Pharmacology Oral

Question 1

What is the MOA of volatile anesthetics?

Answer 1

It is theorized that VA target presynaptic VGNa+ & Ca+ channels, 2- pore K+ channels, antagonizes Glutamate, and acts as agonists at GABA and glycine receptors

Question 2

What is the MOA for Succinylcholine?

Answer 2

Succinylcholine is a depolarizing NMBD that binds to nACHr, mimicking the effects of acetylcholine causing depolarization of the cell resulting in phase I fasciculations and phase II flaccid paralysis.

Question 3

What is the MOA for NonD NMBD?

Answer 3

Nondepolarizing NMBD bind to nAChr, blocking acetylcholine from binding; therefore inhibiting cellular depolarization, which leads to muscle relaxation

Question 4

What is the MOA for opioids?
(except Meperidine)

Answer 4

G-Protein receptors: Opioids activate pre & post-synaptic opioid receptors in the central and peripheral nervous system to either directly decrease the release of neurotransmission or inhibit the release of excitatory neurotransmitters (like Substance P, ACH, norepi), Inhibiting ascending pain pathways

Question 5

What is the MOA for local anesthetics?

Answer 5

Local anesthetics form a selective sodium channel blockade and cause a prolonged inactive state of these channels which prevents excitatory impulse transmission. (Lidocaine can also be a class 1B antiarrhythmic agent by blocking Na+ channels in cardiomyocytes)

Question 6

What is the MOA for Propofol?
(non-barbiturate induction agent)

Answer 6

Propofol decreases the dissociation of GABA from the GABA-A receptor, prolonging the action of GABA and increasing Cl-conduction. This leads to hyperpolarization of the cell and ↓ neuronal transmission.

Question 7

What is the MOA for Etomidate?
(non-barbiturate induction agent)

Answer 7

Etomidate allosterically binds to GABA-A receptor, ↑ the affinity of GABA at the receptor site, ↑ Cl- conduction which hyperpolarizes the cell, ↓ neuronal transmission  Hypnosis

Question 8

What is the MOA for Dexmedetomidine?

Answer 8

Dexmedotomidine is an alpha 2 agonist. It binds to the presynaptic alpha receptor, causing a decrease in Norepi release, which, in turn, decreases excitatory neuronal transmission, resulting in sedation and analgesia.

Question 9

What is the MOA for Ketamine?

Answer 9

Ketamine Blocks NMDA receptors to ↓ ion influx?????????
Analgesic Effects: Interacts with Mu, Kappa, and Delta receptors
* Monoaminergic: descending inhibitory pathways: antinociception
* Muscarinic Receptor Antagonist

Question 10

What is the MOA for Meperidine?

Answer 10

Meperidine acts as an agonist at Mu, Kappa & A2 receptors causing alterations in pain perception and response.

Question 11

What is the MOA for Glycopyrrolate
(Anticholinergic/Antimuscarinic) Quaternary ammonium - does NOT cross BBB

Answer 11

Glycopyrrolate reversibly binds to all muscarinic receptors, causing a competitive blockade of ACH (SNS Predominates). Glycopyrrolate does not cross the BBB.

Question 12

What is the MOA for Atropine?
Anticholinergic/antimuscarinic)
Crosses BBB

Answer 12

Atropine reversibly binds to all muscarinic receptors, causing a competitive blockade of ACH (SNS Predominates).

Question 13

What is the MOA for Scopolamine?(Anticholinergic/antimuscarinic). Tertiary amine crosses BBB

Answer 13

Scopolamine reversibly binds to all muscarinic receptors, causing a competitive blockade of ACH (SNS Predominates). Crosses the BBB

Question 14

What is the MOA for Benzodiazepines?

Answer 14

Benzodiazepines increase the affinity for GABA at the GABAa receptor causing an increase in chloride conductance resulting in anxiolysis

Question 15

What is the MOA for Dantrolene?

Answer 15

Dantrolene works by balancing calcium levels within muscle cells by preventing excessive calcium release from the sarcoplasmic reticulum and blocking calcium entry from outside the cell. It also prevents the flow of calcium through Ryanodine receptors.

Question 16

What is the MOA for anticholinesterases/cholinesterase Inhibitors?
(except for Physostigmine & Pyridostigmine)
These increase SLUDG

Answer 16

Irreversibly binds to and inhibits AChE, thereby increasing the concentration of acetylcholine (ACh) in the synaptic cleft

Question 17

What is the MOA for Physostigmine and Pyridostigmine?

Answer 17

Physostigmine & Pyridostigmine reversibly and competitively inhibit acetylcholinesterase which decreases acetylcholine metabolism and increases acetylcholine levels
Pyridostigmine is a Quaternary Ammonium and does not cross BBB
Physostigmine is a Tertiary Ammonium and crosses the BBB

Question 18

What is the MOA of Suggamedex?

Answer 18

Suggamedex is a highly water-soluble cyclodextrin that forms a tight bond with steroidal NDMB. When binding occurs it creates a concentration gradient away from the NMJ (Greatest Affinity for Rocuronium)

Question 19

What is the MOA for NSAIDS?

Question 20

What is the MOA for beta blockers?

Question 21

What is the MOA for Alpha blockers?

Question 22

What is the MOA for Ephedrine?

Question 23

What is the MOA for Catacholamines?

Question 24

What is the MOA for naloxone?

Answer 24

Naloxone is a Pure Opioid Antagonist: It blocks all three opioid receptor types and displaces opioids from its receptor sites, which reverses respiratory depression and opioid analgesia.

Question 25

What is the MOA for Esmolol?

Answer 25

Esmolol is cardioselective for B1receptors. Competitively inhibits beta1 receptors; resulting in decreased heart rate without a significant decrease in BP

Question 26

What is the MOA for Flumazanil?

Answer 26

Flumazenil competitively inhibits the action of benzos at the recognition site on the GABA receptor, with a high affinity for the receptor.

Question 27

What is the MOA for Ketorolac?

Answer 27

Ketorolac is a non-steroidal anti-inflammatory agent that inhibits COX-1 and COX-2 to decrease pain and the inflammatory response.