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Week 5 - Neuro > Neuro Drugs > Flashcards

Neuro Drugs Flashcards

1
Q

tx for epilepsy

A

antiepileptics, surgical excision of foci, vagus nerve stimulation, removal of causative factors, regulation of physical and mental activity

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2
Q

antiepiletic drugs

A

tx manifestation not cause of seizures, prevents spread of seizure from focus

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3
Q

vagus nerve stimulation (VNS)

A

tx for partial seizures, for refractory cases or if anticonvulsants are poorly tolerated

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4
Q

anticonvulsant drugs

A

used for partial / focal seizures and generalized tonic-clonic seizures

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5
Q

phenytoin

A

for partial and general tonic-clonic seizures, anticonvulsant, non-sedating, target - voltage gated Na channels in presynaptic glutamatergic synapse, alters Na conductance, blocks high frequency repetitive action potentials, decreases glutamate, increases gaba

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6
Q

phenytoin pharmacokinetics

A

well absorbed orally, binds to plasma proteins, need free conc. for clinical effect, excreted in urine, 1st order elimination - as dosage increases metabolism saturates increasing blood conc

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7
Q

phenytoin toxicity

A

nystagmus (early, no need to decrease dosage), diplopia / ataxia (must adjust dose), sedation, gingival hyperplasia, hirsutism (hair growth), long term - coarse facial features, peripheral neuropathy (lessened deep tendon reflexes)

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8
Q

carbamazepine

A

for partial and general tonic-clonic seizures, like tricyclic antidepressants, blocks presynaptic voltage gated sodium channels in glutamatergic neurons, inhibits high-freq repetitive firing, modulates voltage gated Ca channels, increases K conductance, interacts with adenosine receptors

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9
Q

carbamazepine pharmacokinetics

A

slow oral absorption, after meals helps, to all tissues, 70% plasma protein binding, no competition with other protein binding drugs, completely metabolized, induces microsomal enzymes, carbamazepine-10,11 epoxide has anticonvulsant activity, low systemic clearance at first, alters clearance of other drugs, excreted in urine, t 1/2 = 36 hours after first dose / 8-12 hours with continuous tx -> needs adjustment early in tx

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10
Q

carbamazepine drug interaction

A

induction of cytochrome p450, enhances biotransformation of phenytoin, lowers concentrations of valproate / lamotrigine / tiagabine / topiramate, metabolism increased by phenobarbital / phenytoin / valproate

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11
Q

carbamazepine toxicity

A

acute - stupor, come, hyperirritability, convulsions, respiratory depression; long term - drowsiness, vertigo, ataxia, diplopia, blurred vision, more seizures, nausea, vomiting, hematological (aplastic anemia, agranulocytosis), hypersensitivities (skin, eosinophilia, lymphadenopathy, splenomegaly)

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12
Q

oxcarbazepine

A

for partial and general tonic-clonic seizures, blocks presynaptic voltage gated Na channels in glutamatergic neurons, inhibits high-frequency firing, like carbamazepine with less toxicity, weaker inducer of P450, t 1/2 1-2 hours, active metabolite 10-hydroxy oxcarbazepine with t 1/2 8-12 hours

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13
Q

phenobarbital

A

for partial and general tonic-clonic seizures, blocks postsynaptic AMPA receptors in glutamatergic neurons, oldest/safest anticonvulsant, limited sedative effect, barbiturates - choice for infant seizures

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14
Q

phenobarbital mechanism I

A

suppresses abnormal neurons (inhibits spread from foci), inhibits high-freq firing at high conc, decreases Na conductance, blocks some Ca current, only at high conc, improves GABA inhibition and decreases glutamine excitation

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15
Q

phenobarbital mechanism II

A

binds allosteric site for GABAa receptor -> prolongs opening of Cl channels; blocks AMPA receptors -> decreases glutamate release

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16
Q

phenobarbital pharmacokinetics

A

complete oral absorption, slow peak conc, 40-60% bound to plasma protein, 25% pH dependent renal excretion of unchanged drug, 75% inactivated by hepatic microsomal enzymes, induces CYP2C and CYP3A - other drugs metabolized faster by them (oral contraceptive)

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17
Q

phenobarbital toxicity

A

sedation (at first - disappears with chronic), nystagmus and ataxia (high doses), irritability / hyperactivity (children), agitation / confusion (elderly), induces hepatic CYPs, conc elevated by valproic acid

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18
Q

vigabatrin

A

for partial and general tonic-clonic seizures, irreversibly binds GABA-transaminase in GABAergic neurons - prevents degradation of GABA, inhibits vesicular GABA transporter, increased EC GABA conc, desensitization of synaptic GABA receptors, activation of non-synaptic GABA receptors causes tonic inhibition, decreases brain glutamine synthetase, increases GABA conc

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19
Q

lamotrigine

A

for partial and general tonic-clonic seizures, blocks postsynaptic AMPA receptors, suppresses rapid firing, inhibits voltage and use dependent Na channels (go for focal epil), inhibits voltage gated Ca channels (good for gen seizures), decreases synaptic release of glutamate

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20
Q

felbamate

A

for partial and general tonic-clonic seizures, GABA receptors agonist in GABAergic neurons, use-dependent blockage of NMDA receptors in glutamatergic neurons

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21
Q

felbamate drug interactions

A

increases plasma phenytoin and valproic acid leves, decreases carbamazepine

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22
Q

felbamate toxicity

A

aplastic anemia and severe hepatitis

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23
Q

gabapentin and pregabilin

A

for partial and general tonic-clonic seizures, GABA analogs, increase the synaptic / non-synpatic release of GABA, bind voltage gated Ca channels (main MOA), decreases synaptic release of glutamate

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24
Q

gabapentin mechanism of action

A

increases GABA release, binds voltage gated Ca channels decreasing glutamate release in glutamatergic neurons

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25
Q

lacosamide

A

for partial and general tonic-clonic seizures, enhances slow inactivation of voltage gated Na channels, binds collapsin response mediator protein (CRMP2) in presynaptic glutamatergic neurons, blocks neurotrophic factors (BDNF, NT3), affects axonal / dendritic growth

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26
Q

levitiracetam

A

for partial and general tonic-clonic seizures, presynaptic target, binds synaptic vesicular protein SV2A modifying glutamate and GABA release, side effects - somnolence, asthenia, ataxia, dizziness, agitation, anxiety

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27
Q

tiagabine

A

for partial and general tonic-clonic seizures, targets GABA reuptake transporters (GAT-1) increasing GABA at synapse in forebrain and hippocampus, prolongs inhibitory action

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28
Q

topirimate

A

for general and tonic-clonic seizures, post synaptic target, blocks voltage gated Na channels, potentiates inhibitory effect of GABA, works at site different from benzodiazepine and barbiturates, weak carbonic anhydrase inhibitor

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29
Q

ethosuximide

A

for general seizures, presynaptic target, binds voltage gated Ca channels reducing low-threshold Ca (T type) current, pacemaker in thalamus where absence seizures are generated

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30
Q

ethosuximide toxicity

A

gastric distress (pain nausea, vomiting), lethargy, fatigue, headache, dizziness, hiccup, euphoria, improved behavior

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31
Q

valporic acid and sodium valproate

A

for general seizures, solvent for other seizure drugs, anticonvulsant, fully ionized in body

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32
Q

valporic acid and sodium valproate mechanism of action

A

blocks high frequency firing (Na currents), blocks NMDA glutamate receptor excitation, increases GABA levels in brain, faciliatates glutamic acid decarboxylase that synthesizes GABA, inhibits GABA transporter GAT-1, inhibits GABA transaminase that degrades GABA, inhibits histone deacetylase

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33
Q

benzodiazepines

A

for epilepsy, diazepam, lorazepam, clonazepam, nitrazepam, clorazepate, clobazam

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34
Q

diazepam

A

for epilepsy, banzodiazepine, IV or rectal, good at stopping continuous seizure activity (generalized status epilepticus), possibly oral but high tolerance

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35
Q

lorazepam

A

for epilepsy, benzodiazepine, more effective and longer acting than diazepam for status epilepticus, preferred

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36
Q

clonazepam

A

for epilepsy, benzodiazepine, long acting, good for absence seizures, one of most potent antiseizure agents, sedation common on initial therapy

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37
Q

nitrazepam

A

for epilepsy, benzodiazepine, not in US

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38
Q

clorazepate

A

for epilepsy, benzodiazepine, drowsiness, and lethargy common

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39
Q

clobazam

A

for epilepsy, benzodiazepine, not in US

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40
Q

acetazolamide

A

for epilepsy, inhibits carbonic anhydrase (diuretic)

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41
Q

acetazolamide mechanism of action

A

mild acidosis in the brain, diminished depolarizing action of bicarbonate ions moving out of neurons via GABA receptor ion channels

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42
Q

acetazolamide clinical uses

A

all types of seizures, rapid tolerance (return of seizures) in two weeks, may be useful in women who get seizures during their menses

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43
Q

tx tonic-clonic seizures

A

first line - carbamazepine, valproate, phenytoin; second line - lamotrigine, oxcarbazapine

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44
Q

tx myoclonic seizures

A

frist line - valproate; second line - topiramate, levetiracetam, zonisamide

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45
Q

tx partial seizures

A

first line - carbamazepine, phenytoin; second line - valproate, lamotrigine, oxcarbazine, levetiracetam

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46
Q

tx absence seizures

A

first line - valproate; second line - ethosuximide, lamotrigine

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47
Q

tx unclassified seizures

A

first line - valproate; second line - lamotrigine

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48
Q

ethosuximide

A

9 yr old, eyelid flutter every 5-10min, EEG 3Hz synchronously on all leads (generalized), ethosuximide - good tx without effect of excessive sedation / tolerance

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49
Q

lorazepam

A

generalized convulsions / seizure for 45 min in ER, tx IV lorazepam

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50
Q

phenytoin

A

tx for generalized tonic - clonic seizures, 10-20 mg/L plasma level is therapeutic, if inadequate seizure control -> could stop phenytoin and try different drug OR break into 3 daily doses OR increased dose slightly

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51
Q

carbamazepine

A

tx for tonic-clonic seizures, effective because decreases conduction of action potentials

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52
Q

complex partial seizure example

A

abnormal taste/olfaction/lip smacking/epigastric fullness/nausea AND transient loss of consciousness

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53
Q

case - 21 yr old female, lethargic, unresponsive (8 Glasglow Coma Scale), miosis, bradycardia, bradypnea, hypotension

A

methidion overdose, tx - IV fluids, feet in air, naloxone (narcan) pure opioid antagonist, put in floor bed / ICU will need another administration because methidone is long lasting

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54
Q

opioid toxidrome

A

miosis, bradycardia, bradypnea, hypotension, confirm with urine tox screen and responsiveness to naloxone (narcan)

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55
Q

narcan (naloxone)

A

pure opioid antagonist, reverses opioid toxidrome, has no activity when given alone, used in babies after delivery if opioid depression from pain killers given to mom

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56
Q

methadone

A

opioid, tx for opioid addiction, moderate to severe pain reliever, long acting opioid

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57
Q

classes of stimulants

A

sympathomimetics, xanthines, other

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58
Q

sympathomimetics stimulants

A

amphetamine, D- amphetamine, methamphetamine, methylphenidate, cocaine, MDMA - low dose increase release of NE / DA, medium dose blockes NE / DA reuptake, high dose inhibits monoamine oxidase that would break down NE / DA

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59
Q

xanthine stimulants

A

theobromine, theophylline, caffeine

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60
Q

other stimulants

A

nicotine, NE reuptake inhibitors, NE / DA reuptake inhibitors, modafinil, armodafinil

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61
Q

sympathomimetic CNS effects

A

wakeful, alert, increased confidence / motor / speech / accuracy / restless / tremor / respiration rate and depth, decreased eating / tolerance / weight

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62
Q

sympathomimetic non-CNS effects

A

increased systolic / diastolic BP, arrhythmia

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63
Q

acute sympathomimetic toxicity

A

CV headache / arrhythmia / palpitation / angina; CNS dizziness / agitation / confusion, tx antipsychotic, acidify urine so more of active drug is ionized in urine and can not be reabsorbed

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64
Q

chronic sympathomimetic toxicity

A

amphetamine psychosis - hallucinations, paranoid delusions, weight loss - looks like schizo must do urine tox to differentiate

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65
Q

sympathomimetics tolerance / dependence

A

tolerance to effects on appetite / mood, psychological dependence (more with cocaine than amphetamine), withdrawal craving, sleep, fatigue, eating, depression

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66
Q

sympathomimetic therapeutic uses

A

ADHD, narcolepsy, analeptic (reduces drug induced depression)

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67
Q

cocaine

A

alkaloid, crystalline hydrochloride salt, smoke faster pharmkin, injection faster pharmkin, snorting slower pharmkin, 10x potent than amphetamine, <t1/2 than amphetamine (cocaine faster acting, shorter duration)

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68
Q

amphetamine

A

> t1/2 than cocaine (slower acting, longer duration) - methamphetamine is the middle

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69
Q

fastest adminstration / pharmkin

A

IV, smoking

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70
Q

cocaine mechanism of action

A

blocks NE reuptake (motor), blocks DA reuptake motor (euphoria), local anesthetic

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71
Q

cocaine toxicity

A

cardiac arrhythmia, coronary / cerebral thrombosis, in utero - decreased brain size and neuro problems

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72
Q

cocaine tolerance / dependence

A

little tolerance, same daily dose gives same effect, possible physical withdrawal

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73
Q

methylenedioxymethamphetamine (MDMA)

A

from methamphetamine (extra methyl group increases lipophilicity and brain entry), releases and inhibits reuptake of epi / NE / DA, directly stimulates 5HT autoreceptor, stimulates release/inhibits reuptake of serotonin, also affecte histamine / GABA / ACh / DA receptors / NE transporters

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74
Q

bath salts

A

amphetamine-like, stimulants in the brain (cocaine substitute, high abuse / addiction), ingested or snorted, toxicity - chest pain / high BP / high HR / agitation / hallucination

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75
Q

caffiene

A

xanthine, most in starbucks, coffee, nodoz, energy drinks (ER visits)

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76
Q

theophylline

A

xanthine, H in place of R3 group, in tea

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77
Q

theobromine

A

xanthine, H in place of R1 group, in hot cocoa

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78
Q

low dose xanthine

A

clear thought, decreased reaction time, better idea association, less fatigue, improved dexterity for well learned tasks

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79
Q

medium dose xanthine

A

medullary centers affected - increased respiration, increased BP (vasomotor center)

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80
Q

high dose xanthine

A

spinal cord affected - hyperreflexia

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81
Q

other xanthine actions

A

heart stimulation (increased HR, force, output), increased skel muscle work capacity, diuretic, bronchial smooth muscle relaxant (theophylline tx for bronchial asthma), decreased vascular resistance, increased cerebral vascular resistance (tx some headaches)

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82
Q

xanthine mechanism of action

A

unclear, translocation of SR Ca, inhibition of phosphodiesterase - elevated cAMP, adenosine receptor antagonist (inhibits sleepiness adenosine)

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83
Q

xanthine toxicity

A

~ 1mg dose, CNS - insomnia, excitement, convulsions, clonic, death, LD50 150-200 mg/kg, CV - high HR, high resp, extra systoles, decreased clotting, GI - increased secretion

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84
Q

xanthine therapeutic uses

A

cardiac stim for CHF (dilates coronary arteries, increased inotropic forces), paroxysmal dyspnea (left heart failure), analeptic, bronchial asthma, ergot alkaloid (for migraines by vasoconstriction of cerebral arteries)

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85
Q

xanthine tolerance / dependence

A

tolerance to sleep disruption, withdrawal - headache / irritable / low concentration / drowsiness, insomnia, pain - 12-24 hours after not having caffeine

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86
Q

modafinil

A

stimulant, R-modafinil active, L-modafinil not active

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87
Q

modafinil theraputic uses

A

schedule IV controlled, tx - narcolepsy, shift work sleep disorder, daytime sleepiness from sleep apnea, ADHD (not in children - Stevens Johnson syndrome), off-label uses - depression, bipolar, parkinson, schizo, weight loss

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88
Q

modafinil mechanism of action

A

increased DA release in striatum / nucleus accumbens, increases NE release in hypothalamus - all like amphetamine; increased serotonin release in amygdala and frontal cortex, increase hypothalamic histamine, activates glutamatergic receptors, inhibits GABA transmission

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89
Q

modafinil adverse effects

A

headache, nausea, insomnia, low appetite, dizzy, anxiety, high BP — serious dermatologic reaction (Stevens Johnson Syndrome)

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90
Q

cognitive enhancer uses

A

ADHD, alzheimer, smart drug

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91
Q

psychostimulants

A

methylphenidate, amphetamines - first line ADHD tx in children -

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92
Q

amphetamines, methylphenidate

A

psychostimulants, tx ADHD, immediate release and sustained release formulas (only AM administration)

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93
Q

amphetamine ADHD drug names

A

dexedrine, adderall - faster release, shorter acting

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94
Q

methylphenydate ADHD drug names

A

ritalin, concerta - slower release, longer acting

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95
Q

methylphenidate, d-amphetamine, d,l-amphetamine

A

increase DA release and block DA reuptake

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96
Q

d,l amphetamine

A

increases NE release

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97
Q

why stimulants work in tx for ADHD

A

stimulants affect inhibitory areas of the brain first - activation of inhibitory areas help block out other stimuli - low dose stimulants activate prefrontal / limbic inhibitory cortex, higher doses (toxic) - activate motor and euphoria pathways

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98
Q

increasing doses of stimulants (sympathomimetics)

A

low - increased DA / NE release, middle - blockage of NE / DA reuptake, high - inhibition of monoamine oxidase

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99
Q

ADHD tx and tolerance

A

tolerance development is lower in ADHD pt, no psychosis with chronic use

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100
Q

reverse tolerance

A

abuse of amphetamines and cocaine, same dose over long period becomes toxic - eventually become psychotic

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101
Q

atomoxetine (strattera)

A

NE reuptake inhibitor, increases DA in prefrontal cortex (not in nucleus accumbens or striatum - potential for abuse), increases ACh in cortical areas (increasing attention and working memory) tx for adult ADHD, no abuse potential

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102
Q

acetylcholinesterase inhibitors

A

tx for alzheimer, delay death of cholinergic neurons, adverse effects - nausea, anorexia, vomiting, diarrhea - limits max dose, includes donepezil, galanatamine, rivastigmine, tacrine, memantine - increase risk of stomach ulcers (use NSAIDs with caution)

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103
Q

rivastigmine (exelon)

A

acetylcholinesterase inhibitor, tx for alzheimer, 2x day, GI problems, muscle weakness

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104
Q

tacrine (cognex)

A

acetylcholinesterase inhibitor, tx alzheimer, short t1/2 (multiple administrations), many drugs interactions (NSAIDs), liver damage, second choice for AD

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105
Q

galantamine (razadyne)

A

acetylcholinesterase inhibitor, tx alzheimer, stimulates ACh release, do not take with antidepressants

106
Q

memantine (namenda)

A

NMDA glutamate (GLU) receptor antagonist, tx moderate to severe alzheimer, adverse effects - dizzy, headache, constipation, confusion

107
Q

other tx for alzheimer

A

vit E, selegiline, estrogen, NSAIDs, ginko biloba

108
Q

nootropics

A

mind turning, smart drugs, memory enhancers

109
Q

eugeroics

A

wakeful enhancers, modafinil, armodafinil, increase NE and DA release, increase hypothalamic histamine, lower abuse potential, tx for narcolepsy, shift work sleep disorder, daytime sleepiness from sleep apnea, off label uses - ADHD, depression, bipolar, parkinson, schizo, MS - performance enhancing drug at university

110
Q

modafinil

A

eugeroic, wakeful enhancer

111
Q

armodafinil

A

eugeroic, wakeful enhancer

112
Q

general anesthesia

A

CNS depression, absence of sensation, unconscious, controlled, reversible, takes place in brain - equ fast vessel rish

113
Q

stage I of anesthesia

A

analgesia, amnesia, induction, loss of consciousness, reflexes present, can respond to commands, voluntary resistance

114
Q

stage II of anesthesia

A

delirium, loss of consciousness, agitated, combatitive, BP and resp fluctuation, rapid eye movement, breath holding, vomiting, laryngospasm, no memory of this, move through this stage FAST

115
Q

stage III anesthesia

A

surgical anesthesia, regular resp, autonomics depressed due to increasing conc, four planes (light, moderate, deep, excessive)

116
Q

stage IIII anesthesia

A

medullary depression, relative overdose, may result in CV collapse or resp depression

117
Q

goals of general anesthesia

A

loss of consciousness, amnesia, analgesia, blunting of autonomic nervous system, skeletal muscle relaxation

118
Q

balanced general anesthesia

A

general anesthetic -> loss of consciousness, bensodiazepine -> amnesia, opiod -> analgesia and blunting of autonimic system, neuromuscular blocker -> skeletal muscle relaxation

119
Q

inhalation general anesthetics

A

anesthesia machine -> breathing circuit -> lungs -> blood -> brain -> blood -> lungs -> breathing circuit -> anesthesia machine

120
Q

partial pressure

A

additive, P total = P anes + P O2 + P….dosage determined by partial pressure with inhalation, need to leave room for 20% O2

121
Q

Henry’s Law

A

drugs dissolved in fluid do not raise P anes, undissolved drug gives clinical effect, greater sol = slower acting, higher conc, lower sol = faster acting, lower conc

122
Q

induction partial pressures

A

P delivered > P inspired > P alveolar > P arterial > P brain

123
Q

at anesthesia partial pressures

A

P inspired = P alveolar = P arterial = P brain

124
Q

recovery partial pressures

A

P delivered < P expired < P alveolar < P venous < P brain

125
Q

affect P arterial

A

conc of anes in inspired air (higher = faster), pulmonary ventilation (higher = faster), sol of anes in blood (least sol reach equ fastest - N2O, most sol reaches equ slower - halothene)

126
Q

inhalation anesthetics characteristics

A

diverse chem structures, do not interact with defined receptor (injection does), impact all systems, cause physical change (cell membrane?), all but N2O are vaporized (not gaseous)

127
Q

minimum alvoelar concentration (MAC)

A

anes dose in 50% of pop, same as ED50, lowest MAC = most potent, surgical anes 1.3-1.5 MAC (2 MAC = deep anesthesia), effected by age / disease / depressants / ambient temp, MACs are additive leading with on drug can lower the needed MAC of a second drug

128
Q

potency

A

amount to produce specific intensity, function of lipid solubility, correlates with anesthetic potency, more lipid sol = greater potency

129
Q

aqueous solubility

A

determines onset and rate reaching equilibrium, the more soluble a drug the longer it takes to raise its partial pressure in the blood

130
Q

halothene

A

high oil:gas partition coefficient = high potency, high blood:gas paritition coefficient = slow rate of induction

131
Q

N2O

A

low oil:gas paritition coefficient = low potency, low blood:gas partition coefficient = fast induction

132
Q

gas partition coefficient

A

at equilibrium…..blood conc / gas conc

133
Q

second gas effect

A

rapid uptake of first anesthetic creates neg pressure in alveoli causing faster uptake of second anesthetic, ex: N2O rapidly taken up - used first to speed induction, N2O can cause diffusion hypoxia during recovery, lowers required MAC for second anesthetic

134
Q

inhaled anesthetic elimination

A

low aqu sol - leave body fastest, high fat sol - leaves body slowest, lungs and skin/mucous membranes, liberation of halogen can cause kidney / liver / reproductive harm, halothane (poorly metab, consecutive surgery can cause hepatitis), N2O well metabolized

135
Q

ideal inhalation anesthetic

A

stable, compatible, cheap, non-explosive, easily vaporized, low blood sol, potent, no CV depression / airway irritation, good muscle relaxation, minimal metabolism, not toxic to kidney / liver / GI

136
Q

endotracheal intubation

A

may be done for mechanical ventilator, use short acting neuromuscular blocker to relax

137
Q

effects of halogenated hydrocarbon inhalation anesthetics

A

CNS - lower brain metabolism, higher brain blood flow, high ICP; CV - lower contractility / stroke volume / BP (give epi - may increase automaticity), muscle relaxation, malignant hyperthermia (halothane and succinyl choline muscle relaxant)

138
Q

halothane

A

inhalation anesthetic, Adv - potent (low MAC), fast induction / recovery, inexpensive, not irritant, Disadvan - inadequate analgesia / muscle relaxation, low cardiac output, low BP, sensitizes mycardium to catacholamines (give epi -> increased automaticity, cerebral blood flow, ICP), resp depression, heptic toxicity / liver metabolism, malignant hyperthermia (when given with succinyl choline muscle relaxant)

139
Q

isoflurane

A

inhalant anesthetic, ADV - potent, fast induction, no mycardial senstization to catecholamines, less renal/hepatotoxicity; DISADV - rare arrhythmia, pungent odor, malignant hyperthermia

140
Q

sevoflurane

A

high potency, low blood solubility, rapid onset 5-10min, rapid recovery (same day surgery), perfect inhalation anesthetic

141
Q

nitrous oxide

A

only inhalation anesthetic that is gas, ADV - low blood sol, rapid onset, little CV effect, creates second gas effect, mild analgesic; DISADV - high MAC, can’t use as sole anesthetic, no muscle relaxant, diffusion hypoxia if rapidly cut off during recovery

142
Q

IV anesthetics

A

act faster, best for induction of anesthesia, good for short operations, not suitable as single anesthetic due to poor muscle relaxation

143
Q

barbiturates

A

IV anesthetic, thiopental and methohexital, GABA induced Cl- entry into neurons that depresses CNS by hyperpolarizing cells, rapid onset, short action, toxicity - anesthetic dose 50-75% of LD50

144
Q

benzodiazepines

A

IV anesthetic, midazolam (versed) and diazepam (valium), GABA induced entry of Cl- into neurons depressing CNS by hyperolarization, less CV and resp depression (safer), amnestic (memory loss - GOOD), insufficient anesthesia given alone, used as induction agent

145
Q

propofol

A

IV anesthetic, rapid induction and recovery, induces anesthesia, maintains anesthesia alone, given as emulsion, apnea (22-45%) BAD, injection site pain, killed Micheal Jackson

146
Q

ketamine

A

IV anesthetic, dissociative anesthetic (awake, unaware), rapid onset, short duration, emergence reactions (delirium, hallucinations), abused (vet clinics, special K), airway and resp maintained, CV stimulated (good for pt with unstable CV), analgesic, amnestic

147
Q

opiods

A

IV anesthetic, high potency, short acting, fentanyl, sufentanyl, alfentanil, analgesia, hemodynamic stability (good for pt with myocardial dysfunction), depressed resp must be artificially maintained, supplemented with inhaled anesth / benzo / propofol

148
Q

antidepressants

A

tricyclic antidepressants, monoamine oxidase inhibitors, selective serotonin reuptake inhibitors, dual mechanism drugs

149
Q

mood stabilizers

A

lithium carbonate, anticonvulsants, atypical antipsychotics

150
Q

tricyclic antidepressants

A

effect on normal - no stimulation (not abused), sleepiness (tx insomnia); effect in depressed - elevated mood 2-3 wks - in both cases antimuscarinic effects (dry mouth, blurred vision, constipation, urinary retention) - block NE and/or 5HT reuptake, tx depression/anxiety/chronic pain

151
Q

adverse effects of tricyclic antidepressants

A

orthostatic hypotension (NE blocks alpha 1 receptors), antimuscarinic (blocks muscarinic receptor) effects (esp elderly, confusion / constipation / glaucoma), weight gain (block histamine receptor), tachycardia, arrhythmia (block Na channels)

152
Q

tricyclic antidepressant toxicity

A

low therapeutic index 5-10, pts given no more than one week supply, easy to OD in since TI is so low

153
Q

tricyclic antidepressant drug interactions

A

potentiates central depressants - alcohol, sedatives, hypnotics, opioids; decreased gastric emptying increases inactivation of L-DOPA and decreases effectiveness of parkinson tx

154
Q

monoamine oxidase inhibitors

A

irreversibly blocks oxidative deamination of monoamines by monoamine oxidase, increases NT in synpase in 1-2 days, clinical effect 3 wks, tx depression and anxiety

155
Q

MAOa

A

metabolizes NE and 5HT

156
Q

MAOb

A

metabolizes DA

157
Q

monoamine oxidase toxicity

A

low therapeutic index - 5, easy OD

158
Q

monoamine oxidase drug interactions

A

potentiates sympathomimetic amines, esp indirect tyramine that is metabolized by monoamine oxidase in liver, release of NE/EPI/DA, tyramine + monoamine oxidase = hypertensive crisis via adrenergic stimulation

159
Q

pt on monoamine oxidase inhibitor must avoid…

A

foods rich in tyramine - cheese, red wine, beer, broad beans, bananas, avocados, yogurt, sour cream, chocolate, OTC ephedrine / pseudoephedrine

160
Q

selective / reversible monoamine oxidase inhibitors

A

not in US, moderate antidepressant, tyramine food reactions reduced

161
Q

desipramine (norpramin)

A

tricyclic antidepressant, selective NE reuptake inhibitor

162
Q

imipramine (tofranil)

A

tricyclic antidepressant, mixed action NE/5HT reuptake inhibitor

163
Q

phenetzine (nardil)

A

monoamine oxidase inhibitor

164
Q

selective serotonin reuptake inhibitors

A

block serotonin reuptake, not used alone with bipolar disorder - must use mood stabilzer first to prevent rapid mood switch, tx depression and anxiety

165
Q

fluoxetine (prozac)

A

selective serotonin reuptake inhibitor

166
Q

sertraline (zoloft)

A

selective serotonin reuptake inhibitor

167
Q

citalopram (celexa)

A

selective serotonin reuptake inhibitor

168
Q

escitalopram (lexapro)

A

selective serotonin reuptake inhibitor

169
Q

selective serotonin reuptake inhibitor adverse effects

A

nausea, diarrhea, weight loss, stimulation - anxiety / nervousness / insomnia - not sedating like TCAs, risk of suicide because have energy to do so

170
Q

selective serotonin reuptake inhibitor mechanism of action

A

inhibition of 5HT2a - downregulates other receptors, increases NE release, little muscarininic / histaminergic / andrenergic / serotonergic receptor effects (few adverse effects)

171
Q

autoreceptor

A

presynaptic 5HT receptor that inhibits additional 5HT release

172
Q

heteroreceptor

A

NE from neighboring neurons act on alpha2 receptors to inhibit presynaptic release of 5HT

173
Q

atypical antidressants

A

dual/mixed action at 5HT / NE

174
Q

venlafaxine (effexor)

A

selective serotonin and NE reuptake inhibitors, does not have adverse effects due to lack of activity at adrenergic / histaminergic / cholicergic, unlike most antidepressants - increasing dose of this drug increases efficacy due to secondary mechanisms of action (acts at 5HT first, NE second, DA third)

175
Q

desvenlafaxine (pristiq)

A

active metabolite of venlafaxine - longer lasting, tx for adults with major depressive disorder

176
Q

mirtazapine (remeron)

A

blocks presynaptic alpha 2 receptors - autoreceptor on andrenergic neurons increasing NE release and heteroreceptor on serotonergic neurons increasing 5HT release

177
Q

buproprion (wellbutrin)

A

affects both NE and DA transport, adverse - stimulation/agitation/anorexia/insomnia, tx for smoking cessation

178
Q

ketamine

A

IV anesthetic, NMDA receptor antagonist (glutamate), single dose significantly improves depressive symptoms for 2 hrs - 1 wk

179
Q

lithium carbonate

A

tx manic bipolar phase and possible antidepressant, mood stabilizer, no effect in normal people, effect in manic subject, effect seen in 5-21 days, effective in 60-80%, well absorbed by GI, 95% excreted by kidneys - competes with Na reabsorption, Na deficiency increases lithium toxicity

180
Q

lithium carbonate mechanism of action

A

unknown, most likely postsynaptic effect - interferes with production / release of phosphatdylinositol and diacyl glycerol

181
Q

lithium adverse effects

A

fatigue, weakness, slurred speech, ataxia, hand tremor, thirst, urination - no tolerance to hand tremor / thirst / urination, doses >2 mEq/l causes impaired consciousness / coma / rigidity / hyperactive reflexes

182
Q

anticonvulsants for bipolar disorder

A

valproic acid and sodium valproate - good for non-rapid cycling bipolar, better than lithium for rapid-cycling bipolar, carbamazepine aslo approved, phenytoin and phenobarbital no effective

183
Q

atypical antipsychotics for bipolar disorder

A

quetiapine - blocks 5HT 2a receptor, DA antagonist? stabilizes mood

184
Q

antidepressants and bipolar disorder

A

selective serotonin receptor inhibitors should never be used alone - may cause rapid onset mania, should be on mood stabilizer first

185
Q

wake therapy

A

keep pt awake for 24 hrs just starts antidepressant drugs effects, relapse in 24 hrs

186
Q

delay in clinical improvement following tx

A

neurotransmitter and receptor are at start of pathway, there are steps following that maintain mood, neurotransmitter acts through multiple second messangers increasing levels of BDNF which is neuroprotective (increases neuroplasticity, decreases apoptosis, increases neurogenesis)

187
Q

first generation antipsychotics

A

block D2 receptors in limbic system, may make neg symptoms worse, adverse affects due to action at muscarinic / adrenergic / histaminergic receptors

188
Q

first generation antipsychotic muscarinic receptor action adverse effect

A

dry mouth, blurred vision, racing heart, constipation, drowsiness

189
Q

first generation antipsychotics action at adrenergic receptor adverse effect

A

decreased BP, dizziness, drowsiness

190
Q

first generation antipsychotics action at histaminergic receptor adverse effect

A

weight gain, drowsiness

191
Q

first generation anti

A

chloropromazine (thorazine), fluphenazine (prolixin), thioridazine (mellaril), trifluperazine (stelazine), haloperidol (haldol)

192
Q

second generation antipsychotics

A

atypical antipsychotics, block D2 and 5HT receptors

193
Q

second generation antipsychotics

A

clozapine (clozaril), olanzapine (zyprexa), risperidone (risperdal), quetiapine (seroquel), ziprasidone (geodon), aripiprazole (abilify)

194
Q

clozapine

A

second gen antipsychotic, effective on positive and negative symptoms, no parkinsonism, life threatening agranularcytosis - need weekly blood test; ALL other SGA no life threatening effect but not as effective as clozapine, first drug of choice for schizo pt with mod-severe dyskinesia

195
Q

two receptors are better than one - second gen antipsychotics

A

presynaptic 5HT receptors regulate DA release, block presynaptic 5HT 2a receptors increase DA release, improves adverse effects by increasing DA levels, improves both negative and positive symptoms

196
Q

second gen antipsychotics adverse effects

A

weight gain (esp clozapine / olanzapine), type 2 diabetes mellitus, increased lipid levels leading to myocarditis / cardiomyopathy

197
Q

FGA and SGA adverse effect - tardive dyskinesia

A

late onset movement disorder, more with FGA, common in elderly, incidence with clozapine is zero

198
Q

FGS and SGA adverse effects - extrapyramidal side effects

A

seen more with FGA, due to DA receptor blockage, parkinsonism

199
Q

anxiolytic - sedative - hypnotic

A

dose related CNS depression - tranquilization, sedation, hypnosis, general anesthesia, death

200
Q

tranquilization / anxiolytic

A

relaxed, unconcerned with surroundings, fully functional - ideal tx for anxiety

201
Q

sedative

A

decreased activity, calms pt, pt is awake

202
Q

hypnotic

A

drowsiness, onset and maintenance of sleep, pt easily aroused

203
Q

general anesthesia

A

loss of consciousness, pt can’t be aroused

204
Q

barbiturate

A

all similar, only differ on duration of action

205
Q

ultra-short acting barbiturate

A

t1/2 - minutes, very lipid soluble, tx conc reached quickly, redistribution to muscle and other sites causes termination of action

206
Q

thiopental and methohexital

A

ultra-short acting barbiturate

207
Q

short-intermediate action barbiturate

A

t1/2 - hours, depends on metabolism rate

208
Q

secobarbital and pentobarbital

A

short-intermediate acting barbiturate

209
Q

long acting barbiturate

A

t1/2 - days, slow metabolism or excreted uncharged

210
Q

phenobarbital

A

long acting barbituarte, slow and partial metabolism, selective anticonvulsant, less lipid soluble

211
Q

barbiturates action

A

reversible depression of all excitable tissues (skeletal/smooth/cardiac/CNS), skip tranquilization step of depression, like normal sleep, not analgesic until unconscious, paradoxical excitement

212
Q

barbiturates and analgesia

A

hyperalgesic until unconscious, will not sedate in presence of moderate pain

213
Q

barbiturates tolerance

A

tolerance faster - mood, sedation, hypnosis - need to keep increasing dose increasing chance of death, as use increases therapeutic index decreases, highest rate for accidental overdose

214
Q

barbiturates mechanism of action

A

facilitates GABA mediated neuronal hyperpolarization by inflow of Cl-

215
Q

barbiturate effect on organs

A

toxic doses - depresses resp and CV, liver - cytochrome p450 induced causing drug to be broken down faster

216
Q

barbiturate absorption

A

oral - sedative / hypnotic or anticonvulsant; IV - anesthetic induction; IM - not used, too alkaline

217
Q

barbiturate distribution

A

rate of brain up take depends on lipid solubility 30sec - 20min, redistribution causes termination of action for ultra-short acting barbs

218
Q

barbiturate metabolism

A

slower in geriatric and neonatal, decreased t1/2 with repeated administration

219
Q

barbiturate elimination

A

less lipid soluble barbs largely excreted unchanged and active, are weak acids that are reabsorbed at low urine pH

220
Q

tx phenobarbital OD

A

increase urinary pH to 8, causes more drug excreted, less drug reabsorbed, because weak acid drug is turned into ionized form - does not work with more lipid soluble drugs

221
Q

barbiturates adverse effects

A

hangover (extended depression) one day after use, paradoxical excitement (like intoxication) common in geriatric or weak pt

222
Q

barbiturate drug interactions

A

most with similar drugs, induce hepatic enzyme ctyo p450 effecting metabolism of other drugs, compete for metabolic pathways

223
Q

barbiturate clinical uses

A

hypnosis, seizure control, anesthesia induction

224
Q

benzodiazepines

A

tranquilization -> sedation -> hypnosis (no anesthesia step), awareness persists, not relaxed enough for surgery, anterograde amnesia occurs, some block seizures, some relax muscles - depends on partial / full agonist action at specific GABAa receptors

225
Q

benzodiazepine and sleep

A

decreases sleep latency (faster onset), diminished number of awakenings, increases total sleep time, increased REM sleep (fell well rested), partial tolerance develops

226
Q

benzodiazepine mechanism of action

A

facilitates GABA mediated neuronal hyperpolarization by allowing Cl- in

227
Q

benzodiazepine system effects

A

no resp effect unless taken with other depressant drugs, minor CV - decreased BP and increased HR, no liver metabolism effect — little if any effect outside CNS / safer

228
Q

benzodiazepine pharm-kin

A

active metabolites, duration of behavior does not match plasma t1/2 of parent compound, ex: clorazepate decarboxylated in stomach to active metabolite

229
Q

benzodiazepine adverse effect

A

peak hypnotic effect - dizzy, increased reaction time, decreased coordination, confusion; anterograde amnesia at high dose or with alcohol

230
Q

flunitrazepam (rohypnol)

A

benzodiazepine, date rape drug, potent when combined with alcohol, memory loss

231
Q

benzodiazepine toxicity

A

relatively safe, high therapeutic indices, death by OD rare unless combined with other drugs, drug wears off with time, no OD tx needed

232
Q

benzodiazepine OD tx

A

flumazenil, benzo receptor antagonist, IV, reverses effect of benzos and z-sleep aids (zolpidem, zapelon)

233
Q

nezodiazepine clinical uses

A

anxiety, insomnia, seizures, muscle relaxation, preanesthetic med

234
Q

midazolam

A

benzodiazepine, lipid soluble, better sedation - more amnesia, anxiolytic, less pain on injection

235
Q

non-benzodiazepine benzodiazepine-receptor agonist

A

selectively bind benzodiazepine binding site on GABAa receptor, use for sleep, rapid onset, short duration, slow tolerance

236
Q

zolpindem (ambien)

A

non-benzodiazepine benzodiazepine-receptor agonist, sleep aid

237
Q

zaleplon (sonata)

A

non-benzodiazepine benzodiazepine-receptor agonist, sleep aid

238
Q

eszoplicone (lunesta)

A

non-benzodiazepine benzodiazepine-receptor agonist, sleep aid

239
Q

ramelteon (rozemrem)

A

works in suprachiasmatic nucleus, agonist for melatonin MT1 and MT2 receptors, decreased sleep onset time, does not increase total sleep time - longterm use in adults ok

240
Q

diphenydramine

A

OTC, “PM”, for insomnia

241
Q

cholinesterase inhibitors

A

tx alzheimer/parkinson dementia/vascular dementia, alzheimer - reduced choline acetyl transferase = low acetylcholine, prevents breakdown of ACh at synapse, most effective as early tx

242
Q

cholinesterase inhibitors

A

donepezil, galantamine, rivastigmine, tacrine

243
Q

donepezil

A

AChase inhibitor, tx alzheimers/dementia, 1/day dosing, more commonly used, lower side effects

244
Q

galantamine

A

AChase inhibitor, tx alzheimer/dementia

245
Q

rivastigmine

A

AChase inhibitor, tx alzheimer/dementia, patch form

246
Q

tacrine

A

AChase inhibitor, tx alzheimer/dementia, hepatotxicity

247
Q

AChase inhibitor side effects

A

GI upset, rare manic episode

248
Q

memantine (namenda)

A

NMDA receptor antagonist, slows programmed cells death due to excitotoxicity, tx mod to severe dementia, slows decline, side effect - dizzy, BEST USED IN CONJUNCTION WITH ACH inhibitor

249
Q

dementia depression tx

A

SSRI, SNRI - avoid tricyclics with anti-ACh properties (worsen memory / balance)

250
Q

dementia agitation/hallucination tx

A

atypical antipsychotics - risk of mortality in elderly, quetiapine

251
Q

dementia sleep problem tx

A

behavior mod, OTC meds, trazodone or melatonin

252
Q

physical exercise

A

tx dementia, slows decline, less depression, improves functioning - improves cognition, larger hippocampus, less gray matter loss

253
Q

mental exercise

A

tx dementia, slows decline

254
Q

social support

A

tx dementia, greater and more varied social support is protective, less depression, stay in home longer, less hallucination/delusion/psychosis

255
Q

community support

A

tx dementia, help pt stay active and independent, assist with transportation, meds, meals, home help

256
Q

vascular dementia tx

A

prevent - stop risk factors smoking, BP, blood sugar, cholesterol, exercise, mental activity, social activity, fish oil; AChase inhibitors, NMDA antagonists, AND calcium channel blockers (nimodipine)

257
Q

lewy body dementia (parkinson) tx

A

AChase inhibitor, NMDA receptor antagonist, antipsychotics (CAUTION - may cause neuroleptic malignant syndrome), SSRI for depression, AVOID - OTC anticholinergic sleep meds and tricyclics, sleep clonazepam and melatonin

258
Q

frontal temporal dementia tx

A

SSRI - for disinhibition/implusivity (trazodone for aggression/agitation), antypical antipsychotics - olanzipine/quetiapine/abilify help with delusions/agitation (avoid - typical antipsychotics and risperdal), stimulants to increase frontal lobe activity - AChase inhibitors and NMDA receptor antagonists not as helpful

259
Q

dementia general tx tips

A

both behavioral / medical tx, start AChase inhibitor early, manage risk factors, healthy lifestyle, develop community supports, tx symptomatically, add memantine as disease progresses

260
Q

temozolamide (TMZ)

A

tx for gliobalstoma multiforme and melanoma, antineoplastic prodrug that methylates and damages DNA killing tumor cells, only effective if O-methylguanine methyltransferase gene is methylated or it will undo what drug does

261
Q

karnofsky performance scale index

A

classifies pt by functional impairment after tumor resection to determine if they are a good candidate for radiation/chemo, want balance between chemo side effects and benefit of symptom control gained, >80 = normal activity with some symptoms, 50-70 = unable to work can care for oneself with assistance, 0-40 = disabled, requiring increasing degrees of care

262
Q

O-methylguanine methyltransferase gene (MGMT)

A

fixes methylation of DNA, reverses what tx temozolamide does for gliobastoma multiforme does - it methylates tumor cell DNA killing cells

Week 5 - Neuro (3 decks)

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