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Pharmacology #2 > Anti-inflammatories (Non-opioid pain relievers) > Flashcards

Anti-inflammatories (Non-opioid pain relievers) Flashcards

1
Q

NSAID stands for:

A

Non-steroidal Anti-inflammatory drugs

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2
Q

What is the purpose of inflammation?

A

It identifies the injury, helps to remove noxious materials, wards off infection and repairs damaged tissue to restore function.

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3
Q

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

A

True

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4
Q

Injured cells release chemicals called alarmins (I assume these are just cytokines)

A

Okay, got it. It raises the alarm

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5
Q

What can alarmin IL-33 do?

A

It produces degranulation of resident mast cells

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6
Q

What is the most important thing that mast cells release?

A

Histamine- an inflammatory mediator

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7
Q

What effect does histamine have?

A

It acts through a G couple protein receptor to produce local vasodilation and makes the capillaries leaky so that more immune cells can get out of the blood stream and to the injury site (this is what happens in a runny nose!) This results in edema- aka swelling

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8
Q

The histamine receptor activity allows for the freeing of phospholipase C from the membrane which gets cleaved into IP3 and DAG. IP3 increases the concentration of intracellular calcium.

A

Remember that?

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9
Q

When intracellular calcium is increased, what else is made? and what does it do?

A

NO
It is produced in the endothelial cells and travels to the smooth muscles to make them relax, thereby causing vasodilation.

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10
Q

What does MLCK mediated contraction do to the capillary endothelium?

A

It makes the capillary leaky

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11
Q

There are a lot of inflammatory mediators that are released from cells, IE prostaglandins. Do anti-inflammatory drugs work on all of these inflammatory mediators?

A

Nope, they probably just act on one of the inflammatory mediators, most likely prostaglandins

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12
Q

T/F the anti-inflammatory properties and pain relief come from attenuating the production of prostaglandins?

A

True

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13
Q

What are the two main acts of prostaglandins?

A

Pain sensitization and more inflammation

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14
Q

Prostaglandins are all derived from what?

A

arachidonic acid

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15
Q

Arachidonic acid is liberated via the result of some signaling event.

A

Arachidonic acid can be liberated from the cell membrane if I’m not mistaken. If I am mistaken, please edit this card.

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16
Q

T/F cell signaling leads to the liberation of arachidonic acid?

A

TRue

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17
Q

Which enzymes send the arachidonic acids down the path that leads to prostaglandin production?

A

COX1 and COX2

18
Q

Prostaglandins play a key role in generating and maintaining what?

A

The inflammatory response

19
Q

T/F prostaglandins play a key role in pain sensitization?

A

Truth

20
Q

What does pain sensitization mean?

A

It means that after the injury occurs, the prostaglandins make things hurt more. So it makes sense as to why we would want to inhibit them.

21
Q

How is nociceptor activity enhanced?

A

Prostaglandins activate G proteins that lead to the increased activity of PKA. PKA phosphorylates the TRP type nociceptor and enhances its activity leading to increased pain.

22
Q

NSAIDS all work by inhibition of which enzymes?

A

COX

23
Q

What do COX enzymes do?

A

They drive the production of prostaglandins. Inhibit COX enzymes and you inhibit prostaglandins and if you inhibit prostaglandins you inhibit inflammation

24
Q

Aspirin is a 100x better inhibitor of COX___ than COX___.

A

100x better inhibitor of COX-1 than COX-2

25
Q

Aspirin is a reversible or irreversible inhibitor of COX-1 and COX-2?

A

Irreversible

26
Q

Ibuprofen, naproxen, and acetaminophen are all _____ inhibitors of COX-1 and COX-2.

A

reversible

27
Q

Naproxen is most selective for COX-1 or COX-2.

A

COX-2

28
Q

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

A

Analgesia, antipyretic (fever), anti-inflammatory, anti-thrombotic

29
Q

What are the therapeutic effects ibuprofen and naproxen?

A

Analgesia, antipyretic, and anti-inflammatory

30
Q

What are the therapeutic effects of acetaminophen?

A

Analgesia, antipyretic

31
Q

Aspirin inhibits COX enzymes. Inhibition of COX enzymes inhibits what that is crucial for platelet aggregation?

A

Thromboxane A2

32
Q

Even though all of the NSAIDS we’re talking about inhibit COX enzymes, why is aspirin the only one that has a significant effect on platelet formation?

A

Because aspirin is the only one that irreversibly binds. Everything else has a small change in platelet activity, but when the drug leaves the plasma, normal thromboxane A2 production can resume.

33
Q

T/F, only low doses aspirin are effective at preventing thrombotic events?

A

True

34
Q

Is acetaminophen an anti-inflammatory? Why or why not?

A

No because it never reaches the threshold concentration of the drug necessaryf to produce an anti-inflammatory effect, but it does have enough for pain relief

35
Q

Prostaglandins (made primarily from COX-1 activity) stimulates _____ and ______ secretion that comprise the mucus gel that protects the stomach from digesting itself.

A

mucus and bicarbonate

Thanks prostaglandins

36
Q

Why are COX inhibitors potentially bad for your stomach?

A

If you inhibit COX-1, then you inhibit prostaglandins. If you inhibit prostaglandins, then you inhibit the production of the mucous that lines the stomach. This can lead to bleeding, kidney problems, increased blood pressure

37
Q

What is Reye’s syndrome?

A

It is characterized by a fatty change in the liver and edematous encephalopathy following aspirin use. Generally preceded by a mild upper respiratory tract infection that was managed with aspirin at levels that usually aren’t toxic, but in a person with Reye’s syndrome it is toxic

38
Q

What are some precautions and contraindications for aspirin use?

A

Ulcers- internal bleeding
Diabetes- hyper/hypoglycemia
Gout
Hypo coagulation conditions- bleeding without clotting

39
Q

Selective COX-2 inhibitors are bad. Except for celebrex.

A

Liver failure, cardiac problems

40
Q

Which provides more pain relief, opioids or NSAIDS?

A

Opioids.

41
Q

What is the most effective analgesia?

A

An optimum dose of NSAID and some opioids

Pharmacology #2 (11 decks)

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