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Neuro Pharm Flashcards

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1
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MOA - dopamine receptor (D3) agonist ; may be given to patients being treated with levodopa which have started to become tolerant. allows dose of levodopa to be decreased and smooths out response fluctuations. may be give as monotherapy for mild PD ; possible neuroprotective effect due to scavage hydrogen peroxide and enhancement of neurotrophic activity ; ADRs - nausea, vomiting, constipation, dyspepsia, reflux, postural hypotension, arrhythmias, dyskinesias, impulse control, confusion: hallucinations, delusions:: renal insufficiency may require dosage change.

A

Pramipexol

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2
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relatively pure D2 receptor agonist. effective as monotherapy in pts with mild disease and to smooth response to levodopa in pts with more advanced disease and respone fluctuations. biotransformed by CYP1A2; other drugs metabolized by this isoform may significantly decrease its clearance.

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ropinirole

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3
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MOA - dopamine receptor (D2) agonist ; may be given to patients being treated with levodopa which have started to become tolerant ; ADRs - nausea, vomiting, constipation, dyspepsia, reflux, postural hypotension, arrhythmias, dyskinesias, impulse control, confusion, hallucinations, delusions,

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Bromocriptine, pergolide

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4
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MOA - monoamineoxidase-B inhibitor -> inhibits dopamine breakdown into DOPAC ; enhances and prolongs antiparkinsonism effect of levodopa ; Drug interactions -should be used with care in patients recieving TCAs or SSRIs due to theoretical risk of acute toxic interactions of the serotonin syndrome type, may also cause hypertensive crisis when combined with levodopa

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Selegiline, rasagiline

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5
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MOA - CNS and peripheral COMT inhibitor -> inhibits dopamine metabolism into 3-OMD ; may cause URINE to go bright yellow ; ADRs - increased liver enzymes -> acute hepatic failure (must monitor LFTs every 2 weeks during the first year)

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Tolcapone

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6
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MOA - peripheral COMT inhibitor -> prevents decomposition of L-DOPA in the periphery (before crossing BBB) ; may cause URINE to go bright orange

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Entacapone

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7
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MOA - peripheral DOPA decarboxylase inhibitor -> prevents metabolism of L-DOPA to dopamine in the periphery (reducing ADRs of L-DOPA)

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Carbidopa

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8
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MOA - crosses BBB via L-amino acid transporter -> is metabolized to dopamine in the CNS by DOPA decarboxylase ; should be taken 1-2hrs before meal ; NOTE - only 1-3% of _________ enters the brain unchanged (the remainder is biotransformed in the periphery by decarboxylation -> eventually (8hrs) 2/3 of dose ends up in urine as homovanillic acid (HVA) and dihydroxyphenylacetic acid (DOPAC) ; USE - to treat parkinson’s symptoms (especially bradykinesia), approx 1/3 of pts good response ; ADRs - Nausea and vomiting (80% of pts), cardiac arrhythmias, postural hypotension, hypertension (especially with large doses) ; LONG-TERM use -> resistance to drug action causing on-off periods marked by akinesia alternating with increased mobility with significant dyskinesia ; CONTRAINDICATED - psychosis and closed angle glaucoma

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L-DOPA (Levodopa)

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9
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may cause hypertension because of its breakdown to Norepinephrine

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Dopamine in the periphery

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10
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DOPA is metabolized from tyrosine by tyrosine hydroxylase -> which is metabolized by dopa decarboxylase to form this ___________

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Dopamine

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11
Q

These are the two competitive inhibitors to the breakdown of L-DOPA, inhibiting COMT and DOPA decarboxylase respectively

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Entacapone & Carbidopa

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12
Q

pharmacologic doses of pyridoxine (Vit. B6) increase extracerebral biotransformation of ________ -> decreased efficacy unless peripheral decarboxylase inhibitor is also given ; should not admin ___________ to pts taking MAO-A inhibitors or within 2 weeks of DC because of risk of hypertensive crisis

A

Levodopa drug interactions

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13
Q

MOA - potent Dopamine agonist ; effective for temporary relief (rescue) of off-periods of akinesia in pts on optimized dopaminergic Tx ; ADRs - dyskinesias, drowsines, chest pain, sweating, hypotension, bruising at injection, nausea

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Apomorphine

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14
Q

antiviral agent ; serendipitious finding regarding efficacy in parkinsons ; potentiates dopaminergic fucntion by increased synthesis and release, and decreased reuptake ; reported to antagonize adenosine at adenosine A2a receptors which may inhibit D-2 receptor function (inhibition of inhibition) ; less efficatious than levodopa ; ADRs - peripheral edema

A

Amantidine

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15
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can improve tremor and rigidity, minor effect on bradykinesia ; initial Tx with low dose -> increase until benefit ; pts not responding to one agent in this class can be given another ; if drug needs to be withdrawn must do so slowly to decrease likelyhood of exacerbation of parkinson’s disease

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Anticholinergics for treament of Parkinson’s (benztropine)

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16
Q

PHENYTOIN, mephentoin, ethotoin ; MOA - limit the amount of seizure activity in the focus and limit the spread from the focus by inhibiting voltage gated Na+ channels ; Toxicity - nystagmus, diplopia, vertigo, ataxia, hirsurtism, gingival hyperplasia, hepatic microsomal enzyme INDUCTION

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Hydantoins

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17
Q

drug of choice for most types of seizures ; NOTE - not for absence seizures ; MOA - limit the amount of seizure activity in the focus and limit the spread from the focus by inhibiting voltage gated Na+ channels ;

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Phenytoin

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18
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PHENOBARBITAL, metharbital, mephobarbital, primidone (prodrug) ; MOA - limit spread of sizure activity, elevate seizure threshold by enhancing GABA activity ; USE - generalized sizures and partial seizures, NOT for absense seizures ; Toxicity - sedation, exfoliate dermatitis, megaloblastic anemia, hepatic microsomal enzyme INDUCTION

A

Barbituates

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19
Q

ethosyximide, methsuximide, phensuximide ; MOA - unknown (NOT via GABA enhancement or Na+ channels) ; USE - ABSENCE seizure, and may be effective in tonic-clonic seizure ; Toxicities - nvd, diarrhea, sedation, drowsines, inhibits platelet aggregation, hepatotox, teratogenic effects

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Succinimides

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20
Q

MOA - prolongs the refractory period (reduces the rate of firing), decreases the spread of activity from the focus by decreasing excitation of neuron via decreasing Na+ and K+ conductances ; USE - partial seizures, psychomotor, generalized tonic-clonic (NOT for absence seizures) ; Toxicity - blurred, vision, drowsiness, dizziness, ataxia, nausea (tolerance will develop for all of these), also renal and hepatic function and hematological parameters should be monitored due to rare but severe side effects

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Carbamazepine

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21
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USE - absence seizures, generalized seizures, partial seizures, myoclonic seizures, atonic seizures ; prevents Pentylenetetrazol-(PTZ)-induced seizures, blocks electroconvulsive shock (ECS) seizurs, prevents kindled seizures ; MOA - decreases voltage sensitive Na+ channels, and enhances GABA ; Toxicity - anorexia, nausea, vomiting, idiosyncratic hepatotox, high doses may inhibit platelet function ;

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Valproic Acid

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22
Q

USE - absence seizures ; Tox - hemeralopia, hepatitis, nephrosis, bone marrow damage ; MOA - unknown

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Trimethadione

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23
Q

clonazepam, clorazepate, LORAZEPAM, DIAZEPAM ; MOA - enhance GABA, limits spread of activity away from focus ; USE - absence seizures, myoclonic seizures, atonic seizures, status epilepticus ; toxicity - drowsiness, ataxia, personality changes (agression, hyperactivity, irritability - mostly seen in children)

A

Benzodiazepines (BDZs)

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24
Q

condition where seizures persist for a long time ; leads to systemic hypoxia, acidemia, hyperpyrexia, cardiovascular collapse, renal shutdown ; Tx - diazepam or LOREZAPAM other benzodiazepines

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Status epilepticus

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25
Q

MOA - carbonic anhydrase inhibitor, diminishes seizure by production of systemic acidosis ; USE - absence sizures (limited by tolerance) ; Tox - drowsiness, paresthesias

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acetazolamide

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26
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USE - adjunctive treatement in complex partial seizures which are refractory to breakthrough seizures ; Tox - hepatitis, neprhitis, aplastic anemia, psychological effects ; MOA - unknown ; MANDATORY liver, kidney, and bone marrow function

A

Phenacemide

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27
Q

Use - partial seizures, may be used in conjunction with phenytoin or carbamiceptine ; Tox - APLASTIC ANEMIA, ACUTE liver failure ; NOTE - should be limited to most severe and refractive cases ; LAST RESORT

A

Felbamate

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28
Q

carbamazepine, felbamate, phenobarbital, phenytoin, primidone all cause _________________

A

Enzyme induction (specifically anti-epileptics)

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29
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This is caused by BDZs, phenobarbital

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Paradoxical excitement

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30
Q

This is caused by phenytoin, BDZs, phenobarbital,

A

Ataxia

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31
Q

This is caused by carbamazepine, phenytoin, clonazepam

A

Visual distrubances

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32
Q

This is caused by phenytoin

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Gingival hyperplasia, Hirsutism and hypertrichosis

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33
Q

this is caused by phenytoin, primidone, phenobarbital

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Megaloblastic anemia

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34
Q

this is caused by phenytoin, valproic acid, carbamazepine,

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Hepatitis

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35
Q

This is caused by valproic acid also causing this other rare side effect

A

alopecia

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36
Q

ethosuximide (DOC), clonazepam (tolerance limits usefulness), valproic acid (DOC if tonic-clonic present) are used to treat this condition

A

Tx of absence seizures

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37
Q

rates of PO abs depend lipophilicity: triazolam > diazepam > others (lorazepam, chlordiazepoxide) - the higher the lipophilicity = CNS actions more rapidly ; ADRs - sedation, anterograde amnesia, euphoria, hypnosis, decreased REM sleep ; used as an adjunct to general anesthesia pre-operatively

A

Benzodiazepines (BDZs)

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38
Q

does not require breakdown and thus has no metabolites and can be used to substitute diazepam in patients with liver/renal failure

A

oxazepam

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39
Q

synthetic BDZ derivative ; reverses actions of BDZs ; limited clinical data that it also reverses actions of zolpidem, zaleplon, eszopiclone ; does NOT revers effects of barbituates, meprobamate, ethanol ; short half life ; ADRs - agitation, confustion, dizziness, nausea ; may precipitate severe abstinence sydrome in pts who exhibit physiologic BDZ dependence

A

Flumazenil

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40
Q

pharmacokinetics - most barbituates and older sedative-hypnotics are abs rapidly following PO admin like tiobarbituates (thiopental) ; phenobarbital and meprobamate have low lipid solubility and slow penetration of brain ; Biotransformation - hepatic metabolism accounts for clearance these - most undergo Phase I reactions including N-dealkylation and aliphatic hydroxylation - many phase I metabolites are pharmacologically active with long half lives - metabolites are subsequently conjucated (phase II reactions) to form glucuronides -> excreted in urine ; NOTE - elimination half life of parent molecule may have little relationship to time cours of pharmacologic effects

A

Barbituates

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41
Q

barbituate pro-drug

A

Clorazepate

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42
Q

MOA - bind to molecular components of GABA-a receptor (receptor operates as a chloride ion channel and is activated by GABA which causes inhibition) in neuronal membranes of CNS - GABA interacts with alpha and beta subunits causing chloride channel opening and HYPERpolarization ; BDZs increase frequency of channel openings (does NOT directly initiate chloride current) ; Barbituates allow GABA channels to be open for a longer period of time ; allow GABA to act more freely or act like GABA itself - affects all levels of CNS (even spinal cord) ;

A

Pharmacodynamics of Barbiturates, Benzodiazepines, Zolpidem etc

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43
Q

very lipid soluble, enters brain rapidly after IV injection ; use - employed for induction of general anesthesia ; short duration of action due to rapid tissue redistribution from brain, useful in recovery from anesthesia

A

Thiopental (barbituate)

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44
Q

selective anxiolytic effects effects - relieves anxiety without causing marked sedative or euphoric effects ; NO direct interaction with GABAergic systems ; may exert anxiolytic efffects as partial agonist at brain 5HT1A receptors ; also has affinity for D2 receptors ; treated pts have NO rebound anxiety or withdrawal signs after abrupt discontinuance ; NOT effective in blocking acute withdrawal syndrome after abrupt termination of chronic BZ or other sedative-hypnotics ; Minimal abuse liability ; anxiolitic effects may take > 1 week to develop -> NOT useful for Tx of acute anxiety states & NOT effective for panic disorders ; PO abs -> first pass metabolism -> interactions with drugs that increase enzymes such as Rfiampin and those which decrease enzyme levels such as erythromycin and ketoconazole ; NOTE - little or no effecton on driving skills

A

Buspirone

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45
Q

MOA - facilitates GABA mediated neuronal inhibition ; structurally unrelated to BDZ but does have hypnotic activities ; rebound insomnia may occur on abrupt discontinuance of higher doses (abuse) ; NOTE - rifampin decreases T1/2 ; USE - insomnia tx

A

Zolpidem (Ambien)

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46
Q

MOA - binds selectively to BDZ-1 subtype (contain only a-1 subunits) -> facilitates inhibitory actions of GABA ; USE - treat insomnia

A

Zaleplon (Sonata)

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47
Q

MOA - interacts with GABA-benzodiazepine receptor complexes ; USE - treat insomnia

A

Eszopiclone (Lunesta)

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48
Q

MOA - melatonin receptor agonist ; Over the counter ; USE - tx insomnia

A

Ramelteon

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49
Q

very effective in tx of panic disorders and agoraphobia bc of higher selectivity than other BZs ; NOTE - flumazenil can be used to reverse effects

A

Alprazolam

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50
Q

propranolol is an example of this type of drug used as antianxiety agents in situations such as performance anxiety ; sympathetic nervous system overactivity associated with anxiety can be decreased with these meds ; ADRs - lethargy, vivid dreams, hallucination ;

A

Beta blocking drugs Tx for anxiety

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51
Q

MOA - monoclonal antibody causing blockade of integrin on inflammatory cells and vascular endothelial cells and reductino of leukocyte micration into brain and therefore reduced plaque fromation in brain ; ADRs - IMMUNE RECONSTITUTION INFLAMMATORY SYNDROME in pts with MS following cessation of this drug ; May cause progressive multifocal leukoencephalopathy and because of this side effect must have prescribing licence (take class to prescribe)

A

Natalizumab

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52
Q

MOA - Synthetic protain that acts as a decoy for autoimmune antibodies ; ADRs - tiredness and weakness due to overcompensation, TRANSIENT CV (HTN) ; sub q once-a-day

A

Glatiramer acetate (Copaxone)

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53
Q

MOA - antineoplastic that supresses activity of Tcells, Bcells, and macrophages which are the components that attack the myelin system ; ADRs - significant CARDIOTOX, reduced ability to fight infection, birth defects (affects sperm), excreted in breast milk ; NOTE - maximum lifetime dose per patient

A

Mitoxantrone

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54
Q

MOA - mediates antiviral, antiproliferative and immunomodulatory activities ; ADRs - flu-like, depression, HEPATOTOX - monitor LFTs ; produced via recombinant DNA from Ecoli ; sub q every 2 days ; NOTE - compensatory mechanism neutralizing antibodies attack the interferion -> loss of effectiveness of drug (benefit can last upto 5 years)

A

Interferon beta-1b (Betaseron)

55
Q

MOA - binds to type 1 interferion receptors and activates tyrosine kinase, producing antiviral, antiproliferative, and immunomodulatory effects - exact mech unknown ; ADRs - decreased bc longer half life and less injections (1/week) ; 1/3 had fewer attacks and flare-ups vs placebo

A

Interferion beta-1a (Avonex)

56
Q

MOA - phosphate receptor modulator - reduces ability of lymphocytes to leave lymph nodes ; biotransfomred into active metabolite (3A4) with 90% abs and extensive distribution bc highly bound to proteins -> steady state takes 1-2 months (T 1/2 6-9days) ; ADRs - CV first dose effect, increased susceptibility to infection (decreased IgM and IgG titers), macular edema, respiratory ; Interactions - ketoconazole, avoid attenuated vaccines

A

Fingolomid (Gilenya)

57
Q

can cause a convulsant seizure ; one of these medications blocks chloride channels the other interferes with the binding of GABA. what are these respectively

A

Conculsants (CNS excitatory agents) ; Picrotoxin, Bicuculline

58
Q

interferon beta-1a ; resemble the interferon that the body naturally produces during a response by the immune system. It is not known how interferon drugs help people with MS, but they do alter activity of the immune system. The drugs also help the body fight viruses. Another theory is that viruses may trigger relapses in people who already have MS.

A

Avonex ; Extravia

59
Q

galatiramer acetate ; is an artificially made protein that resembles a protein that is part of the myelin that surrounds nerves. It is not known exactly how the drug works, but it appears to alter the activity of the immune system. Unlike the interferon beta drugs, it has not been shown to reduce or delay disability, but it does reduce the frequency of attacks.

A

Copaxone

60
Q

fingolimod ; is biotansformed by sphingosine kinase to the active metabolite, fingolimod-phosphate, which is a sphingosine 1-phosphate receptor modulator – binds with high affinity to sphingosine 1-phosphate receptors 1, 3, 4, and 5 and blocks ability of lymphocytes to exit lymph nodes, reducing lymphocytes in peripheral blood. The mechanism by which fingolimod exerts therapeutic effects in MS may involve reduction of lymphocyte migration into the CNS.

A

Gilenva

61
Q

mitoxantrone ; is an immune system suppressing drug. It is also used to treat some cancers. it reduces neurologic disability and/or the frequency of clinical relapses in patients with secondary progressive, progressive relapsing, or worsening relapsing-remitting MS. It can be given to anyone who is experiencing a worsening of disease.

A

Novantrone

62
Q

FYI - barbituates and benzodiazepines are contraindicated and care must be used when prescribing to pregnant pts respectively

A

FYI - Barbituates & Benzodiazepines

63
Q

most abused bartbituate - due to high lipid solubility

A

Pentobarbital

64
Q

most abused benzodiazepine - due to high lipid solubility ; faster acting ; can cause daytime anxiety bc of short T1/2

A

Triazolam

65
Q

Benzodiazepine that can bue used to treat agoraphobia

A

Alprazolam

66
Q

limited inuse for certain types of epilepsy, inducing a coma, preventing withdrawal from a CNS depressant ; undergo extensive hepatic biotransfromation (except for phenobarbital) bc most of the initial products are not active -> auto-induction ; cumulative effects from multiple dosing ; CONTRAINDICATED in geriatric pts and heptatotoxicity due to significant increase in T1/2 and amplified cummulative effect ; you can increase clearance rate by alkalinizing the urine

A

Barbituates

67
Q

USE - central acting skeletal muscle relaxant, also used to treat pain or spasticity not responsive to tother routes ; MOA - interferes with releases of excitatory NTs ; equal to diazepam in decreaseing spasticity but much less sedation bc it hits the GABAb receptors (most other drugs hit the GABAa receptors) ; ADRs - may lower threshold in ppl with epilepsy

A

Baclofen

68
Q

USE - used to treat neurogenic pain of neuropathy and may also be used as an anti-epileptic in MS pts ; MOA - similar to GABA

A

Gabapentin

69
Q

MOA - an inhibitory amino-acid neurotransmitter

A

Glycine

70
Q

USE - only for ALS ; MOA - reduce glutamine transmission in CNS

A

Riluzole

71
Q

MOA - strong alpha-2- agonists - reduces releases of NT from presynaptic membrane ; related to clonidine ; ADRs - CNS

A

Tizanidine (Zanaflex)

72
Q

MOA - derivative similar to phenytoin, direct action on skeletal muscle by inhibition of excitation-contraction coupling via decreasing the interaction and involvement of Ca2+ (sequester Ca2+ in the sarcoplastic reticulum) ; ADRs - muscle weakness, sedation, hepatotox ; NOTE - the only specific and effective treatment for malignant HYPERthermia and also used for management of neuroleptic malignant sydrome ; USE - muscle spasticity

A

Dantrolene

73
Q

MOA - interfere with release of ACh vesicle at neuromuscular junction

A

Botulinum toxins

74
Q

related to tricyclic antidepressants ; USE - tx of acute local muscle spasm

A

Cyclobenzaprine

75
Q

CNS depress and possible psychological dependence ; USE - tx of acute local muscle spasm ; MOA - anticholnergic drug of the athanolamine antihistamine class

A

Orphenadrine

76
Q

Conclusions: As monotherapy for early PD, pramipexole ER was noninferior (meaning, ER was NOT worse) to pramipexole IR (immediate relase) and significantly more effective than placebo. Tolerability and safety did not differ between the formulations.

A

Article 1 - Extended-release pramipexole in early Parkinson disease a 33-week randomized controlled trial

77
Q

Conclusions: Extended-release pramipexole significantly improved UPDRS (Unified Parkinson’s Disease Rating Scale) score and off-time compared with placebo, with similar efficacy, tolerability, and safety of immediate-release pramipexole compared with placebo. This study provides Class I evidence that the extended-release form of pramipexole, taken once daily, is efficacious as an adjunct to levodopa in advanced PD.

A

Article 2: Extended-release pramipexole in advanced Parkinson disease

78
Q

Conclusions: Long-lasting inhibition of the COMT may limit the efficacy of entacapone by development of a tolerance. Also, an abrupt withdrawal of the treatment will be followed by a dramatic worsening of motor disability.

A

Article 3: Erythrocytes Catechol-O-Methyl Transferase (COMT) Activity Is Up-Regulated After a 3-Month Treatment by Entacapone in Parkinsonian Patients

79
Q

Conclusion: Article describe an unusual patient who had Parkinson’s disease with dropped head syndrome (DHS) caused by amantadine. When the patient, who had DHS while receiving only 2 kinds of antiparkinsonian drugs, was rechallenged with amantadine, DHS developed, accompanied by increased muscle tone in the neck muscles on surface electromyogram. The DHS resolved after the withdrawal of amantadine. Moreover, an IV infusion of levodopa did not alter the DHS. These findings collectively suggest that the DHS in our patient was most likely caused directly by amantadine. Our findings suggest that amantadine may carry the risk of augmenting dystonic syndrome in humans.

A

Article 4: Dropped Head Associated With Amantadine in Parkinson Disease

80
Q

Conclusions: This study evaluated the effects of ropinirole prolonged- release (RPR) in comparison with ropinirole immediate-release (RIR) on sleep-related disorders in Parkinson disease (PD). Ropinirole prolonged-release compared with RIR improved subjective quality of sleep, reduced daytime sleepiness, and led to disappearance of SAs (sleep attacks) in some patients possibly due to a more stable plasma level of ropinirole.

A

Article 5: Effects of Ropinirole Prolonged-Release on Sleep Disturbances and Daytime Sleepiness in Parkinson Disease

81
Q

Conclusion: Levodopa (LD; combined with carbidopa) remains the gold standard for symptomatic treatment of PD, but long-term treatment is associated with complications that may adversely affect QoL.(quality of life) Recent studies have suggested that the addition of a COMT inhibitor may improve QoL through the reduction of some of the motor complications of LD therapy. Further studies are required to determine the full effects of this as well as other treatments that are used to manage LD-associated complications on QoL.

A

Article 6: The Impact of Levodopa on Quality of Life in Patients With Parkinson Disease

82
Q

Abstract: Zolpidem is a hypnotic drug that is chemically distinct from benzodiazepines (BDZ). It has been suggested that it acts selectively on c-aminobutyric acid receptors. However, recent evidence has shown that the behavioural effects of zolpidem are generally similar to those of BDZs. Flumazenil is usually considered to be a BDZ antagonist. Nonetheless, in chronic BDZ users, it acts as a partial, bland agonist. We describe two cases of zolpidem dependence that were detoxified by the use of flumazenil infusion. BDZ dependence is usually treated with tapering of the medication. As an alternative, abrupt discontinuation of the medication and rapid detoxification using flumazenil has been used. Flumazenil may represent an alternative to detoxification treatment by employing a tapering approach, or by replacement therapy with BDZs with a long half-life, particularly where patients are hard to treat or have low compliance to treatment

A

Article 1: Dependence on zolpidem: two case reports of detoxification with flumazenil infusion

83
Q

Conclusion: Recently we reported a study of prescribing patterns of benzodiazepines to elderly patients, using data from in-depth semistructured interviews with physicians. The main finding was that none of the physicians believed that benzodiazepine use was a serious clinical problem in older adults, contrary to all major academically generated guidelines on the subject. In fact, the majority minimized the potential adverse effects of benzodiazepines, while also expressing pessimism about their ability to discontinue use of these medications successfully in long-term users. In addition, we identified an unexpected prescribing pattern using the same methods as described herein. This study used content analysis, a common inductive qualitative analytical technique that involves generating, refining, and condensing themes that appeared in the interviews through a systematic iterative process. The institutional review board of the University of Pennsylvania approved this study. An unexpected pattern emerged when 18 of 33 physicians spontaneously reported prescribing benzodiazepines specifically for acute bereavement. The interview was not designed to investigate bereavement as a potential prescribing indication, and so additional data were not obtained.

A

Article 2: Medicating Grief With Benzodiazepines: Physician and Patient Perspectives

84
Q

Conclusion: Antianxiety agents and sedative–hypnotics, mainly benzodiazepines and also various opiate analgesics, were the scheduled prescription drugs unequivocally identified in blood samples from impaired drivers in Sweden. The contribution of other pharmaceutical agents was relatively small or negligible and did not represent a particular problem for traffic safety. The notion of establishing threshold concentration limits in blood for certain drugs, akin to punishable blood alcohol limits (eg, 0.20 g/L or 0.50 g/L), or enacting graded penalties depending on drug concentration is hard to motivate owing to weak concentration-effect relationships and to the development of tolerance after long-term therapy. Zero-concentration limits or LOQ laws represent a much simpler and more pragmatic way to enforce DUID legislation compared with the traditional impairment laws making it a lot easier to convict an offender.

A

Article 3: Concentrations of Scheduled Prescription Drugs in Blood of Impaired Drivers: Considerations for Interpreting the Results

85
Q

Conclusion: The use of sedatives and hypnotics, antidepressants, and benzodiazepines demonstrated a significant association with falls in elderly individuals.

A

Article 4: Meta-analysis of the Impact of 9 Medication Classes on Falls in Elderly Persons

86
Q

Conclusion: Status epilepticus is a common and serious condition encountered in the neuro-ICU. It is associated with an estimated mortality rate of 20%. Although clinical studies show little evidence to document the effects of permanent neurologic injury in NCSE, prolonged memory dysfunction and the similarities to convulsive status suggest that this condition should be managed expeditiously. Rapid treatment requires prompt recognition of SE’s signs and symptoms and a high index of suspicion for this condition. Ideally, medical care should be guided closely by a neurologic specialist in the ICU. No matter what medications are selected, a goal-directed protocol is essential in facilitating delivery of appropriate treatment as efficiently as possible. As more treatment modalities become available, a focus of newer therapies will be on minimizing the consequences of electrophysiologic insults—in addition to seizure suppression. Neuroprotective agents may become useful to prevent the cascade of delayed neuronal injury In the future, a combination of treatments including seizure suppressants that are capable of becoming maintenance AEDs, neuroprotectants such as N-methyl-D-aspartate antagonists, free radical scavengers, second messenger modulators (ie, nitric oxide or adenosine), and earlier therapies may become available for the many as yet unrecognized incidents of SE in the neuro-ICU.

A

Article 5: Evaluation and Management of Status Epilepticus in the Neurological Intensive Care Unit

87
Q

Conclusion: So what do these study results tell us? In conjunction with previous studies, they augur against the use of benzodiazepines as a first line treatment for any type of BP except in extenuating circumstances. Although this study does not definitively rule out a potential benefit in candidates more amenable to pharmacotherapy, the risks of benzodiazepine therapy must be weighed against the modest benefits. Among the more disconcerting aspects is that between 25% and 76% of patients who start taking benzodiazepines may end up on chronic drug therapy [9]. This suggests that more people may actually be harmed than helped by indiscriminate benzodiazepine use in this population. Hence, careful risk assessment, similar to that employed for opioid trials [3], should be considered before treatment.

A

Article 6: Benzodiazepines for neuropathic back pain: When the cure is worse than the disease

88
Q

Conclusion (final paragraph): Although it is not clear if intranasal midazolam is definitively more effective or associated with fewer adverse effects when compared with rectal diazepam for management of acute seizures, there are significant cost factors and social considerations favoring intranasal midazolam. The current study highlights that an unmet medical need exists to integrate intranasally delivered midazolam into acute seizure management guidelines. Development of a commercial, standardized intranasal benzodiazepine delivery system would provide a useful and more socially acceptable option for community and home management of acute seizures.

A

Article 7: Is Intranasal Midazolam Better Than Rectal Diazepam for Home Management of Acute Seizures?

89
Q

Conclusion: The frequency of reported pain in MS patients was not higher than in the background population. However, pain intensity, the need for analgesic treatment, and the impact of pain on daily life were higher in MS patients.

A

Article 1: Pain in Patients with MS

90
Q

Conclusion: These exploratory findings suggest that testosterone treatment is safe and well tolerated and has potential neuroprotective effects in men with relapsingremitting MS.

A

Article 2: Testosterone Treatment in Multiple Sclerosis

91
Q

Conclusion: In this cohort of patients with MS who had disease refractive to multiple therapeutics before starting natalizumab treatment, magnetic resonance imaging and clinical disease activity returned, often aggressively, following discontinuation of natalizumab therapy. These findings suggest we should consider strategies to minimize the risk of immune reconstitution inflammatory syndrome after natalizumab discontinuation.

A

Article 3: Immune Reconstitution Inflammatory Syndrome in Patients With Multiple Sclerosis Following Cessation of Natalizumab Therapy

92
Q

Conclusion: Anti–interferon beta NAb can persist after interferon beta treatment withdrawal and are associated with overt clinical disease activity. This is made apparent by an increase in relapse rate and faster disability progression and is supported by the observed need for more aggressive therapy after interferon beta treatment cessation. Prospective studies are warranted to confirm these results.

A

Article 4: Clinical Effect of Neutralizing Antibodies to Interferon Beta That Persist Long After Cessation of Therapy for Multiple Sclerosis

93
Q

Conclusion: The story of drug safety issues related to the off-label use of antipsychotics to manage behavioral problems associated with dementia raises some important issues that may be applicable to the larger issue of appropriate prescribing. One issue is that evidence on risks and benefits in younger populations may not be easily generalizable to older adults. Evidence is needed from RCTs and from observational studies on the risks and benefits of drug therapy in the same populations that will be exposed to these drugs. Another issue is the need to develop a system to track off-label use so that efforts can be focused on developing evidence on risks and benefits in indications that have not been assessed through the standard regulatory approval process. This does not mean that off-label use is inappropriate; rather, it means that evidence for off-label use is not normally available through standard processes used by regulators. Finally, and perhaps most importantly, ensuring drug safety in elderly people will require the collaborative effort of researchers, regulators, manufacturers, professional organizations, and health care provider organizations to send the right message to prescribers.

A

Article 1: Prescribing Optimal Drug Therapy for Older People

94
Q

Conclusion: The NH antipsychotic prescribing rate was independently associated with the use of antipsychotics in NH residents. Future research is needed to determine why such a prescribing culture exists and whether it could result in adverse health consequences.

A

Article 2: Unexplained Variation Across US Nursing Homes in Antipsychotic Prescribing Rates

95
Q

Conclusion: The results suggest that frontal cortical serotonin2A receptors are involved in the pathophysiology of schizophrenia.

A

Article 3: Decreased Frontal Serotonin2A Receptor Binding in Antipsychotic-Naive Patients With First-Episode Schizophrenia

96
Q

Abstract: : Several candidate genes have been associated with antipsychotic-induced body weight (BW) gain. Because the endocannabinoid system is deeply involved in BW regulation, endocannabinoid genes may have a role in the antipsychotic-induced weight gain. Therefore, we investigated the 1359 G/A (rs1049353) single nucleotide polymorphisms (SNP) of the cannabinoid receptor 1 (CNR1) gene, which codes the endocannabinoid CB1 receptor, and the complementary DNA (cDNA) 385C/A (rs324420) SNP of the FAAH gene, which codes the endocannabinoid degrading enzyme, for their role in BW changes induced by antipsychotic drugs. Eighty-three white psychotic patients who underwent a naturalistic treatment with different antipsychotics (clozapine, olanzapine, risperidone, quetiapine, and haloperidol) and completed a 24-week treatment period were included into the study together with 80 age- and sexmatched white healthy controls. At the 24th week of treatment, 41 patients gained more than 7% of their baseline BW. No significant differences between patients and controls emerged in genotype and allele frequencies of both SNPs. Genotype and allele frequencies of the FAAH cDNA 385C/ A SNP but not of the CNR1 1359 G/A SNP significantly differed between subjects who gained more than 7% of BWand those who did not, with both AC and AA genotypes and the A allele being significantly more frequent in patients who gained more than 7% of their baseline BW. Present findings, although obtained in a small population and in a naturalistic setting, suggest that the cDNA 385C/A SNP of the FAAH gene may predispose subjects to get a clinically meaningful weight gain after antipsychotic exposure

A

Article 4: Endocannabinoid Pro129Thr FAAH Functional Polymorphism But Not 1359G/A CNR1 Polymorphism Is Associated With Antipsychotic-Induced Weight Gain

97
Q

Conclusion: The FDA advisory was associated with decreases in the use of atypical antipsychotics, especially among elderly patients with dementia.

A

Article 5: Impact of FDA Black Box Advisory on Antipsychotic Medication Use

98
Q

Conclusion: This 13-week, double-blind study evaluated the efficacy and safety of the atypical antipsychotic paliperidone palmitate (recently approved in the United States) versus placebo administered as monthly gluteal injections (after two initial doses given 1 week apart) in acutely symptomatic patients with schizophrenia. Patients (N = 388) were randomly assigned (1 : 1 : 1 : 1) to paliperidone palmitate 50, 100, or 150 mg eq. or placebo. As the 150 mg eq. dose was administered to fewer patients (n = 30) than planned, meaningful and definitive conclusions cannot be drawn from the results of this group. The change from baseline in Positive and Negative Syndrome Scale total score at endpoint showed improvement in both paliperidone palmitate 50 and 100 mg eq. groups but was significant only in the 100 mg eq. group (P = 0.019). The paliperidone palmitate 50 (P = 0.004) and 100 mg eq. (P < 0.001) groups showed significant improvement in the Personal and Social Performance score from baseline to endpoint versus placebo. Common adverse events (in Z2% of patients in any group) more frequent with paliperidone palmitate 50 or 100 mg eq. than placebo (Z5% difference) were headache, vomiting, extremity pain, and injection site pain. Treatment with paliperidone palmitate (100 mg eq.) was efficacious and all doses tested were tolerable

A

Article 6: Efficacy and safety of paliperidone palmitate in adult patients with acutely symptomatic schizophrenia: a randomized, double-blind, placebo-controlled, dose-response study

99
Q

Conclusion: Valproate treatment did not delay emergence of agitation or psychosis or slow cognitive or functional decline in patients with moderate Alzheimer disease and was associated with significant toxic effects.

A

Article 7: Chronic Divalproex Sodium to Attenuate Agitation and Clinical Progression of Alzheimer Disease

100
Q

Abstract: A new analysis by the (FDA) downplays the psychiatric risks of the smoking cessation drug varenicline, but an independent analysis of the agency’s adverse event reports suggests the drug dramatically increases the risk of suicide and suicide-related behavior compared with other cessation medications. Reports of an array of serious adverse events,including suicide, other violence, cardiac problems, and crashes, have dogged vareniclinefor several years. Such reports led the FDA in 2009 to require that the drug’s label carry a black box warning of the risk of severe neuropsychiatric adverse events in patients taking the drug and earlier this year to update the drug’s label to warn of increased risk of cardiac adverse events in patients with cardiovascular disease. Now the new analysisfrom the FDA concludes that varenicline does not increase the risk of hospitalization for psychiatric problems. Meanwhile, though, the independent analysisfound an alarmingly high rate of suicide-related adverse events - predominantly events that would not involve hospitalization

A

Article 8: New Reports Examine Psychiatric Risks of Varenicline for Smoking Cessation

101
Q

Conclusion: Once the most likely etiology is determined, the clinician must discern the mechanism, specific transmitters, and receptors by which this etiology is triggering the symptoms. Subsequent pharmacological management focuses on prescribing the appropriate antagonist to the implicated receptors. If symptoms are refractory despite adequate dosage and around-the-clock prophylactic administration, an empirical trial combining several therapies to block multiple emetic pathways should be attempted. Often, oral administration of medication is not feasible and alternate routes such as rectal suppositories, subcutaneous infusions, and orally dissolvable tablets should be considered.

A

Article 1: Management of Intractable Nausea and Vomiting in Patients at the End of Life “I Was Feeling Nauseous All of the Time . . . Nothing Was Working”

102
Q

Summary: The ability to arrest further vomiting and prevent intravenous fluid therapy and hospitalization aids children with vomiting so they may tolerate oral fluids and be discharged from medical care. This can reduce the medical care burdens and enhance patient satisfaction. This new pharmaceutical therapy may change how gastroenteritis is managed as it is studied further

A

Article 2: Antiemetics for acute gastroenteritis in children

103
Q

Summary: PDNV is an under-recognized problem after outpatient anesthesia. Valid data for the incidence and the best treatment of PDNV after office-based anesthesia are rare. For safety, quality, and patient satisfaction, further research is needed to develop a prediction model to better identify patients at risk for PDNV in order to direct antiemetic prophylaxis for ambulatory patients undergoing office-based anesthesia.

A

Article 3: Nausea and vomiting after office-based anesthesia

104
Q

Conclusion: Promethazine and metoclopramide have similar therapeutic effects in patients who are hospitalized for hyperemesis gravidarum. The adverse effects profile was better with metoclopramide.

A

Article 4: Promethazine Compared With Metoclopramide for Hyperemesis Gravidarum A Randomized Controlled Trial

105
Q

High potency antipsychotic ; acute use in emergency setting due to rapid efficacy ; may be used in cocaine intoxication ; ADRs - extrapyramidal actions - parkinson-like sx

A

Haloperidol

106
Q

Low potency antispychotic ; ADRs - lower risk of agranulocytosis than clozapine ; NOTE - do not administer to geriatric population

A

Chlorpromazine

107
Q

High potency antipsychotic ;

A

Prochlorperazine

108
Q

Low potency antispychotic ; NOTE - do not administer to geriatric population

A

piperidines

109
Q

Atypical antipsychotic ; MOA - 5HT receptor blockade, blockade of D1 receptors and weaker blockade of D2 receptors ; ADRs - higher risk of agranulocytosis than chlorpromazine ; REQUIRED weekly CBC (if there agranulocytosis then can never take med again) ;

A

clozapine

110
Q

Atypical antipsychotic ; NOTE - half the dose is needed for females ; ADRs - weight gain (endocannabinoid endogenous ligands ) -> may lead to diabetes ; caution when prescribing to pt with high BMI ; NO agranulocytosis, NO extrapyramidal actions

A

olanzapine

111
Q

Large dose must be given ; higher incidence of anticholinergic side effects due to higher dose requirements ; ADRs - hypotension, priapism (may be due to the alpha-adrenergic blocking activity -> vasodilation (anti-hypertensive) -> engorgement -> erection), tend to have more anticholinergic activity (more sedating) bc you have to give higher doses (avoid in geriatric pts) ; Examples - chlorpromazine (aliphatics) & piperidines

A

Low potency Antispychotics

112
Q

small dose may be given ; lower incidence of anticholinergic side effects ; ADRs - neuroleptic malignant syndrome, extrapyramidal reactions (more powerful effect on dopamine receptor) ; Examples - haloperidal (butyrophenone), and prochlorperazine (piperazines)

A

High potency Antispychotics

113
Q

variable dosage ; low incidence of anticholinergic side effects ; less ADRs bc they affect DA and 5HT ; Doesnt affect cognitive function ; weight gain bc they are endocannabinoids (munchies) ; Examples - Clozapine (dibenzepines), and Olanzapine (dibenzepines)

A

Atypical antipsychotics

114
Q

cycloplegia, mydryasis, disorientation, flushed skin, increased body temp (decreased sweating), dry mouth, tachycardia, decreased gut motility and decreased urgency ; blind as a bat, mad as a hatter, red as a beet, hot as hell, dry as a bone, the bowel and bladder lose their tone, and the heart runs alone ;

A

Anticholinergic ADRs

115
Q

Alpha-1 adrenergic blockade (vasodilatation -> postural hypotension), Anticholinergic, Antihistamine, Hypothermic (lower body temp), Dopamine blockade of D2 (70-80% blockade - more than this will give parkinsonian sx)

A

MOA of typical anti-psychotics

116
Q

D1 receptor blocker and some D2, AND also serotonin (5HT) receptor blocker -> less ADRs

A

MOA of atypical anti-psychotics

117
Q

tx of positive sx of psychosis (illusions, hallucinations) but do not help with negative sx ; rapid efficacy such as the ED setting, acute mania, alcoholic hallucinations, severe anxiety, anti-emetic, Tourette’s sndrome, Huntingtons, pruritus ; BLACK BOX WARNING - off-label use of anti-psychotics for dementia in the elderly has ben linked to increased mortality

A

Indications for antipsychotics

118
Q

after 1st episode - take antipsychotics for a few months ; after 2nd episode - take longer ; after 3rd episode - lifetime rx

A

Duration of treatment for antipsychotics

119
Q

anticholinergic ADRs, endocrine (amenorrhea, increased production of breast milk in both men and women due to dopamine blockade - not enough dopamine to block prolactin production), gynecomastia, interference with ejaculation, weight gain, hypotention, priapism, hypersensitivity, agranulocytosis, Extrapyramidal reaction (akathisia, Dystonia, parkinson-like sx), tardive dyskinesia, neuroleptic malignant syndrome, elevated core temp (can be resolved with muscle relaxant dantrolene), seizures, pseudodepression ;

A

ADRs of typical antipsychotics

120
Q

more frequent with the high potency antipsychotics ; a life-threatening neurological disorder most often caused by an adverse reaction to neuroleptic or antipsychotic drugs ; typically consists of muscle rigidity, fever, autonomic instability, and cognitive changes such as delirium, and is associated with elevated plasma creatine phosphokinase

A

Neuroleptic malignant syndrome

121
Q

reserved for tx of motor and phonic tics in Tourettes pts ; NOTE - Tourettes is caused by elevated DA

A

Pimozide

122
Q

MOA - blocks 5HT receptors more than D2, also blocks some D1 ; ADRs - cardiac cycle changes and weight gain

A

Resperidone (Risperdal)

123
Q

active metabolite of resperidone ; MOA - blocks 5HT > D2 and some D1 ; ADRs - Weight gain

A

Paliperidone

124
Q

antimanic ; USE - acute mania, manic-depression, anxiety that cant be controled with benzodiazepines ; MOA - unknown ; ADRs - electrolytes must be checked, initially 1-2/week bc this drug is an electrolytes - if concentration is more than 1.5 mEq/L then you may see ataxia, diarrhea, nausea, vomiting, small tremors, sedation - if concentration 1.5-3.5 mEq/L then you may see CNS depression, weight gain, CV, renal and CNS effects, mortality, metalic taste ; drug INTERACTION with diuretics bc Na+ is dumped leaving this drug/electrolyte in the system increasing its relative concentration; NOTE - since the medication normalizes the highs and lows of manic depression som pts may discontinue bc they miss the highs - ALSO - therapeutic incex is between 0.75-1.25mEq/L - can be on this for lifetime bc no cognitive impairments but must be monitored due to low therapeutic index

A

Lithium

125
Q

anticholinergic anti-emetic ; USE - labyrinthine disorders & motion sickness ; MOA - antihistamine, take 1hr before on empty stomach ; ADRs - confusion, disorientation, hallucination, category B - contraindicated in pregnancy ;

A

Meclizine

126
Q

MOA - DA blocking anti-emetic ; USE - drug induced emesis ; ADRs - 2 different dosages of suppositories -> if adult dose given to a child they will develop extrapyramidal sx within hrs

A

Prochlorperazine (Compazine)

127
Q

MOA - bind to dopamine D2 receptors where it is a receptor antagonist, and is also a mixed 5-HT3 receptor antagonist/ 5-HT4 receptor agonist ; USE - acute migranes, abortive ; ADRs - drowsiness, dizziness, dystonia, tardive dyskinesia

A

Metoclopramide (Reglan)

128
Q

MOA - acts primarily as a strong antagonist of the H1 receptor (antihistamine) and a moderate mACh receptor antagonist (anticholinergic), and also has weak to moderate affinity for the 5-HT2A, 5-HT2C, D2, and α1-adrenergic receptors, where it acts as an antagonist at all sites as well ; ADRs - More pronounced than metoclopramide -> drowsiness, dizziness, dystonia, tardive dyskinesia ; NOTE - donot use in children < 2yo bc of potential for fatal resp depression ;

A

Promethazine (Phenegan)

129
Q

USE - anti-emetic for cancer chemotherapy, also decreases emesis after tonsilectomy in children ; MOA - selective blocker of 5HT3 subclass bc enterochromaffin cells of SI release 5HT3 during chemotherapy

A

Ondastron (Zolfran)

130
Q

Cannabinoid ; USE - cancer chemotherapy emesis prophilaxis ; must be taken PO

A

Dronabinol

131
Q

USE - prophylaxis of N/V cause by anestheisa and surgery ; MOA - unknown but has both antihistaminic activity and slight anticholinergic action

A

Benzquinamide

132
Q

hyperosmolar solution -> direct effect on smooth muscle activity ; high CHO load thus contraindicated for diabetics

A

Phosphorated carbohydrate solution

133
Q

MOA - blocks substance P at NK1 receptors in the brain ; USE - in combination with other antiemetics to prevent acute and delayed NV associated with chemo

A

Aprepitant

134
Q

current evidence suggests that schzophrenia is due to hyperactivity of central dopaminergic systems (especially the mesolimbic) -> increased Central dopamine -> higher levels of homovanillic acid (metabolite of DA) in the CSF -> higher level of HVA in plasma

A

Dopamine theory of schizophrenia

Neurology (6 decks)

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