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Surgery > Superficial lesions > Flashcards

Superficial lesions Flashcards

1
Q

To complete general lump exam

A
  • examine draining lymph nodes
  • assess neurovasc
  • look for similar lumps
  • perform general exam as necessary
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2
Q

What is a lipoma?

A

Benign tumour of mature fat cells

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3
Q

Do lipomas undergo malignant change?

A

No, or very rarely.

Liposarcomas arise de novo

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4
Q

How to treat a lipoma?

A
  • watch and wait
  • remove if patient choice, painful, bad cosmesis.
  • need to remove capsule or recurs?
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5
Q

Lipomas variants

A
  • angiolipomas: prominent vasc component
  • hibernomas: brown fat cells
  • Bannayan-Zonana syndrome: multiple lipomas, macrocephaly, haemangiomas
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6
Q

Dercum’s disease

A

aka Adiposis dolorosa: multiple painful lipomas associated with peripheral neuropathy

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7
Q

Liposarcoma classficiation

A

1 - well-differentiated
2 - myxoid and round cell (poor-dif)
3 - pleomorphic

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8
Q

What are the complications of a sebaceous cyst?

A
  • infection
  • ulceration
  • calcification (trichilemmal cyst)
  • sebaceous horn formation
  • malignant change
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9
Q

Sebaceous cyst treatment

A
  • watch and wait if small, asymptomatic

- elliptical skin excision including capsule to prevent recurrence

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10
Q

Different histological subtypes of sebaceous cyst?

A
  • Epidermal: from infundibular portion of hair follicles

- Trichilemmal: from hair follicle epithelium, more common on scalp

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11
Q

Gardner’s syndrome

A
  • multiple epidermal cysts
  • adenomatous polyposis of colon
  • multiple skull osteomata
  • desmoid tumours
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12
Q

What is a ganglion?

A

Cystic swelling related to a synovial lined cavity (joint or tendon sheath).

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13
Q

Ganglion differential

A
  • bursae
  • cystic protrusions from arthritic joints
  • benign giant cell tumours of flexor sheath
  • rarely, malignant e.g. synovial sarcoma
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14
Q

Ganglion treatment

A
  • watch and wait
  • aspiration + 3 weeks immobilisation
  • complete excision including neck at origin
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15
Q

Complications of surgical ganglion treatment

A
  • wound complications e.g. scar, haematoma, infection
  • recurrence
  • damage to adjacent neurovascular structures
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16
Q

Neck triangle borders

A
  • anterior: anterior border of sternocleidomastoid, midline, ramus of mandible
  • posterior: anterior border of trapezius, clavicle, posterior border of sternocleidomastoid
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17
Q

Midline neck lumps DDx

A
  • Solid: thyroid swelling

- Cystic: thyroglossal cyst

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18
Q

Anterior triangle lump DDx

A
  • solid: lymphadenopathy or carotid chemodectoma

- cystic: branchial cyst, cold abscess (TB)

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19
Q

Posterior triangle lump DDx

A
  • solid: lymphadenopathy

- cystic: pharyngeal pouch or cystic hygroma

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20
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

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21
Q

How to complete cervical lymph node exam

A
  • examine face and scalp for primary infection or neoplasia
  • full ENT exam + formal referal
  • examine abdo for hepatosplenomegaly
  • examine breasts and chest
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22
Q

Cervical lymphadenopathy questions

A
  • lump history
  • night sweats, appetite, weight
  • local ENT symptoms
  • systemic disease
  • social hx, foreign travel, TB
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23
Q

Cervical lymphadenopathy causes

A

L - lymphoma, leukaemia
I - infection (tonsillitis, TB, CMV, EBV, HIV)
S - sarcoidosis
T - tumours, primary + secondary

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24
Q

Cervical lymphadenopathy investigations

A

Bloods - FBC, ESR, TFTs, ACE, monospot/paul-bunnell
Radiological - USS, CT, MRI
Histological - FNAC, excision biopsy

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25
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

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26
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
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27
Q

Causes of a solitary thyroid nodule

A
  • prominent nodule in multinodular goitre
  • cyst
  • adenoma
  • cardinoma/lymphoma
  • thyroiditis
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28
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
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29
Q

Investigation of solitary thyroid nodule

A

Triple assessment

  • clinical hx and exam
  • USS
  • FNAC
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30
Q

What do you know about thyroid adenomas?

A
  • most follicular adenomas
  • 2-4cm encapsulated
  • indistinguishable from carcinomas on FNAC
  • need surgical excision to confirm diagnosis
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31
Q

Thyroid malignancy

A
  • 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%
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32
Q

Multiple endocrine neoplasia types

A

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

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33
Q

Feature of multinodular goitre

A
  • 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
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34
Q

MNG management

A
  • 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)
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35
Q

Indications for MNG surgery

A
  • Mechanical - obstructive symptoms
  • Malignancy
  • Medical treatment failure - thyrotoxic
  • Mediastinal extension - unable to FNAC or monitor clinically
  • Marred beauty - cosmetic
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36
Q

Difference between TMNG and Graves’

A

TMNG - older, nodular, no eye signs, AF in 40%, no AI association
Graves’ - younger, diffuse, eyes signs, AF uncommon, associated AI diseases

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37
Q

Causes of diffusely enlarged thyroid gland

A
  • simple colloid goitre
  • Graves’ disease
  • thyroiditis (Hashimoto’s, de Quervain’s, Riedel’s)
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38
Q

What do you know about simple colloid goitres?

A
  • commonest thyroid abnormality
  • physiological hyperplasia or defection hormone production
  • Causes: iodine deficiency, puberty, pregnancy, goitrogens, drugs (lithium, amiodarone), congenital defects (rare)
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39
Q

Graves’ treatment

A
  • 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
40
Q

Thyroidectomy complications

A

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
41
Q

Pathology of thyroid eye disease

A
  • retroorbital inflammation and lymphocyctic infiltration

- sympathetic overstimulation and restrictive myopathy of levator palebrae superioris = lid lag

42
Q

What types of wound are prone to hypertrophic and keloid scar formation?

A

Wounds associated with:

  • infection
  • trauma
  • burns
  • tension
  • flexor surfaces, skin creases = hypertrophic
  • earlobes, chin, neck, shoulder, chest = keloid
43
Q

Clinical course of hypertrophoc and keloid scars

A

Hypertrophic appear soon after injury, usually regress spontaneously.
Keloid scars appear months after injury and continue to grow

44
Q

How to you treat hypertrophic and keloid scars?

A
  • mechanical pressure with topical silicone gel sheets
  • surgical revision with closure aiming to avoid tension
  • intralesional steroid and local anaesthetic injection
45
Q

SCC differential

A 
Benign skin lesions
- keratoacanthoma
- infected seborrhoeic wart
- solar keratosis
- pyogenic granuloma
Malignant skin lesions
- BCC
- Malignant melanoma (amelanotic)
46
Q

Predisposing factors for SCC

A

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)

47
Q

SCC treatment

A 
Primary lesion
- Excision 1 cm margin
- Moh's excision for eyelids, ears, nasolabial folds etc
- Radiotherapy if unresectable
Nodal spread
- Surgical block dissection
- Radiotherapy
48
Q

SCC pathology

A
  • arise from epidermal cells
  • full thickness epidermal atypia
  • extend in all directions into deep dermis and subcut fat
  • well, mod or poorly differentiated
49
Q

Features of a pigmented skin lesion suspicious of malignancy

A
  • loss of normal surface markings around lesion
  • ulceration
  • bleeding
  • variation of colour
  • halo of brown pigment
  • satellite nodules
50
Q

Malignant melanoma differential

A 
Benign
- pigmented naevus aka mole
- freckles
- lentigo
- pigmented seborrhoeic keratoses
- dermatofibromas
- thrombosed haemangiomatas
Malignant
- pigmented BCC
51
Q

Types of malignant melanoma

A
  • 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
52
Q

Predisposing factors of malignant melanoma

A 
Congential
- xeroderma pigmentosum
- dysplastic naevus syndrome
- large congenital naevi
- family history
Acquired
- sunlight
- pre-existing skin lesions: lentigo maligna, >20 naevi
- previous melanoma
53
Q

Malignant melanoma staging

A
  • Clark’s levels of invasion
  • Breslow’s thickeness
  • Beahrs and Myers (combination)
54
Q

Malignant melanoma treatment

A
  • 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
55
Q

BCC differential

A

Benign
- keratoacanthoma
Malignant
- SCC

56
Q

Predisposing factors for BCC

A 
Congenital
- xeroderma pigmentosum
- Gorlin's syndrome
Acquired
- sunlight
- carcinogens: cigarettes, arsenic
- previous radiotherapy
- pre-existing skin lesion: naevus sebaceous
57
Q

BCC treatment

A
  • Nodular tumour, excision with 0.5 cm margin
  • Flat tumour, wider margin
  • Moh’s excision if near delicate structures
  • Radiotherapy
58
Q

Classification of pressure sores

A
  • 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
59
Q

Commonest signs for pressure sores

A

Any bony prominence

  • sacrum
  • greater trochanter
  • heel
  • lateral malleolus
  • ischial tuberosity
  • occiput
60
Q

Conditions with increase risk of pressure sores

A

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

61
Q

Pressure sore treatment

A
  • 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
62
Q

What is a skin graft?

A
  • 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
63
Q

What tissues do skin grafts not take on?

A
  • unhealthy, necrotic, infected tissue
  • irradiated tissue
  • cortical bone without periosteum
  • tendon without peritendon
  • cartilage without perichondrium
64
Q

How do you harvest a skin graft?

A
  • hand-held skin graft knive
  • electric or gas-powered dermatomes
  • donor site usually easily concealed e.g. inner thigh, buttock, inner arm
65
Q

What is a skin flap?

A

Tissue or tissues transfered from one site to another while maintaining a continuous blood supply through a vascular pedicle

66
Q

Classification of skin flaps

A
  • Site: local or distal (free flap)
  • Contents
  • Random or axial (based on a named artery or vein)
67
Q

Indications for flap reconstruction

A
  • 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
68
Q

What is the reconstruction ladder?

A
  • Secondary intention
  • Primary closure
  • Delayed primary closure
  • Split thickness graft
  • Full thickness skin graft
  • Tissue expansion
  • Random flap
  • Axial flap
  • Free flap
69
Q

Ptosis causes

A 
Unilateral
- 3rd nerve palsy
- Horner's syndrome
- Syphilis
Bilateral
- Congenital
- Myopathies: MG, myotonic dystrophy
- Syphillis
70
Q

Ptosis surgical treatment

A

Blepharoplasty - excess eyelid skin and fat removed

71
Q

Facial nerve palsy causes

A
  • Intracranial: vascular, tumour, infection (meningitis)
  • Intratemporal: infection (otitis media, Ramsay Hunt), idiopathic (Bell’s), trauma (surgical, #), tumour
  • Extratemporal: tumour (parotid gland), trauma (surgical, accidental)
72
Q

Branches of facial nerve

A

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

73
Q

Differential of unilateral swelling of parotid gland

A
  • 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
74
Q

Parotid gland swelling features suspicious of malignancy

A
  • history: rapid growth, pain
  • hyperaemic hot skin
  • hard consistency
  • fixed to skin and muscle
  • irregular surface or ill-defined edge
  • facial nerve involvement
75
Q

What is Sjogrens syndrome

A

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

76
Q

Sjogrens syndrome investigations and treatment

A
  • 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)
77
Q

Complications of parotidectomy

A 
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
78
Q

What is a keratoacanthoma?

A

Benign overgrowth of hair follicle cells producing central plug of keratin.
Rapidly forms in 6 weeks, regresses in 6 weeks.
Looks like SCC

79
Q

Keratoacanthoma treatment

A
  • leave alone is asympotmatic

- complete excision + histology (particularly in elderly)

80
Q

What is a neurofibroma?

A

Benign tumour derived from peripheral nerve elements

81
Q

What is neurofibromatosis?

A

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)
82
Q

Neurofibromata complications

A
  • 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
83
Q

Treatment for a single neurofibroma

A
  • leave alone if asympotmatic
  • excision if malignant growth suspected
  • local regrowth is common (unable to detach from underlying nerve)
84
Q

What is a papilloma

A

Overgrowth of all layers of skin with a central vascular core. Increasingly common with age

85
Q

Papilloma treatment

A

Excise with sharp scissors, control bleeding from central vascular core with single stitch or diathermy

86
Q

What is a pyogenic granuloma?

A

Rapidly growing capillary haemangioma, neither pyogenic nor a granuloma!

87
Q

Pygogenic granuloma treatment?

A

Unlikely to regress spontaneously unless arose in pregnancy.

Currettage with diathermy of base or complete excision biopsy

88
Q

What is a seborrhoeic keratosis?

A

Benign overgrowth of basal cell layer of epidermis. Histologically characterised by:

  • hyperkeratosis
  • acanthosis
  • hyperplasia of variably pigmented basaloid cells
89
Q

Seborrhoeic keratosis treatment?

A
  • leave alone if patient wishes

- shave or cauterise off (lies above level of surrounding normal epidermis)

90
Q

What is a solar/actinic keratosis?

A

SCC in situ. Histologically:
- hyperkeratosis
- focal parakeratosis
- irregular acanthosis
- basal layer atypia only (all layers = SCC)
25% progress to invasive SCC if untreated

91
Q

Solar/actinic keratosis treatment

A
  • cryotherapy
  • topical 5-flurouracil
  • photodynamic therapy
  • curretage of affected skin
92
Q

Causes of clubbing

A 
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
93
Q

What is a branchial cyst and how is it diagnosed?

A

Fusion failure of embryonic second and third branchial arches

  • clinical examination
  • FNAC shows opalescent fluid containing cholesterol crystal or pus
94
Q

Branchial cyst treatment

A
  • surgically excised whole if possible
  • injecting dye aids total excision and reduces recurrence
  • treat complicating infections
    Complications: recurrence + chronic, discharging sinus formation
95
Q

Definition of cyst, sinus and fistula

A 
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

Surgery (4 decks)

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