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HEM Exam 1 > Hemolytic Anemias > Flashcards

Hemolytic Anemias Flashcards

1
Q

definition of hemolytic anemias

A
  • a group of disorders characterized by decreased red cell lifespan
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2
Q

normal red cell lifespan

A
  • 120 days
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3
Q

severity of anemia depends on

A
  • ability of bone marrow to compensate
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4
Q

clinical features of hemolytic anemia

A
  • jaundice
  • dark urine
  • pigmented gallstones
  • chronic ankle ulcers
  • splenomegaly
  • requirement for folate

FAP DJS - He (hemolytic) a DJ who Faps

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5
Q

yellowing of sclera called

A
  • scleral icterus
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6
Q

jaundice is

A
  • more generalized yellow discoloration of tissues
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7
Q

what do you want to make sure to do before a splenectomy?

A
  • vaccinate against encapsulated organisms

- spleen required to kill off encapsulated organisms

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8
Q

post-splenectomy blood findings

A
  • Howell-jolly bodies
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9
Q

parvovirus B19 affect on blood cels

A
  • infects and lyses and destroys RBCs in marrow

- causes 7-10 day halt to erythropoiesis

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10
Q

parvovirus B19 in patients with hemolytic anemias

A
  • loss of red cell production causes reticulocyte count and hemoglobin to plummet dramatically
  • aplastic crisis
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11
Q

hemolytic anemias classification schemes

A
  • sites of red cell destruction
  • acquired vs. congenital
  • mechanism of red cell damage
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12
Q

sites of RBC destruction

A
  • extravascular hemolysis

- intravascular hemolysis

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13
Q

extravascular hemolysis

A
  • macrophages in spleen, liver, and marrow removed damaged or antibody-coated red cells
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14
Q

intravascular hemolysis

A
  • red cells rupture within the vasculature, releasing free hemoglobin into the circulation
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15
Q

laboratory evidence for hemolysis

A
  • evidence for increased RBC production

- evidence for increased RBC destruction

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16
Q

evidence for increased RBC production in the blood

A
  • elevated reticulocyte count
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17
Q

evidence for increased RBC production in the bone marrow

A
  • erythroid hyperplasia
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18
Q

evidence for increased RBC production in the bone

A
  • deforming changes in the skull and long bones

- frontal bossing

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19
Q

erythroid hyperplasia

A
  • reduced myeloid/erythroid ratio

- WAY more erythroids

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20
Q

frontal bossing caused by

A
  • increased erythropoietic activity

- marrow space expansion

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21
Q

evidence for increased RBC destruction

A
  • biochemical consequences of hemolysis
  • morphological evidence of RBC damage
  • reduced red cell lifespan
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22
Q

biochemical consequence of hemolysis in general

A
  • elevated LDH levels

- elevated bilirubin

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23
Q

LDH levels high due to

A
  • lysis of any cells
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24
Q

bilirubin is a byproduct of

A
  • heme breakdown
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25
Q

when bilirubin is fractionated, the portion that is elevated is the

A
  • unconjugated bilirubin
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26
Q

biochemical consequences of intravascular hemolysis

A
  • reduced serum haptoglobin
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27
Q

most common hemolytic anemia due to membrane skeleton defects

A
  • hereditary spherocytosis
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28
Q

hereditary spherocytosis defect in

A
  • tethering proteins of membrane skeleton

- ankyrin

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29
Q

lipid microvesicles in heredity spherocytosis

A
  • pinched off in the spleen
  • causes decreased MCV
  • and spherocytic change (spherocytes are engulfed by macrophages which causes the anemia)
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30
Q

hereditary spherocytosis genetic pattern

A
  • autosomal dominant
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31
Q

hereditary spherocytosis patients with trivial infections will develop

A
  • increased hemolysis

- abdominal pain

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32
Q

hereditary spherocytosis and MCHC

A
  • MCHC will be elevated

- ONLY TIME WE CARE ABOUT THIS

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33
Q

hereditary spherocytosis diagnosed by

A
  • osmotic fragility - lysis occurs at higher tonicities
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34
Q

hereditary spherocytosis and parvovirus B19

A
  • causes aplastic crises
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35
Q

hereditary spherocytosis treatment

A
  • folate supplementation

- splenectomy to resolve anemia

36
Q

what cells remain after splenectomy in hereditary spherocytosis

A
  • spherocytes because the cell will still bleb
37
Q

what do RBCs require to maintain biconcave disc shape and hemoglobin in reduced form?

A
  • constant energy
38
Q

what happens if RBC don’t have energy

A
  • they lyse

- or deform

39
Q

two sources of energy for RBCs

A
  • anaerobic glycolysis (Embden-Myerhof pathway)

- aerobic pathway (PPP - G-6-PD)

40
Q

purpose of G-6-PD

A
  • make NADPH and glutathione
41
Q

role of NADPH and glutathione

A
  • detox metabolites of oxidative stress
  • elimination of methemoglobin
  • glutathione neutralizes oxidative metabolites
  • NADPH regenerates glutathione
42
Q

in absence of adequate reducing ability, what will happen to hemoglobin

A
  • will be converted to methemoglobin by oxidizing agents

- then denatured to precipitate as Heinz bodies

43
Q

the spleen’s role on Heinz bodies

A
  • leaves a bite cell or blister cell
44
Q

G6PD deficiency genetic inheritance

45
Q

things to avoid in G6PD deficiency

A
  • oxidizing agents
46
Q

examples of oxidizing agents to avoid

A
  • anti-malarial (quinines)
  • SULFA DRUGS
  • dapsone
  • vit K
  • fava beans
  • naphtha compounds (mothballs)
47
Q

hemolysis in G6PD deficiency is often triggered by

A
  • drugs or infections
48
Q

African American patients G6PD levels immediately after a hemolytic episode

A
  • may be normal since mature cells are lysed

- only younger cell with normal G6PD survive

49
Q

G6PD deficiency symptoms

50
Q

G6PD deficiency reticulocyte count

51
Q

G6PD deficiency bilirubin

52
Q

G6PD deficiency LDH

53
Q

G6PD deficiency haptoglobin

54
Q

G6PD deficiency seen on peripheral smear

A
  • bite and blister cells
55
Q

pathophysiology of acquired hemolytic anemias

A
  • antibodies bind to red cell antigens

- lead to RBC destruction

56
Q

acquired hemolytic anemias - IgG coated RBCs

A
  • interact with Fc receptors on macrophages
  • complete or partial phagocytosis
  • spherocyte formation (extravascular hemolysis)
57
Q

acquired hemolytic anemias - C3-coated red cells

A
  • extravascular hemolysis

- complement mediated RBC lysis (intravascular hemolysis)

58
Q

Immune hemolysis classifications

A
  • autoimmune
  • drug related
  • PNH
59
Q

two types of autoimmune hemolytic anemias

A
  • warm antibody mediated

- cold antibody mediated

60
Q

hallmark of autoimmune hemolytic anemia

A
  • positive Coomb’s test
61
Q

warm antibodies react with RBCs best at

A
  • 37 degrees

- body temp

62
Q

warm antibodies and agglutination of RBC

A
  • do not agglutinate RBCs
63
Q

warm antibody mostly composed of which antibody

64
Q

cold antibodies react best at

A
  • below 32 degrees
65
Q

cold antibodies and RBC agglutination - seen on peripheral blood smear

A
  • cause RBC agglutination

- IgM is pentameric

66
Q

cold antibodies composed mostly of which antibodies

A
  • IgM which fix complement
67
Q

Direct Coomb’s test tests for

A
  • IgG or C3

- DIRECTLY ON RED CELLS

68
Q

Coomb’s reagent contains

A
  • anti-IgG and anti-C3 antibodies

- will cause agglutination

69
Q

if Coomb’s test is positive

A
  • EITHER IgG or C3 on red cells

- follow up with more specific test for anti-IgG or anti-C3

70
Q

warm-antibody hemolytic anemias etiology

A
  • primary or secondary to hematologic malignancy or another autoimmune disease
  • induced by drugs
71
Q

warm-antibody hemolytic anemias symptoms

A
  • splenomegaly
  • jaundice
  • can be VERY symptomatic or not
72
Q

warm-antibody hemolytic anemias - reticulocyte count

73
Q

warm-antibody hemolytic anemias - bilirubin

74
Q

warm-antibody hemolytic anemias - LDH

75
Q

warm-antibody hemolytic anemias - haptoglobin

76
Q

warm-antibody hemolytic anemias - diagnostic test

A
  • positive Coomb’s test
77
Q

warm-antibody hemolytic anemias - seen on peripheral smear

A
  • spherocytes
78
Q

treatment of warm-antibody hemolytic anemias

A
  • may require transfusion

- immunosuppression is mainstay of therapy

79
Q

first line of drugs for warm-antibody hemolytic anemias therapy

A
  • corticostertoids
80
Q

if steroids fail to work in warm-antibody hemolytic anemias

A
  • splenectomy

- rituximab (CD20 - B cell)

81
Q

distal problems with cold agglutinin disease

A
  • distal ischemia

- red cell clumps cannot pass through microvasculature, leading to cyanosis and ischemia in extremities

82
Q

cold agglutinin disease associated with these infections/diseases

A
  • IGM SO ASSOCIATED WITH MMMMM
  • mycoplasma pneumoniae
  • mononucleosis
  • lymphoproliferative diseases
83
Q

cold agglutinin disease treatment

A
  • keep patient warm
84
Q

cold agglutinin disease steroids and splenectomy

A
  • not effective
85
Q

warm antibody hemolytic anemias pathophysiology

A
  • IgG antibodies against RBC surface molecules are formed
  • coat RBC with or without complement
  • IgG coated fragment engulfed by macrophages
  • spherocytes form
86
Q

cold agglutinin disease pathophysiology

A
  • IgM binds to red cells in cooler extremities
  • fix complement
  • lysed directly in vessel
  • or engulfed by complement receptors on macrophages in liver
87
Q

non-immune hemolytic anemias

A
  • MAHA
  • March Hemoglobinuria
  • Infections
  • Drugs, chemicals, and venoms

HEM Exam 1 (22 decks)

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