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S3 Case 4 - Endocrine > Skin Conditions > Flashcards

Skin Conditions Flashcards

(81 cards)

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1
Q

What is psoriasis?

A

Autoimmune disease mediated by T-lymphocytes = vascular + inflammatory changes

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2
Q

Where is psoriasis common?

A

Head
Knees
Elbows

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3
Q

What factors aggravate psoriasis?

A

Stress
Excessive alcohol consumption
Smoking

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4
Q

Who is psoriasis common in?

A

Adults

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5
Q

What is psoriasis thought to be?

A

Hereditary

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6
Q

What is psoriasis characterised by?

A

Thick, silvery scales

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7
Q

Who is eczema common in?

A

Children

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8
Q

What is eczema thought to be?

A

Environmental

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9
Q

What is eczema characterised by?

A

Red, inflamed skin

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10
Q

What can eczema be called?

A

Atopic dermatitis

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11
Q

What are the signs + symptoms of eczema?

A

Red, scaly
Extremely dry
Affect flexures
Vesicles + weeping
Excoriation + thickening of skin

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12
Q

What is eczema?

A

Nonspecific term that refers to group of inflammatory skin conditions characterised by pruritis (itching), erythema (red swelling) + scale

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13
Q

What is dermatitis?

A

Chronic, relapsing inflammation of skin
Broader term than eczema

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14
Q

What may be the causes of AD?

A

Allergy
Irritant
Photodermatitis (sunlight)

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15
Q

What is the pathogenesis of AD?

A

Multifactorial
Combo of genetic + environmental factors

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16
Q

What factors play a role in the pathogenesis of AD?

A

Genetics
Skin barrier dysfunction
Impaired immune response
Environment

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17
Q

What is the filaggrin gene?
Genetic factors of AD

A

Synthesis of a protein that holds the integrity of skin barrier

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18
Q

How many mutations is there of the filaggrin gene?

A

20

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19
Q

What are the environmental factors of AD?

A

Western lifestyle = low exposure to pathogens
Duration of breastfeeding = decreases risk
High social position of parents = in creased risk

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20
Q

What are the 2 hypotheses that have been proposed for pathophysiology of AD?

A

Immunological
Skin barrier

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21
Q

What is the immunological pathogenesis for AD?

A

Results from imbalance of T cells
Th2 predominates + leads to increased production of interleukins
= increased level of IgE + Th1

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22
Q

How many types of hypersensitivity reacts are there?

A

4

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23
Q

What is the timing of Type I hypersensitivity reaction?

A

30 mins

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24
Q

What is the antigen of Type I hypersensitivity reaction?

A

Induces IgE response

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25
What is the timing of Type II hypersensitivity reaction?
Mins to hours
26
What is the antigen of Type II hypersensitivity reaction?
On cell surface
27
What is the timing of Type III hypersensitivity reaction?
3-8hrs
28
What is the antigen of Type III hypersensitivity reaction?
Extracellular-soluble
29
What is the timing of Type IV hypersensitivity reaction?
48-72hrs
30
What is the antigen of Type IV hypersensitivity reaction?
Induces T-cell
31
What is the skin's functions?
Regulates body temp Stores blood Protects body from external environment Detects cutaneous sensations Excretes + absorbs substances Synthesises vit D
32
What are the 3 layers of the skin?
Epidermis Dermis Hypodermis
33
What is the function of the epidermis?
Thin layer of dead cells Defence against outside world
34
What is the function of the dermis?
Made of collagen fibres Keeps skin strong + flexible Houses network of blood vessels = keeps our body temp constant despite external changes
35
What is the function of the hypodermis?
Body fat is stored = energy, sweat glands + new skin manufactured to repair cuts
36
What are the 5 layers of epidermis?
Stratum corneum Stratum lucidum Stratum granulosum Stratum spinosum Stratum basale
37
Describe filaggrin
Helps bind keratinocytes together = intact barrier hydrated stratum corneum Mutation = less filaggrin Itch = impairment of skin
38
What are the 4 things that play into pathogenesis of pruritus?
Barrier dysfunction Environmental factors Immunological factors Pruritus
39
What is involved in barrier dysfunction?
Ceramide reduction = H2O retention = dry Over-desquamation = over-shredding Filaggrin deficiency
40
What is involved in the immunological factors?
Th2 cells Th17 cells Eosinophils Mast cells
41
What is involved in environmental factors?
Climate Smoking Skin pH Microbiome
42
What can the skin be irritated by?
Soap Detergents Wool clothing Hot weather Emotional stress Exposure to triggers
43
Where is AD most common in infants?
Face first Then hands + feet
44
Where is AD most common in older children?
Skin folds (elbows, behind knees)
45
Where is AD most common in adults?
Face + hands
46
What are the side effects of steroids?
Weight gain Osteoporosis Think skin Psychosis
47
What are the aims of treatment for AD?
Treat + control symptoms - eg. itching, pain + discomfort Reduce inflammation Reduce lost moisture Inhibit scratching = decrease infection Improve QoL
48
What are the different treatments for AD?
Reduce contact with irritants (soap substitutes) Identify + reduce exposure to allergen Emollients Topical steroids Antihistamines Antibiotics Systemic steroids Other (herbal/soaps)
49
How do you reduce contact with irritants?
Avoid overheating Avoid direct skin contact with rough fibres Avoid dusty conditions Avoid cosmetics Avoid soap Use gloves to handle chemicals
50
What do emollients do?
Hydrate + soften skin = restore/replace epidermal barrier = protection against pathogen bacterial colonisation
51
What do topical steroids/steroids do?
Up-regulates the expression of anti-inflammatory proteins + represses the expression of proinflammatory proteins in cytosol = prevents translocation of transcription factors
52
What do antihistamines do?
Antagonists acting via histamine H1 receptor
53
What do antibiotics do?
Anti-bacterial properties
54
What are the 4 major components of AD treatment?
Anti-inflammatory Anti-pruritic Moisturiser Anti-bacterial
55
What treatments should be used initially?
Topical skin applications
56
What are ointments for?
Very dry skin
57
What are the properties of ointments?
Greases Occlusive
58
What are pastes?
Ointment suspensions Application of noxious chemicals for localised delivery
59
What are creams for?
Less dry skin
60
What are the properties of creams?
Emulsions Quick absorption
61
What are lotions for?
Less dry skin
62
What are the properties of lotions?
Less messy on wet/hairy surfaces Cooling effect
63
What are the properties of gels?
Hydrophilic/hydrophobic High H2O content
64
What are the properties of emollients?
Hydrophobic Paraffin derivatives Aq. cream alternative
65
What should be used of a corticosteroid ointment if used long term?
Low-potency = decreases risk of side effects
66
What is tachyphylaxis?
More used = daily = less effective = change to weekly = can use longer Even if dose increased wont change the effectiveness
67
What are calcineurin inhibitors?
Steroid free alternative
68
What is an example of calcineurin inhibitors?
Pimecrolimus
69
What are the side effects of calcineurin inhibitors?
Local burning Skin malignancy Infection risk
70
What are tar band properties?
Anti-inflammatory + anti-pruritic
71
What is phototherapy?
Narrow-band UVB
72
What is the aim when using emollients?
To reduce skin H2O loss = protective film
73
What should emollients be used instead of?
Soap Add to bath water/use in shower
74
How do you use emollients?
Use all the time not just with symptoms Large amount at least BD Use after bath/shower Pat dry skin + apply whilst skin is moist Smooth onto skin = do NOT rub Use spoon/pump dispenser Never share
75
What are the different strengths of topical CCS?
Very mild = hydrocortisone Moderate = clobetasone Strong = mometasone Should be prescribed weakest effective treatment to control symptoms
76
How do you use topical CCS?
OD/BD for 1-2 weeks Affected areas Smooth onto skin in direction of hair growth Use emollients first the 30mins later = CCS
77
What is FTU?
Fingertip units 500mg amount required to squeeze a line from tip of adult finger to crease
78
How much topical CCS should be used?
1 FTU to treat area of skin size of two palms
79
What are the side effects of topical CCS?
Burning/stinging = improves with use Less common = inflamed hair follicles, thinning of skin, contact dermatitis, acne + changes in skin colour
80
What are examples of systemic therapy?
Sedative antihistamines = help sleep Immunosuppressant = resistant/rapid relapse Antibacterials = secondary infection
81
What is the treatment for contact dermatitis?
Barrier to irritant Dilute topical CCS Potassium permanganate soaks

S3 Case 4 - Endocrine (17 decks)

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