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HY Cancer Care > Oncology + palliative care > Flashcards

Oncology + palliative care Flashcards

1
Q

NICE definition of neutropenic sepsis?

A

Pt undergoing systemic anti-cancer treatment (SACT)
Temp > 38C
Neutrophil count <0.5x10^9/L
Any clinical features of sepsis

Suspect in all unwell chemo pts- some can’t mount a fever due to corticosteroids

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2
Q

When does neutropenic sepsis typically occur?

A

Average around day 10 post chemo
Range: days 5-14

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3
Q

Clinical features of neutropenic sepsis?

A

Fever
Tachycardia
HYPOTENSION <90 SYSTOLIC = URGENT
RR >20
Symptoms related to specific system eg cough, SoB, line, mucositis
Drowsy
Confused

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4
Q

Risk factors for neutropenic sepsis

A
  • Prolonged neutropenia (>7 days)
  • Severity of neutropenia
  • Significant comorbidities (COPD, DM, renal/hepatic impairment)
  • Aggressive cancer
  • Central lines
  • Mucosal disruption
  • Hospital inpatient
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5
Q

Define neutropenia

A

Fall in the level of circulating neutrophils- defined as absolute neutrophil count (ANC) <1.5x10^9/L
<1: immunocompromise, risk of fatal infection
Severe neutropenia is < 0.5

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6
Q

Describe some causes of neutropenia?

A

Genetic- congenital neutropenia, chediak-Higashi syndrome
Cytotoxic therapies
Diseases of bone marrow- haematological malignancy, tumour infiltration, aplastic anaemia, ionising radiation
Infections- bacterial sepsis, viral infections (Human herpes virus 4&5), malaria, typhoid
Autoimmune- IBD crohns, RA
Vitamin deficiency- B12, folate
Increased neutrophil turnover- bacterial infection, hypersplenism

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7
Q

Most common causative organisms of neutropenic sepsis?

A

Source identified only in 20-30% of patients

Bacteria

  • Increasingly Gpos: staph epidermidis, staph aureus, strep pneumoniae
  • Gneg: E coli, klebsiella, pseudomonas
  • Other: c diff
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8
Q

Name a few complications of neutropenic sepsis. How are patients stratified into who’s at low and high risk of complications?

A

Possible complications of neutropenic sepsis include organ failure, invasive and atypical infection, coagulopathy, encephalopathy and delirium, psychological sequelae and death

Risk stratification using a clinical prediction rule such as the Multinational Association of Supportive Care in Cancer (MASCC) prognostic index to identify people at low risk of complications- takes into account disease burden, co-morbidities (hypotension, COPD, solid tumour, haem malignancy, dehydration), status at onset of fever (ie inpatient or outpatient), age (<60 or >60)
High score = lower risk of severe infection that may be suitable for outpatient care

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9
Q

You suspect a patient may have neutropenic sepsis, what things from the history do you need- from the patient or carer

A
  • Risk factors for neutropenia
  • Recent fever or rigors or hypothermia
  • Symptoms suggesting a focus of infection: dysuria, diarrhoea, productive cough
  • Features of dehydration: reduced UO in past 18hrs
  • Altered behaviour/ mental state/ cognition
  • Type of cancer, timing, duration, intensity of chemo/ RT/ immunosuppressants & when was the last treatment given
  • Recent abx (prophylaxis or therapy)
  • Recent corticosteroid use
  • Recent travel/ infectious contacts/ animal exposure
  • Previous episodes of febrile neutropenia or sepsis?
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10
Q

You suspect neutropenic sepsis in a patient on the ward, what clinical features on examination do you look out for?

A
  • General appearance, level of cognition and consciousness- AVPU or GCS
  • Temperature- high or low
  • HR, RR, signs of resp distress, BP
  • CRT, O2 sats
  • Mottled or ashen skin
  • Pallor or cyanosis of skin/ lips/ tongue, cold peripheries
  • Any rash- non-blanching
  • Any wounds
  • Dry mucous membranes- dehydration
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11
Q

Investigations for suspected neutropenic sepsis?

A

BEDISDE: obs, glucose, pregnancy test

BLOODS:
•FBC (with differential)
•U&Es
•LFTs
•Lactate/ABG
•CRP
Others- bone profile, clotting

CULTURES:
• Blood – central and peripheral
• Urine
• Sputum
• Wound

IMAGING:
• CXR

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12
Q

Management of suspected neutropenic sepsis?

A
  • Prompt assessment by HCPs who are familiar with NS
  • Don’t wait for the FBC
  • Empiric IV broad spectrum antibiotics WITHIN ONE HOUR of hospital admission (use local NICE guidelines)- usually need 5/7 broad spec abx, may switch to oral abx after 48hrs if low risk
  • Fluid resuscitation
  • Oxygen
  • Consider catheterisation
  • Involve senior members of the team – SpR/Consultant
  • Consider need for escalation of care
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13
Q

According to UHL guidelines, what abx do you give within 1 hour for neutropenic sepsis?

A

IV Tazocin
-If penicillin allergic IV Meropenem

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14
Q

Suggest a few ways we can prevent neutropenic sepsis

A
  • Patient education: written and oral information, how and when to contact 24-hour specialist oncology advice/ seek emergency care
  • Antibiotic prophylaxis (versus increased risk of antibiotic resistance)
  • Consider dose reduction for future chemotherapy cycles (palliative chemo)
  • Prophylactic GCSF (curative/adjuvant)
  • ? Stop treatment
  • National chemotherapy alert card
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15
Q

Describe the mechanism of malignant spinal cord compression

A
  • Malignant spinal cord compression (MSCC) occurs when the dural sac and its contents are compressed at the level of the cord or cauda equine
  • 80-85% caused by collapse or compression of a vertebral body that contains metastatic disease (arterial seeding)
  • 10% by direct tumour (paraspinal mass) extension into the epidural space (especially lymphoma)
  • Compression of cord initially causes oedema, venous congestion and demyelination which are reversible
  • Prolonged compression → vascular injury, cord necrosis and permanent damage
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16
Q

Describe the anatomy of the spinal meninges

A

The spinal meninges are three membranes that surround the spinal cord – the dura mater, arachnoid mater, and pia mater. They contain cerebrospinal fluid, acting to support and protect the spinal cord. They are analogous with the cranial meninges.

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17
Q
  1. How many patients are affected by MSCC each year?
  2. What % pts with cancer develop MSCC?
  3. Which types of cancer account for majority of MSCC?
  4. What % pts present with spinal mets have no previous cancer diagnosis?
  5. How many pts who present to their GP w/ back pain have spinal mets?
A
  1. 4000
  2. 5% of all cancers, 15% of advanced cancer
  3. Breast, prostate and lung = 60% cases
    Also common in lymphoma, myeloma, renal & thyroid cancers
  4. About 23%
  5. <0.1%
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18
Q

Commonest site of MSCC?

A
  • Thoracic
  • Up to 50% pts have more than 1 area involved
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19
Q

Clinical features of MSCC?

A

>90% back pain- frequently the first symptom & for 2-3 months ongoing

  • Poorly responsive to analgesia
  • Radiating around chest (band-like) or down legs
  • Radicular component (nerve root)- exacerbated by neck flexion, straight leg raise (SLR), coughing, sneezing, straining
  • May be worse after lying down for a while

Motor symptoms >75%

  • Reduced power
  • Difficulty standing, walking, climbing stairs
  • Often symmetrical

Sensory loss >50%

Sphincter dysfunction

  • Urinary hesitancy
  • Frequency
  • Urinary retention w/ overflow
  • Faecal incontinence

Diminishing performance status, generally unwell

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20
Q

Describe some features you may find on examination of someone with suspected malignant spinal cord compression?

A
  • Acute: flaccid paralysis
  • Over time:
    • Spasticity
    • Hyperreflexia below the level of the lesion with extensor plantar reflex (positive babinski) (UMN lesions)
    • Sensory loss defined within dermatomal level
    • Palpable bladder- UR
  • Cauda equina (not spinal cord; sacral nerves)
    • LBP (lower back pain)
    • Asymmetrical weakness/ sensory deficit
    • Saddle anaesthesia
    • Reduced anal tone
    • Bladder/ bowel dysfunction
      • Painless urinary retention, overflow incontinence

Remember- the disease may affect both the cord and cauda equina leading to a mixed picture

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21
Q

Imaging for MSCC?

A
  • Pain suggesting spinal mets = whole spine MRI within 1 week
  • Signs of MSCC = MRI within 1 day
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22
Q

Management of MSCC?

A
  • Analgesia
  • Dexamethasone 16mg + PPI
    • Glucocorticoids are thought to help reduce oedema helping to relieve compression
  • Swift treatment within 24 hrs of diagnosis
  • Surgery: if limited sites of spinal involvement, radioresistant tumour, if good prognosis (>3/12), cancers such as MM, lymphoma, breast, prostate, renal
    • Surgical decompression & reconstruction
    • Vertebroplasty
    • Balloon kyphoplasty
  • Radiotherapy
    • Within 24 hrs of confirmation
    • Single posterior field, pt usually supine, targets abnormal area + 1-2 vertebra either side
    • Relieves compression of spine & nerve roots by causing cell death of the rapidly dividing tumour cells
    • Relieves pain, stabilises neuro deficit
    • Life expectancy measured in months
  • Other supportive care
    • VTE prophylaxis- TED stockings, prophylactic LMWH
    • Catheter if bladder dysfunction
    • Laxatives
    • Monitor BMs
    • Physiotherapy
    • Occupational therapy
    • Pressure areas- nursing care
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23
Q

Normal range of serum calcium?

A

(corrected): 2.2-2.5 mmol/L

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24
Q

Define malignant hypercalcaemia

How is hypercalcaemia graded?

A

Malignant hypercalcaemia is defined as a serum calcium > 2.6 mmol/L, secondary to a malignant process

The most common malignancies associated with hypercalcaemia are breast cancer, multiple myeloma, lymphoma and lung cancer (e.g. squamous cell carcinoma)

  1. Mild: 2.6-3.0 mmol/L
  2. Moderate: 3.0-3.5 mmol/L
  3. Severe: > 3.5 mmol/L
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25
Q

Calcium physiology: where is calcium stored in the body?

A
  • 99% in bone
  • 1% intracellular
  • 0.1% extracellular
    • 50% ionised- metabolically active, free pool of calcium
    • 41% bound- to albumin (90%) and globulin (10%)
    • 9% complexed- complexes w/ phosphate & citrate
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26
Q

How is the balance between stored calcium and the extracellular pool of calcium maintained?

A
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27
Q

Most cases of hypercalcaemia are caused by what?

A
  1. Primary hyperparathyroidism
  2. Malignant hypercalcaemia
    1. Breast
    2. Myeloma
    3. Lymphoma
    4. Lung cancer
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28
Q

Mechanism of malignant hypercalcaemia?

A
  • PTHrP secretion - “humoral hypercalcaemia of malignancy” (HHM) ~80%
  • Osteolytic metastasis, commonly w/ breast cancer, deposition of tumour cells within bone leads to local production of inflammatory cytokines & other mediators stimulating osteoclasts leading to bone resorption ~20%
  • Production of caltriol (vit D)- Hodgkin’s lymphoma
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29
Q

Clinical features of malignant hypercalcaemia?

A
  • Stones- kidney stones, polyuria, DI
  • Moans- constipation
  • Groans- abdominal pain, N&V, peptic ulcers, pancreatitis
  • Bones- bone pain, muscular weakness
  • Psychiatric overtones- depression, anxiety, impaired cognition, confusion, coma
  • Fatigue, weakness
  • Often non-specific
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30
Q

How to treat malignant hypercalcaemia?

A
  • Aggressive rehydration- IV fluids
  • Bisphosphonates- inhibit osteoclastic bone resorption
    • IV pamidronate or zolendronic acid
    • Can cause renal failure- properly hydrate first
    • Seek advice in renal impairment
    • Take up to 4 days to work, effects last up to 4wks
  • Systemic treatment of malignancy
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31
Q

Suggest some factors affecting the prognosis for patients diagnosed with malignant hypercalcaemia?

A
  • Previous episode of hypercalcaemia?
  • Most patients who develop hypercalcaemia have disseminated disease
  • Many die in < 3/12
  • Px= 52 days for solid organ malignancy
  • Px= 362 days for haematological malignancy
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32
Q

Define SVCO?

A

Malignant superior vena cava obstruction (SVCO) refers to an obstruction to the flow of blood through the superior vena cava (SVC) secondary to a cancer

90% cases are extrinsic compression- intrathoracic primary, lung cancer (80% all cases), mesothelioma

others = mediastinal LN, metastatic or lymphoma (10%)

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33
Q

How many cancer pts are affected by SVCO?

A

3-8% all pts with cancer

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34
Q

What drains into the SVC and what does the SVC drain into?

A

The left & right brachiocephalic veins unite to form the superior vena cava

The SVC travels through the mediastinum and terminates by emptying into the superior aspect of the right atrium

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35
Q

What causes malignant SVCO?

A
  • Lung carcinoma- non small cell more common (although small cell lung carcinoma is less common overall but has a central location & rapid growth so more likely to cause SVCO)
  • Non-Hodgkin’s lymphoma
  • Thymus tumour
  • Breast cancer
  • Mediastinal germ cell tumours
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36
Q

List some signs and symptoms of SVCO?

A

Signs:

  • Facial swelling
  • Distended neck & chest wall veins
  • Upper limb oedema
  • Facial plethora
  • Cyanosis
  • Cognitive dysfunction
  • Can lead to laryngeal oedema, airway obstruction, cerebral oedema

Symptoms:

  • Dyspnoea
  • Facial swelling
  • Head ‘fullness’/ headache
  • Conjunctival swelling & blurred vision
  • Symptoms exacerbated by bending forward/ lying down
  • Cough
  • Dysphagia
  • Lethargy
  • Stridor
  • Hoarse voice
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37
Q

Describe Pemberton’s sign

A
  • Lifting arms above head for 1-2
  • Watch for signs of congestion, facial plethora, cyanosis
  • Resp. distress, inspiratory stridor may occur
  • Venous congestion may be apparent as distension of the neck veins
  • Narrowing of the thoracic inlet against the thyroid
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38
Q

How to investigate suspected SVCO?

A

Imaging is key to diagnosis:

  • CXR- helps exclude other causes of breathlessness
    • Mediastinal widening
    • Malignant pleural effusion
  • URGENT CT- diagnostic
    • Reveals the extent & level of obstruction
    • Presence of collateral vessel formation (is this a chronic obstruction?)
    • Reveals the likely underlying cause
    • Staging for lung cancers
  • Duplex ultrasound
    • To identify SVCO in pts with indwelling catheter
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39
Q

How to manage SVCO?

A
  • Sit upright, elevate head
  • Asses need for O2
  • Dexamethasone 16mg + PPI
  • Opioids
  • Benzodiazepines
  • Stent: if not radio or chemo sensitive- rapid relief of symptoms; doesn’t treat cause
  • Radiotherapy for other malignant causes, response rate 60%
  • Chemotherapy for SCLC, lymphoma, teratoma, response rate >70%
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40
Q

Prognosis for a patient presenting with SVCO?

A

Patients presenting with malignant SVCO have an average life expectancy of six months.

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41
Q

Define tumour lysis syndrome & explain the pathophysiology behind why it happens

A

Tumour lysis syndrome (TLS) results from metabolic disturbances arising from the breakdown of malignant cells following the initiation of treatment for malignancy.

Massive tumour cell lysis → release of large amounts of potassium, phosphate and uric acid into the systemic circulation

  • Hyperuricaemia
  • Hyperkalaemia
  • Hyperphosphataemia
  • AKI from uric acid or calcium phosphate crystals in renal tubules
  • Hypocalcaemia

Sudden death can occur

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42
Q

Which tumours/ cancers are most susceptible to tumour lysis syndrome?

A
  • Greatest risk with haematological malignancy
  • Also seen in other lymhphomas, CLL, myeloma
  • Much less common in solid tumours- germ cell, small cell lung, breast
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43
Q

Clinical risk factors for developing tumour lysis syndrome?

A
  • Pre-existing hyperuricaemia, hyperphosphataemia
  • Renal impairment
  • High volume/ bulky disease
  • Pre-treatment LDH high
  • High circulating WCC
  • Hypovolaemia
  • Pre-treatment diuretic use
  • Urinary tract obstruction from tumour
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44
Q

How do patients with tumour lysis syndrome present?

A
  • Normally day 3-7 post chemotherapy
  • N&V
  • Diarrhoea
  • Anorexia
  • Lethargy
  • Haematuria → oliguria → anuric
  • Fluid overload
  • Cardiac arrhythmia/ arrest- peaked T waves, QTc deranged
  • Muscle cramps, tetany, seizures
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45
Q

How to prevent tumour lysis syndrome?

A

Prevention:

  • Hydrate, maintain UO, lower uric acid levels
    • Pre-hydration & vigorous hydration throughout treatment
    • Keep monitoring electrolytes
  • Allopurinol
    • Xanthine oxidase inhibitor- less hyperuricaemia
    • Doesn’t act on pre-existing uric acid so is used for prophylaxis

Treatment/ prophylaxis:

  • Rasburicase
    • Synthetic uricase- degrades uric acid to allantoin (water soluble)
    • Actively lowers uric acid levels & works on renal deposits, hence can be used prophylactically & for treatment
  • Dialysis
  • Phosphate binders for severe hyperphosphataemia
  • Manage hyperkalaemia- IV calcium gluconate, insulin/ dextrose infusion, nebulised salbutamol & cardiac monitoring for K>6 or 25% increase above baseline
  • Cardiac monitoring for hypocalcaemia; otherwise don’t treat
    • IV replacement if arrhythmias or symptomatic
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46
Q

Essential investigations for suspected tumour lysis syndrome?

A
  • Renal function
  • Electrolytes
  • Serum urate
  • Urine dip
  • Urine microscopy
  • Serum lactate
  • LDH
  • ECG
  • Cardiac monitor
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47
Q

What is the Cairo-Bishop definition?

A

The diagnosis of Tumour Lysis Syndrome is based on the Cairo-Bishop definition

Divides TLS into both a labaroty and clinical definition at presention & within 7 days of treatment

Labaratory diagnosis: 2 or more of

  • Hyperuricaemia
  • Hyperkalaemia- >6 or 25% increase
  • Hyperphosphataemia
  • Low calcium

Clinical diagnosis: 1 or more of

  • Serum creatinine >1.5 x normal
  • Cardiac arrhythmia/ sudden death
  • Seizure

The definition is also used to help stage the TLS

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48
Q

Who gets a 2WW referral for lung cancer?

A
  • CXR findings suggesting lung cancer
  • Unexplained haemoptysis + age >40
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49
Q

What sort of red flag symptoms do you look out for in a GP setting and would warrant an urgent CXR (within 2 weeks)?

A

Age > 40 + 2+ of the following OR if they’ve smoked and have 1 of the following:

  • Cough
  • Fatigue
  • SoB
  • Chest pain
  • Weight loss
  • Appetite loss

Age >40 with ANY of the following:

  • Clubbing
  • Persistent/ recurrent chest infection
  • Supraclavicular lymphadenopathy, or persistent cervixal lymphadenopathy
  • Chest signs consistent with lung cancer
  • Thrombocytosis
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50
Q

What sort of symptoms make you suspect oeseophageal canccer + who gets referred in a GP setting and who are they referred to?

What symptom might warrant a non-urgent referral for oesophageal cancer?

A

Direct + urgent access to upper GI endoscopy for the following:

  • dysphagia
  • age >55 + weight loss + any of the following:
    • upper abdo pain
    • reflux
    • dyspepsia

Non-urgent referral for:

  • Haematemesis
  • Age > 55 + treatment resistant dyspepsia
  • Age > 55 + upper abdo pain w/ one of the following:
    • Low Hb
    • Raised platelet + nausea/ vomiting, wt loss/ reflux/ dyspepsia/ upper abdo pain
    • N&V + wt loss/ reflux/ dyspepsia/ upper abdo pain
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51
Q

Who gets a 2WW referral for pancreatic cancer?

Who gets an urgent direct access scan instead? What scan is performed?

A

Age>40 + jaundice for urgent appointment

For an urgent direct access CT scan:

age >60 + weight loss + any of the following:

  • diarrhoea
  • back pain
  • abdo pain
  • nausea
  • vomiting
  • constipation
  • new-onset diabetes
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52
Q

Patient is referred 2WW for suspected colorectal cancer.

Who are they referred to and what symptoms would warrant this sort of referral?

A
  • age > 40 + unexplained weight loss + abdo pain
  • age > 50 + unexplained rectal bleeding
  • age > 60 with IDA or changes in bowel habit
  • Tests showing occult blood in faeces
  • Rectal or abdominal mass
  • age < 50 + unexplained rectal bleeding + unexplained abdo pain/ change in bowel habit/ weight loss/ IDA
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53
Q

Who gets a 2WW breast cancer referral?

A
  • age > 30 + unexplained breast lump +/- pain
  • age > 50 with discharge/ retraction/ any other concerning symptom in ONE nippple only
  • skin changes suggestive of cancer
  • age > 30 w/ unexplained axillary lump
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54
Q

Who gets urgent 2WW referral for prostate cancer?

Who would you examine instead + send for a blood test?

A
  • Prostate feels malignant on examination
  • PSA levels above the normal for their age

Consider PSA and DRE in:

  • Any LUTs- nocturia, frequency, hesitancy, urgency, retention
  • Erectile dysfunction
  • Visible haematuria
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55
Q

Who would you refer for urgent 2WW bladder cancer?

A

age > 45 +

  • unexplained visible haematuria w/o UTI
  • visible haematuria that persists/ recurs after UTI treatment

age > 60 + unexplained non-visible haematuria + dysuria/ raised WCC

Consider non-urgent referral for recurrent UTIs

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56
Q

Who gets an urgent 2WW referral for malignant melanoma?

A

Using the weighted 7 point checklist, scoring 3 or more

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57
Q

Pt with suspected basal cell carcinoma

Describe features typical of BCC?

Urgent or routine referral?

A

Typical features of basal cell carcinoma include: an ulcer with a raised rolled edge; prominent fine blood vessels around a lesion; or a nodule on the skin (particularly pearly or waxy nodules)

Urgent referral only if a delay will worsen prognosis eg lesion site or size

Otherwise, BCC is a routine referral

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58
Q

Describe the WHO performance status classification

A

0: able to carry out all normal activity without restriction
1: restricted in strenuous activity but ambulatory and able to carry out light work
2: ambulatory and capable of all self-care but unable to carry out any work activities; up and about more than 50% of waking hours
3: symptomatic and in a chair or in bed for greater than 50% of the day but not bedridden
4: completely disabled; cannot carry out any self-care; totally confined to bed or chair.

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59
Q

What is the 4th most common cancer in the UK?

A

Colorectal cancer

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60
Q

Suggest some risk factors for developing colorectal cancer

A
  • Family history
  • Hereditary syndromes (25%)
    • Lynch syndrome is the most common inherited cause (HNPCC)
    • FAP- familiar adenomatous polyposis
      • Autosomal dominant disorder, mutation in APC gene
      • If untreated, almost all develop cancer by age 40
  • Inflammatory bowel disease
  • Ethnicity- more common in white people
  • Radiotherapy
  • Obesity/ diet
    • Low fibre, high fat
    • Red processed meat
    • Garlic, milk, calcium may be protective
  • Diabetes mellitus
  • Smoking
  • Alcohol
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61
Q

What is the most common colorectal cancer pre-disposition syndrome?

What other malignancies can it cause?

Mode of inheritence? Which gene?

A

Lynch syndrome

  • Can also cause endometrial cancer
    • Also, less commonly, ovarian, gastric, small bowel, hpb, brain malignancies
  • Autosomal dominant
  • One of the mismatch repair genes (MMR)
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62
Q

What is colorectal cancer commonly, at a cellular level? Describe how it forms

A

Adenocarcinoma

One of the earliest mutations is to the tumour suppressor adenomatous polyposis coli (APC) which leads to the hyperproliferative epithelium.

One of the key mutations that follows is KRAS, a proto-oncogene, that becomes an oncogene following mutation.

Further mutations to p53 (tumour suppressor and ‘guardian of the genome’) as well as SMAD4 and others leads to the development of a carcinoma from an adenoma.

This is of course a simplification of a much more complex process, but gives an idea of how multiple mutations are required to develop CRC. In inherited conditions, there are often existing mutations along this pathway (e.g. APC in FAP) that predispose individuals to CRC.

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63
Q

Where does colorectal cancer commonly occur?

A

CRC most commonly occurs in the rectum and sigmoid colon (left side of the colon)

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64
Q

How does colorectal cancer occur (pathophysiology)?

A
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65
Q

Approximately how many patients with colorectal cancer have metastasis at diagnosis, and were does it commonly spread to?

Signs/ symptoms of metastatic disease?

A

Approximately 23-26% of CRC have metastatic spread at diagnosis

The liver is the organ most commonly affected

Rectal cancers are more commonly associated with lung metastasis (prior to liver metastasis) due to direct haematogenous spread via the inferior rectal vein and IVC.

Other locations of metastatic spread includes the peritoneum brain and bone.

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66
Q

3 signs and 3 symptoms of colorectal cancer

What symptoms would you expect for Right colon cancer compared to Left and rectum?

A

Signs

  1. Pallor
  2. Abnormal PR exam
  3. Abdominal mass

Symptoms

  1. Change in bowel habit
  2. Malaise
  3. Weight loss
  4. Tenesmus
  5. Abdo pain
  6. Bleeding

Right colon cancer:

  • Weight loss
  • Weakness
  • Rarely obstruction
  • Iron deficiency anaemia

Left colon cancer:

  • Constipation
  • Abdo pain
  • Decreased stool calibre
  • Alternating bowel habit
  • Rectal bleeding
  • Bright red PR bleeding
  • LBO

Rectal cancer:

  • Obstruction
  • Tenesmus
  • Bleeding
  • Bright red PR bleed
  • Palpable mass on rectal exam
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67
Q

Describe the UK screening programme for colorectal cancer

A

The NHS uses the Faecal Immunochemical Test (FIT) to screen for colorectal cancer. This tests for the presence of blood in the stool.

People aged 60-74 (and expanding to 56 years-old from 2021) will be sent a home test kit consisting of a FIT every two years.

After the age of 75, people can request further tests every two years.

Approximately 98% have a normal result.

Those with abnormal results will be invited for colonoscopy.

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68
Q

How is a diagnosis of colorectal cancer made?

A

Colonoscopy = gold standard diagnosis

  • allows visualisation of the colon, identification of malignant lesions and pre-malignant or suspicious polyps
  • risks- perforation- esp. those with diverticular disease
  • bowel prep required- specific diet is followed and agents like Moviprep are given (may have to do this inpatient for some elderly pts)
  • alternatives- CT pneumocolon
    • disadv- can’t visualise polyps or take biopsy, may miss some lesions
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69
Q

Broadly describe the histological and TNM staging of CRC

A

Modified Dukes

  • A: Not into the muscularis propria
  • B: tumour spread beyond muscularis propria
  • C1: LN +ve (apical node spared)
  • C2: LN +ve (apical node involved)
  • D: distant mets

TNM staging-

Tumour

  • TX: Primary tumour cannot be assessed.
  • T0: No evidence of primary tumor
  • Tis: Carcinoma in situ, intramucosal carcinoma (involvement of lamina propria with no extension through muscularis mucosae)
  • T1: Tumor invades submucosa (through the muscularis mucosa but not into the muscularis propria)
  • T2: Tumor invades muscularis propria
  • T3: Tumor invades through the muscularis propria into the pericolorectal tissues
  • T4:
    • T4a: Tumor invades through the visceral peritoneum (including gross perforation of the bowel through tumor and continuous invasion of tumor through areas of inflammation to the surface of the visceral peritoneum)
    • T4b: Tumor directly invades or adheres to other adjacent organs or structures

Node

  • NX: Regional lymph nodes cannot be assessed
  • N0: No regional lymph node metastasis
  • N1: Metastasis in 1 - 3 regional lymph nodes
    • N1a: Metastasis in 1 regional lymph node
    • N1b: Metastasis in 2 - 3 regional lymph nodes
    • N1c: No regional lymph nodes are positive but there are tumor deposits in the subserosa, mesentery or nonperitonealized pericolic or perirectal / mesorectal tissues
  • N2: Metastasis in 4 or more regional lymph nodes
    • N2a: Metastasis in 4 - 6 regional lymph nodes
    • N2b: Metastasis in 7 or more regional lymph nodes

Metastasis

M0: No distant metastasis by imaging; no evidence of tumor in other sites or organs (this category is NOT assigned by pathologists)

  • M1: Nistant metastasis
  • M1a: Metastasis confined to 1 organ or site without peritoneal metastasis
  • M1b: Metastasis to 2 or more sites or organs is identified without peritoneal metastasis
  • M1c: Metastasis to the peritoneal surface is identified alone or with other site or organ metastases

NOTE: Non-regional lymph node spread is considered M1a disease.

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70
Q

Describe treatment options for colorectal cancer

A

Surgery is the mainstay of treatment

  • Laparoscopic > open
  • Stoma- can be temporary
  • Early rectal cancer:
    • Transanal excision
    • Endoscopic submucosal dissection
    • Total mesorectal excision
  • Colonic cancer: offer neo-adjuvant chemotherapy
    • Sigmoid colectomy
    • Right hemicolectomy
    • Left hemicolectomy
    • Subtotal colectomy
    • Total abdominal colectomy
  • Complications of surgery
    • Infection
    • Bleeding
    • Clots
    • ureteric damage
    • Anastomotic leak- commoner in low rectal anastomosis - as such these are often protected with a loop ileostomy
    • Sexual dysfunction
    • Change in bowel habit
  • Neoadjuvant therapy (before surgery)
    • Rectal cancer cT1-T2, cN1-N2, M0, or cT3-T4, any cN, M0 should be offered neoadjuvant radiotherapy or chemoradiotherapy.
    • Colonic cancer with cT4 disease. Consider the use of chemotherapy. There is evidence this improves rate of clear surgical margins and survival.
  • Adjuvant therapy
    • FOLFOX (FOLinic acid, Fluorouracil and OXaliplatin)
    • CAPOX (CAPecitabine and OXaliplatin)
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71
Q

Describe the difference between adjuvant and neoadjuvant therapies

A

Neoadjuvant chemotherapy is delivered before surgery with the goal of shrinking a tumor or stopping the spread of cancer to make surgery less invasive and more effective.

Adjuvant chemotherapy is administered after surgery to kill any remaining cancer cells with the goal of reducing the chances of recurrence.

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72
Q

A patient comes to you and says his best friend recently passed away from colorectal cancer. He asks you if there is anything he can do to reduce his risk of getting colorectal cancer, what do you advise him?

A

Modifiable risk factors

  • Healthy balanced diet, 5 fruits/ veg a day
  • Reduce red meats
  • Stop smoking
  • Maintain healthy weight

Specifically- in people with Lynch syndrome, taking aspirin for >2years has a protective effect

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73
Q

Describe the expected prognosis of CRC

A

Following diagnosis with CRC:

  • 78% survive one year
  • 58% survive five years or more

Prognosis is related to both stage and age at diagnosis. Around 70% of those 15-39 survive 5 years compared to around 40% of those aged over 80. Interestingly survival is also higher in those aged 60-69 - this may be related to the screening programme.

One year survival is around 98% if diagnosed at stage 1, compared to 44% in those with stage 4 disease.

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74
Q

List differential diagnosis for a breast lump + briefly describe features

A
  • Fibroadenoma- mobile, firm breast lumps
  • Breast cyst- smooth discrete lump (may be fluctuant)
  • Epithelial hyperplasia- generalised lumpiness or discrete lumps
  • Fat necrosis- hx of trauma
  • Mammary duct ectasia- may present with a tender lump around the areola +/- a green nipple discharge
  • Duct papilloma- usually present with nipple discharge, if large may be a mass
  • Breast cancer- hard, irregular lump
  • Breast abscess- more common in lactating woman- red, hot tender swelling
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75
Q

Describe some clinical features of breast cancer including features of metastatic spread

A

Breast and/or axillary lump:

  • Often irregular
  • Typically hard/firm
  • May be fixed to skin or muscle
  • Breast pain

Breast skin: change to normal appearance

  • Skin tethering
  • Oedema
  • Peau d’orange

Nipples:

  • Inversion
  • Discharge, especially if bloody
  • Dilated veins

Features may also reflect metastatic spread. The bone (bone pain), liver (malaise, jaundice), lungs (shortness of breath, cough) and brain (confusion, seizures) are most commonly affected

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76
Q

List 6 risk factors for developing breast cancer

A
  • Female gender
  • Age
  • Family history
  • Personal history of breast cancer
  • Genetic predispositions (e.g. BRCA 1, BRCA 2)
  • Early menarche and late menopause
  • Nulliparity
  • Increased age of first pregnancy
  • Multiparity (risk increased in period after birth, then protective later in life)
  • Combined oral contraceptive (still debated, effect likely minimal if present)
  • Hormone replacement therapy
  • White ethnicity
  • Exposure to radiation
  • BRCA
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77
Q

What is BRCA? What cancers does it pre-dispose?

A

BRCA 1:

  • Chromosome 17 mutation
  • 65-80% lifetime risk of breast cancer (normal baseline 12%)
  • Ovarian cancer lifetime risk 40-45% (normal baseline 1.3%)
  • 1% men breast cancer

BRCA 2:

  • Chromosome 13 mutation
  • Lifetime breast cancer risk 45-70%
  • Ovarian cancer risk 11-25%
  • 8% men breast cancer
  • Other malignancies
    • includes peritoneal, endometrial, fallopian, pancreatic and prostate cancer
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78
Q

How many women will develop breast cancer?

A

1 in 8

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79
Q

How are breast cancers classified?

A

Majority are carcinomas

  • Ductal
    • Ductal carcinoma in situ (DCIS)
    • Invasive ductal carcinoma (IDC) (most common invasive breast cancer)
  • Lobular
    • Lobular carcinoma in situ (LCIS) (uncommon)
    • Invasive lobular carcinoma (ILC)

Does it invade the basement membrane?

  • Yes - ‘invasive’
  • No - ‘in situ’
80
Q

Describe the screening programme for breast cancer that the NHS offers

A
  • Ages 50-71
    • Every 3 years
  • Mammogram of each breast
    • Radiologist reviews & says whether it’s satisfactory (96%) or abnormal/ unclear
81
Q

What happens when patients are referred for breast cancer?

A

One-stop breast clinic: triple assessment

  1. Clinical history & examination
  2. Imaging
    1. Mammogram- soft tissue masses and microcalcifications.
    2. USS- used for pts <40
  3. Histopathology
    1. FNA
    2. Core biopsy
82
Q

What is Paget’s disease?

A
  • Paget’s disease of the nipple is an eczematoid change of the nipple associated with an underlying breast malignancy and it is present in 1-2% of patients with breast cancer.
  • In half of these patients, it is associated with an underlying mass lesion and 90% of such patients will have an invasive carcinoma.
  • 30% of patients without a mass lesion will still be found to have an underlying carcinoma.
  • The remainder will have carcinoma in situ.
83
Q

What is inflammatory breast cancer?

A
  • Inflammatory breast cancer where cancerous cells block the lymph drainage resulting in an inflamed appearance of the breast.
  • This accounts for around 1 in 10,000 cases of breast cancer.
84
Q

What surgical options are available for the treatment of breast cancer?

A

Resection of the primary tumour:

  • Mastectomy
    • Multi-focal tumour
    • Central tumour
    • Large lesion in small breast
    • DCIS > 4cm
    • Patient choice
  • Wide local excision (breast conservation)
    • Solitary lesion
    • Peripheral tumour
    • Small lesion in large breast
    • DCIS < 4cm
    • Patient choice
    • Whole breast radiotherapy to reduce the risk of recurrence
85
Q

Besides surgery, what management options are there for breast cancer?

A

Radiotherapy

  • After wide local excision: whole breast radiotherapy- reduces recurrence by 66%
  • After mastectomy: in T3, T4 tumours or if 4+ positive axillary nodes offer RT

Chemotherapy

  • Neoadjuvant: prior to surgery to reduce tumour size, or for pts w/ inflammatory breast cancer
  • Adjuvant: eg FEC (fluorouracil, epirubicin, cylophosphamide) for axillary node disease

Hormone therapy: treatments are for ~ 5 years

  • Pre/peri-menopausal women/ men: tamoxifen (SERM)
    • Side effects of tamoxifen: endometrial cancer risk, VTE, menopausal symptoms, osteoporosis
  • Post-menopausal women: aromatase inhibitors (inhibits peripheral conversion of androgens to oestrogens- not effective in premenopausal women where oestrogens are synthesised primarily by the ovaries) eg anastrozole

Biologics

  • Trastuzumab (Herceptin): HER2 + cancers
    • Contraindicated in heart disease
86
Q

What descriptive terms are used when assessing a skin lesion?

A

Distribution

  • Extensor
  • Flexural
  • Follicular
  • Acral (distal areas of hands and feet)
  • Dermatomal
  • Seborrhoeic

Configuration- shape and outline

  • Discrete
  • Confluent
  • Linear
  • Discoid
  • Target
  • Annular

Colour

  • Erythematous
  • Purpuric
  • Hyperpigmented lesions
  • Hypopigmented lesions
  • Depigmentation

Morphology

  • Macule- flat, <0.5cm
  • Patch- flat, > 0.5cm
  • Papule- solid raised palpable <0.5cm
  • Nodule- > 0.5cn
  • Plaque
  • Vesicle
  • Bulla
  • Pustule
  • Abscess
  • Boil/ furuncle
  • Carbuncle
87
Q

Risk factors for developing skin cancer?

A
  • Exposure to UV light
  • Severe sun burn in childhood (e.g. blistering)
  • Immunosuppression
  • Multiple (>100) or giant (>20 cm) naevi
  • Skin type (Fitzpatrick Skin types I & II)
  • Family history (cyclin-dependent kinase mutations are linked to 20-40% of familial melanoma)
  • Genetic mutations (CDK4, xeroderma pigmentosum, melanocortin 1 receptor)
88
Q

How common is malignant melanoma in the UK?

A

5th most common cancer in the UK

89
Q

Describe the tumour progression of malignant melanoma?

A
  • Benign naevus (typical mole) - controlled proliferation of melanocytes
  • Dysplastic naevus (atypical mole) - abnormal proliferation of melanocytes resulting in a pre-malignant lesion with atypical cellular structure.
  • Radial growth phase - melanomas tend to extend superficially and outwards initially. Melanocytes acquire the ability to proliferate horizontally in the epidermis, but few cells invade the papillary dermis.
  • Vertical growth phase - malignant cells invade the basement membrane and proliferate vertically downwards into the dermis.
  • Metastasis - malignant cells may spread to other areas of body. Typically they travel to regional lymph nodes first; but they may spead to other areas of the skin / soft tissue, or to solid organs (such as the lungs, liver, bone or brain).
90
Q

What is melanoma?

A
  • Melanoma originates from uncontrolled proliferation of melanocytes in the basal epidermis.
  • Melanocytes are specialised melanin-producing cells that are found within the basal epidermis (the deepest layer of the epidermis). The melanin produced is transferred to the mitotically-active keratinocytes above. Here, it protects the nucleus of keratinocytes from UV damage.
91
Q

Describe the ABCDEs of melanoma

A

A - Asymmetry

B - Border irregularity

C - Colour alterations

D - Diameter > 6 mm

E - Evolution

92
Q

What is an excisional biopsy?

A
  • Complete excision with a margin of 1-2mm of healthy surrounding skin
  • Portion of subcut fat- ensuring the full thickness of the dermis has been samples
  • Local anaesthetic; day case procedure
93
Q

Histologically, melanomas are split into 5 major subtypes, what are they?

A
  1. Superficial spreading (70%)
    1. Any location- arms, back, legs, chest
    2. Young pts
    3. Growing moles
    4. Initial radial growth pattern- progresses to invade deep into dermis
  2. Nodular (15%)
    1. Seen at a more advanced stage
    2. Immediately vertical growth
    3. Red or black lump or lump which bleeds or oozes
    4. Sun exposed skin, middle-aged pts
  3. Lentigo maligna (10%)
    1. Elderly pts
    2. Chronically sun-exposed sites
    3. A growing mole
    4. Long period of intraepithelial growth (slow)- better prognosis
  4. Acral lentiginous (<5%) rare
    1. Under nails, palmar/ plantar surfaces of hands/ feet
    2. Subungual pigmentation - Hutchinson’s sign
  5. Desmoplastic melanoma (<1%)
    1. 50% amelanotic
94
Q

Describe the diagnostic features of malignant melanoma?

A

Major criteria

  • Change in size
  • Change in shape
  • Change in colour

Minor criteria

  • Diameter >=7mm
  • Inflammation
  • Oozing or bleeding
  • Altered sensation
95
Q

What is breslow thickness?

A

BT is based on the vertical thickness of malignant melanoma in mm

Measured from stratum granulosum of the epidermis or if the lesion is ulcerated, from the bottom of the ulceration upwards to the point of maximum ulceration

Correlates strongly w/ mortality

96
Q

How is malignant melanoma managed?

A

Surgical

  • Wide local excision
    • Involves removal of the biopsy scar with a surrounding margin of ‘healthy’ skin, with fat, down to muscular fascia.
    • Determined by Breslow thickness (see attached image)
  • Sentinel lymph node biopsy (SLNB)
    • The sentinel node = the 1st lymph node that receives drainage from an affected area
    • Performed under GA
  • Lymphadenectomy
    • Positive SLNB (deposits found within sentinel lymph nodes): usally results in referral for a subsequent lymphadenectomy
      • A lymphadenectomy is performed in an attempt to gain regional control of disease
  • Electro-chemotherapy
    • Locally advanced melanoma
    • Pulses of electricity + chemotherapy- given IV or injected directly into tumour
    • The electricity allows the chemotherapy drug to pass through more effectively

Medical

  • Adjuvant therapy eg interferon alpha
  • Chemotherapy not very good for melanoma
  • Radiotherapy
  • Immunotherapy
97
Q

Where does malignant melanoma metastasise?

A

Spread occurs via lymphatic system/ blood vessels

Can spread to subcut tissue under the skin, lymph nodes, or other organs eg lungs, liver, bone, brain

98
Q

What is the commonest form of skin cancer?

Describe some clinical features of said cancer?

A

Basal cell carcinoma

  • Slow growing
  • Locally invasive
  • Malignant epidermal (basal layer) skin tumour
  • Months- years
  • Sun-exposed areas of the body- 80% head and neck
99
Q

Besides UV light exposure, what are some other risk factors for developing Basal cell carcinoma?

A
  • Skin type
  • Male sex
  • Increasing age
  • Genetics- albinism, Gorlin’s syndrome, zeroderma pigmentosum
  • Previous skin cancers
  • Immunosuppression
  • Carcinogens- ionising radiation
100
Q

Describe the histology of prostate cancers

A
  • Majority adenocarcinomas (95%)
  • Rarer forms- transitional cell, squamous cell, neuroendocrine cancers
  • Majority arise in peripheral zone (70%)
  • 10-20% central zone
  • 10-20% transitional zone
101
Q

Risk factors for developing prostate cancer?

A
  • ↑ Age
  • Black African > White > Asian
  • Family history
    • Prostate cancer in 1st/2nd degree relative
    • Breast cancer in mother
    • 4x increased risk if one 1st degree relative diagnosed with CaP before age 60
  • Obesity
  • Genetics
    • BRCA2 mutation
    • Lynch syndrome
  • Diet
    • Red meat, fat, dairy, calcium
  • Chemicals
    • High pesticide exposure
  • Hormones
    • High levels of IGF-1
102
Q

Clinical features of prostate cancer?

A
  • Frequently asymptomatic
  • LUTS:
    • Nocturia
    • Frequency
    • Hesitancy
    • Urgency
    • Dribbling
    • Overactive bladder
    • Retention
  • Visible haematuria
  • Abnormal DRE (hard, nodular, enlarged, asymmetrical)
  • Symptoms of advanced disease (e.g lower back pain, bone pain, weight loss, anorexia)
  • Ejaculatory symptoms (rare)
103
Q

As a GP, who would you consider doing a DRE (in the context of suspecting prostate cancer)?

A

DRE should be considered in men with:

  • Lower urinary tract symptoms (e.g. nocturia, frequency, hesitancy, urgency or retention)
  • Haematuria
  • Unexplained symptoms that may be explained by advanced prostate cancer (e.g lower back pain, bone pain, weight loss)
  • Erectile dysfunction
  • Other reasons to be concerned of prostate cancer (e.g. elevated PSA)
104
Q

When is a PSA test useful? What are the issues with testing PSA in males?

Suggest some issues for PSA screening?

What to instruct patient prior to PSA test?

A

PSA is produced by normal prostate tissue but levels increase in malignancy, can be used to air diagnosis and surveillance of prostate cancer

Issues-

  • Normal PSA:
    • 1 in 7 (15%) men with normal PSA will have prostate cancer
    • 1 in 50 (2%) will have a higher risk prostate cancer
  • ↑ PSA
    • Age 50-70 10% will have raised PSA
      • PSA 4-10 ng/ml: 25% chance of having CaP
      • PSA>10 ng/ml: 50% chance of having CaP
    • Most, where cancer of the prostate is not detected, will continue to have PSA checked
      • Consider anxiety and uncertainty fears in pts- psychosocial factors

Issues for PSA screening

  • Overdiagnosis
  • Over-treatment
  • QoL- co-morbidities of estabilished treatments
  • Cost-effectiveness

Before testing men should not have:

  • Active or recent UTI (last 6 weeks)
  • Ejaculated for 48 hours
  • Engaged vigorous exercise for 48 hours
  • Had a urological intervention in the past 6 weeks
105
Q

Causes of a raised PSA besides cancer?

A
  • benign prostatic hyperplasia (BPH)
  • prostatitis and urinary tract infection (NICE recommend to postpone the PSA test for at least 1 month after treatment)
  • ejaculation (ideally not in the previous 48 hours)
  • vigorous exercise (ideally not in the previous 48 hours)
  • acute urinary retention
  • instrumentation of the urinary tract
  • prostate cancer
106
Q

First line ix for diagnosis of prostate cancer?

A

Multiparametric MRI

Radiologist reviews & gives it a Likert score

  1. Clinically significant cancer highly unlikely to be present
  2. Clinically significant cancer is unlikely to be present
  3. Chance of clinically significant cancer is equivocal
  4. Clinically significant cancer is likely to be present
  5. Clinically significant cancer is highly likely to be present

Score of 3+ - offer biopsy (guided by the MRI)

107
Q

Management of prostate cancer?

A
  1. Active surveillance- for low risk disease or for those who decline 2 and 3 in intermediate risk, not recommended for high risk disease
    1. 3 monthly PSA
    2. 6 month to yearly DRE
    3. Re-biopsy every 1-3 years
    4. Mp-MRI too
  2. Radical prostatectomy
    1. Removal of prostate gland, resection of the seminal vesicles, along with surrounding tissues +/- dissection of the pelvic lymph nodes
    2. SE- Erectile dysfunction, stress incontinence, bladder neck stenosis
  3. Radical radiotherapy
    1. Offer people with intermediate- and high-risk localised prostate cancer a combination of radical radiotherapy and androgen deprivation therapy
    2. Consider brachytherapy in combination with external beam radiotherapy for people with intermediate- and high-risk localised prostate cancer
    3. Pelvic radiotherapy may be considered in patients who are to have neoadjuvant hormonal therapy and radical radiotherapy and have risk of pelvic wall involvement (>15% risk)
  4. Chemotherapy
    1. Docetaxel
      1. For those who have newly diagnosed non-metastatic prostate cancer + no significant co-morbidities + high risk disease + starting long-term androgen deprivation therapy
      2. Start treatment within 12wks of androgen deprivation therapy
  5. Androgen-deprivation therapies
    1. Prostate cancer is stimulated by circulating androgens (testosterone)
    2. LNrH agonists eg goserelin
    3. GnRH receptor antagonists (LHRH agonists)
108
Q

How is prostate cancer staged?

Risk stratification: how is prostate cancer split into low, intermediate and high risk?

A

Gleason score is used

  • Gleason grade
    • The sum of the most common growth pattern + the second most common growth pattern seen
  • Lowest score an individual with prostate cancer can have is 3+3
  • Sum is inversely proportional to prognosis
    • Gleason X: The Gleason score cannot be determined.
    • Gleason 6 or lower: The cells look similar to healthy cells, which is called well differentiated.
    • Gleason 7: The cells look somewhat similar to healthy cells, which is called moderately differentiated.
    • Gleason 8, 9, or 10: The cells look very different from healthy cells, which is called poorly differentiated or undifferentiated.
109
Q

What’s the difference between active surveillance and watchful waiting?

A
  • Active surveillance: part of a curative strategy aimed at people with localized prostate cancer for whom radical treatments are suitable, keeping them within a window of curability, only those with signs of tumour progression or those with a preference for intervention are considered for radical treatment, active surveillance may avoid or delay the need for RT or surgery
  • Watchful waiting: controlling rather than curing the prostate cancer, for those with localized prostate cancer who don’t want curative treatment/ are unsuitable for it, avoids the use of surgery or radiation but implies that curative treatment will not be attempted
110
Q

How to recognise and refer patients for the following cancers:

  1. Laryngeal
  2. Oral
  3. Thyroid
A

LARYNGEAL CANCER- refer 2WW for pts >45 and:

  • Persistent unexplained hoarseness, or
  • An unexplained lump in the neck

ORAL CANCER- refer 2WW for pts with either:

  • Unexplained ulceration in the oral cavity lasting for more than 3 weeks, or
  • A persistent and unexplained lump in the neck

Refer 2WW for assessment by dentist for pts who have either:

  • A lump on the lip or in the oral cavity, or
  • A red or red and white patch in the oral cavity consistent with erythroplakia or erythroleukoplakia

THYROID CANCER- refer 2WW for people with an unexplained thyroid lump.

111
Q

What type of cancer are head and neck cancers?

A

Mostly SCC- hence often collectively referred to as HNSCCs: Head and Neck Squamous Cell Carcinomas

Common sites-

  • Oral cavity
  • Larynx
  • Nasal cavity
  • Pharynx
  • Middle ear
  • Salivary gland
  • Thyroid glands

Most H&N cancers are of the upper aerodigestive tract- oral cavity, pharynx & larynx

112
Q

Risk factors for developing cancer of the head and neck?

A
  • Smoking (laryngeal cancer)
  • Alcohol excess (pharynx/oral cavity)
  • HPV 16
    • Associated with oropharyngeal cancer
    • Almost always cleared with no adverse affects
    • Presents in younger patients
      • More aggressive, increasing incidence, more amendable to treatment
      • Vaccine available
  • Betel quid (oral cancer)
  • Occupational wood dust exposure (sinonasal cancer)
  • EBV infection (nasopharyngeal cancer)
113
Q

How & where do head and neck cancers spread?

A
  • Different to other cancers
  • Metastasises to cervical LNs first
    • Hard, fixed neck lump
    • Still curable – neck radiotherapy or surgical lymph node clearance (neck dissection)
  • Distant mets usually to lung
114
Q

Many HNSCCs, typically the oral cancers, may begin as a visible premalignant condition, give some examples?

A
  • leukoplakia (white patches)
  • erythroplakia (red patches)
  • erythroleukoplakia (mixed red and white patches)
  • oral lichen planus
  • actinic cheilitis
115
Q

Investigations for head and neck cancers?

A

–US and FNA

–FNE

–CT/MRI scan

–Panendoscopy and biopsy EUA

–PET scan

–P16 staining

116
Q

How are head and neck cancers treated/ managed?

A

Surgical resection +/- adjuvant radiotherapy or chemotherapy or primary radiotherapy +/- adjuvant chemotherapy are the mainstays of treatment for most HNSCCs.

The details:

  • Oral cavity
    • Small tumours - wide local excision +/- neck dissection
    • Large tumours- surgical resection +/- flap reconstruction + neck dissection +/- post operative radiotherapy +/- chemotherapy
  • Oropharynx
    • Small tumours of the tonsil can undergo surgical resection using Laser or Transoral Robotic Surgery +/- neck dissection or primary radiotherapy or both (if margin involved). Larger tumours of the tonsil will undergo solely primary radiotherapy +/- adjuvant chemotherapy
    • Small tumours at the tongue base will undergo surgical resection using Transoral Robotic Surgery with neck dissection or primary radiotherapy or both (if margin involved). Larger tumours at the tongue base will undergo primary radiotherapy +/- adjuvant chemotherapy
  • Larynx
    • Supraglottis-
      • Small tumours will undergo surgical resection using transoral laser microsurgery with bilateral neck dissection or primary radiotherapy +/- adjuvant chemotherapy
      • Larger tumours will undergo laryngectomy with post-operative radiotherapy +/- adjuvant chemotherapy or primary radiotherapy +/- adjuvant chemotherapy
    • Glottis
      • Small tumours will have surgical resection using transoral laser microsurgery with bilateral neck dissection or primary radiotherapy
      • Larger tumours undergo laryngectomy with neck dissection and post-operative radiotherapy +/- adjuvant chemotherapy or primary radiotherapy +/- adjuvant chemotherapy
    • Subglottis- rare. similar principles as glottis
  • Salivary glands
    • Excision
117
Q

Complications following treatment for head and neck cancers?

A
  • Disease recurrence
  • Secondary primary malignancies
  • Dysphagia (secondary to pharyngeal/oesophageal stricture)
  • Pharyngocutaneous fistula (following laryngectomy)
  • Injury to the accessory, vagus, hypoglossal, or marginal mandibular nerves (following neck dissection), or chyle leak (following neck dissection)
  • Mucositis (early complication of radiotherapy) or xerostomia (complication of radiotherapy)
  • Chronic pain, persistent hoarse voice, or hearing loss (following chemoradiotherapy)
118
Q

Classification of thyroid cancer?

A

Thyroid follicular epithelial derived cancer:

  • Papillary- most common, local spread, younger peak incidence compared to follicular, overall good prognosis
  • Follicular- pulmonary & skeletal spread, more common in women
  • Anaplastic- local, skin + brain spread, mean age onset 5, highly aggressive

Medullary thyroid cancer- 25% familial associated with MEN type 2

Primary thyroid lymphoma- treatment normally with chemo/ radiotherapy

119
Q

Risk factors for thyroid cancer?

Clinical features of thyroid cancer?

How is it investigated?

A

The major risk factors are:

  • Radiation exposure (particularly in childhood)
  • Family history / familial thyroid cancer
  • Female sex
  • Other risk factors include obesity, endemic goitre, FAP and Cowden’s syndrome

The most common presentation of differentiated thyroid cancer is a thyroid nodule/mass. Majority thyroid lumps (95%) are benign

  • Thyroid nodule / mass
  • Hoarseness / change in voice
  • Cervical lymphadenopathy
  • Stridor

Investigations- triple assessment

  • Thyroid function tests
  • Ultrasound of thyroid lumps
  • Fine needle aspiration cytology

Then, may need diagnostic hemithyroidectomy

120
Q

How is thyroid cancer treated? Include complications

A

Surgical resection forms the mainstay of management

Post-op: monitor calcium and PTH

Complications of surgery

  • RLN injury
  • Haematoma
  • Hypoparathyroidism

Adjuvant therapy

  • Radioiodine remnant ablation- Iodine mediated destruction of remnant thyroid tissue
  • External beam radiotherapy-may be considered in certain patients with high risk features (high risk of recurrence, local spread, residual/recurrent tumour).
    • Also used in the palliative setting, particularly in cases of bone/spinal and brain metastasis
121
Q

Describe some clinical features of the following HNSCCs

  1. Oral cavity cancer
  2. Pharyngeal cancer
  3. Laryngeal cancer

*Bonus Q- what is Trotters syndrome?

A
  1. Oral cavity cancer
    1. Painless mess, felt on inner lip, tongue, floor of mouth or hard palate
    2. Non-specific- oral cavity bleeding, localised pain in oral cavity, jaw swelling
  2. Pharyngeal cancer
    1. Odynophagia
    2. Dysphgia
    3. Stertor
    4. Referred otalgia
    5. Nasopharyngeal carcinoma- neck lump
  3. Laryngeal cancer
    1. Hoarse voice
    2. Stridor if advanced
    3. Dysphagia
    4. Persistent cough
    5. Referred otalgia
  • *Trotters Syndrome is a triad =* nasopharyngeal malignancy
  • (1) unilateral conductive deafness (secondary to middle ear effusion)*
  • (2) trigeminal neuralgia (secondary to perineural invasion)*
  • (3) defective mobility of the soft palate*
122
Q

Describe briefly the anatomy of the larynx and what region do laryngeal cancers commonly occur?

A

Anatomically, the internal cavity of the larynx can be divided into three sections:

  • Supraglottis – From the inferior surface of the epiglottis to the vestibular folds (false vocal cords)
  • Glottis – Contains vocal cords and 1cm below them. The opening between the vocal cords is known as rima glottidis, the size of which is altered by the muscles of phonation
  • Subglottis – From inferior border of the glottis to the inferior border of the cricoid cartilage

Most malignancies originate in the glottis region

123
Q

What is an MDT made up of?

A
  • Physician
  • Surgeon
  • Radiologist
  • Pathologist
  • Oncologist
  • AHPs (allied health professionals)
124
Q

Some generic side effects of radiotherapy?

What if a patient smokes?

A
  • Skin reaction
  • Mucositis
  • Dry mouth
  • Difficulty swallowing
  • Osteonecrosis
  • Secondary cancers

Smoking causes hypoxia & reduces the effectiveness of radiotherapy

125
Q

What is palliative care?

What is end of life care?

A
  • Palliative care is the active, total care of the patients whose disease is not responsive to curative treatment
  • Control of pain, of other symptoms, and of social, psychological and spiritual problems
  • Patients are ‘approaching the end of life’ when they are likely to die within the next 12 months
  • Palliative care encompasses end of life care and enhanced supportive care
126
Q

Suggest some barriers to recognising deterioration in patients?

A
  • Unclear diagnosis/ prognosis
  • Lack of confidence, knowledge, skill
  • Disease focused vs pt focused
    • Focus on specific results less on overal picture
  • Unrealistic expectations
  • Fear, destroying hope
  • Culture, religious reasons
  • Death anxiety not acknowledged
  • Considered “giving up” on pt?
127
Q

What is the SPICT?

A

SPICT: Supportive and Palliative Care Indicators Tool

  • Used to identify people with deteriorating health due to advanced conditions or serious illness
  • Prompts holistic assessment and future care planning
  • Planning ahead is important for people:
    • whose health is deteriorating gradually
    • who are at risk of an acute illness due to underlying frailty or ill health
    • who are at risk of developing a complication of a LTC
128
Q

What are some indicators of decline in patients?

A
  • Unplanned hospital admissions
  • Performance status poor/ deteriorating
  • Dependent on others for care
  • Carer needs more help + support
  • Significant weight loss
  • Persistent symptoms despite optimal treatment
  • A decision to reduce, stop, or not have treatment
129
Q

What is the clinical frailty scale?

A
  • a judgement-based frailty tool that evaluates specific domains including comorbidity, function, and cognition to generate a frailty score ranging from 1 (very fit) to 9 (terminally ill)
  • Based on 5 indicators
    • weakness, slowness, weight loss, exhaustion and low physical activity
130
Q

Signs a patient is dying

A
  • Bedbound
  • Drowsiness, impaired cognition, leading to coma
  • Difficulty taking oral medications
  • Reduced food and fluid intake, difficulty swallowing
  • Agitation or restlessness
  • Descreased urine output/ incontinence
  • Increasing symptom burden
  • Respiratory secretions
  • Skin colour changes
  • Temperature changes at extremeties
  • Breathing changes:
    • Shallow breathing
    • Use of accessory muscles
    • Cheyne-stokes resp. pattern
131
Q

The Leadership Alliance for the Care of Dying People (LACDP) has identified five priorities for care of the dying person: describe these briefly?

A
  1. The possibility of death is recognised and communicated clearly; decisions are made and actions taken in accordance with the person’s needs and wishes, and these are regularly reviewed and decisions revised accordingly
  2. Sensitive communication takes place between staff and the dying person, and those identified as important to them
  3. The dying person, and those identified as important to them, are involved in decisions about treatment and care to the extent that the dying person wants
  4. The needs of families and others identified as important to the dying person are actively explored, respected and met as far as possible
  5. An individual plan of care, which includes food and drink, symptom control and psychological, social and spiritual support, is agreed, coordinated and delivered with compassion
132
Q

Listed below are some common symptoms in the dying. Name a drug to help them?

  1. Pain
  2. Nausea & vomiting
  3. Breathlessness
  4. Restlessness & agitation
  5. Respiratory tract secretions
A
  1. Pain
    1. Morphine 2.5-5 mg SC PRN
  2. Nausea & vomiting
    1. Levomepromazine 2.5-5mg SC PRN
  3. Breathlessness
    1. Morphine 2.5-5mg
  4. Restlessness & agitation
    1. Midazolam 2.5-5mg SC PRN
    2. Levomepromazine 6.25-12.5mg SC PRN (where delirium and psychosis)
  5. Respiratory tract secretions
    1. Glycopyronium 200-400 mcg SC PRN
133
Q

How is mouth care addressed in end of life care?

A
  • Offer frequent sips if able- use beaker or oral syringe
  • Moisten mouth regularly w/ foam sticks
  • Artificial saliva eg biotene gel
  • Vaseline to lips- KY jelly is using O2
134
Q

Mr Jack Cooper is a 67 -year -old man who was diagnosed with inoperable SCC of right lung cancer 2/12 ago which was treated with 2 fractions of palliative radiotherapy

He was admitted yesterday with increasing breathlessness; drainage of his new pleural effusion is planned for tomorrow

His chest pain is escalating despite regular paracetamol and you (F1) have been asked to review him.

List some possible causes for his pain?

A
  • CANCER related: chest wall invasion, bone metastases, MSCC
  • TREATMENT related: oesophagitis, local reaction to RT
  • OTHER: CAP, PE pneumothorax, MI, anxiety, musculoskeletal
135
Q

What are the different types of pain? How are they described?

A
  • NOCICEPTIVE: normal nervous system, identigiable lesion causing tissue damage
    • Somatic: originates from skin/ muscles/ bone
      • sharp, throbbing, well localised
    • Visceral: originates from hollow viscus or solid organ
      • diffuse ache, difficult to localise
  • NEUROPATHIC: malfunctioning nervous system, nerve structure is damaged
    • stabbing, shooting, burning, stinging, allodynia, numbness, hypersensitivity
  • MIXED: nociceptive and neuropathic
136
Q

Difference between background pain and breakthrough pain?

A

Background pain

  • Persistent baseline pain
  • Regular analgesia

Breakthrough pain

  • Pain breaks through regular pain medicine schedule
  • Quality of pain like background pain but more severe
  • It is managed by as required short acting medications
    • Approx 1/6 of total daily dose
137
Q

Which NSAIDs have no CV or GI risk?

Which have a GI risk only?

Which have a greater CV risk than GI risk?

A
  • No CV or GI risk→ ibuprofen, diclofenac, naproxen
  • GI risk but no CV risk→ cox2; celecoxib
  • CV risk but less GI risk; naproxen or ibuprofen
138
Q

How to manage type 2 diabetes in a dying patient?

A
  • Diet controlled or metformin treated: stop metformin, glucose monitoring required
  • On other tablets or insulin or GLP1 agonist- stop tablets and GLP1 injections, consider stopping insulin if pt only requires small dose
    • If insulin is stopped, check urine for glucose daily, if over 2+ check blood glucose, give rapid acting insulin if blood glucose >20
    • If insulin is continued, prescribe once daily morning dose long acting
139
Q

How to manage type 1 diabetes in a dying patient?

A
  • Do not stop insulin
  • Continue once daily morning dose of insulin, reduce dose
  • Check blood glucose once a day at teatime- if <8, reduce insulin, if >20, increase insulin (to avoid ketosis)
140
Q

What drugs can be used for neuropathic pain?

A
  • Amitriptyline start 10-25mg
  • Gabapentin 300mg TDS over 3/7
  • Pregabalin 75mg BD
  • Full benefit often takes at least 5/7 and may need further titration
141
Q

What are the principles of the WHO pain ladder?

A
  • By the mouth
  • By the clock
  • By the ladder
  • Individual dose titration
  • Use adjuvants at any steps
  • Attention to detail
142
Q

What are adjuvant analgesics?

Name some adjuvant analgesics commonly used?

A
  • Drugs whose primary indications is not for pain
  • Consider for pain that is only partially responsive to opioid analgesia
  • Can have a significant opioid sparing effect

Examples

  • Antidepressants; amitriptyline, duloxetine
  • Anti-convulsants; gabapentin, pregabalin
  • Benzodiazepines; diazepam, clonazepam
  • Steroids; dexamethasone
  • Bisphosphonates for bony pain
143
Q

What are the steps of the WHO pain ladder?

A
  1. Paracetamol, NSAIDs
  2. Dihydrocodeine, codeine phosphate, tramadol, co-codamol
  3. Oxycodone, morphine, fentanyl, diamorphine
144
Q

How are each of the following types of pain managed:

  • Soft tissue pain
  • Visceral pain
  • Bone pain
  • Neuropathic pain
  • Incident pain
A
  • Soft tissue pain
    • Good response to opioid
  • Visceral pain
    • Good/ partial response to opioid
  • Bone pain
    • NSAIDs, RT
    • Bisphosphonate
  • Neuropathic pain
    • Poor response to opioids
    • Adjuvants- amitryptyline, gabapentin, pregabalin
      • Full benefit often takes at least 5 days & may require further titration
    • Early specialist referral required
  • Incident pain
    • IR analgesia
    • Physio/ OT
    • Spinal analgesia
    • Orthopaedic intervention
145
Q

Common side effects of regular use of opioids?

A
  • Constipation
  • Dry mouth
  • N&V
  • Drowsiness/ sedation
146
Q

What to prescribe alongside of opioids?

A

Laxative

Anti-emetic

147
Q

Example of immediate release morphine and example of slow release?

A

IR: Oramorph liquid 10mg/ 5ml

SR: Zomorph capsules BD (10,30,60,100,200mg)

148
Q

How to work out further titrations of opioid dose?

A

Add up 24 hours worth of morphine = TOTAL DAILY DOSE (TDD)

TDD/2 = New Morphine SR dose

TDD/6 = New Morphine IR ‘breakthrough’ (PRN) dose

149
Q

Which opioids are safest in renal impairment?

A

Fentanyl- non-renal excretion

150
Q

How to convert codeine to morphine?

A

codeine to morphine is 10:1

151
Q

How is fentanyl used for pain?

A
  • Transdermal opioid
  • Non-renal excretion
  • 12-24hr to achieve steady state
  • Smallest patch is 12mcg/hr which equates to about 45mg morphine in 24 hours
  • Generally use oramorph as PRN (1/6th of 24 hour morphine equivalent)
152
Q

What can you do for patients who have pain well controlled on zomorph, just started chemo and now can’t keep painkillers down, struggling with n&v?

A

Prescribe syringe driver- via SCSD

153
Q

Signs of opioid toxicity? Causes?

Emergency management of opioid overdose?

A

Signs-

  • Pinpoint pupils
  • Hallucinations
  • Drowsiness
  • Vomiting
  • Confusion
  • Myoclonic jerks
  • Resp. depression

Causes-

  • Dose escalated too quickly
  • Renal impairment
  • Poorly opioid responsive pain but escalated
  • Has had intervention to reduce pain eg nerve block

Emergency management-

  • IV or IM naloxone: has a rapid onset and relatively short duration of action
154
Q

What are the 3 key components of a controlled drug prescription?

A
  1. Drug name
  2. Drug form
  3. Drug strength

Eg

  • Morphine SR (Zomorph) capsules 10mg (Prescribing MR products by brand reduces risk of error)
  • Morphine IR (Oramorph) oral solution 10mg/5ml (Prescribing liquid dose in mg reduces risk of error)
155
Q

What are common causes of N&V in patients with cancer?

A
  • Infection- UTI, pneumonia, gastro-enteritis, thrush
  • Metabolic- renal impairment, hepatic impairment, low Na, high Ca, tumour toxins, sepsis
  • Drug related- opioids, iron, abx, nsaids, diuretics, digoxin, ssri’s, chemo
  • Gastric stasis- pyloric tumour or nodes, ascites, hepatomegaly, opioids, anticholinergics, autonomic neuropathy, gastrostomy
  • GI disturbance- constipation, gastritis, ulceration, obstruction
  • Organ damage- distension, obstruction, RT
  • Neurological- raised ICP, motion sickness, meningeal disease
  • Psychological- anxiety, fear
156
Q

How do the following anti-emetics work- what receptor do they target?

  • Haloperidol
  • Metoclapramide
  • Cyclizine
  • Levomepromazine
  • Ondansetron
  • Domperidone
A
  • Haloperidol-
    • D2 antag in CTZ
  • Metoclapramide-
    • D2 receptor antagonist
    • Acts on gut
    • Increases ACh at muscarinic receptors in gut
    • Promotes gastric emptying
    • Increases peristalsis
  • Cyclizine-
    • H1 receptor antagonist
    • Acts on vestibular nuclei
  • Levomepromazine-
    • D2 receptor antag
    • Acts on CTZ
  • Ondansetron-
    • 5HT3 receptor antagonist
    • Reduces GI motility & secretions
    • Inhibits CTZ centrally
  • Domperidone-
    • Similar to metoclopramide
    • SE: sudden cardiac death, long QT
157
Q

Six potential nausea and vomiting syndromes have been identified in palliative care, with gastric stasis and chemical disturbance being the most common and prominent.

What are the others?

How are they all predominantly treated (name a drug)?

What to use in bowel obstruction nausea/ vomiting?

A
  1. Reduced gastric motility- may relate to opioid use
    1. Metoclopramide, domperidone (not in BO)
  2. Chemically mediated- high Ca, opioids, chemo
    1. Ondansetron, haloperidol
  3. Visceral/ serosal- constipation, oral candidiasis
    1. Cyclizine, levomepromazine
  4. Raised ICP- cerebral mets
    1. Cyclizine
    2. Dexamethasone
    3. RT
  5. Vestibular- ACh and H1 receptors activation, opioid related, can relate to motion too
    1. Cyclizine
    2. Metoclopramide, prochlorperazine
  6. Cortical- anxiety, pain, fear
    1. Benzo eg lorazepam or cyclizine

Other- bowel obstruction: functional- cyclizine

158
Q

Risk factors of chemo induced N&V?

A
  • Female gender
  • Specific chemo agents
  • Age <50
  • past hx of N&V eg pregnancy, prior chemo, motion sickness
159
Q

What is aprepitant & when is it used?

A
  • NK1 antagonist; acts mainly centrally
  • Used for more emetogenic chemo
  • Augments 5HT3 and dex
  • SE: constipation, headache
160
Q

What is the role of anticholinergics in palliative care? Give an example

A

Hyoscine hydrobromide

Controlling respiratory secretions

Also relieving bowel obstruction

161
Q

List potentially reversible causes that may contribute to breathlessness in a patient with advanced malignancy?

A
  • Anaemia- transfusion
  • PE- LMWH, DOAC
  • CCF - diuretics, ACEi
  • COPD- bronchodilators
  • Resp tract infection- abx
  • Pleural effusion- aspirate
  • SVCO- stent, RT, steroids
  • Anxiety- CBT, relaxation, benzodiazepines, SSRIs
162
Q

Why might patients with cancer get breathless?

A

Dyspnoea can result from impaired ventilation or increased ventilatory demand, or both factors. There are multiple possible causes of dyspnoea in people with cancer, including:

  • Direct causes — such as primary lung cancer or lung metastases
  • Indirect effects of cancer — such as pleural effusion, superior vena cava syndrome, anaemia, pulmonary embolism, and surgery
  • Non-malignant causes — such as pneumonia, chronic obstructive pulmonary disease, heart failure, and anxiety
163
Q

How to assess a patient’s breathlessness in a palliative care setting?

A
  • Features of the dyspnoea (for example severity, timing, onset, and precipitating and exacerbating factors)
  • Associated physical symptoms (for example cough, sputum, haemoptysis, wheeze, stridor, pleuritic pain, fatigue, and panic)
  • Effect on the person’s quality of life
164
Q

How is dyspnoea managed in palliative care?

A

Stepwise approach depending on underlying cause + illness

  • Simple measures, such as keeping the room cool, the use of a fan, opening a window, relaxation and breathing techniques
  • Encouraging exercise within the person’s capabilities
  • Adaptations in activities of daily living and lifestyle expectations
  • Strategies to manage other physical symptoms, and the psychological, social, and spiritual needs of the person and their family
  • A strong opioid, such as an immediate-release oral morphine
  • A benzodiazepine short term, especially if dyspnoea is associated with acute anxiety or the person is nearing the end of life
    • Diazepam
    • Lorazepam
  • A bronchodilator if wheeze is thought to be caused by partial airway obstruction from a tumour
  • Oxygen therapy ideally following specialist assessment, especially if the person is at risk of symptomatic hypoxia
165
Q

What does the phrase “advanced care planning” mean?

A

Offers people the opportunity to plan their future care & support, including medical treatment while they have the capacity to do so

  • People at risk of losing mental capacity - for example, through progressive illness.
  • People whose mental capacity varies at different times - for example, through mental illness.
166
Q

What are the following:

  • Mental Capacity Act
  • Advanced Decisions to Refuse Treatment
  • Power of Attorney
A
  • Mental Capacity Act
    • designed to protect and empower people who may lack the mental capacity to make their own decisions about their care and treatment. It applies to people aged 16 and over
  • Advanced Decisions to Refuse Treatment
    • These are for decisions to refuse specific medical treatments and are legally binding
  • Lasting power of Attorney
    • This involves giving one or more people legal authority to make decisions about health and welfare, and property and finances
167
Q

What are the histological types of lung cancer? Describe some key facts about each one.

A
  • Small-cell lung cancer (SCLC)- neuroendocrine cells, produce neuroendocrine hormones- paraneoplastic syndromes- eg ACTH: cushings, siADH,. Grow very fast, poor prognosis, multiple sites, central location near bronchus
  • Non-small cell lung cancer (NSCLC):
    • Adenocarcinoma- most common (38%), more in non-smokers, perioheral, form glands & produce mucin
    • Squamous cell carcinoma- 20%, produce keratin (keratin pearls), central, 98% smokers
    • Large cell- 5%, poorly differentiated, big cells, peripheral, may secrete B-hCG, early mets
  • Mesothelioma
  • Neuroendocrine tumour
168
Q

Risk factors for developing lung cancer?

A
  • Smoking
  • Lung disease eg TB, COPD
  • Radiotherapy
  • Toxins eg asbestos, radon gas, arsenic
  • Pulmonary fibrosis
  • HIV
  • Family history
169
Q

Clinical features of lung cancer? Including emergency presentations and signs of metastases?

Briefly compare the presentation of small cell and non small cell lung cancer

A

Lung cancer is frequently asymptomatic. When symptomatic, cough, malaise and weight loss predominate.

Symptoms

  • Fever
  • Malaise
  • Nausea
  • Cough
  • Haemoptysis
  • Hoarseness
  • Weight loss
  • Anorexia
  • Fatigue
  • Recurrent chest infections
  • Chest pain

Signs

  • Cachexia
  • Anaemia
  • Supraclavicular/ cervical/ axillary lymphadenopathy
  • Stridor
  • Wheeze
  • Clubbing
  • Hypertrophic pulmonary osteoarthropathy (HPOA)
  • Signs of pleural effusion (exudative):
    • Dull (‘stony dull’) percussion
    • Reduced vocal fremitus
    • Reduced breath sounds
  • SVCO
  • Horner’s syndrome

NSCLC

  • Pancoast tumour
    • RLN palsy- hoarse voice
  • Hypercalcaemia (give fluids & zolendronic acid)

Small cell

  • Rapidly progressing symptoms: ~6wks
  • SVCO- headaches, facial swelling, plethora, collaterals over chest walls
  • SiADH- hyponatraemia symptoms
  • Paraneoplastic syndromes
  • Bulky mediastinal disease- dyspnoea, dysphagia due to oeseophageal compression
  • Bone mets- pathological fracture, pain
  • Brain mets- seizure, visual changes, headaches
170
Q

What is a pancoast tumour & how can it present?

A

This is a tumour of the pulmonary apex. Their location means local spread may affect:

  • Brachial plexus
  • Cervical sympathetic trunk and the stellate ganglion
  • Subclavian vein, brachiocephalic vein
  • Subclavian artery
  • RLN
  • Vagus nere

Pancoast tumours are associated with NSCLC

Pancoast tumours are known to cause:

  • Horner’s syndrome
  • Pain in the shoulder that radiates into the arm and hand
  • Atrophy of muscles of the upper limb
  • Oedema of the upper limb
  • Recurrent laryngeal nerve palsy presenting as a hoarse voice

Symptoms

  • Symptoms of lung cancer
  • Pain/ weakness in muscles of arm & hand
  • Hoarse voice
  • Bovine cough
  • SVCO
171
Q

What are paraneoplastic syndromes? Give some examples that are caused by lung cancer?

A

Paraneoplastic syndromes refer to remote effects of tumours unrelated to mass effect, invasion or metastasis.

  1. Hypercalcaemia
    1. May occur due to bony mets or tumour secretion of PTHrP and calcitriol
    2. Stones, bones, groans, thrones, psychiatric moans = renal calculi, bone pain, abdominal pain, polyuria and signs of altered mental status
    3. High calcium seen in 50% of patients with squamous cell carcinoma, 20% of adenocarcinoma and 15% of small cell carcinoma
  2. SiADH
    1. Hyponatraemia
    2. Cerebral oedema if severe
    3. Caused by small cell lung carcinoma
  3. Cushing’s syndrome
    1. Ectopic ACTH released increasing glucocorticoid release
    2. Caused by small cell lung carcinoma
  4. Lambert-Eaton syndrome
    1. Antibodies to voltage-gated calcium channels
    2. 1-3% SClC
    3. Proximal & ocular muscle weakness
    4. Caused by small cell lung carcinoma
  5. Hypertrophic osteoarthropathy
    1. Clubbing & periostitis
    2. Symmetrical, painful arthropathy affecting distal joints
172
Q

What investigations look for evidence of a primary lung cancer?

A

Bedside

  • Observations
  • Blood pressure
  • Lung function tests- spirometry

Bloods

  • FBC
  • U&Es
  • LFTs
  • Bone profile
  • CRP

Imaging

  • CXR
  • CT CAP scan
    • Staging- spread outside chest?
  • PET-CT
    • To see if there’s any hidden disease elsewhere that lights up
  • Bronchoscopy
  • Brain imaging
    • CT head- not good for looking at every single met, so follow up with MRI head
    • MRI head if looking for surgical/ RT curative treatment

Special tests

  • Tissue biopsy
    • Obtained via bronchoscopy, image-guided biopsy, video-assisted thoracoscopic surgery (VATS) or mediastinoscopy
    • Obtained from the tumour, lymph node or metastasis
    • Sometimes pleural fluid is taken
  • Cytology
    • From aspirates, washings, pleural fluids
    • Obtained from the tumour, lymph node or metastasis
173
Q

How is lung cancer staged?

A

TNM staging for NSCLC

Tumour

  • TX: Primary tumour cannot be assessed or tumour proven by presence of malignant cells in sputum or bronchial washings but not visualised by imaging or bronchoscopy
  • T0: No evidence of a primary tumour
  • Tis: Carcinoma in situ
  • T1: Tumour measuring 3 cm or less in greatest dimension surrounded by lung or visceral pleura without bronchoscopic evidence of invasion more proximal than the lobar bronchus (i.e. not in the main bronchus)
  • T2: Tumour > 3 cm but ≤ 5 cm or tumour with any of the following features:
    • Involves the main bronchus regardless of distance from the carina but without the involvement of the carina
    • Invades visceral pleura
    • Associated with atelectasis or obstructive pneumonitis that extends to the hilar region involving part or all of the lung
  • T3: Tumour > 5 cm but ≤ 7 cm in greatest dimension or associated with separate tumour nodule(s) in the same lobe as the primary tumour or directly invades any of the following structure:
    • Chest wall (including the parietal pleura and superior sulcus)
    • Phrenic nerve
    • Parietal pericardium
  • T4: Tumour > 7 cm in greatest dimension or associated with separate tumour nodule(s) in a different ipsilateral lobe than that of the primary tumour or invades any of the following structures: diaphragm, mediastinum, heart, great vessels, trachea, recurrent laryngeal nerve, oesophagus, vertebral body or carina)

Node

  • Nx: Regional lymph nodes cannot be assessed
  • N0: No regional lymph node metastasis
  • N1: Metastasis in ipsilateral peribronchial and/or ipsilateral hilar lymph nodes and intrapulmonary nodes, including involvement by direct extension
  • N2: Metastasis in ipsilateral mediastinal and/or subcarinal lymph node(s)
  • N3: Metastasis in contralateral mediastinal, contralateral hilar, ipsilateral or contralateral scalene, or supraclavicular lymph node(s)

Metastasis

  • M0: no distant metastasis
  • M1: distant metastasis present

Small cell lung carcinoma can be staged in the above TNM staging system too, however the VALSG staging system may be used instead/ in conjunction with it- it better reflects the limited opportunities for treatment with curative intent

  • Limited disease: tumour not spread beyond hemithorax, regional nodes that may be treated with single radiotherapy field.
  • Extensive disease: tumour spread beyond hemithorax or extensively through the hemithorax, distant metastasis, malignant effusions or contralateral hilar/supraclavicular involvement.
174
Q

How are the different types of lung cancers managed?

Include supportive care?

A

NSCLC

  • Surgery
    • Stage I and II disease- lobectomy most often, wedge resection
    • Lymph node sampling to offer prognostic info
  • Chemotherapy
    • Neo-adjuvant (before surgery)
    • Adjuvant (after surgery)
    • Platinum-based regiments
    • MAbs targeting EGFR (e.g. cetuximab) or TKI (e.g. erlotinib)
  • Radiotherapy
    • Often palliative
    • Radical (curative) in early disease

SCLC

  • Surgery
    • Only early disease, small tumour- <5% cases
  • Chemo-radiotherapy
    • Can be given if limited stage- give chemo and radiotherapy
    • Palliative
    • Prophylactic cranial irradiation (PCI) given because those with SCLC are at high risk of brain metastases
  • Immunotherapy

Supportive care

  • Breathlessness
    • Bronchial stent / RT
    • Home O2
    • LOROS breathlessness service
    • Drugs- oramorph, steroids
  • Pain
    • Analgesia
    • Nerve blocks
    • RT
  • Social
    • OT/ PT/ Dietician
    • Psychological support- Macmillan, Support groups, PsychOnc
    • Smoking cessation
    • Financial Support services
175
Q

Epidemiology of lung cancer- average age of presentation? 5 year survival rate?

A

Most diagnosed are >65 years old

One-year survival: 40.6%

Five-year survival: 16.2%

Lung cancer makes up 25% of all cancer deaths

176
Q

Differential of a solitary pulmonary nodule?

Options for management?

A
  • Primary bronchial carcinoma
  • Infection- TB, fungal
  • Non infectious granuloma- granulomatosis with polyangiitis (Wegener’s)
  • Rheumatoid nodule
  • Bronchial carcinoid
  • Haemartoma
  • Metastasis

Management options

  • Sequential CT surveillance over 24 months
  • If patient fit, they may wish to have nodule removed – lobectomy
177
Q

A 78 year old female with known LC (stage IV) presents with leg weakness. On examination there are upper motor neurone signs and sensory loss in the saddle area.

What would you do next?

  1. CT spine
  2. DEXA bone scan
  3. Lumbar spine X-ray
  4. MRI spine
  5. Ultrasound spine

What would be the next management steps?

A
  • This lady has presented with – Cord Compression
  • Urgent MRI spine & discussion with neurosurgeon & oncologist
  • High dose steroids IV or PO dexamethasone
  • RT +/- surgical decompression
  • Urinary catheterisation
  • Delay = paraplegia, loss of bowel & urinary function
178
Q

An 81 year old male patient with LC (stage IV) presents with confusion, nausea and weakness.

What urgent blood test would you arrange?

A

Calcium!

179
Q

Describe the presentation and acute management of the following lung cancer complications-

  1. Hypercalcaemia
  2. SiADH
  3. Brain mets

Besides lung cancer, what else can cause the above?

A
  1. HYPERCALCAEMIA

>3mmol/l usually symptomatic – confusion, weakness, nausea, constipation, reduced fluid intake

  • IV normal saline
  • Bisphosphonates- IV pamidronate
  • Other Causes – Lung Cancer, often squamous cell or bony metastases, raised PTH, sarcoid, vitamin D excess*
    2. SYNDROME OF INAPPROPRIATE ADH RELEASE

Low Sodium & urine osmolality >100 mosmol/kg

Symptoms – Headache, lethargy, confusion, seizures

  • Fluid restrict
  • Consider Demeclocycline (causes diabetes insipidus)
  • Other Causes – Lung cancer (mainly SCLC), pneumonia, drugs (carbamazapine, fluoxetine), stroke*
    3. BRAIN METS
  • Dexamethasone IV or PO 8-12mg/day in morning/early afternoon – avoid in evenings (side effect of insomnia, agitation)
  • Urgent Radiotherapy
180
Q

Describe some of the WHO principles of screening? (1968)

A
  • The condition should be an important health problem
  • There should be a treatment for the condition
  • Facilities for diagnosis and treatment should be available
  • There should be a latent stage of the disease
  • There should be a test or examination for the condition
  • The test should be acceptable to the population
  • The natural history of the disease should be understood
  • There should be an agreed policy on who to treat
  • The total cost of finding a case should be economically balanced in relation to medical expenditure as a whole
  • Case-finding should be a continuous process, not just a “once and for all” project
181
Q

What is the purpose of staging cancers?

A
  • Assessment of local disease
  • Assessment of distant disease

Determines operability & choices of treatment

182
Q

Differential diagnoses of haematuria?

A

Urological

  • Cancer
    • Renal cell carcinoma
    • Upper tract TCC
    • Bladder carcinoma
    • Advanced prostate carcinoma
  • Other
    • Stones
    • Infection
    • Inflammation
    • BPH (large)

Nephrological (glomerular) causes

  • Persistent asymptomatic non visible haematuria, age <40 with associated proteinuria, ↑BP & ↓eGFR is most likely to be nephrological in origin
183
Q

What investigations are done in a Urology Haematuria clinic?

What will primary care have already checked?

A
  • Radiology
    • Ultrasound
  • Endoscopy
    • Flexible cystoscopy
  • Urine
    • Cytology

Primary care will usually have checked eGFR, albumin/creatinine ratio, MSU (if appropriate) before referring to Urology

184
Q

Any lump in the testis is referred via 2WW to Urology. What do the Urologists do?

A
  • Urgent ultrasound of scrotum to confirm diagnosis
  • Check testis tumour markers if testicular mass on ultrasound
    • aFP, hCG, LDH
185
Q

Risk factors for developing bladder TCC?

A
  • Smoking
  • Occupational exposure (20yr latent period)
    • Rubber or plastics manufacture (Arylamines)
    • Handling of carbon, crude oil, combustion, smelting (Polyaromatic hydrocarbons)
    • Painters, mechanics, printers, hairdressers
186
Q

What are some risk factors associated with testicular cancer?

A
  • Cryptorchidism
  • Hypospadias
  • Infertility
  • Klinefelter’s syndrome
  • Tall men
187
Q

Broadly, how is testicular cancer classified?

A
  • The majority of testicular tumours are germ cell in origin (95%)
  • 2 major types-
    • Seminoma
    • Non-seminoma
  • 5% are sex cord/ gonadal stromal tumours eg Leydig cell tumour, Sertoli cell tumour, granulosa cell tumour
188
Q

How does testicular cancer present?

A
  • Commonly as a unilateral scrotal mass
  • Testicular lump, pain, discomfort
  • Back or flank pain (mets)
  • Lymphadenopathy
  • Gynaecomastia (NSGCT)
189
Q

How is a diagnosis of testicular cancer made?

A
  • Testicular USS is the diagnostic modality of choice
190
Q

What tumour markers may be identified in testicular cancer?

A
  • Alpha-fetoprotein (AFP)- NSGCT, particularly yolk sac subtype
  • Beta-HCG- NSGCT, particularly choriocarcinoma subtype, can be seen in seminoma
  • Lactate dehydrogenase- general marker of increased cell turnover, may be raised in seminomas or NSGCTs
191
Q

How is testicular cancer treated?

A
  • Orchidectomy via inguinal approach (to avoid crossing lymph networks)
  • Surveillance, radiotherapy, chemotherapy
192
Q

Where can testicular cancer metastasise to?

A
  • Lung
  • Lymph nodes- pulmonary, pelvic, base of neck
193
Q

How does bladder cancer present?

A
  • Classical presentation: macroscopic (visible) haematuria
  • Dysuria, urgency, urinary frequency
  • Advanced disease- pelvic pain, flank pain, bone pain, peripheral oedema, anorexia, weight loss
194
Q

What is the diagnostic modality of choice for bladder cancer?

A
  • Cystoscopy
    • Allows visualisation of the bladder and for biopsies to be taken
    • Can be therapeutic- allows TURBT to be completed
195
Q

Broadly, how is bladder cancer managed?

A
  • Trans-urethral resection of bladder tumour
  • Intra-vesical BCG (TB live attenuated vaccine) used as immunotherapy
  • Intravesical mitomycin C- antibiotic with anti-neoplastic effects, given following TURBT to reduce recurrence
  • Radical cystectomy
  • Radical radiotherapy
  • Chemotherapy

HY Cancer Care (2 decks)

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