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Neuro Mix Bag > Block 5 Drugs > Flashcards

Block 5 Drugs Flashcards

1
Q

fomepizole

A

treatment for ethylene glycol toxicity, inhibits alcohol dehydrogenase

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2
Q

disulfiram

A

ethanol addiction relapse prevention

Alcohol makes person very sick
Headache, sweating, dizziness, nausea, vomiting, respiratory difficulties, orthostatic hypotension and (very rarely) death
Disulfiram interferes with aldehyde dehydrogenase - leads to ex­cessive acetaldehyde levels

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3
Q

naltrexone

A

ethanol addiction relapse prevention

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4
Q

propromazine/ chlorpromazine (Thorazine)

A

called chlorpromazine in objectives, but propromazine in powerpoint, with thorazine in captions in both cases.
Typical/FGA

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5
Q

First Generation Antipsychotics

A

FGA

First generation anti-psychotic drugs (FGAs), such as haloperidol, act by blocking dopamine receptors in the brain

First generation anti-psychotic drugs are only effective on the positive symptoms of the disease

Block DA receptors everywhere in brain

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6
Q

Haloperidol

A

FGA

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7
Q

Clozapine (Clozaril)

A

Effective for both positive and negative symptoms
NO Parkinson-like symptoms (EPS)
Life threatening adverse effect (agranulocytosis)
Other SGA do not have life-threatening adverse effects but are not as effective as clozapine
SGAs block D2 receptors AND 5-HT receptors

often causes weight gain
No incidence of Tardive Diskinesia

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8
Q

Risperidone

A

SGA

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9
Q

Olanzapine

A

SGA, often causes weight gain

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10
Q

Quetiapine

A

SGA

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11
Q

Aripiprazole

A

SGA with least common occurrence of weight gain

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12
Q

sympathoinmetics

A 
Increased release of NE and DA 
↑ amount of transmitter that can act on postsynaptic receptors 
Blocks NE and DA reuptake
Further ↑NE or DA levels 
Inhibits monoamine oxidase (MAO) 
↑ neurotransmitter levels even higher

Stimulation of medullary respiratory center
Rate and depth
Most effective if respiration is depressed
Decreased food consumption
Feeding center
Tolerance

non-CNS:
Increased systolic and diastolic BP (reflex decrease in HR)
High doses - arrhythmias

THERAPEUTIC USES:
Attention deficit hyperactivity disorder (ADHD)
Narcolepsy
Fatigue
Weight loss
Analeptic - reverses drug induced depression
No longer used
High mortality relative to other measures
With severe depression - risk of cardiac arrhythmias, seizures and delirium

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13
Q

xanthines

A

caffeine and theophylline

Stimulates cerebral cortex
Clearer flow of thought 
Decreased reaction time
Detter association of ideas
Less fatigue
Improved manual dexterity in well learned tasks (e.g., Typing)
Medullary centers affected next
Stimulates respiration
Stimulates vasomotor center
Large doses will affect spinal cord (hyperreflexia)

Direct stimulation of the heart
Theophylline potency > caffeine
Increased rate and force of contraction and cardiac output (CO)
Congestive heart failure,
Rapid and transient increase in CO
Diuresis
Sensitive individuals
Arrhythmias
Premature ventricular contractions (PVCs)
Stimulates skeletal muscle (↑ work capacity)
Smooth muscle relaxant
Theophylline is useful for treatment and prophylaxis of bronchial asthma
↓ Peripheral vascular resistance
↑ Cerebral vascular resistance

MOA:
Translocation of intracellular Ca++ from the sarcoplasmic reticulum
Inhibition of phosphodiesterase
Elevated levels of the second messenger cAMP
Nonselective adenosine receptor antagonist
Inhibit sleepiness-inducing adenosine

Toxicity:

CNS
Insomnia, excitement, mild delirium, sensory disturbances (e.g., ringing in ears, flashes of light)
Followed by convulsions
> 10 gm - clonic convulsions and death

Cardiovascular
Increased HR, extra systoles, increased respiratory rate
Decreased clotting time
Increased gastric secretions 
Also seen with decaffeinated beverages

Therapeutic Uses:

Cardiac stimulation in CHF – controversial
Dilates coronary arteries
Increased coronary blood flow
Increased inotropic and chronotropic forces
Increase O2 demand by the heart
Paroxysmal dyspnea associated with left heart failure
Analeptic
Bronchial asthma
Plus ergot alkaloids for migraine
Vasoconstriction of cerebral vasculature

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14
Q

Amphetimine

A

treats ADHD
Enhances NE release

Amphetamine psychosis:
Vivid hallucinations, paranoid delusions and compulsions
Marked weight loss
Drug screen
Symptoms resolve in 7-10 days
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15
Q

Cocaine

A

More rapid onset due to preferred routes of administration

Mech of Action:
Blocked reuptake of norepinephrine - motor
Blocked reuptake of dopamine - euphoria
Local anesthetic properties

Toxicity:
Cardiac arrhythmias, coronary and cerebral thrombosis
Impairs in utero brain development leading to significantly decreased brain size and neurological manifestations

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16
Q

MDMA (Ecstasy)

A

Very fast action sympathomimeti
Unlike amphetamines:
Directly stimulates 5HT21A autoreceptors
Stimulates the release of serotonin and inhibits its reuptake

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17
Q

Bath salts (Methylenedioxypyrovalerone, Mephedrone)

A

Often contain various amphetamine-like chemicals

Chemicals act in the brain like stimulant drugs

Toxicity associated with Ingesting or snorting "bath salts":
Chest pains
Increased blood pressure
Increased heart rate
Agitation
Hallucinations
Extreme paranoia
Delusions
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18
Q

Caffeine

A

xanthine

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19
Q

Theophylline

A

xanthine

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20
Q

Modafinil

A

Approved by the U.S. Food and Drug Administration (FDA) (DEA Schedule IV Controlled Substance)
Treatment of narcolepsy
Shift work sleep disorder
Excessive daytime sleepiness associated with obstructive sleep apnea
Promoted as a “wakefulness promoting agent” rather than a classic amphetamine-like stimulant
Effective treatment for attention deficit hyperactivity disorder (ADHD)
Discouraged for use by children for any purpose due to cases of severe skin rash

MOA:
Monoamines
Dopamine 
↑ Release in striatum* 
↑ Release in nucleus accumbens*
DA antagonists do not entirely negate the wakefulness-promoting actions of modafinil
May block DA reuptake*
Norepinephrine 
↑ Release in hypothalamus*
Serotonin 
↑ Release in amygdala and frontal cortex 
Elevates hypothalamic histamine levels
Activates glutamatergic circuits 
Inhibits GABAergic neurotransmission
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21
Q

Armodafinil

A

Approved by the U.S. Food and Drug Administration (FDA) (DEA Schedule IV Controlled Substance)
Treatment of narcolepsy
Shift work sleep disorder
Excessive daytime sleepiness associated with obstructive sleep apnea
Promoted as a “wakefulness promoting agent” rather than a classic amphetamine-like stimulant
Effective treatment for attention deficit hyperactivity disorder (ADHD)
Discouraged for use by children for any purpose due to cases of severe skin rash

MOA:
Monoamines
Dopamine 
↑ Release in striatum* 
↑ Release in nucleus accumbens*
DA antagonists do not entirely negate the wakefulness-promoting actions of modafinil
May block DA reuptake*
Norepinephrine 
↑ Release in hypothalamus*
Serotonin 
↑ Release in amygdala and frontal cortex 
Elevates hypothalamic histamine levels
Activates glutamatergic circuits 
Inhibits GABAergic neurotransmission
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22
Q

Atomoxetine

A

Highly selective NE reuptake inhibitor
Atomoxetine also elevates DA levels in the prefrontal cortex
But not in the nucleus accumbens or the striatum
Nucleus accumbens mediates the euphoric properties (i.e., abuse liability) of the psychostimulants
Only first-line ADHD medication that has no abuse potential
Not a DEA Schedule II controlled substance
Only drug approved by the FDA to treat adult ADHD

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23
Q

Methylphenidate

A

treats ADHD

Enhances DA release and blocks reuptake

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24
Q

galanatamine

A

Treatment for Alzheimer

Inhibits AChE
Stimulates nicotinic cholinergic neurons to release more stored ACh
Should be taken cautiously in patients taking…
Antidepressants paroxetine, amitriptyline, fluoxetine and fluvoxamine
Drugs with anticholinergic side effects
These drugs may interfere with the elimination of galantamine from the body
Galantamine and other cholinesterase inhibitors can increase the risk of stomach ulcers

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25
Q

rivastigmine

A

Treatment for Alzheimer
Inhibits both AChE and BuChE

Causes more gastrointestinal problems and cause muscle weakness than other cholinesterase inhibitors

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26
Q

tacrine

A

Treatment for Alzheimer

Short half-life 
Needs to be given multiple times per day
Poor compliance
Many drug interactions 
Especially NSAIDs
May cause liver damage
Second-line therapy for AD
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27
Q

memantine

A

Treatment for Alzheimer

Useful in patients with moderate to severe AD
Mechanism of action
Antagonist at the NMDA subtype of glutamate (GLU) receptor
Found to help patients in the later stages of the disease maintain additional independence
Most common adverse effects of memantine are dizziness, headache, constipation and confusion

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28
Q

ginko biloba

A

May have a modest benefit for AD patients
Serious side effects (bleeding, seizures, coma) have been reported with commercial pharmaceutical-grade ginko biloba preparations

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29
Q

Nootropics

A

Derived from the Greek words nous, or “mind,” and trepein meaning “to bend/turn”
AKA: smart drugs, memory enhancers, cognitive enhancers, and intelligence enhancers

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30
Q

Eugeroics

A 
"Wakefulness Enhancers”
Examples
Modafinil (Provigil)
Armodafinil (Nuvigil)
Mechanism of action ?
Increased release of norepinephrine and dopamine
Elevates hypothalamic histamine levels
Lower abuse potential as compared to traditional stimulant drugs
DEA Schedule IV

FDA approved for
Narcolepsy
Shift work sleep disorder
Excessive daytime sleepiness associated with obstructive sleep apnea

31
Q

Halothane

A

Halogenated Hydrocarbon Inhalation Anesthetic

Advantages
Potent (MAC ranges from 0.7 - 0.9)
Rapid induction and recovery
Among the least expensive volatile anesthetic
Does not irritate larynx - no laryngospasm

Disadvantages
Inadequate analgesia and muscle relaxation
Depresses myocardium and baroreceptor reflexes
↓ Cardiac output
↓ Blood pressure
Sensitizes myocardium to catecholamines
↑ automaticity
Particularly in the presence of adrenergic agonists (e.g., epinephrine) which might be used to raise blood pressure
Increases cerebral blood flow and intracranial pressure
Respiratory depression
Potential for acute or chronic hepatic toxicity
1:35,000 patients develop “halothane hepatitis”
Symptoms include hepatic necrosis, fever, nausea and vomiting, biochemical abnormalities as seen in hepatitis
May progress to complete hepatic failure and death
May be due to significant liver metabolism (~20%)
Malignant hyperthermia

32
Q

Isoflurane

A

Halogenated Hydrocarbon Inhalation Anesthetic

Advantages
Potent
Induction in less than 10 minutes
Doesn’t sensitize the myocardium to catecholamines
Less hepatotoxicity and renal toxicity than halothane (may be related to lower rate of metabolism)

Disadvantages
Rarely arrhythmias
Pungent odor
Potential for malignant hyperthermia

33
Q

Desflurane

A

Halogenated Hydrocarbon Inhalation Anesthetic

34
Q

Sevoflurane

A

Halogenated Hydrocarbon Inhalation Anesthetic

Newest approved inhalation agent for use in North America (1996) 
High potency (low % of inspired gas) 
Low blood solubility 
Rapid onset – 5-10 min 
Rapid recovery – same day surgery
Almost perfect inhalation anesthetic
35
Q

Nitrous oxide

A

Halogenated Hydrocarbon Inhalation Anesthetic

Advantages
Low blood solubility (rapid onset)
Little effect on overall cardiovascular function
Second gas effect
Hastens anesthesia produced by more potent but more soluble inhalation anesthetics
Lowers MAC of other inhalation anesthetics
Mild to moderate analgesic activity

Disadvantages
MAC = 104% - can’t use as sole anesthetic agent
No muscle relaxing effect
Diffusion hypoxia if rapidly discontinued
During recovery, rapid transfer from blood to alveoli, displaces air
Lack of oxygen uptake – hypoxia

36
Q

Pentobarbital

A

Short-intermediate acting barb

Injectable Anesthetics

Unlike Phenobarbitol, increasing urinary pH with sodium bicarbonate is ineffective in treating toxicity, since this requires metabolism before renal excretion

37
Q

Thiopental

A

Injectable Anesthetics
Barbiturate

Mechanism of action
Facilitates GABA induced Cl- entry into neurons, leading to CNS depression

Rapid onset (sec) after iv administration and short action (min) allows quick recovery

Toxicity
anesthetic dose is between 50 and 75% of the LD50

38
Q

Propofol

A

Injectable Anesthetics
Rapid induction (50 seconds) and recovery (4-8 minutes) from anesthesia
May be given alone to maintain anesthesia or used for induction as part of balanced anesthesia technique
May result in injection site pain

39
Q

Etomidate

A

Injectable Anesthetic - best suited for induction of anesthesia, useful for short operative procedures, unsuitable as a single drug anesthetic

40
Q

Midazolam

A

Benzodiazepines

Mechanism of action
Facilitates GABA induced Cl- entry into neurons, leading to CNS depression

Characteristics
Less cardiovascular and respiratory depression than barbiturates
Most important characteristic is amnestic action
Insufficient for anesthesia when given alone
Used as induction agent prior to anesthesia

41
Q

Ketamine

A

Injectable Anesthetics

Dissociative anesthetic
Patient appears to be awake - eyes open
Unaware of environment and doesn’t feel pain

Pharm. Effects:
Principal drawback is the occurrence of emergence reactions (delirium and hallucinations)
Relatively high therapeutic index
Abuse - currently abused in the US

Single dose of ketamine significantly improved symptoms of depression in treatment resistant depressed patients in less than 2 hours and lasts at least one week

42
Q

Fentanyl

A

Opioid

High dose opioids
Analgesia
Anesthesia
Hemodynamic stability - good for patients with compromised myocardial function
Respiration must be maintained artificially and may be depressed into the postoperative period
Usually supplemented with inhalation anesthetic, benzodiazepine or propofol

43
Q

Sufentanil

A

Opioid

High dose opioids
Analgesia
Anesthesia
Hemodynamic stability - good for patients with compromised myocardial function
Respiration must be maintained artificially and may be depressed into the postoperative period
Usually supplemented with inhalation anesthetic, benzodiazepine or propofol

44
Q

Halogenated Hydrocarbon Inhalation Anesthetics

A

Examples - halothane, isoflurane, methoxyflurane (vet), sevoflurane

CNS effects
Decrease brain metabolic rate
Increase cerebral blood flow
Increase intracranial pressure

CV effects
Decreased myocardial contractility and stroke volume leading to lower arterial blood pressure
Sensitizes myocardium to catecholamines
↑ automaticity
Particularly in the presence of adrenergic agonists
Halothane > isoflurane, desflurane, sevoflurane > nitrous oxide

45
Q

Intravenous Anesthetics

A

Injectable anesthetics
Act faster
Best suited for induction of anesthesia
Useful for short operative procedures

Inhalation anesthetics
Maintain anesthesia for longer procedures

Muscle relaxation after IV anesthetics is poor
Unsuitable as a single drug anesthetic for many surgical procedures

46
Q

Desipramine

A

TCA
Block the reuptake of NE
by nerve terminals

47
Q

Imipramine

A

TCA

Block the reuptake of NE and 5-HT by nerve terminals

48
Q

Phenelzine

A

MAO INHIBITOR

49
Q

Fluoxetine

A

SSRI

50
Q

Sertraline

A

SSRI

51
Q

Citalopram

A

SSRI

52
Q

Escitalopram

A

SSRI

53
Q

Venlafaxine

A 
Selective serotonin and norepinephrine reuptake inhibitor (SNRI)
Blocks serotonin reuptake like SSRIs
Also blocks NE reuptake 
So, why isn’t this the same as TCAs?
Venlafaxine does NOT affect 
Adrenergic receptors
Histaminergic receptors 
Cholinergic receptors
Action of the TCAs on these receptors trigger majority of adverse effects

Raising the dose of venlafaxine improves efficacy due to secondary mechanisms of action

54
Q

Desvenlafaxine

A

Active metabolite of venlafaxine
Approved by the FDA in a once-daily formulation for the treatment of adults with major depressive disorder
No evidence that it is any more effective than venlafaxine
Patent for venlafaxine expired in 2010

55
Q

Lithium carbonate

A 
Effect in normal subjects - none
Effect in manic subjects 
Clinical use for over 50 years (30 years in US)
Therapeutic effect seen in 5-21 days 
Effective in 60-80 % of treated patients

Most likely involves effect on postsynaptic rather than presynaptic neuron
Interferes with the production and release of IP3 (phosphatdylinositol-4,5-bisphosphate) and DAG (diacyl glycerol)
May uncouple receptor recognition site from GTP-binding protein (G-protein) by competing with Mg++
May affect several cell or nuclear regulatory factors

Competes with sodium for reabsorption
Sodium deficiency (low sodium diet, diuretics) increases lithium toxicity

TOXICITY
No tolerance to excessive urination and thirst (must regulate H2O intake to prevent washout)
Fatigue, muscular weakness, slurred speech, ataxia, fine tremor of the hands

56
Q

Valproic Acid

A

Anticonvulsant
Good for non-rapid cycling bipolar disorder
Superior to lithium for rapid-cycling bipolar disorder
Anticonvulsants work better for acute manic episodes than for long-term management of bipolar disorder

57
Q

Carbamazepine

A

Anticonvulsant approved by the FDA for prophylaxis of bipolar disorder

58
Q

Quetiapine

A 
Atypical Antipsychotic
Mechanism of action
Blocks 5-HT2A subtype
DA antagonist action ????
Antimanic properties
Stabilizes mood
59
Q

Lurasidone

A

Atypical antipsychotic – 2010
Approved to treat bipolar depression – 2013
Mechanism of action
Central dopamine (D2) and serotonin (5-HT2A) receptor antagonism seem to be involved
Precise mechanism is unknown

60
Q

Tricyclic Antidepressants

A

Effect in normal subjects:
No stimulating or mood elevating effect
Sleepiness and light headedness

Effect in depressed subjects:
Elevation in mood only after 2-3 weeks

Block the reuptake of NE and/or 5-HT by nerve terminals

Orthostatic hypotension
Weight gain
Tachycardia and increased tendency for arrhythmias with high doses

Therapeutic index (TI = LD50 ÷ ED50) between 5-10 
Depressed patients should not be given more than one week supply of TCAs
Drug Interactions
Potentiates central depressants 
Alcohol
Anxiolytic-sedative-hypnotics
Opioids
Antimuscarinic effect may delay gastric emptying time 
↑ Inactivation of levodopa 
Decreases effectiveness when used to treat Parkinsonism
61
Q

Monoamine oxidase (MAO) inhibitors

A

Irreversibly blocks the oxidative deamination of monoamines (e.g., NE and 5-HT)

Changes in neurotransmitters
Occur within 24-48 hr
Clinical improvement usually takes 3+ weeks to begin

Low therapeutic index (less than 5)
Treat:
Symptomatically
Hospitalize 1 week (Why?) (IRREVERSIBLY blocks, needs time to make more)

Potentiates sympathomimetic amines
Particularly indirect acting amines such as tyramine
Dietary tyramine is completely metabolized by hepatic MAO
If patient has taken MAO inhibitor, tyramine enters systemic circulation

Combined effect of tyramine and MAO inhibitor:
Massive adrenergic stimulation
May result in a hypertensive crisis

62
Q

Selective Serotonin Reuptake Inhibitors (SSRIs)

A

WARNING:
SSRIs should not be used alone in bipolar disorder
Need to include a mood stabilizer to prevent rapid mood switch
May cause rapid onset of mania
Patients should be receiving prophylactic mood stabilizer therapy to prevent this from occurring

Depression
Other anxiety disorders

Nausea, diarrhea and weight loss
Stimulation - anxiety, nervousness, insomnia, sufficient to discontinue treatment
SSRIs are not sedating like TCAs or atypical antidepressants
33-50% of those that experience symptoms cannot continue treatment
Sexual dysfunction
MAY CAUSE SUICIDE!

MOA:

Selective inhibition of serotonin reuptake by CNS neurons
Serotonin receptor actions are much more complex than that of other neurotransmitters

5-HT2A – may contribute to clinical improvement seen with SSRIs

5-HT is released and can act…
Postsynaptically to trigger actions in an effector cell
Presynaptically on 5-HT1D autoreceptors to inhibit additional 5-HT release
NE from neighboring neurons act on a2 receptors to inhibit release of 5-HT (heteroreceptors)

63
Q

Phenobarbital

A

Long acting Barb
(slow and partial metabolism)

Phenobarbital is selectively anticonvulsant
The remainder of the barbiturates are relatively unselective in their depression of the CNS

Less lipid soluble (phenobarbital) - 20 min to sleep onset

An overdose of a phenobarbital can be treated by administering sodium bicarbonate intravenously to elevate urinary pH

64
Q

Triazolam

A

benzo

65
Q

Flurazepam

A

Benzo

plasma half-life = 2 -3 hr.; half-life of active metabolite is >50 hr

66
Q

Alprazolam

A

Benzo

67
Q

Diazepam

A

benzo

Preanesthetic medication

68
Q

Lorazepam

A

Benzo

69
Q

Flumazenil

A

Benzodiazepine receptor antagonist

Administered intravenously

Antagonizes sedation, impaired recall, impaired psychomotor function, and respiratory depression

Reverses effects of benzodiazepines, zolpidem, zapelon (see below) but not barbiturates or ethanol

70
Q

Zolpidem

A

Non-Benzodiazepine Benzodiazepine-Receptor Agonists

Mechanism of action
New drugs interact with benzodiazepine binding site on GABAA receptor
Benzodiazepines bind to all GABAA receptor subtypes
Selectively bind to certain subtypes of the receptor

Advantages
Rapid onset
Short duration of action (no residual effects upon wakening)
Slow tolerance development

71
Q

Ramelteon

A 
Mechanism of action
Suprachiasmatic nucleus (SCN) 
Body's "master clock" 
Regulates 24-hour, or circadian, rhythms 
Includes sleep-wake cycle

Ramelton is an agonist at the melatonin MT1 and MT2 receptors located in the brain’s SCN

Adverse effects
Overall adverse events occur at rates generally comparable to placebo
NO evidence of formation of physical dependence or abuse potential, and the drug is not a controlled substance

Approved for long term use in adults

72
Q

Propranolol

A

Useful in treating chronic anxiety, panic attacks and debilitating anxiety
Blocks autonomic signs
Less effective than BZs for anxiety and antidepressants for panic attacks

73
Q

Melatonin

A

Classified as a “dietary supplement” rather than as a drug
Not regulated by FDA
Significant variation in dosages (2-3 mg vs endogenous levels of 0.1 - 0.3 mg) depending on brand
Clinical effectiveness is unclear - doses above 1 mg may disturb sleep

74
Q

Non-Benzodiazepine Benzodiazepine-Receptor Agonists

A

Mechanism of action
New drugs interact with benzodiazepine binding site on GABAA receptor
Benzodiazepines bind to all GABAA receptor subtypes
Selectively bind to certain subtypes of the receptor

Advantages
Rapid onset
Short duration of action (no residual effects upon wakening)
Slow tolerance development

Neuro Mix Bag (8 decks)

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