Reading...
Play button
Play button
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;
28 Cards in this Set
- Front
- Back
|
phenytoin
|
Mechanism of Action: Anticonvulsant, blocks rapidly opening Na channels
Effects: bind open channels selectively, limiting sustained repetitive transmission Indications:use for common seizure types (generalized / focal motor seizures, partial seizures with behavioral manifestations) Metabolism: Saturable hepatic metabolism (low levels = 1st order, high levels = zero order like alcohol – saturate enzymes - can have sudden unexpected toxicity) Toxicity: High levels: ataxia, nystagmus, also gum hypertrophy, increased hair; Bradycardia & cardiac arrhythmias if administration too rapid; Purple glove syndrome with IV phenytoin (skin / venous damage; can use pro-drug “Fosphenytoin” - water soluble with extra PO4 group - to avoid); Induces metabolism of carmazepine; Teratogen Other: less sedating than barbituates |
|
|
dexmedetomidine
|
Mechanism of Action: central alpha-2 adrenergic agonist
Effects:stimulates alpha-2 receptors (pre-synaptic feedback receptors, decreases adrenergic response) Indications & Administration: Long-term ICU sedation (little or no withdrawal after prolonged infusion), combined with opioids for surgery Other effects: keeps resps stable Toxicity: Drops BP, very expensive |
|
|
thiopental
|
Mechanism of Action: GABA agonist IV anesthetic.
Effects: Binds separate site on GABA receptor subunit; increases sensitivity of GABA receptor to GABA, increasing chloride flow & causing more hyperpolarization (inhibitory) in response to GABA. “Group 1” (acts via specific GABA-A receptor) Administration & Indications: Rapid sequence induction (emergency surgery); Continuous infusion (seizures, brain edema) Toxicity: Lowers BP, hypovolemia, apnea, tissue necrosis with extravasation: |
|
|
amantadine (Symmetrel)
|
Mechanism of Action: anti-Parkinson Disease agent, multiple effects (poorly understood)
Effects: weak anti-cholinergic, weak DA-releaser, weak glutamate antagonist Toxicity: hallucinations, insomnia, effects common to other anticholinergics (impaired cognition, dry mouth, constipation, urinary retention) |
|
|
benztropine (Cogentin), trihexyphenidyl (Artane)
|
Mechanism of Action: Anti-cholinergic agents (anti-PD)
Effects: Restores “Ach/DA balance” in theory (less DA, so cut down on ACh Indications: Parkinson Disease, especially in younger patients with tremor as predominant complaint. Generally contraindicated in elderly (cognitive problems) Toxicity: impaired cognition, constipation, urinary retention, dry mouth Other: Use in PD largely supplanted by MAO-i and direct DA agonists |
|
|
entacapone
|
Mechanism of Action: COMT inhibitor.
Effects: helps block hepatic metabolism of L-DOPA (increases half-life in brain, L-DOPA to brain) Administration: with sinemet (L-DOPA + carbidopa, an AADC inhibitor). Need to give 3-4x daily (like L-DOPA Metabolism: don't cross BBB: increase peripheral L-DOPA, helps stabilize concentrations over time Toxicity: generally well tolerated with occasional GI complaints, can cause urine to turn reddish brown |
|
|
lorazepam, diazepam
|
Mechanism of Action: benzodiazepine anticonvulsants
Effects: Enhance GABA activity (bind benzo receptor), increasing inhibitory signalling (hyperpolarizes by increasing Cl influx postsynaptically) Indications: used for rare seizure types, 1st line IV in status epilepticus Toxicity: powerful but sedative, cognitive side effects |
|
|
topiramate
|
Mechanism of Action: Anticonvulsant, blocks AMPA glutamate receptors
Effects: decreases excitatory glutamate signaling Toxicity: Memory & speech problems (AMPA receptors involved in memory formation) |
|
|
etomidate
|
Mechanism of Action: GABA agonist IV anesthetic.
Effects: Binds separate site on GABA receptor subunit; increases sensitivity of GABA receptor to GABA, increasing chloride flow & causing more hyperpolarization (inhibitory) in response to GABA. “Group 1” (acts via specific GABA-A receptor) Indications & Administration: Rapid sequence induction (emergency surgery, esp. in unstable pts) Toxicity: Apnea, inhibits 11-beta hydroxylase, causing drop in cortisol (CONTINUOUS INFUSION CONTRAINDICATED) Other:Hypnosis, amnesia, slowing of cortical EEG (GABA effects) |
|
|
propofol
|
Mechanism of Action: GABA agonist IV anesthetic.
Effects: Binds separate site on GABA receptor subunit; increases sensitivity of GABA receptor to GABA, increasing chloride flow & causing more hyperpolarization (inhibitory) in response to GABA. “Group 1” (acts via specific GABA-A receptor) Indications & Administration: Induction agent, Continuous infusion (alone for diagnostic procedures, + opioid for surgery) Toxicity: Mild drop in BP, decr. respirations, anaphylaxis with egg or soy allergies, burning sensation with injection Other: Hypnosis, amnesia, slowing of cortical EEG (GABA effects) |
|
|
remifentanil
|
Mechanism of Action: opioid receptor agonist
Indications & Administration: Combined with sedative or inhaled anesthetic in surgery, used when very rapid offset desired (metaboilzed by plasma cholinesterase) Toxicity: Apnea, BP drops, chest wall rigidity (need neuromuscular block & endotracheal intubation before ventilating pt). |
|
|
L-DOPA
|
Mechanism of Action: Dopamine receptor agonist (via DA, active metabolite)
Effects: L-DOPA converted to DA via AADC (both peripheral and in nervous tissue), augments DA signalling (decreased in PD) Indications: Parkinson Disease Adminstration: Short half life (1-2 hrs); must give several times throughout day; can result in large swings in serum [L-DOPA] Metabolism: Can cross BBB (DA can't). Less than 2% reaches CNS (rapidly metabolized by AADC in liver, other tissues). Toxicity: big swings are bad: involuntary movements (excessive peak doses); recurrence of symptoms (low trough doses). chronic spiking blood levels may play role in development of delayed dyskinesias. Acute side effects: nausea, orthostatic hypotension, hallucinations Chronic side effects (50% of pts after 5 yrs): wearing-off, on-off phenomenon, disabling dyskinesias |
|
|
pramipexole (Mirapex); ropinirole (Requip)
|
Mechanism of Action:Non-ergot DA receptor agonists (directly stimulate DA receptors). For Parkinson Disease
Indications: Parkinson Disease Adminstration: multiple daily doses (like L-DOPA) Toxicity: Generally well tolerated (alone / in combo). Nausea, somnolence, hallucinations, orthostatic hypertension. Can see mental status changes in elderly, daytime sleepiness, compulsive gambling (unusual side effect) Other: Above info for pramipexole; riponerole is very similar |
|
|
rasagaline (Azilect)
|
MAO-B inhibitor: like selegiline, but once-daily (longer duration of action)
No L-amphetamine / L-methamphetamine metabolites (probably not clinically relevant) |
|
|
selegiline (edepryl)
|
Mechanism of Action: MAO-inhibitor, for Parkinson Disease
Effects: Probably related to irreversible MAO inhibition (increases DA by decreasing breakdown) - symptomatic, not neuroprotective Indications: Parkinson Disease (complements other anti-PD meds) Adminstration: twice daily, generic available Metabolism: Complex pharmacokinetics; L-amphetamine, L-methamphetamine are metabolites; parent compound has MAO-B inhibiting activity too, need to follow MAO-B inhibition as kinetic parameter (not serum levels of drug / dose) Toxicity: well tolerated; rare weight loss Other: shown to prolong time until L-DOPA is needed. |
|
|
sinemet (L-DOPA + carbidopa)
|
Mechanism of Action: L-DOPA: Dopamine receptor agonist (via DA, active metabolite); carbidopa is a peripheral AADC inhibitor
Effects: L-DOPA converted to DA via AADC, augments DA signalling (decreased in PD). . Carbidopa blocks AADC peripherally, increasing delivery to CNS. Effectively reduces rest tremor, rigidity and bradykinesia; less effective in reversing postural instability Indications: Parkinson Disease Adminstration: Short half life (1-2 hrs); must give several times throughout day; can result in large swings in serum [L-DOPA]. Controlled-release preparations help, but slower onset of action, reduced peak blood levels, and longer duration of action Metabolism: Can cross BBB (DA can't). Much still metabolized in liver (COMT) Toxicity: big swings are bad: involuntary movements (excessive peak doses); recurrence of symptoms (low trough doses). chronic spiking blood levels may play role in development of delayed dyskinesias |
|
|
carbamazepine
|
Mechanism of Action: Anticonvulsant, blocks rapidly opening Na channels
Effects: bind open channels selectively, limiting sustained repetitive transmission Indications:use for common seizure types (generalized / focal motor seizures, partial seizures with behavioral manifestations). One of most prescribed anticonvulsants Metabolism: Hepatic metabolism to epoxide metabolite - induces own metabolism; short half-life with sustained release preparation available Toxicity: Few cognitive side effects. Don't use in absence seizures (can make them WORSE!). Teratogen |
|
|
ethosuxamide
|
Mechanism of Action: anticonvulsant, blocks voltage-dependent Ca channels
Effects: Decreases excitatory signaling (blocks Ca reuptake into presynaptic neuron and Ca influx into post-synaptic neuron) Indications:Generalized absence seizures Toxicity: Teratogen |
|
|
lamotrigine
|
Mechanism of Action: Anticonvulsant, blocks Na channels associated with pre-synaptic glutamate release
Effects: limits sustained repetitive transmission Indications:use for common seizure types (generalized / focal motor seizures, partial seizures with behavioral manifestations). also used for less common seizure types (e.g. generalized absence) Metabolism: Hepatic metabolism via glucuronidation; half life prolonged by other drugs (e.g. valproic acid). Teratogen Toxicity: Severe skin rashes in 1% children, 0.3% adults |
|
|
levetiracetam
|
Mechanism of Action: Anticonvulsant, binds SV2A vesicle protein on synaptic vesicles
Effects: inhibits Ca-mediated glutamate exocytosis from pre-synaptic neuron Toxicity: teratogen |
|
|
phenobarbital, primidone
|
Mechanism of Action: barbituate anticonvulsants
Effects: Enhance GABA / benzodiazepine receptor function, increasing chloride influx and causing hyperpolarization / inhibition of synaptic transmission Indications:powerful, use for common seizure types (generalized / focal motor seizures, partial seizures with behavioral manifestations) Metabolism: in liver, long half lives, 1st order kinetics over broad range. Primidone converted to phenobarbital & PEMA (both anticonvulsants) via in vivo metabolism. Toxicity: Cognitive and behavioral side effects, depression. Teratogen |
|
|
valproic acid
|
Mechanism of Action: Anticonvulsant, blocks rapidly opening Na channels, enhances GABA / BZ receptors, may have other mechanisms?
Effects: bind open channels selectively, limiting sustained repetitive transmission; other mechanisms too Indications: useful for all seizure types Metabolism: Hepatic metabolism (as fatty acid) Toxicity: Fatal hepatic necrosis in children < 2 yo, especially if on second anticonvulsant (incidence 2/1000). Slows metabolism of phenobarbital, lamotrigine. Teratogen (strongly associated with spina bifida, can reduce risk with folic acid) |
|
|
ketamine
|
Mechanism of Action: NMDA receptor blocker
Effects:Blocks excitatory glutamate signaling (NMDA) “Group 2” (targets NMDA/AMPA/kainate glutamate receptors, K<sup>+</sup> channels). Produces dissociative anesthesia (eyes open but unresponsive) with profound cutaneous analgesia Indications & Administration: Rapid sequence induction (emergency surgery, esp. unstable pts). Burn dressing changes (cutaneous analgesia). Bronchodilator (used for severe asthma in ICU). Other effects: Stimulates HR, keeps BP & resps stable, stimulates SNS Toxicity: Decreased seizure threshold (contraindicated in epilepsy), increased ICP (contraindicated in head trauma), increased oral secretions |
|
|
desflurane
|
Mechanism of Action: Potent, volatile inhaled anesthetic. Ether.
Effects: “Group 3”: multiple molecular effects (increases inhibitory ion channel flow, depresses excitatory ion channel flow) Special Features: Rapid onset / recovery Toxicity: Laryngospasm (severe airway irritant). Need to use another inducing agent first (to suppress laryngospasm) Other: Hypnosis, amnesia, slowing of cortical EEG (GABA effects). Blood/Gas solubility coefficient: 0.42 |
|
|
halothane
|
Mechanism of Action: Potent, volatile inhaled anesthetic. Alkane.
Effects: “Group 3”: multiple molecular effects (increases inhibitory ion channel flow, depresses excitatory ion channel flow) Special Features: Slow onset / recovery, metabolized (40% elimination - unique among inhaled anesthetics). Toxicity: Myocardial depressant Other: Hypnosis, amnesia, slowing of cortical EEG (GABA effects). Standard to measure solubility, Blood/Gas solubility coefficient: 2.3 |
|
|
isoflurane
|
Mechanism of Action: Potent, volatile inhaled anesthetic. Ether.
Effects: “Group 3”: multiple molecular effects (increases inhibitory ion channel flow, depresses excitatory ion channel flow) Special Features: Medium onset / recovery, slightly pungent odor Toxicity: Airway irritant (coughing) Other: Hypnosis, amnesia, slowing of cortical EEG (GABA effects). Blood/Gas solubility coefficient: 1.4 |
|
|
nitrous oxide (N2O)
|
Mechanism of Action: Potent, volatile inhaled anesthetic. Gas.
Effects: “Group 2”: targets glutamate receptors(NMDA, AMPA, kainate) and two pore K+ channels Toxicity: Need to give with O2 and other anesthetics (high MAC; would need to give lethal dose to achieve total anesthesia) Other: Analgesia (NMDA effect). Blood/Gas solubility coefficient: 0.47 |
|
|
sevoflurane
|
Mechanism of Action: Potent, volatile inhaled anesthetic. Ether.
Effects: “Group 3”: multiple molecular effects (increases inhibitory ion channel flow, depresses excitatory ion channel flow) Special Features: Rapid onset / recovery Toxicity: Emergence delerium Other: Hypnosis, amnesia, slowing of cortical EEG (GABA effects). Blood/Gas solubility coefficient: 0.69 |
