Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Complex Nursing > Exam 3 > Flashcards

Exam 3 Flashcards

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what is hepatitis

A

diffuse inflammation of the liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what causes non-infectious hepatitis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is infectious hepatitis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what are the symptoms of hepatitis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what marks hepatitis on labs

A

albumin decreases
AST/ ALT increased
bilirubin increased
elevating cholestasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

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

A

PT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what does management look like for hepatitis patient

A

volume status
diet
antimetics
IV fluids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what can the liver not metabolize

A

lactate and leads to metabolic acidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

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

A

high calorie, low protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what drug gets rid of urea

A

lactulose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What type of acid/base imbalance would exist with hepatitis

A

metabolic acidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is cirrhosis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what causes cirrhosis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what are the symptoms of cirrhosis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

three hallmark signs of cirrhosis

A

ascites
edema
hypotension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

how do you manage ascites

A

paracentesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

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

A

VP shunt

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

TIPS

A

transjugular intrahepatic portosystemic shunt

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what is hepatic encephalopathy

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

is hepatic encephalopathy reversible

A

yes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what is seen in a patient

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what is. an early sign of hepatic encephalopathy

A

Asterixisis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what is Asterixisis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

how long can a balloon tamponade be inflated

A

24 to 48 hours (due to necrosis or ulcerations)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what is the priority assessment with balloon tamponade

A

respiratory (if the balloon migrates up)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what is the pressure of a balloon tamponade

A

25 to 39 mmHg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what should the head of the bed be with balloon tamponade

A

> 30 degrees

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

what is the treatment for Hepatorenal Syndrome

A

liver renal transplant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

postoperative phase of transplant

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

what does the exocrine fucntion of the pancreas include

A

acinar cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

what do acinar cells do

A

digest proteins, fats, starch

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

what does the endocrine function of the pancreas include

A

islets of langerhans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

what do the islets of langerhans do

A

secrete insulin, glucagon, pancreatic polypetide hormones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

what does insulin do

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

what does glucagon do

A

increases blood sugar levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

what is main consideration with pancreatitis

A

PAIN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

what is acute pancreatitis

A

acute inflammation of the pancreas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

what causes acute pancreatitis mainly

A

gallstones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

what is the second most cause of acute pancreatitis

A

alcohol (direct toxic effect)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

what are the two types of acute pancreatitis

A
  1. interstitial
  2. necrotizing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

what is interstitial pancreatitis

A

mild form of acute inflammtion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

how long does interstitial pancreatitis last

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions