Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Drugs and the Brain > Analgesics > Flashcards

Analgesics Flashcards

1
Q

What is somatosensation?

A

Our sense of touch, pressure and vibration against the skin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is propriosensation?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is nociception?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is pain?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the four types of nocicpetor?

A
  • Thermal
  • Mechanical
  • Polymodal
  • Silent
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What do thermal nocicpetors detect?

A
  • 45 degree (painful heat)
  • 10-15 degree (painful cold)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What do mechanical nociceptors detect?

A
  • Squeezing, streching or penetrating the skin
  • Sharp, intense pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What do polymodal nocicpetors detect?

A

Dull, diffuse burning pain type

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the nociceptor receptor family called?

A

TRP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

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

A

6 that cover a range of temperature sensing thermal nociception

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

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

A
  • TRPv3

-TRPv4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

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

A

TRPA1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Which TRP is active to menthol?

A

TRPM8

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Which TRP is active to camphor?

A

TRPV3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Which TRP is active to capsaicin (chilli)?

A

TRPV1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

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

A

Histamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

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

A
  • Bradykinin
  • Prostaglandin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What does substance P do?

A
  • Dilates the blood vessel
  • Can cause histamine release to potentiate the response
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is mechanical hyperaglesia?

A

The hyper-sensing of pain due to the spreading effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are prostaglandins produced by?

A

COX enzymes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

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

A
  • Glutamate
    co-localised with
  • Substance P
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

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

A

In vesicles in dorsal route ganglion cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Which type of nociceptive fibre causes a wind up effect?

A

Repetative activation of C but NOT alpha delta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What receptors do glutamate and substance P bind to?

A

NK1, NMDA and AMPA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Which axons make up most of the spinothalamic tract?

A
  • Alpha delta fibres
  • C fibres
  • Alpha beta fibre (mechanoreceptor)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

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

A

Layers 1 and 5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is the cause of referred pain?

A

Due to poor localisation, particularly in the viscera

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Where does the nocicpetive tract synapse at the supraspinal level?

A
  • Thalamic level
  • Then project to the other cortices
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

When does nociceptive decussation occur?

A

As soon as information enters te spine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

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

A
  • Insula
  • Hypothalamus
  • Amygdala
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What neurotransmitters do the locus coerleus and the Raphe use?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Which centre drives the LC and Raphe?

A

PAG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What mutations cause insensitivity to pain?

A

Autosomal recessive mutations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What does the gene SCN9A code for?

A

Voltage gated socium channel Nav1.7

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What does the sodium channel Nav1.7 do?

A

Plays an important role in the dorsal route ganglion nociceptive neurons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What is the gene FAAH-OUT associated with?

A

The endocannabinoid system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What can long-term uncontrolled diabetes lead to?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What is parasthesia?

A

Pins and needles sensation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Which COX is the best target for the NSAIDs?

A

COX-2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

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

A
  1. Antipyretic (lower body temp)
  2. Analgesic (reduce pain)
  3. Anti-inflammatory
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What does NSAIDS stand for

A

Non-steroidal anti-inflammatory drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

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

A
  1. Increase heat loss- vasodilation, sweating
  2. Decrease heat production
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What is hyperthermia?

A
  • Thermostat is not increased
  • Too much heat production
  • Feel hot
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What is the area in the hypothalamus involves with heat?

A

Preoptic area hypothalamus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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?

70
Q

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

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?

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?

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?

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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions