Questions for Biochem Midterm ( 851 - 920)

Question 1

851. Which one of following statements about the fed and fasting metabolic states is correct?


Select one:
a. In the fasting state glucagon acts to increase the activity of lipoprotein lipase in adipose tissue.
b. In the fasting state, glucagon acts to increase the synthesis of glycogen from glucose.
c. In the fed state insulin acts to increase the breakdown of glycogen to maintain blood glucose.
d. Ketone bodies are synthesized in liver in the fasting state, and the amount synthesized increase as fasting extends into starvation.
e. In the fed state there is decreased secretion of insulin in response to increased glucose in the portal blood.

Answer 1

d. Ketone bodies are synthesized in liver in the fasting state, and the amount synthesized increase as fasting extends into starvation.

(Fatty acids imported from adipose tissue are converted to ketone bodies for export to the brain)

Question 2

Which one of following statements about the fed and fasting metabolic states is correct?

Select one:
a. In the fed state muscle can take up glucose for use as a metabolic fuel because glucose transport in muscle is stimulated in response to glucagon.
b. In the fed state there is decreased secretion of glucagon in response to increased glucose in the portal blood.
c. In the fed state, glucagon acts to increase the synthesis of glycogen from glucose.
d. Plasma glucose is maintained in starvation and prolonged fasting by gluconeogenesis from ketone bodies.
e. There is an increase in metabolic rate in the fasting state.

Answer 2

b. In the fed state there is decreased secretion of glucagon in response to increased glucose in the portal blood.

Question 3

Which one of following statements about the fed and fasting metabolic states is correct?
Select one:
a. In the fasting state muscle synthesizes glucose from amino acids.
b. In the fed state adipose tissue can take up glucose for synthesis of triacylglycerol because glucose transport in adipose tissue is stimulated in response to insulin.
c. Ketone bodies are synthesized in muscle in the fasting state, and the amount synthesized increases as fasting extends into starvation.
d. Ketone bodies provide an alternative fuel for red blood cells in the fasting state.
e. Plasma glucose is maintained in starvation and prolonged fasting by gluconeogenesis from fatty acids.

Answer 3

b. In the fed state adipose tissue can take up glucose for synthesis of triacylglycerol because glucose transport in adipose tissue is stimulated in response to insulin.

(Insulin
-> activates LPL
-> Fatty acid
-> Acyl-CoA
-> triacylglycerol)

Question 4

Which one of following statements about the fed and fasting metabolic states is correct?
Select one:
a. In the fasting state adipose tissue synthesizes glucose from 
the glycerol released by the breakdown of triacylglycerol.
b. In the fasting state adipose tissue synthesizes ketone bodies.
c. In the fasting state the main fuel for red blood cells is fatty 
acids released from adipose tissue.
d. Ketone bodies provide the main fuel for the central nervous 
system in the fasting state.
e. Plasma glucose is maintained in starvation and prolonged fasting by gluconeogenesis in the liver from the amino acids released by the breakdown of muscle protein.

Answer 4

e. Plasma glucose is maintained in starvation and prolonged fasting by gluconeogenesis in the liver from the amino acids released by the breakdown of muscle protein.

Question 5

Which one of following statements about the fed and fasting metabolic states is correct?

Select one:
a. Fatty acids and triacylglycerol are synthesized in the liver in 
the fasting state.
b. In the fasting state the main fuel for the central nervous 
system is fatty acids released from adipose tissue.
c. In the fasting state the main metabolic fuel for most tissues 
comes from fatty acids released from adipose tissue.
d. In the fed state muscle cannot take up glucose for use as a 
metabolic fuel because glucose transport in muscle is 
stimulated in response to glucagon.
e. Plasma glucose is maintained in starvation and prolonged 
fasting by gluconeogenesis in adipose tissue from the glycerol released from triacylglycerol.

Answer 5

c. In the fasting state the main metabolic fuel for most tissues 
comes from fatty acids released from adipose tissue.

Question 6

A 25-year-old man visits his GP complaining of abdominal cramps and diarrhea after drinking milk. What is the most likely cause of his problem?
Select one:
a. Bacterial and yeast overgrowth in the large intestine
b. Infection with the intestinal parasite Giardia lamblia
c. Lack of pancreatic amylase
d. Lack of small intestinal lactase
e. Lack of small intestinal sucrase-isomaltase

Answer 6

Lack of small intestinal lactase

Question 7

Which one of following statements about glycolysis and gluconeogenesis is correct?
Select one:
a. All the reactions of glycolysis are freely reversible for 
gluconeogenesis.
b. Fructose cannot be used for gluconeogenesis in the liver 
because it cannot be phosphorylated to fructose-6- 
phosphate.
c. Glycolysis can proceed in the absence of oxygen only if 
pyruvate is formed from lactate in muscle.
d. Red blood cells only metabolize glucose by anaerobic 
glycolysis (and the pentose phosphate pathway).
e. The reverse of glycolysis is the pathway for gluconeogenesis 
in skeletal muscle.

Answer 7

d. Red blood cells only metabolize glucose by anaerobic 
glycolysis (and the pentose phosphate pathway).

Question 8

Which one of following statements about the step in glycolysis catalyzed by hexokinase and in gluconeogenesis by glucose 6-phosphatase is correct?

Select one:
a. Because hexokinase has a low Km its activity in liver 
increases as the concentration of glucose in the portal 
blood increases.
b. Glucose-6-phosphatase is mainly active in muscle in the 
fasting state.
c. If hexokinase and glucose-6-phosphatase are both equally 
active at the same time there is net formation of ATP from 
ADP and phosphate.
d. Liver contains an isoenzyme of hexokinase, glucokinase, 
which is especially important in the fed state
e. Muscle can release glucose into the circulation from its 
glycogen reserves in the fasting state.

Answer 8

d. Liver contains an isoenzyme of hexokinase, glucokinase, 
which is especially important in the fed state

Question 9

Which one of following statements about this step in glycolysis catalyzed by phosphofructokinase and in gluconeogenesis by fructose 1,6-bisphosphatase is correct?

Select one:
a. Fructose 1,6-bisphosphatase is mainly active in the liver in the fed state.
b. If phosphofructokinase and fructose 1,6-bisphosphatase are both equally active at the same time, there is a net formation of ATP from ADP and phosphate.
c. Phosphofructokinase is inhibited more or less completely by physiological concentrations of ATP.
d. Phosphofructokinase is mainly active in the liver in the fasting state.

Answer 9

c. Phosphofructokinase is inhibited more or less completely by physiological concentrations of ATP.

Question 10

Which one of the following statements about glucose metabolism in maximum exertion is correct?
Select one:
a. Gluconeogenesis from lactate requires less ATP than is formed during anerobic glycolysis.
b. In maximum exertion pyruvate is oxidized to lactate in muscle.
c. Oxygen debt is caused by the need to exhale carbon dioxide produced in response to acidosis.
d. Oxygen debt reflects the need to replace oxygen that has been used in muscle during vigorous exercise.
e. There is metabolic acidosis as a result of vigorous exercise

Answer 10

e. There is metabolic acidosis as a result of vigorous exercise

(Acidosis is caused by an overproduction of lactic acid that builds up in the blood or an excessive loss of bicarbonate from the blood (metabolic acidosis) or by a buildup of carbon dioxide in the blood that results from poor lung function or depressed breathing (respiratory acidosis).)

Question 11

Which one of following statements about glycogen metabolism is correct?
Select one:
a. Glycogen is synthesized in the liver in the fed state, then exported to other tissues in low density lipoproteins.
b. Glycogen reserves in liver and muscle will meet energy requirements for several days in prolonged fasting.
c. Liver synthesizes more glycogen when the hepatic portal blood concentration of glucose is high because of the activity of glucokinase in the liver.
d. Muscle synthesizes glycogen in the fed state because glycogen phosphorylase is activated in response to insulin.
e. The plasma concentration of glycogen increases in the fed state.

Answer 11

c. Liver synthesizes more glycogen when the hepatic portal blood concentration of glucose is high because of the activity of glucokinase in the liver.
(Glucokinase functions as the glucose sensor in the beta cell by controlling the rate of entry of glucose into the glycolytic pathway (glucose phosphorylation) and its subsequent metabolism. )

Question 12

Which one of following statements about glucose metabolism is correct?

Select one:
a. Glucagon increases the rate of glycolysis.
b. Glycolysis requires NADP+.
c. In glycolysis, glucose is cleaved into two three carbon compounds.
d. Substrate level phosphorylation takes place in the electron transport system.
e. The main product of glycolysis in red blood cells is pyruvate.

Answer 12

c. In glycolysis, glucose is cleaved into two three carbon compounds.

Question 13

Which one of following statements about glycogen metabolism is correct?

Select one:
a. Glycogen synthase activity is increased by glucagon.
b. Glycogen phosphorylase is an enzyme that can be activated by phosphorylation of serine residues.
c. Glycogen phosphorylase cannot be activated by calcium ions.
d. cAMP activates glycogen synthesis.
e. Glycogen phosphorylase breaks the α1-4 glycosidic bonds by hydrolysis.

Answer 13

b. Glycogen phosphorylase is an enzyme that can be activated by phosphorylation of serine residues.

Question 14

Which statements are true for the activity of thrombin?

Select one or more:
a. Conversion of fibrinogen to fibrin
b. Activation of Factor XIII
c. Inactivation of Factor VIII
d. Activation of platelets

Answer 14

a. Conversion of fibrinogen to fibrin
b. Activation of Factor XIII
d. Activation of platelets

(- Activates platelets – GpIb receptor:
Binds to exosite II, which increases FXI and further increases platelet activation by thrombin)

Question 15

Which statements are true concerning the anticoagulant effects of thrombin?

Select one or more:
a. It activates Protein C, which in turn destroys the prothrombinase.
b. Bound to thrombomodulin it is an efficient activator of Protein C
c. It activates Factor XI
d. It inactivates Factor V

Answer 15

a. It activates Protein C, which in turn destroys the prothrombinase.
b. Bound to thrombomodulin it is an efficient activator of Protein C

Question 16

Which compounds are endogenous inhibitors of thrombin?
Select one or more:
a. Heparin
b. Antithrombin
c. Hirudin
d. α1 protease inhibitor
e. 1-protease inhibitor

Answer 16

b. Antithrombin (Serpins)
d. α1 protease inhibitor
e. 1-protease inhibitor

(Antithrombin – Thrombin, (FXa, (FIXa)) – target of heparin therapy
α1 protease inhibitor – Trypsin, elastase, thrombin (Serpins))

Question 17

The Leiden mutation (activated Protein C resistance) is accompanied by thrombophilia, because

Select one:
a. activated Protein C functions efficiently
b. Protein C activation by thrombin is not accelerated by thrombomodulin
c. Factor V activation is facilitated
d. activated Protein C cannot inactivate Factor Va

Answer 17

d. activated Protein C cannot inactivate Factor Va

Question 18

What is true about the tissue factor?

Select one or more:
a. It is a blood coagulation factor with protease activity
b. It is a protein without any enzyme activity
c. It is a cofactor for Factor VIIa
d. It is an activator for Factor XII

Answer 18

b. It is a protein without any enzyme activity
c. It is a cofactor for Factor VIIa

Question 19

What could be a cause of the bleeding trend in hemophilia?
Select one or more:
a. Factor Xa cannot activate prothrombin
b. Factor X is resistant to activated protein C
c. Factor VIII is deficient
d. Factor IX is deficient

Answer 19

c. Factor VIII is deficient
d. Factor IX is deficient

Question 20

What is the importance of phospholipids of the activated platelet?

Select one or more:
a. They form a scaffold for the formation of blood coagulation complexes
b. They serve as a binding site for FXIII
c. They increase the rate of inactivation of blood coagulation enzymes
d. They interact with proteins containing Gla-domain

Answer 20

a. They form a scaffold for the formation of blood coagulation complexes
d. They interact with proteins containing Gla-domain

Question 21

What happens when Gla is not formed?

Select one:
a. Several blood clotting proteins cannot bind to phospholipid surface
b. Several blood clotting proenzymes are rapidly activated
c. The activated blood coagulation factors are efficiently inactivated
d. The inhibitor system of blood coagulation is inactivated

Answer 21

a. Several blood clotting proteins cannot bind to phospholipid surface

Question 22

What impairs the formation of Gla in the blood coagulation proteins?

Select one or more:
a. Vitamin K deficiency
b. Administration of coumarine derivates
c. Liver failure
d. Inhibiition of Vitamin K oxidoreductase

Answer 22

All of them

Question 23

What is true about the prothrombinase complex?

Select one or more:
a. It contains prothrombin. which is bound to Factor Va via its Gla domain
b. Factor Xa hydrolizes two peptide bonds in the prothrombin
c. Factor Va is bound to Factor Xa via its Gla-domain
d. Vitamin K antagonists inhibit the formation of the prothrombinase complex
e. The catalytic efficiency of Factor Xa increases by several orders of magnitude in the complex

Answer 23

b. Factor Xa hydrolizes two peptide bonds in the prothrombin
d. Vitamin K antagonists inhibit the formation of the prothrombinase complex
e. The catalytic efficiency of Factor Xa increases by several orders of magnitude in the complex

Question 24

Which factors contribute to the regulation of the prothrombinase complex?

Select one or more:
a. Activation of Factor V by thrombin
b. Activation of protein C by thrombin
c. Gla-domains Binding of prothrombin and X-factor to phospholipids through Gla-domains
d. Inactivation of Factor Xa by tissue factor pathway inhibitor (TFPI)

Answer 24

All of them

Question 25

What is the role of Factor XIIa in hemostasis?

Select one or more:
a. It initiates the blood coagulation after mechanical injury to prevent bleeding
b. It induces fibrinolysis
c. It may cause vasoconstriction
d. It may cause vasodilation
e. It triggers blood coagulation at sites of inflammation

Answer 25

b. It induces fibrinolysis
c. It may cause vasoconstriction
d. It may cause vasodilation
e. It triggers blood coagulation at sites of inflammation

Question 26

Select the tools for platelet inhibition with therapeutic potential!

Select one or more:
a. Inhibition of TXA2 synthesis
b. Inhibition of the thrombin receptor by heparin
c. Inhibition of ADP release by plasminogen activator
d. Inhibition of platelet aggregation by warfarin
e. Inhibition of cyclooxygenase by aspirin

Answer 26

a. Inhibition of TXA2 synthesis
e. Inhibition of cyclooxygenase by aspirin

Question 27

What is true concerning the hemostatic function of platelets?
Select one or more:
a. They adhere on collagen
b. Platelets form aggregates with other platelets
c. They provide the surface for assembly of blood coagulation complexes
d. ADP is released from platelet granules
e. During activation TXA2 is synthesized

Answer 27

All of them

Question 28

What is true concerning PGI2?

Select one:
a. It is synthesized from free arachidonic acid
b. It is released from phospholipids by phospholipase C.
c. Its synthesis in platelets is catalyzed by prostacycline synthase
d. It inhibits the PAR-1 receptor of platelets

Answer 28

a. It is synthesized from free arachidonic acid

(function: Inhibits platelet aggregation by increasing levels of cAMP)

Question 29

What is true for fibrinolysis?
Select one or more:
a. Fibrin is degraded by proteolytic enzymes
b. Fibrin Crosslinked by Factor XIIIa is not degraded
c. Plasmin is synthesized as a proenzyme
d. Plasmin bound to fibrin is inactivated by α2-plasmin inhibitor more efficiently than free enzyme

Answer 29

a. Fibrin is degraded by proteolytic enzymes
c. Plasmin is synthesized as a proenzyme

Question 30

What is the difference between tissue-type (tPA) and urokinase type (uPA) plasminogen activator?

Select one or more:
a. tPA is active in the presence of tissue factor
b. uPA is an efficient enzyme in the presence of urine
c. tPA activity is equivalent with uPA only in the presence of cofactors
d. uPA is synthesized as a proenzyme
e. The plasminogen activator inhibitor (PAI-1) inactivates only cofactor bound tPA.

Answer 30

c. tPA activity is equivalent with uPA only in the presence of cofactors
d. uPA is synthesized as a proenzyme

Question 31

What is true for streptokinase?

Select one:
a. It belongs to the group of protein kinases
b. It has proteolytic activity
c. It is synthesized by endothelial cell
d. As a fibrinolytic enzyme cleaves peptide bonds in fibrin
e. It forms a complex with human plasminogen. and the complex acts as a plasminogen activator

Answer 31

e. It forms a complex with human plasminogen. and the complex acts as a plasminogen activator

Question 32

What is true about α2-plasmin inhibitor?

Select one or more:
a. One of the most efficient endogenous protease inhibitors
b. It forms an equimolar complex with plasmin.
c. It inhibits fibrin-bound plasmin faster than the free plasmin in circulating blood
d. The inhibitor is covalently bound to fibrin by Factor XIIIa

Answer 32

a. One of the most efficient endogenous protease inhibitors
b. It forms an equimolar complex with plasmin.
d. The inhibitor is covalently bound to fibrin by Factor XIIIa

Question 33

Which inherited defect causes thrombophilia?

Select one or more:
a. Protein C deficiency
b. Antithrombin deficiency
c. Factor VIII deficiency
d. Factor V R506Q mutation
e. Factor XI deficiency

Answer 33

a. Protein C deficiency
b. Antithrombin deficiency
d. Factor V R506Q mutation

Question 34

Which factor inactivates thrombin?

Select one:
a. Activated protein C
b. Antithrombin
c. Heparin
d. α2-plasmin inhibitor

Answer 34

Antithrombin

Question 35

What is true concerning the mechanism of action of drugs used to treat thrombosis?

Select one or more:
a. Heparin dissolves thrombi
b. Heparin directly inhibits thrombin
c. Coumarins dissolve the prothrombinase complex
d. Aspirin prevents platelet aggregation
e. Coumarins inhibit Gla formation

Answer 35

d. Aspirin prevents platelet aggregation
e. Coumarins inhibit Gla formation

Question 36

What is true concerning the function of thrombin?

Select one or more:
a. It converts fibrinogen to fibrin
b. It activates protein C
c. It converts factor VIII to an active enzyme
d. It activates platelets
e. It converts factor XIII to an active protease

Answer 36

a. It converts fibrinogen to fibrin
b. It activates protein C
d. It activates platelets

Question 37

Which process could be a trigger (initial step) of blood coagulation in vivo?

Select one or more:
a. The contact of tissue-factor with blood
b. Conversion of prothrombin to trombin
c. Contact activation of Factor XII on a negatively charged surface
d. Conversion of Factor X to Factor Xa by Factor IXa

Answer 37

a. The contact of tissue-factor with blood
c. Contact activation of Factor XII on a negatively charged surface

Question 38

How do platelets contribute to thrombus formation?

Select one or more:
a. With secretion of ADP
b. With formation of phospholipid surface for assembly of blood coagulation factors
c. With synthesis of thromboxane A2 (TXA2)
d. With secretion of plasminogen activator inhibitor 1 (PAI-1)

Answer 38

All of them

Question 39

What could trigger platelet activation?
Select one or more:

a. Tissue factor
b. Thrombin
c. Collagen
d. ADP
e. Factor XIIa

Answer 39

b. Thrombin
c. Collagen
d. ADP

Question 40

What is the background of the anti-thrombotic action of aspirin?

Select one:
a. Aspirin inhibits the prothrombin activation by Factor Xa
b. Aspirin inhibits the cyclooxygenase activity in endothelial cell
c. Aspirin inhibits the cyclooxygenase activity in platelet
d. Aspirin induces the release of fibrinolytic enzymes from endothelial cell

Answer 40

c. Aspirin inhibits the cyclooxygenase activity in platelet

Question 41

What is the background of the administration of tPA as a safe thrombolytic agent?

Select one or more:
a. tPA is a protease which dissolves fibrin directly
b. tPA is an enzyme which converts plasminogen to plasmin
c. tPA is not inactivated by plasma protease inhibitors
d. fibrin is a cofactor of tPA

Answer 41

b. tPA is an enzyme which converts plasminogen to plasmin
d. fibrin is a cofactor of tPA

Question 42

What is the background of tPA administration as a safe thrombolytic therapy?

Select one:
a. tPA degrades fibrin directly
b. Plasminogen is converted by tPA to plasmin and the latter degrades fibrin
c. tPA inhibits platelet aggregation
d. tPA inactivates α2-plasmin inhibitor, thus plasmin can digest thrombi

Answer 42

b. Plasminogen is converted by tPA to plasmin and the latter degrades fibrin

Question 43

What is true about the mechanism of action of streptokinase?

Select one or more:
a. Streptokinase acts as a fibrinolytic protease and digests fibrin
b. Streptokinase acts as a plasminogen activator and cleaves the activation peptide of plasminogen
c. Streptokinase forms a complex with plasminogen and the complex has the same activity as plasmin
d. Streptokinase forms a complex with plasminogen and the complex acts as plasminogen activator

Answer 43

d. Streptokinase forms a complex with plasminogen and the complex acts as plasminogen activator

Question 44

What is true about urokinase type plasminogen activator (uPA)?

Select one or more:
a. It is a fibrinolytic enzyme, which digests fibrin
b. It is synthesized by endothelial cell and released as an active protease
c. It coverts plasminogen to a fibrinolytic enzyme
d. It is inactivated by PAI-1 (plasminogen activator inhibitor-1)
e. It is synthesized in the form of a single chain proenzyme

Answer 44

c. It coverts plasminogen to a fibrinolytic enzyme
d. It is inactivated by PAI-1 (plasminogen activator inhibitor-1)
e. It is synthesized in the form of a single chain proenzyme

Question 45

What is the function of liver in hemostasis?

Select one or more:
a. It synthesizes blood coagulation factors
b. It modifies Glu to Gla in some proteins
c. It take up removes enzyme-inhibitor complexes from circulating blood
d. It synthesizes inhibitors of the blood coagulation-fibrinolytic system
e. It releases tissue factor in blood circulation

Answer 45

a. It synthesizes blood coagulation factors
b. It modifies Glu to Gla in some proteins
c. It take up removes enzyme-inhibitor complexes from circulating blood
d. It synthesizes inhibitors of the blood coagulation-fibrinolytic system

Question 46

How do coumarins influence blood coagulation?
Select one or more:
a. They block the Vitamin K function
b. They prevent the Gla domain formation
c. They inhibit the γGlu-carboxylase enzyme
d. They inhibit the prothrombinase complex

Answer 46

a. They block the Vitamin K function
b. They prevent the Gla domain formation

Question 47

What is true about the in vivo function of Factor XII?

Select one or more:
a. Initiation of blood coagulation
b. Formation of vasoactive peptides
c. Activation of Factor XI
d. Facilitation of fibrinolysis

Answer 47

All of them

Question 48

What is true about the anti-thrombotic properties of endothelial cells?

Select one or more:
a. They synthesize thrombomodulin, which inactivates thrombin
b. They synthesize plasminogen activators, which initiate fibrinolysis
c. They produce TFPI (tissue factor pathway inhibitor), which inactivates tissue factor
d. They produce TFPI, which inactivates both Factor Xa and Factor VIIa

Answer 48

b. They synthesize plasminogen activators, which initiate fibrinolysis
d. They produce TFPI, which inactivates both Factor Xa and Factor VIIa

Question 49

What is the background of the platelet-inhibiting properties of endothelial cells?

Select one or more:
a. They synthesize and secrete PGI2
b. They express ecto-ADP-ase enzyme on their surface
c. They produce plasminogen activators
d. They generate TFPI, which inactivates tissue factor

Answer 49

a. They synthesize and secrete PGI2
b. They express ecto-ADP-ase enzyme on their surface

(PGI2, a prostaglandin -Inhibits platelet aggregation by increasing levels of cAMP)

Question 50

What is true about the protease-activated receptors (PARs)?
Select one or more:
a. They trigger the blood coagulation cascade
b. Their activation prevents platelet adhesion
c. They trigger platelet aggregation
d. They activate endothelial cells
e. They activate phospholipase C

Answer 50

c. They trigger platelet aggregation
d. They activate endothelial cells
e. They activate phospholipase C

Question 51

Which statements are valid for the lupus anticoagulant?

Select one or more:
a. It is a potent drug for the inhibition of blood clotting
b. Its presence in blood is related to thrombosis
c. It is an immunoglobulin which binds phospholipids
d. It prolongs the laboratory blood clotting assays
e. It shortens the laboratory blood clotting assays

Answer 51

b. Its presence in blood is related to thrombosis
c. It is an immunoglobulin which binds phospholipids
d. It prolongs the laboratory blood clotting assays

Question 52

The clinical symptoms of antiphospholipid syndrome can be treated with

Select one or more:
a. Vitamin K
b. Vitamin K antagonists
c. Folic acid
d. Antifolates
e. Heparin
f. Protamine

Answer 52

b. Vitamin K antagonists
e. Heparin

(Antiphospholipid syndrome (APS), sometimes known as Hughes syndrome, is a disorder of the immune system that causes an increased risk of blood clots. This means people with APS are at greater risk of developing conditions such as: DVT (deep vein thrombosis, a blood clot that usually develops in the leg.)

Question 53

Which statements are true for the activated protein C resistance?

Select one or more:
a. It is a genetic defect of protein C resulting in its decreased activation
b. It is a genetic defect of factor V, which prolongs the action of the prothrombinase complex
c. It is a genetic defect of factor V, which prolongs the action of the tenase complex
d. It is a factor predisposing to hemorrhage
e. It is a factor predisposing to thrombosis

Answer 53

b. It is a genetic defect of factor V, which prolongs the action of the prothrombinase complex
e. It is a factor predisposing to thrombosis

Question 54

Which statement is true concerning the resolution of fibrin clots?

Select one or more:
a. One of the possible products is the D-dimer
b. Plasmin hydrolyzes the bonds connecting fibrin monomers
c. Crosslinked fibrin resists the action of plasmin
d. Cleavage of the Lys-Gln isopeptide bonds is a prerequisite for dissolution
e. Multiple peptide bonds within the fibrin monomers are hydrolyzed

Answer 54

a. One of the possible products is the D-dimer
c. Crosslinked fibrin resists the action of plasmin
e. Multiple peptide bonds within the fibrin monomers are hydrolyzed

Question 55

Which statements are valid for the activation of plasminogen by tissue-type plasminogen activator?

Select one or more:
a. It occurs on a tPA-receptor in platelet membranes
b. Fibrin stimulates it
c. Partial degradation of fibrin stimulates it
d. Carboxypeptidase B stimulates it
e. Some of the plasmic fibrin degradation products stimulate it

Answer 55

b. Fibrin stimulates it
c. Partial degradation of fibrin stimulates it
e. Some of the plasmic fibrin degradation products stimulate it

Question 56

Which factors prolong the life span of fibrin?

Select one or more:
a. Plasmin
b. Factor XIIIa
c. Platelets
d. Neutrophil elastase
e. Plasminogen activator inhibitor 1

Answer 56

b. Factor XIIIa
c. Platelets
e. Plasminogen activator inhibitor 1

Question 57

Which factors limit the propagation of thrombi over the surface of intact endothelium?

Select one or more:
a. Thrombomodulin
b. Tissue-type plasminogen activator
c. Heparan sulfate
d. Plasminogen activator inhibitor 1
e. von Willebrand factor

Answer 57

a. Thrombomodulin
b. Tissue-type plasminogen activator
c. Heparan sulfate

Question 58

Which are substrates of thrombin?

Select one or more:
a. Fibrin
b. Factor V
c. Factor VI
d. Factor VIII
e. Factor XI

Answer 58

b. Factor V
d. Factor VIII
e. Factor XI

Question 59

Thrombin takes part in

Select one or more:
a. Activation of platelets
b. Activation of plasminogen
c. Activation of protein C
d. Activation of protein S
e. Activation of factor V

Answer 59

a. Activation of platelets
c. Activation of protein C
e. Activation of factor V

Question 60

Which statements are valid for the von Willenbrand factor?

Select one or more:
a. It is a cofactor of the tenase complex
b. It is active in a multimeric form
c. It is active in a monomeric form
d. It contributes to the attachment of platelets to the subendothelial matrix
e. It inhibits fibrinolysis

Answer 60

b. It is active in a multimeric form
d. It contributes to the attachment of platelets to the subendothelial matrix

Question 61

Which statements are valid for the von Willenbrand factor?

Select one or more:
a. It is a substrate of thrombin
b. It is produced by endothelial cells
c. It is a cofactor of FXa
d. It contributes to the adhesion of platelets
e. It binds to factor VIII

Answer 61

b. It is produced by endothelial cells
d. It contributes to the adhesion of platelets
e. It binds to factor VIII

Question 62

Which statements are valid for factor XIII?

Select one or more:
a. It is a substrate of thrombin
b. It catalyzes hydrolysis of peptide bonds in fibrin or fibrinogen
c. Its activity facilitates the incorporation of α2-plasmin inhibitor in thrombi
d. Its deficiency causes hemorrhage
e. Its deficiency causes thrombosis

Answer 62

a. It is a substrate of thrombin
c. Its activity facilitates the incorporation of α2-plasmin inhibitor in thrombi
d. Its deficiency causes hemorrhage (an escape of blood from a ruptured blood vessel.)

Question 63

A patient suffers in a severe antithrombin deficiency. What therapeutic strategy can be recommended?

Select one or more:
a. Prothrombin supplementation
b. Heparin injection
c. Oral administration of heparin
d. Vitamin K antagonists
e. Hirudin injection

Answer 63

d. Vitamin K antagonists
e. Hirudin injection (it is used to prevent blood clots following surgery)

Question 64

Endothelial cells release NO, which

Select one or more:
a. activates platelets
b. inhibits platelet activation
c. favours formation of prothrombinase
d. supports the normal blood flow over intact endothelium
e. limits the blood flow to injured blood vessel wall

Answer 64

b. inhibits platelet activation
d. supports the normal blood flow over intact endothelium

Question 65

Thrombin activates platelets through

Select one or more:
a. hydrolysis of a membrane protein
b. binding to a membrane protein
c. receptor-mediated endocytosis
d. increase in the cytosolic Ca2+ concentration
e. increase in the cytosolic cAMP concentration

Answer 65

a. hydrolysis of a membrane protein
b. binding to a membrane protein
d. increase in the cytosolic Ca2+ concentration

Question 66

Which of the following factors produced by endothelial cells contribute to the thromboresistance of endothelium?

Select one or more:
a. von Willebrand factor
b. collagen
c. thrombomodulin
d. prostacyclin
e. plasminogen activators

Answer 66

c. thrombomodulin
d. prostacyclin
e. plasminogen activators

Question 67

The treatment with vitamin K antagonists is monitored with functional coagulation assays, which show decreased plasma levels of the following factors:

Select one or more:
a. factor II
b. factor V
c. factor VIII
d. factor IX
e. factor X

Answer 67

a. factor II
d. factor IX
e. factor X

Question 68

The prothrombin time assay provides information on the plasma levels of the following factors:

Select one or more:
a. Fibrinogen
b. Prothrombin
c. Factor VIII
d. Factor IX
e. Factor XI

Answer 68

a. Fibrinogen
b. Prothrombin

Question 69

The activated partial thromboplastin time assay provides information on the plasma levels of the following factors:

Select one or more:
a. Fibrinogen
b. Prothrombin
c. Factor VIII
d. Factor IX
e. Factor XI

Answer 69

All of them

Question 70

What is the basis of time-dependent changes in membrane permeability?

Select one:
a. Opening of discrete protein pores
b. Changes in the lipid composition of the membrane
c. Changes in ion concentrations
d. Changes in electrical conductivity of the lipid bilayer
e. None of the above

Answer 70

a. Opening of discrete protein pores