General stuff Flashcards
The evidence from published literature supports the treatment of anxiety disorders, but no evidence is yet available for the management of individual symptoms of anxiety or worry.
Reporting of panic-related symptoms by patients does not necessarily lead to the diagnosis of panic disorder or even panic attack.
Patients usually misinterpret heightened anxiety with panic. This has to be clearly differentiated.
It is tempting to diagnose early and quickly in the presence of characteristic symptoms, but it is always good clinical practice to ensure that patients fulfil the required diagnostic criteria for each relevant disorder.
One must take a longer and longitudinal view of the symptoms before prescribing, as the severity of the symptoms will fluctuate with the passage of time and as life circumstances change. This should be carefully considered before prescribing psychotropic drugs.
The first major evidence from literature for the efficacy of antidepressants in GAD came from
imipramine studies.
Various guidelines now recommend SSRIs as first choice due to:
their lesser toxicity in overdose, lesser cardiotoxicity, and a greater tolerability. NICE advised doctors to consider sertraline specifically because of its believed cost effectiveness, although its licence does not include GAD.
The SNRIs venlafaxine and duloxetine now also have good short and medium-term efficacy data.
Antidepressants have a slower onset of action as compared with benzodiazepines; after an average of two to four weeks of treatment:
antidepressants demonstrate greater anxiolytic effects than benzodiazepines.
aglomelatine
imipramine
paroxetine
venlafaxine
trazodone.
All have evidence that shows superior to placebo in the treatment of GAD:
However, aglomelatine, imipramine and trazodone are not licensed for GAD.
The adverse effects of imipramine include:
More serious effects include:
dry mouth
dizziness
constipation
sweating.
sedation
sexual dysfunction
increased risk of falls in the elderly
cardiac toxicity in overdose
seizures.
The adverse effects of SSRIs include:
More serious adverse effects include:
nausea
nervousness
anorexia
insomnia (note: sedation with paroxetine).
decreased libido and delayed orgasm
hyponatreamia
increased risk of GI bleeding in the elderly
extra pyramidal side effects
a citalopram metabolite may increase the QTc interval.
The adverse effects of venlafaxine include:
nausea
dizziness, sweating
insomnia
dry mouth.
More serious adverse effects of venlafaxine include:
sexual dysfunction
elevation of blood pressure (related to dose)
reports of cardiac arrythmias
discontinuation symptoms.
Buspirone:
mechanism of action:
onset of action:
is an azapirone derivative and is a Type 1A Serotonin receptor agonist
has a slow onset of action.
One systematic review found that buspirone is better than placebo at improving symptoms of GAD.
Contrary to popular belief, buspirone does not help patients withdraw from benzodiazepines.
The adverse effects of buspirone include:
dizziness
headache
nausea.
These effects can be minimised by slowly building up the dose, e.g. starting with 10 mg and increasing by 10 mg instalments at weekly intervals up to 40 mg.
Although clinically effective in some patients, beta-blockers are not licensed for use in GAD as there have been no clinical trials in this disorder.
However, they are effective in controlling situational somatic symptoms such as tremor and tachycardia.
People who have social phobia either avoid social situations or endure them with great distress because the fear of embarrassment causes such intense anxiety.
Such avoidance may ultimately interfere with occupational and/or social functioning and lead to significant disability, especially in personal spheres (less than half marry despite most wanting to).
The duration of social phobia is frequently lifelong, and there is a high degree of comorbidity with other psychiatric disorders.
is the most prevalent of any anxiety disorders and is the third most common psychiatric disorder after depression and alcohol abuse
social anxiety
typically begins during childhood with a mean age at onset between 14 and 16 years and is sometimes preceded by a history of social inhibition or shyness.
