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AI Exam 2 > Pain > Flashcards

Pain Flashcards

1
Q

A pain which:
-Comes on suddenly
-Treated by resolving the cause of the pain
-Usually due to trauma, injury or surgery
-Lasts less than 6 months
-OTC treatments / WHO analgesic ladder is used
Is what type of pain?

A

Acute

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2
Q

A pain which:
-Comes on gradually
-Usually the result on a condition that is difficult to treat and diagnose
-Lasts longer than 6 months
-Difficult to find lasting relief
Is what type of pain?

A

Chronic

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3
Q

A pain which is:
-The traditional idea of pain
-Ability to detect and respond to painful stimuli
-Prevents or acts in the response to tissue damage
Is what type of pain?

A

Nociceptive pain

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4
Q

A pain which is:
-A malfunction in the nervous system or damage to the nerves, eg, diabetic neuropathy
-Central pain, peripheral neuropathy, complex regional pain syndrome
-Burning or electric shocks
Is what type of pain?

A

Neuropathic pain

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5
Q

A pain which is:
-Altered nociception in the absence of tissue or nerve damage
-Widespread intense pain
-Exercise / psychological / acupuncture could possibly help
-Antidepressants are used off label
Is what type of pain?

A

Nociplastic pain

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6
Q

What is stage 1 in the WHO analgesic ladder?

A

Non-opioid +/- Adjuvant
-Paracetamol
-NSAIDS/COX2-inhibitors
-Topical treatments

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7
Q

What is stage 2 in the WHO analgesic ladder?

A

Opioid for mild to moderate pain +/- non-opioid. +/- Adjuvant
-Codeine / Dihydrocodeine / Tramadol
= Limited potency at the Mu receptor

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8
Q

What is stage 3 in the WHO analgesic ladder?

A

Opioid for moderate to severe pain +/- non-opioid. +/- Adjuvant
Morphine / Diamorphine / Oxycodone / Fentanyl / Buprenorphine // Alfentanil
= Strong potency at Mu receptor

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9
Q

What anti-epileptic adjuvant therapies could be used for neuropathic pain?

A

-Gabapentin
-Pregabalin
-Carbamazepine

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10
Q

What anti-depressants can be used for pain?

A

Tricyclics
SSRI’s

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11
Q

Why would Dexamethasone be used in palliative care?

A

Bone pain

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12
Q

A patient who is a poor metaboliser would have what benefit from opioids?

A

No benefit - as codeine is converted to morphine in the liver by CYP2D6

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13
Q

A patient who is a super metaboliser would have what benefit from opioids?

A

Lots of benefit

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14
Q

Common side effects of Opioids?

A

Nausea, vomiting, constipation, drowsiness, sedation, respiratory depression

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15
Q

What laxatives should be given for Opioid induced constipation?

A

Stimulant + Osmotic
(Senna + Laxido)

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16
Q

What are the 6 signs of opioid overdose?

A

1) Pinpoint pupils
2) Unconsciousness
3) Shallow / slow breathing
4) Pale skin
5) Blue lips
6) Snoring / rasping breath

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17
Q

What is the reasoning behind pin point pupils?

A

-Stimulation of parasympathetic nervous system
-Contraction causes pinpoint pupils

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18
Q

What is the reasoning for pale skin / blue lips?

A

Hypoxia - low blood oxygen, low blood circulation

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19
Q

What are the pharmacological treatments for Musculoskeletal lower back pain?

A

-NSAIDS
-Weak opioids for acute pain if NSAID not useful
-DO not offer only paracetamol

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20
Q

What shouldn’t be offered for Sciatica?

A

-Gabapentin / Antiepileptics / Benzodiazepines

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21
Q

Should opioids be offered for chronic sciatica?

A

No

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22
Q

What are the long term management options for sciatica?

A

-Epidural injections
*Acute + Severe sciatica
*Local anaesthetic + Corticosteroid

-Spinal decompression surgery

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23
Q

What are the symptoms of Osteoarthritis?

A

-Pain
-Stiffness
-Tenderness
-Grafting sensation (noise)
-Swelling
-Bone spurs

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24
Q

What is the treatment for Osteoarthritis?

A

-Exercise
-Weight loss if needed
-Manual therapies
-Topical NSAIDS
-Paracetamol +/- Opioids
-Intra-articular corticosteroids
-Joint replacement

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25
Q

What drugs can be used for a patient descripting ‘shooting or burning’ pain?
*If one doesn’t work try another

A

-Amitriptyline
-Duloxetine
-Gabapentin
-Pregabalin

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26
Q

If someone with neuropathic pain can’t tolerate oral remedies what should be offered?

A

Capsaicin cream

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27
Q

What drug is used for Trigeminal neuralgia?

A

Carbamazepine

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28
Q

There is NO maximum dose of opioids in palliative care, true or false?

A

True

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29
Q

When someone is made palliative we start with anticipatory (PRN) injection medications , when would a patient be moved onto a syringe driver?

A

3+ injections in 24 hours
*As per NNUH guidance

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30
Q

What is given if a patient is breathless when they are palliative?

A

Opioids / Midazolam - to slow breathing down, comfort patient as less distressed

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31
Q

What do you dilute the medicines with in a syringe driver?

A

Water for injection, remains stable over 24 hours and won’t precipitate

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32
Q

what factors could influence how post operative pain is managed?

A

Comorbidities, renal, liver, age, frailty, allergies

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33
Q

What group of medicines should be avoided if a patient has a fractured hip or pelvis surgeries and why?

A

NSAIDS - affects bone recovery

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34
Q

What should be monitored when a patient has a PCA?

A

Pain score & AVPU & Respiratory rate

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35
Q

When will a patient receive the loading does for a PCA?

A

In recovery

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36
Q

How much does a PCA deliver at a time (mg)?

A

1mg at a time

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37
Q

What is the benefit of a PCA?

A

Smaller dose, more frequently

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38
Q

What are the advantages of a PCA?

A

-Pt ownership and independence
-Faster alleviation of pain
-Reduces distress in waiting for nursing staff
-Less time consuming
-Easy to titrate according to response / need

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39
Q

What are the disadvantages of a PCA?

A

-Patient may not be responsive or dextrous enough to use
-Patient may lack understanding or be scared to use
-Reduced mobility
-Liable to abuse (lock out time)
-Side effects (N&V, low bpm drowsiness, constipation)

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40
Q

What should be monitored hourly for the first 8 hours post PCA insertion?

A

BP
Pulse
RR
Sedation
Pain score
Nausea
(Opioid effects!)

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41
Q

After the first 8 hours of hourly observation, when should they now be done and for how long?

A

Monitor every 2 hours for 24 hours

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42
Q

How is PCA induced nausea and vomiting managed?

A

Cyclizine / Ondansetron

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43
Q

How is PCA induced pruritis managed?

A

Chlorphenamine 4mg TDS

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44
Q

How is PCA induced respiratory depression (RR less than 8) managed?

A

-STOP PCA
-Oxygen and monitor sats
-Consider naloxone 200-400mcg (Short half life)

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45
Q

How should PCA induced excessive sedation be managed?

A

-Remove PCA
-Monitor: Sats, Pain and sedation score
-Ensure adequate non-opioid analgesia is prescribed

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46
Q

Administration of analgesics with or without anaesthetic into the epidural space, is known as what?

A

Epidural

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47
Q

What type of pain does an epidural dampen?

A

Nociceptive transmission

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48
Q

Morphine is in the epidural bag, what is the role of this?

A

-Diffuses into CSF
-Inhibits pain transmission in the spinal cord
-Acts at spinal opioid receptors
-Has no motor or sensory function
-Is reversible
-Doesn’t migrate

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49
Q

What is the role of Bupivocaine in a Epidural bag?

A

-Blocks nerve pulse and contraction
-Diffuses across myelin sheath into nerve cell
-Inhibits sodium channels, preventing depolarisation of the membrane
-Reversible,
-Doesn’t migrate

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50
Q

What two things do we not want an epidural to do?

A

1) Don’t want drugs to travel
2) Lowest concentration in the area we want

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51
Q

If drugs are dense what will happen to them when injected into the spinal column?

A

They will sink downwards
*If less dense will float and reach brain
=Need to find happy medium

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52
Q

Why is Ephedrine prescribed alongside an epidural?

A

RIsk of Hypotenstion

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53
Q

Why is Naloxone prescribed alongside an epidural?

A

It is reversible *just in case of overdose!

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54
Q

What are the advantages of an epidural?

A

-High amounts of pain relief at smaller opioid does than systemic
-Reduced incident of DVT
-Less sedation
-Post - op cover over 24 hours if infusion
-Improved pulmonary function
-Reduced cardiac morbidity and sepsis
-Faster re-establishment of oral intake

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55
Q

What are the disadvantages of an epidural?

A

-Accidental injection into the spinal cord (Total spinal block)
-Risk of permanent spinal damage
-Accidental IV administration
-Dural puncture headache
-Epidural bleed / haematoma
-Migration of drug can lead to respiratory paralysis
-Infection risk

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56
Q

Why is respiratory arrest a side effect on an epidural?

A

Migration of drugs to C3-C5 blocking phrenic nerves

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57
Q

Why can hypotension / hypothermia occur due to an epidural?

A

Vasodilation

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58
Q

Why can there be reduced cardiac output from an epidural?

A

If T1-T4 is affected

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59
Q

If overdose or given IV of the epidural what can this cause?

A

Depression of myocardial excitability

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60
Q

What are the more common side effects of an epidural?

A

Tinnitus, headache, N&V, pruritis, sedation

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61
Q

Can an epidural cause reduced hepatic and renal perfusion?

A

Yes

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62
Q

If Bupivacaine is accidently given via IV what can be given?

A

Intralipid 20% to reverse cardiac arrest risk or life-threatening toxicity

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63
Q

If a dural puncture headache occurs, what should be given?

A

Blood patch: the patients own blood is injected causing a seal around the hole = no more CSF leakage

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64
Q

What are the contraindications of a epidural?

A

-Pt refusal
-Infection at proposed site of infection
-Clotting abnormalities
-Severe respiratory impairment
-Uncorrected hypovolaemia
-Raised intracranial pressure
-Neurological disease
-Difficult anatomy

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65
Q

Can a patient with tattoos have an epidural?

A

Yes/No
*Anaesthetist dependent
-Risk of ink entering epidural space
-If tattoo is old and healed no risk

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66
Q

What type of headache is caused by a muscle spasm in the neck, and could be caused by emotional stress such as tension, anxiety or fatigue,
-Also is non-throbbing, vice like, could be described as tightness or squeezing around the head or a weight pressing down on the head.
-Usually affects both sides of the head
-May worsen throughout the day and made worse by stress.

A

Tension headache

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67
Q

What type of headache is this?
-Excruciating severe unilateral headache
-Accompanied by red eye, lacrimation, nasal congestion, rhinorrhoea, facial sweating, miosis, droopy eye and eye lid oedema?

A

Cluster headaches

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68
Q

Who is more susceptive to a cluster headache?

A

Males

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69
Q

How long does a Cluster headache last?

A

Sudden onset, may way a patient from sleep.
Intermittent onset, can occur up to 8 times a day
-Lasts between 10 mins to 3 hours

70
Q

What needs to be ruled out when a patient has cluster headaches?

A

Meningitis, bleed on head, fever, cranial arthritis

71
Q

What is the dose of paracetamol for a patient aged 4-5?

A

250mg 4-6 hourly QDS

72
Q

What is the dose of paracetamol for a patient aged 6-7?

A

240-250mg 4-6 hourly QDS

73
Q

What is the dose of paracetamol for a patient aged 10-11?

A

480-500mg 4-6 hourly QDS

74
Q

What are the symptoms of a migraine?

A

-Prodrome
-Aura
-Headache
-Postdrome - headache hangover

75
Q

What is a headache, which is lateralised and pulsating, and can cause n&v / photophobia?

A

Migraine

76
Q

A migraine which happens with an aura is called?

A

Classical migraine

77
Q

A migraine which happens without an aura is called?

A

Common migraine

78
Q

A migraine which involves GI symptoms and affects children is known as?

A

Abdominal migraine

79
Q

What causes aura in a migraine?

A

Vasoconstriction across the brain = aura

80
Q

What causes the headache in a migraine?

A

Vasodilation

81
Q

What is the Brain hypothesis of a migraine?

A

An increase in extracellular potassium, decreases blood flow causing a wave of neuronal inhibition

82
Q

What is the Sensory nerve hypothesis of a migraine?

A

Activation of the trigeminal nerve, meaning signals occur, releasing inflammatory mediators such as cytokines, prostaglandins this then causes pain and symptoms to occur.

83
Q

What can be increased during a migraine?

A

Serotonin metabolites

84
Q

What can trigger a migraine?

A

Foods, hormones, environmental,

85
Q

When can a migraine occur?

A

After a stressful period of time

86
Q

What is recommended for a migraine sufferer to do?

A

Keep a headache diary - behaviour, food and what they have done, to try identify triggers!

87
Q

What is phase 1 of a migraine?

A

Prodrome - heightened sensations, foreboding

88
Q

What is phase 2 of a migraine?

A

Aura

89
Q

What is phase 3 of a migraine

A

Headache, photophobia, phonophobia, N&V,

90
Q

What is stage 4 of a migraine?

A

Postdrome - washed out sleepy, post headache hangover

91
Q

What is the diagnosis of a migraine?

A

At least 2 of:
-Unilateral pain
-Throbbing pain
-Aggravated by movement
-Moderate or severe intensity

At least one of:
-N/V
-Phone/photophobia

92
Q

What are five attacks of a migraine called?

A

‘Migraineur’

93
Q

A differential diagnosis for a migraine could be meningitis, what would indicate this?

A

-Non blanching rash *Glass test
-Neck stiffness

94
Q

A differential diagnosis for a migraine could be Subarachnoid haemorrhage, what would indicate this?

A

Worst ever headache feel like they have been hit by a bus, it is in the occipital area (back of the head)

95
Q

A differential diagnosis for a migraine could be temporal arteritis, what would indicate this?

A

Temple/scalp painful to touch, more likely to happen in an older patient.
-Patient need’s a course of steroids

96
Q

If a patient has had a headache for more than 24 hours what should you do?

A

Refer to the GP

97
Q

If a patient has a headache that eases as the day progresses, and effortlessly is vomiting in the morning what should you do?

A

The headache is caused by something else, possibly a tumour hitting the vomit centre
=Refer to GP

98
Q

If a patient has a headache which is causing unsteadiness / clumsiness, especially in children, what should we do?

A

Refer to the GP

99
Q

If a patient under 12 is presenting with a headache that is not easing what should we do?

A

Refer to the GP

100
Q

If a patient has a headache which is a suspected adverse drug reaction, what should we do?

A

Refer to GP

101
Q

How can we manage headaches?

A

1) Shared agreement
2) Eliminate triggers
3) Acute intervention
4) Prophylaxis if 4+ a month

102
Q

What medications should be taken before a headache starts?

A

*Dispersible / effervescent preferred

Aspirin 900mg
Ibuprofen 400mg
Paracetamol 1000mg

103
Q

Why are dispersible / effervescent preferred?

A

If patient is nauseated, the GI tract is not as affected, and therefore the medication can be rapidly absorbed,

104
Q

Should you recommend migraleve to a patient with migraines?

A

NO
Has an antihistamine for sickness as makes the patient drowsy + paracetamol + codeine
*Can buy separate

105
Q

What can be sold OTC to help with sickness in a migraine?

A

Buccastem - 3mg Buccal prochloperazine

106
Q

How does Sumatriptan work?

A

It is a 5-GT1 agonist = constricts blood vessels making them go back to normal

107
Q

Who cannot have Sumatriptan?

A

IHD, uncontrolled BP, over 65+

108
Q

What are the side effects of Sumatriptan?

A

-Tiredness and dizziness
-Heaviness on the chest and throat**Counsel

109
Q

If a patient has taken simple analgesics and a triptan and after 2 hours it still persists what can they do?

A

Can take another triptan if not responded and then sleep off the headache.

110
Q

If a patient is taking 4 or more sumatriptan a month what should we do?

A

Refer to the GP

111
Q

When should prophylaxis be given for headaches?

A

-Functional impairment
-2+ headaches a week
-Amount of acute medication used
-Will the patient comply
-Success or failure of previous therapy

112
Q

Can b-blockers be used in migraine prevention?

A

Yes but can cause fatigue and bronchoconstriction

113
Q

What 5-HT2 antagonist, antihistaminic can be used in prophylaxis of migraines?

A

Pizotifen but can cause weight gain and sedation.

114
Q

What 5-HT2 antagonist can be used in prophylaxis of migraines?

A

Methysergide but can cause N&V, and rare fibrotic conditions

115
Q

What prophylaxis medication is good for, prolonged or atypical migraines with aura (no headache)?

A

Valproate / Topiramate

116
Q

How can BOTOX be used in the prevention of migraines?

A

-Relaxes muscles and blocks pain feedback

117
Q

What two drugs are the future of headache medications?

A

-Serotonin receptor agonists
-Nitric oxide (NO) antagonists

118
Q

What is pain?

A

A protective response, to raise awareness of damage and help to immobilise damaged areas to facilitate healing

119
Q

A pain which comes from cutaneous / musculoskeletal tissue or peritoneal membranes. Most often post-operative, post-exercise or from mild trauma is what?

A

Somatic pain

120
Q

A pain which is in the thoracic or abdominal organs. Most related to post-operative, cancer, or traumatic injury is what type of pain?

A

Visceral

121
Q

A pain which is from injury to the PNS or CNS, most commonly from amputation or T2DM, is known as what type of pain?

A

Neuropathic

122
Q

A pain which is a sensitisation of CNS which causes neuropathic-like pain in distribution of a sympathetic nerve, and can be complex regional pain syndromes (CRPS), is what type of pain?

A

Sympathetically-maintained pain

123
Q

What are the three types of stimuli to pain?

A

-Mechanical
-Thermal
-Polymodal

124
Q

What does polymodal mean?

A

Variety of damaging stimuli

125
Q

What fibres carry noxious stimuli?

A

A and C fibres

126
Q

Informative forces movement away from danger is classed as what pain?

A

First pain

127
Q

Punishing pain that changes behaviour, is classed as what pain?

A

Second pain

128
Q

What are the 4 processes of noiception?

A

1) Detection
2) Transmission
3) Perception
4) Modulation

129
Q

When trauma activates nociceptors, chemical mediators from the brain are released, what are these?

A

ATP, Bradykinin, Prostaglandins, Histamine, 5-HT, H+

130
Q

What do released chemical mediators do in the nociception pain?

A

Activate / sensitise nociceptors = depolarisation and action potential generated

131
Q

What is the major kinin related to pain?

A

Peptide Bradykinin which acts at GPCR’s

132
Q

What kinin is important in Inflammation?

A

Bradykinin

133
Q

What kinin is produced during tissue injury and produced by cleavage of precursor molecules?

A

Bradykinin

134
Q

What kinin causes phosphorylation of the TRPV1 channel increasing the opening of the channel?

A

Bradykinin

135
Q

What kinin causes the release of prostaglandins?

A

Bradykinin

136
Q

What enhances the pain-producing effects of other substances such as bradykinin?

A

Prostaglandins

137
Q

What does activation of PGE2 cause?

A

K+ channel activation and phosphorylation of TRPV1 via EP receptors

138
Q

What ion channels are in Nociceptor terminals?

A

-TRPV1
-P2X
-ASIC
-TRPA1
-TRPM8
-NaV
-K+

139
Q

What activates TRPV1?

A

Heat, chemicals, phosphorylation

140
Q

What activates P2X?

A

ATP

141
Q

What activates ASIC?

A

H+

142
Q

What activates TRPA1 and TRPM8?

A

Cold and chemicals
-pH of less than 5.5
-Heat above 43 deg
-Mustard + Wasabe
-Capsaicin

143
Q

What receptor plays a major role in body temperature regulation and if stimulated leads to a burning sensation?

A

TRPV1 receptor

144
Q

What is the role of C Fibres in peripheral modulation?

A

Chemical mediators reduce the threshold of C fibres, making them more easily activated by a given level of stimulus

145
Q

What is the role of Neuropeptides in peripheral modulation?

A

Increase activity of C fibres leads to the peripheral release of neuropeptides like Substance P and CGRP.

146
Q

What is the role of inflammation in peripheral modulation?

A

These neuropeptides cause the release of inflammatory mediators and NGF, creating a positive feedback loop that increases the sensitivity of neurons

147
Q

What is the role of hyperalgesia in peripheral modulation?

A

Sustained release of C Fibres, Neuropeptides and inflammation mediators can lead to hyperalgesia, which is an increased sensitivity to pain.

148
Q

What is NGF?

A

Nerve growth factor

149
Q

What is the function of NGF?

A

-Acts on TrkA receptors
-Causes upregulation of NaV channels
-Signals to increase TRPV1 activity via tyrosine kinase activity (Phosphorylation)

150
Q

If a patient has a mutation in TrkA, what does this mean?

A

They have a congenital insensitivity to pain

151
Q

What are the NaV channels essential for?

A

Action potential propagation

152
Q

What does a mutation in Nav 1.7 do?

A

Causes erythromelaglgia and paroxysmal extreme pain disorder

153
Q

What does loss of activity at Nac 1.7 do?

A

People do not feel pain

154
Q

What interneurons are present throughout the dorsal horn and common in Substantia Gelatinosa?

A

Inhibitory

155
Q

Activation of nociceptors in viscera result in somatic perception of pain, why does this happen and what causes it?

A

-Referred pain
Possibly due to convergence of multiple nociceptor afferents on a single spinothalamic tract via dorsal horn.

156
Q

What type of pain is rare?

A

Visceral

157
Q

What does the inhibitory interneuron do?

A

Closes the gate and alters info getting into the brain.

158
Q

Neurons that are in the dorsal horn and modulate transmission at the first synapse, and those that also mediate inhibition of transmission are called what?

A

Short inhibitory interneurons
*Enkephalins are important here

159
Q

What is Enkephalin?

A

Endogenous opiate

160
Q

What is something that modulates transmission at the synapse, the pathways originate in the periaquaductal grey (PAG) (5-HT), and the locus ceruleus (NA). Enkephalins are important in stimulation here too!

A

Descending inhibitory pathways

161
Q

Innocuous peripheral stimuli evokes painful sensations such as what?

A

-Hyperalgesia
-Allodynia
-Spontaneous pain
-Neuropathic pain

162
Q

What cells can contribute to increased firing in neuropathic pain?

A

Glial

163
Q

What are the four opioid receptors?

A

All GPCR’s
1) DOR - Delta
2) MOR - Mu
3) KOR - Kappa
4) ORL1 - Orphan

164
Q

What do opioid receptors signal through?

A

Gai/O
= Inhibitory

165
Q

To get morphine induced effects what do we need?

A

MOR

166
Q

What type of drug is morphine?

A

Partial Agonist

167
Q

How does Ziconotide work for neuropathic pain?

A

Inhibits Calcium Channels CaV2.2

168
Q

How does Ketamine work for neuropathic pain?

A

NMDA receptor blocker - suppresses neurotransmission through central synapse

169
Q

How doe Tricyclic antidepressants and SNRIs work for neuropathic pain?

A

Potentiate descending inhibition by modulating 5-HT and NA levels - prevent re-uptake enhance synaptic levels, enhance descending inhibition.

170
Q
A

AI Exam 2 (16 decks)

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