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Semester 3 > Case 2 - Pharmacology > Flashcards

Case 2 - Pharmacology Flashcards

1
Q

how do opioids work

A

by combining with opioid receptors in the brain and spina cord. this blocks transmission of pain signals sent by the nerves to the brain. although the cause of the pain may still remain, but less pain is felt.

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2
Q

what are the 4 types of opioid receptors

A

Mu1,2,3
Delta
Kappa
Nociception

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3
Q

what are mu receptors

A

the receptors responsible for most of the analgesic effects of opioids and for some major unwanted effects

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4
Q

where are mu receptors located

A

in the brain, spinal cord, peripheral sensory neurones and intestinal tract

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5
Q

describe the Mu1 receptor

A

analgesia, physical dependence (this is the unwanted effect, where choleric use of opioid produces tolerance. the negative phyiscal withdrawal symptoms result from the abrupt discontinuation or dosage reduction)

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6
Q

describe the Mu2 receptor

A

respiratory depression, mioisis (contraction of pupil), euphoria, reduced GI mobility, physical dependence - morphine

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7
Q

describe the Mu3 receptor

A

possible vasodilation

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8
Q

describe the delta receptor

A

they can result in analgesia but can also be a proconvulsant. these are located in the brain and the peripheral sensory neurones.

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9
Q

what are the effects of the delta 1 and 2 receptors

A

analgesia, antidepressant effects, convulsant effects and physical dependence

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10
Q

what do kappa receptors do

A

contribute to analgesia at the spinal level and produce relatively few unwanted effects

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11
Q

do kappa receptors contribute to dependence

A

no

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12
Q

where are kappa receptors located

A

in the brain, spinal cord, and the peripheral sensory neurones

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13
Q

exact effects of the kappa1,2,3 receptors

A

analgesia, anticonvulsant effects, depression, hallucinogenic effects, diuresis, sedation and stress

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14
Q

describe the nociception receptors

A

activation results in an anti opioid effect (supra spinal), analgesia, immobility and impairment of learning

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15
Q

examples a nociception receptor

A

ORL1 = anxiety, depression, appetite, development of tolerance to mu-opioid agonists

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16
Q

mechanism of action of opioid receptor activation

A
  1. inhibition of adenylyl cyclaase - opioids reduce the intracellular cAMP content. this affects protein phosphorylation pathways and hence cell function
  2. opiates promote the opening of potassium channels - this reduces synaptic transmission as it causes the axon membrane to be in a state of hyper polarisation
  3. inhibit the opening of calcium channels - this reduces the amount of neurotransmitter released into the synaptic cleft, thus reducing synaptic transmission
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17
Q

what is cocodamol

A

an opioid analgesic derived from morphine but less potent as a pain killer, less sedative and less toxic

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18
Q

does co codamol cause euphoria

A

no - little to non

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19
Q

what does cocodamol contain

A

codeine and paracetamol

20
Q

what is the side effect of co codamol

A

constipation

21
Q

is co codamol a prodrug

A

yes

22
Q

what is the mechanism of action of NSAIDs

A
  • primary effect is inhibition of arachidonic acid oxidation by the fatty acid COX.
  • this inhibits the production of prostaglandins and thromboxane.
  • NSAIDs vary in the degree to which they inhibit each iso form of the COX enzyme.
23
Q

which COX are the anti-inflammatory effects related to

A

COX-2

24
Q

where do their unwanted affects happen

A

COX-1 inhibition

25
Q

what are the three main effects of NSAIDs

A
  1. anti-inflammatory
  2. analgesic effect
  3. antipyretic effect
26
Q

Describe the anti inflammatory effect of NSAIDa

A

modulation of the inflammatory reaction.
- this occurs as a result of a decrease on prostaglandin E2 and prostacyclin PG12

27
Q

describe the analgesic effect of NSIADs

A

it occurs as a result of a decrease in the production of prostaglandins that sensitise nociceptors

28
Q

describe the antipyretic effect of NSAIDs

A

lowering of body temperature when this is raised in disease.
- IL1 releases prostaglandins in the CNS, where they elevate the hypothalamic set point for temperature control
- NSAIDs prevent this completely

29
Q

what are some side effects of NSAIDs

A
  • GI disturbance
  • skin rashes
  • prolonged bleeding
  • increase in the likelihood of thrombotic events such as myocardial infarction by inhibiting prostaglandin I2 synthesis
30
Q

mechanism of ibuprofen

A

weakly COX1 selective: mild short lived anti platelet activity.
- stops production of prostaglandins therefore analgesic aswell

31
Q

mechanism of paracetamol

A

selective through weak COX2 inhibitor. paracetamol does not have any gastric or platelet side effects

32
Q

TCA mechanism in more detail

A

the main effect of TCAs is to block the re uptake of airiness by nerve terminals, by competition for the binding site of the amine transporter.
- most TCAs inhibit noradrenaline and 5-HT reuptake but have much less effect on dopamine re uptake

33
Q

what does inhibiting re uptake mean in simple terms

A

its in the synapse for longer so has a greater effect

34
Q

which receptors do TCAs also effect

A

mostly muscarinic acetylcholine receptors (antagonist). they do not contribute to the antidepressant effects

35
Q

what can TCAs cause when in overdose

A

may cause ventricular dysrhythmias associated with prolongation of the QT interval

36
Q

what is gabapentin

A

an anticonvulsant drug used to treat partial epilepsy and neuropathic pain, including peripheral neuropathy

37
Q

mechanism of action of Gabapentin

A
  • GABA is a neurotransmitter in the CNS, involved with neuronal excitability
  • GABApentin interacts with cortical neurones at auxiliary subunits of voltage sensitive calcium channels - action potentials
  • gabapentin increases the synaptic concentration of GABA, enhances GABA response at non-synaptic sites in neuronal tissues, and reduces the release of mono-amine neurotransmitters
38
Q

what are the three steps of the WHO analgesic ladder

A

mild pain: non-opioid e.g paracetamol
moderate pain: simple analgesic e.g paracetamol + weak opioid like coding
severe pain: strong opioids e.g morphine

39
Q

what is the origin of drug liking in opioid addiction

A
  • when heroin, oxycodone or any other opiate travels through the bloodstream to the brain, the chemicals attach to specialised proteins, called mu opioid receptors, on the surface of opiate sensitive neurones
  • the linkage of these chemicals with receptors triggers the same biochemical brain processes that reward people with feelings of pleasure when they engage in activities that promote basic life functions
  • opioids are prescribed theraputically to relieve pain, but when opioids activate these reward processes in the absence of significant pain, they can motivate repeated use of the drug simply for pleasure
40
Q

what is the main brain circuit activated by opioids

A

the mesolimbic (midbrain) pathway

41
Q

describe the mesolimbic pathway

A

this system generates signals in a part of the brain called the ventral tegmental area, VTA, that results in the release of the chemical dopamine in the nucleus accumbens.
this release of dopamine into the nucleus accumbens causes feelings of pleasure. other areas of the brain create a lasting record to memory that associates these good feelings with the circumstances and environment in which they occur. they are called conditioned associations, often leading to the craving for drugs when the abuser reencounters those persons, places, or things and they drive abusers to seek out more drugs in spite of many obstacles

42
Q

describe opioid withdrawal

A

from a clinical standpoint, withdrawal is one of the most powerful factors in driving opioid dependence and addictive behaviours. treatment of the patients withdrawal systems is based on understanding how withdrawal is related to the brain’s adjustment to opioids.
repeated exposure to escalating dosages of opioids alters the brain so that it functions more or less normally when the drugs are present and abnormally when they are not. two important clinical results of this alteration are opioid tolerance and drug dependence. withdrawal symptoms occur only in patients who have developed tolerance.

43
Q

describe opioid tolerance

A

occurs because the brain cells that have opioid receptors on them gradually become less responsive to the opioid stimulation. for example, more opioid is needed to stimulate the VTA brain cells of the mesolimbic reward stream to release the same amount of dopamine in the NAc. therefore, more opioid is needed to produce pleasure comparable to that provided in previous drug episodes.

44
Q

what does opioid dependence involve

A

the locus ceruleus

45
Q

describe opioid dependence in terms of effects in the locus ceruleus

A

neurones in the LC produce noradrenaline and distribute it to other parts of the brain where it stimulates wakefulness, breathing, BP and general alter ness. when opioid molecules link to the mu receptors on the brain cells in the LC, they suppress the neurones release of NA, resulting in drowsiness, slow respiration, low BP. with repeated exposure to opioids, however the LC neurones adjust by increasing their level of activity.

now, when opioids are present, their suppressive impact is offset by this heightened activity, with the result that roughly normal amounts of noradrenaline are released and the patient feels more or less normal. when opioids are not present to suppress the LC brain cells’ enhanced activity, however, the neurones release excessive amounts of noradrenaline

46
Q

what do these excessive amounts of noradrenaline trigger

A

jitters, anxiety and muscle cramps

47
Q

next…

A

go onto pharmacology notes and study the screenshots I have put in for more detailed learning

Semester 3 (94 decks)

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