All Drugs (by name) Flashcards
Amphetamine
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
D-Amphetamine
Class: sympathomimetic
Enhances DA release and blocks reuptake
Enhances NE release (d,1-amphetamine)
Methamphetamine
Class: sympathomimetic
Methylphenidate
Class: sympathomimetic
Enhances DA release and blocks reuptake
Immediate release: Ritalin
Sustained release: Concerta, Metadate CD
Cocaine
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
MDMA
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
Theobromine
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
THeophylline
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
Caffeine
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
Modafinil
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
Armodafinil
Class: Eugeroics “wakefulness promoter”
Atomoxetine
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
Rivastigmine
Inhibits BOTH AchE and BuChE= increased Ach
Used to treat Alzheimer Disease
Side effects: more GI probs than other cholinesterase inhibitors
Tacrine
AchE inhibitor = increased Ach
Tx for: Alzheimer
short half life
hepatotoxic
second line for Alz
Galantamine
AchE inhibitor
AND stimulates nicotinic cholinergic neurons to release more Ach
Carefull with drugs w/ anticholinergic side fx
cross rx with NSAIDS
Memantine
NMDA antagonist (GLU receptor)
Tx for: moderate to severe Alz
Halothane
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
Isoflurane
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
Desflurane
Inhaled anesthetic
MAC of 7.25 (highish)
Irritant odor
Low blood solubility (0.4)–fast onset
Sevoflurane
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
Nitrous oxide
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
Pentobarbital
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
Thiopental
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
Propofol
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
Etomidate
GABAa modulator (increased Cl- entry–>hyperpolerization)
short-acting intravenous anaesthetic agent used for the induction of general anaesthesia and sedation
Midazolam
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
Ketamine
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????
Fentanyl
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
Sufentanyl
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
Desipramine
Class: Tricyclic Antidepressant
Blocks reuptake of NE
Imipramine
Class: Tricyclic Antidepressant
Blocks reuptake of NE and 5HT
Phenelzine
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)
Fluoxetine
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
Sertraline
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
Escitalopram
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
Venlafaxine
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
Mirtazapine
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
Lithium carbonate
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
Valproic acid
Anticonvulsant
tx of Bipolar disorder
better than Lithium for rapid cycle BD
can be combined with Li after failed monotherapy
Carbamazepine
Anticonvulsant
Prophylactic tx of Bipolar disorder
Phenobarbital
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
Diazapam
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)
Lorazapam
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)
Triazolam
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)
Alprazolam
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)
Flumazenil
Benzo binding site ANTAGONIST (doesn’t block barbiturate function)
tx of benzo OD
Buspirone
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)
Zolpidem
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
Ramelteon
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
Chlorpromazine
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
Halperidol
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
Thioridazine
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
Fluphenazine
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
Clozapine
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
Risperidone
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
Olanzapine
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)
Quetiapine
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)
Ziprasidone
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
Aripiprazole
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
Carbamazepine
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.
Ethosuximide
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)
Levetiracetam
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
Topiramate
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
Phenytoin
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.
Valproic acid
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)
