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Pharmacology > Pharmacology for Hematology > Flashcards

Pharmacology for Hematology Flashcards

1
Q

how does erythropoietin affect RBC values?

A

anemia is caused by low RBC production, causing low oxygen capacity of the blood and decreased tissue oxygenation, this sends a signal to the kidneys causing the kidneys to increase secretion of EPO which stimulates production of RBCs

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2
Q

what is required for RBC production?

A

Iron, B12, Folic acid and Heme

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3
Q

where does Heme iron come from?

A

diet and meat, has a 30-40% absorption

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4
Q

where does non Heme iron come from?

A

vegetarian diet, lentils, 10% absorption

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5
Q

where is iron absorbed?

A

duodenum and proximal jejunum

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6
Q

what is iron absorption regulated by?

A

hepcidin made by liver

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7
Q

how is iron replaced?

A

oral (preferred), IV

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8
Q

who needs IV iron?

A

intolerance to oral products, malabsorption due to IBD or gastric bypass, nonadherence, refusal for blood transfusions

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9
Q

how do you increase iron absorption when takin iron PO?

A

take on empty stomach and with vitamin C

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10
Q

what are some examples of oral iron preparations?

A

ferrous fumarate, ferrous gluconate, ferrous sulfate

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11
Q

what drugs decrease iron absorption?

A

aluminum, magnesium and calcium containing antacids, tetracycline and doxycycline, histamine 2 antagonists, PPI, cholestyramine

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12
Q

when should iron PO be taken?

A

1-2 hours separate from other medications

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13
Q

question about

A

IV iron

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14
Q

question about

A

iv iron

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15
Q

question about iv iron

A

q

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16
Q

question about

A

iv iron

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17
Q

what are adverse reactions associated with PO iron?

A

constipation, tarry stool, nausea, epigastric pain, cramps, diarrhea

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18
Q

what are adverse reactions associated with IV iron?

A

infusion reactions, arthralgia, myalgia, fever, costly

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19
Q

when do you follow up for PO iron and what labs do you get?

A

2 weeks, CBC and reticulocyte count, assess tolerance

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20
Q

when do you follow up for IV iron and what labs do you get?

A

4-8 weeks, CBC, reticulocyte count and iron panel

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21
Q

what are the different colorectal screening guidelines for different organizations?

A

USPSTF: (B) 45, (A) 50
ACG: 45
ACS: (B) 45, (A) 50
ACP/AAFP: 50
discontinue at 75 unless greater than 10 year life expectancy

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22
Q

describe acute iron posioning

A

most commonly an accidental overdose by young children, direct caustic injury to GI mucosa, cellular toxin impairing metabolism

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23
Q

how do you treat acute iron poisoning?

A

whole bowel irrigation NOT activated charcoal, IV iron chelating agents, supportive therapy

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24
Q

describe stage 1 of iron toxicity

A

30 mins - 6 hours
local toxicity, n/v, diarrhea, abdominal pain, GI bleeding

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25
Q

describe stage 2 of iron toxicity

A

6 - 24 hours
latent toxicity, resolution of local toxicity with ongoing cellular toxicity, hypovolemia, poor tissue perfusion, metabolic acidosis and high lactate

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26
Q

describe stage 3 of iron toxicity

A

12- 24 hours
systemic toxicity, shock, acidosis, coagulopathy, coma, multisystem failure

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27
Q

describe stage 4 of iron toxicity

A

2-3 days
hepatic failure

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28
Q

describe stage 5 of iron toxicity

A

3-6 weeks
long term sequelae, gastric outlet obstruction, small bowel obstruction, CNS sequelae

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29
Q

what can cause megaloblastic anemia?

A

vitamin B12, folate or copper deficiency, medications that interfere with DNA synthesis

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30
Q

what are the symptoms of macrocytic anemias?

A

decreased WBC, glossitis, neurocognitive changes with B12 deficiency, neural tube defects with folate deficiency during embryogenesis

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31
Q

describe pernicious anemia

A

auto antibodies against parietal cells that make intrinsic factors causing B12 to not be able to be absorbed

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32
Q

how do you treat vitamin B12 deficiency?

A

supplement - 1000 mcg daily or 2000 if impaired absorption
IM - 1000 mcg weekly for 4 weeks and then monthly

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33
Q

how do you treat folate deficiency?

A

0.2 mg PO is recommended daily for all people, 1-5 mg for deficiency and 0.4 mg for pregnancy, IV

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34
Q

what is important to note in concomitant B12 and folate deficiency?

A

folate supplementation may reverse hematological abnormalities but will not correct or stop neurological manifestations of B12 deficiency

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35
Q

what medications can interfere with folate metabolism?

A

methotrexate, antibiotics (trimethoprim, pyrimethamine), antiseizure agents (phenytoin, valproate, carbamezepine)

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36
Q

when should erythropoietin stimulating agents be considered?

A

when hemoglobin is <10gm/dL, use smallest dose to prevent repeat RBC transfusions

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37
Q

what are erythropoietin stimulating agents contraindicated in?

A

patients with active or recent malignancy due to risk of progression and recurrence

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38
Q

why is there an FDA black box warning for erythropoietin stimulating agents?

A

chronic kidney disease patients experienced greater risks for death, serious adverse cardiovascular reactions and stroke when administered to target a hemoglobin level of greater than 11

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39
Q

describe erythropoietin stimulating agents

A

all are subq
epoetin alfa (epogen, procrit)
epoetin alfa-epbx (retacrit)
darbepoetin alfa (aranesp)
methoxy PEG - epoetin beta (mircera)
dosed 3 times weekly to monthly depending on medication

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40
Q

what is hemostasis?

A

the process of blood clot formation at the site of vessel injury, must be quick, localized and carefully regulated

41
Q

describe primary hemostasis

A

injury leads to platelet adhesion, activation and aggregation, ending with platelet plug

42
Q

what diseases affect primary hemostasis?

A

affects platelets, TIP, TTP, HUS, DIC

43
Q

what stimulates further platelet aggregation?

A

ADP

44
Q

describe secondary hemostasis

A

clotting factors leading to fibrin formation which strengthens platelet plug, coagulation cascade affects extrinsic or intrinsic pathway

45
Q

what diseases affect secondary hemostasis?

A

affects clotting, hemophilia, DIC

46
Q

what happens during thrombosis?

A

high coagulation, high platelets or low fibrinolysis

47
Q

what happens during hemorrhage?

A

low coagulation, low platelets or high fibrinolysis

48
Q

what is the mechanism of arterial thrombosis?

A

typically from endothelial cell injury, causes include vasculitis, rapture of atherosclerotic plaque and trauma, occurs under high flow conditions, platelet adhesion and aggregation, prior activation of coagulation cascade due to platelet activation

49
Q

where does arterial thrombosis usually occur?

A

coronary arteries, cerebral arteries, aorta, left heart chamber, firmly adherent to vessel wall, mostly found in areas with turbulent flow such as bifurcation of arteries

50
Q

what is the composition of arterial thrombosis?

A

platelets > fibrin

51
Q

how do you treat arterial thrombosis?

A

antiplatelets such as aspirin

52
Q

what is the mechanism of venous thrombosis?

A

typically from a combination of factors from Virchow’s triad, occurs under low flow, generates thrombin, prior activation of platelet activation due to coagulation cascade

53
Q

where does venous thrombosis usually occur?

A

venous sinusoids, valves in vein, superficial venous, deep venous, attached loosely, easy to embolize

54
Q

what is the composition of venous thrombosis?

A

fibrin > platelets

55
Q

how do you treat venous thrombosis?

A

anticoagulants such as heparin

56
Q

when do we use antiplatelets?

A

arterial thromboses, peripheral arterial disease, acute coronary syndromes, ischemic stroke, TIA, stable ischemic heart disease

57
Q

when do we use anticoagulants?

A

venous thromboembolism, DVT, DVT prophylaxis, A-fib and PE

58
Q

when do we use fibrinolytics?

A

select patients with venous thromboembolism, stroke, acute myocardial infarction, acute ischemic stroke, massive PE

59
Q

what are the 3 types of antiplatelet drugs?

A

aspirin (dipyridamole + asa/persantine)

P2Y12 inhibitors (clopidogrel/plavix, prasugrel/effient, ticagrelor/brillanta, cangrelor/kengreal (IV))

GP IIb/IIIa inhibitors (eptifibatide/integrilin, tirofiban/aggrasata)

60
Q

what are the indications, MOA and side effects of aspirin?

A

indications: in all spectrums of acute coronary syndromes, secondary prevention for atherosclerotic cardiovascular disease or stroke

MOA: irreversibly binds to COX1 enzyme on platelets ultimately preventing the conversion of arachidonic acid into thromboxane A1 which is responsible for platelet activation and vasoconstriction

Side effects: GI upset, bleeding

61
Q

what are the indications, MOA and side effects of clopidogrel/plavix?

A

Indications: acute coronary syndrome w or w/o percutaneous coronary intervention, recent MI or stroke, peripheral arterial disease

MOA: thienopyridine class, reduces platelet aggregation bu irreversibly blocking the ADP P2Y12 receptor on platelets

Side effects: bleeding, hypersensitivity reaction and morbilliform rash

62
Q

what are the indications, MOA and side effects of prasugrel/effient?

A

indications: acute coronary syndrome w percutaneous coronary intervention

MOA: thienopyridine class, reduces platelet aggregation bu irreversibly blocking the ADP P2Y12 receptor on platelets

Side effects: bleeding

63
Q

what are the indications, MOA and side effects of ticagrelor/brillinta?

A

indications: acute coronary syndrome w or w/o percutaneous coronary intervention, recent MI

MOA: cyclopentyltriazolopyrimidine class, reduces platelet aggregation by reversible binding of the ADP P2Y12 receptor on platelets

Side effects: bleeding, dyspnea, elevated serum creatine and uric acid

64
Q

what are the indications, MOA and side effects of cangrelor/kengreal?

A

MOA: ATP analogue, reduces platelet aggregation by binding selectively and reversibly to P2Y12 receptor

Side effects: bleeding

65
Q

what are the indications, MOA and side effects of Glycoprotein IIb/IIIa inhibitors?

A

Indications: used in certain situations, acute coronary syndrome cath lab, high risk patients (complex lesions, large thrombi hemodynamicallY0

MOA: monoclonal antibodies that bind to glycoprotein IIb/IIIa receptor, blocking the fibrinogen to the receptor preventing the final step of platelet aggregation

Side effects: bleeding, hypotension, bradycardia, thrombocytopenia

66
Q

what causes venous thrombosis?

A

caused by hypercoagulable states which increase the chances of inducing the coagulation cascade

acquired: surgery, trauma, cancer, pregnancy, fracture, immobilization, meds

genetic: factor V leiden, prothrombin gene mutation, protein C or S deficiency, antithrombin III deficiency

67
Q

what is included in Virchow’s triad?

A

hypercoagulability state, vascular wall injury and circulatory stasis

68
Q

what factors does warfarin affect?

A

9a, 10a, 12a and 2a

69
Q

what factors does heparin affect?

A

10a and 2 a

70
Q

what factor does dabigatran affect?

A

2a

71
Q

what factor does apixaban, edoxaban and rivaroxaban affect?

A

10a

72
Q

what does heparin do?

A

brings anti-thrombin (10a) to thrombin, prevents future clots but does not take care of current clot

73
Q

what are the indications, monitoring and side effects of unfractionated heparin?

A

indications: acute inpatient treatment of PE, MI, and acute coronary syndrome

Monitoring: aPTT it anti-factor 10a activity (should be measured at 6 hours, quick elimination)

Side effects: bleeding, heparin induced thrombocytopenia

74
Q

what is the reversal agent for heparin?

A

protamine sulfate

75
Q

describe HIT

A

diagnosed with pre-test probability: thrombocytopenia, timing, thrombosis and other causes of low platelets, HIT antibody assay, if pre-test is high treat empirically, if low wait and watch

treated by stopping heparin, anticoagulant with direct thrombin inhibitors (argatroban, fondaparinux, DOAC) for 3 months or longer

76
Q

what are the indications, monitoring and black box warning for lmw heparin/enoxaprin/lovenox?

A

indications: treatment and prophy for DVT, PE, anticoagulation during pregnancy, bridging for procedures, occasionally MI/acute coronary syndrome

monitoring: none, aPTT is unreliable

black box warning: epidural or spinal hematoma may occur in patients who are anticoagulated with lmw heparin AND are receiving neuraxial anesthesia or undergoing spinal puncture

77
Q

what are the advantages of low molecular weight heparin?

A

better bioavailability, no heparin resistance, can be used outpatient, less dosing frequency, fixed dose without monitoring, lower risk of HIT

78
Q

what are the disadvantages of low molecular weight heparin?

A

slow onset, longer duration of action, less reversible with protamine, longer half life in patients with chronic kidney disease, unreliable monitoring

79
Q

what are the indications, monitoring and black box warning for fondaparinux/arixtra?

A

indications: DVT, PE, thromboprophylaxis, acute coronary syndrome, HIT

no monitoring or reversal agent

black box warning: spinal hematoma

80
Q

what are the indications, MOA and monitoring of warfarin/coumadin?

A

indications: DVT, PE, thromboprophylaxis in A-fib, prosthetic valves, preferred anticoagulant in antiphospholipid antibody syndrome

MOA: Vitamin K antagonist, Inhibits the synthesis of Vitamin K dependent factors II, VII, IX, and X AND endogenous anticoagulant proteins C and S

Monitoring: PT and INR (2-3), check 72 hours after starting

81
Q

what is the reversal agent and pregnancy category for warfarin/coumadin?

A

reversal agent: Vitamin K, PCC and FFP

pregnancy category x: crosses placenta and can cause a hemorrhagic disorder, and serious birth defects characterized by abnormal bone formation

82
Q

warfarin

A

question

83
Q

warfarin

A

question

84
Q

warfrain

A

question

85
Q

what are the 2 types of DOACs?

A

direct thrombin inhibitors and factor 10a inhibitors

86
Q

what are examples of direct thrombin inhibitors?

A

dabigatran/pradaxa, bivaliruden (IV), argatroban (IV)

87
Q

what are examples of factor 10a inhibitors?

A

rivaroxaban/xarelto, apixaban/eliquis, edoxaban/savaysa

88
Q

what is the MOA of direct thrombin inhibitors?

A

bind directly to circulating and clot bound thrombin resulting in inhibition of cleaving fibrinogen (II) to fibrin (IIa)

89
Q

what are the indications for bivaliruden/angiomax?

A

percutaneous coronary intervention and HIT

90
Q

what are the indications for argatroban/argatra?

A

percutaneous coronary intervention and HIT

91
Q

what are the indications, reversal agents and side effects of dabigatran/pradaxa?

A

indications: VTE primary prophylaxis in post surgical patients, treatment and secondary prevention of VTE, stroke prevention in atrial fibrillation (AF)

reversal agent: idarucizumab/praxbind

side effects: dyspepsia, comparable bleeding risk to heparin

92
Q

what are the indications, MOA and reversal agents of direct 10a inhibitors?

A

indications: VTE primary prophylaxis in post surgical patients, treatment and secondary prevention of VTE, stroke prevention in atrial fibrillation (AF) - heparin or coumadin more likely to be used in patients with mechanical heart valves, pregnancy and severe liver disease

MOA: inactivation of circulating and clot-bound factor 10a

reversal agent: Andexanet alfa, PCCs

93
Q

what is tissue plasminogen activator (tPA)?

A

A naturally occurring serine protease that assists in the conversion of plasminogen to plasmin, the main enzyme involved with dissolving blood clots, synthetic tPA drugs are known to recombinant tissue plasminogen activator (rtPA)

94
Q

what are the indications for tPA?

A

ischemic stroke, MI, PE, thrombolysis

95
Q

what are the indications and MOA of fibrinolytic therapy: alteplase/activase?

A

indications: ST Elevation Myocardial Infarction (STEMI), acute Ischemic Stroke, acute massive PE, occluded central venous access

MOA: fibrin specific, almost never associated with allergic reactions, results in a systemic lytic state, with increase fibrin degradation productions (e.g. D-dimer) and a substantial risk of systemic bleeding

96
Q

what are the indication and MOA for fibrinolytic therapy: reteplase/retavase?

A

indication: ST Elevation Myocardial Infarction (STEMI)

MOA: second generation fibrinolytic, almost never associated with allergic reactions, does not bind to fibrin as tightly as alteplase, can diffuse more freely through the clot and at high concentrations, does not compete with plasminogen for fibrin binding sites allowing plasminogen at the site of the clot to be transformed into clot dissolving plasmin

97
Q

describe fibrinolytic therapy: tenecteplase/TNKase

A

used in STEMI, first choice for cardiologists when tPA is needed, greater fibrin specificity and longer plasma half life compared to alteplase, decreased bleeding side effects due to greater fibrin specificity

98
Q

what are the absolute contraindications of fibrinolytic therapy?

A

Prior intracranial hemorrhage, known structural cerebral vascular lesion, known malignant intracranial neoplasm, ischemic stroke within three months (excluding stroke within three hours), suspected aortic dissection, active bleeding or bleeding diathesis (excluding menses), significant closed-head trauma or facial trauma within three months

Pharmacology (4 decks)

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