Superficial lesions Flashcards
(91 cards)
1
Q
What is a lipoma?
A
Benign tumour of mature fat cells
2
Q
Do lipomas undergo malignant change?
A
No, or very rarely.
Liposarcomas arise de novo
3
Q
How to treat a lipoma?
A
- watch and wait
- remove if patient choice, painful, bad cosmesis.
- need to remove capsule or recurs?
4
Q
Lipomas variants
A
- angiolipomas: prominent vasc component
- hibernomas: brown fat cells
- Bannayan-Zonana syndrome: multiple lipomas, macrocephaly, haemangiomas
5
Q
Dercum’s disease
A
aka Adiposis dolorosa: multiple painful lipomas associated with peripheral neuropathy
6
Q
Liposarcoma classficiation
A
1 - well-differentiated
2 - myxoid and round cell (poor-dif)
3 - pleomorphic
7
Q
What are the complications of a sebaceous cyst?
A
- infection
- ulceration
- calcification (trichilemmal cyst)
- sebaceous horn formation
- malignant change
8
Q
Sebaceous cyst treatment
A
- watch and wait if small, asymptomatic
- elliptical skin excision including capsule to prevent recurrence
9
Q
Different histological subtypes of sebaceous cyst?
A
- Epidermal: from infundibular portion of hair follicles
- Trichilemmal: from hair follicle epithelium, more common on scalp
10
Q
Gardner’s syndrome
A
- multiple epidermal cysts
- adenomatous polyposis of colon
- multiple skull osteomata
- desmoid tumours
11
Q
What is a ganglion?
A
Cystic swelling related to a synovial lined cavity (joint or tendon sheath).
12
Q
Ganglion differential
A
- bursae
- cystic protrusions from arthritic joints
- benign giant cell tumours of flexor sheath
- rarely, malignant e.g. synovial sarcoma
13
Q
Ganglion treatment
A
- watch and wait
- aspiration + 3 weeks immobilisation
- complete excision including neck at origin
14
Q
Complications of surgical ganglion treatment
A
- wound complications e.g. scar, haematoma, infection
- recurrence
- damage to adjacent neurovascular structures
15
Q
Neck triangle borders
A
- anterior: anterior border of sternocleidomastoid, midline, ramus of mandible
- posterior: anterior border of trapezius, clavicle, posterior border of sternocleidomastoid
16
Q
Midline neck lumps DDx
A
- Solid: thyroid swelling
- Cystic: thyroglossal cyst
17
Q
Anterior triangle lump DDx
A
- solid: lymphadenopathy or carotid chemodectoma
- cystic: branchial cyst, cold abscess (TB)
18
Q
Posterior triangle lump DDx
A
- solid: lymphadenopathy
- cystic: pharyngeal pouch or cystic hygroma
19
Q
What is a sternomastoid tumour?
A
an ischaemic contracture of a segment of muscle seen in first 1-2 weeks of life following complicated birth. Usually resolves over 4-6 months
20
Q
Cervical lymphadenopathy causes
A
L - lymphoma, leukaemia
I - infection (tonsillitis, TB, CMV, EBV, HIV)
S - sarcoidosis
T - tumours, primary + secondary
21
Q
Cervical lymphadenopathy investigations
A
Bloods - FBC, ESR, TFTs, ACE, monospot/paul-bunnell
Radiological - USS, CT, MRI
Histological - FNAC, excision biopsy
22
Q
Cervical lymphadenopathy FNAC results
A
- if SCC or TB, don’t perform excision biopsy
- if adenocarcinoma, lymphoma or other infection/inflammatory cause, do excision biopsy
23
Q
What is the arterial supply to thyroid gland?
A
- superior thyroid artery from external carotid
- inferior thyroid artery from thyrocervical trunk from subclavian artery
- these two anastamose behind the thyroid gland
24
Q
What do you know about solitary thyroid nodules?
A
- F:M = 4:1
- commonest 40s-50s
- 10% malignant in middle-aged
- 50% malignant in young and elderly
- FNAC most important investigation
25
Investigation of solitary thyroid nodule
Triple assessment
- clinical hx and exam
- USS
- FNAC
26
What do you know about thyroid adenomas?
- most follicular adenomas
- 2-4cm encapsulated
- indistinguishable from carcinomas on FNAC
- need surgical excision to confirm diagnosis
27
Thyroid malignancy
- Papillary - 70%, commonest in young, lymphatic spread
- Follicular - 15%, mean age 50, haematological spread
- Medullary - 8%, parafollicular C cells, calcitonin, 10% MEN2a/b
- Anaplastic - 5%, elderly
- Lymphoma - 2%
28
Multiple endocrine neoplasia types
All Autosomal dominant
MEN 1 - pancreatic islet cell tumour, pituitary adenoma, primary hyperparathyroidism
MEN 2a - phaeo, medullary thyroid Ca, primary hyperparathyroidism
MEN 2b - phaeo, medullary thyroid Ca
29
Feature of multinodular goitre
- progression from smooth goitre to nodular
- middle-aged women
- family history
- malignant change in 5%
- mild hyperthyroidism (Plummer's syndrome) or euthryoid
- no eye signs
30
MNG management
- often no intervention
- investigate prominent nodule or if malignancy features
- TFTs, USS + FNAC, CX
- Remove goitrogens (cabbage)
- Low dose thyroxine causes regression in 50-70%
- If thyrotoxic, treat as Graves
- radioiodine if unfit for surgery
- bilateral subtotal thyroidectomy
- total thyroidectomy + thyroxine reduces maligancy risk (best option)
31
Indications for MNG surgery
- Mechanical - obstructive symptoms
- Malignancy
- Medical treatment failure - thyrotoxic
- Mediastinal extension - unable to FNAC or monitor clinically
- Marred beauty - cosmetic
32
Difference between TMNG and Graves'
TMNG - older, nodular, no eye signs, AF in 40%, no AI association
Graves' - younger, diffuse, eyes signs, AF uncommon, associated AI diseases
33
Causes of diffusely enlarged thyroid gland
- simple colloid goitre
- Graves' disease
- thyroiditis (Hashimoto's, de Quervain's, Riedel's)
34
What do you know about simple colloid goitres?
- commonest thyroid abnormality
- physiological hyperplasia or defection hormone production
- Causes: iodine deficiency, puberty, pregnancy, goitrogens, drugs (lithium, amiodarone), congenital defects (rare)
35
Graves' treatment
- Medical: anti-thyroid drugs (carbimazole, propythiouracil) inhibit thyroid peroxidase, beta-blockers (propanolol) provide symptomatic relief
- Radioiodine: Absolute CI = pregnancy, lactation. Risks = early hyperthyroidism, late hypothyroidism, late hyperparathyroidism
- Surgery: Bilateral subtotal thyroidectomy or total. Good for relapse, pregnant patients, those wanting to get pregnant in next 4 years, large goitres
36
Thyroidectomy complications
General or specific
- Immediate: haemorrhage + airway obstruction, hoarseness (recurrent laryngeal nerve damage), hyperthyroidism (thyroid storm)
- Early: infection, hypoparathryoidism leading to hypocalcaemia
- Late: Recurrence, hypothyroidism, hypertrophic scaring
37
Pathology of thyroid eye disease
- retroorbital inflammation and lymphocyctic infiltration
| - sympathetic overstimulation and restrictive myopathy of levator palebrae superioris = lid lag
38
What types of wound are prone to hypertrophic and keloid scar formation?
Wounds associated with:
- infection
- trauma
- burns
- tension
- flexor surfaces, skin creases = hypertrophic
- earlobes, chin, neck, shoulder, chest = keloid
39
Clinical course of hypertrophoc and keloid scars
Hypertrophic appear soon after injury, usually regress spontaneously.
Keloid scars appear months after injury and continue to grow
40
How to you treat hypertrophic and keloid scars?
- mechanical pressure with topical silicone gel sheets
- surgical revision with closure aiming to avoid tension
- intralesional steroid and local anaesthetic injection
41
SCC differential
```
Benign skin lesions
- keratoacanthoma
- infected seborrhoeic wart
- solar keratosis
- pyogenic granuloma
Malignant skin lesions
- BCC
- Malignant melanoma (amelanotic)
```
42
Predisposing factors for SCC
Congenital: Xeroderma pigmentosum
Acquired
- environmental: sunlight, ionizing radiation, arsenic
- pre-existing skin lesions: solar keratosis, Bowen's disease
- infections: viral warts (HPV 5+8)
- immunosuppression: post-transplant, HIV
- chronic cutaneous ulceration: burns, venous ulcers (Marjolin's ulcer)
43
SCC treatment
```
Primary lesion
- Excision 1 cm margin
- Moh's excision for eyelids, ears, nasolabial folds etc
- Radiotherapy if unresectable
Nodal spread
- Surgical block dissection
- Radiotherapy
```
44
SCC pathology
- arise from epidermal cells
- full thickness epidermal atypia
- extend in all directions into deep dermis and subcut fat
- well, mod or poorly differentiated
45
Features of a pigmented skin lesion suspicious of malignancy
- loss of normal surface markings around lesion
- ulceration
- bleeding
- variation of colour
- halo of brown pigment
- satellite nodules
46
Malignant melanoma differential
```
Benign
- pigmented naevus aka mole
- freckles
- lentigo
- pigmented seborrhoeic keratoses
- dermatofibromas
- thrombosed haemangiomatas
Malignant
- pigmented BCC
```
47
Types of malignant melanoma
- Superficial spreading (70%): legs and back
- Nodular (15-30%): trunk
- Lentigo maligna: face or back of hands
- Acral lentiginous: hairless skin e.g. subungual, palms + soles
- Rare: amelanotic, intracranial, retinal
48
Predisposing factors of malignant melanoma
```
Congential
- xeroderma pigmentosum
- dysplastic naevus syndrome
- large congenital naevi
- family history
Acquired
- sunlight
- pre-existing skin lesions: lentigo maligna, >20 naevi
- previous melanoma
```
49
Malignant melanoma staging
- Clark's levels of invasion
- Breslow's thickeness
- Beahrs and Myers (combination)
50
Malignant melanoma treatment
- Surgery: wide local excision, margin depends on size of main lesion.
- Nodal spread: confirm with FNAC/lymph node biopsy, if palpable - therapeutic block dissection
- Palliation/adjuvants: immunotherapy
- PREVENTION: sun exposure avoidance
51
BCC differential
Benign
- keratoacanthoma
Malignant
- SCC
52
Predisposing factors for BCC
```
Congenital
- xeroderma pigmentosum
- Gorlin's syndrome
Acquired
- sunlight
- carcinogens: cigarettes, arsenic
- previous radiotherapy
- pre-existing skin lesion: naevus sebaceous
```
53
BCC treatment
- Nodular tumour, excision with 0.5 cm margin
- Flat tumour, wider margin
- Moh's excision if near delicate structures
- Radiotherapy
54
Classification of pressure sores
- Stage 1: non-blanching erythema
- Stage 2: partial-thickness skin loss
- Stage 3: full-thickness skin loss, fat at base
- Stage 4: extensive soft tissue loss through deep fascia, often muscle necrosis
55
Commonest signs for pressure sores
Any bony prominence
- sacrum
- greater trochanter
- heel
- lateral malleolus
- ischial tuberosity
- occiput
56
Conditions with increase risk of pressure sores
Immobility and prolonged bed-rest most important factors
- cardiorespiratory disease
- trauma
- neurological disease
- bone and joint disease
- prolonged operative procedures
Impaired wound healing
- metabolic: DM, vit C + zinc deficiencies
- drugs: steroid, chemo, radio
- underlying disease: PVD, CRF, jaundice, malignacy, infection
57
Pressure sore treatment
- Prophylaxis: skin inspection, turning immobile pts, massage, toileting, special mattress + cushions
- Non-surgical: optimize tissue perfusion + oxygenation, treat infection, good nutrition (vit C, zinc, multivits)
- Surgical: debridement + reconstruction with fascia + muscle containing flaps
58
What is a skin graft?
- Transfer of skin from donor sign to recipient site without a blood supply - this is acquired from healthy recipient bed
- Full or partial thickness
- Donor site regenerates from adnexal skin elements
59
What tissues do skin grafts not take on?
- unhealthy, necrotic, infected tissue
- irradiated tissue
- cortical bone without periosteum
- tendon without peritendon
- cartilage without perichondrium
60
How do you harvest a skin graft?
- hand-held skin graft knive
- electric or gas-powered dermatomes
- donor site usually easily concealed e.g. inner thigh, buttock, inner arm
61
What is a skin flap?
Tissue or tissues transfered from one site to another while maintaining a continuous blood supply through a vascular pedicle
62
Classification of skin flaps
- Site: local or distal (free flap)
- Contents
- Random or axial (based on a named artery or vein)
63
Indications for flap reconstruction
- when skin grafts will not take
- to reconstruct like-for-like to promote optimal structure, function and cosmesis
- when blood supply has to be imported to areas of doubtful viability e.g. pressure sores, complex trauma
64
What is the reconstruction ladder?
- Secondary intention
- Primary closure
- Delayed primary closure
- Split thickness graft
- Full thickness skin graft
- Tissue expansion
- Random flap
- Axial flap
- Free flap
65
Ptosis causes
```
Unilateral
- 3rd nerve palsy
- Horner's syndrome
- Syphilis
Bilateral
- Congenital
- Myopathies: MG, myotonic dystrophy
- Syphillis
```
66
Ptosis surgical treatment
Blepharoplasty - excess eyelid skin and fat removed
67
Facial nerve palsy causes
- Intracranial: vascular, tumour, infection (meningitis)
- Intratemporal: infection (otitis media, Ramsay Hunt), idiopathic (Bell's), trauma (surgical, #), tumour
- Extratemporal: tumour (parotid gland), trauma (surgical, accidental)
68
Branches of facial nerve
Motor
- nerve to stapedius
- nerve to posterior belly of digastric
- temporal, zygomatic, buccal, mandibular, cervical
Secretomotor:
- via greater superficial pertrosal nerve to lacrimal, nasal and palatine glands
Taste (anterior 2/3)
- via chorda tympani
Sensory
- anterior wall of external auditory meatus
69
Differential of unilateral swelling of parotid gland
- neoplasia: benign (pleomorphic adenoma), malignant
- stones
- infection/inflammation: mumps, sialadenitis, HIV
- autoimmune: sjogrens
- infiltration: sarcoidosis
- lymph node enlargement
- neural: facial nerve neuroma
- vascular: temporal artery aneurysm
- systemic disease: ALD, DM, pancreatitis, acromegaly, malnutrition
70
Parotid gland swelling features suspicious of malignancy
- history: rapid growth, pain
- hyperaemic hot skin
- hard consistency
- fixed to skin and muscle
- irregular surface or ill-defined edge
- facial nerve involvement
71
What is Sjogrens syndrome
Two of more of:
- keratoconjuctivitis sicca (dry eyes)
- xerostomia (dry mouth)
- associated CTD (RA, scleroderma, SLE, PM, PAN)
Primary if no associated CTD
40x increased risk of developing lymphoma
72
Sjogrens syndrome investigations and treatment
- Antibodies: RhF, anti-salivary, anti-Ro, anti-La
- Schirmer's test
- Slit-lamp
- Lip biopsy
Treatment
- artifical tears and saliva
- systemic steroids
- careful follow-up (lymphoma)
73
Complications of parotidectomy
```
Immediate
- facial nerve transection
- reactionary haemorrhage
Early
- wound infection
- temporary facial weakness
- salivary fistula
- division of greater auricular nerve = numb pinna
Late
- wound dimple
- Frey's syndrome = increased facial sweating when eating due to reinnervation of divided sympathetic nerves to facial skin by fibres of secretomotor branch
```
74
What is a keratoacanthoma?
Benign overgrowth of hair follicle cells producing central plug of keratin.
Rapidly forms in 6 weeks, regresses in 6 weeks.
Looks like SCC
75
Keratoacanthoma treatment
- leave alone is asympotmatic
| - complete excision + histology (particularly in elderly)
76
What is a neurofibroma?
Benign tumour derived from peripheral nerve elements
77
What is neurofibromatosis?
AD cause of multiple neurofibromas with other dermatological manifestations (6 cafe-au-lait spots)
- type 1 (von Recklinghausen's disease) classical cutaneous signs
- Type 2 (MISME syndrome: multiple inherited schwannomas, meningiomas and ependymomas)
78
Neurofibromata complications
- pressure effects: spinal cord or nerve root compression
- deafness: involvement of CN VIII
- sarcomatous transformation: 5-13% in type I
- intra-abdominal effects: obstruction, chronic GI bleeds
- skeletal change: kyphoscholiosis, cystic change, pseudoarthrosis
79
Treatment for a single neurofibroma
- leave alone if asympotmatic
- excision if malignant growth suspected
- local regrowth is common (unable to detach from underlying nerve)
80
What is a papilloma
Overgrowth of all layers of skin with a central vascular core. Increasingly common with age
81
Papilloma treatment
Excise with sharp scissors, control bleeding from central vascular core with single stitch or diathermy
82
What is a pyogenic granuloma?
Rapidly growing capillary haemangioma, neither pyogenic nor a granuloma!
83
Pygogenic granuloma treatment?
Unlikely to regress spontaneously unless arose in pregnancy.
| Currettage with diathermy of base or complete excision biopsy
84
What is a seborrhoeic keratosis?
Benign overgrowth of basal cell layer of epidermis. Histologically characterised by:
- hyperkeratosis
- acanthosis
- hyperplasia of variably pigmented basaloid cells
85
Seborrhoeic keratosis treatment?
- leave alone if patient wishes
| - shave or cauterise off (lies above level of surrounding normal epidermis)
86
What is a solar/actinic keratosis?
SCC in situ. Histologically:
- hyperkeratosis
- focal parakeratosis
- irregular acanthosis
- basal layer atypia only (all layers = SCC)
25% progress to invasive SCC if untreated
87
Solar/actinic keratosis treatment
- cryotherapy
- topical 5-flurouracil
- photodynamic therapy
- curretage of affected skin
88
Causes of clubbing
```
Commonest is idiopathic
Gastrointestinal
- Cirrhosis: esp PBC
- IBD: esp Crohns
- Malabsorption: coeliac
- GI lymphoma
Respiratory
- Bronchial carcinoma: SCC
- Chronic supperative lung disease: abscess, bronchiectasis, CF, empyema
- Fibrosing alveolitis
- Mesothelioma
Caridac
- Cyanotic congenital heart disease
- Infective endocarditis
- Atrial myxoma
Rare causes
- Familial
- Graves
- Axillary artery aneurysm, brachial AV malformation = unilateral
```
89
What is a branchial cyst and how is it diagnosed?
Fusion failure of embryonic second and third branchial arches
- clinical examination
- FNAC shows opalescent fluid containing cholesterol crystal or pus
90
Branchial cyst treatment
- surgically excised whole if possible
- injecting dye aids total excision and reduces recurrence
- treat complicating infections
Complications: recurrence + chronic, discharging sinus formation
91
Definition of cyst, sinus and fistula
```
Cyst = abnormal epithelial lined sac containing gas, fluid, or semisolid material
Sinus = blind-ending tract typically lined by epithelial or granulation tissue, open onto an epithelial surface
Fistula = abnormal communication between two epithelial (or endothelial e.g. AV fistula) surfaces
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