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MS 410 > exam 2 content > Flashcards

exam 2 content Flashcards

1
Q

primary SCI

A

the initial injury

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2
Q

secondary SCI

A

the effects after the initial injury. Edema, swelling, etc.

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3
Q

secondary injury examples

A

hemorrhage, ischemia, hypovolemia, impaired tissue perfusion, edema, anything that worsens primary injury

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4
Q

SCI injuries lead to issues with…

A

mobility, sensory perception, DTR, CV system, RR, bowel/bladder control

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5
Q

c3/c4

A

breathe no more. phrenic nerve runs here and controls breathing and diaphragm

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6
Q

complications of SCI (9)

A

plegia, paresis, hypoesthesia/hyperesthesia, spinal shock, respiratory compromise, immobility, hemorrhagic or hypovolemic shock, autonomic dysreflexia, CV dysfunction

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7
Q

spinal shock

A

occurs immediately after injury
has temporary but complete loss of motor, sense, reflexes and autonomic function
lasts 48 hrs-weeks

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8
Q

respiratory compromise

A

cervical injury at C3-C5
may need trach, vent, respiratory support

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9
Q

what are some things immobility can lead to?

A

fractures (secondary to decreased mobility, think OP), DVT and pressure injuries

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10
Q

autonomic dysreflexia

A

noxious stimuli causes changes in the SNS below the injry

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11
Q

s/s of autonomic dysreflexia

A

increase in SBP, brady, severe HA, congestion, diaphoresis (above injury) and cold below, flushed skin (above) and pale (below)

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12
Q

non surgical tx of SCI

A

stabilization! cervical collar, halo fixator, skeletal traction

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13
Q

spinal precautions

A

support head. firm surfaces, no specialty mattress. no BLT.

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14
Q

focal TBI

A

a specific area of localized damage

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15
Q

diffuse TBI

A

many different areas. may not appear on imaging until necrosis occurs

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16
Q

secondary injury with TBI

A

includes physiological, vascular, and biochemical events as extension of primary injry

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17
Q

some causes of secondary injry with TBI

A

hypotension, MAP < 65, hypoxia, IICP, cerebral edema

O2 AND GLUCOSE NOT GETTING TO BRAIN!

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18
Q

what should the ICP be?

A

10-15 mmHg, > 20 mmHg and neurons start to die.

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19
Q

where does the blood shunt CSF to maintain ICP?

A

to the spinal subarachnoid space, which reduces cerebral blood flow. LEADING TO ISCHEMIA.

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20
Q

s/s of a basilar skull fracture

A

CSF leakage from nose or ears
battle sign
raccoon eyes
loss of smell and hearing
facial nerve dysfunction

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21
Q

what is the battle sign?

A

bruising behind ears

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22
Q

what are raccoons eyes?

A

bruising of the periorbital area

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23
Q

what is a halo’s sign?

A

classic ID of CSF!! put leakage on a piece of paper and a halo will form.

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24
Q

s/s of a mild TBI

A

dazed, disoriented or LOC
may have memory loss > or < event
no evidence of BI on imaging
wide range of physical or cog symptoms
symptoms usually resolve in 72 hrs

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25
Q

s/s of a mod TBI

A

LOC from 30 mins to 6 hrs
GCS 9-12!!
may see focal or diffuse injury on imaging.
may have acute amnesia up to 24 hrs

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26
Q

s/s of a severe TBI

A

LOC of > 6 hrs
GCS 3-8
focal and diffuse damage to brain, vessels and/or ventricles
requires ICU and maybe ICP

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27
Q

what are complications of a TBI (7)?

A

brain bleeds
hydrocephalus
autoregulation impairment
respiratory complications
CSF leak
IICP
herniation

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28
Q

what is cushing’s triad

A

BRADY, HTN, irregular RR (maybe cheynes-stokes)

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29
Q

what is the timeframe of IICP

A

initial injury to 4 days

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30
Q

what is the issue with IICP?

A

ischemia and herniation

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31
Q

what is uncal herination?

A

shift of temporal lobe
DILATED, NONREACTIVE PUPILS

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32
Q

what is central herniation?

A

shift downward in brainstem
cheynes-stokes…
PINPOINT, NONREACTIVE PUPILS

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33
Q

mannitol… what it is? what is it used for? what are some things to note?

A

osmotic diuretic
tx cerebral edema
may cause rebound swelling, requires filter tubing
monitor: renal fxn and osmolatiry, e-, weakness, edema

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34
Q

where can pain be felt with cholecystitis?

A

RUA, may radiate to shoulder! may have rebound tenderness

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35
Q

what is biliary colic?

A

stone moving. super super painful. need OPIOID MANAGEMENT OF PAIN.

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36
Q

how do we help with the shoulder pain associated with CO2 injection during lap chole?

A

walk it off, baby :)

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37
Q

what are the key findings of acute pancreatitis?

A

decreased Ca, Necrotic pancreas, and lots of bleeding

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38
Q

what are some causes of acute panc?

A

biliary tract disease
trauma
alcoholism (worst prognosis)

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39
Q

what happens when the panc can’t do its job

A

CAN’T DIGEST FOOD!

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40
Q

s/s of acute panc

A

N/V/D
abd pain– midepigastric
steatorrhea?
malabsorption?
s/s of DM?
VS!!
diminished or absent bowel sounds
fever
tachy

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41
Q

what is cullen’s sign?

A

bleeding, around the belly button

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42
Q

what is grey-turners sign?

A

bleeding on flanks!

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43
Q

complications of acute panc (9)

A

infection/sepsis
hemorrhage/shock!
necrosis
ARDs/ALI
renal failure
PNA
paralytic ileus
jaundice
DM (rare!)

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44
Q

interventions of acute panc?

A

ABCs AND PAIN MGMT

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45
Q

what is the best way to relieve the stomach for acute panc

A

NPO

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46
Q

what is the best position for a pt in acute panc?

A

not completely supine! leaning forward, sitting up, laying L side in fetal

47
Q

more interventions for acute pan

A

IVF, pain meds
e- replacement
NG tube

48
Q

where should we place the NG tube for someone with acute panc

A

below the ligament of treitz.

49
Q

chronic panc characteristics

A

looks like acute in exacerbations.
leads to loss of exocrine fxn forever…

50
Q

types of chronic panc

A

chronic calfifying panc
chronic obstructive panc
autoimmune panc
hereditary chronic panc

acute can lead to chronic

51
Q

interventions for chronic panc

A

pancreatic enzyme replacement therapy: don’t crush! take with food :)

52
Q

what is the really complication intervention for panc cancer

A

a whipple… removes proximal head of pancreas, duodenum, part of jejunem, part or all of stomach and gallbladder.

53
Q

what are some complications of panc cancer

A

DM, bleeding, infection, bowel obstruction, abscess, PNA, fistula, peritonitis

54
Q

what is the patho for liver disease

A

widespread scarring throughout the liver caused by inflammation (toxins or disease). the scar tissue produces nodules that block blood flow. blood backs up (leading to PHTN)

when cirrhosis starts first the liver gets big and then shrinks!

55
Q

what are the types of liver disease?

A

post-necrotic cirrhosis
laennec’s cirrhosis
biliary cirrhosis

56
Q

what is post-necrotic cirrhosis associated with?

A

Hep C or drug induced

57
Q

what is laennec’s cirrhosis associated with

A

alcoholism

58
Q

what is biliary cirrhosis associated with

A

biliary obstruction
autoimmune

59
Q

what are complications of decompensated liver disease (8)

A

portal HTN, ascites, esophageal varcies, heptorenal syn., hepatic encephalopathy, coag problems, jaundice, peritonitis.

60
Q

what is one of the issues with portal HTN?

A

causes collateral circulation to form, meaning unfiltered blood enters circulation

61
Q

what are early signs of hepatic encephalopathy

A

sleep disturbances, mood disturbances, mental status changes,, speecch problems

62
Q

what are late signs of hepatic encephalopathy?

A

altered LOC, altered cog, neuromuscular problems, coma

63
Q

what are some precipitating factors for hepatic encephalopathy

A

GI bleed, high protein diet, infection, hypovolemia, hypokalemia, constipation

64
Q

what are some characteristics of hepatorenal syndrome?

A

leads to a poor prognosis…
renal vasoconstriction
UO < 500 mL
elevated Cr and BUN

65
Q

what are interventions for ascites

A

nutritional support, Na restriction 1-2 g, paracentesis, vitamin supplements, diuretics

66
Q

what is spontaneous bacterial peritonitis

A

peritonitis that lacks an obvious source, syms may be vague!

67
Q

how do we dx spontaneous bacterial peritonitis

A

paracentesis, get a culture! sample it. could be e.coli from gut..

68
Q

what are interventions for esophageal varices?

A

SCREENING! if haven’t been screened, assume they have it and tx accordingly.
PREVENT BLEEDING
BB: propanolol is the BB of choice for portal HTN, reduces HR and hepatic venous pressure

69
Q

what are interventions for hepatic encephalopathy

A

LACTULOSE
rifaximin
moderate protein diet
promote hydration

70
Q

what hormones live in the anterior pit gland (7)

A

ACTH, GH, TSH, LH, FSH, PL, MSH

71
Q

what does ACTH do?

A

stimulates the adrenals to make cortisol!

72
Q

what do glucocorticoids do?

A

maintain BP
regulate blood glucose
decrease inflammation
promote and regular metabolism
resistance to stress
fluid regulation

73
Q

which hormone is a mineralcorticoid and what does it do?

A

aldosterone
maintains fluid and e- balance

74
Q

what are the two catecholamines?

A

epi and norepi

75
Q

what does GH do in adults

A

maintains muscle, bone and fat distribution, plays a role in metabolism

76
Q

what does TSH do?

A

stimulates the thyroid to produce T3, T4 and calcitonin

77
Q

what are the two hormones the posterior pit gland is responsible for

A

ADH (vasopressin)
oxytocin

78
Q

what are some causes of hypopituitarism (7)?

A

tumor (adenoma)
malnutrition
rapid wt loss
shock
head trauma
brain tumor
brain infection

79
Q

what is sheehan syn

A

pit gland gets bigger during pregnancy, if there is hemorrhagic shock then it can cause ischemia and necrosis of the pit gland

80
Q

what are some early manifestations of hypopit disorders?

A

visual changes!
HA
limited eye mvmt
reduced cognition

81
Q

what are interventions for hypopit disoders

A

HRT!

82
Q

what are causes of hyperpit disorders?

A

TUMORS
hyperplasia

83
Q

what are manifestations of a pit tumor?

A

neuro changes
vision changes
HA
IICP

84
Q

acromegaly is an overgrowth of what

A

GROWTH HORMONE

85
Q

what are the two posterior pit disorders

A

DI and SIADH

86
Q

what is DI

A

ADH deficiency or inability of kidneys to respond to ADH

87
Q

what are characteristics of DI

A

excessive fluid loss, high UOP, dilute urine, dehydration, fluid and e- imbalance

88
Q

what are key findings of DI?

A

hypotension + brady
hemoconcentration
realllllly dilute urine
s/s of dehydration
decreased cog, irritability

89
Q

what should you watch for with DI?

A

hypovolemic shock!!!

90
Q

what are some symptoms of water toxicity?

A

changes in LOC, HA, N/V

91
Q

what is SIADH?

A

excess ADH
leads to water retention, low Na, FVO

92
Q

what is going with SIADH?

A

the feedback loop isn’t working! ADH is secreted despite osmolarity being low or normal.

93
Q

what are some causes of SIADH

A

cancer therapy
pulmonary infection
certain drugs (SSRIs, antianxiety, anticonvulsants?)

94
Q

what are key features of SIADH

A

FVO and everything related to it.

95
Q

what are interventions for SIADH

A

RESTRICT FLUID INTAKE. 500-1000 mL in 24 hrs.
replace Na
daily weights!
mouth care

96
Q

drugs for SIADH with low Na levels and SE

A

Vasopressin antagonist!
SE: rapid increase in Na (leads to demyelination), liver failure, death.

97
Q

drugs for SIADH with normal Na levels

A

diuretics

98
Q

other drugs for SIADH with low Na but not vasopressin and SE

A

hypertonic saline!
SE: pulmonary edema, HF, FVO,
cause caused HF

99
Q

sodium levels below what can lead to seizures

A

120!

100
Q

what should you do when correcting Na levels

A

correct slowly! 8 mmols at a time?
also perform frequent neuro checks!!

101
Q

what are the two adrenal disorders?

A

Addison’s disease
cushings!

102
Q

what is addisons disease?

A

adrenal insufficiency

103
Q

when do we see addisons disease?

A

in response to stress! surgery, trauma, infection!

104
Q

what are the key findings of addison’s disease?

A

fluid depletion
hypotensions
increase K
anorexia, N/V/D, salt cravings! wt loss
hypoglycemia
vitilgo and body hair loss

105
Q

how do we dx addison’s?

A

eosinophil # and ACTH levels

106
Q

what is the ACTH provocation test?

A

give ACTH IV and then look @ cortisol levels 30 and 60 mins later

107
Q

what are interventions for Addisons?

A

hyperkalemia mgmt
tx hypoglycemia
fluid balance
HRT!

108
Q

how do we tx hyperkalemia with Addisons?

A

insulin, diuretics, tele, VS, CV assess

109
Q

what is Cushings disease?

A

excess cortisol and aldosterone

110
Q

what are the key findings of Cushings?

A

excess body fat where it shouldn’t be!
moon face, truncal obesity, wt gain
decreased immunity!
decreased muscle mass!
increased androgen production

111
Q

how do we dx cushings?

A

measure cortisol levels
measure ACTH levels
dexamethasone testing

112
Q

what is dexamethasone testing for cushings?

A

give a dose of dex. collect pee for 24 hours. dex should suppress cortisol levels, if not– positive dx

113
Q

what drugs do we use with cushings?

A

drugs that interfere or inhibit ACTH

MS 410 (2 decks)

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