Week 9

Question 1

Prodromal dementia

Answer 1

Prodromal dementia disease is the very early form of Alzheimer’s or another dementia when memory is deteriorating but a person remains functionally independent.

Signs:
Depression, anxiety, apathy, irritability, agitation, sleep disorders, among other symptoms, have been hypothesized to represent a prodromal stage of dementia or, at least, they increase the risk for conversion from minor neurocognitive disorder to major neurocognitive disorder.

Question 2

Signs of delirium

Answer 2

Delirium is a serious disturbance in mental abilities that results in confused thinking and reduced awareness of the environment. The start of delirium is usually rapid — within hours or a few days, prevalent delirium means that the condition is present on admission, whereas incident delirium occurs during admission.

Usually acute or subacute presentation.
Fluctuating course.
Consciousness is clouded/impaired cognition/disorientation.
Poor concentration.
Memory deficits - predominantly poor short-term memory.
Abnormalities of sleep-wake cycle, including sleeping in the day.
Abnormalities of perception - eg, hallucinations or illusions.
Agitation.
Emotional lability.
Psychotic ideas are common but of short duration and of simple content.
Neurological signs - eg, unsteady gait and tremor.

Question 3

Delirium causes

Answer 3

Acute infections:
Urinary tract infection.
Pneumonia.
Sepsis.
Viral infections.
Meningitis.
Encephalitis.
Cerebral abscess.
Malaria.
Prescribed drugs:
Benzodiazepines.
Analgesics - eg, morphine.
Anticholinergics.
Anticonvulsants.
Anti-Parkinsonism medications.
Steroids.
Surgical:
Postoperative.
Toxic substances:
Substance misuse or withdrawal.
Alcohol - acute intoxication or withdrawal.
Carbon monoxide (CO) poisoning.
Exposure to heavy metals.
Barbiturate withdrawal.
Vascular disorders:
Cerebrovascular haemorrhage or infarction.
Cardiac failure or ischaemia.
Subdural haemorrhage.
Subarachnoid haemorrhage.
Vasculitis - eg, systemic lupus erythematosus (SLE).
Cerebral venous thrombosis.
Migraines.
Metabolic causes:
Hypoxia.
Electrolyte abnormalities - eg, hyponatraemia and hypercalcaemia.
Hypoglycaemia or hyperglycaemia.
Hepatic impairment.
Renal impairment.
Vitamin deficiencies:
Thiamine deficiency.
Nicotinic acid deficiency.
Vitamin B12 deficiency.
Endocrinopathies:
Hypothyroidism and hyperthyroidism.
Hypopituitarism.
Hypoparathyroidism or hyperparathyroidism.
Cushing's disease.
Porphyria.
Carcinoid.
Trauma:
Head injury.
Epilepsy:
For example, postictally.
Neoplasia:
Primary cerebral malignancy.
Secondaries in the brain.
Paraneoplastic syndromes.
Others:
Urinary retention.
Faecal impaction.

Question 4

Types of delirium

Answer 4

Hypoactive subtype - apathy and quiet confusion are present and easily missed. This type can be confused with depression.
Hyperactive subtype - agitation, delusions and disorientation are prominent and it can be confused with schizophrenia.
Mixed subtype - patients vary from hypoactive to hyperactive.

Question 5

Treating delirium

Answer 5

Antipsychotics in a majority are harmful. But can be used for those who are aggressive and do not respond to verbal and non-verbal de-escalation techniques.
Haloperidol or olanzapine are preferred, using the lowest possible dose for the shortest possible time (normally a week or less). The dose should be titrated gradually until symptoms are controlled. It should be noted that neither drug has a UK licence for this use so normal considerations regarding the use of unlicensed medicines should apply. Note that both drugs have the potential to cause extrapyramidal side-effects and should be used in caution or avoided altogether in some patients (eg, people with Lewy-body Parkinson’s disease).
In delirium resulting from alcohol withdrawal (delirium tremens), a benzodiazepine such as diazepam or chlordiazepoxide is preferred. The benzodiazepine is usually used as a reducing course. Large doses may lead to sedation and therefore close observation is required.

Question 6

Common drug causes of delirium (often in elderly) include:

Answer 6

Benzodiazepines.
Narcotic analgesics.
First-generation antihistamines.
Antispasmodics.
Flouroquinolones.
Warfarin.
Captopril.
Theophylline.
Isosorbide dinitrate.
Dipyridamole.
Furosemide.
Lithium.
Tricyclic antidepressants.
Cimetidine.
Anti-arrhythmics.
Statins.
Digoxin.
Steroids.
Beta-blockers.
Over-the-counter medications - eg, liquid medications containing alcohol or chlorphenamine.

Question 7

Drug management of dementia

Answer 7

AChE inhibitor treatment (donepezil, galantamine or rivastigmine) should be considered in patients with mild or moderate Alzheimer’s disease. It should only be started by dementia specialists (psychiatrists, neurologists, and physicians specialising in the care of older people), after appropriate discussion with family and carers. These drugs have cholinergic side-effects and should be started at a low dose, and then be titrated according to response.

Memantine (an NMDA antagonist) is recommended by NICE as a second-line option for managing patients with moderate Alzheimer’s disease where AChE inhibitors are not tolerated or are contra-indicated, or in the treatment of severe Alzheimer’s disease. Memantine can be used in addition to an AChE inhibitor for moderate or severe dementia.

Question 8

Management of vascular dementia

Answer 8

This should only be used if there is severe distress or immediate risk of harm to the patient or others. NICE does not recommend the use of antipsychotics for mild-to-moderate non-cognitive symptoms in dementia with VaD or mixed dementia because of the increased risk of cerebrovascular adverse events and death.

Question 9

Management of dementia with lewy bodies

Answer 9

Avoid neuroleptic drugs for psychiatric and behavioural problems - these commonly induce severe sensitivity reactions in DLB patients - motor and mental impairment is worsened and mortality may be increased. Where these are used, careful monitoring for sensitivity reactions should take place.
Anti-Parkinsonian treatment may also worsen psychosis.
NICE and SIGN guidelines advise that cholinesterase inhibitors - eg rivastigmine - at daily doses of 6 mg and above, can be helpful in treating cognitive decline in people with DLB. However the most recent Cochrane review suggests the evidence of benefit remains unclear.

Question 10

Management of frontotemporal Dementia

Answer 10

Stop drugs which may be exacerbating memory problems or confusion (anticholinergics, CNS drugs).
Selective serotonin reuptake inhibitors (SSRIs) may be helpful in modifying behavioural symptoms. Evidence is limited to small studies.
Atypical antipsychotics are used where there are severe behavioural problems such as agitation and psychosis. These are only used cautiously and when SSRIs have failed, as those with FTD are at higher risk of extrapyramidal side-effects.
Levodopa/carbidopa may be tried where there are Parkinsonian symptoms, and dopamine agonists where this is not effective.

Question 11

Features of Vascular dementia

Answer 11

Presentation varies significantly, as does speed of progression. Presenting features which may suggest a vascular cause include:

Focal neurological abnormalities: visual disturbances (eg, field defects), sensory or motor symptoms (eg, dysphasia, hemiparesis, visual field defects) or extrapyramidal signs (eg, dystonias and Parkinsonian features).
Difficulty with attention and concentration.
Seizures.
Depression and/or anxiety accompanying the memory disturbance.
Early presence of disturbance in gait, unsteadiness and frequent, unprovoked falls.
The patient has bladder symptoms (eg, incontinence) without a demonstrable urological condition.
Features of pseudobulbar palsy
Emotional problems - eg, emotional lability, psychomotor retardation or depression.

Question 12

Features of Lewy body dementia

Answer 12

Dementia is usually the presenting feature, with memory loss, decline in problem solving ability and spatial awareness difficulties.
Characteristically there are fluctuating levels of awareness and attention.
Signs of mild Parkinsonism (tremor, rigidity, poverty of facial expression, festinating gait). Falls frequently occur.
Visual hallucinations.
Sleep disorders including rapid eye movement sleep disorder, restless legs syndrome, nocturnal cramps.
Fainting spells.

Question 13

Features of frontotemporal dementia-

Answer 13

By type:
Behavioural variant frontotemporal dementia.
Loss of inhibition
Inappropriate social behaviour
Poor planning, insight 
Compulsive behaviours

Progressive non-fluent aphasia.
Slow, hesitant, difficult speech.
Grammatical errors in speech.
Impaired understanding of complex sentences, although recognition of individual words is preserved.
Loss of literacy skills.
On examination:

There may be impairment of orofacial movements such as swallowing, coughing or yawning on command (although still present as a reflex).
There may be stuttering, impairment of ability to write or read, or impaired repetition ability

Semantic dementia.
Loss of vocabulary with fluency of speech maintained.
Asking the meaning of familiar words.
Difficulty finding the right word and having to talk around it or describe it.
Loss of recognition of familiar faces or objects.
Memory and visuospatial skills comparatively well preserved.

Question 14

Drugs that cause skin reactions

Answer 14

Penicillin, carbamazepine, allopurinol, gold, sulphonamides, NSAIDs, phenytoin, isoniazid, chloramphenicol, erythromycin, streptomycin.

Question 15

OM+E Glue ear

Answer 15

OME is the most common cause of acquired hearing loss in childhood.
It is more common between the ages of 1 and 6.

pacification of the drum (other than due to scarring).
There are usually no signs of inflammation or discharge on examination.
Loss of the light reflex, or a more diffused light reflex.
Indrawn, retracted, or concave drum.
Decreased or absent mobility of the drum.
Presence of bubbles or fluid level.
Yellow or amber colour change to the drum.
Fullness or bulging of the drum, although this is not typical.
Ear pain, fullness or popping,

NICE recommends that children who most benefit from surgery are those with:

Persistent bilateral OME lasting three or more months.
A hearing loss in the best ear of 25-30 dB or worse, averaged at 0.5, 1, 2 and 4 kHz.
Children with better hearing but who have social, educational or developmental difficulties may exceptionally also benefit from surgical treatment

Question 16

Types of otitis media

Answer 16

There are various subtypes of OM. These include AOM, OME, chronic suppurative otitis media (CSOM), mastoiditis and cholesteatoma. They are generally described as discrete diseases but in reality there is a great degree of overlap between the different types. OM can be seen as a continuum/spectrum of diseases:
AOM is acute inflammation of the middle ear and may be caused by bacteria or viruses. A subtype of AOM is acute suppurative OM, characterised by the presence of pus in the middle ear. In around 5% the eardrum perforates.
OME is a chronic inflammatory condition without acute inflammation, which often follows a slowly resolving AOM. There is an effusion of glue-like fluid behind an intact tympanic membrane in the absence of signs and symptoms of acute inflammation.
CSOM is long-standing suppurative middle ear inflammation, usually with a persistently perforated tympanic membrane.
Mastoiditis is acute inflammation of the mastoid periosteum and air cells occurring when AOM infection spreads out from the middle ear.
Cholesteatoma occurs when keratinising squamous epithelium (skin) is present in the middle ear as a result of tympanic membrane retraction.

Question 17

Mastoiditis

Answer 17

Acute (classic) mastoiditis
History of acute or recurrent episodes of otitis media.
Intense otalgia and pain behind the ear.
Fever.
Infants may present with irritability, intractable crying and feeding problems.
Swelling, redness or a boggy, tender mass behind the ear.
The external ear may protrude forwards; fluctuance can sometimes be demonstrated behind the ear (examine from behind).
Ear discharge may be present and the eardrum may be perforated.
Tympanic membrane bulges and is erythematous.
The patient is unwell.

Chronic mastoiditis
Presents in a subtle or subclinical fashion after an episode of AOM or with history of chronic suppurative otitis media.
Recurrent bouts of otalgia and retro-aural pain.
Recurrent headache.
Episodes of fever.
Infants may present with irritability, intractable crying and feeding problems.
Tympanic membrane may appear infected or may be normal.
May be no external evidence of peri-mastoid inflammation.

Question 18

Treatment of Mastoiditis

Answer 18

The usual initial therapy is high-dose, broad-spectrum intravenous (IV) antibiotics, given for at least 1-2 days (eg, with a third-generation cephalosporin).
Oral antibiotics are usually used after this, starting on IV treatment after 48 hours without fever and continuing for at least 1-2 weeks.
Paracetamol, ibuprofen and other agents may be given as antipyretics and/or painkillers.
Myringotomy ± tympanostomy tube insertion may be performed in some cases as a therapeutic procedure, or to collect middle ear fluid for culture.
Immediate mastoidectomy is usually the method of choice to treat acute mastoiditis with subperiosteal abscess formation[1].
Surgical intervention, usually in the form of mastoidectomy ± tympanoplasty, is also usually suggested if there is:
Mastoid osteitis.
Intracranial extension.
Co-existing cholesteatoma.
Limited improvement after IV antibiotics.

Question 19

Treatment of Otitis Externa

Answer 19

A solution of acetic acid 2% acts as an astringent in the external ear canal by reducing the pH and reducing bacterial and fungal cell growth. It may be used to treat mild otitis externa and is comparable to an anti-infective combined with a corticosteroid; efficacy is reduced if treatment extends beyond 1 week.

If infection is present, a topical anti-infective with or without a corticosteroid may be considered. These are used for a minimum of one week but if symptoms persist they can be used until they resolve, up to a maximum of 2 weeks. Prolonged and extensive use of topical anti-infective or corticosteroid treatment may affect the flora in the ear canal, increasing the risk of fungal infections. If a mild to moderate, uncomplicated fungal infection is suspected in the context of chronic otitis externa, a topical antifungal such as clotrimazole 1% solution, acetic acid 2% spray [unlicensed indication], or clioquinol and a corticosteroid such as flumetasone pivalate with clioquinol can be offered. Sensitivity to topical ear preparations may also occur, especially with prolonged or recurrent use. Astringent agents such as aluminium acetate ear drops are also available.

In view of reports of ototoxicity, treatment with topical aminoglycosides is contra-indicated in patients with a perforated tympanic membrane (eardrum). However, some specialists do use these drops cautiously in the presence of a perforation or patent grommet in patients with chronic suppurative otitis media and when other measures have failed for otitis externa.

Question 20

Causes and Symptoms of otitis externa

Answer 20

Swimming, warm weather, eczema, psoriasis, earwax, middle ear infections.

Common symptoms include itch, ear discharge, temporary dulled hearing and pain. Your ear may feel blocked or full.

Both ears can be affected; however, more often otitis externa affects one ear only. Sometimes the glands in your neck or around your ear can become enlarged and sore.

Sometimes fungal

Question 21

Fungal ear infection/ otomycosis

Answer 21

The typical presentation is with inflammation, pruritus, scaling and severe discomfort. The mycosis results in superficial epithelial exfoliation, masses of debris containing hyphae and suppuration. Pruritus is more marked than with other forms of ear infections and discharge is often a marked feature.

The initial presentation is similar to bacterial otitis externa but otomycosis is characterised by many long, white, filamentous hyphae growing from the skin surface. Suspicion of fungal infection may arise only when the condition fails to respond to antibiotics.

90% of fungal infections involve Aspergillus spp. and the rest Candida spp.

Factors that predispose to otitis externa include absence of cerumen, high humidity, increased temperature and local trauma, water sports, eczema. DIVING.

Burow’s solution or 5% aluminum acetate solution should be used to reduce the swelling and remove the debris.
There is no consensus on treatment but clotrimazole 1% ear drops or flumetasone pivalate 0.02% plus clioquinol 1% ear drops are commonly used.

Question 22

Necrobiosis lipoidica

Answer 22

Necrobiosis lipoidica is an uncommon inflammatory condition in which shiny, red-brown or yellowish patches develop in the skin, usually on the shins. Its significance is that it is often associated with underlying diabetes, both the insulin-dependent and non-insulin-dependent types. Give NSAIDs to steroids depending on severity. Consider cryotherapy. Looks like knee lava patches.

Question 23

Disseminated granuloma annulare

Answer 23

Annular, smooth, discoloured papules and plaques, and necrobiotic granulomas on histology. Granuloma annulare is more correctly known as necrobiotic papulosis.

The disseminated type is composed of small papules, usually arranged symmetrically in poorly-defined rings 10 cm or more in diameter. They are often found around the skin folds of the trunk (armpits, groin). Itch is common. This is the commonest form associated with HIV.

Pink candy floss like patches in areas like chicken skin or in rings.

Question 24

Darier disease

Answer 24

Darier disease is an autosomal dominant skin condition characterized by wart-like blemishes on the body. The most common sites for blemishes are the scalp, forehead, upper arms, chest, back, knees, elbows, and behind the ear, around the nostrils and sides of nose, eyebrows, and beard area)
Skin folds, such as armpits, groin, under the breasts, and between the buttocks
The papules have a firm, harsh feel like coarse sandpaper and may be skin-coloured, yellow-brown, or brown in colour. If several of the small papules grow together they may form larger warty lesions. Hard to the touch, mildly greasy, and can emit a strong odour. There may be a heavily crusted rash similar to seborrheic dermatitis.

Other skin signs may include:

Small pits on the palms and soles
Bleeding under the skin.
Atypical presentations of Darier disease are common:
Flat, freckle-like lesions
Blistered papules
Large, raised, warty lesions
A linear pattern, with papules following the lines of embryonal development of the skin
Cystic acne
Longitudinal stripes on nails and chip in the end.

Severe Darier disease is usually treated with oral retinoids, either acitretin or isotretinoin. Ciclosporin has been reported to be effective in a few patients.

Question 25

Ichthyosis

Answer 25

Ichthyosis is a condition that causes widespread and persistent thick, dry, “fish-scale” skin. The skin of a person with ichthyosis is rough, dry and scaly and needs to be regularly moisturised. Credit: There are at least 20 different types of ichthyosis.

Question 26

Bullous Pemphigoid

Answer 26

Bullous pemphigoid (BP) is a rare, autoimmune, chronic skin disorder characterized by blistering, urticarial lesions (hives) and itching. Less commonly these blisters can involve the mucous membranes including the eyes, oral mucosa, oesophagus and genital mucosa. It typically presents in older adults as a generalized intensely itchy blistering skin condition. 
Sometimes use doxycycline and niacinamide.

Question 27

Stasis dermatitis

Answer 27

Stasis dermatitis is inflammation, typically of the skin of the lower legs, caused by chronic oedema. Symptoms are itching, scaling, and hyperpigmentation. Ulceration can be a complication. Diagnosis is clinical. Treatment is directed at the causes of oedema and preventing ulceration.

Leg elevation and compression are often indicated. Chronic venous insufficiency should be treated.

In addition, noneroded stasis dermatitis often abates with a midpotency topical corticosteroid (eg, triamcinolone acetonide 0.1% cream or ointment). For an eroded (weeping) lesion, a hydrocolloid dressing may be best.

Ulcers are best treated with compresses and bland dressings (eg, zinc oxide paste); other dressings (eg, hydrocolloids) are also effective (see also Direct wound care).

Question 28

Acanthosis nigricans

Answer 28

Acanthosis nigricans is a skin disorder characterised by darkening (hyperpigmentation) and thickening (hyperkeratosis) of the skin, occurring mainly in the folds of the skin in the armpit (axilla), groin and back of the neck.

Acanthosis nigricans is not a skin disease per se but a cutaneous sign of an underlying condition or disease.

There are two important types of acanthosis: benign and malignant. Although classically described as a sign of internal malignancy, this is very rare. Benign types, sometimes described as ‘pseudoacanthosis nigricans’ are much more common.

Question 29

Types of acanthosis nigricans

Answer 29

Obesity-associated acanthosis nigricans
Most common type of acanthosis nigricans
May occur at any age but more common in adulthood
Obesity often caused by insulin resistance
Syndromic acanthosis nigricans
Defined as acanthosis nigricans that is associated with a syndrome, such as hyperinsulinaemia, Cushing syndrome, polycystic ovary syndrome, total lipodystrophy, Crouzon syndrome

Benign acanthosis nigricans
Also referred to as acral acanthotic anomaly
Thick velvety lesion most prominent over the upper surface of hands and feet in patients who are in otherwise good health
Most common in dark-skinned people, especially those of African American descent

Drug-induced acanthosis nigricans
Uncommon, but acanthosis nigricans may be induced by several medications, including nicotinic acid, insulin, systemic corticosteroids and hormone treatments

Hereditary benign acanthosis nigricans
Acanthosis nigricans inherited as an autosomal dominant trait
Lesions may manifest at any age, infancy, childhood or adulthood

Malignant acanthosis nigricans
Acanthosis nigricans associated with internal malignancy
Most common underlying cancer is tumour of the gut (90%) especially stomach cancer
In 25-50% of cases, lesions are present in the mouth on the tongue and lips

Mixed-type acanthosis nigricans
Patients with one type of acanthosis nigricans whom also develop new lesions of a different cause, e.g. overweight patient with obesity-associated acanthosis nigricans who then develops malignant AN

Question 30

Basal cell carcinoma

Answer 30

Basal cell carcinoma (BCC) is a common, locally invasive, keratinocyte cancer (also known as nonmelanoma cancer). It is the most common form of skin cancer.
Inherited syndromes: BCC is a particular problem for families with basal cell naevus syndrome (Gorlin syndrome), Bazex-Dupré-Christol syndrome, Rombo syndrome, Oley syndrome and xeroderma pigmentosum

Slowly growing plaque or nodule
Skin coloured, pink or pigmented
Varies in size from a few millimetres to several centimetres in diameter
Spontaneous bleeding or ulceration

Nodular BCC
Most common type of facial BCC
Shiny or pearly nodule with a smooth surface
May have central depression or ulceration, so its edges appear rolled
Blood vessels cross its surface
Cystic variant is soft, with jelly-like contents
Micronodular, microcystic and infiltrative types are potentially aggressive subtypes
Also known as nodulocystic carcinoma

Superficial BCC
Most common type in younger adults
Most common type on upper trunk and shoulders
Slightly scaly, irregular plaque
Thin, translucent rolled border
Multiple microerosions

Morphoeic BCC
Usually found in mid-facial sites
Waxy, scar-like plaque with indistinct borders
Wide and deep subclinical extension
May infiltrate cutaneous nerves (perineural spread)
Also known as morpheic, morphoeiform or sclerosing BCC

Usually surgically excised.
Imiquimod is an immune response modifier.

Best used for superficial BCCs less than 2 cm diameter
Applied three to five times each week, for 6–16 weeks
Results in a variable inflammatory reaction, maximal at three weeks
Minimal scarring is usual
Fluorouracil cream
5-Fluorouracil cream is a topical cytotoxic agent.

Used to treat small superficial basal cell carcinomas
Requires prolonged course, eg twice daily for 6–12 weeks
Causes inflammatory reaction
Has high recurrence rates

Question 31

Squamous cell carcinoma

Answer 31

Cutaneous squamous cell carcinoma (SCC) is a common type of keratinocyte cancer, or non-melanoma skin cancer. It is derived from cells within the epidermis that make keratin — the horny protein that makes up skin, hair and nails.

Cutaneous SCC is an invasive disease, referring to cancer cells that have grown beyond the epidermis. SCC can sometimes metastasise and may prove fatal. Increased risk with smoking along with the general risk factors.

Cutaneous SCCs present as enlarging scaly or crusted lumps. They usually arise within pre-existing actinic keratosis or intraepidermal carcinoma.

They grow over weeks to months
They may ulcerate
They are often tender or painful
Located on sun-exposed sites, particularly the face, lips, ears, hands, forearms and lower legs
Size varies from a few millimetres to several centimetres in diameter.

Distinct clinical types of invasive cutaneous SCC include:

Cutaneous horn — the horn is due to excessive production of keratin
Keratoacanthoma (KA) — a rapidly growing keratinising nodule that may resolve without treatment
Carcinoma cuniculatum (‘verrucous carcinoma’), a slow-growing, warty tumour on the sole of the foot (meatball)
Marjolin ulcer - a cutaneous SCC that has developed in a scar or chronic ulcer
Multiple eruptive SCC/KA-like lesions arising in syndromes, such as multiple self-healing squamous epitheliomas of Ferguson-Smith and Grzybowski syndrome (burger vs pale pimples)

High-risk cutaneous squamous cell carcinoma has the following characteristics:

Diameter greater than or equal to 2 cm
Location on the ear, vermilion of the lip, central face, hands, feet, genitalia
Arising in elderly or immune suppressed patient
Histological thickness greater than 2 mm, poorly differentiated histology, or with the invasion of the subcutaneous tissue, nerves and blood vessels

Question 32

Squamous cell carcinoma stages and treatments

Answer 32

Metastatic SCC is found in regional lymph nodes (80%), lungs, liver, brain, bones and skin.

T1: Tumour ≤ 2cm without high-risk features

T2: Tumour ≥ 2cm; or; Tumour ≤ 2 cm with high-risk features

T3: Tumour with the invasion of maxilla, mandible, orbit or temporal bone

T4: Tumour with the invasion of axial or appendicular skeleton or perineural invasion of skull base

N1: Metastasis in one local lymph node ≤ 3cm

N2: Metastasis in one local lymph node ≥ 3cm; or; Metastasis in >1 local lymph node ≤ 6cm

N3: Metastasis in lymph node ≥ 6cm

Cutaneous SCC is nearly always treated surgically. Most cases are excised with a 3–10 mm margin of normal tissue around a visible tumour. A flap or skin graft may be needed to repair the defect.

Other methods of removal include:

Shave, curettage, and electrocautery for low-risk tumours on trunk and limbs
Aggressive cryotherapy for very small, thin, low-risk tumours
Mohs micrographic surgery for large facial lesions with indistinct margins or recurrent tumours
Radiotherapy for an inoperable tumour, patients unsuitable for surgery, or as adjuvant

Locally advanced primary, recurrent or metastatic SCC requires multidisciplinary consultation. Often a combination of treatments is used.

Surgery
Radiotherapy
Cemiplimab
Experimental targeted therapy using epidermal growth factor receptor inhibitors

Question 33

Melanoma

Answer 33

Melanoma is a potentially serious type of skin cancer, in which there is uncontrolled growth of melanocytes (pigment cells). Melanoma is sometimes called malignant melanoma.

The main risk factors for developing the most common type of melanoma (superficial spreading melanoma) include:

Increasing age
Previous invasive melanoma or melanoma in situ
Previous basal or squamous cell carcinoma
Many melanocytic naevi (moles)
Multiple (>5) atypical naevi (large or histologically dysplastic moles)
A strong family history of melanoma with 2 or more first-degree relatives affected
White/fair skin that burns easily
Parkinson disease also increases the risk of melanoma.

Precursor lesions include:

Benign melanocytic naevus (normal mole)
Atypical or dysplastic naevus (funny-looking mole)
Atypical lentiginous junctional naevus (flat naevus in heavily sun damaged skin) or atypical solar lentigo
Large or giant-sized congenital melanocytic naevus (brown birthmark).

For superficial melanomas - ABCDE signs

A: Asymmetry of shape and colour
B: Border irregularity including smudgy or ill-defined margin
C: Colour variation and Change
D: Different (formerly diameter)
E: Evolving (enlarging, changing)

For nodular melanoma - EFG signs

E: Elevated
F: Firm to touch
G: Growing

Question 34

Types of melanoma

Answer 34

Superficial spreading melanoma
Lentigo maligna melanoma and lentiginous melanoma (in sun-damaged sites) (looks like red/brown bruise)
Acral lentiginous melanoma (on soles of feet, palms of hands or nails). (often like a red or black bruise)

These superficial forms of melanoma tend to grow slowly, but at any time, they may begin to thicken up or develop a nodule (ie, progress to a vertical growth phase).

Melanomas that quickly involve deeper tissues include:

Nodular melanoma (like a cherry)
Spitzoid melanoma (black dot)
Mucosal melanoma (black patches in mouth)
Neurotropic and desmoplastic melanoma (yellow-white-pink)
Spindle cell melanoma (like a painful spot)
Ocular melanoma. (tumour or black dots in iris)
Combinations may arise, for example, nodular melanoma arising within a superficial spreading melanoma or desmoplastic melanoma arising below a lentigo maligna.