Type II Hypersensitivity Reactions in the Skin Flashcards Preview

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Flashcards in Type II Hypersensitivity Reactions in the Skin Deck (24)
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1
Q

Intrinsic antigen

A

Normal antigen from self protein

2
Q

Extrinsic antigen

A

Could mean foreign OR haptenized/modified self antigen

3
Q

Mechanisms of antibody-dependent cytotoxicity in Type II Hypersensitivity

A
  • Antibody-mediated complement activation and MAC formation, followed by cell swelling and bursting
  • Antibody-mediated complement activation followed by nonspecific neutrophil degranulation (here real damage is mediated by myeloperoxidase, proteinase 3, and peroxidase)
  • Antibodies coating cell attach to C3b and are effectively opsonized and are able to be phagocytosed and destroyed, usually by splenic macrophages
  • Antibody-dependent cell-mediated cytotoxicity (ADCC): NK cells recognize Fc region of IgG and degranulate to kill cell
  • Non-cytotoxic effects (antibody-mediated cellular dysfunction): may result in Grave’s disease hyperthyroidism, mysathenia gravis, etc etc
4
Q

List of some common Type II Hypersensitivity disorders

A
  • autoimmune hemolytic anemia
  • autoimmune thrombocytopenia
  • autoimmune neutropenia
  • Goodpasture syndrome
5
Q

Goodpasture syndrome

A

Type II hypersensitivty reaction against glomerular or alveolar collagen

6
Q

Coomb’s test

A
  1. Purify erythrocytes from blood
  2. Add Coomb’s reagent (anti-human IgG or IgM)
  3. Observe for agglutination (clumping) due to cross-linking
7
Q

Indirect Coomb’s test

A
  1. Purify patient plasma with patient antibodies
  2. Use standardized blood sample from donor
  3. Mix these two, then wait and add Coomb’s reagent
  4. Agglutination indicates anti-erythrocyte antibodies in patient serum

This test is not used to determine self-compatibility, but rather compatibility with exogenous blood samples prior to, for example, transfusion

8
Q
A
9
Q

Desmosome vs Hemidesmosome

A
10
Q

Extracellular desmosome proteins

A
11
Q

Extracellular hemidesmosome proteins

A
12
Q

Pemphigus foliaceus diagram

A
13
Q

Pemphigus foliaceus

A
  • Type II hypersensitivity reaction against desmoglein-1
  • Desmoglein-1 is more concentrated in the stratum corneum and stratum granulosum than in the lower layers, so this usually presents histologically as a superficial-level detachment of epidermis
  • Because these are so superficial, they often erupt before they are ever observed, and so present clinically as erosions
14
Q
A

Pemphigus foliaceus on H and E

15
Q
A

Pemphigus foliaceus patient

16
Q

Pemphigus vulgaris diagram

A
17
Q

Pemphigus vulgaris

A
  • Type II hypersensitivity reaction against desmoglein-3
  • Since desmoglein-3 is found in lower levels of epidermis, like the basal layer, this presents histologically as a low-level epidermal detachment, with acatholysis of keratinocytes within the bulla
  • Clinically presents as flacid blistering which eventually lyses and leaves behind crusting
  • Mucous membrane involvement is an important clinical feature
18
Q
A

Pemphigus vulgaris H and E

Note that the detachment is not quite at the level of the basement membrane, since the hemidesmosomes are still intact. It is at once cell layer just above the basement membrane.

19
Q

Acantholysis

A

The loss of intercellular connections of usually interconnected cells

20
Q
A

Pemphigus vulgaris patient

21
Q

Bullous pemphigoid diagram

A
22
Q
A

Bullous pemphigoid H and E

23
Q
A

Bullous pemphigoid patient

24
Q

Skin diseases with a positive Nikolsky’s sign

A

Pemphigus foliaceus

Pemphigus vulgaris

Staphylococcal Scalded Skin Syndrome

Steven-Johnson Syndrome