Anemias

Question 1

How are RBCs formed?

Answer 1

Stem cell→(Erythropoietin (EP))→proerythroblast

Proerythroblast→(Fe incorporated)→reticulocyte

reticulocyte→(loss of nucleus)→erythrocyte

Question 2

Microcytic anemia

Cause, etiology, treatment

Answer 2

Cause-Relative lack of iron

RBCs small and pale

Etiology:

• Decrease iron intake-diet
  
  • Takes years to occur
• Decrease absorption
  
  • HCL low
  • GI dysfunction
• Increase iron requirement
  
  • Pregnancy–rapid growth
  • Renal disease
• Excessive loss of iron-_chronic blood loss_
  
  • Most common

Treatment:

• Iron-typically FeSO4
  
  • Orally-may cause GI upset
  • Parenteral-sever deficiency

Question 3

Normal iron metabolism/storage

Answer 3

Highly conserved, no mech for removal

Ingest iron→solubilized by HCl in gut, absorbed as Fe++ (ferrous)

Fe++→(transferrin)→Fe+++ (ferric)

Fe+++ not readily absorbed but carried throughout body on transferrin

Transferrin increases during anemia

Excess iron bound to and stored as ferritin–in liver

Question 4

Toxicity of iron

Answer 4

Acute

• Toxic-esp in children
  
  • Lethal in as few as 10 tablets
• Sympt
  
  • Nausea
  • Severe abd pain-mucosal damage
  • Drowsiness
  • Cardiovascular collapse
  • Convulsions
  • Death
• Tx
  
  • Iron chelator-Deferoxamine
  • May pump stomach

Chronic

• Too much iron stored-_Hemochromatosis_
• Tx=phlebotomy (bleeding)

Question 5

Deferoxamine

Answer 5

Tx: Acute iron OD

Mech: Iron chelator

De-Fer-oxamine

_De_toxes _Fer_rous overdose

Question 6

Macrocytic anemia

Answer 6

Characteristics:

• Large RBC precursors
• Multilobed nuclei due to inhibition of DNA syth

Cause: Folic acid deficiency

• Folic Acid necessary for DNA replication
• not enough FA→not enough thymadine→not enough RBCs
• Methionine deficiency may also be present

Etiology:

• Intake deficiency-mainly alcoholics (no green leafy veggies)
  
  • Absorption is rapid
• Drugs can inhibit synth of active form
• Increased requirement
  
  • 1) Infection
  • 2) Pregnancy
    
    • Folic Acid deficiency→neural tube defects
    • Gov’t says all flour products must have FA
  • 3) Renal dialysis
  • Difference b/w macro- and micro here is infection-

Tx:

• Oral therapy usually sufficient
• Parenteral if absorption abnormality
• No contraindications or toxicities
• Only indication is folic acid deficiency

Question 7

B12 deficiency anemia

Answer 7

Function of B12: Ess for DNA synthesis (methionine)

Sympt:

• Megaloblastic anemia-_like folic acid_ def
• Lack of methionine→decrease in myelin synth→ neural damage
  
  • Weakness
  • Spasticity
  • Abnormal gait
  • Irreversible spinal cord damage
  • Ataxia
• Note:
  
  • B12 def=neural defects
  • Folic acid def=neural tube defects

Etiology:

• Insufficient intake rare
• Decrease absorption-most common cause
  
  • Parietal cells make gastric intrinsic factor (GIF)
  • B12 requires GIF for absorption
  • Pt may lack ability to make GIF→pernicious anemia
    
    • Looks like macrocytic anemia so add folic acid
    • No effect because still no B12
    • Fatal if not treated

Tx:

• If deficiency is not due to lack of GIF, just add B12
• If pernicious anemia, B12 give by injection

Pernicious anemia does NOT describe any B12 deficiency, only B12 def. due to lack of GIF

Question 8

“Poetin” and “Pegin”

Answer 8

Epoietin alfa

Darbepoietin

Peginesatide

Tx: Anemia due to chronic renal failure or chemotherapy

Toxicities: Due to excess RBCs

• Increase BP
• Increase clotting
• MI
• Stoke

Question 9

Hemolytic anemia

Cause and tx? Who is at risk?

Answer 9

Cause: Abnormal RBC lysis

Tx: EPO may be useful

Iron not useful

G6PDH deficient patients at risk

Question 10

Sickle cell anemia

Cause and tx

Answer 10

Single nucleotide mutation

Abnormal flow–RBCs get stuck in small vessels

Severe joint pain

Tx: Hydroxyurea

Question 11

Hydroxyurea

Answer 11

Mech: Increase formation of fetal Hb (does not sickle)

SE: Mutagenic

Pregnancy category D