anemia blood drugs Flashcards
erythropoiesis process
kidney sense hypoxia and increase erythropietin. reythropoietin acts on e progenitor cells in bone marrow and produces rbc. kidney sense inreases oxygenation and decreases erythropoietin production
why do we care about anemia?
Lots of your patients will be anemic (renal failure, clinical vampirism, trauma, cancer, pregnant, “little old ladies”.
• YOU will cause anemia (dilutional anemia, hemolysis, stupid perfusion practices)
• Most of your patients only want their blood in their vasculature (Jehovah’s Witnesses, etc.)
• Giving blood (because of anemia) is incredibly, horribly bad. Really bad. Expensive and bad. Bad. Life-threatening bad. Walter White bad
anemia therapeutics
iron, B9, B12, EPOGEN
IRONpotin
Required for the hemoglobin molecule to carry O2.
“Not me!” • Stored in intestinal mucosal cells as ferritin.
• Iron deficiency results from inadequate iron stores &/or intake.
• InjectionsHURT! • Oral iron supplements can cause “GI upset”.
Iron deficiency anemia classically causes a
hypochromic, microcytic anemia. due to bone marrow producing RBC and nom iron to cause pigment
B9 DEFICIENCY CAUSES
pregnancy, lactation, intestinal pathology (Crohn’s Disease, etc.) preventing absorption, alcoholism, certain drugs.
• Folate is require for DNA synthesis
*Folate deficiency anemia classically causes a
megaloblastic anemia. beavuse rate limiting step is production of DNA
B12 DEFICIENCY CAUSES and what ype of anemia is it
Most common cause of deficiency is poor B12 absorption.
• Called“perniciousanemia” and can also cause megoblastic anemia so it is given with B9
erythropoietin
(Epogen, Procrit) • Both are synthetic forms of erythropoietin-
alfa. • Both have identical protein structure
and vary in their glycosylation
darbepotin. why give with iron? why albumin free?
aranesp. is a longer-acting cousin of Epogen and is “albumin-free” (why might that be important?) JEHOVAH
• Part of a comprehensive blood. conservation/blood management program.
• Require week(s) to “kick in” bone marrow so not appropriate for acute blood loss.
• Usually given with iron (why?)
DARBEPOTIN SIDE EFFECTS
High potential for abuse! • INCREASING AWARENESS OF SIDE
EFFECTS: – Stroke – Increased tumor risk
– Thromboembolic events
– Severe HTN – Death
HYDROXYUREA
HYDREA,DROXIA. SICKLE CELL DRUG. airly effective in preventing painful acute “crises” associated with sickling claudication.
(what’s this?) MASSES OF CELLS BLOCK ARTERIES
*Interesting drug…causes sickle cell hemoglobin (HbS) to get diluted by an increased production of fetal hemoglobin (HbF.) particularly when used with epo-alfa.
PETOXIFYLLINE
TRENTAL. It’s a rheologic modifier! cell modifier and makes membrane more flexible
- It increases the “flexibility” of RBC’s so they are less likely to clog capillaries
- Decreases blood viscosity so interesting future possibilities…TIA, strokes, Raynaud’s, diabetic ulcers, etc.
