Pharm - Anemia Flashcards
Drugs we are concerned about causing anemia
chemotherapy, HIV drugs, environmental toxins (lead)
most common cause of anemia
Fe deficiency
CV adaptations to chronic anemia
tachycardia, increased cardiac output (CO), vasodilation
Ferric (3+) or ferrous (2+) iron more efficiently absorbed?
ferrous –> 2 goes in2 the body
2 forms of oral Fe therapy
Ferrous Sulfate, Ferrous Gluconate
Toxicity of oral Fe therapy
GI problems –> nausea, epigastric discomfort, abdominal cramps, constipation, diarrhea
Indications of Parenteral Fe therapy (and not oral)
previous GI surgery, any resection
inflammatory bowel disease
malabsorption syndromes
advanced chronic renal disease requiring hemodialysis and tx w/ EPO
toxic effects of parenteral Fe therapy
IV iron dextran –> HA, light headedness, fever, arthralgias, nausea and vomiting, back pain, flushing, urticaria, bronchospasm
more rare adv effect of parenteral Fe therapy
anaphylaxis –> CV collapse b/c of dec BP –> inc pereability of vasculature –> tachycardia
what must you monitor in a pt who is on parenteral Fe therapy
iron overload/toxicity –> you are bypassing the absorptive regulatory process of oral absorption
kids eat too many iron tabs b/c they look like red M&Ms. what are you worried about
necrotizing gastroenteritis –> vomiting, ab pain, bloody diarrhea, shock, lethargy, dyspnea –> initial improvement followed by severe metabolic acidosis, coma, death
A non drug means of iron overload detox
whole bowel irrigation
what can you not use in iron overload detox
activated charcoal –> will not bind the Fe –> INEFFECTIVE
drug used to detox iron overload
Deferoxamine
MOA of Deferoxamine
potent Fe-chelating compound –> does not effectively chelate other impt trace metals
route of admin for deferoxamine
IV
route of excretion for deferoxamine
urine and bile
weird effect you might see w/ deferoxamine
red piss
actual adverse effects of deferoxamine
tachycardia, hypotension, shock
–> could add to CV collapse caused by Fe toxicity
what is another reason to admin deferoxamine ?
give during transfusion to prevent transfusional Fe overload
most common cause of B12 deficiency
MALABSORPTION
other causes of B12 def
pernicious amenia, being vegan (bacon haters, fucking hippies with their mac computers and shit)
req’d route of administration of B12
parenteral –> IM
why can you not give B12 orally?
most common cause of def is malabsorption, so oral ain’t gonna work
preferred form of B12 to administer
Hydroxocobalamin –> more highly protein bound, will stay in circulation for longer
other form of B12 to administer
cyanocobalamin
pt populations where folate def is common
alcoholics and those w/ liver disease –> diminished hepatic storage of folates
what is folate req’d for
synthesis of amino acids, purines, and DNA
easy correction for folate def
folic acid
what therapeutic process would require supplementation with Folate?
renal dialysis –> removes folate from plasma
Folic acid therapy route of admin
oral –> absorption is high, even w/ pts w/ malabsorption
what risk factors would make you consider folate supplementation?
Supplementation “HALP (help) me!”
H - Hemolytic anemia
A - Alcoholic (Kendall!)
L - Liver disease
Pregnant women (Not Kendall!)
drug induced decificiencies of Folate
think DHFR inhibitors - MTX, trimethoprim (antimicrobial), pyrimethamine (antimalarial), phenytoin (antiepileptic)
which drugs are less likely to induce a folate deficiency ?
trimethoprim, pyrimethamine –> much greater affinity for bacterial and malarial forms of DHFR
rescue therapy for folate antagonist drugs
leucovorin - reduced folate = folinic acid
what therapies do you not give for hemolytic anemia?
iron, B12, folate (it was a clicker question I think)
Erythropoietin site of production
renal tubular cells (I think, I know its in the kidney somewhere)
Erythropoietin upregulated in response to
low pO2 in blood sensed by kidney
Condition that could result in decreased EPO levels
renal failure (There’s really no smoke and mirrors here)
other conditions that could result in decreased EPO
disease, lack of kidney, poor function, on dialysis
what do you give to pts with low levels of epo due to kidney problems
most likely to respond to exogenous EPO
bone marrow disorders and EPO levels
endogenous EPO levels will be high –> not likely to respond to exogenous EPO
drug - agonist of EPO receptors expressed by red cell progenitors
Epoetin alfa
2 main indications of epoetin alfa
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
what do you need to be careful of w/ admin of epoetin alfa?
Hgb levels maintained below 12g/dL, to reduce the risk of serious CV events
epoetin alfa toxicities
CHRONIC KIDNEY DISEASE, CANCER –> proliferation of already present malignancies
What do you want to do to avoid epoetin alfa toxicities
use the lowest dose possible to avoid RBC transfusion –> want to keep Hgb below 12 g/dL
what is the other, non-black box warning for epoetin alfa
perisurgery –> increased risk for DVT, so DVT prophylaxis is recommended (too many RBCs will increase thrombotic risk)
Interference w/ Epoetin response
acute/chronic inflammation, cystic fibrosis, erythrocyte enzyme deficiency
folate of B12 deficiency
hematologic disease, hyperparathyroidism, hypersplenism, occult blood loss
advantages of Darbepoetin alfa
glycosylated form –> persists for longer
less of a problem with renal failure
what drugs are removed by hemodialysis?
NOT epoetin alfa or darbepoetin alfa
drug form of G-CSF
Filgrastim or Pegfilgrastim
drug form of GM-CSF
Sarograstim
what does Filgrastim do?
stimulate proliferation and differentiation of progenitors already committed to neutrophil lineage
what to use Filgrastim for, what does it allow?
permits use of peripheral blood stem cells rather than bone marrow stem cells for autologous and allogenic hematopoietic stem cell transplantation
other clinical utilities of G-CSF
accelerates rate of neutrophil recovery after dose-intensive myelosuppressive ctx
tx for neutropenia –> congential, cyclic, myelodysplasia, aplastic anemia
Megakaryocytic Growth Factors
Oprelvekin
Oprelvekin MOA
induce megakaryocytopoiesis –> increased platelet production
approved use of oprelvekin
secondary prevention of thrombocytopenia in pts receiving cytotoxic ctx for non-myeloid cancers
pharmacodynamics with sargamostim, filgrastim, oprelvekin
dosing a pt on chemo, need to give these drugs separately –> >24 hr prior to and after ctx chemo
Sarograstims interactant
corticosteroid promote leukocytosis
Oprelvekin interactant
thiaxide, loop diuretic –> leads to development of severe hypokalemia (and you do not want to be hypokalemic –> (die like an anorexic)
