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Module 5: GI > Microcytic Anemia II > Flashcards

Microcytic Anemia II Flashcards

1
Q

How does a patient present with anemia?

A

They present with signs of hypoxia:

  • Weakness, fatigue, and dyspnea
  • Pale conjunctiva and skin
  • Headache and lightheadedness
  • Angina, especially with preexisting CAD
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2
Q

What are the Hgb levels considered to be anemic for males and females?

A

Males: Hgb < 13.5g/dl

Females: Hgb < 12.5g/dl

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3
Q

What is the anemia for:

MCV < 80

MCV = 80-100

MCV > 100

A

MCV < 80: Microcytic

MCV = 80-100: Normocytic

MCV > 100: Macrocytic

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4
Q

Why do microcytic anemias occur?

A

Microcytosis is due to an “extra” division in hematopoesis

  • this is due to decreased production of Hgb
  • the cell wants to maintain normal concentrations of Hgb
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5
Q

What is in the differential diagnosis of a person with low Hgb and an MCV < 80?

A

- Iron deficient anemia

- Anemia of chronic disease
(pt is in a state of chronic inflammation and iron is “locked” in macrophages)

- Sideroblastic anemia
(decreased production of protoporphyrin leads to low heme, leads to low Hgb)

- Thalassemia
(decreased production of globin chain = decreased hemoglobin)

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6
Q

What is the most common type of anemia?

A

Iron deficiency anemia

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7
Q

Where does absorption of iron occur?

A

In the duodenum

  • Enterocytes transport iron into blood via ferroportin
  • Transferrin transports iron and delivers it to liver and bone marrow macrophages for storage
  • Stored intracellular iron is bound to ferritin
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8
Q

What molecule is iron bound to in the blood?

A

Transferrin

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9
Q

What is iron bound to in the macrophage?

A

Ferritin

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10
Q

What does serum iron measure?

A

The level of iron in the blood

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11
Q

What does TIBC measure?

A

Total Iron Binding Capacity:

  • Measures transferrin in the blood (bound or unbound)

% saturation measures how much of that transferrin is bound to iron

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12
Q

What does serum ferritin measure?

A

How much iron is present in bone marrow and liver macrophages

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13
Q

How can a person become iron deficient?

What are the most common causes for:
Infants
Children
Adults
Elderly

A

Deficiency can be caused by dietary lack (malnutrition or malabsorption*) or blood loss

Infants = breast feeding (little to no iron in breast milk)

Children = poor diet

Adults = peptic ulcer disease (males); menorrhagia or pregnancy (females)

Elderly = Colon polyps/carcinoma (developed world); hookworm (developing world)

Gastrectomy can be a cause of increased Fe3+; Fe2+ is the form that is absorbed by the duodenum

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14
Q

What are the stages of iron deficiency?

A

Storage iron depleted (serum ferritin decreases; TIBC increases)

Serum iron depleted (serum iron levels decrease; %saturation decreases (< 33%))

Normocytic anemia (bone marrow produces normal sized RBCs, just less of them)

Microcytic, hypochromic anemia (bone marrow is no longer able to make normal RBCs due to decreased iron/heme - central pallor of cells is enlarged due to decreased heme)

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15
Q

What are clinical and lab features of iron deficiency?

A

Anemia

Koilonychia (spoon-shaped nails)

Pica (patients chew on things - dirt, ice, etc)

Microcytic, hypochromic anemia with Increased RDW

Decreased ferritin, Increased TIBC

Decreased serum iron, Decreased % saturation

Increased Free Erythrocyte Protoporphyrin (FEP; blood cell makes heme-iron = protoporphyrin)

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16
Q

What is Plummer-Vinson syndrome?

A

Iron deficiency anema with esophageal web and atrophic glossitis

–> presents with anemia, dysphagia, and beefy-red tongue

17
Q

What is anemia of chronic disease?

A

Chronic diseases with chronic inflammation results in acute phase reactants (i.e. Hepcidin)

  • Hepcidin sequesters iron into storage sites limiting iron transfers from macrophages to erythroid precursors
  • Hepcidin also suppresses EPO production from the kidney
18
Q

What are the lab findings of anemia of chronic disease?

A

Increased ferritin (high stores of ferritin; sequestered by hepcidin)

Decreased TIBC

Decreased serum iron (it’s being used)

Decreased % saturation

Increased Free Erythrocyte Protoporphyrin (FEP)

19
Q

What is the cause of sideroblastic anemia?

A

Defective protoporphyrin synthesis
(no protoporphyrin = no heme; no heme = microcytic anemia)

  • Iron is trapped in RBC mitochondria b/c heme is not produced and released
  • Iron laden mitochondria creates ringed sideroblast
20
Q

What is the most common form of congenital sideroblastic anemia?

A

ALAS deficiency

  • Aminolevulinate synthase is rate limiting enzyme of protoporphyrin production:

Succinyl CoA –> Aminolevulinate
Enzyme: ALAS

21
Q

What are the common causes of acquired sideroblastic anemia?

A

Alcoholism

Lead poisoning (Pb denatures ALAD and Ferrochelatase)

Vitamin B6 deficiency (ALAS requires B6 as a cofactor)

22
Q

What are the laboratory findings of a sideroblastic anemia?

A

Increased ferritin, Decreased TIBC

Increased serum iron, Increased % saturation

Ringed sideroblasts have so much Fe that it starts to create free radicals, causing damage and killing the cell
- free iron is released and taken up by macrophages or leak into blood stream

23
Q

How does thalassemia lead to a microcytic anemia?

A

Thalassemia results in a decreased synthesis of globin chains (as opposed to mutated globin chain like sickle cell)

Alpha thalassemia = decreased alpha globin
Beta thalassemia = decreased beta globin

–> decreased globin leads to decreased hemoglobin; resulting in microcytic anemia

24
Q

Why has thalassemia not be selectively removed from the gene pool?

A

Carriers are protected against Plasmodium falciparum malaria

25
Q

What are the three normal types of hemoglobin?

A

HbF (alpha2gamma2)

HbA (alpha2beta2)

HbA2 (alpha2delta2)

26
Q

What is the cause of alpha-Thalassemia?

A

–> Due to a gene deletion

1 Gene deletion = Asymptomatic

2 Gene deletion (cis or trans) = Mild anemia with slightly Increased RBC count; cis deletion is worse than trans due to increased risk in offspring

3 Gene deletion = Severe anemia; B chains form tetramers (HbH) that damage RBCs

4 Gene deletion = Hydrops fetalis; gamma chains of HbF form tetramers that damage RBCs

(there are normally 4 alpha alleles present on Chr16)

27
Q

What are Hb Barts?

A

Tetramers of gamma chains seen on electrophoresis

–> signature of hydrops fetalis and 4 gene deletion alpha-Thalassemia

28
Q

What is the cause of beta-thalassemia?

A

Beta-thalassemia is due to gene mutations
(Normally, two beta genes are present on Chr11)

  • Mutations result in absent (ßo) or diminished (ß+) production of ß-globin
29
Q

What is Beta thalassemia minor?

A

ß/ß+

  • Mildest form of disease (asymptomatic w/increased RBC count)
  • Microcytic, hypochromic RBCs and target cells
30
Q

What does HgB electrophoresis show for beta thalassemia minor?

A

Slightly decreased HbA

Increased HbA2 to 5% (normal 2.5%)

Increased HbF to 2% (normal 1%)

31
Q

What is Beta thalassemia major?

A

ßo/ßo

  • Most severe form of disease (no HbA)
  • Presents with severe anemia and massive erythroid hyperplasia a few months after birth (HbF is alpha2gamma2; doesn’t require beta)
  • no functional beta chains results in alpha tetramers aggregating to damage RBC
  • -> ineffective erythropoiesis
  • -> extravascular hemolysis
32
Q

What is massive erythroid hyperplasia? What result from this?

A

Expansion of hematopoeisis into marrow of skull (“crew cut” appearance on xray) and facial bones (“chipmunk” appearance)

  • Extramedullary hematopoiesis with Hepatosplenomegally b/c RBCs begin developing in liver and spleen
  • Risk of aplastic crisis with parvovirus B19

Module 5: GI (19 decks)

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