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medicine - gp > Basic Derm 2 > Flashcards

Basic Derm 2 Flashcards

1
Q

What are the general clinical features of rashes caused by insect infections?

A

Insect infections are a common cause of acute (hours-days), very itchy, papular urticarial skin rash. They cause dermal skin lesions (rather than epidermal) that is peripheral

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2
Q

Explain the difference in clinical features between epidermal and dermal skin lesions.

A

Epidermal: any combination of scaling, crusting, weeping and vesiculation.
Dermal: Lump, papule or nodule.
All epidermal lesions also involve the dermis

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3
Q

Differential diagnosis of EPIDERMAL skin lesions?

A

CAT PISS on PWH

Cancers
Atopic dermatitis
Tinea
Psoriasis
Impetigo
Scabies
Solar keratosis
Pityriasis rosacea
Warts
Herpes
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4
Q

Differential diagnosis of DERMAL skin lesions?

A

PISS on IVDU

Pediculosis
Insect bites
Scabies
Skin infiltrations
Viral exanthems
Drugs
Urticaria
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5
Q

Clinical features of flea bites? Management?

A

Arms, forearms, legs and waist (where clothing is tight)
Itchy erythematous maculopapular lesions
Multiple or grouped in clusters

Management is to clear to source of infection

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6
Q

Cause of bed bugs?

A

Cimex lectularius which hides in bedding, mattresses, and travels in baggage into hotels

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7
Q

Clinical features of bed bug bites?

A

Children and teenagers
Maculopapular erythematous lesions +/- wheals, as a linear group of 3 or more bites (along line of superficial blood vessels) over the neck, shoulders, arms, torso and legs
Acute
Extremely itchy

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8
Q

Management of bed bug bites?

A

Clean lesions
Corticosteroid ointment + simple anti-pruritic
Call pest controller

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9
Q

What is the cause of scabies?

A

The mite Sarcoptes scabei

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10
Q

Clinical features of scabies rash?

A

Erythematous papular rash
Male genitalia, elbows, axilla, feet, ankles, female nipples
Symptoms can take weeks to develop
Intense itching worse with warmth and at night

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11
Q

Management of scabies?

A

Scabicidal pharmacotherapy: Permethrin 5% cream (>2 year olds) to whole body from jawline down. Leave overnight and wash off.
Alternatives: benzyl benzoate 25% on for 24h.
Persistence of itch post-treatment is common. Re-treat if itch has not abated after 7 days.
Topical antipruritic: Crotamiton cream 3-5 days + oral antihistamine.
Wash clothing and linen and hang in sun.
Treat all family and close contacts regardless of symptoms.

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12
Q

List the malignant tumours of the skin and mucous membranes?

A

BCC, SCC, malignant melanoma

Bowen skin disease, kaposi sarcoma, secondary tumour

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13
Q

What is the general management approach to skin tumours

A

Surgery is the treatment of choice for most tumours

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14
Q

What is basal cell carcinoma of the skin

A

aka Basal cell epithelioma
It is a common neoplasm related to exposure to sunlight and the the most common skin cancer (80%).
It is locally aggressive but rarely metastasizes.

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15
Q

Pathophysiology of basal cell carcinoma?

A

Repetitive frequent sun exposure –> UV radiation (esp. sunburn wavelength) –> DNA damage to keratinocytes –> thought to affect pluripotent cells lodged in epidermis and follicular epithelium

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16
Q

Clinical features of basal cell carcinoma?

A

Males more frequently
Usually >35 years
Slow growing
Sun exposed areas: mainly FACE (face mask area), neck, upper trunk, limbs
Shape: various forms (nodular, pigmented, ulcerated)
Stretched skin demarcates the lesion, highlights pearliness and distinct margin

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17
Q

List the different clinical presentation types of BCC?

A

Morpheus Cums in CUPS

Morphoeic
Common
Cystic
Ulcerated
Pigmented
Superficial
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18
Q

Management of BCC?

A 
1st line: Simple elliptical excision with 3mm margin.
Biopsy if not excised.
Other Rx:
- radiotherapy (frail patients)
- Photodynamic therapy
- Mohs micrographic surgery
- Cryotherapy
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19
Q

What is squamous cell carcinoma?

A

SCC is the result of atypical, transformed keratinocytes in the skin with malignant behaviour. It ranges from in situ tumours (Bowen’s disease) to invasive tumours and metastatic disease. It tends to arise in premalignant areas (solar/actinic keratoses, burns, chronic ulcers, leucoplakia and Bowen disease) but can arise de novo. It is capable of metastases.

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20
Q

Between BCC and SCC, which is more likely to metastasize?

A

SCC is capable of metastasize. BCC is locally aggressive but rarely metastasizes.

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21
Q

Pathophysiology of SCC?

A

Multifactorial including cumulative sun exposure –> DNA damage to keratinocytes –> malignant transformation

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22
Q

Clinical features of SCC?

A

Usually >50 years age
Sun exposed areas esp. in fair skinned people: head, bald scalp in men, neck, forearms, hands, shin. Other areas: ear and lip (more malignant potential), oral cavity, tongue and genitals are serious and need special management.
Shape:
- Initial firm thickening of skin (esp. in solar keratosis)
- Surrounding erythema
- Hard nodules soon ulcerate
- Ulcers have characteristic everted edge

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23
Q

Management of SCC?

A

Early excision of tumours <1cm with a 4mm margin to deep fat level.
Referral (for specialized surgery/radiotherapy) if: difficult site or lymphadenopathy
- Wedge excision of SCCs of ear and lip
- For SCC over cartilage (central nose or helix) surgery is the only option

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24
Q

What is melanoma?

A

Melanoma is a malignant tumour arising from melanocytes. It is one of the most common forms of cancer in young adults.

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25
Q

List the different types of melanoma.

A

Superficial spreading
Nodular
Lentigo Maligna
Acral lentiginous

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26
Q

Pathophysiology of melanoma?

A

Most arise from apparently normal skin. 30% arise from precursor lesion (benign naevus or solar lentigo) –> mutations (inherited or UV damage) –> malignant change –> radial or vertical growth –> metastases. Tends to spread laterally laterally. Vertical spread is more likely to result in vasculature or lymphatic involvement.

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27
Q

Clinical features of melanoma?

A

30-50 year old (average 40 years)
New or changing deeply pigmented skin lesion (size, shape, colour, surface, border, bleeding or ulceration, itching, satellite nodules, LN involvement).
Sun exposed areas (but can occur anywhere on the body)
- Lower limbs in women
- Upper back in men
Often asymptomatic but can bleed or itch

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28
Q

Risk factors for melanoma?

A 
Increasing age, male
Hx previous melanoma (5x)
Presence of many moles (50+) esp. atypical dysplastic naevi
Family history
Hx of many sunburns
Sun sensitive.fair complexion
Tanning treatments
29
Q

Red flags for melanoma?

A

New or changing lesion
Rapid growing nodule of any colour
Non-healing lump or ulcer
“Ugly Duckling”: Prominent pigmented lesion that stands out from any other
Lesion that concerns the patient
Dermoscopic changes on follow up or poor-dermoscopic-clinical correlation

30
Q

Describe the management approach to suspected melanoma.

A

Suspicious pigmented lesion –> Local excision biopsy 2mm margin to mid fat layer –> histopathology.
If benign/dysplastic naevus, dermatofibroma or pigmented BCC: no further surgery needed.
If malignant melanoma:: re-excision (depending on level and depth)

31
Q

In general, with reference to the anatomy of the nail apparatus, what are the disorders of the nail seen in general practice?

A

Disorders of the:

  • Nail plate
  • Nail folds
32
Q

What are the most probably diagnoses of nail disorders in general practice?

A 
Traumatized fungus POPs
Trauma (nail bed, from biting, habit picking)
Fungal infection (onychomycosis)
Paronychia
Onychogryphosis
Psoriasis
33
Q

What serious disorders of the nail must not be missed?

A

BEG for MILK

  • Bowen disorder
  • Endocarditis (splinter haemorrhages)
  • Glomus tumour
  • Melanoma
  • Iron deficiency anaemia
  • Liver disease (leuconychia)
  • Kidney disease (Chronic - white bands, half and half nail)
34
Q

What are the main nail problems dealt with in general practice?

A 
Trauma
Onychomycosis
Infection
Paronychia
Psorasis
Ingrown toenail
35
Q

What is onychomycosis?

A

Fungal infection of the nail. Onychomycosis affects 3-5% of the population, and 40% of those >60 years. It can be superficial, distal or proximal.

36
Q

Cause of onychomycosis?

A

Trichophyton mentagrophytes var. interdigitale

Trichophyton rubrum

37
Q

Clinical features of onychomycosis?

A

Older age (40% of those >60 are affected)
Distal lateral subungal is most common form
- Lateral onychomycosis: white/yellow opaque streal at one side of nail
- Distal onycholysis: lifting up of end of nail plate, free edge often crumbles
Superficial white onychomycosis: toenails with flaky superficial white plaques and pits on top of the nail plate
- Proximal onychomycosis: yellow spots appear in a half moon
- Total dystrophic onychomycosis: whole nail affected - thickened, opaque and yellow brown

38
Q

Investigations for onychomycosis?

A

Confirm diagnosis by culture and histology of distal nail plate clippings placed in formalin

39
Q

Management of onychomycosis?

A

Non-pharm: regular nail clipping
Pharm:
- Antifungal: Terbinafine 250mg PO daily (12 weeks for toenails, 6 weeks for finger nails)
- Improvement only seen in proximal part of nail is nail takes months to grow
- Evidence for topical treatment is poor

40
Q

Clinical features of psoriasis of nails?

A

Pitting, onycholysis, splinter haemorrhages, distal subungal hyperkeratosis, severe total nail dystrophy.
Can mimic onychomycosis

41
Q

Define acute paronychia

A

Inflammation of the skin around a fingernail or toenail <6 weeks.
Mainly caused by bacterial infection (esp. S. aureus)

42
Q

Clinical features of acute paronychia?

A

Erythema, swelling and pain of the nail fold
There may be localized pus
Subungal extension in more complicated cases

43
Q

Management of acute paronychia?

A

Exclude diabetes
Uncomplicated with localized pus:
- Antiseptic (betadine soaked dressing)
- Elevation of nail fold or puncture the fold to drain pus
- Petroleum gauze dressing
- ABx are rarely necessary
Complicated with subungal extension:
- Small vertical incision alongside the nail or removal of nail
- Nail avulsion helps to establish free drainage of a periungal abscess

44
Q

Define Ingrown toenail.

A

aka onychocryptosis
A common condition typically of the edges of the great toenail, caused by a redundant skin fold –> imbalance between the soft tissues of the nail fold and the growing nail edge. Skin breach can result in infection, oedema and granulation tissue of the nail fold.

45
Q

Causes of ingrown toenail?

A

Injury or deformity of the nail bed

Exacerbated by faulty nail trimming, constricting shoes or poor hygiene

46
Q

How can you advise your patients to prevent ingrown toenail?

A

Prevention is by proper foot and nail care:

  • Hygiene: foot baths, frequent changes of cotton/wool socks and avoid nylon socks. Cotton wool pledget between nail edge can help with separation.
  • Nail care: corners should project beyond the skin, with end of the nail cut squarely
  • Skin fold stretching with thumbs after daily shower
47
Q

Management of ingrown toenail?

A

Surgical management (several options):

  • Excision of ellipse of skin
  • Electrocautery
  • Skin wedge excision
  • Wedge of nail excision and phenolisation
48
Q

Define nail apparatus melanoma.

A

Rare but potentially fatal presentation of melanoma (2-3% of all melanoma) with mortality >50%. and median survival of <12 months after diagnosis. Diagnosis is typically late.

49
Q

When should you suspect nail apparatus melanoma?

A

Any subungal pigmented lesion should be suspect for melanoma.
Subungal haematomas will grow out with the nail. Beware of amelanotic melanoma which can mimic chronic paronychia or pyogenic granuloma. Early referral should be made if there is any suspicion.

50
Q

Clinical features of nail apparatus melanoma?

A

> 70 yrs old, BUT can affect all age groups, races and climates
Longitudinal pigmented streak
+/- Hutchinson sign (pigmentation of proximal nail fold)

51
Q

Management of nail apparatus melanoma?

A

Early recognition and referral is key.
Longitudinal nail biopsy in ALL cases for diagnosis.
Treatment is based on Breslow thickness and level of invasion.
- Level 1 or in situ: whole nail apparatus removal
- Invasive melanoma: amputation of distal phalanx

52
Q

List the general anatomical components of the nail apparatus.

A

Dorsal Surface: distally to proximally: Nail plate, lunula, cuticle. The nail plate is interfaced with the lateral and proximal nail folds.
At the proximal end of the nail plate, deep to the proximal nail fold, is the matrix, underneath which lies the distal phalanx.

53
Q

Define pruritus.

A

Pruritis is latin for itch, end refers to the desire to scratch

54
Q

Define urticaria.

A

aka Hives
A vascular reaction of the skin (dermis) marked by the transient appearance of smooth, slightly elevated papules or wheals that are ertythematous and often attended by pruritus

55
Q

Describe the physiology of pruritus.

A

Pruritus is caused by the same nerve pathway as pain, but with different intensity of stimulus.
It is similar to pain in that it is abolished by analgesia and anaesthesia, decreased by counterirritation, cold, heat and vibration, and can be referred. Histamine may not be the only mediator as evidenced by antihistamines, which act on H1, often being ineffective

56
Q

When assessing pruritus, what is the general diagnostic approach?

A 
By aetiology:
- Primary skin disorder
- Systemic skin disease (broad DDx)
- Psychological/emotional disorder
By ditribution:
- Localized: think primary skin cause
- Generalized: think systemic disease
57
Q

DDx of primary skin disorders causing significant pruritus?

A

Grover’s ACCUSAL of the Pedo Insect

  • Grover’s disease
  • Atopic dermatitis
  • Contact dermatitis
  • Chicken pox
  • Urticaria
  • Scabies
  • Asteatosis (dry skin)
  • Lichen planus
  • Insect bites
  • Pediculosis
58
Q

What are the most probable diagnoses for pruritus in general practice?

A

Atopic dermatitis (eczema)
Old, dry skin (senile pruritus)
Psychological/emotional

59
Q

What serious disorders causing pruritus must NOT be missed?

A 
PRN
- Primary biliary cirrhosis
- Renal failure (chronic)
- Neoplasia (Hodgkin lymphoma, leukaemia, CLL etc..)
Consider excluding pregnancy
60
Q

What is the prevalence if pruritus in patients with Hodgkin lymphoma?

A

The prevalence of itching in Hodgkin lymphoma is 30% (skin often looks normal but patient complains of unbearable itch)

61
Q

Management approach to pruritus?

A

Determine the primary cause!
If no cause found:
Non-pharmacological Rx:
- Env: cooling measures, avoid overheating, avoid known irritants
- Clothing: wear light clothing
- Vasodilatation: avoid vasodilating things like alcohol, hot baths or showers that are too long
Pharmacological Rx:
- Topical: moisturiser (propylene glycol in aqueous cream), emolients to lubricate skin, local soothing lotion (calamine, menthol, phenol). Avoid topical antihistamine. Consider topical corticosteroid.
- Oral: Sedating antihistamine at night (NB not effective for systemic pruritis). Non-sedating antihistamines during the day.

62
Q

Define lichen planus.

A

Lichen planus is an epidermal inflammatory disorder characterised by pruritic, violet, flat-tipped papules, mainly on the wrists and legs.
T-cell autoimmune disease which causes inflammatory cells to attack unidentified protein in the skin and mucosal keratinocytes

63
Q

Clinical features of lichen planus?

A

Young to middle aged adult (Dermnet says >40 yrs mainly)
Small, shiny lichenified plaques on flexor surfaces (wrists, forearms, ankles) but can also affect oral mucosa (white streaks, papules or ulcers), nails and scalp
Chronic

64
Q

Management of lichen planus?

A

Non-pharmacological:
- Education and reassurance: usually resolves over 6-9 months leaving discoloured marks without scarring. Explain recurrence is rare.
- Asymptomatic lesions require no treatment
Pharmacological:
- Topical moderate potency corticosteroids +/- occlusive dressing
- Intralesional corticosteroids for hypertrophic lesions

65
Q

Define dermatitis herpetiformis.

A

aka Duhring-Brocq disease
Rare but persistent, chronic subepidermal vesicular condition that is extremely itchy, whereby HSV-like vesicles (in clusters) erupt at the dermo-epidermal junction - it is not caused by virus.
It is linked to gluten-sensitive enteropathy (coeliac disease)

66
Q

Pathophysiology of dermatitis herpetiformis?

A

Intolerance to gliadin fraction of gluten (in wheat, rye, barley) –> triggers IgA antibody production that targets skin and gut

67
Q

Clinical features of dermatitis herpetiformis?

A

Young adults
(>90% have gluten-sensitive enteropathy)
Vesicles in clusters (usually eroded and crusted due to immediate scratching) on reddened or normal skin over extensor surfaces (elbows, knees) but also scalp, trunk, buttocks and shoulders.
Chronic (lasts for decades)

68
Q

Investigations for dermatitis herpetiformis?

A

Skin biopsy
Screen for nutritional deficiencies (like you would someone with coeliac disease): FBC/EUC/CMP, Fe studies, B12 and folate, TFTs

69
Q

Management of dermatitis herpetiformis?

A

Gluten-free diet

Dapsone 100mg PO daily (usually reduces itch within 3 days)

medicine - gp (3 decks)

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