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Pharmacology > Management of Pain > Flashcards

Management of Pain Flashcards

1
Q

Define pain

A

Pain is an unpleasant sensory + emotional experience associated with actual or potential tissue damage

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2
Q

What are the 2 categories of pain?

A
  • somatogenic

- psychogenic/psychosomatic day

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3
Q

What is somatogenic pain?

A

Pain localised by body tissue. KNOWN cause

  • nociceptive pain - pain caused by inflammation or injury
  • neuropathic pain - generated in nerves itself e.g. shooting pain. Caused by damage to neurones in pain pathway + often doesn’t respond to opioids.
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4
Q

What is psychogenic/psychosomatic pain?

A

Pain for which there is NO known cause, but processing of sensitive information in CNS is disturbed
E.g. common in abdo

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5
Q

What NS response is activated in acute pain?

A

Sympathetic Nervous System

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6
Q

What are the responses to acute pain?

A
  • tachycardia
  • tachypnoea
  • hypertension
  • diaphoresis
  • pallor
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7
Q

What is chronic pain?

A

Pain that is persistent or intermittent for 6months +

  • often unknown cause
  • develops gradually
  • associated with sense of hopelessness/helplessness
  • can lead to sleeping disorders/depression
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8
Q

What is pain tolerance?

A

The duration of time or intensity of pain that an individual will endure before initiation of overt pain responses e.g. seeking pain medication

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9
Q

What influences a persons pain tolerance?

A
  • persons cultural prescription (what’s exceptable)
  • expectations
  • role behaviour
  • physical + mental health (worse if this already exists)
  • age (decrease in tolerance older people)
  • diabetics
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10
Q

What increases a persons pain tolerance?

A
  • alcohol
  • medication e.g. BZs
  • hypnosis
  • warmth + cold
  • distracting activities
  • strong beliefs of faith
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11
Q

What does haemodynamic mean?

A

Relates to flow of blood within body

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12
Q

What are the haemodynamic effects of pain?

A
  • vascoconstriction

- syncope (some Pts under stress have a parasympathetic response, causes BP to drop)

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13
Q

What are cutaneous mechanoreceptors? And how many types are there?

A

4 types, they respond to vibrations/pressure

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14
Q

What are thermoreceptors?

A

They respond to temperature

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15
Q

What do nociceptors + free never endings of sensory cells respond too?

A

Tissue injury

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16
Q

What are the different parts of the reflex arch?

A
  • sensory
  • afferent neurone
  • bridging neurone in spinal cord
  • motor neurone
  • muscle

NOT controlled by brain
If the stimulus is not no it can override spinal reflexes with downward pathways

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17
Q

How does neural transmission occur?

A
  • burn your hand
  • damaged/inflamed tissue releases prostaglandins
  • prostaglandins bind to receptors on nociceptive neurones (activated)
  • transmission goes up spinal cord + initiates firing in primary afferent fibres (release glutamate + peptides) that synapse in laminators I + II of dorsal horn of spinal cord
  • relay neurones in dorsal horn transmit pain information to sensory cortex via neurones in thalamus (goes up somatosensory cortex)
  • activity of relay neurones modulated by inhibitory inputs; local interneurones which release opioid peptides + descending enkephalinergic, noradrenergic + serotonergic fibres - activated by opioid receptors
  • opioid peptide release in both brainstem + spinal cord can reduce activity of dorsal horn relay neurones (cause analgesia)
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18
Q

Why might someone go unconscious when in severe pain?

A

The Collateral to reticular formation, that goes to brainstem is through to do with consciousness.
So if transmission goes to here, people can get responses like increased BP, tachycardia + unconsciousness

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19
Q

If damage to an area increases, how is that reflected in AP?

A

If damage increases, freq of AP increases (AP are all at same amplitude)

  • if it’s a gland + there is high freq = secreted more of gland it produces
  • if it’s an AP in a doperminergic neurones = more dopamine released
  • if it’s an AP in serotonergic neurone = more serotonin released
  • higher freq of AP reaching somatosensory cortex =more pain you will experience. Also affected by number of neurones affected
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20
Q

Why do you not get pain in 3rd degree burns?

A

It destroys nociceptive neurones

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21
Q

Why doesn’t touching cause pain?

A

Nociceptive neurones have a high threshold to depolarisation (small-diameter axons) so non-noxious stimuli (touching) are inadequate (don’t cause pain)

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22
Q

What increases the speed of an AP?

A

Myelinated neurones + larger axon diameter = faster AP

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23
Q

In small diameter neurones, how are AP stimulated?

A

Stimulated by prostaglandins released in injured tissues

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24
Q

What threshold to depolarisation do large diameter neurones have?

A

They have a low threshold to depolarisation (pressure/heat activates them). Large diameter neurones run in parallel

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25
Q

Where do small + large diameter neurones that detect information from the same region, synapse?

A

Synapse in different areas of spinal cord but close to each other.

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26
Q

What are the 3 primary afferent neurones, and ho2 are they stimulated?

A

Beta fibre - stimulated by non-noxious mechanical stimulus. These are LARGE diameter neurones

Delta fibre - stimulated by noxious mechanical stimulus. These are SMALL diameter neurones

C fibre - stimulated by noxious heat + chemical stimuli (e.g. in esophagus, heart burn)

27
Q

What are the spinal cord neurones called that small diameter axons synapse with?

A

T-cells

28
Q

When the gate is closed, what happens to the AP?

A

You don’t get any AP or AP is reduced going up spinal cord =absence sensation of pain

29
Q

What happens when the gate is open?

A

You feel the full effects of nociception e.g. severe pain

30
Q

What is the S neurone?

A

A small neurone between the 2 synapses of spinal cord that had the affect of closing the gate

31
Q

What causes the gate to close?

A

Activity in large diameter axons, close the gate, caused by non-noxious stimuli e.g. ice packs, massage.

Or

Responses from brain sending signals down from spinal cord

32
Q

What does activation of the S neurone do?

A

S neurone releases natural opioid (enkephalins) which either act as an inhibitor +/or blocker in synapse.

Enkephalins bind to small diameter axons terminal or dendrites of transmission neurones = either causes substance P (pain NT) receptor to be deactivated or stops substance P from being released over synapse

33
Q

What hormone in the body can cause the release of enkephalins + endorphins?

A

Adrenaline - helps to escape even if injured (Adrenaline response)

34
Q

Why does IM hurt?

A

Inside of bones don’t have nonciceptive neurones, but you do in the periosteum.

35
Q

How does opioid analgesia work?

A

They mimic endogenous opioid peptides by causing prolonged activation of opioid receptors = produces analgesic, resp depression, euphoria + sedation.

Pain acts as an antagonist to resp depression - if it’s removed e.g. 2oth anaesthetic can be a problem.

36
Q

Why is a side effect of opioids constipation?

A

Gut contains opioid receptors - opioid causes effect on nerve plexuses in gut

37
Q

What are the 2 types of acute pain?

A

somatic e.g. skin, joints
-Superficial coming from skin or close to surface of body

visceral (includes referred)
-pain in internal organs, abdo or chest

38
Q

What is referred pain?

A

Pain that is present in an area removed or distant from its point of origin. The area of referred pain is supplied by the nerves from the same spinal segment at the actual site of pain.

39
Q

What can left shoulder tip pain in trauma be a sign of?

A

Splenic rupture -as blood pushes against spleens capsule, caspusle doesn’t have nonciceptive neurones, the overstretching of capsule causes pain. If it bleeds out onto peritoneum will cause rigidity in that area + cause severe pain

40
Q

What might right shoulder tip pain be a sign of?

A

A liver problem

41
Q

What is deafferentation pain?

A

Pain in an area where there is diminished or abnormal sensation

42
Q

What is compartment syndrome?

A

When you get bleeding in the muscle fibres causing compression

43
Q

What are types of visceral pain? And what receptors are these?

A
  • angina
  • MI
  • acute pancreatitis
  • prosthetic pain
  • renal pain

These receptors are small diameter + unmyelinated C-fibres = AP is slow

NSAIDs are not effective in treatment of visceral pain

44
Q

Where is COX found and what are it’s functions?

A

COX exists in tissues as constitutive isoform (COX-1).

At sites of inflammation, cytokines stimulate induction of second isoform (COX-2).

Inhibition of COX-2 responsible for anti-inflammatory actions of NSAIDs.

Inhibition of COX-1 is response for there GI toxicity.

45
Q

What is the anti-inflammatory action of NSAIDs?

A
  • prostaglandins produce vasodilation + increased vascular permeability
  • inhibition of prostaglandin synthesis reduces inflammation but doesn’t abolish it, because drug doesn’t inhibit other inflammatory mediators
46
Q

What is the antipyretic action of NSAIDs?

A
  • during fever, interleukin 1 is released from leukocytes + acts directly on thermoregulatory centre in hypothalamus to increase body temp
  • aspirin prevents this by preventing the rise in brain prostaglandin levels
47
Q

Why does inhibiting COX 1 affect GI?

A

In the stomach, COX1 produces prostaglandins (PGE2 + PGI2) that stimulate mucus + bicarbonate secretion + cause vasodilation.

Inhibiting this reduces the cytoprotective effects of prostaglandins = causing upper GI side effects e.g. bleeding + ulceration

48
Q

What is the role of misoprostol in previewing GI toxicity from NSAIDs?

A

Misoprostol is a PGE1 derivative. Effecting in preventing GI toxicity in NSAIDs. Used in pts with history of peptic ulcer when NSAID treatment can’t with withdrawn

49
Q

Why can NSAIDs cause nephrotoxicity?

A

Prostaglandins PGE2 + PGI1 are powerful vasodilators (involved in control of renal blood flow + excretion of salt + water).

Inhibition of renal prostaglandin synthesis may result in sodium retention, reduced renal blood flow + renal failure

50
Q

How does Aspirin work?

A
  • inhibits COX 1+2 = blocks synthesis of prostaglandins at injured tissue site
  • also known as acetylsalicylic acid
  • good analgesic + anti inflammatory
  • poor antipyretic
  • reduces blood clothing (COX needed for thromboxane, involved in clotting cascade)
  • half life = 2-3h
  • excreted via urine, sweat, faeces + saliva
51
Q

How does ibuprofen work?

A
  • non selective COX inhibitor
  • caution in asthma (produces inflammatory mediators)
  • good analgesic + anti inflammatory + antipyretic
  • plasma half life = 2h
  • known as acetaminophen in US
  • excreted via urine
52
Q

How does paracetamol work?

A
  • selective COX 2 inhibitor (kind to tum)
  • Good angagesic + antipyretic
  • bad anti inflammatory
  • overdoes of 30 tablets associated with hepatic failure
  • treat fever in children on 38.5C
  • half life 1-4h
  • excreted via urine
53
Q

What are other NSAIDs?

A
  • propionic acids e.g. ibuprofen, fenbufen + naproxen = 1st choice for treatment of inflammatory joint disease
  • selective COX 2 inhibitors e.g. celecoxib, etoricoxib + lumiracoxib = have lowest GI toxicity
  • diclofenac = similar actions to naproxen
  • indometacin = higher incidence of adverse effects e.g. Ulceration, GI bleeding, headaches + dizziness
  • piroxicam -long half-life. High incidence of GI bleeding
54
Q

What is gout?

A

Characterised by deposition of sodium urate crystals in the joint, casing painful arthritis
-acute attacks treated with diplofenac

55
Q

What type of drug is ondansatron?

A

Serotonin receptor antagonist = antiemetic

Dopamine receptor antagonists are also antiemetics

56
Q

What is vertigo?

A

Vertigo is a false sense of rotary movement, associated with sympthathetic overactivity, N&V.

57
Q

What is an important source of stimulation of the vomiting centre?

A

The chemoreceptive trigger zone (CTZ)

58
Q

The vomiting centre receives afferents from where?

A
  • limbic cortex (N+V associated with unpleasant odours + sights)
  • CTZ
  • nucleus solitarius (gag reflex)
  • spinal cord (N associated with physical injury)
  • vestibular System (N+V associated with vestibular disease + motion sickness)
59
Q

What happens when you are sick?

A

Vomiting centre projects to vagus nerve + to spinal motor neurones supplying abdo muscles

  • reverse peristalsis transfers contents of upper intestine to stomach
  • glottis closes
  • breath held
  • oesophagus + gastric sphincter relax
  • abdo muscles contract, ejecting gastric contents
60
Q

Define drug misuse

A

Any drug which harms or threatens to harm the physical or mental health of an individual or other individual, or which is illegal

61
Q

What changes in the brain occur following chronic drug administration?

A
  • increase Ca2+ channels
  • depletion of NT
  • receptor downregulation
  • changes in secondary messenger
  • synthesis of an inverse agonist
62
Q

Why does morphine cause pupil constriction?

A

It has a stimulatory effect on the nucleus of the 3rd cranial nerve

63
Q

Why is morphine the analgesia used in an MI?

A

It stimulates the vagus nerve = bradycardia, lowering BP

64
Q

Why is morphine not given to pts with head injuries?

A
  • causes pupillary responses
  • CO2 retention caused by resp depression = cerebral vasodilation (in pts with raised ICP this can lead to alterations in brain function).

Pharmacology (11 decks)

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