Head and Neck, Skin and Soft Tissue Flashcards

1
Q

What are the differentials of a neck lump based on anatomy?

A

Midline
- Thyroglossal cyst
- Dermoid cyst
- Thyroid swelling (benign or malignant)

Anterior triangle
- Lymphadenopathy (infective, inflammatory, cancer (primary or secondary)
- Branchial cyst
- Carotid body tumour
- Salivary gland pathology (saliadenitis, salialithiasis, ranula, retention cyst, cancer)

Posterior triangle
- Lymphadenopathy (infective, inflammatory, cancer (primary or secondary)
- Cystic hygroma
- Pharyngeal pouch
- Cervical rib

Common to all regions - skin and subcutaneous lesions (lipoma, epidermoid cyst)

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2
Q

What are the differentials for neck lumps based on congenital versus acquired?

A

Congenital (20%)
- Branchial cleft cyst
- Thyroglossal duct cyst
- Dermoid cyst
- Vascular tumours and and malformations (haemangioma, lymphangioma, cystic hygroma).

Acquired (80%)
**Benign **
Skin and subcutaneous (lipoma, sebaceous cyst)
Lymphadenopathy (reactive, infective, inflammatory)
Thyroid (MNG, nodular thyroiditis, cyst, follicular adenoma)
Salivary gland (retention cyst, ranula, sialolithiasis, sialadenitis, adenoma)
Pharyngeal pouch
Vascular (carotid body tumour)
Neuronal (neurofibroma, schwannoma)
**Malignant **
Primary - thyroid, salivary glands, lymphoma, sarcoma
Secondary - SCC, melanoma, thyroid/salivary glands, infraclavicular malignancy

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3
Q

What are the contents of the posterior triangle?

A

**Vessels **- third part of subclavian artery, suprascapular and transverse cervical branches of thyrocervical trunk, external jugular vein, lymph nodes.

Nerves - accessory nerves, brachial plexus trunks, fibers of the cervical plexus

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4
Q

What are the contents of the anterior triangle?

A

Muscles - thyrohyoid, sternothyroid, sternohyoid

Organs - thyroid gland, parathyroid gland, larynx, trachea, oesophagus, submandibular gland, larynx and trachea

Arteries - superior and inferior thyroid a, common carotid, external carotid, internal carotod a, facial, submental and lingual

Veins - anterior jugular veins, internal jugular, common facial, lingual, superior thyroid, middle thyroid, facial veins, submental, lingual veins.

Nerves - vagus nerve, hypoglossal nerve, part of sympathetic trunk, mylohyoid nerve

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5
Q

What are the differentials for lymphadenopathy?

A

**Benign **

Infectious
- Viral
URTIs - adenovirus, rhinovirus, enterovirus
EBV
HSV, CMV, mumps, measles, rubella, HIV
- Bacterial
STaph, strep, toxoplasmosis, brucellosis, cat sratch disease
Mycobacterial infections (TB)

Inflammatory
- Sarcoidosis
- Amyloidosis
- Kawasaki disease

Autoimmune
- SLE
- RA

Medications
- Phenytoin, allopurinol and captopril

Malignant
Primary
- lymphoma
Secondary
- Metastasis

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6
Q

What is a brachial cleft cyst?

A

A congenital epithelial cyst that arises from the lateral aspect of the neck usually due to failure of obliteration/involution of branchial cleft in embryonic development

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7
Q

What is the anatomical pathway of the second brachial cleft cyst?

A

Anterior border of upper 1/3 SCM, deep to platysma, between external and internal carotid arteries, superficial to hypoglossal and glossopharyngeal nerves and ends in tonsillar fossa.

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8
Q

What is a carotid body tumour?

A

This is a paraganglioma of the carotid body derived from chemoreceptor cells
This is the most common head and neck paraganglioma (65%) with 5% bilateral and 5% malignant

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9
Q

What is Merkel cell carcinoma?

A

Rare aggressive cutaneous neuroendocrine malignancy thought to arise from Merkel cells in the epidermis.
Most common site is the head and neck region

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10
Q

What are the 2 main theories for Merkel cell pathogenesis?

A

Traditional -> merkel cells that are located in the basal layer of the epidermis and hair follicles are associated with the mechanoreceptors/sensory neurites in dermal papillae (BUT majority are intradermal as opposed to epidermal)

Alternative -> Arise from totipotential stem cell that acquires neuroendocrine features during malignant transformation

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11
Q

What are the risk factors asscociated with Merkels cell carcinoma ?

A

A - asymptomatic
E - expanding rapidly
I - immunosuppressed
O - older than 50
U - UV radiation exposure

Also , associated with merkel cell polyomavirus

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12
Q

What are the management principles of Merkel cell carcinoma?

A

Surgical excision
- 1-2cm margin (vertical growth, with tendency to invade deep margin)

Radiotherapy - primary radiotherapy for patients who are not surgical candidates

Lymph nodes - only predictive factor of LN mets is tumour size (30% if greater than 1cm)
-> SLNBx - in all patients with negative nodes. For head and neck, variable. If not undergoing SLNBx, radiotherapy. If SLNBx positive, stage patient
-> Regional LND - clincally involved nodes or in +ve SNLBx. Adjuvant RT given. (primary RTx to LNs is an alternative).

Adjuvant radiotherapy post op Ix
- Tumour > 1 cm
- Head and neck primary
- Positive or close resection margins
- LVI, multiple LN involvement
- extracapsular extension of LNs
- immunosuppressed

Systemic therapy
- PD1 inhibitor (pembrolizumab)

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13
Q

What are the prognostic factors for melanoma?

A

Tumour thickness
- > 2mm significantly worse prognosis
Ulceration
Mitotic rate
Lymphatic involvement
Patient related:
- Age (older worse)
- Gender (male worse)
- Site (head, neck, trunk worse)
- Raised LDH

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14
Q

What are the adjuvant treatment options for melanoma?

A

Dependent on patient factors (age, fitness, wishes) and disease factors (node +ve, mets, high risk node -ve

Immunotherapy
- PD-1 receptor (pembrolizumab) - blocks the activity of PD-1 on tumour cells ( PD-1 prevents T cells from recognising and attacking inflammatory and tumour cells). Therefore increasing the immune systems ability to attack melanoma cells.
- CTLA-4 inhibitors (ipilimumab) - present on T cells -> binding to this receptor allows the T cell to remain activated against melanoma.

Targeted therapy (if BRAF mutation present (50% of the time))
- BRAF inhibitors (selectively inhibits mutant BRAF kinase)
- MEK inhibitors

Radiotherapy
- Primary site indications (cant resect, recurrence, positive margins), desmoplastic/neutrotropic features, extensive lymphatic invasion, satellitosis.
- Regional node basins - based on high risk factors for post lymphadenectomy regional recurrence. Number (>1 parotid, >2 cervical, >3 groin nodes), size >3cm neck or axillla or >4cm in groin, extranodal spread, recurrence, unresectable nodal disease.
- Palliative care for brain or spinal mets

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15
Q

What wide local excision margins would you take for melanoma based on the Breslow thickness?

A
  • T1 <1mm = 1cm
  • T2 1-2 mm = 1-2cm Consider narrower for cosemetically or functionally sensitive areas
  • T3/4 >2mm = 2cm
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16
Q

What was the MLST1 trial for melanoma?

A

RCT looking at patients undergoing WLE for melanoma and whether performing SLNBx with reflex LNDx versus nodal observation alone changed melanona specific survival.

Better 10 year disease free survival in those who had SLNBx and LNDx versus those with WLE alone

17
Q

What was the MLST2 trail for melanoma?

A

RCT looking at whether LNDx is required for all patients after SLNBx +ve?

Compared group with routine LNDx after SLNBx +ve versus observation after SLNBx +ve with routine US scan

Results
- no difference in melanoma specific survival
- LN+ve in observation group were able to be successfully salvaged

18
Q

What is a keloid scar?

A

Excessive tissue response to dermal injury characterised by fibroblast proliferation and overproduction of collagen. The tissue extends beyond the borders of the original wound and does not regress spontaneously.

19
Q

What is a hypertrophic scar?

A

Excessive tissue response to dermal injury characterised by fibroblast prolfieration and overproduction of collagen that do not extend beyond the border. Usually undergo partial spontaneous resolution.

20
Q

What are the normal phases of wound healing?

A

1) Inflammation (Day 1-4)
- Haemostasis and inflammation, digestion of necortic debri.

2) Proliferation (Day 5-20)
- Fibroblasts -> angiogenesis -> epithelisation -> collagen formation

3) Remodelling (up to 12 months)
- Collagen production and breakdown with re organisation along the lines of tension

21
Q

What are ways to manage a keloid scar?

A

Intra operatively
- Incisions follow skin crease
- Minimal tension used to close wounds
- Buried sutures used
- Avoid mid chest incisions

Post operatively
- Dressings - occlusive, silicone gel sheets, compressive therapy
- Intra lesional agents - corticosteroid to reduce collagen synthesis, fibroblast proliferation and production of inflammatory mediators. 5-FU can also be used
- ABlative with laser and cryotherapy
- Intralesional interferon, doxorubicin, bleomycin
- Topical imiquimod
- Laser therapy
- Surgical excision (decreased recurrent rate of 100% if combined with therapies listed above)

22
Q

What is the pathogenesis of hidradenitis suppurativa?

A

This is a chronic occlusive disease of hair follicles involving the intertriginous skin of axilla, groin, perineal and inframammary regions.

Accumulation of keratinocytes -> chronic occlusion of the follicular portion of the folliculopilosebaceous units -> stasis and dilatation -> bacteial infection -> wall ruptures -> perifolliculitis -> abscess -> sinuses

If this process is long standing, scarring, contractures and chronic induration of the skin occurs.

23
Q

What are the Hurley classification stages for HS?

A

Stage 1
- Abscess formation with sinus tracts or cicatrisation
- Drug therapy management

Stage 2
- Recurrent abscesses with tract formation and cicatrisation (single or multiple widely seperated lesions)
- Managed with drug therapy +/- limited excision

Stage 3
- Diffuse involvement with multiple interconnected tracts and abscesses
- unlikely to benefit from medical therapy , wide local excision recommended.

24
Q

What are the medical management options for hidradenitis suppurativa?

A

Long term ABs - teracyclines
Antiandrogens -> ciproterone acetate
Oral retinoids
TNF alpha inhibitors -> adalimumab
Prednisone

25
Q

What are the potential causes for a sarcoma?

A

1) Radiation
- tend to follow a aggressive clinical course

2) Other
- angiosarcoma follow chronic lymphodema
- hepatic angiosarcoma - associated with arsenic or vinyl chloride exposure
- Agent organge

3) Genetic
- Lifraumeni p53 miutation
- NF1
- Gardners syndrome (Desmoids)