derm middle tier Flashcards
venous ulcer presentation
Commonly lower leg Takes 2w+ to heal Pain - worse when standing Varicose veins Large, shallow, irregular Normal pulses Warm skin Oedema in other leg
venous ulcer pathophysiology
High pressure (in superficial veins) forces fibrinogen out of vessels → perivascular fibrin deposition → poor oxygenation of skin in this area
venous ulcer risk factors
are they common?
Due to sustained venous hypertension in superficial veins Incompetent valves DVT Atherosclerosis Vasculitis - RA, SLE
common, more common with age
ulcer =
abnormal break in epithelial surface eg skin
arterial ulcer risk factors
Smoking Arterial disease - atherosclerosis ! DM Hypercholesterolemia History of claudication, hypertension, angina
arterial ulcer presentation
Punched out Small, defined Necrotic base Painful - worse at night / legs elevated Higher up on leg / foot Absent peripheral pulses Cold, pale leg No oedema Occurs at pressure/trauma sites
what must not be given to arterial ulcer
compression bandages
what investigation results suggest arterial ulcer
ABPI (ratio of blood pressure at ankle to upper arm). arterial insufficiency <0.8
doppler ultrasound confirms arterial disease
neuropathic ulcer risk factors/causes
DM
Neurological disease
Leprosy
neuropathic ulcer presentation
Painless! Peripheral neuropathy Variable size/depth Warm skin At pressure sites - soles, heels, toes
- vasculitis
ulcer - causes
Vasculitis = Inflammatory disorder of blood vessels → endothelial damage
Mainly idiopathic Drugs Infection Inflammatory disorder Malignant disease
vasculitis ulcer presentation
Usually lower legs Symmetrical Palpable purpura Non-systemic Do not blanch Pyrexia Arthralgia
general ulcer risk factors
Neuropathy eg DM Lymphoedema Vasculitis Malignancy Infection (TB, syphilis) Trauma (pressure sores) Drugs
may be multiple
leg ulcer = most likely to be what
mainly venous disease
some - arterial disease
dermatitis artefacta
ulcer self induced by patient, usually as result of psychological suffering
skin/ ulcer biopsy
ulcer treatment
- Treat cause
- Focus on prevention —Nutrition
- Risk factor control (eg drug addiction)
- Bandages -
- – Compression — Never for arterial ulcers
- Keep it clean and covered
- Antibiotics for infection
- Analgesia
- Steroids - if vasculitis
- Surgery inc debridement , vascular reconstruction
complications of necrotising fascitis
multi organ failure
mortality high
amputation
treatment of necrotising fascitis
Aggressive and immediate treatment
Antibiotics
- Group A strep (pyogenes ) aka type 2 necrotising factor == IV benzylpenicillin + clarithromycin/clindamycin
- Unknown cause = broad spectrum IV antibiotics
Radical debridement
Amputation
investigations and results for necrotising fascitis
X ray - soft tissue gas is seen
Bloods
FBC- v high wbc
Raised CRP
presentation of necrotising fascitis
- Intense pain in area ( Disproportionate to skin findings (initially skin spared))
- Erythematous
- Necrotic (due to vascular supply - may be black and slough (shedding) → dry gangrene
- Blistering
- Sometimes crepitus
- Systemically unwell
- – Fever
- – tachycardia
what is necrotising fascitis
types
- Life threatening infection of the deep fascia causing necrosis of subcut tissue fascia and fat
- Skin is initially spared but is eventually destroyed
- Progresses rapidly
1 : mixture of aerobic and anaerobic bacteria
- Following abdominal surgery
diabetes
2 : Group hemolytic streptococcus (strep pyogenes) (this is aerobic)
- Previously healthy patients
risk factors for necrotising fascitis
Abdominal surgery
Diabetes
comorbidities
Immunosuppression
impetigo seen mainly on what ages
infants kids
impetigo presents
Often on face, hands, feet Itchy Red Growing Weeping Crusting
impetigo treatment
antibiotics
gangrene =
types
Death of tissue from poor vascular supply
Types
- Dry = Necrosis WITHOUT infection
- Wet = Necrosis WITH infection
- – Tissue becomes necrotic, usually after burn/ trauma injury
- – More likely to be infected
amyloidosis =
Misfolded amyloid fibril (protein) deposits
- In multiple organs (systemic)
- In one organ (localised)
name 5 effects of amyloidosis on organs
Kidneys
- Podocyte damage → proteinuria
- Oedema (as result of hypoalbuminemia / lower oncotic pressure)
- –Tiredness
- – Weakness
- – Loss of appetite
- Hyperlipidaemia
Heart
- Stiffens walls → HF
- Interferes with electrical conduction → arrhythmias
- – Oedema
- – SOB
Intestines
- Damages villi → less absorption
- – Weight loss
- – Nausea
- – Diarreha
- – Constipation
- Enlarged liver, spleen, tongue (macroglossia)
Brain
- Alzheimers
- Decreased brain function
- Increase risk of haemorrhage
Nerves
- Damage in somatic (sensory and motor) and autonomic nerves
- – Numbness
Skin
- Purpura esp periorbital
