DLA(3)- Agents Used in Anemia Flashcards

1
Q

Fe deficient anemia is treated with:

  • (1) what supplements / Fe ion form
  • (2) route of administration
  • (3) length of therapy
  • (4) co-administration
A

1- (Fe2+, ferrous iron) ferrous sulfate, ferrous gluconate, ferrous fumarate
2- oral
3- 3-6 mos
4- ascorbic acid / vitC

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2
Q

In patients CRF, Fe deficient anemia treatment:

  • (1) formulations
  • (2) route of administration
A

1- Fe dextran (highes risk of of Type I hypersensitivity), sodium ferric gluconate complex, Fe sucrose

2- parenteral (also for patients with Fe malabsorption)

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3
Q

Fe adverse effects

A

(oral preparations)

  • n/d, constipation, epigastric discomfort + abdominal cramping
  • black stools resembling melena
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4
Q

Acute Iron Toxicity, include Tx

A

(mostly seen in children via accidental ingestion)

  • GI irritant: n/v/d, abdominal pain, mucosal ulceration, bleeding
  • damage to GIT => free Fe into blood => metabolic acidosis (–> coma / death)

Tx:

  • deferoxamine: IV, binds free Fe –> urinary/fecal excretion
  • deferasirox: reduces Fe absorption (w/in 1 hr of ingestion)
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5
Q

Chronic Iron Toxicity, include Tx

A

(mostly genetic predisposition or patients with frequent transfusions => hemochromatosis)
-excess Fe deposition in major organs => cardiomyopathy, cirrhosis, bronze diabetes

Tx: phlebotomy (w/o anemia), for transfusion Pts use oral chelators / deferasirox

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6
Q

B12 is stored in….

A

liver, 2-5 yr stores

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7
Q

blood indications for B12 deficieny

A
  • anemia (macrocytic)
  • elevated homocysteine
  • elevated methyl malonic acid

(possibly: leukopenia, thrombocytopenia, anti-IF Igs)

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8
Q

B12 deficiency therapy (include forms)

A

IM (parenteral) administration of B12, usually monthly

  • hydroxocobalamin
  • cyanocobalamin
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9
Q

drug that impair B9/folate metabolism

A
  • trimethoprim
  • pyrimethamine
  • phenytoin
  • MTX
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10
Q

blood indications of B9 deficiency

A

-macrocytic anemia
-elevated homocystein
(*-normal methyl malonic acid levels)

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11
Q

if macrocytic anemia is evident, what is the immediate treatment protocol

A

B12/B9 co-therapy until methyl malonic acid levels are tested to distinguish the difference

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12
Q

discuss EPO therapy

A
  • Recombinant form EPO (epoetin alfa) –> glycoprotein given IV 3 times a week (1/2 life = 4-13 hrs)
  • Darbepoetic alfa- once a wk (1/2 life x2-3 longer)
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13
Q

EPO:

  • binds (1) receptors on (2) cells
  • (3) and (4) are the main effects
A

1- JAK/STAT receptors
2- RBC progenitors

3- stimulates erythroid proliferation / differentiation
4- release of reticulocytes

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14
Q

list the G-CSF type therapies and their effects

A

(myeloid GFs)
-Filgrastim, G-CSF: neutrophil production

-Sargramostim, GM-CSF: stimulates all myeloid line, including megakaryocyte progenitors

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15
Q

G-CSF therapies are given via (1) route of administration and it activates (2) receptors on (3) cells

A

1- IV, SQ
2- JAK/STAT receptors
3- myeloid progenitors (specifics depend on GF given)

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16
Q

(1) is the main specific Megakaryocyte GF given via (2) route. (1) activates (3) receptors in order to have (4) effect..

A

1- IL-11, oprelvekin
2- SQ
3- CK receptors
4- inc peripheral platelet count and neutrophils

17
Q

(1) is the main SCD treatment which has the following functions, (2)

A

Hydroxyurea:

  • inc HbF –> reduce sickling
  • dec neutrophil adhesion molecule expression (redue vaso-occlusions)
  • inc endothelial production of NO –> vasodilation (reduce vaso-occlusions)
18
Q

Hydroxyurea is administered via (1) route for SCD. It has (2) as the major toxicities.

A

1- oral, well-absorbed

2- leukopenia, induces megaloblastic changes, maculopapular skin rash, painful leg ulcers