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Medicine > Dermatology > Flashcards

Dermatology Flashcards

USMLE

1
Q

List the symptoms for erythroderma (skin failure)

A

Thirst
Fever and chills
Malaise
Dizziness

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2
Q

List the causes for erythroderma

A

Atopic eczema
Seborrhoeic eczema
Psoriasis
Drugs
* Sulphonamides
* Penicillin
* Gold
* Sulphonylureas
* Allopurinol
* Captopril
Idiopathic

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3
Q

List the complications for skin failure

A

High-output cardiac failure (increased blood flow)
Hypothermia (heat loss)
Prerenal acute kidney injury (fluid depletion)
Hypoalbuminemia
Catabolism and increased basal metabolic rate
Secondary bacterial infection
Capillary leak syndrome

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4
Q

List three clinical features of acne

A

Non-inflammatory – open comedones (blackheads) or closed comedones (whiteheads)
Inflammatory – papules, pustules, nodules and cysts
Scars – raised (hypertrophic) or depressed/pitted (box, rolling and ice-pick).

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5
Q

Give the pathophysiology for acne

A

Sebaceous gland hyperplasia and excess sebum production - Stimulated by androgens, most prominent during puberty
Abnormal follicular differentiation - keratinocytes are retained and accumulate due to increased cohesiveness
Cutibacterium acnes colonisation - gram-positive, non-motile rods found deep in follicles and stimulate pro-inflammatory mediators and lipases
Inflammation and immune response - inflammatory cells and mediators efflux into the disrupted follicle, develops papules, pustules, nodules, and cysts

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6
Q

List the risk factors for acne

A

Positive family history
Ethnicity
Diet - high glycaemic index
Hormone
* Hyperandrogenism
* Polycystic ovarian syndrome
* Menstruation

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7
Q

List the presentations for conglobate acne

A

(Found most often in men)
Extensive inflammatory papules
Suppurative nodules (which may coalesce to form sinuses)
Cysts on the trunk and upper limbs.

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8
Q

List the presentations of acne fulminans

A

(variable systemic manifestations)
Fever
Arthralgias, Myalgias
Hepatosplenomegaly
Osteolytic bone lesions

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9
Q

List the drug/toxin causes of acne

A

Glucocorticoids, anabolic steroids
Immunomodulators (azathioprine, EGFR inhibitors, ciclosporin)
Antiepileptic drugs
Isoniazid
Dioxins
Lithium
Iodides
Vitamins B1, B6, B12

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10
Q

List the complication for acne

A

Skin changes
* Scarring
* Post-inflammatory hyper/depigmentation
Psychosocial effects
Systemic comorbidities
* Obesity
* Diabetes mellitus
* Hyperlipidemia
* Hypertension
* Metabolic syndrome

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11
Q

List the first line options for mild to moderate acne

A

(12 week course, once daily in the evening)
Adapalene + benzoyl peroxide (topical)
Tretinoin + clindamycin (topical)
Benzoyl peroxide + clindamycin (topical)

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12
Q

List the first line options for moderate to severe acne

A

Adapalene + benzoyl peroxide (topical)
Tretinoin + clindamycin (topical)
Adapalene + benzoyl peroxide + oral lymecycline/doxycycline
Azelaic acid twice daily + oral lymecycline/doxycycline

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13
Q

What is hidradenitis suppurativa

A

Chronic inflammatory disorder that affects the apocrine pilosebaceous follicles of the axillae, inguinal and breasts

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14
Q

List the presentations for Hidradenitis suppurativa

A

Recurrent abscesses
Draining sinuses
Scarring
Disabling pain
Malodorous discharging lesions
Associated with the metabolic syndrome, obesity and smoking

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15
Q

List the treatment options for Hidradenitis suppurativa

A

Oral tetracycline
Combined rifampicin + clindamycin
Acitretin
Adalimumab (anti-TNF)
Surgery for abscess drainage and excision of affected skin

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16
Q

Where does rosacea predominantly affect

A

The convexities of the centrofacial region (cheeks, chin, nose, and central part of forehead).

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17
Q

Give the diagnostic criteria for rosacea

A

At least one ‘diagnostic’ or two ‘major’ clinical features present:
Diagnostic features
* Phymatous changes - thickened skin with enlarged pores and irregular surface nodularities
* Persistent erythema
Major features
* Flushing/transient erythema
* Papules and pustules
* Telangiectasia
* Eye symptoms (ocular rosacea)
Minor features
* Skin burning/stinging sensation
* Skin dryness
* Oedema

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18
Q

List the signs of ocular rosacea

A

Lid margin telangiectasia
Blepharitis
Conjunctivitis
Keratitis, scleritis, iritis
Anterior uveitis

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19
Q

List the risk factors for rosacea

A

Increasing age.
Photosensitive skin types.
Ultraviolet radiation exposure.
Smoking, alcohol.
Spicy foods and hot drinks.
Heat or cold temperature.
Emotional stress and exercise.
Colonisation with Demodex folliculorum mites.

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20
Q

Give the first line treatment for persistent erythema in rosacea

A

Topical brimonidine 0.5% gel once daily as needed (alpha agonist)

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21
Q

Give the first line treatment for mild-to-moderate papules / pustules.
Give an alternative in pregnancy

A

Topical ivermectin once daily 8-12 weeks
In pregnant/breastfeeding women: metronidazole 0.75% twice daily / azelaic acid 15% twice daily

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22
Q

Give the first line treatment for moderate-to-severe papules / pustules.
Give an alternative in pregnancy

A

Topical ivermectin + oral doxycycline 40mg daily 8–12 weeks

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23
Q

List the endogenous and exogenous classifications for eczema

A

Endogenous
Atopic eczema
Seborrhoeic eczema
Venous (‘gravitational’) eczema
Discoid eczema
Asteatotic eczema
Chronic hand/foot eczema
Lichen simplex/nodular prurigo

Exogenous
Irritant contact eczema
Allergic contact eczema

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24
Q

List the presentations of seborrhoeic eczema

A

Affects greasy areas on the face
Scaling and erythema around the nose, medial eyebrows, hairline and ear canals.

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25
Q

In which diseases are seborrhoeic eczema prevalence increased

A

Parkinson’s disease
HIV

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26
Q

Give the aetiology in seborrhoeic eczema

A

Malassezia (lipophilic commensal yeast) triggers inflammatory skin changes

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27
Q

Give the management in seborrhoeic eczema

A

Topical azole cream (fluconazole, clotrimazole) + short-term mild-moderate-potency steroids

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28
Q

List the presentations for venous eczema

A

Usually elderly and varicose veins / history of venous thrombosis
Involves the inner calf and coexistent signs of venous hypertension
* Hemosiderin deposition
* Lipodermatosclerosis
* Varicose ulceration

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29
Q

Give the management for venous eczema

A

Bland emollients + short-term moderately potent topical steroid

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30
Q

Give the presentations for asteatotic eczema

A

Affects older people in wintertime and can be intensely pruritic.
Involves the lower legs, lower back and other areas that have few sebaceous glands.

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31
Q

Give the management in asteatotic eczema

A

Bland moisturiser and soap substitute

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32
Q

List the presentations for discoid eczema

A

Well-demarcated, inflamed scaly patches, sometimes with tiny vesicles.
Usually affects the limbs and torso, intensely itchy.

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33
Q

Give the management for discoid eczema

A

Potent topical steroids

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34
Q

List the common sites of lichen simplex

A

nape of the neck
outer calves
anogenital area

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35
Q

What is lichen simplex

A

Chronic eczema thickened and lined (lichenified) skin in response to repeated rubbing and scratching.

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36
Q

List the management for lichen simplex

A

Potent / superpotent topical steroid and topical antipruritics (menthol)

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37
Q

What age group does atopic eczema most commonly present

A

Early childhood (< 5 years of age)

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38
Q

What is atopic eczema characterised by

A

Dry, pruritic skin
Episodes of flares and remissions

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39
Q

What is contact dermatitis/eczema caused by

A

External harsh substance (irritant) or allergy-provoking substance (allergen)

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40
Q

List the common contact allergens in contact dermatitis / eczema

A

Fragrance
Rubber chemicals
Metals
Chemical hair dye
Preservative chemicals
Topical antibiotics and antiseptics
Adhesives
Leather and textile dyes
Ingredients in medicated creams - eg. lanolin / hydrocortisone

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41
Q

List the triggering factors in atopic eczema

A

Soap and detergents
Animal dander
House-dust mites
Extreme temperatures
Rough clothing
Pollen
Certain foods
Skin infections
Stress

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42
Q

What makes an individual genetically susceptible to atopic eczema

A

Filaggrin mutation

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43
Q

What are the associated comorbidities in atopic eczema

A

Atopic
* Asthma
* Allergic rhinitis (hay fever)
* Food allergy
* Eosinophilic oesophagitis
Non-atopic
* Allergic contact dermatitis
* Obesity
* Cardiovascular disease

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44
Q

List the complications of atopic eczema

A

S. aureus infection (typical impetigo or worsening of eczema)
Eczema herpeticum
Superficial fungal infections
Psychosocial problems

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45
Q

Lise the presentation for eczema herpeticum

A

Disseminated herpes simplex infection
Fever, lymphadenopathy, malaise

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46
Q

List the risk factors for eczema herpeticum

A

Early-onset and severe atopic eczema
Marked elevations in total IgE
Elevated allergen-specific IgE levels
Peripheral eosinophilia
Presence of filaggrin mutations

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47
Q

Give the management in eczema herpeticum

A

Urgent systemic antiviral therapy

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48
Q

Give the NICE diagnostic criteria for atopic eczema

A

An itchy skin condition plus three or more of the following:
* Visible flexural eczema involving the skin creases
* Personal history of flexural eczema
* Personal history of dry skin in the last 12 months
* Personal history of asthma or allergic rhinitis / history of atopic disease in a first-degree relative of a child < 4 years
* Onset of signs and symptoms before the age of 2 years

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49
Q

List the eczema severity grading

A

Clear - normal skin and no evidence of active eczema
Mild - areas of dry skin, and infrequent itching (with/without small areas of redness)
Moderate - areas of dry skin, frequent itching, and redness (with/without excoriation and localised skin thickening)
Severe - widespread areas of dry skin, incessant itching, and redness (with/without excoriation, extensive skin thickening, bleeding, oozing, cracking, and alteration of pigmentation)
Infected - if eczema is weeping, crusted, or there are pustules, with fever or malaise

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50
Q

List the management for mild, moderate, and severe eczema

A

(Liberal use)

Mild - hydrocortisone 1%
Moderate - betamethasone valerate 0.025% / clobetasone butyrate 0.05%
Severe - betamethasone valerate 0.1%
* 2nd line - Topical calcineurin inhibitors (tacrolimus, pimecrolimus)

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51
Q

List the first line options for infected eczema

A

Flucloxacillin
If penicillin allergy / flucloxacillin resistance: clarithromycin
If penicillin allergy + pregnant: erythromycin
If localised areas of infection: topical fusidic acid

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52
Q

List the classification of topical corticosteroids by potency

A

Very potent
0.05% clobetasol propionate
0.3% diflucortolone valerate
Potent
0.1% betamethasone valerate
0.025% fluocinolone acetonide
Moderately
0.05% clobetasone butyrate
0.05% alclometasone dipropionate
Mild
2.5% hydrocortisone
1% hydrocortisone

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53
Q

List the adverse effects of topical steroids

A

Cutaneous atrophy and telangiectasia
Striae
Steroid-induced rosacea, perioral dermatitis and folliculitis
Tinea incognito
Ocular adverse effects (cataract, glaucoma)
Adrenal suppression (long-term potent steroids)

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54
Q

List the management options for severe itch in atopic eczema

A

Non-sedating antihistamine
* cetirizine
* loratadine
* fexofenadine

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55
Q

List three pathogenic factors in psoriasis

A

Epidermal hyperproliferation
Abnormal keratinocyte differentiation
Lymphocyte inflammatory infiltrate

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56
Q

Give the presentation of Guttate psoriasis

A

small, scattered, round or oval (2mm~1cm in diameter, water drop appearance) scaly papules, which may be pink or red

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57
Q

What is guttate psoriasis strongly associated with

A

Streptococcal URTI

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58
Q

What age group does Guttate psoriasis most commonly affect

A

Children, teenagers and young adults

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59
Q

List the presentations in nail psoriasis

A

Nail pitting
Discolouration (oil drop sign)
Subungual hyperkeratosis - hyperproliferation of the nail bed
Onycholysis - detachment of the nail from the nail bed
Complete nail dystrophy

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60
Q

List the complications of psoriasis

A

Erythrodermic psoriasis
Generalised pustular psoriasis
Pregnancy complications - increased risks of
* Miscarriage / Stillbirth
* Preterm delivery
* Low birthweight
Psychosocial effects

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61
Q

Give the presentations of generalised pustular psoriasis

A

(potentially life-threatening medical emergency)
Rapidly developing widespread erythema
Followed by the eruption of white, sterile non-follicular pustules which coalesce to form large lakes of pus
Associated with systemic illness
* Fever
* Malaise
* Tachycardia
* Weight loss
* Hypothermia

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62
Q

In which type of psoriasis does generalised pustular psoriasis usually present in

A

People with existing / previous chronic plaque psoriasis

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63
Q

List the presentations for erythrodermic psoriasis

A

Diffuse, widespread severe psoriasis that affects > 90% of the body surface area.
High output heart failure
Malabsorption (enteropathy)
Hypothermia
Dehydration
Mild anaemia - (iron deficiency due to skin losses, low vitamin B12 and folate)

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64
Q

Give the management in psoriasis

A

Emollient
Potent topical corticosteroid + topical vitamin D preparation

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65
Q

Give the presentation in chronic plaque psoriasis

A

Monomorphic, erythematous plaques covered by adherent silvery-white scale
Usually on the scalp, behind the ears, trunk, buttocks, periumbilical area, and extensor surfaces.
Symmetrical distribution, can coalesce to form larger lesions.
Auspitz’s sign = If scale is removed, a glossy red membrane with pinpoint bleeding points is revealed
Woronoff’s ring = Halo-like effect around a plaque, due to vasoconstriction

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66
Q

What can erythrodermic psoriasis be precipitated by

A

Systemic infection
Irritants eg. coal tar, ciclosporin
Phototherapy
Sudden withdrawal of corticosteroids

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67
Q

Which age group is Pityriasis rosea most common in

A

Teenagers and young adults (10-35 years)

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68
Q

List the causes of Pityriasis rosea

A

Herpesviruses 6 and 7 (HHV-6/7)
Drugs
* ACEi
* NSAIDs
* hydrochlorothiazide
* gold
* atypical antipsychotics
* barbiturates
* D-penicillamine
* imatinib
* metronidazole
* isotretinoin
Vaccines

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69
Q

What time of the year does pityriasis rosea have increased incidence

A

Spring and autumn

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70
Q

List the characteristics of rash in Pityriasis rosea

A

Most prominent on the torso and proximal limbs
Circular / oval pink macules with collarette of fine scale
Preceded by a larger solitary ‘herald patch’
Christmas tree pattern = Lesions run along dermatome lines of the back

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71
Q

List the presentations in Polymorphic light eruption (‘prickly heat’)

A

Itchy papular rash develops on sun-exposed areas
* ‘V’ of the neck
* Shoulders and arms

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72
Q

Give the management in Polymorphic light eruption (‘prickly heat’)

A

Short course prednisolone

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73
Q

List the presentations in lichen planus

A

Clusters of intensely pruritic, purple–pink, polygonal papules
Flexural aspect of wrists, forearms and lower legs
Fine white streaks (Wickham’s striae)

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74
Q

List the potential triggers for lichen planus

A

Hepatitis B / C
Drugs (antihypertensives, antimalarials, NSAIDs, gold, quinine, quinidine)
Contact allergens
Genetic predisposition
Physical and emotional stress
Injury to the skin (koebnerization)
Localised skin disease eg. herpes zoster

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75
Q

List the typical features of urticaria

A

Central swelling of variable size (red/white), surrounded by an area of redness (flare).
Associated itching/burning sensation.
Fleeting nature - skin returns normal within 1–24 hours.

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76
Q

How does urticaria differentiate from other inflammatory rashes eg. eczema

A

Shorted-lived, lack of skin surface changes

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77
Q

What’s difference between angio-oedema and urticaria

A

Angio-oedema - deeper form of urticaria with transient swellings of deeper dermal, subcutaneous, and submucosal tissues
Often affects the face (lips, tongue, eyelids), genitalia, hands, or feet.

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78
Q

List the classifications for urticaria

A

Acute - < 6 weeks
Chronic - > 6 weeks
* Chronic spontaneous urticaria
* Chronic inducible urticaria

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79
Q

Give the pathophysiology of urticaria

A

Mast cell driven disease - histamine and inflammatory mediators release (eg. leukotrienes, prostaglandins) from activated mast cells results in
* Pruritus
* Vascular permeability (plasma leakage from capillary into skin)
* Oedema

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80
Q

List the acute urticaria triggers

A

Acute viral infection
Certain foods - milk, eggs, peanuts, tree nuts, and shellfish.
Insect bites and stings.
Contact allergens - latex.
Certain drugs - penicillins, aspirin, NSAIDs, vaccinations

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81
Q

What can chronic inducible urticaria caused by

A

Aquagenic urticaria - hot or cold water.
Cholinergic urticaria - active or passive warming.
Cold / Heat urticaria
Symptomatic dermatographism - shear forces
Delayed pressure urticaria - sustained pressure
Solar urticaria - light exposure.
Vibratory angioedema
Contact urticaria - eliciting agent.

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82
Q

List the presentations for vasculitic urticaria

A

Lesions remain for longer than 24 hours
Painful, non-blanching, palpable
Systemic symptoms - fever, malaise, arthralgia

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83
Q

List the management options for urticaria

A

Non-sedating antihistamine (cetirizine, fexofenadine, loratadine)
Prednisolone 40 mg daily for up to 7 days

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84
Q

How long does impetigo heal without treatment

A

7~21 days

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85
Q

Describe the presentation of non-bullous impetigo. Where does it most commonly affect?

A

Thin-walled vesicles / pustules that rupture quickly, forming golden-brown crusts.
Asymptomatic, occasional pruritus
Regional adenopathy common
Systemic symptoms typically absent
Most commonly the face (nose, mouth), limbs, flexures

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86
Q

Describe the presentation of bullous impetigo. Where does it most commonly affect?

A

Large, fragile, flaccid bullae (fluid-filled lesions > 1cm diameter) that rupture and ooze yellow fluid, leaving a scaley collarette
Regional adenopathy rare
Systemic symptoms (fever, lymphadenopathy, diarrhoea, weakness) if large areas affected
Most commonly flexures, face, trunk, and limbs

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87
Q

Give the first line management for localised impetigo

A

Hydrogen peroxide 1% cream

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88
Q

Give the first line management options for widespread non-bullous impetigo

A

(three times daily for 5 days)

Topical fusidic acid 2%
Topical mupirocin 2%

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89
Q

Give the first line management options for non-bullous impetigo + systemically unwell / high risks of complications.
Give the alternatives in penicillin allergy and pregnancy.

A

Flucloxacillin 500 mg four times daily for 5 days
Penicillin allergy: clarithromycin 250 mg twice daily for 5 days
Pregnant: erythromycin 250~500 mg four times daily for 5 days

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90
Q

Give the first line management options for bullous impetigo.
Give the alternatives in penicillin allergy and pregnancy.

A

Flucloxacillin 500 mg four times daily for 5 days
Penicillin allergy: clarithromycin 250 mg twice daily for 5 days
Pregnant: erythromycin 250~500 mg four times daily for 5 days

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91
Q

Give the main causative organism in impetigo

A

S aureus

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92
Q

List the presentation of cellulitis. Where does it most commonly affect?

A

Pain, warmth, swelling, erythema
Blisters, bullae
Fever, malaise, nausea, rigors

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93
Q

How may pseudomonas aeruginosa cellulitis be contacted

A

contaminated hot tubs, sponges, nail puncture wound

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94
Q

How may vibrio vulnificus cellulitis be contacted

A

salt water exposure

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95
Q

How may mycobacterium marinum cellulitis be contacted

A

aquarium keepers

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95
Q

How may aeromonas hydrophila cellulitis be contacted

A

freshwater exposure

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96
Q

List the common causative organisms for cellulitis in people with injury, burns, and co‐existing diseases (immunocompromised, diabetes mellitus, cancer, malnutrition)

A

Streptococcus pneumoniae
Haemophilus influenzae
Gram-negative bacilli
Anaerobes

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97
Q

List the risk factors for cellulitis

A

Break in the skin
* Trauma, surgery
* Leg ulceration
* Maceration/fungal infection between the toes
* Concomitant skin disorder (atopic eczema)
Diabetes mellitus.
Immunocompromise.
Obesity.
Oedema, lymphoedema.
Pregnancy.
Toe web abnormalities.
Venous insufficiency.

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98
Q

List the acute complications for cellulitis

A

Deep-seated infection
* Necrotising fasciitis
* Myositis
Sepsis
Subcutaneous abscess
Post-streptococcal nephritis

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99
Q

List the chronic complications for cellulitis

A

Persistent leg ulceration
Lymphoedema
Recurrent cellulitis

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100
Q

Give the presentation of necrotising fasciitis

A

Severe pain that is out of proportion to the apparent signs of skin inflammation.
Febrile, severely unwell.

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101
Q

Give the management for necrotising fasciitis

A

Surgical debridement / amputation
IV antibiotics - High-dose benzylpenicillin + clindamycin (GAS infection)

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102
Q

Give the classification for cellulitis

A

Eron classification system
Class I - no signs of systemic toxicity and the person has no uncontrolled comorbidities
Class II - either systemically unwell / well but with a comorbidity that may complicate or delay the resolution of infection.
Class III - significant systemic upset that may interfere with a response to treatment, or a limb-threatening infection due to vascular compromise.
Class IV - sepsis or a severe life-threatening infection, such as necrotizing fasciitis.

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103
Q

Give the first line management for cellulitis. Give alternatives in penicillin allergy and pregnancy.

A

Flucloxacillin 500~1000 mg four times daily for 5–7 days

Penicillin allergy
* Clarithromycin 500 mg twice daily for 5–7 days.
* Doxycycline 200 mg on the first day then 100 mg once daily, for a total of 5–7 days.

Pregnancy: Erythromycin 500 mg four times daily for 5–7 days.

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104
Q

Give the first line management for cellulitis near the eyes or nose. Give alternatives in penicillin allergy.

A

Co-amoxiclav 500 mg three times daily for 7 days

Penicillin allergy:
Clarithromycin 500 mg twice daily for 7 days + metronidazole 400 mg three times daily for 7 days

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105
Q

Describe the presentation of boils (furuncles) and carbuncles

A

Boil (furuncle) - deep-seated inflammatory nodule
* infection of the hair follicle with purulent extension into the subcutaneous tissue (small abscess)
Carbuncle - several adjacent boils join beneath the skin, drains pus through many follicular orifices.

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106
Q

List the causes of boils (furuncles) and carbuncles.
What is the most common cause?

A

Staphylococcus aureus - most common
* MRSA
* PVL-SA
Streptococcus pyogenes
Enterobacteriaceae
Enterococci

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107
Q

List the risk factors for Boils (furuncles) and carbuncles

A

Male sex.
Adolescence.
Close personal contact with an infected person
Contact sports
Poor personal hygiene
Pre-existing skin lesions eg. atopic eczema / abrasions.
Corticosteroids
Blood dyscrasias and anaemia.
Immunocompromised
Obesity.
Malnutrition.

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108
Q

Give the complications of Boils (furuncles) and carbuncles

A

Scarring
Infection spread
* Cellulitis
* Thrombophlebitis
* Septic arthritis, osteomyelitis, endocarditis, sepsis, brain abscess
Staphylococcal scalded-skin syndrome
Cavernous sinus thrombosis (boils/carbuncles on the lips, nose, cheek)

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109
Q

Define Staphylococcal carriage

A

Asymptomatic carriage of S aureus on skin or mucous membranes.

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110
Q

List the risk factors for Staphylococcal carriage

A

Healthcare worker.
Age < 30 or > 60 years.
Male sex.
Skin disease eg. atopic dermatitis and psoriasis.
Health conditions eg. HIV, diabetes mellitus, liver dysfunction.
Obesity.
Hormonal contraception.
Recent antibiotic use.
Intravenous drug use.
Hospitalisation or medical intervention (eg. dialysis).
A household member being colonised.
Working with animals and livestock.

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111
Q

List the complications for Staphylococcal carriage

A

Skin and soft tissue infections
* Impetigo
* Boils
* Cutaneous abscess
Surgical site infections
Recurrent skin and soft tissue infections
Invasive infections - bacteraemia, sepsis, endocarditis, osteomyelitis, septic arthritis
Nosocomial infections

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112
Q

What skin conditions is Panton-Valentine leukocidin S. aureus (PVL-SA) associated with

A

Recurrent boils and carbuncles
Necrotizing pneumonia
Necrotizing fasciitis
Osteomyelitis
Septic arthritis
Purpura fulminans

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113
Q

Give the management for nasal Staphylococcal carriage

A

Naseptin cream (chlorhexidine + neomycin)

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114
Q

Give the management for skin Staphylococcal carriage

A

Antiseptic preparation (chlorhexidine 4% body wash + Triclosan 2%) daily as liquid soap for 5 days

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115
Q

Describe the presentation for ecthyma

A

Chronic, well-demarcated, deep ulcers with a necrotic crust and exudate.

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116
Q

What is ecthyma associated with

A

Malnutrition and poor hygiene eg. IVDU

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117
Q

Give the presentation for Ecthyma gangrenosum

A

Distinctive necrotic skin ulcers with central thick, dark brown/black eschar

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118
Q

What is ecthyma gangrenosum typically caused by

A

Pseudomonas septicaemia in an immunocompromised

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119
Q

What is erythrasma

A

superficial skin infection caused by Corynebacterium minutissimum

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120
Q

Describe the presentation for erythrasma

A

Orange–beige scaly plaques in the large flexures (axillae, groin)
Maceration in the toe webs
Corynebacteria show coral-pink fluorescence when examined with Wood’s light (UVA)

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121
Q

Give the management for erythrasma

A

Topical / oral macrolides

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122
Q

List the presentation for Pitted keratolysis

A

Mltiple punched-out areas and maceration of the skin on weight-bearing plantar surfaces
Associated with
* Hyperhidrosis
* Malodour

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123
Q

List the management options for Pitted keratolysis

A

Potassium permanganate soaks
Antiperspirants
Topical imidazoles / fusidic acid

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124
Q

Give the causative organism for head lice infestation

A

pediculosis capitis

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125
Q

List the presentations for head lice

A

Pruritic rash on the back of the neck and behind the ears (hypersensitivity reaction to louse faeces)
Small red papules in the hairline at the nape of the neck
Lymphadenopathy/erythema with a honey-coloured crust on the scalp

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126
Q

List the management options for head lice

A

Wet combing to remove head lice
Physical insecticide - Dimeticone 4% gel (silicone / fatty acid ester-based product)
Chemical insecticide - Malathion 0.5% aqueous liquid

127
Q

Name the causative organism in scabies

A

Sarcoptes scabiei

128
Q

Which type of hypersensitivity is itch in scabies

A

Delayed type-IV hypersensitivity reaction to the mite/mite products (faeces, eggs).

129
Q

How is scabies transmitted

A

Close/prolonged skin contact with infected person
Sexually acquired
Shared clothing/bedding
Dogs and cats

130
Q

List the risk factors for scabies

A

Closed contact with infested person
Poverty and social deprivation
Crowded living conditions
Winter months

131
Q

Give the pathognomonic sign in scabies

A

the burrow (thin, brown-grey line of 0.2–1 cm in length)

132
Q

Give the management in scabies

A

Permethrin 5% cream
* All members of household, sexual partners within the past month, and close personal contacts should also be treated
* Bedding, clothing, and towels should be decontaminated

133
Q

Give the management for resistance scabies

A

Oral ivermectin

134
Q

What is chicken pox caused by

A

varicella-zoster virus

135
Q

When is chicken pox infectious

A

From 24 hours before the rash appears until the vesicles are dry or have crusted over (5 days after the onset of the rash).

136
Q

Where does varicella-zoster virus persist in and years later reactivate to cause herpes zoster (shingles)

A

Sensory dorsal root ganglia

137
Q

List the complications of chicken pox in children

A

Secondary bacterial infection (GAS, S aureus)
* impetigo
* furuncles
* cellulitis
* erysipelas
* necrotizing fasciitis
Neurological complications
* Reye’s syndrome
* Acute cerebellar ataxia
* Encephalitis
* Meningoencephalitis
* Polyradiculitis
* Myelitis

138
Q

List the complications of chicken pox in adults

A

Varicella pneumonia
Hepatitis
Encephalitis

139
Q

List the presentations of Fetal varicella syndrome

A

Infection during the first 28 weeks can lead to intrauterine infection
Skin scarring in a dermatomal distribution
Eye defects:
* Microphthalmia
* Chorioretinitis
* Cataracts
Hypoplasia of the limbs
Neurological abnormalities
* Microcephaly
* Cortical atrophy
* Learning difficulties
* Dysfunction of bowel and bladder sphincters

140
Q

List the complications of chicken pox in immunocompromised

A

Severe disseminated chickenpox with haemorrhagic complications
Varicella pneumonia
Hepatitis
Encephalitis
Disseminated intravascular coagulopathy

141
Q

List the complications of chicken pox in neonates

A

Disseminated / hemorrhagic varicella

142
Q

List the clinical features of chicken pox

A

Small, erythematous macules on the scalp, face, trunk, and proximal limbs
Progress over 12–14 hours to papules, clear vesicles, and pustules.
Crusting occurs within 5 days, and crusts fall off after 1–2 weeks.
Prodromal symptoms:
* Nausea
* Myalgia
* Anorexia
* Headache
* General malaise
* Loss of appetite

143
Q

Give the management for chicken pox

A

Oral aciclovir 800 mg 5 times a day for 7 days

144
Q

List the risk factors for shingles

A

Increasing age
Immunocompromise
Comorbidities
* Rheumatoid arthritis
* Asthma and COPD
* Chronic kidney disease
* Depression
* Diabetes
* Systemic lupus erythematosus
* Granulomatosis with polyangiitis
* Malignancies
Psychological factors
Female sex
Race/ethnicity
Statin use

145
Q

List the complications for shingles

A

Post-herpetic neuralgia
Skin changes
* Scarring
* Changes in pigmentation
* Keloid formation
Secondary infection of the lesions
Herpes zoster oticus (Ramsay Hunt syndrome) - virus infects CNVII
Herpes zoster ophthalmicus - virus infects V1
Peripheral motor neuropathy
CNS complications
* Encephalitis
* Meningoencephalitis
* Myelitis
* Cerebelitis
* Cerebrovascular disease
* Radiculitis
* Guillain–Barré syndrome
Cardiovascular complications
* Stroke / TIA
* MI

146
Q

List the typical clinical features in shingles

A

Prodromal: abnormal sensations and pain in the affected dermatome.
Within 2–3 days, dermatomal rash appears
* Maculopapular lesions develops into clusters of vesicles over 3–5 days.
* usually painful, itchy, tingly, and does not cross the midline of the body.
Vesicles then burst, releasing VZV, and crust over within 7–10 days.
Healing over 2–4 weeks, results in scarring and permanent pigmentation in the affected area.

147
Q

What is Hutchinson’s sign in shingles. What is it a prognostic factor of

A

Rash on the tip/side/root of the nose (nasociliary nerve dermatome)
Prognostic for subsequent eye inflammation and permanent corneal denervation

148
Q

Give the management for shingles

A

Antiviral treatment within 72 hours of rash onset - aciclovir, famiciclovir, valaciclovir

149
Q

What is measles caused by

A

Morbillivirus of the paramyxovirus family

150
Q

How long is the typical incubation period of measles

A

10 days

151
Q

How long are the prodromal symptoms for measles

A

2~4 days

152
Q

When is measles infectious

A

From when symptoms first appear (~4 days before the rash appears) to 4 days after onset of the rash.

153
Q

How is measles transmitted

A

Direct contact with infectious droplets
Airborne (breathing, coughing, sneezing)

154
Q

List the complications for measles

A

Susceptibility to opportunistic infection
Secondary infections of the respiratory tract
* Otitis media
* Pneumonitis
* Tracheobronchitis
* Pneumonia
CNS complications
* Convulsions
* Encephalitis
* Subacute sclerosing panencephalitis
GI complications
* Diarrhoea
* Stomatitis
Ocular - Blindness (measles keratoconjunctivitis)

155
Q

List the presentations for Herpes zoster oticus (Ramsay Hunt syndrome) - virus infects CNVII

A

Lesions in the ear
Facial paralysis
Hearing and vestibular symptoms

156
Q

List the presentation for Herpes zoster ophthalmicus - virus infects V1

A

Keratitis, conjunctivitis, retinitis
Corneal ulceration
Optic neuritis
Glaucoma
Blindness

157
Q

List the typical features in mealses

A

Fever (39C), maculopapular rash, cough, coryzal symptoms, conjunctivitis
The prodromal phase
* Increasing fever to 39C
* Malaise
* Cough
* Rhinorrhoea
* Conjunctivitis
Koplik’s spots appear on the buccal mucosa at the end of the prodromal phase

158
Q

List the characteristics of measles rash

A

Erythematous, maculopapular
On face and behind the ears first
Then descends to the trunk and limbs
On hands and feet last
Rash fades after 5 days, with the total duration up to 1 week.

159
Q

How is measles infection confirmed

A

IgM/IgG
Viral RNA testing

160
Q

List the management plan for measles

A

Notifiable disease
Usually self-limiting
Paracetamol / ibuprofen (symptomatic relief)
Advices
* Rest, drink adequate fluids
* Stay away from school/work at least 4 days after the initial rash
* Avoid contact with susceptible people

161
Q

What is Molluscum contagiosum caused by

A

molluscum contagiosum virus (Poxviridae family)

162
Q

How is Molluscum contagiosum transmitted

A

Direct contact with infected skin
Contaminated fomites
Vertical transmission

163
Q

List the complications for Molluscum contagiosum

A

Pruritus and erythema
Scarring
Secondary bacterial infection
Follicular conjunctivitis
Molluscum dermatitis - molluscum lesions surrounded by a halo of eczema (hypersensitivity)
Psychosocial

164
Q

List the features of Molluscum contagiosum

A

Smooth-surfaced, firm, dome-shaped, flesh-coloured or pearly white papules with a central umbilication.
Commonly 1-30 individual lesions at a time, occurring as clusters.

165
Q

Where is Molluscum contagiosum commonly seen in children

A

trunk, flexures, anogenital

166
Q

How is Molluscum contagiosum managed

A

Self-limiting

167
Q

What is herpes simplex more commonly caused by

A

Usually HSV-1, rarely HSV-2

168
Q

Where does the HSV persist?

A

sensory dorsal root ganglia proximal to the site of infection (typically CNV ganglion)

169
Q

List the presentations for Herpes simplex labialis

A

Prodrome of pain, burning, tingling, itching, and paraesthesia, typically lasts 6-48 hours.
Crops of vesicles that rupture
Leaving superficial ulcers that crust over and heal, typically at the lip mucocutaneous junctions

170
Q

List the presentations for Herpes gingivostomatitis

A

Prodrome of fever, general malaise, sore throat, and cervical/submandibular lymphadenopathy
Sore mouth/throat, excess salivation, drooling
Crops of painful vesicles on a red swollen base that rupture and form pharyngeal/oral mucosa ulcers

171
Q

Give the management for Herpes Simplex

A

aciclovir, valacivlovir

172
Q

List the presentations for ocular herpes simplex

A

Malaise and fever
Eye pain/irritation/photophobia
Keratitis
* Eye watering
* Blurred vision
* Reduced corneal sensitivity
Acute red eye
Crops of vesicles/ulcers on an erythematous base, pustules along the lid margin/periocular skin, eventually crust over.
Hazy cornea/localised creamy opacity (stromal keratitis)
Fixed irregular pupil/erythema around the whole cornea (iritis/uveitis)

173
Q

List the complications for genital herpes simplex

A

Secondary infection with Candida or Streptococcus species
Autoinoculation
Balanitis
Progressive, multifocal, and coalescing mucocutaneous anogenital lesions
Urinary retention
Herpes proctitis
HIV infection
Neonatal HSV if pregnant
Impact on psychosocial functioning
Systemic infection
* Aseptic meningitis
* Encephalitis
* Fulminant hepatitis
* Pneumonitis
* Disseminated infection

174
Q

List the presentations for genital herpes simplex

A

Multiple painful crops of genital blisters which burst to leave erosions and ulcers on the external genitalia/perineum/perianal region.
* Lesions typically develop 4–7 days after exposure
* A primary episode last up to 3 weeks, often more severe than a recurrent episode (6-12 days)
Dysuria, vaginal/urethral discharge
Headache, malaise, fever

175
Q

What are the differences between first and recurrent episodes of genital herpes simplex

A

First episode - Usually bilateral lesions + redness, vesicles, blisters, ulcers.
Recurrent episodes - Usually less severe, unilateral, and localised to the same dermatome during each episode.

176
Q

List the subtypes of tines pedis and the most common causative organism

A

Interdigital - Trichophyton rubrum
Moccasin / dry - Trichophyton rubrum
Vesicobullous - Trichophyton interdigitale

177
Q

List the risk factors for tinea pedis

A

Hot, humid climates, high-temperature environments.
Occlusive footwear - athletes, miners, and soldiers.
Hyperhidrosis
Walking on floor surfaces contaminated with infectious desquamated skin scales
Immunocompromised

178
Q

List the complications for tinea pedis

A

Secondary bacterial infection
Recurrent cellulitis of the lower leg
Tinea manuum - dermatophyte infection of the hands
Dermatophytid reaction - skin eruption on an area that is not where the infection first began
Tinea incognito

179
Q

List the clinical features in Interdigital, Moccasin/dry, and Vesicobullous tinea pedis

A

Interdigital
White or red, fissured, scaling skin or macerated areas between the toes.
Affects the lateral interdigital space between the fourth and fifth toes and then extends medially.

Moccasin / dry
Diffuse, chronic presentation causing scaling, erythema, and hyperkeratosis of the sole and lateral aspect of the foot.
The dorsal surface is usually unaffected.

Vesicobullous
Hard, tense, small vesicles, blisters, bullae, and pustules on an erythematous base, mainly on the arches and soles of the feet.

180
Q

List the management for tinea pedis

A

Topical antifungal cream - clotrimazole, miconazole, econazole
Mildly potent topical corticosteroids - hydrocortisone 1%

181
Q

Give the oral management for severe / extensive tinea pedis

A

Terbinafine
Alternative: oral itraconazole / oral griseofulvin

182
Q

What is candida part of the commensal flora of

A

GI tract
Vagina

183
Q

List the clinical features of candidiasis

A

Soreness and itching
Thin-walled pustules with a red base
Scales may accumulate, producing a white-yellow, curd-like substance over the infected area.

184
Q

What can candidiasis cause

A

Intertrigo (skin fold infections)
Oral candidiasis
Genital infections
* Vulvovaginal candidiasis
* Balanitis
Napkin dermatitis
Onychomycosis (nail plate infection)
Chronic paronychia (nail fold infection)
Chronic mucocutaneous candidiasis

185
Q

List the management for candidiasis in adults

A

Topical imidazole (clotrimazole, econazole, miconazole, ketoconazole)
Terbinafine

186
Q

List the management for candidiasis in children

A

Topical clotrimazole, econazole, miconazole

187
Q

Describe the presentation of erythema nodosum

A

Painful / tender, dusky bruise-like swellings over the shins, which fade over several weeks.
May be associated with arthralgia, malaise and fever.

188
Q

What is Erythema nodosum caused by

A

Infection
* Streptococcal
* Chlamydia
* Fungal (histoplasmosis, blastomycosis)
Idiopathic
Drugs (sulphonamides, oral contraceptive pill)
Bacterial gastroenteritis - Salmonella, Shigella, Yersinia
Inflammatory bowel disease
Sarcoidosis
Tuberculosis
Leprosy

189
Q

Give the inheritance in albinism

A

Autosomal recessive

190
Q

What is albinism caused by

A

Tyrosinase gene mutation

Tyrosinase oxidises L-tyrosine to DOPA
Mutation causes impaired eumelanin synthesis

191
Q

Give the inheritance in piebaldism

A

Autosomal dominant

192
Q

List the presentations in piebaldism

A

isolated congenital leukoderma (white skin) and poliosis (white hair) in a distinct ventral midline pattern

193
Q

List the characteristics of Chediak Higashi syndrome

A

easy bruising
oculocutaneous albinism
recurrent pyogenic infections

194
Q

Give the pathophysiology of vitiligo

A

Autoimmune destruction of melanocytes

195
Q

List the clinical presentation for vitiligo

A

Depigmented macules on extremities and extensor surfaces
Leukotrichia - depigmented hair
Associated with other autoimmune disorders
* diabetes
* hypothyroidism
* pernicious anaemia
* Addison disease

196
Q

List the treatments for vitiligo

A

Topical corticosteroids

197
Q

List the investigations and findings for vitiligo

A

Wood lamp test - blue-white areas
Biopsy - absence of melanocytes

198
Q

What is ash leaf spot a sign of

A

Tuberous sclerosis

199
Q

What is idiopathic guttate hypomelanosis a common finding in

A

Aging

200
Q

Give the pathophysiology in keloid

A

Hyperproliferation of fibroblasts
Results in disorganised overproduction of hyalinised collagens types 1 and 3

201
Q

Which population is keloid seen more commonly in

A

Dark skinned individuals

202
Q

Describe the pathophysiology of senile purpura

A

Loss of elastic fibres in perivascular connective tissue
Minor abrasions can rupture superficial blood vessels
Residual brownish discolouration from hemosiderin deposition

203
Q

What is a sign of malignancy in seborrhoeic keratosis

A

Leser-Trélat sign - abrupt appearance of multiple seborrhoeic keratoses that rapidly increase in their size and number.

204
Q

What is Leser-Trélat sign associated with

A

Malignant acanthosis nigricans

205
Q

List the presentations of seborrhoeic keratoses

A

Benign lesion
Large, greasy, looks stuck on

206
Q

What is keratosis pilaris

A

Retained keratin plugs in the hair follicles

207
Q

List the presentations for keratosis pilaris. Where is it most commonly found? What are the exacerbating factors?

A

Small, painless papules
Roughened skin texture
Mottled perifollicular erythema
Most commonly on the posterior surface of arm
Exacerbated in cold, dry weather

208
Q

What is miliaria

A

Heat rash
Blockage of the eccrine sweat ducts in heat and humidity.

209
Q

How does Miliaria present

A

Small, thin-walled vesicles.
Patches of erythematous papules/pustules.

210
Q

What are glomus tumours (paraganglioma)

A

Benign tumors that arise from modified smooth muscle cells of the glomus body.
(Involved in dermal thermoregulation)

211
Q

Give the presentation of glomus tumours

A

Small, solitary, painful, blue-red papules/nodules located on the hand, foot, or under the nails in the patients 20-40 years of age.
Paroxysmal, severe pain exacerbated by cold.

212
Q

What is pyogenic granuloma

A

Benign vascular skin tumor.
Consists of abnormal capillaries and granulation tissue.

213
Q

Give the presentation of pyogenic granuloma

A

Small red papule that grows rapidly over weeks/months to a pedunculated/sessile shiny mass.
On the hands, trunk, oral mucosa/gingiva.
Bleed with minor trauma.

214
Q

In what population does pyogenic granuloma particularly occur

A

pregnant women

215
Q

What is the most common benign vascular proliferation in adults

A

Cherry hemangioma

216
Q

List the common drugs associated with photosensitivity reactions

A

Tetracyclines eg. doxycycline
Amiodarone
Antipsychotics
* Chlorpromazine
* Prochlorperazine
Diuretics
* Furosemide
* Hydroclorothiazide
Promethazine

217
Q

List the presentations of photosensitivity

A

Erythema
Pain
Bullae formation
Sun-exposed areas

218
Q

Give the presentations of Epidermolysis bullosa

A

Epithelial fragility triggered by minor trauma
Bullae
Erosions
Ulcers.
Friction induced.
Palms and soles.
Chronic thickening of the skin of the feet.
Infants: oral blisters with bottle-feeding.

219
Q

Describe the 4 subtypes of Epidermolysis bullosa. Which subtype is the most common

A

Simplex (most common) - fragility defect in the epidermis (AD)
Junctional - fragility defect in lamina lucida (AR)
Dystrophic - fragility defect below the lamina densa of the basement membrane zone (AD/AR)
Kindler syndrome - fragility in any plane of the dermo-epidermal junction (AR)

220
Q

What conditions are associated with acanthosis nigricans

A

Insulin resistance
Gastrointestinal malignancy

221
Q

What conditions are associated with multiple skin tags

A

Insulin resistance
Pregnancy
Crohn disease (perianal tags)

222
Q

What skin signs are associated with coeliac disease

A

Dermatitis herpetiforms

223
Q

What skin conditions are associated with Hepatitis C

A

Porphyria cutanea tarda
Cutaneous leukocytoclastic vasculitis (palpable pupura) 2ndary to cryoglobulinemia

224
Q

List the skin conditions associated with HIV infection

A

Sudden onset severe psoriasis
Recurrent herpes zoster
Disseminated molluscum contagiosusm
Severe seborrhoeic dermatitis

225
Q

What skin condition is associated with GI malignancy

A

Explosive onset of multiple itchy seborrhoeic keratosis

226
Q

What skin condition is associated with inflammatory bowel disease

A

Pyoderma gangrenosum

227
Q

What is erythema multiforme predominantly caused by

A

HSV1

228
Q

How does erythema multiforme present

A

Classic ‘target’ lesions present as concentric rings of colour variation which develop symmetrically in an acral distribution, with or without involvement of mucous membranes.

229
Q

List the presentation for Epidermal inclusion cyst

A

Dome-shaped, firm, and freely movable cyst or nodule with a central punctum.
Lined with squamous epithelium that contains a semisolid core of keratin and lipid.
On face, neck, scalp, or trunk.
Gradually increases in size and produces a cheesy white discharge.

230
Q

List the presentation for Sweet syndrome (acute febrile neutrophilic dermatosis)

A

Abrupt onset of painful edematous papules, plaques, or nodules on the head, neck, and upper extremities.
High or moderate fever
Tiredness and malaise
Sore eyes and/or mouth ulcers
Arthralgia
Headache

231
Q

What is Sweet syndrome (acute febrile neutrophilic dermatosis) associated with

A

Hematological malignancies
Upper respiratory and GI infections
IBD

232
Q

List the clinical features of dyshidrotic eczema

A

Recurrent, acute episodes
Deep seated, pruritic vesicles and bullae at hands and feet

233
Q

List the biopsy findings in dyshidrotic eczema

A

Intraepideral spongiosis
Lymphocytic infiltrate

234
Q

Which kind of hypersensitivity reaction is urticaria

A

Type 1

235
Q

List the burns severity grading

A

1st degree - superficial epidermis.
o Blanches on pressure and refills.
o Healing within 3 to 6 days without scarring.

2nd degree - dermis.
o 2a blanches on pressure and refills, 2b doesn’t.
o Both have vesicles/ bullae.
o Healing takes 3 weeks or more, with hypopigmentation/hyperpigmentation.
o Scarring with 2b.

3rd degree - Subcutaneous tissue.
o No pain. Black, white, leather-like skin (eschar).
o Does not heal by itself.

4th degree - muscle, fat, bone.
o Charred tissue.
o Dead needs amputation.

236
Q

List the systemic effects of burns

A

SIRS and DIC
ARDS and hypovolemic shock.
Hypermetabolic state.
Hypothermia, dehydration due to evaporative fluid loss.
Hemoglobinuria, myoglobinuria due to hemolysis and muscle
damage - acute tubular necrosis.

237
Q

When does systemic effects occur in burns

A

Burns more than 30% of BSA

238
Q

When does Hypermetabolic response in burn injury occur

A

Within 5 days of injury, after an initial 24-48 hours of shock.

239
Q

Give the pathophysiology of Hypermetabolic response in burn injury

A

Increased inflammatory mediators results in increased catecholamines, glucocorticoids and glucagon

240
Q

List the clinical features of Hypermetabolic response in burn injury

A

Hyperdynamic circulatory response: tachycardia, hypertension
Increased Gluconeogenesis and insulin resistance - hyperglycemia
Increased Basal metabolic rate - increased basal body temperature
Increased Protein and lipid catabolism - increased lean muscle wasting

241
Q

List the management options in Hypermetabolic response in burn injury

A

Beta blockade to blunt the catecholamine effect.
Earty burn excision and grafting
Glycemic control - insulin
Nutritional support and anabolic steroid therapy

242
Q

What should patients with inhalation injury receive empirical treatment with? What is it for?

A

Cyanide toxicity.
IV hydroxocobalamin (binds cyanide and excreted in urine)

243
Q

What is the preferred fluid for burn victims

A

Lactated Ringer solution

244
Q

What is inhalation injury in burns caused by

A

Glottic edema from the heat and airway irritation due to particulate matter found in smoke
Oedema may cause airway obstruction

245
Q

List the causative organisms for burn wound sepsis by timeline

A

Immediately after burn: gram-positive organisms.
After more than 5 days: gram-negative organisms / fungi.

246
Q

What population is at high risks for burn wound sepsis

A

> 20% surface area burns

247
Q

List the clinical presentations for burn wound sepsis

A

Earliest sign: change in appearance of the wound or loss of viable skin graft.
Temperature <36.5 or >39.
Progressive tachycardia; HR >90.
Progressive tachypnea; RR >30.
Refractory hypotension; SBP <90.
Signs of SIRS:
▪ Oliguria.
▪ Hyperglycemia.
▪ Thrombocytopenia.
▪ Altered mental status.
▪ Hypothermia (<36)

248
Q

Describe two categories of burn wound sepsis

A

Invasive:
▪ Systemic manifestations - confusion and tachycardia.
▪ Biopsy - microbial invasion into unburned tissue.
Noninvasive:
▪ Minimal or no systemic symptoms.

249
Q

List the investigations for burn wound sepsis

A

Quantitative wound culture (>10^5 bacteria/g of tissue).
Biopsy for histopathology to determine depth

250
Q

Give the treatment in burn wound sepsis

A

Broad-spectrum IV antibiotics
* Pip-tazo
* Carbapenem

251
Q

What are dermatophytes

A

Fungal organisms that require keratin for growth

252
Q

List the host factors for dermatophyte infection

A

Genetic susceptibility, including atopy
Ethnicity
Immunosuppression (HIV, corticosteroids)
Skin diseases that disrupt the epidermis (eg. atopic dermatitis)
Predisposing illnesses
* diabetes mellitus
* peripheral vascular disease

253
Q

List the local factors for dermatophyte infection

A

Sweating
Occlusion
Occupational exposure
High humidity
Exposure to infected animals, fomites, skin contact with the floors of public bathing facilities
Contact sports

254
Q

List the sites of dermatophyte infections

A

Hair, hair follicle and perifollicular skin
* tinea capitis
* tinea barbae
* Majocchi’s (trichophytic) granuloma
Keratinised epidermal skin
* tinea faciale
* tinea corporis
* tinea cruris
* tinea manuum
* tinea pedis
Nail apparatus: tinea unguium

255
Q

List the presentations for tinea corporis

A

Scaly, erythematous, pruritic patch with centrifugal spread
Subsequent central clearing with raised,
annular border

256
Q

Give the first line management for localised and extensive tinea coporis

A

Localised: Topical antifungals (clotrimazole, terbinafine)
Extensive: Oral antifungals (terbinafine, griseofulvin)

257
Q

What is tinea corpora’s commonly caused by

A

Trichophyton rubrum

258
Q

What is tinea versicolor commonly caused by

A

Malassezia furfur

259
Q

List the presentations for tinea versicolor

A

Hypo- or hyperpigmented coalescing scaly macules on the trunk and upper arms
Most common in the summer months in adolescents and young adults
Relapsing

260
Q

Give the investigation and findings in tinea versicolor (pityriasis versicolor)

A

KOH preparation shows hyphae and yeast cells in a spaghetti and meatball pattern

261
Q

List the treatments for tinea versicolor (pityriasis versicolor)

A

Topical ketoconazole, terbinafine, selenium sulfide

262
Q

In what population is tinea capitis most common in

A

African American children

263
Q

List the clinical features in tinea capitis

A

Scaly, erythematous patch with hair loss on scalp
Black dots in affected area
Tender lymphadenopathy

264
Q

Give the management options in tinea capitis

A

Oral griseofulvin or terbinafine

265
Q

Give the pathophysiology for pemphigus

A

IgG autoantibodies against desmoglein 3 (Dsg3) and/or desmoglein 1 (Dsg1) on the cell surface of epidermal keratinocytes.

266
Q

List the three classes of pemphigus. Which one is the most common?

A

pemphigus vulgaris (most common)
pemphigus foliaceus
paraneoplastic pemphigus

267
Q

Give the presentation for pemphigus vulgaris

A

Oral mucosal lesions - painful, persisting erosions that interfere with eating.
Flaccid blisters with clear content. Blisters develop on non-erythematous skin, quickly transforming into postbullous erosions.
Blisters and erosions predominate at seborrhoeic areas (chest, face, scalp, interscapular region) and on the extremities.

268
Q

List the investigations and findings for pemphigus vulgaris

A

IgG autoantibodies against desmoglein 3 (Dsg3)
Histology - acantholysis (loss of cell-cell adhesion) superior to the basement membrane of the skin in the lower portion of the epidermis

269
Q

List the presentations for Pemphigus foliaceus

A

Transient, flaccid blisters or crusty erosions in seborrhoeic skin areas (chest, scalp, face, interscapular region).
No mucosal involvement.

270
Q

List the investigations and findings for Pemphigus foliaceus

A

IgG autoantibodies against desmoglein 1 (Dsg1)
Histology - acantholysis at the level of the stratum corneum

271
Q

When does paraneoplastic pemphigus occur?

A

Presents in the context of concomitant malignancy
* Non-Hodgkin’s lymphoma
* Chronic lymphocytic leukaemia
* Thymoma
* Castleman’s disease

272
Q

List the presentations for Paraneoplastic pemphigus

A

Mucosal involvement: cheilitis and/or ulcerative stomatitis, persisting painful erosions that lead to severe dysphagia
Cicatricial conjunctivitis, keratitis, and genital and pharyngeal involvement
Cutaneous polymorphic lesions

273
Q

What is a characteristic and life-threatening complication of Paraneoplastic pemphigus

A

Pulmonary involvement
* Alveolitis
* Bronchiolitis obliterans
* Pulmonary fibrosis

274
Q

List the histology findings in Paraneoplastic pemphigus

A

Epidermal acantholysis, dyskeratosis, and vacuolar interface changes
Epidermal intercellular deposition of IgG and C3, with or without linear deposition at the basement membrane zone
Serum autoantibodies to epithelia
Autoantibodies to several cytoplasmic proteins of the plakin family

275
Q

List the first line management options in pemphigus

A

Rituximab
Corticosteroids

276
Q

List the risk factors for Porphyria cutanea tarda

A

Alcohol use
Smoking
Hepatitis C
HIV
Iron overload
* Haemochromatosis
* Myelofibrosis
* End-stage renal disease
Oestrogen treatment
Uroporphyrinogen decarboxylase (UROD) mutations

277
Q

List the pathophysiology for Porphyria cutanea tarda

A

In iron overload and oxidative stress, uroporphyrinogen is partially oxidised to form uroporphomethene, which is a competitive inhibitor of hepatic UROD.
UROD deficiency in the liver
Substrates for the deficient UROD, porphyrinogens (reduced porphyrins), accumulate in the liver, are oxidised to porphyrins, transported to the skin, and cause photosensitivity.

278
Q

List the clinical features of Porphyria cutanea tarda

A

Blistering and crusted skin lesions on the back of hands and other sun-exposed areas of the body.
Skin fragility, with minor trauma causing blister formation
Hypertrichosis
Skin hyperpigmentation
Dark or reddish urine (porphyrin)

279
Q

List the investigations and findings for Porphyria cutanea tarda

A

Urine / plasma porphyrin levels - elevated
Serum ferritin and liver biopsy - elevated
Elevated LFT

280
Q

List the management for Porphyria cutanea tarda

A

(Remission usually within 6 months)
Repeated phlebotomy - reduce iron stroes
Low-dose hydroxychloroquine / chloroquine

281
Q

What is the most common non-melanoma skin cancer

A

basal cell carcinoma

282
Q

List the medical risk factors for basal cell carcinoma

A

xeroderma pigmentosum
nevoid basal cell carcinoma (Gorlin-Goltz) syndrome
transplantation (particularly solid organ)

283
Q

List the presentations for xeroderma pigmentosum

A

severe photosensitivity
skin pigmentary changes
malignant tumor development
occasionally progressive neurologic degeneration

284
Q

Give the inheritance and genetic defect in xeroderma pigmentosum

A

autosomal recessive, mutations in nucleotide excision repair

285
Q

List the presentations for nevoid basal cell carcinoma (Gorlin-Goltz) syndrome

A

development of multiple BCCs often at a young age
associated with skin tags and cysts, jaw cysts, skin pits, bone changes, fibromas, and medulloblastoma

286
Q

List the clinical presentations for basal cell carcinoma

A

Pearly white/pink papulo-nodule or firm plaque.
Prominent solar damage or history of considerable UV radiation exposure.

287
Q

List the histology findings in basal cell carcinoma

A

Dermal masses of varying sizes and shapes composed of basophilic cells with large oval rather uniform nuclei and scant cytoplasm.
Peripheral palisading

288
Q

Name the precursor lesion in squamous cell carcinoma

A

actinic keratosis

289
Q

List the risk factors for squamous cell carcinoma

A

UV exposure
Ionising radiation
Burns
Hereditary skin conditions
Environmental toxins eg. arsenic, soot, tar
Human papillomavirus
Immunocompromised states

290
Q

List the classifications for squamous cell carcinoma

A

Actinic keratosis: precursor lesions to SCCs
SCC in situ (Bowen’s disease): confined to outer layer of skin
Invasive SCC: spread into deeper layers of skin
Metastatic SCC: spread to other parts of body

291
Q

List the presentation for actinic keratosis

A

skin-coloured, yellowish, or erythematous, irregularly shaped, small, “sandpaper” scaly macules or plaques localised to sun-exposed areas of the body

292
Q

List the presentations for SCC in situ (Bowen’s disease). Where is it most commonly found?

A

thin, flesh-coloured or erythematous plaques that often have scale or haemorrhagic crust

Most commonly detected on head and neck (84%) and extensor upper extremities (13%)

293
Q

List the presentations for invasive SCC

A

exophytic and sometimes ulcerated tumours.

294
Q

Where does metastatic SCC commonly spread to

A

Regional lymph nodes (85%)
Lungs, liver, brain, skin, bone

295
Q

List the symptoms for metastatic SCC

A

lymphadenopathy, bone pain, hepatomegaly

296
Q

List the three variants of SCC

A

Keratoacanthoma
Verrucous carcinoma
Marjolin ulcer

297
Q

List the presentations for Keratoacanthoma

A

Rapidly growing, dome-shaped nodule with a central keratin-filled crater.
Usually grows over weeks to months and involutes after 2 to 3 months.

298
Q

List the presentations for Verrucous carcinoma

A

Exophytic, fungating, verrucous nodules, or plaques on skin or mucosa.
Usually occurs in oral cavity, genitals, and feet

299
Q

List the presentations of Marjolin ulcer

A

Aggressive, ulcerating SCC that arises in chronic wounds, burns, scars, or ulcers

300
Q

List the histology findings in actinic keratosis

A

Atypical keratinocytes that appear to crowd the basal layer and lower levels of the epidermis, but do not extend to full thickness.

301
Q

List the histology findings in invasive SCC

A

Extend beyond the basement membrane, penetrate into the dermis, and may invade deeper structures.
Atypical keratinocytes have variable large, hyperchromatic nuclei, and mitotic figures
May present as spindle cell tumours
Solar elastosis

302
Q

List the histology findings in SCC in situ (Bowen’s disease)

A

Full-thickness atypia in the epidermis, with an intact basement membrane.

303
Q

List the managements in SCC

A

Topical chemotherapy with fluorouracil-based regimens
Surgical excision
Radiotherapy

304
Q

In which age group does melanoma incidence peak?

A

> 70 years

305
Q

List the risk factors for melanoma

A

Personal or family history of melanoma
Personal history of skin cancer (including actinic damage)
Fitzpatrick skin type I or II (white skin)
Light eye colour
High freckle density
Red or blond hair
Prior sunbed use
Childhood history of sunburns
Large number of melanocytic naevi
Presence of atypical melanocytic naevi (dysplastic naevi)
Presence of large (>20 cm) congenital melanocytic naevi
Genetic syndromes with skin cancer predisposition (e.g., xeroderma pigmentosum)
Immunosuppression

306
Q

List the four types of melanoma

A

Superficial spreading melanoma (MOST COMMON)
Nodular melanoma
Lentigo maligna melanoma
Acral lentiginous melanoma

307
Q

Where is Superficial spreading melanoma most commonly found in men and women

A

Torso in men
Legs in women

308
Q

Where does acral lentiginous melanoma arise from

A

Palms, soles, and nail apparatusL

309
Q

List the clinical features of melanoma

A

ABCDE
Asymmetry
Border irregularity
Colour variability
Diameter >6 mm
Evolution over time

310
Q

List the common metastasis sites of melanoma

A

Skin and subcutaneous tissue
Lungs
Liver
Bones
Brain

311
Q

List the dermoscopy findings in melanoma

A

Atypical globules and dots of different sizes and shapes
Patches of atypical network
Blue-white veil

312
Q

Give the aetiology of Kaposi’s sarcoma

A

human herpesvirus-8 (HHV-8) + immunodeficiency

313
Q

List four epidemiological forms of Kaposi’s sarcoma

A

Classic (sporadic)
Endemic (observed in sub-Saharan Africa)
Epidemic (AIDS-related)
Iatrogenic (transplant-related)

313
Q

List the presentations for Kaposi’s sarcoma

A

Cutaneous lesions - painless, non-pruritic
Gastrointestinal KS
* Weight loss
* Abdominal pain
* Nausea and vomiting
* Ileus
* Upper or lower GI tract bleeding
* Malabsorption
* Intestinal obstruction
Pulmonary KS
* Dyspnoea
* Fever
* Cough
* Haemoptysis
* Chest pain

314
Q

List the investigations of Kaposi’s sarcoma

A

HIV test
CD4+ T-cell count and HIV viral load
Skin biopsy

315
Q

What causes chloracne

A

Dioxins (Halogenated aromatic hydrocarbon)
* Most commonly found in fungicides, insecticides, herbicides

Medicine (8 decks)

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