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Neuro, respiratory, genomics
most common causes of seizures
brain trauma from injury, stroke or sodium imbalance
abnormal HTT assessment findings r/t seziures
asymmetrical rhythmic twitching, ALOC, disorientation, altered RR - depth and pattern, low SpO2, incontinence.
are all seizures treated the same
no, determining the type of seizure and triggers determines the meds used
what is an aura r/t seizures
a visual change/disturbance AND/OR physical (scent, sensation, sound) that appears as a PRECURSOR to a seizure
what is the post-ictal period
the period of time for a patient following their seizure
what to do if your patient has a sizure (4 do’s, 2 do not’s)
turn the patient to the side to keep airway clear, protect the patient from injury
loosen any restrictive clothing (around chest/neck), record start and end times of seizures
what not to do if/when your patient has a seizure
do not hold the patinet down and do not force anythring into the patient’s mouth
expected assessment findings during post-ictal period
sleepy, disoriented, headache, may not communicate verbally, may take hours to return to baseline (hours-days is common)
what are dangers that seizures can cause in everyday life
drowning, burns, falls from stairs or ladders, driving
what are seizures
sudden electrical firing of nuerons in the brian causing a change in function and ehavior.
what are common seizure triggers
alcohol, sleep deprivation, stress, light/patterns
what is epilepsy
a chronic disorder where repeated, unprovoked seizure activity occurs
pt education r/t seizure medications
meds must be taken EVERYDAY at SAME TIME → compliance is crucial
often more than one med is needed, and it is important to manage side effects (sometimes can’t drive bc of specific meds)
how long do you usually need to stay on seizure meds
for life
what is alzheimers disease
irreversible dementia caused by nerve cell death, loss of acetylcholine and brain atrophy
loss of neurons = loss of synapses and Ach = brain atrophy
what are key physiological findings found in alzheimers disease
BETA AMYLOID PLAQUES - they accumulate outside of nuerons, thus interfering with nerve stimulation
TAU proteins accumulate inside neurons to form NEUROFIBRILLARY TANGLES - that interfere with conduction and cuase DEATH of neurons
Manifestations (S+S) of alzheimers disease
loss of short-term memory and denial of memory loss with eventual disorientatin, impaired abstract thinking
progressive forgetfulness, disorientation, confusion, loss of problem solving and judgement, behavior changes - agitation, restlessness (with little/no emotional regulation)
what are manifestations of LATE STAGE (near EOL) alzheimer’s disease
non-verbal, non-ambulatory state with difficulty swallowing and eating
how do you diagnose alzheimers?
there are no biological markets, so confirmation is only with autopsy to see beta amyloid plaques and neurofibrillary tangles
CT/MRI can provide some answers by helping R/O other causes
treatment/plan of care for pt with alzheimer’s
ensure safety (major fall risk), memory aids, maintaining unimpaired cognitive functions, maintaining or improving the general state of hygiene, nutrition and health (involve them in their ADLs), pharmacolgic treamtnets
do you try to reorient a patient with late-stage alzheimers
no, just be a caring and soft pressure and play into their reality
what can cause a decline in functioning for a pt in early stage alzheimers
a major event, hospitalization or injury can cause a patient to often have significant decline that never returns to the patient’s previous baseline
what is the medication prototype for alzheimers
donepezil, an acetylcholinesterase inhibitor
MOA for donepezil
it prevents the breakdown of acetylcholine, which increases the amount of Ach available and results in increased nerve impulses
SE of donepezil
nausea, diarrhea and slow heart rate (bradycardia)
how fast does donepezil work in the body
improvement of memory is seen in 1-4 weeks
what medication is used only for Moderate to Severe Alzheimers
memantine, a n-methyl0d0aspartate (NDMA) recpetor antagonist
what is the MOA for memantine
it blocks glutamate activity, so it can slow the progression of disease in moderate to severe alzheimers
what is the pathophysiology of Parkinson’s disease & what does it cause
the degeneration of basal ganglia, leading to DOPAMINE depletion (and relative excess of acetylcholine
causes fine tremors, motor dysfunctinoo and coordination issues
what are the two types of Parkinson’s disease
primary = onset before age 40, common in men and is the progressive degenerative disorder of basal ganglia
secondary = Caused by external or known triggers, such as side effects from certain medications, head trauma, or vascular issues (strokes)
symptoms of Parkinson’s Disease
tremors (PILL ROLLING) in hands and fingers at rest
tremors increase when fatigued
bradykinesia, abnormal slowness of movement, sluggish physical/mental responses, rigidity with jerky movements, shuffle steps w/ stooped position, blank facial expression with MASKLIKE FACES, loss of coordination and balence.
class + MOA for benztropine mesylate
ant9cholinergic that restores balance of neurotransmitters in the CNS to reduce the rigidity and tremors in patients with Parkinson’s
cautions/CI for beztropine mesylate
patients with angle closure glaucoma, myasthenia gravis or a bowel obstruction
SE of benztropine mesylate
disorientation, confusion, dry eyes and mouth, constipation (antichol)
evaluate for effectivess of benztropine mesylate
causes a decrease in parkinsonian symptoms (mask like face, rigidity, shuffle gait)
patient education for benztropine mesylate
address dry mouth, maintain good oral hygiene - drinking water frequently and use hard candy to stimulate salivation, rinse mouth
if alertness is impaired, avoid use of machinery/cars
MOA of carbidopa/levodopa
levodopa increases the amount of DOPAMINE available in the CNS. Carbidopa prevents levodopa from being metabolized before it enters the CNS (allowing for lower dosages of levodopa to be administered to achieve the same effect)
cautions for carbidopa/levodopa
patients with cardiac, renal or psychiatric disorders
recurrence of parkinsonian symptoms appears after a few years of levodopa therapy, so it is reserved for patients with significant symptoms
SE/AE of carbidopa/levodopa
depression, involuntary movements/dyskinesias, orthostatic hypotension
NC/pt education for carbidopa/levodopa
monitor for efficacy/relief of symptoms, change positions slowly (ortho hypo), do NOT administer with a high protein meal, take at regular intervals to maximize benefit, recurrence of parkinsonian symptoms appear after a few years → USE FOR PTS WITH SEVERE SYMPTOMS
S+S of ADHD (attention0deficit Hyperactivity Disorder)
easy distractibility, failure to receive instructions properly, inability to focus on one task at a time, difficulty remembering loss/misplacement of personal items, excessive talking or interrupting, inability to sit still, impulsiveness, sleep disturbance.
how ADHD affects life (not S+S)
affects friendships, causes self esteem issues, diminished social success
treatment basics of ADHD
about 70% of children with ADHD are treated with meds
pharmacotherapy = STIMULANT MEDICATIONS
self medicate → alcohol, drugs later in life
MOA of methylphenidate
activates the RAS in the brain, releases dopamine and norepinephrine → SYMPATHOMIMETIC
uses for methylphenidate
ADHD, narcolepsy, obesity treatment (helps bc stimulant = increased metabolism, and bc helps with satiation)
administration of methylphenidate
sustained release tablets must be swallowed whole
SE/AE of methylphenidate
increase HR, BP and liver toxicity
high abuse potential → heavily regulated
what is bipolar disorder
aka manic depression, a condition with alternating episodes of mania and depression
S+S of mania r/t bipolar
inflated self esteem or grandiosity, decreased need for sleep, increased talkativeness, flight of ideas (changing topic frequently), distracted or increased goal-directed activity (esp with grandiose ideas), excessive involvement in pleasurable activities (shopping, sex, etc)
what is the general term for the class of meds used to treat bipolar
mood stabilizers
what classes of medications can be used to treat bipolar disorder
some anytiseizure drugs, some antipsychotic medications, lithium
why isn’t lithium used much anymore to treat bipolar disorder
it has a narrow therapeutic index so blood levels constantly need to be evaluated, like every 4-5 days, and if there is a overdose it requires hemodialysis and supportive care
class of olanzapine (zyprexa)
atypical antipsychotic
uses of olanzapine (zyprexa)
schizophrenia and bipolar 1 disorder , along with psychosis/delirium if indicated
MOA of olanzapine/zyprexa
binds to dopamine and serotonin receptors. It leads to a decrease in positive symptoms in patients, including hallucinations, delusions and disorganized speech, though and behavior (DECREASES PSYCHOSIS SYMPTOMS)
AE of olanzapine/zyprexa
drowsiness (most common), weight gain, DECREASED insulin sensitivity (monitor BG levels), can cause dopamine blockade = increased risk of dyskinesia and extrapyramidal symptoms (tongue clicking, eye twitch, other physical movements)
class of lithium
antischizophrenic, mood stabilizer, anti-inflammatory properties
uses of lithium
bipolar 1 disorder, adjunct for refractory depression in patients with mood disorders
MOA for lithium
not well studied, but increased inhibitory neurotransmitters and decreases excitatory neurotransmitters in the brain
AE of lithium
amount of salt in the body indfluences effects of this medication and it ca increase salt lsos from the body → causing electrolyte imbalences
QT elongation (risk for V-tach_)
hand tremor in 25-50% of pts
NARROW THERAPEUTIC INDEX = MONITOR FOR TOXICITY
ringing of ears, loss of coordination, diarrhea, vomiting, serotonin syndrome
S+S of lithium toxicity
ringing of ears, loss of coordination, diarrhea, vomiting, serotonin syndrome (also confusion and disorientation)
patient education/NC for lithium
take at same time each day in morning, encourage salt-steady diet (do not use salt substitutes bc need Na in the body not K), drink plenty of fluids (avoid caffeine), educate of toxicity S+S, and constant checking of lithium levels
what is serotonin syndrome & what can it be caused by
high levels of serotonin the body, causing altered mental status
can be from lithium toxicity, SSRI & MAOI medications
S+S of serotonin syndrome
AMS (altered mental status), hyperthermia, sweating, myoclonus/ocular clonus (rhythmic muscle twitching), rigidity (that can cause rhabdo bc extended period of use from being stiff), diarrhea, restlessness.
S+S of depression
difficulty sleeping (or excessive sleeping), feeling tired/fatigued, abnormal eating, inability to concentrate or make decisions, feelings of despair, guilt and misery/lack of self-worth, lack of interest in personal appearance/sex/doing hobbies, delusions or hallucinations
what are the different types of depression
situational (loss of job/loved one), postpartum, seasonal effective disorder, psychotic depression
what do antidepressants do / used for
to enhance/stabilize mood, may be prescribed for other disorders (phobias, panic, anxiety, etc)
what is the major BBW for all antidepressants
closely monitor adults and children taking antidepressants FOR WARNING SIGNS OF SUICIDE. weekly (or daily) checks are required until mood elevates → which can be up to 12 weeks.
children and adolescents are at HIGHER RISK
what is a common side effect between antidepressants
weight gain
long long does it take for meds to cause full effects
several weeks
pharmacologic class of sertraline (zoloft)
SSRI - selective serotonin re-uptake inhibitor
uses of sertraline (zoloft)
for depression, social anxiety and obsessive-compulsive disorder
has both antidepressant and anxiolytic properties
MOA of sertraline (zoloft)
prevents the reuptake of serotonin from the synapse, which leads to increased levels of serotonin → making people often feel better bc serotonin = feel-good neurotransmitter
administration of sertraline (zoloft)
abrupt discontinuation can cause withdrawal symptoms (nausea, sweating, agitation, tremors, seizures)
BBW for suicide/worsening mental health
SE of sertraline (zoloft)
decreased libido (experienced by 70% of people on it), weight gain
class of buproprion (wellbutrin)
atypical antidepressant
uses for buproprion (wellbutrin)
used for treatment of depression and to assist in smoking cessation (r/t dopamine), off-label use for children with ADHD
MOA for buproprion (wellbutrin)
not well understood, known to inhibit the reuptake of norepinephrine and dopamine weakly.
SE/AE of buproprion (wellbutrin)
many, most notable = lowered seizure threshold (more likely to occur if you have epilepsy/seizure condition), worsening of suicidal ideation, weight loss
how long does wellbutrin (buproprion) take to take effect in the body
full effect is seen around 4 weeks.
what do MAOIs do
monoamine oxidase inhibitors terminate the action of neurotransmitters such as dopamine, norepinephrine and epinephrine
when is treatment with MAOIs indicated
because of their low safety margin, they are used only when SSRI’s or other meds have NOT WORKED !! (not first line medications)
what is the major food/drug interaction with MAOIs?
any foods with TYRAMINE
a form of amino acid tyrosine, when taken with MAOIs - there is a sudden release of norepinephrine which leads to acute HYPERTENSION accompanied by stuff neck, HA, flushing, palpitations, diaphoresis and nausea
what foods have tyramine (to educate patients on MAOIs)
avoado’s, bananas, cheese, yogurt, alcohol, deli meats, raisins or papaya
class of methylprednisolone
corticosteriod
uses for methylprednisolone
anti-inflammatory, immunosuppressive (used for spinal cord injury!)
MOA for methylprednisolone
modifies protein synthesis in leukocytes, to inhibit leukocyte (WBC) infiltration at inflammation site, interfere with the function of mediators of inflammatory response and suppress humoral immune responses
AE of methylprednisolone
long term use → can cause Kaposi’s sarcoma = cancer
myopathy (muscle breakdown because decreased protein = decreased repair), impaired wound healing, osteoporosis, risk of INFECTION, HYPERGLYCEMIA, mood swings/irritability
risk factors for respiratory disorders
allergies, chest injury, crowded living conditions, exposure to chemical and pollutants, family history of infectious diseases, frequent respiratory illness, travel to foreign country, smoking, surgery, viral syndromes
what is pnenumonia (and its pathophysiology)
infection of the lower respiratory tract that causes:
widespread inflammation in the lungs
increased neutrophils
T cells and B cells arrive, causing tissues to fill with debris and exudate
microorganism release toxins and further damage the lung tissue
how does the inflammation r/t pneumonia worsen the condition
edema caused by inflammation stiffens the lung, thus decreasing lung compliance (ability of lungs to move) and vital capacity → causing HYPOXEMIA
what is pneumonia caused by
bacteria, viruses, fungi, protozoa or parasites
can be from inhalation of microorganism
aspiration of secretions/food (that can become infected over time)
what are three common types of pneumonia
community acquired, nosocomial, ventilator acquired (VAP)
community acquired pneumonia
MRSA, INFLUENZA!!!, streptococcus oneumoniae = most common
Nosocomial pneumonia
hospital acquired, r/t staphylococcus aureus & MRSA
Ventilator acquired pneumonia
subtype of nosocomial, d’t bacteria on bottom cuff of ET (endotracheal) tube
clinical manifestations (S+S) of pneumonia
URI (upper respiratory tract infection), fever, chills, PRODUCTIVE cough, pleural pain = dyspnea, hemoptysis, pulmonary consolidation (fluid in air sacs), inspiratory crackles, rhonchi and wheezing
how do you diagnose pneumonia
CXR - chest xray, looking for pulmonary consolidation/cloudy lung fields, elevated EBC, sputum cultres positive
what two general classes of medications are used to treat pneumonia
antibiotics, antivirals
most common cause of bacterial pneumonia and its treatment
streptococcus pneumonia
treat with antibiotics