Antidepressants Flashcards
(111 cards)
1
Q
When given at equivalent and target doses, most antidepressants are _______ efficacious in treating major depressive disorder, but patient responses _____.
A
Equally
Differ
2
Q
Side effect profiles vary greatly from class to class and individual ______ responses to drug therapy varies from class to class
A
Patient
3
Q
A response is considered a reduction in symptoms but not?
A
Complete remission
4
Q
Antidepressant therapy is often chosen based on what two things?
A
Adverse effects and individual response
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
6
Q
Medication compliance is influenced greatly by ________.
A
Tolerability
7
Q
It is important to consider side effects occur much _____ than the positive therapeutic effects, making adherence a common problem
A
Sooner
8
Q
_____ ______ is most commonly associated with tricyclics antidepressants, monoamine oxidase inhibitors, and mirtazapine
A
Weight gain
9
Q
What is recommended as a first line to managing weight gain?
A
Diet and exercise
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.
11
Q
What antidepressant is less likely to cause weight gain?
A
Bupropion
12
Q
What two medications were associated with higher incidence of sexual side effects?
A
Paroxetine and citalopram
13
Q
What SSRI is associated with less sexual dysfunction?
A
Fluoxetine
14
Q
Antidepressants not associated with sexual side effects are what two?
A
Bupropion and Mirtazapine
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
16
Q
Nausea with antidepressant therapy is _______ in nature
A
Transient
17
Q
To prevent nausea due to antidepressants it is recommended to start therapy with ____ dose and titrate ____.
A
Low
Slowly
18
Q
Taking antidepressant with food will make nausea better or worse
A
Better
19
Q
When should you take antidepressants to help prevent nausea?
A
Before bed
20
Q
Sleep disturbances with antidepressants involves what sleep disturbances?
A
Insomnia
Inability to fall asleep
Difficulty staying awake
21
Q
First action of the provider when a patient complains of sleep disturbances with an antidepressant is to?
A
Assess the dosing schedule
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
23
Q
If the patient reports insomnia or difficulty sleeping, when should the patient take the antidepressant?
A
In the morning
24
Q
What SSRI is commonly associated with insomnia?
A
Fluoxetine
25
Bupropion, venlafaxine, and SNRIs are associated with what sleep disturbance?
Insomina
26
Why would SNRI cause insomina?
Because they are increasing norepinephrine
27
Where do antidepressants need to be distributed in the body to produce their antidepressant effects?
CNS,
28
To reach the CNS the antidepressant must cross the?
Blood brain barrier
29
How does the blood brain barrier limit permeability?
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
30
The rate and amount of antidepressant that crosses the blood brain barrier involves two mechanisms what are they?
Passive diffusion - b/c they are small molecules and highly lipophilicity
Active transport from the BBB into the peripheral blood supply by P-glycoprotein.
31
P-glycoprotein is a _______ protein
Efflux
32
P-glycoprotein works to _____ drug from the body or from specific areas in the body, such as the brain
Exclude
33
Most antidepressants increase the concentration monoamine neurotransmitters such as serotonin, norepinephrine, and dopamine within the?
Synaptic cleft
34
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
Neurotransmitter
Reuptake
Reuptake transport inhibitors
35
How long does the initial response take with a antidepressant therapy?
2-4 weeks for an initial response
36
How long does a fully response take for antidepressants?
4-6 weeks
37
What is the reasons for the delay in therapeutic effect in antidepressants?
Initially synaptic neurotransmitter concentration stimulations an additional mechanism which is involved in the antidepressant effect.
38
Most antidepressants are _________ at one or more of the receptors in both the CNS and PNS
Antagonist
39
List three major receptor classes blocked by antidepressants?
Alpha adrenergic receptors
Cholinergic receptors
Histamine receptors
40
What determines a large portion of the adverse effect profile of each medication?
What degree does the antidepressant block a receptor and which receptors are blocked
41
Abrupt discontinuation of antidepressant can result in what?
Serotonin withdrawal syndrome
42
Antidepressant therapy gradually results in changes in __________ over the course of weeks of drug therapy.
Neurotransmission
43
CNS and PNS become somewhat dependent on what?
Antidepressant action
44
if antidepressant therapy is withdrawn abruptly or the doses decreased too rapidly what will develop? what is another name for it?
serotonin withdrawal syndrome
| discontinuation syndrome
45
list the signs and symptoms of serotonin withdrawal syndrome?
```
remember finish
f- flu like symptoms
i- irritabile/anxious
n- nausea
i - insomnia
s- sensory disturbances
h- hormonal (crying spells)
```
46
serotonin withdrawal syndrome is a high risk with what groups?
specifically SSRIs and specific SNRI (venlafaxine)
| however all antidepressants are at risk
47
serotonin syndrome is caused by?
increase in intrasynaptic serotonin which results in excessive serotonin in the periphery
48
serotonin syndrome is the result of what?
a pharmacodynamic drug interaction between SSRI and other medications that augment serotonergic function
49
what are non antidepressant medications implicated in serotonin syndrome?
tramadol, meperidine, and fentanyl.
50
what are the signs and symptoms of serotonin syndrome?
```
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
treatment resistant depression is generally defined as failure at?
two antidepressants
52
treatment resistant depression can affect up to 1/3 of patients with depression and leads to more comorbities and what else?
increased hospitalizations
| increased suicide rate
53
what is a common solution for truly refractory patients?
electroconvulsive therapy
54
the response and remission rate in patients treated with ECT is _______ to those treated with antidepressants alone
superior
55
ECT functions by?
applying electrodes to the patient head and by initiating a electrical current that produces a generalized seizure in a controlled environment
56
what medications may a patient be given preoperative for ECT?
anticholinergic medication
anesthetic
muscle relaxant
57
the muscle relaxant given prior to ECT can prevent full expression of what?
seizure throughout the body
58
what are the theories for how ECT improves depression
increase of monoamines such as dopamine and serotonin and neuropeptides
59
ECT si considered safe, yet it can still cause?
transient increase in blood pressure, pulse, and ICP
60
when performing ECT special precautions should be taking in which patients?
heart conditions
61
ECT treatments are usually ____ times per week and responses vary from ___ to ___ treatments
3
| 4 to 20
62
the most common side effect of ECT are ? (2)
confusion and memory loss
63
what is the typical first line treatment for depression?
SSRI
64
SSRI are a popular drug class due to an improved ______ and ______ when compared to TCA and MAOIs
safety and adverse effect profile
65
what is the mechanism of action of SSRIs?
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
what does it mean SSRIs are halogenated? why is it beneficical?
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
adverse effects of SSRIs are?
remember BAD SSRI
body weight increase
anxiety/agitation
diarrhea
serotonin syndrome
sexual dysfunction
really got to poop
Insomnia/sedation
68
SSRIs are more prone to ?
serotonin withdrawal syndrome
69
what drug class of antidepressants is the most selective for serotonin?
SSRIs
70
Antidepressants with a shorter half-life, have a greater risk for causing withdrawal syndrome. Why
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
name a antidepressant with a long elimination half-life?
fluoxetine
72
what is the benefit of long elimination half-life antidepressants?
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
what is the mechanism of action for SNRIs
have an affinity for both serotonin and norepinephrine reuptake transporters which will block the reuptake of both neurotransmitters
74
the adverse effects of SNRIs are relatively mild, partially due to what?
the low affinity for blocking muscarinic alpha adrenergic and histamine receptors
75
name the side effects of SNRIs have the same side effects as ______. which are?
SSRIs
stomach (nausea, constipation, diarrhea)
sexual (decreased libido/erectile dysfunction)
sleep (insomnia)
76
Abrupt withdrawal of Venlafaxine can lead to ?
serotonin withdrawal syndrome
77
venlafaxine can also cause a rise in _____ due to norepinephrine levels increased. so the patient should do what?
blood pressure
| regularly monitor their blood pressure
78
gastrointestinal symptoms are common in SNRIs how can a patient combat this?
take with food
| Take the extended release formulation of venlafaxine has fewer GI adverse effects than the immediate release
79
levomilnacipran is contraindicated in patients with _______________ due to increased risk of _________.
uncontrolled narrow angle glaucoma
| mydriasis
80
what is the mechanism of action for TCA?
block the reuptake of both serotonin and norepinephrine
81
TCA adverse effect profile is _____ than SNRIs
worse
82
Tertiary amine tricyclic antidepressants are more ________ blockade of the reuptake of ___________, which secondary amine TCA are more selective for the blockade of reuptake of ________________
selective
serotonin
norepinephrine
83
name two tertiary amine tricyclic antidepressants
amitriptyline and imipramine
84
Name two secondary amine tricyclic antidepressants
thing NA for new edition
nortriptyline
azipramine
85
why were SSRIs and SNRIs first developed?
because TCAs have a worse adverse effect profile
86
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.
alpha adrenergic
muscarinic
histamine
87
alpha adrenergic receptors constrict smooth muscle resulting in vasoconstriction, so TCA's blockade of this receptor would cause?
postural hypotension due to vasodilation
88
what precautions should a patient perform during the initial dosing of TCAs until the body can compensate?
monitor blood pressure
89
what disorder can be prevalent with TCAs as well?
cardiovascular disorders causing arrhythmias.
90
blockage of muscarinic receptors produce effects referred to as? list them
```
anticholinergic effects
dry mouth
constipation
blurred vision
urinary retention
confusion
hallucination
```
91
what histamine receptors are TCAs known to block
H1 and H2
92
When psychiatric drugs are said to have an antihistamine property , this refers to ?
blockade of H1 receptors in the CNS
93
antihistamine effects of antidepressants include _________ from the blockade of these receptors.
excessive drowsiness
94
the adverse effect profile of secondary tricyclic antidepressants is _____than that of tertiary tricyclic antidepressants
milder
95
what is bupropion mechanism of action?
blocks reuptake of dopamine and norepinephrine in the CNS
96
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
smoking
| limbic
97
a major risk of buproprion is?
risk for causing seizures
98
the seizure risk for buproprion is ______ dependent. what does that mean?
dose, meaning it goes up with increasing dose once a dose reaches a certain level, the risk for seizures increases exponentially.
99
name the three absolute contraindications fro buproprion for the risk of seizure?
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
mirtazapine is a _________ antidepressants with structural features of _________.
TCA
| serotonin
101
name the two atypical antidepressants
buproprion and mirtazapine
102
what is the mechanism of action for mirtazapine?
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
mirtazapine is a potent H1 receptor antagonist which often leads to what two symptoms
sedation and weight gain
104
mirtazapine binds to ________ receptors with a low affinity, which is why ________ effects are minimal
muscarinic receptors
| anticholinergic
105
the combination of monoamine oxidase inhibitors with ________ rich foods may result in life threatening reactions
tyramine
106
tyramine is a precursor for the biosynthesis of __________ neurotransmitters
catecholamine
107
tyramine obtained from the diet is metabolized by _____________ in the GI tract
monoamine oxidase
108
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
tyramine
catecholamines
hypertensive
109
name three catecholamines increased with tyramine rich foods?
norepinephrine
dopamine
and epinephrine
110
patients taking monoamine oxidase inhibitors should avoid ______ rich foods
tyramine
111
name three tyramine rich foods?
picked foods
red wine
hard cheeses
