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Flashcards in Pharmacology Deck (55)
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1
Q

Where can analgesics act?

A

Site of injury- Decrease sensitisation by decreasing prostaglandins
Block nerve conduction- Block Na channels (lidocaine)
Block synapse transmission in dorsal horn
Activate inhibitory descending path
Ion channels upregulated in nerve damage

2
Q

What are the rungs of the analgesic ladder?

A

NSAIDs/paracetamol
Weak opioid
Strong opioid

3
Q

Give some examples of NSAIDs

A

Aspirin
Diclofenac
Ibruprofen

4
Q

Give some examples of weak opioids

A

Codeine

Tramadol

5
Q

Give some examples of strong opioids

A

Morphine

Oxycodone

6
Q

Whats the difference between opiates and opioids?

A

Opiates- Substances from or structurally similar to opium.

Opioids- Anything acting on opioid receptors

7
Q

What are endogenous opioids called?

A

Enkephalins

8
Q

How does the body naturally modulate nociception?

A

Descending pathways from the brainstem (Supraspinal Antinociception)

9
Q

Where does the Supraspinal Antinociception system arise?

A

Periaqueductal grey (midbrain)

10
Q

Where does the supraspinal antinociception system ultimately project to?

A

Spinal cord

11
Q

Where does the PAG project to?

A
Locus ceruleus (pons)
Nucleus raphe magnus (medulla)
12
Q

What activates the PAG?

A

Opioids and electrical input

13
Q

What does activation of nucleus raphe magnus do?

A

Release 5-HT (serotonin) and enkephalins onto dorsal horn to modulate nociception.

14
Q

What chemical can activate the NRM?

A

Opioids (morphine)

15
Q

What does activation of the locus ceruleus do?

A

Release NA onto dorsal horn to modulate nociception.

16
Q

What kind of receptors are opioid receptors?

A

GCPR

17
Q

What kind of GCPR are opioid receptors?

A

Gi/o

18
Q

What does activation of GCPR do?

A

Inhibit presynaptic VGCC channel opening (By SU. Block vesicle release).
Open postsynaptic K+ channels to hyperpol (By SU)
Inhibit adenylate cyclase (a SU. Needed for long term effects)

19
Q

What are the three main categories of opioid receptor?

A

Mu- Main but lots of side effects
Delta
Kappa

20
Q

What are some side effects of opioids?

A
Addiction
Resp depression
Constapation
N+V
Orthostatic hypotension
Confusion
Hallucinations
21
Q

Name six key opioid R agonists

A
Mrorphine
Diamorphine
Codeine
Fentanyl
Tramadol
Methadone
22
Q

How can morphine be given?

A

IV
Oral
IM
Subcut

23
Q

What receptor does morphine preferentially act on?

A

Mu

24
Q

Where is morphine metabolised?

A

Liver

25
Q

What is a difference between morphine and diamorphine?

A

Diamorphine is more lipophilic

26
Q

How does codeine compare to morphine?

A

Weaker

27
Q

How is codeine usually given?

A

Orally

28
Q

IN addition to analgesia what other effects does codeine have?

A

Anti-diarrhoeal

Antitussive

29
Q

What are two variations of codeine?

A

Oxycodone

Hydrocodone

30
Q

How does fentanyl compare to morphine?

A

100x more potent

31
Q

When and how is fentanyl used?

A

IV for maintenance analgesia

Transdermal for chronic pain

32
Q

Describe tramadol

A

Weak muR agonist.

Most effects by activating NRM

33
Q

What patient group should avoid tramadol?

A

Epileptics

34
Q

Describe methadone

A

Weak mu R agonist. Long half life.

Good for chronic pain and addiction

35
Q

Name two important opioid receptor antagonists

A

Naloxone

Naltrexone

36
Q

How does naloxone work?

A

Competitive mu antagonist

37
Q

When is naloxone used?

A

To reverse opioid toxicity. Short HL so must monitor closely to check doesn’t wear off too quickly.
Newborn babies with opioid toxicity from birth process

38
Q

Describe naltrexone

A

Similar to naloxone but longer HL and oral availability

39
Q

Broadly how do NSAIDs work?

A

Decrease nociceptor sensitisation

40
Q

When are NSAIDs used?

A

To treat mild inflammatory pain

41
Q

What effects do NSAIDs have?

A

Analgesic
Antipyretic
Anti Inflammatory

42
Q

How do NSAIDs decrease nociceptor sensitisation

A

By decreasing prostaglandin synthesis

43
Q

Which enzymes do NSAIDs inhibit to block prostaglandin synthesis?

A

COX1 and 2

44
Q

What do prostaglandins do?

A

Hyperalgesia
Allodynia
Pain

45
Q

What is the difference between COX1 and 2

A

COX1 always active

COX2 only activated locally to damage by cytokines

46
Q

Is paracetamol a NSAID and why?

A

No because it doesn’t have any anti-inflammatory effects

47
Q

Where does paracetamol work?

A

Centrally

48
Q

What is neuropathic pain?

A

Pain from damaged nerves

49
Q

Does neuropathic pain respond to NSAIDs and opioids?

A

No

50
Q

What does neuropathic pain respond to?

A

Gabapentin
Pregabalin
Amitriptyline
Carbamazepine

51
Q

How do gabapentin and pregabalin work?

A

Decrease the expression of the a2d SU of VGCC which is upregulated in damaged sensory nerves

52
Q

Name a condition gabapentin is used for

A

Migraine profolaxis

53
Q

Name a condition pregabalin is used for

A

Diabetic neuropathy

54
Q

How does amitriptyline work?

A

Decrease reuptake of NA

55
Q

How does carbamazepine act?

A

Blocks VGNC subtype that is upregulated in damaged nerves.