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)
2
Q
What symptoms does Eicosanoids treat?
A
- Inflammation (OA, RA)
- Gastroprotection
Osteoarthritis: OA, Rheumatoid arthritis: RA
3
Q
List the drugs that are Salicylates
A
- Aspirin
- Salicylates
4
Q
List the drugs that are Arylproionic acids
A
- Ibuprofen
- Naproxen
- Ketoprofen
- Flurbiprofen
- Fenoprofen
- Oxaprozin
Target both COX1/2
5
Q
List the drugs that are Indoleacetic acids
A
- Indomethacin
- Sulindac
- Etodolac
Target both COX1/2
6
Q
List the drugs that are Anthranilic acids
A
Meclofenamate
Target both COX1/2
7
Q
List the drugs that are Enolic acids
A
- Piroxicam
- Meloxicam
Target both COX1/2
8
Q
List the drugs that are Alkanones
A
Nabumatone
Target both COX1/2
9
Q
List the drugs that are Heteroaryl acetic acids
A
- Diclofenac
- Ketorolac
Target both COX1/2
10
Q
List the drugs that are COX-2 selective
A
- Celecoxib (First COX-2 Selective)
11
Q
List the drugs that are Analgesic and Antipyretic
A
Acetaminophen
12
Q
What is a important fact about Acetaminophen?
A
It is NOT an NSAIDs, does not have any anti-imflammatory properties
13
Q
What are Eicosanids?
A
- An Autocoid: local hormone (autocrine, paracrine)
- Oxygenated products of polyunsaturated fatty acids (diverse biological
- Short t1/2
14
Q
Explain the mechanism for Eicosanoid synthesis
A
- Arachidonic acid is released from the membrane by lipases, Phospholipase A2 (PLA2) and phospholipase C & DAG lipase
- Arachnoid is then oxygenated by four separate routes
- Lipoxygenase
- Expoxygenase
- Cyclooxygenase (COX)
- Free Radicals (nonenzymatic)
- Phospholipids: phospholipase A2 (PLA2)
- Phosphatidylinositides: phospholipase C & DAG lipase
15
Q
What factors determine the type of Eicosanoid that will be synthesized?
A
- The type of cell (neuron vs. hepatocyte)
- Cell phenotype (cell subtypes)
- Type of cellular stimulation (trauma vs. housekeeping)
- Type of polyunsaturated long chain fatty acid (impact of diet)
16
Q
What are the 3 isozymes produced by cyclooxygnease?
A
- COX-1
- COX-2
- COX-3
Enzyme needed: PGH synthase
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
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.
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?
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
21
Q
What is the function of the ligand PGI2?
PGI2=Prostacyclin
A
Prevents Platelet Aggregation
22
Q
What is the function of the ligand TXA2?
TXA2=Thromboxane
A
Platelet aggregation
23
Q
What is the function of PGE2?
PGE2=Prostaglandin E2
A
Gastric Protection
24
Q
What are the three phases of Inflammation?
A
Acute →Immune →Chronic
25
Explain what happens during Acute Inflammation
* Initial response to tissue injury, **mediated by autacoids**
* Usually precede the immune response, PGI2 & PGE2 mediate vasodilation, vascular permeability, chemotaxis (Attraction to site) & **pain**
26
Explain what occurs during the Immune Response of Inflammation including the benefical and deleterious effects
* Activation of **T-cells & B-cells** in response to foreign substance
* **Beneficial:** kill foreign organisms
* **Deleterious:** Chronic inflammation without resolution
## Footnote
* T-cells (T-lymphocytes, cell mediated immunity)
B-cells (B-lymphocytes, produce antibodies)
27
Explain what occurs during Chronic Inflammation
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**
28
What does prostagladins do for the GI tract
Provide gastroduodenal cytoprotection
29
List the different ways prostagladins provide gastroduodenal cytoprotection to GI tract (5)
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
30
What occurs when prostaglandins decrease d/t use of NSAIDs?
Negative GI effects
31
What is Rheumatoid arthritis (RA)? Which ages does it affect? Which bones does it affect?
* 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
## Footnote
Synovial tissue lines the joints capsule
32
What is Osteoarthritis (OA)? Which ages does it affect? Which bones does it affect?
* **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**
33
True or False. NSAIDs prevent and reverese RA and OA
FALSE
only alleviate some symptoms
34
What is the mechanism of action for Aspirin (ASA)
| Everything that has to do w/ ASA is HIGH yield
## Footnote
Also known as Acetylsalicylic Acid
* **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**
35
Explain the anti-inflammatory therapeutic uses of Aspirin
* **Treatment for RA and OA**
* MOA
1. **↓ PG synthesis**
2. **Interferes with the kallikren system**
36
Explain the Kallikrein system that aspirin interferes with
## Footnote
HIGH yield
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)
37
A majority of aspirin goes through what chemical mechanism?
* Glycine conjugation
* 75% becomes Salicyluric acid
38
List other chemical outcomes for aspirin
* 30% turns into NaHCO3 (sodium bicarb)
* 10% is renally eliminated as free salicylate
* 4% turns into NH4Cl
| Review Slide 17
39
What DO you give a patient if they come in w/ an aspirin overdose?
NaHCO3 (sodium bicarb)
40
What do you NOT give a patient if they come in w/ an aspirin overdose?
NH4Cl (ammonium chloride)
41
Explain the antipyretic uses of Aspirin
* **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)**
42
Explain the analgesic and antithrombotic uses of Aspirin
* **Analgesic**: Effective in **reducing pain** of mild to moderate intensity of varying causes
* **Antithrombotic**: **↓TXA2**
| Review Slide 19 for a list of varying causes
## Footnote
TXA2= platelet aggregator
43
List the side effects on the Gl tract caused by Aspirin
* **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
44
List the side effects on the CNS caused by Aspirin
* **Salicylism**: at higher doses, reversible (e.g. tinnitus, ↓ hearing, vertigo)
* **Hyperpnea**: direct affect on the medulla oblongata, ↑ ventilation
45
List the side effects on the kidneys caused by Aspirin
* Reversible **↓ of glomerular filtration rate**, especially in patients with underlying renal disease or elderly
* Inhibition of PG’s (E1,E2,I1)
46
What drug interaction causes cross reactivity and which drug(s) does not?
* **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
47
What is Reye Syndrome?
* Aspirin side effect
* Acute potentially **fatal illness** occurring almost exclusively in children under 15 y/o
48
What happens w/ Reye Syndrome?
## Footnote
ASA side effect
* 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
How can Reye Syndrome be avoided?
**Give children Acetaminophen (APAP) or Ibuprofen (IBU) during viral infections**
## Footnote
Usually don't give children ASA
50
At low doses, what are the effects and complications of Aspirin?
Effects
* Analgesic
* Antipyretic
* Antiplatelet
Complications
* **Gastric intolerance**
* **Bleeding**
* Hypersensitivity reactions
* Impared hemostatsis
## Footnote
Another complication: ↓ elimation of uric acid causes problem w/ gout
51
At higher doses, what are the effects of Aspirin?
* Anti-inflammatory
* Uricosuric (↑ elimation of uric acid)
52
At mild intoxication of Aspirin what are the complications?
* **Central hyperventilation**
* **Tinnitus**
53
At moderate intoxication of ASA, what are the complications?
* Fever (d/t decoupling of protons)
* Dehydration
* **Metabolic acidosis**
## Footnote
Salicylates impair cellular respiration by uncoupling oxidative phosphorylation which is a possible mechanism for hyperthermia at toxic doses
54
At severe intoxication of ASA what are the complications?
* Vasomotor collapses
* **Coma**
* Hypoprothrombinemia
55
At lethal intoxication of ASA what are the complications?
**Renal and respiratory failure**
56
List the drug interactions that can occur w/ Aspirin
* Ethanol
* Methotrexate
* Warfin
* Valproic acid
* Spironlactione
* Sulfonylureas & exogenous insulin
57
What are the effects of the drug interaction btw Aspirin and Ethanol?
## Footnote
HIGH yield
* Ethanol: ↑ GI bleeding
58
What are the effects of the drug interaction btw Aspirin and Methotrexate?
## Footnote
HIGH yield
* Displaced from protein binding site
* **↓ renal excretion, therefore ↑ its concentration**
* i.e. pancytopenia
59
What are the effects of the drug interaction btw Aspirin and Warfin?
## Footnote
HIGH yield
Additive effects on bleeding
60
What are the effects of the drug interaction btw Aspirin and Valproic acid?
* Displaced from protein binding sites
* **↓ clearance, therefore ↑ free concentrations**
* i.e. drowsiness
## Footnote
Valproic acid used to treat seizures
61
What are the effects of the drug interaction btw Aspirin and Spironolactone?
## Footnote
HIGH yield
Inhibits its diuretic effects
## Footnote
Antagonizes aldosterone
62
What are the effects of the drug interaction btw Aspirin and Sulfonylureas & exogenous insulin?
Additive hypoglycemic effects (@ doses > 2 g/d)
## Footnote
* Hypoglycemia effects with sulfonylureas may be synergetic inhibition of K(ATP) activity
* Glyburide (sulfonylureas)
63
What are some contraindications of Aspirin?
* Patients with **hemophilia (bleeding)**
* **Pregnant women (bleeding to both)**
64
What is the treatment for an Aspirin overdose? What age group is affected the most?
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
List the druges that are Nonacetyled Salicylates
* **Choline** Salicylate
* **Magnesium** Salicylate
* **Sodium** Salicylate
* Sodium Thiosalicylate
* Salsalate
* **Methyl** Salicylate
## Footnote
Oil of wintergreen = methyl salicylate, Bengay brand, topical analgesic contains methyl salicylate
66
What types of drugs are Nonacetylated Salicyates?
Effective anti-inflammatory drugs (Not really pain)
## Footnote
Less effective analgiscs than ASA, b/c they are less effective COX1/2 inhibitors
67
When are non-acetylated salicylates preferable compared to ASA?
When COX 1/2 irreversible inhibiton is undesirable, **more preferable for asthma, bleeding, renal**
## Footnote
Similar problems as with ASA, except for specific acetylation problems
68
Which drug is a Salicylate derivative?
Diflunisal
69
For Difunisal explain:
* Mechanism of Action
* Therapeutic use
* Side effects
* 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
Explain the mechanism of action for Ibuprofen
| Arylprpropionic Acids
## Footnote
HIGH yield
* **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
What are the therapeutic uses of Ibuprofen?
* RA, OA
* Analgesia (Tx of mild to moderate pain, More effective in men?)
* Primary dysmenorrhea
* Antipyretic (Fever)
72
What is an important structutral features of NSAIDs?
Have to be an acid
| Review Slide 29
73
List the side effects of Ibuprofen?
## Footnote
HIGH yield
* **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
List some drug interactions of Ibuprofen and their effects?
| Drugs to not take together
* **Digoxin, Lithium & Methotrexate:** ↑plasma conc.
* **Diuretics, ACE inhibitors, & beta-blockers:** antagonize blood pressure loweing effects
* **ETOH:** ↑ bleeding time
75
Is it possible to overdose on Ibuprofen? and what is the treatment?
* Minimal signs of toxicity and rarely fatal (VERY HARD TO OVERDOSE)
* Treatment: Activated charcoal
76
What type of drug is Na**pro**xen and what is its therapeutic use?
* Arylpropionic acid, similar to **ibuprofen**
* Treatment: Gout Pain
* **!One of the safest NSAIDs for patients with cardiovascular disease!**
| Also known as Aleve
77
Which drug is one of the safest NSAIDS in patients w/ cardiovascular disease?
Naproxen
78
What type of drug is Ket**pro**fen? And explain its mechanism of action
* 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
List the Arylpronic Acids drugs that are used to treat RA, OA (anti-inflammation)
## Footnote
LOW yield
* Flur**pro**fen
* Fen**pro**fen
* Oxa**pro**zin
80
Explain the mechanism of action of Inodomethacin
| Indole Acetic Acid
## Footnote
HIGH yield
**Inhibitor:**
* **COX inhibitor (COX-1 > COX-2)**
* **Potent COX-3 inhibitor**
* **Lipoxygenase inhibitor**
81
List the Therapeutic uses of Indomethacin
## Footnote
HIGH yield
* RA, OA
* **Gout: acute pain**
* **Patent Ductus Arteriosus** (non-surgical closure)
* Extra-articular inflammation, **e.g., pericarditis, pleurisy**
82
List the side effects of Indomethacin:
* GI
* CNS
Hematologic
Renal
* GI: Diarrhea, Abdominal pain, Hemorrhage, Pancreatitis
* **CNS (15-25% incidence)**: Headache, Confusion, Depression, Psychosis
* Hematologic: Thrombocytopenia, Aplastic anemia
* Renal: Hyperkalemia (decreased GFR)
83
What are the contraindication of Indomethacin?
* Contraindicated during pregnancy
* Use with caution in patients with psychiatric illness & Peptic ulcer disease (PUD)
84
What type of drug is Sulindac?
## Footnote
HIGH yield
**sulfoxide prodrug reduced to active sulfide**
| Indole Acetic Acids
85
Explain the mechanism of action of Sulindac
**COX inhibitor (COX-1 > COX-2)**
86
What are the therapeutic uses of Sulindac?
* RA, OA
* Gout: acute pain
87
List the side effects of Sulindac (4)
* GI & renal
* **Stevens-Johnson syndrome,** Toxic epidermal necrolysis
* Thrombocytopenia, Agranulocytosis
* Nephrotic syndrome: Proteinuria
* Cholestatic liver damage: ↑ bile acid, bilirubin
88
For Etodolac explain:
* what type of drug?
* Mechanism of action
* Therapeutic use
* SIde effects
| Indole Acetic Acid
## Footnote
Low yield
* **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
For Tolmetin explain:
* Mechanism of action
* Therapeutic use
* SIde effects
| Heteroaryl acetic acid
## Footnote
Low yield
* 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
What is the most frequently used NSAID worldwide?
Diclofenac
91
Explain the mechanism of action for Diclofenac
| Heteroaryl acetic acid
## Footnote
HIGH yield
* **Nonselective inhibitor of COX-1/2**
* **Potent COX-3 inhibitor**
* **Lipoxygenase inhibitor**
92
What are the therapeutic uses for Diclofenac?
## Footnote
HIGH yield
* RA, OA
* Analgesia
* Primary dysmenorrhea: painful menstruation b/c of XS PG’s e.g., N/V, faintness
93
What are the side effects of Diclofenac?
Similar to other NSAIDs e.g., GI , renal, hepatotoxic (4%)
94
What is the treatment for arthritis in patients w/ an ulcer risk?
## Footnote
HIGH yield
**Arthrotec®: (Diclofenac & Misoprostol)**
95
Explain the mechanism of action for Ketorolac
| Heteroaryl acetic acid
## Footnote
HIGH yield
**Inhibitor of COX-1/2/3**
96
What are the therapeutic use(s) of Ketoralac?
* Analgesia
The Tx postoperative **acute pain that !requires analgesia at an opioid level!** moderately severe pain
97
What are the side effects to Ketoralac?
* 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
For Piroxicam explain:
* Mechanism of action
* Therapeutic use
* Side effects
* Miscellaneous
| Enolic Acids (Oxicams)
## Footnote
HIGH yield
* 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
For Meloxicam explain:
* Mechanism of action
* Therapeutic uses
* Side effects
* Miscellaneous
| Enolic Acid
## Footnote
HIGH yield
* 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
For Nabumetone explain:
* What type of drug?
* Mechanism of action
* Therapeutic uses
* Side effects
* Miscellaneous
| Alkanone
## Footnote
Low yield
* **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
For Mefenamic Acid explain:
* Mechanism of action
* Therapeutic uses
* Side effects
* Miscellaneous
| Anthranilic Acid
## Footnote
Low yield
* 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
For Meclofenamate explain:
* Mechanism of action
* Therapeutic uses
* Side effects
* Miscellaneous
| Anthranilic Acids
## Footnote
Low yield
* 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
Why was the COX-2 selective drug, Celecoxib created?
* Scientisy thought being more selective for COX 2 would be a great innovation
* To lessen GI Side Effects
| Review Slide 45
104
What type of drug is Celecoxib? and explain its mechanism of action?
| COX-2 Selective
## Footnote
HIGH yield
* Sulfonamide
* MOA: **COX-2 selective inhibitor**
105
What are the therapeutic uses of Celecoxib?
* RA, OA
* **Familial Adenomatous Polyposis (FAP)**, Pre-cancerous colorectal lesions, at 40-50 yrs can develop cancer (inhibition of COX-2 mediated angiogenesis)
106
List the side effects caused by Celecoxib
* **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
Is Acetaminopen (APAP) an NSAID?
NO, it is a N-aceyl-para-amino-phenol (AM404)
108
Explain the mechanism of action of APAP
## Footnote
APAP-Acetaminopen
* **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
What are the therapeutic use(s) for APAP?
## Footnote
APAP-Acetaminopen
* **Analgesia, Antipyretic**
* Very weak peripheral anti-inflammatory effects
110
What are the side effects caused by APAP?
## Footnote
APAP-Acetaminopen
* **Hepatotoxic**
* **Nephrotoxic**
* **Rash (SJS, TEN)**
## Footnote
SJS- Steven Johnson Syndrome
TEN-Toxic epidermal necrolysis
111
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. Decreased TXA2
112
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
C. Diclofenac and misoprostal
113
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
b. Naproxen
114
2. 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
e. Two of the above
(COX1 & COX3)
115
3. Reye syndrome is a potential side effect for which drug?
a. Aspirin
b. Ibuprofen
c. Acetaminophen
d. All of the above
a. Aspirin
116
4. 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
c. Ketorolac
117
Which of the following can be used for Patent Ductus Arteriosus?
a. Indomethacin
b. Diflunisal
c. Ibuprofen
d. Sulindac
a. Indomethacin
