Treatment of Anemia CIS Flashcards
(33 cards)
Case 1: 5 year hx of peptic ulcer disease, heavy menstruation, blood in stools, low ferritin, low HCT, low Hgb. She has been taking NSAIDs. What should be given to pt orally?
NSAIDs and peptic ulcer disease can reduce iron absorption
heavy menstruation - can predispose to anemia
Ferrous Sulfate: given orally
- since she has children, need to warn her about poisoning from iron if they get into the bottle.
- she should take it separately from tetracycline and be taken with food.
when would parenteral iron therapy be indicated?
malabsorption - parenteral iron is given in ferric form,
other indications: intolerance to oral therapy, advanced chronic renal disease, small bowel resection, inflammatory bowel disease, malabsorption syndromes
what to give when suffering acute iron toxicity?
deferoxamine - its an iron chelator
activated charcoal is not effective in iron poisoning
case 2: 38 y/o female with cancer that is in the middle of chemo. She c/o SOB and her Hgb is low, Hct is low, MCV and MCHC are normal. peripheral smear shows normochromic, normocytic RBCs. What kind of anemia?
Anemia of chronic disease
Which agent will stimulate an increase in the production of retics and is most appropriate tx for this patient?
Epoetin alpha
Cyanocobalamin?
used for B12 deficiency
Oprelvekin
Megakaryocyte growth factor
Pegfilgrastim
G-CSF
Filgrastim
G-CSF
what drug should you not choose if pt. is on chemotherapy?
erythrocyte stimulating agents: Epoetin alph and darbepoetin alpha - see increased risk of progression or recurrence of anemic pts with cancer, and is not recommended
megaloblastic anemia tx?
assoc. with Vit B12 deficiency or folic acid deficiency.
Give either cyanocobalamin, hydroxocobalamin or folic acid
an anemia (of macrocytic classification) that results from inhibition of DNA synthesis during red blood cell production.[1] When DNA synthesis is impaired, the cell cycle cannot progress from the G2 growth stage to the mitosis (M) stage. This leads to continuing cell growth without division, which presents as macrocytosis. Megaloblastic anemia has a rather slow onset, especially when compared to that of other anemias. The defect in red cell DNA synthesis is most often due to hypovitaminosis, specifically a deficiency of vitamin B12 and/or folic acid.
vit B12 deficiency?
often see neurological problems, if give folic acid, will probably rescue the anemia, but the neurologic sx will most likely progress
signs of anemia?
pallor, fatigue, dizziness, exertional dyspnea, hypoxia, tachycardia, increased CO and vasodilation
inadquate iron intake?
microcytic hypochromic anemia
ferrous sulfate, ferrous gluconate, ferrous fumarate
oral preparations of iron
- should be taken with water
AE’s= nausea, epigastric discomfort, ab cramps, constipation, black stools, diarrhea
free iron levels
if have high iron levels, then see increase in apoferritin (stimulate apoferritin synthesis)
if have low iron levels, then see increase in transferrin (low levels inhibit apoferritin synthesis)
parenteral iron therapy
iron dextran, iron-sucrose complex, sodium ferric gluconate complex
Use: given to pts that are unable to tolerate/absorb oral iron or with extensive chronic anemia (i.e. advanced CRD, small bowel resection, IBD, malabsorption syndromes)
AE’s: (esp. of iron dextran) = h/a, light headedness, fever, arthralgias, back pain, flushing, urticaria, bronchospasm * anaphlylaxis, death!
- = less likely to cause hypersensitivity rxns
Acute iron toxicity
seen in children who ingest iron tablets => necrotizing gastroenteritis, vomiting, bloody diarrhea –> shock, lethargy, dsypnea –> severe met. acidosis, death
** give parenteral deferoxamine (iron chelating that promotes excretion)**
chronic iron toxicity
deposits in heart, liver, pancreas –> organ failure and death
(2) Toxicity is most common in patients with inherited hemochromatosis, a disorder characterized by excessive iron absorption, and in patients who receive many red cell transfusions over a long period of time
(3) Efficiently treated with intermittent phlebotomy (deferoxamine is not effective, only used in last case effort)
(4) Oral iron chelator deferasirox reduces liver iron concentrations but data in removing iron from heart is lacking
what does VitB12 deficiency lead to? tx?
megaloblastic macrocytic anemia (often associated with mild/moderate leukopenia/thrombocytopenia),
GI sx, neurologic abnormalities
iv) Neurologic syndrome associated with B12 deficiency usually begins with paresthesias in peripheral nerves and weakness and progresses to spasticity, ataxia, and other CNS dysfunctions (B12 treatment stops the progression of neurologic disease but may not fully reverse neurologic symptoms)
obtained in meat, eggs, dairy products
defiency usually due to malabsorption due to lack of intrinsic factor or loss of distal ileum function
- seen in pernicioius anemia, gastrectomy, IBD, small bowel resection
tx: Cyanocobalamin, Hydroxocobalamin
deferoxamine
iron chelator used to tx acute iron toxicity
deferasirox
iron chelator used to tx chronic iron overload
Cyanocobalamin, Hydroxocobalamin
tx of Vit B12 deficiency
reqd for synthesis of amino acid methionine and synth of succinyl CoA
almost all cases are due to malabsorption - so these are given parenterally
Folic Acid
Folic acid is reqd for synth. of amino acids, purines, and DNA
**Major consequence of deficiency is anemia; folic acid deficiency is implicated as a cause of congenital malformations in newborns and may play a role in vascular disease
Obtained through yeast, liver, kidney and green veggies!
folic acid deficiency results in megaloblastic anemia! (same as B12) - but does not cause the neurologic sx as seen in B12 deficiency
deficiency seen in : inadequate dietary intake of folates (e.g., alcoholics with poor diet and diminished hepatic storage, pregnant women and patients with hemolytic anemia with increased folate requirements, patients with malabsorption syndromes, patients undergoing renal dialysis have folates removed from plasma)
iv) Drugs that can cause folic acid deficiency include methotrexate, trimethoprim, and pyrimethamine (all inhibit dihydrofolate reductase) and long-term therapy with phenytoin
