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Pharmacology III > Anxiety > Flashcards

Anxiety Flashcards

1
Q

What is a drug that has a calming effect, relieving anxiety and tension.?

A

Sedative

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2
Q

What is A drug that produces sleep by depressing brain function?
Often cause hangover effects in the morning

A

Hypnotic

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3
Q

What is a drug that reduces anxiety?

A

Anxiolytic

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4
Q

What is a normal emotional state in response to a stressful situation that;s usually transient and commonly caused by the perception of real or potential danger?

A

Anxiety

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5
Q

What are the general medical conditions that cause anxiety?

A

MI, asthma, hyperthyroidism (usually when tx the anxiety improves), migraine, pain

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6
Q

What are the psychiatric disorders that cause anxiety?

A

Mood disorders, schizophrenia, delirium, dementia, substance abuse

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7
Q

What are the medication induced causes of anxiety?

A

Depressants, stimulants

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8
Q

When does anxiety become pathological?

A
  • Pathological anxiety occurs when safe stimuli acquire a meaning of danger
  • Anxiety is excessive, inappropriate or generalized
  • Responses to feared stimuli are maladaptive
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9
Q

When does anxiety become a disorder?

A

Becomes a DISORDER when source of significant subjective distress or functioning impaired

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10
Q

What are the neurochemical theories?

A 
--Noradrenergic Model
Hypersensitive autonomic nervous system
--Benzodiazepine Receptor Model
Inhibitory pathway
Deficit in patients with anxiety disorders
--Serotonin Model
Primarily an inhibitory neurotransmitter
May help to reduce ANS hyperactive state
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11
Q

What are the anxiety associated neurotransmitter systems?

A

GABA
Norepinephrine model
Serotonin model

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12
Q

What is the gamma-aminobutyric acid (GABA) receptor?

A

High affinity sites, adjacent to GABA receptors, for benzodiazepine and barbiturates on the cell membrane in the CNS.

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13
Q

What is the MOA of benzodiazepines?

A

The binding of benzodiazepines enhances the action of GABA, resulting in a greater entry of chloride ion

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14
Q

What are the anxiety disorders?

A 
Panic disorder (+/-)
Social anxiety disorder (SAD)
Specific phobia
Generalized anxiety disorder (GAD)
Obsessive-compulsive disorder (OCD)
Posttraumatic stress disorder (PTSD)
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15
Q

What is literally the fear of market place or open spaces, also anxiety about being in situations that escape is difficult?

A

Agoraphobia

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16
Q

What do people with agoraphibia avoid?

A

Driving, bridges, tunnels, elevators, airplanes, malls, long lines, sitting in middle of row

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17
Q

Are males or females more affected by anxiety?

A

Females

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18
Q

What are panic attacks?

A 
Sudden onset with no warning
Usually last no more than 20-30mins
Can occur at anytime
Overwhelming sense of doom
Fear of dying or losing control
Physical sx
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19
Q

What is a panic attack under the DSM-IV criteria?

A 
Period of intense fear or discomfort, in which at least 4 of the following sx developed abruptly and peaked w/in 10 minutes:
Palpitation
Sweating
Trembling
Sensations of SOB
Feeling of choking
CP or discomfort
Nausea or abd distress
Dizziness, lightheadedness, feeling faint
Fear or losing control or going crazy
Fear of dying
Numbness or tingling
Chills or hot flashes
Derealization of depersonalization
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20
Q

What is Generalized anxiety disorder (GAD)?

A

Excessive anxiety and worry about a number of events or activities on most days for at least 6 mo.
Associated w/ 3 or more sx- restlessness, easily fatigued, difficulty concentration, irritability, muscle tension, sleep disturbance.
Significant distress at work and socially
Typically present with somatic complaints

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21
Q

What are the nonphamarcologic therapy options for GAB?

A

Lifestyle changes

CBT

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22
Q

What are the pharmacotherapy tx for GAD?

A 
Antidepressants
Benzodiazepines
Buspirone
Pregabalin
Beta Blockers
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23
Q

What should patients with GAD avoid?

A

Caffeine
OTC cold preparations
Marijuana
Excess alcohol or use for sleep

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24
Q

What are the advantages of CBT?

A 
It works
It may have low relapse rate when d/c
MOst people like it
TIme-limietd
Overall low price
few side effects
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25
Q

What are the disadvantages of CBT?

A 
Harder to admin than meds
Limited availability
More effort than taking meds
Lack of 3rd party coverage
Not all patients willing or able
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26
Q

What are the benzodiazepines used to tx anxiety?

A 
Alprazolam (Xanax)
Clonazapam (Klonopin)
Chlordiazepoxide (Librium)
Cloraze[ate (Tranxene)
Diazepam (Valium)
Halazepam (Paxipam)
Lorazepam (Ativan)
Oxazepam (Serax)
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27
Q

What are the most effective and safe medications for acute anxiety sx?

A

Benzodiazepines

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28
Q

Benzodiazepines (-pams)- ROA and absorption

A 
Route of Admin
Oral, IV, IM, rectal
Absorption
Rapidly and completely
Lipophilic agents-distributed throughout the body
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29
Q

Benzodiazepines (-pams)- duration of action and metabolism

A 
Short, intermediate, long
Long-acting form active metabolites with long half-lives
Metabolism
Hepatic (active metabolites)
Excreted in urine; redistributed
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30
Q

What are the long acting 1-3 day benzodiazepines?

A

Clorazepate- not used often don’t worry about this one.
Chlordiazepoxide
Diazepam
Flurazepam

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31
Q

What are the intermediate 10-20 hour acting benzodiazepines?

A

Alprazolalm
Lorazepam
Temazepam

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32
Q

What are the short acting 3-8 hour acting benzodiazepines?

A

Oxazepam

Triazolam

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33
Q

Benzodiazepine (-pams)- MOA

A

Potentiate the inhibitory activity of GABA
Binds to the GABA-BDZ receptor complex
-Facilitates the opening of Cl- channels
Prevents further release of excitatory neurotransmitters (hyperpolarization)

*Bind to the allosteric site!

34
Q

What should dosing of benzos be related back to?

A

Lorazepam

35
Q

What is the onset of high potency benzos?

A

Fast

36
Q

Benzodiazepine (-pams)- ADRs

A

SEDATION
Fatigue
Weakness
Psychomotor impairment (decreased memory and decreased recall, ataxia and mental confusion)
Paradoxical reactions (mostly in special populations like elderly, brain injured, MR, kids)
Rebound anxiety and insomnia

37
Q

Benzodiazepines (-pams)- tapering

A

<10-25% every 1-2 wks
At 50% initial dose, slow taper further
Maintain multiple dosing to minimize taper-related plasma level fluctuations
Discontinuation is less difficult over the first 50% of the dose
A longer taper period is needed for the final 50% of the dose to avoid potentially severe withdrawal sx

38
Q

Benzodiazepines (-pams)- drug interactions

A

–Other CNS depressants – ETOH, opiates
–Cimetidine –Inhibits metabolism of longer acting BZDs
–Fluoxetine–Decreases clearance of diazepam
–CYP3A4 inhibitors (fluoxetine, fluvoxamine, grapefruit juice, ketoconazole, nefazodone)
Decrease clearance of alprazolam

39
Q

What are the three big disadvantages of benzodiazepines?

A

Physiologic dependence
Risk for withdrawal reactions with abrupt discontinuation
Concern over abuse potential

40
Q

What results from abrupt withdrawal from benzodiazepines?

A

Abrupt withdrawal results in withdrawal symptoms– confusion, anxiety, agitation, restlessness, insomnia, tension
Long-acting tend to withdrawal themselves
Short-acting more severe withdrawal treatment = long t1/2 benzo

41
Q

When is a benzo overdose lethal?

A

Benzo overdose seldom lethal unless combined with other central depressants ie., ETOH

42
Q

What is The antidote for a benzodiazepine overdose?

A

FLUMAZENIL** rapidly reverses effects of benzos
IV
May require frequent administration
May precipitate withdrawal in dependent patients or cause seizures in epileptics

43
Q

Are barbutrates used for insomnia and anxiety?

A

No

44
Q

Barbiturates- ADRs

A

Induce tolerance, physical dependency, severe withdrawal symptoms
Potentially Fatal Respiratory Depression
Suppresses hypoxic and chemoreceptor response to CO2
narrow therapeutic range

45
Q

Why do barbiturates have alot of drug interactions?

A

They are p450 inducers

46
Q

Barbiturates- indications

A

Ultra-short t1/2: IV General Anesthesia
thiopental
Sedative/hypnotic
At low doses, sedation (calming, reduced excitement) higher doses hypnosis anesthesia coma and death
Amobarbital (amytal), pentobarbital, secobarbital
Anticonvulsant
–Treatment of tonic-clonic, status epilepticus, eclampsia
–DOC in children with recurrent febrile SZ
Phenobarbital

47
Q

What is the drug of choice for a child with recurrent febrile sz?

A

Phenobarbital

48
Q

Barbiturates- MOA

A

Potentiates GABA action on chloride entry into neuron ->hyperpolarization
Barb receptor on GABA different than Benzo
Block excitatory glutamate receptors
Anesthetic concentrations block Na+ channels

49
Q

What are the long acting (1-2days) barbiturates?

A

Phenobarbital

50
Q

What are the short-acting (3-8 hours) barbiturates?

A

Pentobarbital
Secobarbital
Amobarbital

51
Q

What are the ultra short-acting (20 min) barbiturates?

A

Thiopental

52
Q

Barbiturates- pharmakokinetics

A 
PO
Redistribute in body from brain to splanchnic areas to skeletal muscle then adipose tissue
Metabolized in liver
P450 inducer drug-drug interactions
Renal excretion
53
Q

Barbiturates- ADRs

A

Drowsiness, impaired concentration, mental/physical sluggishness
Synergizes ETOH
Drug hangover
Nausea and dizziness

54
Q

Are barbiturates a P450 inducer?

A

Increase porphyrin synthesis contraindicated in patients with acute intermittent porphyria

55
Q

What happens with abrupt withdrawal of barbiturates?

A

Abrupt withdrawal-> tremors, anxiety, weakness, restlessness, N/V, SZ, delerium, cardiac arrest
More severe than opiate withdrawal, can result in death

56
Q

What occurs with OD of barbiturates?

A

Severe respiratory depression coupled with CV depression-> shock; shallow, infrequent breathing

57
Q

What is the tx of a barbiturate OD?

A

No antagonist available

Ventilation; purge stomach; hemodialysis; alkalinization of urine with phenobarbital

58
Q

What components of anxiety does a beta blocker help with?

A

Physiologic component of anxiety:
tachycardia, palpitations, tremor, sweating

No CNS depression
non-addicting, no drowsiness

Do not use in asthma, diabetes, CHF
monitor BP, pulse

Helpful for performance anxiety:
propranolol 10 mg prn

59
Q

When should beta blockers be used to tx anxiety?

A

When you have a patient that has stage fright or anxiety in front of a crowd. Not a regular medication to manage anxiety

60
Q

Buspirone (Buspar®)- indications

A

Treat anxiety d/o

61
Q

Buspirone (Buspar®)- MOA

A

Reduce 5-HT transmission by acting as partial agonist at these receptors
Some affinity for DA receptors also

62
Q

Buspirone (Buspar®)- advantages and disadvantages

A

Advantages:
Dependence unlikely; minimal sedation

Disadvantages:
Only effective in GAD; doesn’t work in severe anxiety
Slow onset of action
CAUSES HYPOTHERMIA; INCREASED PROLACTIN/GH
P450 metabolism- chance of drug interactions.

63
Q

Buspirone (Buspar®)- ADRs

A

HA, dizziness, nausea

64
Q

How long does it take for buspirone to start working?

A

1 week

65
Q

Pregabalin-MOA

A

Similar to gabapentin
Site of action- Alpha(2) delta subunit of voltage dependent calcium channels
Reduces calcium influx into the neuron and inhibits neuronal excitability
Reduces the release of glutamate, NE, and substance P

66
Q

Pregabalin- ADRS (in GAD)

A 
Dizziness
Somnolence
Dry Mouth
Abnormal Thinking
Blurred vision
Diarrhea
Incoordination
Ataxia
67
Q

What type of antidepressant is able to be used in all anxiety disorders?

A

SSRIs

68
Q

What is considered the DOC for GAD?

A

SSRI

69
Q

What is DOC for panic disorder?

A

SSRI (FLX, SERT, PAR)

70
Q

What can a combination of benzos and antidepressants cause?

A

Jitteriness syndrome or hyperrsensitivity reaction– jitteriness, shakiness, increased anxiety, and insomnia.
Start low and go slow!

71
Q

What are the advantages of SSRI/VLFX in panic disorder treatment?

A

Effective for comorbid depression
Effective in managing mixed patients- especially with PD, GAD, OCD
Lower risk in suicidal patients
Generally well tolerated and no abuse potential
Once daily dosing
Relapse prevention

72
Q

What are the disadvantages of SSRI/VLFX for treating panic disorder-GAD?

A

Delayed onset (days to weeks)
Transient activation early in therapy
SE: GI, sexual dysfunction, discontinuation syndrome
Withdrawal reactions when discounted

73
Q

What is SSRI induced anxiety?

A

Enhanced 5-HT release or have supersenstive 5-HT2 receptors, which increases glutamate
High potency BZDs have rapid anxiolytic effects and also reduce early SSRI-induced anxiety

74
Q

Who needs long term medications for anxiety?

A

The majority of anxiety and panic disorder patients need long-term tx
Relapse rates after discontinuation of medication are significant
Tapering needs to be very gradual (3-6mo)

75
Q

What antihistamines are used to tx anxiety and insomnia?

A

Diphenhydramine (Benadryl)

Hydroxyzine (Atarax)

76
Q

What are the side effects of antihistamines?

A

Non- addicting

Some anticholinergic effects

77
Q

ETOH- MOA

A

Antianxiety and sedative effects
CNS depressant producing sedation then hypnosis with increasing doses
Shallow dose-response curve
Sedation over wide dose range

78
Q

ETOH- pharmacokinetics

A 
PO; readily absorbed
Vd close to total body water
Metabolized by liver
ETOH->acetaldehyde-> acetate
Eliminated via kidneys and lungs
Synergizes other sedative agents
Severe CNS depression with barbs and antihistamines
79
Q

ETOH- ADRs

A

Chronic consumption: gastritis, nutritional deficiencies, severe liver disease, cardiomyopathy

80
Q

What medications are involved with the treatment of alcohol withdrawal?

A

-Benzodiazepines
-Carbamazepine for SZ during withdrawal
-Disulfiram (Antabuse)
Conditioned avoidance response
Blocks oxidation of acetaldehyde to acetate
Accumulation of acetaldehyde flushing, TACHY, hyperventilation, nausea

Pharmacology III (19 decks)

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