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Pharmacology Test 3 > Antidepressants > Flashcards

Antidepressants Flashcards

1
Q

When given at equivalent and target doses, most antidepressants are _______ efficacious in treating major depressive disorder, but patient responses _____.

A

Equally

Differ

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2
Q

Side effect profiles vary greatly from class to class and individual ______ responses to drug therapy varies from class to class

A

Patient

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3
Q

A response is considered a reduction in symptoms but not?

A

Complete remission

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4
Q

Antidepressant therapy is often chosen based on what two things?

A

Adverse effects and individual response

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5
Q

List the five general properties common to all antidepressants?

A 
Drug distribution
Effects on monoamine neurotransmitters: evidence for the monoamine theory of depression
Time course of drug action
Effects at receptors
Discontinuation/withdrawal syndrome
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6
Q

Medication compliance is influenced greatly by ________.

A

Tolerability

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7
Q

It is important to consider side effects occur much _____ than the positive therapeutic effects, making adherence a common problem

A

Sooner

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8
Q

_____ ______ is most commonly associated with tricyclics antidepressants, monoamine oxidase inhibitors, and mirtazapine

A

Weight gain

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9
Q

What is recommended as a first line to managing weight gain?

A

Diet and exercise

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10
Q

If the patient is non compliant with diet/exercise or they are unsuccessful, the patient should be?

A

Switched to an alternative agent that is less likely to cause weight gain.

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11
Q

What antidepressant is less likely to cause weight gain?

A

Bupropion

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12
Q

What two medications were associated with higher incidence of sexual side effects?

A

Paroxetine and citalopram

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13
Q

What SSRI is associated with less sexual dysfunction?

A

Fluoxetine

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14
Q

Antidepressants not associated with sexual side effects are what two?

A

Bupropion and Mirtazapine

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15
Q

So if you have a patient being non compliant with antidepressants due to sexual side effects what would be the best two medications to switch him to?

A

Bupropion and mirtazapine

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16
Q

Nausea with antidepressant therapy is _______ in nature

A

Transient

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17
Q

To prevent nausea due to antidepressants it is recommended to start therapy with ____ dose and titrate ____.

A

Low

Slowly

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18
Q

Taking antidepressant with food will make nausea better or worse

A

Better

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19
Q

When should you take antidepressants to help prevent nausea?

A

Before bed

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20
Q

Sleep disturbances with antidepressants involves what sleep disturbances?

A

Insomnia
Inability to fall asleep
Difficulty staying awake

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21
Q

First action of the provider when a patient complains of sleep disturbances with an antidepressant is to?

A

Assess the dosing schedule

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22
Q

If the patient is experiencing difficulty staying awake during the day, be sure that the patient is taking the antidepressant when?

A

At nighttime before bed

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23
Q

If the patient reports insomnia or difficulty sleeping, when should the patient take the antidepressant?

A

In the morning

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24
Q

What SSRI is commonly associated with insomnia?

A

Fluoxetine

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25
Q

Bupropion, venlafaxine, and SNRIs are associated with what sleep disturbance?

A

Insomina

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26
Q

Why would SNRI cause insomina?

A

Because they are increasing norepinephrine

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27
Q

Where do antidepressants need to be distributed in the body to produce their antidepressant effects?

A

CNS,

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28
Q

To reach the CNS the antidepressant must cross the?

A

Blood brain barrier

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29
Q

How does the blood brain barrier limit permeability?

A

It is a specialized layer of endothelial cells lining the capillaries of intracranial vessels that uses tight junctions and a basement membrane to limit permeability

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30
Q

The rate and amount of antidepressant that crosses the blood brain barrier involves two mechanisms what are they?

A

Passive diffusion - b/c they are small molecules and highly lipophilicity
Active transport from the BBB into the peripheral blood supply by P-glycoprotein.

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31
Q

P-glycoprotein is a _______ protein

A

Efflux

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32
Q

P-glycoprotein works to _____ drug from the body or from specific areas in the body, such as the brain

A

Exclude

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33
Q

Most antidepressants increase the concentration monoamine neurotransmitters such as serotonin, norepinephrine, and dopamine within the?

A

Synaptic cleft

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34
Q

Most antidepressants produce their effect by inhibiting the transporter that takes up the ____________ from the synaptic cleft back into the presynaptic neuron. This is known as? Medications that work like this are called

A

Neurotransmitter
Reuptake
Reuptake transport inhibitors

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35
Q

How long does the initial response take with a antidepressant therapy?

A

2-4 weeks for an initial response

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36
Q

How long does a fully response take for antidepressants?

A

4-6 weeks

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37
Q

What is the reasons for the delay in therapeutic effect in antidepressants?

A

Initially synaptic neurotransmitter concentration stimulations an additional mechanism which is involved in the antidepressant effect.

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38
Q

Most antidepressants are _________ at one or more of the receptors in both the CNS and PNS

A

Antagonist

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39
Q

List three major receptor classes blocked by antidepressants?

A

Alpha adrenergic receptors
Cholinergic receptors
Histamine receptors

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40
Q

What determines a large portion of the adverse effect profile of each medication?

A

What degree does the antidepressant block a receptor and which receptors are blocked

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41
Q

Abrupt discontinuation of antidepressant can result in what?

A

Serotonin withdrawal syndrome

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42
Q

Antidepressant therapy gradually results in changes in __________ over the course of weeks of drug therapy.

A

Neurotransmission

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43
Q

CNS and PNS become somewhat dependent on what?

A

Antidepressant action

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44
Q

if antidepressant therapy is withdrawn abruptly or the doses decreased too rapidly what will develop? what is another name for it?

A

serotonin withdrawal syndrome

discontinuation syndrome

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45
Q

list the signs and symptoms of serotonin withdrawal syndrome?

A 
remember finish
f- flu like symptoms
i- irritabile/anxious
n- nausea
i - insomnia
s- sensory disturbances
h- hormonal (crying spells)
46
Q

serotonin withdrawal syndrome is a high risk with what groups?

A

specifically SSRIs and specific SNRI (venlafaxine)

however all antidepressants are at risk

47
Q

serotonin syndrome is caused by?

A

increase in intrasynaptic serotonin which results in excessive serotonin in the periphery

48
Q

serotonin syndrome is the result of what?

A

a pharmacodynamic drug interaction between SSRI and other medications that augment serotonergic function

49
Q

what are non antidepressant medications implicated in serotonin syndrome?

A

tramadol, meperidine, and fentanyl.

50
Q

what are the signs and symptoms of serotonin syndrome?

A 
remember Harmful!
H- hyperthermia
A- anti-cognitive (delirium/ confusion/agitation)
reflexes - hyperreflexia
myoclonus - hyperreflexia
fast heart rate
unconsciousness - coma
loss of GI control nausea/diarrhea
51
Q

treatment resistant depression is generally defined as failure at?

A

two antidepressants

52
Q

treatment resistant depression can affect up to 1/3 of patients with depression and leads to more comorbities and what else?

A

increased hospitalizations

increased suicide rate

53
Q

what is a common solution for truly refractory patients?

A

electroconvulsive therapy

54
Q

the response and remission rate in patients treated with ECT is _______ to those treated with antidepressants alone

A

superior

55
Q

ECT functions by?

A

applying electrodes to the patient head and by initiating a electrical current that produces a generalized seizure in a controlled environment

56
Q

what medications may a patient be given preoperative for ECT?

A

anticholinergic medication
anesthetic
muscle relaxant

57
Q

the muscle relaxant given prior to ECT can prevent full expression of what?

A

seizure throughout the body

58
Q

what are the theories for how ECT improves depression

A

increase of monoamines such as dopamine and serotonin and neuropeptides

59
Q

ECT si considered safe, yet it can still cause?

A

transient increase in blood pressure, pulse, and ICP

60
Q

when performing ECT special precautions should be taking in which patients?

A

heart conditions

61
Q

ECT treatments are usually ____ times per week and responses vary from ___ to ___ treatments

A

3

4 to 20

62
Q

the most common side effect of ECT are ? (2)

A

confusion and memory loss

63
Q

what is the typical first line treatment for depression?

A

SSRI

64
Q

SSRI are a popular drug class due to an improved ______ and ______ when compared to TCA and MAOIs

A

safety and adverse effect profile

65
Q

what is the mechanism of action of SSRIs?

A

they are highly selective for binding to the SERT (serotonin reuptake transporter) relative to the NERT (norepinephrine reuptake transporter) , which only blocks the reuptake of serotonin resulting in increased serotonin concentrations at the synaptic cleft

66
Q

what does it mean SSRIs are halogenated? why is it beneficical?

A

increased halogen groups present
it will increase SSRIs ability to interact with lipophilic compounds allowing for increased penetration across the blood brain barrier into the CNS

67
Q

adverse effects of SSRIs are?

A

remember BAD SSRI
body weight increase
anxiety/agitation
diarrhea

serotonin syndrome
sexual dysfunction
really got to poop
Insomnia/sedation

68
Q

SSRIs are more prone to ?

A

serotonin withdrawal syndrome

69
Q

what drug class of antidepressants is the most selective for serotonin?

A

SSRIs

70
Q

Antidepressants with a shorter half-life, have a greater risk for causing withdrawal syndrome. Why

A

due to a short elimination half-life leaving the body rapidly resulting in blood levels falling quickly for withdrawal of therapy or dose reduction

71
Q

name a antidepressant with a long elimination half-life?

A

fluoxetine

72
Q

what is the benefit of long elimination half-life antidepressants?

A

they leave the body more slowly and blood concentration decreases in a slower manner, causing less likely change of a rapid decrease in drug effect

73
Q

what is the mechanism of action for SNRIs

A

have an affinity for both serotonin and norepinephrine reuptake transporters which will block the reuptake of both neurotransmitters

74
Q

the adverse effects of SNRIs are relatively mild, partially due to what?

A

the low affinity for blocking muscarinic alpha adrenergic and histamine receptors

75
Q

name the side effects of SNRIs have the same side effects as ______. which are?

A

SSRIs
stomach (nausea, constipation, diarrhea)
sexual (decreased libido/erectile dysfunction)
sleep (insomnia)

76
Q

Abrupt withdrawal of Venlafaxine can lead to ?

A

serotonin withdrawal syndrome

77
Q

venlafaxine can also cause a rise in _____ due to norepinephrine levels increased. so the patient should do what?

A

blood pressure

regularly monitor their blood pressure

78
Q

gastrointestinal symptoms are common in SNRIs how can a patient combat this?

A

take with food

Take the extended release formulation of venlafaxine has fewer GI adverse effects than the immediate release

79
Q

levomilnacipran is contraindicated in patients with _______________ due to increased risk of _________.

A

uncontrolled narrow angle glaucoma

mydriasis

80
Q

what is the mechanism of action for TCA?

A

block the reuptake of both serotonin and norepinephrine

81
Q

TCA adverse effect profile is _____ than SNRIs

A

worse

82
Q

Tertiary amine tricyclic antidepressants are more ________ blockade of the reuptake of ___________, which secondary amine TCA are more selective for the blockade of reuptake of ________________

A

selective
serotonin
norepinephrine

83
Q

name two tertiary amine tricyclic antidepressants

A

amitriptyline and imipramine

84
Q

Name two secondary amine tricyclic antidepressants

A

thing NA for new edition
nortriptyline
azipramine

85
Q

why were SSRIs and SNRIs first developed?

A

because TCAs have a worse adverse effect profile

86
Q

the adverse effects of TCAs are dependent on the fact that TCAs block both neurotransmitter receptors in the CNS and PNS, name the three major receptors blocked.

A

alpha adrenergic
muscarinic
histamine

87
Q

alpha adrenergic receptors constrict smooth muscle resulting in vasoconstriction, so TCA’s blockade of this receptor would cause?

A

postural hypotension due to vasodilation

88
Q

what precautions should a patient perform during the initial dosing of TCAs until the body can compensate?

A

monitor blood pressure

89
Q

what disorder can be prevalent with TCAs as well?

A

cardiovascular disorders causing arrhythmias.

90
Q

blockage of muscarinic receptors produce effects referred to as? list them

A 
anticholinergic effects
dry mouth
constipation
blurred vision
urinary retention
confusion
hallucination
91
Q

what histamine receptors are TCAs known to block

A

H1 and H2

92
Q

When psychiatric drugs are said to have an antihistamine property , this refers to ?

A

blockade of H1 receptors in the CNS

93
Q

antihistamine effects of antidepressants include _________ from the blockade of these receptors.

A

excessive drowsiness

94
Q

the adverse effect profile of secondary tricyclic antidepressants is _____than that of tertiary tricyclic antidepressants

A

milder

95
Q

what is bupropion mechanism of action?

A

blocks reuptake of dopamine and norepinephrine in the CNS

96
Q

the blockage of dopamine in bupropion can decrease craving symptoms for _______ cessations, as blockade of dopamine reuptake in the ________ system may ease symptoms of cravings in cases of drug addiction

A

smoking

limbic

97
Q

a major risk of buproprion is?

A

risk for causing seizures

98
Q

the seizure risk for buproprion is ______ dependent. what does that mean?

A

dose, meaning it goes up with increasing dose once a dose reaches a certain level, the risk for seizures increases exponentially.

99
Q

name the three absolute contraindications fro buproprion for the risk of seizure?

A

pt. with a history of a seizure disorder
patients with bulimia or anorexia nervosa (higher risk of electrolyte abnormalities, which can lead to seizure)
pt. undergoing withdrawal of ETOH or anxiolytic medications such as benzos.
- this is because ETOH withdrawal can lead to seizures if it is not properly treated.

100
Q

mirtazapine is a _________ antidepressants with structural features of _________.

A

TCA

serotonin

101
Q

name the two atypical antidepressants

A

buproprion and mirtazapine

102
Q

what is the mechanism of action for mirtazapine?

A

an alpha 2 adrenergic antagonist and antagonist at several post synaptic serotonin receptors including 5 HT2A, 5HT2C, 5HT3 receptors, resulting in the increase of serotonin and norepinephrine

103
Q

mirtazapine is a potent H1 receptor antagonist which often leads to what two symptoms

A

sedation and weight gain

104
Q

mirtazapine binds to ________ receptors with a low affinity, which is why ________ effects are minimal

A

muscarinic receptors

anticholinergic

105
Q

the combination of monoamine oxidase inhibitors with ________ rich foods may result in life threatening reactions

A

tyramine

106
Q

tyramine is a precursor for the biosynthesis of __________ neurotransmitters

A

catecholamine

107
Q

tyramine obtained from the diet is metabolized by _____________ in the GI tract

A

monoamine oxidase

108
Q

inhibition of monoamine oxidase in the GI tract by monoamine oxidase inhibitors may result in excessive __________ absorption into the body, which results in biosynthesized into __________. resulting in ______ crisis and other life threatening events

A

tyramine
catecholamines
hypertensive

109
Q

name three catecholamines increased with tyramine rich foods?

A

norepinephrine
dopamine
and epinephrine

110
Q

patients taking monoamine oxidase inhibitors should avoid ______ rich foods

A

tyramine

111
Q

name three tyramine rich foods?

A

picked foods
red wine
hard cheeses

Pharmacology Test 3 (4 decks)

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