Digestion & Elimination Disorders PDF

DISORDERS OF DIGESTION & E L I M I N AT I O N Dr. Madelyn Carey Spring 2024 STRUCTURE & FUNCTION COMPONENTS OF GI TRACT A hollow, muscular tube extending from the mouth to the anus Mouth Esophagus Stomach Small intestine Large intestine Anus C O N S I D E R AT I O NS IN AGING Tooth enamel and dentin...

DISORDERS OF DIGESTION & E L I M I N AT I O N Dr. Madelyn Carey Spring 2024 STRUCTURE & FUNCTION COMPONENTS OF GI TRACT A hollow, muscular tube extending from the mouth to the anus Mouth Esophagus Stomach Small intestine Large intestine Anus C O N S I D E R AT I O NS IN AGING Tooth enamel and dentin wear down Teeth are lost Periodontal disease Gum recession Osteoporotic bone changes Number of tastebuds decline Sense of smell diminishes Salivary secretion decreases Decreased esophageal and gastric motility DISORDERS OF UPPER AND LOWER GASTROINTESTINAL SYSTEMS OVERVIEW Upper and lower GI system disorders Clinical manifestations Often nonspecific May be related to a number of impairments Four cardinal signs and symptoms Pain Altered ingestion Altered motility: diarrhea vs constipation Bleeding: Upper GI (melena) vs Lower GI (hematochezia) Digestive Pathway ESOPHAGEAL DEFECTS Food and liquids enter the mouth Mastication and addition of salivary enzymes Voluntary transport of food and liquids Positioned at back of throat for esophageal entry Pushed into the esophagus Involuntary transit to the stomach Cardinal Symptoms Pain Alteration in ingestion Bleeding ESOPHAGEAL RING Circumferential, nondistensible narrowing of esophageal lumen Manifestations May be asymptomatic (e.g., Schatzki B rings) Dysphagia symptoms depend degree of obstruction Dysphagia is often chronic and episodic May cause symptoms heartburn or regurgitation Treatment Dietary restrictions First-line treatment : Endoscopic dilation therapy Endoscopic incisional therapy ESOPHAGEAL WEBS Etiology Congenital – Malformed embryonic esophageal structures Acquired – Complex etiologies Manifestations Frequently asymptomatic Typical presentation: Dysphagia for solids May present with acute food impaction Can develop nasopharyngeal reflux and aspiration Spontaneous perforation may occur Treatment Dietary restrictions First-line treatment : Endoscopic dilation therapy ESOPHAGITIS Etiology Eosinophilic esophagitis (EoE) – Cause unknown; many associated factors Radiation esophagitis – Radiation treatment of thoracic cancers; exacerbated by chemotherapeutic agents Corrosive esophagitis – Ingestion of strong alkaline or acid substances Pill esophagitis – Swallowed pill lodges transversely in esophageal lumen and causes inflammation Manifestations Vary based on etiology Treatment Varies based on etiology Thorough history and physical exam is required ESOPHAGEAL DIVERTICULA Etiology Acquired condition Most common cause: Impaired esophageal motility May be caused by traction on esophagus due to inflammatory disease of mediastinum (e.g., tuberculosis) Manifestations Most often asymptomatic Manifestations vary based on location of diverticula May produce dysphagia and heartburn Gurgling sound may be audible during swallowing Neck mass may develop with large diverticula Treatment May not require intervention Treatment depends on size and location Surgical intervention may be needed for large diverticula ESOPHAGEAL P E R F O R AT I O N Etiology Primarily iatrogenic causes (e.g., endoscopy, nasogastric tube insertion, intraoperative injury) Foreign body or caustic substance ingestions Blunt or penetrating trauma Esophageal malignancy or infection Conditions that impair esophageal wall strength Forceful vomiting Manifestations Signs and symptoms vary based on location of perforation Most frequent complaint: Pain Pneumomediastinum and crepitus may be present Systemic infection or septic shock may develop Hematemesis (Mallory-Weiss tear) Treatment Varies based on severity and associated conditions NPO status (no food or fluids by mouth) Decompressive therapies, esophageal stent, surgery H I ATA L H E R N I A Etiology Multifactorial May involve genetic link Manifestations May be asymptomatic Frequently involves symptoms of gastroesophageal reflux May produce dyspnea, reduced exercise tolerance, syncope, and audible bowel sounds at the left lung base Treatment Structure and severity categorized by type (I through IV) Medications for symptomatic gastric reflux Surgery may be indicated GASTROESOPHAGEAL REFLUX DISEASE (GERD) Etiology Multifactorial Risk factors include decreased LES tone, pregnancy, obesity, impaired gastric motility, surgical vagotomy, and decreased endogenous gastrin levels Manifestations Most common: heartburn, epigastric pain, regurgitation (often after meals) Patients complain of a burning sensation in the throat and a sour taste in the mouth. Extraesophageal symptoms include acid injury to tooth enamel, throat pain, hoarseness, dysphonia, excessive throat clearing, chronic cough, globus, and dysphagia Serious complications include esophageal cancer Treatment Medication: antacids, H-2 blockers, PPI Diet: avoiding fat, chocolate, peppermint, alcohol, coffee, acidic foods Behavioral changes: weight loss, smaller meals, avoidance of the supine position BARRETT ESOPHAGUS Etiology Also known as Barrett metaplasia Complication of GERD Manifestations Often asymptomatic Common symptoms include heartburn and regurgitation Treatment Aggressive treatment of GERD (medication and surgery) Endoscopic surveillance and biopsies If dysplasia present : Endoscopic eradication therapy and intensive surveillance Surgical intervention may be indicated ESOPHAGEAL CANCER Etiology Most likely multifactorial Environmental factors combined with genetic factors Main risk factors: GERD, cigarette smoking, obesity Manifestations Esophageal adenocarcinoma and SCC – Similar symptoms Progressive dysphagia for solids, weight loss, heartburn Less common: hoarseness, dry cough, pneumonia, odynophagia Treatment Endoscopic mucosal resection and ablation Chemotherapy, radiation, and surgical resection Palliative endoscopic esophageal stenting Main categories of stomach disorders DISORDERS OF THE STOMACH Disorders of secretion Disorders of motility Associated Cardinal GI symptoms Pain Altered ingestion Altered digestion Gastrointestinal tract (GIT) bleeding PEPTIC ULCER DISEASE Etiology Various causes Most common: H. pylori infection and NSAID use Contributing factors include smoking, excessive alcohol use, drug use, emotional stress, and psychosocial components Manifestations May be asymptomatic Common manifestations – Epigastric pain and dyspepsia Common complications – Bleeding, perforation, obstruction Treatment Identify causative factor H. pylori – Triple or quadruple therapy NSAID-induced – H2 receptor antagonist and cease NSAID GASTRITIS ACUTE GASTRITIS CHRONIC GASTRITIS Etiology Etiology Infection-induced – Usually due to H. pylori Infection-induced – Usually due to H. pylori Drug-induced – NSAIDs, steroids, some chemotherapeutic drugs, alcohol, and iron supplements Chemical and caustic agents (NSAIDs, excessive alcohol ingestion, radiation exposure) Occurs with critical illness; due to physiologic stress and ischemic changes caused by shock, hypotension, or release of vasoactive substances Autoimmune disease (e.g., Crohn disease, Wegener granulomatosis, and sarcoidosis) Pathogenesis Acute imbalance between mucosal injury and repair mechanisms Development of mucosal hyperemia and erosive changes with histologic presence of inflammation Pathogenesis Begins with superficial gastritis Advances to gastric atrophy Gastric glandular structures are lost and/or converted to intestinal phenotypes (metaplasia) Gastric atrophy is precursor to gastric cancer T R E AT M E N T ACUTE GASTRITIS CHRONIC GASTRITIS Elimination of causative agent or exacerbating factors Elimination of causative agent or exacerbating factors Eradication of H. pylori infection if indicated Eradication of H. pylori infection if indicated Surgical intervention for GI bleeding Medications to enhance protection of gastric mucosa (e.g., sucralfate and misoprostol) Acupuncture Surgical intervention for GI bleeding GASTRIC OUTLET OBSTRUCTION Etiology Includes gastric, duodenal, and/or extraluminal pathology Malignancies of digestive organs Surgical- and interventional-induced obstructions Metastatic cancer Manifestations Abdominal pain, distention or bloating Vomiting, dehydration, and weight loss May include early satiety and nausea Treatment Benign cases – Nasogastric tube suction, medications to suppress gastric acid production, IV fluid and electrolyte replacement, nutritional supplementation, trial liquid diet, endoscopic balloon dilation or surgery Malignant cases – Based on underlying cause; may include stenting, chemotherapy, endoscopic balloon dilation, or surgery Advanced cancers - Palliative procedures may be preferred I N FA N T I L E H Y P E R T R O P H I C P Y L O R I C STENOSIS Etiology Frequently affects young infants Unknown; linked to genetic and environmental factors Manifestations Manifestations begin at 4–6 weeks of age Gradual onset of worsening nonbilious projectile vomiting Hunger/eagerness to feed after vomiting Dehydration or weight loss Peristalsis may be visible in upper abdomen Palpable mass may be present in right upper abdomen Laboratory findings include hypochloremia, hypokalemia, and metabolic alkalosis Treatment Surgical intervention STOMACH CANCER Etiology Risk factors include H. pylori infection, cigarette smoking, high alcohol ingestion, excessive dietary salt, inadequate fruit and vegetable consumption, and pernicious anemia High-nitrate diet may also increase risk Manifestations Clinical manifestations are known as alarm features Most common: Weight loss and abdominal pain May include dysphagia, nausea, early satiety, occult GI bleeding, and palpable abdominal mass Treatment Treatment depends on cancer staging Upper endoscopy may be used for palliative procedures May require endoscopic resection, radiation, chemotherapy, and/or surgical resection Absorption in the lower gastrointestinal tract Chyme enters small bowel via the duodenum DISORDERS OF THE SMALL INTESTINE, LARGE INTESTINE, AND RECTUM Bowel is primary site of absorption Nutrients and vitamins Electrolytes Water Impaired motility may cause multiple alterations Malabsorption Malnutrition Dehydration I N F L A M M AT O RY B O W E L D I S E A S E Chronic inflammatory disorder involving the GI tract Two major IBD disorders Ulcerative colitis (UC) Crohn disease (CD) U L C E R AT I V E C O L I T I S ( U C ) Limited to mucosal layers of colon and rectum. Characterized by relapsing and remitting episodes of inflammation Develops as a continuous lesion Clinical Manifestations Fever, loss of appetite, weight loss, fatigue and night sweats Bloody and/or mucoid, diarrhea, dehydration, and anemia Crampy abdominal pain, pain with defecation, and tenesmus Involvement of the rectum may also lead to constipation Toxic megacolon – May need blood transfusion or surgery CROHN’S DISEASE (CD) May involve any portion of the GIT – mouth to anus Most commonly affects ileum and proximal colon Characterized by transmural inflammation of the bowel Lesions are not always continuous (skip lesions) Clinical Manifestations Fever, loss of appetite, weight loss, fatigue and night sweats Nausea, vomiting, and diarrhea with or without blood Abdominal pain and pain with defecation due to anorectal fissures Complications include bowel strictures, obstructions, perforations in the bowel and intra-abdominal abscesses T R E AT M E N T F O R I B D Optimize quality of life by treating acute processes Induce and maintain remission Wholesome nutrition and healthy lifestyle habits Probiotics APPENDICITIS Appendicitis is the infectious inflammation of the appendix. Obstruction is thought to lead to bacterial overgrowth and luminal distention Increased intraluminal pressure and/or excessive inflammation can inhibit blood flow causing vascular compromise to the affected tissue Appendix may become gangrenous and can rupture Manifestations Cramping abdominal pain, tenderness with palpation of the right lower abdominal quadrant, nausea or vomiting, increased white blood cell count, and low-grade fever Treatment Gold standard – Laparoscopic surgery BOWEL OBSTRUCTION Etiology Most often due to adhesions (75% of cases) Other common causes include HANG IV (Hernia, Adhesions Neoplasm/tumor, Gallstone ileus, Intussusception, Volvulus) Manifestations Abdominal pain, nausea, vomiting, abdominal distention, and inability to satisfactorily pass gas or stool Hyperactive, high-pitched bowel sounds often present Bowel sounds will be absent if ileus develops Treatment Medical management includes gastric decompression, intravenous fluids, and serial physical and serum tests Surgery may be indicated if medical management fails If strangulation and bowel ischemia present – Emergent surgery needed I R R I TA B L E B O W E L S Y N D R O M E Etiology Abnormal gut motor and sensory activity, central neural dysfunction, psychologic disturbances, mucosal inflammation, stress, and luminal factors Manifestations Abdominal pain, cramps, or discomfort Change in bowel habits and bloating Symptoms may be triggered after eating Symptoms may also include nausea, lethargy, backache, and bladder symptoms Treatment Depends on type and severity of IBS Education, reassurance, and dietary/lifestyle changes Diverticula DIVERTICUL AR DISEASE Small outpouchings (herniations) of colonic mucosa Protrude through muscle layers of the colon wall Diverticulosis Diverticula without evidence of inflammation Diverticulitis Inflamed diverticula DIVERTICULAR DISEASE Associated factors include alterations in colonic wall resistance, alterations in colonic motility, low-fiber diets, NSAID use, advanced age, obesity, and lack of exercise Manifestations Sudden, constant abdominal pain in left lower quadrant Abdominal distention and nausea Diarrhea, constipation, and decreased appetite Fever, tachycardia, and hypotension Treatment Outpatient management: Clear liquid diet, oral broad-spectrum antibiotics, and follow-up care Inpatient treatment required if suspected peritonitis or complications present Inpatient treatment: Administration of intravenous fluids and antibiotics, no food or drink by mouth Surgery may be indicated HEMORRHOIDS Etiology Straining during bowel movement Risk factors include conditions that increase intraabdominal pressure and/or impede venous return (e.g., pregnancy or portal hypertension) Manifestations Hematochezia, itching, perianal discomfort and soiling Large hemorrhoids may produce sensation of rectal fullness or of incomplete evacuation Hemorrhoids may be internal or external Treatment Depends on severity Stages I and II: Diet modification, topical glucocorticoids, vasoconstrictors, analgesics, and sclerotherapy Stages III and IV: Procedural interventions (e.g., hemorrhoidal banding and surgical hemorrhoidectomy) Adenomas Polyps of the colon Precursors to most colorectal cancers (CRCs) Benign tumors Form in glandular structures in intestinal mucosal epithelium CRC CANCER Colon Cancer Malignant growth or tumor Results from division of abnormal cells in the colon Occurs in ascending, transverse, or descending colon Rectal Cancer Malignant growth or tumor Located up to 15 cm from the anal opening R I S K FA C T O R S & P R O T E C T I V E FA C T O R S Modifiable Risk Factors LEADING CAUSE: Moderate to heavy alcohol ingestion Obesity Sedentary lifestyle Smoking Heavy consumption of red and processed meats Low consumption of fruits and vegetables Hereditary/Medical Risk Factors Family history of CRC and/or polyps Certain genetic factors Inflammatory bowel disease (UC or CD) Type 2 diabetes mellitus Aging Protective Factors Diet rich in whole-grain fiber Use of NSAIDs (e.g., aspirin) C L I N I C A L M A N I F E S TAT I O N S E A R LY A D VA N C E D Typically asymptomatic Unique manifestations based on location of cancer Numerous potential manifestations Hematochezia and symptoms of anemia Distended abdomen Change in bowel habits Palpable abdominal mass and lymph nodes Weight loss and fatigue Generalized or localized abdominal pain Palpable mass on digital exam (rectal) Blood in stool SCREENING Early detection is essential Screening methods Colonoscopy, fecal tests for occult blood and DNA testing for mutant genes Screening recommendations All men and women Begin screening at age 50 Individuals with predisposing genetic factors Begin screening earlier than age 50 S TA G I N G Used to determine treatment Usually includes TNM classification Tumor, lymph nodes, and metastases Endoscopy may be used for staging Surgery may be needed for advanced stages Depends on nature and metastasis of CRC Surgery Most often used to treat CRC that has not spread Adenomas may be removed during endoscopy If cancer extends beyond the bowel wall Additional interventions may be indicated Chemotherapy with or without radiation Organ- or tissue-specific therapy T R E AT M E N T DISORDERS OF THE E X O C R I N E PA N C R E AT I C & H E PAT O B I L I A R Y S Y S T E M S ACCESSORY O RG ANS OF THE GI TRACT Liver Produces bile Synthesizes plasma proteins Metabolizes and eliminates drugs and toxins Stores vitamins, glucose, and blood Detoxification and coagulation Gallbladder Stores bile Pancreas Exocrine functions Aids in digestion of carbohydrates, fats, and proteins Involved in production of enzymes and bicarbonate Endocrine functions Produces hormones C O M P L I C AT I O N S – L I V E R D I S O R D E R S Develop as a result of liver impairment or failure More than 80-90% hepatic function must be compromised for symptoms to appear. Most common complications Portal hypertension, which is associated with: Splenomegaly Esophageal varices Ascites Hepatic encephalopathy COMMON MA NIFESTATIONS OF LIVER DISORDERS Vague abdominal pain Indigestion Hepatomegaly Abnormally enlarged liver (palpation of the liver below the costal margin) Advanced symptoms Esophageal varicies: Increased pressure on lining of vessels in esophagus Melena vs bright red rectal bleeding Hematemesis Decreased H/H levels Dyspnea Fatigue Jaundice: hyperbilirubinemia Yellowing of skin Dark urine Light stools Vitamin deficiency Ascites: abdominal swelling caused by accumulation of fluid Weight gain Bulging flanks Decreased appetite Abdominal discomfort Dyspnea P O RTA L H Y P E RT E N S I O N Increased portal venous pressure > 5mmHg Normal = 3 mmHg Results from increased resistance of blood flow through the portal venous system Most common cause is cirrhosis Scarring of hepatic tissue Decreased intrahepatic blood flow Manifestations: ABCDE: “A” stands for Ascites, “B” for Bleeding, “C” for Caput medusae, “D” for Diminished liver function, and “E” for Enlarged spleen A C U T E L I V E R FA I L U R E Loss of liver function Elevated liver tests from inflammation or hepatocyte destruction Prolonged coagulation Altered mental status Decreased toxin clearance M A N I F E S TAT I O N S O F A C U T E L I V E R FA I L U R E Hallmark signs Coagulopathy Altered mental status Jaundice Acetaminophen overdose: Massively increased liver enzymes and decreased bilirubin Virus-induced: Increased bilirubin Severe cases: Encephalopathy or hepatic coma neurologic checks are necessary to monitor for additional changes in mental status T R E AT M E N T Diagnosis: History (drug overdose, viral exposure, etc.) AST/ALT levels Bilirubin level Presence of coagulopathy and altered mental status Treatment: Elevate head of bed to decrease aspiration Frequent neuro checks Volume resuscitation as needed N-acetylcysteine for acetaminophen overdose Blank HAV HBV HCV HDV Mode of Fecal–oral transmissio Spread through contaminated n water Parenteral, Parenteral sexual, perinatal Incubation 30 days 28–180 days 35–72 days 30–180 days 15–60 days Acute Insidious Insidious Insidious Acute No Yes Yes Yes No May also be spread by eating contaminated shellfish such as oysters, mussels, or clams that are raw or undercooked or via infected workers in the food industry. Onset Chronic Infection Spread through infected blood or body fluids Major cause of liver disease Parenteral, sexual, perinatal HEV Occurs only in those with HBV Fecal– oral Waterborne transmission C L I N I C A L M A N I F E S TAT I O N S O F V I R A L H E PAT I T I S Prodromal Begins about 2 weeks after exposure Client highly contagious Nonspecific symptoms Nausea, vomiting, anorexia, cough, low-grade fever Icterus Begins 2 weeks after prodromal phase Can last up to 6 weeks Jaundice, tea-colored urine, clay-colored stools, enlarged/tender liver, prolonged PT/INR Recovery Begins as jaundice resolves, usually 6-8 weeks after exposure Enlarged and tender liver may continue Liver profile usually returns to normal within 12 weeks after onset of jaundice T R E AT M E N T Vaccine: HAV and HBV Supportive care Rest, fluids, nutrition Oral based therapies: HCV LIVER CANCER Also called hepatoma or hepatocellular carcinoma Fifth most commonly diagnosed cancer Poor survival rate worldwide Second most common cause of death in men Hepatocellular carcinoma Most common form of liver cancer (80% of cases) Intrahepatic cholangiocarcinoma Second most common form of liver cancer R I S K FA C T O R S F O R H E P A T O C E L L U L A R CARCINOMA H E A LT H A LT E R AT I O N S L I F E S T Y L E / E N V I R O N M E N TA L Cirrhosis Excess alcohol consumption Hemochromatosis Excess coffee consumption Carriers of hepatitis B or hepatitis C virus Exposure to aflatoxins Obesity Oral contraceptive use M A N I F E S TAT I O N S O F H E PAT O C E L L U L A R C A N C E R Weakness Weight loss Abdominal bloating and discomfort Often described as aching or feeling of fullness Jaundice (due to elevated bilirubin) Mild if present in early stages Liver dysfunction Disturbances in clotting factors and hormones Bruising and bleeding (decreased prothrombin) Elevated liver enzymes Elevated alkaline phosphatase (ALP) Elevated gamma-glutamyl transferase (GGT) Elevated aspartate aminotransferase (AST) Elevated alanine aminotransferase (ALT) T R E AT M E N T Surgery Local therapy Regional Therapy May be curative Hepatic resection Preferred method of treatment - High incidence of postoperative morbidity and recurrence Transplantation May be curative If lesions are small and complete ablation is achieved Radiofrequency ablation (RFA) Cryotherapy Transcatheter arterial chemoembolization Percutaneous ablation External beam radiation therapy CIRRHOSIS Late stage of scarring of the liver Fibrosis leads to constriction and increased vessel pressures. Causes Alcohol consumption (most common) Chronic viral hepatitis Chronic obstruction of bile ducts Genetic diseases Wilson disease, hemochromatosis, glycogen storage disease,alpha-1 antitrypsin deficiency, and autoimmune hepatitis End Stage Liver Failure Scarring of liver due to poor liver function Increased vascular permeability Systemic changes due to portal hypertension A L C O H O L - R E L AT E D L I V E R D A M A G E May be acute or chronic Severity Pattern of drinking Amount of alcohol consumed Number of years of alcohol consumption Immunity Humoral disorders Genetic and biochemical makeup Overall nutrition, diet, and health status M A N I F E S TAT I O N S A L C O H O L - I N D U C E D CIRRHOSIS E A R LY PROGRESSIVE Increased serum ammonia Splenomegaly/ Hepatomegaly Restlessness RUQ abdominal discomfort Vague, early symptom of systemic toxicity Agitation Progressive impairment in judgment Nausea Spider angioma Jaundice Ascites/Dyspnea Abnormal liver function tests T R E AT M E N T Diagnosis: History of alcohol abuse and elevated liver enzymes Most important: Abstinence from alcohol Improving overall health and nutrition Liver transplant Option available only if patient maintains sobriety Prevention and treatment of serious complications Bleeding Esophageal varices Swollen rectal veins Ascites Strongly linked to obesity Fatty liver becomes insulin resistant, increasing risk for disease Deposit of lipids in the liver Mild: steatosis NONALCOHOLI C FA T T Y L I V E R DISEASE (NAFLD) >5% hepatic lipid accumulation Severe: nonalcoholic steatohepatitis (NASH) Inflammation and damage of hepatocytes May progress to cirrhosis Manifestations: Few symptoms in mild disease Elevated AST and ALT Metabolic syndrome symptoms: obesity, diabetes, dyslipidemia T R E AT M E N T Diagnosis: Evidence of fatty liver without history of chronic alcohol abuse Treatment: Weight loss Vitamin E Bariatric surgery if indicated GALLBLADDER DISORDERS Stores and concentrates bile Cholelithiasis Gallbladder stone formation (gallstones) Most common gallbladder disorder CHOLELITHIASI S Five F’s Pathogenesis of gallstones Forty Typically formed in the gallbladder Migrate to bile ducts Produce obstruction and inflammation Formed from cholesterol or pigment 80% of the stones formed from cholesterol Risk Factors Changes in metabolism Biliary stasis or obstruction Hypertriglyceridemia Sedentary lifestyle Diabetes mellitus Family history of cholelithiasis Fertile Female Fair Fat M A N I F E S TAT I O N S O F C H O L E L I T H I A S I S E A R LY A C U T E R E L AT E D T O OBSTRUCTION Often vague Severe and sudden onset of radiating pain Indigestion or mild gastric distress after fatty meal Originates in mid-epigastric region Extends to RUQ and right subscapular region and to back or shoulder Biliary colic Nausea, vomiting, sweating, and tachycardia May cause jaundice, pain, and hepatocyte damage T R E AT M E N T Asymptomatic patients with low risk for complications Medications Decrease cholesterol production in the liver Dissolve the stone Symptomatic patients Surgical intervention Laparoscopic cholecystectomy Open cholecystostomy ADDITIONAL GALLBLADDER DISORDERS Choledocholithiasis Gallstone in the common bile duct Can cause complications for the liver and pancreas Cholangitis Inflammation of the common bile duct M A N I F E S TAT I O N S O F CHOLEDOCHOLITHIASIS & CHOLANGITIS Similar to cholelithiasis and acute cholecystitis RUQ pain and abdominal tenderness Fever Jaundice Pruritus Dark-colored urine and clay-colored stools Due to increased bilirubin Advanced cholangitis Clinical signs consistent with sepsis T R E AT M E N T Surgery Choledocholithotomy Supportive therapy Analgesics Antihistamines Nutrition Antibiotics Antiemetics Early treatment of sepsis if indicated CHOLECYSTITIS Acute or chronic inflammation of the gallbladder Associated conditions Gallstones Other alterations that damage the gallbladder walls Etiology Cystic duct stone - Most common Trauma Infection of the gallbladder Sepsis M A N I F E S TAT I O N S O F C H O L E C Y S T I T I S Intolerance of dietary fat Epigastric heaviness or RUQ abdominal pain Symptoms typically occur after eating Flatulence, belching, and regurgitation Colicky pain due to obstruction of bile flow Steatorrhea and amber-colored urine Due to biliary obstruction Bleeding, jaundice, and pruritus may be present Fever and chills T R E AT M E N T Surgery Laparoscopic cholecystectomy Antibiotics CANCER OF GALLBLADDER Typical site of origination Surface lining or epithelium of gallbladder Can originate in other locations (e.g., biliary tract) Gallbladder damage Injury to inner mucosal lining or bile ducts Potential sources of damage Gallstones, toxins, bacteria, or parasites Main risk factor: Gallstones M A N I F E S TAT I O N S O F G A L L B L A D D E R CANCER E A R LY L AT E Often subtle Intense RUQ abdominal pain Coexisting cholelithiasis frequently present Jaundice Weight loss Palpable gallbladder T R E AT M E N T Surgical removal of carcinoma Laparoscopic cholecystectomy Open cholecystectomy Indicated for removal of large, advanced tumor Whipple resection Removal of surrounding diseased tissues DISORDERS OF T H E PA N C R E A S Divided into three sections Head, midsection, and tail Examples of pancreatic disorders Acute and chronic pancreatitis Pancreatic cysts Cancer of the pancreas A C U T E PA N C R E AT I T I S Inflammation or necrosis of the pancreas Usually mild Leading causes: Alcohol abuse and gallstones Serious and painful inflammation may occur Develops in 20% of cases of pancreatitis M A N I F E S TAT I O N S O F A C U T E PA N C R E AT I T I S Abdominal pain Changes in vital signs Jaundice Paresthesia Cullen sign Turner sign Steatorrhea Critical warning signs Low urine output, hypoxemia, restlessness, confusion Worsening tachypnea and tachycardia May indicate hypovolemic shock T R E AT M E N T Depends on patient’s condition and response Early treatment is essential to prevent complications Oxygen as needed to maintain oxygenation Opioid analgesic as needed – very painful!! Intravenous hydration Complete bowel rest and NPO status Nasogastric suctioning may be ordered Prevent stimulation of digestive processes C H R O N I C PA N C R E AT I T I S Similar to acute pancreatitis Pain with chronic pancreatitis is often less severe Tissue damage is irreversible Most common cause: Alcohol abuse Calculi (stones), pseudocysts, or tumors Smoking Cystic fibrosis Primary cholangitis Exposure to toxic metabolites Inflammatory bowel disease Genetics Familial hyperlipidemia M A N I F E S TAT I O N S O F C H R O N I C PA N C R E AT I T I S Anorexia and malabsorption of fats and proteins Weight loss Steatorrhea Dull, constant abdominal pain Left upper quadrant (LUQ) or epigastric area Often precipitated by alcohol intake T R E AT M E N T Elimination of alcohol and smoking Low-fat diet Oral enzyme replacements Insulin injections Surgery Pain control PA N C R E AT I C C A N C E R Risk factors Cigarette smoking – Most significant risk factor Obesity Diet Nitrates, preservatives, and high fat Diabetes mellitus Chronic pancreatitis Genetic predisposition M A N I F E S TAT I O N S O F PA N C R E AT I C CANCER E A R LY L AT E Abdominal and epigastric discomfort Portal vein hypertension Malabsorption and weight loss Due to decreased pancreatic enzyme production Back pain Nausea and vomiting Bile duct obstruction Dark urine, steatorrhea, jaundice, and pruritus Diabetes mellitus Both a risk factor and consequence of pancreatic cancer Ascites Hepatomegaly and splenomegaly Esophageal varices T R E AT M E N T Surgery Radiochemotherapy