Module 4 - the Digestive System D: Intestines, Bile, Liver (4/3 and 4/6 lectures)

small intestine

  • ~6-7m following the stomach

  • consists of duodenum, jejunum, ileum

duodenum basics

  • first part of the small intestine

  • related to L1-L3 vertebrae, partly to T12

  • 4 parts

    • 1st: superior

      • has common bile duct and duodenal cap

        • duodenal cap is site of ulcers

    • 2nd: descending (where the magic happens)

      • has major duodenal papilla

        • common opening for CBD and main pancreatic duct

        • in posteromedial wall

        • w/in wall, common opening dilates → forms ampulla of Vater

          • ampulla is surrounded by sphincter of Oddi

      • has minor duodenal papilla

    • 3rd: horizontal

    • 4th: ascending

  • functions:

    • digestion and absorption of food

      • digestion: enzymatic breakdown of nutrients into absorbable components

        • pancreas is most important source of digestive enzymes

        • peristalsis is stimulated, with pancreatic and gallbladder secretion, by endocrine cells of intestinal mucosa

    • regulate stomach and gallbladder emptying in response to chyme

    • secrete secretin → inhibits gastric acid secretion

      • due to high acid and fatty acids in lumen

    • secrete CCK in response to fatty chyme → induces gallbladder contraction

    • secrete enterogastrone → inhibits stomach peristalsis

  • epithelium has villi with capillaries inside

    • food content moves from lumen → epithelial cells → villi → nutrients get absorbed by capillaries → nutrients get released into portal system → liver

      • refresher: portal system is L gastric v., superior and inferior mesenteric vs., splenic v.

        • L gastric reabsorbs 10% of digested food/nutrients from stomach

        • sup. mesenteric reabsorbs from small intestine, cecum, ascending colon, R 2/3 of transverse colon

        • inf. mesenteric reabsorbs from L 1/3 of transverse colon, descending colon, sigmoid colon, upper rectum

        • splenic v. carries bilirubin, etc. from spleen → portal system

    • villi increase surface area available for absorption

small intestine motility

  • small intest. mixes nutrients with digestive enzymes, exposes digested nutrients to absorptive mucosa, propels non-absorbed material to large intestine

  • BER: basic electrical rhythm

    • set up by slow saves (12/min), like in stomach

    • APs occur on top of slow waves, lead to contraction

  • segmental contractions

    • contraction and relaxation of small ~1cm segments mixing chyme without net forward movement

    • occur ~8-12/min to create chopping/churning

  • propulsive contraction: peristalsis

    • net forward movement after digestion and absorption

    • runs 3-5cm over m. before fading

    • propels chyme toward large intestine

    • from pylorus to ileocecal valve (through whole small intestine): 3-5hrs

    • reflex is controlled by enteric NS

  • gastroileal reflex: presence of food in stomach triggers increased peristalsis in ileum and relaxation of IC sphincter

    • mediated by ANS and gastrin

ileocecal valve

  • sphincter between ileum and cecum (separates small and large intestines)

  • function: prevent backflow of fecal content into small intestine

  • normally closed (under tonus except after a meal)

    • relaxes by gastroileal reflex (by gastrin)

      • GI reflex also increases terminal ileal peristalsis

vomiting

  • a wave of reverse peristalsis beginning in small intestine

  • irritation and inflammation by bacteria, fungus, virus, autoimmune disease that causes irritation of GI tract (especially upper) → increased intrabdominal pressure → pushes up lower LES

    • retching occurs if upper esoph. sphincter remains closed

    • vomiting occurs if pressure in esoph. is great enough to open the UES

  • vomiting center: in medulla oblongata

    • stimulated by tickling the back of the throat, gastric distention, and vestibular stimulation (motion sickness)

  • chemoreceptor trigger zone in 4th ventricle

    • activated by emetics, radiation, vestibular stimulation

large intestine (colon) basics

  • ~1m long after small intestine, “framing” small intestine

    • connected to small intestine by ileocecal valve

  • parts: cecum, ascending colon, transverse colon, descending colon, sigmoid colon, rectum

  • 90% of fluid in fecal material is reabsorbed here

large intestine motility

  • similar to movement in small intestine, but to propel fecal material from cecum → colon

  • slow waves are pacemaker → segmental contraction → peristalsis

  • in cecum and proximal colon: when distended w/ feces, IC sphincter contracts to prevent reflux into ileum

    • segmental contractions in proximal colon mix contents

      • responsible for appearance of haustra

    • mass movements occur 1-3x/day

      • cause colonic contents to move distally for long distances

  • in distal colon: fecal material becomes semisolid

    • moves slowly because most water absorption occurs in proximal colon

    • moved to rectum by mass mvmts

  • defecation:

    • rectum fills w/ feces → contracts → internal anal sphincter relaxes

      • rectosphincteric reflex

    • rectum fills to ~25% capacity → urge to defecate

      • defecation is prevented because of external anal sphincter

        • under voluntary control, tonic contraction

    • to defecate: EAS relaxes (voluntary) → rectal smooth m. contracts → forces feces out of body

      • Valsalva maneuver: intra-abdominal pressure increases by expiring against a closed glottis

pancreas basics

  • elongated, pinkish, glandular accessory digestive gland

  • retroperitoneal, transverse btwn duodenum and spleen, posterior to stomach

  • has endocrine and exocrine function

    • endocrine function will be covered later (secretion of insulin, glucagon, somatostatin)

  • 4 parts: head, neck, body, tail

    • uncinate process is an extension of the lower part of the head

  • exocrine function: secretion of pancreatic enzymes for digestion

  • main duct opens into second part of duodenum by sphincter of Oddi

pancreatic secretion

  • pancreas has high [HCO3-]

    • purpose: neutralize acidic chyme reaching duodenum

  • contains enzymes essential for digestion of carbs, proteins, fat

  • composition/characteristics of secretion:

    • high volume

    • same [Na+ and K+] as plasma

    • much higher [HCO3] than plasma

    • much lower [Cl-] than plasma

    • isotonic

    • contains pancreatic lipase, amylase, proteases

  • secretion formation:

    • exocrine part resembles a bunch of grapes

    • acinar cells produce small V of initial secretion (mainly Na+ and Cl-)

      • cells make up most of the pancreas’s weight, despite producing small V

    • ductal cells modify initial secretion

      • secrete HCO3- and absorb Cl- via exchange mechanism in luminal membrane

    • ducts are water-permeable: water moves into lumen → makes secretion isosmotic

  • stimulation of secretion:

    • secretin

      • secreted by S cells in duodenum in response to H+ in duod. lumen

      • acts on pancreatic ductal cells to increase HCO3- secretion

        • in response to H+ content of chyme entering duod.

      • result: HCO3- is secreted from pancreas into duod. to neutralize HCO3-

    • CCK

      • secreted by I cells in duod. in response to small peptides, AAs, and fatty As in duod. lumen

      • acts on pancreatic acinar cells to increase enzyme secretion

        • amylase, lipases, proteases

    • ACh (by vagovagal reflexes)

      • released in response to H+, small peptides, AAs, and fatty As in duod. lumen

      • stimulates enzyme secretion by acinar cells, potentiates effect of secretin on HCO3- secretion

        • like CCK

      • note: both afferent and efferent fibers are by vagus n., hence vasovagal reflex name

bile

  • composition: bile salts, phospholipids, cholesterol, bilirubin (bile pigments)

    • bilirubin is product of damaged RBCs (Hb becomes bilirubin → gives greenish-yellowish color to bile)

  • function: emulsification of fats

  • formation: produced continuously by hepatocytes

    • 1* bile acids are synth. from cholesterol by hepatocytes

      • cholic acid, chenodeoxycholic acid

    • in intestine, bacteria convert a portion of each of 1* bile acids → 2* bile acids

      • deoxycholic acid, lithocholic acid

    • synth. of new bile acids occurs as needed to replace bile acids that get excreted in feces

    • bile acids conjugate w/ glycine or taurine → form bile salts (named for parent bile acid)

      • water-soluble → better than bile acids

      • e.g. taurocholic acid is cholic acid conjugated w/ taurine

    • electrolytes and water are added to bile

    • in interdigestive period: gallbladder relaxes, sphincter of Oddi is closed, gallbladder fills w/ bile

    • bile is concentrated in gallbladder as result of isosmotic absorption of solutes and water

    • bile and bile salts are essential to digestive and absorptive activity

    • bile and bile salts are vehicle for excretion of bilirubin and other waste products/toxins

  • drains into hepatic ducts, stored in gallbladder for release

gallbladder contraction

  • CCK

    • released in response to small peptides and fatty acids in duod.

    • informs gallbladder: bile is needed to emulsify and absorb lipids in duod.

    • causes contraction of gallbladder and relaxation of sphincter of Oddi

  • ACh

    • causes gallbladder contraction

bilirubin

  • damaged RBCs are accumulated by spleen

  • in spleen: damaged RBCs release Hb

  • Hb becomes biliverdin (green), still in spleen

  • biliverdin becomes unconjugated bilirubin, still in spleen

  • blood carries unconj. bilirubin to liver

  • in liver, glucoronic acid conjugates bilirubin

  • conjugated bilirubin moves into intestine, becomes urobilinogen

  • urobilinogen converts into stercobilinogen → oxidized to stercobilin (brownish color of feces)

    • or not converted → gets oxidized to urobilin (yellowish color of urine)

liver physiological anatomy

  • functional unit: liver lobule

    • liver has 50-100,000 lobules

  • cells are organized in plates and sinuses radiating out around a central vein → vein drains the lobule

    • bile canaliculi are btwn plates

    • 2 types of cells in plates: endothelial and Kupffer

  • lobule is fed blood from portal system and arteriole circulation

    • blood supply travels within fibrous septa that delineates lobule

  • bile canaliculi flow outward to bile ductules in septa

blood flow into liver

  • blood flow into liver is ~1450ml/min

    • portal v. carries 1100ml/min

    • hepatic a. carries 350-ml/min

  • blood flow into liver

    • filtration: harvest/sequestering of nutrients, and screen/filter for bacterial

    • portal blood shows colonic bacteria, systemic blood doesn’t

    • Kupffer cells: specialized macrophages that ingest bacteria in 1/100th second → liver can effectively screen >99% of bacteria in blood during transit through liver

liver metabolic functions

  • regarding carbs: glycogen storage, gluconeogenesis, glycogenolysis, glycogenesis, breakdown of insulin and other hormones

  • storage of vitamins

    • stores A for 10 months, D for 3-4 months, B12 for 1 yr

  • formation of plasma proteins: coagulation proteins

    • synth of 7 clotting proteins: prothrombin, factors VII, IX, and X, protein S, protein Z (accelerator globulin)

      • vit K is required^

  • erythropoietin formation

  • storage of iron

  • removal/excretion of drugs, hormones

    • detox/excrete many drugs via bile

      • sulfonamides, penicillin, ampicillin, erythromycin

    • hormones and metabolites are reduced and excreted (thyroxine, steroids)

      • e.g. estrogen, cortisol, aldosterone

    • excess plasma Ca2+ is excreted via bile

clinical points (including pathologies)

  • how to tell difference btwn rectum and sigmoid colon: color, tenia coli on intestine but not on rectum, blood supply

  • refresher: main abdominal blood supply

    • abdominal aorta → 3 branches: celiac, superior mesenteric, inferior mesenteric as.

    • celiac a. → L gastric, splenic, common hepatic, hepatopancreatic as., and a tiny branch to upper duodenum

    • superior mesenteric supplies lower duodenum, jejunum, ileum, appendix, cecum, ascending colon, R 2/3 of transverse colon

    • inferior mesenteric supplies L 1/3 of transverse colon, descending colon, sigmoid colon, and upper rectum

  • blood supply of rectum:

    • superior rectal a. (a branch of superior mesenteric)

    • middle and inferior rectal as. are branches of iliac a. (direct and indirect)

  • jaundice: high bilirubin content → yellow tint to skin

    • normal level is 0.5mg/dl, jaundice occurs at 1.5mg/dl

    • human can survive 40mg/dl

    • common causes:

      • increased RBC lysis → hemolytic jaundice

      • blockage of bile duct or liver damage → blocked bilirubin excretion to GI → obstructive jaundice

  • gallbladder pathologies

    • cholelithiasis: gall stones

      • formed due to imbalance in [cholesterol and bile salts] in bile

      • bile salts are no longer in suspension → salts or cholesterol precipitate

    • acute cholecystitis: acute inflammation of gallbladder wall

      • usually due to cystic duct obstruction by a gallstone

      • bile accumulates in gallbladder → enlargement, pain in epigastric and R hypochondriac in transpyloric line

      • pain, nausea, vomiting, involuntary muscle guarding, painful splinting of respiration during deep inspiration in palpation of R upper quadrant

        • Murphy’s sign

    • treatment: cholecystectomy

      • removal of gallbladder due to severe biliary colic

        • e.g. cystic duct obstruction, cholecystitis, etc

  • liver damage can cause a buildup of toxins/hormones/metabolites in the liver → lead to toxicity or hyperactivity

    • not the same as overdose or overproduction, but can make Pts more prone to overdose?

  • liver pathologies

    • jaundice: a sign of liver damage because of lack of storage of bilirubin → builds up in blood

    • hepatitis: inflammation of liver

      • caused mainly by various viruses

      • can be caused by some poisons, autoimmunity, hereditary conditions

    • cirrhosis: formation of fibrous tissue in liver → replaces dead liver cells

      • death of liver cells can be caused by viral hepatitis, alcoholism, or contact w/ other liver-toxic chemicals, e.g.

      • liver cannot receive lots of blood from portal system → backflow of blood into portal system → portal hypertension

    • hemochromatosis: accumulation of iron in body → liver damage

      • hereditary

    • cancers

      • primary hepatocellular carcinoma, cholangiocarcinoma, or metastatic cancers

        • usually from other parts of GI tract

    • Wilson’s disease: body retains copper

      • hereditary

clinical cases

  • A surgeon removes a pt’s entire duodenum because of a tumor. What are side symptoms post-op?

    • lack of I cells → lack of CCK → lack of bile released from gallbladder, sphincter of Oddi will not relax

    • lack of S cells → lack of secretin

    • malabsorption

    • early gastric emptying with fatty chyme

    • oversecretion of gastric acid → gastritis

  • What happens if we have no closure of upper esoph. sphincter?

    • vomiting, not retching, if vomiting center is stimulated

    • dysphagia

    • gastric reflux → retrosternal pain

    • possible weight loss later on due to malabsorption and dysphagia

      • ^but this symptom is not acute

  • If there is congenital closure of pyloric sphincter, what will happen to pt?

    • malabsorption, lack of digestion

    • increased risk of gastritis → risk for gastric ulcers if left untreated

    • accumulation of food in stomach → severe abdominal pain, maldigestion, malabsorption, constipation

    • nonbilious vomit