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32 Cards in this Set
- Front
- Back
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What are the six anxiety disorders characterized by DSM-IV?
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1) Generalized anxiety disorder
2) Social phobias 3) Simple phobias 4) Panic disorder 5) Post-traumatic stress disorder 6) Obsessive-compulsive disorder |
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Describe generalized anxiety disorder
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Characterized by excessive, unrealistic and long lasting worrying
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Describe social phobias
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Characterized by fear or embarrassment in social or performance situations
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Describe simple phobias
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Characterized by fear and aversion in response to specific objects or places, such as blood, spiders, bridges, or elevators
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Describe panic disorders
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Characterized by brief, recurrent and unexpected episodes of terror
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Describe post-traumatic stress disorder (PTSD)
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Characterized by recurrent episodes of fear often triggered by reminders of an extremely stressful trauma
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Describe obsessive-compulsive disorder
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Characterized by consuming, disturbing and insuppressible obsessive thoughts and compulsive activities.
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Describe how anxiety levels shift throughout a persons life and what determines the anxiety level
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Individuals appear to have rather consistent anxiety levels over their lifetime suggesting that levels of anxiety behavior persist over long periods of time and reflect fundamental differences in brain composition or wiring. Such differences in brains of high anxiety versus low anxiety individuals are likely to have developed as a result of differences in both the genetic makeup of each individual as well as the environment they have experienced during their lifetime.
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What genes have been linked to increased anxiety in humans? Describe this gene
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The serotonin transporter (SERT) gene. There are two alleles: s and l. s/s/ individuals have lower cellular SERT activity and have higher neuroticism and lower agreeableness scores than s/l and l/l individuals.
The s/s allele may also be associated with increased amygdala activity. This means that SERT influences anxiety-related behaviour by modulating the excitability of specific fear circuits in the brain. |
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What determines the expression of SERT polymorphisms?
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The permissive rearing environment
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What is the relationship between MAO-A activity and childhood experiences?
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The biochemical consequences of high MAO-A activity are sufficient to protect the brain against the long-term consequences of childhood abuse.
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Describe the genetics of depression
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Rates of major depression at age 26 were found to be strongly influenced by the number of stressful life events in individuals carrying the s/s and l/s alleles of the 5-HTT promoter polymorphism, but not in those carrying the l/l alleles. Notably, predisposition to depression was not further modified by the MAO-A polymorphism, suggesting different molecular mechanisms for MAO-A and 5-HTT mediated susceptibilities.
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Who gets PTSD?
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PTSD develops in approximately 15% of individuals who experience or witness severe trauma such as rape, murder, or military combat
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What is the relationship between PTSD and the brain?
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One of the most consistent findings in PTSD is a tendence for a decrease in volume of the hippocampus, a structure in the medial temporal lobe of the brain required for associative memory. The hippocampus is known to be easily damaged by stress hormones.
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What drugs have been used to treat excessive anxiety? Which ones have been shown to be most specific and effective?
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-Alcohol
-Barbituates -Opiates -Beta-blockers -Benzodiazepines (Best choice) |
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Besides anxiety effects, what are the other therapeutic uses of benzodiazepines?
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-Central muscle relaxation in spastic diseases such as cerebral palsey
-Anticonvulant effects particularly for status epilepticus -Hypnotic activity for sleep induction in insomniacs -Alcohol detoxification |
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How do benzodiazepines work?
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They increase the potency of the major inhibitory neurotransmitter in the brain, gamma-amino-butyric acid (GABA) by modulating the function of GABA-A receptors.
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What are the possible explanations for the anxiolytics activity of benzodiazepines?
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a. Anxiety is probably associated with an excessive neuronal firing rate
b. Normally GABA binds to its receptors nad opens a chloride channel which results in inhibiton of neuronal firing nad a consequent reduction in anxiety c. When a benzodiazepine binds to its site on the GABA receptor, it enhances hte binding of GABA, thereby potentiating its effect and consequently, neuronal firing rate is further inhibited d. GABA does not compete with radioactive diazepam for binding to the benzodiazepine receptor |
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What is the critical physiological hallmark of anxiety?
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Excessive excitatory neurotransmission. However, the precise anatomical location and nature of this brain hyper-excitability is not known.
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How often are long-acting benzodiazepines given? What are the consequences of this?
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The long-acting compounds can be given once a day since considerable drug accumulation occurs and consequently there is persistence of the drug and/or of the active metabolites throughout the day. Therefore, even if a patient were to miss a dose, or an entire day of drug, the blood levels would not fall precipitously, and so, rapid recrudescence of symptoms would not be likely to occur. However, the rate and extent of drug accumulation with long-acting compounds can be unpredictable and, in some cases, excessive drug can accumulate.
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What are the symptoms of generalized anxiety? What is the incidence? What are the treatments?
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Symptoms: Unrealistic, excesive and long lasting worry. Motor tension. Autonomic hyperactivity. Hypervigilance
Incidence: 5% Treatment: Benzodiazepines, SRIs |
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What are the symptoms of panic disorder? What is the incidence? What are the treatments?
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Symptoms: Brief, recurrent, unexpected episodes of terror (15-30 min). Sympathetic crisis. Dyspnea (shortness of breath). Fear of dying
Incidence: 3.5% Treatment: SRI, behavioral therapy |
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What are the symptoms of post traumatic stress disorder? What are the treatments?
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Symptoms: After extremely stressful event recurrent episodes of fear often triggered by reminders of initial trauma
Treatment: Behavioral therapy |
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What are the symptoms of social phobia? What is the incidence? What are the treatments?
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Symptoms: In specific social situation: aversion, fear, and automatic arousal
Incidence: 13.3% Treatment: SRIs, behavioral therapy |
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What are the symptoms of specific phobia? What is the incidence? What are the treatments?
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In the presence of specific animals, blood, or situations: aversion, fear and automatic arousal
Incidence: 11.3% Treatment: Behavioral therapy |
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What are the symptoms of obsessive-compulsive disorder? What is the incidence? What are the treatments?
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Symptoms: Recurrent obsessions and compulsions
-Obsession: persistent doubt or fears -Compulsion: repetitive acts to alleviate the anxiety Incidence: 2-3% Treatment: SRIs, behavioral therapy |
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What are the side effects of benzodiazepines?
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-Sedation
-Ataxia -Dependence liability - more limited than the general CNS depressants -Even large oral doses of diazepam are not lethal. When combined with other CNS depressants, e.g., alcohol, death can occur |
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What is the cardinal principle in treating patients with benzodiazepines?
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To administer the lowest effective dose for the shortest period of time. This will minimize physical dependency and reduce the discontinuance syndrome.
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What is the critical factor in reducing discontinuance syndromes?
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Slow tapering. Patients often require weeks to months to be weaned from benzodiazepines. Fortunately, serious withdrawal events such as seizures or hallucinations are extremely rare.
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What drugs have started to replace benzodiazepines for many kinds of anxiety? How do they work?
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SRIs
They likely dampen excessive brain excitability |
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Describe the time course of SRI action
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Benzodiazepines act rapidly, within minutes of administration, while SSRIs act much more slowly, with therapeutic effects developing only two to four weeks after the beginning of treatment (Figure 3). The slow therapeutic onset of SSRIs suggests that the anxiolytic effect of these drugs depends on inducing long-term plastic changes in the brain.
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What is a possible mechanism for the actions of SRIs?
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Several molecular markers of such plastic changes have been identified and recently an increase in the proliferation of new neurons in the rodent hippocampus has been shown to contribute to the behavioral effects of SSRIs. Such changes gradually induced by SSRIs could provide the mechanism by which these drugs are able to counteract the excessive excitability associated with anxiety disorders.
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