Anxiety Disorders Flashcards

(38 cards)

1
Q

List the components of the current understanding of the biological basis of anxiety and anxiety disorders

A

Neuroanatomy: hippocampus, amygdala, PFC
NT’s
Hypothalamic-Pituitary-Adrenal Axis (HPA)
Anxious temperament

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2
Q

Explain the current understanding of the biological basis of anxiety and anxiety disorders based on neuroanatomy

A
Hippocampus 
•	In temporal lobe
•	Involved in memory and learning
•	Sensors for cortisol
•	May become dysregulated in anxiety and depression 

Amygdala
• Processes sensory info
• Role in negative emotions = fear and learning new fear associations
• Activation → activates HPA → autonomic and behavioral responses
• Responses = innate (evolutionarily conserved); selective (genetically determined)

PFC
• Inhibits amygdala → regulates expression of fear
• Helps “unlearn” fear associations

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3
Q

Explain the current understanding of the biological basis of anxiety and anxiety disorders based on neurotransmitters

A

o Glutamate = excitatory; GAGA = inhibitory

o Noradrenergic and serotonergic systems likely involved in anxiety disorders

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4
Q

Explain the current understanding of the biological basis of anxiety and anxiety disorders based on the HPA axis

A

o Normal stress response = activates HPA:
• Result: metabolic mobilization; increased HR, BP and respiration; redistribution of blood flow; suppression of immune, inflammatory, and digestive systems

o Chronic stress = abnormal HPA activation
• Result: HT, obesity, diabetes, osteoporosis, suppressed immune function, memory impairment, changes in brain structure, depression, anxiety
• Adrenal cortex hypertrophy
• Hippocampus neuronal atrophy and volume reduction

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5
Q

Explain the current understanding of the biological basis of anxiety and anxiety disorders based on temperament

A

Genetically determined = 40% heritable
• Hippocampus = heritable determinants
• Amygdala = not heritable

o Have extreme behavioral inhibition (freezing) in response to new situations or strangers
o Can be identified early in life (2 years old)
o Predicts development of anxiety, depression, co-morbid substance use

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6
Q

Describe agoraphobia

A
  • Intense anxiety about 2 or more of: using public transportation, being in open spaces, being in enclosed spaces, standing in line or being in a crowd, being outside of home alone
  • May be co-morbid with panic disorder, social phobia, GAD, MDD, PTSD, alcohol use disorder
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7
Q

Recognize the substance­ and medication­ induced and other medical etiologies of anxiety.

A
Medical conditions
o	Hyperthyroidism
o	Hyperparathyroidism
o	Pheochromocytoma
o	Hypoglycemia 
o	Cardiac arrhythmias
o	Mitral valve prolapse
o	Pulmonary embolus
o	Myocardial infarction 
Substance-induced
o	Caffeine intoxication
o	Stimulant abuse
o	Alcohol withdrawal
o	Sedative-hypnotic withdrawal
Medications
o	Asthma drugs (albuterol)
o	Steroids (prednisone)
o	Thyroid drugs 
o	Some antidepressants (bupropion)
o	Stimulants (methylphenidate)
o	Decongestants (pseudoephedrine)
o	Caffeine-containing drugs (No-Doz)
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8
Q

Panic disorder: epidemiology

A

Lifetime prevalence: 2-3% females; 0.5-15% males

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9
Q

Panic disorder: pathophysiology

A
Biological disturbances:
•	Increased catecholamines in CNS
•	Abnormal locus ceruleus (area in brainstem regulating alertness and procuces NE)
•	CO2 hypersensitivity 
•	Lactate metabolism disturbances
•	Abnormal GABA NT system 

Abnormal brain structure:
• Temporal lobe (hypothalamus)
• Cerebral vasoconstriction

Hereditary
• Risk = 20% in 1st-degress relatives

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10
Q

Panic disorder: common comorbidities

A

Higher rates peptic ulcer disease, HT, death

Increased risk of other psychiatric conditions
o Depression
o Alcohol abuse

Higher rates suicide

Other types anxiety disorders

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11
Q

GAD: epidemiology

A

Lifetime prevalence: 4-7%

More common in women

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12
Q

GAD: pathophysiology

A
  • Unknown underlying cause
  • Environmental factors > hereditary role
  • Frontal lobe and limbic system disturbances in NE, GABA, and serotonin may be factors
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13
Q

GAD: common comorbidities

A
  • Often exists with other psychiatric disorder

* Increased risk depression and substance abuse

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14
Q

OCD: epidemiology

A

Lifetime prevalence: 2-3%

Equally prevalent in males and females

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15
Q

OCD: pathophysiology

A
  • Serotonin dysfunction
  • Associated neurological disorders: TBI, epilepsy, Huntington’s
  • Genetically linked to Tourette’s

Other findings:
• Abnormal electroencephalographic findings
• Abnormal auditory evoked potentials
• Growth delays
• Abnormal neuropsychological test results

PANDAS (Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal Infections)
• Strong heritable component

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16
Q

ODC: common comorbidities

A
  • Recurrent major depression episodes (70-80%)
  • History of tics (20-30%)
  • Tourette’s (5-7%)
17
Q

OCD: prognosis

A
Poor prognostic indicators:
•	Yielding to compulsions
•	Childhood onset
•	Bizarre compulsions
•	Need for hospitalization 
•	Coexisting major depression or personality disorder

Favorable indicators:
• Good social and occupational adjustment
• Presence of precipitating event
• Episodic symptom course

18
Q

Recognize the clinical presentations of social phobia and specific phobias.

A
  • Social phobia: strong persisting fear of situations in which embarrassment can occur
  • Specific phobia: strong persisting fear of an object or situation
  • Both result in avoidance, anxious anticipation, or distress
19
Q

Somatization disorder

A

o Presence of distressing and impairing somatic symptoms that can’t be explained on basis of physical and lab exam
o Ex: pain, GI symptoms, sexual symptoms, neurological symptoms
o Lifetime prevalence = 0.2-2%; 5:1 female to male ratio
o Begins before age 30
o Course can be chronic and debilitating
o Episodes typically last 6-9 months, may be separated periods of 9-12 months
o Genetic component; otherwise etiology is unclear
o Must rule out other medical disorders: MS, myasthenia gravis, SLE, HIV/AIDS, acute intermittent porphyria, hyperthyroidism, hyperparathyroidism and chronic systemic infections

20
Q

Conversion disorder

A

Presents with one or more neurological symptoms without identifiable neurological cause; caused by psychological factors

21
Q

GAD: treatment

A

o Combo of medication and psychotherapy
o 1st line = SSRIs
o Also effective = SNRIs
o May use SSRI and benzodiazepine, then taper benzodiazepine once SSRI has taken effect
o CBT: restructure patient’s distortion about environment
o Other behavioral interventions: deep breathing, progressive muscle relaxation, imagery

22
Q

Panic disorder: treatment

A

o Combo of medication and psychotherapy
o 1st line = SSRIs
o Also effective = SNRIs; may use older tricyclic and MAOI antidepressants but not as safe or tolerable
o Benzodiazepines to prevent attacks
o CBT: education to help make more appropriate attributions to somatic symptoms
o Exposure therapy: expose to feared stimulus to desensitize themselves

23
Q

OCD: treatment

A

o Combo of medication and psychotherapy
o 1st line = SSRIs
o Clomipramine = gold standard but lots side effects so try SSRIs first
o Refractory OCD: antidepressants + antipsychotics; psychosurgery (cingulotomy)
o CBT: Exposure and response prevention; family therapy to prevent reinforcement of compulsions

24
Q

List the benzodiazepines

A
Alprazolam
Clonazepam
Diazepam
Lorazepam
Midazolam
Oxazepam
25
List the benzodiazepine antagonists
Flumazenil
26
List the serotonergic anxiolytic
Buspirone
27
List the hypnotics
Eszopiclone | Zolpidem
28
MOA of benzodiazepines vs barbiturates
Overall MOA: o Affect GABAA receptors o GABA = major inhibitory NT in CNS o Stimulate GABAA receptors → opens Cl- pore → Cl- entry into neuron → hyperpolarization → less likely to fire Benzodiazepine agonists o Positive GABAA receptors modulators o Increase affinity of GABAA receptors for GABA o Increase frequency of GABA-induced Cl- channel opening o Do NOT directly activate GABAA receptor Barbiturates o Increase duration of GABA-induced channel opening o At high concentrations = directly activate GABAA receptor • Overall result: neuron hyperpolarized, less excitable
29
Benzodiazepines: effects & uses
Agonist effects: sedating, hypnotic, anxiolytic, amnesiac, spasmolytic, anti-seizure ``` Therapeutic uses Do NOT: • Produce surgical anesthesia • Depress respiration in normal patients • Induce CYP enzymes Indicated for short-term use (2-4 weeks) ```
30
Benzodiazepines: adverse effects
o Minimal effects on CV function, slight decrease in BP o Withdrawal syndrome with sudden DC: insomnia, anxiety, seizures (Need to taper to avoid) o Paradoxical excitement especially in children and elderly CNS: • Dose related effects: drowsiness, ataxia, slurred speech • Additive CNS depression with ethanol and other sedatives and hypnotics o Highly teratogenic (Pregnancy Risk Category D and X)
31
Buspirone
Serotonergic anxiolytic • Non-Benzodiazepine anxiolytic • Partial agonist at 5-HT1A receptors; moderate affinity/partial agonist effects for D2 receptors • Treats GAD • NO sedation, anticonvulsant effects or psychomotor impairment
32
Explain why there is a difference in the duration of action of diazepam and lorazepam when these drugs are administered chronically.
Diazepam o Long-acting o Hepatic metabolism via CYP2C19 & CYP3A4 o Has two active metabolites Lorazepam o Metabolized by glucuronidation o Glucuronide excreted in urine o No active metabolites (avoids hangover effect)
33
Explain why the benzodiazepines are not the drugs of choice for the chronic treatment of generalized anxiety disorder and insomnia.
* Adverse effects * Tolerance and dependence with chronic use * Withdrawal symptoms = occur more commonly with shorter-acting drugs like benzodiazepines
34
Explain why the benzodiazepines may be the drugs of choice the treatment of acute anxiety.
• Shorter acting
35
List other clinical uses of benzodiazepines
Insomnia Sedation Anesthesia = at higher doses Alcohol withdrawal o Benzodiazepines can substitute for alcohol o Treat with long-acting benzodiazepine to prevent withdrawal o Gradually taper dose Antispasmodic = treatment for seizure disorders; need higher doses so also get sedative effect
36
Describe the types of insomnia
Transient insomnia • Lasts 3 weeks • Caused by major psychiatric illnesses (e.g. mania), sleep apnea, chronic medical illnesses (e.g. CHF) • "Learned" insomnia
37
Describe the 2 hypnotics
Zolpidem • Non-benzodiazepine sedative-hypnotic for short-term treatment • MOA: within GABAA receptor complex • Both immediate and controlled release forms Eszopiclone • Non-benzodiazepine sedative-hypnotic for long-term treatment • MOA: within GABAA receptor complex
38
Describe the indications for the use of flumazenil and potential hazards associated with its use.
Indications: o Treats benzodiazepine overdoses o Reverses benzodiazepine sedation during anesthesia o Antagonizes sedative actions of zolpidem and eszopiclone o No effect on barbiturate activity Adverse reactions o CNS: dizziness, headache o Injection site pain o Patients shouldn’t engage in activities requiring complete alertness (residual sedative effects from benzodiazepines)