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MBBS IV - Junior Clerkship WCS > JC85 (Medicine) - Urticaria, Angioedema, Anaphylaxis > Flashcards

JC85 (Medicine) - Urticaria, Angioedema, Anaphylaxis Flashcards

1
Q

Clinical definition of wheals

A
  1. Central swelling (palpable)
  2. Pruritus
  3. Fleeting nature - Resolution < 24 hours
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2
Q

Compare wheals with urticarial vasculitis

A

Wheals:

  • Pruritic lesion with central swelling
  • Resolution under 24 hours

Urticarial vasculitis:

  • Painful lesion
  • Last > 24 hours
  • Constitutional symptoms and post-inflammatory hyperpigmentation
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3
Q

Clinical definition of angioedema

A

Swelling of deep dermis/ Subcutaneous tissue
Painful (c.f. pruritic wheals)
Slow resolution through 72 hours (c.f. Wheals)

Angioedema with wheals or without wheals are two entities

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4
Q

Clinical definition of anaphylaxis

A

Serious, acute, life-threatening systemic hypersensitivity reaction

Involvement of two or more organ systems

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5
Q

Name one guideline and outline the diagnostic criteria for anaphylaxis

Onset time limit for anaphylaxis

A

EAACI guideline

Acute onset of illness with skin, mucosa or both involvement

AND at least one of following

  • Respiratory compromise: dyspnea, wheezing, bronchospasm, stridor…etc
  • Hypotension and end-organ dysfunction: hypotonia, syncope, incontinence

Time limit:
S/S within 2 hours of exposure
S/S within 30 mins of food allergy
S/S within minutes of IV medication or insect stings

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6
Q

2 patho-mechanisms/ Endotypes of Urticaria

A

Histaminergic - Mast cell mediated type

Bradykinergic - Kinin mediated type

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7
Q

Pathophysiology of histaminergic urticaria

A

Classic allergic histaminergic urticaria:

  • Exposure to allergen activates Th cell and stimulate IgE class switch in B cells
  • IgE bind to FceRI on mast cell surface
  • Repeat exposure to allergen causes IgE Ab cross-link and activation of mast cell degranulation
  • Release vasoactive amines and cytokines e.g. histamine
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8
Q

Downstream physiological response to histamine release from Mast cells

A

GIT:
Increase fluid secretion and peristalsis&raquo_space; diarrhea and vomiting

Airway and eyes:
Increase mucus secretion, narrow airway&raquo_space; airway congestion and blockage
Contract bronchial smooth muscles

Blood vessels: increase vascular permeability
Increase fluid retention in interstitium
Increase lymphatic flow
Hypotension and anaphylatix shock

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9
Q

Compare the clinical presentation of histaminergic vs Bradykinergic urticaria

How to differentiate the two?

A

Histaminergic urticaria:

  • Angioedema with or without hives present
  • Pruritic
  • Faster onset and offset
  • Responsive to antihistamines or steroids
  • May have systemic symptoms (anaphylaxis)
  • Related to allergen exposure

Bradykinergic urticaria:

  • Angioedema WITHOUT hives
  • Not Pruritic
  • Only responsive to bradykinin antagonists

HIVES = Histaminergic
Challenge with antihistamines/ steroids or Bradykinin antagonist

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10
Q

Pathophysiology of bradykinergic urticaria

A

Mast cell independent

Bradykinin produced through activation of plasma contact system:

  • Prekallikrein&raquo_space; Kallikrein&raquo_space; Increase conversion of high molecular weight kinin (HMWK) to Bradykinin
  • Regulated by C1-Esterase inhibitor
  • Bradykinin causes vasodilation, Increase vascular permeability, Increase nociceptor stimulation for pain sensation
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11
Q

Causes of Bradykinergic urticaria

A

Hereditary C1-esterase inhibitor defect/ deficiency

Acquired: most commonly ACEi-related
ACE normally inhibits bradykinin
ACEi&raquo_space; remove normal inhibition on bradykinin

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12
Q

Differentials of histaminergic urticaria

A

Allergic, Type I HS reaction - Allergen caused

**Spontaneous or autoimmune urticaria and angioedema/ Chronic spontaneous urticaria (CSU) - No allergen needed

Inducible urticaria and angioedema

Urticarial vasculitis

Auto-inflammatory syndromes

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13
Q

4 clinical groups of anaphylaxis

A

IgE mediated
- Food, venom, medications, occupational allergen, radiocontrast

IgE independent
- Radiocontrast, NSAID, Dextrans, Biologic

Non-immunologic, Direct mast cell activation

  • Physical factors: exercise, cold, heat, UV
  • Ethanol
  • Medication

Idiopathic (20%)

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14
Q

Mimics of anaphylaxis

A 
Acute urticaria/ angioedema 
Asthmatic attack 
Vasovagal syncope 
Panic attacks 
Shock 
Other causes of sudden collapse or respiratory distress
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15
Q

Anaphylaxis

First investigations and acute management

A

Acute serum tryptase test***

  • Must measure within 6 hours of onset
  • Save blood immediately upon admission

Find potential allergen/ triggers

  • Within one hour of onset
  • e.g. food, drugs, venom, NSAIDs, exercise…etc

Acute treatment:

  • Anti-histamine, Steroids
  • Intramuscular adrenaline*** 1:1000 solution or Auto-injector

Observe for biphasic reaction

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16
Q

Cut-off for serum tryptase

A

Cut-off depends on base-line
e.g. baseline - 1.0 ng/mL
Cut-off = 1.0 +20% + 2 = 3.2ng/mL

OR

> 11.4ng/mL

17
Q

Monitoring time for anaphylaxis

A

Always observe for biphasic reaction

Respiratory S/S = observe for at least 6-8 hours
Hypotension or collapse = observe for at least 12-24 hours

18
Q

Preventative measures against worsening anaphylaxis

A
  1. Strictly avoid allergen
  2. Anti-histamines and close observation for mild reactions
  3. Adrenaline auto-injectors and emergency medical Tx
19
Q

Outline the QMH anaphylaxis pathway for prevention

A

Pre-discharge checklist:

  • Comprehensive and targeted allergy history
  • Tryptase test
  • Patient education and avoidance advice
  • Adrenaline Autoinjector admin and training
  • Trigger allergist referral
20
Q

Differentials of bradykinergic urticaria

A

ACEi-induced angioedema (most common)

Hereditary angioedema

Acquired C1-esterase inhibitor deficiency

21
Q

Most common causes of non-allergic histaminergic urticaria

A

Acute or Chronic spontaneous urticaria

Inducible urticarias

  • Physical: vibration, cold or heat, sunlight, delayed pressure urticaria
  • Cholinergic, Exercise-induced, contact, aquagenic
22
Q

Chronic spontaneous urticaria

  • Trigger?
  • Pathophysiology
  • Concomitant conditions
  • Tx
A

No exogenous trigger/ spontaenous!!!

Pathophysiology:

  • AutoAb against IgE or FceRI&raquo_space; activate basophils and mast cells
  • Mast cell degranulation releases histamine and other mediators
  • Histamine binds to H-receptors in endothelial cells and sensory nerves

Concomitant: Autoimmune thyroid disease (10%)

23
Q

Chronic spontaneous urticaria

Treatment options

A

Tx:
2nd generation anti-histamine (do not cross BBB)
Increase dosage up to 4 times if unresponsive

Add: Anti-IgE antibody Omalizumab, Ciclosporin

24
Q

Monitoring method for disease activity of urticaria

A

UAS-7
Urticaria Activity Score

Keep diary of score over 7 days

MBBS IV - Junior Clerkship WCS (131 decks)

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