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59 Cards in this Set

  • Front
  • Back
Phenytoin
-Mechanism
Use-dependent blockade of Na+ channels; inhibition of glutamate release from excitatory presynaptic nuerons
Phenytoin
-Clinical use
Tonic-clonic seizure; also class 1B antiarrhythmic
Phenytoin
-Toxicity
*Chronic use produces gingival hyperplaisa in children
-Peripheral neuropathy,
-megaloblastic anemia (decreases folate absorption)
-Teratogenic (fetal hydanton syndrome)
Nystagmus, ataxia, diplopia sedation, SLE-like symptoms; induction of cytochrome p-450.
Barbiturate
-Mechanism
Facilitate GABAa action by increasing duration of Cl- channel opening, thus decreasing neuron firing
(Ending with barbital)
Barbiturate
-Clinical use
Sedative for anxiety, seizures, insomnia, induction of anesthesia (thiopental)
Barbiturate
-Toxicity
Dependence, additive CNS depression effects with Alcohol, respiratory or cardiovascular depression (can lead to death), drug interactions owing to induction of liver microsomal enzymes (cytochrome p450)
How do you treat Barbiturate overdose?
Symptom management (Assist respiration, increase BP)
Benzodiazepine
-Mechanism
Facilitate GabaA action by increasing frequency of Cl- channel opening. MOst havne long half-lifes and active metabolites (most examples end with zepam (Lorazepam))
Which drug has an effect on sleep cycle?
Benzodiazepine decreases REM sleep
Benzodiazepine
-Clinical use
Anxiety, spasticity, status epilepticus (lorazepam and diazepam), detoxification especially alcohol withdrawl-DT's), night terrors, sleep walking
Benzodiazepines
-Toxicity
Dependence, additive CNS depression effect with alcohol. Less risk of respiratory depression and coma than with barbiturates
Which Benzodiazepine have the highest addictive potential?
Short acting- TOM traizolam, oxazepam, Midazolam
What do you treat Benzodiazepine with?
Flumazenil (Competitive antagonist at GABA receptors
What are the requirements of CNS drugs?
Lipid-Soluble--> Go through CNS (blood-brain barrier)
CNS drugs with decrease blood solubility has what effect
Decrease solubility in blood causes rapid induction and recovery
Drugs with increase solubility in lipids have what effect
Increase potency= 1/MAC
MAC=Minimal alveolar concentration at which 50% of the popoulation is anesthesized decrease with age
N20 low blood and lipid solublitiy means
fast induction and low potency
Inhaled anesthetics
-Examples
Halothane, -flurane, Nitrous oxide
Inhaled anesthetics
-Effects
-Brain
-Body
Myocardial depression, respiratory depression, nausea/emesis, increase cerebral blood flow (decrease cerebral metabolic demand)
Halothane and methyoxyflurane
-Toxicity
*Hepatotoxicity (halothane), nephrotoxicity (methyoxyflurane)
Proconvulsant (enflurane)
Thiopental
-Potency and lipid solubility
Benzodiazepin High potency and high lipid solublity used for short surgical procedures
Midazolam
-Uses of and what type of drug
Benzodiazepines, most common drug for endoscopy used with gasesous anesthestics and narcotics.
Can cause respiratory depression, decrease BP and Amnesia
Ketamine
-Use
PCP analog acts as a dissociative anesthetics. Blocks NMDA receptors. Cardiovascular stimulants. Increase cerebral blood flow
Ketamine
-Side effects
Disorientaion, hallucination, and bad dreams
Morphine
-Use
Opiate during general anesthesia (fentanyl as well)
Propofol
-Use
Used for rapid anesthesia induction and short procedures. Potentiates GABAa
Why would propofol be used instead of thiopental?
Less post-op nausea
Esters vs. Amides idenitifying
Esters one I and Amides hae two I's
Esters and Amides
-Mechanisms
Blocks Na+ channels by binding to specific receptors on inner portion of channel. Preferentially binds to activated Na+ channels so most effective in rapidly firing neurons. third degree amine local anesthetics penetrate membrane in uncharged form then bind to ion channels as charged form
Procaine
-Category
Ester
Thiopental
-Type
Barbiturate
Lidocaine
-Type
Amide
Esters and amides
-Allergic
If your allergic to one give the other
Esters and amides
-Infected tissues
In infected tissue its acidic so the alkaline anesthetic are charged and cannot penetrate membrane effectively (Give more anesthetic)
Esters and amides
-Order of nerve blockade
small diameter myelinated fiber> small unmyelinated fiber> large myelinated fiber> large unmyelinated fiber
Size predominates over myelination
Esters and amides
-Order of losses of temp, pain, pressurem touch
Pain (lose first) > temp> touch> pressure (lose last)
Esters and amides
-How do you enhance local action
Give with vasoconstrictors (usually epi) to decrease bleeding, Increase anesthesia by decreasing systemic concentration
Succinylcholine
-Complications
Hyperkalemia and hypercalcemia
Succinylcholine
-stages and reversibility
Considered a depolarizing drug
Nicotinic
Phase I (prolonged depolarization): no anitdote block potentiated by cholinesterase inhibitors
Phase II: (repolarized by blocked)- antidote consist of cholinesterase inhibitors (eg. Neostigmine)
Tubocurarine
-Mechanism
Non-depolarizing compete with Ach for receptors (nicotinic)
Tubucurarine
-Agents for Reversal of blockade
neostigmine, edrophonium, and other cholinesterease inhibitors
Dantrolene
-Used in treatment of
Malignant hyperthermia (causesd by concominant use of inhalation anesthetics (halothane, not n20) and succinyl choline
Also used to treat neuroleptic malignant syndrome
Dantrolene
-Mechanism
prevents release of Ca2+ from the sarcoplasmic reticulum of skeletal muscles (muscle relaxer)
Drugs used in parkinsons
Bromocriptine
Amatadine
Levdopa
Selegline
Anticholinergic
Bromocriptine
-Function
Agonize dopamine receptors
Amatidine
-Function
Increase dopamine release (also antiviral against influenza and rubella)
Levdopa
-Mechanism
Converted to dopamine in CNS given with Carbidopa. Can cross blood-brain barrier and converted to Dopa-decarboxylase in the CNS to dopamine
Selegline
-Function
Prevent dopamine breakdown (selective MAO type B inhibitor)
Benztropine
-Function
Curb excess cholinergic activity (antimuscarininc- improves tremor and rigidity but little effect on bradykinesia)
For essential or familial tremor use
Beta-Blockers
Levdopa
-Toxicity
Arrhythmias from peripheral conversion to dopamine
Long-term use--> dyskinesia following administration, akinesia between doses
Why is Carbidopa given with L-Dopa?
Carbidopa (peripheral decarboxylase inhibitor) to increase the bioavailability of L-dopa in the brain and limit peripheral side effects
Sumatriptan
-Mechanism
5-HT (1b/1d) agonist causes vasoconstriction, inhibition of trigeminal activation and vasoactive peptide release:
Sumatriptan
-Clinical use
Acute Migraine, cluster headache attacks
Sumatriptan
-Toxicity
Coronary vasospasm (contraindicatied in patients with CAD or Prinzmental's angina), mild tingling
Memantine
-Mechanism
NMDA receptor antagonist; (prevents too much glutamate which can hurt the brain) helps prevent excitotoxicity (mediated by Ca2+)
Memantine
-Toxicity
Dizziness, confusion, hallucinations
Donepezil
-Mechanism
Acetylcholinesterase inhibitor
Alzheimers
Donepezil
-Toxicity
Nausea, dizziness, insomnia