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year 2 core concepts > derm > Flashcards

derm Flashcards

1
Q

what is the immune response in atopy? how does that play a role in dermatitis

A

CD4+ Th2 lymphocytes detect allergen causing exaggerated igE response to allergen (perfume, foods, clothes)

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2
Q

how does genetic play an role in atopic dermatitis

A

mutation of FLG gene that encode for filaggrin (protein for skin barrier)

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3
Q

what are the histological progression in atopic dermatitis?

A
  1. inflammatory infiltrate of CD4+ Th2 lymphocytes in the upper dermis which can diffuse into epidermis
  2. keratinocyte apoptosis
  3. Spongiosis-> vesicles
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4
Q

define keratocyte apoptosis in context of dermatitis

A
  • process that regulates cell death
  • can be activated by inflammation and help attract more inflammatory cells
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5
Q

define spongiosis

A
  • intercellular edema or accumulation of fluid between the cells of the epidermis
  • enough fluid=vesicle with WBC and proteinaceous fluid
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6
Q

how does keratinocyte apoptosis lead to spongiosis

A

As keratinocytes die and become detached from each other, the spaces between them fill with fluid, leading to spongiosis

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7
Q

what are the histological changes in chronic atopic dermatitis

A

lichenification, plaques

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8
Q

Symptoms of dermatitis in acute vs chronic phase?

A
  • Acute: oozing, vesicles, swelling, blistering
  • Chronic: plaques, skin thickening
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9
Q

children vs Enfant presentation of atopic dermatitis & associated conditions

A
  • Children: dry, itchy, erythematous rash, no well defined border in flexor areas (ie, bends of elbow, behind knees)
  • babies: face, trunk & extensor areas
  • May also have asthma or allergic rhinitis (history of atopic disease)
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10
Q

How is the severity of atopic dermatitis/eczema defined?

A
  • Mild: localized areas of dry skin, infrequent itching
  • Moderate: localized areas of dry skin, frequent itching, redness
  • Severe: widespread areas of dry skin, excessive itching, redness
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11
Q

what are the step by step treatments of atopic dermatisit/ eczema

A
  1. Emollients (ie, Dermol 200, E45 lotion)
  2. Topical hydrocortisone
  3. Topical betamethasone or clobetasol (can be titrated up except in private areas)
  4. Topical calcineurin inhibitors (inhibition of T-lymphocytes activation)
  5. phototherapy, systemic therapy
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12
Q

what are the primary and secondary complications of atopic dermatitis

A
  • Primary infection: eczema herpeticum
  • Secondary infection: staph aureus (crusty, oozing rash)
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13
Q

what is eczema herpeticum?

A

skin infection caused by HPV 1 & 2
seen in children with atopic eczema

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14
Q

what is the presentation of eczema herpeticum

A

rapid progressing painful rash with punched out erosions and vesicles

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15
Q

what is the treatment for eczema herpeticum

A

IV aciclovir

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16
Q

What are the cause & disease associated with dermatitis herpetiformis?

A
  • deposition of IgA in the dermis
  • associated with celiac disease (weight loss)
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17
Q

what is the presentation of dermatitis herpetiformis

A

Itchy small red vesicular lesions on extensor surfaces (ie, elbow, knee, butt, torso)

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18
Q

what is this?

A

dermatitis herpitformis

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19
Q

What is the diagnosis of dermatitis herpetiformis?

A
  • Skin biopsy: igA in a granular pattern in upper dermis
  • bloods: Anti-tissue transglutaminase (anti-TTG)
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20
Q

what is the treatment for dermatitis herpetiformis

A

gluten free diet
dapsone

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21
Q

What is the cause & associated conditions of seborrhoeic dermatitis?

A
  • Inflammation from proliferation of Malassezia furfur fungus
  • HIV, Parkinson’s disease
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22
Q

what are the symptoms of seborrhoeic dermatitis

A

itchy lesions on sebum-rich areas (ie, scalp, around eye, nose, ears)
may cause infections

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23
Q

How is seborrhoeic dermatitis treated?

A
  • zinc pyrithione (‘Head & Shoulders’)
  • topical ketoconazole, Topical steroids for short periods
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24
Q

how is seborrhoea dermatitis treated in babies

A

baby shampoo & oil, mild topical steroid (1% hydrocortisone)

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25
Q

what is the cause of irritant contact dermatitis

A

non-allergic reaction to weak acids or alkalis (ie, soap)

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26
Q

what is the presentation of irritant contact dermatitis

A

usually on hands, erythema will be present but usually no crusting and vesicles

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27
Q

cause & symptoms of allergic contact dermatitis

A
  • type 4 hypersensitivity
  • acute weeping eczema (dry, rashes, erythema, crusting & vesicles),
  • ie, hairline & scalp following hair dye use
28
Q

investigation & treatment allergic contact dermatitis

A
  • skin patch test
  • topical potent steroids (betamethasone)
29
Q

can you define psoriasis?

A
  • Epidermal proliferation/ thickening esp in keratin layer
  • triggered by immune cells causing scaly plaques
30
Q

what are the causes of psoriasis?

A
  • Genetics: HLA-B, identical twins
  • activated by Environmental trigger: trauma, injury, infection, sunburn
31
Q

explain the pathophysiology of psoriasis

A
  • environmental trigger
  • keratinocytes to release chemicals that activate Th 1 & Th17 lymphocytes and neutrophils
  • inflammatory response and keratinocyte proliferation
32
Q

what is the function of T cells (Th1 and Th17) in activating psoriasis

A
  • trigger inflammation
  • keratinocyte growth & division
  • breakdown of the protective barrier.
33
Q

what is the function of neutrophils in activating psoriasis

A
  • attracted by complement system to keratin layer/ stratum corneum
  • build up forming muno micro abscess
  • causes keratinocyte proliferation
34
Q

what is the function of the complement system

A

innate immune system
helps to eliminate pathogens and damaged cells from the body.

35
Q

what are the histological presentations of psoriasis

A
  1. parakeratosis: nuclei in keratinocytes due to rapid differentiation
  2. micro-abscess: retention of neutrophils
  3. elongated rete pegs: epidermis concave down to dermis become thicker and longer
36
Q

What is the typical presentation of psoriasis? (skin and nail)

A
  • raised, itchy, scaly, well-defined plaques w/ symmetrical distribution in the scalp, extensor surfaces, trunk, gluteal
  • Nails: hyperkeratosis, pitting
37
Q

What are the two signs of psoriasis?

A
  1. Koebner phenomenon: psoriasis that develops in an area of trauma
  2. Auspitz sign: bleeding points where surface scale is removes
38
Q

what is plaque psoriasis

A
  • Plaque psoriasis: well-demarcated red, scaly patches affecting extensor surface, sacrum and scalp
39
Q

what is flexural and guttate psoriasis

A
  • Flexural psoriasis: skin is smooth
  • Guttate psoriasis: many small red psoriatic rash on torso/ trunk & limb, triggered by streptococcal infection
40
Q

What are the exacerbating factors of psoriasis?

A
  • trauma, alcohol
  • Beta blockers, lithium, chloroquine, hydroxychloroquine, ACE inhibitors
  • Withdrawal of systemic steroids
41
Q

What is the management plan for psoriasis?

A
  1. topical Potent corticosteroid + vitamin D analog applied once per day
  2. Vitamin D analogue twice
  3. topical Potent corticosteroid twice for 4 weeks
    (emollients given to all)
42
Q

give me an examples of topical potent corticosteroid and vitamin D analogue combo

A

topical betamethasone + calcipotriol

43
Q

What is the cause + patient profile of impetigo?

A
  • staph aureus or strep pyogenes
  • Children during warm weathers, very contagious spread via toys & clothing
44
Q

what is the presentation of impetigo

A
  • Golden-crusted skin lesions and red sores around the mouth, Face, flexures limbs
45
Q

what is this?

A

impetigo

46
Q

what is the investigation for impetigo? when is it done?

A
  1. clinical diagostic
  2. bacterial swab for culture if its extensive or severe, suspect MRSA (antibiotic resistant bacteria), recurrent
47
Q

What is the treatment for impetigo? Can the patient go to school?

A
  1. hydrogen peroxide 1% cream
  2. topical fusidic acid
  3. Oral flucloxacillin or erythromycin
    (No school until lesions are crusted & healed or 48 hours after starting antibiotics treatment)
48
Q

What is the typical presentation of basal cell carcinoma skin?

A
  • Rodent ulcer that is slow progressive
  • Telangiectasia, ill- defined border
  • papule then becomes nodular (raised)
49
Q

What is the histological presentation of basal cell carcinoma skin?

A
  • Basal nest in the dermis
  • Irregular strands invading dermis and palisading nucleus
50
Q

What are the risk factors and treatment of basal cell carcinoma skin?

A

Sun exposed skin (scalp, arms)
Routine referral
Surgical excision
Topical imiquimod if no risk of metastasis

51
Q

What are actinic keratoses?

A
  • Partial dysplasia of epidermal keratinocytes due to chronic sun exposure
  • Less than 1% may develop into squamous cell carcinoma
52
Q

What is the presentation of actinic keratoses?

A
  • Scaly erythema papules or patches, gritty and rough
  • Occurs on sun exposed skin like scalp, face, hands, ear
53
Q

What is the treatment for actinic keratoses?

A
  • Sun avoidance and sunscreen
  • Fluorouracil cream
  • Topical diclofenac and imiquimod
  • Cryotherapy
54
Q

What is bowen’s disease

A
  • Full thickness dysplasia of epidermal keratinocytes
  • can develop in squamous cell carcinoma (5-10%)
  • Seen commonly in fair skinned women
55
Q

What is the typical presentation of bowen’s disease

A
  • Women (fair skin, red hair) present with slow growing lesion
  • Scaly red patch/ plaque, well-demarcated with irregular border
56
Q

Are there any variants of bowen’s disease?

A
  • Neoplasia in genital mucosa (vulval, penile, anal, intraepithelial)
  • Linked to HPV-16 and 18, common in HIV
57
Q

How is Bowen’s disease managed?

A

Topical 5- fluorouracil
Cryotherapy and excision

58
Q

What is the typical presentation of squamous cell carcinoma of the skin?

A
  • Rapid expanding ulcerative nodule w/ well defined border
  • May bleed, central erythema, red scaling plaques
  • Can be on face, lip, ear
59
Q

What are the risk factors of squamous cell carcinoma of the skin?

A
  • Sun exposed skin
  • Immunosuppression (HIV, renal transplant)
    Smoker
  • Pre-malignancy: actinic keratosis and Bowen’s disease
60
Q

What is the treatment for squamous cell carcinoma of the skin

A

Surgical excision
4mm margin for -20mm
6 mm margin for +20mm

61
Q

What is the typical presentation of lichen planus?

A
  • Itchy papular rash in palms, forearm, legs flexor surfaces, gentility
  • Polygonal, violaceous papules
  • White lines in buccal mucosa in mouth
62
Q

What is the treatment for lichen planus?

A
  • Potent topical steroids (ie, betamethasone, clobetasone)
  • Benzydamine mouthwash or spray for oral lichen planus
63
Q

What is the cause and risk factor of cellulitis?

A

Mainly Strep pyogenes
staph aureus
Risk factor: Diabetes

64
Q

What are the clinical presentations of cellulitis?

A

Swelling in legs
Macular hot erythema with ill defined margins that spread
Fever, rigors, nausea

65
Q

what is this?

A

cellulitis

66
Q

What are the investigations for cellulitis?

A
  • Clinical diagnosis, ERON classification
  • Blood culture/ swab only if patient is not responding to treatment or atypical presentation
67
Q

What is the management for cellulitis?

A
  • Rest, elevation, analgesia, splint
  • Flucloxacillin
  • Doxycycline, clarithromycin for pen allergy
  • IV flucloxacillin (confusion, tachycardia, sepsis)

year 2 core concepts (9 decks)

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