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PHAR 358 - Therapeutics (Dr. K. Halpape) > Anxiety > Flashcards

Anxiety Flashcards

1
Q

What brain circuit regulates the fear response?

A

Amygdala-Centered Circuit

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2
Q

What brain circuit regulates the worry response?

A

Cortico-Striato-Thalamo-Cortical Circuit

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3
Q

If the amygdala senses a fear response is needed, where does it mobilize signals towards?

A

Prefrontal Cortex

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4
Q

Which brain structure initiates “fight or flight” or “freeze” motor responses?

A

Periaqueductal Gray

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5
Q

The Amygdala targets the ________ nucleus to increase RR during fear responses.

A

parabrachial

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6
Q

What are some of the long term repercussions of poorly managed anxiety?

A

-Increased atherosclerosis

-Increased cardiac ischemia

-Increased BP

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7
Q

Which neurotransmitter (unique to the worry response) influences experienced symptoms?

A

Dopamine… Others are the same across both fear & worry response pathways (ie. Serotonin, NE, GABA, Glutamate, Voltage-Gated Ca2+ Channels).

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8
Q

T or F: Gabapentin & Pregabalin work on the GABA pathway.

A

FALSE… Act upon voltage-gated Ca2+ channels.

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9
Q

What types of Voltage-Sensitive Calcium Channels (VSCCs) do Gabapentin & Pregabalin act upon? What subunits do they bind to?

A

N, P, Q
A2 Delta

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10
Q

What Serotonin receptor does Buspirone agonize?

A

5-HT1A

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11
Q

What is the only condition in which Buspirone shows effectiveness in?

A

Generalized Anxiety Disorder

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12
Q

T or F: SNRI initiation can actually worsen the fear / worry response of patients who struggle with anxiety.

A

True… LTU we see downregulation of B1 receptors & improved response, but initial NE activity increases can worsen anxiety.

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13
Q

Prazosin manages hyperarousal / nightmarish symptoms by blocking what receptor?

A

Alpha 1

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14
Q

Which class of medications should be avoided in the treatment of PTSD?

A

Benzos

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15
Q

In what situations should Bupropion use be avoided?

A

-Seizure Hx
-Head Trauma
-Eating Disorders
-Electrolyte Disturbances

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16
Q

Is Bupropion more sedating or activating?

A

Activating

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17
Q

Is Buspirone’s OOA fast or slow?

A

Slow (can take up to 2wks or even longer to see a response)

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18
Q

When should Buspirone use be avoided in the treatment of anxiety-related conditions?

A

Comorbid Depression

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19
Q

In comparison to other SSRIs, does Duloxetine cause more or less insomnia & agitation?

A

More

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20
Q

When should Duloxetine use be avoided?

A

-Liver Dx
-Heavy EtOH use

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21
Q

Mirtazapine & Hydroxyzine are useful in treating anxious patients with comorbid ______.

A

insomnia

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22
Q

Is Paroxetine more or less sedating compared to other SSRIs?

A

More

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23
Q

Paroxetine has been demonstrated to cause what prenatal defect?

A

Cardiac Septal Defects

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24
Q

What other unique side effect (compared to other SSRIs) does Paroxetine demonstrate?

A

Greater Wt Gain

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25
Q

For anxious patients with concerns about sexual dysfunction, what AD agents can be used?

A

Desvenlafaxine
Bupropion
Mirtazapine
Vortioxetine

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26
Q

Does Generalized Anxiety Disorder (GAD) affect men or women more?

A

Women (2:1)… However, very likely that stats are underreported.

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27
Q

Provide some examples of medications that can bring upon symptoms of anxiety.

A

Bupropion
Prednisone
Ecstasy
Marijuana
Ma Huang
Ginseng
Ephedra
Pseudoephedrine
Phenylephrine
Levothyroxine

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28
Q

What are the more common symptoms associated with GAD?

A

Racing Thoughts
Dizzy / Disoriented
Excessive Sweating
Trembling / Shaking
Irritable
Sleep Disturbances

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29
Q

What screening tool can we use in the pharmacy for those whom we suspect have GAD?

A

GAD-7

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30
Q

A score of >/= ____ on the GAD-7 indicates that a patient may have GAD & requires further evaluation by a psychiatrist.

A

10

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31
Q

What are good non-pharmacological interventions that can be used in treating somebody with GAD?

A

-Reduce substance use (ie. Caffeine, Alc, Nic)

-Routine Exercise

-CBT / Psychotherapy

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32
Q

What are the first line treatment options for GAD?

A

SSRIs: Escitalopram, Sertraline, Paroxetine

SNRIs: Duloxetine, Venlafaxine

VSCC: Pregabalin

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33
Q

What are the 2nd line options for treating GAD?

A

BZDs: Alprazolam, Lorazepam, Diazepam (short-term)

SNRI: Bupropion

5-HT1A: Buspirone

H1A: Hydroxyzine

34
Q

What is considered to be an adequate trial for a therapy in treatment of GAD?

A

8-12wks

35
Q

What is the MOA of Benzos?

A

Bind Benzo Receptor on GABAa neuron, increases frequency of Cl- channel opening, hyperpolarized state of neuron = less excitable.

36
Q

Although no RCTs assessing Clonazepam use in GAD are published, what benefits might it have over other Benzos in practice?

A

Longer t1/2, so effects are maintained within the entire dosing window & avoid peaks / troughs in concentrations seen with other shorter acting Benzos.

37
Q

What are the short-acting Benzos? Long-acting?

A

SA: Alprazolam, Lorazepam

LA: Clonazepam, Diazepam

38
Q

Side effects of Benzos?

A

-Dizzy / Drowsy
-Ataxia
-Paradoxical (kids)
-Memory Impairment
-Worsening Depression

39
Q

What some factors that increase the dependency risk of Benzos?

A

-LTU & increasing dose
-Hx SUD
-Hx Personality Disorders

40
Q

Withdrawal Benzo symptoms can occur following discontinuation within as little as ____ week(s).

A

one week

41
Q

What Benzos are preferred in those whom are either elderly or have liver dysfunction?

A

LOT

L - Lorazepam
O - Oxazepam
T - Temazepam

42
Q

What are the signs of somebody going through Benzo withdrawal?

A

-Seizures (within 1-2d stop)
-Sweats
-Tremors
-N / V
-Rebound Anxiety
-Tachycardia
-Insomnia / Agitation
-Hallucinations

43
Q

What percentage of patients experience Benzo withdrawals if their therapy is stopped suddenly within 8wks of starting?

A

30% (hence why tapering is very important)

44
Q

Which Benzo is favored in situations where a taper is needed?

A

Diazepam (decrease 10-20% q1-2wks)

45
Q

What patient demographics would we caution against using Benzos?

A

Sleep Apnea / COPD (increased risk of respiratory drive depression)

Opioid Users (same as above)

Old (fall risk)

Pregnancy (multiple risk factors & teratogenic)

46
Q

Name of Benzo antidote using in the emergency department?

A

Flumazenil

47
Q

What are some of the clinical presentations of a ‘panic attack’?

A

-Abdom / Chest Pains
-Chills
-Dizzy
-Choking Feeling
-Palpitations
-Nauseous
-SOB
-Sweating
-Increase HR
-Trembles / Shakes

48
Q

What is the likelihood of a patient with Panic Disorder achieving remission?

A

1/3 (most require LT treatments, but possible someone can go into remission without therapies).

49
Q

A score of </= ___ on the Panic Disorder Severity Scale (PDSS) indicates a patient may have achieved remission.

A

3

50
Q

1st line options for Panic Disorder?

A

SSRIs: Citalopram, Escitalopram, Fluoxetine, Paroxetine, Sertraline

SNRIs: Duloxetine, Venlafaxine

51
Q

2nd line options for Panic Disorder?

A

TCAs: Clomipramine, Imipramine

Augmented Benzos: Alprazolam, Clonazepam

52
Q

3rd line option for Panic Disorder?

A

Phenelzine (if no response to anything else)

53
Q

T or F: Benzos are effective in the treatment of acute panic attacks.

A

FALSE… OOA of the drugs are often too slow (kick in after the panic attack has passed).

54
Q

What is a suitable timeframe for tapering maintenance therapies used in Panic Disorder?

A

4 - 6mths (greatly reduces risk of relapse)

55
Q

What percentage of patients with Social Anxiety Disorder (SAD) seek treatment, and after what length of time would they consider seeking out treatment?

A

~50%; 15 - 20yrs of living with symptoms

56
Q

What are some proposed dysregulated neurotransmitter theories for why people experience SAD?

A

Dopamine - Reduced D2 receptor binding, lower levels

Serotonin - Hypersensitive 5HT2 receptors

57
Q

___ - ___ % of patients with SAD have a history of concurrent anxiety, depression, and SUD.

A

70 - 80%

58
Q

How does Generalized SAD differ from Non-Generalized SAD?

A

Generalized: Fear & avoidance of wide range of social situations

Non-Generalized: Fear limited to one or two situations

59
Q

CBT treatment for those with SAD should be initiated for at least what length of time?

A

12wks

60
Q

In addition to CBT / SSRIs / SNRIs, what other pharmacological therapy is considered 1st line in treating SAD?

A

Pregabalin

61
Q

What other unique agents can be used for performance-induced SAD situations?

A

Atenolol, Propranolol (as they can help to reduce tremors, palpitations, blushing)

62
Q

Are Canadian men or women more commonly affected by PTSD?

A

Women

63
Q

What types of traumatic events show the highest rates of PTSD prevalence?

A

Childhood Trauma / Rapes

64
Q

What are the strongest predictors of PTSD?

A

1) Lack of Social Support following exposure to trauma

2) Life Stressors following exposure to trauma

3) Severity of the trauma itself

65
Q

Describe what happens in various brain regions (ie. PFC, LC, Amygdala) during a PTSD stressor response.

A

Amygdala - Activate catecholamines, target Periaqueductal Gray to induce “freezing” response.

Locus Coeruleus - Tonic firing increases, which strengthens memory consolidation.

Prefrontal Cortex - Weakened response in presence of high NE levels (leading to less regulation of behavior & emotions).

66
Q

What is the PTSD triad?

A

1) Re-experience of the event

2) Avoidance of stimuli that invite memories or experiences of the trauma

3) Increased arousal

67
Q

1st line PTSD drugs?

A

SSRIs: Fluoxetine, Paroxetine, Sertraline

SNRI: Venlafaxine

Prazosin (trauma-related nightmares & sleep improvements)

68
Q

Which drugs would NOT be recommended for treating PTSD?

A

Benzos (no evidence, worsens severity of PTSD, increased risk of developing PTSD if used shortly after trauma, development of SUD / aggression / depression).

69
Q

PTSD treatment timelines (OOR, max response, duration)?

A

OOR: 2-8wks
Max Response: 12wks
Duration: 12-24mths

70
Q

What are some of the theorized pathologies underlining OCD?

A

-Serotonin Neurotransmission

-Dopamine Transmission (espec. comorbid tics & Tourette’s)

-Glutamate

71
Q

What are some known / suspected OCD causes?

A

PANDAS (Peds Autoimmune Neuropsychiatric Disorder Assoc. with Strep Infections)

Pregnancy

Temperamental

Environmental (abuse, trauma)

72
Q

In what percentage of OCD patients do suicidal thoughts occur at some point?

A

50% (attempts in 25%)

73
Q

Who is more likely to have comorbidities associated with OCD: Males or Females?

A

Males

74
Q

In kids, a comorbid triad of OCD, __ ______, and ____ is often seen.

A

Tic Disorder; ADHD

75
Q

What other disorders are more often seen in OCD patients?

A

Body Dysmorphia
Skin Picking
Hair Plucking

76
Q

What is the 1st line treatment strategy for OCD?

A

SSRIs: Escitalopram, Fluoxetine, Paroxetine, Sertraline

SNRI: Venlafaxine

CBT (or combo of both)

77
Q

What is an appropriate length of time to have considered CBT an ‘adequate trial’ in managing OCD? SSRI?

A

CBT: 13 OW sessions
SSRI: 12wks

78
Q

What pharmacotherapy is recommended in OCD treatment upon failure of two different SSRIs?

A

Clomipramine (TCA)

79
Q

T or F: CBT has a stronger effect on OCD “obsessions” than it does on “compulsions”.

A

False… Stronger effect on compulsions.

80
Q

The underlying dopamine effects of what two drugs gives them more of an adjunctive role in treating OCD than other mental health disorders?

A

Aripiprazole, Risperidone

81
Q

Timeframes for OCD (OOR, Max Response, Duration)?

A

OOR: 2-4wks
Max Response: 10-12wks
Duration: 1-2yrs

PHAR 358 - Therapeutics (Dr. K. Halpape) (8 decks)

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