All Drugs (by name) Flashcards

(65 cards)

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
Etomidate
GABAa modulator (increased Cl- entry-->hyperpolerization) short-acting intravenous anaesthetic agent used for the induction of general anaesthesia and sedation
26
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
27
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????
28
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
29
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
30
Desipramine
Class: Tricyclic Antidepressant Blocks reuptake of NE
31
Imipramine
Class: Tricyclic Antidepressant Blocks reuptake of NE and 5HT
32
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)
33
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
34
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
35
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
36
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
37
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
38
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
39
Valproic acid
Anticonvulsant tx of Bipolar disorder better than Lithium for rapid cycle BD can be combined with Li after failed monotherapy
40
Carbamazepine
Anticonvulsant Prophylactic tx of Bipolar disorder
41
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
42
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)
43
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)
44
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)
45
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)
46
Flumazenil
Benzo binding site ANTAGONIST (doesn't block barbiturate function) tx of benzo OD
47
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)
48
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
49
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
50
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
51
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
52
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
53
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
54
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
55
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
56
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)
57
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)
58
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
59
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
60
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.
61
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)
62
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
63
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
64
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.
65
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)