CTB8 Flashcards
What is anaphylaxis?
A severe systemic allergic reaction involving respiratory and cardiovascular systems.
What triggers anaphylaxis?
Allergens such as foods, insect stings, drugs (e.g., penicillin), and latex.
How does IgE contribute to anaphylaxis?
IgE binds mast cells and basophils, causing degranulation upon antigen exposure.
What mediators are released during mast cell degranulation?
Histamine, leukotrienes, prostaglandins, and cytokines.
What is the physiological effect of histamine?
Vasodilation, increased vascular permeability, bronchoconstriction, and itching.
What are the four classical signs of acute inflammation?
Rubor (redness), calor (heat), tumor (swelling), and dolor (pain).
What is loss of function (functio laesa)?
A fifth sign of inflammation; severe dysfunction results in systemic collapse in anaphylaxis.
How does anaphylaxis affect the cardiovascular system?
Systemic vasodilation causes hypotension and shock.
What happens to the respiratory system during anaphylaxis?
Bronchoconstriction, airway oedema, and mucus production cause dyspnoea.
Why is adrenaline the first-line treatment for anaphylaxis?
It reverses hypotension (vasoconstriction), bronchodilation, and mast cell stabilisation.
What are the ABC principles of anaphylaxis treatment?
Airway, Breathing, and Circulation.
What is the role of leukotrienes in anaphylaxis?
They sustain bronchoconstriction, inflammation, and increased vascular permeability.
What happens to mast cells during anaphylaxis?
They degranulate, releasing preformed and newly synthesised mediators.
How is anaphylactic shock defined?
Severe hypotension and tissue hypoperfusion due to systemic vasodilation.
What is the function of basophils in anaphylaxis?
They complement mast cell responses, releasing histamine and other mediators.
What is the role of prostaglandins in anaphylaxis?
They induce pain, vasodilation, and inflammation.
What pathway leads to IgE production?
Th2 cells stimulate B cells to switch to IgE production in response to antigens.
What are the symptoms of anaphylaxis?
Rashes, swelling, hypotension, bronchospasm, gastrointestinal distress, and dizziness.
How is anaphylaxis diagnosed clinically?
By acute onset of symptoms involving skin, respiratory, cardiovascular, or gastrointestinal systems.
What is the incidence of anaphylaxis in the population?
Approximately 0.05-2% of people experience anaphylaxis.
What does adrenaline act on to restore cardiovascular function?
Alpha-1 receptors (vasoconstriction) and beta-2 receptors (bronchodilation).
Why does vascular permeability increase in anaphylaxis?
Histamine and leukotrienes induce endothelial cell contraction, causing leakage.
How can anaphylaxis cause laryngeal oedema?
Increased vascular permeability causes fluid leakage into airway tissues.
What is biphasic anaphylaxis?
A recurrence of symptoms hours after the initial reaction, even with treatment.
Why are antihistamines used in anaphylaxis management?
They block histamine action, reducing swelling, itching, and rash.
What is the role of glucocorticoids in anaphylaxis?
They reduce late-phase inflammation and prevent recurrent symptoms.
What are lipid mediators?
Molecules like leukotrienes and prostaglandins produced from arachidonic acid.
Why is oxygen therapy important in anaphylaxis?
It counters hypoxaemia caused by bronchoconstriction and airway oedema.
What is the role of tryptase in anaphylaxis?
Tryptase is a mast cell-specific enzyme that can confirm mast cell activation.
Why is mast cell activation rapid in anaphylaxis?
Pre-formed mediators (e.g., histamine) are released immediately upon antigen binding.
What are the key inducers of anaphylaxis?
Foods, drugs, insect stings, and latex.
What mechanisms cause hypotension in anaphylaxis?
Systemic vasodilation and increased capillary permeability reduce blood volume.
How does anaphylaxis affect gastrointestinal function?
Smooth muscle contraction causes nausea, vomiting, abdominal pain, and diarrhoea.
How does IgE-mediated hypersensitivity differ from other types?
It is immediate, mediated by IgE, and causes mast cell degranulation.
How are adrenaline auto-injectors used in emergency management?
They deliver intramuscular adrenaline to quickly reverse symptoms.
Why does anaphylaxis sometimes cause wheezing?
Bronchoconstriction reduces airway diameter, increasing airflow resistance.
How do cytokines contribute to anaphylaxis?
They amplify inflammation by recruiting immune cells.
What are common anaphylaxis risk factors?
Previous allergic reactions, atopy, asthma, and exposure to known allergens.
Why does anaphylaxis need rapid treatment?
It can progress rapidly to shock, respiratory failure, and death if untreated.
What long-term strategies help prevent anaphylaxis?
Allergen avoidance, desensitisation therapy, and carrying an adrenaline auto-injector.
What is the role of IL-4 in IgE production?
IL-4 promotes B-cell class switching to produce IgE antibodies.
Why is adrenaline given intramuscularly in anaphylaxis?
IM administration provides rapid absorption and onset of action.
What causes skin rashes and urticaria in anaphylaxis?
Histamine induces vasodilation and increased capillary permeability.
How does hypoxaemia occur during anaphylaxis?
Airway obstruction and bronchospasm limit oxygen delivery to alveoli.
How does anaphylaxis affect heart rate?
Tachycardia occurs due to compensatory sympathetic activation.
Why can anaphylaxis lead to unconsciousness?
Severe hypotension and hypoperfusion impair brain function.
How does adrenaline stabilise mast cells?
It reduces mediator release by acting on beta-2 receptors.
What are the emergency steps for suspected anaphylaxis?
Administer adrenaline, call emergency services, provide oxygen, and monitor vitals.
Why are beta-blockers risky in anaphylaxis?
They block adrenaline’s effects, reducing treatment efficacy.
How does leukotriene receptor antagonism benefit anaphylaxis patients?
It blocks leukotriene activity, reducing bronchoconstriction and inflammation.
