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]

Historical slide algorithm:

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]

This flowchart is useful for understanding the lecture, but it is not a current stand-alone protocol. History and examination alone are often inaccurate, and more than one cause may coexist. Current CDC guidance recommends that every genital ulcer be assessed with syphilis serology plus a direct lesion test where available, and type-specific HSV-1/HSV-2 nucleic-acid amplification testing (NAAT) or culture; offer HIV testing and tailor other STI tests to exposure sites and local epidemiology. Lesion HSV NAAT is preferred because culture sensitivity falls as lesions heal. Start presumptive treatment promptly when infectious syphilis or a first episode of genital herpes is clinically suspected rather than waiting for every result ^[7].

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

Key facts from the lecture slides (retain the exact numerical claims as historical teaching):

• The slide states HSV-2 90% / HSV-1 10% ^[1], but those proportions are not universal; either type can cause genital herpes.
• 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]

Clinical photographs show grouped, clear vesicles on an erythematous base and a disseminated monomorphic, crusted/punched-out eruption over the face. Grouping of same-stage vesicles is the visual clue; widespread painful punched-out erosions in eczematous skin should raise concern for eczema herpeticum and urgent antiviral assessment ^[1].

First clinical episodes are often more severe and prolonged, whereas recurrences are commonly shorter and more localized. This reflects the host response and reactivation of latent virus from sensory ganglia, but prior unrecognized infection means a “first recognized episode” is not always a true primary infection.

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]

• Lesion NAAT/PCR is now the preferred, most sensitive direct test; culture is less sensitive, especially in recurrent or healing lesions ^[7].
• The microscopy slide shows a Tzanck smear with multinucleated giant keratinocytes. This may support a herpesvirus infection but cannot distinguish HSV-1, HSV-2, or varicella-zoster virus, so it does not replace type-specific NAAT.
• Type-specific serology cannot prove that a current ulcer is herpetic, but it can be useful in selected patients (for example, recurrent atypical symptoms with negative lesion testing); interpretation and confirmatory testing may be needed ^[7].

Management:

The slide lists symptomatic control, systemic antivirals, topical antibiotics, contact tracing, and screening for other STIs ^[1]. In current practice, treat a first clinical episode with an oral antiviral (acyclovir, valacyclovir, or famciclovir); topical antivirals offer little benefit, and topical antibiotics are reserved for clinically infected secondary lesions rather than given prophylactically ^[7].

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]

The photograph shows the classic solitary round ulcer with a clean, indurated base. A chancre is classically painless, but morphology is not sufficiently reliable to exclude coinfection. It may heal spontaneously without treatment; this does not mean the infection is cured, because dissemination can already have occurred ^[7].

The later truncal photograph demonstrates the diffuse papular eruption of secondary syphilis, linking the local chancre to subsequent systemic disease ^[1].

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 slide's fibrin-cuff theory (Browse's hypothesis). Treat it as one historical mechanistic model, not the whole modern explanation: sustained ambulatory venous hypertension drives inflammation, microcirculatory dysfunction, oedema, tissue remodelling, and impaired healing.

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 and visual pattern:

After minor injury; shallow ulcer with yellowish/exudative base; medial and lateral malleoli (gaiter area) ^[1]

The slide photographs show an irregular shallow gaiter-area ulcer within brown haemosiderin pigmentation, oedema, and stasis eczema. Venous ulcers may ache or be painful; “painless” is a comparison with ischaemic rest pain, not a rule.

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]

The images make the vascular pattern explicit: distal toe/heel ulcers, dry black eschar or gangrene, shiny hairless skin, and pressure-point tissue loss. Do not apply strong compression before vascular assessment; threatened limb, gangrene, or rest pain requires urgent vascular review ^[9].

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

In the photographs, the key discriminator is a deep irregular ulcer with a violaceous, undermined edge, sometimes with adjacent pustules or multiple lesions. The active inflammatory rim is more diagnostically useful than the nonspecific necrotic centre.

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. Biopsy of the active ulcer edge is primarily used to exclude mimics; histology is not uniquely diagnostic. Antibiotics are used only for proven secondary infection, and aggressive debridement of active PG can worsen disease through pathergy. Wound care and any necessary debridement should be individualized with dermatology/surgical input; systemic anti-inflammatory or immunosuppressive therapy treats the underlying process.

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]

Nocturnal itch is a useful clue but is not specific. Classic adult scabies often spares the head and neck; however, the scalp, face, palms, and soles may be involved in infants, older adults, immunocompromised people, and crusted scabies.

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.
• The lecture photographs show the practical spectrum: a serpiginous scaly burrow, small papules and excoriations, persistent genital/breast nodules, and a mite removed from the end of a burrow. Secondary scratch marks may dominate even when primary lesions are sparse ^[1].

DDx:

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

Treatment:

The slide lists benzyl benzoate, gamma benzene hexachloride (lindane), permethrin, malathion, and monosulfiram ^[1]. Current CDC guidance uses permethrin 5% cream as first-line therapy for classic scabies (neck down for 8–14 hours, commonly repeated about one week later). Oral ivermectin is an effective alternative in appropriate patients, but its safety is not established in pregnancy or children weighing under 15 kg. Lindane is no longer first-line because of neurotoxicity and important contraindications ^[10].

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]

The photograph shows widespread excoriated papules and scratch marks rather than a diagnostic primary eruption. “No rash” therefore means no primary dermatosis: secondary excoriation, crusting, lichenification, or prurigo-like lesions may still be prominent.

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

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

The slide panel is a useful starting checklist, but current staged assessment also emphasizes medication review, xerosis, complete skin/lymph-node/abdominal examination, ferritin/iron status, and targeted tests driven by history and examination. Abnormalities or persistent unexplained itch determine the second-line work-up ^[11].

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]

“Chronic idiopathic” is now generally termed chronic spontaneous urticaria (CSU). Functional autoantibodies and other autoimmune mechanisms are demonstrable in a subset, but the lecture's “about half” is not a diagnostic rule. CSU can coexist with angioedema. Do not equate chronic wheals alone with anaphylaxis: acute urticaria may occur during anaphylaxis, which is defined by systemic airway, breathing, circulation, or severe gastrointestinal involvement and requires emergency treatment ^[12].

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]

That list reflects broad historical screening. Current guidance recommends history and examination first, with limited basic tests in CSU and additional allergy, infection, autoimmune, complement, or biopsy investigations only when the clinical story indicates them. For recurrent angioedema without wheals, assess for bradykinin-mediated angioedema with C4 plus C1-inhibitor level/function; this is not a routine screen for every patient with wheals ^[12].

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

• First-line: 2nd generation H1 antihistamines (cetirizine, loratadine), can uptitrate to 4× standard dose
• If control remains poor: omalizumab; ciclosporin is a later specialist option
• Avoid long-term systemic corticosteroids; a brief rescue course may be used for a severe acute exacerbation under clinical supervision
• Acute anaphylaxis: IM adrenaline

This stepwise sequence—second-generation H1 antihistamine, up-dosing to as much as fourfold if needed, then omalizumab and later ciclosporin—is the current international guideline pathway. The slide-era H2-blocker/ranitidine step is not part of that core algorithm ^[12].

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]

• Palmoplantar psoriasis: the sole and palm images show symmetric, sharply marginated hyperkeratosis, erythema, scale, and painful fissuring. Thick acral scale can obscure the classic silvery plaque appearance; inspect nails and other extensor/scalp sites and exclude tinea when unilateral or atypical.
• Guttate/Koebner pattern: the truncal photograph contains numerous drop-like plaques, with linear lesions at sites of trauma illustrating the Koebner phenomenon.
• Generalized pustular psoriasis (GPP): innumerable superficial non-follicular pustules arise on diffuse erythema and coalesce into “lakes of pus,” followed by crusting/desquamation. The visual pattern plus fever/systemic illness distinguishes this from ordinary plaque psoriasis ^[1].
• Visual differentials: the AGEP photograph also shows many small non-follicular pustules, often accentuated in flexures, so a new-drug timeline is crucial. The SSSS image shows superficial tender exfoliation in a child rather than discrete sterile pustules.

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:

The historical case used bed rest, clarithromycin while cultures were pending, bland wash/emollient care, IV fluids, and careful fluid balance ^[1]. The antibiotic was case-specific empirical cover, not treatment for sterile GPP. Use systemic antibiotics only when bacterial infection is suspected or cannot yet be excluded ^[13].

Treat or withdraw the provoking factor (e.g. stop systemic steroids that triggered the flare). ^[1]

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

Current framing: a significant GPP flare needs urgent specialist/inpatient assessment of temperature, haemodynamics, hydration, electrolytes, renal/hepatic function, and infection/organ complications, with bland supportive skin care. Systemic treatment depends on severity, contraindications, and local availability. Specialist options include ciclosporin, acitretin, methotrexate, and biologic therapy; spesolimab, an IL-36-receptor antagonist, is specifically approved in the United States for GPP in adults and adolescents aged 12 years or older who weigh at least 40 kg, with indications and availability varying by jurisdiction ^[13][14].

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]

This is a historical regimen, not a dosing template. Methotrexate is prescribed once weekly under a specialist protocol, after checking contraindications/interactions and with blood-count, liver, and renal monitoring.

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
• Hepatic fibrosis assessment — the slide's mandatory liver biopsy after a cumulative 1.5 g is outdated. Current AAD guidance uses risk-based monitoring and incorporates non-invasive fibrosis assessment; biopsy is not triggered solely by reaching that cumulative dose ^[15].