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An RN working in the Intensive Care Unit (ICU) is caring for a patient with an acute gastrointestinal hemorrhage related to liver failure that resulted from alcoholic cirrhosis. During hand-off report at the end of the shift, the outgoing RN states to the incoming RN, “I have been in that room all day, transfusing blood products and giving medications. It’s so much work for really no reason. I don’t know why this patient drank to the degree he did to destroy his liver. He did this to himself. What a waste of resources. I heard his family wants to get him on a list for a liver transplant.”

Address the following:

1. What is the most appropriate way for the incoming RN to approach this situation? Include ethical and legal considerations.

2. What is the role of the RN in regard to addressing the value system of other health care workers that may have a negative impact of the delivery of patient care? Include ethical and legal considerations.

minimum 250 words and references

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Casey Durgan
Casey DurganLv2
28 Sep 2019

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Case 2 (7.5 pts)

R. S., a 55-year-old man, has been admitted to the hospital for treatment of acute gastrointestinal bleed. He is well known to the medical community for his chronic alcohol abuse and encephalopathy.

Past History: R. S. has been hospitalized four times in the past 24 months; most recently he was discharged 12 weeks ago for treatment of upper gastrointestinal bleeding. He has a 40-year history of smoking and drinks an unknown quantity of liquor daily. On previous admissions he has been treated for pancreatitis, alcohol withdrawal seizures, cirrhosis and associated ascites, coagulopathy, esophageal varices, anemia, gastrointestinal bleed, and gastritis.

Current Status: His current problems include hepatic encephalopathy, gastrointestinal bleed, coagulopathy, jaundice, history of tuberculosis (age 15 with treatment), and hypoxia; all present were on previous admission. Medications at last discharge included spironolactone (25 mg twice a day), ranitidine (150 mg twice a day), antacid (Maalox), and multivitamins.

R. S. was found unconscious in a pool of blood and vomitus. He was taken to the hospital and admitted to the medical intensive care unit. Initial vital signs were as follows: blood pressure 90/60, heart rate 112, and respirations 12. Intravenous infusion with normal saline was begun through a central line; oxygen was started at 3 L by nasal cannula. Physical examination revealed icteric sclera, clear lungs, grade Ill/TV systolic ejection murmur, and abdomen soft and without masses, liver percussed at 12 cm below the costal margin, and skin markedly jaundiced. Deep tendon reflexes were brisk and equal bilaterally.
Lab tests revealed the following: sodium 137 mEq/L, potassium 4.8 mEq/L, chloride 102 mEq/L, carbon dioxide 23 mEq/L, blood urea nitrogen 132 mg/dl, creatinine 1.3 mg/dl, glucose 115 mg/dl, hematocrit 27.7%, hemoglobin 9.3 g, white blood cell count 17,800 mm3, platelets 259,000 mm3, direct bilirubin 7.8 mg/dl, total bilirubin 16.4 mg/dl, amylase 42 somogyi units/dl, alkaline phosphatase 127 mu/dl, ammonia level 200 mg. Blood gases were as follows: Po.2 85 mm Hg, PCO2 30 mm Hg, pH 7.35, prothrombin time (PT) patient 17 sec., prothrombin time (PT) control 12.3 sec., partial prothrombin time (PIT) 46/36 sec.
Treatment with blood replacement was initiated; it included transfusion of 6 units fresh frozen plasma and 5 units packed red blood cells, with antacids, ranitidine, vitamin K, thiamine, and lactulose by nasogastric tube.
On the following day R. S.’s mental status was improved and his laboratory studies were as follows: sodium 133 mEq/L. potassium 3.5 mEq/L, chloride 105 mEq/L, blood urea nitrogen 15 mg/dl, creatinine 0.7 mg/dl, glucose 114 mg/dl, hematocrit 38.7%, white blood cell count 5200 mm3, PT 15.7/12 sec., ammonia 93 mg, alkaline phosphatase 92 m/dl. Vital signs were as follows: blood pressure 116/72, heart rate 72, respirations 15, afebrile.
On day 2 he was oriented X3 and was transferred from the intensive care unit. During the course of his hospitalization his total bilirubin ranged from 16.4 mg/dl down to 10.7 mg/dl at discharge.

What is the physiological benefit of having a hepatic portal system?

Does R.S have elevated bilirubin? If yes, does the portion of the total bilirubin that is direct indicate pre hepatic, post hepatic or an intrahepatic problem?

What is ascites? How do hypoalbuminemia and increased serum aldosterone levels contribute to the development of ascites?

Explain the cause of the patients’ clotting defects.

The sclera of R. S.’s eyes are icteric and his skin yellowed. What is the cause of

these discolorations, and what do they indicate about his pathophysiology?

Explain why esophageal varices are the leading cause of death in patients with cirrhosis

Roger Maxwell is very health-conscious. He runs, swims, and hikes; follows a lowcarbohydrate diet; and generally feels great. He sees a physician when he needs to, in addition to annual physical exams at the large company where he is an engineer. He'd never allow himself to get so out of shape that heart disease would be a risk. Because of his strict adherence to this healthy lifestyle, Roger is surprised when a medical intern, gazing at his yearly elecfrocardiogram (ECG) at his work physical, clearly picks up on something.

"What? What are you looking at?" Roger blurts out while buttoning up his shirt.

"Oh, it's probably nothing." But she doesn't look like it's probably nothing.

"The heart murmur? My mom's been telling me about it since childhood. Not a big deal. The doctors called it something last year, something I never heard of." "Did you check it out?" asks the intern.

"Nah. It wasn't bothering me, so I forgot about it. Why? What's wrong?"

"Well, maybe you should ask the doctor to explain it again and suggest what to do."

"About what?"

"The doctor will explain it. Please don't worry, though," says the intern as she rushes off to the next patient.

Roger's electrocardiograms had in fact been showing that he has had long QT syndrome, and not a heart murmur, for many years. The doctor explains that this is a problem with the heart's rhythm, and not its valves. Roger goes home and Googles long QT syndrome right away. What he finds concerns him enough to alert his relatives.

Long QT syndrome is a lengthening in the time that it takes the ventricles (the lower two heart chambers) to recover after a contraction, called the QT interval on an electrocardiogram. This delay is called torsade de pointes, and it causes lightheadedness upon standing or even fainting, as blood pressure drops when the heart rhythm becomes abnormal. If the arrhythmia turns into the more erratic condition called ventricular fibrillation, it can be deadly. Some cases •of sudden cardiac arrest in people who apparently do not have heart disease are in fact due to long QT syndrome. This 'may have been the case with Roger's aunt, Amelia, his mother's sister, who died at age 34 of what was thought to be a heart attack, but, now Roger realizes, was more likely an arrhythmia. Still, with only one affected relative, Roger had never thought of his aunt's •early demise as a family history, especially since his mother is healthy.

Roger reads that in people with some forms of long QT syndrome, fatal arrhythmia can be triggered by intense emotions or a sudden loud sound. The first recorded case of the condition was a little girl, who collapsed dead •when her teacher suddenly yelled at her. Her older brother had died in a similar circumstance. Suddenly, Roger remembers that his daughter Sheila faints very easily. She even passed out once at a rock concert because she got so excited. He'd never panicked over it because his mother fainted easily, too. A pattern was emerging.

Long QT syndrome is caused by mutations in any of at least 10 genes that encode either proteins that form parts of ion channels (potassium, sodium, or calcium) or proteins that affect the functioning of these channels. Ion channels control the spread of nerve impulses and the resulting muscle contraction. The time for the heart's reeovery after a beat, called repolarization, extends the period when ions are trapped inside heart muscle cells because the channels are blocked, too slow to open, or too quick to close in people who are at elevated risk due to inheriting a mutation. People with long QT syndrome can experience arrhythmia if they take certain drugs that prolong the QT interval. These drugs include certain antibiotics, antidepressants, and diuretics ("water pills").

Roger reads about the different genes and drug combinations that cause long QT syndrome on Wikipedia, and then he scans www.genetests.org to find labs that test for all of them. Only then does he make an appointment with a cardiologist, and he arranges to have his blood and that of his daughter and mother sent to one of the labs. Two weeks later, he learns that they all have a dominant mutation in a gene called HERG (for "human ether-a-go-go") that causes long QT syndrome type 2 (LQT2). Even healthy family members could have inherited the mutation, because 15 percent of people with long QT syndrome do not have symptoms. The concern is their increased risk of developing symptoms in the future—perhaps suddenly.

Question 1 : Roger is upset that in the past doctors had not been more insistent that he follow up on the abnormal ECG pattern. When he mentions this to his primary care physician, she answers, "I didn't say anything because you are so healthy, and people who have cardiac arrest from long QT do so in young adulthood. You're too old to worry about it." But Roger should be worried, because

a. he looks younger than he is, so could still be at risk

b. the condition can be inherited, so others in the family could be affected.

c. he could die at any time.

d. he can no longer take antibiotics.

e. long QT syndrome can cause cholesterol to build up in his coronary arteries.

2. Individuals who should take genetic tests for long QT syndrome are

a. all the people in generation IV.

b. Eric, Joan and Peter, and then Dylan, Anika, Sean, Keri, and Anna if a parent has the mutation.

c. Juanita, Larry, Joan, Peter, and Ellie.

d. Abe, Sara, Craig, Philip, Edwin, and Yvonne.

e. Only those who are athletic.

3. The mode of inheritance of long QT syndrome in the Maxwell family is

a. X-Iinked recessive

.b. autosomal recessive.

c. autosomal dominant.

d. sex-limited.

e. X-Iinked dominant.

4. Some people who inherit the same mutation as Roger do not experience any symptoms. This means that the mutation is

a. variably expressive.

b. genetically heterogeneic.

c. polygenic.

d. incompletely penetrant.

e. dominant.

5). The fact that mutations in any of several genes can cause long QT syndrome means that the condition is

a. variably expressive.

b. genetically heterogeneic.

c. polygenic.

d. incompletely penetrant.

e.recessive.

6). The risk that Sean, Keri, or Anna has inherited the family's mutation for long QT syndrome is

a. 1

b. ¾

c. ¼

d. ¼

e. 1/8

7) Roger is relieved that he does not have- LQT7, which affects skeletal as well as cardiac muscle, causing short stature and scoliosis. He is also glad that he doesn't have LQT8, which causes many symptoms, or either of two types that also cause deafness. These other forms of the condition, with more than one symptom, exhibit

a. invariable expressivity.

b. complete penefrance.

c. genetic homogeneity.

d. pleiotropy.

e. phenocopy.

8) The reason that mutations in different genes all cause the same phenotype of extended QT interval on an ECG is that

a. the heart is an extremely complex organ.

b. the genes all encode proteins that affect ion channels essential for maintaining heartbeat.

c. the genes all encode the same protein.

d. the mutations all affect the genes in the same way.

e. the QT interval is highly variable, even within individuals at different times.

9). A phenotypic pattern in a family that could be due to inherited long QT syndrome is

a. sudden cardiac death in one or more young people and individuals who faint easily.

b. many individuals who eat a very fatty diet and are sedentary but do not develop heart disease.

c. many individuals with hypertension.

d. many individuals who suffer heart attacks after age 50.

e. a family with rnany athletes who have very low heart rates because of intense and frequent exercise.

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