Flood Chapter 43 Flashcards
1
Q
Elderly patients taking antidepressant therapy are at particular risk for?
A
toxicity
2
Q
Drugs used for psychopharmacologic therapy include? (5)
A
antidepressants, anxiolytics, lithium, antipsychotics, and anticonvulsants.
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
4
Q
What drugs are useful for treatment of bipolar disorders and psychotic disorders including schizophrenia?
A
Lithium, anticonvulsants, and antipsychotic
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
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.
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
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
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.
10
Q
Antidepressants are logically classified based on their?
A
chemical structures and their acute neuropharmacologic effects.
11
Q
The precise mechanism by which antidepressants work is
A
unknown
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.
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.
14
Q
What are the drugs of choice for the treatment of mild to moderate depression
A
selective serotonin reuptake inhibitors (SSRIs)
15
Q
First-line pharmacotherapy for panic disorder and obsessive-compulsive syndrome are?
A
SSRIs
16
Q
SSRIs are also effective in treatment of social phobia and posttraumatic stress disorder. T/F
A
True
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).
18
Q
Newer SSRIs are believed to act on ________ and _________ pathways in the brain.
A
serotonin and norepinephrine
19
Q
MOA of newer SSRIs include
A
Dual serotonin and norepinephrine reuptake blockade (venlafaxine) and α2-receptor blockade (mirtazapine).
20
Q
SSRIs that share the ability to block the reuptake of serotonin include (6 Older SSRIs)
A
fluoxetine paroxetine sertraline fluvoxamine citalopram escitalopram.
21
Q
This newer SSRI may cause hypertension it some individuals
A
Venlafaxine.
It has dual serotonin and norepinephrine reuptake blockade.
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.
23
Q
There is abundant evidence that _______ receptors are involved in the etiology of anxiety.
A
serotonin
24
Q
Potent inhibition of serotonin reuptake appears to be necessary for effectiveness in the treatment of ___________.
A
obsessive-compulsive disorders
25
Compared with tricyclic antidepressants, SSRIs are preferred because?
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.
26
The most important advantage of SSRIs compared with tricyclic antidepressants is
the relative safety of SSRIs when taken in overdose.
27
This SSRI may be similar to tricyclic antidepressants with respect to elevated overdose-associated risk associated with proconvulsant and cardiac side effects.
Venlafaxine
28
Common side effects of SSRIs include?
insomnia, agitation, headache, nausea, and diarrhea.
29
Should SSRIs be suddenly discontinued?
Tapering all SSRIs before discontinuance is recommended especially for drugs with short elimination half-times.
30
Abrupt discontinuation of SSRIs with short elimination half-times (paroxetine, venlafaxine) may be associated with?
dizziness, paresthesias, myalgias, irritability, insomnia, and visual disturbances.
31
Abrupt discontinuation of SSRIs with short elimination half-times (paroxetine, venlafaxine) may be associated with?
dizziness, paresthesias, myalgias, irritability, insomnia, and visual disturbances.
32
First SSRI introduced in US is?
Fluoxetine
33
How often can you increase the dose of Fluoxetine
once every 4 weeks
34
Therapeutic effect of fluoxetine is evident in what time?
2-4 weeks
35
What is the elimination half time of fluoxetine
1-3 days for acute administration
| 4-6 days for chronic administration
36
This metabolite of Fluoxetine has an elimination half time of 4-16 days
norfluoxetine
37
Fluoxetine is often administered once in the morning because
May cause insomnia. Day time admin reduces risk of insomnia.
38
The most common side effects of fluoxetine are
nausea, anorexia, insomnia, sexual dysfunction, agitation, and neuromuscular restlessness, which may mimic akathisia.
39
Fluoxetine can promote weight loss by
Appetite suppression associated with fluoxetine therapy may help patients achieve weight loss.
40
Like tricyclic antidepressants, fluoxetine may be an effective analgesic for treatment of chronic pain as may be associated with rheumatoid arthritis. T/F
True
41
Does fluoxetine cause hypotension?
Fluoxetine does not cause hypotension, and changes in conduction of cardiac impulses seem infrequent.
42
Fluoxetine should be discontinued for how long before starting an MAOI?
5 weeks due to long elimination half time
43
Will abrupt discontinuation of fluoxetine lead withdrawal symptoms?
No:
The long elimination half-time of fluoxetine appears to prevent withdrawal symptoms induced by abrupt discontinuance of the drug.
44
An overdose with fluoxetine alone is associated with the risk of cardiovascular and central nervous system (CNS) toxicity. True/ False
False.
| It is not associated with CVS or CNS toxicity
45
This drug can cause bradycardia resulting in syncope occasional elderly patients.
Fluoxetine
46
What drugs will cause serotonin syndrome when combined with Fluoxetine
The combination of fluoxetine and lithium or carbamazepine may also provoke this potentially fatal syndrome.
47
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.
Fluoxetine
48
The addition of fluoxetine to treatment with a tricyclic antidepressant drug may result in _______ increase in the plasma concentration of the tricyclic drug.
a two- to fivefold
49
__________drugs may inhibit the metabolism of fluoxetine or vice versa.
Neuroleptic
50
What is the effect of Fluoxetine on beta-blockers and antidysrhythmic drugs
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.
51
MAO inhibitors combined with fluoxetine may cause
serotonin syndrome
52
What are the symptoms of serotonin syndrome.
anxiety, restlessness, chills, ataxia, and insomnia.
53
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.
Sertraline
54
The recommended washout period for sertraline before starting an MAO inhibitor is
14 days
55
Compared with fluoxetine, sertraline may cause more _________but may be less likely to cause ________and___________
gastrointestinal symptoms (nausea, diarrhea)
insomnia and agitation.
56
Elimination half time of Sertraline is?
25 hrs
57
_________ was the third SSRI introduced in the United States and has an efficacy similar to that of fluoxetine.
Paroxetine
58
This drug has a relatively short elimination half-time (24 hours), and there are no active metabolites.
Paroxetine
59
compared to other SSRIs paroxetine has increased or decreased incidence of sedation?
increased
60
Compared to other SSRIs, paroxetine concentration in breast milk is?
The levels of paroxetine in breast milk are greater than levels in patients receiving fluoxetine or sertraline.
61
Compared to Fluoxetine, paroxetine has more or less inhibition of CYP450
Paroxetine produces less inhibition of hepatic cytoplasmic P-450 enzymes than is fluoxetine.
62
The recommended washout period for paroxetine before starting an MAO inhibitor is?
14 days.
63
This SSRI enhances the anticoagulant effects of Warfarin
Paroxetine
64
Enhancement of the anticoagulant effect of warfarin by paroxetin reflects
competition for common protein-binding sites
65
What is the elimination half time of paroxetine
20 hrs
66
This drug is simply the S isomer of another SSRI, which is the more pharmacologically active stereoisomer.
Escitalopram (S-Citalopram)
67
Citalopram should be used with caution in patients at risk for prolonged QT intervals. because
Citalopram causes dose-dependent QT interval prolongation, which can place patients at risk for torsades de pointes.
68
Escitalopram may prolong the QT interval more than Citalopram. True/False
False: Escitalopram has les QT prolongation
69
SSRIs in their order of introduction to US
First: Fluoxetine
Second: Sertraline
Third: Paroxetine
Fourth: Citalopram
70
Compared to other SSRIs, fluvoxamine may produce more or less CYP450 inhibition?
Less
may still cause clinically significant drug interactions.
71
Fluvoxamine is effective in the management of?
OCD
72
This SSRI is associated with a common side effect of nausea, vomiting with a possibly greater frequency than with other SSRIs
fluvoxamine
73
Besides N/V, other side effects of Fluvoxamine are?
headache, sedation, insomnia, and sexual dysfunction.
74
administration of Bupropion in combination with an MAO inhibitor may result in?
Ataxia and myoclonus rarely.
Elevated blood pressure
Serotonin syndrome
75
This SSRI is structurally related to amphetamines
Bupropion
76
This SSRI is effective for smoking cessation.
bupropion
77
The mechanism of action of bupropion is obscure but may include
inhibition of dopamine and norepinephrine reuptake.
78
This drug does not inhibit MAO. It is associated with a greater incidence of seizures (about 0.4%) than other antidepressants.
Bupropion
79
What characteristic advantage of SSRIs does Bupropion also possess
Lack of postural hypotension
Lack of anticholinergic effects
Lacks significant effects on conduction of cardiac impulses
80
What is the advantage of Bupropion when compared to other SSRIs
Unlike the SSRIs, bupropion is not associated with significant drug interactions and is not commonly associated with sexual dysfunction.
81
Some patients experience stimulant-like effects early in therapy with this antidepressant
Bupropion
82
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.
Venlafaxine
83
What is the perceived MOA of Venlafaxine
Like the tricyclic antidepressants, this drug inhibits the reuptake of norepinephrine and serotonin and may potentiate the action of dopamine in the CNS.
84
Unlike tricyclic antidepressants, venlafaxine does not produce _______ and _________.
anticholinergic effects or postural hypotension.
85
Side effects of venlafaxine include?
insomnia, sedation, and nausea.
86
The recommended washout period of Venlafaxine is______
14 days.
87
Venlafaxine is metabolized by _________ and also acts as a weak inhibitor of these enzymes.
cytochrome P-450 enzymes
88
The elimination half-time of Venlafaxine is _____ hours and that of its active metabolite is ________ hours.
5 hours
| 11 hours
89
At high doses Venlafaxine can cause what in 5% to 7% of patients?
a modest but persistent increase in diastolic blood pressure
90
This drug should be avoided in patients with severe renal dysfunction and chronic liver disease.
Duloxetine
91
This drug acts as a serotonin reuptake inhibitor and a serotonin agonist via an active metabolite.
Trazodone
92
Trazodone lacks effects on conduction of cardiac impulses but on rare occasions has been associated with cardiac dysrhythmias. True/False?
True
93
Common side effects of trazodone include
sedation
orthostatic hypotension
nausea, and vomiting
Priapism in males.
94
This antidepressants' greatest efficacy may be treatment of insomnia induced by SSRIs or bupropion.
Trazodone
95
The elimination half-time of Trazodone is
3 to 9 hours
96
Toxicity associated with a Trazodone overdose is less than what accompanies an overdose of tricyclic antidepressants and MAO inhibitors. T/F
True
97
Why should you consider holding antiplatelet medication perioperative setting for a patient on SSRIs?
They have antiplatelet activity
98
What is the risk of discontinuing an SSRI for surgery
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
Withdrawal symptoms associated with sudden discontinuation of TCA are?
chills
coryza
muscle aches
100
Tricyclic antidepressants have been supplanted as the first line because
Unfavourable side effects due to anticholinergic, antiadrenergic, and antihistaminic properties
Narrow therapeutic index
101
Normal plasma concentration of this tricyclic antidepressant is 50 to 150 ng/mL.
nortriptyline
102
Narrow therapeutic index of tricyclic antidepressants that make them lethal in overdose is due to?
inhibition of sodium ion channels reflecting a slowing of conduction of cardiac impulses and appearance of life-threatening cardiac dysrhythmias.
103
Normal plasma concentration of this tricyclic antidepressant should not exceed 225 ng/mL.
imipramine
104
Normal plasma concentration of this tricyclic antidepressant should not exceed 125 ng/mL.
desipramine
105
It is preferable to taper tricyclic and tetracyclic antidepressants during a ___________period to avoid the risk of withdrawal symptoms
4-week
106
Withdrawal symptoms of tricyclic antidepressants have been attributed to?
supersensitivity of the cholinergic nervous system.
107
It is possible that tricyclic antidepressants produce antiinflammatory effects similar to local anesthetics because?
Because of their structural similarities to local anesthetics and known sodium channel blockade.
108
The efficacy of tricyclic antidepressants on chronic pain syndromes may be limited by?
a narrow therapeutic index
| intolerability of side effects
109
TCAs are believed to produce pain relief by?
Serotonin activity and reuptake inhibition
Potentiation of CNS endogenous opioids
Antinflammatory effects.
110
The structure of tricyclic antidepressants resembles that of _________ and ____________.
local anesthetics and phenothiazines
111
____________ is the prototype of the tricyclic antidepressants,
Imipramine
112
Similar to local anesthetics, tricyclic antidepressants structure include?
hydrophobic portion linked to an amide via a linear intermediate moiety.
113
___________________ denotes the three-ring chemical structure of the central portion of the molecule
Tricyclic
114
List 10 TCAs (3 -tyline, 3 -pine, 4, -pramine)
```
Amitriotyline
Nortriptyline
Protriptyline
Amoxapine
Mirtzapine
Doxepine
Desipramine
Clomipramine
Imipramine
Trimipramine
```
115
Name 3 MOIs
Phenelzine
Tranylcypromine
Isocarboxazid
116
Tricyclic antidepressants act at
several transporters and receptors
117
Antidepressant effect of TCAs is likely produced by?
blocking the reuptake (uptake) of serotonin and/or norepinephrine at presynaptic terminals, thereby increasing the availability of these neurotransmitters.
118
What is the difference between TCAs classified as Tertiary Amines and secondary amines
Tertiary amines inhibit reuptake of both serotonin and norepinephrine and secondary amines are primarily norepinephrine reuptake inhibitors.
119
Identify 3 TCAs classified as tertiary amines
amitriptyline, imipramine, clomipramine
120
Chronic administration of TCAs will affect which receptors and how?
Decreased sensitivity of postsynaptic β1 and 5HT2 receptors and of presynaptic α2 receptors.
Increased sensitivity of postsynaptic α1 receptors.
121
TCA are effective at once daily dose because?
Long elimination half life 17-30 hrs
Wide range of therapeutic plasma concentration
122
Toxicity with TCAs is likely to occur at what plasma concentration? What conc is acceptable?
Therapeutic plasma conc = 100-300 ng/ML
Toxicity > 500ng/mL
123
Individual variation in rate of metabolism for TCAs is ______
10 to 30 fold
124
Metabolism of TCAs is increased in the elderly. T/F?
False, its decreased
125
Metabolism of TCAs
Oxidation in liver by microsomal enzymes
Conjugation with glucuronic acid
126
Elimination period of TCAs
≥1week
127
What is the
CNS effects
CVS effects
Anticholinergic effects
128
This TCA produces the most anticholinergic effects
Amitriptyline
129
This TCA produces the least anticholinergic effects
Desipramine
130
What is true of anticholinergic effects of TCAs in adults
- 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
What are the most common CV effects of TCAs
Orthostatic hypotension
Moderate increase in HR
132
Risk for hypotension during GA in patients taking TCAs is High. T/F
False, the risk is low
133
Tricyclic antidepressants increase the risks of cardiac dysrhythmias and sudden death. True/False
False:
In the absence of drug overdose, this has not been substantiated
134
What is the effect of TCA on left ventricular function?
In the absence of severe preexisting cardiac dysfunction, tricyclic antidepressants lack adverse effects on left ventricular function.
135
In the absence of severe preexisting cardiac dysfunction, TCAs may possess cardiac antidysrhythmic properties. T/F?
true
136
Tricyclic antidepressants produce depression of conduction of cardiac impulses through the atria and ventricles, manifesting on the electrocardiogram (ECG) as
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
TCA enhance depressant cardiac effects of anesthetics. T/F
True
138
Quinidine-like properties of tricyclic antidepressants are thought to reflect
Slowing of sodium ion flux into cells, resulting in altered repolarization and conduction of cardiac impulses.
139
What TCAs produce the highest sedation
Amitriptyline and doxepin
140
What TCAs lower the seizure threshold
maprotiline and clomipramine
141
How does TCAs affect enflurane
may enhance the CNS-stimulating effects of enflurane.
142
TCA are fatal in overdose because?
Cardiac toxicity
Tendency to cause seizures
Depressant properties on the CNS
143
The combination of a tricyclic antidepressant and an MAO inhibitor may result in CNS toxicity manifesting as?
hyperthermia
seizures
coma
144
What properties are most likely to be responsible for drug interactions of tricyclic antidepressants?
Anticholinergic effects and catecholamine uptake blocking properties
145
TCA drug interactions may be prominent with which drugs (5)
(a) sympathomimetics
(b) inhaled anesthetics
(c) anticholinergics
(d) antihypertensives
(e) opioids.
146
Binding of tricyclic antidepressants to plasma albumin can be decreased by competition from other drugs, including ______
phenytoin
aspirin
scopolamine.
147
indirect-acting sympathomimetics may produce exaggerated pressor responses in patients taking TCAs due to?
an increased amount of norepinephrine available to stimulate postsynaptic adrenergic receptors
148
What is the effects of acute administration of tricyclic antidepressants on sympathetic nervous system
increases sympathetic nervous system synaptic activity due to norepinephrine reuptake blockade,
149
What is the effects of Chronic administration of tricyclic antidepressants on sympathetic nervous system
chronic administration of these drugs may result in decreased sympathetic nervous system transmission due to downregulation of β-adrenergic receptors.
150
Why will Acute admin of TCAs cause increased sympathetic nervous system activity
due to an increased amount of norepinephrine available to stimulate postsynaptic adrenergic receptors
151
Why will chronic admin of TCAs cause decreased sympathetic nervous system activity
due to downregulation of β-adrenergic receptors
152
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 ___________.
an indirect-acting drug such as ephedrine.
153
What is the appropriate use of vasopressors in patients recently started on tricyclic antidepressants?
Titrate smaller than usual doses of direct-acting sympathomimetics.
154
Chronic TCA use is _____ weeks
6
155
What is the appropriate use of vasopressors in patients on chronic tricyclic antidepressants?
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
For a patient on chronic TCA, hypotension may not respond to conventional sympathomimetic because?
adrenergic receptors are either desensitized or catecholamine stores are depleted
157
Induction of anesthesia may be associated with an increased incidence of _____________ in patients treated with tricyclic antidepressants.
cardiac dysrhythmias
158
Dose of exogenous epinephrine necessary to produce cardiac dysrhythmias during anesthesia with a volatile anesthetic is ___________ by tricyclic antidepressants
decreased
159
MAC for patient treated with TCA is increased or decreased?
Increased:
Theoretically, increased availability of norepinephrine in the CNS could result in increased anesthetic requirements for inhaled anesthetics.
160
TCA may interact with pre-op anticholinergics to cause delirium confusion (central anticholinergic syndrome) , to avoid this use?
Glycopylorate
Remember
Atropine is a useful treatment when tricyclic antidepressants dangerously slow atrioventricular or intraventricular conduction of cardiac impulses.
161
What is the effect of TCA on clonodine
accentuated rebound hypertension after abrupt dc of clonodine
162
Effect of TCAs on opioids
Augment analgesic and ventilatory depressant effect
163
Abrupt dc of TCAs may result in?
Malaise
Chills
Coryza
Skeletal muscle aching
164
Tricyclic antidepressant overdose is life-threatening, as the progression from an alert state to unresponsiveness may be _________.
rapid
165
___________ are the most frequent terminal events after TCA overdose.
Intractable myocardial depression or ventricular cardiac dysrhythmias
166
Presenting features of tricyclic antidepressant overdose include?
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
Plasma concentrations of tricyclic antidepressants do not allow prediction of the likely occurrence of seizures or cardiac dysrhythmias. T/F?
True
168
he comatose phase of tricyclic antidepressant overdose lasts _________________ hours
24 to 72 hours
169
After TCA overdose, risk of life-threatening cardiac dysrhythmias persists for up to ________, necessitating continued monitoring of the ECG in these patients.
10 days
170
Treatment of a life-threatening overdose of a tricyclic antidepressant is directed toward management of ____________.
CNS and cardiac toxicity
171
Treatment of anticholinergic psychosis after TCA overdose may be indicated. What is the treatment drug?
Physostigmine, 0.5 to 2 mg given intravenously
172
Hypotension after TCA OD may be the result of
direct tricyclic antidepressant–induced vasodilation, α-adrenergic blockade, or myocardial depression.
173
Hypotension after TCA OD may be treated with?
Fluids
Alkalinization of plasma (HCO3/Hyperventilation)
Sympathomimetic
Inotropes
174
MAO inhibitors are used less commonly because
Their administration is complicated by side effects (hypotension)
lethality in overdose
lack of simplicity in dosing.
175
The dosage of MAO inhibitors is the same in the elderly as in younger adults because
elderly persons often have higher levels of MAO and because the metabolism of these drugs does not seem to be affected by age.
176
Patient should avoid tyramine containing foods when taking MAOI because
interactions with tyramine that can result in systemic hypertension
177
MAO inhibitors approved in the United States for the treatment of depression or panic disorder are?
phenelzine, tranylcypromine, and isocarboxazid.
178
What drugs are contraindicated with MAO inhibitors
Cyclic antidepressants
179
This MAOI may be indicated for early parkinson's disease
Selegiline which is an MAO-B selective inhibitor
180
Describe the structure and function of MAO
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
MAO-A preferentially deaminates
serotonin
norepinephrine
epinephrine
182
AO-B preferentially deaminates
phenylethylamine
183
MAO is divided into two subtypes (MAO-A and MAO-B) based on _______
different substrate specificities
184
What is the MOA of MAOIs
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
The most serious common side effects of MAOI is
orthostatic hypotension, which may be especially prominent in elderly patients
186
Orthostatic hypotension from MAOI may reflect accumulation of _____________?
false neurotransmitter octopamine in the cytoplasm of postganglionic sympathetic nerve endings which is released in response to neural impulse.
187
This MAOI has anticholinergic-like side effects and may produce sedation in some patients.
Phenelzine
188
This MAOI has no anticholinergic side effects but has mild stimulant effects, which may cause insomnia.
Tranylcypromine
189
Impotence and anorgasmy are side effects of _______ MAO inhibitors.
All
190
Compared to TCAs, MAOI effect on EEG is?
Minimal and not seizure-like
191
Compared to TCAs, MAOI effect on cardiac rhythm is?
MOAI do not produce cardiac dysrhythmias
192
Patients taking this MAO-B inhibitor do not need to follow a tyramine diet and doses <30mg/day
Selegiline
193
Patients treated with MAOIs should avoid tyramine- containing foods because
They cannot metabolize dietary tyramine
Tyramine be taken up by SNS and hence causing a massive release of endogenous catecholamines
194
Dietary tyramine induced HTN resembles that of pheochromocytoma and should be treated with?
Nitropruside
Beta blockers for persistent dysrhythmias after BP is controlled
195
In patient taking MAOI decrease the dose to about one-third of normal, with additional titration of doses based on cardiovascular responses. T/F
True
196
Overdose with an MAO inhibitor is reflected by
Signs of excessive sympathetic nervous system activity (tachycardia, hyperthermia, mydriasis)
seizures
coma
197
Serotonin syndrome occurs when
When there is an excess of serotonin agonism in the central and peripheral nervous systems.
198
SSRIs, tricyclic antidepressants, and MAO inhibitors, particularly in combination, have all been associated with serotonin syndrome. T/F
True
199
The differential diagnosis for suspected serotonin syndrome includes
malignant hyperthermia, neuroleptic malignant syndrome, and anticholinergic poisoning
200
The principal disadvantage of Buspirone seems to be _______--
a slow onset of effect (1 to 2 weeks), which may be interpreted as ineffectiveness by patients experiencing acute anxiety.
201
Drug of choice for treatment of Bipolar
Lithium
202
The Lithium therapeutic range for acute mania is __________, with oral doses averaging 900 to 1,800 mg per day
1.0 to 1.2 mEq/L
203
What is the effect of loop diuretics on lithium
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
What is the effect of thiazide diuretics on lithium
renal excretion is not enhanced by thiazide diuretics, which act selectively on the distal renal tubules. May increase conc due to volume depletion
205
What is the effect of potassium sparing diuretics on lithium
do not facilitate reabsorption of lithium and, in fact, may increase excretion.
206
What is the effects of NSAIDs on lithium
by altering renal blood flow, may produce marked increases in the plasma concentration of lithium and should be used with care.
