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Bood and Lymph > Anemias > Flashcards

Anemias Flashcards

1
Q

What are the four types of microcytic anemias?

A
  • Iron deficiency anemia
  • Anemia of chronic disease
  • Sideroblastic anemia
  • Thalassemias
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2
Q

What are the lab findings associated with iron deficiency anemia?

A
  • Low ferritin / high TIBC
  • Low serum iron and low iron saturation
  • High FEP
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3
Q

What are the lab findings associated with anemia of chronic disease?

A
  • High ferritin / low TIBC
  • Low serum iron and low iron saturation
  • High FEP
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4
Q

What are the lab findings associated with sideroblastic anemia?

A
  • High ferritin / low TIBC

- High serum iron and high iron saturation

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5
Q

What are the different causes of sideroblastic anemia?

A
  • Congenital (ALAS)
  • Alcoholics (mitochondria)
  • B6 deficiency (ALAS)
  • Lead poisoning (ALAD and ferrochelatase)
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6
Q

What is sideroblastic anemia? and how can it be identified on bone marrow smear?

A
  • Disruption in pathway of porphyrin synthesis and fusion to Fe to make heme.
  • Prussian-blue stain will display ring sideroblasts (iron accumulation in mitochondria in ring around nucleus).
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7
Q

What are the different types of alpha thalassemias?

A
  • Single deletion: asymptomatic
  • Double deletion: asymptomatic or mild anemia slightly increased RBC count, cis- more severe due congenital transmission- asians, trans- african americans
  • Triple deletion- severe anemia, HbH (B tetramer)–> destruction of RBC.
  • 4 deletions- lethal (hydrops fetalis), Hb Barts (gamma tetramer)
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8
Q

What are the different types of hemoglobin?

A
  • Hb A- A2B2
  • Hb F- A2G2
  • Hb A2- A2 D2
  • Hb H- B4
  • Hb Barts- G4
  • A4
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9
Q

What are the two main types of B thalassemias?

A
  • B thalassemia minor- B/B+, asymptomatic with increased RBC count, target cells on blood smear due to decreased cytosolic volume from reduced hemoglobin. elevated Hb A2
  • B thalassemia major- B0/B0, on set a few months after birth, ineffective erythropoiesis and extravascular hemolysis, extramedually hematopoiesis (HSM), expanded bone marrow into skull (crew cut) and face (chipmunk cheeks), aplastic crisis with parvo B19. Require transfusions–> secondary hemachromatosis risk. blood smear with target cells and nucleated RBC’s (production of RBC outside marrow).
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10
Q

What are the two types of macrocytic anemia?

A
  • Folate
  • Vitamin B12 deficiency
  • Alcoholism
  • Liver disease
  • Drugs (5-FU)
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11
Q

What causes megaloblastic anemia?

A
  • DNA synthesis impairment
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12
Q

What are the lab findings for folate deficiency?

A
  • Macrocytic anemia
  • Hypersegmented neutrophils
  • Glossitis
  • Decreased serum folate
  • Increased homocysteine (increase risk thrombosis)
  • Normal methylmalonic acid
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13
Q

What are the findings for B12 deficiency?

A
  • Macrocytic anemia
  • Hypersegmented neutrophils
  • Glossitis and subacute spinal cord degeneration
  • Decreased serum B12
  • Increased homocysteine (increase risk thrombosis)
  • Increased methylmalonic acid
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14
Q

What are the different causes of vitamin B12 deficiency?

A
  • Pernicious anemia
  • Pancreatic insufficiency
  • Crohn’s and Diphyllobothrium Latum
  • Dietary (vegans)
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15
Q

Where are folate and B12 absorbed?

A
  • Duodenum

- Ileum

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16
Q

What are the common laboratory findings shared by intra and extravascular hemolysis?

A
  • Anemia, splenomegaly and jaundice caused by increase in unconjugated bilirubin as well as increased risk of bilirubin gallstones.
  • Bone marrow hyperplasia.
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17
Q

What are the findings unique to intravascular hemolysis?

A
  • Hemoglobinemia
  • Hemoglobinuria
  • Hemosiderinuria
  • Decreased free haptoglobin
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18
Q

What diseases are predominantly extravascular hemolysis normocytic anemias?

A
  • Hereditary spherocytosis
  • Sickle cell anemia
  • Hemoglobin C
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19
Q

Defects in which proteins cause hereditary spherocytosis?

A
  • Spectrin
  • Ankyrin
  • Band 3.1
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20
Q

What are the clinical and laboratory findings in hereditary spherocytosis?

A
  • Spherocytes with loss of central pallor on peripheral blood smear.
  • High RDW and MCHC
  • Anemia, jaundice and increase risk of gallstones and splenomegaly.
  • Increased risk of aplastic crisis with Parvovirus B19 infection.
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21
Q

How is hereditary spherocytosis diagnosed?

A
  • Osmotic fragility test
22
Q

How is hereditary spherocytosis treated and what would you see on blood smear following treatment?

A
  • Splenectomy

- Howell-Joley bodies due to the absence of spleen which normally removes them.

23
Q

What is the genetic cause sickle cell anemia?

A
  • Mutation in the B globulin chain of one (trait) or both alleles (disease). The mutation is the replacement of a glutamic acid (hydrophilic) with valine (hydrophobic).
24
Q

What environmental factors cause cell sickling?

A
  • Hypoxia, dehydration and acidosis

- Only when >50% HbS

25
Q

What are the clinical and lab findings of sickle cell?

A
  • Anemia, jaundice and increase risk of gallstones.
  • Increased risk of aplastic crisis with Parvovirus B19 infection.
  • Decrease haptoglobin due to intravascular hemolysis.
  • Massive erythroid hyperplasia leading to hematopoiesis expansion into skull, facial bones and liver (hepatomegaly)
26
Q

What are the complications with sickle cell induced vaso-occlusion?

A
  • Dactylitis- infarcts in bones of hands and feet, common in infants
  • Autosplenectomy- Shrunken, fibrotic spleen.
  • Acute chest syndrome- occlusion of pulmonary microcirculation. Common after infection. Chest pain, SOB, lung infiltrates.
  • Pain crisis
  • Renal papillary necrosis- Hematuria, and proteinuria.
27
Q

What is primary concern for patients with sickle cell trait?

A
  • Hypoxia and hypertonicity in the renal medulla induce sickling–> mircoinfarctions–> hematuria and eventually in ability to concentrate urine.
28
Q

How can sickle trait and disease be tested for?

A
  • Metabisulfite screen
  • Hb electrophoresis- disease (90%), trait (45%)
  • Blood smear shows sickle cells and target cells in sickle cell disease only.
29
Q

What is the genetic cause and features of hemoglobin C?

A
  • B globin glutamic acid replaced with lysine (rather than valine in sickle)
  • Mild anemia with characteristic crystals on blood smear.
30
Q

What are the primarily intravascular normocytic anemias?

A
  • Paroxysmal nocturnal hemoglobinuria (PNH)
  • G6PD deficiency
  • Immune hemolytic anemia (IHA)
  • Microangiopathic hemolytic anemia
  • Malaria
31
Q

What is the cause of PNH?

A
  • Acquired myeloid defect in GPI resulting in the absence decay accelerating factor (DAF) on the surface of RBC. Absence of DAF allows C3 and complement activation resulting in the intravascular destruction of RBC. This occurs especially at night when shallow breathing produces blood acidosis and induction of complement. RBC, WBC and platelets are lysed.
32
Q

How is PNH tested for?

A
  • Sucrose test for sceening

- Acidified serum or flow cytrometry for CD55 (DAF)

33
Q

What are the complications of PNH?

A
  • Iron deficiency anemia

- Acute myeloid leukemia (10%)

34
Q

What is the most common cause of death in PNH?

A
  • Thrombosis of hepatic, portal or cerebral veins. Due to destroyed platelets release of cytoplasmic contents.
35
Q

What is the cause of hemolysis in G6PD deficiency?

A
  • X-linked disorder
  • Reduced half-life of G6PD–> reduced NADPH–> reduced Glutathione–> increased oxidative stress of H2O2–> hemolysis in circulation.
36
Q

What are the two variants of G6PD deficiency?

A
  • African (mild)
  • Mediterranean
  • Both protect against malaria
37
Q

What are the laboratory features of G6PD?

A

Smear shows

  • Heinz bodies (precipitated hemoglobin) can be seen with stain.
  • Bite cells
38
Q

What causes of oxidative stress?

A
  • Infections, drugs, and fava beans
39
Q

How does the patient present with G6PD deficiency?

A
  • Hemoglobinuria and back pain hours after exposure to oxidative stress.
40
Q

How is G6PD tested for?

A
  • Heinz prep for screening

- Enzyme study to confirm, must be performed weeks after episode.

41
Q

What are the 2 types of immune hemolytic anemia?

A
  • IgG (warm agglutinin)

- IgM (cold agglutinin)

42
Q

What are the causes of warm agglutinin IHA?

A
  • SLE, CLL and drugs (penicillin, cephalosporin, alpha- methyldopa (induce production of auto antibody))
43
Q

What is IgM IHA associated with?

A
  • Mycoplasma pneumonia

- Infectious mononucleosis

44
Q

What is the difference between direct and indirect Coombs tests?

A
  • Direct - Confirms antibodies on surface of RBC’s.

- Indirect - Confirms antibodies in serum

45
Q

What are the anemias due to under production?

A
  • Parvo B19
  • Aplastic anemia
  • Myelophthisic process (metastatic cancer)
46
Q

What causes Parvo B19 anemia?

A
  • Infection of progenitor cells in bone marrow halts production of RBC
  • Worse when combined with other marrow stress (I.E. sickle cell)
47
Q

What is the treatment for IgG IHA?

A
  • Cessation of drug
  • Steroids
  • IVIG
  • Splenectomy last resort
48
Q

What is the pathology of aplastic anemia?

A
  • Destruction of hematopoietic stem cells–> pancytopenia (anemia, thrombocytopenia and leukopenia) with low production of reticulocytes.
49
Q

What are the potential causes of aplastic anemia?

A
  • Drugs or chemicals, viral, autoimmune damage.
50
Q

What would a bone marrow biopsy reveal in a patient with aplastic anemia?

A
  • Empty, fatty marrow.
51
Q

What are the treatment for aplastic anemia?

A
  • Transfusions
  • Bone marrow stimulating factors (EPO, GM-CSF, G-CSF)
  • Immunosuppressants
  • Bone marrow transplant

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