LIVER AND PORTAL HYPERTENSION

Liver and Portal Hypertension
Afroz Lakhani, RN,BScN
Pathophysiology 2009

Liver
The liver is the largest organ in the body, normally weighing about 1 to 2.3kg (although this can increase to over 10kg in chronic cirrhosis). The liver is the main organ of metabolism and energy production; its other main functions include:
Bile production
Storage of iron, vitamins and trace elements
Detoxification
Conversion of waste products for excretion by the kidneys

Functions of Liver
Carbohydrate metabolism: Maintains plasma glucose levels. Post-meal when glucose levels rise, glucose with the influence of insulin is converted to glycogen for storage.
When glucose levels falls, the hormone glucagon stimulates glycogen into glucose again. That’s how our glucose levels stays in normal range.
Fat metabolism: Excess dietary carbs or protein will store as fat. (under the skin, around kidneys)
Digested fat convert triglycerides for energy and storage.

Protein metabolism:
Deamination of amino acids: a)Nitrogenous portion is removed to form into urea, excreted into urine.
b) nucleic acids breaks down to uric acidsurine.
Transamination: removal of nitrogenous portion of amino acids and attaches to carb moleculenon-essential amino acids.
Synthesis of plasma proteins and most blood clotting factors from amino acids.

Portal Circulation




The liver is unusual has a double blood supply; the right and left hepatic arteries carry oxygenated blood to the liver, and the portal vein carries venous blood from the GI tract to the liver.
Portal vein enters the liver, the blood drains into the hepatic sinusoids, where it is screened by specialized macrophages (Kupffer cells) to remove any pathogens that manage to get past the GI defenses. The plasma is filtered through the endothelial lining of the sinusoids and bathes the hepatocytes; these cells contain vast numbers of enzymes capable of breaking down and metabolizing most of what has been absorbed.
The portal venous blood contains allof the products of digestion absorbed from the GI tract, so all useful and non-useful products are processed in the liver before being either released back into the hepatic veins which join the inferior vena cava just inferior to the diaphragm, or stored in the liver for later use.














Liver Cirrhosis

Scarring of the Liver
Cx: alcoholism, viral hepatitis, toxic reaction to drugs, biliary obstruction
S/S: wt loss, anorexia, weakness, hepatomegaly, jaundice, abdominal pain (stretching of Glisson’s cap)





Pathophysiology Liver Cirrhosis






Portal Hypertension
Obstructed blood flow through the damaged liver results in increased blood pressure (portal hypertension) throughout the portal venous system.
Pressure normally 3mm Hg;
portal HTN at least 10 mmHg
Cx: thrombosis, inflammation, fibrosis of sinusoids, viral hepatitis, cardiac disorders, most common is cirrhosis of liver.
Long term PHTN can lead to Ascites, Varices, Splenomegaly, Hepatic encephalopathy.


Ascites






Pathophysiology

PHTN and decreased serum albumin capillary hydrostatic pressure to exceed capillary osmotic pressure and causes fluid into peritoneal cavity.
The failure of the liver to metabolize aldosterone increases sodium and water retention by the kidney.
Loss of fluid into the peritoneal space causes further sodium and water retention by the kidney in an effort to maintain the vascular fluid volume.
Treatment
No salt diet
Diuretics: Spironolactone (Aldactone), an aldosterone blocking agent.
Ammonium chloride and acetazolamide are contraindicated because of the possibility of precipitating hepatic coma.
Bed rest
Paracentesis
Insertion of a peritoneovenous shunt to redirect ascitic fluid from the peritoneal cavity into the systemic circulation.



Caput medusae is the appearance of distended and engorged paraumbilical veins which are seen radiating from the umbilicus across the abdomen to join systemic veins
Esophageal Varices
Are extremely dilated sub-mucosal veins in the esophagus.
Bleeding or hemorrhage from esophageal varices occurs in approximately one third of patients with cirrhosis and varices.
The mortality rate resulting from the first bleeding episode is 45% to 50%;
It is one of the major causes of death in patients with cirrhosis
Pathophysiology EV
Increased obstruction of the portal vein causes venous blood from the intestinal tract and spleen seeks an outlet through collateral circulation (new pathways of return to the right atrium).
The effect is increased pressure, particularly in the vessels in the of the lower esophagus and upper part of the stomach.
These collateral vessels are not very elastic but rather are tortuous and fragile and bleed easily.
Treatment:
Prevent hemorrhage
Straight to ICU
potential hypovolemia
Oxygen
Intravenous fluids with electrolyte
Blood transfusion
Strict I/O
vasopressin, vasopressin with nitroglycerin, somatostatin, balloon tamponade, TPSS (transhepatic portosystemic shunt), transhepatic catheter embolization, shunt surgery, gastric stapling and sclerotherapy


Splenomegaly
an enlargement of the spleen.
Caused by increased pressure in the splenic vein, which branches from the portal vein.

Hepatic Encephalopathy
CNS totality
Lack of mental alertness, confusion, coma, convulsions.
Flapping tremor called asterixis (liver flap)
Memory loss



Pathophysiology HEn

Ammonium ion produced in the intestinal tract, abundance in colon by bacterial degradation of luminal proteins and amino acids.
Normally: Ammonium ion diffuse into portal blood, transported to the liver, where they converted to urea.
When the blood from intestines bypass the liver, ammonia is not converted to urea, and ammonia moves directly into general circulation then to cerebral circulation thus hepatic encephalopathy occurs.
Treatment
No big protein diet
Prevent GI bleeding
No narcotics or tranquilizers
Nonabsorbable antibiotic like neomycin (to eradicate bacteria from the colon)
Lactulose (acts in Large intestine, low ph)

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Kozier & Erb. (2008). Fundamentals of Nursing (8th edition) New Jersy: Pearson.
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Ross and Wilson. (2006). Anatomy and physiology (10th edition) Churchill Livingstone