Dermatology Flashcards

1
Q

what is Auspitz sign?

A

it is seen in psoriasis when pinpoint bleeding occurs on removal of a layer of scale

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2
Q

what is Koebner phenomenon?

A

where skin lesions in psoriasis occur at sites of skin injury in otherwise healthy skin

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3
Q

what is eczema herpeticum caused by?

A

herpes simplex virus

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4
Q

what is the treatment of eczema herpeticum?

A

IV aciclovir

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5
Q

what are the situations for using:

  1. patch testing
  2. skin prick testing
  3. skin scrapings
A
  1. identify allergens that cause a type 4 hypersensitivity reaction - takes 2 days for a reaction
  2. identify allergens which cause a type 1 hypersensitivity reaction (IgE antibodies) e.g. asthma or anaphylaxis
  3. when fungal infection is suspected
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6
Q

which organism is seborrheic dermatitis associated with?

A

malassezia fungus

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7
Q

what is the treatment of infantile seborrheic dermatitis?

A

topical olive oil

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8
Q

which condition is acne vulgaris associated with?

A

PCOS - polycystic ovarian syndrome

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9
Q

what are the treatments for acne vulgaris?

A
  1. conservative
  2. salicylic acid and benzoyl peroxide
  3. topical retinoids
  4. Abx - tetracyclines and erythromycin/clindamycin
  5. systemic: anti-adrenergic like OCP and spironolactone
  6. isotretinoin
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10
Q

what is the problem with retinoids?

A

they are teratogenic

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11
Q

what are the complications of acne rosacea?

A

rhinophyma (skin thickening, enlargement and disfiguration of the nose)
blepharitis, conjunctivitis, keratitis

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12
Q

what is the treatment of acne rosacea?

A

general: sun protection, avoid spicy foods
emollients
topical: Abx = metronidazole; azelaic acid, brimonidine…
laser therapy for telangiectasia
surgery for rhinophyma

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13
Q

which mite is commonly found in sebaceous follicles of individuals with rosacea?

A

demodex folliculorum

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14
Q

what lesions can herpes simplex cause?

A
oral lesions
genital lesions
aphthous ulcers
herpes keratitis
herpetic whitlow
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15
Q

what are the investigations for herpes simplex?

A

usually clinical diagnosis

swab for HSV NAAT (PCR test)

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16
Q

what is the treatment of herpes simplex?

A

aciclovir

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17
Q

what is the advice for patients who have ongoing herpes simplex?

A

sex should be avoided when there is a prodrome and or genital lesions are present

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18
Q

what are the 3 major signs of chicken pox?

A

rash, fever and malaise

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19
Q

which organism causes chicken pox?

A

varicella zoster virus

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20
Q

how long does prodrome in chicken pox last?

A

up to 4 days

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21
Q

how do you know when chicken pox is not contagious anymore?

A

the lesions have crusted over

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22
Q

what is the treatment for chicken pox?

A

hydration, avoid scratching, avoid high-risk groups
paracetamol
sedating antihistamines (chlorphenamine) for itch
emollients and calamine lotion for itch
oral aciclovir if severe or high-risk group

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23
Q

which drug should not be given with chicken pox?

A

NSAIDs!!!

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24
Q

which organism causes shingles?

A

varicella zoster virus

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25
Q

what is the presentation of shingles?

A
dermatomal distribution - never crosses the midline
pain
rash - vesicular, fluid-filled
can be a/w flu-like symptoms
can involve the eye
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26
Q

what is Ramsey-Hunt syndrome?

A

facial nerve involvement with the varicella zoster virus

this leads to skin lesions in the ear, hearing and vestibular problems and facial paralysis

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27
Q

what is the treatment of shingles?

A

oral antivirals - valaciclovir

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28
Q

which organism causes molluscum contagiosum?

A

poxvirus

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29
Q

what is the presentation of molluscum contagiosum?

A

lesions are small, smooth, pearly coloured papules with a central area of umbilication

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30
Q

which organisms cause impetigo?

A

STAPH AUREUS!!

also strep pyogenes

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31
Q

which organisms cause cellulitis?

A

group A- beta haemolytic strep - strep pyogenes
staph aureus

less common:
strep pneumonia
haemophilus influenza
gram negative bacilli
anaerobes
MRSA
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32
Q

what type of infection is a dermatophyte?

A

fungal infection

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33
Q

what is another name for dermatophyte?

A

tinea or ringworm

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34
Q

where are the following located?

  1. tinea capitis
  2. tinea pedis
  3. tinea cruris
  4. tinea corporis
  5. onychomycosis
A
  1. scalp
  2. foot (athlete’s)
  3. groin
  4. body
  5. fungal nail infection
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35
Q

what is the most common dermatophyte?

A

trichophyton rubrum

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36
Q

what increases the risk of tinea?

A

occlusive footwear, excess sweating…
use of steroids
diabetes
immunosuppression

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37
Q

what are the presentations of tinea corporis, tinea capitis and tinea pedis?

A

tinea corporis: itchy rash, scaly, red, well-demaracted rings
tinea capitis: well-demarcated hair loss; itchy, dry, red
tinea pedis: white/red, flaky, cracked, itchy between toes

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38
Q

what investigations are needed for tinea?

A

skin scrapings - microscopy and culture

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39
Q

what is the management of tinea?

A

general: hygiene, footwear, don’t share clothing…
topical anti-fungals: terbinafine, clotrimazole, miconazole (both creams), ketoconazole (shampoo)
oral anti-fungals: terbinafine, fluconazole, itraconazole
for a fungal nail infection: amorolfine nail laquer 6-12 months; if resistant = oral terbinafine

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40
Q

what do you need to check when giving oral terbinafine for tinea?

A

need to check LFTs

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41
Q

what is the most common candidiasis?

A

candidiasis albicans

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42
Q

what is the cause of nappy rash?

A

Nappy rash is an irritant contact dermatitis that occurs in the nappy area. Secondary infection with Candida albicans or bacteria (Staphylococcal aureus or streptococcus) can occur

43
Q

what is Intertrigo?

A

candidiasis in the skin folds e.g. nappy rash

44
Q

what is the pathology of candidiasis?

A

candida needs a host to survive
it is a normal organism in the GI tract
most often associated with immunosuppression

45
Q

what is the treatment of candidiasis?

A

topical: Nystatin liquid drops OR miconazole 2% gel (oral and swallowed)
emollients
intertrigo: miconazole or clotrimazole cream

46
Q

which 2 conditions are associated with malassezia fungus?

A

seborrheic dermatitis and pityriasis versicolor

47
Q

what is the cause of pityriasis versicolor?

A

malassezia produces acetic acid
this diffuses through the skin and affects melanocyte function
the infection causes pale patches on the skin

48
Q

what is the presentation of pityriasis versicolor?

A
flaky skin with pale white, brown or pink patches
can be months/years
in light-skinned: patch darker than skin
in dark-skinned: patch lighter than skin
well-demarcated, circular
affects trunk
NOT USUALLY ITCHY
49
Q

what are the investigations of pityriasis versicolor?

A

skin scrapings
affected areas will fluoresce blue or green on Wood’s lamp exam
spaghetti and meatball appearance: potassium hydroxide shows clusters of yeast cells and long hyphi

50
Q

what is the treatment of pityriasis versicolor?

A

topical agents x2 weeks: selenium shampoo, miconazole/ketoconazole shampoo, sodium thiosulphate

oral: fluconazole, ketoconazole
prophylaxis: itraaconazole

51
Q

which infection and mite is scabies?

A

parasitic infection

sarcoptes scabiei mite

52
Q

what is the presentation of scabies?

A

found in webbing and sides of fingers, wrists, elbows, axillae, feet and genitals
rash due to hypersensitivity reaction
erythematous papules or vesicles and surrounding dermatitis
burrows = irregular tracks

53
Q

what is the treatment of scabies?

A

1: permethrin 5% cream
2: benzyl benzoate 25% emulsion

systemic: oral ivermectin

54
Q

what is erythroderma?

A

intense redness of skin covering 90% of skin

usually 2nd to pre-existing inflammatory skin disease e.g. psoriasis

55
Q

what is the presentation of erythroderma?

A

red, painful, itchy skin
malaise
peeling of skin
lymphadenopathy

56
Q

are females or males more likely to get SJS/TEN?

A

females

57
Q

what are the causes of SJS/TEN?

A

meds: allopurinol, anti-epileptic drugs, sulfonamides, antivirals, NSAIDs, salicylates, sertraline, imidazole, beta-lactams…
infections: herpes simplex, mycoplasma pneumonia, HIV, cytomegalovirus

58
Q

what kind of reaction is SJS/TEN?

A

immune-complex mediated hypersensitivity reaction

type 4 hypersensitivity

59
Q

what is the presentation of SJS/TEN?

A

history: prodromal flu-like/URTI, painful rash starting at trunk > spreads to face and limbs, mouth ulcers or soreness, painful or irritated eyes
exam: rash starts as macules > blisters > desquamation (peeling), positive Nikolsky’s sign, ulceration/erythema and blistering of oral cavity, conjunctivitis or corneal ulceration

60
Q

what is a positive Nikolsky’s sign?

A

gentle rubbing > peeling

seen in SJS/TEN

61
Q

what are the investigations of SJS/TEN?

A

skin biopsy!!!!

body surface area (to see if SJS or TEN)

62
Q

which investigation is not useful in SJS/TEN?

A

patch testing

63
Q

what is the management of SJS/TEN?

A

hospital admin, urgent derm referral, burns unit/ICU
stop causative meds
fluid and electrolytes maintained
ophthalmology
analgesia (steroids), immunoglobulins, immunosuppressants

64
Q

which is the most dangerous skin cancer?

A

melanoma

65
Q

what are the RF of melanoma?

A

FH, white skin, increasing age, PMH melanoma, multiple naevi (moles), sun (UVB whereas UVA for SCC/BCC), sun burn, males

66
Q

what is the acronym used for melanomas?

A
Asymmetry
Border - irregular
Colour variation
Diametes (>6mm)
Evolution
67
Q

which are the investigations for melanoma?

A

Breslow thickness and histology

biopsy if thickness >1mm possibly

68
Q

what is the pathology of BCC?

A

locally invasive keratinocyte cancer
slow growing
arise from epidermal basal cells

69
Q

which is the most common skin cancer?

A

BCC

70
Q

what is the presentation of BCC?

A
pearly nodule with a raised red edge
rolled border/edges
may be scaly
often on face
can also be ulcerated and can crust over
71
Q

what is the treatment of BCC?

A

excision
treat topically (not for head or neck): Imiquimod
cryotherapy
Mohs

72
Q

what is the presentation of SCC?

A

typically: irregular, ill-defined red nodule with scale and ulceration
on face, scalp, ears, hands and shins (sun exposed areas)
solitary nodules, often eroded at centre with crust and bleeding
fleshy
may be painful

73
Q

what is erythema nodosum?

A

a form of panniculitis (inflammation of the fat under the skin) resulting in tender, raised, red nodules that usually affect the shin

74
Q

what are the causes of erythema nodosum?

A
NODOSUM:
NO cause (idiopathic 50%)
Drugs: sulfonamides, dapsone
OCP
Sarcoidosis
Ulcerative colitis/Crohn's
Micro: TB, strep, toxoplamosis
75
Q

what is the presentation of erythema nodosum?

A

lesions are tender nodules for 1-2 weeks
as they resolve they bruise, but do not scar
most common on shin
most common in women

76
Q

which conditions cause acanthosis nigricans?

A

type 2 diabetes, Cushing’s, PCOS, steroids, OCP, underactive thyroid

77
Q

what is vitiligo?

A

an acquired depigmentation disorder of the skin where there is a loss of melanocytes in the epidermis leading to a loss of pigmentation

78
Q

which conditions are associated with vitiligo?

A

thyroid (Grave’s), type 1 diabetes, rheumatoid arthritis, pernicious anaemia, myasthenia gravis, psoriasis, alopecia…

79
Q

what is the presentation of vitiligo?

A

well-demarcated, smooth flat patches of depigmentation
may be segmented (children) or non-segemented/generalised (adults)
Koebner phenomenon
body hair white in vitiligo

80
Q

what are the investigations for vitiligo?

A

Wood lamp > lesions fluoresce

histology shows loss of melanocytes and depigmentation

81
Q

what is alopecia areata?

A

chronic hair loss disorder that is non-scarring and localised

82
Q

what is the presentation of alopecia areata?

A
well-defined localised loss of hair
often caused by tinea capitis!
exclamation mark hairs
hair loss not always complete
NO erythema, inflammation or scarring
pitting of nails
83
Q

what is the treatment of alopecia areata?

A
topical corticosteroids
corticosteroids injected intralesionally
systemic corticosteroids
immunotherapy
phototherapy and laser therapy
84
Q

what is SLE?

A

systemic lupus erythematous
it is a multisystem autoimmune disease
type 3 hypersensitivity reaction

85
Q

what is the cause of SLE?

A

unknown
genetic factors: HLA-DR2/3
environmental triggers: terbinafine, phenytoin, sulfsalazine, carbamazepine
EBV
combo of these causes breakdown of tolerance to self-antigens

86
Q

what are the RF of SLE?

A
African American
females (9:1)
childbearing age
HLA-DR2/3
sunlight exposure
87
Q

what is the presentation of SLE?

A

90% have: fatigue, fever, weight loss
malar rash, discoid rash, oral ulcers, scarring alopecia, photosensitivity
MSK: non-erosive arthritis of small joints of hands and feet; early morning stiffness
Cardiac: all 3 layers of heart; pericarditis, coronary artery disease, endocarditis
Lung: pleuritis, pulmonary hypertension
Neuro: seizures
GI: abo discomfort, N/V
kidneys: lupus nephritis > haematuria and proteinuria
haem penias (antiphospholipid syndrome)

88
Q

what is the typical history and exam of SLE?

A

history: fatigue, weight loss, arthralgia, joint stiffness, chest pain, SOB, haematuria, abdo pain, dry eyes and mouth, skin and mucosal ulceration
exam: fever and hypertension, malar rash, discoid rash, oral ulcers, alopecia, led oedema, joint tenderness (fibromyalgia), Raynaud’s

89
Q

which conditions are associated with Raynaud’s?

A

systemic sclerosis, SLE, RA, Sjogrens, thrombocytosis…

90
Q

what are the investigations for SLE?

A

bedside: urinalysis (haematuria and proteinuria)
lab: FBC (anaemia), elevated ESR with possible normal CRP, anti-nuclear, anti-dsDNA, anti-smith and antiphospholipid antibodies screen
imaging: MRI brain, echo

91
Q

what is the treatment of SLE?

A

avoid sun exposure, wear high SPF suncream, exercise and smoking cessation

mild: hydroxychlorine and methotrexate (inflammation), NSAIDs (inflammation and pain), low-dose prednisolone oral/intra-articular injection, methotrexate (skin and joint disease)
moderate: immunosuppressants e.g. azathioprine and ciclosporine, high-dose prednisolone
severe: (also lupus nephritis and CNS) high-dose oral prednisolone/IV methylprednisolone, in combo with immunosuppresants e.g. cyclophosphamide; possible biologics e.g. rituxmiab

92
Q

what is dermatomyositis?

A

idiopathic inflammatory myopathy with chronic inflammation of skin and muscles

93
Q

what is the cause of dermatomyositis?

A

genetic: PTP22 gene and HLA
triggers: meds, malignancy, viral infections, silica exposure
most have disease associated antibodies
can be due to malignancy = paraneoplastic syndrome

94
Q

what does myositis mean?

A

proximal muscle weakness and myalgia

95
Q

which cancers cause dermatomyositis?

A

lung, breast, ovarian and gastric

96
Q

what is the presentation of dermatomyositis?

A

muscle pain, fatigue and weakness
bilateral and proximal muscles affected
mostly affects shoulder and pectoral girdles
develops over weeks

heliotrope rash (purple rash on eyelids), Gottron’s papules (red papules on dorsum of finger joints, elbows and knees), shawl rash (erythema across upper back and shoulders), nailfold erythema

97
Q

what are the investigations for dermatomyositis?

A

muscle biopsy = definitive diagnosis
auto-antibody screen: anti-Jo-1, anti-Mi-2
creatine kinase >1000!

98
Q

what is the treatment of dermatomyositis?

A
guided by rheumatologist
physio and occupational therapy
1. corticosteroids (oral)
other: immunosuppressants (azathioprine), IV immunoglobulins, biological therapy (infliximab)
screen for underlying malignancy
99
Q

what is vasculitis?

A

inflammation of blood vessels

small, medium and large

100
Q

what are the different types of vasculitis and give examples

A

small: Henoch-Schonlein purpura, Churg-Strauss, microscopic polyangitis, Wegener’s granulomatosis
medium: poyarteritis nodosa, Churg-Strauss, Kawasaki
large: giant cell arteritis, Takayasu’s arteritis

101
Q

what is the presentation of vasculitis?

A

purpura (purple coloured non-blanching spots), joint and muscle pain, peripheral neuropathy, renal impairment, GI disturbance, anterior uveitis and scleritis, hypertension
also: fatigue, fever, weight loss, anorexia, anaemia
Kawasaki: strawberry tongue

102
Q

what are the investigations for vasculitis?

A

CRP and ESR elevated
anti-neutrophil cytoplasmic antibodies (ANCA):
2 types = p-ANCA (anti-MPO) and c-ANCA (anti-PR3)
p-ANCA: microscopic polyangitis and Churg-Strauss
c-ANCA: Wegener’s granulomatosis

103
Q

what is the treatment of vasculitis?

A

refer to rheumatology
treatment= steroids and immunosuppressants
steroids: oral prednisolone, IV hydrocortisone, nasal sprays, inhaled for lung e.g. Churg-Strauss
immunosuppressants: cyclophosphamide, methotrexate, azathioprine, rituximab
Henoch-Schonlein: supportive, simple analgesia, hydration
Kawasaki: aspirin and IV immunoglobulins

104
Q

what is Peutz-Jeghers syndrome?

A

a rare autosomal dominant condition that has intestinal polyps and lentigines in and around the mouth. intestinal polyps can cause intestinal obstruction