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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
what are these things LMWH heparin apixaban, rvaroxaban fonraparinus
Xa inhibitors
26
list hte LMWH anticoagulatns
dalteparin | enoxapain
27
what are dalteparin and enoxaparin
APAEIN | LMWH
28
what are argatroban, bivalirudin, dabigatran
direct thrombin inhibitors
29
list the direct thrombin inhibitors
argatroban, bivalirudin, dabigatran
30
list the direct Xa inhibitors
XABANs apixaban rivarozaban
31
what are apixaban and rivaroxaban
direct Xa inhibitors
32
what are dealteparin and enosparin
APARIN - LMWh
33
list the thromballytics and their MOA
alteplase, reteplase, streptokinase, tenecteplace - stimulatse tPA to increased plasmin - causes degradation of the fibrin mesh
34
what are atelplase, reteplase, streptokinase, tenecteplase,
stimulate tPA - increases plasmin - increase degradation of fibrin mesh
35
what is aminocaprioc acid
inhibits tPa - less fibirn - less breakdown of fibrin mesh
36
enyzme and inheritance pattern of hemophilia A
AR | VIII
37
enzyme and inheritance patter of hemophilia B
AR | IX
38
enzyme and inheritance pattern of hemophilia C
AD | XI
39
role of vitamin K in coagulation please
oxidized vitamin k -- (epoxide reductase) -- reduced vitamin K -- (cofactor for) -- II, VII, IX and X, protein C and S
40
what is the MOA fo warfarin
inhibits vitamin K epoxide reuctase - less gamm carboxylation of II, VII, IX, X - less coagulation
41
describe vitamin K deficiency
decreased synthesis of factors II, VII, IX, X, protein C and protein S
42
what is the role of vWF
initial platelet to collagen and carries/protects VIII
43
what does protein C do?
protein C -- (thrombin-thrombomodulin complex from endothelial cells) -- activated protein C -- (with protein S) -- cleaves and inactivatesa Va and VIIIa
44
how do endothelial cells play a role in protein C
thrombin-thrombomodulin complex activates protein C
45
role of plasminogen
plasminogen -- (tPA) -- plasmin --- fibrinolysis
46
role of plasmin pelase
fibrinolysis due to cleavage of fibrin mesh, destruction of coagulation factors
47
what is the MOA fo heparin
heparin enhances the activity of antithrombin
48
what does antithrombin do?
II, VII, IX, X, XI, XII
49
what are the main targets of antithrombin?
thrombin and factor Xa
50
what happens in factor V leiden
mutation produces a factor V that is resistant to inhibition by activater protein C
51
what is tPA used for
clinically as a thrombolytic
52
what does plasmin do?
cleavage of fibrin mesh | destruction fo coagulation factors
53
action of antithrombin
II, VII, IX, X, XI XII | but mainly II and X
54
primary hemostasis aka?
platelet plug formation
55
what are the five steps in primary hemostasis
injury -- exposure -- adhesion -- activation -- aggregation
56
describe the injury phase of primary hemostasis/platelet plug formation
endothelial damamge - transient vasoconstriction via neural stimulation reflex and endothelin - released from the damagede cell
57
describe the exposure phase of primary platelet hemostasis/platelet plug formation
vWF binds to exposed collagen | vWF is release from a) platelets alpha granules and b) vWF from weibel palade bodies in endotenlail cells
58
describe the adhesion phase of pirmary hemostasis/platelet plug formation
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
describe the activation phase of primary hemostasis/platelet plug formation
ADP binding to receptor induces GpIIb/GpIIIa expression at platelet surface
60
descrieb the aggregation phase of primary hemostasis/platelet plug formation
finbrinogen binds GpIIb/GpIIIa receptors and links platelets
61
what is aggregation in primary hemostasis a balance between?
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
what is the result of primary hemostasis/platelet plug formation
temporary plug stops bleeding - unstable - easily dislodged
63
describe the platelet plug
temporary that stops bleeding | unstable and easily disolged
64
what comes after primary hemostasis
secondary hemostasis and coagulation casciase
65
what is thrombogenesis?
foration of insoluble fibrin mesh
66
what does aspirin do?
aspirin inhibits cyclooxygenase (TXA2 synthesis prevented = no primary plug/platelt plug formation0
67
what is the MOA of ticlopidine, prasugrel, clopidogrel
inhibit ADP induced expression of GpIIb/IIIa
68
list the drugs that inhibit ADP induced expression fo GpIIb/IIIa
ticlopdine prasugrel clopidogrel
69
what is ristocetin
activates vWF to bind GpIb
70
what to suspect when there is a failure of agglutination in a ristocentin assay
von willdebrane - no vWF | bernard soulier syndrome - no GpIb
71
what activates vWF to bind GpIb
ristocetin
72
enzyme deficiency in glanzmann thrombasthenia
GpIIb/IIIa deficiency - no aggregation stage - no fibrinogne binds GpIIb/IIIA and platelets
73
what step of primary hemostasis doesnt occur at vWF deficienty and bernard soulier syndrome
on injury and expsoure where vWF binds to exposed collagen.
74
how do endothelial cells contribute to thrombogenesis
in weibel-palade bodies - vWF and factor VIII, thromboplastin (activates VIII), tPa and PGI2
75
what are in endothelial cells
weibel palade bodies - vWF, factor VIII, thromboplastin, (coagulant) tPA, PGI2 (anticoagulant)

Haematology and Oncology - step (5 decks)

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