Inflammation Exemplars Notes PDF

INFLAMMATION EXEMPLARS LECTURER: BETH FLOTT, EDD, RN INFLAMMATION - EXEMPLARS  Cirrhosis (anemia, GI bleed)  Hepatitis  Pancreatitis  Glomerulonephritis  Crohn’s Disease/Ulcerative Colitis (Inflammatory Bowel Disease)  Ulcers (gastritis, gastric, duodenal, stress)  Diverticulosis/Dive...

INFLAMMATION EXEMPLARS LECTURER: BETH FLOTT, EDD, RN INFLAMMATION - EXEMPLARS  Cirrhosis (anemia, GI bleed)  Hepatitis  Pancreatitis  Glomerulonephritis  Crohn’s Disease/Ulcerative Colitis (Inflammatory Bowel Disease)  Ulcers (gastritis, gastric, duodenal, stress)  Diverticulosis/Diverticulitis  Cholecystitis/Cholelithiasis  Acute/Erosive Sudden onset - acute mucosal injury and inadequate mucosal repair GASTRITIS Causes – H. Pylori, medications including NSAIDs and corticosteroids Chronic Gastritis: Presence of chronic inflammatory cells in gastric mucosa causing inflammation and/or metaplasia Two phases: Non-atrophic/superficial – damage to surface of mucosa Atrophic –damage is deeper, secretory glands affected, lack of intrinsic factor, cancer risk Causes - H. Pylori, medications including NSAIDs and corticosteroids, autoimmune conditions Presence of inflammatory response evidenced on biopsies ULCERS  Peptic Ulcer Disease – imbalance between potent gastric acid and the protective mucosal barrier lining  Gastric  Duodenal GASTRIC ULCERS  Typically occurs later in life; peak incidence in 60’s  Causes  Duodenal reflux of bile  H. pylori  NSAID induced - associated with normal to decreased gastric acid secretion  Symptoms  Burning or gnawing discomfort; may be precipitated by food; nausea and weight loss frequently accompany this type of ulcer   Typically occur in first portion of duodenum DUODENAL ULCERS  Causes  H. Pylori  NSAID use  Symptoms  Burning or gnawing discomfort with empty stomach and during the night  Tend to occur after severe trauma, severe illness/infection, or neurological injury Develops acutely STRESS ULCERS Causes Think about - how does stress impact the GI system? Hospitalized patients – why is this population at risk? Subtype of stress ulcer Cushing’s Ulcer – related to neurological injury, overstimulation of vagus nerve, increased secretion of gastric acid ULCERS – INTER-RELATED CONCEPT: PERFUSION COMPLICATION: GI BLEEDING Upper GI bleeding – Lower GI bleeding – Response to GI bleeding bleeding in the bleeding from the Occult bleeding dependent upon the esophagus, stomach or jejunum, ileum, colon or duodenum rectum amount and rate Hematemesis Caused by polyps, Usually caused by slow, Compensatory Hematochezia (bright diverticulitis, chronic blood loss that mechanisms manifest – red stools) inflammatory disease, is not obvious what are these? What cancer or hemorrhoids signs/symptoms will be Melena see with bleeding? ULCERS – DIAGNOSIS & TREATMENT Diagnosis History – asking about NSAID use Upper GI endoscopy (NOT If suspected perforation)  Treatment Testing for H. Pylori Labs  Medications that inhibit acid  Antibiotics WBC level  Discontinuing NSAIDS Hemoglobin – measures the protein in RBCs that binds to oxygen 12-17.4 g/dL 13.5 – 18 g/dL (males); 12 – 16 g/dL (females) Hematocrit – proportion of RBCs to total blood cell population 36%-52% 40% – 52% (males); 36% - 47% (females) INFLAMMATION  H. Pylori is discovered in the GI tract of a client experiencing an inflammation of the gastric mucosa. These findings support which diagnosis? A. Chronic diarrhea B. Paralytic ileus C. Chronic gastritis D. Pyloric obstruction INFLAMMATORY Both include an inappropriate Symptoms BOWEL DISEASES immune response in the GI tract -pain and fever -environmental factors -bleeding -genetic predisposition CHRON’S -altered motility -microbial imbalance in the gut -loss of appetite and weight loss DISEASE ULCERATIVE COLITIS Intermittent diseases - periods of remission when no symptoms are present SIMILARITIES INFLAMMATORY BOWEL DISEASES - DIFFERENCES Ulcerative Colitis Chron’s Disease  Typically involves the rectum  Transmural inflammation of the bowel with skip lesions  Continuous lesion involving mucosal and  Most commonly affects ileum and proximal colon submucosal layers  Extends through layers of the bowel, can result in  Inflammation, epithelial cell damage, loss of goblet fissures and fistulas cells  Bowel wall thickening, ulcerations  Bloody diarrhea, crampy abdominal pain,  “Cobblestone appearance” dehydration  Nausea, vomiting, diarrhea, bowel obstructions  Toxic megacolon  Perforations INFLAMMATORY BOWEL DISEASE  Comparison of effects in ulcerative colitis and Chron’s disease DIAGNOSTICS & TREATMENT Diagnostics Treatment Stool sample (rule out other Anti-inflammatory agents disease processes) Immunosuppressants CRP and ESR – elevated Surgery H&H – anemia Lower endoscopy studies and biopsies INFLAMMATION  Which of the following is a TRUE statement regarding Crohn disease? A. It involves the mucosa only B. Skip lesions are common C. It affects only the rectum D. The most common site is the rectum  Diverticula – small outpouchings of mucosa through muscle layers of the colon wall DIVERTICULAR Diverticulosis – no or low-grade DISEASE inflammation present (stable) Diverticulitis – highly inflamed diverticula (unstable)  Formation of diverticula - Mucosal Formation of diverticula - Feeder Development of chronic low-grade herniation develops due to high- artery penetrates through the inflammation (uncomplicated amplitude contractions at an area of muscle layer of colon wall diverticulosis weakness Complicated diverticulitis: With diet, stress, and other risks - Complicated diverticulitis: Feeder Inflammation associated with obstruction, stasis, altered local artery may become compressed or formation of an abscess, fistula, bacteria, or ischemia of the eroded, leading to perforation or obstruction, bleeding, or a diverticula lead to diverticulitis bleeding perforation DIVERTICULAR DISEASE DIVERTICULAR DISEASE   Symptoms/Manifestations DIVERTICULAR  Sudden, constant left lower quadrant abdominal pain, nausea diarrhea, DISEASE tachycardia, fever, hypotension  Diagnostics  Imaging for complicated cases  Urinalysis to rule out other conditions  Stool sample for occult blood  Treatment  Clear liquid diet  Antibiotics  Surgery INFLAMMATION A client is diagnosed with hematochezia. Which assessment finding confirms this diagnosis? A. Bloody vomitus B. Bright red rectal bleeding C. Presence of tarry stools D. Positive testing for occult blood CHOLELITHIASIS/CHOLECYSTITIS  Gallbladder  Cholelithiasis – stone formation in the gall bladder; can be acute or chronic  Cholecystitis – stones can block the ability for bile to leave gallbladder, causing inflammation of the gallbladder; can be acute or chronic CHOLELITHIASIS/CHOLECYSTITIS  Cholecystokinin stimulates gallbladder and pancreas to contract, releasing digestive juices and bile  Gallstones form and can block bile, leading to initiation of inflammatory process (cholecystitis)  Increased pressure from buildup of bile leads to damage, resulting in tissue ischemia  Damage to walls of gall bladder and surrounding mucosa  Can lead to perforation of gallbladder and necrosis  Risk factors  Diet high in fat and cholesterol  Hyperlipidemia  Sedentary lifestyle  Females more at risk particularly those with use of estrogen replacement, multiparous CHOLELITHIASIS/CHOLECYSTITIS   Clinical Manifestations  Mild gastric distress in RUQ after fatty meal  Blocked  Severe and sudden onset of midepigastric pain (biliary colic); radiates to right shoulder blade CHOLELITHIASIS/CHOLECYSTITIS  Nausea  Tachycardia  Steatorrhea, dark urine  Fever, chills  Common bile duct blocked - choledocholithiasis  Back-up into pancreas – pancreatic enzyme back-up leads to autodigestion, pancreatitis  Back-up into liver – jaundice, pain CHOLELITHIASIS/CHOLECYSTITIS Diagnostics Treatment Elevated WBC Medications to decrease cholesterol Elevated amylase and lipase – if pancreas Healthy lifestyle habits involved Surgery - cholecystectomy Elevated conjugated bilirubin, AST, ALT – if liver involved Abdominal x-ray; gallbladder scan   Acute  Inflammation or necrosis of the pancreas  Severe cases – 20% of cases  Pro-inflammatory cytokines released widely, massive vasodilation leading to shock PANCREATITIS -  Alcohol abuse ACUTE  Ethanol metabolized and tissues are injured by toxins that release enzymes  Partial sphincter obstruction and tissue irritation  Gallstones  Traps the enzymes (trypsin) autodigests tissue causing inflammatory response   Manifestations  Pain – deep epigastric pain  Abdominal distention, tenderness PANCREATITIS -  Fever ACUTE  Cullen Sign  Grey-Turner Sign  Paresthesias   Diagnostics  WBC - elevated  Amylase – produced by pancreas and salivary glands for digestion and excreted by kidneys  25 – 151 units/L  Elevation begins 3-6 hours after pain begins, peaks in 24 hours and returns to normal in 2-3 days  Lipase – produced by the pancreas to break down fats and PANCREATITIS - triglycerides into fatty acids and glycerol ACUTE  10 – 140 units/L Treatment Pain Relief NPO status Fluid Replacement PANCREATITIS - CHRONIC  Pain is less severe – dull, constant, and located in LUQ; alcohol induces pain  Long-term inflammation leads to irreversible damage  Causes  Alcoholism  Obstruction/stricture of pancreatic duct – cystic fibrosis, genetic hyperlipidemia  Diagnostics/Treatment  Elevated WBC, amylase, and lipase  Low-fat diet  Enzymes – replaced by oral replacements taken before or during a meal  Surgery GLOMERULONEPHRITIS Inflammation of glomeruli and capillaries – characterized by proteinuria, hematuria, and edema Leads to deposit of antigen/antibody complexes Activation of phagocytes & platelets leads to injury to cells & membrane of glomerulus Increased permeability allows passage of RBCs, protein into urine Capillaries occluded with WBCs leading to decreased blood flow to glomeruli, ischemia, and retention of water and wastes Primary Limited to the kidneys, usually idiopathic, include minimal change disease, IgA nephropathy, autoimmune conditions Secondary Result of another disease process (diabetes, lupus, postinfectious – Group A Beta Hemolytic Streptococcus) GLUMERULONEPHRITIS GLOMERULONEPHRITIS  Acute – most cases  Rapidly Progressive – syndrome that is a medical emergency, leads to AKI, crescents often present  Chronic – few cases that can progress over many years  Focal vs Diffuse GLOMERULONEPHRITIS  Manifestations  Nephritic Syndrome presentation – hematuria, proteinuria, RBC casts, and dysmorphic RBCs  Nephrotic Syndrome presentation – hyperlipidemia, hypoalbuminemia, edema, proteinuria, and fatty casts in urine  Can have both syndromes present  All types – if diffuse, decreased renal function is present  Diagnostics  Labs  Urinalysis – expected is no evidence of protein, 0-3 RBCs, 0-4 WBCs, and occasional casts  Blood Urea Nitrogen (BUN) – formed in the liver as an end product of protein metabolism; excreted via kidneys  8-22 mg/dl  Must be assessed with serum creatinine if BUN and creatinine rise together = renal insufficiency/failure  Serum Creatinine – end product of creatine metabolism is muscles – elevated levels indicate renal insufficiency/failure GLOMERULONEPHRITIS  0.6 – 1.3 mg/dL  Albumin – plasma protein that maintains oncotic pressure (to prevent edema) and transports water-soluble substances such as fatty acids, hormones, bilirubin and drugs  3.5 – 5.0 gr/dL  Total Protein – consists of circulating albumin and globulins in serum  6.0 – 8.0 gr/dL  Treatment  Primary – BP control, medication for hyperlipidemia  Secondary – treating primary cause HEPATITIS – REVIEW OF LIVER FUNCTIONS  Liver Functions  Storage of blood – in case of hemorrhage or hypovolemia  Storage of fat-soluble vitamins (A, D, E, K)  Storage of minerals (copper, iron, glucose, fat)  Storage of glycogen  Filtration of blood  Kupffer cells – phagocytes assist in removing bacteria and foreign substances  Synthesis of clotting factors (Factors I, II, VII, IX, and X)  Secretion and congregation of bilirubin  Breaks down and detoxifies substances  Production of albumin  Converts ammonia to urea HEPATITIS  Inflammation of the liver  Causes  Viral – five main different types  Acute Alcoholic Hepatitis  Lipids accumulate in liver cells as byproduct of alcohol metabolism. GI tract bacteria degradation also induces inflammation d/t increased permeability after alcohol consumption  Autoimmune  Progressive, typically chronic inflammatory disease  Significantly elevated immunoglobulin levels Virus Type HAV HBV HCV HDV HEV Type RNA DNA RNA RNA RNA Mode Fecal-oral Parenteral, Parenteral Parenteral, Fecal-oral sexual, sexual, perinatal perinatal Incubation 30 days 28-180 35-72 days 30-180 15-60 days days days Onset Acute Insidious Insidious Insidious Acute Chronicity No Yes Yes Yes No Patho Hepatocyte Viral Hepatocyte Co-infection Viral HEPATITIS injury replication, injury with HBV, replication, caused by co-infection caused by severe cell liver is cellular with viral immune injury, cytotoxic, immune mutation, response, inflammati immune responses inflammati inflammati on response on and on and progressing causes cellular fibrosis to cirrhosis inflammati necrosis leading to on and cirrhosis cholestasis Severity Mild Severe Severe Severe Severe in pregnancy  Prodromal – From 2 weeks after initial exposure until jaundice occurs. Fatigue, nausea, vomiting, low-grade fever. Highly infectious HEPATITIS - Icteric – Can last up to 6 weeks, starts when PHASES jaundice develops. Jaundice, clay-colored stools, liver enlarged Recovery/Post-icteric – Starts 6-8 weeks after exposure. Jaundice starts to resolve. Labs begin to improve Diagnostics Viral hepatitis - positive antibodies for different types Bilirubin - a by-product of hemoglobin breakdown Consists of total, direct (conjugated) and indirect (unconjugated) Total: 0.1–1.2 mg/dL, μ Direct (conjugated): 0.1–0.3 mg/dL, μ Alanine aminotransferase (ALT) – enzyme found primarily in liver cells 10-35 u/L HEPATITIS Aspartate aminotransferase (AST) – enzyme found primarily in liver and rises with cellular injury 8-35 units/L Treatment Vaccines for HAV and HBV Rest, nutrition, symptom management INFLAMMATION A patient is diagnosed with hepatitis A. Transmission of this form of hepatitis occurs via: A. fecal-oral route B. Infected blood or body fluids C. Sexual contact D. Intravenous drug use CIRRHOSIS  Late stage scarring of the liver  Causes – alcohol consumption, hepatitis, chronic obstruction of bile ducts  Risk factors – male, countries with higher alcohol consumption per capita CIRRHOSIS CIRRHOSIS LIVER DISEASE - ASCITES  Albumin – protein produced in liver  Essential for increased oncotic pressure  Liver damage stops albumin production, fluid leaks into interstitial spaces  Dyspnea can occur d/t pressure on diaphragm LIVER DISEASE - JAUNDICE  Bilirubin – waste product of RBC production  Albumin required to carry unconjugated bilirubin back to liver to conjugate into water-soluble product for elimination JAUNDICE  Other causes of jaundice  Hemolytic  Obstructive  Extrahepatic  Intrahepatic LIVER DISEASE – PORTAL HYPERTENSION AND ESOPHAGEAL VARICES  When hepatocytes are eventually replaced by scar tissue, the fibrous connective tissue leads to constriction. This forces blood out of the liver to vessels that have a lower pressure, including vessels surrounding the esophagus and spleen  Major risk of GI bleeding – liver does not produce enough clotting factors  Normal portal pressure = 3 mmHg; Increased > 5 mmHg; Complications with pressure > 10 mmHg LIVER DISEASE – HEPATIC ENCEPHALOPATHY  Ammonia – by-product of protein metabolism; converted to urea in liver  When liver not functioning, ammonia accumulates in bloodstream  Impacts brain function – confusion, disorientation LIVER – INTERRELATED CONCEPTS CIRRHOSIS  Diagnostics  AST – elevated  ALT – elevated  Bilirubin – elevated  Albumin – - decreased - plasma protein that maintains oncotic pressure (to prevent edema)  3.5 – 5.0 gr/dL  Total Protein – decreased - consists of circulating albumin and globulins in serum  6.0 – 8.0 gr/dL  Ammonia – elevated – end-product of nitrogen breakdown during protein metabolism  15-45 micrograms/dL  Coagulation tests – increased  Prothrombin Time (PT) – 10 – 13 seconds QUESTIONS??