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Pharmacology Step 1 > Pharmacology CNS and PNS > Flashcards

Pharmacology CNS and PNS Flashcards

1
Q

Neurotransmitters Levels in Disease
-Acetylcholine, Dopamine, GABA, Glutamate, Norepinephrine, Serotonin (5-HT)

FA-OS p. 512

A

Acetylcholine
-Low in: Alzheimer’s

Dopamine

  • Low in: Parkinson’s
  • High in: Schizophrenia, mania, psychosis

GABA
-Low in: Anxiety, epilepsy

Glutamate
-High in: Alzheimer’s, Schizophrenia, epilepsy

Norepinephrine

  • Low in: Major depressive disorder
  • High in: Anxiety

Serotonin (5-HT)

  • Low in: Major depressive disorder, bipolar disorder, anxiety
  • High in: Schizophrenia
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2
Q

Neurotransmitter Levels in Alzheimer’s

FA-OS p. 512

A
  • Low Acetylcholine

- High Glutamate

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3
Q

Neurotransmitter Levels in Schizophrenia

FA-OS p. 512

A
  • High Dopamine
  • High Glutamate
  • High Serotonin
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4
Q

Neurotransmitter Levels in Parkinson’s

FA-OS p. 512

A

-Low Dopamine

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5
Q

Neurotransmitter Levels in Mania

FA-OS p. 512

A

-High Dopamine

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6
Q

Neurotransmitter Levels in Psychosis

FA-OS p. 512

A

-High Dopamine

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7
Q

Neurotransmitter Levels in Anxiety

FA-OS p. 512

A
  • Low GABA
  • High Norepinephrine
  • Low Serotonin
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8
Q

Neurotransmitter Levels in Epilepsy

FA-OS p. 512

A
  • Low GABA

- High Glutamate

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9
Q

Neurotransmitter Levels in Major Depressive Disorder

FA-OS p. 512

A
  • Low Norepinephrine

- Low Serotonin

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10
Q

Neurotransmitter Levels in Bipolar Disorder

FA-OS p. 512

A

-Low Norepinephrine

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11
Q

An important site for the production of ACh in the brain

A

nucleus basalis of Meynert

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12
Q

Important sites of dopaminergic neurons in the brain

A
  • Substantia nigra pars compacta

- Ventral tegmental area

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13
Q

Location of histaminergic neurons in the brain

A

-Ventral posterior hypothalamus (tuberomammillary nucleus)

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14
Q

Primary site of norepinephrine synthesis in the brain

A

-Locus ceruleus (found in the upper pons)

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15
Q

Area that releases serotonin to projections throughout the brain

A

-Raphe nucleus

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16
Q

General characteristics of neuromuscular junction blocking agents

A
  • Used for skeletal muscle relaxation
  • Site of action = neuromuscular junction
  • Do NOT cause analgesia or unconsciousness (only paralysis)
  • Structurally resemble ACh
  • Bind ACh receptors on muscle
  • Two classes: depolarizing agents and nondepolarizing agents
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17
Q

Depolarizing agent drug name

A

Succinylcholine

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18
Q

Succinylcholine mechanism

A
  • Short acting (works within 30 sec and last 10 min)
  • Depolarizing agent
  • ACh receptor agonist
  • Resistance to AChE allows it to remain bound to the receptor
  • Limited by diffusion away from endplate
  • Metabolized by pseudocholinesterase before it reaches site of action
  • Two phases:
    1. drug binds aggressively to ACh receptor, triggering depolarization at the motor endplate. Remains bound, so Na channels cannot depolarize.
    2. after the drug has been bound for a while, induces conformational change–>nondepolarizing block that is irreversible
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19
Q

Succinylcholine uses

A

Temporary muscle paralysis in surgery and intubation

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20
Q

Succinylcholine side effects

A

-Cardiovascular: low dose-nagative chronotropic and inotropic effects
high dose-positive chronotropic and inotropic effects, raises catecholamine levels
-Fasciculations during phase 1 (visible motor unit contractions)
-Myalgia
-Hyperkalemia- especially concerning in setting of burns, trauma, spinal cord injury, cardiac disease and metabolic abnormalities
-Malignant hyperthermia

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21
Q

Nondepolarizing agent drug names

A
  • Mivacurium (short acting)
  • Vecuronium (intermediate acting)
  • Rocuronium (intermediate acting)
  • Atracurium (intermediate acting)
  • Pancuronium (long acting)
  • Doxacurium (long acting)
    (obvious) NOTE: they all end in -curonium or -curium
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22
Q

Nondepolarizing agent mechanisms

A
  • ACh receptor competitive antagonists
  • Bind to ACh receptor, but does not cause depolarization and blocks ACh from binding
  • Most depend on hepatic or renal elimination to terminate effect (exception=mivacurium which is metabolized by pseudocholinesterase and thus safe for pts with renal or hepatic disease
  • Can give AChE inhibitor to reverse effects
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23
Q

Nondepolarizing agent uses

A
  • Muscle relaxant during intubation, surgery
  • Can be used in place of depolarizing agent
  • Decreases the amount of required inhalational agents and helps maintain paralysis
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24
Q

Nondepolarizing agent side effects

A
  • Respiratory failure secondary to diaphramatic paralysis
  • Tachycardia (pancuronium)
  • Histamine release (Mivacurium)
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25
Q

Cholinesterase inhibitor drug names

A
  • Neostigmine
  • Pyridostigmine
  • Edrophonium
  • Physostigmine
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26
Q

Cholinesterase inhibitor mechanism

A
  • Inactivate AChE by electrostatic or covalent binding

- Prevents ACh degradation at the neuromuscular junction

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27
Q

Cholinesterase contraindications

A

-With depolarizing agents: by inhibiting cholinesterase and pseudocholinesterase, it prolongs the phase 1 block

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28
Q

Cholinesterase uses

A
  • Reverse effects of nondepolarizing agents during surgery

- Used to diagnose (edrophonium) and treat (neostigmine) myasthenia gravis

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29
Q

Cholinesterase side effects

A
  • Bradycardia
  • Bronchospasm
  • Excitation (physostigmine)
  • Intestinal spasm
  • Increased bladder tone
  • Pupillary constriction
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30
Q

Anticholinergic drug names

A
  • Atropine
  • Scopolamine
  • Benztropine
  • Glycopyrrolate (charged and cannot cross the BBB)
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31
Q

Anticholinergic drug mechanism

A

-Complete block of ACh receptors

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32
Q

Anticholinergic uses

A
  • Primary use: anesthesiology
  • Scopolamine is antiemetic
  • Atropine: generally used for cardiovascular effects (reverses vagal-stimulated bradycardia, decreases respiratory secretions, relaxes bronchial smooth muscle, reversal of antipsychotic extrapyramidal effects) or with pralidoxime for organophosphate poisoning
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33
Q

Anticholinergic side effects

A

-CNS stimulation
-Cutaneous blood vessel dilation
-Urinary retention
-Cycloplegia (paralysis of ciliary muscle–>blocks eye accommodation)
-Decreased secretions
Mnemonic: “blind as a bat, dry as a bone, red as a beet, mad as a hatter and hot as a hare”

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34
Q

Barbiturate drug names

A

-Phenobarbital
-Pentobarbital
-Thiopental
-methohexital
-Secobarbital
Obvious NOTE: all end in -tal

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35
Q

Barbiturate mechanism

A

-Increase duration of Cl channel opening on GABAa receptors–>enhanced GABAergic transmission
Mneumonic: “BarbiDURATe increases the DURATion of GABAa receptor Cl channel opening)
-Can block excitatory glutamate receptors
-CYP450 inducer
-Phenobarbital is 75% metabolized in the liver and 25% excreted unchanged by the kidney

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36
Q

Barbiturate uses

A
  • Short term agents (thiopental, methohexital) used in anesthesia
  • Tonic-clonic seizure prevention, status epilepticus, exlampsia (phenobarbital)
  • Mild sedative
  • Relieve anxiety
  • Insomnia (but not recommended because suppresses REM sleep>other stages)
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37
Q

Barbiturate side effects

A
  • Dependence
  • Synergy with alcohol and benzodiazepines (cross-tolerance)
  • Respiratory, cardiovascular and CNS depression that can cause coma or death
  • CYP450 induction alters other drug metabolism
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38
Q

Barbiturate contraindications

A

-Acute intermittent porphyria (barbiturates activate ALA synthase, the rate-limiting enzyme of heme synthesis)

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39
Q

Treatment of barbiturate overdose

A
  • Manage symptoms (ABCs)
  • Hemodialysis in severe cases
  • Alkalization of urine to help with elimination (phenobarbital)
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40
Q

Symptoms of barbiturate withdrawal

A
  • Anxiety
  • Irritability
  • Elevated heart and respiration rate
  • Muscle pain
  • Nausea
  • Tremors
  • Hallucinations
  • Confusion
  • Seizures
  • Death if untreated
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41
Q

Benzodiazepine drug names

A

-Diazepam
-Lorazepam
-Triazolam
-Temazepam
-Oxazepam
-Midazolam
-Chlordiazepoxide
Alprazolam
NOTE: most end in -zolam

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42
Q

Benzodiazepine mechanism

A
  • Increased frequency of Cl channel opening with binding to GABA receptors
  • Cl entry–>hyperpolarization which reduces excitability
  • Effect terminated through redistribution and excretion (metabolized by hepatic microsomal system into active metabolites)
  • Can cross the placental barrier
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43
Q

Benzodiazepine uses

A
  • Anxiolytics via inhibition of lymbic circuit
  • Muscle relaxant to treat spasms
  • Amnesic agents for endoscopy
  • Anticonvulsant
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44
Q

Short acting benzodiazepines

A

(Not great) Mnemonic: “TOM thumb”

  • Triazolam
  • Oxazepam
  • Midazolam
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45
Q

Benzodiazepine side effects

A
  • Synergistic with alcohol and barbiturates (cross-tolerance)
  • Respiratory depression and coma (much less than barbiturates)
  • Drowsiness/confusion
  • Tolerance
  • Dependence
  • Decrease latency to sleep onset and increase stage 2 sleep. REM sleep and stages 3 and 4 sleep are decreased
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46
Q

Benzodiazepine competitive antagonist

A

Flumazenil

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47
Q

Benzodiazepine withdrawal

A

-Confusion
-Anxiety
-Agitation
-Restlessness
-Insomnia
-Tension
Note: similar to barbiturate withdrawal, but less severe

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48
Q

Opiod drug names

A
  • Morphine
  • Hydromorphine
  • Oxymorphone
  • Methadone
  • Meperidine
  • Fentanyl
  • Sufentanil
  • Alfentanil
  • Remifentanil
  • Codeine
  • Hydrocodone
  • Oxycodone
  • Buprenorphine
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49
Q

Neuroleptics (definition)

A
  • Classified as first generation and second generation (atypical) anti-psychotics
  • Block type 2 dopamine receptors (D2)
  • Most effective against the positive symptoms of schizophrenia (such as hallucinations and delusions)
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50
Q

First-generation anti-psychotics drug names

A 
Low potency group
-Chlorpromazine
-Thioridazine
High potency group
-Haloperidol
-Trifluoperazine
-Pimozide
-Perphenazine
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51
Q

Mechanism of first-generation anti-psychotics and difference between low and high potency drugs in this group

A
  • All work in the mesolimbic system by blocking post-synaptic D2 receptors
  • Low-potency drugs have an affinity for muscarinic ACh receptors, alpha-adrenergic receptors, and histaminergic receptors (note: this causes side effects)
  • High potency drugs have a greater affinity for D2 receptors
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52
Q

Uses of first-generation anti-psychotic drugs

A
  • Treatment of acute psychosis
  • Treat of schizophrenia
  • Treatment of bipolar disorder
  • Haloperidol used in Tourette syndrome (to control tics) and Huntington disease (to control choreiform movements)
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53
Q

Side effects of first-generation anti-psychotic drugs

A

All 1st gen drugs:

  • Neuroleptic malignant syndrome
  • Hyperprolactinemia (amenorrhea, galactorrhea, gynecomastia)

High-potency anti-psychotics

  • Extrapyramidal signs (Parkinsonism, akathisia, tremor)
  • Movement disorders (tardive dyskinesia, dystonia)

Low-potency anti-psychotics

  • Sedation
  • -> *Blockade of histamine receptors causes weight gain, sedation, orthostatic hypotension, tremor, and sexual dysfunction
  • Anticholinergic side effects
  • -> *Blockade of muscarinic receptors causes facial flushing, dry mouth, urine retention, constipation

Thioridazine (additional side effects)

  • Sudden death from prolongation of the QT interval, leading to torsades de points
  • Irreversible retinal pigmentation

Chlorpromazine (additional side effects)
-Deposits in the lens and cornea

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54
Q

Second-generation (atypical) anti-psychotic drug names

A

-Clozapine
-Risperidone
-Olanzapine
-Quetiapine
-Ziprasidone
Aripiprazole

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55
Q

Mechanism of second-generation (atypical) anti-psychotic drugs

A
  • Effects on the serotonergic, dopaminergic (with D2 affinity), and noradrenergic systems
  • Each medication has a different neuroreceptor profile (leading to different therapeutic action and different side effects)
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56
Q

Advantages of second-generation (atypical) anti-psychotic drugs over first-generation anti-psychotic drugs

A
  • Second-generation drugs are more effective with negative and chronic symptoms of schizophrenia (avolition, alogia, flattened affect)
  • Second-generation drugs have a lower risk of tardive dyskinesia, neuroleptic malignant syndrome, and extra-pyramidal signs
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57
Q

Uses of second-generation (atypical) anti-psychotic drugs

A
  • Treatment of schizophrenia
  • Treatment of psychosis
  • Treatment of bipolar disorder
  • Risperidone used for antidepressant augmentation
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58
Q

Selective serotonin reuptake inhibitor side effects

A
  • Few side effects, so safe in pregnancy
  • Diarrhea
  • Sexual dysfunction (decreased libido, erectile dysfunction, anorgasmia)
  • Weight gain
  • Fatigue
  • Discontinuation syndrome (worse with short-acting): dizziness, vertigo, nausea, fatigue, headache, insomnia, shock-like sensations, paresthesia, visual disturbances, muscle pain, chills, irritability, agitation and suicidal thoughts
  • Birth defects–most commonly ventral septal defects–can happen (greatest risk with paroxetine)
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59
Q

Monoamine oxidase inhibitor (MAOI) drug names

A
  • Phenelzine
  • Tranyleypromine
  • Isocarboxazid
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60
Q

Opiod mechanism

A
  • Analgesics that act on the CNS
  • Endogenous endorphins are formulated from proopiomelanocortin (POMC), which is also the precursor for the formation of adrenocorticotropic hormone (ACTH), melanocyte-stimulating hormone (MSH) and lipotropin (LPH)
  • Synthetic opiods structurally resemble endogenous opiods
  • Most bind to the Mu-opiod receptor either as full or partial agonists
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61
Q

Opiod uses

A
  • Local analgesia (regional nerve blocks, epidural nerve blocks, spinal nerve blocks)
  • Systemic pain relief (patient controlled analgesia)
  • Chronic pain management
  • Used in antitussives (e.g. dextromethorphan)
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62
Q

Opiod side effects

A
  • Tolerance
  • Dependence
  • Overdose potential
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63
Q

Buspirone mechanism

A
  • Partial serotonin 1A agonist (5HT-1A) receptor agonist in the CNS
  • Does not affect GABAergic receptors, so it does not interact with ethanol, is non-sedating and has low risk of dependence as it does not cause the euphoria associated with benzodiazepines and barbiturates
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64
Q

Buspirone uses

A

-Generalized anxiety disorder

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65
Q

Buspirone side effects

A
  • May stimulate the locus ceruleus–>increased norepinephrine release–>increased anxiety
  • May not work for patients with a history of benzodiazepine use or severe anxiety
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66
Q

Selective serotonin reuptake inhibitor drug names

A
  • Citalopram
  • Fluoxetine
  • Paroxetine
  • Sertraline
  • Fluvoxamine
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67
Q

Selective serotonin reuptake inhibitor mechanism

A
  • Prevent reuptake of serotonin by the presynaptic terminal–>increased availability of serotonin to the postsynaptic membrane
  • Takes 3-6 weeks to get desired effect clinically
  • Does not increase mood in non-depressed patients
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68
Q

Selective serotonin reuptake inhibitor uses

A
  • First line for depressive and anxiety disorders
  • Panic disorder
  • obsessive-compulsive disorder
  • Post-traumatic stress disorder
  • Eating disorders
  • Trichotillomania (impulsive hair eating)
  • Prevents post-stroke depression and improves morbidity and mortality even in the absence of depression
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69
Q

Selective serotonin reuptake inhibitor side effects

A
  • Few side effects, so safe in pregnancy
  • Diarrhea
  • Sexual dysfunction (decreased libido, erectile dysfunction, anorgasmia)
  • Weight gain
  • Fatigue
  • Discontinuation syndrome (worse with short-acting)
  • Birth defects can happen (greatest risk with paroxetine)
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70
Q

Monoamine oxidase inhibitor (MAOI) drug names

A
  • Phenelzine
  • Tranyleypromine
  • Isocarboxazid
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71
Q

MAOI mechanism

A
  • Irreversibly inhibits Monoamine oxidase-A from breaking down norepinephrine–>increased norepinephrine levels
  • MAO-A also breaks down serotonin and tyramine, so there are increased levels of these neurotransmitters as well
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72
Q

MAOI side effects

A 
Use with tyramine causes potentially fatal side effects and the following symptoms:
-Hypertensive crisis
-Diaphoresis
-Headache
-Vomiting
MUST AVOID: cheese (pizza), Pepperoni, Beer, Wine, Smoked/pickle meat, Liver, Spoiled foods
Use with SSRIs can cause serotonin syndrome:
-Confusion
-Hyperthermia
-Myoclonus
-diaphoresis
-Hyperreflexia
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73
Q

Side effects of second-generation (atypical) anti-psychotics

A

All 2nd generation drugs:

  • Cardiotoxicity
  • Abnormal ECG
  • Neuroleptic malignant syndrome
  • Hyperprolactinemia (gynecomastia, galactorrhea, and amenorrhea)
  • Extrapyramidal signs (Parkinsonism, akathisia, tremor)
  • Increased chance of seizures
  • Insulin intolerance, T2D (unrelated to weight gain)
  • Hyperlipidemia

Clozapine (additional side effects)

  • Agranulocytosis
  • Weight gain

Olanzapine (additional side effects)
-Weight gain

Risperidone (additional side effects)
-Especially prone to hyperprolactinemia

Ziprasidone (additional side effects)
-Prolongation of QT and PR intervals

Note: Ziprasidone and aripiprazole have fewer metabolic side effects than other 2nd-generation drugs

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74
Q

Names of Mood Stabilizing Drugs

A

Lithium

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75
Q

Mechanisms of Mood Stabilizing Drugs (Lithium)

A
  • Exact mechanism of lithium unknown

- It is believed that lithium interferes with monoamine synthesis, release, and reuptake

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76
Q

Uses of Mood Stabilizing Drugs (Lithium)

A
  • Treatment of Bipolar Disorder
  • Used to augment antidepressants in major depressive disorder
  • May take 2-3 weeks for effects of lithium to manifest
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Perfectly
77
Q

Precautions with Lithium (lab tests to follow)

A
  • Lithium has a low therapeutic index
  • Must follow blood levels of lithium to keep them to the minimum therapeutic level
  • Regularly follow creatinine (renal function) and TSH (thyroid function)
78
Q

Side effects of Mood Stabilizing Drugs (Lithium)

A
  • Hypothyroidism & goiter
  • Thirst
  • Renal dysfunction (nephrogenic diabetes insipidous results in increased creatinine kinase and eventual kidney failure)
  • Tremor
  • Diarrhea
  • Increased appetite and weight gain
  • Cardiac conduction problems
  • Mild cognitive impairment
  • CNS depression (at toxic levels)
  • Congenital abnormalities
79
Q

Anticonvulsants (definition and 3 basic mechanisms)

A
  • These agents suppress uncontrolled neuronal discharge in epileptic seizures
  • Anticonvulsants inhibit neuronal firing through 3 different mechanisms to reduce the likelihood that a seizure will occur:
    1. Increasing GABAergic activity
    2. Blocking voltage-gated sodium channels
    3. Blocking voltage-gated calcium channels
80
Q

Types of seizures (categories)

A

2 general categories: partial and generalized

Partial Seizures include:

  • Simple seizure
  • Complex seizure
  • Partial seizure with secondarily generalized tonic-clonic seizure

Generalized Seizures include:

  • Absence seizure
  • Myoclonic seizure
  • Tonic-clonic seizure
  • Atonic seizure
  • Status epilepticus
81
Q

Names of anticonvulsants that target presynaptic and postsynaptic GABA and the GABA receptor (anticonvulsant mechanism #1: increase GABAergic activity)

A
  • Vigabatrin (inhibit GABA-T, which metabolizes GABA)
  • Valproate (inhibit GABA-T, which metabolizes GABA)
  • Tiagabine (activate GAT-1, which reuptakes GABA)
  • Barbiturates (GABA receptor)
  • Benzodiazepines (GABA receptor)

Note: These drugs increase CNS inhibition and raise the seizure threshold

82
Q

Names of anticonvulsants that target and extend sodium sodium channel inactivation (anticonvulsant mechanism #2: block voltage-gated Na+ channels)

A
  • Carbamazepine
  • Phenytoin
  • Topiramate
  • Lamotrigine
  • Valproate
  • Zonisamide

Note: All work on intracellular side of inactivated Na+ channel

Note: These drugs block the rapid successive firing of action potentials (which is classically associated with partial seizures and generalized tonic-clonic seizures)

83
Q

Names of anticonvulsants that target and reduce current through T-type calcium channels (anticonvulsant mechanism #3: block voltage-gated Ca2+ channels)

A
  • Ethosuximide
  • Valproate

Note: These drugs on the extracellular side of the Ca2+ channel, specifically T-type calcium channels

Note: These drugs are used in treatment of generalized absence seizures

  • These drugs reduce calcium current in thalamic neurons
  • Thalamic neurons are responsible for the generation of the 3-Hz spike-and-wave rhythms seen in absence seizures
  • Reduction of T-type currents in thalamic neurons stops the rhythmic discharge associated with absence seizures
84
Q

Mechanism of Valproic Acid (or valproate, which is the ionized form)

-Mainly mechanism #2 for anticonvulsant drugs

A
  • Binds to voltage-gated Na+ channels and favors the inactivated state
  • Decreases Ca2+ influx across T-type Ca2+ channels in the membrane (this reduces the calcium current in thalamic neurons)
85
Q

Uses of Valproic Acid

A
  • Treatment of partial and generalized tonic-clonic seizures
  • Second-line treatment for generalized absence seizures (ethosuximide is first line)
  • Treatment of bipolar disorder (mood-stabilizing properties)
  • Treatment of intermittent explosive disorder (a behavioral disorder characterized by extreme expression of anger that is disproportionate to the inciting cause)
  • Used as prophylaxis for migraines

Note: Use of this drug is decreasing due to high # side effects and lower efficacy compared with other medications

86
Q

Side effects of Valproic Acid

A
  • GI upset (stomach pain, nausea, diarrhea)
  • Increased appetite, leading to weight gain
  • Tremor
  • Sedation
  • Alopecia
  • Hepatotoxicity
  • Decreased platelet count
  • Possible polycystic ovarian sydrome (PCOS)
  • Congenital neural tube defects (folate antagonist)
87
Q

Mechanism of ethosuximide

-Mainly mechanism #3 for anticonvulsant drugs

A
  • Decreases Ca2+ influx across T-type Ca2+ channels in the membrane (this reduces the calcium current in thalamic neurons)
  • This is why ethosuximide is used for absence seizures (because absence seizures are associated with rhythmic discharge through T-type currents in the thalamus)
88
Q

Uses of ethosuximide

A

-First-line treatment for absence seizures

89
Q

Side effects of ethosuximide

A
  • GI distress
  • Lethargy
  • Headache
  • Urticaria
  • Steven-Johnson syndrome
90
Q

Mechanism of phenobarbitol

-Mainly mechanism #1 for anticonvulsant drugs

A
  • Part of barbiturate drug class

- Acts on the GABA-A receptor to increase CNS inhibition and raise the seizure threshold

91
Q

Uses of phenobarbitol

A

-Many uses but role in anticonvulsant therapy is specific to treatment of status epilepticus

92
Q

Side effects of phenobarbitol

A
  • Sedation
  • Tolerance
  • Dependence
  • Induction of cytochrome P450 system
93
Q

Mechanism of carbamazepine

-Mechanism #2 for anticonvulsant drugs

A
  • Reduces the rate of recovery of voltage-gated sodium channels (like phenytoin & lamotrigine)
  • -> This blocks the rapid successive firing of action potentials that is classically associated with partial seizures and generalized tonic-clonic seizures)
94
Q

Uses of carbamazepine

A
  • First-line treatment for partial seizures and tonic-clonic seizures
  • Treatment of bipolar disorder
  • Treatment of trigeminal neuralgia
95
Q

Side effects of carbamazepine

A
  • Aplastic anemia
  • Agranulocytosis
  • Hyponatremia
  • Induces cytochrome P450 system (increases metabolism of itself and oral contraceptives)
96
Q

Mechanism of phenytoin

-Mechanism #2 for anticonvulsant drug

A
  • Slows the rate of recovery of voltage-gated sodium channels (like carbamazepine & lamotrigine)
  • -> this blocks the rapid successive firing of action potentials
97
Q

Uses of phenytoin

A
  • Treatment of all types of partial and generalized seizures (EXCEPT absence seizures)
  • First line treatment for prophylaxis against status epilepticus
98
Q

Side effects of phenytoin

A

Toxicity (at high levels)

  • Nystagmus
  • Diplopia
  • Ataxia
  • Sedation
  • Gingival hyperplasia
  • Megaloblastic anemia
  • SLE-like syndrome
  • Induction of cytochrome P450
  • Fetal hydantoin syndrome
99
Q

Mechanism of Lamotrigine

A
  • Slows the rate of recovery of voltage-gated sodium channels (like carbamazepine & phenytoin)
  • -> This blocks the rapid successive firing of action potentials
  • May also reduce the amount of released glutamate
100
Q

Uses of Lamotrigine

A
  • Treatment of partial seizures and generalized tonic-clonic seizures
  • Treatment of focal epilepsy
  • Treatment of Lennox-Gastaut syndrome (type of childhood-onset epilepsy)
  • Treatment of bipolar disorder
101
Q

Side effects of Lamotrigine

A
  • Dizziness
  • Nausea
  • Headache
  • Skin rash (hypersensitivity reaction)
  • Stevens-Johnson syndrome (avoided by increasing the dose very slowly)
102
Q

Mechanism of Pregabalin

-Mainly anticonvulsant mechanism #1

A
  • Binds to alpha2-delta subunit for high-voltage-activated Ca2+ channels
  • Increases the density of GABA transporter protein and increases the rate of functional GABA transport
  • Decreases pre-synaptic release of glutamate, NE, and substance P

Note: These mechanisms produce both anticonvulsant and anti-nociceptive effects

103
Q

Uses of Pregabalin

A
  • Treatment of neuropathic pain associated with diabetic neuropathy and post-herpetic neuralgia
  • Adjunctive treatment of fibromyalgia
  • Adjunctive treatment of partial seizures

Note: Compared to gabapentin, pregabalin is more potent, absorbs faster and has greater bioavailability

104
Q

Side effects of Pregabalin

A
  • Dizziness
  • Somnolence
  • Weight gain
105
Q

Mechanism of Gabapentin

A
  • Was designed to be a GABA analog, but it does not modulate GABA receptors
  • Avidly binds to the alpha2-delta subunit for high-voltage-activated Ca2+ channels
  • -> This may increase the synaptic concentration of GABA and enhances GABA responses at non-synaptic sites in neuronal tissues
  • Decreases presynaptic release of glutamate
106
Q

Uses of Gabapentin

A
  • Treatment of partial seizures
  • Treatment of pain (including neuropathic) and peripheral neuropathy
  • Treatment of bipolar disorder
  • Treatment of anxiety
  • Used for sedation (because it is highly lipid soluble)
107
Q

Side effects of Gabapentin

A
  • Sedation

- Weight gain

108
Q

Tricyclic antidepressant drug names

A

-Amitriptyline
-Imipramine
-Amoxapine
-Clomipramine
-Desipramine
-Doxepin
-Nortriptyline
-Protriptyline
NOTE: All but Doxepin end in -ptyline or -ine

109
Q

Tricyclic antidepressant mechanism

A
  • Increase synaptic concentration of serotonin and NE in the CNS
  • Inhibit serotonin and NE reuptake by presynaptic terminal
110
Q

Tricyclic antidepressant uses

A
  • Chronic pain
  • Major depression
  • Anxiety disorders
  • Enuresis in children historically, but risk of sudden death means that this is not first line
111
Q

Tricyclic antidepressant side effects

A

3 C’s:

  • Constipation
  • Cardiac arrhythmias
  • Coma (overdose potential)

Others:

  • Sudden death in children (imipramine and desipramine)
  • Sedation
  • Tremor
  • Insomnia
  • Orthostatic hypotension
  • Psychosis
  • Seizures
  • Weight gain
112
Q

Bupropion mechanism

A
  • Heterocyclic antidepressant
  • Mechanism is mostly unknown–thought to have to do with blocking NE and dopamine reuptake (depression) and action on nicotinic ACh receptor antagonism (smoking cessation)
113
Q

Bupropion uses

A

2nd and 3rd line for:

  • Smoking cessation
  • Major depression
114
Q

Bupropion side effects

A
  • Stimulant effects
  • Tachycardia
  • Insomnia
  • Headaches
  • Seizure risk is higher than other antidepressants
115
Q

Bupropion contraindications

A
  • Anorexia
  • Bulimia
  • Seizure disorders (lowers seizure threshold)
  • MAO inhibitor treatment within the past 2 weeks
116
Q

Venlafaxine mechanism

A
  • Converted to active metabolite O-desmethylvenlafaxine

- Inhibit presynaptic reuptake of serotonine>NE

117
Q

Duloxetine mechanism

A

-Inhibit presynaptic reuptake of serotonine>NE

118
Q

Venlafaxine uses

A
  • Major depression
  • Melancholia
  • Anxiety disorders
  • Chronic pain associated with depression
119
Q

Duloxetine uses

A
  • Major depression
  • Anxiety disorders
  • Chronic pain associated with depression
  • Diabetic peripheral neuropathic pain
120
Q

Duloxetine side effects

A
  • Sedation
  • Nausea
  • Constipation
  • Elevated bp
  • Sweating
121
Q

Venlafaxine side effects

A
  • Sedation
  • Nausea
  • Constipation
  • Elevated bp
  • Sweating
122
Q

Nefazodone mechanism

A
  • Serotonin modulator

- Blocks 5HT2 receptor and inhibit reuptake of 5-HT and NE

123
Q

Trazodone mechanism

A
  • Serotonin modulator
  • Blocks 5HT2 receptor and inhibit reuptake of 5-HT and NE
  • Antagonizes serotonin at low doses and acts as a serotonin agonist at high doses
  • Effects histamine blockade
124
Q

Mirtazapine mechanism

A
  • Serotonin modulator
  • Blocks 5HT2 receptor and inhibit reuptake of 5-HT and NE
  • Antagonizes histamine H1 receptors
  • Weakly blocks peripheral alpha1-adrenergic and muscarinic receptors
125
Q

Nefazodone uses

A
  • Major depression

- Anxiety

126
Q

Trazodone uses

A
  • Major depression
  • Anxiety
  • Insomnia
127
Q

Mirtazapine uses

A
  • Major depression

- Anxiety

128
Q

Nefazodone side effects

A
  • Sedation
  • Increased appetite
  • Weight gain
  • Dry mouth
  • Hepatotoxicity
  • Visual trails
  • Postural hypotension
129
Q

Trazodone side effects

A
  • Sedation
  • Increased appetite
  • Weight gain
  • Dry mouth
  • Priapism (persistent and painful erection of the penis)
  • Postural hypotension
130
Q

Mirtazapine side effects

A
  • Sedation
  • Increased appetite
  • Weight gain
  • Dry mouth
  • Postural hypotension
131
Q

Maprotiline mechanism

A
  • Tetracyclic antidepressant
  • Selectively prevents the reuptake of NE
  • Unlike other antidepressants, does NOT prevent serotonin reuptake
132
Q

Maprotiline uses

A

-Major depression

133
Q

Maprotiline side effects

A
  • Sedation

- Orthostatic hypotension

134
Q

Define neuroleptics

A
  • First and second-generation antipsychotics
  • Block D2 (dopamine type 2) receptors
  • Most effective against the positive symptoms of schizophrenia, such as hallucinations and delusions
135
Q

First generation antipsychotic drug names

A
  • Chlorpromazine (low potency)
  • Thioridazine (low potency)
  • Haloperidol (high potency)
  • Trifluoperazine (high potency)
  • Pimozide (high potency)
  • Perphenazine (high potency)
136
Q

First generation antipsychotic mechanism

A
  • Work in the mesolimbic system
  • Block postsynaptic D2 receptors
  • The low potency drugs (Chlorpromazine and Thioridazine) also have affinity for muscarinic ACh, alpha-adrenergic and histaminergic receptors
  • High potency drugs (e.g. Haloperidol) have greater D2 affinity
137
Q

First generation antipsychotic uses

A
  • Acute psychosis
  • Schizophrenia
  • Bipolar disorder
  • Tourette syndrome to control ticks (Haloperidol)
  • Huntington disease (to control movements)
138
Q

First generation antipsychotic side effects

A
  • Extrapyramidal signs (Parkinsonism, akathisia, tremor)–especially high potency
  • Movement disorders (tardative dyskinesia, dystonias)–esp high potency
  • Sedation (low potency)
  • Neuroleptic malignant syndrome
  • Hyperprolactinemia (amenorrhea, galactorrhea, gynecomastia)
  • Anticholinergic side effects–low potency
  • Sudden death from prolongation of QT interval–> torsades de pointes (thioridazine)
  • Irreversible retinal pigmentation (thioridazine)
  • Deposits in the lens and cornea (chlorpromazine)
139
Q

Drug classes used to treat Alzheimer’s disease

A
  1. Block NMDA receptors (which are activated by excess glutamate associated with disease)
    -Memantine
  2. Block AChE (AChE breaks down ACh into choline and acetate; ACh is low in AD)
    -Tacrine, donepezil, rivastigmine, galantamine
    Note: To date, no FDA-approved rug modifies the disease progression
140
Q

Mechanism of Memantine

A
  • During depolarization of neuronal cells, the magnesium blockade of NMDA receptors is relieving, thus allowing calcium to enter the cell
  • Over time, calcium influx leads to neuronal damage
  • Memantine non-competitively blocks NMDA receptors in the CNS, thus preventing stimulating by glutamate. This results in less intracellular calcium. Less intracellular calcium prevents further damage to the neurons
141
Q

Uses of Memantine

A
  • Used to treat moderate to severe Alzheimer’s disease

- May be used to treat vascular dementia

142
Q

Side effects of Memantine

A
  • Agitation
  • Insomnia
  • Urinary incontinence
  • Diarrhea
143
Q

Drug names of selective inhibitors of AChE in the CNS

A
  • Tacrine
  • Donepezil
  • Rivastigmine
  • Galantamine
144
Q

Mechanism of selective inhibitors of AChE in the CNS (tacrine, donepezil, rivastigmine, galantamine)

A
  • By selectively inhibiting AChE in the CNS, levels of ACh increase, which has been shown to improve cognition
  • Centrally acting AChE inhibitors improve efficacy and decrease peripheral side effects
145
Q

Uses of selective inhibitors of AChE in the CNS (tacrine, donepezil, rivastigmine, galantamine)

A

-Treatment of Alzheimer’s disease (because they are centrally acting and can cross the BBB)
Note: Other AChE inhibitors, like those neostigmine used for myasthenia gravis, cannot cross the BBB, and thus, are not used for Alzheimer’s disease

146
Q

Side effects of selective inhibitors of AChE in the CNS (tacrine, donepezil, rivastigmine, galantamine)

A
  • Nausea
  • Vomiting
  • Diarrhea
  • Insomnia
147
Q

Drug classes used to treat Parkinson’s disease

A

Strategies to increase levels of CNS dopamine:

  1. increase endogenous dopamine by preventing its degradation
    - MAO-B inhibitors (selegiline, rasagiline)
  2. add an exogenous precursor of dopamine that is converted to dopamine centrally
    - Levodopa
  3. give dopamine agonists that directly stimulate D2 receptors
    - Bromocriptine, pergolide, ropinirole, pramipexole
148
Q

Cause of Parkinson’s disease

A
  • Loss of dopaminergic neurons in the substantia nigra pars compacta
  • This results in lower levels of dopamine in the CNS
149
Q

Clinical manifestations of decreased dopamine

A
  • Mask-like facies
  • Bradykinesia
  • Resting tremor
  • Muscle rigidity
  • Shuffling gait
  • Postural instability
150
Q

Drug names of dopamine receptor agonists used in Parkinson’s disease

A
  • Bromocriptine
  • Pergolide
  • Ropinirole
  • Pramipexole
151
Q

Mechanism of dopamine receptor agonists used in Parkinson’s disease (bromocriptine, pergolide, ropinirole, pramipexole)

A
  • These drugs all work as dopamine receptor agonists, but each drug has different effects on the different types of dopamine receptors
  • Pergolide: agonist of D1 and D2 receptors
  • Ropinirole and Pramipexole: agonist of only D2 receptors
  • Bromocriptine: D2 receptor agonist and D1 receptor antagonist (can antagonize D1 receptors in the hypothalamus)
152
Q

Uses of dopamine receptor agonists (bromocriptine, pergolide, ropinirole, pramipexole)

A
  • Used to treat Parkinson’s disease

- Bromocriptine can be used to reduce the rate of growth of pituitary adenomas (prolactinomas) and to treat acromegaly

153
Q

Side effects of dopamine receptor agonists (bromocriptine, pergolide, ropinirole, pramipexole)

A
  • Headache
  • Nausea
  • Vomiting
  • Epigastric pain
  • Hypotension/syncope initially (leading to hypertension over time)
154
Q

Mechanism of Levodopa (L-Dopa)

A
  • Levodopa is a metabolic precursor to dopamine that enters the brain through an L-amino acid transporter (dopamine itself cannot cross the BBB)
  • Once in the CNS, levodopa is further decarboxylated to dopamine
155
Q

How does levodopa (L-dopa) appear in the urine?

A

-Appears as the metabolites homovanillic acid (HVA) and dihydroxyphenylacetic acid (DOPAC)

156
Q

Uses of Levodopa (L-Dopa)

A

-First-line treatment for Parkinson’s disease

157
Q

What is Levodopa (L-Dopa) given with and why?

A

-Given with carbidopa to reduce peripheral conversion of L-dopa to dopamine, which decreases the side effects and increases the availability of L-dopa for the CNS

158
Q

Side effects of Levodopa (L-Dopa)

A

-Nausea and vomiting
-Tachycadia
-Atrial fibrillation
-Dyskinesias
-Agitation
-Confusion
Note: L-Dopa is CONTRAINDICATED in psychosis and close-angle glaucoma

159
Q

What are the two types of monoamine oxidase in the nervous system?

A
  • MAO-A metabolizes NE and serotonin

- MAO-B metabolizes dopamine

160
Q

Drug names of MAO-B inhibitors

A
  • Selegiline

- Rasagiline

161
Q

Mechanism of MAO-B inhibitors (Selegiline)

A

-Selegiline is an irreversible selective inhibitor of MAO-B (which is found in the striatum and metabolizes dopamine in the brain)

162
Q

Uses of MAO-B inhibitors (Selegiline)

A
  • Treatment of Parkinson’s disease
  • Note: A selegiline preparation (Emsam) is available in a skin patch that allows the drug to bypass the GI tract. Its low dose does not have tyramine food interactions as seen with other MAO inhibitors
163
Q

Side effects of MAO-B inhibitors

A

-Serotonin syndrome (can occur when taken in combination with meperidine, TCAs, or SSRIs)

164
Q

Drug names of catechol-o-methyltransferase (COMT) inhibitors

A
  • Tolcapone (central and peripheral)

- Entacapone (peripheral)

165
Q

Mechanism of catechol-o-methyltransferase (COMT) inhibitors

A

-COMT inhibitors can prolong the action of levodopa by decreasing its peripheral (tolcapone and entacapone) and central (tolcapone) activity

Note: Entacapone is preferred to tolcapone even though it only has peripheral activity because it also has less hepatotoxicity

166
Q

Uses of catechol-o-methyltransferase (COMT) inhibitors

A

-Used to increase the levels of levodopa in the treatment of Parkinson disease

167
Q

Side effects of catechol-o-methyltransferase (COMT) inhibitors

A
  • Dyskinesias
  • Nausea
  • Confusion
168
Q

What are general anesthetics?

A
  • They cause analgesia, amnesia, and unconsciousness (essential to surgery)
  • They also cause muscle relaxation and suppression of reflexes
169
Q

What are the four sequential stages of anesthesia?

A

Stage 1. Analgesia: “conscious and conversational”
Stage 2. Disinhibition: autonomic variations (changes blood pressure, heart rate, and respiratory rate)
Stage 3. Surgical anesthesia: Unconscious with relaxed muscles
Stage 4. Medullary depression: Respiratory and vasomotor center depression

170
Q

What are the methods of delivery of general anesthetics?

A
  • Inhaled agents (volatile, halogenated hydrocarbons)

- IV drugs (common property of rapid induction)

171
Q

Tradeoff between potency and speed of induction in general anesthetics

A
  • Drugs with low solubility in blood have rapid induction and recovery times
  • Drugs with high solubility in oil or lipids have increased potency
  • “Anesthetics with greater solubility in oil tend to also have greater solubility in blood and vice versa, implying that there is a tradeoff between potency and speed of induction”
172
Q

Properties of inhaled anesthetics

A

-Depth of anesthesia can be rapidly altered by changing the inhaled concentration of the drug (making it suitable for maintaining anesthesia)

  • Speed of induction of inhaled anesthetics depends on:
    1. The alveolar gas and venous blood partial pressures
    2. The solubility of the anesthetic agent in the blood
    3. The alveolar blood flow

-The minimum alveolar concentration (MAC) is very similar to ED50 and is equal to the alveolar concentration of an inhaled anesthetic that stops movement in 50% of patients in response to incision

173
Q

Properties of drugs that cross the BBB

A

-Drug must penetrate through lipid membranes (lipophilic) or must be actively transported

174
Q

Drug names of inhaled anesthetics

A
  • Halothane
  • Isoflurane
  • Sevoflurane
  • Desflurane
175
Q

Mechanism of inhaled anesthetics (halothane, isoflurane, sevoflurane, desflurane)

A
  • The mechanism of inhaled anesthetics is poorly understood

- Derived from early research and clinical experience with ether and chloroform

176
Q

Side effects of inhaled anesthetics (halothane, isoflurane, sevoflurane, desflurane)

A
  • Respiratory depression
  • Nausea
  • Emesis
  • Hypotension
177
Q

Toxicity of inhaled anesthetics (halothane, isoflurane, sevoflurane, desflurane)

A
  • Hepatotoxicity (halothane)
  • Nephrotoxicity (methoxyflurane - no longer used in the US)
  • Convulsions (enflurane)
  • Malignant hyperthermia (all agents except nitrous oxide)
178
Q

What drug is used to treat malignant hyperthermia?

A
  • Dantrolene
  • This drug interferes with calcium release from the sacroplasmic reticulum of muscle cells by binding to ryanodine receptors
179
Q

Properties of intravenous anesthetics

A
  • Used to rapidly induce anesthesia

- Propofol has the ability to both induce and maintain anesthesia

180
Q

Types of intravenous anestheics

A
  • Barbiturates
  • Benzodiazepines
  • Ketamine
  • Opiates
  • Propofol
  • Etomidate
181
Q

Properties of barbiturates (thiopental) for intravenous anesthesia

A
  • Highly lipid-soluble and enters brain rapidly (making them suitable for induction of anesthesia and short surgical procedures)
  • Redistribution from brain to other tissues causes loss of effects
  • Not analgesic (therefore, they require a supplementary analgesic)
  • IV barbituates can cause severe hypotension in patients who are hypovolemic or in shock
  • Anesthetic concentrations of pentobarbitol block high-frequency sodium channels
182
Q

Properties of benzodiazepines (midazolam) for intravenous anesthesia

A
  • Most common drug used for endoscopy
  • Used with inhalation anesthetics and narcotics
  • Midazolam can cause severe postoperative respiratory depression and amnesia
183
Q

Properties of ketamine (arylcyclohexylamine) for intravenous anesthesia

A
  • This is a PCP analog that acts as a dissociative anesthetic (very high affinity for NMDA receptors)
  • It causes sedation, amnesia, immobility, disorientation, and hallucinations
184
Q

Properties of opioids (morphine, fentanyl, sufentanil) for intravenous anesthesia

A
  • Used with other CNS depressants during general anesthesia
  • Toxicity involves hypotension, respiratory depression, and muscle rigidity
  • Opioids are reversed with naloxone or naltrexone (which antagonize the mu-opioid receptor)
185
Q

Properties of propofol for intravenous anesthesia

A
  • Used for rapid induction of anesthesia and short surgical procedures
  • An excitatory phase may occur (causing muscle twitching, spontaneous movements, and hiccups)
  • It can also reduce ICP
  • Used in the resection of spinal cord tumors (since it has much less effect than volatile anesthetics on CNS-evoked potentials, it can be used when assessing spinal cord function)
186
Q

OCD treatment

A

-Tricyclic antidepressants and SSRIs
Treatment of choice:
-Clomipramine (TCA)
-Fluoxetine

187
Q

Meds to abort migraines

A
  • Sumatriptan
  • Almotriptan
  • Rizatriptan
  • Zolmitriptan
188
Q

Which drug(s) should be given to reverse anesthesia caused by fentanyl, propofol and midazolam?

A

-Naloxone and Flumazenil

189
Q

Mood stabilizers

A
  • Lithium

- Lamotrigine

190
Q

Lithium

A
  • Inhibits andrenergic, muscarinic adn serotonergic neurotransmission in the brain
  • Alters serotonin, norepinephrine and dopamine neurotransmission
  • Common adverse effects: acute lithium intoxication [nausea, vomiting, diarrhea, renal failure, ataxia, tremor), bradyarrhythmia, hypotension, hyperkalemia, nephrogenic diabetes insipidous, hypothyroidism, goiter, ECG and EEG abnormalities are rare, acne
191
Q

Lamotrigine

A
  • Inhibits neurotransmission by blocking neuronal Na channels
  • Adverse reactions: rash, ataxia, somnolence, blurred vision
192
Q

Methylphenidate

A

-Increase catecholamine release from the synaptic terminal
-Block catecholamine reuptake
-Weakly inhibit MAO
Adverse effects: hypertension, tachyarrhythmia, restlessness, loss of appetite, addiction potential

Pharmacology Step 1 (6 decks)

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