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Sem 3, Case 5 (stroke, memory and GAD) > GAD > Flashcards

GAD Flashcards

1
Q

What structures make up the lambic system?

A

Hippocampus
Amygdala
Thalamus
Hypothalamus
Cingulate gyrus

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2
Q

Define GAD…

A

A condition of stress/anxiety that is persistent, excessive and disproportionate/unrealistic

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3
Q

Which area of the brain integrates the emotional response from the limbic system into the process of decision making?

A

The prefrontal cortex

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4
Q

Which area of the brain is overactive in GAD?

A

The amygdala

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5
Q

How does GABA relate to GAD?

A

A reduction of GABA causes decreased inhibition to the Amygdala
This causes overactive amygdala, releasing more stress hormones/increased fear response
= disproportionate/unnecessary anxiety

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6
Q

What is the pathophysiology of GAD?

A

Dysregulation (decrease) in GABA-A secretion
This causes reduced inhibition on the amygdala
Causes amygdala to become over active
Generates a disproportionate/unnecessary stress and fear response

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7
Q

Which neurotransmitter is associated with GAD?

A

GABA-A

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8
Q

What is the increased risk of GAD if a first degree relative has GAD?

A

2.5x increased risk

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9
Q

What factors cause an increased chance of GAD?

A

Genetic:
- first degree relative has GAD
- mutations in the chromosomes: 2p21 and 2q12

Environmental:
- childhood trauma (parental neglect or over-control)
- major distressing life events

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10
Q

What must the symptoms cause in order to be diagnosed with GAD?

A

Significant distress
Impairment of daily functioning

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11
Q

What are the DSM5 criteria for a diagnosis of GAD?

A
  1. Persistent fear and worry
  2. Plus at least 3 of:
    • poor concentration
    • restlessness
    • fatigue
    • muscle tension
    • initial insomnia (difficulty getting to sleep)

Symptoms must be prevalent for 6+ months

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12
Q

How long must symptoms have persisted for in order to diagnose GAD?

A

6+ months

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13
Q

What are 3 other conditions that could be misdiagnosed as GAD?

A
  1. Alcohol/drug misuse
  2. Hypothyroidism
  3. Phaecochromocytoma (adrenal gland cancer)
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14
Q

What are some psychological symptoms of GAD?

A
  • constant worries/intrusive thoughts
  • feelings of apprehension and dread
  • poor concentration
  • depersonalisation, derealisation (if severe GAD)
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15
Q

What are some physical symptoms of GAD?

A
  • tremors, butterflies, palpitations
  • sweating
  • dry mouth
  • muscle tension, tension headaches
  • hyperventilation (difficulty taking breath, stabbing chest pain, parasthesia)
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16
Q

What are the features of hyperventilation?

A
  • difficulty taking a breath
  • “atypical” chest pain = stabbing, non radiating, not central (usually on left)
  • parasthesia in hands, feet, lips
  • respiratory acidosis
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17
Q

What are some behavioural symptoms of GAD?

A
  • putting things off because of anxiety
  • avoiding particular situations
  • self medication to relieve anxiety (alcohol, drugs)
18
Q

What is the epidemiology of GAD?

A
  • Almost 2x more common in women
  • median onset age = 30
  • most common diagnosis in young adult life
  • most commonly recognised due to physical symptom presentation
19
Q

What is the most common mammalian structure of the GABA-A receptor?

A

Subunits:
2x alpha-1
2x beta-2
1x gamma-2

Chloride ion in middle

20
Q

Describe the (chemical) synthesis of GABA?

A

Glutamate (Glutamic acid) => decarboxylase => GABA

21
Q

How is GABA removed from the synapse?

A

Re-uptake into PRE-SYNAPTIC terminal and surrounding GLIAL CELLS

22
Q

What are the 2 classes of GABA receptors?

A

GABA-A
GABA-B

23
Q

How does GABA binding to GABA-A receptors cause hyperpolarisation (inhibition)?

A

GABA-A receptor structure = 5 subunits surrounding a chloride ion

  • GABA binds to receptor
  • activating chloride ions to travel through into neurone
  • decreases charge inside neurone = hyperpolarisation
24
Q

What are the main treatment options for GAD?

A
  • medication (diazepam, pregabalin, SSRIs, SNRIs, TCAs)
  • psycho therapies (CBT, counselling, group therapy)
  • lifestyle changes (exercise, avoiding caffeine/alcohol etc)
25
Q

What is the maximum amount of time a person can be on benzodiazapines for?

A

No longer than 2 weeks

(They are very addictive)

26
Q

How long does NICE recommend a course of CBT should be for GAD?

A

12-15 hour long sessions over 4 months

27
Q

What % of GAD patients respond well to CBT?

A

60%

28
Q

Compare medication Vs CBT in efficacy of treating GAD?

A

Both have similarly high efficacy!

Recommended to use both for best results
Means treatment route is a patient decision as both are effective methods

29
Q

What is the action do benzodiazepines in GAD?

A

Positive allosteric modulator of GABA-A receptor = INCREASES GABA ACTION

Binds to allosteric site on GABA-A
UP-regulates GABA action
= increases chloride transmission
= restores inhibitory action of GABA

30
Q

What is the first-line pharmacological treatment for GAD? Why?

A

SSRIs

  • not addictive
  • fewer side effects
  • safer in overdose
31
Q

Describe what a course of SSRIs would entail?

A
  • effective after 1-2 weeks of use
  • continue for at least 6 MONTHS if effective
  • mild withdrawals = TAIL OFF at end of course
32
Q

What are the side effects of SSRIs?

A
  • nausea, diarrhoea
  • sexual dysfunction
  • dry mouth
  • dizziness
  • loss of appetite
  • insomnia
33
Q

In what’s % of GAD cases are SSRIs effective?

A

70%

34
Q

What other conditions can be treated by Pregabalin?

A
  • Epilepsy
  • Neuropathic pain

Pregabalin = anticonvulsant

35
Q

What is the MOA of pregabalin?

A
  • Decreases release of glutamate, Substance P and NA (excitatory)
  • Similar structure to GABA

Specific action is unknown

36
Q

What is the main difference between each benzodiazepine drug?

A

The length of their half life

  • diazepam = 30 hours
  • triazolam = 2 hours
37
Q

How quickly do the effects of benzodiazepines kick in in GAD?

A

Within 30-60 mins

38
Q

What are side effects of benzodiazepines?

A
  • addiction/dependence (withdrawal can include seizures)
  • tolerance
  • sedation
  • impaired cognition
39
Q

What are Beta-Blockers effective at treating in GAD?

A

PHYSICAL symptoms (tremors, sweating…)

Not psychological

40
Q

What is the MOA of beta-blockers?

A

Beta-adrenergic ANTAGONISTS on smooth muscle (heart…)

41
Q

Name one condition that beta-blockers are contraindicated in?

A

Asthma

42
Q

What is agoraphobia?

A

Fear of crowded places

Sem 3, Case 5 (stroke, memory and GAD) (3 decks)

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