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PHAR 370 > Module 3: Drugs that Influence the CNS > Flashcards

Module 3: Drugs that Influence the CNS Flashcards

1
Q

What is the main excitatory neurotransmitter in the brain?

A

Glutamate

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2
Q

What is the main inhibitory neurotransmitter in the brain?

A

Gamma-aminobutyric acid (GABA)

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2
Q

How do drugs increase the GABA inhibitory signalling in the brain?

A

The drugs mimic the inhibitory effects of GABA by binding onto the chloride channel, slowing excitatory CNS transmission

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3
Q

What is the definition of Drug Classes?

A

A class of drugs is a group of drugs that have the same mechanism of action and similar pharmacological properties

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4
Q

T/F Each class of sedative-hypnotic agents bind to a different site on the chloride channel

A

True!

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5
Q

What are the three main classes of sedative-hypnotic drugs that bind to the chloride ion channel?

A

Benzodiazepines, barbiturates, the “Z” drugs

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6
Q

What are the three classes of barbiturates?

A

Long acting (1-2 days)
Short acting (3-8 hours)
Ultrashort acting (20 minutes)

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6
Q

What receptor do benzodiazepines bind of the chloride ion channel? What happens when it binds?

A

The benzodiazepine receptor. Upon binding, benzodiazepines increase the frequency of the opening of the chloride channel, enhancing GABA’s effect

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6
Q

What are some of the pharmacological properties of Benzodiazepines?

A

High therapeutic index, relieve anxiety, produce sedation, decrease aggression, minimal suppression of REM sleep, skeletal muscle relaxation

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6
Q

How do benzodiazepines negatively effect pregnant/breastfeeding individuals?

A

Benzodiazepine freely crosses the placenta and distributes to the fetus. In the first trimester, can cause fetal abnormalities. Also transfers through the milk, which can expose infants to doses, leading to sedation or death

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6
Q

Which of the GABA modifying drugs are used to treat insomnia? Why?

A

The “Z” drugs and short-acting benzodiazepines; The depressive nature makes users feel drowsy

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6
Q

Describe the pharmacology of barbiturates

A
  • Low therapeutic index
  • Suppress REM type sleep
  • Lethality is common when combined with alcohol
  • No antidote
  • Death can occur from withdrawl
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6
Q

Why do benzodiazepines have a high misuse potential?

A

They are wildly prescribed and are often used with other CNS depressants (alcohol) or stimulants

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6
Q

Describe the clinical use of barbiturates

A

Ultrashort and short acting can be used to induce anesthesia.
Long acting have been used as anti-seizure medications
Limited clinical use

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6
Q

How do benzodiazepines work?

A

They bind to the chloride channel at the barbiturate receptor, and act as an allosteric activator, increasing the duration of the opening of the chloride channel, increasing GABA effects

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6
Q

How do benzodiazepines negatively effect the elderly?

A

Can produce cognitive dysfunction. Due to slower metabolism, are more likely to experience over-sedation and falls

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7
Q

Why do barbiturates have a high misuse potential?

A

They have quite a bit of pleasurable effects, tolerance is rapidly made

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7
Q

T/F Benzodiazepines are first line of treatment for anxiety? Explain.

A

False. They are second-line due to their potential for over-sedation, cognitive impairment, and psychomotor incoordination

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8
Q

Which of the GABA modifying drugs are used to treat anxiety?

A

Benzodiazepines

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9
Q

Which of the GABA modifying drugs are used to treat seizures?

A

Long acting barbiturates for partial seizures, benzodiazepines for status epilepticus

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9
Q

Which of the GABA modifying drugs are used to treat skeletal muscle spasm (e.g., cerebral palsy). Why?

A

Benzodiazepines; relax the muscles

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9
Q

Which of the GABA modifying drugs are used to treat alcohol withdrawl syndrome? Why?

A

Benzodiazepines; have cross tolerance with alcohol

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9
Q

What are generalized seizures?

A

Involve the entire CNS, accompanied by loss of consciousness. Subdivided based on the type of movement and duration of loss of consciousness that occurs during the seizure

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10
Q

What are the three ways anti-seizure drugs decrease glutamate-induced excitation?

A

Increasing the inhibitory input (GABA)
Blocking electrical activity of the nerve to slow nerve impulses (blocking sodium channel activity)
Decreasing excitatory transmission (decreasing the release of glutamate at the synapse)

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10
Q

What are partial (focal) seizures?

A

Involve focal areas of the brain and have more restricted symptoms. May involve motor disturbances, as well as alterations of perceptions or behaviour

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11
Q

What are some of the adverse effects of anticonvulsants?

A

Sedation, tremor, cognitive impairment, nausea, vomiting, diarrhea, elevated hepatic enzymes, skin rashes

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12
Q

How are adverse effects of anticonvulsants minimzied?

A

By starting with a low dose and slowly increasing; administering with meals

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13
Q

T/F Most anticonvulsants reduce biotransformation enzymes

A

False! They induce biotransformation enzymes - so the metabolism of concurrently administered drugs is also increased

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14
Q

What are the three types of depression?

A

Reactive (secondary) depression
Major depression
Depression associated with dipolar disorder

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15
Q

What are the three theories surrounding the cause of major depression? Give a brief description

A

The amine hypothesis
Neurotrophic hypothesis
Neuroendocrine hypothesis

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16
Q

Give a brief description of the amine hypotheisis

A

Suggests that depression is the result of a deficiency of the excitatory neurotransmitters in the CNS (norepinephrine, serotonin, and dopamine)

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16
Q

Give a brief description of the neurotrophic hypothesis

A

Depression is associated with reduced neurotrophic support characterized by a decrease in neurogenesis and synaptic connectivity

16
Q

Give a brief description of the neuroendocrine hypothesis

A

Depression may be due to an abnormality in hormones affecting mood

16
Q

What are the three ways antidepressants work?

A

Via blocking neurotransmitter reuptake systems
Blocking neurotransmitter metabolism - increasing the amount released
Directly increasing the amount of neurotransmitter released

17
Q

What is the overall end goal of antidepressants?

A

To increase the amount of neurotransmitter within the synaptic cleft

17
Q

What are the three kinds of antidepressants that function by blocking the neurotransmitter reuptake systems?

A

Tricyclic antidepressants (TCAs)
Serotonin reuptake inhibitors (SSRIs)
Serotonin norepinephrine reuptake inhibitors (SNRIs)

17
Q

How do SNRIs work?

A

They block the transporters for both serotonin and norepinephrine

17
Q

How do tricyclic antidepressants (TCAs) work?

A

Inhibit the reuptake of transporters of both serotonin and norepinephrine into the presynaptic axon, causing an increased concentration of the neurotransmitters left in the synaptic cleft

17
Q

What are some adverse effects of SSRIs?

A

Nausea, headache, nervousness, insomnia, sexual dysfunction, decreased metabolism

Key: Serotonin syndrome, sexual dysfunction

17
Q

What are some of the common adverse effects of TCAs

A

Anticholinergic effects (dry mouth, constipation)
Hypotension when standing uo
Sedation
block sodium channels; arrhythmias, seizures
Weight gain

Key: Anticholinergic, antiadrenergic and antihistaminic effects; weight gain

17
Q

How do SSRIs work?

A

Block the serotonin transporter protein in the presynaptic terminal

17
Q

When are TCAs used over other drugs of this class?

A

Only used when other drugs fail to control the symptoms of depression, due to their intense adverse effects

17
Q

When are SSRIs used over other drugs?

A

First line of treatment for depression due to their high safety profile

17
Q

What is serotonin syndrome?

A

Something that occurs due to concurrent use of multiple drugs that increase serotonin. Characterized by muscle rigidity, elevated body temp, confusion, agitation

17
Q

What are the adverse effects of SNRIs?

A

Key: Same as SSRIs and Increased BP and heart rate

18
Q

When are SNRIs used over other drugs?

A

When they don’t respond to SSRIs

19
Q

What is the common example of antidepressants that function by blocking the neurotransmitter metabolism?

A

Monoamine oxidase (MAO) inhibitors

20
Q

How do MAO inhibitors work?

A

MAO inhibitors block the enzyme that metabolizes norepinephrine, serotonin, and tyramine (MAO-A) and dopamine (MAO-B). This allows for more amines to accumulate in the presynaptic stores, so more can be released when the nerve impulse reaches the presynaptic neuron

21
Q

What are some key adverse effects of MAOis?

A

Hypertensive crisis (severe increase in BP)
Serotonin syndrome

22
Q

When are MAOIs used over other drugs?

A

Are second line therapy; used when other drugs have failed

23
Q

What is the common antidepressant that functions by directly increasing the amount of neurotransmitter released from the presynaptic nerve?

A

Autoreceptor antagonists

24
Q

How do autoreceptor antagonists work?

A

Inhibits the activation of a2 receptors, which removes a negative feedback loop in the neuronal membrane, allowing the presynaptic neuron to release more neurotransmitter

25
Q

What is a key adverse effect of Autoreceptor antagonists?

A

Are also an antagonist at some serotonin and histamine receptors

26
Q

When are autoreceptor antagonists used over other drugs?

A

Prescribed if they don’t response to SSRI therapy

27
Q

What is electroconvulsive therapy? When is it used?

A

ECT are electrodes that are put on the head and spark a brief seizure. Has minimal adverse effects, and is valuable in those who have psychotic depression

28
Q

What are the two phases of treatment in bipolar disorder?

A

Reduction of patient’s mood to a “normal” range with antipsychotics
Stabilization of a patient’s mood within “normal” range with a mood stabilizers

29
Q

T/F Antidepressants can make the depressive phase of bipolar disorder worse

A

True

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PHAR 370 (3 decks)

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