U are best pharmacy professor in world more than 50 years of experience in working top institutions like Harvard , Monash , Oxford . Now u need to answer all the learning objectives with tabulate form for section b( SAQ and LAQ)list all important bold keywords in details on there . Give me easy memory trick to remember these for my exam . Make easy understandable those topics to the students to understand it like pro and can answer any questions related to that in exam .

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🎓 PHAR1612 - PATHOPHYSIOLOGY OF SKIN DISORDERS

Complete Section B (SAQ & LAQ) Study Guide

Prof-Level Notes with Memory Tricks — Ready for Exam

📋 MASTER TABLE OF ALL LEARNING OBJECTIVES — SECTION B

🔷 TOPIC 1: SKIN LESIONS (Primary & Secondary)

Learning Objective	Key Bold Terms	Details
Define skin lesion	Skin lesion	Any area of skin that differs from surrounding skin in color, size, shape, or texture
Describe causes	Hereditary, Viral, Bacterial, Fungal, Allergic, Drug reaction, UV exposure, Burns, Autoimmune	Causes include: herpes simplex/HPV (viral), Staph/Strep (bacterial), Candida albicans (fungal), SLE (autoimmune), melanoma (cancer)
Define & describe PRIMARY lesions	Macule, Patch, Papule, Plaque, Nodule, Vesicle, Bulla, Pustule, Wheal, Cyst	Earliest basic lesion related to a disease — original, first-appearing
Define & describe SECONDARY lesions	Scale, Crust, Erosion, Ulcer, Fissure, Scar, Lichenification, Atrophy, Keloid	Arise FROM primary lesions — by natural progression, scratching, rubbing, infection

Primary Lesions Breakdown Table:

Lesion	Description	Example
Macule	Flat, <1 cm, color change, no elevation	Freckle, petechiae
Patch	Flat, >1 cm, color change	Vitiligo, Mongolian spot
Papule	Elevated, solid, <1 cm	Wart, acne (early)
Plaque	Elevated, solid, >1 cm, flat top	Psoriasis
Nodule	Elevated, solid, deeper, >1 cm	Lipoma, rheumatoid nodule
Vesicle	Elevated, fluid-filled, <0.5 cm, CLEAR fluid	Herpes simplex, chickenpox
Bulla	Elevated, fluid-filled, >0.5 cm, CLEAR fluid	Burns, pemphigus
Pustule	Elevated, filled with PURULENT fluid (pus)	Acne vulgaris, impetigo
Wheal	Transient elevated lesion with EDEMA and PRURITUS	Urticaria (hives)
Cyst	Elevated, semisolid/fluid contents, enclosed	Sebaceous cyst

Secondary Lesions Breakdown Table:

Lesion	Description	Example
Scale	Dead skin cells flaking	Psoriasis, dandruff
Crust	Dried serum/blood on surface	Impetigo
Erosion	Loss of epidermis only, moist	Ruptured vesicle
Ulcer	Loss of epidermis + dermis, deeper	Pressure sore, diabetic ulcer
Fissure	Linear crack through epidermis/dermis	Athlete's foot
Scar	Fibrous tissue replacement after healing	Post-surgical, post-burn
Lichenification	Thickened skin from chronic scratching	Chronic eczema
Keloid	Overgrowth of scar tissue beyond wound margins	Post-burn/surgical hypertrophic scar

🧠 MEMORY TRICK - Primary Lesions: "Many Patients Prefer Noting Vital Bugs, Pustules While Crying"

Macule, Patch, Papule, Plaque, Nodule, Vesicle, Bulla, Pustule, Wheal, Cyst

🧠 MEMORY TRICK - Secondary Lesions: "Silly Cats Eat Ugly Fish, Sometimes Licking Keloids"

Scale, Crust, Erosion, Ulcer, Fissure, Scar, Lichenification, Keloid

🔷 TOPIC 2: WOUND HEALING

Learning Objective	Key Bold Terms	Details
Describe aetiology of wound	Mechanical injury, burns, chemical, pressure, ischemia	Skin injuries from cuts, burns, chemicals, pressure necrosis
Name & describe the 4 phases	Haemostasis, Inflammatory, Proliferative, Remodelling	Sequential overlapping phases of tissue repair
Differentiate 1st, 2nd, 3rd intention	Primary, Secondary, Tertiary intention	Differs by wound size, closure method, scarring outcome

Wound Healing Phases - Master Table:

Phase	Timing	Key Events	Key Cells/Molecules
Haemostasis	Immediate (0-few hrs)	Vasoconstriction, platelet aggregation, clot/thrombus formation, fibrin mesh	Platelets, Thrombin, Fibrin, TXA2
Inflammatory	Day 1-4	Vasodilation, neutrophils clean debris, then macrophages arrive, phagocytosis	Neutrophils, Macrophages, Histamine, Prostaglandins, IL-1, TNF-α
Proliferative	Day 4-21	Fibroblasts produce collagen, angiogenesis (new blood vessels), granulation tissue, re-epithelialization	Fibroblasts, Collagen (Type III initially), VEGF, Keratinocytes, Granulation tissue
Remodelling	Week 3 - 2 years	Type III collagen replaced by Type I collagen, scar matures, wound contracts, tensile strength increases	Type I Collagen, MMPs, Myofibroblasts — Max strength = 80% of original

1st vs 2nd Intention Healing:

Feature	First Intention	Second/Third Intention
Wound type	Small, clean, minimal tissue loss (surgical cut, slit)	Large wound, extensive necrosis (burn, diabetic ulcer)
Edges	Approximated (can be closed with sutures)	Cannot be approximated, gap too large
Re-epithelization	Rapid, direct	Slow, requires granulation tissue fill first
Scarring	Minimal or none	Extensive, visible scar
Healing time	Days to weeks	Weeks to months
Risk	Low infection risk	High infection risk, delayed healing, more necrosis in diabetics

🧠 MEMORY TRICK - 4 Phases: "HIPR" = "Healing Is Properly Renewed"

Haemostasis → Inflammation → Proliferation → Remodelling

🔷 TOPIC 3: BURNS

Learning Objective	Key Bold Terms	Details
Aetiology of burns	Thermal, Chemical, Electrical, Radiation (UV), Abrasion	Hot objects, scalding liquids, explosions, electrical injury, harsh chemicals, sunburn
Three degrees of burn	First-degree, Second-degree (superficial/deep partial thickness), Third-degree (full thickness)	Categorized by depth of tissue destruction
Pathophysiology	Protein denaturation, Inflammation, Fluid loss, Infection risk	Cell death, vascular damage, systemic response
Complications	Infection, Respiratory complications, Circulatory problems, Electrolyte imbalance, PTSD
Management	Respiratory care, Fluid replacement, Wound care, Pain control, Rule of Nines

Burns Classification Master Table:

Degree	Old Name	Depth	Appearance	Pain	Example
1st degree	Superficial	Epidermis ONLY	Red, DRY, NO blisters	Mild pain	Mild sunburn, brief heat exposure
2nd degree (superficial partial thickness)	Superficial partial	Epidermis + superficial dermis	RED, BLISTERED, MOIST, weeping	Very painful	Severe sunburn, scalding
2nd degree (deep partial thickness)	Deep partial	Epidermis + deep dermis	Blistered, may be DRY (sweat glands damaged)	LESS painful (nerve damage)	Scalding, flame, hot grease
3rd degree	Full thickness	Full skin + sometimes subcutaneous/bone	Dry, pale, CHARRED, broken	Painless (nerve destroyed)	Prolonged flame, chemical burns

Rule of Nines:

Body Area	% BSA
Head & neck	9%
Each arm	9%
Anterior trunk	18%
Posterior trunk	18%
Each leg	18%
Perineum	1%

🧠 MEMORY TRICK - Burn Degrees: "RED, BLISTERED, CHARRED"

1st = Red (dry, painful)
2nd = Blistered (very painful = superficial; less painful = deep)
3rd = Charred (painless, full thickness)

🔷 TOPIC 4: SKIN ERUPTIONS

4A: PSORIASIS

Learning Objective	Key Bold Terms	Details
Definition	Psoriasis, Chronic inflammatory skin disease, Autoimmune	Chronic relapsing autoimmune disorder causing hyperproliferation of keratinocytes
Clinical presentation	Plaques, Silvery-white scales, Erythema, Auspitz sign, Pruritus, Nail pitting, Psoriatic arthritis	Thick red plaques covered by silvery scales, especially on elbows, knees, scalp
Pathophysiology	T-cell activation (Th1/Th17), Keratinocyte hyperproliferation, IL-17, IL-23, TNF-α, Dendritic cells	Antigen triggers DC activation → T-cell (Th17) activation → cytokines (IL-17, IL-23, TNF-α) → keratinocytes multiply 28x faster than normal → scale formation

Psoriasis Pathophysiology Step-by-Step:

Step	Event
1	Trigger (infection, stress, drugs like lithium/beta-blockers, trauma - Koebner phenomenon)
2	Dendritic cells activated → present antigens to T-cells
3	Th1 & Th17 T-cells activated → release cytokines: IL-17, IL-23, TNF-α, IFN-γ
4	Cytokines → keratinocyte hyperproliferation (cycle: normal 28 days → abnormal 3-4 days)
5	Abnormal keratinocytes → incomplete differentiation → parakeratosis (nuclei retained in stratum corneum)
6	Acanthosis (epidermal thickening) + Munro microabscesses (neutrophil collections in stratum corneum)
7	Result: thick silvery-white plaques on red erythematous base

4B: DERMATITIS (Eczema)

Atopic Dermatitis:

Feature	Details
Definition	Chronic, relapsing inflammatory skin disease with intense pruritus, associated with atopy (IgE-mediated hypersensitivity)
Triad of Atopy	Asthma + Allergic rhinitis + Atopic dermatitis
Pathophysiology	Filaggrin gene mutation → impaired skin barrier → allergen penetration → Th2-dominant response → IL-4, IL-5, IL-13, IgE elevation → mast cell degranulation → histamine release → intense itch
Clinical features	Pruritus (severe), erythema, dry skin (xerosis), lichenification (chronic scratching), oozing vesicles in acute phase
Trigger	Food allergens (milk, eggs, nuts), dust mites, pollen, stress, irritants
Distribution	Infants: face/extensor surfaces; Children/Adults: flexural areas (antecubital, popliteal fossa)

Contact Dermatitis:

Type	Mechanism	Example	Key Feature
Irritant Contact Dermatitis (ICD)	Non-immunological - direct chemical damage to skin cells	Soaps, detergents, acids	No prior sensitization needed; affects anyone
Allergic Contact Dermatitis (ACD)	Type IV hypersensitivity (delayed, T-cell mediated)	Nickel, rubber, poison ivy, latex	Requires prior sensitization; reaction 48-72 hrs after re-exposure

Seborrheic Dermatitis:

Feature	Details
Definition	Chronic inflammatory condition affecting sebaceous gland-rich areas
Cause	Malassezia furfur (yeast overgrowth on sebum-rich areas) + immune response
Clinical features	Greasy yellowish scales, erythema, on scalp (dandruff), face (nasolabial folds, eyebrows), chest
Pathophysiology	Malassezia metabolizes sebum triglycerides → oleic acid → skin barrier disruption → inflammatory response

🧠 MEMORY TRICK - Dermatitis Types: "ACS" = Atopic, Contact, Seborrheic

Atopic = Allergy (Th2, IgE, filaggrin)
Contact = Chemical or T-cell (Type IV)
Seborrheic = Scalp, Sebum, Malassezia

🔷 TOPIC 5: ACNE VULGARIS (Disorders of Sebaceous Glands)

Learning Objective	Key Bold Terms	Details
Define pilosebaceous unit	Pilosebaceous unit	Hair follicle + sebaceous gland + arrector pili muscle = one unit
Aetiology	Sebum overproduction, Cutibacterium acnes (C. acnes), Keratin plugging, Androgens, Genetics	Multifactorial
Pathogenesis	Follicular hyperkeratinization, Sebum excess, C. acnes colonization, Inflammation	4-step process
Types of acne	Comedone (open/closed), Papule, Pustule, Nodule, Cyst	Non-inflammatory vs Inflammatory

Acne Pathogenesis - 4 Steps:

Step	Event	Key Term
1	Androgens (at puberty) stimulate sebaceous glands → excess sebum	Seborrhoea
2	Abnormal keratinization of follicular lining → keratin plug blocks follicle	Comedone formation (blocked follicle)
3	Trapped sebum + keratin = ideal medium for C. acnes overgrowth	Bacterial colonisation
4	C. acnes releases lipases → free fatty acids → inflammatory cascade → papules, pustules, nodules, cysts	Inflammation

Acne Types Table:

Type	Features	Non-/Inflammatory
Closed comedone (whitehead)	Blocked follicle, covered with skin, white bump	Non-inflammatory
Open comedone (blackhead)	Blocked follicle, open to surface, oxidized melanin = black	Non-inflammatory
Papule	Red, solid, elevated, inflamed	Inflammatory
Pustule	Pus-filled, yellow center, inflamed	Inflammatory
Nodule	Large, deep, solid, painful	Inflammatory
Cyst	Deep, pus-filled, most severe, leads to scarring	Inflammatory (Severe)

🧠 MEMORY TRICK - Acne Pathogenesis: "SACK"

Sebum overproduction
Abnormal keratinization (comedone)
C. acnes colonization
Kindles inflammation

🔷 TOPIC 6: DISORDERS OF HAIR

Disorder	Key Bold Terms	Definition	Pathophysiology	Management
Alopecia areata	Idiopathic, Catagen phase, Autoimmune, Anagen	Disease causing patchy hair loss, most on scalp/beard	Autoimmune T-cell attack on hair follicles; inhibition of progression to catagen phase (idiopathic); follicle stuck in catagen/telogen	Topical minoxidil, Oral finasteride (low dose)
Hirsutism	Androgens, PCOS, Terminal hair	Excessive male-pattern hair growth in women (face, chest, back)	Excess androgens (from PCOS, adrenal tumors, drugs) → conversion of vellus to terminal hair in androgen-sensitive areas	Anti-androgens (spironolactone), OCP, treat underlying cause
Hypertrichosis	Non-androgen-dependent, Lanugo, Vellus	Excessive hair growth in non-androgen-dependent pattern (can be generalized or localized)	NOT driven by androgens - may be congenital or due to drugs (cyclosporine, minoxidil, phenytoin), malnutrition	Treat underlying cause, laser hair removal

🧠 MEMORY TRICK - Hair Disorders: "AAH" (like saying "Aah!" when you see hair problems)

Alopecia areata (hair LOSS, autoimmune)
Androgen = Hirsutism (male-pattern in females)
Hypertrichosis (excessive hair, NON-androgen)

🔷 TOPIC 7: DISORDERS OF NAILS

Disorder	Key Bold Terms	Description	Common Causes
Onycholysis	Nail plate separation, Distal/lateral detachment	Separation of nail plate from nail bed, starting distally	Psoriasis, fungal infection (onychomycosis), trauma, hyperthyroidism
Clubbing	Hyponychial angle >180°, Lovibond angle, Drumstick fingers, Schamroth sign	Bulbous enlargement of fingertip with loss of normal nail angle - angle between nail and proximal fold becomes >180°	Chronic hypoxia (lung cancer, COPD, cyanotic heart disease), liver cirrhosis, IBD
Pitting	Punctate depressions, Thimble pitting	Small pit-like depressions on nail surface due to defective nail matrix keratinization	Psoriasis (most common), alopecia areata, eczema

🧠 MEMORY TRICK - Nail Disorders: "OCP" (like Oral Contraceptive Pill, something pharma students know well!)

Onycholysis = nail lifts OFF the bed
Clubbing = CHRONIC hypoxia (think lung cancer)
Pitting = Psoriasis (P for P)

🔷 TOPIC 8: DRUG ERUPTION — SJS & TEN

Learning Objective	Key Bold Terms	Details
Definition	Stevens Johnson Syndrome (SJS), Toxic Epidermal Necrolysis (TEN)	Severe, life-threatening mucocutaneous reactions — SJS: <10% BSA; SJS/TEN overlap: 10-30%; TEN: >30% BSA
Clinical manifestations	Prodrome, Erythema, Blisters/Bullae, Mucous membrane involvement, Nikolsky sign, Skin detachment	Flu-like prodrome → target lesions → blistering → massive epidermal detachment
Pathophysiology	CD8+ T-cells, Cytotoxic attack, Keratinocyte apoptosis, FasL-Fas pathway, Granulysin	Drug-specific CD8+ T-cells attack keratinocytes expressing drug antigens → massive keratinocyte apoptosis → epidermal necrolysis
Causative drugs	Allopurinol, Carbamazepine, Phenytoin, Sulfonamides, NSAIDs, Lamotrigine, Nevirapine
Genetic risk	*HLA-B1502 (carbamazepine in Asians), HLA-B5801* (allopurinol in Asians)	Pharmacogenomics marker

SJS vs TEN Comparison:

Feature	SJS	SJS-TEN Overlap	TEN
BSA detachment	< 10%	10-30%	> 30%
Mortality	~5%	~15%	~30-40%
Severity	Moderate	Severe	Life-threatening

SJS/TEN Pathophysiology Step-by-Step:

Step	Event
1	Causative drug taken by genetically susceptible patient
2	Drug or its metabolite acts as hapten → binds to MHC I on keratinocytes
3	Drug-specific CD8+ cytotoxic T-cells activated
4	Granulysin (cytotoxic protein) + FasL (Fas ligand) released
5	FasL binds Fas on keratinocytes → apoptosis cascade → massive keratinocyte death
6	Epidermal-dermal separation → blistering, skin peeling (Nikolsky sign positive)
7	Mucous membranes (mouth, eyes, genitalia) also involved

Clinical Features to Know:

Sign/Symptom	Description
Nikolsky sign	Gentle pressure on skin causes it to peel/slough - POSITIVE in TEN
Target lesions	Classic "bull's eye" erythematous macules in SJS
Prodromal symptoms	Fever, malaise, sore throat (flu-like) 1-3 days before skin eruption
Mucous membrane	Oral, ocular, genital erosions — CRITICAL distinguishing feature from other drug rashes

🧠 MEMORY TRICK - SJS/TEN Drugs: "A Can Prevent Serious Liver Necrosis"

Allopurinol
Carbamazepine
Phenytoin
Sulfonamides
Lamotrigine
Nevirapine

🔷 TOPIC 9: SKIN TUMOURS

Tumour	Key Bold Terms	Origin	Clinical Features	Risk Factors
Squamous Cell Carcinoma (SCC)	Keratinocytes, Actinic keratosis, UV radiation, Bowen's disease	Malignant keratinocytes (epidermal cells)	Scaly, ulcerated, firm nodule; can metastasize; on sun-exposed areas	UV exposure, HPV, immunosuppression, burns/scars
Basal Cell Carcinoma (BCC)	Most common skin cancer, Pearly papule, Telangiectasia, Rolled border, NEVER metastasizes	Basal cells of epidermis	Pearly/translucent nodule with rolled borders, central ulcer, telangiectasia ("rodent ulcer")	UV exposure (most common skin cancer worldwide), fair skin
Melanoma	Melanocytes, ABCDE rule, Breslow thickness, Clark level, Most aggressive, Metastasis	Malignant melanocytes	Irregular, asymmetric pigmented lesion; can metastasize widely	UV exposure, fair skin, family history, dysplastic naevi

Melanoma ABCDE Rule:

Letter	Stands for	Warning sign
A	Asymmetry	One half does not match the other
B	Border	Irregular, ragged, notched edges
C	Colour	Multiple shades of brown, black, red, white, blue
D	Diameter	> 6mm (size of a pencil eraser)
E	Evolution	Changing in size, shape, color; new bleeding/itching

🧠 MEMORY TRICK - 3 Skin Cancers: "BMS = Be More Scared" (in order of severity/aggressiveness)

BCC = Basal (most common, least dangerous - NEVER metastasizes)
SCC = Squamous (middle - can metastasize locally)
Melanoma = Most aggressive (metastasizes widely)

🏆 GRAND MASTER MEMORY TRICKS SUMMARY

Topic	Memory Trick	What It Covers
Primary lesions	"Many Patients Prefer Noting Vital Bugs, Pustules While Crying"	Macule, Patch, Papule, Plaque, Nodule, Vesicle, Bulla, Pustule, Wheal, Cyst
Secondary lesions	"Silly Cats Eat Ugly Fish, Sometimes Licking Keloids"	Scale, Crust, Erosion, Ulcer, Fissure, Scar, Lichenification, Keloid
Wound healing phases	HIPR = "Healing Is Properly Renewed"	Haemostasis, Inflammation, Proliferation, Remodelling
Burn degrees	"RED, BLISTERED, CHARRED"	1st (red/dry), 2nd (blistered), 3rd (charred/painless)
Dermatitis types	"ACS"	Atopic, Contact, Seborrheic
Acne pathogenesis	"SACK"	Sebum, Abnormal keratinization, C. acnes, Kindles inflammation
Hair disorders	"AAH"	Alopecia areata, Androgen=Hirsutism, Hypertrichosis
Nail disorders	"OCP"	Onycholysis, Clubbing, Pitting
SJS/TEN drugs	"A Can Prevent Serious Liver Necrosis"	Allopurinol, Carbamazepine, Phenytoin, Sulfonamides, Lamotrigine, Nevirapine
Skin cancers	"BMS = Be More Scared"	BCC (least dangerous), SCC, Melanoma (most dangerous)
Melanoma check	ABCDE	Asymmetry, Border, Colour, Diameter, Evolution

⚡ EXAM LIGHTNING QUICK-REFS

Q: What is the key difference between SJS and TEN?

% BSA skin detachment: SJS <10%, TEN >30%. Both involve mucous membranes and have +ve Nikolsky sign.

Q: Name the 4 phases of wound healing IN ORDER with key events:

Haemostasis (platelet plug, fibrin) → Inflammation (neutrophils clean, macrophages arrive) → Proliferation (fibroblasts lay collagen III, angiogenesis, re-epithelialization) → Remodelling (collagen III → collagen I, scar matures, 80% tensile strength)

Q: Differentiate Hirsutism from Hypertrichosis:

Hirsutism = androgen-dependent, male-pattern in females (PCOS most common cause). Hypertrichosis = non-androgen, generalized excess hair (congenital or drug-induced by minoxidil, cyclosporine).

Q: What is the key pathophysiology of psoriasis?

Th17/Th1 T-cell activation → IL-17, IL-23, TNF-α → keratinocyte hyperproliferation (28x faster) → parakeratosis + Munro microabscesses → silvery plaques on erythematous base.

Q: Difference between atopic dermatitis and contact dermatitis?

Atopic = Th2, IgE-mediated, filaggrin mutation, chronic, flexural areas. Contact = either direct chemical (ICD) or Type IV delayed hypersensitivity T-cell mediated (ACD), needs allergen exposure.

Q: Name the pilosebaceous unit and acne pathogenesis:

Pilosebaceous unit = hair follicle + sebaceous gland. Acne: SACK - Sebum overproduction (androgens) → Abnormal keratinization → C. acnes colonization → Kindles inflammation.

Q: What is Nikolsky sign?

Gentle lateral pressure causes skin to peel/slough - positive in TEN/SJS, indicating epidermal-dermal separation.

Q: Describe clubbing:

Bulbous enlargement of fingertip, loss of nail angle (>180°), Schamroth sign. Caused by chronic hypoxia: lung cancer, COPD, cyanotic congenital heart disease, liver cirrhosis.

📌 BOLD KEYWORDS QUICK-SCAN LIST (for last-minute revision)

Skin Lesions: Macule Patch Papule Plaque Nodule Vesicle Bulla Pustule Wheal Cyst Scale Crust Erosion Ulcer Fissure Scar Lichenification Keloid

Wound Healing: Haemostasis Platelets Fibrin Inflammatory phase Neutrophils Macrophages Proliferative phase Fibroblasts Collagen III → I Granulation tissue Re-epithelialization VEGF Remodelling MMPs Myofibroblasts First intention Second intention

Burns: Superficial (epidermis) Partial thickness (dermis) Full thickness BSA Rule of Nines Nikolsky Skin grafting Electrolyte imbalance

Psoriasis: Th17 IL-17 IL-23 TNF-α Keratinocyte hyperproliferation Parakeratosis Munro microabscesses Auspitz sign Koebner phenomenon Silvery plaques

Atopic Dermatitis: Filaggrin mutation Th2 response IL-4 IL-5 IL-13 IgE Mast cells Histamine Xerosis Lichenification Atopy triad

Contact Dermatitis: ICD (irritant) ACD (allergic) Type IV hypersensitivity Sensitisation phase Elicitation phase CD4+ T-cells

Seborrheic Dermatitis: Malassezia furfur Sebaceous glands Oleic acid Dandruff Nasolabial folds

Acne: Pilosebaceous unit Sebum Androgens Follicular hyperkeratinization Comedone Cutibacterium acnes Lipases Free fatty acids Non-inflammatory vs Inflammatory acne

Hair: Alopecia areata Catagen phase Minoxidil Finasteride Hirsutism PCOS Terminal hair Hypertrichosis Lanugo Vellus hair

Nails: Onycholysis Nail plate Nail bed Clubbing Lovibond angle Schamroth sign Pitting Psoriasis association

SJS/TEN: CD8+ T-cells Granulysin FasL-Fas pathway Keratinocyte apoptosis Nikolsky sign HLA-B*1502 HLA-B*5801 Mucous membrane Allopurinol Carbamazepine % BSA

Skin Tumours: BCC (pearly papule, rolled border, telangiectasia) SCC (actinic keratosis, UV) Melanoma ABCDE Breslow thickness Metastasis Melanocytes Keratinocytes Basal cells

Good luck in your exam! Use the HIPR, SACK, ABCDE, OCP, BMS mnemonics when you blank out - they will unlock the full answer every time. The key to SAQ/LAQ success is always: Definition → Pathophysiology (step-by-step) → Clinical Features → Examples. Follow that structure and you will answer any question like a pro. 💪

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