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Medicine - Finals > Oncology > Flashcards

Oncology Flashcards

1
Q

Define oncological emergency

A

Acute medical problem related to cancer (or its treatment), which may result in serious morbidity/mortality if not treated quickly

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2
Q

3 main categories of oncological emergency?

A

Metabolic
Structural/obstructive
Treatment-related

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3
Q

Main oncological emergencies?

A 
Hypercalcaemia
SIADH
Spinal cord compression
SVC obstruction
Neutropenic sepsis
Tumour lysis syndrome
Raised ICP
Airway obstruction
Anaphylaxis
Extravasation
Tamponade
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4
Q

Definition of hypercalcaemia?

A

Serum corrected calcium > 2.6 mmol/L

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5
Q

What is meant by corrected calcium?

A

4% circulating Ca is bound to albumin
Unbound, ionised Ca is physiologically important

To correct Ca levels, add 0.1mmol/L to Ca level for every 4g/L that albumin levels are <40g/L

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6
Q

What are the corrected calcium levels (mmol/L) for hypercalcaemia that is:

a) Mild
b) Moderate
c) Severe

A

a) Mild: 2.6-3.0
b) Moderate: 3-3.4
c) Severe: >3.4

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7
Q

Causes of hypercalcaemia?

A 
Bone destruction (e.g. bony mets)
PTH-related protein (released by some tumours)
Primary hyperparathyroidism
Sarcoidosis
Vit D intoxication
Thyrotoxicosis
Lithium
Tertiary hyperparathyroidism
Dehydration
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8
Q

What is the cause of hypercalcaemia if PTH is high-normal/raised?

A

Hyperparathyroidism

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9
Q

What are the possible causes of hypercalcaemia if PTH is low/low-normal?

A 
Malignancy
Drugs (thiazides, high dose vit D, Li)
Thyrotoxicosis
Adrenal insufficiency
Sarcoidosis or TB
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10
Q

How does hypercalcaemia present?

A 
Painful bones
Urinary stones
Abdominal groans (abdo pain, constipation, N+V, etc)
Psychic moans
Fatigue
HTN
Ectopic calcification
Cardiac arrest
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11
Q

What investigations should be done for hypercalcaemia?

A 
Corrected calcium levels (Ca and albumin)
ECG (shortened QT interval)
Chloride
ABG
K+
Phosphate
Alkaline phosphatase
PTH
Protein electrophoresis
CXR - sarcoidosis
Isotope bone scan (?bony mets)
24hr urinary Ca2+ excretion (for familial hypocalciuric hypercalcaemia)
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12
Q

What are some pointers on investigation towards malignancy as the cause of hypercalcaemia?

A

Low albumin, Cl-, K+
Alkalosis
Raised phosphate, alk phos
PTH normal

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13
Q

Pointers on investigation towards hyperparathyroidism as cause of hypercalcaemia?

A

Raised PTH

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14
Q

How is hypercalcaemia treated?

A

1) Diagnose and Rx underlying cause
2) Correct dehydration (IV 0/9% saline, 3L over 24h)
3) Bisphosphonates (pamidronate, zolendronic acid)

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15
Q

How do bisphosphonates work to treat hypercalcaemia?

A

Inhibit osteoclasts - reduces bone turnover

Reduces Ca2+ levels over several days

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16
Q

Side effects of bisphosphonates?

A 
Flu-like Sx
Oesophagitis
Osteonecrosis of the jaw
Bone pain, myalgia
Reduced phosphate levels
Nausea and vomiting
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17
Q

Other than treating the underlying cause, correcting dehydration, and giving bisphosphates, what else can be done to manage hypercalcaemia associated with malignancy?

A

1) Denosumab (inhibits RANK ligand to inhibit osteoclast maturation)
2) Chemotherapy may help
3) Furosemide (promotes renal excretion of Ca2+)

Steroids may be used in sarcoidosis

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18
Q

What is Denosumab, and what is it used for?

A

Human monoclonal antibody
Inhibits RANK ligand (inhibits osteoclast maturation)
Used to treat hypercalcaemia of malignancy

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19
Q

What is SIADH?

A 
Syndrome of inappropriate ADH secretion
Excess ADH
Failure to excrete dilute urine - water retention
Low serum sodium and plasma osmolarity
High urine osmolarity
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20
Q

How is the osmolarity affected in SIADH:

a) plasma
b) urine

A

a) plasma osmolarity low

b) urine osmolarity high

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21
Q

What are the causes of SIADH?

A 
Cancer:
Small cell lung cancer
Pancreatic
Lymphoma (NHL and Hodgkin's)
Prostate

Non-cancer:
Neuro (stroke, SAH, SDH, meningitis, etc)
Infections (TB, pneumonia)
Drugs (sulfonylureas, SSRIs, TCAs, carbamazepine, vincristine, cyclophosphamide)
Other causes: PEEP, porphyrias

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22
Q

How does SIADH present?

A

Fatigue
N+V
Confusion
Coma

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23
Q

What investigations should be done for SIADH?

A 
Serum Na (low, dilutional)
Plasma osmolarity (low)
Urine Na (high, concentrated)
Urine osmolarity (high)

CT scan - look for underlying cause

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24
Q

How is SIADH managed?

A

1) Fluid restriction
2) Demeclocycline
3) ADH receptor antagonists
4) Treat underlying cause where possible

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25
Q

What is demeclocycline? How does it work to treat SIADH?

A

Tetracycline antibiotic
Causes reversible nephrogenic diabetes insipidus
Kidneys excrete too much water - compensates for excess ADH secretion

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26
Q

How is SIADH managed in an emergency?

A

Slow IV infusion NaCl 1.8%

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27
Q

Why is it important to correct SIADH slowly?

A

To avoid precipitating central pontine myelinolysis

Neurological disorder caused by severe damage of the myelin sheath of nerve cells in the pons

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28
Q

What is spinal cord compression?

A

1) Pressure from tumour between vertebral bodies

2) Collapsed vertebral bodies (ie due to bone cancer) on the spinal cord of caudal equina

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29
Q

Briefly describe the anatomy of the spinal cord

A

Extends from base of skull
Terminates at L1
Cauda equina extends below L1 and contains lumbar, sacral and coccygeal spinal nerves

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30
Q

Which spinal nerves are responsible for the knee and ankle jerk reflexes?

A

Knee: L3-4

Ankle: S1

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31
Q

What are the causes of spinal cord compression?

A 
Malignancy (primary or secondary)
Trauma
Disc prolapse
Inflammatory disease, esp in RA
Spinal infection
Epidural or subdural haematoma
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32
Q

Which types of cancer most commonly cause spinal cord compression?

A 
Breast
Lung
Thyroid
Kidney
Prostate
Bowel
Melanoma
Myeloma
Lymphoma
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33
Q

In women with bony mets, where is the cancer most likely to have originated?

A

Breast

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34
Q

How does spinal cord compression present?

A

Back pain
Radicular pain (radiates to lower extremity via nerve route)
Weakness + sensory loss below level of compression
Difficulty walking
Bladder/bowel dysfunction
Erectile dysfunction
Abnormal neuro exam (LMN signs at level of compression, UMN signs below)

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35
Q

How are the following affected in UMN vs LMN lesions?

1) tone
2) power
3) reflexes
4) wasting
5) fasciculations

A

1) inc vs dec
2) dec and dec
3) brisk vs absent
4) absent vs present
5) absent vs present

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36
Q

How is spinal cord compression investigated?

A

MRI whole spine

Bloods - FBC, U&Es, LFTs (could indicate liver mets)

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37
Q

How is spinal cord compression managed?

A

High-dose corticosteroids - PO DEXAMETHASONE 8mg BD (one at 8am, one at 12pm - do not give after noon as will keep them up all night)
PPI cover whilst on steroids
Bed rest if spinal instability
Neurology assessment
Definitive treatment depends on: site and extent of lesion, overall prognosis, fitness for GA, neurological ability, functional status

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38
Q

When would surgery be indicated for spinal cord compression?

A

Single area of compression - decompress then radiotherapy

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39
Q

What is the role of radiotherapy in the management of spinal cord compression?

A

Needed ASAP to prevent deterioration of neurology
Aims to shrink tumour that causes the symptoms
For patients that require definitive therapy but aren’t suitable for surgery
Can be used for pain control

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40
Q

What are some other methods of treatment for spinal cord compression?

A 
Chemotherapy (if tumour chemo-sensitive)
Hormone deprivation (in prostate ca patients)

Other measures: bisphosphonates, VTE prophylaxis, pressure sore prevention, manage bladder and bowel dysfunction, plan for rehab

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41
Q

What is the prognosis of spinal cord compression?

A

Related to severity of the neurological deficit at the time of presentation

If paraplegia and sphincter involvement has occurred, recovery is uncommon

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42
Q

What is superior vena cava obstruction (SVCO)?

A

Compression, invasion or occasionally intra-luminal obstruction of the SVC

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43
Q

Describe the anatomy of the SVC.

Is it in the R or L side of the mediastinum?

A

Provides venous drainage for head, neck, upper limbs, upper thorax
Extends from the junction of the R and L innominate veins into the right atrium
Surrounded by sternum, trachea, R bronchus, aorta, pulmonary artery, and perihilar and peritracheal nodes
The SVC runs along the R side of the mediastinum
In SVCO, collateral pathways form to provide alternative route for blood to return to RA

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44
Q

What are the main causes of SVCO?

A

90% due to:
Small cell lung cancer
Non-SCLC
Lymphoma

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45
Q

What are the other causes of SVCO?

A

Thymoma
Germ-cell tumours

Others, e.g. thrombus, direct tumour invasion, etc.

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46
Q

What are the symptoms of SVCO?

A

Can have sudden or insidious onset

DYSPNOEA = most common symptom
Chest pain (often at rest)
Cough
Oedema (neck, face, arm)
Dizziness, headache (worse in AM), visual disturbance, nasal stuffiness, syncope
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47
Q

What are the signs of SVCO?

A

Dilated veins over arms, neck and anterior chest wall
Oedema of upper torso, arms, neck and face
Severe respiratory distress
Cyanosis
Engorged conjunctiva
Convulsions and coma

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48
Q

Pemberton’s sign is positive in SVCO. What does this mean?

A

You ask the patient to raise their arms up to the side of their face until they touch.

If they develop cyanosis, worsening SoB or facial congestion, it is said to be positive

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49
Q

What investigations are done for SVCO?

A 
Clinical diagnosis
CXR - widened mediastinum or mass on R side of heart
CT scan
Biopsy of any mass for histopathology
Doppler studies
Invasive contrast-venography
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50
Q

How is SVCO managed?

A

Symptomatic relief (elevation of bed head + O2)
Steroids - Dexamethasone 8mg BD PO
Endovascular stenting
Anticoagulation

Ultimate Rx depends on cause (radio vs chemo) - radio indicated in some lung cancers. Chemo useful in chemo-sensitive tumours, e.g. SCLC

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51
Q

Normal value for intracranial pressure in adults?

A

<15 mmHg

Vol inside cranium is fixed, so any increase in the contents can lead to raised ICP
This can be mass effect, oedema, or obstruction to fluid outflow

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52
Q

What are the causes for raised ICP?

A 
Brain tumours/mets
Cerebral oedema
Haemorrhage (SD, ED, SAH, IC, IV)
Infection (meningitis, encephalitis, brain abscess)
Status epilepticus
Idiopathic intracranial hypertension
Head injury
Hydrocephalus
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53
Q

How does raised ICP present?

A 
Headache (worse on bending forwards)
Vomiting
Visual disturbance (reduced acuity and peripheral field loss)
Hx trauma
Reduced GCS
Falling pulse and rising BP (Cushing's response)
Cheyne-stokes respiration 
Pupil changes 
Papilloedema
54
Q

What pupil changes can be seen with raised ICP?

A

Constriction at first
Later filatation

Important to not mask these signs by using agents which dilate the pupil to aid fundoscopy (e.g. tropicamide)

55
Q

What investigations need doing for raised ICP?

A

CT/MRI to determine underlying lesion
Fundoscopy
U+E, FBC, LFT, glucose, serum osmolality, clotting, blood cultures
Consider toxicology screen
CXR - any source of infection that may indicate abscess
Consider LP if safe, measuring opening pressure

56
Q

What is the immediate management for raised ICP?

A 
ABCDE
Avoid pyrexia and maintain normoglycemia 
Manage seizures and keep MAP >90
CSF drainage
Elevate head of bed 30-40 degrees
Analgesia and sedation (IV propofol etc)
Neuromuscular blockade 
Mannitol
Hyperventilation (if intubated)

Diagnose and Rx underlying cause and exacerbating factors

57
Q

What is the role of mannitol in raised ICP?

A

Osmotic agent - used to ‘suck’ water out of the brain

Can be used initially but may lead to rebound raised ICP after prolonged use (12-24 hrs)

58
Q

What is the role of corticosteroids in raised ICP?

A

ONLY useful if the cause of raised ICP is cancer

Not effective in reducing ICP except for oedema surrounding tumours

Dexamethasone 10mg IV

59
Q

What are the 3 main herniation syndromes associated with raised ICP?

A

1) Uncal herniation
2) Cerebellar tonsil herniation
3) Subfalcian (cingulate) herniation

60
Q

What is uncal herniation? Symptoms?

A

Caused by a lateral supratentorial mass (pushes uncus against midbrain)

3rd nerve compressed - causes dilated ipsilateral pupil, ophthalmoplegia

Followed by contralateral hemiparesis due to pressure on the cerebral peduncle

Coma from pressure on the ascending reticular activation system (ARAS) in the midbrain

61
Q

What is cerebellar tonsil herniation? Symptoms?

A

INCREASED PRESSURE IN THE POSTERIOR FOSSA (ie posterior mass), forcing the cerebellar tonsils through the foramen magnum

Symptoms: ataxia, 6th nerve palsies, upgoing plantars, loss of consciousness, irregular breathing, apnoea

Syndrome may proceed v rapidly given the small size and poor compliance of posterior fossa

62
Q

What is subfalcian (cingulate) herniation?

A

FRONTAL MASS
May be silent unless ACA is compressed and causes a stroke
Symptoms: contralateral leg weakness, abulia (inability to make decisions)

63
Q

What may cause airway obstruction in cancer?

A

Pressure from a tumour, e.g. bronchial carcinoma compressing trachea

Rx: ABCDE, intubate/cricothyroid

64
Q

What is neutropenic sepsis?

A

Emergency caused by chemotherapy

Neut <1 + Fever >37.5
OR
Unwell in absence of fever

65
Q

What can cause neutropenic sepsis?

A

Current/recent chemotherapy regime - particularly for blood cancers (also lung, breast, ovarian, colorectal)

66
Q

What is the definition for sepsis?

A

Life-threatening organ dysfunction due to dysregulated host response to infection

67
Q

What is septic shock?

A

Hypotension despite adequate fluid resus along with perfusion abnormalities leading to end-organ dysfunction (lactic acidosis, oliguria, altered mental state)

68
Q

What investigations need to be done for neutropenic sepsis?

A

FBC!!

Identify source (CXR, Urine MC+S, Blood cultures)
May also want to rule out DIC
69
Q

How is neutropenic sepsis managed?

A 
ABCDE and Sepsis 6 (?HDU)
IV access - 500ml NaCl fluid challenge
O2 if hypoxic
15 min obs
Consider GCSF 
IV ABx (Tazocin, +/- gentamicin)
Review regularly
70
Q

What is GCSF, and why would you consider it in the management of neutropenic sepsis?

A

Granulocyte macrophage colony stimulating factor

Stimulates bone marrow to produce granulocytes and stem cells and release them into bloodstream

71
Q

How is neutropenic sepsis prevented in patients undergoing chemotherapy with a high risk of developing it?

A

Fluoroquinolone

72
Q

What is anaphylaxis?

What type of hypersensitivity reaction is it?

A

Acute, life-threatening, multi-system severe reaction of the body’s immune system
Type 1 hypersensitivity

73
Q

What causes anaphylaxis?

A

Exposure to trigger (allergen) to which they have already been sensitised

Can occur in response to chemotherapy

74
Q

Give 4 differentials for anaphylaxis

A

Carcinoid
Phaeochromocytoma
Systemic mastocytosis
Hereditary angioedema

75
Q

How is anaphylaxis managed?

A 
STOP OFFENDING AGENT and call for help
ABCDE
Resus - O2, IV saline
0.5mg 1 in 1000 adrenaline IM
IV hydrocortisone
IV piriton
Fluid resus
76
Q

What is tumour lysis syndrome?

A

Sudden tumour necrosis due to cancer treatment
Leading to metabolic abnormalities
Caused by abrupt release of large quantities of cellular components into blood following rapid lysis of malignant cell

77
Q

What metabolic disturbances are seen in tumour lysis syndrome?

A

Hyperkalaemia/phosphataemia/uricaemia
Hypocalcaemia
Raised lactate, LDH

AKI (raised urea and Creat, reduced UO)

78
Q

What causes tumour lysis syndrome?

A

Usually treatment-mediated (may be spontaneous)

79
Q

Which type of malignancies is tumour lysis most commonly seen in?

A

Haematological (Burkitt’s lymphoma, ALL)

Other bulky chemo-sensitive tumours (leukaemia, germ cell tumours)

80
Q

What are the RFs for tumour lysis syndrome?

A

Volume depletion (dehydration, bleeding)
Renal impairment
Treatment-sensitive tumours
High pre-treatment rate, lactate and LDH levels

Elevated LDH levels on blood tests predicts increased risk (LDH is a product of cell breakdown, so increased levels can indicate tumour breakdown)

81
Q

How does tumour lysis syndrome present?

A 
Weakness
Constipation, vomiting, nausea
Abdominal pain (paralytic ileus)
Palpitations, chest pain, collapse (cardiac arrhythmias due to metabolic abnormalities)
Seizures
Reduced urine output, lethargy
AKI
82
Q

Why can tumour lysis syndrome lead to AKI?

A

Deposition of uric acid and calcium phosphate crystals in the renal tubules can cause acute renal failure

This can be exacerbated by concomitant intravascular depletion

83
Q

What investigations need to be done for tumour lysis syndrome?

A

FBC
U+E
Serum LDH, phosphate, urate
Calcium profile

84
Q

How can tumour lysis syndrome be prevented?

A

IV fluids
Rasburicase (recombinant urate oxidase) - catalyses uric acid conversion to allantoin
Allopurinol (xanthine oxidase inhibitor) - prevents uric acid production from xanthines

85
Q

How does rasburicase work to prevent tumour lysis syndrome?

A

Catalyses the oxidation of uric acid into allantoin (more soluble)

86
Q

How is acute tumour lysis syndrome treated?

A 
Vigorous hydration - IV fluids 
Correct hyperkalaemia
Rasburicase (stop allopurinol)
Acetazolamide (alkalinise urine - makes uric acid more soluble)
Phosphate binders
Dialysis
87
Q

How does acetazolamide help in the treatment of tumour lysis syndrome?

A

Alkalinises urine (makes uric acid more soluble)

88
Q

What type of shock is caused by cardiac tamponade?

A

Obstructive shock

89
Q

What are the signs of tamponade?

A

Becks triad:

1) Falling BP
2) Rising JVP
3) Muffled heart sounds

Kussmaul's sign (increased JVP on inspiration)
Pulsus paradoxus (pulse fades on inspiration)
90
Q

What investigations should be done in cardiac tamponade?

A

Echo
CXR (globular heart, L heart border convex/straight, R cardiophrenic angle <90)
ECG (electrical alternans)

91
Q

How is cardiac tamponade treated?

A 
Early senior involvement 
Give O2, monitor ECG, set up IVI
Group and save
Pericardiocentesis
Cardiothoracic surgery (CABG, ventricular repair, etc)
92
Q

Give some examples of complementary therapies that may be used alongside traditional cancer treatment?

A 
Acupuncture
Aromatherapy/massage
Clinical hypnosis
Reflexology
Shiatsu
Healing/Reiki
Western herbal medicine
Manipulative therapies (osteopathy, chiropractic)
Homeopathy
93
Q

What is the conversion factor between codeine and morphine?

A

Codeine to morphine - divide by 10

94
Q

Which chemotherapy is commonly associated with peripheral neuropathy?

A

Vincristine

Urinary hesitancy may also develop secondary to bladder atony

95
Q

What treatments are there for a patient who is experiencing bony mets?

A

NSAIDs (diclofenac)
Bisphosphonates
Radiotherapy

96
Q

What are the 5 most common sites for bony mets?

A

Desc. order:

1) spine
2) pelvis
3) ribs
4) skull
5) long bones

97
Q

Which is the most common cancer causing bony mets?

A

Prostate

98
Q

What are the side effects associated with cyclophosphamide?

A

Haemorrhagic cystitis
Myelosuppression
Transitional cell carcinoma

99
Q

What are the side effects associated with:

1) Bleomycin?
2) Doxorubicin

A

1) Lung fibrosis

2) Cardiomyopathy

100
Q

What are the side effects associated with methotrexate?

A

Myelosuppression
Mucositis
Liver fibrosis
Lung fibrosis (methotrexate cough!)

101
Q

What are the side effects associated with 5-fluorouracil?

A

Myelosuppression
Mucositis
Dermatitis

102
Q

Which tumour marker is raised in pancreatic cancer?

A

CA19-9

remember - 9 looks a bit like a pancreas?

103
Q

Which tumour marker is raised in breast cancer?

A

CA15-3

3 looks like boobs?

104
Q

What should the breakthrough morphine dose be for breakthrough pain compared to the normal daily dose?

A

1/6th

ie if someone is taking 30mg BD (60mg total), breakthrough dose is 10mg

105
Q

Which opioids are safest to use in patients with CKD?

A

Alfentanil
Buprenorphine
Fentanyl

106
Q

Define neoplasm

A

A new and abnormal growth of tissue in the body

107
Q

What are the 6 hallmarks of cancer?

A

1) Evading growth suppressors
2) Activating invasion and metastasis
3) Enabling replicative immortality
4) Inducing angiogenesis
5) Resisting cell death
6) Sustained proliferative signalling

108
Q

Define:

1) pharmacodynamics

2) pharmacokinetics

A

1) what the drug does to the body

2) what the body does to the drug

109
Q

What are the 3 features of chemotherapy that must be present for a treatment to be effective?

A

1) the drug must reach cancer cells
2) the cell must be sensitive to the cytotoxicity of the drug
3) the toxic effect must be minimal to the benefit of the drug

110
Q

Define screening

A

A process of identifying apparently healthy people who may be at increased risk of a disease or condition

111
Q

Who does the MDT comprise of in cancer care?

A 
Oncologist
Surgeon specific to the body system affected by the cancer
Clinical nurse specialist
Macmillan team
Patient and their family
112
Q

What is the purpose of neoadjuvant chemotherapy?

A

Given before surgery/radical Rx to shrink the tumour - makes it easier to operate on

Can eradicate micro-metastatic disease and can allow some tumours to be downstages before the definitive/curative treatment

113
Q

Give 3 possible downsides to neo-adjuvant chemotherapy

A

1) delays the definitive treatment
2) adds the risk of potentially fatal chemotherapy related complications (eg neutropenic sepsis)
3) may cause a decrease in patient performance status which may mean they are no longer fit for surgery

114
Q

What is the purpose of adjuvant chemotherapy?

A

Given after surgery
To ensure any margins or micrometastatic sites are free from disease
In some cancers (breast, colorectal), it can improve survival

115
Q

Possible limitation with adjuvant chemo?

A

Morbidity from surgery may mean patients are not fit for chemo within an appropriate timeframe

116
Q

What are the side effects of radiotherapy?

A 
Nausea, vomiting or anorexia
Mucositis (esp with ENT tumours - PEG may be advised)
Oesophagitis
Diarrhoea
Skin rashes

Early SE involve local inflammation
Late SE involve local fibrosis

117
Q

What are the 3 different groups of systemic anti-cancer treatment?

A

1) Cytotoxic chemotherapy
2) Hormone therapy
3) Molecularly-targeted therapy

118
Q

What are the 3 main groups of cytotoxic chemotherapy agents?

A

1) Alkylating agents (not cell-cycle phase specific), e.g. Cyclophosphamide
2) Antimetabolites (target S phase of cell cycle), e.f. Fluorouracil, methotrexate, hydroxycarbamide
3) Natural products, e.g. Bleomycin, Doxorubicin

119
Q

What are some general side effects of chemotherapy?

A 
Nausea
Taste changes
Hepatic/renal impairment
Immune suppression
Peripheral neuropathy
Constipation
Hair loss
Skin rashes
Infertility
Heart failure
120
Q

Lung cancer. What are the 3 main subtypes of NSCLC?

A

Squamous cell cancer
Adenocarcinoma
Large cell lung carcinoma

121
Q

Lung cancer. Which type of NSCLC is most seen in non-smokers?

A

Adenocarcinoma

122
Q

Which tumour marker is raised in ovarian cancer?

A

CA 125

123
Q

Which tumour marker is raised in prostatic carcinoma?

A

PSA

124
Q

Which tumour marker is raised in hepatocellular carcinoma and teratomas?

A

Alpha-feto protein (AFP)

125
Q

Which tumour marker is raised in colorectal cancer?

A

Carcinoembryonic antigen (CEA)

126
Q

Lung cancer. Which type of lung cancer is most associated with smoking?

A

Squamous cell

127
Q

Other than bone pain, what signs/symptoms may a patient with bony mets suffer?

A

Pathological fractures
Hypercalcaemia
Raised ALP

128
Q

Common side effects of chemotherapy are nausea and vomiting. How could these be managed?

A

Metoclopramide (if low risk of symptoms)

Ondansetron (if high risk of symptoms)

129
Q

How does ondansetron work?

A

5HT3 antagonist

130
Q

What are the 5 most common causes of cancer in the UK?

A 
Desc order:
Breast 
Lung
Colorectal
Prostate
Bladder

Medicine - Finals (13 decks)

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