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Finals > Palliative and oncology > Flashcards

Palliative and oncology Flashcards

1
Q

Neoplastic spinal cord compression

When to suspect?

A

In all lower back pain in cancer

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2
Q

Neoplastic spinal cord compression

Which cancers is it most commonly associated with?

A
  • Lung
  • Liver
  • Breast
  • Prostate
  • Myeloma
  • Melanoma
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3
Q

Neoplastic spinal cord compression

Causes

A
  • Collapse or compression of a vertebral body due to metastases (common)
  • Direct extension of a tumour into the vertebral column (rare)
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4
Q

Neoplastic spinal cord compression

Presentation

A
  • Back pain, may be worse on lying down/straining/coughing
  • Lower limb weakness
  • Sensory loss and numbness
  • Lesions > L1 –> UMN signs in leg, sensory level
  • Lesions < L1 –> LMN signs in legs, perianal numbness
  • Tendon reflexes INCREASED BELOW, ABSENT AT LEVEL
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5
Q

Neoplastic spinal cord compression

Investigations

A
  • Urgent whole spine MRI scan (within 24 hrs)
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6
Q

Neoplastic spinal cord compression

Management

A
  • High-dose dexamethasone (16 mg / 24 hrs PO)
  • With prophylactic GI protection (PPI) and blood glucose monitoring
  • Refer urgently to oncology MDT for consideration of radiotherapy or surgery
  • Radiotherapy should be given within 24 hrs of MRI diagnosis
  • May need decompressive surgery depending on the prognosis
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7
Q

Neoplastic spinal cord compression

Prognosis

A

Patients with loss of motor function after 48 hrs are unlikely to recover function

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8
Q

Neoplastic spinal cord compression

Differentiating from cauda equina

A

Cauda equina presents with lower motor neuron signs (reduced tone and reduced reflexes). The nerves being compressed are lower motor neurons that have already exited the spinal cord.
- When the spinal cord is being compressed higher up (above L1) by metastatic spinal cord compression, upper motor neuron signs (increased tone, brisk reflexes and upping plantar responses) will be seen.

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9
Q

Neutropenic sepsis

Presentation

A
  • Neutrophil count < 0.5 x 10^9/L

- Temp > 38 degrees OR other sign/symptom consistent with clinically significant sepsis

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10
Q

Neutropenic sepsis

Who should you suspect this in?

A
  • IN all patients unwell within 6 weeks of receiving chemo (most common 7-14 days after)
  • Examine indwelling catheter sites
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11
Q

Neutropenic sepsis

Management

A
  • IMMEDIATE TX
  • Treat post-chemo fever before WBC results
  • Tazocin (Piperacillin/Tazobactam)
  • If still febrile/unwell after 48 hours try meropenem +/- vancomycin
  • If not responding after 4-6 days investigate for fungal disease
  • Fluoroquinolone if suspect they might develop it as prophylaxis
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12
Q

Drugs that can cause neutropenic sepsis

A
  • Anti-cancer chemotherapy
  • Clozapine (schizophrenia)
  • Hydroxychloroquine (rheumatoid arthritis)
  • Methotrexate (rheumatoid arthritis)
  • Sulfasalazine (rheumatoid arthritis)
  • Carbimazole (hyperthyroidism)
  • Quinine (malaria)
  • Infliximab (monoclonal antibody use for immunosuppression)
  • Rituximab (monoclonal antibody use for immunosuppression)
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13
Q

Superior vena cava syndrome

Pathophysiology

A

Reduced venous return from head, neck and upper limbs

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14
Q

Superior vena cava syndrome

Causes

A

Common = extrinsic compression from malignancy (90%):

  • Lung (small cell) = most common cause
  • Others: lymphoma, metastatic, lymphoma, germ cell

Less common = venous thrombosis
- If current/past central venous access

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15
Q

Superior vena cava syndrome

Signs and symptoms

A
  • SOB = most common
  • Swelling of face, neck, arms
  • May see periorbital or conjunctival oedema
  • Headache - worse in the mornings
  • Visual disturbances - blurred vision
  • Pulseless jugular venous distension
  • Distended chest veins
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16
Q

Superior vena cava syndrome

What is Pemberton’s sign?

A
  • Raising the hands over the head –> facial congestion and cyanosis
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17
Q

Superior vena cava syndrome

Management

A
  • Prop patient up
  • High dose Dexamethasone = 16 mg OD
  • Oxygen if needed
  • CT to define anatomy of obstruction
  • SUPERIOR VENA CAVA STENTING and balloon venoplasty
  • Treat w radio/chemotherapy depending on the sensitivity of underlying cancer (e.g. SCLC, lymphoma)
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18
Q

Malignancy-associated hypercalcaemia

Epidemiology

A
  • 10-20% of cancer patients

- 40% of myeloma

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19
Q

Malignancy-associated hypercalcaemia

Causes

A

PTH-related protein produced by tumour causing local osteolysis

  • MYELOMA
  • Bone mets (lung, breast, kidney, thyroid, prostate)
  • Squamous cell lung cancer (PTHrP)
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20
Q

Malignancy-associated hypercalcaemia

Presentation

A
  • BONES (painful)
  • STONES (kidney)
  • GROANS (GI disturbance)
  • MOANS (psychiatric)
  • Shortened QT interval
  • HTN
  • Corneal calcification
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21
Q

Malignancy-associated hypercalcaemia

Management

A
  • Aggressive rehydration with normal saline
  • Bisphosphonates (if eGFR > 30) -)> IV Zolendronic acid for 3 days
  • Calcitonin - short-term, tolerance can develop
  • Long term = control of underlying malignancy
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22
Q

Malignancy-associated hypercalcaemia

Prognosis

A

`- Poor prognostic sign

- 75% mortality within 3 months

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23
Q

Brain metastases

Epidemiology

A

Up to 40% of patients with cancer

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24
Q

Brain metastases

Which cancers?

A
  • Lung = most common
  • Breast
  • Colorectal
  • Melanoma
  • Kidney
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25
Q

Brain metastases

Presentation

A
  • Headache - worse in the morning, coughing, bending
  • Focal neurological symptoms
  • Ataxia
  • Fits
  • Nausea and vomiting
  • Papilloedema
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26
Q

Brain metastases

Investigations

A

URGENT CT/MRI

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27
Q

Brain metastases

Management

A
  • High dose dexamethasone –> reduce cerebral oedema

- Stereotactic radiotherapy

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28
Q

Brain metastases

Prognosis

A
  • Poor prognosis
  • Median survival = 1-2 months
  • Better prognosis if single lesion or breast cancer
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29
Q

Tumour lysis syndrome

Pathophysiology

A

Chemo for rapidly proliferating tumours (leukaemia, lymphoma, myeloma) leads to:

  • Cell death
  • Increased urate
  • Increased potassium
  • Increased phosphate
  • Decreased calcium
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30
Q

Tumour lysis syndrome

Presentation

A
  • Increased urate
  • Increased potassium
  • Increased phosphate
  • Decreased calcium
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31
Q

Tumour lysis syndrome

Associated risks

A
  • Arrhythmias

- Renal failure

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32
Q

Tumour lysis syndrome

Management

A
  • Hydration
  • Uricolytics - Rasburicase, Allopurinol
  • Monitor K+, Ca2+ and phosphate levels
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33
Q

Massive haemorrhage

Which tumours?

A
  • Head and neck tumours

- Lung/GI tumours with Hx of bleeding

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34
Q

Massive haemorrhage

When to suspect?

A
  • Suspect massive occult bleed if patient suddenly in shock
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35
Q

Massive haemorrhage

Management

A
  • Stop any anticoagulation
  • Palliative - remain with patient, dark towels
  • Midazolam 10 mg STAT
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36
Q

Nausea and vomiting

Reduced gastric motility (gastric stasis)

A
  • Domperidone

- Metoclopramide

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37
Q

Nausea and vomiting

Bowel obstruction WITHOUT colic

A
  • Metoclopramide
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38
Q

Nausea and vomiting

Bowel obstruction WITH colic

A
  • HYOSCINE BUTYLBROMIDE/HYDROBROMIDE
  • Haloperidol
  • Cyclizine
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39
Q

Nausea and vomiting

Chemically-mediated

A
  • Haloperidol

- Ondansetron

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40
Q

Nausea and vomiting

Raised ICP

A
  • Cyclizine

- +/- Dexamethasone

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41
Q

Nausea and vomiting

Vestibular

A
  • Cyclizine
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42
Q

Nausea and vomiting

Cortical

A
  • Benzodiazepine

- Cyclizine

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43
Q

5-HT3 antagonists

Examples
SEs

A
  • Ondansetron, Granisetron

- SEs: constipation, headache, flushing

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44
Q

Anti-histamines

MoA
Examples
SEs

A
  • Act on H1-receptors centrally and peripherally
  • Cyclizine, Promethazine, Cinnarizine
  • SEs: anti-muscarinic effects, palpitations & arrhythmias, sleep disturbances, EPSEs
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45
Q

D2 receptor antagonists

Haloperidol
MoA
SEs

A
  • MoA: acts on D2 receptors in chemo-receptor trigger zone

- SEs: EPSEs, sedation, QT prolongation, depression

46
Q

D2 receptor antagonists

Domperidone
MoA
SEs

A
  • MoA: Act on D2 receptors PERIPHERALLY

- SEs: QT prolongation, drowsiness, dry mouth, diarrhoea, malaise

47
Q

D2 receptor antagonists

Metoclopramide
MoA
SEs

A
  • MoA: Act on D2 receptors CENTRALLY

- SEs: EPSEs, drowsiness, diarrhoea, gynaecomastia, galactorrhoea, hyperprolactinaemia

48
Q

Levomepromazine, Prochlorperazine

MoA
Indications
SEs

A
  • MoA: act on dopamine, H1 and Ach-receptors
  • Used when non-specific or multi-factoral N+V cause
  • SEs: EPSEs, drowsiness, anti-muscarinic SEs, postural hypotension, QT prolongation
49
Q

Hyoscine butylbromide/hydrobromide, Glycopyrronium bromide

MoA
Indications

A
  • MoA: muscarinic receptor antagonist
  • Used in cases of smooth muscle spasm (bladder, GI tract), excessive secretions including sialorrhoea, drooling, death rattle and inoperable bowel obstruction)
50
Q

Pain relief in palliative stomatitis/mucositis?

A

Benzydamine 0.15% mouthwash (Difflam®)

51
Q

First-line pain relief in palliative care

A
  • Offer patients with advanced and progressive disease regular oral modified-release (MR) or oral immediate-release morphine (depending on patient preference)
  • With oral immediate-release morphine for breakthrough pain
52
Q

Firs-line doses of morphine

A

If no comorbidities use 20-30mg of MR a day with 5mg morphine for breakthrough pain

53
Q

Co-prescribing with opioids

A
  • Laxatives should be prescribed for all patients initiating strong opioids
  • Patients should be advised that nausea is often transient. If it persists then an antiemetic should be offered.
  • Drowsiness is usually transient - if it does not settle then adjustment of the dose should be considered
54
Q

Breakthrough dose of morphine

A

1/6th of total 24 hrs dose

55
Q

Opioids in renal impairment

A

Mild –> Moderate:
- OXYCODONE

Severe (< 10):
- BUPRENOPRHINE
- FENTANYL
(not renally excrete so less likely to cause toxicity)

56
Q

When else might you consider using oxycodone?

A

Oxycodone generally causes less sedation, vomiting and pruritis than morphine but more constipation, so can be used in anyone complaining from these morphine SEs

57
Q

Pain management in bone mets

A

Strong opioids
Bisphosphonates
Radiotherapy
Denosumab

58
Q

Oral morphine to SC morphine

A

Divide by 2

59
Q

How much to increase morphine dose by?

60
Q

Oral morphine to SC diamorphine

A

Divide by 3

61
Q

Oral oxycodone to SC diamorphine

A

Divide by 1.5

62
Q

Oral codeine to oral morphine

A

Divide by 10

63
Q

Oral tramadol to oral morphine

A

Divide by 10

64
Q

Management of hiccups

A
  • Chlorpromazine
  • Haloperidol
  • Gabapentin
  • Dexamethasone
65
Q

Management of agitation and confusion

A
  • Find cause and treat this
  • Environmental factors

If require meds:

  • 1st line = haloperidol
  • Others: chlorpromazine, levomepromazine

In terminal phase:
- Midazolam

66
Q

Management of secretions

A
  • Avoid fluid overload
  • Educate the family that they are not likely to be troubled by them
  • HYOSCINE HYDROBROMIDE or HYOSCINE BUTYLBROMIDE
  • Also glycopyrroinum bromide
67
Q

Which HPV subtypes are most significant RFs for cancer?

A
  • 16
  • 18
  • 33

Though it should be noted that the majority of healthy women will spontaneously clear HPV within 2 years without developing cervical cancer

68
Q

Which HPV subtypes cause warts?

69
Q

Which lung cancer is most commonly associated with smoking?

A

Squamous cell carcinoma

70
Q

Lung cancer

Adenocarcinoma vs squamous cell carcinoma

A
  • Squamous cell lung cancer is more commonly found near large airways, unlike adenocarcinoma which is more commonly peripheral
  • Squamous cell = most common in smokers
  • Adenocarcinoma = most common in non-smokers
71
Q

Most common tumour causing bone metastases (in descending order)

A
  • Prostate
  • Breast
  • Lung
72
Q

Most common site (in descending order)

A
  • Spine
  • Pelvis
  • Ribs
  • Skull
  • Long bones
73
Q

Other than bone pain, features may include?

A
  • Pathological fractures
  • Hypercalcaemia
  • Raised ALP
74
Q

Cytotoxic agents

Cyclophosphamide
MoA

A
  • Alkylating agent

- Causes cross-linking in DNA

75
Q

Cytotoxic agents

Cyclophosphamide
Adverse effects

A
  • Haemorrhagic cystitis
  • Myelosuppression
  • Transitional cell carcinoma
76
Q

Cytotoxic agents

Bleomycin
MoA

A
  • Degrades performed DNA
77
Q

Cytotoxic agents

Bleomycin
Adverse effects

A
  • Lung fibrosis
78
Q

Cytotoxic agents

Anthracyclines, e.g. Doxorubicin
MoA

A
  • Stabilizes DNA-topoisomerase II complex inhibits DNA and RNA synthesis
79
Q

Cytotoxic agents

Anthracyclines, e.g. Doxorubicin
Adverse effects

A
  • Cardiomyopathy
80
Q

Cytotoxic agents

Methotrexate
MoA

A
  • Inhibitis dehydrofolate reductase and thymidylate synthesis
81
Q

Cytotoxic agents

Methotrexate
Adverse effects

A
  • Myelosuppression
  • Mucositis
  • Liver fibrosis
  • Lung fibrosis
82
Q

Cytotoxic agents

Fluorouracil (5-FU)
MoA

A

Pyrimidine analogue inducing cell cycle arrest and apoptosis by blocking thymidylate synthase (works during S phase)

83
Q

Cytotoxic agents

Fluorouracil (5-FU)
Adverse effects

A
  • Myelosuppression
  • Mucositis
  • Dermatitis
84
Q

Cytotoxic agents

6-mercaptopurine
MoA

A

Purine analogue that is activated by HGPRTase, decreasing purine synthesis

85
Q

Cytotoxic agents

6-mercaptopurine
Adverse effects

A
  • Myelosuppression
86
Q

Cytotoxic agents

Cytarabine
MoA

A

Pyrimidine antagonist. Interferes with DNA synthesis specifically at the S-phase of the cell cycle and inhibits DNA polymerase

87
Q

Cytotoxic agents

Cytarabine
Adverse effects

A
  • Myelosuppression

- Ataxia

88
Q

Cytotoxic agents

Vincristine/blastine
MoA

A

Inhibits formation of microtubules

89
Q

Cytotoxic agents

Vincristine/blastine
Adverse effects

A
  • Vincristine: peripheral neuropathy (reversible), paralytic ileus
  • Vinblastine: myelosuppression
90
Q

Cytotoxic agents

Docetaxel
MoA

A

Prevents microtubule depolymerisation & disassembly, decreasing free tubulin

91
Q

Cytotoxic agents

Docetaxel
Adverse effects

A
  • Neutropenia
92
Q

Cytotoxic agents

Irinotecan
MoA

A

Inhibits topoisomerase I which prevents relaxation of supercoiled DNA

93
Q

Cytotoxic agents

Irinotecan
Adverse effects

A
  • Myelosuppression
94
Q

Cytotoxic agents

Cisplatin
MoA

A

Causes cross-linking in DNA

95
Q

Cytotoxic agents

Cisplatin
Adverse effects

A
  • Ototoxicity
  • Peripheral neuropathy
  • Hypomagnesaemia
96
Q

Cytotoxic agents

Hydroxyurea
MoA

A

Inhibits ribonucleotide reductase, decreasing DNA synthesis

97
Q

Cytotoxic agents

Hydroxyurea
Adverse effects

A
  • Myelosuppression
98
Q

PET Scan

A
  • Form of nuclear imaging which uses fluorodeoxyglucose (FDG) as the radiotracer
  • Allows a 3D image of metabolic activity to be generated using glucose uptake as a proxy marker
  • The images obtained are then combined with a conventional imaging technique such as CT to decide whether lesions are metabolically active
  • Used to evaluate primary and possible metastatic disease
99
Q

Tumour markers

CA 19-9

A

Pancreatic cancer

100
Q

Tumour markers

CA 125

A

Ovarian cancer

101
Q

Tumour markers

CA 15-3

A

Breast cancer

102
Q

Tumour markers

PSA

A

Prostate carcinoma

103
Q

Tumour markers

alpha-feto protein (AFP)

A
  • Hepatocellular carcinoma

- Teratoma

104
Q

Tumour markers

Carcinoembryonic antigen (CEA)

A

Colorectal cancer

105
Q

Tumour markers

S-100

A
  • Melanoma

- Schwannoma

106
Q

Tumour markers

Bombesin

A
  • Small cell lung carcinoma
  • Gastric cancer
  • Neuroblastoma
107
Q

BRCA 1 and 2

A
  • Carried on chromosome 17 (BRCA 1) and Chromosome 13 (BRCA 2)
  • Linked to developing breast cancer (60%) risk.
  • Associated risk of developing ovarian cancer (55% with BRCA 1 and 25% with BRCA 2).
  • BRCA2 mutation is associated with prostate cancer in men
108
Q

Gardners Syndrome

A
  • Autosomal dominant familial colorectal polyposis
  • Multiple colonic polyps
  • Extra colonic diseases include: skull osteoma, thyroid cancer and epidermoid cysts
  • Desmoid tumours are seen in 15%
  • Mutation of APC gene located on chromosome 5
  • Due to colonic polyps most patients will undergo colectomy to reduce risk of colorectal cancer
  • Now considered a variant of familial adenomatous polyposis coli
109
Q

Amsterdam criteria

A
  • Three or more family members with a confirmed diagnosis of colorectal cancer, one of whom is a first degree (parent, child, sibling) relative of the other two.
  • Two successive affected generations.
  • One or more colon cancers diagnosed under age 50 years.
  • Familial adenomatous polyposis (FAP) has been excluded.
110
Q

Lynch Syndrome

A
  • Autosomal dominant
  • Develop colonic cancer and endometrial cancer at young age
  • 80% of affected individuals will get colonic and/ or endometrial cancer
  • High risk individuals may be identified using the Amsterdam criteria
111
Q

Li-Fraumeni Syndrome

A
  • Autosomal dominant
  • Consists of germline mutations to p53 tumour suppressor gene
  • High incidence of malignancies particularly sarcomas and leukaemias

Diagnosed when:

  • Individual develops sarcoma under 45 years
  • First-degree relative diagnosed with any cancer below age 45 years and another family member develops malignancy under 45 years or sarcoma at any age
112
Q

What sort of bone lesions would be seen in metastases?

A

focal sclerotic bony lesions

Finals (21 decks)

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