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pharacology > NSAIDS > Flashcards

NSAIDS Flashcards

1
Q

Immune response is the body’s way to defend itself
from invading bacteria, fungi, viruses, and nonliving substances that appear foreign and harmful
(toxins, chemicals, drugs, and foreign particles.

A

INFLAMMATION

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2
Q

Steps in the process of inflammation

A
  1. Histamine and prostaglandin release
  2. capillaries dilate clotting begins
  3. chemotactic factors attract phagocytic cells
  4. Phagocytes consume pathogens and cell debris
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3
Q

5 cardinal signs of inflammation

A
  1. Pain (Dolor)
  2. Heat (Calor)
  3. Redness (Rubor)
  4. Swelling (Tumor)
  5. Loss of function (functio laesa)
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4
Q

is an abnormally high temperature
associated with infection and is triggered by the release of prostaglandins.

A

FEVER

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5
Q

Steps in the process of fever

A
  1. Pathogens activate leukocytes
  2. Leukocytes relese cytokines
  3. Cytokines stimulate hypothalamus
  4. Hypothalamus release Prostaglandin
  5. Prostaglandins trigger fever
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6
Q

Enzyme that is Responsible for the synthesis of Prostaglandins
(PGs)

A

CYCLOOXYGENASE (COX)

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7
Q

mediators of pain, inflammation and fever.

A

Prostaglandins

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8
Q

Constitutive Enzyme
responsible for the Maintenance function

A

COX1

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9
Q

Constantly expressed even there are no inflammation

A

COX1

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10
Q

what are the maintenance COX1 is responsible for

A
  1. Platelet aggregation
    (TXA2)
  2. Cytoprotection
    (PGE)
  3. Vasodilation
    (PG1)
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11
Q

ADR of NSAID when it
is overuse:

A

PUD (Peptic
Ulcer Disease)

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12
Q

Inducible Enzyme

A

COX-2

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13
Q

 Low at normal states
but increases during
inflammatory
processes.

A

COX- 2

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14
Q

Alternative splice
variant of COX-1

A

COX-3

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15
Q

Potently inhibited by
Paracetamol

A

COX-3

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15
Q

Very abundant in
CNS
(HYPOTHALAMUS)

A

COX -3

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16
Q

DRugs that produce Symptomatic relief
NOT ALL OTC

A

NSAIDS

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17
Q

Indications of NSAIDS

A
  1. Analgesic
  2. Antipyretic
  3. Anti-inflammatory
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18
Q

TRue or false
As the dose increases in NSAIDs it will become a prescription drug (Rx)

A

True

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19
Q

MECHANISM OF ACTION of NASAIDS

A

Inhibitors of COX

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20
Q

EFFECTS of NSAIDS

A

Decreased Prostaglandin synthesis

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21
Q

SIDE/ADVERSE EFFECTS of NSAIDS

A
  1. GASTROINTESTINAL ULCERATION
  2. SODIUM AND WATER RETENTION
  3. Low renal vasodilation
  4. ↑Uric Acid
  5. HYPERSENSITIVITY REACTIONS
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21
Q

SIDE/ADVERSE EFFECTS of NSAIDS

A
  1. GASTROINTESTINAL ULCERATION
  2. SODIUM AND WATER RETENTION
  3. Low renal vasodilation
  4. ↑Uric Acid
  5. HYPERSENSITIVITY REACTIONS
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22
Q

True or false

NSAID - should be taken with
meals

A

true

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23
Q

Weakly acidic in nature

A

NSAIDS

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24
Q

Risk Factors of NSAIDS

A

Risk Factors:
o Old age
o High dose NSAIDs
o Multiple NSAID therapy
o Prior history of PUD o Concurrent use of steroids

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25
Q

true or false
NSAIDS are responsible in increase in PG-induced inhibition of renal Chloride reabsorption.

A

false

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26
Q

what are the drugs that contraindicated in
patients with gout.

A

ASA and Tolmetin

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27
Q

Non-Selective COX Inhibitors of NSAIDS

A

METHYL SALICYLATE
BISMUTH SUBSALICYLATE
ASPIRIN (ASA)

INDOMETHACIN

PIROXICAM

DICLOFENAC
SULINDAC
NABUMETONE
KETOROLAC

IBUPROFEN
NAPROXEN
TOLMETIN

PHENYLBUTAZONE
OXYPHENBUTAZONE

MEFENAMIC ACID

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28
Q

NSAIDs Selective COX-2 Inhibitors

A

MELOXICAM
ETODOLAC

CELECOXIB
ETORICOXB
PARECOXIB
ROFECOXIB
VALDECOXIB

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29
Q

Non-Acetylated SAlicylates

A

METHYL SALICYLATE
BISMUTH SUBSALICYLATE

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30
Q

Acetylated Salicylates

A

ASPIRIN (ASA)

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31
Q

Pharmacokinetics of Aspirin

A

Absorption: Absorbed in the stomach and intestines unhydrolyzed.

Distribution: Highly protein bound; hydrolysed to its active form.

Metabolism: LT 600mg/day →First order kinetics
MT 600mg/day →Zero order kinetics

Excretion: Enhanced by urinary alkalinization

32
Q

Aspirin therapeutics

A
  1. Analgesic
  2. Antipyretic
  3. Anti-inflammatory
  4. Antiplatelet
33
Q

true and false

ASPIRIN is the only drug that is
utilized as antiplatelet in high doses

A

false

34
Q

responsible for platelet aggregation that synthesized by PG

A

TXA2

35
Q

true or false

Low doses of aspirin have been found to
non-selectively inhibit the synthesis of TXA2
without having as much effect on
prostacyclin, whereas higher doses inhibit the
synthesis of both prostaglandins.

A

false

36
Q

true of false

aspirin inhibits platelet aggregation for the life of the platelet and effectively reduces platelet aggregation when administered twice a day or every other day.

A

false

37
Q

dose of aspirin that produces anti platelet effect

A

80-160 mg

38
Q

dose of aspirin that produces analgesic and antipyretic effect

A

650-975 mg

39
Q

dose of aspirin that produces salicylism

A

3-30 g

40
Q

dose of aspirin that produces anti inflammatory effect and tinnitus

A

3-6 g

41
Q

dose of aspirin that produces hyperventilation and respiratory alkalosis

A

6-10 g

42
Q

dose of aspirin that produces fever, dehydration and metabolic acidosis

A

10-20 g

43
Q

dose of aspirin that produces shock coma, respiratory and renal failure and death

A

20-30 g

44
Q

(early sign of salicylate toxicity)

A

Tinnitus 3-6 g

45
Q

(stimulation of medulla leading to
exhalation of carbon dioxide)

A

Hyperventilation

46
Q

Treatment of salicylism

A
  1. Emesis and gastric lavage to remove
    unabsorbed drug.
  2. IV NaHCO3.
  3. Administration of fluid, electrolytes, and
    supportive care.
47
Q

ADVERSE EFFECTS of ASA

A
  1. Salicylism
  2. Severe Anaphylactic Reactions
  3. Reye’s Syndrome
48
Q

adverse effect of ASA if Children is given aspirin while having viral
infection (chicken pox, flu) or recovering from it

A

Reye’s syndrome

49
Q

Reye’s syndrome manifestation

A

Hepatic failure and
Encephalopathy

50
Q

One of the most potent inhibitors of CCX isozymes.

A

INDOLE DERIVATIVE

51
Q

Non- selective CoX inhibitor that Closes the Ductus Arteriosus

A

INDOMETHACIN

52
Q

PG analog used to maintain the potency
of Ductus Arteriosus

A

ALPROSTADIL

53
Q

→ Selective COX-1 inhibitor.
→ Long half-life: 50 hours
→ Higher risk for PUD.

A

PIROXICAM

54
Q

First NSAID for parenteral use.
available also as ophthalmic solution

A

Ketorolac

55
Q

PHENYLACETIC ACID Derivatives

A

DICLOFENAC
SULINDAC
NABUMETONE
KETOROLAC

56
Q

PHENYLACETIC ACID Derivatives that used for less than 5 days only (toxic: hematologic toxicity )

A

Ketorolac

57
Q

The only non-acidic NSAID

A

NABUMETONE

58
Q

IBUPROFEN brand name

A

(Advil®, Medicol®)

59
Q

NAPROXEN brand name

A

(Skelan®, Flanax®)

60
Q

test that rapidly screen out infection
versus neoplastic disease and significantly
narrow the differential diagnoses.

A

Naproxen test

61
Q

Contraindicated in patients with gout

A

TOLMETIN

62
Q

Non- selective CoX inhibitor that Withdrawn from the market.

A

PHENYLBUTAZONE
OXYPHENBUTAZONE

63
Q

Non- selective CoX inhibitor that Withdrawn from the market.

A

PHENYLBUTAZONE
OXYPHENBUTAZONE

64
Q

MEFENAMIC ACID brand names

A

Ponstan®
Dolfenal®

65
Q

COX 2 inhibitor that is Withdrawn

A

ROFECOXIB
VALDECOXIB

66
Q

Specific COX-2 inhibitors.
Lesser risk for NSAID induced PUD

A

true

67
Q

Disadvantage of COX-2 inhibitors : chronic thrombotic events → stroke and MI

A

false - acute

68
Q

what are the most important prostaglandins affecting platelet aggregation

A

PROSTACYCLIN (also called
prostaglandin I2 [PGI2])
TXA2.

69
Q

synthesized by vascular endothelial cells and inhibits
platelet aggregation

A

Prostacyclin

70
Q

it is synthesized by platelets and promotes platelet aggregation.

A

TXA2

71
Q

Aka Acetaminophen (present in USP)

A

PARACETAMOL

72
Q

Not an NSAID
 analgesic and antipyretic activity
 weak anti-inflammatory activity

A

PARACETAMOL

73
Q

Weak peripheral inhibitor of COX at the peripheral circulation.
Inhibits COX-3

A

Paracetamol

74
Q

true or false
A minor pathway involves oxidation of acetaminophen by cytochrome P450 enzymes (CYP1A2, CYP2E1, and CYP3A isozymes) to form a potentially non-toxic intermediate, N-acetyl-pbenzoquinone imine (NAPQI).

A

false - toxic

75
Q

paracetamol toxicity result

A

hepatic necrosis.

76
Q

given to treat acetaminophen overdose protects the liver by maintaining or restoring the glutathione levels, or by acting as an alternative substrate for conjugation with and thus detoxification of the reactive

rich in SH

A

Acetylcysteine (Mucomyst)

77
Q

Acetaminophen is primarily metabolized by what

A

conjugation with sulfate and glucuronide.

78
Q

is an unpleasant sensory and emotional
experience that serves to alert an individual to actual or potential tissue damage.

A

Pain

pharacology (3 decks)

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