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Drug Action > NSAIDs: Non-Steroidal Anti-inflammatory Drugs > Flashcards

NSAIDs: Non-Steroidal Anti-inflammatory Drugs Flashcards

1
Q

What is the traditional NSAID?

A

Aspirin (ASA)
(aspirin, motrin, aleve)

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2
Q

Salicylates vs. non-salicylates?

A

Salicylates – aspirin
Non-salicylates – ibuprofen (Advil)

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2
Q

When was aspirin first produced?

A

Purified acetyl salicylic acid (ASA) helps with pain
Modified structure gave us aspirin (1897), the first synthetic drug to help diminish side effects

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2
Q

Who and which company is aspirin associated with?

A

1894 Bayer pharmaceuticals with Felix Hoffman
Wanted to find something to deal with chronic pain and made a big breakthrough

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3
Q

History of NSAIDS, what plants was ASA/salicin first discovered?

A

1428: white willow extracted
1839: meadowsweet
Extract was salicin

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3
Q

When and how was aspirin’s mechanism of action found?

A

1971 found out the mechanism of action because of John Robert Vane’s research on prostaglandins

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4
Q

Pharmacodynamics of NSAIDs?

A

The cell membrane has a lot of arachidonic acid (fatty acid) which are used to make prostaglandins (EICOSANOIDS, 20 carbon structure)
Phospholipase A removes them from the membrane
Cox 1 and cox 2 are used to make prostaglandins which help with gastrointestinal protection and inflammation and pain

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4
Q

What are prostaglandins?

A
  • Made by almost all cells
  • Autocrine and paracrine functions (act on the same cell and neighboring cells)
  • Rapidly inactivated
    Prostaglandins have multiple roles in normal physiology and pain reaction and inflammation, initiate fever
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5
Q

What is a cyclooxygenase?

A

Cyclooxygenase is a dimer in the ER that forms a ring by adding 2 oxygens
- AA enters one of the two active sites
- It is converted to prostaglandin
- Further modifications to make different subtypes

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6
Q

What are the 2 major cyclooxygenases?

A
  • Cox-1: active all the time, protects the stomach by making gastric mucous
  • Cox-2: inducible after injury, involved un chronic inflammation
    NSAIDS block both types of cyclooxygenases
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7
Q

What do prostaglandins act on?

A
  • Act on GPCRs
  • Subgroups, PGD, PGE, PGF, PGI, PGT (receptors DP1, DP2, …, EP1, EP2…TP1)
  • Different receptors do different things, they are differentially expressed in different parts of the body
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8
Q

Role of prostaglandins, pathologic and physiologic?

A

Pathologic:
Fever, asthma, ulcers, diarrhea, dysmenorrhea, inflammation, bone erosion, pain
Physiologic:
Temperature control, bronchial tone, cytoprotecting, intestinal mobility, myometrial tone, semen viability
Concerned with pathological role when giving drugs
We are Concerned with pathological role when giving drugs

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9
Q

NSAIDS block prostaglandin synthesis to treat 3 main effects?

A

Inflammation – anti inflammatory
Pain – analgesic
Fever – antipyretic

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10
Q

How do prostaglandins create a pain response in the periphery

A

(nerve endings are more sensitized to other mediators because of prostaglandins)
Nociceptors: prostaglandins sensitize to other mediators

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11
Q

How do NSAIDs reduce pain?

A

Pain is initiated in the periphery, travels to spinal cord, then brain
NSAIDS in the periphery start action
Injured cells release PGE2 and other Prostaglandins as well as other mediators, NSAIDs inhibit their production, to prevent them from sensitizing nerve endings to pain.

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12
Q

What type of pain are NSAIDS useful for treating?

A

-Temporary pain, not severe pain
- If more serious or persisting pain use miso
- If cancer pain use opioids but can also use NSAIDS as a mix

  • Relief of mild/moderate pain (headache, toothache, myalgia)
  • Relief of inflammatory disorders (arthritis, osteoarthritis, gout)
  • Reduce fever
13
Q

What other effect does aspirin have?

A

Prophylaxis of myocardial infraction (heart attack) and stroke (aspirin only)
prevents these by reducing blood clots

14
Q

Tissue injury causes?

A

COX activated, prostaglandins synthesized at injury site, sensitize nerve endings to activity of other mediators

15
Q

acute vs chronic inflammation?

A

Acute inflammation: small cut, goes away quickly
Chronic inflammation: arthritis, cardiovascular disease, chronic inflammatory disease, bone muscular and skeletal disease (osteoporosis), cancer

16
Q

What NSAIDs are toxic to cats?

A

ASA and acetaminophen

17
Q

How is fever produced in the body?

A

Fever: produced by activity in hypothalamus (temperature control)
PGE2 raises temperature, (COX-2, PGE2)

18
Q

How is inflammation produced in the body?

A

Take in liquid mediators, monocytes, basophils, neutrophils that release Brady Kinin and PGE2

19
Q

NSAIDs upper GI tract and renal side effects?

A

Stomach creates mucus that sits on top of cells to protect them from the HCl acid in the stomach
Chronic NSAIDS interfere with prostaglandins that make mucus, making the cells exposed to HCl acid
Frequent and serious side effects with chronic use, even make Ulcers
(can antacids be used to prevent this)

20
Q

Therapeutic effects of ASA? (4)

A

Analgesic, anti-inflammatory, and antipyretic effects (usual effects of NSAIDS)
Antithrombotic effects – blocks blood clots

21
Q

How does Aspirin block prostaglandin formation?

A

Acetyl group bound in COX enzyme, serine binds irreversibly
COX can no longer make prostaglandins
Aspirin binds both COX1 and COX2

22
Q

How does aspirin lower risk of thrombosis?

A

Aspirin permanently inactivates platelets (because platelets have no nucleus), but it does not block other cell types
If aspirin inactivates enough platelets, there will be a low risk of thrombosis
Thromboxane A2 activate platelets, fibrinogen binds and can form a clot
Aspirin blocks thromboxane A2 no platelet conformational change, so cannot bind fibrinogen
Long term use lowers colon cancer risk

23
Q

Aspirin metabolism?

A

Metabolism:
Low dose – half life is first order, 3 hours
High dose – half life is zero order, 15 hours

24
Q

aspirin excretion?

A

Excreted: by itself in the kidneys
Depending on the pH, the aspirin will be reabsorbed more or less
Alkaline urine will cause more aspirin to be excreted

25
Q

Aspirin toxicity and OD (salicylism)?

A
  • Headache, tinnitus (ear ringing), dizziness, dim vision, hearing impairment
  • Confusion and drowsiness
  • Sweating and hyperventilation
  • Nausea and vomiting
  • Acid base disturbance

Child resistant lids helped with problems of kids overdose deaths

26
Q

What is Reye’s syndrome?

A

Inflammation in the brain, kids given aspirin, rare, so kids not given aspirin anymore
(this was discovered in phase 4 clinical trials)

27
Q

What do traditional NSAIDs block?

A

cox-1 and cox-2 blockers, ratio varies in amount of blockage

28
Q

Ibuprofen?

A

Temporarily binds to cox, if take aspirin after Ibuprofen, aspirin is blocked and will not go in
Pharmacokinetics:
Metabolism in liver
Excretion in the urine
Most drugs act mostly on cox 1 (aspirin), ibuprofen activity is in the middle

29
Q

VIOXX (Rofecoxib) a Cox2 inhibitor, effects?

A

VIOXX (Rofecoxib) little side effects
After monitored the use in the public
There was a small increase in the rate of cardiovascular problems instead of using cox1 inhibitor
Taken off market
Another drug is left on the market because can be beneficial in some people

30
Q

COX2 inhibitors?

A

Mainly involved with inflammation
- Cox2 inhibitor: vasoconstriction, greater ability for platelet aggregation from cox1 activity
binding site of cox 2 is bigger than cox1

31
Q

Why is acetaminophen not really an NSAID?

A

Acetaminophen (Tylenol):
- Sold even more than aspirin, Ibuprofen
- Analgesic, antipyretic effects
- No anti-inflammatory effects
Acetaminophen only acts in some tissues, endothelial cells and neurons, not platelets or inflammatory cells

32
Q

What does Acetaminophen block to prevent prostaglandin formation?

A

Blocks POX further down in the process of prostaglandin synthesis
NSAIDS block COX further up in the process
Active in the brain and the periphery

33
Q

Acetaminophen metabolism?

A

Short half life
Toxic intermediate (glutathione) conjugation to be excreted
Hepatoxic metabolite, liver makes more and more, liver gets damaged
Alcohol induced CYP2E1, that breaks down acetaminophen to its toxic intermediate

34
Q

Acetaminophen poisoning?

A

0-24 hours: anorexia, nausea, vomiting
24-72 hours: abdominal pain, liver injury
72-96 hours: liver failure

35
Q

Acetaminophen overdose cure?

A

If someone overdoses, give n acetylcysteine – antidote glutathione precursor

Drug Action (18 decks)

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