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Liver Largest gland of the body and a major organ Receives nutrient-rich blood directly from the GI tract Stores or transforms nutrients into chemical substances Manufactures and secretes bile Removes waste products from the bloodstream and secretes them into the bile Bile produced by the liver is stored temporarily in the gallbladder When needed for digestion, the gallbladder empties and bile enters the intestine Important in the regulation of glucose and protein Anatomy of the Liver The liver is a large, vascular organ located behind the ribs in the upper right abdomen, weighing 1200- 1500 g and divided into four lobes. Each lobe is divided into functional units called lobules, surrounded by connective tissue. Blood enters the liver from two sources: 80% from the nutrient-rich but oxygen-poor portal vein, and the rest from the oxygen-rich hepatic artery. These blood vessels form sinusoids, which bathe liver cells (hepatocytes) in a mixture of venous and arterial blood. The sinusoids drain into central veins, which join to form the hepatic vein, draining into the inferior vena cava near the diaphragm. Kupffer cells, a type of phagocyte, engulf bacteria and other particles from portal blood. The smallest bile ducts, called canaliculi, carry secretions from hepatocytes to larger bile ducts, forming the hepatic duct. The hepatic duct and cystic duct from the gallbladder merge to form the common bile duct, which empties into the small intestine. -The sphincter of Oddi controls bile flow from the common bile duct into the duodenum. Functions of the Liver Glucose Metabolism The liver regulates blood glucose levels by converting glucose into glycogen (stored in hepatocytes) after meals. When needed, glycogen is converted back to glucose (glycogenolysis) and released into the bloodstream. When glycogen stores are insufficient, the liver produces glucose via gluconeogenesis, using amino acids or lactate, especially during hypoglycemia. Ammonia Conversion Ammonia, a by-product of amino acid breakdown, is converted into urea by the liver. Ammonia from intestinal bacteria is also removed from portal blood and converted into urea for excretion via urine. Protein Metabolism The liver synthesizes most plasma proteins, including albumin, globulins, clotting factors, and transport proteins. It requires Vitamin K for the synthesis of clotting factors, such as prothrombin. Amino acids are used for protein synthesis in the liver. Fat Metabolism The liver breaks down fatty acids for energy and produces ketone bodies (acetoacetic acid, beta-hydroxybutyric acid, acetone) during times of limited glucose (e.g., starvation or diabetes). Fatty acids also help in synthesizing cholesterol, lecithin, lipoproteins, and other lipids. Vitamin and Iron Storage The liver stores vitamins A, B, D, and B- complex vitamins, as well as iron and copper. Bile Formation Bile is continuously produced by hepatocytes and stored in the gallbladder for digestion. Bile aids in fat emulsification and the excretion of waste products like bilirubin. Bilirubin Excretion Bilirubin, from the breakdown of hemoglobin, is processed in the liver and excreted in bile. In the intestine, bilirubin is converted to urobilinogen, partially excreted in feces, and reabsorbed into portal blood for reuse or excretion through the kidneys. Drug Metabolism The liver metabolizes many drugs (e.g., barbiturates, opioids, sedatives) by conjugating them with compounds for excretion. First-pass metabolism reduces the bioavailability of some oral drugs, meaning larger doses may be needed to achieve the desired effect compared to parenteral routes. Assessment of Liver Health History Past Medical History: Check for liver diseases or past issues (e.g., hepatitis, cirrhosis). Lifestyle: Look at alcohol use, diet, exercise, and toxin exposure. Medications: Review drugs that may affect liver health. Family History: Ask about liver problems or genetic liver conditions. Physical Assessment Skin: Look for jaundice (yellow skin/eyes), swelling (edema), or spider veins. Tremor and Asterixis: Check for hand tremors or involuntary hand flapping (signs of liver issues). Abdominal Assessment Fluid Wave: Check for fluid buildup in the abdomen (ascites). Palpation: Liver Size: Feel for the liver in the right upper abdomen. Tenderness: Look for pain when touching the liver. Palpable Liver: If the liver is enlarged, it may feel firm and sharp Diagnostic Evaluation Liver Function Tests
Liver function tests may not show abnormal results until more than 70% of liver tissue is damaged. Tests measure enzyme activity and serum levels of proteins, bilirubin, ammonia, clotting factors, and lipids. ALT (Alanine Aminotransferase): Increased in liver disorders, used to monitor conditions like hepatitis, cirrhosis, or liver damage from medications. AST (Aspartate Aminotransferase) : Elevated levels can indicate damage to organs like the heart, liver, muscles, or kidneys. Not specific to liver disease but may increase in cirrhosis, hepatitis, or liver cancer. GGT (Gamma Glutamyl Transferase) : High levels are linked to cholestasis and alcoholic liver disease. Liver Biopsy A liver biopsy involves removing a small sample of liver tissue for examination. It helps diagnose liver conditions when clinical findings and lab tests aren’t enough. Often used to evaluate liver disorders or detect lesions . Other Diagnostic test Ultrasonography, CT Scans, and MRI: Used to identify normal liver structures and abnormalities in the liver and biliary tree. Radioisotope Liver Scan: Assesses liver size, blood flow, and possible obstructions. Laparoscopy: A fiberoptic endoscope is inserted through a small abdominal incision to: Jaundice Occurs when bilirubin concentration in the blood increases due to liver disease, bile flow obstruction (e.g., gallstones), or excessive red blood cell destruction. With bile duct obstruction, bilirubin cannot enter the intestine, leading to a decrease in urobilinogen in the stool and absence in the urine. Jaundice becomes visible when serum bilirubin exceeds 2.0 mg/dL, resulting in a yellow or greenish-yellow tint to the skin and sclerae (the white part of the eyes). Types of Jaundice Hemolytic Jaundice Cause: Increased red blood cell destruction, leading to excess bilirubin in the blood. Bilirubin: Predominantly unconjugated (free) bilirubin. Fecal and Urine Urobilinogen: Increased, but urine is free of bilirubin. Symptoms: Mild jaundice, unless bilirubin levels are extremely high (over 20-25 mg/dL), which can lead to central nervous system effects. Complications: Long-term mild jaundice can lead to pigment stones in the gallbladder. Hepatocellular Jaundice Cause: Liver cell damage prevents proper clearance of bilirubin from the blood. Common causes include hepatitis, viral infections, alcohol abuse, and chemical toxins. Associated with: Cirrhosis (often due to excessive alcohol intake or viral infections). Symptoms: Lack of appetite, nausea, fatigue, weakness, and possible weight loss. In some cases, jaundice may not be obvious. Bilirubin and Urobilinogen: Serum bilirubin and urine urobilinogen levels may be elevated. Liver Enzymes: AST and ALT levels increase, indicating liver cell damage. Other Symptoms: Headache, chills, and fever, particularly if the cause is infectious. Prognosis: Hepatocellular jaundice may be reversible depending on the cause and extent of liver damage. Obstructive Jaundice Cause: Extrahepatic Obstruction: Blockage outside the liver (e.g., gallstones, inflammation, tumors, or pressure from an enlarged organ). Intrahepatic Obstruction: Blockage inside the liver’s small bile ducts (e.g., inflammation or certain medications like some antibiotics and hormones). Effects: Bile backs up into the liver and enters the bloodstream, causing jaundice (yellowing of skin, mucous membranes, and eyes). Urine turns deep orange and foamy due to bilirubin. Stools become light or clay-colored because of a lack of bile in the intestine. Symptoms: Itching from bile buildup in the skin. Fatty food intolerance and indigestion due to impaired fat digestion. Lab Results: Moderate increase in AST, ALT, and GGT. High bilirubin and alkaline phosphatase levels. Hyperbilirubinemia (high bilirubin levels) can be caused by inherited disorders, leading to jaundice. Gilbert Syndrome: Increased unconjugated bilirubin causes jaundice. Liver function and histology are normal, with no hemolysis. Affects 3-8% of the population, mostly males. Other Inherited Conditions: Dubin-Johnson Syndrome: Chronic jaundice with liver pigment. Rotor Syndrome: Chronic conjugated hyperbilirubinemia, no liver pigment. Benign Cholestatic Jaundice of Pregnancy: Due to sensitivity to pregnancy hormones. Benign Recurrent Intrahepatic Cholestasis: A genetic condition affecting bile flow. Portal Hypertension increased pressure in the portal venous system due to liver damage, commonly caused by cirrhosis but can occur in non-cirrhotic liver disease. Key Features: Splenomegaly (enlarged spleen) with possible hypersplenism (overactive spleen). Major complications include ascites (fluid buildup in the abdomen) and varices (enlarged veins, often in the esophagus, which can bleed). Ascites is the buildup of fluid in the abdomen, often due to liver problems. Causes: High pressure in the liver (portal hypertension) leads to fluid leakage.
Reduces risk of: Post-paracentesis circulatory dysfunction Renal dysfunction Hyponatremia Rapid fluid reaccumulation Benefits of Albumin Improves: Hemodynamic stability Renal function Possibly cardiac function Decreases arterial vasodilation Refractory Ascites Ascites that does not respond to diuretics + sodium restriction for 2 weeks or more Can cause serious complications like respiratory distress Needs rapid intervention Body’s Misinterpretation in Cirrhosis Despite excess fluid, kidneys think there’s low blood volume Triggers: Renin–angiotensin–aldosterone system (RAAS) → sodium retention Antidiuretic hormone (ADH) → water retention Can cause dilutional hyponatremia Esophageal Varices Varicose veins (varicosities) in the esophagus Develop due to elevated pressure in veins draining into the portal system Commonly located in the lower esophagus, but may: Extend higher up the esophagus Spread into the stomach Varicose veins (varicosities) in the esophagus Develop due to elevated pressure in veins draining into the portal system Commonly located in the lower esophagus, but may: Extend higher up the esophagus Spread into the stomach High risk of rupture Can cause massive GI bleeding from: Upper GI tract Rectum Bleeding risk increases with clotting abnormalities seen in severe liver disease Prevalence 30% of patients with compensated cirrhosis 60% of patients with decompensated cirrhosis at diagnosis Pathophysiology Caused by portal hypertension Results from obstruction in portal venous circulation due to liver damage Clinical Manifestations Signs of Bleeding Hematemesis (vomiting blood) Melena (black, tarry stools) General deterioration in mental or physical status Often associated with alcohol abuse history Signs of Shock Cool, clammy skin Hypotension (low blood pressure) Tachycardia (increased heart rate) Assessment and Diagnostic Findings Endoscopy: Primary method to identify bleeding site Ultrasonography, CT Scanning, Angiography: Used for additional imaging Endoscopic Video Capsule: Can detect esophageal varices but not a substitute for standard endoscopy unless endoscopy is not possible Endoscopy Screening for Cirrhosis Patients with cirrhosis should undergo screening endoscopy If no varices found: Repeat in 2–3 years If small varices found: Repeat in 1–2 years Large varices (found on endoscopy) are at higher risk for bleeding Portal Hypertension Measurements Indicators of Portal Hypertension Dilated abdominal veins Hemorrhoids Splenomegaly (enlarged spleen) Ascites (fluid in the abdomen) Procedure for Hepatic Venous Pressure Gradient (HVPG) Measurement Catheter insertion: A catheter is inserted into the antecubital or femoral vein. Advanced under fluoroscopy to reach the hepatic vein. Fluid infusion: Fluid is infused to inflate the balloon once the catheter reaches the hepatic vein. Obtaining the measurement: “Wedged” pressure: Occludes the blood flow in the vessel to measure pressure, similar to pulmonary artery wedge pressure. Pressure is measured in the unoccluded vessel. Hepatic venous pressure gradient (HVPG) is calculated. Interpretation: HVPG > 10 mm Hg = clinically significant portal hypertension. Though this method may underestimate portal pressure, it can be repeated to monitor the effectiveness of treatment. Direct Measurement of Portal Pressure Methods for direct portal vein pressure: Catheter insertion directly into the portal vein or one of its branches. Endoscopic Pressure Measurement: Used only with endoscopic sclerotherapy to measure pressure within varices. Laboratory Tests Liver Function Tests Serum aminotransferases (AST, ALT) Bilirubin Alkaline phosphatase Serum proteins Imaging Tests Splenoportography: Serial or segmental X-rays to detect collateral circulation in esophageal vessels → indicates presence of varices
Hepatoportography and Celiac Angiography: Usually performed in the OR or X-ray department Medical Management Bleeding varices = Medical emergency Can lead to hemorrhagic shock Patient is critically ill and usually transferred to the ICU Requires aggressive medical and nursing care Continuous monitoring of vital signs Especially when hematemesis or melena is present IV fluids to restore volume Electrolytes to correct imbalances Volume expanders Blood transfusions if needed Urinary catheter inserted for frequent urine output monitoring Avoid overhydration → may increase portal pressure and worsen bleeding Pharmacologic Approach Endoscopic Surgical Pharmacologic Therapy Start vasoactive drugs immediately, before endoscopy, in suspected variceal bleeding. Medications are fast-acting and can be started quickly in active bleeding situations. Octreotide (Preferred First-Line) Synthetic somatostatin analog Reduces variceal bleeding by causing selective splanchnic vasoconstriction → inhibits glucagon release Vasopressin (Urgent Situations Only) Causes splanchnic arterial constriction → lowers portal pressure Constricts distal esophageal & proximal gastric veins Beta-Blockers (Long-Term Prevention) Propranolol, Nadolol, Carvedilol Reduce portal pressure Prevent first bleeding in patients with known varices Prevent rebleeding after an initial bleed ***** _Do not use during active bleeding. Nitrates (e.g., Isosorbide) Lower portal pressure through Venodilation and Decreased cardiac output Contraindicated in coronary artery disease it can cause coronary vasoconstriction and myocardial infarction_* Balloon Tamponade Purpose: Temporarily control massive bleeding from esophageal varices Stabilize patient before definitive treatment Procedure: Tube inserted through nose to stomach Has 2 balloons: esophageal & gastric Inflated externally to compress bleeding varices Risks : Airway obstruction (if balloon shifts into oropharynx or ruptures) Aspiration of blood/secretions (especially in stuporous/comatose patients) Ulceration or necrosis (if tube is in too long or overinflated) Precautions : Test balloons before insertion Use <12 hours (preferably less) Consider endotracheal intubation to protect airway Other Treatments Endoscopic Sclerotherapy Injection of a sclerosing agent into varices using an endoscope Promotes thrombosis to stop bleeding Endoscopic Variceal Ligation (Banding) First-line treatment for acute bleeding Also used to prevent first and recurrent bleeding episodes TIPS (Transjugular Intrahepatic Portosystemic Shunt) Used for uncontrolled variceal bleeding not responding to drugs/endoscopy Creates a shunt within the liver to lower portal pressure Surgical Management Includes: Surgical ligation of varices Shunts: splenorenal, mesocaval, portacaval Esophageal transection with devascularization Surgical Bypass (Shunt Surgery) Decompresses portal circulation Works well in stopping bleeding, but worse survival vs. TIPS No longer used for prevention of bleeding Consider when MELD score <15, Not eligible for transplant and No access to TIPS or follow-up. Hepatic Encephalopathy and Coma Also known as Portosystemic Encephalopathy A life-threatening and reversible neuropsychiatric complication of severe liver failure May show no clear signs, but abnormalities appear on neuropsych testing Caused by liver failure, portal hypertension, and shunting of blood from portal to systemic circulation Begins subtly, often called minimal or subclinical HE Pathophysiology (Two main causes) Hepatic insufficiency- Liver can't detoxify harmful substances (especially ammonia) Portosystemic shunting - Blood bypasses liver, allowing toxins into systemic circulation _Ammonia – The Main Culprit. Comes from digestion of dietary & blood proteins in GI tract_** Other Contributing Factors Not directly related to ammonia but can still trigger HE: Excessive diuresis Dehydration Infections Surgery Fever Certain meds (sedatives, tranquilizers, analgesics, diuretics causing K ⁺loss) Other Toxic Substances Involved Manganese buildup Mercaptans (from sulfur compounds) Changes in amino acids and false neurotransmitters like dopamine Clinical manifestation Early symptoms: Mental status changes (e.g., confusion) Motor disturbances Altered mood and sleep patterns (e.g., daytime sleepiness, nighttime restlessness and insomnia) Progression of symptoms: Increased difficulty in awakening Disorientation to time and place Eventual coma and possible seizures Neurological signs:
Usually managed at home unless symptoms are severe Assist patient and family in coping with temporary disability and fatigue Educate on diet, rest, follow-up blood work, and avoiding alcohol Provide guidelines on sanitation and hygiene to prevent disease spread Emphasize hand hygiene after bowel movements and before eating Educate on safe food and water supply, and effective sewage disposal Dietary Management Hepatitis B HBV is primarily transmitted through blood (percutaneous and permucosal routes). Can be found in blood, saliva, semen, and vaginal secretions. Transmission occurs through mucous membranes and breaks in the skin. Carrier mothers can transfer HBV to their infants, especially in high-incidence areas (e.g., Southeast Asia). Infection is typically not transmitted via the umbilical vein but during birth and close contact afterward. HBV has a long incubation period and replicates in the liver, remaining in the serum for extended periods, allowing for transmission. Screening of blood donors has significantly reduced the occurrence of HBV after blood transfusion Risk Factors Clinical Manifestations Incubation period of HBV is 1 to 6 months. Fever and respiratory symptoms are rare; some patients may experience arthralgias and rashes. Symptoms may include loss of appetite, dyspepsia, abdominal pain, generalized aching, malaise, and weakness. Jaundice may or may not be evident; if present, light- colored stools and dark urine may accompany it. The liver may be tender and enlarged (12 to 14 cm vertically). The spleen may be enlarged and palpable in a few patients; posterior cervical lymph nodes may also be enlarged. Assessment and Diagnostic Finding: HBV is a DNA virus with several antigenic particles: HBcAg (hepatitis B core antigen) – antigenic material in the inner core. HBsAg (hepatitis B surface antigen) – antigenic material on the viral surface, a marker of active replication and infection. HBeAg – an independent protein circulating in the blood. HBxAg – gene product of the X gene of HBV DNA. Specific antibodies are markers for different stages of the disease: anti-HBc – antibody to core antigen, present during the acute phase of illness, may indicate ongoing HBV in the liver. anti-HBs – antibody to surface determinants, usually detected during late convalescence, indicating recovery and immunity. anti-HBe – antibody to hepatitis B e-antigen, typically signifies reduced infectivity. anti-HBxAg – antibody to the hepatitis B x- antigen, may indicate ongoing replication of HBV. Prevention Screening of blood donors Proper disposal of sharps Wearing of gloves Needless IV administration Disinfection Patient education Active Immunization Active Immunization: HBV Hepatitis B vaccine is recommended for high-risk people like healthcare workers and those on hemodialysis. People with chronic liver diseases, like HCV, should also get vaccinated. In 2018, HEPLISAV-B, a new hepatitis B vaccine, was approved for adults 18 and older, given in two doses 1 month apart. Before 2019, a yeast-based vaccine was used, with over 90% protection in healthy people. Immunity can last 5-10 years, even if antibody levels drop. Booster shots are not needed for most people but are recommended for the immunocompromised. A plasma-based vaccine is only used for people allergic to yeast-based vaccines or with immunodeficiencies. The vaccine is given in the deltoid muscle for adults. Passive Immunity: Hepatitis B Immune Globulin HBIG gives passive immunity to people who haven't had hepatitis B or the vaccine. It's used after exposure to HBV from needlesticks, splashes, sexual contact, or from an infected mother to baby. It's made from plasma with high anti-HBs antibodies. HBIG should be given as soon as possible after exposure. Both HBIG and the vaccine are given for protection. They should be given in different spots with separate syringes. HBIG is safe and doesn't transmit infections. Medical management Minimize infectivity and liver inflammation Decrease symptoms Alpha-interferon is the most promising treatment, with a regimen of 5 million U daily or 10 million U three times a week for 16 to 24 weeks. This regimen results in remission in about one-third of patients.
Nursing Management Convalescence can be prolonged, requiring 3 to 4 months or more for full recovery. Gradual return to physical activity is encouraged after jaundice resolves. Psychosocial concerns include potential isolation due to hospitalization or inability to work. Planning is important to address social isolation and avoid sexual contact. HEPATITIS C VIRUS HCV is transmitted through blood, including sharing needles, unprotected sex, and needlesticks in healthcare. High-risk groups include IV drug users, people with multiple sexual partners, frequent blood transfusion recipients, and healthcare workers. Incubation period ranges from 15 to 160 days. Symptoms are usually mild or absent, but many people develop chronic infection. Chronic HCV can lead to liver damage, cirrhosis, or liver cancer. High-risk groups should be screened for HCV. Avoid alcohol and liver-affecting medications to prevent disease progression. Risk Factors Management Rest, vitamins, and diet are not beneficial for treating HCV. HCV treatment has improved with the introduction of protease inhibitors in 2011. Current therapies can achieve a sustained virologic response (SVR), meaning the virus is undetectable 12 weeks after treatment, indicating a cure. Over 90% of HCV patients can be cured, regardless of the HCV genotype, with 8 to 12 weeks of oral therapy. Blood screening has reduced HCV transmission through blood transfusions. Public health programs are helping reduce HCV cases related to shared needles in IV or injection drug use. Hepatitis D Hepatitis D virus (HDV) infection occurs in some cases of hepatitis B. HDV requires hepatitis B surface antigen (HBsAg) for replication, so only people with hepatitis B are at risk. Diagnosis is confirmed by the presence of anti-delta antibodies and HBsAg. Hepatitis D is common among IV drug users, hemodialysis patients, and recipients of multiple blood transfusions. Sexual contact with individuals infected with hepatitis B is a key mode of transmission for both hepatitis B and D. The incubation period for hepatitis D ranges from 30 to 150 days. Symptoms of hepatitis D are similar to hepatitis B but patients are more likely to develop acute hepatic failure, chronic active hepatitis, and cirrhosis. Interferon alfa is the only licensed drug available for treating hepatitis D infection Hepatitis E HEV is primarily transmitted through the fecal-oral route, often via contaminated water in areas with poor sanitation. The incubation period for HEV ranges from 15 to 65 days. Hepatitis E generally resembles hepatitis A and has a self-limited course with abrupt onset Jaundice is almost always present in hepatitis E. Chronic forms of hepatitis E do not develop. Prevention focuses on good hygiene practices, especially handwashing, to avoid contact with the virus. The effectiveness of immune globulin in preventing hepatitis E is uncertain. Hepatitis G Virus And GB Virus-C A non-A–E agent causing hepatitis has been suspected for some time. The incubation period for posttransfusion hepatitis is 14 to 145 days, longer than hepatitis B or C. In the U.S., about 5% of chronic liver disease cases are cryptogenic (unknown cause), with 50% of these patients having had blood transfusions. Hepatitis G virus (HGV) or GB virus-C (GBV-C) is thought to be the cause, transmitted percutaneously. Risk factors for HGV/GBV-C are similar to those for hepatitis C. There is no clear link between HGV/GBV-C infection and liver disease progression, though persistent infection may occur without affecting the clinical course. Non-viral Hepatitis Certain chemicals, like carbon tetrachloride and phosphorus, can cause toxic hepatitis when inhaled, injected, or ingested. These chemicals are true hepatotoxins and lead to acute liver cell necrosis. Some medications can induce hepatitis, but they act as sensitizers rather than toxins. Drug-induced hepatitis is similar to viral hepatitis, but it causes more extensive liver damage. Medications that can cause hepatitis include isoniazid, halothane, acetaminophen, methyldopa, and certain antibiotics, antimetabolites, and anesthetics. Toxic Hepatitis Toxic hepatitis starts similarly to viral hepatitis with symptoms like loss of appetite, nausea, vomiting, jaundice, and an enlarged liver. A history of exposure to harmful chemicals or drugs helps in early diagnosis and treatment. Severity of symptoms depends on the level of toxicity. Early removal of the toxin leads to faster recovery; delayed exposure makes recovery harder. There is no specific antidote for toxic hepatitis. In severe cases, symptoms may include fever, vomiting with blood, bleeding, and shock, leading to coma and death without a liver transplant. Treatment focuses on supporting the body with fluids, blood replacement, and comfort measures. Some patients may recover but later develop chronic liver disease. Drug-induced Hepatitis Drug-induced liver disease is a common cause of acute liver failure. Symptoms may appear quickly or after months of using a medication.
Connected to the common bile duct (CBD) by the cystic duct. Pancreas Located in the upper abdomen. Has both exocrine and endocrine functions: Exocrine: Secretes pancreatic enzymes into the GI tract via the pancreatic duct. Endocrine: Secretes insulin, glucagon, and somatostatin directly into the bloodstream. Disorders of the Gallbladder Disorders include inflammation and carcinoma that obstruct the biliary tree. Gallbladder disease with stones is the most common biliary system disorder. Not all cholecystitis cases are related to stones (cholelithiasis or choledocholithiasis). Most people with gallstones (15 million Americans) experience no pain and are unaware of their presence. Cholecystitis Gallbladder Inflammation Can be acute or chronic. Causes pain, tenderness, and rigidity in the upper right abdomen, radiating to the midsternal area or right shoulder. Associated with nausea, vomiting, and typical signs of acute inflammation. An empyema occurs if the gallbladder fills with purulent fluid (pus). Calculous Cholecystitis Over 90% of cases are caused by a gallbladder stone obstructing bile outflow. Bile remaining in the gallbladder triggers chemical reactions, autolysis, and edema. Blood vessels in the gallbladder become compressed, compromising vascular supply. Gangrene and perforation of the gallbladder may occur. Bacteria play a minor role, but secondary infection of bile happens in about 50% of cases. Acalculous Cholecystitis Acute inflammation of the gallbladder without gallstone obstruction. Often occurs after major surgeries, orthopedic procedures, severe trauma, or burns. Thought to be caused by changes in fluids, electrolytes, and regional blood flow in the visceral circulation. Bile stasis and increased bile viscosity are also contributing factors. Diagnosis is challenging, especially in cases following major surgeries or trauma. Cholelithiasis Stones form in the gallbladder from solid constituents of bile. Vary in size, shape, and composition. Uncommon in children and young adults, but more prevalent with age. Prevalence: 5%-20% in women aged 20-55 years, 25%-30% in women over 50 years. Affects about 50% of women by age 70. Pathophysiology Two Types of Gallstones: Pigment Stones (10%-25% of cases): Form when unconjugated pigments in bile precipitate. Increased risk in patients with cirrhosis, hemolysis, and biliary tract infections. Cannot be dissolved, must be surgically removed. Cholesterol Stones (75% of cases): Form due to supersaturation of bile with cholesterol, resulting from decreased bile acid synthesis and increased cholesterol synthesis in the liver. Cholesterol precipitates out of bile, leading to stone formation. The saturated bile also causes irritation and inflammation in the gallbladder mucosa. Risk Factors Clinical Manifestations of Gallbladder Disease: Pain and Biliary Colic Occurs when gallstone obstructs the cystic duct, causing gallbladder distension, inflammation, and possible infection (acute cholecystitis). Symptoms : Fever, palpable abdominal mass, excruciating upper right abdominal pain radiating to the back or right shoulder, nausea, vomiting, and restlessness. Pain typically occurs after a heavy meal and can be constant or colicky. Jaundice Caused by obstruction of the common bile duct, resulting in bile being absorbed into the bloodstream, giving the skin and mucous membranes a yellow color. Often accompanied by itching (pruritus). Changes in Urine and Stool Color Dark urine due to bile pigments being excreted by the kidneys. Clay-colored or grayish stools due to lack of bile pigments. Vitamin Deficiency: Obstruction of bile flow impairs the absorption of fat-soluble vitamins A, D, E, and K. Prolonged obstruction can lead to deficiencies, such as vitamin K deficiency causing bleeding problems. Medical Management Reduce pain and inflammation. Manage with diet and support. Surgery or medications to remove the cause. Cholecystectomy:
Laparoscopic surgery preferred (less risk, faster recovery). Open surgery if needed. Supportive Care: Rest, fluids, pain relief, and antibiotics often help. Surgery after symptom improvement. Post-surgery diet: low-fat liquids. Pharmacologic Therapy Ursodeoxycholic acid (UDCA) and chenodeoxycholic acid (CDCA): Used to dissolve small, cholesterol- based gallstones; not for frequent symptoms, cystic duct occlusion, or pigment stones. Nonsurgical Gallstone Removal Dissolving Stones: Solvents like mono-octanoin or MTBE can be infused into the gallbladder via percutaneous tube, T-tube tract, or ERCP. Stone Removal by Instrumentation: Used for stones not removed during cholecystectomy or lodged in the CBD. T-tube Tract Procedure: A catheter with a basket is used to retrieve stones from the common bile duct through the T-tube tract or fistula. ERCP Procedure: An endoscope is used with a cutting instrument to enlarge the sphincter of Oddi, allowing stones to pass into the duodenum, or with a basket/balloon to retrieve the stones. Intracorporeal Lithotripsy: Uses laser pulse technology under fluoroscopic guidance to fragment gallstones in the gallbladder or CBD. Extracorporeal Shock Wave Lithotripsy (ESWL): A noninvasive procedure that uses shock waves to fragment gallstones, transmitted through a fluid- filled bag or water bath. Surgical Management: Surgery is performed to relieve symptoms, remove the cause of biliary colic, and treat acute cholecystitis, either as elective or emergency procedure. Cholecystectomy Removal of the gallbladder through an abdominal incision after ligating the cystic duct and artery, performed for acute and chronic cholecystitis. A drain may be placed if there's a bile leak. Performed when extensive surgery isn't possible, the gallbladder is opened, stones and drainage are removed, and a drainage tube is secured. Choledoctostomy Reserved for seriously ill patients, involves making an incision in the common duct for stone removal, followed by tube insertion for bile drainage until swelling subsides, with laparoscopic cholecystectomy planned later. Endoscopic Ultrasound (EUS) A guided gallbladder drainage procedure with success rates comparable to percutaneous drainage. Disorders of the Pancreas Acute pancreatitis: A serious condition that can be life-threatening, often a medical emergency. Chronic pancreatitis: May go undetected in early stages, with about 90% loss of exocrine function by the time symptoms appear. It can present with acute episodes but doesn't typically result from acute pancreatitis unless complications occur. Cause: Often described as autodigestion of the pancreas due to temporary obstruction of the pancreatic duct, hypersecretion of pancreatic enzymes, and reflux of enzymes into the pancreatic duct. Acute Pancreatitis Mild (Interstitial Edematous Pancreatitis): Most common, with no pancreatic necrosis, diffuse gland enlargement due to inflammation. Mild symptoms, with return to normal function within 6 months. Severe (Necrotizing Pancreatitis): Involves tissue necrosis, severe complications like organ failure (e.g., pulmonary insufficiency, shock, kidney disease), pancreatic cysts, abscesses, or bleeding Pathophysiology Self-digestion of the pancreas by its own enzymes (especially trypsin). Gallstones or bile reflux can activate enzymes prematurely, causing inflammation. Clinical Manifestations Main symptom: Severe abdominal pain, often in the mid-epigastrium, worsened after meals and unrelieved by antacids. Other symptoms: Nausea, vomiting (gastric or bile- stained), abdominal distention, guarding, rigidity (indicating peritonitis), fever, jaundice, confusion, and agitation. Assessment and Diagnostic Findings Diagnosis Criteria: Requires two out of three: History of upper abdominal pain. Elevated serum amylase or lipase levels (greater than 3 times the normal limit). Typical findings on imaging (CT, MRI, or ultrasound). Lab Findings Serum amylase usually rises within 24 hours and normalizes in 48-72 hours. Serum lipase remains elevated longer than amylase, often for several days. Ranson Criteria Medical Management Oral Intake: Withheld to reduce pancreatic enzyme stimulation. Enteral feedings are recommended when possible, as they prevent infections and are cost-effective. Pain Management: Parenteral opioids (morphine, fentanyl, hydromorphone) are used for adequate pain relief. Intensive Care: Fluid and blood loss correction, low albumin levels management. Hemodynamic and arterial blood gas monitoring in the ICU. Antibiotics prescribed if infection is present, but not as prophylaxis. Surgical Intervention: Surgery may be required for diagnosis (diagnostic laparotomy), pancreatic drainage, or to remove infected/necrotic pancreatic tissue Nursing Management
Support for home and transitional care Tumors of the Head of the Pancreas: Tumors in the head of the pancreas account for 60%- 80% of all pancreatic tumors. These tumors often obstruct the common bile duct, leading to issues with bile flow. Clinical Manifestations Jaundice, clay-colored stools, dark urine Malabsorption of nutrients and fat-soluble vitamins Abdominal pain, pruritus, anorexia, weight loss, malaise Jaundice must be differentiated from that caused by gallstones. Includes duodenography, angiography, pancreatic scanning, PTC, ERCP, and percutaneous needle biopsy. Medical Management Preoperative preparation is essential, focusing on nutritional support and correction of deficiencies. High-protein diet and pancreatic enzymes may be prescribed. Hydration, correction of prothrombin deficiency with vitamin K, and treatment of anemia are crucial. Enteral or parenteral nutrition and blood therapy may be necessary. Pancreatic Islet Tumors Types of Tumors Insulinomas: Produce excess insulin, leading to hypoglycemia and symptoms like weakness, confusion, and seizures. Nonfunctioning Islet Cell Tumors (NETs): Do not affect insulin secretion. The 5-hour glucose tolerance test helps diagnose insulinoma and distinguish it from other causes of hypoglycemia. Surgical Management Tumors are usually benign but can be malignant. Surgical removal is recommended and usually provides immediate symptom relief. If hypertrophy rather than a tumor is present, a partial pancreatectomy (removal of the tail and part of the body of the pancreas) is performed. Nursing Management Preoperative care includes monitoring for hypoglycemia and administering glucose as needed. Postoperative care focuses on managing serum glucose levels and monitoring recovery from abdominal surgery. Patient education is tailored to the extent of surgery and changes in pancreatic function. Hyperinsulinism Cause: Overproduction of insulin by pancreatic islets. Symptoms: Hunger, nervousness, sweating, headache, faintness, seizures, and unconsciousness. Diagnosis: Hyperplasia or tumors of the islets of Langerhans may be found at surgery or autopsy. Treatment: Surgery to remove hyperplastic or neoplastic pancreatic tissue is the main treatment. Severe hypoglycemia is treated with glucose. Complications: 15% of patients with functional hypoglycemia may develop diabetes later. Ulcerogenic Tumors (Zollinger-Ellison Syndrome) Cause: Tumors of the islets of Langerhans that cause excessive gastric acid secretion, leading to ulcers in the stomach, duodenum, and jejunum. Symptoms: Nausea, vomiting, diarrhea, and burning upper abdominal pain. Diagnosis: Blood gastrin level measurement, CT scan, MRI, EUS, or upper endoscopy. Treatment: Surgery and management of excessive acid production. Diabetes A metabolic disorder with high blood glucose (hyperglycemia) due to problems with insulin secretion, insulin action, or both. Main Types of Diabetes Type 1 Diabetes – Autoimmune destruction of insulin- producing cells; usually early onset. Type 2 Diabetes – Insulin resistance and relative insulin deficiency; common in adults. Gestational Diabetes – Occurs during pregnancy. LADA (Latent Autoimmune Diabetes in Adults) – Slow-progressing form of type 1 in adults. Secondary Diabetes – Associated with other medical conditions or syndromes. Risk Factors Pathophysiology Insulin (from beta cells) lowers blood sugar by: Moving glucose into cells for energy. Storing glucose as glycogen (in liver/muscles). Helping store fat and protein. Preventing breakdown of stored glucose, fat, and protein. Glucagon (from alpha cells) raises blood sugar by: Stimulating the liver to release stored glucose. Balance between insulin and glucagon keeps blood glucose levels stable during eating and fasting. Type 1 Diabetes Autoimmune destruction of pancreatic beta cells → no insulin production. Caused by genetics, immune response, and possibly viral infections. People inherit a risk, not the disease itself. Requires lifelong insulin therapy. Type 2 Diabetes More common in people over 30 and those with obesity (now rising in younger age groups). Caused by: Insulin resistance (body cells don’t respond well to insulin). Impaired insulin secretion (pancreas doesn’t make enough insulin). Often related to genetics, lifestyle, and obesity. Can be managed with lifestyle changes, oral meds, or insulin. Diabetic Ketoacidosis (DKA) – Mostly in Type 1 Caused by insulin deficiency → body breaks down fat for energy → ketones build up. Key issues: Hyperglycemia Ketosis Metabolic acidosis Symptoms: Polyuria, polydipsia, nausea, vomiting, fatigue, fruity-smelling breath, coma if untreated. Hyperglycemic Hyperosmolar Syndrome (HHS) – In Type 2 Severe hyperglycemia without ketones.
Enough insulin is present to prevent fat breakdown (no ketones), but not enough to control blood sugar. Can lead to dehydration, altered mental status, and coma. Gestational Diabetes (GDM) Glucose intolerance during pregnancy, especially in the 2nd and 3rd trimesters. Caused by placental hormones → insulin resistance. High-risk women are screened early; all average-risk women are screened at 24–28 weeks. Risk Factors Obesity History of GDM Family history of diabetes Glycosuria Poor obstetric outcomes Diagnosis Glucose challenge test (if >140 mg/dL → oral glucose tolerance test). Management First-line: Diet + blood glucose monitoring Insulin if needed (70–85% manage with lifestyle only) Target BG in pregnancy: 140–180 mg/dL After Pregnancy: Blood glucose usually returns to normal Higher risk of developing type 2 diabetes later → screen every 3 years Latent Autoimmune Diabetes in Adults (LADA) A slow-progressing autoimmune diabetes (shares features of type 1 and type 2). Beta-cell destruction happens gradually. May be misdiagnosed as type 2 at first. Common Features Onset before age 50 BMI < 25 kg/m² Personal or family history of autoimmune disease Sudden symptoms before diagnosis Risk Patients will likely require insulin over time. Clinical Manifestation Polyuria (increased urination) Polydipsia (increased thirst) Polyphagia (increased appetite) Fatigue Weakness Vision changes Sudden weight loss at times with Type 1 Diabetes Criteria For Diagnosing Diabetes Goal of Treatment To control blood glucose levels (euglycemic state) Normalize insulin activity Reduce the development of complications Diabetes management Nutritional therapy Exercise Monitoring Pharmacologic therapy Education Pharmacologic therapy Insulin: Secreted by beta cells of the pancreas. Lowers blood glucose after meals by facilitating glucose uptake in muscle, fat, and liver cells. Essential when insulin production is insufficient. Insulin therapy Type 1 diabetes: Requires lifelong exogenous insulin, as the body cannot produce insulin. Type 2 diabetes: Insulin may be required long-term when oral medications and diet fail, or if insulin deficiency occurs. Diabetes management Nutritional therapy Exercise Monitoring Pharmacologic therapy Education Diabetic Ketoacidosis (DKA) Result of a significant insulin deficit, leading to disturbances in carbohydrate, protein, and fat metabolism. Main Clinical Features Hyperglycemia (high blood glucose) Dehydration and electrolyte loss
Monitoring frequency: Check ECGs and potassium levels every 2 to 4 hours during the first 8 hours of treatment. Cautions: Potassium replacement is withheld if: Hyperkalemia (high potassium) is present. The patient is not urinating. Hyperglycemic Hyperosmolar Syndrome (HHS) Definition: A metabolic disorder primarily seen in type 2 diabetes, often triggered by an illness that increases insulin demand. Key features Hyperglycemia and hyperosmolality (increased blood concentration). Minimal or absent ketosis (no significant buildup of ketones). Alterations in sensorium (mental state, confusion). A relative insulin deficiency due to insulin resistance is the root cause. Pathophysiology Persistent hyperglycemia leads to osmotic diuresis, where glucose is excreted in urine, pulling water and electrolytes along. Water shifts from intracellular to extracellular space to maintain osmotic balance, leading to dehydration. Hypernatremia (high sodium) and increased osmolarity occur due to water loss and glucose presence. Key Differences Between DKA and HHS: DKA: Common in type 1 diabetes, with ketoacidosis, often presents with rapid onset. HHS: Typically seen in type 2 diabetes, with minimal ketosis, often presents with gradual onset. Clinical Manifestations of HHS: Low blood pressure (hypotension) Severe dehydration (dry mouth, skin loses elasticity) Rapid heart rate (tachycardia) Changes in mental status (confusion, drowsiness, or even coma) Assessment and Diagnosis of HHS: Blood glucose: Greater than 600 mg/dL Osmolality: Over 320 mOsm/kg Ketoacidosis: Absent Electrolytes and BUN: Consistent with severe dehydration Neurologic signs: Mental status changes, focal deficits, hallucinations due to cerebral dehydration Orthostatic hypotension: Present with dehydration Management of HHS: Fluid replacement: To rehydrate Electrolyte correction: For balance Insulin administration: To lower blood sugar Close monitoring to prevent fluid overload, heart failure, and cardiac arrhythmias. This is especially important as patients are typically older. Macrovascular Diabetes Atherosclerotic changes: Blood vessels thicken, sclerose, and become occluded by plaque, blocking blood flow. Increased risk: These changes happen earlier and more frequently in diabetic patients, leading to: Coronary artery disease Cerebrovascular disease Peripheral vascular disease Key Complications Myocardial Infarction (MI): Twice as common in men with diabetes, three times more common in women. Increased risk of complications and a second MI. Patients with diabetes may experience "silent" MIs without typical ischemic symptoms, often detected only on ECG. Cerebrovascular Disease: Accelerated atherosclerosis affects cerebral blood vessels. Increased risk of transient ischemic attacks and strokes. Diabetics are twice as likely to develop cerebrovascular disease and have a higher risk of death from stroke. Role of Diabetes in Macrovascular Disease Elevated blood glucose: While hyperglycemia is a key feature, there's no direct link found between high blood sugar and atherosclerosis. Independent risk factor: Diabetes itself accelerates atherosclerosis. Other contributing factors: Platelet and clotting abnormalities Decreased red blood cell flexibility Impaired oxygen release Arterial wall changes due to hyperglycemia Possibly hyperinsulinemia Management Risk factor modification: Focus on aggressive management to reduce atherosclerosis risk factors. MNT (Medical Nutrition Therapy) and exercise: Key for managing obesity, hypertension, and hyperlipidemia. Medications: Used to control hypertension and hyperlipidemia. Smoking cessation: Essential for reducing cardiovascular risk. Blood glucose control: Helps reduce triglyceride levels and the risk of complications. Microvascular Complications Diabetic microvascular disease (microangiopathy): Characterized by thickening of the capillary basement membrane due to prolonged elevated blood glucose levels. This thickening affects small blood vessels in areas like the retina and kidneys. Diabetic Retinopathy: Leading cause of blindness in individuals aged 20- in the U.S. Affects both type 1 and type 2 diabetes. Caused by changes in small blood vessels in the retina (the part of the eye that sends visual information to the brain). The retina has various blood vessels that can be damaged in this condition. Stages of Diabetic Retinopathy Nonproliferative (background): Early stage, with microaneurysms, hemorrhages, and hard exudates. Preproliferative: Progression with worsening changes in retinal blood vessels.
Proliferative: Advanced stage with the growth of new, fragile blood vessels that can cause bleeding and vision loss. Macular edema: A complication of nonproliferative retinopathy, affecting around 10% of diabetic patients, leading to visual distortion and central vision loss. Retinopathy in Diabetes Nearly all patients with type 1 diabetes and most patients with type 2 diabetes will have some degree of retinopathy after 20 years of diabetes. Ocular Complication Advanced Stages of Diabetic Retinopathy Preproliferative Retinopathy: Considered a precursor to proliferative retinopathy. More widespread vascular changes in the retina. Loss of nerve fibers in the retina. Macular edema may cause visual changes, similar to background retinopathy. 10% to 50% of patients with preproliferative retinopathy may develop proliferative retinopathy within a short period, potentially as soon as 1 year. Proliferative Retinopathy: Most severe stage, representing the greatest threat to vision. Characteristics: New blood vessels proliferate from the retina into the vitreous (the gel-like substance in the eye). These new blood vessels are fragile and prone to bleeding. Consequences of proliferative retinopathy: Vitreous hemorrhage: The blood from the ruptured vessels clouds the vitreous, impairing the transmission of light to the retina, leading to vision loss. Retinal detachment: Scar tissue from resorbed blood can cause traction on the retina, leading to detachment and further vision loss. Clinical Manifestations Painless Process: Retinopathy itself typically does not cause pain. Non- and Preproliferative Retinopathy: Blurry vision may occur due to macular edema. Many patients are asymptomatic, and retinopathy may progress without noticeable symptoms. Proliferative Retinopathy: Despite hemorrhaging, some patients may not experience significant changes in vision. Symptoms of hemorrhaging include: Floaters or cobwebs in the visual field. Sudden visual changes, such as spotty or hazy vision. Complete vision loss in severe cases. Assessment and Diagnostic Findings: Direct visualization of the retina using an ophthalmoscope after dilating the pupils. Fluorescein angiography: A technique where a dye is injected into the vein, allowing the ophthalmologist to see detailed images of the retinal vessels. Fluorescein angiography helps identify the type and activity of retinopathy, providing more detailed information than an ophthalmoscope alone. Medical Management Control of hypertension. Blood glucose management to prevent further damage. Smoking cessation, which is crucial for reducing vascular damage. Argon laser photocoagulation: Used to treat advanced retinopathy. The laser destroys leaking blood vessels and areas of neovascularization (new blood vessels). Nursing Management Promoting Home, Community-Based, and Transitional Care: Encourage regular eye exams, especially for diabetic patients, to detect early signs of retinopathy. Educate patients on managing blood glucose, blood pressure, and the importance of smoking cessation. Support the patient in managing lifestyle changes and understanding treatment options. Nephropathy Nephropathy refers to kidney disease that results from diabetic microvascular changes in the kidneys. This is a common and serious complication of diabetes. Early detection and management of nephropathy can help reduce the risk of kidney failure. Clinical Manifestations The signs of kidney dysfunction in diabetic patients are similar to those seen in non-diabetic patients. As kidney failure progresses, insulin breakdown decreases, leading to more frequent hypoglycemic episodes. Albumin leakage into the urine is one of the earliest signs of kidney damage, and its presence in the urine is a key indicator of nephropathy. If microalbuminuria (albumin in the urine) exceeds 30 mg/24 hours on two consecutive tests, further testing with a 24-hour urine sample is needed. Kidney function should be monitored annually with tests for BUN and creatinine levels. Management Along with maintaining blood glucose control, managing diabetic nephropathy includes controlling hypertension with ACE inhibitors like captopril.
Medical Management Foot exams: The feet should be examined during every healthcare visit or at least once per year by a podiatrist, physician, or nurse. More frequent exams may be necessary for higher-risk individuals. Neuropathy assessment: All patients should be evaluated for neuropathy using a monofilament device by an experienced examiner. Foot care: Pressure areas like calluses and thick toenails should be treated by a podiatrist. Routine nail trimming is also necessary. Blood glucose control: Maintaining blood glucose levels is critical to prevent infections and reduce the risk of diabetic neuropathy. Nursing Management Foot assessment: Nurses should conduct or facilitate foot assessments at each visit. Patient education: Educating patients about proper foot care is a key nursing responsibility to prevent complications, disability, and painful conditions. Endocrine System Involves hormone release by endocrine glands (pituitary, thyroid, parathyroid, adrenal glands, pancreatic islets, ovaries, testes) and specialized tissues (e.g., GI system, kidneys, white blood cells). Hormones are secreted into the bloodstream (endocrine) or through ducts to epithelial surfaces (exocrine). Types of Hormones: Amines and Amino Acids: E.g., epinephrine, norepinephrine, thyroid hormones. Peptides, Polypeptides, Proteins, and Glycoproteins: E.g., thyrotropin-releasing hormone (TRH), follicle-stimulating hormone (FSH), growth hormone (GH). Steroids: E.g., corticosteroids produced by the adrenal cortex. Fatty Acid Derivatives: E.g., eicosanoids, retinoids. Pituitary Gland Health History: Assess symptoms related to hormonal imbalances. Physical Examination: Check for signs of hormone deficiency or excess. Diagnostic Evaluation: Blood tests (for hormone levels), urine tests (for hormone excretion), and imaging studies (e.g., MRI) can aid in diagnosis. Master Gland: Controls secretion of hormones from other endocrine glands. Location and Control: Controlled by the hypothalamus, connected via the pituitary stalk. Anterior Pituitary Hormones FSH, LH, PRL, ACTH, TSH, GH: Regulate other glands and growth/metabolism. GH: Affects growth in children and metabolism in adults. Hypersecretion: ACTH Excess: Leads to Cushing’s syndrome, a group of symptoms caused by overproduction of ACTH. GH Excess: Leads to Acromegaly in adults (enlargement of peripheral body parts and soft tissues). GH Excess in Children: Results in Pituitary Gigantism (excessive growth before epiphyseal plates fuse). GH Deficiency in Children: Leads to Pituitary Dwarfism with limited growth. Posterior Pituitary Hormones Vasopressin (ADH): Regulates water excretion by kidneys. Oxytocin: Facilitates childbirth and lactation. Diabetes Insipidus (DI): Caused by deficient vasopressin (ADH) production. Results in large volumes of dilute urine. Can occur due to brain surgery, tumors, traumatic injury, infections, post-hypophysectomy, or medication use. Pathophysiology Hypopituitarism: Underproduction of pituitary hormones, can be due to pituitary or hypothalamus issues. Causes: Radiation, trauma, tumors, or vascular lesions leading to hormone deficiencies. Symptoms of Hypopituitarism: Extreme weight loss, atrophy of endocrine organs, hair loss, impotence, amenorrhea, and hypoglycemia. If untreated, coma and death can occur. Pituitary Tumors Types of Pituitary Tumors: Functional Tumors: Secrete pituitary hormones. Nonfunctional Tumors: Do not secrete hormones. Tumors may arise from eosinophilic, basophilic, or chromophobic cells. Clinical Manifestations Eosinophilic Tumors In children: Result in Gigantism (exceptionally tall, but weak and lethargic). In adults: Lead to Acromegaly (enlarged feet, hands, nose, chin, etc.). Headaches and visual disturbances (color discrimination, diplopia, blindness). Basophilic Tumors ( Cause Cushing’s Syndrome, with symptoms like:) Hyperadrenalism: Truncal obesity, hypertension, osteoporosis, masculinization in females, amenorrhea. Chromophobic Tumors Most common (90%).
Typically nonfunctional, but can cause hypopituitarism (obesity, somnolence, fine hair, dry skin, loss of libido, headaches, visual defects). Assessment & Diagnostic Findings History & Physical Examination: Including visual acuity and fields. Imaging: CT and MRI scans to locate the tumor. Hormonal Testing: Serum levels of pituitary and target organ hormones (e.g., thyroid, adrenal) to help confirm diagnosis. Medical Management Hypophysectomy: Surgical removal of the pituitary gland, typically via a transsphenoidal approach. This is the treatment of choice for conditions like Cushing’s disease caused by excessive ACTH production. Stereotactic Radiation Therapy: Used for precise targeting of pituitary tumors, minimizing damage to normal tissue. Surgical Management Hypophysectomy is also used to relieve bone pain from metastatic tumors (e.g., from breast or prostate cancer). Diabetes Insipidus (DI) Cause: Deficiency of ADH (vasopressin) leading to large volumes of dilute urine and extreme thirst. Types of DI: Central DI: Caused by damage to the hypothalamus or pituitary (e.g., from trauma, surgery, tumors). Nephrogenic DI: Due to kidney injury, medications (e.g., lithium), or electrolyte imbalances (hypokalemia, hypercalcemia). Dipsogenic DI: Caused by hypothalamic dysfunction, often linked to injury, surgery, or inflammation. Differentiation: DI needs to be differentiated from diabetes mellitus, which also causes polydipsia and excessive urination but due to different causes. Clinical Manifestations Excessive Urine Output: More than 250 mL/hour of dilute urine with a specific gravity between 1. and 1.005. Intense Thirst: Patients often drink 2 to 20 liters of fluid daily, craving cold water. Fluid Imbalance: Restricting fluid intake doesn't control the disease and can cause hypernatremia and severe dehydration due to continued high urine output. Assessment and Diagnostic Findings Fluid Deprivation Test: Withholding fluids for 8- hours or until 3-5% of body weight is lost, while monitoring weight and performing plasma and urine osmolality studies. Characteristics of DI: Inability to concentrate urine (specific gravity and osmolality don't increase), weight loss, high serum osmolality, and elevated serum sodium levels. Monitoring: Vital signs, weight, and serum levels are closely monitored during the test. The test is stopped if complications like tachycardia, excessive weight loss, or hypotension develop. Medical Management Main Goals: Replace ADH, ensure adequate fluid replacement, and address any underlying intracranial pathology. Nephrogenic DI: Requires a different approach, not involving ADH replacement, but may focus on managing kidney response and electrolyte balance. Pharmacologic Therapy Central DI: Desmopressin: The drug of choice, a synthetic vasopressin, administered orally or intranasally. It lacks the vascular effects of natural ADH. Vasopressin: Not recommended in patients with coronary artery disease due to its vasoconstrictive effects. Chlorpropamide and Thiazide Diuretics: Used for mild cases, as they potentiate vasopressin's effects but can cause hypoglycemia. Nephrogenic DI: Thiazide Diuretics: Help manage fluid balance. Mild Salt Depletion: Aids in managing fluid retention. Prostaglandin Inhibitors (e.g., Indomethacin, Aspirin): Used to treat nephrogenic DI but not effective for central DI. Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH): Cause: Result of failure in the negative feedback system regulating ADH release, leading to water retention and dilutional hyponatremia. Possible Causes: Nonendocrine Origins: Bronchogenic carcinoma (malignant lung cells release ADH), pneumonia, pneumothorax, and other lung-related issues. Central Nervous System Disorders: Head injuries, brain surgery, tumors, infections. Medications: Vincristine, phenothiazines, tricyclic antidepressants, thiazide diuretics, and nicotine may stimulate ADH release or increase renal sensitivity to ADH. SIADH Medical Management Fluid Restriction: The primary treatment, helping to gradually correct hyponatremia as retained water is slowly excreted. Diuretics: Furosemide may be used to help remove excess fluid. Hypertonic NaCl (3%): Administered intravenously in severe hyponatremia to increase sodium levels. Treating the Underlying Cause: Eliminate or address the underlying issue, such as a tumor, medication, or CNS disorder. Thyroid Gland The thyroid is a butterfly-shaped gland located in the lower neck, anterior to the trachea. It is the largest endocrine gland. Hormones Produced by the Thyroid Gland Thyroxine (T4) Triiodothyronine (T3) Calcitonin Thyroid Hormone (T3 and T4) Composition: Both T3 and T4 are amino acids containing iodine atoms: T4 (Thyroxine): Contains four iodine atoms in each molecule. T3 (Triiodothyronine): Contains three iodine atoms in each molecule. Synthesis and Storage: These hormones are synthesized in the thyroid gland and stored until needed. They are bound to proteins (thyroxine- binding globulin [TBG], transthyretin, and albumin) to be transported in the bloodstream.
