Exam 3 Study Guide PDF

Exam 3 Study guide 1 GI 1. Know about the infectious agents (for Vibrio cholera and Norwalk Virus) and pathophysiologic rationale for the clinical manifestation of diarrhea; a. Diarrhea: increase in frequency of defecation and fluidity, volume, and we...

Exam 3 Study guide 1 GI 1. Know about the infectious agents (for Vibrio cholera and Norwalk Virus) and pathophysiologic rationale for the clinical manifestation of diarrhea; a. Diarrhea: increase in frequency of defecation and fluidity, volume, and weight of feces. b. Acute - Non-inflammatory (large-volume) diarrhea: bacteria disrupts normal absorption i. Vibrio cholera: toxins binds to ATP pump causing water, Na+, Cl- loss in stool (not able to reabsorb sodium à not able to reabsorb water. If ATP pump is broken, water stay in the intestine causing diarrhea) ii. Norwalk virus: Infects small intestine mucosa, damages microvilli, causes malabsorption lactose and fat (malabsorption issue) c. Chronic diarrhea: i. Excessive fluid drawn into intestinal lumen by osmosis (osmotic diarrhea) d/t poorly absorbed solutes such as Mg++, lactose ii. Excessive secretion of fluids by intestinal mucosa (secretory diarrhea) d/t bacterial overgrowth, hormone secreting tumors such as Zollinger-Ellison iii. Inflammatory or intrinsic disease of colon (ulcerative colitis, Crohn’s – inflammatory diarrhea) 2. Be able to compare the causes and manifestations of the different forms (i.e., acute versus chronic) of gastritis; a. Inflammatory disorder of gastric mucosa b. Manifestations: vague abdominal discomfort, epigastric tenderness, fullness, N/V, anorexia, gastric bleeding c. Acute gastritis: i. Transient inflammation – irritants: NSAIDs, alcohol, bacterial toxins (H. pylori) d. Chronic gastritis: i. Chronic Inflammation – progressive ii. Type A, immune (fundal) 1. Most rare and severe type 2. Autoimmune response to parietal cells à decreased Vit B12 absorption à pernicious anemia (d/t decrease in acid, iron deficiency anemia can result) iii. Type B, nonimmune (antral): 1. NSAIDs – block prostaglandin synthesis à decreased mucosal protein (prostaglandin stimulates mucous secretion) 2. alcohol, tobacco – stimulates acid secretion à irritate stomach lining 3. H. pylori – releases cytokine that damages gastric epithelium  Exam 3 Study guide 2 e. Note: chronic gastritis type b and acute gastritis same causes i. HCL enters mucosa à mucosal cell damage à inflammation à released histamine à histamine binds to H2 receptors à increase acid secretion à further damage à ulceration 3. Know the predisposing factors (to include infectious agents) development of peptic ulcers; a. Break in ulceration in protective lining, stomach (gastric), or duodenum (duodenal) b. H.pylori – damages gastric epithelium making it susceptible to HCL c. Habitual use of NSAIDs d. Smoking, alcohol, caffeine: stimulates HCL secretion e. Steroids (glucocorticoids): Decrease renewal of mucosa and increase HCL secretion. Also have vasoconstrictor effects similar to NE/EPI (on alpha receptors) leaving cells susceptible to HCL f. Stress: similar to steroids 4. Know the complications of peptic ulcer disease (duodenal vs. gastric); a. Duodenal i. Chronic intermittent pain right epigastric area ii. Pain begins when stomach is empty (2-3 h after eating) iii. Typical “pain-food-relief” pattern iv. Most absorption happens in duodenal area (small intestine) v. When you eat, you have no pain b. Gastric – i. Severe pyrosis (epigastric pain) during or immediately after eating. ii. Nausea, vomiting, weight loss c. PUD complications: i. Hemorrhage: d/t erosion of ulcer into an arterial vein (hematemesis melano) ii. Obstruction of pylorus: caused by edema, spasm, or scar tissue (fullness, vomiting) iii. Perforation: caused by ulcer eroding through all layers of stomach and duodenum wall (severe abdominal pain, rigidity, absent bowel sounds, signs of shock) iv. Dumping Syndrome: Rapid emptying of hypertonic chyme into small intestines → fluid drawn into bowel by osmosis → decreased blood volume (HTN, increased pulse, dizziness) and intestinal dilation (N/V, abdominal cramping, diarrhea) v. Monitor for symptoms related to these!  Exam 3 Study guide 3 5. Understand and be able to compare the pathophysiologic mechanisms and characteristics (signs & symptoms) of inflammatory bowel disease (Crohn’s disease and ulcerative colitis) Crohn’s (chronic inflammatory disorder affects both large and small intestine) i. Inflammation begins in lymph tissue in the intestinal submucosa ii. Inflammation spreads to mucosa and serosa (can completely penetrate bowel wall) iii. Fissures and crevices develop →Lesions are surrounded by inflamed tissue and edema creating a cobblestone appearance iv. Lesions may “skip” around (some haustral areas inflamed and some are not) v. Fistulas and abscesses may form vi. Bowel wall thickens and lumen narrows causing “string sign” b. S/S: i. Diarrhea ii. abd pain, >5 stools/day (nonbloody) iii. wt loss (malabsorption), fever, malaise, chronic UTIs iv. Folic acid, vit d deficiency v. Hypoalbunemia c. Begins in the submucosa and spreads to all layers d. Most often found in ilieum  Exam 3 Study guide 4 Ulcerative Colitis – ulceration of colonic mucosa in rectum and sigmoid colon ○ Patho Inflammation begins in the rectum and spreads throughout colon Lesions form in the crypts of Lieberkuhn in the base of the mucosal layer (most severe at sigmoid colon) Inflammation → pinpoint mucosal hemorrhages → overtime crypt abscesses form Inflammatory lesions become necrotic and ulcerate Starts in the innermost layer (mucosa - crypt of lieberkuhn) ○ S/S: 30-40 stools/day (bloody and contains mucus), mild abd cramping, anorexia, weakness, fatigability, fever, dehydration 6. Study the clinical manifestations and pathophysiologic rationale for diseases of the esophagus (understand the mechanical & neural etiologies of dysphagia; and understand the disease process in GERD); a. Dysphagia - difficulty swallowing i. Mechanical Obstruction (strictures, tumors, diverticula) 1. Intrinsic – originate in wall of esophageal lumen 2. Extrinsic – outside of esophageal lumen and narrow esophagus by pressing inward on the esophagus wall – commonly caused by tumors 3. Inflammatory injury and healing → repeated inflammatory injury and healing, reinjury and re- healing → Scarring occurs in the form of fibrous bands (becomes stiff)→ narrowing of the esophagus in the area (from build-up) → swallowing difficulties 4. Often has to be surgically corrected ii. Neural/functional (Parkinson’s or achalasia-failure to relax) → sphincters not relaxing and allowing things to pass 1. Impaired relaxation of LES → Food obstructed into lower esophagus → Esophagus dilates (distends),  Exam 3 Study guide 5 swallowing difficulties → retrosternal pain, regurgitation of undigested food, unpleasant taste, vomiting, weight loss 7. GERD: regurgitation of chyme (acid, pepsin, bile salts) into esophagus a. Transient LES relaxation or weakness (d/t pregnancy, obesity, genetic, diet, nicotine) → reflux of (acidic) chyme into the unprotected lining of the esophagus inflammation → heartburn, frequent belching, increased salivation, dysphagia due to strictures b. Complications: Strictures, ulcers, Barrett esophagus c. Symptoms worsen upon lying down or if intra-abdominal pressure increases, alcohol, citrus fruits can cause discomfort 8. Discuss diverticular disease, clinical and age alerts, causes, pathophysiology, signs and symptoms (of diverticulitis), complications, treatment, and special considerations; Diverticular disease – diverticulosis (asymptomatic, outpouching of mucosa through muscle layer of the colon) Diverticulitis - inflammation of the diverticulum (inflamed pockets) Causes o Predisposing factors: § Age, genetics, obesity, smoking, diet, lack of physical activity, medication use (aspirin NSAIDs) § Low fiber diet; constipation and the presence of weakness in muscle layer of the bowel can lead to outpouching [weak GI tissue + low fiber in diet = things not moving out, gets stuck in pouches] S/S: may be asymptomatic Constipation, LLQ pain, distension, flatulence [diverticulosis ] elevated WBC Patho o Thickening of circular muscles and shortening of longitudinal muscles in diverticula à pressure of narrow lumen increases à rupture diverticula à inflammation/diverticulitis 8. Know the major complications of liver dysfunction, liver failure: portal hypertension, ascites, hepatic encephalopathy, jaundice, and hepatorenal syndrome (include liver function tests and blood studies in discussion on liver failure). Also, include percutaneous liver biopsy in discussion; a. liver dysfunction b. portal hypertension – study ninja nerd video?  Exam 3 Study guide 6 i. Cause by any disorder that obstructs or impedes blood flow through liver = high pressure in portal veins ii. Prehepatic - iii. Intrahepatic – 1. Inflammation, thrombosis, cirrhosis, viral hepatitis iv. Posthepatic 1. Hepatic vein thrombosis, cardiac disorders that impair pumping ability of the right side of the heart à blood collects and increases pressure in veins of portal system c. Ascites – see map d. hepatic encephalopathy i. May occur d/t portal HTN or other hepatic diseases (hepatitis) 1. May develop in fulminant hepatits a. Fulminant hepatitis develops 6-8 wks after initial symptoms of hepatitis: anorexia, vomiting, abdominal pain, progressive jaundice→ ascites, GI bleeding, lethargy, and hepatic encephalopathy ii. Liver failure→ ammonia buildup (d/t liver necrosis causing liver failure)--> encephalopathy→ hepatic coma→ death e. jaundice i. Bilirubin metabolism: RBC destruction à unconjugated bilirubin (lipid soluble) à passes through liver à conjugated bilirubin (water soluble and now able to be excreted in feces) ii. Hemolytic jaundice (Prehepatic/nonobstructive jaundice)  Exam 3 Study guide 7 1. Excessive lysis of RBC = elevated unconjugated iii. Intrahepatic jaundice 1. Both conjugated and unconjugated 2. Damage to liver cells or obstruction of bile canaliculi iv. Extrahepatic jaundice 1. Elevated conjugated (already gone through liver) f. hepatorenal syndrome g. LFTs: i. AST, ALT, Alkaline Phosphatase – markers of injury 1. Liver related AST/ALT higher than alk phos 2. Biliary related Alk phos most elevated ii. Bilirubin, albumin, Prothrombin Time 1. True measures of liver function tests 9. Focus on the clinical manifestations of different types viral hepatitis. In other words know the three stages of viral hepatitis (prodromal, clinical, & recovery) and know signs and symptoms that occur in these stages; 10. Understand the pathophysiologic processes that occur in the different types of cirrhosis; and a. Cirrhosis: irreversible inflammatory, fibrotic liver disease b. Scarring of liver tissues which interferes with normal liver functions and results in structural changes within lobes of liver, characterized by  Exam 3 Study guide 8 structural and functional disorganization as a result of fibrosis and nodules of regenerated tissue c. Pathophysiology i. Protein synthesis: decreased albumin (hypoalbuminemia)→ edema (fluids stays in the third space because there is no albumin to pull up the fluid) ii. Alcoholic cirrhosis: alcohol is transformed into acetaldehyde, and excessive amounts significantly alter the liver cell function. Acetaldehyde will inhibit the export of proteins from the liver It will alter metabolism of vitamins and minerals and introduce, or induce malnutrition. So cellular damage initiates an inflammatory response along with necrosis. It'll result in excessive collagen formation, fibrosis, and scarring at the structure of the liver, and obstruction of the biliary vasculature channels. Alcoholic cirrhosis progresses to fatty infiltration, fibrosis, and cirrhosis. iii. Bile production: fat malabsorption (steatorrhea) 1. Fat deposition within the liver is caused primarily by increased lipogenesis and decreased fatty acid oxidation by the, liver cells. So with biliary cirrhosis, that differs from alcoholic cirrhosis and that the damage and inflammation leading to cirrhosis begins in the bile canaliculi, rather than the hepatocytes. iv. Hormone accumulation 1. Estrogen level: gynecomastia, altered hair distribution, testicular atrophy 2. Increased MSH: dark pigment 3. Increased aldosterone and ADH: edema v. Ammonia build up → hepatic encephalopathy, coma, death vi. Decreased bilirubin metabolism → jaundice, hyperbilirubinemia vii. Decreased vitamin K clotting factor → bleeding → anemia viii. Portal hypertension; ascites, varices, splenomegaly 11. Obstructing bile canaliculi 12. Discuss the causes; pathophysiology and manifestations of acute versus chronic pancreatitis, pancreatic enzyme therapy in chronic pancreatitis; Just know the basic patho given in class and the enzymes that you would expect to see elevated in lab results Chronic pancreatitis  Exam 3 Study guide 9 a. Inflammation of pancreas – life threatening disorder 13. Elevated enzymes in lab results a. Serum bilirubin b. Serum and urinary amylase levels 14. Chronic pancreatitis: chronic or functional impairment of pancreas, most commonly associated with chronic alcohol abuse. a. Inflammation occurs over weeks to months b. Destruction of exocrine parenchyma and deposition of calcifications c. Toxic metabolites and chronic release of inflammatory cytokines contribute to destruction of acinar cells and islets of Langerhands à pancreatic parenchyma destroyed and replaced by fibrous tissues, strictures, calcification, ductal obstruction à cysts walled off areas or pockets of pancreatic juice, necrotic debris, or blood within or adjacent to pancreas 15. s/s: due to chronic inflammation and destruction Islets of Langerhans a. Diabetes, malabsorption→ weight loss, pain (upper left abdomen and radiates to back): n/v, flatulence, constipation, steatorrhea 16. Assessment: pain, GI complaints, stool characteristics, bleeding-positive Turner’s sign/Cullen’s sign 17. Medications: Pancrelipase (pancreatic enzyme replacement) Renal 1. Know the manifestations of kidney disease and the clinical significance of abnormal lab findings associated with renal/urinary dysfunction; UA o Amber, protein present o RBC > 3 = hematuria – bleeding in urinary system o WBC > 5 = infection/inflammation of urinary system o Casts > 0-few = kidney disease o Crystals = increased d/t infection/inflammation in urinary system Blood Test o BUN increased > 20 mg/dl = increased protein breakdown, decreased renal function, decreased renal perfusion o Creatinine > 1.5 mg/dl = renal impairment o CBC – decreased (decreased erythropoietin) - anemia o ABGs – metabolic acidosis o Electrolytes: § Increased potassium – hyperkalemia (kidney excretes K, increased levels = kidneys not working properly) § Decreased Na+ (water retention during late stages of renal failure)  Exam 3 Study guide 10 Blood cell, cast à upper infection à pyelonephritis Blood cell, crystals à lower infection à bladder 4. Study the causes and effects patho and clinical manifestations of obstruction in various locations within the urinary tract kidney stones (renal calculi); Causes o Familial genetics (inherited or shared diet) o Diet § High protein (purines - uric acid) – alcohol, canned, seafood, organ meat, salt, milk (excessive Ca++), animal fat, oxalate (collards, spinach, some tree nuts, black tea) o High mineral content water: “hard” (excessive CaSO4) or “soft” (NaCO3) water o Climate: high temp à dehydration à decreased urine volume and increased solutes in urine o Residents of SE US: high mineral content water, flimate, diet o pH of urine: “alkaline” (less soluble Ca++ and PO43-) or “acidic” (less soluble uric acid and cystine) o Alcohol: may promote purine production in body o Diseases: gout and UTI o Sedentary lifestyle, immobility à increases stasis o Lack of inhibitors in diet: citrate and magnesium prevent stone-forming particles from aggregating Theories for stone formation: o Saturation theory: stone formation occurs when there is supersaturation of one or more salts in the urine o Matrix theory: Mucopolysaccharides secreted by epithelial cells in kidney tubules act as a nidus for stone formation o Inhibitor theory: lack of stone inhibiting substances in urine increases the risk of stone formation Patho o Formation requires – supersaturated urine (w/ stone components), nidus (nucleus that facilitates crystal aggregation)  Exam 3 Study guide 11 Clinical manifestations o Calcium stone – calcium phosphate or calcium oxalate § Caused by hypercalciuria (excess calcium) o Struvite stone – composed of magnesium, ammonia, phosphate § Result of UTI à bacteria produces ammonia à struvite stone o Uric acid stone – cause by hyperuricosuria (gout, high purine diet) 5. Understand the etiology, infectious agents, manifestations, and complications of urinary tract infections. Also, be familiar with the defense mechanisms against urinary tract infections outlined in your lecture slides; Classified by: Location: Bladder (cystitis) Lower vs Upper urinary tract (pyelonephritis) Complicating factors: Uncomplicated vs Complicated UTI Etiology o UTI risk factors § Diabetes mellitus § Neurogenic bladder § Sexually active women § Diminished ureteral peristalsis (pregnant women) § Urinary obstruction (calculi, BPH) § Indwelling catheters § Urinary stasis (bacterial growth) § Vesicoureteral reflux of urine (congenital)  Exam 3 Study guide 12 § Bladder distension (caused by BPH, bladder cancer, or MS decreases blood flow→ ischemia of bladder tissue) all increase susceptibility of organism invasion Infectious agents, Manifestations  Exam 3 Study guide 13 Complications Defense mechanisms o Washout phenomenon: bacteria removed from bladder and urethra during voiding o Protective mucin layer: lines bladder and protects against bacterial invasion o Local immune responses: Normal phagocytic activity of bladder mucosa. Also, acid urine and urea produce hostile environment for bacteria o Ureterovesical junction competence: Prevents reflux of urine from bladder to ureters and kidneys (urine will leave the body) o Peristaltic movement by ureters: Facilitate movement of urine from renal pelvis through ureters and into bladder o Prostatic secretions (bacteriostatic) and Longer urethra in males 6. Know the etiology, pathophysiology, clinical manifestations, complications, treatment of glomerular disorders (glomerulonephritis, nephrotic syndrome); o Causes o Infection o Immunologic abnormalities (most common cause)  Exam 3 Study guide 14 o Drugs o Toxins o Systemic disorders (diabetes mellitus and lupus) Most common cause of CKD and end-stage renal failure Epithelial or podocyte layer of glomerular capillary is disturbed Clinical manifestations o Proteinuria o Hematuria o Edema o HTN (RAAS activation) o Oliguria from decreased GFR o Increased BUN and Cr 7. Differentiate between prerenal, intrarenal, and postrenal causes of acute renal failure; o Prerenal – caused by hypoperfusion from renal vasoconstriction, hypotension, hypovolemia (dehydration, hemorrhage), inadequate cardiac output (HF) o Decreased blood flow à decreased GFR à accumulate toxins (azotemia), oliguria o RAAS turns on – sodium and water retention – regulatory mechanism o Intrarenal – caused by functional and structural damage to the nephron o Tubular injury (acute tubular necrosis)  Exam 3 Study guide 15 § Postischemic: persistent hypoperfusion § Nephrotoxic: nephrotoxins (abx such as aminoglycosides, radiocontrast media, myoglobin – rhabdo, MSK injury, falls, heavy metals, bacterial toxins) à accumulate in renal cortex o Glomerular injury (glomerulonephritis) § Infectious event → immunologic process affects glomeruli → filtration abnormalities → hematuria, proteinuria o Postrenal – occurs from obstruction that affects kidneys bilaterally o Causes of Obstruction § Bilateral ureteral obstruction § Bladder outlet obstruction (ex: BPH, tumor, neurogenic bladder, urethral obstruction) SEE DRAWING IN NOTES 8. Discuss the clinical manifestations (including laboratory, urinalysis, and EKG findings), treatment, special considerations, age and clinical alerts, and complications of acute renal failure (acute kidney injury); use your “stages of AKI” slides (as a guide); and o LAB: Decrease GFR and azotemia, elevation BUN and Cr o UA  Exam 3 Study guide 16 o EKG o COMPLICATIONS o Oliguric stage o UOP falls below