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INI CET Dermatology Syllabus

The Dermatology syllabus for INI CET in full: 10 chapters, 28 topics and 108 sub-topics, every one listed below, plus 50 Dermatology flashcards with answers.

10Chapters
28Topics
108Sub-topics
50Flashcards

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

INI CET Dermatology flashcards — 50 questions with answers

  1. Name the three primary layers of the skin from superficial to deep, and the predominant cell type of the epidermis.

    Epidermis (mainly keratinocytes), dermis (collagen/elastin with fibroblasts), and subcutis/hypodermis (adipose tissue). The epidermis is composed predominantly of keratinocytes.

  2. List the five layers of the epidermis from deep to superficial.

    Stratum basale (germinativum), stratum spinosum, stratum granulosum, stratum lucidum (only in thick/palmoplantar skin), and stratum corneum.

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

    Normal epidermal turnover is about 28 days (~28-56 days cited). In psoriasis it is markedly shortened to about 3-4 days due to hyperproliferation.

  4. Differentiate the dermo-epidermal junction antigens targeted in the two major autoimmune blistering groups.

    Pemphigus targets intraepidermal desmosomal cadherins (desmoglein 1 and 3), causing acantholysis. Pemphigoid targets hemidesmosomal antigens at the basement membrane (BP180/BPAG2 and BP230), causing subepidermal blisters.

  5. Define the following primary skin lesions: macule, papule, nodule, plaque, vesicle, bulla, pustule, wheal.

    Macule = flat color change <1 cm; Papule = raised <1 cm; Nodule = raised >1 cm with dermal involvement; Plaque = flat-topped elevation >1 cm; Vesicle = fluid-filled <1 cm; Bulla = fluid-filled >1 cm; Pustule = pus-filled; Wheal = transient edematous plaque (urticaria).

  6. Define these secondary skin lesions: scale, crust, erosion, ulcer, lichenification, excoriation.

    Scale = flakes of stratum corneum; Crust = dried exudate/serum/blood; Erosion = loss of epidermis only (heals without scar); Ulcer = loss extending into dermis/deeper (scars); Lichenification = thickened skin with accentuated markings from chronic rubbing; Excoriation = scratch-induced linear erosion.

  7. For a skin biopsy, when is a punch vs. an excisional biopsy preferred, and what is the minimum punch size for adequate dermal sampling?

    Punch biopsy (typically 3-4 mm; minimum useful ~3 mm) samples epidermis to subcutis for inflammatory dermatoses; excisional biopsy is preferred for suspected melanoma to assess full depth/Breslow thickness. Shave biopsy is for superficial/exophytic lesions.

  8. Which type of biopsy and transport medium is required for direct immunofluorescence (DIF) in autoimmune bullous disease?

    A perilesional biopsy is taken and transported in Michel's medium (or normal saline if processed quickly), NOT formalin, because formalin destroys the immunoreactants needed for DIF.

  9. What is patch testing used to diagnose, and which type of hypersensitivity reaction does it detect?

    Patch testing diagnoses allergic contact dermatitis. It detects Type IV (delayed, T-cell mediated) hypersensitivity.

  10. Describe the standard reading schedule and grading principle for patch testing.

    Patches are applied for 48 hours, then removed; readings are done at 48 hours (Day 2) and again at 72-96 hours (Day 3-4) for delayed reactions. Reactions are graded from doubtful (?+), weak (+, erythema/papules), strong (++, vesicles), to extreme (+++, bullous/spreading).

  11. In dermoscopy, what is the pigment network and what does a typical (regular) vs. atypical network suggest?

    The pigment network is a honeycomb-like grid of brown lines (melanin in rete ridges). A regular, uniform network suggests a benign melanocytic nevus; an atypical/irregular network with variable thickness and abrupt cutoff raises suspicion for melanoma.

  12. What classic dermoscopic features differentiate basal cell carcinoma from a melanocytic lesion?

    BCC shows arborizing (branching) telangiectatic vessels, blue-gray ovoid nests, leaf-like areas, spoke-wheel structures, and ulceration, with absence of a pigment network.

  13. Name three classic clinical signs of psoriasis (including the bleeding-point sign).

    Auspitz sign (pinpoint bleeding when scale is removed), Koebner phenomenon (lesions at sites of trauma), and the candle-grease sign (waxy scale on scratching). Histology shows Munro microabscesses.

  14. What is the histopathological hallmark tetrad of plaque psoriasis?

    Parakeratosis, acanthosis with regular elongation of rete ridges, thinning of suprapapillary plates, Munro microabscesses (neutrophils in stratum corneum), and dilated dermal capillaries. Spongiform pustules of Kogoj may be present.

  15. State the diagnostic criteria framework and characteristic morphology/distribution of atopic dermatitis in adults vs. infants.

    Diagnosed by Hanifin and Rajka criteria (pruritus is essential). Infants: face, scalp, and extensor surfaces. Adults/children: flexural involvement (antecubital and popliteal fossae). It is part of the atopic triad with asthma and allergic rhinitis.

  16. What is the role of filaggrin in atopic dermatitis pathogenesis?

    Loss-of-function mutations in the filaggrin (FLG) gene impair the skin barrier, increasing transepidermal water loss and allergen penetration, predisposing to atopic dermatitis and ichthyosis vulgaris.

  17. Outline the four key pathogenic factors in acne vulgaris.

    (1) Follicular hyperkeratinization (comedo formation), (2) increased sebum production (androgen-driven), (3) colonization by Cutibacterium acnes (formerly Propionibacterium acnes), and (4) inflammation.

  18. What is the primary (non-inflammatory) lesion of acne, and what is the first-line topical agent that targets it plus its mechanism?

    The comedo (open = blackhead, closed = whitehead) is the primary lesion. Topical retinoids (e.g., adapalene, tretinoin) are first-line and act as comedolytics by normalizing follicular keratinization.

  19. What are the monitoring requirements and main contraindication for oral isotretinoin?

    Monitor liver enzymes and fasting lipids (triglycerides). It is a potent teratogen — absolutely contraindicated in pregnancy; pregnancy prevention/iPLEDGE-type programs with two contraception methods are mandatory.

  20. Name the causative organisms and key features of impetigo (contagiosa) vs. erysipelas.

    Impetigo: Staphylococcus aureus and Streptococcus pyogenes; superficial, honey-colored crusts. Erysipelas: Streptococcus pyogenes; sharply demarcated, raised, bright-red plaque of the upper dermis (commonly face/legs) with fever.

Show the other 30 Dermatology flashcards

  1. What organism causes staphylococcal scalded skin syndrome (SSSS) and what is the target of its toxin?

    Staphylococcus aureus producing exfoliative (epidermolytic) toxins A/B, which cleave desmoglein 1, causing superficial subcorneal splitting and a positive Nikolsky sign, sparing mucosae.

  2. Distinguish the lesions of herpes simplex, varicella, and herpes zoster.

    HSV: grouped vesicles on an erythematous base (recurrent, localized). Varicella (chickenpox): generalized lesions in different stages simultaneously ('dew drop on a rose petal'). Herpes zoster (shingles): painful dermatomal vesicles from VZV reactivation.

  3. What virus causes molluscum contagiosum, and what is its characteristic histologic inclusion body?

    Molluscum contagiosum virus (a poxvirus). Lesions are umbilicated papules; histology shows intracytoplasmic Henderson-Paterson (molluscum) inclusion bodies.

  4. How do you confirm a dermatophyte infection at the bedside, and what is the classic morphology of tinea corporis?

    KOH (potassium hydroxide) mount of skin scrapings shows septate branching hyphae. Tinea corporis presents as an annular plaque with a raised, scaly, active advancing border and central clearing ('ringworm').

  5. Differentiate the clinical presentation and KOH finding of pityriasis (tinea) versicolor.

    Caused by Malassezia (furfur/globosa). Presents as hypo- or hyperpigmented scaly macules on the trunk; KOH shows the 'spaghetti and meatballs' appearance (short hyphae plus round yeast). Fluoresces yellow-green/coppery-orange under Wood's lamp.

  6. What are the diagnostic autoantibodies for systemic lupus erythematosus, including the most specific ones?

    ANA is the most sensitive screening test. Anti-dsDNA (correlates with renal disease) and anti-Smith (anti-Sm) are the most specific for SLE. Anti-Ro/SSA is associated with subacute cutaneous LE and neonatal lupus.

  7. Describe the lupus band test and the characteristic cutaneous lesion of discoid lupus erythematosus.

    Lupus band test: DIF showing granular IgG/IgM and C3 deposition along the dermo-epidermal junction. Discoid LE shows well-defined erythematous plaques with adherent scale, follicular plugging, and scarring/atrophy.

  8. List the characteristic cutaneous signs of dermatomyositis (including eponymous signs).

    Heliotrope rash (violaceous periorbital eyelid erythema with edema), Gottron's papules (violaceous papules over knuckles/MCP-PIP joints), shawl sign (V-neck/upper back erythema), and periungual telangiectasia with ragged cuticles. Associated with proximal muscle weakness and elevated CK; paraneoplastic in adults.

  9. Which autoantibodies are associated with limited (CREST) vs. diffuse systemic sclerosis (scleroderma)?

    Limited cutaneous SSc/CREST: anti-centromere antibody. Diffuse cutaneous SSc: anti-Scl-70 (anti-topoisomerase I), associated with interstitial lung disease. Anti-RNA polymerase III is linked to renal crisis.

  10. What does the CREST syndrome acronym stand for?

    Calcinosis cutis, Raynaud's phenomenon, Esophageal dysmotility, Sclerodactyly, and Telangiectasia.

  11. What is the pathophysiology of vitiligo and the characteristic Wood's lamp finding?

    Vitiligo is autoimmune destruction of melanocytes causing well-demarcated depigmented (chalk-white) macules. Under Wood's lamp the lesions show bright/sharply accentuated blue-white fluorescence and clearer margins. Koebner phenomenon is positive.

  12. Differentiate melasma from post-inflammatory hyperpigmentation in terms of cause and distribution.

    Melasma: symmetric, blotchy facial hyperpigmentation (malar, centrofacial, mandibular) triggered by UV, pregnancy/hormones, and is acquired/chronic. PIH: hyperpigmentation following inflammation/injury (e.g., acne, eczema) located at prior lesion sites; epidermal PIH improves faster than dermal.

  13. What is the cornerstone topical depigmenting agent for melasma and the classic combination formulation?

    Hydroquinone (tyrosinase inhibitor) is first-line. The Kligman's formula combines hydroquinone, tretinoin, and a topical corticosteroid. Strict broad-spectrum photoprotection is essential.

  14. Describe the classic clinical features and prognostic sign of alopecia areata.

    Alopecia areata: non-scarring, well-circumscribed round patches of hair loss with 'exclamation mark' hairs at the margins. It is autoimmune (T-cell mediated against the hair follicle). Ophiasis pattern and nail pitting indicate poorer prognosis; alopecia totalis/universalis are extensive variants.

  15. What is the pattern and pathogenesis of androgenetic alopecia, and the two FDA-approved treatments?

    Androgenetic alopecia is patterned hair loss from dihydrotestosterone (DHT)-mediated miniaturization of follicles: bitemporal recession/vertex in men (Norwood scale), diffuse crown thinning sparing frontal line in women (Ludwig scale). FDA-approved: topical minoxidil and oral finasteride (5-alpha-reductase inhibitor).

  16. Name the most common dermatophyte causing onychomycosis, the most common clinical subtype, and the gold-standard treatment.

    Trichophyton rubrum is the most common cause; distal lateral subungual onychomycosis (DLSO) is the most common subtype. Oral terbinafine is the treatment of choice (most effective for dermatophyte nail infection).

  17. What is the basic defect in epidermolysis bullosa, and how are the three classic types distinguished by level of cleavage?

    EB is a group of inherited mechanobullous disorders with blistering from minor trauma. EB simplex: cleavage within the basal keratinocytes (keratin 5/14 defect, intraepidermal). Junctional EB: split within the lamina lucida (laminin-332 defect). Dystrophic EB: split below the lamina densa (type VII collagen/anchoring fibril defect, scarring/milia).

  18. List the diagnostic criteria features of neurofibromatosis type 1 (NF1).

    NF1 (von Recklinghausen): >=2 of - >=6 cafe-au-lait macules (>5 mm prepubertal, >15 mm postpubertal); >=2 neurofibromas or 1 plexiform neurofibroma; axillary/inguinal freckling (Crowe's sign); optic glioma; >=2 Lisch nodules (iris hamartomas); a distinctive bony lesion; and a first-degree relative with NF1.

  19. What is the most common skin cancer overall, its typical clinical appearance, and its metastatic potential?

    Basal cell carcinoma is the most common. Classic nodular BCC: a pearly/translucent papule with rolled borders, telangiectasia, and central ulceration ('rodent ulcer'). It is locally invasive but rarely metastasizes.

  20. What are the key risk factors and precursor lesion for cutaneous squamous cell carcinoma?

    Risk factors: chronic UV exposure, immunosuppression (transplant patients), HPV, chronic wounds/scars (Marjolin's ulcer), and arsenic. The precursor is actinic keratosis; SCC in situ is Bowen's disease. SCC has higher metastatic potential than BCC, especially on lip/ear.

  21. What are the ABCDE criteria for melanoma and the single most important histologic prognostic factor?

    ABCDE: Asymmetry, Border irregularity, Color variegation, Diameter >6 mm, Evolution/change. The most important prognostic factor is Breslow thickness (tumor depth in mm); ulceration and mitotic rate also matter.

  22. Name the four major clinicopathologic subtypes of melanoma and which is most common vs. most aggressive.

    Superficial spreading (most common, ~70%), nodular (most aggressive, vertical growth from onset), lentigo maligna (sun-damaged skin of elderly, best prognosis), and acral lentiginous (palms/soles/nails; most common type in dark-skinned and Indian patients).

  23. What is the mechanism of action of botulinum toxin type A in cosmetic use?

    Botulinum toxin A cleaves SNAP-25, a SNARE protein, blocking presynaptic release of acetylcholine at the neuromuscular junction, causing temporary chemodenervation/muscle relaxation. Effect onset is ~3-7 days and lasts ~3-4 months.

  24. For cosmetic botulinum toxin, name the most common treated areas and a serious complication to avoid in the upper face.

    Common areas: glabellar frown lines, forehead horizontal lines, and lateral canthal lines (crow's feet). A key complication is eyelid/brow ptosis from diffusion to the levator palpebrae superioris or frontalis muscle; injections must respect safe distances from the orbital rim.

  25. What is the most commonly used dermal filler material, what enzyme reverses it, and a feared vascular complication?

    Hyaluronic acid (HA) is the most common dermal filler; it is reversible with hyaluronidase. The most feared complication is intravascular injection causing vascular occlusion, leading to skin necrosis or blindness (retinal artery occlusion), most dangerous in the glabella and nose.

  26. Classify chemical peels by depth and give a representative agent for each.

    Superficial (epidermis): glycolic acid, salicylic acid, Jessner's solution, 10-30% TCA. Medium (papillary to upper reticular dermis): 35-50% TCA, often combined with Jessner's. Deep (mid-reticular dermis): phenol (Baker-Gordon). Deeper peels give better results for scarring/wrinkles but higher complication (scarring, dyspigmentation) risk.

  27. What is the frosting endpoint in TCA chemical peeling and what does it indicate?

    Frosting is whitening of the skin from protein coagulation/keratin denaturation by trichloroacetic acid. The degree of frosting (Level I = erythema with streaky frost; II = white frost with erythema; III = solid white frost) correlates with peel depth.

  28. What Wood's lamp color is characteristic of erythrasma, and what organism causes it?

    Erythrasma fluoresces coral-red/pink under Wood's lamp due to coproporphyrin III produced by Corynebacterium minutissimum. It presents as well-demarcated reddish-brown patches in intertriginous areas.

  29. What is the Nikolsky sign and in which conditions is it positive?

    Nikolsky sign is dislodgement/sliding of the superficial epidermis with lateral shearing pressure on perilesional skin, indicating epidermal fragility/acantholysis. Positive in pemphigus vulgaris, staphylococcal scalded skin syndrome, and toxic epidermal necrolysis.

  30. Compare the targeted molecular cytokines in biologic therapy for psoriasis (TNF, IL-17, IL-23, IL-12/23).

    TNF-alpha inhibitors: adalimumab, etanercept, infliximab. IL-12/23 (p40): ustekinumab. IL-17 inhibitors: secukinumab, ixekizumab. IL-23 (p19): guselkumab, risankizumab. The IL-23/Th17/IL-17 axis is central to psoriasis pathogenesis.

Same Dermatology syllabus in other exams

The Dermatology outline above is identical in these 3 exams:

INI CET Dermatology FAQ

What is in the INI CET Dermatology syllabus?

INI CET 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 INI CET Dermatology?

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

Are there flashcards for INI CET Dermatology?

Yes — a 50-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.