Skin Flashcards
1
Q
What is the approximate surface area of the skin?
A
1.8m sq, 16% bodyweight
2
Q
Three main layers of the skin?
A
epidermis, dermis and hypodermis (subcutis)
3
Q
Which skin layer is the epidermis?
A
Outermost layer
4
Q
Main functions of the epidermis?
A
replace damaged cells to maintain protective properties
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
6
Q
Secondary function of the epidermis?
A
produce melanin to protect skin from UV radiation
7
Q
What cells is the epidermis made up of?
A
Mostly keratinocytes, with some melanocytes and Langerhans cells
8
Q
What do melanocytes do?
A
produce melanin
9
Q
What do Langerhans cells do?
A
inolved in immune response
10
Q
How are nutrients etc transported in the epidermis?
A
diffusion - there are no blood vessels
11
Q
What are the four layers of the epidermis? innermost -> outermost
A
stratum basale
stratum spinosum
stratum granulosum
stratum corneum
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
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
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
15
Q
Structure of stratum corneum?
A
dead cells which are flattened with densely packed keratin (corneocytes) - which are then shed from the skin
16
Q
Structure of the dermis?
A
contains sweat glands, hair, sebaceous glands, smooth muscle (goosebumps), lymphatics and nerves
17
Q
Functions of the dermis?
A
strength (from collagen and fibroblasts) and elasticity (elastin)
18
Q
Structure of the hypodermis?
A
contains nerves, blood supplies and fat
19
Q
function of the hypodermis?
A
cushion and insulate the tissue beneath the hypodermis
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
21
Q
what is the real name of vit D3
A
cholecalciferol
22
Q
what produces vitamin D3 in the skin?
A
7-dehydrocholesterol
23
Q
where is vitamin D3 obtained ?
A
most from sunlight. can also get from eggs and fish
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
25
how does vitamin d raise plasma calcium levels?
stimulates intestinal epithelium to make more calcium transport proteins
26
consequences of vit d deficiency?
inadequate calcium absorption and deposition in bone
bone deformity in children (rickets) and bone pain/tenderness in adults (osteomalacia)
27
how much sun exposure is enough to prevent vit d deficiency?
10-15 minutes on hands and face a few times a week
28
what sensory receptors detect touch in the skin?
machanoreceptors
29
what receptors detect temperature changes in the skin?
thermoreceptors
30
what receptors detect pain in the skin?
nociceptors
31
What makes the fingertips so sensitive?
large numbers and overlapping sensory neurones
32
how does the skin control body temperature
vasodilation or vasoconstriction
sweating when internal temp reaches over 37 degrees
33
How does newborn fat help insulate?
brown fat - gets oxidised to produce more heat than ATP to stay warm
34
what does the skin act as a barrier against?
bacteria and toxins, dehydration, UV radiation, mechanical damage/trauma
35
what is the first immune mechanism of skin?
physical barrier to pathogens
36
what happens (immune) when the skin is broken?
- recognises foreign matter and initates inflammatory response
- Langerhans cells ingest particle and present antigens to the T and B cells to produce a resposne
37
What are the four stages of the skin healing process
1. haemostasis
2. inflammatory phase
3. proliferative phase
4. maturation phase
38
what happens if an injury only affects the epidermis?
keratinocytes break from basement membrane, then enlarge until they meet another cell (contact inhibition).
39
for what types of injury do the 4 stages of healing occur?
lacerations etc that affect the dermis and epidermis
40
What is the main function of the haemostasis phase in skin healing?
clot formation
41
What happens during the haemostasis phase in skin healing?
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
42
what is the main function of the inflammatory phase in skin healing?
cleans the wound to prepare for healing
43
What happens during the inflammatory phase in skin healing?
- 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
44
What is the function of the proliferative phase in skin healing?
dermis repaired and epidermis regenerated - this stage is initiated by presence of macrophages
45
What happens during the proliferative phase in skin healing?
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
46
What happens in the maturation phase of skin healing?
scar formation - can take up to two years
collagen is re-aligned to improve strength, and pulled inwards. extra blood vessels close
47
What are intrinsic patient factors that affect wound healing?
patient nutrition, skin perfusion, age, weight, co-morbidity (incl. medication), smoking
48
How does patient nutrition affect wound healing?
- protein is needed to produce antibodies, leukocytes, collagen and fibroblasts
- vitamin ABCE zinc and iron are all involved
49
How does skin perfusion affect wound healing?
- oxygen and nutrient supply is required
| - compromised blood supply e.g. peripheral vascular disease will delay healing
50
How does age affect wound healing?
younger patients are more likely to have better nutrition, better perfusion and fewer co-morbidities
51
How does weight affect wound healing?
- collagen structure is altered in obese BMIs
| - likely to be reduced tissue perfusion
52
How do co-morbities affect wound healing?
- 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
53
How does smoking affect wound healing?
impairs wound contraction, nicotine is a vasoconstrictor, reduces oxygen and causes platelet aggregation
54
What are extrinsic wound factors that affect wound healing?
moist wound, wound temperature, tissue oxygenation, pH, infection, clean wound surface
55
How does a moist wound affect wound healing?
moisture helps progression of epithelialisation, diffusion of growth factors and enzymes
too moist can encourage infection
56
How does wound temperature affect wound healing?
body enzymes are at optimum at 37 degrees
57
How does tissue oxygenation affect wound healing?
more oxygen is required at epithelialisation than at granulation
58
How does pH affect wound healing?
lactic acid rises when oxygen falls, reduced pH causes oxygen to dissociate from Hb, reducing oxygenation
59
How does infection slow wound healing?
The bacteria outweigh the body's own immune resposne, so wound healing slows
60
How does a clean wound surface affect wound healing?
foreign matter increases the length of the inflammatory phase so delays healing
61
What is the management of eczema focused around?
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
62
What are the types of trigger factors for eczema flare ups?
Irritation, physoclogical, food hypersensitivity, allergens
63
In what ways can irritation cause an eczema flare-up?
e.g. soaps (remove skin lipids, activate proteases), abrasive clothing, temperature/humidity extremes
64
In what ways can psychological stress cause an eczema flare up?
can cause habitual scratching which worsens eczema
65
In what ways can food hypersensitivity cause an eczema flare up?
very rarely, 10% of children and most of these under 3
66
In what ways can allergens cause an eczema flare up?
house dust mites, animals, toiletries/cosmetics, moulds, pollens
67
What is the significance of emollients in eczema treatment?
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
68
What evidence is there to support the use of emollients?
little. but also little doubt about their usefulness
69
How to emollients help to protect skin?
forms an oily layer that prevents water evaporation, so water stays in stratum corneum and enters cells
70
What is complete emollient therapy?
frequent application of creams and ointments as well as bath oil and soap substitute
71
How much cream/ointment should be applied per week in complete emollient therapy?
500g
72
What counselling points should be given for emollient application?
- 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)
73
How are soap substitutes used for complete emollient therapy?
instead of all conventional soaps, appy to dry skin then rinsed off
74
How are bath oils used for complete emollient therapy?
about 15mL in a warm (not hot) bath
forms a fine emollient film on the skin
75
What balance must be struck between patient preference and efficacy?
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
76
What types of lanolin treatments can be used for eczema?
highly purified and hypoallergenic - not as poorly tolerated as made out
77
What is the role of humectants in eczema therapy, and what are some examples?
draw water from the dermis to the epidermis to hydrate it
e.g. glycerin, urea, polyethylene glycol
78
What is the role of colloidal oatmeal in eczema treatment?
soothing and anti-itch properties
79
What is the role of lauromacrogols in eczema treatment?
Anti-itch
80
What is the role of antiseptics in eczema treatment?
useful in controlling flares
81
What excipients in creams can be irritant, and therefore unsuitable for eczema treatment?
sodium lauryl sulfate, chlorocresol, phenoxyethanol
82
How does emollient use affect the need for corticosteroids?
good emollient use can reduce the need for corticosteroids
83
What ratio of emollient to steroid should be used throughout eczema treatment?
10x more emolllient than steroid
84
What balance must be struck regarding potency of corticosteroids?
least potent steroid vs. undertreating
it is better to have a shorter course of a more potent steroid
85
When should mild corticosteroids be used, and what is an example of one?
on thin skin, e.g. face, genitals
86
When should moderate corticosteroids be used, and what is an example of one?
mild to moderate eczema with 1-2 weeks. e.g. clobetasone butyrate
87
When are potent steroids required and what is an example of one?
e.g. mometasone
on thick skin or severe eczema
88
What determines the potency of a steroid?
the steroid and the formulation (e.g. cream vs. ointment)
89
When should the varying formulations be used?
ointments can be used for dry skin
creams etc. for oozing or infected, as these shouldn't be occluded
90
What steroids are available OTC, and when can it be supplied?
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
Who can you not supply OTC corticosteroids to?
u10s or pregnant women, unless recommended by GP
92
Stepped care plan: treamtent when clear
emollients only
93
Stepped care plan: treatment when mild flare
emollients + maybe mild corticosteroids
94
Stepped care plan: treatment when moderate flare
emollients, steroid, can add in: topical calcineurin inhibitors, bandages
95
Stepped care plan: treatment when severe flare
everything from moderate, plus phototherapy and/or systemic therapy
96
What potency steroids and duration should be used for a moderate flare on face and neck?
mild potency for 3-5 days
97
What potency steroids and duration should be used for a moderate flare on the body?
moderate potency for 7-14 days
98
What potency steroids and duration should be used for a severe flare on face and neck?
moderate potency for 3-5 days
99
What potency steroids and duration should be used for a severe flare on the body?
high potency for 7-14 days
100
Incidence of the long term effects of steroid use?
well recognised but often exaggerated - usually only occur after a long period of use
101
What determines the incidence of the effects of steroid use?
area and thickness of skin, potency, duration of use.
greater absorption when the skin is raw
102
What counselling points are important when supplying corticosteroids?
- 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
Importnat difference between clobetasol and clobetasone?
clobetasol is v potent, clobetasone is moderate
104
What should be used to treat a bacterial infection of eczema (and why)?
oral antibiotics - no evidence that topical are better and resistance risk is high
105
Why are sedating antihistamines useful for eczema? Examples?
Anti-itch as well as helping sleep
promethazine & alimemazine not suitsble for under 2s
hydroxyzine licensed from 6m
106
What are topical immunomodulators and when should they be used?
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
Mechanism of action of calcneurin inhibitors?
inhibit calcineurin phosphatase - enzyme involved in activation of T cells and propagation of inflammatory response
108
What are the three situations according to NICE when calcineurin inhibitors can be used?
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
What else are calcineurin inhibitors licensed for?
maintenance therapy (2x a week) to prevent flares for up to 12 months
110
What is the main side effect of calcineurin inhibitors?
burning, but this disppears after a few days
111
When can systemic immunosuppression be used for eczema therapy?
severe atopic eczema
112
Examples of systemic immunosuppressants?
ciclosporin, methotrexate, azatioprine and systemic corticosteroids
113
How does phototherapy work for eczema treatment?
UVA alone has little effect, given with a psoralen photosensitiser
- mechanism is not fully understood, maybe immunosuppression
114
Why is close monitoring required for UV therapy?
Skin cancer risk
115
What is wet wrapping?
emollient or corticosteroid, wet tubular bandage, dry wrap
| can be used on the whole body except the scalp
116
WHen is wet wrapping used?
Extensive and severe eczema, esp in children
117
Why is supervision required when using frequent wet wrapping?
over-absorption of steroid due to occlusion
118
When can behvaioural therapy be used for eczema?
Adjunct to other treatment. help patient cope with the chronic illness impact on their life
119
What should patients be educated on regarding their eczema?
- 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
Incidence of psoriasis?
affects 2-5% of the population, usuallystarts in 20s-30s (but can be any age)
inheritance appears to play a role
121
What are the different types of psoriasis?
chronic plaque, guttate, pustular and erythrodermic
122
What does chronic plaque psoriasis look like?
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
What body parts is chronic plaque psoriasis most common on?
scalp, exterior of limbs (shins, elbows) and lower back
also flexures (groin, elbows, under breasts) - shiny, red and moist, no scales
124
Pathology of chronic plaque psoriasis?
- 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
What is guttate psoriasis?
an accute form, commonly follows strep throat (more common in children and young adults)
appearance - small scaly lesions, widespread
126
How to treat guttate psoriasis?
Usually clears in 8 weeks with topical therapy
127
What is pustular psoriasis?
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
What is erythrodermic psoriasis?
red and inflamed patches all over body, usually scaly. precipitated by withdrawal of corticosteroid
129
What effect does psoriasis have on nails?
affected in 50% of cases
- small pits
- onchylosis (partial separation from nail bed)
- oil spots (salmon coloured patches from discolouration of skin)
130
What are the precipitating factors for psoriasis?
- 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
What factors are used to determine the severity of psoriasis?
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
What are the general points surrounding management of psoriasis?
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
What are some second line treatments for psoriasis?
phototherapy, photochemotherapy, systemic drugs
134
How likely is it that psoriasis clears completely?
for chronic plaque, rarely clears completely but can have periods where it is confined to a small patch
135
What isthe use of emollients in psoriais treatment?
All patients should use regularly, restores pliability of skin and reduces shedding of scales
136
What is the role of vitamin D analogues in psoriasis treatment?
mainstay - can clear large portions within 6-8 weeks
137
How do vitamin D analogues work to treat psoriasis?
inhibit keratinocyte differentiation and proliferation
weaker effects on calcium levels than vitamin D
138
What is the evidence base for using vitamin D analogues in psoriasis treatment?
at least as effective as corticosteroids, with longer remission periods on discontinuation
most effective regimen is emollients + steroids + vit D analogue
139
What are two examples of vitamin D analogues?
calcipotriol (dryness and stinging, not suitable on face)
| calcitriol (far less irritant)
140
How much vitamin D analogue should be applied to psoriaisis?
thicker than steroids - 1 FTU does approx one palm (twice as thick as Cx)
141
What is the place of steroid therapy in psoriasis treatment?
tolerance can be an issue, and more is required to be effective
mild - face and genitals
potent - recalcitrant lesions on trunk and limbs
142
What steroid cannot be used for psoriaisis?
clobetasone butyrate 0.05%
143
What is tazarotene and what is its place in psoriasis therapy?
a topically active retinoid, affecting keratinocyte differentiation (antiproliferative and anti-inflammatory effects)
144
Disadvantages of tazarotene therapy?
Irritant, causes photosensitivity, teratogenic
145
Place of tar in psoriasis therapy?
mechanism unknown, believed to be keratinolytic and antiproliferative
often used in combination with UVB phototherapy
146
Types of preparations of tar for psoriasis treatment?
propietary preps, or 1-5% in paraffin
147
Disadvantages of tar for psoriasis treatment?
stains, less effective, unpleasant smells
148
What is dithranol?
Yellow powder, very irritant to skin (inflammatory, causes blisters)
149
How is dithranol used in psoriasis treatment?
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
What is micanol?
temp sensitive, releases dithranol at skin temp then washed off to prevent further release. response in 20 days
151
Presentation of scalp psoriasis?
extends about 1cm from the hairline, doesnt normally affect hair growth but can cause temp. thinning
152
Special treatment mild for sclp psoriasis?
tar containing shampoo enough usually
153
Treatment steps for severe scalp psoriasis?
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
Importance of selecting the correct dressings?
- can interact with medications
| - different aims of treatment will need different dressings
155
What three factors need to be considered when selecting a wound dressing?
wound related issues, clinical effectiveness, economic factors
156
How will dead tissue behave in a wound?
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
Complications of an eschar?
delays autolysis indefinitely, the shrinking can cause pain
158
Primary interventions for necrotic wounds?
rehydrating the wound, removing dead tissue (can be done by surgical debridement)
159
What are hydrogel dressings?
60-90% water content to draw moisture through the wound, making eschar easier to remove
160
In what forms are hydrogel dressings available?
amorphous gel (most commonly used), impregnated non-woven dressings, sheets
161
How are hydrogel dressings used?
covered with a secondary dressing to hold in place and prevent moisture evaporation
162
What secondary dressings can be used with hydrogels?
plastic film adsorbent dressings (eg, Melonin, Telfa) or vapour-permeable films (eg, Tegaderm, OpSite, Bioclusive)
163
What cannot be done to further treat the wound if a hydrogel dressing is used?
larvae therapy - hydrogels contain propylene glycol which is toxic to larvae
164
What is a suitable alternative to hydrogel dressings?
Hydrocolloid dressings
165
How do hydrocolloid dressings work?
occlusive and waterproof, so promote moisture accumulation
166
What type of wounds are hydrocolloid dressings not suitable for?
Dry ones, or over exposed bone/muscle
contraindicated in infected wounds as encourage bacterial growth
most contain gelatin so not veggie
167
What type of dressing would be suitable for a necrotic wound with a high level of exudate?
alginate dressing - more than hydrogel/colloid
168
How are alginate dressings used and how do they work?
derived from seaweed, absorb a lot but maintain a moist environment
assortment of ribbons and sheets should be used to pack the wound
169
What types of wounds are alginates not suitable for?
dry ones - can stick and cause trauma when removed
170
What is slough?
left behind after eschar separates from healthy tissue - yellowish partly liquified material
171
How should necrotic digits be treated compared to necrotic wounds?
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
How must slough be managed in a wound?
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
What dressings are best for sloughy wounds?
alginate covered with a semipermeable film dressing or hydrocolloid
heavy exudate: hydrofibre dressing with absorbent secondary dressing
174
What is biosurgery?
Larval therapy - suitable for necrotic and sloughy wounds
175
How does larval therapy work to improve wound healing?
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
Why is analgesia often requires for biosurgery?
pain caused by pH changes in the wound - pain decreases with bacterial load
177
What treatment is needed for infected wounds?
systemic antibiotics (swab for sensitivity tests) plus antimicrobial dressing
topical antibiotics are rarely used due to resistance concerns
178
Which topical antibiotic is still used regularly for wounds?
0.75% metronidazole, for reducing odour of fungating wounds colonised w anaerobes
179
Uses and disadvantages of charcoal dressings?
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
What ingredients can antimicrobial dressings contain?
- 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
What is granulation tissue?
fragile mix of proteins and polysaccharides linked with collagens to form a vascular gel-like matrix.
182
How must granulating wounds be managed?
must be kept warm and moist, and exudates managed
183
How to dress low-depth granulating wounds?
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
How often should dressings on granulating wounds be changed?
as infrequently as possible, to avoid damage to the fragile tissue
185
How to dress deep cavity granulating wounds?
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
When do wounds stop granulating?
when the base of the wound cavity is almost level with the surrounding skin, when epithelialisation begins
187
What is epithelialisation?
- 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
What dressings are suitable for epithlialising wounds?
- hydrocolloids or semi-permeable dressings
189
Other dressings suitable in the final stages of healing?
- soft silicone dressings, knotted viscose preparations, knitted viscose, nylon sheet dressings
must be checked regularly for allergies, infection and signs of deterioration
190
What are complex dermatology therapies?
carry a high risk of toxicity (narrow therapeutic index), require intensive monitoring
- high cost, specialist prescribing, not first line
191
What is isotretinoin used for?
severe acne unresponsive to tpoical treatments and antibiotics
192
How does isotretinoin work?
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
What risks does isotretinoin carry?
- 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
At what point do complex therapies start to form part of treatment in psoriasis?
from moderate disease onwards
195
What is PUVA treatment?
Psoralens + UVA
oral 8-methoxypsoralen 0.6mg/kg
196
Dosing of psoralens in PUVA treatment?
2 hours before UVA exposure, treatment 3x weekly, usually clears in 5-6 weeks (20-30 exposures)
197
How does PUVA treatment work?
disrupts DNA synthesis, inhibits basal cell proliferation - slows basal cell growth to normal speeds
198
Adverse effects of PUVA treatment?
- psoralens is teratogenic
| - premature skin ageing, pigmentation, cataracts
199
What is acitretin?
Similar to isotretinoin (retinoid), normalises skin cell proliferation and differentiation
similar side effect profile to isotretinoin, longer half-life, prolonged therapy
200
What precautions are needed with acitretin therapy?
Pregnancy prevention for 3 years, hyperlipidaemia (CVD risk assessment, monitor lipid profile, hepatoxic (regular LFTs, avoid alcohol)
201
Place of methotrexate in skin conditions?
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
What risks does methotrexate carry?
```
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
Place of calcineurin in psoriasis therapy?
blocks calcineurin-dependent factor - blocking IL-2 and proliferation of T-lymphocytes, cytokines and keratinocytes
204
Adverse effects of ciclosporin?
Nephrotoxic (associated hypertension too), teratogenic, immunosuppressant
205
Dosing of ciclosporin?
2.5 - 5mg/kg daily (must be emphasised as patients may have had methotrexate weekly
206
Role of biologics in psoriasis treatment?
Target TNF - used as a last resort when other treatments ineffective
207
Examples of the biologics used for psoriasis?
infliximab, adalimumab, ustekinumab, secikinumab, etanercept (GM fusion protein)
208
Effectiveness of biologics for psoriasis?
response usually seen in 6 weeks, very effective. 6months-2 years continuation
risk that patients can develop antibodies
209
Risks associated with use of biologics?
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)
