WK 4: Delirium&Dementia/Depression/Pain/Sz Flashcards
how does delirium present in a patient?
transient acute confusional states that can come on abruptly or gradually over time
-usually associated with other medical conditions
What are the two main types of delirium states?
hyperactive
hypoactive
what is HYPERactive delirium?
Acute ( happens quickly ) disturbance in attention/awareness
-develops in 2-3 days
“excited delirium”/combative
what are some examples of patients who might experience hyperactive delirium?
ICU pt, post surgery, someone withdrawing, hospitalized elderly
what are some risk factors associated with hyperactive delirium?
medications (benzos/narcotics)
acute infection/ if a pt is septic
surgery
hypoxia
electrolyte/ metabolic dysfunction
insomnia
what are some manifestations that can occur due to hyperactive delirium?
restlessness, irritability, difficulty concentrating, insomnia, tremulous, poor appetite.
-distressed, very confused
how does a person with hyperactive delirium think?
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)
hyperactive delirium can lead to __________, which can cause death. along with symptoms of combativeness, aggression, pain and rapid breathing.
excited delirium syndrome (ExDS)
(most common in those with mental illness or drug abuse)
how long do hyperactive delirium states last?
2-3 days then they resolve on their own
-occasionally if in the hospital it can last a few weeks
what is HYPOactive delirium?
assoc. with right sided frontal basal-ganglion disruption (coordination/movement).
-common with liver/kidney failure pt
“catatonic” delirium, obtunded
some manifestations of hypoactive delirium
decreased alertness & attention span, decreased ability of perception/interpretation of the environment, forgetfulness, apathetic, slow speech, frequently falls asleep
what the the goal for treating someone with delirium?
to identify the cause and remove it
-> modify any risk factors
Trx with anti-psychotics
What is the difference between delirium and dementia?
delirium is preventable, acute, and treatable
dementia is unavoidable and usually progressively worsens
BUT pt’s with dementia are MORE likely to have delirium
what is dementia?
progressive failure of cerebral functioning
-memory, language, judgement, decision making, and orientation all may be impaired
-Sx are irreversible
-causes not fully understood
how does one develop dementia?
pathophysiology
neurons degenerate, brain tissue compresses, atherosclerosis of cerebral vessels, brain trauma, infection, or neuro-inflammation
-can have a genetic predisposition
treatment for dementia
no cure
-Trx directed at optimizing functional capacity and accommodating to loosing abilities
what are the four types of dementia?
- Alzheimer’s (most common)
- Vascular
- Lewy Body
- Frontotemperal
*can have a combo of more than one kind
what is the leading cause of severe cognitive dysfunction in elderly?
Alzheimer’s Dz (AD)
What is the process of diagnosing someone with Alzheimer’s dz?
by ruling out other conditions that could be causing the same Sx: tumors, meningitis, etc..
What are some risk factors for Alzheimer’s Dz?
> 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
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.
4 is the highest risk
- Unhealthy lifestyle, lives alone
- age, FHx
- age, down syndrome
- age, inherited gene, and shut off from community
what do tau protein do?
facilitate nerve cell degeneration
pathophysiology of AD
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
vascular dementia
-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
what are some risk factors for vascular dementia?
- DM
- HPL
- HTN
- being a smoker
frontotemporal dementia
familial association w/ age onset <60
rare
r/t gene mutation of encoding the tau protein
what are the three clinical syndromes related to frontotemporal dementia
1.behavioral variant
2. progressive non-fluent behavior
3. semantic dementia
what are two medications that can aid in the treatment of dementia?
Donepezil and Memantine
they slow the progression, neither are cure, don’t help longterm
when is the best time to give donepezil?
at bedtime best to eat with food to minimize GI effects
- which medication is better for moderate to severe AD?
- which medication is better for mild to moderate AD?
- memantine
- donepezil
what are neurotransmitters?
chemicals that enable neurotransmission, path of electrical impulses from neuron to neuron
what are the four major neurotransmitters?
- dopamine
- norepinephrine
- serotonin (5HT)
- GABA
imbalance in one can affect the other
deficits in dopamine lead to what symptoms/ reactions?
-parkinson-like symptoms: slow reaction time, anergia (abnormal lack of energy)
-anhedonia: “pleasure center” dysfunction. inability to experience pleasure
deficits in serotonin lead to what symptoms/reactions?
-OCD sx: obsessive thoughts, compulsive behavior
-impulsivity: suicide, aggression, susceptibility to “cue triggers”
GABA dysfunction is associate with what kind of disorders?
anxiety disorder
panic disorders
and recently major depressive disorder
NOREPI is an excitatory neurotransmitter that is associated with what?
fight or flight response
high levels of NOREPI are associated with what symptoms?
anxiety, stress, hyperactivity
low levels of NOREPI are associated with what symptoms?
lack of energy, focus or motivation
low=lack of
what is the diagnosis requirement for depression?
presence of symptoms intense enough to cause distress and persistently impair psychosocial functions
Sx of depression
loss of interest/ pleasure
fatigue
restlessness, irritability
impaired concentration
low self esteem
negative thinking
sleep disturbances
appetite disturbances
-these Sx interfere with living
how does someone treat their depression?
-medications
-psychotherapy
-psychoeducation
-support groups
-brain stimulation
*best treatment is a combo of treatments
panic disorder is characterized by what two psychological symptoms?
- anticipatory anxiety: fearful expectation of panic anxiety onset
- avoidance anxiety: personal strategies to decrease risk of panic anxiety and increase feeling of control
overwhelming stress can induce circulating stress hormones which stimulates _______, the must abundant neurotransmitter
glutamate
how would you describe “panic”
unexpected & out of proportion reaction to events happening to or around the patient.
panic attack symptoms
palpitations, CP, SOB, dizziness, N, fear of loosing control, tingling of extremities, flushing, chills
what are some treatments used for panic disorders ?
cognitive behavioral therapy
anti-depressants
Benzo’s (second line/acute situations)
generalized anxiety disorder
chronic
anxiety >6 Mo
excessive/uncontrolled/unrealistic worry
Physical Sx of generalized anxiety disorder
muscle tension, autonomic hyperactivity, exaggerated startle, difficulty concentrating
risk factors for developing generalized anxiety
-excessive substance use
-childhood abuse/family trauma
-genetics
Trx for generalized anxiety disorders
-cognitive behavioral therapy
-anti-depressants (SNRI/SSRI)
-Buspirone
-benzo’s (acute)
what are the three main/core symptoms of PTSD?
hyper-arousal
avoidance of reminders
experiencing the events
definition of PTSD
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
PTSD treatments
psychotherapy
EMDR
SSRI/SNRI medications
what is social anxiety disorder?
intense fear of being criticized by others
-fear of humiliation
-withdraw from situations or experiences with intense discomfort
caused of social anxiety disorder
-inherited trait
-brain structure
-environment/ learned behavior
Trx of social anxiety
-cognitive behavioral therapy
-SSRI
Benzos
propranolol (1-2hrs before activity)
OCD
repetitive unwanted thoughts/obsessions
repeated activities/rituals
compulsions
time consuming and distressing to Pt
what are some subtypes of OCD
cleaning compulsion
hoarding
symmetry obsessions
harm obsessions
obsessions without visible compulsions
what are the four classifications of antidepressant medications that we need to know?
SSRI
SNRI
TCA
MAOI
what are some general considerations the nurse needs to discuss/ go over when a patient is taking an antidepressant ?
-SSRI and SNRI are first line treatment
-all take 4-8 wks to work efficiently
-assess SI risk/ mental imbalance
what is the MOA for SSRI medications
inhibitors of serotonin at nerve endings
= increased amount of serotonin available
what is the MOA for SNRI medications?
blocks neuronal activity of serotonin and norepinephrine
when a patient is on an SNRI medication, what kind of lab value should you check?
LFT’s, which is a liver function test
-not a good medication for Pts with liver issues
TCA’s are an older generation of antidepressant medications and not typically used because ?
they can caused fatal overdoses. if patient has increased SI it is not a good option for them
what is the MOA of TCA medications?
blocks reuptake of norepinephrine and serotonin, making them more available in the synapse
anticholinergic side effects
hot as a hare
dry as a bone
blind as a bat
red as a beet
mad as a hatter
What is the MOA of an MAOI drug?
inhibits MAO enzymes found in the liver, intestinal walls and terminals of neurons
-decreased MAO increases availability of neurotransmitters at nerve endings
what are the three atypical antidepressents?
buproprion
ketamine
trazadone
what is the MOA of benzodiazepines?
they enhance the inhibitory effects of GABA (relaxation)
what are some nursing considerations when using Bezo’s?
-teratogenic
-schedule 4 drug
-cant mix with other drugs that ALSO decrease CNS
-avoid grapefruit and fatty foods
what is the antidote to Benzo’s?
flumazenil
substance use disorder
rewarding effects of drugs from large amount of dopamine getting released
-mimics and enhances pleasure response
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
false
function can be gained back
what are some treatment options for a person suffering from substance use disorder?
cognitive behavior therapy
medications
motivation enhancement therapy
family therapy
12 step programs
medically assisted detox
*Trx must address the whole person
MOA of methadone
synthetic opioid analgesic, mu-agonist
what is the MOA of Buprenorphine ?
partial opioid agonist
-> blocks receptors r/t craving
what the the MOA of Naloxone ?
opioid antagonist, blocks opioid receptors
why is buprenorphine and naloxone combined to create Suboxone?
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
opioid withdrawal timeline
-starts in 12-24 hrs
-lasts 5-10 days
-peaks at 72 hours
opioid withdrawal symptoms
flu-like, N/V/D, cramping, goosebumps, depression, drug cravings, anxiety, diaphoresis, myalgias, fever
Benzo and alcohol withdrawal is similar because they both act on ____receptors
GABA
-therefore they are treated the same
S/Sx of Benzo and alcohol withdrawal
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
Wernicke’s encephalopathy
-dangerous S.E. of benzo/alcohol withdrawal
-encephalopathy, disorientation, indifference, inattention, nystagmus, conjugate gaze palsy, gait ataxia
delirium tremens
hallucinations, disorientation, tachycardia, HTN, fever, agitation, diaphoresis
Benzo withdrawal timeline
onset: 6-12 hours
peak: 2 weeks, then start to subside
*if not addressed professionally then Sx can last months/years
alcohol withdrawal timeline
onset: 8 hours
peaks: 1-3 days
starts to taper off after one week
how do you treat alcohol and benzo withdrawal ?
with Benzo taper to prevent Sz and DT severity
-vitamin supplements for alcohol
3 parts of the nervous system that are involved in sensation, perception and response to pain
- afferent pathways
- interpretive centers
- efferent pathways
nociception
impulses traveling to and from the brain
process of feeling pain/sensations
-pain receptors
nociceptors
pain receptors
what are nociceptive stimuli
stimuli that cause or are close to causing tissue injury
-> an unpleasant sensation telling up to react
endorphines
natural neurochemicals that aid in inhibiting the pain response
(endogenous opioids)
physiology of pain
transduction
transmission
perception
modulation
