Hypersensitivites

Question 1

What activates the coagulation system?What is the main peptide released by the kinin system? What are the effects?

Answer 1

Injury to the blood vessel
Bradykinin
Increases vascular permeability, vasodilation, causes pain. GOAL= keep pathogen contained, stop bleeding

Question 2

What mechanisms are in place to prevent inflammation from becoming chronic?

Answer 2

1. Eliminating the offending agent
2. Short life span of PMN
3. Short half life of mediator molecules
4. Anti-inflammatory cytokines like TGF-beta and IL10

Question 3

What defines Hypersensitivity I?

Answer 3

Anaphylactic- system wide response to exogenous Ag.
IgE is released and bound to mast cells.
Only takes 15-30 min.
Examples: allergic asthma, hay fever

Question 4

What defines Hypersensitivity II?

Answer 4

Cytotoxic
IgG and IgM
Cell surface Ag
minutes to hours
Examples: erythroblastosis fetalis, Graves

Question 5

What defines Hypersensitivity III?

Answer 5

Immune complex
IgG and IgM
soluble
3-8 hours
Examples Lupus

Question 6

What defines Hypersensitivity IV?

Answer 6

Delayed
tissues and organs
48-72 hours
TB tes, poison ivy, granuloma

Question 7

Define atopic.

Answer 7

Tendency to be hyperallergic…produce much more IgE than normal. Genetic component.

Question 8

What are common allergens that induce type I?

Answer 8

Anaphylaxis
Proteins: vaccines
Plant pollen: rye grass, ragweed, timothy grass, birch tress
Drugs: penicllin, sulfonamides, local anesthetics
Foods: nuts, seafood, eggs, milk
Insect products
Mold
Animal hair and dander
Latex

Question 9

What is anaphylaxis? What are some symptoms?

Answer 9

Systemic response to allergen (pollens rarely cause though).
Ab pain, nausea, vomitting
difficulty breathing/swallowing cough
anxiety, confusion
fainting
hives, itchiness
nasal congestion

Question 10

What is the test called for allergens?

Answer 10

Skin prick= wheal and flare from histamine release is positive

Question 11

Describe how type II mechanism works.

Answer 11

IgG reacts with Ag bound to cell surface on self cell and activates complement to destroy via phagocytosis

Question 12

Give the specific examples of the mechanism for type II.

Answer 12

1. Phagocytosis
   A. Transfusion rxn- destroys RBCs
   B. Hemolytic disease of newborn- 1st pregnancy mom Rh- and baby Rh+ blood mix= mom makes Ag for Rh= subsequent pregnancy mom’s Ab attack baby’s RBC (treatment anti-Rh Ab
2. ADCC
   A. acute rheumatic fever- Ab against sore throat
   cross react with heart and joint cells
3. Cellular Dysfunction
   A. Myasthenia gravis-Ab binds to Ach R
   B. Graves

Question 13

Describe the mechanism of type III.

Answer 13

Lots of soluble self Ag= small immune complexes that are harder to recognize and transport to liver so they get caught in smaller structures (like kidney)

Question 14

How is type IV different from the other hypersensitivities?

Answer 14

Mediated by T cells and MO and late onset (>12 hrs). Causes chronic inflammatory disease.
Contact dermititis-Ag binds to self proteins= taken up by APC= activate Th1 cells to produce INF-gamma