Metabolism Rapid Reasoning
NURS 2900
10 Points
III. Developing Nurse Thinking by Identifying Clinical RELATIONSHIPS
What is the RELATIONSHIP of the past medical history and current illness? 1 Point
Past Medical History:
Current Illness:
Patient is a 27-year-old male who
immigrated to America from Somalia
and is currently living in New York.
His past medical history relates to his current illness for several reasons.
Patient is unable to identify his medical
history or treatment, He states he had a
liver problem where he was hospitalized,
and it was viral in nature. He does not
recall the treatment.
He chews khat which is a caffeinated
chew that could be related to the poor
dentition as well as poor nutrition and
limited access to resources. He denies the
use of alcohol or other drugs. He has a
history of taking ibuprofen and Tylenol
for joint paint. He was previously healthy
with no other symptoms.
He has a history of smoking 1 pack per
day since he was a teenager
It should be noted there is a potential
that the patient has been walking around
with a hepatitis virus and because he has
been asymptomatic as evidenced by
previous statement of healthy until
recently, he has not been aware that he is
still carrying the virus.
© 2014 Keith Rischer/www.KeithRN.com
1. He grew up and immigrated he from a country that is
underdeveloped and lacking in resources especially for health care.
Hepatitis vaccination rates are lower in other countries that have
poor medical care.
2. He does not have a good understanding of his medical history. He is
unable to identify whether he had treatment or not or what his
illness is even called. This is relevant currently because it indicates
he still has significant barriers to accessing medicine for one reason
or another. His inability to recall information could also potentially
be correlated to a decrease in level of awareness. Knowing that he
was hospitalized one year ago helps indicate a level of chronicity of
the disease etiology.
3. If he had received treatment and continued education about his
illness, he could have potentially mitigated his disease progression
and lived a more full and normal life. if the patient has hepatitis b
he could have been walking around with it from the time of birth
unaware minus the one prior sickness from it.
4. He does not have a history of alcohol or drug use which indicates
that again this is not necessarily caused by needles although he
could have been nicked or scraped by someone infected. It is more
liable that he contracted it either through birth or blood
contamination through poor sanitary living conditions.
Metabolism Rapid Reasoning
NURS 2900
10 Points
What is the RELATIONSHIP between each physician order and Abdi’s problem? 2.5 Points
Care Provider Orders:
1. Seizure precautions
2. Esophagogastroduodenoscopy (EGD)
with Biopsy
3. Neurological assessment Q2 hours
4. Daily Weight
5. Paracentesis
6. Bed rest
7. Dietician consult
List 3 best practice screenings that you will
implement and why
Rationale for why the primary care provider ordered this?
1.Seizure precautions are put into place because the patient is
developing hepatic encephalopathy. Studies vary on the proportion
of patients that develop seizures due to hepatic encephalopathy
some studies suggest it is an uncommon event and others suggest
approximately 1/3 of patients with liver failure and hepatic
encephalopathy will develop seizures. The development of seizure
due to hepatic encephalopathy is increased poor outcomes. because
little is known about this patient’s medical history and because of
the severity of his cirrhosis/liver failure he should be put on seizure
precautions as a standard safety protocol.
2. Esophagogastroduodenoscopy (EGD) is a diagnostic endoscopic
procedure used to visualize the oropharynx, esophagus, stomach,
and proximal duodenum. The purpose of this procedure is to detect
the presence of esophageal varices, ulcerations of the stomach,
duodenal ulcers and bleeding. The EDG is considered a lower risk
procedure for patients with liver failure.
3. Neuro checks every two hours are indicated for patients
displaying signs of hepatic encephalopathy. The patient is exhibiting
signs of lowered consciousness, as well as asterixis, coupled with
high levels of ammonia in the blood. Excess ammonia in the blod
stream results in increased glutamine production and accumulation
in astrocytes.
This creates an osmotic gradient that promotes (brain cells)
astrocytic swelling Elevated glutamine levels also result in a process
that contributes to the neuronal dysfunction in hepatic
encephalopathy. These processes facilitated ammonia crossing the
blood brain barrier and cause cerebral edema. Neuro checks are
required to monitor for progression because without monitoring
neurological function in the presence of excess ammonia the patient
will ultimately end up in a coma and die, through organ failure.
4. daily weights are necessary currently because the patient is
retaining fluid. He has peripheral edema, he has ascites in his
abdomen, his sodium levels are elevated, potassium levels are low
and he is oliguric, and displaying all indications of hepatorenal
syndrome.
5.Paracentesis is indicated in patients with later stages of cirrhosis,
liver failure, the goal is to remove fluid off the belly and relieve the
ascites, the fluid removed can also be measures, and sent to the lab
to look for infection. With ascites
© 2014 Keith Rischer/www.KeithRN.com
Metabolism Rapid Reasoning
NURS 2900
10 Points
6.Bed rest should be prescribed for him due to the increasing
cerebral edema, or hepatic encephalopathy. He is hypotensive and
has lowered level of consciousness so the safest thing for him to do
is just rest and not try to get up.
7.needs a dietary consult to determine what he should be eating and
discuss how to get nutrients adequately. He is now having issues
with both his liver and his kidneys and will need a low sodium diet,
with the appropriate amount of protein for where his liver and
kidney function are at.
Three best practice screenings for him would be
Fall risk: he should be on falls precautions due to hypotension and
increased icp.
Nursing Delirium scale or Neecham confusion scale to measure
Delirium is considered as an altered mental state, which is
somewhere between between coma and stupor at one end and
normal wakefulness and alertness at the other. This is indicated for
patients with hepatic encephalopathy.
Pain scale : he should be on a pain scale because elevated pain
increases blood pressure which can elevate intracranial pressure.
Glasgow coma scale: he should have the Glasgow comas scale being
utilized each shift or assessment due to the hepatic encephalopathy.
This will allow them to monitor his level or consciousness and
neurological functioning and correlate to other findings.
What is the rationale for why each of the medications are being administered? 1.5 Points
© 2014 Keith Rischer/www.KeithRN.com
Metabolism Rapid Reasoning
NURS 2900
10 Points
Medication Orders:

Lactulose 10 g/15 mL Solution- Administer 30 mL
orally TID

Lansoprazole 30 mg tablet- Administer 1 tablet
orally AC BID

Potassium Replacement Protocol

Lasix 20 mg tablet- Administer 1 tablet orally BID

Spironolactone 12.5 mg tablet- Administer orally
Daily

Propranolol 20 mg tablet- Administer 1 tablet orally
TID
Rationale:
Lactulose is used to prevent and treat clinical portalsystemic encephalopathy it acts to decrease the intestinal
production and absorption of ammonia. Lactulose catalyzes
increases in uptake of ammonia by bacteria found in the
colon. The bacteria utilize the trapped ammonia as a
nitrogen source for protein synthesis. This causes a
decrease in the intestinal ph. which allows the conversion
of NH3 to NH4+ the ionized form of ammonium is unable
to cross the blood brain barrier thereby inhibiting the
continued development of hepatic encephalopathy.
Lactulose also decreases the production of ammonia in the
intestines by destroying the bacteria responsible for the
production of ammonia.
Lansoprazole selectively inhibits membrane enzymes in
gastric parietal cells and reducing gastric acid secretion. It
is effective at treating acid secretions in the stomach and
esophagus. This is important because the patient has
coagulation problems currently and is at an increased risk
of esophageal varices or bleeding.
Potassium replacement protocol the potassium replacement
protocol is indicated because he has a low potassium level
currently at 2.9 and he is going to be taking Lasix and
undergoing a paracentesis. All of these factors are going to
put his fluid and electrolyte status at greater risk. He is also
having little urine output and hepatorenal syndrome. when
he beings to urinate the fluid out he will need to have his
potassium levels monitored closely
Lasix: the furosemide is high ceiling loop diuretic that acts
at the distal loops of Henle to block the absorption of
sodium and water from the filtered fluid in the kidneys.
Water follows sodium and to potassium follows sodium.
Spironolactone is prescribed in combination with Lasix to
diurese the patient more effectively this is a common
prescription for causing an increased diuretic effect and it is
potassium sparing to hopefully preserve some of the
potassium that will be lost due to the Lasix.
Propranolol is a non-selective beta blocker that is readily
prescribed for the treatment of esophageal varices and
portal hypertension. propranolol works by reducing the
hepatic venous pressure and decreasing it to below
12mmHG leads to a reduction in the risk of variceal
bleeding.
© 2014 Keith Rischer/www.KeithRN.com
Metabolism Rapid Reasoning
NURS 2900
10 Points
What is the priority problem (Diagnosis) that your patient is most likely presenting with? 0.5 Point
Acute liver failure which could be leading to cirrhosis or end stage liver disease. This is most likely secondary to a
hepatitis infection that remained in the body latent and had an acute onset.
It would be difficult to conclude that he does in fact have end stage liver disease without a biopsy and several other
diagnostic labs used to verify cirrhosis.
What is the underlying cause/pathophysiology of this primary problem? 0.5 Point
Viral hepatitis------- infection causes the host to mount a response against viral proteins that are expressed by
infected hepatocytes. This process proliferates and creates a cascade where pro- apoptosis (death) t cells
recognize antigen on hepatocytes and triggers an inflammatory necrotizing disease pathway. This can be
chronic or acute depending on the type and the bodies immune response. In the case of this patient, he
developed acute potentially on chronic liver failure (some people can have hepatitis chronically and be
asymptomatic unaware).
Viral Hepatitis especially B in this patients case can leave a patient asymptomatic for years and then
develop fulminant liver failure or acute liver failure. ---Acute liver failure: - this is caused by
proinflammatory viral response that destroys a significant number of hepatocytes. The hepatocytes are replaced
by a fibrous tissue which are then unable to function and serve the purposes of a functioning liver. – this leads
to cirrhosis which is end stage liver failure. There are several system issues that occur to facilitate acute liver
failure and make it worse.
A significant amount of blood is being circulated through the liver at any given time for detoxification and other
processes. The destruction of hepatocytes leads to fibrosis of the liver.
The changes in structure of the liver caused by the destruction of hepatocytes cause an increase in the vascular
resistance in the liver which causes portal hypertension. The increase in portal pressure decreases the blood
flow in the portal system causing blood to shunted and enter into the splenic circulation overall (gi circulation).
The body tries to compensate by and dilating the blood vessels which leads to pooling of platelets being
sequestered into the spleen. (splenomegaly). This with poor protein blood levels (low albumin) leads to poor
© 2014 Keith Rischer/www.KeithRN.com
Metabolism Rapid Reasoning
NURS 2900
10 Points
perfusion of renal system and the RASS system activates and fluid is retained. This process leads to
thrombocytopenia, anemia, leukopenia, as well as initiates the hepatorenal syndrome.
The vasodilation that occurs in gi or splanchnic circulation along with the decreased blood flow the portal
system causes the blood to pool which creates a hypovolemic effect in the central circulatory system. This
causes the sympathetic nervous system to respond inappropriately to angiotensin II leading to worsened blood
pressures. The complexity of the circulatory dysregulation leads to a prerenal injury of the kidney. This process
is proliferated by the continuous shunting of blood due to portal hypertension. Increased intra-abdominal
pressure can cause venous congestion and a decline in GFR. In addition, organ compression can stimulate the
RAAS system as well.
Bilirubin which is the end product of heme is converted i to urobilinogen and excreted from the body when this
process is disrupted patients develop jaundice.
Ammonia is another ion that builds up in the body, ammonia is the byproduct of gluconeogenesis in protein
synthesis. However, ammonia builds up due to the shunting that occurs in the liver and is not converted
appropriately to urea and removed from the body. The result of a build up in ammonia levels lead to an increase
in cerebral edema, or hepatic encephalopathy.
What nursing priority will guide your plan of care? Provide rationale. 1 Point
The major priority currently for this patient will be decreasing intracranial pressure.
Decreasing the level of ammonia in the body will undo the cerebral edema he is developing the rationale
behind this is that increases in ICP will ultimately lead to coma and death for the patient and without treatment
that is the trajectory his disease will take.
What THREE interventions will you initiate based on this priority? 3 Points
Nursing Interventions:
© 2014 Keith Rischer/www.KeithRN.com
Rationale:
Metabolism Rapid Reasoning
NURS 2900
10 Points
Evaluate serum ammonia levels daily and administer lactulose as
Administer lactulose and monitor prescribed. Lactulose converts ammonia to ammonium which inhibits it
from crossing the blood brain barrier thereby decreasing the patient’s
ammonia levels via labs
hepatic encephalopathy it also decreases the overall production of
ammonia by the gut.
Monitor neurologic status for
Monitoring for neurologic status changes is necessary because as
changes
ammonia levels improve or worse so will the patients neurological
functioning. The patient currently has decreased level of consciousness
and asterixis which are associated with stage two hepatic
encephalopathy.
Monitor protein levels in hepatic
encephalopathy patients
Patients with hepatic encephalopathy should have low to moderate
amounts of protein especially if they are headed towards coma due to
the production of ammonia as a byproduct in cellular respiration.
Lowered levels of protein lead to lowered amounts of ammonia
production but this is a catch 22 in patients because cellular processes
require added amounts of protein to heal in the presence of injury.
Maintain bedrest
Reduce metabolic and hepatic demands on the body which decreases the
risk of increased ammonia build up.
Have the patient write there
name each day
Monitor fluid and electrolyte
balance.
© 2014 Keith Rischer/www.KeithRN.com
Decreases in ability to write ones name or increases in the ability of
patient to write clearly can be an indicator of neurological function
Monitoring fluid and electrolyte balance will decrease excess energy
expenditure which will result in worsened ammonia levels.
Metabolism Rapid Reasoning
NURS 2900
10 Points
© 2014 Keith Rischer/www.KeithRN.com