Anxiety Flashcards
(36 cards)
what is anxiety?
Anxiety is a normal, physiological response to threatening situations that serves a protective function.
Anxiety is pathological when there is a bias to interpret non-threatening situations as threatening
what are the different types of anxiety?
1Simple/Specific phobias
2Social phobia/ Social anxiety disorder (SAD)
3Panic disorder (PD)
4Posttraumatic stress disorder (PTSD)
5Generalized anxiety disorder (GAD)- diffused worries (MOST COMMON)
6Obsessive compulsive disorder (OCD)- repetitive behaviour
(Premenstrual dysphoric disorder (PMDD))
DSM criteria for generalized anxiety disorder include:
Excessive anxiety and worry about things most days of the week for at least 6 months
Difficulty controlling feelings of worry
At least 3 of the following symptoms in adults: (motor symptoms) restlessness, fatigue, trouble concentrating, irritability, muscle tension or sleep problems
Anxiety that interferes with daily life
Core features of anxiety disorders are common which are NPA
Negative cognition: Ability to interpret unthreatening situations as threatening (bias)
Physiology: feel panic/ anxiety (sympathetic) HR, RR, BP increase, NA released, sweating
Avoidance: obv in PTSD, avoid situation which will trigger anxiety disorder
describe the innate/ secondary pathway of feeling anxious
innate: sensory- thalamus- amygdala (fear centre) - release of amine NT, increase alert, attention
amygdala- PAG- release of 5HT,NA- avoidance
amygdala- HPA- stress hormone cortisol and A- automonic fight or flight resp
2ndary: sensory- prefrontal cortex and hippocampsus- relate to previous memory and associtated emotions- TOP DOWN CONTROL- make decision whether to worry or not
aetiology of anxirty disorder (GAD)
- Largely unknown
- Abnormal regulation of brain areas involved in stress/fear (amygdala)
- NT systems implicated:
1 Underactivity of 5HT system? (poor appetite)
2 Overactivity of NA system? (too alert)
3 Disruption in level of GABA inhibition?
1) reduced expression of GABAA-receptors
2) reduced function/regulation of GABAA-receptors by benzodiazepines, neurosteroids - Genetic and environmental (stress) factors play a role
trt for GAD
ABB
β-blockers (propanolol) – target autonomic symptoms
Benzodiazepines*
Antidepressants (SSRIs)1st line
Buspirone (partial agonist at 5-HT1A receptors) alternative trt
Evidence-based psychological interventions (same for depression)
Specific NICE guidance for different anxiety disorders, Stepped-care approach
functions of BB (antihypertensive) in GAD
treat autonomic sympathetic symptoms of anxiety e.g. stress response, increased HR,BP
no effect on the brain region amygdala
treat phobias, PTSD: memory consolidation
BZ and barbiturates e.g pentobarbital, which is safer and why
BZ is safer
both give relief of anxiety but BZ make you fully aware of the environemnt. barbiturates- NOT in touch with the environement.
chemical structure of BZ
a benzene ring joint to a 7 membered 1,4 diazepine ring (N on C1, 4)
how do the R1-8 substituents of the ring influence BZ’s PK
- affinity to allosteric GABAa rec (b.w a and gamma subunit)
- efficacy
what is the efficacy for GABAa, BZ agonist/ inverse agonist / antagonist
BZ agonist- 100% efficacy in enhancing GABA response
BZ inverse agonist- negative -100% efficacy in opposing GABA repsonse
antagonist- 0% efficacy, as unable to activate the rec
BZ can modulate GABA response only when…
GABA is present
what are GABA inverse agonist used for clincally and why
inverse agonist- reversal of respiratory depression.
GABA response is inhibitory
inverse agonist gives opposite GABA response which is stimulatory
what are the use of BZ agonists? give exmaples
anxiolytic - diazepam, clonzepam
Pre op sedation -midazolam
what are the side effects of BZ (MS-double-A-W)
memory loss - useful pre-op med for anaesthesia. BUT Flunitrazepam used to spike drinks
sedation- on target s/e bc CNS depression
abuse - build up tolerance
addiction - not psychological drug seeking but bc of anxiety relief
withdrawal syndrome - physical dependence with long term: irritability, insomnia, dsyphoria = similar to anxiety sym that we trying to trt
major clinical uses of BZ
their MOA
anxiolytic- diazepam, lorazepam
sedative
hypnotic- nitrazepam, flurazepam, temazepam
(increasing CNS depression)
enhance GABAnergic inhibitory effect on the brain, cause CNS depression
3 Sub-classes of BZs
2-keto–> longest half life 40h, keto gp oxidised in liver- active metab- oxidised again
3-hydroxyl–> shortest half life, not metabolised but conjugated with glucuronide and rapidly excreted
triazole–> moderate half life, oxidised in liver but fewer active metabolites
is BZ long term or short term trt option for anxiety
short term ONLY to avoid w/d
adjunct to AD
Drug interactions of BZ
similar CNS depressants e.g. ethanol, barbiturates –> additive effect
Inhibitors of cytochrome P450 (3A3/4)- phenytoin –> metab by oxidation in liver
why does alcohol cause mood elevation when it is a CNS depressant
apprently stimulatory effect caused by depression of inhibitory control mechanism in brain
why do we sleep?
Cortical recovery Organizing/storing memories Metabolism/weight homeostasis Sleep deprivation may provide clues (dizzy, visual disturbances) Cortex is always active and alert
Electroencephalogram (EEG) records
the activity of populations of neurones
what are the eeg rthymns?
fast- alpha, beta- high amp
slow- delta, theta
