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First Aid > Heme/Onc 1 > Flashcards

Heme/Onc 1 Flashcards

1
Q

What is the first line defense against bleeding?

A

Vasoconstriction

Key mediator: Endothelin

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2
Q

What is Endothelin?

A

Potent vasoconstrictor released by endothelial cells near site of damage

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3
Q

Endothelin receptor blockers are used to treat what condition?

A

Pulmonary hypertension

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4
Q

Where are coagulation factors synthesized?

A

Liver

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5
Q

What do many coagulation factors activate to become?

A

Serine proteases

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6
Q

What do coagulation factors form when triggered by endothelial damage?

A

Fibrin to prevent blood loss

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7
Q

What is Tissue Factor?

A

Glycoprotein

Constitutively expressed in sub-endothelial cells

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8
Q

What is the major activator of the coagulation system?

A

Tissue factor (exposed by tissue damage)

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9
Q

How is Prothrombin Time and INR measured?

A

Tissue factor added to blood sample, time to clot = PT

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10
Q

How does thrombin make more thrombin?

A

Activates cascade via positive feedback: Activates Factor V, XI, and VIII

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11
Q

Where is Factor VIII produced?

A

Endothelial cells (not the liver)

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12
Q

Von Willebrand Factor is produced by?

A

Endothelial cells and megakaryocytes

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13
Q

Factor VIII circulates bound to what?

A

Von Willebrand Factor

Increases Factor VIII plasma half life

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14
Q

What are the 2 multicomponent complexes that convert X to Xa?

A

Extrinsic Xase, Intrinsic Xase

Require phospholipids (TF bearing cells or platelets) and calcium

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15
Q

What is Extrinsic Xase comprised of?

A

Phospholipid: TF-bearing cells, Enzyme: Factor VIIa, Co-factor: Tissue factor, Substrate: Factor X

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16
Q

What is Intrinsic Xase comprised of?

A

Phospholipid: Platelets, Enzyme: Factor IXa, Co-factor: Factor VIII (VIIIa), Substrate: Factor X

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17
Q

What is added to blood samples to prevent clotting?

A

EDTA (binds calcium)

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18
Q

Calcium is also called?

A

Factor IV (required for clot formation)

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19
Q

What is the function of Factor XIII?

A

Crosslinks fibrin and stabilizes fibrin plug

Requires Ca2+

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20
Q

What activates Factor XIII formation?

A

Thrombin (IIa) formation

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21
Q

What is Factor XII also called?

A

Hageman factor

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22
Q

What activates Factor XII?

A

Contact with negatively charged substances

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23
Q

How is the Activated Partial Thromboplastin Time (PTT) measured?

A

Add plasma to (-) charge substance (silica), time to form clot = PTT

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24
Q

What peptide hormone is required for normal function of the intrinsic pathway?

A

Kinins (circulate as inactive precursors due to short half life)

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25
Q

What activates kininogens?

A

Kallikreins

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26
Q

What are 3 effects of bradykinin?

A

Vasodilator, Increases vascular permeability, Pain

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27
Q

Bradykinin is degraded by?

A

ACE and C1 inhibitor protein (part of complement system)

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28
Q

What is a dangerous side effect of ACE inhibitors?

A

Angioedema

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29
Q

What can C1 inhibitor deficiency lead to?

A

Hereditary angioedema

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30
Q

What are 2 functions of Factor XII?

A

Activates clotting and produces bradykinin

Does not have a lot of physiologic significance

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31
Q

What happens in Prekallikrein Deficiency?

A

XII cannot activate normally, markedly prolonged PTT

No bleeding problems because Factor XII does not have a lot of physiologic significance

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32
Q

What activates the Kinin System?

A

Factor XII

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33
Q

What are 3 important deactivators of coagulation?

A

Antithrombin III, Proteins C and S, Tissue factor pathway inhibitor

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34
Q

Antithrombin III inhibits what proteins?

A

Serine proteases

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35
Q

Which factors are inhibited by Antithrombin III?

A

Factors II, VII, IX, X, XI, XII

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36
Q

What produces and activates Antithrombin III?

A

Liver

Activated by heparin sulfate molecules made by the endothelium

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37
Q

What is the basic mechanism of heparin drug therapy?

A

Mimics heparin sulfate and activates antithrombin III

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38
Q

What does deficiency of Antithrombin III lead to?

A

A hypercoagulable state

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39
Q

What produces Protein C and S?

A

Liver

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40
Q

What activates Protein C?

A

Thrombomodulin (cell membrane protein on endothelial cells) and Thrombin Complex

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41
Q

Activated Protein C primarily inactivates which factors?

A

Va and VIIIa

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42
Q

What does Tissue factor pathway inhibitor inactivate?

A

Xa

Mechanisms: directly binds, Binds TF/VIIa complex → prevents X activation

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43
Q

What plasma levels are increased with heparin administration?

A

Tissue factor pathway inhibitor (may contribute to antithrombotic effect)

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44
Q

Are Protein C and Protein S zymogens?

A

Yes, No

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45
Q

Where is Plasminogen synthesized?

A

Liver (as a zymogen)

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46
Q

What is the main role of plasmin?

A

Breakdown of fibrin

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47
Q

What are 3 plasminogen activators?

A

Tissue plasminogen activator (tPA), Urokinase, Streptokinase (streptococcal protein)

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48
Q

Tissue plasminogen activator (tPA) and urokinase are used as drug therapy for?

A

Acute MI and stroke

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49
Q

What does plasmin break down fibrin into?

A

Fibrin degradation products and D-dimers

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50
Q

What does the presence of D-dimers indicate?

A

Clot breakdown (indicates breakdown of crosslinked fibrin from XIII)

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51
Q

Fibrin degradation products (FDPs) can be elevated in the absence of a clot from?

A

Fibrinogen breakdown

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52
Q

What is the underlying mechanism of Primary Fibrinolysis?

A

Overactive plasmin causes ↑ FDP with normal D-dimer

Hyperfibrinolysis: Plasmin breakdown of fibrinogen but not fibrin (no clot present)

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53
Q

What is a complication of Primary Fibrinolysis?

A

Can deplete clotting factors → increase PT/PTT with bleeding

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54
Q

What are 2 conditions that can lead to Primary Fibrinolysis?

A

Prostate cancer: release of urokinase, Cirrhosis: Loss of alpha2 antiplasmin from liver

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55
Q

Which clotting factors are Vitamin K dependent?

A

II, VII, IX, X, C/S

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56
Q

What does Vitamin K deficiency lead to?

A

Bleeding

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57
Q

What is the mechanism of Warfarin?

A

Vitamin K antagonist

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58
Q

What is Erythrocyte Sedimentation Rate increased in?

A

Inflammatory conditions (factors stick together and settle faster)

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59
Q

What are acute phase reactants?

A

Serum proteins from the liver that rise in inflammation or tissue injury

Driven by cytokines

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60
Q

What are 3 examples of acute phase reactants?

A

Ferritin, Plasminogen, C reactive protein (binds bacteria; activates complement)

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61
Q

What forms a thrombus?

A

Fibrin and Activated platelets

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62
Q

What drives platelet production?

A

Thrombopoietin (TPO), produced mostly in liver

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63
Q

What can activate platelets?

A

Endothelial injury (exposure to subendothelial collagen) and stimuli from other activated platelets

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64
Q

What are the 3 steps to form a platelet plug?

A

Adhesion to sub-endothelium, Aggregation: Platelet-platelet binding, Secretion: Release of granule content

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65
Q

Von Willebrand Factor is synthesized by?

A

Endothelial cells and megakaryocytes

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66
Q

Where is Von Willebrand Factor stored?

A

Weibel–Palade bodies in endothelial cells, Alpha granules in platelets, Some found in plasma

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67
Q

When is Von Willebrand Factor released?

A

During vascular injury

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68
Q

What are 3 functions of Von Willebrand Factor?

A

Carrier protein for VIII, Binds platelets to damaged epithelium, Binds activated platelets together (aggregation)

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69
Q

What is the mechanism of platelet adhesion?

A

Vascular damage exposes subendothelial collagen → collagen binds vWF → vWF binds GP1b

70
Q

Platelet Aggregation is mediated by what receptor?

A

GPIIb/IIIa receptor

71
Q

What is the mechanism of Platelet aggregation?

A

Platelet activation → GPIIb/IIIa changes conformation and becomes capable of binding → binds fibrinogen or vWF → links platelets together

72
Q

What activates platelet granules?

A

Platelet binding to collagen and granule contents from other platelets

73
Q

What granules are most abundant in Platelets?

A

Alpha granules- Fibrinogen, vWF, and platelet factor 4

74
Q

What do Dense granules in platelets contain?

A

ADP, Calcium, Serotonin

75
Q

What is the mechanism of Heparin induced thrombocytopenia?

A

Antibodies formed against PF4/heparin complex → platelet activation → diffuse thrombosis + low platelets from consumption

76
Q

What is the serotonin release assay?

A

Screening test for Heparin induced thrombocytopenia (HIT)

Donor platelets radiolabeled with 14C-serotonin → add patient serum and heparin → excessive serotonin release if HIT antibodies present

77
Q

Adenosine Diphosphate (ADP) binds to what 2 receptors?

A

P2Y1 and P2Y12 (GPCR)

78
Q

What happens when ADP binds P2Y1 or P2Y12 receptor?

A

↓ cAMP formation

P2Y1: Calcium release, change in platelet shape; P2Y12: Platelet degranulation, ↑ aggregation

79
Q

Clopidogrel, prasugrel, ticlopidine, and ticagrelor are what type of drugs?

A

P2Y12 receptor blockers

80
Q

What is thromboxane A2?

A

A powerful platelet activator

81
Q

What is the mechanism of Aspirin in platelet activation inhibition?

A

Inhibits COX → ↓ TXA2 → inhibits platelet activation

82
Q

How is thromboxane formed?

A

Lipids in cell membrane → arachidonic acid (AA) via phospholipase A2 in endothelial cells near damaged endothelium → AA released and converted to TXA2 by platelets (COX)

83
Q

What does the bleeding time test?

A

Test of platelet function

Small cut on patient’s arm, filter paper applied until bleeding stops (rarely done in modern era)

84
Q

Arterial thrombosis can present as?

A

Stroke, Myocardial infarction, Ischemic limb

85
Q

What is Virchow’s triad?

A

3 factors that lead to formation of a thrombus: Endothelial damage, Stasis of blood, Hypercoagulability

86
Q

What are Common Hypercoagulable States?

A

Post Op, Fall/Hip Fracture/Trauma, Long plane flight, Malignancy, Decreased activity, surgery, bed rest, Pregnancy, OCP, Elevated homocysteine, Nephrotic syndrome, Smoking

87
Q

Why does OCP cause a Hypercoagulable State?

A

Estrogen increases production of coagulation factors

88
Q

During pregnancy, which clotting factors are increased/decreased?

A

Increased fibrinogen, Decreased protein S

89
Q

What can increase the levels of homocysteine?

A

Folate/B12/B6 deficiency, Homocystinuria (cystathionine beta synthase deficiency)

90
Q

What can lower the levels of homocysteine?

A

Folate

91
Q

Why is Nephrotic syndrome a Hypercoagulable state?

A

Loss of anti-clotting factors in urine (ATIII)

92
Q

What are 4 Inherited Hypercoagulable Conditions?

A

Factor V Leiden, Prothrombin 20210 gene mutation, Protein C deficiency, Antithrombin III deficiency

93
Q

What inhibits Factor V normally?

A

Activated protein C (APC)

94
Q

What is the mechanism of Factor V Leiden Mutation?

A

Abnormal factor V, not inactivated by APC → hypercoagulability

Point mutation in factor V gene → single amino acid change

95
Q

What is Prothrombin 20210 gene mutation?

A

Guanine to adenine change in prothrombin gene

Leads to increased prothrombin levels → hypercoagulable state

96
Q

What are 3 causes of acquired Antithrombin III Deficiency?

A

Impaired production (liver disease), Protein losses (nephrotic syndrome), Consumption (DIC)

97
Q

How does Antithrombin III Deficiency classically present?

A

Heparin resistance

98
Q

What condition is Protein C Deficiency associated with?

A

Warfarin skin necrosis

Thrombosis of the skin tissue (large dark purple skin lesions)

99
Q

What is the mechanism of Antiphospholipid Syndrome?

A

Caused by antiphospholipid antibodies

Occur in association with lupus

100
Q

What are 3 clinical consequences of Antiphospholipid Syndrome?

A

Increased risk of venous and arterial thrombosis, Increased PTT, False positive syphilis (RPR/VDRL)

101
Q

What are the 3 antibodies in Antiphospholipid Syndrome?

A

Anti-cardiolipin, Lupus anticoagulant, Anti-β2 glycoprotein

102
Q

Which antibody in Antiphospholipid Syndrome causes a false positive syphilis test?

A

Anti-cardiolipin

103
Q

Lupus anticoagulant interferes with which coagulation assay?

A

Falsely elevated PTT

Lupus Anticoagulant binds Phospholipid, which is required in coagulation cascade

104
Q

How are antibodies detected in Antiphospholipid Syndrome?

A

Anti-cardiolipin, Anti-β2 glycoprotein: ELISA testing, Lupus anticoagulant: Detected indirectly through coagulation assays

105
Q

What is needed to perform PTT assay?

A

Patient serum, Contact factor i.e. silica, Phospholipid, Ca2+

106
Q

What is a Mixing study?

A

Add patient’s serum with normal serum, measure if PTT remains abnormal or is normalized

107
Q

What is the result of a mixing study in Antiphospholipid Syndrome?

A

Falsely elevated PTT

108
Q

What is Anti-β2 glycoprotein testing?

A

ELISA testing

109
Q

How is Lupus anticoagulant detected?

A

Detected indirectly through coagulation assays

110
Q

What is needed to perform a PTT assay?

A

Patient serum, Contact factor (i.e. silica), Phospholipid, Ca2+

111
Q

What is the result of a mixing study in Antiphospholipid Syndrome?

A

PTT will not correct

112
Q

What is the result of a mixing study in a clotting factor deficiency?

A

PTT corrects to normal

113
Q

What are 2 other tests to detect Lupus Anticoagulant if PTT is normal?

A

Dilute Russell viper venom time, Kaolin clotting time

114
Q

What is the diagnostic criteria for Antiphospholipid Syndrome?

A

One laboratory plus one clinical criteria: Lab criteria: 2 positive results of antibody detection, Clinical: thrombosis, fetal death after 10 weeks, >3 consecutive fetal loss before 10 weeks

115
Q

What is Hypercoagulable Workup?

A

Panel of tests for hypercoagulable states

Controversial because expensive and rarely changes management

116
Q

What tests are included in Hypercoagulable Workup?

A

Antithrombin level, Protein C and S levels, Factor V Leiden gene mutation, Prothrombin gene mutation, Antiphospholipid antibodies, Cancer screening

117
Q

What is Normal PT/PTT? What is INR?

A

PT: ~10s, PTT: ~30s

INR = Patient PT/Control PT

118
Q

What is the common type of bleeding with abnormal platelets?

A

Tends to be more superficial: Mucosal bleeding, skin bleeding, petechiae

119
Q

What is the common type of bleeding with abnormal coagulation factors?

A

Joint bleeding, deep tissue bleeding

120
Q

What is the inheritance pattern of hemophilias?

A

X-linked recessive (mutations can run in family or occur de novo)

121
Q

What factor deficiency is seen in Hemophilia A/B?

A

Hemophilia A: Deficiency of factor VIII, Hemophilia B: Deficiency of factor IX

122
Q

What are 2 common symptoms of Hemophilia?

A

Recurrent joint bleeds, Spontaneous or easy bruising

123
Q

What coagulation assay(s) are abnormal in Hemophilia?

A

Prolonged PTT, PT, bleeding time, platelet count all normal

124
Q

What is the treatment for Hemophilias?

A

Replacement factor VIII and IX, Desmopressin, Aminocaproic acid, Cryoprecipitate

125
Q

What is Cryoprecipitate used as a source of?

A

Fibrinogen

Used in DIC, massive trauma with blood transfusions

126
Q

What are 2 side effects of desmopressin?

A

Flushing, Headache

has vasodilating properties

127
Q

Desmopressin can also be used to treat what 3 conditions besides Hemophilia?

A

Central diabetes insipidus, von Willebrand disease, Bed wetting (decreases urine volume)

128
Q

What are Coagulation Factor Inhibitors?

A

Antibodies that inhibit activity or increase clearance of clotting factors

129
Q

Which Coagulation Factor Inhibitor is most common?

A

Inhibitors of factor VIII most common

130
Q

Coagulation Factor Inhibitors often occur in association with what 3 conditions?

A

Malignancy, Post-partum, Autoimmune disorders

131
Q

What is the clinical presentation of Coagulation Factor Inhibitors?

A

Similar to hemophilia, bleeding + prolonged PTT

132
Q

What is the result of a mixing study in a patient with Coagulation Factor Inhibitors?

A

PTT will still be elevated because the VIII is being inhibited/cleared

133
Q

What are 3 key lab findings in Vitamin K Deficiency?

A

Elevated PT/INR, Elevated PTT (less sensitive), Normal bleeding time

134
Q

What are 4 common causes of Vitamin K Deficiency?

A

Antibiotics, Newborn, Malabsorption, Warfarin

135
Q

Why can Blood Transfusion sometimes cause coagulopathy?

A

Large volume transfusions dilute the clotting factors

Packed RBCs have no plasma/platelet, Saline or IV fluids also have no clotting factors

136
Q

What is the treatment for Blood Transfusion Coagulopathy?

A

Fresh frozen plasma

137
Q

Which clotting factor is not produced in the liver?

A

Factor VIII

138
Q

What coagulation assay findings would you see in liver disease?

A

Increased PT (more sensitive, VII is first to decrease), Increased PTT

139
Q

Where is Thrombopoietin produced?

A

Liver

140
Q

What is the mechanism of Glanzman’s Thrombasthenia?

A

Deficiency IIb/IIIa → no platelet aggregation

141
Q

What is the mechanism of Bernard-Soulier?

A

Deficiency Ib → Platelets cannot bind vWF (no adhesion)

142
Q

What is the mechanism of Wiscott Aldrich?

A

Impaired T cell cytoskeleton function → Immunodeficiency

143
Q

What is the inheritance pattern of Glanzman’s Thrombasthenia?

A

Autosomal recessive

144
Q

What is the inheritance pattern of Bernard-Soulier?

A

Autosomal recessive

145
Q

What is the inheritance pattern of Wiscott Aldrich?

A

X linked

146
Q

What are key diagnostic findings in Glanzman’s Thrombasthenia?

A

Prolonged bleeding time, Blood smear: Isolated platelets (no clumping), Absent platelet aggregation in response to stimuli

147
Q

What are 3 key diagnostic findings in Bernard-Soulier Syndrome?

A

Results in large platelets on blood smear, Prolonged bleeding time, Thrombocytopenia

148
Q

What is the classic triad seen in Wiskott-Aldrich Syndrome?

A

Immune dysfunction, Eczema, decreased platelets

149
Q

What is Idiopathic thrombocytopenic purpura (ITP)?

A

Disorder of decreased platelet survival

Commonly caused by anti-GPIIB/IIIA antibodies → platelet consumption by splenic macrophages

150
Q

How to diagnose Idiopathic thrombocytopenic purpura (ITP)?

A

Diagnosis of exclusion

151
Q

What are 3 treatments for Idiopathic thrombocytopenic purpura (ITP)?

A

Steroids, IVIG, Splenectomy

152
Q

What is Thrombotic thrombocytopenic purpura?

A

Disorder of small vessel thrombus formation which consumes platelets → thrombocytopenia

153
Q

What protein is defective in Thrombotic thrombocytopenic purpura?

A

ADAMTS13: vWF cleaving protease, prevents thrombotic occlusion

154
Q

Where are large multimers of vWF stored?

A

Endothelial Weibel-Palade bodies, Platelet α-granules

released into serum as multimers

155
Q

What is the usual cause of Thrombotic thrombocytopenic purpura?

A

Acquired autoantibody to ADAMTS13

156
Q

What causes Microangiopathic hemolytic anemia (MAHA)?

A

Shearing of RBCs as they pass through thrombi in small vessels

157
Q

What is seen on blood smear in Microangiopathic hemolytic anemia (MAHA)?

A

Schistocytes

158
Q

Microangiopathic hemolytic anemia (MAHA) is seen in what 3 conditions?

A

TTP, DIC, HUS

159
Q

What are the 4 clinical features of Thrombotic thrombocytopenic purpura?

A

Fever, Neurological symptoms: HA, confusion, seizures, Renal failure, Petechiae

160
Q

What are 5 lab findings in Thrombotic thrombocytopenic purpura?

A

Hemolytic anemia, Thrombocytopenia, Schistocytes on blood smear, Normal PT/PTT, May see elevated d-dimer

161
Q

What is the clinical presentation of Hemolytic Uremic Syndrome?

A

MAHA, thrombocytopenia, acute kidney injury

Usually no fever or CNS symptoms

162
Q

Hemolytic Uremic Syndrome is a complication of what infection?

A

E. Coli O157:H7 infection (Shiga-like toxin causes microthrombi)

163
Q

Hemolytic Uremic Syndrome is commonly seen in what age group?

A

Children

164
Q

What is the underlying mechanism in Disseminated Intravascular Coagulation?

A

Widespread activation of clotting cascade, Diffuse thrombi (platelets/fibrin) → ischemia, Destruction of red blood cells → anemia (MAHA), Consumption of clotting factors and platelets

165
Q

What 4 conditions can lead to Disseminated Intravascular Coagulation?

A

Obstetrical emergencies, Sepsis, Leukemia (especially acute promyelocytic leukemia), Rattlesnake bites

166
Q

What are lab findings in Disseminated Intravascular Coagulation?

A

Prolonged PT/PTT, bleeding time, thrombin time, Elevated D-dimer, Anemia (MAHA, schistocytes), Thrombocytopenia, low fibrinogen

167
Q

What is the treatment for Disseminated Intravascular Coagulation?

A

Treat underlying disorder, Fresh frozen plasma, RBCs, platelets, Cryoprecipitate (for low fibrinogen)

168
Q

What are 3 underlying mechanisms of Thrombocytopenia?

A

Decreased production, Platelet sequestration, Platelet destruction

169
Q

What is normal platelet count?

A

150,000-400,000 /ml

170
Q

When does bleeding occur in relation to platelet count?

A

Bleeding occurs when platelet count is <10,000

First Aid (18 decks)

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