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Biochemistry > Semester 3, midterm 2: Extra q's > Flashcards

Semester 3, midterm 2: Extra q's Flashcards

1
Q

Heparin is one of the most frequently used drugs in the treatment of thrombosis, because heparin

  1. Inactivates thrombin directly
  2. Inhibits prothrombin activation by thrombin
  3. Facilitates thrombin inactivation by antithrombin
  4. Increases thrombus dissolution by plasmin
A

3

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2
Q

Which statement is valid for the von Willenbrand factor?

  1. It is a substrate of thrombin
  2. It is produced by endothelial cells
  3. It contributes to the disaggregation of platelets
  4. It contributes to the adhesion of platelets
  5. It binds to factor VIII
A

2,4,5

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3
Q

It is characteristic for PGI2, that

  1. It is synthesized from free arachidonic acid
  2. It is released from phospholipid by phospholipase C
  3. Its synthesis in platelets is catalyzed by prostacycline synthase
  4. It inhibits PAR-1 receptor of platelets
A

1

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4
Q

How does thrombomodulin (TM) modify blood coagulation?

  1. It accelerates protein C activation by thrombin
  2. It inhibits fibrinogen conversion to fibrin
  3. Activation of platelet by thrombin is inhibited by TM
  4. It inactivates thrombin
A

1, 2, 3

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5
Q

What is the trigger for platelet activation?

  1. Tissue factor
  2. Thrombin
  3. Collagen
  4. PAF
  5. Factor XIIa
A

2, 3, 4

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6
Q

Why is aspirin used in the prevention of myocardial infarction? Because aspirin:

  1. Inhibits prothrombin activation by factor Xa
  2. Inhibits cyclooxygenase activity in endothelial cell
  3. Inhibits cyclooxygenase activity in platelet
  4. Induces release of fibrinolytic enzymes from endothelial cell
A

3

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7
Q

Why do you treat patients with tPA? Because tPA:

  1. Is a protease which dissolves fibrin directly
  2. Is an enzyme which converts plasminogen to plasmin
  3. Is not inactivated by plasma protease inhibitors
  4. Acts primarily at the location of fibrin
A

2, 4

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8
Q

The endothelial cell is antithrombotic, because:

  1. On its surface there is heparan sulfate which increases the rate of thrombin inactivation by antithrombin
  2. It is able to synthesize tPA and uPA
  3. It synthesizes PAI-1
  4. It is able to synthesize tissue factor
  5. It can release PGI2
A

1, 2, 5

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9
Q

What are the difficulties with the fibrinolytic therapy?

  1. Plasmin formed in the blood is inactivated immediately by the inhibitor system
  2. Only plasmin bound to fibrin is protected against the inhibitor system
  3. Application of plasminogen activators is not sufficient because they are inactivated by endogenous plasminogen activators inhibitors
  4. During fibrinolysis, thrombin may be released from a thrombus and it may provoke an additional thrombus
A

1,2,3

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10
Q

Which phases of biotransformation is mediated by transporters?

A

3rd phase

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11
Q

What is the dominant chemical reaction in the 1st phase of biotransformation?

A

Oxidation

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12
Q

What is the cofactor of glucuronidation?

A

UDP-glucuronic acid

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13
Q

Which enzymes catalyze glucuronidation?

A

UDP-glucuronosyl transferases (UGTs)

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14
Q

Which are the most important ligands of the nuclear receptors?

A

Hormones, drugs, fatty acids, eicosanoids

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15
Q

List at least two types of pattern recognition receptors involved in the patomechanism of atherosclerosis

A

Scavanger, TLRs, NLRP

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16
Q

Which enzymes catalyze the majority of reactions in 1st phase of biotransformation?

A

P450 monooxygenase isoenzymes

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17
Q

What is the electron donor for monoogygenases in drug metabolism?

A

NADPH

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18
Q

Which are the most important xenobiotic inducers of CYP1 isoenzymes?

A

Methylcholanthrene, dioxin derivatives, cigarette smoke

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19
Q

What is the dominant type of conjugation in case of electrophilic intermediates?

A

GSH (glutathion) conjugation

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20
Q

How is the formation of blood coagulation complexes inhibited in the clinic?

A

By Heparin, Vitamin K antagonists - coumarins

Marevan, Warfarin

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21
Q

What activates protein C?

A

Thrombin in complex with thrombomodulin

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22
Q

How is plasmin formed?

A

From plasminogen in the presence of plasminogen activator (tPA, uPA, streptokinase)

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23
Q

How is fibrinolysis terminated?

A

Alpha2-antiplasmin, alpha2-macroglobulin, plasmin acivator inhibiting factor 1+2, TAFI

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24
Q

Give the name of at least one drug that can inhibit platelet activation

A

Aspirin (inhibits COX -> AA to prostaglandins)

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25
Q

Is it possible that the thrombin exerts any antithrombotic effects? Explain.

A

The thrombin and thrombomodulin complex activates protein C, which inhibits FVa+VIIIa

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26
Q

What is the background of the activated Protein C resistance?

A

The inability of Protein C to cleave Va and VIIIa, leads to hypercoagulability

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27
Q

Which diagnostic assay is based on the intrinsic pathway? List examples of its application!

A

APTT - Activated partial thromboplastin time
Can detect these def. if prolonged time: vWF disease, hemophilia, factor XII def. (APTT prolonged, but PT time is still normal)

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28
Q

What initiates blood coagulation at sites of vessel injury?

A

By factor VIIa if tissue factor is also present

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29
Q

Where isnt tissue factor present under normal conditions?

A

Healthy endothelial cells, blood

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30
Q

How does Hirudin act? When may its action be exploited therapeutically?

A

It is an inhibitor of Thrombin. Has a negatively charged tail, it binds to active site of thrombin and inactivates it. (it has a specific activity on fibrinogen) Hirudin prevent formation of blood clots and thrombus, do not interfere with ability of serum proteins.

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31
Q

What kind of plasminogen activators are used in thrombolytic therapy?

A

TPA (Tissue type Plasminogen Activators)
UPA (Urokinase Plasminogen Activators)
Streptokinase

32
Q

What is the kinetic significance of the phospholipid bound complexes in blood coagulation?

A

The extreme increase of reaction rates

33
Q

How can tPA be increased?

A

Pos. feedback from plasmin, increased conc. of cofactor (fibrin)

34
Q

Primary thrombin inhibitor in blood? How is effect enhanced pharmacologically

A

Antithrombin with heparin

35
Q

List at least 3 triggers of platelet activation

A

Thrombin, collagen, thromboxan, ADP, PAF

36
Q
  1. Describe the composition of prothrombinase complex

2. What are the structurally important elements of complex formation

A
  1. Composed by activated factor X and V

2. These factors are bound to Ca-ions to the negative phospholipid membrane on platelets

37
Q

What are the substrates for thrombin in blood coagulation system?

A

Factor V, VIII, XI, XIII, fibrinogen, protein C (thrombomodulin)

38
Q

What are the enzymes that degrades fibrin clots?

A

Plasmin

39
Q

Which is a typical phase II reaction?

  1. Glucuronidation
  2. Carboxylation
  3. Conjugation with Glutathione
  4. Oxidation
  5. Acetylation
A

1, 3, 5

40
Q

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

  1. Fibrinogen stimulates it
  2. Fibrin stimulates it
  3. Partial degradation of fibrin stimulates it
  4. Carboxypeptidase B stimulates it
  5. Some of the plasmic fibrin degradation products stimulate it
A

2

41
Q

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

  1. Thrombomodulin
  2. tPA
  3. Heparan sulfate
  4. Plasminogen activator inhibitor 1
  5. Von Willenbrand factor
A

1, 2, 3

42
Q

Thrombin takes part in:

  1. Activation of platelets
  2. Activation of plasminogen
  3. Activation of protein C
  4. Activation of protein S
  5. Activation of factor V
A

1, 3, 5

43
Q

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

  1. Prothrombin supplementation
  2. Heparin injection
  3. Oral administration of heparin
  4. Vitamin K antagonists
  5. Hirudin injection
A

4, 5

44
Q

What is the function of thrombin receptor?

  1. To initiate blood coagulation cascade
  2. To prevent platelet adhesion
  3. To induce platelet aggregation
  4. To activate endothelial cells
  5. To activate phospholipase C
A

3, 4, 5

45
Q

Which, if any of the following compunds are inhibitors of platelet aggregation?

  1. Adenosine diphosphate
  2. Aspirin
  3. Thromboxane A2
  4. Clopidogrel
  5. Prostacyclin
A

2, 4, 5

46
Q

Which, if any of the following statements is/are true of classical hemophilia (factor VIII deficiency)?

  1. Autosomal dominant inheritance
  2. Prolonged prothrombin time
  3. Prolonged activated partial thromboplastin time
  4. Aspirin administration is safe
  5. Prolonged skin bleeding time
A

3

47
Q

True for tissue-type plasminogen activator (tPA)?

  1. Used in treatment of acute myocardial infarction
  2. Inhibited by alpha2 antiplasmin
  3. Synthesized by vascular endothelial cells
  4. Activity is stimulated by fribrin
  5. High therapeutic doses can cause excessive bleeding
A

1, 3, 4, 5

48
Q

True for antithrombin?

  1. Cofactor for the anticoagulant drug, warfarin
  2. Inactivates coagulation factor VIII
  3. Inactivates coagulation factor X
  4. Congenital deficiency causes excessive bleeding
  5. Inheritance of deficiency is autosomal dominant
A

3, 5

49
Q

True for thrombin?

  1. It stimulates platelet aggregation
  2. Its formation is reduced by warfarin
  3. Its formation is reduced in patients with protein C deficiency
  4. It promotes activation of protein C
  5. It promotes crosslinking of fibrin strands
A

1, 2, 4,

50
Q

What are the roles of platelets?

A
  1. Adhesion: stick to exposed collagen of the subendothelial layer
  2. Activation: change shape, turn on receptors and secrete chemical messengers (ADP, vWF, thrombin, growth factors)
  3. Aggregation: they stick to each other
51
Q

What is the purpose of having phospholipids on the platelet membrane?

A

The negativity of the phospholipids make them ideal for binding of Ca of the prothrombinase complex. The phospholipids are also used for thromboxane production.

52
Q

What is Leiden mutation?

A

An SNP mutation in FV (arginine exchanged for glutamine) that makes FV hard to degrade by APC -> APC resistance

53
Q

Effect of Coumarin; after how long is the effect of Coumarin observable?

A

Coumarins inhibits Vit K Epoxide Reductase responsible for Glu to Gla change of factors II, VII, IX, X
Takes about 3 days to see the effects (max. 60hours half life) (Use heparin the first few days)

54
Q

What are the substrates of factor VII?

A

Exposure of TF, which binds VIIa, causing activation of IX + X

55
Q

How does endothelial cells initiate coagulation formation?

A
  1. Damaged endothelia: Attract/activate platelets + coagulation factors
  2. By exposure of collagen, TP, PAI-1
56
Q

Which receptor mediates dioxin toxicity?

A

Aryl Hydrocarbon receptor (AhR)

57
Q

What is the molecule that regulates the intracellular calcium levels directly?

A

Ip3

58
Q

What kind of metabolizer phenotypes are known due to SNPs of drug metabolizing enzymes?

A

Poor metabolizers, extensive metabolizers, ultrarapid metabolizers

59
Q

Which if any of the following statements is/are true for vitamin K?

  1. Def. reduces prothrombin levels
  2. Def. reduces antithrombin levels
  3. It can be given to treat excessive Warfarin activity
  4. Def. reduces protein C levels
  5. Low levels are observed in patients with liver disease
A

1, 3, 4 (5?)

60
Q

How is blood coagulation initiated in vivo?

  1. By the contact of tissue factor with blood
  2. By the conversion of prothrombin to thrombin
  3. By the activation of factor XII
  4. By the conversion of factor X to factor Xa in the presence of factor VIIa
A

1, 4

61
Q

Which are substrates of thrombin?

  1. Fibrin
  2. Factor V
  3. Factor VI
  4. Factor VIII
  5. Factor XI
A

2, 4, 5 (+ FXIII)

62
Q

The following defects cause thrombophilia:

  1. Protein C def.
  2. Antithrombin def.
  3. Factor VIII def.
  4. Factor V resistance against activated protein C (APC-resistance)
  5. Factor XI def.
A

1, 2, 4

63
Q 
The prothrombin time assay provides information on the plasma levels of the following factors:
1. Fibrinogen
2. Prothrombin
3. FVIII
4. FIX
5 FXI
A

1, 2 (+ FV, FVII, FX)

64
Q

Thromboxane is inhibited by:

  1. Prostacyclin
  2. Heparin
  3. Aspirin
A

3

65
Q

The clinical symptoms of antiphospholipid syndrome can be treated with

  1. Vitamin K
  2. Vitamin K antagonists
  3. Folic acid
  4. Antifolates
  5. Heparin
  6. Protamine
A

2, 5

66
Q

Which statements are valid for the dissolution of fibrin?

  1. Plasmin hydrolyzes the bonds connecting the fibrin monomers
  2. Leukocytes participate in this process
  3. Cleavage of the Lys-Gln isopeptide is a prerequest for dissolution
  4. Multiple peptide bonds within fibrin monomers are hydrolyzed
  5. One of the possible products is the D-dimer
A

1, 4, 5

67
Q

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

  1. Fibrinogen stimulates it
  2. Fibrin stimulates it
  3. Partial degradation of fibrin stimulates it
  4. Carboxypeptidase B stimulates it
  5. Some of the plasmic fibrin degradation products stimulate it
A

2

68
Q

What happens to a patient with streptokinase?

  1. Streptokinase, as a fibrinolytic protease digests fibrin directly
  2. Streptokinase, as a plasminogen activator, converts directly plasminogen to plasmin
  3. Streptokinase forms a complex with plasminogen, which becomes plasmin
  4. Human plasminogen in a complex with streptokinase becomes a plasminogen activator
A

4

69
Q

Which statements are valid for factor XIII?

  1. Its a substrate of thrombin
  2. It catalyzes hydrolysis of peptide bonds in fibrin of fibrinogen
  3. Its activity facilitates the incorporation of plasmin inhibitor in thrombi
  4. Its def. causes hemorrhage
  5. Its def. causes thrombosis
A

1, 3, 4

70
Q

Thrombin activates platelets through

  1. Hydrolysis of a membrane protein
  2. Binding to a membrane protein
  3. Receptor mediated endocytosis
  4. Increasing cytosolic calcium level
  5. Increase in the cytosolic cAMP concentration
A

1, 2, 4

71
Q

How does coumarins influence blood coagulation?

  1. They inhibit vit. K function
  2. They prevent Gla domain formation in some blood coagulation factors
  3. They inactivate carboxylase enzyme directly to prevent Glu conversion to Gla
  4. They prevent prothrombinase complex formation
A

1, 2, 4

72
Q

Inhibitors of thrombin?

  1. Antithrombin
  2. Protein C
  3. Heparin
  4. Aspirin
A

1

73
Q

Hemophilia A

  1. Autosomal dominant
  2. Prolonged prothrombin time (PT)
  3. Prolonged activated partial thromboplastin time (aPTT)
  4. Aspirin administration is safe
  5. Prolonged skin bleeding time
A

3,5

74
Q

Tissue plasminogen activator (tPA)

  1. Used in treatment of acute myocardial infarction
  2. Inhibited by alpha-2 antiplasmin
  3. Synthesized by vascular endothelial cells
  4. Stimulated by fibrin
  5. High therapeutic doses can cause excessive bleeding
A

All except 2

75
Q

Protein C activation resistance, which of the following are NOT correct?

  1. Problem is in prothrombinase time
  2. Mutation in protein C
  3. Mutation in FVIII
  4. Mutation in FX
A

1, 2, 4 (?)

76
Q

Prerequisites for thromboxane synthesis are:

  1. Availability of PL-containing arachidonate for phospholipase A2
  2. Active lipoxygenase
  3. Functional cyclooxygenase
  4. Corticosteroids dont inhibit COX
A

1, 3

Biochemistry (9 decks)

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