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Flashcards in hypersensitivity Deck (32)
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1
Q

what can trigger hypersensitivity

A

infection
environmental substances
self antigen

2
Q

hypersensitivity due to influenza

A

exaggerated immune resposne to damaged epithelium in resp tract
cytokine storm –> hypotension and coagulation

3
Q

hypersensitivity due to dust

A

can get to lower extremities of resp tract –> area rich in adaptive immune cells

if IgE mediated = allergy symptoms
if IgG mediated = farmers lung

4
Q

hapten hypersensitivity

A

haptens are small molecules that bind to proteins and elicit immune response
small environmental antigens can diffuse into skin and act like these
delayed hypersensitivity

5
Q

T1 hypersensitivity

A

IgE, eosinophils
degranulation of mast cells
immediate sensitivity, allergy

6
Q

atopy

A

genetic tendency to produce IgE to normally innocuous environmental allergens

7
Q

allergy

A

clinical expression of atopy

urticaria
angioedema
asthma
dermatitis, eczema

8
Q

T1: degranulating cells

A

release of mediators cause allergy

mast cells release after IgE and allergen interact

9
Q

T1: IgE required, how is it produced

A

IgE is produced by B cells when they are co-stimulated with IL-4

10
Q

mast cell mediators

A

stored: histamine, heparin
new: prostaglandins, leukotrienes

11
Q

T1: drug Rx

A
B2 agonists 
epinephrine 
antihistamines
specific receptor antagonists
corticosteroids
12
Q

T1: how do B2 agonists work

A

mimic effects of sympathetic nervous system

prevent smooth muscle bronchial contraction in asthma

13
Q

T1: how does epinephrine work

A

lifesaving in anaphylaxis

stimulates alpha and beta adrenergic receptors, decreased vascular permeability, inc BP and reverses airway obstruction

14
Q

T1: how do antihistamines work

A

block specific histamine receptors

15
Q

T1: how do specific receptor antagonists work

A

block effects of leukotrienes

16
Q

TII hypersensitivity

A

IgM or IgG react with antigen present on surface of cells

antigen can be self or exogenous - distinction between hypersensitivity and autoimmunity can be blurred

e.g. ABO blood group reaction

17
Q

TII: how is damage caused

A

when antibody binds damage arises through:

  • complement activation
  • Fc binding and stimulation of phagocytes
  • antibody dependent cellular toxicity
  • effects on target cell: inhibitory, stimulatory
18
Q

TII: immune mediated haemolysis

A

alloimmune haemolysis
autoimmune haemolysis
drug induced haemolysis

19
Q

TII: good pasture’s syndrome

A

IgG binds glycoprotein in basement membrane of lungs and glomeruli

20
Q

TII: Grave’s disease

A

antibodies affecting cell function
hyperthyroidism
thyroid stimulated when autoantibodies bind to TSH receptor

21
Q

TIII hypersensitivity

A

IgG antibody reaction to self or exogenous antigen

abnormal deposition of antigen-antibody immune complexes in the tissues

22
Q

normal immune complex formation

A
  • kept soluble in blood by activated complement components
  • travel in blood to liver, spleen
  • phagocytes take up complexes
  • complexes destroyed once phagocyte has taken up antigen
23
Q

normal immune complex clearance

A

complement breaks down large complexes

complement receptor 1 transfers complexes to phagocytes

24
Q

pathological immune complexes: antigen factors

A

chronic persistence
abnormal ratio of antigen to antibody
rate of complex formation

25
Q

pathological immune complexes: host factors

A

antibody defects
complement defects
Fc or phagocyte defects

26
Q

TIII: serum sickness

A

systemic illness

complexes distributed widely throughout many tissues

27
Q

TIII: arthus reaction

A

localised disorder

complexes formed in tissues

28
Q

TIII: clinical disorders

A

extrinsic allergic alveolitis e.g. Farmer’s lung

post-strep glomerulonephritis

29
Q

TIII: immune complex disease in kidney

A

cause of renal failure

glomerulonephritis

30
Q

TIII: Rx

A

antigen elimination
removal complexes
immunosuppressive Rx

31
Q

TIV hypersensitivity

A
delayed hypersensitivity (2-3days) 
mediated by Th1 and Th17 cells and the cytokines they secrete
32
Q

TIV pathophys

A
  • initiated when macrophages recognise danger signals and initiate inflammatory response
  • dendritic cell presents antigen to T cell
  • TNF secreted by T cells and macrophages