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Pharmacology > NSAIDS > Flashcards

NSAIDS Flashcards

1
Q

Which 3 symptoms do NSAIDS treat?

A

inflammation
fever
pain

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2
Q

What are the 3 classes of NSAIDS?

A

1) Aspirin and Salicylic Acids
2) Non-selective and traditional NSAIDS
3) COX-2 specific inhibitors

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3
Q

What is the shared mechanism of all NSAIDS?

A

inhibiting activity of cylooxygenase enzymes

prevent conversion of arachadonic acid to prostaglandins and thromboxane

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4
Q

COX-1 is associated with _____________________ while COX-2 is associated with _____________________.

A

1: regulating homeostasis
2: inflammatory response

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5
Q

How do NSAIDS prevent conversion of arachadonic acid into prostaglandins and thromboxane?

A

prevent binding of arachadonic acid to active site

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6
Q

What are 2 aspirin specific indications?

A

1) Stroke/MI prevention

2) inhibition of platelet activaion

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7
Q

Other than inflammation, pain, fever, what are some lesser known indications of NSAIDS?

A

promote closure of patent ductus arteriosus

cancer prevention

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8
Q

True or False: all NSAIDS act as competitive COX enzyme inhibitors?

A

FALSE; aspirin is non-competitive (covalently modifies enzyme permanently)

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9
Q

What is aspirin’s mechanism of action?

A

irreversible non-competitive COX inhibitor

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10
Q

Which Cox enzyme is inducible?

A

2 (induced in response to pro-inflammatory stimuli)

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11
Q

Where is Cox1 located? Cox2?

A

1: ubiquitously
2: induced in macs, monocytes (low level constitutive expression in kidney and endothelium)

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12
Q

What 3 housekeeping functions does COX-1 perform?

A

1) platelet regulation
2) kidney function
3) stomach acid/mucous production

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13
Q

What 3 effects do prostaglandins produced by Cox-2 have on the body?

A

1) increased vasodilation (increased blood flow)
2) increased migration of phagocytes
3) increased vascular permeability (increased edema)

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14
Q

True or false: PGs generate pain response

A

FALSE; they increase response to painful stimuli (decrease activation threshold for pain stimuli)

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15
Q

How do NSAIDS impair fever generation?

A

Fever: caused by IL-1 and TNF being produced in periphery and go to CNS to induce COX2 to make PGE2 which causes fever

NSAIDS inhibit COX2

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16
Q

What 5 housekeeping functions is COX1 responsible for?

A

1) GI tract (cytoprotective for stomach lining)
2) cardiovascular system (regulates BP)
3) Kidney (PGs promote vasodilation, GFR, maintain normal renal blood flow)
4) Female reproduction (PGs cause too many cramps, helps birth)
5) Control of ductus arteriosus (PGs keep this open)

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17
Q

What is aspirin’s mechanism of action?

A

irreversibly inhibits COX-1 by acetylating the enzyme within its active site

(also inhibits COX-3 but much less potently)

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18
Q

What is the predominant COX in the stomach?

A

COX-1

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19
Q

What do PGs do in the stomach?

A

1) inhibit gastric acid section
2) increase gastric bicarb production
3) increase gastric mucous production
4) increase vasodilation

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20
Q

Platelets only express ______ and produce ____________.

A

COX-1

Thromboxane

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21
Q

Endothelial cells express __________ and produce _______________

A

COX-1 and 2

PGI2

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22
Q

True or false: endothelial cells produce thromboxane

A

FALSE; lack TXA2 synthase

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23
Q

Which PG promotes platelet aggregation? Which one inhibits it?

A

Thromboxane promotes

PGI2 (prostacyclin) inhibits platelet agg

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24
Q

Can NSAIDS delay or promote labor?

A

DELAY (because prostaglandins are needed in labor)

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25
Q

When is it appropriate to give NSAIDS to an infant?

A

in cases where ductus does not close spontaneously (after 12-24 hours)

PGs keep it open so you want to block those

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26
Q

Rank these 3 drugs with their specificity for COX1 inhibition?
ibuprofen, naproxen, aspirin

A

strongest to least

aspirin>naproxen>ibuprofen

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27
Q

Is aspirin an acid or a base?

A

weak acid (rapidly absorbed in stomach)

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28
Q

True or false: both aspirin and salicylic acid inhibit COX1 and 2 and are anti-inflammatory

A

true

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29
Q

Where is aspirin metabolized?

A

serum (rapidly to salicylic acid and acetic acid)

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30
Q

True or false: aspirin is equally potent inhibitor of Cox1 and 2

A

FALSE (more potent for 1)

31
Q

What are 5 indications for aspirin?

A

1) muscle pain
2) inflammatory disease (RA)
3) fever reduction
4) prophylactic prevention of cardiovascular events
5) cancer prevention?

32
Q

What are the doses for aspirin effects?

A

anti-platelet: 80mg
analgesic: 2400mg
anti-inflammatory: 4000-6000mg

33
Q

Describe the unique indication for aspirin?

A

1) treatment in stroke
2) secondary prevention of CVID after stroke
3) prophylactic treatment for primary prevention of stroke and MI in high risk individuals

34
Q

Describe the mechanism of action in low dose aspirin?

A

first acetylates COX1 in platelets PERMANENTLY inhibiting activity and production of pro-thrombic agent TXA2 (LASTS FOR LIFETIME OF PLATELET - 7 DAYS)

Overall: inhibits TXA2 and spares PGI2 promoting anti-thrombogenic environment

35
Q

Why does the baby aspirin not affect endothelial cells as much?

A

they can re-synth COX1 so they can still make PGI2 (an inhibitor of platelet aggregation)

36
Q

What happens at high doses of aspirin?

A

anti-platelet effect of inhibiting TXA2 is offset by increased inhibition of PGI2 (which inhibits platelet aggregation — therefore, you now promote platelet aggregation)

37
Q

Why is Diflusinal NOT given to patients running a fever?

A

does not cross BBB

38
Q

What group is diflusinal in?

A

salicylic acids

39
Q

When are salicylic acids preferred to aspirin?

A

1) increased risk of GI complications

2) increased risk of bleeding

40
Q

True or false: salicylates are protein bound

A

true (compete with warfarin and sulfonylureas)

41
Q

Can aspirin be toxic?

A

YES! at 10-30g in adult; 3 in child - metabolised by 1st order kinetics but switch to zero at high dose

42
Q

How do you treat salicylate toxicity?

A

alkalinization of urine with sodium bicarb

43
Q

What are traditional NSAIDS used for that aspirin is not?

A

treatment of acute gout

44
Q

What is the main hallmark to ibuprofen?

A

RAPID ONSET (15-30 mins) ideal for fever treatment/acute pain

45
Q

What is the hallmark of Naproxen?

A

LONG HALF LIFE (twice daily dosing) and RAPID ONSET (60 mins)

46
Q

What is the hallmark of Oxaprozin?

A

VERY LONG HALF LIFE (50-60 hours - once daily dosing)

47
Q

What are the hallamarks of Indomethacin?

A

10-40X MORE POTENT THAN ASPIRIN (not tolerated as well) but used to promote DUCTUS CLOSING

48
Q

What is the hallmark of Ketorolac?

A

IV ANALGESIC FOR POST SURGICAL PAIN (replacement for morphine)

49
Q

What is the hallmark of diclofenac?

A

most potent but selective for COX2

50
Q

What are 2 biggest concerns for adverse effects of aspirin and tNSAIDS?

A

1) GI toxicity
2) kidney impairment

(also Reye’s and increased risk of gout - specific to aspirin)

51
Q

What is the most common adverse effect of all NSAIDS?

A

GI toxicity (direct damage to epithelial cells due to ion trapping. Also inhibiting COX1 in stomach blocks gastric protective effect of PGs)

52
Q

What drug can help mitigate gastric toxicity caused by NSAIDS?

A

Misprostol (PGI analog)

Omeprazole (proton pump inhibitor)

53
Q

True or false: all patients experience adverse NSAID effects on kidneys

A

FALSE (PGs do not normally play a major role in renal hemodynamics)

54
Q

What do adverse kidney effects look like on patients with NSAIDS?

A

vasoconstriction (renal ischemia, decreased GFR)

55
Q

What is a rare but clinically important effect of NSAIDs on the kidney?

A

acute interstitial nephritis and nephrotic syndrome (inflammatory cell infiltration many months after exposure)

analgesic nephropathy/chronic interstitial nephritis (with chronic daily overuse of drug over many years)

56
Q

True or false: NSAIDS increase risk of heart attack and stroke?

A

TRUE except aspiring (and naproxen)

only in high dose and chronic treatment

57
Q

Do high dose aspirin/NSAIDS promote vasoconstriction or dilation?

A

constriction (exacerbating hypertensive patients)

58
Q

Why can you not take NSAIDS before surgery?

A

increases chances of bleeding

59
Q

What does a hypersensitivity reaction to NSAIDS look like?

A

severe asthma attack (aspirin patients are sensitive to all NSAIDS)

caused by build up of leukotrienes made by build up of arachidonic acid

60
Q

When are NSAIDS not allowed during pregnancy?

A

after 30 weeks (close ductus)

can delay labor too though (block stimulatory PGs)

61
Q

What is Reye’s

A

fatal liver degenerative disease and associated encephalitis

62
Q

How does aspirin increase risk of gout?

A

inhibits renal anion transporter responsible for uric acid excretion

63
Q

What are the clinical effects of NSAIDS primarily due to?

A

inhibition of COX2

64
Q

What is the reasoning for COS2 selective inhibitors

A

they should exhibit potent anti-inflammatory effects without adverse COX1 inhibition effects

65
Q

What are COX2 inhibitors primarily used for? (celecoxib)

A

RA and osteoarthritis

66
Q

What are the adverse effects of celecoxib?

A

renal toxicity

CARDIOVASCULAR (why they are not a first choice)

67
Q

What causes the increased CVID risk in celecoxib?

A

more thromboxane rich environment

68
Q

What are 6 contraindications to NSAIDS?

A

1) history of GI ulcers
2) patients with renal disorders
3) bleeding disorders
4) history of CVD
5) patients with hypersensitivity to an NSAID
6) pregnancy

69
Q

what are 3 important NSAID drug interactions?

A

1) Lithium - decreased renal clearance of lithium (increased lith tox)
2) Methotrexate - impaired clearance (increased meth tox)
3) aminoglycosides - decreased clearance

70
Q

What 3 things should dictate choice of NSAID?

A

1) clinical efficacy
2) safety
3) cost effectiveness

71
Q

How does Acetaminophen work?

A

inhibit COX1/2 in the CNS

72
Q

what is the functional part of acetaminophen?

A

the active metabolite AM404

73
Q

What enzyme antagonizes effects of acetaminophen?

A

hydroperoxidase

74
Q

True or false: acetaminophen inhibits COX in peripheral tissues

A

FALSE

Pharmacology (21 decks)

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