WK 4: Delirium&Dementia/Depression/Pain/Sz Flashcards

1
Q

how does delirium present in a patient?

A

transient acute confusional states that can come on abruptly or gradually over time
-usually associated with other medical conditions

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2
Q

What are the two main types of delirium states?

A

hyperactive
hypoactive

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3
Q

what is HYPERactive delirium?

A

Acute ( happens quickly ) disturbance in attention/awareness
-develops in 2-3 days
“excited delirium”/combative

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4
Q

what are some examples of patients who might experience hyperactive delirium?

A

ICU pt, post surgery, someone withdrawing, hospitalized elderly

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5
Q

what are some risk factors associated with hyperactive delirium?

A

medications (benzos/narcotics)
acute infection/ if a pt is septic
surgery
hypoxia
electrolyte/ metabolic dysfunction
insomnia

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6
Q

what are some manifestations that can occur due to hyperactive delirium?

A

restlessness, irritability, difficulty concentrating, insomnia, tremulous, poor appetite.
-distressed, very confused

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7
Q

how does a person with hyperactive delirium think?

A

They cannot rationalize and are usually completely inattentive with a grossly altered perception of what is happening.

(physical symptoms: diaphoretic, tachycardia, increased temperature, and dilated pupils)

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8
Q

hyperactive delirium can lead to __________, which can cause death. along with symptoms of combativeness, aggression, pain and rapid breathing.

A

excited delirium syndrome (ExDS)

(most common in those with mental illness or drug abuse)

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9
Q

how long do hyperactive delirium states last?

A

2-3 days then they resolve on their own

-occasionally if in the hospital it can last a few weeks

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10
Q

what is HYPOactive delirium?

A

assoc. with right sided frontal basal-ganglion disruption (coordination/movement).
-common with liver/kidney failure pt
“catatonic” delirium, obtunded

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11
Q

some manifestations of hypoactive delirium

A

decreased alertness & attention span, decreased ability of perception/interpretation of the environment, forgetfulness, apathetic, slow speech, frequently falls asleep

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12
Q

what the the goal for treating someone with delirium?

A

to identify the cause and remove it
-> modify any risk factors
Trx with anti-psychotics

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13
Q

What is the difference between delirium and dementia?

A

delirium is preventable, acute, and treatable
dementia is unavoidable and usually progressively worsens

BUT pt’s with dementia are MORE likely to have delirium

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14
Q

what is dementia?

A

progressive failure of cerebral functioning
-memory, language, judgement, decision making, and orientation all may be impaired
-Sx are irreversible
-causes not fully understood

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15
Q

how does one develop dementia?
pathophysiology

A

neurons degenerate, brain tissue compresses, atherosclerosis of cerebral vessels, brain trauma, infection, or neuro-inflammation
-can have a genetic predisposition

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16
Q

treatment for dementia

A

no cure
-Trx directed at optimizing functional capacity and accommodating to loosing abilities

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17
Q

what are the four types of dementia?

A
  1. Alzheimer’s (most common)
  2. Vascular
  3. Lewy Body
  4. Frontotemperal

*can have a combo of more than one kind

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18
Q

what is the leading cause of severe cognitive dysfunction in elderly?

A

Alzheimer’s Dz (AD)

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19
Q

What is the process of diagnosing someone with Alzheimer’s dz?

A

by ruling out other conditions that could be causing the same Sx: tumors, meningitis, etc..

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20
Q

What are some risk factors for Alzheimer’s Dz?

A

> 65 y/o
FHx
inheriting genes from family
existing mild cognitive impairment
down syndrome
unhealthy lifestyle
previous head trauma
being shut off from the community

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21
Q

who is at a higher risk for AD?
1. a 55 y/o female that is obese due to being sedentary and lives alone in an apartment.
2. an 88 y/o male who’s mother has AD. He currently lives with his wife and son.
3. a 66 year old male with down syndrome who lives with his caretaker and is on a bland diet.
4. a 77 year old male with a the gene for AD, but denies any immediate family that he knows of with the condition. He lives alone 50 miles outside of Lexington.

A

4 is the highest risk

  1. Unhealthy lifestyle, lives alone
  2. age, FHx
  3. age, down syndrome
  4. age, inherited gene, and shut off from community
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22
Q

what do tau protein do?

A

facilitate nerve cell degeneration

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23
Q

pathophysiology of AD

A

build up of neuritic plaques
neurofibrillary tangles of tau protein
plaque disrupts nerve impulse transmission -> kills neurons (mainly in cerebral cortex and hippocampus/ areas related to memory)
leads to brain atrophy
changes occur over decades

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24
Q

vascular dementia

A

-2nd most common
-r/t cerebrovascular dz
-r/t large artery Dz, cardioembolism, small vessel dz, strokes
pretty much anything that can cause hypo-perfusion to the brain

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25
Q

what are some risk factors for vascular dementia?

A
  1. DM
  2. HPL
  3. HTN
  4. being a smoker
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26
Q

frontotemporal dementia

A

familial association w/ age onset <60
rare
r/t gene mutation of encoding the tau protein

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27
Q

what are the three clinical syndromes related to frontotemporal dementia

A

1.behavioral variant
2. progressive non-fluent behavior
3. semantic dementia

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28
Q

what are two medications that can aid in the treatment of dementia?

A

Donepezil and Memantine
they slow the progression, neither are cure, don’t help longterm

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29
Q

when is the best time to give donepezil?

A

at bedtime best to eat with food to minimize GI effects

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30
Q
  1. which medication is better for moderate to severe AD?
  2. which medication is better for mild to moderate AD?
A
  1. memantine
  2. donepezil
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31
Q

what are neurotransmitters?

A

chemicals that enable neurotransmission, path of electrical impulses from neuron to neuron

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32
Q

what are the four major neurotransmitters?

A
  1. dopamine
  2. norepinephrine
  3. serotonin (5HT)
  4. GABA

imbalance in one can affect the other

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33
Q

deficits in dopamine lead to what symptoms/ reactions?

A

-parkinson-like symptoms: slow reaction time, anergia (abnormal lack of energy)
-anhedonia: “pleasure center” dysfunction. inability to experience pleasure

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34
Q

deficits in serotonin lead to what symptoms/reactions?

A

-OCD sx: obsessive thoughts, compulsive behavior
-impulsivity: suicide, aggression, susceptibility to “cue triggers”

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35
Q

GABA dysfunction is associate with what kind of disorders?

A

anxiety disorder
panic disorders
and recently major depressive disorder

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36
Q

NOREPI is an excitatory neurotransmitter that is associated with what?

A

fight or flight response

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37
Q

high levels of NOREPI are associated with what symptoms?

A

anxiety, stress, hyperactivity

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38
Q

low levels of NOREPI are associated with what symptoms?

A

lack of energy, focus or motivation

low=lack of

39
Q

what is the diagnosis requirement for depression?

A

presence of symptoms intense enough to cause distress and persistently impair psychosocial functions

40
Q

Sx of depression

A

loss of interest/ pleasure
fatigue
restlessness, irritability
impaired concentration
low self esteem
negative thinking
sleep disturbances
appetite disturbances

-these Sx interfere with living

41
Q

how does someone treat their depression?

A

-medications
-psychotherapy
-psychoeducation
-support groups
-brain stimulation

*best treatment is a combo of treatments

42
Q

panic disorder is characterized by what two psychological symptoms?

A
  1. anticipatory anxiety: fearful expectation of panic anxiety onset
  2. avoidance anxiety: personal strategies to decrease risk of panic anxiety and increase feeling of control
43
Q

overwhelming stress can induce circulating stress hormones which stimulates _______, the must abundant neurotransmitter

A

glutamate

44
Q

how would you describe “panic”

A

unexpected & out of proportion reaction to events happening to or around the patient.

45
Q

panic attack symptoms

A

palpitations, CP, SOB, dizziness, N, fear of loosing control, tingling of extremities, flushing, chills

46
Q

what are some treatments used for panic disorders ?

A

cognitive behavioral therapy
anti-depressants
Benzo’s (second line/acute situations)

47
Q

generalized anxiety disorder

A

chronic
anxiety >6 Mo
excessive/uncontrolled/unrealistic worry

48
Q

Physical Sx of generalized anxiety disorder

A

muscle tension, autonomic hyperactivity, exaggerated startle, difficulty concentrating

49
Q

risk factors for developing generalized anxiety

A

-excessive substance use
-childhood abuse/family trauma
-genetics

50
Q

Trx for generalized anxiety disorders

A

-cognitive behavioral therapy
-anti-depressants (SNRI/SSRI)
-Buspirone
-benzo’s (acute)

51
Q

what are the three main/core symptoms of PTSD?

A

hyper-arousal
avoidance of reminders
experiencing the events

52
Q

definition of PTSD

A

the chronic activation of stress response in relation to exposure to potentially life threatening event (fight or flight is always on)
-affects: memory, sleep, depression issues
-includes: flashbacks, nightmares, emotional blunting, irritability and exaggerated startle

53
Q

PTSD treatments

A

psychotherapy
EMDR
SSRI/SNRI medications

54
Q

what is social anxiety disorder?

A

intense fear of being criticized by others
-fear of humiliation
-withdraw from situations or experiences with intense discomfort

55
Q

caused of social anxiety disorder

A

-inherited trait
-brain structure
-environment/ learned behavior

56
Q

Trx of social anxiety

A

-cognitive behavioral therapy
-SSRI
Benzos
propranolol (1-2hrs before activity)

57
Q

OCD

A

repetitive unwanted thoughts/obsessions
repeated activities/rituals
compulsions
time consuming and distressing to Pt

58
Q

what are some subtypes of OCD

A

cleaning compulsion
hoarding
symmetry obsessions
harm obsessions
obsessions without visible compulsions

59
Q

what are the four classifications of antidepressant medications that we need to know?

A

SSRI
SNRI
TCA
MAOI

60
Q

what are some general considerations the nurse needs to discuss/ go over when a patient is taking an antidepressant ?

A

-SSRI and SNRI are first line treatment
-all take 4-8 wks to work efficiently
-assess SI risk/ mental imbalance

61
Q

what is the MOA for SSRI medications

A

inhibitors of serotonin at nerve endings
= increased amount of serotonin available

62
Q

what is the MOA for SNRI medications?

A

blocks neuronal activity of serotonin and norepinephrine

63
Q

when a patient is on an SNRI medication, what kind of lab value should you check?

A

LFT’s, which is a liver function test
-not a good medication for Pts with liver issues

64
Q

TCA’s are an older generation of antidepressant medications and not typically used because ?

A

they can caused fatal overdoses. if patient has increased SI it is not a good option for them

65
Q

what is the MOA of TCA medications?

A

blocks reuptake of norepinephrine and serotonin, making them more available in the synapse

66
Q

anticholinergic side effects

A

hot as a hare
dry as a bone
blind as a bat
red as a beet
mad as a hatter

67
Q

What is the MOA of an MAOI drug?

A

inhibits MAO enzymes found in the liver, intestinal walls and terminals of neurons
-decreased MAO increases availability of neurotransmitters at nerve endings

68
Q

what are the three atypical antidepressents?

A

buproprion
ketamine
trazadone

69
Q

what is the MOA of benzodiazepines?

A

they enhance the inhibitory effects of GABA (relaxation)

70
Q

what are some nursing considerations when using Bezo’s?

A

-teratogenic
-schedule 4 drug
-cant mix with other drugs that ALSO decrease CNS
-avoid grapefruit and fatty foods

71
Q

what is the antidote to Benzo’s?

A

flumazenil

72
Q

substance use disorder

A

rewarding effects of drugs from large amount of dopamine getting released
-mimics and enhances pleasure response

73
Q

T/F: if someone suffers from substance use disorder, then becomes sober, they are unable to gain back function in their brain that was previously lost

A

false
function can be gained back

74
Q

what are some treatment options for a person suffering from substance use disorder?

A

cognitive behavior therapy
medications
motivation enhancement therapy
family therapy
12 step programs
medically assisted detox

*Trx must address the whole person

75
Q

MOA of methadone

A

synthetic opioid analgesic, mu-agonist

76
Q

what is the MOA of Buprenorphine ?

A

partial opioid agonist

-> blocks receptors r/t craving

77
Q

what the the MOA of Naloxone ?

A

opioid antagonist, blocks opioid receptors

78
Q

why is buprenorphine and naloxone combined to create Suboxone?

A

because even though buprenorphine can stand on its own as a treatment option, when combined it helps the patient recover quicker since its an agonist and antagonist

79
Q

opioid withdrawal timeline

A

-starts in 12-24 hrs
-lasts 5-10 days
-peaks at 72 hours

80
Q

opioid withdrawal symptoms

A

flu-like, N/V/D, cramping, goosebumps, depression, drug cravings, anxiety, diaphoresis, myalgias, fever

81
Q

Benzo and alcohol withdrawal is similar because they both act on ____receptors

A

GABA

-therefore they are treated the same

82
Q

S/Sx of Benzo and alcohol withdrawal

A

can be deadly

sleep disturbance, dry retching, irritability, N, tension, weight loss, anxiety, palpations, panic attacks, anxiety, HA, myalgias, diaphoresis, unable to concentrate, perceptual changes

dangerous symptoms: Sz, hallucinations, delirium tremens, wernicke’s encephalopathy

83
Q

Wernicke’s encephalopathy

A

-dangerous S.E. of benzo/alcohol withdrawal
-encephalopathy, disorientation, indifference, inattention, nystagmus, conjugate gaze palsy, gait ataxia

84
Q

delirium tremens

A

hallucinations, disorientation, tachycardia, HTN, fever, agitation, diaphoresis

85
Q

Benzo withdrawal timeline

A

onset: 6-12 hours
peak: 2 weeks, then start to subside

*if not addressed professionally then Sx can last months/years

86
Q

alcohol withdrawal timeline

A

onset: 8 hours
peaks: 1-3 days
starts to taper off after one week

87
Q

how do you treat alcohol and benzo withdrawal ?

A

with Benzo taper to prevent Sz and DT severity
-vitamin supplements for alcohol

88
Q

3 parts of the nervous system that are involved in sensation, perception and response to pain

A
  1. afferent pathways
  2. interpretive centers
  3. efferent pathways
89
Q

nociception

A

impulses traveling to and from the brain
process of feeling pain/sensations
-pain receptors

90
Q

nociceptors

A

pain receptors

91
Q

what are nociceptive stimuli

A

stimuli that cause or are close to causing tissue injury

-> an unpleasant sensation telling up to react

92
Q

endorphines

A

natural neurochemicals that aid in inhibiting the pain response

(endogenous opioids)

93
Q

physiology of pain

A

transduction
transmission
perception
modulation