 37a, 38ab, 39a, 40c.
PATHOPHYSIOLOGY OF THE LIVER. JAUNDICE
Tests:
1.
The use of glucose in the treatment of hepatic patients is conditioned by:
a) energy source
b) stimulates ammonia neutralisation
c) activates glyconeogenesis in a liver
d) source for formation of glucuronic acid
2.
Name three basic indicative enzymes of the liver damage:
a) LDH (lactate dehydrogenase)
b) ALT (alanine aminotransferase)
c) AST (aspartate aminotransferase)
d) hexokinase
e) glycogensintase
3.
In diffusive lesion of hepatocytes following changes of protein level are
observed:
a) hypoalbuminemia
b) hypergammaglobulinemia
c) hyperalbuminemia
d) hypogammaglobulinemia
4.
How is the level of amino acids in blood variated in liver pathology?
a) increases
b) it is depressed
c) does not variate
5.
Urea level in blood in liver pathology:
a) increases
b) it is depressed
c) is not variated
6.
How is ammonia level in blood variated in liver pathology?
a) it is depressed
b) raises
c) does not variate
7.
Fatty infiltrations of hepatocytes promote development of:
a) increased mobilisation of fats from the depot
b) lipakaine deficiency
c) yield of fat from the liver
d) intensifying lipolisis in the liver
e) lack of ferments β - oxidations of fatty acids
8.
What is the main factor in development of ascites in cirrhosis?
a) decrease in osmotic pressure of blood
b) augmentation of permeability of pots
c) portal hypertensia
d) Increased secretion of atrial natriuretic factor
9.
Termination of bile inflow into the duodenum causes the deficiency of
following vitamins:
a) В1
b) A
c) D
d) В12
10. Lipolysis disturbances are caused инвуашсше ща following substances in the
intestine:
a) bile acids
b) bilirubin
c) cholesterol
11. Decrease of pancreatic lipaseactivity is connected with disturbances in
synthesis of:
a) bile acids
b) bilirubin
c) cholesterol
12. Biochemical composition of blood in haemolytic jaundice is characterised by
increase of:
a) indirect bilirubin
b) direct bilirubin
c) direct and indirect bilirubin
13. Biochemical composition of blood in obstructive (mechanical) jaundice is
characterised by maintenance increase of:
a) indirect bilirubin
b) direct bilirubin
c) direct and indirect bilirubin
14. Biochemical composition of blood in hepatic (hepatocellular) jaundice is
characterised by increased content of:
a) indirect bilirubin
b) direct bilirubin
c) direct and indirect bilirubin
15. Biochemical composition of urine in haemolytic jaundice is characterised by
presence of:
a) indirect bilirubin
b) direct bilirubin
c) urobilin
16. Biochemical composition of urine in obstructive (mechanical) jaundice is
characterised by presence of:
a) direct bilirubin
b) urobilin
c) indirect bilirubin
d) verdoglobin
17. Biochemical composition of urine in hepatic (hepatocellular) jaundice is
characterised by presence of:
a) direct bilirubin
b) indirect bilirubin
c) urobilin
18. Of which jaundicу type cholemia syndrome is characteristic?
a) haemolytic
b) obstructive (mechanical)
c) the hepatic (hepatocellular)
19. What change of heart rhythm activity is characteristic of obstructive
(mechanical) jaundice?
a) tachycardia
b) bradycardia
c) sinus arrhythmia
20. What causes changes in heart rhythm activity in obstructive (mechanical)
jaundice?
a) indirect bilirubin
b) direct bilirubin
c) bile acids
d) cholesterol
21. Which changes of hemostasis characterize hepatic jaundice?
a) increased hemorrhage
b) intravascular thrombosis
22. What manifestations are characteristic of obstructive (mechanical) jaundice?
a) increase of bile acids in blood
b) hypercholesterinemia
c) skin itch
d) tachycardia
e) decrease of direct bilirubin in blood
24. The itch in mechanical jaundice is connected with:
a) hyperbilirubinemia
b)cholemia
c) Infringement of lipids exchange
d) hyperpotassemia
23. What changes in blood are detected in hepatic jaundice?
a) augmentation of direct bilirubin
b) augmentation of indirect bilirubin quantity
c) cholemia
d) urobilinogen augmentation
e) hyperalbuminemia
24. What is characteristic of hepatic insufficiency:
a) augmentation of glycogen synthesis
b) reduction of glycogen synthesis
25. What set of biochemical composition changes of blood characterizes hepatic
coma?
a) hypoglycemia, increased level of amino acids, increased level of ammonia
b) hyperglycemia, reduction of ammonia level
c) hypoglycemia, reduction of amino acids level, increased level of ammonia
d) hyperglycemia, increased amino acids level, reduction of ammonia level.
26. Which of the following substances has the greatest value in pathogeny of
hepatic coma?
a) bilirubin
b) bile acids
c) ammonia
d) urea
27. What clinical symptoms are caused by cholemia?
a) dermal itch
b) bradycardia
c) tachycardia
d) diarrhoeia
e) depressing of arterial pressure
29. How does residual nitrogen variate in liver diseases?
a) does not variate
b) raises
c) drops
30. Portal hypertensia developes if blood preassure in the portal vein is more than:
a) 36 mm Hg
b) 26 mm Hg
c) 16 mm Hg
d) 8 mm Hg
e) 0 mm Hg
31. Liver blood-flow volume in direct Eck fistula is:
a) reduced
b) increased
c) not variated
32. Liver blood-flow volume in inverse Eck-Pavlov fistula is:
a) reduced
b) increased
c) not variated
33. Cholemia syndrome is characterised by increase of following components in
blood:
a) bile acids
b) cholesterol
c) chylomicrons
d) muriatic acid
Answers:
1аd, 2abc, 3ab, 4a, 5b, 6b, 7abе, 8c, 9bc, 10a, 11a, 12a, 13b, 14c, 15c, 16a, 17ac,
18bc, 19b, 20c, 21a, 22abc, 23b, 24abcd, 25b, 26а, 27c, 28abe, 29b, 30d, 31a, 32b,
33ab
PATHOPHYSIOLOGY OF DIGESTION
Tests:
1. Pathological intensifying of appetite is designated by the term:
a) hyperrexia
b) polyphagia
c) disphagia
d) aphagia
e) anorexia
2. Anorexia – is:
a) absence of appetite
b) difficulty in swallowing
c) pathologically increasing of appetite
d) increase of food intake
e) bulimia
3. Bulimia is:
a) absence of appetite
b) difficulty in swallowing
c) pathologically increasing of appetite
d) increase of food intake
e) disturbance of salivation
4. Polyphagia is:
a) absence of appetite
b) difficulty in swallowing
c) pathologically increasing of appetite
d) increase of food intake
e) chewing disorder
5. Dysphagia is:
a) absence of appetite
b) pathologically increasing of appetite
c) increase of food intake
d) difficulty in swallowing
6. Anorexia nervosa occurs in:
a) enteric infection
b) diabetes mellitus
c) hysteria
d) intoxication
e) vomiting
7. Causes of hyperrexia are:
a) diabetes mellitus
b) intoxication
c) pain syndrome
d) suppression of food centre
e) damage of ventrolateral nuclei hypothalami
8. Pararexia is:
a) perversion of appetite
b) fast satiation
c) difficulty in swallowing
d) increasing of appetite
e) decreasing of appetite
9. Causes of hypersalivation are:
a) fever
b) parotitis
c) sialoadenitis
d) sialolithiasis
e) sialolithiasis, toxicosis of pregnancy
10. Consequences of hypersalivation are:
a) scurf on tongue
b) lack of K+
c) caries
d) inflammation in oral cavity
e) xerostomia
11. Hyposalivation leads to:
a) neutralisation of gastric juice
b) maceration of skin around mouth
c) hypokaliemia
d) ptyalism (sialorrhea)
e) xerostomia
12. What is the main effect of leptin, synthesised in adipcytes?
a) it enhances inhibition in CNS
b) it activates excitation in CNS
c) it oppresses appetite
d) it increases appetite
13. Where neuropeptid Y – the basic activator of sense of hunger - is developed?
a) stomach
b) small intestine
c) adipocytes
d) hypothalamus
14. How does appetite change in ventrolateral nucleus of hypothalamus irritation?
a) does not change
b) increases
c) reduces
15. Hyposalivation causes:
a) acidity reduction in the stomach
b) swallowing disorders
c) organism dehydration
d) gastroesophagal reflux
16. Caries is promoted by intake of:
a) sweet
b) salty
c) fat
17. Incoercible vomiting causes:
a) metabolic acidosis development
b) development nongaseous alkalosis
c) increase of arterial pressure
d) hyperglycemia
e) hyperchlorhydria
18. Vomiting causes:
a) hypernatriemia
b) hypochloremia
c) metabolic acidosis
d) hyperosmolar dehydration
19. Vomiting has protective-adaptive value in:
a) pregnancy toxicosis
b) reception of substandard nutrition
c) brain tumours
d) emotional shock
e) hydrocephaly
20 Stomach gases cause:
a) hiccups
b) vomiting
c) eructation
d) nausea
e) heartburn
21. The heartburn developes in:
a) achylia
b) depressing of esophagus receptors sensitivity to stomach contents
c) low intragastric pressure
d) gastroduodenal reflux
22. In insufficiency of ezofago-gastric sphincter occurs:
a) regurgitation of stomach content into the esophagus
b) decrease in peristalsis of the esophagus;
c) difficulty in peristaltic activity
d) Food ingestion disturbances
e) Congestion and rotting of food in the esophagus.
23. What substances activate stomach secretion?
a) somatostatin
b) gastrin
c) acetylcholine
d) histamine
e) adrenaline
24. What substances stimulate stomach motility?
a) adrenaline
b) noradrenaline
c) acetylcholine
d) motiline
e) cholecystokinin
25. What of substences stimulate secretion of pancreatic juice ?
a) somatostatin
b) acetylcholine
c) secretin
d) adrenaline
e) motiline
26. What material stimulates secretion and motility of all departments of the
gastrointestinal tract?
a) adrenaline
b) acetylcholine
c) hydrocortisone
d) histamine
e) gastrin
27. What hormone inhibits secretion of all departments of the gastrointestinal tract?
a) hydrocortisone
b) heparin
c) somatostatin
d) vasoactive intestinal peptide
e) serotonin
28.
The absence of enzymes and hydrochloric acid in gastric juice is called?
a) achlorhydria
b) acholia
c) achylia
29.
How is the activity of peptases changed in hypoacidosis state?
a) is depressed
b) increases
c) is not changed
30.
How is the activity of peptases changed in hyperacidosis state?
a) is depressed
b) increases
c) is not changed
31.
What changes in the stomach are caused by excessive increase of
parasympathetic nerves tone?
a) reduction of muriatic acid formation
b) increased secretion of gastric juice
c) reduction of histamine allocation
d) increased histamine allocation
e) hydrochloric acid hypersecretions
32.
Specify the possible causes of stomach hypersecretion development:
a) excessive parasympathetic stimulation of the stomach
b) excessive sympathetic stimulation of the stomach
c) increased gastrin synthesis
d) gastrin synthesis deficiency
e) increase of histamine synthesis in the stomach wall
33.
Specify the possible causes of stomach hyposecretion development:
a) stomach excessive parasympathetic stimulation
b) decrease in gastrin synthesis
c) increase of histamine synthesis
d) decrease of secretin synthesis
34.
Specify consequences of achlorhydria:
a) depressing of secretin synthesis by duodeni mucosa
b) decrease of gastric juice peptic ferments activity
c) inhibition of food evacuation from the stomach into the intestine
35.
The mechanism of stomach ulcer occurrence in a stress includes:
a) ischemia of the mucous
b) hyperemia of the mucous
c) intensifying of secretion of gastric mucosa
d) increased endorpines secretion
e) oppression of regeneration properties of epithelium
36.
Absorption of which vitamins is considerably disturbed in acholia?
a) vitamin A
b) vitamin В1
c) vitamin D
d) vitamin E
e) vitamin K
37. Which hormones stimulate mucous and bicarbonate secretion in the
stomach?
a) prostaglandin F2α
b) prostaglandin Е
c) somatostatin
d) hydrocortisone
38. What mechanisms promote hypersecretion and hyperchlorhydria of
gastric juice?
a) intensifying of parasympathetic influences on a stomach
b) intensifying of sympathetic influences on a stomach
c) increase formation of a somatostatin
d) increase formation of histamine
39.
Which substances stimulate insulin development?
a) glucose
b) somatostatin
c) lipids
d) antibodies
40.
The intolerance of milk can cause allergy to:
a) polysaccharides
b) ovalbumin
c) β-laktoglobulin
d) lactose
41.
Stomach ulcer causes:
a) high gastric acidity
b) low activity of factors of protection
c) low gastric acidity
d) blood-flow intensifying in stomach wall
42.
Which hormones reduce the activity of protective factors in the stomach?
a) gastrin
b) secretin
c) hydrocortisone
d) thyroxine
43.
Factors causing the development of stomach ulcer are:
a) increased formation of mucosa in the stomach
b) hypersecretion of bicarbonates
c) increased formation of Prostaglandins Е1 and Е2
d) depressed regeneration of mucosa
44.
Following factors lead to stomach ulcer:
a) blood-flow increase in stomach wall
b) increase of PgЕ formation
c) helycobacter pylori
d) aspirin use
45.
What hormones stimulate secretion of pancreatic juice?
a) somatostatin
b) acetylcholine
c) secretin
d) adrenaline
e) motiline
46
What hormones stimulate secretion and motility of all departments of the
gastrointestinal tract?
a) adrenaline
b) acetylcholine
c) hydrocortisone
d) histamine
e) gastrin
47.
What hormone inhibits secretion of all departments of the gastrointestinal
tract?
a) hydrocortisone
b) heparin
c) somatostatin
d) vasoactive intestinal peptide (VIP)
e) serotonin
48.
The causes of acute pancreatitis are:
a) organism overheating
b) sweet nutrition
c) cholelithiasis
d) alcohol abuse
49.
Give pathogenic stages of acute pancreatitis:
a) activation of ferments in gland
b) increase of arterial preassure
c) increase of pressure in pancreatic ducts
d) hypovolemic shock
50.
Name the principal cause of chronic pancreatitis:
a) mechanical traumas
b) alcohol abuse
c) cholelithiasis
d) heritable disease
51.
More severe clinical course has obstruction of:
a) small intestine
b) large intestine
52.
Malabsorbtion is a syndrome caused by:
a) increased bile inflow into the intestine
b) disturbed absorption of nutrients in the small intestine
c) fasting
d) endocrine function disturbance in the pancreas
53.
The malabsobtion syndrome is characterised by nutritive absorption
disorder in:
a) the stomach
b) the small intestine
c) the thick intestine
d) the rectum
54.
Steatoreja is:
a) allocation of fat with urine
b) fat accumulation in blood
c) allocation of fat with feces
d) allocation stercobilin with feces
e) allocation of urobilin with feces
55. Steatorrhea occurs in:
e)
a) gastric juice hypersecretions
b) acholia
c) high activity of intestinal lipases
d) difficulty of the intestine motility
extra protein in human organism
56. Mechanical intestinal obstruction developes in:
a) spastic stricture or paralysis of intestinal musculation
b) thrombosis of intestinal wall vessels
c) paresis of intestinal muscles
d) tumors and helminthosis an intestine
e) paralysis of intestinal wall vessels
57.
The pathogeny of intestinal autointoxication is caused by toxic influence of:
a) products of rotting of protein in an intestine and biogenic amines
(pentamethylenediamine, putrescin)
b) indirect bilirubin
c) ketone bodies
d) bile acids
e) direct bilirubin
Answers:
1a, 2a, 3c, 4d, 5e, 6c, 7a,8a, 9e, 10b, 11e, 12c, 13d, 14c, 15b, 16a, 17b, 18b, 19b,
20c, 21d, 22a, 23bcd, 24cd, 25bc, 26b, 27c, 28c, 29a, 30b, 31bde, 32ace, 33b,
34ab, 35a, 36acde, 37b, 38ad, 39a, 40c, 41ab, 42c, 43cd, 44cd, 45bc, 46b, 47c,
48cd, 49acd, 50b, 51a, 52b, 53b, 54c, 55b, 56d, 57a.
CONTENTS
DISORDERS OF PERIPHERAL CIRCULATION .............................. 1
INFLAMMATION. ALTERATION AND EXUDATION .................. 6
INFLAMMATION. PROLIFERATION AND REGENERATION
............................................................... Ошибка! Закладка не определена.
THERMAL REGULATORY DYSFUNCTION. FEVER.
HYPERTHERMIA. HYPOTHERMIA ......................................................... 15
IMMUNOLOGICAL DISORDERS. CATEGORIZATION. AIDS ... 21
ALLERGY ........................................................................................... 79
DISORDERS OF CARBOHYDRATE METABOLISM .................... 30
DISORDERS OF LIPID METABOLISM .......................................... 39
DISORDERS OF PROTEIN METABOLISM. GOUT ....................... 47
DISORDERS OF WATER-MINERAL METABOLISM ................... 58
DISORDERS OF ACID-BASE BALANCE ....................................... 65
PATHOLOGY OF VITAMINES ………...
163
CELL PATHOLOGY
…………
HYPOXIA. HYPEROXIA ................................................................... 82
ROLE OF HEREDITY IN PATHOLOGY ……………………..90
EXTREME CONDITIONS. STRESS. SHOCK. COMA. COLLAPSE .
TUMOR GROWING ......................................................................... 101
RADIATION SICKNESS .................................................................. 104
PATHOLOGY OF CIRCULATING BLOOD VOLUME.
BLEEDING…………
ANEMIA…………………
QUANTITATIVE DISORDERS OF NEUTROPHILS.
LEUKOCYTOSIS AND
LEUKOPENIA……………………………………
LEUKEMIA …
DISORDERS OF HEMOSTASIS. THROMBOPHILIC
DISORDERS OF HEMOSTASIS. THROMBOSIS AND EMBOLISM.
DISORDERS OF HEMOSTASIS. HEMORRHAGIC DISORDERS
OF HEMOSTASIS.…
PATHOPHYSIOLOGY OF NERVOUS SYSTEM
PATHOPHYSIOLOGY OF HIGH NERVOUS SYSTEM
ACTIVITY…
PATHOPHYSIOLOGY OF ENDOCRINE SYSTEM. PITUITARY
GLAND AND SUPRARENAL GLAND FUNCTIONS
INFRINGEMENTS…
PATHOPHYSIOLOGY OF ENDOCRINE SYSTEM. PATOLOGY
OF THYROID, PARATHYROID GLANS AND SEX GLANDS
INSUFFICIENCY OF BLOOD CIRCULATION. MYOCARDIAL
INFARCTION…..
PATHOLOGY OF HEART RATE. ARTERIAL HYPERTENSION
PATHOLOGY OF RESPIRATORY SYSTEM…
KIDNEY PATHOLOGY…….
PATHOPHYSIOLOGY OF LIVER. JANDINCE……
PATHOPHYSIOLOGY OF DIGESTION