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Nervous system > Analgesic agents > Flashcards

Analgesic agents Flashcards

1
Q

What are the three types of pain and what are opioids used for?

A

Nociceptive (tissue damage)
Inflammatory
Neuropathic pain

Opioids for nociceptive and inflammatory

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2
Q

How do opioids work?

A

Bind to their receptor in the presynaptic neuron, reduces the function of the Ca2+ channel.
It also binds to receptors in the postsynaptic neuron to increase the conducation of the K+ channel resulting in hyerpolarisation.

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3
Q

What are agonists, antagonists, agonist-antagonists and partial agonists of the opioid receptors?

A

Agonists: morphine, fentanyl, pethadine
Antagonists: naloxone, naltrexone
Agonist-antagonist (depending on the receptor): Nalorphine, pentazocine
Partial agonist: buprenorphine

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4
Q

What are the adverse effects of opioids?

A

Respiratory depression, nausea nad vomiting, drowsiness, constipation, itching, ilius, hypotension, bradycardia

Caution with COPD, sleep apnoea, elderly

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5
Q

What do you do for someone who is addicted?

A

Give methadone or buprenorphine,
Give clonidine to reduce the autonomic symptoms of withdrawal.
Give anti-diarrhea and anti-nausea/vomiting, and something for muscle cramps

OR do rapid detoxification, when patient is under general give lots of naltrexone.

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6
Q

What are the features of morphine?

A 
Powerful analgesia, sedation,
Cough suppression,
miosis
altered mood (euphoria and tranquility)
Large volume of distribution
Half-life of 3 hours.

Side effects: respiratory depression, nausea adn vomiting, constipation, addiction, pruritus, bradycardia, hypotension, biliary colic

IV, IM, oral

Oral bioavailability (25%)

Metabolised in the liver - some biproducts have analgesic effects.

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7
Q

What are the features of pethadine?

A

It is synthetic, less miosis, less biliary spasm
Causes dry mouth and tachycardia

Oral bioabailability 50%
Highly lipid soluble - fast onset.

IV and oral

Same side effects as other opioids.

One byproduct of metabolisim is a problem for patients with renal failure because it will accumulate.

Interacts with monoamine oxidase inhibitors (MAOI)

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8
Q

What are the features of fentanyl?

A

High lipid solubility (fast onset)
80-100 times more potent than morphine
IV, IM, transmucosal lozenges, nasal and sublingual spray, sublingual tablets, transdermal patches - but this is slow and cant rapidly change doses.
Transdermal iontophoresis - trnsdermal administration of ionizable drugs. Electrically cgarged components are propelled through the skin by an external electric field - patient has some control.

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9
Q

What are the features of methadone?

A

Fully synthetic
Well absorbed from all roues - oral (70%), rectal, subcutaneous, IV, sublingual,
Rapid onset of analgesia (30-60 mins)
No cognitive impairment or euphoria, safe in liver and renal failure.

Used for chronic pain, neuopathic pain (better than the others)
For opioid withdrawal or detox.

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10
Q

What are the features of tramadol?

A

Synthetic
Oral (70%)
Not strrong
Inhibit uptake of noradrenaline and serotonic,
Causes the release of endogenous opioids.

Side effects N and V
May cause serotonin syndrome (careful with antidepressants)
little respiratory depression, caution with epilepsy patients.

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11
Q

What are the features of codine?

A

Opiate

Mild to moderate pain,
Suppresses cough, anti-diarrhoeal

Drowsiness and constipation
Can cause dependence

Codeine is metabolised to morphine - ultra-rapid metabolisers are at a higher risk of toxic opioid effects and slow metabolisers may not receive adequate effects

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12
Q

What are coanalgesics and some examples?

A

adjuvant drugs whose primary purpose is not for pain relief by they can enhance the function of analgesics.

Tricyclic antidepressants, anticonvulsants, corticosteroids, clonidine

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13
Q

What is the other name for aspirin?

A

acetyl salicylic acid

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14
Q

What is the mechanism of action of NSAIDs?

A

They inhibit the cyclooxygenase enzymes, leading to suppression of prostanoids production in cells.

Newer agents only inhibit COX2.

This process is reversible for all drugs except for aspirin,

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15
Q

What do NSAIDs do?

A

Decrease inflammation by decreasing prostaglandins.
Reduce mild pain by decreasing by decreasing prostaglandins.
Anti-pyretic by decreasing PGE2
Anticoagulation by decreasing thromboxane A2 in platelets.

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16
Q

What are prostaglandins?

A

A large group of lipid compounds derrive from fatty acids.

Highly potent with many actions, short half life, produced by all cells

17
Q

What are eicosanoids made out of?

A

Arachidonic acid. It is esterfied to the phospholipids of the cell membrane.
Activation of phospholipase releases arachadonic acid from the cell membrane. This is stimulated by
Thrombin, bradykinin 5HT, NO, cell damage

18
Q

What is the pathway for prostanoid synthysis?

A

Arachidoni acid is released by activation of phospholipase A2. Arachadonic acid is converted by COX1 and COX2 into Thrombonane A2 in platelets, prostacycline in endothelial cells and prostaglandins in other cells

19
Q

What does COX1 do?

A

It has a homeostatic function.
COX1 is constitutive (always in cells).
Production of prostaglands for normal function (thomboxane A2).

20
Q

When is COX1 expressed?

A

During inflammation. Induced by IL-1, TNF, GF.
Produces inflammatory prostaglands that cause pain and inflammation.
NSAIDs or steroids are taken to depress these prostaglandins.

Most NSAIDs block both COX1 and COX2

21
Q

What are the side effects of COX-2 inhibitors?

A

Gastric side effects

Increase in heart attaks and strokes

22
Q

What are the pharmacokinetics of NSAIDs?

A

Highly lipophilic
Rapid and complete oral absorption, little first pass metabolism (95% oral bioavailibility).
High degree of protein binding.

Onset is slow, metabolized in the liver.

23
Q

What are the side-effects of NSAIDs?

A

Due to blockage of COX1

Gastric disorders - decrased protection against stomach acid.
Bleeding - decreased thromboxane A2- implcations for surgery
Renal problems - analgesic nephropathy

24
Q

What happens to aspirin after taken?

A

It is absorbed by passive diffusion in the stomach and upper intestine. Once in the blood it is deacetylated to salicylic acid, which is responsible for the analgesic and anti-inflammatory effects.
It is bound to serum albumin.
In the liverit is conjugated to glycine and excreted in the urine (10% excreted unchanged). It competes with uric acid for secretion in the kidneys. Therefore it exacerbates gout.

25
Q

What can taking aspirin daily do?

A

Low doses block thromboxane A2 to decrease platelet adhesion, which reduces the risk of heart attack and stroke. But the prostaglands that cause vasodilation are not inhibited at low concentrations.

26
Q

What is the function of prostanoids on the GI track and what is the impact of NSAIDs?

A

Gastric cytoprotective prostanoid protects against acid damage by increasing mucus synthasis and thickness, increasing bicarbonate secretion, decreasing acid secretion,dilates gastric blood vessels to feed mucosa of the stomach.

NSAIDs reducethese features and can cause ulcers. Can also cause vomiting, nausea and diarrhoea

27
Q

What are the side effects of aspirin?

A

Aspirin induced asthma - triggered within 1-3 ho ingestion. PGE2 is a bronchodilator that is lost. Leucotrines ar bronchoconstrctors

Rhinitis (sneezing, nasal obstruction)
Facial flushing
Nasal polyps - later stage

28
Q

What is reyes syndrome?

A

Children given aspirin after a viral infection can get Reys syndrome. Causes encephalopathy

29
Q

What do prostaglandins do in pregnancy?

A

Establish and maintain labor, increase uterine smooth muscle contraction, maintains patency of the ductus arteriosis

NSAIDs given to patient will inhibit labor

In a premature child, NSAIDs will cause closure of the ductus arteriosus

30
Q

Is paracetamol a NSAID?

A

No

31
Q

What does an overdoes of paracetamold do and what is th antedote?

A

Fatal hepatic damage.

N-acetyl-cystiene

Nervous system (20 decks)

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