Dermatology Flashcards

(253 cards)

1
Q

What is urticaria and what are its causes?

A

urticaria describes a local or generalised superficial swelling of the skin.

causes:
- allergy
- non-allergic seen sometimes

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2
Q

Clinical features of urticaria

A

pale pink raised skin
variously described as hives, wheals or nettle rash
pruritic (itchy)

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3
Q

How is urticaria managed?

1st line
additional for troublesome symptoms?
Treatment for severe/resistant episodes

A

1st:
- non-sedating antihistamines (loratadine, cetirizine)
- continue for up to 6 weeks following an episode of acute urticaria

troublesome symptoms:
- sedating antihistamine (chlorphenamine) - use at night in addition to daytime non-sedating

severe/resistant episodes:
- oral prednisolone

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4
Q

What is tinea, what does the term describe and what are the main types of tinea infection?

A

dermatophyte (fungus that infects keratinised tissue (skin, hair nails) fungal infection.

main types:
- tinea capitis - scalp
- tinea corporis - trunk legs or arms
- tinea pedis - feet

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5
Q

What are the key features, causes, and possible complications of tinea capitis if you dont treat?

tell me how you would diagnose it too?

A

clinical features:
- cause of scarring alopecia (mainly in children) if you dont treat.
- if untreated, may form a raised, pustular , spongy/boggy mass - KERION

causes:
- MC in UK/USA: Trichophyton Tonsurans
- Can be caused by Microsporum Canis (from cats or dogs)

how to diagnose:
- wood’s lamp: Microsporum Canis lesions show green fluorescence.
- Trichophyton species: don’t fluoresce under Wood’s Lamp.
- Most useful ix: scalp scrapings

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6
Q

How is tinea capitis managed?

A

oral antifungals:
- terbinafine - for trichophyton tonsurans
- Griseofulvin: for Microsporum infections.

Topical adjunct:
- Ketoconazole shampoo - for the first 2 weeks to reduce transmission.

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7
Q

What are the causes and clinical features of tinea corporis (ringworm) and how is it managed?

A

causes:
- trichophyton rubrum
- trichophyton verrucosum (eg from contact with cattle)

Clinical features:
- well-defined annular erythematous lesions
- associated pustules and papules

Management:
- oral fluconazole

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8
Q

What are the features of tinea pedis (athlete’s foot) and in which group is it most common?

Mx?

A

itchy peeling skin between toes

common in adolescence

Mx:
- First line: Topical antifungal cream (e.g. clotrimazole, terbinafine).

If severe or resistant: Oral antifungal (terbinafine or itraconazole)

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9
Q

What is Bowen’s Disease , who is it most common in and what is the risk if left untreated?

A

types of precancerous dermatosis that is a precursor to squamous cell carcinoma.

mc in elderly

5-10% chance of developing invasive skin cancer if untreated

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10
Q

Clinical features of Bowen’s Disease?

A

Lesion characteristics:
- red, scaly patches
- often 10-15mm in size
- slow- growing

Typical Sites:
- sun-exposed areas like head (temples), neck and lower limbs

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11
Q

How would you manage options for Bowen’s Disease and how are they typically used?

A

can be diagnosed in primary care if diagnosis is clear or repeat episode.

tx:
- topical 5- fluorouracil (5-FU) : twice daily for 4 weeks.
- can cause significant inflammation/erythema - topical steroids given to control. (clobetasol propionate or betamethasone valerate short term)

cryotherapy
excision

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12
Q

What is squamous cell carcinoma (SCC) how common is metastasis and what are the main risk factors?

A

common variant of skin cancer.

rare but occurs in 2-5% of pts.

rf:
- excessive sunlight exposure/psoralen UVA therapy
- actinic keratoses and Bowen’s disease
- immunosuppression ( following renal transplant, HIV)
- smoking
- long-standing leg ulcers (Marjolijn’s ulcer)
- Genetic Conditions: xeroderma pigmentosum, oculocutaneous albinism.

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13
Q

Clinical Features of squamous cell carcinoma (SCC)?

A

sites:
- typically on sun-exposed areas - head, neck , dorsum of hands and arms

lesion characteristics:
- rapidly expanding painless ulcerated nodules
- cauliflower-like appearance
- areas of bleeding may be present.

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14
Q

How is squamous cell carcinoma treated and what are the margin recommendations?

A

Surgical Excision is mainstay:
- Lesion <20mm : excision with 4mm margins
- Lesion >20mm : excision with 6mm margins

Mohs micrographic surgery:
- Used in high-risk patients and in cosmetically important sites.

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15
Q

What are the prognostic factors for squamous cell carcinoma (SCC)?

A

Good Prognosis:
Well-differentiated tumours
- <20mm diameter
- <2mm deep
- No associated diseases

Poor Prognosis:
- >20mm diameter
- >4mm deep
- immunosuppression for whatever reason

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16
Q

What causes scabies, how is it transmitted, who does it typically affect?

A

cause:
- scabies is caused by the mite sarcoptes scabiei

transmission:
- spread by prolonged skin contact

epidemiology:
- typically affects children and young adults

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17
Q

What is the mechanism behind the associated pruritus with scabies?

A

the mite burrows into the skin and lays eggs in the stratum corneum

the intense pruritus is due to a delayed type IV hypersensitivity reaction to mites/eggs

This reaction occurs about 30 days after the initial infection

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18
Q

What are the clinical features of scabies, including primary and secondary signs, and how many infants be affected differently?

A

primary features:
- widespread pruritus
- linear burrows ( thin threads) on:
- sides of fingers
- interdigital webs
- flexor aspects of the wrist

in infants:
- The face and scalp may also be affected

Secondary features (from scratching):
- excoriation (scratch mark/skin break caused by scratching/rubbing)
- infection

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19
Q

How is scabies managed, including first-line and second-line agents, and what is the expected course of symptoms post-treatment?

A

1st line: permethrin 5%
2nd line: malathion 0.5%
pruritus: may persist for 4-6 weeks post-eradication

general guidance:
- avoid close physical contact with others until treatment is complete
- all household and close contacts should be treated simultaneously, even if asx
- on 1st day of tx, launder, iron, or tumble-dry clothing, bedding and towels to kill mites.

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20
Q

What specific instructions should patients be given on how to apply insecticide treatment for scabies?

A

Apply insecticide to all areas ( including face and scalp - contrary to manufacturer’s advice)

Apply to cool, dry skin

Pay close attention to :
- between fingers and toes, under nails, armpits, creases of skin so wrists and elbows.

Allow to dry and leave on for 8-12 hrs for permethrin and 24 hours for malathion

wash off after the specified periuod

reapply if insecticide is removed ( eg hand washing, nappy change)

repeat tx 7 days later

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21
Q

What is crusted (Norwegian) scabies, who is most at risk, what are its features, and how is it managed?

A

severe form of scabies with heavy infestation

pts with suppressed immunity like HIV

features:
- crusted skin full/overflowing with hundreds of thousands of organisms

mx:
- ivermectin
- isolation!!

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22
Q

What is psoriasis, how common is it, what is the typical skin presentation and what systemic risks are associated with it?

A

definition: chronic skin disorder.

prevalence: 2%

typical skin presentation: red scaly patches on skin

systemic risks: increased risk of arthritis and cardiovascular disease

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23
Q

key aspects of psoriasis pathophysiology (genetic, immunological and environmental)?

A

multifactorial - not fully understood

genetic:
- Associated with HLA-B13, HLA-B17, HLA- Cw6
- strong concordance (approx 70%) in identical twins

immunological:
- Abnormal t-cell activity stimulates keratinocyte proliferation
-TH17 cells producing IL-17 play a role (in addition to Th1 and Th2)

Environmental influences:
- Worsening: skin trauma, stress
- Triggers: streptococcal infection
- Improvement: sunlight

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24
Q

What factors may exacerbate psoriasis and what infection may trigger guttate psoriasis?

A

exacerbators:
- trauma
- alcohol
- drugs : beta blockers, lithium, antimalarials (chloroquine, hydroxychloroquine), nsaids, acei, infliximab.
- Withdrawal of systemic steroids.

Trigger: streptococcal infection can trigger guttate

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25
What are the recognised subtypes of psoriasis and their key features?
plaque psoriasis: most common : well-demarcates red scaly patches on extensor surfaces, sacrum, scalp flexural psoriasis: smooth lesions in flexural areas guttate psoriasis: transient rash, often after strep infection, multiple red, teardrop lesions on body Pustular psoriasis: often affects palms and soles
26
What are the clinical features of chronic plaque psoriasis?
Appearance: Erythematous plaques with silvery-white scale Sites: extensor surfaces ( elbows, knees), scalp, trunk, buttocks, peri-umbilical area Borders: clear delineation between normal and affected skin size : plaques range 1-10 cm Auspitz's sign: removing scale reveals red membrane with pinpoint bleeding points
27
What is guttate psoriasis, who does it affect, how is it triggered, and what are its clinical features? tell me the difference between chronic plaque psoriasis (standard) and guttate?
epidemiology: more common in children/adolescents trigger: streptococcal infection 2-4 weeks before onset features: - tear drop (gutta= drop) papules on trunk/limbs - pink, scaly patches or plaques - acute onset over days chronic plaque: large well defined thick silvery scaly plaques on extensor surfaces. guttate: sudden outbreak of small drop shaped scaly lesions often after strep throat infection usually in children/young adults.
28
How is guttate psoriasis managed?
most resolve spontaneously in 2-3 months abx to eradicate strep: no firm evidence topical agents as per psoriasis UVB phototherapy Tonsillectomy may be needed in recurrent episodes
29
What even if pityriasis rosea? How can guttate psoriasis be differentiated from pityriasis rosea (prodrome, appearance, distribution, natural history)?
pityriasis rosea: self limiting skin rash resolves on own within 6-12 weeks and starts with single "herald patch" (large oval scaly lesion) and then followed by multiple smaller oval patches on trunk, often in Christmas tree pattern. cause is usually viral Prodome : - Guttate: classically strep sore throat 2-4 weeks earlier - pityriasis rosea : may follow URTI but not typical in exams Appearance : - Guttate - tear drop scaly papules trunk/limbs - Pityriasis rosea : herald patch then multiple oval lesions with fine peripheral scale. Distribution: - guttate: scattered papules - pityriasis rosea: lesions follow langer's lines : giving "fir-tree" pattern. Natural History: Guttate: resolves in 2-3 months: treat with topical/UVB pityriasis : self-limiting resolves approx 6 weeks.
30
What is pityriasis rosea and who does it usually affect and what is thought to play a role in its aetiology? treatment?
acute self limiting rash so no treatment resolves in 6-12 weeks. affects younger adults not fully understood - thought that human herpes virus HHV-7 might play a role
31
Clinical features of pityriasis rosea including prodrome, characteristic lesions and distribution?
prodrome: - most patients: none - minority: recent viral infection herald patch: - usually on the trunk subsequent rash: - eythematous , oval, scaly patches - characteristic distribution: lesions run parallel to langer's lines: produces a "fir- tree" appearance. langers lines are: natural skin tension lines.
32
What additional features may be seen in psoriasis beyond skin lesions?
nail signs: pitting onycholysis : separation of nail plate from nail bed. arthritis (psoriatic arthritis)
33
What are the main complications associated with psoriasis?
psoriatic arthropathy (approx. 10% of patients) metabolic syndrome: cluster of conditions that increase risk of cvd and t2dm: key features 3 or more: central obesity, high bp, high triglycerides, low hdl cholesterol, high fasting glucose/insulin resistance cardiovascular disease venous thromboembolism psychological distress
34
What systemic complications are patients with psoriasis at increased risk of?
cardiovascular disease hypertension venous thromboembolism depression ulcerative colitis Crohn's disease non-melanoma skin cancer other cancers: liver lung upper Gi
35
tell me the stepwise management process of managing chronic plaque psoriasis in primary care?
general: regular emollients to reduce scale/pruritus 1st line (up to 4 weeks) : - potent corticosteroid once daily + vit d analogue once daily - apply separately (1 morning 1 evening) 2nd line (after 8 weeks no improvement) : - vit d analogue twice daily 3rd line (after 8-12 weeks no improvement) : - potent corticosteroid twice daily up to 4 weeks or coal tar preparation once/twice daily - short-acting dithranol can also be used.
36
Secondary care management options for psoriasis and tell me if they have any adverse effects too.
phototherapy: - Narrowband UVB : treatment of choice - 3 times a day -PUVA (psoralen+ UVA) also used Adverse effects: skin ageing , increased risk of SCC (not melanoma) Systemic therapy: - methotrexate (1st-line, esp with joint disease) - ciclosporin - systemic retinoids - biologics : infliximab, etanercept, adalimumab - ustekinumab (IL-12/IL-23 blocker, promising in trials)
37
How is scalp psoriasis managed?
1st line: potent topical corticosteroid once daily for 4 weeks if no improvement after 4 weeks: - switch to different formulation (Shampoo/mousse) and/or - use agents to remove adherent scale before steroid (e.g. salicylic acid, emollients, oils)
38
How is psoriasis affecting the face, flexures, and genital areas managed?
mild/moderate potency corticosteroid once or twice daily max 2 weeks.
39
What important safety considerations apply to topical corticosteroids in psoriasis?
Risks: skin atrophy, striae, rebound symptoms Areas at risk: scalp, face, flexures → max 1–2 weeks/month Systemic risk: if potent steroids applied to >10% body surface area NICE limits: Potent steroids: ≤8 weeks at a time Very potent steroids: ≤4 weeks at a time Aim for a 4-week break before restarting
40
What are the features, mechanism, pros/cons, and precautions of vitamin D analogues in psoriasis?
Examples: calcipotriol, calcitriol, tacalcitol Mechanism: ↓ cell division/differentiation → ↓ epidermal proliferation Pros: long-term use possible, no smell/staining, uncommon adverse effects Cons: reduce scale/thickness but not erythema Precautions: avoid in pregnancy; max adult weekly dose = 100 g
41
What is dithranol, how is it used in psoriasis, and what are its adverse effects?
Mechanism: inhibits DNA synthesis Use: short-contact treatment, wash off after ~30 mins Adverse effects: burning, staining
42
What is coal tar, how does it act, and what are its limitations in psoriasis?
Mechanism: not fully understood, likely inhibits DNA synthesis Limitations: unpleasant smell, staining of skin/clothing
43
What are the NICE indications for referral of a patient with psoriasis to secondary care?
Diagnostic uncertainty Severe/extensive disease (>10% BSA affected) Cannot be controlled with topical therapy, or if: Acute guttate psoriasis requires phototherapy Nail disease causes major functional/cosmetic impact Any type has major physical, psychological, or social impact Children/young people: refer to specialist at presentation
44
Which types of psoriasis require same-day referral?
Erythroderma (widespread redness and scaling affecting > 90% of BSA. Generalised pustular psoriasis.
45
What are the NICE criteria for starting non-biological systemic therapy in psoriasis?
Psoriasis cannot be controlled with topical therapy and Has significant physical/psychological/social impact and One or more of: Extensive psoriasis (>10% BSA or PASI >10) Localised psoriasis with significant functional impairment/distress (e.g. severe nail disease, high-impact sites) Phototherapy ineffective, not possible, or relapse within 3 months (>50% return of baseline severity)
46
Which agents are used for non-biological systemic therapy in psoriasis, and when might ciclosporin be preferred over methotrexate?
Agents: methotrexate, ciclosporin Methotrexate: generally first-line Ciclosporin preferred if: Need rapid/short-term control (e.g. flare) Palmoplantar pustulosis - a chronic skin condition with recurrent sterile pustules on the palms and soles, often on a red, scaly base. Patient considering conception (male or female) and systemic therapy cannot be avoided
47
What biological systemic therapies are used in psoriasis, how are they given, and what prerequisites are required before use?
Agents & routes: Adalimumab – subcutaneous injection Etanercept – subcutaneous injection Infliximab – intravenous infusion Ustekinumab – subcutaneous injection Prerequisite: Failed trial of methotrexate, ciclosporin, and PUVA (non-biologics and phototherapy)
48
nail changes in psoriasis - where is affected? does it reflect severity of psoriasis? what nail changes seen?
doesn't reflect severity affects both fingers and toes strong association with psoriatic arthropathy: 90-90% pts of psoriatic arthropathy have nail changes. pitting onycholysis (separation of nail from nail bed) subungual hyperkeratosis loss of the nail
49
What are pressure ulcers, where do they typically develop, and what factors predispose patients to them?
pressure ulcers develop in patients unable to move parts of their body due to illness, paralysis, or advancing age. typical sites: over bony prominences (eg sacrum, heel) predisposing factors: - malnourishment - incontinence (urinary and faecal) - lack of mobility - pain (reduced mobility)
50
What scoring system is widely used to screen for patients at risk of pressure ulcers, and what factors does it assess?
Scoring System: Waterlow Score Factors included: - BMI - Nutritional Status - Skin type - Mobility - Continence
51
How are pressure ulcers graded according to the European pressure ulcer advisory panel classification system?
Grade 1 : non-blanchable erythema of intact skin. other possible indicators (esp in darker skin): discolouration, warmth, oedema, induration, hardness Grade 2 : partial thickness skin loss involving epidermis or dermis (or both). Clinically appears as abrasion or blister. Grade 3: Full thickness skin loss with damage/necrosis of subcutaneous tissue. May extend down to (but not through) underlying fascia. Grade 4: Extensive destruction, tissue necrosis, or damage to muscle, bone, or supporting structures, with or without full thickness skin loss
52
How are pressure ulcers managed?
maintain a moist wound environment to encourage healing : hydrocolloid dressings and hydrogels may help avoid use of soap - to prevent drying the wound. wound scabs: not routinely done (ulcers usually colonised with bacteria) - systemic abx only if clinical evidence of infection (Surrounding cellulitis) - consider referral to a tissue viability nurse. - surgical debridement may be beneficial in selected wounds
53
What is erythema nodosum , what are its typical features, where does it occur and how does it resolve?
inflammation of subcut fat lesion: tender, erythematous, nodular lesions typical sites: usually on the shins, but may also occur on forearms and thighs course: usually resolves within 6 weeks healing: lesions heal without scarring.
54
what are the causes of erythema nodosum?
Infection: Streptococci Tuberculosis Brucellosis Systemic disease: Sarcoidosis - inflammatory disease where the body forms non-caseating granulomas (tiny clumps of immune cells) in organs, most often the lungs and lymph nodes. Inflammatory bowel disease Behçet’s disease - rare inflammatory condition causing recurrent mouth ulcers, genital ulcers, eye inflammation, and skin lesions, due to blood vessel inflammation. Malignancy/lymphoma Drugs: Penicillins Sulphonamides Combined oral contraceptive pill Other: Pregnancy
55
What is erythema multiforme, how is it classified and how does it differ from stevens-Johnson syndrome (SJS)?
hypersensitivity reaction, most commonly triggered by infections major and minor major is with mucosal involvement relation to sjs: they thought it was just a very severe form of EM but proved otherwise
56
clinical features of erythema multiforme?
target lesions initially appear on back of hands/feet, then spread to torso upper limbs more commonly affected than lower limbs pruritus: occasionally present, usually mild.
57
causes of erythema multiforme?
viruses: - herpes simplex virus (MC) - ORF - skin disease of sheep/goats, parapox virus idiopathic bacteria: mycoplasma, streptococcus drugs: - penicillin -sulphonamides -carbamazepine -allopurinol - nsaids -oral contraceptive pill - nevirapine connective tissue disorder like SLE other: sarcoidosis, malignancy
58
What are keloid scars and how do they differ from the original wound?
tumour-like lesions that arise from connective tissue of a scar extent: extend beyond dimensions of the original wound.
59
what are the predisposing factors for keloid scars?
more common in people with dark skin more common in young adults , rare in elderly common sites (Decreasing frequency): - sternum - shoulder - neck - face - extensor surface of limbs - trunk
60
how does incision placement affect the likelihood of keloid formation?
keloid scars are less likely if incisions are made along relaxed skin tension lines. langer lines (based on cadaver studies) aren't as reliable: incisions along skin tension lines give better cosmetic results.
61
How are keloid scars treated?
early keloids: intra-lesional steroids (triamcinolone) excision: sometimes required, but risk of stimulating further keloid scarring : consider carefully
62
What are head lice , what organism causes them, and how do they live and reproduce on humans?
definition: head lice (pediculosis capitis (nits)) - common condition in kids caused by : parasitic insect: pediculus capitis - lives on and amongst scalp hair. lifestyle: live only on humans. feed on human blood. eggs: - grey/brown pinhead-sized - glued close to the scalp , hatch in 7-10 days nits: - empty egg shells white and shiny - found further along hair shaft as hair grows.
63
How are head lice transmitted and what are the typical symptoms and timing of onset?
transmission: - spread by direct head to head contact - cannot jump fly or swim - more common in children due to close play symptoms: - initially asx when newly infected - itching and scratching on scalp occur 2-3 weeks after infection. incubation period: none
64
How is head lice diagnosed?
fine-toothed combing of wet/dry hair
65
How are head lice managed and what advice should be given about contacts and school attendance?
tx indicated only if living lice found tx options: - malathion - wet combing - dimeticone -isopropyl myristate -cyclomethicone contacts: - household contacts do not need treatment unless also affected school: - children with head lice shouldnt be excluded from school.
66
What is folliculitis, what causes it, how severe can it be and how does a furuncle differ?
inflammation of hair follicles can result from infection, chemical irritation or physical injury can be mild, superficial form to severe deep infections that can cause scarring or permanent hair loss. furuncle is a boil: deeper more pronounced infection of hair follicle
67
tell me the infectious and non-infectious causes of folliculitis?
bacterial: - mc: staphylococcus aureus - pseudomonas aeruginosa: hot tub folliculitis fungal : candida species, dermatophytes (Esp in immunocompromised) viral : herpes simplex virus : herpetic folliculitis non-infectious : - chemical folliculitis: from topical steroids, oils, tar - physical folliculitis: shaving, tight clothing, occlusive dressings
68
what are the general clinical features of folliculitis?
small red bumps or white-headed pimples around hair follicles itching or tenderness pus-filled blisters that may rupture and crust over
69
what are the common specific presentations of folliculitis and how do they differ?
folliculitis barbae: lesions in bearded area caused by staphylococcus aureus infection pseudofolliculitis barbae: bearded area, caused by irritation, predominantly affects men of black African or African Caribbean ancestry.
70
How would you manage folliculitis: general measures bacterial hot tub (pseduomonas) fungal viral (hsv) non infectious
General measures: Maintain good hygiene Avoid shaving/irritants and tight clothing Use warm compresses to relieve discomfort Bacterial folliculitis: Mild → topical antibiotics (e.g. fusidic acid, clindamycin) Severe/recurrent → oral antibiotics (e.g. flucloxacillin) Hot tub folliculitis (Pseudomonas): Usually self-limiting; avoid contaminated pools/hot tubs Fungal folliculitis: Topical or systemic antifungals (depending on severity) Viral folliculitis (HSV): Oral antivirals (e.g. aciclovir) Non-infectious folliculitis: Remove/avoid triggers (e.g. stop topical steroids, avoid oils/tar, loosen clothing, modify shaving practices)
71
What are the 2 main types of contact dermatitis and how do they differ in cause, mechanism and presentation?
irritant: - cause : non allergic reaction to weak acids/alkalis (eg detergents) - epidemiology: common, often seen on the hands - features: erythema typical: crusting and vesicles rare allergic: - mechanism: type iv hypersensitivity reaction - epi: uncommon, often seen on head following hair dyes - features: acute wheeping eczema, mainly at hairline margins ( not the hairy scalp itself) - tx: topical potent corticosteroid
72
how can cement cause both irritant and allergic contact dermatitis?
Irritant contact dermatitis: From the alkaline nature of cement Allergic contact dermatitis: From dichromates present in cement
73
What is basal cell carcinoma and what are its key characteristics, how common is it?
1 of 3 main types of skin cancer. other name: rodent ulcer characteristics: - slow growing -locally invasive - metastases are extremely rare epi: most common type of cancer in western world
74
clinical features of nodular basal cell carcinoma which is the most common subtype?
Site: Sun-exposed areas, especially head and neck Appearance: Initially: Pearly, flesh-coloured papule with telangiectasia Later: May ulcerate, leaving a central crater
75
referral pathway if bcc is suspected
routine referral
76
mx of bcc
Surgical removal (mainstay) Curettage Cryotherapy Topical creams: imiquimod, fluorouracil Radiotherapy
77
what systemic conditions are associated with pruritus and what non systemic ones
systemic: (whole body problem) liver disease, iron def anaemia, polycythaemia, ckd, lymphoma, hyperthyroidism, hypothyroidism, diabetes pregnancy non: (local skin problem) - senile pruritus, urticaria, eczema, scabies, psoriasis, pityriasis rosea
78
liver disease can be associated with pruritus - what are the key clinical features that'll help identify it?
hx of alcohol excess stigmata of chronic liver disease: spider naevi, bruising, palmar erythema, gynaecomastia signs of decompensation: ascites, jaundice, encephalopathy
79
iron deficiency anaemia can be associated with pruritus - what are the key clinical features that'll help identify it?
pallor koilonychia, atrophic glossitis, post-cricoid webs, angular stomatitis
80
polycythaemia can be associated with pruritus - what are they key clinical features thatll help identify it?
itching esp with a warm bath ruddy complexion (reddish healthy and flushed) may have gout or peptic ulcer disease
81
ckd can be associated with pruritus - what are they key clinical features thatll help identify it?
Lethargy, pallor Oedema, weight gain Hypertension
82
lymphoma can be associated with pruritus - what are they key clinical features thatll help identify it?
Night sweats Lymphadenopathy Splenomegaly, hepatomegaly Fatigue
83
what is onycholysis and what are the causes?
Onycholysis describes the separation of the nail plate from the nail bed Causes idiopathic trauma e.g. Excessive manicuring infection: especially fungal skin disease: psoriasis, dermatitis impaired peripheral circulation e.g. Raynaud's ( fingers toes change colour response to cold or stress due to spasm of small blood vessels reducing blood flow) systemic disease: hyper- and hypothyroidism
84
of these nail signs tell me which conditions they are seen in : nail pitting blue nails leuconychia half and half (lindays nails) nail patella syndrome yellow nail syndrome (thick yellow slow growing nails)
nail pitting: psoriasis and alopecia areata blue nails: Wilsons disease leukonychia: hypoalbuminemia, less common is fungal disease or lymphoma half and half: distal portion brown and proximal portion pale. chronic renal failure nail patella syndrome: rare genetic with abnormal nails might be missing ridged or small. knee problems - absent or underdeveloped patellae. yellow nail syndrome: associated with congenital lymphoedema, pleural effusions, bronchiectasis and chronic sinus infections
85
What is onychomycosis, which nails are most commonly affected, and what are the main causative organisms?
Definition: Fungal nail infection that may involve any part of the nail or the entire nail unit Epidemiology: Toenails are much more likely to be infected than fingernails Causative organisms: Dermatophytes (type of fungi that infect keratinised tissue so skin hair nails) (~90% of cases, mainly Trichophyton rubrum) Yeasts (~5–10% of cases, e.g. Candida) Non-dermatophyte moulds
86
rf for onychomycosis?
Increasing age Diabetes mellitus Psoriasis Repeated nail trauma
87
What are the clinical features of onychomycosis?
Most patients present due to “unsightly” nails Thickened, rough, opaque nails are the most common finding
88
main differential diagnoses for onychomycosis
Psoriasis Repeated trauma Lichen planus Yellow nail syndrome
89
How should onychomycosis be investigated, and what is a key limitation of the tests?
Investigations: Nail clippings ± scrapings Microscopy and culture Indication: Should be done in all patients if antifungal treatment is being considered Limitation: False-negative rate of cultures is ~30% → repeat samples may be needed if clinical suspicion remains high
90
How is onychomycosis managed, and how does treatment vary depending on severity and causative organism?
No treatment needed if asymptomatic and patient not bothered by appearance If dermatophyte or Candida infection confirmed: Limited involvement (≤50% nail, ≤2 nails affected, superficial white onychomycosis): Topical amorolfine 5% nail lacquer Duration: 6 months (fingernails), 9–12 months (toenails) Extensive involvement due to dermatophyte infection: Oral terbinafine (first-line) Duration: 6 weeks–3 months (fingernails), 3–6 months (toenails) Extensive involvement due to Candida infection: Oral itraconazole (first-line, pulsed weekly therapy)
91
What is a lipoma, whats it pathophysiology and how common is malignant transformation? epidemiology
common benign tumour of adipocytes usually in subcut tissues. rarely in deeper adipose tissue. malignant transformation : very rare to liposarcoma 1 in 1000 mc in middle aged adults
92
characteristic clinical features of a lipoma how to diagnose?
lump characteristics: smooth mobile painless clinical diagnosis
93
how to manage a lipoma
observation if asx removal if diagnosis is uncertain or compressing surrounding structures
94
features suggesting possible sarcomatous change in a lipoma and what is their significance?
features suggestive of liposarcoma: size> 5cm increasing size pain deep anatomical location if all 4 features present : upto 85% risk of sarcoma in 1 series
95
What is the main cause of venous leg ulcers, and what are other possible causes?
Main cause: venous hypertension secondary to chronic venous insufficiency Other causes: calf pump dysfunction or neuromuscular disorders.
96
how do venous leg ulcers form pathophysiologically?
In chronic venous hypertension, pressure in the veins → capillaries also get over-pressurised. Plasma (including fibrinogen) leaks out of those tiny capillaries. Fibrinogen becomes fibrin, and wraps around the capillaries like a thin cuff. That “fibrin cuff” makes it harder for oxygen and nutrients to diffuse into the skin → poor healing and ulceration. leucocyte sequestration too : venous htn so blood flow in capillaries slows then wbc(leucocytes) stick to capillary walls (endothelium) and become trapped (sequestered) and release inflammatory mediators and enzymes. both lead to microcirculatory damage, poor oxygenation and poor tissue healing so tissue breakdown.
97
key features of venous insufficiency (veins have trouble returning blood back to heart)
oedema brown pigmentation (haemosiderin deposition which is iron containing pigment coming from rbc breakdown) lipodermatosclerosis (fibrosis and hardening of skin) venous eczema
98
What are the typical clinical features and location of venous leg ulcers?
usually above the ankle (gaiter area and just above the medial malleolus) painless shallow ulcer with irregular edges surrounding skin often shows venous changes (pigmentation, eczema, swelling, oedema, fibrosis)
99
what conditions are associated with deep vs superficial venous insufficiency?
deep venous insufficiency: usually due to previous dvt superficial venous insufficiency: often due to varicose veins.
100
What imaging ix are used for venous leg ulcers, and what do they assess?
Doppler ultrasound: detects presence of reflux Duplex ultrasound: assesses anatomy and venous flow.
101
What is the purpose of an ankle-brachial pressure index (ABPI) and what are its key values?
used to assess for arterial disease in non-healing ulcers (as poor arterial flow impairs healing) normal ABPI: 0.9-1.2 <0.9 : suggests arterial disease >1.3 : may also indicate arterial disease due to arterial calcification (false-negative result eg in diabetics)
102
How are venous leg ulcers managed? main tx surgical adjuncts what doesnt work?
Main treatment: 4 layer compression bandaging but only after excluding arterial disease. (check ABPI before applying compression) Surgical Options: consider surgery for venous insufficiency If ulcer fails to heal after 12 weeks or is >10cmsquared , skin grafting may be required. adjuncts: oral pentoxifylline: peripheral vasodilator that improves healing rate. flavonoids: some evidence of benefit though limited hydrocolloid dressings, topical growth factors, ultrasound therapy, intermittent pneumatic compression - all have little evidence for efficacy.
103
What is a Marjolin's Ulcer, and where does it usually occur?
squamous cell carcinoma developing at sites of chronic inflammation (eg old burns, chronic osteomyelitis) usually appears 10-20 years later, most commonly on the lower limb.
104
What are the typical sites and features of arterial ulcers?
sites: toes and heels appearance: deep punched out ulcers with well defined angles pain: painful (Especially at night or when legs elevated) associated findings: cold limbs, no palpable pulses, possible gangrene, and low ABPI measurements.
105
Where do neuropathic ulcers commonly occur and what causes them?
commonly on plantar surface of the metatarsal heads and plantar surface of the hallux (big toe) - l shape kinda caused by pressure and loss of protective sensation due to peripheral neuropathy (commonly diabetic)
106
common condition leading to amputation in diabetic patients
plantar neuropathic ulcer
107
how to manage neuropathic ulcer?
use cushioned shoes and pressure relieving footwear to reduce callous formation and redistribute pressure
108
what is pyoderma gangrenosum and with which conditions is it associated?
neutrophilic dermatosis causing rapidly enlarging ulcers. (inflammatory skin disease) associated with inflammatory bowel disease (especially ulcerative colitis and rheumatoid arthritis) can occur at stoma sites.
109
What are the typical clinical features of pyoderma gangrenosum?
start as erythematous nodules or pustules that ulcerate, often with painful, undermined (edge with the red bit being inside) , violaceous edges.
110
What are arterial ulcers and what causes them?
arterial (ischaemic) ulcers are chronic wounds caused by insufficient arterial blood supply, most commonly bc of peripheral arterial disease(PAD) result from tissue ischaemia and necrosis secondary to reduced arterial blood flow. typically painful slow to heal and can impair QoL
111
pathophysiology of arterial ulcer formation
caused by reduced arterial perfusion which causes tissue ischaemia which causes necrosis and ulceration. primary cause: atherosclerosis, narrowing and hardening of arteries other factors: thrombosis, embolism, trauma ischaemia deprives tissue of oxygen and nutrients impairs healing and leads to ulcer formation.
112
risk factors for arterial ulcer formation
SAME AS CV DISEASE smoking diabetes htn hyperlipidemia obesity sedentary lifestyle
113
typical locations and appearance of arterial uclers
found on lower extremities, especially over bony prominences: lateral malleolus toes anterior tibial area appearance: small round with well-defined, "punched-out" edges. base: pale, dry or necrotic often surrounded by shiny, thin, hairless, pale skin
114
key symptoms and signs associated with arterial ulcers
pain: severe, often worse at night or when leg is elevated (relieved by hanging leg down) surrounding skin: shiny, thin, hairless, with atrophy and pallor pulses: diminished or absent peripheral pulses (dorsalis, pedis, posterior tibial) temperature: cool limb due to poor perfusion may be associated with areas of gangrene.
115
how would you diagnose an arterial ulcer?
physical exam: inspect ulcer characteristics and assess peripheral pulses. ABPI: non-invasive test comparing ankle and arm blood pressures. ABPI < 0.9 indicates PAD. doppler ultrasound: assesses arterial blood flow and detects stenosis or occlusion. imaging: MRA or CTA to visualise arterial anatomy and localise blockages blood tests: lipid profile, blood glucose, and other tests to identify modifiable cv risk factors.
116
what are main goals in managing arterial ulcers?
improve blood supply, promote ulcer healing, and prevent recurrence.
117
What are the key management strategies for arterial ulcers?
risk factor modification: - smoking cessation - diet change ( reduce saturated fats, improve cv health) - regular exercise (As tolerated) - control comorbidities : DM, HTN, HYPERLIPIDEMIA Optimisation of blood flow: - revascularisation procedures: angioplasty,stenting,bypass surgery to restore arterial flow. -pharmacotherapy so antiplatelets like aspirin or clopidogrel or statins for lipid control and atherosclerosis management. Wound care: - debridement: remove necrotic tissue (surgical, enzymatic or with specialised dressings) - dressings: maintain moist wound environment and protect against infection (hydrocolloid, alginate or foam dressing) - infection control: topical/systemic abx if infection evidence. monitor for comps: - watch for osteomyelitis, gangrene and critical limb ischaemia
118
Why should compression bandaging not be used in arterial ulcers?
compression further reduces arterial perfusion so worsens ischaemia. always exclude arterial disease (ABPI) before applying compression - only indicated in venous ulcers.
119
What are actinic (solar) keratoses and what causes them?
premalignant skin lesion caused by chronic sun exposure (UV damage) result from cumulative uv radiation = keratinocyte dysplasia. happens in fair skinned older adults - esp those with outdoor occupations. POTENTIAL TO PROGRESS TO SCC.
120
characteristic features of actinic keratoses?
small crusty scaly lesions on sun-exposed skin. colour: pink red brown or same as surrounding skin surface: rough sandpaper like texture. location: commonly on temples face scalp(bald men), ears forearms and dorsum of hands often multiple lesions may be present simultaneously
121
what are key management options for actinic keratoses?
prevent further damage: avoid sun, protective clothes, regular sunscreen (spf 30+) topical therapy: - fluorouracil (5-FU) cream : 2-3 week course. can cause redness and inflammation during tx. give topical hydrocortisone after to reduce inflammation - topical diclofenac: for milk AK. moderate efficacy but fewer side effects. - topical imiquimod: - good efficacy shown in trials. stimulates local immune response to abnormal cells. procedural options: - cryotherapy (liquid nitrogen) for isolated lesions. - curettage and cautery for thicker or resistant lesions. (scrape of cancerous tissue and then apply heat to destroy)
122
why is treatment of actinic keratoses important?
because AK premalignant - can progress to SCC if left untreated
123
What is impetigo and what are its main causative organisms?
superficial bacterial skin infection. usually caused by staphylococcus aureus or streptococcus pyogenes (Group A b-haemolytic streptococcus) can be primary (on normal skin) or secondary to other skin conditions like eczema scabies or insect bites
124
who is most commonly affected by impetigo and under what conditions?
common in children esp in warm weather when bacterial growth and skin contact increase
125
where on the body does impetigo usually occur?
can appear anywhere but commonly on: face flexures exposed limbs - areas not covered by kapreh
126
how is impetigo spread and what is its incubation period?
direct contact with discharges from lesions/scbas bacteria enter via minor abrasions and spread through scratching. mainly transmitted via hands, but also toys clothing equipment and the environment. incubation: 4-10 days
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key clinical features of impetigo?
golden crusted skin lesions typically around mouth andnose. lesions may start as vesicles that rupture and form honey coloured crusts. highly contagious. usually painless, but may cause mild itching or irritation. systemic symptoms are rare.
128
how is limited localised impetigo managed? if its extensive then?
1st line: hydrogen peroxide 1% cream - if not systemically unwell or at high risk of comps. - recommended to reduce abx resistence and is just as effective as topical abx for non-bullous impetigo. alternative if topical abx required: topical fusidic acid. topical mupirocin if fusidic acid resistance is suspected. MRSA: resistant to fusidic acid and retapamulin = use topical mupirocin instead. EXTENSIVE: - -1ST LINE - ORAL FLUCLOXACILLIN. - IF PENICILLIN ALLERGY: ERYTHROMYCIN (MACROLIDE ALTERNATIVE)
129
what are the school exclusion recommendations for children with impetigo?
exclude from school until lesions are crusted and healed or 48 hrs after starting abx treatment (whichever comes first)
130
why is proper hygiene important in impetigo mx? key measures to prevent spread
prevent spread to other body areas and contacts. key measures: - handwashing - avoid sharing towels - cover lesions
131
tell me the key priorities in the immediate mx of burns
airway breathing circulation (ABC) - assess first! stop burning process and prevent further injury
132
tell me the correct first aid for thermal (heat) burns
remove from heat source. within 20 mins of injury irrigate with cool (not iced) water for 10-30 mins. dont use ice. cover the burn with cling film - apply in layers not wrapped around limbs (to allow for swelling)
133
tell me the key first aid steps for electrical and chemical burns
electric: switch off power supply first then remove person from source. chemical: - brush off any dry/powder chemicals then irrigate thoroughly with water. - don't attempt neutralisation of chemical.
134
what methods are used to estimate burn surface area
wallaces rule of nines: - head and neck: 9% - each arm : 9% - each anterior leg - each posterior leg - anterior chest - posterior chest - anterior abdomen - posteriori abdomen lund and browder chart: most accurate, adjusts for age and body proportions palmar surface method: patients palm is like 1% total body surface area (TBSA) - useful for small burns under 15%.
135
when figuring out depth of burns tell me what theyre called and the appearance
1st degree: superficial epidermal: red painful dry no blisters 2nd degree: partial thickness (superficial dermal) - pale pink painful blistered slow capillary refill 2nd degree: partial thickness deep dermal - white or mottled reduced sensation painful to deep pressure non-blanching erythema. 3rd degree - full thickness - white(waxy) , brown(leathery) or black , no blisters painless (nerve destruction)
136
Which burns should be referred to a specialist burns unit or secondary care?
all deep dermal and full-thickness burns superficial dermal burns over 3 % tbsa adult or 2% tbsa for children. burns involving face, hands, feet, perineum, genitalia, flexures or circumferential burns of limbs torso or neck. inhalation injury suspected electrical/chemical burns. suspicion of non-accidental injury.
137
outline the initial management steps for burns
immediate first aid (cooling, covering, ABCs) review referral criteria - ensure appropriate setting. superficial epidermal burns: symptomatic relief - analgesia, emolients, etc superficial dermal burns: - cleanse wound leave blisters intact apply non-adherent dressing, avoid topical creams and then review in 24 hrs
138
what are the systemic effects and pathophysiology of severe burns?
local response: progressive tissue loss, release of inflammatory cytokines. systemic effects: - fluid loss and third spacing: hypovolemia, shock - catabolic state: protein breakdown, metabolic stress - immunosuppression, leading to bacterial translocation from gut into normally sterile tissue (cross the intestinal barrier into like liver, portal venous system, mesenteric lymph nodes) : sepsis (common cause of death in major burns)
139
tell me priorities in management of a severe burn? ABC when to transfer to burns unit?
stop burning process and resuscitate. airway: - assess for smoke inhalation and airway oedema. - early intubation if facial/neck burns, stridor, or oropharyngeal blistering. breathing/circulation: - iv fluids if >10% TBSA in children or >15% in adults. - use parkland formula for resuscitation: volume (ml) = % TBSA* weight(kg) * 4 - give half in first 8 hours half over next 16 hours. - insert urinary catheter for monitoring output. - analgesia as needed. transfer if: - complex burns, hands/perineum/face - over 10% in adults 5% in children.
140
when is an escharotomy indicated? what is it?
escharatomy: surgery where burn eschar ( tough leathery dead skin) cut open to relieve pressure and restore circulation or ventilation to underlying tissues. do if: - circumferential full-thickness burns to limbs or torso that: - restrict respiration (if chest/torso) or - cause compartment syndrome (if limb) procedure is careful division of burnt tissue (eschar) to relieve pressure and improve perfusion * compartment syndrome - high pressure in closed muscle compartment cutting blood flow = ischaemia = emergency fasciotomy needed
141
principles of wound care in burns
superficial burns: conservative management most heal within 2 weeks. deep/complex: possible excision and skin grafting required. primary close : not usually performed due to high infection risk. no evidence prophylactic systemic or topical abx. maintain strict asepsis, pain control and nutritional support.
142
What is acanthosis nigricans and how does it present clinically?
skin condition characterised by symmetrical, brown, velvety, hyperpigmented plaques. common sites: neck, axillae, groin ( can affect elbows, knees, or umbilicus) lesions are typically painless, thickened with velvety texture.
143
Describe the pathophysiology of acanthosis nigricans
caused by insulin resistance = leads to hyperinsulinemia Excess insulin stimulates keratinocyte and dermal fibroblast proliferation via insulin-like growth factor receptor-1 (IGFR1). Leads to epidermal thickening (acanthosis) and increased pigmentation.
144
What are the main causes and associations of acanthosis nigricans?
Endocrine/metabolic causes: - obesity - T2DM - Polycystic ovary syndrome (PCOS) - Cushing's syndrome - Acromegaly - Hypothyroidism Genetic/Familial causes: - Familial acanthosis nigricans - Prader-Willi Syndrome Malignant Cause: - Gastrointestinal (especially gastric) adenocarcinoma - particularly if onset is sudden in an older patient. Drug Induced: - Combined Oral Contraceptive pill (COCP) - Nicotinic Acid (niacin)
145
What is the significance of sudden-onset acanthosis nigricans in an older adult?
suggests a paraneoplastic cause, most commonly gastrointestinal adenocarcinoma (Especially gastric cancer) should prompt evaluation for malignancy.
146
How is acanthosis nigricans managed?
Identify and treat the underlying cause: - Weight loss for obesity - Improved glycaemic control in T2DM. - Manage associated endocrine disorders. Symptomatic treatment: - Topical keratolytics such as topical retinoids may help smooth thickened skin. Screen for malignancy: - Especially in sudden-onset cases or older patients without clear metabolic cause.
147
What is lichen planus and what is its likely cause?
Inflammatory skin disorder of unknown aetiology, most likely immune-mediated (T-cell driven autoimmune reaction against basal keratinocyte (bottom layer cells of epidermis - stem cells that divide and move upward becoming the different layers of skin as they mature.) can affect skin, oral mucosa, genitalia, nails and occasionally the scalp.
148
what are the characteristic features of lichen planus?
itchy, papular rash - often intensely pruritic. Common sites: palms, soles, genitalia, and flexor surfaces of the arms (especially wrists) papules are polygonal (flat-topped) and may merge into plaques. Wickham's Striae: fine white lacy lines visible on the surface of the lesions. Koebner phenomenon: new lesions appear at sites of trauma.
149
What mucosal and nail changes can occur in lichen planus?
oral involvement : - occurs in approx 50% of pts. - white lace(reticular) pattern on buccal mucosa : sometimes erosive or ulcerative. Nail Changes: - thinning of the nail plate - Longitudinal ridging. - In severe cases, nail loss or pterygium formation (adhesion of proximal nail fold to nail bed)
150
Which drugs are known to cause lichenoid eruptions?
Gold Quinine Thiazide Diuretics (Acei, B-blockers, and antimalarials.)
151
How is Lichen Planus Managed?
1st line: - Potent Topical Corticosteroids (eg betamethasone, clobetasol) - mainstay of treatment. Oral Involvement : - Benzydamine mouthwash or spray for pain and inflammation. Extensive or resistant disease: - oral corticosteroids or immunosuppressants (eg azathioprine, ciclosporin) Supportive: - Antihistamines for itching. - Avoid trauma or scratching (Koebner phenomenon).
152
What is the prognosis of lichen planus?
Chronic but usually self-limiting within 1-2 years. Recurrences can occur. Oral lichen planus may persistent longer and rarely carry a small risk of malignant transformation to oral squamous cell carcinoma.
153
What is rosacea who does it typically affect?
Chronic inflammatory skin disorder of unknown aetiology, mainly affecting the face (nose, cheeks, forehead) common in middle - aged fair-skinned adults. more severe in men, especially with rhinophyma. Triggered by sunlight, alcohol, spicy foods, stress, and extremes of temperature.
154
What are the key clinical features of rosacea?
Flushing - often the earliest symptom. Persistent erythema over central face (nose, cheeks, forehead) Telangiectasia (visible small blood vessels) Papules and Pustules develop later (acneiform but no comedones, unlike acne vulgaris) Rhinophyma: thickened, bulbous, nodular nose (advanced stage) Ocular involvement: blepharitis, conjunctivitis, or keratitis. Sunlight and heat may exacerbate symptoms.
155
What is thought to underlie rosacea pathogenesis?
likely immune dysregulation with vascular hyperreactivity and chronic inflammation. Demodex folliculorum mites and UV exposure may contribute.
156
What are the key general measures for managing rosacea?
avoid triggers: sunlight spicy food alcohol hot drinks and stress. apply high-factor sunscreen daily (spf30+) camouflage creams may help conceal redness. gentle skincare: avoid alcohol based or irritating products.
157
How is predominant erythema/flushing managed? for rosacea
topical brimonidine gel (a-adrenergic agonist) : - used as required to temporarily reduce redness. - reduces erythema within 30 mins, peaks at 3-6 hours and redness returns gradually to baseline. - effective for flushing with limited telangiectasia.
158
How are mild-to-moderate papules and pustules managed? for rosacea
1st line: topical ivermectin. alternative: topical metronidazole or topical azelaic acid. continue general skin care and sun protection.
159
How are moderate to severe papules and pustules managed in rosacea?
combination therapy: topical ivermectin + oral doxycycline (tetracycline antibiotic with anti-inflammatory effect)
160
when should patients with rosacea be referred to secondary care or dermatology?
no improvement with optimal primary care mx. prominent telangiectasia- may benefit from laser therapy prescence of rhinophyma (may require surgical or laser treatment.) severe ocular involvement.
161
How can rosacea be distinguished from acne vulgaris?
rosacea: no comedones (blackheads/whiteheads) , central facial redness, flushing, telangiectasia and ocular involvement. acne vulgaris: comedone always present, affects wider areas ( face, back, chest) not triggered by flushing.
162
What is seborrheic dermatitis and what causes it?
chronic eczematous dermatitis affect sebum-rich areas of skin. thought to be inflammatory reaction to malassezia furfur fungus (formerly pityrosporum ovale) common - affects about 2% of general population.
163
What are the characteristic features of seborrheic dermatitis in adults?
Eczematous lesions on sebum-rich areas: - scalp - dandruff - periorbital area - auricular folds - around ears - nasolabial folds - sides of nose may be associated with otitis externa or blepharitis. chronic recurrent course.
164
What conditions are associated with seborrhoeic dermatitis in adults?
HIV infection - can be severe or extensive Parkinson's disease ( due to increased sebum production)
165
How is seborrheic dermatitis of the scalp managed in adults?
1st line: ketoconazole 2% shampoo (antifungal to reduce malassezia) alternatives/adjuncts: - OTC shampoos containing zinc pyrithione ( eg head and shoulders) - tar-based shampoos ( neutrogena T/gel) - Selenium sulphide may be useful. - Topical corticosteroids for short-term control of inflammation.
166
How is seborrhoeic dermatitis affecting the face or body managed?
topical antifungals eg ketoconazole cream. topical corticosteroids: short courses to reduce inflammation. difficult to treat - recurrences are common. maintain skin hygiene and avoid irritants.
167
How does seborrhoeic dermatitis present in infants?
common infant skin condition, typically affects: - scalp (cradle cap) - nappy area - face - limb flexures cradle cap: erythematous rash with coarse yellow scales, developing in the first few weeks of life.
168
How is seborrheic dermatitis managed in infants?
reassure parents - its harmless and resolves spontaneously (usually by 8 months of age) conservative care: - massage topical emollient into scalp to loosen scales. - gently brush with a soft brush. - wash off with mild shampoo. if severe or persistent: - topical imidazole ( antifungal) cream may be used.
169
What is the prognosis of seborrheic dermatitis in children?
usually resolves spontaneously by around 8 months of age. recurrence after infancy is rare.
170
What are the most common types of animal bites seen in clinical practice and what organisms are usually involved?
most common: dog and cat bites. infections are usually polymicrobial, but the most frequent isolate is pasteurella multocida ( especially from cat bites)
171
How should animal bites be managed?
Wound care: - thoroughly cleanse and irrigate the wound. - do not suture puncture wounds (unless required for cosmetic or functional reasons, eg face) Antibiotic prophylaxis/treatment: 1st line: co-amoxiclav. if penicillin-allergic: doxycycline + metronidazole. assess tetanus vaccination status and update if required.
172
What organisms are commonly found in human bite infections?
usually multimicrobial, including both aerobic and anaerobic bacteria: - streptococcus spp. - staphylococcus aureus - eikenella corrodens - Fusobacterium - Prevotella
173
How are human bites managed?
Cleanse wound thoroughly and avoid primary closure unless necessary for cosmesis. Antibiotic of choice: co-amoxiclav (as for animal bites) if penicillin-allergic: doxycycline + metronidazole assess for viral transmission risk : consider HIV, hepatitis B, and hepatitis C exposure. Consider HIV post-exposure prophylaxis (PEP) if high-risk source.
174
What are bed bugs and what clinical problems can they cause?
bed bugs describe a variety of clinical problems including itchy skin rashes, bites, allergic symptoms secondary to infestation with Cimex Lectularius.
175
How common are bed bug infestations and where do they thrive?
Increasingly common presentation in uk gp. bedbugs thrive in matresses or fabrics and can be extremely difficult to eradicate.
176
How is the itch from bed bug bites managed?
topical hydrocortisone is suitable to control itch.
177
what is the definitive management for bed bug infestation?
pest management company involvement and fumigation of the house.
178
what measures can help control bed bug numbers?
hot-washing bed linen and using mattress covers.
179
What causes Lyme disease and how is it transmitted?
caused by the spirochaete borrelia burgdorferi. spread by ticks (Ticks are blood-sucking arachnids (parasites) that attach to the skin of animals or humans to feed.)
180
What is the characteristic rash of early Lyme disease and its features?
erythema migrans (bull's- eye rash) at the site of the tick bite. develop 1-4 weeks after the initial bite ( may present sooner) usually painless, >5cm in diameter , and slowly increases in size. present in around 80% of patients.
181
What systemic features may be seen early in Lyme disease?
headache lethargy fever arthralgia
182
What are the cardiovascular manifestations of late lyme disease?
heart block peri/myocarditis
183
What are the neurological manifestations of late lyme disease?
facial nerve palsy radicular pain - pain radiating along a nerve root due to irritation or compression of a spinal nerve. meningitis
184
when can lyme disease be diagnosed clinically, and what is the first-line investigation if needed?
erythema Migrans is diagnostic - start antibiotics without further tests. first line test: ELISA antibodies to Borrelia Burgdorferi.
185
What should be done if the initial ELISA is negative by Lyme disease is still suspected?
if tested within 4 weeks of symptom onset - repeat ELISA in 4-6 weeks. if symptoms for 12 weeks or more and still suspected then perform immunoblot test. if positive or equivocal ELISA, perform immunoblot test for confirmation.
186
How should an attached tick be removed, and are antibiotics indicated?
Use fine-tipped tweezers, grasp tick close to skin, and pull upwards firmly. wash the area afterwards. routine antibiotic treatment is not recommended for patients with tick bites.
187
What are the antibiotic options for lyme disease?
doxycycline for early disease. amoxicillin if doxycycline is contraindicated ( eg pregnancy) ceftriaxone for disseminated disease. people with erythema migrans should be started on antibiotics without further testing.
188
What reaction may occur after initiating therapy for Lyme disease?
jarisch-herxheimer reaction : fever, rash, tachycardia after the first antibiotic dose. more commonly seen in syphilis (another spirochaetal infection)
189
in which group of women does atrophic vaginitis most commonly occur
post menopausal women
190
what are the typical symptoms of atrophic vaginitis?
vaginal dryness dyspareunia - pain during sex occasional spotting
191
what are the examination findings in atrophic vaginitis?
vagina appears pale and dry
192
how is atrophic vaginitis treated?
vaginal lubricants and moisturisers are 1st line if they dont help use topical oestrogen cream
193
How common is vaginal itching and how does it differ from pruritus ani (anus)
vaginal itching common- 1in 10 women seek help at some point. pruritus vulvae usually has underlying cause but pruritus ani doesnt.
194
What are the common causes of pruritus vulvae?
irritant contact dermatitis - eg latex condoms, lubricants - mc cause atopic dermatitis seborrheic dermatitis lichen planus lichen sclerosus psoriasis - seen in approx. 1/3 of patients with psoriasis.
195
What general advice should be given to women with pruritus vulvae?
take showers rather than baths. clean the vulval area with an emolient such as epaderm or diprobase. clean only once daily - repeated cleaning can worsen symptoms.
196
how are underlying causes of pruritus vulvae treated?
most conditions respond to topical steroids. combined steroid-antifungal cream may be used if seborrhoeic dermatitis is suspected.
197
What is acne and what structure of the skin does it affect?
disease of pilosebaceous unit. several different types of acne lesions are usually seen in each patient.
198
How are comedones formed and what are the types? (Acne vulgaris)
comedones are due to a dilated sebaceous follicle. if the top is closed, whitehead is seen. if the top opens blackhead forms
199
what causes inflammatory lesions in acne?
inflammatory lesions form when the follicle bursts, releasing irritants. types: papules and pustules
200
what lesions may result from an excessive inflammatory response?
nodules cysts
201
what can acne ultimately cause,and what are the types of scars?
scarring types: icepick scars hypertrophic scars
202
how does drug induced acne differ from typical acne?
drug induced acne is often monomorphic (eg pustules are characteristically seen in steroid use)
203
What is acne fulminans?
very severe acne associated with systemic upset eg fever hospital admission often required usually responds to oral steroids
204
what is acne vulgaris and where does it typically occur?
common skin disorder usually occurring in adolescence. typically affects the face, neck and upper trunk. characterised by obstruction of pilosebaceous follicles with keratin plugs, resulting in comedones, inflammation, and pustules.
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How is acne classified?
Mild: open and closed comedones with or without sparse inflammatory lesions. Moderate: Widespread non-inflammatory lesions and numerous papules and pustules. Severe: Extensive inflammatory lesions, which may include nodules, pitting, and scarring.
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What are the first-line treatment options for mild to moderate acne?
12 week course of topical combination therapy should be tried 1st line: - fixed combination of topical adapalene with topical benzoyl peroxide. - fixed combo of topical tretinoin with topical clindamycin. - fixed combo of topical benzoyl peroxide with topical clindamycin topical benzoyl peroxide can be used as monotherapy if these options are contraindicated or the person wishes to avoid using topical retinoid or antibiotic.
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What are the treatment options for moderate to severe acne?
12 week course of one of following options: - fixed combo of topical adapalene with topical benzoyl peroxide - fixed combination of topical tretinoin with topical clindamycin - fixed combo of topical adapalene with topical benzoyl peroxide + either oral lymecycline or oral doxycycline - topical azelaic acid + either oral lymecycline or oral doxycycline.
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important points about oral abx usage in acne?
avoid tetracyclines in pregnant and breasfeeding women in children under 12 - erythromycin in pregnancy is good to use. minocycline now considered less appropriate due to possibility of irreversible pigmentation. only continue abx treatment ( topical or oral) for over 6 months in exceptional circumstances. topical retinoid ( if not contraindicated) or benzoyl peroxide should always be co-prescribed with oral abx to reduce abx resistance. topical and oral abx shouldnt be used together. gram negative folliculitis may occur as a complication of long-term abx use - high dose oral trimethoprim is effective if this occurs.
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What are the alternative options to oral abx in women with acne?
combined oral contraceptives (COCP) can be used as an alternative to oral abx in women. as with abx, they should be used in combo with topical agents. dianette ( co-cyprindiol) is sometimes used because of its anti-androgen properties but: - has increased risk of VTE compared to other COCPs. - Should generally be used 2nd line - only for 3 months and women should be counselled about risks
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when should oral isotretinoin be considered in acne?
only under specialist supervision. pregnancy is contraindication to topical and oral retinoid tx.
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Which abx approaches should be avoided to reduce abx resistance?
monotherapy with topical abx. monotherapy with oral abx combination of topical abx and oral abx.
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which patients should be referred to a dermatologist for acne?
acen conglobata: rare severe form ( mainly in men) with extensive inflammatory papules, suppurative nodules ( may coalesce to form sinuses) and cysts on the trunk. nodulo-cystic acne.
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when should referral for acne be considered:
mild to moderate acne that hasnt responded to 2 completed courses of tx. moderate to severe acne that hasnt responded to previous tx including an oral abx. acne with scarring. acne with persistent pigmentary changes. acne causing or contributing to persistent psychological distress or a mental health disorder.
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How common in acne vulgaris and who in?
80-90% of teenagers, 60% seek medical advice. could persistent beyond adolescence affecting 10-15% of females and 5% of males over 25 yrs old.
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what are the main pathological mechanisms of acne?
follicular epidermal hyperproliferation leads to formation of keratin plug leads to obstruction of the pilosebaceous follicle. activity of sebaceous glands may be controlled by androgens although levels are often normal in patients. colonisation by proprionibacterium acnes ( anerobic bacterium) inflammation
216
What is eczema herpeticum and what causes it?
severe primary infection of the skin by herpes simplex virus 1 or 2. more commonly seen in children with atopic eczema and presents as a rapidly progressing painful rash.
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what are the examination findings in eczema herpeticum?
monomorphic punched-out erosions ( circular depressed ulcerated lesions) usually 1-3mm in diameter
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how is eczema herpeticum managed?
potentially life threatening - children should be admitted for iv aciclovir.
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Hoe common is eczema in children and when does it usually present?
occurs in around 15-20% of children and is becoming more common. typically presents before 2 yrs of age. clears in around 50% of children by 5 years, and 7% by 10 years of age
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what are the features of eczema in children?
itchy erythematous rash. repeated scratching may exacerbate affected areas. in infants, the face and trunk are often affected. in younger children eczema often occurs on the extensor surfaces. in older children, more typical flexor distribution is seen, affecting creases of face and neck
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How is eczema in children managed?
avoid irritants. simple emolients: - large quantities should be prescribed ( eg 250g/week) roughly in a 10:1 ratio with topical steroids. apply emolient first, then wait 30 mins before applying topical steroid. creams soak in faster than ointments. avoid contamination: dont insert fingers into pots - many have pump dispensers. topical steroids wet wrapping: - large amounts of emolient ( and sometimes topical steroids) applied under wet bandages. in severe cases, oral ciclosporin may be used
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What are the key components of eczema mx?
avoidance of triggers and skin care education: avoid known irritants and allergens. provide guidance on gentle skin care routines .
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what is the role of emolients in eczema mx?
integral to all tx plans regardless of severity. use liberally and regularly, even when skin is clear, to maintain hydration and barrier function. selection should be based on pt preference to improve adherence. creams are generally preferred by most people- adherence is key. ointments provide the strongest emolient effect and may be more effective, but are greasy and better at night.
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What topical therapies are used for eczema?
Topical corticosteroids: - vital for managing flare-ups, with potency tailored to severity and site. example treatments (NICE): - mild eczema : hydrocortisone 1% - moderate eczema : betamethasone valerate 0.025% or clobetasone butyrate 0.05% - severe eczema : betamethasone valerate 0.1% topical calcineurin inhibitors: - suitable for sensitive skin regions, include tacrolimus and pimecrolimus. topical antimicrobials: - used when there is clinical evidence of secondary infection.
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What systemic therapies may be used for eczema?
indicated for severe or unresponsive cases. oral corticosteroids: - used cautiously for acute severe exacerbations. immunosuppressants: - ciclosporin, methotrexate, or azathioprine for chronic severe eczema. biologic therapies: - dupilumab for cases unresponse to conventional therapy.
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What other treatment may be considered for extensive eczema?
phototherapy
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What prognostic markers are associated with severe disease in acne?
onset at age 3-6 months. severe disease in childhood. associated asthma or hay fever. small family size. high IgE serum levels.
228
what is the general principle for using topical steroid creams? and give me examples of them too pls
use the weakest steroid that control symptoms. 1 finger tip unit (FTU) = 0.5g , sufficient to treat a skin area about twice the size of the flat of an adult hand. mild : hydrocortisone 0.5-2.5% moderate: betamethasone valerate 0.0o25% (betnovate RD) clobetasone butyrate 0.05% (eumovate) fluticasone propionate (0.05%) cutivate potent: betamethasone valerate 0.1% (betnovate) very potent: clobetasol proprionate 0.05% (dermovate)
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With steroid applications how many finger tip units for : Hand and fingers (front and back) A foot (all over) Front of chest and abdomen Back and buttocks Face and Neck An entire arm and hand An entire leg and foot
hand and fingers (front and back) : 1.0 a foot (all over) : 2.0 front of chest and abdomen: 7.0 back and buttocks: 7.0 face and neck: 2.5 an entire arm and hand : 4.0 an entire leg and foot : 8.0
230
For the following what quantities of topical steroids for a single daily application for 2 weeks?
Face and Neck: 15 to 30g Both hands: 15 to 30g Scalp: 15 to 30g Both arms: 30 to 60g Both legs: 100g Trunk: 100g Groin and Genitalia: 15 to 30g
231
What is cellulitis and which layers of the skin does it affect?
bacterial infection affecting the dermis and deeper subcutaneous tissues. clinical diagnosis
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tell me the most common causative organisms of cellulitis
streptococcus pyogenes - most common staphylococcus aureus - less common
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How do most cases of cellulitis resolve?
majority of cases with oral abx
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most common clinical features of cellulitis
commonly occurs on the shins usually unilateral - bilateral cellulitis is rare and suggests alternative diagnosis. erythema - generally well defined margins, could present with diffuse erythema. blisters and bullae may be seen with severe disease. swelling. systemic upset: fever malaise nausea
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How is cellulitis diagnosed and when are ix required?
clinical diagnosis. no further ix required in primary care. bloods and blood cultures may be requested if pt is admitted and septicaemia is suspected
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What is the eron classification system for celllulitis and what are its classes?
1 - no signs of systemic toxicity and no uncontrolled co-morbidities. 2 - systemically unwell or systemically well but with co-morbidity like peripheral arterial disease, chronic venous insufficiency, morbid obesity - which may complicate or delay resolution. 3. - significant systemic upset (acute confusion tachycardia tachypnoea hypotension) or unstable co-morbidities that may interfere with response to treatment, or limb threatening infection due to vascular compromise. 4 - sepsis syndrome or severe life threatening infection such as necrotizing fasciitis.
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which patients should be admitted for iv antibiotics according to eron classification?
eron class 3 or 4 cellulitis. severe or rapidly deteriorating cellulitis ( eg extensive skin involvement) very young ( under 1 yr) or frail patients. immunocompromised patients. significant lymphoedema. facial cellulitis (unless very mild) or periorbital cellulitis.
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what is recommended for eron class 2 cellulitis?
admission may not be necessary if community facilities and expertise are available to give iv abx and monitor the patient (check local guidelines)
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how should patients not requiring admission for cellulitis be treated?
oral abx
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how is cellulitis mx guided?
eron classification
241
tell me the nice recommendations for eron class 1 cellulitis tx?
oral flucloxacillin: 1st line for mild/moderate cellulitis if penicillin allergic: oral clarithromycin, erythromycin (in pregnancy) or doxycycline.
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tell me the nice recommendations for eron class 2 cellulitis?
admission may not be necessary if community facilities are available give iv abx and monitor pt. check local guidlines.
243
nice recommendations for eron class 3-4 cellulitis
admit. oral/iv co-amoxiclav, oral/iv clindamycin, iv cefuroxime, or iv ceftriaxone.
244
How many main subtypes of melanoma are there, which is the most aggressive?
4 main types: superficial spreading, nodular, lentigo maligna, acral superficial spread 70% of cases. then nodular , then lentigo (less common) then acral (rare)
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with melanoma (the 4 types) tell me the areas they typically affect
superficial spreading: arms legs back and chest, young people nodular: sun exposed skin, middle aged people lentigo maligna: chronically sun-exposed skin, older people acral: nails palms or soles, people with darker skin pigmentation
246
with 4 main types of melanoma tell me their appearances
superficial spreading: growing mole with diagnostic features nodular: red or black lump or lump that bleeds and oozes lentigo maligna: growing mole with diagnostic features acral lentiginous: subungal pigmentation ( hutchinsons sign) or on palms and feet.
247
other than the main types of melanoma, give me 3 others
desmoplastic melanoma amelanotic melanoma ocular melanoma (melanoma arising in other parts of the body)
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what are the major diagnostic features of melanoma?
change in size change in shape change in colour
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what are the minor diagnostic features of melanoma?
diameter of 7mm or more. inflammation oozing or bleeding altered sensation.
250
if you suspect melanoma what to do ? once reviewed, melanoma diagnosis confirmed then what to do?
excision biopsy remove lesion completely as incision biopsy can make histopathological assessment difficult. once confirmed: remove pathology report to determine whether futher re-excision of margins is needed.
251
based on breslow thickness, what are the recommended margins of excision for melanoma?
lesion thickness: 0-1mm: 1cm 1-2mm: 1-2 cm - depending on site and pathological features 2-4mm: 2-3cm - depending on site and pathological features over 4mm: 3cm
252
what further treatments may be selectively applied in melanoma management?
sentinel lymph node mapping isolated limb perfusion block dissection of regional lymph node groups
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What is the single most important factor in determining prognosis for patients with malignant melanoma? how does breslow thickness relate to prognosis in malignant melanoma? approx 5 year survival for breslow thickness under 0.75mm and 0.75-1.50mm and 1.5-4mm and over 4mm?
invasion depth of the tumour called breslow depth or breslow thickness thicker tumours have worse prognosis and lower 5 year survival. 95-100% 80-96% 60-75% 50%