Exam 3 Flashcards

(138 cards)

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
What is the nursing care for fluid overload?
diuretics, albumin, protein supplements
26
What is a Sengstaken-Blakemore tube used for?
To control bleeding from Varices
27
What are some complications of liver disease?
Cirrhosis Hepatic Encephalopathy (HE) Hepato-renal syndrome Spontaneous bacterial peritonitis Hepatocellular carcinoma
28
What is the most common form of cirrhosis in the US?
Laennecs (portal alcoholic or severe malnutrition)
29
What cardiac complication comes from liver disease?
Cardiocirrhosis: Cirrhosis complicating heart disease, with recurrent intractable congestive heart failure
30
What is post-necrotis cirrhosis?
Cirrhosis following submassive necrosis of the liver (subacute yellow atrophy) due to toxic or viral hepatitis
31
What causes biliary cirrhosis?
Caused by obstruction or infection of the major extra or intrahepaticbile ducts
32
What can cause cirrhosis?
Caused by chronic hepatitis virus, alcohol abuse, nonalcoholic steatohepatitis, hereditary hemochromatosis, Wilson’s disease, and alpha1-antitrypsin deficiency
33
What is the patho of cirrhosis?
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
34
What are the s/s of cirrhosis?
-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
35
What are complications of cirrhosis?
-Portal Hypertension -Ascites -Bleeding Esophageal Varices -Coagulation Defects -Jaundice -Hepatic Encephalopathy -Hepatorenal Syndrome
36
What is the nursing care for cirrhosis?
-Monitor nutrition, fluid balance, urine output, electrolytes, PT/PTT, platelet function, hematocrit. -Monitor LOC, abdominal girth. -CVP -Manage ascites
37
What are ways in which ascites is managed?
paarecentesis (percutaneous needle aspiration) venous peritoneal shunt (used when resistant to other therapies; rare)
38
What is TIPS?
procedure to decompress portal venous system
39
How do you assess worsening cirrhosis?
early recognition of neurological and mental status changes, increasing ascites, and hepatorenal syndrome
40
What does TIPS stand for?
transjugular intrahepatic portosystemic shunt
41
RWhat happens during a TIPS procedure?
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
42
Which vein carries blood from the digestive organs to the liver?
Portal vein
43
Which veins carry blood away from the liver back to the heart?
Hepatic veins
44
What are normal ammonia levels?
9.5-49 mcg/dL
45
Which hepatic disorder is commonly related to the accumulation of toxins such as ammonia?
Hepatic encephalopathy
46
What diet is a someone with hepatic encephalopathy likely on?
Low protein diet
47
What medications are used for patients with hepatic encephalopathy?
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
48
What is an early sign of hepatic encephalopathy?
Asterixisis: asking pt to hold hand out, like stopping traffic, and watch for involuntary flapping motion Also assess for hyperreflexia and muscle rigidity
49
What causes portal hypertension?
-Increase intrahepatic resistance (decreased outflow) -Splanchnic arteriolar vasodilation (increased inflow)
50
What is cirrhosis characterized?
increased intrahepatic vascular resistance d/t (1) architectural distortion and (2) deficiency of nitric oxide
51
What are the three ports of a Sengstaken Blakemore tube?
Gastric aspiration port Esophageal balloon Gastric balloon
52
What is a balloon tamponade?
Refers to the use of balloons inserted into the esophagus, stomach or uterus, and inflated to alleviate or stop refractory bleeding
53
What are other ways to treat portal hypertension?
Blood transfusion Drug therapy Injection sclerotherapy
54
What is the most frequently fatal complication of cirrhosis?
Hepatorenal syndrome
55
What is the treatment for hepatorenal syndrome?
liver/kidney transplant
56
What is the range for a MELD score?
6 to 40
57
What is a MELD score?
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
What should be monitored during the postoperative phase of a liver transplant?
Hemodynamic status, oxygenation and electrolyte balance. Monitoring of adequate oxygenation Coagulation studies Hyperglycemia Hyperkalemia Metabolic acidosis Calcium, phosphorus, and magnesium
59
Why might vasopressors and fluid boluses be required during the postoperative phase of a liver transplant?
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
What hormones are secreted by the pancreas?
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
What is the difference between interstitial and necrotizing pancreatitis?
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
What are causes of acute pancreatitis?
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
What are hallmark symptoms of pancreatitis?
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
What are normal blood amylase levels?
23-85 U/L
65
What are normal lipase levels?
0-160 U/L
66
What is the most sensitive indicator for acute pancreatitis?
Lipase levels (normal is 0-160 U/L)
67
In pancreatitis, what do the increases in BUN, AST, ALT, and WBC indicate?
Increased BUN – suggests hypovolemia AST increase – indicates damage to liver cells ALT – indicates gallstone pancreatitis WBC – related to inflammation
68
What is the criteria for acute pancreatitis diagnosis?***
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
What are the priorities in the ED for acute pancreatitis?
-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
What meds are given for acute pancreatitis?
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
What is the difference between using CT with contrast and MRCP for imaging of acute pancreatitis?
CT with contrast: 90% specific and sensitive MRI w/ MRCP: helpful in patients with a contrast allergy and renal insufficiency
72
What are the nursing care for pancreatitis?
-Fluid/electrolyte replacement -Pain control -Nutrition -Pancreatic rest -ERCP/Surgery
73
What are signs to look for in severe hemorrhagic pancreatitis?
Turner's Sign Cullen's Sign
74
Define Turner's sign.
bruising of the flanks, retroperitoneal hemorrhage
75
Define Cullen's sign.
edema and bruising around the umbilicus
76
What are signs of hypocalcemia/hypomagnesemia?
Chvostek's Sign Trousseau's Sign
77
Describe Chvostek's sign.
twitching of the facial muscles in response to tapping over the area of the facial nerve
78
Describe Trousseau's sign.
carpopedal spasm caused by inflating the Bp cuff to a level above the sysltolic pressure for 3 minutes; more sensitive for hypocalcemia
79
What is the difference between Type I and Type II DM?
Type I (Insulin dependent) — no production of insulin Type II (Insulin resistance) — hyperglycemia, hyperinsulinemia, and consequent Beta cell exhaustion
80
What is the most common cause of DKA?
Infection (30-50% of cases); UTI and PNA account for most
81
What type of DM is DKA more commonly seen?
Type I
82
What is necessary for diagnosis of DKA?
Hyperglycemia Acidosis Ketosis
83
What are physical findings of a patient with DKA?
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
What lab values are often associated with DKA?
Blood glucose > 250mg/dL pH < 7.30 Anion gap >10 Urinalysis: ketones and glucose present Serum creatinine: elevated WBC: elevated
85
What are normal anion gap levels?
Less than 11
86
What is the nursing care for DKA?
-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
T/F: There are ketones present in HHS.
False
88
What are hallmarks of HHS?
Marked hyperglycemia Hyperosmolality No ketoacidosis
89
Between HHS and DKA, which has higher mortality?
HHS
90
Which type of DM is more common in HHS?
Type II
91
What are physical findings of a patient with HHS?
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
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?
HHS
93
What are common lab results of a patient with HHS?
-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
What is the nursing care for HHS?
-Correct volume depletion -Control hyperglycemia -ID underlying cause and treat -Patient education
95
What is the order of priority for DKA? (check)
#1: insulin therapy #2: fluid replacement
96
What is the only type of insulin that can be given IV?
Regular
97
What happens to K+ levels as you administer insulin?
Insulin drives potassium into the cells – causing it to decrease rapidly.
98
Why is insulin continued even after BG decreases in DKA?
By giving D5 ½ NS infusion with the insulin, we can continue to bring down the acidosis process while maintaining safe blood sugars.
99
What should be included in patient education of DKA?
-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
What do you do if a patient comes in with an insulin pump?
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
What population is often affected by HHS?
Fairly common in older adults with other co-morbidities (CHF, CKD) Nursing homes: severe elevated glucose in setting of dehydration = high mortality
102
What are functions of the skin?
-Protects against Infection -Prevents loss of body fluids -Controls body temperature -Functions as a sensory and excretory organ -Produces Vitamin D -Determines identity
103
What are the different categories of burn depth?
-Superficial (First Degree) -Partial Thickness (Second Degree) -Full Thickness (Third Degree) -Fourth Degree
104
In the rule of nines, what percentage are both arms?
18%, 9% for each arm
105
In the rule of nines, what percentage is one leg?
18%, both legs are 36%
106
What is the breakdown of the rule of nines?
Head and Neck: 9% Arms: 9% each Ant. trunk: 18% Post trunk: 18% Legs: 18% each Perineum: 1%
107
What part of the body getting burned will have increased mortality rates?
Upper part of the body
108
What part of the body getting burned will most likely lead to pulmonary complications?
Head, neck, chest
109
What part of the body getting burned will make the patient more prone to infection?
Perineum
110
Burn patients have a higher mortality at what ages?
Adults over 60 and children under two (thinner skin, more body surface)
111
What are the different causes of burns?
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
What percentage of TBSAB in adults is life threatening?
Greater than 25%
113
What percentage of TBSAB in children is life threatening?
Greater than 20%
114
What burn circumstances are life threatening?
-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
What is the treatment for thermal burns?
-Irrigate -Remove Wet Clothing -Transport -High oxygen concentration if the fire was in a closed space
116
What is the treatment for chemical burns?
-Dilute the chemical when appropriate -Remove contaminated clothing -Flush for at least twenty to thirty minutes
117
What is the treatment for electrical burns?
-Turn off Source of Current -Use non-conductive materials to remove from electricity source -Immobilize
118
What are the three phases of burn care?
Emergent Phase Acute Phase Rehabilitative Phase
119
Describe the phases of burn care.
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
What are the priorities during the emergency phase of burn care?
-Institute and Maintain Strict -Isolation -Institute Fluid Resuscitation -Gastric Intubation -Foley Catheter -Tetanus -Wound Cultures -Tubbing
121
What is Parkland's formula?
Lactated Ringers: 4cc. X body weight (kg) X TBSAB
122
From when should fluid resuscitation be calculated?
Fluids must be calculated from the time of burn occurrence as most of the fluid is lost in the initial 8 hours
123
How much of the calculated fluid should be given in the first 8 hours?
1/2 of the calculated fluid for the first 24 hours is given in that initial 8 hours
124
What are signs that show an adaptive fluid level?
-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
Define allograft, xenograft, and autograft.
Allograft: from another human Xenograft: from an animal Autograft: from self
126
What is escharotomy?
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
What are complications from burns?
-Hypovolemic Shock -Wound Infection -Respiratory Complications -Curlings Ulcer -Electrolyte Alterations -Cardiovascular Problems
128
What are management priorities in the acute phase of burns?
-Fluid -Wound Care (debridement, dressings, medications) -Hydrotherapy -Nutrition
129
What medication is given for burns?
Silvadene: antimicrobial properties -softens eschar -can cause leukopenia
130
What is a side effect of silvadene?
Can cause leukopenia
131
How often should tubbing occur for a burn patient?
At least once a day
132
What are the downsides of tubbing?
-Loss of body heat -Painful, stressful -Loss of sodium
133
What is the purpose of tubbing for burn patients?
-Removes topical agents and cleanses -Softens the eschar, increasing range of motion
134
During the emergent phase, what is the psychological impact of burns?
Psychological "shutdown"
135
During the acute phase, what is the psychological impact of burns?
Pain, depression, regression
136
During the recuperative phase, what is the psychological impact of burns?
Apprehension
137
What is the intervention for the psychological impact of burns?
Burn support group
138
What are the priorities in the recuperative phase of burns?
-Jobst garments -Splinting (for contractures)