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PCL200 > Drugs for Depression & Anxiety > Flashcards

Drugs for Depression & Anxiety Flashcards

1
Q

_____ & ______ are essential emotions for survival - much of the neuron circuitry regulating these emotions is subcortical (subconcious)

A

fear, anxiety

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2
Q

state the part of the brain that is our thinking mind

A

cortex

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3
Q

________ is a powerful motivator of behaviour

A

emotion

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4
Q

define fear

A

an emotional state aroused by specific external stimuli that gives rise to defensive and escape behaviours

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5
Q

define anxiety

A

a generalized response to an unknown threat or internal conflict - Concern about a future event that might be threatening - when we don’t have a feeling of control

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6
Q

define anxiety disorders

A

psychiatric conditions characterized by overactivity (dysregulation) of the autonomic nervous system (fight or flight), expectation of an impending threat, and continuous vigilance for danger (not caused by drug intoxication or drug withdrawal)

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7
Q

define panic disorder

A

characterized by episodic periods of intense fear and ANS over activation

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8
Q

what are the signs of panic disorder/ANS overactivation

A
  • fast heartbeat
  • short breath
  • patients sincerely believe they are dying
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9
Q

define generalized anxiety disorder

A

persistent state of excessive worry and anxiety serious enough to cause a disruption in normal activities

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10
Q

define anticipatory anxiety

A

a fear of having a panic attack; may lead to the development of agoraphobia

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11
Q

define agoraphobia

A

a fear of being away from home or other protected place

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12
Q

define social anxiety disorder

A

excessive fear of being exposed to the scrutiny of other people that leads to avoidance of social situations

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13
Q

define post traumatic stress disorder

A

a reaction to a terrifying event that occurs to or is witnessed by the patient

Everyone experienced a traumatic event but only a portion has a persistent debilitating syndrome from it

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14
Q

what are the signs of ptsd

A
  • flashbacks
  • nightmares
  • anxiety
  • compulsive thoughts about the event/rumination
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15
Q

what is the lifetime prevalence of anxiety disorders

A

at least 20% (high!)

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16
Q

what may anxiety disorders be comorbid with

A

depression

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17
Q

females are ______ as likely as males to develop an anxiety disorder - emphasizes biological nature but gender may also play a role

A

twice

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18
Q

what is the heritability to anxiety disorders

A

0.3 (based on family and twin studies, quite low)

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19
Q

bdnf (gene) and val66met allele may play a role for what disorder (and what does val66met do)

A

ptsd, val66met may impair the ability to forget a fear memory in humans and mice

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20
Q

why might ptsd be easier to understand

A

bc they can see the genetic differences in people who can move on and those who cannot

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21
Q

chronic psychological stress persistently increases _______ and effects _________ _________ numbers

A

cortisol, neuron synapse

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22
Q

what happens in the brain during periods of stress

A

there is increased connectivity = you learn about what the stress is. But enduring consistent stress leads to persistent increase in cortisol and effects the connections in the synaptic connections = possible loss in volume of the cortex (decreases synapse number in hippocampus and cortex) = fear not working properly

stress affects hypothalamus –> anterior pituitary –> adrenal gland –> cortisol (long term has much dire affects)

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23
Q

what devices provides the best evidence for the neurobiology of anxiety disorders

A

fMRI - functional magnetic resonance imaging

DTI - diffusion tensor imaging

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24
Q

what can you see in the fMRI regarding anxiety disorders

A

Sees blood flow - when neurons fire it has blood sent to the area and the iron in the blood gets picked up

brain regions that are activated have increased blood flow

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25
Q

name the part of the brain that patients w anxiety disorders have an overactivation of

A

the amygdala

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26
Q

what does the amygdala do

A

regions for fear, anger, negative emotions

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27
Q

describe what the DTI studies

A

white matter tracts and connectivity

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28
Q

anxiety disorders reduce connectivity between _____ ____ and the _________

A

frontal cortex and amygdala

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29
Q

which is easier to treat, anxiety disorders or depression

A

anxiety disorders

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30
Q

for anxiety disorders, __________ has similar efficacy to pharmacotherapy

A

psychotherapy

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31
Q

describe the first line therapy for anxiety disorders

A

SSRIs (selective serotonin reuptake inhibitors) and antidepressants that are actually more effective for anxiety than they are for depression - the effect of increasing serotonin is particularly effective in anxiety disorders

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32
Q

what might be used as alternate treatment for GAD (generalized anxiety disorder) and PD

A

benzodiazepines

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33
Q

why might benzodiazepines be limited in treating GAD and PD

A
  • tolerance
  • withdrawal
  • rebound effect: If you stop taking it then you get a return on the anxiety and it may be worse
  • abuse liability: Need more and more and more to control the anxiety
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34
Q

list the characteristics of major depressive disorder (MDD) (9)

A
  • depressed mood most of the day
  • diminished interest or pleasure in all or most activities
  • significant unintentional weight loss or gain
  • insomnia or sleeping too much
  • agitation or psychomotor retardation noticed by others
  • fatigue or loss of energy
  • feelings of worthlessness or excessive guilt
  • diminished ability to think or concentrate, or indecisiveness
  • recurrent thoughts of death
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35
Q

state the most common brain disorder, based on WHO

A

depression, over 350 million people of all ages globally

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36
Q

what is the leading cause of disability world wide, based on WHO

A

depression

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37
Q

based on WHO, how is disability measured

A

DALYs - disability adjusted life years: how many years of healthy life are lost to the disease

DALY=YLL+YLD

38
Q

which sex is more affected by depression

A

women

39
Q

how many people globally die from suicide, based on WHO

A

1 million

40
Q

what may prevent people from accessing therapies for depression

A

cultural stigmas

41
Q

state the heritability of depression

A

30%-40%

42
Q

what are some risks/what are some factors that determines prevalence

A
  • environmental risk, psychological stress
  • age; early adulthood onset mostly but can occur anything
  • gender; more females than males
  • marital status; divorced, widowed, single, married
  • education
  • socioeconomic status
43
Q

describe how stress reduces synapses

A
  • chronic stress induces depression
  • production of cortisol causes a decrease in brain derived neurotrophic factor (protein)
  • decrease in bdnf causes a decrease in new neurons and retraction of dendrites
  • can be reversed w antidepressant treatment
  • the synpases have significantly less dendritic sprouts
44
Q

t/f can the process of stress induced synapse reduction be reversed

A

yes, by antidepressants

45
Q

how can antidepressants reverse the synapse reduction due to chronic stress

A

New connections forming and an increase in new born neurons (stem cells waiting to be differentiated into a neuron - not common but there is a low level of neurogenesis) - when you take antidepressants, you see an increase in neurogenesis

46
Q

state the psychotherapy treatment for depression

A

cognitive behavioural therapy

47
Q

list the 5 pharmacotherapies as treatments for depression

A
  1. tricyclic antidepressants (tcas)
  2. monoamine oxidase inhibitors (MAOi’s)
  3. selective serotonin reuptake inhibitors (SSRIs)
  4. serotonin/norepinephrine reuptake inhibitors (SNRIs)
  5. hallucinogens (ket (most researched), psilocybin, MDMA) - work much quicker than 1-4
48
Q

other than psychotherapy and pharmacotherapy, what might be another treatment for depression

A

electroconvulsive therapy (ECT and TMS) and deep brain stimulation (Helen Mayberg)

49
Q

monoamines are _________ for their receptors, and their receptors are the _______________

A

agonists, g-protein coupled receptors

50
Q

list 6 monoamines relevant to this

A
  1. dopamine (DA)
  2. norepinephrine (NE)
  3. serotonin (5HT)
  4. melatonin
  5. histamine
  6. trace amines
51
Q

what do monoamines regulate (10)

A
  • mood
  • sleep
  • appetite
  • peristalsis
  • arousal (awakeness)
  • sexual function
  • cognition
  • reward
  • motivation
  • aggression
    (sometimes w opposing effects between dopamine and serotonin)
52
Q

state the similarities/features of monoamines (4)

A
  • all derived from amino acids in similar synthetic processes and are degraded by the same/similar enzymes
  • all packaged into synaptic vesicles by VMAT2 (vesicular monoamine transporter 2)
  • act on metabotropic, g-protein coupled receptors
  • all cleared from the synapse by plasma membrane transporters; another way to clear is through enzymes that will degrade them (monoamine oxidase)
53
Q

what does monoamine oxidase degrade

A

serotonin, norepinephrine, adrenaline, dopamine, tyramine (cheese effect is too much tyramine)

54
Q

how do monoamine oxidase inhibitors affect levels of nt (serotonin, norepinephrine, adrenaline, dopamine, tyramine)

A

they increase levels of this bc monoamine oxidase is what degrades them; more serotonin means you can package more and so it increases levels of the NT

55
Q

what are 2 examples of monoamine oxidase inhibitors

A

phenelzine (also a drug for tb) and moclobemide (reversible)

56
Q

what is the moa of phenelzine (MAOI)

A

irreversible inhibitor of monoamine oxidase, once it binds the enzyme it permanently inactivates it and there is no more enzyme until the cell makes more

57
Q

describe the concerns of phenelzine (MAOI)

A

highly effect but only used as last resort bc nuremous drug drug interactions that cause hypertensive crisis (excess adrenaline) and serotonin syndrome (too much) that can be fatal

High BP = brain cannot handle a “firehouse” of blood going through it. The blood vessels will burst = stroke

58
Q

describe the relationship of hypertensive crisis and tyramine

A

tyramine can cause hypertensive crisis

foods that contain tyramine are cheese wine beer sauerkraut thus you have to have a strict diet while on MAOIs

59
Q

compare reversible and irreversible MAOIs

A

phenelzine is irreversible and reversible is moclobemide.

phenelzine is highly effective with serious adverse effects and moclobemide are also effective and much safer but doctors have reluctance prescribing

they have the same drug drug interactions and diet

60
Q

how were tricyclic antidepressant discovered

A

the drugs were initially made for schizophrenia patients. After chlorpromazine (schizophrenia med) was discovered - all pharma companies wanted chlorpromazine made many chemicals similar (imipramine) –> gave it to psychiatrist, tried it on schizophrenia patients and didn’t work, and just randomly tested out on his depressed patients.

didn’t want to make more bc there was no market, but a stockholder and pharma owner had a wife w depression so they kept it.

61
Q

what is the primary therapeutic benefit of TCAs

A

they have several targets. primary benefit is thought to be due to blocking (antagonist) the reuptake of both serotonin and norepinephrine (inhibit NET and SERT)

62
Q

list the receptors (7) and channels (2) that TCAs are antagonists for

A

receptors:
1. 5ht2a
2. 5ht2c
3. 5ht6
4. 5ht7
5. a1 adrenergic
6. antihistamine
7. anticholinergic
channels
1. sodium
2. calcium

63
Q

what are the adverse effects of TCAs blocking ion channels

A

cause of death from overdose is from cardiotoxicity, prolonged heart rhythms

64
Q

what are the adverse effects of TCAs antagonizing the receptors

A

histamine receptor antagonist causes drowsiness, anti-muscarinic cholinergic receptor causes dry mouth and dry eyes

65
Q

safety profile of ________ preferred over TCAs

A

SSRIs

66
Q

name 2 examples of tcas

A

imipramine, amitriptyline

67
Q

what are the first line of treatment for depression and anxiety

A

ssri

68
Q

list examples of ssri (4)

A

fluoxetine eg prozac
paroxetine eg paxil
citalopram eg celexa
sertraline eg zoloft

69
Q

fluoxetine is the ________ selective and first line for __________ and have a ______ half life

A

least, adolescents, long (the lost half life may lead to dosing problems

70
Q

paroxetine has _______________ effects, _____ weight gain

A

anti-cholinergic effects, most

71
Q

t/f we know how ssri causes weight gain, if so, how

A

false, we don’t know, all of them cause weight gain after 6 months

72
Q

citalopram is the _____ selective for SERT

A

most

73
Q

sertraline is an __________ of DAT (dopamine transporter)

A

antagonist

74
Q

ssris were the first class of drugs developed by what design, and what did this design mean

A

rational drug design; screened for ability to inhibit sert and elevate serotonin based on actions of tcas and maois

75
Q

what is the typical half life of ssri and what is the outlier

A

around 24-30 hours, fluoxetine is 48-96 hours, active metabolites have half lives of several days

76
Q

contrast between the timelines of adverse effects and beneficial effects of ssris

A

Beneficial effects take several weeks to occur and you get the adverse effects from day 1 (the weight gain is later)

note that many or most of the adverse effects diminish with continued use

77
Q

list the adverse effects of ssris (11)

A
  • headache
  • insomnia
  • gi disturbance (nausea, cramping, diarrhea)
  • sexual dysfunction (reduced libido, anorgasmia)
  • weight gain
  • dizziness
  • weakness
  • fatigue
  • tremor
  • agitation
  • anxiety
    Note that the less common effects are at the end of the list
78
Q

how to deal with discontinuation syndrome and its effects

A

effects: anxiety, insomnia, headache, nausea

how to deal: taper off treatment by reducing dose and then taking on alternating days

79
Q

snri inhibits what transporters

A

sert and net

80
Q

for depression, are ssri or snri more effective

A

snri

81
Q

examples of snris 2

A

venlafaxine (effecor)
duloxetine (cymbalta)

82
Q

why is bupropion (wellbutrin) a different kind of antidepressant (diff class altogether)

A

little action on sert, but blocks dat and net

83
Q

what is serotonin syndrome caused by

A

drug drug interactions of ssri and maoi –> too much released that you can’t clear it

ssri + cough med (dextromethorphan)

ssri + tryptans (migraine med) or some opiods (aalgesics)

can also be caused by ecstasy (mdma)

84
Q

what are the adverse effects of serotonin syndrome (10) and the fatal effects (3)

A

adverse:
agitation or restlessness, hyper reflexes, diarrhoea, fast heart beat, high bp, hallucinations, increase body temperature, loss of coordination, nausea, vomiting

fatal: hyperthermia, tachycardia, lactic acidosis (too acidic) from muscle contraction

85
Q

list the related disorders that also respond to anti-depressants (8)

A

dysthymia, postpartum depression, atypical depression (overeat, oversleep, inability to react positively, oversensitivity to rejection), SAD, anxiety disorders (gad, panic, ptsd, social), ocd, neuropathic pain, eating disorders (bulimia but not anorexia nervosa)

86
Q

hallucinogens (as antidepressants) have more ______ antidepressants effects

A

rapid

87
Q

how must hallucinogens (as antidepressants) be delivered

A

in a clinic with someone guiding them

88
Q

how might ketamine act as an antidepressant

A

antagonist of nmda type of glutamate receptors - increases synapse density within 1h of treamtent. given intravenously every 1-4 weeks

89
Q

how might psilocybin act as an antidepressant

A

chemical in psilocybes (magic mush) converted to psilocin in body - agonist of 5ht2a serotonin receptor

90
Q

how might lsd (lysergic acid diethylamide) act as an antidepressant

A

chemical dervied from ergot mold - agonist of 5ht2a serotonin receptor

91
Q

how might mdma (3,4-methylenedioxymethamphetamine) act as an antidepressant

A

acts in same way as amphetamine

selective for sert - reverse transports serotonin

PCL200 (5 decks)

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