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Step 1 Immunology > Coagulation > Flashcards

Coagulation Flashcards

1
Q

Main actor in primary hemostasis

A

platelets

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2
Q

Main actor in primary hemostasis

A

platelets

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3
Q

Main actor in secondary hemostasis

A

fibrin

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4
Q

First phenomenon observable at damaged vessel

A

transient vasoconstriction, mediated by:

1) reflex neural stimulation
2) endothelin release

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5
Q

How does platelet adhesion occur (3 steps)

A

1) vWF is released from Weibel-Palade bodies and PLT α-granules
2) vWF binds exposed subendothelial collagen
3) PLT GP1b binds vWF

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6
Q

How does platelet activation occur? (3 steps)

A

1) Adhesion induces PLT shape-change
2) PLTs release ADP from dense granules, promoting GPIIb/IIIa expression
3) PLTs produce TXA2 with COX, promoting aggregation
4) PLTs release Ca+2, enabling coagulation cascade

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7
Q

How does platelet aggregation occur?

A

GPIIb/IIIa binds fibrinogen, crosslinking PLTs

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8
Q

Aspirin in primary hemostasis

A

Inhibits COX → ↓TXA2

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9
Q

Drugs that inhibit ADP-signaling in PLTs

A

Clopidogrel, prasugrel, ticlopidine (inhibits GPIIb/IIIa expression)

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10
Q

Drugs that directly inhibit GPIIb/IIIa

A

Abciximab, eptifibatide, tirofaban

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11
Q

Ristocetin mechanism

A

Causes vWF to bind GPIIb/IIIa

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12
Q

Failure to aggregate in ristocetin assay occurs in

A

von Willebrand disease and Bernard-Soulier syndrome

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13
Q

Clinical features in disorders of primary hemostasis (8)

A

Mucosal bleeding:

1) Intracranial bleeding (most important)
2) Epistaxis (most common)
3) Others: menorrhagia, hematuria, GI bleeds, hemoptysis

Skin bleeding:

1) petechiae, purpura, ecchymosis
2) easy bruising

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14
Q

petechiae are usually seen in ______ PLT disorders

A

Quantitative

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15
Q

PLT count at which Sxs are seen

A
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16
Q

Most common cause of thrombocytopenia in children and adults?

A

ITP

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17
Q

Pathogenesis of ITP

A

Anti-GPIIb/IIIa antibodies cause PLT destruction in spleen

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18
Q

Causes of ITP?

A

Acute: viral infection, immunization
Chronic: SLE or idiopathic in women of childbearing age

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19
Q

Complication associated with ITP in pregnancy

A

Transient thrombocytopenia in newborn (IgG crosses placenta)

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20
Q

Tx of ITP

A

1) Corticosteroids (less long term effectiveness in adults)
2) IVIG
3) Splenectomy (refractory)

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21
Q

Tx of ITP

A

1) Corticosteroids (less long term effectiveness in adults)
2) IVIG
3) Splenectomy (refractory)

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22
Q

Main actor in secondary hemostasis

A

fibrin

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23
Q

First phenomenon observable at damaged vessel

A

transient vasoconstriction, mediated by:

1) reflex neural stimulation
2) endothelin release

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24
Q

How does platelet adhesion occur (3 steps)

A

1) vWF is released from Weibel-Palade bodies and PLT α-granules
2) vWF binds exposed subendothelial collagen
3) PLT GP1b binds vWF

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25
Q

How does platelet activation occur? (3 steps)

A

1) Adhesion induces PLT shape-change
2) PLTs release ADP from dense granules, promoting GPIIb/IIIa expression
3) PLTs produce TXA2 with COX, promoting aggregation
4) PLTs release Ca+2, enabling coagulation cascade

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26
Q

How does platelet aggregation occur?

A

GPIIb/IIIa binds fibrinogen, crosslinking PLTs

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27
Q

Aspirin in primary hemostasis

A

Inhibits COX → ↓TXA2

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28
Q

Drugs that inhibit ADP-signaling in PLTs

A

Clopidogrel, prasugrel, ticlopidine (inhibits GPIIb/IIIa expression)

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29
Q

Drugs that directly inhibit GPIIb/IIIa

A

Abciximab, eptifibatide, tirofaban

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30
Q

Ristocetin mechanism

A

Causes vWF to bind GPIIb/IIIa

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31
Q

Failure to aggregate in ristocetin assay occurs in

A

von Willebrand disease and Bernard-Soulier syndrome

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32
Q

Clinical features in disorders of primary hemostasis (8)

A

Mucosal bleeding:

1) Intracranial bleeding (most important)
2) Epistaxis (most common)
3) Others: menorrhagia, hematuria, GI bleeds, hemoptysis

Skin bleeding:

1) petechiae, purpura, ecchymosis
2) easy bruising

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33
Q

petechiae are usually seen in ______ PLT disorders

A

Quantitative

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34
Q

PLT count at which Sxs are seen

A

Less than 50

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35
Q

Most common cause of thrombocytopenia in children and adults?

A

ITP

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36
Q

Pathogenesis of ITP

A

Anti-GPIIb/IIIa antibodies cause PLT destruction in spleen

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37
Q

Causes of ITP?

A

Acute: viral infection, immunization
Chronic: SLE or idiopathic in women of childbearing age

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38
Q

Complication associated with ITP in pregnancy

A

Transient thrombocytopenia in newborn (IgG crosses placenta)

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39
Q

Lab findings in ITP (4)

A

1) ↓ PLT
2) NL PT/PTT
3) ↑ BT
4) ↑ Megakaryocytes in marrow

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40
Q

Tx of ITP

A

1) Corticosteroids (less long term effectiveness in adults)
2) IVIG
3) Splenectomy (refractory)

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41
Q

Schistocytes on smear imply

A

microangiopathic hemolytic anemia

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42
Q

Cause of thrombocytopenia in Microangiopathic Hemolytic Anemia

A

Consumption of platelets in microthrombus formation

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43
Q

Anti-ADAMTS13 antibodies are seen in

A

Thrombotic Thrombocytopenic Purpura

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44
Q

Pathogenesis of TTP

A

Acquired anti-ADAMTS13 antibody prevents cleavage of vWF multimers → hypercoagulability

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45
Q

Pathogenesis of HUS

A

EHEC expresses shiga-like toxin → glomerular endothelial damage → microthrombus formation

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46
Q

Labs in TTP (6)

A

1) ↓PLT
2) NL PT/PTT
3) ↑LDH
4) ↑BT
5) Schistocytes
6) ↑Megakaryocytes in marrow

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47
Q

Labs in HUS (6)

A

1) ↓PLT
2) NL PT/PTT
3) ↑LDH
4) ↑BT
5) Schistocytes
6) ↑Megakaryocytes in marrow

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48
Q

Clinical findings in HUS and TTP

A

1) Skin and mucosal bleeding
2) Hemolytic anemia
3) Fever
4) Renal insufficiency (more in HUS)
5) CNS abnormalities (more in TTP)

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49
Q

Complications in FV Leiden

A

1) DVT
2) cerebral vein thrombosis
3) recurrent pregnancy loss

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50
Q

Pathogenesis in Bernard-Soulier syndrome

A

Congenital GPIb deficiency → defect in primary hemostasis

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51
Q

Smear findings in Bernard-Soulier syndrome

A

Enlarged platelets: splenic destruction of dysfunction platelets → compensatory marrow hyperplasticity → immature platelets in circulation

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52
Q

Lab findings in Bernard-Soulier syndrome

A

1) ↓/NL PLT
2) ↑BT
3) No aggregation in Ristocetin assay

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53
Q

Tx in TTP

A

plasmapheresis, steroids

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54
Q

Pathogenesis in Glanzmann thrombasthenia

A

Genetic GPIIb/IIIa deficiency → defective platelet aggregation

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55
Q

Labs in Glanzmann thrombasthenia

A

1) NL PLT
2) ↑BT
3) Aggregation on Ristocetin assay

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56
Q

Chemical agents causing defective primary hemostasis

A

Aspirin (aggreagation)

Uremia (aggregation and adhesion)

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57
Q

Activation of extrinsic pathway requires

A

1) TF and FVII
2) Platelet phospholipid surface
3) Calcium (dense granules)

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58
Q

Activation of intrinsic pathway requires

A

1) Subendothelial collagen and FXII
2) Platelet phospholipid surface
3) Calcium (dense granules)

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59
Q

Extrinsic pathway

A

1) TF:FVIIa
2) → FVa:FXa
3) → Thrombin (FII)
4) → FVIIIa:FIXa
5) → ↑ FVa:FXa
6) → ↑↑ Thrombin
7) → fibrin
8) Fibrin crosslinking via FXIII

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60
Q

Intrinsic pathway

A

1) Subendothelial collagen → XIIa
2) → XIa
3) → FVIIIa:FIXa
4) → FVa:FXa
5) → Thrombin (FII)
6) → fibrin
7) Fibrin crosslinking via FXIII

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61
Q

Vitamin K dependent coagulation factors

A

II, VII, IX, X, C, S

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62
Q

t(1/2) of FVIII is dependent on

A

binding to vWF

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63
Q

Protein C pathway

A

1) Activated by thrombin:thrombomodulin complex
2) complexes with protein S
3) Inactivates FVa, VIIIa

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64
Q

Activation of vit K dependent coagulation factors

A

1) VitK -[epoxide reductase]→ Reduced VitK

2) Precursors -[Reduced VitK, γ-glutamyl transferase]→ mature factors

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65
Q

Mechanism of Warfarin action

A

Inhibits epoxide reductase

66
Q

Cause of heparin induced thrombocytopenia

A

Heparin binds PF-4 on PLT surface → antibodies bind complex → splenic destruction of PLTs

PLT fragments may activate coagulation and cause thrombosis

67
Q

Cause of hypocoagulability in newborns

A

Lack enteric flora, which produce vit K

68
Q

Lab findings in DIC

A

1) ↑ D-dimers
2) Schistocytes
3) ↓PLTs
4) ↑PT/PTT
5) ↓ fibrinogen, FV, FVIII

69
Q

Tx in DIC

A

Frozen plasma

70
Q

Causes of antithrombin deficiency

A

1) inherited

2) Renal failure (loss to urine)

71
Q

Labs in antithrombin deficiency

A

1) PT/PTT NL

2) PTT following thrombin less increased than expected

72
Q

Thrombotic skin necrosis and hemorrhage after Warfarin administration may be observed in

A

Protein C or S deficiency

73
Q

Deficiency in Hemophilia A

A

FVIII; X-linked

74
Q

Deficiency in Hemophilia B

A

FIX; X-linked

75
Q

Deficiency in Hemophilia C

A

FXI; autosomal recessive

76
Q

PT measures

A

Extrinsic pathway

77
Q

PTT measures

A

Intrinsic pathway

78
Q

Lab findings in hemophilia

A

1) ↑PTT, NL PT

2) NL PLT

79
Q

Tx in hemophilia

A

1) Desmopressin

2) Deficient factor concentrate

80
Q

Hemophilia presentation

A

1) Easy bruising
2) Bleeding after surgery
3) Hemarthrosis

81
Q

Autoimmune disease with similar findings to Hemophilia A

A

Anti-FVIII antibody

82
Q

Lab distinguishing FVIII inhibitor from Hemophilia A

A

1) Inhibitor: Mixing normal plasma with patient plasma does not correct PTT
2) Hemophilia A: mixing study corrects PTT

83
Q

von Willebrand Disease defect

A

vWF deficiency; most commonly autosomal dominant

84
Q

Labs in von Willebrand disease

A

1) NL PT/↑PTT (due to ↓FVIII)

2) No aggregation on ristocetin screen

85
Q

Tx in von Willebrand disease

A

Desmopressin

86
Q

Cause of heparin induced thrombocytopenia

A

Heparin binds PF-4 on PLT surface → antibodies bind complex → splenic destruction of PLTs

PLT fragments may activate coagulation and cause thrombosis

87
Q

Common causes of DIC (7)

A

1) Obstetric complications (amniotic TF)
2) Sepsis (esp. E Coli/N meningitidis)
3) Adenocarcinoma (Mucin)
4) APL (abnormal primary granules)
5) Rattlesnake bite
6) Nephrotic syndrome (loss of ATIII)
7) Pancreatitis

88
Q

Lab findings in DIC

A

1) ↑ D-dimers
2) Schistocytes
3) ↓PLTs
4) ↑PT/PTT
5) ↓ fibrinogen, FV, FVIII

89
Q

Tx in DIC

A

Frozen plasma

90
Q

Plasmin pathway

A

1) Activated by tPA
2) cleaves fibrin and fibrinogen, destroys coag factors, blocks PLT aggregation
3) inactivated by α2-antiplasmin

91
Q

Causes of plasmin overactivity

A

1) Radical prostatectomy (uPA release)

2) Liver cirrhosis (↓ α2-antiplasmin)

92
Q

Labs in plasmin overactivity

A

1) ↑ PT/PTT (loss of plasma factors)
2) ↑ BT
3) NL PLT
4) 0 D dimers

93
Q

Tx in plasmin overactivity

A

aminocaproic acid

94
Q

Features distinguishing postmortem clot from thrombus

A

1) Lines of Zahn

2) Attachement to vessel wall

95
Q

Mechanisms by which endothelial cells prevent clotting (5)

A

1) Conceal subendothelial collagen and TF
2) Production of PGI2 and NO
3) Secretion of heparin-like molecules
4) Secretion of tPA
5) Secretion of thrombomodulin

96
Q

Mechanism of ↑ thrombosis risk in B12/folate deficiency

A

Elevated homocysteine damages endothelial cells

97
Q

Findings in Cystathione β Synthase deficiency

A

CBS deficiency inhibits conversion of homocysteine into cystathione, →

1) Homocysteinuria
2) Vessel thrombosis
3) mental retardation
4) lens dislocation
5) long, slender fingers

98
Q

Prothrombin 20210A

A

Point mutation increasing expression of prothrombin → hypercoagulable state

99
Q

Effects of oral contraceptives on coagulation

A

Estrogen increases coagulation factor production → hypercoagulable state

100
Q

Histological finding in atherosclerotic embolus

A

cholesterol clefts

101
Q

Dyspnea and petechiae on skin overlying the chest following trauma

A

Fat embolus

102
Q

Caisson disease

A

Chronic decompression sickness, characterized by multifocal ischemic necrosis of the bone

103
Q

Histological findings in amniotic fluid embolus

A

squamous cells and keratin debris

104
Q

Cause of sudden death in PE

A

R heart pumping against complete occlusion

105
Q

Packed RBCs: effect

A

↑ Hb and O2 carrying capacity

106
Q

Packed RBCs: use

A

acute blood loss, severe anemia

107
Q

Platelet transfusion: use

A

Stop bleeding in thrombocytopenia/PLT defects

108
Q

Fresh frozen plasma: effect

A

↑ Coagulation factor levels

109
Q

Fresh frozen plasma: use

A

DIC, cirrhosis, warfarin reversal

110
Q

Cryoprecipitate: contains

A

Fibrinogen
FVIII, FXIII
vWF
Fibronectin

111
Q

Electrolyte imbalances caused by blood transfusion

A

Hypocalcemia (chelated by citrate, anticoagulant)
Hyperkalemia (lysed RBCs)
iron overload

112
Q

Conditions causing appropriate absolute polycythemia (3)

A

Lung Dz
Congenital heart disease
High altitude

113
Q

Unfractionated heparin mechanism

A

Binds ATIII, increasing irreversible inhibition of clotting factors, esp. FII and FX

114
Q

Heparin clinical use (4)

A

1) DVT prophylaxis
2) PE prophylaxis and acute Tx
3) Acute MI
4) Pregnancy (doesn’t cross placenta)

115
Q

Heparin adverse affects (4)

A

1) Bleeding
2) HIT
3) Osteoporosis
4) Hyperkalemia (aldosterone suppression)

116
Q

Pathogenesis of heparin induced thrombocytopenia

A

IgG antibodies against heparin-PF4 complex → PLT destruction and hypercoagulability

117
Q

Reversal of heparin

A

Protamine sulfate (unfractionated only)

118
Q

Heparin monitoring is done via

A

PTT

119
Q

Differences between LMWH and unfractionated heparin (6)

A

1) Action at FX only
2) Longer half-life
3) Renal elimination
4) Cannot be monitored via PTT
5) Lower HIT risk
6) Not reversible by protamine sulfate

120
Q

Tx in HIT

A

DC heparin, start direct thrombin inhibitors (e.g. bivalirudin, argatroban/dabigatran)

121
Q

Direct thrombin inhibitors

A

Bivalirudin

Argatroban/Dabigatran

122
Q

Direct FXa inhibitors

A

Apixaban, rivaroxaban

123
Q

Clinical use of Direct FXa Inhibitors

A

Tx/prophylaxis for DVT and PE

Prophylaxis in A-fib

124
Q

Warfarin MOA

A

inhibits vitamin K epoxide reductase →↓ production of FII, VII, IX, X, C, S

125
Q

Warfarin monitoring is done via

A

PT/INR

126
Q

First factors affected by Warfarin

A

C, S, VII

127
Q

INR goal in most warfarin therapy

A

2 - 3

128
Q

Warfarin use

A

Chronic anticoagulation (esp. DVT and A-Fib prophylaxis)

129
Q

Rxn inhibited by warfarin

A

γ-carboxylation

130
Q

Pathogenesis and Tx of warfarin induced skin necrosis

A

Transient hypercoagulable state caused by loss of Protein C/S
Prevent w/heparin bridge

131
Q

time to onset of Warfarin effects

A

8-12 hours

132
Q

Warfarin reversal

A 
Vit K (delayed)
FFP (immediate)
133
Q

Warfarin in pregnancy

A

Teratogenic

134
Q

Warfarin elimination

A

Hepatic - CyP450

135
Q

Warfarin route of administration

A

oral

136
Q

Heparin route of administration

A

IV/SC

137
Q

Site of warfarin action

A

Liver

138
Q

ADP receptor inhibitors (4)

A

1) Clopidogrel
2) prasugrel
3) ticagrelor
4) ticlopidine

139
Q

Ticagrelor: difference from other ADP receptor inhibitors

A

Allosteric binding site; reversible inhibition

140
Q

ADP receptor inhibitors MOA

A

Irreversibly (or reversibly - ticagrelor) inhibits P2Y12 → ↓GPIIb/IIIa expression

141
Q

Adverse effects of ADPr inhibitors (2)

A

Neutropenia (ticlopidine)

TTP

142
Q

Use of ASA/ADPr inhibitor therapy (3)

A

1) Prophylaxis in PAD/CAD/Cerebrovascular disease
2) Prophylaxis for coronary stent thrombosis (dual therapy)
3) Acute MI (chewable aspirin)

143
Q

ASA mechanism

A

irreversibly inhibits COX-1 and COX-2 by acetylation → ↓TXA2

144
Q

Substances released in PLT degranulation (3)

A

TXA2, ADP, 5-HT

145
Q

ASA adverse effects

A

“Pseudo-allergy” due to ↑LT synthesis

146
Q

Phosphodiesterase inhibitors (2)

A

cilostazol, dipyridamole

147
Q

Phosphodiesterase inhibitor MOA

A

↑cAMP in PLTs → inhibition of PLT aggregation; vasodilation

148
Q

Phosphodiesterase inhibitor Use (4)

A

1) Intermittent claudication
2) Coronary vasodilation
3) Angina prophylaxis
4) Stroke/TIA prophylaxis

149
Q

Phosphodiesterase inhibitor adverse effects (3)

A

1) Coronary steal
2) Flushing, hypotension
3) Abdominal pain

150
Q

GPIIb/IIIa inhibitors (3)

A

ABCiximab
eptiFIBatide
tiroFIBan

151
Q

GPIIb/IIIa inhibitor MOA

A

bind GPIIb/IIIa, preventing aggregation

152
Q

GPIIb/IIIa inhibitor use (2)

A

1) Unstable angina

2) Percutaneous transluminal angioplasty

153
Q

GPIIb/IIIa inhibitor adverse effects (2)

A

Thrombocytopenia, bleeding

154
Q

Fibrinolytics (4)

A

tPA (alteplase)
rPA (reteplase)
TKA-tPA (tenecteplase)
Streptokinase

155
Q

Fibrinolytic MOA

A

Aid conversion of plasminogen to plasmin

156
Q

Fibrinolytics clinical use (3)

A

1) Ischemic stroke (3 - 4.5 hrs after Sxs appear)
2) Acute MI (if PCI not available w/in 2 hours)
3) Severe PE/DVT

157
Q

Fibrinolytics: contraindications (4)

A

1) Severe HTN
2) Head trauma or intracranial bleeding
3) Recent surgery
4) Hypocoagulability disorders

158
Q

Tx of bleeding as a result of fibrinolytic therapy

A

1) Aminocaproic acid
2) Tranexamic acid
3) Cryoprecipitate
4) FFP

159
Q

Labs in fibrinolytic therapy

A

1) ↑ D-dimers

2) ↑ PT/PTT

160
Q

Adverse effects in fibrinolytic therapy

A

1) Bleeding (esp intracranial)

2) Anaphylaxis (streptokinase)

Step 1 Immunology (13 decks)

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