Anxiety (DONE) Flashcards
(33 cards)
Consequences of excessive anxiety
Decreased capacity for skilled motor movements
Decreased complex intellectual tasks
Decreased perception of new information
Normal and clinical anxiety
A normal, protective psychological response to an unpleasant/threatening situation
However, excessive anxiety can lead to severe distress and impair social functioning
The distinction between a pathological and a normal state of anxiety is difficult to make but represents the point at which the symptoms interfere with normal, productive activities
The term anxiety is applied to several different disorders
Generalised anxiety disorder (GAD)
Persistent anxiety, unlikely to have specific triggers
Diagnosis made after more than 6 months of excess worry or anxiety on most days
Patient cannot control it easily
3 or more of the following are present for more than 6 months: restless/on edge, easily fatigued, difficulty concentrating, irritability, muscle tension, sleep disturbances
Panic disorder
Recurrent panic attacks
Worry about future attacks, or consequences of one, change in behaviour as a result
Specific phobias
Excessive fear of specific situations or objects, avoidance behaviour, change in social functioning
Social anxiety disorder
Similar to phobias but triggered by social situations
Obsessive Compulsive Disorder
Preoccupation and recurrent thoughts with an object or activity
Obsessions- stress and anxiety from persistent thoughts or impulses, not explained by specific life events, recognised as a product of their own mind
Compulsions- driven to repetitive behaviours, unrealistic avoidance methods
Post traumatic stress disorder
Reaction to a traumatic event
Continued experience with triggers
Two or more for more than a month of: insomnia, irritability, poor concentration, increased vigilance, exaggerated response to non-threatening stimuli
Who suffers from anxiety?
Most commonly reported mental illness- lifetime prevalence of 21%
Age of onset typically in young adulthood (20s and 30s)
Female to male ration 2:1
Often more than one anxiety disorder and 2/3 of sufferers will have another mental illness, most commonly depression
Manifestations of anxiety
Verbal complaints
Social effects
Somatic and autonomic effects
Symptoms of anxiety
Over-activity on the sympathetic nervous system
Palpitations, breathlessness, faintness, dizziness, sweating, flushes, dry mouth, cold extremities, piloerection, fatigue
Over-activity in the parasympathetic nervous system
Frequency/urgency of micturition, diarrhoea
Over-activity in the somatic efferent nervous system
Increased muscle tension, headache, facial pain, chest pain/tightness, trembling, fatigue
Pathophysiology
Anxiety occurs when there is a disturbance of the arousal systems in the brain
Arousal maintained by at least three interconnected systems: a general arousal system, an emotional arousal system, an endocrine/autonomic arousal system
Excess activity on the general arousal system can lead to the hyperarousal- mediated by the brainstem reticular formation, thalamic nuclei and basal forebrain bundle
Increased activity in the emotional arousal system associated with anxiety and panic attacks
Neurotransmitters pathophysiology
Several neurotransmitters implicated
ACh is the main neurotransmitter maintaining general arousal
NA and 5HT are associated with heightened emotional arousal, innervating the hippocampus, amygdala, FC and hypothalamus
GABA inhibits other neurotransmitter pathways- increased GABA activity may have a protective effect against excessive stress reactions
Causes of anxiety
Genetic factors- trait anxiety
Medical- psychological, metabolic disturbances, temporal lobe lesions, depressive disorder
Drugs- CNS stimulants e.g. caffeine, amphetamines
Drug withdrawal- from CNS depressants e.g. alcohol, hypnotics, anxiolytics
Treatment of anxiety
Psychotherapy Benzodiazepines Antidepressants Anti-epileptics Antipsychotics Buspirone Propranolol Barbiturates
NICE stepped care plan for GAD
Step 1: all known and suspected presentations of GAD- identification
Step 2: Diagnosed GAD that has not improved after step 1 interventions- low intensity psychological interventions for GAD
Step 3: GAD with marked functional impairment or that has not improved after step 2 interventions- offer either an individual high intensity psychological intervention or drug treatment
Step 4: Complex treatment refractory GAD and very marked functional impairment, such as self neglect or a high risk of self harm- highly specialist treatment
Psychotherapy
First line treatment in all anxiety disorders
CBT/ applied relaxation
Self help
Psychoeducational groups
Little evidence for other psychotherapies
Medications in the treatment of anxiety: benzodiazepines
The most commonly used anxiolytics and hypnotics
Short term relief (two to four weeks only) of anxiety that is severe, disabling, or causing the patient unacceptable distress
Use to treat short term mild anxiety is inappropriate
Schedule 3 and 4 CDs
Pharmacological effects of benzodiazepines
Sedation, sleep induction
Sleep, but permitting arousal
Decreased anxiety, amnesia at higher doses
Muscle relaxation (both midbrain and spinal effects)
Anticonvulsant activity
Reduced aggression
Pharmacology of BZDs
Modulate the action of GABA at GABA-a receptors
Single-channel studies show: an increased frequency of channel openings, no change in conductance, no change in mean open time- indicating that BZDs stabilise the active form of the receptor
Classification of BZDs
Short acting (half life < 8 hours): triazolam, temazepam, oxazepam, lormetazolam Intermediate (10-18 hours): lorazepam Long acting (>20 hours): diazepam, chlordiazepoxide, nitrazepam, flurazepam, flunitrazepam
BZD metabolism
Most are well absorbed after oral dosing
All are widely distributed
Plasma levels decline due to hepatic metabolism- to intermediates that may be active finally to inactive water soluble conjugates
Renal excretion of inactive glucuronides
Hepatic function, not renal function, is the important determining factor for potency and duration of action
Adverse effects
Sedation
Ataxia (unsteady gait with high doses)
Potentiation of alcohol and other CNS depressants
Interference with motor skills- impaired dexterity and speed of response, reduced awareness
Tolerance
Withdrawal syndrome and dependence
Anxiety and aggression
Paradoxically, in some individuals BZDs can induce irritability and aggression
Particularly marked with the ultra-short acting BZD, triazolam, which led to it being withdrawn in the UK
Probably withdrawal syndrome, more acute with drugs whose action wears off rapidly
