01291430 - Mfm Ii - Hypersensivity Ii - Iv (Alley)

Front 1

What isotype mediates Type II and III hypersensitivity?

Back 1

IgG

Front 2

What is significant about Type II hypersensitivity and the site of reaction?

Back 2

occurs on the cell surface of an RBC or platelet. LARGE CELL SURFACE = type 2

Front 3

What is the most common type 2 hypersensitivity and how does it work?

Back 3

penicillin.
penicillin usually binds to a bacteria surface, but sometimes it can bind to an RBC or a platelet that generates an complement/IgG response and against self-cell with modified surface that leads to RBC lysis or phagocytosis.

Front 4

What is the difference of the ABO blood groups?

Back 4

there are different antigens that are on the RBCs that determine blood type.
O - carbohydrate tail, Anti-A, Anti-B Abs
A - carb tail + GalNAc, Anti-B Abs
B - carb tail + Gal, Anti-A Abs
AB - carb tail + GalNAc & Gal, no Abs

Front 5

What does type 3 hypersensitivity target?

Back 5

soluble antigen

Front 6

What is the problem with type 3 hypersensitivity?

Back 6

so many immune complexes form that activate so much complement that they cannot be cleared fast enough to not prevent detrimental inflammation.

Front 7

What anaphylatoxin generated by complement is most problematic in type 3 hypersensitivity?

Back 7

C5a can, on it's own, cause macrophage to degranulate and cause a fast increase in local inflammation

Front 8

What is serum sickness and how does it present?

Back 8

serum sickness is the unclearable build-up of immune complexes in the serum which presents as a cutaneous rash. it is usually self-limiting (will clear once more Ab is made and complexes are cleared) type 3 hypersensitivity response.

Front 9

What are the three types of type 4 hypersensitivity?

Back 9

1. delayed-type
2. contact
3. gluten-sensitivity enteropathy

Front 10

What is the process of delayed type hypersensitivity?

Back 10

1. antigen is introduced sub-cu and is processed by APCs like macrophage
2. APC presents to memory T cell which differentiates into an effector TH1 and releases cytokines (IFN-gamma) to produce inflammation
3. inflammation occurs and recruits to cause localized edema and reaction

Front 11

What excreted molecules occur from TH1 and macrophage during a delayed type reaction?

Back 11

1. chemokines - recruit macrophage
2. IFN-gamma - activate macrophage, release inflammatory mediators
3. TNF-alpha, LT - adhesion molecules for extravasation, local tissue destruction
4. IL-3 - monocyte production by bone marrow stem cells

Front 12

What is a common example of contact sensitivity?

Back 12

poison ivy

Front 13

What is the process of contact sensitivity?

Back 13

1. contact sensitizing agent penetrates skin
2. csa binds to self proteins which are identified and taken up by Langerhans cells
3. Langerhans presents csa:self protein to Th1 which secretes IFN-gamma
4. inflammation occurs involving IL-1, TNF-alpha, CXCL8, 1, 9 secreted from epithelial layer which can cause blistering from the exudate and CTL destroyed tissue/contact agent

Front 14

What is celiac disease?

Back 14

hypersensitivity 4/autoimmune reaction to gluten in the jejunum

Front 15

What is the process of celiac disease reaction?

Back 15

1. gluten is degraded to gluten fragments in the gut lumen
2. fragments enter gut tissue and are deaminated by trans-glutaminase
3. naive CD4+ t cells responds to deaminated peptides presented by HLA-DQ8 or DQ2 and differentiates into TH1
4. subsequent inflammation causes villous atrophy

Front 16

What do some people NOT have celiac disease?

Back 16

HLA-DQ8 or HLA-DQ2 absence

Front 17

What is SJS?

Back 17

steven johnson's syndrome caused by drug hypersensitivity of carbamazepine or allopurinol which presents with sloughing of skin. similar to TEN, but TEN has higher body surfaces affected.