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Dermatology > 6- Dermatology (Inflammatory conditions) > Flashcards

6- Dermatology (Inflammatory conditions) Flashcards

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Dermatology Board Prep flashcards
1
Q

Atopic Eczema
Background

A
  • Inflammatory skin condition
  • Chronic, relapsing atopic condition caused by defects in the normal continuity of the skin barrier, leading to inflammation in the skin
  • Significant variation in the severity of the condition
  • Can become infected e.g. cellulitis
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2
Q

Pathophysiology of eczema

A

The simplified pathophysiology is that eczema is caused by defects in the barrier that the skin provides. Tiny gaps in the skin barrier provide an entrance for irritants, microbes and allergens that create an immune response, resulting in inflammation and the associated symptoms.

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3
Q

Causes/ risk factors for eczema

A
  • Genetic influence
  • Atopic- dust, fur
  • Environmental triggers
    o Cold
    o Dietary products
    o Washing powders
    o Stress
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4
Q

presentation of eczema

A

Presentation
- Presents in infancy
- Acute: itchy papules and vesicles
- Dry, red, itchy and sore patches of skin
- Flexor surfaces e.g. elbow, knees, face and neck
- Nail signs- pitting and ridging
- Can appear as flares rather than being constant

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5
Q

management of eczema is split into

A

maintenance and management of flares

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6
Q

maintenance management of eczema

A
  • Provoking factors avoided
  • Emollients used to create an artificial barrier over the skin to compensate for the defective skin barrier
  • Used as often as possible, particularly after washing and before bed (3-4 times a day)

AVOID
- Hot baths
- Scratching
- Soaps which remove natural oils

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7
Q

Management of Eczema Flares

A
  • Thicker emollients and “wet wraps’ (applying a wrap to areas covered in emollient overnight)
  • Topical steroids (oral if severe)
  • Antibiotics to treat infections e.g. fluxcloxacillin
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8
Q

Specialist treatment for severe non responsive eczema

A
  • Phototherapy
  • Topical tacrolimus
  • Oral corticosteroids
  • Methotrexate
  • Azathioprine
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9
Q

types of emollients

A

The thicker the more effective
- Ointments- has the highest oil content, therefor most effective at treating dry skin
- Creams- lighter and easier to leave on skin (less oil on skin)
o Lots of people use creams in the day and ointment at night
- Lotions (least oil content)- least effect on dry skin

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10
Q

examples of emollients

A

Thin creams:
* E45
* Diprobase cream
* Oilatum cream
* Aveeno cream
* Cetraben cream
* Epaderm cream
Thick, greasy emollients:
* 50:50 ointment (50% liquid paraffin)
* Hydromol ointment
* Diprobase ointment
* Cetraben ointment
* Epaderm ointment

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11
Q

How to use emollients?

A
  • Always wash and dry hands first (best after a shower)
  • Never use fingers to decant emollient from a tub (bacteria can get into ointment)- use spatula or clean spoon
  • How much? Depends on condition of skin
    o For adults with very dry skin use 500-1000g per week
  • Follow the direction the hair lies and apply emollients with stroking motion
  • If using a steroid cream or another treatment for skin condition, wait at least 30 mins after putting emollient on before applying (avoids dilution)
  • Can be applies as often as you like (3-4 times a day
    o Esp hands and face
  • Can use before swimming
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12
Q

topical steroids rules

A
  • use weakest steroid for shorted period of time to get the skin under control.
  • Mild: for face and flexure
  • Stronger: thicker skin
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13
Q

steroid ladder

A
  • Mild: Hydrocortisone 0.5%, 1% and 2.5%
  • Moderate: Eumovate (clobetasone butyrate 0.05%)
  • Potent: Betnovate (betamethasone 0.1%)
  • Very potent: Dermovate (clobetasol propionate 0.05%)
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14
Q

side effective of steroids

A
  • Thinning of the skin
  • Telangiectasia

Systemic absorption of steroid
- Slower growth
- Weight gain
- Roundness of face
- Mood changes

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15
Q

how to apply steroid creams

A
  • Wash and dry hands
  • Squeeze out about the same amount as the tip of your finger (this I enough for the same area as if you put your two hands flat together)
  • Only apply to effected areas
  • Avoid applying steroids with emollients (dilution)
  • Dry and wash hands thoroughly after
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16
Q

Eczema and infections

A

Bacterial
- Most commonly staphylococcus aureus
- Oral antibiotics: flucloxacillin
- Severe cases may require admission and IV abx

Eczema herpeticum
- Viral skin infection cause by HSV or VZV

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17
Q

Eczema herpeticum

Background

A
  • Widespread eruption
  • Serious complication of atopic eczema
  • Occurs in those with pre-existing skin conditions where the virus an enter the skin and cause infection
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18
Q

causes of eczema herpeticum

A

Causes
- Herpes simplex virus (HSV 1)
o May be associated with a coldsore
- Varicella zoster virus

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19
Q

Presentation of eczema herpeticum

A
  • Extensive crusted papules, blisters and erosions
    o Will burst
  • Systemically unwell with fever and malaise
  • Lymphadenopathy
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20
Q

management of eczema herpticum

A

First line: Acyclovir
- Oral if moderate
- IV if severe (will need admitting)

Antibiotic for secondary bacterial infection

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21
Q

Complications of eczema herpeticum

A
  • Herpetic hepatitis
  • Encephalitis
  • Bacterial superinfection
  • DIC
  • Death
22
Q

Psoriasis
Background

A
  • Psoriasis is a chronic, autoimmune skin condition that can also affect the nails and joints. It tends to flare up from time to time. (psoriatic arthritis- pitting, onycholysis = nail signs))
  • Increases risk of arthritis and CVD- inflammation of vasc
23
Q

pathophysiology of psoriasis

A
  • Occurs due to increased production of skin cells- keratinocytes
  • Skin cells normally replaced every 3-4 weeks, however in this chronic condition it only takes 3-7 days
  • Underlying cause not fully understood- to do with immune system mistaking healthy cells
24
Q

triggers for psoriasis

A

o Injury to skin- Koebner phenomenon
o Throat infection- step
o Medications
o Stress
o Infection
o Smoking and alcohol

25
Q

risk factors for psoriasis

A
  • fairer complections
  • genetic risk
26
Q

presentation of psoriasis

A
  • Usually extensor e.g. elbows and knees and scalp region (as opposed to eczema)
  • Erythematous, crusty skin covered with silvery scales
  • Raised and rough plaques
  • Guttate more common in children, my be preceded by strep throat infection
  • Nail psoriasis e.g. pitting, thickening, oncolysis
  • Psoriatic arthritis 10-20% (usually middle age starts)
  • Auspitz sign – scratch and gentle removal of scales cause capillary bleeding
27
Q

Auspitz sign

A

scratch and gentle removal of scales cause capillary bleeding

28
Q

management of psoriasis

A

Management
- Emollient
- Topical corticosteroids
- Topical Vitamin D analogues (Calcipotriol)
- Second line
o Phototherapy (narrow band UV B)
- Unlicenced treatments for severe psoriasis
o Methotrexate, cyclosporine, retinoids, biologic medications such as DMARDs e.g. TNF antagonist adalimumab
- Psychosocial counselling

29
Q

types of psoriasis

A

plaque
guttate
flexutal
pustular
erythroderma

30
Q

Plaque psoriasis

A

the most common sub-type resulting in the typical well-demarcated red, scaly patches affecting the extensor surfaces, sacrum and scalp

31
Q

Guttate psoriasis:

A

transient psoriatic rash frequently triggered by a streptococcal infection.

Multiple red, teardrop lesions appear on the body-> especially trunk
o second most common
o children
o small raised papules

32
Q

Flexural psoriasis

A

in contrast to plaque psoriasis the skin is smooth

33
Q

Pustular psoriasis

A

commonly occurs on the palms and soles
o Rare
o Pustules form under erythematous skin
o Not infectious
o Medical emergency and usually require hospital admission

34
Q

Erythroderma psoriasis

A
  • Rare form of psoriasis with extensive erythematous inflamed areas covering most of the surface area of the skin
  • Skin falls away in large patches resulting in raw exposed areas
  • Medical emergency
35
Q

Koebner phenomenon

A

refers to the development of psoriatic lesions to areas of skin affected by trauma

36
Q

Residual pigmentation

A

of the skin after the psoriatic lesions resolve

37
Q

Acne vulgaris
Background

A
  • Very common condition
  • Acne – comedowns
  • Open comedowns- blackheads
  • Closed comedowns- whiteheads
38
Q

pathophysiology of acne vulgaris

A

Pathophysiology

  • Caused by chronic inflammation, with or without localised infection, in pockets of skin known as pilosebaceous unit
  • Acne results from increased production of sebum, trapping keratin and blocking the pilosebaceous unit
  • Leads to swelling and inflammation
  • Androgenic hormones increase production of sebum- therefore exacerbated by puberty and improves with anti-androgenic hormonal contraception
  • Bacteria: Propionibacterium acnes – bacteria which colonises the skin and can contribute to acne
39
Q

sk factors for acne vulgaris

A

Risk factors
- Puberty and adolescence
- Family history

40
Q

Presentation of acne vulgaris

A
  • Significant variation in severity of acne
  • Red, inflamed and sore spots on the skin
  • Typically distributed
    o Face
    o Upper chest
    o Upper back
  • In darker skin -> hyperpigmented lesiosn
41
Q

Management of acne vulgaris
Stepwise

A
  • No treatment if mild
  • Psychosocial counselling
  • Topical benzoyl peroxide
  • Topical retinoids (chemicals related to vitamin A)- slows production of sebum
  • Topical antibiotics – clindamycin (prescribed with benzoyl peroxide t reduce bacterial resistance
  • Oral antibiotics such as lymecycline (make sure not pregnant- tetracycline is a teratogen)
  • Oral contraceptive pill e.g. Co-cyprindiol (Dianette)- COCP)
  • Oral retinoids e.g. isotretinoin
42
Q

Describing acne lesions

A
  • Pustules are small lumps containing yellow pus
  • Comedomes are skin coloured papules representing blocked pilosebaceous units
  • Blackheads are open comedones with black pigmentation in the centre
  • Ice pick scars are small indentations in the skin that remain after acne lesions heal
  • Hypertrophic scars are small lumps in the skin that remain after acne lesions heal
  • Rolling scars are irregular wave-like irregularities of the skin that remain after acne lesions heal
43
Q

Oral retinoids

A

Isotretinoin i.e. Roaccutane
- Effective last line option
- Prescribed by specialist
- Highly teratogenic
- Women must have reliable contraception and do regular pregnancy tests
o And agree to termination if gets pregnant
o Stop a month before trying to get pregnant

44
Q

retinoids MOA

A
  • Reduce production of sebum, reducing inflammation and bacterial growth
45
Q

Side effects of oral retinois

A
  • Dry skin and lips
  • Photosensitivity of the skin to sunlight
  • Depression, anxiety, aggression and suicidal ideation. Patients should be screened for mental health issues prior to starting treatment.
  • Rarely Stevens-Johnson syndrome and toxic epidermal necrolysis
46
Q

Contact dermatitis
Background

A
  • Itchy rash caused by direct contact with allergen
  • Delayed Type 4 hypersensitivity reaction
  • Types
    o Chemical burns
    o Irritant contact dermatitis
    o Allergic contact dermatitis
47
Q

Pathophysiology of contact dermatitis

A

Common in children because skin is easily sensitised:
- Thinner skin than adults
- Can absorb more applied substances
- More likely to have underlying atopic dermatitis which facilitates sensitisation due to impaired skin barrier
- Sensitization can occur in newborns from ages 0-3, prevalence of subsequent allergic contact dermatitis increases with age

48
Q

common allergens which cause contact dermatitis

A
  • Nickel (piercings, buttons, fasteners, clips, toys)
  • Fragranced products
  • Colophonium found in plasters
49
Q

presentation of contact dermatitis

A
  • Shows up on skin after direct contact e.g. face, hands, feet, arms, legs
  • When allergen is removed, rash slowly resolves over several days to several weeks and will reappear with further contact
  • Always itchy
  • Erythematous blisters
  • Oedema
  • Dryness
  • Fissuring
  • Lichenification
  • Pigmentation increase or decrease
50
Q

investigations for contact dermatitis

A
  • Patch testing
51
Q

management of contact dermatitis

A

Management
- Once cause has been identified, avoid direct contact (lifelong)
- Avoid soap and dry skin carefully after washing
- Short course of topical corticosteroid cream
o Hydrocortisone for face
- Emollients frequently applies
- Severe: oral corticosteroids e.g. prednisone
- Second line: calcineurin inhibitor

Dermatology (9 decks)

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