Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
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
Normal Size Small Size show me how
CNS DRUGS
Kaplan
| Question | Answer |
|---|---|
| What are the types of GABA receptors and their MOA? (2) | 1. GabaA - increase Cl- influx (inotrophic channel) 2. GabaB - increase K efflux (Baclofen is an agonist) (G-protein coupled) Both cause hyperpolarization |
| How does Benzodiazepam and Barbiturates work? | Benzo: increase frequency of Cl- channel (potentiate GABA) Barbs: increase duration of Cl- channel |
| What are the Benzo drugs? | -lams and -pams Alprazolam Diazepam |
| Flumazenil MOA | BZ receptor antagonist (used in reversal of Benzo overdose) |
| Which part of the GabaA receptor does Benzos work on? | On the BZ 1 and BZ2 (Barbs does NOT work on these) |
| What does BZ1/BZ2 mediate? | BZ1- sedation/sleep BZ2- antianxiety and impaired cognitive functions |
| Benzos vs Barbs which are more dangerous and why? | Barbs bc they do not have a plateu and they can work independently of GabaA receptor at high doses |
| Which Benzos are safe to use in liver dysfunction and why? | Outside The Liver Oxazepam Temazepam Lorazepam They are not metabolized by the liver |
| What are the withdrawal signs of Barbs and ethanol? | Anxiety Agitation Seizure (life threatening) |
| What are the medication used in withdrawal of Barbs and ethanol? | Benzos Think your CNS is a car that’s gotten used using powerful brakes (barbs) If you suddenly cut the brake line ,car flies out of control = seizures. Benzos are emergency brakes that let you slow the car down while restoring normal brake function |
| What are the non- Benzos drugs that work on BZ1 receptor? (2) | The Z’s 1. Zaleplon 2. Zolpidem |
| What are the usage of Zaleplon and Zolpidem and their side effect? | Use: Sedation/ sleep for sleep disorders S/e: Sleepwalking |
| What is a drug used in generalized anxiety that does not depress the CNS (so no effect on GABA) ? | Buspirone (Serotonin receptor partial agonist) |
| What is the MOA of Buspirone? | 5 HT 1a (serotonin) agonist |
| Is Buspirone used for acute anxiety attack or preventative and why? | Buspirone is used as a PREVENTIVE MEDICATION. (Bc Serotonin is Slow) BZs are couple to ion channel so they work faster so you use them as a acute treatment -serotonin plays a role in sleep, mood and pain inhibition |
| Drug used for Insomia? | Suvorexant |
| Suvorexant MOA | Orexin receptor antagonist (orexin promote wakefulness) S/e somnolence |
| What other drug besides BZs can be antidoted by Flumazenil? | The Zs. ZALEPLON and ZOLIPIDEM Bc they work on BZ1 receptors |
| What are the 3 types of alcohols? | 1. Ethylene glycol 2. Methanol 3. Ethanol |
| What is the enzyme that breakdown the alcohols and for which alcohol does it have the highest affinity for? | ALCOHOL DEHYDROGENASE Highest affinity for ETHANOL (compared to ethylene glycol and methanol) |
| What is the main side effect of GLYCOALDEHYDE accumulation? | Nephrotoxicity |
| What is the main side effect of FORMALDEHYDE accumulation? (Met. Of Methanol) | Ocular damage (blurry vision) |
| What is the main side effects of ACETALDEHYDE? (Met. Of Ethanol) | Nause, vomiting and Headache |
| What is the treatment for alcohol toxicity (overdose)? (2) | 1. Ethanol (bc alcohol dehydrogenase has higher affinity for it and has the lesser 2. FOMEPIZOL (plus hemodialysis bc there will be accumulation of the alcohols itself. R side effect of the other -aldehydes) |
| Which drug causes “hangover” symptoms (nausea,vomiting, headache) and it works by inhibiting what enzyme? | DISULFIRAM blocks ACETALDEHYDEDEHYDROGENASE |
| What other (2) drugs cause Disulfiram like effects? | 1. Metronidazole 2. Griseofulvin |
| Alcohol work through which receptor? | Alcohols works through GABA mimetic activity so that makes all alcohols an CNS depressant (Alcohol also decreases ADH secretion) |
| What is the ‘Amine’ hypothesis of Depression? | Hypothesis is that Depression is caused dt a decrease in monoamine neurotransmitters (5 HT, NE, Dopamine) Monoamine nueurotransmitters are neurotransmitters derived from aminoacids |
| What are the acute mechanism of antidepressants? | Increase 5HT, NE, DA (sometimes) |
| Which drug depletes all the neurotransmitters (5HT,NE,DA)? | Reserpine (old HTN drug) |
| What are the SSRIs (6) | 1. Citalopram 2. Escitalopram 3. Fluoxetine 4. Paroxetine 5. Sertraline 6. Fluvoxamine |
| What are the most common reason for discontinuation of SSRIs? | Sexual dysfunction |
| What is the MOA of SSRIs? | Block 5HT reuptake |
| What is the drug interaction of SSRIs? | Inhibit cytochrome P450 enzymes (except CITALOPRAM/ ESCITALOPRAM) -that’s why it can cause sexual dys. b/c cyp450 makes testosterone + cortisol |
| What are the TCAs (3) | 1. Clomipramine 2. Imipramine 3. Amitriptyline |
| What is the MOA of TCAs? | Blockage of 5HT and NE reuptake |
| What are the side effects of TCAs? | Muscarinic and alpha blocking properties |
| What are the SNRIs (3)? | 1. Venlafaxine 2. Desvenlafaxine 3. Duloxetine |
| SNRIs MOA | Inhibit 5HT and NE reuptake |
| What is the difference between TCAs and SNRIs? | SIDE EFFECT PROPERTIES. (Bc they work through the same MOA, SNRIs have LESS ANS effect) |
| What are the Mono amino oxidase (MAO) inhibitors? (2) | 1. Phenelzine 2. Tranylcypromine |
| MAO inhibitors mechanism of action | Irreversible INHIBITION OF MAO-A and MAO-B MAO-A breakdown tyramine, NE, 5HT MAO-B breakdown DA |
| Which drug do a pt switch to when they been on a 5HT drug and get sexual dysfunction? | BUPROPION (it PROPs you up) an NDRI -decrease the threshold for seizure |
| Bupropion MOA | DA and NE reuptake blocker (also used for smoking cessation) |
| Trazodone | Antidepressant. Associated w cardiac arrhythmias and priapism |
| Mirtazapine | Alpha 2 antagonist also used as antidepressant (increase NE release in post synaptic cleft) |
| What drug is a partial agonist of nicotine receptors? And its usage? | Varenicline. Used in smoking cessation Bc it’s a partial agonist when pt is not smoking it acts on the nicotine receptors bring sense of smoking. When pt is smoking it work as an antagonist (Bupropion) |
| Drugs working on NE only for depression? (2) | 1. Mirtazapine (2. Bupropion) |
| Drugs working on 5HT only for depression ? (1) | SSRIs |
| What is the drug of choice for Bipolar disorders? | Lithium |
| What is the MOA of Lithium? (2) | 1. Prevent recycling of inositol ( decrease IP2) by blocking inositol monoposphate - affects Gq pathway 2. Decrease cAMP - blocks V2 receptors |
| What are the side effects of Lithium? | Narrow therapeutic index Tremor Hypothyroidism with goiter Ebstein anomaly |
| What are the Amphetamine like drugs use in ADHD? (2) and their MOA | 1. Methylphenidate 2. Amphetamine MOA: increase NE and DA |
| What is a selective NE reuptake inhibitor used for ADHD? | Atomoxetine |
| What is the difference between Amphetamines and Atomoxetine? | Atomoxetine lacks abuse potential because it does not increase dopamine such as Amphetamines |
| What type of G protein are D1 and D2 receptors coupled to? | D1: Gs coupled D2: Gi coupled |
| Nigrostriatal pathway has which subtype of D2 receptor? | D2A |
| MesolimbiC pathway has which subtype of D2 receptor? | D2C |
| What are the 3 neural pathways that DA work on? | 1. Nigrostriatal tract 2. Mesolimbic- Mesocortical tract 3. Tuberoinfundibular tract |
| What is the role of DA in the Nigrostriatal pathway? | Inhibits GABA-ergic neurons. Responsible for movement Cell bodies in substantia nigra project to striatum where they release dopamine. |
| What is the role of DA in the Mesolimbic- Mesocortical tract pathway? | Increase reinforcement ( make a behavior likely to occur again) and Psychosis Cell bodies in midbrain project to cerebrocortical and limbo structures |
| What is the role of DA in the Tuberoinfundibular pathway? | Decrease prolactin. Cell bodies in hypothalamus project to anterior pituitary |
| What is the role of DA on the Chemoreceptor Trigger Zone? | Increase Emesis |
| What is the imbalance in Parkinson’s Disease? | LOW DOPAMINE, high Ach |
| What is the aim in pharmacotherapy of Parkinson’s Disease ? (2) | 1. Increase DA 2. Block muscarinic receptor (to decrease Ach effects) Both (DA and Ach should be balanced always) |
| Which drug can be given to a schizophrenic patient suffering from drug induced Parkinsonism if the offending drug cannot be stopped? | Muscarinic antagonist (to decrease Ach effects, staying in balance w DA) |
| Levodopa MOA and what is it combined with and why? | MOA: prodrug converted to Dopamine Given w CARBIDOPA |
| Carbidopa MOA | PERIPHERAL dopa decarboxylase (AAAD) inhibitor |
| Benefits of Levodopa+ Carbidopa? (2) | 1. Increase Levodopa in the brain 2. Less DA in the periphery—> fewer dopamine s/e |
| What are the drugs that inhibit COMT(2) and what does COMT do? | “Capone” 1. Tolcapone (centrally) 2. Entacapone COMT MOA: converts L-dopa to 3-O- Methyldopa |
| What is a MAO-B selective inhibitor? | Selegiline (Gets metabolized into an amphetamine) MAO - B breakdown DA |
| What are the 3 DA receptor agonists? | 1. Pramipexole 2. Ropinirole 3. Bromocriptine (older drug less commonly used) |
| What are the 3 drugs that ‘decrease Ach function’ ? (Muscarinic blockers) | 1. Benztropine 2. Trihexyphenidyl 3. Amantadine (cause livedo reticularis= red blueish net like lesion on skin) All are MUSCARINIC BLOCKERS |
| What is meant with “positive” and “negative” symptoms of schizophrenia? | Positive: symptoms that are present but should not be. easier to treat with antipsychotic drugs Negative: symptoms that are present but should be absent |
| What are the positive symptoms of schizophrenia? | Thought disorders Delusions Hallucinations Paranoia |
| What are the negative symptoms of schizophrenia? | Amotivation Social withdrawal Flat effect Poverty of speech |
| What is the “dopamine hypothesis” of schizophrenia? | Symptoms arise dt excessive dopamine in the mesolimbic-Mesocortical pathway |
| Why are the 2 roles of antipsychotic drugs? | 1. Block dopamine receptors (typical) 2. Block 5HT receptors (atypical) |
| What are the “typical”/ DA receptor blockers? (4) | 1. Chlorpromazine 2. Thioridazine 3. Fluphenazine 4. Haloperidol |
| What are the “atypical”/ 5HT receptor blockers ? (4) | 1. Clozapine 2. Olanzapine 3. Risperidone 4. Aripiprazole |
| Which ANTIPHSYCHOTIC drugs cause increase prolactin? | The TYPICALS and Risperidone (D2 receptor antagonists) |
| What is a Seizure? | An EXCESSIVE activity of cortical neurons that results in transient symptoms |
| What are the main Mechanisms in which Anticonvulsants drugs work? (4) | 1. Decrease axonal conduction by preventing Na influx through fast Na channels 2. Increased inhibitory tone by facilitation of GABA hyper polarization 3. Decrease excitatory effects of glutamic acid 4. Decreased presynaptic Ca influx (type T channel) |
| Which anticonvulsants work through decreasing axonal conduction? (2) | 1.Carbamazepine 2. Phenytoin |
| Which anticonvulsants work through increasing GABA hyperpolarization? (2) | 1. Barbiturates 2. Benzodiazepines |
| Which anticonvulsants work through decreasing glutamic acid effects? (3) | 1. Lamotrigine, 2.Topiramate (blocks AMPA receptors- migraine prophylaxis) 3. Felbamate (blocks NMDA receptors) NMDA= glutamate |
| Which anticonvulsants drug works through decreasing presynaptic Ca influx? (2) | 1. Ethosuximide 2. Valproate acid (Used in Absence seizure) |
| DOC for Absence seizure? | Ethosuximide (and Valproic acid) |
| DOC for Status epilepticus? | Lorazepam (and Diazepm |
| What are the major side effects of Phenytoin? (3) | 1. Gingiva hyperplasia 2. Hirsutism 3. Osteomalacia (decrease vitamin D) Tetarogenicity |
| Major side effects of Carbamazepine? (2) | 1. Megaloblastic anemia 2. Exfoliative dermatitis (DOC for trigeminal neuralgia) Can also cause SIADH by making the tubules sensitive to ADH |
| What is a side effect of Lamotrigine? | Steven’s-Johnson syndrome |
| Gabapentin MOA | Targets α2δ-1 subunit of PRESYNAPTIC Calcium channel —> Decrease Ca influx (Used in post herpetic neuralgia) |
| What are the drugs that DECREASE the efficacy of oral contraceptives? (3) | 1. CARBAMAZEPINE 2. Phenytoin 3. Phenobarbitol |
| What are the Inhaled Anesthetics? (3) | Nitrous and the “ane’s” 1. Nitrous oxide 2. Sevoflurane 3.Desflurane |
| Which inhaled anesthetic has the LEAST potency? | Nitrous Oxide |
| What is the Mac Value? | Gives the POTENCY of the anesthetic (MAC= minimal alveolar anesthetic concentration) |
| What is the ED50? | QUANTITY of anesthetic agent required to anesthetize the patient by 50% of desired response |
| What is the Blood-Gas ratio? | Solubility of drug in blood. The lower the blood-gas ratio the faster the onset of action and the faster the elimination of the drug (lower solubility in blood faster gets into tissue, you can think of it like that) |
| MAC (minimal alveolar anesthetic concentration) are lower in 2 populations, which are? | 1. Elderly 2. Presence of Opiates/ Sedative-hypnotics |
| What are the Intravenous Anesthetics? (5) | 1. Midazolam (a benzo) 2. Propofol 3. Fentanyl 4. Ketamine 5. Etomidate |
| Which Intravenous anesthetic is best for Asthmatic patients? | Ketamine (Bc little effect of respiration) |
| Which Intravenus anesthetic is best for patients with cardiovascular disease? | Etomidate |
| What effect does Midazolam cause? | Anterograde amnesia (It’s a benzo) |
| Which type of anesthetic is Ketamine? | Dissociative anesthetic (NO SENSORY INPUT) |
| What is used to reverse Fentanyl overdose? | Naloxone |
| What are the 2 groups of local Anesthetics? | 1. Esters 2. Amides |
| What are the Ester anesthetics? (3) | 1. Procaine 2. Cocaine 3. Benzocaine |
| What are the Amide anesthetics? (3) | 1. Lidocaine 2. Bupivacaine 3. Mepivacaine |
| Are local Anesthetics bases or acids? | BASES with Pka of -8 |
| Where does the local anesthetics block Na channels (inside or outside)? | INSIDE (blocks the inactivated Na channels) (Ionized drug= active. Ionized drug does not cross the lipid membrane easily) In infected tissue(acidic) anesthetic does not work properly bc ionized form cannot enter cell |
| What is the order of sensitivity of the nerve fibers? | Type B and C —> type A delta —> type A beta and gamma —> type A alpha |
| Local anesthetics is COADMINISTERED with what other drug and WHY? | W/ Alpha 1 agonists (Ephylephrine) . To VASOCONSTRICT and keep the drug localized and decrease systemic effects. |
| What are the side effects of Local anesthetics? | Bradycardia Allergies (with ESTERS) |
| What type of channel is the nicotine receptor? | Na/K+ channel (Found in ganglia) |
| How many subunits does the nicotinic receptor have? | 5 subunits (2 of them are alpha subunits where Ach binds to and open the channel and depolarize the muscle) |
| What are the 2 group types we have for skeletal muscle relaxants? | 1. Nondepolarizing (competitive) nicotinic antagonists 2. Depolarizing (noncompetitive) nicotinic agonists |
| What is train-of-four stimulation? | Stimulation of peripheral nerves to assess the degree of neuromuscular blockage |
| What are the Nondepolarizing nicotinic antagonists? (3) | “-Curium” 1. Rocuronium 2. Atracurium 3. Cisatracurium |
| Which substance can reverse the Nm blockers? | Sugammadex |
| What are the Depolarizing nicotinic agonists? (1) | Succinylcholine |
| Depolarizing nicotinic agonists has 2 phases what are they? | Phase 1: Depolarization (fasciculation, prolong depolarization, flaccid paralysis) Phase 2: Desensitization |
| Which Nondepolarizing nicotinic antagonists is safe in hepatic and renal impairment but makes a metabolite, and which metabolite? | ATRACURIUM Metabolite: Laudanosine (cause SEIZURE) |
| What is the fade with train-of-four stimulation in Nondepolarizing vs Depolarizing skeletal muscle relaxants? | Nondepolarizing: PROGRESSIVE paralysis Depolarizing: IMMEDIATE paralysis |
| Side effects of Succinylcholine? (2) | 1. Malignant hyperthermia 2. Hyperkalemia |
| What is the characteristics of Malignant hyperthermia? | Muscle rigidity Hyperthermia Hypertension Acidosis (accum of CO2 + lactic ) Hyperkalemia (dt rhabdomyolysis) |
| Which drug is used in extreme muscle rigidity and its MOA? | Dantrolene MOA: directly on skeletal muscle to decrease contractility by blocking Ca release from the sarcoplasmic reticulum. |
| What is the treatment for Malignant hyperthermia dt Serotonin syndrome? (2) | Cyproheptadine (5HT Antagonist) Benzodiazepines |
| What is the most important Opioid receptor? | Mu RECEPTOR (there are 3 in total) |
| What is the prototype mu receptor agonist? | MORPHINE |
| Where does Morphine work? (2locations) | 1. Presynaptic 2. Postsynaptic Through Gi coupling receptor |
| How does the pre- and post synaptic receptors of opioid work? | Presynaptic: auto receptors (decrease release of pain transmitters) Postsynaptic: increase K efflux(membrane hyperpolarization —> decrease pain signal) |
| What are the pain neurotransmitters? (2) | 1. Glutamate 2. Substance P |
| Which drug should be avoided in head trauma? | Morphine (Because it causes vasodilation which can increase the intracranial pressure) |
| How does Morphine act as an analgesia? | INCREASE pain tolerance and DECREASE perception and reaction to pain |
| How is Morphine overdose reversed? | NALOXONE |
| What is the effect of Morphine on smooth muscle? (4) | 1. GI: DECREASE PERISTALSIS 2. GU: URINARY RETENTION 3. Biliary: INCREASE PRESSURE (biliary colic) 4. Pupils: MIOSIS RELAXATION |
| How is Morphine metabolized? | By GLUCURONIDATION (Morphine-6-glucuronidase is active, careful in renal patients) |
| How is seizures caused by Meperdine treated? | Benzodiazepines |
| What are the full agonist opioids? (3) | 1. Meperdine 2. Methadone 3. Codeine |
| What are the partial agonist opioid? (1) | BUPRENORPHINE |
| What are the 2 Mixed agonist-antagonist opioids? | 1. Nalbuphine 2. Pentazocine |
| What are the 3 opioid antagonists? | 1. Naloxone 2. Naltrexone 3. Methyl naltrexone |
| Opioids are contraindicated in? (5) | 1. Head injury 2. Pulmonary dysfunction (except pulmonary edema) 3. Hepatic/Renal dysfunction 4. Adrenal or thyroid deficiencies 5. Pregnancy (neonatal dependence or depression) |
| Which full opioid agonist can cause serotonin syndrome and HOW? | Meperdine (bc it is metabolized to NORMEPERDINE which is a serotonin reuptake inhibitor) |
| Which full agonist opioid is a prodrug? | Codeine (metabolized by CYP2D6) |
| Mixed opioid agonist-antagonists are agonist and antagonist at which receptors? | Agonist at Kappa receptors (Pain relief) Antagonist at Mu receptors |
| What are the major 3 side effects of opioid analgesics? | 1. Pinpoint pupils 2. Respiratory depression 3. Coma |
| Tolerance of opioid occurs everywhere EXCEPT | Miosis and CONSTIPATION |
| How is opioid withdrawal treated ? (3) | 1. Clonidine (a alpha 2 agonist) 2. Methadone 3. Supportive (Withdrawal of opioid analgesics cause decrease sympathetic like effects) |
| Loperamide (opioid) used for | to treat DIARRHEA |
| Dextromethorphan (opioid) used to treat | COUGH |
| What causes withdrawal on a patient on full opioid mu agonist drug? | Partial or mixed opioid causes withdrawal in those patients |
| What are the common and different features of Serotonin Syndrome and Neuroleptic Malignant Syndrome? | Common: 1. Fever 2. Tachycardia 3. Hypertension SS 1. Clonus (hyperreflexia) 2. Diarrhea NMS 1. Rigidity 2. CK, WBC |
| Which drug is used to treat Multiple Sclerosis spasticity? | GABA B Agonist (BACLOFEN) to treat MS during flares is Interferon- beta |
Created by:
DVD27