gastrointestinal physiology Flashcards
Normal gastrointestinal embryology
Foregut—esophagus to upper duodenum.
Midgut—lower duodenum to proximal 2 /3 of transverse colon.
Hindgut—distal 1 /3 of transverse colon to anal canal above pectinate line.
Midgut development:
. 6th week—physiologic midgut herniates through umbilical ring
. 10th week—returns to abdominal cavity + rotates around superior mesenteric artery (SMA),
total 270° counterclockwise
Ventral wall defects-Developmental defects due to failure of rostral fold closure (eg, sternal defects [ectopia cordis]), lateral fold closure (eg, omphalocele, gastroschisis), or caudal fold closure (eg, bladder exstrophy).
Gastroschisis-
Etiology-Extrusion of abdominal contents through
abdominal folds (typically right of umbilicus
coverage- Not covered by peritoneum or amnion; “the
abdominal contents are coming out of the Ǥ ”
Assoication- Not associated with chromosome abnormalities
Omphalocele-
Etiology- Failure of lateral walls to migrate at umbilical
ring –>persistent midline herniation of
abdominal contents into umbilical cord
coverage- Surrounded by peritoneum (light gray shiny
sac); “abdominal contents are seal ed in the Ɵ ”
Association- Associated with congenital anomalies (eg,
trisomies 13 and 18, Beckwith-Wiedemann
syndrome) and other structural abnormalities
(eg, cardiac, GU, neural tube)
NOTE:
Congenital umbilical hernia-Failure of umbilical ring to close after physiologic herniation of the intestines. Small defects usually close spontaneously.
Tracheoesophageal anomalies- Esophageal atresia (EA) with distal tracheoesophageal fistula (TEF) is the most common (85%) and often presents as polyhydramnios in utero (due to inability of fetus to swallow amniotic fluid). Neonates drool, choke, and vomit with first feeding. TEFs allow air to enter stomach (visible on CXR). Cyanosis is 2° to laryngospasm (to avoid reflux-related aspiration). Clinical test: failure to
pass nasogastric tube into stomach
In H -type, the fistula resembles the letter H . In pure EA, CXR shows gasless abdomen.
intestinal atresia
hypertrophic pyloric stenosis
pancreas and spleen embryology
Intestinal atresia-
Presents with bilious vomiting and abdominal distension within first 1–2 days of life.
Duodenal atresia —failure to recanalize. Associated with “double bubble” (dilated stomach,
proximal duodenum) on x-ray A). Associated with Down syndrome.
Jejunal and ileal atresia —disruption of mesenteric vessels –> ischemic necrosis –> segmental
resorption (bowel discontinuity or “apple peel”).
Hypertrophic pyloric stenosis-
Most common cause of gastric outlet obstruction in infants (1:600). Palpable olive-shaped mass in
epigastric region, visible peristaltic waves, and nonbilious projectile vomiting at ∼ 2–6 weeks old.
More common in firstborn males; associated with exposure to macrolides. Results in hypokalemic
hypochloremic metabolic alkalosis (2° to vomiting of gastric acid and subsequent volume
contraction). Ultrasound shows thickened and lengthened pylorus A . Treatment is surgical
incision (pyloromyotomy).
Pancreas—derived from foregut. Ventral pancreatic buds contribute to uncinate process and main
pancreatic duct. The dorsal pancreatic bud alone becomes the body, tail, isthmus, and accessory
pancreatic duct. Both the ventral and dorsal buds contribute to pancreatic head.
Annular pancreas—abnormal rotation of ventral pancreatic bud forms a ring of pancreatic tissue
encircles 2nd part of duodenum; may cause duodenal narrowing (arrows in A ) and vomiting.
Pancreas divisum—ventral and dorsal parts fail to fuse at 8 weeks. Common anomaly; mostly
asymptomatic, but may cause chronic abdominal pain and/or pancreatitis.
Spleen—arises in mesentery of stomach (hence is mesodermal) but has foregut supply (celiac trunk
–> splenic artery).
Retroperitoneal structures-structures that lack a mesentery. injuries to these structres can cause blood or gas accumulation in retroperitoneal space
SAD PUCKER
Suprarenal (adrenal) glands [not shown]
Aorta and IVC
Duodenum (2nd through 4th parts)
Pancreas (except tail)
Ureters [not shown]
Colon (descending and ascending)
Kidneys
Esophagus (thoracic portion) [not shown]
Rectum (partially) [not shown]
Important gastrointestinal ligaments
Falciform ligament-
connect-Liver to anterior abdominal wall
Structure contained- Ligamentum teres hepatis (derivative of fetal umbilical vein), patent paraumbilical veins
Notes: Derivative of ventral mesentery
Hepatoduodenal ligament
connect- Liver to duodenum
Structures contained- Portal triad: proper hepatic artery, portal vein, common bile duct
NOTE: Pringle maneuver—ligament may be compressed between thumb and index finger
placed in omental foramen to control bleeding
- Borders the omental foramen, which connects the greater and lesser sacs
- Part of lesser omentum
Gastrohepatic ligament
connects- Liver to lesser curvature of
stomach
structures contained: Gastric vessels
NOTE: Separates greater and lesser sacs on the right
-May be cut during surgery to access lesser sac Part of lesser omentum
Gastrocolic ligament (not shown)
connect- Greater curvature and transverse colon
structures contained- Gastroepiploic arteries
NOTE: Part of greater omentum
Gastrosplenic ligament
connects- Greater curvature and spleen
structures contained- Short gastrics, left gastroepiploic vessels
NOTE: Separates greater and lesser sacs on the left
-Part of greater omentum
Splenorenal ligament
connects- Spleen to posterior abdominal wall
structures contained: Splenic artery and vein, tail of pancreas
Digestive tract anatomy
Layers of gut wall (inside to outside—MSMS ):
.M ucosa—epithelium, lamina propria, muscularis mucosa
. S ubmucosa—includes S ubmucosal nerve plexus (Meiss ner), S ecretes fluid
.M uscularis externa—includes M yenteric nerve plexus (Auerbach), M otility
. S erosa (when intraperitoneal), adventitia (when retroperitoneal)
Ulcers can extend into submucosa, inner or outer muscular layer. Erosions are in the mucosa only.
Digestive tract histology
Esophagus-Nonkeratinized stratified squamous epithelium. Stomach Gastric glands.
Duodenum-Villi and microvilli increased absorptive surface.
Brunner glands (HCO3−-secreting cells of submucosa) and crypts of Lieberkühn (contain stem cells
that replace enterocytes/goblet cells and Paneth cells that secrete defensins, lysozyme, and TNF).
Jejunum- circulares (also present in distal duodenum) and crypts of Lieberkühn.
Ileum-Peyer patches (lymphoid aggregates in lamina propria, submucosa), plicae circulares (proximal ileum), and crypts of Lieberkühn.
Largest number of goblet cells in the small intestine.
Colon-Crypts of Lieberkühn but no villi; abundant goblet cells.
Abdominal aorta and branches
Arteries supplying GI structures are single andbranch anteriorly.
Arteries supplying non-GI structures are pairedand branch laterally and posteriorly.
Superior mesenteric artery syndrome— characterized by intermittent intestinal obstruction symptoms (primarily postprandial pain) when SMA and aorta compress transverse (third) portion of duodenum. Typically occurs in conditions associated with diminished mesenteric fat (eg, low body weight/malnutrition).
Two areas of the colon have dual blood supply from distal arterial branches (“watershed regions”) –> susceptible in colonic ischemia:
. Splenic flexure—SMA and IMA
. Rectosigmoid junction—the last sigmoid arterial branch from the IMA and superior rectal artery
Gastrointestinal blood supply and innervation
Foregut is supplied by celiac artery, parasympathetic innervation was vagus, vertebral level at T12/L1, structures supplied- pharynx (vagus nerve only) and lower esophagus (celiac artery only) to proximal duodenum; liver, gallbladder, pancreas, spleen (mesoderm)
Midgut is supplied by SMA, vagus at L! and supplies distal duodenum to proximal 2/3 of transverse colon
Hindgut- is supplied by IMA and pelvic nerve for parasympathetic innervation at L3 supplying structures like the distal 1/3 of transverse colon to upper portion of rectum
Branches of celiac trunk: common hepatic, splenic, and left gastric. These constitute the main blood supply of the stomach.
Strong anastomoses exist between:
. Left and right gastroepiploics
. Left and right gastrics
Posterior duodenal ulcers penetrate gastroduodenal artery causing hemorrhage.
Anterior duodenal ulcers perforate into the anterior abdominal cavity, potentially leading to
pneumoperitoneum
Portosystemic anastomoses
site of anastomosis: Esophagus clinical sign: Esophageal portal-> symstemic: varices Left gastric ↔ azygos
site of anastomosis: Umbilicus Clinical sign: Caput medusae portal–> systemic: Paraumbilical ↔ small epigastric veins of the anterior abdominal wall.
site of anastomosis: Rectum Clinical sign: Anorectal varices Portal–> systemic: Superior rectal ↔ middle and inferior rectal
The functional unit of the liver is made up of hexagonally arranged lobules surrounding the central vein with portal triads on the edges (consisting of a portal vein, hepatic artery, bile ducts, as well lymphatics
Apical surface of hepatocytes faces bile canaliculi. Basolateral surface faces sinusoids
Kupffer cells, which are specialized macrophages, are located in the sinusoids
Hepatic stellate (Ito) cells in space of Disse store vitamin A (when quiescent) and produce extracellular matrix (when activated). Responsible for hepatic fibrosis
Zone I—periportal zone:
. Affected 1st by viral hepatitis
. Ingested toxins (eg, cocaine)
Zone II —intermediate zone:
. Yell ow fever
Zone III—pericentral vein (centrilobular) zone:
. Affected 1st by ischemia
. High concentration of cytochrome P-450
. Most sensitive to metabolic toxins (eg,
ethanol, CCl4 , halothane, rifampin)
. Site of alcoholic hepatitis
Biliary structures
Gallstones that reach the confluence of the common bile and pancreatic ducts at the ampulla of
Vater can block both the common bile and pancreatic ducts (double duct sign), causing both
cholangitis and pancreatitis, respectively.
Tumors that arise in head of pancreas (usually ductal adenocarcinoma) can cause obstruction of
common bile duct –> enlarged gallbladder with painless jaundice (Courvoisier sign).
Cholangiography shows filling defects in gallbladder (blue arrow) and cystic duct
Femoral region
organized from lateral to medial: nerve, artery, Veins
the femoral triangle contains the femoral nerve, arterm veins
the femoral sheath does not contain the femoral nerve
hernias- Protrusion of peritoneum through an opening, usually at a site of weakness. Contents may be at risk for incarceration (not reducible back into abdomen/pelvis) and strangulation (ischemia and necrosis). Complicated hernias can present with tenderness, erythema, fever.
Abdominal structures enter the thorax; may occur due to congenital defect of pleuroperitoneal membrane or from trauma. Commonly occurs on left side due to relative protection of right hemidiaphragm by liver.
Most commonly a hiatal hernia , in which stomach herniates upward through the esophageal hiatus of the diaphragm
Sliding hiatal hernia—gastroesophageal junction is displaced upward as gastric cardia slides into hiatus; “hourglass stomach.” Most common type.
Paraesophageal hiatal hernia— gastroesophageal junction is usually normal but gastric fundus protrudes into the thorax.
Direct inguinal hernia- Protrudes through the inguinal (Hesselbach) triangle. Bulges directly through parietal peritoneum medial to the inferior epigastric vessels but lateral to the rectus abdominis.
Goes through the external (superficial) inguinal ring only. Covered by external spermatic fascia. Usually occurs in older men due to an acquired weakness in the transversalis fascia.
Medial to inferior epigastric vessels = Direct hernia.
Lateral to inferior epigastric vessels = Indirect hernia.
Femoral hernia- Protrudes below inguinal ligament through femoral canal below and lateral to pubic tubercle. More common in fem ales, but overall inguinal hernias are the most common
More likely to present with incarceration or strangulation than inguinal hernias.
Inguinal (Hesselbach) triangle:
. Inferior epigastric vessels
. Lateral border of rectus abdominis
. Inguinal ligament
Vitamin/mineral absorption
iron is absorbed in duodenum
folate is absorbed in small bowel
B12 absorbed in terminal ileum along with bile salts, requires intrinsic factor
Peyer patches
Unencapsulated lymphoid tissue found in
lamina propria and submucosa of ileum.
Contain specialized M cells that sample and
present antigens to iM mune cells.
B cells stimulated in germinal centers of Peyer
patches differentiate into IgA-secreting plasma
cells, which ultimately reside in lamina
propria. IgA receives protective secretory
component and is then transported across the
epithelium to the gut to deal with intraluminal
antigen.
Bile
Composed of bile salts (bile acids conjugated to glycine or taurine, making them water soluble), Cholesterol 7α -hydroxylase catalyzes rate‑limiting step of bile acid synthesis.
Functions:
. Digestion and absorption of lipids and fatsoluble
vitamins
. Cholesterol excretion (body’s 1° means of
eliminating cholesterol)
. Antimicrobial activity (via membrane
disruption)
decreased absorption of enteric bile salts at distal ileum
(as in short bowel syndrome, Crohn disease)
prevents normal fat absorption. Calcium,
which normally binds oxalate, binds fat
instead, so free oxalate is absorbed by gut
–> increased frequency of calcium oxalate kidney
stones.
Bilirubin
Heme is metabolized by heme oxygenase to biliverdin, then reduced to bilirubin.
Unconjugated bilirubin is removed from blood by liver, conjugated with glucuronate, and excreted
in bile.
Direct bilirubin—conjugated with glucuronic acid; water soluble.
Indirect bilirubin—unconjugated; water insoluble.
Gastrointestinal regulatory substances
go to page 365 FA 2019
Gastrointestinal secretory products
go to page 366
Pancreatic secretions
go to page 367
