Dermatology > Module 1: Case Studies > Flashcards

Module 1: Case Studies Flashcards

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1
Q

What is the morphology of Ms NS’s skin lesions?

A

Multiple erythematous papules and pustules on the cheeks, chin, and forehead, with presence of open and closed comedones, areas of inflammation, and possible post-inflammatory hyperpigmentation.

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2
Q

What is the most probable diagnosis for Ms NS?

A

Inflammatory acne vulgaris.

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3
Q

What features suggest that Ms NS does not have rosacea?

A

Absence of central facial flushing, telangiectasia, and lack of triggers like heat, alcohol, or spicy food.

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4
Q

Why is folliculitis considered in the differential diagnosis?

A

Because folliculitis presents with pustules, but it is usually more pustular than papular and may have bacterial or fungal causes.

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5
Q

What lifestyle factors has Ms NS attempted to modify?

A

Avoiding chocolate, pizza, and chips, using Dettol soap, and applying regular moisturiser.

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6
Q

What key lesion types differentiate acne vulgaris from other facial eruptions?

A

Presence of comedones (open and closed) combined with inflammatory papules and pustules.

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7
Q

What aspects of Ms NS’s history are important to explore further

A

Menstrual cycle regularity, skincare products and makeup use, stress and sleep patterns, family history of acne, medications (like corticosteroids or androgens), and dietary habits.

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8
Q

Why is menstrual history important in acne assessment?

A

Irregular cycles may indicate hormonal influence, such as polycystic ovary syndrome (PCOS), which can exacerbate acne.

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9
Q

What general skincare measures are recommended for acne?

A

Avoid harsh soaps (e.g., Dettol), wash with gentle aqueous cream, avoid picking lesions, use oil-free non-comedogenic moisturizers and sunscreen, manage stress, and maintain healthy sleep.

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10
Q

Which dietary factors might influence acne?

A

High-glycemic foods and possibly dairy products can trigger or worsen acne in some individuals.

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11
Q

What is the first-line topical treatment for mild inflammatory acne?

A

Topical benzoyl peroxide (2.5–5%) in the morning to reduce inflammation and bacterial growth.

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12
Q

What is the role of topical retinoids in acne management?

A

Topical retinoids (like tretinoin) applied at night prevent new comedones and improve skin cell turnover.

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13
Q

When are oral antibiotics indicated in acne?

A

For moderate to severe inflammatory acne not responding to topical therapy; commonly doxycycline for 3–6 months.

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14
Q

How can oral contraceptives help in acne management?

A

Combined oral contraceptives (e.g., Diane-35, Yasmin) can reduce androgen-mediated acne in females, if not contraindicated.

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15
Q

Why should harsh soaps like Dettol be avoided in acne care?

A

They disrupt the skin barrier, increase dryness, and may worsen irritation and inflammation.

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16
Q

What is the morphology of Mr IA’s skin lesions?

A

Well-demarcated, erythematous plaques with thick, silvery-white scales; possible nail involvement (pitting or onycholysis); symmetrical distribution on hands, arms, elbows, knees, lower legs, lower back, and scalp; chronic course with fissuring, dryness, and erythema.

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17
Q

What is the most likely diagnosis for Mr IA?

A

Chronic plaque psoriasis (psoriasis vulgaris)

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18
Q

Which features in the history support a diagnosis of psoriasis?

A

Chronic progressive course over 12 years, symmetrical distribution, involvement of extensor surfaces and scalp, partial response to topical corticosteroids, family history (father affected).

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19
Q

What are key differential diagnoses to consider?

A

• Eczema (but typically flexural, less scaly, more pruritic)
• Fungal infections (tinea, usually unilateral or annular)
• Lichen planus (violaceous, polygonal, less scaling)

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20
Q

What is the significance of nail changes in psoriasis?

A

Nail pitting or onycholysis indicates involvement of the nail matrix or bed and can correlate with severity; may affect diagnosis and treatment choice.

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21
Q

Why might topical fluocinolone and aqueous cream have limited benefit?

A

Chronic plaque psoriasis often requires stronger topical corticosteroids, combination therapy, or systemic treatments; lesions may be resistant due to chronicity.

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22
Q

What lifestyle or psychosocial factors are important to explore?

A

Impact on self-esteem, work-related stress, triggers (trauma, infection, alcohol, smoking), and adherence to treatment.

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23
Q

What general skin care measures are recommended for psoriasis?

A

Regular emollient use (Vaseline or aqueous cream), gentle skin cleansing, avoiding scratching, and managing dryness and fissuring.

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24
Q

Which body sites are most commonly affected in plaque psoriasis?

A

Extensor surfaces (elbows, knees), scalp, lower back, and hands.

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25
What features differentiate psoriasis from eczema?
Psoriasis: well-demarcated plaques, thick silvery scales, extensor surfaces, chronic course, family history. Eczema: ill-defined plaques, less scaling, often flexural, more pruritus, acute flares.
26
What is the likely diagnosis for Mr IA and why?
Psoriasis vulgaris. Justification: chronic 12-year history, classic extensor/scalp distribution, well-demarcated scaly plaques, family history, and resistance to mild topical corticosteroids.
27
Which bedside test can help confirm psoriasis?
Auspitz sign—gentle scraping reveals silvery scales with pinpoint bleeding.
28
What is the Koebner phenomenon in psoriasis?
Development of new psoriatic lesions at sites of skin trauma or injury.
29
How should you counsel Mr IA about the nature of psoriasis?
It is a chronic, lifelong condition with periods of remission and flare-ups; not contagious and not due to poor hygiene.
30
What triggers can worsen psoriasis that Mr IA should be aware of?
Stress, infections, smoking, alcohol, cold weather, and certain medications like beta-blockers and NSAIDs.
31
Why is psychosocial support important for patients with psoriasis
Because visible lesions can affect self-esteem and social interactions; support groups or counselling may help cope with psychological impact.
32
What is the first-line topical treatment for active psoriatic plaques?
High-potency corticosteroids (e.g., clobetasol propionate 0.05%) applied short-term to reduce inflammation.
33
Which topical agents are preferred for maintenance therapy in psoriasis?
Vitamin D analogs (e.g., calcipotriol or calcitriol) to slow skin turnover and prevent new plaques.
34
How do keratolytic agents help in psoriasis management?
Topical coal tar or salicylic acid reduce scaling and soften plaques, improving penetration of other treatments.
35
What types of moisturizers are recommended for psoriatic skin?
Moisturizers containing urea or lactic acid to improve hydration and reduce dryness and fissuring.
36
How should scalp psoriasis be managed?
Use medicated shampoos (coal tar, salicylic acid, or ketoconazole) and apply high-potency corticosteroid lotions (e.g., clobetasol or betamethasone) for flare-ups.
37
Why are high-potency corticosteroids used only short-term in psoriasis?
To minimize risks of skin atrophy, telangiectasia, and systemic absorption.
38
What is the role of phototherapy in psoriasis management?
Narrowband UVB phototherapy is effective for widespread psoriasis when topical treatments fail.
39
Which systemic therapy is considered first-line for severe psoriasis?
Methotrexate, which suppresses the overactive immune response.
40
When is ciclosporin used in psoriasis treatment?
For severe cases needing rapid disease control, often short-term due to toxicity risks.
41
Which biologics are used for psoriasis and when?
Adalimumab, secukinumab, infliximab, and ustekinumab—used for treatment-resistant psoriasis or psoriasis with arthritis.
42
What lifestyle modifications support psoriasis management?
Avoid triggers (smoking, alcohol, stress, infections), maintain a healthy diet (rich in omega-3, low processed foods), regular exercise, and controlled sunlight exposure
43
Why is sunlight recommended but with caution in psoriasis?
Sunlight helps reduce inflammation and plaques, but overexposure can cause sunburn and worsen skin damage
44
How do lifestyle factors complement pharmacological therapy in psoriasis?
They reduce triggers and systemic inflammation, improve overall skin health, and may enhance treatment response.
45
What is the morphology of Mr JM’s rash?
Large, well-demarcated, erythematous, scaly plaques with a serpiginous border, central clearing (annular pattern), prominent peripheral scaling, extremely pruritic, located on the hip.
46
What is the most likely diagnosis?
Tinea corporis (ringworm).
47
Which clinical features support a diagnosis of tinea corporis?
Annular lesions with raised, scaly borders and central clearing, severe pruritus, chronic course, and poor response to topical corticosteroids.
48
Why did fluocinolone ointment not improve the rash?
Corticosteroids do not treat fungal infections; they may suppress inflammation temporarily but can worsen dermatophyte infections.
49
What key symptom is most characteristic of tinea corporis?
Intense itching (pruritus).
50
Which other areas are commonly affected by tinea corporis?
Trunk, limbs, and sometimes intertriginous areas (groin, underarms).
51
What are important risk factors in this patient for fungal infections?
Diabetes mellitus (immunosuppression) and previous inappropriate corticosteroid use.
52
What bedside tests can aid in confirming tinea corporis?
• KOH (potassium hydroxide) preparation: shows fungal hyphae under the microscope. • Wood’s lamp: may help with some dermatophytes (though many species are non-fluorescent).
53
Why is central clearing significant in annular lesions?
It helps differentiate tinea (fungal) lesions from other dermatoses like eczema or psoriasis, which usually lack central clearing.
54
What is the role of lesion borders in diagnosing fungal infections?
Raised, scaly edges indicate active fungal growth, while central clearing shows where infection is resolving.
55
What risk factors make Mr JM more susceptible to tinea corporis?
Type 2 diabetes, which increases susceptibility to fungal infections, and possible undiagnosed immunosuppression.
56
What are the most common causative organisms of tinea corporis
Dermatophytes, primarily Trichophyton rubrum and Trichophyton mentagrophytes.
57
How does diabetes contribute to increased risk of fungal infections?
High blood sugar impairs neutrophil function and reduces immune response, allowing fungal infections to persist or worsen.
58
Why is it important to consider immunosuppression in chronic fungal infections?
Immunosuppressed individuals are more likely to develop severe, extensive, or recurrent infections.
59
What clinical feature differentiates tinea corporis from eczema or psoriasis?
The annular lesion with raised, scaly borders and central clearing is characteristic of fungal infection.
60
How does diabetes worsen fungal skin infections?
Impaired immune function and poor glycaemic control create an environment that favors fungal overgrowth.
61
What is the effect of prolonged topical corticosteroid use on fungal infections?
Suppresses inflammation but worsens fungal infections, leading to “tinea incognito.”
62
Which lifestyle or environmental factors may contribute to tinea corporis?
Obesity, excessive sweating, contaminated clothing or gym equipment, and close contact with infected individuals or animals.
63
Which diagnostic tests can confirm tinea corporis?
• Fungal culture on Sabouraud’s agar to identify the species. • HbA1c or fasting blood glucose to assess diabetes control.
64
What advice should be given to Mr JM regarding the cause and contagiousness of his condition?
It is likely a fungal skin infection worsened by steroid use. Avoid sharing towels, clothing, or bedding as it is contagious.
65
What hygiene measures help prevent spread or recurrence of tinea corporis?
Keep the skin dry, wear loose cotton clothing, and change clothes frequently.
66
How does diabetes management relate to treatment of tinea corporis?
Poorly controlled diabetes can worsen infections; optimizing blood glucose helps improve treatment outcomes.
67
What should Mr JM do about using fluocinolone?
Stop using it, as corticosteroids worsen fungal infections.
68
What is the first-line treatment for mild to moderate tinea corporis?
Topical antifungals such as clotrimazole 1% cream, applied twice daily for 2–4 weeks, extending 2 cm beyond visible lesions, and continued for at least 2 weeks after lesion resolution.
69
When is systemic antifungal therapy indicated?
For extensive, refractory, or severe cases not responding to topical treatment.
70
Which systemic antifungals are commonly used for tinea corporis?
• Oral terbinafine 250 mg daily for 2–4 weeks (first-line) • Oral itraconazole 100–200 mg daily for 1–2 weeks (resistant cases) • Oral fluconazole 150–200 mg once weekly for 4 weeks
71
What monitoring is required for prolonged systemic antifungal therapy?
Liver function tests to detect hepatotoxicity.
72
What adjunctive measures help prevent recurrence of tinea corporis?
Use antifungal powders in socks and shoes, disinfect personal items like clothing, bedding, and towels, and maintain good diabetes control.
73
Why should topical antifungal treatment extend beyond the visible lesion?
Fungal hyphae can spread beyond visible lesions; extending treatment prevents recurrence.
74
How does improving diabetes control aid in treatment of tinea corporis?
Optimizing blood glucose strengthens immune response and reduces fungal overgrowth, improving treatment outcomes.
75
What is the morphology of Sipho’s skin lesions?
Firm, hyperkeratotic, rough, warty papules on the hand with black dots (thrombosed capillaries), gradually enlarging and multiplying over months, non-tender, and without signs of inflammation.
76
What is the most likely diagnosis?
Common warts (verruca vulgaris)
77
What key clinical feature distinguishes warts from other skin lesions?
Rough, hyperkeratotic surface with tiny black dots representing thrombosed capillaries.
78
What is the typical cause of common warts?
Human papillomavirus (HPV), usually types 2 or 4.
79
How are warts transmitted?
Through direct skin-to-skin contact or indirectly via contaminated surfaces (e.g., towels, toys, or school equipment).
80
Why might other children avoid playing with Sipho?
Due to the visible, contagious nature of the warts and misconceptions about infection or hygiene.
81
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What are common sites for warts in children?
Hands, fingers, knees, and elbows — areas prone to trauma or friction.
83
Are warts painful?
Usually painless but may cause discomfort, especially if located on pressure areas or near nail beds.
84
What is the likely diagnosis for Sipho’s skin lesions?
Common warts (Verruca vulgaris).
85
What features support the diagnosis of common warts?
Rough, hyperkeratotic papules; slow progression over months; location on the hands; spreading pattern; and social stigma due to visibility.
86
What is the causative organism of common warts?
Human papillomavirus (HPV), most commonly types 1, 2, 4, and 7.
87
What is the pathogenesis of warts?
HPV infects the basal layer of the epidermis, causing excessive keratinocyte proliferation and formation of warty papules.
88
How are warts transmitted?
Through direct skin-to-skin contact or contact with contaminated objects and surfaces (e.g., towels, toys, or school desks).
89
Why are warts more common in children?
Because children have an immature immune system and frequent minor skin trauma that facilitates viral entry.
90
What social or psychological effect can warts have in children?
They can cause embarrassment, social isolation, and teasing from peers.
91
Are common warts self-limiting?
Yes, most warts resolve spontaneously within 1–2 years as the immune system clears the virus.
92
When is treatment indicated for warts?
When warts are persistent, painful, spreading, or causing social distress.
93
What is the first-line treatment for common warts?
• Soaking in warm water. • Topical salicylic acid (17–40%) applied daily for several weeks. • Cryotherapy with liquid nitrogen.
94
How does salicylic acid work in wart treatment?
It gradually removes the thickened keratin and promotes viral clearance by exposing infected tissue.
95
What is cryotherapy and how does it help?
It involves freezing the wart with liquid nitrogen, causing destruction of infected tissue and stimulating immune response.
96
What are second-line treatments for resistant or widespread warts?
• Cantharidin (causes blistering of wart tissue). • Electrocautery or laser therapy. • Immunotherapy (e.g., imiquimod or intralesional Candida antigen).
97
What advice should be given to Sipho’s parents about prognosis?
Warts are benign and common in children; they usually disappear over time as immunity develops.
98
What preventive advice should be given to Sipho and his parents?
• Avoid scratching or picking warts to prevent spreading. • Maintain good hand hygiene. • Do not share towels or personal items.
99
How should parents reassure Sipho about his condition?
Explain that warts are common, not dangerous, and will likely go away; social support helps reduce embarrassment.
Dermatology
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