PL505

Cirrhosis and Portal

Hypertension
 NARS: National Academic Reference Standards
‫المعايير القومية المرجعية االكاديمية‬
It is the minimum level of knowledge and skills that a graduate must possess to ensure good practice of his profession.
These standards have been set by the National Authority for Quality Assurance of Education and Accreditation agency
(NAQAAE)

NARS Programme Course LOs

LOs

Learning outcomes (Knowledge and skills ): measurable achievements that the learner will be able to
understand after learning processes is completed

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 NAQAAE issued two versions of these standards in 2009 (outcome based) and 2017 (competency based) consecutively, as a result of upgrading and
updating the attributes of pharmacy graduates globally.

Competency: the capability of applying the acquired skills and knowledge that enable the student to successfully perform in professional and educational
contexts.

NARS 2009 (Outcome based) NARS 2017 (Competency based)

It depends on make use of all the information the

Depends on gaining a huge amount of information with student acquired during the study period to solve
minor applications professional problems that he encounters through
his/her work, whether in private pharmacies, hospitals
or research centers through integrating the knowledge
and skills the student gain to solve such problems

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 Liver disease
The liver has considerable reserve capacity reflected in its ability to function normally despite surgical
removal of 70–80% of the organ or the presence of significant disease. Itis noted for its capacity to
regenerate rapidly. However, once it has been critically damaged multiple complications develop involving
many body systems.
Acute liver disease
Acute liver disease is a self-limiting episode of hepatocyte damage which in most cases resolves
spontaneously without clinical sequelae. This is a rare condition in which there is a rapid deterioration in
liver function with associated encephalopathy (altered mentation) and coagulopathy.
Chronic liver disease
Chronic liver disease occurs when permanent structural changes within the liver develop secondary to
long-standing cell damage, with the consequent loss of normal liver architecture. In many cases, this
progresses to cirrhosis, where fibrous scars divide the liver cells into areas of regenerative tissue called
nodules.
 Liver cirrhosis
• CIRRHOSIS
• is a diffuse injury to the liver characterized by fibrosis and a conversion of the
normal hepatic architecture into structurally abnormal nodules. The resulting
resistance to blood flow results in portal hypertension
 Clinical Picture of Hepatic cirrhosis

Compensated Cirrhosis often is a silent disease, Some cases may have anorexia, loss of
weight, dizziness, fatigue and osteoporosis as a result of Vitamin D malabsorption and calcium
deficiency.

Decompensation clinical symptoms may include jaundice of the eyes or skin, pruritus,
gastrointestinal bleeding, coagulopathy, increasing abdominal girth, and mental status changes.
Almost all of the mortality and morbidity resulting from cirrhosis is caused by the
decompensated type.

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 Diagnosis of liver cirrhosis

Liver cirrhosis is diagnosed by several criteria as follow:

 Previous history of chronic liver diseases, such as viral hepatitis, alcohol abuse, chronic
drug abuse, and family history of liver diseases.

 Clinical examination of patients with cirrhosis may reveal a variety of findings such as:
Abdominal wall vascular collaterals (caput medusa), jaundice, ascites, clubbing, fetor
hepaticus (a sweet, pungent breath odor), gynecomastia, hepatomegaly and splenomegaly.

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 Diagnosis of liver cirrhosis
 Investigations

Biochemical tests

 Which reflect alterations in the function of hepatocytes include:-

The serum (AST), alanine transaminase (ALT), alkaline phosphatase, and g-
glutamyltransferase; total, direct and indirect serum bilirubin; and serum albumin. Complete
blood count (CBC) with platelets, and a prothrombin time test .

 Synthetic function capacity Albumin and coagulation factors are markers of hepatic
synthetic activity and are used to estimate hepatocyte functioning in cirrhosis.
• Thrombocytopenia is a relatively common feature in chronic liver disease and is found in
15% to 70% of cirrhotic patients.
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 Diagnosis of liver cirrhosis

Imaging studies
• Abdominal ultrasonography with Doppler.
• Computed tomography (CT), and magnetic resonance imaging (MRI)
• Liver biopsy is an invasive procedure with an associated morbidity and mortality.
Nevertheless, it remains the gold standard in establishing a diagnosis and assessing the
severity of chronic liver disease.

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 Clinical Picture of Hepatic cirrhosis

Cirrhosis is a silent disease, most patients remaining

asymptomatic until decompensation occurs.
Decompensation is usually defined as the first
occurrence of ascites, oesophageal variceal bleeding
and hepatic encephalopathy.
• CIRRHOSIS
Clinical Presentation of Cirrhosis
 TREATMENT
• CIRRHOSIS
Goals of Treatment:
• Treatment goals are clinical improvement or resolution of acute
complications, such as variceal bleeding, and resolution of hemodynamic
instability for an episode of acute variceal hemorrhage.
• Other goals are prevention of complications, adequate lowering of portal
pressure with medical therapy using β-adrenergic blocker therapy, and
support of abstinence from alcohol
 1- Portal hypertension
• is characterized by hypotension, and decreased systemic vascular resistance.
 Patients with portal hypertension are often asymptomatic, while others may present
with bleeding varices, ascites and/or encephalopathy.
 TREATMENT of Ascites
• Avoid alcohol intake, sodium restriction (to 2 g/day), and diuretics. Fluid loss and
weight change depend directly on sodium balance in these patients

• Diuretic therapy should be initiated with single morning doses of spironolactone, 100 mg,
and furosemide, 40 mg, titrated every 3 to 5 days, with a goal of 0.5 kg maximum daily
weight loss.

• The dose of each can be increased together, maintaining the 100:40 mg ratio, to a
maximum daily dose of 400 mg spironolactone and 160 mg furosemide.

• • If tense ascites is present, paracentesis should be performed prior to institution of

diuretic therapy and salt restriction.

• • Liver transplant should be considered in patients with refractory ascites.

 3- SPONTANEOUS BACTERIAL PERITONITIS (SBP)
A- Treatment :
• Patients with documented or suspected SBP should receive broad-spectrum antibiotic
therapy to cover Escherichia coli, Klebsiella pneumoniae, and Streptococcus pneumoniae
• Cefotaxime, 2 g every 8 hours, or a similar third-generation cephalosporin for 5 days is
considered the drug of choice. Oral ofloxacin, 400 mg every 12 hours for 8 days, is
equivalent to IV cefotaxime.
B- Prophylaxis:
• Antibiotic prophylaxis for those who experience a prior episode of SBP indefinite Can
also consider indefinite antibiotic prophylaxis in patients without GI bleeding if ascitic
fluid protein concentration is less than 1.5 g/dL and at least one of the following is
present: SCr > 1.2 mg/dL, BUN > 25 mg/dL, sodium < 130 mg/dL, or Child-Turcotte-Pugh score > 9 with bilirubin
> 3 mg/dL and if variceal hemorrhage for 7 days
• should receive long-term antibiotic prophylaxis with daily ciprofloxacin 500 mg or
double-strength trimethoprim-sulfamethoxazole.
 4- The management of varices
(A) primary prophylaxis to prevent bleeding.
(B) treatment of variceal hemorrhage.
(C) secondary prophylaxis to prevent rebleeding in patients who have already
bled.
A- Primary Prophylaxis

The mainstay of primary prophylaxis is the use of a nonselective β-adrenergic

blocking agent such as propranolol or nadolol. These agents reduce portal
pressure by reducing portal venous inflow via two mechanisms:
• decrease in cardiac output and
• decrease in splanchnic blood flow.
 B- Management of variceal hemorrhage.

(ABCs, airway, breathing, and circulation; TIPS, transjugular intrahepatic

portosystemic shunt.)
Airway management is critical.

Blood volume
• maintain hemoglobin of 8 g/dL with volume expansion to maintain
systolic blood pressure of 90 to 100 mm Hg and heart rate of less than
100 beats/min is recommended.
• Fluid resuscitation involves colloids initially and subsequent blood
products.
• Vigorous resuscitation with saline solution should generally be avoided.
 B- Management of variceal hemorrhage
• Vasoactive drug therapy (usually octreotide) Somatostain analogue
• To stop or slow bleeding is initiated early to control bleeding and
facilitate endoscopy. IV bolus of 50 mcg followed by a continuous
infusion of 50 mcg/h. It should be continued for 5 days after acute
variceal bleeding.
• Patients should be monitored for hypo- or hyperglycemia.
• Vasopressin causes nonselective vasoconstriction and can result in
myocardial ischemia or infarction, arrhythmias, mesenteric ischemia,
ischemia of the limbs, or cerebrovascular accidents.

• Antibiotic therapy should be used early to prevent sepsis in patients with signs
of infection or ascites. A short course (up to 7 days) of IV ceftriaxone twice daily
or IV ciprofloxacin is recommended.
 B- Management of variceal hemorrhage
• Endoscopic Variceal ligation(EVL )is the recommended form of endoscopic
therapy for acute variceal bleeding, although endoscopic injection
sclerotherapy (injection of 1–4 mL of a sclerosing agent into the lumen of the
varices) may be used.

• If standard therapy fails to control bleeding, a salvage procedure such as

balloon tamponade (with a Sengstaken-Blakemore tube) or transjugular
intrahepatic portosystemic shunt (TIPS) is necessary.