Dermatology Flashcards
(117 cards)
1
Q
What are the functions of skin
A
protection, regulation and sensation
Protection: physical and immunological barruer
- Primary function of skin
- protects underlying organs from mechanical impact
- protects and detects pressure
- detects variations in extreme temperature and is a berrier to micro-organisms
- barrier to UV radiation/chemicals
Regulation: physiological
- body temp via sweat, hair and changes in peripheral circulation (constriction/dilation)
- fluid balance via sweat and insensible loss
- synthesis of Vitamin D
Sensation: network of nerve cells that detect and relay changes in the environment (heat, cold touch, pain)
2
Q
Describe the normal anatomy of the skin
A
3 layers: epidermis, dermis and hypodermis (subcutaneous tissue)
Epidermis:
- stratified squamous keratinocytes, melanocytes, Langerhan cells and merkel cells
- Layers from outermost: stratum corneum, stratum granulosum, stratum spinosum, stratum basale
Dermis:
- fibroblasts, mast cells, blood vessels and skin appendages (hair follicles, sebaceous and sweat glands, nails)
- superficial papillary layer and inner reticular layer
Subcutaneous tissue:
- where bigger blood vessels are found and is a major store of adipose tissue
3
Q
Describe embryoloigcal development of the skin
A
- Epidermis is derived from the ectoderm
- Week 5: embryo covered by simple cubodial epithelium
- Week 7: single squamous layer (periderm) and a basal layer
3rd month: hair appears as epidermal proliferation into dermis
4th month: intermediate layer forms between basal layer and periderm
- Sweat glands develop as downgrowth’s of epithelial cords into the dermis
4
Q
What is the role of langerhan cells (LC)?
A
- members of the dendritic family, residing in basal layers
- specialise in antigen presentation: acquire antigens in peripheral tissues, travel to regional lymph nodes, present to naive t cells and initiate adaptive immune response and potent cytokine release
- involved in antimicrobial immunity, skin immunosurveillance, induction of hypersensitivity and the pathogenesis of chronic inflammatory diseases of the skin
5
Q
How does a skin allergy develop?
A
- Skin irritation by non-allergenic and allergenic compounds, inducing Langerhan cell migration and maturation
- Langerhans from epidermis to regional lymph nodes
- Sensitisation takes 10-14days from initial exposure to allergen
- Once sensitised to a chemical, allergic contact dermatitis can develop within hours of repeat exposure
6
Q
How does ultraviolet affect the skin?
A
Direct cellular damage and alterations in immunogenic fxn
- P53 tumour suppressor genes mutated due to DNA damage: leads to poor suppression of tumour growth and implicated in development of melanoma and non-melanoma skin cancers
Chronic UV exposure: loss of skin elasticity, fragility, abnormal pigmentation, haemorrhage of blood vessels, wrinkles and premature aging
7
Q
How is the skin protected from UV damage?
A
- Keratinocytes and melanocytes protect against UV DNA damage: melanocytes are dendritic and protect DNA in keratinocyte nuclei
- Release melanosomes to protect underlying nucleus
8
Q
How is Vitamin D synthesised in skin?
A
- During sunlight exposure, solar UVB photons are absorbed by skin and converted to pre-vitamin D(3)
- Pre-vitamin D3 undergoes transformation within plasma membrane to active Vitamin D(3)
9
Q
What are the different types of cutaneous receptors?
A
- Meissner corpuscles
- Pacini corpuscles
- Ruffini corpuscles
- Free nerve endings associated with merkel cells
10
Q
Where are each of the different cutaneous receptors found and what is their function?
A
Merkel cell free nerve endings:
- Base of epidermis
- Respond to sustained gentle and localised pressure
Meissner Corpuscles
- Below the epidermis, especially on palmar surfaces
- Light touch
Ruffini’s Corpuscles
- Dermis; Deep pressure and stretching
Pacini’s Corpuscles
- Deep dermis
- Sensitive to deep touch, rapid deformation of skin surface and around joints for position/proprioception
Other free nerve endings: pain, temperature
11
Q
What cutaneous receptor(s) sense gentle touch?
A
- Merkel cell free nerve endings and Meissner corpuscles
12
Q
What cutaneous receptor(s) sense deep pressure?
A
- Ruffini and Pacini corpuslces
13
Q
What cutaneous receptor(s) sense position/proprioception around a joint?
A
- Pacini Corpuscles
14
Q
What are the cateogories in the Fitzpatrick skin colour types?
A
- Very fair - always burn, can’t tan
- Fair - usually burns, sometimes tans
- Medium - sometimes burns, usually tans
- Olive - rarely burns, always tans
- Brown - never burns, always tans
- Black - never burns, always tans
15
Q
Define a macule
A
Flat area of skin change, pale, red, pigmented, usually small
16
Q
Define a papule
A
Raised lesion on skin about 5mm in size
17
Q
Define a pustule
A
Small pus-filled lesion usually around 5mm or less
18
Q
Define a vesicle
A
Tiny fluid-filled blister normally 5mm or less
19
Q
Define a plaque
A
Elevated area of skin change and redness
20
Q
Define a bulla
A
Large blister usually 1cm or more
21
Q
Define erythematous
A
Abnormal redness of the skin
22
Q
Define ulceration of the skin
A
Loss of epidermis or a skin break
23
Q
Define acne vulgaris
A
A skin condition characterised by papules, pustules and comedones (white/black heads), especially on the face due to inflamed or infected sebaceous glands and prevalent among adolescents
24
Q
What is the clinical presentation of acne?
A
- Pustules, papules and comedones: need all 3 to be diagnosed acne
- May also have erythema, cysts, scarring
In darker skins: hyperpigmentation (harder to diagnose)
Distribution: face, chest, back/shoulders, legs, scalp
25
List 3 acne subtypes
- Papulopustular
- Nodulocystic
- Comedonal
- Steroid induced
- Acne fulminans: severe, sudden onset (hrs), progressive acne
(- Acne rosacea: adult acne, doesn't fit criteria for acne \*NOT acne\*. Nose, forehead, cheeks distribution)
26
Which of the following is not a subtype of acne?
A. Acne fulminans
B. Acne rosecea
C. Comedonal
D. Nodulocystic
B. Acne rosecea
27
What is the general pathophysiology of acne?
- Glandular follicular disorder
- Lining of sebaceous gland thickens and the oil produced by the sebaceous gland can't escape
- Bacteria on the skin loved trapped oil and provoke an inflammatory reaction (red, inflamed spot)
- Everything builds up from behind until it eventually pops
- The longer the gland in inflamed, the more trauma there is and more likely to cause scarring
28
List 3 causes of acne
- Excess oil production
- Hair follicles clogged by oil and dead skin cells
- Bacteria
- Excess androgen production
29
What treatment options are available for acne vulgaris, and what is their main aim?
Reduce plugging (mild)
- Topical retinoid: slows turnover of follicle lining
- Topical benzoyl peroxide: dissolves the plug
Reduce bacteria
- Dual-action antibiotics that reduce bacteria on skin and work as anti-inflammatory agents
- Topical antibiotics (erythromycin, clindamycin)
Reduce sebum production (moderate)
- Antiandrogen hormones (OCP)
- Reduces bacterial resistance
Dietary modification
- Reduce dairy/glycaemia load eg. milk, chocolate
Isotretinoin (severe)
- Reduces sebum production, plugging and bacteria
30
What is isotretinoin?
How does it work?
- Oral retinoid lisenced for **severe** acne vulargis
- Concentrated form of Vitamin A
- Reduces sebum production, plugging (stops blockage of the gland) and bacteria
- Remission for 80% teenagers
- 16 week course
31
List 3 side effects of isotretinoin
Trivial: dry mouth, nose bleeds, dry skin
Serious:
- Deranged liver function
- Raised lipids
- Mood disturbance
- Tetatogenicity (birth defects) therefore need to be on 2 forms of contraceptive and pregnancy test before and every 4 weeks during treatment and one a month after finishing treatment
32
Define eczema
- Interchangable with dermatitis = inflammation of the skin
- Inflammatory skin condition of the epidemis in which patches of skin become inflamed, **itchy**, red and rough (if not itchy - not eczema)
- Eczema: atopic type from childhood
(Atopy is the genetic tendancy to develop allergic diseases)
- Dermatitis: exogenous (allergic/contact dermatitis)
33
What are the causes of eczema?
- Combination of genetic, immune and reactivity to a variety of stimuli
- Inflammation in eczema primarily due to inherited abnormalities in skin, leading to increased permeability and reduced antimicrobial function
- Primary cause: abnormalities of Filaggrin (proteins which bind keratin fibres in epidermal cells)
34
How is eczema classified and list 2/3 examples of each type
Endogenous: internal without external trigger
- Atopic, seborrheic, varicose
Exogenous (Dermatitis): external trigger
- Contact (allergic, irritant)
- Photoreaction (allergic, drug)
35
What is atopic eczema?
Presentation?
Aetiology?
Pathology?
Associations?
- Itchy inflammatory skin condition
- Bilateral, flexural sites (cubital and popliteal fossa)
- Aetiology: genetic and immune aetiology
- Pathology: IgE immunologulins
- Associations: hayfever, asthma, allergic rhinitis, conjunctivitis
36
List 3 complications of atopic eczema
Bacterial infection (Staph. aureus)
Viral infection
Fatigue
Growth reduction
Psychological impact
37
How would you manage atopic eczema?
- Emollients (greasy moisturiser)
- Topical steroids: encourage protective barrier film to redevelop and reduces abnormal immune response
- Bandages
- Anti-histamines
- Antibiotics/antivirals
- Avoid exacerbating factors
38
What are the types of contact dermatitis?
- Precipitated by an exogenous agent
- Irritant contact dermatits: direct noxious effect on skin barrier (due to noxious chemical)
- Allergic contact dermatitis: Type IV hypersensitivity reaction (immune pathway)
39
List 3 common causes of allergic contact dermaitits
- Nickel: jewellery, coins
- Chromate: cement, tanned leather
- Cobalt: pigment/dyes
- Colophony: glue, adhesive tape
- Fragrance: cosmetics, creams, soaps
40
# Define seborrhoeic dermatitis
Aetiology
Typical presentation
Management
- Chronic, **scaly** inflammatory skin condition
Aetiology: disproportional immune reaction to a small amount of yeast
Presentation
- Typically face, eyebrows, scalp (often thought to be dandruff) - Worse in teenagers
- Diagnostic feature for HIV
Management: medicated anti-yeast shampoo (scalp) and anti-microbial, mild steroid moisturiser (face)
41
Define psoriasis
Chronic relapsing and remitting scaling skin disease which may appear at any age and affect any part of the skin
42
How does psoriasis present?
Age: two peaks at 20-30 and 50-60yrs
- Usually bilateral with **extensor** surface pattern
- Thickness and scaling: keratinocyte proliferation
**-** Redness and inflammation: inflammatory infiltrate
- Red patches of skin covered with thick, silvery scaling
- Dry cracked skin
- Swollen and stiff joints
43
What is the pathogenesis of psoriasis?
- T cell mediated autoimmune disease
- Abnormal T cell infiltration: release of inflammatory cytokines including interferon, interleukins and TNF causing redness and inflammation
Increased keratinocyte proliferation: causing thickening and scaling
44
What other conditions is psoriasis connected with?
- Psoriatic arthritis: erosive, inflammatory, destructive arthritis
- Metabolic syndrome
- Liver disease
- Depression
45
List 3 subtypes of psoriasis
- Erythrodermic
- Pustular
- Flexural/Inverse (more psoriasis is extensor driven)
46
What is management of psoriasis based on?
- Severity
- Patient preference
- Patient tolerability
- Presence of arthropathy
47
What is the management for psoriasis?
**1. Topical creams and ointments**
- Moisturisers: reduce dryness and flakiness
- Steroids: reduce autoimmune response, redness, inflammation
- Salicylic acid: dissolves thick dead skin
**2. Phototherapy light treatment (UVB)**
- Non-specific immunosuppressant therapy
- Can reduce T cell proliferation
- Encourages vitamin D and reduces skin turnover
- Risks: burning (short term), skin cancer (long term)
**3. Systemic therapy**
- Immunosuppressants: methotrexate
- Oral retinoid
**4. Biologics**
48
What are 3 main skin cancer types?
- Basal cell carcinoma: *most common type of skin cancer, develops from basal cells at the bottom of epidermis*
- Squamous cell carcinoma: *develops from squamous cells or keratinocytes in upper layers of epidermis*
- Malignant melanoma: *Develops from melanocytes (not just unique to skin - brain/bowel)*
49
What are the risk factors for developing basal cell carcinoma?
- Caused when a basal cell (at the bottom of the epidermis) develops a mutation in its DNA ie. DNA damage
RFs:
- Chronic UV radiation exposure from the sun / tanning beds
- Fair skin
- Increasing age and male
- Immunosuppressant drugs
- Previous BCC or other skin cancer type
- Repeated prior episodes of sunburn
50
What is the pathogenesis of basal cell carcinomas (BCC)?
- Basal cells are found at the bottom of the epidermis
- The process of creating new skin cells is controlled by a basal cell's DNA
- A mutation in the DNA causes the basal cells to multiply rapidly and continue growing when it would normally die
- Eventually the accumulating abnormal cells may form a tumour
- 80% are **found on the head and neck ie. UV exposed sites**
51
What is the porgnosis of basal cell carcinomas
- Most common type of skin cancer
- Cured in almost every case
- Metastatic spread is rare
- Good prognosis
52
What are the subtypes of basal cell carcinomas?
Nodular
Superficial
Pigmented
Morphoeic/Scleroitc
53
How do nodular BCCs present?
- Nodule \>0.5cm **raised** lesion
- **Shiny 'pearly'** (characteristic feature)
- Can see cluster of red lines (blood vessels over top)
- Often ulcerated/depressed centrally, giving rolled edge appearance
- **N****eat, rolled edge**
- Commonly seen on the face
54
How do superficial BCCs present?
- Flattened patch
- Scaly, irregular plaque
- Rolled, translucent edge with broken blood vessels
- Stereotypical distribution: sun-exposed sites (shoulders and upper trunk)
55
How do pigmented BCCs present?
- Shiny, raised lesion
- Domed edge
- Presence of broken blood vessels
- Could be mistaken for melanoma due to pigmentation but melanomas aren't shiny like BCC
56
How do morphoeic/sclerotic BCCs present?
- Waxy, scar like lesion
- Indistinct margin
- Shiny, some broken blood vessels
- Could infiltrate subcutaneous nerves
- Difficult to diagnose
57
What are the treatment options for a basal cell carcinoma?
Gold standard: **Surgical excision with 2-4mm margin**
- Highest chance of complete removal and it not returning
- If large, skin graft may be required
Mohs microscopic surgery: surgery under the microscope in fragile areas eg. tip of nose, around eyes
Curettage and cautery
- Superficial skin surgery, just need local anaesthesia and no sutures required
- Appropriate for elderly patients with distinct, small BCC and unfit for bigger surgery
- Suitable for well-defined, small nodular or superficial BCC
Cyrotherapy
- Freezing a superficial skin lesion with liquid nitrogen
- Appropriate for small superficial BCCs on trunk/shoulders
Photodynamic therapy: for low-risk, small superficial BCCs
Liquid imiquimoid/5-fluorouracil cream
58
What are the risk factors for developing a squamous cell carcinoma (SCC)?
- Increasing age and male
- **Sun exposed skin**
**- Any type of damaged skin**: radiotherapy, thermal burn, leg ulcer
- Previous SCC or other form of skin cancer
- Atinic keratoses (pre-malignant variant)
- Smoking
59
What are the clinical features of a squamous cell carcinoma (SCC)?
- Squamous looking ie. keratin crust (NOT skiny)
- Rolled margin but no broken blood vessels
- Background skin is more sun-exposed (sub damage)
- Can ulcerate
- Proressive type (grows more rapidly than a BCC)
Commonly: face, lips, ears, hands
60
What is the prognosis for a squamous cell carcinoma?
- Good prognosis (99% survival rate if caught early)
- Cured mostly by surgery
- Rarely metastasises
61
What are the treatment options for a SCC?
How are SCC in-situs treated?
How can you prevent SCC development?
Almost all: **surgical excision with _4mm_ margin**
Other options: Curettage and cautery, aggressive cyrotherapy or radiotherapy (if tumour is inoperable, patient is unsuitable for surgery or used as an adjuvant)
For SCC insitu
- topical imiquimod or 5-fluorouracil cream
- cyrotherapy
- photodynamic therapy
Prevention: sub protection
62
What are the risk factors for developing malignant melanoma?
- UV irradiation
- Sunburns during childhood
- Fair skin (Skin Type I or II)
- Genetic markers
- Personal history of melanoma
- Immunosuppression
- Number (\>5) and size (\>5mm) of melanocytic naevi (moles, non-malignant melanoma)
63
What is the pathogenesis of malignant melanoma?
- Uncontrolled proliferation of melanocytic stem cells that have undergone a genetic transformation due to DNA damage
- Radial growth phase followed by vertical growth
- Vertical growth has a worse prognosis
- Depth of melanoma called Breslow's depth
Metastatic spread via lymphatics
- Lymphovascular invasion: tumour cells destroy local blood vessels therefore increasing the risk of spread
- Lymphatic spread: cells usually metastasis to draining lymph nodes
64
What is the prognosis for malignant melanoma?
Prognosis is determined by depth of the melanoma: Breslow's depth = the depth of the lowest atypical melanocyte
- Risk of metastasis increases as thickness of melanoma increases
65
What is the progression of melanomas?
- Benign melanocytic naevi and atypical/dysplastic melanocytic naevi are precancerous lesions and spread through the dermis
66
Define Breslow's depth and Clark's levels of melanoma
Brewlow's depth (mm): the depth of the lowest atypical melanocyte
Clark's levels: correlate to the specific layer of skin the tumour has grown into (not as specific as Breslow)
- Good to combine the two
67
What is the presentation of a melanoma?
- Occur anywhere in the body
- 1st sign: atypical melanocytic naevi (mole)
- Pigmented, NOT shiny lesion
- During radial growth: flat (not invasive/malignant)
- With vertical growth, it becomes raised: malignant
Symmetry is very important, signs of malignancy:
- **irregular shape, different shades of pigment and tumour lump in the centre**
- ABCDE criteria: asymmetry, border irregularity, colour variation, diameter \>6mm, evolving (enlarging, changing)
68
List 3 subtypes of melanomas
- Superficial spreading malignany melanoma: commonest subtype, irregular brown patch
- Nodular melanoma
- Acral melanoma (hands, feet, nails)
- Subungual melanoma (under the nail)
Amelanotic melanoma (no pigment)
69
What are the treatment options for melanomas?
Surgical exision
- Breslow depth \<1mm: 1cm margin
- Breslow depth \>1mm: 2cm margin
Immunotherapy
Biologic antibodies
Assessment of lymph nodes and organ spread
Long-term follow-up up to 5 years
70
Outline the function of the skin and identify three organisms found in the normal skin flora
Skin: acts as a physical barrier to the environment to prevent infection
- Colonised with many bacteria
Organisms:
- Staphococci (S. aureus)
- Streptococci (A, B, C, G)
- Anaerobes
- Yeasts
71
Define cellulitis
A spreading bacterial infection of the dermis and subcutaneous tissue, characterised by redness, warmth, swelling and pain. It commonly appears in areas where there is a break in the skin
72
Outline two general and local modifiable and non-modifiable risk factors for developing cellulitis
General:
- Modifiable: venous insufficiency, lymphoedema, immunocompromise, obesity
- Non-modifiable: pregnancy, Causacian
Local:
- Modifiable: ulcers, eczema, althlete's foot, burns, surgical
- Non-modifiable: trauma, animal/insect bites, tattoos
73
Outline the clinical presentation of cellulitis
Local:
- usually unilateral, usually lower limbs
- oedema, pain, erythma, warmth (inflammation)
- dimpled skin
- treated with oral antibiotics
Can progress into invasive disease (bacteraemia):
- systemic: fever, chills, hypotension
- treated with IV antibiotics
74
Outline the pathophysiology of cellulitis
There is a break in the skin barrier
- organisms from the normal skin flora can invade the subcutaneous tissue, potentially into the dermis
- can breach the deeper dermis
- can become invasive if they reach the blood supply, then disseminate to the rest of the body
75
Identify 3 causative organisms of cellulutis
**- Strepococcus pyogenes**
**- Staph. aureus (inc. MRSA)**
Rarer causes:
- haemophilus influenza
- strep. viridans
- Pasteurella multiocida (cat/dog bite)
- clostridium perfringes
76
Outline the diagnostic process for cellulitis
**Clinical diagnosis**
Investigations may reveal:
- leucocytosis
- elevated CRP
- the causative organism on blood culture
77
Outline the basis for management decisions for cellulitis and the management options
Basis:
- Assess severity: *how much of the body is it encompassing, mark the borders and assess over a few days*
- Anatomical site: *facial cellulitis can be devastating*
- Co-morbidity: *eg. obesity, venous insufficiency*
- Healthcare associated infection: *is this necrotising*
Options:
- Surgery (necrotising fasciitis)
- HDU (High dependency unit)
- Abx: IV/oral, which abx
78
Identify three causes for hospital admission for a patient with cellulitis
- Significant systemic illness
- Sepsis syndrome / necrotising fasciitis
- Severe / Rapidly deteriorating cellulitis
- Very young or frail
- Co-morbidities
- Immunocompromised
- Facial cellulitis
79
What is the antibiotic recommendation for the following causative agents of cellulitis
S. pyogenes
S. aureus / MRSA
Penicillin allergy
Pasteurella multocida
Clostridium perfringes
S. pyogenes: flucloxacillin
S. aureus: flucloxacillin
MRSA: vancomycin
Penicillin allergy: doxycycline, clindamycin or vancomycin
Pasteurella multiocida: co-amoxiclav or doxycycline and metronidazole
Clostridium perfringes: pencillin + flucloxacillin + clindamycin + gentamicin + metronadazole
80
What is the most common causative agent for the follow:
- Typical cellulitis
- Typical cellulitis with pus formation
- Cat/Dog bite
- Necrotising fasciitis
And what antibiotics are used to treat each
Typical cellulitis: strep. pyogenes
- Flucloxacillin
Typical cellulitis pus forming: S. aureus / MRSA
- S. aureus: flucloxacillin
- MRSA: vancomycin
cat/dog bite: pasteurella multocida
- co-amoxiclav OR doxycycline and metronadazole
necrotising fasciitis: s. pyogenes or clostridium perfringes
- penicillin + flucloxacillin + clindamycin + gentamicin + metronadazole
81
Identify three complications of cellulitis
- Necrotising fasciitis
- Gangrene
- Severe sepsis
- Infection of other organs eg. osteomyelitis, meningitis
- Endocarditis
82
Outline the differential diagnosis for suspected cellulitis
Statis dermatitis
- skin condition due to chronic venous insufficiency
- absense of fever, circumferential, **bilateral**
Acute arthritis
- usually poly-joint involvement
- **joint** involvement, pain on movement
Pyoderma Gangrenosum
- associated with IBD
- ulceration on legs, **history of IBD**
Hypersensitivity/Drug reaction
- exposure to allergens, **itch**, absence of fever and pain
DVT
- **absence of skin changes** or fever
- just painful, swollen area
Necrotising fasciitis
- severe pain out of proportion
- swelling, fever, **rapid progression, systemic toxicity**
83
Define necrotising fasciitis
Very severe, rapidly spreading bacterial infection of the soft tissue and fascia over hours
- medical emergency
84
Outline the clinical presentation of necrotising fasciitis, to differentiate it from typical cellulitis
Initially (Hours)
- Commonly lower leg
- severe pain at time of presentation and worsens with time
- erythema and swelling
- systemically unwell (fever, chills, hypotension)
After a few days
- Area becomes blackened (necrosis)
- Skin crepitus
- Severe pain continues until necrosis/gangrene destroys peripheral nerves, rendering the site painless
Progression:
Painful → painless
Red/Purple → Black
85
Outline the management for necrotising fasciitis
Mainstay: **surgery**
- Early suspicion and surgical debridement
5 abs used until surgery (Given **IV**):
- penicillin
- flucloxacillin
- gentamicin: *Gram -ve cover*
- clindamycin: *switches of exotoxin production and improves mortality*
- metronadazole
Need oxygen and fluids to raise BP
Abx adjusted once blood culture returned with causative organism
86
# Define impetigo
Outline the clinical presentation and causative agent
What is the management
Def: acute superficial bacterial skin infection (pyoderma)
Clinical presentation:
- typically children or sports people
- peri-oral
- 'honey-coloured' crusted lesion and pustules
Causative agent:
- Staph. aureus (any staph species)
Management:
- Remove the crust gently, apply anti-septic for 3-5 days and cover the affected area
- Flucloxacillin indicated if: severe symptoms (fever), more the 3 lesions, high risk of complications, unresolving infection
87
Define scarlet fever and what causes it
Def: bacterial infection that presents with a distinctive rash of tiny pink-red spots that cover the entire body
Cause:
- Group A Streptococcal infection
- Affects those who have recently had a strep A throat infection or impetigo caused by strains of Group a strep
- a toxin produced by the bacteria produce the distinctive rash
88
Outline the clinical presentation of scarlet fever
- Usually post-pharyngitic presentation
- Sudden fever with a sore throat, swollen neck glands, headache, nausea
- Diffuse red blush
- Starts on the upper chest and spreads to the trunk, neck and extremeties
- rash fades over the course of a week and starts to desquamate (peel) over several weeks
- occlusion of sweat glands gives the skin a sandpapery touch
- circum-oral pallor
- red strawberry tongue
Severe cases: high fever and systemic toxicity
89
Outline the management for scarlet fever
Once, culture of strep is diagnosed, a course of penicillin is usually started
Other:
- paracetamol for fever, headache
- oral antihistamines and emollients
90
Identify the common causative agent causing infection after a bite and outline the management for bites
Management
- Routine prophylaxis only indicated if: deep bite, on the hands, splenectomised or immunocompromised patient
- Gram stain of wound and blood cultures if systemically unwell
- Treatment: abx +/- surgical involvement if deep infection
- Aggressive debridement and abscess drainage
Causative agent: pasteurella multocide
91
Outline the classification of burns
1st degree: Superficial (Epidermis only)
- Dry/red
- blanches on pressure, painful
- heals in 7 days
2nd degree: Partial thickness (epidermis and dermis)
- superficial v deep (involves dermis)
- blisters
- progression of superficial to deep: painful to painless
- heals in \<21 days +/- abx/surgery/grafting
3rd degree: full thickness (to subcutaneous tissue)
- painless, non-blanching
- requires surgery
4rd degree: involves fascia/muscle/bone
- healing requires surgery
92
Outline the diagnosis and treatment of infected burns
Diagnosis:
- rapid bacterial colonisation esp. due to hospital organisms
- diagnosed clinically
Management:
- need to monitor: infection, hypothermia, acid-base abnormalities and dehydration with burns
- involves plastic surgeons and microbiology team early
- surgery
Infected Burns:
- cleaning, dressing
- topical antimicrobials
- Oral/IV abx (directed by culture results)
93
Define tinea, it's characterisation and classifications
Tinea: a skin infection with a dermatophyte (ringworm) fungus
Characterisation:
- scaly, inflammatory or non-inflammatory patches
- fungal
- limited to the epidermis
- preferentially inhabits warm, moist areas of the skin
Classification:
- Tinea pedis: foot (athlete's foot)
- Tinea corporis: body
- Tinea capitis: head/scalp
- Tinea cruris: jock itch
94
Outline the types and presentation of Herpes Simplex Virus (HSV)
What is the diagnosis and treatment?
Type 1: stomatitis 'cold sore'
Type 2: genital herpes
Presentation:
- primary infection asymptomatic in 60%
- vesicular, may be painful
Diagnosis: clinical, blood for PCR
Treatment: acyclovir (topical, oral, IV)
95
What conditions can be caused by varicella zoster virus?
Chicken Pox
- self-limiting childhood infection
- highly infectious, needs a side room
- Diagnosis: PCR of vesicle fluid
- In adults: can cause pneumonitis
- treat at risk individuals with acyclovir
Shingles
- Reactivation of dormant VZV
- may be very painful
- treat at risk patients with acyclovir
96
Identify 3 cutaneous changes seen with thyroid disease
Hypothyroidism: dry skin
Grave's disease: autoimmune hyperthyroidism
- pretibial myxoedema: characterised by localised thickening of the skin in the pretibial area and localised skin lesions due to the deposition of hyaluronic acid
- thyroid acropachy: nail changes specific to Grave's
97
Identify 3 cutaneous changes seen with diabetes
- Necrobiosis lipoidica: waxy appearance, yellow decolouration often on the skins, occassionally ulcerates
- Diabetic dermopathy
- Scleredema: cutaneous skin disorder with loss of elasticity
- Leg ulcers
- Granuloma annulare
98
Identify 3 cutaneous changes seen with steroid excess
Ie. Cushing's excess
- Acne: back and chest
- Striae: exaggerated stretch marks
- erythema
- gynaecomastia
99
Identify 2 cutaneous changes with steroid insufficiency
- hyperpigmentation
- acanthosis nigricans: brown velvety skin in folds eg. axilla, groin
100
Identify 3 cutaneous presentations of Cushing's Disease
- inc. central adiposity
- Moon facies and buffalo hump
- Global skin atrophy: epidermal and dermal components
- Straie on abdominal flanks, arms, thighs
- Purpura with minor trauma
101
Identify two cutaneous presentations of excess testosterone and excess progesterone
Testosterone:
- Acne and hirsutism
Progesterone:
- Acne and dermatitis
102
Identify 3 cutaneous presentations that may indicate underlying systemic infection
- necrolytic migratory erythema: *erythematous, scaly plaques found on acral, intriginous and periorificial areas*
- erythema gyratum repens: *reddened concentric bands whorled woodgrain pattern. Severe pruritus and peripheral eosinophila*
- acanthosis nigricans: *smooth, velvet hyperkeratotic plaques in intertiginous areas eg. axilla, groin*
- erythema annulare
- sweet's syndrome
103
How does necrolytic migratory erythema look?
What else can it present with?
How is it treated
Morphology:
- erythematous, scaly plaques found on acral (extremity), intertriginous (eg. axilla) and periorifical areas
- associated with an islet cell tumour of the pancreas
- other signs: hyperglycaemia, diarrhoea, weight loss, glossitis
Treatment: removal of the tumour
104
Describe the morphology of erythema gyratum repens.
What condition is it associated with?
How is it treated?
Morphology:
- Reddened concentric bands whorled woodgrain pattern
- Severe pruritis and pheripheral eosinophila
Condition: strong association with lung cancer
Treat: treat the underlying malignancy
105
Describe the morphology of acanthosis nigricans and identify 3 associated conditions
Morphology:
- Smooth, velvet-like hyperkeratotic plaques in intertriginour areas eg. groin, axilla, neck
Type I: associated with malignancy adenocarcinoma
Type II: familial type
Type III: Associated with obesity and insulin resistance
106
Identify the cutaneous changes seen with Vitamin B deficiency
Dementia, diarrhoea, dermatitis
107
Identify 3 cutaneous changes seen with zinc deficiency
Outline 1 cause of zinc deficiency in adults
- pustules
- bullae
- scaling
- acral (extremeties) and perioral distribution
Causes in adults:
- alcoholism
- malabsorptive states
- bowel surgery
- IBD
108
Outline the clinical presentation of Vitamin C deficiency
Scurvy
- punctate purpura/bruising
- corkscrew spiral curly hairs
- patchy hyperpigmentation
- dry skin and hair
- non-healing wounds
- inflamed gums
109
Identify 3 cutaneous changes seen with erythema nodosum and 3 conditions in which it develops
Cutaneous changes:
- tender bilateral erythematous subcutaneous nodules
- usually found on anterior lower legs, knees and arms
- ill-defines, warm, oval lesions without ulceration
- bright red
Conditions it's associated with:
- Strep infection
- pregnancy/ OCP
- sarcoidosis
- IBD
110
Identify 3 cutaneous changes seen with pyoderma gangrenosum and 3 conditions in which it may develop
Cutaneous changes:
- rapidly enlarging, very painful ulcer
- sudden onset at site of minor injury
- may start as a small pustule, red bumb or blood-blister
- edge of ulcer: purple and undermined
Associated with:
- IBD: Crohn's disease and ulcerative colitis
- Rheumatoid arthritis
- Myeloma
111
What conditions are the following associated with:
Alopexia areata hair loss
Hair thinning
Male pattern balding
Alopexia: autoimmune
Hair thinning: B12 def, lupus, iron deficiency, hypothyroidism
Male pattern balding: androgen excess
112
What are the two most common skin presentations to primary care?
- Ezcema
- Psoriasis
113
Identify 3 common benign and 3 worrying skin lesions that GPs see
Worrying:
- melanoma
- squamous cell carcinoma
- basal cell carcinoma
* Any changing pigmented lesion should be referred to dermatology - urgent cancer suspicion*
Benign:
- Warts
- Seborrhoeic warts
- Skin tags
- Seborrhoeic keratosis
- Pyogenic granuloma
114
How are the following benign skin lesions managed?
Warts
Seborrhoeic warts
Skin tags
Warts: topical salicylic acid or cyrotherapy (freezing)
Seborrhoeic warts: cyrotherapy
Skin tags: do nothing or private sector that bitch
115
Define and outline the clinical presentation of psoriasis
# Define: a chronic inflammatory skin condition characterised by clearly defined, red and scaly plaques (thickened skin)
- Overproduction of skin cells causing red, scaly patches
Clincial presentation:
- Symmetrically distributed red, scaly plaques with well-defined edges
- Scale is typically silvery-white
- Common sites: extensor surfaces (elbow, knee), scalp, nails, joints
116
Outline the management for psoriasis
Lifestyle: smoking, weight alcohol
Mild: topical agents alone
- Emollients
- Salicylic acid
- topical corticosteroids
- coal tar
Widespread / Not reponding:
- Phototherapy, often in combo with topical or systemic agents
- commonly methotrexate, ciclosporin
117
