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First Aid > Heme/Onc 2 > Flashcards

Heme/Onc 2 Flashcards

1
Q

von Willebrand Factor is synthesized by what 2 cells?

A

endothelial cells and megakaryocytes

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2
Q

What are the 2 roles of von Willebrand Factor in hemostasis?

A
  • Binds platelets to endothelium and other platelets
  • Carrier of factor VIII
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3
Q

How does Von Willebrand Disease present?

A
  • Usually mild, non-life threatening bleeding
  • Easy bruising, skin bleeding
  • Prolonged bleeding from mucosal surfaces → menorrhagia
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4
Q

What are normal/abnormal lab findings present in Von Willebrand Disease?

A
  • Increased PTT and bleeding time
  • Normal PT and normal platelet count
  • No aggregation with Ristocetin cofactor activity assay
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5
Q

What is Ristocetin cofactor activity assay?

A
  • Ristocetin is an antibiotic that binds vWF and glycoprotein GPIb
  • If vWF is present → platelet aggregation
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6
Q

What is the most common inherited bleeding disorder? What is the inheritance pattern?

A
  • Von Willebrand Disease
  • Most cases autosomal dominant
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7
Q

What are 3 treatments for Von Willebrand Disease?

A

vWF concentrate
Desmopressin
Aminocaproic acid

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8
Q

What is the mechanism of Aminocaproic acid?

A

Inhibits plasminogen activation to plasmin (antifibrinolytic)

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9
Q

What is Heyde’s Syndrome? What are 2 features?

A

GI bleeding associated with aortic stenosis

  • Angiodysplasia
  • High shearing force caused by aortic stenosis uncoils vWF multimers → cleaved by ADAMST13 → vWF deficiency
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10
Q

What is the treatment for Heyde’s Syndrome?

A

aortic valve surgery

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11
Q

↓cAMP lead to [increased/decreased] platelet activation

A

increased

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12
Q

Aspirin inhibits the production of [2]

A

Thromboxane A2
Prostaglandins

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13
Q

What are 5 effects of PGE2?

A
  • Redness (Vasodilation)
  • Edema (Increased permeability)
  • Fever (hypothalamus)
  • Pain
  • Afferent Renal vasodilation
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14
Q

What is the effect of PGE2/PGI2?

A

protects the GI mucosa

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15
Q

NSAIDS [reversibly/irreversibly] inhibit COX-1 and COX-2; Aspirin [reversibly/irreversibly] inhibits COX-1 and COX-2

A

reversibly, irreversibly

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16
Q

What is the lifespan of a platelet?

A

7-10 days

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17
Q

Naproxen and Indomethacin are

A

NSAIDs

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18
Q

What are common uses of aspirin?

A
  • Reduce inflammation, pain, fever
  • Coronary disease: Acute MI, secondary prevention
  • Stroke: acute ischemic stroke, secondary prevention
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19
Q

What are 4 possible adverse effects of Aspirin?

A
  • Bleeding
  • Gastritis/Ulcers
  • Tinnitus: caused by salicylate
  • Reye’s syndrome: liver failure and encephalopathy in with aspirin use in children
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20
Q

Aspirin is given to children in what rare condition?

A

Kawasaki

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21
Q

What are 2 drugs classified as Thienopyridines?

A

Clopidogrel, Prasugrel

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22
Q

What is the mechanism of Thienopyridines (Clopidogrel, prasugrel)?

A

Irreversible P2Y12 receptor blockers

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23
Q

What are 2 side effects of Thienopyridines?

A
  • Bleeding
  • Thrombotic Thrombocytopenic Purpura (rare)
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24
Q

What is the mechanism of Ticagrelor? What is a unique side effect?

A
  • Reversible P2Y12 receptor blocker (inhibits platelet activation)
  • Dyspnea
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25
Q

What is the mechanism of Dipyridamole? Indications (2)?

A
  • PDE III inhibitor and blocks adenosine uptake by cells
  • Indication: stroke prevention with aspirin, chemical cardiac stress testing
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26
Q

Adenosine is a [vasoconstrictor/vasodilator]

A

Vasodilator

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27
Q

What is the mechanism of Cilostazol? Indication?

A
  • PDE III inhibitor (raises cAMP in platelets and vascular smooth muscle)
  • Indication: peripheral arterial disease (rarely used for anti-platelet effects)
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28
Q

What are 3 side effects of PDE inhibitors?

A
  • Flushing
  • Headache
  • Hypotension

*due to vasodilation

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29
Q

What is the mechanism of Abciximab, eptifibatide, tirofiban? Indication?

A
  • IIB/IIIA receptors blockers → prevent aggregation
  • Abciximab: Fab fragment
  • IV drugs used in acute coronary syndromes/stenting
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30
Q

What is a side effect of IIB/IIIA receptors blockers? Name 3 of the drugs

A

Thrombocytopenia (must monitor platelet count after administration)

Abciximab, Tirofiban, Eptifibatide

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31
Q

What are 2 components that form a thrombus?

A

fibrin and activated platelets

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32
Q

Heparin is found naturally in what type of cells?

A

mast cells

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33
Q

Heparin is used in what two forms?

A
  • Unfractionated: widely varying polymer chain lengths
  • Low molecular weight: smaller polymers only
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34
Q

What is the mechanism of Unfractionated Heparin?

A

Activates Antithrombin III

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35
Q

Antithrombin III inhibits what 5 coagulation factors?

A

XII, XI, IX, Xa, and Thrombin

*12, 11, 9, 10a

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36
Q

Heparin will increase which coagulation assays?

A
  • Increases PTT and Thrombin time
  • Can increase PT at high dosages
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37
Q

Dosing of Unfractionated Heparin

A

Response is highly variable from patient to patient due to binding to plasma proteins and cells
- Dose must be adjusted

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38
Q

What is the mechanism of Protamine? What is it used for?

A
  • Binds heparin → neutralizes drug
  • Reversal agent for heparin overdose (most effective against unfractionated heparin) i.e. in cardiac surgery
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39
Q

Why is protamine used in cardiac surgery?

A

High dose heparin is administered for heart-lung bypass → quick reversal at completion of case

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40
Q

What are 2 uses for Unfractionated Heparin?

A
  • Acute management: DVT/PE, MI, Stroke
  • Prophylaxis for DVT in hospitalized patients
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41
Q

What are 3 side effects of Unfractionated Heparin?

A
  • Mainly bleeding and thrombocytopenia
  • Osteoporosis (long term use)
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42
Q

Direct suppressive effect of platelet production with heparin is called

A

“Non-immune” thrombocytopenia

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43
Q

Heparin-induced thrombocytopenia (HIT) is what type of hypersensitivity reaction?

A

Type II

(Immune complexes bind platelet factor 4-heparin)

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44
Q

What is the mechanism of Heparin-induced thrombocytopenia (HIT)?

A

IgG-Hep-PF4 Complexes → bind to platelet surface → 1) removal by splenic macrophage 2) Platelet aggregation/activation

*lead to diffuse arterial/venous thrombosis and thrombocytopenia

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45
Q

When does Heparin-induced thrombocytopenia (HIT) occur?

A

5-10 days after heparin exposure

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46
Q

How to definitively diagnose Heparin-induced thrombocytopenia?

A

HIT antibody testing

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47
Q

What is the mechanism of Enoxaparin?

A

Activates ATIII to a less degree → only inhibits Xa

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48
Q

Dosing of Low Molecular Weight Heparin

A

Dosed based on weight (reduced plasma proteins and cells)
- Usually no monitoring required

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49
Q

What are 2 benefits to using Low Molecular Weight Heparin vs UF Heparin?

A
  • Do not need to adjust dose or monitor PTT
  • Lower incidence of HIT
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50
Q

Unlike UF heparin, LMWH only effects _____. How does this affect coagulation assays?

A
  • Factor X
  • Thrombin test will not change
  • PTT is NOT sensitive to LMWH
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51
Q

Low Molecular Weight Heparin use should be monitored in what 2 conditions? What test is used?

A
  • Obesity, Renal failure
  • Anti Xa level test
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52
Q

How is Anti Xa Level measured? What is it used for?

A
  • Pt sample is added to Xa substrate + cromophore (illuminates when Xa substrate is split)
  • High Xa activity = high illumination
  • Used to monitor LMWH effect in patients with obesity or renal failure
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53
Q

What is the mechanism of Rivaroxaban and Apixaban?

A

Factor Xa inhibitors

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54
Q

Rivaroxaban and Apixaban are used in

A
  • Used in A Fib as alternatives to warfarin (do not require monitoring)
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55
Q

What are the effects of Rivaroxaban and Apixaban on PT and PTT?

A

Increase (Xa in both pathways)

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56
Q

What is the mechanism of Lepirudin, Bivalirudin, and Desirudin?

A

Direct Thrombin Inhibitors

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57
Q

What is the mechanism of Argatroban?

A

Direct Thrombin Inhibitor

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58
Q

What is the mechanism of Dabigatran?

A

Direct Thrombin Inhibitor

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59
Q

How do Direct Thrombin Inhibitors affect coagulation assays?

A
  • Prolong PT, PTT, and thrombin time
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60
Q

Which 2 Anticoagulants prolong thrombin time?

A

Direct Thrombin Inhibitors
UF Heparin

(inhibit thrombin function)

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61
Q

Patients with HIT should be initiated on which drug?

A

Direct Thrombin Inhibitors

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62
Q

Bivalirudin is used in

A

Acute coronary syndromes

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63
Q

Dabigatran is used to treat

A
  • A fib, as an alternative to warfarin
  • does not require monitoring
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64
Q

What is the mechanism of Warfarin?

A

Inhibits Vitamin K epoxide reductase → ↓ vitamin K dependent factors (II, VII, IX, X)

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65
Q

What is the role of Vitamin K in activating clotting factors?

A

Forms γ-carboxyglutamate(Gla) residues in the clotting factors

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66
Q

What are the 2 forms of vitamin K? Where are they found?

A

K1: found in green leafy vegetables
K2: synthesized by GI bacteria

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67
Q

Why does Warfarin take days to achieve its effect?

A

Inhibits formation of clotting factors, no effect on already circulating clotting factors

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68
Q

[PT/PTT] is more sensitive to the effects of Warfarin

A

PT (extrinsic pathway)

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69
Q

Dosing of Warfarin? Why?

A
  • Dose monitored and adjusted to reach target PT/INR
  • Drug effect varies with amount of Vitamin K in the body
70
Q

Which coagulation factor is the first to fall with Warfarin use? Why?

A

Factor VII (shortest half life)

71
Q

Thrombin time with Warfarin use?

A

Normal

72
Q

What is the underlying mechanism of the prothrombotic effects of Warfarin?

A
  • Warfarin also inhibits production of Vitamin K dependent Protein C (anti-clotting factor with short half life)
  • Initial Warfarin Rx → Protein C deficient
73
Q

Warfarin is often started without heparin in what condition?

A

A Fib

74
Q

What are adverse effects of Warfarin?

A
  • Crosses placenta → fetal warfarin syndrome
  • Bleeding
  • Skin necrosis
75
Q

[Unfractionated heparin/Warfarin] is often used in pregnancy. Why?

A

UF heparin, does not cross placenta

76
Q

Who is at risk for Warfarin Skin Necrosis? What symptoms does this cause?

A
  • Patients with protein C deficiency
  • Thrombosis of skin tissues → large purple skin lesions
77
Q

What are 3 uses for Warfarin?

A
  • Stroke prevention atrial fibrillation
  • Mechanical heart valves
  • DVT/PE
78
Q

What is a downside of Warfarin use?

A

requires INR checks (monthly blood draw)

79
Q

What are Novel Oral Anticoagulants? Examples?

A
  • Alternative to Warfarin

Factor Xa inhibitors: Rivaroxaban, Apixaban
Direct Thrombin inhibitors: Dabigatran

80
Q

What is the upside to using Novel Oral Anticoagulants vs Warfarin? Downside?

A
  • No INR checks, consistent dose
  • Expensive, no reversal agent (except for Dabigatran)
81
Q

What is the reversal agent for Dabigatran?

A

Idarucizumab

82
Q

What are 3 thrombolytics drugs? What is a side effect?

A
  • tPA, Urokinase, Streptokinase
  • MAJOR bleeding risk
83
Q

What are the reversal agent for Anticoagulants?

A

Fresh frozen plasma: corrects deficiencies of any clotting factor

84
Q

What are 2 reversal agents for Warfarin? When are they used?

A
  • Fresh frozen plasma (used with severe bleeding + ↑INR)
  • Vitamin K (used with ↑ INR in absence of serious bleeding)
85
Q

What is the target INR for most patients on Warfarin?

A

3-Feb

86
Q

Increasing INR levels and Warfarin use

A

INR 3-5: Hold warfarin
INR 5-9: Hold warfarin, Oral vitamin K
INR >9: Consider IV vitamin K, FFP

87
Q

Normocytic anemia may result from what 2 mechanisms?

A

Non-hemolytic (low production)
Hemolytic (increased destruction)

88
Q

What are 3 extrinsic causes of Hemolysis?

A
  • Antibodies
  • Mechanical trauma (narrow vessels)
  • RBC infection
89
Q

What are intrinsic causes of Hemolysis? What are examples?

A

Failure of membrane, hemoglobin, or enzymes
- Membrane: Hereditary spherocytosis
- Enzyme: G6PD deficiency
- Hemoglobin: Sickle cell anemia (Abnormal Hgb)

90
Q

What are 6 hallmarks of Hemolysis?

A
  • Normocytic anemia
  • Elevated plasma LDH (Converts pyruvate to lactate, spills out of RBC)
  • Increased reticulocyte count (hemolysis → increase EPO → increase reticulocyte)
  • Elevated indirect bilirubin → jaundice
  • Increased risk of pigment stones
  • Decreased Haptoglobin (lower in intravascular)
  • Urine Hgb and hemosiderin (intravascular)
91
Q

What is a key blood test in normocytic anemias? What does this differentiate?

A

Corrected Reticulocyte Count (corrected for degree of anemia)
- Low: underproduction
- High: increased destruction (hemolysis)

92
Q

How do you calculate the Corrected Reticulocyte Count? What does <2% mean?

A

<2% = inadequate bone marrow response, underproduction

reticulocyte % × (patient Hct/normal Hct)

93
Q

What is the purpose of Reticulocyte Production Index (RPI)? How to calculate?

A

Corrects longer life of reticulocytes

94
Q

What does a low corrected reticulocyte count indicate?

A

Underproduction of reticulocytes.

95
Q

What does a high corrected reticulocyte count indicate?

A

Increased destruction (hemolysis) of red blood cells.

96
Q

How do you calculate the Corrected Reticulocyte Count?

A

Reticulocyte % × (patient Hct/normal Hct).

97
Q

What does a corrected reticulocyte count of <2% mean?

A

<2% indicates inadequate bone marrow response, underproduction.

98
Q

What is the purpose of the Reticulocyte Production Index (RPI)?

A

It corrects for the longer life of reticulocytes in anemia.

99
Q

What does an RPI of <2% suggest?

A

<2% suggests bone marrow failure.

100
Q

Where does extravascular hemolysis occur?

A

In the liver and spleen.

101
Q

What type of anemia is caused by increased hemolysis?

A

Normocytic anemia.

102
Q

What are the Cords of Billroth?

A

Vascular channels in the spleen that end blindly, where old/damaged RBCs are phagocytosed.

103
Q

What is a main cause of intravascular hemolysis?

A

Narrowed vessels leading to mechanical trauma, such as thrombus in small vessels.

104
Q

What is haptoglobin and how does its level change with hemolysis?

A

Haptoglobin is a plasma protein that binds free hemoglobin and is removed by the liver. Its levels decrease with hemolysis.

105
Q

What are haptoglobin levels in intravascular vs extravascular hemolysis?

A

Intravascular: low or indetectable; Extravascular: low or normal.

106
Q

What organ produces haptoglobin?

A

The liver.

107
Q

What is haptoglobin classified as?

A

An acute phase reactant that increases with inflammation.

108
Q

What are three urine findings seen in hemolysis?

A

No bilirubin, hemoglobinuria when haptoglobin is saturated, and hemosiderinuria.

109
Q

What can cause urine to turn red/brown?

A

Hemolysis (Hgb) and rhabdomyolysis (myoglobin).

110
Q

What does a urine dipstick with no red cells plus + Hgb suggest?

A

Hemolysis or rhabdomyolysis.

111
Q

What type of cells does Parvovirus B19 replicate in?

A

RBC progenitor cells.

112
Q

What does Parvovirus B19 infection lead to in patients with chronic hemolysis?

A

Severe anemia (‘Aplastic crisis’).

113
Q

What are two reasons for back/abdominal pain in some hemolytic disorders?

A

Splenomegaly and decreased nitric oxide leading to smooth muscle spasm.

114
Q

What are two hemolytic disorders that commonly present with back/abdominal pain?

A

G6PD deficiency and paroxysmal nocturnal hemoglobinuria (PNH).

115
Q

What is Autoimmune Hemolytic Anemia?

A

RBC destruction from autoantibodies, resulting in extravascular hemolysis.

116
Q

What are the two types of Autoimmune Hemolytic Anemia?

A

Warm and Cold; warm is more common.

117
Q

What characterizes Warm Autoimmune Hemolytic Anemia?

A

IgG antibodies against RBC surface antigens that bind at body temperature (37C).

118
Q

What symptoms are seen in Warm Autoimmune Hemolytic Anemia?

A

Anemia, jaundice, splenomegaly, pallor, fatigue, tachycardia, dyspnea.

119
Q

What are two diagnostic findings of Warm AIHA?

A

Spherocytes on blood smear and positive Direct Antiglobulin Test (DAT).

120
Q

How is a direct Coombs test performed?

A

Patient RBCs plus anti-IgG antiserum; positive if agglutination occurs.

121
Q

What does the Indirect Antiglobulin Test/Indirect Coombs test for?

A

It tests for antibodies in the patient’s serum.

122
Q

What does the Direct/Indirect Coombs test test for?

A

Direct tests for antibodies bound to RBC; Indirect tests for antibodies in the serum.

123
Q

Which Coombs test is commonly used in hemolytic anemia?

A

Direct Coombs test.

124
Q

What conditions is Warm AIHA associated with?

A

Lupus, Non-Hodgkin lymphoma, Chronic lymphocytic leukemia (CLL), Methyldopa use.

125
Q

What is the mechanism of action of Methyldopa?

A

CNS α2 receptor agonist; antihypertensive drug of choice in pregnancy.

126
Q

Why is Methyldopa associated with Warm Autoimmune Hemolytic Anemia?

A

It triggers production of RBC antibodies and may alter Rh antigen on red cells.

127
Q

What adverse effect can high doses of penicillin lead to?

A

Hemolytic anemia.

128
Q

What is the underlying mechanism of hemolytic anemia with high dose penicillin use?

A

Penicillin binds to RBC, forming a haptan that elicits an immune response.

129
Q

What are two drugs that can lead to a positive direct Coombs test?

A

Penicillin and Methyldopa.

130
Q

What are three treatments for Warm Autoimmune Hemolytic Anemia?

A

Glucocorticoids, immunosuppressants, splenectomy.

131
Q

What is Cold Autoimmune Hemolytic Anemia?

A

Large IgM antibodies bind at <30C, leading to complement fixation and RBC agglutination.

132
Q

Where does Cold Autoimmune Hemolytic Anemia occur in the body?

A

In limbs, fingertips, toes, nose, and ears.

133
Q

What unique symptoms are seen in Cold Autoimmune Hemolytic Anemia?

A

Purple discoloration and pain in fingers/toes, symptoms associated with cold exposure.

134
Q

What protein is Cold Autoimmune Hemolytic Anemia Direct Coombs positive for?

A

C3, because IgM is lost in warm central organs.

135
Q

What antibodies are added in Direct Coombs for Cold Autoimmune Hemolytic Anemia?

A

Anti-C3.

136
Q

What type of hemolysis does Cold Autoimmune Hemolytic Anemia cause?

A

Extravascular hemolysis.

137
Q

Why does Cold Autoimmune Hemolytic Anemia rarely cause intravascular hemolysis?

A

RBC has complement inhibitory molecules (CD55/CD59).

138
Q

What conditions is Cold Autoimmune Hemolytic Anemia associated with?

A

Chronic lymphocytic leukemia (CLL), Mycoplasma pneumonia, Epstein-Barr virus.

139
Q

What is the treatment for Cold Autoimmune Hemolytic Anemia?

A

Avoid the cold and immunosuppressants.

140
Q

What causes Microangiopathic hemolytic anemia?

A

Thrombi in microvasculature cause narrowing and shearing of RBCs.

141
Q

What is a characteristic finding of Microangiopathic hemolytic anemia on blood smear?

A

Schistocytes.

142
Q

What conditions is Microangiopathic hemolytic anemia seen in?

A

TTP, HUS, DIC, Malignant Hypertension.

143
Q

What is Mechanical hemolysis?

A

Shear forces destroy RBCs in large blood vessels.

144
Q

What conditions is Mechanical hemolysis seen in?

A

Aortic stenosis, mechanical heart valves, left ventricular assist devices.

145
Q

What are two classic infectious agents that cause Red Blood Cell Infections?

A

Malaria and Babesia.

146
Q

What is Paroxysmal Nocturnal Hemoglobinuria?

A

RBC destruction via the complement system due to a genetic mutation.

147
Q

What is the mechanism of disease in Paroxysmal Nocturnal Hemoglobinuria?

A

Loss of GPI anchor leads to loss of DAF/CD55 and CD59 on RBC membranes.

148
Q

What type of hemolysis does Paroxysmal Nocturnal Hemoglobinuria predominantly cause?

A

Intravascular hemolysis.

149
Q

What is the clinical presentation of Paroxysmal Nocturnal Hemoglobinuria?

A

Sudden hemolysis at night, fatigue, dyspnea, abdominal pain, thrombosis.

150
Q

What deficiency is common in Paroxysmal Nocturnal Hemoglobinuria?

A

Iron deficiency.

151
Q

What is the leading cause of death in Paroxysmal Nocturnal Hemoglobinuria?

A

Thrombosis.

152
Q

What diagnostic test confirms Paroxysmal Nocturnal Hemoglobinuria?

A

Flow cytometry.

153
Q

What are four lab findings seen in Paroxysmal Nocturnal Hemoglobinuria?

A

Elevated LDH, low haptoglobin, hemoglobinuria/hemosiderinuria, negative direct Coombs test.

154
Q

What is the mechanism of Eculizumab?

A

It binds complement component C5, blocking formation of the membrane attack complex.

155
Q

What type of hemolysis does Eculizumab protect against?

A

Intravascular hemolysis.

156
Q

What are the results of treating Paroxysmal Nocturnal Hemoglobinuria with Eculizumab?

A

Stable Hgb levels and fewer transfusions.

157
Q

What cells are most affected by Pyruvate Kinase Deficiency?

A

RBCs, as they require PK for anabolic metabolism.

158
Q

What does membrane failure with RBC commonly lead to?

A

Phagocytosis in the spleen.

159
Q

What is the inheritance pattern of Pyruvate Kinase Deficiency?

A

Autosomal recessive.

160
Q

When does Pyruvate Kinase Deficiency usually present?

A

In newborns.

161
Q

What type of hemolysis does Pyruvate Kinase Deficiency cause?

A

Extravascular hemolysis.

162
Q

What physical finding is commonly associated with Pyruvate Kinase Deficiency?

A

Splenomegaly.

163
Q

What is Glucose-6-Phosphate Dehydrogenase’s role?

A

It is a key enzyme in the HMP shunt.

164
Q

What is the HMP shunt necessary for?

A

The generation of NADPH.

165
Q

What does NADPH protect RBCs from?

A

Oxidative stress.

166
Q

What is the inheritance pattern of G6PD Deficiency?

A

X-linked recessive.

167
Q

What does G6PD Deficiency present with?

A

Recurrent hemolysis after exposure to triggers.

168
Q

What type of hemolysis is seen in G6PD Deficiency?

A

Mostly extravascular, with some intravascular.

169
Q

What are three triggers for G6PD Deficiency?

A

Infection, fava beans, and certain drugs.

170
Q

Where is G6PD deficiency highly prevalent?

A

Africa and the Mediterranean.

171
Q

What are two classic findings on blood smear in G6PD deficiency?

A

Heinz bodies and bite cells.

First Aid (18 decks)

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