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Hemostasis Flashcards

1
Q

What is the first step of hemostasis? What are the two mediators of this?

A

Transient vasoconstriction mediated by a neural reflex arc and endothelin release

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2
Q

What is the molecule that is on endothelium and causes vasoconstriction?

A

Endothelin

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3
Q

What is the molecule on platelets that binds vWF?

A

GPIb

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4
Q

Where does vWF come from (which cells)? (2)

A
  • Weibel-Palade bodies within Endothelium

- Platelets

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5
Q

What is step II of hemostasis?

A

vWF binding to GPIb

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6
Q

What is in Weibel-Palade bodies?

A

vWF

P-selectin

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7
Q

What is released from platelets when the bind vWF?

A

ADP

TXA2

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8
Q

What is the enzyme that makes TXA2?

A

COX

platelet cyclooxygenase

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9
Q

What is the receptor on platelets that ADP induces? What does this do?

A

GpIIb/IIIa

Causes platelet-platelet binding

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10
Q

What does TXA2 do in platelets?

A

Causes platelet linking

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11
Q

What is the linker molecule between platelets that is used in aggregation?

A

fibrinogen + GPIIb/IIIa

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12
Q

What are the two, broad types of disorders of primary hemostasis?

A

Qualitative

Quantitative

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13
Q

What is the most common symptom of hemostasis disorders?

A

Mucosal and skin bleeding (epistaxis, hemoptysis etc)

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14
Q

What is the most feared complication of platelet defects?

A

Intracranial bleeding

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15
Q

Are petechia usually seen in qualitative or quantitative disorders?

A

Quantitative (thrombocytopenia)

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16
Q

Petechiae are characteristic of what hematological defect?

A

Quantitative Platelet issues

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17
Q

What is the drug that binds to and inhibits GpIIa/IIIb?

A

Abciximab

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18
Q

Define primary and secondary hemostasis

A 
Primary = platelet plug
Secondary = Fibrinogen cross linking
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19
Q

What are the four useful lab studies for hemostasis disorders?

A
  • Platelet count
  • Bleeding time
  • Blood smear
  • Bone marrow biopsy
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20
Q

What are the cells that produce platelets?

A

Megakaryocytes

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21
Q

What is immune thrombocytopenic purpura (ITP)?

A

Autoimmune production of IgG against platelet antigens (e.g. GPIIb/IIIa)

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22
Q

What is the most common cause of thrombocytopenia in adults?

A

ITP

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23
Q

What organ makes the IgG in ITP?

A

Spleen

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24
Q

What is the acute form of ITP? What is the treatment?

A

Develops weeks after viral infection/immunization

Usually self-limited, thus supportive treatment

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25
Q

What is the chronic form of ITP? Who is this usually seen in (disease/age group)?

A

Usually women of childbearing age, associated with SLE.

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26
Q

What is the problem with ITP in pregnant women?

A

IgG that is produced can cross the placenta, and resulting in thrombocytopenia in fetus

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27
Q

What is the platelet count in ITP (up, down, or normal)?

A

Down

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28
Q

What is the PT/PTT in ITP (up, down, or normal)?

A

Normal

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29
Q

What is the megakaryocyte count in ITP (up, down, or normal)?

A

Up

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30
Q

What is the treatment for the fetus in ITP?

A

Corticosteroids

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31
Q

What is the treatment for symptomatic ITP? Why does this work?

A

IVIG–causes macrophages to eat IG, not bound to platelets (effect is short lived)

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32
Q

What is the treatment of refractory ITP? Why?

A

Splenectomy–eliminates the site of antibody production, and the site of destruction

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33
Q

What is microangiopathic hemolytic anemia?

A

Pathologic formation of platelet microthrombi in small vessels, causing RBCs to rupture d/t platelet microthrombi

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34
Q

What is the characteristic finding of a blood smear in microangiopathic hemolytic anemia?

A

Sheared RBCs (schistocytes)

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35
Q

Helmet cell = ?

A

Schistocyte (seen in microangiopathic anemia)

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36
Q

What are the two diseases that cause microangiopathic anemia?

A

Thrombocytopenic purpura (TTP)

Hemolytic uremic syndrome (HUS)

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37
Q

What is the deficient enzyme in TTP? What does this do?

A

Decrease in ADAMTS13 enzyme, which normally cleaves vWF for degradation, causing abnormal platelet adhesion on uncleaved monomers

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38
Q

What causes the decrease in ADAMS-13 in TTP?

A

Acquired antibody; most commonly seen in females

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39
Q

What causes HUS?

A

E.coli OH157:H7 verotoxin damages endothelial cells, resulting in platelet microthrombi

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40
Q

What is the bacteria that causes HUS? Who is affected, and where does this bacteria come from?

A

E.coli OH157:H7

Children affected when eating undercooked beef

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41
Q

What are the clinical findings of HUS? (4)

A
  • Dysentery
  • Skin and mucosal bleeding
  • Renal damage
  • CNS dysfunction
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42
Q

What is the predominant problem in TTP and HUS respectively?

A 
TTP = CNS dysfunction
HUS = Renal insufficiency
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43
Q

Why is the PT/PTT normal in HUS/TTP?

A

No activation of the coagulation cascade

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44
Q

What are the findings of a blood smear with TTP/HUS?

A

Schistocytes

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45
Q

What are the findings of a bone biopsy with TTP/HUS?

A

Increased megakaryocytes

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46
Q

What happens to bleeding time with TTP/HUS?

A

Increased

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47
Q

What is the treatment for TTP?

A

Plasmapheresis and corticosteroids

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48
Q

What is the cause of Bernard-Soulier syndrome?

A

Genetic GP1b deficiency; platelet adhesion is impaired

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49
Q

What are the findings of a blood smear with Bernard-Soulier syndrome?

A

Mild thrombocytopenia with enlarged platelets

(Big Suckers with Bernard-Soulier)

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50
Q

What is the cause of Glanzmann thrombasthenia?

A

Genetic GIIb/IIIa causing platelet aggregation impairment

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51
Q

What is the MOA of ASA in preventing platelet aggregation?

A

Lack of TXA2 d/t irreversible inhibition of COX

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52
Q

What is the coagulation problem with uremia?

A

Uremia disrupts platelet function; both adhesion and aggregation is impaired

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53
Q

What is the goal of secondary hemostasis?

A

Stabilize the platelet plug

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54
Q

What is the end product of coagulation?

A

Thrombin/fibrin

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55
Q

What protein connects the GPIIb/IIIa proteins on platelets together? What forms this, and what enzyme activates it?

A

Fibrin, which is formed from fibrinogen by thrombin

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56
Q

What produces fibrinogen, and where does it go (before activation?

A

Liver, floats around in the blood stream until activated

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57
Q

What are the three things that are needed to activate the coagulation cascade?

A
  1. Activating substance
  2. Ca
  3. Phospholipid surface of platelets
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58
Q

What are the two activating substances of the coagulation cascade?

A
  1. Tissue thrombin activator (VII)

2. Subendothelial collagen activates factor XII

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59
Q

What causes disorders of secondary hemostasis?

A

Usually d/t factor abnormalities

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60
Q

What are the clinical features of secondary hemostasis disorders?

A
  • Deep tissue bleeding into muscles/joints

- Rebleeding after procedures

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61
Q

What does PT measure (intrinsic or extrinsic pathway)?

A

The extrinsic pathway

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62
Q

What does PTT measure (intrinsic or extrinsic pathway)?

A

The intrinsic pathway (“has more factors, so has an extra T”)

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63
Q

What are the factor steps of the intrinsic pathway?

A

12, 11, 9, 8, 10

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64
Q

What are the factor steps of the extrinsic pathway? Common pathway?

A

3, 7, 10

Common = 5, 2, 1

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65
Q

What activates factor 12?

A

Subendothelial collagen

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66
Q

What activates the extrinsic pathway?

A

Tissue thromboplastin (factor 3)

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67
Q

Which lab value measures the effect of heparin (PT or PTT)?

A

PTT (HEP and PTT both have three letters)

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68
Q

Which lab value measures the effect of warfarin (PT or PTT)?

A

PT

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69
Q

What is the factor that has a genetic defect in hemophilia A?

A

Factor VIII (“Hemophilia aaa–eeeight”)

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70
Q

What is the inheritance pattern of hemophilia A?

A

X-linked recessive or new mutation

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71
Q

What are the PT and PTT findings of hemophilia A?

A

Increased PTT

Normal PT

72
Q

What is the platelet count and bleeding time in hemophilia A? (up, down, normal)

73
Q

What is the treatment for hemophilia A?

A

Recombinant factor 8

74
Q

What is the factor deficiency for hemophilia B (“Christmas disease”)?

75
Q

What is the cause of coagulation factor inhibitor? Which factor is affected most commonly?

A

Acquired antibody against coagulation factor, resulting in impaired factor function

Factor VIII most commonly affected

76
Q

How do you distinguish between hemophilia A caused by a coagulation factor inhibitor vs a factor deficiency (since both have increased PTT)?

A

PTT does not correct upon mixing normal plasma with pts plasma (mixing study) if caused by a coagulation factor inhibitor (since antibodies are in serum)

77
Q

What is von Willebrand disease? Symptoms?

A

Deficiency of vWF

Mucosal and skin bleeding

78
Q

What is the most common inherited coagulation factor disorder?

A

Genetic vWF deficiency

79
Q

What is the most common type of vWF disease? Inheritance pattern?

A

AD decrease in vWF levels (quantitative, not qualitative defect)

80
Q

What happens to bleeding time, PTT, and PT in vWF disease?

A
  • Increased bleeding time
  • Increased PTT
  • Normal PT
81
Q

Why does the PTT increase in vWF disease?

A

vWF is needed to stabilize factor 8

82
Q

What is the ristocetin test, and what is the result in vWF disease?

A

Ristocetin induces platelet agglutination by causing vWF to bind to platelet GPIb; thus abnormal test

83
Q

What is the treatment for vWF disease? MOA?

A

desmopressin

Increases the release of vWF from WP bodies

84
Q

What are the factors that need vitamin K for gamma carboxylation?

A

10, 9, 7, 2 (vitamin K was born in 1972)

protein C and S

85
Q

Why are newborns susceptible to vitamin K deficiency, as well as pts on long term abx?

A

Lack of bacterial colonization in the gut that make vit K

86
Q

How does liver failure lead to coagulation disorders? How about abx therapy? Malabsorption?

A
  • Decreased production of coagulation factors
  • Decreased vit K from bacteria
  • Decrease in fat soluble vitamin (K) absorption
87
Q

What is the enzyme the liver produces that activates vitamin K?

A

Epoxide reductase

88
Q

What lab value is followed in liver damage-caused coagulation disorders?

A

PT (same as warfarin)

89
Q

Why does large volume transfusion cause secondary coagulation defects?

A

Dilution of coag factors

90
Q

What is the cause of heparin induced thrombocytopenia (HIT)?

A

Antibodies to Hep-PF4 complex

Fragments of destroyed platelets may activated remaining platelets, leading to thrombosis

91
Q

What, generally, is DIC caused by?

A

Pathologic activation of the coagulation cascade, leading to the consumption of factors and platelets

92
Q

What are the two major problems with DIC?

A
  1. Widespread microthrombi

2. Thrombocytopenia

93
Q

What causes DIC in sepsis?

A

Cytokines and induction of coag by bacteria

94
Q

What happens to platelet count in DIC (up, down, nl)?

95
Q

What happens to PT/PTT in DIC (up, down, nl)?

96
Q

What happens to fibrinogen in DIC (up, down, nl)?

97
Q

What is the screening lab test for DIC?

A

D-Dimer (elevated fibrin split products)

98
Q

Microangiopathic hemolytic anemia is found in DIC. What is the blood smear finding to confirm this?

A

Schistocytes

99
Q

What is the treatment for DIC?

A

Transfuse blood products or cryoprecipitate

100
Q

What is the function of fibrinolysis normally?

A

Remove thrombus after damaged vessel heals

101
Q

What is the function of plasmin? (3)

A
  • Degrades fibrin/fibrinogen
  • Shuts down clotting factors
  • Blocks platelet aggregation
102
Q

What do endothelial cells release to activate plasmin from plasminogen?

103
Q

What is the endogenous molecule that inactivates plasmin?

A

alpha-2-antiplasmin

104
Q

What are disorders of fibrinolysis caused by, generally?

A

Plasmin overactivity, resulting in excessive cleavage of fibrinogen

105
Q

What is the chemical released during a radical prostatectomy that activates plasmin?

106
Q

Why does liver cirrhosis lead to fibrinolysis disorder?

A

Loss of alpha-2 antiplasmin

107
Q

Disorders of fibrinolysis present similar to what other process?

108
Q

What are happens to PT/PTT with disorders of fibrinolysis? Why?

A

increase–cleavage of coaulation factors

109
Q

What happens to bleeding time and platelet count with disorders of fibrinolysis? Why?

A

Increased bleeding time

Normal platelet count–inhibition of platelet aggregation

110
Q

What is the difference between DIC and fibrinolysis disorders in terms of platelet count? D-dimer?

A

DIC has reduced platelets with increased d-dimer

Both normal with fibrinolysis

111
Q

Why is the d-dimer not elevated with disorders of fibrinolysis?

A

No clot formed, just overactivation of plasmin

112
Q

What is the treatment for disorders of fibrinolysis? MOA?

A

Aminocaproic acid–blocks activation of plasminogen

113
Q

What are the two characteristics that distinguish a thrombus from a post mortem clot?

A
  • Lines of Zahn

- Attachment to the blood vessel walls

114
Q

What are the three major risk factors for thrombosis?

A
  1. Disruption of blood flow
  2. Endothelial cell damage
  3. Hypercoagulable state
115
Q

What protects blood vessels from thrombosis? (4)

A
  1. Barrier via endothelial cells does not allow attachment
  2. PGI2
  3. NO
  4. Heparin-like molecules
116
Q

What is the function of PGI2 that endothelial cells release?

A

Prevents coagulation and dilates vessels

117
Q

What is the function of antithrombin III?

A

Inactivates thrombin and coagulation factors

118
Q

What are lines of Zahn?

A

Alternating layers of RBCs, platelets, and fibrin in a thrombus

119
Q

What is the function of tPA that endothelial cells secrete?

A

Activates plasminogen to plasmin, which will cleaves fibrin and fibrinogen to prevent clot formation

120
Q

What is the function of plasmin? (3)

A
  1. Cleaves fibrin & fibrinogen
  2. Destroys coag factors
  3. Blocks platelet aggregation
121
Q

What is the function of thrombomodulin?

A

Redirect thrombin to activate protein C

122
Q

What is the action of protein C once activated by thrombomodulin/thrombin?

A

Inactivates factors V and VIII

123
Q

What are the ways that we can develop elevated levels of homocysteine? (recall that this damages endothelial cells)

A
  1. Vitamin B12/folate deficiency

2. Cystathionine beta synthase (CBS) deficiency (homocysteine)

124
Q

Why does a Vit B12/folate deficiency lead to increased levels of homocysteine?

A

THF needs to hand off a methyl group to vit B12, which hands off to homocysteine, which produces methionine

125
Q

What is the enzymatic deficiency that leads to high levels of homocysteine, and is the cause of homocystinuria?

A

Cystathionine beta synthase (CBS)

126
Q

What are the symptoms of homocystinuria?

A
  • Vessel thrombosis
  • MR
  • Long, slender fingers
  • Lens dislocation
127
Q

What are the two ways that can result in a hypercoagulable state?

A
  1. Excessive procoagulant factors

2. Lack of anticoagulant factors

128
Q

What is the classic presentation for patients with a hypercoagulable state?

A

Recurrent DVTs, or DVTs at a young age

129
Q

Deficiencies in protein C or S leads to what? Why? How is this inherited?

A

Hypercoagulable state, since protein C will not block factors 5 and 8.

AD

130
Q

Patients with deficiencies in protein C or S are more likely to have a complication with what drug? Why?

A

Warfarin (coumadin) since protein C and S are lost first, and these are already defective or deficient

131
Q

What is the treatment that we start patients with when starting coumadin?

A

Heparin first

132
Q

What is factor V leiden? Does this lead to a hypercoagulable state or a bleeding disorder?

A

Mutated form of factor V that prevents deactivation by protein C

Leads to a hypercoagulable state

133
Q

What is the most common cause of a hypercoagulable state?

A

Factor V leiden

134
Q

What is the prothrombin 20210A defect?

A

Inherited point mutation in prothrombin, leading to increased gene expression, and thus a hypercoagulable state

135
Q

What does an antithrombin III deficiency lead to?

A

Decreases the protective effect of heparin-like molecules produced by the endothelium, increasing the risk for thrombus

136
Q

What normally activates antithrombin III? What does activation of antithrombin III lead to?

A

Heparin like molecules activates it

inactivates thrombin and coagulation factors

137
Q

Why doesn’t the PTT rise when patients with antithrombin III deficiency are given heparin? What is given to these patients instead?

A

Limited number of ATIII

Warfarin

138
Q

Why are oral contraceptives associated with a hypercoagulable state?

A

Estrogen induces an increased production of coagulation factors

139
Q

What is an atheroscleotic embolus? How can you differentiate this from a normal embolus?

A

One that results from an arthresclerotic plaque

Will see cholesterol crystals in the embolus

140
Q

Fat emboli are associated with what?

A

Bone fractures

141
Q

What are the signs/symptoms of a fat embolus?

A

-Dyspnea and petechiae on the skin overlying the chest

142
Q

Gas emboli are classically seen in what condition?

A

Decompression sickness

143
Q

What causes decompression sickness?

A

N gas precipitates out of the blood due to rapid ascent by a diver

144
Q

What are the two symptoms that decompression sickness can present with?

A

Bends or the chokes

145
Q

What is Caisson’s disease?

A

Chronic form of gas emboli that is characterized by multifocal ischemic necrosis of bone

146
Q

Why can gas emboli result from laparoscopic surgery?

A

Air is pumped into the abdomen

147
Q

What are the symptoms that occur when amniotic fluid enters maternal circulation?

A
  • Dyspnea
  • DIC
  • Neuro symptoms
148
Q

What is found within amniotic fluid that causes an embolism?

A

-Tissue thromboplastin
-Squamous cells
Keratin debris

149
Q

What are the three veins usually associated with DVTs?

A

Iliac
Popliteal
Femoral

150
Q

Why are PEs usually silent? (2)

A
  1. Dual blood supply to the lung

2. Usually small embolus

151
Q

When do pulmonary infarction usually occur with PEs?

A

Obstruction of medium to large vein

Pre-existing cardiopulmonary compromise

152
Q

Why is the D-dimer elevated with DVTs or a PE?

A

Clot is actively being lysed, resulting in fibrin breakdown products

153
Q

Why is the characteristic shape of infarcts caused by PEs? Why is it hemorrhagic?

A

Wedge

Hemorrhagic d/t other blood supply and loose CT d/t infarct

154
Q

What is a saddle embolus?

A

Blockage of both pulmonary arteries by a clot

155
Q

What is the major complication of chronic pulmonary emboli?

A

Pulmonary HTN (type IV)

156
Q

What is the most common cause of a systemic thromboembolism?

A

Thrombus that arose from the left heart

157
Q

What drug should never be given to patients with HIT?

158
Q

What causes DIC in the obstetric setting?

A

Amniotic fluid contains tissue thromboplastin, which can activate the coag cascade if exposed in maternal blood

159
Q

How can adenocarcinoma cause DIC?

A

Mucin production causes activation of coagulation cascade

160
Q

How can acute promyelocytic leukemia cause DIC?

A

Auer rods in cells leak out of cells and activate the coagulation cascade

161
Q

How can rattle snake bite cause DIC?

A

Toxin causes activation of coag

162
Q

What is the MOA of heparin?

A

Binds to and activates ATIII

163
Q

What is the MOA of vincristine and vinblastine? Use? Side effects?

A

bind to beta-tubulin, and inhibit polymerization into microtubules

Solid tumors, leukemias/lymphomas

Neurotoxic and myelosuppression

164
Q

What is the MOA, use, and side effects of: paclitaxel and other taxols?

A
  • Hyper Stabilize polymerized tubules
  • Ovarian and breast cancer
  • Myelosuppression and alopecia
165
Q

What is the MOA, use, and side effects of: cisplatin and carboplatin?

A
  • Cross link DNA
  • Testicular, bladder, and ovarian cancer
  • Nephrotoxic and acoustic nerve damage
166
Q

What is the MOA, use, and side effects of: Irinotecan and topotecan?

A
  • Topoisomerase II inhibitors
  • Solid tumors
  • Myelosuppression, alopecia
167
Q

What is the MOA, use, and side effects of: hydroxyurea

A

Inhibits ribonucleotide reductase (S phase specific)

  • Melanoma, CML
  • Myelosuppression
168
Q

What is the MOA, use, and side effects of: cyclophosphamide

A
  • Covalently linking DNA
  • Solid tumors
  • Myelosuppression, hemorrhagic cystitis
169
Q

What is the MOA, use, and side effects of: Nitrosoureas (carmustine, lomustine)

A
  • Cross BBB and covalently links DNA
  • Brain tumors
  • CNS toxicity
170
Q

What is the MOA, use, and side effects of: busulfan

A
  • Cross links DNA
  • CML, and bone marrow ablation
  • Pulmonary fibrosis
171
Q

What is the MOA, use, and side effects of: bleomycin

A
  • Induces free radical damage to cause breaks in DNA
  • Testicular cancer
  • Pulmonary fibrosis
172
Q

What is the MOA, use, and side effects of: doxorubicin

A
  • Generates free radicals and intercalates DNA
  • Solid tumors, leukemia
  • Cardiotoxic
173
Q

What is dexrazoxane used for?

A

Prevent cardiotoxicity from doxorubicin

174
Q

What is the MOA, use, and side effects of: 5-FU

A
  • Pyrimidine analog, inhibits thymidylate synthase
  • Colon cancer
  • Photosensitivity and myelosuppression
175
Q

What is the MOA, use, and side effects of: ritixumab

A
  • Anti CD20
  • RA, non-hodgkin’s lymphoma
  • PML
176
Q

What is the MOA, use, and side effects of: Vemurafeib

A
  • BRAF kinase inhibitor

- Metastatic melanoma

177
Q

What is the MOA, use, and side effects of: bevacizumab

A
  • Monoclonal ab against VEGF
  • Solid tumors
  • Hemorrhage

All the things (36 decks)

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