Anxiety (DONE) Flashcards

1
Q

Consequences of excessive anxiety

A

Decreased capacity for skilled motor movements
Decreased complex intellectual tasks
Decreased perception of new information

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2
Q

Normal and clinical anxiety

A

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

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3
Q

Generalised anxiety disorder (GAD)

A

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

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4
Q

Panic disorder

A

Recurrent panic attacks

Worry about future attacks, or consequences of one, change in behaviour as a result

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5
Q

Specific phobias

A

Excessive fear of specific situations or objects, avoidance behaviour, change in social functioning

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6
Q

Social anxiety disorder

A

Similar to phobias but triggered by social situations

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7
Q

Obsessive Compulsive Disorder

A

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

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8
Q

Post traumatic stress disorder

A

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

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9
Q

Who suffers from anxiety?

A

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

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10
Q

Manifestations of anxiety

A

Verbal complaints
Social effects
Somatic and autonomic effects

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11
Q

Symptoms of anxiety

A

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

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12
Q

Pathophysiology

A

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

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13
Q

Neurotransmitters pathophysiology

A

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

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14
Q

Causes of anxiety

A

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

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15
Q

Treatment of anxiety

A
Psychotherapy
Benzodiazepines
Antidepressants
Anti-epileptics
Antipsychotics
Buspirone
Propranolol
Barbiturates
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16
Q

NICE stepped care plan for GAD

A

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

17
Q

Psychotherapy

A

First line treatment in all anxiety disorders
CBT/ applied relaxation
Self help
Psychoeducational groups
Little evidence for other psychotherapies

18
Q

Medications in the treatment of anxiety: benzodiazepines

A

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

19
Q

Pharmacological effects of benzodiazepines

A

Sedation, sleep induction
Sleep, but permitting arousal
Decreased anxiety, amnesia at higher doses
Muscle relaxation (both midbrain and spinal effects)
Anticonvulsant activity
Reduced aggression

20
Q

Pharmacology of BZDs

A

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

21
Q

Classification of BZDs

A
Short acting (half life < 8 hours): triazolam, temazepam, oxazepam, lormetazolam
Intermediate (10-18 hours): lorazepam
Long acting (>20 hours): diazepam, chlordiazepoxide, nitrazepam, flurazepam, flunitrazepam
22
Q

BZD metabolism

A

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

23
Q

Adverse effects

A

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

24
Q

Anxiety and aggression

A

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

25
Q

Tolerance and dependence to BZDs

A

Dependence is uncommon with long acting drugs, unless used at high doses
Rapid removal is more likely to precipitate withdrawal
Ultra short acting drugs e.g. triazolam may cause withdrawal within a few hours of a single dose
Patients with a history of drug abuse are at greater risk

26
Q

BDZ withdrawal syndrome symptoms

A
Increased anxiety/insomnia
Dysphoria
Irritability
Sweating
Unpleasant dreams
Tremors
Anorexia
Faintness/dizziness
27
Q

Withdrawal effects and dependence can be prevented or reduced by:

A

Avoiding when history of alcohol abuse or previous problems with prescribed sedatives
Not prescribing short acting drugs for continuous medication
Not prescribing other agents at high doses
Arranging a planned withdrawal using a reducing regime with a long acting BZD
Substituting with sedative TDA antidepressants or antipsychotic

28
Q

Withdrawal protocol

A

A BZD can be withdrawn in steps of about one-eighth of the daily dose every fortnight. For patients who have difficulty:
Transfer patient to equivalent daily dose of diazepam preferably taken at night
Reduce dose every 2-3 weeks, if withdrawal symptoms occur maintain this dose until symptoms improve
Reduce dose further, if necessary in small steps, it is better to reduce too slowly than too quickly
Stop completely, full withdrawal can take 4 weeks to a year or more

29
Q

Antidepressants

A

SSRIs e.g. paroxetine, citalopram, sertraline
First line drug options in GAD, panic disorder, social phobia, PTSD and OCD
Evidence also for fluoxetine and fluvoxamine in OCD
Produce delayed anxiolytic effect (>2 weeks)
Initial worsening of symptoms is common

30
Q

Mechanism of action of SSRIs

A
SSRIs inhibit 5-HT transporter
Initial increase of synaptic 5-HT less than expected, due to inhibitory 5-HT1a autoreceptors on the soma and dendrites of 5-HT containing neurons, which reduce 5-HT release
Prolonged treatment (>2 weeks) thought to produce desensitisation of somatodendritic 5-HT1a autoreceptors resulting in heightened excitation of serotonergic neurons and enhanced 5-HT release
31
Q

Side effects of SSRIs

A

Can cause nausea, anorexia, insomnia, loss of libido
Interact with several different drugs e.g. NSAIDs which can lead to increased GI bleeding, gastroprotective drug such as PPI could be prescribed
Also a withdrawal issue with short acting SSRIs

32
Q

Buspirone

A

5-HT1a partial agonist licensed for short term use in anxiety
Mechanism thought to be the same as SSRIs
Studies have shown that it is effective on GAD but less effective than BZDs
Causes nausea and dizziness, does not cause sedation, tolerance or withdrawal
Not recommended by NICE

33
Q

Propranolol

A

Propranolol and oxprenolol are both licensed for anxiety
Useful for physical symptoms such as palpitations, tremor, sweating and shortness of breath
Beta blockers do not have sufficient evidence to support their inclusion in NICE guideline
However, small studies indicate that giving propranolol immediately after a traumatic event may prevent emerging PTSD