Nutritional Anemia Flashcards

1
Q

What are the disorders you think of for DDX of Macrocytic Anemia?

A

Vit B12 Deficiency

Folate Deficiency

Myelodysplastic disorders

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2
Q

What causes the cells, on a structural level, to become macrocytic?

A

-lack of either vitamin B12 or folate slows the synthesis of DNA but not RNA, so the RBC increases in size before dividing resulting in macrocytic RBC

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3
Q

Where do we get our Vitamin B12 from?

A

-meat and dairy products only!

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4
Q

How does a person develop a Vit. B deficiency macrocytic anemia?

A

-Vitamin B is unable to be absorbed or you have severe inadequate intake of dietary B12 for several years.

Dietary intake» R factor»> Intrinsic Factor»> IF-CBL»> ileum»>absorption

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5
Q

What is pernicious anemia?

A
  • autoimmune attack on gastric Intrinsic Factor
  • -anti-IF abys block the attachment of Cbl to IF
  • -attachment of Cbl-IF to ileal receptors are blocked.
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6
Q

What is chronic atrophic gastritis?

A

leads to the decline of IF production, associated w/ autoantibodies against gastric parietal cells, results in less acidic pH in stomach.

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7
Q

Etiologies of B12 Deficiency

A
  • pernicious anemia*
  • Chronic Atrophic Gastritis*
  • chronic alcoholism*
  • gastrectomy*
  • HIV infection
  • crohns
  • inadequate dietary intake (vegans, pregnancy)
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8
Q

Clinical presentation of Vit B12 Anemia

A
  • macrocytic, MCV>100, elevated iron levels, indirect bilirubin & LDH (indicating increased RBC breakdown)
  • peripheral smear: megaloblastic, hypersegmented neutrophils, & macrocytosis
  • thrombocytopenia and neutropenia–bone marrow gets suppress over all leading to decreased cells.

-homocysteine levels increased (both folate and vit B12 required to convert homocysteine to methionine); build up leads to venous thromboembolism and
atherosclerosis

  • neurologic changes; d/t defect in myelin formation, peripheral neuropathy (burn, numb, tingle, sting), weakness, spasticity, memory loss, irritability, and dementia
  • increased risk of osteoporosis (d/t suppression of osteoblast activity)
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9
Q

Folate Deficiency Etiologies

A
  • poor nutrition (folate found in meat, green leafy veggies, nuts, fruit)
  • alcoholism
  • infants fed primarily fed goats milk
  • drugs interfering w/ folate metabolism– trimethoprim, methotrexate, phenytoin
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10
Q

Folate Deficiency Presentation

A
  • macrocytic anemia
  • hyperhomocysteinemia
  • NO neurologic findings
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11
Q

After how much time may folate deficiency occur? B12?

A
  • 4-5 months

- YEARS!!!

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12
Q

If pt has borderline abnormal vitamin values (B12 and folate) what do you test next?

A

-metabolites! methymalonic acid and homocysteine

–if BOTH are ELEVATED then B12 deficiency

–if MMA is normal and homocysteine is increased FOLATE deficiency.

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13
Q

What test used to be used to test pernicious anemia?

A

-schilling test

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14
Q

Treatment of Folate Deficiency ?

What is something to look for in particular?

A

-folic acid po daily for 1-4mo or until complete hematologic recovery

** if they have B12 deficiency!
always rule out B12 deficiency before administering folic acid because folic acid can partially reverse some of the hematologic effects of B12 deficiency. If you only treat for folic acid and they have B12 deficiency as well their neurologic sx will progress and become permanent after 6mo
-if urgent draw blood prior to tx to test B12 deficiency and then treat BOTH folic acid and B12 until tests are known.

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15
Q

Treatment of B12 Deficiency

A

-IM or deep SQ injections of Cobalamine –1000mcg every day for 1 week, 1mg every week for 4 weeks, if underlying disorder persisits» 1mg/mo.

–other preparations: oral Cbl, sublingual, and nasal spray

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16
Q

Response to Tx in B12 Deficiency

A
  • elevated serum iron, indirect bilirubin and LDH fall rapidly in 1-2days
  • bone marrow changes from megaloblastic to normoblastic
  • hypokalemia is common during early response d/t the marked increase in K+ utilization in the production of new hematopoietic cells, SO PATIENTS SHOULD BE MONITORED!!!
17
Q

What are the etiologies of Iron deficiency ?

A
  • poor dietary intake
  • reduced iron absorption
  • increased blood loss ( overt blood loss: surgery, menometrorrhagia, pregnancy AND/OR occult bleeding: assume GI cancer until proven otherwise!!)
  • intravascular hemolysis
  • congenital iron deficiency
18
Q

What is absolute iron deficiency?

A

iron stores in the bone marrow & liver/spleen are ABSENT

Serum ferritin is LOW

19
Q

What are in your DDx of Microcytic Anemia?

A
  • iron deficiency
  • thalassemia
  • anemia of chronic disease
  • sideroblastic
20
Q

What causes anemia of chronic disease?

A

-inflammation, infection, malignancy

hepcidin-induced block in the release of iron from the Mf back into circulation, makes iron less available for RBC production

21
Q

Treatment of Anemia of Chronic Disease

A

treat with EPO stimulating agents

22
Q

Clinical Manifestation of Iron deficiency

A
  • asymptomatic
  • weakness
  • fatigue
  • HA
  • irritability
  • exercise intolerance
  • Pica
  • Restless leg syndrome***
  • glossal pain/smooth tongue**
23
Q

What is tests are included in an iron study? What would these look like with Iron deficiency anemia?

A
  • serum iron (decreased)
  • ferritin (decreased)
  • Transferrin/Total iron binding capacity (THIS GOES UP!!)
  • transferrin saturation (decreased)
24
Q

What are the lab findings in:

  • thalassemia
  • anemia of chronic disease
  • siderblastic anemias
A

thalassemia:
- serum Fe= normal to high
- Hgb A2 increased
- RBC count is high

Chronic:

  • serum Fe and TIBC are low
  • normal to increased ferritin
  • eval for chronic inflammation**

Sideroblastic:
-peripheral smear indicating ringed sideroblasts on prussian blue staine of bone marrow

25
Q

What pt population is IV iron effective in?

A

-unresponsive or intolerant to iron

26
Q

When is IV iron required?

A

-when the amount of iron loss through daily blood loss exceeds the capacity of the GI tract to absorb oral iron

27
Q

What are in your DDx of Microcytic Anemia?

A
  • iron deficiency
  • thalassemia
  • anemia of chronic disease
  • sideroblastic
28
Q

What causes anemia of chronic disease?

A

-inflammation, infection, malignancy

hepcidin-induced block in the release of iron from the Mf back into circulation, makes iron less available for RBC production

29
Q

Treatment of Anemia of Chronic Disease

A

treat with EPO stimulating agents

30
Q

Clinical Manifestation of Iron deficiency

A
  • asymptomatic
  • weakness
  • fatigue
  • HA
  • irritability
  • exercise intolerance
  • Pica
  • Restless leg syndrome***
  • glossal pain/smooth tongue**
31
Q

What is tests are included in an iron study? What would these look like with Iron deficiency anemia?

A
  • serum iron (decreased)
  • ferritin (decreased)
  • Transferrin/Total iron binding capacity (THIS GOES UP!!)
  • transferrin saturation (decreased)
32
Q

What are the lab findings in:

  • thalassemia
  • anemia of chronic disease
  • siderblastic anemias
A

thalassemia:
- serum Fe= normal to high
- Hgb A2 increased
- RBC count is high

Chronic:

  • serum Fe and TIBC are low
  • normal to increased ferritin
  • eval for chronic inflammation**

Sideroblastic:
-peripheral smear indicating ringed sideroblasts on prussian blue staine of bone marrow

33
Q

What pt population is IV iron effective in?

A

-unresponsive or intolerant to iron

34
Q

When is IV iron required?

A

-when the amount of iron loss through daily blood loss exceeds the capacity of the GI tract to absorb oral iron