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pt > L18 and L19 NSAIDS > Flashcards

L18 and L19 NSAIDS Flashcards

1
Q

inflammation

A

-Occurs upon infections or noxious stimuli.
-Eliminates harmful agents (e.g. microbes, toxins) and necrotic cells.
-Initiates the healing process.
-May injure normal tissues

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2
Q

how may an infection injure normal tissues

A

-Too strong response (severe infection)
-Prolonged response (persistent or recurrent infection)
-inappropriate response (self-antigens in autoimmune diseases)

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2
Q

signs of inflammation

A

-Heat (calor)
-Redness (rubor)
-Swelling (tumor)
-Pain (dolor)
-Loss of function (functio laesa)

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3
Q

chemical mediator of inflammation

A

-vasoactive amines
-eicosandoids
-platelet-activating factor (PAF)
-cytokines
-complement components
-coagulation and kinin systems

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4
Q

what are kinds of eicosanoids of inflammation

A

protaglandins, leukotrienes, and lipoxins

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4
Q

what are vasoactive amines of inflammation

A

histamines and sertonin

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5
Q

what are cytokines that cause acute inflammation

A

-tumor necrosis factor (TNF), interleukin-1 (IL-1), chemokines

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6
Q

what are the chemokine that cuase chronic inflammation

A

interferon-y (IFN-y)

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7
Q

what are the kinds of complement compounds of inflammation

A

C3a and C5a

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8
Q

what are the coagulation and kinin systems of inflammation

A

bradykinin, thrombin, and fibrinopeptides

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9
Q

eicosanoid

A

-short lived mediators (second to minutes)
-autocrine and paracrine signaling
-bind to G-proteins coupled receptors (GPCRs) in the target cells
*generation of cAMP (Gs)–> dilation
* release of calcium (Gq)–> constriction

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10
Q

eicosanoid: PGE2

A

-dilation of blood vessels, bronchi
-oxytocic dilation in uterus

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11
Q

eicosanoids: PGF2a

A

-constriction of blood vessels, bronchi
-oxytocic constriction of uterus

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12
Q

eicosanoids: PGI2

A

-dilation of blood vessels
-inhibits aggregation in platelets

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13
Q

eicosanoids: TXA2

A

-constriction of blood vessels
-aggregation of platelets

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14
Q

arachidonic acids

A

-20-carbon polyunsaturated fatty acids
-Essential fatty acids
-Most abundant and important precursor of eicosanoids
-Released from membrane phospholipids by phospholipase A2 (PLA 2 ).
-Corticosteroids suppresses the production of phospholipase A2 .

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14
Q

oxygenation of arachidonic acid

A

-PGH synthase (COX) pathway
-Lipoxygenase pathway
-Epoxygenase (cytochrome p450) pathway
-Isoprostane pathway (free radical reaction

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15
Q

PGH synthase

A

-PGH synthase has both cyclooxygenase and hydroperoxidase activities.
-Cyclooxygenase (COX) reaction
*Radical-mediated oxidation
-Hydroperoxidase reaction
*Conversion of a hydroperoxyl group (-OOH) to a hydroxyl group (-OH

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16
Q

what are the two isoforms of PGH synthase

A

-PGH synthase 1
-PGH synthase 2
-inhibited by nonsteridal anti inflammatory drugs (NSAIDS)

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16
Q

PGH synthase 1

A

-COX-1
-Constitutively expressed in various tissues.
-“Housekeeping” functions, e.g. gastric cytoprotection

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17
Q

PGH synthase 2

A

-COX-2
-Expressed upon stimulus in inflammatory and immune cells.
-Stimulated by growth factors, tumor promoters, and cytokines.

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18
Q

alprostadil

A

-eicosanoid drug
-PGE 1
-Relaxes smooth muscles and expand blood
vessels.
-used for erectile dysfunction by injection or as a suppository

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19
Q

misoprostol

A

-eicosanoid drug
-PG F 1 derivative
-cytoprotective
-prevents peptic ulcers
-terminated early pregnancy in combination with mifeprestone

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20
Q

latanoprost

A

-eicosanoid drug
-Topically active PGF 2a derivative (prodrug)
-Constrict blood vessels.
-Used in ophthalmology to treat high pressure
inside the eye (ex. glaucoma)

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20
Q

prostacyclin

A

-eicosanoid drug
-PGI 2
-Powerful vasodilator
-Inhibitor of platelet aggregation
-Used to treat pulmonary arterial hypertension
by IV injection or inhalation.
-Should not be used with anticoagulants.

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21
Q

activites of NSAIDs

A

-Anti-inflammatory
-Analgesic
-Antipyretic

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22
Q

uses of NSAIDs

A

-Treatment of moderate pain, fever, and inflammation from acute inflammation
-Treatment of early-stage rheumatoid arthritis and osteoarthritis
-Cancer preventio

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23
Q

mechanisms of action NSAIDs

A

-Inhibition of prostaglandin endoperoxide H synthase (PGHS or COX), which catalyzes the formation of prostaglandins.
-Many NSAIDs inhibit both COX-1 and COX-2

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24
Q

classes of NSAIDs

A

-salicylates
-arylacetic acids
-arylpropionic acids
-non carboxylase NSAIDs
-COX 2 selective NSAIDs

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25
Q

Gastrointestinal side effects of NSAIDs

A

-Mild (common): dyspepsia, nausea, vomiting
-severe (rare: blood loss, ulcer, GI hemorrhage
-administration with food may decreases GI side effects.
-Aspirin ~ indomethacin > naproxen > sulindac

26
Q

mechanisms of gastrointestinal effects of NSAIDs

A

-Acidity of many NSAID –> primary insult
-Inhibition of synthesis of cytoprotective prostaglandins (PGEs) in gastric mucosa->secondary insult
-Inhibition of platelet aggregation (increased tendency of bleeding)

27
Q

blood coagulation side effects of NSAIDs

A

-Aspirin prolongs bleeding time by irreversible inhibition of platelet COX-1 and the consequent reduced formation of thromboxane.
-Aspirin use before surgery or tooth extraction is contraindicated.
-can be used to some patients with cardiovascular disease to prevent blood
coagulation.

28
Q

renal side effects of NSAIDs

A

-Little effect in normal patients.
-Renal failure in patients with cardiovascular, hepatic, and renal diseases

29
Q

Hypersensitivity side effects of NSAIDs

A

-Characterized by skin rashes, hives, angioedema, and an asthma-like syndrome
(blocked by 5-lipoxygenase inhibitors).
-Occurs in 0.3% of the population (10% in asthmatics).

30
Q

reye’s side effects of NSAIDs

A

-specific to salicylates
-A rare, acute, life-threatening condition characterized by vomiting, delirium, an coma (20-30% mortality)
-Brain damage is common in survivors.
-Occurs in children who have had the flu or chicken pox.
-Aspirin should not be given to anyone under the age of 12 who has a fever

31
Q

CNS side effects of NSAIDs

A

-Tinnitus
-Dizziness
-Headache

32
Q

misoprostol prevention of GI side effects

A

-Synthetic PGE1 analog
-Used prophylactically to prevent NSAID-induced gastric ulcers in patients at high risk

33
Q

Proton pump inhibitors (e.g. esomeprazole) prevention of GI side effects

A

-Greatly reduce acid secretion in stomach and protect against ulceration in the
absence of COX-1 activity.

34
Q

drug interactions of NSAIDs

A

-Many NSAIDs are highly bound to serum albumin (typically 90-99%).
-NSAIDs may compete for serum albumin binding sites with other drugs that are
highly bound to these sites

34
Q

combination products to prevent GI side effects

A

-Naproxen/esomeprazole
-Naproxen/misoprostol
-Diclofenac/misoprosto

35
Q

examples of drug interactions of NSAIDs

A

– combination with oral anticoagulants
-Increases the plasma concentration of free anticoagulant.
-The ability of salicylate to produce GI bleeding and inhibit the clotting mechanism aggravates the problem.
-Necessitates a possible decrease in the dosage of anticoagulant

36
Q

structure activity relationships in NSAIDs

A

-Commonly contains an acidic group (e.g. carboxylic acid)
-the acidic group is located one carbon atom adjacent to an aromatic or heteroaromatic ring.
-Substitution of a methyl group on the carbon atom separating the acidic group from the aromatic ring (acetyl  propionic) tends to increase activity (“profens”).
-A second area of lipophilicity (aromatic or alkyl) that is noncoplanar with the aromatic or heteroaromatic ring generally enhances activity

37
Q

salicylates

A

-salicylic acid
-aspirin
-salsalate
-disunisal

38
Q

salicylic acid

A

-salicylate
-First obtained in 1838 from salicin, a glycoside present in willow and poplar bark (from Latin salix, willow tree).
-Hippocrates prescribed chewing willow bark for pain relief in the 5th century BC (no formal record).
-Sodium salicylate was used as an antipyretic /antirheumatic agent in 1875.
-Slightly acidic (pKa = 3.0)
-absorbed as an ionic form from the small intestine and, to lesser extent, from the stomach as an acid form.
-Inhibits COX-1 and COX-2 reversibly.
-May suppress COX-2 induction.

39
Q

aspirin (acetylsalicylic acid)

A

-salicylate
-prepared in 1853 but was used as a drug in 1899.
-The only NSAID that irreversibly inhibits COX by acetylating a serine residue in the active site.
-Absorbed largely as the intact form but hydrolyzed rapidly to salicylate by plasma esterase.
-2-fold more potent than salicylic acid as analgesic/antipyretic.
-Blocks platelet-aggregating factor TXA 2 effectively; increases the risk of bleeding
but also reduces the risk of myocardial infarction.
-Not stable in solutions

40
Q

salsalate

A

-salicylate
-Dimer of salicylic acid
-Hydrolyzed to two salicylates in the small intestine and absorbed.
-Does not cause GI bleedin

41
Q

diflunisal

A

-salicylates
-More potent analgesic than aspirin, but produces fewer side effects.
-Less antipyretic activity than aspirin.
-3-4 fold longer t 1/2 than aspiri

42
Q

arylacetic acids

A

-indomethacin
-sulindac
-etodolac
-diclofenac

43
Q

indomethacin

A

-One of the most potent NSAIDS in use
-High incidence of side effects
-Not suitable for a long-term use.
-Not stable in solution due to the hydrolysis of the amide bond.

44
Q

sulindac

A

-Prodrug; the sulfoxide group is reduced to the active sulfide intermediate in the circulatory
system.
-Less GI side effects.
-Suitable for a long-term use to treat chronic inflammation

45
Q

etodolac

A

-Pyranocarboxylic acid
-As potent as indomethacin.
-Somewhat selective for COX-2.
-Less GI bleeding
-suitable for long-term use to manage osteoarthritis

46
Q

diclofenac

A

-The most widely used NSAID in the world.
-As potent as indomethacin
-Somewhat selective for COX-2.
-inhibits both COX and lipoxygenase pathways

47
Q

arylpropionic acid

A

-ibuprofen
-naproxen
-ketorolac

47
Q

ibuprofen

A

-Popular OTC analgesic
-More potent than aspirin, but less potent than indomethacin.
-Moderate degrees of gastric irritation
-α-Methyl group enhances it activity and reduces many side effects.
-Bioequivalent racemic mixture
-S-(+)-enantiomer possesses greater activity in vitro.
-R-(-)-enantiomer is converted to S-(+)-enantiomer enzymatically in vivo.

48
Q

ketorolac

A

-Cyclized heteroarylpropionic acid derivative
-Short-term management of moderate to severe pain.
-Analgesic activity similar to centrally acting analgesics.
-Widely accepted alternative to narcotic analgesics.

49
Q

naproxen

A

-S-(+)-enantiomer
-More potent than ibuprofen.
-Moderate degrees of gastric irritation.
-Used to treat rheumatoid arthritis and osteoarthritis

50
Q

non-carbocylates

A

-nabumetone
-meloxicam

50
Q

nabumetone

A

-Nonacidic prodrug
-Metabolized rapidly to 6-methoxynaphthalene-acetic acid (6-MNA), which is an effective inhibitor
of COX.
-Minimum gastric side effects.
-Potent anti-inflammatory, but weak analgesic activity

51
Q

meloxicam

A

-Belongs to the oxicam class, which resembles the peroxy radical intermediate in COX.
-Enolic acid
-Long acting; single daily dose.
-As potent as indomethacin.
-Somewhat selective for COX-2

52
Q

consequences of COX-1 inhibition

A

-Stomach irritation and ulceration
*Decreased production of cytoprotective prostaglandins
*Bleeding from inhibition of thromboxane formation
-Blockade of platelet aggregation
-inhibition of uterine motility
-Inhibition of prostaglandin-mediated renal function
-Hypersensitivity reactions
-Preferential inhibition of COX-2 gives anti-inflammatory effects with lower incidence of gastric ulceration

52
Q

selectivity COX-2 inhibitors

A

-Valine in the NSAID binding site of COX-2 is substituted for isoluecine in that of COX-1.
-Selective COX-2 inhibitors exploit the larger NSAID binding site in COX-2 with larger and relatively rigid substituents.
-FDA classifies only celecoxib, rofecoxib, and valdecoxib as selective COX-2 inhibitors (“coxib”)

53
Q

side effects of selectivity COX-2 inhibitors

A

-Selective inhibition of COX-2 results in elevated
blood pressure and accelerated atherogenesis.
-Constitutive expression of COX-2 in endothelium is critical for production of PGI2 (prostacyclin)
-selective COX-2 inhibitors do not affect the
production of TXA2 by COX-1; heightened
thrombotic response on the rupture of
atherosclerotic plaque.
-Selective COX-2 inhibitors increase
cardiovascular hazard (heart attack and stroke).
-Merck withdrew rofecoxib from the US market
in 2004.
-Pfizer withdrew valdecoxib from the US market
in 2005.

53
Q

celecoxib

A

-First NSAID to be marketed as selective COX-2 inhibitor.
-Used for osteoarthritis and rheumatoid arthritis.
-Good efficacy against pain, inflammation, and fever.
-As potent as naproxen.
-Less risk of GI side effects.
-No antiplatelet activity

54
Q

activities of acetaminophen

A

-Analgesic and antipyretic effects similar to aspirin.
-Much weaker as an anti-inflammatory agent

55
Q

mechanisms of action of acetaminophen

A

-Does not inhibit arachidonic acid binding to PGHS.
-Scavenges peroxynitrite required for PGH synthase activity.
-Peroxynitrite is the major oxidant for PGH synthase activity in the CNS.
-In inflammation, high concentrations of peroxides are present, and
acetaminophen scavenging is overwhelmed

56
Q

fewer adverse effects compared to aspirin

A

-Lower incidence of gastrointestinal disturbance.
-Tolerated in patients with blood coagulation disorders.
-Not associated with Reye’s syndrome.
-May cause a rash but a low incidence of hypersensitivity.
-Does not cross-react with aspirin

57
Q

hepatoxicity at toxic dose acetaminophen

A

-Cytochrome P450-mediated N-hydroxylation to form N-acetylimidoquinone,
which reacts with glutathione.
-toxic doses overload the glutathione, and cell damage occurs in the liver.

58
Q

eicosanoids

A

-Alprostadil (Edex®)
-Misoprostol (Cytotec®)
-Latanoprost (Xalatan® , Monopost ®)
-Prostacyclin (Epoprostenol ®

59
Q

salicylates

A

-Salicylic acid
-Aspirin
-Salsalate (Disalcid®)
-Diflunisal (Dolobid ®

60
Q

arylacetics acids

A

-Indomethacin (Indocin®, Tivorbex®)
-Sulindac (Clinoril ®)
-Etodolac (Lodine®)
-Diclofenac (Cataflam® ,Voltaren®

61
Q

arylpropioic acids

A

-Ibuprofen (Advil ®, Motrin®)
-Naproxen (Aleve ®)
-Ketorolac (Toradol ®, Biorolac®

61
Q

Selective COX-2 inhibitor

A

Celecoxib (Celebrex ®)

62
Q

non-carboxylates

A

-Nabumetone (Relafen®)
-Meloxicam (Mobic®, Vivlodex®)

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