Liver and Pancreas Anatomy and Function PDF

Liver and Pancreas Anatomy and Function Lecture Number 5.2 Status Done Type Lecture 5.2 Liver and Pancreas Anatomy and Function Overview This lecture discusses the liver and pancreas's anatomy and functions, highlighting their roles in metabolism, digestion,...

Liver and Pancreas Anatomy and Function Lecture Number 5.2 Status Done Type Lecture 5.2 Liver and Pancreas Anatomy and Function Overview This lecture discusses the liver and pancreas's anatomy and functions, highlighting their roles in metabolism, digestion, and detoxification. Focus areas include the liver's unique blood supply and lobular zonation, bile synthesis, fatty acid metabolism, and glucose regulation, alongside the pancreas’s exocrine function in enzyme secretion and bicarbonate release for digestion. Pathological contexts like liver steatosis, toxic injury, and diabetes-related metabolic changes are integrated to illustrate clinical relevance. Learning Objectives Objective 1: Describe the position and functional anatomy of the liver. Objective 2: Outline major liver functions (e.g., storage, synthesis, biotransformation). Objective 3: Explain venous drainage pathways from the foregut, midgut, and hindgut to the hepatic portal vein. Objective 4: Describe the position and functional anatomy of the pancreas. Objective 5: Discuss the exocrine functions of the pancreas, including enzyme and bicarbonate production by acinar and duct cells. Key Concepts and Definitions Liver Anatomy: Located in the right upper quadrant (RUQ), largely intraperitoneal except areas in contact with the diaphragm; weighs ~1.5 kg. Divided into four anatomical lobes (right, left, caudate, quadrate) by the falciform ligament, with no functional distinctions between lobes. Portal Venous System : Major blood supply (60-70%) to the liver, formed by the confluence of the splenic and superior mesenteric veins, draining GI tract blood to the liver. Hepatocytes: Principal liver cells responsible for carbohydrate (CHO), fatty acid (FA), and protein metabolism, detoxification, and albumin production, forming 80% of liver mass. Pancreas Anatomy: Situated in the C-shaped curve of the duodenum, mainly exocrine (85%) but with critical endocrine roles (insulin, glucagon production). Liver Zonation : Hepatic lobules contain three zones with varying oxygenation and metabolic function; Zone 1 is oxygen- rich and prone to toxin exposure, while Zone 3 is susceptible to ischemic injury. Clinical Applications Case Study: Paediatric steatosic liver disease often shows Zone 1 injury, contrasting with Zone 3 injury in adults, reflecting differences in metabolic activity. Diagnostic Approach: Recognize zonal injury patterns (toxic injury in Zone 1, ischemic injury in Zone 3) to aid in diagnosing liver pathologies. Treatment Options: Lifestyle modifications, particularly dietary adjustments, are critical for managing fatty liver disease, with focus on reducing saturated fat intake. Complications/Management: Steatosis and insulin resistance can progress to type 2 diabetes, necessitating careful monitoring of metabolic functions and liver health. Pathophysiology  Liver Zonation and Injury Mechanisms: Blood flow in hepatic lobules initiates from the portal triad (oxygen/nutrient- rich) and flows towards the central vein, creating zones with unique oxygen and nutrient profiles. Zone 1 performs oxidative metabolism, while Zone 3 handles glycolysis and other non-oxidative processes. Zone 1 is also first to encounter toxins, leading to a higher likelihood of toxic injury, whereas Zone 3 is more vulnerable to ischemic injury. Hepatic Fatty Acid Metabolism : Fatty acids enter the liver via dietary fat, chylomicron remnants, or systemic NEFA (non-esterified fatty acids) from adipose tissue. Hepatocytes manage fatty acids through de novo lipogenesis (DNL) and disposal via oxidation or storage as triglycerides in very low-density lipoproteins (VLDL), with systemic implications for lipid metabolism. Pharmacology VLDL Synthesis and Metabolism : Begins with ApoB100 assembly in the rough ER, followed by triglyceride lipidation via microsomal transfer protein (MTP). Insulin resistance, calorie excess, high free sugar intake, and physical inactivity all increase VLDL production, linking to elevated cardiovascular risk. Bile Acid Synthesis: Two pathways exist: the classical pathway, initiated by cholesterol 7α-hydroxylase (CYP7A1) in the liver, producing primary bile acids cholic acid (CA) and chenodeoxycholic acid (CDCA); and the alternative pathway, contributing