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Block 3 > Pain & Pharmacology Of Analgesics > Flashcards

Pain & Pharmacology Of Analgesics Flashcards

1
Q

What are the 2 types of pain?

A
  1. Nociceptive

2. Neuropathic

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2
Q

What is nociceptive pain?

A

The result of tissue damage, often acute, short-term and relatively easy to treat (physiological)

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3
Q

What is neuropathic pain?

A

The result of damage to neurons, often chronic and difficult to locate + treat

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4
Q

Define hyperalgesia.

A

When something that is moderately painful normally becomes excruciating i.e. patient is over-sensitized to it

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5
Q

Define allodynia.

A

When something that is not noxious, causes a painful response in the patient e.g. putting a T-shirt on when sunburnt - it shouldn’t hurt you but it does!

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6
Q

How does nociceptive pain occur?

A

Physical damage or response to inflammatory soup (immune response) results in activation of free-nerve endings which respond to mechanical, chemical, pressure + temperature changes

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7
Q

What pharmacological options exist for nociceptive pain?

A

NSAIDs + opioids:

  • Ibuprofen
  • Co-codamol
  • Morphine (gold-standard opioid)
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8
Q

What are some examples of nociceptive pain?

A

Low-back pain
Myofascial pain
Arthritis
Visceral pain (pancreatitis, interstitial cystitis, endometriosis etc.)

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9
Q

How does neuropathic pain occur?

A

Damage/changes in the pain neurons themselves but mechanism is unclear -wind-up of activity through pathways

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10
Q

List some classic symptoms of neuropathic pain.

A

Shooting/burning pain

Paraesthesias (pins + needles): tingling, numbness, burning + throbbing

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11
Q

Give some examples of conditions that cause neuropathic pain.

A 
Phantom limb
Trigeminal neuralgia
Post-stroke pain
Post-herpetic pain (shingles)
Complex regional pain syndrome
Malignant pain
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12
Q

What is complex regional pain syndrome (CRPS)?

A

Massive autonomic activation in 1 limb causing burning pain, redness etc.

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13
Q

What is referred pain?

A

Sensory info from ANS travels alongside sympathetic (pain/temp) and parasympathetic neurons (other sensation) entering at the same level so pain/temp for example can be referred to cutaneous region where it enters

E.G. heart = T1-5 + kidneys = T10-L1

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14
Q

How do you treat referred pain?

A

Treat the underlying cause i.e. figure out the organ innervated by this dermatome and treat the organ issue

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15
Q

What is a tension headache? How do you treat it?

A

Presents on frontal lobe and back of neck

Treat with NSAIDs, maybe codeine + keep a diary to determine trigger factors as avoidance may be possible

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16
Q

What is a sinusitis headache? How do you treat it?

A

Presents in a typical butterfly pattern across the front of the face

Treat with decongestants, antihistamine or steroids

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17
Q

What are migraine headaches? How do you treat them?

A

Unilateral headache presenting with nausea and photophobia perhaps due to vaso-constriction

Prophylaxis = β-blockers or amitriptyline

Treat with 3 step approach:

  1. NSAIDs +/- antiemetics
  2. Rectal NSAIDs + antiemetic
  3. Anti-migraine drugs (5HT1B/1D agonists e.g. sumatriptan + naratriptan)

AVOID OPIOIDS

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18
Q

What are cluster headaches? How do you treat them?

A

Unilateral symptoms behind 1 eye with sympathetic involvement causing runny eyes/nose

Prophylaxis = verapamil

Treatment = sumatriptan

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19
Q

What are the different types of headache?

A
  1. Tension
  2. Sinus
  3. Migraine
  4. Cluster
  5. Medication over-use
  6. Sub-arachnoid haemorrhage
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20
Q

What are sub-arachnoid haemorrhage headaches? How do you treat it?

A

Worst ever rapid onset thunderclap headache

This is an emergency so get them a CT scan ASAP

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21
Q

Where in the body can the pain pathway be modulated?

A
  1. Periphery
  2. Spinal cord
  3. Centrally
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22
Q

Give some drug development targets for pain treatment.

A

Rubefacients
Capsaicin
Topical analgesics

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23
Q

How do rubefacients work?

A

Distract area around inflammatory soup e.g. when you rub an area making it less painful - work around the gate control theory

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24
Q

How does capsaicin work?

A

Causes enough pain to distract focus of pain

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25
Q

How is nociceptive pain sensed and carried to brain?

A
  1. Sensed by free nerve endings on C (groan) and Aδ (ouch) fibres (1st order neurons)
  2. Synapse at substantia gelatinosa onto 2nd order neurons
  3. Carried via lateral spinothalamic tracts (trigeminothalamic tract if in face) to thalamus and on to cortex
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26
Q

What is the difference between C and Aδ pain fibres?

A

C: longer and slower pain response as they have no myelin sheath

Aδ: shorter and quicker pain response as they have myelin sheath

27
Q

What is the gate control theory of pain?

A

Input from 1st order pain fibres (Aδ/C) activates 2nd order cells and inhibit local interneurons so pain signal can travel onwards

However, mechanical stimulation of area activates inhibitory interneurons reducing pain transmission by inhibiting 2nd order cells

28
Q

What are the main higher pain centres sending output to descending tracts?

A

Hypothalamus
Periaqueductal gray (defense region)
Brainstem nuclei

29
Q

What brainstem nuclei send output to descending pain tracts?

A

Nucleus raphe paragigantocellularis, nucleus raphe magnus + locus coeruleus that produce 5-HT

Dorsolateral funiculus which contains descending inhibition tract

30
Q

What are some important higher integration centres?

A

Parietal lobe:
Frontal cortex
Prefrontal cortex
Amygdala

31
Q

What is descending inhibition?

A

Higher centres (e.g. limbic system) modify response to painful stimuli and this travels to ANS and spinal lamina of dorsolateral funiculus (brainstem nuclei) dampening down the pain

Many transmitters and neuromodulators involved particularly 5HT and NA

32
Q

Why does neuropathic pain remain chronic?

A

Because so much information is going through that there is reduced descending inhibition due to confusion and pain gate is left open

33
Q

Why does neuropathic pain occur?

A 
Badly managed acute pain
Emotionally sensitive patient
Poor coping skills
Previous bad pain experiences
Pain goes on for longer 
Surgical complications
Genetic predisposition
34
Q

What part of the spinal cord does pain travel through?

A

Dorsal horn

35
Q

Describe the biopsychosocial model of pain perception.

A

Incorporates all aspects of pain and associated behaviour such as:

  • Biological pain (varies e.g. when women are on cycle + thought that women have higher pain thresholds than men)
  • Psychological e.g. attitudes/beliefs, psychological distress + illness behaviour
  • Social
36
Q

What are the non-pharmacological options used to treat pain?

A 
Exercise
Physiotherapy
Acupuncture
Transcutaneous Electrical Nerve Stimulation (TENS)
Behavioural therapy
37
Q

What are the invasive procedures used to treat pain?

A

Nerve blocks/injections at trigger points or joints

Ablation

Implants of pumps releasing drugs e.g. neuromodulators

38
Q

What pharmacological options exist for neuropathic pain?

A

TCAs and anti-epileptics:

  • Nortriptyline/amitriptyline
  • Gabapentin/pregabalin +/- nortriptyline (better tolerated in combo than amitriptyline)
  • Carbemazepine alone (never in combo - good for trigeminal neuraligia)
39
Q

Describe the WHO ladder for cancer pain control.

A
  1. Pain-free: no medication
  2. More pain: administer non-opioid analgesic (paracetamol/NSAID) +/- adjuvant (e.g. caffeine)
  3. More pain: administer weak opioid (e.g. codeine, co-codamol) +/- non-opioid +/- adjuvant
  4. More pain: strong opioid (morphine + related e.g. fentanyl, methadone) +/- non-opioid +/- adjuvant
40
Q

How do non-steroidal anti-inflammatory drugs (NSAIDs) work?

A
  1. Rapid uptake into stomach + SI
  2. Block production of pro-inflammatory PGs by inhibiting COX so AA is not broken down
  3. Metabolites excreted in urine
41
Q

What are the different forms of cyclooxygenase (COX)?

A

COX1: normal cell function
COX2: inflammation
COX3: fever? Does it exist?

42
Q

What are the commonly used non-steroidal anti-inflammatory drugs (NSAIDs)?

A

Aspirin (also used as CV drug)

Ibuprofen (weak)

Naproxen (strong + lower side effects)

Diclofenac (stronger but like naproxen)

Indomethacin (strong, good for arthritis but high side effects)

43
Q

What non-steroidal anti-inflammatory drugs (NSAIDs) can a patient with gut problems take?

A

COX-2 inhibitors e.g. Celecoxib, Etoricoxib + Paracoxib

Similar to naproxen but with lower GI effects

44
Q

What class of drug does paracetamol come under?

A

It is part of the NSAID family but it is kind of isolated - thought that it might be working on COX-3 if it exists - it is a anti-pyretic but not anti-inflammatory which is why it doesn’t quite fit into NSAID category

45
Q

What do prostaglandins (PGs) do?

A

PGs work on prostanoid receptor increasing activation of Na channels casing depolarisation, AP firing + pain

46
Q

List the side effects of non-steroidal anti-inflammatory drugs (NSAIDs).

A 
GI problems (heartburn, nausea, vomiting, diarrhoea, bleeding/ulceration)
CV incidents (thrombosis esp. COX-2)
Headache
Tinnitus
Dizziness
Insomnia 
Nervousness
Depression
Vertigo
Photosensitivity
Renal impairment 
Hypertension
Hypersensitivity (skin rashes + eruptions, angioedema, bronchospasm)
47
Q

What is a common indicator of salicylate toxicity?

A

Tinnitus (esp. with salicylate NSAIDs e.g. aspirin) - common in patients on consistent low doses but also high acute dose

Salicylism has 1% mortality

48
Q

What happens to the gut with long-term use of non-steroidal anti-inflammatory drugs (NSAIDs)?

A

Holes start to form in gut lining, mucus becomes stringy with bacteria on it and ulcer formation occurs

After a very long-time, the reticular structure underlining the normal gut cells has come out to the surface

49
Q

What is Reye’s syndrome?

A

A condition causing swelling in liver and brain (can cause death) as a result of aspirin use in children under 16 years old if they have had a virus before hand

50
Q

What can you prescribe non-steroidal anti-inflammatory drugs (NSAIDs) with to reduce side effects?

A

PPIs

51
Q

What are the symptoms of severe non-steroidal anti-inflammatory drugs (NSAIDs) toxicity?

A

Auditory (ototoxicity, tinnitus, deafness)
Pulmonary (apnoea, aspiration pneumonitis, pulmonary oedema, alkylosis, respiratory arrest)
CV (tachycardia, hypotension, asystole, dysrhythmias)
CNS (depression, seizure, encephalopathy, delirium, hallucinations)
GI (pancreatitis, hepatitis)
Renal failure
Coma

52
Q

What is chronic non-steroidal anti-inflammatory drugs (NSAIDs) intoxication? How is it treated?

A

Plasma levels more than 300mg/kg

Treatment:

  • Fluid replacement
  • Haemodialysis
  • Activated charcoal
  • Lorazepam/diazepam i.v. for seizures
53
Q

What are the 4 opioid receptors?

A

μ (MOP/OP3)
κ (KOP/OP2)
δ (DOP/OP1)
ORL1 (OP4)

54
Q

What are the opioid agonists?

A

Strong: morphine (T1/2 = 3-4hrs) , diamorphine (T1/2 = 3-4hrs) + tramadol (acts on 5-HT receptor + has disturbing hallucinogenic side effects)

Weak: codeine (T1/2 = 3-4hrs)+ dihydrocodeine

55
Q

What are the opioid partial agonists/mixed agonist-antagonists?

A

Nalorphine
Pentazocine
Buprenorphine (T1/2 = 12hrs)

= mixed affect

56
Q

What are the opioid antagonists?

A

Naloxone (T1/2 = 1-2hrs like Fentanyl)

Naltrexone (T1/2 = 10hrs)

57
Q

What are the 4 main groups of opioid synthetic derivatives?

A
  1. Phenylpiperidine e.g. pethidine (T1/2 = 2-4hrs)
  2. Methadone e.g. dextropropoxyphene (T1/2 = more than 24hrs)
  3. Benzomorphan e.g. cyclazocine
  4. Thebaine e.g. buprenorphine (T1/2 = 12hrs)
58
Q

How do opioids work?

A

Thought to act by mimicking endogenous opioids in the CNS e.g. brainstem pain nuclei

59
Q

How do opioids decrease neuronal transmission?

A

Decreasing opening of voltage-dependent Ca2+ channels

Increasing K+ outflow via K/ATP + K/IR channels hyperpolarising cell so less likely to fire when stimulus appears

Decreasing Ca2+ release from IC stores via cAMP reduction (can increase it too)

Decreased exocytosis of transmitter vesicles

60
Q

What are the side effects of opioid toxicity?

A

Cardinal: respiratory depression, conscious depression/mood alterations, miosis + coma (GCS less than 7)

Others: reduced gastric motility, nausea/vomiting, SM spasm, anaphylaxis, psychiatric changes (pentazocine, tramadol) + tolerance/dependency (addiction/withdrawal)

61
Q

If a white Caucasian person is not responding to a opioid dose, what should you do?

A

Do not just keep upping the dose as a high % of the Caucasian population are unresponsive and you will induce toxicity

62
Q

How do you treat opioid overdose?

A

Opioid antagonists: naloxone (short-lasting) + naltrexone (longer-lasting)

If conscious and within 1hr of OD give activate charcoal + 0.8-2mg naloxone every 2-3mins for respiratory depression

Combo to resolve coma = naloxone, O2, glucose + thiamine(in case there is more than 1 cause)

63
Q

What is the problem with including barbiturate antagonist flumazenil or benzo clomazinole in the coma cocktail?

A

Can result in rebound seizures or potentiate seizures in susceptible people

64
Q

What other drugs can be used for trigeminal neuralgia if carbamazepine is not well tolerated?

A

Oxcarbazepine
Gabapentin
Pregabalin

Block 3 (40 decks)

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