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PDA Block 3 > Intro to Neuropsychopharmacology Part 2 > Flashcards

Intro to Neuropsychopharmacology Part 2 Flashcards

1
Q

Bipolar I Disorder

A

-one or more manic episodes

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2
Q

Bipolar II Disorder

A

-at least one hypomanic episode and one major depressive disorder

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3
Q

Cyclothymic Disorder

A

-2 years, periods with hypomanic and depressive symptoms not meeting criteria for hypomania or major depressive episodes

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4
Q

Criteria for manic episode

A
  • inflated self-esteem/grandiosity
  • decreased need for sleep
  • talkativeness
  • flight of ideas/racing thoughts
  • distractibility
  • increased goal directed activity/psyhomotor agitation
  • excessive involvement in pleasurable activities with potential for adverse consequences
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5
Q

lithium

A
  • monovalent cation of the lightest alkali metal
  • one of few psychotherapeutic drugs that has no behavioral effects in “normals”
  • blocks manic behavior
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6
Q

Lithium act by blocking enzymes in neurotransmission explain how

A

-lithium inhibits the phosphatase that converts IP2 to IP1

  • PLC converts PIP2 to IP3 and DAG
  • the IP3is then converted to IP2 i
  • IP2 is then converted to IP1 and then inositol. this is where lithium blocks. therefore it is stopping the recycling
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7
Q

Describe lithium pharmacokinetics

A

-readily absorbed after oral administration
-eliminated in urine approximately 95%
-extensive tubular reabsorption
-Na levels affect Li levels. increased Na excretion causes clinically significant increases in Li levels
ie thiazide diuretics, losses of fluids or electrolytes
-narrow therapeutic window so important to monitor levels
-ACE inhibitors and Angiotensin II receptor blockers can also raise Li levels

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8
Q

Why is it important to monitor li levels

A

-it has a low therapeutic window and the Li levels in the body can change if someone takes and ACE inhibitor or if someone uses a diuretic or change their electrolyte levels in anyway

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9
Q

side effects and toxic reactions

A
  • fatigue and muscular weakness
  • tremor: may be treated with beta blockers
  • GI symptoms
  • slurred speech and ataxia
  • serious toxicity at plasma levels about 2 to 3 times therapeutic levels
  • impaired conciousness
  • rigidity and hyperactive deep reflexes
  • coma
  • lithium levels are affected by plasma sodium levels thus interactions with diuretics and some antihypertensives
  • narrow therapeutic window. important to monitor lithium blood levels
  • should be used in caution in pregnant women
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10
Q

Clinical uses of lithium

A
  • treat mania and prevent recurrences of bipolar disease

- may be useful in preventing recurrences of unipolar depression in some patients

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11
Q

alternatives to lithium

A
  • anitseizure agents
  • valproic acid, divalproex
  • lamotrigene
  • haloperidol
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12
Q

Valproic acid, divalproex

A
  • used as first line drug in bipolar disease

- blocks sodium channel and may increase synaptic GABA; sedating

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13
Q

Lamotrigene

A

-acts at sodium channel- similar mechanism for carbamazepine

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14
Q

Haloperidol

A

initial control of manic symptoms

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15
Q

Key syndrome for anxiety disorders

A
  • excessive fear and anxiesty manifest by:
  • symptoms of flight or fight (ANS and arousal and escape)
  • muscle tension and vigilance (musculoskeletal and avoidance)
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16
Q

disorder in the classification of anxiety disorders

A
  • separation anxiety disorder
  • selective mutism
  • specific phobia
  • social anxiety disorder
  • agoraphobia
  • generalized anxiety disorder
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17
Q

Generalized anxiety disorder

A
  • generalized persistent anxiety for at least 1 months duration
  • absence of the specific symptoms and patterns that characterize other anxiety disorders such as phobias, panic attacks, or OCD
  • psychological correlates include apprehensive expectation with worry fear and anticipation of misfortune to self and others, hyperattensiveness, distractibility, difficulty in concentrating, insomnia, feeling on edge and impatience
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18
Q

ANS arousal with anxiety

A
  • sweating
  • tachycardia and palpitations
  • cold and clammy hands
  • dry mouth and lump in throat feeling
  • GI upset
  • frequent urination and diarrhea
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19
Q

Voluntary muscle activation

A

-jitteriness and an inability to relax

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20
Q

complications to anxiety

A

-abuse of alcohol, sedatives and antianxiety medications are common

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21
Q

Sleep disorders

A
  • insomnia-disorders of initiating and maintaining sleep

- hypersomnia- disorders of excessive sleep or sleepiness

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22
Q

treatment of anxiety and insomnia

A
  • benzodiazepines and related drugs
  • SSRIs
  • Buspirone
  • classical antihistamines
  • alcohol, cannabis, opiates
  • barbiturates
23
Q

GABA localization

A
  • substantia nigra
  • globus pallidus
  • hippocampus
  • limbic structures: amygdala
  • hypothalamus
  • spinal cord
24
Q

describe the GABA channel

A
  • it is like the nicotinic channel
  • it is a pore
  • when GABA binds to it it opens and allows CL to rush into the cell hyperpolarizing it
25
Q

how do benzodiazepenes influence GABA binding

A

they increase GABA binding

26
Q

ligands of the benzodiazepine receptor

  • agonist
  • antagonist
A
  • agonists: clinically useful benzodiazepines ie Diazepam, Zolpidem
  • antagonists: block the action of benzodiazepines at the receptor, Flumazenil
27
Q

Benzodiazepines used to treat anxiety

A
  • Alprazolam
  • Diazepam
  • Lorazepam
28
Q

Flurazepam

  • onset of action
  • duration of action
  • active metabolites
A
  • rapid onset
  • long duration of action
  • active metabolite is Desalkylflurazepam
29
Q

Lorazepam

A

both anxiety and insomnia!!

30
Q

Describe the role of lipophilicity in Diazepam

A
  • fast onset of action: oral
  • high lipid solubility: rapid absorption and entry into the brain
  • rapid redistribution after single dose
  • active metabolites change this in multiple dose situation
31
Q

Lorazepam

A
  • less lipophilic than diazepam
  • absorption and onset of action are slower
  • longer duration of action after single dose
  • no active metabolites
32
Q

what is the only benzodiazepine that is not metabolized to an active metabolite

A

Lorazepam

33
Q

CNS effects of the benzodiazepines

A
  • decreased anxiety
  • sedation
  • hypnosis
  • muscle relaxation
  • anterograde amnesia-IV administration
  • anticonvulsant action
  • minimal CV and respiratory actions at therapeutic doses
34
Q

drug interactions for benzodiazepines

A
  • produce additive CNS depression with most other depressant drugs such as ethanol, other sedative hypnotics and sedating antihistamines
  • drugs that affect hepatic metabolism such as cimetidine
35
Q

clinical uses of benzodiazepines

A
  • anxiety states (short term)
  • sleep disorders
  • muscle relaxant (Diazepam)
  • seizure treatment
  • intravenous sedation and anesthesia
  • alcohol withdrawal-chlordiazepoxide
36
Q

Benzodiazepine withdrawal

A
  • anxiety
  • insomnia
  • irritability
  • headache
  • hyperacusis
  • hallucinations
  • seizures
37
Q

How do you treat abuse of benzodiazepines

A

-gradual reduction in dose, switch to longer acting drugs

38
Q

Buspirone

A
  • not related chemically or pharmacologically to the benzodiazepines
  • high affinity for 5-HT1A receptos
  • less sedating than benzodiaepines
  • no cross-tolerance with benzodiazepines
  • does not potentiate other sedative hypnotics and depressants nor suppress symptoms of their withdrawal
  • used in the treatment of generalized anxiety syndrome
  • therapeutic effects may take 1 t 2 weeks to occur
39
Q

other treatments for anxiety besides benzodiazepines and buspirone

A
  • SSRIs and SNRIs-panic attacks and GAD

- Beta blockers: performance anxiety

40
Q

Describe the dimesions of insomnia

A
  • symptoms may be mild or severe, or transient, chronic or intermittent
  • can’t fall asleep and/or stay asleep
  • daytime sequelae: tired, fatigued, sleepy, anxious, depressed
41
Q

Effects of benzodiazepines on sleep

A
  • decreased latency to sleep
  • increase in stage 1 and stage 2 sleep
  • decreased time in stage 3 and stage 4 and REM sleep
  • rebound insomnia upon withdrawal
42
Q

adverse effects of using a benzodiazepine for sleep

A
  • daytime sedation
  • ataxia
  • rebound insomnia
  • tolerance and dependence
  • occasional idiosyncratic excitement and stimulation
43
Q

Zolpidem

A
  • not benzodiazepine chemically
  • but bind to the Benzodiazepine receptor on GABA complex
  • weak anxiolytic, muscle relaxant and anticonvulsant at hypnotic dose
  • stage 3 and 4 sleep preserved, minor effect on REM sleep
  • typical duration is 5 to 6 hours. sustained release preparation, duration of action 7 to 8 hours, also available.
  • also available as an oral spray targeted at problems of sleep initiation and sublingual tablets for middle of the night waking . some forms are approved for longer term use
44
Q

Barbiturate metabolism, pharmacokinetics and interactions

A
  • rapidly absorbed and distributed
  • highly lipid soluble compounds such as thiopental distribute rapidly to the brain. action terminated by redistribution
  • can induce own metabolism and that of other drugs
  • eliminated primarily by renal excretion
45
Q

Where do barbiturates act

A
  • GABAa receptor

- Cl ion channel complex binding to a barbiturate site, enhance action of GABA and increase inhibition

46
Q

pharmacological actions and adverse effects for barbiturates

A

-general CNS depression
*sedation, hypnotic action, anesthesia
-anticonvulsant
-respiratory depression
-tolerance
physical dependence
-actue poisoning
additive with other CNS depressants such as alcohol other sedative hypnotics and antihistamines
-interact with drugs that affect microsomal drug metabolism

47
Q

Describe tolerance of barbiturates

A

-both metabolic and pharmacodynamic. it is not uniform to all drug effects

48
Q

describe physical dependence of barbiturates

A

-repeated use of barbiturates may result in withdrawal symptoms upon cessation of use. similar to BDC life threatening seizures may occur. abrupt withdrawal in chronic users is contraindicated

49
Q

describe acute poisoning in barbiturate use

A

-stupor, coma and respiratory depression . treatment involves removing any unabsorbed drug, supporting respiration and preventing complications

50
Q

Skeletal muscle relaxants

A
  • drugs used to reduce muscle tone associated with spasticity related to multiple sclerosis injuries and other muscular skeletal disorders
  • spasticity is characterized by increases in tonic stretch reflexes and flexor muscle spasms together with a possible muscle weakness
  • mechanisms underlying spasticity involve both the stretch reflex arc itself and higher centers in the brain
  • pharmacological treatment of spasticity targets both sites
51
Q

GABAergic agent

A
  • Diazepam

- Baclofen

52
Q

Diazepam

A
  • its action in reducing spasticity is at least partly mediated in the spinal cord
  • it can be used in patients with muscle spasm of almost any origin including local trauma
  • it produces sedation in most patients at the doses required to reduce muscle tone
53
Q

Baclofen

A
  • GABA-mimetic agent that works at GABA B receptors. this results in hyperppolarization, causing presynaptic inhibition
  • this can result in decreased release of excitatory transmitters such as glutamate
  • Baclofen is at least as effective as diazepam in reducing spasticity and produces much less sedation
54
Q

Tizanidine

A
  • an alpha2 adrenergic agonist that is related to clonidine. it may enhance both presynaptic and postsynaptic inhibition
  • may have similar efficacy to diazepam and baclofen in relieving muscle spasms
  • side effects include drowsiness, hypotension, dry mouth and asthenia

PDA Block 3 (16 decks)

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