Pain drugs Flashcards
(34 cards)
How do NSAIDS work?
Inhibit prostaglandin synthesis by inhibiting COX enzyme
COX1 is constitutive form: It stimulates prostaglandin synthesis which is essential for gastric mucosa, renal function and preventing thrombus formation
COX2 is expressed in response to inflammatory stimuli. Stimulates prostaglandins whichproduce inflammation and pain
What causes NSAIDS benefits and side effects
Benefits: COX2 inhibition
Side effects: COX1 inhibition
Who are at risk of the side effects of NSAIDS, and when can they definitely not be used in:
Risk: peptic ulcer disease, GI bleed, cardiovascular disease
No No: Severe renal impairment, heart failure, liver failure, NSAID hypersensitivity
Name some side effects of NSAIDS
Indegestion GI toxicity renal impairment hypersensitivity fluid retension
What would you tell someone who is going to start taking NSAIDS?
For pain relief, don’t stop cause
Indigestion is common, stop if it happens
Long term use not recommended
How do opioids work?
Activate opioid U centres in CNS, with several effects that reduce neuronal exciteability and pain transmission.
In medulla, they blunt the response to hypoxia and hypercapnoea, reducing respiratory drive and breathlessness.
Reduce sympathetic activity.
When would you use opioids?
Rapid relief of acute severe pain
Chronic pain when others are insufficient (rung 3 of who pain ladder). Weak in mild-moderate pain (rung2 of pain ladder)
Breathlessness relief in EOL care
What are some contraindications to taking opioids?
Hepatic and renal failure - need to metabolise
Respiratory failure-
Tramadol lowers seizure potential
Long term- addiction
Do opioids interact with anything?
monitor closely with other sedatives
What are the main side effects of opioids?
Addictive! Respiratory depression Euphoria, detachment Neurological depression in higher doses Nausea and vomiting, activates chemoreceptor trigger zone pupillary constriction constipation
How does paracetamol work?
Poorly understood
Weak cox-2 inhibitor - so is antiinflammatory
Cox inhibition increases pain threshold and reduces prostaglandins in the thermoregulatory centre in hypothalamus, reducing fever
When is paracetamol used?
First line for most types of acute and chromic pain.
Antipyretic
When is paracetamol contraindicated?
Reduce dose in liver toxicity due to either NAPQI production (eg from excess alcohol misuse) or reduced glutamine stores (eg malnourished)
Why could someone suffering seizures be at higher risk of paracetamol toxicity?
Phenytoin and carbemazepine (antiepileptics) are cytochrome p450 inducers which increase the rate of NAPQI production and therefore risk of liver toxicity after overdose.
How safe is paracetamol at theraputic dose?
Very
How does a paracetamol overdose result in liver toxicity?
Metabolised by cytochrome p450 into NAPQI which is toxic, and conjugated with glutathione before elimination
Overdose floods this pathway, NAPQI accumilation causes hepatocellular necrosis
How would you prevent paracetamol toxicity?
Prevent with glutathione precursor acetylcystine
What is allopurinol used for?
Preventing acute attacks of gout
Prevent calcium oxalate and uric acid renal stones
What kind of drug is Allopurinol, and how does it work?
xanthine oxidase inhibitor
stops xanthine oxidase converting xanthines into uric acid
Reducing precipitation or uric acid in joints and kidneys
When wouldn’t you start someone on allopurinol?
During an acute attack of gout (can continue if already on it)
Recurrent skin rash / hypersensitivity reactions
What does Allopurinol interact with?
Amoxycillin- increases chance of skin rash
ACE inhibitors and thiazides increase risk of hypersensitivity reactions
What are some possible side effects of allopurinol
Skin rash, usually mild but can be hypersensitivity
Can actually trigger an attack of gout
Name an alpha blocker and what it does
Doxazosin
Improves symptoms in benign prostatic hyperplasia
Add-on treatment in hypertension
How do alpha blockers work?
Highly selective for alpha-1 adrenoreceptor, found mainly in smooth muscles in blood vessels and urinary tract.
Alpha blockers block this receptor, causing vasodilation and fall in BP as well as widening lumen, reducing resistance to bladder outflow.
