Causes of upper gastrointestinal bleeding (UGIB) in patients with liver cirrhosis can be grouped

into two categories: the first includes lesions that arise by virtue of portal hypertension, namely
gastroesophageal varices and portal hypertensive gastropathy; and the second includes lesions
seen in the general population (peptic ulcer, erosive gastritis, reflux esophagitis, Mallory–Weiss
syndrome, tumors, etc.).

Emergency upper gastrointestinal endoscopy is the standard procedure recommended for both
diagnosis and treatment of UGIB. The endoscopic treatment of choice for esophageal variceal
bleeding is band ligation of varices. Bleeding from gastric varices is treated by injection with
cyanoacrylate. Treatment with vasoactive drugs as well as antibiotic treatment is started before or
at the same time as endoscopy. Bleeding from portal hypertensive gastropathy is less frequent,
usually chronic and treatment options include β-blocker therapy, injection therapy and
interventional radiology.

The standard of care of UGIB in patients with cirrhosis includes careful resuscitation, preferably in
an intensive care setting, medical and endoscopic therapy, early consideration for placement of
transjugular intrahepatic portosystemic shunt and, sometimes, surgical therapy or hepatic
transplant.

Gastrointestinal bleeding is common among people with cirrhosis due to a complication called
portal hypertension. This is elevated blood pressure in the veins that lead to your liver

Cirrhosis is severe and permanent scarring of your liver. It’s also called end-stage liver disease
because it’s the most severe form of liver damage.

It’s estimated that more than half a million people in the United States have cirrhosis. Cirrhosis
has many causes, but heavy alcohol use and viral infections are among the most common.
Portal hypertension, meanwhile, raises your risk of developing conditions like stomach and
esophageal varices that can lead to bleeding. Gastrointestinal bleeding is a serious medical
condition that requires prompt medical attention. If left untreated, it can be life threatening.

The esophagus is the hollow, muscular tube that moves food and liquid from the throat to the
stomach. The wall of the esophagus is made up of several layers of tissue, including mucous
membrane, muscle, and connective tissue

Esophageal varices are enlarged veins in the esophagus, the tube that connects the throat and
stomach. Esophageal varices most often happen in people with serious liver diseases.

Esophageal varices develop when regular blood flow to the liver is blocked by a clot or scar
tissue in the liver. To go around the blockages, blood flows into smaller blood vessels that aren't
designed to carry large volumes of blood. The vessels can leak blood or even burst, causing
life-threatening bleeding.

A few medicines and medical procedures are available to help prevent or stop bleeding from
esophageal varices.

Symptoms

Esophageal varices usually don't cause symptoms unless they bleed. Symptoms of bleeding
esophageal varices include:
  Vomiting large amounts of blood.
 Black, tarry or bloody stools.
 Lightheadedness due to blood loss.
 Loss of consciousness in severe cases.

Your doctor might suspect esophageal varices if you have signs of liver disease or been
diagnosed with liver cirrhosis, including:

 Yellow coloration of the skin and eyes, known as jaundice.

 Easy bleeding or bruising.
 Fluid buildup in the abdomen, called ascites (uh-SY-teez).

Causes

Esophageal varices sometimes form when blood flow to your liver is blocked. This is most often
caused by scar tissue in the liver due to liver disease, also known as cirrhosis of the liver. The
blood flow begins to back up. This increases pressure within the large vein, known as the portal
vein, that carries blood to your liver. This condition is called portal hypertension.

Portal hypertension forces the blood to seek other pathways through smaller veins, such as
those in the lowest part of the esophagus. These thin-walled veins balloon with the added blood.
Sometimes they rupture and bleed.

Causes of esophageal varices include:

 Severe liver scarring, called cirrhosis. Several liver diseases — including

hepatitis infection, alcoholic liver disease, fatty liver disease and a bile duct
disorder called primary biliary cholangitis — can result in cirrhosis.
 Blood clot, also called thrombosis. A blood clot in the portal vein or in a vein that
feeds into the portal vein, known as the splenic vein, can cause esophageal
varices.
 Parasitic infection. Schistosomiasis is a parasitic infection found in parts of Africa,
South America, the Caribbean, the Middle East and East Asia. The parasite can
damage the liver, as well as the lungs, intestine, bladder and other organ
Vit k

Indications

Vitamin K is a fat-soluble vitamin that affects coagulation pathways within the body. Vitamin K is found
in foods and can be a dietary supplement. Vitamin K is essential for the synthesis of coagulation proteins.
It is a co-factor for vitamin K-dependent carboxylation, which includes various enzymes. The process of
vitamin K carboxylation allows the coagulation factors to bind calcium ions, which further facilitates the
cascade pathways. Vitamin K deficiency impairs the coagulation process leading to issues with bleeding.
Recent research has linked vitamin K deficiency to issues with osteoporosis and cystic fibrosis.[1][

Continuing Education Activity

Vitamin K is a medication used to manage and treat bleeding due to the coagulation disorder caused by
warfarin and vitamin K deficiency. It is in the fat-soluble vitamin class of drugs. This activity outlines the
indications, actions, and contraindications for vitamin K as a valuable agent in managing coagulation
disorders caused by warfarin or vitamin K deficiency.

gamma-Carboxyglutamate

Found in various tissues, particularly in four blood-clotting proteins including prothrombin, in

kidney protein, in bone protein, and in the protein present in various ectopic calcifications.

Chelation- is a type of bonding of ions and molecules to metal ions.

Coagulation -consists of three pathways, the extrinsic, intrinsic, and common pathways, that
interact together to form a stable blood clot.

carboxylation,-control blood coagulation, vascular calcification, bone metabolism,

and other important physiological processes.

Coagulation- in physiology, the process by which a blood clot is

formed
TRANEXAMIC ACID 500MG

Contraindications
 In patients with subarachnoid hemorrhage, due to risk of cerebral edema
and cerebral infarction. (4)
 In patients with active intravascular clotting. (4)
 In patients with severe hypersensitivity reactions to tranexamic acid or any
of the ingredients. (4)

Antifibrinolytic agents (tranexamic acid, aminocaproic acid, nafamostat and aprotinin)

are drugs that act by inhibiting the process that dissolves clots, thereby reducing bleeding.

Tranexamic acid is a competitive inhibitor of plasminogen activation and at much higher concentrations
a noncompetitive inhibitor of plasmin, thus implying that tranexamic acid interferes with the fibrinolytic
process in the same way as aminocaproic acid. Tranexamic acid is about 10 times more potent in vitro
than aminocaproic acid. Tranexamic acid binds considerably more strongly than aminocaproic acid to
both the strong and weak sites of the plasminogen molecule in a ratio corresponding to the difference in
potency between the compounds. Tranexamic acid in a concentration of 1 mg/mL does not aggregate
platelets in vitro. Tranexamic acid in concentrations up to 10 mg/mL blood has no influence on the
platelet count, the coagulation time or various coagulation factors in whole blood or citrated blood in
normal subjects. On the other hand tranexamic acid in concentrations of 10 mg/mL and 1 mg/mL blo

What causes liver cirrhosis?it