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Peer Teaching
Dermatology
&
Miscellaneous
Basic skin structure
Ulcers
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Arterial
Venous
Neuropathic
Traumatic
Vasculitic
Arterial Vs Venous
ARTERIAL
VENOUS
Gaiter area above lateral malleolus
Tips of toes
To start with irregular then becomes
demarcated
Deep ulcer, round
Pre tibial areas
Peripheral on borders or sides of feet.
Large but shallow
cool, shiny pale or dusky skin with loss of
hair.
Peripheral gangrene
Reduced peripheral pulses
Delayed cap refill
BETTER WITH LEG DOWN
PAIN HIGH
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 head
surrounded by callus
limited joint mobility?
Deformity? Ie Charcots joints
Check footwear for source of trauma/ pressure
NB: osteomyelitis complicates deep neuropathic ulcers
Traumatic
Including IV drug abuse
Vasculitic
Purpuric wound edges
Palpable purpura
Nodules
Livedo
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
TYPES
ATOPIC
EXOGENOUS
Hereditary
Acute or chronic skin inflammation
Abnormal epithelial barrier function 
antigenic and irritant agents to penetrate
and come into contact with immune cells.
Due to primary chemical irritants such as:
Primary irritants
-acids & alkalis
-detergents
-petroleum
Delayed Type IV hypersensitivity
-nickel
-rubber additives
-hair dyes
-topical medicaments
Filaggrin mutation (Caucasians)
 IgE in serum
Preferential activation of Th2 CD4
lymphocytes
ATOPIC
• Itchy
• Erythematous
• Scaly patches  seen in flexures behind
knees and around the neck.
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Can become secondarily infected by Staph Aureus (crusted, weeping
impetigo-like lesion) OR
herpes 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
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EDUCATION – family AND patient
Emollients (aqueous cream or emulsifying ointments)
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Mild steroids (hydrocortisone) used for face
Potent steroids used for body and soles (betamethasone)
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Topical immunomodulators ie calcineurin inhibitors (tacrolimus and pimecrolimus)
for eyelids
Abx if superinfection
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• 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
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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.
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• Third-line:
• Oral retinoid (isotretinoin or acitretin)
Side effects of Isotretinoin
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mild alopecia
dry skin
raised blood fat levels
teratogenicity
psychological disturbances
Skin Cancer
• Malignant melanoma
• Squamos cell cancer
• Basal cell carcinoma (rodent )
Malignant Melanoma
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Sunlight is major cause
F>M
Metastasise early!!
Can occur in pre-existing moles
Nodular melanomas: invade deeply and metastasise
early
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• Superficial spreadingmelanomas: grow slowly and
metastasise
GLASGOW SCALE
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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)
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Ulcerated lesion
Hard, raised edges
Sun-exposed sites
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Treatment:
Excision (curretage)
Photodynamic therapy (PDT) for superficial tumours
Keratotic nodule with granulating base and rolled border
Regional lymphadenopathy
Mohs microscopic surgery if need to preserve skin in recurrent
cancers e.g. eyelid
Squamos cell cancer
Basal cell carcinoma (rodent )
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Very slow grower
Never metastasizes
Locally invasive (hence rodent)
Middle aged
Caucasians
Types
• Nodulocystic:
• Dome shaped pearly papule
• Telangiecstasia across surface
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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 SKIN
Necrotizing fasciitis
Cellulitis & erysipelas
LIFE-THREATENING soft tissue infection
rapidly progressive necrosis that spreads
subcutaneously to deep fascia
Due to streptococcus pyogenes (or
staph.aureus if immunosuppressed)
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
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 trauma
Ill patient with high temp, tachycardia,
low BP
Pain> signs
Altered LoC
Rapidly spreading poorly demarcated
purplish erythema
Erythema in involved area
Poorly demarcated margins
Swelling
Warmth
Tenderness
Dishwater pus (malodorous
serosanguineous exudate)
Crepitation in soft tissue (gas from
aerobic/anaerobic)
blisters
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
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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 nausea
Vomiting
Lethargy
malaise
24-72 h
Asymptomatic
Mild nausea
Vomiting
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 Ca
Staging
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Confined to breast
mobile
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Growth confined to breast
Mobile
Lymph nodes in ipsilateral axilla
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Tumour fixed to muscle (not chest wall)
Ipsilateral lymph nodes matted/fixed
Skin involved> tumour
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Complete fixation chest wall
Distant METS
Management is MDT-based!
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Surgery: wide local excision OR masectomy + breast reconstruction
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Radiotherapy: post-op to avoid recurrence
If lymph node +ve also
(SE: pneumonitis, pericarditis, rib fractures, lymphoedma, brachial plexopathy)
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Chemotherapy: good if younger and lymph node +ve
 Antrhacycline
5FU
cyclophosphamide
Methotrexate
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Endocrine agents:
To decrease oestrogen (ER) activity:
Tamoxifen (ER blocker)
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Reconstruction: implants
Latissimus dorsi flap
TRAM flap
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
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
Pathophysiology
1. GP120 – CD4+
2. CD4+ migrates
Lymphoid tissue
3. Replication, producing billions
virions
4. New CD4+ cells infected, numbers
delete
5. Immune function falls.
Stages
1. Acute infection
Asymptomatic
2. Seroconversion
2-6 weeks post exposure.
3. Asymptomatic phase
* can get PGL
4. AIDS
CD4+ count <200mm3
HIV
Diagnosis
ELISA = HIV-Ab if 1-3 weeks post exposure
PCR = 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
Management
HAART: 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