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
2
Q
Steps in the process of inflammation
A
- Histamine and prostaglandin release
- capillaries dilate clotting begins
- chemotactic factors attract phagocytic cells
- Phagocytes consume pathogens and cell debris
3
Q
5 cardinal signs of inflammation
A
- Pain (Dolor)
- Heat (Calor)
- Redness (Rubor)
- Swelling (Tumor)
- Loss of function (functio laesa)
4
Q
is an abnormally high temperature
associated with infection and is triggered by the release of prostaglandins.
A
FEVER
5
Q
Steps in the process of fever
A
- Pathogens activate leukocytes
- Leukocytes relese cytokines
- Cytokines stimulate hypothalamus
- Hypothalamus release Prostaglandin
- Prostaglandins trigger fever
6
Q
Enzyme that is Responsible for the synthesis of Prostaglandins
(PGs)
A
CYCLOOXYGENASE (COX)
7
Q
mediators of pain, inflammation and fever.
A
Prostaglandins
8
Q
Constitutive Enzyme
responsible for the Maintenance function
A
COX1
9
Q
Constantly expressed even there are no inflammation
A
COX1
10
Q
what are the maintenance COX1 is responsible for
A
- Platelet aggregation
(TXA2) - Cytoprotection
(PGE) - Vasodilation
(PG1)
11
Q
ADR of NSAID when it
is overuse:
A
PUD (Peptic
Ulcer Disease)
12
Q
Inducible Enzyme
A
COX-2
13
Q
Low at normal states
but increases during
inflammatory
processes.
A
COX- 2
14
Q
Alternative splice
variant of COX-1
A
COX-3
15
Q
Potently inhibited by
Paracetamol
A
COX-3
15
Q
Very abundant in
CNS
(HYPOTHALAMUS)
A
COX -3
16
Q
DRugs that produce Symptomatic relief
NOT ALL OTC
A
NSAIDS
17
Q
Indications of NSAIDS
A
- Analgesic
- Antipyretic
- Anti-inflammatory
18
Q
TRue or false
As the dose increases in NSAIDs it will become a prescription drug (Rx)
A
True
19
Q
MECHANISM OF ACTION of NASAIDS
A
Inhibitors of COX
20
Q
EFFECTS of NSAIDS
A
Decreased Prostaglandin synthesis
21
Q
SIDE/ADVERSE EFFECTS of NSAIDS
A
- GASTROINTESTINAL ULCERATION
- SODIUM AND WATER RETENTION
- Low renal vasodilation
- ↑Uric Acid
- HYPERSENSITIVITY REACTIONS
21
Q
SIDE/ADVERSE EFFECTS of NSAIDS
A
- GASTROINTESTINAL ULCERATION
- SODIUM AND WATER RETENTION
- Low renal vasodilation
- ↑Uric Acid
- HYPERSENSITIVITY REACTIONS
22
Q
True or false
NSAID - should be taken with
meals
A
true
23
Weakly acidic in nature
NSAIDS
24
Risk Factors of NSAIDS
Risk Factors:
o Old age
o High dose NSAIDs
o Multiple NSAID therapy
o Prior history of PUD o Concurrent use of steroids
25
true or false
NSAIDS are responsible in increase in PG-induced inhibition of renal Chloride reabsorption.
false
26
what are the drugs that contraindicated in
patients with gout.
ASA and Tolmetin
27
Non-Selective COX Inhibitors of NSAIDS
METHYL SALICYLATE
BISMUTH SUBSALICYLATE
ASPIRIN (ASA)
INDOMETHACIN
PIROXICAM
DICLOFENAC
SULINDAC
NABUMETONE
KETOROLAC
IBUPROFEN
NAPROXEN
TOLMETIN
PHENYLBUTAZONE
OXYPHENBUTAZONE
MEFENAMIC ACID
28
NSAIDs Selective COX-2 Inhibitors
MELOXICAM
ETODOLAC
CELECOXIB
ETORICOXB
PARECOXIB
ROFECOXIB
VALDECOXIB
29
Non-Acetylated SAlicylates
METHYL SALICYLATE
BISMUTH SUBSALICYLATE
30
Acetylated Salicylates
ASPIRIN (ASA)
31
Pharmacokinetics of Aspirin
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
Aspirin therapeutics
1. Analgesic
2. Antipyretic
3. Anti-inflammatory
4. Antiplatelet
33
true and false
ASPIRIN is the only drug that is
utilized as antiplatelet in high doses
false
34
responsible for platelet aggregation that synthesized by PG
TXA2
35
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.
false
36
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.
false
37
dose of aspirin that produces anti platelet effect
80-160 mg
38
dose of aspirin that produces analgesic and antipyretic effect
650-975 mg
39
dose of aspirin that produces salicylism
3-30 g
40
dose of aspirin that produces anti inflammatory effect and tinnitus
3-6 g
41
dose of aspirin that produces hyperventilation and respiratory alkalosis
6-10 g
42
dose of aspirin that produces fever, dehydration and metabolic acidosis
10-20 g
43
dose of aspirin that produces shock coma, respiratory and renal failure and death
20-30 g
44
(early sign of salicylate toxicity)
Tinnitus 3-6 g
45
(stimulation of medulla leading to
exhalation of carbon dioxide)
Hyperventilation
46
Treatment of salicylism
1. Emesis and gastric lavage to remove
unabsorbed drug.
2. IV NaHCO3.
3. Administration of fluid, electrolytes, and
supportive care.
47
ADVERSE EFFECTS of ASA
1. Salicylism
2. Severe Anaphylactic Reactions
3. Reye’s Syndrome
48
adverse effect of ASA if Children is given aspirin while having viral
infection (chicken pox, flu) or recovering from it
Reye's syndrome
49
Reye's syndrome manifestation
Hepatic failure and
Encephalopathy
50
One of the most potent inhibitors of CCX isozymes.
INDOLE DERIVATIVE
51
Non- selective CoX inhibitor that Closes the Ductus Arteriosus
INDOMETHACIN
52
PG analog used to maintain the potency
of Ductus Arteriosus
ALPROSTADIL
53
→ Selective COX-1 inhibitor.
→ Long half-life: 50 hours
→ Higher risk for PUD.
PIROXICAM
54
First NSAID for parenteral use.
available also as ophthalmic solution
Ketorolac
55
PHENYLACETIC ACID Derivatives
DICLOFENAC
SULINDAC
NABUMETONE
KETOROLAC
56
PHENYLACETIC ACID Derivatives that used for less than 5 days only (toxic: hematologic toxicity )
Ketorolac
57
The only non-acidic NSAID
NABUMETONE
58
IBUPROFEN brand name
(Advil®, Medicol®)
59
NAPROXEN brand name
(Skelan®, Flanax®)
60
test that rapidly screen out infection
versus neoplastic disease and significantly
narrow the differential diagnoses.
Naproxen test
61
Contraindicated in patients with gout
TOLMETIN
62
Non- selective CoX inhibitor that Withdrawn from the market.
PHENYLBUTAZONE
OXYPHENBUTAZONE
63
Non- selective CoX inhibitor that Withdrawn from the market.
PHENYLBUTAZONE
OXYPHENBUTAZONE
64
MEFENAMIC ACID brand names
Ponstan®
Dolfenal®
65
COX 2 inhibitor that is Withdrawn
ROFECOXIB
VALDECOXIB
66
Specific COX-2 inhibitors.
Lesser risk for NSAID induced PUD
true
67
Disadvantage of COX-2 inhibitors : chronic thrombotic events → stroke and MI
false - acute
68
what are the most important prostaglandins affecting platelet aggregation
PROSTACYCLIN (also called
prostaglandin I2 [PGI2])
TXA2.
69
synthesized by vascular endothelial cells and inhibits
platelet aggregation
Prostacyclin
70
it is synthesized by platelets and promotes platelet aggregation.
TXA2
71
Aka Acetaminophen (present in USP)
PARACETAMOL
72
Not an NSAID
analgesic and antipyretic activity
weak anti-inflammatory activity
PARACETAMOL
73
Weak peripheral inhibitor of COX at the peripheral circulation.
Inhibits COX-3
Paracetamol
74
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).
false - toxic
75
paracetamol toxicity result
hepatic necrosis.
76
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
Acetylcysteine (Mucomyst)
77
Acetaminophen is primarily metabolized by what
conjugation with sulfate and glucuronide.
78
is an unpleasant sensory and emotional
experience that serves to alert an individual to actual or potential tissue damage.
Pain
