Exam 2 Flashcards
causes of secondary TBI (4)
- hypotension
- hypoxia
- increased ICP
- cerebral edema
= all the things we try to manipulate when someone has a TBI
mild TBI
(loss of consciousness, GCS, presentation, resolution)
may or may not have loss of consciousness (but will be < 30 mins)
2. dazed, disoriented
3. resolves in ~72 hrs
moderate TBI
(loss of consciousness, GCS)
loss of consciousness > 30 mins up to 6 hrs
GCS 9-12
severe TBI
(loss of consciousness, GCS)
loss of consciousness > 6 hrs
GCS 3-8
normal ICP
10-15
therapeutic CPP
greater than 70
how to calculate CPP
MAP - ICP
how to calculate MAP
(systolic + (2)diastolic) / 3
CSF will have which characteristics? (3)
- clear fluid (can have some blood)
- halo
- glucose present
if someone has a CSF leak, what are they at increased risk for?
infection
if someone had a brain injury, what hormonal complications could develop r/t the body’s response to the injury?
DI or SIADH
r/t pressure on the pituitary gland from inflammation
what is most common cause of death with TBI?
increased ICP
term:
brain tissue shifts to accommodate for inc. ICP
herniation
(imminent death)
term:
temporal lobe shift to the R or L
uncal herniation
pupil presentation with uncal herniation
dilated non reactive = “blown” (mydriasis)
term:
shift of brain tissue downward towards brainstem
central herniation
pupil presentation + other changes with central herniation
pinpoint/nonreactive (miosis)
cheyne stones respers (b/c pushing on brainstem)
components of cushing’s triad
- widening pulse pressure
- bradycardia
- changes in RR
poor prognosis of TBI (6)
fever ***
GCS change of 2 points
hypoxia
CPP <70
cushing’s triad
fixed/blown pupils
how is CO2 r/t cerebral blood flow and ICP ?
CO2 is vasodilator. we want to keep this at the low side of normal to prevent vasodilation and further increasing the ICP
ways to prevent increases in ICP (4)
- avoid coughing, sneezing, bending, etc
- DON’T cluster care
- turn down lights
- limited suction
what should SBP and MAP be maintained at for TBIs?
SBP >100
MAP >65-70 (in messer lecture she said both were ok)
what drug are we using to reduce ICP?
mannitol (osmotic diuretic)
brain death components (3)
- apnea
- loss of brainstem reflexes
- irreversible/unresponsive coma
w/ SCI, C3-C5 injury is concern for what?
respiratory compromise
where does the phrenic nerve (controls diaphragm) connect to spinal cord?
C3
with SCI, if pt can’t cough + suction isn’t enough, what can we do to help them?
quad cough - forcefully push on chest during exhalation
SCI @ T6 is a concern for what?
CV compromise (hypotension, brady, dysrhythmias)
plegia =
paralysis
paresis =
weakness
term:
temporary loss of sensation + movement after SCI
spinal shock
(not true shock)
term:
loss of SNS innervation to heart and vasculature –> bradycardia, hypotension
neurogenic shock
(actual shock)
autonomic dysreflexia happens with injury where on spinal cord?
T6 and above
autonomic dysreflexia happens with noxious stimuli where on spinal cord? what are some of the stimuli? (5)
T6 and BELOW
- distended bladder
- constipation
- restrictive clothing
- pressure / pain
- temperature
what s+s do you see with autonomic dysreflexia?
severe HTN, bradycardia,
vasodilation ABOVE injury: sweating, flushed skin
vasoconstriction BELOW injury: goosebumps, pale, cool
what is the 1st thing you should do if a patient presents with signs of autonomic dysreflexia?
ASSESS + correct/remove noxious stimuli
spine precautions (4)
- no BLT (bend, lift, twist)
- log roll
- firm mattress
- cervical stabilization
condition:
Autoimmune disease of CNS that destroy Myelin Sheaths (slowing of conduction + formation of white plaques)
MS
s+s of MS
- mobility issues
- sensory issues **
- pain
- visual changes **
- cognitive changes **
** differences from ALS
aggravating factors of MS (4)
- extreme temps
- stress
- fatigue
- overepxertion
aggravating factors of MS (4)
- extreme temps
- stress
- fatigue
- overexertion
patients with MS are at high risk for what? why? (3 reasons)
infection
PNA risk b/c of dysphagia, UTI risk b/c of bladder retention, taking immunosuppressants
med therapy for MS
immunosuppressants
also may have pain meds, muscle relaxants
condition:
Degenerative disease of CNS → muscle weakness + atrophy (progressive, rapid, fatal)
ALS
what type of muscle movement does ALS impact?
voluntary
mnemonic for s+s of ALS
“All Muscles Stopping”
compared to MS, ALS does NOT impact which fxn?
bladder/sensory
priority complication for ALS
respiratory failure
(will eventually need trach)
condition:
Autoimmune disorder of the peripheral nervous system attacking nerves → damage to myelin sheaths → motor weakness + sensory abnormalities
GBS
which neuro condition is associated with remyelination? (in the recovery stage)
GBS
GBS is often preceded by what?
infection (respiratory or GI)
or vaccination
describe presentation and s+s of GBS
ascending paralysis - starts with tingling or paralysis of feet/legs
does GBS have bowel and bladder issues?
YES
does ALS have cognitive changes?
NO
does GBS have cognitive changes?
NO
what is priority complication for GBS?
respiratory distress syndrome
describe lumbar puncture findings between MS and GBS
MS: protein, increased WBCs
GBS: protein, normal WBCs
priority intervention for GBS
airway management (HOB, O2, suction, mech vent PRN)
tx for GBS
plasmapheresis (remove antibodies that are attacking myelin sheaths of PNS)
condition:
excessive firing of CN 5 causing sudden facial pain with spasms
trigeminal neuralgia
pain descriptors for trigeminal neuralgia
electric, shooting, sharp
people with trigeminal neuralgia are at an increased risk for what?
self harm
(very painful and debilitating condition)
ways to manage pain with trigeminal neuralgia
avoid triggers as much as possible
meds: anticonvulsants, gabapentin, muscle relaxers, nerve blocks)
condition:
Chronic autoimmune disease of peripheral nervous system where acetylcholine receptors get blocked or attacked by antibodies
myasthenia gravis
s+s of myasthenia gravis (3)
- weakness
- ptosis (eyelid drooping)
- eventual… respiratory dysfunction
with myasthenia gravis, activity _______ weakness and resting _______ weakness
activity: worsens
rest: improves
cholinergic test for MG results
given cholinergic drug + MG improves (b/c has more ACh)
tensilon test for MG results
given cholinesterase inhibitor + MG improves (b/c has more ACh)
med therapy for MG
cholinesterase inhibitors + immunosuppressants
cholinergic crisis vs myasthenic crisis (in terms of the neurotransmitter and drugs)
cholinergic: too much ACh (from too much cholinesterase inhibitor drug)
myasthenic: too little ACh (not enough cholinesterase inhibitor drug)
= both still with severe muscle weakness. cholinergic is from excessive stimulation and muscles are depleted, whereas myasthenic is from under stimulation.
s+s of cholinergic crisis
PsNS on overdrive (rest and digest symptoms)
tx for cholinergic crisis
atropine (dry shit up)
tensilon test: what is it?
if cholinergic crisis, what will you see?
if myasthenic crisis, what will you see?
given cholinesterase inhibitor drug
cholinergic crisis: will get worse (b/c essentially given more ACh)
myasthenic crisis: will improve (b/c given ACh and there was previously not enough)
tx for myasthenic crisis
neostigmine (cholinesterase inhibitor)
cirrhosis most commonly caused by what?
chronic etoh use
hepatitis
decompensated liver disease is what?
when symptoms develop and liver is chirrotic
what are the 5 main complications of liver disease?
- portal vein HTN
- ascites
- esophageal varices
- hepatorenal syndrome
- hepatic encephalopathy
why does ascites happen with liver disease?
liver can’t produce albumin so fluid leaks out of vessels
protein is leaking, which also prevents fluid from staying in vessels
esophageal varices put pt at risk for what?
BLEEDING!
what happens with portal HTN? (simple patho)
blood, nutrients, toxins all back up into other organs and cause HTN of the vessels supplying those organs
hepatic encephalopathy is r/t what? how do we tx it?
build-up of ammonia, toxins
tx: lactulose (3-4 stools/day) + rifaximin (reduces ammonia production)
what lab/patient presentation would you see with hepatorenal syndrome?
elevated BUN/creatinine
UO < 500mL/day
s+s of liver disease (there’s 14 listed - 3 are labs. try your best ◡̈ )
jaundice
RUQ pain
fatigue
wt changes
palmar erythema
asterixis
itchy skin
hypotension
petichiae
ascites
low protein/albumin
increased bilirubin
elevated liver enzymes (early)
esophageal varices
what Na restriction should pt with liver disease / ascites be on?
1-2g/daily
what are protein requirements for pt with liver disease?
moderate protein
what is priority concern with ascites?
respiratory fxn
(HOB, O2)
tx for ascites (2)
- diuretics
- paracentesis
for patients with liver disease, all of them should be screened for what?
esophageal varices !!
if patient is found to have esophageal varices, they should have what medication therapy?
BB - control HTN and prevent rupture
what 2 precautions should someone with liver disease be on if they have ascites and esophageal varices?
fall precautions (center of gravity is off)
bleeding (esophageal varices)
if someone with esophageal varices starts to bleed, what do you do? (4 - 1 of them is meds)
- turn on side (protect airway)
- lower HOB (prevent shock)
- 2 large bore IVs (for fluids + blood)
- meds: vasopressors + ocreotide + ABX
what supplements should pt with liver disease be given?
multivitamin, thiamine, folate
what electrolyte should we monitor with lactulose therapy?
K+
sudden abd pain w/ board-like abd. what are you worried about? what is tx?
peritonitis
tx: ABX
cholecystitis puts a patient at high risk for what?
peritonitis
nutritional risk factor for cholecystitis
high fat, low fiber diet
s+s of cholecystitis (7)
- RUQ pain radiating to shoulder
- clay colored stool
- jaundice
- dark urine
- fever
- chills
- tachycardia
for dx of cholecystitis, ultrasound can show us _____ and xray can show us _______
US: inflammation
xray: stones
if patient has shoulder pain after cholecystectomy, what should you do?
educate them this is normal r/t CO2 from surgery and best tx is AMBULATE ◡̈
term:
Remove part of pancreas and connect to small intestine
whipple procedure for pancreatic cancer
assessments after whipple (4)
- leaking at site
- peritonitis
- sepsis
- infection
condition:
premature activation of pancreatic enzymes → inflammation of pancreas
acute pancreatitis
what 2 general things happen with acute pancreatitis?
- cannot digest food
- pancreas starts to autodigest itself
2 most common causes of acute pancreatitis
- alcoholism
- stones
why can we see hypocalcemia with acute pancreatitis?
b/c fatty acids (from lipolysis) bind with Calcium, leading to low serum levels
s+s of acute pancreatitis (7)
- epigastric LUQ pain that’s described as “boring” through their body to their back
- steatorrhea
- pain with eating
- gas
- bloating
- respiratory issues (r/t ALI from close proximity)
- gray turner
- cullen’s sign
what lab findings would you see with acute pancreatitis? (3)
- elevated lipase + amylase
- elevated glucose (b/c pancreas cannot produce enough insulin)
- elevated bilirubin
interventions for acute pancreatitis
- ABC
- pain mngmnt
- NPO
re: chronic pancreatitis, what do you need to know for enzyme replacement? (4)
- lifetime need
- do not crush
- take with food
- WIPE YA LIPS!!!
ACTH stimulated to produce:
cortisol
posterior pituitary controls which 2 hormones?
oxytocin + ADH
“AO PO”
condition:
overproduction of GH. + what presentation do you see?
acromegaly
enlargement of bodily features
re: acromegaly, which changes are permanent? which are reversible?
permanent: skeletal
reversible: tissue
tx for acromegaly
dopamine agonists (suppress GH)
term:
removal of pituitary gland / tumors
hypophysectomy
what is post op care for hypophysectomy? (3)
- nasal packing
- special mouth care (use mouthwash, no brushing)
- avoid increased ICP
if someone has a hypophysectomy, what will be required for the pt?
lifelong HRT
condition:
adrenal gland hypofunction. low levels of cortisol + aldosterone
addison’s
s+s of addison’s (6)
- hyponatremia –> salt cravings
- hyperkalemia –> dysrhythmias
- hypoglycemia –> GI upset, sweat, tremors
- hypotension
- hypovolemia
- bronze pigmented skin
pharm interventions for addison’s (4)
- kayexolate
- insulin
- steroid (“sone”)
- aldosterone
condition:
adrenal gland hyperfunction (excess cortisol)
cushing’s disease
s+s of cushing’s disease (14)
- moon face
- buffalo hump
- thin hair
- hyperglycemia
- truncal obesity
- striae
- thin extremities
- OP
- frail skin
- impaired immunity
- hirsutism
- HTN
- GI ulcers
- psychosocial disturbances
interventions for cushing’s disease (7)
- reduce cortisol
- address HTN
- fluid restriction
- Na restriction
- calcium + vit D
- no NSAIDs
- infection prevention
med therapy for cushing’s
inhibit or block ACTH (ex: ketoconazole)
SIADH is excess of which hormone?
ADH
(“syndrome of INCREASED ADH”)
s+s of SIADH (think general)
general:
fluid overload (you know these s+s) + low Na (neuro s+s)
+ high urine specific gravity
tx for SIADH (4)
- fluid restriction (500-1000mL)
- hypertonic saline (if low Na)
- diuretics (if Na normal)
- med: vasopressin antagonists
if patient with SIADH (and fluid volume overload), presented with pulmonary edema, what would your interventions be?
raise HOB, give O2, get fluid off
diabetes insipidus is caused by what?
deficiency of ADH
s+s of DI (5)
- extreme UO
- hypernatremia
- intense thirst
- dehydration s+s
- low urine specific gravity (very diluted)
tx for DI
desmopressin (synthetic ADH) and fluids
when treating DI, we should be mindful of which complication?
water toxicity (HA, N/V, changes in LOC)
