Drugs Test 5 Flashcards
Benzedrine
Amphetamine
MOA: Increased release of NE and DA (low dose) Blocks NE and DA reuptake (medium dose) Inhibits MAO (high dose)
Therapeutic uses: ADHD, narcolepsy, rarely fatigue, never weight loss.
Behavioral effects: Decreased fatigue; Increased wakefulness and alertness; restlessness
Other CNS effects: Stimulation of medullary respiratory sydrome (increase breath rate and depth). Decreased food consumption.
Other non CNS effects: Increased systolic and diastoic BP (reflex decrease in HR) Arrhythmias at high dose.
Toxicity: Headaches, palpitations, hyperthermia, dizziness, agitation, confusion (treat with antipsychotics/ acidification of urine)
Treatment = AAAA = Amphetamines –> Acidify Urine –> Anitpsychotics –> Alpha-Blockers.
Chronic abuse: Vivid hallucinations (ddx vs psychoses via drug screen. Symptoms resolve in 7-10 days.
Tolerance: Develops to appetite and mood.
Dependence: Psychological (mainly)
Cocaine
MOA block reuptake of NE (motor) and DA (euphoria)
Uses: Local anesthesia.
Toxicity: cardiac arrrhthmias, coronary and cerebral thrombosis. Impairs UTERO BRAIN DEVELOPMENT.
Tolerance: May develop, but same dose for same effect
Dependence: Psychological; Physical is disputed
MDMA
MOA: Stimulates release and inhibits reuptake of Epi, NE, and DA. Very rapid entry into the brain due to lipophilicity. Unlike amphetamines it directly stimulates 5HT-2(1a) receptor.
Effects: CNS stimulant and empathogen
Possible use for as empathogen to treat PTSD?
Bath Salts
Very dangerous uncontrolled drug that causes agitation, hallucination, paranoia, etc.
Caffeine
MOA: Not well understood. Translocation of of intracelluar Ca from the sarcoplasmic retic? Inhibition of phosphodiesterase? Nonselective adenosine receptor antagonist?
Actions: Stimulates cerebral cortex. Clearer thoughts. Less fatigue, Improved dexterity. Increased respiration.
Uses: Anti-asthmatic = Smooth muscle relaxant
Anti Migraine = Increase cerebral vascular resistance
CHF? = Cardiac stim; dialation of coronaries; increased O2 demand by heart.
Toxicities: hyperreflexia (high doses); Increased HR and contractility; diuretic, smooth muscle relaxant,
Tolerance: some developetolerance to sleep disrupting effects, withdrawal symptoms (headache, irritability, drowsiness etc.)
Modafinil
Provigil
MOA: Increase DA, NE, 5-HT, Histamine, Glutamine, Inhibits GABA
Uses: Narcolepsy, Shift work sleep disoreder, Excessive daytime sleepiness, MS, ADHD (mainly adult), many off-label uses
Side effects: Headache, nausea, insomnia, lack of appetite, anxiety, severe dermatologic rxns.
Methylphenidate
Ritalin = Immediate release Concerta = sustained release
Enhances DA release and blocks reuptake.
Low concentrations: Activate areas of prefrontal and limbic cortex to improve attention, diminish impulsivity, decrease hyperactivity, and calming effect
High concentrations: motor arousal
Atomoxetine
MOA: Highly selective NE reuptake inhibitor. Elevates DA in frontal cortex.
*Only first-line ADHD medication that has no abuse potential. Only drug approved to treat adult ADHD
Adverse Effects: difficulties in working memory.
Rivastigmine
MOA: Inhibits AChE and BuChe
Administered BID
Adverse effects: more GI problems and muscle weakness than other anticholinesterases.
Used to treat early AD
Tacrine
MOA: Centrally acting anticholinesterase and indirect cholinergic agonist
Short half life
Many drug interactions - especially NSAIDs, and may cause liver damage.
Second-line therapy for AD
Galantamine
MOA: Inhibits AChE and stimulates nicotinic cholinergic neurons to release more stored ACh.
Interactions: Antidepressants, drugs with anticholinergic side effects. NSAIDs (stomach ulcers)
Memantadine
MOA: Antagonist at the NMDA receptor.
Useful for later stage patients. (moderate to sever AD)
Adverse effects: dizziness, headache, constipation, and confusion.
Ginko Biliboa
MOA: unknown. May have modest benefits for AD patients.
Serious side effects. (likely not worth the risk)
Halothane
MOA: actions on multiple ion channels, which ultimately depresses nerve conduction, breathing, cardiac contractility. Binds to potassium channels in cholinergic neurons (immobilizing effects).
Advantages: potent, rapid induction and recovery, cheap, non-volatile, no laryngospasm.
Disadvantages: Inadequate analgesia and muscle relaxation. Cardiac depression. Sensitizes myocardium to epi., respiratory depression.
Highest blood solubility and lowest MAC.
Acute hepatic toxicity and Malignant hypothermia.
Isoflurane
MOA: actions on multiple ion channels, which ultimately depresses nerve conduction, breathing, cardiac contractility. Binds to potassium channels in cholinergic neurons (immobilizing effects).
Advantages: potent (low MAC), fast induction (not very soluble), less cardiac sensitization and hepatotoxicity
Disadvantages: Rarely arrhthmias, malignant hyperthermia
Sevoflurane
MOA: actions on multiple ion channels, which ultimately depresses nerve conduction, breathing, cardiac contractility. Binds to potassium channels in cholinergic neurons (immobilizing effects).
Advantages: High potency (low MAC), Rapid onset (Low blood solubility)
“almost perfect inhaled anesthetic”
Nitrous Oxide
Only inhalation anesthetic that is a gas.
Advantages: Very low blood solubility (rapid onset), little CV affects, Second gas effect, mild to moderate analgesia
Disadvantages: MAC = 104% (can’t be used alone), No muscle relaxing effect, Diffusion hypoxia if rapidly discontinued
Thiopental
Barbituate - intravenous anesthetic
MOA: Facilitates GABA induced Cl entry into neurons leading to CNS depression. (Increase duration of channel openings)
Rapid onset and short action.
Toxicity: Anesthetic dose is between 50 and 75% of LD50.
Diazepam (Also Lorazopam, Triazolam, and Alprazolam)
“Valium”
Benzodiazapines- intravenous anesthetic; Also anxiolytic, sedative, and hypnotic. Anticonvulsive as well.
First line anti-seizure for status epilepticus (IV) or any other active seizures.
MOA: Facilitates GABA induced Cl entry into neurons via allosteric modification leading to CNS depression. (increase frequency of channel openings)
Characteristics: Less CV and respiratory depression than barbs. Insufficient for anesthesia alone (used as induction agent)
Most important action for anesthesia is AMNESTIC action. Anterograde amnesia is also side effect of benzos.
More rapid oral absorbtion than other benzos.
Hepatic metabolism. Many have pharmacologically active metabolites, some with long half lifes.
Tolerance is pharmacodynamic. (no induction of CYP 450)
Dependence: mental and physical (withdrawal) dependence
Toxic doses can reversibly depress excitable tissues (myocardial contractility, vascular tone –> circulatory collapse)
Propofol
Rapid induction and recovery from anesthesia.
MOA: Unknown; possibly GABAergic or Na+ blocker. Possible Opiod link.
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
Abuse potential = very risky.
Ketamine
Dissociative anesthetic. Patient appears awake.
MOA: NMDA antagonist
Pharmacological effects: anesthetic, analgesic, amnestic, and sedative. No CV depression or respiratory probs.
Adverse effects: Delirium and hallucinations after emergence. Abuse (Special K)
High therapeutic index
Possible depression treatment.
Fentanyl
Potent opioid used in anesthesia for analgesia and anesthesia. Usually supplemented with inhalation anesthetic, benzo, or propofol.
Notes: Hemodynamically stable (good for CV patients). Respiration must be maintained artificially and may be depressed post-op.
Sulfentyl
Potent opioid used in anesthesia for analgesia and anesthesia. Usually supplemented with inhalation anesthetic, benzo, or propofol.
Notes: Hemodynamically stable (good for CV patients). Respiration must be maintained artificially and may be depressed post-op.
Midazolam
Versed
Benzodiazapene- intravenous anesthetic
MOA: Facilitates GABA induced Cl entry into neurons leading to CNS depression. (increase frequency of channel openings)
Characteristics: Less CV and respiratory depression than barbs. Insufficient for anesthesia alone (used as induction agent)
Most important action is AMNESTIC action
Haloperidol
Typical Antipsychotic
Blocks Dopamine D2 receptor decreasing dopamine caused psychoses.
Only effective vs positive symptoms and in some instances worsens negative symptoms (increased 5-HT)
Side effects: Big one is tardive dyskinesia (abnormal facial movements/twitches that persist even after stopping the drug.) Parkinsonism (blocking Nigrostriatal pathway). Galactorrhea, Amenorrhea, and Sexual dysfunction (blocking tuberoinfundibular pathyway). Negative symptoms due to Mesocortical overactivity.
Olanzapine
Atypical antipsychotic
Works in three areas:
- ) Blocking Dopamine receptors
- ) Blocking 5-HT receptors
- ) Blocks reuptake of Glutamate
Side effects: Weight gain and sedation
Risperidone
Most common used. First choice.
Atypical Antipsychotic. Effective for both positive and negative symptoms.
- ) Blocking Dopamine receptors
- ) Blocking 5-HT receptors
- ) Blocks reuptake of Glutamate
Useful for motor and pschiatric problems.
Side effects: Weight gain (most common reason for poor compliance). Increase in type 2 DM.
Tetrabenzine
Dopamine depleting agent that inhibits their transport inot presynaptic vesicles w/ highest binding density in caudate, putamen, and nucleus accumbens.
Used to treat chorea in HD.
Side effects: Extra-pyramidal Symptoms, anxiety/depression, sedation, insominia, nausea/vomitting
Clozapine (Clozaril)
Atypical Antipsychotic. Effective for both positive and negative symptoms.
- ) Blocking Dopamine receptors
- ) Blocking 5-HT receptors
- ) Blocks reuptake of Glutamate
Especially DA (D4) antagonist. Works primarily on psychiatric symptoms.
Risk of agranulocytosis –> Get WBC before Rx.
Valproic Acid (Depakote)
MOA (HD): Enhances GABA effects.
Usually anti-siezure, but can help chorea.
First line for convulsive seizures.
MOA (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
Essentially every antiseizure drug can cause side effects/adverse effects of:
GI upset (nausea, vomiting and so forth)
CNS effects (like mental status changes, headache dizziness, drowsiness, ataxia, vision changes)
Rash; when severe, patients can develop stevens-johnson syndrome
Hematologic problems (anemia, agranulocytosis, cytopenias etc)
Benzodiazepines
First line usage to treat chorea. See other uses in other cards.
Lithium
MOA: Unkown exactly. Influences re-uptake of 5HT, NE.
Affects post synaptic D2R
Old mood stabilizer. Used in Bipolar and HD
Therapeutic effect seen in 5-21 days.
Adverse effects: Fatigue, muscular weakness, slurred speech, ataxia, fine tremor of hand.
Presymptomatic Genetic Testing (HD)
Purpose: accurate risk assessment (very accurate)
Desire: Reduce M & M (No decrease possible)
Value of testing depends on effectiveness of prevention/management/treatment (None for HD)
Must be tailored to individual’s preferences/family needs/ and experience (Crucial Aspect for HD)
Can be prenatal to assure non-affected child (Can be done/ also IVF option)
Differs from Diagnostic Genetic Testing - already showing symptoms (Will tell number of repeats?)
Non affected child IVF
Used when parent does not want to know personally, but doesn’t want to pass HD onto kids.
Transfer only unaffected embryos to the patient. Parents are blind.
Electroencephalography (EEG)
A number of electrodes are placed on the scalp and the underlying active synapses are monitored.
Beta wave = Eyes open, acitve thinking. Low amplitude and high frequency. (Awakeand REM)
Alpha wave = Eyes closed, relaxed. Second highest frequency and second lowest amplitude (Stage 1)
Theta wave = Drowsiness, meditation. Second lowest frequency and second highest amplitude. (Stage 2)
Delta wave = Slow-wave sleep. lowest frequency and highest amplitude. (Sleep stage 3 and 4)
at night, BATS Drink Blood = Beta, Alpha, Theta, Sleep spindles, Delta, Beta
Phenobarbital
Barbituate
MOA: Bind to molecular components of GABA-A receptor (Cl- channel –> hyperpolarizes) in neuronal membranes in CNS. Potentiate GABA action by increasing the duration of the GABA-gated channel opening.
Primary uses: Hypnosis, seizure control, and anesthesia induction.
Not as selective as newer drugs.
First line for pregnant women and children w/ seizures.
Absorbed rapidly into the blood following oral administration.
Less lipid soluble (20 min to sleep onset)
Major metabolic pathway involves oxidation via hepatic enzymes.
Water-soluble metabolites are excreted via kidney. Phenobarbital has a significant percentage (25%) excreted unchanged.
Overdose think BBBB –> Barbituates, Basic urine –> push Bicarb –> (increase BP).
Activity of CYP-450 enzymes may be increased (drug-drug and drug-self reactions.
Tolerance common. Due to both kinetic and dynamic changes.
Dependence: both mental and physical dependence. Shorter half life = more severe withdrawal (thiopental)
Pentobarbital
Barbituate
MOA: Bind to molecular components of GABA-A receptor (Cl- channel –> hyperpolarizes) in neuronal membranes in CNS. Potentiate GABA action by increasing the duration of the GABA-gated channel opening.
Primary uses: Hypnosis, seizure control, and anesthesia induction.
Not as selective as newer drugs.
Absorbed rapidly into the blood following oral administration.
Less lipid soluble (20 min to sleep onset)
Major metabolic pathway involves oxidation via hepatic enzymes.
Water-soluble metabolites are excreted via kidney. Phenobarbital has a significant percentage (25%) excreted unchanged.
An overdose of a phenobarbital can be treated by administering sodium bicarb IV to elevate urinary pH.
Activity of CYP-450 enzymes may be increased (drug-drug and drug-self reactions.
Tolerance common. Due to both kinetic and dynamic changes.
Flumazenil
Benzodiazepine binding site antagonist (doesn’t block barbituate)
Used to treat post-op respiratory depression caused by benzodiazapines.
Zolpidem
MOA: Interact with benzo binding site on GABA-A receptro at certain subtypes.
Advantages: Rapid onset, short duration, and slow tolerance development.
Only used for sedation/hypnotic activities (no anxiolytic usage)
Buspirone
Selective anxiolytic effects without significant sedative or hypnotic effects.
MOA: not directly w/ GABA. Unknown.
Anxiolytic effects may take more than a week to become established. Used for generalized anxiety, not attacks.
Rapidly absorbed orally but undergoes significant first pass metab. Half life 2-4 hours.
Inhibitors of CYP3A4 (i.e. erythromycin, ketoconazole, grafefruit juice etc.) can markedly increase plasma levels.
Ramelteon
Hypnotic drug specifically useful for patients who have difficulty FALLING asleep.
MOA: Agonist of melatonin receptors are involved in maintaining circadium rhythms underlying the sleep-wake cycle.
No rebound insomnia or withdrawal. Low abuse potential.
Cholpromazine (Thorazine)
Typical Antipsychotic
Blocks Dopamine D2 receptor decreasing dopamine caused psychoses.
Only effective vs positive symptoms and in some instances worsens negative symptoms (increased 5-HT_
Side effects: Big one is tardive dyskinesia (abnormal facial movements/twitches that persist even after stopping the drug.) Parkinsonism (blocking Nigrostriatal pathway). Galactorrhea, Amenorrhea, and Sexual dysfunction (blocking tuberoinfundibular pathyway)
-one, -apine
Atypical Antipsychotic. Effective for both positive and negative symptoms.
- ) Blocking Dopamine receptors
- ) Blocking 5-HT receptors
- ) Blocks reuptake of Glutamate
Useful for motor and pschiatric problems.
Side effects: Weight gain (most common reason for poor compliance). Increase in type 2 DM.
-azine
Typical Antipsychotic
Blocks Dopamine D2 receptor decreasing dopamine caused psychoses.
Only effective vs positive symptoms and in some instances worsens negative symptoms (increased 5-HT)
Side effects: Big one is tardive dyskinesia (abnormal facial movements/twitches that persist even after stopping the drug.) Parkinsonism (blocking Nigrostriatal pathway). Galactorrhea, Amenorrhea, and Sexual dysfunction (blocking tuberoinfundibular pathyway). Negative symptoms due to Mesocortical overactivity.
Carbamazepine
Anti-seizure
MOA: -stabilizes “inactivated” state of VG Na+ channels –> decrease in repetitive firing
First line for focal, local (simple partial siezure) and complex partial seizures.
Induces CYP enzymes (Chris Paul induces good offense. Carbamazepine and Phenytoin are the only inducers.)
Essentially every antiseizure drug can cause side effects/adverse effects of:
GI upset (nausea, vomiting and so forth)
CNS effects (like mental status changes, headache dizziness, drowsiness, ataxia, vision changes)
Rash; when severe, patients can develop stevens-johnson syndrome
Hematologic problems (anemia, agranulocytosis, cytopenias etc)
Ethosuximide
Anti-seizure
MOA: 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
First line for generalized non-convulsive (absence) therapy
Essentially every antiseizure drug can cause side effects/adverse effects of:
GI upset (nausea, vomiting and so forth)
CNS effects (like mental status changes, headache dizziness, drowsiness, ataxia, vision changes)
Rash; when severe, patients can develop stevens-johnson syndrome
Hematologic problems (anemia, agranulocytosis, cytopenias etc)
First line for absence seizures.
Levetiracetam
Anti-Seizure
Affects synaptic vesicle protein SV2A, resulting in decreased glutamate release but increased GABA release
First line for simple partial, complex partial, and convulsive seizures.
Essentially every antiseizure drug can cause side effects/adverse effects of:
GI upset (nausea, vomiting and so forth)
CNS effects (like mental status changes, headache dizziness, drowsiness, ataxia, vision changes)
Rash; when severe, patients can develop stevens-johnson syndrome
Hematologic problems (anemia, agranulocytosis, cytopenias etc)
Topiramate
Anti-Seizure
MOA: 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
Essentially every antiseizure drug can cause side effects/adverse effects of:
GI upset (nausea, vomiting and so forth)
CNS effects (like mental status changes, headache dizziness, drowsiness, ataxia, vision changes)
Rash; when severe, patients can develop stevens-johnson syndrome
Hematologic problems (anemia, agranulocytosis, cytopenias etc)
Phenytoin
Anti-siezure
MOA:Prolongs Inactivation phase of v-gated sodium channels which prevents rapid firing of action potentials; also see decreased glutamate release
Induces CYP enzymes (Chris Paul induces good offense. Carbamazepine and Phenytoin are the only inducers.)
Essentially every antiseizure drug can cause side effects/adverse effects of:
GI upset (nausea, vomiting and so forth)
CNS effects (like mental status changes, headache dizziness, drowsiness, ataxia, vision changes)
Rash; when severe, patients can develop stevens-johnson syndrome
Hematologic problems (anemia, agranulocytosis, cytopenias etc)
Gabapentin
Anti siezure (neuropathic pain first line too!)
Inhibits high-voltage-activated Ca2+ channels (decreases Ca2+ entry)
Ethanol
Generalized CNS Depressant.
Amphophilic –> complete abosrption
Initial stimulation due to the depression of inhibitory control “disinhibition euphoria”
Thought and motor processes that are most dependent on training and previous experience are first affected
Perception and reaction to pain are diminished
Systemic effects: vasodilation (loss of body heat/ sense of warmth). Chronic use is major cause of cardiomyopathy –> many defects seen in chronic alcoholics.
Chronic low dose usage raises HDL and lowers LDL. (Don’t let patient’s use this excuse for alcoholism).
Increases production of TPA.
Effects: on liver:
Acute - interferes w/ oxidative metab of other drugs.
Chronic- Increases oxidative metab (inducer). Increases hepatic synthesis of fats –> accumulation of fat can lead to cirrhosis and alcoholic hepatitis. Usually reversible with abstinence.
On kidney: diuretic –> blocks ADH release from pituitary
On GI tract: 1-3 alcholoics suffers from chronic erosive gastritis
On pancreas: Etiological factor in acute and chronic pancreatitis
Risk of FAS.
Metabolized to acetaldehyde by alcohol dehydrogenase. First order ( about a shot an hour)
Therapeutic uses: Antiseptic, antidote to methanol intoxication.
Physical dependence and tolerance.
Disulfiram interferes w/ aldehyde dehyrdogenous leads to excessive acetaldehyde.
Methanol
Toxic drug that causes blindness, severe acidosis, coma, and death.
Acidosis and retinal damage due to formation of formic acid.
Treatment: most important therapeutic goal reduce acidosis w/ bicarb until urinary pH = 7.5. Administer ethanol (lower Km for enzyme)
Ethylene Glycol
Toxicity: renal failure- blockade due to calcium oxate crystals. Vomitting. Acidosis (formic acid)
Early sx: vomitting, depression, ataxia, weakness and flaccid paralysis, convulsions followed by coma or death.
Later symptoms: renal failure, emesis, dehydration, coma, death.
Cause of death: Metabolic acidosis, cardio dysfunction, and acute kidney failures. Due to glyoxylic and oxalic acid.
Treatment: Emesis, acidosis, and convulsion management. Metabolic competion with ethanol or Fomepizol (expensive!)
Fomepizol
Expensive inhibitor of alcohol dehyrdogenase used to treat ethylene glycol metabolism (or methanol?)
Disulfiram
Interferes w/ aldehyde dehyrdogenous leads to excessive acetaldehyde.
Used to treat alcohol addiction by preventing relapse and reversing skinnerian conditioning.
Naltrexone
Used to prevent alcohol relapse. Oral antagonist of opiod receptors.
Decreases cravings.
Desipramine
NE- selective Tricyclic Antidepressant
MOA: Block the reuptake of NE by nerve terminals resulting in increased NE concentrations.
Effects: Normal person- No stimulation or mood elevating effect. Sleepiness. Depressed subjects: elevation of mood only after 2-3 weeks (need to convince to stay on drugs)
Take once a day before bed.
Adverse effects: Orthostatic hypotension (blockade of alpha adrenoceptors), antimuscarinic effects (Dry mouth, blurry vision, constipation, urinary retention), Weight gain, tachycardia
Low therapeutic index (5-10) (can only give 1 week of dose at a time)
Metabolized by CYP2D6 which is inhibited by fluoxetine. (concurrent fluoxetine and TCA could lead to TCA toxicity)
Use primarily in depression that is unresponsive to more commonly used antidepressants (SSRIs, SNRIs)
Imipramine
NE / 5-HT mixed action Tricyclic antidepressant
MOA Block the reuptake of NE and 5-HT
Adverse effects: Orthostatic hypotension (blockade of alpha adrenoceptors), antimuscarinic effects (Dry mouth, constipation, blurry vision, urinary retention), Weight gain, tachycardia
Low therapeutic index (5-10) (can only give 1 week of dose at a time)
Take orally once a day before bed
Metabolized by CYP2D6 which is inhibited by fluoxetine. (concurrent fluoxetine and TCA could lead to TCA toxicity)
Use primarily in depression that is unresponsive to more commonly used antidepressants (SSRIs, SNRIs)
Phenelzine
MAOIs
Irreversibly blocks the oxidative deamination of monoamines. Nonselectively inhibits both MAO-A (NE and 5-HT) and MAO-B (DA).
Clinically improvement usually takes 3+ weeks to begin.
Low therapeutic index (less than 5)
SSRIs should not be started until at least 14 days following discontinuation of treatment with an MAOIs. (reverse is also true!)
Can cause serotonin syndrome. (administer serotonin antagoinist = cyproheptadine)
Potenentiates sympathomimetic amines –> combined with tiyramine can cause hypertensive crisis. (avoid foods rich in tyramine) Also OTC cold preparations w/ ephiderine, pseudoephedrine.
Fluoxetine
Prozac –> SSRI
MOA: Selectively blocks the reuptake of serotonin. Increases 5-HT postsynaptically to trigger actions in an effector cell. Presynaptically on 5-HT(1) autoreceptors to inhibit additional 5-HT release.
5-HT2A is important receptor type for clinical effect.
Adverse effects: nausea, diarrhea, and weight loss. Stimulation - anxiety, nervousness, insominia –> sufficient to discontinue treatment. SSRIs are not sedating like TCAs. (33-50% of those w/ symptoms can’t continue treatment) Sexual dysfunction. INCREASED SUICIDE RISK.
Side effects decrease after a few weeks.
SSRIs should not be used alone for bipolar disoreder.
Sertraline
Zoloft
MOA: Selectively blocks the reuptake of serotonin. Increases 5-HT postsynaptically to trigger actions in an effector cell. Presynaptically on 5-HT(1) autoreceptors to inhibit additional 5-HT release.
5-HT2A is important receptor type for clinical effect.
Adverse effects: nausea, diarrhea, and weight loss. Stimulation - anxiety, nervousness, insominia –> sufficient to discontinue treatment. SSRIs are not sedating like TCAs. (33-50% of those w/ symptoms can’t continue treatment) Sexual dysfunction. INCREASED SUICIDE RISK.
Side effects decrease after a few weeks.
SSRIs should not be used alone for bipolar disorder.
Escitalopram
Lexapro
MOA: Selectively blocks the reuptake of serotonin. Increases 5-HT postsynaptically to trigger actions in an effector cell. Presynaptically on 5-HT(1) autoreceptors to inhibit additional 5-HT release.
5-HT2A is important receptor type for clinical effect.
Adverse effects: nausea, diarrhea, and weight loss. Stimulation - anxiety, nervousness, insominia –> sufficient to discontinue treatment. SSRIs are not sedating like TCAs. (33-50% of those w/ symptoms can’t continue treatment) Sexual dysfunction. INCREASED SUICIDE RISK.
Side effects decrease after a few weeks.
SSRIs should not be used alone for bipolar disorder.
Venlafaxine
Effexor
Atypical (Dual/Mixed Action) Antidepressants
Serotninin-norepinepherine reuptake inhibitor (SNRI)
Blocks serotonin reuptake like SSRIs
Also blocks NE reuptake
Different than TCAs: adrenergic, histamine, cholinergic receptors.
Contraindicated in patients with MAOIs and vice versa.
Raising dose of venlafaxine improves efficacy due to secondary mechanisms of action. Serotonin –> NE –> DA.
Mirtazapine
Atypical Antidepressant
Blocks presynaptic alpha-2 on adrenergic neurons (autoreceptors) and on serotnergic neurons (heteroreceptors). This increases NE and 5-HT.
Buproprion
Atypical Antidepressant - Wellbutrin
Enhances both NE and DA neurotransmission via reuptake inhibition.
Adverse effects: stimulation (agitation, anorexia, insomnia)
Often used in combination w/ SSRIs to obtain greater response. (very limited data supporting this)
Also used for smoking cessation (Zyban)
Cidofovir
Anitviral that is given as prodrug. Host cells phosphorylate drug to active form. Then preferentially bound by viral DNA polymerase (600x). Chain terminator.
Used for JC polymyxovirus and second line for alpha-herpes viruses that have become resistant to acyclovir (both resistance due to thymidine kinase changes and DNA polymerase changes.)
Thymidine analog
Cyproheptadine
Blocks 5-HT2A receptor.
Given to treat serotonin syndrome caused by MAOI (especially if you start SSRIs too soon) and MDMA.
Vecuronium
Muscle relaxant only given w/ anesthesia for optimal surgical outcomes.
Theophylline
Stronger potency xanthine than caffeine.
Uses: Anti-asthmatic = Smooth muscle relaxant
Anti Migraine = Increase cerebral vascular resistance
CHF? = Cardiac stim; dialation of coronaries; increased O2 demand by heart.
