A 35-year-old businessman with painful penile shaft rash starting as vesicles then developing into ulcers. Travels to China frequently, denies exposure to sex workers but has a girlfriend in China. ^[1]

Infective: Syphilis, Herpes, Chancroid, Lymphogranuloma venereum (LGV). Non-infective: Malignancy, Trauma, Fixed drug eruption, Behçet's syndrome, Erythema multiforme. ^[1]

The lecture provides a specific investigation flowchart for genital sores:

1. If vesicles present → Swab for HSV culture → Herpes
2. If no vesicles → Dark Ground Examination (DGE) x3 + VDRL/FTA/TPHA → Syphilis
3. If DGE negative → Swab + culture for H. ducreyi → Chancroid
4. If all tests negative → Consider non-infective causes; specific test for LGV ^[1]

Why DGE x3? Treponema pallidum is extremely difficult to culture. Dark-ground microscopy visualizes the spirochete directly from the ulcer exudate. You need three attempts because the sensitivity of a single DGE is only ~50%. This is why you also send serology (VDRL = non-treponemal screening; FTA-ABS and TPHA = treponemal confirmatory tests).

Herpes is the commonest cause of genital ulcer in Hong Kong ^[1]

Key facts from the lecture slides:

• HSV-2 accounts for 90%, HSV-1 for 10% of genital herpes ^[1]
• Incubation period: 2–5 days ^[1]
• Primary attack: particularly painful, tender inguinal lymphadenopathy, lasts ~3 weeks ^[1]
• Recurrent infection: HSV remains latent in sensory and autonomic ganglia → reactivation gives local, less symptomatic, shorter episodes ^[1]
• Reactivation triggers: trauma, menstruation, stress ^[1]

Why does primary herpes hurt more? The initial infection triggers a full-blown immune response because the host has no pre-existing antibodies. Recurrent episodes are attenuated because of partial immunity — the virus reactivates from the sacral dorsal root ganglion (S2-S4) and tracks along peripheral nerves to cause a localized eruption.

Complications of herpes:

Cutaneous dissemination, encephalitis, sacral radiculomyelopathy, urinary retention, bacterial superinfection, erythema multiforme, neonatal herpes ^[1]

• Sacral radiculomyelopathy — HSV can cause an ascending myelitis affecting S2-S4 → urinary retention, constipation, saddle anesthesia. This is an emergency.
• Neonatal herpes — Life-threatening in neonates; acquired during vaginal delivery if mother has active lesions. Mortality up to 30% in disseminated form.
• Erythema multiforme — HSV is the commonest cause of recurrent EM. The target lesions of EM are an immune-complex–mediated response to HSV antigens.

Investigations for herpes:

Viral antigen detection, viral culture, immunoassay (detect viral antibody), EM (electron microscopy), PCR, serology (inaccurate) ^[1]

• Viral culture remains important for typing but takes days.
• PCR is now the most sensitive and specific test — detects HSV DNA.
• Serology is inaccurate because it cannot distinguish current vs. past infection, and cross-reactivity between HSV-1 and HSV-2 is common.

Management:

Symptomatic control, antiviral agents (acyclovir/valacyclovir), topical antibiotics to reduce superimposed infection, contact tracing, screen for other STDs ^[1]

Treponema pallidum; IP 9–90 days; can be congenital or acquired; classified as primary/secondary/tertiary and early/latent ^[1]

Primary syphilis (chancre): solitary, painless ulcer with indurated base at site of trauma during sexual intercourse. Inguinal lymphadenopathy: non-tender, discrete, rubbery ^[1]

Why is the chancre painless? T. pallidum evades the immune system initially by lacking surface lipoproteins that activate toll-like receptors. The chancre heals spontaneously in 3–6 weeks even without treatment — this does not mean the patient is cured. The spirochete has already disseminated.

If left untreated, syphilis progresses: Primary → Secondary (widespread rash, mucous patches, condylomata lata) → Latent → Tertiary (gummas, cardiovascular syphilis, neurosyphilis). This natural history is beyond this specific lecture but is heavily tested elsewhere.

55-year-old lady with leg ulcers for several years ^[1]

Venous, Arterial, Pyoderma gangrenosum, Dysglobulinaemias, Sickle cell and thalassaemia, Basal cell carcinoma, Squamous cell carcinoma, Panniculitis, Vasculitis, Pressure ^[1]

Pathophysiology — from first principles:

Venous hypertension → distension and elongation of capillary loops → fibrinogen leaks into tissue → forms pericapillary fibrin cuffs → prevents diffusion of O₂ and nutrients to skin → local ischaemia → ulceration ^[1]

This is the fibrin cuff theory (Browse's hypothesis). Essentially, incompetent venous valves → ambulatory venous hypertension → capillary damage → extravasation of macromolecules → tissue hypoxia → ulcer.

Clinical features:

Eczema, atrophie blanche, oedema, pigmentation (haemosiderin), ulceration, venous flare, varicosities ^[1]

• Atrophie blanche = white, atrophic, scarred areas with surrounding telangiectasia — a sign of healed venous ulceration
• Haemosiderin pigmentation = brown discolouration from breakdown of extravasated red blood cells
• Lipodermatosclerosis = fibrosis of subcutaneous tissue causing an "inverted champagne bottle" leg appearance

Ulcer characteristics:

After minor injury; often painless; well-defined border; shallow ulcer with yellowish base; medial and lateral malleoli (gaiter area) ^[1]

Treatment:

Rest and leg elevation, compression dressing, exercise, diet to reduce weight, treatment of eczema, antibiotic if superimposed infection, cleansing agent, surgical ^[1]

Arterial insufficiency → skin ulceration. Risk factors: smoking, diabetes, hypertension. Painful ulcer worse at night. Other ischaemic symptoms: intermittent claudication, coldness, numbness. ^[1]

Signs:

Skin dry and scaly; hair sparse or absent; toenail thickened; deep punch-out ulcer; absent pulse; gangrene ^[1]

This table is directly from the lecture slides and is extremely high-yield: ^[1]

Management of arterial ulcers:

Doppler US, arteriographic assessment, control of risk factors, surgical assessment. Elastic stocking CONTRAINDICATED. ^[1]

Painful nodule or pustule breaks down to form a progressively enlarging ulcer. Single or multiple. Irregular, purplish border. Known association with systemic diseases. ^[1]

Associated systemic diseases:

Inflammatory bowel disease, connective tissue diseases, arthritis, gammopathy, haematological malignancy, Behçet's disease ^[1]

A useful mnemonic: IBAG-H — IBD, Arthritis, Gammopathy, Haematological malignancy.

Why does PG matter? It exhibits pathergy — trauma or surgical debridement worsens the ulcer. This is the opposite of what you'd normally do for an ulcer. If a surgeon debrides a PG lesion thinking it's a simple wound, it will rapidly enlarge.

Investigation: exclude infection by skin swab and tissue culture; skin biopsy; pathergy test; investigate for associated conditions. Treatment: systemic immunosuppressive agents and treat underlying disease. ^[1]

Key principle: PG is a diagnosis of exclusion (must rule out infection). It's treated with immunosuppression (corticosteroids, ciclosporin, dapsone, biologics), NOT antibiotics or surgery.

65-year-old elderly home resident with itchiness affecting the whole body but sparing the face. Symptoms worse at night. ^[1]

Infestation with Sarcoptes scabiei mite that burrows into the stratum corneum. Transmitted by physical contact. Itchiness due to immune response to the mite. Itchiness develops several weeks after infestation and will persist for weeks/months after treatment. ^[1]

Why does it spare the face in adults? The face has a higher density of pilosebaceous units and a different immune microenvironment. In infants, the immune system is immature, so the mite can infest any area including the face and scalp.

Why worse at night? The mite is more active at higher temperatures (under bedcovers). Also, cortisol levels drop at night → reduced natural anti-inflammatory state → itch worsens.

Clinical features:

Itchy rash that spares the face in adults but can affect the face in infants. Burrows especially in finger and toe webs. Scabies nodules in genitalia and breasts. Excoriation marks without much inflammation. ^[1]

• Burrows = pathognomonic finding — thin, wavy, greyish lines 5-15 mm long, often in web spaces. These are where the female mite tunnels to lay eggs.
• Scabies nodules = firm, pruritic, reddish-brown nodules, typically on male genitalia. They represent a hypersensitivity reaction and can persist long after the mite is eradicated.

DDx:

Eczema, generalised pruritus of systemic disease, urticaria ^[1]

Treatment:

Benzyl benzoate, gamma benzene hexachloride (lindane), permethrin, malathion, monosulfiram. Treat the whole family. 2x applications. ^[1]

Post-treatment pruritus:

Eurax (crotamiton), topical steroid. Scabies nodules can be very resistant and need potent topical steroid. ^[1]

Why does itching persist after treatment? The itch is an immune response to mite antigens embedded in the skin. Even after all mites are dead, the antigens remain and continue to provoke a Type IV hypersensitivity reaction for weeks. This does NOT mean treatment failure. Counsel the patient about this.

65-year-old elderly home resident with itchiness affecting the whole body INCLUDING the face. Persistent despite topical steroid. ^[1]

Note how this case parallels Case 3 but differs: face is involved, and treatment-resistant. This should shift your differential away from scabies toward systemic causes.

Generalized itchiness affecting the whole body without inflammatory dermatoses. Need to DDx from scabies, mild asteatotic eczema, dermatographism. Difficult to manage. ^[1]

Thyroid disease, parathyroid diseases, hepatic disease (especially obstructive jaundice), lymphoma, uraemia, iron deficiency, myeloproliferative diseases ^[1]

CBP, RFT, LFT, Ca, TSH, ESR ^[1]

Why each test:

• CBP — Iron deficiency (low MCV/Hb), lymphoma (lymphocytosis, eosinophilia), myeloproliferative disease (raised Hb/WBC/platelets)
• RFT — Uraemia
• LFT — Obstructive jaundice (raised ALP, GGT, bilirubin)
• Ca — Hyperparathyroidism, malignancy
• TSH — Thyroid disease
• ESR — Non-specific marker for lymphoma, connective tissue disease

Idiopathic, Infection (hepatitis, fungal, H. pylori, parasites), Systemic disease (SLE, autoimmune), Immunological (food, drug allergy), Physical, Genetic ^[1]

40% resolve within 1 year. Associate with deep pressure urticaria. About half of patients have antibody against IgE or IgE receptor. Can associate with angioedema and anaphylactic shock. ^[1]

Why do autoantibodies cause urticaria? Anti-IgE or anti-FcεRI antibodies bind to mast cells and cross-link IgE receptors → mast cell degranulation → histamine release → wheals. This is an autoimmune mechanism (Type II hypersensitivity) and explains why these patients are often refractory to simple antihistamines.

Cholinergic, deep pressure, dermographism, cold, heat, aquagenic, vibratory ^[1]

• Dermographism = writing on skin → wheal appears along the stroke. Most common form of physical urticaria. Test by firmly stroking skin with a blunt object.
• Cholinergic urticaria = triggered by rise in core body temperature (exercise, hot bath, emotion). Tiny 2–4 mm wheals ("micropapular").
• Cold urticaria = wheals on cold exposure. Dangerous because swimming in cold water can cause massive histamine release → anaphylaxis/drowning.

History and examination, physical challenge, CBP/RFT/LFT/ESR/ANA/C3/C4/C1-esterase inhibitor/stool for ova, prick test/RAST, skin biopsy, oral challenge test ^[1]

Why C3/C4/C1-esterase inhibitor? To exclude hereditary angioedema (HAE), which presents with recurrent angioedema WITHOUT urticaria. Low C4 is a screening test; low C1-esterase inhibitor confirms the diagnosis.

Why ANA? Chronic urticaria can be associated with SLE and other autoimmune diseases.

Management principles (from supporting lectures ^[5]):

• First-line: 2nd generation H1 antihistamines (cetirizine, loratadine), can uptitrate to 4× standard dose
• Add-on: H2 blockers (ranitidine) — some mast cells in skin express H2 receptors
• Refractory: omalizumab (anti-IgE biologic), ciclosporin
• Acute anaphylaxis: IM adrenaline

66-year-old man with several years history of rash affecting extensor surfaces of elbows and knees. Mildly itchy. Marked dandruff and nail changes affecting fingers and toes. ^[1]

37-year-old male with long history of skin problems, recent deterioration. Seen by GP, given medication and injection. Developed extensive rash with pustules. ^[1]

These patients suffer from the same condition ^[1]

Chronic inflammatory skin condition affecting 2–3% of the population. Two peaks of onset: young and late middle age. Earlier onset tends to be associated with worse prognosis. Triggers: genetic, drugs, infection (streptococcal), stress. ^[1]

Pathophysiology (from first principles): Psoriasis is a T-cell–mediated autoimmune disease. Th1 and Th17 cells produce TNF-α, IL-17, and IL-23 → stimulate keratinocyte hyperproliferation. Normal epidermal turnover is ~28 days; in psoriasis, it's ~4 days. This rapid turnover produces the thick silvery scale because keratinocytes don't have time to mature properly and shed.

Chronic large plaque, guttate, pustular, erythroderma. Nail: pitting, onycholysis. Scalp, joints. Auspitz sign, Koebner phenomenon. ^[1]

Key signs:

• Auspitz sign = removal of psoriatic scale → pinpoint bleeding (you've exposed the dilated capillaries at the tips of elongated dermal papillae)
• Koebner phenomenon = new psoriatic lesions appearing at sites of skin trauma (also seen in lichen planus, vitiligo)
• Nail pitting = punctate depressions from psoriatic involvement of the nail matrix
• Onycholysis = separation of the nail plate from the nail bed

Diagnosis is clinical. Management by topical agents: (1) Diprosalic ointment in the morning (betamethasone + salicylic acid), (2) Daivonex ointment at night (calcipotriol — vitamin D analogue), (3) Polytar shampoo (for scalp psoriasis). ^[1]

Treatment ladder:

1. Topical — emollients, topical steroids (with salicylic acid for descaling), vitamin D analogues (calcipotriol), tar preparations, dithranol
2. Phototherapy — UVB (narrowband), PUVA
3. Systemic — methotrexate, acitretin, ciclosporin
4. Biologics — anti-TNF (infliximab, adalimumab), anti-IL-17 (secukinumab), anti-IL-23 (guselkumab)

General: counselling, avoid aggravating factors, eradicate infection ^[1]

Pustular psoriasis, drug-induced acute pustular eruption (AGEP), staphylococcal scalded skin syndrome (SSSS), subcorneal pustular dermatosis, dermatitis herpetiformis, pemphigus foliaceus ^[1]

Sudden onset of sterile pustules with fever. Erythema surrounds pustules. Become extensive and confluent. Nail involvement common. Unusual to see other forms of psoriasis at the same time. Often provoked by infection, drugs (steroid withdrawal, lithium, oral contraceptive). ^[1]

Investigation findings in Case 6:

Skin swab and blood culture: negative (sterile pustules!). CBP: WBC 15 (leukocytosis from systemic inflammation). RFT/LFT: normal. Ca: 2.0 (low — can be low in generalized pustular psoriasis due to albumin loss). CXR: normal. Drug history: IMI steroid PRN for years for "psoriasis." Skin biopsy: suggestive of pustular psoriasis. ^[1]

Management of Case 6:

Bed rest, clarithromycin 500mg BD (empirical antibiotic cover while awaiting cultures), emulsifying ointment as soap, aqueous cream LA BD, IV fluids, careful fluid balance. ^[1]

Avoid irritants: tar, dithranol, phototherapy (in the acute phase — these would worsen inflammation). ^[1]

Systemic treatment: methotrexate (MTX), iso-acitretin, ciclosporin. ^[1]

Started MTX 2.5mg as testing dose, increased gradually to 15mg/week. Careful monitoring of CBP, RFT, LFT. Aim to gradually withdraw MTX. Patient warned of adverse effects and need for liver biopsy if cumulative dose reaches 1.5g. ^[1]

Why these precautions?

• MTX inhibits dihydrofolate reductase → suppresses rapidly dividing cells (including bone marrow and GI mucosa)
• CBP monitoring — for pancytopenia
• LFT monitoring — for hepatotoxicity (MTX causes hepatic fibrosis)
• RFT monitoring — MTX is renally excreted; renal impairment → toxicity
• Liver biopsy at 1.5g cumulative dose — to assess for hepatic fibrosis (though this threshold is somewhat historical; newer guidelines use Fibroscan/elastography)