Patient sem 1 SKIN Flashcards

1
Q

Describe the structure of skin?

A

3 major layers:
epidermis, dermis and hypodermis/subcutis
epidermis made of 4 layers

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2
Q

What is the function of the epidermis? Describe the structure

A

The epidermis’ main function is to replace damaged cells to maintain protective properties

4 layers: stratum basal, stratum spinous, stratum granulosum, stratum cornea

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3
Q

Describe the form and function of the stratum basal

A

the stratum basal is the lowest layer, comprising of a single row of keratinocytes. constant cell division pushes older cells up . melanocytes are found here and produce melanin when skin is exposed to UV lighr

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4
Q

Describe the form and function of the stratum spinosum

A

this layer anchors cells cells together by interlocking cytoplasmic processes. these cells are called prickle cells

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5
Q

Describe the form and function of the stratum granulosum

A

cells undergo enzyme induced destruction, loosing nuclei and cytoplasmic organelle. lipid rich secretion acts a water sealant for skin, keratin is laid down meshing structures together

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6
Q

Describe the form and function of the stratum cornea

A

layer of dead flattened cells, with densely packed keratin (corneocytes). corneocytes then shed from skin

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7
Q

Describe the form and function of the dermis

A

Provides strength to skin (by providing collagen and fibroblasts) and elasticity by providing elastin.

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8
Q

what are the impacts of skin conditions on patients and society?

A

Can be associated with severe psychological impact

Emerging evidence: increased risk of cardiovascular disease

Development issues in children

Many suffers experience low quality of life, bullying

Huge burden in society and impact on health services

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9
Q

what are the different types of eczema?

A

Atopic, (main focus)
asteatotic, lichen(thick hardned skin brought by scratching), gravitationa (linked to venous pressure, fluid leaks and shiny red l, herpeticum, discoid, seborrhoea, pomphoylx
IgE antibody link

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10
Q

what other conditions are commonly associated with eczema?

A

asthma and hay fever

IgE antibody link

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11
Q

eczema epidemiology

A

affects all ages, mainly children
Most cases before age 5
More in urban areas, higher socioeconomic groups
Many cases clear in late childhood/adolescence, but not all

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12
Q

eczema pathophysiology

A

Dysfunctional skin barrier (altered conversion of keratinocytes to protein lipid scales)
causes :
water loss from skin
hyper- reactivity (inflammation, itch)
infection (staphylococcus aureus )
Thelper cell dysregulation thought to involved (IgE and mast cells)

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13
Q

risk factors for eczema?

A

stress, genetics, pollen and pets, rough clothes, contact allergens, soap, extreme temperatures , skin infection, hormones, certain foods

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14
Q

how does eczema present?

A

v young - face ,cheeks, scalp and skin

growing kids - fletchers, wrists and ankles

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15
Q

how is eczema diagnosed?

A

itch, early onset, involvement of the fletchers, asthma if older,

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16
Q

why is it not advised to scratch eczema

A

lichenifies skin over time

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17
Q

treatment of mild eczema

A

Emollients

Mild topical steroid if inflamed skin, spread thinly using fingertip u

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18
Q

treatment of moderate eczema

A

Increase use of emollients
Use emollients quickly if you spot a flare coming on
Increase potency of steroid
Neck, face, genitals – may use mild steroid i. e. hydrocortisone
Loratidine, Ranitidine – non-sedating antihistamine – evidence is low which is why it is only on trial
*You can only use mild steroids on patients who are really young
Under 12 months old only use mild steroids

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19
Q

treatment of severe eczema

A

Emollients. Increase use
Potent topical steroid. Start with moderate potency on sensitive areas. Aim for maximum 7-14 days (5 if sensitive areas)
Consider trial of non-sedating antihistamine if itch present, review 3/12

If itch affecting sleep, consider sedating antihistamine
Consider oral corticosteroid if severe symptoms and distress.

bandages, oral steroids,photherapy
between flares:
lower potency steroid (intermittently) ,topical cacinuirn inhibitors (tacrolimus) review 3/6 months

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20
Q

describe what different severities of eczema will present like

A

Mild:Some dry skin, some itching, a little redness

Moderate
Dry skin, itching, redness, some thickening

Severe
Widespread as above, skin thickening, bleeding, oozing, etc.

Infected
Weeping, crusted, pustules, +/- systemic symptoms

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21
Q

treatment for infected eczema

A

Weeping, crusted, pustules, +/- systemic symptoms

Oral antibiotics may be required, if localised infection use topical

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22
Q

give an example of a low potency topical steroid

A

Hydrocortisone 0.1, 0.5, 1, 2.5%

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23
Q

give an example of a moderate potency topical steroid

A

Clobetasone butyrate 0.05%

Betamethasone valerate 0.025%

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24
Q

give an example of a potent potency topical steroid

A

Betamethasone Valerate 0.1%

Betamethasone dipropionate 0.05%

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25
Q

what counselling is given to patients with eczema?

A

use emollients liberally and frequently
continue steroids for 48hr after reduced inflammation
scratch mittens, cut nails
discard old products after infective episode
ointments less well tolerated - use at night (v good at managing dry hard thickened skin
Creams and lotions – better if not wanting occlusive barrier e.g. weeping

26
Q

what are important things to remember about emollients

A

fire hazard - paraffin based
steroid sparing
urea and lanolin reactions
aq cream avoided due to sodium laurel sulphate irritation
pump tub to decrease cross contamination
after wash, gently dry skin and stroke in following hair growth

27
Q

what is psoriasis

A

Chronic, inflammatory disorder of skin and joints

Relapsing remitting in nature

28
Q

what is the main type of psoriasis?

A

vulgaris ( chronic plaque )

29
Q

where does vulgarisms affect mainly ?

A

scalp, knees, elbows,

30
Q

what is the prevalence of psoriasis in the UK?

what age demographic are affected ?

A

1-2%

15-25 (75% of cases)

31
Q

pathophysiology of psoriasis

A

Inflammatory cells present in all layers of psoriatic skin leading to epidermal hyper proliferation and vascular changes.

Particularly important role for T cells, TNF alpha and interleukins

32
Q

risk factors for psoriasis

A

Healthy diet and exercise improves symptoms
Stopping smoking can improve disease status
Alcohol excess is a trigger
Genetics – family history 70%
Pregnancy can be a protective factor
Puberty and menopause is a risk factor – hormonal changes
Skin injuries e.g. Burns, cuts  psoriasis

33
Q

what are some complications of psoriasis?

A

Psoriatic arthritis – screening for symptoms and use of PEST tool
Depression/anxiety – screening at appointments for symptoms
Metabolic syndrome and CVD – lifestyle modification, screening

34
Q

how do you treat psoriasis of the trunk and limb?

A

adults: potent corticosteroid and vitamin D analogue (calcipitrol)
coal tar if above not effective

35
Q

how do vitamin d analogues work

A

reduce cell proliferation

36
Q

how do you treat psoriasis of the scalp

A

Potent corticosteroid.
If not effective try a different formulation and/or salicylic acid/emollients.

Combine steroid with calcipotriol or use vitamin D analogue alone if not effective/tolerated

37
Q

how to treat psoriasis of face, flexures or genitals

A

Mild-moderate steroid
Short term treatment

If not effective/long term treatment needed, use calcineurin inhibitor (tacrolimus)

38
Q

how does salicylic acid help treat psoriasis?

A

removes scales which prevent treatment from properly penetrating

39
Q

how is mild psoriasis treated :

A

emollients, topical corticosteroid alone or with vitamin D analogue

calcinurin inhibitor

coal tar

40
Q

how is moderate psoriasis treated?

A

Phototherapy plus topical treatments
oral methotrexate or cyclosporin plus topical

oral acitretin plus topical

41
Q

how is severe psoriasis treated?

A

add biological agent

42
Q

how is severity measured?

A

covering 10% of body

patient very distressed

43
Q

name 3 vitamin d analogues?

A

calcipqotriol
calcitriol
tacalitol

44
Q

patient advice for psoriasis?

A

emollients use liberally
care with prolonged steroid use
continue steroids 48 hours after reduced inflammation
Skin irritation and photosensitivity with vitamin D analogues
Several weeks for effect to be seen, persevere
Avoid scratching and picking
Report joint symptoms immediately
Importance of review after 4 weeks – toxicity, adherence, effectiveness
Combination steroid and calcipotriol product better than each alone
Emollients for daily use, other treatments for flares
Treatment break in between steroid courses, in between could use Vit D

45
Q

what types of acne are there?

A

vulgaris
rosacea
conglobata
fulminant

46
Q

where does acne affect most

A

face back chest

47
Q

pathophysiology of acne

A

pilosebaceous follicles involved
increased hyperplasia of cells secreting hair sebum
enlarge, turnover increase
composition of substrate ideal for bacterial growth

bacteria stimulates inflammation - production of fatty acids - stimulate keratincye proliferation and differentiation
grow over follicle and block causing inflammation

48
Q

what is comodogensis?

A

blocked follicles

49
Q

presentation of acne?

A

Open follicle – blackheads (close to the skin, melanin in the skin interact with the atmosphere and turns black)
Closed follicle – whiteheads (lower down and they can progress into acne lesions)
Can also get hypercornification – hardening of the skin

50
Q

risk factors for acne

A

Family members with acne
High glycaemic index foods - inc androgens
Medications (not technically acne!)
Polycystic ovary syndrome (PCOS) - 30% affected
Smoking?
Stress
Cosmetics – look for those that are labelled non-comedogenic

51
Q

treating mild to moderate acne

A
Topical retinoid (adapaline 0.1% gel/cream, isotretinoin)
Benzoyl peroxide (BPO - 4% cream or 5% gel/wash) 
Azelaic acid (20% cream, 15% gel)
Topical antibiotic (clindamycin 1%) always with BPO
52
Q

treating moderate acne

A

Oral antibiotic and topical retinoid . doxycycline, linocycline with topical retinoid
Can add BPO - reduces incidence of resistance to the antimicrobials
Treat for 6-8 weeks can repeat course
may need maintenance treatment i.e BPO and azaelic acid or retinoid

53
Q

treating severe acne

A

oral isotretinoin

54
Q

how does BPO / benzyl peroxide treat acne?

A

anti-bacterial and uses free radical oxidation

55
Q

why is azaelic acid preferable for mild - moderate acne

A

less skin irritation and for milder acne

56
Q

what are common drug combinations for treating mild to moderate acne?

A

Antibiotics + BPO

Retinoids + BPO

57
Q

patient advice for acne

A

Do not over clean the skin
Do not pick/squeeze lesions – scarring risk
Use non-comedogenic / no oil products (uncertain benefit for facial cleansers)
Bleaching of hair and clothing – BPO
Skin irritation, if severe reduce application frequency/switch – all
Avoid contact with eyes and mucous membranes - all treatments

Sunscreen and avoid sunbeds – retinoids/BPO/oral antibiotics

Avoid in pregnancy – retinoids/oral antibiotics

Apply to whole affected area, not just individual lesions

For gels: apply after washing and then remove a few hours later to avoid irritation

For washes: apply and leave on for a few minutes, then rinse off

Apply pea sized amount to entire affected area, wash off after 30-60 mins (retinoids)
Lifestyle advice important

58
Q

What are the 3 main functions of the skin

A

barrier to protect tissues and organs
temperature control
sensory organ for touch, pain,temperature
production of vitamin D

59
Q

How does vitamin D production occur?

A

7-dehydrocholesterol in the skin produces vitamin D3 (cholecalciferol) in the presence of ultraviolet radiation in sunligh

60
Q

What can lack of vitamin D leas too?

A

nadequate calcium absorption and lack of deposition in bone, causing bone deformity in children (rickets) and bone pain and tenderness in adults (osteomalacia).