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HEMATOLOGY AND ONCOLOGY > HEMATOLOGY AND ONCOLOGY- Physiology > Flashcards

HEMATOLOGY AND ONCOLOGY- Physiology Flashcards

1
Q

What composes Blood group A?

A

A antigen on RBC surface and anti-B antibody in plasma

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2
Q

Which is the antigen of Blood group B?

A

B antigen on RBC surface

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3
Q

Whcih is the antibody of Blood group B?

A

anti A antibody in plasma

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4
Q

Which antigens do Blood group AB have on RBC surface?

A

A and B antigens on RBC surface

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5
Q

What kind of antibodies do AB blood group have?

A

No antibodies in plasma

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6
Q

“Universal recipient” of RBCs

A

AB blood groups

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7
Q

Which is the antibody of Blood group B?

A

anti A antibody in plasma

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8
Q

“Universal recipient” of RBCs

A

AB blood group

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9
Q

“Universal donor” of plasma

A

AB blood group

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10
Q

Which antigens does O blood group has?

A

Neither A nor B antigen on RBC surface

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11
Q

Which antibodies does O blood group has?

A

Both antibodies in plasma A and B

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12
Q

Which antibodies does O blood group has?

A

Both antibodies in plasma A and B

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13
Q

“Universal donor” of RBCs

A

O blood groups

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14
Q

“Universal recipient” of plasma

A

O blood groups

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15
Q

What can Incomplatible blood transfusions cause?

A

Immunologic response, hemolysis, renal failure, shock, and death

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16
Q

Do anti-A and anti-B antibodies-IgM cross the placenta?

A

No

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17
Q

Which antibodies are anti A and anti B antibodies?

A

IgM

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18
Q

Do anti-Rh- IgG cross the placenta?

A

Yes

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19
Q

Do anti-Rh- IgG cross the placenta?

A

Yes

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20
Q

Which antibodies does anti Rh has?

A

IgG

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21
Q

Where are Rh antigen?

A

On RBC surface

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22
Q

Where are Rh antigen?

A

On RBC surface

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23
Q

What happens in Rh disease?

A

Rh- mothers exposed to fetal Rh+ blood (often during delivery) may make anti-Rh IgG

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24
Q

What happens in subsequent pregnancies in Rh disease?

A

Anti-Rh IgG crosses the placenta, causing hemolytic disease (Erythroblastic fetalis) of the newborn in the next fetus that is Rh+

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25
Q

Hemolytic disease of the newborn

A

Erythroblastic fetalis

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26
Q

Treatment for Rh disease

A

Rho (D) immune globulin for mother during every pregnancy to prevent initial sensitization of Rh- mother to Rh antigen

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27
Q

What happens in Hemophilia A?

A

Deficiency of factor VIII

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28
Q

What happens in Hemophilia B?

A

Deficiency of Factor IX

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29
Q

What activates bradykinin?

A

Kallikrein

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30
Q

What inactivates bradykinin

A

Angiotensin-converting enzyme (ACE)

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31
Q

What is the effect of epoxide reductase?

A

Acts in procoagulation

Converts Oxidized vitamin K → reduced vitamin K

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32
Q

What is the function of reduced vitamin K?

A

Acts as a cofactor in procoagulation

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33
Q

Vitamin K acts in the precursors of these coagulation factors

A

II, VII, IX, X, C, S

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34
Q

What does Warfarin inhibits?

A

The enzyme vitamin K epoxide reductase

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35
Q

What is the relationship of vitmain K and neonates?

A

Neonates lack enteric bacteria, which produces vitamin K

36
Q

What happens in Vitmain K defiency?

A

↓ synthesis of factors II, VII, IX, X, protein C, protein S

37
Q

Which coagulation factor is related to vWF?

A

vWF carries/ protects VIII

38
Q

What activates Protein C?

A

Thrombin thrombomodulin complex

39
Q

Where is Thrombin thrombomodulin complex produce?

A

In endothelial cells

40
Q

What is the function of Protein S?

A

From activated protein C, cleaves and inactivates Va, VIIIa

41
Q

What is the product of Plasminogen?

A

Plasmin

42
Q

What activates Plasminogen?

A

Tissue plasminogen activator

43
Q

What is the function of plasmin?

A

Fibrinolysis:

  1. cleavage of fibrin mesh
  2. destruction of coagulation factors
44
Q

What is the function of Antithrombin?

A

Inhibits activated forms of factors II, VII, IX, X, XI, XII

45
Q

Who enhances the activity of antithrombin?

A

Heparin

46
Q

Principal targets of Antithrombin

A

Thrombin and Factor Xa

47
Q

What do Factor V Leiden mutation leads to?

A

Produces a factor V resistant to inhibition by activated protein C

48
Q

What is the function of Tissue plasminogen activator (tPA)?

A

Used clinically as a thrombolytic

49
Q

Who manage primary hemostasis?

A

Platelet plug formation

50
Q

Which is the process of platelet plug formation?

A

Injury → Adhesion → Activation → Aggreagation

51
Q

Who mediates the injury phase of primary hemostasis?

A

vWF binds to exposed collagen upon endothelial damage

52
Q

Who mediates the injury phase of primary hemostasis?

A

vWF binds to exposed collagen upon endothelial damage

53
Q

Which is the first step of adhesion in primary hemostasis?

A

Platelets bind vWF via GpIb receptor at the site of injury only (specific)

54
Q

In Adhesion phase of primary hemostasis, what happens next after platelets bind to vWF via GpIb receptor?

A

Platelets release ADP and Ca2+

55
Q

What is the function of ADP and Ca2+ in Primary hemostasis?

A

Necessary for coagulation cascade

56
Q

What is the function of ADP in primary hemostasis?

A

ADP helps platelets adhere to endothelium

57
Q

What is the function of ADP in primary hemostasis?

A

ADP helps platelets adhere to endothelium

58
Q

In primary activation what happens during activation phase?

A

ADP binding to receptor indices GpIIb/IIIA

59
Q

What is the main event in Aggregation on primary hemostasis?

A

Fibrinogen binds GpIIb/IIIa receptors and links platelet

60
Q

In primary hemostasis, who are pro-aggregation factors?

A

TXA2
↓ Blood flow
↑ platelet aggregation

61
Q

During primary aggregation, who are anti- aggregation factors?

A

PGI2 and NO
↑ blood flow
↓ platelet aggregation

62
Q

Who release TXA2?

A

Platelets

63
Q

During primary hemostasis, who release PGI2 and NO?

A

Endothelial cells

64
Q

What is the final result of primary hemostasis?

A

Temporary plug stops bleeding

65
Q

What is the final result of primary hemostasis?

A

Temporary plug stops bleeding

66
Q

What is Thrombogenesis?

A

Formation of insoluble fibrin mesh

67
Q

What is the main function of Aspirin?

A

Inhibits cyclooxygenase (TXA2 synthesis)

68
Q

Inhibit ADP- induced expression of GpIIb/IIIa

A

Ticlopidine/ Clopidogrel

69
Q

What is the effect of Ticlopidine/ Clopidogrel?

A

Inhibit ADP- induced expression of GpIIb/IIIa

70
Q

What is the effect of Abciximab?

A

Inhibits GpIIb/IIIa directly

71
Q

Inhibits GpIIb/IIIa directly

A

Abciximab

72
Q

What is the effect of Ristocetin?

A

activates vWF to bind to GpIb

73
Q

What other useful effect does Ristocetin has?

A

Useful for diagnosis: normal paltelet aggreagation response is not seen in von Willebrand disease

74
Q

Irreversibly block ADP receptor

A

Clopidogrel and Ticlopidine

75
Q

Deficiency of GpIb, who binds to vWF

A

Bernard Soulier syndrome

76
Q

What is deficient in von Willebrand disease?

A

vWF

77
Q

Precursor of TXA2

A

Arachidonic acid

78
Q

Which factor promotes the conversion from arachidonic acid to TXA2?

A

COX

79
Q

Deficiency of GpIIb/IIIa

A

Glanzmann thrombasthenia

80
Q

What is erythrocyte sedminatation rate?

A

During acute phase reactants in plasma can cause RBC aggregation, thereby ↑ RBC sedimentation rate

81
Q

Example of Acute phase reactatn

A

Fibrinogen

82
Q

Who has higher density between plasma and RBC aggragates?

A

RBC aggregates

83
Q

When is erythrocyte sedminatation rate increased?

A

Infections, autoimmune diseases (eg SLE, rheumathoid, rheumatoid arthritis, temporal arteritis), malignant neoplasms, GI disease (ulcerative colitis), pregnancy

84
Q

When is erythrocyte sedminatation rate decreased?

A

Polycythemia, sickle cell anemia, CHF, microcytosis, hypofibrinogenemia

85
Q

When is erythrocyte sedminatation rate decreased?

A

Polycythemia, sickle cell anemia, CHF, microcytosis, hypofibrinogenemia

86
Q

When is erythrocyte sedminatation rate decreased?

A

Polycythemia, sickle cell anemia, CHF, microcytosis, hypofibrinogenemia

HEMATOLOGY AND ONCOLOGY (4 decks)

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