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Anxiety Disorders Flashcards

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
Q

List the benzodiazepine antagonists

A

Flumazenil

26
Q

List the serotonergic anxiolytic

A

Buspirone

27
Q

List the hypnotics

A

Eszopiclone

Zolpidem

28
Q

MOA of benzodiazepines vs barbiturates

A

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
Q

Benzodiazepines: effects & uses

A

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
Q

Benzodiazepines: adverse effects

A

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
Q

Buspirone

A

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
Q

Explain why there is a difference in the duration of action of diazepam and lorazepam when these drugs are administered chronically.

A

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
Q

Explain why the benzodiazepines are not the drugs of choice for the chronic treatment of generalized anxiety disorder and insomnia.

A
  • Adverse effects
  • Tolerance and dependence with chronic use
  • Withdrawal symptoms = occur more commonly with shorter-acting drugs like benzodiazepines
34
Q

Explain why the benzodiazepines may be the drugs of choice the treatment of acute anxiety.

A

• Shorter acting

35
Q

List other clinical uses of benzodiazepines

A

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
Q

Describe the types of insomnia

A

Transient insomnia
• Lasts 3 weeks
• Caused by major psychiatric illnesses (e.g. mania), sleep apnea, chronic medical illnesses (e.g. CHF)
• “Learned” insomnia

37
Q

Describe the 2 hypnotics

A

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
Q

Describe the indications for the use of flumazenil and potential hazards associated with its use.

A

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)

Neuro (20 decks)

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