Dermatology > Module 1: Basic Derm > Flashcards

Module 1: Basic Derm Flashcards

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1
Q

What is acne vulgaris?

A

Acne vulgaris is a chronic inflammatory disorder of the pilosebaceous unit (hair follicle and sebaceous gland), commonly seen in adolescents.

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2
Q

What are the four main pathogenic factors in acne vulgaris?

A

Increased sebum production (due to androgens)

Follicular hyperkeratinization (blockage of follicles)

Colonization by Cutibacterium acnes (formerly Propionibacterium acnes)

Inflammation of the follicle wall.

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3
Q

Which age group is most commonly affected by acne vulgaris?

A

Adolescents and young adults, typically between 12 and 25 years.

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4
Q

What are the clinical features of acne vulgaris?

A

Comedones (open = blackheads; closed = whiteheads)

Papules and pustules

Nodules or cysts in severe cases

Commonly affects the face, chest, back, and shoulders.

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5
Q

What causes comedone formation in acne?

A

Hyperkeratinization and sebum retention block the pilosebaceous duct, forming comedones.

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6
Q

Which bacterium plays a major role in acne pathogenesis?

A

Cutibacterium acnes, which promotes inflammation by releasing enzymes and inflammatory mediators.

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7
Q

What are the main types of acne based on severity?

A

Mild: Comedonal acne

Moderate: Papulopustular acne

Severe: Nodulocystic or conglobate acne

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8
Q

What topical treatments are used for mild acne?

A

Topical retinoids (e.g., adapalene, tretinoin)

Benzoyl peroxide

Topical antibiotics (e.g., clindamycin, erythromycin)

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9
Q

What systemic treatments are used for moderate to severe acne?

A

Oral antibiotics (e.g., doxycycline, minocycline)

Hormonal therapy in females (e.g., combined oral contraceptives, anti-androgens like cyproterone acetate)

Oral isotretinoin for severe or resistant acne.

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10
Q

What precautions are required when prescribing isotretinoin?

A

Teratogenicity: strict pregnancy prevention

Monitor liver function and lipids

Avoid in pregnancy and breastfeeding

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11
Q

What non-drug measures can help manage acne?

A

Gentle cleansing (avoid scrubbing)

Avoid picking or squeezing lesions

Use non-comedogenic skincare products

Manage stress and diet (limit high glycaemic foods).

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12
Q

What are potential complications of acne vulgaris?

A

Post-inflammatory hyperpigmentation

Scarring (atrophic or keloid)

Psychological distress (low self-esteem, anxiety, depression)

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13
Q

Further History to Consider in acne vulgaris :

A
  • Menstrual cycle regularity (to rule out hormonal influence, e.g., PCOS).
  • Use of skincare products and makeup (potential irritants or occlusive agents).
  • Stress levels and sleep patterns.
  • Family history of acne.
  • Any medications (e.g., corticosteroids, androgens).
  • Dietary habits (though diet has limited but possible influence).
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14
Q

Why should harsh cleansers like Dettol soap be avoided in acne management?

A

Harsh soaps can disrupt the skin barrier, increase dryness, and cause irritation, which may worsen acne

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15
Q

What type of cleanser is recommended for patients with acne?

A

Use a gentle cleanser, such as aqueous cream, to wash the face without stripping the skin’s natural oils.

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16
Q

Why should patients avoid touching or picking acne lesions?

A

Picking or squeezing lesions can lead to inflammation, infection, and permanent scarring.

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17
Q

What type of moisturizers and sunscreens are suitable for acne-prone skin?

A

Use oil-free, non-comedogenic moisturizers and sunscreens to avoid clogging pores and worsening acne.

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18
Q

How can diet influence acne severity?

A

Dairy and high-glycaemic foods may trigger or worsen acne in some individuals; reducing these can help in management.

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19
Q

Why is stress management and good sleep hygiene important in acne?

A

Stress and poor sleep can increase hormonal fluctuations and inflammation, leading to acne flare-ups

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20
Q

What is the first-line treatment for mild inflammatory acne (papules and pustules)?

A

Combination of topical benzoyl peroxide in the morning and a topical retinoid at night.

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21
Q

What is the role of benzoyl peroxide in acne treatment?

A

Benzoyl peroxide (2.5–5%) reduces inflammation and kills C. acnes bacteria, preventing resistance to antibiotics.

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22
Q

Why are topical retinoids such as tretinoin used in acne?

A

Retinoids normalize follicular keratinization, preventing new comedone formation and improving skin turnover.

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23
Q

When are oral antibiotics indicated in acne treatment?

A

Used in moderate to severe inflammatory acne or when topical therapy fails; typically for 3–6 months (e.g., doxycycline).

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24
Q

What are key precautions when using oral antibiotics for acne?

A

Always combine with benzoyl peroxide to prevent bacterial resistance

Limit duration to 3–6 months

Avoid prolonged or repeated courses

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25
When can oral contraceptive pills (OCPs) be considered for acne?
In females with hormonal acne or menstrual flares, OCPs like Diane-35 or Yasmin can help reduce androgen-related sebum production.
26
What are contraindications for using oral contraceptives in acne?
Smoking (especially >35 years), history of thromboembolism, uncontrolled hypertension, or estrogen-dependent cancers.
27
What are two common conditions that can mimic acne vulgaris?
Rosacea and Folliculitis.
28
How does rosacea differ from acne vulgaris?
Rosacea typically presents with central facial flushing and telangiectasia, which are absent in acne vulgaris.
29
How does folliculitis differ from acne vulgaris?
Folliculitis usually presents with more pustular lesions that are often bacterial or fungal in origin, unlike acne which involves comedones (blackheads and whiteheads).
30
What is the key feature present in acne but absent in both rosacea and folliculitis?
The presence of comedones (open and closed) is characteristic of acne vulgaris.
31
What is rosacea?
Rosacea is a chronic inflammatory skin condition that primarily affects the central face, causing redness, flushing, papules, pustules, and visible blood vessels (telangiectasia).
32
Who is most commonly affected by rosacea?
It typically affects fair-skinned adults aged 30–60, especially women; however, men may have more severe phymatous (thickened skin) forms.
33
What areas of the face are most commonly involved?
The cheeks, nose, chin, and forehead are most often affected.
34
What are the four main subtypes of rosacea?
Erythematotelangiectatic – persistent redness and visible vessels. Papulopustular – red bumps and pustules resembling acne. Phymatous – thickened skin, often on the nose (rhinophyma). Ocular – eye irritation, dryness, and conjunctivitis
35
What distinguishes rosacea from acne vulgaris?
Rosacea lacks comedones (blackheads/whiteheads) and often shows flushing and telangiectasia.
36
What symptoms are commonly associated with rosacea?
Facial burning, stinging, dryness, and sensitivity to topical products.
37
What are common triggers that worsen rosacea?
Hot drinks and spicy foods Alcohol (especially red wine) Sun exposure Heat or cold weather Emotional stress Topical steroids or irritating cosmetics
38
What are the general measures for managing rosacea?
Avoid triggers (sun, heat, alcohol, spicy foods) Use gentle cleansers and non-irritating moisturizers Daily broad-spectrum sunscreen Avoid topical steroids on the face
39
What is the first-line topical treatment for mild rosacea?
Topical metronidazole, azelaic acid, or ivermectin applied once or twice daily.
40
What systemic treatments can be used for moderate to severe rosacea?
Oral tetracyclines (e.g., doxycycline) for anti-inflammatory effects
41
How is flushing and persistent erythema managed?
Topical brimonidine (α2-agonist) or laser therapy for visible blood vessels.
42
How is phymatous rosacea (rhinophyma) treated?
Surgical excision, laser therapy, or dermabrasion may be needed for cosmetic improvement.
43
How is ocular rosacea managed?
Lubricating eye drops, oral doxycycline, and ophthalmology referral for persistent symptoms.
44
Why should topical corticosteroids be avoided in rosacea?
They can worsen inflammation, cause rebound flares, and induce steroid rosacea.
45
What is psoriasis?
Psoriasis is a chronic, immune-mediated inflammatory skin disease characterized by hyperproliferation of keratinocytes, leading to well-demarcated, scaly plaques.
46
What type of hypersensitivity reaction is psoriasis?
It is a Type IV (T-cell–mediated) hypersensitivity reaction.
47
What is the typical age of onset for psoriasis?
It has bimodal peaks: Early-onset: 15–35 years (genetic) Late-onset: 50–60 years (often milder)
48
What causes the characteristic thick plaques in psoriasis?
ccelerated keratinocyte turnover due to immune activation by Th1, Th17, and dendritic cells, resulting in increased epidermal proliferation
49
Which cytokines are key in psoriasis pathogenesis?
TNF-α, IL-17, and IL-23 are central to inflammation and keratinocyte activation
50
What are the classic features of psoriatic plaques?
Well-demarcated, erythematous plaques with silvery-white scales, commonly on extensor surfaces (elbows, knees), scalp, and sacrum.
51
What is Auspitz’s sign?
Pinpoint bleeding when psoriatic scales are removed — due to exposure of dilated dermal capillaries.
52
What is the Koebner phenomenon?
Appearance of new psoriatic lesions at sites of skin trauma
53
Name common types of psoriasis.
Chronic plaque (vulgaris) – most common Guttate – small drop-like lesions, often after strep throat Inverse (flexural) – in skin folds Pustular – sterile pustules on palms/soles Erythrodermic – generalized redness, scaling, and systemic illness
54
What nail changes are seen in psoriasis?
Pitting Onycholysis (nail lifting) Subungual hyperkeratosis “Oil-drop” discoloration
55
What is psoriatic arthritis?
An inflammatory arthritis associated with psoriasis, presenting as asymmetric oligoarthritis, DIP joint involvement, or spondyloarthritis.
56
What factors can trigger or worsen psoriasis?
Infections (e.g., streptococcal throat infections) Stress Cold weather Skin trauma (Koebner phenomenon) Medications (β-blockers, lithium, NSAIDs, antimalarials, withdrawal of corticosteroids)
57
What are general measures for psoriasis management?
Avoid triggers Regular emollients to reduce scaling Psychological support
58
What are the first-line topical treatments for mild psoriasis?
Topical corticosteroids Vitamin D analogues (calcipotriol) Tar preparations or salicylic acid (for scaling)
59
What are systemic treatment options for moderate-to-severe psoriasis?
Methotrexate Cyclosporine Acitretin (oral retinoid) Biologic agents (anti-TNF, anti-IL-17, anti-IL-23)
60
When are biologics indicated in psoriasis?
For moderate-to-severe or treatment-resistant psoriasis, or psoriatic arthritis.
61
What is guttate psoriasis associated with?
Streptococcal throat infection, usually in children or young adults.
62
What is pustular psoriasis?
A severe form with sterile pustules that can be localized (palms and soles) or generalized with systemic symptoms
63
What is erythrodermic psoriasis?
A life-threatening form with widespread erythema, scaling, and systemic involvement (fever, dehydration, infection risk).
64
What key patient education point should always be emphasized?
Psoriasis is chronic and relapsing—treatment controls symptoms but does not cure the disease
65
What is the diagnosis for a patient with chronic, scaly plaques on extensor surfaces, scalp, and lower back?
Psoriasis vulgaris.
66
What key feature supports the diagnosis of psoriasis based on duration?
The chronic and progressive 12-year history of the skin condition supports psoriasis.
67
What is the typical distribution pattern of psoriasis vulgaris?
Extensor surfaces (elbows and knees), scalp, lower back, and hands.
68
What lesion characteristics are typical of psoriasis vulgaris
Well-demarcated, erythematous plaques with silvery-white scales — the hallmark of psoriasis.
69
How does family history support the diagnosis?
A positive family history (e.g., father with similar skin condition) suggests a genetic predisposition to psoriasis
70
Why does lack of response to fluocinolone and aqueous cream support psoriasis?
Failure to respond to mild topical corticosteroids or emollients indicates a chronic inflammatory condition like psoriasis rather than eczema or dermatitis.
71
What is the first-line treatment for active psoriatic plaques?
High-potency topical corticosteroids (e.g., clobetasol propionate 0.05%) are used short-term to reduce inflammation and plaque thickness.
72
Why should high-potency corticosteroids be used only short-term?
Prolonged use can cause skin atrophy, tachyphylaxis, and systemic absorption, especially on thin skin areas
73
What is the role of vitamin D analogs in psoriasis treatment?
Calcipotriol or calcitriol slow keratinocyte proliferation and normalize differentiation — ideal for maintenance therapy after initial control.
74
Why are vitamin D analogs preferred for long-term use?
They have a good safety profile, cause less skin thinning, and can be used continuously to prevent relapses
75
How do topical coal tar and salicylic acid help in psoriasis?
They act as keratolytics, reducing scaling and plaque thickness, and help enhance penetration of other topical agents.
76
What is the function of moisturizers in psoriasis management?
Urea or lactic acid–based moisturizers help hydrate the skin, reduce scaling, and improve barrier function.
77
What topical agents are recommended for scalp psoriasis?
Medicated shampoos containing coal tar, salicylic acid, or ketoconazole to help reduce scaling and inflammation.
78
What is used for flare-ups of scalp psoriasis?
Clobetasol or betamethasone scalp lotion, applied short-term, to control inflammation during flares
79
Why is scalp psoriasis often more challenging to treat?
Hair coverage limits topical penetration, and chronic irritation from scratching can worsen lesions (Koebner phenomenon).
80
How is moderate to severe psoriasis defined?
Involvement of more than 10% of body surface area (BSA) or cases where topical therapy is inadequate.
81
When is phototherapy indicated in psoriasis?
When psoriasis is widespread or unresponsive to topical treatments
82
What is the preferred form of phototherapy for psoriasis?
Narrowband UVB (NB-UVB) phototherapy — effective and safer than PUVA (psoralen + UVA).
83
How does phototherapy help in psoriasis?
It reduces T-cell activity and slows keratinocyte proliferation, leading to improvement in lesions.
84
What is the first-line systemic treatment for severe psoriasis?
Methotrexate, which suppresses the overactive immune response and reduces skin cell turnover.
85
What systemic drug is used for rapid control in severe psoriasis flares?
Ciclosporin, due to its potent immunosuppressive action, providing fast symptom relief.
86
When are biologics indicated in psoriasis management?
In treatment-resistant cases or when psoriasis is associated with psoriatic arthritis.
87
Give examples of biologic agents used in psoriasis.
TNF-α inhibitors: adalimumab, infliximab IL-17 inhibitor: secukinumab IL-12/23 inhibitor: ustekinumab
88
What lifestyle factors should psoriasis patients avoid?
Smoking, alcohol, stress, and infections — all known to exacerbate flares.
89
What dietary advice is beneficial for psoriasis patients?
Healthy diet rich in omega-3 fatty acids and low in processed foods to reduce systemic inflammation.
90
How can exercise benefit psoriasis patients?
Regular exercise helps reduce inflammation, improves mood, and lowers cardiovascular risk.
91
What is the role of sunlight in psoriasis management?
Controlled sunlight exposure can help improve lesions, but sunburn must be avoided as it can worsen psoriasis.
92
What is Tinea corporis?
Tinea corporis (ringworm) is a superficial fungal infection of the body skin, caused by dermatophytes (Trichophyton, Microsporum, or Epidermophyton species).
93
Why is it called "ringworm"?
Because the infection produces ring-shaped, scaly lesions that resemble a worm under the skin — although no actual worms are involved.
94
Who is most commonly affected by Tinea corporis?
It can affect all ages, but is more common in children and athletes (especially those with close skin contact like wrestlers)
95
How is Tinea corporis transmitted?
Through direct contact with an infected person, animal (cats, dogs), or contaminated objects such as towels or clothing
96
Which fungal organisms most commonly cause Tinea corporis?
Trichophyton rubrum Trichophyton mentagrophytes Microsporum canis (animal-associated)
97
What are the characteristic skin lesions in Tinea corporis?
Annular (ring-shaped) erythematous plaques Raised, scaly, active borders with central clearing Often itchy (pruritic)
98
How can Tinea corporis be distinguished from eczema or psoriasis?
The well-defined advancing edge with central clearing is typical of Tinea, while eczema/psoriasis have diffuse, non-annular lesions.
99
What areas of the body are commonly affected?
Trunk, limbs, neck, and face (but not scalp, groin, hands, or feet — which have their own specific “tinea” names).
100
How is Tinea corporis diagnosed?
Clinical appearance is often diagnostic. Microscopy (KOH prep) shows branching septate hyphae. Fungal culture confirms species if uncertain.
101
When should additional testing (e.g., fungal culture) be done?
When the diagnosis is unclear, the infection is widespread, or resistant to treatment.
102
What is the first-line treatment for localized Tinea corporis?
Topical antifungals such as: Clotrimazole, miconazole, or terbinafine cream (applied twice daily for 2–4 weeks, continuing 1 week after clearance)
103
When is oral antifungal therapy indicated?
For extensive, refractory, or hair-bearing area infections. Examples: Oral terbinafine Oral itraconazole Oral fluconazole
104
Why should topical corticosteroids be avoided in Tinea corporis?
They suppress inflammation, worsen fungal growth, and can mask symptoms — leading to tinea incognito.
105
What preventive measures can help avoid Tinea corporis reinfection?
Keep skin dry and clean Avoid sharing towels or clothing Treat infected pets Wash bedding and clothing in hot water
106
What is tinea incognito?
A modified or atypical presentation of Tinea caused by misuse of topical steroids, resulting in less scaling but deeper infection.
107
Why is adherence to treatment duration important?
Stopping treatment too early can lead to recurrence, as fungal spores persist even after visible improvement.
108
What are the main causative organisms of Tinea Corporis?
Dermatophyte fungi, especially Trichophyton rubrum and Trichophyton mentagrophytes.
109
How can topical corticosteroids worsen a fungal infection?
They suppress local immune and inflammatory responses, allowing the fungus to proliferate. This can lead to Tinea incognito — an atypical, less scaly form of Tinea.
110
What lifestyle or environmental factors may predispose to Tinea Corporis?
Obesity and excessive sweating (warm, moist skin environment). Close contact with infected people or animals. Use of contaminated clothing, towels, or gym equipment.
111
Which diagnostic tests confirm Tinea Corporis?
Fungal culture on Sabouraud’s agar – identifies the exact dermatophyte species. KOH microscopy – shows branching septate hyphae. HbA1c or fasting glucose – checks for underlying diabetes or poor glycaemic control.
112
What should patients with Tinea Corporis be told about contagion?
It is contagious — avoid sharing towels, clothing, or bedding, and wash items in hot water.
113
What hygiene advice helps control Tinea Corporis
Keep affected skin clean and dry. Wear loose, breathable cotton clothing. Change clothes frequently, especially after sweating. Disinfect personal and gym items.
114
What should patients be advised about topical steroid use?
Stop using fluocinolone or other steroids. Steroids worsen fungal infections and mask symptoms.
115
How does controlling diabetes help treat Tinea Corporis?
Good glycaemic control improves immune function and reduces fungal overgrowth, aiding faster healing.
116
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.
117
How should topical antifungals be applied to prevent recurrence?
Apply beyond the visible edge of the lesion by at least 2 cm and continue for at least 2 weeks after lesion resolution.
118
When is systemic antifungal therapy indicated?
For extensive, refractory, or severe cases, or when lesions involve hair-bearing areas.
119
What is the first-line systemic antifungal for Tinea Corporis?
Oral terbinafine 250 mg daily for 2–4 weeks
120
What are alternative systemic treatments for resistant cases?
Oral itraconazole 100–200 mg daily for 1–2 weeks Fluconazole 150–200 mg once weekly for 4 weeks Note: Monitor liver function if prolonged treatment is required.
121
What adjunct measures help prevent reinfection?
Use antifungal powders (e.g., clotrimazole powder) in socks and shoes. Disinfect personal items (clothing, bedding, towels). Maintain good hygiene and control diabetes if present.
122
Why is continuing treatment beyond lesion resolution important?
To eradicate remaining fungal spores, prevent recurrence, and ensure complete cure.
123
How does controlling diabetes help in Tinea Corporis management?
Good glycaemic control improves immune response and reduces the favorable environment for fungal growth, aiding treatment efficacy.
124
What are common warts (Verruca Vulgaris)?
Benign hyperkeratotic skin lesions caused by human papillomavirus (HPV), mostly types 1, 2, and 4.
125
Who is most commonly affected by common warts?
Children and young adults; more frequent in immunocompromised individuals
126
How are common warts transmitted?
Via direct skin-to-skin contact or contact with contaminated surfaces, especially in warm, moist environments (e.g., swimming pools, gyms).
127
What are the characteristic features of common warts?
Hyperkeratotic, rough-surfaced papules Well-defined margins Often skin-colored, gray, or brown May have black punctate dots (thrombosed capillaries)
128
Where are common warts usually found?
Hands, fingers, knees, elbows, and dorsal surfaces of feet.
129
Are common warts painful?
Usually painless, but pressure areas (soles, fingers) can be tender.
130
How is the diagnosis of common warts made?
Mostly clinical, based on appearance and distribution. Dermoscopy can show thrombosed capillaries. Biopsy is rarely needed unless atypical features are present.
131
Do all warts require treatment?
Not always — many spontaneously resolve within 1–2 years. Treatment is indicated for pain, cosmetic concern, or functional impairment.
132
What are common topical treatments for warts?
Salicylic acid 17–40% (keratolytic) applied daily Cantharidin (blistering agent, usually in clinics) Imiquimod (immune response modifier, for resistant cases)
133
What procedural treatments are available for warts?
Cryotherapy (liquid nitrogen) Electrocautery or curettage Laser therapy for refractory warts
134
How can recurrence be prevented?
Avoid skin trauma and sharing personal items Maintain good hand hygiene Treat immunosuppression or underlying conditions if present
135
What advice should patients with warts receive?
Warts are contagious; avoid direct contact and sharing towels or shoes. Cover warts with plasters in public areas (pools, gyms). Do not pick or scratch, as it may spread infection. Be patient — treatment may take weeks to months, and multiple sessions may be needed.
136
What causes common warts (Verruca Vulgaris)?
Human papillomavirus (HPV), most commonly types 1, 2, 4, and 7.
137
How does HPV cause wart formation?
HPV infects the basal layer of the epidermis, inducing excessive keratinocyte proliferation, leading to hyperkeratotic papules.
138
How is HPV transmitted in common warts?
By direct skin-to-skin contact or via contaminated surfaces, such as shared school items or towels.
139
Why are common warts more frequent in children?
Because children have an immature immune system, making them more susceptible to infection.
140
Do all warts require treatment?
No — most warts are self-limiting, resolving within 1–2 years. Treatment is indicated if persistent, painful, or socially distressing.
141
What are first-line, home or over-the-counter treatments for common warts?
Soaking in hot water to soften lesions Salicylic acid (17–40%) solution or patches applied daily for several weeks Cryotherapy (liquid nitrogen) to destroy infected tissue
142
What are second-line treatments for warts if first-line fails?
Cantharidin (blistering agent, applied in clinic) Electrocautery or laser therapy for resistant warts Immunotherapy (e.g., imiquimod or intralesional Candida antigen) to stimulate immune response
143
What is the usual prognosis of common warts in children?
Most warts resolve spontaneously within 1–2 years as the child’s immunity develops.
144
How long does treatment usually take?
Treatment can be slow, often taking weeks to months, and multiple sessions may be required.
145
What hygiene advice should be given to prevent spread?
Avoid picking or scratching warts Encourage good hand hygiene Avoid sharing towels, clothing, or personal items
146
How should parents be reassured about warts in children?
Warts are common, benign, and not a serious condition, especially in children
Dermatology
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