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Hematology > Disorders of Iron Metabolism > Flashcards

Disorders of Iron Metabolism Flashcards

1
Q

Anemia

  • Definition
  • Causes
A
  • Anemia is when RBCs aren’t supplying enough oxygen to body

- Causes include decreased production of RBC or increased loss.

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2
Q

Hypoproliferative Anemia

A
  • Decreased production of RBC
  • Causes include: Nutritional deficiency, Bone marrow replacement, Stem cell arrest or damage, and Hereditary or acquired defect
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3
Q

Causes of increased loss of RBC

A
  • Blood loss

- Accelerated destruction

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4
Q

Patient History that effects Anemia

A
  • When anemia began? (Congenital or Acquired )
  • Severity of symptoms (Mild - Severe)
  • Chronic blood loss?
  • Hemolysis?
  • Neurologic symptoms
  • Underlying disease
  • Prior anemia or therapy
  • Medications, drugs, toxins
  • Dietary history
  • Family history
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5
Q

Physical Exam of Anemia

A 
Skin: pallor, jaundice, petechiae
Mouth: smooth tongue
Heart: cardiac dilatation
Abdominal: splenomegaly
Lymph nodes
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6
Q

Initial Lab testing of Anemia

A
  • CBC
  • Differential
  • Reticulocyte count
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7
Q

Classification of anemia

A

2 types:

  1. Functional - PA uses this.
  2. Morphologic - we in the lab do this.
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8
Q

Functional Classification of anemia

A
  • Maturation: Cytoplasmic, Nuclear
  • Hypoproliferative: Decreased EPO, Iron Depletion, Marrow damage
  • Hemolysis or hemorrhage
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9
Q

Morphologic Classification of anemia

A
  • Microcytic
  • Normocytic
  • Macrocytic
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10
Q

Microcytic Anemia

A

Most common anemia

  • Iron deficiency
  • Anemia of chronic inflammation
  • Thalassemia/ Some Hemoglobinopathies
  • Anemia of chronic blood loss
  • Sideroblastic anemia: Lead poisoning, Porphyrias
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11
Q

Normocytic Anemia

A
  • Acute blood loss
  • Hemolysis
  • Bone marrow failure
  • Dyserythropoiesis
  • Infection
  • Malignancy
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12
Q

Macrocytic Anemia

A
  • Megaloblastic anemia: B12/Folate Deficiency, Myelodysplastic syndromes, Medication or chemotherapy
  • Marked reticulocytosis
  • Liver disease
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13
Q

Peripheral blood smear with anemia

A
  • Coexisting leukopenia or thrombocytopenia (decrease in WBC and Platelets)
  • Size and shape of RBC
  • RBC inclusions
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14
Q

Bone Marrow Examination

A
  • used to compare with the PBS, but is usually used in WBC disorders.
  • Maturation of RBC and WBC
  • Presence of megakaryocytes
  • M:E Ratio
  • Iron stores
  • Presence of abnormal elements
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15
Q

Disorders of Iron and Heme Metabolism

A
  • Iron Deficiency
  • Anemia of Chronic Inflammation
  • Sideroblastic Anemias: Lead poisoning, Porphyrias
  • Iron Overload
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16
Q

Normal Iron Metabolism

A
  • Total body iron is 3 - 4 g
  • More than 2/3 is contained within the RBC
  • Each mL of blood contains 1 mg of Fe
  • Ten to twenty times more Fe is used in RBC production than is absorbed each day
  • Most comes from RBC degradation: Transferrin carries Fe from macrophages in spleen to bone marrow
17
Q

Iron Absorption

A
  • Hepcidin: peptide produced by the liver regulates iron absorption.
    Hepcidin functions:
    1. Signal that limits intestinal iron absorption.
  • Increased levels – iron deficiency
  • Decreased levels – iron overload
    2. Inhibits iron release from hepatic stores
18
Q

Iron Deficiency causes

A
  1. Increased need: Pregnancy, Growth spurts
  2. Increased loss: Menstruation, Chronic bleeding
  3. Decreased intake (diet)
19
Q

Stages of Iron Depletion

A

Stage 1. Ferrotin decreases
Stage 2. Serum iron decreases and TIBC increases with the decreased Ferritin
Stage 3. Hemaglobin decreases with the above.

20
Q

Clinical Signs of Iron Deficiency

A
  • Fatigue
  • Pallor
  • Koilonychia
  • Craving unusual foods – ice, clay, starch, pickles
  • Pica
21
Q

Pica

A
  • craving unusual non-food material for iron
22
Q

Lab Values of Iron Deficiency

A
  • Absence of stainable iron stores (hemosiderin)
  • Hemoglobin <10 g/dL
  • Microcytic (first), hypochromic
  • Increased RDW
23
Q

Treatment of Iron Deficiency

A
  • Treat underlying disorder
  • Iron supplements: Retic counts begin rising in 5-10 days, Hemoglobin rises in 2-3 weeks
  • Nutritional counseling: Lean meats, eggs, whole grains, green leafy vegetables, legumes
24
Q

Anemia of Chronic Disease

A
  • Anemia that occurs in patients with chronic infections, inflammation or neoplastic disorders
  • Cytokine inhibition of EPO production with impaired erythropoiesis
  • Impaired release of iron from macrophages
  • Mild anemia, normo to microcytic, normo to hypochromic
  • Anemia precedes microcytosis
  • Iron studies: Plasma iron - decreased; TIBC - decreased: Ferritin - normal or increased
25
Q

Hepcidin in Anemia of Chronic Disease

A
  • Explains error in ferrokinetics: Decreased serum iron with abundant iron stores.
  • Hepcidin is an acute phase reactant
  • Levels increase in inflammation: Decrease in iron absorption in intenstine. Decreased iron release from macrophages.
26
Q

Sideroblastic Anemia

A
  • Diseases that interfere with heme production
  • Increase in total body iron
  • Ringed sideroblasts in bone marrow
  • *Dimorphic RBC population: Normochromic and hypochromic
27
Q

Heredity and Acquired Sideroblastic Anemia

A

Hereditary:

  • Sex-linked disorder affecting men
  • Due to decreased activity of ALA synthetase
  • About 50% respond to Vitamin B6

Acquired:

  • Refractory anemia with ringed sideroblasts – stem cell disorder
  • Secondary to drugs or toxins – interference: Lead, Alcohol - inhibition of B6
  • Malignancy - abnormal stem cells
28
Q

Lead Poisoning

A
  • Inhibition of heme synthesis by accumulated lead: ALA dehydrase and heme synthetase
  • Interferes with iron storage
  • Microcytic, hypochromic anemia?? May indicate concommitant disorder
  • Coarse basophilic stippling
29
Q

Porphyrias

A
  • Disease characterized by impaired heme production
  • Many caused by deficiencies of enzymes on heme synthetic pathway:
    • Causes accumulation of products from earlier stages
  • Causes sideroblastic anemia
30
Q

Hemochromatosis

A
  • Hereditary disorder – autosomal recessive
  • HFE gene linked to class I HLA
  • Deposition of Fe in organ tissues: Pancreas, liver, spleen
  • Iron release into the plasma affected by hepcidin levels
  • “Bronze diabetes” skin discolorization due to Fe related fibrosis of the pancreas
  • Treatment – therapeutic removal of Fe through phlebotomy or chelation therapy

Hematology (20 decks)

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