Dermatology

Question 1

Presentation and pathogenesis of Bullous Impetigo

Answer 1

S. Aureus –> toxin A. Act on demoglein 1.
Presentation: Local vesicles and bullae

Question 2

Presentation and pathogenesis of Staphylococcal scalded skin syndrome

Answer 2

Staph –> Toxin B –> Desmoglein 1 –> separation of superficial epidermis
Presentation: Erythema, sandpaper rash +/- systemic
No scarring

Question 3

Presentation and pathogenesis of Pemphigoid

Answer 3

Auto-antibodies against diff. layers of skin. Superficial to deep: Pemphigus foliceus –> pemphigus vulgaris –> pemphigoid (sub-epidermal)
Blistering - more fragile if more superficial. Tense if deeper. Pemphigoid scars.

Question 4

Inherited blistering skin conditions

Answer 4

• Epidermolysis bullosa simplex (D) - defect to keratin. intra-epidemal separation.
• Junctional epidermolysis bullosa (R) - mutation to laminin and collagen genes. Mucosal, nail and teeth involvment. Dermal-epidermal junction.
• Dystrophic epidermolysis bullosa (R/D) - defect collagen VII gene. Separation below epidermal junction.
  NB require skin biopsy and genetic testing

Question 5

Presentation and pathogenesis of toxic epidermolysis bullosa / SJS

Answer 5

TEN: >30% skin detachment
Patho: Reaction to trigger –> apoptotic keratinocyte cell death –> dermal - epidermal separation
Presentation: Widespread erythema, exfoliation. Mucosal and systemic involvement.
Tx: Supportive, wound care, prevent infection

SJS: Tender macules, target lesions, blusters + mucosal involvement. 10% skin detachment

Question 6

Pathophysiology and presentation of Icthyoses

Answer 6

Patho: Genetic mutation –> defective production of epidermis and keratinocytes –> impaired barrier
Presentation: Thickened stratum corneum –> dry, rough, fish like scales

Question 7

Acne treatment and mechanism

Answer 7

• Benzyl peroxide/ axalaic acid/ topical ABx - reduced P. Acne and bacteria
• Salicylic acid - Keratinolytic
• Topical retinoid - reduced comedones, reduced inflammation

Question 8

Pathophysiology of Albinism

Answer 8

= Partial / total absence of melanin
Usually genetic (OCA1A, OCA1B, OCA2)

Question 9

Presentation of different types of Albinism

Answer 9

Oculocutaneous (OCA1A) - White hair/ skin, grey eyes. Absence of tyrosinase activity
Oculuocutaneous (OCA1B) - Reduced tyrosinase activity, some pigmentation. Worse in warm areas.
Ocular (OCA2) - Normal tyrosinase activity, lack of functional P proteins –> pigmented over time. Ocular Sx.
Sign = congenital nystagmus

Question 10

Pathophysiology and presentation of erythema multiforme

Answer 10

Patho: Self-limiting hypersensitivity reaction to trigger (infection, HSV, mycoplasma, drugs, idiopathic)
Presents: Red papules –> target lesions +/- mucosal involvement. Typically symmetrical lesions on limbs.

Question 11

Pathophysiology and presentation of erythema nodosum

Answer 11

Patho: Hypersensitivity reaction to - TB, strep, mycoplasma, IBD, viruses, sulphonamides, idiopathic
Presents: Older children. Multiple, discrete, large, hot, red, tender nodules, usually on shins. Fever, malaise, arthraligia

Question 12

Presentation of Measles

Answer 12

Cold like Sx –> 5 days later get maculopapular rash (palmar sparing_
Koplik spots

Question 13

Complications of Measles

Answer 13

Otitis media, deafness
LRTI
Encephalitis, seizures, LD
Subacute sclerosis panencephalitis - dormant in CNS –> 7y later –> neuro failure and death

Question 14

Mumps complications

Answer 14

Parotiditis
Orchitis
Meningism
Liver involvement

Question 15

Presentations and complications of rubella

Answer 15

Arthraligia
Maculopapular rash
Lymphadenopathy
Risks: Arthritis, in utero malformations

Question 16

Fifth disease : organism and presentation

Answer 16

Parvovirus B19
“Slapped cheeks”
Lace like rash, sparing palms and soles

Question 17

Roseola: organism and presentation

Answer 17

Human herpes virus 6/7
Fever, coryza, irritability. Rash on recovery
Risks: liver damage, encephalitis

Question 18

Scarlet fever: organism and presentation

Answer 18

Strep pyrogenes
Pyrexia
Rash - sandpaper. Periorbital sparing.
Strawberry tongue
Risk: rheumatic fever

Question 19

Scarlet fever treatment

Answer 19

10 days Pen V

Question 20

Chickenpox rash characteristics

Answer 20

Pruritic vesicular rash. Evolves at diff rates:
Macules / Papules / Vesicles / Pustules

Question 21

Common organisms causing cellulitis / erisipelas

Answer 21

Staph. Aureus
Strep Pyogenes
H. Influenza
Strep

Question 22

What is Incontinentia pigmenti and how does it present?

Answer 22

X-linked dominant multisystem disorder. Lethal for males.
Hypopigmented and hairless streaks
Alopecia and wiry hair
Dental and ocular anomalies
Seizures in 30%
Skin biopsy – marble like lesions. Skin may appear blistered. Large number of intradermal eosinophils.

Question 23

Molluscum contagiosum: Pathogen and presentation

Answer 23

Pox virus
Appear in clusters due to autoinoculation of virus to nearby skin.
Patients with atopic eczema / immunosuppressed may develop molluscum.
Usually go by self (6-18m). ?Tx in older children – potassium hydroxide, podophyllotoxin, imiquimod.

Question 24

Types of collagen and associated defects

Answer 24

I – Bone. Osteogenesis imperfecta.
II – Cartilage. Achondroplasia, Stickler syndrome.
III – BV eg vascular type Ehlers-Danlos
IV – Basal lamina. Alport syndrome, Goodpasture syndrome. Kidney, hearing and eye abnormalities.
V- Skin. Ehler-Danlos.

Question 25

What is Pityriasis Rosea and how does it present?

Answer 25

= Post-viral rash
Sx – eruption of erythematous plaques.
May start with solitary ‘Herald patch”, followed in few days by a widespread eruption of small scaly lesions, mostly on trunk. Usually oval with long axis running along dermatomes.
May be itchy.