3a: Sedative-Hypnotics, Antianxiety, Antidepressants Flashcards

1
Q

purpose of CNS drugs

A

to modify the activity of the neurons in the CNS, treat CNS disorders, and change the arousal levels of the CNS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

neurotransmitters

A

released by neurons to cause excitation or inhibition to other neurons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

examples of neurotransmitters in the CNS

A

ACh, monoamines, amino acids, peptides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

mechanism of CNS drugs

A

modification of the synaptic transmission, which is done by altering the quantity of the neurotransmitter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

two categories of Sedative-Hypnotics

A

benzodiazepines and nonbenzodiazepines (both used to promote sleep, specifically in short-term situations like hospital stays)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

benzodiazepines

A

used for anxiety and promoting sleep, considered safer than barbiturates (nonbenzos), less chance of lethal overdose, and can cause tolerance and physical dependence with long-term use

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

mechanism of benzos

A

increased inhibition at the CNS synapses that use GABA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

side effects of benzos

A

drowsiness, decreased motor performance, hang-over effect, anterograde amnesia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

suffix for benzos

A

(-am)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

nonbenzodiazepines (barbiturates)

A

used for sleep-hypnosis, CNS depressants, very small therapeutic index, very addictive, not commonly used

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

mechanism of barbiturates

A

not entirely clear but do bind to GABA receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

side effects of barbiturates

A

very addictive, drug abuse, hang-over effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

suffix for barbiturates

A

(-al)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

other compounds that can cause sedation-hypnosis

A

alcohol, antihistamines, antidepressants, antipsychotics, anticonvulsants, opioid analgesics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

pharmacokinetics of sedation-hypnosis drugs

A

very lipid-soluble, administered orally one dose at bedtime, absorbed from the GI tract, distributed uniformly throughout the body, metabolized in the liber, excreted through the kidneys

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

side effects of all sedative-hypnotics

A

tolerance and dependence, complex motor behaviors (sleep walking, sleep driving, etc.), GI discomfort, dry mouth, sore throat, muscular incoordination

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

indications for anti anxiety drugs

A

generalized anxiety, social anxiety, panic disorder, OCD, PTSD

18
Q

what is the most common benzo for treating anxiety?

A

Valium

19
Q

Valium is not good for what population, and why?

A

not good for the elderly, because it has a long half-life, and they cause sedation, confusion, and memory problems (associated with increased fall risk and hip fractures)

20
Q

what is rebound anxiety (related to benzos)?

A

removal of benzo that causes anxiety levels to return to pre-treatment levels

21
Q

mechanism of BuSpar

A

increases the effects of the neurotransmitter serotonin

22
Q

side effects of BuSpar

A

headache, dizziness, nausea, restlessness, hypothermia, low risk of abuse

23
Q

why are antidepressants an effective way to treat anxiety?

A

they typically have fewer side effects and lower risk of addiction than anti-anxiety medications

24
Q

examples of antidepressants

A

Paxil, Effexor, Zoloft

25
Q

indications for beta-blockers

A

arrhythmias, hypertension, and other cardiac issues (decreases anxiety without the sedation)

26
Q

symptoms of depression

A

inappropriate disposition, feeling unreasonably sad or discouraged, fluctuating between periods of depression and excessive excitation

27
Q

biological cause of depression

A

disturbance in CNS neurotransmission involving neurotransmitters serotonin, norepi, dopamine

28
Q

four categories of antidepressants

A

SSRIs, SNRIs, tricyclics, MAOs

29
Q

what is the key neurotransmitter that helps regulate mood and depression?

A

serotonin

30
Q

mechanism of SSRIs

A

block the reuptake of serotonin into the presynaptic terminals (allowing serotonin to stay in the synaptic cleft and exert its effect longer)

31
Q

mechanism of SNRIs

A

same as SSRIs, but also blocks reuptake of norepinephrine

32
Q

mechanism of tricyclics

A

block reuptake of all three synapses: serotonin, norepinephrine, and dopamine

33
Q

mechanism of MAO inhibitors

A

prevents MAO enzyme from breaking down neurotransmitters, therefore keeping neurotransmitters in the synaptic cleft for longer

34
Q

pharmacokinetics of antidepressants

A
  • typically administered orally
  • small dosages initially, increased slowly
  • metabolized in liver
35
Q

side effects of antidepressants

A

most common: nausea, vomiting, diarrhea, constipation
less common: anticholinergic, cardiac effects, orthostatic hypotension

36
Q

What is the most serious side effect of SSRIs and SNRIs?

A

serotonin syndrome

37
Q

mechanism and symptoms of serotonin syndrome

A

excessive serotonin built up in brain can lead to sweating, restlessness, tremor, clonus, rigidity, progressing to seizures, coma, death

38
Q

what else are antidepressants used to treat?

A

chronic pain

39
Q

what is the primary drug used to treat bipolar disorder?

A

lithium

40
Q

side effects of lithium

A

possible toxicity (since lithium is not metabolized, only excreted in urine)

41
Q

four systems affected by lithium toxicity

A

CNS, GI, CV, renal

42
Q

rehab implications of antidepressants

A
  • 2-4 week delay from start until effects
  • depression may increase during this time
  • 1/3 of patients with depression do not respond to meds