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PA2203- Final > Hypersensitivity Rxns > Flashcards

Hypersensitivity Rxns Flashcards

1
Q

what is a hypersensitivity run and what do they require

A

Over rxn of the immune system to self or non self antigens

-require a sensitized host (prior exposure)

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2
Q

What are type 1 hypersensitivities mediated by

A

IgE mediated

-soluble antigens cross link IgE antibodies bound to mast cels/basophils

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3
Q

examples of type 1 hypersensitivites (4)

A

atopy
allergies
acute allergic asthma
anaphylaxis

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4
Q

How are IgE antibodies developed : what cells stim them and ILs needed

A

B cells stimed by Th2 cells

need IL4,5,13

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5
Q

Steps to get mast cells sensitized

A
  1. APC present to Th2
    2.Th2 acctivate b cells
  2. B cells proliferate into plasma cells and secrete IgE
    4 IgE bind to mast cells sensitizing them
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6
Q

What does reexposure to antigens bind to

A

preexposure of certain antigens bind IgE and crosslink FceRI receptors

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7
Q

What is released in the immediate type 1 hypersensitivity and what occurs (2)

A

immediately after exposure histamine and leukotriene released which causes: vasodilation of arterioles and increased permeability, airway smooth mm contraction, leukocyte extravasation to affected site

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8
Q

When does late phase type 1 hypersensitivity occur and what is released

A

2-6 hrs post

-cytokines (IL4,5,13) amplifies type 1 rxn (activate eosinophils, neutrophils, monocytes etc)

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9
Q

Natural hx of type 1 hypersensitivity

A

12hrs- 3days

acute rxn

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10
Q

What percentage of people have atopy and why

A

10-20%

-higer total lvl of IgE in circulation, more eosinophils

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11
Q

What is the clinical manifestation to atopy

A

allergy

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12
Q

What leads to atopy

A
  1. genetics (components of immune system)
  2. Environment (infection)
  3. Lifestyle (stress, obesity)
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13
Q

What is allergy mediated by

A

IgE antibodies

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14
Q

Effect of type 1 hypersensitivity on nasal passages and eyes

A

eyes: redness, itchy, watery eyes, conjunctiva
nasal: allergic rhinitis, sneezing, runny nose, coughing etc, respiratory distress etc

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15
Q

What is asthma

A

disease of the bronchi and bronchioles causing attacks/paroxysms of reversible airflow obstruction (airway inflammation, bronchospasm, mucus hyper production)

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16
Q

What are the primary clinical manifestations on the skin of type 1 hypersensitivities

A
  1. dermatitis (eczema)- red area of superficial skin that is often itchy
  2. Urticaria (hives)- raised areas surrounded by a red base, itchy, typically lasts <24hrs
17
Q

Food allergy vs food intolerance

A

allergy- IgE mediated process

intolerance- IgG mediated process

18
Q

What is anaphylazis and how is it mediated

A

IgE mediated- widespread basophil degranulation+ systemic inflammation
-itchy hives,dyspenia, light-headedness, low bp

19
Q

common characteristics of allegens (5)

A
  • low molecular weight
  • highly soluble
  • multivalent antigens
  • enzymatically active
  • stable chem structue
20
Q

What is the major allergen of house dust mite and what does it do

A

Der p1

Break up tight junctions getting increased access to APCs in mucosal tissues

21
Q

Gold standard of allergy testing

A

blood testing: cells timed with antigen under investigation and IgE antibodies measured

22
Q

What are drugs to treat allergies

A 
Antihistamines
Leukotriene inhibitors
Inhaled bronchodialators
Epinephrine- relaxes sm mm
Allergy shots- (expand tolergenic responses)
23
Q

What are type II hypersensitivities mediated by

A

IgG or IgM antibodies directed against cell associated antigens or ECM antigens

24
Q

What do type II hypersensitivities result in

A

Cytotoxic responeses

  • activation of classic complement path
  • antibody dependent cell mediated cytotoxicity
  • Phagocytosis
25
Q

What are isoantibodies

A

IgM/IgG antibodies against blood antigens you don’t have

26
Q

What do isoantibodies do when blood is mismatched (3)

A
  1. Agglutination
  2. Clumps activate classical complement pathway
  3. Hemolysis by MAC/inflammation/opsinization
27
Q

When does hemolytic disease of the fetus and newborn occur

A

if mother is rh- and child is rh+, mother may generate anti rh IgG antibodies and if next child is rh+ it will initiate hemolytic rxn

28
Q

what occurs in myasthenia gravis

A

type II hypersensitivity
IgG autoantibodies target nicotinic act receptors on neuromuscular junction blocking action pot/ activate classical complement pathway

29
Q

What occurs in Graves disease

A

Type II hypersensitivity
-autoimmune disorder where IgG antibodies bind to thyroid stem hormone receptor causing over prod of T3/T4 (hyperthyroidism)

30
Q

Symptoms of Graves disease

A

Unexplained weight loss, elevated HR, high BP, anxiety/irratability etc

31
Q

What are type III hypersensitivities and what do they activate

A

formation of small immune complexes between IgG antibodies and soluble antigens (deposits in walls of blood v)
-activate classical complement pathway, inflammation

32
Q

What is arthur’s reaction and serum sickness due to and what do they do

A

type III hypersensitivity
-small immune complexes in tissues causing inflammation/tissue damage
Arthus- localized
serum- systemic

33
Q

What is systemic lupus erythematosus and what causes it

A

Type III hypersensitivity (IgG autoantibodies and soluble nuclear antigens)-deposit in tissues and activate complement/inflammation

-fatiue, fever, jt pain/swelling, rashes, any organ targeted

34
Q

What is required for a type 4 hypersensitivity and timeframe

A
  • delayed hypersensitivity (>24hrs)

- Requires prior exposure to antigen and sensitization to generate antigen specific t cells

35
Q

What type of antigen specific t cell is required for TB type 4 hypersensitivity

A

Th1 cells

36
Q

What type of antigen specific t cell is required for chronic asthma and what does it cause

A

Th2 cells

-airway remodelling, hyperresponsitivness (to irritation) and obstruction

37
Q

What type of antigen specific t cells are required for poison ivy (type 4) and what do each do

A

th1 cells= activate macrophages

clts- induce apoptosis

PA2203- Final (11 decks)

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