1
Q
What is anaphylaxis?
A
A severe, life-threatening, systemic hypersensitivity reaction with rapid onset, causing airway, breathing, and/or circulatory compromise.
2
Q
What type of reaction is anaphylaxis?
A
A Type I (immediate) hypersensitivity reaction.
3
Q
What are the two main immunologic mechanisms of anaphylaxis?
A
IgE-mediated and non-IgE-mediated mechanisms.
4
Q
What is IgE-mediated anaphylaxis?
A
An allergic reaction where IgE antibodies bind to mast cells and basophils, triggering mediator release after re-exposure to an allergen.
5
Q
What is non-IgE-mediated anaphylaxis?
A
Direct mast cell activation without IgE involvement, often triggered by drugs, contrast media, or physical factors.
6
Q
Which cells are central to anaphylaxis?
A
Mast cells and basophils.
7
Q
What happens during mast cell and basophil degranulation?
A
Rapid release of inflammatory mediators into the circulation.
8
Q
What is the role of histamine in anaphylaxis?
A
Causes vasodilation, increased vascular permeability, bronchoconstriction, pruritus, and urticaria.
9
Q
What is the role of leukotrienes in anaphylaxis?
A
Cause potent and prolonged bronchoconstriction, increased mucus production, and airway oedema.
10
Q
What is the role of prostaglandins in anaphylaxis?
A
Contribute to vasodilation, bronchospasm, and inflammation.
11
Q
How do these mediators cause shock in anaphylaxis?
A
By causing systemic vasodilation and capillary leak, leading to hypotension and reduced organ perfusion
12
Q
Why does anaphylaxis progress rapidly?
A
Because mediator release is sudden and systemic.
13
Q
Why is adrenaline effective in anaphylaxis?
A
It counteracts mediator effects by causing vasoconstriction, bronchodilation, and stabilisation of mast cells.
14
Q
One-line pathophysiology summary?
A
Trigger → mast cell degranulation → mediator release → airway, breathing, and circulatory failure.
15
Q
What are the most common food triggers of anaphylaxis?
A
Nuts (especially peanuts and tree nuts)
Shellfish (prawns, crab, lobster)
Eggs
📌 Food is the most common trigger in children
16
Q
Which drugs commonly cause anaphylaxis?
A
Penicillins (most common drug cause)
NSAIDs (e.g. ibuprofen, aspirin)
Radiological contrast media
📌 Always ask about previous drug reactions
17
Q
Which insects are common triggers of anaphylaxis?
A
Bees
Wasps
📌 Venom-induced anaphylaxis is more common in adults
18
Q
How does latex cause anaphylaxis and who is at risk?
A
Triggered by natural rubber latex exposure
High-risk groups:
Healthcare workers
Patients with multiple surgeries (e.g. spina bifida)
19
Q
What is idiopathic anaphylaxis?
A
Anaphylaxis with no identifiable trigger despite full evaluation
📌 Diagnosis of exclusion
20
Q
Can anaphylaxis occur without skin signs?
A
Yes. Skin signs may be absent, especially in severe or rapidly progressive anaphylaxis.
21
Q
Which body systems are typically involved in anaphylaxis?
A
Airway
Breathing
Circulation
Skin/mucosa
Gastrointestinal (GI)
22
Q
What are the key airway features of anaphylaxis?
A
Hoarseness
Stridor
Tongue swelling
→ Suggest upper airway oedema and impending obstruction
23
Q
What are the main breathing features of anaphylaxis?
A
Wheeze
Bronchospasm
Hypoxia
→ Due to lower airway constriction
24
Q
What circulatory signs indicate anaphylaxis?
A
Hypotension
Shock
Collapse
→ From vasodilation and capillary leak
25
What skin and mucosal features may be seen in anaphylaxis?
Urticaria
Angioedema
Flushing
⚠️ May be absent in severe cases
26
hat gastrointestinal symptoms occur in anaphylaxis?
Vomiting
Abdominal pain
Diarrhoea
→ Due to smooth muscle contraction
27
How is anaphylaxis clinically diagnosed?
By acute onset of illness with airway, breathing, or circulatory compromise, with or without skin features
28
How is anaphylaxis diagnosed?
Clinically.
👉 Do NOT wait for tests to make the diagnosis or start treatment.
29
What is the first major diagnostic criterion for anaphylaxis?
Sudden onset of illness with airway, breathing, or circulation compromise
30
What is the second diagnostic criterion for anaphylaxis?
Two or more organ systems involved after exposure to a likely allergen
(e.g. skin + breathing, GI + circulation)
31
What is the third diagnostic criterion for anaphylaxis?
Hypotension after exposure to a known allergen
(even if other features are mild or absent)
32
Are skin features required to diagnose anaphylaxis?
No.
Anaphylaxis can occur without rash, urticaria, or angioedema.
33
What is the key mistake to avoid when diagnosing anaphylaxis?
Delaying treatment while waiting for blood tests (e.g. tryptase)
34
Complete the sentence: “Anaphylaxis is a ______ diagnosis.”
Clinical diagnosis
35
What is the first priority in managing anaphylaxis?
ABC approach (Airway, Breathing, Circulation)
36
What is the first-line treatment for anaphylaxis?
IM adrenaline (epinephrine)
37
What is the recommended adult dose of IM adrenaline in anaphylaxis?
0.5 mg IM
38
Where should IM adrenaline be given?
Mid-anterolateral thigh (vastus lateralis)
39
How often can IM adrenaline be repeated?
Every 5 minutes if there is no clinical response
40
Why is adrenaline the drug of choice in anaphylaxis?
Reverses airway oedema
Treats bronchospasm
Restores blood pressure via vasoconstriction
41
What supportive oxygen therapy is indicated?
High-flow oxygen
42
What circulatory support should be given in anaphylaxis?
IV access
Rapid IV fluid bolus (for hypotension/shock)
43
How should the patient be positioned during anaphylaxis?
Lie flat
Left lateral position if pregnant
44
What is the most common cause of death in anaphylaxis management?
Delayed or inadequate adrenaline administration
45
Are antihistamines, steroids, or beta-agonists lifesaving in anaphylaxis?
No.
👉 Adrenaline is the only lifesaving drug.
46
What is the role of antihistamines in anaphylaxis?
Relieve skin symptoms only
Urticaria, itching, flushing
❌ Do NOT treat airway, breathing, or circulation
47
Do antihistamines prevent progression of anaphylaxis?
No.
They are symptomatic only, not disease-modifying
48
What is the role of corticosteroids in anaphylaxis?
May reduce delayed or biphasic reactions
Evidence is weak
49
Why are corticosteroids NOT first-line in anaphylaxis?
Slow onset of action
Do not treat acute airway or shock
50
What is the role of beta-agonists (e.g. salbutamol)?
Treat bronchospasm only
Adjunct to adrenaline, not a substitute
51
Can beta-agonists replace adrenaline in wheezy anaphylaxis?
No.
Adrenaline must always be given first.
52
What is the most dangerous misconception in anaphylaxis management?
Using antihistamines or steroids instead of adrenaline
53
Why is early airway assessment essential in anaphylaxis?
Because airway oedema can progress rapidly, leading to sudden obstruction.
54
Which airway features suggest impending obstruction in anaphylaxis?
Hoarseness
Stridor
Tongue or lip swelling
Difficulty speaking or swallowing
55
What is the key airway danger in anaphylaxis?
Rapidly progressive upper airway oedema
56
Why should you assume a difficult airway in anaphylaxis?
Distorted anatomy from oedema
Poor laryngoscopic view
Rapid deterioration possible
57
What airway preparations should be made early in anaphylaxis?
Call for senior help early
Prepare difficult airway equipment
Have a surgical airway kit ready
58
What is the role of adrenaline in airway management?
Reduces airway oedema
May delay or prevent intubation
59
When should you consider early intubation in anaphylaxis?
Progressive airway swelling
Worsening voice or stridor
Inability to lie flat
Poor response to IM adrenaline
60
Why is delayed intubation dangerous in anaphylaxis?
Airway oedema may progress to a “can’t intubate, can’t oxygenate” (CICO) situation
61
When must you escalate to a surgical airway?
Failed intubation + failed oxygenation
Severe upper airway obstruction not relieved by adrenaline
62
What is the single biggest airway mistake in anaphylaxis?
Underestimating how fast airway oedema can progress
63
What is refractory anaphylaxis?
Persistent or worsening symptoms despite appropriate IM adrenaline.
64
What must be confirmed before calling anaphylaxis refractory?
Correct IM adrenaline dose
Correct site (mid-anterolateral thigh)
Repeated doses given at appropriate intervals
65
What is the next step if anaphylaxis is refractory to IM adrenaline?
IV adrenaline infusion
⚠️ Expert / ICU / monitored setting only
66
Why is IV adrenaline restricted to expert settings?
High risk of arrhythmias
Requires continuous monitoring and titration
67
Which patients are at higher risk of refractory anaphylaxis?
Patients on beta-blockers
Severe asthma
Delayed adrenaline administration
68
Why can beta-blockers worsen anaphylaxis?
They blunt the response to adrenaline, making hypotension and bronchospasm harder to treat.
69
What drug should be considered in anaphylaxis patients on beta-blockers?
Glucagon
70
How does glucagon help in beta-blocker–associated anaphylaxis?
Increases heart rate and contractility
Works independently of beta-adrenergic receptors
71
True or False: Failure of antihistamines and steroids defines refractory anaphylaxis.
False.
Refractory anaphylaxis is defined by failure of adrenaline.
72
Complete the sentence: “Refractory anaphylaxis requires escalation to ______.”
IV adrenaline ± glucagon (expert care)
73
What is a biphasic reaction in anaphylaxis?
Recurrence of anaphylactic symptoms after initial recovery, without re-exposure to the allergen.
74
When do biphasic reactions typically occur?
Hours after initial resolution, usually within 4–12 hours, but can occur later.
75
Do biphasic reactions require re-exposure to the trigger?
No—they occur without further allergen exposure.
76
Which symptoms can recur in a biphasic reaction?
Any anaphylactic features, including airway, breathing, and circulatory compromise.
77
Why are biphasic reactions clinically important?
Because patients may deteriorate after appearing stable, potentially outside hospital.
78
Why is observation required after anaphylaxis?
To detect and treat biphasic reactions early.
79
What is the minimum observation period after mild anaphylaxis?
At least 4 hours after symptom resolution.
80
When is prolonged observation (≥12 hours) required?
In patients with:
Severe or refractory anaphylaxis
Multiple doses of adrenaline required
Hypotension or airway involvement
Asthma or high-risk comorbidities
81
Do steroids reliably prevent biphasic reactions?
No—evidence is weak.
82
Key exam rule about discharge after anaphylaxis?
Never discharge immediately after symptom resolution—observe first.
83
One-line takeaway?
Anaphylaxis can return hours later—observe every patient appropriately.
84
Are investigations required to diagnose anaphylaxis?
No.
👉 Anaphylaxis is a clinical diagnosis – do NOT delay treatment for tests.
85
What is serum tryptase?
A marker of mast-cell degranulation released during anaphylaxis.
86
Is serum tryptase used for acute diagnosis of anaphylaxis?
No.
It is NOT helpful acutely and does not rule out anaphylaxis if normal.
87
Why can serum tryptase be normal in true anaphylaxis?
Food-related anaphylaxis may not raise tryptase
Early or delayed sampling
Non–mast-cell-dominant reactions
88
When should serum tryptase be taken?
1–2 hours after symptom onset (peak level)
A baseline sample later (e.g. ≥24 hours after recovery)
89
Why is a baseline tryptase level useful?
Confirms a true rise from baseline
Helps identify mast cell disorders if persistently elevated
90
What is the main purpose of measuring serum tryptase?
Retrospective confirmation of anaphylaxis
Medico-legal documentation
Allergy specialist assessment
91
What is the biggest mistake regarding tryptase in anaphylaxis?
Using it to exclude anaphylaxis or delaying adrenaline while waiting for results
92
Complete the sentence: “Serum tryptase is for ______, not ______.”
Confirmation, not acute diagnosis
93
What is the most important medication to prescribe on discharge after anaphylaxis?
Adrenaline auto-injector
94
How many adrenaline auto-injectors should patients usually be prescribed
Two
→ In case symptoms recur or the first dose fails
95
What education must be given about the adrenaline auto-injector?
When to use it
How to use it
Inject into outer thigh
Use immediately if symptoms recur
96
Why is trigger avoidance education essential after anaphylaxis?
To prevent recurrence of a potentially fatal reaction
97
What trigger-related advice should be given to patients?
Identify likely allergens
Read food/medication labels
Inform healthcare providers
Avoid known triggers
98
Who should all patients with anaphylaxis be referred to?
Allergy specialist
99
Why is allergy referral important?
Confirm trigger
Perform formal allergy testing
Guide long-term prevention
100
What is the most common discharge error after anaphylaxis?
Discharging without an adrenaline auto-injector and education
101
What is the most common and dangerous error in anaphylaxis management?
Delaying adrenaline
102
What is the correct route for first-line adrenaline in anaphylaxis?
IM adrenaline
⚠️ Giving IV adrenaline initially is a major exam and clinical error.
103
Why is IV adrenaline inappropriate as first-line therapy?
High risk of arrhythmias
Requires expert monitoring
IM is safer and effective
104
Why is relying on antihistamines a management pitfall?
They treat skin symptoms only and do not reverse airway or shock.
105
What position should a hypotensive anaphylaxis patient be placed in?
Lie flat
❌ Sitting upright can cause sudden cardiovascular collapse.
106
When is an upright position acceptable in anaphylaxis?
Never if hypotensive
(Left lateral only if pregnant)
107
Why is missing anaphylaxis without rash a common pitfall?
Because skin signs may be absent, especially in severe or rapidly progressive cases.
108
Which systems matter more than the presence of a rash?
Airway, Breathing, Circulation
109
True or False: Absence of urticaria excludes anaphylaxis.
False
110
Complete the sentence: “When in doubt, give ______.”
Adrenaline
111
Which investigation best supports the diagnosis of recent anaphylaxis?
Question 1 options:
Serum tryptase measured several hours after onset
Patch testing
Eosinophil count
Serum IgE at presentation
Serum tryptase measured several hours after onset
Why?
Serum tryptase is released from mast cells during anaphylaxis
It peaks ~1–2 hours
112
Question 2 (1 point)
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A rash recurs at the same site every time a patient takes a particular antibiotic.
What is the most likely diagnosis?
Question 2 options:
Acute eczema
Urticarial vasculitis
Toxic epidermal necrolysis
Fixed drug eruption
Fixed drug eruption
Why?
Classic feature: lesions recur at exactly the same site with re-exposure to the drug
Commonly due to antibiotics (e.g. sulfonamides), NSAIDs
Lesions are well-demarcated, erythematous ± blistering, leaving post-inflammatory hyperpigmentation
Why the others are wrong:
❌ Acute eczema → diffuse, not site-specific
❌ Urticarial vasculitis → painful, persistent wheals, systemic features
❌ Toxic epidermal necrolysis → widespread epidermal necrosis, very severe
113
Saved
A 75 kg adult with anaphylaxis requires adrenaline.
What is the correct initial intramuscular dose?
Question 3 options:
5 mg
1 mg
0.5 mg
0.05 mg
0.5 mg
Why?
Adult anaphylaxis IM adrenaline dose = 0.5 mg IM
This corresponds to 0.5 mL of 1:1000 (1 mg/mL) adrenaline
Given into the anterolateral thigh
Can be repeated every 5 minutes if no clinical improvement
Why the others are wrong:
❌ 5 mg → dangerously high (cardiac arrest dosing)
❌ 1 mg → IV cardiac arrest dose, not IM anaphylaxis
❌ 0.05 mg → underdosing (paediatric range)
In adults, the IM adrenaline dose for anaphylaxis is fixed (0.5 mg) — not weight-based.
114
Question 4 (1 point)
Saved
A patient collapses minutes after a bee sting with stridor, wheeze, and hypotension.
What is the single most appropriate immediate treatment?
Question 4 options:
Nebulised salbutamol
Intravenous antihistamine
Intravenous adrenaline
Intramuscular adrenaline
Intramuscular adrenaline
Why?
This is classic anaphylaxis (airway + breathing + circulation involvement).
IM adrenaline is:
First-line
Fastest safe route
Reduces airway oedema, bronchospasm, and hypotension
Given into the anterolateral thigh.
Why the others are wrong:
❌ Nebulised salbutamol → adjunct only (bronchospasm), does not treat shock
❌ Intravenous antihistamine → slow onset, adjunct only
❌ Intravenous adrenaline → not first-line; reserved for refractory cases in expert settings due to arrhythmia risk
115
Question 5 (1 point)
Which feature best distinguishes hereditary angio-oedema from allergic angio-oedema?
Question 5 options:
Pruritus
Non-itchy swelling lasting several days
Rapid response to antihistamines
Presence of urticaria
Non-itchy swelling lasting several days
Why?
Hereditary angio-oedema (HAE) is bradykinin-mediated, not histamine-mediated.
Key distinguishing features:
Non-pruritic (not itchy)
No urticaria
Swelling develops slowly and lasts 2–5 days
Poor or no response to antihistamines, steroids, or adrenaline
Why the others are wrong:
❌ Pruritus → suggests allergic (histamine-mediated) angio-oedema
❌ Rapid response to antihistamines → allergic angio-oedema
❌ Presence of urticaria → allergic, excludes HAE
Exam pearl 🧠:
Angio-oedema without itch or urticaria = think bradykinin (HAE, ACE-inhibitors).
116
Question 6 (1 point)
Saved
Which clinical feature increases the probability of asthma in a wheezing adult?
Question 6 options:
Chronic productive cough without wheeze
Prominent dizziness
Symptoms only during viral infections
Personal or family history of atopy
Personal or family history of atopy
Why?
Asthma is strongly associated with atopy:
Eczema
Allergic rhinitis
Food or drug allergies
A personal or family history of atopy significantly increases the likelihood that wheeze is due to asthma.
Why the others are wrong:
❌ Chronic productive cough without wheeze → suggests COPD or bronchiectasis
❌ Prominent dizziness → non-specific, not suggestive of asthma
❌ Symptoms only during viral infections → more typical of viral-induced wheeze, not asthma
Exam pearl 🧠:
Adult wheeze + atopy = asthma until proven otherwise.
117
Saved
A 22-year-old woman with no previous allergy history develops generalized erythema, wheeze, hypotension, and vomiting shortly after receiving intravenous acetylcysteine.
Which mechanism best explains this reaction?
Question 7 options:
Immune-complex deposition
Direct mast-cell mediator release without antibody involvement
IgE-mediated hypersensitivity requiring prior sensitisation
Delayed T-cell mediated hypersensitivity
Direct mast-cell mediator release without antibody involvement
Why?
This is an anaphylactoid (non–IgE-mediated) reaction.
IV acetylcysteine commonly causes direct mast-cell degranulation.
No prior sensitisation is required.
Clinically indistinguishable from anaphylaxis.
Why the others are wrong:
❌ Immune-complex deposition → type III hypersensitivity (e.g. serum sickness)
❌ IgE-mediated hypersensitivity requiring prior sensitisation → unlikely with first exposure
❌ Delayed T-cell mediated hypersensitivity → occurs days later (e.g. contact dermatitis)
Exam pearl 🧠:
First exposure + anaphylaxis-like picture = think non–IgE-mediated mast-cell activation (anaphylactoid).
118
A patient has recurrent urticarial lesions lasting over 24 hours, leaving bruising, with associated arthralgia.
What is the most likely diagnosis?
Question 8 options:
Cholinergic urticaria
Dermographism
Contact dermatitis
Urticarial vasculitis
Urticarial vasculitis
Why?
Key distinguishing features of urticarial vasculitis:
Lesions persist > 24 hours
Often painful or burning rather than itchy
Heal with residual bruising or hyperpigmentation
Systemic symptoms common (arthralgia, fever, abdominal pain)
It is a small-vessel vasculitis rather than simple urticaria.
Why the others are wrong:
❌ Cholinergic urticaria → small, short-lived wheals (<1 hour), exercise/heat triggered
❌ Dermographism → transient wheals after scratching, no bruising
❌ Contact dermatitis → eczematous rash, delayed, not migratory wheals
Exam pearl 🧠:
Urticaria that lasts >24 h + bruising = vasculitis until proven otherwise
119
Question 9 (1 point)
Saving...
Which group is permitted to administer intramuscular adrenaline in the community?
Question 9 options:
Doctors only
Nurses only
Trained laypersons
Paramedics only
Trained laypersons
Why?
IM adrenaline (e.g. via adrenaline auto-injectors like EpiPen®) can be legally and safely administered in the community by trained laypersons.
This includes:
Patients themselves
Parents/caregivers
Teachers or first aiders with training
Early administration is life-saving and should not be delayed waiting for medical professionals.
Why the others are wrong:
❌ Doctors only → too restrictive; delays treatment
❌ Nurses only → incorrect
❌ Paramedics only → incorrect; community use is encouraged
Exam pearl 🧠:
If you can recognise anaphylaxis and you are trained, you can give IM adrenaline.
120
A patient with anaphylaxis is taking a beta-blocker and responds poorly to adrenaline.
Which medication should be considered?
Question 10 options:
Hydrocortisone
Salbutamol
Noradrenaline
Glucagon
Glucagon
Why?
Beta-blockers blunt the effect of adrenaline (β-receptor antagonism).
Glucagon increases intracellular cAMP independently of β-adrenergic receptors, restoring:
- Inotropy
- Chronotropy
- Blood pressure
It is the recommended rescue drug in adrenaline-resistant anaphylaxis due to beta-blockers.
Why the others are wrong:
❌ Hydrocortisone → delayed effect; prevents biphasic reactions, not acute reversal
❌ Salbutamol → adjunct for bronchospasm only
❌ Noradrenaline → may be used in ICU for refractory shock, but does not overcome β-blockade
Exam pearl 🧠:
Anaphylaxis + β-blocker + poor adrenaline response = glucagon
121
Question 11 (1 point)
Saving...
Which discharge measure most effectively reduces the risk of fatal recurrence after anaphylaxis?
Question 11 options:
Routine ENT referral
Oral antihistamines
Adrenaline autoinjector prescription and training
Avoidance advice only
Adrenaline autoinjector prescription and training
122
Saving...
Which drug reaction is characterised by widespread epidermal sloughing involving more than 30% of body surface area?
Question 12 options:
Fixed drug eruption
Erythema multiforme
Toxic epidermal necrolysis
Stevens–Johnson syndrome
Toxic epidermal necrolysis
Why?
Toxic epidermal necrolysis (TEN) is defined by:
>30% body surface area epidermal detachment
Full-thickness epidermal necrosis
High mortality
It is most commonly drug-induced (e.g. sulfonamides, anticonvulsants, allopurinol).
Key distinctions (exam favourite):
Stevens–Johnson syndrome (SJS): <10% BSA
SJS–TEN overlap: 10–30% BSA
TEN: >30% BSA
Why the others are wrong:
❌ Fixed drug eruption → localized, recurrent lesions
❌ Erythema multiforme → target lesions, minimal epidermal loss
❌ Stevens–Johnson syndrome → less extensive skin involvement
Exam pearl 🧠:
Think of SJS and TEN as a spectrum — % skin loss defines the diagnosis.
123
Question 13 (1 point)
Saving...
Which screening investigation is most appropriate when hereditary angio-oedema is suspected?
Question 13 options:
Serum tryptase
Serum C4 level
Skin-prick testing
Serum IgE
Serum C4 level
Why?
Hereditary angio-oedema (HAE) is due to C1 esterase inhibitor deficiency or dysfunction.
Serum C4 is persistently low, even between attacks.
It is the best initial screening test for suspected HAE.
Why the others are wrong:
❌ Serum tryptase → elevated in mast-cell–mediated anaphylaxis, not HAE
❌ Skin-prick testing → assesses IgE-mediated allergy
❌ Serum IgE → usually normal in HAE
Exam pearl 🧠:
Recurrent angio-oedema without urticaria → check C4 first
124
Question 14 (1 point)
Saving...
Which clinical scenario does NOT meet diagnostic criteria for anaphylaxis?
Question 14 options:
Urticaria with wheeze and hypotension
Acute hypotension after allergen exposure without skin features
Vomiting, wheeze, and collapse after food ingestion
Facial swelling alone with no systemic features
Facial swelling alone with no systemic features
Why?
Anaphylaxis requires systemic involvement, typically affecting ≥2 organ systems (skin, respiratory, cardiovascular, gastrointestinal) or isolated hypotension after a known allergen.
Isolated facial swelling (angio-oedema) without respiratory compromise, hypotension, or GI symptoms does not meet criteria.
Why the others DO meet criteria:
✅ Urticaria + wheeze + hypotension → skin + respiratory + cardiovascular
✅ Acute hypotension after allergen exposure without skin features → diagnostic on its own
✅ Vomiting + wheeze + collapse after food ingestion → GI + respiratory + cardiovascular
Exam pearl 🧠:
Skin signs are common but not mandatory for anaphylaxis — systemic involvement is the key.
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Question 15 (1 point)
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After the first adrenaline dose, a patient remains hypotensive and wheezy.
What is the most appropriate next step?
Question 15 options:
Repeat intramuscular adrenaline after 5 minutes if needed
Give antihistamines before further adrenaline
Observe for 30 minutes
Switch immediately to intravenous adrenaline
Repeat intramuscular adrenaline after 5 minutes if needed
Why?
IM adrenaline is first-line and may be repeated every 5 minutes if there is ongoing airway, breathing, or circulatory compromise.
Many patients require multiple IM doses before stabilising.
This should be done while providing high-flow oxygen, IV fluids, and calling for senior help.
Why the others are wrong:
❌ Give antihistamines before further adrenaline → antihistamines are adjuncts and must never delay adrenaline
❌ Observe for 30 minutes → inappropriate in ongoing anaphylaxis
❌ Switch immediately to intravenous adrenaline → IV adrenaline is reserved for refractory cases in expert/monitored settings
Exam pearl 🧠:
Persistent anaphylaxis = repeat IM adrenaline first, not antihistamines or IV adrenaline.
126
Question 16 (1 point)
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A patient develops non-itchy facial swelling shortly after starting an ACE inhibitor.
Which mediator is primarily responsible?
Question 16 options:
Histamine
Serotonin
Bradykinin
IgE
Bradykinin
Why?
ACE inhibitors reduce breakdown of bradykinin.
Accumulated bradykinin increases vascular permeability → angio-oedema.
Features:
Non-pruritic
No urticaria
Poor response to antihistamines, steroids, or adrenaline
Why the others are wrong:
❌ Histamine → allergic/IgE-mediated angio-oedema
❌ Serotonin → not a key mediator here
❌ IgE → requires allergic sensitisation
Exam pearl 🧠:
ACE-inhibitor angio-oedema = bradykinin, not histamine.
127
Question 17 (1 point)
Saving...
A patient develops small, intensely itchy papules shortly after exercise that resolve within hours.
What is the most likely diagnosis?
Question 17 options:
Cold urticaria
Stevens–Johnson syndrome
Urticarial vasculitis
Cholinergic urticaria
Cholinergic urticaria
Why?
Cholinergic urticaria is triggered by:
Exercise
Heat
Emotional stress
Typical features:
Small (1–3 mm) intensely pruritic papules
Rapid onset
Short duration (minutes to a few hours)
Often surrounded by erythema
Why the others are wrong:
❌ Cold urticaria → triggered by cold exposure
❌ Stevens–Johnson syndrome → severe mucocutaneous reaction, not transient papules
❌ Urticarial vasculitis → lesions last >24 hours, bruise, systemic features
Exam pearl 🧠:
Exercise + tiny itchy papules + quick resolution = cholinergic urticaria
128
Question 18 (1 point)
Saving...
Which additional treatment is appropriate in anaphylaxis with persistent hypotension?
Question 18 options:
Furosemide
0.9% saline bolus
Morphine
Fluid restriction
0.9% saline bolus
Why?
Anaphylaxis causes profound vasodilation and capillary leak, leading to relative hypovolaemia.
Rapid IV isotonic crystalloid (0.9% saline) is essential when hypotension persists despite adrenaline.
Large volumes may be required (e.g. 1–2 L in adults, titrated to response).
Why the others are wrong:
❌ Furosemide → worsens hypovolaemia
❌ Morphine → causes histamine release and hypotension
❌ Fluid restriction → dangerous in shock
Exam pearl 🧠:
Anaphylaxis shock = adrenaline + fluids
129
Question 19 (1 point)
A teenager with asthma has recurrent wheeze, mucus plugging, eosinophilia, very high IgE, positive Aspergillus testing, and bronchiectasis.
What is the most likely diagnosis?
Question 19 options:
Severe asthma
Allergic bronchopulmonary aspergillosis (ABPA)
Bronchiolitis obliterans
Pulmonary tuberculosis
Allergic bronchopulmonary aspergillosis (ABPA)
Why?
Classic constellation for ABPA:
Underlying asthma
Very high IgE
Eosinophilia
Positive Aspergillus sensitisation
Mucus plugging and central bronchiectasis
Represents a hypersensitivity reaction to Aspergillus fumigatus colonising the airways.
Why the others are wrong:
❌ Severe asthma → does not explain very high IgE + Aspergillus positivity + bronchiectasis
❌ Bronchiolitis obliterans → post-infectious, fixed airflow obstruction, no high IgE/eosinophilia
❌ Pulmonary tuberculosis → constitutional symptoms, cavities/nodes, not this immunologic profile
Exam pearl 🧠:
Asthma + high IgE + eosinophilia + bronchiectasis = ABPA
130
General Medicine
flashcards
Decks in class (37)
# Cards
-
EOB Exams659
-
ECG Module 196
-
ECG Module 2153
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ECG Module 3: normal sinus rhythm284
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ECG Module 4: Wave abnormalities324
-
ECG Module 5: Rhythm abnormalities243
-
Chest X- ray165
-
Hypertension52
-
Advanced Airway Management341
-
CPR48
-
Post Cardiac Arrest Care35
-
CardioPulmonary Resuscitation532
-
Basic Airway Management122
-
Capnography41
-
Ventilator Settings27
-
Ventilation15
-
Anaphylaxis130
-
Cardiac Infections75
-
Benzodiazepine Overdose112
-
Iron Overdose92
-
Opioid Overdose122
-
Paracetamol Overdose107
-
TCA Overdose80
-
Bradycardia198
-
Tachycardia251
-
Hyponatremia121
-
Hyperthermia27
-
Hypothermia71
-
Hypertensive Emergency146
-
Delirium127
-
Sepsis105
-
Status Epilepticus108
-
Snack bites155
-
Acute Kidney Injury101
-
Pneumonia22
-
Bronchiectasis23
-
COPD40
