infection - Allergies Flashcards
what is hypersensitivity?
the antigen-specific immune responses that are either inappropriate or excessive and result in harm to host
what are the mechanisms underlying the inappropriate / excessive immune responses?
the mechanisms employed by the host to fight infections
what are the phases of hypersensitivity reactions?
sensitisation phase - 1st encounter with antigen
effector phase - re-exposure to same antigen
what are the types of hypersensitivity reactions?
type 1 - immediate <30mins - allergies (environmental non-infectious)
type 2: antibody mediated (5-12 hours)
type 3: immune complexes mediated (3-8 hours)
type 4: cell-mediated (24-48 hours) - environmental infectious agents & self antigens
which gene means people get allergies?
TH2 phenotype
IgE production
which gene means people don’t get allergies?
TH1 phenotype
what are the environmental factors which means people are less likely to get allergies?
developing countries large family size rural homes, livestock low Abx use poor sanitation intestinal microflora variability high oralfaecal & helminth burden
what are the environmental factors which pre-disposes people to allergies?
westinised countries small familu size affluent urban homes high Abx use good sanitation
what are common allergens?
house dust mite (faeces) animals (hair) tree & grass pollen inset venom - bee stings medicines - Abx penicillin chemicals - latex foods e.g. milk, peanuts, seafood
what is clinical cross-reactivity?
if you are allergic to one thing, you have an increased risk of being allergic to another e.g. cow’s milk predisposes to goat’s milk
what are some toxic mast cell mediators? function?
histamine & heparin - increase vascular permeability & cause SM contraction
what are some mast cell cytokines mediators?
- TNF-alpha: promotes inflammation, stimulates cytokine production
- IL-3, IL-5: promote eosinophil production & activation
- IL-4, IL-13: stimulate & amplify TH2 cell response (extracellular microbes) - eosinophils, B cell, mast cells
what are some lipid mediators of mast cell?
- leukotrienes C4 (released by eosinophils?) - SM contraction, increase vascular permeability, stimulate mucus secretion
(toxic to epithelium - shedding, asthma) - platelet- activating factor
what is the immune mechanism of allergic reaction on 2nd exposure?
allergen bind to mast cell, causing degranulation of histamine & chemokines
and synthesis of new mediators: leukotrienes, prostaglandins
(allergen cross-linking on 2nd exposure)
what does mast cell degranulation of histamine, chemokines, prostaglandins & leukotrienes lead to?
increased vascular permeability
vasodilation
bronchial constriction (SM)
what is the difference between 1st & 2nd exposure (mechanism)?
1st: IgE-mediated triggering of mast cell, plasma B cell finds the antigen-specific IgE which activates the mast cell
2. irritant directly activates mast cell
how does mast cells in EPIDERMIS activated manifest itself?
urticaria
how does mast cells in face activated manifest itself?
angioedema
mast cells in DEEP dermis
lips, eyes, tongue, upper resp airways
what is the systemic manifestations of allergic reaction?
anaphylaxis: systemic activation of mast cells hypotension CVS collapse generalised urticaria angioedema
breathing problems (broncho SM constriction)
what are signs & symptoms of anaphylaxis?
- CNS: lightheadedness, confusion, loss of consciousness, headache
- resp: SoB, wheeze (high pitch expiratory), stridor (harsh sound during inspiration), cough
- swelling of conjunctiva, lips, tongue (throat)
- skin: hives, itchiness, flushing
- CVS: tachy/bradycardia, LOW BP
- GI: D&V
what are the 3 rules of anaphylaxis?
- sudden onset, rapid progression
- involves at least 2 organs (one is skin / mucosa)
- 70% CVS involvement, drop in BP enough to make diagnosis
what is the treatment of anaphylactic shock? what is it’s MoA?
IM adrenaline:
- reversis peripheral vasodilation, reduces oedema & alleviates HYPOtension
- reverses airway obstruction / bronchospasm
- increases force of myocardial contraction
- inhibits mast cell degranulation (via ß2-receptor)
what are the things you need to monitor for a patient with anaphylactic shock?
pulse, BP, ECG, oximetry
DO NOT DELAY TREATMENT
how do you diagnose allergy?
- history: allergens, seasonal
- blood tests: serum allergen-specific IgE, serum mast cell tryptase, histamine
- skin prick test: wheal & flare reaction (>3mm) - mast cell in epidermis
- challenge tests: food & drug allergy (risk of anaphylaxis - trained personnel)
management of allergy?
- allergen avoidance / elimination
- education - recognise symptoms & EPIPEN use
- medic alert identification e.g. wrist-band
- drugs: anti-histamines, corticosteroids, IM adrenaline
- allergen desensitisation: specialist hospital based-unit with resus equipmen
what is allergen desensitisation / immunotherapy?
involves the administration of increasing doses of allergen extracts over a period of years
given to patients by injection / sublingual
(effective in bee / wasp venom stings)
what are the potential mechanisms of desensitisation?
shifts TH2 to TH1
inhibitory anti-inflammatory cytokines
allergen specific blocking IgG
CD4+CD25 regulatory T cells
