249/250 - Other Anemias (Iron/Chronic Disease, Megaloblastic) Flashcards

1
Q

List 3 acquired and 2 hereditary causes of megaloblastic anemia

A
  • Acquired
    • B12 deficiency
    • B9 (folic acid) deficiency
    • Pharmacologic
  • Hereditary
    • Orotic aciduria
    • Lesch-Nyhan syndrome

B9 and B12 deficiency are the most common causes overall

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2
Q

When is it appropriate to use iron to treat anemia of inflammation?

A

When there is a concurrent iron deficient state

If it’s just anemia of inflammation, don’t sue iron

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3
Q

What findings on peripheral blood smear are indicative of megaloblastic anemia? (3)

A
  • Hypersegmented neutrophils
  • Macro-ovalocytes
    • Large, oval-shaped blood cells
  • Low blood counts overall
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4
Q

How can levels of homocystine and methylmalonate differentiate between folate (B9) vs. B12 deficiency?

A
  • B9 deficiency
    • High homocysteine
    • Normal methylmalonate
  • B12 deficiency
    • High homocysteine
    • High methylmalonate

Both will have megaloblastic anemia; only B12 deficiency will have neurologic sx (subacute combined degeneration)

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5
Q

Is pure dietary deficiency more likely to cause B9 or B12 deficiency?

A

B9 deficiency

  • B9 is found in leafy green vegetables; 3-4 months of body stores*
  • B12 is found in meat, eggs, dairy; 2-4 years of body stores => deficiency likely results from malnutrition and malabsorption; look fo other deficiencies*
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6
Q

Describe the pathogenesis of anemia of inflammation (aka anemia of chronic disease)

A

It all starts with inflammatory stress

  • -> Increased hepcidin
  • -> Ferroportin is degraded
  • -> Iron cannot be absorbed from the GI tract, and it is sequestered as ferrtin
  • -> Ferritin increases, but cannot be delivered to erythroid marrow (also, ferritin is an acute phase reactant)
    • vs. IDA, where ferritin is reduced
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7
Q

What are the dietary sources of B12?

A

Meat, eggs, dairy

Body can store 3-4 years => dietary deficiency alone usually does not cause B12 deficiency

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8
Q

How will the following vary in a patient with anemia due to rheumatoid arthritis?

  • Iron:
  • % saturation:
  • Iron binding capacity (IBC or TIBC):
  • Ferritin:
A
  • Iron: Low
  • % saturation: Low
  • Iron binding capacity (IBC or TIBC): Normal
  • Ferritin: High
  • Inflammatory disease*
  • -> Increased hepcidin*
  • -> Iron sequestration in storage sites (Ferritin), but cannot be used bc hepcidin is degrading ferroportin*
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9
Q

List 2 clinical scenarios where we would expect hepcidin to be suppressed

A

Iron deficiency

Hypoxia

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10
Q

What is the first line treatment for hemochromatosis?

A

Phlebotomy

Only use iron chelation if a pt has concurrent anemia (low hemoglobin), and never use with hereditary hemochromatosis

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11
Q

What CNS manifestation results from B12 deficiency?

A

Subacute combined degeneration

  • Loss of dorsal column, corticospinal tract, spinocerebellar tract
    • Decreased sensation, weakness, ataxia
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12
Q

How will the following vary in a patient with hemochromatosis?

  • Iron:
  • % saturation:
  • Iron binding capacity (IBC or TIBC):
  • Ferritin:
A
  • Iron: High
  • % saturation: High
  • Iron binding capacity (IBC or TIBC): Normal or decreased
  • Ferritin: High
  • Hemochromatosis = defect in hepcidin*
  • -> Ferroportin is able to absorb a ton of iron from the gut*
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13
Q

List 4 risk factors for copper deficiency

A
  • Gastric bypass
  • Celiac disease
  • Excess zinc
  • TPN

Presents similarly to bone marrow disease (MDS); rule out before beginning aggressive tx

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14
Q

List 2 clinical scenarios in which we would expect hepcidin to be upregulated

A

Iron sufficiency/overload

Inflammation (IL-6)

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15
Q

What is the next step in evaluating a patient who has a new iron deficiency anemia?

A

Rule out bleeding

Then, figure out the underlying disease process

IDA is always caused by an underlying disease or bleeding

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16
Q

Will the bone marrow be hypercellular or hypocellular in B12/folate deficiency?

A

Hypercellular

Low peripheral blood counts with hypercellular marrow => megaloblastic anemia

17
Q

What is the most common type of anemia worldwide?

A

Iron deficiency anemia

18
Q

What is the treatment for anemia of inflammation?

A

Treat whatever is causing the inflammation

(Interrupt IL-6 signaling)

Don’t give iron unless there is a concurrent iron-deficiency anemia

19
Q

Supplementing folate (B9) in vitamin B12 deficiency will improve which symptoms of B12 deficiency?

A

Hematologic (megaloblastic anemia)

Folate will NOT have any effect on the neurologic symptoms of B12 deficiency!

20
Q

Will hepcidin be upregulated or downregulated in iron deficiency anemia?

How would this affect ferroportin?

A

Downregulated hepcidin

  • > Ferroportin channel expressed
  • Hepcidin puts the brakes on iron absorption by inhibiting iron transport through ferroprotin (Hepcidin causes degradation of ferroportin)*
21
Q

List 2 functions of ferroportin

A

Iron transport from hepatocytes -> macrophages

Iron absorption from gut enterocytes -> plasma

Inhibited by hepcidin

22
Q

What is the difference between absolute and functional iron deficiency anemia?

A
  • Absolute = truly there is not enough iron in the body
  • Functional = Iron is there, but not available for use
    • Anemia of inflammation
    • Increased EPO (enough iron, but cannot keep up with new demand)
23
Q

What does % saturation measure? (In terms of iron stores)

A

Total iron / iron binding capacity

24
Q

Describe the absorption of B12

A
  • B12 is liberated from binding proteins by gastric acid
  • B12 binds salivary haptocorrin (HC)
  • B12 released from HC by pancreatec proteases
  • B12 binds intrinsic factor (from gastric parietal cells)
  • B12-IF complex is absorbed in the ilium
  • 3-4 years of body stores; malabsorption is more likely than malnutrition*
  • Malabsorption may be caused by low gastric acid, gastric bypass, deficient IF, pancreatic insufficiency, intestinal diseases*
25
Q

Vocabulary review:

  • Ferritin:
  • Transferrin:
  • TIBC:
A
  • Ferritin: Storage form of iron (in macrophages)
  • Transferrin: Transport protein for iron
    • When it’s time to use the iron, ferritin is bound to transferrin and it gets shipped wherever it needs to go
  • TIBC: Total iron binding capacity
    • The amount of iron (ferritin) that the body’s transferrin is capable of binding

Note: As lab values, transferrin and TIBC measure essentially the same thing; transferrin is a direct measurement, and TIBC is an indirect measurement

26
Q

What are the dietary sources of folate?

A

Leafy green vegetables

27
Q

What protein transports iron?

A

Ferroportin

Iron transport through ferroportin is regulated by hepcidin

28
Q

Which protein is the major regulator of iron absorption?

A

Hepcidin

  • Iron is absorbed through ferroportin
  • Hepcidin decides if this happens or not
29
Q

List the symptoms of iron deficiency anemia (4)

A
  • Anemia sx
    • Lightheaded, fatigued, dizzy, difficulty breathing
  • Epithelial depletion sx (cannot replenish)
    • Brittle nails, cracked lips, tongue sensitivity
  • Pica
    • Eating dirt or ice
  • Sx of underlying disease
30
Q

What is pernicious anemia?

How does it affect B12?

A
  • Auto-antibodies destroy gastric parietal cells and intrinsic factor
    • -> Less HCL
    • -> Less intrinsic factor
  • Results in impaired B12 absorption
    • Megaloblastic anemia
    • Subacute combined degeneration