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Supp Neuro 5 > All Drugs (by name) > Flashcards

All Drugs (by name) Flashcards

1
Q

Amphetamine

A

Class: sympathomimetic

Low dose:
Increased release of NE and DA
↑ amount of transmitter that can act on postsynaptic receptors

Medium dose:
Blocks NE and DA reuptake
Further ↑NE or DA levels

High dose:
Inhibits monoamine oxidase (MAO)
↑ neurotransmitter levels even higher

Immediate release: Dexedrine

Sustained release: Dexedrine Spansules, Adderall XR

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2
Q

D-Amphetamine

A

Class: sympathomimetic

Enhances DA release and blocks reuptake

Enhances NE release (d,1-amphetamine)

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3
Q

Methamphetamine

A

Class: sympathomimetic

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4
Q

Methylphenidate

A

Class: sympathomimetic

Enhances DA release and blocks reuptake

Immediate release: Ritalin

Sustained release: Concerta, Metadate CD

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5
Q

Cocaine

A

Class: sympathomimetic

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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6
Q

MDMA

A

Class: sympathomimetic

Derived from methamphetamine

Increases lipophilicity–Very rapid entry into the brain

Stimulates release and inhibits reuptake of
Epinephrine
Norepinephrine
Dopamine

Unlike amphetamines
Directly stimulates 5HT21A autoreceptors
Stimulates the release of serotonin and inhibits its reuptake

MDMA also directly affects other neurotransmitters
Histamine
GABA
Acetylcholine
Dopamine receptors
Binds to the norepinephrine transporter protein

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7
Q

Theobromine

A

Class: Xanthines

Proposed MOA:
Translocation of intracellular Ca2+ from the sarcoplasmic reticulum
Inhibition of phosphodiesterase
Elevated levels of the second messenger cAMP
Nonselective adenosine receptor antagonist
Inhibit sleepiness-inducing adenosine

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8
Q

THeophylline

A

Class: Xanthines

greater potency than caffeine

Proposed MOA:
Translocation of intracellular Ca2+ from the sarcoplasmic reticulum
Inhibition of phosphodiesterase
Elevated levels of the second messenger cAMP
Nonselective adenosine receptor antagonist
Inhibit sleepiness-inducing adenosine

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9
Q

Caffeine

A

Class: Xanthines

Proposed MOA:
Translocation of intracellular Ca2+ from the sarcoplasmic reticulum
Inhibition of phosphodiesterase
Elevated levels of the second messenger cAMP
Nonselective adenosine receptor antagonist
Inhibit sleepiness-inducing adenosine

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10
Q

Modafinil

A

Class: Eugeroic “wakefullnes promoter”

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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11
Q

Armodafinil

A

Class: Eugeroics “wakefulness promoter”

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12
Q

Atomoxetine

A

Highly selective NE reuptake inhibitor

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

Increased Ach release only when both a1-NE receptors AND D1-DA receptors simultaneously activated in prefrontal cortex (improved working memory)

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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13
Q

Rivastigmine

A

Inhibits BOTH AchE and BuChE= increased Ach

Used to treat Alzheimer Disease

Side effects: more GI probs than other cholinesterase inhibitors

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14
Q

Tacrine

A

AchE inhibitor = increased Ach

Tx for: Alzheimer

short half life

hepatotoxic

second line for Alz

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15
Q

Galantamine

A

AchE inhibitor

AND stimulates nicotinic cholinergic neurons to release more Ach

Carefull with drugs w/ anticholinergic side fx

cross rx with NSAIDS

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16
Q

Memantine

A

NMDA antagonist (GLU receptor)

Tx for: moderate to severe Alz

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17
Q

Halothane

A

Class: Inhaled 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
May be due to significant liver metabolism (~20%)

Malignant hyperthermia
Potentially fatal hypermetabolic reaction in skeletal muscle
Cool patient
treat with dantrolene – blocks Ca release from sarcolplasmic reticulum in muscle cells

Shivering during recovery - mechanism is unknown

Prolonged drowsiness for several hours after recovery

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18
Q

Isoflurane

A

Inhaled 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

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19
Q

Desflurane

A

Inhaled anesthetic

MAC of 7.25 (highish)

Irritant odor

Low blood solubility (0.4)–fast onset

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20
Q

Sevoflurane

A 
New approved inhalation agent (1996) for use in North America 
High potency (low % of inspired gas) 
Low blood solubility (0.7)
Rapid onset – 5-10 min 
Rapid recovery – same day surgery
Pleasant odor
Almost perfect inhalation anesthetic
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21
Q

Nitrous oxide

A

Only inhalation anesthetic that is a gas

Advantages
Low blood solubility (rapid onset)
Little effect on overall cardiovascular function
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

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22
Q

Pentobarbital

A

Class: 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

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23
Q

Thiopental

A

Class: 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

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24
Q

Propofol

A

Class: sedative?

Rapid induction (50 seconds) and recovery (4-8 minutes) from anesthesia

given alone to maintain anesthesia or used for induction as part of balanced anesthesia technique

Must be given as emulsion patients generally awaken from anesthesia feeling more “clear headed” and are not nauseous (anti-emetic action)

Most significant respiratory effect is apnea (22-45%)

May result in injection site pain

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25
Q

Etomidate

A

GABAa modulator (increased Cl- entry–>hyperpolerization)

short-acting intravenous anaesthetic agent used for the induction of general anaesthesia and sedation

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26
Q

Midazolam

A

Versed

Class: Benzodiazapines

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

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

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27
Q

Ketamine

A

Class: dissociative agent?

Structurally and pharmacologically related to phencyclidine (PCP)

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

Pharmacological effects
Anesthetic, analgesic, amnestic and sedative

Airway reflexes and respiration is maintained
Cardiovascular system is not depressed and may actually be stimulated (↑ HR and BP) – ideal for patients with unstable CV function

Mechanism of action – NMDA Glutamate receptors ???

Rapid onset of action (1-2 min) when given intravenously or intramuscularly

Relatively short duration of action (approximately 20 min)

Principal drawback is the occurrence of emergence reactions (delirium and hallucinations)

Relatively high therapeutic index

Abuse - currently abused in the US

Depression treatment????

28
Q

Fentanyl

A

Class: opiod

High dose opioid
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

29
Q

Sufentanyl

A

Class: opiod

High dose opioid
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

30
Q

Desipramine

A

Class: Tricyclic Antidepressant

Blocks reuptake of NE

31
Q

Imipramine

A

Class: Tricyclic Antidepressant

Blocks reuptake of NE and 5HT

32
Q

Phenelzine

A

Class: MAO inhibitor

tx: depression

Non-selectively inhibits both MAO-A and B
-irreversibly blocks deamination of monoamines

increases DA, NE, 5HT

Low therapeutic index

***don’t mix with SSRIs

Watch out food tyramine rich foods (aged cheese, red wine, beer, bananas)

33
Q

Fluoxetine

A

Prozac

Class: SSRI

5-HT is released and can act…

Postsynaptically to trigger actions in an effector cell

Presynaptically on 5-HT1 autoreceptors to inhibit additional 5-HT release

Reuptake process can remove 5-HT from the synapse
This is blocked by SSRIs

34
Q

Sertraline

A

Class: SSRI

5-HT is released and can act…

Postsynaptically to trigger actions in an effector cell

Presynaptically on 5-HT1 autoreceptors to inhibit additional 5-HT release

Reuptake process can remove 5-HT from the synapse
This is blocked by SSRIs

35
Q

Escitalopram

A

Class: SSRI

5-HT is released and can act…

Postsynaptically to trigger actions in an effector cell

Presynaptically on 5-HT1 autoreceptors to inhibit additional 5-HT release

Reuptake process can remove 5-HT from the synapse
This is blocked by SSRIs

36
Q

Venlafaxine

A

Effexor

Class: Atypical (Dual/mixed action) Antidepressant

Serotonin-norepinephrine reuptake inhibitor (SNRI)
Blocks serotonin reuptake like SSRIs
Also blocks NE reuptake

How different than TCAs?
Venlafaxine does NOT affect 
  Adrenergic receptors
  Histaminergic receptors 
  Cholinergic receptors
       ***Action of the TCAs on these receptors trigger majority of adverse effects

Contraindicated in patients on MAOIs, and vice versa

***raising dose improves efficacy due to secondary MOAs

37
Q

Mirtazapine

A

Cymbalta

Class: Atypical (Dual/mixed action) Antidepressant

Blocks presynaptic a2 receptors

  • On adrenergic neurons (autoreceptors)
  • On serotonergic neurons (heteroceptors)

Blocking a2 receptors increases NE and 5-HT levels

38
Q

Lithium carbonate

A

Treats Bipolar Disorder

Mechanism of action is unknown

  • 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)
  • Can inhibit norepinephrine-sensitive adenylyl cyclase
  • May uncouple receptor recognition site from GTP-binding protein (G-protein) by competing with Mg++
  • May affect several cell or nuclear regulatory factors
  • Working hypothesis: alters gene expression implicated in long-term neuroplastic events that could underlie long-term mood stabilization

***low therapeutic index

39
Q

Valproic acid

A

Anticonvulsant

tx of Bipolar disorder

better than Lithium for rapid cycle BD

can be combined with Li after failed monotherapy

40
Q

Carbamazepine

A

Anticonvulsant

Prophylactic tx of Bipolar disorder

41
Q

Phenobarbital

A

Class: Barbiturate

increase DURATION of GABA-gated Cl- channel openings

at high conc, may also directly activate chloride channels

also depress excitatory GLU by binding AMPA receptors

ability to induce full surgical anesthisia

more pronounced CNS depression –>low margin of safety

effective tx of tonic-clonic seizures

respiration fx are dose related

42
Q

Diazapam

A

Class: Benzodiazapine

Enhance GABA’s effects allosterically without directly activating GABAA receptors or opening the associated chloride channels.

Increase in the FREQUENCY of chloride channel-opening events.

Unlike barbiturates, benzodiazepines have little impact on hepatic drug-metabolizing enzyme activity with continuous use.

Also exert dose-dependent anterograde amnesic effects (inability to remember events occurring during the drug’s duration of action)

43
Q

Lorazapam

A

Class: Benzodiazapine

Enhance GABA’s effects allosterically without directly activating GABAA receptors or opening the associated chloride channels.

Increase in the FREQUENCY of chloride channel-opening events.

Unlike barbiturates, benzodiazepines have little impact on hepatic drug-metabolizing enzyme activity with continuous use.

Also exert dose-dependent anterograde amnesic effects (inability to remember events occurring during the drug’s duration of action)

44
Q

Triazolam

A

Class: Benzodiazapine

Enhance GABA’s effects allosterically without directly activating GABAA receptors or opening the associated chloride channels.

Increase in the FREQUENCY of chloride channel-opening events.

Unlike barbiturates, benzodiazepines have little impact on hepatic drug-metabolizing enzyme activity with continuous use.

Also exert dose-dependent anterograde amnesic effects (inability to remember events occurring during the drug’s duration of action)

45
Q

Alprazolam

A

Class: Benzodiazapine

Enhance GABA’s effects allosterically without directly activating GABAA receptors or opening the associated chloride channels.

Increase in the FREQUENCY of chloride channel-opening events.

Unlike barbiturates, benzodiazepines have little impact on hepatic drug-metabolizing enzyme activity with continuous use.

Also exert dose-dependent anterograde amnesic effects (inability to remember events occurring during the drug’s duration of action)

46
Q

Flumazenil

A

Benzo binding site ANTAGONIST (doesn’t block barbiturate function)

tx of benzo OD

47
Q

Buspirone

A

Selective anxiolytic effects
Relieves anxiety without significant sedative or hypnotic effects
No anticonvulsant or muscle relaxant properties.
Buspirone does not interact directly with GABAergic systems

Mechanism?
Partial agonist at brain 5-HT1A receptors
Also has affinity for brain dopamine D2 receptors

Minimal abuse liability

Anxiolytic effects may take more than a week to become established

unsuitable for management of acute anxiety states

Used in generalized anxiety states but is less effective in panic disorders.

Less psychomotor impairment than benzodiazepines (does not affect driving skills)

48
Q

Zolpidem

A

Ambien

Mechanism of action
New drugs interact with benzodiazepine binding site on GABAA receptor
Non-benzo chemical structure
Benzodiazepines bind to all GABA-A receptor subtypes
These selectively bind to certain subtypes of the receptor

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

49
Q

Ramelteon

A

Ramelteon (Rozerem), a novel hypnotic drug specifically useful for patients who have difficulty in falling asleep

Melatonin receptors are involved in maintaining circadian rhythms underlying the sleep-wake cycle

Ramelteon is an agonist at MT1 and MT2 melatonin receptors located in the suprachiasmatic nuclei (“master clock”) of the brain

No direct effects on GABAergic neurotransmission in the CNS

No rebound insomnia or significant withdrawal symptoms

Minimal potential for abuse, regular use does not result in dependence

Adverse effects of ramelteon include dizziness, drowsiness, fatigue, and endocrine

50
Q

Chlorpromazine

A

Thorazine

Class: First Gen Antipsychotic

FGA block D2 in 4 out of 4 Pathways
• Decreasing DA activity has been shown to increase 5-HT
• Increase in 5-HT inhibits DA release

  • Mesolimbic
  • Blocking D2 decreases positive symptoms

• Mesocortical
• Blocking D2 receptors here does not improve negative symptoms, in
fact can worsen negative symptoms (increases in 5-HT?)

  • Nigrostriatal
  • Blocking D2 receptors here causes Parkinsonism (EPSE)
  • Tuberoinfundibular
  • DA inhibits prolactin
  • Blocking D2 receptors here causes:
  • Galactorrhea
  • Amenorrhea
  • Sexual dysfunction
51
Q

Halperidol

A

Haldol

Class: First Gen Antipsychotic

FGA block D2 in 4 out of 4 Pathways
• Decreasing DA activity has been shown to increase 5-HT
• Increase in 5-HT inhibits DA release

  • Mesolimbic
  • Blocking D2 decreases positive symptoms

• Mesocortical
• Blocking D2 receptors here does not improve negative symptoms, in
fact can worsen negative symptoms (increases in 5-HT?)

  • Nigrostriatal
  • Blocking D2 receptors here causes Parkinsonism (EPSE)
  • Tuberoinfundibular
  • DA inhibits prolactin
  • Blocking D2 receptors here causes:
  • Galactorrhea
  • Amenorrhea
  • Sexual dysfunction
52
Q

Thioridazine

A

Mellaril

Class: First Gen Antipsychotic

FGA block D2 in 4 out of 4 Pathways
• Decreasing DA activity has been shown to increase 5-HT
• Increase in 5-HT inhibits DA release

  • Mesolimbic
  • Blocking D2 decreases positive symptoms

• Mesocortical
• Blocking D2 receptors here does not improve negative symptoms, in
fact can worsen negative symptoms (increases in 5-HT?)

  • Nigrostriatal
  • Blocking D2 receptors here causes Parkinsonism (EPSE)
  • Tuberoinfundibular
  • DA inhibits prolactin
  • Blocking D2 receptors here causes:
  • Galactorrhea
  • Amenorrhea
  • Sexual dysfunction
53
Q

Fluphenazine

A

Prolixin

Class: First Gen Antipsychotic

FGA block D2 in 4 out of 4 Pathways
• Decreasing DA activity has been shown to increase 5-HT
• Increase in 5-HT inhibits DA release

  • Mesolimbic
  • Blocking D2 decreases positive symptoms

• Mesocortical
• Blocking D2 receptors here does not improve negative symptoms, in
fact can worsen negative symptoms (increases in 5-HT?)

  • Nigrostriatal
  • Blocking D2 receptors here causes Parkinsonism (EPSE)
  • Tuberoinfundibular
  • DA inhibits prolactin
  • Blocking D2 receptors here causes:
  • Galactorrhea
  • Amenorrhea
  • Sexual dysfunction
54
Q

Clozapine

A

Clozaril

Class: Atypical/Second Gen Antipsychotic

Effective for both positive and negative symptoms
o No Parkinson’s disease like side effects

o SGA mechanism of action
o Block D2 receptors AND 5-HT2A receptors

  • No D2 activation
  • DA release into the synapse (not inhibited by 5-HT anymore)

No EPSE

***AGRANULOCYTOSIS

55
Q

Risperidone

A

Risperidal

Class: Atypical/Second Gen Antipsychotic

Effective for both positive and negative symptoms
o No Parkinson’s disease like side effects

o SGA mechanism of action
o Block D2 receptors AND 5-HT2A receptors

  • No D2 activation
  • DA release into the synapse (not inhibited by 5-HT anymore)

**EPSE and hypotension at higher doses

56
Q

Olanzapine

A

Zyprexa

Class: Atypical/Second Gen Antipsychotic

Effective for both positive and negative symptoms
o No Parkinson’s disease like side effects

o SGA mechanism of action
o Block D2 receptors AND 5-HT2A receptors

  • No D2 activation
  • DA release into the synapse (not inhibited by 5-HT anymore)
57
Q

Quetiapine

A

Seroquel

Class: Atypical/Second Gen Antipsychotic

Effective for both positive and negative symptoms
o No Parkinson’s disease like side effects

o SGA mechanism of action
o Block D2 receptors AND 5-HT2A receptors

  • No D2 activation
  • DA release into the synapse (not inhibited by 5-HT anymore)
58
Q

Ziprasidone

A

Geodon

Class: Atypical/Second Gen Antipsychotic

Effective for both positive and negative symptoms
o No Parkinson’s disease like side effects

o SGA mechanism of action
o Block D2 receptors AND 5-HT2A receptors

  • No D2 activation
  • DA release into the synapse (not inhibited by 5-HT anymore)

**less weight gain

59
Q

Aripiprazole

A

Abilify

Class: Atypical/Second Gen Antipsychotic

Effective for both positive and negative symptoms
o No Parkinson’s disease like side effects

o SGA mechanism of action
o Block D2 receptors AND 5-HT2A receptors

  • No D2 activation
  • DA release into the synapse (not inhibited by 5-HT anymore)

**less weight gain

60
Q

Carbamazepine

A

Indication: partial (focal) and secondarily generalized tonic-clonic seizures; (but may make absence or myoclonic seizures worse.)

stabilizes “inactivated” state of VG Na+ channels –> decrease in repetitive firing

Adverse Effects: Mild leukopenia and hyponatremia common.

61
Q

Ethosuximide

A

Indication: Primary tx for Absence (generalized, non-convulsive) seizures; ethosuximide is NOT effective in generalized tonic-clonic or partial (focal) seizures.

Bocks VG T-type dependent calcium channel, disrupting pacemaker activity; Works on thalamic neurons, which may stop them from generating rhythmic cortical discharges that occur during absence seizures

Adverse effects: behavorial changes, Psychotic behavior, systemic lupus erythematosus (SLE)

62
Q

Levetiracetam

A

Indication: primary therapy for focal seizures, primary or secondary generalized tonic-clonic seizures and myoclonic seizures.

Affects synaptic vesicle protein SV2A, resulting in decreased glutamate release but increased GABA release

Adverse effects: behavioral changes, psychosis, especially in patients with underlying psych diagnoses.

***NO drug interactions

63
Q

Topiramate

A

Indications: focal and primarily generalized tonic clonic seizures

Increased inactivation of VG Na+ channels

  • blocks presynaptic (N; P/Q) VG Ca2+ channels
  • enhances GABAa-receptor currents (not via BZD receptor)
  • limits activation of AMPA-kainate subtypes of the glutamate receptor

Adverse effects: Psychomotor slowing

64
Q

Phenytoin

A

Indication: partial and secondarily generalized tonic-clonic seizures, but is no longer considered a drug of first choice

Prolongs Inactivation phase of v-gated Na+ channels

prevents rapid firing of action potentials

decreased glutamate release

Adverse effects: Nystagmus common; Cerebellar atrophy has been reported with long-term use and after acute intoxication. Gingival hyperplasia, coarsening of facial features and hirsutism can also occur.

65
Q

Valproic acid

A

Indication: works for most! Drug of choice for primarily generalized tonic-clonic seizures

Decreases repetitive firing, potentially via multiple mechanisms: block of VG Na+, NMDA receptor block, decreases GABA reuptake (GAT-1); reduces the flow of Ca2+ through T-type Ca2+ channels

Adverse effects: Alopecia, appetite stimulation, weight gain. Elevation of hepatic transaminases (indicator or liver damage)

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