Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
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
|