Brainscape's Knowledge GenomeTM

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


See full index

Advanced Pharmacology > Exam 4 - NSAIDS/Non-Opiods/Opiods > Flashcards

Exam 4 - NSAIDS/Non-Opiods/Opiods Flashcards

1
Q

What are NSAIDS?
Examples?

A

Non-steroidal Anti-Inflammatory Drugs that relieve pain and fever by supressing inflammation via COX-1, COX-2, and/or LOX inhibition

Aspirin, ibuprofen, ketorolac, naproxen

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

Diagram the cell damage pathways (COX and LOX)

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

Describe the two different COX isoforms?

A
  • COX-1 – Always present allows for important homeostatic functions in the GI tract, renal tract, platelet function, and macrophage differentiation. Inhibition undesirable
  • COX-2 - expressed due to stimulation and leads to inflammatory response
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the pharmcokinetics of NSAIDS?

A
  • Weak acids
  • Well absorbed
  • Highly metabolized
  • Highly protein bound
  • Renally and hepatically cleared
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the major side effects of NSAIDS?

A
  • Gastic irritation by decreasing gastic mucous production leading to ulcers
  • Nephrotoxicity
  • Hepatotoxicity
  • Thrombosis
  • Rare hypersensitivity reactions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Describe the MOA of aspirin’s irreversible inhibition?

A

Irreversibly blocks COX-1 by acetylation of serine 529.
This prevents arachidonic acid interacting with COX.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Categorize the NSAIDS based on selectivity of COX and LOX inhibition.

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

Describe the MOA of NSAIDS to reduce fever?

A

Mediated by inhibition of COX and IL-1
PG inhibition in the hypothalamus leads to peripheral vasodilation causing dissipation of heat.
NSAIDS cause cerebral vasoconstriction

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

Describe the MOA of GI upset that occurs with all NSAIDS?

A

Inhibits GI protective prostaglandin produced by COX-1, causing irritation of gastric mucosa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the black box warning for NSAIDS?

A

Increased risk of cardiovascular events (MI, stroke) and GI bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What would the toxicity of aspirin be at a level of 70 24 hours after ingestion?

A

Severe toxicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the benefits and drawbacks of COX-2 selective inhibitors?
Drug?

A

Benefits: No effect on COX-1 functions (less GI upset, no impact on platelet aggregation)
Drawbacks: Increased risk of serious CV events due to inhibition of PGI2
Celecoxib

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

What are the indications for diclofenac and indomethacin?

A

Indomethacin
* Rheumatism
* Gout
* Patent ductus arteriosus
Diclofenac
* Reduce arthritic pain
* Comes in a topical form

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Why is acetaminophen not an NSAID?

A

It selectively inhibits COX-2 in the CNS and does not have much effect on the arachidonic acid pathway in the periphery
It has no anti-inflammatory effects

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

Describe the selection criteria for NSAIDS?

A

All are roughly equal in efficacy, comes down to:
* Personal factors
* Cost
* Toxicities
- Most: Indomethacin, meclofenamate
- Least: Aspirin and ibuprofen
- COX-2 better for patients high risk for stomach bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Describe the acute and chronic effects of glucocorticoids?

A

Acute is good, chronic is bad
Attributed to cortisol levels

17
Q

What is the MOA of glucocorticoids?

A
  • Inhibit immune response by blocking transcription/translation
  • Increases Annexin-1 which suppresses phospholipase A2 and leukotriene response
  • Increases secretory leukoprotease inhibitor (SLPI)
  • Increases IL-10 - immunosuppressive enzyme
  • Decreases NFkB which is proinflammatory
18
Q

What are DMARDs?

A

Disease Modifying Anti-Rheumatic Drugs
Used to reduce inflammation and decrease damage to bones and joints

19
Q

List the 3 biologic DMARDs and their MOA?

A
  • Abatacept (Orencia) - Blocks T cell activation
  • Rituximab (Rituxan) - Depletes B-lymphocytes
  • Adalimumab (Humira) - anti TNF-alpha
20
Q

What are the endogenous opiods and their receptors?

A
  • Endorphins – highest affinity for mu opioid receptors
  • Enkephalins – highest affinity for delta receptors
  • Dynorphins – Highest affinity for kappa receptors

All ligands can bind to each receptor, they differ in affinity

21
Q

What are the components of pain and pain signaling?

A
  • Components: Sensory and emotional
  • Pain is sensed by nociceptors (free nerve endings) with specialized receptors that when bound, initiate an action potential in an afferent neuron.
  • Pain signals arrive at the dorsal horn of the spinal cord where they ascend to the somatosensory cortex.
22
Q

Describe the 3 main fibers for sensation transmission?

A
  • A beta fiber (myelinated) – transmits non-noxious mechanical stimuli
  • A delta fiber (myelinated) - transmits noxious heat and mechanical stimuli like sharp pain. Produces initial reflex response.
  • C fiber (unmyelinated) - transmits noxious heat, chemical, and mechanical stimuli (slow, burning pain).
23
Q

Describe the 3 tracts in the CNS?

A
  • Spinothalamic - (primary pain pathway) transmits signal through the thalamic nuclei to the somatosensory cortex.
  • Spinoreticular - (emotional sensation) transmits signal through the reticular formation of the pons, then thalamus, then somatosensory cortex.
  • Spinomesencephalic - Mu opiod receptors in the periaqueductal (PAD) grey matter of the brainstem can release endorphins to supress pain signaling.
24
Q

What are the pharmacokinetics of opiods?

A

A: well absorbed, many routes
D: Highly perfuses tissues; accumulates
M: Varies
E: mainly urine (drug tests)

25
Q

What are the different organ system effects of the opiods?

A
  • CNS - analgesia, euphoria, sedation, respiratory depression, miosis (always, no tolerance)
  • CV - bradycardia (CNS), tachycardia (meperidine, demerol)
  • GI - constipation (no tolerance)
26
Q

What are the specific applications for opioids?

A
  • Analgesia
  • Acute Coronary Syndrome
  • Acute pulmonary edema
  • Cough
  • Diarrhea (loperamide)
  • Shivering (demerol)
  • Anesthesia
27
Q

What is opiod toxicity?

A

An extension of an opiods therapeutic effects
* Respiratory depression
* Nausea and vomiting
* Postural hypotension
* Constipation
* Itch (mast cell degranulation)

28
Q

What is the difference between tolerance and withdrawl?

A

Toleance is when the body requires more of the drug to achieve the desired effect
Withdrawl stems from chemical and physical dependence leading to physical symptoms

29
Q

What is the degree of tolerance for the different opiod effects?

A
30
Q

What drugs are phenanthrenes?

A
  • Morphine, codeine, oxycodone
  • Dilaudid
  • Heroin
31
Q

What drugs are phenylheptylamines?

A

Methadone

32
Q

What drugs are phenylpiperidines?

A
  • Fentanyl
  • Meperidine (Demerol)
  • Tramadol
33
Q

What are the opiod antagonists?

A

Naloxone - opiods
Naltrexone - EtOH
Naloxegol - antagonizes GI effects

34
Q

What are the treatments for post-op shivering?

A

Meperidine and ondansetron

35
Q

What are the use and class of buprenorphine, butorphanol, and dextromethorphan?

A

buprenorphine - partial agonist, for opioid abuse
butorphanol - partial agonist. Post op shivering
Dextromethorphan - antitussive

Advanced Pharmacology (17 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions