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I3 Exam 1 > Anemia of Chronic Disease and Hemolytic Anemias > Flashcards

Anemia of Chronic Disease and Hemolytic Anemias Flashcards

1
Q

is there low iron in anemia of chronic disease

A

no, there is normal iron but there is an inability to incorporate iron into the
RBC

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2
Q

What do the cells look like in ACD

A

normocytic, can sometimes look microcytic which looks like iron def anemia sometimes

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3
Q

what is the retic count in the ACD

A

low or normal, not elevated to compensate for the anemia

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4
Q

what are the causes of ACD

A

infection, viral (HIV, bacterial, fungal, parasitic)

  • malignancy - lose blood
  • autoimmune like IBD
  • ESRD (decreased production of EPO)
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5
Q

what will the ferritin levels look in ACD

A

normal because not iron deficiency

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6
Q

what is the difference in the CBC of patients with ACD vs iron def anemia

A

RDW is normal in the ACD and WBC is elevated in ACD but both have elevated platelets (thrombocytosis)

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7
Q

what will be ferritin in levels in ACD vs iron deficiency

A

elevated serum ferritin in ACD because normal iron but it isn’t being utilized
- but decreased ferritin in iron def

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8
Q

what is the treatment for ACD

A

transfusion
- but also need to give chelating agents for transfusion

  • erythropeitic stimulating agents
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9
Q

what is the target Hb for patients with ACD

A

target Hb of 10

- overcorrection can lead to increased neurological and cardiovascular mortalities

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10
Q

what type of anemia is hemolytic anemia

A

hyperproliferative

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11
Q

what is happening to the RBC in hemolytic anemia

A

bone marrow is producing RBC but the RBC are living shorter lifespan than they should

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12
Q

what is the retic count for patients with hemolytic anemia

A

increased retic count, responding to the loss of RBC

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13
Q

what are the Hb degradation products you would expect to see in hemolytic anemia

A

increased indirect bilirubin and LDH

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14
Q

what will the haptoglobin level be in hemolytic anemia

A

decreased haptoglobin

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15
Q

what is the role of haptoglobin

A

binds to free Hb, you will have lots of Hb from hemolysis which saturates the haptoglobin

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16
Q

What are the three most common features of hemolytic anemia

A

high bilirubin, high LDH and decreased haptoglobin

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17
Q

what are the symptoms of hemolytic anemia

A
  • tired, fautigue

- jaundice because high bilirubin

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18
Q

what is intravascular hemolysis

A

when RBC are hemolysing in the blood

  • more acute
  • disintegration of RBC in the peripheral blood and free Hb will go to kidneys and shut them down
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19
Q

what is extravascular hemolysis

A

typically takes place in spleen and liver

  • abnormal RBC
  • when they go through the spleen the spleen kills them
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20
Q

What will you find in the urine of a patient with hemolytic anemia

A

Hb in the urine and hemosiderin

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21
Q

What are the findings on the peripheral smear of a patient with hemolytic anemia

A

immature nucleated RBC (bone marrow sending out immature cells to compensate)

  • microspherocytes
  • schistocytes - destroyed RBC
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22
Q

What are the findings on the marrow biopsy of a patient with hemolytic anemia

A

increased production of RBC = erythroid hyperplasia

- compensate for loss of RBC

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23
Q

what are the two hereditary RBC enzyme defects causing hemolytic anemia

A

G6PD def

pyruvate kinase def

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24
Q

what are the two hereditary RBC membrane defects causing hemolytic anemia

A

spherocytosis and ovalocytosis

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25
Q

what are the two Hb defects causing hemolytic anemia

A

amino acid subtitutions = sickle cell

and production defects = alpha and beta thal

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26
Q

what sort of anemia can result from mechanical stress?

A

acquired hemolytic anemia can be caused by mechanical stress due to abnormal aortic valve that destroys RBC and there is fragmentation of the cells

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27
Q

paroxysmal nocturnal hemoglobinuria

A

acquired

- defects in the complement that lead to destruction of RBC

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28
Q

what test do you use for immune hemolytic anemia

A

direct antiglobulin test, Coomb’s test

29
Q

What is the direct Coombs test

A

Red blood cells are incubated with an anti-compliment or anti-IGG and they will agglutinate if positive if patients RBC is coated with IGG or complement

30
Q

What is the indirect Coombs test

A

detect antibodies in the serum, want to make sure that any transfusions don’t interact with antibodies in the patients blood

  • bring RBC from donor and incubate with serum of the patient
  • add anti-IGG or anti-complement and if cells agglutinate then you have indirect evidence that patient has antibodies in the serum to make sure that the cells aren’t destroyed if you do a transfusion
31
Q

what causes autoimmune hemolytic anemia

A

and IGG that will attach to RBC and will lead to removal of that RBC by macrophages
- spleen will recognize as abnormal = extravascular hemolysis

32
Q

what is warm AIHA

A

hemolysis usually happens in warm environment

37 C, usually igG

33
Q

what is cold AIHA

A

hemolysis usually happens in cold environment

usually igM, usually fixes complement, destroy RBC = intravascular hemolysis

34
Q

what is leading to RBC destruction in AIHA

A

red cells react with antibody and may have complement fixation which leads to RBC destruction

  • igG and or complement coated RBC interact with FC receptors on macrophages
  • lead to absorption of cell, destruction or spherocyte formation from spleen = acquired
35
Q

heriditary spherocytosis

A

congenital, inherited
- known since childhood
as opposed to AIHA usually caused by warm reactive IGG that leads to spherocyte formation in the spleen

36
Q

where does complement mediated RBC lysis tend to usually happen

A

intravascular, doesn’t require spleen

37
Q

disorders associated with warm IAHA

A
  • idiopathic (40%)
  • lymphoid malignancies (CLL)
  • autoimmune disorder = SLE
38
Q

what drugs can cause warm IAHA

A

methyl dopa, penicillin

39
Q

what disorders are associated with cold IAHA

A
  • lymphoid malignancies

- infections (mycoplasma pneumo, EBV)

40
Q

Which temperature does IGG typically react at

A

warm temperature

- warm IAHA

41
Q

what is the clinical presentation of IAHA

A

anemia, jaundice (hemolysis), cardiopulm collapse, hepatosplenomegaly, thrombosis (clotting), acrycyanosis - bluish discoloration upon exposure to cold weather

42
Q

how is warm IAHA treated

A
  • steroids
  • rituximad (anti-antibody)
  • splenectomy = increased risk of infection, more risk for thrombosis
43
Q

What is rituximab used for

A

warm IAHA as an anti-antibody

44
Q

what is the treatment for cold AIHA

A
  • plasma exchange in rare cases
  • administer RBC through blood warmer
  • steroids do not work
  • splenectomy not useful
  • avoid exposure to cold
45
Q

Do patients with cold IAHA respond to steroids or splenectomy?

A

no, only patients with warm IAHA

46
Q

G6Pd deficiency

A

G6PD is important for protecting RBC for ox. phos and NADPH levels

  • patients sensitive to oxidant exposure
  • can stimulate hemolysis
47
Q

What type of inheritance pattern is a G6PD deficiency

A

X linked disorder

48
Q

What is the A1 type of G6PD

A
  • African men
  • mild hemolysis
  • enzyme levels low
  • self-limited
49
Q

When should you check on the G6PD levels in the A1 type?

A

don’t check in the acute phase, need to give them some time to use the supplemented enzyme and then it is usually self limiting
- wait until crisis has resolved

50
Q

When should you check on the G6PD levels in the mediterranean type?

A

they always have low levels, not self limiting

  • severe hemolysis
  • always have low levels of enzymes
  • life threatening
51
Q

What drugs can cause a G6PD deficiency

A

sulfonamides, anti malarial drugs

52
Q

What can fava bean ingestion cause?

A

can lead to severe hemolysis in mediterranean type of G6PD deficiency

53
Q

What would lab tests show for somebody with G6PD deficiency

A

denatured Hb in RBC early in hemolysis

- Heinz bodies

54
Q

What do heinz bodies show us

A
  • G6Pd deficiency
    bite cells
  • denatured Hb
  • macrophages take a bite out of the cell
55
Q 
25 y/o patient with mild jaundice, gallstones, anemia
CBC showed anemia
Coomb's test was negative
LDH was elevated
low haptoglobin
A

hereditary spherocytosis

56
Q

what would you see in iron deficiency anemia

A

area of central pallor and microcytic cells

57
Q

what is hereditary spherocytosis

A
  • autosomal dominant inheritance

- defect that affects Ankyrin protein

58
Q

What does a defect in Ankyrin protein cause

A

hereditary spherocytosis

59
Q

What are the clinical manifestations of hereditary spherocytosis

A

chronic anemia, splenomegaly, gallstones

60
Q

What is the difference in the lab tests in AIHA and hereditary spherocytosis

A
  • you can also have spherocytes on lab smear but different clinical setting
61
Q

What is the treatment for hereditary spherocytosis

A

replace with folic acid

  • extravascular hemolysis
  • splenectomy to resolve hemolysis but will still have spherocytosis
  • gall bladder removal because of gall stones
62
Q

With extravascular hemolysis do you lose Hb or become iron deficient?

63
Q

What will a splenectomy cure for a patient with hereditary spherocytosis

A

you will cure the hemolysis but not the sphereocytosis

64
Q

43 y/o female with a history of jaundice and lupus. you decide to obtain a coomb’s test. test is positive IgG coomb’s test

A

warm auto-immune hemolytic anemia

65
Q

52 y/o patient with a diagnosis of Non-Hodgkin’s lymphoma

- CBC shows agglutination of cells at cold temperature

66
Q

What history indicates G6Pd deficiency

A

infection or drugs : sulfonamides, anti malarial drugs

67
Q

27 y/o male taking bactrim (sulfa drug), dark urine, isteric sclerae (yellowing of eyes), Hb of 10, high bilirubin, LDH elevated, blister cell on blood smear

what do you want to check for with this patient?

A

check G6PD level

  • African American always think G6PD
  • new history of antibiotic use
  • blister cells on blood smear
68
Q

What are blister cells on blood smear indicative of?

A

G6PD deficiency

I3 Exam 1 (12 decks)

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