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MD3 > AC - Palliative Care > Flashcards

AC - Palliative Care Flashcards

1
Q

What are some key components of palliative care?

A

Can be introduced at any stage of disease/age - can even be introduced along side life-prolonging Rx. Early assessment & strategies better outcome

Doesn’t intend to hasten or prolong death

Aims to improve QOL, prevent suffering and support maximal functioning

Holistic - psychological, physical & spiritual

Team based care - disciplinary and disciplinary

Needs to be culturally safe

Needs to involve family, carers/supports as well as patient

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2
Q

What factors may influence perception & experience of dying process?

A

Age - age can influence whether people view it as expected or not - this can influence the level of support given

Previous experiences with death - patient may have had a positive or negative experience with relative/friend which impacts on their attitude and coping skills

Culture & religion - may positively or negatively influence coping ability and attitudes - i.e. some cultures may experience distress associated with ‘after-life’

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3
Q

Common palliative care issues which need to be considered/discussed?

A

Physical, psychological and spiritual problems
Financial & ‘getting affairs in order’ - i.e. wills, POA
Education about the diagnosis & its relation to prognosis
How disease/Rx will impact on function - sexual, social, work, home
How they will manage/cope with symptoms and when they become very ill
Whether they should be managed at home or in hospital
Discussion of possible ethical issues - advanced care directives, when to withdraw certain treatments and when/how to discuss imminent death
Assess carer stress and how family will cope

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4
Q

Define pain

A

Unpleasant emotional and sensory experience in response to actual or perceived tissue damage

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5
Q

What is nociceptive and neuropathic pain?

A

Nociocpetive pain - noxious stimuli acting on peripheral nociceptors (small unmyelinated c-fibres)
- can be somatic (localised, sharp) or visceral (vague, dull)

Neuropathic pain - dysfunction within PNS or CNS (unmyelinated c-fibres + alpha-delta myelinated fibres)

  • pain in distribution of nerve root/dermatome/peripheral nerve
  • shooting, burning, electric shock pains
  • may be spontaneous or associted with allodynia or hyperalgesia
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6
Q

Define acute vs. chronic pain

A

Acute - temporary, usually serves physiological purpose

Chronic - persists beyond expected normal recovery or > 3 months, usually not serving physiological purpose

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7
Q

How can cancer/tumours cause pain?

A

Hypercalcaemia - generalised muscle aches/pains
Infiltrative or compressive - of nerve
Involvement of bone, soft tissue and viscera
Space occupying - pressure, stretching capsule
Ulceration
Peripheral neuropathy
Obstruction of hollow viscera

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8
Q

What are risk biological risk factors to developing pain

A

Acute pain - poor response to initial analgesia, initially poorly managed or inadequate initial analgesia

Underlying comorbidities - may restrict Rx available/prevent effective management

Mechanism of pain - Neuropathic pain higher risk

Multiple pains and pain mechanisms

Nature of underlying pathology

Refractory adverse effects from analgesia

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9
Q

What are psychosocial risk factors to developing chronic pain?

A

ABCDE
A - attitudes to recovery
B - beliefs about seriousness of underlying cause (i.e. catastrophising
C - ongoing compensation/cover claim
D - understanding of the disease/diagnosis, hx of drug/alcohol use
E - emotional, family, work, financial related stressors

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10
Q

What are the general principles of chronic pain mangaement?

A

4Ps - physical, psychological, pharmacological and procedures/other

Physical - physical reactivation - increase exercise, core strength, stretching/flexibility - consider physio and exercise physiologist referrals

Psychological - CBT, acceptance-based Rx, stress management, mindfulness - consider referral to psychology

Procedures - consider other useful interventions i.e. surgical, nerve blocks, intra-articular steroid injections
Other - modification of the environment, advice on safe lifting/bending etc

Goals need to be realistic - may not be able to completely eliminate pain
Reduce pain to tolerable level and support to develop skills/strategies to cope with pain and limit pain-related handicaps
GP management plan/TCA valuable

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11
Q

What are the general pharmacological options for pain management?

A
  1. Simple analgesia - paracetamol, NSAIDs
  2. Opioids
  3. Neuropathic pain agents
  4. Steroids (dexamethasone)
  5. Bisphosphonates
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12
Q

Describe the WHO analgesia ladder

A
  1. Simple analgesia +/- adjunct (i.e. antiemetic, laxative, antidepressant, anticonvulsant)
  2. ADD weak opioid (codeine, tramadol)
  3. REPLACE weak opioid for strong opioid (morphine, oxycodone, hydromorphone, fentanyl, buprenorphine)
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13
Q

What are important features on Pain history?

A

4Ps

  1. Pain - cardinal features
  2. Pathology/past hx - treating comorbidities may improve QOL and improve ability to cope or may need to be considered with pain management
  3. Performance - effect on social, physical and occupational function, severity, any fear avoidance
  4. Psychological - how they are coping, any co-existing or underlying psychological/psychiatric issues (esp. anxiety & depression)
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14
Q

What are pharm Rx options for neuropathic pain?

A

1st line = amitriptyline (TCA)
2nd line = pregabalin or gabapentin
3rd line = duloxetine

Anticonvulsants and MAOI inhibitors can also be used
Carbamezepine - trigeminal neuralgia
Pregabalin - diabetic neuropathy

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15
Q

What pain is dexamethasone useful in relieving?

A

Raised ICP - headache
Pain due to stretching of liver capsule
Inflammatory pain

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16
Q

What can improve bony pain/hypercalcaemia pain?

A

Bisphosphonates

Paliative RTx - especially bony mets to spine

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17
Q

How can severity of pain be assessed/rated?

A

Visual analogue, numerical and verbal scales
Face scale - esp. in peadiatric, aged care and language barrier
Clinical/behavioural observation (Abbey Scale) - particularly in cognitive impairment
- Verbal, non-verbal cues
- New or increased behavioural issues/disturbances
- Social, food or treatment refusal
- Sleep disturbance

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18
Q

What is PRN dosing in pal care for opioids?

A

1/6th of daily dose

19
Q

What are the adverse effects of NSAIDs?

A

CV (embolic events, worsening of HTN, HF)
GI (PUD)
Renal (reduced eGFR, AKI, worsening of CKD)

20
Q

What are key characteristics of tramadol?

A

Weak opioid
Long acting - 12 hrs
Has SSRI effect also
Less constipation & respiratory effects but greater other S/E

Avoid in elderly as increases risk of delirium

21
Q

What are key characteristics of morphine?

A

Avoid in renal impairment (metabolites accumulate) but safer in liver impairment

Long (MS contin, 12 hrs) and short acting (3-4 hrs)

22
Q

What is the conversion of sub/cut to oral morphine and ratio of morphine to oxycodone?

A

1mg sub/cut = 3mg oral

1:1.5 ratio morphine:oxycodone

23
Q

Compare use of oxycodone & morphine

A

Oxycodone used more frequently than morphine as it has less cognitive side effects and more predictable serum levels

It is safer in liver impairment (except targin)

It is stronger than morphine (1.5:1 ratio)

Short acting is oxycodone longer effect than morphine

24
Q

What are the types of oxycodone?

A 
Short acting (oxynorm, endone, 4-6 hrs)
Long acting (targin, oxycontin, 12 hrs)

Targin has naloxone - supposed to reduce constipation effects by reducing GIT absorption. If liver impairment it is absorbed systemically - withdrawal if tolerant, less analgesia

25
Q

What is the sub/cut to oral conversion of oxycodone?

A

1mg s/c = 2mg oral

26
Q

What is the sub/cut to oral conversion of hydromorphone and the conversion to morphine?

A

1mg sub/cut = 3.5mg oral

1mg hydromorphone = 5mg morphine

27
Q

What is the conversion of fentanyl to morphine?

A

12mcg (smallest patch dose)/hr = 15mcg s/c morphine over 24 hrs

28
Q

What is the conversion of buprenorphine to morphine?

A

5mcg/hr buprenorphine = 5mg over 24 hrs of morphine

29
Q

Compare use of hydromorphone & fentanyl

A

Fentanyl long acting comes in 3day patch (lowest dose 12mcg/hr)
Long acting hydromorphone is s/c or oral lasting 24 hrs

Fentanyl is safer in renal impairment but hydromorphone can still be used in renal impairment

Hydromorphone has less side-effects and is easier to use than fentanyl

30
Q

How can dyspnoea be managed in pal care?

A

Non-pharm

  • Decrease work of breathing - positioning/posturing
  • Increase perception of air - sit near open windows, fan blowing on face

Pharm

  • O2
  • Morphine (short-acting)
  • Benzos (lorazapam, midazolam - medium acting)
31
Q

How are partial BO managed in pal care?

A

Chance of spontaneous resolution therefore give some active treatment

Supportive - some oral intake, fluids

Pharm - metoclompramide
- Antiemetic (reduces symptoms), prokinetic (improves motility which may help resolve obstruction)

32
Q

How is a complete BO managed in pal care?

A

Need to be sure complete as active Rx may lead to risk of perforation and non-active may reduce chance of clearing - terminal event

Hyoscine butylbromide (buscapan) - antispasmodic (releives colicky pain), reduces secretions (reduces vomiting), antiemetic

Dexamethasone - minimal evidence but still usually given

Octreotide - reduces blood flow to gut - less secretions and vomiting

33
Q

what is the most common clinical presentation of spinal cord compression in pal care?

A

Usually insidious, chronic compression rather than acute event

Thoracic > lumbar > cervical

Usually a result of compression from extra-dural mass which impairs vascular in/out-flow leading to cord ischaemia

Will have localised pain and tenderness on examination

May have radicular pain/symptoms

34
Q

Spinal cord compression vs. cauda equina syndrome

A

Compression above L2 = spinal cord compression

compression below L2 = cauda equina syndrome

35
Q

What are the 4 general causative mechanisms of nausea, the receptors and stimuli that affect them?

A
  1. GIT - inflammation (toxins, infection), mechanical (obstruction, ileus, gastroparesis), dopamine receptors
  2. CTZ - biochemical (metabolic, drugs), dopamine and serotonin receptors
  3. Vestibular system - motion and viruses, histamine, muscarinic and dopamine receptors
  4. Higher CNS - anxiety, anticipatory, raised ICP
36
Q

What drugs are effective on GIT mediated nausea?

A

Domperidone

Metoclopromide

37
Q

What drugs are effective on CTZ mediated nausea?

A

1st line = metoclopromide, haloperidol
2nd = prochlorpromezine

Also ondanestron (5-HT3 antagonist) 
Dexamethasone
38
Q

What drugs are effective on vestibular mediated nausea?

A 
Cyclizine (antihistamine)
Hyoscine butylbromide (anticholinergic)
promethazine (dopamine)
39
Q

What drugs are effective on higher-CNS mediated nausea?

A

Alprazolam (anxiety)

Dexamethasone

40
Q

What is a good approach to breaking bad news/talking about death?

A

SPIKES

  1. Set-up - appropriate environment, significant others, privacy, manage time restraints
  2. Perception - check patients understanding of situation and what they’re expecting
  3. Invitation - obtain patient’s invitation to discuss difficult topic
  4. Knowledge - provide information about diagnosis, sign post bad news is coming
  5. Emotions - identify and acknowledge emotions, be empathetic and give them some time
  6. Summary & strategy - ask if patient wants to discuss treatment plan, check their understanding and manage their expectations
41
Q

What are appropriate steps and discussions to be taken when discussing end-of-life care?

A
  1. communicate to pt and family that they are dying (SPIKES)
  2. counsel pt and family on - getting affairs in order, process of dying and what to expect, symptoms that may occur and how will be managed/reassure, discuss nutrition and fluids
  3. Rationalise medications, observations and procedures - only perform those directly impacting/improving symptoms
  4. Nutrition - remove artificial if not contributing to comfort, other strategies (ice chips, damp sponge in mouth)
  5. prescribe PRN medications - benzos, opioids, antiemetic, antipsychotic, anti-secretions (buscapan, atropine, glycoparylate)
42
Q

How would you describe the process of dying to a patient?

A

Will gradually become less and less aware of surroundings and hunger and thirst will diminish
Will become more tired and sleepy, spending more and more time in bed and asleep than awake
Eventually will become unconscious

43
Q

What is the process of confirming a death?

A
  1. Before - check resus/ACD status, circumstances of death & patient background
  2. Address family/friends if present - respect
  3. General inspection - signs of life - movement, colour
  4. Respiration - signs of respiratory effort
  5. Response - verbal and pain stimuli
    6 . Pupils - fixed and dilated after death
  6. Circulation - palpate carotid artery, heart sounds (1min), lung (3mins)
  7. Documentation and communication

MD3 (21 decks)

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