Allergic rhinitis and histamine Flashcards
(25 cards)
What is histamine
Histamine is a small, monoamine signalling molecule derived from histidine
Acts both as a neurotransmitter and immune modulator
What are the 4 receptor types
H1 - Inflammation
H2 - gastric acid secretion
H3 - Neurotransmission
H4 Immunomodulation
What is the mechanism behind H1 receptors
Alteration of vascular permeability > extravasation> causes oedema > adhesion molecules> inflammatory cell migration
How common are allergies and how do allergies occur
Allergies affect 1 in 4 people due to environmental and genetic factors. It is when the immune system overreacts to innocuous harmless antigens (allergens)
What is Atopy and give examples of Atopic disorders
Atopy = genetic tendency to produce excessive IgE in response to innocuous antigens
Atopic disorders: eczema, asthma, allergic rhinitis
Risk of atopy doubles with each atopic parent
What genetic factors affect atopy
Childs risk is doubled with each atopic parent.
What non genetic factors affect atopy
overly clean environments, low infections in childhood, exposure to smoke, reduced nutrients, stress. No siblings
What is allergic rhinitis (hay fever) and how is it triggered
Allergic inflammation of the nasal airways (turbinate and olfactory nerves)
Triggered when a sensitised immune system inhales an allergen
What are the 3 kinds of allergic rhinitis
Seasonal (pollens, spores grasses, trees and weeds) = hay fever (aka pollinosis)
Perennial (dust mites, animal dander, mould spores)
Occupational (chemicals in workplace)
What are the symptoms of allergic rhinitis
Sneezing, rhinorrhoea (clear, watery nasal discharge)
Itching (eyes, nose, ears)
Congestion, mouth breathing, snoring, halitosis
Eye involvement: bilateral itching, allergic conjunctivitis, eyelid swelling, “allergic shiners”
Ear issues: middle ear effusion,
infections
Post-nasal drip → cough, nausea
What do the turbinates do and how does their structure
Contains turbinates (superior, middle, inferior) = bony projections that:
Create turbulent airflow and filter air.
Narrow orifice
Large surface area
Mucus and Cillia
Turbulent airflow
What happens to the nasal turbinates during allergic rhinitis and how can they be seen
Swollen nasal turbinates can be seen via nasal endoscopy.
The septum and middle turbinate swell and pus enters the airt spaces between them (meatus) restricting airflow
What is rhinorrhoea and what are the symptoms of it
Excess nasal secretion
Clear thin colourless secretion (suggests rhinits rather than infection)
Persistent nasal discharge can cause post nasal drip (excess mucus draining through the back of the nose to throat, potential for cough, throat inflammation, nausea.
Allergic salute (horizontal crease)
What re the immunoglobulin classes and why is IgE important in the allergic response
5 different classes of immunoglobulin. IgE is comparatively absent in serum.
IgE’s antiparasitic and allergy roles require mast cells and basophils
How does IgE work in antiparasite targeting
IgE molecules specific to parasite antigen and formed during first exposure
Constant domain of IfE can attach to receptors on the surface of mast cells arming the cell to recognise a futute target
IgE normally on last 2 days in the blood but once attached to a mast cell, their half life is weeks or months
When next exposed to sufficient antigen, antibody binding triggers cargo release at the site of parasite infection
What is the immunological mechanism behind allergic histamine release
- Sensitisation (First exposure)
Allergen → presented to plasma B cells → plasma B cells produce large amounts of anti allergen IgE (class switching)
IgE binds to mast cells & basophils
Mast cells and basophils become “sensitised”
- Degranulation (Re-exposure)
Allergen cross-links IgE on mast cells and phosphorylates specific proteins→ triggers PLC to convert PIP 2 to IP3 and DAG → Causes release of calcium from endoplasmic reticulum → histamine and cytokine release
What triggers degranulation
Allergen binding via IgE
Trauma(burnt, blunt force)
Side effects of drugs (e.g. morphine)
What happens after degranulation
Mast cells deposit histamine, heparin,
cytokines and growth factors
Allergic response is mediated by H1 receptor
H1 activates PLC
How are symptoms caused by the IgE response
Nerve stimulation : Itching and sneezing
Vasodilation : Erythema
Leaking fluid from blood vessels: Rhinorrhea Nasal congestion eyelid swelling Allergic shiners
What is urticaria (hives) and how is it caused
Histamine- caused blotches and bumps.
Most likely to occur from skin contact with pollen than breathing in pollen. More commonly associated with foold allergies or insect bites
How does preventing histamine release aid allergic rhinitis
(Mast Cell Stabilisers)
e.g. Sodium cromoglycate
Blocks degranulation, though mechanism unclear
Non-steroidal; used in nasal sprays, eye drops
Especially useful in children and for ocular allergy
How does blocking histamine effects assist allergic rhinitis
Target: H1 receptor antagonists/inverse agonists
Sedating (1st gen): e.g. Diphenhydramine
Cross blood-brain barrier → drowsiness
Non-sedating (2nd gen): e.g. Loratadine, Cetirizine
Don’t cross BBB
Ketotifen: dual action (antihistamine + mast cell stabiliser)
How does supressing inflammation (glucocorticoids) treat allergic rhinitis and what are the side effects
Increase anti-inflammatory proteins, reduce pro-inflammatory ones
Topical administration
Delayed onset of action
Side effect: risk of infections, especially with eye use (bc of immuno suprresants
How does physiological counteraction treat allergic rhinitis (α-Adrenoceptor Agonists) and what are the risks
e.g. Phenylephrine, Xylometazoline
Alpha1 adrenoreceptor Cause vasoconstriction to oppose histamine-induced vasodilation
Don’t use long-term → risk of rebound congestion
