Type I Immunopathology Flashcards Preview

Blood and Lymph Unit 2 > Type I Immunopathology > Flashcards

Flashcards in Type I Immunopathology Deck (13)
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1
Q

What normally happens during worm infestation?

A
  1. ) Make IgE and IgG against worms. IgG binds to worm/ova (opsonizes,) activates complement, C3a and C5a attract neutrophils. This doesn’t work. :(
  2. ) Worm sheds antigen -> diffuse to nearby mast cells (who have FceR loaded w/ anti-helminth IgE) -> antigen corsslings w/ IgE, mast cells release histamine -> smooth muscle contraction and peristalsis TO pOOP em out
  3. ) MOST IMPORTANT!!!!!!!!!! late-phase response. Mast cells secrete ECF-A2 (which is prostaglandins and leukotrienes) -> attract huge number of eosinophils (which have Fc receptors for IgG, which, on step 1, coat the worm!) Eosinophils contain MAJOR BASIC PROTEINS which is hella toxic to helminths.
  4. ) Th2 finds helminth antigens presented by APC, attracts both eosinophils and macrophages. Th2’s lymphokines (IL-4, IL-5, IL-13) activate M2 macrophages which heal damage and wall-off resistant invaders.
2
Q

Anaphylaxis

A

IgE binds strongly to FcR1 receptors, bound IfE are crosslinked by allergen, mast cells signalled to secrete histamine.

If systemic, causes vasodilation and broncho/gut constriction which is no good

3
Q

Allergic rhinitis

A

Runny nose and itchy eyes lol

4
Q

Eczema

A

chronic dry skin, bacterial secondary infection is common

5
Q

Oral Allergy Syndrome

A

food allergy, antigens pass through mucous membranes w/ rapid access to local mast cells.

Tingling tongue, mouth, lips, itching and swelling yay.

6
Q

Hyper IgE syndrome

A

We probs don’t have to know this

Also called Job Syndrome, autosomal dominant, inability to make IFNgamma effectively. Poor Th1 response, results in high serum IgE, skin abscesses, and fungal/pseudomonal penumonia

7
Q

What is IgE development dependent on?

A

Thf and IL-4. Takes 5-ever to make (7 yrs if you move to a new continent or w/e)

8
Q

Describe Immediate reaction in atopic state

A

IgE binds mast cells and basophil IgE receptor FceRI with small association factor

IgE laden mast cells must be triggered by cross-linking of antigen. (antigen must be at least divalent)

Degranulation releases histamine, heparin, enzymes and TNF. Responsible for hives, or the wheel and flare response

9
Q

Describe late phase reaction in atopic state

A

Activated mast cells initiates a series of enzymatic steps

1.) Phospholipase PLA2 cleaves arachidonic acid from membrane phospholipids.
(can be converted by cyclooxygenase pathway into prostaglandins and lipooxygenase pathway into leukotrienes.) 5-15 min. Anti-histamine

2.) This initiated inflammation, constricts bronchioles (ECF-A) and attracts eosinophils! 4-10 hrs. Anti-inflammatory

10
Q

Describe allergen skin testing

A

Drip the allergen on skin! Poke it through! See if u react.

11
Q

What is CAP-FEIA

A

Flourescent Enzyme Immunoassay, where allergen is fixed into a capsule, patient’s serum is added and unbound proteins are washed away. Bound IgE is quantified.

12
Q

Asthma! Tests, aggravators

A

Asthma is both bronchoconstrictive and inflammatory (leads to fibrosis)

Tested by spirometry: tests FEV1. Volume of air that can be exhaled from lungs in 1 sec. Measured at baseline, give bronchodilators and see if it improves.

Over time FEV1 decreases b/c fibrosis. To decrease this, use inhaled glucocorticoids.

13
Q

Potential treatments to type I immunopathology

A

Avoid it!

Anti-histamines!

Epinephrine! (for anaphylactic shock!)
Glucocorticoids! (mostly for topical/pulmonary inhalents b/c systemic has a lot of problems)

Leukotriene inhibitors!

LABAs (long acting beta-2 agonists -> rapidly reduce bronchoconstriction, given in combination w/ inhalable steroid)

IgE blocker (treatment for asthma for kids 12 and older who dont respond to steroids)

Immunotherapy - “allergy shots” maybe increase your tolerance, maybe desensitizes mast cell, maybe increases T-reg. Nobody knows!