Neuro drugs 2 Flashcards
other inhaled anesthetic other than the -anes?
Nitrous oxide (N2O)
inhaled anesthetic mechanism?
unknown
Effects of inhaled anesthetics
1) myocardial depression
2) respiratory depression
3) nausea/emesis
4) increased cerebral blood flow (due to decreased cerebral metabolic demand)
methoxyflurane AE
nephrotoxic
nitrous oxide AE
expansion of trapped gas in a body cavity
what else can cause malignant hyperthermia?
succinylcholine
malignant hyperthermia genetics and inheritance
1) autosomal dominant with variable penetrance
2) mutations in voltage-sensitive ryanoidine receptor causing increased calcium release.
Dantrolene mechanism
Ryanodine receptor antagonist
IV anesthetics
The Mighty King Proposes Foolishly to Oprah Barbiturates (thiopental) Benzos (Midazolam) Arylcyclohexylamines (Ketamine) Propofol Opioids
thiopental profile
1) High potency, high lipid solubility, rapid entry of brain
2) Effect terminated by rapid redistribution into tissue and fat.
3) decreased cerebral blood flow.
thiopental uses
Induction of anesthesia and short surgical procedures.
Midazolam use
endoscopy; used adjectively with gaseous anesthetics and narcotics.
midazolam AE’s
1) severe postoperative respiratory depression.
2) drops BP
3) anterograde amnesia
ketamine mechanism
PCP analog, thus blocks NMDA receptors. Cardiovascular stimulant.
ketamine effects
1) disorientation
2) hallucination
3) bad dreams
4) increased cerebral blood flow.
propofol uses
1) sedation in ICU
2) rapid anesthesia induction
3) short procedures
nice thing about propofol
less postop nausea than thiopental
opioid IV anesthetics and use
morphine, fentanyl used with other CNS depressants during general anesthesia.
NMDA receptor structure
Glutamate receptor and ion channel protein. Glutamate and glycine bind.
- magnesium ion.
esters vs. amides nomenclature
Amides have 2 I’s. Esters have 1.
use of neuromuscular blocking drugs?
muscle paralysis in surgery or mechanical ventilation.
depolarizing neuromuscular blocking drug?
succinylcholine
succinylcholine MOA
Strong ACh receptor agonist; produces sustained depolarization.
succinylcholine complicatoins
1) hypercalcemia
2) hyperkalemia
3) malignant hyperthermia
Reversal of depolarizing blockade: Phase I
Phase I = prolonged depolarization.
No antidote. Block potentiated by cholinesterase inhibitors.
Reversal of depolarizing blockade: Phase II
Phase iI = Repolarized but blocked; ACh receptors available but desensitized)—may be reversed with cholinesterase inhibitors.
non depolarizing NMJ drugs
Tubocurarine Atracurium Mivacurium Pancuronium Vecuronium Rocuronium
non depolarizing NMJ drug MOA
competitive ACh antagonists
How do you reverse blockade with non depolarizing drugs?
Neostigmine + atropine (need to give atropine to prevent muscarinic effects such as bradycardia) OR edrophonium Or other cholinesterase inhibitors
baclofen MOA
GABA B agonist
ergot dopamine agonists
bromocriptine
non-ergot dopamine agonists
pramipexole, ropinirole
which dopamine agonists are preferred for PD?
non-ergot (pramipexole, ropinirole)
Amantadine MOA for PD
increases dopamine availability (increases dopamine release and decreases dopamine reuptake)
amantadine toxicity
1) Ataxia
2) livedo reticularis
carbidopa MOA
blocks peripheral conversion of L-DOPA to dopamine by inhibiting DOPA decarboxylase.
Other benefit of carbidopa
Reduces side effects of peripheral L-dopa conversion into dopamine (nausea, vomiting)
entacapone, tolcapone MOA
inhibit COMT
COMT action
degrades peripheral L-dopa to 3-O-methyldopa (3-OMD)
selegiline MOA
inhibits MAO-B
MAO-B action
converts dopamine to DOPAC
Why is benztropine used?
curbs excess cholinergic activity, thus improving tremor and rigidity. *no effect on bradykinesia.
Difference between L-dopa and dopamine
L-dopa can cross BBB and is converted by dopa decarboxylase to dopamine.
AE’s of levodopa/carbidopa
- Arrhythmias from increased peripheral formation of catecholamines.
- long-term use can lead to dyskinesia following administration (“on-off” phenomenon).
- akinesia between doses.
other drug like selegiline?
rasagiline
selegiline/rasagiline AE
May enhance adverse effects of L-dopa.
Memantine use
AD
memantine MOA
1) NMDA receptor antagonist
2) helps prevent excitotoxicity (mediated by Ca2+)
memantine AE’s
Dizziness + confusion + hallucinations
other AChE inhibitor used for AD?
tacrine
AChE inhibitor (donepezil AE’s)..
1) nausea
2) dizziness
3) insomnia
HD drugs?
1) tetrabenazine
2) reserpine
3) haloperidol
haloperidol MOA
D*2 receptor antagonist
tetrabenazine/reserpine MOA
Inhibit VMAT, leading to decreased dopamine vesicle packaging and release.
Riluzole MOA
decreases glutamate excitotoxicity via an unclear mechanism.
Efficacy of riluzole?
not great, only modestly increases survival.
What serotonin receptor do triptans target?
5-HT*1B/1D
Triptan effects?
1) inhibit trigeminal nerve activation
2) prevent vasoactive peptide release
3) induce vasoconstriction
triptan AE’s
1) coronary vasospasm
2) mild paresthesia
triptans AE’s
1) CAD
2) prinzmetal angina
