Liver Cirrhosis: Physiology & Anatomy

Liver Cirrhosis Physiology

• Hepatocytes detoxify the blood facilitated by sinusoid
• Ammonia, a byproduct of protein metabolism, is converted into urea for excretion
• Bile; bile salt and bilirubin (due to RBC breakdown) are excreted, causing yellowish stool
• Vitamins ADEK, B12 (cobalamin), B9 (folate), Iron, and glucose (glycogen) are stored
• Albumin is produced to maintain oncotic pressure and prevent blood vessel leakage
• Clotting factors like fibrinogen and prothrombin are produced
• Estrogen is metabolized and eliminated
• The liver facilitates blood flow through the hepatic portal vein

Liver Anatomy

• Hepatic portal vein drains blood which is rich with nutrients but low in oxygen
• Superior mesenteric vein drains the small intestine, pancreas, and large intestine
• Inferior mesenteric vein drains the large intestine and rectum
• Splenic vein drains the spleen and pancreas
• Gastric and Cystic veins drain the stomach and gallbladder
• Hepatic artery supplies oxygenated blood to the liver

Liver Cirrhosis Pathophysiology

• Liver cirrhosis is characterized by inflammation, fibrosis (liver scarring), and altered liver function
• Obesity, alcohol consumption, and Hepatitis B and C are common risk factors

Liver Cirrhosis Manifestation

• Intoxication occurs due to impaired detoxification through the sinusoid
• Hepatic encephalopathy (asterixis) and confabulation results from impaired ammonia conversion
• Jaundice, no ADEK absorption, and steatorrhea result from impaired bile production
• Malnutrition and impaired glucose regulation results from impaired vitamin and glycogen storage
• Ascites results in decreased production of albumin
• Bleeding/coagulopathy results in decreased production of clotting factors
• Spider angioma and palmar erythema results from impaired estrogen metabolism
• Portal hypertension and esophageal & gastric varices are dilated veins which may lead to bleeding due to impaired facilitation of blood through the hepatic portal vein

Liver Cirrhosis Management

• Avoid hepatotoxic drugs to prevent intoxication
• Lactulose is administered for hepatic encephalopathy (asterixis) and confabulation
• Intravenous (IV) fat emulsion is administered in the case of no ADEK absorption and steatorrhea
• Nutritional supplements are recommended for malnutrition
• Monitor for signs of hyperglycemia/hypoglycemia for glucose regulation
• Diuretics and paracentesis are administered for ascites
• Bleeding precautions, BT, IVF are applied for bleeding
• Beta-blockers are administered and straining is avoided for portal hypertension, esophageal & gastric varices

Liver Cirrhosis Diagnostics

• Increased AST (Aspartate Aminotransferase) and ALT (Alanine Aminotransferase) indicates impaired liver function
• International Normalized Ratio (INR) is elevated; normal range is 10–14 seconds
• Prothrombin Time (PT) is elevated; normal range is 0.8–1.2
• Platelet, WBCs and hemoglobin counts are decreased indicating splenic sequestration
• Albumin levels are decreased
• Ammonia levels are increased

Cholecystitis Physiology

• Bile is stored for fat digestion/emulsification
• Bilirubin, a brownish/yellow fluid (byproduct of RBC breakdown), is carried and excreted through the gastrointestinal (GI) tract (feces)

Cholecystitis Pathophysiology

• Gallstone (cholelithiasis), obesity, high fat diet and skipping meals may cause cholecystitis
• Obstruction or no contraction could lead to increased pressure in the gallbladder wall
• Inflammation of the gallbladder
• Altered gallbladder function

Cholecystitis Manifestation

• Steatorrhea, vitamin ADEK deficiency/malnutrition are symptoms of cholecystitis
• Clay-colored stool, jaundice, and dark urine are manifestations of cholecystitis
• Pain in the right upper back/shoulder (referred pain) is known as Boas sign, and occurs due to phrenic nerve irritation
• Murphy's sign is right upper quadrant (RUQ) pain upon inspiration
• Biliary colic is RUQ pain triggered by fat ingestion

Cholecystitis Management

• Chenodeoxycholic acid (chenodiol) is administered as a gallstone dissolution agent
• Laparoscopic Cholecystectomy may cause shoulder pain
• Open Cholecystectomy is a treatment option

Cholecystitis Diagnostics

• ERCP Endoscopic Retrograde Cholangiopancreatography) is used for diagnostics
• Abdominal Ultrasound is used for diagnostics
• Increased bilirubin is a diagnostic measure

Pancreatitis Physiology

• Acinar cells produce lipase, protease (trypsin and chymotrypsin), and amylase
• Insulin, a hormone or 'key', is produced in the Islet of Langerhans, and facilitates entry of blood glucose into the cell
• Glucagon, a hormone, stimulates stored glucose (glycogen) in the liver

Pancreatitis Pathophysiology

• Obstruction in pancreatic duct/common bile duct/sphincter of Oddi (gallstone, cystic fibrosis) and alcohol can cause pancreatitis
• Acinar cell damage results in premature activation of pancreatic juices
• Autodigestion is a pancreatic enzyme that leads to inflammation of the pancreas and possible hemorrhage
• Thick mucus can obstruct the pancreas
• Blocked pancreatic duct
• All of the above contribute to altered function of the pancreas

Pancreatitis Manifestation

• Postprandial pain
• Vitamin ADEK malabsorption/malnutrition, steatorrhea are manifestations of pancreatitis
• Hyperglycemia (Type 3c Diabetes/T3cD) is when blood sugar is too high
• Hypoglycemia is when blood sugar is too low
• Bleeding due to autodigestion
  • Cullen's sign: bluish discoloration on the umbilicus
  • Grey Turner sign: bluish discoloration on the flank area

Pancreatitis Management

• Acute condition: NPO (nothing by mouth)
• Nutritional support
• Monitor blood glucose
• Pancrelipase (should not be mixed with alkaline liquids)
• Low fat, no alcohol consumption, and limit simple carbohydrates

Pancreatitis Diagnostics

• CT scan or Ultrasound
• Elevated White Blood Cell (WBC) count
• Elevated C-Reactive Protein (CRP)
• The findings above are not only limited to pancreatitis, but are indicative

Appendicitis Pathophysiology

• Fecalith due to low fiber intake is the main cause
• Bacterial Infection
• Inflammation of the appendix, leading to rupture

Appendicitis Manifestation

• McBurney's point tenderness: RLQ pain when pressed
• Rovsing's sign: pain in RLQ when pressing the LLQ
• Psoas sign: pain in RLQ when extending the right leg
• Obturator sign: pain in RLQ when internally rotating the right hip

Appendicitis Management

• Laparoscopic Appendectomy is a treatment option
• Open Appendectomy is a treatment option
• Antibiotics
• Analgesics are prescribed for pain
• Elevated WBC and C-Reactive Protein are indicative of appendicitis