PHL 532

Lecture 1
Cirrhosis and Portal
Hypertension
⚫The Faculty of Pharmacy of October University for Modern Sciences and Arts is nationally accredited, has
British partnership, and is committed to producing graduates who are able to compete in national and
international job markets and entrepreneurship, and to be an effective member of the medical team
providing best medical care, while heeding professional ethics, through an outstanding academic
programme and proficient academic staff. The faculty is devoted also to provide effective community
services, and exceptional applied scientific research.
‫الرسالة‬
‫ تلتزم بتخريج صيدلى لادر على المنافسة فى أسواق العمل‬،‫ بشراكة بريطانية‬،‫• كلية الصيدلة جامعة أكتوبر للعلوم الحديثة واآلداب معتمدة محليا‬
‫ من خالل‬،‫ مراعيا ً أخالليات المهنة‬،‫ و أن يكون عضو فعال فى الفريك الطبى بتمديم أفضل رعاية صحية‬،‫المحلية و الدولية و ريادة األعمال‬
.‫ وكذلن تلتزم الكليه بمديم خدمات مجتمعية فعالة و أبحاث علمية تطبيمية متميزة‬،‫برنامج تعليمى متميز و أعضاء هيئة تدريس أكفاء‬
⚫The Faculty of Pharmacy of October University for Modern Sciences and Arts is a
pioneer in tutelage, scientific research, and community service at the local and regional
levels, and holds an advanced position among its counterparts in international
Pharmacy subject ranking.

‫الرؤية‬
 ‫( كلية الصيدلة جامعة اكتوبر للعلوم الحديثة و اآلداب‬MSA)‫كلية رائدة فى مجال‬
‫التعليم و البحث العلمى و المشاركة المجتمعية على المستوى المومى و اإللليمى و لها‬
‫ترتيب متمدم فى التصنيف العالمى لكليات الصيدلة‬
 – Overall Aims of Course
• The aims of this course are to help the student recall, comprehend and relate
management concepts, functions and skills to pharmacy practice. Topics taught
to the students will provide the facts and knowledge to make therapeutic
decisions. Analytical skills, however, are attained through case studies and
problem-oriented discussions. It is expected that the students will develop
competence in developing the most patient-specific therapeutic plans by
integration of the knowledge obtained in this course, other courses in
biochemistry and information given in pharmacology.
1. Mapping CLO to programme and NARS key elements
NARS Key element Programme Key element Course learning outcome (CLO)
1-1-4- Articulate knowledge from fundamental sciences to explain 1-1-4-2 Utilize knowledge from fundamental sciences to select suitable drug 1.1.4.2.1. Choose latest evidence-based pharmacologic treatments for different
drugs’ actions and evaluate their appropriateness, effectiveness, and based on evaluation of its suitability, effectiveness, and safety in individuals studied diseases (infectious , DM, renal and hepatic diseases )
safety in individuals and populations. and community.

1-1-5- Retrieve information from fundamental sciences to solve 1-1-5-1 Extract information from basic sciences to efficiently deal with 1.1.5.1.1 Integrate the laboratory and other diagnostic markers for the diagnosis,
therapeutic problems therapeutic (pathophysiological) problems. management and follow up of the disease process and treatment.

1-1-6- Utilize scientific literature, and collect and interpret 1-1-6-1- Utilize scientific literature and collect and interpret information to 1.1.6.1.1 Use evidence based medicine steps to provide the patient with most
information to enhance professional decision. take proper decision to save patient life and to prevent the spreading of suitable and safest drug regimen
diseases.

2-1-3 Recognize own personal and professional limitations and accept 2-1-3-1- Recognize own personal and professional limitations. 2.1.3.1.1. Differentiate between drug related problems and disease deterioration
the conditions of referral to or guidance from other members of the issues requires referral to other health care provider
health care team.

2-4-3 Take actions to solve any identified medicine-related and 2-4-3-1- Take actions to solve any identified medicine-related problems. 2.4.3.1.1. Analyze medical and clinical information and their utilization in
pharmaceutical care problems. patient's therapy.

2-5-2 Retrieve, interpret, and critically evaluate evidence-based 2-5-2-2- Retrieve, interpret, and critically evaluate evidence-based 2.5.2.2.1. Provide appropriate treatment for individualized patient based on the
information needed in pharmacy profession information needed in clinical pharmacy practice. recent guidelines

3-1-4 Relate etiology, epidemiology, pathophysiology, laboratory 3-1-4-2- Select the proper pharmacotherapeutic approach to treat 3.1.4.2.1. Review of all patient related information and the disease process of
diagnosis, and clinical features of infections/diseases and their infections/diseases based on their etiology, epidemiology, pathophysiology (infectious , DM, renal and hepatic diseases ) to provide the patient with most
pharmacotherapeutic approaches and clinical features. suitable drug

4-2-1 Demonstrate effective communication skills verbally, non- 4-2-1-1-Effectively communicate verbally, non-verbally, and in writing with 4.2.1.1.1. Develop comprehensive presentation skills , encourage team work
verbally, and in writing with professional health care team, patients, professional health care team. capabilities and practice open discussion with students
and communities.
8. Assessment Methods and Tools:
Assessment Method/s Assessment Type Timing Weight
Tutorial exam SUMMATIVE Week 10 25

Quiz 1,2 SUMMATIVE WEEKs 4 & 9 5

Assignment SUMMATIVE Due variable 10

Mid-term exam SUMMATIVE Weeks 7&8 20

Final written exam SUMMATIVE Weeks 14 40

Formative Formative During the 0
semester
Total 100
Liver
• The largest internal organ, up to 1500 gm.
• It is formed of 2 lobes, right (large) & left
(small)
• Dual blood supply, hepatic artery and portal
vein
 Functions of the Liver
Performs over 500 chemical processes
Produces over 160 different proteins
Makes clotting factors for the blood
Stores & releases sugar as glycogen
Metabolizes, detoxifies, synthesizes

DRUG DISPOSITION

The liver's rich enzyme system allows the metabolism of many drugs,
including alcohol.
The liver detoxifies noxious substances arriving from the splanchnic
circulation, preventing them from entering the systemic circulation.
The liver converts some lipophilic compounds into more water-soluble
agents to be easily excreted in bile and urine.
Others are metabolized to less active agents.
 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.
 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
2/20/2024 12
 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.

2/20/2024 13
Laboratories, Radiological and Histological Evaluations
 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.

2/20/2024 15
 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.
2/20/2024 16
 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.

2/20/2024 17
Criteria and Scoring for the Child–Pugh Grading of Chronic
Liver Disease
 prevention and treatment Hepatic cirrhosis

Cirrhosis isn't curable, but it’s treatable. Once cirrhosis develops, the treatment of
compensated stage directs to preventing the progression into decompensation stage, and that of
decompensated stage focuses on preventing the development of complications of cirrhosis.
Treatment of the underlying disease can often halt or even reverse the progression of early-
stage cirrhosis. Therefore, it is evident that the elimination or reduction of viral load by anti-
viral drugs, the removal of hepatic parasites, or the withdrawal of any drug or toxin leading to
parenchymal damage ,immune suppression in autoimmune hepatitis, treatment of iron overload
in hemochromatosis and copper overload in Wilson disease.

2/20/2024 19
2/20/2024 20
 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
• 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
 2- Ascites
• CIRRHOSIS
is the pathologic accumulation of lymph fluid within the peritoneal cavity.
It is one of the earliest and most common presentations of cirrhosis.

• The development of ascites is related to systemic arterial vasodilation that

leads to the activation of the baroreceptors in the kidney and an activation of
the renin–angiotensin–aldosterone system, activation of the sympathetic
nervous system, and release of antidiuretic hormone in response to the arterial
hypotension. These changes cause sodium and water retention
 Clinical Picture of Ascites

Patients typically report progressive abdominal distension that

may be painless or associated with abdominal discomfort, weight
gain, early satiety, shortness of breath, and dyspnea resulting
from fluid accumulation and increased abdominal pressure

Patients with ascites typically will have flank dullness on

examination and a fluid wave

25
 Diagnosis of liver Ascites

1.Signs and symptoms

2.Chest x-ray may reveal elevated diaphragm.
3.Ultrasound is the most sensitive test to detect
ascites.
4. Paracentesis, use to determine serum-ascites albumin
gradient (SAAG), calculated by subtracting the ascites
albumin concentration from the serum albumin
concentration; a value greater than 1.1 indicates ascites
caused by portal hypertension. 26
 TREATMENT of Ascites
• Diuretic therapy
Spironolactone alone may be sufficient for an initial episode of ascites

Or combination

should be initiated with single morning doses of spironolactone, 100 mg, and furosemide, 40
mg, titrated every 72 hrs , 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.
the goal No upper limit of weight loss if massive edema is present, 0.5 kg/day in patients
without edema
 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

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

therapy and salt restriction. Administer albumin at a dose of 6–8 g/L of ascitic fluid removed if
more than 5 L is removed at one time.

Discontinue drugs associated with sodium/water retention, such as NSAIDs. Avoid angiotensin
converting enzyme inhibitors and angiotensin receptor blockers to prevent renal failure.
Box 16.1 The sequential approach to the management
of cirrhotic ascites

Bedrest and sodium restriction (60–90 mEq/day, equivalent

to 1500–2000 mg of salt/day)

Spironolactone (or other potassium-sparing diuretic)

Spironolactone and loop diuretic

Large-volume paracentesis and colloid replacement

Other measures
Transjugular intrahepatic portosystemic shunt (TIPS)
Peritonovenous shunt
Consider orthotopic liver transplantation
 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

Regimen: 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.
 3- SPONTANEOUS BACTERIAL PERITONITIS (SBP)
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

Regimen :
should receive long-term antibiotic prophylaxis with daily ciprofloxacin 500
mg or double-strength trimethoprim-sulfamethoxazole.

• If variceal hemorrhage for 7 days

Regimen: of IV ceftriaxone twice daily or IV ciprofloxacin is recommended.
 4- HEPATIC ENCEPHALOPATHY
• CIRRHOSIS
• Hepatic encephalopathy (HE) is a metabolically induced functional disturbance of the
brain that is potentially reversible.

• The symptoms of HE are thought to result from an accumulation of gut-derived

nitrogenous substances in the systemic circulation as a consequence of shunting
through portosystemic collaterals bypassing the liver. These substances then enter the
central nervous system (CNS) and result in alterations of neurotransmission that affect
consciousness and behavior.

• Thought to be secondary to the accumulation of nitrogenous substances (mainly NH3)

arising from the gut. Other theories are related to the activation of γ-aminobutyric
acid receptors by endogenou benzodiazepine-like substances, possible zinc deficiency,
or altered cerebral metabolism.
 Encephalopathy associated with cirrhosis may develop as a result of specific
precipitating factors or spontaneously.
Box 16.2 Precipitating causes of hepatic encephalopathy

• Gastro-intestinal bleeding
• Infection (spontaneous bacterial peritonitis, other sites of
sepsis)
• Hypokalaemia, metabolic alkalosis
• High protein diet
• Constipation
• Drugs, opioids and benzodiazepines
• Deterioration of liver function
• Post-surgical TIPS
4- HEPATIC ENCEPHALOPATHY SYMPTOMS
 4- HEPATIC ENCEPHALOPATHY Diagnosis
• CIRRHOSIS

1- Signs and symptoms

2- Ammonia level
3- Rule out other causes
 4- Hepatic Encephalopathy Treatment
Treatment approaches include

reduction in blood ammonia concentrations by dietary restrictions, with drug therapy

aimed at inhibiting ammonia production or enhancing its removal (lactulose and
antibiotics).

• To reduce blood ammonia concentrations in patients with episodic HE, protein intake
is limited or withheld (while maintaining caloric intake) until the clinical situation
improves. Protein intake can be titrated back up based on tolerance to a total of 1 to
1.5 g/kg/day.
 Treatment of Hepatic Encephalopathy(HE).
a- Reduce blood ammonia concentrations,
• lactulose is initiated at 45 mL orally every hour (or 300 mL lactulose syrup with 700
mL water given as a retention enema held for 60 minutes) until catharsis begins. The
dose is then decreased to 15 to 30 mL orally every 8 to 12 hours and titrated to
produce two or three soft stools per day.
 Treatment of Hepatic Encephalopathy(HE).
b- Antibiotic therapy with
• metronidazole or neomycin is reserved for patients who
have not responded to diet and lactulose.
• Rifaximin 550 mg twice daily plus lactulose can be used for
patients with inadequate response to lactulose alone.

C-Check for vitamins and minor elements deficiencies (e.g. Zinc

acetate supplementation (220 mg twice daily) is recommended for
long-term management in patients with cirrhosis who are zinc
deficient
 Drug therapies for encephalopathy

Table 16.5 Drugs commonly used in the management of encephalopathy

Drug Dose Comment Side effects

Lactulose 15–30 mL orally Aim for 2–3 soft stools daily Bloating, diarrhoea
2–4 times daily

Metronidazole 400–800 mg orally daily in Metabolism impaired in liver Gastro-intestinal disturbance

divided doses disease

Neomycin 2–4 g orally daily in divided doses Maximum duration of 48 h Potential for nephro- and ototoxicity
Used less frequently now

Rifaxamin 550 mg twice daily Benefit demonstrated over Allergic reactions, gastro-intestinal
6 months use disturbance
May permit overgrowth
Clostridium difficile
 5- PORTAL HYPERTENSION AND VARICES
• CIRRHOSIS
• Portalhypertension lead to development of varices
and alternative routes of blood flow resulting in
acute variceal bleeding.

• Progression to bleeding can be predicted by Child-

Pugh score, size of varices, and the presence of red
wale markings on the varices.
 5- 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.
• CIRRHOSIS

A- Primary Prophylaxis
• Therapy should be initiated with propranolol, 20 mg twice daily, or nadolol, 20
to 40 mg once daily, and titrated every 2 to 3 days to maximal tolerated dose to
heart rate of 55 to 60 beats/min. β-Adrenergic blocker therapy should be
continued indefinitely.

• Patients with contraindications to therapy with nonselective β-adrenergic

blockers (ie, those with asthma, insulin-dependent diabetes with

episodes of hypoglycemia, and peripheral vascular disease) or
intolerance to β-adrenergic blockers should be considered for alternative
prophylactic therapy with EVL.
B- Management of variceal
hemorrhage.
 B- Management of variceal hemorrhage.

(ABCs, airway, breathing, and circulation 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 decrease
blood flow to portal system
• 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.
Table 16.6 Drugs used in the treatment of acute bleeding
varices

Drug Dosage and administration

Terlipressin 1–2 mg bolus 4–6 hourly for 48 h

Octreotide 50 cg/h i.v. infusion for 48 h or

longer if patient rebleeds
 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.
 Upper GI bleed

Resuscitation/fluid replacement

Vasoactive therapy (e.g. terlipressin)

Endoscopy delayed Diagnostic endoscopy

Oesophageal varices
Torrential bleed
identified

Balloon tamponade Banding/sclerotherapy

Bleeding Bleeding
continues stops

Salvage therapy Repeat banding/sclerotherapy

with TIPS/surgery to obliterate varices
Long-term -blocker

Fig. 16.7 Management of oesophageal variceal haemorrhage.

 C- Prevention of Rebleeding
• A nonselective β-adrenergic blocker along with EVL is the best treatment
option for prevention of rebleeding.

• Propranolol may be given at 20 mg twice daily (or nadolol, 20–40 mg once

daily) and titrated weekly to achieve a goal of heart rate 55 to 60 beats/min
or the maximal tolerated dose. Patients should be monitored for evidence of
heart failure, bronchospasm, or glucose intolerance.

• The combination therapy of a nonselective β-blocker with isosorbide

mononitrate can be used in patients unable to undergo EVL.
Mr. W.S is a 48-year-old divorced father of 2 teenagers. He has
been diagnosed with cirrhosis of the liver 2 years ago and has
recently been admitted to the community hospital for ascites and
malnutrition. He is lethargic but responds appropriately to verbal
stimuli. He complains of ‘spitting up blood the past week or so”
and states “I just don’t feel hungry”. He has lost 20 pounds in the
last 3 months and has 3+ pitting pretibial edema, as well as
abdominal edema. The liver is palpable at 5 cm below the right
costal margin; the spleen is also enlarged. VS: T-37 c, BP-110/70, P-
110, R-24.WBCs, RBCs and platelets, are decreased, while serum
ammonia and total bilirubin are mildly elevated. O2 sat is 88%.
What is the nutritional advice that you recommend? (3 marks)
1. Avoid alcohol intake ( 0.5 mark)
2. Sodium restriction (to 2 g/day) (1 mark)
3. To reduce blood ammonia concentrations, protein intake is limited or
withheld (while maintaining caloric intake) until the clinical situation
improves. Protein intake can be titrated back up based on tolerance to a
total of 1 to 1.5 g/kg/day.( 1 mark)
4. Check for vitamins deficiencies (e.g. Zinc acetate supplementation (220 mg
twice daily) is recommended for long-term management in patients with
cirrhosis who are zinc deficient( 0.5 mark)

What is the cause in that case that may precipitate hepatic encephalopathy?
How can this cause be managed and prevented? (9 marks)
• Spitting up blood the past week may indicate esophageal bleeding that may
precipitate HE (2 marks)
Management
Blood volume ( 1.5 marks)
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.

Vasoactive drug therapy (usually octreotide) Somatostain analogue (1.5 marks)

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 oral norfloxacin 400 mg twice daily or IV ciprofloxacin is recommended ( 1 mark)
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. (1.5 mark)

Prevention (1.5 marks)

A nonselective β-adrenergic blocker along with EVL is the best treatment option for prevention of rebleeding