Non-opioid Analgesics Flashcards

1
Q

What is local inflammation?

A

The body’s response to an injury

  • ID the injury
  • remove noxious materials
  • ward off infection
  • repair damage to tissue/restore function
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Injured cells release what?

A

Alarmins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

T/F - pathogens can sneak through an injury site?

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Alarmin Il-33 can produce what?

A

Degranulation of mast cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Histamine

A

One of the more important initial mediators of the inflammatory response released by mast cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How does Histamine act?

A

Through a GPCR to produce vasodilation and render the capillaries ‘leaky’
This allows more immune cells to enter the injury site and produce edema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is Histamine-H1 receptors activity

A

Increase intracellular Ca to produce two major effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What two major effects are the result of the increase of intracellular Ca by Histamine-H1 receptor activity?

A

1) NO mediated relaxation of smooth muscle, causing vasodilation
2) MLCK mediated contraction of the capilary endothelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What does MLCK mediated contraction of the capillary endothelium cause?

A

It makes the capillaries leaky

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

As more immune cells are recruited to the injury site, what happens?

A

The inflammatory response is ramped up

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What role does inflammation play in nociceptive pain?

A

Inflammatory mediators interact with receptors and facilitate the transmission of pain signals throughout the nervous system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the major inflammatory mediators that can cause pain?

A
Prostaglandins
Substance P
TNF-a
IL-16
IL-6
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

T/F - Local inflammation adds to the pain felt at the injury site

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

T/F - Excessive inflammation is not beneficial to the host

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What’s the goal of anti-inflammatory drugs?

A

Attenuate the inflammatory response

Attenuate pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

The anti-inflammatory properties and pain relief comes from what?

A

Attenuating the production of prostaglandins

17
Q

What are prostaglandins synthesized from?

A

Arachidonic acid

18
Q

What are the principle prostaglandins?

A

PGE2
PGD2
PGF2
PGI2

19
Q

What do Cox1 and Cox 2 do?

A

They send arachadonic acid down the path leading to the production of prostaglandins

20
Q

How do prostaglandins enhance pain sensitization?

A

They activate Gas, which increases PKA activity, which phosphorylates TRP nociceptors - enhancing pain sensitization

21
Q

How do NSAIDs wrk?

A

Inhibiting COX enzymes, diminishing the production of prostaglandins

22
Q

What is acetylsalicylic acid’s (asprin) mechanism of action?

A

Irreversible inhibitor of Cox1 and Cox2

About 100x better inhibitor of Cox1

23
Q

What is Ibuprofen, Naproxen, and Acetaminophen’s mechanism of action?

A

Reversible inhibitors of Cox1 and Cox2

Naproxen are most selective for Cox2

24
Q

What are the therapeutic effects of acetylsalicylic acid?

A

Analgesia
Antipyretic (fever)
Anti-inflammatory
Anti-thrombolytic (clotting)

25
Q

What are the therapeutic effects of ibuprofen and naproxen?

A

Analgesia
Antipyretic (fever)
Anti-inflammatory

26
Q

What are the therapeutic effects of acetaminophen?

A

Analgesia

Antipyretic (fever)

27
Q

Why is acetylsalicylic acid able to produce anti-thrombosis?

A

Because it is an irreversible inhibitor of the Cox enzymes, knocking out ALL enzyme activity

28
Q

Why is acteaminophen not an anti-inflammatory?

A

Several possibilities

1) Unique Cox enzyme in the CNS is the target
2) Acetaminophen’s mechanism is different
3) Provides relief through an entirely different mechanism (cannabinoid receptor)

29
Q

How can NSAIDs disrupt mucosal defense in the stomach?

A

Prostaglandins (primarily from Cox1) stimulate mucus and bicarbonate secretion to help make the ‘mucus gel’ protecting the stomach from digesting itself

30
Q

What are some adverse affects of NSAIDs

A
Decreased mucosal stomach defense
Increases bleeding time (acetylsalicylic acid)
Kidney problems
Increased BP
Heart failure (rare)
31
Q

What are some precaustions and contraindications for acetylsalicylic acid

A

Ulcer
Diabetes
Gout
Hypocoagulation conditions

32
Q

What is important to know for combining opioids and non-opioid pain relievers?

A

It can be done
NSAIDS have a ceiling effect - maximum pain relief achieved is higher for opioids
They work by different mechanisms

33
Q

What is the most effect analgesia?

A

Optimum dose of NSAID and an additional opioid