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Cancer care > Key topic lectures > Flashcards

Key topic lectures Flashcards

1
Q

How much does 1 bag of red cells raise the Hb

A

10 g/L (in 70 kg male)

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2
Q

What are some long term lines that can be inserted for cancer treatment

A

Tunnelled central lines (between chest wall and superior vena cava)

PICC line (between anterior cubital fossa and heart)

Implantable ports

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3
Q

What is tumour lysis syndrome

A

Tumour lysis releases cellular components into circulation

Imbalance: high uric acid, high potassium, high phosphorus, low calcium

Can cause: arrhythmias, sudden death, seizures

Management: allopurinol (blocks uric acid production), rasburicase (urate oxidase)

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4
Q

What is the guidance around pregnancy and chemotherapy

A

Avoid pregnancy whilst on chemotherapy

Can use norethisterone (stops periods)

Avoid COCP (high thrombotic risk)

Advise barrier protection (to protect partners)

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5
Q

What is criteria for neutropenic sepsis

A

Fever > 38

Fever > 37.5 for > 1 hour

Neutropenia < 0.5

Neutropenia < 1 and falling

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6
Q

What is the management for neutropenic sepsis

A

Follow hospital neutropenic sepsis protocol (similar to sepsis 6)

G-CSF (granulocyte colony stimulating factor): SC injection, can reduce severity and duration of neutropenia, side effects (bone pain, headaches, nausea, fever)

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7
Q

Which cells come from the myeloid line

A

Megakaryocytes (thrombocytes)

Erythrocytes

Mast cells

Myeloblasts (basophils, neutrophils, eosinophils, monocytes (macrophages))

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8
Q

Which cells come from the lymphoid line

A

Small cells (B cells (plasma cells), T cells)

Natural killer cells

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9
Q

What are the symptoms of hypercalcaemia

A

Fatigue

Abdominal pain

Nausea and vomiting

Constipation

Confusion

Headaches

Polydipsia

Polyuria

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10
Q

What are the symptoms of hyperviscosity

A

Headaches

Somnolence

Visual disturbance

Ischaemic events

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11
Q

Which drugs are now potentially curable for CML

A

Tyrosine kinase inhibitors (imatinib)

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12
Q

What are the properties of cancer cells that promote growth

A

Evade apoptosis

Self-sufficiency in growth signal

Insensitive to anti-growth signal

Tissue invasion and metastasis

Limitless replicative potential

Sustained angiogenesis

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13
Q

What is neoadjuvant therapy

A

Given before definitive management

Shrink tumour

Optimise outcome

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14
Q

What is adjuvant therapy

A

Given after treatment

Reduce risk of recurrence

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15
Q

What is palliative care

A

Symptom relief

Improve quality of life

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16
Q

What is 5-fluorouracil

A

Inhibits thymidylate synthesis

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17
Q

How do cancer cells develop drug resistance

A

Decreased uptake of drug

Increased drug metabolism

Altered drug targets

Impaired apoptotic pathways

Altered cell cycle checkpoints

Efflux pumps

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18
Q

What things are important to remember when prescribing chemotherapy drugs

A

Narrow therapeutic index

Alter doses based on: BMI, renal/hepatic function, performance status

Often give drugs in combination (synergistic effecr)

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19
Q

What are the side effects of chemotherapy

A

Brain (chemo-brain, peripheral neuropathy, fatigue)

Hair (alopecia)

Circulation (neutropenic sepsis, cardiomyopathy, myelosuppression)

GI tract (vomiting, mucositis)

Bladder (haemorrhagic cystitis)

Large intestine (diarrhoea, constipation)

Skin (rash, nail ridging/loss)

Reproductive organs (impaired fertility, decreased libido, premature menopause)

Kidneys (AKI, electrolyte disturbance)

Liver (deranged LFTs)

Lungs (pneumonitis, PE)

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20
Q

What are some examples of antiemetics used in cancer treatment

A

5HT3 antagonists (ondansetron)

Dopamine receptor antagonists (metoclopramide)

Steroids (dexamethasone)

Antihistamines (cyclizine)

NK1 receptor antagonists (aprepitant)

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21
Q

How do monoclonal antibodies work

A

Bind to cancer cell antigen

Block downstream signalling pathways

Arrest cell cycle proliferation

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22
Q

What are the side effects of immunotherapy

A

Skin toxicity

Hair growth disorders

Pruritus

Nail changes

Fatigue

Myelosuppression

Diarrhoea

Nausea and vomiting

Hypertension

Proteinuria

GI perforation

Delayed wound healing

Arterial thromboembolic events

Cardiac ischaemia

Abnormal LFTs

Allergic reaction

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23
Q

What are immunotherapy checkpoint inhibitors

A

Aid binding of PD-1 (on T cell) and PD-L1 (on tumour cell)

Block proteins that stop immune system from killing cancer cells

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24
Q

What are the aims of radiotherapy

A

Deliver maximum dose to tumour

Minimise dose to surrounding normal tissue

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25
Q

What is radical radiotherapy

A

Aim to cure

4 - 7 weeks

20 - 37 individual sessions

Small fields of irradiation

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26
Q

What is palliative radiotherapy

A

Alleviates symptoms

1 - 10 individual sessions

Large field of irradiation

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27
Q

What are the short-term side effects of radiotherapy

A

Fatigue

Hair loss

Dysphagia

Sore throat

Oral mucositis

Diarrhoea

Sterility

Dysuria

Radiation cystitis

Pancytopenia

Lymphoedema

Erythema

Nausea and vomiting

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28
Q

What are the late side effects of chemotherapy

A

Skin pigmentation/necrosis/ulceration

Bone necrosis/fracture/impaired growth

Mouth ulcers/dryness

Cataracts

Loss of sight

Lung fibrosis

Cardiomyopathy

Pericardiafibrosis

Infertility

Menopause

Bowel strictures/adhesions/fistulas

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29
Q

What is imitinib

A

A BCR-ABL tyrosine kinase inhibitor

‘Magic bullet’

Very tumour selective

Has very few side effects

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30
Q

What is growth fraction

A

The proportion of cells dividing at any given time

Useful indicator of the sensitivity of cancer cells to chemo drugs (large growth fraction = more responsive)

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31
Q

Which cancers are highly sensitive to chemotherapy

A

Lymphomas

Germ cell tumours

Small cell lung cancers

Neuroblastomas

Wilm’s tumours

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32
Q

Which cancers have a moderate sensitivity to chemotherapy

A

Breast

Colorectal

Bladder

Ovary

Cervix

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33
Q

Which cancers have a low sensitivity to chemotherapy

A

Prostate

Renal

Brain

Endometrial

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34
Q

What is the main side effect of cisplatin and carboplatin

A

Ototoxicity

Nephrotoxicity

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35
Q

What is the main side effect of vincristine

A

Peripheral neuropathy

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36
Q

What is the main side effect of bleomycin and busulfan

A

Pulmonary fibrosis

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37
Q

What is the main side effect of transtuzuman and doxorubicin

A

Cardiotoxicity

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38
Q

What is the main side effect of cyclophosphamide

A

Haemorrhagic cystitis

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39
Q

What is the main side effect of methotrexate, 5-FU and 6-MP

A

Myelosuppression

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40
Q

What are the risk factors for prostate cancer

A

Increasing age

Family history

Genetic conditions (BRCA2…)

Ethnicity (black > white > asian)

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41
Q

How might a patient with prostate cancer present

A

Often asymptomatic

Raised PSA

LUTS

Bone pain

Ejaculatory symptoms (rare)

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42
Q

What investigations are needed for suspected prostate cancer

A

DRE

PSA

MRI prostate/pelvis (usually pre-biopsy)

Biopsy (TRUS (transrectal ultrasound), transperineal)

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43
Q

What are the common causes of raised PSA

A

Prostate cancer

Urinary infection

Prostatitis

BPH

Acute urinary retention

Intense exercise

Sexual activity

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44
Q

What is the management for metastasis of prostate cancer

A

Hormones (surgical/medical castration)

Palliation (single-dose radiotherapy, bisphosphonates)

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45
Q

What is the management for locally advanced prostate cancer

A

Radical radiotherapy

Adjuvant hormones

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46
Q

What is the management for localised prostate cancer

A

Criteria: T1/2, N0, M0, PSA < 20

Curative intent (active surveillance, radical prostatectomy, radiotherapy)

Palliative care

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47
Q

What are the cancer-related differentials of haematuria

A

Renal cell carcinoma

Transitional cell carcinoma

Bladder carcinoma

Advanced prostate carcinoma

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48
Q

What are the non-cancer differentials of haematuria

A

Stones

Infection

Inflammation

Large BPH

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49
Q

What investigations are needed for haematuria

A

Ultrasound

Flexible cystoscopy

Urine cytology

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50
Q

What are the tumour markers for testicular cancer

A

aFP

hCG

LDH

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51
Q

When should cancer be suspected in a penile lump/ulcer

A

STI ruled out

Persistent despite treatment

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52
Q

What are the risk factors for bladder transitional cell carcinoma

A

Male

White

Smoking

Occupational exposure (rubber/plastic manufacturing, painting, hairdressing…)

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53
Q

What is the management for bladder transitional cell carcinoma

A

Low risk, non-muscle invasive (monitoring cystoscopies)

Intermediate/high risk, non-muscle invasive (monitoring cystoscopies, intravesical chemotherapy/immunotherapy)

Muscle invasion (neoadjuvant chemotherapy, radical cystectomy/radiotherapy, palliative care)

Metastasis (systemic chemotherapy, immunotherapy, palliation)

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54
Q

Give an overview of renal cell carcinoma

A

95% of upper urinary tract tumours

Presentation: haematuria, incidental, palpable mass

M>F

White > non-white

Risk factors: smoking, obesity, dialysis

Management: surveillance, excision, biological therapies, palliation

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55
Q

Give an overview of testicular cancer

A

Germ cell tumour

Usually <45

Risk factor: undescended testis

Treatment: inguinal orchidectomy

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56
Q

What are the risk factors for penile cancer

A

Phimosis (hygiene, smegma)

HPV (16 and 18)

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57
Q

How quickly does cancer treatment need to start

A

62 days from GP referral to treatment

31 days from diagnosis to treatment

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58
Q

What are the risk factors for lung cancer

A

High smoking pack years

Airway obstruction

Increasing age

Family history

Exposure to carcinogens (asbestos…)

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59
Q

How might a patient with lung cancer present

A

Often asymptomatic

Unexplained cough

Weight loss

Shortness of breath

Lethargy

Weakness

Hoarse voice

Dysphagia

Chest pain

Wheeze

Fever

Clinical signs of: SVCO, hypercalcaemia, anaemia, SIADH, Cushing’s, VTE

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60
Q

How is the T staging for lung cancer calculated

A

T1 - < 3 cm

T2 - 3 - 7 cm, invades visceral pleura/main bronchus

T3 - > 7 cm, invades phrenic nerve/diaphragm/chest wall/mediastinal pleura

T4 - invades mediastinal organs/vertebral bodies/carina/different lobes

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61
Q

How is the N staging for lung cancer calculated

A

N0 - no nodal involvement

N1 - ipsilateral bronchopulmonary/hilar nodes

N2 - ipsilateral mediastinal/subcarinal nodes

N3 - contralateral/supraclavicular nodes

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62
Q

What are the common sites of metastases in lung cancer

A

Liver

Adrenals

Lung

Lymph nodes

Pleura

Brain

Bone

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63
Q

What diagnostic tests are needed for lung cancer

A

Bloods (routine, calcium, INR)

CXR

Staging CT

Histology (ultrasound guided FNA, bronchoscopy, CT biopsy, thoracoscopy)

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64
Q

What is a malignant pleural effusion

A

Diagnosed by ultrasound-guided aspirate

Exudate

Indicates advanced disease (M1)

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65
Q

What are the differentials for incidental pulmonary nodes on CT

A

Primary bronchial carcinoma

Infection (TB, fungal)

Non-infectious granuloma (granulomatosis with polyangiitis)

Rheumatoid nodules

Bronchial carcinoid

Hamartoma

Metastasis

Management: CT surveillance for 24 months, consider removal

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66
Q

How is SIADH related to lung cancer

A

Due to paraneoplastic syndrome

Get hyponatraemia

Presentation: headache, lethargy, confusion, seizures

Management: fluid restriction, hypertonic saline, diuretics

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67
Q

What is the management for brain metastasis

A

Dexamethasone

Urgent radiotherapy

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68
Q

What is mesothelioma

A

Cancer of pleura

Due to asbestos exposure

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69
Q

What is Horner syndrome

A

Due to compression of sympathetic ganglion by Pancoast’s tumour

Ptosis, miosis, anhidrosis, exophthalmos

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70
Q

How might non-small cell lung cancer present

A

Horner syndrome

Hypercalcaemia

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71
Q

How might small cell lung cancer present

A

Rapidly progressing symptoms

SVCO

SIADH

Paraneoplastic syndrome

Bulky mediastinal disease

Bone metastasis

Brain metastasis

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72
Q

What are the tumour markers for lung cancer

A

(All non-specific)

CEA

Ca 19-9

Ca 125

PSA

aFP

b-HCG

73
Q

What are the types of non-small cell lung cancer

A

Adenocarcinoma

Squamous cell carcinoma

Large cell carcinoma

Large cell with neuroendocrine features

Adenosquamous

74
Q

What are the genetic conditions that can increase the risk of colorectal cancer

A

Familial adenomatous polyposis (autosomal dominant, develop cancer by 40 if untreated)

Hereditary non-polyposis colorectal cancer (aka Lynch syndrome, autosomal dominant, 85% cancer by age 70)

Familial colorectal cancer

Inflammatory bowel disease

75
Q

What lifestyle factors increase the risk of colorectal cancer

A

Western diet (low fibre, high fat, red meat)

Obesity

Smoking

Alcohol

Lack of exercise

76
Q

How might a patient with right colon cancer present

A

Weight loss

Fatigue

Obstruction rare

Iron deficiency anaemia

77
Q

How might a patient with left colon cancer present

A

Constipation

Abdominal pain

Alternating bowel habits

Bright red rectal bleeding

Large bowel obstruction

78
Q

How might a patient with rectal cancer present

A

Obstruction

Tenesmus

Bright red rectal bleeding

Palpable mass

79
Q

What investigations are needed for colorectal cancer

A

Baseline bloods

Tumour markers (CEA)

Colonoscopy

Flexible sigmoidoscopy

Barium enema

CT colonography

Biopsy

CT CAP

80
Q

What is the management of liver metastasis in colorectal cancer

A

Surgical resection

Microwave ablation

Radiofrequency ablation

Selective internal radiotherapy

81
Q

What are the common sites of metastasis from prostate cancer

A

Liver

Bone

Bladder

Lymph nodes

82
Q

How is the Gleason’s pattern calculated in prostate cancer

A

1 - small, uniform glands

2 - more stroma between glands

3 - distinctly infiltrative margins

4 - irregular masses of neoplastic glands

5 - only occasional gland formation

83
Q

What is the relationship between grade and Gleason’s score for prostate cancer

A

Grade 1 - 3+3

Grade 2 - 3+4

Grade 3 - 4+3

Grade 4 - 4+4

Grade 5 - Gleason 9-10 (lack of gland formation)

84
Q

What is the difference between active surveillance and watchful waiting for PSA testing

A

Active surveillance - closely monitor, regular examinations and tests, give potentially curative treatment if have progression

Watchful waiting - less intense follow-up, few tests, aim to control symptoms

85
Q

What is the management for prostate cancer

A

Brachytherapy (for small, solid tumours that have not spread)

Radical prostatectomy

External beam radiation therapy

Androgen deprivation therapy (GnRH analogues - suppress FSH)

86
Q

Head and neck cancers are mainly what type of cancer

A

Squamous cell carcinoma

87
Q

What are the risk factors for developing head and neck cancers

A

Smoking

Alcohol

Betel nuts

HPV

EBV

Asbestos exposure

Formaldehyde exposure

88
Q

What do head and neck cancers often present with

A

Lymphadenopathy

Difficulty breathing

Dysphagia

Difficulty speaking

89
Q

What are the NICE guidelines for likely presentations of head and neck cancers

A

Lip/oral cavity lump - oral cancer

Persistent/unexplained neck lump - oral cancer

Unexplained neck lump in > 45 - laryngeal cancer

Persistent and unexplained hoarse voice in > 45 - laryngeal cancer

Read and white patches in oral cavity - oral cancer

Unexplained ulceration in oral cavity for > 3 weeks - oral cancer

90
Q

Where do head and neck cancers commonly metastasise to

A

Lymph nodes

Lung

Bone

Liver

Brain

91
Q

What is the management for head and neck cancers

A

Surgery (resection, laser, excision)

Radiotherapy

Chemotherapy

Biological therapies

Immunotherapy

92
Q

What is the criteria for neutropenic sepsis

A

Undergoing systemic anticancer treatment

Temperature > 38

Neutrophil count > 0.5

93
Q

When should neutropenic sepsis be suspected

A

In all chemotherapy patients who become unwell

Some may not have a fever due to corticosteroid use

94
Q

When are patients usually most susceptible to neutropenic sepsis

A

Around day 10

Bigger range for haematological malignancy

95
Q

What are the signs and symptoms of neutropenic sepsis

A

Fever

Tachycardia > 90

Hypotension < 90

Respiratory rate > 20

Symptoms related to specific systems (cough, shortness of breath, mucositis)

Drowsiness

Confusion

96
Q

What factors increase the risk of infection in cancer patients

A

Prolonged neutropenia (> 7 days)

Severe neutropenia

Significant co-morbidities

Aggressive cancer

Central lines

Mucosal disruption

Hospital admission

97
Q

What investigations are needed in neutropenic sepsis

A

Bloods

Blood cultures (often negative)

Swabs

CXR

98
Q

What are the common causative organisms of neutropenic sepsis

A

Staph aureus

Staph epidermidis

Enterococcus

Streptococcus

80% due to endogenous flora

99
Q

What is the management for neutropenic sepsis

A

Don’t wait for FBC to confirm neutropenia

Empirical IV broad spectrum antibiotics within 1 hour

Sepsis 6

Involve seniors early

100
Q

What is the further management for neutropenic sepsis

A

Granulocyte colony stimulating factor

Patient education

Antibiotic prophylaxis

Dose reduction for further chemotherapy

Stop treatment

101
Q

Why does metastatic spinal cord compression need to be urgently treated

A

To preserve function

102
Q

How does metastatic spinal cord compression occur

A

Dural sac and its contents compressed at level of spinal cord/corda equina

80-85% due to collapse/compression of vertebral bodies that have metastatic spread

10% due to direct spread of tumour into epidural space (especially lymphomas)

103
Q

What are the signs of the reversible stage of metastatic spinal cord compression

A

Oedema

Venous congestion

Demyelination

104
Q

What are the signs of the irreversible stage of metastatic spinal cord compression

A

Prolonged compression

Vascular injury

Cord necrosis

105
Q

Which cancers commonly cause metastatic spinal cord compression

A

Breast

Prostate

Lung

Lymphoma

Myeloma

Renal

Thyroid

106
Q

How might a patient with metastatic spinal cord compression present

A

Motor symptoms (reduced power, difficulty standing/walking/climbing stairs, often symmetrical)

Sensory loss

Sphincter dysfunction (hesitancy, frequency, retention, overflow, incontinence)

Reduced performance status

Back pain

Poor response to normal analgesia

Exacerbated by: neck flexion, coughing, sneezing, straining, lying down

107
Q

What are the investigations for metastatic spinal cord compression

A

Pain suggestive of spinal metastasis - MRI spine within 1 week

Signs of metastatic spinal cord compression - MRI within 24 hours

108
Q

What is the management for metastatic spinal cord compression

A

Within 24 hours of diagnosis

Dexamethasone

Analgesia

Surgery

Radiotherapy

109
Q

What is the prognosis for metastatic spinal cord compression

A

Depends on mobility at presentation

Loss of sphincter control - poor sign

Good in radiosensitive tumours - lymphoma, myeloma, breast, prostate, NSCLC

110
Q

Which cancer types does hypercalcaemia commonly occur in

A

Breast

SCLC

Renal

Myeloma

Lymphoma

111
Q

What are the causes of hypercalcaemia in cancer patients

A

Humeral (80%, chemicals released by tumour affect calcium levels (PTH-related protein, vitamin D))

Bone invasion (20%, osteolytic metastasis with local release of cytokines)

20% do not have bone metastasis

112
Q

How might a patient with hypercalcaemia present

A

Nausea

Anorexia

Thirst

Polydipsia

Polyuria

Fatigue

Constipation

Confusion

Poor concentration

Drowsiness

Bone pain

Severe: nausea, vomiting, ileus, delirium, coma, death

113
Q

What is the treatment for hypercalcaemia

A

Rehydration

Bisphosphonates (inhibit osteoclastic bone resorption)

Denosumab (SC)

Systemic treatment of malignancy

Consider: regular blood tests, bisphosphonate infusions

114
Q

What is the prognosis for cancer patients with hypercalcaemia

A

Many die within 3 months

115
Q

How might a patient with superior vena cava obstruction present

A

Swelling in face/neck/arms

Distended neck and chest veins

Shortness of breath

Cyanosis

Stridor

Hoarse voice

Lethargy

Headaches

Confusion

Conjunctival swelling

Blurred vision

Pemberton’s sign

116
Q

How can superior vena cava obstruction lead to death

A

Laryngeal oedema

Airway obstruction

117
Q

What investigation is needed for superior vena cava obstruction

A

CT with contrast

118
Q

What is the management for superior vena cava obstruction

A

Sit upright, elevate head

Oxygen

Dexamethasone

Opioids

Benzodiazepines

Stent insertion

Anticoagulation (if due to thrombosis)

119
Q

What are the features of tumour lysis syndrome

A

Hyperuricemia

Hyperkalaemia

Hyperphosphatemia

AKI (uric acid or calcium phosphate in renal tubules)

Hypocalcaemia

120
Q

Which cancers are most susceptible to tumour lysis syndrome

A

Haematological malignancy

Bulky chemo-responsive tumours

121
Q

What are the risk factors for developing tumour lysis syndrome

A

High volume/bulky disease

Pre-treatment LDH high

High circulating WCC

Pre-existing renal dysfunction/nephropathy

Pre-treatment hyperuricaemia

Hypovolemia

Diuretic use

Urinary tract obstruction from tumour

122
Q

How might a patient with tumour lysis syndrome present

A

3-7 days after chemotherapy

Nausea and vomiting

Diarrhoea

Anorexia

Lethargy

Haematuria

Anuria

Fluid overload

Cardiac arrhythmias (tented T waves, QTc derangement)

Muscle cramps

Tetany

Seizures

123
Q

What is the treatment for tumour lysis syndrome

A

Good hydration and fluid balance

Monitor electrolytes

Allopurinol (xanthine oxidase inhibitor, get less hyperuricemia)

Rasburicase (degrades uric acid)

Dialysis

124
Q

What is palliative care

A

Active, total care of patients whose disease is not responsive to curative treatment

Aim to control pain and other symptoms

Deal with social, psychological, and spiritual issues

125
Q

When is a patient said to be end of life

A

Likely to die within the next 12 months

126
Q

What are the general indicators of decline

A

Unplanned hospital admissions

Poor/deteriorating performance status

Dependence on carers

Carers need more help and support

Significant weight loss

Persistent symptoms despite optimal treatment

Decision to reduce/stop treatment

127
Q

What are the stages of the clinical frailty score

A

1 - very fit

2 - well

3 - managing well

4 - vulnerable

5 - mildly frail

6 - moderately frail

7 - severely frail

8 - very severely frail

9 - terminally ill

128
Q

What are the factors that indicate that death is approaching

A

Bedbound

Drowsiness

Impaired cognition

Difficulty taking oral medications

Reduced food and fluid intake

Increased symptom burden

129
Q

What are the signs that a patient is entering the dying phase

A

Shallow breathing

Use of accessory muscles

Respiratory secretions

Skin colour changes

Temperature at extremes

Decreased consciousness

Agitation

Restlessness

Decreased urine output

Incontinence

Decreased/absent oral intake

Difficulty swallowing

130
Q

What are some commonly used medications in the last few days of life

A

Morphine (pain and breathlessness)

Midazolam (anxiety, agitation, seizures)

Levomepromazine (nausea, vomiting, hallucinations)

Glycopyrronium (respiratory secretions)

131
Q

What are the features of pain in advanced disease

A

Usually persistent

Can have multiple aetiologies

Impairs function

Threatens independence

Invokes fear of further suffering

Aim to optimise quality of life right up until death

132
Q

What are the types of pain

A

Nociceptive

Neuropathic

Mixed

133
Q

What is nociceptive pain

A

Normal nervous system, pain due to tissue damage

Somatic - from skin/muscle/bone, sharp/throbbing/well-localised

Visceral - from hollow viscus/solid organ, diffuse ache, difficult to localise

134
Q

What is neuropathic pain

A

Malfunctioning nervous system

Nerve structure damaged

Stabbing, shooting, burning, stinging, numbness, hypersensitivity

135
Q

Which NSAIDs/COX-2 inhibitors should be prescribed when there is no cardiovascular/GI risk

A

Ibuprofen

Diclofenac

Naproxen

136
Q

Which NSAIDs/COX-2 inhibitors should be prescribed when there is GI risk

A

Celecoxib

137
Q

Which NSAIDs/COX-2 inhibitors should be prescribed when there is cardiovascular risk

A

Naproxen

Ibuprofen

138
Q

What should be prescribed alongside all NSAIDS/COX-2 inhibitors

A

PPI

139
Q

What are some adjuvant (co-analgesic) medications

A

Antidepressants (amitriptyline, duloxetine)

Anticonvulsants (gabapentin, pregabalin)

Benzodiazepines (diazepam, clonazepam)

Steroids (dexamethasone)

Bisphosphonates

140
Q

Which medications are on step 1 of the WHO pain ladder

A

Paracetamol

NSAIDs

141
Q

Which medications are on step 2 of the WHO pain ladder

A

Dihydrocodeine

Codeine phosphate

Tramadol

Co-codamol

142
Q

Which medications are on step 3 of the WHO pain ladder

A

Oxycodone

Morphine

Fentanyl

Diamorphine

143
Q

How does pain respond to opioids in different parts of the body

A

Soft tissue - good response

Viscera - good/partial response

Bone - partial response

Neuropathic - poor response

144
Q

What is the codeine to morphine conversion ratio

A

10 : 1

145
Q

How is the morphine dose calculated

A

TDD / 2 = slow release dose

TDD / 6 = PRN dose

146
Q

Which is the name of the slow release morphine

A

Zomorph

147
Q

What is the name of the immediate release morphine

A

Oramorph

148
Q

What are the common side effects of opioids

A

Constipation (give laxatives)

Dry mouth

Nausea (give antiemetics)

Vomiting

Drowsiness

Sedation

149
Q

What are fentanyl patches

A

Transdermal opioid

Non-renal excretion

12-24 hours to reach steady state

Use oramorph PRN for breakthrough pain

150
Q

What are the signs of opioid toxicity

A

Pinpoint pupils

Hallucinations

Drowsiness

Vomiting

Confusion

Myoclonic jerks

Respiratory depression

151
Q

Why does opioid toxicity occur

A

Fast dose escalation

Renal impairment

Poor response to pain

Given with a nerve block

152
Q

How is breathlessness as a palliative symptom managed

A

Stay calm

Sit upright

Air flow across face

Oxygen

Consider medications: morphine, lorazepam, midazolam

153
Q

Which receptors are found in the chemoreceptor trigger zone of the brain

A

NK1

D2

5HT3

154
Q

Which receptors are found in the vomiting centre of the brain

A

NK1

ACh

H1

5HT2

155
Q

What factors increase the risk of chemo-induced nausea and vomiting

A

Specific chemo drugs

Female

< 50

Past history of nausea and vomiting

156
Q

What are the causes of constipation in cancer patients

A

Disease-related

Fluid depletion

Weakness

Intestinal obstruction

Medications

Biochemical (hypercalcaemia, hypokalaemia)

Pain

157
Q

How is malignant bowel obstruction managed

A

Non-surgical: rest bowel, limit oral fluids, NG tube for vomiting, correct electrolyte imbalance, analgesia, trial dexamethasone

Surgical: endoscopic stenting, venting gastrostomy (to decompress)

158
Q

What are the principles of the double effect

A

Action must be morally good

Only good effect must be intended

Good effect must not be achieved by way of bad effect

Good result must outweigh the bad effect

159
Q

How does alkylating agent chemotherapy work

A

Makes cross-links between DNA stands

Prevents DNA replication

160
Q

How does platinum agent chemotherapy work

A

Makes cross-links between DNA stands

Prevents DNA replication

161
Q

How does antimetabolite chemotherapy work

A

Acts as substitute for metabolites needed for DNA synthesis

162
Q

How does topoisomerase inhibitor chemotherapy work

A

Prevents unwinding of DNA strands for replication

163
Q

How does tubulin-active agent chemotherapy work

A

Stops spindle formation

164
Q

What are the immediate side effects of chemotherapy

A

(Within minutes)

Extravasation (leaking of chemo drug into adjacent tissue)

Facial/body flushing

Cardiac arrhythmias

Hypotension

Hypersensitivity

Anaphylaxis

Haemorrhagic cystitis

165
Q

What are the short-medium term side effects of chemotherapy

A

(Hours - 7 days)

Discolouration of urine

Tumour lysis syndrome

Nausea and vomiting

Mucositis

Constipation

Diarrhoea

Fatigue

166
Q

What are the medium-long term side effects of chemotherapy

A

(> 7 days)

Bone marrow suppression

Alopecia

Liver dysfunction

Renal toxicity

Cardiac toxicity

Peripheral neuropathy

Pulmonary fibrosis

Changes in fertility

167
Q

What are the modes of chemotherapy resistance

A

Modified cell membrane composition

Reduced drug transporters

Increased efflux pumps

Drug inactivation mechanisms develop

Drug target modification/loss

Up-regulation of pro-survival genes

168
Q

How does checkpoint inhibitor immunotherapy work

A

Decrease suppression of T cell immune response (encourage immune cells to kill cancer cells)

169
Q

How does adoptive cell therapy immunotherapy work

A

T cells isolated from patient, modified, multiplied, re-injected

170
Q

How does cancer vaccine immunotherapy work

A

Use patient’s own dendritic cells

Used in metastatic prostate cancer

171
Q

How does cytokine immunotherapy work

A

Increase signalling between immune cells and other body cells

172
Q

How does oncolytic virus immunotherapy work

A

Viruses target particular cancer cells

173
Q

What is the main side effect of immunotherapy

A

Organitis

174
Q

What is the NICE urgent CXR criteria for lung cancer

A

> 40 and 2 of (or smoker and 1 of): cough, fatigue, shortness of breath, chest pain, anorexia, weight loss

> 40 and: persistent/recurrent chest infections, finger clubbing, persistent lymphadenopathy, chest signs consistent with lung cancer, thrombocytosis

175
Q

Give an overview of small cell lung cancer

A

Rare in non-smokers

60% metastatic at presentation

Aggressive

Poor prognosis

Very sensitive to chemotherapy

High relapse rate

Often use radiotherapy

Give prophylactic cranial irradiation

176
Q

What are radiosensitizers

A

Drugs that make cancer cells more susceptible to radiotherapy

177
Q

Which cancers are commonly treated with chemoradiotherapy

A

Head and neck cancers

Cervical cancer

Bladder cancer

Anal cancer

178
Q

What are the side effects of radiotherapy

A

Hair loss

Dysphagia

Sore throat

Oral mucositis

Diarrhoea

Sterility

Dysuria

Radiation cystitis

Low blood counts

Lymphoedema

Erythema

Nausea and vomiting

Fatigue

Cancer care (8 decks)

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