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SIU5 Neurology > Anxiety > Flashcards

Anxiety Flashcards

1
Q

what is anxiety?

A

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

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2
Q

what are the different types of anxiety?

A

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))

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3
Q

DSM criteria for generalized anxiety disorder include:

A

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

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4
Q

Core features of anxiety disorders are common which are NPA

A

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

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5
Q

describe the innate/ secondary pathway of feeling anxious

A

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

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6
Q

aetiology of anxirty disorder (GAD)

A
  • 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
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7
Q

trt for GAD

ABB

A

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

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8
Q

functions of BB (antihypertensive) in GAD

A

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

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9
Q

BZ and barbiturates e.g pentobarbital, which is safer and why

A

BZ is safer
both give relief of anxiety but BZ make you fully aware of the environemnt. barbiturates- NOT in touch with the environement.

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10
Q

chemical structure of BZ

A

a benzene ring joint to a 7 membered 1,4 diazepine ring (N on C1, 4)

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11
Q

how do the R1-8 substituents of the ring influence BZ’s PK

A
  • affinity to allosteric GABAa rec (b.w a and gamma subunit)

- efficacy

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12
Q

what is the efficacy for GABAa, BZ agonist/ inverse agonist / antagonist

A

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

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13
Q

BZ can modulate GABA response only when…

A

GABA is present

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14
Q

what are GABA inverse agonist used for clincally and why

A

inverse agonist- reversal of respiratory depression.
GABA response is inhibitory
inverse agonist gives opposite GABA response which is stimulatory

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15
Q

what are the use of BZ agonists? give exmaples

A

anxiolytic - diazepam, clonzepam

Pre op sedation -midazolam

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16
Q

what are the side effects of BZ (MS-double-A-W)

A

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

17
Q

major clinical uses of BZ

their MOA

A

anxiolytic- diazepam, lorazepam
sedative
hypnotic- nitrazepam, flurazepam, temazepam
(increasing CNS depression)
enhance GABAnergic inhibitory effect on the brain, cause CNS depression

18
Q

3 Sub-classes of BZs

A

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

19
Q

is BZ long term or short term trt option for anxiety

A

short term ONLY to avoid w/d

adjunct to AD

20
Q

Drug interactions of BZ

A

similar CNS depressants e.g. ethanol, barbiturates –> additive effect
Inhibitors of cytochrome P450 (3A3/4)- phenytoin –> metab by oxidation in liver

21
Q

why does alcohol cause mood elevation when it is a CNS depressant

A

apprently stimulatory effect caused by depression of inhibitory control mechanism in brain

22
Q

why do we sleep?

A 
Cortical recovery
Organizing/storing memories
Metabolism/weight homeostasis
Sleep deprivation may provide clues (dizzy, visual disturbances)
Cortex is always active and alert
23
Q

Electroencephalogram (EEG) records

A

the activity of populations of neurones

24
Q

what are the eeg rthymns?

A

fast- alpha, beta- high amp

slow- delta, theta

25
Q

describe the stages of sleep

A

repeated cycles of REM and non-REM

each cycle has a shorter and shallower (no longer reach stage 4) non REM period and longer REM

26
Q

REM SLEEP

A 
EEG shows brain is awake
high oxygen consumption of brain
Vivid dreaming
Loss of skeletal muscle tone (atonia)
Bursts of rapid eye movements
Sympathetic predominates- high hr, rr
"an active hallucinating brain in a paralyzed body"
27
Q

NREM SLEEP

A

a rest period (better to take longer nap and get to this stage)
Muscle tension reduced, - Leg twitching
Body temperature lowered
Energy consumption lowered
Increase in parasympathetic (rest and digest)
Brain rhythms slow (“slow wave sleep”), larger amp, delta rthymn
“a resting brain in a movable body”

28
Q

Brain mechanisms of sleep

A

RAS- THALAMUS- CORTEX
Ascending reticular activating system (RAS)
Locus coeruleus – noradenaline
Raphe nuclei – serotonin
Brainstem/forebrain – acetylcholine
Midbrain – histamine
high Firing of these neurons = awakening
low Firing of these neurons = falling asleep

29
Q

REM-on cells are

REM-off cells are

A

(acetyl)cholinergic neurons in the brainstem

serotoninergic and noradrenergic neurons in the brainstem

30
Q

what is the name of Subjective rating scale for sleepiness

A

Epworth sleepiness scale

31
Q

use of hypnotic

A
  • intermittent (for reccurent short term insomnia)
  • short term (< 2 weeks) if daytime impairment is severe
  • tolerance may develop
  • withdrawal syndromes
32
Q

Treatment aims to

A

shorten time to sleep, increase total duration of sleep, maintain the structure of REM cycle

33
Q

what are the Non-benzodiazepine hypnotics

-MOA

A

Zaleplon, zolpidem, zopiclone (“Z drugs”)

  • bind to GABAA receptor, gabanergic, CNS depressant
  • short action, no rebound insomnia, less w/d, may dependent
34
Q

sleep regulating sub

A

Interleukins (ILs) immune mediators- (sleep inducer) if fighting off infections, body needs time to repair by sleeping
Melatonin derived from 5-HT in endocrine pineal gland- (sleep inducer) MA hormone NT, production is switched on at night time in the dark, switched off in morning.
Hypocretin-orexin (2 names 1 protein)
Hypothalamic neuropeptide (sleep inducer) regulates appetite, metabolism- orexingenic, stimulate feeding and sleeping.
Stimulants e.g. caffeine, cocaine, amphetamine- external mostly. Increase NA (and 5HT) release, keep alert.

35
Q

Benzodiazepine hypnotics
Long acting - 2 keto
Short acting - 3 oh

A

diazepam, nitrazepam and flurazepam

temazepam/ Restoril, triazolam/ Halcion

36
Q

Over the counter “sleep remedies”

important to make sure pt is not…

A 
Antihistamines 
Promethazine (Phenergan)
Diphenhydramine (Nytol)
‘Natural remedies’
Melatonin (Circadin) short ½ life, extended release product needed.
Chamomile tea ?
Lavender? 
Evening primrose oil?
Valerian? herbal sedarting essential oils 
Not very evidence based
pt is not taking any CNS suppresant POM

SIU5 Neurology (13 decks)

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