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Med Surg II > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

causes of secondary TBI (4)

A
  1. hypotension
  2. hypoxia
  3. increased ICP
  4. cerebral edema

= all the things we try to manipulate when someone has a TBI

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2
Q

mild TBI

(loss of consciousness, GCS, presentation, resolution)

A

may or may not have loss of consciousness (but will be < 30 mins)
2. dazed, disoriented
3. resolves in ~72 hrs

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3
Q

moderate TBI

(loss of consciousness, GCS)

A

loss of consciousness > 30 mins up to 6 hrs
GCS 9-12

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4
Q

severe TBI

(loss of consciousness, GCS)

A

loss of consciousness > 6 hrs
GCS 3-8

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5
Q

normal ICP

A

10-15

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6
Q

therapeutic CPP

A

greater than 70

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7
Q

how to calculate CPP

A

MAP - ICP

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8
Q

how to calculate MAP

A

(systolic + (2)diastolic) / 3

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9
Q

CSF will have which characteristics? (3)

A
  1. clear fluid (can have some blood)
  2. halo
  3. glucose present
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10
Q

if someone has a CSF leak, what are they at increased risk for?

A

infection

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11
Q

if someone had a brain injury, what hormonal complications could develop r/t the body’s response to the injury?

A

DI or SIADH

r/t pressure on the pituitary gland from inflammation

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12
Q

what is most common cause of death with TBI?

A

increased ICP

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13
Q

term:
brain tissue shifts to accommodate for inc. ICP

A

herniation

(imminent death)

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14
Q

term:
temporal lobe shift to the R or L

A

uncal herniation

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15
Q

pupil presentation with uncal herniation

A

dilated non reactive = “blown” (mydriasis)

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16
Q

term:
shift of brain tissue downward towards brainstem

A

central herniation

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17
Q

pupil presentation + other changes with central herniation

A

pinpoint/nonreactive (miosis)
cheyne stones respers (b/c pushing on brainstem)

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18
Q

components of cushing’s triad

A
  1. widening pulse pressure
  2. bradycardia
  3. changes in RR
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19
Q

poor prognosis of TBI (6)

A

fever ***
GCS change of 2 points
hypoxia
CPP <70
cushing’s triad
fixed/blown pupils

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20
Q

how is CO2 r/t cerebral blood flow and ICP ?

A

CO2 is vasodilator. we want to keep this at the low side of normal to prevent vasodilation and further increasing the ICP

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21
Q

ways to prevent increases in ICP (4)

A
  1. avoid coughing, sneezing, bending, etc
  2. DON’T cluster care
  3. turn down lights
  4. limited suction
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22
Q

what should SBP and MAP be maintained at for TBIs?

A

SBP >100

MAP >65-70 (in messer lecture she said both were ok)

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23
Q

what drug are we using to reduce ICP?

A

mannitol (osmotic diuretic)

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24
Q

brain death components (3)

A
  1. apnea
  2. loss of brainstem reflexes
  3. irreversible/unresponsive coma
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25
Q

w/ SCI, C3-C5 injury is concern for what?

A

respiratory compromise

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26
Q

where does the phrenic nerve (controls diaphragm) connect to spinal cord?

A

C3

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27
Q

with SCI, if pt can’t cough + suction isn’t enough, what can we do to help them?

A

quad cough - forcefully push on chest during exhalation

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28
Q

SCI @ T6 is a concern for what?

A

CV compromise (hypotension, brady, dysrhythmias)

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29
Q

plegia =

A

paralysis

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30
Q

paresis =

A

weakness

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31
Q

term:
temporary loss of sensation + movement after SCI

A

spinal shock
(not true shock)

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32
Q

term:
loss of SNS innervation to heart and vasculature –> bradycardia, hypotension

A

neurogenic shock
(actual shock)

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33
Q

autonomic dysreflexia happens with injury where on spinal cord?

A

T6 and above

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34
Q

autonomic dysreflexia happens with noxious stimuli where on spinal cord? what are some of the stimuli? (5)

A

T6 and BELOW

  1. distended bladder
  2. constipation
  3. restrictive clothing
  4. pressure / pain
  5. temperature
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35
Q

what s+s do you see with autonomic dysreflexia?

A

severe HTN, bradycardia,

vasodilation ABOVE injury: sweating, flushed skin

vasoconstriction BELOW injury: goosebumps, pale, cool

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36
Q

what is the 1st thing you should do if a patient presents with signs of autonomic dysreflexia?

A

ASSESS + correct/remove noxious stimuli

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37
Q

spine precautions (4)

A
  1. no BLT (bend, lift, twist)
  2. log roll
  3. firm mattress
  4. cervical stabilization
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38
Q

condition:

Autoimmune disease of CNS that destroy Myelin Sheaths (slowing of conduction + formation of white plaques)

A

MS

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39
Q

s+s of MS

A
  1. mobility issues
  2. sensory issues **
  3. pain
  4. visual changes **
  5. cognitive changes **

** differences from ALS

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40
Q

aggravating factors of MS (4)

A
  1. extreme temps
  2. stress
  3. fatigue
  4. overepxertion
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41
Q

aggravating factors of MS (4)

A
  1. extreme temps
  2. stress
  3. fatigue
  4. overexertion
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42
Q

patients with MS are at high risk for what? why? (3 reasons)

A

infection

PNA risk b/c of dysphagia, UTI risk b/c of bladder retention, taking immunosuppressants

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43
Q

med therapy for MS

A

immunosuppressants

also may have pain meds, muscle relaxants

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44
Q

condition:

Degenerative disease of CNS → muscle weakness + atrophy (progressive, rapid, fatal)

A

ALS

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45
Q

what type of muscle movement does ALS impact?

A

voluntary

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46
Q

mnemonic for s+s of ALS

A

“All Muscles Stopping”

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47
Q

compared to MS, ALS does NOT impact which fxn?

A

bladder/sensory

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48
Q

priority complication for ALS

A

respiratory failure
(will eventually need trach)

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49
Q

condition:

Autoimmune disorder of the peripheral nervous system attacking nerves → damage to myelin sheaths → motor weakness + sensory abnormalities

A

GBS

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50
Q

which neuro condition is associated with remyelination? (in the recovery stage)

A

GBS

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51
Q

GBS is often preceded by what?

A

infection (respiratory or GI)
or vaccination

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52
Q

describe presentation and s+s of GBS

A

ascending paralysis - starts with tingling or paralysis of feet/legs

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53
Q

does GBS have bowel and bladder issues?

A

YES

54
Q

does ALS have cognitive changes?

A

NO

55
Q

does GBS have cognitive changes?

A

NO

56
Q

what is priority complication for GBS?

A

respiratory distress syndrome

57
Q

describe lumbar puncture findings between MS and GBS

A

MS: protein, increased WBCs

GBS: protein, normal WBCs

58
Q

priority intervention for GBS

A

airway management (HOB, O2, suction, mech vent PRN)

59
Q

tx for GBS

A

plasmapheresis (remove antibodies that are attacking myelin sheaths of PNS)

60
Q

condition:

excessive firing of CN 5 causing sudden facial pain with spasms

A

trigeminal neuralgia

61
Q

pain descriptors for trigeminal neuralgia

A

electric, shooting, sharp

62
Q

people with trigeminal neuralgia are at an increased risk for what?

A

self harm
(very painful and debilitating condition)

63
Q

ways to manage pain with trigeminal neuralgia

A

avoid triggers as much as possible
meds: anticonvulsants, gabapentin, muscle relaxers, nerve blocks)

64
Q

condition:

Chronic autoimmune disease of peripheral nervous system where acetylcholine receptors get blocked or attacked by antibodies

A

myasthenia gravis

65
Q

s+s of myasthenia gravis (3)

A
  1. weakness
  2. ptosis (eyelid drooping)
  3. eventual… respiratory dysfunction
66
Q

with myasthenia gravis, activity _______ weakness and resting _______ weakness

A

activity: worsens

rest: improves

67
Q

cholinergic test for MG results

A

given cholinergic drug + MG improves (b/c has more ACh)

68
Q

tensilon test for MG results

A

given cholinesterase inhibitor + MG improves (b/c has more ACh)

69
Q

med therapy for MG

A

cholinesterase inhibitors + immunosuppressants

70
Q

cholinergic crisis vs myasthenic crisis (in terms of the neurotransmitter and drugs)

A

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.

71
Q

s+s of cholinergic crisis

A

PsNS on overdrive (rest and digest symptoms)

72
Q

tx for cholinergic crisis

A

atropine (dry shit up)

73
Q

tensilon test: what is it?

if cholinergic crisis, what will you see?

if myasthenic crisis, what will you see?

A

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)

74
Q

tx for myasthenic crisis

A

neostigmine (cholinesterase inhibitor)

75
Q

cirrhosis most commonly caused by what?

A

chronic etoh use

hepatitis

76
Q

decompensated liver disease is what?

A

when symptoms develop and liver is chirrotic

77
Q

what are the 5 main complications of liver disease?

A
  1. portal vein HTN
  2. ascites
  3. esophageal varices
  4. hepatorenal syndrome
  5. hepatic encephalopathy
78
Q

why does ascites happen with liver disease?

A

liver can’t produce albumin so fluid leaks out of vessels

protein is leaking, which also prevents fluid from staying in vessels

79
Q

esophageal varices put pt at risk for what?

A

BLEEDING!

80
Q

what happens with portal HTN? (simple patho)

A

blood, nutrients, toxins all back up into other organs and cause HTN of the vessels supplying those organs

81
Q

hepatic encephalopathy is r/t what? how do we tx it?

A

build-up of ammonia, toxins

tx: lactulose (3-4 stools/day) + rifaximin (reduces ammonia production)

82
Q

what lab/patient presentation would you see with hepatorenal syndrome?

A

elevated BUN/creatinine

UO < 500mL/day

83
Q

s+s of liver disease (there’s 14 listed - 3 are labs. try your best ◡̈ )

A

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

84
Q

what Na restriction should pt with liver disease / ascites be on?

A

1-2g/daily

85
Q

what are protein requirements for pt with liver disease?

A

moderate protein

86
Q

what is priority concern with ascites?

A

respiratory fxn
(HOB, O2)

87
Q

tx for ascites (2)

A
  1. diuretics
  2. paracentesis
88
Q

for patients with liver disease, all of them should be screened for what?

A

esophageal varices !!

89
Q

if patient is found to have esophageal varices, they should have what medication therapy?

A

BB - control HTN and prevent rupture

90
Q

what 2 precautions should someone with liver disease be on if they have ascites and esophageal varices?

A

fall precautions (center of gravity is off)

bleeding (esophageal varices)

91
Q

if someone with esophageal varices starts to bleed, what do you do? (4 - 1 of them is meds)

A
  1. turn on side (protect airway)
  2. lower HOB (prevent shock)
  3. 2 large bore IVs (for fluids + blood)
  4. meds: vasopressors + ocreotide + ABX
92
Q

what supplements should pt with liver disease be given?

A

multivitamin, thiamine, folate

93
Q

what electrolyte should we monitor with lactulose therapy?

A

K+

94
Q

sudden abd pain w/ board-like abd. what are you worried about? what is tx?

A

peritonitis

tx: ABX

95
Q

cholecystitis puts a patient at high risk for what?

A

peritonitis

96
Q

nutritional risk factor for cholecystitis

A

high fat, low fiber diet

97
Q

s+s of cholecystitis (7)

A
  1. RUQ pain radiating to shoulder
  2. clay colored stool
  3. jaundice
  4. dark urine
  5. fever
  6. chills
  7. tachycardia
98
Q

for dx of cholecystitis, ultrasound can show us _____ and xray can show us _______

A

US: inflammation
xray: stones

99
Q

if patient has shoulder pain after cholecystectomy, what should you do?

A

educate them this is normal r/t CO2 from surgery and best tx is AMBULATE ◡̈

100
Q

term:
Remove part of pancreas and connect to small intestine

A

whipple procedure for pancreatic cancer

101
Q

assessments after whipple (4)

A
  1. leaking at site
  2. peritonitis
  3. sepsis
  4. infection
102
Q

condition:
premature activation of pancreatic enzymes → inflammation of pancreas

A

acute pancreatitis

103
Q

what 2 general things happen with acute pancreatitis?

A
  1. cannot digest food
  2. pancreas starts to autodigest itself
104
Q

2 most common causes of acute pancreatitis

A
  1. alcoholism
  2. stones
105
Q

why can we see hypocalcemia with acute pancreatitis?

A

b/c fatty acids (from lipolysis) bind with Calcium, leading to low serum levels

106
Q

s+s of acute pancreatitis (7)

A
  1. epigastric LUQ pain that’s described as “boring” through their body to their back
  2. steatorrhea
  3. pain with eating
  4. gas
  5. bloating
  6. respiratory issues (r/t ALI from close proximity)
  7. gray turner
  8. cullen’s sign
107
Q

what lab findings would you see with acute pancreatitis? (3)

A
  1. elevated lipase + amylase
  2. elevated glucose (b/c pancreas cannot produce enough insulin)
  3. elevated bilirubin
108
Q

interventions for acute pancreatitis

A
  1. ABC
  2. pain mngmnt
  3. NPO
109
Q

re: chronic pancreatitis, what do you need to know for enzyme replacement? (4)

A
  1. lifetime need
  2. do not crush
  3. take with food
  4. WIPE YA LIPS!!!
110
Q

ACTH stimulated to produce:

A

cortisol

111
Q

posterior pituitary controls which 2 hormones?

A

oxytocin + ADH

“AO PO”

112
Q

condition:
overproduction of GH. + what presentation do you see?

A

acromegaly

enlargement of bodily features

113
Q

re: acromegaly, which changes are permanent? which are reversible?

A

permanent: skeletal

reversible: tissue

114
Q

tx for acromegaly

A

dopamine agonists (suppress GH)

115
Q

term:
removal of pituitary gland / tumors

A

hypophysectomy

116
Q

what is post op care for hypophysectomy? (3)

A
  1. nasal packing
  2. special mouth care (use mouthwash, no brushing)
  3. avoid increased ICP
117
Q

if someone has a hypophysectomy, what will be required for the pt?

A

lifelong HRT

118
Q

condition:

adrenal gland hypofunction. low levels of cortisol + aldosterone

A

addison’s

119
Q

s+s of addison’s (6)

A
  1. hyponatremia –> salt cravings
  2. hyperkalemia –> dysrhythmias
  3. hypoglycemia –> GI upset, sweat, tremors
  4. hypotension
  5. hypovolemia
  6. bronze pigmented skin
120
Q

pharm interventions for addison’s (4)

A
  1. kayexolate
  2. insulin
  3. steroid (“sone”)
  4. aldosterone
121
Q

condition:
adrenal gland hyperfunction (excess cortisol)

A

cushing’s disease

122
Q

s+s of cushing’s disease (14)

A
  1. moon face
  2. buffalo hump
  3. thin hair
  4. hyperglycemia
  5. truncal obesity
  6. striae
  7. thin extremities
  8. OP
  9. frail skin
  10. impaired immunity
  11. hirsutism
  12. HTN
  13. GI ulcers
  14. psychosocial disturbances
123
Q

interventions for cushing’s disease (7)

A
  1. reduce cortisol
  2. address HTN
  3. fluid restriction
  4. Na restriction
  5. calcium + vit D
  6. no NSAIDs
  7. infection prevention
124
Q

med therapy for cushing’s

A

inhibit or block ACTH (ex: ketoconazole)

125
Q

SIADH is excess of which hormone?

A

ADH

(“syndrome of INCREASED ADH”)

126
Q

s+s of SIADH (think general)

A

general:
fluid overload (you know these s+s) + low Na (neuro s+s)

+ high urine specific gravity

127
Q

tx for SIADH (4)

A
  1. fluid restriction (500-1000mL)
  2. hypertonic saline (if low Na)
  3. diuretics (if Na normal)
  4. med: vasopressin antagonists
128
Q

if patient with SIADH (and fluid volume overload), presented with pulmonary edema, what would your interventions be?

A

raise HOB, give O2, get fluid off

129
Q

diabetes insipidus is caused by what?

A

deficiency of ADH

130
Q

s+s of DI (5)

A
  1. extreme UO
  2. hypernatremia
  3. intense thirst
  4. dehydration s+s
  5. low urine specific gravity (very diluted)
131
Q

tx for DI

A

desmopressin (synthetic ADH) and fluids

132
Q

when treating DI, we should be mindful of which complication?

A

water toxicity (HA, N/V, changes in LOC)

Med Surg II (6 decks)

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