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MNI (pain pharm) > L38- NSAIDs > Flashcards

L38- NSAIDs Flashcards

1
Q

define NSAIDs and indicate prototype

A

group of drugs involved in antipyretic, analgesic, anti-inflammatory activity

ASA / aspirin is prototype

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2
Q

(1) is the main source of eicosanoids, with (2) as the structural elements. It is converted from cell membrane to (1) by (3), which can be inhibited by (4) drugs.

A

1- arachidonic acid
2- 20C unsaturated FA with 4 double bonds

3- PLA2
4- steroids (inhibition, downregulation)

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3
Q

NSAIDs generally inhibit ______ reaction / cascade- include all components

A

COX-1/2 = cyclooxygenase

-arachidonic acid —-> Prostaglandins: prostacyclin, thromboxanes

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4
Q

arachidonic acid is converted to LTs via ______

A

lipoxygenases

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5
Q

(1) = prostacyclin

(2) is the main thromboxane

A

1- PG-I2

2- TX-A2

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6
Q

______ is mainly responsible for fever and pain responses, include brief mechanism

A

PG-E2:

  • Fever via hypothalamus / anterior pituitary pathway
  • Pain via sensitization of peripheral nerves to pain stimulation
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7
Q

COX-1:

  • (constitutive/inducible) enzyme
  • (2) main location
  • (3) main function
  • major source of (4)
A

1- constitutive
2- gastric epithelium, platelets
3- tissue homeostasis
4- cytoprotective PG formation

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8
Q

COX-2:

  • (constitutive/inducible) enzyme, (2) is the exception
  • major source of (3) and (4)
A

1- inducible via GFs, tumor promoters, CKs
2- constitutive in brain, kidneys

3- eiconasoids in cancer / inflammation
4- prostacyclin (PG-I2)

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9
Q

anti-inflammatory of NSAIDs mostly results from action on COX-(1/2) inhibition

A

COX-2

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10
Q

gastric damage from NSAIDs results from ______ actions

A

COX-1 inhibition + direct irritation

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11
Q

list the all the NSAIDs

A

Selectives (for COX-2): celecoxib, meloxicam

Non-Selectives (PAINKID): piroxicam, aspirin, ibuprofen, naproxen, ketorolac, indomethacin, diclofenac

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12
Q

______ is the main specific use for NSAIDs

A

mild-to-moderate pain: especially inflammatory pain, eg. MSK disorders (RA, OA)

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13
Q

list the two main uses of aspirin beyond its NSAID activity, explain (hint- not post-MI use)

A

1) 50% dec in colon cancer risk

2) adjunct with Niacin (anti-dyslipidemia, lows serum cholesterol) in order to prevent PG mediated intense flushing

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14
Q

______ can be used to close persistent PDA in neonatal life (drug of choice)

A

indomethacin

note- ibuprofen has shown to have equal efficacy and safety

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15
Q

list the main systems that NSAID AEs mostly affect

A
  • GI
  • renal
  • CVS
  • respiratory (NERD)
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16
Q

describe the main GI AE with NSAID use, include mechanism

A

Ulceration:
1) inhibition of COX-1 –> dec in protective components for GI lining (seen in non-selective NSAIDs)

2) direct local irritation of gastric mucosa

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17
Q

to prevent GI AEs, NSAIDs can be co-administered with….

A

misoprostol (PG-E1)
PPIs
H2R blockers

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18
Q

______ has highest risk for GI AEs with NSAID use, ______ has the lowest risk

A

high- Piroxicam (non-selective)

low- celecoxib (COX-2 selective)

19
Q

describe the main CVS AE with NSAID use, include mechanism and if more in selective or non-selective NSAIDs

A

Mostly selective NSAIDs, celecoxib > meloxicam in terms of COX-2 selectivity:

  • Platelets (COX-1) –> inc TX-A2 (selective) –> vasoconstriction, platelet aggregation
  • Endothelial cells can replenish COX-2, but still overall –> dec PG-I2 –> dec vasodilation, dec inhibition of platelet aggregation

=> thrombosis formation —> inc risk of MI, CVA, death

20
Q

compare GI and CVS AEs between selective and non-selective NSAIDs

A

selective: mostly GI issues via COX-1 inhibition

non-selective / coxibs: mostly CVS via only COX-2 inhibition

21
Q

list the two major adverse renal effects from NSAIDs

A
  • dec renal blood flow

- analgesic nephropathy

22
Q

describe mechanism of decreased renal blood flow from using NSAIDs

A

Normal Situations:

  • PGs dilate afferent arterioles => inc RBF
  • Angiotensin II (AGII) constricts efferent arterioles –> inc RBF

CHF / CKD Pts:

  • inc PGs are more important than AGII at maintaining RBF/GFR
  • *-if given NSAID –> dec PGs => dec RBF
23
Q

prolonged and excessive use of NSAIDs may lead to….

A

chronic interstitial nephritis —- papillary necrosis

**use acetaminophen

24
Q

______ is the NSAID that most commonly causes hypersensitivity reactions, explain

A

Celecoxib- contains Sulfonamide –> rxn via allergy

25
Q

NSAID effects on respiratory system:

  • inc in (1) causes (2) response in lungs and (3) symptoms
  • inc in (4) causes (5) response in lungs and (6) symptoms
A

NERD: NSAID exacerbated respiratory disease

1/2/3- inc LT-C4, LT-B4 –> bronchoconstriction:
-wheezing, dyspnea

4/5/6- inc LT-C4, LT-B4 –> vasodilation:

  • flushing, hypotension, shock
  • vasomotor rhiniti, angioedema, urticaria
26
Q

list the drugs that are most concerning when used with NSAIDs

A

ACE inhibitors
corticosteroids
warfarin

27
Q

describe the effect of ACE inhibitors and NSAIDs when co-administered

A

ACEI alone:

  • dec angiotensin II
  • dec inactivation of bradykinin => inc PGs –> vasodilation + dec BP

ACEI w/ NSAID –> dec PG production –> diminishes effects of ACEIs

28
Q

describe ‘triple whammy’ drug interactions

A

Triple Whammy: ACEI + diuretic + NSAID => acute renal injury

  • NSAID –> dec PG => afferent vasoconstriction –> dec GFR
  • ACEI –> dec AG II => efferent vasodilation –> dec GFR
  • diuretic –> dec plasma volume –> dec GFR
29
Q

______ is the main risk with using NSAIDs + corticosteroids

A

inc risk of GI ulceration:

-do not take on empty stomach if they must be taken together

30
Q

______ is the main risk with using NSAIDs + warfarin

A

inc risk of bleeding- especially in susceptible patients (von Willebrand’s, hemophilia)

31
Q

list and explain the contraindications for NSAIDs (hint- 2)

A

1) children/young adults (no ASA or salicylate derivatives):
-Reye’s syndrome = fever + viral-like illness
(use acetaminophen)

2) pregnancy, especially near term
- may cause premature PDA closure

32
Q

list the salicyclates

A

ASA
magnesium choline salicylate
sodium salicylate
salicyl salicylate

33
Q

______ is the major unique feature of ASA compared to other salicylates

A

irreversible inhibition of COX-1/2

34
Q

ASA is metabolized into (1), which may cause (2) casade depending on dosage

A

1- ASA –> **salicylate + acetic acid

2- salicyclare is oxidative phosphorylation uncoupler:

i) inc CO2
ii) at high doses, inc CO2 => hyperventilation
iii) at toxic doses, over stimulation of ventilation => desensitization –> hypoventilation

35
Q

ASA has a (1) effect on platelets, lasting for (2) duration and having (3) as main result

A

1- irreversible inhibition of COX-1
2- 5-7 days = platelet lifespan
3- dec TX-A2 (usually vasoconstriction + platelet aggregation) => prolonged bleeding time

Note- endothelial cells are not as affected at low doses b/c they can make their own COX enzymes

36
Q

describe the relative effects of each of the following on PG-I2/prostacyclin levels and TX-A2 levels:

  • (1) low dose ASA
  • (2) convention NSAIDs
  • (3) COX-2 inhibitors
A

1- slight dec PG-I2, major dec TX-A2

2- major dec in PG-I2 and TX-A2

3- major dec PG-I2, no effect TX-A2

37
Q

ASA:

  • (1) major clinical use
  • (2) CVS use
A

1- mild to moderate pain: RA and other anti-inflammatory + antipyretic

2- cardioprotective –> inhibits platelet aggregation at low doses

38
Q

list the effects of ASA as dose increases

A
  • low dose 81mg, antiplatelet
  • moderate dose 650-1000mg, antipyretic + analgesic
  • high doses 1-6g, anti-inflammatory + tinnitus
  • 6-10g, hyperventilation / respiratory alkalosis
  • 10-20g, fever, dehydration, metabolic acidosis
  • 20-30g, shock, coma, respiratory / renal failure, death
39
Q

describe the metabolism of ASA

A

<1g, first-order kinetics; half-life 3.5hrs
>1g, zero-order kinetics

metabolized by liver –> metabolites excreted by urine

40
Q

list the many AEs of ASA

A
  • GI distress (ulceration)
  • prolonged bleeding time
  • Reye’s syndrome (young people)
  • hypersensitivity
  • hepatic injury at high doses
  • anti-uricosuric effect (inc serum uric acid)
  • salicylism
41
Q

describe the anti-uricosuric effect

A

with use of ASA:

  • uric acid is excreted into renal tubule via OAT (organic acid transporter)
  • ASA competes with uric acid for OAT
  • dec uric acid secretion
  • hyperuricemia

(avoid use in gout Pts)

42
Q

(1) describe salicylism

(2) describe acute salicylate intoxication

A

1- (mild chronic salicylate intoxication) HA, dizziness, tinnitus, mental confusion, hyperventilation

2:

  • mixed respiratory alkalosis and metabolic acidosis
  • respiratory failure is usual cause of death
  • circulatory collapse may occur
43
Q

Acetaminophen is a metabolite of (1) and its MOA is (2), giving it (3) activity in terms of clinical use, but not (4).

A

1- phenacetin
2- weak COX-1/2 inhibitor
3- analgesic, antipyretic
4- anti-inflammatory

44
Q

______ may accumulate in acetaminophen overdose

A

NAPQI = N-acetyl-p-benzoquinone imine

MNI (pain pharm) (8 decks)

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