Non-Opioid Pain Relievers Flashcards

1
Q

Local ___ is the body’s response to injury.

A

inflammation

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2
Q

What is the point of inflammation?

A
  1. identify injury
  2. remove noxious materials
  3. ward off infection
  4. repair damage to tissue/restore function
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3
Q

Injured cells release certain chemicals called ___. ___ ___ can produce ___ of resident immune cells called ___ cells.

A

alarmins; Alarmin IL33; degranulation

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4
Q

___ is released by mast cells and acts through ____ to produce local ___ and render the ___ ‘leaky’. This will allow more immune cells to enter the injury site and also produce ___.

A

Histamine; GPCR; vasodilation; capillaries; edema

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5
Q

Where is the histamine receptor found and what does it do upon activation?

A

Histamine-H1 receptor activity on vascular endothelium and increases Ca2+

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6
Q

What are the two major effects that Histamine stimulated increase in Ca2+ cause?

A
  1. NO produced in endothelial cells travels to smooth muscle. Once there, NO relaxes the smooth muscle (vasodilation)
  2. MLCK mediated contraction of the capillary endothelium makes the capillary leaky
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7
Q

T/F. Inflammation adds to the pain felt at the injury site and excessive inflammation is not beneficial to the host.

A

True.

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8
Q

What is the goal of anti-inflammatory drugs?

A
  1. attenuate the inflammatory response

2. attenuate pain

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9
Q

The anti-inflammatory properties and pain relief comes from attenuating the production of ___, which are involved in pain ___ and more ___.

A

prostaglandins; sensitization; inflammation

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10
Q

Prostaglandins are derived from ___ ___. What are the four principle prostaglandins?

A

arachidonic acid

PGE2, PGD2, PGF2, PGI2

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11
Q

T/F. Prostaglandins are not stored prior to signal but instead made in response to cell signal.

A

True.

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12
Q

Which is more important in inflammation, COX-1 or COX-2? Which COX is constitutively active?

A

cox-2

COX-1 is constitutive. COX-2 is induced

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13
Q

The action of the enzymes ___ and ___ sends the arachidonic acid down the path leading to production of the ___.

A

COX1; COX2; prostaglandins

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14
Q

What does COX stand for?

A

cyclooxygenase enzyme

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15
Q

What are the undesirable affects of inhibiting COX-1?

A
COX-1 is involved in homeostatic functions so its inhibition affects the following:
GI tract
Renal tract
Platelet function
Macrophage differentiation
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16
Q

The 4 different prostaglandins interact with ___ different GPCRs. PGE2 interacts with ___ different GPCRs, therefore some effects are in direct opposition to each other.

A

8; 4

17
Q

T/F. Prostaglandins play a key role in generating and maintaining the inflammatory response and in pain sensitization.

A

True.

18
Q

Where do prostaglandins act to sensitize pain responses?

A

via their GPCRs at peripheral nerve endings

19
Q

___ mediated activation of G-alpha-___ leads to increased activity of PKA. PKA mediated ___ of the ___ type nociceptor enhances its activity leading to a sensitized pain response.

A

PGE2; s; phosphorylation; TRP

20
Q

T/F. Prostaglandins can only sensitize pain via peripheral nerve endings.

A

False, they can also work via central mechanisms which could make things feel more painful

21
Q

How do all NSAIDS work?

A

by inhibition of COX enzymes and diminishing the production of prostaglandins

22
Q

___ acid or aspirin is a ___ inhibitor that works 100X better on ___-_. It is the ___ selectivity of the commonly used NSAIDS. COX-2 inhibition produces __-____ acid after inhibition.

A

Acetylsalicylic; irreversible; COX-1; worst; 15-hydroxyeicosatetraenoic

23
Q

Which drugs are the reversible inhibitors of COX-1 and -2? Which one is more selective for COX-2 (inducible form)?

A

Ibuprofen, Naproxen, and Acetaminophen

Naproxen

All inhibit COX-1 at lower concentrations than COX-2 except naproxen

24
Q

What are the therapeutic effects of acetylsalicylic acid (aspirin)?

A

analgesia
anti-pyretic (fever)
anti-inflammatory
anti-thrombolytic

25
Q

What are the therapeutic effects of ibuprofen and naproxen?

A

analgesia, antipyretic (fever) and anti-inflammatory

They do not keep platelets from aggregating at low concentrations (anti-thrombolytic)

26
Q

What are the therapeutic effects of acetaminophen?

A

analgesia and antipyretic

27
Q

Platelet aggregation is mediated in part through the ___ production of ___ and ___ of COX enzymes inhibit its production.

A

autocrine; thromboxane; inhibition

28
Q

Why does aspirin have an anti-thrombolytic affect?

A

Since acetylsalicylic acid inhibits COX enzyme IRREVERSIBLY, a low dose will knock out all the enzyme activity and continue to inhibit after the drugs has left the plasma. This is not the case for reversible inhibitors.

29
Q

Why is acetaminophen not anti-inflammatory?

A
  1. there is a unique COX enzyme in the CNS for acetaminophen
  2. diff mechanism of action on COX
  3. provides pain relief through another mechanism
  4. never reaching threshold to produce anti-inflammatory effects
30
Q

What is the adverse affects on the stomach?

A

disruption of mucosal defence

31
Q

Prostaglandins (made primarily from ___-_ activity) stimulate ___ and ___ secretion that help comprise the ‘___ ___’ that protects the stomach from ___ itself. Digestion of the stomach due to inhibition of COX-1 has nothing to do with aspirin being ___.

A

COX-1; mucus; bicarbonate; mucus gel; digesting; acidic

32
Q

In addition to stomach issues, what are other adverse effects of aspirin?

A

increases in bleeding time (acetylsalicylic acid)
kidney problems (water, Na+ retention)
increased BP
heart failure (rare)

33
Q

What disease is characterized by fatty change in the liver and edematous encepalopathy following aspirin use 3-5 days later?

A

Reye’s syndrome

34
Q

What age group is affected by Reye’s syndrome? What is it preceded by? How many progress to coma and death or permanent neurologic impairments?

A

children age 6 months to 15 yrs

mild upper respiratory tract infection managed with aspirin administration at levels that are not ordinarily toxic

25%

35
Q

What are some precautions or contraindications for acetylsalicylic acid?

A

ulcer
diabetes
gout
hypocoagulation conditions

36
Q

Which is the only COX-2 inhibitor still on the market?

A

Celecoxib

37
Q

T/F. NSAIDS are good at what they do at low concentrations but can’t achieve levels of relief like opioids.

A

True.

38
Q

T/F. The most effective analgesia is an optimum dose of NSAID + additional opioid.

A

True.