Prepared by: BSN 408 - GROUP 2
Post necrotic cirrhosis - in which
HEPATIC LIVER CIRRHOSIS
Question: What is the function of the liver?
a. The liver regulates most chemical levels in the
blood and excretes a product called bile.
b. The liver helps in digestion and an endocrine
function that regulates blood sugar.
c. The liver carries the major digestion and
absorption of digestion food.
Answer: A. The liver regulates most chemical
levels in the blood and excretes a product called
bile. This helps carry away waste products from
the liver because all the blood leaving the
stomach and intestines passes through the liver.
I. NATURE OF DISEASE
Chronic liver disease (CLD) or
cirrhosis of the liver is one of the leading causes
of death in the Philippines. Hepatic failure also
results from chronic liver disease or the result of
persistent liver damage over many years, in
which healthy liver tissue is replaced by fibrotic
tissue. This form of liver failure is called
cirrhosis. Finally, liver cells can be replaced by
fatty cells or tissue and is known as fatty liver
disease.
1.1 Three (3) Types of Cirrhosis
1. Alcoholic cirrhosis - in which the scar
tissue characteristically surrounds the
portal areas. This is most frequently
caused by chronic alcoholism and is
the most common type of cirrhosis.
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2.
there are broad bands of scar tissue. This
is a late result of a previous bout of acute
viral hepatitis.
3. Biliary cirrhosis - in which scarring
occurs in the liver around the bile ducts.
This type of cirrhosis usually results from
chronic biliary obstruction and infection
(cholangitis); it is much less common
than the other two types.
1.2 Risk Factors
A. Modifiable Risk Factors
1. Drinking too much alcohol
2. Being overweight
3. Having viral hepatitis
B. Non-Modifiable Risk Factors
1. Gender - women are more prone to liver
cirrhosis
2. Age - 30 to 60 y/o
3. Genetics
1.3 Mortality Rate
Cirrhosis is relatively common and is a
significant cause of hospitalization and death,
especially after middle age because it develops
gradually over time. According to recent data
from the Philippine Statistics Authority, liver
diseases accounted for 27.3 cases per 1000
deaths in the country in 2020. Liver cirrhosis
accounts for 31.8% of liver-related deaths in the
country, while malignant disease of the liver
comprises 35.8%. Viral hepatitis comprises
5.3% of liver-related deaths (Ornos et al., 2023).
 When cells are damaged and die off, the
II. PATHOGENESIS OF THE
dead tissue that was previously full of living cells
DISEASE
becomes fibrotic, meaning it becomes
thickened with a large amount of protein and
Question: CIRRHOSIS is a/an _______
forms scar tissue.
formation of fibrosis, within which hepatic cell
regeneration is _______ to form nodules of
_____-functioning cells.

a. Irreversible, restricted, poorly

functioning cells

b. Reversible, unrestricted, rich-

functioning cells

Answer: A. Cirrhosis is an irreversible

formation of fibrosis, within which hepatic cell
regeneration is restricted to form nodules of
poorly functioning cells.
This happens when the liver is constantly
forced to process alcohol like in alcoholic liver
disease, or become subjected to a viral attack
for a long time like in Hepa-B Virus (HBV),
Drug overdose (i.e. Acetaminophen), or
anything else that causes a long-term or chronic
state of a liver cell or hepatocyte destruction and
inflammation, the liver can become seriously
scarred and damaged to the point where it is
no longer reversible, at which point it
becomes fibrotic and in the liver it is called
cirrhosis.

Figure 1: Pathogenesis of Liver Cirrhosis

Synthesis

As it is usually irreversible, cirrhosis is

often referred to as the “end-stage” or “late-
stage” liver damage. When liver cells are
injured, they start to come together and form
what are called regenerative nodules. These
are like colonies of living liver cells.

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 produce collagen, which is the main ingredient
in extracellular matrix, fibrosis, and scar tissue.
As this fibrotic tissue builds up, it starts to
compress the central veins and sinusoids.

In a healthy, normal state, these cells

play key roles in the natural wound-healing
process, but when the liver cells are constantly
Regenerative nodules are one of the
injured, the stellate cells are constantly
classic signs of cirrhosis and are the reason why
activated and so they constantly produce
a cirrhotic liver is more bumpy as opposed
collagen and factors that lead to fibrosis.
to a smooth, healthy liver. Also with cirrhotic
liver tissue, it is evident that in between these And this is when complications due to
clumps of cells or nodules, is fibrotic tissue and cirrhosis start to crop up.
collagen.

Fibrosis is a process mediated by

special cells called stellate cells, which sit
between the sinusoid and hepatocyte, known as
the perisinusoidal space. The portal vein and
As the central veins and sinusoids
hepatic artery is combined into a sinusoid,
become compressed and push on the fluid
which then goes into the central vein, and these
inside, their pressure starts to build up, leading
are all lined with hepatocytes. Along with these
to intrasinusoidal (or portal)
though is a bile duct, and all three constitute a
hypertension, which is this higher pressure
portal triad.
in the portal veins. Higher portal vein
The perisinusoidal space, which means pressure means that fluid in blood vessels is
“around the sinusoidal space”, and stellate cells more likely to get pushed into tissues and across
are located just in the middle, and usually in tissues into large open spaces like the peritoneal
healthy tissue, their main function is to store cavity. That’s why cirrhosis leads to excess
vitamin A and are otherwise considered peritoneal fluid, a condition called ascites, and
dormant. When the hepatocytes are injured, can result in other complications like
they secrete paracrine factors that “activate” and congestive splenomegaly and
change the stellate cells. When activated, the hypersplenism, where the spleen becomes
stellate cells lose vitamin A, proliferate, and enlarged because all this fluid and blood cannot
start secreting transforming growth factor get into the liver and backs up into the spleen.
beta1, or TGF-beta, which then causes them to
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 In the same way, your circulatory system
starts diverting blood away from the liver
because of the high liver pressures, this is
known as a portosystemic shunt. Blood flow
follows the path of least resistance and shunts
away from the portal system and towards the
systemic system of circulation.
These changes in portal flow ultimately
trigger renal vasoconstriction, so increased
resistance in the renal circulation, which
decreases blood flow through the kidneys,
leading to decreased filtration hepatorenal
failure, where kidney failure follows liver
failure.
The fibrotic tissue, pressure buildup, and
diversion of blood from the hepatic circulation
essentially reduces the number of functional
sinusoidal veins, and the number of functional
portal triads in general.
As you have less and less of these basic
liver functional units, your liver becomes less
and less able to do its job of detoxification.
When your liver is not detoxifying your blood,
these toxins can get into the brain and start
causing mental deficits, a condition known as
hepatic encephalopathy.
Although there are several neurotoxins
that are thought to contribute to the
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development of these mental changes, the best-
understood factor is ammonia in the blood,
which is produced mainly in the gastrointestinal
tract; usually the liver plays a vital role in
removing ammonia and stopping it from going
into the systemic circulation. As more of these
and other toxins get into the brain, patients
might develop asterixis, where they experience
tremors or jerky hands when outstretched, and
as even more toxins build up, eventually
patients can progress to a coma.
Also, since the liver plays a big role in
metabolizing estrogen into inactive metabolites
that can be removed from the blood and
excreted, patients can also experience
complications due to increased estrogen in the
blood, like gynecomastia, spider
angiomata, and palmar erythema.
And, since the liver usually conjugates
bilirubin, increased unconjugated bilirubin in
the blood from a less functional liver can lead to
jaundice.
Another important job of the liver is
producing albumin, so again, if the liver is not
functioning right, you can have a decreased
amount of albumin in the blood, or
hypoalbuminemia.
Finally, the liver helps in making clotting
factors or proteins that help coagulate your
blood, so when you are not producing these
coagulation factors, you can develop issues
related to your ability to coagulate blood,
which you need in order to stop blood loss after
an injury.

Answer: A. Ultrasonogram (UGS)
3.1 Blood Tests
Compensated Cirrhosis (Stage 3)
- early on, with a small amount of
scarring and fibrosis. The liver can
still do a lot of its job.
- Non-specific symptoms like weight
loss, weakness, or fatigue.
Decompensated Cirrhosis (Stage 4)
- Later on, with extensive scarring, the
liver progresses to decompensated
cirrhosis, and cannot function properly.
- Described symptoms - jaundice and
pruritus or itchy skin, ascites, hepatic
encephalopathy leading to confusion,
and easy bruising from low
coagulation factors.
III. DIAGNOSTICS AND LABORATORY
STUDIES
Question: Which of these diagnostic and
laboratory studies uses sound waves to locate
liver pathology?
a. Ultrasonogram (UGS)
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b. CT Scan
c. MRI
1. Serum enzymes – Aspartate
Aminotransferase (AST) and ALT or
Alanine Aminotransferase are elevated in
serum when liver damage or
inflammation is present. Both alcoholic
and non-alcoholic fatty liver disorders
can cause elevated liver enzyme levels.
2. Alkaline phosphatase and Gamma
Glutamyl Transferase (GGT) - also
produced from bile ducts and may also
elevate, indicative of a presence of liver
disorders.
3. Protein and albumin levels – when
these are present in the liver, it is a sign
of a healthy liver. These levels are out of
balance when there is liver disease.
4. Prothrombin Time Test – if a liver
disease is present, prothrombin time is
prolonged.
5. Bilirubin Level – when old blood cells
are destroyed, a yellow pigment remains.
Bilirubin is often excreted in the feces by
the liver after being removed from the
blood circulation. However, bilirubin
builds up in the blood when the liver fails
to function properly, which can result in
yellowing of the skin and eyes known as
jaundice.
6. Creatinine - this is a byproduct that
your muscles produce. It is often
removed from your blood by your
kidneys. In the late stages of cirrhosis or
 when the disease has progressed, kidney
damage can be detected by a high
creatinine level.
7. Sodium Blood Test – the level of
sodium in the blood may be a sign that a
person has cirrhosis if it is insufficient, a
condition called hyponatremia.
3.2 Radiological Studies
1. Ultrasonogram (USG) of the
abdomen – this useful, non-invasive,
and inexpensive method uses sound
waves to locate liver pathology.
2. CT Scan – also known as Computed
Axial Tomography Scan or Image is done
to diagnose a variety of liver diseases by
closely examining deeper liver tissues.
3. MRI – Magnetic Resonance Imaging
method is used to examine the
pathologically damaged liver tissues.
4. Endoscopy – it makes use of a flexible
tube that has a camera and light on one
end. It can be used to search for varices,
which are abnormal blood vessels. These
develop when cirrhosis scars in the portal
vein, which supplies blood to your liver,
then obstructs blood flow. In this vein,
pressure increases with time and results
in blood accumulating in blood vessels in
the stomach, esophagus, or intestines.
5. Endoscopic Retrograde
Cholangiopancreatography
(ERCP) – a procedure in which a long,
thin tube with camera is inserted into the
gastrointestinal tract to view the bile and
pancreatic ducts where any pathology is
possible to find.
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6. Magnetic resonance elastography
and transient elastography – these
more recent tests search for stiffness in
your liver brought on by scarring from
cirrhosis. It is less invasive than a liver
biopsy yet is not generally accessible.
3.3 Liver Biopsy
- sections of the liver tissue are aspirated
using a long, thin needle under a local
anesthetic agent with the help of USG or
CT scan. This is done to validate the
diagnosis. Under a microscope, the
aspirated sample gets examined.
IV. Treatment Modalities
Question: Is liver cirrhosis curable?
a. Yes
b. No
Answer: B. No. Liver cirrhosis is not curable,
but it is treatable. The treatment of liver
cirrhosis primarily focuses on managing its
underlying causes, preventing further
complications, and providing supportive care.
4.1 Pharmacological Treatment
Modalities
1. Antacids and/or histamine-2 (H2)
antagonists:
Antacids are over-the-counter
medications that neutralize stomach acid
and provides relief from symptoms of
heartburn and acid indigestion. Patients
with liver cirrhosis may experience
gastrointestinal symptoms, such as acid
reflux, which may be due to various
factors, including portal hypertension,
 esophageal varices, and ascites. Ascites is
often a complication of cirrhosis, where it
causes fluid buildup in the abdomen, and
the pressure of fluid in the abdomen may
contribute to GERD-like symptoms.
With that, antacids are typically used for
symptom management rather than as a
direct treatment for cirrhosis itself.
2. Histamine-2 Receptor Antagonists:
These are medications that reduce
the production of stomach acid by
blocking the action of histamine on H2
receptors in the stomach. In some cases,
patients with cirrhosis may experience
peptic ulcer or acid related diseases as
complications, or as a side effect of
medications used to manage cirrhosis-
related issues, and H2 antagonists can be
used to manage such symptoms.
3. Vitamins and nutritional
supplements:
4. Potassium-sparing
Patients with liver cirrhosis often
have special dietary needs and may
benefit from certain vitamins and
nutritional supplements, such as:
a. Vitamin D. Liver cirrhosis can
potentially impact vitamin D
metabolism and lead to vitamin D
deficiency. When the liver is
damaged, it may not convert the
precursor to vitamin D into its
active form, resulting in lower
levels, which can have various
health implications.
b. Omega-3 Fatty Acids,
inflammation is a common feature
of liver cirrhosis, and excessive
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inflammation can contribute to
the progression of the disease.
And with the anti-inflammatory
properties of Omega 3 fatty acids,
this may help reduce
inflammation in the liver.
c. Zinc, liver cirrhosis can lead to
various complications, including
esophageal varices, which can
rupture and cause bleeding. And
with the wound healing and tissue
repair ability of Zinc, this can
prevent such complications.
d. Antioxidants, Liver cirrhosis is
often associated with increased
oxidative stress due to factors like
inflammation and impaired liver
function. And with antioxidants, it
can help mitigate this oxidative
stress by neutralizing free radicals
and reducing cell damage.
diuretics
(Spironolactone) or triamterene
(Dyrenium):
Liver cirrhosis can slow the
regular flow of blood through the liver.
This increases the pressure in the vein
that brings blood to the liver. The
increased pressure in the portal vein can
cause fluid to accumulate in the legs,
called edema, and in the abdomen, called
ascites.
a. Spironolactone is an
aldosterone receptor antagonist
primarily works by blocking the
effects of aldosterone, a hormone
that promotes sodium and water
retention. This is often the
 preferred diuretic for cirrhosis-
related ascites, as it does not only
reduce the fluid buildup in the
abdomen, but also it has a
potassium-sparing effect that
helps retain potassium, thereby is
beneficial in cirrhosis where
electrolyte imbalances are
common.
b. On the other hand, Triamterene
(Dyrenium) primarily works by
inhibiting sodium reabsorption in
the distal tubules of the kidneys.
However, although it is effective in
reducing fluid retention, it lacks
some benefits of Spironolactone,
such as its ability to block the
aldosterone, thereby making it to
not be the first choice of
potassium-sparing diuretics for a
patient with liver cirrhosis.
5. Immunosuppressants
In some cases, such as
autoimmune hepatitis or primary biliary
cirrhosis, immunosuppressant therapy
may be prescribed to manage and slow
down the progression of liver cirrhosis.
Autoimmune hepatitis is initially
managed with a glucocorticoid, such as
Prednisone, that controls the
inflammation in the liver thereby
preventing further scarring.
4.2 Procedural Treatment Modalities
1. Esophageal variceal banding or
litigation – Small rubber bands are
wrapped around varices, which are
swollen veins in the esophagus, by
doctors using a thin tube. When the
blood pressure in the liver is too high,
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veins may hemorrhage. Bleeding is
stopped by a band.
2. Paracentesis — medical professionals
can remove fluid from the peritoneal
cavity, the area of the stomach where
your liver is located. Ascites is a
consequence of liver cirrhosis that is
evaluated by doctors. Ascites is a fluid
that accumulates in the cavity.
3. Thoracentesis – During this
procedure, doctors use a needle to
remove fluid from the pleural cavity, or
the area between the tissue lining the
lungs and the chest wall. This fluid
accumulates due to a cirrhosis condition
termed hepatic hydrothorax.
4.3 Surgical Treatment Modalities
Liver Transplant
- A surgery that removes a liver that no
longer functions properly and replaces it
with a healthy liver from a deceased
donor or a portion of a healthy liver from
a living donor.
○ Treatment option for people who
have significant complications
due to end-stage chronic liver
disease.
○ Treatment option in rare cases of
sudden failure of a previously
healthy liver
1. Cadaveric liver transplants are also
known as deceased donor liver
transplantation. The livers that are
transplanted come from brain-dead
organ donors where consent is given.
The donor’s whole liver will be
transplanted to the patient.
 2. Living donor liver transplants: The
donor's healthy liver will be partially
removed and transplanted to the patient.
This can be done because the liver has a
remarkable ability to regenerate itself.
Both the transplanted liver and the
portion left behind in the donor are able
to regrow rapidly. Even with 70% of its
mass removed, the remaining 30% of the
liver will function adequately to support
life for the donor, and the liver will
regenerate to 100% functionality within
4 – 6 weeks.
4.4 Post op responsibilities:
1. Monitor liver enzymes, bilirubin, protein
synthesis markers, and coagulation
factors to detect early graft dysfunction.
2. Immunosuppressive therapy to prevent
rejection (e.g. calcineurin inhibitors,
Tacrolimus)
a. Tacrolimus 1st day of post op 4mg
BID (a goal through is typically
10-12 ng/mL
b. After 4 weeks of initial treatment,
Tacrolimus trough goal will
stabilize to maintain a lifelong
goal 5-8 ng/mL
c. Corticosteroid such as
methylprednisolone will be given
intraoperatively and transitioned
to prednisone to complete their
tape over the course of 3-6 months
d. Mycophenolate is given if there’s
an infection
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3. Watch out for diarrhea, headaches,
tremors from the neurotoxicity risk of
tacrolimus and insomnia.
V. Nursing Management
Question: For the client with liver failure,
what nursing intervention would be most
appropriate to control fluid accumulation in
the abdominal cavity?
A. Monitoring intake and output
B. Providing a low sodium diet
C. Increasing PO fluid intake
D. Weighing the client daily
Answer: B. Low-sodium diet
1. Promote Rest
- Optimize the positioning of the bed to
enhance breathing efficiency.
- Encourage the patient to do mild
exercises.
- Keep the head of the bed elevated to 30
degrees.
- Provide oxygen therapy.
- Reduce the frequency of suctioning to
decrease stimulation.
2. Improve Nutritional Status
- High-protein diet supplemented by B-
complex vitamins and others, including
A, C, and K.
- Encourage patient to eat: Provide small,
frequent meals, consider patient
preferences, and provide protein
supplements, if indicated.
- Restrict sodium.
 - A low-sodium diet is one means of
controlling abdominal fluid collection.
Sodium intake may be restricted to 500
mg to 1 g daily.
3. Providing Skin Care
- Frequent change in position.
- Avoid using irritating soaps and adhesive
tape.
- Provide lotion to soothe irritated skin.
4. Reducing Risk of Injury
- Protect the patient from falls and other
injuries.
- Orient to time, place, and procedures.
- Advise the patient to call for help getting
out of bed.
5. Monitoring and Managing
Complications
- Monitor the patient’s mental status
closely and report changes.
- Carefully monitor serum electrolyte
levels.
- Record the amount of fluid intake and
output, daily weight changes, changes in
abdominal girth, and edema formation.
- Monitor patients for the presence of
nocturia, followed by oliguria, since both
conditions are indicative of progressive
liver failure.
- END -

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 REFERENCES

Khatri, M. (2023, May 28). What are the tests for cirrhosis? WebMD.

https://www.webmd.com/digestive-disorders/tests-for-cirrhosis#

Mandal, A. (2023, June 12). Liver disease diagnosis. https://www.news-

medical.net/health/Liver-disease-diagnosis.aspx#

MEH. (n.d.). Liver transplant. https://www.mountelizabeth.com.sg/conditions-

treatments/transplant/liver-

transplant?gclid=CjwKCAjw3dCnBhBCEiwAVvLcu2Q13wg_Mw6lVBqN_Fg7vDVxKJ

h6zLKu8JAVEpTY9AaPUPTPtqo_2BoCdAgQAvD_BwE

Ornos et al., (2023, June). Liver diseases: Perspective from the Philippines. Science Direct.

https://doi.org/10.1016/j.aohep.2023.101085

Osmosis from Elsevier. (2017, September 5). Cirrhosis - causes, symptoms, diagnosis,

treatment, pathology [Video]. YouTube.

https://www.youtube.com/watch?v=f46VFQG2S84

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