Busy. Please wait.
or

show password
Forgot Password?

Don't have an account?  Sign up 
or

Username is available taken
show password

why


Make sure to remember your password. If you forget it there is no way for StudyStack to send you a reset link. You would need to create a new account.
We do not share your email address with others. It is only used to allow you to reset your password. For details read our Privacy Policy and Terms of Service.


Already a StudyStack user? Log In

Reset Password
Enter the associated with your account, and we'll email you a link to reset your password.
Don't know
Know
remaining cards
Save
0:01
To flip the current card, click it or press the Spacebar key.  To move the current card to one of the three colored boxes, click on the box.  You may also press the UP ARROW key to move the card to the "Know" box, the DOWN ARROW key to move the card to the "Don't know" box, or the RIGHT ARROW key to move the card to the Remaining box.  You may also click on the card displayed in any of the three boxes to bring that card back to the center.

Pass complete!

"Know" box contains:
Time elapsed:
Retries:
restart all cards
share
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.

  Normal Size     Small Size show me how

Pharm - Neuro/DA

Neuro/Drug Abuse Pharmacology from First Aid 2013

QuestionAnswer
Name five classes of drugs used in the treatment of glaucoma. Alpha-agonists - dec aqueous humor secretion Beta-blockers - dec aqueous humor secretion Acetazolamide - dec synthesis via CA enzyme Cholinomimetics - contract ciliary muscle to increase outflow Prostaglandin PGF2 - increase outflow
What are the side effects of epinephrine, brimonidine (a2) in glaucoma? Mydriasis; do NOT use in closed-angle glaucoma. Blurry vision, ocular hyperemia, ocular pruritis.
What are some beta blockers used in glaucoma? What are their side effects? Timolol, betaxolol, carteolol: no ocular SFX
What are the side effects of using acetazolamide to treat glaucoma? Nothing.
What are some cholinergics used to treat glaucoma? What are their side effects? Direct: Pilocarpine, carbachol Indirect: physostigmine, echothiophate Use pilocarpine in emergencies. All may cause miosis and ciliary muscle contraction, increasing outflow, but not halting secretion.
Which is the drug name of the prostaglandin PGF2 that is used in glaucoma to increase outflow? What is its side effect? Latanoprost - darkening of the iris
What are the three opioid receptor classes? What is their cellular MOA? Mu, kappa, and delta: they open K+ channels, close Ca2+ channels, and decrease synaptic transmission. They also inhibit the release of most NT's and substance P.
Name several full opioid agonists. Morphine, fentanyl, codeine, heroin, methadone, meperidine, dextramethorphan, diphenoxylate.
Which opiates are used for: 1. Diarrhea? 2. Cough suppression? 3. Addiction maintenance? 4. Acute pulmonary edema 1. loperamide, diphenoxylate 2. dextramethorphan 3,4. methadone
What are the signs of opioid toxicity? What would you use to treat overdose? respiratory depression, constipation, miosis ("pinpoint pupils"). Treat with: Naloxone, naltrexone
Butorphanol: MOA, Use, Tox MOA: mu-opioid partial agonist, kappa agonist Use: severe pain (labor, migraine), less risk of respiratory depression Tox: Competes with full agonists and so can produce withdrawal symptoms if taken with other opiates. Not easily reversed.
Tramadol: MOA, Use, Tox MOA: weak agonist, also an SNRI Use: chronic pain Tox: decreases seizure threshold
What are the symptoms of opioid withdrawal? Sweating, dilated pupils, piloerection, vomiting, diarrhea, stomach cramps, rhinorrhea
What are the uses for Naloxone, Naltrexone? Opioid toxicity.
What is the treatment for opioid withdrawal? Nothing; treat symptoms.
What is the first-line treatment for simple, complex, and tonic-clonic seizures, and trigeminal neuralgia? Carbamazepine
What is the first-line treatment for tonic-clonic seizures alone? Valproate
What is the first-line treatment for absence seizures? Ethosuximide
What is the treatment for status epilepticus? Benzodiazepines (diazepam or lorazepam)
Seizures occurring as part of ecclampsia are classically treated with what? What epilepsy drugs may be added? MgSO4, may add benzodizepines
Phenytoin: MOA, Use MOA: blockade of Na channels and Glut release Use: Tonic-clonic szs, or as Class IB AA
What are some toxicities and side effects of phenytoin use? Upreg CYP450, SLE-like syndrome, nystagmus, ataxia, diplopia, sedation, gingival hyperplasia, peripheral neuropathy, magaloblastic anemia, hirsutism, FHS
What is fetal hydantoin syndrome? Maternal phenytoin use --> microcephaly, hypoplastic nails and phalanges, cardiac defects
Carbamazepine: MOA, Use, Tox MOA: Na+ channel inactivation Use: 1st line for everything exc Absence sz Tox: diplopia, ataxia, blood dyscrasias, CYP450, SIADH, SJS
Ethosuximide: MOA, Use, Tox MOA: blocks thalamic Ca2+ channels Use: absence seizures Tox: E-->FGH: Fatigue, GI, Headache
Valproate: MOA, Use, Tox MOA: block Na, increase GABA Use: tonic-clonic or myoclonic seizures migraine prophylaxis Tox: GI, hepatotox, NT defects if pregnant weight gain
Topiramate: MOA, Use, Tox MOA: block Na, increase GABA Use: 2nd line seizures, migraine prevention Tox: sedation, mental dulling, kidney stones, WEIGHT LOSS
Benzodiazepines: naming, MOA Nom: -zepam, -zolam MOA: increase FREQUENCY of Cl- channel opening at GABA-A receptor
What are the clinical uses for benzodiazepines? Anxiety, spasticity, status epilepticus, night terrors, sleep walking, hypnotic, alcohol withdrawal/detox
What are the toxicities of benzodiazepines? Addiction, CNS depression with alcohol, less risk of respiratory depression than with barbiturates.
What is the treatment for benzodiazepine toxicity/overdose? Flumazenil - competitive antagonist for GABA receptor
What is the treatment for alcohol withdrawal? Benzodiazepines
What are the symptoms of benzodiazepine withdrawal? Delirium, respiratory depression, seizure, anxiety, autonomic instability, cardiac arrest
Barbiturates: naming, MOA Nom: -barbital, -pental MOA: increase DURATION of Cl- channel opening at GABA-A receptor
What are the clinical uses for barbiturates? Anxiety, seizures, insomnia, induction of anesthesia (thiopental).
What are the toxicities of barbiturates? Respiratory and CV depression, CNS depression with EtOH use, addiction, CYP450 interactions
What is the treatment for barbiturate toxicity/overdose? Nothing; assist respiration and maintain BP
What are the symptoms for barbiturate withdrawal? Same as for benzos: delirium, respiratory and cardiac depression, seizure, anxiety, autonomic dysregulation
What are some examples of non-benzo hypnotics? Ambien (zolpidem), zaleplon, eszopliclone
How do non-Benzo hypnotics work? What are they used for? They act via the BZI subtype of GABA receptors to treat insomnia.
What are the toxicities for non-benzo hypnotics, and how are they treated? Ataxia, headaches, confusion. All of shorter duration and with less risk of dependence than other hypnotics. Immediately reversed with flumazenil.
General anesthetic induction, duration, and potency is governed by what variable? Lipid-solubility: more hydrophobic = slower onset but high potency; less hydrophobic = faster onset and recovery time
In general anesthesia, what is MAC, and what is its relationship to potency? Mean alveolar concentration = the concentration at which 50% are anesthetized. Potency = 1/[MAC]
Compare the potency and solubility of halothane vs. nitrous oxide. Halothane (lipid solb) - slow induction, high potency N2O (less solb) - fast induction and recovery
Inhaled anesthetics: naming, MOA Nom: halothane, N2O, "-flurane" MOA: unknown
Inhaled anesthetics: Effects, Tox Eff: CV/Resp depression, N/V, increased cerebreal blood flow with decreased cerebral metabolic demand Tox: liver(halothane), kidney(methoxyflurane), convulsant(enflurane), malignant hyperthermia (all exc N2O)
How do you treat malignant hyperthermia, and what is its MOA? Dantrolene: blocks the Ryr Ca2+ channel in the sarcoplasmic reticulum
What are the two classes of local anesthetics? Esters: procaine, cocaine, teracaine Amides: lidocaine, et al (two I's in name)
What is the MOA and effect of local anesthetics? MOA: block Na+ channels Block small nerve > larger nerve, myelinated > unmyelinated; lose pain, then temperature, then touch, then pressure. Need more with infected (acidic) tissue. Enhanced effect with vasoconstrictors.
Local anesthetics: Use, Tox Use: minor surgeries, spinal anesthesia Tox: CNS excitation, HTN/hypoTN, cardiac toxicity, arrhythmias
What are the two classes of neuromuscular blocking agents? Depolarizing (Succinylcholine) Non-depolarizing (-curium, -curonium)
Succinylcholine: MOA, Effect, Tox MOA: Ach agonist, initial fasiculations, then blockade Phase 1: prolonged, depolarized Phase 2: repolarized but blocked Cholinesterase inhibitors will potentiate Phase 1, and reverse Phase 2. Tox: hyperCa, hyperK, malignant hyperthermia
Non-depolarizing NM blocking drugs: MOA, Tox Competitive Ach antagonists, reversible with neostigmine or edrophonium
What are the symptoms of LSD intoxication? CNS depression, anxiety, hallucination, delusion, flashbacks when sober, pupil dilation.
What are the symptoms of PCP/ketamine abuse? Belligerence, fever, agitation, violent psychosis, vertical and horizontal nystagmus.
What are the symptoms of PCP/ketamine withdrawal? Depression, anxiety, restlessness, disturbed sleep.
What is the treatment for PCP/ketamine withdrawal? Benzodiazepines and haloperidol.
What are the symptoms for stimulant drug abuse? increased mood, psychomotor agitation, insomnia, cardiac arrhythmia, tachycardia, anxiety, pupil dilations (cocaine and amphetamines)
What are the symptoms for stimulant withdrawal? Depression, lethargy, somnolence, weight gain/hunger, headache, craving, suicidality (esp. cocaine)
What are the symptoms for depressant drug abuse? Euphoria, decreased anxiety, sedation, behavioral disinhibition, respiratory depression.
What are the symptoms for depressant withdrawal? Anxiety, tremor, seizures, insomnia
What is delirium tremens? What is its treatment? Usually alcohol withdrawal with formication "crawlies," nightmares, hallucinations, diaphoresis, tremors, dysphoria. Treat with benzodiazepines.
What is the treatment strategy for Parkinson's Disease? BALSA: B-Bromocriptine A-Amantadine L-L-Dopa (with Carbidopa) S-Selegiline A-Antimuscarinics
Bromocriptine: MOA, Use, Tox Ergot-derived DA agonist. Used to increase DA in Parkinson's. Non-ergots (pramipexole, ropinirole) are preferred because ergots can cause vasoconstriction (CREST, Buergher's).
Amantidine: MOA, Use, Tox MOA/Use: inc DA release in Parkinson's, also an antiviral for Influenza A and rubella Tox: ataxia
What is L-Dopa/Carbidopa used for? L-DOPA: Converted to DA in Parkinson's. Carbidopa: peripheral decarboxylase inhibitor limits DA side effects peripherally
Selegiline: MOA, Use, Tox? MOA: MAO-B inhibitor, prevent DA breakdown Also, COMT inhibitors Use: Parkinson's Tox: May enhance adverse effects of DA
What are side effects of long-term L-DOPA use? Arrhythmia, dyskinesia, akinesia between doses
Which anti-muscarinic is used in Parkinson's? Benzotropine: improves tremor and rigidity, no effect on bradykinesia
What two drug classes are given in Alzheimer's disease? (1) NMDA antagonists: Memantine (2) Ach inhibitors
Memantine: MOA, Use, Tox MOA: NMDA antagonist, prevents cytotoxicity Use: Alzheimers Tox: Dizziness, confusion, hallucination
Donezipil, galantamine, rivastigmine: Use, Tox Use: Ach inhibitors for Alzheimer's Tox: Nausea, dizziness, insomnia
What drugs are used in the treatment of Huntington's? In the dz: dec GABA, dec ACh, inc DA...so: Tetrabenazine and reserpine (inhibit VMAT to decrease DA packaging) Haloperidol (DA receptor antagonist)
Sumatripan: MOA, Use, Tox MOA: 5HT agonist inhibits CN-V activation and induces vasoconstriction Use: acute migraines and cluster headaches Tox: Prinzmetal's vasospasm
Created by: wmwebb89