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PHAR370- Fundamentals of Pharmacology and Therapeutics > Module 3- Drugs that Influence the CNS > Flashcards

Module 3- Drugs that Influence the CNS Flashcards

1
Q

Excessive CNS excitation can lead to…

A

Deleterious effects including

  1. anxiety
  2. insomnia
  3. seizures
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2
Q

Neurochemistry of brain is dependent on

A

The balance between excitatory and inhibitory signals

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2
Q

What is the primary excitatory neurotransmitter in the brain?

A

Glutamate

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3
Q

What is the primary inhibitory neurotransmitter in the brain?

A

Gamma-aminobutyric acid (GABA)

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4
Q

Treatment for anxiety and insomnia?

A

Appropriate treatment can include

  1. behavioural changes (i.e. stress reduction and physical exercise)
  2. Prescription medication (i.e. sedative hypnotic agents)
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5
Q

Sedative Hypnotic agent examples

A
  1. anti-anxiety effect- used to treat anxiety disorders (OCD)
  2. sedation: relieve anxiety, decrease activity, moderate excitement and calm individual
  3. hypnosis: produce drowsiness and aid in the onset and maintenance of sleep
  4. general anesthesia: state of unconsciousness with absence of pain sensation
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6
Q

Examples of anxiety disorders sedative hypnotics treat

A
  1. generalized anxiety
  2. obsessive compulsive disorder
  3. panic disorder
  4. post traumatic stress disorder
  5. phobias
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7
Q

How doe sedative hypnotics treat anxiety?

A

Reduces the amount of glutamate-induced neural excitation by increasing the GABA inhibitory signalling in the brain

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8
Q

The Chloride ion channel

A
  • GABA binds to chloride channel on the membrane of neuron in the brain and spinal cord
  • binding causes channels to open and allows negatively charged ions to flow into the cell, resulting in an inhibitory effect
  • SHAs also bind here, on a different site on the chloride channel -> resulting in an increase in synaptic inhibition and dampening neuronal responses
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9
Q

Drugs that bind to the chloride channel

A
  1. benzodiazepines
  2. Barbiturates
  3. The “Z” drugs
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10
Q

Where do benzodiazepines bind

A

bind to the chloride channel at the benzodiazepine receptor, and increases the frequency of GABA receptor mediated opening of the chloride channel

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11
Q

How are benzodiazepines classified?

A

Allosteric activator

Benzos bind to and activate a separate receptor on the chloride channel than the neurotransmitter GABA, which makes it an allosteric activator

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12
Q

Pharmacokinetics of benzodiazepines

A

absorption: usually taken as a capsule, or tablet

metabolism: have different durations of action, determined by the rate of liver metabolism and formation of, or lack of formation of pharmacologically active metabolites

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13
Q

Pharmacological properties of Benzodiazepines

A
  • possess very high therapeutic index
  • relieve anxiety
  • produce sedation and amnesia
  • decreased aggression
  • some are effective hypnotics
  • minimal suppression of REM type sleep
  • skeletal muscle relaxation
  • anticonvulsant action
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14
Q

Short term use of benzodiazepines

A

Produces: relaxation, calmness, and relieve from anxiety of tension

Adverse effects: drowsiness, lethargy, impairment of thinking/memory, nausea, and constipation

Moderate doses can impair motor coordination and driving, so patients should refrain

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15
Q

Long term use of benzodiazepines

A

Varies between individuals
- some take large amounts for long periods of time without major evidence of intoxication
- others demonstrate symptoms of chronic-sedative hypnotic intoxication (i.e. impaired thinking, poor memory/judgement, disorientation and incoordination)

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16
Q

Elderly and benzodiazepines

A

can produce cognitive dysfunction, because benzos metabolize more slowly than young adults, often leading to over-sedation, falls and injury

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17
Q

Pregnant/breastfeeding women and benzodiazepines

A

benzos freely cross the placenta and distribute int the fetus
- risk of fetal abnormalities

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18
Q

lethality and benzodiazepines

A

Death from overdose is rare, but does occur following ingestion of enormous doses

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19
Q

Flumazenil

A

Benzodiazepine receptor antagonist that blocks the effect of benzodiazepines

  • Antidote for benzo overdosing
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20
Q

Benzodiazepines misuse potential

A

Low- as they are weaker reinforcing properties than barbiturates, opioids, and stimulants

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21
Q

Benzodiazepine use disorder

A

Low misuse, but high degree of cross tolerance among benzos and other sedative-hypnotic drugs

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22
Q

Barbiturates

A

Potent CNS depressants

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23
Q

Classes of barbiturate

A

Long acting (1-2 days)- phenobarbital

Short acting (3-8 hours)- secobarbital

ultrashort acting (20 mins)- thiopental

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24
Q

Where do barbiturates bind to?

A

bind to chloride channel at barbiturate receptor, and increase the duration that the channel is open

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25
Q

Pharmacological properties of barbiturates

A
  • low therapeutic index
  • suppress REM type sleep
  • lethality is common (especially combined w alcohol)
  • death can occur from withdrawal
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26
Q

Barbiturate antidote

A

There is none

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27
Q

Clinical use of barbiturates

A

Limited use since replaced with safer drugs

Ultrashort and short acting can be used to induce anesthesia,

Long acting agents- anti seizure drugs

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28
Q

Barbiturate misuse potential

A

equal to or greater than alcohol

  • pleasurable effects
  • inherent harmfulness is high
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29
Q

barbiturate use disorder

A

tolerance develops very rapidly to sleep induction and mood effects, often within a few weeks of nightly administration

  • addiction can result from regular use
  • withdrawal syndrome occurs after discontinuation of chronic use
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30
Q

The “Z” drugs

A

Zolpidem
zopiclone
similar drugs that start w “Z”

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31
Q

Where do the “Z” drugs bind

A

Bind to a subset of the GABA receptors, causing sedation and minimal REM disruption

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32
Q

What do “Z” drugs have advantages over benzodiazepines as a hypnotic?

A

they disturb sleep patterns (REM) even less than benzos

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33
Q

Therapeutic uses of GABA-modifying drugs

A

Anxiety- benzos effective in reducing symptoms of anxiety

Insomnia- “Z” drugs or short acting barbiturates (cause drowsiness)

Seizures- long acting barbiturates (i.e. phenobarbital) used to treat partial seizures
- benzos used for status epilepticus

Skeletal muscle spasms- benzos

Alcohol withdrawal syndrom- benzos due to cross tolerance

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34
Q

Seizure disorders

A

second most common neurological disorder after a stroke

  • Generalized seizures
  • partial seizures
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35
Q

General seizures

A

account for 40% of all seizures

involve the entire CNS, arising in both cerebral hemispheres, and are accompanied by loss of consciousness

Can be subdivided into several classes based on the type of movement and duration of loss of consciousness

  1. tonic-clonic
  2. status epilepticus
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36
Q

Partial seizures

A

account for the other 60% of seizures

May involve motor disturbances and alterations of perception or behaviour

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37
Q

How do seizures happen?

A

Result from a sudden repeated spontaneous discharge of groups of excitatory neurons on CNS, that may radiate to involve surrounding areas of the brain

  • must involve glutamatergic neurons since they are major excitatory neurons in CNS
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38
Q

Treatment of seizures

A

Mechanism 1-increasing inhibitory input

Mechanism 2- blocking electrical activity of nerve

Mechanism 3- decrease excitatory transmission

39
Q

Seizure treatment- mechanism 1

A

Increasing inhibitory input to the neuron to suppress firing
- accomplished by increasing GABA activity in the brain

i.e. valproate, phenobarbital, and benzodiazepines

40
Q

Seizure treatment- mechanism 2

A

blocking electrical activity of nerve to slow the nerve impulses
- accomplished by blocking sodium channel electrical activity, which will slow the conduction of the nerve impulse

i.e. lamotrigine and valproate

41
Q

Seizure treatment- mechanism 3

A

Decrease excitatory transmission
- accomplished by decreasing the release of glutamate at the synapse

i.e. lamotrigine

42
Q

Pharmacokinetics of anticonvulsants

A

Regardless of specific drug, most anti-seizure medications have similar pharmacokinetics since they all must cross the blood-brain barrier and enter the CNS

absorption rate= 80-100%

Cleared= mostly by liver

43
Q

Adverse effects of anticonvulsants

A

CNS- sedation, tremors, ataxia, and cognitive/visual impairment

Immune system: benign skin rashes occur in 5-20% of patients

Hepatic: enzymes may become elevated, but generally asymptomatic

GI: nausea, vomiting, and diarrhea

44
Q

Anticonvulsants and drug interactions

A

most anticonvulsants induce biotransformation enzymes, the metabolism of concurrently administered drugs is increased, resulting in a decrease in the duration of action of concurrent drugs

45
Q

Toxicity and overdose in anticonvulsants

A

Even though they act by decreasing CNS activity, they are rarely lethal

most dangerous effect = respiratory depression, which can be potentiated by other CNS depressants

Overdose treatments = supportive therapy

46
Q

Withdrawal and anticonvulsants

A

does occur, and severity depends on the drug being withdrawn

withdrawal can cause increased frequency and severity of seizures

47
Q

Depression

A

Mental illness affecting 10-15% of the population over a lifetime

Feeling of intense
- sadness
- hopelessness
- despair
- self-disproval
- physical and mental slowing
- sometimes suicidal thoughts

48
Q

Types of depression

A
  1. Major depression (25%)
  2. Depression associated with bipolar disorder (10-15%)
  3. Reactive depression (60%)
49
Q

Major Depression

A

Characterized by depressed mood for at least 2 weeks and/or a loss of interest or pleasure in activities

associated with significant morbidity and mortality

50
Q

The amine hypothesis

A

depression may be due to a reaction in the activity of one or more neurotransmitter systems in the CNS

  1. serotonin + norepinephrine are released from presynaptic neuron
  2. neurotransmitters are removed from synaptic cleft via SERT and NET, this terminating their action
  3. MAO-A inactivates the neurotransmitters, and they cannot be repackaged into vesicles for subsequent release
  4. theorizes that in depression, the levels of released neurotransmitters fall below normal levels, leading to impaired excitation of neurons… depression
51
Q

What does SERT and NET stand for?

A

SERT- serotonin reuptake transporters

NET- norepinephrine uptake transporters (NET)

52
Q

What does MAO stand for?

A

enzyme monoamine oxidase

53
Q

Neurotrophic hypothesis

A

Depression may be due to a loss of neurotrophic support characterizes by a decrease in neurogenesis and synaptic connectivity

A reduction in nerve growth factors are responsible for a loss of neural plasticity and neurogenesis, and antidepressants stimulate neurogenesis and synpatic connectivity in cortical areas of the brain is a protein required for neural growth and axon sprouting within the NS

54
Q

Nerve growth factors and major depression

A

brain derived neurotrophic factors (BDNF) is a protein required for neural growth and axon sprouting within the nervous system

changes in trophic factors (BDNF) plays a major role in the development of MDD

55
Q

the neuroendocrine hypothesis

A

depression may be due to an abnormality in hormones affecting mood

56
Q

Hormones affecting mood

A
  1. cortisol
  2. thyroid hormones
  3. sex hormones
57
Q

Mechanism of action of antidepressants

A
  1. block neurotransmitter reuptake systems
  2. block metabolism of neurotransmitters, thereby increasing amount of neurotransmitter released
  3. directly increasing the amount of neurotransmitter released
58
Q

Types of antidepressants that block neurotransmitter reuptake systems

A
  1. tricyclic antidepressants (TCAs)
  2. serotonin reuptake inhibitors (SSRIs)
  3. serotonin norepinephrine reuptake inhibitors (SNRIs)
59
Q

Tricyclic antidepressants

A

inhibit the reuptake transporters of both serotonin and norepinephrine (SERT/NET) into presynaptic axon, causing increased concentration of these neurotransmitters to be present in the synaptic cleft

example: Nortriptyline; tricyclic antidepressant used to treat depression

60
Q

Adverse effects of tricyclic antidepressants

A
  1. anticholinergic effects (dry mouth, urinary retention, constipation, blurred vision)
  2. antiadrenergic (alpha) effects (hypotension when standing)
  3. antihistaminic actions (sedation)
  4. block sodium channels (arrhythmias, seizures, fatal in overdose)
  5. weight gain
61
Q

Serotonin reuptake inhibitors (SSRIs)

A

most widely used class of drugs in treatment of depression

much less of an effect on ANS than TCAs

Example: Fluoxetine

62
Q

Adverse effect of SSRIs

A

Cause nausea, headaches, nervousness, and insomnia more commonly than TCAs

High incidence of sexual dysfunction

63
Q

Drug-drug interactions of SSRIs

A
  1. decreased metabolism
    • SSRIs inhibit the CYP450 enzymes, so metabolism of concurrently administered drugs is altered
    • may lead to drug toxicity or loss of drug efficacy
  2. serotonin syndrome
    • occurs due to concurrent use of multiple drugs that increase serotonin
64
Q

Serotonin norepinephrine reuptake inhibitors (SNRIs)

A

block the transporters for both serotonin and norepinephrine

Unlike TCAs, these drugs do not have effects at autonomic and histaminic receptors

taken if patients do not respond to SSRIs

Example: venlafaxine

65
Q

Adverse effects of SNRIs

A

increase in blood pressure and heart rate

66
Q

types of antidepressants that block neurotransmitter metabolism

A

Monoamine oxidase (MAO) inhibitors

67
Q

Monoamine oxidase (MAO) inhibitors

A

by blocking a major pathway for the monoamine neurotransmitters, the MAO inhibitors allow more amines to accumulate in presynaptic stores, resulting in more to be released when the nerve impulse reaches the presynaptic neuron

68
Q

MAO-A

A

enzyme primarily responsible for metabolism of norepinephrine, serotonin and tyramine

69
Q

MAO-B

A

more selective for metabolism of dopamine

70
Q

Drug-drug interactions of MAOIs

A

if MAO inhibitors are prescribed, patients must be warned that they interact with many other drugs and w tyramine-containing foods

  • a MAO inhibitor can cause serotonin syndrome
71
Q

antidepressants that increase the amount of neurotransmitter released

A

autoreceptor antagonists

72
Q

autoreceptor antagonists

A

new drug that inhibits the activation of alpha-2 receptors

  • alpha-2 receptors located on the presynaptic neuronal membrane are autoreceptors, meaning that activation of these receptors inhibits the release of neurotransmitter from the presynaptic neuron
  • drugs that block alpha-1 autoreceptors remove this negative feedback loop, allowing the presynaptic neuron to release more neurotransmitter into the synaptic cleft

Example: mirtazapine

73
Q

Electroconvulsive therapy

A

patients are given a muscle relaxant to prevent movement and are put under general anesthesia
- electrodes are then placed on the head to sent ~500-900 milliamo current through brain, sparking a brief seizure

74
Q

Bipolar disorder

A

brain disorder characterized by manic and depressive phases

Symptoms of manic phase:
- elation
- excitement
- hyperactivity
- disinhibition
- aggression
- some psychotic symptoms

Symptoms of depressive phase:
- depressed mood
- sleep disturbances
- anxiety

75
Q

Treatment of manic phase of BPD

A
  1. reduces the patient’s mood to a “normal” range with antipsychotic medications such as haloperidol, chlorpromazine, or new typical antipsychotics
  2. stabalize the patient’s mood within “normal” range with a mood stabilizer
76
Q

treatment of depressive phase of BPD

A

The depressive phase is not the same as MDD, antidepressants are sometimes used, but may actually make matters worse. Mood stabilizers tend to be effective

77
Q

Antipsychotics

A

class of drugs used to reduce psychotic symptoms caused by a variety of disorders, including bipolar disorder, schizophrenia, and drug-induced psychoses

78
Q

Three classes of antipsychotics

A
  1. phenothiazine
  2. Haloperidol
  3. Atypical antipsychotics
79
Q

Phenothiazine antipsychotics

A

block dopamine receptors in different regions of the CNS

Not highly specific to dopamine receptors, therefore some effects are related to the antagonism of other receptor systems, such as cholinergic, histaminic, and alpha-adrenergic receptors

80
Q

Adverse effects of phenothiazine

A

antagonism of dopamine receptors in the
- nigrostriatal system of the brain results in extrapyramidal movement disorders (tremor, rigidity of limbs and slowing of movement, reduction in spontaneous activity, dystonia)

  • hypothalamus will result in the excess release of prolactin
81
Q

Blockade of cholinergic (muscarinic) receptors due to phenothiazine

A

Therapeutic effects: reduction of extrapyramidal adverse effects

Adverse effects: blurred vision, dry mouth, constipation, difficulty urinating

82
Q

Blockade of histamine receptors due to phenothiazine

A

Adverse effects: sedation, drowsiness, and weight gain

83
Q

Blockade of a-adrenoreceptors due to phenothiazine

A

adverse effects: postural hypotension, dizziness, reflex tachycardia

84
Q

Haloperidol

A

Like phenothiazines, it competitively blocks dopamine receptors

Useful alternative for patients who do not respond to or cannot tolerant phenothiazines

85
Q

Second-generation antipsychotics (i.e. atypical antipsychotics)

A

Produce less extrapyramidal side effects

Have dual action by blocking dopamine and serotonin receptors

86
Q

Examples of second generation antipsychotics

A

clozapine, risperidone, and olanzapine

87
Q

Side effects of atypical antipsychotics

A

weight gain, increased risk of developing diabetes, and sudden cardiac death due to abnormality in the rhythm of the heart

88
Q

Other uses for atypical antipsychotics

A
  • schizoprenia
  • delusions and aggression associated with dementia in the elderly
  • autism spectrum disorder
  • developmental disorder
  • posttraumatic stress disorder (as an alternate to antidepressants)
  • obsessive compulsive disorder
  • borderline personality disorder
89
Q

Mood stabilizers

A

Second category, used to prevent mania (highs) and depression (lows)

90
Q

Two categories

A
  1. Lithium carbonate
  2. Anticonvulsants
91
Q

Lithium carbonate

A

mood stabilizing agent used to prevent mood swings in patients, also used to treat mania

92
Q

Mechanism of action of lithium carbonate

A

not yet resolved but 2 possibilities under consideration…
1. Effect on electrolytes and ion transport
2. Effect on second messengers that mediate terminate transmitter action

93
Q

Pharmacokinetics of lithium

A
  • period of 2-4 weeks of administration may be required for lithium to have a full therapeutic effect
  • body elims lithium as if it were sodium
  • increased sodium intake increases lithium excretion

-narrow therapeutic index

94
Q

Adverse effects of lithium

A
  • tremour, thirst, excessive urination, edema, and weight gain
  • confusion and loss of muscle coordination
  • mild hypothyroidism
  • toxic kidney effects are observed in some individuals treated chronically with lithium, but are uncommon
  • when taking during pregnancy, it can cause cardiac malformations in the fetus
95
Q

Anticonvulsants as mood stabilizers

A

(i.e. valproic acid) have a more rapid onset of action than lithium, and are often preferred

Note: not all anticonvulsants are mood stabilizers

PHAR370- Fundamentals of Pharmacology and Therapeutics (5 decks)

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