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Phase 2a - Systems > Dermatology > Flashcards

Dermatology Flashcards

1
Q

what organism causes acne and what type of organism is it?

A

propionibacterium acnes - gram -ve anaerobic bacteria

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2
Q

list the 4 processes involved in development of acne

A

follicular epidermal hyperproliferation
blockage of pilosebaceous units with surrounding inflammation
increased sebum production
infection with P. acne

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3
Q

give 3 cardinal features of acne

A

blackheads/whiteheads (open/closed comedones), inflammatory papules and pustules

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4
Q

where does acne most commonly develop?

A

face, back and sternal area

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5
Q

name 2 clinical variants of acne

A

infantile acne, oil acne (occupational oil exposure), acne fulminans

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6
Q

what are the different treatment options for acne?

A

1st line - topical keratolytics (benzoyl peroxide), retinoids (tretinoin) or abx (erythromycin).
2nd line - low dose oral abx (tetracycline, trimethoprim).
3rd line - retinoid drug (tretinoin) but only in severe cases

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7
Q

what are retinoids and what must be monitored in a patient using them?

A

synthetic vitamin A analogues.

highly teratogenic - monitor bloods/do pregnancy tests

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8
Q

explain the pathophysiology underlying atopic eczema

A

abnormal epithelial barrier function allows antigenic/irritant agents to reach immune cells
(mutations in filaggrin).
Th2 activation initially, then Th0 and Th1 drive chronic phase.
high serum IgE.

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9
Q

list some possible exacerbating factors of atopic eczema

A

strong detergents and chemicals, cat and dog fur, some dietary allergens, infection, woolen clothes, anxiety/stress

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10
Q

when taking a history for a possible diagnosis of atopic eczema, would the family history be more significant if the patient’s mother or father has atopic eczema?

A

mother - strong maternal predominance in family histories

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11
Q

describe the rash that eczema produces

A

itchy erythematous scaly patches, especially in flexures.
skin thickening.
can weep/exudate - infection.

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12
Q

give 3 features associated with atopic eczema apart from the rash

A

pitting and ridging of nails, prominent skin creases, dry scaling of skin, follicular hyperkeratosis

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13
Q

give a complication of atopic eczema

A

infections - usually S aureus, appear as yellow lesions.
cutaneous viral infections - HSV (can lead to Kaposi’s sarcoma).
cataracts, conjunctival irritation.

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14
Q

give 3 investigations you might perform to confirm eczema as a diagnosis, or to confirm atopy

A

skin-prick testing.
RAST tests.
bloods - raised serum IgE or eosinophilia.

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15
Q

what is the triple combination treatment of eczema?

A 
topical steroid (hydrocortisone = mild, betamethasone = potent).
frequent emollient (e.g. aqueous cream).
bath oil/soap subsitutes.
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16
Q

for severe cases of atopic eczema, in which triple combination therapy has failed, what could you prescribe?

A

topical immunomodulators - tacrolimus ointment.

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17
Q

what causes contact dermatitis?

A

substance in contact with the skin - either a chemical irritant or a type IV hypersensitivity reaction.

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18
Q

how would you identify contact dermatitis?

A

rash with clear demarcation/odd-shaped areas - patch test to identify allergen

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19
Q

how would you treat contact dermatitis?

A 
remove cause(s)
steroids, antipuritic agents
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20
Q

explain the underlying pathology of psoriasis

A

T lymphocyte driven.
increased cell turnover - epidermal rete ridges appear elongated and clubbed, capillary dilatation, mixed neutophil and lymphohistiocytic infiltration

21
Q

give 4 clinical features of chronic plaque psoriasis

A

well demarcated, red scaly plaques with silver scale.
found on extensor surfaces, lower back, ears and scalp.
Kobner phenomenon - new plaques arise if there’s skin trauma.
can be itchy and sore.

22
Q

name 3 triggers of psoriasis

A

infection (Strep group A), drugs (lithium), UV light, alcohol, stress

23
Q

name 4 features associated with psoriasis

A

nail pitting, distal separation of nail plate, yellow brown dicolouration, damaged nail matrix and lost nail plate.
psoriatic arthritis.

24
Q

how would you manage psoriasis?

A

emollients to hydrate skin.
moderate - use topical steroids, vit D analogues and purified coal tar.
tazaroten - a retinoid.
salicylic acid, phototherapy.
severe (ulceration, pyrexia) - methotrexate.

25
Q

what are the two peaks in age of onset of psoriasis?

A

16-22yrs and 55-60yrs

26
Q

how would flexural psoriasis present?

A

red glazed, non-scaly plaques in flexures - groin, natal cleft, sub-mammary

27
Q

how would guttate or “raindrop psoriasis” present?

A

explosive eruption of small circular/oval plaques appear on trunk 2wks after strep throat

28
Q

how do venous ulcers develop?

A

sustained venous hypertension in superficial veins due to incompetent valves in deeper veins - this increased pressure causes extravasation of fibrinogen through capillary walls, giving rise to perivascular fibrin deposition leading to poor oxygenation of the skin

29
Q

give 3 clinical features of a venous ulcer

A

oedema, venous eczema, brown pigmentation, varicose veins, lipodermatosclerosis, scarring white atrophy with telangiectasia

30
Q

how would you manage a venous ulcer?

A

high compression bandaging with leg elevation.
Doppler to exclude arterial disease.
diuretics for oedema, analgesia if painful, compression stockings to reduce recurrence.

31
Q

give 4 clinical features of arterial ulcers

A

punched-out painful ulcers, higher up the leg or on feet, cold and pale, absent peripheral pulses, arterial bruits.
Doppler US to confirm.

Hx of claudication, angina, hypertension and smoking.

32
Q

what treatment must NEVER be given to arterial ulcers?

A

compression stockings.

33
Q

in what group of people do neuropathic ulcers develop most commonly?

A

diabetics with peripheral neuropathy

34
Q

how does a patient with cellulitis normally present?

A

hot, tender area of erythema of skin due to infection of deep subcutaneous layer - poor margins.
upward spread with blistering and oedema.
px is unwell with fever.
prefers lower limb.

35
Q

what is the usual causative organism of cellulitis?

A

strep pyogenes.

36
Q

give 2 risk factors for cellulitis

A

lymphoedema, venous insuffiency, leg oedema, obesity.

site of entry - leg ulcer, trauma, tinea pedis (athletes foot).

37
Q

what is the main differential of cellulitis?

A

DVT

38
Q

how would you treat cellulitis?

A

phenoxymethylpenicillin and flucloxacillin.

erythromycin if penicillin allergy.

39
Q

how would you confirm a diagnosis of cellulitis due to strep pyogenes?

A

serological streptococcal titres

40
Q

what is the likely causative organism of necrotising fasciitis? how does it present?

A

group A beta haemolytic strep.

arises spontaneously with intense pain of affected skin and muscle.

41
Q

how would you treat necrotising fasciitis?

A

radial debridement ± amputation.

IV - benzylpenicillin and clindamycin

42
Q

which skin cancer is most associated with excessive sunlight exposure?

A

basal cell carcinoma

43
Q

what does a basal cell carcinoma look like?

A

pearly nodule with rolled telangiectasia edge, erodes and ulcerates

44
Q

what does a squamous cell carcinoma look like?

A

ulcerated lesion with hard raised edges

45
Q

which types of skin cancer metastasise, and which one is the most serious?

A

squamous cell and melanoma metastasise.

melanoma is most serious - early mets.

46
Q

how are all skin cancers treated?

A

surgical excision ± radiotherapy

47
Q

what are the components of the ABCDE criteria for moles?

A 
Asymmetry of mole
Border irregularity
Colour - non-unifrom
Diameter >6mm
Elevation
48
Q

what are the components of the Glasgow 7 point mole checklist?

A

Major - change in colour/size/shape (2pts).
Minor - diameter >6mm, inflammation/crusting/bleeding, sensory change (e.g. itch).

need 3+ to refer.

Phase 2a - Systems (18 decks)

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