Palliative Care Flashcards
(141 cards)
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)
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
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)
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
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)
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
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.
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)
9
Q
Name 2 NSAIDs
A
Naproxen (250-500 mg bd)
Ibuprofen (400mg tds)
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
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
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
13
Q
What particular patients would you prescribe NSAIDs in with caution?
A
Renally impaired
Uncontrolled HTN
HF
14
Q
What are the weak/moderate opioids?
A
Codeine
Dihydrocodeine
Tramadol
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
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
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
18
Q
What are the strong opioids?
A
Morphine
Diamorphine
Oxycodone (synthetic)
Fentanyl
Alfentanil
Hydromorphone
Burenorphine
Methadone (specialist only)
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
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
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
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)
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
24
Q
If taking modified release morphine, what else should patients be prescribed with?
A
PRN for breakthrough pain (immediate release morphine)
25
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)
26
How should opoids be prescribed - mg or ml?
mg! (as differing strenghts avaliable)
27
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)
28
What should the dose be if the patient is elderly/frail?
Halve stating dose
29
What should you do to opoid dose if patient has renal impairment/failure?
Dose reduction
Seek specialist advice - alternative opioids
30
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**
31
How often should patients have their doses reviewed after being initiated on morphine?
Every 24 hrs - if pain inadequately controlled, ↑ background dose ( \< 30%)
32
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)
33
How strong is oxycodone?
1.5x more potent than oral morphine (∴ divide MST by 1.5 to get equavalent dose)
34
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.
35
What should the dose of PRN immediate release oxycodone be relative to the 24hr oxycocone dose?
1/6th
36
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)
37
What opioids can be given via SC/continuous SC infusion (via syringe driver)? What is the duration of action for each?
Diamorphine
Morphine sulfate
Oxycodone
SC - 4 hrs
CSCI - 24 hrs
38
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
39
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*
40
What is the most commonloy used syringe driver?
McKinley T34
41
Where are the recommended sites for insertion of SC cannula for syringe drivers?
Anterior chest wall
Upper arms
Abdo wall
Thighs
42
What other drugs can be given as SC infusion via syringe driver? (AVOID mixtures of \>3 compatiable drugs if possible)
43
WHat drugs are not suitable for syringe drivers? Why?
Due to irritation...
* diazepam
* chlorpromazine
* prochlorperazine.
44
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
45
Why shouldnt transdermal preperations be used in unstable pain or in last days of life?
Due to long titration period and duration of action
46
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)
47
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
48
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.
49
What are the other routes strong opioids can be administered?
* Sublingual
* Buccal
* Nasal fentanyl
For specific situations. Seek specialist adivce
50
What are the equivalent opioid doses accross different routes of administration?
51
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?**
52
Who might be able to offer help if you are unable to control patients pain?
* Senior colleagues
* Hospital/community palliative care team
* Local hospice
53
What adjuvant analgesia could you offer for cancer induced bone pain?
Consider:
* NSAIDs
* Bisphosphonates
* Palliative radiotherapy
* Corticosteroids
54
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 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
55
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
56
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)
57
What is the normal starting dose for anticonvulsants (i.e. gabapentin, pregabalin)
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
Name some important corticosteroids
* Dexamethasone \*\*
* Prednisolone
* Hydrocortisone
\*\*1st choice due to:
* high anti-inflamm potency (1mg dex = 7mg pred)
* high solubility
* Low mineralocorticoid effects\*\*
59
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
60
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
61
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)
62
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**
63
When should corticosteroids be cautioned?
Infection
Children
64
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
65
What time should you give corticosteroids?
Morning - prevent insomnia
66
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
67
In the context of N&V, what four main mechanisms contribute to stimulation of the vomiting centre?
68
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)
69
WHat are the causes of gastric irritation/stasis?
* Tumour
* Hepatomegaly
* Ascites (‘squashed stomach’)
* Dysmotility (drugs, autonomic failure).
70
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.
71
What are the CFs for toxic causes of N&V?
* Persistent or intermittent nausea
* Small vomits, ‘possets’, and retching
72
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).
73
WHat is the Tx for toxic related N&V?
Haloperidol 1 - 5mg PO or SC
74
What are the cerebral causes for N&V?
* ↑ICP
* Anxiety, anticipatory N&V
* Interdeterminate
75
What are the CFs of ↑ICP?
* Early morning headache
* Vomiting
* Little nausea
* Associated focal neurological Sx/signs
76
What is the Tx for ↑ICP related N+V?
* Dexamethasone 8-16mg po
* +/- Cyclizine
* 50mg TDS PO
* 150mg/24hrs SC
77
WHat are the CFs for anxiety/anticipatory related N+V?
* Specific precipitants
* Overly anxious
* Depression
78
What are the Txs for anxiety related/anticipatory N+V?
* Benzodiazepines (lorazepam)
* CBT
* Complementary therapies
79
What is the treatment for multifactorial/indeterminate N+V?
Consider levomepromazine 6.25-12.5mg PO or SC
80
What type of antiemetic is metoclopramide and domeridone?
* Dopamine D2 receptor antagonist
81
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**
82
What are the SEs of Metoclopramide and domperidone?
* **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
What are the CIs for using metoclopramide/domperidone?
* Avoid in children and young adults (↑ extrapyramidial Sx)
* **GI obstruction** (can cause **perforation**)
84
What are the improtant drug interactions for metoclopramide?
**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
WHat type of anti-emetic is cyclizine/cinnarizine/promethazine?
* Histamine H1 receptor antagonist
86
What is the indication for using cyclizine?
* Prophylaxis and Tx of N&V in a wide range of contexts, particularly motion sickness and vertigo
87
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
88
What are the main SEs of Histamine H1 receptor antagonists?
* Drowsiness (cyclizine = least sedating)
* Dry mouth and throat (anticholinergic effects)
* IV - transient tachycardia (**Palpatations**)
89
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)
90
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
91
What is the mechism by which haloperidol and other first-generation antipsychotics (chlorpromazine, prochlorperazine) work in reducing N&V?
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
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)
93
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
94
What are the important drug interactions forthe antipsychotics?
* Extensive list!
* Avoid in combo with drugs that ↑QT interval
* antipsychotic, amiodarone, ciprofloxcin, macrolides, quinine, SSRIs
95
What type of antiemetic is ondansetron?
* Serotonin 5-HT receptor antagonist
96
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
97
What are the SEs of ondansetron?
* Rare but can cause:
* constipation
* Diarrhoea
* Headaches
98
What are the warnings of ondansetron?
* May prolong QT interval (but only at high doses)
99
WHat are the improtant drug interactions of oldansetron?
* Avoid 5HT anatagonists when PTs taking drugs that ↑QT interval
* e.g. antipsychotics, quinine, SSRIs
100
What are the two main types of GI obstruction?
* Mechanical
* Functional
Can be partial, complete or intermittent at single or multiple sites
101
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
* 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
What bowel sounds would you hear with mechanical and functional intestinal obstruction?
* Functional - no bowel sounds
* Mechanical - high pitched, tinkling
103
What types of cancers does intestinal obstruction most take place?
* Ovarian
* Bowel
104
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
105
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
106
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.
107
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
108
How should dull aching pain with intestinal obstruction be managed?
* Diamorphine or morphoine SC/CSCI
109
How should pain from a tumour mass be managed?
* Consider dexamethasone/chemo/radio - ↓tumour/peri-tumour oedema
110
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
111
Name 2 bulk forming laxatives
Fybogel, ispaghula husk
112
What are the SEs of bulk forming laxative/fybogel
* Abdo distention
* flactulence
* Rarely cause:
* Faecal impaction
* GI obstruction
113
What are the CIs for bulk forming laxatives?
* Subacute/established **intestinal obstruction or faecal impaction**
* Caution with **ileus**
* **RARELY APPROPRIATE IN PALLIATIVE CARE SETTINGS**
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WHat are the improtant interactions of bulk forming laxatives?
No clinically significant ones
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Name 5 stool softening laxatives
* Docusate
* Lactulose
* Macrogol
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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
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What are the important SEs of stool softening laxatives?
* Flactulence/bloating (especially lactulose)
* Abdo cramos
* Nausea
* Diarrhoea
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What are the CIs for stool softening laxatives?
* Bowel obstruction (↑risk of perforation)
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What are the interactions of stool softening laxatives? (lactulose, macrogel, movicol, magnesium salts)
No significant drug interactions
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Name 2 stimulant laxativesd
* Senna
* Bisacodyl
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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)
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WHat are the SEs of stimulant laxatives?
* Abdo **pain/cramping**
* STOP if patient has **COLIC**
* **Diarrhoea**
* **Melanosis coli** (long term use)
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What are the important interactions of stimulant laxatives?
No important ones
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What are the CIs for stimulant laxatives?
* **Intestinal obstruction** - ↑risk of perforation
* Avoid rectal preperations if **haemorrhoids** or **anal fissures** present
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WHen should you avoid
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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
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Name 2 combination laxtives (i.e. both stimulant and softener)
* Movicol
* Co-danthrusate (dantron + docusate)
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What are the best laxatives for opioid-induced constipation?
* Co-danthrusate
* Co-danthramer
* Movicol
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How often should laxatives be reviewed?
Every 2 days
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What is the definition of dyspnoea?
* Uncomfortable awareness of breathing
* Occurs in patients with advanced cancer and in cardioresp and neurological disease
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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
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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
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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)
**10/20 Lung carcinoma** **►** Resection, RT, or chemoT
**Carcinomatous Lymphangitis ►** Trial dexamethasone (8-12mg O.M)
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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
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What pharmacological treatment would you consider for irreversible breathlessness in palliative settings?
**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
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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
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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
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What is the Tx for oral oral candidosis?
* Systemic antifungals (**Fluconazole - 50mg/7 days**)
* Topical agents (**Nystatin** oral suspension)
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What are the Tx for sore, ulcerated mouth?
* Topical analgesia (paracetamol mouth rinse)
* Topical anaesthetics (e.g. lidocaine)
* Systemic preperations
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