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109 Cards in this Set
- Front
- Back
The 3 Neurotransmitters of the PNS |
Acetylcholine, Norepinephrine, and Epinephrine |
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Motor symptoms of Parkinson's Disease are mainly treated with drugs that activate ___________ receptors. |
Dopamine |
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Motor symptoms of Parkinson's disease are treated with drugs that block ________________ receptors. |
Cholinergic |
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Most effective treatment for motor symptoms of Parkinson's. |
Levodopa |
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Enzyme that converts Levadopa to Dopamine |
decarboxylase |
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These drugs block dopamine receptors in the striatum and can negate the effects of Levodopa |
First-generation antipsychotics |
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These second-generation antipsychotics can be used to treat levodopa-induced psychosis |
Clozapine and Quetiapine |
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Levodopa with an MAOI can result in |
hypertensive crisis |
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What is the effect of taking levodopa with a high protein meal? |
Reduced therapeutic effects. Amino acids compete with levodopa for absorption from the intestine and transport across the BBB |
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How does Carbidopa enhance the effects of Levodopa? |
It prevents the decarboxylation of levodopa in the intestine and peripheral tissues, and since it cannot cross the BBB, it does not prevent the conversion of levodopa to dopamine in the brain
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Can Carbidopa cross the blood-brain barrier? |
No. All of its actions take place in the intestine and peripheral tissues. |
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Pramipexole is an oral ______________ agonist |
nonergot dopamine |
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_________________ is a first-line drug for motor symptoms in Parkinson's disease and can be used for mono therapy early on. |
Pramipexole |
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Mechanism by which dopamine agonists relieve motor symptoms of Parkinson's: |
They cause direct activation of dopamine receptors in the striatum |
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Nausea, dyskinesia, postural hypotension, and hallucinations result from excessive activation of _____________ receptors. |
Dopamine |
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Entacapone is a __________________________. |
COMT inhibitor |
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This drug is combined with levodopa to inhibit metabolism by COMT in the intestine and peripheral tissue, thereby making more levodopa available to the brain. |
Entacapone |
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MAO-B inhibitors that can enhance responses to levodopa (name 2) |
Selegiline and Rasagiline |
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Which BRAIN enzyme inactivates dopamine? |
MAO-B |
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Spherical, extracullar bodies that consist of a beta-amyloid core surrounded by remnants of axons and dendrites |
Neuritic plaques |
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In patients with Alzheimer's ________________ is present in high levels and may contribute to neuronal injury. |
beta amyloid
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Neurofibrillary tangles result from production of a faulty form of this protein, that in healthy neurons serves to maintain the orderly arrangement of neurotubules |
tau |
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Alzeheimer's dementia can be treated with _______________ or ____________________. |
cholinesterase inhibitors; memantadine (Namenda) |
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Donepezil is an example of a |
cholinesterase inhibitor |
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Cholinesterase inhibitors increase the availability of __________ at synapses? |
acetylcholine |
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Peripheral cholinergic side effects include: |
nausea, vomiting, dyspepsia, diarrhea |
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Cardiac cholinergic side effects include: |
bradycardia |
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First generation antihistamines, tricyclic antidepressants, and conventional antipsychotics can reduce responses to these drugs: |
cholinesterase inhibitors
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Memantadine modulates the effects of glutamate at _____________ receptors. |
NMDA |
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The only drug approved for severe Alzheimer's Disease |
Memantadine |
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Significant side effects of Memantadine |
no clinically significant adverse effects |
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In this type of seizure, excitation undergoes limited spread from the focus to adjacent cortical areas |
partial |
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In this type of seizure excitation spreads widely throughout both hemispheres of the brain |
generalized |
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Phenytoin is active against ___________ and ___________ seizures but not ___________ seizures. |
tonic-clonic;partial;absence |
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therapeutic phenytoin range |
10-20 mcg/mL |
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If phenytoin levels rise above _______ mcg/mL, CNS toxicity develops |
20 |
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Phenytoin toxicity signs: |
nystagmus, sedation, ataxia, diplopia, cognitive impairment |
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Gingival hyperplasia is caused in 20 percent of patients on this drug |
phenytoin |
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Carbamezapine is active against ____________ and _________ seizures. |
partial;tonic-clonic |
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Often the preferred seizure drug |
Carbamezapine |
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When initiating carbamezapine and periodically, this should be checked. |
CBC (can cause leukopenia, anemia, and thrombocytopenia; and RARELY, fatal aplastic anemia) |
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Seizure drug that can sometimes cause hematologic toxicity |
Carbamezapine |
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This drug has activity against all types of seizures |
Valproate |
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In children under 2 taking valproic acid, especially when taking other AEDs, this is a risk |
Fatal liver injury |
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This AED can cause potentially fatal pancreatitis |
Valproate |
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Phenobarbitol is sometimes used for seizures in contrast other barbiturates because |
it does not cause generalized CNS depression at these doses |
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These three AEDs INDUCE the synthesis of hepatic drug-metabolizing enzymes and accelerate inactivation of other drugs (oral contraceptives;warfarin) |
Phenytoin, carbamezapine, phenobarbitol |
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What is the deal with AEDs and pregnancy |
All are potentially dangerous, but not as dangerous as having seizures during pregnancy |
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How to minimize fetal risk while taking AEDs? |
AVOID VALPROATE; use just one AED if possible at lowest effective dose |
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We know initial treatment of status epilepticus is with a benzodiazapine, but follow-up treatment usually consists of: |
phenytoin or fosphenytoin |
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3 drugs used for spasticity: |
Baclofen, diazepam, and dantrolene |
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These two muscle relaxants relieve spasticity by mimicking the inhibitory actions of GABA in the CNS |
Baclofen and diazepam |
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This drug acts directly on muscle to promote relaxation |
Dantrolene |
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Abrupt discontinuation of intrathecal baclofen can lead to ________________, organ failure, and fatality. |
rhabdomyolysis |
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Prolonged use of dantrolene can cause |
liver damage (monitor LFTs and minimize dose) |
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This CNS muscle relaxant can be used to treat malignant hyperthermia |
dantrolene |
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First-generation antipsychotics carry a higher risk than second-generation for |
EPS |
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Second-generation antipsychotics carry a higher risk than first-generation for |
metabolic effects |
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Thought to relieve symptoms of schizophrenia by causing strong blockade of D2 receptors: |
First-generation antipsychotics |
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Thought to relieve the symptoms of schizophrenia by causing moderate blockade of D2 receptors and strong blockade of 5-HT3 receptors |
Second-generation antipsychotics |
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Anticholinergic drugs are effective against these particular extrapyramidal side effects |
acute dystonia; parkinsonism {akathisia is harder to treat but may respond to anticholinergics, beta blockers, or benzodiazapines) |
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Although there really is no treatment for tardive dyskinesia, this could POSSIBLY help: |
switching to a second-generation antipsychotic |
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Is the risk of EPS higher with high or low potency first-generation antipsychotics? |
high-potency |
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Of the first-generation antipsychotics, do high or low potency have a greater risk of tardive dyskinesia? |
equal with both groups |
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The risk of sedation, orthostatic hypotension, and anticholinergic effects is greater with ________ potency FGAs. |
low |
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If a person on a FGA is experiencing muscle rigidity, high fever, and autonomic instability, they could be experiencing this potentially fatal adverse effect. |
neuroleptic malignant syndrome |
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These two drugs are used to treat neuroleptic malignant syndrom |
dantrolene and bromocriptine |
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How do antipsychotics affect circulating levels of prolactin? |
They increase it by blocking the inhibitory actions of dopamine on prolactin release |
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This drug can counteract the beneficial effects of FGA drugs and vice versa (dopamine receptors) |
levodopa (levodopa activates them, FGAs block them) |
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Haldol is a ________________. |
high-potency FGA |
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These two SGAs carry the greatest risk of metabolic effects |
Clozapine and Olanzapine |
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This is the most effective antipsychotic drug available. |
Clozapine ( second-generation antipsychotic) |
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The major adverse effect of Clozapine |
agranulocytosis |
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In general, antidepressant therapy should continue for how long after symptoms resolve? |
4 to 9 months |
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Agitation, confusion, hallucinations, hyperreflexia, tremor, and fever are a sign of: |
serotonin syndrome |
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TCAs block reuptake of: |
NE and 5-HT |
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Most common side effects of TCAs |
sedations, orthostatic hypotension, anticholinergic effects |
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Most serious adverse effect of TCAs |
cardiotoxicity |
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TCAs and MAOIs taken concurrently can cause: |
a hypertensive crisis |
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How do TCAs affect responses to direct-acting sympathomimetics (e.g. epinephrine)? |
They intensify response |
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How do TCAs affect responses to indirect-acting sympathomimetics (eg, amphetamine) |
diminish response |
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With antidepressants, it's not the inhibition or accumulation of MAOs that causes the antidepressant effect, but: |
the adaptive cellular responses that relieve depression |
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What do MAOIs do? |
Increase neuronal stores of NE and 5-HT and intensity transmission at noradrenergic and serotonergic synapses |
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main neurotransmitters MAOIs and TCAs work on |
NE and serotonin (5-HT) |
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MAOIs are first-line drugs for this condition ONLY |
atypical depression |
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This class of antidepressants does NOT cause direct CNS stimulation |
TCAs (SSRIs and MAOIs do cause direct CNS stimulation) |
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_________ and ___________ cause orthostatic hypotension. |
TCAs and MAOIs |
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If a patient taking an MAOI is admitted with a hypertensive crisis, treatment is: |
an IV vasodilator (nitroprusside, labetalol, phentolamine) or sublingual nifedepine |
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MAOIs and ___________-acting sympathomimetics can result in hypertensive crisis |
indirect (amphetaine, cocaine) |
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MAOIs plus SSRIs could equal |
serotonin syndrome |
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The three types of drugs used to treat bipolar disorder: |
mood stabilizers, antipsychotics, antidepressants |
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Lithium trough levels should be less than : |
1.5 mEq/L |
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When should lithium level be measured? |
12 hours after evening dose |
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common side effects of lithium at therapeutic doses: |
tremor, goiter, polyuria |
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Reduction in sodium levels will_________ lithium excretion. |
reduce (causing lithium to accumulate, possibly to toxic levels) Maintain normal sodium intake levels. |
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Lithium levels can be increased by _________ and ___________. |
diuretics (thiazides, especially) and NSAIDs |
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Barbiturates often _____________ hepatic drug-metabolizing enzymes, and benzodiazapenes do not. |
induce |
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Selection of a particular benzodiazapene relies heavily on a preference for |
time-course |
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This drug can be used to treat benzodiazapene overdose |
Flumazenil (benzodiazapene receptor antagonist) |
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Benzodiazapines, Buspar, and these four antidepressants are first-line drugs for generalized anxiety disorder |
Venlafaxine, Paroxetine, Escitalopram, Duloxetine |
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Buspirinone levels can be increased by: |
erythromycin, ketoconazole, and grapefruit juice |
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The best treatment for PTSD |
exposure therapy |
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These drugs are approved for PTSD, although there isn't proof that drugs are particularly effective: |
Paroxetine and Sertraline |
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Amphetamines work primarily by promoting neuronal release of ______ and ________, and partly by blocking their reuptake. |
NE and dopamine |
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How do amphetamines cause vasoconstriction and cardiac effects (increased heart rate, increased AV conduction, increased contractility)? |
by promoting release of norepinephrine from peripheral neurons |
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These are the only three non-stimulants approved for ADHD: |
atomoxetine, guanfacine, and clonidine |
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Caffeine is a |
methylxanthine |
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Caffeine and other drugs in its class act primarily by |
blocking adenosine receptors |
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Two principal uses of caffeine: |
treatment of apnea in premature infants and reversal of drowsiness |