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CIRRHOSIS OF THE LIVER WITH PORTAL

HYPERTENSION

Sushma Preethi. K1* Priyanka. K1 Harshith. K2

Department of Pharm-d, CMR college of pharmacy, kandlakoya, Hyderabad-501401, India.
Department of Pharm-d, CMR college of pharmacy, kandlakoya, Hyderabad-501401, India.
Department of Pharm-d, CMR college of pharmacy, kandlakoya, Hyderabad-501401, India.

ABSTRACT:
Portal hypertension is an increase in the blood pressure within the system of veins called the portal venous
system. Veins coming from the stomach, intestine, spleen, and pancreas merge into the portal vein which
then branches into smaller vessels and travels through the liver. The most common cause of portal
hypertension is cirrhosis of the liver. Here we report a case of an old female patient with cirrhosis of the
liver with portal hypertension. Cirrhosis is scarring that accompanies the healing of liver injury caused by
hepatitis, alcohol, or other less common causes of liver damage. Portal hypertension is the most common
for cirrhosis such as ascites and gastroesophageal varices as well as hepatic encephalopathy. The
medications prescribed to the patient were Diuretics, Beta- Blockers, Antibiotics, and Laxatives. Inj.
furosemide 40mg, Inj. Monocef 1gm, Syp. Lactulose, Tab. Ciplar 40mg is prescribed and based on the
patient’s condition the dose will be adjusted.

Keywords:

Portal hypertension, Cirrhosis.

INTRODUCTION:

Portal hypertension is an increase in the blood pressure within the system of veins called the portal venous
system. Due to impaired hepatic sinusoidal circulation, portal hypertension develops intrahepatic vascular
resistance.[1] Chronic liver disease causes structural alterations of the liver via increased extracellular
matrix and changes of the cellular phenotypes, associated with dysfunction of liver sinusoidal endothelial
cells.[2] Portal hypertension is the most common for cirrhosis such as ascites and gastroesophageal varices
as well as hepatic encephalopathy.[3]

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Cirrhosis is caused by Alcohol, Viral Hepatitis, Hemochromatosis, Biliary obstruction, Drugs, and Toxins.
The pathophysiology involves there will be a hepatocellular injury, there will be inflammatory response
with cytokine and there will be the destruction of hepatocytes, bile ducts, and vascular endothelial cells.
There will be repair through cellular proliferation and regeneration by the following formation of fibrous
scars. There will be the response for fibrosis which leads to the increased expression of fibril forming
collagen, the process influenced by the Kupffer cells which activate stellate cells by eliciting the production
of cytokines, thereby preventing normal flow to hepatocytes and increasing vascular resistance. Initially,
fibrosis may be reversible if inciting events are removed. The process of cirrhosis may be irreversible and
leads to cirrhosis.[4]

CASE REPORT:

A 51year old female patient was unconscious when came to hospital with history of giddiness from
6months, On examination the temperature was afebrile, Pulse Rate- 77/min, Blood Pressure- 130/80mmhg,
Laboratory Findings: WBC- 3.57, RBC-3.85, HB-13.1, MCV- 104.7, PT- 52, Differential Count: N-
1.96%, L- 0.97%, M- 0.52%, E- 0.10%, B- 0.2%, Blood Sugar: Blood Urea- 24.77mg%, Serum Creatinine-
0.64mg%, Serum Calcium- 7.9mg%, Serum Proteins: Total- 6.70gm%.

The patient was started with the treatment on admission were Monocef 1gm twice a day, Lasix 40mg, and
Optineuron 1amp were given by intravenous route once a day. Rifagut 400mg and Ciplar LA 40mg were
given by oral route once a day. After administrating the drugs patient started reacting positively, physician
advised MRI where the patient was conscious with Pulse Rate- 24bpm, Blood Pressure- 110/90mmhg, The
drugs were continued till DAY-7 vitals are stable and the same drugs were prescribed. The discharge
medication was: Monocef 1gm given intravenous twice a day, Lasix 40mg given intravenous once a day,
and Syrup. Lactulose and Ciplar 40mg are given by oral route once a day.

DISCUSSION:

Early detection of cirrhosis and portal hypertension is now possible using simple non-invasive methods,
leading to the advancement of individualized risk stratification in clinical practice. Despite previous
assumptions, cirrhosis can regress if its etiologic cause is effectively removed. Nevertheless, while this is
now possible for cirrhosis caused by chronic hepatitis C, the incidence of cirrhosis due to non-alcoholic
steatohepatitis has increased dramatically and effective therapies are not yet available. New drugs acting
on the dynamic component of hepatic vascular resistance are being studied and will likely improve the
future management of portal hypertension.

CONCLUSION:

Cirrhosis is considered a dynamic disease able to progress and regress. In this new way of understanding
the spectrum of changes characterizing ACLD, early diagnosis, before the occurrence of decompensation,
is an important step to achieving a reduction in mortality due to CLD since several different

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pharmacological and non-pharmacological approaches can be used during this phase to prevent
decompensation. Ultrasound elastography of the liver allows accurate non-invasive identification of
patients with ACLD, with the additional advantage of providing a numerical surrogate of the risk of portal
hypertension and complications. Prevention of decompensation is possible by reducing portal pressure
through measures aimed at eliminating all the possible sources of injury reducing intrahepatic resistance
and at reducing Porto collateral flow. Long-standing drugs, such as NSBBs, remain the mainstay for portal
pressure reduction and can prevent not only variceal bleeding but also other more frequent decompensating
events such as ascites. After decompensation, therapy should be aimed toward avoiding further
decompensation and death, with statins being promising in these cases.

REFERENCES:

1. Bosch J, Groszmann RJ, Shah VH. Evolution in the understanding of the pathophysiological
basis of portal hypertension: How changes in paradigm are leading to successful new
treatments. J Hepatol. 2015 Apr;62(1 Suppl): S121-30. DOI: 10.1016/j.jhep.2015.01.003.
PMID: 25920081; PMCID: PMC4519833.

2. Iwakiri Y, Groszmann RJ. The hyperdynamic circulation of chronic liver diseases: from the
patient to the molecule. Hepatology. 2006 Feb;43(2 Suppl 1): S121-31. DOI:
10.1002/hep.20993. PMID: 16447289.

3. Trebicka J, Reiberger T, Laleman W. Gut-Liver Axis Links Portal Hypertension to Acute-

on-Chronic Liver Failure. Visc Med. 2018 Aug;34(4):270-275. doi: 10.1159/000490262.
Epub 2018 Jul 13. PMID: 30345284; PMCID: PMC6189544.

4. Bosch J, Pizcueta P, Feu F, Fernández M, García-Pagán JC. Pathophysiology of portal

hypertension. Gastroenterol Clin North Am. 1992 Mar;21(1):1-14. PMID: 1568769.

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