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Y4 NSS > Derm > Flashcards

Derm Flashcards

1
Q

How would you define acne?

A

common chronic disorder of the pilo-sebaceous unit, resulting in blockage of the follicle, formation of comedones and inflammation

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2
Q

how would you describe the appearance of acne?

A
  • comedones can be open blackheads or closed whiteheads
  • papules - small, raised, erythematous, inflammatory lesions that do not contain pus
  • pustules - similar to papules but with pus
  • nodules - large, painful, solid lesions deep within skin which can lead to scarring
  • cysts - pus filled lesions that can lead to scarring, severe form
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3
Q

what are the classifications for acne?

A
  • non-inflammatory: blackheads, whiteheads
  • inflammatory: papules, pustules, nodules and cysts
  • mild: non-inflammatory lesions
  • moderate: inflammatory papules and pustules
  • severe: codules, scarring, acne fulminans and conglobata
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4
Q

what is the pathophysiology of acne?

A
  • follicular epidermal hyperproliferation resulting in formation of keratin plug
    • this obstructs pilosebaceous follicle
  • activity of sebaceous glands may be controlled by androgen
  • leads to colonisation by anaerobic bacterium
  • inflammation
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5
Q

what are some risk factors for acne?

A
  • hormonal changes - puberty, menstrual cycle, PCOS
  • increased sebum production
  • blockage of hair follicles and sebaceous glands by keratin and sebum
  • bacterial colonisation
  • family history
  • certain medications like steroids, hormonal tx
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6
Q

how might acne present?

A
  • self confidence issues
  • scarring
  • post-inflammatory hyperpigmentation
  • mental health
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7
Q

how is acne investigated?

A
  • clinical
  • swabs if uncertain
  • pre-isotretinoin ix
  • PCOS mx etc
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8
Q

how is acne managed?

A

12w course of management
- mild to moderate: topical benzyl peroxide, topical abx, topical retinoids
- moderate to severe: topical retinoids with topical benzoyl or abx, second line oral abx, COCP, isotretinoin
- referrals

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9
Q

how is acne complicated?

A
  • Post-inflammatory erythema
  • Post-inflammatory hyper- and hypo- pigmentation
  • Psycho/social/sexual dysfunction
  • Scars (atrophic, hypertrophic, keloid)
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10
Q

how would you describe psoriatic lesion?

A

clearly defined, dry, erythematous and scaly plaques, symmetrical distribution, scale silvery white and appears shiny on skin folds common on scalp, elbows, knees on extensor surfaces

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11
Q

what is the pathophysiology of psoriasis?

A
  • systemic chronic relapsing inflammatory condition affecting skin, nails, joints and scalp with faster skin cell turnover
  • hyperproliferative skin epidermis causes rapid regeneration of new skin cells, causing abnormal buildup and thickening of skin in those areas
  • inflammatory cell infiltration
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12
Q

what are the various types of psoriasis?

A

plaque
guttate
pustular
erythrodermic

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13
Q

what are some triggers for psoriasis?

A
  • Skin trauma (Koebner phenomenon)
  • Infection: Streptococcus, HIV
  • Drugs:B-blockers,Anti-malarials,Lithium,Indomethacin/NSAIDs (BALI)Withdrawal of steroids
  • Stress
  • Alcohol + smoking
  • Cold/dry weather
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14
Q

how does psoriasis present?

A
  • extensor surfaces
  • itch, skin cracks, stress induced flare ups
  • nail changes: pitting, thickening, discolouration, ridging
  • joint involvement
  • signs: auspitz (small points of bleeding where plaques scraped off), koebner (lesions affected by trauma), residual (skin after lesions)
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15
Q

how is psoriasis managed?

A

lifestyle - WL, stopping smoking, managing stress, topicals
- potent topical corticosteroid OD (eg Betnovate) + topical vitamin D OD (eg Dovonex)
- phototherapy
- systemic
- biologics

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16
Q

what are some complications of psoriasis?

A
  • psychosocial
  • CVS risk
  • systemic tx side effects: pneumonitis, hepatotoxic, myelosuppression
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17
Q

what are the two types of contact dermatitis?

A
  • Irritant - Eczema due to contact with an irritant. There may be burning, pain, and stinging. Eczematous rash appears localised to the direct area of contact
  • Allergic - Presents as an itchy, eczematous rash (vesicles, fissures, erythema), typically 24-48 hours after exposure. The rash may extend beyond the boundaries of immediate contact
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18
Q

what is the pathophysiology of allergic contact dermatitis?

A
  • delayed type 4 hypersensitivity reaction
  • exposure to allergen sensitises immune system overtime
  • Upon re-exposure (e.g. after repeated hair dyes), an immune response is triggered, leading to inflammation and the characteristic skin rash
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19
Q

what is the pathophysiology of irritant contact dermatitis?

A

natural barrier disrupted resulting in direct damage to skin cells and inflammation

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20
Q

how does contact dermatitis present?

A
  • irritant: hairdressers, healthcare staff, builders and cleaners using irritants like bleach or detergents
  • allergic: nickel, acrylates, fragrance, hair dye, henna
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21
Q

how is contact dermatitis investigated?

A

patch testing
skin biopsy

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22
Q

how is contact dermatitis managed?

A
  • AVOIDANCE effective
  • liberal emollient and soap substitutes to repair barrier
  • topical steroids
  • oral antihistamines
  • occupational dermatitis, workplace modifications
  • derm referral if - severe, recurring and persistent, no response to mx, associated with occupation
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23
Q

what are some complications of contact dermatitis?

A
  • Secondary bacterial or fungal skin infections due to scratching
  • Scarring or post-inflammatory hyperpigmentation
  • Chronic or recurrent dermatitis
  • Impact on quality of life, especially in individuals with severe or chronic forms
  • Potential complications related to occupational dermatitis, such as work disability
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24
Q

what is the pathophysiology of eczema?

A
  • chronic inflammatory disorder of the skin characterized by dermal inflammation leading to histological changes in the epidermis such as spongiotic change, acanthosis, hyperkeratosis
  • as a result of abnormal barrier function of epidermis causing easy skin irritation
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25
Q

how might eczema present?

A
  • 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, a more typical distribution is seen, with flexor surfaces affected and the creases of the face and neck
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26
Q

how is eczema managed?

A
  1. emollients to prevent water loss and allow repair
  2. middle potent topical corticosteroids
    itch - non-sedating antihistamines
  3. topical calcineurin inhibitors
  4. phototherapy
  5. oral steroids
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27
Q

how would you advise application of topical steroids?

A
  • apply sparingly on affected areas (about an amount from last crease of finger to tip enough for area covering both palms of hand, wash hands before applying, don’t use with emollient as may dilute, no more than twice a day during flare ups

long term use can lead to side effects due to systemic absorption hence give lowest potency controlling the eczema, advice on side effects such as transient burning, acne, or even systemic side effects such as adrenal suppression

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28
Q

when would you refer someone with eczema?

A

referral to dermatology is diagnosis uncertain, eczema not controlled with current treatment, recurrent secondary infection, high risk complications or for bandage advice

  • referral to immunologist if food allergy trigger and not available in primary care
  • referral to clinical psychologist if psychological wellbeing affected or not improving
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29
Q

what is a complication of eczema to be aware of?

A

eczema herpeticum (rapidly worsening, painful eczema, clustered blisters and punched out erosions)

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30
Q

describe the appearance of urticaria?

A

urticarial weals can be few centimetres in diameter, coloured white or red, with or without red flare

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31
Q

how does urticaria present?

A

superficial swelling of the skin (epidermis and mucous membranes) resulting in red, raised and itchy rash

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32
Q

what would you focus on when examining someone with urticaria?

A
  • time of onset, severity using urticaria activity score
  • any known causes or triggers like food allergies - especially if occuring 1h after exposure to food
  • family history of atopy
  • consider possiblity of angio-oedema and offer non-sedating antihistamines and remove offensive cause
  • acute urticaria with fever can be the first sign of covid, in children caused by infection
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33
Q

how is urticaria managed?

A
  • suspected anaphylaxis or angio-oedema different
  • identify trigger or underlying cause, symptoms diary
  • non-sedating antihistamine, if severe oral corticosteroid
  • arrnage referral if painful and persistent, not controlled with antihistamines, angio-oedema
  • clinical psychologist for quality of life affected
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34
Q

what is the name of the pathogen head lice?

A

pediculosis capitis - infests hairs on scalp and feeds on human blood

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35
Q

what are some risk factors of catching head lice?

A
  • age 4-11
  • female
  • sharing beds, clothing, hairbrushes
  • greater number of children in family
  • overcrowded living conditions
36
Q

how does headlice present?

A
  • scalp pruritus
  • feeling of things moving in hair
  • scratching, causing crusting and scale

*small red papules under hairline at nape of neck and behind ears = louse bites

37
Q

how is headlice managed?

A
  • topical insecticide and wet combing
    • demiticone - physical barrier to cause suffocation
    • second application 7-10 days after first
    • wet combing - most effective
      • four session over 2 weeks
      • good for pregnant or lactating women
  • oral ivermectin
38
Q

describe the appearance of a scabies lesion?

A

rash - erythematous papules, excoriations which may appear as vesicles if complications like infection. granulomatous nodules on dark skin and may appear grey not red

39
Q

what is the pathogen responsible for scabies?

A

transmissable disease caused by parasitic mite infests humans ‘sarcoptes scabiei’ 5-15 per host

40
Q

what are some risk factors for scabies?

A

risk factors include contact with infected, poverty and social deprivation, institutionalisation, winter

41
Q

how might scabies present?

A
  • ‘itchy rash’ 4-6w after initial infection, symmetrical lesions, hands, wrists, axillae, thighs, buttocks and genitalia. neck and above spared and may appear aczematous
    • crusted scabies in immunocompromised, elderly with neck and above
42
Q

how is scabies managed?

A
  • good prognosis given compliance, treat pt and family, itching treatment, permethrin cream (insecticide) onto cool skin and wash off after 8h then next week, decontaminate bedding clothes etc, sedating antihistamine to help sleep
  • re-treat if persisting 2-4 weeks or new burrows, dermatology referral for persistent nodular scabies for steroid treatment, specialist advice if child under 2
43
Q

describe the appearance of a candidiasis lesion?

A

erythematous maculopapular lesions with satellite pustules in the intertriginous areas

lesions are moist, eroded, and accompanied by fine scaling and pruritus

44
Q

what are some risk factors for candidiasis?

A
  • infancy or old age
  • warm climate
  • broad-spectrum abx
  • DM
  • iron deficiency
  • immunosuppression
    • cancer, malnutrition, HIV
  • chemo etc
45
Q

how is candidiasis managed?

A
  • skin - imidazole creams
  • mouth - nystatin oral suspension
  • vagina - imidazole cream +/- pessary
46
Q

what is dermatophytosis?

A

ringworm and tinea

fungal infection caused by dermatophytes - a group of fungi that invade and grow in dead keratin

47
Q

what is the appearance of tinea or ringworm?

A
  • round and well defined, annular, erythematous lesions with papules and pustules with a more inflamed edge
  • rash scaly, dry, swollen or itchy
48
Q

how does tinea present?

A
  • described differently depending on where it affects - scalp/ trunk, legs. arms / feet
    • tinea pedis, cruris, capitis, unguigum, corporis
49
Q

how is tinea investigated?

A
  • skin scrapings sent from edge of lesion
  • scalp brushings
  • nail clippings
  • culture
50
Q

how is tinea managed?

A
  • take measures to prevent spread by washing clothes, bedding etc and not sharing towels etc
  • confirm diagnosis before tx
  • topical anti-fungal eg: terbenafine, clotrimazole twice daily for 2w
  • may be managed with oral fluconazole
51
Q

describe the appearance of shingles?

A
  • dermatomal distribution of blisters confined to cutaneous distribution of one or two adjacent sensory nerves
    • starts off as red papules
    • each blistering or becomes pustular and then crusts over
  • unilateral, with a sharp cut-off at the anterior and posterior midlines
52
Q

what is the pathophysiology of shingles?

A
  • localised, blistering and painful rash caused by reactivation of varicella-zoster virus (VZV)
  • VZV remains dormant in dorsal root ganglia in spine for years before it is reactivated and migrates down sensory nerves to skin to cause herpes zoster
53
Q

how does shingles present?

A
  • localised pain without tenderness or any visible skin change
    • pain might be one spot or it may spread out
  • unwell with fever, headache, LN enlarged
  • within one to three days of the onset of pain, a blistering rash appears in the painful area of skin
  • complete within 2–3 weeks in children and young adults, and within 3–4 weeks in older patients
54
Q

how is shingles managed?

A
  • rest, pain relief
  • protective ointment applied to the rash like petroleum jelly
  • oral abx for secondary infections
  • Antiviral treatment can reduce pain and the duration of symptoms if started within one to three days after the onset
    • Aciclovir 800 mg 5 times daily for seven days
    • steroids unproven
55
Q

what are some complications of shingles?

A
  • eye complications
  • deep blistters
  • muscle weakness
  • ramsay hunt
  • infections
  • post-herpetic neuralgia
56
Q

what is post-hepatic neuralgia?

A
  • persistence or recurrence of pain in the same area, more than a month after the onset of herpes zoster
  • could be an itch

mx: early antivirals, local anaesthetic, topical capsaicin, amitryptylline

57
Q

how does molluscum contagiosum?

A

pink or pearlish white papules with central umbilication, upto 5mm in diameter which appear anywhere except palms and sole of feet

58
Q

what is the pathophysiology of molluscum contagiosum?

A
  • Molluscum contagiousum caused by poxvirus
  • transmission via direct close contact
    • skin to skin
    • shared towels
    • auto-inoculation by scratching
    • sexual
  • mostly in pre-school children
59
Q

how does molluscum present?

A
  • common viral skin infection of childhood that causes localised clusters of umbilicated epidermal papules.
  • affects young children under age of 10
    • more in warm climates, overcrowded environments
  • commonly in warm, moist places, armpit, behind knees, groin, genital
  • induces dermatitis skin becomes pink dry and itchy
60
Q

what are the investigations done for molluscum contagiosum?

A

White molluscum bodies can often be expressed from the centre of the papules

skin biopsy
histopathology

61
Q

how is molluscum managed?

A
  • reassure as self limiting, about 18m, treatment if troublesome with itching or if inflammation develops
    • referrals if HIV positive or anogenital lesions to GUM clinic
  • physical: cryotherapy, laser ablation
  • medical: antiseptic like hydrogen peroxide
  • topical corticosteroid for secondary dermatitis
62
Q

how can you prevent molluscum?

A
  • Keep hands clean
  • Avoid scratching or shaving
  • Cover all visiblelesionswith clothing or watertight bandages
  • Dispose of used bandages
  • Do not share towels, clothing, or other personal effects
  • Adults should practice safesexor abstinence
63
Q

what are some complications of molluscum?

A
  • secondary infection
  • conjunctivitis
  • disseminated secondary eczema
  • scarring
64
Q

how would you describe chicken pox lesions?

A

vesicular rash, small erythematous macules on scalp, face, trunk and proximal limbs and may progress to papules, clear vesicles and pustules with fever and malaise

65
Q

what is the pathophysiology of chicken pox?

A
  • primaryinfection with the varicella-zoster virus, of theHerpesviridaefamily → This virus is sometimes called herpesvirus type 3
  • transmission via contact or droplet spread where infectious 1-2 days before rash and until vesicles dry and crusted over 5 days since rash onset
66
Q

how will chicken pox present?

A
  • itchy red papules progressing to vesicles on the stomach, back and face, and then spreading to other parts of the body
  • Blisters can also arise inside the mouth
  • high fever, headache, cold-like symptoms, vomiting and diarrhoea
  • prodromal symptoms for up to 48 hours before breaking out in the rash. These include fever, malaise, headache, loss of appetite and abdominal pain
  • blisters clear up within one to three weeks but may leave a few scars
67
Q

how is chickenpox investigated?

A
  • A clue to the diagnosis is in knowing that the patient has been exposed to an infected contact within the 10–21 day incubation period
  • Patients may also have prodromal signs and symptoms
  • PCR
  • culture of blister fluid
  • serology IgM, IgG
68
Q

how is chickenpox managed?

A
  • specialist care if pregnant, immunocompromised etc
  • self limiting in children, analgesia
  • keep cool, trim nails
  • calamine lotion
  • antivirals for immunocompetent adult or adolescent if 24h within rash onset, if high risk of complications, topical calamine lotion, chlorphenamine
69
Q

what are School exclusion criteria for chickenpox?

A

Advise that the most infectious period is 1-2 days before the rash appears, but infectivity continuesuntil all the lesions are dry and have crusted over (usually about 5 days after the onset of the rash)

70
Q

what are the complications of chickenpox?

A
  • may complicate to bacterial infection, lung involvement in adults or varicella pneumonia in immunocompromised
  • secondary infection - NSAIDs increase risk
  • dehydration
  • exacerbation of asthma
  • viral pneumonia
  • encephalitis
  • disseminated haemorrhagic chickenpox
  • scarring
71
Q

what are some pregnancy associated of chickenpox?

A

spontaneous abortion, fetal chorioretinitis, cataracts, limb atrophy, cerebral cortical atrophy and microcephaly, cutaneous scars, and neurological disability

72
Q

how does herpes simplex lesions appear?

A
  • cluster of small, fluid-filled vesicles on an erythematous base
    • vesicular eruptions with crusting
73
Q

how is herpes simplex lesions managed?

A
  • avoid sunlight, reduce stress
  • acyclovir - oral, IV, ointment
    • for bothersome sx, prevent transmission
74
Q

how does cellulitis look?

A
  • localised area of red, painful, swollen skin and systemic symptoms
  • mostly on limbs
  • goes hand in hand with Erysipelas → superficial form of cellulitis in the upper dermis
75
Q

how is cellulitis investigated?

A
  • FBC, CRP
  • blood culture
  • CXR
  • USS doppler
  • MRI
76
Q

how is cellulitis managed?

A

MDR
elevate limb
mark edges
analgesia, hydration
IV abx fluclox
switch to oral when fever settles

77
Q

what are some complications of cellulitis?

A
  • necrotising fasciitis
    • more serious soft tissue infection recognised by severe pain, skin pallor, loss of sensation, purpura, ulceration and necrosis
  • gas gangrene
  • severe sepsis
  • infection of other organs, eg pneumonia, osteomyelitis, meningitis
  • endocarditis
78
Q

how does folliculitis look?

A

inflamed hair follicles with or without pus
- tender red spot, often with a surface pustule
- may be superficial or deep, affecting anywhere there are hairs, including chest, back, buttocks, arms and legs

79
Q

how is folliculitis managed?

A
  • bacterial boil - hygiene, antiseptic cleanser, abx ointment, oral abx
  • viral severe - antivirals
80
Q

how does impetigo appear?

A

well defined lesions usually starting around nose and face with honey-coloured crusts on erythematous base

bullous - superficial, small or large thin roofed bullae which tend to spontaneously rupture and ooze yellow fluid leaving scaley rim

81
Q

what are some risk factors for impetigo?

A
  • skin conditions - atopic dermatitis
  • skin trauma
  • immunosuppression
  • warm, humid climate
  • poor hygiene
  • crowded environments
82
Q

how might impetigo present?

A
  • 2-5 year olds
  • non-bullous - face or extremities but any involved
  • bullous - face, trunk, extremities, buttocks, perineal
    • systemic malaise, fever, lymphadenopathy
83
Q

how is impetigo investigated?

A
  • clinical
  • skin swab for cultures and sensitivity for MRSA
  • nasal swabs to identify staph nasal carriage
  • rarely biopsy
84
Q

how is impetigo managed?

A

*self-limiting in 2-3w

  • localised - antiseptic
  • topical fusidic acid for localised
  • oral antibiotics eg: flucloxacillin QDS for 7 days if severe
  • hygiene advice - hand washing, gentle cleansing, watertight dressing
85
Q

what are some complications of impetigo?

A
  • cellutlitis
    • scarlet fever
    • staphylococcal scalded skin syndrome - detachment of the outermost skin layer

Y4 NSS (11 decks)

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