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Neuro Mike Rose > Drugs Test 5 > Flashcards

Drugs Test 5 Flashcards

1
Q

Benzedrine

A

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)

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2
Q

Cocaine

A

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

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3
Q

MDMA

A

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?

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4
Q

Bath Salts

A

Very dangerous uncontrolled drug that causes agitation, hallucination, paranoia, etc.

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5
Q

Caffeine

A

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.)

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6
Q

Modafinil

A

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.

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7
Q

Methylphenidate

A 
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

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8
Q

Atomoxetine

A

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.

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9
Q

Rivastigmine

A

MOA: Inhibits AChE and BuChe

Administered BID

Adverse effects: more GI problems and muscle weakness than other anticholinesterases.

Used to treat early AD

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10
Q

Tacrine

A

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

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11
Q

Galantamine

A

MOA: Inhibits AChE and stimulates nicotinic cholinergic neurons to release more stored ACh.

Interactions: Antidepressants, drugs with anticholinergic side effects. NSAIDs (stomach ulcers)

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12
Q

Memantadine

A

MOA: Antagonist at the NMDA receptor.

Useful for later stage patients. (moderate to sever AD)

Adverse effects: dizziness, headache, constipation, and confusion.

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13
Q

Ginko Biliboa

A

MOA: unknown. May have modest benefits for AD patients.

Serious side effects. (likely not worth the risk)

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14
Q

Halothane

A

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.

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15
Q

Isoflurane

A

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

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16
Q

Sevoflurane

A

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”

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17
Q

Nitrous Oxide

A

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

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18
Q

Thiopental

A

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.

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19
Q

Diazepam (Also Lorazopam, Triazolam, and Alprazolam)

A

“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)

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20
Q

Propofol

A

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.

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21
Q

Ketamine

A

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.

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22
Q

Fentanyl

A

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.

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23
Q

Sulfentyl

A

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.

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24
Q

Midazolam

A

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

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25
Q

Haloperidol

A

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.

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26
Q

Olanzapine

A

Atypical antipsychotic

Works in three areas:

  1. ) Blocking Dopamine receptors
  2. ) Blocking 5-HT receptors
  3. ) Blocks reuptake of Glutamate

Side effects: Weight gain and sedation

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27
Q

Risperidone

A

Most common used. First choice.

Atypical Antipsychotic. Effective for both positive and negative symptoms.

  1. ) Blocking Dopamine receptors
  2. ) Blocking 5-HT receptors
  3. ) 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.

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28
Q

Tetrabenzine

A

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

29
Q

Clozapine (Clozaril)

A

Atypical Antipsychotic. Effective for both positive and negative symptoms.

  1. ) Blocking Dopamine receptors
  2. ) Blocking 5-HT receptors
  3. ) Blocks reuptake of Glutamate

Especially DA (D4) antagonist. Works primarily on psychiatric symptoms.

Risk of agranulocytosis –> Get WBC before Rx.

30
Q

Valproic Acid (Depakote)

A

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)

31
Q

Benzodiazepines

A

First line usage to treat chorea. See other uses in other cards.

32
Q

Lithium

A

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.

33
Q

Presymptomatic Genetic Testing (HD)

A

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?)

34
Q

Non affected child IVF

A

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.

35
Q

Electroencephalography (EEG)

A

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

36
Q

Phenobarbital

A

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)

37
Q

Pentobarbital

A

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.

38
Q

Flumazenil

A

Benzodiazepine binding site antagonist (doesn’t block barbituate)

Used to treat post-op respiratory depression caused by benzodiazapines.

39
Q

Zolpidem

A

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)

40
Q

Buspirone

A

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.

41
Q

Ramelteon

A

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.

42
Q

Cholpromazine (Thorazine)

A

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)

43
Q

-one, -apine

A

Atypical Antipsychotic. Effective for both positive and negative symptoms.

  1. ) Blocking Dopamine receptors
  2. ) Blocking 5-HT receptors
  3. ) 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.

44
Q

-azine

A

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.

45
Q

Carbamazepine

A

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)

46
Q

Ethosuximide

A

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.

47
Q

Levetiracetam

A

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)

48
Q

Topiramate

A

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)

49
Q

Phenytoin

A

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)

50
Q

Gabapentin

A

Anti siezure (neuropathic pain first line too!)

Inhibits high-voltage-activated Ca2+ channels (decreases Ca2+ entry)

51
Q

Ethanol

A

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.

52
Q

Methanol

A

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)

53
Q

Ethylene Glycol

A

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!)

54
Q

Fomepizol

A

Expensive inhibitor of alcohol dehyrdogenase used to treat ethylene glycol metabolism (or methanol?)

55
Q

Disulfiram

A

Interferes w/ aldehyde dehyrdogenous leads to excessive acetaldehyde.

Used to treat alcohol addiction by preventing relapse and reversing skinnerian conditioning.

56
Q

Naltrexone

A

Used to prevent alcohol relapse. Oral antagonist of opiod receptors.

Decreases cravings.

57
Q

Desipramine

A

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)

58
Q

Imipramine

A

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)

59
Q

Phenelzine

A

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.

60
Q

Fluoxetine

A

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.

61
Q

Sertraline

A

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.

62
Q

Escitalopram

A

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.

63
Q

Venlafaxine

A

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.

64
Q

Mirtazapine

A

Atypical Antidepressant

Blocks presynaptic alpha-2 on adrenergic neurons (autoreceptors) and on serotnergic neurons (heteroreceptors). This increases NE and 5-HT.

65
Q

Buproprion

A

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)

66
Q

Cidofovir

A

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

67
Q

Cyproheptadine

A

Blocks 5-HT2A receptor.

Given to treat serotonin syndrome caused by MAOI (especially if you start SSRIs too soon) and MDMA.

68
Q

Vecuronium

A

Muscle relaxant only given w/ anesthesia for optimal surgical outcomes.

69
Q

Theophylline

A

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.

Neuro Mike Rose (21 decks)

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