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Neuro Pt 4 > Pharm Review Yellow Slides > Flashcards

Pharm Review Yellow Slides Flashcards

1
Q

How does the reactive reward pathway work?

A

VTA activation releases DA onto NA neurons so pleasure perceived and identifies stimulating activity as one to be repeated

Drugs of abuse share this final common pathway and also increase DA release in the nucleus accumbens

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2
Q

Mechanism of actions of hallucinogens

A

Partial agonist at 5HT2 receptors (DA releaser)

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3
Q

Acute toxicity opioids and treatment

A

Respiratory depression-pinpoint pupils-coma

Treatment: naloxone

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4
Q

Acute toxicity CNS depressants and treatment

A

Respiratory depression, coma (extremely rare with BDZs)

Treatment

Ethanol: supportive plus fluids-electrolytes-thiamine

Benzodiazepines: flumazenil

Barbiturates: supportive

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5
Q

CNS stimulants acute toxicity and treatment

A

SNS overactivity, increased HR-BP-temp, chest pain-MI, psychosis

Treatment: CVS support, vasodilators for BP, BDZs for agitation-seizures

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6
Q

Nicotine acute toxicity and treatment

A

rare – ingestion of insecticide or cigarettes by children

Nausea-vomiting, diarrhea, CVP collapse, convulsions

Treatment: CVS support, emetics-gastric lavage-charcoal

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7
Q

Cross tolerance

A

Tolerance develops to one drug – then will be seen to other drugs of the same class - same target

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8
Q

Tolerance and opioids

A

Develops rapidly (up to 100-fold); not to constipation

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9
Q

Tolerance and CNS Depressants

A

Rapid to barbiturates > ethanol, benzodiazepines

Significant to sedation-intoxication, less to lethal dose

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10
Q

Tolerance and CNS stimulants

A

develops to euphoria-anorexia-hyperthermia, but can see supersensitivity to paranoia

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11
Q

Tolerance and nicotine

A

Develops to subjective effects and nausea

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12
Q

Tolerance to hallucinogens

A

Not common, since repeated use minimal

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13
Q

Tolerance to cannabinoids

A

Rapid to most effects, also disappears rapidly

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14
Q

Cross dependence

A

Ability of one drug to suppress the withdrawal associated with physical dependence on another drug

Related to pharmacological effects at target – not chemical similarities

Ex: BDZ used for ethanol withdrawal

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15
Q

Do tolerance and dependence necessarily coexist? What about addiction and physical dependence?

A

NO! and No!

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16
Q

Withdrawal from opioids and treatment

A

Rarely life-threatening: insomnia, diarrhea, irritability, cramps, muscle aches, increased BP

Treatment: clonidine, methadone

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17
Q

Withdrawal from CNS depressants and treatment

A

Significant risk of mortality due to seizures (monitor)

Treatment: substitution with BDZs: loading dose - then taper to prevent seizures

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18
Q

Withdrawal from CNS stimulants and treatment

A

Sleepiness, fatigue, depression, hyperphagia, craving

Treatment: largely behavioral

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19
Q

Side effects of ethanol metabolism

A

increased NADH Hepatic Metabolic Disruption

increased levels of NADH leads to decreased Krebs activity -> decreased gluconeogenesis -> hypoglycemia

increased levels blood lactate leads to acidosis, behavioral disturbances

Increased Mg++ excretion can lead to convulsions

Increased Acetyl CoA leads to increased F.A. synthesis + decreased fat breakdown leading to a fatty liver

Decreased uric acid excretion may precipitate gout attacks

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20
Q

Ethanol and tolerance

A

Development of tolerance occurs - limited relative to opioids

Cross tolerance with other CNS depressants (BDZs-GAs)

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21
Q

Drugs used for reducing alcohol consumption

A

Disulfiram [Antabuse]

Opioid antagonists (Naltrexone)

NMDA receptor drugs (Acamprosate)

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22
Q

Positive symptoms of schizophrenia

A

Increased dopamine in the Nucleus Acumbens

Delusions
Hallucinations
Disordered thoughts

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23
Q

Negative symptoms of schizophrenia

A

Decreased DA in the prefrontal cortex

Blunted affect-anhedonia
Alogia - Asociality

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24
Q

Effects of Antipsychotic Receptor Block (D2) on Mesolimbic pathway

A

Decrease + symptoms of schizophrenia

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25
Q

Effects of Antipsychotic Receptor Block (D2) on Mesocortical pathway

A

Increase − symptoms of schizophrenia

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26
Q

Effects of Antipsychotic Receptor Block (D2) on Nigrostriatal pathway

A

Increase Extrapyramidal Side Effects

loss of inhibition of inhibitory indirect pathway leads to drug-induced movement disorder (pseudoparkinson’s)

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27
Q

Effects of Antipsychotic Receptor Block (D2) on Tuberoinfindibular pathway

A

Hyperprolactinemia

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28
Q

Effects of Antipsychotic Receptor Block (D2) on Hypothalamus

A

Poikilothermia, Weight Gain

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29
Q

Effects of Antipsychotic Receptor Block (D2) the Chemoreceptor Trigger Zone

A

Anti-Emetic Effect

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30
Q

D2 block side effects and treatments

A

Extrapyramidal Side Effects - increased with typical-high potency

Acute dystonia (onset 1-5 days): Torticollis, trismus, opisthotonos

Treatment: anticholinergic agents [diphenhydramine-benztropine]

Akathisia (onset 6-60 days): Motor restlessness – “can’t sit still”

Treatment: reduce dose – change drug – anticholinergic – β blocker, benzodiazepine

Pseudoparkinsonism (onset 5-90 days): Tremor, bradykinesia, rigidity, shuffling gait

Treatment: anticholinergic agents

Tardive dyskinesia (onset 3-6 months or longer, 20-40% incidence in elderly females): D2 receptor supersensitivity?

Involuntary movements of orofacial muscles, choreathetoid movements

Treatment: rarely effective, prevention best strategy

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31
Q

5HT2A Receptor Block effects

A

Mesocortical pathway: decreased negative schizophrenia symptoms

CNS: Weight gain

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32
Q

Muscarinic Cholinergic Block side effects

A

ANS: Blurred vision, dry mouth, constipation, difficulty urinating

CNS: Toxic-confusional state

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33
Q

Alpha-1 Receptor Block side effects

A

ANS: Orthostatic hypotension, impotence, failure to ejaculate

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34
Q

Histamine H1 Receptor Block side effects

A

CNS: Weight gain, sedation

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35
Q

What drug causes agranulocytosis?

A

clozapine - dose-related

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36
Q

Galactorrhea

A

excessive or inappropriate production of milk.

due to block of hypothalamic DA receptors

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37
Q

Lowered seizure threshold with antipsychotics

A

1-4% with clozapine

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38
Q

Neuroleptic malignant syndrome

A

Similar to malignant hyperthermia

Treat with dantrolene sodium

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39
Q

First line therapy for depression

A

Generic SSRIs

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40
Q

Bupropion

A

Equal efficacy as SSRIs

Less weight gain and sexual side effects

Not effective in anxious depression

41
Q

SNRIs

A

May be more effective than SSRIs

Side effects > SSRIs

42
Q

SSRIs side effects

A

Acute (diminishes over time): nausea, diarrhea, active-insomnia, somnolence

Delayed onset: weight gain, sexual dysfunction, cognitive blunting

43
Q

Weight gain with antidepressants

A

More: TCADs – mirtazapine – paroxetine

Less: fluoxetine – sertraline – venlafaxine

Least: bupropion

44
Q

Sexual dysfunction with antidepressants

A

Less with bupropion and mirtazapine

45
Q

Anticholinergic side effects and antidepressants

A

Concern with TCADs (

46
Q

Arrhythmias as side effect of antidepressants

A

Concern with TCADs (avoid if cardiac disease - ↑ QT)

47
Q

Orthostatic hypotension as side effect of antidepressants

A

Trazodone - TCADs - MAOIs

48
Q

Hypertension as a side effect of antidepressants

A

Venlafaxine

49
Q

Withdrawal syndrome and antidepressants

A

Paroxetine and venlafaxine most likely

Fluoxetine least likely

50
Q

Most common drug-drug interaction of antidepressants

A

Additive CNS depressant effects when used with other sedatives

51
Q

Drug-drug interactions and MAOIs

A

Hypertensive crisis with drugs (meperidine, decongestants) or with foods high in tyramine (beer-wine-cheese) [results from acute increase in NE release]

52
Q

serotonin syndrome

A

SSRIs + MAOIs

Hyperthermia, muscle rigidity, myoclonus

Rapid changes in mental status (confusion / agitation) and vital signs (hypertension and tachycardia)

53
Q

Lithium mechanism of action

A

Slow onset

Effects greatest on cells with highest level of activity (use-dependence)

Enhance 5HT action and/or diminish NE and DA effect – most favored MOA:

Interference with PIP recycling (Gq protein: IP3 and DAG)
Also interference with Gs and Gi (adenylyl cyclase) can lead to side effects

In thyroid leads to anti-TSH release, leading to hypothyroidism

In kidney leads to anti-ADH release leading to polyuria-polydipsia

May affect gene regulation for growth factors and neuronal plasticity

54
Q

Lithium uses

A

Prevention (maintenance use) of both manic and depressive episodes

Commonly used in combination with other agents

55
Q

Lithium food interactions

A

Competes with sodium for reabsorption - Food-Drug

Interactions possible

Increase in dietary Na+: decreased Li+ Cp

Na+ restriction: increased Li+ Cp

56
Q

Adverse effects of lithium

A

Related to plasma concentration - narrow therapeutic index

Decrease in thyroid function (weight gain possible)

Polyuria, polydipsia (anti-ADH action) (12%)

Moderate toxicity: Confusion, sedation, lethargy, twitching

Severe toxicity: Seizures, stupor, coma

57
Q

Lithium drug interactions

A

Drug Interactions:

Diuretics can decrease renal clearance by 25%

Increase in lithium levels also seen with NSAIDs

58
Q

Treatment of anxiety

A
  1. Antidepressants are first line (SSRIs, SNRIs, NOT NDRIs)
  2. BDZ (abuse potential): limits use to acute and situational anxiety
  3. Busprione: Weaker anxiolytic effect than benzodiazepines, but fewer side effects
  4. Barbiturates: Rarely used for anxiety because of low safety margin - drug interactions - high abuse potential
59
Q

Buspirone

A

Alternative as an anxiolytic agent

5HT1A partial agonist - NOT a benzodiazepine

Moderate D2 receptor block so monitor for possible extrapyramidal system side effects

NO sedation or additive CNS depression or anticonvulsant or myorelaxant action

Requires 2 weeks for onset of anxiolytic effect and 4-6 weeks for maximal efficacy

More useful and effective in chronic anxiety

Less patient acceptance

Must be administered on routine schedule - not prn use

60
Q

How does the GABA Receptor-Cl Ion Channel Complex work and how to BDZ, barbiturates, and ethanol interact with it?

A

GABA binds to receptor which opens Cl channel leading to ↓ Em and ↓ excitability

BDZs bind to site on α subunit [α1 and α2-5] intensifying the action of GABA. Presence of GABA required for BDZ effect.

BARBs bind to distinct site on channel
Low dose: action similar to BDZs
Higher doses: direct interaction with channel – NO GABA required - plus inhibition of excitatory NTs

Ethanol binds both specifically and non-specifically at distinct sites so action similar to barbiturates

61
Q

Z drugs

A

(structurally distinct from BDZs) bind to same site as BDZs [only α1] - same action

62
Q

What is the antagonist that binds to same site as BDZs and “Z”-drugs and is used in the treatment of benzodiazepine overdose toxicity?

A

Flumazanil

63
Q

Alpha 1 GABA receptors (agonist, location in brain, and actions)

A

Agonists: BDZ and “z-drugs”

Location: cortex

Actions: Sleep, anticonvulsant, amnesia, additive CNS depression

64
Q

Alpha 2-5 GABA receptors (agonist, location in brain, and actions)

A

Agonists: BDZ

Location: limbic system, brain stem

Actions: Anxiolytic, Myorelaxant, motor incoordination, tolerance, dependence, addiction, decreased REM

65
Q

Effects of BDZ and Z-drugs on sleep stages

A

Sleep Latency: Both BDZ and z-drug decrease latency
Stage I: Both increase it
Stage 2: Both increase it
Stages 3-4: BDZ decrease it and z-drugs have no effect
REM: BDZ decrease it and z drugs have no effect

66
Q

Tolerance to effects of BDZ and z drugs

A

BDZ: if used for more than one week

Z-drugs: very little tolerance

67
Q

Triazolam

A

A BDZ

Rapid oral absorption

Short t1/2: 1.5-5 hrs - eliminated in 1 dosing cycle

Less daytime sedation (hangover)

Rebound insomnia next day due to rapid elimination

Use cautiously in elderly – dosage reduction

68
Q

Temazepam

A

Slow absorption - minimal effect on sleep latency

Intermediate t1/2 (9-13 hrs)

69
Q

Flurazepam

A

Long t1/2 + active metabolite (75-90 hrs) - low tolerance

Can accumulate in elderly - impaired hepatic clearance leads daytime sedation (“hangover”) / overdosage

70
Q

Zolpidem and Zaleplon

A

Z drugs

Rapid oral absorption

Shortest durations of action (6-8 hours) and half-lives of available agents (zolpidem: 2-2.5 hrs - zaleplon: 1 hr)

71
Q

Eszopiclone

A

Z-drug

Structurally different from zolpidem or zaleplon with longer t1/2 (approximately 6 hrs)

72
Q

BDZ: adverse rxns

A

Daytime sedation and performance impairment

Anterograde amnesia (triazolam > temazepam)

Rebound insomnia

Psychologic and physiologic dependence – schedule IV

73
Q

Z-drugs: adverse rxn

A

Safety similar to benzodiazepines

Common side effects: drowsiness, amnesia, headache, GI complaints – rarely bizarre behavioral disturbances

Rebound effects or next-day psychomotor performance alteration appear minimal with zolpidem and zaleplon

Increased with eszopiclone (longer t1/2) at higher doses

Tolerance-dependence-withdrawal are possible but less likely than with BDZs - BUT they are Schedule IV

74
Q

Are fatal overdoses common with BDZ and Z drugs?

A

No, overall pretty safe

75
Q

What’s the most widely prescribed agent for insomnia and what are its effects?

A

Zolpidem

Effective for:

Reducing sleep latency (immediate release formulation - Ambien®)

Reduce nocturnal awakenings (sustained release formulation - Ambien CR®)

Insomnia associated w/ middle-of-the-night awakening (low dose sublingual formulation - Intermezzo®)

76
Q

Clinical use of zaleplon

A

Effective for:

Decreasing time to sleep onset – rapid oral onset

NOT for reducing nocturnal awakenings - short half-life

BUT is suitable to aid sleep onset for middle-of-the-night awakenings with elimination by morning

77
Q

Clinical use of Eszopiclone

A

Effective for:

Sleep maintenance – longest half-life of “Z”-drugs

Safe for long-term use (6 months) – little evidence for tolerance-dependence-abuse – BUT Schedule IV

78
Q

What is general anesthetic potency proportional and inversely proportional to?

A

Potency proportional to Lipid Solubility (O/W)

INVERSELY proportional to MAC

79
Q

What factors affect the rate of onset of anesthetic action?

A

Concentration of anesthetic in the inspired air (higher conc increases rt of onset)

Solubility of the anesthetic in blood: Lower the blood solubility of the gas the faster the rate of induction

80
Q

Drugs for treatment of grand mal (tonic clonic) seizures

A

Phenytoin
Carbamazepine
Valproate
Levetiracetam

81
Q

Treatment for seizures: broad spectrum

A

Phenobarbital
Diazepam
Valproate
Divalproex

82
Q

Treatment for absence seizures

A

Ethosuximide

Valproate

83
Q

Treatment for partial seizure

A

Levetiracetam

84
Q

Treatment for status epilepticus

A

Diazepam / Lorazepam / Midazolam

85
Q

Antiseizures meds that increase inhibition of Sodium Channel Function

A

Block sustained high-frequency repetitive firing of APs that can initiate seizure formation

Blockade is use-dependent (blocks the ones firing too much, while leaving normal neurons alone)

Prolongs the inactivated state of the sodium channel and prolongs refractoriness

Phenytoin, carbamazepine, valproate

86
Q

Mechanisms of antiseizure meds

A

Inhibition of Sodium Channel Function

Decrease in low-threshold Ca++ (T-type) current

Inhibition of high-voltage activated Ca++-channels

Inhibits function of synaptic vesicle protein SV2A

Enhancement of GABA Action

87
Q

Antiseizure meds that cause a decrease in low-threshold Ca++ (T-type) current

A

Oscillatory currents in thalamic neurons are abnormal in absence seizures -

blocked by ethosuximide-valproate

88
Q

Antiseizure meds that cause inhibition of high-voltage activated Ca++-channels

A

VSCC (aka N-type) involved in regulation of glutamate neurotransmitter release

89
Q

Antiseizure meds that inhibit function of synaptic vesicle protein SV2A

A

Impairs Ca++-mediated neurotransmitter release -

levetiracetam

90
Q

Antiseizure meds that enhance GABA Action

A

Benzodiazepines and phenobarbital enhance the inhibitory effect of GABA (increased opening of Cl- channels)

Valproate appears to act partly by this mechanism

91
Q

Carbamazepine

A

A drug of choice for partial seizures

Often tried first in tonic-clonic seizures

Pharmacokinetics:
Strong inducer of CYP450 enzymes leads to self-induction + drug-drug interactions

Adverse Drug Reactions:
Diplopia-ataxia-sedation (dose-related), GI upset

Rare but serious adverse drug rxns:

Aplastic anemia-agranulocytosis: monitor CBC

Hepatotoxicity: monitor liver function tests

92
Q

Phenytoin

A

Very effective against partial and tonic-clonic seizures

Pharmacokinetics:
Oral absorption is formulation dependent – concern with generic switching

IM absorption erratic (better with prodrug Fosphenytoin)

Zero-order (saturation) metabolism in therapeutic range

Strong inducer of CYP450 enzymes: DDIs

Adverse Drug Reactions:
Nystagmus-diplopia-ataxia-sedation (dose-related), Rash; gingival hyperplasia-hirsutism develop gradually

Long-term use: osteomalacia, peripheral neuropathy

93
Q

Lamotrigine

A

Newer AED

Effects on VSSCs (suppress repetitive APs) and VSCCs (decrease Glu release) - broad spectrum

1st line for partial or generalized seizures - better tolerated than phenytoin or carbamazepine

ADRs: Similar to phenytoin (lower incidence): diplopia, ataxia, dizziness, skin rashes, sedation

94
Q

Levetiracetam

A

Newer AED

Precise mechanism unknown - affects Ca++ channels

1st line in treatment of generalized tonic-clonic seizures

ADRs: Somnolence, asthenia, dizziness

Low incidence of cognitive effects

No CYP450 metabolism - minimal DDIs

95
Q

Ethosuximide

A

Drug of choice in absence seizures

Adverse Drug Reactions – generally few side effects

Possible DDIs with CYP inhibitors or inducers

Dose-related gastric distress most common (nausea-vomiting, pain)

Less common: transient lethargy-fatigue, dizziness, headache

96
Q

Valproate

A

Broad spectrum agent with efficacy against the most common seizure types

Pharmacokinetics: Administered as enteric-coated and delayed-release formulations

Inhibits metabolism of other AEDs: phenytoin, lamotrigine, carbamazepine, phenobarbital, ethosuximide

Adverse Drug Reactions – generally few side effects

Dose-related GI upset (nausea-vomiting, pain)

Weight gain common

Black Box Warnings: Hepatic failure (deaths [increased risk

97
Q

Phenobarbital

A

Used for: Neonatal status epilepticus and as an adjunct for partial and tonic-clonic seizures

Pharmacokinetics: Metabolized slowly by P450 system - t1/2 of 4-5 days

Classic enzyme inducer

Adverse Drug Reactions: Irritability - overactivity in many children, sedative effects in others; Mild ataxia, nystagmus, skin rash, osteomalacia; May interfere with learning (cognitive deficits)

98
Q

Status Epilepticus

A

State of recurrent major motor seizures between which patient does not regain consciousness

Mortality of 20-25% - death can occur from respiratory arrest or circulatory collapse

Treatment Options:

Initial therapy IV diazepam (lorazepam or midazolam) until seizures stop or 20 mg given

Then start phenytoin or fosphenytoin slow infusion

If seizures persist IV phenobarbital until seizures stop

If seizures still continue, pentobarbital or propofol infusion with pressor support

Neuro Pt 4 (25 decks)

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