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Pathophysiology - Midterm > Lecture 5: Depression & Anxiety > Flashcards

Lecture 5: Depression & Anxiety Flashcards

1
Q

What is wellness based on?

A

The integrated and coordinated function of many neurotransmitter systems

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2
Q

What is the broad definition of a disorder?

A

Imbalance impairing function and quality of life

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3
Q

What are psychiatric disorders?

A

CNS diseases characterized by disturbances in emotion, cognition, motivation, and socialization

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4
Q

True or false: psychiatric disorders are homogeneous syndromes, meaning they are the same in every case

A

False, they are heterogeneous syndromes, meaning they are different in every case/patient

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5
Q

How are psychiatric disorders diagnosed?

A

Clinical observations and criteria

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6
Q

How often do anxiety and sleep disorders co-occur?

A

Very often

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7
Q

What kind of neural flow is found in sleep disorders?

A

Stimulating more than calming

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8
Q

What are characteristics of NORMAL anxiety?

A

Adaptive and temporary

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9
Q

What are characteristics of EXCESSIVE anxiety?

A

Persistent, severe, and impairs function

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10
Q

What is anxiety good for?

A

Preparing for/reacting to environmental changes

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11
Q

What is the diagnostic criteria for generalized anxiety disorder (GAD)?

A

1) Excessive anxiety and worry, occurring more-days-than-not for at least 6 months, about a number of issues
2) Patient finds it difficult to control the worry
3) Exhibits 3 of the symptoms: restlessness, easily fatigued, difficulty concentrating, irritability, muscle tension, or sleep disturbance

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12
Q

What are the stages of a sleep cycle?

A

Stage 1, 2, 3, 4, and REM

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13
Q

What is delta sleep?

A

The most restorative sleep; difficult to arouse; muscle atonia

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14
Q

How many sleep cycles does a typical person go through each night?

A

4-6

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15
Q

Where does the circadian rhythm come from?

A

Suprachiasmic nucleus

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16
Q

What is the target of the majority of sleep medications?

A

Alter sleep cycles

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17
Q

What triggers non-REM sleep?

A

Primary serotonergic tracts in medulla and dorsal raphe nucleus

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18
Q

What enables REM sleep?

A

Cholinergic tracts

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19
Q

What turns off REM sleep?

A

Noradrenergic areas

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20
Q

What 6 hormones produce an “alerting” effect?

A

1) Dopamine
2) Norepinephrine
3) Acetylcholine
4) Histamine
5) Substance P
6) CRH (cortisol)

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21
Q

What 4 factors can cause insomnia?

A

Situational, medical, psychiatric, or pharmacological factors

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22
Q

What are the common problems in sleep disorders?

A
  • Difficulty falling asleep
  • Difficulty maintaining sleep
  • Non-restorative sleep
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23
Q

What is the ideal treatment for sleep disorders?

A

Improvement without medication

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24
Q

What are some situational causes of insomnia?

A

Stressors, jet lag, shift work

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25
Q

What are some medical causes of insomnia?

A

Cardiovascular, respiratory, pain, endocrine, GI, neurologic, pregnancy

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26
Q

What are some psychological causes of insomnia?

A

All disorders including substance abuse

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27
Q

What are some pharmacological causes of insomnia?

A

Anticonvulsants, adrenergic blockers, diuretics, SSRI, seriods, stimulants

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28
Q

What 4 conditions are all linked?

A

Anxiety, sleep disorders, chronic pain, and depression

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29
Q

What are 3 treatment targets in insomnia?

A

1) Address reversible causes and utilize sleep hygiene techniques
2) Enhance GABA and serotonin
3) Inhibit histamine, ACh, NE, dopamine, substance P and cortisol

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30
Q

What are 2 medications that are GABA agonists?

A

Benzodiazepines and zopiclone

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31
Q

What other medications besides GABA agonists can be used in the treatment of insomnia?

A

Antihistamines, antidepressants, and melatonin or related agonists

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32
Q

What types of drugs can cause anxiety?

A

Antidepressants, bronchodilators, steroids, herbals, thyroid, and stimulants

33
Q

Withdrawal from ____ can cause anxiety

A

Sedatives

34
Q

Describe the noradrenergic model of anxiety

A

ANS is overactive causing excessive NE and glutamate

35
Q

Describe the GABA model of anxiety

A

Increased GABA can favourable impact 5HT, NE, and dopamine

36
Q

Describe the serotonin model of anxiety

A

Increasing 5HT causes decreased LC firing and NE “excess”, which causes decreased overstimulation

37
Q

What is the main goal of anxiety treatment?

A

Define condition and focus on reduction of reversible factors, as well as decrease duration and severity of symptoms to improve overall functioning

38
Q

What are some physical symptoms of anxiety?

A

Restlessness, fatigue, muscle tension, sleep disturbance, and irritability

39
Q

What type of treatment do physical symptoms of anxiety respond quickly to?

A

GABAa agonists

40
Q

What type of treatment has better long-term effects for physical symptoms of anxiety, but what is the drawback to them?

A
  • Antidepressants

- Can increase physical symptoms at first and benefits take time

41
Q

What is a disadvantage to benzodiazepines in anxiety?

A

Have a dependence liability because of fast onset and rapid elimination

42
Q

What are cognitive symptoms of anxiety?

A

Worries hard to control, on edge, poor concentration

43
Q

What can cause quick easing of cognitive symptoms of anxiety?

A

Benzodiazepines

44
Q

What is the treatment of choice for chronic anxiety symptoms?

A

Antidepressants

45
Q

What non-pharm treatments are essential for optimal management of anxiety disorders?

A

Psychoeducation, psychotherapy, meditation, and exercise

46
Q

What are properties of benzodiazepines?

A

Muscle relaxant, anxiolytic, sedative, and anticonvulsant

47
Q

What is the main function of benzodiazepines?

A

GABA agonist (decreases CNS excitability by increasing GABA)

48
Q

What does the onset speed of benzodiazepines correlate with?

A

Lipid solubility

49
Q

What does a longer half-life mean?

A

Slower drug elimination and longer “hangover” effect

50
Q

What does a shorter half-life mean?

A

Fast drug elimination and increased rebound symptoms, leading to a risk of dependency

51
Q

What types of benzodiazepines have a short half-life?

A

Lorazepam and alprazolam

52
Q

What is the role of pharmacists in sleep and anxiety disorders?

A

1) Educate about non-drug strategies
2) Educate about importance of thorough assessment and appropriate pharmacologic strategies
3) Educate about appropriate time-frames
4) Promote adherence

53
Q

What does a major depressive episode cause?

A

Significant distress or dysfunction

54
Q

What does NOT cause major depressive episodes?

A

Medication, mental illness, drug of abuse, or bereavement

55
Q

What must be included in a major depressive episode?

A

Depressed mood and anhedonia (lack of pleasure in otherwise pleasurable activities) and must include 5 symptoms consistently in a 2 week period

56
Q

What are the symptoms of a major depressive episode?

A

Depressed most of the day; anhedonia; weight loss; sleep disturbance; psychomotor changes; fatigue; feelings of worthlessness; inability to concentrate; suicidal thoughts

57
Q

What is noticed in the neuropathology of anxiety disorders?

A
  • Small decrease in hippocampal size
  • Increased activation of amygdala (centre for emotions and motivation) by negative stimuli
  • Decreased activation of nucleus accumbens by rewarding stimuli
58
Q

How is depression diagnosed?

A

Validated questionnaires or scales to screen for and measure severity

59
Q

What must be included in a medical workup for depression?

A

Thyroid function

60
Q

What is the function of St. John’s Wort for depression?

A

Impacts many neurotransmitters

61
Q

What is St. John’s Wort effective for?

A

Mild to moderate depression

62
Q

What is a disadvantage to St. John’s Wort?

A

Potential for interacting with prescription medications

63
Q

What are 10 potential sites for drug action?

A

Action potentials in presynaptic fiber; synthesis of neurotransmitter; storage; metabolism; release; reuptake into nerve ending or uptake into glial cell; degradation; receptor for the transmitter; receptor-induced increase or decrease in ionic conductance; retrograde signalling

64
Q

What is the most common site of drug action in antidepressants?

A

Reuptake into nerve ending or uptake into glial cell

65
Q

What does more storage mean?

A

More release

66
Q

What does less metabolism mean?

A

More neurotransmitter

67
Q

What does more release mean?

A

More signalling

68
Q

What is degradation used for?

A

Treatment resistant patients because it has a number of side effects

69
Q

How can you minimize side effects of an antidepressant?

A

Start with a low dose and work up

70
Q

True or false: antidepressants cause addiction or dependency

A

False

71
Q

What is needed for full and optimal benefits of antidepressants?

A

Long-term administration

72
Q

What is serotonin involved in regulating?

A

Impulsivity, anxiety, irritability, sex, appetite, aggression, mood, emotion, and cognitive function

73
Q

What is norepinephrine involved in regulating?

A

Energy, interest, motivation, anxiety, irritability, mood, emotion, and cognitive function

74
Q

What is dopamine involved in regulating?

A

Drive, motivation, sex, appetite, agression, mood, emotion, and cognitive function

75
Q

What are markers of poor outcomes of depression?

A

More severe presentation, longer time untreated, number of episodes, and frequency of relapse

76
Q

What are factors that are consistent with better outcomes in patients with depression?

A

Access to supports, adherence to treatment, a history of “more rapid” response, and lower life stressors

77
Q

Is adherence or compliance more important?

A

Adherence

78
Q

What are 4 factors that impact our “psychiatric immune system”?

A

1) Psycho-social elements like feeling connected, valued, supported, threatened, and vulnerable
2) Life events and stressors
3) Socio-economic factors
4) Overall physical and mental health

Pathophysiology - Midterm (11 decks)

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