Stiner

Question 1

T1H (Type 1 Hypersensitivity) referred to as

Answer 1

allergy, atopy, or immediate hypersens.

Question 2

How long after RE-exposure does T1H occur

Answer 2

minutes

Question 3

Ex of T1H

Answer 3

hives, hay fever, food allergies, bronchial asthma, anaphylaxis

Question 4

T1H sequence of events

Answer 4

1) Initial exposure to antigen causes IgE antibody production
2) IgE binds to Fc receptor on mast cell
3) Reexposure causes cross linking of bound IgE
4) Release of mast cell mediators
5) Immediate response-vasodilation and permeability, smooth m contraction
6) Late response-inflam

Question 5

What mediates immediate response to mast cell degranulation?

Answer 5

Vasoactive amines (serotonin and histamine)
Lipid mediators (prostaglandins and leukotrienes)

Question 6

Prostaglandins

Answer 6

• Vasoconstriction in lungs
• Vasodilation in smooth m
• constriction or dilation of bronchioles
• aggregation or disaggregation of platelets

Question 7

Leukotrienes

Answer 7

• Bronchoconstriction
• increased vascular permeability
• increased mucus
• referred to as slow reacting substance of anaphylaxis (SRS-A)

Question 8

What mediates late response to mast cell degranulation?

Answer 8

• Cytokines and chemokines

- Infiltration of eosinophils, monocytes, and neutrophils (release ROS)

Question 9

How is asthma treated?

Answer 9

• Inhaled corticosteroids
• Leukotriene modifiers
• Inhaled long acting beta2 agonists
• Cromolyn
• Theophylline

Question 10

Most severe form of immediate hypersens.

Answer 10

anaphylaxis

Question 11

What is anaphylaxis? Symptoms? Treatment?

Answer 11

• Response driven by systemic release of vasoactive amines and lipid mediators from mast cells
• Causes life threatening drop in BP and severe bronchoconstriction
• Treated w/ epinehprine and antihistamine

Question 12

What happens with T2H

Answer 12

• Ab bind to foreign or self Ag
• Primarily IgG or IgM
• Activate complement cascade–>MAC

Question 13

T2H diseases

Answer 13

Hemolytic disease of Newborn
Hemolytic anemia
Blood transfusion rxns
Graves disease
Myasthenia gravis

Question 14

Hemolytic disease of newborn and treatment

Answer 14

1st child has Rh
Mother makes anti-Rh antibody
2nd child has Rh and its RBCs are attacked
*Treated w/ rhogam

Question 15

Hemolytic anemia and treatment

Answer 15

Auto antibodies produced against self Ag on RBC. Destruction of RBC–>anemia
*Prednisone or blood trans

Question 16

Graves disease and treatment

Answer 16

TSH receptor stimulated by Ab. Overproduction of thyroid hormone
*radioactive iodine, anti-thyroid drugs, thyroid removal

Question 17

Myasthenia gravis and treatment

Answer 17

ACh receptor blocked by Ab

*cholinesterase inhibitors and corticosteroids

Question 18

What happens with T3H

Answer 18

Ab and Ag bind forming immune complexes that deposit in blood vessels or tissues causing inflam.
Can be caused by exogenous or endogenous Ag

Question 19

How do small immune complexes affect WBCs?

Answer 19

Ligate Fc receptors, causing activation and tissue damage

Question 20

Examples of T3H

Answer 20

SLE, Arthus rxn, serum sickness, lupus nephritis, rheumatoid arthritis

Question 21

How long after exposure does T3H occur?

Answer 21

3-10 hrs

Question 22

What mechanisms do immune complexes use to trigger inflam?

Answer 22

1)Mast cell activation
2)Macrophages release TNF-alpha and IL-1 (induce inflam. cascase
C3a,4a,5a-stim mast cells to release more vasoactive amines, and chemotatic factors.
Fc receptors for IgG may be crucial for antibody complex mediated hypersens.

Question 23

Arthus rxn mechanism and cause

Answer 23

• Triggered in skin by IgG and immune complexes form
• Complexes bind Fc receptors on mast cells and leukocytes
  
  • Local inflam rxn w/ vascular perm.
  • C5a activates leukocytes
• Occurs in vessel walls, pleura, pericardium, synovium, or glomeruli
• Repeated subQ injections of tetanus or diptheria vaccines
• If high levels of IgG immune complex and subsequent exposure of that Ag occurs

Question 24

Arthus reaction symptoms and treatment

Answer 24

• Swelling, induration, pain, edema, hemorrhage, necrosis

- Anti-inflamm agents

Question 25

Serum sickness mechanism and cause

Answer 25

- Caused by foreign protein injection that leads to antibody response * Antivenin * Anti-lymphocyte globulin * antibiotics * Streptokinase - Immune complexes form, deposit in vessels, and activate complement and phagocytes - Although this is T3H, symptoms occur days or weeks after injection of serum

Question 26

serum sickness symptoms and treament

Answer 26

- Chills, fever, rash, nephritis, lymphadenopathy, and arthritis * Rash from mast cell degran due to ligation of FcRy - Self limiting due to secondary Ab response - Antihistamines, corticosteroids

Question 27

SLE

Answer 27

- IgG Ab against self Ag in all nucleated cells - Complexes deposit in blood vessels, kidney, joints and other tissues - Phagocytes activated by Fc receptors - Autoreactive T cells produce more Ab and destroy tissues - NSAIDs, corticosteroids, immunosuppressive agents

Question 28

Immune complexes directed against DNA and histones are deposited in ________

Answer 28

skin, joints, kidney, and choroid plexus

Question 29

What happens with T4H?

Answer 29

Ag specific T cells induce macrophage infiltration in sensitized individual Activated CD8 T cells destroy target cells Generally activated by haptens AKA DTH

Question 30

How long after exposure does T4H occur

Answer 30

2-3 days

Question 31

DTH ex

Answer 31

``` Tuberculin (TH1) Contact dermatitis (TH1 or CTLs) Chronic asthma (TH2) Gluten sens (TH1 and TH2) Graft rejection (TH2) ```

Question 32

TB test and therapy

Answer 32

Tuberculin injected TH1 mediated response if individuals have been exposed in past *self limiting

Question 33

Contact dermatitis

Answer 33

- Haptens complexed w/ skin become internalized (think poison ivy) - Elicited by CD4 or CD8 - Two phases: sensitization and elicitation * corticosteroids, antihistamines

Question 34

Sensitization

Answer 34

``` First exposure to antigen 10-14 days to develop Langerhans cells in skin APC present Ag to T cell CD4 Memory cells form ```

Question 35

Elicitation

Answer 35

``` Reexposure 24-48 hrs LC Ag presentation to memory T cells at site of Ag entry T cells release IFN gamma and cytokines Leads to inflam and recruitment ```

Question 36

Chronic asthma

Answer 36

DTH Mast cell degranulation leads to TH2 and eosinophil influx Eosinophils degranulate->damage tissue and recruit Chronic inflammation can cause irreversible damage and death *corticosteroids, bronchodilators, cromolyn

Question 37

Crohn's disease

Answer 37

Thought to be due to unresolved DTH Initial presentation may be in oral cavity Chronic inflam of bowel mucosa *corticosteroids, immunosppresants