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Pharmacology > Exam3Lec3Nsaids > Flashcards

Exam3Lec3Nsaids Flashcards

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
Q

Salicylates impair cellular respiration by doing what?

A

uncoupling oxidative phosphorylation which is a possible mechanism for hyperthermia at toxic doses

can also eliminate uric acid at low dose

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26
Q

Aspirin (Acetylsalicylic Acid, ASA)
Drug Interactions

A
  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

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27
Q

Aspirin (Acetylsalicylic Acid, ASA)
A. Contraindication
B. Overdose
C. Treatment for overdose

A

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)

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.

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28
Q

What are the nonacetylated salicylates?

A
  1. Choline Salicylate
  2. Magnesium Salicylate
  3. Sodium Salicylate
  4. Sodium Thiosalicylate
  5. Salsalate
  6. Methyl salicylate
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29
Q

Are nonacetylated salicylates effective anti-inflammatory drugs? Why or why not?

A

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.

Similar problems as with ASA, except for specific acetylation problems

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30
Q

Which drug is a salicylate derivative?

A

Diflunisal

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31
Q

Diflunisal
1. MOA
2. Therapeutic use
3. Side effects
4. Miscellaneous

A
  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
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32
Q

Which drugs are Arylpropionic Acids?

A

Ibuprofen (hy)
Naproxen
Ketoprofen
Flurbiprofen
Fenoprofen
Oxaprozin

-profen or =-pro

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33
Q

Ibuprofen
1. MOA
2. Therapeutic use
3. Side effects

A
  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)**

Caution in patients with renal disease or CHF because of incr renal blood flow & GFR because inhibits renal PG synthesis

34
Q

Ibuprofen
1. Drug interactions
2. Miscellaneous

A
  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

Digoxin, Lithium & Methotrexate: incr plasma conc.
Diuretics, ACE inhibitors, & beta-blockers: it can antagonize blood pressure lowering effects
ETOH can incr bleeding time

35
Q

Can you take ketoprofen whille breast feeding?

A

NO

Similar to ibuprofen, although it should not be taken during breast feeding

36
Q

Which is one of the safest NSAIDs in patients with cardiovascular disease?

A

Naproxen

Similar to ibuprofen, Tx of gout pain

37
Q

Which drug(s) are indole acetic acids?

A

Indomethacin (hy)
Sulindac(hy)
Etodolac

38
Q

Indomethacin
MOA:
Therapeutic use:

A

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”

Patent Ductus Arteriosus close this so the baby can breath

39
Q

Indomethacin
Side effects
Contraindications

A

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

In=INsanity=no psychiatric illness
pud: peptic ulcer disease

40
Q

Indole Acetic Acids: Sulindac
MOA
Therapeutic use

A

sulfoxide prodrug reduced to active sulfide
MOA: COX inhibitor (COX-1 > COX-2)
Therapeutic use: RA, OA, Gout

41
Q

Indole Acetic Acids: Sulindac
Side effects

A
  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
Q

Indole Acetic Acids: Etodolac
1. MOA
2. Therapeutic use
3. Side effects

A
  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

racemic mixture, R = inactive, S = active

43
Q

Which drug(s) are Hetereoaryl acetic acids?

A

Tolmetin
Diclofenac hy
Kerorolac hy

44
Q

Hetereoaryl acetic acids: Tolmetin
1. MOA
2. Therapeutic use
3. Side effects

A
  1. MOA: Nonselective inhibitor of COX-1/2
  2. Therapeutic use: RO, OA
  3. Side effects: similar to other NSAIDS
45
Q

Hetereoaryl acetic acids: Diclofenac
1. MOA
2. Theapeutic use
3. Side effects

A
  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

DI=DYsmenorrhea
Primary dysmenorrhea: painful menstruation b/c of XS PG’

46
Q

What is a frequently used NSAID used worldwide?

A

Diclofenac

47
Q

What can be used as a treat of arthritis in patients with an ulcer risk?

A

Arthrotec: Diclofenac & Misoprostol

brand name: Arthrotec
Misoprostol is a PG derivative (analog) and has beneficial effects in GI tract

48
Q

Hetereoaryl acetic acids: Ketorolac
1. MOA
2. Therapeutic use
3. Side effects

A
  1. MOA: Nonselective inhibitor, potent inhibitor cox-3
  2. Therapeutic use:analgesia AT AN OPIOD LEVEL
  3. Side effects: similar to other nsaids

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
Q

Which drug(s) are the enolic acids (oxicams)?

A
  1. Piroxicam hy
  2. Meloxicam
50
Q

Piroxicam
1. MOA
2. Therapeutic use
3. Side effects
4. Miscellaneous

A
  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
Q

Meloxicam
1. MOA
2. Therapeutic use
3. Side effects
4. Contraindications

A
  1. MOA: nonselectvive inhibitorof cox1/2
  2. Therapeutic use: OA
  3. Side effects: similar to NSAIDs
  4. Contraindications: no pregnancy
52
Q

Which drug(s) is an Alkanone?

A

Nabumetone

53
Q

Nabumetone
1. MOA
2. Therapeutic use
3. Side effects
4. Half life

A

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
Q

Which drug(are) are an Anthranilic acid?

A
  1. Mefenamic Acid
  2. Meclofenamate
55
Q

Mefenamic Acid
1. MOA:
2. Therapeutic use:
3. Side effect:

A
  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

LESS EFFECTTIVE THAN ASA FOR TX OF INFLAMMATION

56
Q

Meclofenamate
1. MOA:
2. Therapeutic use:
3. Side effect:
4. Excretion

A
  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
Q

Which Cox is imperative for maintainingg normal fxn of the body?

A

COX1

if inhibites by a cox inhibitor it can lead to kident failure, GI problems, etc

58
Q

Which drug(s) is a cox-2 selective inhibitor?

A

Celecoxib (sulfonamide)

hy

59
Q

Celecoxib
1. MOA
2. Therapeutic use
3. Side effects

A
  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

Familial Adenomatous Polyposis (FAP): Pre-cancerous colorectal lesions, At 40-50 y/o can develop cancer

60
Q

Does Celecoxib or Ibuprofen cause more ulcers?

A

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
Q

What is metabolized by CYP2C9 & inhibitor of CYP2D6

A

Celecoxib

62
Q

Which drug (s) is a N-Acetyl-Para-Amino-Phenol?

A

Acetaminophen, APAP

hy

63
Q

Acetaminophen, APAP
1. MOA
2. Therapeutic Use
3. Side effects

A
  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

endocannabinoids=anandamide & 2-arachidonylglyeride

64
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

we decr formation of this aggregating factor which is a prostaglandin produced thru cyclooxygenase

65
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

azrotec

66
Q

Which of the following is a mu receceptor agonist?
A. Acetominophen
B. Benzodiazepines
C. Morphine
D. Bradifacoum

A

C. Morphine

67
Q

Which of the following NSAIDS irreversible acetylates the COX enzyme?
A. Aspirin
B. Ibuprofen
C. Indomethacin
D. Ketorolac

A

A. Aspirin

68
Q

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

A

C. Ibuprofen

69
Q

Which of the following NSAIDs is a selective COX-2 inhibitor?
A. Aspirin
B. Celecoxib
C. Piroxicam
D. Ketorolac

A

B. Celecoxib

70
Q

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

A

D. Acetaminophen

71
Q

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

A. Ibuprofen

72
Q

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

A. Aspirin

73
Q

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

A

C. Ketorolac

74
Q

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

A. Mefanamic acid

remember “mefs are toxic”

75
Q

Is Acetominphen anti-inflam

A

NO

76
Q

What can directly cause sulfa allergy?

A

Celecoxib

77
Q

Which of the following is the safest NSAID for patients with a medical history of cardiovascular disease?
Aspirin
Naproxen
Ketoprofen
Indomethacin

A

Naproxen

78
Q

Which medication is Cyclooxygenase isozymes are expressed from the COX 1 Gene?
COX1
COX2
COX 3
All of the above
Two of the above

A

Two of the above

cox 1 and cox 3

79
Q

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

A

a. Aspirin

80
Q

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

A

c. Ketorolac

81
Q

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

A

Indomethacin

Pharmacology (26 decks)

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