Module 4 Flashcards
What is hyperactive confusional state? How long does this develop over?
Acute disturbances in attention / awareness - develops over 2-3 days
What are the risk factors for hyperactive confusional state?
Medications, acute infection, surgery, hypoxia, electrolyte imbalances, and insomnia
How does hyperactive confusional state manifests?
Restless, irritable, difficulty concentrating, insomnia, tremors, poor appetite
What is fully developed delirium?
Hallucinations, completely inattentive, grossly altered perception
What is excited delirium syndrome
Combative, aggressive, pain, rapid breathing, can lead to death
How to treat hyperactive confusional state
Remove risk factors when possible
What is hypoactive confusional state associated with?
Right sided frontal basal-ganglion disruption
How does hypoactive confusional state manifest?
Decreased alertness and attention span, forgetfulness, apathetic, slow speech, frequently falls asleep
How do you treat hypoactive confusional state?
Remove causative agents if possible
Compare the onset of delirium and dementia
Dementia: slow and progressive
Delirium: acute (r/t hospitalizations)
Compare the course of delirium and dementia
Dementia: chronic, slow decline
Delirium: fluctuating and reversible
Compare the attention level for delirium and dementia
Dementia: intact early but declines later
Delirium: inability to focus or sustain attention
Compare the alertness and orientation level of dementia and delirium
Dementia: intact early and can be variable in later stages
Delirium: impaired
Compare the behavior between dementia and delirium
Dementia: intact early on
Delirium: agitated, withdrawn, depressed
Compare the speech habits between delirium and dementia
Dementia: word finding problems / aphasia
Delirium: incoherent, disorganized
What are the risk factors for Alzheimers
65+, family hx, existing mild cognitive impairment, head trauma, and isolation
What is the patho behind Alzheimers
Accumulation of neuritic plaques and intraneuronal neurofibrillary tangles of tau protein
In frontotemporal dementia what is progressive non-fluent behavior and semantic dementia
Progressive : problems with language and writing
Semantic: problems forming words and sentences
What is dopamine responsible for
pleasure, satisfaction
what is norepinephrine responsible for
increases alertness, arousal, and attention
what is serotonin responsible for
mood, sleep, sexual desire
what is GABA responsible for
reduces neuronal excitability by inhibiting nerve transmission
How does a dopamine deficit manifest
parkinson’s like symptoms and pleasure center dysfunction
how does a serotonin deficit manifest
OCD like symptoms and impulsivity
together how do serotonin and dopamine deficit manifest
depression and cravings
what is anticipatory anxiety
fearful expectation of panic anxiety onset
what is avoidance anxiety
personal strategies used to increase feelings of control and decrease the risk of panic
what is used as a second line therapy for panic disorders
benzos
what is generalized anxiety disorder and how long does it take to be diagnosed
excessive, uncontrolled, unrealistic worry accompanied by muscle tension, autonomic hyperactivity, exaggerated startle, difficulty concentrating
anxiety present for more than 6 months
what are the risk factors for GAD
excessive use of certain substances, childhood abuse / family trauma, genetics
what are the key characteristics of PTSD
vivid flashbacks, nightmares, emotional blunting, irritability, and exaggerated startle
what are the 4 main causes of PTSD in men and women
Men: rape, combat, childhood neglect, and childhood physical abuse
Women: rape, sexual molestation, physical attack, being threatened with a weapon
If a person takes propranolol for social anxiety how long before should they take it?
1-2 hours before
compare obsessions and compulsions
obsessions - repetitive unwanted thoughts
compulsions - repeated activities or rituals
What is a second line treatment (pharm) for OCD
Clomipramine
How does the brain pathways change with addiction
Addiction decreases dopamine pathways but with abstinence they do regenerate
What are the risk and protective factors of substance abuse?
Risk: aggressive behavior as children, lack of parental supervision, poor social skills, drug experimentation, availability of drugs at school
Protective: good self control, parental monitoring and support, positive relationship, good grades, school anti-drug policies
What is the safest way to manage acute withdrawal symptoms
medically assisted detoxification
treatment programs for substance use also need to test patients for what
diseases that are associated with substance use disorders - like HIV / ADIS, hepatitis, TB, and endocarditis
Antagonist or agonists - for buprenorphine and naloxone
Buprenorphine: partial opioid agonist
Naloxone: opioid antagonist
What is the opioid withdrawal timeline
begins 12-24 hours after last dose, peaks at 72 hours, physical symptoms start to lessen at 1 week
cravings and depression can last through months
What is included in supportive treatment for opioid withdrawal
Tylenol and anti-diarrhea
what are the serious symptoms related to benzo and alcohol withdrawal
seizures, hallucinations, delirium tremens (tachycardia, hypertension, fever, agitation, diaphoresis), wernikes encephalopathy (profound disorientation, inattention, oculomotor dysfunction)
What is the benzo withdrawal timeline
first symptoms start 6-12 hours after last dose, peaks at 2 weeks
what is the alcohol withdrawal timeline
8 hours - anxiety, insomnia, nausea, and abdominal pain
1-3 days is the peak - high blood pressure, increased body temperature
with alcohol withdrawal what vitamin needs supplementation
B1
What is the purpose of acute pain
protective, promotes withdrawal from painful stimuli, teaches avoidances, allows injured parts to heal
what are the three pathways that are involved with pain sensation, perception, and response
afferent pathways - take impulses from spinal cord to cortex
interpretive centers - interpret impulse as pain
efferent pathways - physical / mental response to pain
what is nociceptive pain
stimuli of a certain intensity that causes or could potentially cause tissue injury
what happens at the transduction phase of pain
stimuli converted to action potentials - happens at A-delta and C-fibers
What does prostaglandin do when activated
lowers the pain threshold - when prostaglandin is suppressed it decreases the pain by raising the pain threshold.
promotes inflammation, pain, and fever
protects lining of stomach from acid, promotes clotting factors (activates platelets), and affects kidney function
what fibers are myelinated
a-delta
what fibers are non-myelinated
C-fibers
if pain activate the a-delta fibers what does the pain feel like
sharp, stinging, cutting, and pinching - these are localized
if pain activates the c-fibers what does the pain feel like
dull, burning, aching - these are poorly localized
what fibers do not transmit pain
A-alpha and A-beta
compare tolerance and threshold in relation to pain
tolerance - greatest intensity of a pain a person can handle
threshold - lowest intensity of pain that a person can recognize
intense pain at one location may decrease or increase the pain threshold in another site
decreases
what is the gate control theory
if we block the pain before it gets to the brain we can stop/lower the pain perception
pain < 3 months is considered
acute
pain >3-6 months is considered
chronic
what type of pain stimulates the ANS
acute - can change HR, BP, sweating, and cause dilated pupils
compare the stimuli for nociceptive and neuropathic pain
nociceptive - outside the CNS
neuropathic - inside the CNS
compare the causes of nociceptive and neuropathic pain
nociceptive - activated in response to actual / impending tissue injury
neuropathic - arises from direct injury to NERVES
visceral pain activates only which pain fiber
C
cutaneous / somatic pain involves what system and has what complaints
musculoskeletal pain
constant, achy
what is the localization of cutaneous / somatic pain
well localized in skin and subcutaneous tissue but less well localized for bones
visceral pain involves what system and has what complaints
involves organs
cramping, splitting, N/V, diaphoresis
what is the localization of visceral pain
poorly localized
neuropathic pain involves what system and has what complaints
nerves
shooting, burning, electric shock, sharp, numb, weakness
what is the localization of neuropathic pain
poorly localized
compare referred and phantom pain
referred - pain felt at a distance from the actual pathology (common in visceral pain)
phantom - sensation of pain that originates from an amputated part
nonselective COX inhibitors decrease what
gastric acid protection and platelet function
does acetaminophen have anti-inflammatory effects
no
what enzyme is responsible for the production of prostaglandins
COX
chronic alcohol users should limit their acetaminophen to how much
2 g / day
when administering an opioid when should you wait and assess for level of sedation
if RR is less than 10
how does initial drowsiness change with more doses of opioids
diminishes
0.1 mg of IV fentanyl is how much morphine
10 mg IV morphine
define myoclonic
brief, shock-like jerks of a muscle of groups
what is the cause of primary seizures
don’t know the cause - they are idiopathic
what is the etiology of secondary seizures
chemical imbalances, fever, brain injuries
What is the caveat to diagnosing epilepsy
must have no evidence of a reversible metabolic cause
what is seizure threshold
persons likelihood to have a seizure
what is a generalized onset seizure
neuronal activity simultaneously in both hemispheres on the brain
tonic vs clonic
tonic - prolonged skeletal muscle contraction
clonic - alternating skeletal muscle contraction and relaxation
what are absence seizures
brief loss of awareness that commonly occurs with repetitive spasmodic eyes blinking for up to 30 seconds
what is a focal onset seizure
seizure originating in a localized part of the brain (one lobe)
what is the prodromal phase of seizure
signs / activities that usually come before a seizure starts
what is that aural, ictal, and post-ictal phases of seizures
aural - sensory warning
ictal - seizure
post-ictal - recovery
what is status elipepticus
a continuing series of multiple seizure without a recovery period, lasts 30 minutes or more and can lead to respiratory arrest
how long must a patient go without a seizure to be be eligible to decrease dose or stop their anti-epileptic meds?
1-2 years
are pregnant women able to take anti-epileptic drugs
no, they are teratogenic