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Yr3 Pharmacology > Pain drugs > Flashcards

Pain drugs Flashcards

1
Q

How do NSAIDS work?

A

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

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2
Q

What causes NSAIDS benefits and side effects

A

Benefits: COX2 inhibition

Side effects: COX1 inhibition

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3
Q

Who are at risk of the side effects of NSAIDS, and when can they definitely not be used in:

A

Risk: peptic ulcer disease, GI bleed, cardiovascular disease

No No: Severe renal impairment, heart failure, liver failure, NSAID hypersensitivity

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4
Q

Name some side effects of NSAIDS

A 
Indegestion
GI toxicity
renal impairment
hypersensitivity
fluid retension
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5
Q

What would you tell someone who is going to start taking NSAIDS?

A

For pain relief, don’t stop cause
Indigestion is common, stop if it happens
Long term use not recommended

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6
Q

How do opioids work?

A

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.

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7
Q

When would you use opioids?

A

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

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8
Q

What are some contraindications to taking opioids?

A

Hepatic and renal failure - need to metabolise
Respiratory failure-
Tramadol lowers seizure potential
Long term- addiction

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9
Q

Do opioids interact with anything?

A

monitor closely with other sedatives

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10
Q

What are the main side effects of opioids?

A 
Addictive!
Respiratory depression
Euphoria, detachment
Neurological depression in higher doses
Nausea and vomiting, activates chemoreceptor trigger zone
pupillary constriction
constipation
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11
Q

How does paracetamol work?

A

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

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12
Q

When is paracetamol used?

A

First line for most types of acute and chromic pain.

Antipyretic

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13
Q

When is paracetamol contraindicated?

A

Reduce dose in liver toxicity due to either NAPQI production (eg from excess alcohol misuse) or reduced glutamine stores (eg malnourished)

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14
Q

Why could someone suffering seizures be at higher risk of paracetamol toxicity?

A

Phenytoin and carbemazepine (antiepileptics) are cytochrome p450 inducers which increase the rate of NAPQI production and therefore risk of liver toxicity after overdose.

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15
Q

How safe is paracetamol at theraputic dose?

A

Very

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16
Q

How does a paracetamol overdose result in liver toxicity?

A

Metabolised by cytochrome p450 into NAPQI which is toxic, and conjugated with glutathione before elimination
Overdose floods this pathway, NAPQI accumilation causes hepatocellular necrosis

17
Q

How would you prevent paracetamol toxicity?

A

Prevent with glutathione precursor acetylcystine

18
Q

What is allopurinol used for?

A

Preventing acute attacks of gout

Prevent calcium oxalate and uric acid renal stones

19
Q

What kind of drug is Allopurinol, and how does it work?

A

xanthine oxidase inhibitor
stops xanthine oxidase converting xanthines into uric acid
Reducing precipitation or uric acid in joints and kidneys

20
Q

When wouldn’t you start someone on allopurinol?

A

During an acute attack of gout (can continue if already on it)
Recurrent skin rash / hypersensitivity reactions

21
Q

What does Allopurinol interact with?

A

Amoxycillin- increases chance of skin rash

ACE inhibitors and thiazides increase risk of hypersensitivity reactions

22
Q

What are some possible side effects of allopurinol

A

Skin rash, usually mild but can be hypersensitivity

Can actually trigger an attack of gout

23
Q

Name an alpha blocker and what it does

A

Doxazosin
Improves symptoms in benign prostatic hyperplasia
Add-on treatment in hypertension

24
Q

How do alpha blockers work?

A

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.

25
Q

When is doxazosin contrainducated?

A

Postural hypertension

26
Q

What drugs do alpha blockers have dangerous interactions / combined effects?

A

Antihypertensives, particularly beta blockers, causing dangerously low BP, dizziness, syncope

27
Q

Name some side effects of doxazocin, and when can they be especially bad?

A

Postural hypertension, dizziness, syncope

Usually worst after first dose

28
Q

What kind of drug is finasteride?

A

5-alpha reductase inhibitor

29
Q

How does finasteride work?

A

Reduces the size of the prostate by inhibiting 5 alpha reductase, which convert testosterone to the more active dihydrotestosterone
Inhibition of this slows growth and improves urinary flow

30
Q

Why is an alpha blocker usually preffered to finasteride?

A

Finasteride takes longer to work

31
Q

When is finasteride indicated?

A

benign prostatic hypertrophy (2nd line)

32
Q

When should finasteride never be indicated?

A

pregnant women or men who may have sex with a pregnant woman, as it causes fetal genital abnormalities

33
Q

What are the side effects of 5-alpha reductase inhibitors?

A

Anti-androgens, so rediced libido and impotency
Hair growth - antibaldness!
Nipple / breast growth and tenderness

34
Q

What would you tell a patient starting on finasteride?

A

takes up to 6 months to get working,
Reduced libido and possible impotence (usually transient, goes away once body is used to it)
Nipple / breast growth / tenderness
Condom if having sex

Yr3 Pharmacology (6 decks)

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