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Dermatology > Pathology > Flashcards

Pathology Flashcards

1
Q

What is the visual presentation of hyperkeratosis

A

A scaly skin rash

Build up of keratin layer

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2
Q

What are the 4 main reaction patterns of inflammatory skin diseases

A

Spongiotic-intraepidermal oedema e.g. eczema
Psoriasiform- elongation of the rete ridges e.g. psoriasis
Lichenoid-basal layer damage e.g. lichen planus and lupus
Vesiculobullous- blistering e.g. pemphigoid, pemphigus

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3
Q

What is the characteristic of lichenoid disorders

A

Damage to basal epidermis - between epi and dermis
Most common condition is lichen planus
Can be a lichenoid drug reaction

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4
Q

How does lichen planus present

A

Itchy flat topped pink/purple papules
Very ithcy
Affects wrists, forearms, shins and ankles
May get lacy, white streaks in cheeks or on papules- Wickham’s striae

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5
Q

what is the main feature of immunobullous diseases

A

Blisters

vesicles and bullae

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6
Q

What is pemphigus

A

Rare autoimmune bullous disease
Autoantibodies cause damage to the junctions between skin cells - intrepidermal
Loss of junction integrity causes severe blisters

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7
Q

How can you treat pemphigus

A

Responds to steroids

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8
Q

What is the most common subtype of pemphigus

A

Pemphigus vulgaris

80% of cases

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9
Q

Describe the cause of pemphigus vulgaris

A

IgG autoantibodies made against desmoglein 3 which forms the desmosomes
Immune complexes form and complement is activated
Proteases are released and dissolve the attachments between cells - leads to acantholysis
Occurs within the epidermis itself

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10
Q

what is acantholysis

A

Breakdown of intercellular adhesion sites

common to all types of pemphigus

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11
Q

What causes bullous pemphigoid

A

IgG antibodies attack the hemidesmosomes that attach the basal cells to the basement membrane
This breaks down the DEJ and causes separation of dermis and epidermis
Complement is activated and the surrounding tissues are damaged

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12
Q

How does bullous pemphigoid present

A

Can present with itchy red plaques and papules before the blisters develop
Subepidermal blisters - deep
Large, tense blisters on normal, red or urticarial base
When they burst, they leave erosisons but do not scar
Unlikely to affect mucosa (mouth only if at all)
typically localised to one area or widespread on trunk/ limbs
Nikolsky sign negative

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13
Q

What would show up if you did immunofluorescence on a bullous pemphigoid sample

A

Linear pattern of IgG antibodies would show up along the basement membrane - solid typically green line alone BM
Would also pick up complement

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14
Q

What condition is dermatitis herpetiformis associated with

A

Coeliac disease

Personal or family history

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15
Q

How does dermatitis herpetiformis present

A

Extremely itchy lesions - typically preceeds blisters
Small blisters on erythematous urticarial base - often scratched off leaving crusts or excoriation
Symmetrical
Often affects the elbows, extensor forearms, knees, buttocks, face and scalp
The hallmark is papillary dermal microabscesses

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16
Q

Which HLA group is dermatitis herpetiformis associated with

A

HLA-DQ2 haplotype

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17
Q

What would a dermatitis herpetiformis sample look like under immunofluorescence

A

IgA deposits seen at the tips of the dermal papillae

Granular IgA deposits

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18
Q

What is the aetiology of acne

A

It is a chronic inflammatory disease of the pilosebaceous units.
Increased androgens during puberty cause increased activity of sebaceous glands
Keratin and sebum plugs the pilosebaceous unit
Glands get blocked, inflamed then rupture
Infection with other bacteria (p acnes) causes further inflammation

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19
Q

What is the normal distribution of acne

A

face, upper back, anterior chest

High concentration of sebaceous glands

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20
Q

What is the clinical presentation of rosacea

A

Recurrent facial flushing - exacerbated by sudden change in temperature , alcohol & spicy food
Erythema
Visible blood vessels
Pustules and papules
Thickening of skin Rhinophyma - enlarged red nose
Affects nose, chin, cheeks and forehead

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21
Q

How can you differentiate between acne and rosacea

A

Rosacea does not have comedones - black/white heads

Also normal sebum excretion rates

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22
Q

What are some triggers of rosacea

A 
Sunlight
Alcohol
Spicy foods
Stress
Sudden temperature changes
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23
Q

List some topical treatments for acne

A

Bezoyl peroxide
Antibiotics
Retinoids

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24
Q

How do topical retinoids work

A

Dry skin up by shrivelling the sebaceous glands and reducing secretion
Anticomedonal

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25
Q

Describe the presentation of acne vulgaris

A

Comedones - black/white heads
Pustules and papules
cysts
erythema

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26
Q

What is a potential complication of acne

A

Scarring
Can be atrophic (shallow/ice pick) or hypertrophic (keloid)
Usually after deep lesions

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27
Q

Where on the body does rosacea normally appear

A

Nose, chin, cheeks and forehead

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28
Q

How can you treat rosacea

A 
Reduce exposure to triggers - diet, wear suncream 
Topical = metronidazole, ivermectin 
Oral tetracycline - long term
Roacccutane if severe 
Vascular laser for telengectasia 
Rhinophyma - surgery
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29
Q

How do you treat lichen planus

A

Symptomatically
Usually burns out after 12-18 months
Can use topical steroids
Oral if very severe

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30
Q

what is Nikolsky’s sign

A

When the top layer of skin slips away from the lower ones when rubbed slightly
Positive in pemphigus

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31
Q

Which areas of the body are typically affected by pemphigus vulgaris

A 
Scalp, face, axillae, groins 
Mucosal involvement (eyes, genitals) is very common 
May also appear on pressure points
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32
Q

Which condition has higher risk, pemphigus or pemphigoid?

A

Pemphigus

Very high mortality if untreated - 75-99%

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33
Q

How do you treat pemphigus

A

First line - oral steroids (pred)
Typically start steroid as inpatient – may be IV

Then can add another immunosuppressive agent - usually azathioprine

Topical steroids and anaesthetics are symptomatic treatment only

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34
Q

List physical causes of skin blistering

A

Insect bites
Burns
Friction - particularly in elderly as friable skin

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35
Q

List infectious causes of skin blistering

A

HSV – cold sores, eczema herpeticum
VZV – chickenpox, zoster
Coxsackie virus – hand-foot-and-mouth disease

Staph aureus – bullous impetigo, SSSS
Strep pyogenes – bullous cellulitis

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36
Q

List genetic causes of skin blistering

A

Epidermolysis bullosa (EB)

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37
Q

Which drug reactions can cause skin blistering

A

EM / Stevens-Johnson syndrome
Toxic epidermal necrolysis (TEN)
Fixed drug eruption

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38
Q

What is the role of desmosomes

A

Hold adjacent epidermal cells together

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39
Q

What is the role of the hemidesmosomes

A

Hold the epidermis to the dermis at the DEJ

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40
Q

How would you investigate suspected bullous disease

A

History and examination
Bloods – Usual set with inflammatory markers – ESR/CRP
May do swabs to rule out infection
Biopsy with IMF - this will be your diagnostic test

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41
Q

which age group is most affected by bullous pemphigoid

A

Age >60 years in majority

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42
Q

How do you treat bullous pemphigoid

A

Topicals: emollients, topical antisepsis / hygiene measures

First-line – topical steroid + doxycycline for localised disease

Second line – oral steroid + steroid sparing like doxy for generalised disease
May use doxy alone if disease is not severe

Rest are 3rd line onwards that isn’t responding - azithioprine, dapsone, biologics

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43
Q

Bullous pemphigoid is typically self limiting - true or false

A

True
However it is chronic and can take months to years to resolve without treatment
Treatment reduces recovery to 3-6 months

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44
Q

which age group is most affected by pemphigus vulgaris

A

Usually a disease of middle age

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45
Q

How does pemphigus vulgaris present

A

Flaccid vesicles/bullae
Includes oral, throat and genital lesions
They rupture easily leaving raw, denuded erosions
Nikolsky sign positive

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46
Q

How would pemphigus vulgaris present on immunofluorescence

A

Would see IgG deposits outlining epidermal cells

Looks like chicken wire

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47
Q

Which age group is most affected by dermatitis herpetiformis

A

Mainly young adults

Can affect all ages though!

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48
Q

How would you investigate dermatitis herpetiformis

A

Coeliac serology – IgA antibodies to tissue transglutaminase (tTG)

Histology of lesion- subepidermal blisters, microabscesses in dermal papillae

Biopsy uninvolved skin for detection of granular deposits of dermal papillary IgA on immunofluorescence

Small intestinal scope + biopsy

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49
Q

How do you treat dermatitis herpetiformis

A

Gluten-free diet - mainstay

Drugs: dapsone, Tetracyclines

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50
Q

How do you treat mild acne

A

Topical treatment only
e.g. Benzoyl peroxide
Topical antibiotics, retinoids

Range of anti-comedonal, inflammaotry and microbial effects

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51
Q

What are comedones

A

Blocked pores bascially
If closed - whitehead
If open - blackhead

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52
Q

What can cause an increase in sebum production

A

Androgen effect as sebaceous unit had androgen receptors

Increased androgen production - seen in puberty or androgenic hormone imbalance in females

Increased availability - decreased SHBG

Increased androgen receptor responsiveness

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53
Q

The more bacteria present in acne, the worse it is - true or false

A

False!
No relationship between # of bacteria and acne severity
More related to amount of sebum and ductal cornification

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54
Q

Which bacteria commonly colonise acne

A

Propionobacterium acnes
Staph. epidermidis
Malassezia furfur

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55
Q

How do you grade acne

A

Mild- scattered papules and pustules

Moderate- numerous papules, pustules and
mild atrophic scarring

Severe - as above, cysts, nodules and significant scarring

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56
Q

What factors can aggravate acne

A 
Poor diet 
Being pre-menstrual = common to flare
Sweating 
 UV 
Steam or oil in environment 
Stress
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57
Q

How do you treat moderate acne

A

Topical treatment and oral antibiotics or Dianette® (females)

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58
Q

How do you treat severe acne

A

Isotretinoin (Roaccutane®)

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59
Q

What are the side effects of benzoyl peroxide for acne

A

Erythema and peeling

Bleaches clothes, hair, bedlinen and towels

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60
Q

Retinoids should be avoided in pregnancy - true or false

A

True

Systemic absorption of topicals not significant but still avoid

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61
Q

What are the side effects of topical retinoids for acne

A

Stinging, irritation, erythema and peeling

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62
Q

Which antibiotics are used for acne

A

Topical:
Erythromycin
Tetracycline
Clindamycin

Oral: 
Erythromycin	
Oxytetracycline	
Doxycycline 
Minocycline - needs LFT monitoring
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63
Q

What is the main skin side effect of tetracyclines

A

Photosensitivity

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64
Q

If antibiotic therapy isnt working for acne should you try another

A

Yes

Try a second antibiotic after 3-6 months

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65
Q

Can contraception be used to treat acne

A

Yes - combined pills
Typically use dianette
Oestrogen decreases androgen production
Takes 6 months to lower sebum though

Progesterone rich / Only contraceptives may exacerbate acne

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66
Q

What are the indications for starting someone on roaccutane

A

Nodulo-cystic acne
Inadequate response to conventional therapy
Relapse after adequate antibiotics
Significant scarring
Severe psychological impairment (dysmorphophobia)
post-inflammatory hyperpigmentation

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67
Q

How does roaccutane work

A

Reduces sebaceous gland activity

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68
Q

List side effects of roaccutane

A 
Dry skin, lips, eyes, nose 
Skin fragility
Hyperlipidaemia
Abnormal liver function
Teratogenesis- contraception
Mood alteration
Arthralgia
Acne fulminans
Hair thinning
Benign intracranial hypertension
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69
Q

How does tuberous sclerosis present in the skin

A 
Multiple hamartomas
Angiofibromas
Peri-ungual fibromas
Shagreen patches
Ash leaf macules
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70
Q

What causes tuberous sclerosis

A

Autosomal dominant mutation

2/3 are de-novo

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71
Q

What causes neurofibromatosis

A

Autosomal dominant

Mutation in neurofibromin gene (tumour suppressor) on chromosome 17

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72
Q

How does neurofibromatosis present in the skin

A

Neurofibromas
Cafe au lait macules
Axillary freckling
Lisch nodules

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73
Q

List skin manisfestations of diabetes

A

Infections
Leg ulcers and other complications
Some specific disease related to diabetes - Necrobiosis Lipoidica etc

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74
Q

What is erysipelas

A

skin infection in upper dermis - typically strep
Seen in diabetics

Confluent erythema
Well demarcated
Not raised, scaly or crusty
Would be tender, hot, painful, patient may feel unwell

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75
Q

How do you treat erysipelas

A

Need oral or IV antibitoics as deep

Would probably use IV if on the face/periorbital

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76
Q

Candida is common in diabetes - true or false

A

True
Occurs in warm moist areas
Also seen around nails
Hyperglycaemia favours growth

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77
Q

Describe the appearance of Necrobiosis Lipoidica

A

Bilateral lesions - tyipcally on shins
Smooth skin surface = deeper issue
Epidermal issue will typically be dry and scaly
Erythema and yellowing seen - subcutus peeks through

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78
Q

What causes Necrobiosis Lipoidica

A

Technically unknown
Most patients are diabetics - ?microvascular cause

Granulomatous inflammatory reaction around destroyed collagen

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79
Q

How do you treat Necrobiosis Lipoidica

A

Inject steroids around lesion

Can use tacrolimus - calcineurin inhibitor

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80
Q

How might psoriasis present in the nails

A

Pitting
Onycholysis (lifting of the nail plate off the nail bed)
Subungual hyperkeratosis– keratin build up below the nail
Longitudinal ridging
Thickening
Crumbling
Colour changes

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81
Q

How can you treat psoriatic nail disease

A

Topical steroids
Intralesional if a few nails affected
Calcipotriol
PUVA - systemic psoriasis treatment

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82
Q

How do you diagnose fungal nail disease

A

Take clippings

Assess for skin involvement

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83
Q

How do you treat fungal nail disease

A

Topical or oral antifungals

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84
Q

How does fungal nail disease present

A

Thickened nails
Brittle
Yellow discoloration

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85
Q

What is a subungual haematoma

A

Bleeding under the nail

Typically after obvious trauma but repeated microtrauma can be enough

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86
Q

What must be ruled out before diagnosing simple subungal haematoma

A

Subungual melanoma
They can bleed too
Dermoscopy can help clarify

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87
Q

How does subungal melanoma present

A 
Irregular pigmentation under nail 
Typically a brown/black stripe down nail
Extends to involve proximal nail fold 
May bleed, ulcerate,
Abnormalities of the nail plate
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88
Q

How do you manage subungal melanoma

A

May require excision of the entire nail apparatus if not amputation

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89
Q

What is a myxoid pseudocyst

A

A benign, painless cyst (though lacks capsule) at the edge of the nail
Treat by draining - may recur

90
Q

What causes lichen planus

A

T cell mediatedautoimmunedisorder

Inflammatory cells attack an unknownproteinwithin the skin and mucosalkeratinocytes

91
Q

How does lichen planus present in the nails

A 
Thinning
Onycholysis
Pterygium(fusion of nail with nail bed)
Loss of nail 
Ridges
92
Q

What are Beau’s lines

A

Transverse lines secondary to nail growth arrest, usually at a time of severe illness, chemotherapy
Deep grooved lines horizontal on nail

93
Q

What is paronychia

A

Infection in the skin around a nail
Acute may be due to trauma, nail biting and usually bacterial
Chronic is typically a fungal infection

94
Q

How do you differentiate between scarring and non-scarring alopecia

A

Non-scarring alopecia’s demonstrate visible follicular units on dermoscopy, while scarring alopecia’s are devoid of follicular units

95
Q

What is androgenic alopecia

A

Typical male or female pattern baldness

Likely due to androgen sensitivity and genetics

96
Q

How can you manage androgenic alopecia

A

Monoxodil 5%(vasodilatory effects)
Males – finasteride (stops testosterone being converted to DHT)
Spironolactone
Hair transplant
Camoflage: nanogen fibres, hair piece, wig
Psychological support

97
Q

What is telogen effluvium

A

Hair loss related to stressful events
Hair suddenly moves from the anagen to telogen phase causing mass hair shedding
Can be due to pregnancy, surger, illness, stress
Usually corrects itself with time

98
Q

What causes alopecia areata

A

Autoimmune condition

T-cell mediated

99
Q

How does alopecia areata present

A

May have preceding tingling, ‘trichodynia’
Focal patches of confluent hair loss.
Exclamation mark hairs - thinner at base, thicker at top

100
Q

How do you manage alopecia areata

A 
Potent topical steroids
Intralesional steroids
DCP
JAK inhibiors
Camoflage
101
Q

What is traction alopecia

A

Hair loss caused by traction

Usually due to tight hairstyles or headgear

102
Q

What is trichotillomania

A

Irresistible urge to pull at hair

Associated with OCD, stress and anxiety - treat these to treat

103
Q

How does trichotillomania present

A

Temples and vertex common sites - often on side of dominant hand
Irregularly shaped patches of hair loss
Varying lengths

104
Q

Tinea capitis can lead to alopecia - true or false

A

True

Can even scar if extensive + chronic (called kerion - highly inflamed TC lesion)

105
Q

List 3 main causes of scarring alopecia

A

Discoid SLE
Lichen planopilaris
Folliculitis decalvans and Dissecting Cellulitis of the scalp

106
Q

How does discoid lupus present on the scalp

A

Persistent, scaly, discoid lesions on the head and neck area
Inflammatory plaques present
Can cause scarring, discolouration
May be triggered by sunlight

107
Q

How do you treat discoid lupus

A

High potency steroids
Intralesional steroids
Protopic

Systemic treatment: hydroxychloroquine, oral pred, methotrexate, other immunosuppressives

Sun protection

108
Q

How does Lichen planopilaris present

A

Symptoms: itch, pain, tenderness, burning
Significant loss of hair - scarring/permanent
Common sites: forehead, nape of neck, sides of scalp
Slow to progress
Trichoscopyreveals absentfollicles, white dots, tubularperifollicularscale and perifollicularerythema

109
Q

How does folliculitis decalvanspresent

A

Follicular pustules and scarring alopecia

Characteristically, several or many hairs can be seen coming out of a single follicle, so the scalp looks”tufted”

110
Q

How does dissecting cellulitis of the scalp present

A 
Perifollicular and follicular pustules
Nodules and pseudocysts, often with purulent exudate
Abscess
Hair loss - scarring/permanent
Keloid scars
111
Q

What is hirsutism

A

Male pattern of secondary or post-pubertal hair growth occurring in women
May develop thicker hairs, across the moustache and beard area, lower abdomen etc

112
Q

What can cause hirsutism

A

PCOS
Cushings
Congenital adrenal hyperplasia

Caused by increased androgens or stronger response to them

113
Q

How do you manage hirsutism

A

COCP
Spironolactone
Metformin
Hair removal - many types

114
Q

What is hypertrichosis

A

Non-hirsute excessive hair growth over and above the normal for the age,sexand race of a male or female

Can be congenital, associated with naevi or spina bifida
Aquired - malnutrition, malignancy and certain drugs

115
Q

Which drugs can cause hypertrichosis

A

Ciclosporin
Phenytoin
Minoxidil - used for hair loss

116
Q

What is DRESS

A

Drug exanthem with eosinophilia and systemic symptoms
Red rash skin reaction with additonal symptoms

Facial swelling
Lymphadenopathy
Liver involvement - check LFT
Morbilliform rash
Fever

May even go on to need organ transplant if multiple organ involvement

117
Q

What is a drug exanthem

A

Erthematous macular + papular rash in response to medication
Usually then becomes confluent
Usually blanches
Axillae, groins hands and feet often spared.

118
Q

How do you treat drug exanthems

A

Stop the offending drug
Treat symptoms - antihistamine & topical steroids, regular emollient
If DRESS give oral steroids

119
Q

Which drugs often cause exanthem reactions

A

Antibitoics - penicillins, cephalasporins
Allopurinol
Anti-epileptics
NSAIDs

120
Q

What is the main difference between SJS and TEN

A

SJS – mucosal involvement more likely <10% skin involved

TEN - >30% skin involved

121
Q

Describe the presentation of SJS

A

Characteristic prodrome of respiratory symptoms, followed up to 14 days later by erosions of at least 2 mucosal surfaces with variable skin involvement

Pyrexia, systemic upset especially in children
May be dehydrated

Target like lesions, blisters etc
Epidermal detachment - desquamation affecting up to 10% of body
Nikolskys sign – positive, detachment of epidermis on light lateral pressure

122
Q

How do you treat SJS and TEN

A

Stop any offending drug or treat underlying cause
Needs HDU or ICU as very dangerous
May have burns unit input
Supportive treatment:
Fluid management, thermoregulation, regular emollient, dressing care etc
Prevent secondary infection

123
Q

Which drugs can cause urticaria

A

Can be any drug if patient is truly IgE allergic

NSAIDs and aspirin can induce a pseudourticaria

124
Q

Describe erythema multiform

A

Hypersensitivity reaction to some drugs or infection
Forms target lesion on skin
Usually acute and self limiting
Can involve mucosa and lead to fever

125
Q

List causes of erythema multiform

A

Idiopathic
Drugs - sulphonamides, penicillin, phenytoin
Viral infections – common with HSV in children

126
Q

What is a fixed drug eruption

A

A T cell mediated reaction to a specific drug
Recurrent and fixed site when exposed to offending drug.
Erythema, oedema, bruised appearance, blistering

127
Q

Which drugs commonly cause a fixed drug eruption

A

Tetracyclines
Paracetamol
Sulphonamides
NSAIDS

128
Q

Which drugs commonly cause a phototoxic drug reaction

A

Quinine
Doxycycline
NSAIDS
Retinoids

129
Q

Describe the appearance of erythema nodusum

A

Tender nodules usually on shins

Deep - nodules felt on palpation, may not be visible

130
Q

Which drugs can cause eryhtema nodusum

A 
Sulfonamide
Amoxicillin
Oral contraceptive
Non-steroidalanti-inflammatorydrugs
Bromide
Salicylate
131
Q

Which drugs can induce bullous pemphigoid

A

Frusemide, penicillamine, penicillin, sulphonamides

Younger demographic compared to BP

132
Q

How can amiodarone affect the skin

A

Can cause blue/black discoloration

133
Q

How does pityriasis rosea present

A

Solitary lesion appears 2-4 days before onset of rash – herald patch
Truncal eruption – small pink oval lesions with peripheral “micca” scale

134
Q

How do you treat pityriasis rosea

A

Self-limiting - likely viral cause

Can use topical steroids

135
Q

What causes vitiligo

A

Loss of melanocytes from affected areas
May be assoc with other autoimmune conditions
Around 30% have a family history

136
Q

How can you treat vitiligo

A

Topical steroids / phototherapy may help

Consider cosmetic camouflage

137
Q

Which skin conditions often have a psychological component

A

Urticarias
Pruritis
Flushing reactions
Sweat gland disorders

Stress can also trigger flare of many skin diseases - it is an inflammatory process

138
Q

What are salmon patches

A

Very common birthmark - 50% of babies
Either on face or back of neck
Thought to be due to persistant foetal circulation rather than a malformation. Tend to resolve
Neck lesions more persistant, around 10% into adulthood

139
Q

What are haemangiomas

A

Vascular tumours confined to children - benign

They occur during early childhood and most will regress and disappear

140
Q

Describe the appearance of a port wine stain

A 
Macular red birthmark 
They don’t extend outwith the initial area but may thicken
These lesions persist for life
Common on the face 
Typically unilateral
141
Q

What causes a port wine stain

A

Vascular malformation of capillaries

142
Q

When is a port wine stain associated with epilepsy

A

If their PWS is in the distribution of CN V1 - nose
Associated with ipsilateral vascular malformation in brain
Called Sturge Weber syndrome

143
Q

What conditions are seen in Sturge Weber syndrome

A

Causes seizures, intellectual impairment, hemi-paresis and glaucoma
Will have a port wine stain in V1 distribution

144
Q

What is Klippel-Trenauney

syndrome

A

Port wine stain on limb
The associated vascular malformation involves many vessels
Leads to progressive limb overgrowth and thickening

145
Q

Where do most infantile haemangiomas appear

A

Commonest on head and neck

146
Q

Which babies are at higher risk of infantile haemangiomas

A

Commoner in prems & females

147
Q

What are some of the complications of infantile haemangiomas

A

Can be very painful if they become ulcerated
Risk of infection
Bleeding
Compression
Obstruction of vision if around the eye or airway if near it

148
Q

What does a tumour type lesion over the spinal cord in an infant suggest

A

Spina bifida

May have an overlying haemangioma - rare

149
Q

How would you treat a serious infantile haemangioma

A

Topical or Intra-lesional corticosteroids
Systemic corticosteroids
Propranolol @ 2-3 mgs /Kg for several months

Used if in a high risk area

150
Q

What is a mongolian blue spot

A

Blueish birthmark
Common over buttock but can be seen anywhere
Common in black and asian skin
Can be confused with NAI - need to document when you find one

151
Q

Congenital Melanocytic Naevi have a risk of developing into melanoma - true or false

A

True
Around 4 fold risk
Higher for larger lesion

152
Q

What is a Congenital Melanocytic Naevus

A

A melanocytic (pigmented) mole
Aquired in childhood
May become warty or hairy

153
Q

When would you consider an underlying cause of cafe au lait macules in a child

A

If they have 2 or more under the age of 2 then you would consider neuroectodermal disease

154
Q

Which type of cell is primarily responsible for the development of urticaria, angioedema and anaphylaxis

A

Mast cells

Found in the dermis

155
Q

Histamine release from mast cells can have which cutaneous effects

A

Urticarial lesions or wheals due to superficial dermal oedema

Angioedema due to deep dermal or subcutaneous swelling

156
Q

Meningococcal meningitis is associated with what type of rash

A

Non-blanching purpuric rash
Caused by damage of the dermal vessel walls by bacteria in the endothelial cell walls
Check with glass test

157
Q

How do you treat suspected meningococcal disease in primary care

A

IV / IM Benzylpenicillin as soon as possible

Transfer to hospital ASAP

158
Q

How do you treat suspected meningococcal disease in secondary care

A

Ceftriaxone or Cefotaxime are the antibiotics of choice

159
Q

What can cause SJS

A

Most commonly drugs - NSAIDs, sulphonamides, anticonvulsants and other antibiotics
Typically occurs 2-8 weeks after ingestion

May be caused by infections in some

160
Q

How long does SJS typically last

A

4 - 6 weeks

161
Q

Describe the presentation of TEN

A

May have initial fever, sore eyes
Rapidly spreading skin lesions, initially dusky-red macules which coalesce, leading to necrosis and detachment
Large areas of epidermal and mucosal detachment affecting >30 % body surface area
Nikolskys sign – positive, detachment of epidermis on light lateral pressure
Pain is major feature
May be resp / GI epithelial involvement
Rapidly progressing

162
Q

What causes TEN

A

Almost always due to drugs

Develops 1-3 weeks after taking the drug

163
Q

What is erythroderma

A

Defined as erythema, often with scale, of at least 90% of the body surface area
Descriptor not diagnosis

164
Q

What can cause erythroderma

A 
Can be idiopathic 
Dermatitis
Psoriasis
Drug reactions
Cutaneous T-cell lymphoma - may have overlying ulcerating tumours

Though to be due to reduced cell transit time and increased mitotic rate

165
Q

Which drugs are common causes of erythroderma

A

Allopurinol
Antibiotics
Carbamazepine
PPIs

166
Q

How do you manage erythroderma

A

Initial management supportive and symptomatic - fluids, temp regulation etc
Emollients +++
May need antihistamines for associated pruritus
Specific treatment for underlying condition

167
Q

List some complications of erythroderma

A

Tachycardia and enter high output cardiac failure - due to increased blood flow to skin
Disturbed thermoregulation - hyperthermia
Compensatory hypermetabolism due to loss of heat

168
Q

Describe the appearance of eczema herpeticum

A

Multiple, monomorphic crusted vesicles are seen
Often haemorrhagic,
May be associated bacterial infection

May also have fever, malaise, lymphadenopathy

169
Q

What is eczema herpeticum

A

Widespread infection with Herpes Simplex

Most commonly seen in children and young adults with atopic eczema

170
Q

How do you treat eczema herpeticum

A

Prevention - avoid contact with friends and family with H Simplex infection
Severe cases – IV antiviral ASAP
Less severe cases – oral Rx

171
Q

How does pustular psoriasis present

A

Sterile pustules on skin surface
Often surrounded by red, inflamed skin
May be localized, usually to the hands and feet
Can be widespread - this is life threatening
Usually an acute presentation

172
Q

What can trigger pustular psoriasis

A 
Pregnancy
Withdrawal of corticosteroids
Infections
Hypocalcaemia
Other drugs eg salicylates, lithium
173
Q

List potential complications of pustular psoriasis

A 
Can be fatal! 
Hypoalbuminaemia
Hypocalcaemia
Acute renal tubular necrosis
Liver failure
Secondary infection
174
Q

How do you treat pustular psoriasis

A

Remove any triggers if possible
Supportive treatment
Most cases require systemic therapy - Acitretin or Methotrexate
Consider PUVA

175
Q

What is necrotising faciitis

A

Infection in the deep dermis, subcutaneous fat and fascia

Group A strep is a common aetiological agent but often multiple organisms involved

176
Q

Which factors can predispose to necrotising fasciitis

A

Trauma
Diabetes
Surgery

177
Q

How does necrotising fasciitis present

A

painful, hot skin which is erythematous / dusky
Bullae and necrosis develops
Rapidly progressive cellulitis and necrosis
Patient is generally severely ill

178
Q

How do you treat necrotising fasciitis

A

Urgent management with surgical debridement and high dose IV antibiotics is essential

179
Q

How do you differentiate between venous and arterial ulcers

A

Venous – malleolus, superficial

Arterial – distal, deeper

180
Q

How can you treat acanthosis nigricans

A

Can try topical retinoids / vit D analogues, sal. acid

181
Q

What can cause acanthosis nigricans

A

Insulin resistance is the main cause - seen in diabetes

Can be paraneoplastic

182
Q

What causes pretibial myxoedema

A

Graves disease

Auto-antibodies cross-react with the fibroblasts and cause thickening of the skin and fluid accumulation

183
Q

How do you treat pretibial myoedema

A

Treat underlying Graves

Correct circulation – compression stocking

184
Q

What skin signs may be seen in hyperthyroidism

A 
Warm, moist smooth skin
Hyperhidrosis
Facial flushing, palmar erythema
 Fine, thin hair. Diffuse alopecia 
Pruritus 
Pretibial myoedema seen in Graves
185
Q

What skin signs may be seen in hyperthyroidism

A

Cold, dry pale skin
Dry, coarse brittle hair, diffuse alopecia
Loss of lateral 1/3 eyebrow
Periorbital oedema and generla puffiness
Thickened brittle nails

186
Q

What skin signs may be seen in Addison’s

A

Increased pigmentation - due to MSH release alongside the ACTH

Seen all over but especially in palmar creases and buccal mucosa

187
Q

Which tumours can cause increased pigmentation in the skin

A

Pituitary
Lung

Due to MSH release

188
Q

Which tumours can cause hirsutism

A

Ovarian

Other androgenic effects like acne and baldness may be seen

189
Q

What are the 3 types of lupus skin disease

A

Cutaneous / Chronic Discoid LE - only in skin

Subacute cutaneous LE

Systemic LE - typical CTD with skin signs

190
Q

How do you treat Cutaneous / Chronic Discoid LE

A

Reduce sun exposure - can be a trigger
Use potent topical steroids – only condition where you start with potent in the face due to scarring risk and high inflammation
Then Hydroxycholroquine – oral

Also true for subacute type

191
Q

How does Cutaneous / Chronic Discoid LE present

A

Erythematous indurated plaques on sun exposed sites
Heals with scarring
If on hairy site will lead to permanent hair loss

192
Q

How does subacute cutaneous LE present

A

Usually ring-shaped erythematous scaly plaques, not indurated
Symmetrical.
Photosensitive - on sun exposed sites
Heal without scarring

193
Q

Which conditions is more associated with the development of SLE - Cutaneous / Chronic Discoid LE or subacute cutaneous LE

A

Subacute

Also more likely to be antibody positive

194
Q

What skin signs are seen in SLE

A

Butterfly ‘malar’ rash is classic - spares nasolabial folds
Photosensitive
Nail fold capillaries prominent
May have widespread DLE type rash

195
Q

Describe the skin changes seen in systemic sclerosis

A

Scleroderma
No surface change - deeper in dermis
Very hard and no give in skin – can be very restrictive
Common in fingers - sclerodactyly

Will also see telengectasia and Raynaud;s

196
Q

List the skin features of dermatomyositis

A

Photosensitivity rash like that of L.E
Shawl like pattern
Heliotrope oedema of eyelids
Linear finger rash with Gottron’s papules

197
Q

Describe the appearance of erythema multiforme

A

Target lesions

Often affects knees, elbows, palms, soles and mucosal areas

198
Q

What can cause erythema multiforme

A

90% due to infection – HSV
Often follows a coldsore

Some meds - sulphonamide

199
Q

Describe the appearance of erythema nodusum

A

Red, tender, diffuse nodules
Will be able to feel nodules deep in skin
Typically on shins

200
Q

What can cause erythema nodusum

A

Infections – Strep, TB, EB, fungal
Drugs – OCP, sulphonamides
Inflammatory bowel disease
Sarcoidosis

201
Q

Describe the appearance of cutaneous vasculitis

A

Non-blanching, purpuric rash ± bullae and necrosis.

Lower legs usually worst

202
Q

What is livedo reticularis

A

Mottled cyanotic network exacerbated by cold - purple/blue lines of veins

Can be caused by hot water bottle exposure!
Also heart failure, emboli, drugs etc

203
Q

What is Mycosis Fungoides

A

A cutaneous T cell lymphoma
Presents first with a reddish patch and then becomes a plaque
Can then erupt and cause erythroderma

204
Q

Which cancers often met to the skin

A

Breast, lung, colon, stomach, uterus, kidney,, lung, colon

205
Q

What is a sister mary joseph nodule

A

A malignant metastatic nodule found around the umbilicus

Sign of advanced cancer

206
Q

Which primary cancer is associated with generalised pruritis

A

lymphoma

207
Q

What is pityriasis versicolor

A

A common yeast infection of the skin which can affect melanocyte function leading to variable pigmentation

208
Q

What is urticaria

A

A transient (individual lesions last <24 hours) eruption of erythematous and oedematous swellings of the dermis, usually associated with itching

Also called hives or wheals

209
Q

What is angioedema

A

Transient (24 to 48 hours at most) swellings in the deeper dermal, subcutaneous and submucosal tissues.
Often seen in lips and tongue

210
Q

Urticaria is seen in which autoimmume disease

A

SLE

211
Q

Which drug is associated with angioedema

A

ACE inhibitors

212
Q

What can cause urticaria and angioedema

A 
Allergy 
Drugs - salicylates 
Physical urticarias - solar, cold, water etc. 
SLE 
Infections 
Idiopathic - chronic type
213
Q

How do you treat urticaria

A

Allergen avoidance if trigger identified

If no trigger then suppressive therapy

  • antihistamines (H1 and H2)
  • leukotrine antagonists
  • serotonin antagonists
  • UV phototherapy
214
Q

How do antihistamines work

A

Reversible competetitive inhibitors of histamine - bind to histamine receptors
Reduces the action of histamne

215
Q

How do you differentiate anaphylaxis from urticaria and angioedema

A

Will also present with respiratory compromise and hypotension - they will be shocked

216
Q

What are the 4 main types of itch

A

Pruritoceptive - triggered by something in skin

Neuropathic - damage to C or P nerves

Neurogenic - no C/PNS damage but still nerves that are triggering itch

Psychogenic - psychological cause with no CNS damage

217
Q

Which nerve fibres transmit the sensation of itch

A

unmyelinated C fibres

218
Q

Which chemical mediators in the skin can trigger itch

A

Histamine
Tryptase
Interleukin 2
Substance P

219
Q

What treatments are available for non-specific itch

A

Sedative anti-histamines
Emollients - with menthol or cooled in fridge
Antidepressants can work for neuropathic itch
Photo therapy
Opiate antagonists, serotonin (5HT3 receptor) antagonists

220
Q

Which type of antihistamines are good for treating itch - sedative or non-sedative

A

Sedative

non-sedative antihistamines useless for most itch except in urticaria and insect bites

Dermatology (14 decks)

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