TO DO DERMATOLOGY Flashcards

1
Q

ACNE VULGARIS
Briefly describe the pathophysiology of acne

A

comedones are non-inflammatory lesions and can be open (blackheads) or closed (whiteheads). When the follicle bursts, inflammatory lesions such as papules and pustules may form. Excessive inflammation results in nodules, and cysts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

ACNE VULGARIS
Describe the signs of acne

A

MILD
- non-inflamed lesions (open + closed comedones) with few inflammatory lesions

MODERATE
- more widespread
- increased inflammatory papules + pustules

SEVERE
- widespread inflammatory papules pustules, nodules or cysts
- scarring

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

ACNE VULGARIS
Describe the treatment for acne

A

1st line
- topical retinoid +/- benzoyl peroxide,
- topical antibiotic (clindamycin)
- topical azelaic acid 20%

2nd line
- oral tetracycline (doxycycline, lymecycline) with topical benzoyl peroxide +/- topical retinoid
- COCP (co-cyprindiol)

3rd line
- isotretinoin (accutane)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

ECZEMA
what is the management?

A

MILD
- emollients
- mild corticosteroids (hydrocortisone 1%)

MODERATE
- emollients
- moderate corticosteroids (betamethasone 0.025% or clobetasone 0.05%)
- antihistamines

SEVERE
- emollients
- potent corticosteroid (betamethasone 0.1%)
- oral corticosteroid
- antihistamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

BCC
what are the risk factors for BCC?

A
  • male
  • UV exposure
  • fair skin
  • xeroderma pigmentosa
  • immunosuppression
  • arsenic exposure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

BCC
what is the clinical presentation?

A
  • pearly indurated flesh-coloured papule with rolled border
  • covered in telangiectasia
  • may ulcerate + create central crater
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

CELLULITIS
what are the most common causes?

A
  • s.aureus
  • s.pyogenes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

CELLULITIS
what are the risk factors?

A
  • break in cutaneous barrier
  • immunocompromise
  • other skin conditions (eczema, shingles)
  • history of cellulitis
  • obesity
  • venous insufficiency
  • lymphoedema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

CELLULITIS
how is it classified?

A

Erons classification

CLASS 1 - no systemic signs (outpatient/oral abx)

CLASS 2 - systemically unwell or systemically well but have comorbidity (possible admission)

CLASS 3 - significant systemic upset (admission required)

CLASS 4 - sepsis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

CELLULITIS
what is the management?

A

antibiotics
- 1st line = flucloxacillin
- if penicillin allergic = clarthromycin/erythromycin/doxycycline
- 1st line if near eyes/nose = co-amoxiclav
- severe infection = co-amoxiclav/cefuroxime/clindamycin
- MRSA = add vancomycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

CONTACT DERMATITIS
give some examples of common allergens that cause contact dermatitis

A

nickel sulfate
neomycin
formaldehyde
sodium gold thiosulfate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

CONTACT DERMATITIS
what are the risk factors?

A
  • occupation with frequent exposure to water and caustic materials e.g. labourers, chefs, farmers
  • history of atopic eczema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

CONTACT DERMATITIS
how long do symptoms last for?

A
  • ICD takes 3-6 weeks to resolve
  • ACD typically resolves within a few days
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

CONTACT DERMATITIS
what is the management for irritant contact dermatitis (ICD)?

A

1st line
- avoidance of irritant
- skin emollients

2nd line
- topical corticosteroids (hydrocortisone, betamethasone)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

CONTACT DERMATITIS
what is the management of allergic contact dermatitis (ACD)?

A

1st line
- avoidance of allergen
- topical corticosteroids (hydrocortisone, betamethasone)

2nd line
- topical calcineurin inhibitors (tacrolimus, pimecrolimus)

3rd line
- oral corticosteroids (prednisolone, dexamethasone)
- phototherapy (BUVB, PUVA)
- immunosuppressants (azathioprine, ciclosporin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

CUTANEOUS WARTS
what is the pathophysiology?

A

they are caused by human papillomavirus (HPV) types 2 and 4

The virus invades the skin through small cuts or abrasions and causes rapid growth of cells on the outer layer of the skin, leading to the formation of a wart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

CUTANEOUS WARTS
what are the risk factors?

A
  • use of public showers
  • close contact with a person with warts
  • skin trauma
  • immunosuppression
  • meat handlers
  • Caucasian ethnicity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

CUTANEOUS WARTS
what are the clinical features?

A

often asymptomatic
- firm rough papules or nodules
- interrupted skin lines over warts
- black dots within wart (thrombosed capillaries)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

CUTANEOUS WARTS
what is the management?

A

1st line
- watchful waiting
- topical salicylic acid

2nd line
- cryotherapy (freezing with liquid nitrogen)
- immunotherapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

FOLLICULITIS
what are the risk factors?

A
  • trauma (shaving, hair extraction)
  • topical corticosteroid use
  • diabetes mellitus
  • immunosuppression
  • drug-induced (corticosteroids, androgenic hormones, isoniazid, lithium)
  • hot tub use
    chronic inflammatory skin disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

FOLLICULITIS
what is hot tub folliculitis caused by?

A

pseudomonas aeruginosa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

FOLLICULITIS
what are the clinical features?

A

SYMPTOMS
- erythema
- papules (small, clusters)
- pustules (small, whiteheads)
- pruritis (localised)

SIGNS
- localised to shaving area
- blistering if severe
- subdermal mass (abscess if severe)
- raised eosinophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

FOLLICULITIS
what is the management?

A

CONSERVATIVE
- use clean sterile razors for shaving
- wear loose clothing
- antibacterial soap
- avoid hot tubs

MEDICAL
- mild = no treatment or topical antibiotics
- moderate bacterial = oral flucloxacillin (s.aureus) or oral ciprofloxacin (pseudomonas)
- moderate viral = oral aciclovir
- moderate fungal = ketoconazole, fluconazole, itraconazole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

CUTANEOUS FUNGAL INFECTION (RINGWORM)
what are the risk factors?

A
  • close contact with infected individuals or animals
  • damp, warm environments
  • participation in contact sports
  • shared facilities
  • immunocompromised states
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

CUTANEOUS FUNGAL INFECTION (RINGWORM)
what are the clinical features?

A

SYMPTOMS
- itching
- discomfort
- hair loss

SIGNS
- annular (ring shaped lesions)
- central clearing of the rash
- scaling of the skin
- erythema
- nail thickening and crumbling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

CUTANEOUS FUNGAL INFECTION (RINGWORM)
what is the management?

A

1st line
- topical antifungals (clomitrazole, terbinafine)
- skin care (avoid sharing towels, keep area clean and dry)

2nd line
- oral antifungals (terbinafine, itraconazole, fluconazole)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

HEAD LICE
what causes head lice?

A

parasites (Pediculus humanus capitis) cause an infestation called pediculosis capitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

HEAD LICE
what is the management?

A

1st line
- medicated lotions/sprays (dimeticone, isopropyl myrisate, cyclomethicone)
- wet combing (over 2 week period, days 1, 5, 9 and 13)
- insecticide (malathion)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

IMPETIGO
what are the most common causative organisms?

A

s.aureus = most common
s.pyogenes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

IMPETIGO
what is the management?

A

non-bullous
- localised = hydrogen peroxide 1% cream or topical antibiotic (fusidic acid, mupirocin)
- widespread = topical (fusidic acid or mupirocin) or oral antibiotics (flucloxacillin, clarithromycin or erythromycin)

bullous
- oral antibiotics (flucloxacillin, clarithromycin or erythromycin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

IMPETIGO
what is the general advice for school/work?

A
  • avoid sharing towels
  • stay away until lesions have healed, dry and crusted over or 48 hours after initiation of antibiotics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

LICHEN PLANUS
what is the pathophysiology?

A

immune response leading to T-cell mediated inflammation and keratinocyte apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

LICHEN PLANUS
what are the risk factors?

A
  • ages 40-60
  • hep C
  • drugs (thiazide diuretics, beta-blockers, NSAIDS and antimalarials)
  • vaccinations
  • stress
  • family history
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

LICHEN PLANUS
what are the clinical features?

A

SYMPTOMS
- itching
- oral discomfort
- hair loss

SIGNS
- purple, polygonal, flat-topped papules on wrists, ankles and lower back
- wickhams striae (white streaks overlying rash)
- rough thinning nails with grooves
- sore, red patches on vulva
- ring-shaped (annular) purple/white patches on penis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

LICHEN PLANUS
what is the management?

A

1st line
- topical corticosteroids
- conservative (wash with warm water, emollients, avoid tight clothing)

2nd line
- oral corticosteroids
- topical calcineurin inhibitors (tacrolimus)
- phototherapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

MALIGNANT MELANOMA
why can it affect GI tract and brain?

A

melanocytes are derived from neural crests
melanoma can occur anywhere neural cells migrate such as GI tract and brain

37
Q

MALIGNANT MELANOMA
what is the most common gene mutation associated with melanomas?

A

BRAF gene mutation - found in 50% of cases

38
Q

MALIGNANT MELANOMA
what are the risk factors?

A
  • increasing age
  • family history
  • pale skin (fitzpatrick type I and II)
  • red/blonde/light coloured hair
  • UV exposure
  • precursor lesions (dysplastic naevi)
  • previous skin cancer
  • immunosuppression
  • xeroderma pigementosum
39
Q

MALIGNANT MELANOMA
how do you assess a nevus?

A

ABCDE
A - asymmetry of lesion
B - border irregular
C - colour non-uniform
D - diameter >6 mm
E - evolution: changing shape, size or colour

40
Q

MALIGNANT MELANOMA
what are the different types?

A
  • superficial spreading (most common, horizontal growth)
  • nodular (may ulcerate + bleed, vertical growth)
  • lentigo maligna (seen in elderly, on face)
  • acral lentiginous (palms, soles and nailbed, more common in darker skin)
  • amelanotic (pink, lack pigment)
41
Q

MALIGNANT MELANOMA
what is the diagnostic criteria?

A

MAJOR (2 points each)
- change in size
- irregular shape/border
- irregular colour

MINOR (1 point each)
- largest diameter >7mm
- inflammation
- oozing or crusting
- change in sensation (including itch)

> 3 points = strong concerns about cancer

42
Q

MALIGNANT MELANOMA
what are the investigations?

A
  • dermoscopy (ABCDE)
  • excision biopsy

to consider
- sentinel node biopsy
- CT chest, abdomen and pelvis
- genetic studies

43
Q

MALIGNANT MELANOMA
how is it staged?

A

AJCC staging system

0 = confined to epidermis, melanoma in situ
1 = breslow thickness <2mm, no nodal involvement/mets
2 = breslow thickness 1-2mm with ulceration, or >2mm with/without ulceration, no nodal involvement/mets
3 = any thickness, involvement of local skin/LN
4 = any thickness, distant mets/LN

44
Q

MALIGNANT MELANOMA
what is the management?

A

EARLY STAGE (0-2)
- excision with adequate margin
- topical imiquimod

STAGE 3
- LN dissection
- radiotherapy
- resection of mets

STAGE 4
- systemic treatments (chemo/immunotherapy)
- radiotherapy
- resection of mets

45
Q

MALIGNANT MELANOMA
where does it tend to spread to?

A

lymph nodes
brain
bones
liver
lung
GI tract

46
Q

PITYRIASIS ROSEA
what is it?

A

inflammatory skin condition of uncertain aetiology, though an association with human herpesviruses 6 and 7

47
Q

PITYRIASIS ROSEA
what is the characteristic feature?

A

herald patch - single, oval scaly patch up to 10cm diameter and appears 2 weeks before rest of rash

48
Q

PITYRIASIS ROSEA
what are the clinical features?

A
  • herald patch
  • itchy rash (erythematous, oval, papular scaly patches on trunk + extremities)
  • fir tree appearance
49
Q

PITYRIASIS ROSEA
what is the management?

A
  • emollients
  • topical steroid = mild (hydrocortisone 1%) or moderate (betamethasone valerate 0.025%)
  • antihistamine (chlorphenamine) if itching affects sleep
50
Q

PITYRIASIS VERSICOLOR
what is it?

A

common superficial fungal infection caused by the Malassezia species, a yeast that is part of the normal skin flora

51
Q

PITYRIASIS VERSICOLOR
what are the risk factors?

A
  • hot and humid climates
  • excessive sweating
  • oily skin
  • immunocompromised
  • age (teenagers + young adults)
52
Q

PITYRIASIS VERSICOLOR
what are the clinical features?

A
  • itching (may also be asymptomatic)
  • rash on back, chest and upper arms
  • well-demarcated round/oval scaly patches
  • rash worsens with sun exposure
  • colour variation
53
Q

PITYRIASIS VERSICOLOR
what is the management?

A

1st line
- topical antifungals (ketonazole, selenium sulphide shampoo)
- sun protection

2nd line
- oral antifungals (fluconazole)

54
Q

PSORIASIS
what is the pathophysiology?

A
  • immune-mediated
  • abnormal T-cell activity that stimulates proliferation of keratinocytes
55
Q

PSORIASIS
what are the genetic factors that are strongly associated with psoriasis?

A

HLA-B13
HLA-B17

56
Q

PSORIASIS
what are the risk factors?

A
  • family history
  • obesity
  • smoking and alcohol consumption
  • medications (ACEi, BB, NSAIDs, lithium, hydroxychloroquine, steroid withdrawal, abx)
57
Q

PSORIASIS
what are the nail changes?

A
  • pitting
  • onycholysis
  • subungual hyperkeratosis
  • nail loss
58
Q

PSORIASIS
what is the management?

A

1st line
- patient education
- regular emollients
- topical corticosteroids + vit D for 4 weeks

  • if poor response, continue for 4 more weeks
  • if poor response after 8 weeks, stop corticosteroid + take vit D BD
  • if poor response after 12 weeks, potent topical steroid BD for 4 weeks

2nd line
- short-acting dithranol
- phototherapy

3rd line
- DMARDS (methotrexate, apremilast, ciclosporin)
- biologics (adalimumab, infliximab)

59
Q

SCABIES
what is the pathophysiology?

A
  • infestation with Sarcoptes scabiei
  • type IV hypersensitivity reaction
60
Q

SCABIES
how long does it take for symptoms to develop?

A
  • 1st time exposure = 3-6 weeks
  • it is contagious before the rash develops
  • in cases of re-infestation = 1-3 days
61
Q

SCABIES
what is the management?

A

1st line
- permethrin 5% cream
- topical crotamiton cream (symptomatic relief)

2nd line
- malathion aqueous 0.5%

62
Q

SCC
what is the pre-cancerous form of SCC?

A

actinic keratosis

63
Q

SCC
what are the invasive forms of SCC?

A
  • cutaneous horn
  • marjolin ulcer
  • keratoacanthoma
64
Q

SCC
what are the risk factors?

A
  • sun exposure and history of sunburns
  • use of tanning beds
  • chronic skin inflammation or injury
  • HPV infection
  • immunosuppression
65
Q

SCC
what are the clinical features?

A

SYMPTOMS
- itchy, tender or painful lesions
- ulcerating lesions
- lesions on sun-exposed areas

SIGNS
- scaly or erythematous lesions
- crusted or indurated lesions
- bleeding lesions
- irregular borders

66
Q

SCC
what is the management?

A
  • surgical excision (wide local or Mohs)
  • agressive cryotherapy
  • topical 5-fluorouracil
  • imiquimod
  • radiotherapy
67
Q

NECROTISING FASCIITIS
what are the different types?

A

it is classified according to causative organism
type 1 = polymicrobial (most common)
type 2 = group A haemolytic strep (s.pyogenes)
type 3 = gas gangrene
type 4 = fungal

68
Q

NECROTISING FASCIITIS
what are the risk factors?

A
  • recent trauma, burns or skin infection
  • increasing age
  • immunosuppressed
  • DM
  • SGLT-2 inhibitors
  • marine exposure
  • close contact with someone with necrotising fasciitis
69
Q

NECROTISING FASCIITIS
what are the clinical features?

A

EARLY
- intense pain
- skin puncture or injury
- flu-like symptoms
- erythema, warmness, swelling, tenderness
- hypersensitive site
- fever

LATE
- gas or crepitus
- skin necrosis
- fever
- purple/blue skin discolouration
- reduced sensation
- hypotension + tachycardia

70
Q

NECROTISING FASCIITIS
what is the management?

A
  • immediate surgical debridement
  • IV antibiotics (broad-spectrum)
  • supportive care
  • amputation
71
Q

URTICARIA AND ANGIOEDEMA
what are the causes?

A
  • viral infection
  • idiopathic
  • cold
  • heat
  • exercise
  • stress
  • medications - NSAIDS, antihypertensives
  • thyroid function
72
Q

URTICARIA AND ANGIOEDEMA
what is the management?

A
  • 1st line = non-sedating antihistamines (cetirizine, loratadine and fexofenadine)
  • 2nd line = leukotriene receptor antagonists - montelukast, or omalizumab

if symptoms persist a short course of oral corticosteroid can be used in addition to above

SYMPTOMATIC RELIEF
- calamine lotion
- topical menthol 1% aqueous cream
- sedating antihistamines (chlorphenamine) if disturbing sleep

73
Q

GANGRENE
what are the different types?

A

wet gangrene = infectious gangrene (necrotising fasciitis, gas gangrene)

dry gangrene = ischaemic gangrene secondary to reduced blood flow

74
Q

GANGRENE
what are the causes of dry gangrene?

A

atherosclerosis
peripheral artery disease
thrombosis
vasculitis
vasospasm

75
Q

GANGRENE
what are the clinical features of dry gangrene?

A

well-demarcated necrotic area without signs of infection

76
Q

GANGRENE
what are the clinical features of wet gangrene?

A

necrotic area is poorly demarcated from surrounding tissue
patients present with fever + sepsis

77
Q

GANGRENE
what are the investigations for wet gangrene?

A

BLOODS
- FBC
- blood cultures
- inflammatory markers (CRP + ESR)

IMAGING
- X-ray, USS or CT scan (to assess extent of disease)

TISSUE BIOPSY
- to identify causative organism

78
Q

GANGRENE
what are the investigations for dry gangrene?

A

BLOODS
- FBC
- inflammatory markers (CRP + ESR)
- glucose level
- coagulation profile

IMAGING
- doppler USS or angiography

TISSUE BIOPSY
- not typically needed

79
Q

GANGRENE
what is the management of wet gangrene?

A
  • surgical debridement
  • amputation
  • broad-spectrum antibiotics
80
Q

GANGRENE
what is the management of dry gangrene?

A
  • surgical debridement
  • amputation
81
Q

GANGRENE
what is the cause of gas gangrene?

A

clostridium perfringens

82
Q

GANGRENE
what are the clinical features of gas gangrene?

A
  • acute onset severe localised pain
  • minimal local inflammation
  • skin darkening + spreading erythema
  • fever (hot to touch)
  • gas production in affected area
  • distinctive potent smell from infected area
83
Q

URTICARIA AND ANGIOEDEMA
what are the risk factors?

A
  • allergens (food, medications, insect stings)
  • physical stimuli (pressure, cold, heat)
  • infections (viral, bacterial)
  • autoimmune processes
  • stress + emotional factors
84
Q

ONYCHOMYCOSIS
what are the causative organisms?

A
  • dermatophytes (trichophyton rubrum) = most common
  • yeasts (candida)
  • non-dermatophyte moulds
85
Q

ONYCHOMYCOSIS
what are the risk factors?

A
  • increasing age
  • diabetes mellitus
  • psoriasis
  • repeated nail trauma
86
Q

ONYCHOMYCOSIS
what is the management?

A
  • asymptomatic = not treatment

limited involvement (<50% nail affected, <2 nails affected, superficial)
- 1st line = topical amorolfine 5% nail lacquer, 6m for hands + 9-12m for feet

extensive dermatophyte infection
- 1st line = oral terbinafine, 6w-3m for hands + 3-6m for feet

extensive candida infection
- 1st line = oral itraconazole, ‘pulsed’ weekly therapy

87
Q

ROSACEA
what are the clinical features?

A
  • typically affects nose, cheeks + forehead
  • flushing is often 1st symptom
  • telangiectasia
  • later develops into persistent erythema with papules + pustules
  • rhinophyma
  • ocular involvement (blepharitis)
  • sunlight may exacerbate symptoms
88
Q

ROSACEA
what is the management?

A

CONSERVATIVE
- high factor sun cream
- camouflage cream to conceal redness

SYMPTOM CONTROL
- flushing = topical brimonidine gel or oral propranolol
- telangiectasia = laser therapy
- papules/pustules
- mild-moderate = 1st line - ivermectin (other options = topical metronidazole, topical azelaic acid)
- mod-severe = topical ivermectin + oral doxycycline