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Module- CNS Flashcards

1
Q

Anxiety definition

A

refers to a state of tension, apprehension, or uneasiness that stems from the anticipation of danger - the source of which is largely unknown or unrecognized

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2
Q

Anxiety Disorder definition

A

When anxiety impairs a person’s ability to engage in normal day-to-day functions

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3
Q

T or F:

There are clear bounds between normal and abnormal anxiety

A

False

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4
Q

What is an anxiety disorder?

A

Any disorder that shares features of excessive fear and anxiety accompanied by behavioural disturbances.

They differ from one another in the types of objects or situations that induce this anxiety.

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5
Q

How are anxiety disorders diagnosed

A
  • Diagnosis should only be made when the client’s behaviours symptoms cannot be better explained by another mental disorder or attributed to the physiological effects of an existing medical condition or to the adverse effects of a substance or medications
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6
Q

Separation Anxiety Disorder

A

Feelings of fear or anxiety about separation from attachment figures

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7
Q

Selective Mutism

A

Consistent failure to speak in social situations where speaking is expected

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8
Q

Specific Phobia

A

Fearful or anxious feelings about a particular situation or object

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9
Q

Social Anxiety Disorder

A

Fear, anxiety and avoidance of social interactions and situations

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10
Q

Panic Disorder

A

Intense feelings of immediate apprehension, terror, or impending doom accompanied by increased autonomic nervous system activity

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11
Q

Agoraphobia

A

A fear of open spaces; trying to escape and concerns that help might not be available

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12
Q

Generalized Anxiety Disorder

A

Anxiety symptoms are the physiology consequence of another medical condition

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13
Q

Substance or medication-induced anxiety disorder

A

Anxiety due to intoxication or withdrawal from a substance or prescribed medication

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14
Q

Pathophysiology of anxiety

A

· Norepinephrine is an excitatory neurotransmitter
· Gamma-aminobutyric acid (GABA) is an inhibitory neurotransmitter
· Stimulation of the Hypothalamus-Pituitary-Adrenal (HPA) axis induces, corticotropin-releasing factor (CRF) release.

CRF release stimulates the locus ceruleus and induces norepinephrine release thereby activating the limbic system and cerebral cortex.

This generates the feelings of anxiety

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15
Q

What is the Cerebral Cortex

A
  • The “thinking” or conscious portion of the brain.
  • This brain region processes sensory inputs, regulates voluntary muscle action,
  • is responsible for intellect, memory, learning, decision making, and other higher level brain functions
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16
Q

What is the Locus ceruleus

A

A brain stem nucleus that contains many noradrenergic neurons and has extensive projections to the limbic system, cerebral cortex and cerebellum

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17
Q

What is the limbic system?

A

An area in the middle of the brain responsible for emotional expression, learning and memory. Includes the amygdala (not shown)

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18
Q

What is the Hypothalamus

A

Responsible for unconscious responses to stress such as elevated blood pressure, respiratory rate, and dilated pupils

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19
Q

GABA Hypothesis

A

People with anxiety disorders release an excess of the excitatory neurotransmitter norepinephrine in response to normal stimuli

In combo with a deficiency in GABA release we see an exaggerated response htat is disproportioned to the threat of the activity

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20
Q

What is GABA? Where are thier receptors located?

A

· GABA serves as the major inhibitory neurotransmitter the brain and spinal cord
· Their receptors are located throughout the brain, and are associated with chloride channels

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21
Q

What is the effect when GABA binds to their receptor

A

When GABA binds to its receptor, the channel opens, allowing chloride to move into the neuron

Movement of chloride ions across the membrane hyperpolarizes the neuron

As a result, the cell membrane is less responses to excitatory neurotransmitters such as norepinephrine

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22
Q

role of the Reticular Activating system

A

Stimulation of the RAS produces increased alertness and arousal

Inhibition of the RAS results in sedation and sleep

Proper functioning of this system is vital for us being alter and sleeping when needed

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23
Q

What innervates the RAS, What does this cause?

A

The HPA axis innervates the reticular activating system.

When stimulated, the RAS activates the cerebral cortex resulting in increased alertness and arousal

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24
Q

Two results of the Activation of the hypothalamus

A
  1. Increased limbic activity thereby producing an increased fear and anxiety response
  2. Increased reticular activating system activity, which results in increased alertness and an interrupted sleep pattern
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25
True or False: the RAS stimulation can account for both the increased risk of sleep disturbances and the finding that people find it harder to get a good nights sleep
true
26
How is Insomnia characterized?
characterized by a dissatisfaction with sleep quantity or quality, associated with one (or more) of the following symptoms: 1. Difficulty initiating sleep, 2. Difficulty maintaining sleep, characterized by frequent awakenings or problems returning to sleep after awakenings or, 3. Early-morning awakenings with an inability to return to sleep
27
True or false: Episodic or behavioural insomnia is often attributed with mood disorders?
No Normally attributed to normal stressors or specific activities that can interfere with sleep. mood disorder = long term, persistent insomnia
28
causes of long-term + persistent insomnia
mood disorders such as depression, anxiety disorders, bipolar disorder or chronic pain due to illness
29
How long does Episodic or behavioural insomnia last for?
Symptoms last at least 1 month, but less than 3 months
30
what is the recommended first line of treatment for situational anxiety and episodic insomnia?
non-pharmacological therapies such as changes in lifestyles, medication, exercise and improved diet are often sufficient to relive mild cases
31
True or false: | Antidepressants are prescribed for the short-term treatment of anxiety disorders
False For long-term treatment
32
What are prescribed for the short-term treatment of anxiety and insomnia?
Selective central nervous system depressants Ex. Benzodiazepines
33
Long half-life benzodiazepines: who are they better and worse for?
Benzodiazepines with a long half-life produce active metabolites & accumulate in plasma Better for: those with anxiety disorders as longer half-life can stabilize mood and reduce risk of withdrawal symptoms Worse for: elderly, those with insomnia and those with impaired liver function
34
who are Short half-life benzodiazepines not suited for?
· Poor choice for anxiety treatment as it has a short effect and can experience spurts of anxiety between doses
35
What are the differences in benzos based on?
1. plasma half life 2. production of active metabolizes 3. clinical uses
36
What are Anti-anxiety drug vs. Sedative-hypnotics used to treat?
Sedative-hypnotics = Insomnia Anti-anxiety drug = anxiety
37
How do benzodiazepines work?
Inhibit GABA neurons, which decreases neuron firing When they bind to the receptor, the activity of GABA at its receptor in enhanced, increasing the entry of chloride ions into the neuron This causes hyperpolarization Enhances inhibitory effects of GABA to relive anxiety, tension and nervousness and to produce sleep
38
Why are benzos well absorbed with oral administration?
Highly lipid soluble + Highly bound to lipid proteins
39
What benzos can be administered through IV
Diazepam, lorazepam and midazolam
40
how are ·long plasma half-life Benzodiazepines metabolzied and what does this mean for the client?
metabolized in the liver by Cytochrome P450 enzymes into active metabolites, conjugated through glucuronidation into highly water-soluble inactive metabolites that are then excreted via the kidneys no appropriate for elderly, those with liver disease or for use with drugs that inhibit oxidation
41
Why do most short half-life benzodiazepines undergo glucuronic acid conjugation only?
They do not produce active metabolites
42
Administration of benzos
Lowest effective dose should be used to avoid adverse effects (Like daytime drowsiness and impaired mobility) Can be increased based on patient response to relieve symptoms while avoiding adverse drug effects
43
True or false: | Benzodiazepines show effect on mood 1-3 days after administration
false Does not show an effect on mood until approx. 4- 6 weeks after administration
44
Insomnia and Benzodiazepines
Benzodiazepines should be taken on an as needed basis Daily benzodiazepine use worsens insomnia + increases risk of dependence Benzodiazepines lose their effectiveness at producing sleep after 2 - 4 weeks of daily use
45
Adverse Effects of Benzodiazepines
· Over sedation · Dizziness · Confusion · Impaired mobility
46
Why are effects are rare with benzodiazepines? when can they happen?
Effects are rare when mediation is taken as prescribed o Effects are more commonly seen in the elderly due to impaired drug metabolism and excretion o Elderly can become agitated, confused, and irritable with use o Can be confused with dementia
47
What is rebound insomnia? when does it occur
· Occurs with abrupt discontinuation of the drug · Symptoms of insomnia and anxiety worsen within the first 2 days of drug discontinuation · Increases the risk of dependence to benzodiazepines · Effects are reversed once drug administration is resumed
48
What is flumazenil used for?
Flumazenil is a benzodiazepine antagonist used for the management of benzodiazepine overdose Once administered, client may awaken abruptly with dysphoria, agitation, anxiety, cardiac arrhythmias and seizures o Should be used cautiously
49
Does flumazenil reverse the depressed respiration characteristic of overdose?
no, must be managed separately
50
Symptoms of benzodiazepine withdrawal and how long they last
· Increased heart rate, loss of appetite, tremor, abdominal and muscle cramps, vomiting, sweating, insomnia, agitation, anxiety and panic · Symptoms can persist for 2 - 4 weeks
51
when are the most severe withdrawal symptoms seen?
· Severe symptoms are seen with short acting benzos like lorazepam and triazolam unless they are gradually discontinued · Long acting symptoms might not appear until 4-5 days after discontinuing the drug due to their longer half life
52
Why does the client get a physical dependance to benzos?
· An altered physical condition caused by the nervous system adapting to repeated substance use · Over a prolonged period of time, the cells of the body function as though it is normal for the drug to be continually present · Thought that it could be because of the abrupt separation of the benzo molecules from their receptors, resulting in a acute decrease in GABA transmission Less GABA = Less inhibition of the central nervous system = hyperarousal
53
how long do you need to taper benzos for to prevent withdrawal?
· Need to taper use for 4 - 16 weeks to prevent withdrawal
54
Important considerations: age
sedative-hypnotic drugs like benzodiazepines are metabolized and excreted more slowly in older adults, and thus accumulate in the plasma easily. elderly patients are at an increased risk of developing adverse effects to the drug.
55
Important considerations: Gender
Women are prescribed benzodiazepines at twice the rate as men. dependence is unrecognized in approximately 75% of women who are addicted to the drug.
56
Important considerations: short vs. long acting
Benzodiazepines with a short half-life are associated with an increased risk of dependence, compared to benzodiazepines with a longer half-life
57
Important considerations: daily administration
should only be taken on an "as needed basis" for the treatment of insomnia. Daily administration worsens insomnia and increases the risk of dependence
58
Important considerations: Abrupt discontinuation
Results in "rebound insomnia" Patients who abruptly discontinue their prescription are at increased risk of experiencing withdrawal effects of the drug and are more likely to resume the medication, thereby increasing their risk for benzodiazepine dependence
59
Important considerations: Inappropriate prescription
CNS depressants should never be the first line of therapy for insomnia, especially if the cause can be so clearly identified (grief associated with the loss of her husband).
60
Role of the Nurse in Benzodiazepine Therapy
Patient monitoring and education related to drug regimen · Assess patient's need, including intensity and duration of symptoms · Identify factors that precipitate patient's anxiety or insomnia · Drug history · Assess likelihood for drug abuse or dependence · Assess patients for side effects
61
Which type of anxiety manifests with other mental illnesses such as depression or psychosis
Panic disorders
62
T/F: Generalized anxiety is known as anxiety that lasts for 6 months or more
TRUE
63
T/F: Generalized anxiety interferes with ADLS
TRUE
64
Who is more likely to experience GAD? and what age group?
- women | - 20-35 age group
65
anxiety disorders related to other medical conditions
- asthma - arthritis - ulcers - hypertension
66
In anxiety which substance is being overstimulated and which is being understimulated?
- excitatory NE is being overstimulated | - GABA is being understimulated
67
Where is nor epinephrine released from?
locus coeruleus
68
What is the stress response mediated by?
HPA axis
69
What neurotransmitter is being inhibited? Which is being excitatory?
- excitatory is NE | - inhibitory is GABA
70
Stimulation of RAS results inn
alertness and arousal
71
Inhibition of RAS results in
sleep and sedation
72
Which is insomnia more prominent in? Men or women?
Women
73
T/F: the first line of therapy for treatment of insomnia or anxiety is pharmacological
false: should only be used if it is significantly impacting ADL'S
74
Which drug class is used for chronic anxiety and persistant insomnia
antidepressants
75
T/F: non benzodiazepines anxiolytics are used for insomnia
true
76
Where are effects of diazepam pronounced?
amygdala in temporal lobe
77
How is flumazenil admin?
RAPID IV INFUSION
78
T/F: Severe withdrawal symptoms are not associated with short acting benzos
false: most often associated with short acting
79
How should benzos withdrawal symptoms be prevented?
- slow tapered in dose and gradually discontinued | - reduce does by 10-25% each week for 4-16 weeks

PHARMACOLOGY (27 decks)

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