Dermatology Flashcards
1
Q
Define basal cell carcinoma.
A
The commonest form of skin malignancy.
= rodent ulcer
2
Q
Explain the aetiology / risk factors of basal cell carcinoma.
A
- Prolonged sun exposure or UV radiation
- Photosensitizing pitch
- Tar
- Arsenic
Associated with abnormalities of the patched / hedgehog intracellular signaling cascade as seen in Gorlin’s Syndrome (naevoid basal cell carcinoma syndrome).
3
Q
Summarise the epidemiology of basal cell carcinoma.
A
Common in those with fair skin and areas of high sunlight exposure, elderly, rare before 40 years
Lifetime risk in Caucasians = 1:3
4
Q
Recognize the presenting symptoms of basal cell carcinoma.
A
A chronic slowly progressive skin lesion usually on the face but also on the scalp, ears or trunk.
5
Q
Recognize the signs of basal cell carcinoma on physical examination.
A
Nodulo-Ulceractive:
- Small glistening translucent skin over a coloured papule
- Slowly enlarged (early)
- Central ulcer with raised pearly edges
- Fine telangiectatic vessels run over the tumour surface
- Cystic changes in larger, more protuberant lesions
Morphoeic:
- Expanding
- Yellow / white waxy plaque
- Ill-defined edge - more aggressive
Superficial:
- Most often on trunk
- Multiple pink / brown scaly plaques with a fine whipcord edge expanding slowly
- Can grow to more than 10cm in diameter
Pigmented:
- Specks of brown or black pigment
6
Q
Identify appropriate investigations for basal cell carcinoma and interpret the results.
A
Biopsy rarely necessary - diagnosis based on clinical suspicion.
7
Q
Define burns injury.
A
Predominantly to the skin and superficial tissues, caused by heat from hot liquids, flame, or contact with heated objects, electrical current or chemicals.
8
Q
Explain the aetiology / risk factors of burns injury.
A
Severity assess by burn size (% total body surface area) and depth (1st to 4th degree)
Risk Factors:
- Young children
- Age > 60 years
- Male sex
9
Q
Summarise the epidemiology of burns injury.
A
Very common injuries
10
Q
Recognize the presenting symptoms of burns injury.
A
- Dry and painful burns
- Wet and painful burns
- Dry and insensate burns
11
Q
Recognize the signs of burns injury on physical examination.
A
- Erythema
- Clouded cornea
- Cellulitis
- Burns affecting subcutaneous tissue, tendon or bone
12
Q
Identify appropriate investigations for burns injury and interpret the results.
A
- FBC - low haematocrit, hypovolaemia, neutropenia, thrombocytopenia
- Metabolic panel - high urea, creatinine, glucose, hyponatraemia, hypokalaemia
- Carboxyhaemoglobin - high levels in inhalation injury
- Arterial blood gas - metabolic acidosis in inhalation injury
- Fluorescein staining - damaged corneal epithelial cells in corneal burns
- CT scan of head and spine - brain injury, fracture in head or spine trauma
- Wound biopsy culture - positive for the causative organism in wound infection sepsis
- Wound histology - show wound infection
13
Q
Define cellulitis and erysipelas.
A
Cellulitis - an acute spreading infection of the skin with visually indistinct borders that principally involves the dermis and subcutaneous tissue, characterised by redness, swelling, heat and tenderness and usually occurs in an extremity.
Erysipelas - a distinct form of superficial cellulitis with notable lymphatic involvement, that is raised and sharply demarcated from uninvolved skin.
14
Q
Explain the aetiology / risk factors of cellulitis and erysipelas.
A
Often results from penetrating injury (e.g. IV cannulation), local lesions (e.g. insect bites, sebaceous cysts, surgery) or fissuring (e.g. in anal fissured, toe web spaces), which allows pathogenic bacteria to enter the skin.
In rare cases of septicaemia, it can arise spontaneously from blood-borne sources.
Most common organisms: Streptococcus pyogenes, Staphylococcus aureus. (MRSA not uncommon)
If occuring in orbit, Haemophilus influenzae is most common cause, arising from adjacent sinuses.
Risk Factors:
- Diabetes
- Venous insufficiency
- Eczema
- Oedema
- Lymphoedema
15
Q
Summarise the epidemiology of cellulitis and erysipelas.
A
Very common.
Main risk factors - skin break poor hygiene, poor vascularization of tissue (e.g. DM)
16
Q
Recognise the presenting symptoms of cellulitis and erysipelas.
A
History of cut, scratch or injury.
Periorbital:
- Painful swollen red skin around eye
Orbital cellulitis:
- Painful or limited eye movements
- Visual impairment
17
Q
Recognize the signs of cellulitis and erysipelas on physical examination.
A
Cellulitis - acute onset of red, painful, hot, swollen skin
Erysipelas - well-demarcated, bright-red raised skin
Lesion:
- Erythema
- Oedema
- Warm tender indistinct margins
- Pyrexia (may indicate systemic spread)
- Orange-peel appearance
- Bistering & bleeding
Exclude Abscess:
- Test for fluid thrill or fluctuation
- Aspirate if pus suspected
Periorbital:
- Swollen eyelids
- Conjunctival injection
Orbital Cellulitis:
- Proptsis - protrusion of the eyeball
- Impaired acuity and eye movement
- Test for relative afferent pupillary defect, visual acuity and colour vision (to monitor optic nerve function)
18
Q
Identify appropriate investigations for cellulitis and erysipelas and interpret the results.
A
Bloods
- WCC / CRP / ESR
- U&E
- Blood culture
Discharge
- Culture & sensitivity
- Skin swab and biopsy
Aspiration
- Often non-purulent, not usually necessary
CT/MRI Scan
- When orbital cellulitis is suspected - to assess the posterior spread of infection
19
Q
Generate a management plan for cellulitis and erysipelas.
A
Medical:
- Oral penicillins - e.g. flucloxacillin, benzylpenicillin, coamoxiclav (community)
- Tetracyclines (community)
- Hospital - treat empirically using local microbiological guidelines but change depending on sensitivity of any cultured organisms
- IV use may be necessary
Surgical
- Orbital decompression if orbital cellulitis (emergency)
Abscess
- Can be aspirated, incised and drained or excised completely
20
Q
Identify the possible complications of cellulitis and erysipelas and its management.
A
- Sloughing of overlying skin
- Localised tissue damage
- Orbital cellulitis - permanent vision loss, spread to brain, abscess formation, meningitis, carvenous sinus thrombosis
21
Q
Summarise the prognosis for patients with cellulitis and erysipelas.
A
Good with treatment
22
Q
Define eczema (including atopic, contact, discoid, dyshidrotic, herpeticum, seborrhoeic).
A
A pruritic papulovesicular skin reaction to endogenous or exogenous agents.
Discoid = Nummular
Dyshidrotic = Pompholyx
Herpeticum - a disseminated viral infection characterised by fever and clusters of itchy blisters or punched-out erosions (complication of atopic eczema)
23
Q
Explain the aetiology / risk factors of eczema (including atopic, contact, discoid, dyshidrotic, herpeticum, seborrhoeic).
A
Numerous varieties caused by a diversity of triggers.
Exogenous:
- Irritant - prolonged contact with a cell-damaging irritant (e.g. ammonia in nappy rash)
- Contact - Type IV Delayed Hypersensitivity reaction to allergen (e.g. nickel, chromate, perfumes, latex, plants)
- Phototoxic
Endogenous:
- Atopic
- Seborrhoeic - Pityrosporum yeast
- Pomphloyx (dyshidrotic)
- Varicose - increased venous pressure in lower limbs
- Lichen simplex
Atopic:
- Impaired epidermal barrier function due to intrinsic structural and functional skin abnormalities (predominant model)
- Immune function disorder in which Langerhans cells, T-cells and immune effector cells modulate an inflammatory response to environmental factors
Lichen Simplex:
- Thickening of skin secondary to a cycle of itch, scratch, itch
- Characterised by well-demarcated hyperpigmented lichenified plaques
24
Q
Summarise the epidemiology of eczema (including atopic, contact, discoid, dyshidrotic, herpeticum, seborrhoeic).
A
Contact - prevalence 4%
Atopic - onset in 1st year of life, childhood incidence 10-20%
25
Recognise the presenting symptoms of eczema (including atopic, contact, discoid, dyshidrotic, herpeticum, seborrhoeic).
- Itching
- Heat
- Tenderness
- Redness
- Weeping
- Crusting
- Enquire into occupational exposures or irritants used at home (e.g. bleach)
- Enquire into family / personal history of atopy (e.g. asthma, hay fever, rhinitis)
26
Recognise the signs of eczema (including atopic, contact, discoid, dyshidrotic, herpeticum, seborrhoeic) on physical examination.
Acute
- Poorly demarcated erythematous oedematous dry scaling patches
- Papules
- Vesicles with exudation and crusting
- Excoriation marks
Chronic
- Thickened epidermis
- Skin lichenification
- Fissures
- Change in pigmentation
Contact and Irritant:
- Eczema reaction occurs where irritant / allergen comes into contact with skin
- Autosensitization (spread to other sites)
Atopic:
- Face and flexures
Seborrhoeic:
- Yellow greasy scales on erythematous plaques
- Nasolabial folds, eyebrows, scalp, presternal area
Pompholyx (Dyshidrotic):
- Acute and often recurrent painful vesiculobullous eruption on palms and soles
Varicose:
- Excema of lower legs
- Associated with marked varicose veins
Nummular (Discoid) :
- Coin shaped, on legs and trunks
Asteatotic:
- Dry
- Crazy paring pattern
27
Identify appropriate investigations for eczema (including atopic, contact, discoid, dyshidrotic, herpeticum, seborrhoeic) and interpret the results.
Contact:
- Skin patch testing - disc conatining postulated allergen is diluted and applied to back for 48h
- Positive if allergen induces a red raised lesion
Atopic:
- Laboratory testing not routinely used- including IgE levels
- Swab for infected lesions (bacteria, fungi, viruses)
28
Define epidermoid and pilar cysts (sebaceous cysts).
A closed sac found under the skin, usually on the trunk, neck or face. They are filled with cheese-like matter and usually are painless.
Epidermoid cyst - a cyst where the cyst sac forms from cells that normally occur on the top layer of the skin (the epidermis).
Pilar cyst - a cyst where the cyst sac forms from cells similar to those that are in the bottom of the hair follicles (where hairs grow from).
29
Explain the aetiology / risk factors of epidermoid and pilar cysts (sebaceous cysts).
Risk Factors:
- Hereditary tendency to form cysts - e.g. Gardner Syndrome, Gorlin Syndrome
- High levels of testosterone
- Male gender
- Skin trauma
- Swollen hair follicles
30
Summarise the epidemiology of epidermoid and pilar cysts (sebaceous cysts).
Epidermoid - most common cutaneous cysts, 3-4th decades of life, rare before puberty, M:F 2:1
31
Recognise the presenting symptoms of epidermoid and pilar cysts (sebaceous cysts).
- Small, round bump under the skin, usually on the face, neck or trunk
- Tiny blackhead plugging the central opening of the cyst
- Thick, yellow, smelly material that sometimes drains from the cyst
- Redness, swelling and tenderness in the area, if inflamed or infected
History:
- How long has it been there?
- Does it hurt?
- Any other symptoms, e.g. itch?
- Any other lumps?
- Is it getting bigger?
- Ever been abroad?
- Otherwise well?
32
Recognise the signs of epidermoid and pilar cysts (sebaceous cysts) on physical examination.
Appear as firm, round, mobile subcutaneous nodules of varying size.
Common on face, scalp, neck and trunk.
Characteristic central punctum.
Infection common, foul pus exits through the punctum.
33
Identify appropriate investigations for epidermoid and pilar cysts (sebaceous cysts) and interpret the results.
- Examination of the skin
- Biopsy - rule out other skin growths
- Skin culture - determine type of infection
34
Define erythema multiforme.
An acute hypersensitivity reaction of the skin and mucous membranes.
Stevens-Johnson Syndrome - severe form with bullous lesions and necrotic ulcers.
35
Explain the aetiology / risk factors of erythema multiforme.
Degeneration of basal epidermal cells and development of vesicles between the cells and the underlying basement membrane.
Lymphocytic infiltrate is seen around the blood vessels, and at the dermal-epidermal junction.
Immune complex deposition is variable and non-specific.
Precipitating factor only identified in 50% of cases.
Drugs:
- Sulphonamides
- Penicillin
- Phenytoin
- Barbiturates
Infection:
- Viral - HSV, EBV, coxsackie, adenovirus, ORF
- Bacterial - Mycoplasma pneumoniae, Chlamydiae
- Fungal - Histoplasmosis
Inflammatory:
- Rheumatoid arthritis
- SLE
- Sarcoidosis
- Ulcerative colitis
- Systemic vasculitis
Malignancy:
- Lymphomas
- Leukaemia
- Myeloma
Radiotherapy
36
Summarise the epidemiology of erythema multiforme.
Any age group
| M:F 2:1
37
Recognize the presenting symptoms of erythema multiforme.
- Non-specfic prodromal symptoms of URTI
- Sudeen appearance of itching, burning, painful skin lesion
- May fade, leaving behind pigmentation
38
Recognize the signs of erythema multiforme on physical examination.
- Classic target (bulls eye) lesions
- Rim of erythema surrounding a paler area
- Vesicles / bullae
- Urticarial plaques
- Symmetrical
- Distributed over arms, legs, palms, soles, extensor surface
Stevens-Johnson Syndrome
- Affecting > 2 mucous membranes - conjunctiva, cornea, lips (haemorrhagic crusts), mouth, genitalia
- Systemic symptoms - sore throat, cough, fever, headache, myalgia, arthralgia, D&V
- Shock - hypotension, tachycardia
39
Identify appropriate investigations for erythema multiforme and interpret the results.
Usually unnecessary as erythema multiforme and Stevens-Johnson Syndrome are clinical diagnoses.
Blood:
- High WCC, eosinophils, ESR, CRP
- Throat swab
- Serology
- Low albumin - in extensive exudation
- High urea - due to catabolic state and dehydration
- Autoantibodies
Imaging
- CXR - to exclude sarcoidosis and atypical pneumonias
Skin Biopsy
- Histology and direct immunofluorescence may be indicated in cases of diagnostic doubt
40
Define erythema nodosum.
Panniculitis (inflammation of the subcutaneous fat tissue) presenting as red or violet subcutaneous nodules.
41
Explain the aetiology / risk factors of erythema nodosum.
Delayed hypersensitivity reaction to antigens associated with various infectious agents, drugs and other diseases.
Infection:
- Bacterial - Streptococcus, TB, Yersinia, rickettsia, Chlamydia, leprosy
- Viral - EBV
- Fungal - histoplasmosis, blastomycosis, coccidioidomycosis
- Protozoal - toxoplasmosis
Systemic Disease:
- Sarcoidosis
- IBD
- Behcet's disease
Malignancy:
- Leukaemia
- Hodgkin's disease
Drugs
- Sulphonamides
- Penicillin
- Oral contraceptive pills
Pregnancy
42
Summarise the epidemiology of erythema nodosum.
25% of cases have no underlying cause.
Usually young adults.
M:F 3:1
43
Recognize the presenting symptoms of erythema nodosum.
- Tender red or violet nodules
- Bilaterally
- Shins, thighs, forearms
- Fatigue
- Fever
- Anorexia
- Weight loss
- Arthralgia
- Symptoms of underlying aetiology
44
Recognise the signs of erythema nodosum on physical examination.
- Crops of red or violet dome-shaped nodules
- Present on both shins, thighs, forearms
- Tender to palpation
- Low-grade pyrexia
- Tender joints, painful on movement
- Signs of underlying aetiology
45
Identify appropriate investigations for erythema nodosum and interpret the results.
Determine underlying aetiology.
Bloods
- Anti-streptolysin-O titre at diagnosis and 2-4 weeks later to assess for antecedent streptococcal infection
- FBC
- U&E
- CRP
- ESR
- LFTs
- Serum ACE - high in sarcoidosis
Throat Swab
- Culture
Mantoux / Heaf Skin Testing
- For TB
CXR
- To look for hilar adenopathy or other evidence of pulmonary sarcoidosis, TB and fungal infections
46
Define herpes simplex virus.
Includes HSV1 and HSV2.
47
Explain the aetiology / risk factors of herpes simplex virus.
Alpha-herpes virus with double-stranded deoxyribonucleic acid (dsDNA). Transmitted via close contact with an individual shedding the virus (e.g. kissing, sexual intercourse).
Multiply in epithelial cells of mucosal surface.
Produces vesicles or ulcers.
Lifelong latent infection when virus enters sensory neurons at infection site.
Can then reactivate, replicate and infect surrounding tissue - occurs in response to physical, emotional stresses or immunosuppression.
Disseminated infection if impaired T-cell immunity - e.g. pneumonitis, hepatitis, colitis
Risk Factors:
- HIV infection
- Immunosuppressive medications
- High-risk sexual behaviour
- Female sex
- Black race
- Increasing age
- Lack of condom use
48
Summarise the epidemiology of herpes simplex virus.
HSV1 - infection in 2/3 of world's population (approx 3.7 billion <50 years)
HSV2 - infection in 11% of world's population ( approx 400 million)
90% adults seropositive for HSV1 by 30 years.
35% adults >60 years seropositive for HSV2.
1/3rd population recurrent HSV infections.
49
Recognise the presenting symptoms of herpes simplex virus.
HSV1 Primary Infection:
- Asymptomatic
- Pharyngitis
- Gingivostomatitis - may make eating very painful
- Herpetic whitlow - inoculation of virus into a finger
Recurrent infection / reactivation:
- Prodrome (6h) peri-oral tingling and burning
- Vesicles appear (48h), ulcerate and crust over
- Complete healing 8-10 days
HSV2
- Very painful blisters and rash in genital, perigenital and anal area
- Dysuria
- Fever
- Malaise
HSV Keratoconjunctivitis:
- Epiphoria - watering eyes
- Photophobia
50
Recognise the signs of herpes simplex virus on physical examination.
Primary Infection:
- Subclinical or sensory nerve prodrome (tingling)
- Vesicles
- Shallow ulcers
Systemic Symptoms:
- Fever
- Malaise
- Tender cervical lymphadenopathy
- Heals 8-12 days
Reactivation:
- Usually less severe unless immunosuppressed
Herpes Labialis:
- Cold sore lesion at lip border, predominantly HSV1
Genital Herpes:
- Predominantly HSV2
Gingivostomatitis:
- Fever
- Sore throat
- Tender oropharyngeal vesicles
- Yellow slough filled ulcers
Keratoconjunctivitis:
- Corneal dendritic ulcers
- Avoid steroids
Herpetic Whitlow:
- Painful vesicles on distal phalanx due to inoculation through a break in the skin
Herpes Encephalitis:
- Most common treatable viral encephalitis
- Transfer of virus from peripheral site to brain via neuronal transmission
- Prodrome - fever, malaise, headache, nausea
- Encephalopathy - general/ focal signs of cerebral dysfunction including psychiatric symptoms, seizure, focal neurology (temporal involvement in 60%), memory loss (HSV1 in immunocompetent patients)
51
Identify appropriate investigations for herpes simplex virus and interpret the results.
- Clinical diagnosis
- Confirmation required in encephalitis, keratoconjunctivitis or immunosuppression
- Viral PCR of CSF, swab or vesicle scraping
- Culture
- Immunofluorescence
- Serology
52
Define lipoma.
Slow growing, benign, mesenchymal tumours that form well-circumscribed, lobulated lesions composed of adipocytes.
53
Explain the aetiology / risk factors of lipomas.
- Demarcated from surrounding fat by a thin, fibrous capsule
- 50% soft-tissue neoplasms
- Encountered by primary care physicians, surgeons and pathologists
- Usually arise in subcutaneous tissues
- Can occur in any area of the body, most frequently trunk and proximal limbs
- No malignant potential
- DD - liposarcomas
Risk Factors:
- Genetic predisposition
- Trauma
- Heavy alcohol consumption
54
Summarise the epidemiology of lipomas.
1% prevalence.
Incidence of 2.1 per 1000 per year.
5% of patients present with multiple lipomas.
55
Recognise the presenting symptoms of lipomas.
- Soft, mobile, superficial cutaneous mass <5cm
- Painless
- Gastrointestinal obstruction
- GI bleeding
- Abdominal mass
- Muscle weakness
- Paraesthesia
56
Recognise the signs of a lipoma on physical examination.
- Soft, mobile, superficial cutaneous mass <5cm
- Painless
- Gastrointestinal obstruction
- GI bleeding
- Abdominal mass
- Muscle weakness
- Paraesthesia - burning or prickling sensation that is usually felt on hands, arms, legs or feet
57
Identify appropriate investigations for a lipoma and interpret the results.
- MRI if lesion >3cm and deep to the superficial fascia
- CT
- USS
- Core needle biopsy
- Incisional biopsy
- Excisional biopsy
- UGI contrast study - shows submucosal mass with no invasion of surroudning muscle layers or with evidence of mucosal involvement
58
Define melanoma and melanocytic lesions.
Malignancy arising from neoplastic transformation of melanocytes, the pigment-forming cells of the skin. The leading cause of death from skin disease.
59
Explain the aetiology /risk factors of melanoma and melanocytic lesions.
DNA damage in melanocytes caused by UV radiation results in neoplastic transformation.
50% arise in pre-existing naevi, 50% in previously normal skin.
4 Histopathological Types:
1) Superficial spreading (70%)
- Typically arises in a pre-existing naevus
- Expands in radial fashion before vertical growth phrase
2) Nodular (15%)
- Arises de novo
- Agressive
- No radial growth phrase
3) Lentigo Maligna (10%)
- More common in elderly with sun damage
- Large flat lesions
- Follow an indolent growth course
- Usually on the face
4) Acral Lentiginious (5%)
- Arise on palms, soles and subungual areas
- Most common type in non-white populations
60
Summarise the epidemiology of melanoma and melanocytic lesions.
Steadily increasing incidence
6000 per year diagnosed in the UK
Lifetime risk 1 in 80 in US
Whte races x20 risk to non-white races
61
Recognize the presenting symptoms of melanoma and melanocytic lesions.
Change in size, shape or colour of a pigmented skin lesion, redness, bleeding, crusting, ulceration
62
Recognise the signs of melanoma and melanocytic lesions on physical examination.
ABCDE
```
A = Asymmetry
B = Border irregularity / bleeding
C = Colour variation
D = Diameter >6cm
E = Elevation
```
63
Identify appropriate investigations for melanoma and melanocytic lesions and interpret the results.
1. Excisional Biopsy
2. Lymphoscintigraphy
3. Sentinel Lymph Node Biopsy
4. Staging
5. Blood
Excisional Biopsy
- For histological diagnosis and determination of Clark's Levels or Breslow Thickness
Lymphoscintigraphy
- Radioactive compound injected around lesion
- Dynamic images taken over the course of 30 mins to trace the lymph drainage and the sentinel nodes
Sentinel Lymph Node Biopsy
- Dissected and histologically examined for metastatic involvement
Staging
- Imaging by ultrasound, CT, MRI, CXR
Blood
- LFT - common site of metastasis
64
Define molluscum contagiosum.
Caused by the molluscum contagiosum virus, a ubiquitous poxvirus that escapes immune destruction for months to years.
65
Explain the aetiology / risk factors of molluscum contagiosum.
Lesions are cutaneous (less commonly mucosal).
Henderson-Patterson bodies - virally infected keratinocytes with central orifice (epidermal collections of molluscum bodies)
Caused via skin-to-skin or fomite contact in children, and by sexual transmission in adults.
Risk Factors:
- Close contact with infected individual
- Sexual contact with infected individual
- HIV infection
- Tropical climate
- Swimming
- Atopic dermatitis
66
Summarise the epidemiology of molluscum contagiosum.
1/3 patients develop symptoms of local erythema, swelling or pruritus.
67
Recognise the presenting symptoms of molluscum contagiosum.
- Pearl-like, smooth papules
- Umbilicated
- Central dell
- Surrounding erythema
- Facial or groin distribution of lesions
- Pruritus
- Atopic dermatitis
68
Recognise the signs of molluscum contagiosum on physical examination.
- Pearl-like, smooth papules
- Umbilicated
- Central dell
- Surrounding erythema
- Facial or groin distribution of lesions
- Pruritus
- Atopic dermatitis
69
Identify appropriate investigations for molluscum contagiosum and interpret the results.
- Curettage biopsy
- Tzanck stain
- Haematoxylin and eosin staining
- HIV test
70
Define pressure sores.
Localised injury to the skin and / or underlying tissue usually over a body prominence, as a result of pressure or of pressure in combination with shear stress.
Most common over body prominence, but can develop on any part of the body, including mucosal surfaces.
Can be small, superficial wounds or blisters involving only epidermal elements or larger wounds, covered or filled with necrotic tissue and involving deeper tissues such as fascia, muscle or bone.
71
Explain the aetiology / risk factors of pressure sores.
Stage 1 - non-blanchable redness of intact skin, typically over a bony prominence
Stage 2 - partial thickness loss of dermis presenting as a shallow, open ulcer with a red/pink wound bed, without slough, or an intact or open / ruptured sero-sanguinous blister
Stage 3 - full thickness skin loss with visible subcutaneous fat, bone/tendon/muscle not exposed
Stage 4 - full thickness tissue loss with exposed bone/tendon/muscle
Risk Factors:
- Immbolity
- Sensory impairment
- Older age
- Surgery
- Intensive care stay
- Malnourishment
- History of previous pressur ulcers
- Environmental factors - e.g. the nature of the surface on which the pateint has been sitting or lying
- Faecal or urinary incontinence
- Diabetes
- Peripheral vascular disease
72
Recognise the presenting symptoms of pressure sores.
- Use of non-pressure-relieving support surface
- Localised skin changes on areas subjected to pressure
- Shallow open wound or tissue loss on areas subjected to pressure
- Full-thickness wound on areas with involvement of major tissues on areas subjected to pressure with or without undermining (tunnelling)
- Localised tenderness and warmth around area of wound
- Increased exudate and / or foul odour
73
Recognise the signs of pressure sores on physical examination.
- Use of non-pressure-relieving support surface
- Localised skin changes on areas subjected to pressure
- Shallow open wound or tissue loss on areas subjected to pressure
- Full-thickness wound on areas with involvement of major tissues on areas subjected to pressure with or without undermining (tunnelling)
- Localised tenderness and warmth around area of wound
- Increased exudate and / or foul odour
74
Identify appropriate investigations for pressure sores and interpret the results.
- Clinical diagnosis
- Wound swab
- ESR - >100mm/hour in osteomyelitis
- WBC - >15.0 x 10^9/L in osteomyelitis
- Serum glucose - elevated in diabetes
- Deep tissue biopsy
- MRI
75
Define psoriasis.
A chronic inflammatory skin disease, which has characteristic lesions and may be complicated by arthritis.
76
Explain the aetiology / risk factors of psoriasis.
Unknown. Genetic, environmental factors and drugs (e.g. may be triggered by Streptococcal infections, antimalarial agents, B-blockers, lithium).
Excess proliferation of epidermal cells (rapid cell turnover possible mediated by cytokines released by lymphocytes in the dermis) and accelerated upward migration of immature keratinocytes.
Risk Factors:
- Guttate psoriasis - Streptococci sore throat
- Palmoplantar pustulosis - smoking, middle-aged women, autoimmune thyroid disease, SAPHO
- Generalised pustular - hypoparathyroidism
SAPHO = synovitis, acne, palmoplantar pustulosis, hyperostosis, osteitis - chronic recurrent multifocal inflammation of bones (e.g. sternoclavicular, sacroiliac joint)
77
Summarise the epidemiology of psoriasis.
1-2% population
| Peak age of onset = 20 years
78
Recognise the presenting symptoms of psoriasis.
- Itching
- Tender skin
- Pinpoint bleeding with removing scales (Auspitz phenomenon)
- Skin lesions may develop at the site of trauma / scars (Koebner phenomenon)
79
Recognise the signs of psoriasis on physical examination.
Discoid / Nummular Psoriasis:
- Symmetrical
- Well-demarcated
- Erythematous plaques
- Silvery scales over extsnor surface - knee, elbows, scalp, sacrum
Flexural Psoriasis:
- Less scaly plaques in axilla , groins, perianal, genital skin
Guttate:
- Small (<1cm) drop-like lesions over trunk, limbs
Palmoplantar:
- Erythematous plaques
- Pustules
- Palms and soles
Generalized Pustular Psoriasis:
- Pustules distributed over limbs and torso
Nail:
- Pitting
- Oonycholysis - lifting off of the nail plate from the nail bed
- Subungual hyperkeratosis
- Salmon patch on the nail
Joints:
- Seronegative arthritis with 6 possible presentations:
1) Monoarthritis
2) Distal asymmetrical oligoarthritis (distal interphalangeal joints)
3) Dactylitis (interphalangeal arthritis and flexor tenosynovitis)
4) Rheumatoid arthritis-like (symmetrical polyarthritis)
5) Arthritis mutilans (telescoping of the digits)
6) Anklyosing spondylitis
Poor correlation between joint and skin involvement.
80
Identify appropriate investigations for psoriasis and interpret the results.
Majority of patients do not need any investigations.
Guttate Psoriasis:
- Anti-streptolysin-O titre
- Throat swab
Flexural Lesions:
- Skin swabs - exclude candidiasis
Nail:
- Analyse nail clippings to exclude onychomycosis (fungal infection)
Joint Involvement:
- Rhuematoid factor (negative)
- Radiographs (distal interphalangeal joints)
- Erosions
- Perarticular osteoporosis
- Pencil-in-cup deformity - whittling and cupping of the phalanges
- Sacroilitis
81
Define squamous cell carcinoma.
Malignancy of the epidermal keratoinocytes of the skin.
Marjolin's Ulcer - a squamous cell carcinoma that arises in an area of chronically inflammed or scarred skin.
82
Explain the aetiology / risk factors of squamous cell carcinoma.
Bowen's Disease - intra-epidermal carcinoma in situ
- Proliferation of atypical keratinocytes
- Basement membrane intact
- Solitary or multiple red-brown scaly patches
Squamous Cell Carcinoma
- Malignant keratinocytes invade locally into the dermis
- Spread to local lymph nodes
- Distally metastasies - e.g. lungs, liver
- Staging on TNM
Risk Factor:
- UV radiation from sunlight exposure
- Actinic keratoses - sun-induced precancerous lesions
- Radiation
- Carcinogens - e.g. tar derivatives, cigarette smoke, soot, industrial oils, arsenic
- Chronic skin disease - e.g. lupus, peukoplakia
- Human Papilloma Virus
- Long-term immunosuppression - e.g. transplant recipients, HIV
- DNA repair genetic defects - e.g. xeroderma pigmentosum
83
Summarise the epidemiology of squamous cell carcinoma.
2nd most common cutaneous malignancy - 20% of skin cancer
Often occurring in middle-aged and elderly light-skinned individuals.
Incidence 1 in 4000 annually
M:F 2-3:1
84
Recognise the presenting symptoms of squamous cell carcinoma.
- Skin lesion
- Ulcerated
- Recurrent bleeding or non-healing
85
Recognise the signs of squamous cell carcinoma on physical examination.
- Variable appearance
- Ulcerated
- Hyperkeratotic
- Crusted or scaly
- Non-healing lesion
- Often on sun-exposed areas
- Palpate for local lymphadenoapthy
86
Recognise the signs of squamous cell carcinoma on physical examination.
- Variable appearance
- Ulcerated
- Hyperkeratotic
- Crusted or scaly
- Non-healing lesion
- Often on sun-exposed areas
- Palpate for local lymphadenopathy
87
Define urticaria (acute, chronic).
A skin condition consisting of erythematous, blanching, oedematous, non-painful, pruritic lesions that develop rapidly, usually over minutes.
Typically lasts less than 24hours and leaves no residual skin markings upon resolutions.
Acute episodes - period of less than 6 weeks, caused by specific stimulus and are self-limiting.
Chronic episodes - period of over 6 weeks, not attributable to a specific stimulus.
88
Explain the aetiology / risk factors of urticaria (acute, chronic).
Acute:
- Lasts less than 6 weeks
- Hypersensitivity reaction to a specific trigger
- Viral infections
Chronic :
- Daily or near-daily episodes of hives occuring for 6 weeks or more
- Complex aetiology
Risk Factors:
- Positive family history
- Female sex
- Exposure to drug or food trigger
- Recent viral infection
- Recent insect bite or sting
89
Summarise the epidemiology of urticaria (acute, chronic).
A recent studies reported that the lifetime prevalence of all types of urticaria was 8.8% to 10.8%, with a female predominance and a mean age of 35 to 39 years.
Angio-oedema - swelling involving the deeper layers of the subdermis and occurs in association with urticaria in 40% of cases. Involves face and neck, potentially compromise airway.
90
Recognise the presenting symptoms of urticaria (acute, chronic).
- Pruritus - unpleasant sensation of the skin that provokes the urge to scratch
- Resolution in 24 hours
- Swelling of face, tongue or lips
- Erythematous oedematous lesions
- Blanching lesions
- Stridor
91
Recognise the signs of urticaria (acute, chronic) on physical examination.
- Pruritus - unpleasant sensation of the skin that provokes the urge to scratch
- Resolution in 24 hours
- Swelling of face, tongue or lips
- Erythematous oedematous lesions
- Blanching lesions
- Stridor
92
Identify appropriate investigations for urticaria (acute, chronic) and interpret the results.
- FBC - normal, eosinophilia, neutrophilia
- ESR - elevated or normal
- CRP - elevated or normal
- C4 - decreased in hereditary and acquired angio-oedema
- TSH - elevated or normal
- ANA - anti-nuclear antibodies - positive in rheumatological disease
- Skin prick testing - may be positive
- Allergen avoidance diet
- Serum tryptase
- Skin biopsy
- C1 esterase inhibitor level and function, C1q levels
- Specific IgE to suspected allergen
93
Define varicella zoster.
Primary infection is called vaircella (chicken pox).
Reactivation of the dormant virus in the dorsal root ganglia, causes zoster (shingles).
94
Explain the aetiology / risk factors of varicella zoster.
- Herpes ds-DNA virus
- Highly contagious
- Transmission by aerosol inhalation or direct contact with vesicular secretions
Viral inhalation and infection of the URT.
Replication in regional lymph nodes, liver and spleen.
Week 2-3 - spreads to skin, producing rash and then leading to clinical resolution.
Remains latent in dorsal root ganglia.
Reactivation causes virus to travel down sensory axon to produce dermatomal shingles rash.
95
Summarise the epidemiology of varicella zoster.
Chickenpox peak incidence occurs at 4-10 years.
Shingles peak incidence at >50 years.
90% of adults are VZV IgG positive (previously infected).
96
Recognise the presenting symptoms of varicella zoster.
- Incubation period 14-21 says
Chicken Pox:
- Prodromal malaise
- Mild pyrexia
- Sudden appearance of an intensely itchy spreading rash
- Affecting the face and trunk more than the extremities, the oropharynx, conjunctivae, genitourinary tract
- Vesicles weep and crust over, forming new vesicles
- Contagious from 48h before the rash and until all the vesicles have crusted over - within 7-10 days
Shingles:
- May occur after a period of stress
- Tingling / hyperaesthesia in a dermatomal distribution
- Painful skin lesions
- Recovering in 10-14 days
97
Recognise the signs of varicella zoster on physical examination.
Chicken Pox:
- Macular papular rash
- Evolves into crops of vesicles
- Areas of weeping and crusting
- Skin excoriation - from scratching
- Mild pyrexia
Shingles:
- Vesicular macular papular rash
- Dermatomal distribution
- Skin excoriation
98
Identify appropriate investigations for varicella zoster and interpret the results.
Both chickenpox and shingles usually clinical diagnosis.
Vesicle Fluid
- Electron microscopy
- Direct immunofluorescence
- Cell culture
- Viral PCR - all rarely necessary
Chicken Pox
- Consider HIV testing
- Especially in adults with prior history of varicella infection
99
Generate a management plan for varicella zoster.
Chicken Pox:
- Children - treat symptoms with calamine lotion, analgesia, antihistamines
- Adults - consider aciclovir, valaciclovir, famciclovir if within 24h of rash onset especially if elderly, smoker, immunocompromised or pregnant
Shingles:
- Aciclovir, valaciclovir, famciclovir if within 72h of rash onset if elderly, immunocompromised or ophthalmic involvement
- Low-dose amitriptyline if in moderate / severe discomfort
- Simple analgesia (paracetamol)
Prevention:
- VZIG may be indicated in immunosuppressed and pregnant women exposed to varicella zoster
- Chickenpox vaccine licensed in the UK, but no guidelines avaliable for appropriate use
100
Identify the possible complications of varicella zoster and its management.
Chicken Pox:
- Secondary infection
- Scarring
- Pneumonia
- Encephalitis
- Cerebellar syndrome
- Congenital varicella syndrome
Shingles:
- Postherpetic neuralgia
- Zoster opthalmicus - rash involves ophthalmic division of Trigeminal Nerve (CN V)
- Ramsay Hunt's Syndrome - reactivation in geniculate ganglion causing zoster of the ear and facial nerve palsy (vesicles behind pinna of ear or in canal)
- Sacral zoster may lead to urinary retention
- Motor zoster - muscle weakness of myotome at the similar level as involved dematome
101
Summarise the prognosis for patients with varicella zoster.
Depends on complications.
Worse in pregnancy, elderly and immunocompromised.
102
Define candidiasis.
Infection with candida, especially as causing oral or vaginal thrush.
103
Explain the aetiology / risk factors of candidiasis.
Dimorphic fungus (yeast) colonizes approx. 30% individuals.
- Colonization begins shortly after birth and persists throughout life
- Found in respiratory, GI, genitourinary tracts and the skin and mucous membranes
- Exists in both yeast (blastospore) phase and hyphal (mycelial) phase, depending on surrounding conditions
- Immunocompetent individuals provide effective immune surveillance against Candida
- Any immune defect can lead to infection and visible disease
Risk factors:
- Antibiotics
- Corticosteroids
- Dental prostheses
- Chemotherapy
- Radiation treatment
- HIV
104
Summarise the epidemiology of candidiasis.
Rise in Candida infections - due to diabetes, malignancy, chemotherapy, human immunodeficiency virus
200 species - most common C. albicans.
105
Recognise the presenting symptoms of candidiasis.
- Areas of heat and humidity and maceration
- Burning
- Itching
- Irritation
- Redness and swelling
- Pain and soreness
- Rash
106
Recognise the signs of candidiasis on physical examination.
Cutaneous
- Under breasts
- In gluteal and inguinal folds
- Diaper area
- Under pannus
- Armpit
- Erythema with satellite papules
- Overlying white plaques - intertrigo
Oral
- Thrush
- Infants and elderly
107
Identify appropriate investigations for candidiasis and interpret the results.
- Superficial scraping
- Add saline - see pseudohyphae and yeast under microscope
- KOH added to nail or skin specimens to help dissolve the keratin and visualise the yeast
- Calcolfluor white - rapid diagnosis with a fluorescent microscope
- Culture and sensitivities
Skin biopsy with periodic acid-Schiff (PAS) staining
