Dermatology Flashcards
USMLE (317 cards)
1
Q
List the symptoms for erythroderma (skin failure)
A
Thirst
Fever and chills
Malaise
Dizziness
2
Q
List the causes for erythroderma
A
Atopic eczema
Seborrhoeic eczema
Psoriasis
Drugs
* Sulphonamides
* Penicillin
* Gold
* Sulphonylureas
* Allopurinol
* Captopril
Idiopathic
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
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).
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
6
Q
List the risk factors for acne
A
Positive family history
Ethnicity
Diet - high glycaemic index
Hormone
* Hyperandrogenism
* Polycystic ovarian syndrome
* Menstruation
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.
8
Q
List the presentations of acne fulminans
A
(variable systemic manifestations)
Fever
Arthralgias, Myalgias
Hepatosplenomegaly
Osteolytic bone lesions
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
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
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)
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
13
Q
What is hidradenitis suppurativa
A
Chronic inflammatory disorder that affects the apocrine pilosebaceous follicles of the axillae, inguinal and breasts
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
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
16
Q
Where does rosacea predominantly affect
A
The convexities of the centrofacial region (cheeks, chin, nose, and central part of forehead).
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
18
Q
List the signs of ocular rosacea
A
Lid margin telangiectasia
Blepharitis
Conjunctivitis
Keratitis, scleritis, iritis
Anterior uveitis
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.
20
Q
Give the first line treatment for persistent erythema in rosacea
A
Topical brimonidine 0.5% gel once daily as needed (alpha agonist)
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
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
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
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.
25
In which diseases are seborrhoeic eczema prevalence increased
Parkinson's disease
HIV
26
Give the aetiology in seborrhoeic eczema
Malassezia (lipophilic commensal yeast) triggers inflammatory skin changes
27
Give the management in seborrhoeic eczema
Topical azole cream (fluconazole, clotrimazole) + short-term mild-moderate-potency steroids
28
List the presentations for venous eczema
Usually elderly and varicose veins / history of venous thrombosis
Involves the inner calf and coexistent signs of venous hypertension
* Hemosiderin deposition
* Lipodermatosclerosis
* Varicose ulceration
29
Give the management for venous eczema
Bland emollients + short-term moderately potent topical steroid
30
Give the presentations for asteatotic eczema
Affects older people in wintertime and can be intensely pruritic.
Involves the lower legs, lower back and other areas that have few sebaceous glands.
31
Give the management in asteatotic eczema
Bland moisturiser and soap substitute
32
List the presentations for discoid eczema
Well-demarcated, inflamed scaly patches, sometimes with tiny vesicles.
Usually affects the limbs and torso, intensely itchy.
33
Give the management for discoid eczema
Potent topical steroids
34
List the common sites of lichen simplex
nape of the neck
outer calves
anogenital area
35
What is lichen simplex
Chronic eczema thickened and lined (lichenified) skin in response to repeated rubbing and scratching.
36
List the management for lichen simplex
Potent / superpotent topical steroid and topical antipruritics (menthol)
37
What age group does atopic eczema most commonly present
Early childhood (< 5 years of age)
38
What is atopic eczema characterised by
Dry, pruritic skin
Episodes of flares and remissions
39
What is contact dermatitis/eczema caused by
External harsh substance (irritant) or allergy-provoking substance (allergen)
40
List the common contact allergens in contact dermatitis / eczema
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
41
List the triggering factors in atopic eczema
Soap and detergents
Animal dander
House-dust mites
Extreme temperatures
Rough clothing
Pollen
Certain foods
Skin infections
Stress
42
What makes an individual genetically susceptible to atopic eczema
Filaggrin mutation
43
What are the associated comorbidities in atopic eczema
Atopic
* Asthma
* Allergic rhinitis (hay fever)
* Food allergy
* Eosinophilic oesophagitis
Non-atopic
* Allergic contact dermatitis
* Obesity
* Cardiovascular disease
44
List the complications of atopic eczema
S. aureus infection (typical impetigo or worsening of eczema)
Eczema herpeticum
Superficial fungal infections
Psychosocial problems
45
Lise the presentation for eczema herpeticum
Disseminated herpes simplex infection
Fever, lymphadenopathy, malaise
46
List the risk factors for eczema herpeticum
Early-onset and severe atopic eczema
Marked elevations in total IgE
Elevated allergen-specific IgE levels
Peripheral eosinophilia
Presence of filaggrin mutations
47
Give the management in eczema herpeticum
Urgent systemic antiviral therapy
48
Give the NICE diagnostic criteria for atopic eczema
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
49
List the eczema severity grading
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
50
List the management for mild, moderate, and severe eczema
(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)
51
List the first line options for infected eczema
Flucloxacillin
If penicillin allergy / flucloxacillin resistance: clarithromycin
If penicillin allergy + pregnant: erythromycin
If localised areas of infection: topical fusidic acid
52
List the classification of topical corticosteroids by potency
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
53
List the adverse effects of topical steroids
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)
54
List the management options for severe itch in atopic eczema
Non-sedating antihistamine
* cetirizine
* loratadine
* fexofenadine
55
List three pathogenic factors in psoriasis
Epidermal hyperproliferation
Abnormal keratinocyte differentiation
Lymphocyte inflammatory infiltrate
56
Give the presentation of Guttate psoriasis
small, scattered, round or oval (2mm~1cm in diameter, water drop appearance) scaly papules, which may be pink or red
57
What is guttate psoriasis strongly associated with
Streptococcal URTI
58
What age group does Guttate psoriasis most commonly affect
Children, teenagers and young adults
59
List the presentations in nail psoriasis
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
60
List the complications of psoriasis
Erythrodermic psoriasis
Generalised pustular psoriasis
Pregnancy complications - increased risks of
* Miscarriage / Stillbirth
* Preterm delivery
* Low birthweight
Psychosocial effects
61
Give the presentations of generalised pustular psoriasis
(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
62
In which type of psoriasis does generalised pustular psoriasis usually present in
People with existing / previous chronic plaque psoriasis
63
List the presentations for erythrodermic psoriasis
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)
64
Give the management in psoriasis
Emollient
Potent topical corticosteroid + topical vitamin D preparation
65
Give the presentation in chronic plaque psoriasis
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
66
What can erythrodermic psoriasis be precipitated by
Systemic infection
Irritants eg. coal tar, ciclosporin
Phototherapy
Sudden withdrawal of corticosteroids
67
Which age group is Pityriasis rosea most common in
Teenagers and young adults (10-35 years)
68
List the causes of Pityriasis rosea
Herpesviruses 6 and 7 (HHV-6/7)
Drugs
* ACEi
* NSAIDs
* hydrochlorothiazide
* gold
* atypical antipsychotics
* barbiturates
* D-penicillamine
* imatinib
* metronidazole
* isotretinoin
Vaccines
69
What time of the year does pityriasis rosea have increased incidence
Spring and autumn
70
List the characteristics of rash in Pityriasis rosea
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
71
List the presentations in Polymorphic light eruption (‘prickly heat’)
Itchy papular rash develops on sun-exposed areas
* ‘V’ of the neck
* Shoulders and arms
72
Give the management in Polymorphic light eruption (‘prickly heat’)
Short course prednisolone
73
List the presentations in lichen planus
Clusters of intensely pruritic, purple–pink, polygonal papules
Flexural aspect of wrists, forearms and lower legs
Fine white streaks (Wickham’s striae)
74
List the potential triggers for lichen planus
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
75
List the typical features of urticaria
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.
76
How does urticaria differentiate from other inflammatory rashes eg. eczema
Shorted-lived, lack of skin surface changes
77
What's difference between angio-oedema and urticaria
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.
78
List the classifications for urticaria
Acute - < 6 weeks
Chronic - > 6 weeks
* Chronic spontaneous urticaria
* Chronic inducible urticaria
79
Give the pathophysiology of urticaria
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
80
List the acute urticaria triggers
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
81
What can chronic inducible urticaria caused by
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.
82
List the presentations for vasculitic urticaria
Lesions remain for longer than 24 hours
Painful, non-blanching, palpable
Systemic symptoms - fever, malaise, arthralgia
83
List the management options for urticaria
Non-sedating antihistamine (cetirizine, fexofenadine, loratadine)
Prednisolone 40 mg daily for up to 7 days
84
How long does impetigo heal without treatment
7~21 days
85
Describe the presentation of non-bullous impetigo. Where does it most commonly affect?
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
86
Describe the presentation of bullous impetigo. Where does it most commonly affect?
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
87
Give the first line management for localised impetigo
Hydrogen peroxide 1% cream
88
Give the first line management options for widespread non-bullous impetigo
(three times daily for 5 days)
Topical fusidic acid 2%
Topical mupirocin 2%
89
Give the first line management options for non-bullous impetigo + systemically unwell / high risks of complications.
Give the alternatives in penicillin allergy and pregnancy.
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
90
Give the first line management options for bullous impetigo.
Give the alternatives in penicillin allergy and pregnancy.
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
91
Give the main causative organism in impetigo
S aureus
92
List the presentation of cellulitis. Where does it most commonly affect?
Pain, warmth, swelling, erythema
Blisters, bullae
Fever, malaise, nausea, rigors
93
How may pseudomonas aeruginosa cellulitis be contacted
contaminated hot tubs, sponges, nail puncture wound
94
How may vibrio vulnificus cellulitis be contacted
salt water exposure
95
How may mycobacterium marinum cellulitis be contacted
aquarium keepers
95
How may aeromonas hydrophila cellulitis be contacted
freshwater exposure
96
List the common causative organisms for cellulitis in people with injury, burns, and co‐existing diseases (immunocompromised, diabetes mellitus, cancer, malnutrition)
Streptococcus pneumoniae
Haemophilus influenzae
Gram-negative bacilli
Anaerobes
97
List the risk factors for cellulitis
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.
98
List the acute complications for cellulitis
Deep-seated infection
* Necrotising fasciitis
* Myositis
Sepsis
Subcutaneous abscess
Post-streptococcal nephritis
99
List the chronic complications for cellulitis
Persistent leg ulceration
Lymphoedema
Recurrent cellulitis
100
Give the presentation of necrotising fasciitis
Severe pain that is out of proportion to the apparent signs of skin inflammation.
Febrile, severely unwell.
101
Give the management for necrotising fasciitis
Surgical debridement / amputation
IV antibiotics - High-dose benzylpenicillin + clindamycin (GAS infection)
102
Give the classification for cellulitis
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.
103
Give the first line management for cellulitis. Give alternatives in penicillin allergy and pregnancy.
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.
104
Give the first line management for cellulitis near the eyes or nose. Give alternatives in penicillin allergy.
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
105
Describe the presentation of boils (furuncles) and carbuncles
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.
106
List the causes of boils (furuncles) and carbuncles.
What is the most common cause?
Staphylococcus aureus - most common
* MRSA
* PVL-SA
Streptococcus pyogenes
Enterobacteriaceae
Enterococci
107
List the risk factors for Boils (furuncles) and carbuncles
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.
108
Give the complications of Boils (furuncles) and carbuncles
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)
109
Define Staphylococcal carriage
Asymptomatic carriage of S aureus on skin or mucous membranes.
110
List the risk factors for Staphylococcal carriage
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.
111
List the complications for Staphylococcal carriage
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
112
What skin conditions is Panton-Valentine leukocidin S. aureus (PVL-SA) associated with
Recurrent boils and carbuncles
Necrotizing pneumonia
Necrotizing fasciitis
Osteomyelitis
Septic arthritis
Purpura fulminans
113
Give the management for nasal Staphylococcal carriage
Naseptin cream (chlorhexidine + neomycin)
114
Give the management for skin Staphylococcal carriage
Antiseptic preparation (chlorhexidine 4% body wash + Triclosan 2%) daily as liquid soap for 5 days
115
Describe the presentation for ecthyma
Chronic, well-demarcated, deep ulcers with a necrotic crust and exudate.
116
What is ecthyma associated with
Malnutrition and poor hygiene eg. IVDU
117
Give the presentation for Ecthyma gangrenosum
Distinctive necrotic skin ulcers with central thick, dark brown/black eschar
118
What is ecthyma gangrenosum typically caused by
Pseudomonas septicaemia in an immunocompromised
119
What is erythrasma
superficial skin infection caused by Corynebacterium minutissimum
120
Describe the presentation for erythrasma
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)
121
Give the management for erythrasma
Topical / oral macrolides
122
List the presentation for Pitted keratolysis
Mltiple punched-out areas and maceration of the skin on weight-bearing plantar surfaces
Associated with
* Hyperhidrosis
* Malodour
123
List the management options for Pitted keratolysis
Potassium permanganate soaks
Antiperspirants
Topical imidazoles / fusidic acid
124
Give the causative organism for head lice infestation
pediculosis capitis
125
List the presentations for head lice
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
126
List the management options for head lice
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
Name the causative organism in scabies
Sarcoptes scabiei
128
Which type of hypersensitivity is itch in scabies
Delayed type-IV hypersensitivity reaction to the mite/mite products (faeces, eggs).
129
How is scabies transmitted
Close/prolonged skin contact with infected person
Sexually acquired
Shared clothing/bedding
Dogs and cats
130
List the risk factors for scabies
Closed contact with infested person
Poverty and social deprivation
Crowded living conditions
Winter months
131
Give the pathognomonic sign in scabies
the burrow (thin, brown-grey line of 0.2–1 cm in length)
132
Give the management in scabies
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
Give the management for resistance scabies
Oral ivermectin
134
What is chicken pox caused by
varicella-zoster virus
135
When is chicken pox infectious
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
Where does varicella-zoster virus persist in and years later reactivate to cause herpes zoster (shingles)
Sensory dorsal root ganglia
137
List the complications of chicken pox in children
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
List the complications of chicken pox in adults
Varicella pneumonia
Hepatitis
Encephalitis
139
List the presentations of Fetal varicella syndrome
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
List the complications of chicken pox in immunocompromised
Severe disseminated chickenpox with haemorrhagic complications
Varicella pneumonia
Hepatitis
Encephalitis
Disseminated intravascular coagulopathy
141
List the complications of chicken pox in neonates
Disseminated / hemorrhagic varicella
142
List the clinical features of chicken pox
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
Give the management for chicken pox
Oral aciclovir 800 mg 5 times a day for 7 days
144
List the risk factors for shingles
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
List the complications for shingles
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
List the typical clinical features in shingles
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
What is Hutchinson's sign in shingles. What is it a prognostic factor of
Rash on the tip/side/root of the nose (nasociliary nerve dermatome)
Prognostic for subsequent eye inflammation and permanent corneal denervation
148
Give the management for shingles
Antiviral treatment within 72 hours of rash onset - aciclovir, famiciclovir, valaciclovir
149
What is measles caused by
Morbillivirus of the paramyxovirus family
150
How long is the typical incubation period of measles
10 days
151
How long are the prodromal symptoms for measles
2~4 days
152
When is measles infectious
From when symptoms first appear (~4 days before the rash appears) to 4 days after onset of the rash.
153
How is measles transmitted
Direct contact with infectious droplets
Airborne (breathing, coughing, sneezing)
154
List the complications for measles
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
List the presentations for Herpes zoster oticus (Ramsay Hunt syndrome) - virus infects CNVII
Lesions in the ear
Facial paralysis
Hearing and vestibular symptoms
156
List the presentation for Herpes zoster ophthalmicus - virus infects V1
Keratitis, conjunctivitis, retinitis
Corneal ulceration
Optic neuritis
Glaucoma
Blindness
157
List the typical features in mealses
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
List the characteristics of measles rash
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
How is measles infection confirmed
IgM/IgG
Viral RNA testing
160
List the management plan for measles
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
What is Molluscum contagiosum caused by
molluscum contagiosum virus (Poxviridae family)
162
How is Molluscum contagiosum transmitted
Direct contact with infected skin
Contaminated fomites
Vertical transmission
163
List the complications for Molluscum contagiosum
Pruritus and erythema
Scarring
Secondary bacterial infection
Follicular conjunctivitis
Molluscum dermatitis - molluscum lesions surrounded by a halo of eczema (hypersensitivity)
Psychosocial
164
List the features of Molluscum contagiosum
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
Where is Molluscum contagiosum commonly seen in children
trunk, flexures, anogenital
166
How is Molluscum contagiosum managed
Self-limiting
167
What is herpes simplex more commonly caused by
Usually HSV-1, rarely HSV-2
168
Where does the HSV persist?
sensory dorsal root ganglia proximal to the site of infection (typically CNV ganglion)
169
List the presentations for Herpes simplex labialis
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
List the presentations for Herpes gingivostomatitis
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
Give the management for Herpes Simplex
aciclovir, valacivlovir
172
List the presentations for ocular herpes simplex
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
List the complications for genital herpes simplex
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
List the presentations for genital herpes simplex
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
What are the differences between first and recurrent episodes of genital herpes simplex
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
List the subtypes of tines pedis and the most common causative organism
Interdigital - Trichophyton rubrum
Moccasin / dry - Trichophyton rubrum
Vesicobullous - Trichophyton interdigitale
177
List the risk factors for tinea pedis
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
List the complications for tinea pedis
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
List the clinical features in Interdigital, Moccasin/dry, and Vesicobullous tinea pedis
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
List the management for tinea pedis
Topical antifungal cream - clotrimazole, miconazole, econazole
Mildly potent topical corticosteroids - hydrocortisone 1%
181
Give the oral management for severe / extensive tinea pedis
Terbinafine
Alternative: oral itraconazole / oral griseofulvin
182
What is candida part of the commensal flora of
GI tract
Vagina
183
List the clinical features of candidiasis
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
What can candidiasis cause
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
List the management for candidiasis in adults
Topical imidazole (clotrimazole, econazole, miconazole, ketoconazole)
Terbinafine
186
List the management for candidiasis in children
Topical clotrimazole, econazole, miconazole
187
Describe the presentation of erythema nodosum
Painful / tender, dusky bruise-like swellings over the shins, which fade over several weeks.
May be associated with arthralgia, malaise and fever.
188
What is Erythema nodosum caused by
Infection
* Streptococcal
* Chlamydia
* Fungal (histoplasmosis, blastomycosis)
Idiopathic
Drugs (sulphonamides, oral contraceptive pill)
Bacterial gastroenteritis - Salmonella, Shigella, Yersinia
Inflammatory bowel disease
Sarcoidosis
Tuberculosis
Leprosy
189
Give the inheritance in albinism
Autosomal recessive
190
What is albinism caused by
Tyrosinase gene mutation
Tyrosinase oxidises L-tyrosine to DOPA
Mutation causes impaired eumelanin synthesis
191
Give the inheritance in piebaldism
Autosomal dominant
192
List the presentations in piebaldism
isolated congenital leukoderma (white skin) and poliosis (white hair) in a distinct ventral midline pattern
193
List the characteristics of Chediak Higashi syndrome
easy bruising
oculocutaneous albinism
recurrent pyogenic infections
194
Give the pathophysiology of vitiligo
Autoimmune destruction of melanocytes
195
List the clinical presentation for vitiligo
Depigmented macules on extremities and extensor surfaces
Leukotrichia - depigmented hair
Associated with other autoimmune disorders
* diabetes
* hypothyroidism
* pernicious anaemia
* Addison disease
196
List the treatments for vitiligo
Topical corticosteroids
197
List the investigations and findings for vitiligo
Wood lamp test - blue-white areas
Biopsy - absence of melanocytes
198
What is ash leaf spot a sign of
Tuberous sclerosis
199
What is idiopathic guttate hypomelanosis a common finding in
Aging
200
Give the pathophysiology in keloid
Hyperproliferation of fibroblasts
Results in disorganised overproduction of hyalinised collagens types 1 and 3
201
Which population is keloid seen more commonly in
Dark skinned individuals
202
Describe the pathophysiology of senile purpura
Loss of elastic fibres in perivascular connective tissue
Minor abrasions can rupture superficial blood vessels
Residual brownish discolouration from hemosiderin deposition
203
What is a sign of malignancy in seborrhoeic keratosis
Leser-Trélat sign - abrupt appearance of multiple seborrhoeic keratoses that rapidly increase in their size and number.
204
What is Leser-Trélat sign associated with
Malignant acanthosis nigricans
205
List the presentations of seborrhoeic keratoses
Benign lesion
Large, greasy, looks stuck on
206
What is keratosis pilaris
Retained keratin plugs in the hair follicles
207
List the presentations for keratosis pilaris. Where is it most commonly found? What are the exacerbating factors?
Small, painless papules
Roughened skin texture
Mottled perifollicular erythema
Most commonly on the posterior surface of arm
Exacerbated in cold, dry weather
208
What is miliaria
Heat rash
Blockage of the eccrine sweat ducts in heat and humidity.
209
How does Miliaria present
Small, thin-walled vesicles.
Patches of erythematous papules/pustules.
210
What are glomus tumours (paraganglioma)
Benign tumors that arise from modified smooth muscle cells of the glomus body.
(Involved in dermal thermoregulation)
211
Give the presentation of glomus tumours
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
What is pyogenic granuloma
Benign vascular skin tumor.
Consists of abnormal capillaries and granulation tissue.
213
Give the presentation of pyogenic granuloma
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
In what population does pyogenic granuloma particularly occur
pregnant women
215
What is the most common benign vascular proliferation in adults
Cherry hemangioma
216
List the common drugs associated with photosensitivity reactions
Tetracyclines eg. doxycycline
Amiodarone
Antipsychotics
* Chlorpromazine
* Prochlorperazine
Diuretics
* Furosemide
* Hydroclorothiazide
Promethazine
217
List the presentations of photosensitivity
Erythema
Pain
Bullae formation
Sun-exposed areas
218
Give the presentations of Epidermolysis bullosa
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
Describe the 4 subtypes of Epidermolysis bullosa. Which subtype is the most common
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
What conditions are associated with acanthosis nigricans
Insulin resistance
Gastrointestinal malignancy
221
What conditions are associated with multiple skin tags
Insulin resistance
Pregnancy
Crohn disease (perianal tags)
222
What skin signs are associated with coeliac disease
Dermatitis herpetiforms
223
What skin conditions are associated with Hepatitis C
Porphyria cutanea tarda
Cutaneous leukocytoclastic vasculitis (palpable pupura) 2ndary to cryoglobulinemia
224
List the skin conditions associated with HIV infection
Sudden onset severe psoriasis
Recurrent herpes zoster
Disseminated molluscum contagiosusm
Severe seborrhoeic dermatitis
225
What skin condition is associated with GI malignancy
Explosive onset of multiple itchy seborrhoeic keratosis
226
What skin condition is associated with inflammatory bowel disease
Pyoderma gangrenosum
227
What is erythema multiforme predominantly caused by
HSV1
228
How does erythema multiforme present
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
List the presentation for Epidermal inclusion cyst
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
List the presentation for Sweet syndrome (acute febrile neutrophilic dermatosis)
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
What is Sweet syndrome (acute febrile neutrophilic dermatosis) associated with
Hematological malignancies
Upper respiratory and GI infections
IBD
232
List the clinical features of dyshidrotic eczema
Recurrent, acute episodes
Deep seated, pruritic vesicles and bullae at hands and feet
233
List the biopsy findings in dyshidrotic eczema
Intraepideral spongiosis
Lymphocytic infiltrate
234
Which kind of hypersensitivity reaction is urticaria
Type 1
235
List the burns severity grading
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
List the systemic effects of burns
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
When does systemic effects occur in burns
Burns more than 30% of BSA
238
When does Hypermetabolic response in burn injury occur
Within 5 days of injury, after an initial 24-48 hours of shock.
239
Give the pathophysiology of Hypermetabolic response in burn injury
Increased inflammatory mediators results in increased catecholamines, glucocorticoids and glucagon
240
List the clinical features of Hypermetabolic response in burn injury
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
List the management options in Hypermetabolic response in burn injury
Beta blockade to blunt the catecholamine effect.
Earty burn excision and grafting
Glycemic control - insulin
Nutritional support and anabolic steroid therapy
242
What should patients with inhalation injury receive empirical treatment with? What is it for?
Cyanide toxicity.
IV hydroxocobalamin (binds cyanide and excreted in urine)
243
What is the preferred fluid for burn victims
Lactated Ringer solution
244
What is inhalation injury in burns caused by
Glottic edema from the heat and airway irritation due to particulate matter found in smoke
Oedema may cause airway obstruction
245
List the causative organisms for burn wound sepsis by timeline
Immediately after burn: gram-positive organisms.
After more than 5 days: gram-negative organisms / fungi.
246
What population is at high risks for burn wound sepsis
>20% surface area burns
247
List the clinical presentations for burn wound sepsis
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
Describe two categories of burn wound sepsis
Invasive:
▪ Systemic manifestations - confusion and tachycardia.
▪ Biopsy - microbial invasion into unburned tissue.
Noninvasive:
▪ Minimal or no systemic symptoms.
249
List the investigations for burn wound sepsis
Quantitative wound culture (>10^5 bacteria/g of tissue).
Biopsy for histopathology to determine depth
250
Give the treatment in burn wound sepsis
Broad-spectrum IV antibiotics
* Pip-tazo
* Carbapenem
251
What are dermatophytes
Fungal organisms that require keratin for growth
252
List the host factors for dermatophyte infection
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
List the local factors for dermatophyte infection
Sweating
Occlusion
Occupational exposure
High humidity
Exposure to infected animals, fomites, skin contact with the floors of public bathing facilities
Contact sports
254
List the sites of dermatophyte infections
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
List the presentations for tinea corporis
Scaly, erythematous, pruritic patch with centrifugal spread
Subsequent central clearing with raised,
annular border
256
Give the first line management for localised and extensive tinea coporis
Localised: Topical antifungals (clotrimazole, terbinafine)
Extensive: Oral antifungals (terbinafine, griseofulvin)
257
What is tinea corpora's commonly caused by
Trichophyton rubrum
258
What is tinea versicolor commonly caused by
Malassezia furfur
259
List the presentations for tinea versicolor
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
Give the investigation and findings in tinea versicolor (pityriasis versicolor)
KOH preparation shows hyphae and yeast cells in a spaghetti and meatball pattern
261
List the treatments for tinea versicolor (pityriasis versicolor)
Topical ketoconazole, terbinafine, selenium sulfide
262
In what population is tinea capitis most common in
African American children
263
List the clinical features in tinea capitis
Scaly, erythematous patch with hair loss on scalp
Black dots in affected area
Tender lymphadenopathy
264
Give the management options in tinea capitis
Oral griseofulvin or terbinafine
265
Give the pathophysiology for pemphigus
IgG autoantibodies against desmoglein 3 (Dsg3) and/or desmoglein 1 (Dsg1) on the cell surface of epidermal keratinocytes.
266
List the three classes of pemphigus. Which one is the most common?
pemphigus vulgaris (most common)
pemphigus foliaceus
paraneoplastic pemphigus
267
Give the presentation for pemphigus vulgaris
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
List the investigations and findings for pemphigus vulgaris
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
List the presentations for Pemphigus foliaceus
Transient, flaccid blisters or crusty erosions in seborrhoeic skin areas (chest, scalp, face, interscapular region).
No mucosal involvement.
270
List the investigations and findings for Pemphigus foliaceus
IgG autoantibodies against desmoglein 1 (Dsg1)
Histology - acantholysis at the level of the stratum corneum
271
When does paraneoplastic pemphigus occur?
Presents in the context of concomitant malignancy
* Non-Hodgkin's lymphoma
* Chronic lymphocytic leukaemia
* Thymoma
* Castleman’s disease
272
List the presentations for Paraneoplastic pemphigus
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
What is a characteristic and life-threatening complication of Paraneoplastic pemphigus
Pulmonary involvement
* Alveolitis
* Bronchiolitis obliterans
* Pulmonary fibrosis
274
List the histology findings in Paraneoplastic pemphigus
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
List the first line management options in pemphigus
Rituximab
Corticosteroids
276
List the risk factors for Porphyria cutanea tarda
Alcohol use
Smoking
Hepatitis C
HIV
Iron overload
* Haemochromatosis
* Myelofibrosis
* End-stage renal disease
Oestrogen treatment
Uroporphyrinogen decarboxylase (UROD) mutations
277
List the pathophysiology for Porphyria cutanea tarda
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
List the clinical features of Porphyria cutanea tarda
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
List the investigations and findings for Porphyria cutanea tarda
Urine / plasma porphyrin levels - elevated
Serum ferritin and liver biopsy - elevated
Elevated LFT
280
List the management for Porphyria cutanea tarda
(Remission usually within 6 months)
Repeated phlebotomy - reduce iron stroes
Low-dose hydroxychloroquine / chloroquine
281
What is the most common non-melanoma skin cancer
basal cell carcinoma
282
List the medical risk factors for basal cell carcinoma
xeroderma pigmentosum
nevoid basal cell carcinoma (Gorlin-Goltz) syndrome
transplantation (particularly solid organ)
283
List the presentations for xeroderma pigmentosum
severe photosensitivity
skin pigmentary changes
malignant tumor development
occasionally progressive neurologic degeneration
284
Give the inheritance and genetic defect in xeroderma pigmentosum
autosomal recessive, mutations in nucleotide excision repair
285
List the presentations for nevoid basal cell carcinoma (Gorlin-Goltz) syndrome
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
List the clinical presentations for basal cell carcinoma
Pearly white/pink papulo-nodule or firm plaque.
Prominent solar damage or history of considerable UV radiation exposure.
287
List the histology findings in basal cell carcinoma
Dermal masses of varying sizes and shapes composed of basophilic cells with large oval rather uniform nuclei and scant cytoplasm.
Peripheral palisading
288
Name the precursor lesion in squamous cell carcinoma
actinic keratosis
289
List the risk factors for squamous cell carcinoma
UV exposure
Ionising radiation
Burns
Hereditary skin conditions
Environmental toxins eg. arsenic, soot, tar
Human papillomavirus
Immunocompromised states
290
List the classifications for squamous cell carcinoma
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
List the presentation for actinic keratosis
skin-coloured, yellowish, or erythematous, irregularly shaped, small, “sandpaper” scaly macules or plaques localised to sun-exposed areas of the body
292
List the presentations for SCC in situ (Bowen's disease). Where is it most commonly found?
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
List the presentations for invasive SCC
exophytic and sometimes ulcerated tumours.
294
Where does metastatic SCC commonly spread to
Regional lymph nodes (85%)
Lungs, liver, brain, skin, bone
295
List the symptoms for metastatic SCC
lymphadenopathy, bone pain, hepatomegaly
296
List the three variants of SCC
Keratoacanthoma
Verrucous carcinoma
Marjolin ulcer
297
List the presentations for Keratoacanthoma
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
List the presentations for Verrucous carcinoma
Exophytic, fungating, verrucous nodules, or plaques on skin or mucosa.
Usually occurs in oral cavity, genitals, and feet
299
List the presentations of Marjolin ulcer
Aggressive, ulcerating SCC that arises in chronic wounds, burns, scars, or ulcers
300
List the histology findings in actinic keratosis
Atypical keratinocytes that appear to crowd the basal layer and lower levels of the epidermis, but do not extend to full thickness.
301
List the histology findings in invasive SCC
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
List the histology findings in SCC in situ (Bowen's disease)
Full-thickness atypia in the epidermis, with an intact basement membrane.
303
List the managements in SCC
Topical chemotherapy with fluorouracil-based regimens
Surgical excision
Radiotherapy
304
In which age group does melanoma incidence peak?
>70 years
305
List the risk factors for melanoma
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
List the four types of melanoma
Superficial spreading melanoma (MOST COMMON)
Nodular melanoma
Lentigo maligna melanoma
Acral lentiginous melanoma
307
Where is Superficial spreading melanoma most commonly found in men and women
Torso in men
Legs in women
308
Where does acral lentiginous melanoma arise from
Palms, soles, and nail apparatusL
309
List the clinical features of melanoma
ABCDE
Asymmetry
Border irregularity
Colour variability
Diameter >6 mm
Evolution over time
310
List the common metastasis sites of melanoma
Skin and subcutaneous tissue
Lungs
Liver
Bones
Brain
311
List the dermoscopy findings in melanoma
Atypical globules and dots of different sizes and shapes
Patches of atypical network
Blue-white veil
312
Give the aetiology of Kaposi's sarcoma
human herpesvirus-8 (HHV-8) + immunodeficiency
313
List four epidemiological forms of Kaposi's sarcoma
Classic (sporadic)
Endemic (observed in sub-Saharan Africa)
Epidemic (AIDS-related)
Iatrogenic (transplant-related)
313
List the presentations for Kaposi's sarcoma
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
List the investigations of Kaposi's sarcoma
HIV test
CD4+ T-cell count and HIV viral load
Skin biopsy
315
What causes chloracne
Dioxins (Halogenated aromatic hydrocarbon)
* Most commonly found in fungicides, insecticides, herbicides
