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Surgery > Skin > Flashcards

Skin Flashcards

1
Q

Lymphatic drainage of skin

A

Above umbilicus: axillary nodes
Below umbilicus except over popliteal fossa: superficial inguinal nodes
Skin over popliteal fossa: popliteal nodes

Right lymphatic duct drains everything above umbilicus on right
Thoracic duct drains everything else

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2
Q

What are school sores

A

Impetigo = infection of superficial layers of epidermis

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3
Q

MC skin infection in children

A

Impetigo

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4
Q

Aetiology of impetigo

A

Staph aureus (consider MRSA)
GAS (strep pyogenes)

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5
Q

Forms of impetigo and characteristics

A

Bullous (staph aureus only)
- Neonates
- Trunks and limbs
- Flaccid bullae that rupture and release exudate forming honey coloured crust

Non-bullous (MC)
- Children aged 2-5yo
- Nares and around mouth and @ sites of trauma (insect bites, abrasions, burns etc - ESP 2˚ infection of scabies)

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6
Q

Clinical features of impetigo

A

Erythematous (2-4mm) macules/vesicles/bullae –> exudate and honey coloured crust
Rapid spread to adjacent skin

No pain but can be very itchy
Usually no systemic features

Usually no scarring but GAS more likely to + can get post-inflammatory pigmentation in darker skin

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7
Q

Investigations for impetigo

A

Usually clinical Dx

If Tx fails: lift corner of crusted lesion and swab for MC&S

If recurrent: consider nasopharyngeal/axillary/perineal swab for MRSA carriage

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8
Q

DDx of impetigo

A

HSV (esp. bullous lesions around mouth)
VZV
Scabies
Staphylococcal scalded skin syndrome
Childhood discoid lupus
Insect bites
Bullous pemphigoid
Eczema or contact dermatitis

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9
Q

Features, cause, epidemiology of staphylococcal scalded skin syndrome

A

Syndrome 2˚ to staphylococcal infection resulting in fever and generalised erythematous rash with sloughing of superficial skin layers and + Nikolsky sign.

Staph exotoxin causes destruction of keratinocyte attachments in stratum granulosum only.

Affects neonates and pts with renal impairment

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10
Q

What is Nikolsky sign

A

Epidermal separation on manual stroking of skin

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11
Q

Complications of impetigo

A
  • Scarlett fever
  • PSGN
  • ARF
  • SSS
  • STSS
  • Lymphadenitis
  • Osteomyelitis
  • Septic arthritis
  • Pneumonia
  • Septicaemia
  • Eczema pts: rapidly spreading infection and worse Sx
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12
Q

What is Scarlett fever

A

Syndrome characterised by blanching, sandpaper like body rash, circumoral pallor and strawberry tongue in setting of GAS pharyngitis

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13
Q

Mx of impetigo

A
  • 2% mupirocin ointment TDS for 7 days
  • Exclusion from school/daycare until 24 hours after Tx and until all lesions are no longer weeping and have crusted over
  • Hygeine (water and soap wash, airdrying, handwashing) and no sharing towels, bed linen etc.
  • If widespread, systemic features, complications, recurrent etc: PO cephalexin
  • Can use dilute bleach baths to soften crusts if extensive
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14
Q

When is impetigo no longer infectious

A

Once all lesions are crusted over and no longer weeping

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15
Q

What is cellulitis

A

Infection of deep dermis and SC tissues

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16
Q

What is erysipelas

A

Infection of upper dermis and superficial lymphatics

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17
Q

Aetiology of cellulitis and erysipelas

A

MC = staph aureus and strep pyogenes (MC in erysipelas)

May be an obvious entry to skin providing entry point for infection e.g., abrasian/laceration/bite

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18
Q

Clinical features of cellulitis and erysipelas

A

Erythema
Swelling
Warmth
Acute pain and tenderness
+/- Dischage

Rapidly spreading to surrounding skin

Erysipelas = infected skin is demarcated from non-infected skin

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19
Q

Investigations for cellulitis and erysipelas

A

Usually none required

Systemic Sx: FBC, CRP, blood cultures
Close to bone/OM risk: XR or MRI
Discharge: swab for MC&S and HSV PCR if vesicles
Consider biopsy if immunocompromised or subacute/chronic

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20
Q

Management of cellulitis in <1 mo neonate

A

< 1mo: admit for IV antibiotics in consultation with ID

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21
Q

Mx of mild cellulitis in infant/child/adult >1mo

A

PO cefalexin or flucloxacillin as outpatient
+ cotrimoxazole if MRSA

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22
Q

Mx of moderate cellulitis in infant/child/adult > 1mo

A

Admit for IV flucloxacillin 2g (50mg/kg in chikd) 6 hourly and lignocaine/prilocaine gel
+ cotrimoxazole if MRSA

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23
Q

Mx of severe cellulitis in infant/child/adult > 1mo

A

Rapidly progressive or high temp/HR despite 24 hour Tx

Admit for IV flucloxacillin and vancomycin and lignocainne
+ clindamycin if shock
+ surgical review to exclude deeper infection/NF

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24
Q

Mx of erysipelas or if Streptococcus pyogenes suspected in cellulitis

A

No systemic features: phenoxymethylpenicillin (V) 500 mg (child: 12.5 mg/kg) 6 hourly for 5 days

Systemic features: IV benzylpenicillin 1.2 g (child: 50 mg/kg) 6-hourly

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25
Q

Complications of cellulitis

A

Recurrent infection

Deeper infection e.g., OM/NF
Abscess

Systemic: septicaemia, IE, septic arthritis, STSS, ARF, PSGN

Thrombophlebitis
Lymphodema

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26
Q

Complications of orbital cellulitis

A

Cavernous sinus thrombosis
IC abscess
Blindness

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27
Q

What is necrotising fasciitis

A

Deep rapidly spreading tissue infection resulting in necrosis of subcutaneous tissue, fascia, and muscle

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28
Q

What causes necrotising fasciitis

A

MC: 2˚ strep pyogenes or anaerobes

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29
Q

How does necrotising fasciitis present

A

Severe pain/tenderness out of proportion with examination findings
Palpable crepitus (subcutaneous gas)
Violaceous bullae and necrosis
Hard (‘wooden’) subcutaneous tissue that is painful on palpation
Oedema beyond the margin of erythema
Cutaneous anaesthesia

Fever and systemic Sx (tachycardia, tachypnoea, hypotension, palpitations, light-headed, N, V)

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30
Q

Mx necrotising fasciitis

A

Emergent surgical consultation: fasciotomy and debridement

IV meropenem, vancomycin, clindamycin and analgesia

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31
Q

What is folliculitis

A

Inflammatory reaction of hair follicle presenting as pustules/papules on erythematous base

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32
Q

Causes of folliculitis

A

Non-infective: maceration, obesity, heavy sweating, contact with occlusive substances (eg oils), shaving/ waxing, drugs e.g., steroids

Infective: staph aureus, pseudomonas (hot tubs/spas), malassezia, dermatophytes, HSV

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33
Q

Ix of infective folliculitis

A

Swab for MC&S +/- HSV PCR +/- fungal culture request

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34
Q

Tx infective folliculitis:

A

Warm compresses, antiseptic washes, clean sharp razors when shaving

ABx guided by susceptibility results e.g., fluclox if staph aureus

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35
Q

Initial episode HSV Tx

A

Topical LA
Severe: Valaciclovir 1 g orally, 12-hourly for 7 days

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36
Q

Cutaneous manifestations of HSV

A

Herpetic whitlow
Eczema herpeticum

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37
Q

Wart aetiology

A

HPV 1, 2, 4, 27, 57

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38
Q

Wart Tx

A

Usually resolve spontaneously within a few months to 2 years, so in most cases treatment is not needed

Topical salicylic acid
Liquid nitrogen cryotherapy

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39
Q

What is this

A

Pityriasis veriscolor

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40
Q

What is pityriasis versicolor

A

Common chronic condition presenting as hyper or hypopigmented patches caused by Malassezia yeasts, which are normal skin commensal organisms

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41
Q

Dx and Mx of pityriasis versicolor

A

Diagnosis is usually clinical.

General measures (eg showering after excessive sweating) can help.

Can Tx with econazole 1% topical solution and ketoconazole 2% shampoo –> oral fluconazole if not responding

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42
Q

What is tinea

A

Tinea (ringworm) is caused by dermatophytes, which can infect the skin, scalp or nails and usually presents as an annular or arcuate rash (definite edge and central clearing) that is scaly and itchy

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43
Q

What is a kerion

A

Acute form of tinea capitis, presenting as a boggy, painful, inflammatory pustular mass with associated alopecia
MC in children

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44
Q

Dx of tinea

A

Skin scrapings, subungual debris, nail clippings or plucked hair: MC&S

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45
Q

When is topical Tx used in tinea

A

Recent onset of localised tinea affecting the trunk (including groin), limbs, face, or between the fingers or toes

46
Q

When is oral Tx used in tinea

A

Tinea that:
- is widespread or established (particularly on the feet)
- has not responded to topical antifungal therapy
- recurs soon after treatment
- has been inappropriately treated with a topical corticosteroid
- is on the scalp, palms or soles
- is inflammatory, hyperkeratotic, vesicular or pustular

Must have MC&S before commencing oral Tx

47
Q

Tx for tinea

A

Topical = terbinafine 1% cream or gel once or twice daily for 7-14 days

Oral: terbinafine 250mg PO once daily for 2 weeks

48
Q

Causes of necrotising fasciitis

A

Type I: polymicrobial infection caused by an anaerobe (e.g., bacteroides) plus a facultative anaerobe (e.g., escherichia coli, enterobacter, klebsiella, proteus) or non-group A streptococcus with or without Staphylococcus aureus.

Type II: monomicrobial infection –> MCC = Streptococcus pyogenes (GAS)
- or staph aureus/MRSA

49
Q

Necrotising fasciitis pathophysiology

A

Bacteria introduced into skin and soft tissue from minor trauma, puncture wounds, or surgery (or no ID’d cause)

Infection extends through the fascia but not into the underlying muscle, and tracks along fascial planes extending beyond the area of overlying cellulitis.

50
Q

Necrotising fasciitis Ix

A

Immediate surgical exploration
- finger test performed under LA at bedside involving 2cm incision to deep fascia –> minimal resistance to finger dissection, abscence of bleeding, presence of necrotic tissue, murky/greyish dishwater fluid = suggests

MC&S from blood cultures and tissue specimens obtained in surgical debridement

FBC, UEC, CRP, CK, LFT, coags, VBG/ABG

51
Q

What is gangrene

A

Subtype of coagulative necrosis/complication of necrosis characterised by the decay of body tissues

52
Q

What are the types and causes of gangrene

A

Infectious/wet: caused by NF or gas gangrene (clostridium perfringens)

Ischaemic/dry: atherosclerosis, diabetes-associated microangiopathy, thrombosis in hypercoagulable states (APS, IVDU, vasculitis, malignancy), vasospasm (raynaud, coacaine)

53
Q

Clinical presentation of gangrene

A

Pain
Oedema, swelling
Skin discolouration
Crepitus in gas gangrene

54
Q

Ix of gangrene

A

FBC, CRP, UEC, LFT, LDH, coags (baseline)
Blood cultures (+ in wet)
Plain XRs (may demonstrate gas in soft tissues)
CT or MRI of affected site (abscess/enhancement/oedema/thickening in fascia)
Doppler USS (ischaemic type)

55
Q

Tx of gangrene

A

NF as per NF
Gas gangrene: IV benzylpenicillin and clindamycin, supportive therapy +/- debridement/amputation
Ischaemic: IV heparin + surgical revascularisation/thrombolysis

56
Q

What is Fournier gangrene

A

Synergistic gangrene of the genitalia, usually following genital trauma (eg postpartum) or spread from a perianal, retroperitoneal or urinary tract infection.
Can rapidly spread to anterior abdominal wall and gluteal muscles

Ix and Mx as per NF

57
Q

Risk factors for melanoma

A

UVB induced DNA damage: chronic sun exposure or intermittent high intensity exposure

Fair skin
Xeroderma pigmentosa
Albinism

PMHx of NMSC
FHx of melanoma

Multiple dysplastic naevi
Familial atypical mole melanoma syndrome

Immunosuppression

58
Q

What is the UV signature in melanoma

A

C > T or CC > TT nucleotide substitutions

59
Q

What is a common naevus and it’s pathophys

A

Benign neoplasm at dermal-epidermal junction

BRAFV600E expression in melanocytes –> limited period of proliferation followed by permanent growth arrest secondary to accumulation of p16 (cyclin dependent kinase inhibitor –> cell cycle arrest). Other protective/attritional factors include p14 accumulation (induces apoptosis), replicative senescence (telomere shortening) and immune surveillance

60
Q

Types of common naevi

A

Junctional: nest of round melanocytes at dermal-epidermal junction
Compound: extension into dermis
Intradermal: loss of epidermal nests/junctional component

61
Q

What is melanoma in situ

A

Intraepidermal malignant melanocytes = definitive precursor lesion to malignant melanoma

62
Q

Which type of melanoma is not associated with MIS

A

Nodular

63
Q

What are the types of MIS

A

Lentigo maligna
- Lentiginous growth: linear pattern of proliferation of melanocytes along basal cell layer of epidermis
- CSD melanoma

MIS with pagetoid growth
- Pagetoid growth: upward spreading of melanocytes along adnexal structures into epidermis
- Non-CSD melanoma and BRAF V600E

64
Q

What is malignant melanoma

A

Malignant proliferation of melanocytes breaching dermis

65
Q

What are the growth patterns of malignant melanoma

A

Radial: horizontal spread along superficial dermis and epidermis
Vertical: downwards invasion into deep dermis as expansile mass (Breslow thickness)

66
Q

What are the types of malignant melanoma

A

Superficial spreading (MC)
Nodular
Lentigo maligna
Acral lentiginous

67
Q

Describe superficial spreading melanoma

A

Flat irregular macule with variable pigmentation MCly on back or chest in men and extremities women

68
Q

Describe nodular melanoma

A

Smooth nodule appearing on back/chest in men or extremities in women

Most aggressive form with worst prognosis and no MIS or radial growth phase

69
Q

Describe lentigo maligna

A

Large irregular patch with irregular pigmentation MCly on face in elderly men

70
Q

Melanoma clinical features

A

A = asymmetry
B = irregular borders
C = colour is variegated
D = diameter > 6mm
E = evolving

71
Q

Describe acral lentiginous melanoma

A

Occurs as a brown-black macule on glabrous skin (palms/soles), nail bed, and mucous membranes in non-Caucasians and is unrelated to UVB exposure

72
Q

Histology of melanoma

A

Melanocytes with atypia: large N-C ratio, rregular shape, clumped chromatin
Asymmetry
Poor circumscription
Absent maturation
> 6mm

73
Q

Prognostic factors for melanoma

A

Breslow thickness
Ulceration
Degree of LN involvement
Distant metastases?
Mitoses
Clark level

74
Q

Describe Breslow Thickness stages

A

Stage 1: 0-1mm
Stage 2: 1-2mm
Stage 3: 2-4mm
Stage 4: > 4mm

75
Q

Describe the Clark Levels

A

1 = confined to epidermis
2 = invaded papillary dermis
3 = contact with reticular dermis
4 = invaded reticular dermis
5 = invaded hypodermis

76
Q

Where does melanoma metastasise and how

A

LNs, liver, lungs, brain, bone

Parallel dissemination via vascular and lymphatic routes rather than in serial

77
Q

Dx and staging of melanoma

A
  1. Examination and dermatoscopy
  2. Excisional biopsy with 2mm lateral margins in ellipsoid shape and depth should include upper layer of SC fat using Langer lines as a guide
  3. Melanoma confirmed: wide local excision with margins determined by tumour thickness, site, age, type, comorbidities etc. (depth same as lateral margin but not deeper than deep fascia)
  4. Breslow thickness > 1mm or lymphadenopathy/signs of mets: Lymphatic mapping with LN scintigraphy and sentinel node biopsy
  5. Staging with CT and PET if metastatic disease
78
Q

Mx of melanoma

A
  1. Wide local excision
  2. Refer to MDT or oncologist if metastasis
  3. Systemic therapies include BRAF inhibitors, Treg stimulators, KIT inhibitors etc depending on subtype
    - CTLA4 antibody = ipilimumab
    - PD1 antibody = nivolumab
  4. Regular skin checks: every 3 months for 2 years –> every 6 months for 2 years –> yearly
79
Q

What is squamous cell carcinoma

A

Malignant proliferation of squamous cells that crosses epidermal BM into dermis

80
Q

Epidemiology of SCC

A

2nd MC skin cancer
2M > F

81
Q

Risk Factors SCC

A
  • UVB-induced skin damage
    o Exacerbated by Fitzpatrick skin types I and II, xeroderma pigmentosa, albinism
  • Chemical exposure e.g., arsenic, coal tars from smoking, hydrocarbons
  • Human papillomavirus
    o 1, 2, 4, 11 –> warts
    o 16, 18, 31, 33 –> oncogenic
  • Immunosuppression (HIV, transplant)
  • Chronic inflammation –> burns, draining sinus, scars, ulcers, Lichen planus, TB, leprosy = Marjolin ulcer
  • Exposure to ionising radiation (x-ray)
82
Q

Precursors and variants for SCC

A
  • Actinic keratosis –> scale/plaque on face, back, or neck
  • Squamous cell carcinoma in situ –> atypical keratinocytes confined to surface (not through BM) appearing as scaly red plaques
  • Keratoacanthoma –> grows rapidly then regresses over months (cup filled with keratin debris)
83
Q

Clinical features of SCC

A
  • Ulcerated nodular hyeperkeratotic scale
  • Red everted edges, easily bleeds, edges are like granulation tissue
  • MC sites = face, lower lip, ears, hands, neck
  • Unlikely to metastasise (MC if on scar or skin not exposed to sun) –> LN, liver, lung, bone, brain
84
Q

Histopathology of SCC

A
  • Atypical squamous cells, keratinisation (keratin pearls), invasion of dermis
  • Actinic keratosis: dermal elastosis, some cytologic atypia in lower epidermal layers, hyperkeratosis etc.
  • SCCIS: atypical cells involve entire epidermis
85
Q

Prognosis for SCC

A

usually good unless metastasised

86
Q

Epidemiology of BCC

A

MC malignant skin Ca
MC in Aus
2M > F

87
Q

Risk factors for BCC

A
  • UBV-induced DNA damage (++ if albinism, xeroderma pigmentosa, Fitzpatrick skin types I and II)
  • Nevoid BCC/Gorlin syndrome (AD)  PTCH1 mutation associated with multiple BCCs at young age + other malformations
  • Scars, immunosuppression, chemicals (arsenics, tars)
  • P53 abnormality in 50%
88
Q

Clinical features BCC

A
  • Pearly nodule with rolled borders and central ulceration, surrounded by telangiectasia
  • MC sites = upper lip, around eyelids, forehead, nose
  • Nodular and superficial types
89
Q

Histology of BCC

A
  • Proliferating basal cells, retraction artefact, peripheral palisading nuclei (long axes run in parallel alignment)
  • Nodular may extend deep into dermis as cords with hyperchromatic nuclei surrounded by LOs and fibroblasts while superficial (often mistaken for psoriasis or seborrheic keratosis) extends over surface only
90
Q

Prognosis/complications of BCC

A

Excellent; low metastasis; but can be deeply infiltrative/perineural invasion
- Great nerve insertion area on face is infraorbital foramen: BCC can get in via infraorbital nerve which is a branch of maxillary from trigeminal nerve –> MUST travel with stroma to invade –> meningitis

91
Q

What is a Merkel Cell tumour

A

Worst prognosis
- Painless firm non-tender red-blue nodule on head/neck
- May be associated with polyomavirus

92
Q

NMSC Mx

A
  1. Excision biopsy (otherwise shave for a thin lesion and punch for a thick lesion) with margins of 3-5mm (5mm for scc 2-3mm for BCC but 4-5 if unclear BCC borders)
    - Punch biopsy favoured for non-pigmented lesions cos allows adequate depth
  2. Mohs micrographical if large/difficult
  3. Consider liquid nitrogen cryotherapy, imiquimod, curettage, cautery in superficial
  4. Radiotherapy as an adjunct if perineural spread or risk of metastasis
  5. In SCC suspected LN mets should be confirmed with FNA cytology
93
Q

What are furuncles

A

Deep folliculitis beyond dermis with abscess formation in subcutaneous tissue

94
Q

What are complications of facial furuncles

A

Periorbital cellulitis
Cavernous sinus thrombosis

95
Q

What are carbuncles

A

Confluent furuncles forming an inflammatory mass (abscess and skin necrosis may be present)

96
Q

Complications of necrotitis fasciitis

A

Severe necrosis resulting in amputation of affected limb, sepsis, DIC, organ dysfunction e.g., AKI, death even with adequate Tx

97
Q

Tx of carbuncles and furuncles

A

Incision and drainage

Adjunctive antibiotic treatment increases cure rate and prevents recurrence and should be considered for abscesses with diameter > 5cm
- dicloxacillin/flucloxacillin 500 mg PO 6-hourly for 5 days
- trimethoprim + sulfamethoxazole 160mg + 800mg PO 12 hourly for 5 days if MRSA suspected

98
Q

How does tetanus occur

A

Clostridium tetani neurotoxins = tetanospasmin reaches CNS through retrograde axonal transport –> inhibits release of inhibitory NTs e.g., GABA and glycine –> uninhibited activation of alpha motor neurons resulting in muscle spasms, rigidity and autonomic instability

99
Q

Clinical features of tetanus

A
  • Triad of trismus, risus sardonicus, opisthotonos
  • Triggers = noise, handling, light etc.
100
Q

Complications of tetanus

A

o Laryngospasm/respiratory muscle spasm  hypoxia or resp failure
o Autonomic dysfunction (tachycardia, labile BP, sweating, arrhythmia) circulatory arrest and shock
o Oesophageal spasm  dysphagia
o Urethral spasm  urinary retention
o Aspiration
o Exhaustion

101
Q

What is pilonidal disease

A

Local inflammation of superior midline gluteal cleft

102
Q

Risk factors and pathophys for pilonidal disease

A
  • M > F, 15 -25yo, deep gluteal cleft, hairy, obese, poor anal hygiene/local irritation, sedentary, FHx
  • Sitting  breakage of hair follicles in vulnerable skin with a deep natal cleft  open pore/pit  collect debris/broken hair  negative pressure on movement  further penetration of hair into local SC tissue  pilonidal sinus  local tissue inflammation within sinus
103
Q

Presentation and complications of pilonidal disease

A
  • Complications = acute infection (abscess) or fistula
  • Presentation:
    o May be asymptomatic
    o Sinus tract opening in sacrococcygeal region
    o Acute e.g., abscess  purulent discharge, fever, pain, fluctuant erythematous swelling
    o Chronic  mucoid/purulent/blood-stained discharge from abscess/fistula, localised pain
104
Q

Tx for pilonidal disease

A
  • Treatment: incision and drainage
  • A pilonidal sinus is a cyst or abscess in the natal cleft. Treatment is primarily surgical. Antibiotics are not indicated unless cellulitis is present, and therapy should be guided by the results of cultures and susceptibility testing. If cultures are not available, treat as for uncomplicated (nonsevere) diverticulitis (ETG)
105
Q

What is Hidradenitis Suppurativa

A

Occlusion of apocrine pilosebaceous follicles of axillae, inguinal area, and around breasts  painful lumps under skin in these areas

106
Q

Presentation and complications of Hidradenitis Suppurativa

A
  • inflammatory cysts, discharge, odour, pain
  • abscesses, sinus tracts, scarring
107
Q

What is Hidradenitis Suppurativa associated with

A
  • metabolic disease, obesity, smoking
108
Q

Tx of Hidradenitis Suppurativa

A

o Wear lose clothing, lose weight, eat healthy, stop smoking
o Topical clindamycin
o Doxycycline PO +/- oral corticosteroids +/- oral retinoids +/- biologics e.g., infliximab +/- spironolactone
o I&D relieves abscess Sx immediately but can cause scarring/recurrence

109
Q

What is an epidermal cyst and how does it present

A

Keratin-filled cyst lined by stratified squamous epithelial
Slow-growing painless, firm, mobile, nodule MC on head/face/neck/back/genitals

110
Q

How is an epidermoid cyst Tx

A
  • Asymptomatic  none
  • Inflamed  intralesional steroids
  • Infected/pressure Sx  PO Abx and total surgical excision
111
Q

What is a lipoma and how does it present

A

Common benign tumour of SC soft tissue made up of mature fat cells
- Non-tender, slow growing, soft, rubbery, round tumour
- MC on shoulders, back, head, neck

112
Q

How is lipoma Tx

A

Surgical excision considered if painful, for cosmetic reasons or if growing rapidly or firm on palpation

Surgery (17 decks)

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