Respiratory + Pain Drugs Flashcards
What do you use paracetamol for
1) 1st line - acute and chronic pain
2) Antipyretic
How does paracetamol work
Weak inhibitor of COX
In the CNS COX Inhibition appears to increase the pain threshold and reduce prostaglandin concentration in the thermoregulatory centre of the hypothalamus
Which COX is paracetamol specific for?
COX 2 –> however it is only a weak inhibitor as its actions are inhibited by peroxides
What inhibits the action of paracetamol
peroxides
Adverse effects of paracetamol
Generally very safe
This is because lack of COX-1 inhibition prevents, GI, renal and CV implications
How is paracetamol metabolised
By CP450 enzymes in the liver
Metabolised to NAPQI that is conjugated with glutathione
In overdose NAPQI builds up causing hepatocellular necrosis
When should we reduce paracetamol dose
In those at risk of liver toxicity e.g.
Increased NAPQI production –> chornic excessive alcohol use or inducing enzymes
Decreased glutathione stores –> malnutrtion, low body weight, severe hepatic impairment
What does patacetaml interact with
CP450 Inducers e.g. carbamazepine and phenytoin
This increase the rate paracetamol is metabolised hence increased NAPQI production and risk of liver toxicity
How do we establish the efficacy of n-acetylcysteine in treating paracetamol overdose?
Test INR, ALT and creatinine
Name strong opioids
Morphine, Oxycodone
What do we use strong opioids for
Acute severe pain - rapid onset e.g. post-op and MI
Chronic pain –> step 3
Breathlessness –> relieves it in end of life care
Acute pulm oedema –> with furosemide and oxygen and nitrates
How do strong opioids work
Activation of opioud mu receptors in the CNS
Decreases neuronal excitability and pain transmission
In the medulla they blunt the response to hypoxia and hypercapnia –> hence redce breathlessness
AS they relieve pain also decrease sympathetic stimulation –> this may reduce cardiac work and oxygen demand hence relieving symptoms in MI and pulm. oedema
Adverse effects of strong opiods
1) Respiratory depression
2) Neurological symptoms
3) Nausea and vomiting –> as they activate chemoreceptor trigger zone –> usually decreases with time but offer them an anti-emetic
4) Pupillary constriction –> activate the Edinger-Westphal nucleus
5) Constipation –> decrease motility and increase smooth muscle tone
6) itching, urticaria, vasodilation and sweating –> as may cause histamine release
7) Toelrance
8) Withdrawal reaction –> anxiety, pain, breathlessness, pupils dilate, cold and dry skin
Warnings of strong opioids
Redice dose in hepatic or renal impairment
Avoid in respiratory failure
Avoid in biliary colic –> can cause smooth muscle contraction and spasm of Sphincter of Oddi –> worsens pain
Interactions of strong opioids
Dont use with other sedating drugs e.g. anti-psychotics, benzodiazepines or tricyclic antidepressants.
Name opiate compounds
Co-codamol
Co-dydamol
Indications for opiate compounds
Treatment of mild-moderate pain –> when paracetamol is insufficient
Overdose effects of opiate compounds
Hepatotoxicity - paracetamol
Neurological and respiratory depression - opiods
Warnings of opiate compounds
Extreme caustion in significant respiratory disease
Dose reductin in renal/hepatic impairment
What should we avoid prescribing opiate compounds with
Other sedating drugs (tricyclic antidepressants, benzodiazepines, antipsychotics)
Name weak opiods
Codeine, Dihydrocodeine, Tramadol
How do weak opiates work
Codeine and dihydrocodeine metabolised by the liver to produce small amounts of morphine/dihydromorphine
Why do some poeple find opiates ineffective
10% of caucasians have an enzyme CP450 2D^ that is less active hence don’t metablise it
What is tramadol
Synthetic analogue of codeine