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The Patient > Skin > Flashcards

Skin Flashcards

1
Q

What is the approximate surface area of the skin?

A

1.8m sq, 16% bodyweight

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2
Q

Three main layers of the skin?

A

epidermis, dermis and hypodermis (subcutis)

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3
Q

Which skin layer is the epidermis?

A

Outermost layer

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4
Q

Main functions of the epidermis?

A

replace damaged cells to maintain protective properties

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5
Q

How does the epidermis carry out its main function and how long does it take?

A

continually produces keratinocytes and pushes them up through the 4 layers of the epidermis until they are shed

28 days

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6
Q

Secondary function of the epidermis?

A

produce melanin to protect skin from UV radiation

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7
Q

What cells is the epidermis made up of?

A

Mostly keratinocytes, with some melanocytes and Langerhans cells

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8
Q

What do melanocytes do?

A

produce melanin

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9
Q

What do Langerhans cells do?

A

inolved in immune response

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10
Q

How are nutrients etc transported in the epidermis?

A

diffusion - there are no blood vessels

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11
Q

What are the four layers of the epidermis? innermost -> outermost

A

stratum basale
stratum spinosum
stratum granulosum
stratum corneum

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12
Q

structure of the stratum basale?

A

a single layer of keratinocytes that are constantly undergoing division and pushing up into spinosum. also contains melanocytes that distribute melanin to keratinocytes

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13
Q

structure of stratum spinosum?

A

cells anchored together by interlocking cytoplasmic processes
cells called prickle cells (due to their appearance)

also contains Langerhans cells

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14
Q

what happens in stratum granulosum?

A

enzyme induced destruction of cells - lose nuclei and organelles

  • contains a lipid rich secretion to act as the water sealant
  • keratin meshes the strcutures together further
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15
Q

Structure of stratum corneum?

A

dead cells which are flattened with densely packed keratin (corneocytes) - which are then shed from the skin

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16
Q

Structure of the dermis?

A

contains sweat glands, hair, sebaceous glands, smooth muscle (goosebumps), lymphatics and nerves

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17
Q

Functions of the dermis?

A

strength (from collagen and fibroblasts) and elasticity (elastin)

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18
Q

Structure of the hypodermis?

A

contains nerves, blood supplies and fat

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19
Q

function of the hypodermis?

A

cushion and insulate the tissue beneath the hypodermis

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20
Q

What are the functions of the skin?

A

vitamin D production, sensory organ for touch/temp/pain, control of body temperature, protecting organs

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21
Q

what is the real name of vit D3

A

cholecalciferol

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22
Q

what produces vitamin D3 in the skin?

A

7-dehydrocholesterol

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23
Q

where is vitamin D3 obtained ?

A

most from sunlight. can also get from eggs and fish

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24
Q

how is vit D3 converted to active vit D?

A

D3 –> calcidol in the liver, then hydroxylated to calcitriol in the kidney to make active vit D

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25
Q

how does vitamin d raise plasma calcium levels?

A

stimulates intestinal epithelium to make more calcium transport proteins

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26
Q

consequences of vit d deficiency?

A

inadequate calcium absorption and deposition in bone

bone deformity in children (rickets) and bone pain/tenderness in adults (osteomalacia)

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27
Q

how much sun exposure is enough to prevent vit d deficiency?

A

10-15 minutes on hands and face a few times a week

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28
Q

what sensory receptors detect touch in the skin?

A

machanoreceptors

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29
Q

what receptors detect temperature changes in the skin?

A

thermoreceptors

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30
Q

what receptors detect pain in the skin?

A

nociceptors

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31
Q

What makes the fingertips so sensitive?

A

large numbers and overlapping sensory neurones

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32
Q

how does the skin control body temperature

A

vasodilation or vasoconstriction

sweating when internal temp reaches over 37 degrees

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33
Q

How does newborn fat help insulate?

A

brown fat - gets oxidised to produce more heat than ATP to stay warm

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34
Q

what does the skin act as a barrier against?

A

bacteria and toxins, dehydration, UV radiation, mechanical damage/trauma

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35
Q

what is the first immune mechanism of skin?

A

physical barrier to pathogens

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36
Q

what happens (immune) when the skin is broken?

A
  • recognises foreign matter and initates inflammatory response
  • Langerhans cells ingest particle and present antigens to the T and B cells to produce a resposne
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37
Q

What are the four stages of the skin healing process

A
  1. haemostasis
  2. inflammatory phase
  3. proliferative phase
  4. maturation phase
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38
Q

what happens if an injury only affects the epidermis?

A

keratinocytes break from basement membrane, then enlarge until they meet another cell (contact inhibition).

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39
Q

for what types of injury do the 4 stages of healing occur?

A

lacerations etc that affect the dermis and epidermis

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40
Q

What is the main function of the haemostasis phase in skin healing?

A

clot formation

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41
Q

What happens during the haemostasis phase in skin healing?

A

1 platelets in blood recognised exposed collagen (from exposed dermis)
2 platelets become sticky and release thromboxane A2 (activated platelets) which aggregatewith collagen and form a plug on the wound
3 activated platelets release serotonin which reduces blood supply to the wound
4 damaged tissue releases thromboplastin - combines w calcium to produce insoluble fibrin at the end of clotting cascade. combines with platelet aggregate, dries and scabs

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42
Q

what is the main function of the inflammatory phase in skin healing?

A

cleans the wound to prepare for healing

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43
Q

What happens during the inflammatory phase in skin healing?

A
  • Langerhans cells release inflammatory mediators
  • bradykinin increases pain, leukotrienes increase blood flow to area
  • capillaries become more permeable to increase white blood cell traffic to the wound, plasma movement to tissue causes swelling
  • neutrophils digest bacteria and particles, monocytes move to wound & mature into macrophages that clean the wound
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44
Q

What is the function of the proliferative phase in skin healing?

A

dermis repaired and epidermis regenerated - this stage is initiated by presence of macrophages

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45
Q

What happens during the proliferative phase in skin healing?

A

if low oxygen - macrophages release angiogenic growth factors to develop new blood vessels to bring oxygen and nutrients

  • macrophages also release chemicals to attract granulation tissue to produce new connective tissue
  • platelet derived growth factors and macrophages activate fibroblasts which grow and divide to produce a collagen network to strengthen the wound
  • Specialised fibroblasts (myofibroblasts) act like a muscle and can contract the edges of the wound, closing the wound
  • epithelial cells move over granulation tissue, then stop through contact inhibition
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46
Q

What happens in the maturation phase of skin healing?

A

scar formation - can take up to two years

collagen is re-aligned to improve strength, and pulled inwards. extra blood vessels close

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47
Q

What are intrinsic patient factors that affect wound healing?

A

patient nutrition, skin perfusion, age, weight, co-morbidity (incl. medication), smoking

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48
Q

How does patient nutrition affect wound healing?

A
  • protein is needed to produce antibodies, leukocytes, collagen and fibroblasts
  • vitamin ABCE zinc and iron are all involved
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49
Q

How does skin perfusion affect wound healing?

A
  • oxygen and nutrient supply is required

- compromised blood supply e.g. peripheral vascular disease will delay healing

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50
Q

How does age affect wound healing?

A

younger patients are more likely to have better nutrition, better perfusion and fewer co-morbidities

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51
Q

How does weight affect wound healing?

A
  • collagen structure is altered in obese BMIs

- likely to be reduced tissue perfusion

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52
Q

How do co-morbities affect wound healing?

A
  • diabetes: hypoglycaemia affects leukocyte phagocytosis
  • anaemia, ischaemia, jaundice and cancer will adversley affect healing
  • cytotoxics and PG inhibitors (e.g. steroids) will reduce wound healing - antagonism of growth factors, affecting inflammation, fibroblast proliferation, collagen synthesis etc
  • vasoconstrictors: nicotine, cocaine, adrenaline etc. tissue hypoxia
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53
Q

How does smoking affect wound healing?

A

impairs wound contraction, nicotine is a vasoconstrictor, reduces oxygen and causes platelet aggregation

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54
Q

What are extrinsic wound factors that affect wound healing?

A

moist wound, wound temperature, tissue oxygenation, pH, infection, clean wound surface

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55
Q

How does a moist wound affect wound healing?

A

moisture helps progression of epithelialisation, diffusion of growth factors and enzymes

too moist can encourage infection

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56
Q

How does wound temperature affect wound healing?

A

body enzymes are at optimum at 37 degrees

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57
Q

How does tissue oxygenation affect wound healing?

A

more oxygen is required at epithelialisation than at granulation

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58
Q

How does pH affect wound healing?

A

lactic acid rises when oxygen falls, reduced pH causes oxygen to dissociate from Hb, reducing oxygenation

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59
Q

How does infection slow wound healing?

A

The bacteria outweigh the body’s own immune resposne, so wound healing slows

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60
Q

How does a clean wound surface affect wound healing?

A

foreign matter increases the length of the inflammatory phase so delays healing

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61
Q

What is the management of eczema focused around?

A

Reducing relapses and treating them promptly when they arise

  • identify and avoid triggers
  • implementing stepped care plan
  • referral to specialists when conventional treatment doesn’t work
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62
Q

What are the types of trigger factors for eczema flare ups?

A

Irritation, physoclogical, food hypersensitivity, allergens

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63
Q

In what ways can irritation cause an eczema flare-up?

A

e.g. soaps (remove skin lipids, activate proteases), abrasive clothing, temperature/humidity extremes

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64
Q

In what ways can psychological stress cause an eczema flare up?

A

can cause habitual scratching which worsens eczema

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65
Q

In what ways can food hypersensitivity cause an eczema flare up?

A

very rarely, 10% of children and most of these under 3

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66
Q

In what ways can allergens cause an eczema flare up?

A

house dust mites, animals, toiletries/cosmetics, moulds, pollens

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67
Q

What is the significance of emollients in eczema treatment?

A

the mainstay. restore integrity of the skin barrier, should be used even when skin is good

can reduce Cx requirements, restore suppleness and improve appearance of skin

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68
Q

What evidence is there to support the use of emollients?

A

little. but also little doubt about their usefulness

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69
Q

How to emollients help to protect skin?

A

forms an oily layer that prevents water evaporation, so water stays in stratum corneum and enters cells

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70
Q

What is complete emollient therapy?

A

frequent application of creams and ointments as well as bath oil and soap substitute

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71
Q

How much cream/ointment should be applied per week in complete emollient therapy?

A

500g

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72
Q

What counselling points should be given for emollient application?

A
  • apply quickly but gently with clean hands
  • 30 mins before corticosteroid
  • can be warmed for easier application
  • can be cooled to soothe itch
  • frequent application (3-4 times a day)
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73
Q

How are soap substitutes used for complete emollient therapy?

A

instead of all conventional soaps, appy to dry skin then rinsed off

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74
Q

How are bath oils used for complete emollient therapy?

A

about 15mL in a warm (not hot) bath

forms a fine emollient film on the skin

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75
Q

What balance must be struck between patient preference and efficacy?

A

The thicker, greasier emollients are more effective but patients often dislike greasiness etc

best results come from frequent application which only happens if well tolerated by patient

might need different preparations for different body parts. patients may be happier using heavier preps at night

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76
Q

What types of lanolin treatments can be used for eczema?

A

highly purified and hypoallergenic - not as poorly tolerated as made out

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77
Q

What is the role of humectants in eczema therapy, and what are some examples?

A

draw water from the dermis to the epidermis to hydrate it

e.g. glycerin, urea, polyethylene glycol

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78
Q

What is the role of colloidal oatmeal in eczema treatment?

A

soothing and anti-itch properties

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79
Q

What is the role of lauromacrogols in eczema treatment?

A

Anti-itch

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80
Q

What is the role of antiseptics in eczema treatment?

A

useful in controlling flares

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81
Q

What excipients in creams can be irritant, and therefore unsuitable for eczema treatment?

A

sodium lauryl sulfate, chlorocresol, phenoxyethanol

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82
Q

How does emollient use affect the need for corticosteroids?

A

good emollient use can reduce the need for corticosteroids

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83
Q

What ratio of emollient to steroid should be used throughout eczema treatment?

A

10x more emolllient than steroid

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84
Q

What balance must be struck regarding potency of corticosteroids?

A

least potent steroid vs. undertreating

it is better to have a shorter course of a more potent steroid

85
Q

When should mild corticosteroids be used, and what is an example of one?

A

on thin skin, e.g. face, genitals

86
Q

When should moderate corticosteroids be used, and what is an example of one?

A

mild to moderate eczema with 1-2 weeks. e.g. clobetasone butyrate

87
Q

When are potent steroids required and what is an example of one?

A

e.g. mometasone

on thick skin or severe eczema

88
Q

What determines the potency of a steroid?

A

the steroid and the formulation (e.g. cream vs. ointment)

89
Q

When should the varying formulations be used?

A

ointments can be used for dry skin

creams etc. for oozing or infected, as these shouldn’t be occluded

90
Q

What steroids are available OTC, and when can it be supplied?

A

1% hydrocortisone

shouldn’t be used for more than 1 week without Dr advice. refer anyone who is widespread or not been diagnosed.

clobetasone 0.05% for over 12s

91
Q

Who can you not supply OTC corticosteroids to?

A

u10s or pregnant women, unless recommended by GP

92
Q

Stepped care plan: treamtent when clear

A

emollients only

93
Q

Stepped care plan: treatment when mild flare

A

emollients + maybe mild corticosteroids

94
Q

Stepped care plan: treatment when moderate flare

A

emollients, steroid, can add in: topical calcineurin inhibitors, bandages

95
Q

Stepped care plan: treatment when severe flare

A

everything from moderate, plus phototherapy and/or systemic therapy

96
Q

What potency steroids and duration should be used for a moderate flare on face and neck?

A

mild potency for 3-5 days

97
Q

What potency steroids and duration should be used for a moderate flare on the body?

A

moderate potency for 7-14 days

98
Q

What potency steroids and duration should be used for a severe flare on face and neck?

A

moderate potency for 3-5 days

99
Q

What potency steroids and duration should be used for a severe flare on the body?

A

high potency for 7-14 days

100
Q

Incidence of the long term effects of steroid use?

A

well recognised but often exaggerated - usually only occur after a long period of use

101
Q

What determines the incidence of the effects of steroid use?

A

area and thickness of skin, potency, duration of use.

greater absorption when the skin is raw

102
Q

What counselling points are important when supplying corticosteroids?

A
  • importance of not using as an emollient
  • difference between potency and concentration
  • amount to apply (FTU should cover an area twice teh size of flat of hand
103
Q

Importnat difference between clobetasol and clobetasone?

A

clobetasol is v potent, clobetasone is moderate

104
Q

What should be used to treat a bacterial infection of eczema (and why)?

A

oral antibiotics - no evidence that topical are better and resistance risk is high

105
Q

Why are sedating antihistamines useful for eczema? Examples?

A

Anti-itch as well as helping sleep

promethazine & alimemazine not suitsble for under 2s
hydroxyzine licensed from 6m

106
Q

What are topical immunomodulators and when should they be used?

A

Calcineurin inhibitors
pimecrolimus (for mild to mod), tacrolimus (for mod to severe)

used when side effect risk of steroids is serious, or they aren’t effective

107
Q

Mechanism of action of calcneurin inhibitors?

A

inhibit calcineurin phosphatase - enzyme involved in activation of T cells and propagation of inflammatory response

108
Q

What are the three situations according to NICE when calcineurin inhibitors can be used?

A
  1. alternative to corticosteroids that would be inappropriate
  2. potent steroids would otherwise be needed most of the time
  3. there is evidence of steroid induced skin damage
109
Q

What else are calcineurin inhibitors licensed for?

A

maintenance therapy (2x a week) to prevent flares for up to 12 months

110
Q

What is the main side effect of calcineurin inhibitors?

A

burning, but this disppears after a few days

111
Q

When can systemic immunosuppression be used for eczema therapy?

A

severe atopic eczema

112
Q

Examples of systemic immunosuppressants?

A

ciclosporin, methotrexate, azatioprine and systemic corticosteroids

113
Q

How does phototherapy work for eczema treatment?

A

UVA alone has little effect, given with a psoralen photosensitiser
- mechanism is not fully understood, maybe immunosuppression

114
Q

Why is close monitoring required for UV therapy?

A

Skin cancer risk

115
Q

What is wet wrapping?

A

emollient or corticosteroid, wet tubular bandage, dry wrap

can be used on the whole body except the scalp

116
Q

WHen is wet wrapping used?

A

Extensive and severe eczema, esp in children

117
Q

Why is supervision required when using frequent wet wrapping?

A

over-absorption of steroid due to occlusion

118
Q

When can behvaioural therapy be used for eczema?

A

Adjunct to other treatment. help patient cope with the chronic illness impact on their life

119
Q

What should patients be educated on regarding their eczema?

A
  • patients and carers should be fully involved with care and decisions, with importance of adherence enforced at every consultation
  • how to recognise a flare early
  • how to use stepped care plan to manage a flare
  • starting treatment immediately and continuing for 48 hours past symptoms resolving
120
Q

Incidence of psoriasis?

A

affects 2-5% of the population, usuallystarts in 20s-30s (but can be any age)
inheritance appears to play a role

121
Q

What are the different types of psoriasis?

A

chronic plaque, guttate, pustular and erythrodermic

122
Q

What does chronic plaque psoriasis look like?

A

well defined thickened red plaques, silvery scales (dark red and grey on black skin)

can get pinpoint bleeding if scales are stretched or removed

123
Q

What body parts is chronic plaque psoriasis most common on?

A

scalp, exterior of limbs (shins, elbows) and lower back

also flexures (groin, elbows, under breasts) - shiny, red and moist, no scales

124
Q

Pathology of chronic plaque psoriasis?

A
  • hyperproliferation of the epidermis - up to 16x thicker than normal. (NOT an acceleration of growth, more cells enter the growth phase)
  • abnormal differentiation of keratinocytes
  • granular layer missing
  • stratum corneum thickened, many cells still have nuceli
  • infiltration of dermis and epidermis w T lymphocytes and neutrophils
  • cutaneous vasculature stimulation, new blood vessels form in plaques
125
Q

What is guttate psoriasis?

A

an accute form, commonly follows strep throat (more common in children and young adults)

appearance - small scaly lesions, widespread

126
Q

How to treat guttate psoriasis?

A

Usually clears in 8 weeks with topical therapy

127
Q

What is pustular psoriasis?

A

Localised: yellow/brown pustules on soles of feet or palms
Generalised: v rare. clusters of pustules develop on already raw skin - acute onset and severe, hospital admission required

128
Q

What is erythrodermic psoriasis?

A

red and inflamed patches all over body, usually scaly. precipitated by withdrawal of corticosteroid

129
Q

What effect does psoriasis have on nails?

A

affected in 50% of cases

  • small pits
  • onchylosis (partial separation from nail bed)
  • oil spots (salmon coloured patches from discolouration of skin)
130
Q

What are the precipitating factors for psoriasis?

A
  • trauma (wounds, scratches, tattoos)
  • infection (guttate triggered by strep usually)
  • hormonal events
  • sunlight (usually improves, but can worsen in 10% of cases)
  • drugs (lithium, Ace inhibs, antimalarials, beta blockers)
  • alcohol and smoking
  • profound stress
131
Q

What factors are used to determine the severity of psoriasis?

A

disease activity, response to treatment and impact on the individual

generally, more than 15-20% of body coverage is severe, but smaller patches can have a huge impact (visible or sensitive)

132
Q

What are the general points surrounding management of psoriasis?

A

most patients w chronic plaque have mild disease managed in primary care with topical treatment

moderate to severe disease can require second line, under dermatologist supervision

133
Q

What are some second line treatments for psoriasis?

A

phototherapy, photochemotherapy, systemic drugs

134
Q

How likely is it that psoriasis clears completely?

A

for chronic plaque, rarely clears completely but can have periods where it is confined to a small patch

135
Q

What isthe use of emollients in psoriais treatment?

A

All patients should use regularly, restores pliability of skin and reduces shedding of scales

136
Q

What is the role of vitamin D analogues in psoriasis treatment?

A

mainstay - can clear large portions within 6-8 weeks

137
Q

How do vitamin D analogues work to treat psoriasis?

A

inhibit keratinocyte differentiation and proliferation

weaker effects on calcium levels than vitamin D

138
Q

What is the evidence base for using vitamin D analogues in psoriasis treatment?

A

at least as effective as corticosteroids, with longer remission periods on discontinuation

most effective regimen is emollients + steroids + vit D analogue

139
Q

What are two examples of vitamin D analogues?

A

calcipotriol (dryness and stinging, not suitable on face)

calcitriol (far less irritant)

140
Q

How much vitamin D analogue should be applied to psoriaisis?

A

thicker than steroids - 1 FTU does approx one palm (twice as thick as Cx)

141
Q

What is the place of steroid therapy in psoriasis treatment?

A

tolerance can be an issue, and more is required to be effective
mild - face and genitals
potent - recalcitrant lesions on trunk and limbs

142
Q

What steroid cannot be used for psoriaisis?

A

clobetasone butyrate 0.05%

143
Q

What is tazarotene and what is its place in psoriasis therapy?

A

a topically active retinoid, affecting keratinocyte differentiation (antiproliferative and anti-inflammatory effects)

144
Q

Disadvantages of tazarotene therapy?

A

Irritant, causes photosensitivity, teratogenic

145
Q

Place of tar in psoriasis therapy?

A

mechanism unknown, believed to be keratinolytic and antiproliferative

often used in combination with UVB phototherapy

146
Q

Types of preparations of tar for psoriasis treatment?

A

propietary preps, or 1-5% in paraffin

147
Q

Disadvantages of tar for psoriasis treatment?

A

stains, less effective, unpleasant smells

148
Q

What is dithranol?

A

Yellow powder, very irritant to skin (inflammatory, causes blisters)

149
Q

How is dithranol used in psoriasis treatment?

A

combined in Zn and salicylic acid paste to be applied to affected areas. concn increased according to patient response

traditional inpatient regimen: applied, leave for 12-24 hours, tar bath, UVB irradiation

new regimen: short contact dithranol therapy (SCDT) - up to 8% for 15-30 mins, with or without UVB. suitable for home use

150
Q

What is micanol?

A

temp sensitive, releases dithranol at skin temp then washed off to prevent further release. response in 20 days

151
Q

Presentation of scalp psoriasis?

A

extends about 1cm from the hairline, doesnt normally affect hair growth but can cause temp. thinning

152
Q

Special treatment mild for sclp psoriasis?

A

tar containing shampoo enough usually

153
Q

Treatment steps for severe scalp psoriasis?

A
  1. soften scales - oil massage then leave for an hour. keratinolytic agents (e.g. salicyllic acid, sulfur) can help lift scales
  2. active vit d treatment or steroid
154
Q

Importance of selecting the correct dressings?

A
  • can interact with medications

- different aims of treatment will need different dressings

155
Q

What three factors need to be considered when selecting a wound dressing?

A

wound related issues, clinical effectiveness, economic factors

156
Q

How will dead tissue behave in a wound?

A

In ideal conditions, will autolytically debride itself. if exposed to a drying atmosphere, can dehydrate and shrink to form a hard black/olive eschar

157
Q

Complications of an eschar?

A

delays autolysis indefinitely, the shrinking can cause pain

158
Q

Primary interventions for necrotic wounds?

A

rehydrating the wound, removing dead tissue (can be done by surgical debridement)

159
Q

What are hydrogel dressings?

A

60-90% water content to draw moisture through the wound, making eschar easier to remove

160
Q

In what forms are hydrogel dressings available?

A

amorphous gel (most commonly used), impregnated non-woven dressings, sheets

161
Q

How are hydrogel dressings used?

A

covered with a secondary dressing to hold in place and prevent moisture evaporation

162
Q

What secondary dressings can be used with hydrogels?

A

plastic film adsorbent dressings (eg, Melonin, Telfa) or vapour-permeable films (eg, Tegaderm, OpSite, Bioclusive)

163
Q

What cannot be done to further treat the wound if a hydrogel dressing is used?

A

larvae therapy - hydrogels contain propylene glycol which is toxic to larvae

164
Q

What is a suitable alternative to hydrogel dressings?

A

Hydrocolloid dressings

165
Q

How do hydrocolloid dressings work?

A

occlusive and waterproof, so promote moisture accumulation

166
Q

What type of wounds are hydrocolloid dressings not suitable for?

A

Dry ones, or over exposed bone/muscle

contraindicated in infected wounds as encourage bacterial growth

most contain gelatin so not veggie

167
Q

What type of dressing would be suitable for a necrotic wound with a high level of exudate?

A

alginate dressing - more than hydrogel/colloid

168
Q

How are alginate dressings used and how do they work?

A

derived from seaweed, absorb a lot but maintain a moist environment

assortment of ribbons and sheets should be used to pack the wound

169
Q

What types of wounds are alginates not suitable for?

A

dry ones - can stick and cause trauma when removed

170
Q

What is slough?

A

left behind after eschar separates from healthy tissue - yellowish partly liquified material

171
Q

How should necrotic digits be treated compared to necrotic wounds?

A

shouldn’t be rehydrated as may become a focus for infection, should be left exposed to air for auto-amputation (surgery used if extensive tissue destruction)

172
Q

How must slough be managed in a wound?

A

support natural processes that debride slough, manage exudates from the inflammatory stage of wound healing

important not to over-hydrate as this can cause maceration

173
Q

What dressings are best for sloughy wounds?

A

alginate covered with a semipermeable film dressing or hydrocolloid

heavy exudate: hydrofibre dressing with absorbent secondary dressing

174
Q

What is biosurgery?

A

Larval therapy - suitable for necrotic and sloughy wounds

175
Q

How does larval therapy work to improve wound healing?

A

larvae exude enzymes that break down dead tissue - combat odour and kill bacteria (healthy tissue is not affected

a secondary dressing should be used to absorb exudates and keep larvae in the wound - must be non-occlusive as they require oxygen

176
Q

Why is analgesia often requires for biosurgery?

A

pain caused by pH changes in the wound - pain decreases with bacterial load

177
Q

What treatment is needed for infected wounds?

A

systemic antibiotics (swab for sensitivity tests) plus antimicrobial dressing

topical antibiotics are rarely used due to resistance concerns

178
Q

Which topical antibiotic is still used regularly for wounds?

A

0.75% metronidazole, for reducing odour of fungating wounds colonised w anaerobes

179
Q

Uses and disadvantages of charcoal dressings?

A

can be used to remove odour, but some are only suitable as a secondary dressing. stick to wounds if allowed to dry out so cause trauma when removed

180
Q

What ingredients can antimicrobial dressings contain?

A
  • iodine: contraindicated in hypertension, pregnancy, breastfeeding, thyroid disease and renal impairment
  • silver: release silver when coming into contact with exudates. expensive but a good supplement to systemic therapies where circulation may limit therapeutic levels in wound
  • honey: moist healing environment, eliminate odour, stimulate new tissue growth and aid debridement. limited by pain on application, high cost and bee sting allergies
181
Q

What is granulation tissue?

A

fragile mix of proteins and polysaccharides linked with collagens to form a vascular gel-like matrix.

182
Q

How must granulating wounds be managed?

A

must be kept warm and moist, and exudates managed

183
Q

How to dress low-depth granulating wounds?

A

low or non adherent dressing, or a hydrocolloid. occlusive dressings are particularly effective as they create a hypoxic environment which promotes granulation. use alginates if exudate is heavy

184
Q

How often should dressings on granulating wounds be changed?

A

as infrequently as possible, to avoid damage to the fragile tissue

185
Q

How to dress deep cavity granulating wounds?

A

polyurethane foam dressing can be used to pack the wound
important not to overpack the wound because this can cause wound distortion leading to ischaemia, necrosis, cosmetic defects and patient discomfort

186
Q

When do wounds stop granulating?

A

when the base of the wound cavity is almost level with the surrounding skin, when epithelialisation begins

187
Q

What is epithelialisation?

A
  • epithelial cells advance in a sheet across the wound, meeting in the middle
  • doesn’t tend to produce much exudate
  • must keep wound moist until it closes
188
Q

What dressings are suitable for epithlialising wounds?

A
  • hydrocolloids or semi-permeable dressings
189
Q

Other dressings suitable in the final stages of healing?

A
  • soft silicone dressings, knotted viscose preparations, knitted viscose, nylon sheet dressings

must be checked regularly for allergies, infection and signs of deterioration

190
Q

What are complex dermatology therapies?

A

carry a high risk of toxicity (narrow therapeutic index), require intensive monitoring
- high cost, specialist prescribing, not first line

191
Q

What is isotretinoin used for?

A

severe acne unresponsive to tpoical treatments and antibiotics

192
Q

How does isotretinoin work?

A

reduces skin sebum production by up to 90% after 6 weeks (apoptosis of sebocytes, reduces conc of P. acnes on the skin)

lowers hyperkeratinisation - interferes with comedogenesis (white heads)

anti-inflammatory properties

193
Q

What risks does isotretinoin carry?

A
  • v. teratogenic - requires full contraception for 1 month either side of treatment
  • mental health effects (depression, suicidal ideation), full psych history needed, refer to psych if MH deteriorates and stop drug
  • impaired night vision (it’s a retinoic acid) - must inform DVLA if affected
  • dry skin and mucous membranes - joint pain is common
  • fragile skin: use spf 50 in summer, no wax, dermabrasion or laser treatments for 6 months after
194
Q

At what point do complex therapies start to form part of treatment in psoriasis?

A

from moderate disease onwards

195
Q

What is PUVA treatment?

A

Psoralens + UVA

oral 8-methoxypsoralen 0.6mg/kg

196
Q

Dosing of psoralens in PUVA treatment?

A

2 hours before UVA exposure, treatment 3x weekly, usually clears in 5-6 weeks (20-30 exposures)

197
Q

How does PUVA treatment work?

A

disrupts DNA synthesis, inhibits basal cell proliferation - slows basal cell growth to normal speeds

198
Q

Adverse effects of PUVA treatment?

A
  • psoralens is teratogenic

- premature skin ageing, pigmentation, cataracts

199
Q

What is acitretin?

A

Similar to isotretinoin (retinoid), normalises skin cell proliferation and differentiation

similar side effect profile to isotretinoin, longer half-life, prolonged therapy

200
Q

What precautions are needed with acitretin therapy?

A

Pregnancy prevention for 3 years, hyperlipidaemia (CVD risk assessment, monitor lipid profile, hepatoxic (regular LFTs, avoid alcohol)

201
Q

Place of methotrexate in skin conditions?

A

Eczema and psoriasis - folic acid antagonist

blocks DNA synthesis (folates are co-factors for many enzymes) - slows basal cell proliferation in psoriasis

enzyme inhibition leads to increased adenosine - inhibits neutrophil chemotaxis and cytokine secretion - anti-inflammatory in eczema

202
Q

What risks does methotrexate carry?

A 
Liver cirrhosis (monthly LFTs, step down to 3 monthly later on)
blood disorders (thrombocytopaenia, leukopaenia, anaemia) - weekly FBC then monthly
GI symptoms (stomatitis, nausea) - folic acid 5mg weekly
alopecia, family planning (affects sperm for 3 months after), infection risk
203
Q

Place of calcineurin in psoriasis therapy?

A

blocks calcineurin-dependent factor - blocking IL-2 and proliferation of T-lymphocytes, cytokines and keratinocytes

204
Q

Adverse effects of ciclosporin?

A

Nephrotoxic (associated hypertension too), teratogenic, immunosuppressant

205
Q

Dosing of ciclosporin?

A

2.5 - 5mg/kg daily (must be emphasised as patients may have had methotrexate weekly

206
Q

Role of biologics in psoriasis treatment?

A

Target TNF - used as a last resort when other treatments ineffective

207
Q

Examples of the biologics used for psoriasis?

A

infliximab, adalimumab, ustekinumab, secikinumab, etanercept (GM fusion protein)

208
Q

Effectiveness of biologics for psoriasis?

A

response usually seen in 6 weeks, very effective. 6months-2 years continuation

risk that patients can develop antibodies

209
Q

Risks associated with use of biologics?

A

infection:
- particular concern of reactivation of latent TB
- salmonella/listeria - patients should avoid raw/part cooked meat, fish, eggs and dairy
CV risks
- dont use in severe heart failure, monitor patients with existing CVD
worsening of neurological disease (dont use in demyelating disease like MS)
conflicting evidence about malignancy (lymphoma)

The Patient (8 decks)

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