Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharm III > Flood Chapter 43 > Flashcards

Flood Chapter 43 Flashcards

1
Q

Elderly patients taking antidepressant therapy are at particular risk for?

A

toxicity

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

Drugs used for psychopharmacologic therapy include? (5)

A

antidepressants, anxiolytics, lithium, antipsychotics, and anticonvulsants.

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

______and ________are the drugs most likely to be prescribed by primary care physicians for the treatment of depression in adults.

A

Antidepressants and anxiolytics

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

What drugs are useful for treatment of bipolar disorders and psychotic disorders including schizophrenia?

A

Lithium, anticonvulsants, and antipsychotic

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

Antidepressant therapy side effects may be less well tolerated among the elderly population due to age. True/False

A

False: They are less tolerated due to coexisting disease

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

It is estimated that up to 50% of the population is treated for a depressive illness at some time in life. True or False?

A

False: Its 10% of the population not 50% of the population.

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

It is well accepted that anesthesia can be safely administered to patients being treated with drugs used to treat mental illness. True/False

A

True

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

Clinical uses of antidepressant drugs include?

A 
Childhood ADHD
Bulimia
PTSD
Unipolar and Bipolar depression
OCD
Migraine prophylaxis
Neuropathic pain
Social Phobia
Panic disorder
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Neurobiologically, reuptake blockade or monoamine oxidase (MAO) inhibition occurs promptly after initiation of antidepressant therapy, but clinical improvement typically does not occur for 2 to 4 weeks. This could be explained by?

A

Perhaps adaptive changes including downregulation of neurotransmitter receptors are necessary before evidence of clinical improvement appears.

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

Antidepressants are logically classified based on their?

A

chemical structures and their acute neuropharmacologic effects.

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

The precise mechanism by which antidepressants work is

A

unknown

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

Antidepressants appear to act by

A

altering noradrenergic neurotransmission and/or serotoninergic neurotransmission thereby increasing the amount of norepinephrine and serotonin in synapses.

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

What is the black box warning on Newer SSRIs

A

Increased suicidal tendencies in children and adolescents.

Nevertheless, the risk is small and many patients benefit from treatment with SSRIs emphasizing the need to individualize therapy.

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

What are the drugs of choice for the treatment of mild to moderate depression

A

selective serotonin reuptake inhibitors (SSRIs)

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

First-line pharmacotherapy for panic disorder and obsessive-compulsive syndrome are?

A

SSRIs

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

SSRIs are also effective in treatment of social phobia and posttraumatic stress disorder. T/F

A

True

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

A prominent cause of noncompliance with SSRI therapy in both men and women is?

A

drug-induced sexual dysfunction in both men and women (delayed ejaculation, anorgasmia, decreased libido).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Newer SSRIs are believed to act on ________ and _________ pathways in the brain.

A

serotonin and norepinephrine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

MOA of newer SSRIs include

A

Dual serotonin and norepinephrine reuptake blockade (venlafaxine) and α2-receptor blockade (mirtazapine).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

SSRIs that share the ability to block the reuptake of serotonin include (6 Older SSRIs)

A 
fluoxetine
paroxetine
sertraline
fluvoxamine
citalopram
escitalopram.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

This newer SSRI may cause hypertension it some individuals

A

Venlafaxine.

It has dual serotonin and norepinephrine reuptake blockade.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Standard practice dictates trying several SSRIs before moving to another class of medication because?

A

Different SSRIs have different side effect profiles.

Patients who do not respond to one drug or who fail to tolerate the drug may do well on a different SSRI.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

There is abundant evidence that _______ receptors are involved in the etiology of anxiety.

A

serotonin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Potent inhibition of serotonin reuptake appears to be necessary for effectiveness in the treatment of ___________.

A

obsessive-compulsive disorders

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Compared with tricyclic antidepressants, SSRIs are preferred because?

A

Lack anticholinergic properties

Do not cause postural hypotension or delayed conduction of cardiac impulses

Do not appear to have a major effect on the seizure threshold.

Are relatively safe when taken in overdose except for Venlafaxine.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

The most important advantage of SSRIs compared with tricyclic antidepressants is

A

the relative safety of SSRIs when taken in overdose.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

This SSRI may be similar to tricyclic antidepressants with respect to elevated overdose-associated risk associated with proconvulsant and cardiac side effects.

A

Venlafaxine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Common side effects of SSRIs include?

A

insomnia, agitation, headache, nausea, and diarrhea.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Should SSRIs be suddenly discontinued?

A

Tapering all SSRIs before discontinuance is recommended especially for drugs with short elimination half-times.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Abrupt discontinuation of SSRIs with short elimination half-times (paroxetine, venlafaxine) may be associated with?

A

dizziness, paresthesias, myalgias, irritability, insomnia, and visual disturbances.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Abrupt discontinuation of SSRIs with short elimination half-times (paroxetine, venlafaxine) may be associated with?

A

dizziness, paresthesias, myalgias, irritability, insomnia, and visual disturbances.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

First SSRI introduced in US is?

A

Fluoxetine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

How often can you increase the dose of Fluoxetine

A

once every 4 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Therapeutic effect of fluoxetine is evident in what time?

A

2-4 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is the elimination half time of fluoxetine

A

1-3 days for acute administration

4-6 days for chronic administration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

This metabolite of Fluoxetine has an elimination half time of 4-16 days

A

norfluoxetine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Fluoxetine is often administered once in the morning because

A

May cause insomnia. Day time admin reduces risk of insomnia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

The most common side effects of fluoxetine are

A

nausea, anorexia, insomnia, sexual dysfunction, agitation, and neuromuscular restlessness, which may mimic akathisia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Fluoxetine can promote weight loss by

A

Appetite suppression associated with fluoxetine therapy may help patients achieve weight loss.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Like tricyclic antidepressants, fluoxetine may be an effective analgesic for treatment of chronic pain as may be associated with rheumatoid arthritis. T/F

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Does fluoxetine cause hypotension?

A

Fluoxetine does not cause hypotension, and changes in conduction of cardiac impulses seem infrequent.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Fluoxetine should be discontinued for how long before starting an MAOI?

A

5 weeks due to long elimination half time

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Will abrupt discontinuation of fluoxetine lead withdrawal symptoms?

A

No:
The long elimination half-time of fluoxetine appears to prevent withdrawal symptoms induced by abrupt discontinuance of the drug.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

An overdose with fluoxetine alone is associated with the risk of cardiovascular and central nervous system (CNS) toxicity. True/ False

A

False.

It is not associated with CVS or CNS toxicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

This drug can cause bradycardia resulting in syncope occasional elderly patients.

A

Fluoxetine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What drugs will cause serotonin syndrome when combined with Fluoxetine

A

The combination of fluoxetine and lithium or carbamazepine may also provoke this potentially fatal syndrome.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Among the SSRIs, this drug is the most potent inhibitor of certain hepatic cytochrome P-450 enzymes hence increasing concentration of drugs that are dependent on hepatic metabolism for clearance.

A

Fluoxetine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

The addition of fluoxetine to treatment with a tricyclic antidepressant drug may result in _______ increase in the plasma concentration of the tricyclic drug.

A

a two- to fivefold

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

__________drugs may inhibit the metabolism of fluoxetine or vice versa.

A

Neuroleptic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What is the effect of Fluoxetine on beta-blockers and antidysrhythmic drugs

A

Several cardiac antidysrhythmic drugs as well as some β-adrenergic antagonists may be metabolized by the same enzyme system that is inhibited by fluoxetine, resulting in potentiation of these drug effects.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

MAO inhibitors combined with fluoxetine may cause

A

serotonin syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What are the symptoms of serotonin syndrome.

A

anxiety, restlessness, chills, ataxia, and insomnia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

This drug has a shorter elimination half-time (25 hours) than fluoxetine and is a less potent inhibitor of hepatic microsomal enzymes. A potentially active metabolite has an elimination half-time of 60 to 70 hours.

A

Sertraline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

The recommended washout period for sertraline before starting an MAO inhibitor is

A

14 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Compared with fluoxetine, sertraline may cause more _________but may be less likely to cause ________and___________

A

gastrointestinal symptoms (nausea, diarrhea)

insomnia and agitation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Elimination half time of Sertraline is?

A

25 hrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

_________ was the third SSRI introduced in the United States and has an efficacy similar to that of fluoxetine.

A

Paroxetine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

This drug has a relatively short elimination half-time (24 hours), and there are no active metabolites.

A

Paroxetine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

compared to other SSRIs paroxetine has increased or decreased incidence of sedation?

A

increased

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Compared to other SSRIs, paroxetine concentration in breast milk is?

A

The levels of paroxetine in breast milk are greater than levels in patients receiving fluoxetine or sertraline.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Compared to Fluoxetine, paroxetine has more or less inhibition of CYP450

A

Paroxetine produces less inhibition of hepatic cytoplasmic P-450 enzymes than is fluoxetine.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

The recommended washout period for paroxetine before starting an MAO inhibitor is?

A

14 days.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

This SSRI enhances the anticoagulant effects of Warfarin

A

Paroxetine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Enhancement of the anticoagulant effect of warfarin by paroxetin reflects

A

competition for common protein-binding sites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What is the elimination half time of paroxetine

A

20 hrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

This drug is simply the S isomer of another SSRI, which is the more pharmacologically active stereoisomer.

A

Escitalopram (S-Citalopram)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Citalopram should be used with caution in patients at risk for prolonged QT intervals. because

A

Citalopram causes dose-dependent QT interval prolongation, which can place patients at risk for torsades de pointes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Escitalopram may prolong the QT interval more than Citalopram. True/False

A

False: Escitalopram has les QT prolongation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

SSRIs in their order of introduction to US

A

First: Fluoxetine
Second: Sertraline
Third: Paroxetine
Fourth: Citalopram

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Compared to other SSRIs, fluvoxamine may produce more or less CYP450 inhibition?

A

Less

may still cause clinically significant drug interactions.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Fluvoxamine is effective in the management of?

A

OCD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

This SSRI is associated with a common side effect of nausea, vomiting with a possibly greater frequency than with other SSRIs

A

fluvoxamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Besides N/V, other side effects of Fluvoxamine are?

A

headache, sedation, insomnia, and sexual dysfunction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

administration of Bupropion in combination with an MAO inhibitor may result in?

A

Ataxia and myoclonus rarely.
Elevated blood pressure
Serotonin syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

This SSRI is structurally related to amphetamines

A

Bupropion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

This SSRI is effective for smoking cessation.

A

bupropion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

The mechanism of action of bupropion is obscure but may include

A

inhibition of dopamine and norepinephrine reuptake.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

This drug does not inhibit MAO. It is associated with a greater incidence of seizures (about 0.4%) than other antidepressants.

A

Bupropion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

What characteristic advantage of SSRIs does Bupropion also possess

A

Lack of postural hypotension
Lack of anticholinergic effects
Lacks significant effects on conduction of cardiac impulses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

What is the advantage of Bupropion when compared to other SSRIs

A

Unlike the SSRIs, bupropion is not associated with significant drug interactions and is not commonly associated with sexual dysfunction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Some patients experience stimulant-like effects early in therapy with this antidepressant

A

Bupropion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

This antidepressant is perceived to have a profile of efficacy similar to that of the tricyclic antidepressants but has a more favorable side effect profile.

A

Venlafaxine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

What is the perceived MOA of Venlafaxine

A

Like the tricyclic antidepressants, this drug inhibits the reuptake of norepinephrine and serotonin and may potentiate the action of dopamine in the CNS.

84
Q

Unlike tricyclic antidepressants, venlafaxine does not produce _______ and _________.

A

anticholinergic effects or postural hypotension.

85
Q

Side effects of venlafaxine include?

A

insomnia, sedation, and nausea.

86
Q

The recommended washout period of Venlafaxine is______

A

14 days.

87
Q

Venlafaxine is metabolized by _________ and also acts as a weak inhibitor of these enzymes.

A

cytochrome P-450 enzymes

88
Q

The elimination half-time of Venlafaxine is _____ hours and that of its active metabolite is ________ hours.

A

5 hours

11 hours

89
Q

At high doses Venlafaxine can cause what in 5% to 7% of patients?

A

a modest but persistent increase in diastolic blood pressure

90
Q

This drug should be avoided in patients with severe renal dysfunction and chronic liver disease.

A

Duloxetine

91
Q

This drug acts as a serotonin reuptake inhibitor and a serotonin agonist via an active metabolite.

A

Trazodone

92
Q

Trazodone lacks effects on conduction of cardiac impulses but on rare occasions has been associated with cardiac dysrhythmias. True/False?

A

True

93
Q

Common side effects of trazodone include

A

sedation
orthostatic hypotension
nausea, and vomiting
Priapism in males.

94
Q

This antidepressants’ greatest efficacy may be treatment of insomnia induced by SSRIs or bupropion.

A

Trazodone

95
Q

The elimination half-time of Trazodone is

A

3 to 9 hours

96
Q

Toxicity associated with a Trazodone overdose is less than what accompanies an overdose of tricyclic antidepressants and MAO inhibitors. T/F

A

True

97
Q

Why should you consider holding antiplatelet medication perioperative setting for a patient on SSRIs?

A

They have antiplatelet activity

98
Q

What is the risk of discontinuing an SSRI for surgery

A

may take 2-3 weeks for full washout and 2-4 weeks for reestablishment which may predispose the patient to a major depressive episode.

99
Q

Withdrawal symptoms associated with sudden discontinuation of TCA are?

A

chills
coryza
muscle aches

100
Q

Tricyclic antidepressants have been supplanted as the first line because

A

Unfavourable side effects due to anticholinergic, antiadrenergic, and antihistaminic properties

Narrow therapeutic index

101
Q

Normal plasma concentration of this tricyclic antidepressant is 50 to 150 ng/mL.

A

nortriptyline

102
Q

Narrow therapeutic index of tricyclic antidepressants that make them lethal in overdose is due to?

A

inhibition of sodium ion channels reflecting a slowing of conduction of cardiac impulses and appearance of life-threatening cardiac dysrhythmias.

103
Q

Normal plasma concentration of this tricyclic antidepressant should not exceed 225 ng/mL.

A

imipramine

104
Q

Normal plasma concentration of this tricyclic antidepressant should not exceed 125 ng/mL.

A

desipramine

105
Q

It is preferable to taper tricyclic and tetracyclic antidepressants during a ___________period to avoid the risk of withdrawal symptoms

A

4-week

106
Q

Withdrawal symptoms of tricyclic antidepressants have been attributed to?

A

supersensitivity of the cholinergic nervous system.

107
Q

It is possible that tricyclic antidepressants produce antiinflammatory effects similar to local anesthetics because?

A

Because of their structural similarities to local anesthetics and known sodium channel blockade.

108
Q

The efficacy of tricyclic antidepressants on chronic pain syndromes may be limited by?

A

a narrow therapeutic index

intolerability of side effects

109
Q

TCAs are believed to produce pain relief by?

A

Serotonin activity and reuptake inhibition

Potentiation of CNS endogenous opioids

Antinflammatory effects.

110
Q

The structure of tricyclic antidepressants resembles that of _________ and ____________.

A

local anesthetics and phenothiazines

111
Q

____________ is the prototype of the tricyclic antidepressants,

A

Imipramine

112
Q

Similar to local anesthetics, tricyclic antidepressants structure include?

A

hydrophobic portion linked to an amide via a linear intermediate moiety.

113
Q

___________________ denotes the three-ring chemical structure of the central portion of the molecule

A

Tricyclic

114
Q

List 10 TCAs (3 -tyline, 3 -pine, 4, -pramine)

A 
Amitriotyline
Nortriptyline
Protriptyline
Amoxapine
Mirtzapine
Doxepine
Desipramine
Clomipramine
Imipramine
Trimipramine
115
Q

Name 3 MOIs

A

Phenelzine
Tranylcypromine
Isocarboxazid

116
Q

Tricyclic antidepressants act at

A

several transporters and receptors

117
Q

Antidepressant effect of TCAs is likely produced by?

A

blocking the reuptake (uptake) of serotonin and/or norepinephrine at presynaptic terminals, thereby increasing the availability of these neurotransmitters.

118
Q

What is the difference between TCAs classified as Tertiary Amines and secondary amines

A

Tertiary amines inhibit reuptake of both serotonin and norepinephrine and secondary amines are primarily norepinephrine reuptake inhibitors.

119
Q

Identify 3 TCAs classified as tertiary amines

A

amitriptyline, imipramine, clomipramine

120
Q

Chronic administration of TCAs will affect which receptors and how?

A

Decreased sensitivity of postsynaptic β1 and 5HT2 receptors and of presynaptic α2 receptors.

Increased sensitivity of postsynaptic α1 receptors.

121
Q

TCA are effective at once daily dose because?

A

Long elimination half life 17-30 hrs

Wide range of therapeutic plasma concentration

122
Q

Toxicity with TCAs is likely to occur at what plasma concentration? What conc is acceptable?

A

Therapeutic plasma conc = 100-300 ng/ML

Toxicity > 500ng/mL

123
Q

Individual variation in rate of metabolism for TCAs is ______

A

10 to 30 fold

124
Q

Metabolism of TCAs is increased in the elderly. T/F?

A

False, its decreased

125
Q

Metabolism of TCAs

A

Oxidation in liver by microsomal enzymes

Conjugation with glucuronic acid

126
Q

Elimination period of TCAs

A

≥1week

127
Q

What is the

A

CNS effects
CVS effects
Anticholinergic effects

128
Q

This TCA produces the most anticholinergic effects

A

Amitriptyline

129
Q

This TCA produces the least anticholinergic effects

A

Desipramine

130
Q

What is true of anticholinergic effects of TCAs in adults

A
  • Anticholinergic delirium at therapeutic doses
  • Serious anticholinergic toxicity due to polypharmacy
  • They have greater sensitivity to anticholinergic and other receptor effects compared to younger patients on TCAs
131
Q

What are the most common CV effects of TCAs

A

Orthostatic hypotension

Moderate increase in HR

132
Q

Risk for hypotension during GA in patients taking TCAs is High. T/F

A

False, the risk is low

133
Q

Tricyclic antidepressants increase the risks of cardiac dysrhythmias and sudden death. True/False

A

False:

In the absence of drug overdose, this has not been substantiated

134
Q

What is the effect of TCA on left ventricular function?

A

In the absence of severe preexisting cardiac dysfunction, tricyclic antidepressants lack adverse effects on left ventricular function.

135
Q

In the absence of severe preexisting cardiac dysfunction, TCAs may possess cardiac antidysrhythmic properties. T/F?

A

true

136
Q

Tricyclic antidepressants produce depression of conduction of cardiac impulses through the atria and ventricles, manifesting on the electrocardiogram (ECG) as

A

prolongation of the P-R interval

widening of the QRS complex

flattening or inversion of the T wave

changes on the ECG are probably benign and gradually disappear with continued therapy

137
Q

TCA enhance depressant cardiac effects of anesthetics. T/F

A

True

138
Q

Quinidine-like properties of tricyclic antidepressants are thought to reflect

A

Slowing of sodium ion flux into cells, resulting in altered repolarization and conduction of cardiac impulses.

139
Q

What TCAs produce the highest sedation

A

Amitriptyline and doxepin

140
Q

What TCAs lower the seizure threshold

A

maprotiline and clomipramine

141
Q

How does TCAs affect enflurane

A

may enhance the CNS-stimulating effects of enflurane.

142
Q

TCA are fatal in overdose because?

A

Cardiac toxicity
Tendency to cause seizures
Depressant properties on the CNS

143
Q

The combination of a tricyclic antidepressant and an MAO inhibitor may result in CNS toxicity manifesting as?

A

hyperthermia
seizures
coma

144
Q

What properties are most likely to be responsible for drug interactions of tricyclic antidepressants?

A

Anticholinergic effects and catecholamine uptake blocking properties

145
Q

TCA drug interactions may be prominent with which drugs (5)

A

(a) sympathomimetics
(b) inhaled anesthetics
(c) anticholinergics
(d) antihypertensives
(e) opioids.

146
Q

Binding of tricyclic antidepressants to plasma albumin can be decreased by competition from other drugs, including ______

A

phenytoin
aspirin
scopolamine.

147
Q

indirect-acting sympathomimetics may produce exaggerated pressor responses in patients taking TCAs due to?

A

an increased amount of norepinephrine available to stimulate postsynaptic adrenergic receptors

148
Q

What is the effects of acute administration of tricyclic antidepressants on sympathetic nervous system

A

increases sympathetic nervous system synaptic activity due to norepinephrine reuptake blockade,

149
Q

What is the effects of Chronic administration of tricyclic antidepressants on sympathetic nervous system

A

chronic administration of these drugs may result in decreased sympathetic nervous system transmission due to downregulation of β-adrenergic receptors.

150
Q

Why will Acute admin of TCAs cause increased sympathetic nervous system activity

A

due to an increased amount of norepinephrine available to stimulate postsynaptic adrenergic receptors

151
Q

Why will chronic admin of TCAs cause decreased sympathetic nervous system activity

A

due to downregulation of β-adrenergic receptors

152
Q

patients recently started on tricyclic antidepressants, exaggerated pressor responses should be anticipated whether or not direct-acting or indirect-acting sympathomimetics are administered, although pressor responses may be more pronounced with ___________.

A

an indirect-acting drug such as ephedrine.

153
Q

What is the appropriate use of vasopressors in patients recently started on tricyclic antidepressants?

A

Titrate smaller than usual doses of direct-acting sympathomimetics.

154
Q

Chronic TCA use is _____ weeks

A

6

155
Q

What is the appropriate use of vasopressors in patients on chronic tricyclic antidepressants?

A

administration of either a direct-acting or indirect-acting sympathomimetic is acceptable

decrease the initial dose of drug to about one-third the usual dose.

Hypotension may not respond to conventional sympathomimetic hence may have to use norepi.

156
Q

For a patient on chronic TCA, hypotension may not respond to conventional sympathomimetic because?

A

adrenergic receptors are either desensitized or catecholamine stores are depleted

157
Q

Induction of anesthesia may be associated with an increased incidence of _____________ in patients treated with tricyclic antidepressants.

A

cardiac dysrhythmias

158
Q

Dose of exogenous epinephrine necessary to produce cardiac dysrhythmias during anesthesia with a volatile anesthetic is ___________ by tricyclic antidepressants

A

decreased

159
Q

MAC for patient treated with TCA is increased or decreased?

A

Increased:

Theoretically, increased availability of norepinephrine in the CNS could result in increased anesthetic requirements for inhaled anesthetics.

160
Q

TCA may interact with pre-op anticholinergics to cause delirium confusion (central anticholinergic syndrome) , to avoid this use?

A

Glycopylorate

Remember
Atropine is a useful treatment when tricyclic antidepressants dangerously slow atrioventricular or intraventricular conduction of cardiac impulses.

161
Q

What is the effect of TCA on clonodine

A

accentuated rebound hypertension after abrupt dc of clonodine

162
Q

Effect of TCAs on opioids

A

Augment analgesic and ventilatory depressant effect

163
Q

Abrupt dc of TCAs may result in?

A

Malaise
Chills
Coryza
Skeletal muscle aching

164
Q

Tricyclic antidepressant overdose is life-threatening, as the progression from an alert state to unresponsiveness may be _________.

A

rapid

165
Q

___________ are the most frequent terminal events after TCA overdose.

A

Intractable myocardial depression or ventricular cardiac dysrhythmias

166
Q

Presenting features of tricyclic antidepressant overdose include?

A

agitation and seizures followed by coma, depression of ventilation, hypotension, hypothermia, and striking evidence of anticholinergic effects including mydriasis, flushed dry skin, urinary retention, and tachycardia.

167
Q

Plasma concentrations of tricyclic antidepressants do not allow prediction of the likely occurrence of seizures or cardiac dysrhythmias. T/F?

A

True

168
Q

he comatose phase of tricyclic antidepressant overdose lasts _________________ hours

A

24 to 72 hours

169
Q

After TCA overdose, risk of life-threatening cardiac dysrhythmias persists for up to ________, necessitating continued monitoring of the ECG in these patients.

A

10 days

170
Q

Treatment of a life-threatening overdose of a tricyclic antidepressant is directed toward management of ____________.

A

CNS and cardiac toxicity

171
Q

Treatment of anticholinergic psychosis after TCA overdose may be indicated. What is the treatment drug?

A

Physostigmine, 0.5 to 2 mg given intravenously

172
Q

Hypotension after TCA OD may be the result of

A

direct tricyclic antidepressant–induced vasodilation, α-adrenergic blockade, or myocardial depression.

173
Q

Hypotension after TCA OD may be treated with?

A

Fluids
Alkalinization of plasma (HCO3/Hyperventilation)
Sympathomimetic
Inotropes

174
Q

MAO inhibitors are used less commonly because

A

Their administration is complicated by side effects (hypotension)

lethality in overdose

lack of simplicity in dosing.

175
Q

The dosage of MAO inhibitors is the same in the elderly as in younger adults because

A

elderly persons often have higher levels of MAO and because the metabolism of these drugs does not seem to be affected by age.

176
Q

Patient should avoid tyramine containing foods when taking MAOI because

A

interactions with tyramine that can result in systemic hypertension

177
Q

MAO inhibitors approved in the United States for the treatment of depression or panic disorder are?

A

phenelzine, tranylcypromine, and isocarboxazid.

178
Q

What drugs are contraindicated with MAO inhibitors

A

Cyclic antidepressants

179
Q

This MAOI may be indicated for early parkinson’s disease

A

Selegiline which is an MAO-B selective inhibitor

180
Q

Describe the structure and function of MAO

A

Flavin-containing enzyme found principally on outer mitochondrial membranes.

Functions via oxidative deamination to inactivate several monoamines including dopamine, serotonin (5-hydroxytryptamine), norepinephrine, and epinephrine.

181
Q

MAO-A preferentially deaminates

A

serotonin
norepinephrine
epinephrine

182
Q

AO-B preferentially deaminates

A

phenylethylamine

183
Q

MAO is divided into two subtypes (MAO-A and MAO-B) based on _______

A

different substrate specificities

184
Q

What is the MOA of MAOIs

A

Act by forming a stable, irreversible complex with MAO enzyme, especially with cerebral neuronal MAO thereby increasing the amount of neurotransmitter (norepinephrine) available for release from CNS neurons increases

185
Q

The most serious common side effects of MAOI is

A

orthostatic hypotension, which may be especially prominent in elderly patients

186
Q

Orthostatic hypotension from MAOI may reflect accumulation of _____________?

A

false neurotransmitter octopamine in the cytoplasm of postganglionic sympathetic nerve endings which is released in response to neural impulse.

187
Q

This MAOI has anticholinergic-like side effects and may produce sedation in some patients.

A

Phenelzine

188
Q

This MAOI has no anticholinergic side effects but has mild stimulant effects, which may cause insomnia.

A

Tranylcypromine

189
Q

Impotence and anorgasmy are side effects of _______ MAO inhibitors.

A

All

190
Q

Compared to TCAs, MAOI effect on EEG is?

A

Minimal and not seizure-like

191
Q

Compared to TCAs, MAOI effect on cardiac rhythm is?

A

MOAI do not produce cardiac dysrhythmias

192
Q

Patients taking this MAO-B inhibitor do not need to follow a tyramine diet and doses <30mg/day

A

Selegiline

193
Q

Patients treated with MAOIs should avoid tyramine- containing foods because

A

They cannot metabolize dietary tyramine

Tyramine be taken up by SNS and hence causing a massive release of endogenous catecholamines

194
Q

Dietary tyramine induced HTN resembles that of pheochromocytoma and should be treated with?

A

Nitropruside

Beta blockers for persistent dysrhythmias after BP is controlled

195
Q

In patient taking MAOI decrease the dose to about one-third of normal, with additional titration of doses based on cardiovascular responses. T/F

A

True

196
Q

Overdose with an MAO inhibitor is reflected by

A

Signs of excessive sympathetic nervous system activity (tachycardia, hyperthermia, mydriasis)

seizures

coma

197
Q

Serotonin syndrome occurs when

A

When there is an excess of serotonin agonism in the central and peripheral nervous systems.

198
Q

SSRIs, tricyclic antidepressants, and MAO inhibitors, particularly in combination, have all been associated with serotonin syndrome. T/F

A

True

199
Q

The differential diagnosis for suspected serotonin syndrome includes

A

malignant hyperthermia, neuroleptic malignant syndrome, and anticholinergic poisoning

200
Q

The principal disadvantage of Buspirone seems to be _______–

A

a slow onset of effect (1 to 2 weeks), which may be interpreted as ineffectiveness by patients experiencing acute anxiety.

201
Q

Drug of choice for treatment of Bipolar

A

Lithium

202
Q

The Lithium therapeutic range for acute mania is __________, with oral doses averaging 900 to 1,800 mg per day

A

1.0 to 1.2 mEq/L

203
Q

What is the effect of loop diuretics on lithium

A

depletion of sodium as produced by dehydration, decreased sodium intake, and thiazide and loop diuretics may increase reabsorption of lithium by proximal renal tubules, resulting in as much as a 50% increase in the plasma concentration of lithium.

204
Q

What is the effect of thiazide diuretics on lithium

A

renal excretion is not enhanced by thiazide diuretics, which act selectively on the distal renal tubules. May increase conc due to volume depletion

205
Q

What is the effect of potassium sparing diuretics on lithium

A

do not facilitate reabsorption of lithium and, in fact, may increase excretion.

206
Q

What is the effects of NSAIDs on lithium

A

by altering renal blood flow, may produce marked increases in the plasma concentration of lithium and should be used with care.

Pharm III (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions