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BIOM 3090 > Unit 05: Depression and Anxiety > Flashcards

Unit 05: Depression and Anxiety Flashcards

1
Q

how id depression treated

A
  • varies depending on degree of the disorder
  • psychotherapy can be effective alone or in combination with medication
  • drugs used to treat depression act on one or more monoamine systems
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2
Q

what are commonly prescribed antidepressants

A

Tricyclics, selective serotonin reuptake inhibitors (SSRIs) and monoamine oxidase inhibitors (MAOIs)

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3
Q

what are Tricyclics, what do they do and give an example

A
  • Tricyclic antidepressants are heterocyclic compounds (name based on their 3 ringed structure)
  • inhibit reuptake of norepinephrine and serotonin - elevate the conc of them
  • effective in more than 70% of patients but are not used as first lines of treatment due to side effects and drug-drug interactsions
    ex: Imipramine
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4
Q

what are the adverse effects associated with tricyclics

A
  • adverse effects are due to effects on several other receptors and prtoeins
  • affect cardiovasucalr system - block cardiac sodium channels (do this in manner similar to the anti-arrhythmic quinidine)
  • high affinity for antagonising muscarinic, H1 and α1 receptors: potent antihistamines, anticholinergics and vasodilators

*not desirable properties and contribute to adverse affects

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5
Q

what are SSRIs

A

selective serotonin reuptake inhibitors - mos widely prescribed antidepressants in north america

ex: fluoxitine (prozac)

used to treat depression, panic disorder, anxiety, OCD and bulimia

  • fewer side effects than other antidepressants but can cause insomia and sexual dysfunction

*also inc sucide rate in children/adolescents so not prescribed to youth

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6
Q

what are the drug interacts of SSRIs

A
  • inhibit CYP2D^ which is responsible for metabolicm or tricyclic antidepressants
  • NEVER TAKE SSRIs and tricyclic antidepressants together, if making the switch need to wean off first
  • SSRIs inc level of serotonin so should not be taken in combintion with drugs that increase serotonin via another mechanisms like MAOI inhibitors

^can cause serotonin syndome

  • not dangerous drugs unless combined with other antidepressants
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7
Q

describe Monoamine Oxidase Inhibitors, give an example of one

A
  • used to treat depression and inhibit both MAO-A and MAO-B
  • Norepinephrine, serotonin and dopamine apthways are all affected
  • MAOIs onyl used if tricyclic antidepressants not effective
    ex: Phenelzine - non selective irreversible MAOI
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8
Q

what does MAO-A metabolize? what does MAO-B metabolize?

A

MAO-A which metabolizes norepinephrine, serotonin, dopamine and tyramine

MAO-B which only metabolizes dopamine.

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9
Q

what is phenelzine

A

non-selective and irreversible MAOI

*most widely used MAOI for the treatment of depression

  • decreases metabolism of morepinephrine, dopamine and serotonin
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10
Q

what are side effects of MAOIs

A
  • do not have significant side effects on their own but are not used as first line drugs bc of dietary interactions
  • can cause hypertensive crisis if ingest tyramine containing foods: foods that have bene pickled, aged, smoked like meats and alc
  • hypertensive crisis can also occur if individual is taking CNS stimulants like cocaine or amphetamine
  • Sympathomimetics are also contraindicted if taking MOAIs - cause sympathetic excess

* do not take MAO inhibiots with serotonergic agents bc combination can cause serotonin syndrom

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11
Q

what are the newer classes of antidepressants

A
  • seroronin and norepinephrine reuptake inhibitors (SNRIs), 5-HT2 receptor antagonists and tetracyclic and unicyclic agents
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12
Q

what is bupropion

A
  • knwon as wellbutrin
  • example of one of the more commonly prescribed newer atypical antidepressants
  • mechanisms of poorly understoof but modest inhibitor of re-uptake and stimulates release of dopamine and norepinephrine
  • does not block histaminic, adrenergic or muscarinic receptors but still increases dopamine levels (do not use in patietns with psychosis)

*like SSRIs it inhibits CYP2D6 so do not take with other drugs metabolised by that enzyme

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13
Q

long term treatment with antidepressants

A

alter the sensitivity or levels of a variety of CNS receptors and neuronal growth factors.

It is unknown if long-term changes can result in complete recovery or cure from depression.

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14
Q

How are antidepressants used clinically?

A
  • SSRIs prescribed first bc few side effects and generally safer if overdoses occur
  • therapy starts as low dose
  • dosing antidepressants is balance between clincial effectiveness and averse effects - dosage can be gradually increased
  • if patients does not respond to one ro two SSRIs they are switch to a drug in a different drug class

*monoamine levels are changed after single dose but benefit not observed for weeks - prob due to adaptive changes from sustained elevations in monoamines

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15
Q

What is Anxiety

A

unpleasent state or feelings of apprehension, tension, uncertainty, dissatisfaction and fear

  • anxiey disorders include panic disorders, phobias, obsessive compulsive disorders and generalized anxiety
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16
Q

how is anxiety treated

A
  • psychotherapy, behavioural intervention and medication like sedatives or hypnotics

*If anxiety is secondary to other disorders such as psychosis or depression, it is best treated by controlling the primary illness.

17
Q

what are Sedatives, hypnotics and anxiolytics

A
  • all used to treat anxiety disorders

Anxiolytics or sedatives = drugs that produce a calming effect and provide relief of anxiety with little or no effect on moror or mental functions

Hypnotics = drugs that produce drowsiness and induce sleep

*many are both sedatives and hypnotics with effects of drugs being dopse dependent

18
Q

what are Benzodiazepines and barbiturates

A

common drugs with sedative, hypnotic and anxiolytic properties

19
Q

what do benzodiazepines do? give an example

A
  • enhance the effect of GABA at the GABAA receptor
  • results in sedative, hypnotic (sleep inducing) and anxiolytic (anti-anxiety) effect
    ex: diazepam
20
Q

how are benzodiazepines metabolized

A

CYP450 and excreted as glucuronides or oxidized metabolites

* first pass metabolism for many benzodiazepines is oxidation to form an active metabolite

21
Q

MOA of benzodiazepines

A
  • binds to GABAA receptors at site that is distincy from GABA
  • binding of drug to benzodiazepine site does not activate GABAA receptors but increases frequency of GABA mediated opening of the CL- channel

*mechanis requires GABA for effect to take place

  • by increasing the frequency of channel opening, benzodiazepines enhance Cl- conductance which increases inhibtion of many neurons in diff brain regions
22
Q

what are barbiturates

A
  • drugs that act to depress the CNS producing a wide spectrum of effects from mild-sedation to total anesthesia
  • have sedative, hypnotic and anxiolytic activity and also nehance GABA neurotransmission

ex = phenobarbital

*not barbiturates are often replaced with benzodiazepines bc they are safer esp with regards to overdose

23
Q

pharmacokinetics of barbituarates

A

similar to benzodiazepines, phase I reactions (oxidation by cytochrome P450) are followed by phase II reactions involving conjugation with glucuronide

In contrast to benzodiazepines, the metabolites produced are generally not active

  • barbiturates increase expression of some cytochrome P450 enzymes.
24
Q

MOA of barbituates

A
  • bind to GABAA receptors at distinct site on the receptor
  • the binding site id different than the site for GABA and benzodiazepines
  • binding of barbiturates increases the duration of the opening of GABA-mediated Cl- channels
  • this inc Cl- conductance and enhances the inhibition of many neurons
  • at high doses can directly activity GABAA recepotrs and inhibit glutamate receptors and high frequency sodium channels
25
Q

describe the clinical use and toxicology of sedative hypnotics

A
  • toxicolgy is dose dependent and based on CNS depressive effects
  • can cause imapired judgement and motor skills to amensia, coma and even death
  • addictive CNS depression can occur with the combindation of toher drugs that despress the activity of the CNS liek opiates and alc
  • prolonges use can result in dependance and symptoms of withdrawal when medication is stopped
  • tolerance to anxiolytics can also arise
26
Q

what effect do barbiturates have on CP450 enxymes and what must be kept in mind

A
  • increase the levels of some cytochrome P450 enzymes - enhances metabolism of other drugs
  • higher doses of other drugs needed to reach therapeutic effect
  • also enhanced toxicity in individuals with impaired liver function
27
Q

describe ethanol

A
  • can induce the same effets as sedativev-hypnotics
  • effects are dose-dependent and cause CNS depressino via decreased memrbane excitability and increased GABAA and decrease NMDA receptor activation
  • other effects include:diuresis, decreased myocardial contractility, slurred speech, and impaired judgment.

chronic effects: impact the liver and cause fatty liver which can lead to hepatitis, cirrhosis, liver failure, pancreatitis, and gastritis malnutrition.

28
Q

metabolism of ethanol

A
  • metabolized in liver through oxidation reactions
  • major pathway involved the enzyme alcohol dehyrogenase and minor pathway utilizes CYP 450 (Microsomal ethanol oxidizing system)
  • remaining ethanol thats not metabolized by liver is excreted unchanged by kidneys and lungs
  • clearance rate follows 0 order kinetics - the higher the consumption of hiher quantities of ethanol causes blood levels to continue to rise
29
Q

describe methanol

A

metabolied to formic acid which is toxic to the CNS

  • if it accumulates in retina can cause blindess
  • methanol poisoning can be treated with ethanol bc it has a higher affinity for alcohol dehydrogenase - slows down methanol metabolism to formic acid

BIOM 3090 (22 decks)

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