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Exam3Lec3Nsaids Flashcards

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1
Q

What are eicosanoids? 4 points

all eicosanoids LY

A
  1. autocoids: local hormone, aurtocrine, paracrine
  2. Oxygenated products of polyunsat long chain fatty acids
  3. Large family of compouinds
  4. Short 1/2 life
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2
Q

What needs to occur in order for eicosanoid synthesis to occur?

A

arachidonic acid that is stored in the phospholipid bilayer but be released by Phospholipids: phospholipase A2 (PLA2).

arachidonic acid is the precursor

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3
Q

After arachidonic is released from the cell membrane, it be oxygenated by four separate routes, what are they?

A

Lipoxygenase
Epoxygenase
Cyclooxygenase
Free Radicals (nonenz)

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4
Q

What an important target for Nsaids and acetominophens?

A

Cyclooxygenase

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5
Q

What are 4 factors that determine the type of eicosanoid synthesized from arachidonic acid?

A
  1. The type of cell
  2. Cell phenotype
  3. Type of cellular stimulation(trauma vs. housekeeping)
  4. Type of polyunsaturated long chain fatty acid.
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6
Q

What are the 3 isoxymes of Cyclooxygenase (PGH synthase)?

A

Cox-1
Cox-2
Cox-3

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7
Q

Cox-1 (3 points)

A
  1. Constitutively expressed (always turned-on)
  2. Important hosukeeping functions
  3. Gastric protection

housekeeping

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8
Q

Cox-2 (3 points)

A
  1. Inducible
  2. Early response gene product to inflammation & immune cells
  3. Incr in expression by growth factors, tumors, cytokines

trauma

cox2 is induced of there is inflammation and infection of cell

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9
Q

Cox-3

A
  1. Shares the catalytic & key structural features of COX-1/2
  2. Expressed by the COX-1 gene
  3. APAP inhibitor of CNS COX-3 → analgesia.

gene product of Cox-1

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10
Q

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

A
  1. DP1->PGD2
  2. EP1->PGE2
  3. FPA,B->PGF2α
  4. IP ->PGI2
  5. TPα,β->TXA2

all the same letters

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11
Q

What are the three phases of Inflammation?

A
  1. Acute
  2. Immune
  3. Chronic
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12
Q

What is acute inflammation?

A
  1. Initial response to tissue injury, releases autocoids
  2. PGI2 & PGE2 mediate vasodilation, vascular permeability, chemotaxis & pain

mediated by autocoids

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13
Q

What is the immune response for inflammation?

A
  1. Acitvation of T-cells and B-cells
  2. Benefiical: kill foreign organisms
  3. Deleterious: perpetuates chronic inflammation without resolution
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14
Q

What is chronic inflammation?

A
  1. Release of mediators (unique to this phase)
  2. Interleukins 1,2,3 cause lymphocyte activation & prostaglandin production
  3. Tumor necrosis factor (TNF) from macrophages can cause prostaglandin production
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15
Q

What are 5 mechansisms of gastroduodenal cytoprotection?

A
  1. Maintaining mucosal blood flow → Counteracts mucosal ischemia by ulcerogens
    2.Increased mucus secretion → Maintain neutral pH at cell surface
    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

if any of these are damaged it can lead to ulcers
if we decr prostaglandins, w/nsaids we see neg GI effects

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16
Q

What is Rheumatoid arthritis (RA)?

A
  • Chronic inflammation of the synovial tissue lining the joint capsule resulting in the proliferation of this tissue (pannus)
  • This leads to destruction of small joints in hands,wrist, and feet

can occur at any age

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17
Q

What is Osteoarthritis (OA) ?

A
  • Affects primarily the weight-bearing joints.
  • Causes pain, limitation of motion, deformation & progressive disability, e.g., knees, hips & spine

most common form of joint disease

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18
Q

What drugs are salicylates?

A

Aspirin (hy), Salicylate

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19
Q

Aspirin (Acetylsalicylic Acid, ASA)
MOA

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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20
Q

Aspirin (Acetylsalicylic Acid, ASA)
Therapeutic use #1

A

Antinflammatory so its a treatment for RA and OA. It decr PG synthesis and interferes with the kallikrein system:
* Inhibit granulocyte adherence to damaged vasculature
* Stabilize lysosomes
* Inhibit the migration of leukocytes & macrophages to site of inflammation
* ↓ Bradykinin (9AA)

“aspirin does not like kalli and brady”

Bradykinin (9AA) is a potent pain modulator as well

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21
Q

Aspirin (Acetylsalicylic Acid, ASA)
Therapeutic use #2

A

Antipyretic(tx of fever)
ASA blocks
* Production of prostaglandins in response to pyrogens
* Interleukin-1 in the hypothalamus which is produced by macrophages (released during inflammation to activate lymphocytes)

Elevated body temperature caused by an infection is caused by the 2 bullet points

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22
Q

Aspirin (Acetylsalicylic Acid, ASA)
Therapeutic use #3 and 4

A
  • Analgesic: Effective in reducing pain of mild to moderate intensity. Acts peripherally on inflammation & probably inhibits pain stimulation, centrally, subcortical site
  • Antithrombotic: ↓ TXA2
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23
Q

After Asprin is converted to Salicylate, what products can it turn to and mention the percentages

A
  1. Ester and ether glucuronides (5-10%)
  2. MAJORITY Undergo conjugation w/ glycine to become Salicyluric Acid (75%)
  3. Free salicylate (10%)-renally eliminated
  4. undergo oxidation to become Genstisic Acid (1%)
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24
Q

Aspirin (Acetylsalicylic Acid, ASA)
SIde effects
A. Gastric
B. CNS
C. Kidney
D. Allergy
E. Syndrome
F. Liver

A

A. Gastric: Undissolved tablet directly irritates the gastric mucosa and incr incidence of gastric & duodenal ulcers
B. CNS: salicylism at high doses, reversible tinnitus hyperpnea incr ventilation
C. Kidney: reversible decr of glomerular filtration rate by Inhibition of PG’s E1, E2, I2
D. Allergy: Urticaria, edema, bronchospasm, rhinitis
E. Syndrome: Reye Syndrome for ages <15, fatal
F. Liver: fatty liver with encephalopathy, viral infection follows

to avoid viral inf give children APAP or IBU during viral infections

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25
Salicylates impair cellular respiration by doing what?
uncoupling oxidative phosphorylation which is a possible mechanism for hyperthermia at toxic doses ## Footnote can also eliminate uric acid at low dose
26
**Aspirin (Acetylsalicylic Acid, ASA)** Drug Interactions
1. *Ethanol*: incr GI bleeding 2. *Methotrexate*: Displaced from protein binding sites & decr renal excretion (incr concern which is pancytopenia) 3. *Warfarin*: Additive effects on bleeding 4. *Valproic acid*: Displaced from protein binding sites & incr clearance(more drowsiness) 5. *Spironolactone*: Inhibit its diuretic effects 6. *Sulfonylureas (glyburide)* & exogenous insulin: salicylates (adds more glucose) Ethan Met War and Val Surprisingly Spiraled
27
**Aspirin (Acetylsalicylic Acid, ASA)** A. Contraindication B. Overdose C. Treatment for overdose
A. Contraindication: pregnancy and pt's with hemophilia (bleeding), **strong cross rxn with ibuprofen** B. Overdose: A frequent cause of poisoning in young children C. Treatment for overdose: * Activated charcoal * Hyperthermia: alcohol sponges or ice packs * **Maintain a high urine output with sodium bicarbonate (alkalinize the urine and incr salicylate excretion) ** ## Footnote if you overdose in aspirin, give sodium bicarb (NaHCO3) becuase it a base and it will neutralize the acidity by incr elimination. It cleaves protein off so you have more of the ionized form.
28
What are the nonacetylated salicylates?
1. Choline Salicylate 2. Magnesium Salicylate 3. Sodium Salicylate 4. Sodium Thiosalicylate 5. Salsalate 6. **Methyl salicylate**
29
Are nonacetylated salicylates effective anti-inflammatory drugs? Why or why not?
They are effective anti-inflamm but they are less less effective analgesics than ASA because they are less effective COX-1/2 inhibitors. Therefore, these are more preferable for pts that have asthma, bleeding, renal, etc. ## Footnote Similar problems as with ASA, except for specific acetylation problems
30
Which drug is a salicylate derivative?
Diflunisal
31
**Diflunisal** 1. MOA 2. Therapeutic use 3. Side effects 4. Miscellaneous
1. MOA: Nonselective COX-1/2 inhibitor 2. Therapeutic use: Analgesia, RA, OA 3. Side effects: Similar to ASA, except for specific acetylation problems 4. Miscellaneous:Very little antipyretic activity, Not metabolized to salicylate
32
Which drugs are Arylpropionic Acids?
Ibuprofen (hy) Naproxen Ketoprofen Flurbiprofen Fenoprofen Oxaprozin ## Footnote -profen or =-pro
33
**Ibuprofen** 1. MOA 2. Therapeutic use 3. Side effects
1. *MOA*:A non-selective inhibitor of COX-1/2, A potent COX-3 inhibitor. **More potent anti-inflammatory effect than ASA** 2. *Therapeutic use*: RA, OA, analgesia, Primary dysmenorrhea, Antipyretic 3. *Side effects*: Less GI bleeding than ASA, **97% cross reactivity in patients with ASA allergy**, contraindicated in 3rd trimester of pregnancy,** Caution in patients with renal disease or CHF (can inhibit prostaglandins in kidney)** ## Footnote Caution in patients with renal disease or CHF because of incr renal blood flow & GFR because inhibits renal PG synthesis
34
**Ibuprofen** 1. Drug interactions 2. Miscellaneous
1. *Drug interactions*: Digoxin, Lithium & Methotrexate. Diuretics, ACE inhibitors, & beta-blockers. ETOH 2. *Miscellaneous*: Overdose: minimal signs of toxicity & rarely fatal, treat with activated charcoal ## Footnote Digoxin, Lithium & Methotrexate: incr plasma conc. Diuretics, ACE inhibitors, & beta-blockers: it can antagonize blood pressure lowering effects ETOH can incr bleeding time
35
Can you take ketoprofen whille breast feeding?
NO ## Footnote Similar to ibuprofen, although it should not be taken during breast feeding
36
Which is one of the safest NSAIDs in patients with cardiovascular disease?
Naproxen ## Footnote Similar to ibuprofen, Tx of gout pain
37
Which drug(s) are indole acetic acids?
**Indomethacin (hy)** **Sulindac(hy)** Etodolac
38
**Indomethacin** MOA: Therapeutic use:
MOA: COX inhibitor (COX-1 > COX-2), potent COX-3 inhibitor, Lipoxygenase inhibitor Therapeutic use: RA, OA, **gout**, **patent ductus arteriosus**(non-surgical closure), **pericarditis, pleurisy** "GPPP" ## Footnote Patent Ductus Arteriosus close this so the baby can breath
39
**Indomethacin** Side effects Contraindications
*Side effects*: 1. GI 2. CNS 3. Hematologic: Thrombocytopenia, Aplastic anemia 4. Renal: Hyperkalemia (COX inhibition) can lead to arrthymias *Contraindications*: no pregnancy, no psychiatric illness, no PUD ## Footnote In=INsanity=no psychiatric illness pud: peptic ulcer disease
40
**Indole Acetic Acids: Sulindac** MOA Therapeutic use
**sulfoxide prodrug** reduced to active sulfide MOA: COX inhibitor (COX-1 > COX-2) Therapeutic use: RA, OA, Gout
41
**Indole Acetic Acids: Sulindac** Side effects
1. GI & renal 2. **Stevens-Johnson syndrome**, Toxic epidermal necrolysis 3. Thrombocytopenia, Agranulocytosis 4. Nephrotic syndrome: Proteinuria 5. Cholestatic liver damage: incr bile acid, bilirubin
42
**Indole Acetic Acids: Etodolac** 1. MOA 2. Therapeutic use 3. Side effects
1. MOA: racemic mixture, Nonselective inhibitor of COX-1/2 (COX-2 > COX-1) 2. Therapeutic use: OA, Analgesia, Gout pain 3. Side effects: Similar to other NSAIDs with less GI toxicity ## Footnote racemic mixture, R = inactive, S = active
43
Which drug(s) are Hetereoaryl acetic acids?
Tolmetin **Diclofenac hy** **Kerorolac hy**
44
**Hetereoaryl acetic acids: Tolmetin** 1. MOA 2. Therapeutic use 3. Side effects
1. MOA: Nonselective inhibitor of COX-1/2 2. Therapeutic use: RO, OA 3. Side effects: similar to other NSAIDS
45
**Hetereoaryl acetic acids: Diclofenac** 1. MOA 2. Theapeutic use 3. Side effects
1. MOA: non selective Cox inhibitor, potent Cox3 inhibitor, lipoxygenase inhibitor 2. Theapeutic use: RA, OA, analgesia,Primary dysmenorrhea, N/V, faintness 3. Side effects: similar to other NSAIDS ## Footnote DI=DYsmenorrhea Primary dysmenorrhea: painful menstruation b/c of XS PG’
46
What is a frequently used NSAID used worldwide?
Diclofenac
47
What can be used as a treat of arthritis in patients with an ulcer risk?
Arthrotec: Diclofenac & Misoprostol ## Footnote brand name: Arthrotec Misoprostol is a PG derivative (analog) and has beneficial effects in GI tract
48
**Hetereoaryl acetic acids: Ketorolac** 1. MOA 2. Therapeutic use 3. Side effects
1. MOA: Nonselective inhibitor, potent inhibitor cox-3 2. Therapeutic use:**analgesia AT AN OPIOD LEVEL** 3. Side effects: similar to other nsaids ## Footnote The Tx postoperative acute pain that requires analgesia at an opioid level, e.g., moderately severe pain short tern use only up to 5 days b/c of toxicity
49
Which drug(s) are the enolic acids (oxicams)?
1. **Piroxicam hy** 2. Meloxicam
50
**Piroxicam** 1. MOA 2. Therapeutic use 3. Side effects 4. Miscellaneous
1. MOA: non selective inhib of Cox1/2 2. Therapeutic use: RA, OA 3. Side effects: sinilar to other NSAIDs 4. Miscellaneous: Primary glucuronide metabolite **Long 1/2 life = 42-76 h** piro=primary, if you are primary, you are long
51
**Meloxicam** 1. MOA 2. Therapeutic use 3. Side effects 4. Contraindications
1. MOA: nonselectvive inhibitorof cox1/2 2. Therapeutic use: OA 3. Side effects: similar to NSAIDs 4. **Contraindications: no pregnancy**
52
Which drug(s) is an Alkanone?
Nabumetone
53
**Nabumetone** 1. MOA 2. Therapeutic use 3. Side effects 4. Half life
**Prodrug: Ketone -> Acetic acid** 1. MOA: nonselective inhibitor of cox1/2 2. Therapeutic use: RA, OA 3. Side effects: similar to other nsaids 4. Half life : >24hrs
54
Which drug(are) are an Anthranilic acid?
1. Mefenamic Acid 2. Meclofenamate
55
**Mefenamic Acid** 1. MOA: 2. Therapeutic use: 3. Side effect:
1. MOA:nonselective inhibitor of cox1/2, less effective than ASA 2. Therapeutic use: Analgesia, Primary dysmenorrhea 3. Side effect: similar to other NSAIDs, **more TOXIC than ASA**, no pregnacy ## Footnote LESS EFFECTTIVE THAN ASA FOR TX OF INFLAMMATION
56
**Meclofenamate** 1. MOA: 2. Therapeutic use: 3. Side effect: 4. Excretion
1. MOA: nonselective inhibtor of cox1/w 2. Therapeutic use: RA, OA, analgesia, Primary dysmenorrhea 3. Side effect: simi;ar to nsaids, no pregnancy **4. Excretion: Excreted in the urine as a glucuronide metabolite**
57
Which Cox is imperative for maintainingg normal fxn of the body?
COX1 ## Footnote if inhibites by a cox inhibitor it can lead to kident failure, GI problems, etc
58
Which drug(s) is a cox-2 selective inhibitor?
Celecoxib (sulfonamide) | hy
59
Celecoxib 1. MOA 2. Therapeutic use 3. Side effects
1. MOA: COX-2 selective inhibitor 2. Therapeutic use: RA, OA, **Familial Adenomatous Polyposis (FAP)**, angiogenesis 3. Side effects: Ulcers, MI (decr PGI2, and Incr TXA2=more platelet aggregation), **Sulfa allergy** ## Footnote Familial Adenomatous Polyposis (FAP): Pre-cancerous colorectal lesions, At 40-50 y/o can develop cancer
60
Does Celecoxib or Ibuprofen cause more ulcers?
With the Celecoxib Long-term Arthritis Safety Study, it wac shown that the incidence of ulcers for Celecoxib was 1.3% vs. Ibuprofen 3.0%. So it causes less ulcers. This is b/c there is less inhibition of COX1 so its preserving good activty of PG
61
What is metabolized by CYP2C9 & inhibitor of CYP2D6
Celecoxib
62
Which drug (s) is a N-Acetyl-Para-Amino-Phenol?
Acetaminophen, APAP | hy
63
**Acetaminophen, APAP** 1. MOA 2. Therapeutic Use 3. Side effects
1. MOA: CNS cox-3 inhibitor, **AM404 inhibits the re-uptake of endocannabinoids → ↑ CB1 activity → ↑ 5-HT in descending pain pathways** 2. Therapeutic Use:**Analgesia, Antipyretic** 3. Side effects: **Hepatotoxic, Nephrotoxic, Rash (SJS, TEN)** | NOT anti-inflamm ## Footnote endocannabinoids=anandamide & 2-arachidonylglyeride
64
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 ## Footnote we decr formation of this aggregating factor which is a prostaglandin produced thru cyclooxygenase
65
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 ## Footnote azrotec
66
Which of the following is a mu receceptor agonist? A. Acetominophen B. Benzodiazepines C. Morphine D. Bradifacoum
C. Morphine
67
Which of the following NSAIDS irreversible acetylates the COX enzyme? A. Aspirin B. Ibuprofen C. Indomethacin D. Ketorolac
A. Aspirin
68
Which of the following should not be given to a patient with an Aprin allergy due to its 97% cross reactivity? A. Indomethacin B. Sulindac C. Ibuprofen D. Diclfenac
C. Ibuprofen
69
Which of the following NSAIDs is a selective COX-2 inhibitor? A. Aspirin B. Celecoxib C. Piroxicam D. Ketorolac
B. Celecoxib
70
Which of the following drugs has a mechanism of action of incr serotonin in the descending pain pathways to treat pain? A. Sulindac B. Piroxclam C. Ketorolac D. Acetaminophen
D. Acetaminophen
71
All of the following drugs should not be given to a patients with a sulfa allergy due to theIr possible side effects of SJS EXCEPT? A. Ibuprofen B. Sulindac C. Acetaminophen D. Celecoxib
A. Ibuprofen
72
A 7 yr old has experienced a viral inf and in a effort to treat his fever and pain, his parents adminiters an NSAID. The child then develops fatty liver with encephalopthay and is thought to have Reye syndrome. Which of the following NSAID was the child likey given? A. Aspirin B. Sulindac C. Piroxicam D. Acetaminophen
A. Aspirin
73
Which of the following NSAIDs is used for the treatment of post-operative pain that requires analgesia at an opiod lvl? A. Aspirin B. Sulindac C. Ketorolac D. Diclofenac
C. Ketorolac
74
Which of the following NSAIDs should be used sparingly as it is more toxic than Aspirin? A. Mefanamic acid B. Acetominophen C. Celecoxib D. Piroxicam
A. Mefanamic acid ## Footnote remember "mefs are toxic"
75
Is Acetominphen anti-inflam
NO
76
What can directly cause sulfa allergy?
Celecoxib
77
Which of the following is the safest NSAID for patients with a medical history of cardiovascular disease? Aspirin Naproxen Ketoprofen Indomethacin
Naproxen
78
Which medication is Cyclooxygenase isozymes are expressed from the COX 1 Gene? COX1 COX2 COX 3 All of the above Two of the above
Two of the above ## Footnote cox 1 and cox 3
79
Reye syndrome is a potential side effect for which drug? a. Aspirin b. Ibuprofen c. Acetaminophen d.All of the above
a. Aspirin
80
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 Ibuprofen Meloxicam Ketorolac Meclofenamate
c. Ketorolac
81
Which of the following can be used for Patent Ductus Arteriosus? a. Indomethacin b. Diflunisal c. Ibuprofen d. Sulindac
Indomethacin

Pharmacology (26 decks)

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