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Biochemistry Theory Semester 1 > Blood Coagulation > Flashcards

Blood Coagulation Flashcards

1
Q

1 What is the primary role of Factor XIII in blood clotting? A Conversion of fibrinogen to fibrin B Inhibition of thrombin C Cross‑linking of fibrin monomers D Activation of platelets

A

CCross‑linking of fibrin monomers

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2
Q

2 Which enzyme is responsible for the cross‑linking of fibrin monomers? A Transglutaminase B Protease C Kinase D Phosphatase

A

ATransglutaminase

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3
Q

3 Haemophilia A is mainly due to a deficiency of which clotting factor? A Factor VIII B Factor IX C Factor XI D Factor X

A

AFactor VIII

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4
Q

4 Haemophilia B is commonly caused by the deficiency of which factor? A Factor VIII B Factor V C Factor IX D Factor XIII

A

CFactor IX

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5
Q

5 Which plasma protein (heparin cofactor) inactivates thrombin? A Protein C B Antithrombin III C Protein S D Plasminogen

A

BAntithrombin III

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6
Q

6 Mechanism of heparin in anticoagulation: A Binds platelets B Promotes fibrinolysis C Accelerates thrombin‑antithrombin complex D Inhibits vitamin‑K epoxide reductase

A

CAccelerates thrombin‑antithrombin complex

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7
Q

7 Inactive precursor of plasmin: A Plasminogen B Thrombinogen C Proplasmin D Fibrinogen

A

APlasminogen

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8
Q

8 TPA plays a major role in: A Clot formation B Fibrinolysis C Platelet aggregation D Fibrin cross‑linking

A

BFibrinolysis

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9
Q

9 Thrombolytic agent for acute MI: A Aspirin B Warfarin C Streptokinase D Heparin

A

CStreptokinase

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10
Q

10 Substance enhancing plasmin generation at injury sites: A Thrombin B TPA C Factor XIII D Antithrombin III

A

BTPA

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11
Q

11 Natural inhibitor neutralizing activated clotting factors: A Plasmin B Antithrombin III C Protein C D Tissue factor

A

BAntithrombin III

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12
Q

12 Aspirin inhibits synthesis of: A Prostacyclin B Thromboxane A₂ C Fibrin D Plasminogen

A

BThromboxane A₂

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13
Q

13 Role of thromboxane A₂: A Inhibits clotting B Promotes platelet aggregation & vasoconstriction C Lyses fibrin D Activates fibrinolysis

A

BPromotes aggregation & vasoconstriction

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14
Q

14 Direct outcome of heparin: A ↓ Antithrombin III B Fibrin clot formation C Rapid neutralization of thrombin D ↑ Fibrinogen

A

CNeutralizes thrombin

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15
Q

15 Enzyme converting fibrinogen to fibrin: A Thrombin B Plasmin C Transglutaminase D Factor XIII

A

AThrombin

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16
Q

16 Degradation of fibrin into soluble peptides is: A Coagulation B Fibrinolysis C Transamidation D Hemolysis

A

BFibrinolysis

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17
Q

17 Effect of Factor XIII deficiency on clots: A Overly rigid B No clot C Unstable (no cross‑link) D Resist fibrinolysis

A

CUnstable (no cross‑link)

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18
Q

18 Inherited bleeding disorder due to absent clotting factors: A Thrombophilia B Hemophilia C Leukemia D Hypercoagulability

A

BHemophilia

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19
Q

19 ‘Antithrombin III’ is: A Coagulation factor B Fibrinolytic enzyme C Natural thrombin inhibitor D Platelet activator

A

CNatural inhibitor of thrombin

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20
Q

20 Endothelial substance binding fibrin to accelerate fibrinolysis: A Urokinase B Heparin C TPA D Vitamin K

A

CTPA

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21
Q

21 Aspirin inhibits which platelet enzyme? A COX‑1 B Phospholipase A₂ C Thrombin D Transglutaminase

A

ACOX‑1

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22
Q

22 Fibrinolysis defined as: A Stable fibrin network B Fibrin → degradation products C Cross‑linking fibrin D Platelet activation

A

BFibrin → degradation products

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23
Q

23 Cross‑linking of fibrin monomers is essential for: A Initiating coagulation B Clot stabilization C Inducing fibrinolysis D Inhibiting thrombin

A

BStabilizing the clot

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24
Q

24 Structure that limits coagulation by adsorbing thrombin: A Fibrin B Plasmin C Antithrombin III D Factor XII

A

AFibrin

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25
25 Haemophilia C involves deficiency of: A Factor VIII B Factor IX C Factor XI D Factor XIII
C Factor XI
26
26 Assertion–Reason: Factor XIII cross‑links fibrin → clot stability; transglutaminase forms covalent bonds.
AR Type A (Both true & explains)
27
27 Assertion–Reason: Heparin anticoagulation via enhanced antithrombin III; increases thrombin‑AT III complex.
AR Type A
28
28 In coagulation cascade, step directly inhibited by heparin: A Fibrinogen→fibrin B Prothrombin→thrombin C Cross‑linking fibrin D Plasminogen→plasmin
B Activation of prothrombin
29
29 Assertion–Reason: TPA dissolves clots; binds fibrin & converts plasminogen to plasmin.
AR Type A
30
30 Component directly breaking down fibrin clots: A Thrombin B Plasmin C Factor XIII D Fibrinogen
B Plasmin
31
31 Molecule most directly inhibited by aspirin in platelet pathway: A Thromboxane A₂ B ADP receptors C GPIIb/IIIa D Serotonin
A Thromboxane A₂
32
32 Assertion–Reason: Inhibitors of activated factors confine clotting; factors inactivated by dilution/inhibitors/clearance.
AR Type A
33
33 Clinical fibrinolytic agent example: A Heparin B Streptokinase C Warfarin D Aspirin
B Streptokinase
34
34 Assertion–Reason: Factor VIII deficiency → haemophilia A; Factor VIII essential for intrinsic pathway.
AR Type A
35
35 Low‑dose aspirin antiplatelet effect: A ↑ Plasmin B Irreversibly acetylates COX‑1 C Blocks thrombin D ↓ Fibrinogen
B Irreversible COX‑1 inhibition
36
36 Role of Ca²⁺ in clotting: A Inhibit clotting B Cofactor in many reactions C Directly converts fibrinogen D Enhances fibrinolysis
B Cofactor
37
37 Factor directly converting prothrombin to thrombin: A VIIa B Xa C V D XII
B Factor Xa
38
38 Assertion–Reason: Plasmin degrades fibrin; generated from plasminogen by TPA/urokinase.
AR Type A
39
39 Function of antithrombin III: A Promote fibrin B Degrade factors C Bind & inactivate thrombin (esp. w/ heparin) D Enhance TPA
C Binds & inactivates thrombin
40
40 Enzyme activity of Factor XIII for cross‑linking fibrin: A Protease B Transglutaminase C Kinase D Phosphatase
B Transglutaminase
41
41 Assertion–Reason: Hemarthrosis in haemophilia due to unstable clots.
AR Type A
42
42 Factor initiating extrinsic pathway: A IX B Tissue factor C XI D XIII
B Tissue factor
43
43 Assertion–Reason: Urokinase activates plasminogen; kidney‑secreted to prevent urinary clots.
AR Type A
44
44 Molecule binding fibrin to localize plasminogen activation: A Heparin B Thrombin C TPA D AT III
C TPA
45
45 Assertion–Reason: Short half‑life of activated factors limits coagulation; rapid inactivation & clearance.
AR Type A
46
46 Body mechanism limiting clot propagation: A Continual XIII B Removal of activated factors by RES C Enhanced aggregation D ↑ Fibrinogen
B Removal by RES
47
47 Diagram showing TPA action illustrates: A Clot stabilization B Fibrinolysis C Platelet activation D XII activation
B Fibrinolysis
48
48 Assertion–Reason: Cross‑linked fibrin resists fibrinolysis; covalent bonds ↑ stability.
AR Type A
49
49 Component initiating extrinsic pathway in cascade diagram: A Tissue factor B IX C AT III D Plasmin
A Tissue factor
50
50 Mechanism of streptokinase: A Inhibits thrombin B Binds plasminogen → plasmin C Prevents fibrin formation D ↑ AT III
B Activates plasminogen
51
51 Molecular basis of clot stabilization: A Ionic interactions B Covalent bonds via transglutaminase C Continuous aggregation D Thrombin inactivation
B Covalent bonds (transglutaminase)
52
52 Step generating thrombin on cascade schematic: A X activation intrinsic B Prothrombinase complex formation C Tissue factor release D AT III‑heparin binding
B Prothrombinase complex
53
53 Assertion–Reason: Heparin enhances AT III via conformational change ↑ affinity for proteases.
AR Type A
54
54 Diagram with coag & fibrinolysis: structure showing clot breakdown: A Fibrin mesh B Plasminogen→plasmin by TPA C Fibrin cross‑link D Thrombin‑fibrin binding
B Plasminogen→plasmin
55
55 Rapid clearance of activated factors due to: A Platelet binding B Dilution + inhibitors + RES/Liver removal C Continuous TF D Splenic storage
B Dilution & inhibitors
56
56 Irreversible COX‑1 acetylation by aspirin results in: A ↑ TxA₂ B ↓ TxA₂ → ↓ aggregation C ↑ Fibrin D ↑ TPA activity
B Decreased TxA₂
57
57 Assertion–Reason: Short half‑life of activated factors prevents systemic coagulation; rapid inhibitor & hepatic removal.
AR Type A
58
58 Fibrinolysis best defined: A Fibrinogen→fibrin B Enzymatic breakdown of cross‑linked fibrin C Fibrin formation D Platelet activation
B Breakdown of cross‑linked fibrin
59
59 Key interaction for rapid thrombin inactivation (diagram): A Heparin‑thrombin B Heparin‑induced AT III conformational change binding thrombin C Fibrinogen competitive D Plasminogen activation
B Heparin‑AT III‑thrombin
60
60 Assertion–Reason: Streptokinase lyses clots; forms complex with plasminogen → plasmin.
AR Type A
61
61 Final result of plasmin activity: A Fibrinogen→fibrin B Cross‑linked fibrin C Fibrin degradation products D Thrombin activation
C Fibrin degradation products
62
62 Why clots remain localized: A Rapid inactivation & removal of activated factors B Excess fibrinogen C Continuous TxA₂ D Systemic TF
A Rapid inactivation/removal
63
63 Assertion–Reason: Antiplasmin regulates fibrinolysis; quickly inhibits plasmin.
AR Type A
64
64 Key link between coagulation and fibrinolysis: A Factor XIII B TPA C TxA₂ D AT III
B TPA
65
65 Component binding fibrin to localize fibrinolysis (schematic): A Heparin B TPA C Plasminogen D AT III
B TPA
66
66 Assertion–Reason: TPA deficiency impairs clot lysis; TPA converts plasminogen to plasmin.
AR Type A
67
67 Event terminating coagulation: A Excess TxA₂ B Adsorption of thrombin by fibrin C Continued X activation D ↑ Platelet adhesion
B Thrombin adsorption by fibrin
68
68 Inherited bleeding due to Factor XI deficiency is: A Hemophilia A B Hemophilia B C Hemophilia C D vWD
C Hemophilia C
69
69 Assertion–Reason: Excessive fibrinolysis causes bleeding; plasmin degrades fibrin & factors V/VIII.
AR Type A
70
70 Anticoagulant inhibiting vitamin‑K epoxide reductase: A Heparin B Warfarin C Streptokinase D Aspirin
B Warfarin
71
71 Role of Ca²⁺ in coagulation: A Unnecessary B Cofactor for X activation & prothrombinase C Direct fibrin formation D Inhibits TPA
B Cofactor
72
72 Assertion–Reason: Cascade self‑amplifying, needs regulation; activated factors propagate and are neutralized by inhibitors.
AR Type A
73
73 Process blocked by α₂‑antiplasmin: A Platelet aggregation B Inhibition of thrombin C Plasmin activity D Factor XIII activation
C Blocks plasmin
74
74 Clinical purpose of streptokinase: A Prevent clots B Lyse clots via plasminogen activation C Enhance platelets D Inhibit AT III
B Clot lysis (plasminogen→plasmin)
75
75 Assertion–Reason: Bone‑marrow transplant cures genetic clotting defects; donor stem cells make normal factors.
AR Type A

Biochemistry Theory Semester 1 (12 decks)

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