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Exam 3 Flashcards

1
Q

What are the functions of the liver?

A

-Metabolism of glucose, proteins, lipids, vitamins
-Detoxification of medications, ETOH, ammonia, toxins, and hormones
-Synthesis of clotting factors
-Conjugation and secretion of bilirubin-
-Synthesis of bile acids (or salts)-break down dietary fats and oils

-Formation, excretion of bile
-Carbohydrate Metabolism
-Lipid Metabolism
-Protein Metabolism
-Metabolism of Steroid Hormones
-Metabolism of Drugs
-Synthesis of plasma proteins, clotting factors
-Filtration of Blood

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2
Q

What are common nursing diagnoses for hepatic disorders?

A

Fluid Volume Excess
Altered Tissue Perfusion
Altered Thought Process
Altered Nutrition
Ineffective Breathing Pattern
Pain
Risk for Fluid Volume Deficit
Risk for Infection

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3
Q

What are some symptoms of hepatitis?

A

Yellow skin and eyes
Dark urine
Light-colored stools
N/V
Loss of appetite
Extreme fatigue
Diarrhea
Low-grade fever
Malaise

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4
Q

What are non-infectious reasons for hepatitis?

A

Excessive ETOH
Other toxins (Bacterial, fungal, parasitic)
Autoimmune Diseases (primary biliary cirrhosis)
Congenital (Willson’s disease, hemochromatosis)
R-sided HF (related to back up of fluid)
Non-ETOH fatty liver (NASH)

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5
Q

What are infectious reasons for hepatitis?

A

Acute or chronic A-E
Other viral syndromes (herpes, Epstein-Barr, coxsackievirus, and varicella-zoster)

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6
Q

At what point does liver failure occur?

A

occurs when there is a loss of 60% or greater of hepatocytes

symptoms develop when > 75% hepatocytes injured/killed

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7
Q

How does acute liver failure transition into chronic?

A

becomes chronic, or results in patient death as fulminant liver failure progressing to cerebral edema, coma, and death from brain stem herniation

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8
Q

What history assessment questions must be asked when caring for hepatitis?

A

-ETOH and illicit IV drug use
-Use of rxs or OTC meds such as herbal supplement
-transfusion hx
-Occupational/travel exposure
-Sexual hx

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9
Q

When should a patient be hospitalized for hepatitis?

A

Once hepatic decompensation with portal vein HTN, ascites, encephalopathy, and coagulopathy, should be hospitalized

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10
Q

What are liver function lab tests should be assessed in hepatic disorders?

A

Total Protein
Albumin
Total Bulirubin
Direct Bulirubin
AST
ALT
Alkaline Phosphatase

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11
Q

In advanced liver disease, what happens to albumin?

A

Low levels

Albumin responsible for coloid osmotic pressure, so leads to leakage of intravas to interstitial spaces/peripheral edema

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12
Q

What lab result measures the liver’s capacity to synthesize clotting factors?

A

PT

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13
Q

What are the markers of dysfunction of liver synthetic function?

A

Albumin
PT
Total bilirubin

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14
Q

What are markers for hepatocellular injury?

A

AST/ALT: released when hepatocytes are injured or die.

Used to evaluate acute liver injury, response to treatment, and monitoring those at risk

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15
Q

What lab results are used to evaluate cholestasis (excretory function)?

A

Alkaline phosphatase: Damage to bile duct or obstruction of bile flow
Bilirubin: Elevation is proportional to amt of liver dysfunction.

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16
Q

When is jaundice present in a patient with declined excretory function?

A

Jaundice when > 2.5 mg/dL

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17
Q

What is the nursing care for hepatitis?

A

Supportive.

Providing rest and adequate nutrition
Preventing further liver injury by avoiding hepatotoxic meds/substances like ETOH

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18
Q

What does nursing care for hepatitis include in the hospital?

A

BP, HR, dysrhythmias, urine output-IVF
Daily weights , strict I.Os, abd girth measurements
High calorie, low protein in small freq meals with antiemetics for N/V
Monitor for bleeding-gums, epistaxis, eccyhmosis, petechiae, hematuria, melena

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19
Q

What is the diet for a patient with hepatitis?

A

High calorie, low protein in small freq meals with antiemetics for N/V

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20
Q

What is lactulose used for?

A

for ammonia, acidifies the colon to prevent the absorption of ammonia

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21
Q

What medications are used for hepatitis?

A

Lactolose for ammonia
Antibiotics to clear colon of bacteria that produce ammonia
Treat pruritis from the jaundice with cream or bile salt sequestering agent like Cholestryramine

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22
Q

What is choletyramine used for?

A

Treat pruritis from the jaundice

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23
Q

Why do you give saline and not LR for a patient with hepatitis?

A

Liver cannot metabolize lactate, and this could cause worsening metabolic acidosis

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24
Q

What is the acid/base imbalance in hepatitis?

A

metabolic acidosis

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25
Q

What is the nursing care for fluid overload?

A

diuretics, albumin, protein supplements

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26
Q

What is a Sengstaken-Blakemore tube used for?

A

To control bleeding from Varices

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27
Q

What are some complications of liver disease?

A

Cirrhosis
Hepatic Encephalopathy (HE)
Hepato-renal syndrome
Spontaneous bacterial peritonitis
Hepatocellular carcinoma

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28
Q

What is the most common form of cirrhosis in the US?

A

Laennecs (portal alcoholic or severe malnutrition)

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29
Q

What cardiac complication comes from liver disease?

A

Cardiocirrhosis: Cirrhosis complicating heart disease, with recurrent intractable congestive heart failure

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30
Q

What is post-necrotis cirrhosis?

A

Cirrhosis following submassive necrosis of the liver (subacute yellow atrophy) due to toxic or viral hepatitis

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31
Q

What causes biliary cirrhosis?

A

Caused by obstruction or infection of the major extra or intrahepaticbile ducts

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32
Q

What can cause cirrhosis?

A

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

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33
Q

What is the patho of cirrhosis?

A

Inflammation, fibrotic changes, and increased intrahepatic vascular resistance cause compression of the liver lobule, leading to increased resistance or obstruction of normal blood flow through the liver, which is normally a low-pressure system

Results in splenomegaly, varices, hemorrhoids, cardiac dysfunction

Unstable glucose levels, fatigue/decreased activity tolerance

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34
Q

What are the s/s of cirrhosis?

A

-Decreased synthesis of albumin leads to interstitial edema and deceased plasma volume
-Clotting dysfunction–>bruising–> hemmorahge–>low-grade DIC
-Portal HTN with ascites and LE edema

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35
Q

What are complications of cirrhosis?

A

-Portal Hypertension
-Ascites
-Bleeding Esophageal Varices
-Coagulation Defects
-Jaundice
-Hepatic Encephalopathy
-Hepatorenal Syndrome

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36
Q

What is the nursing care for cirrhosis?

A

-Monitor nutrition, fluid balance, urine output, electrolytes, PT/PTT, platelet function, hematocrit.
-Monitor LOC, abdominal girth.
-CVP
-Manage ascites

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37
Q

What are ways in which ascites is managed?

A

paarecentesis (percutaneous needle aspiration)
venous peritoneal shunt (used when resistant to other therapies; rare)

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38
Q

What is TIPS?

A

procedure to decompress portal venous system

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39
Q

How do you assess worsening cirrhosis?

A

early recognition of neurological and mental status changes, increasing ascites, and hepatorenal syndrome

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40
Q

What does TIPS stand for?

A

transjugular intrahepatic portosystemic shunt

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41
Q

RWhat happens during a TIPS procedure?

A

IR ppl use image guidance to make a tunnel through the liver to connect the portal vein to one of the hepatic veins (three veins that carry blood away from the liver back to the heart).

This reduces portal HTN and variceal bleeding

Improved survival rates

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42
Q

Which vein carries blood from the digestive organs to the liver?

A

Portal vein

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43
Q

Which veins carry blood away from the liver back to the heart?

A

Hepatic veins

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44
Q

What are normal ammonia levels?

A

9.5-49 mcg/dL

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45
Q

Which hepatic disorder is commonly related to the accumulation of toxins such as ammonia?

A

Hepatic encephalopathy

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46
Q

What diet is a someone with hepatic encephalopathy likely on?

A

Low protein diet

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47
Q

What medications are used for patients with hepatic encephalopathy?

A

Lactulose: facilitate BM and clear nitrogenous products, decreases the colonic pH to prevent absorption of ammonia
Neomycin or metronidazole: clear the gut of bacteria that promotes nitrogen production

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48
Q

What is an early sign of hepatic encephalopathy?

A

Asterixisis: asking pt to hold hand out, like stopping traffic, and watch for involuntary flapping motion

Also assess for hyperreflexia and muscle rigidity

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49
Q

What causes portal hypertension?

A

-Increase intrahepatic resistance (decreased outflow)
-Splanchnic arteriolar vasodilation (increased inflow)

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50
Q

What is cirrhosis characterized?

A

increased intrahepatic vascular resistance d/t
(1) architectural distortion and (2) deficiency of nitric oxide

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51
Q

What are the three ports of a Sengstaken Blakemore tube?

A

Gastric aspiration port
Esophageal balloon
Gastric balloon

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52
Q

What is a balloon tamponade?

A

Refers to the use of balloons inserted into the esophagus, stomach or uterus, and inflated to alleviate or stop refractory bleeding

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53
Q

What are other ways to treat portal hypertension?

A

Blood transfusion
Drug therapy
Injection sclerotherapy

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54
Q

What is the most frequently fatal complication of cirrhosis?

A

Hepatorenal syndrome

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55
Q

What is the treatment for hepatorenal syndrome?

A

liver/kidney transplant

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56
Q

What is the range for a MELD score?

A

6 to 40

57
Q

What is a MELD score?

A

Ranks your degree of sickness, which shows how much you need a liver transplant. The higher the number, the more urgent your case is.

58
Q

What should be monitored during the postoperative phase of a liver transplant?

A

Hemodynamic status, oxygenation and electrolyte balance.

Monitoring of adequate oxygenation
Coagulation studies
Hyperglycemia
Hyperkalemia
Metabolic acidosis
Calcium, phosphorus, and magnesium

59
Q

Why might vasopressors and fluid boluses be required during the postoperative phase of a liver transplant?

A

May be required the first 24-48 hours

High cardiac outputs and low systemic vascular resistance related to the effects of end-stage liver disease that continues immediately after surgery

60
Q

What hormones are secreted by the pancreas?

A

Insulin (increase uptake of glucose into cells; promote glycogenesis)
Glucagon (promotes glycogenolysis; increase blood sugar levels)
Somatostatin (mild inhibition of insulin and glucagon; decrease gut motility and secretion of digestive juices)

61
Q

What is the difference between interstitial and necrotizing pancreatitis?

A

Interstitial: Mild cases – no end-organ damage and have low mortality rates; self-limiting with full recovery.

Necrotizing or Severe: Often develop SIRS and end-organ dysfunction.

62
Q

What are causes of acute pancreatitis?

A

Gallstones and excessive alcohol intake are responsible for 70-80% of the cases

10% of the time: biliary tract disease, trauma, infection, shock, and certain medications (steroids, diuretics, transplant meds, TPN)

63
Q

What are hallmark symptoms of pancreatitis?

A

Epigastric or left upper quadrant pain.

Pain is described as a deep, sharp, constant with radiation to the back, chest, or flanks, and increases within minutes of eating food high in fat content

64
Q

What are normal blood amylase levels?

A

23-85 U/L

65
Q

What are normal lipase levels?

A

0-160 U/L

66
Q

What is the most sensitive indicator for acute pancreatitis?

A

Lipase levels (normal is 0-160 U/L)

67
Q

In pancreatitis, what do the increases in BUN, AST, ALT, and WBC indicate?

A

Increased BUN – suggests hypovolemia
AST increase – indicates damage to liver cells
ALT – indicates gallstone pancreatitis
WBC – related to inflammation

68
Q

What is the criteria for acute pancreatitis diagnosis?***

A

Presence of 2 of the 3 following criteria:
(i) abdominal pain consistent with the disease
(ii) serum amylase and/or lipase greater than three times the upper limit of normal
(iii) characteristic findings from abdominal imaging

69
Q

What are the priorities in the ED for acute pancreatitis?

A

-Volume resuscitation (several liters of isotonic crystalloids solution, followed by 200-300ml/hour)
-Stabilization of vitals (can quicky decompensate with hypovolemic shock, pulm compromise, renal failure, and GI bleeding)
-Begin pain relief

70
Q

What meds are given for acute pancreatitis?

A

Priority: Pain relief with opioids (Dilaudid or morphine)
Anticholinergics – decreases GI motility and pancreatic enzyme release
Anti-spasmodics – relaxes the smooth muscle, relaxes sphincter of Oddi
H2 blockers/PPI – decrease GI acid secretions
Antibiotics – if have necrotizing pancreatitis

71
Q

What is the difference between using CT with contrast and MRCP for imaging of acute pancreatitis?

A

CT with contrast: 90% specific and sensitive

MRI w/ MRCP: helpful in patients with a contrast allergy and renal insufficiency

72
Q

What are the nursing care for pancreatitis?

A

-Fluid/electrolyte replacement
-Pain control
-Nutrition
-Pancreatic rest
-ERCP/Surgery

73
Q

What are signs to look for in severe hemorrhagic pancreatitis?

A

Turner’s Sign
Cullen’s Sign

74
Q

Define Turner’s sign.

A

bruising of the flanks, retroperitoneal hemorrhage

75
Q

Define Cullen’s sign.

A

edema and bruising around the umbilicus

76
Q

What are signs of hypocalcemia/hypomagnesemia?

A

Chvostek’s Sign
Trousseau’s Sign

77
Q

Describe Chvostek’s sign.

A

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

78
Q

Describe Trousseau’s sign.

A

carpopedal spasm caused by inflating the Bp cuff to a level above the sysltolic pressure for 3 minutes; more sensitive for hypocalcemia

79
Q

What is the difference between Type I and Type II DM?

A

Type I (Insulin dependent) — no production of insulin
Type II (Insulin resistance) — hyperglycemia, hyperinsulinemia, and consequent Beta cell exhaustion

80
Q

What is the most common cause of DKA?

A

Infection (30-50% of cases); UTI and PNA account for most

81
Q

What type of DM is DKA more commonly seen?

A

Type I

82
Q

What is necessary for diagnosis of DKA?

A

Hyperglycemia
Acidosis
Ketosis

83
Q

What are physical findings of a patient with DKA?

A

Hyperventilation, Kussmauls (acetone/fruity breath), dehydration, abd distention, dry mucous membranes, flushed skin, poor skin turgor, decreased perfusion, hypotension, tachycardia, altered mental status, stupor, coma

84
Q

What lab values are often associated with DKA?

A

Blood glucose > 250mg/dL
pH < 7.30
Anion gap >10
Urinalysis: ketones and glucose present
Serum creatinine: elevated
WBC: elevated

85
Q

What are normal anion gap levels?

A

Less than 11

86
Q

What is the nursing care for DKA?

A

-Improve circulatory volume and tissue perfusion (Fluid resuscitation)
-Correct electrolyte imbalances (K+/Phosphate replacement)
-Correct serum glucose (Insulin therapy; slowly)
-Correct ketoacidosis (Bicarb replacement in severe acidosis)
-Treat precipitating event (re-establish metabolic fx)
-Patient education

87
Q

T/F: There are ketones present in HHS.

A

False

88
Q

What are hallmarks of HHS?

A

Marked hyperglycemia
Hyperosmolality
No ketoacidosis

89
Q

Between HHS and DKA, which has higher mortality?

A

HHS

90
Q

Which type of DM is more common in HHS?

A

Type II

91
Q

What are physical findings of a patient with HHS?

A

weakness, polyuria, polydipsia, impaired mental state (confusion to coma) with dehydration S/S include tachycardia, hypotension, low CO, poor skin turgor, rapid resps, non-Kussmauls, warm, flushed skin

92
Q

An older adult, over past few days, appears more drowsy, is eating, sleeping more, and difficult to wake up. This is consistent with hx for what disease?

A

HHS

93
Q

What are common lab results of a patient with HHS?

A

-BG 400-4000mg/dL
-High NA and serum osmolality
-Not acidotic, so pH low-ish
-Bicarb normal
-Anion gap is not elevated
-Serum osmolality is very high (reflects the severe dehydration)
-High Na

94
Q

What is the nursing care for HHS?

A

-Correct volume depletion
-Control hyperglycemia
-ID underlying cause and treat
-Patient education

95
Q

What is the order of priority for DKA? (check)

A

1: insulin therapy

#2: fluid replacement

96
Q

What is the only type of insulin that can be given IV?

A

Regular

97
Q

What happens to K+ levels as you administer insulin?

A

Insulin drives potassium into the cells – causing it to decrease rapidly.

98
Q

Why is insulin continued even after BG decreases in DKA?

A

By giving D5 ½ NS infusion with the insulin, we can continue to bring down the acidosis process while maintaining safe blood sugars.

99
Q

What should be included in patient education of DKA?

A

-When you are ill, you should check your blood sugar more often
-Notify your provider if you’re ill
-Notify your provider or go to the ED at the FIRST indication of DKA (fruity breath, heavy breathing, feeling dry and hot, excessive urination, blurry vision, or a blood glucose over 400 mg/dL or over your meter MAX)
-If you have an insulin pump, make sure it is working appropriately

100
Q

What do you do if a patient comes in with an insulin pump?

A

If a patient comes in with an insulin pump, it should always be turned OFF – we will manage their sugars with SubQ insulin and don’t want them to receive a double dose.

101
Q

What population is often affected by HHS?

A

Fairly common in older adults with other co-morbidities (CHF, CKD)

Nursing homes: severe elevated glucose in setting of dehydration = high mortality

102
Q

What are functions of the skin?

A

-Protects against Infection
-Prevents loss of body fluids
-Controls body temperature
-Functions as a sensory and excretory organ
-Produces Vitamin D
-Determines identity

103
Q

What are the different categories of burn depth?

A

-Superficial (First Degree)
-Partial Thickness (Second Degree)
-Full Thickness (Third Degree)
-Fourth Degree

104
Q

In the rule of nines, what percentage are both arms?

A

18%, 9% for each arm

105
Q

In the rule of nines, what percentage is one leg?

A

18%, both legs are 36%

106
Q

What is the breakdown of the rule of nines?

A

Head and Neck: 9%
Arms: 9% each
Ant. trunk: 18%
Post trunk: 18%
Legs: 18% each
Perineum: 1%

107
Q

What part of the body getting burned will have increased mortality rates?

A

Upper part of the body

108
Q

What part of the body getting burned will most likely lead to pulmonary complications?

A

Head, neck, chest

109
Q

What part of the body getting burned will make the patient more prone to infection?

A

Perineum

110
Q

Burn patients have a higher mortality at what ages?

A

Adults over 60 and children under two (thinner skin, more body surface)

111
Q

What are the different causes of burns?

A

Thermal (flame, hot liquid, hot object)
Chemical (tissue destruction secondary to chemical, liquid, or acid)
Electrical (only entrance and exit wounds apparent)
Radiation (localized)

112
Q

What percentage of TBSAB in adults is life threatening?

A

Greater than 25%

113
Q

What percentage of TBSAB in children is life threatening?

A

Greater than 20%

114
Q

What burn circumstances are life threatening?

A

-Greater than 25% TBSAB in adults
-Greater than 20% TBSAB in children
-Full thickness greater than 10%
-Burn of face, hands, eyes, ears, perineum
-Inhalation, electrical burn
-Burn with extenuating circumstances

115
Q

What is the treatment for thermal burns?

A

-Irrigate
-Remove Wet Clothing
-Transport
-High oxygen concentration if the fire was in a closed space

116
Q

What is the treatment for chemical burns?

A

-Dilute the chemical when appropriate

-Remove contaminated clothing

-Flush for at least twenty to thirty minutes

117
Q

What is the treatment for electrical burns?

A

-Turn off Source of Current

-Use non-conductive materials to remove from electricity source

-Immobilize

118
Q

What are the three phases of burn care?

A

Emergent Phase
Acute Phase
Rehabilitative Phase

119
Q

Describe the phases of burn care.

A

Emergent Phase: Begins with the injury and lasts 24-48 hours or, in the critically ill patient, up to two weeks

Acute Phase: Begins when initial fluid replacement is complete and fluid shifts from interstitial back to vascular space

Rehabilitative Phase: From hospital admission to resumption of functioning level in society

120
Q

What are the priorities during the emergency phase of burn care?

A

-Institute and Maintain Strict -Isolation
-Institute Fluid Resuscitation
-Gastric Intubation
-Foley Catheter
-Tetanus
-Wound Cultures
-Tubbing

121
Q

What is Parkland’s formula?

A

Lactated Ringers:
4cc. X body weight (kg) X TBSAB

122
Q

From when should fluid resuscitation be calculated?

A

Fluids must be calculated from the time of burn occurrence as most of the fluid is lost in the initial 8 hours

123
Q

How much of the calculated fluid should be given in the first 8 hours?

A

1/2 of the calculated fluid for the first 24 hours is given in that initial 8 hours

124
Q

What are signs that show an adaptive fluid level?

A

-Lucid Mental Status
-Adaptive Vital Signs
-Adequate Peripheral -Perfusion
-Adequate Urinary Output
-Return to Normal Weight
-Pulse Rate Less than 120
-Normal CVP
-Clear Lungs

125
Q

Define allograft, xenograft, and autograft.

A

Allograft: from another human
Xenograft: from an animal
Autograft: from self

126
Q

What is escharotomy?

A

Emergency surgical procedure involving incising through areas of burnt skin to release the eschar and its constrictive effects, restore distal circulation, and allow adequate ventilation.

127
Q

What are complications from burns?

A

-Hypovolemic Shock
-Wound Infection
-Respiratory Complications
-Curlings Ulcer
-Electrolyte Alterations
-Cardiovascular Problems

128
Q

What are management priorities in the acute phase of burns?

A

-Fluid
-Wound Care (debridement, dressings, medications)
-Hydrotherapy
-Nutrition

129
Q

What medication is given for burns?

A

Silvadene: antimicrobial properties

-softens eschar
-can cause leukopenia

130
Q

What is a side effect of silvadene?

A

Can cause leukopenia

131
Q

How often should tubbing occur for a burn patient?

A

At least once a day

132
Q

What are the downsides of tubbing?

A

-Loss of body heat
-Painful, stressful
-Loss of sodium

133
Q

What is the purpose of tubbing for burn patients?

A

-Removes topical agents and cleanses
-Softens the eschar, increasing range of motion

134
Q

During the emergent phase, what is the psychological impact of burns?

A

Psychological “shutdown”

135
Q

During the acute phase, what is the psychological impact of burns?

A

Pain, depression, regression

136
Q

During the recuperative phase, what is the psychological impact of burns?

A

Apprehension

137
Q

What is the intervention for the psychological impact of burns?

A

Burn support group

138
Q

What are the priorities in the recuperative phase of burns?

A

-Jobst garments
-Splinting (for contractures)

Complex (2 decks)

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