Pain killing Meds Flashcards Preview

Pharmacology > Pain killing Meds > Flashcards

Flashcards in Pain killing Meds Deck (32):
1

Do prostaglandins produce pain?

NO, but they potentiate the pain caused by other  mediators of inflammation (e.g. histamine, bradykinin).

Prostaglandins sensitize sensory nerve endings to nociceptive stimuli.

 

2

Do NSAIDs have an antipyretic action?

Indirectly, yes.

Fever - endogenous pyrogen (interleukin I) released from leucocytes - these act on thermoregulatory centre in hypothalamus.

This effect also causes a rise in hypothalmus prostaglandins which are pyogenic.

3

Can you use aspirin for gout?

No because they raise plasma urate levels at low doses by inhibiting uric acid secretion in the renal tubules.

4

Do prostaglandins cause inflammation?

Yes;

they are released from cells in response to chemical/ physical trauma.

they stimulate inflammatory cell chemotaxis (vasodilation, >> permeability >> oedema

  • they sensitize sensory nerve endings to nociceptive stimuli.

 

5

Relationship of COX (cyclooxygenase Isozymes)

and NSAIDs

NSAIDS are non-selective inhibitors of COX-1 and COX-2.

 

COX-1 has a protective effect on GI tract. COX1 is involved with synthesis of prostaglandins that are cytoprotective.

COX-2 - normally levels are low, it is up-regulated in the inflammatory process by substances such as cytokines, endotoxins.

6

Relationship between NSAIDs and lithium

NSAIDs inhibit the renal excretion of lithium and can increase lithium levels and toxicity.

7

Can you combine Spironolactone with NSAIDs?

Not advisable due to increased risk of hyperkalaemia.

8

Why is it advisable for children not to have salicylates?

Increase risk of Reye's syndrome

 

(salicylates; aspirin - salicyclic acid)

9

Relationship of aspirin levels to pharmological and toxic effects

A image thumb
10

Adverse effects of aspirin

Reye's syndrome

GI bleeding

>> does; tinnitus, hyperventilation, fever, dehydration, metabolic acidosis, organ failure, death

hypoprothrombinaemia - impairment of haemostasis.

11

Tx of salicylate overdose

induce vomiting

IV Sodium bicarbonate

dehyration support

12

Celecoxib - what's special about this NSAID?

Is the first selective COX-2 inhibitor (therefore doesn't affect cytoprotective effects of COX-1).

Less risk of GI bleeding.

 

>>> risk of cardiovascular events

13

NSAIDs has two unusual indications, what are they?

Alzheimer's

(neurogeneration is accomopanied by inflammatory COX mechanisms)

Colon cancer

(angiogensis of tumour growth requires COX-2 activity)

14

antidote to acetaminophen overdose

acetylcysteine

15

what is >>>> acetaminophen toxic?

due to depletion of hepatic glutathione that converts the hepatotoxic quinone intermediate.

16

Adverse effects of acetaminophen?

long term use is associated with an increased risk of renal dysfunction.

17

What is COX? 

cyclooxygenase

an enzyme that catalyzes the first step in the synthesis of prostaglandins from arachidonic acid

 

Found in endoplasmic reticulum

18

How do NSAIDS work?

decrease COX activity by competitive inhibition.

(non-selective, therefore affects the cytoprotective GI aspect of COX-1)

Except aspirin; forms a covalent, irreversible inhibition of COX.

Net effect << prostaglandin production

19

Why does APAP (acetaminophen) only have a WEAK anti-inflammatory effect? 

Because it inhibits COX-3 only.

20

Can you give NSAIDs in pregnancy?

NO, especially in the second half of pregnancy.

Acetaminophen can be safely given for analgesia and antipyresis.

21

What are the two groups of analgesics?

  • opiods
  • nonopiods (also called NSAIDs because of significant anti-inflammatory effect)

22

MOA of opioids?

Act primarily in the spinal cord and brain to inhibit the neurotransmission of pain.

23

MOA of nonopioids?

Act primarily on peripheral tissues to inhibit the formation of algogenic or pain-producing substances such as prostaglandins?

24

Three origins of pain, what are they?

somatic

visceral

neurogenic

25

Why are drugs like codeine (moderate opiod agonist) best combined with acetaminophen or a NSAID?

Moderate opioid agonists cause intolerable adverse effects if given in high doses for severe pain.

Therefore best given submaximally with another drug for best clinical effectiveness.

 

(NB. strong opioid are better tolerated, therefore use for severe pain)

26

Strong Opioid Agonists include:

Morphine

Methadone

Oxycodone

Fentanyl

Meperidine

 

27

CNS effects of Morphine (7)

  1. analgesia
  2. sedation
  3. euphoria/ dyphoria
  4. miosis
  5. nausea/ vomiting
  6. respiratory depression
  7. inhibition of cough reflex

28

What is the importance of miosis if a patient has taken opioids?

It's a diagnositic sign of opioid overdose because little/ no tolerance developes to miosis

29

What is the cardiovascular effect of morphine (and other opioids)?

VASODILATION

- orthostatic hypotension (careful with this)

- it would helps patients with coronary artery disease due to << peripheral resistance

Therefore: << Cardiac work, << myocardial oxygen demand.

30

How do opioids depress respiratory function?

Reduce hypercapnic drive

Reduce tidal volume and rate

 

IMP. cerebral circulation is very sensitive to CO2 levels and responds with incrase in cerebral blood flow, therefore >> pressure.

DON'T use opioids with closed-head injuries.

31

What's the antidote to opioid overdose?

Naloxone

32

Other effects of opioids (except CV and cns):

 

nausea and vomiting (opiods stimulate chemoreceptor trigger zone in the medulla)

Pruritus (due to release of histamine)

Flushing and warmth of upper torso (due to histamine)