Unit 06: drugs Flashcards
1
Q
what is yohimbine
A
Alpha 2 receptor antagonist
- can reverse effects of alpha2 receptor agonists
- drugs can reverse sedation and most cardiovascular effects
2
Q
what is atipamezole
A
Alpha 2 receptor antagonist
- can reverse effects of alpha2 receptor agonists
- drugs can reverse sedation and most cardiovascular effects
3
Q
what is dexmedetomidine
A
sedative
- alpha-2 agonist
4
Q
A
5
Q
what is diazepam
A
sedative
benzodiazepine
6
Q
what is medetomidine
A
- mixture of 2 enantiomers - dexmedetomidine and levomedetomidine
(dexmedetomidine is the biologically active)
- when ued at moderate dosages with general anesthetic there is usually no significant change in BP
7
Q
what is flumazenil
A
- GABA R antagonist: competitive inhibitor of benzodiazepine site
- reverses overall effects of benzodiazepines
- used to reverse benzodiazepine overdose
8
Q
what is fentanyl
A
mu receptor agonist with intense analgesic effect, known as the “full Mu agonist”.
9
Q
what is pentazocine
A
opioid
kappa agonist with good analgesic effect
also produces a weak effect at mu receptors, making it act like an antagonist to other mu opioids
10
Q
A
11
Q
what is loperamide?
A
- reduce propsulive gut motility in large bowel, decrease gut secretions and cause constiction of anal spincter
- stool remians in large colon longer which allows more water to be reabsorbed - potent constipating effect
12
Q
what is Diphenoxylate?
A
- reduce propsulive gut motility in large bowel, decrease gut secretions and cause constiction of anal spincter
- stool remians in large colon longer which allows more water to be reabsorbed - potent constipating effect
13
Q
A
14
Q
Ether
A
early general anesthetic
- inhalant introducted in 1846
- demonstrated little respiratroy or cardiovascular depression and relatively non-toxic
- does have pungent odour and expolsive properties
- now used as starter fluid in combustion engines
15
Q
chloroform
A
CHCl3
early general anesthetic
- inhalant introducted in 1847
- non pungent odor and non explosive
- can be hepatotoxic resulting in severe cardiovascular depresion
- was preferred inhalant until almost 1950
16
Q
what is nitrous oxide
A
- AKA laughing gas
- weak CNS depressant, cannot produce general anesthesia even when 100% NO is administered
- used to reduce amount of other inhalants requires, speeds up uptake of gas anesthetics
- can be used of analgesia, no respiratory depression is assocaited with it suse as longa s you dont go above 50-60% which would dispalce O2 ausing asphyxiation
- little effect on cardiovascular system at lower conc
- adverse effects include increasing uptake of other anesthetics, and effects on GI system (formation of gas pockets causing bloating), N2O outflow can cause hypoxia during recovery
- todau used in dental clinics, hospitals and few veterinary clinics to reduce amount of hydrocarbon anesthetic required
17
Q
what is cyclopropane?
A
- early general anesthetic
- used to be most populat
- associated with explosions in operating room bc has flammable properties
18
Q
sodium pentobarbital
A
- barbiturate that is effective and relatively safe if used with caution (narrow safty margin)
- elimination of drug requries hepatic metabolism- metabolism is too slow in emergency situations
- injectible anesthetic
19
Q
halogenated hydrocarbon anesthetics
A
- isoflurance, sevoflurane and desflurane
- all inhalants
20
Q
what is sodium thiopental
A
- barbiturate adiminstered via IV
- ultra short duration with rapid induction and recovery rate
The physiological effects on the CNS include dose dependent depression in 10-30 seconds, and unconsciousness for 1½ - 3 minutes.
If a partial dose is administered, it is likely to cause excitement as opposed to induction.
21
Q
what is propofol
A
one of the most popular intravenous anesthetics
- offers sedation and anesthesia but has poor analgesic effects
- mainly used for induction and has short duration (2-5min) so can be utilized during short painful procedures
- premedation should be used first sot hat less propofol is needed for respiratory induction- resulting in less blood pressure depression
- half life of drug increases with age so can be problematic in geriatirc patients
22
Q
what is propofol
A
- one of most popular intravenous anesthetics
- offers sedation and anestheria btu has poor analgesic effects
- short duration of action, should also use a premedication so less propofol is needed (minimize effects of blood pressure depression
- actcs by slowing dissocition of GABA from tis receptor- longer inhibition of action potentials
- can cause apnea for 30-60sec and dose dependent respiratroy despression but not usually a problem
- can cause dope dependent depression of blood rpessure causing peripheral vasodilation
23
Q
what is ketamine
A
dissociateive anesthetic, only IV anesthetic with analgesic properties
GABA and NMDA antagonist (GABA is inhibitory so if u ihibt that get inc SNS activity)
- can increase HR and BP due to SNS stimulation, can use this to advantage in patietns in cardiovascular shock
- can rise intracranial pressue causing seizures, hallucinations and excitment during recovery phase
- use with diazepam to rpoduce rapid, smooth induction with little effect on cardiovascualr system
*never used alone
24
Q
what is dantrolene
A
administer is patietn is suspected to be experiencing malignant hyperthermia (potential effect of halothane)
25
Q
what is Haloethane
A
- inhalant anesthetic
- 25% is metabolized, hepatotoxic metabolites
- can cause hypoxia and increased CO2 causing epinephrine release, deos not change HR but CO can decrease (reduces BP)
- can cause arrhythmias due to sensitivity of the myocardium to epinephine
- can depress thermoregulation resulting in hypothermia or malignant hyperthermia (very dangerous but need to ahve a genetic mutation for that)
- can result in liver damage bc hepatotoxic
26
Q
what is isoflurane
A
- most common anesthetic
- alsmot no toxicity since very little is metabolized
- low solubiltiy in tissues so moves in and out of bdoy quickly
- causes less depression of CO than halothane but does ccase vasodilation which can result in dose dependent drop in blood pressure
- post anesthetic hepatic necrosis has been reported in 1/500,000 pateints
- less potent than halothane and has pungent odour (only real drawback)
27
Q
what is sevoflurane
A
- Inhalant anesthetic
- less stable than isoflurane, breaks fown when exposed to CO2 abosrbent in anestheic machine amkign it worse when the oxygen flow rate is low
- as result nephrotoxic ocmound is release “compound A” (MOA somewhat unknwon)
- human metbaolize up to 5% producing fluride ions that are released and thought to damage renal tubules, this sint supported by data
28
Q
what is tubocurarine
A
- non depolarizing NM blocker
- also idnuced histamine relase which lowers bp
29
Q
what is pancuronium
A
NM blocker agent
- replaced tubocurarine but tends ot be vagolytic (inhibits pSNS signaling in the vagus nerve causing increased HR)
- has been replaced with rocuronium, mivacurium and atracirium
30
Q
what are currently used NM blocker agents
A
rocuronium, mivacurium and atracurium
- differ mainly in duration of action and route of elimination
31
Q
what is atracurium
A
NM blocker agent
- used to prevent eye movement during ocular surgery
- chemically similar to acetylcholine and competitively blocks nicotinic receptors at neuromuscular junction
- causes intense relaxation or paralysis of voluntary muscle
- intensity of effect depends on dose
- safer than other non depolarizing blockers like tubucurauine and pancuronium and depolarizing blockers like succinyl chlone which is now barely used
32
Q
what is cisatracurium
A
- same advantages of atracurium but less liekly to cause adverse effects
33
Q
what is procain
A
- first cocaine substitute
- main local anesthetic until lidocaine
- known as Novocain and still used but less frequently
- problem is that its an ester which is cleaved by plasma esterases and has a short duration of action (15-60min)
esters are more allergenic then amides but are sometimes still use wen rapid onset but short duration is desired
34
Q
what is lidocaine
A
- most widely used local anesthetic
- numerous routes of administration and applications
- overdose can cause drowsiness or seizures, muscle twitching, possible cardiac arrest and death
- usualy administered via injection and has duration of action of 30-60 min
- onset following infiltration is approx 3 min
- can aso be topical gel or topical spray
35
Q
what is bupivacaine
A
- antoher widely used local anesthetic
- slower onset (15min) but logner duration (2-4 hours)
- longer effects come with greater cardiovascular toxicity if an IV bolus forms, can cause severe ventricular arrhythias
- lecobupivacaine is the s(-) enantiomer and does not dsitribute well to CNS and heart
- **levobupivacaine has replaced bupivacaine for regional, IV use in human medicine.
