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MLSCI 270 > AIHA > Flashcards

AIHA Flashcards

1
Q

theories of autoimmunity

A
  • malfunctioning T cells
  • cross-reactivity
  • molecular mimicry
  • alteration of self-antigens
  • secondary to disease
  • inherited tendency
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2
Q

primary idiopathic autoimmunity

A
  • Ab against own RBCs
  • unknown cause
  • 60 y/o +
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3
Q

autoimmunity secondary to diseas

A
  • viral or bacteriogenic disease
  • often 2y to CLL
  • WBC problems (ex: B cell lymphoma = can make Ab that’s not quite right, if malignant = makes a whole lot)
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4
Q

three main types of AIHA

A
  • WAIHA = 70%
  • cold autoimmune hemolytic anemia
    > cold hemagglutinin disease (CHD) = 16%
    > paroxysmal cold hemoglobinuria = 1-2%
  • drug-related hemolytic anemia = 12%
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5
Q

instances when DAT is positive

A
  • patient alloantibodies bind donor cells
  • maternal Abs bind fetal cells
  • passive antibodies (blood products/IVIg)
  • autoantibodies
  • antibodies/complement due to drugs
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6
Q

in vivo binding of immunoglobulins, complement components, or both

A

DAT positive

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7
Q

if a DAT is positive, what follow-up testing is needed

A

elution

Ab ID

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8
Q

warm autoimmune hemolytic anemia

A
  • often in elderly patients
  • primary idiopathic
  • secondary
    > white cell malignancies (CLL, lymphoma, MDS)
    > autoimmune diseases (Lupus, rheumatoid arthritis)
    > viral infections (children or adults)
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9
Q

clinical symptoms of WAIHA

A
  • pallor
  • weakness
  • shortness of breath
  • dizziness
  • jaundice (EVH)
  • fever
  • splenomegaly
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10
Q

hematology results of WAIHA

A 
CBC
- hemoglobin and hematocrit decreased
- peripheral smear
 > nRBC
 > polychromasia
 > spherocytosis
 > HJ bodies (seen in asplenic individuals)

other indicators of EVH

  • increase bilirubin
  • increase LDH
  • decease haptoglobin
  • high RDW
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11
Q

T or F. autoadsorptions cannot be performed if the patient has been transfused in the past three months

A

T as alloantibodies might be removed by donor cells

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12
Q

cold autoantibodies general characteristics

A
  • IgM
  • thermal range = 4C (<15C; sometimes RT; up to 32C)
  • binds complement
  • specificities
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13
Q

harmless autoanti-I

A
  • titre <64
  • max thermal range (20-24C; most below)
  • rxn not readily enhanced by albumin
  • polyclonal
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14
Q

pathological autoanti-I

A
  • titre >1000
  • max. thermal range (30-32C)
  • rxn enhanced by albumin
  • monoclonal (one B cell going out of control => making this autoAb)
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15
Q

cold AIHA

A
  • primary idiopathic = tend to see in older people
  • secondary to disease
    > Mycoplasma pneumonia = anti-I
    > use erythromycin
    > EBV = anti-i
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16
Q

CHD

A

cold hemagglutinin disease
- symptoms: tingle due to lack of O2 = go inside = warm up; IgM pops off BUT complement stays and works more efficiently

  • when blood cools down to 30C = ears, nose, etc first things to go down => auto anti I attaches at 30C = decreased blood flow; O2 used up from those cells unable to move freely
    => binds complement
  • no spherocytosis
  • increased polychomasia
  • anemia symptoms (fatigue, etc.)
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17
Q

treatment for CHD

A

just avoid the cold

18
Q

ACROCYANOSIS

A

bluish discoloration of the extremities due to decreased amount of oxygen delivered to the peripheral part

19
Q

CHD investigation

A

identify autoAb

  • panel
  • auto control (at room temp = pos)
  • cord cells (without autoanti-I = neg)
  • titration (>1000)

DAT = pos

  • polyspecific pos
  • monospecific = only pos for C3
20
Q

cold agglutinin titration

A
  • pre-warmed patient plasma is serially diluted
  • test with adult O cells, patient cells, and cord cells at various temps (37C, RT, 4C)
  • determine titre at 4C
  • use strength of adult vs cord cells to determine identity (anti-I vs anti-i)
21
Q

finding compatible blood (follow-up CHD investigation

A
  • prewarm
  • use autoadsorbed plasma
  • ensure monospecific anti-IgG used (don’t want to pick up complement binding)
  • ensure EDTA sample used
  • transfuse using blood warmer if necessary
22
Q

PCH

A

paroxysmal (sudden onset) cold hemoglobinuria (Hb in urine through IVH)

  • antibody specificity is anti-P
  • AKA Donath-Landsteiner Ab
  • IgG that reacts in the cold!
  • binds complement right to C9
  • hemolysis (IVH bc of C9)
23
Q

PCH etiology

A

often 2ry to MMRV; often was found in children

24
Q

symptoms of PCH

A

intermittent hemolysis with exposure to cold = anemia hemolysis, etc.

25
Q

lab findings for PCH

A

similar to CHD

- decrease Hb, haptoglobin; increase LDH, bilirubin (takes a while to increase)

26
Q

treatment for PCH

A

wait for underlying infection to clear; avoid cold

27
Q

Donath-Landsteiner Test

A
  • PCH
  • collect blood, keep warm, and allow to clot (37C)
  • incubate serum with P(+) RBCs and normal serum at 4C
  • warm to 37C
  • spin and read for hemolysis

hemolysis = anti-P present
no hemolysis = anti-P not present

28
Q

why can’t we use EDTA to test for PCH?

A
  • always serum! bc EDTA will cause a false negative as it would get rid of Ca 2+ and Mg 2+ which complement needs
29
Q

why do we add normal serum in the Donath-Landsteiner test?

A

to supply complement

- ensuring that there is enough complement source; bc in vivo, patient may have used up all of the complement

30
Q

Often a cold agglutinin screen is performed before doing a ______. if the patient plasma does not react with O adult cells at 4 degrees when diluted at _____, there is no need for _______ _______

A

titration
1/40
serial dilutions

31
Q

drug induced HA

A
  • positive DAT could be caused by dug
  • rarely leads to hemolysis
  • more often seen as interference
  • should be considered in DAT workup
32
Q

when are blood products used as drugs?

A
  • RhIg given to Rh pos patients with ITP
  • IVIg therapy
    > monitor Hb
    > drop in Hb (<100g/L); perform DAT, Bili, LD
33
Q

methyldopa HA

A
  • antihypertensive drug used in pregnancy: Aldomet
  • autoantibody related to dose and time
  • positive DAT
  • anemia
  • autoAb produced
  • serologically indistinguishable from WAIHA
    > panreacting
    > specificity
  • substance sensitizing cells
  • treatment = take them off drug
34
Q

drug adsorption (penicillin)

A
  • IV (massive doses)
  • drug binds to RBC
  • drug/RBC complex stimulates immune response
  • IgG Ab attaches to penicillin
35
Q

lab results for drug adsorption

A
  • DAT = pos; due to IgG; neg for C3d
  • antibody screen = negative bc screen cells do not have penicillin
  • Eluate = neg
36
Q

immune complex “innocent bystander”

A

Quinidine = antimalarial drug

37
Q

Quinidine AIHA

A
  • patient maks drug Ab
  • Ab-Ag complex binds; RBC activates complement
  • RBC destroyed by complement
  • IVH
38
Q

immune complex lab results

A
  • DAT = pos (for complement only)
  • Ab scr = neg
  • Eluate = NOT done; even if w did = still neg
39
Q

if complement is only positive from DAT

A

either cold auto, drug-induced, or immune complex

40
Q

membrane modification (cephalosporins) AIHA

A
  • uses adsorption mechanism
  • modifies RBC membrane (makes it sticky)
  • nonspecific protein binding
    > complement, IgG, IgM, IgA
41
Q

lab results for membrane modification

A
  • DAT = pos (due to IgG and complement)
  • Abscr = neg
  • eluate = neg

bc drug Abs not specific Abs

MLSCI 270 (15 decks)

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