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Medicine finals Prithvi > Derm > Flashcards

Derm Flashcards

1
Q

wht is skin and what are skin appendages?

A

skin = epidermis + dermis +overlying subcutaneous tissue.

skin appendages are structures formed by skin derived cells such as nails, hair, sweat glands and sebaceous glands

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2
Q

major cell types of epidermis

A

there are 4

  1. keratinocytes- produce keratin as a protective barrier
  2. langerhans’ cells - present antigens and activeate T cells for immune protection
  3. melanocytes - produce melanin which gives pigment to skin and protects cell nuclei from UV radiation induced DNA damage
  4. merkel cells - contain specialised nerve endings for sensation
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3
Q

average epidermal turnover time

A

migration of cells from basal layer to horny layer. it is about 30 days

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4
Q

different epidermal layers and their composition

A 
stratum basale (basal cell layer) -actively dividing deepest layer
stratum spinosum (prickle cell layer)- differentiating cells
stratum granulosum (granular cell layer)- cells here lose their nuclei and contain granules of keratohyaline. they secrete lipid into intercellular spaces
stratum corneum (horny layer) - layer of keratin. most superficial layer

**in areas of thick skin such as palms, soles and digits there is a 5th layer called stratum lucidum beneath stratum corneum and it consists of paler, compact keratin.

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5
Q

contents of dermis

A

mainly made of collagen along with elastin and glycosaminoglycans which are synthesised by fibroblasts. the dermis also contains immune cells, nerves, skin appendages as well as lymphatic and blood vessels.

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6
Q

3 main types of hair

A
  1. lanugo hair (fine long hair in fetus)
  2. vellus hair (fine short hair on all body surfaces)
  3. terminal hair (coarse long hair on scalp, eyebrows, eyelashes and pubic areas)
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7
Q

what does each hair consist of

A

each hair is made of modified keratin and has a shaft and hair bulb (actively dividing cells and ,melanocytes which give pigment to the hair)

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8
Q

growth cycle of hair follicles

A

each hair follicle enters its own growth cycle -

  1. anagen - long growing phase
  2. catagen - short regressing phase
  3. telogen - resting/shedding phase
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9
Q

types of sweat glands

A

eccrine sweat glands - distributed universally in the skin
apocrine sweat glands - found in the axillae, areolae, genitalia and anus, and modified sweat glands are found in the external auditory canal. they only function from puberty onwards and action of bacteria on the sweat produces body odour

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10
Q

4 phases of wound healing

A

haemostasis
iflammation
prolifereation
remodelling

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11
Q

causes of urticaria, angioedema and anaphylaxis

A
  • idiopathic
  • foods (nuts, sesame, shellfish, dairy products)
  • drugs (penicillin, contrast media, NSAIDs, morphine, ACEis)
  • insect bites
  • contact (eg latex)
  • viral or parasitic infections
  • autoimmune
  • hereditary - in some cases of angioedema
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12
Q

what is the major mediator of urticaria?

A

histamine derived from skin mast cells

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13
Q

urticaria presentation

A

itchy wheals. due to swelling involving superficial dermis, raising the epidermis

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14
Q

angioedema presentation

A

swelling of tongue and lips - deeper swelling involving dermis and subcutaneous tissue

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15
Q

presentation of anaphylaxis

A

can present initially with urticaria and angioedema
bronchospasm, hypotension, facial and laryngeal oedema

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16
Q

management of urticaria, angioedema and anaphylaxis

A

mild-moderate urticaria - antihistamines
severe acute urticaria and angioedema - corticosteroids
anaphylaxis - adrenaline, corticosteroids and antihistamines

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17
Q

complications of urticaria, angioedema and anaphylaxis

A

urticaria is usually uncomplicated
angioedmea and anaphylaxis can lead to asphyxia, cardiac arrest and death

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18
Q

lesion?

A

an area of altered skin

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19
Q

rash?

A

an eruption

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20
Q

naevus?

A

a localised malformation of tissue structures

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21
Q
A

naevus

pigmented melanocytic naevus (mole)

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22
Q

comedone?

A

a plug in a sebaceous follicle containing altered sebum, bacteria and cellular debris. can present as either open (blackheads) or closed (whiteheads)

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23
Q
A

open comedone (in acne)

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24
Q
A

closed comedones (in acne)

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25
Q

generalised vs widespread pattern of distribution of lesions?

A

generalised= all over body

widespread= extensive spread

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26
Q

flexural areas

A

body folds - groin, neck, behind ears, antecubital fossa, popliteal fossa

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27
Q

extensor surfaces

A

knee, elbows, shins

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28
Q

pressure areas

A

saccrum, buttocks, ankles and heels

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29
Q

dermatome

A

A dermatome is an area of skin in which sensory nerves derive from a single spinal nerve root

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30
Q

photosensitive

A

affects sun exposed areas such as face, neck and back of hands

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31
Q
A

sunburn

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32
Q

Köebner phenomenon

A

a linear eruption arising at site of trauma

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33
Q
A

koebner phenomenon (in psoriasis)

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34
Q
A

target lesions (erythema multiforme)

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35
Q
A

annular lesion (tinea corporis)

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36
Q
A

discoid/nummular lesion (discoid eczema) ie coin shaped/round lesion

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37
Q

erythema?

A

redness which blanches on pressure

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38
Q
A

palmar erythema

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39
Q
A

purpura

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40
Q

petichiae vs ecchymoses

A

petechiae - small pinpoint purpuric macules

ecchymoses - large bruise like purpuric patches

remember purpura does not blanch

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41
Q
A

hypopigmentation

in this case - pityriasis versicolor (superficial fungal infection)

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42
Q
A

depigmentation

(here vitiligo - loss of melanocytes)

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43
Q
A

hyperpigmentation

(here cause was melasma - increased melanin pigmentation)

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44
Q
A

macules (freckles)

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45
Q
A

patchy morphology - this is vascular malformation - naevus flammeus/ port wine stain

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46
Q
A

papules

here xanthomata

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47
Q

nodule?

A

solid raised lesion more than 0.5cm in diameter with a deeper component

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48
Q
A

nodule

here Pyogenic granuloma(granuloma telangiectaticum)

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49
Q

plaque

A

palpable scaling raised lesion >0.5cm in diameter

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50
Q
A

psoriatic plaque

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51
Q

papule vs vesicle?

A

papule - raised solid lesion <0.5cm in diameter

vesicle - raised clear fluid filled leasion <0.5cm in diameter. aka small blister

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52
Q
A

vesicles in acute hand eczema (pompholyx)

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53
Q

bulla

A

raised clear fluid filled lesion >0.5cm in diameter

aka large blister

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54
Q
A

bulla

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55
Q

pustule

A

pus containing lesion<0.5cm in diameter

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56
Q
A

pustules in acne

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57
Q

abscess

A

localised accumulation of pus in the dermis or subcutaneous tissue

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58
Q
A

periungual abscess

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59
Q

wheal

A

transient raised lesion due to dermal oedema

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60
Q
A

wheal in urticaria

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61
Q

boil/furuncle

A

staphylococcal infection around or within a hair follicle

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62
Q

carbuncle

A

staphylococcal infection of adjacent hair follicles (multiple boils/furuncles)

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63
Q

excoriation

A

loss of epidermis following trauma

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64
Q
A

excoriations

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65
Q

lichenification

A

well defined roughening of skin with accentuation of skin markings

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66
Q
A

lichenification (here has happend due to chronic rubbing in eczema)

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67
Q

scales

A

flakes of stratum corneum

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68
Q
A

psoriatic scales

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69
Q

crust

A

Rough surface consisting of dried serum, blood, bacteria and cellular debris that has exuded through an eroded epidermis(e.g.from a burst blister)

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70
Q
A

crust (in impetigo)

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71
Q

scar

A

new fibrous tissue which occurs post wound healingand may be atrophic (thinning), hypertrophic (hyperproliferation within wound wall) or keloid (hyperproliferation beyond wound wall)

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72
Q
A

keloid scar

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73
Q

ulcers

A

loss of epidermis and dermis (heals with scarring)

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74
Q
A

leg ulcers

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75
Q

fissure

A

epidermal crack often due to excess dryness

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76
Q
A

fissure in eczema

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77
Q

striae

A

linear areas which progress from purple to pink to white with the histopathological appearance like a scar (associated with excessive steroid use, glucocorticoid production, pregnancy and growth spurts)

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78
Q
A

striae

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79
Q
A

alopecia areata (well defined patch of complete hair loss)

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80
Q

hirsutism

A

androgen dependent hair growth in females

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81
Q
A

hirsutism

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82
Q

hypertrichosis

A

non androgen dependent pattern of excessive hair growth eg in a pigmented naevii

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83
Q
A

hypertrichosis

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84
Q

clubbing?

A

loss of angle bw posterior nail fold and nail plate

associations include suppurative lung disease, cyanotic heart disease, idiopathic and IBD

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85
Q
A

clubbing

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86
Q
A

koilonychia - spoon shaped depression of the nail plate

associations include Fe deficiency anaemia, congenital and idiopathic

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87
Q
A

onycholysis - separation of the distal end of the nail plate from the nail bed

associated with fungal nail infection, trauma, psoriasis and hyperthyroidism

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88
Q
A

nail pitting - punctuate depressions on nail plate

associated with psoriasis, eczema and alopecia areata

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89
Q

what do sweat glands do?

A

regulate body temperature and are innervated by the sympathetic nervous system

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90
Q

what is the nail made of?

A

nail matrix

nail plate (which in turn arises from the nail matrix at the posterior nail fold) - hard keratin

nail bed - contains blood capillaries

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91
Q

pilosebaceous unit?

A

sebaceous gland + hair follicle are collectively called a pilosebaceous unit.

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92
Q

what are sebaceous glands stimulated by?

A

sebaceous glands are stimulated by conversion of androgens to dihydrotestosterone and therefore become active at puberty

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93
Q

what causes erythema nodosum

A

it is a hypersensitivity response to a variety of stimuli. some causes are - group A beta haemolytic streptococcus, malignancy, sarcoidosis, primary TB, pregnancy, IBD, chlamydia and leprosy

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94
Q

presentation of erythema nodosum

A

discrete erythematous tender nodules which may become confluent. the shins are the most common site. lesions continue to appear for 1-2 weeks and leave bruise like discolouration as they resolve. they do not ulcerate and resolve without atrophy or scarring.

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95
Q

erythema multiforme

A

an acute self limiting inflammatory condition presenting as target lesions. herpes simplex virus is the main precipitating factor but other causes include idiopathic, other infections and drugs.

mucosal involvement is absent or limited to 1 mucosal surface

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96
Q

stevens-johnson syndrome

A

characterised by mucocutaneous necrosis with at least 2 mucosal sites involved.

main associations are drugs or combinations of infections or drugs.

histopathology shows epithelial necrosis with few inflammatory cells

extensive necrosis differentiates it from erythema multiforme

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97
Q

toxic epidermal necrosis

A

an acute severe disease characterised by extensive skin and mucosal necrosis accompanied by systemic toxicity.

usually drug induced

histopathology shows full thickness epidermal necrosis with subepidermal detachement

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98
Q

mx of erythema multiforme, SJS and TEN?

A

early recognition and call for senior help

full supportive care to maintain haemodynamic stability

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99
Q

complications of of erythema multiforme, SJS and TEN?

A

mortality rates 5-12% with SJS and >30% with TEN

death often due to sepsis, electlyte imbalance and multi-organ failure

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100
Q

how is acute meningococcaemia transmitted?

A

via respiratory secretions

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101
Q

cause of acute meningococcaemia

A

Neisseria meningitidis

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102
Q

presentation of

A

meningitis - headache, neck stiffness and fever

septicaemia - hypotension, fever, myalgia, etc

non-blanching purpuric rash on trunks and extremities, which may be preceeded by blanching maculopapular rash, and, can rapidly progress to echhymoses, haemorrhagic bullae and tissue necrosis

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103
Q

management of acute acute meningococcaemia

A

abx - eg benzylpenicillin

prophylactic abx for close contacts eg rifampicin (ideally within 14 days of exposure)

supportive care if required - IV fluids, analgesia, etc.

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104
Q

complications of acute acute meningococcaemia

A

septicaemic shock, DIC, multi organ failure and death

105
Q

what is erythroderma? causes?

A

exfoliative dermatitis involving at least 90% of skin surface

causes - previous skin disease (eg eczema, psoriasis), lymphoma, drugs (sulphonylureas, gold, sulphonamides, allopurinol, penicillin, captopril) and idiopathic

106
Q

presentation of erythroderma

A

skin appears inflammed, oedematous and scaly

systemically unwell with lymphadenopathy and malaise

107
Q

mx of erythroderma

A

treat underlying cause where known

emollients and wet wraps to maintain skin moisture

topical steroids may help relieve inflammation

108
Q

complications of erythroderma

A

secondary infection

fluid loss and electrolyte imbalance

hypothermia

high output cardiac failure

capillary leak syndrome (most severe)

prognosis depends on underlying cause. 20-40% mortality

109
Q
A

erythema nodosum

110
Q
A

erythema multiforme

111
Q
A

Stevens-Johnson syndrome

112
Q
A

erythroderma

113
Q

eczema herpeticum?

A

aka kaposi’s varicelliform eruption

it is a serious complication of atopic eczema or other skin conditions (less common) where there is widespread eruption caused by herpes simplex virus

114
Q

presentation of eczema herpeticum

A

extensive crusted papules, blisters and erosions

systemically unwell with fever and malaise

115
Q

mx of eczema herpeticum

A

antivirals (aciclovir) and antibiotics if secondary bacterial infection

116
Q

complications of eczema herpeticum

A

herpes hepatitis, encephalitis, DIC and rarely death

117
Q
A

eczema herpeticum

118
Q

necrotising fasciitis? cause and RFs

A

rapidly spreading infection of the deep fascia with secondary tissue necrosis

caused by group a beta haemolytic strep, or a mix of anaerobic and aerobic bacteria

50% of cases occur in previously healthy individuals.

RFs include abdominal surgery and medical co-morbidities (diabetes, malignancy)

119
Q

presentation of nec fasc

A

severe pain

systemically unwell with fever and tachycardia

erythematous, blistering and necrotic skin

presence of crepitus (subcutaneous emphysema)

x-ray may show soft tissue gas (absence does not exclude diagnosis)

120
Q

mx of nec fas

A

urgent referral for extensive surgical debridement

IV abx

remember mortality up to 76%

121
Q

what is this and what is imp to do in this pt?

A

herpes zoster (shingles) infection due to varicella zoster virus affecting the distribution of the ophthalmic division of the trigeminal nerve.

examination for eye involvement is important

122
Q

what are erysipelas and cellulitis?

causes?

presentation?

Mx?

complications?

A

they are spreading bacterial infections of the skin

cellulitis involves the deep subcutaneous tissue

erysipelas is an acute superficial form of cellulitis and involves the dermis and upper subcutaneous tissue

they are caused by staphylococcus aureus and streptococcus pyogenes. RFs - minor skin injury, immunosuppresion, wounds, leg ulcers, toe web intertrigo

presentation - most commonly inflammation in the lower limbs. swelling, erythema, warmth, pain. may be associated with lymphangitis. sytemically unwell with fever, malaise or rigors. erysipelas is distinguished from cellulitis by a well defined, red raised border

mx - abx (fluclox or benzylpenicillin). supportive care including rest, leg elevation, sterile dressings and analgesia

complications - local necrosis, abscess and septicaemia

123
Q
A

erysipelas

124
Q

staphylococcal scalded skin syndrome

A

skin disorder seen in infancy and early childhood caused by the production of a circulating epidermolytic toxin from phage group II, benzylpenicillin resistant (coagulase +ve) staphylococci.

125
Q

presentation of staphylococcal scalded skin syndrome

A

develops within a few hrs to a few days and may be worse over face, axillae, groins or neck.

a scald like appearance is followed by large flaccid bulla

perioral crusting is typical

there is intraepidermal blistering

lesions are very painful

sometimes the eruption is more localised

recovery is usually within 5-7 days

126
Q

mx of staphylococcal scalded skin syndrome

A

abx - eg a systemic penicillinase-resistant penicillin (flucloxacillin), fusidic acid, erythromycin or appropriate cephalosporin

analgesia

127
Q
A

staphylococcal scalded skin syndrome

128
Q

superficial fungal infections and causes

A

common and mild infection of the superficial layers of skin, nails and hair but can be severe in immunocompromised individuals.

causes - 3 main groups -

dermatophytes (tinea/ringworm), yeast (candidiasis, malassezia) and moulds (aspergillus)

129
Q

presentation of fungal skin infections (superficial)

A

varies with site of infection but usually itchy and unilateral

130
Q

tinea corporis

A

tinea infection of trunk and limbs

itchy circular or annular lesions with a cleaarly defined, raised and scaly edge is typical

131
Q

tinea cruris

A

tinea infection of groin and natal cleft

very itch, circular or annular lesions with clearly defined rasied and scaly edge is typical

132
Q

tinea pedis

A

athlete’s foot

moist scaling and fissuring in toe webs, spreading to sole and dorsal aspect of the foot

133
Q

tinea manuum

A

tinea infection of the hand

scaling and dryness in the palmar creases

134
Q

tinea capitis

A

scalp ringworm

patches of broken hair, scaling and inflamaation

135
Q

tinea unguium

A

tinea infection of the nail

yellow discolouration, thickened and crumbly nail

136
Q

tinea incognioto

A

inappropriate treatment of tinea infection with topical or systemic steroids leading to ill defined and less scaly lesions

137
Q

candidiasis

A

candidal skin infection - white plaques on mucosal areas, erythema with satellite lesions in flexures

138
Q

pityriasis/tinea versicolor

A

infection with malassezia furfur

scaly pale brown patches on upper trunk that fail to tan on sun exposure, usually asymptomatic

139
Q

mx of fungal skin infections

A

establish diagnosis by skin scrapings, hair or nail clippings (for dermatophytes) or skin swabs (for yeasts)

general measures - treat known precipitating factor (eg underlying immunosuppressive condition, moist environment)

topical antifungal agents (eg terbinafine cream)

oral antifungal agents (eg itraconazole) for severe, widespread, or nail infections

AVOID topical steroids - can lead to tinea incognito

140
Q
A

tinea infection

141
Q
A

tinea capitis

142
Q
A

tinea manuum of right hand

143
Q
A

tinea pedis associated with tinea unguium

144
Q
A

right axilla candidiasis

145
Q
A

pityriasis versicolor

146
Q

generally skin cancer are of 2 types?

A

non-melanoma (BCC and SCC) and melanoma (malignant melanoma)

147
Q

which is the most life threatening type of skin cancer

A

malignant melanoma

it is one of the few cancers affecting the younger population

148
Q

1 RF for skin cancer

A

sun exposure is the single most preventable risk factor for skin cancer

149
Q

Basal cell carcinoma

A

a slow growing, locally invasive malignant tumour of the epidermal keratinocytes normally in older individuals. only rarely metastasises

it is the most common malignant skin tumour

150
Q

RFs for BCC

A

increasing age

male sex

immunosuppression

previous hx of skin cancer

genetic predisposition

skin type I (always burns, never tans)

hx of frequent or severe sunburn in childhood

UV exposure

151
Q

presentation of BCC

A

various morphological types - nodular (most common), superficial (plaque like), cystic, morphoeic (sclerosing), keratotic and pigmented

nodular basal cell carcinoma is a small skin coloured papule or nodule with surface telangiectasia, and a pearly rolled edge; the lesion may have a necrotic or ulcerated centre (rodent ulcer)

most common over head and neck

152
Q

mx of BCC

A

surgical excision - tx of choice as it allows histological examination of tumor and margins

mohs micrographic surgery (excision of lesion and tissue borders are progressively excised until specimens are microscopically free of tumour) - for high risk, recurrent tumours

radiotherapy where surgery is not appropriate

other - cryotherapy, curretage and cautery, topical photodynamic therapy, and topical treatment (eg imiquimod cream) for small and low-risk lesions

153
Q

complications of BCC and prognosis

A

local tissue invasion and destruction

prognosis depends on tumor size, site, type, growth pattern/histological subtype, failure of previous tx, recurrence and immunosuppression

154
Q
A

basal cell carcinoma - nodular type

155
Q

Squamous cell carcinoma

A

locally invasive malignant tumour of the epidermal keratinocytes or its appendages which has the potential to metastasise

156
Q

RFs for SCC

A

genetic predisposition

immunosuppression

chronic inflammation (eg leg ulcers, wound scars)

pre-malignant skin conditions (eg actinic keratoses)

excessive UV exposure

157
Q

presentation of SCC

A

keratotic (scaly, crusty), ill defined nodule which may ulcerate

158
Q

mx of SCC

A

surgical excision is the tx of choice

mohs micrographic surgery may be necessary for ill defined, large, recurrent tumours

radiotherapy for large non-resectable tumours

159
Q

prognosis of SCC

A

depends on tumour size, site, histological patttern, depth of invasion, perineural involvement and immunosuppression

160
Q
A

SCC adjacent to ear

161
Q
A

SCC on glans penis

162
Q

malignant melanoma

A

an invasive malignant tumour of the epidermal melanocytes which has the potential to metastasise

163
Q

RFs for malignant melanoma

A

family hx or previous hx of melanoma

hx of multiple moles or atypical moles

skin type I (always burns, never tans)

excessive UV exposure

164
Q

presentation of malignant melanoma

A

“ABCDE symptoms” rule -

Asymmetrical shape

Border irregularity

Colour irregularity

Diameter>6mm

Evolution of lesion (eg change in size and/or shape)

Symptoms (eg bleeding, itching)

MAJOR SUSPICIOUS FEATURES - asymmetrical shape, colour irregularity and evolution of lesion (ACE)

more common on the legs in women and trunk in men

165
Q

types of malignant melanoma

A
  1. superficial spreading melanoma (70%of all melanomas) - common on lower limbs, in young and middle aged adults; related to intermittent high-intensity UV exposure
  2. nodular melanoma - common on the trunk, in young and middle aged adults; related to intermittent high intensity UV exposure
  3. lentigo maligna melanoma - common on the face, in elderly population; related to long term cumulative UV exposure
    1. acral lentiginous melanoma - common on the palms, soles and nail beds, in elderly population; no clear relation with UV exposure
166
Q

mx of malignant melanoma

A

depends on staging of melanoma - currently used system in the UK is American Joint Committee of Cancer Staging System (AJCC).

satges I-IV are based on primary tumour Breslow thickness, lymph node involvement and evidence of metastases. stage I is the earliest and stage IV is the most advanced

In general, surgical excision is the definitive treatment (often a second surgery, wide local excision is needed after initial excision biopsy)

radiotherapy may sometimes be useful. chemotherapy is used for metastatic disease

167
Q

prognosis of malignant melanoma

A

depends on stage of melanoma and breslow thickness

in general, 90% of ppl diagnosed with melanoma in England and Wales survived 10yrs or more

168
Q
A

acral lentiginous melanoma

169
Q
A

lentigo maligna melanoma

170
Q
A

nodular melanoma

171
Q
A

superficial spreading melanoma

172
Q

what does management of inflammatory conditions such as eczema and psoriasis aim at?

A

management is aimed at achieving control and not providing a cure. important to address the psychosocial complications of the illnesses.

patient education is important in these chronic skin conditions

173
Q

atopic eczema

A

eczema (or dermatitis) is characterised by papules and vesicles on an erythematous base

atopic eczema is the most common type - usually develops by early childhood and resolves during teenage years (but may recur). 20% prevalence in <12 yr olds in UK.

174
Q

cause of atopic eczema

A

+ve family hx of atopy (eczema, asthma, allergic rhinits) is often present

a primary genetic defect in skin barrier function (loss of functional variants of the protein filaggrin) appears to underlie atopic eczema

exacerbating factors - infections, allergens (eg chemicals, food, dust, pet fur), sweating, heat and severe stress

175
Q

presentation of atopic eczema

A

commonly present as itchy, erythematous dry scaly patches

more common on face and extensor aspects of limbs in infants and flexor aspects in children and adults

acute lesions are erythematous, vesicular and weepy (exudative)

chronic scratching/rubbing can lead to excoriations and lichenification

may show nail pitting and ridging of nails

176
Q

mx of atopic eczema

A
  • general measures - avoid known exacerbating factors, frequent emollients +/- bandages and bath oil/soap substitute
  • topical therapies - topical steroids for flare ups; topical immunomodulators (eg tacrolimus, pimecrolimus) can be used as steroid sparing agents
  • oral therapies - antihistamines for symptomatic releif, abx (eg flucloxacillin) for 2ndary bacterial infection and antivirals (eg aciclovir) for 2ndary herpes infection
    • phototherapy and immunosuppressants (eg oral prednisolone, azathioprine, ciclosporin) for severe non-responsvive cases
177
Q

complications of atopic eczema

A

2ndary bacterial infection (crusted weepy lesions)

2ndary viral infection - eczema herpeticum, molluscum contagiosum (pearly with central umbilication) and viral warts

178
Q
A

atopic eczema

179
Q
A

atopic eczema

180
Q

acne vulgaris

A

an inflammatory disorder of the pilosebaceous follicle

over 80% of teenagers aged 13-18 yrs

181
Q

causes of acne vulgaris

A

hormonal (androgen)

contributing factors - increased sebum production, abnormal follicular keratinization, bacterial colonization (propionibacterium acnes) and inflammation

182
Q

presentation of acne vulgaris

A

non-inflammatory lesions (mild acne) - open and closed comedones

inflammatory lesions (moderate and severe acne) - papules, pustules, nodules and cysts

commonly affects face, chest and upper back

183
Q

mx of acne vulgaris

A

general measures - no specific food has been identified to cause acne.

tx needs to be continued for atleast 6 weeks to produce effect

topical therapies (mild acne) - benzoyl peroxide and topical abx and topical retinoids (comedolytic and anti-inflammatory properties)

oral therapies (mod to severe acne) - oral abx and anti-androgen (in females)

oral retinoids (for severe acne)

184
Q

complications of acne

A

post inflammatory hyperpigmentation, scarring, deformity, psychological and social effects

185
Q
A

acne vulgaris - comedones

186
Q
A

acne vulgaris - papules and nodules

187
Q

psoriasis

A

chronic inflammatory skin condition due to hyperproliferation of keratinocytes and inflammatory cell infiltration

affects abt 2% of UK population

188
Q

types of psoriasis

A

chronic plaque psoriasis is the most common type

other types include guttate (raindrop lesions), seborrhoeic (naso-labial and retro-auricular), flexural (body folds), pustular (palmar-plantar) and eryhtrodermic (total body redness)

189
Q

cause of psoriasis

A

complex interaction bw genetic, immunological and environmental factors

precipitating factors include trauma (which may produce a Koebner phenomenon), infection (eg tonsillitis), drugs, stress and alcohol

190
Q

presentation of psoriasis

A

well demarcated erythematous scaly plaques

lesions can sometumes be itchy, burning or painful

common on the extensor surfaces of the body and over scalp

auspiz sign (scratch and gentle removal of scales causes capillary bleeding)

50% have assocaited nail changes (eg pitting, onycholysis)

5-8% suffer from associated psoriatic arthropathy - symmetrical polyarthritis, asymmetircal oligomonoarthritis, lone distal interphalangeal disease, psoriatic sondylosis and arthritis mutilans (flexion deformity of distal interphalangeal joints)

191
Q

mx of psoriasis

A

general measures - avoid known precipitants. use emollients to reduce scales

topical therapies (localised and mild psoriasis)- vitamin D analogoues, topical corticosteroids, coal tar preparations, dithranol, topical retinoids, keratolytics and scalp preparations

phototherapy (extensive disease) - UVB and photochemotherapy ie psoralen + UVA

oral therapies (extensive and sever psoriasis or psoriasis with systemic involvement) - methotrexate, retinoids, ciclosporin, mycophenolate mofetil, fumaric acid esters and biologics (etanercept, adalimumab, ustekinumab)

192
Q

complications of psoriasis

A

erythroderma

psychological and social effects

193
Q
A

plaque psoriasis

194
Q
A

nail changes and arthropathy (in psoriasis)

195
Q
A

psoriasis (with scalp involvement)

196
Q

what can blistering skin disorders be divided into?

A

in general, blistering skin conditions can be divided into -

  1. immunobullous diseases (eg bullous pemphigoid, pemphigus vulgaris)
    1. blistering skin infections(eg herpes simplex)
      1. other blistering disorders (eg porphyria cutanea tarda)
197
Q

what does the fragility of blisters depend on?

A

depends on level of split within the skin -

an intra-epidermal split causes blisters to rupture easily

a sub-epidermal split (split bw epidermis and dermis) causes blisters to be less fragile

198
Q

common causes of blisters

A

impetigo

insect bites

herpes simplex infection

herpes zoster infection

acute contact dermatitis

pompholyx (vesicular eczema of the hands and feet )

burns

**bullous pemphigoid and pemphigus vulgaris are uncommon conditions due to immune reaction within the skin

199
Q
A

bullous impetigo (in a new tatto)

200
Q
A

pompholyx

201
Q

bullous pemphigoid

A

blistering disorder which usually affects the elderly

caused by autoantibodies against antigens bw the epidermis and dermis causing a subepidermal split in the skin

202
Q

presentation of bullous pemphigoid

A

tense fluid filled blisters on an erythematous base

lesions are often itchy

may be preceeded by a non-sepcific itchy rash

usually affects trunk and limbs (mucosal involvement less common)

203
Q

mx of bullous pemphigoid

A

general measures - wound dressings where required and monitor for signs of infection

topical therapies for localised diseases - topical steroids

oral therapies for widespread disease - oral steroids, combination of oral tetracycline and nicotinamide, immunosuppressive agents (eg azathioprine, mycophenolate mofetil, methotrexate, etc)

204
Q
A

bullous pemphigoid

205
Q

pemphigus vulgaris

A

blistering skin disorder usually affecting the middle aged

caused by autoantibodies against antigens within the epidermis causing an intraepidermal split in the skin

206
Q

presentation of pemphigus vularis

A

flaccid easily ruptured blisters forming erosions and crusts

lesions often painful

usually affects the mucosal areas (can precede skin involvement)

207
Q

mx of pemphigus vulgaris

A

general measures - wound dressings where required, monitor for signs of infection and good oral care (if oral mucosa is involved)

oral therapies - high dose oral steroids, immunosuppressive agents (eg MTX, azathioprine, cyclophosphamide. mycophenolate mofetil, etc)

208
Q
A

pemphigus vulgaris

209
Q
A

pemphigus vulgaris affecting the oral mucosa

210
Q

types/ddx of leg ulcers

A

3 main types

  1. venous
  2. arterial
  3. neuropathic

other causes - vasculitic ulcers (purpuric, punched out lesions), infected ulcers (prurulent discharge, may have systemic signs) and malignancy (eg SCC in long standing non-healing ulcers)

In clinical practice there can be mixture of arterial, venous and/or neuropathic components in an ulcer

211
Q
A

venous ulcer

212
Q
A

arterial ulcer

213
Q
A

neuropathic ulcer

214
Q

venous leg ulcers

A
  1. hx - often painful, worse on standing. hx of venous disease - varicose veins, DVT
  2. common sites - malleolar areas (more common over medial than lateral malleolus)
  3. lesion - large, shallow irregular ulcer. exudative and granulating base
  4. associated features - warm skin, normal peripheral pulses, leg oedema, haemosiderin and melanin deposition (brown pigment), lipodermatosclerosis, atrophie blanche (white scarring with dialted capillaries)
  5. possible ix - normal ankle/brachial pressure index (ie ABPI 0.8-1)
  6. management - compression bandaging (only after excluding arterial insufficiency)
215
Q

arterial leg ulcers

A
  1. hx - painful esp at night, worse when legs elevated. hx of arterial disease eg atherosclerosis
  2. common sites -pressure and trauma sites eg pretibial, supramalleolar (usually lateral), and at distal points eg toes
  3. lesion - small, sharply defined, deep ulcer, necrotic base
  4. associated features - cold skin, weak or absent peripheral pulses, shiny pale skin, loss of hair
  5. possible ix - ABPI <0.8 - presence of arterial insufficiency. doppler studies and angiography
  6. mx - vascular reconstruction. *compression bandaging is CONTRAINDICATED*
216
Q

neuropathic leg ulcer

A
  1. hx - often painless, abnormal sensation, hx of diabetes or neurological disease
  2. common sites - pressure sites eg soles, heels, metatarsal heads, toes
  3. lesion - variable size and depth, granulating base, may be surrounded by or underneath a hyperkeratotic lesion (callus)
  4. associated features - warm skin, normal peripheral pulses but cold weak/absent pulses if it is a neuroischaemic ulcer, peripheral neuropathy
  5. possible ix - ABPI <0.8 implies neuroischaemic ulcer, X-ray to exclude osteomyelitis
  6. mx - wound debridement, regular repositioning, appropriate footwear and good nutrition
217
Q

causes/ddx for an itchy eruption

A

inflammatory condition (eg eczema), infection (eg varicella), infestation (eg scabies), allergic reaction (eg some cases of urticaria), idiopathic or autoimmune (eg lichen planus)

218
Q
A

(chronic fissured) hand eczema

219
Q
A

scabies

220
Q
A

urticaria

221
Q
A

lichen planus

222
Q
A

wickham’s striae

223
Q

eczema

A
  1. hx - personal or family hx of atopy. exacerbating factors (eg allergens, irritants)
  2. common sites - variable (eg flexor aspects in children and adults but extensor aspects and face in infants)
  3. lesion - dry erythematous patches. acute eczema is erythematous, vesicular and exudative
  4. assoc features - 2ndary bacterial or viral infections
  5. possible ix - patch testing. serum IgE lvls. skin swab
  6. mx - emollients, corticosteroids, immunomodulators, antihistamines
224
Q

scabies

A
  1. hx - pruritis worse at night. may have hx of contact with symptomatic individuals
  2. common sites - sides of fingers, finger webs, wrists, elbows, ankles, feet, genitals, nipples
  3. lesions - linear burrows (may be tortuous) or rubbery nodules
  4. assoc features - 2ndary eczema and impetigo
  5. ix- skin scrape, extraction of mite and view under microscope
  6. mx - scabicide (eg permethrin or malathion). antihistamines
225
Q

urticaria

A
  1. hx -precipitating factors (eg food, drugs, contact)
  2. common sites - no specific tendency
  3. lesions - pink wheals (transient). may be round, annular or polycyclic
  4. assoc feautres - may be associated with angioedema or anaphylaxis
  5. ix - bloods and urinalysis to exclude systemic cause
  6. mx - antihistamines, corticosteroids
226
Q

lichen planus

A
  1. hx -family hx in 10%. may be drug induced
  2. common sites - forearms, wrists and legs. always examine oral mucosa
  3. lesions - violaceous (lilac) flat topped papules. symmetrical distribution
  4. assoc features - nail changes and hair loss. lacy white streaks on oral mucosa and skin lesions (wickham’s striae)
  5. ix - skin biopsy
  6. mx - corticosteroids, antihistamines
227
Q

ddx/causes for a changing pigment lesion

A

benign - melanocytic naevi, seborrhoeic wart

malignant - malignant melanoma

228
Q
A

congenital naevus

229
Q
A

seborrhoeic keratosis

230
Q
A

malignant melanoma

231
Q

malignant melanoma

A
  1. hx - tend to occur in adults or middle aged. hx of evolution of lesion. may be symptomatic (bleeding, itching). presence of RFs
  2. common sites - more common on legs in women and trunk in men
  3. lesions - features of ABCDE - asymmetrical shape, border irregularity, color irregularity, diameter > 6mm, evolution of lesion
  4. mx - excision
232
Q

melanocytic naevi

A
  1. hx - not usually present at birth but develop during infancy, childhood or adolescence. asymptomatic.
  2. common sites - variable
  3. lesions - congenital naevi may be large, protuberant, hairy and pigmented. junctional naevi are small, flat and dark. intradermal naevi are usually dome shaped papules or nodules. compound naevi are usually raised, warty, hyperkeratotic, and/or hairy
  4. mx - rarely needed
233
Q

seborrhoeic wart

A
  1. hx - tend to arise in middle aged or elderly. often multiple and asymptomatic
  2. common sites - face and trunk
  3. lesions - warty greasy papules or nodules. ‘stuck on’ appearance with well defined edges
  4. mx - rarely needed
234
Q

ddx/ causes of purpuric eruption

what ix are important?

A

thrombocytopaenic (meningococcal septicaemia, DIC, ITP)

non-thrombocytic causes (trauma, drug (eg steroids), aged skin, vasculitis (eg HSP))

platelet count and clotting screen is required to rule out coagulation disorders

235
Q
A

HSP

236
Q
A

senile purpura

237
Q

meningococcal septicaemia

A
  1. hx - acute onset. sx of meningitis and septicaemia
  2. common sites - extremities
  3. lesion - petechiae, ecchymoses, haemorrhagic bullae and/or tissue necrosis
  4. assoc features - systemically unwell
  5. ix - bloods, LP
  6. mx - abx
238
Q

disseminated intravascular coagulation

A
  1. hx - hx of trauma, malignancy, liver failure, obstetric complications, transfusions or sepsis
  2. common sites - spontaneous bleeding from ear, nose, throat, GI tract, respiratory tract or wound site
  3. lesion - petechiae, ecchymoses, haemorrhagic bullae and/or tissue necrosis
  4. assoc features - systemically unwell
  5. ix - bloods (clotting screen is imp)
  6. mx -treat underlying cause, transfuse for coagulation deficiencies and anticoagulants for thrombosis
239
Q

vasculitis

A
  1. hx - painful lesions
  2. common sites - dependent areas (eg legs, buttocks, flanks)
  3. lesion - palpable purpura (often painful)
  4. assoc features - systemically unwell
  5. ix - bloods and urinalysis. skin biopsy
  6. mx - treat underlying cause. steroids and immunosuppressants if there is systemic involvement
240
Q

senile purpura

A
  1. hx - arise in the elderly population with sun damaged skin
  2. common sites - extensor surfaces of hands and forearms. such skin is easily traumatised.
  3. lesion- non-palpable purpura. surrounding skin is atrophic and thin
  4. assoc features - systemically well
  5. ix - none req
  6. mx - none req
241
Q

ddx for red swollen leg

A

cellulitis

erysipelas

Venous thrombosis

chronic venous insufficiency

242
Q

cellulitis/erysipelas

A
  1. hx - painful spreading rash. hx of abrasion or ulcer
  2. lesion -erysipelas - well-defined edge. cellulitis - diffuse edge
  3. assoc features - systemically unwell with fever and malaise. may have lymphangitis
  4. ix - skin swab. anti-streptococcal O titre (ASOT)
  5. mx - abx
243
Q

venous thrombosis

A
  1. hx - pain with swelling and redness. hx of prolonged bed rest, long haul flights or clotting tendency
  2. lesion - complete venous occlusion may lead to cyanotic discolouration
  3. assoc features- usually systemically well. may present with PE
  4. ix- d-dimer. doppler US and/or venography
  5. mx - anticoagulants
244
Q

chronic venous insufficiency

A
  1. hx - heaviness or aching of leg which is worse on standing and relieved by walking. hx of venous thrombosis
  2. lesion - discoloured (purple-blue), oedema (improved in the morning), venous congestion and varicose veins
  3. assoc features - lipodermatosclerosis (erythematous induration creating ‘champaigne bottle’ appearance). stasis dermatitis (eczema with inflammatory papules, scaly and crusted erosions). venous ulcer.
  4. ix - doppler ultrasound and/or venography
  5. mx - leg elevation and compression stockings. sclerotherapy or surgery for varicose veins
245
Q

what tx modalities exist for skin diseases

A

medical - topical and systemic

physical therapy (eg cryotherapy, phototherapy, photodynamic therapy, lasers and surgery)

246
Q

contents of topical treatments

A

active constituents which are transported into the skin by a base (aka vehicle)

active constituents eg - steroids, tar, immunomodulators, retinoids, abx

base eg - lotion(liquid), cream (oil in water), gel (organic polymers in liquid, transparent), ointment (oil with little or no water), paste (poder in ointment)

247
Q

emollients eg, indications, SEs

A

eg- Aqueous cream,emulsifying ointment,liquid paraffin and white soft paraffin in equal parts (50:50)

indications - to rehydrate skin and re-establish surface lipid layer.

useful for dry scaling conditions and as soap substitutes

SEs - reactions may be irritant or allergic (eg due to preservants or perfumes in creams)

248
Q

topical/oral corticosteroids eg, indications, SEs

A

topical steroids - classed as mildly potent (hydrocortisone), moderately potent (clobetasone butyrate (eumovate)), potent(betamethasone valerate(Betnovate)) and very potent (clobetasol propionate(dermovate))

oral steroids - prednisolone

indications - anti-inflammatory and anti-proliferative effects

useful for allergic and immune reactions, inflammatory skin conditions, vasculitis, blistering disorders, connective tissue diseases.

SEs -

local SEs - skin atrophy (thinning), telangiectasia, striae, may mask, cause or exacerbate skin infections, acne or perioral dermatitis, and allergic contact dermatitis

systemic SEs (from oral prednisolone) - cushing’s syndrome, immunosuppression, diabetes, hypertension, osteoporosis, cataract and steroid induced psychosis

249
Q

oral aciclovir indications, SEs

A

indications - viral infections due to herpes simplex and herpes zoster virus

SEs - GI upset, raised liver enzymes, reversible neurological reactions, haematological disorders

250
Q

oral antihistamines eg, indications, SEs

A

eg - non sedative (cetirizine, loratadine)

sedative (chlorpheniramine, hydroxyzine)

indications - block histamine receptors producing an anti-pruritic effect

useful for type 1 hypersensitivity reactions and eczema (esp sedative antihistamines for children)

SEs - sedative antihistamines can cause sedation and anticholinergic effects (dry mouth, blurred vision, urinary retention, constipation)

251
Q

topical/oral abx eg, indications, SEs

A

topical abx: fusidic acid, mupirocin, neomycin

oral abx: u know them

indications: bacterial skin infections and some used for acne

SEs: local - local skin irritation/allergy

systemic: GI upset, rashes, anaphylaxis, vaginal candidiasis, abx-associated infection such as C.diff and abx resistance (rapidly appears to fusidic acid)

252
Q

topical antiseptics eg, indications, SEs

A

chlorhexidine, cetrimide, povidone-iodine

indications: tx and prevention of skin infection

SEs: local skin irritation/allergy

253
Q

oral retinoids eg, indications, SEs

A

eg: isotretinoin, acitretin
indications: acne, psoriasis, disorders of keratinisation

SEs: mucocutaneous reactions such as dry eyes, dry lips and dry skin, disordered liver function, hypercholesterolaemia, hypertrigylceridaemia, myalgia, arthralgia and depression

teratogenicity: effective contraception must be practiced at least 1 month before, during and 1 month after isotretinoin, but for 2 yrs after acitretin

254
Q

biological therapy eg, indications, SEs

A

eg - monoclonal antibodies (eg.,Infliximab,,Adalimumab,,Ustekinumab,,
Certolizumab,,Gorlilumab), Fusion,antibody proteins (eg.,Etanercept),
Recombinant human cytokines and growth factors (eg.,Interleukins)

indications: mainly for psoriasis, atopic eczema and hidradenitis suppurativa

SEs - local - redness, swelling and bruising at site of injection

systemic: allergic reactions, antibody formation, flu-like symptoms, infections, hepatitis, demyelinating disease, heart failure, blood problems, rare reports of cancers (non-melanoma skin cancers, lymphoma)

255
Q

functions of normal skin

A

i) protective barrier against environmental insults
ii) temp regulation
iii) Sensation
iv) Vitamin D synthesis
v) Immunosurveillance
vi) Appearance/cosmesis

256
Q

what does varicella-zoster virus cause?

A

Herpes zoster, also known as shingles, is caused by the reactivation of the varicella-zoster virus (VZV), the same virus that causes varicella (chickenpox). Primary infection with VZV causes varicella. Once the illness resolves, the virus remains latent in the dorsal root ganglia.

257
Q

shingles

A

In immunocompetent patients, the most frequent site of reactivation is the thoracic nerves followed by the ophthalmic division of the trigeminal nerve (ophthalmic shingles), which can progress to involve all structures of the eye. If the mucocutaneous division of the VII cranial nerve is involved, the lesions in the ear, facial paralysis and associated hearing and vestibulary symptoms are known as Ramsay Hunt syndrome

Chickenpox can rarely be acquired from a patient with active shingles, as the lesions shed virus (transmission is by direct contact or droplet spread) but shingles is not caught from contact with a person with chickenpox.

HIV, Hodgkin’s lymphoma and bone marrow transplants all present a high risk

post herpetic neuralgia - PHN, is persistent or recurring pain lasting 30 days or more after the acute infection or after all lesions have crusted.

Ophthalmic herpes is a danger to sight and the patient should see an ophthalmologist the same day. Antiviral therapy is mandatory for this at any age.

If the tip of the nose has a rash, the nasociliary branch of the trigeminal nerve is involved. This branch supplies the globe and so it is very likely that the eye will be affected (at least 75% of cases). This is called Hutchinson’s sign. The eye can be seriously affected with little evidence of a shingles rash.

Mx -

rash should be kept clean and dry to avoid secondary bacterial infection. If the rash can be covered, or if the lesions have all crusted, there is no need to avoid school or work. If the rash is weeping and not in a covered part of skin, however, the person should stay off school or work.

analgesia (paracetamol or co-codamol or nsaids)

Prescribe an oral antiviral treatment (aciclovir, valaciclovir) within 72 hours of rash onset for people with any of the following criteria:

Immunocompromise
Non-truncal involvement (such as shingles affecting the neck, limbs, or perineum).
Moderate or severe pain.
Moderate or severe rash.

Consider prescribing oral antiviral treatment within 72 hours of rash onset for all people aged over 50 years to reduce the incidence of post-herpetic neuralgia

In the UK, there is a shingles vaccination programme for people aged 70 years and above. The programme began in September 2013. It is not recommended for people aged 80 years or more.

258
Q

ramsay hunt syndrome

A

he Ramsay Hunt syndrome described here occurs when the varicella-zoster virus (chickenpox) becomes reactivated in the geniculate ganglion of the VIIth cranial nerve (facial nerve) causing facial paralysis, loss of taste, vestibulocochlear dysfunction and pain.

Presentation -

pain deep within the ear. after a day or two, the pain often radiates outward into the pinna and there is a more constant, diffuse and dull background pain.

The following may also be presenting features:

  • Vertigo and ipsilateral hearing loss or hyperacusis.
  • Tinnitus.
  • Facial weakness or face drop.
  • Rash or blisters, which may be on the skin of the ear canal, auricle or both.
  • A rash or herpetic blisters in the distribution of the nervus intermedius -
    • The anterior two thirds of one side of the tongue.
    • The soft palate.
    • The external auditory canal, visible only with an otoscope.
    • The pinna.

Mx - aciclovir and prednisolone asap

If there is problem with closing the eye, a pad will protect the cornea, and eye lubricants should be prescribed.

Medicine finals Prithvi (22 decks)

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