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Flashcards in Palliative Care Deck (141):

What are the different types of analgesia?

Non-opioid (simple analgesia) eg paracetamol or NSAIDS

Opioids (weak and strong)

Adjuvant (co analgesics)


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

- 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


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

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)


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

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


Which analgesic should be prescribed?

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)


How does paracetamol exert its action? 

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


What are the SEs of paracetamol? 

  • 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. 


WHat are the CIs for paracetamol? 

Risk of liver toxicity due to:

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


Name 2 NSAIDs 

Naproxen (250-500 mg bd)

Ibuprofen (400mg tds)



How do NSAIDs exert their action? 

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

Benefits from blocking COX2, SEs from COX1



WHat are the SEs of NSAIDs? 

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


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

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


What particular patients would you prescribe NSAIDs in with caution?

Renally impaired

Uncontrolled HTN



What are the weak/moderate opioids?





How do weak opioids exert their action? 

- Broken down to morphine (codeine) and dihydromorphine (dihydrocodeine) which are agonists of U receptors in CNS

- reduce pain transmission


Why doesn't codeine or dihydrocodeine work in everyone?

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

10% Caucasians have less active metabolising enzyme  ∴ ineffective


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

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



What are the strong opioids?



Oxycodone (synthetic) 





Methadone (specialist only)


How do strong opioids exert their action? 

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


How does tramadol exert its actions? 

- 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 


What are the side effects of Opioids?

  • 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


What are the signs of opioid toxicity?

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


What types of morphine sulphate preperations are there? 

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


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

PRN for breakthrough pain (immediate release morphine)


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

  • 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)


How should opoids be prescribed - mg or ml? 

mg! (as differing strenghts avaliable)


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)

  • 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)


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

Halve stating dose


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

Dose reduction

Seek specialist advice - alternative opioids


What is the starting regimen of morphine sulphate?

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



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

Every 24 hrs - if pain inadequately controlled, ↑ background dose (


What is oxycodone? When is it used?

  • 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)


How strong is oxycodone?

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


WHat are the avalaible formulations for oxycodone?

  • 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. 


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



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

  • 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) 


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


Morphine sulfate 



SC - 4 hrs

CSCI - 24 hrs 


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

SC morphine - 2x more potent

SC diamorphine - 3x more potent


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


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

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


What is the most commonloy used syringe driver? 

McKinley T34 


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

Anterior chest wall

Upper arms

Abdo wall



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


WHat drugs are not suitable for syringe drivers? Why?

Due to irritation...

  • diazepam
  • chlorpromazine
  • prochlorperazine. 



What are transdermal (patch) preperations of morphine indicated?

Patients with:

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




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

Due to long titration period and duration of action


What should patients with transdermal patches be prescribed along with?

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


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

12, 25, 50, 75 or 100µg per hour

Applied every 72 hrs


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

  • 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. 


What are the other routes strong opioids can be administered?

  • Sublingual
  • Buccal 
  • Nasal fentanyl 

For specific situations. Seek specialist adivce 


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


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

  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? 


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

  •  Senior colleagues
  • Hospital/community palliative care team
  • Local hospice


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


  • NSAIDs
  • Bisphosphonates
  • Palliative radiotherapy
  • Corticosteroids 


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

Consider patients Sx, SEs and co-morbidities when Rx

  • 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 


What is the mechanism by which gabapentin and pregabalin work?

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


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

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


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

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


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


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


Name some important corticosteroids

  • Dexamethasone **
  • Prednisolone
  • Hydrocortisone


**1st choice due to:

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


What is the mechanism by which corticosteroids exert their action?

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 


What are the important SEs of corticosteroids

  • 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 



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

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)


What are the important interactions of corticosteroids?

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


When should corticosteroids be cautioned?




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

  • 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 


What time should you give corticosteroids?

Morning - prevent insomnia 


What other non-pharmacological Txs are avaliable for pain?  

  • 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 



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


What are the CFs of gastric stasis/irritation? 

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


WHat are the causes of gastric irritation/stasis?

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


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

  • 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.  



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

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


WHat are toxic causes of N&V?

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


WHat is the Tx for toxic related N&V?

Haloperidol 1 - 5mg PO or SC


What are the cerebral causes for N&V?

  • ↑ICP
  • Anxiety, anticipatory N&V
  • Interdeterminate 


What are the CFs of ↑ICP?

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


What is the Tx for ↑ICP related N+V?

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


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

  • Specific precipitants 
  • Overly anxious
  • Depression


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

  • Benzodiazepines (lorazepam)
  • CBT
  • Complementary therapies 


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

Consider levomepromazine 6.25-12.5mg PO or SC


What type of antiemetic is metoclopramide and domeridone? 

  • Dopamine D2 receptor antagonist 


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

  • 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


What are the SEs of Metoclopramide and domperidone?

  • 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



What are the CIs for using metoclopramide/domperidone?

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


What are the improtant drug interactions for 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


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

  • Histamine H1 receptor antagonist


What is the indication for using cyclizine?

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


What is the mechanism by which cyclizine works?

  • 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


What are the main SEs of Histamine H1 receptor antagonists?

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


What are the warnings for Histamine H1 receptor antagonists?

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


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

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


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


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


  • 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)


What are the SEs of haloperidol, prochlorperazine and chlorpromazine?

  • 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)


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

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


What are the important drug interactions forthe antipsychotics?

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


What type of antiemetic is ondansetron?

  • Serotonin 5-HT receptor antagonist


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

  • 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


What are the SEs of ondansetron?

  • Rare but can cause:
    • constipation
    • Diarrhoea
    • Headaches


What are the warnings of ondansetron?

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


WHat are the improtant drug interactions of oldansetron?

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


What are the two main types of GI obstruction?

  • Mechanical 
  • Functional

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


What are the CFs of intestinal obstruction?

  • 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
  • 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 


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

  • Functional - no bowel sounds
  • Mechanical - high pitched, tinkling


What types of cancers does intestinal obstruction most take place?

  • Ovarian
  • Bowel


How is intestinal obstruction diagnosed?

  • 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


What are is the surgical management of intestinal obstruction?

  • 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



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

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. 


How should colicky pain with intestinal obstruction be managed?

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


How should dull aching pain with intestinal obstruction be managed?

  • Diamorphine or morphoine SC/CSCI


How should pain from a tumour mass be managed?

  • Consider dexamethasone/chemo/radio - ↓tumour/peri-tumour oedema 


How do bulk forming laxatives work?

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


Name 2 bulk forming laxatives 

Fybogel, ispaghula husk


What are the SEs of bulk forming laxative/fybogel 

  • Abdo distention
  • flactulence
  • Rarely cause:
    • Faecal impaction
    • GI obstruction


What are the CIs for bulk forming laxatives?

  • Subacute/established intestinal obstruction or faecal impaction 
  • Caution with ileus


WHat are the improtant interactions of bulk forming laxatives?

No clinically significant ones


Name 5 stool softening laxatives

  • Docusate
  • Lactulose
  • Macrogol


What is the mechanism by which stool softening laxatives work?

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


What are the important SEs of stool softening laxatives?

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


What are the CIs for stool softening laxatives?

  • Bowel obstruction (↑risk of perforation)


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

No significant drug interactions


Name 2 stimulant laxativesd

  • Senna
  • Bisacodyl


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

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


WHat are the SEs of stimulant laxatives?

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


What are the important interactions of stimulant laxatives?

No important ones


What are the CIs for stimulant laxatives?

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


WHen should you avoid 


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

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


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

  • Movicol
  • Co-danthrusate (dantron + docusate)


What are the best laxatives for opioid-induced constipation?

  • Co-danthrusate
  • Co-danthramer
  • Movicol


How often should laxatives be reviewed?

Every 2 days


What is the definition of dyspnoea?

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


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

Asthma  ► Bronchodilators, corticosteroids, physio 

Pulmonary oedema ► Diuretics, morphine 

Pneumonia ► ABx, physio

PE ► anticoagulants, morphine 

Pneumothorac ► chest drainage 


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

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 


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

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)

10/2Lung carcinoma ► Resection, RT, or chemoT

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


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

  • 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 


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


  • 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


  • 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 


What mouth problems can you get in palliative care?

  • 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 



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

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


What is the Tx for oral oral candidosis?

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


What are the Tx for sore, ulcerated mouth?

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