Examius

🇮🇳 FMGE · subject

FMGE Dermatology Syllabus

The Dermatology syllabus for FMGE in full: 10 chapters, 28 topics and 108 sub-topics, every one listed below, plus 51 Dermatology flashcards with answers.

10Chapters
28Topics
108Sub-topics
51Flashcards

Dermatology syllabus: all 10 chapters

Expand any chapter to see its topics and sub-topics.

  1. Introduction to Dermatology

     2 topics
    • Anatomy and physiology of the skin
      • Layers of the skin (epidermis, dermis, subcutaneous tissue)
      • Appendages (hair, nails, sweat glands)
      • Functions of the skin (protection, thermoregulation, sensation)
    • Classification of skin lesions
      • Primary lesions (macule, papule, plaque, nodule, vesicle, bulla)
      • Secondary lesions (scale, crust, erosion, ulcer, atrophy)

  2. Basic Dermatological Procedures

     3 topics
    • Skin Biopsy
      • Techniques (punch biopsy, shave biopsy, incisional biopsy)
      • Indications
      • Interpretation of histopathological findings
    • Patch Testing
      • Diagnosis of allergic contact dermatitis
      • Interpretation of patch test results
    • Dermoscopy
      • Use of dermoscopy for the diagnosis of melanocytic lesions
      • Use of dermoscopy for the diagnosis of non-melanocytic lesions
      • Use of dermoscopy for the diagnosis of inflammatory skin conditions

  3. Inflammatory Skin Disorders

     3 topics
    • Psoriasis
      • Clinical features
      • Plaque psoriasis
      • Guttate psoriasis
      • Pustular psoriasis
      • Topical therapy
      • Phototherapy
      • Systemic therapy
    • Eczema (Atopic Dermatitis)
      • Clinical features
      • Acute eczema
      • Subacute eczema
      • Chronic eczema
      • Emollients
      • Topical corticosteroids
      • Calcineurin inhibitors
    • Acne Vulgaris
      • Pathogenesis
      • Comedones
      • Papules
      • Pustules
      • Nodules
      • Topical retinoids
      • Benzoyl peroxide
      • Oral antibiotics

  4. Infectious Skin Disorders

     3 topics
    • Bacterial infections
      • Impetigo
      • Cellulitis
      • Erysipelas
      • Folliculitis
      • Furuncles
      • Carbuncles
    • Viral infections
      • Herpes simplex virus (HSV) infection
      • Herpes zoster (shingles)
      • Molluscum contagiosum
      • Common warts
      • Plantar warts
    • Fungal infections
      • Dermatophytosis
      • Candidiasis
      • Pityriasis versicolor

  5. Autoimmune and Connective Tissue Disorders

     3 topics
    • Lupus erythematosus
      • Systemic lupus erythematosus (SLE)
      • Discoid lupus erythematosus (DLE)
      • Subacute cutaneous lupus erythematosus (SCLE)
    • Dermatomyositis
      • Clinical features
      • Skin manifestations (heliotrope rash, Gottron's papules)
      • Management
    • Scleroderma
      • Localized scleroderma (morphea)
      • Systemic sclerosis (limited cutaneous, diffuse cutaneous)

  6. Pigmentary Disorders

     3 topics
    • Vitiligo
      • Pathogenesis
      • Clinical features
      • Depigmented macules
      • Patches
      • Topical corticosteroids
      • Phototherapy
    • Melasma
      • Clinical features
      • Topical depigmenting agents
      • Chemical peels
    • Post-inflammatory hyperpigmentation
      • Causes
      • Clinical features
      • Management

  7. Hair and Nail Disorders

     3 topics
    • Alopecia areata
      • Pathogenesis
      • Clinical features (well-defined patches of non-scarring alopecia)
      • Management (topical corticosteroids, intralesional corticosteroids)
    • Androgenetic alopecia
      • Clinical features
      • Pattern of hair loss (male pattern baldness, female pattern hair loss)
      • Management (topical minoxidil, oral finasteride)
    • Onychomycosis
      • Fungal nail infection
      • Clinical features (thickened, discolored nails)
      • Management (oral antifungal therapy, topical therapy)

  8. Genodermatoses

     2 topics
    • Epidermolysis bullosa
      • Clinical features
      • Epidermolysis bullosa simplex
      • Dystrophic epidermolysis bullosa
      • Wound care
      • Genetic counseling
    • Neurofibromatosis
      • Neurofibromatosis type 1 (von Recklinghausen disease)
      • Clinical features
      • Management

  9. Skin Cancer

     3 topics
    • Basal cell carcinoma
      • Clinical features
      • Risk factors
      • Management
    • Squamous cell carcinoma
      • Clinical features
      • Risk factors
      • Management
    • Melanoma
      • Clinical features
      • Staging
      • Management

  10. Cosmetic Dermatology

     3 topics
    • Botulinum toxin injections
      • Indications (dynamic wrinkles)
      • Technique
      • Complications
      • Contraindications
    • Fillers
      • Hyaluronic acid fillers
      • Calcium hydroxylapatite fillers
      • Poly-L-lactic acid fillers
      • Volume restoration
      • Wrinkle correction
    • Chemical peels
      • Superficial peels (alpha hydroxy acids)
      • Medium-depth peels (trichloroacetic acid)
      • Deep peels (phenol)
      • Skin rejuvenation

FMGE Dermatology flashcards — 51 questions with answers

  1. What are the three main layers of the skin from superficial to deep, and which germ layers do they derive from?

    Epidermis (ectoderm), dermis (mesoderm), and subcutaneous tissue/hypodermis (mesoderm). Melanocytes and nerves are neuroectodermal.

  2. Name the five layers (strata) of the epidermis from deep to superficial.

    Stratum basale (germinativum), stratum spinosum, stratum granulosum, stratum lucidum (only in thick/palmoplantar skin), and stratum corneum. Mnemonic: 'Come, Let's Get Sun Burned' (reversed).

  3. What is the approximate epidermal turnover (transit) time from basal layer to shedding, and how is it altered in psoriasis?

    Normal turnover is about 28 days; in psoriasis it is drastically accelerated to roughly 3-4 days, causing scaling.

  4. Which cell types reside in the epidermis and what is each one's function?

    Keratinocytes (keratin/barrier), melanocytes (melanin), Langerhans cells (antigen presentation), and Merkel cells (touch mechanoreceptors).

  5. Define a macule versus a papule.

    A macule is a flat, circumscribed change in skin color <1 cm (a patch if >1 cm). A papule is a solid, raised lesion <1 cm (a nodule if larger/deeper, a plaque if a flat-topped elevation >1 cm).

  6. Distinguish a vesicle, bulla, and pustule.

    A vesicle is a fluid-filled blister <1 cm; a bulla is a fluid-filled blister >1 cm; a pustule is a circumscribed lesion filled with pus.

  7. Differentiate primary from secondary skin lesions.

    Primary lesions arise de novo from the disease process (e.g., macule, papule, vesicle); secondary lesions result from evolution or external manipulation (e.g., scale, crust, erosion, ulcer, scar, lichenification).

  8. What is the difference between an erosion and an ulcer?

    An erosion is loss of epidermis only and heals without scarring; an ulcer is loss extending into the dermis or deeper and heals with scarring.

  9. Which skin biopsy technique is best for a deep/subcutaneous panniculitis or evaluating the full skin thickness?

    An incisional or excisional biopsy (or a deep punch reaching subcutaneous fat). Punch and shave biopsies may miss deep pathology.

  10. When is a shave biopsy appropriate versus contraindicated?

    Appropriate for raised/superficial/exophytic lesions (e.g., suspected BCC, seborrheic keratosis). Contraindicated when melanoma is suspected, because it can transect the lesion and prevent accurate Breslow depth measurement.

  11. What is patch testing used to diagnose, and what type of hypersensitivity does it detect?

    Patch testing diagnoses allergic contact dermatitis, a Type IV (delayed-type, T-cell mediated) hypersensitivity reaction.

  12. What is the standard reading schedule for patch test results?

    Patches are applied for 48 hours, then read at 48 hours (initial removal) and again at 72-96 hours (delayed reading) to detect late reactions.

  13. What is dermoscopy and what key advantage does it offer?

    Dermoscopy is non-invasive in vivo examination of skin using a magnifying dermatoscope with polarized/immersion light, visualizing subsurface structures (pigment network, vessels) to aid diagnosis of melanocytic and other lesions, improving melanoma detection.

  14. On dermoscopy, what is the 'blue-white veil' a clue to?

    A blue-white veil (confluent blue pigmentation with overlying white haze) is a dermoscopic feature suggestive of melanoma.

  15. What is the pathophysiologic hallmark of psoriasis on histology?

    Hyperproliferation of keratinocytes with parakeratosis, acanthosis, elongated rete ridges, thinned suprapapillary plates, and neutrophil collections (Munro microabscesses in stratum corneum).

  16. What are the Auspitz sign and Koebner phenomenon in psoriasis?

    Auspitz sign = pinpoint bleeding when psoriatic scale is removed (due to thin suprapapillary plates over dilated capillaries). Koebner phenomenon = appearance of new lesions at sites of trauma.

  17. Name the classic clinical type and typical distribution of plaque psoriasis.

    Chronic plaque psoriasis (psoriasis vulgaris): well-demarcated erythematous plaques with silvery-white scale on extensor surfaces (elbows, knees), scalp, and lumbosacral region.

  18. What cytokine pathway is central to psoriasis and is the target of modern biologics?

    The IL-23/IL-17 (Th17) axis, along with TNF-alpha; biologics target TNF-alpha, IL-12/23, IL-17, and IL-23.

  19. What is the underlying barrier/immune defect in atopic dermatitis (eczema)?

    A filaggrin gene mutation causing impaired skin barrier function, combined with a Th2-skewed immune response (elevated IL-4, IL-13, IgE).

  20. Describe the age-related distribution of atopic dermatitis.

    Infants: face and extensor surfaces; children/adults: flexural areas (antecubital and popliteal fossae, neck, wrists).

Show the other 31 Dermatology flashcards

  1. What triad of atopic conditions is associated with atopic dermatitis?

    The atopic triad: atopic dermatitis (eczema), allergic rhinitis (hay fever), and asthma.

  2. What are the four pathogenic factors in acne vulgaris?

    (1) Increased sebum production (androgen-driven), (2) follicular hyperkeratinization, (3) Cutibacterium acnes (Propionibacterium acnes) colonization, and (4) inflammation.

  3. Differentiate open and closed comedones in acne.

    Open comedones = blackheads (dilated follicle with oxidized melanin/keratin); closed comedones = whiteheads (obstructed follicle with a closed surface).

  4. What is the first-line oral treatment for severe nodulocystic acne, and what key precaution is required?

    Oral isotretinoin; it is highly teratogenic, requiring strict contraception and pregnancy monitoring (e.g., iPLEDGE), plus monitoring of lipids and liver function.

  5. What organism causes impetigo and what is its classic clinical sign?

    Staphylococcus aureus (and Streptococcus pyogenes); classic sign is honey-colored (golden) crusting, often perioral/perinasal.

  6. Differentiate erysipelas from cellulitis.

    Erysipelas involves the upper dermis and superficial lymphatics with a sharply demarcated, raised, bright-red border (usually Strep pyogenes); cellulitis involves deeper dermis and subcutaneous fat with poorly defined borders.

  7. What is staphylococcal scalded skin syndrome (SSSS) and which toxin causes it?

    SSSS is widespread superficial epidermal blistering/desquamation caused by S. aureus exfoliative toxins (A and B) cleaving desmoglein-1; Nikolsky sign is positive, mucosa is spared.

  8. Which virus causes molluscum contagiosum and what is its characteristic lesion?

    A poxvirus; lesions are dome-shaped, pearly, umbilicated (central dimple) papules; histology shows Henderson-Paterson (molluscum) bodies.

  9. What is the difference between HSV-1 and HSV-2 typical sites and reactivation patterns?

    HSV-1 classically causes orolabial herpes (cold sores) and latency in the trigeminal ganglion; HSV-2 causes genital herpes with latency in sacral ganglia. Both can reactivate with stress, illness, UV, or immunosuppression.

  10. What rash distribution characterizes herpes zoster (shingles)?

    Painful grouped vesicles on an erythematous base in a unilateral dermatomal distribution (does not cross the midline), from reactivation of varicella-zoster virus in a dorsal root ganglion.

  11. What organism causes tinea (dermatophytosis) and which test confirms it?

    Dermatophytes (Trichophyton, Microsporum, Epidermophyton); confirmed by KOH (potassium hydroxide) wet mount showing septate branching hyphae, plus fungal culture.

  12. How does tinea versicolor present, what causes it, and what is its KOH finding?

    Caused by Malassezia (Pityrosporum); presents as hypo- or hyperpigmented scaly macules on the trunk; KOH shows 'spaghetti and meatballs' (hyphae and spores).

  13. What are the cutaneous hallmarks of acute systemic lupus erythematosus?

    A photosensitive malar ('butterfly') rash sparing the nasolabial folds, discoid lesions, photosensitivity, and oral ulcers; ANA and anti-dsDNA/anti-Smith antibodies are markers.

  14. Differentiate discoid lupus from systemic lupus skin involvement.

    Discoid lupus erythematosus (DLE) is chronic cutaneous lupus with scarring, atrophic, hyperpigmented plaques and follicular plugging, often without systemic disease; SLE malar rash is non-scarring.

  15. What are the characteristic cutaneous signs of dermatomyositis?

    Heliotrope rash (violaceous periorbital edema/discoloration) and Gottron's papules (violaceous papules over knuckles/MCP and PIP joints), plus shawl sign and proximal muscle weakness.

  16. Which autoantibody is associated with dermatomyositis and increased malignancy risk?

    Anti-Jo-1 (associated with antisynthetase syndrome/ILD); anti-TIF1-gamma and anti-NXP2 are associated with malignancy. Dermatomyositis warrants age-appropriate cancer screening.

  17. Differentiate limited from diffuse systemic sclerosis (scleroderma).

    Limited cutaneous scleroderma = CREST syndrome (Calcinosis, Raynaud's, Esophageal dysmotility, Sclerodactyly, Telangiectasia), anti-centromere antibody; diffuse = widespread skin and early internal organ involvement, anti-Scl-70 (anti-topoisomerase I) antibody.

  18. What is the pathophysiology of vitiligo?

    Autoimmune destruction of melanocytes producing well-demarcated, depigmented (chalk-white) macules/patches; associated with other autoimmune disease (thyroid). Wood's lamp accentuates lesions.

  19. What is melasma and what are its main triggers?

    Melasma is acquired symmetric hyperpigmentation of sun-exposed facial skin (cheeks, forehead, upper lip); triggers include UV exposure, pregnancy ('chloasma'/mask of pregnancy), and oral contraceptives/hormones.

  20. What causes post-inflammatory hyperpigmentation (PIH) and who is most affected?

    PIH results from increased melanin production/deposition following cutaneous inflammation or injury (acne, eczema, trauma); it is more common and persistent in darker skin types (Fitzpatrick IV-VI).

  21. What is alopecia areata and its characteristic clinical/dermoscopic finding?

    Autoimmune non-scarring hair loss producing smooth, round patches; characteristic 'exclamation mark' hairs at the margin; alopecia totalis (whole scalp) and universalis (whole body) are severe forms.

  22. Describe the pattern and key mediator of androgenetic alopecia.

    Genetically determined, androgen (dihydrotestosterone/DHT)-driven hair miniaturization; men: bitemporal recession and vertex thinning (Norwood-Hamilton); women: diffuse central thinning sparing frontal hairline (Ludwig). Treated with topical minoxidil and oral finasteride (5-alpha-reductase inhibitor).

  23. What is onychomycosis, its most common cause, and first-line systemic treatment?

    Fungal infection of the nail, most often by Trichophyton rubrum; presents with thickened, discolored, dystrophic nails; first-line oral therapy is terbinafine. Diagnosis confirmed by KOH/culture/PAS of nail clippings.

  24. What is epidermolysis bullosa and what distinguishes its main types by cleavage plane?

    A group of inherited blistering disorders from mutations in structural skin proteins. EB simplex: cleavage within basal keratinocytes (keratin 5/14). Junctional EB: within lamina lucida (laminin-332). Dystrophic EB: below lamina densa (type VII collagen), heals with scarring.

  25. What are the diagnostic cutaneous features of neurofibromatosis type 1 (NF1)?

    Six or more cafe-au-lait macules, axillary/inguinal freckling (Crowe's sign), multiple neurofibromas, and Lisch nodules (iris hamartomas); NF1 is autosomal dominant (neurofibromin gene, chromosome 17).

  26. What is the most common skin cancer, its typical appearance, and its behavior?

    Basal cell carcinoma (BCC); presents as a pearly, translucent papule with rolled borders, telangiectasias, and possible central ulceration ('rodent ulcer'); locally invasive but rarely metastasizes.

  27. What are the risk factors and key behavior of squamous cell carcinoma (SCC) of the skin?

    Risk factors: chronic UV exposure, actinic keratoses (precursor), immunosuppression, chronic wounds/scars (Marjolin ulcer); SCC can metastasize, more readily than BCC, especially on lip/ear.

  28. What is the ABCDE rule for melanoma, and what histologic measurement guides prognosis?

    Asymmetry, Border irregularity, Color variation, Diameter >6 mm, Evolving. Breslow thickness (depth in mm) is the most important prognostic factor; greater depth means worse prognosis.

  29. How does botulinum toxin work cosmetically and which lines does it best treat?

    Botulinum toxin (Botox) cleaves SNAP-25, blocking acetylcholine release at the neuromuscular junction, causing temporary muscle relaxation; best for dynamic wrinkles (glabellar frown lines, forehead lines, crow's feet). Effect lasts about 3-4 months.

  30. What are dermal fillers commonly made of, and what is the main reversible agent for the most common type?

    Most dermal fillers are hyaluronic acid (HA)-based, used to restore volume and soften static wrinkles/folds; HA fillers can be dissolved with hyaluronidase, important for managing vascular occlusion complications.

  31. Classify chemical peels by depth and give an example agent for each.

    Superficial (epidermis): glycolic acid, salicylic acid, Jessner's solution; Medium (papillary-upper reticular dermis): trichloroacetic acid (TCA 35-50%); Deep (mid-reticular dermis): phenol (Baker-Gordon). Deeper peels treat deeper lines but carry higher scarring/pigment risk.

Same Dermatology syllabus in other exams

The Dermatology outline above is identical in these 3 exams:

FMGE Dermatology FAQ

What is in the FMGE Dermatology syllabus?

FMGE Dermatology is split into 10 chapters: Introduction to Dermatology, Basic Dermatological Procedures, Inflammatory Skin Disorders, Infectious Skin Disorders, Autoimmune and Connective Tissue Disorders, Pigmentary Disorders, Hair and Nail Disorders, Genodermatoses, Skin Cancer and Cosmetic Dermatology. Together they contain 28 topics and 108 sub-topics.

How many chapters are in FMGE Dermatology?

10 chapters, containing 28 topics and 108 sub-topics. The largest chapter is Basic Dermatological Procedures, with 3 topics.

Are there flashcards for FMGE Dermatology?

Yes — a 51-card Dermatology deck, printed in full in the flashcards section of this page and available in the Examius app with spaced repetition. The free plan covers one exam of your choice, including its flashcards; Examius Pro, a one-time purchase, unlocks every other exam and deck.