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Pharmacology: Exam 3 > Lecture 3: NSAIDs > Flashcards

Lecture 3: NSAIDs Flashcards

1
Q

What does NSAIDs stand for?

A

Non-Steroidal Anti-Inflammatory Drugs

Anti-inflammatory
Analgesic (no pain)
Antipyretic (no fever)

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2
Q

What symptoms does Eicosanoids treat?

A
  • Inflammation (OA, RA)
  • Gastroprotection

Osteoarthritis: OA, Rheumatoid arthritis: RA

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3
Q

List the drugs that are Salicylates

A
  • Aspirin
  • Salicylates
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4
Q

List the drugs that are Arylproionic acids

A
  • Ibuprofen
  • Naproxen
  • Ketoprofen
  • Flurbiprofen
  • Fenoprofen
  • Oxaprozin

Target both COX1/2

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5
Q

List the drugs that are Indoleacetic acids

A
  • Indomethacin
  • Sulindac
  • Etodolac

Target both COX1/2

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6
Q

List the drugs that are Anthranilic acids

A

Meclofenamate

Target both COX1/2

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7
Q

List the drugs that are Enolic acids

A
  • Piroxicam
  • Meloxicam

Target both COX1/2

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8
Q

List the drugs that are Alkanones

A

Nabumatone

Target both COX1/2

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9
Q

List the drugs that are Heteroaryl acetic acids

A
  • Diclofenac
  • Ketorolac

Target both COX1/2

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10
Q

List the drugs that are COX-2 selective

A
  • Celecoxib (First COX-2 Selective)
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11
Q

List the drugs that are Analgesic and Antipyretic

A

Acetaminophen

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12
Q

What is a important fact about Acetaminophen?

A

It is NOT an NSAIDs, does not have any anti-imflammatory properties

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13
Q

What are Eicosanids?

A
  • An Autocoid: local hormone (autocrine, paracrine)
  • Oxygenated products of polyunsaturated fatty acids (diverse biological
  • Short t1/2
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14
Q

Explain the mechanism for Eicosanoid synthesis

A
  1. Arachidonic acid is released from the membrane by lipases, Phospholipase A2 (PLA2) and phospholipase C & DAG lipase
  2. Arachnoid is then oxygenated by four separate routes
  • Lipoxygenase
  • Expoxygenase
  • Cyclooxygenase (COX)
  • Free Radicals (nonenzymatic)

  • Phospholipids: phospholipase A2 (PLA2)
  • Phosphatidylinositides: phospholipase C & DAG lipase
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15
Q

What factors determine the type of Eicosanoid that will be synthesized?

A
  1. The type of cell (neuron vs. hepatocyte)
  2. Cell phenotype (cell subtypes)
  3. Type of cellular stimulation (trauma vs. housekeeping)
  4. Type of polyunsaturated long chain fatty acid (impact of diet)
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16
Q

What are the 3 isozymes produced by cyclooxygnease?

A
  • COX-1
  • COX-2
  • COX-3

Enzyme needed: PGH synthase

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17
Q

For COX-1:

  • How is it expressed?
  • How is it distributed?
  • Explain its function(s)
A
  • Constitutively expressed (always turned-on)
  • Widely distributed in the body
  • Function(s): Important housekeeping functions, Gastric protection
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18
Q

For COX-2:

  • How is it expressed?
  • Explain its function(s)
A
  • Inducible (its expression depends on certain stimulation)
  • Function(s):
    1. Early response gene product to inflammation & immune cells
    2. ↑ in expression by growth factors, tumor promoters, cytokines & endotoxins (lipopolysaccharides)

Cytokines ad Endotoxins could possibly cause the increased temp.

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19
Q

For COX-3:

  • How is it expressed?
  • Explain its function(s)
A
  • Expressed by the COX-1 gene
  • Functions:
    1. Role in CNS mediated pain & fever?
    2. Acetaminophen inhibitor of CNS COX-3 → analgesia, antipyretic
    3. Very weak anti-inflammatory?
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20
Q

What are the 5 GPCR receptors for Eicosanoids and their respective ligand?

A
  • DP1→PGD2
  • EP1→PGE2
  • FP(A,B)→PGF(2⍺)
  • IP→PGI2
  • TP(⍺,β)→TXA2

Pharmacologic effect: Determined by receptor density & type on different cells

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21
Q

What is the function of the ligand PGI2?

PGI2=Prostacyclin

A

Prevents Platelet Aggregation

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22
Q

What is the function of the ligand TXA2?

TXA2=Thromboxane

A

Platelet aggregation

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23
Q

What is the function of PGE2?

PGE2=Prostaglandin E2

A

Gastric Protection

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24
Q

What are the three phases of Inflammation?

A

Acute →Immune →Chronic

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25
Q

Explain what happens during Acute Inflammation

A
  • Initial response to tissue injury, mediated by autacoids
  • Usually precede the immune response, PGI2 & PGE2 mediate vasodilation, vascular permeability, chemotaxis (Attraction to site) & pain
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26
Q

Explain what occurs during the Immune Response of Inflammation including the benefical and deleterious effects

A
  • Activation of T-cells & B-cells in response to foreign substance
  • Beneficial: kill foreign organisms
  • Deleterious: Chronic inflammation without resolution

  • T-cells (T-lymphocytes, cell mediated immunity)
    B-cells (B-lymphocytes, produce antibodies)
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27
Q

Explain what occurs during Chronic Inflammation

A

Release of mediators, which are unique to this phase

  • Interleukins 1, 2, 3 from macrophages & T-cells can cause lymphocyte activation & prostaglandin production
  • Tumor necrosis factor (TNF) from macrophages can cause prostaglandin production
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28
Q

What does prostagladins do for the GI tract

A

Provide gastroduodenal cytoprotection

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29
Q

List the different ways prostagladins provide gastroduodenal cytoprotection to GI tract (5)

A
  1. Maintaining mucosal blood flow
  2. Increased mucus secretion → Maintain neutral pH
  3. Increased bicarbonate secretion→ Neutralize gastric acid
  4. Reduced epithelial H+ permeability → Protect mucosa from H+ permeability
  5. Increased cell turnover → Replace damaged cells with new cells
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30
Q

What occurs when prostaglandins decrease d/t use of NSAIDs?

A

Negative GI effects

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31
Q

What is Rheumatoid arthritis (RA)? Which ages does it affect? Which bones does it affect?

A
  • Chronic inflammation of the synovial tissue results in proliferation of this tissue (pannus) leading to destruction of the joint, e.g., small joints of the hands, wrists & feet
  • Occurs at any age

Synovial tissue lines the joints capsule

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32
Q

What is Osteoarthritis (OA)? Which ages does it affect? Which bones does it affect?

A
  • Most common form of joint disease,
  • It affects nearly 50% of the population older than 65 y/o & virtually everyone over the age of 75
  • Affects primarily the weight-bearing joints, knees, hips & spine
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33
Q

True or False. NSAIDs prevent and reverese RA and OA

A

FALSE
only alleviate some symptoms

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34
Q

What is the mechanism of action for Aspirin (ASA)

Everything that has to do w/ ASA is HIGH yield

Also known as Acetylsalicylic Acid

A
  • Non-selective inhibitor of COX-1/2
  • Irreversibly acetylates COX→No enzymatic activity
  • More potent inhibitor of COX-1/2 than is its salicylate metabolite
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35
Q

Explain the anti-inflammatory therapeutic uses of Aspirin

A
  • Treatment for RA and OA
  • MOA
    1. ↓ PG synthesis
    2. Interferes with the kallikren system
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36
Q

Explain the Kallikrein system that aspirin interferes with

HIGH yield

A
  1. Inhibit granulocyte adherence to damaged vasculature
  2. Stabilize lysosomes
  3. Inhibit the migration of leukocytes & macrophages to site of inflammation
  4. ↓ Bradykinin (9AA) (potent mediator for pain)
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37
Q

A majority of aspirin goes through what chemical mechanism?

A
  • Glycine conjugation
  • 75% becomes Salicyluric acid
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38
Q

List other chemical outcomes for aspirin

A
  • 30% turns into NaHCO3 (sodium bicarb)
  • 10% is renally eliminated as free salicylate
  • 4% turns into NH4Cl

Review Slide 17

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39
Q

What DO you give a patient if they come in w/ an aspirin overdose?

A

NaHCO3 (sodium bicarb)

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40
Q

What do you NOT give a patient if they come in w/ an aspirin overdose?

A

NH4Cl (ammonium chloride)

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41
Q

Explain the antipyretic uses of Aspirin

A
  • Tx for fever
  • Elevated body temp. caused by an infection results from:
    1. Production of prostagladin in response to pyrogens
    2. Interluekin-1 in the hypothalamis which is produced by machrophages
  • Asprin blocks both effects (1 and 2)
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42
Q

Explain the analgesic and antithrombotic uses of Aspirin

A
  • Analgesic: Effective in reducing pain of mild to moderate intensity of varying causes
  • Antithrombotic: ↓TXA2

Review Slide 19 for a list of varying causes

TXA2= platelet aggregator

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43
Q

List the side effects on the Gl tract caused by Aspirin

A
  • Gastritis: at higher doses
  • Undissolved tablet directly irritates the gastric mucosa (↓ by taking w/ meals & water)
  • Non-ionized ASA absorbed in the stomach (acidic)
  • ASA inhibits the protective prostaglandins (PGEs)
  • ↑ incidence of gastric and duodenal ulcers
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44
Q

List the side effects on the CNS caused by Aspirin

A
  • Salicylism: at higher doses, reversible (e.g. tinnitus, ↓ hearing, vertigo)
  • Hyperpnea: direct affect on the medulla oblongata, ↑ ventilation
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45
Q

List the side effects on the kidneys caused by Aspirin

A
  • Reversible ↓ of glomerular filtration rate, especially in patients with underlying renal disease or elderly
  • Inhibition of PG’s (E1,E2,I1)
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46
Q

What drug interaction causes cross reactivity and which drug(s) does not?

A
  • HIGH CROSS REACTIVITY WITH IBUPROFEN
  • Little to no cross reactivity with non-acetylated salicylates

Review Slide 21 for other allergies that could occur in <1% of pts

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47
Q

What is Reye Syndrome?

A
  • Aspirin side effect
  • Acute potentially fatal illness occurring almost exclusively in children under 15 y/o
48
Q

What happens w/ Reye Syndrome?

ASA side effect

A
  • Produces fatty liver with encephalopathy, onset usually follows a viral infection (e.g. Influenza A or B, chicken pox) who took ASA
  • With in 1–7 days, persistent vomiting generally occurs with stupor (near unconsciousness), with possible seizures & coma
49
Q

How can Reye Syndrome be avoided?

A

Give children Acetaminophen (APAP) or Ibuprofen (IBU) during viral infections

Usually don’t give children ASA

50
Q

At low doses, what are the effects and complications of Aspirin?

A

Effects

  • Analgesic
  • Antipyretic
  • Antiplatelet

Complications

  • Gastric intolerance
  • Bleeding
  • Hypersensitivity reactions
  • Impared hemostatsis

Another complication: ↓ elimation of uric acid causes problem w/ gout

51
Q

At higher doses, what are the effects of Aspirin?

A
  • Anti-inflammatory
  • Uricosuric (↑ elimation of uric acid)
52
Q

At mild intoxication of Aspirin what are the complications?

A
  • Central hyperventilation
  • Tinnitus
53
Q

At moderate intoxication of ASA, what are the complications?

A
  • Fever (d/t decoupling of protons)
  • Dehydration
  • Metabolic acidosis

Salicylates impair cellular respiration by uncoupling oxidative phosphorylation which is a possible mechanism for hyperthermia at toxic doses

54
Q

At severe intoxication of ASA what are the complications?

A
  • Vasomotor collapses
  • Coma
  • Hypoprothrombinemia
55
Q

At lethal intoxication of ASA what are the complications?

A

Renal and respiratory failure

56
Q

List the drug interactions that can occur w/ Aspirin

A
  • Ethanol
  • Methotrexate
  • Warfin
  • Valproic acid
  • Spironlactione
  • Sulfonylureas & exogenous insulin
57
Q

What are the effects of the drug interaction btw Aspirin and Ethanol?

HIGH yield

A
  • Ethanol: ↑ GI bleeding
58
Q

What are the effects of the drug interaction btw Aspirin and Methotrexate?

HIGH yield

A
  • Displaced from protein binding site
  • ↓ renal excretion, therefore ↑ its concentration
  • i.e. pancytopenia
59
Q

What are the effects of the drug interaction btw Aspirin and Warfin?

HIGH yield

A

Additive effects on bleeding

60
Q

What are the effects of the drug interaction btw Aspirin and Valproic acid?

A
  • Displaced from protein binding sites
  • ↓ clearance, therefore ↑ free concentrations
  • i.e. drowsiness

Valproic acid used to treat seizures

61
Q

What are the effects of the drug interaction btw Aspirin and Spironolactone?

HIGH yield

A

Inhibits its diuretic effects

Antagonizes aldosterone

62
Q

What are the effects of the drug interaction btw Aspirin and Sulfonylureas & exogenous insulin?

A

Additive hypoglycemic effects (@ doses > 2 g/d)

  • Hypoglycemia effects with sulfonylureas may be synergetic inhibition of K(ATP) activity
  • Glyburide (sulfonylureas)
63
Q

What are some contraindications of Aspirin?

A
  • Patients with hemophilia (bleeding)
  • Pregnant women (bleeding to both)
64
Q

What is the treatment for an Aspirin overdose? What age group is affected the most?

A

Treatment

  • Activated charcoal
  • Hyperthermia: alcohol sponges or ice packs
  • Maintain a high urine output with sodium bicarbonate (alkalinize the urine→ ↑ salicylate excretion)
  • A frequent cause of poisoning in young children
65
Q

List the druges that are Nonacetyled Salicylates

A
  • Choline Salicylate
  • Magnesium Salicylate
  • Sodium Salicylate
  • Sodium Thiosalicylate
  • Salsalate
  • Methyl Salicylate

Oil of wintergreen = methyl salicylate, Bengay brand, topical analgesic contains methyl salicylate

66
Q

What types of drugs are Nonacetylated Salicyates?

A

Effective anti-inflammatory drugs (Not really pain)

Less effective analgiscs than ASA, b/c they are less effective COX1/2 inhibitors

67
Q

When are non-acetylated salicylates preferable compared to ASA?

A

When COX 1/2 irreversible inhibiton is undesirable, more preferable for asthma, bleeding, renal

Similar problems as with ASA, except for specific acetylation problems

68
Q

Which drug is a Salicylate derivative?

A

Diflunisal

69
Q

For Difunisal explain:

  • Mechanism of Action
  • Therapeutic use
  • Side effects
A
  • Mechanism of Action: Nonselective COX-1/2 inhibitor
  • Therapeutic use: Analgesia (Tx for mild to moderate pain-NO fever), RA, OA
  • Side effects: Similar to ASA, except for specific acetylation problems
70
Q

Explain the mechanism of action for Ibuprofen

Arylprpropionic Acids

HIGH yield

A
  • A non-selective inhibitor of COX-1/2
  • A potent COX-3 inhibitor
  • More potent anti-inflammatory effect than ASA (need less of a dose)
71
Q

What are the therapeutic uses of Ibuprofen?

A
  • RA, OA
  • Analgesia (Tx of mild to moderate pain, More effective in men?)
  • Primary dysmenorrhea
  • Antipyretic (Fever)
72
Q

What is an important structutral features of NSAIDs?

A

Have to be an acid

Review Slide 29

73
Q

List the side effects of Ibuprofen?

HIGH yield

A
  • Less GI bleeding than ASA
  • Caution in patients with renal disease or CHF (b/c of ↓ renal blood flow & GFR)
  • !97% cross reactivity in patients with ASA allergy!
  • Contraindicated during the 3rd trimester of pregnancy b/c of ↑ bleeding time, OK during breast feeding
74
Q

List some drug interactions of Ibuprofen and their effects?

Drugs to not take together

A
  • Digoxin, Lithium & Methotrexate: ↑plasma conc.
  • Diuretics, ACE inhibitors, & beta-blockers: antagonize blood pressure loweing effects
  • ETOH: ↑ bleeding time
75
Q

Is it possible to overdose on Ibuprofen? and what is the treatment?

A
  • Minimal signs of toxicity and rarely fatal (VERY HARD TO OVERDOSE)
  • Treatment: Activated charcoal
76
Q

What type of drug is Naproxen and what is its therapeutic use?

A
  • Arylpropionic acid, similar to ibuprofen
  • Treatment: Gout Pain
  • !One of the safest NSAIDs for patients with cardiovascular disease!

Also known as Aleve

77
Q

Which drug is one of the safest NSAIDS in patients w/ cardiovascular disease?

78
Q

What type of drug is Ketprofen? And explain its mechanism of action

A
  • Arylpropionic acid, similar to ibuprofen, although it should NOT be taken during breast feeding
  • MOA: Nonselective COX-1/2 inhibitor & an inhibitor of lipoxygenase
79
Q

List the Arylpronic Acids drugs that are used to treat RA, OA (anti-inflammation)

LOW yield

A
  • Flurprofen
  • Fenprofen
  • Oxaprozin
80
Q

Explain the mechanism of action of Inodomethacin

Indole Acetic Acid

HIGH yield

A

Inhibitor:

  • COX inhibitor (COX-1 > COX-2)
  • Potent COX-3 inhibitor
  • Lipoxygenase inhibitor
81
Q

List the Therapeutic uses of Indomethacin

HIGH yield

A
  • RA, OA
  • Gout: acute pain
  • Patent Ductus Arteriosus (non-surgical closure)
  • Extra-articular inflammation, e.g., pericarditis, pleurisy
82
Q

List the side effects of Indomethacin:

  • GI
  • CNS
    Hematologic
    Renal
A
  • GI: Diarrhea, Abdominal pain, Hemorrhage, Pancreatitis
  • CNS (15-25% incidence): Headache, Confusion, Depression, Psychosis
  • Hematologic: Thrombocytopenia, Aplastic anemia
  • Renal: Hyperkalemia (decreased GFR)
83
Q

What are the contraindication of Indomethacin?

A
  • Contraindicated during pregnancy
  • Use with caution in patients with psychiatric illness & Peptic ulcer disease (PUD)
84
Q

What type of drug is Sulindac?

HIGH yield

A

sulfoxide prodrug reduced to active sulfide

Indole Acetic Acids

85
Q

Explain the mechanism of action of Sulindac

A

COX inhibitor (COX-1 > COX-2)

86
Q

What are the therapeutic uses of Sulindac?

A
  • RA, OA
  • Gout: acute pain
87
Q

List the side effects of Sulindac (4)

A
  • GI & renal
  • Stevens-Johnson syndrome, Toxic epidermal necrolysis
  • Thrombocytopenia, Agranulocytosis
  • Nephrotic syndrome: Proteinuria
  • Cholestatic liver damage: ↑ bile acid, bilirubin
88
Q

For Etodolac explain:

  • what type of drug?
  • Mechanism of action
  • Therapeutic use
  • SIde effects

Indole Acetic Acid

Low yield

A
  • Racemic mixture R = inactive, S = active
  • Mechanism of action
    Nonselective inhibitor of COX-1/2 (COX-2 > COX-1)
    Therapeutic use :OA, Analgesia,
    Gout pain
  • Side effects: Similar to other NSAIDs with less GI toxicity
89
Q

For Tolmetin explain:

  • Mechanism of action
  • Therapeutic use
  • SIde effects

Heteroaryl acetic acid

Low yield

A
  • Mechanism of action: Nonselective inhibitor of COX-1/2
  • Therapeutic use: Rheumatoid arthritis, Osteoarthritis
  • Side effects: Similar to other NSAIDs (e.g., GI, renal)
90
Q

What is the most frequently used NSAID worldwide?

A

Diclofenac

91
Q

Explain the mechanism of action for Diclofenac

Heteroaryl acetic acid

HIGH yield

A
  • Nonselective inhibitor of COX-1/2
  • Potent COX-3 inhibitor
  • Lipoxygenase inhibitor
92
Q

What are the therapeutic uses for Diclofenac?

HIGH yield

A
  • RA, OA
  • Analgesia
  • Primary dysmenorrhea: painful menstruation b/c of XS PG’s e.g., N/V, faintness
93
Q

What are the side effects of Diclofenac?

A

Similar to other NSAIDs e.g., GI , renal, hepatotoxic (4%)

94
Q

What is the treatment for arthritis in patients w/ an ulcer risk?

HIGH yield

A

Arthrotec®: (Diclofenac & Misoprostol)

95
Q

Explain the mechanism of action for Ketorolac

Heteroaryl acetic acid

HIGH yield

A

Inhibitor of COX-1/2/3

96
Q

What are the therapeutic use(s) of Ketoralac?

A
  • Analgesia
    The Tx postoperative acute pain that !requires analgesia at an opioid level! moderately severe pain
97
Q

What are the side effects to Ketoralac?

A
  • Similar to other NSAIDs, e.g., GI , renal, bleeding, allergy, Toxic to the neonate
  • Short term use only, i.e., up to 5 days (d/t toxicity)
98
Q

For Piroxicam explain:

  • Mechanism of action
  • Therapeutic use
  • Side effects
  • Miscellaneous

Enolic Acids (Oxicams)

HIGH yield

A
  • Mechanism of action: Nonselective Inhibitor of COX-1/2 (COX-1>COX-2)
  • Therapeutic use: RA, OA
  • Side effects: Similar to other NSAIDs (GI, renal)
  • Miscellaneous: Primary glucuronide metabolite, Long t1/2 = 42-76 hrs
99
Q

For Meloxicam explain:

  • Mechanism of action
  • Therapeutic uses
  • Side effects
  • Miscellaneous

Enolic Acid

HIGH yield

A
  • Mechanism of action: Nonselective inhibitor of COX-1/2 (COX-2 >COX-1)
  • Therapeutic use: OA
  • Side effects: Similar to other NSAIDs (GI, renal)
  • Miscellaneous: Contraindicated during pregnancy
100
Q

For Nabumetone explain:

  • What type of drug?
  • Mechanism of action
  • Therapeutic uses
  • Side effects
  • Miscellaneous

Alkanone

Low yield

A
  • Prodrug: Ketone→Acetic acid
  • Mechanism of action: Nonselective inhibitor of COX-1/2, (COX-2 > COX-1)
  • Therapeutic use :RA, OA
  • Side effects: Similar to other NSAIDs, e.g., GI, renal
  • Miscellaneous: t1/2 > 24hrs
101
Q

For Mefenamic Acid explain:

  • Mechanism of action
  • Therapeutic uses
  • Side effects
  • Miscellaneous

Anthranilic Acid

Low yield

A
  • Mechanism of action: Inhibitor of COX-1/2 less effective than ASA for Tx of inflammation
  • Therapeutic use: Analgesia- moderate pain, < 1 week of Tx, Primary dysmenorrhea
  • Side effects: Similar to other NSAIDs, e.g., GI, renal, !More toxic than ASA!
  • Miscellaneous: Contraindicated during pregnancy
102
Q

For Meclofenamate explain:

  • Mechanism of action
  • Therapeutic uses
  • Side effects
  • Miscellaneous

Anthranilic Acids

Low yield

A
  • Mechanism of action: Inhibitor of COX-1/2 (COX-1 = COX-2)
  • Therapeutic use: RA, OA, Analgesia: mild to moderate pain, Primary dysmenorrhea
  • Side effects: Similar to other NSAIDs (e.g., GI ,renal), Contraindicated during pregnancy
  • Miscellaneous: Excreted in the urine as a glucuronide metabolite
103
Q

Why was the COX-2 selective drug, Celecoxib created?

A
  • Scientisy thought being more selective for COX 2 would be a great innovation
  • To lessen GI Side Effects

Review Slide 45

104
Q

What type of drug is Celecoxib? and explain its mechanism of action?

COX-2 Selective

HIGH yield

A
  • Sulfonamide
  • MOA: COX-2 selective inhibitor
105
Q

What are the therapeutic uses of Celecoxib?

A
  • RA, OA
  • Familial Adenomatous Polyposis (FAP), Pre-cancerous colorectal lesions, at 40-50 yrs can develop cancer (inhibition of COX-2 mediated angiogenesis)
106
Q

List the side effects caused by Celecoxib

A
  • Ulcers: Celecoxib 1.3% vs. Ibuprofen 3.0% (MORE)
  • MI: (MORE) Celecoxib > Ibuprofen, ↓ PGI2 & ↑ TXA2
  • (FDA suggests no difference in GI toxicity with older NSAIDs)
  • Sulfa allergy
107
Q

Is Acetaminopen (APAP) an NSAID?

A

NO, it is a N-aceyl-para-amino-phenol (AM404)

108
Q

Explain the mechanism of action of APAP

APAP-Acetaminopen

A
  • Inhibitor of CNS COX-3?
  • AM404 inhibits the re-uptake of endocannabinoids → ↑ CB1 activity →→ ↑ 5-HT in descending pain pathways? (which ↓ ascending pain pathway)
109
Q

What are the therapeutic use(s) for APAP?

APAP-Acetaminopen

A
  • Analgesia, Antipyretic
  • Very weak peripheral anti-inflammatory effects
110
Q

What are the side effects caused by APAP?

APAP-Acetaminopen

A
  • Hepatotoxic
  • Nephrotoxic
  • Rash (SJS, TEN)

SJS- Steven Johnson Syndrome
TEN-Toxic epidermal necrolysis

111
Q

A 55-year-old man is prescribed low dose aspirin for myocardial infarction prevention. Which of the following is the most likely mechanism of action?
A. Decreased TXA2
B. Decreased PGI2
C. Increased PGE2
D. Increased PGFα

A

A. Decreased TXA2

112
Q

A 75-year-old woman is diagnosed with rheumatoid arthritis, and she has a history of peptic ulcer disease. Which of the following would provide the best treatment for this patient?
A. Acetaminophen and indomethacin
B. Ketorolac and aspirin
C. Diclofenac and misoprostal
D. Celecoxib and prednisone

A

C. Diclofenac and misoprostal

113
Q
  1. Which of the following is the safest NSAID for patients with a medical history of cardiovascular disease?
    a. Aspirin
    b. Naproxen
    c. Ketoprofen
    d. Indomethacin
A

b. Naproxen

114
Q
  1. Which medication is Cyclooxygenase isozymes are expressed from the COX 1 Gene?
    a. COX1
    b. COX2
    c. COX 3
    d. All of the above
    e. Two of the above
A

e. Two of the above
(COX1 & COX3)

115
Q
  1. Reye syndrome is a potential side effect for which drug?
    a. Aspirin
    b. Ibuprofen
    c. Acetaminophen
    d. All of the above
A

a. Aspirin

116
Q
  1. A 50-year-old male post-op wants a pain killer but refuses any opioids due to history of abuse. Which of the following NSAIDs can be prescribed?
    a. Ibuprofen
    b. Meloxicam
    c. Ketorolac
    d. Meclofenamate
A

c. Ketorolac

117
Q

Which of the following can be used for Patent Ductus Arteriosus?
a. Indomethacin
b. Diflunisal
c. Ibuprofen
d. Sulindac

A

a. Indomethacin

Pharmacology: Exam 3 (8 decks)

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