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Dermatology Physiology for MRCP Part 1

TL;DR

Dermatology questions in MRCP Part 1 revolve around mechanisms, not memorising rashes. This guide summarises dermatology physiology & pathophysiology: what MRCP Part 1 expects, focusing on barrier function, keratinocyte biology, cutaneous immunology, pigmentation, and blistering disorders. A short case-based question, pitfalls, and a practical checklist reinforce the essentials. Use it alongside structured revision through a QBank and mock tests.


Why this matters

Dermatology contributes only a small slice to the MRCP Part 1 blueprint, but the concepts frequently overlap with immunology, genetics, infectious disease, and connective tissue disorders. Many stems appear dermatology-light at first glance but hinge on understanding barrier physiology, inflammatory pathways (e.g., IL-23/Th17), and keratinocyte biology.

If you need a full exam overview, see our MRCP Part 1 overview:👉 https://crackmedicine.com/mrcp-part-1/


What MRCP Part 1 typically tests in dermatology

Below is a concise breakdown of recurring exam themes. These align with study expectations outlined by MRCP(UK):Official exam information → https://www.mrcpuk.org/mrcpuk-examinations/part-1-examination

1) Skin barrier physiology

  • The stratum corneum is a lipid–protein barrier; dysfunction increases transepidermal water loss.

  • Filaggrin mutations impair barrier formation → predispose to atopic dermatitis (confirmed in dermatology literature by the British Association of Dermatologists: https://www.bad.org.uk).

  • Conditions driven by barrier failure include eczema and ichthyoses.

2) Keratinocyte biology

  • Disorders of keratin pairs (e.g., K5/K14) produce epidermolysis bullosa simplex.

  • Hyperproliferation and parakeratosis are hallmark processes in psoriasis.

  • Cytokines IL-17, IL-23, TNF-α contribute to the psoriatic inflammatory environment.

3) Cutaneous immunology

  • Langerhans cells provide antigen presentation → key to allergic contact dermatitis.

  • T-cell–mediated (Type IV) hypersensitivity drives many drug eruptions.

  • Autoimmune blistering conditions differ in their targets:

    • Pemphigus vulgaris: desmoglein-3 (intraepidermal)

    • Bullous pemphigoid: BP180/BP230 (subepidermal)

NICE overview of autoimmune blistering disease management:https://www.nice.org.uk/guidance/ng190

4) Pigmentation physiology

  • Melanin production occurs in melanocytes → packaged into melanosomes and transferred to keratinocytes.

  • Albinism: impaired tyrosinase or melanosome function.

  • Vitiligo: autoimmune melanocyte destruction (NHS overview: https://www.nhs.uk/conditions/vitiligo/).

5) Microvascular / inflammatory processes

  • Mast-cell degranulation → urticaria; C1 inhibitor defects → angio-oedema.

  • In vasculitis, patterns reflect vessel size and immunopathology (immune complex vs ANCA-associated).


High-yield list (exam-focused)

  1. Transepidermal water loss increases with stratum corneum lipid disruption.

  2. Filaggrin mutations → atopic dermatitis susceptibility.

  3. Parakeratosis is a hallmark of psoriasis.

  4. BP180/BP230 are targets in bullous pemphigoid (subepidermal blister).

  5. Desmoglein-3 → pemphigus vulgaris (flaccid blisters).

  6. Type IV hypersensitivity underpins contact dermatitis and many drug eruptions.

  7. Melanogenesis impairment → albinism; melanocyte destruction → vitiligo.

  8. Keratin 5/14 mutations → epidermolysis bullosa simplex.

  9. Dermatophytes invade keratin; yeasts like Candida invade intertriginous skin/mucosae.

  10. Mast-cell–driven urticaria improves with antihistamines; C1 inhibitor deficiency → bradykinin-mediated swelling (non-responsive to antihistamines).


Five key subtopics you must master

1) Atopic dermatitis physiology

Barrier defect + Th2-skewed inflammation.Filaggrin-linked predisposition heavily tested.

2) Psoriasis

Rapid keratinocyte turnover, parakeratosis, IL-17/IL-23 pathways.Focus on mechanism → therapy logic.

3) Autoimmune blistering

Know the histological level (intra vs subepidermal).Pemphigus = acantholysis; BP = tense blisters.

4) Drug eruptions

From morbilliform reactions to SJS/TEN: keratinocyte apoptosis pathways (FasL, granulysin).

5) Pigmentation disorders

Autoimmune (vitiligo), genetic (albinism), post-inflammatory pathways.

A quick reference table: blistering disorders

Disorder

Target Antigen

Level of Split

Typical Feature

Pemphigus vulgaris

Desmoglein-3

Intraepidermal

Flaccid blisters

Bullous pemphigoid

BP180/BP230

Subepidermal

Tense bullae

Dermatitis herpetiformis

IgA at dermal papillae

Subepidermal

Coeliac-linked, grouped vesicles

Study workflow graphic highlighting QBank practice, spaced repetition and mock exams for MRCP Part 1 revision.

Practical examples / mini-cases

Mini-MCQ

A 68-year-old man presents with generalised pruritus and tense blisters. Mucosal involvement is absent. Skin biopsy shows a subepidermal split with eosinophils. Which structure is most likely targeted by autoantibodies?

A. Desmoglein-3B. Desmoglein-1C. BP180D. Keratin 14

Answer: C. BP180Tense bullae and subepidermal blistering strongly indicate bullous pemphigoid. BP180 (type XVII collagen) is the major antigen. Desmogleins would suggest pemphigus, which presents with flaccid lesions.


Practical study checklist (dermatology for MRCP Part 1)

  • ☐ Review barrier physiology and filaggrin pathways.

  • ☐ Memorise blistering disorders by antigen + depth of split.

  • ☐ Learn cytokine pathways involved in psoriasis.

  • ☐ Revise hypersensitivity types and drug eruption mechanisms.

  • ☐ Do 50–100 dermatology QBank questions for pattern recognition.

  • ☐ Use mock tests to rehearse multi-system stems (derm + immunology).

  • ☐ Read one authoritative guideline (BAD/NICE) for real-world context.

If you need MCQ practice:👉 https://crackmedicine.com/qbank/

For timed simulations:👉 https://crackmedicine.com/mock-tests/


Common pitfalls (5 bullets)

  • Confusing antigen targets in blistering disorders.

  • Over-relying on rash memorisation without understanding mechanisms.

  • Missing systemic clues in vasculitic or connective-tissue disorders.

  • Ignoring cytokine biology in psoriasis.

  • Forgetting pigmentation physiology (melanocyte vs melanin defects).


FAQs

1) How much dermatology appears in MRCP Part 1?

A small proportion, but questions often integrate immunology, genetics, and infectious disease. Knowing core mechanisms covers most stems.

2) Do I need to memorise rare dermatoses?

No. MRCP Part 1 focuses on common mechanisms—barrier dysfunction, psoriasis physiology, vitiligo, blistering disease basics, and drug reactions.

3) What is the best way to learn autoimmune blistering diseases?

Anchor them to antigen + level of split. This alone answers 80% of blister questions.

4) Should I learn NICE/BAD guidance?

Only high-level concepts. These help with mechanism-based reasoning but are not tested for detailed protocol knowledge.

5) Are images heavily tested?

Not in Part 1. Pattern recognition still helps, but questions are typed, mechanism-driven stems.


Ready to start?

If you're building your dermatology foundations for MRCP Part 1, pair this guide with structured practice. Try our Free MRCP MCQs (https://crackmedicine.com/qbank/) and run a timed mock at Start a mock test (https://crackmedicine.com/mock-tests/). Continue exploring MRCP guidance here: https://crackmedicine.com/mrcp-part-1/.


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