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Mental Health > Pham of Depression and Anxiety > Flashcards

Pham of Depression and Anxiety Flashcards

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
Q

List some drugs which inhibit both Noradrenalin and Serotonin; what are there drug classes

A

Amitriptyline (TCA); Imipramine (TCA); Clomipramine (TCA)

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27
Q

List some drugs that are selective for the Serotonin Reuptake transporter; what are there drug classes

A

Venlafaxine (serotonin-norepinephrine reuptake inhibitor): Paroxetine (SSRI); Fluvoxamine (SSRI); Citalopram (SSRI)

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28
Q

what are some benefits of Mixed Serotonin?norepinephrine reuptake inhibitors

A

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

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29
Q

List some Serotonin?norepinephrine reuptake inhibitors

A

Reboxetine (Noradrenaline selective); Venlafaxine (Serotonin selective); Duloxetine (mixed); Milnacipram (Mixed)

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30
Q

Other than depression what can venlafaxine and duloxetine be prescribed for?

A

Anxiety disorders

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31
Q

Other than depression what can duloxetine and Milnacipram be prescribed for?

A

neuropathic pain and fibromyalgia

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32
Q

describe the mechanism of action of reboxetine? What are peripheral side effects?

A

Highly selective inhibitor of the Noradrenaline uptake transporter; dizziness and insomnia

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33
Q

describe the mechanism of action of Bupropion; what are some other conditions it can be used to treat?

A

Inhibits both noradrenaline and dopamine (but not serotonin) but their efficacy in depression is less than that of TCAs; Nicotine dependence

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34
Q

Describe the actions of MAOIs

A

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

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35
Q

MAO-a and -b both degrade what? What is most degraded; least?

A

Dopamine; tyramine; and tryptamine; all are degraded equally

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36
Q

MAO-a mainly degrades what? What is most degraded; least?

A

serotonin; melatonin; noradrenaline; adrenalin; in that order leading to grater increase in Serotonin than noradrenaline

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37
Q

what do MOAs prevent the degradation of what three transmitters? What neurotransmitter presence increases the most when MAOs are given?

A

Serotonin > Noradrenaline > Dopamine;

38
Q

Phenelzin is a __________ binder of which MAO subtype?

A

Irreversible; both MAO-a and MAO-b

39
Q

what are some side effects of Phenelzin?

A

Anticholinergic side effects; hypotension; insomnia; weight gain; “Cheese-reaction”

40
Q

moclobemide is a _________ inhibitor of which MAO subtype?

A

Reversible competitive; MAO-a

41
Q

what are some side effects of Moclobemide?

A

Nausea; insomnia; agitation

42
Q

Other than the brain where is MAO-a located? What issues does this cause?

A

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
Q

What does Tyramine cause the release of? What does this cause

A

Tyramine causes the realise if stirred noradrenaline; triggering a sudden and dangerous sever increase in blood pressure

44
Q

What are some foods that people on tyramine-restricted diets need to avoid?

A

Cheese; yeast (vegemite); beer; chianti wine; avocados; yogurt; soy sauce; bean pods; banana skins; some medications (SSRIs)

45
Q

What are some basic signs of the “Cheese reaction”

A

skin flushing and strong headaches

46
Q

MAOs such as phenelzine are often ?

A

the last resort; used only after the SSRIs and TCAs have been unsuccessful

47
Q

Mirtazapine is what class of antidepressant

A

Tetracyclic antidepressant

48
Q

Approximately how long should anti-depressant be used for? And at what dose? After this time how should the drug be discontinued?

A

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
Q

How long after a MAOI should a patient wait before eating food rich in tyramine?

A

Approx.. 2-3 weeks

50
Q

St. john’s wort is a very popular what? What effect does it have?

A

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
Q

Prophylaxis with lithium salts is effective against what?

A

it is effective against manic and depressive phases

52
Q

What are some basic benefits of therapy with lithium salts?

A

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
Q

What are some of the side effects of lithium salts

A

Lethargy; muscle weakness; oedema; slow weight gain

54
Q

at the most basic level what do anti-depressants do? What are the three main ways they can they accomplish this

A

Antidepressants increase synaptic transmitters levels; mainly by blocking presynaptic Alpha2 receptors OR inhibiting Monoamine oxidase OR by inhibiting Transmitter re-uptake

55
Q

What are some drugs that block Presynaptic alpha2 receptors?

A

Tetracyclic antidepressant

56
Q

what are the two types of antidepressants which act on Monoamine oxidase?

A

Reversible inhibitors of MAO; Non-selective MAOIs

57
Q

What are the four types of antidepressants which act by inhibiting transmitter reuptake?

A

Selective noradrenaline reuptake inhibitors; Tricyclic antidepressants; selective Serotonin reuptake inhibitors; Serotonin and noradrenaline reuptake inhibitors

58
Q

describe the interrelationship between anxiety and depression?

A

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
Q

What are the three main treatments for anxiety historically? What is the common pathway for them?

A

Alcohol; Barbiturates; opium; all of these drugs generally “slow down” the nervous system; leading to drowsiness; impaired memory: tolerance; physical dependence

60
Q

on the GABA-alpha what does the binding of GABA do? How does this affect the passage of what ion?

A

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
Q

What ion does the GABA-alpha receptor admit? Which way does the ion flow? What does this effect?

A

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
Q

If GABA-alpha receptors activity is increased generally what will this lead to

A

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
Q

what are some drug classes that activate The GABA-alpha receptor?

A

Benzodiazepines; z-drugs; ethanol; barbiturates

64
Q

Benzodiazepines do not directly do what? Instead they?

A

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
Q

What are some of the effects of benzodiazepines?

A

Induction of sleep and sedation; reduction of anxiety and aggression; reduction of muscle tone and coordination; anticonvulsant effects; anterograde amnesia

66
Q

what are the two main hypnotic drugs classes? What are some drugs in those classes

A

Z-drugs; zolpidem; zopiclone; Benzodiazepines; lorazepam; Temazepam

67
Q

What are some general pitfalls with drugs acting on the BZD site?

A

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
Q

generally what are some of the benefits of using BDZs over barbiturates?

A

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
Q

Chronic use of BDZs leads to issues with?

A

Tolerance and dependence

70
Q

The innervation of the parasympathetic nervous system from the limb structures is thought to mediate what?

A

The visceral symptoms associated with anxiety

71
Q

The Dorsal motor nucleus of the valgus is associated with

A

Fear induced parasympathetic nervous system activation

72
Q

The Lateral Hypothalamus is associated with?

A

Fear induced sympathetic nervous system activation

73
Q

the Serotonin 1-alpha receptor is found where? What kind of receptor is it? What does there activation lead to?

A

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
Q

Buspirone is a potent partial agonist of? It is an effective treatment for?

A

5-ht 1-alpha; it is effective in Generalised anxiety disorder

75
Q

Describe the what and how activation of 5-HT 1-alpha receptor does

A

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
Q

when do anxiolytic effects occur when starting buspirone?

A

Anxiolytic effects occur after weeks

77
Q

Why is there a delay of anxiolytic effects when starting buspirone?

A

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
Q

Buspirone is an effective _________ but not ___________

A

Buspirone is an effective anxiolytic but not anti-depressant

79
Q

What are some advantages of buspirone?

A

Minimal risks of dependence and withdrawal; not a muscle relaxant; not sedative; not anticonvulsant

80
Q

what are the major Anxiolytics? What is there mechanism of action? What are they used for?

A

Benzodiazepines (Diazepam; alprazolam) :-: Act on the GABA Receptor :-: Short term treatment of anxiety;;;Buspirone :-: acts on serotonin receptor :-: May be effective in GAD

81
Q

what are the major Autonomic suppression? What is there mechanism of action? What are they used for?

A

Propranolol :-: Acts by inhibiting beta adrenoceptors:-: useful for some social/performance anxiety disorders

82
Q

Imipramine has some positive effects in what disorder? What is the catch with this treatment?

A

Panic disorders; need a higher does than used in treating depression

83
Q

Other than depression MAOIS can be used to treat what conditions?

A

PTSD; Agoraphobia; Panic disorder; social phobia

84
Q

what is considered the best pharmacological treatment for OCD?

A

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
Q

Why do we have overlap in the treatment of depression and anxiety disorders?

A

Often patients have a mixed profile of depression and anxiety; their drug regiments address both

86
Q

What is the most effective treatment for anxiety?

A

Combining medication and therapy

87
Q

why Cognitive-Behavioural Therapy is very useful in treating anxiety disorders?

A

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
Q

In Anxiety disorder we have a shift in what? What does this result in? how can we counter this?

A

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
Q

what are some indication for GABA alpha receptor enhancing drugs?

A

Insomnia anxiety seizures muscle spasms;

90
Q

ethanol enhances what receptor activity?

A

GABA-alpha

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