Card Set Information
Eczema psoriasis lesions
A chronic, relapsing and remitting scaling skin disease
What is the pathogenesis of psoriasis?
T-cell mediated autoimmunity
Abnormal T cell infiltration releases cytokines = increased keratinocyte proliferation
What are some co-morbidities of psoriasis?
: Arthritis in 30% of chronic psoriasis
What are the frequent ages of onset of psoriasis?
Between 20-30 and 50-60
Outline the common clinical presentation of psoriasis
Discrete, circular, pink patches/plaques from hyperkeratosis
Found on extensor surfaces, scalp, buttocks (trauma sites)
Nail features; onycholysis, pitting
Describe the subtypes of psoriasis
: Pink/red scaly plaques
: 'Raindrop' like, very small, circular plaques on trunk. Related to strep throat
: Diffuse redness with blisters on palms and feet soles + exfoliation
: Generalised redness, extreme keratosis
What factors affect the treatment choice for psoriasis?
Outline the treatment choices for psoriasis
(in order of toxicity)
Outline the pathophysiology of eczema
Inherited abnormalities in the skin; irregular fillagrin expression
Creates a 'barrier defect'
Increased permeability reduces antimicrobial function
Describe some endogenous causes of eczema?
: Allergy = itchines. Managed with moisturisers + antihistamines, maybe topical steroids
: Yeast infection; anti-fungal shampoo and moisturiser given
: Vein incompetence = hydrostatic pressure = stretched dry skin. Compression socks
What are common causes of exogenous eczema?
Contact allergies the main cause; nickel, chromate, cobalt, fragrance etc.
Photosensitivity due to drugs
What is native joint septis arthritis?
A medical emergency, where one of the patient's joints becomes infected.
Loss of cartilage and osteoarthritis
What is the clinical presentation of septic arthritis?
Single or polyarticular
Knee and hip
Can develop into severe sepsis and septic shock
What investigations are useful in septic arthritis?
: gram stain, microscopy for crystals (gout) and cultures
: colony and sensitivity testing
: in osteomyelitis
Outline some causative organisms of septic arthritis
Strep pyogenes, pneumococcus
How is septic arthritis treated?
Minimum of two weeks IV antibiotics
Afterwards, 3 weeks oral antibiotics
What is the definition of osteoarthritis?
Progressive infection of bone, characterised by necrosis and sequestra formation
Outline the causes of oseoarthritis
Similar organisms to septic arthritis
Local spread from overlying infection (e.g. cellulitic ulcer)
Trauma (compound fracture)
How is osteoarthritis investigated and treated?
MRI the image of choice
Antibiotic choice depends on culture; eithe oral or 4-6 weeks IV
Outline the use of surgery in osteomyelitis
Debulk infection back to healthy bone
Manage dead space that remains
Stabilise infected fractures
Outline the pathogenesis of prosthetic joint infections
Usually caused by coagulase negative Staph aureus; gram negative bacilli, S. Viridans.
In local spread, it may be anything
Prosthesis has no blood supply, so infections common
How are infections commonly introduced in prosthetic joint infections?
Local spread in 60-80%; skin organisms
Haematogenous in 20-40%
Outline the clinical presentation of prosthetic joint infections
Inflammation; pain, effusion, warmth
Fever and systemic symptoms
Loosening on radiograph/mechanical dysfunction
What investigations are used in prosthetic joint infections?
Macroscopic appearance, histopathology and microbiology
Cultures are not definitive due to contamination
Tissue, fluid or pus samples preferable to swabs
What prophylaxis is commonly used in preventing PJIs?
Given 30mins before incision, for <24 hours
Cephalosporins used, unless C.Diff present
If MRSA, glycopeptides used (vanco or teico)
What treatments are used in PJIs?
: Debride, antibiotics and implant retained
: If infection >30 days after surgery, joint may not be functional. Prosthesis/cement removed
Give the definition of:
- Resection arthroplasty
- Revision arthroplasty
- Pseudo arthrosis
Putting in an artificial joint
Replacing a diseased joint with an artificial one
Re-operating on an artificial joint
Fusing two bones together
Allowing two bones to articulate, without a joint
Spreading infection of the dermis and subcutaenous tissue
Often affects lower limb
Outline the clinical presentation of cellulitis
Spreading, diffuse edge
Systemic symptoms in 40% (fever, nausea)
Outline the diagnosis of cellulitis
Usually clinical, not laboratory
If below the waist or in diabetis, expect gram negative
In IVDUs, it can be anything
Outline the management of cellulitis
: Flucloxacilllin, penicillin V (clinda/vanco if allergy)
Mark area of inflammation to monitor progress
If refractory, consider; resistance/admission/underlying condition/incorrect diagnosis (e.g. DVT, erysipelas)
Streptococcus infection of dermis, especially face and eyes
Similar to cellulitis
Well demarcated edge, raised
Describe impetigo, including treatment
Staph infection of epidermis
Often peri-oral, honey coloured skin crusting
Gentle crust removal, flucloxacillin
Describe methods of reducing surgical infection likelihood
Define necrotising fasciitis
Rapidly spreading infection of subcutaneous fascia, occurs over hours
Outline the pathophysiology of necrotising fasciitis
Toxin or mixed mediated
Toxins a superantigen; cytokines released + toxic shock syndrome
Medical emergency; 70% mortality if untreated
What are the characteristics of necrotising fasciitis?
Intitially painful, becomes painless in later stages
Very rapid spread of dusty, necrotis skin
Skin crepitus can occur, due to air entry into subcutaneous tissue
How is necrotising fasciitis treated?
Rapid surgical assessement and debridement of all necrotic tissue
Tissue samples sent from theatre for cultures and sensitivity
Broad IV antibiotics cover helpful; penicillin, fluclox, clinda, metro, genta
Describe the cause, presentation and treatment of abscesses
Causes include IVDU, trauma
Presents with pain, swelling
Aspirated and cultured
How are burns managed?
Cultures rarely sterile, due to rapid colonisation