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Pharm Block 3 > 4 - Neuropsychopharmocology 2 > Flashcards

4 - Neuropsychopharmocology 2 Flashcards

1
Q

What is the prevalence of bipolar disorder?

A

Affects less than 3% of the population in a year.

Over 80$ of those cases are classified as severe and use a disproportionate amount of mental and general health resources.

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2
Q

Describe bipolar I, II, and cyclothymic disorder?

A

I: one or more manic episodes, coded by severity and current episode.

II: at least one hypomanic episode and one major depressive episode

Cyclothymic: 2 yrs, periods with hypomanic and depressive symptoms not meeting criteria for hypomania or MDD, specify is with anxious distress

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3
Q

What are the criteria for manic episodes?

A

Inflated self-esterrm/grandiosity
Decreased need for sleep
talkativeness
Flight of ideas/racing thoughts
Distractability
Increased goal directed activity/psychomotor agitation
Excessive involvement in pleasurable activities with potential for adverse consequences

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4
Q

What monovalent cation is one of the few psychotherapeutic drugs with no behavior effects on people without a mental disorder and works to block manic behavior?

A

Lithium

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5
Q

What is the function of lithium?

A

Lithium inhibits a phosphatase that converts IP2 to IP1 for recycling of phosphoinositol.

Also effects glycogen synthase kinase

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6
Q

What are the pharmacokinetics of lithium? What increases and decreases Lithium levels in the body?

A

Absorbed orally, elim in urine 95%, extensive tubular reabsorption

Na levels affect Li levels. Increased NA excretion causes clinically significant increases in Li levels (Thiazide diuretics). ACE inhibitor and AngII receptor blockers raise Li levels.

Narrow therapeutic window, monitor levels.

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7
Q

What are the side effects of lithium?

A

Fatigue/muscle weakness
Tremor
Gi symptoms
Slurred Speech

Toxicity at plasma levels 2-3x the therapeutic levels cause impaired consciousness, rigidity, and coma.

Do not use in pregnant women or caution with those taking diuretics or some antihypertensives.

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8
Q

What are the clinical uses of lithium?

A

Treats mania and prevents reoccurrences of bipolar disease.

May be useful in preventing reoccurrences of unipolar depression in some pts (off-label)

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9
Q

What two antiseizure agents are used as first line drugs in bipolar disorder and work by blocking sodium channels? What is an important consideration for one of these drugs?

A

Valproic acid and Divalproex

Valproic acid is teratogenic and can cause neural tube defects.

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10
Q

What other drug acts as a sodium channel blocker to treat bipolar disorder similarly to valproic acid and divalproex? What is a consideration when treating a patient with this?

A

Lamotrigene

Antiseizure agents can cause suicidal ideations.

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11
Q

How common are anxiety disorders?

A

18% of the us pop has a diagnosable anxiety disorder, with about 1/5 of those regarded as severe.

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12
Q

How does the DSM-5 classify anxiety disorders? What are some examples?

A

Key syndrome is excessive fear and anxiety that manifests by: symptoms or fight or flight (AND arousal and escape) and muscle tension and vigilance (musculoskeletal and avoidance)

GAD, agoraphobia, panic disorder, social anxiety disorder, phobias, selective mutism, separation anxiety.

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13
Q

What are the characteristics for generalized anxiety disorder (GAD)?

A

Generalized persistent anxiety for at least 1 month.

Absence of phobias, panic attacks, or OCD.

Apprehensive expectation with worry fear and anticipation of misfortune to self and others, hyper-attentiveness, distractibility, difficulty in concentrating, insomnia, feeling on edge and impatience.

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14
Q

What are some somatic correlated of anxiety? What are some complications?

A

ANS arousal: sweating, tachy, palpitations, clammy hands, dry mouth, GI upset, freq urination and diarrhea.

Voluntary mule activation: jitteriness and inability to relax.

Complications: abuse of alcohol, sedatives and anti-anxiety medications are common.

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15
Q

Describe the stages of sleep?

A

Awake: random fast activity and low voltage (amplitude) and fast activity

Drowsy: alpha wave range and more voltage

Stage 1 (Light sleep): theta waves, slows down

Stage 2 (Deep sleep):slower waves with high amp signals with sleep spindles and K complexes

Delta deepest sleep: slow waves with very high amplitude

REM sleep: similar pattern to when you’re awake

  • Eyes moving muscles tense
  • Dreaming
  • Rapid eye movement sleep
  • Necessary and restorative
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16
Q

What are two types of sleep disorders?

A
  1. Insomnia:L disorders of initiating and maintaining sleep

2. Hypersomnia: disorders of excessive sleep or sleepiness

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17
Q

What are the different treatments for anxiety and insomnia?

A
  1. Benzodiazepines and related drugs
  2. SSRIs commonly used
  3. Buspirone
  4. Classical antihistamines
  5. Alcohol, cannabis, opiates
  6. Barbituiates
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18
Q

What occurs at the GABAergic synapse?

A

Dietary glutamate is converted into GABA and then packaged into vesicles.

When the neuron is depolarized, GABA is released into the synapse and can bind to GABA A and B receptors.

GABA A receptor is most important for drugs.

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19
Q

Where is GABA localized? What is the importance of it?

A

Primary inhibitory nt in the brain.

Hypothalamus, hippocampus, limbic system (amygdala), spinal cord, globus pallidus, substantia nigra.

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20
Q

What is the structure and function of the GABA A receptor? Where does GABA bind and what happens when it binds?

A

It’s an ANION channel made up of 4 or 5 transmembrane regions (depending on the location) with a pore in the center.

When GABA binds between the alpha and beta subunit, the channel opens up and allows chloride into the neuron to hyperpolarize the cell. This is why GABA is inhibitory.

21
Q

What happens when benzodiazepines bind to the GABA A receptor?

A

Benzodiazepines binding to the receptor improves GABAs ability to bind to the receptor.

This results in greater entry of chloride into the cell, and further hyperpolarization causing sleep and relaxation.

22
Q

What else can bind to GABA receptors? What does this tell us?

A

Barbiturates, benzodiazepines, alcohol, and neurosteroids.

This means there is a potential for drug interaction and additive effects that may be harmful because they all act on the same common pathway (the GABA receptor).

23
Q

What drugs are agonists of the benzodiazepine receptor?

A

Diazepam and zolpidem

24
Q

What drug is a benzodiazepine receptor antagonist that blocks the action of benzodiazepines at the GABA receptor?

A

Flumazenil

25
Q

What drug is a partial agonist for 5HT1A and inhibits adenylate cyclase and opens K+ channels? What else does this drug do?

A

Buspirone

Also binds to dopamine receptors.

Used to treat GAD.

26
Q

What benzodiazepines are used to treat anxiety? How are these given when treating anxiety?

A

Alprazolam
Diazepam
Lorazepam

Much lower doses to relieve anxiety than for a hypnotic dose (sleep).

27
Q

What benzodiazepine has a rapid onset of action, long duration of action, and is converted to an active metabolite?

A

Flurazepam

Active metabolite: desalkylflurazepam.

28
Q

What benzodiazepine is approved to treat both anxiety and insomnia? Which newer drug is preferred over diazepam and is primarily used to induce sleep?

A

Treat anxiety and insomina: lorazepam

Newer drug to induce sleep: zolpidem

29
Q

What role does lipophilicity play in the pharmacokinetics of diazepam and lorazepam?

A

Diazepam: high lipid solubility and rapid absorption/action and entry into the brain. Rapid redistribution after single dose, but active metabolites build up with more doses.

Lorazepam: less lipophilic, absorption and onset of action slower. Longer duration of action after single dose. No active metabolites.

ie lipophilicity determines speed of onset.

30
Q

What long-acting active metabolite is made from diazepam?

A

Desmethyldiazepam

31
Q

What are the CNS effects of benzodiazepines? What are the CN and respiratory actions?

A

Decreased anxiety
Sedation
Hypnosis
Muscle relaxation (higher doses)
Anterograde amnesia (IV) - for conscious sedation
Anticonvulsant
Minimal CV and respiratory actions at therapeutic doses.

32
Q

Can you kill yourself if you overdose on benzodiazepines alone?

A

NO. These will just make you very very sleepy but will not kill you when taken alone.

When alcohol or other drugs are added on, that’s when it can kill you.

33
Q

What drugs interact with benzodiazepines?

A

Other depressants such as ethanol, sedative hypnotics, and sedating antihistamines can cause additive CNS depression.

Combining benzodiazepines with opioids can be fatal (FDA black box warning).

Drugs that affect hepatic metabolism such as cimetidine can alter the metabolism of benzos.

34
Q

What are the clinical uses of benzodiazepines?

A 
Anxiety states 
Sleep disorders 
Muscle relaxant (diazepam)
Seizure treatment 
IV sedation and anesthesia 
Alcohol withdrawl (Chlordiazepoxide).
35
Q

What benzodiazepine can be used to treat alcohol withdrawal? How does this work?

A

Chlordiazepoxide

Cross tolerance/cross dependence occurs with everything that binds the GABA receptor. If you have physical dependence on one drug, other drugs with same action can be used to keep you out of withdrawal.

Need to do slow alcohol withdrawal to prevent seizures, so you switch to equiv amount of a long acting drug and then slowly withdraw this drug.

36
Q

What are symptoms of benzodiazepine withdrawal? How do you treat benzodiazepine abuse?

A

Anxiety, insomnia, irritability, headache, hyperacusis, hallucinations, seizures.

To treat abuse, gradually reduce dose and switch to longer acting drugs.

37
Q

What are characteristics of buspirone? What is it used to treat?

A

Not related to benzos, high affinity for 5HT1A receptors.

Less sedating than benzos, no cross tolerase. Does not potentiate other sedative-hypnotics or depressants not suppress symptoms of their withdrawl.

Treats GAD, therapeutic effects make take 1-2 wks.

38
Q

How do beta-b lockers treat anxiety?

A

They can be used for performance anxiety to decrease the autonomic effects associated with anxiety.

39
Q

What effects do benzodiazepines have on sleep?

A

Decreased latency to sleep (go to sleep faster).

Increases in stage 1 and 2, decreased time in stage 4, 4, and REM sleep (but this is made up for with the longer time spend sleeping).

Rebound insomnia upon withdrawal.

40
Q

What are adverse effects of benzodiazepines?

A

Daytime sedation, ataxia, rebound insomnia, tolerance and dependence, occasional idiosyncratic excitement and stimulation.

41
Q

What is the function of Zolpidem? What is the duration of action>?

A

Non-benzodiazepine that binds the BDZ receptor on the GABA receptor complex.

Weak anxiolytic (not good for anxiety), muscle relaxant and anticonvulsant at hypnotic dose.

DOA 5-6 hrs, extended release for 7-8 hours. Also available in oral spray or sublingual for nighttime waking.

42
Q

What are the pharmacokinetics of barbiturates? How are they metabolized?

A

Rapidly absorbed/distributed.
High lipid soluble compounds such as thiopental distribute to brain. Action terminated by redistribution.

Can induce own metabolism and that of other drugs.

Renal elim.

43
Q

What do barbiturates act on and what are their effects? What are some adverse effects?

A

GABA A Cl- ion channel and enhance action of GABA to increase inhibition.

  1. sedation
  2. Hypnotic action
  3. Anesthesia
  4. Anticonvulsant

Respiratory depression, tolerance, physical dependence, acute poisoning (coma, rep depression).

44
Q

Why are barbiturates rarely used? How does this compare to benzodiazepines?

A

Because they can cause coma and/or death at higher doses.

Benzodiazepines cannot kill you by themselves, they can only cause hypnosis and anesthesia. (but they can kill you when used with other depressants, alcohol, or opioids).

45
Q

What other drugs can be used as sedative-hypnotics?

A

Hydroxyzine: sedating H1 blocker

OTC sleep mediation that contain antihistamines such as diphenhydramine.

46
Q

What are skeletal muscle relaxants used for?

A

Reduce muscle tone associated with spasticity related to MS or of musculoskeletal disorders.

Spasticity is increases in tonic stretch reflexes and flexor muscle spasms.

47
Q

What GABAergic agent reduces spasticity partly mediated in the spinal cord and can be used in patients with muscle spasm of almost any origin including trauma? What other symptoms occur with this drug?

A

Diazepam - skeletal muscle relaxant

Produces sedation in post patients at the doses required to reduce muscle tone.

48
Q

What GABA-mimetic agent works at the GABA B receptor to cause hyperpolarization and presynaptic inhibition? What else does this drug result in?

A

Baclofen - skeletal muscle relaxant

Can result in decreased release of excitatory transmitters such as glutamate.

At least as effective as diazepam but with much less sedation.

49
Q

What drug is an alpha2 adrenergic agonist that’s related to clonidine and may enhance presynaptic and postsynaptic inhibition? What is this drug used for? What are side effects?

A

Tizanidine - skeletal muscle relaxant

May have similar efficacy to diazepam and baclofen for muscle spasms.

Side effects include drowsiness, hypotension, dry mouth, and asthenia (weakness).

Pharm Block 3 (15 decks)

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