Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

PHAR 230 > M6 L2 Non-narcotic Analgesics > Flashcards

M6 L2 Non-narcotic Analgesics Flashcards

1
Q

COX-1

A

widely distributed enzyme
- has all effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

COX-2

A

limited distribution enzyme
(macrophages and at sites of inflammation)
- for inflammatory processes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what does “COX” stand for

A

cyclooxygenase enzyme

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

COX-3

A

mainly in brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

3 isoenzymes of cyclooxygenase enzyme

A

COX-1, COX-2, COX-3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

3 types of antipyretics

A
  1. non-steroidal anti-inflammatory drugs (NSAIDS)
  2. Acetaminophen (tylenol)
  3. Selective COX-2 inhibitors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

NSAIDS examples

A

aspirin, ibuprofen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

example of selective COX-2 inhibitor

A

celecoxib

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

how does acetylsalicylic acid (aspirin) work

A
  • irreversible inhibition of COX -1 and -2 (decreases production of prostaglandins and thromboxanes
  • other NSAIDs cause reversible inhibition of COX enzyme
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

pharmacological action of acetylsalicylic acid

A
  • analgesic
  • antipyretic
  • antiplatelet
  • anti inflammatory (high dose)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

NSAIDS in general are used for…

A

mild to moderate pain (less effective than opioids)
- do this through inhibition of PG’s synthesis
1. peripheral action: prevents sensation of pain-transmitting nerve fibres to chem mediators released by tissue injury
2. central action: inhibits action of transmitters involved in pain pathways

  • no tolerance, addiction, or dependence
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what do NSAIDs do for fever

A

by inhibition of PG’s synthesis
- reset temp center in hypothalamus
- no effect on normal body temp

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what do NSAIDS do on thromboembolic disease

A
  • through antiplatelet effect
  • treatment or prophylaxis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

how do NSAIDS help inflammation

A

need a high dose
- rheumatic fever
- rheumatoid arthritis
- gout (high dose)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

adverse effects of NSAIDs

A
  • bleedings (commonly GI)
  • GI upset (when you block the prostaglandins this can affect the mucosa of the stomach)
  • bronchial asthma
  • tinnitus (ringing of ears)
  • acid base imbalance
  • chronic nephritis
  • hypersensitivity
  • reyes syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

adverse effects of aspirin

A
  • swelling of eyes, face, lips, tongue, or throat
  • wheezing, diff breathing, hoarseness, fast breathing
  • tachycardia
  • cold, clammy skin
  • hives/rash
  • ear ringing
  • bloody vomit
  • bleeding
17
Q

contraindications of using aspirin and other NSAIDS

A
  • bleeding tendencies
  • peptic ulcer
  • bronchial asthma
  • allergy to aspirin or other NSAIDs
  • chronic renal disease
  • children or adolescents w fever and viral infection
18
Q

absorption, protein bound, metabolism, and excretion of aspirin

A

absorption: stomach - small intestine
protein bound: 50-80%
metabolism: liver (80%)
excretion: kidney

19
Q

acute aspirin toxicity manifestations

A
  • vomiting, abdominal pain
  • tinnitus
  • hypoglycemia, hypokalemia
  • hyperthermia, hyperventilation
  • metabolic acidosis, respiratory alkalosis
  • confusion, seizures, coma
  • pulmonary edema, hypotension, CV collapse } cause death
20
Q

acute aspirin toxicity treatment

A
  • no specific antidote
  • provide supportive measures: ABC’s, fluids and electrolytes, restore pH, glucose
  • alkalinization of urine
21
Q

Commonly used other NSAIDs besides aspirin

A
  • ibuprofen (advil) } OTC
  • naproxen (aleve) } OTC
  • indomethacin
  • ketorolac
  • diclofenac (can be linked to heart attack and stroke risk)
22
Q

acetaminophen

A

(not an acid, not an NSAID)
- mech of action is not fully understood (inhibits COX enzyme…but has other unknown actions ?? COX-3 inhibition
- no anti-inflammatory or anti-platelet action
- safe if you have a bleeding tendency, or pregnancy
- absorption: GIT
- metabolism: liver
- excretion: kidney

23
Q

adverse effects/pros of acetaminophen

A
  • safe if taken in proper dose
  • safe in preg
  • causes liver and renal damage possibly
24
Q

end products of acetaminophen metabolism

A

NAPQI: N-acetyl-p-benzoquinoneimine (bad for liver)
GSH: glutathione

25
Q

acute acetaminophen toxicity

A
  • commonly due to suicide
  • acute liver damage (may be fatal)
  • antidote: N-acetylcysteine (NAC)
  • supportive measures
  • +/- charcoal ingestion
  • +/- gastric lavage
26
Q

N-acetylcysteine (NAC)

A
  • antidote of acetaminophen
  • source of glutathione -> decreased NAPQI -> decreased liver damage
  • most effective within 8 hrs of exposure
  • oral or IV
27
Q

COX-2 inhibitors

A
  • selective inhibitors of COX-2 isozyme
  • less COX-1 induced side effects: asthma, gastric irritation and bleeding, more theoretical!!
  • more risk of thrombosis and cardiovascular morbidity and mortality
  • ex: celecoxib

PHAR 230 (31 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions