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OTHERS Flashcards

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Dermatology Board Prep flashcards
1
Q

What causes scabies?

A

The mite sarcoptes scabiei and its spread by prolonged skin contact

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2
Q

What age does scabies typically affect?

A

Children and young adults

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3
Q

Pathophysiology of scabies?

A

The scabies mite burrows into the skin, laying its eggs in the stratum corneum
The intense pruritus associated with scabies is due to a delayed type 4 hypersensitivity reaction to mites/eggs which occurs about 30 days after the initial infection

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4
Q

Clinical features of scabies?

A

Widespread pruritus
Linear burrows on the sides of fingers, interdigital webs and flexor aspects of the wrist
Secondary features due to scratching - excoriations and infection

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5
Q

Management of scabies?

A

Permethrin 5% is first line - apply to all areas paying close attention to between fingers/toes, under nails, armpit area, creases of skin. Allow to dry and leave on skin for 8-12 hours before washing off. Reapply if washed off during treatment period.
Repeat treatment 7 days later

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6
Q

How long does pruritus last in scabies?

A

Usually 4-6 weeks post eradication

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7
Q

Advice for household members when scabies is diagnosed?

A

avoid close physical contact with others until treatment is complete
all household and close physical contacts should be treated at the same time, even if asymptomatic
launder, iron or tumble dry clothing, bedding, towels, etc., on the first day of treatment to kill off mites.

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8
Q

What us crusted scabies?

A

Aka Norwegian scabies
This is seen in patients with suppressed immunity, especially HIV
The crusted skin will be teeming with hundreds and thousands of organisms

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9
Q

Management of crusted scabies?

A

Ivermectin
Isolation is essential

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10
Q

Clinical features of lichen planus?

A

An itchy, papular rash most common on the palms, soles, genitalia and flexor surfaces of arms
Rash is polygonal in shape with white-lines pattern on the surface
Koebner phenomenon may be seen
Oral involvement in 50% of cases - white-lace pattern
Nail changes - thinning of nail plate and longitudinal ridging

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11
Q

What causes lichen planus?

A

Unknown aetiology, most probably immune-mediated

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12
Q

Drug causes of lichen planus?

A

Gold
Quinine
Thiazides

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13
Q

Management of lichen planus?

A

Potent topical steroids
Benzydamine mouthwash or spray for oral lichen planus

If extensive it may require oral steroids or immunosuppression

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14
Q

What is Henoch-schonlein purpura?

A

An IgA mediated small vessel vasculitis
Usually seen in children following an infection

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15
Q

Clinical features of HSP?

A

Palpable purpuric rash with localise oedema - over buttocks and extensor surfaces of arms and legs
Abdominal pain
Polyarthritis
Features of IgA nephropathy may occur e.g. haematuria

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16
Q

Management of HSP?

A

Analgesia if arthalgia
Supportive

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17
Q

Prognosis of HSP?

A

Excellent - usually a self-limiting condition especially in children without renal disease
Bp and urinalysis should be monitored to detect progressive renal involvement
1/3rd of patients have a relapse

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18
Q

What can cause purpura in children?

A

Meningococcal septicaemia
ALL
Congenital bleeding disorders
ITP
HSP
Non-accidental injury

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19
Q

Causes of purpura in adults?

A

ITP
Bone marrow failure e.g. leukaemia or myelodysplasia
Senile purpura
Drugs e.g. anti thrombotic
Nutritional deficiencies e.g. vit B12 or C or folate

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20
Q

What is senile purpura?

A

Aka actinic purpura
A common benign condition characterised by recurrent purple ecchymoses on extensor surfaces of foreharms following minor trauma

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21
Q

What are keloid scars?

A

Tumour-like lesions that arise from the connective tissue of a scar and extend beyond the dimensions of the original wound

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22
Q

Predisposing factors for keloid scars?

A

Ethnicity: dark skin
Young adults

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23
Q

Common sites for keloid scars?

A

In order of decreasing frequency:
Sternum
Shoulder
Neck
Face
Extensor surface of limbs
Trunk

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24
Q

Treatment of keloid scars?

A

If early it may be treated with intra-lesional steroids e.g. triamcinolone
Excision is sometimes required but careful consideration is needed for the potential to create further keloid scarring

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25
Q

What is a a thesis nigricans?

A

Symmetrical brown velvety plaques found often on the neck, axilla and groin

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26
Q

Causes of acanthosis nigricans?

A

T2DM
GI cancer
Obesity
PCOS
Acromegaly
Cushing disease
Hypothyroidism
Familial
Prader-Willi syndrome
Drugs - COCP and nicotinic acid

27
Q

Pathophysiology of acanthosis nigricans?

A

insulin resistance → hyperinsulinemia → stimulation of keratinocytes and dermal fibroblast proliferation via interaction with insulin-like growth factor receptor-1 (IGFR1)

28
Q

What are headline?

A

Pediculus humanus capitis parasite

29
Q

Management of head lice?

A

Dimeticone 4% lotion - apply to hair leave for 8 hours then wash off. Repeat 7 days later
Special fine combs

NICE recommend the Bug Buster Kit

30
Q

What is erythema about igne?

A

A. Skin disorder caused by over-exposure to infrared radiation
Typically an elderly woman who always sits next to an open fire

31
Q

Presentation of erythema ab igne?

A

Reticulated, erythematous patches with hyperpigmentation and telangiectasia

32
Q

Tx of erythema ab igne?

A

Stop exposure To the heat source

33
Q

Why is erythema ab igne important to treat?

A

If the cause is not treated then patients may go on to develop squamous cell skin cancer.

34
Q

What is hirsutism?

A

Androgen-dependant hair growth in women

35
Q

What is hypertrichosis?

A

Androgen-independant hair growth

36
Q

Causes of hirsutism?

A

PCOS - most common
Cushing
Congenital adrenal hyperplasia
Androgen therapy
Obesity
Adrenal tumour
Androgen secreting ovarian tumour
Drugs: phenytoin or corticosteroids

37
Q

Scoring system for assessing hirsutism?

A

Ferriman-Gallwey scoring system

38
Q

Management of hirsutism?

A

Advise weight loss if overweight
Waxing/bleaching
COCP such as co-cyprindiol (dianette) or yasmin
Topical eflornithine can be used for facial hirsutism

39
Q

Causes of hypertrichosis?

A

Drugs: minoxidil, Ciclosporin, diazoxide
Congenital hypertrichosis lanuginosa
Congenital hypertrichosis terminal is
Porphyria cutanea tarda
Anorexia nervosa

40
Q

What is hyperhidrosis?

A

Excessive sweat production

41
Q

Management options for hyperhidrosis?

A

topical aluminium chloride - first line
preparations are first-line
iontophoresis - weak electric current passes through water to temporarily stop sweat glands
botulinum toxin
surgery e.g. Endoscopic transthoracic sympathectomy

42
Q

What are milia and who are they most common in?

A

Small, benign, keratin-filled cysts that typically appear around the face
Most common in newborns

43
Q

What is pellagra?

A

A niacin deficiency that causes the 3 Ds: dermatitis, diarrhoea and dementia

44
Q

What can cause pellagra?

A

Isoniazid therapy (as isoniazid’s inhibits the conversion of tryptophan to niacin)
Alcoholics

45
Q

What is pyoderma gangrenosum?

A

A rare, non-infectious, inflammatory disorder that causes a very painful skin ulceration

46
Q

Where is pyoderma gangrenosum most commonly found?

A

The lower legs

47
Q

Causes of pyoderma gangrenosum?

A

Idiopathic
IBD
Rheumatological - arthritis, SLE
Haematological - lymphoma, myeloproliferative disorders, myeloid leukaemias, monoclonal gammopathy
Granulpmatosis with polyangiitis
PBC

48
Q

Features of pyoderma gangrenosum?

A

Sudden small pustule, red bump or blood blister
Late the skin breaks down resulting in a p flu ulcer. The edge of the ulcer is often purple and the ulcer itself may be deep and necrotic
May be accompanied by fever and myalgia

49
Q

Diagnosis of pyoderma gangrenosum?

A

Histology can be done but is not specific
Would show dense infiltration of neutrophils as its a neutrophilic dermatosis

50
Q

Management of pyoderma gangrenosum?

A

Oral steroids
As potential for rapid progression is high!

51
Q

Why should surgery be postponed until all pyoderma gangrenosum is completely controlled on immunosuppression?

A

To prevent worsening the disease
Pathergy - this is when trauma of the skin leads to ulcers/inkjury that may be resistant to healing

52
Q

What is a salmon patch?
Who are they common in?
How do they present?

A

A vascular birthmark see in 50% of newborn babies
Pink and blotchy
Fade over a few months
Commonly on forehead, eyelids and nape of neck

53
Q

What are port wine stains
How do they present?
Treatment?

A

Vascular birthmarks
Unilateral, deep red or purple mark that darkens and raises over time
Cosmetic camouflage or laser therapy can treat it

54
Q

DDx of shin lesions?

A

Erythema nodosum
Pyoderma gangrenosum
Pretibilial myxoedema
Necrobiosis lipoidica diabeticorum

55
Q

How does pretibial myxoedema present?

A

Symmetrical, erythematous lesions
Shiny, orange peel skin

56
Q

What is necrobiosis lipoidica diabeticorum?

A

A skin rash often on the shins
Rare

Presents with shiny, painless areas of yellow/red skin
Associated with telangiectasia

57
Q

Skin manifestations of SLE?

A

photosensitive ‘butterfly’ rash - nasolabial sparing
discoid lupus
alopecia
livedo reticularis: net-like rash

58
Q

Features of atopic eruption of pregnancy?

A

is the commonest skin disorder found in pregnancy
it typically presents as an eczematous, itchy red rash.
no specific treatment is needed

59
Q

Features of polymorphic eruption of pregnancy?

A

pruritic condition associated with last trimester
lesions often first appear in abdominal striae
management depends on severity: emollients, mild potency topical steroids and oral steroids may be used

60
Q

Features of pemphigoid gestationis?

A

pruritic blistering lesions
often develop in peri-umbilical region, later spreading to the trunk, back, buttocks and arms
usually presents 2nd or 3rd trimester and is rarely seen in the first pregnancy
oral corticosteroids are usually required

61
Q

Causes of spider naevi?

A

Liver disease
Pregnancy
COCP

62
Q

What are spider naevi?

A

Central red papules with surrounding capillaries that blanch on pressure
Almost always found on upper part of body

63
Q

How can spider naevi be differentiated from telangiectasia?

A

Spider naevi can be differentiated from telangiectasia by pressing on them and watching them fill. Spider naevi fill from the centre, telangiectasia from the edge .

64
Q

What is thr most common malignancy associated with acanthosis nigricans?

A

Adenocarcinoma

DERMATOLOGY (14 decks)

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