Dermatology > Module 8 > Flashcards

Module 8 Flashcards

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1
Q

What are common localised causes of hyperpigmentation?

A

Melasma – brown patches, often on face, hormonally influenced

Ochronosis – blue-black pigmentation, often from hydroquinone overuse

Post-inflammatory hyperpigmentation – after skin injury or inflammation

Acanthosis nigricans – velvety hyperpigmented plaques, often in neck/folds, associated with insulin resistance

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2
Q

What are generalised causes of hyperpigmentation?

A

Hormonal (e.g., Addison’s disease, pregnancy)

Drugs (e.g., minocycline, antimalarials)

Neurofibromatosis (café-au-lait spots)

Liver diseases (cholestasis, chronic liver disease)

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3
Q

What is the difference between hypopigmentation and depigmentation?

A

Hypopigmentation: Reduced pigment, skin is lighter but not completely colorless

Depigmentation: Complete loss of pigment, skin is entirely pale or white

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4
Q

What are common causes of depigmentation?

A

Vitiligo – autoimmune destruction of melanocytes, well-defined patches

Albinism – congenital absence of pigment throughout the skin, hair, and eyes

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5
Q

Which pigment in epidermal cells primarily determines skin colour?

A

Melanin

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6
Q

How does UV light affect skin colour?

A

UV light oxidizes melanin, causing tanning or pigmentary darkening

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7
Q

How does haemoglobin contribute to skin colour?

A

Red blood cells in the dermis give a pink to red hue; breakdown products like bilirubin can cause yellowing (jaundice)

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8
Q

What is pigment incontinence, and how does it affect skin colour?

A

Occurs when basal keratinocytes are damaged

Melanin falls into the dermis, taken up by macrophages

Leads to post-inflammatory hyperpigmentation

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9
Q

How does epidermal thickness affect skin colour?

A

Thicker epidermis, as seen in lichenification, can alter apparent skin colour, making it appear darker or more opaque

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10
Q

A 40-year-old woman presents with dark marks on her face. How would you describe the morphology?

A

Brown hyperpigmented patches on the malar area

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11
Q

What are three possible causes for these hyperpigmented facial patches?

A

Melasma – more common in women, linked to oestrogen, aggravated by sunlight

Ochronosis – blue-black pigmentation, often from topical hydroquinone overuse

Post-inflammatory hyperpigmentation – following inflammation or injury to the skin

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12
Q

How would you treat hyperpigmentation in this patient?

A

Sun protection – physical methods, broad-spectrum sunscreen with iron oxide

Topical retinoid cream at night to increase skin turnover

Chemical peels or acids for exfoliation (in selected patients)

Skin bleaching agents (e.g., hydroquinone) if indicated

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13
Q

Which hormonal factors can contribute to facial hyperpigmentation?

A

Pregnancy (melasma)

Oestrogen-containing oral contraceptives

Other hormonal imbalances affecting pigmentation

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14
Q

How can topical agents affect facial pigmentation?

A

Soaps, moisturisers, perfumes, aero-allergens – may aggravate pigmentation indirectly via irritation

Skin lightening agents (e.g., hydroquinone) – can cause acquired ochronosis

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15
Q

Which oral medications can contribute to facial hyperpigmentation?

A

Thiazide diuretics

Hypoglycaemic drugs

Non-steroidal anti-inflammatory drugs (NSAIDs)

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16
Q

How does post-inflammatory hyperpigmentation occur on the face?

A

Following excoriations or scratching

After acne

Lichenoid eczema

Lichen planus or discoid lupus erythematosus

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17
Q

What is the morphology of lichenoid eczema?

A

Purple patches in a photo-distribution

Increased skin markings (lichenification)

Sun-exposed areas: malar area, arms, chest

Spares areas shielded from sun (folds, creases, under chin)

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18
Q

What is a common cause?
Lichenoid Eczema

A

Thiazide diuretics and other photosensitizing agents

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19
Q

How is it managed?
Lichenoid Eczema

A

Stop the offending drug and use topical corticosteroids if needed

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20
Q

What is the morphology of lichen planus?

A

Purple, planar, pruritic, polygonal papules (4 P’s)

Can coalesce into plaques with hyperpigmentation (slate grey)

Inflammatory and very itchy

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21
Q

How is lichen planus treated?

A

Potent topical corticosteroids

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22
Q

What is the morphology of acanthosis nigricans?

A

Brown, velvety patches

Usually in neck, axilla, sometimes with skin tags

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23
Q

How is acanthosis nigricans managed?

A

Responds to lifestyle modification (weight loss, control of insulin resistance)

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24
Q

What are freckles and where do they usually occur?

A

Brown macules caused by increased melanin production (not increased melanocytes)

Usually in type 1 and 2 skin

Symptomless

Commonly on the face

Indication of UV/solar damage

Solar protection is recommended

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25
How do freckles compare with solar lentigines?
Freckles: small, uniform brown macules; fade without sun exposure; no melanocyte proliferation Solar lentigines: larger, persistent pigmented patches; accumulate with age; also UV-induced
26
A woman develops axillary freckling and hypertension. What is the probable underlying disorder?
Neurofibromatosis type 1 (NF1)
27
What other skin changes are likely in neurofibromatosis?
Café-au-lait macules – light-brown patches on trunk and limbs Neurofibromas – soft, benign tumors along nerves
28
What is the shared feature in these patients?
Depigmentation – complete or near-complete loss of pigment in affected areas
29
What is the diagnosis for patient A with well-defined depigmented patches on the skin?
Vitiligo Cause: Autoimmune destruction of melanocytes Management: Topical corticosteroids, UV therapy
30
What is the diagnosis for patient B with generalized depigmentation from birth?
Oculocutaneous albinism Cause: Normal melanocytes but cannot produce melanin (tyrosinase enzyme defect) Management: Photoprotection, skin cancer surveillance, eye monitoring
31
How can you help these patients reduce complications?
Sun protection (especially in albinism) Regular skin cancer surveillance Ophthalmology follow-up for albinism
32
What is the morphology seen in tinea versicolor, pityriasis alba, and post-inflammatory hypopigmentation?
Hypopigmented patches – areas of skin lighter than surrounding skin
33
What are the key features of Tinea versicolor?
Hypopigmented patches on the back or trunk Fine scale (may be elicited by stretching the skin) Usually occurs in older children or adolescents Treatment: Only treat if there is active scale (e.g., topical antifungals)
34
What are the key features of Pityriasis alba?
Occurs on the face of children, more frequent in darker skin types Not fungal, mild phenotype of eczema Treatment: Moisturiser or mild corticosteroid if scale present
35
What are the key features of Post-inflammatory hypopigmentation?
Occurs after previous skin inflammation, e.g., psoriasis, seborrheic dermatitis History of prior lesion at the same site Usually resolves over time, no active treatment needed unless underlying inflammation persists
36
What is the first step in evaluating a patient with localised hypopigmentation?
Assess the presence or absence of scale on the lesions
37
Why is the site of the lesion important?
Certain conditions affect specific areas: Face: pityriasis alba Trunk/back: tinea versicolor Sites of previous inflammation: post-inflammatory hypopigmentation
38
What other patient factors should you consider?
Presence or absence of other diseases (eczema, psoriasis, fungal infections) Age and skin type may help differentiate causes
39
How is treatment decided in hypopigmentation
Based on findings: Scale present: treat active condition (e.g., topical antifungals, corticosteroids, moisturiser) No scale: often resolves spontaneously
40
What are the common causes of localised hypopigmentation?
Pityriasis alba Tinea versicolor Post-inflammatory hypopigmentation
41
What is the morphology and key feature of Vitiligo?
Depigmented patches with sharply defined borders Follicular repigmentation: darker patches appear as melanocytes from hair follicles repopulate the skin
42
Which rare conditions can cause hypopigmented skin lesions?
Cutaneous T-cell lymphoma – may present with hypopigmented patches, often in children or young adults Sarcoidosis – granulomatous lesions can cause localized hypopigmentation Photo-lichenoid dermatitis – drug-induced (e.g., thiazide diuretics), often sun-exposed areas Discoid lupus erythematosus – inflammatory plaques with depigmentation and scarring Flat warts – slightly hypopigmented, smooth papules
43
What is the general principle in evaluating less common hypopigmentation?
Consider history of drugs, systemic disease, or chronic inflammatory conditions Look for associated signs (scaling, plaques, follicular involvement, systemic symptoms) Biopsy if the diagnosis is uncertain
44
What are common causes of increased pigmentation?
Tanning – UV-induced darkening of melanin Acanthosis nigricans – velvety hyperpigmentation in neck/axilla, insulin resistance Post-inflammatory hyperpigmentation – after chronic eczema or other inflammation Melasma – brown facial patches, hormonally influenced Acquired ochronosis – due to prolonged hydroquinone use Disorders of the dermal-epidermal interface: -Discoid lupus erythematosus (DLE) - Lichen planus
45
What are common causes of decreased pigmentation?
Albinism – congenital absence of melanin Vitiligo – autoimmune destruction of melanocytes Post-inflammatory hypopigmentation – after skin injury or inflammation Tinea versicolor – hypopigmented fungal patches Eczema – mild hypopigmentation in chronic lesions Leukomelanoderma of HIV – hypopigmented macules Plane warts – slightly hypopigmented papules Leprosy, cutaneous lymphoma, sarcoid – can cause localized hypopigmentation
46
What are the first steps in evaluating hair loss?
Pattern: Localised vs diffuse Scarring: Scarring vs non-scarring Skin conditions: Presence of inflammation, scale, or other dermatologic signs
47
Describe patient A with hair loss in areas of traction. What is the likely diagnosis?
Clinical features: Hair loss in areas under repeated tension Diagnosis: Traction alopecia Prognosis: Good if caught early; may become scarring and permanent if late Treatment: Stop the traction
48
Describe patient B with a widened part. What is the likely diagnosis?
Clinical features: Widened hair part, diffuse thinning over the crown Diagnosis: Female pattern alopecia (androgenic) Prognosis: Lifelong treatment needed to prevent progression Treatment: Topical minoxidil (lifelong), finasteride if male
49
Describe patient C with non-scarring patches of hair loss. What is the likely diagnosis?
Clinical features: Patchy, non-scarring hair loss Diagnosis: Alopecia areata (autoimmune) Prognosis: Good, often patchy regrowth Treatment: Ultrapotent topical corticosteroids
50
Describe patient D with a moth-eaten pattern. What is the likely diagnosis?
Clinical features: Irregular, patchy hair loss resembling moth-eaten appearance Diagnosis: Secondary syphilis Prognosis: Resolves with treatment Treatment: Benzathine penicillin
51
What is the term for hair loss involving the whole scalp?
Alopecia totalis.
52
How do the patches of alopecia areata appear on the scalp?
Smooth, normal skin, non-scarring, well-defined patches.
53
What is the term for hair loss involving the whole body?
Alopecia universalis.
54
Which other body sites can be affected in alopecia areata?
Eyebrows, eyelashes, axillae, and beard.
55
What is a treatment option for alopecia areata?
Methotrexate
56
What are common triggers for telogen effluvium?
Drugs, iron deficiency, other nutritional deficiencies, and thyroid disorders
57
What is the normal hair growth and shedding phase ratio?
90% of hair is in the growth phase (anagen), 10% is in the shedding phase (telogen).
58
When is hair shedding noticed in telogen effluvium?
Shedding is noticed when the balance between growth and shedding is disrupted.
59
What happens to hair in telogen effluvium if the trigger is reversible?
Hair growth returns to normal once the trigger is removed.
60
Which medication can be used to stimulate hair growth in telogen effluvium?
Minoxidil
61
What pattern of hair loss is seen in a man with hair loss over the occiput?
Scarring alopecia with shiny areas lacking hair follicles, often with nodules and papules.
62
What condition commonly causes hair loss over the occiput in males with curly hair?
Folliculitis keloidalis.
63
What is the prognosis for folliculitis keloidalis?
Poor; it usually leads to permanent hair loss.
64
Why should the occiput not be shaved down to a 0 in folliculitis keloidalis?
Shaving too close can worsen scarring and prevent hair regrowth.
65
What type of treatment is used for folliculitis keloidalis?
Anti-inflammatory therapy.
66
What are the signs of secondary impetiginisation on the scalp?
Honeycomb crusting due to secondary infection.
67
How is secondary impetiginisation managed?
Stop the irritant (e.g., hair dye) and treat with a topical corticosteroid.
68
What are the features of discoid lupus erythematosus (DLE) on the scalp?
Photo-distributed lesions, scarring alopecia, and erythema.
69
How is discoid lupus erythematosus (DLE) of the scalp treated?
Sun protection and topical corticosteroids.
70
What are the scalp features of psoriasis?
Scaly scalp with silvery, prolific scale and erythematous border.
71
How is scalp psoriasis managed?
Use a keratolytic (e.g., salicylic acid) and topical corticosteroid.
72
What are the features of scalp eczema?
Lichenification, more crust than scale, dried fluid, and irritated skin.
73
What should you avoid in the treatment of scalp eczema and why?
Avoid keratolytics because they irritate and burn the skin.
74
What is chronic paronychia and who is at risk?
Eczema of the nail fold, commonly seen in people with repeated exposure to water, detergents, or irritants (e.g., fish factory workers).
75
How is chronic paronychia treated?
Topical corticosteroids and drying agents.
76
What nail changes are seen in psoriasis?
Pitting and onycholysis (nail lifting).
77
What additional features may accompany nail psoriasis?
Dactylitis (sausage digits), arthritis, and involvement of other nails.
78
Which other conditions can cause dactylitis besides psoriasis?
Sarcoidosis and tuberculosis (TB).
79
What are other possible nail changes in psoriasis?
Subungual hyperkeratosis, nail plate thickening, and discoloration.
80
What are the common features of onychomycosis?
Nail discoloration, thickening, and onycholysis (nail lifting).
81
Does onychomycosis affect all nails symmetrically?
No, it often affects several nails but not all, and involvement is usually asymmetrical.
82
Which other areas may be involved in onychomycosis?
Toe web spaces and soles.
83
When is systemic treatment indicated for onychomycosis?
Oral antifungal treatment is used if there is nail involvement or concurrent scalp fungal infection.
84
What does white nails indicate?
Hypoalbuminaemia
85
What does “half and half” nails indicate?
Renal disease.
86
What does blue discoloration of nails indicate?
HIV infection or use of AZT.
87
What do Beau’s lines indicate?
A systemic issue affecting nail growth.
88
What does koilonychia (spoon-shaped nails) indicate?
Iron deficiency.
89
What are the most common causes of abnormal nail growth?
Paronychia, psoriasis, and tinea (onychomycosis).
90
Do nail color changes always indicate disease?
No, some color changes may have no significance, but they can be markers for systemic disease.
Dermatology
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