Non-Opioid Lecture

Question 1

Define Analgesia:

Answer 1

Absence of pain in response to a stimulus that is normally painful

Question 2

Define Pain:

Answer 2

An unpleasant sensory or emotional experience associated with actual or potential tissue damage, or described in terms of such damage

Question 3

Define Anesthesia:

Answer 3

Absence of all sensory modalities

Question 4

3 endogenous responses to pain:

Answer 4

1. Endorphins
2. Enkephalins
3. Dynorphins

Question 5

Location and function of endorphins

Answer 5

Mainly concentrated in the central nervous system, activates opioid receptors, provides analgesia, euphoria at mu receptor

Question 6

What was the first endorphin to be purified? What receptor does it activate?

Answer 6

Enkephalins, activates delta receptor

Question 7

Dynorphins have a high affinity for which receptor?

Answer 7

kappa-opioid receptor

Question 8

2 types of pain

Answer 8

1. Dull, aching, inflammatory (NSAIDS most effective)

2. Sharp, piercing, lancinations (Opiates most effective)

Question 9

Most dental pain is which of the two types?

Answer 9

Mostly dull,aching, inflammatory pain

- NSAIDS are most effective against this type of pain

Question 10

Degrees of pain and what is most effective for each?

Answer 10

1. Mild = Salicylates, NSAIDS most effective
2. Moderate = Salicylates, NSAIDS most effective
3. Severe = opiates are best

Question 11

Locus of action for non-opioid analgesics and Mechanism?

Answer 11

• Act primarily at peripheral nerve endings
• Antipyretic effect mediated centrally
  Mechanism: inhibit prostaglandin synthesis

Question 12

Locus of action for opioid analgesics and mechanism?

Answer 12

• Act primarily within CNS

Mechanism: depress CNS which reduces response to pain (pain reaction)

Question 13

T or F, All non-opioid analgesics work on the peripheral nervous system

Answer 13

True

Question 14

T or F, Opiates = more side effects

Answer 14

True

Question 15

Why are NSAIDS considered true analgesics?

Answer 15

They stop the pain from where it is occurring. Opiates are not considered true analgesics because they simply DIMINISH your awareness of pain, so they only act as analgesics (don’t feel the pain)

Question 16

NSAIDS inhibit the synthesis of what? How is this done?

Answer 16

Inhibit prostaglandin synthesis

• Inhibit the important enzyme: cyclooxygenase (COX) so that prostaglandins are not formed
• Inhibit cytoprotective PG as well as PG associated with inflammation (These are the good guys that our bodies need)

Question 17

3 main non-opioid analgesic classes that we talked about

Answer 17

1. Salicylates = aspirin
2. Non-steroidal anti-inflammatory drugs (NSAIDS) - includes ibuprofen
3. Acetaminophen (Tylenol) = Not an NSAID. Classified as a miscellaneous analgesic

Question 18

Why is Acetaminophen not considered an NSAID

Answer 18

It works on COX 3 in the CNS, and is not anti-inflammatory

Question 19

How many different NSAIDS are approved in the U.S.

Answer 19

22

Question 20

What are the affects of prostacyclin?

Answer 20

Vasodilation
Inhibits platelet aggregation

-*** Opposite of thromboxane effects

Question 21

What are the effects of prostaglandins

Answer 21

Cytoprotective

Inflammatory mediators

Question 22

What are the effects of thromboxane?

Answer 22

Vasoconstriction
Platelet aggregation

-*** Opposite of prostacyclin effects

Question 23

COX 1 maintains what 5 things on a normal physiologic basis?

Answer 23

1. Renal blood flow
2. Body temperature
3. Blood pressure
4. Heart rate
5. Reproduction

Question 24

If you take NSAIDs and Aspirin, what happens by blocking COX?

Answer 24

Block formation of both cytoprotective prostaglandins and prostaglandins associated with inflammation (Blocks COX 1 and 2)

Question 25

What adverse effect is present if COX 1 is blocked by aspirin or NSAIDS?

Answer 25

Decreases production of protective mucous = GI ulceration and bleeding.
**Remember: COX 1 regulates the amount of stomach acid produced. Stomach has thick mucous lining to protect gastric mucosa from HCl

• Chronic use of NSAIDS is associated with GI ulceration and bleeding

Question 26

When is COX 2 produced?

Answer 26

Produced when you experience trauma and need inflammatory response for healing.
- This is the “inducible” form of COX

Question 27

T or F, Blocking COX 2, like COX 1, will have an adverse effect on the stomach by blocking the cytoprotective prostaglandins.

Answer 27

False, COX 2 have no effect on the stomach = leave cytoprotective prostaglandins intact. They only alter prostaglandins associated with inflammation.

Question 28

Drugs that block COX 2 are primarily used for what?

Answer 28

Arthritis

-***Celebrex is a common brand of COX 2 inhibitors used for arthritis

Question 29

COX 3 is found where?

Answer 29

Only in the CNS

Question 30

COX 3 function

Answer 30

It works centrally but has no anti-inflammatory effects. It does suppress prostaglandin synthesis.

• *** This is how acetaminophen works. Pain control but no anti-inflammatory effects

Question 31

Why can tylenol be used for fever reduction?

Answer 31

It works centrally and can act on the hypothalamus

Question 32

Non-selective NSAIDS block which COX?

Answer 32

Both COX-1 and COX-2

Question 33

Selective NSAIDS block which COX?

Answer 33

Block COX-2 only. Only one available in US = celecoxib (Celebrex)