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corness blk 4
| Question | Answer |
|---|---|
| The attempted focus of antipsychotic treatment is to treat psychosis while (2): | a) not exacerbating or b) actually alleviating concomitant mood disorders |
| Postive sxms of Schizophrenia (4) | 1.Hallucinations 2.Delusions 3.Disorganised speech/thought 4.Disorganized motor behaviour or catatonic behaviour |
| What sxms of Schizophrenia are caused by to much D2 | Hallucinations Delusions Disorganised speech/thought |
| what are the negative symptoms of schizophrenia (5) | 1.Loss of interest/ detachment from pleasure (Anhedonia) 2.Blunted emotions (Blunted Affect) 3.Limited communication (Alogia) 4.Dysfunctional motivation (Alvolition) 5.Dysfunction of socialization/interaction (Asociality) |
| What sxms of schizophrenia are caused by to little D1 (mainly in the prefrontal cortex)? | 1.Loss of interest/ detachment from pleasure (Anhedonia) 2.Blunted emotions (Blunted Affect) 3.Limited communication (Alogia) 4.Dysfunctional motivation (Alvolition) 5.Dysfunction of socialization/interaction (Asociality) 6.disorganized motor/cata |
| Pychosis is caused by over activity or dopamine where in the brain? | nucleus accumbens |
| All known antipsychotics have had significant affinity to D__ | 2 |
| drug induced psychosis is caused by degeneration of neurons from ______________ to the dorsal rache nuclues and VTA | Habenula |
| D1 and D2 receptors what tract in the substantia nigra innervates what part of the brain and cause what function? | Nigrostriatal, Caudate & Putamen; Extra pyramidal motor control |
| D2 receptors what tract in the VTA innervates what part of the brain and cause what function? | Mesolimbic; nucleus accumbens; arousal, memory, motivation |
| D1 receptors what tract in the VTA innervates what part of the brain and cause what function? | Mesocortical; Frontal and prefrontal cortex; cognition, communications, emotions, |
| D2 receptors what tract in the hypothalamus innervates what part of the brain and cause what function? | Tubero-infundibular; pituitary; inhibits prolactin secretion |
| What part of he brain should neurleptics increase dopamine? | Prefrontal cortex in the mesocortical tract |
| Side effects of typical antipsychotics (4 | 1.Extrapyramidal and Parkinsons-like symptoms 2.)Tardive dyskinesia 3.Endocrine dysfunction 4.Dysphoria |
| what endocrine dysfunctions occur with the side effects of typical antipsychotics | 1.Increased prolactin levels 2.Neuroleptic malignant syndrome (NMS) 3.SIADH (excess ADH and hyponatremia) |
| what tardive dyskinesia occur with the side effects of typical antipsychotics | 1.Involuntary excessive movement 2.Can be long-lasting or permanent |
| what extrapyramidal and parkinsons-like sxms occur with the side effects of typical antipsychotics | 1.Dystonia 2.Muscle rigidity, bradykinesia and tremor 3.Akathisia (restlessness) |
| What two drugs have sedation(H1 block), Hypotension (alpha blockade), Anti –muscarinic effects* | Chlorpromazine; Thioridazine |
| What 2 drugs help EPS (Parkinsonism) via D1 and D2 block | Fluphenazine; Haloperidol |
| Antipsychotics are lipophilic, orally effective However, ___________ and ____________ are available as IM long acting preparations (2-4 weeks); hence rapid initiation of treatment and maintenance is possible in noncompliant patients | Haloperidol; Fluphenazine |
| What are the acute EPS adverse effects of typical antipsychotics and there timelines | 3.Acute muscular dystonia – 4 hours 2.Akinesia - 4 days – can not initiate movements -Pseudo-parkinsonism symptoms- 1-4 weeks (rigidity, tremor, hypokinesia, mask like face, shuffling gait) - pill-rolling 3.Akathisia- 4 weeks |
| what is the timeline for chronic tardive diskinesia? | 4 months |
| what causes chronic tardive dyskinesia? | supersensitivity of DA receptors due to chronic blockade (months or years) of DA receptors in caudate, putamen |
| How do you treat neuroleptic malignant syndrome? | stop offending antipsychotic drug and start bromocriptine (DA receptor agonist) /Amantadine/Dantrolene and Diazepam, along with symptomatic management |
| what causes life-threatening condition , extreme muscle rigidity, hyperthermia, autonomic dysfunction. Altered level of consciousness, associated with 20% mortality rate. Occurs due to rapid and excessive blockade of postsynaptic DA receptors | Neuroleptic malignant syndrome (NMS) |
| What antipyschotic ADR do you treat with beta blockers? | Akathisia |
| What pathway (direct/indirect) does D1 (stimulate/inhibit)? What about D2? What pathway facilitates motion and what pathway involves tonic inhibition? | D1:direct; stimulate; motion D2: indirect; inhibit; tonic |
| If D2 is blocked or lost, this inhibition is more sensitive. ____________ block is needed when D2 stimulation is down | Muscarinic M1 |
| DAergic that stimulates DA release and inhibits reuptake and manages L-dopa off periods | Amantadine |
| DAergic that is a D2 agonist and weak partial D1 agonist and manages L-dopa off periods | Bromocriptine |
| Ca release inhibition that is a ryanodine receptor type 1 (RYR-1) and is a muscle relaxant | Dantrolene |
| antiAch is a muscarinic antagonist for Parkinson’s Disease | Biperiden |
| antiACh is a M1/H1 antagonist for second line Parkinson's disease | Benztropine |
| antiAch is a M/H1 antagonist which is a antihistamine | Diphen-hydramine |
| Benzo that facilitates GABA-induced Cl influx that is a anxiolytic muscle relaxant | Diazepam |
| -generation anti-psychotics target D2 as antagonists, and also manage to reduce or eliminate extrapyramidal symptoms (EPS). | __________ |
| Most atypical neuroleptics now show a narrow range of ___-___% D2 receptor occupancy at the optimal therapeutic dose. | 60-65; Higher affinity for D2 = greater occupancy by the neuroleptic = greater EPS |
| High or Low 5HT2A/D2 ratio means most likely chance of EPS. | high |
| Clozapine is a better anti-psychotic than its binding affinity to D2 would suggest for two reasons? | 1.Clozapine shows rapid dissociation from D2 binding sites 2.Clozapine in an atypical neuroleptic and atypicals tend to antagonizes more than just D2. |
| Serotonin acting through 5HT2A has an inhibitory effect on DA release in which two brain areas? | dorsal striatum and prefrontal cortex |
| Blocking 5HT2A increases DA release in dorsal striatum and prefrontal cortex improves what? | EPS and mood and cognitive symptoms (negative symptoms). |
| _________ receptor activation by serotonin in the NAc would normally stimulate DA release but _________ receptor blockade achieved by atypical neuroleptics allows the same neuroleptic dose to occupy a greater number of D2 receptors. | 5HT2A |
| antipsychotic antagonism of what receptors causes appitite stimulation (3)? | 1.Histamine H1 2.5HT2A 3.5HT2C |
| what is a main feature of atypical neuroleptics and is related to their binding profile? | show clinical efficacy at dosing levels which do not show extensive EPS |
| What side effect is respiradone known for? | hyperprolactinemia and EPS side effec |
| what side effects are , olanzapine and clozapine known for? | weight gain, hyperglycemia and sedation |
| What 4 Atypical Neuroleptics features that affect EPS | 1.They target D2 (little or no affinity to D1) 2.They all have very low affinity to D2 3.They almost all have affinity to 5HT2A (antagonists) 4.Atypicals with anti-muscarinic actions show added benefits against EPS |
| what 3 Atypical Neuroleptics features affect negative symptoms? | 1.target D2 (little affinity to D1) 2.They all appear to have affinity to 5HT2A *3.Atypicals with partial 5HT1A agonist actions show added benefits against negative symptoms |
| name 2 D2 recpetor blockade side effects | EPS; prolactin elevation |
| name 3 H1 receptor blockage side effects | weight gain, dizziness, sedation |
| name a 5-HT2C receptor blockage side effects | satiety blockade (leads to weightgain) |
| which Antipyschotic drug has a prolonged QT interval side effect? | thioridazine*, rispiradone, ziprasidone, clozapine, quetiapine, haloperidol, |
| which antipyschotic drug has agranulocytosis side effect? | clozapine |
| what is the Poikilothermic effect | temperature (body temp varies with environment) ie chlorpromazine) |
| Primarily a sodium channel blocker that may also increase GABA transmission used in the treatment of Bipolar disorder | Valproate / Valproic acid |
| drug that may modulate glutamate and GABA transmission. Interferes with IP3 turnover (affecting M1, M3, alpha1, 5HT1A. Used to treat Bipolar Disorder | Lithium |
| dry mouth, increased thirst or urination; diabetes insipidus diarrhea are side effects of what bipolar drug? | Lithium |
| What Bipolar drugs are C.I.'s during pregnancy? which drug should be used instead? | Valproate and Lithium; Quetiapine is considered safer during pregnancy |
| What drug(s) can only use in patients with normal cardiac and renal function? and which drug(s) ADRs include hepatotoxicity and pancreatitis | Valproate; Valproate |
| Drugs for absence siezures (petit mal) (2) | Valproate, ethosuxemide |
| drugs for myoclonic siezures (2) | Valproate clonazepam |
| drugs for tonic-clonic (grand mal) (3) | Valproate, phenytoin, carbamazepine --> (pediatric) |
| drugs for partial (focal) seizures | Carbamazepine, phenytoin, valproate |
| what drugs ↓axonal conduction by preventing Na+ influx through fast Na+ channels-? (6) | 1.phenytoin 2.carbamazepine 3.valproate 4.topiramate 5.lamotrigine 6.zonisamide |
| what drugs ↑inhibitory tone by facilitation of GABA-mediated hyperpolarization? (2) | 1.) Benzo's 2.) Barbiturates |
| what anti-epileptic drugs ↓ excitatory effects of glutamic acid? (2) | 1. topiramate (block AMPA receptor) 2.felbamate (blocks NMDA receptors) |
| what drugs↓ presynaptic Ca2+ influx through type-T channels in thalamic neurons? (2) | ethosuximide and valproic acid |
| what is the mechanism for valproate? and what enzyme does it inhibit? | 1.Prolongs inactivation of Na+ channel (similar to phenytoin and carbamazepine)- hence blocks sustained high-frequency repetitive firing of neurons 2.Blocks T-type Ca2+ channels 3.)inhibits Cyp450-2C9 |
| what is Divalproex sodium? | 1.a combination of sodium valproate and valproic acid 2.reduced to valproate when it reaches GIT 3.better GI tolerance hence preferred by patients |
| What is the mechanism for Phenytoin | blocks axonal Na+ channels in their inactivated state (prolongs the inactivated state) and slows its rate of recovery ---> prevents seizure propagation |
| which drug needs plasma monitoring (Therapeutic range - 10-20μg/mL) b/c Small increases in a daily dose can produce large increases in the plasma concentration, resulting in drug-induced toxicity | Phenytoin |
| toxicity from what drug causes Gingival hyperplasia (Gum hypertrophy) and Hirsutism, Megaloblastic anemia, Aplastic anemia, Osteomalacia (interferes with Vit. D, Inhibition of ADH release | Phentoin |
| is a prodrug of Phenytoin, rapidly converted to phenytoin in plasma. Intravenous _____________ can be used as a substitute for Phenytoin AND neurosurgery and status epilepticus. | fosphenytoin |
| DoC for Trigeminal neuralgia | Carbamazepine |
| The following ADR's are associated with what drug? 1.Dilutional hyponatremia (↑ADH secretion/sensitivity) 2.may cause an increase in seizures 3.Exfoliative dermatitis 4.Fetal malformations | Carbamazepine |
| A prodrug with improved toxicity profile than carbamazepine does not produce the epoxide metabolite, which is largely responsible for the ADR of carbamazepine | Oxcarbazepine |
| Drug? blocks Na+ channels, high voltage-dependent Ca2+ channels effective in a variety of seizure disorders: partial seizures, generalized seizures, absence seizures,Lennox-Gastaut syndrome (as adjunct). approved for bipolar (maintenance) | LAMOTRIGINE |
| broad-spectrum anticonvulsant delays the recovery of the inactivated Na+ channels enhance GABA activity by binding to the GABA receptor blocks the activation of AMPA receptors add on therapy for Partial seizures prophylaxis for migraine | TOPIRAMATE |
| What is the consensus mechanistic goal of the antipsychotic agents to treat the positive symptoms of schizophrenia | Decrease DA in NAc |
| What advantage do the atypical neuroleptics have over the typical neuroleptics and how do they achieve this? | Treat – sxm’s and EPS |
| What Drug can be used for bipolar maintenance, acute bi-polar mania, and bi-polar depression? | Quetiapine |
| What neuroepileptic can be used in children and adolescence (4) | Aripriprazole; Lurasidone; Olanzapine; Quetiapine |
| what's the difference between sedatives and hypnotics | Sedatives: decrease activity, moderate excitement and calm the recipient. Hypnotics: Produce drowsiness and facilitate the onset and maintenance of a state of sleep that resembles natural sleep and from which the recipient can be easily aroused. |
Created by:
moore420
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