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NSAIDS Flashcards

1
Q

common uses for NSAIDS

A

acute and chronic pain conditions
cancer-associated pain syndromes
treatment of dysmenorrhea
prevention of thrombosis

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2
Q

example of carboxylic acid

A

acetylated: ASA
nonacetylated: sodium salicylate, salicylamide, difunisal

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3
Q

examples of acetic acids

A

indomethicin, sulindac, tolmetin

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4
Q

examples of proprionic acids

A

ibuprofen, naproxen, COX 2 inhibitors

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5
Q

examples of enolic acids

A

phenylbutazone, piroxicam

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6
Q

examples of pyrrolopyrrole

A

ketorolac

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7
Q

common therapuetic actions of NSAIDS

A

analgesic, antiinflammatory, antipyretic, platelet inhibitory effects

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8
Q

MOA of COX inhibition

A

resulting in decrease in peripheral synthesis of prostaglandins, inhibition of prostaglandin synthesis decreases inflammatory response to surgical trauma, thus decreases peripheral nocioception and pain perception

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9
Q

Two forms of COX

A

COX-1 is present in all tissues

COX-2 inhibitor-specific dugs reduced likelihood of GI toxicity. Is produced primarily at the site of inflammation

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10
Q

NSAID pharmacokinetics

A
  • well absorbed from the GI tract
  • low first pass hepatic extraction
  • highly bound (>95%) to plasma albumin
  • exhibit small volumes of distribution
  • most are weakly acidic. with pK of 3-5
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11
Q

NSAID adverse reactions

A

dyspepsia, renal problems, skin reactions, CNS issues, inhibition of platelet aggregation

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12
Q

rare NSAID reactions

A

blood dyscrasias, erythema, uticaria, pneumonitis, aseptic meningitis, aplastic anemia

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13
Q

NSAIDS and gastric acid

A

prostaglandins go to the paraietal cells and block gastric acid production. If COX is blocked so is prostaglandins, so acid will keep building up causing dyspepsia

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14
Q

NSAID and renal

A

rarely have effects on renal function in healthy individuals.
Renal toxicity can occur, which is likely due to NSAID induced inhibition of prostaglandin synthesis, which inhibits the compensatory mechanism response for renal medullary ischemia.

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15
Q

What NSAID can be prescribed with absolute safety with respect to renal effects

A

ASA

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16
Q

NSAIDS and HTN

A

prostaglandins modulate systemic BP by effects on vascular tone in arteriolar smooth muscle and control of extracellular fluid volume.
Prostaglandins counteract response to vasoconstrictor hormones and can influence sodium balance
NSAIDS may interfere with the pharmacologic control of HTN
Usually clinically insignificant

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17
Q

NSAIDS and coags

A

due to the reversable inhibition of COX NSAIDS inhibit platelet aggregation, lasts about 5 elimination half times (24-96hrs)
Increasing period use, especially ketorolac has sparked debates among surgeons regarding postop bleeding…
conversely- useful after microvascular surgery

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18
Q

ASA and coags

A

ASA induces irreversible inactivation of platelet COX

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19
Q

NSAIDS and aseptic meningitis

A

may follow systemic drug administration especially ibuprofen and H2 receptor agonists
Syndrome is greater in females with underlying autoimmune or collagen vascular disease.
S/S appear within hours but may delay for weeks
Most patietns recover fully when drug is discontinued
Fever is common
Other usual features of meningitis, periorbital edema, conjunctivitis, hypotension, parotitis, fatigue, and seizure

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20
Q

NSAIDS and drug reactions

A

elderly patients are at greatest risk:
most common- oral anticoags and NSAIDS= increased risk of GI hemorrhage
Potassium sparing diuratics + NSAIDS= increased risk of hyperkalemia

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21
Q

NSAID induced decrease in renal function may interfere with clearance of:

A

digoxin, lithium, amoniglycoside antibiotics

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22
Q

NSAIDs may interfere with the antihypertensive actions of

A

beta blockers, diuretics, and ACEI

23
Q

Periop considerations of NSAIDS

A

decrease postop pain and requirements for opioids
adjuvants with neuroaxial opioids
IV is better than IM
exhibit ceiling effect when used for post op pain

24
Q

ASA

A

a salicylate that produces analgesia through its ability to irreversibly acetylate the COX enzyme, leading to a decrease in the synthesis and release of prostaglandins
The leukotriene pathway remains intact in the presence of ASA.
ASA does OT interact with opioid receptors.
And has LITTLE effect on release of histamine or serotonin.

25
ASA pharmacokinetics
Rapidly absorbed from the small intestine Alkalinization of urine may increase urinary excretion, requiring larger doses to achieve plasma concentration. Buffered effervescent preparations undergo a more rapid absorption and achieve higher plasma concentrations with less GI irritation.
26
Is ASA a weak acid or weak base?
Weak acid. pKa 3.5
27
ASA clearance
After absoprtion into systemic circulation, ASA is rapidly hydrolyzed in the liver to salicylic acid. Metabolism occurs in the liver where it conjugates with glycine to form salicylic acid Renal excretion of free s.a. is highly variable from up to 85% of alkaline to as low as 5% in acidic Plasma concentrations increase in presence of renal dysfunction. Elimination half time is 2/3 hours.
28
Clinical uses of ASA
A) analgesic for symptomatic relief of low-intensity pain associated with: HA and arthritis B) Antipyretic C) Anti-platelet- mainstay therapy/prevention of MI and angina and some ischemic strokes.
29
ASA side effects
GI upset, hemorrhagic events, easy bruising, melena, epistaxis, CNS stim, hepatic and renal dysfunction, metabolic alterations, uterine effects, allergic rxn
30
how does ASA increase bleeding time
induces functional defect in platelets that is clinically detectable as prolonged bleeding time. prevention of the formation of thromboxane, platelets are sensitive to small doses. irreversible, lasts the lifespan of the platelet.
31
Avoid is ASA in patients with...
severe hepatic dysfunction, vit K deficiency, hypoprothrombinemia, hemophelia
32
ASA and CNS stim
excessive dosing of ASA may produce: - hyperventilation due to direct stim of medullary vent center - seizures - tinnitus - hyperthermia and dehydration may be the life threatening result of salicylate overdose - metabolic and resp acidosis
33
ASA hepatic dysfunction
salicylates can be associated with increased plasma concentrations of transminase enzymes, indicating hepatic damage is usually reversible
34
ASA Renal Dysfunction
chronic use of ASA has not been shown to increase the incidence of ESRD
35
ASA and metabolic alterations
large doses of salicylates may cause hyperglycemia and glycosuria and may deplete liver and skeletal muscle glycogen Salicylates decrease lipogenisis by partially blocking incorporation of free fatty acids
36
ASA and uterine effects
prolongation of labor by salicylates may reflect loss of uterotropic effects of prostaglandins ASA use is notmally d/c'd before anticipated time of delivery to avoid the potential of postpartum hemorrhage and prolonged labor
37
ASA allergic rxn
rare and life threatening | vasomotor rhinitis, laryngeal edema, bronchoconstriction, CV collapse
38
ASA induced asthma
occurs in 8-20% of al asthmatic adults -greater incidence with rhinosinitus and nasal polyps Occurs within an hour on ingestion -life threatening bronchospasm and hypotension Cross sensitivity between ASA and other NSAIDS must be considered with pts with asthma Not an allergy- response is not immunologic
39
Acetaminophen
``` alternative to ASA -analgesic -antipyretic Especially in patients where salicylates are not recommended -peptic ulcer disease -prolongation of bleeding time ```
40
Acetaminophen Pharmacokinetics
nearly complete after oral administration -no significan binding to serum protiens Converted by conjugation and hydroxylation in the liver to inactive metabolites -only small amount of drug excreted unchanged
41
Acetaminophen side effects
reduction consumption could lower incidence of ESRD 8-10% | Hepatic necrosis and death may accompany a single dose of acetaminophen of >15g
42
indomethacin
methylated inderole derivative -analgesic, antipyretic, an anti-inflammatory MOST potent inhibitor of COX known useful management of arthritis drug of choice for treatment of ankylosing spondylitis Single dose controls cardiac failure in neonates with PDA
43
Indomethacin side effects
severe adverse effects limit the usefulness - GI upset and frontal HA - inhibition of platelet aggregation - allergic rxn and cross sensitivity with salicylates - LFTs may become abnormal - preexisting renal disease patients may experience exacerbation - neutropenia, thrombocytopenia, and aplastic anemia are rare
44
Propionic acid derivatives
Ibuprofen, naproxen, -prominent analgesic, antipyretic and anti-inflammatory agents -useful in treating various form of arthritis NAPROXEN has linger elimination half life
45
side effects of propionic acids
GI and mucosal ulcerations are less than with salicylates platelet function is altered but varies with specific drug assume a hypersensitive to salicylates may also be allergic to propionic acids derivatives
46
what propioic acid is most associated with adverse renal effects?
fenoprofen
47
side effects with warfarin of propionic acids
extensive plasma protein binding to albumin, must decrease dose of warfarin
48
ibuprofen problem
hematopoietic suppression characterized by agranulocytosis and bone marrow granulocytic aplasia associated with chronic use of ibuprofen
49
Ketorolac
Potent analgesic but only moderate anti-inflammatory activity IM or IV - potentiates the anti-nocioceptive actions of opioids - exhibit ceiling effect with respect to post op analgesia - absence of ventilatory or CV depression, little or no effect on biliary tract dynamics
50
Ketorolac dose
30mg= 10mg MSO4 or 100mg Meperidine
51
Ketorolac side effects
inhibits platelet thromboxane production and platelet aggregation bleeding time may be increased increased post op blood loss must be considered and discussed Bronchospasm may occur in patient with nasal polyps, asthma, and ASA sensitivity Cross tolerance between ASA and olther NSAIDS occur regularly
52
Gabapentin (neurontin)
originally for anticonvulsant purposes actual MOA unknown, but believed to act on N type voltage gated calcium channels in the CNS -Many uses including neuropathic pain -Has undergone scrutiny lately for marketing it's off label uses -most common side effects are dizziness and drowsiness little to no abuse potential.
53
Pregabalin (Lyrica)
originally for anticonvulsant purposes - actual MOA unknown but believed to act on N type voltage gated channels in the CNS - many uses including neuropathic pain - little or no abuse potential but has been labeled V by FDA - most common side effects: drowsiness, dizziness

anesthesia pharm (10 decks)

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