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Drugs and the Brain > Analgesics > Flashcards

Analgesics Flashcards

1
Q

What is somatosensation?

A

Our sense of touch, pressure and vibration against the skin

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2
Q

What is propriosensation?

A

Our sense of where our body parts are (a subtype of somatosensation)

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3
Q

What is nociception?

A

Our sense of tissue damage and the neural processes of encoding and processing noxious stimuli

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4
Q

What is pain?

A

Our perception of nociception that is in the brain (the sensory input)

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5
Q

Is pain made up of peripheral or central elements?

A

BOTH

Pain is the result of damaging processes and our interpretation of them

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6
Q

What are the four types of nocicpetor?

A
  • Thermal
  • Mechanical
  • Polymodal
  • Silent
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7
Q

What do thermal nocicpetors detect?

A
  • 45 degree (painful heat)
  • 10-15 degree (painful cold)
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8
Q

What do mechanical nociceptors detect?

A
  • Squeezing, streching or penetrating the skin
  • Sharp, intense pain
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9
Q

What do polymodal nocicpetors detect?

A

Dull, diffuse burning pain type

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10
Q

Where are silent nocicpetors found and what do they detect?

A
  • Found in the viscera
  • Respond to (over) distension/swelling
  • Intense poorly localised pain
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11
Q

What do mechanical alpha delta fibres respond to?

A
  • Do not respond to strong pressure from a blunt probe
  • If equal pressure is applied all over a small area (pin prick, causing damage) they show a robust response
  • Increased by pinching (damaging) a larger area
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12
Q

What is the nociceptor receptor family called?

A

TRP

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13
Q

How many heat sensing alpha delta TRP’s are there?

A

6 that cover a range of temperature sensing thermal nociception

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14
Q

Which two thermal TRP’s are activated at normal temperatures (more somatosensory than nocicpetive)?

A
  • TRPv3

-TRPv4

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15
Q

What TRP is activated by chemicals such as garlic and radish?

A

TRPA1

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16
Q

Which TRP is active to menthol?

A

TRPM8

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17
Q

Which TRP is active to camphor?

A

TRPV3

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18
Q

Which TRP is active to capsaicin (chilli)?

A

TRPV1

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19
Q

Which chemical causes the spreading of local projections away from the site of injury?

A

Histamine

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20
Q

Which two chemicals are involved in exacerbating the nocicpetive response locally?

A
  • Bradykinin
  • Prostaglandin
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21
Q

What does substance P do?

A
  • Dilates the blood vessel
  • Can cause histamine release to potentiate the response
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22
Q

What is mechanical hyperaglesia?

A

The hyper-sensing of pain due to the spreading effect

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23
Q

What are prostaglandins produced by?

A

COX enzymes

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24
Q

What are the two neurotransmitters which project up the spinal cord?

A
  • Glutamate
    co-localised with
  • Substance P
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25
Q

Where are glutamate and substance P stored in the spinal cord?

A

In vesicles in dorsal route ganglion cells

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26
Q

How does Substance P act on glutamate?

A
  • Causes depolarisation as it slows and prolongs the action of glutamate
  • As it is not easily broken down, it can also act on neighbouring neurons (paracrine)
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27
Q

Why does substance P make it hard to localise some pain?

A
  • Because it activates neighbouring synapses (paracrine)
  • Regions in the spinal cord are being activated so the damage seems to spread out as there are other inputs and over estimation
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28
Q

Which type of nociceptive fibre causes a wind up effect?

A

Repetative activation of C but NOT alpha delta

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29
Q

What is the wind-up effect (steps)?

A
  1. Activation which projects to neurons in the spinal cord
  2. Second order neurons
  3. Input from C fibres and alpha delta fibres
  4. As alpha delta fibres are myelinated, the signal jumps across the nodes
  5. Because C fibres are un-myelinated, the signal has to be regenerated
  6. The initial reaction is the A volley because the AD fiibres get the information the quickest
  7. The A volley remains steady throughout
  8. Later on, the C volley starts earlier and lasts longer on every stimulus because there is priming input from the AD fibre
  9. When the C input comes along, there is plasticity from the C fibre and this increases the response of the neuron to the C fibre
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30
Q

What are the two second order neurons in the dorsal horn called?

A
  • A-Volley from alpha delta
  • C-Volley from C fibre
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31
Q

What receptors do glutamate and substance P bind to?

A

NK1, NMDA and AMPA

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32
Q

Why is AMPA the primary glutamate receptor in nocicpetive transmission?

A

The A fibre alone is not enough to release the Mg molecule from the NMDA receptor

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33
Q

How does the wind-up from the C fibre increase the firing at the synapse?

A
  • The increased input the receptor receives means there is enough depolarisation for the NMDA to displace the Mg molecule
  • Lots of calcium then enters
  • This can cause the post-synaptic ion channels more likely to fire
  • This then causes more C fibre response
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34
Q

Which axons make up most of the spinothalamic tract?

A
  • Alpha delta fibres
  • C fibres
  • Alpha beta fibre (mechanoreceptor)
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35
Q

What layers of the spinal cord do the alpha delta and c fibres project into?

A

Layers 1 and 5

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36
Q

How does gating pain at the spinal cord level work?

A
  • If drive the alpha beta mechanoreceptors by rubbing the area, they drive interneurons to become more active
  • This increases the inhibition and reduces the excitability of the inhibitory neurons
  • This reduces the projection neuron action the the C fibre
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37
Q

What is the cause of referred pain?

A

Due to poor localisation, particularly in the viscera

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37
Q

What is an example of referred pain?

A

Pain from a myocardial infarction can be felt away from the heart such as in the jaw

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38
Q

Where does the nocicpetive tract synapse at the supraspinal level?

A
  • Thalamic level
  • Then project to the other cortices
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39
Q

When does nociceptive decussation occur?

A

As soon as information enters te spine

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40
Q

What is the spinoreticular transmission system?

A
  • Runs to the reticular formation from the spinal cord
  • Then into the medulla and PONS
  • Next into the thalamus and the cortex
  • Lastly into the periaqueductal grey
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41
Q

Which regions of the brain project into the periaqueductal grey (PAG)?

A
  • Insula
  • Hypothalamus
  • Amygdala
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42
Q

What are three bits of evidence that there is top-down modulation of pain?

A
  • Electrical stimulation of the PAG
  • Effect of opioids
  • PAG through locus coereleus and raphe
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43
Q

What neurotransmitters do the locus coerleus and the Raphe use?

A

Noradrenaline (second order projection) and serotonin (projection neurons)

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44
Q

How do the pontine and 5HT neurons top-down regulate?

A
  • They drive the interneuron which contains an endogenous opioid
  • This decreases the excitability by reducing calcium entry and reduces activity
  • This will turn off the synapse, reducing the nocicpetive information flowing into the brain
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45
Q

Which centre drives the LC and Raphe?

A

PAG

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46
Q

What mutations cause insensitivity to pain?

A

Autosomal recessive mutations

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47
Q

What can individuals with congenital pain sensitivity not detect?

A

Severe damage such as broken bones, burns, or even self inflicted injuries such as biting off the tip of their tongue

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48
Q

What does the gene SCN9A code for?

A

Voltage gated socium channel Nav1.7

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49
Q

What does the sodium channel Nav1.7 do?

A

Plays an important role in the dorsal route ganglion nociceptive neurons

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50
Q

What is the gene FAAH-OUT associated with?

A

The endocannabinoid system

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51
Q

What can long-term uncontrolled diabetes lead to?

A

Neuropahthy (nerve damage) with the legs and feet often the first tissues affected

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52
Q

What is parasthesia?

A

Pins and needles sensation

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53
Q

What are the steps to prostaglandin synthesis?

A
  • Tissue damage to the cell membranes
  • Arachidonic acid is converted to prostaglandin
  • Leaves prostaglandin H2 and G2
  • These are converted into a various group of compounds (icodomoids) such as prostaglandin E2
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54
Q

Where do the NSAID drugs act on prostaglandin synthesis?

A

When arachidonic acid is converted to prostaglandin G2 and H2 by targetting cyclooxygenases

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55
Q

What are three types of cyclooxygenases and when are they expressed?

A
  • COX-1: constitutively expressed
  • COX-2: Induced in damaged/infected cells
  • COX-3: (splice varient of COX-1)
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56
Q

Which COX is the best target for the NSAIDs?

A

COX-2

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57
Q

What are the main therpeutic roles of NSAIDS (3)?

A
  1. Antipyretic (lower body temp)
  2. Analgesic (reduce pain)
  3. Anti-inflammatory
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58
Q

What does NSAIDS stand for

A

Non-steroidal anti-inflammatory drugs

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59
Q

What needs to happen when the core temperature is too low?

A
  1. Increase heat conservation- vasoconstriction (piloerection)
  2. Increase heat production- shivering, exercise
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60
Q

What needs to happen when the core temperature is too high?

A
  1. Increase heat loss- vasodilation, sweating
  2. Decrease heat production
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61
Q

Outline pyresis (fever)

A

CAUSE
Body thermostat is raised (hypothalamus is too high because of inflammatory response)

Core temp is sensed as too low

EFFECT
Increase heat gain/conservation

SYMPTOMS
Feel cold

WHY
Because prostaglandin E2 has been released in the periphery and this has an effect on increasing the set point of the thermostat

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62
Q

What is hyperthermia?

A
  • Thermostat is not increased
  • Too much heat production
  • Feel hot
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63
Q

What is the area in the hypothalamus involves with heat?

A

Preoptic area hypothalamus

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64
Q

Where do TRP thermoreceptor channels run to?

A
  • Run through the peripheral nervous system into the POA in the hypothalamus (central thermostat site)
65
Q

How does the hypothalamus cause the production of prostaglandin E2?

A

Generates in response to interleukin-1 and released by macrophages

or

Via the blood

66
Q

How do NSAIDs reduce fever (pyrexia)?

A
  • Inflammatory mediators (PGE2, IL-1) raise the preoptic areas set point (thermostat)
  • NSAIDs reduce the set point back down to a normal level
67
Q

Will NSAIDs reduce core temperature in hyperthermia?

A

No, because there is no raised thermostat

68
Q

How does bradykinn work?

A
  • It is potentiated by prostaglandin E2 and released by damaged or infected tissue
  • The effect of the PGE2 is to sensitise the C fibre to bradykinin
69
Q

Which NSAID is selective for COX2?

A

Celecoxib

70
Q

Which NSAID us used more as an anti-platelet drug?

A

Aspirin

71
Q

Name five NSAID drugs

A
  • Aspirin
  • Ibuprofen
  • Diclofenac
  • Naproxen
  • Celecoxib
72
Q

How does aspirin function at COX?

A

Irreversible on both COX1 and 2

73
Q

How does Ibuprofen act at COX?

A

Is reversible, non-competative and weakly selective at COX1

74
Q

What are some common NSAID side-effects?

A
  • GI upsets (dyspepsia, nausea, ulcers)
  • Aspirin inhibits platelet aggregation, prolongs clotting time
  • Skin reactions
  • Renal damage
  • Bronchospasm in aspirin sensitive asthmatics
75
Q

What is aspirin and reyes syndrome?

A

Rare disorder occuring in children- hepatic encephalopathy with 20-40% mortality (aspirin is no longer given to under 16s)

76
Q

What is salicylism?

A

Salicylate overdose (non-fatal) produces symptoms of 8th cranial nerve damage- tinnitus, vertigo, nausea and vomiting

77
Q

What is an uncommon heart side effect of NSAIDs?

A

Cardiovascular effects including MI and stroke

78
Q

How does paracetamol act?

A
  • Potentially onlt central action
  • Antipyretic analgesic, not anti-inflammatory (not a classic NSAID)
  • Reversably competative at COX3, splice variant of COX1
79
Q

What are the side-effects of paracetamol?

A
  • None at therpeutic doses
  • Toxic at high doses, may be hepatotoxic if taken at max
  • In overdose, it is metabolised to a toxic metabolite which causes liver necrosis
80
Q

What is neuropathic pain?

A
  • Damage to neural tissue
  • Signals nociceptive reaction inappropriately as there is no local damage
  • Cannot be treated with NSAIDs
81
Q

What are the treatments for neuropathic pain?

A
  • May respond to opioids
  • Generally managed with tricyclic antidepressant or anti-epileptics
  • Capsaicin cream is licensed for the symptomatic relief of postherepetic neuralgia or pain in diabetic neuropathy
  • Lidocaine can be used for localised pain
82
Q

How does ketamine act as an analgesic?

A
  • Is an NMDA antagonist/dissociative anaesthetic at higher doses
  • Can be used for brief painful procedures
83
Q

How is Nitrous oxide used as an analgesic?

A
  • Not anaesthetic in hmans- is a powerful analgesic which can be used alone or to augment anaesthetics
  • May be an NMDA antagonist but hard to identify the precise pharmacology
84
Q

What are three types of neuropathic pain?

A
  • Ongoing
  • Allodynia
  • Hyperaglasia
85
Q

What is allodynia?

A

Where a normally non painful stimulus such as light touch produces pain

86
Q

What is hyperaglasia?

A

Where pain sensations aree heightened

87
Q

What can trigger neuropathic pain?

A
  • Viral infections (shingles)
  • Autoimmine disease (MS)
  • Strokes
  • Diabetes
  • Cancer
  • Etc
88
Q

What is trigeminal neuraglia?

A
  • Common form of neuropathic pain that is caused by the compression of the trigeminal nerve
  • Results in excruciating face pain
  • Sometimes attacks of pain can be triggered by even the slightest pressure on the face
89
Q

Why are peptide toxins attractive candidates for drugs?

A

Because, unlike small molecule inhibitors of ion channels, they are highly selective

90
Q

What kinds of molecules do cone snails release?

A

Peptide toxins

91
Q

What toxins does the conus magus produce?

A
  • Peptide toxins that target nicotinic ACh receptors
  • Voltage gated sodium channels
  • Calcium channels
  • Possibly potassium channels
92
Q

What is the name of the conus magus’s toxin?

A

Nicotinic selective toxin a-conotoxin M1

93
Q

What is the C magus toxin omega-conotoxin MVIIA selective for?

A

N-type calcium channels

94
Q

What is a synthetic version of What is the C magus toxin omega-conotoxin MVIIA?

A

Ziconotide (prialt)

95
Q

How is ziconotide administered?

A
  • Intrathecally (directly into the CSF) becasue it is a peptide and cannot cross the BBB
96
Q

How does ziconotide act?

A
  • Inhibiting neurotransmitter released by nociceptive neurons at the level of the spinal cord
  • Shows relatively good efficacy against neuropathic pain
97
Q

What are some side effects of ziconotide?

A
  • Dizzines
  • Nausea
  • Anxiety
  • Insomnia
  • Psychosis
  • Suicide
  • Depression
  • Seizures
98
Q

What are Endogenous Opioids?

A

Neurotransmitters in specialised CNS tracts

99
Q

Where are endogenous opioid cell bodies found?

A
  • Rostral ventral medulla
  • PAG
  • Spinal cord laminae 1 and 2
100
Q

Where so the endogenous opioids axons project to?

A
  • To/within the PAG
  • LC
  • Raphe
  • Within the spinal cord
101
Q

How do the endogenous opioids work?

A
  • Through the descending pathway
  • From PAG, it recruits seretonergic and dopiminergic neurons to reduce the activity of second order neurons in the laminae
102
Q

What are three opioid peptides?

A
  • Endorphins
  • Enkephalins
  • Dynorphins
103
Q

What is the role of the opioid peptides?

A
  • Released in the prescence of pain (endogenous system)
  • Released in accupuncture/sport
104
Q

What are the three traditional opioid receptors?

A
  • Mu
  • Delta
  • Kappa
105
Q

What are the re-classified, new opioid receptors?

A
  • MOPr (Mu opioid receptor)
  • DOPr
  • KOPr
  • NOPr
106
Q

What are Mu Opioid receptor subtypes?

A

1, 2 and 3

107
Q

What are Mu Opioid receptor mechanisms?

A
  • Open up K channels in the membrane
  • Causes hyperpolarisation
  • Reduces neuronal activity
  • Inhibit neurotransmitter release (especially ACh, glutamate and substance P)
  • Produces analgesia
108
Q

What are Mu Opioid receptor side effects?

A
  • Respiratory depression
  • Constipation
  • Euphoria
  • Sedation
  • Dependence
109
Q

What are Delta Opioid receptor subtypes?

A

1 and 2

110
Q

How do Delta Opioid receptors act?

A
  • Similarly to Mu receptors
  • Produces analgesia
  • Can be proconvulsant (too much excitation)
111
Q

What are Kappa Opioid receptor subtypes?

A

1, 2 and 3

112
Q

How do Kappa Opioid receptors work?

A
  • Reduce calcium channel activity presynaptically
  • Means less depolarisation because they inhibit neurotransmitter release
  • Analgesia at the spinal level
113
Q

What are side effects of Kappa opioid receptors?

A
  • Sedation
  • Dysphoria/hallucinations
114
Q

What type of receptors are opioid receptors linked with?

A
  • GPCR family
  • Often negatively linked to adenylyl cyclase (decrease cAMP)
115
Q

How much homology do the opioid receptors show?

A

65%

116
Q

Where is pain management located?

A

In the dorsal horm of the spinal cord

117
Q

How do analgesias act to manage pain?

A
  • Enhance the transmission from the PAG to the other sites (LC, Raphe)
  • This inhibits the projection neurons by increasing inhibition and increasing the response
  • There is then lots of converging responses of opioids in increasing sensitivity and directly inhibiting the potentiation of the descending pathways
118
Q

What are three groups of opioid receptor targetting compounds with examples?

A
  1. Agonists (morphine and codeine)
  2. Antagonists (naloxone and naltrxone)
  3. Mixed action compounds (buprenorphine and pentazocine)
119
Q

What are some central morphine like side effects?

A
  • Analgesia
  • Sedation
  • Cough- suppression (anti-tussive)
  • Euphoria
  • Respiratory depression
  • Nausea
  • Itch
120
Q

What is peripheral and what does it do?

A
  • Morphine like analgesia
  • Reduces inflammation
  • Increases the threshold for pain
  • Action on the GI tract (Mu and Delta receptors)
121
Q

What is Ioperamide?

A
  • Morphine-like drug
  • Mu agonist, cannot cross the BBB (not analgesic)
  • Causes constipation (imodium)
122
Q

Where do opioid agonists act?

A
  • Spinal level (dorsal horn) Mu2. delta2, Kappa1
  • At the supraspinal level (brain) Mu1, Delta 1&2, Kappa3
123
Q

What do opioid agonists do?

A
  • Raise the pain threshold
  • Increase the pain tolerance
  • Are better against dull, constant pain than sharp, stinging pain
124
Q

What is the ‘classic opiate’ and how does it act?

A
  • Morphine
  • Mu agonist
125
Q

What are some side-effects of morphine?

A
  • Analgesia
  • Euphoria
  • Anti-tussive
  • Sedative
  • Nausea
  • Constipation
  • Pupillary constriction
  • Bronchoconstriction
  • Hypotension
  • Respiratory depression
126
Q

What is a potential new synthetic morphine-like drug with fewer side effects?

A

Morphine 6 glucuronide

127
Q

What 4 areas do opioid agonists vary in?

A
  • Analgesic efficacy
  • Absorption/distribution
  • Duration of effect
  • Side effects
128
Q

What is diamorphine

A
  • Heroin
  • Pre-cursor to morphine (de-acetlyated)
  • Is faster and more potent than morphine
129
Q

What is Fentanyl

A
  • An agonist with similar actions to morphine
  • Rapid onset
  • Used in chronic cancer pain and post-surgical analgesia
  • Can be given by patch
130
Q

What is Methodone?

A
  • Used to ‘wean’ dependents away from opioid addiction
  • Longer duration of action and lessened withdrawal symptoms than morphine
131
Q

What is Oxycodone?

A
  • Used for acure/chronic pain
  • Now widely abused
132
Q

What is an opioid?

A

A drug that acts at opioid receptors

133
Q

What is an opiate?

A
  • Is an opioid derved from opium poppies
  • Such as morphine, codeine and thebaine
134
Q

What is Heroin?

A

A semisynthetic opioid produced by chemically modifying morphine that has been purified from opium poppies

135
Q

What is Buprenorphine?

A

A partial Mu agonist

136
Q

What are side-effects of buprenorphine?

A
  • Analgesia
  • Sedation
  • Nausea
  • Respiratory depression not fully reversed by naloxone
137
Q

What is Buprenorphine used to treat?

A
  • Opioid dependence
  • As reduced abuse potential and less intense withdrawal than morphine
138
Q

What is Nalorphine?

A
  • A mixed action compound as it was initially regarded as a Mu antagonist but is now seen to be: delta, kappa partial agonist
139
Q

What are side-effects of nalorphine?

A
  • Some Analgesia (lower abuse potential)
  • Dysphoria (depression)
140
Q

What is Pentazocine?

A
  • A mixed action compound which combines:
  • Mu antagonism and Kappa agonist
  • Reduces euphoria, abuse potential and limits respiratory depression, however Kappa agonist means analgesia
141
Q

What is Tramadol?

A
  • A mixed action compound that combines:
  • Weak Mu agonist and weak inhibition of monoamine reuptake
  • Is used therapeutically as analgesic for moderate to severe pain
142
Q

What are some side-effects of Tramadol?

A
  • Anti-tussive
  • Nausea
  • Tolerance/dependence
143
Q

How do many of the Opioid drugs have cough suppressive effects?

A

Action at cough centres in the CNS via Mu or delta receptors

144
Q

How can we seperate the anti-tussive elements from the analgesic ones in opioid drugs?

A
  • Quantitatively, by adding a large subsituent at position 3 on the morphine molecule
145
Q

What is Dextromethorphan?

A

A cough suppressant without the analgesia

146
Q

How do opioids trigger nausea?

A
  • Endogenous toxins trigger the opioid receptors in the chemoreceptor trigger zone
  • This is located the medulla oblongata
  • Crosses the BBB
  • Triggers the vomit reflex
147
Q

How are motion sickness and opioid nausea related?

A
  • Motion sickness in detected by the vestibular nuclei signals to the chemoreceptor trigger zone
  • Opioid receptors in the medulla oblongata trigger the chemoreceptor trigger zone
  • Both then cause the vomit reflex
148
Q

What is a study done on mice into tolerance of opioids?

A
  • Give mouse a treatment of morphine
  • Then wait a period of time and give a second treatment whilst it is on a hot plate
  • Mouse will not sense the hot plate
  • Continue to dose the mouse and measure how much morphine is needed to give the same analgesic effect for it not to feel the hot plate
  • Need to increase the dosage each time to cause the same effect
149
Q

How does tolerance to morphine lead to dependence?

A
  • Morphine inhibits cAMP production
  • System responds by increasing Adenylate cyclase expression (tolerance)
  • When remove the morphine, there is a spike in cAMP production (dependence)
150
Q

How are narcotic antagonists formed?

A
  • Synthesised by modification of the structure of morphine and other agonists
  • Usually by substitution of large groups on the N atom at position 17 in morphine
151
Q

What is an example of a narcotic antagonist?

A

Naloxone

152
Q

How does Naloxone act?

A

Competative antagonist at all 3 opioid receptors but particularly Mu

153
Q

What are three potential therapeutic ways to use naloxone?

A
  1. Alone
  2. After an agonist
  3. Used in a patient dependent on opioids
154
Q

What occurs when naloxone is given alone?

A
  • Very little effect

BUT

  • Respiratory depression in drug addicts
  • Respiratory depression in newborns
155
Q

What occurs when naloxone is given after an agonist?

A
  • Reverses all effects of full agonists
  • Reverses agonist actions of mixed action compounds (need lagrer dose)
  • Used to treat respiratory depression (in opioid overdose)
  • Short action (longer than agonist), metabolized in the liver
156
Q

What occurs when naloxone is given to dependent patients?

A
  • Precipitate withdrawal syndrome
  • Used to treat overdose in dependent patients but have to titrate carefully to do this without precipitating withdrawal
  • Used in ‘treatment’ of dependence?
157
Q

What is Oxycontin?

A

A synthetic opioid

158
Q

How long did Purdue marketer state that oxycontin was effective for compared to reality?

A
  • Claimed to be a ‘12 hour drug’
  • Actually 4-6 hours
159
Q

What is a pill mill?

A
  • A clinic that specialises in prescribing opioids to patients that do not need them
  • Patients are bought in by drug dealers where they buy medication for them or exchange other drugs
160
Q

What is Oxycontin’s nickname?

A

Hillbilly heroin

161
Q

What is Fentanyl?

A

A synthetic opioid with 50-100 times the potency of morphine

Drugs and the Brain (9 decks)

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