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2ND YR DERM > WEEK 2 > Flashcards

WEEK 2 Flashcards

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Dermatology Board Prep flashcards
1
Q

advantages of topical treatments?

A
  • direct application
  • reduced systemic effects
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2
Q

disadvanates of topical

A

tim consuimgn

correct dosage

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3
Q

what is a cream?

A
  • semisolid of oil in water
  • contain emilsifier and preservative
  • non greasy
  • high water content
  • cool and moisturise
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4
Q

what is an ointment?

A
  • semi solid grease/oil
  • no preservative
  • occlusive and emollient
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5
Q

what is a lotion?

A
  • liquid formualtion
  • suspension or solution of medication in water, alcohol or other liquids
  • treat scalp or hairy areas
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6
Q

what is a paste?

A
  • stiff
  • greasy
  • contain finely powdered material
  • protective, occlusive, hydrating
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7
Q

advantage of using a foam?

A
  • increased penetration of active agents
  • can easily spread over large areas of skin, no greasy oil/film
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8
Q

main classes of topical therapies?

A
  • emollients
  • topical steroids
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9
Q

why re emollients used?

A
  • prescribed for all dry scaley conditions
  • enhance rehydation of epidermis
  • need frequent application
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10
Q

how much emollient should be prescribed per week?

A

300-500g per week for extensive asthma

  • apply frequently
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11
Q

what is one risk when using an emollient?

A

highly flammable

  • smoking is not reccommended
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12
Q

what is the term given to very dry skin?

A

xerotic

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13
Q

give 4 possible side effects of topical steroids

A
  • v
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14
Q

mode of action of topical steroids?

A
  • reduce inflammation
  • cause immune suppression
  • vasoconstrictive
  • anti proliferative
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15
Q

give a mild topical steroid?

A

hydrocrotisone

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16
Q

give a name of a potent steroid?

A
  • betnovate
  • mometasone
  • valerate
  • betamethasone
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17
Q

uses of topical steroids?

A
  • eczema
  • psoriasis
  • other non-infective inflammatory dermatoses
  • keloid scars
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18
Q

how much steroid should be applied to the whole body?

A

20-30g tube for one week

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19
Q

side effects of topical steroids?

A
  • steroid rosacea
  • perioral dermatitis
  • thinning of the skin
  • purpura
  • stretch marks
  • may worsen or mask infections
  • systemic absorption
  • tachyphylaxis
  • rebound flare of disease
  • glaucoma and cataract
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20
Q

name an ultra potent steroid

A

clobetasol propionate

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21
Q

what effects do antiseptics have?

A
  • bacteriocidal affects
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22
Q

give an example of an antiseptic

A
  • providone iodine skin cleanser (betadine)
  • hibitane, savlon
  • triclosan
  • hydrogen perooxide
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23
Q

when would antibiotics be used?

A
  • acne/roascea
  • skin infection
  • infected eczematous process
  • otitis externa
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24
Q

name conditions in which topical antifungals would be used

A
  • candida (thrush)
  • dermatophytes (ringworm)
  • pityriasis versicolour (use cream or shampoo)
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25
Q

name some good antipruritics

A
  • menthol
  • capsaicin (from red chilli peppers)
  • camphor / phenol
  • crotamiton
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26
Q

what are keratolytics used for?

A

used to soften keratin

e.g….

  • viral warts
  • hyperkeratotic eczema / psoriarsis
  • corns / calluses
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27
Q

side effects of topical therapies?

A
  • burning or irritation
  • contact allergic dermatitis
  • local toxicity
  • systemic toxicity
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28
Q

what cell type lines the normal epidermis?

A
  • epidermis-stratified keratinising squamous epithelium
29
Q

function of langerhans cells in epidermis?

A
  • act as sentinels monitoring environment for antigens
  • important in initiating inflammation
  • located in upper and mid-epidermis
  • dendritic cells
30
Q

which part of the dermis are the appendages and pilosubaecous usints found?

A

in the reticular dermis

31
Q

where are the malnocytes?

A

the purple dots with the white halos around them

  • highly dendritic
  • pigment synthesisers
  • act as a UV barrier
32
Q

what is acanthosis?

A

increased thickness of the epithelium (to basal layer) really just hyperplasia

33
Q

what is parakeratosis?

A

perisistence of nuclei in the keratin layer

34
Q

what is hyperkeratosis?

A

increased thickness of keratin layer

35
Q

what is papillomatous?

A

irregular epithelial thickening

36
Q

what is spongiosis?

A
  • oedema fluid between squames appears to increase prominence of intercellular prickles
  • if severe filled by oedema flui will develop
37
Q

what are the 4 main recation patterns of inflammatory skin disease?

A
  • spongiotic intraepidermal oedema (e.g. oedema)
  • psoriaform-elongation of the rete ridges (e.g. psoriasis)
  • lichenoid-basal layer damage (e.g. lichen planus and lupus)
  • vesiculobullous-blistering (e.g. phemphigoid, phemphigus and dermatitis herpetiformis)
38
Q
  • conditions characterised by damage to the basal epidermis
  • protypic condition is lichen planus
  • itchy flat topped violaceous papules
A

lichenoid disorders

39
Q

what does lichen planus histology look like?

A
  • irregular saw tooth acnthosis
  • hypergranulosis and orthohyperkeratosis
  • band like upper dermal infiltrate of lymphocytes
  • basal damage with formation of cytoid bodies
40
Q
  • blisters are the primary feature of this disease
  • caused by disroders of the immune system

Examples

  • pemphigus
  • bullous pemphigoid
  • dermatitis herpetiformis
A

immunobullous diseases

41
Q

pathology behind pemphigus?

A

loss of integrity of epidermal cell adhesion

42
Q

what is pemphigus vulgaris?

A
  • autoimmune condition
  • IgG auto-antibodies made against desmoglein 3 (like a glue in the eoidermis)
  • immune comlexes form on cell surface disrupting desmosome attachments
  • end result is acantholysis
43
Q

symptoms of pemphigus vulgaris?

A
  • involves skin (scalp, face, axillae, groin, trunk)
  • may affect mucosa (e.g. mouth, resp. tract, extensive mucosal involvement may be fatal)
  • produces fluid filled blisters which rupture to form shallow erosions
44
Q

what is the histological hallmark for dermatitis herpetiformis?

A
  • papillary dermal microabscesses
45
Q

what antibody should be looked for in dermatitis herpetiformis?

A

IgA in dermal papillae

46
Q

give the aetiology of acne?

A
  1. increased androgens at puberty
  2. increased androgen sensitivity of sebaceous glands]keratin plugging of pilsubaecous units
  3. infection with anaerobic bacterium corynebacterium acnes
47
Q

what is rosacea?

A
  • scaley erythamatoeus eruptions
  • patchy inflammation with plasma cells
  • pustules
  • demodex mite in subaecous duct
48
Q

type 1 allergy

A
  • causes an immediate reaction (minutes - 2hrs)
  • may routes of exposure
  • must have a consistent reaction with every exposure
49
Q

what must occur with all allergies

A

you must be sensitised to the allergy first

50
Q

common clinical presentations of allergies?

A
  • urticaria
  • angioedema
  • wheezing/asthma
  • anaphylaxis (circulartory collapse)
51
Q

investigations of allergies?

A
  • history
  • specific IgE
  • skin prick or prick prick testing
  • challenge test
  • serum mast cell tryptase level
52
Q

manageeent of allergies?

A
  • allergen avoidance
  • orevent affects of mast cell activation (anti-histamines)
  • anti-inflammatory agent (corticosteroid)
  • adrenaline autoinjector (for anaphylaxis)
53
Q

type IV allergy

A
  • delayed hypersensitivity
  • antigen specific
  • T cell mediated
  • allergic contact dermatitis
  • onset reaction typically 24-48 hrs after exposure
54
Q

what is done when bacteria is suspected?

A

put swab on agar plate

55
Q
  • gramp oisitive cocci in clusters
  • aerobic and faculatively anaerobic
  • 2 important ypes (staph. arueus: coagulase positive + coagulase negative staph)
A

staphylococcus sp.

56
Q

only ever prescribe or take a swab when???!!

A

THERE IS A CLINICAL SIGN OF INFECTION

  • dont assume just because there is a culture swab carried out
57
Q
  • common human pathogen
  • prodces enzymes including coagulase, an enzyme that clots plasma
  • distinguishes it from all other staph. species^^
  • causes wound, skin, bone and joint infections
  • flucloxacillin reccommended to treat
  • resistent starins (methicillin resistant)
  • some strains produce toxins
A

staphylococcus aureus

58
Q

what does methiccilin resistent staph aureus mean?

A

flucloxacillin resistent

use e.g.

  • doxycycline
  • co-trimoxazole
  • vancomycin
59
Q

what does it mean by staph. epidermidis being a skin commesnal?

A

NOT PATHOGENIC

60
Q

when should yu swab a leg ulcer

A

when there is high suspcicion of infection as there are usually commensals living there whcih is okay

61
Q

what happens if you think a patient has measles?

A

in negative pressure room

need to be isolated

62
Q

what is urticaria?

A

erythema with a well defined edge

63
Q

what does eczema look like?

A

ill defined, scaley

64
Q

give 3 cutaneous examples of type 1 hypersensitivity

A
  • urticaria (red wehals caused by blood vessel dilation + leakage into surrounding tissue)
  • angio-oedema (swelling of subcutaenous tissues)
  • anaphylaxis
65
Q

cutaneous examples of type 4 (delayed) hypersensitivity?

A
66
Q

give the factors increasing the potential of topical steroids to cause side effects

A
67
Q

side effects of steroids?

A
  • contact allergy to hydrocortisone
  • acneifrom eruptions
  • tachyphylaxis
  • pigmentary changes
  • poor wound healing
  • modification of existing disease
  • unstable pustular psoriasis
  • steroid roascea
  • atrophy, bruising
  • gaucoma
  • hirsutism
  • poor owund healing
  • striae (stretch marks)
  • growth retardation (systemic effect)
68
Q

what can be done to reduce the risk of side effects from steroids?

A
  • dont use topical steroids where they wnt work
  • use least potent preparation that is effective
  • know quanitites required for appropriate use
69
Q
A

2ND YR DERM (6 decks)

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