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Mental Health > Pham of Depression and Anxiety > Flashcards

Pham of Depression and Anxiety Flashcards

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2
Q

Describe the monoamine Hypothesis

A

There is a deficiency in the brain of the neurotransmitters Noradrenaline and Serotonin

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3
Q

According the monoamine hypothesis what is the mechanism of drugs that cause depression

A

Drugs which depilate the stories of noradrenaline and serotonin

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4
Q

According the monoamine hypothesis what is the mechanism of drugs that are anti-depressants?

A

Drugs which elevate the stores of noradrenaline and serotonin

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5
Q

explained the stress hypothesis of depression

A

it is an observation that there are high cortisol levels in depression patents, also the cortisol levels tend to fail to respond with the normal fall when a synthetic steroid such as dexamethasone is given.

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6
Q

what two enzymes break down Noradrenaline and serotonin? Where are they located

A

Mona-amine oxidase and Catechol-o-methyl transferase; both are present both externally and in the presynaptic neuron

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7
Q

what are the general roles of serotonin

A

Eating; regulation of sleep; libido ejaculation and orgasm; impulsive behaviour; aggression

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8
Q

what are the general roles of noradrenaline

A

Regulation of vigilance; attention; motivation and aggression

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9
Q

Describe the basic mechanism of Tricyclic antidepressants

A

TCAs inhibit there reuptake of both serotonin and noradrenaline by blockading the presynaptic uptake receptors; this action increases the concentration of both noradrenaline and serotonin in the synaptic cleft

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10
Q

Why are TCAs considered dirty drugs?

A

because they interact with several other cellular systems causes a verity of side effects

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11
Q

List five classical TCAs

A

imipramine; desipramine; clomipramine; amitriptyline; nortriptyline

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12
Q

TCAs have variation in there ability to?

A

selectively inhibit noradrenaline or serotonin transporters

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13
Q

TCAs are not ideal antidepressants due to?

A

they are long acting and are often converted to active metabolites; they have many side effects; they are easy to overdose on; the interact with many other drugs;

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14
Q

what are some common side effects of TCAs

A

Tachycardia; Dysrhythmias; tremors; hypertension; hypotension; gig disturbances; sexual dysfunction; sedation; muscarinic inhibition (dry mouth; blurred vision); occasionally mania and convulsions

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15
Q

what type of drugs can TCAs interact with

A

alcohol; anaesthetics; hypotensive drugs; and NSAIDs; MAOIs

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16
Q

TCAs can to used to treat what? (not depression)

A

neuropathic pain

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17
Q

Describe the mechanisms of SSRIs

A

Similar to TCAs but are selective for serotonin reuptake only

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18
Q

What are some common SSRIs

A

Fluoxetine; escitalopram sertraline; fluvoxamine; paroxetine; citalopram

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19
Q

other than depression what other conditions can SSRIs be used for

A

anxiety with panic attacks; OCD

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20
Q

SSRIs have several side effects what are they

A

Nausea and anorexia; diarrhea; insomnia restlessness; loss of libido failure of orgasm; overdose and drug interaction (serotonin syndrome)

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21
Q

describe the symptoms of serotonin syndrome

A

Abdominal pain; diarrhoea; sweating; changes in mental state; convulsions; renal failure; cardiovascular shock; possible death

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22
Q

describe some of clinical signs of serotonin syndrome

A

tremor (greater in the lower extremities); clonus (greater in the lower extremities); hyper-reflexia (greater in the lower extremities); increased bowel sounds; agitation; tachycardia; mydriasis; autonomic instability (hypertensive)

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23
Q

Serotonin syndrome can be caused by taking SSRIs in combination with?

A

MAOIs; TCAs; any other serotonergic agonists; procovulsive opiates; St. johns wort

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24
Q

the theory of mechanism of action of many antidepressant drugs is that they restore the levels of serotonin in the synaptic cleft; what are some of the issues with this theory?

A

Onset of anti-depressant effects often take 2-3 weeks; the fast effects are limited to increased energy levels; serotonergic agonists are not effective in depression (triptanes; buspirone); Neuroadaptive changes appear to be necessary for anti-depressant effects of SSRIs

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25
Q

List some drugs that are selective for the Noradrenaline reuptake transporter; what are there drug classes

A

Maprotiline (TCA); desipramine (TCA); reboxetine (Norepinephrine Reuptake Inhibitor); protriptyline (TCA)

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26
List some drugs which inhibit both Noradrenalin and Serotonin; what are there drug classes
Amitriptyline (TCA); Imipramine (TCA); Clomipramine (TCA)
27
List some drugs that are selective for the Serotonin Reuptake transporter; what are there drug classes
Venlafaxine (serotonin-norepinephrine reuptake inhibitor): Paroxetine (SSRI); Fluvoxamine (SSRI); Citalopram (SSRI)
28
what are some benefits of Mixed Serotonin?norepinephrine reuptake inhibitors
Generally similar to TCAs but no major receptor blocking actions resulting in fewer side effects; less of a risk of cardiac effects leading to less risk of overdose
29
List some Serotonin?norepinephrine reuptake inhibitors
Reboxetine (Noradrenaline selective); Venlafaxine (Serotonin selective); Duloxetine (mixed); Milnacipram (Mixed)
30
Other than depression what can venlafaxine and duloxetine be prescribed for?
Anxiety disorders
31
Other than depression what can duloxetine and Milnacipram be prescribed for?
neuropathic pain and fibromyalgia
32
describe the mechanism of action of reboxetine? What are peripheral side effects?
Highly selective inhibitor of the Noradrenaline uptake transporter; dizziness and insomnia
33
describe the mechanism of action of Bupropion; what are some other conditions it can be used to treat?
Inhibits both noradrenaline and dopamine (but not serotonin) but their efficacy in depression is less than that of TCAs; Nicotine dependence
34
Describe the actions of MAOIs
Inhibits the Monoamine oxidase enzyme from breaking down serotonin; melatonin; noradrenaline and adrenaline; by preventing its degradation the postsynaptic cell has more serotonin and noradrenaline for each release; additionally prevents degradation in the synaptic cleft causes an increase in concentration
35
MAO-a and -b both degrade what? What is most degraded; least?
Dopamine; tyramine; and tryptamine; all are degraded equally
36
MAO-a mainly degrades what? What is most degraded; least?
serotonin; melatonin; noradrenaline; adrenalin; in that order leading to grater increase in Serotonin than noradrenaline
37
what do MOAs prevent the degradation of what three transmitters? What neurotransmitter presence increases the most when MAOs are given?
Serotonin > Noradrenaline > Dopamine;
38
Phenelzin is a __________ binder of which MAO subtype?
Irreversible; both MAO-a and MAO-b
39
what are some side effects of Phenelzin?
Anticholinergic side effects; hypotension; insomnia; weight gain; "Cheese-reaction"
40
moclobemide is a _________ inhibitor of which MAO subtype?
Reversible competitive; MAO-a
41
what are some side effects of Moclobemide?
Nausea; insomnia; agitation
42
Other than the brain where is MAO-a located? What issues does this cause?
it is also located in the gut among other places; irreversible inhibition of MAO-b means the tyramine is not broken down in the GI tract and unaltered tyramine can readily enter the blood stream.
43
What does Tyramine cause the release of? What does this cause
Tyramine causes the realise if stirred noradrenaline; triggering a sudden and dangerous sever increase in blood pressure
44
What are some foods that people on tyramine-restricted diets need to avoid?
Cheese; yeast (vegemite); beer; chianti wine; avocados; yogurt; soy sauce; bean pods; banana skins; some medications (SSRIs)
45
What are some basic signs of the "Cheese reaction"
skin flushing and strong headaches
46
MAOs such as phenelzine are often ?
the last resort; used only after the SSRIs and TCAs have been unsuccessful
47
Mirtazapine is what class of antidepressant
Tetracyclic antidepressant
48
Approximately how long should anti-depressant be used for? And at what dose? After this time how should the drug be discontinued?
Anti-depressant in use should be continued for at least nine months at the dose which maintains normal mood; the dose should be gradually reduced over a six weeks period to avoid symptoms such as anxiety; agitation; mood swings; nausea
49
How long after a MAOI should a patient wait before eating food rich in tyramine?
Approx.. 2-3 weeks
50
St. john's wort is a very popular what? What effect does it have?
Very popular OTC ant depressive medication with people holding strong beliefs in natural medicine; it has a very strong placebo effect but Hyperforin; a constituent of the extract has been shown to inhibit the uptake of serotonin
51
Prophylaxis with lithium salts is effective against what?
it is effective against manic and depressive phases
52
What are some basic benefits of therapy with lithium salts?
Reduces manic and depressive episodes; reduction of suicide attempts; no psychotropic effect in healthy people; there are many side effects but none are really severe
53
What are some of the side effects of lithium salts
Lethargy; muscle weakness; oedema; slow weight gain
54
at the most basic level what do anti-depressants do? What are the three main ways they can they accomplish this
Antidepressants increase synaptic transmitters levels; mainly by blocking presynaptic Alpha2 receptors OR inhibiting Monoamine oxidase OR by inhibiting Transmitter re-uptake
55
What are some drugs that block Presynaptic alpha2 receptors?
Tetracyclic antidepressant
56
what are the two types of antidepressants which act on Monoamine oxidase?
Reversible inhibitors of MAO; Non-selective MAOIs
57
What are the four types of antidepressants which act by inhibiting transmitter reuptake?
Selective noradrenaline reuptake inhibitors; Tricyclic antidepressants; selective Serotonin reuptake inhibitors; Serotonin and noradrenaline reuptake inhibitors
58
describe the interrelationship between anxiety and depression?
Chronic stress and anxiety are strongly associated with depression; theses disorders appear to result from the stresses of life as well as an individual's coping mechanisms and genetic predisposition; This suggests that there may be common Neuroadaptive pathology with theses disorders; therefore some of the some medication are sued in the treatment of both anxiety and depression
59
What are the three main treatments for anxiety historically? What is the common pathway for them?
Alcohol; Barbiturates; opium; all of these drugs generally "slow down" the nervous system; leading to drowsiness; impaired memory: tolerance; physical dependence
60
on the GABA-alpha what does the binding of GABA do? How does this affect the passage of what ion?
Binding of GABA alters the shape of the central pore through the middle of the GABA-0alpha receptor complexes; this allows Cl ions to pass down there concentration gradient into the neuronal cytoplasm
61
What ion does the GABA-alpha receptor admit? Which way does the ion flow? What does this effect?
CL-; into the cell; the influx of Cl- ions increases the negative membrane potential of the postsynaptic neuron and essentially makes it less likely to fire an action potential
62
If GABA-alpha receptors activity is increased generally what will this lead to
if GABA-alpha receptor activity is increased it is less likely that neurons will fire and an action potential resulting in decreased neuronal activity and a sense of calm
63
what are some drug classes that activate The GABA-alpha receptor?
Benzodiazepines; z-drugs; ethanol; barbiturates
64
Benzodiazepines do not directly do what? Instead they?
Benzodiazepines do not have ANY effect on the GABA-alpha receptor themselves; but they allosterically enhance the affinity of the receptor for GABA; this causes the chloride channel to open more frequently resulting in larger hyperpolarisations of adult neurons
65
What are some of the effects of benzodiazepines?
Induction of sleep and sedation; reduction of anxiety and aggression; reduction of muscle tone and coordination; anticonvulsant effects; anterograde amnesia
66
what are the two main hypnotic drugs classes? What are some drugs in those classes
Z-drugs; zolpidem; zopiclone; Benzodiazepines; lorazepam; Temazepam
67
What are some general pitfalls with drugs acting on the BZD site?
chronic use may cause withdrawal symptoms hypnotic drugs should be tapered off slowly over time; Never mix with alcohol; hypnotic drugs can cause anterograde amnesia this can lead to double dosing
68
generally what are some of the benefits of using BDZs over barbiturates?
BDZs have less toxicity; less physical dependence; less tolerance than barbiturates if used for 2-4 weeks; BDZs do not produce the life threatening respiratory depression on there own even if taken in large amounts
69
Chronic use of BDZs leads to issues with?
Tolerance and dependence
70
The innervation of the parasympathetic nervous system from the limb structures is thought to mediate what?
The visceral symptoms associated with anxiety
71
The Dorsal motor nucleus of the valgus is associated with
Fear induced parasympathetic nervous system activation
72
The Lateral Hypothalamus is associated with?
Fear induced sympathetic nervous system activation
73
the Serotonin 1-alpha receptor is found where? What kind of receptor is it? What does there activation lead to?
5-HT 1-alpha receptors are found in the cortex and amygdala; these receptors are auto-inhibitory; their activation causes a decrease in release of serotonin
74
Buspirone is a potent partial agonist of? It is an effective treatment for?
5-ht 1-alpha; it is effective in Generalised anxiety disorder
75
Describe the what and how activation of 5-HT 1-alpha receptor does
The inhibitory g-protein alpha subunit of the 5-HT1-alpha receptor binds to and inhibits adenylate cyclase; this prevents the conversion of ATP to cAMP; this inhibits the cell depolarization and release of 5-HT;
76
when do anxiolytic effects occur when starting buspirone?
Anxiolytic effects occur after weeks
77
Why is there a delay of anxiolytic effects when starting buspirone?
One theory of how buspirone and SSRIs produce their delayed anxiolytic effects is that over time they induce desensitisation of somatodendritic 5HT 1-alpha auto-receptors resulting in heightened excitation of serotonergic synapses
78
Buspirone is an effective _________ but not ___________
Buspirone is an effective anxiolytic but not anti-depressant
79
What are some advantages of buspirone?
Minimal risks of dependence and withdrawal; not a muscle relaxant; not sedative; not anticonvulsant
80
what are the major Anxiolytics? What is there mechanism of action? What are they used for?
Benzodiazepines (Diazepam; alprazolam) :-: Act on the GABA Receptor :-: Short term treatment of anxiety;;;Buspirone :-: acts on serotonin receptor :-: May be effective in GAD
81
what are the major Autonomic suppression? What is there mechanism of action? What are they used for?
Propranolol :-: Acts by inhibiting beta adrenoceptors:-: useful for some social/performance anxiety disorders
82
Imipramine has some positive effects in what disorder? What is the catch with this treatment?
Panic disorders; need a higher does than used in treating depression
83
Other than depression MAOIS can be used to treat what conditions?
PTSD; Agoraphobia; Panic disorder; social phobia
84
what is considered the best pharmacological treatment for OCD?
SSRIs such as fluoxetine and the TCA clomipramine; although they are need at higher doses and over 1-3 months for the effects to be seen
85
Why do we have overlap in the treatment of depression and anxiety disorders?
Often patients have a mixed profile of depression and anxiety; their drug regiments address both
86
What is the most effective treatment for anxiety?
Combining medication and therapy
87
why Cognitive-Behavioural Therapy is very useful in treating anxiety disorders?
The cognitive part helps people change the thinking patterns that support their fears; the behavioural part helps people change the way they react to anxiety-provoking situations
88
In Anxiety disorder we have a shift in what? What does this result in? how can we counter this?
In anxiety disorder we have a shift in the balance of the CNS and Neurotransmitters resulting in over excitation; to counter this effect we need to decrease or slow the neuronal and synaptic activity of the nervous systems.
89
what are some indication for GABA alpha receptor enhancing drugs?
Insomnia anxiety seizures muscle spasms;
90
ethanol enhances what receptor activity?
GABA-alpha

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