Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

HemOnc > 11 - Nutritional Anemias > Flashcards

11 - Nutritional Anemias Flashcards

1
Q

Iron Functions in the body

A
  • Hemoglobin
  • Myoglobin
  • Cellular enzymes
  • Electron transport (aerobic respiration)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Dietary Iron Sources

A
  • Animal sources - heme; ferrous (2+) iron
  • Liver, mollusks, beef, shrimp, sardines, turkey
  • Plant sources - non-heme; ferric (3+) iron
    -Enriched cereals/pasta, beans, lentils, pumpkin
    seeds, blackstrap molasses
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Iron Absorption

A
  • Absorbed in duodenum and proximal jejunum
  • Enhanced by acidity
  • Ascorbic acid increases the absorption of non-heme
    iron
  • Heme iron is absorbed more efficiently than non-
    heme iron
  • 10-15% of total iron intake is in heme form and 85-
    90% in non-heme.
  • Molecules involved in absorption
  • Heme transporter
  • Duodenal cytochrome B
  • Divalent metal transporter 1 (DMT1)
  • Ferroportin 1
  • Hepcidin
  • Hephaestin
  • Transferrin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Iron Distribution

A
  • Red blood cells – 65%
  • Storage – 30%
  • Myoglobin – 3.5%
  • Enzymes – 0.5%
  • Transferrin-bound – 0.1%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Storage of Iron/Iron carriers in the body

A
  • Ferritin – organized, globular protein complex, readily
    mobilized iron, also in circulation
  • Hemosiderin – disorganized, insoluble, less able to
    mobilized, stain with Prussian blue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Iron Uptake by Cells mechanisms

A
  • Surface transferrin receptors
  • Endocytosis by clathrin-coated pits
  • Release of iron to cytoplasm (DMT1)
  • Recycling of transferrin receptor and transferrin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Iron Deficiency effect

A
  • Interference with heme synthesis
  • Decreased intracellular hemoglobin
  • Microcytic, hypochromic anemia
  • Causes: Chronic bleeding – gyne, GI, GU
    Malabsorption, gastric bypass
    Vegetarian - diet
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Iron Deficiency - Clinical Findings

A
  • Weakness, fatigue, headache, difficulty with
    concentration, angina, myalgias
  • Pica (craving for non-nutritive substances)
  • Brittle nails/hair
  • Atrophic tongue
  • Cheilosis
  • Koilonychia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Sequential Iron Changes

A
  • Iron depletion
  • Iron deficient erythropoiesis
  • Iron deficiency anemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Morphology of Iron Deficiency

A
  • Blood
  • Microcytic, hypochromic anemia
  • Anisopoikilocytosis with ovalocytes, “pencil” cells
  • Low reticulocyte count
  • Bone marrow
    -Poorly-hemoglobinized erythroid precursors with
    “ragged” cytoplasm
  • Absent stainable iron
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Iron deficiency - Laboratory findings

A
  • Iron studies
    – Decreased serum iron
  • Increased total iron binding capacity (TIBC)
  • Decreased % saturation
  • Decreased ferritin (acute phase protein)
  • Increased soluble transferrin receptors
  • Increased free erythrocyte protoporphyrin
  • Increased zinc protoporphyrin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Iron Deficiency Treatment

A
  • Identify source of iron deficiency
  • Oral ferrous iron (ferrous sulfate)
  • every other day
  • correction of CBC in 3 months
  • Continue for 6 months
  • Intravenous iron
  • Only in selected cases (malabsorption, compliance)
  • Risk of allergic reaction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Hereditary Hemochromatosis (HH)

A
  • HFE gene mutation (chromosome 6) (C282Y, H63D)
  • Autosomal recessive
  • 10% Europeans are carriers, 0.25-0.5% affected
  • Other mutations (juvenile hemochromatosis):
  • Hepcidin gene
  • Hemojuvelin gene
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Hereditary hemochromatosis Pathophysiology

A
  • Down regulation of hepcidin synthesis
  • Dysregulation of ferroportin
  • Increased iron absorption and release from storage
    sites
  • Full saturation of transferrin
  • Increased accumulation of parenchymal iron
  • Toxic cell injury
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Hereditary hemochromatosis - Clinical Findings

A
  • Presentation between age 40-60 (men > women)
  • End-organ damage
  • Cirrhosis
  • Bronze diabetes
  • Heart failure
  • Testicular atrophy
  • Amenorrhea
  • Arthropathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Hereditary Hemochromatosis - Lab Findings

A
  • Liver biopsy – increased parenchymal iron (replaced
    by MRI)
  • Iron studies
    – Increased serum iron
  • Decreased total iron binding capacity (TIBC)
  • Increased % saturation
  • Increased ferritin
17
Q

Hereditary Hemochromatosis - Treatment

A
  • Weekly phlebotomy
  • Chelation therapy
  • SQ/IV
    (deferoxamine/Desferal)
  • Oral (Deferiprone/Ferraprox,
    Deferasirox/Exjade, Jadenu)
18
Q

Hemosiderosis

A
  • Secondary iron overload
  • Multiple transfusions (250 mg iron per unit)
  • Chronic alcohol use
  • Ineffective erythropoiesis (thalassemia major)
  • Iron accumulates in macrophages and Kupffer cells
    (rather than parenchymal cells)
  • Less cell toxicity and organ damage
19
Q

Anemia of Chronic Disease (ACD)

A
  • Chronic inflammatory, infectious, or neoplastic
    disease
  • Upregulation of hepcidin (acute phase protein)
  • interferes with iron release from cells
  • “functional” iron deficiency
  • Blunted erythropoietin synthesis
  • Impaired erythropoietin binding to erythroid
    precursors
20
Q

Anemia of Chronic Disease - Laboratory findings

A
  • Mild-moderate normocytic/microcytic anemia
  • Normal red cell morphology (normal RDW)
  • Iron studies
    – Decreased serum iron
  • Decreased total iron binding capacity (TIBC)
  • Decreased normal % saturation (variable)
  • Increased ferritin
  • Increased C-reactive protein and sedimentation rate
21
Q

difference between anemia of chronic disease and iron-deificiency anemia

A
22
Q

Sideroblastic Anemia - appearance and basis

A
  • Ringed sideroblasts
  • Impaired iron incorporation into heme

-Abnormal erythroid precursors with excess iron in
mitochondria

  • Perinuclear “ring-like” distribution
23
Q

Sideroblastic Anemia - genetic and acquired

A
  • Inherited
  • δ-aminolevulinate synthase 2 (heme synthesis)
  • Acquired
  • Chronic alcohol use
  • Pyridoxine deficiency
  • Lead poisoning
  • Copper deficiency
  • Drugs (isoniazid, chloramphenicol)
  • Myelodysplastic syndromes
24
Q

Sideroblastic Anemia - Laboratory Findings

A
  • Moderate-severe microcytic anemia
  • Dimorphic red cell population
  • Basophilic stippling, Pappenheimer bodies
  • Iron studies
    – Increased serum iron
  • Decreased total iron binding capacity (TIBC)
  • Increased % saturation
  • Increased ferritin
25
Q

Sideroblastic Anemia Treatment

A
  • High dose pyridoxine (some cases respond)
  • Transfusion support
  • Bone marrow/stem cell transplant (congenital cases)
26
Q

B12 and folic acid

A
  • Prevalence of B12 deficiency is 1-2% in the general population and 10-15% in older and
    hospitalized people.
  • Total body stores of vitamin B12 are in the range of 2 to 5 mg, with approximately half of this
    stored in the liver. If vitamin B12 intake or absorption ceases, deficiency typically does not
    develop for at least one to two years, sometimes longer.
  • Folate acid deficiency is uncommon in people eating a varied diet and is added to many
    prepared foods.
  • Total body folate stores are estimated to be approximately 500 to 20,000 mcg (0.5 to 20 mg).
    If folate intake ceases, deficiency may develop within weeks to months, or more rapidly if
    demands for folate are increased.
  • Testing includes: CBC and smear, serum B12 and folate levels to start.
  • Autoantibodies to intrinsic factor – obtain if no other cause for deficiency, as the diagnosis of
    pernicious anemia
  • Consider MMA (methyl malonic acid) and homocysteine for patients whose initial tests are
    borderline .
    MMA and homocysteine NML – no deficiency
    MMA and homocysteine elevated – B12 deficient but does not exclude folate deficiency
    MMA NML and homocysteine elevated – folate deficiency
27
Q

cobalamin processing in the body

A
28
Q

methionine and folate cycle

A
29
Q

B12, methylmalonic acid, and folic acid

A
30
Q

causes of b12 deficiency

A
31
Q

causes of folic acid deficiency

A
32
Q

Changes in erythrocytes with B12 or folate deficiency - megaloblastic

A
33
Q

treatment of b12 deficiency in adults

A
34
Q

treatment of folic acid deficiency

A

Give the patient 1-5 mg PO daily
Tell them to eat a better diet

(bean, eggs, and leafy greens)

HemOnc (29 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions