Disorders of Elimination Slides (1) PDF

Week 7 Disorders of Elimination Disorders of Upper and Lower GI Bleeding in the GI Tract: Frank hematemesis: bright red blood from above the stomach Coffee ground emesis: bleeding in stomach with partial digestion of blood Occult blood: Blood from intestine mixing into the stool and...

Week 7 Disorders of Elimination Disorders of Upper and Lower GI Bleeding in the GI Tract: Frank hematemesis: bright red blood from above the stomach Coffee ground emesis: bleeding in stomach with partial digestion of blood Occult blood: Blood from intestine mixing into the stool and not seen by the naked eye Melena: intestinal hemorrhage with large amounts of blood Frank blood in stool: hemorrhage in the rectal/anal area Esophagitis Etiology: Causes can be multifactoral Radiation esophagitis: associated with thoracic cancers and exacerbated by chemo Corrosive esophagitis: Ingestion of strong alkaline or acidic substances Pill esophagitis: Pill lodged in lumen can cause inflammation Pathogenesis: Irritation and inflammation of esophageal tissue may lead to damage Manifestations: Depends on the etiology Treatment: Varies depending on etiology; thorough H&P is necessary Esophageal Diverticula Etiology Acquired through changes in esophageal motility and inflammatory disease of the mediastinum Pathogenesis: Pressure increases esophageal lumen and mucosa protrudes through weakened esophageal wall and produces outpouching Manifestations: Often asymptomatic. May produce dysphasia and heartburn, gurgling may be heard during swallowing, and neck mass may be observed Treatment: Depends on size and location, may require surgery Esophageal Perforation Etiology Mostly iatrogenic (endoscopy, NG tube insertion, intraoperative) Trauma Cancer or infection Forceful vomiting Pathogenesis: tear or rupture creates hole in esophagus Manifestations: Pain, crepitus may occur, infection or shock, hemataemesis Treatment: varies depending on size. NPO. May require surgery Hiatal Hernia Etiology: multifactoral, may be genetic Pathogenesis: Herniation of stomach through diaphragm Manifestations May be asymptomatic, GERD, may produce dyspnea Treatment: treatment for GERD, surgery may be indicated GERD Etiology: multifactoral Risks: pregnancy, obesity, decreased gastric motility Pathogenesis: failure of lower esophageal sphincter to keep gastric contents in the stomach. Reflux of acid, pepsin, and bile into esophagus. Can develop esophageal erosions and ulceration Manifestations Heartburn, epigastric pain. If it comes to top of esophagus: dysphasia, throat pain, cough, sore throat Treatment: medication, dietary changes, behavioral changes (smoking, alcohol consumption). Surgery may be indicated Barrett Esophagus Etiology: also know as Barrett’s metaplasia; complication of GERD Pathogenesis: chronic inflammatory changes to esophageal mucosa, carcinoma may develop If GERD is treated, metaplasia will regress. If left untreated, metaplasia will become dysplasia Manifestations: often no symptoms. Heartburn may develop Treatment: aggressive treatment of GERD, serial endoscopy to evaluate changes in tissues, surgery may be necessary Esophageal Cancer Etiology: can be genetic Risk factors: GERD, smoking, obesity Pathogenesis SCC and adenocarcinoma comprise 95% of esophageal cancers Manifestations Progressive dysphasia, weight loss, heartburn Treatment Mucosal resection and ablation, chemo/radiation, endoscopic stents Disorders of the Stomach Main categories of stomach disorders Disorders of secretion Disorders of motility Associated cardinal symptoms Pain, altered ingestion and digestion, GI bleeding Types of Disorders Type of Disorder Examples PUD Ulcers Secretion Gastritis Stomach cancer Gastroparesis Motility Pyloric stenosis Gastric outlet syndrome Peptic Ulcer Disease (PUD) Etiology H.pylori and NSAID use Contributing factors: smoking, alcohol, emotional stress Pathogenesis Increased gastric acid or weakened mucosal barrier leading to mucosal erosion and possible ulceration of GI tract Manifestations Can be asymptomatic. Epigastric pain, dyspepsia Complications: Bleeding, perforation, obstruction Treatment Identify causative factor, treatment of H.Pylori, medications to reduce stomach acid or repair mucosa Gastritis Gastritis can be acute or chronic Gastric Cancer Etiology: Risk factors include H.pylori, smoking, ETOH abuse, inadequate fruit and vegetable consumption and pernicious anemia Pathogenesis Tumors arise from gastric mucosa (adenocarcinoma), connective tissue of gastric wall, neuroendocrine tissues or lymphoid tissues Manifestations Most common is weight loss and abdominal pain but may also include: Dysphagia, nausea, occult GI bleeding, early satiety, and palpable abdominal mass Inflammatory Bowel Disease Inflammatory Bowel Disease (IBD) Chronic inflammation in the lower GIT Two major disorders Ulcerative colitis Crohns disease IBD Ulcerative Colitis: Etiology: Not well understood Environment, genetics, autoimmune disorder, microbial imbalance in the gut Pathogenesis Inflammation of the mucosal and submucosal layers that is one continuous lesion and can affect the entire colon. Manifestations Fever, weight loss, fatigue, bloody and mucous diarrhea, dehydration, anemia, abdominal pain IBD Crohns Etiology: not completely understood Environmental, genetic, microbial imbalance, autoimmune Pathogenesis Inflammation causing granulomatous lesions and destruction of the bowel Manifestations Abdominal pain, fever, weight loss, fatigue, N/V, diarrhea Complications include bowel strictures, obstruction, perforation, Appendicitis Etiology: believed to be due to obstruction and inflammation within the appendix Pathogenesis: Obstruction will lead to bacterial growth and inflammation, can inhibit perfusion to the tissue, appendix can become gangrenous and rupture Manifestations: Abdominal pain, tenderness in RLQ, N/V, increased WBC count and low grade fever Bowel Obstruction Etiology Adhesions are the cause 75% of cases Other causes: HANG IV (hernia, adhesions, neoplasia/tumor, gallstone ileus, intussusception, volvulus Pathogenesis Above etiology causes GIT blockage, 80% are in small intestine Manifestations Abd pain, N/V, abd distention, decreased BM, hyperactive bowel sounds; if ileus develops, bowel sounds will be absent Bowel Obstruction Complications: bowel necrosis, perforation, sepsis, death Treatment: Decompress the bowel, IVF, nothing by mouth (NPO) until it resolves, surgery may be necessary Irritable Bowel Syndrome Etiology Abnormal gut motility, psychological disturbances, inflammation, stress Pathogenesis Altered discomfort with alternating bowel habits (constipation to diarrhea) Manifestations: Abd pain, cramping, change in bowel habits, bloating, often triggered after eating. Diverticula Disease Diverticula Small outpourings of colonic mucosa Diverticulosis Diverticula without evidence of inflammation Diverticulitis Inflamed diverticula Pathogenesis of Diverticula Disease Mucosa herniation develops at areas of weakened bowel Feeder arteries can become compressed or eroded leading to perforation or bleeding Development of chronic low grade inflammation Development of obstruction, stasis, altered local bacteria, or ischemia lead to diverticulitis Complicated diverticulitis is an inflammation with the formation of an abscess, fistula, obstruction, bleeding, or perforation Diverticula Disease Etiology weakened bowel wall, low fiber diet, NSAID use, advanced age, obesity, sedentary lifestyle Manifestations Sudden onset of LLQ pain, abd distention, nausea, change in bowel habits, fever, tachycardia, hypotension Hemorrhoid Disease Etiology: Straining during bowel movements Risk factors include: increased intraabdominal pressure, or impeded venous return Pathogenesis: Abnormal enlargement of vascular mucosal cushions that assist with anal continence Manifestations: Hematochezia, anal itching and discomfort, soiling, feeling of rectal fullness Can be internal or external  Colorectal Cancer Precursor to cancer Adenoma (polyps) Benign tumors Malignant growth in the colon Results from division of abnormal cells in the Colon Cancer colon Occurs in the ascending, transverse, or descending colon Malignant growth in the rectum Located up to 15 cm from the anal Rectal Cancer opening Modifiable risk factors Obesity, sedentary lifestyle, smoking, moderate alcohol consumption, high consumption of red meats, low consumption of fruit and vegetables Hereditary or medical risk factors Family history of CRC, inflammatory bowel disease, T2DM, aging Protective factors Diet rich in whole grain fiber, use of NSAIDS Manifestations of early CRC Often asymptomatic Other symptoms Hematochezia and symptoms of anemia Change in bowel habits, weight loss, and fatigue Abdominal pain Manifestations of advanced CRC Depends on the location of the cancer Physical assessment Distended abdomen, palpable mass Rectal cancer-palpable mass on rectal exam Right sided cancers (ascending colon) Usually silent, may develop abd pain, tumors stay on one side of the colon wall. Unlikely to develop bowel obstruction, dark red blood in stool Left sided cancers (descending colon) Tumors grow circumferential around the colon. Stool becomes long and pencil like, can lead to intestinal obstruction, bright red blood in stool Screening for CRC Early detection is essential Screening methods Lower GI endoscopy, fecal tests for occult blood, and DNA testing for mutant genes Screening recommendations All men and women should begin screening at age 50 Individuals with predisposing factors should begin screening earlier Disorders of the Exocrine Pancreatic and Hepatobilary System  Cancer of the Liver Liver cancer Also called hepatocellular cancer 5th most commonly diagnosed cancer Poor survival rate worldwide Risk factors: Cirrhosis and carriers of Hep B & C Overconsumption of alcohol and coffee, obesity, oral contraceptive use Potential manifestations of liver cancer Weakness and fatigue Weight loss Abdominal bloating and distention Jaundice Liver dysfunction Disturbances in clotting factors Bleeding and bruising Elevated liver enzymes ALP, GGT, AST and ALT Metabolic Disorders Cirrhosis Late stage scarring of the liver Causes Alcohol consumption (the most common) Chronic viral hepatitis Chronic obstruction of bile ducts Genetic disorders (Wilson disease, alpha-1 antitrypsin deficiency, and autoimmune hepatitis) Alcohol related liver damage May be acute or chronic Acute liver damage Alcoholic hepatitis Chronic liver damage Cirrhosis, steatosis, steatohepatitis, fibrosis Effects of alcohol on the liver Progressive deterioration of liver cells Accumulation of fat in the liver Early stage: steatosis (fatty liver) Progressive stage: Cirrhosis Hepatocytes are replaced by scar tissue Metabolic function of the liver is impaired Development of secondary conditions: portals hypertension and other systemic effects Severity of alcohol induced liver damage Contributing factors Pattern of drinking Amount of alcohol consumed Number of years of alcohol consumption Immunity Genetic and biochemical makeup Overall nutrition, diet, and health status Potential early manifestations of alcohol induced cirrhosis Increased serum ammonia Restlessness Vague, early symptom of systemic toxicity Agitation Progressive impairment in judgment Examples of Progressive Cirrhosis Anorexia and Weight Loss Ascites Esophageal varices Portal hypertension Jaundice RUQ pain Asterixis (flapping tremor) Bruising and bleeding Nausea Confusion/Mental status changes Elevated liver enzymes Cholelithiasis Pathogenesis Typically formed in the gall bladder Migrates to bile ducts and produces obstruction and inflammation Formed from cholesterol or pigment Conditions associated with excess cholesterol Obesity Diets high in fat and cholesterol Use of medications that lower serum cholesterol Risk factors for cholelithiasis Changes in metabolism Biliary stasis or obstruction Hypertriglyceridemia Sedentary lifestyle Diabetes mellitus Family history of cholelithiasis Risk factors for cholelithiasis among women Multiparous Use of estrogen replacement therapy/OCP Five F’s Female, fair, fat, fertile, and forty Early signs of gall stones Often vague Indigestion or mild gastric distress after a fatty meal Acute manifestations of duct obstruction Severe and sudden onset of midepigastric pain Pain can extend to RUQ and subscapular region and to back and shoulder N/V, diaphoresis, and tachycardia Manifestations of bile reflux into the liver May cause jaundice, pain, or hepatocyte damage Consequences of common bile duct obstruction May cause reflux of pancreatic enzymes Can lead to pancreatitis Steatorrhea Due to lack of bile for fat digestion Pruritus Due to accumulation of bile salts in the blood  Cholecystitis Cholecystitis Acute or chronic inflammation of the gall bladder Associated conditions Gall stones (cholelithiasis) Other alterations that damage gall bladder walls Etiology Cystic duct stone (most common) Trauma Infection of gall bladder Sepsis Pathogenesis of cholecystitis Inflammation develops Caused by both the stone and digestive juices Bile builds up Creates increased pressure in the gall bladder Causes chemical damage to gall bladder Tissue ischemia occurs Damage to gall bladder walls and mucosa Potential for gall bladder perforation and necrosis Acute cholecystitis Results from blockage of cystic duct; causes pain and biliary colic Chronic cholecystitis Occurs due to untreated acute cholecystitis Gall bladder becomes scarred with fibrosis Bile may contain pathogens and cause infection Impaired circulation and edema cause ongoing issues Gangrene, abscess, perforation with peritonitis and sepsis Clinical manifestations of cholecystitis Intolerance of dietary fat Epigastric heaviness or RUQ pain Flatulence, belching, GERD Colicky pain Steatorrhea Bleeding, jaundice, pruritus may be present Fever and chills  Acute Pancreatitis Acute Pancreatitis Inflammation or necrosis of the pancreas Can contribute to pancreatic ischemia Serious and painful inflammation may occur Early treatment is necessary to prevent complications Etiology of Acute Pancreatitis Most common: ALCOHOL Viral infections Trauma/Abdominal Surgery Hyperlipidemia Medications Pathogenesis of alcohol induced pancreatitis Ethanol is metabolized and toxic metabolites are released causing tissue injury and partial obstruction Pathogenesis of gall stone induced pancreatitis Obstruction of pancreatic ducts and trapping of digestive enzymes Autodigestion of pancreatic tissue Acute inflammatory response is triggered SIRS and multiple organ failure may occur Manifestations of Acute Pancreatitis Abdominal Pain: LUQ with Changes in Vitals: distention & tenderness Hypotension Critical Warning Signs: Tachycardia Oliguria Fever Paresthesia Hypoxemia Restlessness Jaundice Confusion Steatorrhea Worsening tachypnea and tachycardia May evolve to hypovolemic shock Turner sign: Cullen sign: Bruising and bluish discoloration Bruising and edema in the flank areas caused around umbilicus by bleeding in the peritoneum Chronic Pancreatitis Chronic pancreatitis Similar to acute pancreatitis, pain is often less severe Tissue damage becomes irreversible Etiology of pancreatitis Most common: alcohol abuse Calculi and tumors Smoking Cystic fibrosis Exposure to toxic metabolites Inflammatory bowel disease Pathogenesis of chronic pancreatitis Obstruction of pancreatic duct—>chronic pancreatitis develops Manifestations of chronic pancreatitis Anorexia and malabsorption of fats and proteins weight loss and steatorrhea Dull, constant abdominal pain LUQ pain, often precipitated by alcohol intake Pancreatic Cancer Etiology Generally unknown Risk factors Smoking Obesity Diet: nitrates, preservatives, and high fat Diabetes mellitus Chronic pancreatitis Genetic predisposition Pathogenesis of pancreatic cancer Pancreatic cancer spreads easily Demonstrates early invasion to lymphatic system Factors that promote metastasis Infiltration to major vessels Lack of well developed pancreatic capsule May obstruct common bile duct and portal vein Jaundice and liver damage can develop Manifestations of pancreatic cancer Systems are slow to develop Contributes to delayed diagnosis and treatment Factors that influence clinical presentation Size and extent of cancer Metastasis to other organs and tissue Early manifestations of pancreatic cancer Abdominal pain and discomfort Malabsorption and weight loss, N/V Back pain Bile duct obstruction Dark urine, steatorrhea, jaundice, pruritus Diabetes mellitus Both a risk factor and a consequence of pancreatic cancer Late manifestations of pancreatic cancer Portal vein hypertension Ascites Hepatosplenomegaly Esophageal varices Liver Failure Liver Functions Detoxification Coagulation Nutrition Storage Metabolism of medications Production of many substances Normal Liver Blood Vessels Dual Blood Supply Hepatic artery and portal vein carry approximately 25% of body’s total cardiac output Hepatic artery Supplies ~30% of blood to the liver, branches from aorta (oxygenated) Portal vein Supplies ~70% of blood to liver, branches from splenic vein and inferior/ superior mesenteric veins-Supplies deoxygenated, nutrient rich blood Portal Hypertension Increased portal venous pressure (>5 mmHg) Normal is 3 mmHg >10 mmHg is associated with complications 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 Non-cirrhosis causes Prehepatic: portal vein thrombosis, narrowing of portal vein Posthepatic: severe R-sided HF, hepatic vein outflow obstruction Conditions associated with increased portal pressure Esophageal varices and hemorrhage Rectal varices Splenomegaly Complications of Liver Failure Melena Hematemesis Esophageal Varices Decreased Hgb/Hct levels Dyspnea Fatigue Increased abdominal girth Weight gain Decreased appetite Ascites Abdominal discomfort Dyspnea  Serum Creatinine >2.5 Hepatorenal syndrome No evidence of renal disease, shock, or nephrotoxic drugs Nonspecific Dyspnea Heptaopulmonary syndrome Digital clubbing Hypoxemia Dyspnea at rest or exertion Chest pain Portopulmonary syndrome Syncope JVD/Peripheral edema Jaundice Dark urine and clay stools Jaundice and Cholestasis NAFLD Strongly linked to obesity Fatty liver becomes insulin resistant and increases risk for morbidity Deposit of lipids in the liver Mild: Steatosis (>5% hepatic lipid accumulation) Severe: Inflammation and damage to liver cells and may progress to cirrhosis  Etiology & Pathogenesis of Acute Liver Failure Loss of hepatocyte function without cirrhosis Damage occurs over days/weeks Drugs account for >60% of cases Acetaminophen is most common Other factors : Viruses, toxins, autoimmune responses High Mortality Rate Diagnosis H&P AST/ALT Bilirubin Presence of coagulopathy and altered mental status Disorders of Kidney and Urinary Tract Function Concepts Related to Disorders of the Urinary Tract Acute kidney injury (AKI) Rapid decrease in kidney function Chronic kidney disease (CKD) Loss of kidney function over time Results from a failure of the body to remove waste products End stage renal disease (ESRD) Occurs is CKD is not treated Results from a failure of the body to remove waste products Concepts Related to Disorders of Urinary Tract Elimination of waste products Without blood flow to the kidneys, urine output decreases Acid-base balance Bicarbonate acts as a buffer to maintain acid-base balance In acidosis, kidneys reabsorb bicarbonate In alkalosis, kidneys excrete more bicarbonate Diabetic Nephropathy CKD resulting from hyperglycemia Leading cause of ESRD Proteinuria Risk factors Poor glycemic control Uncontrolled hypertension Obesity Smoking Genetics Race  Hyperglycemia Polyuria Increased renal blood flow Glomerular Hypertrophy Glomerular Hypertension Hyperfiltration Hypertensive Nephropathy CKD resulting from long standing HTN Second leading cause of ESRD Affects glomerulus, tubules, and vasculature of kidneys Risk factors Genetics Diabetes More prevalent in African Americans Urinary Tract Infection (UTI) UTI Infection of the lower urinary tract or kidneys Cystitis Infection of the bladder Most common bacterial infection Risk factors Gender DM Obstruction Neurogenic bladder Use of spermicides and diaphragms Pyleonephritis Infection of the kidney Risk factors Female gender GU abnormalities Neurogenic bladder Immunosuppression DM Etiology: Ascending bacterial colonization from urethra to the bladder to the kidney Most common caused by E. Coli Other causes Obstructions Urinary retention Instrumentation Clinical Manifestations Cystitis Dysuria, urgency, frequency, confusion (older adults) Pyleonephritis CVA tenderness Fever, chills Renal Calculi Results from formation of crystals into larger stones Common in males Risk factors: Previous stones Dehydration High calcium levels High oxalate diet Most are calcium based Can be uric acid, cysteine stones Stone formation Damage to lining of the urinary tract Crystal aggregation Slow urine flow allows crystallization Excretion of large amounts of calcium Clinical manifestations Acute, unilateral flank pain N/V Colicky pain that comes and goes Hematuria Diagnosis H&P, Ultrasound and/or X-Ray Renal Cancer Malignant tumor in the kidney Risk factors HTN and obesity Clinical Manifestations Painless hematuria, weight loss, dull aching abdominal pain, can be asymptomatic AKI and CKD Concepts Related to Kidney Disease Normal kidney function Regulation of fluid and electrolytes Excretion of waste Control of blood pressure Regulation of acid-base balance This is all accomplished by perfusion to the kidneys AKI Alteration of kidney function Spectrum of risk to overt failure Often results from infection/inflammation Can often be reversed if caught early CKD Alteration in kidney function with vague symptoms Systemic changes due to portal hypertension Long-term damage from diseases such as DM or HTN AKI Abrupt reduction of kidney function Often reversible Characterized by azotemia Accumulation of nitrogenous waste Three main etiologies: Prerenal, intrinsic, and postrenal  Etiology Pathogenesis Responsible for 60% of cases Usually reversible Prerenal Increased Cr and BUN Oliguria