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Liz's Hematology Module 1 > N/N Anemias > Flashcards

N/N Anemias Flashcards

1
Q

Aplastic anemia

  • Common cause
A

Idiopathic (unknown cause)

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2
Q

Aplastic anemia

  • 4 secondary causes
A
  • Chemicals (benzene, arsenic, insecticides, weed killers)
  • Drugs (chloramphenical)
  • Radiation (long term, low dose)
  • Infections, esp. chronic ( Hepatitis C, EBV, CMV, HIV)
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3
Q

Aplastic anemia

  • Name of most comon congenital disorder associated w/ it
A

Fanconi’s anemia

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4
Q

Aplastic anemia

  • BM cellularity
A

Hypocellular

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5
Q

Aplastic anemia

  • CBC
A
  • WBC < 1500/cumm
  • ↓ RBC
  • Hb < 7 g/dL
  • ↓ Hct
  • ↓ PLT
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6
Q

Aplastic anemia

  • Characteristic RBC morphology
A

None, just few present

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7
Q

Aplastic anemia

  • Retic count
A

Decreased to absent

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8
Q

Aplastic anemia

  • Treatment
A
  • Take away offending agent, if applicable
  • “support” therapy as needed (antibiotics, blood products esp. plts, use of growth factors)
  • immunosuppressive therapy to stimulate BM
  • Only cure is BM transplant
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9
Q

Type of poik found in most every hemoglobinopathy

A

Sickle cells

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10
Q

Amino acid substitution found in sickle cell anemia

A

Glutamic acid replaced by valine

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11
Q

3 factors contributing to sickling process

A
  • Hypoxia
  • Acidosis
  • Dehydration
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12
Q

Sickle cell anemia

  • Cause of “painful crises”
A

Tissue damage from hypoxia

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13
Q

Sickle cell anemia

  • Cause of “acute chest syndrome”
A

Infarction of organs

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14
Q

Sickle cell anemia

  • Cause of high risk of infections
A

Splenomegaly to autosplenectomy

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15
Q

Sickle cell anemia

  • Inheritance
A

Abnormal gene from both parents

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16
Q

Sickle cell anemia

  • Hemoglobin nomenclature
A

SS

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17
Q

Sickle cell anemia

  • Solubility (Sickledex) results
A

Hemoglobin S is insoluble → precipitates in solution = turbid (+)

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18
Q

Sickle cell anemia

  • Hemoglobin electrophoresis results
A

S > F (no A)

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19
Q

Sickle cell anemia

  • RBC morphology
A
  • Poik → “targets plus” sickles, schistos, spheres
  • Polychromasia (increased retic count)
  • RBC inclusions → H-J bodies, Pappenhemier
  • nRBCs
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20
Q

Sickle cell anemia

  • Treatment
A
  • Adequate hydration
  • Pain relief from crises (morphine)
  • Antibiotics
  • Blood transfusions
  • Hydroxyurea to increase hemoglobin F…relieve sickling
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21
Q

Sickle cell trait

  • Inheritance
A

Abnormal gene from one parent

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22
Q

Sickle cell trait

  • Hemoglobin nomenclature
A

AS

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23
Q

Sickle cell trait

  • Solubility (Sickledex) results
A

Hemoglobin A is soluble = solution remains clear (-)

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24
Q

Sickle cell trait

  • Hemoglobin electrophoresis results
A

A > S

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25
Q

Sickle cell trait

  • RBC morphology
A
  • Slight targets
  • No sickles (treatment may occur under severe hypoxic states)
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26
Q

Sickle cell trait

  • Treatment
A

No treatment necessary

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27
Q

Sickledex solubility (screening) test

  • Principle
A

Blood added to buffered solution of reducing agent

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28
Q

Sickledex solubility (screening) test

  • Reducing agent
A

Sodium dithionite or sodium metabisulfite

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29
Q

Sickledex solubility (screening) test

  • Causes for false positive results
A
  • Proteinemia
  • > 18 g/dL hemoglobin
  • Other sickling hemoglobins
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30
Q

Sickledex solubility (screening) test

  • Causes for false negative results
A
  • Testing a newborn
  • < 7 g/dL hemoglobin
  • Multiple transfusions
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31
Q

Amino acid substitution found in hemoglobin C disease

A

Glutamic acid substituted w/ lysine

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32
Q

Hemoglobin C disease

  • Clinical presentation
A

Mildly hemolytic anemia

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33
Q

Hemoglobin C disease

  • Hemoglobin nomenclature
A

CC

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34
Q

Hemoglobin C disease

  • Hemoglobin electrophoresis results
A

100% C (no A)

35
Q

Hemoglobin C disease

  • RBC morphology
A
  • Poik → “targets plus” C crystals
  • Polychromasia (increased retic count)
36
Q

Hemoglobin C trait

  • Clinical presentation
A

Asymptomatic

37
Q

Hemoglobin C trait

  • Hemoglobin nomenclature
38
Q

Hemoglobin C trait

  • Hemoglobin electrophoresis results
39
Q

Hemoglobin C trait

  • RBC morphology
A

Targets only

40
Q

Hemoglobin SC disease

  • Inheritance
A
  • Lysine substitution (C) from one parent
  • Valine substitution (S) from the other
41
Q

Hemoglobin SC disease

  • Clinical presentation
A

Less severe than sickle cell disease (SS), but still mild-moderately (severe) hemolytic anemia w/ painful crises

42
Q

Hemoglobin SC disease

  • Hemoglobin electrophoresis results
43
Q

Hemoglobin SC disease

  • RBC morphology
A
  • Poik → “targets plus” sickles, C crystals, and SC crystals
  • Polychromasia (increased retic count)
  • RBC inclusions (H-J bodies, Pappenheimer)
  • nRBCs
44
Q

Sickle cell ß thal

  • Inheritance
A
  • Valine substitution from one parent
  • ß0 or ß+ from the other
45
Q

Sickle cell ß thal

  • Clinical presentation (sickle ß0 thal vs. sickle ß+ thal)
A
  • ß0 → severe hemolytic anemia
  • ß+ → mild to moderate hemolytic anemia
46
Q

Sickle cell ß thal

  • Hemoglobin electrophoresis results (sickle ß0 thal vs. sickle ß+ thal)
A
  • ß0 → S > F (↑) > A2 (↑) w/ no A
  • ß+ → S > A > F (↑) > A2 (↑)
47
Q

Sickle cell ß thal

  • RBC morphology (sickle ß0 thal vs. sickle ß+ thal)
A
  • ß0 and ß+ → “targets plus” sickles (sickles may be absent w/ mild ß+), schistos, spherocytes, nRBCs
48
Q

2 ways that hemoglobin D may be differentiated from hemoglobin S since they both migrate to the same point on cellulose acetate electrophoresis

A
  • Solubility testing (hemoglobin D will be negative)
  • Citrate (acid) electrophoresis
49
Q

World’s third most common abnormal hemoglobin (behind Hb S and Hb C) and indicate the geographic ara in which it commonly occurs

A
  • Hemoglobin E
  • Common in SE Asia
50
Q

Physiological mechanism for predominant type of poik found in hereditary spherocytosis

A

↓ spectrin causes ↑ permeability of sodium into cell

51
Q

Physiological mechanism for predominant type of poik found in hereditary elliptocytosis

A

↓ cholesterol in cell membrane causes Hb to polarize to opposite ends

52
Q

Physiological mechanism for predominant type of poik found in hereditary stomatocytosis

A

Defect in NaK-ATPase pump → ↓ Na+ in and ↑ K+ out → abnormal slit-like pallor

53
Q

Hereditary spherocytosis

  • Clinical presentation
A

Anemia, jaundice, splenomegaly

54
Q

Hereditary spherocytosis

  • RBC indices
A
  • ~12 g/dL hemoglobin
  • MCHC = 36-38%
55
Q

Hereditary spherocytosis

  • RBC morphology
A
  • Variable # in spheres
  • Polychromasia (increased retic count)
56
Q

Osmotic fragility test

  • Principle
A

Blood is added to series of hypotonic salt solutions, beginning and completion of hemolysis are noted

57
Q

Osmotic fragility

  • Conditions that show “increased osmotic fragility”
A

Hereditary spherocytosis

58
Q

Osmotic fragility test

  • Conditions that show “decreased osmotic fragility”
A
  • Thalassemia
  • Sickle cell anemia
  • Any hypochromic anemia
59
Q

Osmotic fragility test

  • Conditions that show “decreased resistance to hemolysis”
A

Hereditary spherocytosis

60
Q

Osmotic fragility test

  • Conditions that show “increased resistance to hemolysis”
A
  • Thalassemia
  • Sickle cell anemia
  • Any hypochromic anemia
61
Q

Osmotic fragility test

  • NaCl concentration when hemolysis should begin (in a normal person)
A

0.45-0.5% NaCl

62
Q

Osmotic fragility test

  • NaCl concentration when hemolysis should be completed (in a normal person)
A

0.3-0.35% NaCl

63
Q

Type of poik that demonstrates greatest resistance to hemolysis

A

Target cells, hypochromic sickles

64
Q

Expected results that occur w/ any hemolytic anemia

  • Plasma haptoglobin
65
Q

Expected results that occur w/ any hemolytic anemia

  • Retic count
66
Q

Expected results that occur w/ any hemolytic anemia

  • Serum bilirubin
67
Q

G-6-PD deficiency

  • Result of deficient enzyme
  • Type of poik or inclusion bodies present
  • Triggering factor
A
  • Glutathione is not reduced
  • Heinz bodies, bite cells
  • Administration of new drug, infection, ingestion of fava beans, ingestion of moth balls
68
Q

PK deficiency

  • Result of deficient enzyme
  • Type of poik or inclusion bodies present
  • Triggering factor
A
  • Decreased capacity to generate ATP
  • Burr cells
  • Triggering factors?
69
Q

Methemoglobin reductase deficiency

  • Result of deficient enzyme
  • Type of poik or inclusion bodies present
  • Triggering factor
A
  • Increased levels of methemoglobin
  • Poik?
  • Triggering factors?
70
Q

Paroxysmal Nocturnal Hemoglobinuria (PNH)

  • Etiology
A
  • Causes cells, esp. RBCs, to be more sensitive than normal to lytic action of complement (in an acid environment)
71
Q

Paroxysmal Nocturnal Hemoglobinuria (PNH)

  • Clinical presentation
A
  • “sleep-induced hemolytic anemia” → bloody first morning urine, clears throughout day
72
Q

Paroxysmal Nocturnal Hemoglobinuria (PNH)

  • CBC
A

Pancytopenia

73
Q

Paroxysmal Nocturnal Hemoglobinuria (PNH)

  • RBC morphology
74
Q

Paroxysmal Nocturnal Hemoglobinuria (PNH)

  • Ham’s test results
75
Q

Principle of Ham’s test

A

Due to intrinsic membrane defect, PNH red cells are more sensitive to lysis by complement. A pH of 6.7-7.0 and 37°C provide optimum conditions for complement activation via alternate pathway and subsequent lysis fo PNH red cells

76
Q

3 conditions that may cause an alloimmune hemolytic anemia to develop

A
  • Transfusions
  • Pregnancy (HDFN)
  • Organ transplantation
77
Q

Abnormality in immune system whereby the ability for self-recognition of an individual’s own red cell Ags is lost

A

Autoimmune hemolytic anemia

78
Q

Abs produced by one individual react w/ Ags of another individual

A

Alloimmune hemolytic anemia

79
Q

Cold agglutinin

  • Alloimmune vs. autoimmune
A

Cold autoimmune

80
Q

Cold agglutinin

  • CBC results
A

↓ RBC, Hb, Hct

↑ MCV and RDW

81
Q

Cold agglutinin

  • RBC morphology
A

Clumping of RBCs due to IgM Ab

82
Q

Ab associated with paroxysmal cold hemoglobinuria

83
Q

2 disorders commonly associated w/ microangiopathic hemolytic anemia (MAHA)

A
  • Hemolytic uremic syndrome (HUS)
  • Thrombotic thrombocytopenic purpura (TTP)
  • Disseminated intravascular coagulation (DIC)
84
Q

Predominant type of poik found in MAHA

A

Schistocytes

Liz's Hematology Module 1 (15 decks)

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