Neurology Flashcards
Acetazolamide
Glaucoma also diuretic
Decrease aqueous humor synthesis via inhibition of carbonic anhydrase
NO PUPILLARY OR VISION CHANGES
Methadone
Opioid analgesic
Majority of OD related deaths
Acts at mu receptors: efflux K+, close Ca2+ channels:decreasing synaptic transmison
Inhibit release of ACh, norepinephrine, 5-HT, glutamate, substance P
Clinical: pain, acute pulmonary edema, HEROIN ADDICTS
Toxicity: Respiratory depression, block urinary voiding reflexes
Constipation and miosis no tolerance!
Fentanyl
Opioid analgesic
Majority of OD related deaths
Acts at mu receptors: efflux K+, close Ca2+ channels:decreasing synaptic transmison
Inhibit release of ACh, norepinephrine, 5-HT, glutamate, substance P
Clinical: pain, acute pulmonary edema
Toxicity: Respiratory depression, block urinary voiding reflexes
Constipation and miosis no tolerance!
Loperamide
Opioid analgesic
Majority of OD related deaths
Acts at mu receptors: efflux K+, close Ca2+ channels:decreasing synaptic transmison
Inhibit release of ACh, norepinephrine, 5-HT, glutamate, substance P
Clinical: pain, acute pulmonary edema, DIARRHEA
Toxicity: Respiratory depression, block urinary voiding reflexes
Constipation and miosis no tolerance!
Brimonidine
Glaucoma
Decrease aqueous humor synthesis
Side effects: Mydriasis; not used in closed angle glaucoma
ocular hyperemia, foreign body sensation, allergy reactions, ocular pruritus
Meperidine
Opioid analgesic
Majority of OD related deaths
Acts at mu receptors: efflux K+, close Ca2+ channels:decreasing synaptic transmison
Inhibit release of ACh, norepinephrine, 5-HT, glutamate, substance P
Clinical: pain, acute pulmonary edema
Toxicity: Respiratory depression, block urinary voiding reflexes. DILATES pupils in overdose.
DOESN’T CAUSE BILIARY COLIC
Constipation and miosis have no tolerance!
Timolol, betaxolol, carteolol
Glaucoma
Decrease aqueous humor synthesis
NO PUPILLARY OR VISION CHANGES
Latanoprost (PGFalpha)
Glaucoma: Prostaglandin
Increase outflow of aqueous humor
Darkens color of iris
Codeine
Opioid analgesic
Majority of OD related deaths
Acts at mu receptors: efflux K+, close Ca2+ channels:decreasing synaptic transmison
Inhibit release of ACh, norepinephrine, 5-HT, glutamate, substance P
Clinical: pain, acute pulmonary edema
Toxicity: Respiratory depression, block urinary voiding reflexes
Constipation and miosis no tolerance!
Diphenoxylate
Opioid analgesic
Majority of OD related deaths
Acts at mu receptors: efflux K+, close Ca2+ channels:decreasing synaptic transmison
Inhibit release of ACh, norepinephrine, 5-HT, glutamate, substance P
Clinical: pain, acute pulmonary edema, DIARRHEA
Toxicity: Respiratory depression, block urinary voiding reflexes
Constipation and miosis no tolerance!
Physostigimine, echothiophate
Use in pilocarpine emergencies,
very effective at opening meshwork into canal of Schlemm
Glaucoma: Epinephrine
Alpha Agonist
Decrease aqueous humor synthesis via vasconstriction
Side effects: Mydriasis; not used in closed angle glaucoma
ocular hyperemia, foreign body sensation, allergy reactions, ocular pruritus
Morphine
Opioid analgesic
Majority of OD related deaths
Acts at mu receptors: efflux K+, close Ca2+ channels:decreasing synaptic transmission, inhibit adenylate Cyclase
Inhibit release of ACh, norepinephrine, 5-HT, glutamate, substance P
Clinical: pain, acute pulmonary edema
Toxicity: Respiratory depression, block urinary voiding reflexes
Constipation and miosis no tolerance!
Naloxone
Opioid receptor antagonist
treats opioid toxicity
Displaces morphine from receptors (used acutely)
reverses analgesia, sedation, hypotension and respiratory depression
dextromethorphan
Opioid analgesic
Majority of OD related deaths
Acts at mu receptors: efflux K+, close Ca2+ channels:decreasing synaptic transmison
Inhibit release of ACh, norepinephrine, 5-HT, glutamate, substance P
Clinical: pain, acute pulmonary edema, COUGH SUPPRESSION
Toxicity: Respiratory depression, block urinary voiding reflexes
Constipation and miosis no tolerance!
Tramadol
Weak opioid receptor agonist
Inhibits serotonin and NE reuptake
Clinical: chronic pain
Decreases seizure threshold, serotonin syndrome
Pentazocine
mu receptor agonist and weak antagonist
Competitively inhibits mu receptors and produces antagonistic effects leading to decreased opioid analgesic effects
Designed to produce analgesic effects with little abuse potential
Naltrexone
opioid receptor antagonist
Treats opioid toxicity
Ethosuximide
MOA: blocks thalamic T-type Ca2 channels
Clinical: absence seizures
Side effects: Fatigue, GI distress, Headache, Itching and Stevens-Johnson Syndrome
FGHIJ
Pilocarpine, carbachol
Glaucoma: cholnomimetic
increase outflow of aqueous humor via contraction of ciliary muscle and opening of trabecular meshwork
Side effects: miosis and cyclospasm
Benzodiazepines-seizure (diazepam, loazepam)
MOA: increase GABA action
Clinical: status epilepticus, eclampsia seizures, night terrors and sleepwalking, anxiolytic (Generalized anxiety disorder and panic attacks), short term for insomnia, seizures due to alcohol withdrawal, spasticity (muscle relaxant)
Side effects: sedation, tolerance, dependence, respiratory depression, impairs balance, decrease memory and concentration.
CI: alcohol, barbiturates, neuroleptics, and 1st gen antihistamines
Phenytoin
MOA: increased Na channel inactivation
Increase refractory period
Clinical: simple, complex, TONIC CLONIC (1st line), status epilepticus (1st line prophylaxis)
Side effects: ataxia, nystagmus, gingival hyperplasia (increased expression of PDGF), hirsutism, megaloblastic anemia (folate deficiency) fetal hydantoin syndrome, SLE-like syndrome, induction of cytocrhome P-450, lymphadenoapthy, SJ syndrome, osteopenia
Carbamazepine
MOA: increase Na channel inactivation
Clinical: first line for simple, complex and tonic clonic
Side effects: diplpia, agraunulocytosis, aplastic anemia, liver toxicity, teratogensis, induction of cytochrome P-450, SIADH, SJ syndrome
Monitor blood and LFTs
1st line for tirgeminal neuralgia
Valproic acid-seizures
MOA: increase Na channel inactiavtion
Increase GABA concentration by inhibiting GABA transminase
Clinical: Simple, complex, TONIC CLONIC (1st line), absence, juvenile myoclonic epilepsy
Side effects: GI distress, fatal hepatotoxicity, neural tube defects in fetus, weight gain, contraindicated in pregnancy
Also used for myoclonic seizures and bipolar disorder
Drug of choice for absence seizures associated with tonic clonic seizures
Gabapentin
MOA: Inihibits voltage activated Ca channels
GABA analog
Clinical: Simple, complex, tonic clonic
Side effects: sedation, ataxia
also used for peripheral neuropathy, postherpetic neuralgia, migraine prophylaxis, bipolar disorder
Phenoarbital
MOA: increase GABA action
Clinical: simple, complex, tonic-clonic
Side effects: sedation, tolerance, induction of cytochrome P-450, cardiorespiratroy depression
1st line in neonates
Topiramate
MOA: blocks Na channels
Increase GABA action
Clinical: simple, complex, tonic clonic
Side effects: mental dulling, kidney stones, weight loss
Used for refractory partial seizures, and migraine prevention
Tiagabine
MOA: Increase GABA by inhbiting re-uptake
Clinical: simple and complex
Also used for refractory partial seizures
Vigabatrin
MOA: increase GABA by irreversibly inhibiting GABA transaminase
Clinical: simpe and complex
Also used for refratory partial seizures
Barbituates
Phenoarbital, pentoarbital, thiopental, secobarbital
MOA: facilitate GABA by increasing DURATION of Cl- channel opening decreasing neuron firing
Contraindicated in porphyria
Clinical: sedative for anxiety, seizures, insomnia, induction of anesthesia (theopental)
Toxicity: respiratory and cardiovascular depression (can be fatal), CNS depression (exacerbated by alcohol use), dependence
Induce cytochrome P-450
Overdose treatment is supportive (assist respiration and maintain BP)
Halothane
Inhaled anesthetic
MOA: unknown
Effects: myocardial depression (increase atrial and ventricular pressures), respiratory depression, nausea/emesis, increased cerebral blood flow (increase intracranial pressure), decrease metabolic demand, decrease mucociliary clearance (atelectasis), decrease GFR, decrease hepatic flow
Bronchodilation properties used in patients with asthma
Toxicity: Hepatotoxicity-extensive hepatic necrosis (autoAb damage), Increased AST, ALT and bilirubin Malignant hyperthermia (+succinylcholine) induce fever and severe muscle contractions-Treat with dantrolene
Levetiracetam
MOA: Unknown
Clinical: Simple, complex, tonic clonic
Long acting Benzodiazepines
Diazepam, temazepam, Chlorodiazepoxide, clorazepate, flurazepam
MOA: Facilitate GABA by increasing frequency of Cl- channel opening
Decreases REM sleep
Clinical: anxiety, spasticity, status epilepticus (diazepam), detoxification from alcohol delirum tremens, general anesthetic (amnesia muscle relaxation), hypnotic (insomnia)
Diazepam and chlrodizepoxide are first line treatment for seizures assoicated with alcohol withdrawal
Toxicity: Less dependence (due to slower clearance), Higher daytime drowsiness (increased chance of falls), additive CNS ddepression effects with alcohol, less risk of respiratory depression and coma than barbiturates, sedation impairs coordination and balance (avoid in elderly) decreased memory and concentration
Avoid with alcohol, barbituates, neuroleptics and 1st gen antihistamines
Treat overdose with flumazenil (competitive antagonist at GABA benzodiazepine receptor)
Medium acting Benzodiazepines
Estazolam, lorazepam, temazepam
10-20 hour duration
MOA: facilitate GABA action by increasing frequency of CL- channel opening
Decrease REM sleep
Clinical: anxiety, spasticity, status epilepticus (lorazepam), detoxification from alcohol delirum tremens, general anesthetic (amnesia muscle relaxation), hypnotic (insomnia)
Toxicity: dependence, additive CNS depression with alcohol, less respiratory depression and coma than barbiturates, sedation impairs coordination and balance (avoid in elderly), decreased memory and concentration
Treat overdose with flumazenil (competitive antagonist at GABA benzodizepine receptor)
isoflurane
Inhaled anesthetic
MOA: unknown
Effects: myocardial depression (increase atrial and ventricular pressures), respiratory depression, nausea/emesis, increased cerebral blood flow (increase intracranial pressure), decrease metabolic demand, decrease mucociliary clearance (atelectasis), decrease GFR, decrease hepatic flow
Toxicity: malignant hyperthermia AD (+succinylcholine) induces fever and severe muscle contractions-treat with dantrolene
Butorphanol
Mu-opioid receptor partial agonist and kappa-opioid receptor agonist, produces analgesia
Clinical: severe pain (migraine, labor)
Toxicity: less respiratory depression
can cause opioid withdrawal symptoms
Sevoflurane
Inhaled anesthetic
MOA: unknown
Effects: myocardial depression (increase atrial and ventricular pressures), respiratory depression, nausea/emesis, increased cerebral blood flow (increase intracranial pressure), decrease metabolic demand, decrease mucociliary clearance (atelectasis), decrease GFR, decrease hepatic flow
Bronchodilation properties used in patients with asthma
Toxicity: Malignant hyperthermia-AD (+succinylcholine) induces fever and severe muscle contractions-treat with dantrolene
Short acting benzodiazepines
Triazolam, Oxazepam, midazolam and alprazolam (TOM and Al are short)
MOA: facilitate GABA action by increasing frequency of Cl- channel opening
Decrease REM sleep
Clinical: anxiety, spasticity, detoxification from alcohol delirum tremens, general anesthetic (amnesia muscle relaxation), hypnotic (insomnia)
Toxicity: dependence, additive CNS depression with alcohol, less respiratory depression and coma than barbiturates, sedation impairs coordination and balance (avoid in elderly), decreased memory and concentration
LESS DROWSINESS
SEVERE WITHDRAWAL SYMPTOMS AND HIGHER ADDICTIVE POTENTIAL
Treat overdose with flumazenil (competitive antagonist at GABA benzodiazepine receptor)
Midazolam
Benzodiazepine used for IV anesthetics
Used for endoscopy
Used with gaseous anesthetics and narcotics
may cause severe postop respiratory depression
Decrease BP (treat overdose with flumazenil)
anterograde amnesia
Nonbenzodiazepine hypnotics
Zolpidem (Ambien), Zaleplon, eszopiclone
MOA: act via the BZ1 subtype of the GABA receptor. Effect reversed by flumazenil
Rapid onset of action
Clinical: insomnia
Toxicity: ataxia, headaches confusion
less risk of dependence than benzodiazepines
No antconvulsant or muscle relaxing acitivity
Rapid metabolism by liver enzymes
Nitrous oxide
Inhaled anesthetic
MOA: unknown
Effects: myocardial depression (increase atrial and ventricular pressures), respiratory depression, nausea/emesis, increased cerebral blood flow (increase intracranial pressure), decrease metabolic demand, decrease mucociliary clearance (atelectasis), decrease GFR, decrease hepatic flow
Toxicity: expansion of trapped gas in a body cavity
Arylcyclohexylamines
Ketamine
PCP analogs that act as dissociateive aneshtetics
MOA: block NMDA recpetors
Cardiovascular stimulants
Cause disorientation, hallucination and bad dreams
Increase cerebral blood flow
Also used in treating morphine tolerance
Thiopental
Barbiturate IV anesthetic
High potency and high lipid solubility-rapidly enters brain
Great for recovery
used of induction of anesthesia and short surgical procedures
effect terminated by rapid redistribution into tissue (skeletal muscle and fat)
Decreased cerebral blood flow
Propofol
Used for sedation in ICU
Rapid anesthesia induction and short procedures
less postop nausea than thiopental
Potentiates GABA
Local Anesthetics
Esters: procaine, cocaine, tetracaine
Amides: lidocaine, mepivacaine, bupivacaine (amides have 2 i’s)
MOA: block Na channels by binding to receptors on inner portion of channel
Preferentially bind to activated Na channels so most effective in rapidly firing neurons
Clinical: with epinephrine to enhance local action leading to decrease bleeding, increase anesthesia by decreasing systemic concentration
Cannot penetrate membrane effectively in infected tissue due to acidic environment
Affect small diameter fibers and myelinated fibers (size matters more) more than large and unmyelinated
Order of loss: pain-temp-touch-pressure
Use: minor surgical procedures, spinal anesthesia
Toxicity: CNA excitation, severe cardiovacular toxicity (bupivacaine), hypertesnion, hypotension and arrhytmmias (cocaine)
l-dopa/carbidopa
MOA: increase dopamine in brain
l-dopa can cross BBB and converted by dopa decarbocylase in the CNS to dopamine
Carbidopa: peripheral decarboxylase inhibitor-increases L-dopa bioavalability in the brain
limits peripheral side effects not anxiety, agitation, insomnia, confusion, delusions and hallucinations
Clinical: parkinsons-will experience on/off phenomenon (unpredictable)
Toxicity: arrhytmias from increase peripheral formation of catecholamines
can lead to dyskinesia following administartion and akinesia bewtee doses also dystonia (all occur after 5-10 years of use)
Somnolence, confusion, hallucinations (first in older people)
Do not take with vitamin B6 due to increase peripheral metabolism of levodopa decreasing its effectiveness
Fastest induction and recovery times for anesthetics
Low solubility in blood
Greatest potency of anesthetics
Increased solubility in lipids (1/MAC)
Succinylcholine
Depolarizing neuromuscular blocking drug
MOA: strong ACh receptor agonist: produces sustained depolarization and prevents muscle contraction
-Not degraded by AChE
Reversal of blockade
Phase I: (prolonged depolarization)-no antidote potentiated by cholinesterase inhibitors
Phase II: (repolarized but blocked-Ach receptors are available but desensitized)-antidote cholinesterase inhibitors
Clinical: muscle paralysis in surgery or mechanical ventilation-selective for motor nicotinic receptor
Complications: hypercalcemia, hyperkalemia (can lead to rhabdomyolysis especially with halothane) and malignant hyperthermia
arrhythmias
Lamotrigine
MOA: blocks voltage gated Na channels
Clinical: simple, complex, tonic clonic, absence
Side effects: SJ syndrome
Also used for refractory partial seizures, and Bi-polar disorder
Enflurane
Inhaled anesthetic
MOA: unknown
Effects: myocardial depression (increase atrial and ventricular pressures), respiratory depression, nausea/emesis, increased cerebral blood flow (increase intracranial pressure), decrease metabolic demand, decrease mucociliary clearance (atelectasis), decrease GFR, decrease hepatic flow
Toxicity: proconvulsant
Malignant hyperthermia: AD (+succinylcholine) induces fever and severe muscle contractions-treatment dantrolene
Bromocriptine, pergolide, pramipexole, ropinirole
Bromocriptine, pergolide-ergot
pramipexole, ropinirole-non-ergot
Non ergots perferred due to longer half life
MOA: dopamine agonists
Treats parkinsons
Methoxyflurane
Inhaled anesthetic
MOA: unknown
Effects: myocardial depression (increase atrial and ventricular pressures), respiratory depression, nausea/emesis, increased cerebral blood flow (increase intracranial pressure), decrease metabolic demand, decrease mucociliary clearance (atelectasis), decrease GFR, decrease hepatic flow
Toxicity: nephrotoxicity
Malignant hyperthermia-AD (+succinylcoline) induce fever and severe muscle contractions-treat with dantrolene
Dantrolene
MOA: prevent release of Ca2+ from the sarcoplasmic reticulum of skeletal muscle
Clinical: treat malignant hyperthermia and neuroleptic malignant syndrome-toxicity of antipsychotic drugs
Selegiline
MOA: selectively inhibits MAO-B which metabolizes dopamine over NE and 5HT increasing the availability of dopamine
Clinical: adjunctive agent to L-dopa in treatment of Parkinson
toxicity: may enhance adverse effects of L-dopa
MPTP produces Parkionsonism (MPP+ created by MAO-B causes damage) can be prevented by pretreatment with selegiline
Entacapone, tolcapone
MOA: COMT inhibitors prevent L-dopa degradation via methylation leading to dopamine availability
Clinical: parkinsons
Tolcapone can lead to hepatoxicity
Dyskinesia, hallucinations, confusion, nausea and ORTHOSTATIC hypotension.
Benzotropine and trihexyphenidyl
MOA: antimucarinic
Clinical: improves tremor and rigidity but has little effect on bradykinesia in Parkinson’s
Drug induced Parkinson’s
AE: dry mouth, blurred vision, constipation, nausea and urinary retention
Amantadine
treats Parkinsons
MOA: may increase dopamine release
AE: ankle edema and livedo reticularis
Tubbucurarine, atracurium, mivacurium, pancuronium, vercuronium, recoroniuum
Nondepolarizing neuromuscular blocking drugs
MOA: competitive antagonists of ACh receptors
Reversal of blockade:
neostigmine (given with atropine to prevent muscarinic effects), edrophonium and other cholinesterase inhibitors
Clinical: muscle paralysis in surgery or mechanical ventilation-selective for motor nicotinic receptor
Use vecuronum or recuroniium in burns, myopathies, crush injuries and denervation to avoid hyperkalemia
Memantine
MOA: NMDA receptor antagonist, helps prevent excitotoxicity mediated by Ca2+
Clinical: Alzheimer
Toxicity: dizziness, confusion, hallucinations
Donepezil, galantamine, rivastigmine
MOA: AChE inhibitors
Clinical: Alzheimers
Toxicity: nausea, dizziness, insomnia
Vitamin E-antoxidant helps slow functional loss of Alzheimers
Tetrabenzine and reserpine
MOA: inhibit vesicular monoamine transporter (VMAT
Limit dopamine vesicle packaging and release
Clinical: Huntingtons
Sumatriptan
MOA: 5Ht agonist Inhibits trigeminal nerve activation prevents vasoactive peptide release Induces vasoconstriction half-life < 2 hours
Clinical: acute migraine and cluster headache attacks
Toxicity: coronary vasospasm (contraindicated in patients with coronary artery disease or Prinzmetal angina), mild tingling
Increases BP
Avoided in cardiac or cerebrovascular disease,
Ranibizumab
Anti VEGF
Used for age related wet macular degeneration
slows choroidal neovascularization
Pryaptanib
Anti VEGF
Used for age related wet macular degeneration
slows choroidal neovascularization
Riluzole
Modestly increases survival of Lou Gehrig disease by decreasing presynaptic glutamate release
Primidone
Metabolized to phenobarbital and phenylethylmalonamide (PEMA) both of which are anticonvulsants
Used for epilepsy, 2nd line essential tremor
Causes lethargy, acute intermittent porphyria (abdom pain, neuro, psych)
