Pharm lc 17 Analgesia

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  • Created by: Amh
  • Created on: 17-04-16 17:28
What are pain receptors called
nocioceptive receptors
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What are the important neurotransmitters for nocioreceptrors
5HT, Enkephalins
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Outline the nocireceptive pathway
enough stimulus to activate nerve ending, bradykinin, prostaglandins, generalised inflammatory process, ATP nociceptor inflammation passes up through the spinal cord to higher centre of the brain
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Can we differentiate between nociception and pain
yes (nocicpetion - peripheral pain - effective component of nociceptive input )
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where does information travel
goes u p descending inhibitory action - which can modulate actiitygoing up. hypothalamus, amygdala, pag
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how are nocireceptors different from other mechanical/ thermal receptors?
They are much thinner, have a higer threshold, stimulated by noxious threshold.
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What are the 2 types of nocireceptors
(Adelta)Myelinated and unmyelinated (C fibres)
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What sort of pain does C fibres elicit
dull burning pain
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What sort of pain do A delta fibres elicit
Sharp localised pain
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where are the cell bodies of spinal nociceptive afferent fibres
dorsal root ganglia (end in dorsal horn)
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Where does acute pain come from
excessive noxious
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how does capsaicin affect nociception
Excites nociceptive nerve terminals. Binds to vanilloid receptor. Which is a ligand gated cation channel. Capsaicin is an agonist. It opens th channels which is permeable to na and ca causing depolarisation, and initiation of AP
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What else is the vanilloid receptor sensitive to
temperatures in excess oof 45 degrees , and increased H+ concentration
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How is the vanilloid receptor modulated
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How do several pain-producing substances affect vanilloid (VR1)
Work through GPCR to sensitize VR1
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What are the most active kinins
Bradykinin and kallidin
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when are Bradykinin and kallidin produced
produced under situations of tissue injury
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what is Bradykinin
a potent pain producing substance
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How does Bradykinin work
Causes the release of prostuglandins, and combines with GPCRs. it brings its effect via intracellular mesages
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what is Bradykinin receptors coupled to
Bradykinin receptors are couple to activation of Protein Kinase C (PKCe) which phosphorylates VR1 and opens VR1 channel propigating an AP
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Do prostuglandins cause pain
no, but they enhance the pain producing effect of 5-HT and Bradykinin
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What are mediators of nociception
TRP, ATP, Kinins, Prostuglandins
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What is TRP
Transient receptor potential. Channel family including TRPV1. Vanniloids.
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How is TRP activated
Activated by capsaicin, temperature and acidity - causing subsquent peptide release. direct effect on depolarisation, lso causes peptide release aCRPG release too
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Where does ATP act
purinergic receptors
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What are NSAIDs
Aspirin, and ibuprofen
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How do NSAIDs do
Inhibitors of cyclooxygenase, reduce production of prostaglandins
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What are some non selective NSAIDs
Aspirin, Ibruprofen, Diclofenac
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What are some selective NSAIDs
Coxibs, and paracetemol
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Where are the endings of C fibres and A delta fibfres
Peripheral tisse
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Where do the afferent C fibres and A delta fibres project o after the dorsal horn
the thalamus
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What is lamina 2 rich in
Opioid receptors
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What do descendin inhib pathways do
reduice transmission of pain
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What is the periaquiductal grey rich in
Opioid receptors
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What are some endogenous opioid peptides
Enkephalins, Endorphins and Dynorphins
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What are the dif types of Enkephalins
leu-Enkephalins and met-Enkephalins
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Outline Enkephalins
pentapeptides, endogenous ligands at the u & delta receptors,widley distributed in CNS, synthesised in cell body, processed during axonal transport
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what happens when opiod receptors are activated
They inhibit adenylate cyclase reducing cAMP
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What is morphine
An alkaloidexrtact from opium
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What are the actions of morphine
Analgesic, antidiarrheal, antitussic, sedation, cough suprresion, euphoria, stimulation of CTZ
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How does opioid tolerance build up
The initial decrease in cAMP means that the body starts up regulating it. So eventually loads or morphine is needed to over come this excess cAMP
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What is withdrawal a symptom of
rebound from increased cAMP
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What are some other key opiods
Codeine, diamorphine (heroin)
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What is codeine metabolised to and how
metabolised to morphine by CYP2D6
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What is codeine used in conjunction with
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What is diamorphie
A semi synthetic prodrug - it is also metabolised to morphine
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why is diamorphine heroin used
It has better oral asorption than plain old morphine - so is given to terminally ill patients
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What are some other agonists of opioid receptors
Pethidine, Fentanyl, methadone
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is Pethidine shorter or longer acting then morphine
Shorter acting than morphine
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What is the active metabolite of Pethidine
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what does Pethidine interact with
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when is Pethidine used
1st stage of labour
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When is fentanyl used
with general anaesthetics
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Is fentanyl shorter or longer acting then morphine, and why
shorter acting deu to redisribution.
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When is methadone used
in addicts to help ween of morphine - it is longer lasting
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What are the side effects of theses
respiratory depression
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What is a partial opioid agonist
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What does Buprenorphine do
Produces strong analgesia, limits resp distress
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Does Buprenorphine have a long duration of action
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Why is Buprenorphine used in addicts
reduces heroin euphoria and less ersp side effects and long lasting
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What are some opioid antagonist
Namoxone, and Naltrexone
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Why would you use opioid antagonists
to reverese opiate overdose
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How do you trea neuropathic pain conditions (nerve damaged individuals/opiod resistant)
Tricyclic antidepressants like amitriptyline - effects inhibition of NA reuptake. and anticonvulsants that inhibit calcium channel opening like gabapenitin
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What are the important neurotransmitters for nocioreceptrors


5HT, Enkephalins

Card 3


Outline the nocireceptive pathway


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Card 4


Can we differentiate between nociception and pain


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Card 5


where does information travel


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