Peer Teaching

Dermatology &

Miscellaneous

Ulcers

• Arterial• Venous• Neuropathic• Traumatic• Vasculitic

Arterial Vs VenousARTERIAL VENOUS

Gaiter area above lateral malleolusTips of toesTo start with irregular then becomes demarcatedDeep ulcer, round

cool, shiny pale or dusky skin with loss of hair.Peripheral gangreneReduced peripheral pulsesDelayed cap refill

BETTER WITH LEG DOWN

PAIN HIGH

Pre tibial areasPeripheral on borders or sides of feet. Large but shallow

Haemosiderin deposits on tibial areas varicose eczema with hyperpigmentation and lipodermatosclerosis

BETTER WITH LEG UP

MINIMAL PAIN

Type of Ulcer What to know:

Neuropathic Pressure sites on foot:under second metatarsal headsurrounded by calluslimited joint mobility?Deformity? Ie Charcots joints Check footwear for source of trauma/ pressureNB: osteomyelitis complicates deep neuropathic ulcers

Traumatic Including IV drug abuse

Vasculitic Purpuric wound edgesPalpable purpuraNodulesLivedo Ass.w/ connective tissue disorders

What might delay healing?

• oedema• immobility (poor calf muscle pump and

oedema)• anaemia or malnutrition• corticosteroids• repetitive trauma• heavy colonization with bacteria

ECZEMA

• Superficial skin inflammation with vesicles (when acute)

• redness• oedema• oozing• scaling• pruritus

TYPESATOPIC EXOGENOUS

Hereditary

Abnormal epithelial barrier function antigenic and irritant agents to penetrate and come into contact with immune cells. Filaggrin mutation (Caucasians) IgE in serumPreferential activation of Th2 CD4 lymphocytes

Acute or chronic skin inflammation

Due to primary chemical irritants such as:Primary irritants-acids & alkalis-detergents-petroleumDelayed Type IV hypersensitivity-nickel-rubber additives-hair dyes-topical medicaments

ATOPIC

• Itchy• Erythematous• Scaly patches seen in flexures behind knees

and around the neck. • Can become secondarily infected by Staph Aureus (crusted, weeping

impetigo-like lesion) ORherpes simplex virus (small blisters or punched out lesions = eczema herpeticum which is FATAL)

EXOGENOUS

• Unusual pattern of rash with clear-cut demarcation

• Odd-shaped areas of erythema and scaling

Treatment• EDUCATION – family AND patient• Emollients (aqueous cream or emulsifying ointments) • Mild steroids (hydrocortisone) used for face • Potent steroids used for body and soles (betamethasone)

• Topical immunomodulators ie calcineurin inhibitors (tacrolimus and pimecrolimus) for eyelids

• Abx if superinfection

• Second line: If severe and unresponding • prednisolone• azathioprine• ciclosporin

• For exogenous eczema:

!!Remove causative agents!!

ACNE

• Increased sebum production by sebaceous glands

• Blockage of pilosebaceous units

• Follicular epidermal hyperproliferation

• Infection with propionibacterium

• Androgens (in normal amounts) stimulate increased sebum production• Hair follicles with large sebaceous glands (face, neck, chest & back)

become blocked due to hyperkeratosis• closed ‘comedo’• Within the follicle an obligate anaerobe proprionibacterium acnes

proliferates• Acts on sebum releasing inflammatory chemicals• Leak into surrounding dermis• Body mounts an intense acute inflammatory response• PAPULE: rapid pustular development. Red base. • PUSTULE: evolved papules• NODULES: increasing severity to become deep-seated nodule V.

uncomfortable and cysts develop.

COMEDONES OPEN

Felt rather than seen dilated blocked hair follicles. Always seen in acne in younger patients.

WORST CASE SCENARIO

• ACNE FULMINANS = young man develops severe nodulocystic acne +

• fever• malaise• joint pain• swelling

Treatment• First-Line• Keratolytics (benzoyl peroxide)• Topical retinoids (tretinoin or isotretinoin)• Retinoid-like agents (adapalene)• Abx (erythromycin, clindamycin)• • Second-line:• Low dose oral Abx (oxytetracycline, trimethoprim)• • Hormonal Rx + cyproterone acetate + co-cyprindol is good if CI to oral

contraceptive.• • Third-line: • Oral retinoid (isotretinoin or acitretin)

Side effects of Isotretinoin

• mild alopecia• dry skin• raised blood fat levels• teratogenicity• psychological disturbances

Skin Cancer

• Malignant melanoma • Squamos cell cancer • Basal cell carcinoma (rodent )

Malignant Melanoma

• Sunlight is major cause• F>M• Metastasise early!!• • Can occur in pre-existing moles• • Nodular melanomas: invade deeply and metastasise early• • Superficial spreadingmelanomas: grow slowly and

metastasise

GLASGOW SCALE

• Assymetry• Border-irregular• Colour – non uniform• Diameter >7mm• Elevation

• (=Glasgow scale) + Clarks staging to stratify depth URGENT EXCISION

Squamos cell cancer

• Begins as solar (actinic) keratoses on the forehead

• OR• Found on lips of life-long smokers • OR • In long-standing ulcers (marjolin’s)

• Ulcerated lesion• Hard, raised edges• Sun-exposed sites• • Keratotic nodule with granulating base and rolled border• Regional lymphadenopathy

• Treatment:• Excision (curretage)• Photodynamic therapy (PDT) for superficial tumours• • Mohs microscopic surgery if need to preserve skin in recurrent

cancers e.g. eyelid

Squamos cell cancerBasal cell carcinoma (rodent )

• Very slow grower• Never metastasizes• Locally invasive (hence rodent)• • Middle aged• Caucasians

Types• Nodulocystic:• Dome shaped pearly papule• Telangiecstasia across surface

• Superficial:• 1 + scaly erythematous plaques (on trunk)• well-defined raised pearly edges• Bowen’s or fungal??

• Pigmented: if heavily pigmented then think malignant melanoma. • Morphoeic: waxu indurated plaque that looks like a scar

Treatment:

• Excision (curretage)• Photodynamic therapy (PDT) for superficial

tumours

INFECTIONS OF SKINNecrotizing fasciitis Cellulitis & erysipelas

LIFE-THREATENING soft tissue infectionrapidly progressive necrosis that spreads subcutaneously to deep fascia Secondary to organ failure AND streptococcal toxic shock syndrome (TSS) Consider if sick patient not responding to treatment for cellulitis and pain out of proportion to signs

Due to streptococcus pyogenes (or staph.aureus if immunosuppressed) Erysipelas = often involves the face. Due to group A streptococci beta-haemolytic. Cellulitis = lower extremities normally. Common in patients with chronic lymphoedema. Due to streptococcus or sometimes CA-MRSA.

Necrotizing fasciitis Cellulitis & erysipelas

Hx of recent traumaIll patient with high temp, tachycardia, low BPPain> signsAltered LoCRapidly spreading poorly demarcated purplish erythema Dishwater pus (malodorous serosanguineous exudate) Crepitation in soft tissue (gas from aerobic/anaerobic)blisters

Erythema in involved areaPoorly demarcated marginsSwellingWarmthTenderness Low-grade fever

Necrotizing fasciitis Cellulitis & erysipelas

MISCELLANEOUS

Paracetamol OD

• Exceed max recommended dose =2 X 500mg QDS in 24h • Intake of >12g or >150mg/kg hepatic necrosis

• Risk factors:• alcohol abuse• enzyme inducing drugs (anticonvulsants or anti-TB drugs)• malnourished• anorexia nervosa• HIV more susceptible to toxic

• Paracetamol metabolized in liver by conjugation with glucoronate or sulphate excreted by kidneys.

• Cytochrome P450 metabolises some of it to highly reactive N-acetyl-p-benzoquinonimine (can inactivated by conjugation with glutathione)

0-24 h Asymptomatic or mild nauseaVomitingLethargymalaise

24-72 h AsymptomaticMild nauseaVomiting Liver enlargement & tenderness

> 72 h Increasing confusion (encephalopathy) Jaundice, coagulopathy, hypoglycaemia, renal angle pain

• WITHIN 8 HOURS OF OD:N-acetylcysteine IV

Breast Cancer

STAGING OF BREAST CaStaging

1 Confined to breastmobile

2 Growth confined to breastMobileLymph nodes in ipsilateral axilla

3 Tumour fixed to muscle (not chest wall)Ipsilateral lymph nodes matted/fixedSkin involved> tumour

4 Complete fixation chest wallDistant METS

Management is MDT-based!• Surgery: wide local excision OR masectomy + breast reconstruction

• Radiotherapy: post-op to avoid recurrence• If lymph node +ve also• (SE: pneumonitis, pericarditis, rib fractures, lymphoedma, brachial plexopathy)

• Chemotherapy: good if younger and lymph node +ve• Antrhacycline• 5FU• cyclophosphamide• Methotrexate

• Endocrine agents:• To decrease oestrogen (ER) activity:• Tamoxifen (ER blocker)• • Anastrozole (aromatase inhibitors that target ER synthesis good if post-menopausal• • Ovarian ablation or GnRH analogues ‘GOSERELIN’ if young and ER +ve tumour. • • Support: breast care nurses • Reconstruction: implants• Latissimus dorsi flap• TRAM flap

Mental Capacity Act 2005

5 magic principles – learnt them!

• 1. Presumption of capacity – everyone has the capacity to make their own decision until proven otherwise

• 2. The right for support to be given to help make those decision – ie get all info before conclude they are incapable.

• 3. Individuals retain right to make what might seem like unwise decisions

• 4. Must retain patients best interests if make it on their behalf ie they lack capacity

• 5. The least restrictive option in their best interested must be chosen on their behalf.

HIV Human immunodeficiency virus

Transmission

Sexual intercourse/Infected blood/IVDU/Vertical

Stages 1. Acute infection Asymptomatic2. Seroconversion 2-6 weeks post exposure. 3. Asymptomatic phase * can get PGL4. AIDSCD4+ count <200mm3

Pathophysiology

1. GP120 – CD4+2. CD4+ migrates Lymphoid tissue3. Replication, producing billions

virions4. New CD4+ cells infected, numbers

delete5. Immune function falls.

HIVDiagnosisELISA = HIV-Ab if 1-3 weeks post exposurePCR = HIV RNA or core p24 antigen- All HIV diagnoses given tuberculin test.

Complications• LUNGS: Pneumocystis jiroveci

pneumonia - give IV co-trimoxazole and pred• GI: candidiasis, HSV, anorexia, weight

loss, Diarhhoea, hepatomegaly, anaemia

• EYE: CMV retinitis. Fudoscopy shows ‘mozzarella pizza’ sign

• CNS: - acute= transient meningoencephalitis - chronic= dementia, meningitis, CMV encephalitis

ManagementHAART: highly active antiretroviral therapy

1 NNRTI ( non - nucleoside reverse transcriptase inhibitor) e.g NEVIRAPINE and EFAVIRENZ 2 NRTI e.g ZIDOVUDINE

OR

PI (protease inhibitor) e.g INDINAVIR 2 NRTI