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Haematology and Oncology - step > physiology > Flashcards

physiology Flashcards

1
Q

describe ABO classification: type A

A

antigen: A
antibody: anti B IgM
clinical relevance: if receive B ro AB = hemolytic reaction

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2
Q

describe ABO classification: type B

A

antigen: B
antibody: anti A IgM
clinical relevance: if receive A or AB = hemolytic reaction

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3
Q

describe ABO classification: type AB

A

antigen: A and B
antibody: no IgM
clinical relevance: universal acceptor of blood, universal donor of plasma

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4
Q

describe ABO classification: type O

A

antigen: none
antibody: anti-A and anti-B IgM
clinical relevance: universal donor of blood, universal acceptor of plasma

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5
Q

what Ig crosses the placenta

A

IgG crosses

IgM does not

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6
Q

describe the pathogenesis of hemoytic disease of the newborn

A

Rh- mothers exposed to fetal Rh+ blood (often during delivery) may make anti-D IgG.
subsequent pregnancies anti-D IgG crosses the placenta - hemolytic disease of the newborn in the next fetus that is Rh+

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7
Q

how do you prevent hemolytic disease of the newborn

A

giev RhoGAM to Rh - pregnant women during third trimester - prevents maternal anti Rh IgG produciton.

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8
Q

when will Rh- mothers have anti-D igG?

A

only ir previously exposed to Rh+ blood

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9
Q

list the coagulation factors in the intrinsic pathways

A

XII
XI
IX
VIII

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10
Q

list the colagulaiton factors in the extrinsic pathway

A

VII

thromboplastic = tissue factor

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11
Q

what stimulates the intrinsic coagulation pathway

A

colagen
basement membrane
activated platelets
HMWK

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12
Q

what does bardykinin do?

A

vasodilation
permeabiltiy
pain

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13
Q

what causes vasodilation, permeability, pain

A

bradykinin

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14
Q

what activates HWMK to bradykinin

A

HWMK to brandykinin by kallikrien

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15
Q

list the factors in the common coagulation pathway

A 
X
V
II
I
XIII
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16
Q

describe the finbirnoytic pathway

A

plasminogen – tPA - plasmin - dissolves the fibrinn mesh that stabilized the platelet plug resulting in fibrin degradation products

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17
Q

list the cofactors of the coagulation cascade

A

V
VIII
XIII

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18
Q

what does thrombin do

A

activates V, VIII, XIII, and fibrinogne to fibrin monomers

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19
Q

what does V do?

A

Xa to II

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20
Q

what does VIII do?

A

IX to X

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21
Q

what steps use Ca and phospholipids

A

the ones involving vitamin K dependent factors II , VII, IX, X
VII and IX activating X
X activating II and XIII satbilizing fibring momnets to fibrin mesh

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22
Q

list the anticoagulnts that affect thrombin

A

heparin - greatest efficacy
LMWH - dalteparin, enoxaparin
direct thrombin inhibitiors: argatroban, bivalirudin, dabigatran

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23
Q

list the anticoagulants that affect factor Xa

A

LMWH (fgreaset efficacy)
heparin
direct Xa inhibitors: apixaban, rivaroxaban
fonfaparinus

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24
Q 
what are these things
heparin
dalteparin
enoxaparin
argatroban
bivalirudin
dabigatran
A

IIa inhibitors

anticoagulants

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25
Q

what are these things
LMWH
heparin
apixaban, rvaroxaban fonraparinus

A

Xa inhibitors

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26
Q

list hte LMWH anticoagulatns

A

dalteparin

enoxapain

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27
Q

what are dalteparin and enoxaparin

A

APAEIN

LMWH

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28
Q

what are argatroban, bivalirudin, dabigatran

A

direct thrombin inhibitors

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29
Q

list the direct thrombin inhibitors

A

argatroban, bivalirudin, dabigatran

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30
Q

list the direct Xa inhibitors

A

XABANs
apixaban
rivarozaban

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31
Q

what are apixaban and rivaroxaban

A

direct Xa inhibitors

32
Q

what are dealteparin and enosparin

A

APARIN - LMWh

33
Q

list the thromballytics and their MOA

A

alteplase, reteplase, streptokinase, tenecteplace - stimulatse tPA to increased plasmin - causes degradation of the fibrin mesh

34
Q

what are atelplase, reteplase, streptokinase, tenecteplase,

A

stimulate tPA - increases plasmin - increase degradation of fibrin mesh

35
Q

what is aminocaprioc acid

A

inhibits tPa - less fibirn - less breakdown of fibrin mesh

36
Q

enyzme and inheritance pattern of hemophilia A

A

AR

VIII

37
Q

enzyme and inheritance patter of hemophilia B

A

AR

IX

38
Q

enzyme and inheritance pattern of hemophilia C

A

AD

XI

39
Q

role of vitamin K in coagulation please

A

oxidized vitamin k – (epoxide reductase) – reduced vitamin K – (cofactor for) – II, VII, IX and X, protein C and S

40
Q

what is the MOA fo warfarin

A

inhibits vitamin K epoxide reuctase - less gamm carboxylation of II, VII, IX, X - less coagulation

41
Q

describe vitamin K deficiency

A

decreased synthesis of factors II, VII, IX, X, protein C and protein S

42
Q

what is the role of vWF

A

initial platelet to collagen and carries/protects VIII

43
Q

what does protein C do?

A

protein C – (thrombin-thrombomodulin complex from endothelial cells) – activated protein C – (with protein S) – cleaves and inactivatesa Va and VIIIa

44
Q

how do endothelial cells play a role in protein C

A

thrombin-thrombomodulin complex activates protein C

45
Q

role of plasminogen

A

plasminogen – (tPA) – plasmin — fibrinolysis

46
Q

role of plasmin pelase

A

fibrinolysis due to cleavage of fibrin mesh, destruction of coagulation factors

47
Q

what is the MOA fo heparin

A

heparin enhances the activity of antithrombin

48
Q

what does antithrombin do?

A

II, VII, IX, X, XI, XII

49
Q

what are the main targets of antithrombin?

A

thrombin and factor Xa

50
Q

what happens in factor V leiden

A

mutation produces a factor V that is resistant to inhibition by activater protein C

51
Q

what is tPA used for

A

clinically as a thrombolytic

52
Q

what does plasmin do?

A

cleavage of fibrin mesh

destruction fo coagulation factors

53
Q

action of antithrombin

A

II, VII, IX, X, XI XII

but mainly II and X

54
Q

primary hemostasis aka?

A

platelet plug formation

55
Q

what are the five steps in primary hemostasis

A

injury – exposure – adhesion – activation – aggregation

56
Q

describe the injury phase of primary hemostasis/platelet plug formation

A

endothelial damamge - transient vasoconstriction via neural stimulation reflex and endothelin - released from the damagede cell

57
Q

describe the exposure phase of primary platelet hemostasis/platelet plug formation

A

vWF binds to exposed collagen

vWF is release from a) platelets alpha granules and b) vWF from weibel palade bodies in endotenlail cells

58
Q

describe the adhesion phase of pirmary hemostasis/platelet plug formation

A

platelets bind vWF via GpIb receptors at site of inury - specifi c– platelets undergo conformational change – platelets release ADP and CA from the delta granmoesl that are necssary for coagulation cascause and TXA2 – ADP helps platelets adhere to endothelium

59
Q

describe the activation phase of primary hemostasis/platelet plug formation

A

ADP binding to receptor induces GpIIb/GpIIIa expression at platelet surface

60
Q

descrieb the aggregation phase of primary hemostasis/platelet plug formation

A

finbrinogen binds GpIIb/GpIIIa receptors and links platelets

61
Q

what is aggregation in primary hemostasis a balance between?

A

proaggregation: TXA2 release by platelets, decreased blood flow and increased platelet aggreatgion
antiaggregation: PGI2 and NO release by enothelial cells, increased blood flow and decreased platelet aggregation.

62
Q

what is the result of primary hemostasis/platelet plug formation

A

temporary plug stops bleeding - unstable - easily dislodged

63
Q

describe the platelet plug

A

temporary that stops bleeding

unstable and easily disolged

64
Q

what comes after primary hemostasis

A

secondary hemostasis and coagulation casciase

65
Q

what is thrombogenesis?

A

foration of insoluble fibrin mesh

66
Q

what does aspirin do?

A

aspirin inhibits cyclooxygenase (TXA2 synthesis prevented = no primary plug/platelt plug formation0

67
Q

what is the MOA of ticlopidine, prasugrel, clopidogrel

A

inhibit ADP induced expression of GpIIb/IIIa

68
Q

list the drugs that inhibit ADP induced expression fo GpIIb/IIIa

A

ticlopdine
prasugrel
clopidogrel

69
Q

what is ristocetin

A

activates vWF to bind GpIb

70
Q

what to suspect when there is a failure of agglutination in a ristocentin assay

A

von willdebrane - no vWF

bernard soulier syndrome - no GpIb

71
Q

what activates vWF to bind GpIb

A

ristocetin

72
Q

enzyme deficiency in glanzmann thrombasthenia

A

GpIIb/IIIa deficiency - no aggregation stage - no fibrinogne binds GpIIb/IIIA and platelets

73
Q

what step of primary hemostasis doesnt occur at vWF deficienty and bernard soulier syndrome

A

on injury and expsoure where vWF binds to exposed collagen.

74
Q

how do endothelial cells contribute to thrombogenesis

A

in weibel-palade bodies - vWF and factor VIII, thromboplastin (activates VIII), tPa and PGI2

75
Q

what are in endothelial cells

A

weibel palade bodies - vWF, factor VIII, thromboplastin, (coagulant)
tPA, PGI2 (anticoagulant)

Haematology and Oncology - step (5 decks)

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