Shelbye's CSON Notes Blog



Gastrointestinal A&PFunction:Mechanical & chemical breakdown of foodAbsorption of nutrientsGI tract: Hollow tube from mouth to anusMouth:Breakdown begins w/chewing + salivation (α-amylase→CHO digestion)Esophagus:Transports bolus via swallowingOropharyngeal (voluntary)Esophageal (involuntary)Lower esophageal sphincter (opens to allow food into stomach; closes to prevent regurgitation into esophagus)Stomach:Secretes digestive juices + HCL + pepsinMixes/stores food; propels chyme into duodenum via peristalsisGastrointestinal A&PSmall intestine: (5 meters long!)Duodenum→Receives chyme through pyloric sphincter→bile (fats) + pancreatic enzymes (proteins, CHOs, fats) + intestinal enzymes (proteins, CHOs, fats)Jejunum→Sugars & proteins absorbedIleum→Bile salts, Vit B12, chloride absorbedLarge intestine: (“leftovers” enter via ileocecal valve)Cecum, appendix, colon (ascending, transverse, descending, sigmoid), rectumWhen Things Go Wrong—GI DisordersMotility disordersGastritisPeptic ulcer diseaseMalabsorption syndromesInflammatory bowel diseaseAppendicitisVascular insufficiencyDisorders of nutritionMotility DisordersA)Dysphagia Difficulty swallowingCauses:Mechanical obstruction of esophagus (tumors inside or outside, strictures, diverticular herniations)Impairment of esophageal motility (CVA, Parkinson disease, achalasia)Achalasia: nerve dysfunction→failure of muscular ring at end of esophagus to relax→lower esophagus becomes distendedIn a condition called?achalasia, the lower esophageal sphincter fails to relax; food that has been swallowed has difficulty passing into the stomach, and the esophagus above the lower esophageal sphincter becomes enlarged. One or several meals may lodge in the esophagus and pass slowly into the stomach over time. There is danger of aspiration of esophageal contents into the lungs when the person lies downB) Gastroesophageal RefluxReflux of chyme into esophagus from the stomachCommon symptom: “Heartburn”If long term→esophageal inflammation & erosion→fibrosis & thickeningCauses: Obesity, smoking, delayed gastric emptying (ulcers, pyloric stricture, hiatal hernia)C) Hiatal HerniaPotrusion of ↑ stomach thru diaphragmSliding (congenital, short esophagus, trauma, weak diaphragm muscles)S/S: GER, esophagitisParaesophageal(curvature of stomach herniates alongside of esophagus)S/S: Discomfort after eating, dysphagiaD) Pyloric ObstructionNarrowing / blocking of pyloric sphincterCongenital Acquired (PUD, carcinoma of pylorus)S/S: (early) vague epigastric fullness—worse after meals & late in day; nausea; epigastric painS/S: (late) gastric distention; vomiting; infrequent, small stoolsE) Intestinal ObstructionSimple: mechanical blockageAcute: Torsion, intussusception, herniationChronic: Tumor, inflammatory disorderFunctional: ↓ motility (Ex—paralytic ileus)S/S: “Colicky” pain + vomitingMay become necrotic, perforate → peritonitis (infection)2) GastritisInflammation of gastric mucosaAcute: Erosions usually superficial. Acute gastritis refers to a transient inflammation of the gastric mucosa. It’s most commonly associated with local irritants such as bacterial endotoxins, alcohol, and aspirin. Cause: Chemicals, drugs (NSAIDS)S/S: Vague abdominal discomfort; epigastric tenderness; BLEEDING (bleeding and hematemesis are associated with alcohol consumption, vauge s/s associated with NSAID use)Chronic: Age=thinning/degeneration of stomach wall=loss of chief & parietal cells→ ↓ acid→ ↑ gastrin in plasma→ pernicious anemia (↓Vit. B12 absorbed). It’s characterized by the absence of grossly visible erosions and the presence of chronic inflammatory changes leading eventually to atrophy of the glandular epithelium of the stomach.Cause: ?Autoimmune, H. pylori3) Peptic Ulcer DiseaseBreak / ulceration in protective mucosal lining of stomach, duodenumSubmucosa exposed to gastric secretions → autodigestion↑ Risk: Smoking, ↑ age, NSAIDS, alcohol, H. pylori, chronic diseasesGastric/Duodenal UlcersCauses:NSAIDS→ inhibits prostaglandins + ↓mucus productionH. pylori→ stimulates gastrin production→ ↑acid production/ulcer formation S/S: Chronic intermittent pain relieved by food intake/antacid use; 1st clinical manifestation may be hemorrhage / perforation4) Malabsorption SyndromesInterfere with nutrient absorption in small intestinePancreatic insufficiency→ Deficient production of pancreatic enzymes (affects digestion of proteins, CHO, fats)Lactase deficiency→ Lactose not broken down Bile salt deficiency→ Fats not digested / absorbed5) Inflammatory Bowel DiseaseUlcerative colitis—chronic, inflammatory→ulceration of mucosa in colon (usually in sigmoid & rectum)Crohn disease—inflammatory, affects both small & large intestine (rectum is seldom involved)Diverticular disease—herniations / saclike outpouchings of mucosa thru muscle layers (usually wall of sigmoid colon)6) AppendicitisInflammation of vermiform appendixMost common surgical emergency of abdomenGenerally 20-30 years of age (can happen at any ageCause: ?obstruction of lumen w/stool, foreign bodies, tumors → bacterial infectionObstruction → appendix can’t drain → ↑pressure → appendix becomes hypoxic → mucosa ulcerates → bacteria invasion → inflammation → gangrene → perforation 7) Vascular InsufficiencyGastrointestinal system extremely vascularAtherosclerotic lesions, emboli, thrombi can occlude blood flow anywhereChronic mesentary insufficiency can develop as result of cardiovascular disorders—cardinal s/s: Colicky abdominal pain after eating8) Disorders of NutritionObesityComplex disorderNumerous theoriesIncreases risk for CAD, DM, gallstones, HTN, CVD; breast/cervical/endometrial/ liver CA in women; prostate/colon/rectal CA in menAnorexia nervosa / bulimia nervosaPsychologic syndromesStarvation—short-term vs long-termLiver, GB, Pancreas A&P ReviewContribute enzymes, bile, hormonesAll three organs vital to digestionDeliver secretions to the duodenum through duct systemLiver StructureLargeHighly VascularEnclosed in upper right abdomenLiver has blood supply from the heart and from the GI tract. GI tract blood supply provides the nutrients and low oxygenated bloodGlisson capsule covers liver (blood vessels, lymphatics, nerves) When the liver is diseased or swollen, distention of the capsule causes pain et the lymphatics may ooze fluid into the peritoneal space Hepatic artery (oxygenated blood)from the heartPortal vein (some oxygen + nutrients)from the GI tractLiver lobules – smaller anatomic unitsMetabolic functions of the liver require a large amount of blood. The liver receives blood from both arterial and venous sources. The hepatic artery branches from the abdominal aorta and provides oxygenated blood (400-500ml/min). The hepatic portal vein, which receives blood from the inferior and superior mesenteric veins and the splenic vein, delivers about 1000-1200ml/min to the liver. Portal venous blood constitutes 70% of the blood supply to the liver. This blood carries some oxygen and is rich in nutrients that have been absorbed from the digestive tract.Hepatocytes “plates” (functional cells of liver) – can regenerate, therefore damaged or resected liver tissue can regrow Sinusoids (capillaries between plates of hepatocytes) – located between the plates of hepatocytes, receive mixture of arterial and venous blood from branches of the hepatic artery and portal vein. Blood from the sinusoids drains to a central vein in the middle of each lobule. Venous blood from all the lobules then flows into the hepatic vein, which empties into the IVCKupffer cells (mononuclear phagocyte system) immunity cellsThe sinusoids of the liver lobules are lined with highly permeable endothelium. This permeabilityenhances the transport of nutrients from the sinusoids into the hepatocytes, where they aremetabolized. The sinusoids are also lined with phagocytic Kupffer cells, which are part of the mononuclear phagocyte system.These Kupffer cells remove foreign substances from the blood and trap bacteria. Disse space (hepatic lymph system) drainage Between the endothelial lining of the sinusoid and the hepatocyte is the Disse space, which drains interstitial fluid into the hepatic lymph system.Bile canaliculi (channels that conduct bile to bile ducts)Common bile duct >Sphincter of Oddi Liver FunctionPerforms numerous complex & important functionsMany related to digestion & nutritionA large, highly vascular organ, the liver is enclosed in a fibrous capsule in the upper right area of the abd. The liver performs numerous complex and important functions, many of which are related to digestion and nutritionLiver Function #1Filters/detoxifies bloodMetabolic detoxification / biotransformation (cuts down reabsorption of potentially toxic substances, then facilitates their excretions through the intestines or kidneysAlchohol, barbiturates, amphetamines, steroids and hormones (estrogens, aldosterone, ADH, testosterone) are metabolized, preventing excessive accumulation and AE Alters chemicals to make less toxic, or biologically active *****However, sometimes the end products of this process themselves can become toxins. For example, end products of alcohol metabolism are acetaldehyde and hydrogen. Excessive alcohol intake over a prolonged period causes these end products to damage hepatocytes. Acetaldehyde (poison) damages cellular mitochondria, and the excess hydrogen promotes fat accumulation. This is how alcohol impairs the liver’s ability to function. Diminishes intestinal reabsorption Diminishes renal tubular reabsorption Liver Function #2Removes ammonia from body fluidsProcess called deamination (amino acids converted to carbohydrates, or ketoacids, by removal of ammonia)Converts to urea, then passes into the bloodExcreted in urineLiver Function #3Produces bileContains bile salts, bilirubin, etc. Emulsifies fats Helps in absorption of fatsThe liver secretes 700 to 1200 ml of bile per day. Bile contains bile salts, cholesterol, bilirubin, electrolytes, water.It is formed by hepatocytes & secreted into the canaliculi. Bile salts (conjugated bile acids), are needed for emulsifying and absorption of fats. After this work is done, most bile salts are actively absorbed in the terminal ileum and returned to the liver through the portal circulation for resecretion.This recycling of bile salts is called the enterohepatic circulation.Conjugation, or binding of bile acids with amino acids, makes the bile acids more water soluble, thus keeping them from being diffused in the duodenum & ileum.Intestinal bacteria will deconjugate some bile salts back into bile acids (secondary bile acids). These acids diffuse passively into the portal blood from both small & large intestines. An increase in the plasma concentration of bile acids accelerates the uptake and resecretion of bile acids and salts by the hepatocytes. The cycle of hepatic secretion, intestinal absorption, and hepatic resecretion of bile acids completes the enterohepatic circulation.Bile secretion is called choleresis. A choleretic agent stimulates the liver to secrete bile. One strong stimulus is a high concentration of bile salts. Other choleretics include secretin, which increases the rate of bile flow by promoting the secretion of bicarbonate from canaliculi and other intrahepatic bile ducts; cholecystokinin; and vagal stimulation. See Figure 29-4, p. 636 in Porth Liver Function #4Produces plasma proteinsAlbumins and globulins (synthesized by liver) Maintains blood volume & pressureSynthesizes nonessential amino acids (tested with liver function test)AST, ALT, LDH, alkaline phosphatase Can store vitamin A for several yearsLiver Function #5Plays important role in carbohydrate metabolismReleases glucose during hypoglycemiaTakes up glucose during hyperglycemiaThe liver MANAGES (contributes to the stability of blood glucouse leves by releasing glucose during times of low blood sugar and taking up glucose during time of high blood sugar Liver Function #6Converts glucose to glycogenGlyconeogenesisStores it for fuel for musclesOr, converts glucose to fatCan convert amino acids & glycerol to glucoseGluconeogenesisLiver Function #7Stores essential nutrientsIron (as ferritin) & copper – released as needed for red blood cell production Vitamin B12 & D—stores for several monthsVitamin A – stores for several years Vitamins E & KThe liver stores these and in times of excessive intake and releases them in times of need Liver Function #8Stores fats – synthesized from carbs and proteinFat absorbed by lacteals in the intestinal villi enter the liver through the lympatics, primarily as triglycerides. Triglycerides can be hydrolyzed to glycerol and free fatty acids and used to produce ATP (for cellular use) Converts excess sugars to fats – Stored in adipose tissueLiver Functions #9, #10, #11Storage of large volumes of bloodRemoval of bacteria & foreign particlesSynthesizes prothrombin, fibrinogen, factors I, II, VII, IX, XBecause of its extensive vascular network, the liver can store a large volume of blood. The amount stored at any one time depends on pressure relationships in the arteries and veins. The liver also can release blood to maintain systemic circulatory volume in the event of hemorrhage.Kupffer cells in the sinusoids of the liver remove bacteria and foreign particles from the portal blood. Because the liver receives all the venous blood from the gut and pancreas, the Kupffer cells play an important role in destroying intestinal bacteria and preventing infections.The liver also has hemostatic functions. It synthesizes prothrombin, fibrinogen, and factors I, II, VII, IX, and X, all of which are necessary for effective clotting. Vitamin K, a fat-soluble vitamin, is essential for the synthesis of other clotting factors. Because bile salts are needed for reabsorption of fats, vitamin K absorption depends on adequate bile production in the liver. Liver Function #12Metabolism of bilirubin By-product of destruction of old rbc’s Gives bile greenish black colorProduces yellow tinge of jaundiceSee Handouts re: Enterohepatic circulation of bile salts & Bilirubin MetabolismLiver DisordersViral hepatitisFulminant hepatitis Alcoholic cirrhosisBiliary cirrhosisViral hepatitisRelatively commonAffects primarily the liverAll five types (A, B, C, D, E) can cause acute, icteric (jaundice) illnessPathologic lesions similar to other viral infections (“you’ve seen one…”)Hepatic cell necrosisKupffer cell hyperplasiaInfiltration by mononuclear phagocytes (varying severity)An inflammatory processCan damage/obstruct bile canaliculiLeads to cholestasis & obstructive jaundiceIn milder cases, liver parenchyma (functional tissue) not damagedDamage tends to be most severe in Hep B & Hep CHep B can result in acute fulminating hepatitisWide spectrum of manifestationsAbsence of symptoms→fulminating hepatitis with liver failure & comaCauses abnormal liver function test results: ↑serum aminotransferase, ↑AST, ↑ALTAST = aspartate transaminase ALT = alanine transaminase Clinical course:Prodromal phase—begins @ 2 weeks post exposure; ends w/appearance of jaundiceClinical (Icteric) phase—begins 1-2 weeks after prodromal phase; lasts 2-6 weeksRecovery phase—begins w/resolution of jaundice, @ 6-8 weeks post exposureViral hepatitis—Clinical ManifestationsProdromal phase:Appearance of jaundiceFatigue / malaise (caused by systemic effects of liver inflammation) Anorexia (caused by systemic effects of liver inflammation on the GI system) Nausea/vomitingArthralgia / Myalgia HeadacheChanges in sense of taste and smell Hyperalgia (extreme sensitivity to pain)CoughLow-grade feverClinical phase:(actual phase of illnesss)Worsening of all symptoms of the prodromal stageJaundiceItching Dark urineClay-colored stoolsEnlarged, smooth liver Liver tender, painful to percussionRecovery phase:Begins w/resolution of jaundiceSymptoms diminishLiver remains enlarged/tenderLiver function returns to normalViral hepatitis--ComplicationsChronic active hepatitis (if it happens at least twice)CirrhosisHepatic failure & deathPrimary hepatocellular carcinomaFulminant hepatitisClinical syndromeResults in severe liver impairment / necrosis of liver cellsHigh potential for liver failureMay occur as complication of:HCV infectionHBV infectionCombination HBV / HDV infectionRarely occurs with HAV infectionsMay also occur as a result of:Toxic reactions to drugs (eg. Tylenol)Congenital metabolic disordersClinical course:Develops 6-8 weeks post initial symptomsMany of same symptoms + ascites & GI bleedHepatic encephalopathyHepatic necrosis irreversible, 60% to 90% dieAcute liver failure usually develops within 6-8 weeks after the initial symptoms of viral hepatitis or a metabolic liver disorder. Anorexia, vomiting abdominal pain, & progressive jaundice are initial signs, followed by ascites & GI bleed. Hepatic encephalopathy is manifested as lethargy, altered motor functions, and coma & is related to cerebral edema, ischemia, & brain stem herniation. Liver function tests show elevations of both direct & indirect serum bilirubin, serum transaminases, & blood ammonia. Prothrombin time (PT) is prolonged. Renal failure & pulmonary distress can occur.Antiviral reverse transcriptase inhibitors are available to treat chronic hepatitis B or C. Treatment of acute liver failure is supportive. The hepatic necrosis is irreversible, & 60% to 90% of affected children die. Liver transplantation may be lifesaving & should be considered early. It’s amazing, but survivors usually do not develop cirrhosis or chronic liver disease.CirrhosisChronic liver disease—develops slowlyWidespread destruction of hepatic cells + collapse of supporting structureReplaced by fibrous cellsLiver develops “cobbly” appearanceCirrhosis is a chronic liver disease. It’s characterized by widespread destruction of hepatic cells, which are replaced by fibrous cells. This process is called fibrotic regeneration. Cirrhosis is a common cause of death in the U.S. It’s twice as common in men as in women, and is especially prevalent among malnourished persons over age 50 with chronic alcoholism. Mortality is high; many patients die within 5 years of onset.IT’S INTERESTING TO ME THAT DEATHS FROM ALCOHOL-RELATED LIVER DISEASE HAVE INCREASED OVER THE LAST DECADE. HOWEVER, HIGH ALCOHOL CONSUMPTION AMONG WOMEN LEADS TO EARLIER & MORE SEVERE CIRRHOSIS. ALTHOUGH ALCOHOLIC CIRRHOSIS IS THE MOST PREVALENT OF THE DIFFERENT TYPES OF CIRRHOSIS, THE OCCURRENCE OF CIRRHOSIS AMONG PERSONS WITH ALCOHOLISM IS RELATIVELY LOW (@25%).Cirrhosis--TypesClassified by “cause” (See Handout of Cirrhosis of the liver) Most common:Laennec’s (also called alcoholic, portal, fatty cirrhosis)PostnecroticBiliaryMetabolicAlcoholic (Laennec’s) cirrhosisAlcohol transformed into acetaldehydeExcessive acetaldehyde:↓hepatocyte function↓oxidation of fatty acids↓enzyme/protein synthesis↓ammonia breakdown↓proteins leaving liver (albumin…)↓metabolism of vitamins/minerals (malnutrition)Damage to hepatocytes leads to:Inflammatory responseResults in excessive collagen formationFibrosis/scarring alter liver structureLeads to bile canaliculi/duct obstructionAs well as sinusoid (capillary) obstructionAlcoholic cirrhosis (Cont’d)Begins with fatty liver↑Lipogenesis ↓Fatty acid oxidationPossible mobilization of lipids from adipose tissueFatty accumulation reversible w/cessation of alcohol consumption Fibrosis/liver damage irreversibleAlcoholic cirrhosis—symptomsEnlarged liver (initially—fatty infiltrationMany of same s/s of hepatitis (fatigue, anorexia, nausea, etc)Later s/s—ascites, esophageal varices, testicular atrophy, splenomegalyPostnecrotic cirrhosisDevelops from chronic hepatitisExposure to arsenic, carbon tetrachloride, other toxinsMore common in womenMost common type worldwideBiliary cirrhosis (primary)Damage begins in bile canaliculi / bile ducts (inflammation, then destruction)Primary—idiopathic (we don’t know why)Pruritis/hyperbilirubinemia/jaundice→light-colored stools → cirrhosis → portal hypertension→encephalopathy Biliary cirrhosis (primary) Affect women & those > 30 years old. Life expectancy is 5-10 years after onset of symptoms.Disease specific antibodies can be detected—Antiretroviral treatment is being tried—Liver transplant is very effective– Biliary cirrhosis (Secondary)Prolonged obstruction of bile duct branches / common bile ductSecondary biliary cirrhosis can be caught and managed by endoscopic removal of stones/stent placement, or by surgery GallstonesTumorsChronic pancreatitisFibrotic strictureCystic fibrosis (children)Biliary atresia (children)Metabolic cirrhosisMetabolic diseases can lead to cirrhosis:Wilson’s disease (copper not being excreted in the bile)Alpha?-antitrypsin (hereditary disease, not putting out alpha1 antitrypsin)Hemochromatosis (iron overload) Portal HypertensionCause: Any disorder that slows (impedes) or blocks (obstructs) blood flow through any part of portal venous systemCan result from:Inflammation (hepatitis, etc.)Fibrosis of sinusoids (cirrhosis)Thrombosis (blood clots)Long-term portal hypertension causes:Ascites Varices (esophageal, gastric, rectal)Splenomegaly Hepatic encephalopathy ................
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