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Hypersensitivity II Flashcards

1
Q

What two Abs does Type II hypersensitivity involve?

A

IgG

IgM

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2
Q

Where is the Ag located?

A

surface of cell in circulation (soluble phase)

in a tissue

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3
Q

what two main things are involved in Type II

A

circulating Ab

its target Ag

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4
Q

What is often the result of type II

A

Cytotoxicity

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5
Q

Mechanisms of Type II

A

complement- and Fc receptor- mediated inflammation

opsonization and phagocytosis

ADCC, macs, NK cells

Abnormal physiologic responses without cell/tissue injury

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6
Q

ADCC: which Ab serve as bridges

A

IgG

links target cells to effector cells

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7
Q

what are the effector cells in ADCC

A

Macs
NK
Neutrophils
Eosinophils

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8
Q

What are two examples of abnormal physiologic responses without cell/tissue injury seen in Type II

A
  • Ab stimulates TSH receptor w/o hormone (Graves)

- Ab inhibits binding of ACh to ACh receptor (Myasthenia Gravis)

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9
Q

What are some diseases associated with Type II?

A
  • Transfusion reaction
  • Hemolytic disease of the new born
  • Autoimmune hemolytic anemia
  • goodpasture’s disease
  • pemphigus vulgaris
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10
Q

Important tests used in Type II diseases

A
  • Coombs test

direct vs indirect

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11
Q

What does Coomb test detect?

A

Anti-RBC antibodies

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12
Q

Direct Coombs test

A

picks up Ab DIRECTLY on the surface of RBC

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13
Q

What is the resulting effect of coombs test

A

agglutination of RBC

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14
Q

What does direct coombs test help detect?

A
  • Hemolytic disease of the the newborn
  • Autoimmune hemolytic anemia
  • transfusion reaction
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15
Q

Indirect coombs

A

two step

Measures Anti-RBC Abs in the SERUM

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16
Q

Basically what is happening with the coombs test?

A

Antibody on RBC (direct or indirect) – then add Anti Ig —> agglutination of RBC

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17
Q

when is indirect coombs used?

A

blood banking:

  • cross-matching
  • blood typing
  • Ab detection
  • Ab identification
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18
Q

What type of reaction does transfusion reaction cause?

A

Type II

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19
Q

Blood group AB has what Ags? what are the Abs in serum?

A

Ag: AB
Ab: none

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20
Q

Blood group O has what Ags? what are the Abs in serum?

A

Ag: H
Ab: anti-A, Anti-B

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21
Q

What is the Ig antibodies found in blood?

A

IgM antibodies

22
Q

If the potential donor is O type, do you have to worry about a transfusion reaction?

23
Q

Why do you not have a transfusion reaction against any donors with AB type recipient?

A

Recepient has no Abs against A or B

24
Q

What are the clinical symptoms of transfusion reaction?

A

Fever
Low BP
Nausea, vomiting
Back/chest pain

25
Hemolytic disease of the newborn
Type II Erthoblastosis fetalis Ag on RBC - RhD
26
When does Hemolytic disease of the newborn occur?
second pregnancy of women who is RhD NEG and has RhD POS baby. The anti-Rh affects the RhD+ fetus -- lysis occurs
27
In HDN, mother is RhD ___? | Baby?
Negative mom positive baby
28
What do you see in HDN?
elevated Bilirubin Large liver/spleen Petechiae Positive Direct coombs test
29
What test is used for HDN?
direct coombs test
30
When does sensitization occur in HDN?
Postpartum - Ab formed against the RhD+ RBC from the baby in the FIRST pregnancy
31
What can be given to destroy the fetal blood cells that leaked into maternal circulation?
Anti-D(Rh) injections: Rhogam
32
What is the Anti-D treatment?
Passive immunization: inject Rh- mothers with preformed Anti-RhD --- so that - No sensitization occurs destorys RhD+ in MATERNAL circulation repeat each pregnancy and after procedures
33
Autoimmune Hemolytic Anemia
Anti-RBC antibodies produced hemolysis of RBC Pos. direct coombs
34
Drug induced hemolytic rxn
DRUG binds surface protein on RBC (seen with penicillin) IgG sp to drug prodcued -- binding of the IgG: Complement mediated lysis Opsonization/phagocytosis (C3b/IgG via Macs)
35
Pemphigus vulgaris
Ag is FIXED tissue Ag (autoabs against inTERcellular subs) Autoimmune blistering disease IgG Ab affects skin/mucus membranes separation of epidermal layers/epithelial cells
36
Immunofluorescence of Pemphigus vulgaris/Goodpasture's syndrome?
Type II so linear staining pattern AB to FIXED AG ***
37
Goodpasture's syndrome
Ag in kidney/lung - basement membrane (BM) - Circulating Ab to glomerular BM (Anti-GBM abs) cross reacts with alveolar BM -- leads to pulm hemorrhage Autoimmune IgG abs Anti-tissue Ab -- > activate complement and recruit inflammatory cells
38
What are two main clinical presentations for Goodpasture's
Acute Glomerulonephritis Pulmonary hemorrhage Males
39
Treatment of Goodpasture's
remove anti-GMB ab by PLASMAPHERESIS Immunosuppressant drugs
40
Example of cross-reactivity with Ag from infectious agent
ARF
41
ARF
GAS Ag (throat infection) --> cross react with myocardial Ag - cardiac manifestations - migratory arthiritis
42
Ab interference with cell function
Perinicious anemia : intrinsic factor of gastric parietal cells gets neutralized --> dec Vit B12 absorption Autoimmune
43
What is the result of lack of intrinsic factor?
dec Vit B12 absorption Abnormal erythropoiesis and anemia
44
Two diseases with Anti-receptor Abs?
- Myasthenia gravis (inhibition) | - Grave's Disease (stimulation)
45
Clinical presentation of myasthenia gravis
Ptosis muscular weakness respiratory problems (receptor # dec or destoryed in addition inhibition of NT binding)
46
who is more affected by Grave's?
20-30 yo women
47
Clinical presentation of Grave's disease?
Hyperthyroidism Exophthalmos Myxedema heat intolerance, anxiety
48
What occurs in Grave's disease?
Anti-TSH receptor Antibody ---> stimulates receptor and mimics action of TSH Continuous release of T3 and T4 (normally, T3 and T4 signals pituitary to stop releasing TSH)
49
Treatment of type II hypersensitivity
Plasmapheresis | Immunosuppression
50
What does plasmapheresis do?
Gets rid of Abs by removing affected plasma and replacing with good plasma
51
what is immumosuppression used for?
for reactions against self Ag

POD Exam 3 (6 decks)

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