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Complex Nursing > Exam 3 > Flashcards

Exam 3 Flashcards

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1
Q

what is the function of the liver

A
  1. metabolism of glucose, proteins, lipids, vitamins
  2. detoxification
  3. synthesis of clotting factors
  4. synthesis of bile acids
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2
Q

what is hepatitis

A

diffuse inflammation of the liver

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3
Q

what is the time line for non infectious

A

can be acute, lasting less than 6 months or can develop into chronic hepatitis

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4
Q

what causes non-infectious hepatitis

A

excessive ETOH, toxic exposures, autoimmune diseases, bacterial, fungal, parasitic

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5
Q

what is infectious hepatitis

A

acute or chronic caused by viral syndromes of herpes, Epstein Barr, varciella Zoster

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6
Q

what history should be considered for hepatitis

A

ask about ETOH and illicit drug usage, use of Rxs or OTC meds, tranfusion hx, occupational or travel history

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7
Q

what are the symptoms of hepatitis

A

yellowing of skin
dark urine
clay colored stool
N/V
loss of apetite
extreme fatigue

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8
Q

what other physical findings may be seen with hepatitis

A

bruising and bleeding tendencies
tongue changes
nutritional changes
spider nevi
sparse body hair
aterial brewery

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9
Q

what marks hepatitis on labs

A

albumin decreases
AST/ ALT increased
bilirubin increased
elevating cholestasis

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10
Q

what would be used to measure liver capacity to synthesize clotting factors

A

PT

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11
Q

what does management look like for hepatitis patient

A

volume status
diet
antimetics
IV fluids

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12
Q

what can the liver not metabolize

A

lactate and leads to metabolic acidosis

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13
Q

why do you need to watch volume status

A

daily weights due to the low colloid osmotic pressure so leads to leaking of intravenous fluid to interstitial spaces

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14
Q

what type of diet would you want to give someone with heptatitis

A

high calorie, low protein

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15
Q

what drug gets rid of urea

A

lactulose

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16
Q

What type of acid/base imbalance would exist with hepatitis

A

metabolic acidosis

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17
Q

What is cirrhosis

A

severe scarring of the liver that can occur due to hepatitis or chronic alcoholism

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18
Q

what causes cirrhosis

A

chronic hepatitis virus
alcohol abuse
nonalcoholic steatohepatitis
hereditary hemochromatosis
Wilson’s disease and alpha1-antitrypsin deficiency

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19
Q

what are the symptoms of cirrhosis

A

low blood pressure
lightheadedness
postural hypertension
positive orthostatic
edema
worsening signs of volume overload

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20
Q

three hallmark signs of cirrhosis

A

ascites
edema
hypotension

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21
Q

what are the labs associated with cirrhosis

A

low albumin
increased AP
increased AST and ALT
increased coagulants
increased bili
hypo-osmolality
high ammonia levels

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22
Q

what is supportive care for cirrhosis

A

there is no cure, reaction to the ongoing signs and symptoms = monitor BP, oxygenation, strict IO, neuro assessments

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23
Q

how do you manage ascites

A

paracentesis

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24
Q

what is used as a therapy when treatments are not working for cirrhosis

A

VP shunt

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25
Q

TIPS

A

transjugular intrahepatic portosystemic shunt

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26
Q

what is hepatic encephalopathy

A

related to the accumulation of toxins (amonia) and changes in neurologic levels

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27
Q

is hepatic encephalopathy reversible

A

yes

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28
Q

what is seen in a patient

A

a decrease in neurological function that is subtle including memory, personality, concentration, reaction times

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29
Q

what is. an early sign of hepatic encephalopathy

A

Asterixisis

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30
Q

what is Asterixisis

A

a clinical sign that describes the inability to maintain sustained posture with subsequent brief, shock-like, involuntary movements

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31
Q

how long can a balloon tamponade be inflated

A

24 to 48 hours (due to necrosis or ulcerations)

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32
Q

what is the priority assessment with balloon tamponade

A

respiratory (if the balloon migrates up)

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33
Q

what is the pressure of a balloon tamponade

A

25 to 39 mmHg

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34
Q

what should the head of the bed be with balloon tamponade

A

> 30 degrees

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35
Q

what is Hepatorenal Syndrome

A

Most frequently fatal complication of cirrhosis

Development of renal failure in pts with severe liver disease in the absence of other identifiable causes for renal pathology.

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36
Q

what is compensatory mechanisms related to Hepatorenal Syndrome

A

get extreme systemic vasodilation which decreases circulating blood volume; compensatory action is CO increases and maximal renal vasoconstriction occurs which reduces renal perfusion and results in renal failure

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37
Q

what symtpoms will a patient with Hepatorenal Syndrome present with

A

Reduced renal blood flow
Ascites
Jaundice
Hypotension
Decreasing urine output
Increased serum creatine
SBP = spontaneous bacterial peritonitis

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38
Q

what is the treatment for Hepatorenal Syndrome

A

liver renal transplant

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39
Q

what is the MELD score

A

used to predict a 3 month mortality of patients with severe cirrhosis and resulting in kidney failure

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40
Q

postoperative phase of transplant

A

the nursing focuses on hemodynamic stability, adequate oxygenation, fluid and electrolyte balance

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41
Q

following a transplant what drugs may be needed

A

vasopressors and fluid boluses may be required the first 24 to 48 hours related to high cardiac outputs and low systemic vascular resistance

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42
Q

what does the exocrine fucntion of the pancreas include

A

acinar cells

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43
Q

what do acinar cells do

A

digest proteins, fats, starch

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44
Q

what does the endocrine function of the pancreas include

A

islets of langerhans

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45
Q

what do the islets of langerhans do

A

secrete insulin, glucagon, pancreatic polypetide hormones

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46
Q

what does insulin do

A

increase uptake of glucose into the cells, promotes glycogenesis, lowers blood sugar levels

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47
Q

what does glucagon do

A

increases blood sugar levels

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48
Q

what is main consideration with pancreatitis

A

PAIN

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49
Q

what are other nursing considerations for pancreatitis

A

altered tissue perfusion
impaired gas exchange
decreased cardiac output
fluid volume deficit
infection
knowledge deficit
altered nutrition

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50
Q

what is acute pancreatitis

A

acute inflammation of the pancreas

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51
Q

what causes acute pancreatitis mainly

A

gallstones

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52
Q

why do gallstones cause pancreatitis

A

block the pancreatic secretions from emptying into the duodenum and this causes inflammation (the reflux of bile causes the inflammation)

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53
Q

what is the second most cause of acute pancreatitis

A

alcohol (direct toxic effect)

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54
Q

what are the two types of acute pancreatitis

A
  1. interstitial
  2. necrotizing
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55
Q

what is interstitial pancreatitis

A

mild form of acute inflammtion

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56
Q

how long does interstitial pancreatitis last

A

self limiting with full recovery
last a few weeks and then goes away

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57
Q

what happens to a patient that develops necrotizing acute pancreatitis

A

irreversible damage caused by this and Most patients end up with sepsis, then MODS

58
Q

what should you ask a patient about when gathering history related to acute pancreatitis

A

alcohol consumption
diabetes
gallbladder disease
medications
recent anorexia, N/V, weight loss

59
Q

what is the hallmark sign of acute pancreatitis

A

Pain

60
Q

where is pain felt with acute pancreatitis

A

persistent epigastric to the left upper quadrant, constant and radiating to the back, can be described as non-specific, severe pain (10/10)

61
Q

what other S/S are seen with acute pancreatitis

A

abdominal guarding
Illeus
Diarrhea
Bleeding
Foul smelling bowels
dehydration
decreased BP (increased HR)

62
Q

what is a key lab value for acute pancreatitis

A

amylase and lipase elevation 3 times normal

63
Q

normal amylase level is

A

23 to 85 unites per liter

64
Q

normal lipase levels

A

0 to 160 U/L

65
Q

how will acute pancreatitis impact BUN

A

increased

66
Q

what does an increased BUN suggest

A

hypovolemia

67
Q

AST and ALT in relation to acute pancreatitis

A

Increased

68
Q

AST suggests

A

indicates damage to liver cells

69
Q

WBC related to

A

inflammation

70
Q

the three diagnostic criteria for acute pancreatitis

A

(i) abdominal pain consistent with the disease
(ii) serum amylase and/or lipase greater than three times the upper limit of normal, and/or
(iii) characteristic findings from abdominal imaging

71
Q

acute pancreatitis patient enters the ED

A

establish the diagnosis

72
Q

if the patient is determined to have AP what is next step to be done in ED

A

volume resuscitation then stabilization of vital signs

73
Q

the priority pain relief drug for AP is

A

opioids (dilaudid / morphine)

74
Q

why would an AP patient get anti- cholinergic

A

decrease Gi motility and pancreatic enzyme release

75
Q

why would an AP patient get anti-sporadics

A

relax the smooth muscles

76
Q

why would an AP patient get H2 blockers

A

decrease GI acid secretions

77
Q

if the patient has necrotizing pancreatitis what medication may they require

A

antibiotics

78
Q

three complications of liver disease

A
  1. cirrhosis
  2. Hepatic Encephalopathy
  3. Hepto-renal syndrome
79
Q

Laenacks Cirrhosis

A

seen in middle age men who are alcoholics

80
Q

Post Necrotic Cirrhosis

A

cirrhosis that develops after sub massive necrosis of liver due to nasty toxin or viral hepatitis, not common

81
Q

Biliary Cirrhosis

A

obstruction or infection of extra or intra hepatic bile ducts so bile cant drain, marked by jaundice, abdominal pain, steatorrhea, enlargement of liver and spleen

82
Q

cardiac cirrhosis

A

related to recurrent and tractable CHF (from left sided heart failure moves into right sided heart failure), output decreases and perfusion decreases

83
Q

acute pancreatitis is a _________ problem

A

exocrine

84
Q

diabetes mellitus is a ____________ problem

A

endocrine

85
Q

N/V can lead to what electrolyte imbalance

A

hypokalemia

86
Q

what electrolyte imbalance may be seen with acute pancreatitis due to loss of fat

A

hypocalemia

87
Q

Endoscopic retrograde cholangiopancreatography (ERCP)

A

Procedure to diagnose and treat problems in the liver, gallbladder, bile ducts, and pancreas

88
Q

when may a patient need ERCP to be performed

A

Necessary if massive pancreatic necrosis and patient has worsening clinical picture (tachycardia, other organ failure, supplemental O2 required and not maintaining good O2, intubation required)

89
Q

what are some complications of ERCP

A

can precipitate acute pancreatitis and introduce infection to sterile area, risks/complications include bleeding and using contrast dye (dye load)

90
Q

severe hemorrhagic pancreatitis two signs

A
  1. Turner’s Sign
  2. Cullen’s Sign
91
Q

turner’s sign

A

bruising of the flanks, retroperitoneal hemorrhage

92
Q

cullen’s sign

A

edema and brusing around the umbillicus

93
Q

chvostek’s sign

A

twitching of the facial muscles in response to tapping over the area of the facial nerve

94
Q

○ Trousseau’s Sign

A

carpopedal spasm caused by inflating the BP cuff to a level above the systolic pressure for 3 minutes, more sensitive to hypocalcemia

95
Q

type 1 diabetes

A

autoimmune, no insulin production, often first diagnosis of diabetes comes with an episode of DKA especially in children

96
Q

type 2 diabetes

A

insulin resistance, hyperglycemia, hyperinsulinemic, beta cells don’t work well

97
Q

complications of diabetes

A

○ Diabetic retinopathy: #1 cause of blindness
○ Premature coronary artery disease
○ HTN
○ Autonomic dysfunction with gastroparesis
○ Diarrhea
○ Nephropathy
○ Infertility issues
○ Increased risk of infection
○ Hyperlipidemia
○ Peripheral vascular disease
○ Poor wound healing - osteomyelitis

98
Q

metabolic syndrome

A

High triglyceride
low HDL
HTN
Hyperglycemia
Central Obesity

99
Q

When do we do impaired glucose tolerance test?

A

pregnant

100
Q

nursing diagnosis to consider

A

Fluid Volume Deficit
Decreased Cardiac Output
Altered Nutrition
Risk for altered tissue perfusion: cerebral

101
Q

DKA is common with what type of diabetes

A

Type 1

102
Q

what is the most common cause of DKA

A

infection

103
Q

other factors that can lead to DKA (beyond #1 reason)

A

drugs, trauma, stroke, MI, Pancreatitis

104
Q

biggest concern with DKA

A

Blood glucose level and dehydration

105
Q

three hallmark signs of DKA

A

polyuria, polydipsia, polyphagia

106
Q

what is the cornerstone of management with DKA

A

Insulin therapy

107
Q

hyperglycemia leads to

A

hyperosmolality

108
Q

the accumulation of keto-acids leads to

A

metabolic acidosis

109
Q

what is the breathing seen with DKA patients

A

kussmaul respiratory pattern (to compensate for metabolic acidosis)

110
Q

what are the other symptoms would be seen with DKA

A

fruity breath
dry mucous membranes
flushed skin
hypotension
tachycardia
poor ski turgor

111
Q

what medications may be used for DKA

A

diuretics, beta blockers, corticosteroids, anti-psychotics

112
Q

two priority management for DKA

A

fluid resuscitation and insulin therapy

113
Q

HHS is more common with what type of diabetic

A

Type 2

114
Q

HHS is secondary to

A

some sort of physiologic stress

115
Q

examples of some sort of physiologic stress

A

illness, infections, trauma, UTI, surgery

116
Q

HHS is known for

A

marked hyperglycemia
hyperosmolality
no ketoacidosis

117
Q

DKA or HHS lead to more mortality

A

HHS

118
Q

what is the typical HHS patient present with

A

Older adult pt with type 2 diabetes, drowsy, eating less, sleeping more, impaired neuralgic function

119
Q

the BG of a patient with HHS is

A

BG 400-4000 (mean is 1100 mg/dL),

120
Q

sodium levels of HHS patient is

A

high NA and serum osmolarity

121
Q

is a HHS acidotic

A

NO

122
Q

what will not be considered with HHS patient

A

pH, anion gap, bicarb, ketones

123
Q

what is the priority management of HHS

A

Fluid resuscitation and insulin therapy are two priorities in management

124
Q

what is more dangerous hypoglycemia or hyperglycemia

A

hypoglycemia

125
Q

hypoglycemia can lead to

A

death, coma, injury

126
Q

what causes hypoglycemia

A

stress, weight loss, insulin shock, excessive alcohol, sepsis

127
Q

hypoglycemia is a _______ mimicer

A

stroke

128
Q

signs of hypoglycemia

A

hypothermia
tachypnea
tachycardia
HTN
dysrthmias
diaphoresis
hunger

129
Q

what is the role of your skin barrier

A

protects against infections
prevents fluid losses
controls body temperature
produces vitamin D

130
Q

Allograft

A

AKA homograft, temporary wound covering, donor is cadaver, temporary

131
Q

Xenograft

A

AKA heterograft, skin taken from another species usually pigs, temporary

132
Q

Autograft

A

skin taken from themselves, permanent

133
Q

Physiologic Dressing

A

allograft, xenograft, autograft are all examples of physiologic dressing

134
Q

Eschar

A

AKA scab, dark dead slothy layer of skin/tissue, associated with escharotomy, can strangle circulation

135
Q

granulation

A

when taking off eschar, healthy pink skin is called granulation skin, when you see it you know burn is ready for permanent graft

136
Q

Debridement

A

removal of eschar, can happen naturally, with enzymes, or done surgically by burn nurse

137
Q

Escharotomy

A

incision into eschar to expose healthy skin to relieve pressure that may result in strangulation of circulation

138
Q

most severe types of burns

A

combination of partial and full thickness

139
Q

Superficial burn

A

Only involve epidermis !!!!
○Has a dry appearance without blistering
○Skin appears pink, red, blanches when you apply pressure (when release it fills up again)
○May be mild edema

140
Q

examples of superficial burn

A

sunburn, splashes from hot liquid

141
Q

partial thickness superficial includes

A

epidermis and superficial dermis

Complex Nursing (2 decks)

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