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Basic Pharmacology > 13. Analgesics > Flashcards

13. Analgesics Flashcards

1
Q

List medical analgesics

A
  • non steroidal anti-inflammatories
  • pioid analgesics
  • general anaesthetics
  • local anaesthetics
  • anxiolytics
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2
Q

List non-medical analgesics

A
  • alcohol
  • nicotine/caffeine
  • cocaine
  • LSD
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3
Q

Why do dentists need to understand analgesics?

A
  • prescribed for post operative dental pain
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4
Q

Noxious stimuli are sensed by …
Process?

A
  • peripheral receptors/nociceptors
  • nociceptive fibres travel to CNS (dorsal horn) and excite transmission fibres running to the thalamus
  • nociception is process whereby noxious peripheral stimuli transmitted to CNS
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5
Q

Are pain and nociception the same thing?

A
  • no
  • pain is subjective and amount of pain a stimuli produces depends on more than stimulus itself
  • pain has sensory and emotional components
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6
Q

Chemical mediators for nociception/pain

A
  • in most cases, stimulation of nociceptive endings in periphery is chemical in origin
  • mechanical and thermal stimuli can cause acute pain but chronic pain results due to chemical mediators
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7
Q

Polynodal nociceptors are what?

A

receive afferent fibres in high proportions in periphery to send to brain
high receptor threshold

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8
Q

3 types of afferent fibres in nociception

A
  • C fibres
  • A delta
  • A beta fibres
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9
Q

Where are C fibres?

A

outer dorsal horn

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10
Q

Properties of C fibres

A
  • non-myelinated
  • low conduction velocity
  • nociceptor/thermoreceptor/machanoreceptor
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11
Q

Properties of A-delta fibres

A
  • myelinated
  • rapid conduction velocity
  • nociceptor/mechanoreceptor
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12
Q

What kind of receptor is A-beta fibres

A

mechanoreceptors

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13
Q

Explain the neural pathway of nociception from primary afferent neurons to superficial lamina of dorsal horn of spinal cord

A
  • signal goes from pain trigger to PAN, to dorsal horn to brainstem (pons/medulla) to midbrain
  • goes to thalamus to the cingulate and somatosensory cortexes and the limbic system
  • ## negative feeback system from limbic system to PAG, down RVM to dorsal horn
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14
Q

Chemical mediators (stimulate pain endings in skin) include …

A
  • 5-HT
  • kinins like bradykinin
  • metabolites of intermediary metabolism e.g lactic acid
  • capsaicin (responsible for burning taste of chilli peppers)
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15
Q

… is a chemical mediator that enhances the pain producing effects of other agents but they do not …

A
  • eicosanoids
  • stimulate nociceptive endings
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16
Q

4 properties of NSAIDS

A
  • analgesic - relieve pain
  • anti-inflammatory - reduce inflammation
  • antipyretic - decrease elevated body temp
  • antiplatelet - reduce platelet aggregation
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17
Q

Mechanism of action of NSAIDs

A
  • inhibit prostaglandin (eicosanoid) production by irreversibly inhibiting cyclooxygenase (COX) function
  • therapeutic effects related to inhibition of COX 2 (induced in activated inflammatory cells)
  • unwanted side effects related to inhibition of COX1 - enzyme expressed in most tissues
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18
Q

Prostaglandin synthetic pathway

A
  • phospholipids in cell membrane
  • get phospholipase A2 and related enzymes
  • arachidonic acid (goes to lipoxygenase then leukotrines) or cyclo-oxygenase (COX)
  • various intermediates (PGG2, PGH2) like thrombocanes, prostaglandins and prostacyclin
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19
Q

Where do NSAIDs work in prostaglandin synthetic pathway?

A
  • NSAIDs act on cyclo-oxygenase inhibiting COX or its reduction
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20
Q

How does aspirin fill the 4 NSAIDs properties?

A
  • analgesic as has decreased prostanoid synthesis leads to less sensitisation of nociceptors to effects of mediators like 5-HT, kinins etc
  • anti-inflammatory same as above
  • antipyretic - centre in hypothalamus regulates body temp, in fever temp is raised due to synthesis of PGE2 due to pyrogens
  • aspirin decreases this PGE2 synthesis
  • antiplatelet - from blood clotting
21
Q

When would aspirin be the first choice of drug?

A
  • in mild analgesia
  • cheap and effective
22
Q

ADME of aspirin

A
  • orally taken
  • rapidly hydrolysed by esterases to salicylate
  • half life of 4-15 hrs - dose dependent
23
Q

Unwanted effects of aspirin

A
  • low doses gives GI irritation, hypersensitivity
  • salicylism in high doses - tinnitus, vertigo, decreased hearing
  • Reye’s syndrome, rare childhood disorder
  • interacts with warfarin
24
Q

How does Reye’s manifest?

A
  • massive brain and liver swelling in children coming out of heightened immune state
25
Q

How does ibuprofen fill the NSAID categories?

A
  • decreased prostanoid synthesis leads to less sensitisation of nociceptors to effects of mediators e.g 5-HR, kinins makes it analgesic and anti-inflammatory
  • antipyretic as centre in hypothalamus regulates body temp. In fever, temp raised due to synthesis of PGE2 due to pyrogens and ibuprofen decreases this
  • no antiplatelet vibes
26
Q

When is ibufropen first choice NSAID?

A
  • for inflammatory joint disease
  • effective and better tolerated than most
27
Q

ADME of ibuprofen

A
  • oral, topical, rectal
  • rapid absorption in 1-2 hours
28
Q

Unwanted effects of ibuprofen

A
  • uncommon and mild
  • local sensitivity reactions
  • less gastric irritation than aspirin
  • suitable for kids
29
Q

How is paracetamol still an NSAID when it’s not anti-inflam or antiplatelet?

A
  • analgesic and antipyretic in exact same ways as aspirin and ibuprofenW
30
Q

When would paracetamol be the first choice NSAID?

A
  • safe and effective mild analgesic at therapeutic dose
  • less analgesic activity in inflammatory conditions
31
Q

ADME for paracetamol

A
  • oral, rectal, IV
  • peak plasma conc within 30-60 mins
  • half life 2-4 hrs
  • mainly conjugated to glucuronic acid/sulphates
32
Q

Unwanted effects of paracetamol

A
  • uncommon
  • hepatotoxicity in overdose or chronic usage
  • allergic skin reactions
33
Q

Morphine analogues OPIOIDS

A
  • diamorphine (heroin)
  • codeine
34
Q

Synthetic derivatives OPIOIDS

A
  • pethidine
  • dextropropoxyphene
35
Q

Opioid neurotransmitters

A
  • enkephalins
  • endorphins
  • dynorphins
36
Q

Opioid receptors

A
  • mu, delta and kappa
  • mu responsible for most analgesic effects
  • opioid analgesics act as agonists at mu
  • all opioid receptors linked through G-proteins to inhibition of denylate cyclase
37
Q

Therapeutic effects of opioid analgesics

A
  • analgesia
  • euphoria and sedation
38
Q

ADME of opioid analgesics

A
  • oral, rectal, IV, IM
  • erratic absorption from gut
  • extensive first pass metabolism
39
Q

Indications of opioid analgesics

A
  • moderate to severe pain with strong opioids e.g morphine, pethidine
  • mild to moderate pain/cough suppressive/antidiarrhoel - weak opioids e.g codeine
40
Q

Adverse CNS effects of opioid analgesics

A
  • drowsiness and sedation
  • respiratory depression
  • tolerance and dependence
  • cough suppression
  • nausea-vomiting
41
Q

Adverse PNS effects of opioid analgesics

A
  • constipation
  • histamine release
  • pinhole pupils
42
Q

Give 2 strong opioids

A
  • morphine
  • pethidine
43
Q

Give 2 weak opioids

A
  • dextropropoxyphene
  • dihydrocodeine
44
Q

Explain morphine

A
  • most valuable for severe pain relief
  • terminal care
45
Q

Explain pethidine

A
  • more lipid soluble than morphine
  • rapid onset/short duration
  • less constipation than morphine
  • prescribed by dentists
46
Q

Explain dextropropoxyphene

A
  • very mild analgesic
  • used in combo with aspirin and paracetamol
47
Q

Expplain dihydrocodeine

A
  • pharmacologically similar to codeine
  • nausea and constipation limit dose and duration of use
48
Q

Tolerance with opioids

A
  • detected in 12-24 hrs
  • sensitivity will return on withdrawel
  • extends to all pharmacological actions
49
Q

Dependence on opioids

A
  • following abrupt withdrawal after chronic treatment
  • abstinence syndrome after acute treatment

Basic Pharmacology (16 decks)

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