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4th Year Drugs > Palliative Care > Flashcards

Palliative Care Flashcards

1
Q

What are the different types of analgesia?

A

Non-opioid (simple analgesia) eg paracetamol or NSAIDS

Opioids (weak and strong)

Adjuvant (co analgesics)

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2
Q

What is the analgesia ladder? What are the main principles of the ladder?

A
  • Increasing pain -> up rung of ladder
  • Reducing pain -> down rung of ladder
  • Rx from different classes are used alone or in combo according to type of pain and response
  • Two medicines of same class (eg NSAIDS) should not be given concurrently
  • However, immediate release and sustained release opioids may be prescribed together
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3
Q

What type of pains are only partially responsive to opioids? What should be used instead?

A

Chemotherapy-induced neuropathy

Pains unrelated to underlying illness eg tension H/A

  • post-herpetic pain
  • muscle spasms
  • nerve damage/compression
  • Bone pain
  • visceral pain
  • tenesmus pain
  • activity provoked pain
  • adjuvants, nerve blockage or oncological treatments (if cancer related)
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4
Q

To manage pain effectively, what things are important to establish?

A

1. Cause of pain

  • Ix eg x-ray, USS/CT, MRI for MSCC
  • non- malignant causes (eg arthritis, tension H/A, infections)
  • multiple causes in advanced, progressive disease

2. Type of pain

  • acute vs chronic
  • nociceptive vs neuropathic vs inflammatory vs visceral - breakthrough pain
  • incident pain

3 severity of pain (eg facial expression, groaning, ability to move, timing, number of sites, patient pain-rating scales)

4. What helps? What exacerbates/relieves? Effects of pain/analgesia

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5
Q

Which analgesic should be prescribed?

A

BY MOUTH - where possible

BY THE CLOCK - regular, as well as PRN dose

BY THE LADDER - assess pain severity and identify appropriate analgesic for level of pain.

INDIVIDUAL DOSE TITRATION - titrate dose against effect, with no upper limit for most opioids (except buprenorphine, codeine and tramadol)

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6
Q

How does paracetamol exert its action?

A
  • Weak, specific inhibitor of COX2
  • ↓ pain (increases pain threshold)
  • ↓ temperature (reduces fever)
    • ↓ prostaglandins in the thermoregulatory area of the hypothalamus
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7
Q

What are the SEs of paracetamol?

A
  • Usually well tolerated - COX2 inhibitor (no effect on gastric mucosa, renal perfusion)
  • OVERDOSE - paracetamol metabolised by CYP450 –> NAPQI (toxic) — glutathione —> conjugated, excreted form
  • NAPQI -> hepatocellular necrosis. If overdose, pathway above is overwhelmed.
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8
Q

WHat are the CIs for paracetamol?

A

Risk of liver toxicity due to:

  • ↑ NAPQI production (chronic alcohol disease)
  • ↓ glutathione (malnutrition, reduced body weight, excess alcohol intake)
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9
Q

Name 2 NSAIDs

A

Naproxen (250-500 mg bd)

Ibuprofen (400mg tds)

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10
Q

How do NSAIDs exert their action?

A

COX inhibitor - COX2 - inhibit prostaglandins synthesis from ARACHIDONIC ACID .

Benefits from blocking COX2, SEs from COX1

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11
Q

WHat are the SEs of NSAIDs?

A

COX1: prostaglandins essential for:

  • Maintaining gastric mucosa
  • Maintaining renal perfusion
  • Preventing thrombus formation in vascular endothelium

∴

  • Peptic ulceration/GI bleeds
  • Hypersensitivity (bronchospasm)
  • Renal impairment (↑H2O/Na -> ↑BP)
  • ↑ CV events risk (↑BP)

Ibuprofen is safest NSAID

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12
Q

What should you consider co-prescribing alongside NSAIDs in patients with cancer/advanced disease?

A
  • High risk for GI effects
  • Consider co-prescribing H2-receptor antagonist or PPI
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13
Q

What particular patients would you prescribe NSAIDs in with caution?

A

Renally impaired

Uncontrolled HTN

HF

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14
Q

What are the weak/moderate opioids?

A

Codeine

Dihydrocodeine

Tramadol

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15
Q

How do weak opioids exert their action?

A
  • Broken down to morphine (codeine) and dihydromorphine (dihydrocodeine) which are agonists of U receptors in CNS
  • reduce pain transmission
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16
Q

Why doesn’t codeine or dihydrocodeine work in everyone?

A

Metabolised to morhpine or dihydromorphine which are agonists of U receptors in CNS

10% Caucasians have less active metabolising enzyme ∴ ineffective

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17
Q

What is co-codamol? What doses are they avaliable in?

A
  • Codeine + paracetamol
  • 3 strengths:
    • Weak - 8mg cod + 500mg para
    • Strong - 15mg cod and 500mg para OR 30mg codeine and 500mg paracetamol
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18
Q

What are the strong opioids?

A

Morphine

Diamorphine

Oxycodone (synthetic)

Fentanyl

Alfentanil

Hydromorphone

Burenorphine

Methadone (specialist only)

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19
Q

How do strong opioids exert their action?

A

Activate CNS U (mu) receptors which ↓ pain transmission and ↓ excitability

Medulla - ↓ response to hypoxia and hypercapnia, ↓ respiratory drive and SOB

↓ pain, SOB and anxiety -> ↓ sympathetic drive -> ↓cardiac work and oxygen demand

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20
Q

How does tramadol exert its actions?

A
  • Tramadol - synthetic codiene - moderate strength opoid
  • Tramadol and its active metabolite are agoinsts of the U receptor which reduces pain transmission
  • Also reduces the re-uptake of serotonin and noradrenaline ∴ avoid combo with drugs that reduce seizure threshold e.g. SSRI, tricyclic antidepressants
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21
Q

What are the side effects of Opioids?

A
  • Constipation- ALWAYS prescribe laxative
  • N&V - ALWAYS prescribe PRN anti-emetic
  • Drowsiness (dose related, usually temporary. If persistent ?overdose ?renal impairment) - DO NOT DRIVE
  • Confusion, hallucinations and delirium (usually if opioid toxicity ∴ ↓dose or change opioid
  • Respiratory depression - rare if titrated properly - ↓RR and ↓O2 sats
  • Papillary constriction - ↓ sympathetic drive and activation of Erdinger Westphal nucleus
  • Histamine release - sweating, rashes, urticaria, vasodilation

Neither TOLERANCE nor ADDICTION are signficiant problems in patients with end of life

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22
Q

What are the signs of opioid toxicity?

A
  • N&V
  • Drowsy
  • Confusion
  • Visual hallucinations
  • Monoclonic jerks
  • ↓RR
  • Pinpoint pupils (not useful sign if on long term opioids)
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23
Q

What types of morphine sulphate preperations are there?

A

Immediate release tablets and liquids- effective after 20-30mins and last for 4-6 hrs e.g.

  • Oramorph (10mg/5ml, 20mg/1ml)
  • Sevredol tablets (10mg, 20mg, 30mg)

Modified (slow) release tablets, granules or capsules - effective after 4 hrs and last for 12 hrs e.g.

  • MST MR
  • Zomorph capsules
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24
Q

If taking modified release morphine, what else should patients be prescribed with?

A

PRN for breakthrough pain (immediate release morphine)

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25
Q

What should PRN (immediate release morphine) medications constitute in relation to total dose?

A
  • 1/6th of total 24hr dose
  • e.g. MST 30mg bd
    • ie. 60mg in 24hrs
    • ∴ PRN = 10mg
  • Should be individually titrated - if dose effective for patient, do not change PRN dose (irrespective of background dose)
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26
Q

How should opoids be prescribed - mg or ml?

A

mg! (as differing strenghts avaliable)

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27
Q

What should you do if there is a partial response to opioids or inadequate duration of pain relief? (i.e pain returns in <4 hrs after immediate or <12hrs after modified release)

A
  • Increase background dose by 30%-50% increments or until adverse SEs occur
  • Check PRN dose = adequate for background dose (i.e. 1/6th of background)
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28
Q

What should the dose be if the patient is elderly/frail?

A

Halve stating dose

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29
Q

What should you do to opoid dose if patient has renal impairment/failure?

A

Dose reduction

Seek specialist advice - alternative opioids

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30
Q

What is the starting regimen of morphine sulphate?

A

If opoid-naive..

  • start weak opoids ± paracetamol and/or adjuvant drugs

If optimal dose of weak opoid ± others does not control pain

  • Change to morphine (slow/immediate release) at dose which = equivalent to dose of weak opioid (MST ~20mg bd usually appropriate). STOP WEAK OPOID
  • e.g. 60mg codeine phosphate qds -> slow release MST 10mg BD + PRN (2mg). Immediate = 5mg oramorph/4 hrs
  • ↓ dose elderly/frail (1/2) and ↓dose/non-renally exreted alternative in renal failure

If started on immediate release, once stable dose achieve, convert to equivalent dose of slow release preperations

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31
Q

How often should patients have their doses reviewed after being initiated on morphine?

A

Every 24 hrs - if pain inadequately controlled, ↑ background dose ( < 30%)

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32
Q

What is oxycodone? When is it used?

A
  • Synthetic morphine - strong opoid with similar dosing schedule to morphine
  • 2nd line if:
    • Intolerant to morphine (oxy = ↑expensive!)
  • 1st line if:
    • Moderate renal impairment (metabolised by liver)
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33
Q

How strong is oxycodone?

A

1.5x more potent than oral morphine (∴ divide MST by 1.5 to get equavalent dose)

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34
Q

WHat are the avalaible formulations for oxycodone?

A
  • Immediate release (oxynorm) - lasts 4-6hrs
  • Modified/slow release (Oxycontin) - lasts 12hrs
  • SC oxycodone (10mg/ml or 50mg/ml) - for equivalent dose, SC = ½ oral dose
    • Check SEs after 24hrs due to inter-individuals variability. Co-prescribe with PRN analgesia.
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35
Q

What should the dose of PRN immediate release oxycodone be relative to the 24hr oxycocone dose?

A

1/6th

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36
Q

What are the indications for continuous SC infusion (via a syringe driver)?

A
  • Patient unable to take oral medication or concerns about absorption due to
    • persistent voming
    • GI obstruction
    • Dysphagia
    • Weakness
    • Unconscious
    • Mouth/throat/oesphageal lesions

Inadequate pain control NOT indication for SC infusion (unless there is reason for oral opioids not being absorbed)

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37
Q

What opioids can be given via SC/continuous SC infusion (via syringe driver)? What is the duration of action for each?

A

Diamorphine

Morphine sulfate

Oxycodone

SC - 4 hrs

CSCI - 24 hrs

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38
Q

Compared to oral morphine, what are the relative strengths of SC (parenteral) morphine and SC diamorphine?

A

SC morphine - 2x more potent

SC diamorphine - 3x more potent

∴ to convert oral to SC, divide oral by 2 and 3 respectively

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39
Q

What are good starting doses for SC/continuous SC infusion in a) opioid naive and b) patients with opoid receptive pain?

A

SC morphine/diamorphine (PRN)

  • 1 - 2.5mg SC (opioid naive) OR
  • 1/6th of 24hr dose

CSCI morphine/diamorphine

  • 5 - 10 mg /24hrs (opoid naive)
  • Diamorphine - 1/3 previous 24hr oral dose
  • Morphine - 1/2 previous 24hr oral dose

At start, consider stat PRN dose as syringe pump may take several hours to reach therapeutic levels

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40
Q

What is the most commonloy used syringe driver?

A

McKinley T34

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41
Q

Where are the recommended sites for insertion of SC cannula for syringe drivers?

A

Anterior chest wall

Upper arms

Abdo wall

Thighs

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42
Q

What other drugs can be given as SC infusion via syringe driver? (AVOID mixtures of >3 compatiable drugs if possible)

A
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43
Q

WHat drugs are not suitable for syringe drivers? Why?

A

Due to irritation…

  • diazepam
  • chlorpromazine
  • prochlorperazine.
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44
Q

What are transdermal (patch) preperations of morphine indicated?

A

Patients with:

  • chronic pain already stabilised on other opoids
  • Poor compliance
  • swallowing/absorption probs
  • Severe renal impairment/renal failure
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45
Q

Why shouldnt transdermal preperations be used in unstable pain or in last days of life?

A

Due to long titration period and duration of action

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46
Q

What should patients with transdermal patches be prescribed along with?

A

Immediate release PRN preperations (dependent on patch strength - work out conversion and aim for 1/6th of 24 hr dose)

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47
Q

What strengths do fentanyl patches (SEE-THROUGH) come in? How often should they be applied?

A

12, 25, 50, 75 or 100µg per hour

Applied every 72 hrs

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48
Q

What doses do transdermal buprenorphine patches (BROWN) come in? How often should they be applied?

A
  • Low dose patches - 5, 10, 20 µg per hour. Applied every 7 days. Patients with poor compliance requiring low dose
  • High strength patches - 35, 52.5, 70 µg per hour. Applied every 96 hrs, changed twice a week.
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49
Q

What are the other routes strong opioids can be administered?

A
  • Sublingual
  • Buccal
  • Nasal fentanyl

For specific situations. Seek specialist adivce

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50
Q

What are the equivalent opioid doses accross different routes of administration?

A
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51
Q

If the opioids do not work, work things do you need to think about?

A
  1. Is opioid analgesia of choice? - not all pain = opioid responsive. Consider aetiology.
  2. Is dose high enough? If partial response or inadequate pain relief duration, consider ↑ background dose by 30% (ensure PRN = adequate for background dose)
  3. Is drug being absorbed? Vomiting, dysphagia, high stoma output - consider alternative delivery routes e.g. SC , IV, transdermal
  4. Is pain breaking through with movement or painful procedures? Identify and ↓provoking factors. Consider PRN opioids, consider NSAIDs
  5. Are adjuvants required?
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52
Q

Who might be able to offer help if you are unable to control patients pain?

A
  • Senior colleagues
  • Hospital/community palliative care team
  • Local hospice
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53
Q

What adjuvant analgesia could you offer for cancer induced bone pain?

A

Consider:

  • NSAIDs
  • Bisphosphonates
  • Palliative radiotherapy
  • Corticosteroids
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54
Q

What drugs could you consider for neuropathic pain? Wat do you need to consider? What are the relevent SEs for each in palliative care?

A

_Consider patients Sx, SEs and co-morbidities when R_x

  • TCA Anti-depressants (e.g. amitriptyline, duloxetine)
    • SEs: anti-cholinergic (can’t see, can’t pee, can’t shit, can’t spit), postural ↓BP
  • Anticonvulsants e.g. gabapentin, pregabalin
    • SEs: (usually at start) sedation, dizziness, ataxia
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55
Q

What is the mechanism by which gabapentin and pregabalin work?

A
  • Binds to voltage gated Ca channels, preventing inflow of Ca, inhibiting NT release
  • ∴ ↓synaptic transmission and neuronal excitability
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56
Q

What is a normal starting dose for anti-depressants in the context of neuropathic pain?

A
  • Start with low dose and titrate gradually every 2-5 days
  • e.g. Amitriptyline - start from 10mg —> up to 75mg at night (if tolerated)
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57
Q

What is the normal starting dose for anticonvulsants (i.e. gabapentin, pregabalin)

A

Start lowest dose - titrate slowl. Caution/↓dose in elderly/frail/renally impaired

Gabapentin

  • start 100mg t.d.s.
  • Slowly titrate assessing efficacy/SEs (max 600mg qds)

Pregabalin

  • Start 25 - 75 mg bd
  • Slowly titrate assessing efficacy/SEs (max 300 mg bd)
58
Q

Name some important corticosteroids

A
  • Dexamethasone **
  • Prednisolone
  • Hydrocortisone

**1st choice due to:

  • high anti-inflamm potency (1mg dex = 7mg pred)
  • high solubility
  • Low mineralocorticoid effects**
59
Q

What is the mechanism by which corticosteroids exert their action?

A

Modify the immune response

  • Upregulate anti-inflammtroy genes
  • Downregulate pro-inflammatory genes (e.g. cytokines, TNFa)
  • ↓ circulating inflamm cells (eosinphils, monocytes)

Metabolic effects

  • ↑ gluconeogenesis - ↑gluconeogenesis from catabolism of muscle (AAs) and fat (fatty acids)

Mineralocorticoid effect

  • ↑Na and H2O retention and ↑K+ excretion in renal tubule
60
Q

What are the important SEs of corticosteroids

A
  • Immunosuppression
  • Metabolic - hyperglycaemia**, DM, osteoperosis
  • ↑ catabolism - prox muscle weakness, skin thinning, easy bruising, gastritis
  • Mood and behavioural changes - insomnia, confusion, psychosis, suicidal ideas
  • Mineralcorticoid - ↑BP, ↓K+, oedema
61
Q

What are the long term side effects of steroid use?WHat could happen if you withdraw steroids too quickly?

A

Suppressed ACTH secretion ► adrenal atrophy ► ↓endogenous cortisol production ► chronic glucocorticoid def (fatigue, ↓weight loss, arthralgia)

  • If withdrawn suddenly - ADDISONIAN CRISIS
  • ∴ slow withdrawal required to ↑adrenal funct
  • (not necessary if Tx duration <2 weeks)
62
Q

What are the important interactions of corticosteroids?

A
  • NSAIDs - ↑risk of peptic ulcer/GI
  • ß2-agonists, theophylline, loop/thiazide diuretics - ↑risk of hypo-K taking
  • Metabolised by P450
  • ↓immune response to vaccines
63
Q

When should corticosteroids be cautioned?

A

Infection

Children

64
Q

What indications might corticosteroids be used for in palliative care? What doses might you use?

A
  • Bronchial obstruction (16mg od + early RT)
  • Superior vena caval obstruction (Dex 16mg od - urgent stent)
  • ↑ICP (Dex 4-8mg, unless severe Sx/risk of coning - 16mg)
  • Neuropathic pain - may reduce nerve compress
  • Carcinomatous lymphangitis (dex 8-12mg o.m)
  • Liver capsule pain (Dex 4-8mg od)
  • Pelvic pain
  • Exacerbation of COPD/asthma
65
Q

What time should you give corticosteroids?

A

Morning - prevent insomnia

66
Q

What other non-pharmacological Txs are avaliable for pain?

A
  • Palliative radiotherapy e.g. bone pain
  • Palliative chemotherapy e.g. for tumour masses compressing viscera or nerves
  • Surgery e.g. intramedullary nail for pain from a femoral metastasis
  • Anaesthetic and neurosurgical interventions e.g. paravertebral nerve block
  • Psychological interventions e.g. CBT
  • TENS
  • Complementary therapies e.g. aromatherapy
67
Q

In the context of N&V, what four main mechanisms contribute to stimulation of the vomiting centre?

A
68
Q

What are the CFs of gastric stasis/irritation?

A
  • Early satiety
  • Epigastric fullness
  • Hiccups
  • Heartburn
  • Large amount of vomit - often min nausea between vomits (vomiting relieves)
69
Q

WHat are the causes of gastric irritation/stasis?

A
  • Tumour
  • Hepatomegaly
  • Ascites (‘squashed stomach’)
  • Dysmotility (drugs, autonomic failure).
70
Q

What is the Tx for N&V relating to gastric stasis/irritation?

A
  • Metoclopramide
    • 10-20 mg po/sc 30 minutes before meals
    • 30-60 mg SC /24hrs
  • Stop any causative drugs if possible
  • Tx any treatble causes e.g. drain ascites
  • Consider proton pump inhibitor/H2 receptor antagonist if gastric irritation.
71
Q

What are the CFs for toxic causes of N&V?

A
  • Persistent or intermittent nausea
  • Small vomits, ‘possets’, and retching
72
Q

WHat are toxic causes of N&V?

A
  • Drugs (opioids, digoxin, antiepileptics)
  • Hypercalcaemia - nausea, constipation, confusion, polyuria/dipsia
  • Uraemia (nausea, fatigue, itch) - ↓renal funct
  • Infections (UTI, pneumonia).
73
Q

WHat is the Tx for toxic related N&V?

A

Haloperidol 1 - 5mg PO or SC

74
Q

What are the cerebral causes for N&V?

A
  • ↑ICP
  • Anxiety, anticipatory N&V
  • Interdeterminate
75
Q

What are the CFs of ↑ICP?

A
  • Early morning headache
  • Vomiting
  • Little nausea
  • Associated focal neurological Sx/signs
76
Q

What is the Tx for ↑ICP related N+V?

A
  • Dexamethasone 8-16mg po
  • +/- Cyclizine
    • 50mg TDS PO
    • 150mg/24hrs SC
77
Q

WHat are the CFs for anxiety/anticipatory related N+V?

A
  • Specific precipitants
  • Overly anxious
  • Depression
78
Q

What are the Txs for anxiety related/anticipatory N+V?

A
  • Benzodiazepines (lorazepam)
  • CBT
  • Complementary therapies
79
Q

What is the treatment for multifactorial/indeterminate N+V?

A

Consider levomepromazine 6.25-12.5mg PO or SC

80
Q

What type of antiemetic is metoclopramide and domeridone?

A
  • Dopamine D2 receptor antagonist
81
Q

What is the mechanism by which metoclopramide/domperidone (dopamine D2 receptor antagonists) work?

A
  • Chemoreceptor Trigger Zone - inputs in vomiting centre
    • responsible for sensing emetogenic substances in blood e.g. drugs
    • D2 receptor main receptor in CTZ.
    • Dopamine also promotes relaxation of stomach and lower oesphageal sphincter
  • Blocking D2 receptors = ↓ CTZ stimulation and prokinetic effect (promotes gastric emptying)
  • ∴ metoclopramide/domperidone = effective in N&V due to CTZ stimulation (e.g. drugs) and ↓ gastric motility
82
Q

What are the SEs of Metoclopramide and domperidone?

A
  • DIARRHOEA
  • Metoclopramide - Long term use - extrapyramidal syndromes (e.g. tardive dyskinesia)
    • Short term Tx - acute dystonic disorders e.g. oculogyric crisis
  • Doperidone - does not cross BBB ∴ does not cause Extra-P Sx
83
Q

What are the CIs for using metoclopramide/domperidone?

A
  • Avoid in children and young adults (↑ extrapyramidial Sx)
  • GI obstruction (can cause perforation)
84
Q

What are the improtant drug interactions for metoclopramide?

A

Metoclopramide

  • Co-prescribed with antipsychotics ↑risk of extrapyramidial SE
  • Do NOT combine with dopaminergic agents for Parkinson’s disease (antagonise effects)

Domperidone - not subject to above interactions

85
Q

WHat type of anti-emetic is cyclizine/cinnarizine/promethazine?

A
  • Histamine H1 receptor antagonist
86
Q

What is the indication for using cyclizine?

A
  • Prophylaxis and Tx of N&V in a wide range of contexts, particularly motion sickness and vertigo
87
Q

What is the mechanism by which cyclizine works?

A
  • Histamine (H1) and Acetylcholine receptors - predominate in vomiting centre and in its communication with vestibular system
  • Blocks BOTH receptors - ↓N&V in wide range of conditions
    • e.g. drugs, post-op, radiotherapy
    • MAINLY vertigo/motion sickness
88
Q

What are the main SEs of Histamine H1 receptor antagonists?

A
  • Drowsiness (cyclizine = least sedating)
  • Dry mouth and throat (anticholinergic effects)
  • IV - transient tachycardia (Palpatations)
89
Q

What are the warnings for Histamine H1 receptor antagonists?

A
  • Sedating - avoid driving and avoid in patients at risk of hepatic encephalopathy
  • Prostatic hypertrophy (may develop urinary retention)
90
Q

What are the important interactions of Cyclizine/histamine H1 receptor antagonists?

A
  • Sedation ↑ in combo with other sedatives (benzos, opioids)
  • ↑anticholinergic effects taking ipratropium and tiotropium
91
Q

What is the mechism by which haloperidol and other first-generation antipsychotics (chlorpromazine, prochlorperazine) work in reducing N&V?

A

Haloperidol

  • Blockage of dopamine D2 receptor in the CTZ and gut
  • ↓ CTZ stimulation and promotes gastric emptying

Prochlorperazine/chlorpromazine

  • Block D2 receptors and, to lesser extent, histamine (H1) and acetylcholine receptors in vomiting centre and vestibular system
  • ↓N&V in wide variety of different situations e.g. chemoT, radioT, vertigo)
92
Q

What are the SEs of haloperidol, prochlorperazine and chlorpromazine?

A
  • Extrapyramidial effects
    • Acute
      • dystonic reaction
      • Akathisia (restlessness)
      • Neuroleptic malignant syndrome (rare SE: rigidity, confusion, autonomic dysregulation, pyrexia)
    • Chronic
      • Tardive dyskinesia
  • Drowsiness
  • postural ↓BP
  • QT-interval prolongation
  • Erectile dysfunctiin
  • Hyperprolactinaemia (tuberhypophyseal D2 blockage)
93
Q

What are the warnings for using haloperidol, prochlorperazine and chlorpromazine?

A
  • Avoid in severe liver disease (sedating effect, pot for hepatotoxicity
  • Prostatic hypertrophy (urinary retention - anticholinergic)
  • Elderly - ↓dose
94
Q

What are the important drug interactions forthe antipsychotics?

A
  • Extensive list!
  • Avoid in combo with drugs that ↑QT interval
    • antipsychotic, amiodarone, ciprofloxcin, macrolides, quinine, SSRIs
95
Q

What type of antiemetic is ondansetron?

A
  • Serotonin 5-HT receptor antagonist
96
Q

What is the mechanism by which ondansetron/5HT receptor antagonists work?

A
  • High density serotonin (5HT) receptors in CTZ
  • Serotonin key NT released by gut in response to emetogenic stimuli ► stimulates vagus nerve ► activates vomiting centre
  • ∴ effective for N&V due to CTZ stimulation (e.g. drugs) and visceral stimuli (e.g. gut infection, radioT),
    • but NOT motion sickness
97
Q

What are the SEs of ondansetron?

A
  • Rare but can cause:
    • constipation
    • Diarrhoea
    • Headaches
98
Q

What are the warnings of ondansetron?

A
  • May prolong QT interval (but only at high doses)
99
Q

WHat are the improtant drug interactions of oldansetron?

A
  • Avoid 5HT anatagonists when PTs taking drugs that ↑QT interval
    • e.g. antipsychotics, quinine, SSRIs
100
Q

What are the two main types of GI obstruction?

A
  • Mechanical
  • Functional

Can be partial, complete or intermittent at single or multiple sites

101
Q

What are the CFs of intestinal obstruction?

A
  • Nausea - often postprandial, intermittent and relieved by voming undigested food
  • Vomiting - may be faeculent
  • Dull aching pain due to tumour mass and/or nerve infiltration
  • COLICKY PAIN
  • Altered bowel sounds (diarrhoea and/or constipation)
  • Abdo distention (May be absent in high obstruction)
  • Paradoxical disarrhoea and/or constipation
  • Other Sx: no flatus, anorexia, dry mouth, dehydration
102
Q

What bowel sounds would you hear with mechanical and functional intestinal obstruction?

A
  • Functional - no bowel sounds
  • Mechanical - high pitched, tinkling
103
Q

What types of cancers does intestinal obstruction most take place?

A
  • Ovarian
  • Bowel
104
Q

How is intestinal obstruction diagnosed?

A
  • Hx and Physical exam
    • Complete obstruction - flatus/stools absent
    • ΔΔ constipation (faecal impaction)
  • Contrast radiography - may help define site and extent
  • CT scan - assist in choice
  • AXR (supline and erect) may help - but ‘normal appearance’ on AXR does not exclude obstruction
105
Q

What are is the surgical management of intestinal obstruction?

A
  • Difficult to select patients appropriate. Depends on:
    • Patient disease (performance status, prognosis e.g. ascites = poor prognosis, Tx)
    • Comorbidity
    • Level of obstruction
    • Co-existing Sx.
  • Bowel resection or by-pass +/- stoma formation - single-site obstruction without other life threatening disease
106
Q

What is the management if surgery for intestinal obstruction is inappropriate/not possible?

A

Medical symptom management - aimed at ↓Sx and ↑QoL:

  • Mouth care
  • Small amounts of oral fluid/food if desired - often well tolerated. Patient decides if risk of vomiting outweighs pleasure of eating
  • IV fluids and NG tube (TPN) - short term intervention (rarely appropriate for long term management).
  • Rx - generally by continuous SC infusion - antiemetics, analgesics, antispasmotics.
107
Q

How should colicky pain with intestinal obstruction be managed?

A
  • STOP stimulant laxatives/prokinetic drugs e.g. metoclopramide.
  • Use antispasmodics e.g. hyoscine butylbromide 60-120mg/24hrs
108
Q

How should dull aching pain with intestinal obstruction be managed?

A
  • Diamorphine or morphoine SC/CSCI
109
Q

How should pain from a tumour mass be managed?

A
  • Consider dexamethasone/chemo/radio - ↓tumour/peri-tumour oedema
110
Q

How do bulk forming laxatives work?

A
  • Contains HYDROPHILIC substance e.g. cellulose, polysaccharide
  • Attracts water into the stool ► ↑stool mass ► ↑peristalsis
  • Relieves constipation and useful for chronic diarrhoea
111
Q

Name 2 bulk forming laxatives

A

Fybogel, ispaghula husk

112
Q

What are the SEs of bulk forming laxative/fybogel

A
  • Abdo distention
  • flactulence
  • Rarely cause:
    • Faecal impaction
    • GI obstruction
113
Q

What are the CIs for bulk forming laxatives?

A
  • Subacute/established intestinal obstruction or faecal impaction
  • Caution with ileus
  • RARELY APPROPRIATE IN PALLIATIVE CARE SETTINGS
114
Q

WHat are the improtant interactions of bulk forming laxatives?

A

No clinically significant ones

115
Q

Name 5 stool softening laxatives

A
  • Docusate
  • Lactulose
  • Macrogol
116
Q

What is the mechanism by which stool softening laxatives work?

A
  • Osmotically active substances = not digested/absorbed and remain in gut lumen
  • Hold water in the stool ► ↑stool volume ► ↑peristalsis
117
Q

What are the important SEs of stool softening laxatives?

A
  • Flactulence/bloating (especially lactulose)
  • Abdo cramos
  • Nausea
  • Diarrhoea
118
Q

What are the CIs for stool softening laxatives?

A
  • Bowel obstruction (↑risk of perforation)
119
Q

What are the interactions of stool softening laxatives? (lactulose, macrogel, movicol, magnesium salts)

A

No significant drug interactions

120
Q

Name 2 stimulant laxativesd

A
  • Senna
  • Bisacodyl
121
Q

How do stimulant laxatives (e.g. senna, bisacodylo, sodium picosulphate) work?

A
  • ↑H2O and electrolytes secretion from colonic mucosa ► ↑colonic content volume ► ↑peristalsis
  • Also has pro-peristaltic action (exact mechanism differs between agents)
122
Q

WHat are the SEs of stimulant laxatives?

A
  • Abdo pain/cramping
  • STOP if patient has COLIC
  • Diarrhoea
  • Melanosis coli (long term use)
123
Q

What are the important interactions of stimulant laxatives?

A

No important ones

124
Q

What are the CIs for stimulant laxatives?

A
  • Intestinal obstruction - ↑risk of perforation
  • Avoid rectal preperations if haemorrhoids or anal fissures present
125
Q

WHen should you avoid

A
126
Q

What should you do if a patient bowel has not opened in 3 days despite laxatives?

A
  • Perform PR exam (if safe/appropriate)
  • Consider use of suppositories/enemas
127
Q

Name 2 combination laxtives (i.e. both stimulant and softener)

A
  • Movicol
  • Co-danthrusate (dantron + docusate)
128
Q

What are the best laxatives for opioid-induced constipation?

A
  • Co-danthrusate
  • Co-danthramer
  • Movicol
129
Q

How often should laxatives be reviewed?

A

Every 2 days

130
Q

What is the definition of dyspnoea?

A
  • Uncomfortable awareness of breathing
  • Occurs in patients with advanced cancer and in cardioresp and neurological disease
131
Q

What are the possible reversible causes of sudden onset breathlessness? What Txs could be considered?

A

Asthma ► Bronchodilators, corticosteroids, physio

Pulmonary oedema ► Diuretics, morphine

Pneumonia ► ABx, physio

PE ► anticoagulants, morphine

Pneumothorac ► chest drainage

132
Q

What are the possible reversible causes of breathlessness arising over several days? What Txs could you consider treating these causes?

A

COPD exaccerbation ► ABx, Bronchodilators, corticosteroids

Pneumonia ► ABx, physio

Bronchial obstruction by tumor ► dexamethasone 16mg O.D, early radiotherapy, consider laser or stents

Superior vena caval obstruction ► Dexamthasone 16mg OD. Urgent stent

133
Q

What are the possible reversible causes for breathlessness of more gradual onset? WHat treatments might you consider?

A

Congestive HF ► diuretics, digoxin, ACEi

Anaemia ► Transfusion may help if Hb<80g/l

PE ► pleural aspiration and follow with pleurodesis if appropriate

Pulmonary fibrosis ► Hx of cytotoics or lung radiotherapy

Ascites ► Paracentesis if appropriate (drain into peritoneum)

10/20 Lung carcinoma ► Resection, RT, or chemoT

Carcinomatous Lymphangitis ► Trial dexamethasone (8-12mg O.M)

134
Q

If there is no reversible cause for breathlessness, what is the non-pharmacological palliative manegement?

A
  • Reassure and explain to patient and family
  • Modification of lifestyle, breathing retraining, relaxation and tailored exercise may be beneficial
  • Consider Physio referral or OT
  • Oxygen may help acute dyspnoea BUT long term O2 therapy not beneficial
  • Fan in face often helps dyspnoea
135
Q

What pharmacological treatment would you consider for irreversible breathlessness in palliative settings?

A

Opioids

  • MST MR (5-10mg BD) + laxative
    • titrate by 5-10mg bd every 7 days until SEs or total dose = 30mg
  • Oramorph - if opioid naive/renally impaired
    • 2.5mg four hourly - gradually titrate upwards according to response

Benzodiazepines

  • Lorazepam (0.5-1.0 mg Sub-lingually) may give rapid relief during panic attacks/↓SOB
  • Midazolam (2.5mg SC) may benefit patients who cannot tolerate oral/sublingual route
136
Q

What mouth problems can you get in palliative care?

A
  • Dry mouth (xerostomia) - ↓fluid intake and SEs of drugs
    • ↓taste, anorexiam, halitosis, dysphagia, infection
  • Coated mouth - poor salivary function
  • Sore/ulcerated mouth
    • Infection (oral candidiosis) - coats mouth, SPARES LIPS
      • ​altered taste, soreness, pain
    • Mucositis - post-chemo/radiotherapy
    • Tumour
    • Aphthous ulcers
    • Vitamin deficiency
137
Q
A
138
Q

What is the treatment for a dry mouth in palliative care?

A
  • Frequent sips of cold unsweetened drink
  • Sugar free chewing gum/low sugar pastilles/boiled sweets
  • Artifical saliva substitutes
139
Q

What is the Tx for oral oral candidosis?

A
  • Systemic antifungals (Fluconazole - 50mg/7 days)
  • Topical agents (Nystatin oral suspension)
140
Q

What are the Tx for sore, ulcerated mouth?

A
  • Topical analgesia (paracetamol mouth rinse)
  • Topical anaesthetics (e.g. lidocaine)
  • Systemic preperations
141
Q
A

4th Year Drugs (7 decks)

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