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HEME > Pharm - Anemia > Flashcards

Pharm - Anemia Flashcards

1
Q

Drugs we are concerned about causing anemia

A

chemotherapy, HIV drugs, environmental toxins (lead)

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2
Q

most common cause of anemia

A

Fe deficiency

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3
Q

CV adaptations to chronic anemia

A

tachycardia, increased cardiac output (CO), vasodilation

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4
Q

Ferric (3+) or ferrous (2+) iron more efficiently absorbed?

A

ferrous –> 2 goes in2 the body

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5
Q

2 forms of oral Fe therapy

A

Ferrous Sulfate, Ferrous Gluconate

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6
Q

Toxicity of oral Fe therapy

A

GI problems –> nausea, epigastric discomfort, abdominal cramps, constipation, diarrhea

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7
Q

Indications of Parenteral Fe therapy (and not oral)

A

previous GI surgery, any resection
inflammatory bowel disease
malabsorption syndromes
advanced chronic renal disease requiring hemodialysis and tx w/ EPO

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8
Q

toxic effects of parenteral Fe therapy

A

IV iron dextran –> HA, light headedness, fever, arthralgias, nausea and vomiting, back pain, flushing, urticaria, bronchospasm

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9
Q

more rare adv effect of parenteral Fe therapy

A

anaphylaxis –> CV collapse b/c of dec BP –> inc pereability of vasculature –> tachycardia

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10
Q

what must you monitor in a pt who is on parenteral Fe therapy

A

iron overload/toxicity –> you are bypassing the absorptive regulatory process of oral absorption

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11
Q

kids eat too many iron tabs b/c they look like red M&Ms. what are you worried about

A

necrotizing gastroenteritis –> vomiting, ab pain, bloody diarrhea, shock, lethargy, dyspnea –> initial improvement followed by severe metabolic acidosis, coma, death

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12
Q

A non drug means of iron overload detox

A

whole bowel irrigation

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13
Q

what can you not use in iron overload detox

A

activated charcoal –> will not bind the Fe –> INEFFECTIVE

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14
Q

drug used to detox iron overload

A

Deferoxamine

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15
Q

MOA of Deferoxamine

A

potent Fe-chelating compound –> does not effectively chelate other impt trace metals

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16
Q

route of admin for deferoxamine

A

IV

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17
Q

route of excretion for deferoxamine

A

urine and bile

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18
Q

weird effect you might see w/ deferoxamine

A

red piss

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19
Q

actual adverse effects of deferoxamine

A

tachycardia, hypotension, shock

–> could add to CV collapse caused by Fe toxicity

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20
Q

what is another reason to admin deferoxamine ?

A

give during transfusion to prevent transfusional Fe overload

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21
Q

most common cause of B12 deficiency

A

MALABSORPTION

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22
Q

other causes of B12 def

A

pernicious amenia, being vegan (bacon haters, fucking hippies with their mac computers and shit)

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23
Q

req’d route of administration of B12

A

parenteral –> IM

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24
Q

why can you not give B12 orally?

A

most common cause of def is malabsorption, so oral ain’t gonna work

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25
Q

preferred form of B12 to administer

A

Hydroxocobalamin –> more highly protein bound, will stay in circulation for longer

26
Q

other form of B12 to administer

A

cyanocobalamin

27
Q

pt populations where folate def is common

A

alcoholics and those w/ liver disease –> diminished hepatic storage of folates

28
Q

what is folate req’d for

A

synthesis of amino acids, purines, and DNA

29
Q

easy correction for folate def

A

folic acid

30
Q

what therapeutic process would require supplementation with Folate?

A

renal dialysis –> removes folate from plasma

31
Q

Folic acid therapy route of admin

A

oral –> absorption is high, even w/ pts w/ malabsorption

32
Q

what risk factors would make you consider folate supplementation?

A

Supplementation “HALP (help) me!”

H - Hemolytic anemia
A - Alcoholic (Kendall!)
L - Liver disease
Pregnant women (Not Kendall!)

33
Q

drug induced decificiencies of Folate

A

think DHFR inhibitors - MTX, trimethoprim (antimicrobial), pyrimethamine (antimalarial), phenytoin (antiepileptic)

34
Q

which drugs are less likely to induce a folate deficiency ?

A

trimethoprim, pyrimethamine –> much greater affinity for bacterial and malarial forms of DHFR

35
Q

rescue therapy for folate antagonist drugs

A

leucovorin - reduced folate = folinic acid

36
Q

what therapies do you not give for hemolytic anemia?

A

iron, B12, folate (it was a clicker question I think)

37
Q

Erythropoietin site of production

A

renal tubular cells (I think, I know its in the kidney somewhere)

38
Q

Erythropoietin upregulated in response to

A

low pO2 in blood sensed by kidney

39
Q

Condition that could result in decreased EPO levels

A

renal failure (There’s really no smoke and mirrors here)

40
Q

other conditions that could result in decreased EPO

A

disease, lack of kidney, poor function, on dialysis

41
Q

what do you give to pts with low levels of epo due to kidney problems

A

most likely to respond to exogenous EPO

42
Q

bone marrow disorders and EPO levels

A

endogenous EPO levels will be high –> not likely to respond to exogenous EPO

43
Q

drug - agonist of EPO receptors expressed by red cell progenitors

A

Epoetin alfa

44
Q

2 main indications of epoetin alfa

A

1) prevention of the need of transfusion in patients undergoing certain types of surgery
2) tx of anemia, especially secondary to renal failure, HIV, cancer and prematurity

45
Q

what do you need to be careful of w/ admin of epoetin alfa?

A

Hgb levels maintained below 12g/dL, to reduce the risk of serious CV events

46
Q

epoetin alfa toxicities

A

CHRONIC KIDNEY DISEASE, CANCER –> proliferation of already present malignancies

47
Q

What do you want to do to avoid epoetin alfa toxicities

A

use the lowest dose possible to avoid RBC transfusion –> want to keep Hgb below 12 g/dL

48
Q

what is the other, non-black box warning for epoetin alfa

A

perisurgery –> increased risk for DVT, so DVT prophylaxis is recommended (too many RBCs will increase thrombotic risk)

49
Q

Interference w/ Epoetin response

A

acute/chronic inflammation, cystic fibrosis, erythrocyte enzyme deficiency
folate of B12 deficiency
hematologic disease, hyperparathyroidism, hypersplenism, occult blood loss

50
Q

advantages of Darbepoetin alfa

A

glycosylated form –> persists for longer

less of a problem with renal failure

51
Q

what drugs are removed by hemodialysis?

A

NOT epoetin alfa or darbepoetin alfa

52
Q

drug form of G-CSF

A

Filgrastim or Pegfilgrastim

53
Q

drug form of GM-CSF

A

Sarograstim

54
Q

what does Filgrastim do?

A

stimulate proliferation and differentiation of progenitors already committed to neutrophil lineage

55
Q

what to use Filgrastim for, what does it allow?

A

permits use of peripheral blood stem cells rather than bone marrow stem cells for autologous and allogenic hematopoietic stem cell transplantation

56
Q

other clinical utilities of G-CSF

A

accelerates rate of neutrophil recovery after dose-intensive myelosuppressive ctx
tx for neutropenia –> congential, cyclic, myelodysplasia, aplastic anemia

57
Q

Megakaryocytic Growth Factors

A

Oprelvekin

58
Q

Oprelvekin MOA

A

induce megakaryocytopoiesis –> increased platelet production

59
Q

approved use of oprelvekin

A

secondary prevention of thrombocytopenia in pts receiving cytotoxic ctx for non-myeloid cancers

60
Q

pharmacodynamics with sargamostim, filgrastim, oprelvekin

A

dosing a pt on chemo, need to give these drugs separately –> >24 hr prior to and after ctx chemo

61
Q

Sarograstims interactant

A

corticosteroid promote leukocytosis

62
Q

Oprelvekin interactant

A

thiaxide, loop diuretic –> leads to development of severe hypokalemia (and you do not want to be hypokalemic –> (die like an anorexic)

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