Microcytic Anemia Flashcards

1
Q

What is microcytic anemia?

A

Deficiency in oxygen carrying erythrocytes Microcytic & hypochromic → small erythrocytes w/insufficient Hb (hence pale)

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2
Q

What is a common cause of microcytic anemia?

A

iron deficiency

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3
Q

Who is at risk for microcytic anemia?

A

→ increased Fe requirements (e.g. pregnancy) → Fe malabsorption → Blood loss *consider those on PPIs have decreased stomach acid (stomach acid increases Fe bioavailability)

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4
Q

Expected lab values w/microcytic anemia

A

Mean Cell Volume (MCV): <80fL
Mean Cell Hemoglobin Concentration (MCHC): <30%
Serum Iron (SI): <30 mcg/dL
Transferrin saturation: <10%
Serum ferritin: <20 mcg/L

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5
Q

Where does iron absorption take place?

A

intestine, primarily in duodenum

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6
Q

Dietary sources of iron

A

organ meats, brewer’s yeast, wheat germ, egg yolks, oysters, green leafy veggies

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7
Q

Difference between heme and non heme iron absorption

A

→ Heme Fe in meat well absorbed → non-heme Fe 1st reduced by ferrireductase to ferrous Fe before absorption

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8
Q

How is iron transported?

A

Transferrin: beta globulin that binds 2 molecules of ferric Fe→ transports Fe in plasma to maturing erythroid cells in bone marrow

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9
Q

How is iron stored?

A

Fe primarily stored as ferritin in intestinal mucosal cells, macrophages in liver, spleen, and bone, parenchymal liver cells

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10
Q

Significance of serum ferritin

A

estimate of total body Fe stores

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11
Q

How is iron eliminated?

A

• No mech for Fe excretion → small loss in feces, trace in bile, urine, sweat • why hepcidin is imp – main Fe hormone, decreases absorption

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12
Q

How much iron is lost/excreted daily?

A

• ~1mg iron lost daily • 10% women lose >2mg/day on menses

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13
Q

Types of PO iron

A

Ferrous sulfate (Feosol) Ferrous gluconate (Fergon) Ferrous fumarate (Feostat)

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14
Q

PO iron: adverse reactions

A

Nausea, epigastric discomfort, abdominal cramps, constipation, diarrhea, black stools GI upset: Fumarate causes most

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15
Q

Which type of PO iron is preferred?

A

Ferrous sulfate

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16
Q

What is the benefit of slow release PO iron?

A

marketed as less GI upset, but releases in ileum, late for absorption. NOT preferred.

17
Q

When is iron best absorbed?

A

on empty stomach but may take w/food to minimize GI effects

18
Q

How long should iron supplementation continue in IDA?

A

3-6mths after correcting IDA cause

19
Q

What happens in acute iron toxicity?

A

causes GI tract corrosion & direct cellular damage

20
Q

Who is most at risk for acute iron toxicity?

A

Almost exclusively occurs in young kids so store out of reach!

21
Q

How is acute iron toxicity treated?

A

whole bowel irrigation and iron-chelating agents (e.g., IV deferoxamine)

22
Q

Types of IV Iron

A

Iron dextran (INFeD)

Sodium ferric gluconate (Ferrlecit)

Iron sucrose (Venofer)

23
Q

What are the indications for the different types of IV iron?

A

INFeD: IDA

Ferrlecit & Venofer: CKD pts on hemodialysis

24
Q

Side effects of INFed?

A

HA, lightheadedness, fever, arthralgias, anaphylaxis/death

25
Q

Side effects of Ferrlecit and Venofer

A

N/V, injection site reaction, hypotension, cramps, dizziness, chest pain, back pain

26
Q

Why choose IV iron over PO iron?

A

PO Failure OR Extensive chronic anemia unable to be maintained on PO Fe (Fe malabsorption, hemodialysis and/or on erythropoietin, severe PO intolerance )

27
Q

Special consideration for INFed?

A

requires test dose prior to 1st admin