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Neurology
FA complete review part 4 Pharmacology
| Question | Answer |
|---|---|
| List of Epilepsy drugs: | 1. Benzodiazepines 2. Carbamazepine 3. Ethosuximide 4. Gabapentin 5. Lamotrigine 6. Levetiracetam 7. Phenobarbital 8. Phenytoin, fosphenytoin 9. Tiagabine 10. Topiramate 11. Valproic acid 12. Vigabatrin |
| What is the main use for Benzodiazepines as an epileptic agent? | Acute status epilepticus |
| What is the mechanism of action of Benzodiazepines? | Increase GABA-A action |
| What epilepsy drugs can be used a secondary treatment of Eclampsia seizures? | Benzodiazepines |
| What are side effects associated with Benzodiazepines? | Sedation, tolerance, dependence, and respiratory depression |
| Which could be the most fatal or severe adverse effect of benzodiazepine overdose? | Respiration depression |
| Which epilepsy drug(s) MOA is to increase the actions GABA-A? | Benzodiazepines and Phenobarbital |
| What is the common use of Carbamazepine? | Treatment of Partial (focal) seizures |
| Which type of generalized seizures can be treated, not commonly, with Carbamazepine? | Tonic-clonic seizures |
| What is MOA of Carbamazepine? | Blocks Na+ channels |
| Which partial seizure medication MOA is to block the sodium cation channels? | Cabazempine |
| List of known adverse effects caused by Carbamazepine? | 1. Diplopia 2. Ataxia 3. Blood dyscrasias 4. Liver toxicity 5. Teratogénesis 6. Induction of CYP450 7. SIADH 8. Stevens-Johnson syndrome |
| What is a severe cutaneous adverse effect of Carbamazepine? | Stevens-Johnson syndrome |
| What are the common blood dyscrasias caused by Carbamazepine? | Agranulocytosis and Aplastic anemia |
| What are the teratogenic side effects associated with the use of Carbamazepine? | Cleft lip/palate, and spina bifida |
| A newborn with cleft lip and palate, and a turf of hair in the lower back, was born to a mother with seizure hx. What is the most likely medication she was taking? | Carbamazepine |
| SIADH, SJS, and blood dyscrasias are known adverse effects of whichani-epilepsy drug? | Carbamazepine |
| What is the 1st line of treatment for Trigeminal neuralgia? | Carbamazepine |
| Besides focal seizures, what non-epileptic condition , is primarily treated with Carbamazepine? | Trigeminal neuralgia |
| What is treated with Ethosuximide? | Absence seizure |
| What drug is used to treat Absence seizures? | Ethosuximide |
| MOA of Ethosuximide | Blocks thalamic T-type Ca+ channels |
| Which anti-epilepsy drug works by blocking the Thalamic T-Type calcium cation channels? | Ethosuximide |
| A list of all adverse effects associated with Ethosuximide: | EFGHIJ: - Ethosuximide causes: Fatigue, GI distress, Headache, Itching (and urticaria) Stevens-Johnson syndrome |
| Thalamic T-type Ca2+ channel blocker epileptic | Ethosuximide |
| Which the only type of seizures treated with Gabapentin? | Partial (focal) seizures |
| What is the MOA of Gabapentin? | Primarily inhibits high-voltage-activated Ca2+ channels |
| Which antiepileptic was designed as a GABA analog? | Gabapentin |
| Inhibition of high-voltage-activated Ca2+ channels. | MOA of Gabapentin |
| Common side effects of Gabapentin | Ataxia and Sedation |
| What are non-epileptic uses of Gabapentin? | 1. Peripheral neuropathy 2. Postherpetic neuralgia |
| Which seizures are can be treated with Lamotrigine? | Partial seizures, Tonic-Clonic , and Absence seizures |
| MOA of Lamotrigine | - Blocks voltage-gated Na+ channels - Inhibits the release of glutamate |
| What NT release is inhibited by Lamotrigine? | Glutamate |
| Which channels are blocked by Lamotrigine? | Voltage-gated Na+ channels |
| What is the associated adverse effect of Lamotrigine? | Stevens-Johnson syndrome |
| How is SJS prevented when taking Lamotrigine? | Slow titration |
| Blocks voltage-gated Na+ channels and inhibits release of glutamate. | Mechanism of action of Lamotrigine |
| What is a possible effect of the mode of action of Levetiracetam? | Possible modulation of GABA and glutamate release |
| What are the adverse effects seen with Levetiracetam? | 1. Neuropsychiatric symptoms 2. Fatigue, drowsiness, and headache |
| Personality changes are seen in a person taking which antiepileptic? | Levetiracetam |
| What is the mode of action of Phenobarbital? | Increase GABA-A action |
| Phenobarbital share MOA with which other type of epilepsy medications? | Benzodiazepines |
| First line of seizures (focal, tonic-clonic) in neonates is: | Phenobarbital |
| What is probably the most severe side effect of Phenobarbital? | Cardiorespiratory depression |
| As side effects, both, benzodiazepines and Phenobarbital have certain organ depressons: Benzodiazepines cause __________________ depression. Phenobarbital causes___________________ depression. | Respiratory Cardiorespiratory |
| Which epilepsy drugs are known to cause induction of the CYP450 system? | Carbamazepine and Phenobarbital |
| 1st line of treatment for recurrent status epilepticus | Phenytoin |
| What is Fosphenytoin? | Water-soluble phenytoin prodrug used only in hospitals for the treatment of epileptic seizures. |
| Water-soluble phenytoin | Fosphenytoin |
| What is the mode of action of Phenytoin? | Blocks Na+ channels |
| What is the order kinetics of Phenytoin? | Zero |
| Zero order kinetics antiepileptic | Phenytoin |
| Which antiepileptics or seizure medication block Na+ channels as mechanism of action? | Carbamazepine, Phenytoin, and Topiramate |
| Blocks Na+ channels; zero order kinetics | Phenytoin |
| List of side effects associated with Phenytoin: | 1. P450 system induction 2. Hirturism 3. Enlarged gums 4. Nystagmus 5. Yellow-brown skin 6. Teratogenicity 7. Osteopenia 8. Inhibited folate absorption 9. Neuropathy |
| What rare adverse effects associated with Phenytoin? | Stevens-Johnson syndrome, DRESS syndrome, and SLE-like syndrome |
| Phenytoin is used as 1st line of treatment of acute ----> | Tonic-clonic seizures |
| Phenytoin is used as 1st line of treatment for which recurrent seizure type? | Status epilepticus |
| What is the main agent used for prophylaxis of Status epilepticus? | Phenytoin |
| Phenytoin is an inducer or inhibitor of the CYP450 system? | Inducer |
| Which anti-seizure medication is associated with possible development of SLE-like syndrome? | Phenytoin |
| What is the teratogenic effect caused by Phenytoin? | Fetal hydantoin syndrome |
| A newborn with Fetal Hydantoin syndrome most likely had a mother that took what medication during pregnancy? | Phenytoin |
| What is the common use of Tiagabine? | Partial (focal ) seizures |
| What is the MOA of Tiagabine? | Increasing GABA by inhibiting reuptake |
| MOA- inhibiting GABA reuptake, thus increasing GABA concentration. | Tiagabine |
| What is the mode of action of Topiramate? | 1. Blocks Na+ channels 2. Increases GABA action |
| This drug works by blocking Na+ channels and also by increasing GABA action. | Topiramate |
| Valproic acid is 1st line of treatment of acute -----> | Tonic-clonic seizures |
| What are the two parts of the MOA of Valproic acid? | 1. Increases Na+ channel inactivation 2. Increases GABA concentration by inhibiting GABA transaminase |
| Which enzyme is inhibited by Valproic acid? | GABA Transaminase |
| How does Valproic acid increases the concentration of GABA? | Inhibiting GABA transaminase |
| Which antiepileptic works by Increasing the Na+ channel inactivation? | Valproic acid |
| What are the associated adverse effects of Topiramate? | Sedation, mental dulling, word-finding difficulty, kidney stones, weight loss, and glaucoma. |
| A person with a seizure disorder started to complain about not remembering or finding the right words. She had been an avid writer and poet. What medication can cause this? | Topiramate |
| What is an non-seizure related use of Topiramate? | Migraine prevention |
| What are other uses for Valproic acid, other than as antiepileptic medication? | Myoclonic seizures, bipolar disorder, migraine prophylaxis |
| What teratogenic defects are expected for the use of Valproic acid? | Neural tube defects |
| Irreversible GABA transaminase inhibitor. | Vigabatrin |
| What is the associated black box warning of Vigabatrin? | Permanent visual loss |
| Permanent visual loss may be caused by which antiepileptic? | Vigabatrin |
| What are some common Barbiturates? | Phenobarbital, pentobarbital, thiopental, and secobarbital |
| What is the detailed MOA of Barbiturates? | Facilitate GABA-A action by increasing DURATION of Cl- channel opening, thus decreasing neuron firing. |
| Barbiturates increase or decrease, duration of Cl- opening? | Increase |
| Which type of drugs are known to increase DURATION of Cl-channel opening? | Barbiturate |
| What is the result of the increased duration of Cl- channel opening by Barbiturates? | Facilitation of GABA-A action |
| What are the clinical uses for barbiturates? | Sedative for anxiety, seizures, insomnia, induction of anesthesia |
| Which barbiturate is used as to induce anesthesia? | Thiopental |
| Thiopental is a _____________________. | Barbiturate |
| Increase duration of Cl- channel opening | Barbiturate |
| Barbiturates are to be avoided in people with _________________. | Porphyria |
| A patient with a known porphyria should avoid which type of drugs? | Barbiturate |
| CNS depression by barbiturates can be exacerbated by: | Alcohol use |
| What is the overdose by Barbiturates treatment? | Supportive (assist respiration and maintain BP) |
| List of common Benzodiazepines: | Diazepam, Lorazepam, Triazolam, Temazepam, Oxazepam, Midazolam, Chlordiazepoxide, Alprazolam |
| What is the mechanism of action of Benzodiazepines? | Facilitate GABA-A action by increasing frequency of Cl- channel opening |
| Which, benzodiazepines or barbiturates, enhance GABA-A action, by increasing the frequency of Cl- channel opening? | Benzodiazepines |
| Most Benzodiazepines have: | Long half-lives and active metabolites |
| Which mnemonic may be used to remember those Benzodiazepines with SHORT half-lives? | ATOM |
| What does the mnemonic ATOM stands for? | Short half-life benzodiazepines Alprazolam, Triazolam, Oxazepam, Midazolam |
| What is a risk or adverse effect of short half-live benzodiazepines? | Higher addictive potential |
| Which drugs are known to increase the frequency of Cl- channel opening? | Benzodiazepines |
| What drugs and substances bind to GABA-A receptors? | Benzodiazepines, Barbiturates, and Alcohol |
| GABA-A receptor is a : | Ligand-gated Cl- channel |
| Why are Oxazepam, Temazepam, and Lorazepam used to treat alcohol withdrawal safer than other benzodiazepines? | Due to minimal first-pass metabolism |
| What are some important Nonbenzodiazepine hypnotics? | Zolpidem, Zaleplon, and esZopiclone |
| What is the MOA of nonbenzodiazepines hypnotics? | Act via BZ1, subtype of GABA receptor |
| What is the GABA subtype used by nonbenzodiazepine hypnotics? | BZ1 |
| Nonbenzodiazepine hypnotic effects are reversible with: | Flumazenil |
| Why are nonbenzodiazepines hypnotics used for sleep? | They affect less the sleep cycle as compared to Benzodiazepines |
| Clinical use for Zolpidem? | Insomnia |
| What is the mechanism of action of Suvorexant? | Orexin (hypocretin) receptor antagonist |
| Orexin receptor antagonist | Suvorexant |
| What is the clinical use for Suvorexant? | Insomnia |
| Suvorexant is contraindicated in patients with _________________. | Narcolepsy |
| What are conditions are have Suvorexant administration contraindicated? | 1. Narcolepsy 2. Liver disease 3. Strong CYP3A4 inhibitors |
| What is the MOA of Ramelteon? | Melatonin receptor agonist, binds MT1 and MT2 in suprachiasmatic nucleus. |
| Ramelteon binds to: | MT1 and MT2 in the Suprachiasmatic nucleus |
| What is the clinical use of Ramelteon? | Insomnia |
| What is the most common Triptan? | Sumatriptan |
| Common 5-HT 1B/1D agonist. | Sumatriptan |
| What is the MOA of Triptans? | Inhibit trigeminal nerve activation Prevent vasoactive peptide release Induce vasoconstriction |
| What is the clinical use for Triptans? | - Acute migraine - Cluster headache attacks |
| What some adverse effects of Triptan therapy? | Coronary vasospasm, mild paresthesia, and serotonin syndrome |
| Which type of patients are at higher risk of coronary vasospasms due to Triptan intake? | CAD and/or Prinzmetal angina paites |
| When is it possible to develop serotonin syndrome with the use of Triptans? | When used in combination with other 5-HT agonists. |
| List of Na+ channel blocker epileptics: | 1. Carbamazepine 2. Fosphenytoin 3. Lamotrigine 4. Phenytoin 5. Topiramate 6. Valproic acid |
| SV2A receptor blocker (antiepileptic). | Levetiracetam |
| List of GABA-A agonists: | 1. Benzodiazepines 2. Topiramate 3. Phenobarbital 4. Propofol |
| Which epileptics are Ca2+ channel blockers? | Ethosuximide and Gabapentin |
| GABA reuptake inhibitor epileptic | Tiagabine |
| Which antiepileptics are GABA transaminase inhibitors? | Valproic acid and Vigabatrin |
| Parkinsonism is due to: | Loss of dopaminergic neurons and excess cholinergic activity |
| Parkinson drugs are categorized in strategies, which are: | 1. Dopamine agonists 2. Increase dopamine availability 3. Increase L-DOPA availability 4. Prevent dopamine breakdown 5. Curb excess cholinergic activity |
| The Dopamine agonists used for Parkinson disease are divided into: | 1. Ergot and, 2. Non-ergot |
| Which type of Dopamine agonist are preferred in treating of Parkinson disease? | Non-ergot |
| Which is the Ergot dopamine agonist used for Parkinson disease? | Bromocriptine |
| What are the Non-ergot dopamine agonists in Parkinson disease treatment? | Pramipexole and Ropinirole |
| Ropinirole and Pramipexole are: | Non-ergot Dopamine agonists |
| What are symptoms are included in Non-ergot dopamine agonist toxicity? | Impulse control disorder, postural hypotension, and hallucinations/confusion. |
| A person with a movement disorder is treated with a commonly used drug for such, but later develops a gambling problem. What are the more likely drugs given? | Pramipexole and Ropinirole |
| Parkinson drug that works by increasing dopamine availability. | Amantadine |
| How does Amantadine increase dopamine availability? | Increase dopamine release and decrease dopamine uptake |
| What are signs of Amantadine toxicity? | Ataxia and livedo reticularis |
| What is the mode of action of drugs that increase L-DOPA availability? | Prevent peripheral (pre-BBB) L-DOPA degradation, which increases the L-DOPA entering the CNS ---> increase central L-DOPA available for conversion to dopamine |
| What are the main drugs that increase L-DOPA availability? | Levodopa, Carbidopa, and Entacapone |
| Levodopa and Entacapone --> | Increase L-DOPA availability |
| MOA of Carbidopa: | Blocks peripheral conversion of L-DOPA to dopamine by inhibiting DOPA decarboxylase |
| Which enzyme is inhibited by Carbidopa? | DOPA decarboxylase |
| How does Entacapone prevent peripheral L-DOPA degradation? | Inhibiting COMT |
| Which drug is used in conjunction with Entacapone? | Levodopa |
| Which enzyme is inhibited by Entacapone? | COMT |
| Peripheral COMT is inhibited by ____________________. | Entacapone |
| Entacapone prevents the degradation of L-DOPA into: | 3-O-methyldopa (3-OMD) |
| A reduction in 3-OMD levels might be seen with the use of which Parkinson disease drug? | Entacapone |
| Agents that inhibit or prevent dopamine breakdown, work pre- or post-BBB? | Post-BBB |
| Which are the two types of agents that prevent dopamine breakdown post-BBB? | MAO-B inhibitors and Central COMT inhibitor |
| A central COMT inhibitor means: | It prevents that breakdown of Dopamine post BBB into 3-methoxytyramine (3-MT) |
| Central or Peripheral COMT inhibitors prevent conversion of dopamine into 3-MT? | Central COMT inhibitors |
| Which is a common central COMT inhibitor used in Parkinson disease? | Entacapone |
| What is the overall purpose of Selegiline and Rasagiline? | Prevent dopamine breakdown post-BBB |
| How does Selegiline prevent Dopamine breakdown? | Block conversion of dopamine into DOPAC by selectively inhibiting MAO-B. |
| Which enzyme is selectively inhibited by selegiline and rasagiline, in the treatment of Parkinson disease? | MAO-B |
| How do MAO-B inhibitors help in treating Parkinson disease symptoms? | Prevent dopamine breakdown post-BBB |
| Which Parkinson drugs are known to curb excess cholinergic activity? | Benztropine, trihexyphenidyl |
| Benztropine and Trihexyphenidyl are ________________________. | Antimuscarinics |
| How do antimuscarinics help in Parkinson symptoms relief? | Improve tremors and rigidity but has little to no effect in bradykinesia |
| What is intended to "better" by the use of Benztropine in Parkinson disease? | Tremor and rigidity |
| What enzyme in the CNS converts L-DOPA into dopamine? | DOPA decarboxylase |
| What long term adverse effects of Levodopa/Carbidopa administration? | Dyskinesia following administration ("on-off" phenomenon), akinesia between doses |
| What is the function of MAO-B? | Metabolize dopamine |
| What is a possible adverse effect of Selegiline and Rasagiline? | May enhance adverse effects of L-DOPA |
| Tetrabenazine and Reserpine clinical uses are: | Huntington chorea and Tardive dyskinesia |
| MOA of Tetrabenazine and reserpine: | Inhibit vesicular monoamine transporter (VMAT) dopamine |
| What is the result of the inhibition of VMAT dopamine? | Decrease vesicle packaging and release |
| Which drugs may cause decrease vesicle packaging and release due to VMAT dopamine inhibition? | Tetrabenazine and reserpine |
| What is the use for Riluzole? | ALS |
| MOA of Riluzole? | Decreased neuron glutamate excitotoxicity |
| What medication is used to treat Lou Gehrig disease? | Riluzole |
| List of common Alzheimer drugs: | 1. Memantine 2. Donepezil, Rivastigmine, and Galantamine |
| What is the mechanism of action of Memantine? | NMDA receptor antagonist |
| NMDA receptor antagonist used to treat Alzheimer? | Memantine |
| What are the two types of Alzheimer disease drugs? | 1. NMDA receptor antagonists 2. AChE inhibitors |
| CNS drugs must be: | 1. Lipid soluble, in order to cross the BBB, or, 2. Actively transported across the BBB |
| Drugs with low solubility in blood = | Rapid induction and recovery times |
| Drugs with high solubility in lipids = | Increase in potency |
| 1 -------------- = MAC | Potency |
| What does MAC in anesthetics stand for? | Minimal Alveolar Concentration |
| What is MAC? | Minimal Alveolar Concentration required to prevent 50% of subjects from moving in response to noxious stimulus |
| Which anesthetic is an example of decreased blood and lipid solubility? | Nitrous oxide (N2O) |
| Halothane, propofol, and thiopental have: | Increase lipid and blood solubility, and thus high potency and slow induction. |
| Which anesthetics have high potency and slow induction? | Halothane, propofol, and thiopental |
| What are inhaled anesthetics examples? | Desflurane, halothane, enflurane, isoflurane, sevoflurane, methoxyflurane, and N2O. |
| What are the physiological effects of inhaled anesthetics? | Myocardial depression, respiratory depression, nausea/emesis, increased cerebral blood flow. |
| Halothane adverse effect | Hepatotoxicity |
| What adverse effect is seen with Methoxyflurane? | Nephrotoxicity |
| Which inhaled anesthetics are proconvulsant if toxic levels are reached? | Enflurane and Epileptogenic |
| What is a possible adverse effect of the use of N2O as an inhaled anesthetic? | Expansion of trapped gas in a body cavity |
| What is Malignant hyperthermia? | Rare, life-threatening condition in which inhaled anesthetics or succinylcholine induce fever and severe muscle contractions. |
| What are the genetic principles associated with Malignant hyperthermia? | The susceptibility of Malignant hyperthermia, is often inherited as AD with variable penetrance. |
| What type of mutations induced or cause increase levels of Ca2+ release from Sarcoplasmic Reticulum? | Voltage-sensitive Ryanodine receptor (RYR1 gene) mutations |
| A mutated RYR1 gene causes --> | Increase release of Ca2+ from SR |
| A mutated RYR1 gene may increase the subject's susceptibility to develop which anesthetic-induced emergency? | Malignant hyperthermia |
| What is the treatment for Malignant hyperthermia? | Dantrolene |
| Dantrolene is used to treat: | Malignant hyperthermia |
| A person under surgery spikes fever > 104 F and has muscle twitches, is going to be treated with: | Dantrolene |
| What is the MOA of Dantrolene? | Ryanodine receptor antagonist |
| Ryanodine receptor antagonist | Dantrolene |
| Is malignant hyperthermia associated with Intravenous (IV) or Inhaled anesthetics? | Inhaled anesthetics |
| What are the common Intravenous anesthetics? | Thiopental, Midazolam, Propofol, and Ketamine |
| Thiopental is a _______________________ anesthetic. | Intravenous anesthetic |
| Which IV anesthetic is a barbiturate? | Thiopental |
| Which IV anesthetic is a Benzodiazepine? | Midazolam |
| NMDA receptor antagonist IV anesthetic | Ketamine |
| What is the mode of action of Propofol? | Pontentiates GABA-A |
| Which GABA receptor type, is targeted by IV anesthetics, A or B? | GABA-A |
| Thiopental is used for long or short, surgical procedures? | Short |
| How is the effect of Thiopental quickly terminated? | Rapid redistribution into tissue and fat |
| Cerebral blood flow with Thiopental is increased or decreased? | Decreased |
| Which IV anesthetic decreases cerebral blood flow? | Thiopental |
| What are severe or significant adverse effects of IV anesthetic, Midazolam? | Severe postoperative respiratory depression, hypotension, and anterograde amnesia |
| What kind of amnesia may be provoked as adverse effect of Midazolam? | Anterograde amnesia |
| What are the common uses for Midazolam? | 1. Procedural sedation (endoscopy) 2. Anesthesia induction |
| Which IV anesthetic may be used in the ICU setting? | Propofol |
| Which IV anesthetic is used to rapid anesthesia induction? | Propofol |
| MOA of Ketamine | NMDA receptor antagonist |
| What are the anesthetic uses of Ketamine? | 1. Dissociative anesthesia 2. Sympathomimetic |
| Increased or Decreased. Cerebral blood flow with Ketamine? | Increased |
| What is a possible emergence reaction to Ketamine anesthesia? | Disorientation, hallucination, and vivid dreams |
| Which IV anesthetic is known to increase the cerebral blood flow? | Ketamine |
| What are the two types of local anesthetics? | Esters and Amides |
| List of Ester Local anesthetics: | Procaine, Tetracaine, Benzocaine, and Chloroprocaine |
| List of Amide Local anesthetics: | Lidocaine, Mepivacaine, Bupivacaine, and Ropivacaine |
| What is the MOA of Local anesthetics? | Block Na+ channels by dingin to specific receptors on inner portion of channels |
| On which neuros a local anesthetics the most effective? | Rapidly firing neurons |
| What can be given along with a local anesthetic to enhance the local action? | Epinephrine |
| How does the co administration of local anesthetic + epinephrine help to enhance effect? | Decrease bleeding, increase anesthesia by systemic concentration |
| What is the order of loss when a local anesthetic is administered? | Pain --> Temperature --> Touch --> Pressure |
| What is the first scenario that is loss or blocked by local anaesthetics? | Pain |
| What type of anesthetics are used for spinal anesthesia? | Local anesthetics |
| What is an bupivacaine specific adverse effect? | Cardiovascular toxicity |
| Which local anesthetic is known to cause Methemoglobinemia? | Benzocaine |
| Selective for Nm nicotinic receptors at NMJ but not autonomic Nn receptors. | Neuromuscular blocking drugs |
| Neuromuscular blocking drugs are divided into ________________ and _________________. | Depolarizing and Non-depolarizing |
| What are complications of Depolarizing neuromuscular blocking drugs? | Hypercalcemia, hyperkalemia, and malignant hyperthermia. |
| What is the most common Depolarizing neuromuscular blocking agent? | Succinylcholine |
| Succinylcholine is a strong___________________________________. | ACh receptor agonist |
| MOA of Succinylcholine: | ACh receptor agonist that produces sustained depolarizing and prevents muscle contraction |
| The reversal of blockade caused by Succinylcholine is reversed in how many phases? | 2 phases |
| Which phase pf Succinylcholine blockade is definced a prolonged depolarization? | Phase I |
| Phase II of Succinylcholine blocked is: | Repolarized but blocked; ACh receptors are available, but desentized |
| What some common Nondepolarizing Neuromuscular blocking drugs? | Atracurium, Cisatracurium, Pancuronium, and Vecuronium |
| What is MOA of Non-depoloarizing nuromulsclar blcking agents? | Competitive with ACh for receptors |
| What are some drugs used to reverse the Nondepolarizing neuromuscular drug blockade? | Neostigmine and Edrophonium |
| Why is neostigmine must be given with atropine or glycopyrrolate? | To prevent muscarinic effects such as bradycardia |
| Which drugs must be administered with Neostigmine in order to prevent muscarinic effects? | Atropine or Glycopyrrolate |
| _______________________, prevents the release of Ca2+ from the SR of skeletal muscle by binding to the ryanodine receptor. | Dantrolene |
| What are the two clinical sues for Dantrolene? | 1. Malignant hyperthermia, 2. Neuroleptic malignant syndrome |
| What is a severe toxicity of antipsychotic drugs treated with Dantrolene? | Neuroleptic malignant syndrome |
| MOA of Baclofen: | Skeletal muscle relaxant. GABA-B receptor agonist in spinal cord |
| What is the clinical use for Baclofen? | Muscle spasticity, dystonia, and multiple sclerosis |
| GABA-B receptor agonist in spinal cord | Baclofen |
| Which GABA receptor is used by Baclofen? | GABA-B |
| Skeletal muscle relaxant that acts within CNS | Cyclobenzaprine |
| What is the clinical use for Cyclobenzaprine? | Muscle spasms |
| List of antispasmodics or Spasmolytics: | - Baclofen - Cyclobenzaprine - Dantrolene - Tizanidine |
| What is the mechanism of action of Tizanidine? | a-2 agonist, acts centrally |
| What conditions which produce spams, are treated with Tizanidine? | Muscle spasticity, multiple sclerosis, ALS, and cerebral palsy |
| Which spasmolytics work centrally? | Cyclobenzaprine and Tizanidine |
| Back muscle pain/spasm is commonly treated with: | Baclofen |
| On which opioid receptors does opioid analgesics work? | u, g, and k |
| Which is the B-endorphin opioid receptor? | u |
| What is mechanism of action of opioid analgesics? | Agonists at opioid receptors to modulate synaptic transmission, which leads to closure of presynaptic Ca2+ channels and open K+ channels leading to a decrease in synaptic transmission. |
| What are common Opioid analgesics Full agonists? | Morphine, heroin, meperidine, methadone, codeine, and fentanyl |
| Which is a common Opioid analgesics Partial agonist? | Buprenorphine |
| Mixed agonist/antagonist opioid analgesics? | Nalbuphine, pentazocine, and butorphanol |
| Common Opioid analgesics antagonists | Naloxone, naltrexone, and methylnaltrexone |
| Clinical uses for Opioid analgesics: | - Moderate to severe or refractory pain - Diarrhea - Acute pulmonary edema - Maintenance programs for heroin addicts |
| Which opioid analgesics are used for maintenance programs for heroin addicts? | Methadone, buprenorphine + naloxone |
| What are some adverse effects of opioid analgesics? | N/V, pruritus, addiction, respiratory depression, constipation, sphincter of Oddi spasms, miosis, additive CNS depression with other drugs |
| What is used to treat Opioid analgesic toxicity? | Naloxone |
| What is used to treat relapse of a detoxified Opioid analgesic? | Naltrexone |
| What are the two common Mixed and antagonist opioid analgesics? | Pentazocine and Butorphanol |
| What is the mechanism of action of PENTAZOCINE? | 1. k-opioid receptor agonist and , - u-opioid receptor weak antagonist or partial agonist |
| What is the clinical use for Pentazocine? | Analgesia for moderate to severe pain |
| What is a severe adverse effect or result from the use of Pentazocine? | Opioid withdrawal symptoms if patient is also taking full opioid agonist. |
| What are the mechanisms of action of Butorphanol? | 1. k-opioid receptor agonist and, 2. u-opioid receptor partial agonist |
| What are common instances in which Butorphanol is used? | In severe pain such as migraines and labor. |
| What is the MOA of Tramadol? | Very weak opioid agonist |
| Which opioid analgesic is known to inhibit the reuptake of norepinephrine and epinephrine? | Tramadol |
| Very weak opioid agonist | Tramadol |
| What is the use for Tramadol? | Chronic pain |
| What are two specifics adverse effects of Tramadol? | - Decreases seizure threshold - Serotonin syndrome |
| What is the purpose of Glaucoma therapy? | Decreases IOP via decreased amount of aqueous humor |
| How is the aqueous humor decreased in Glaucoma therapy? | Inhibition of synthesis/ secretion or increase drainage of aqueous humor. |
| Which drug classes are in Glaucoma therapy are used to decrease aqueous humor synthesis? | B-blockers, a-agonists, and diuretics. |
| Which beta-blockers are used in Glaucoma? | Timolol, betaxolol, and carteolol |
| How do beta-blockers mechanism of action work for Glaucoma treatment? | Decreases aqueous humor synthesis |
| Which are common alpha-agonists used in Glaucoma therapy? | Epinephrine, apraclonidine, and Brimonidine |
| Decreases aqueous humor synthesis via vasoconstriction. | Epinephrine |
| Which a-agonist is contraindicated in treatment of closed-angle glaucoma? | Epinephrine |
| What is an adverse effect of Epinephrine in association of Glaucoma treatment? | Mydriasis |
| What are the adverse effects seen with Apraclonidine and Brimonidine, as they treat glaucoma? | Blurry vision, ocular hyperemia, foreign body sensation, ocular allergic reactions, and ocular pruritus. |
| Which a common diuretic used for Glaucoma? | Acetazolamide |
| How does Acetazolamide help in treating glaucoma? | Decreases aqueous humor synthesis via inhibiting carbonic anhydrase |
| Which common prostaglandins are used in treating Glaucoma? | Bimatoprost, and Latanoprost |
| How do Prostaglandins MOA contribute to Glaucoma treatment? | 1. Increase outflow of aqueous humor via a decreaed resistace of flow through uveoscleral pathway |
| What are adverse effects of Glaucoma treating Prostaglandins? | 1. Darkens color of iris (browning) 2. Eyelash growth |
| Direct Cholinomimetics that are used to treat Glaucoma: | Pilocarpine and Carbachol |
| Pilocarpine and Carbachol are: | Direct cholinomimetics that are used to treat glaucoma |
| Which receptor are the cholinomimetics use to treat glaucoma? | M3 |
| Which are the Indirect cholinomimetics that treat glaucoma? | Physostigmine and Echothiophate |
| MOA of Cholinomimetics treating Glaucoma: | Increase outflow of aqueous humor via contraction of ciliary muscle and opening of trabecular meshwork |
| Why is Pilocarpine widely used in Closed-angle glaucoma? | Very effective at opening meshwork into canal of Schlemm |
| Which cholinomimetic is very effective in treatment of Closed-angle glaucoma? | Pilocarpine |
| What are the two main adverse effects of Glaucoma-treating cholinomimetics? | Miosis and cyclospasm |
| What causes the cyclospasms when using Cholinomimetics to treat glaucoma? | Contraction of ciliary muscle |
| Which muscle is stimulated to contract in order for cholinomimetics to treat Glaucoma? | Ciliary muscle |
| Which Glaucoma therapy drug classes work by increasing the outflow of aqueous humor? | Prostaglandins and Cholinomimetics (M3) |
Created by:
rakomi
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