GI Flashcards
Foregut
Pharynx to duodenum
Midgut
duodenum to transverse colon
Hindgut
Distal transverse colon to rectum
Failure of rostral fold closure
Sternal defects
Failure of lateral fold closure
Omphalocele, Gastroschisis
Gastroschisis
Extrusion of abdominal contents through abdominal folds; NOT covered by peritoneum
Omphalocele
Persistence of herniation of abdominal contents into umbilical cord, COVERED BY PERITONEUM
Failure of caudal fold closure
Bladder extrosphy
Penile abnormality associted with bladder extrosphy
Epispadas
Duodenal atresia
failure to recanalize
* seen in trisomy 21
Jejunal, ileal, colonic atresia
due to vascular accident (apple peel atresia)
Midgut development
6th week - midgut herniates through umbilical ring
10th week - returns to abdominal cavity + rotates around SMA
Pathology of GI development
Malrotation of midgut, omphalocele, intestinal atresia or stenosis, volvulus
Most common tracheoesophageal anomaly
Esophageal atresia with distal tracheoesophageal fistula (TEF)
Sx of esophageal atresia w/ TEF
Newborn baby with drooling, choking, vomiting on first feeding. TEF allows air to ender stomach (visible on CXR). Cyanosis is secondary to laryngospasm (to avoid reflux-related aspiration)
Clinical test of esophageal atresia w/ TEF
Failure to pass NG tube into stomach
CXR of gasless abdomen
Pure atresia (isolated) esophageal atresia
Congenital pyloric stenosis
hypertrophy of pylorus causes obstruction. Palpable “olive” mass in epigastric region and nonbilious projectile vomiting at 2 weeks of age. Treatment is myoectomy. Usually in first born males.
Embryo origin of pancreas
derived from foregut.
Ventral pancreatic buds contribute what?
Pancreatic head and main pancreatic duct. Uncitate project
Dorsal pancreatic buds form what?
Pancreatic body, tail, isthmus, and accessory pancreatic duct
Annular pancreas
ventral pancreatic bud abnormally encircles 2nd part of duodenum; forms a ring of pancreatic tissue that causes duodenal narrowing
Pancreas divisim
ventral and dorsal root fail to fuse at 8 weeks
Embryo origin of spleen
Arises from mesentery of stomach (hence is mesodermal) but is supplied by foregut (celiac artery)
Retroperitoneal structures
Include GI structures that lack a mesentary and non-GI structures
Result of injury to retroperitoneal structures
Cause blood or gas accumulation in retroperitoneal space
Name retroperioneal structures
"SAD PUCKER" S-uprarenal (adrenal) gland A-orta and IVC D-uodenum (2nd and 3rd parts) P-ancreas (EXCEPT TAIL) U-reters C-olon (decending and ascending) K-idneys E-sophageus (lower 2/3) R-ectum (lower 2/3)
Falciform ligaments
connects liver to anterior abdominal wall
contains ligamentum teres hepatis (derivative of fetal umbilical vein)
- derivative of ventral mesentary
Hepatoduodenal ligament
connects liver to duodenum
contains: Portal triad (hepatic artery, portal vein, common bile duct)
- can do Pringle maneuver
- connects greater and lesser sacs
Pringle maneuver
Hepatoduodenal ligament may be compressed between thumb and index finger placed in omental foramen to control bleeding.
Gastrohepatic ligament
connects liver to lesser curvature of stomach
- contains gastric arteries
- separates greater and lesser sacs on RIGHT
- may be cut during surgery to access lesser sac
Gastrocolic
connects greater curvature to transverse colon
- structures contain gastroepiploic artery
- part of greater omentum
Gastrosplenic
connects greature curvature and spleen
- contains short gastrics, LEFT gastroepiploic vessels
- seperate greater and lesser sacs on LEFT
Splenorenal
connect spleen to posterior abdominal wall
- contains splenic artery and vein, tail of pancreas
Layers of gut wall (inside to outside)
"MSMS" - inside to outside M-ucosa S-ubmucosa M-uscularis externa S-erosa
Musosa of gut
- epithelium (absorption)
- lamina propria (support)
- muscularis mucosa (motility)
Submucosa of gut
- submucosal nerve plexus (Meissner’s) - controls secretory activity
Muscularis externa of gut
include Myenteric nerve plexus (Auerbach’s)
Serosa of gut
- serosa when intraperitoneal
- adventitia when retroperitoneal
Ulcers of gut are found in which gut layers?
Can extend into submucosa, inner or out muscular layer
Erosions are found in which gut layers
Only in mucosa
Frequencies of basal electric rhythm
Stomach - 3 waves/min
Duodenum - 12 waves/min
Ileum - 8-9 waves/min
Esophagus: Histology
Nonkeratinized stratified squamous epithelium
Stomach: Histology
Gastric glands
Duodenum: Histology
Villi and microvilli for increased absorptive surface
Brunner’s glands (submucosa) and crypts of Lieberkuhn
Jejunum: Histology
Plicae circulares and crypts of Liberkuhn
Ileum: Histology
Peyer’s patches (lamina propria, submucosa), plicae circularis (proximal ilum) and crypts of Liberkuhm
Colon: Histology
has crypts but no villi, numerous goblet cells
Four sites of portosystemic anastomoses
- Esophagus
- Umbilicus
- Rectum
- TIPS (artificial transjugular intrahepatic portosystemic shunt - used for tx of portal hypertension)
Esophagus anastomosis
Clinical sign: esophageal varices
Connects left gastric to esophageal
Umbilical anastomosis
Clinical sign: caput medusae
Below umbilicus: connects paraumbilical to superficial and inferior epigatric
Above umbilicus: connects paraumbilic to superior epigastric and lateral thoracic
Rectum
Clinical sign: internal hemorrhoids
Connects superior rectal to middle and inferior rectal
Common sx of portal hypertension
Varices of gut, butt, and caput (medusae)
Tx of portal hypertension
TIPS - transjugular intrahepatic porosystemic shunt between portal vein and hepatic vein percutaneously relieves portal hypertension by shunting blood to systemic circulation
Pectinate (dentate) line
where endoderm (hindgut) meets ectoderm
Pathology ABOVE pectinate line
Internal hemorrhoids, Adenocarcinoma
Receives arterial supply from superior rectal artery (branch of IMA)
Venous drainage is superior to rectal vein –> inferior mesenteric vein –> portal vein
Pathology BELOW pectinate line
External hemorrhoids, squamous cell carcinoma
Arterial supply: Inferior rectal artery (branch of internal pudendal artery)
Venous drainage to inferior rectal vein –> internal illiac ven –> IVC
Internal hemorrhoids (painful or not painful?
NOT PAINFUL, because receives visceral innervation. Lymphatic drainage to deep nodes
External hemorrhoids
PAINFUL. Receive somatic innervation (inferior rectal branch of pudendal nerve)
Lymphatic drainage to superficial inguinal nodes
Apical surface of hepatocytes
face bile canaliculi
Basolateral surface of hepatocytes
face sinusoids
Zone I of liver
Periportal zone - affected first by viral hepatitis. Areas in which branch of portal vein/ hepatic artery are located)
Zone II of liver
Intermediate zone
Zone III - Pericentral vein (Centrilobular zone)
affected 1st by ischemia - farthest away from hepatic artery
- contains P-450 system
- most sensitive to toxic injury
- site of alcoholic hepatitis
Result of gallstone blocking ampulla of Vater
blocks bile and pancreatic ducts
Result of tumor arising in head of pancreas (near duodenum)
Can cause obstruction of common bile duct
Femoral region organization
Lateral to medial: "NAVEL" N-erve A-rtery V-ein E-mpty pace L-ymphatics
Femoral triangle
contains femoral vein, artery, nerve
Femoral sheath
Fascial tube 3-4 cm BELOW inguinal ligamen. Contains femoral vein, artery, and canal (deep inguinal lymph nodes) BUT NOT FEMORAL NERVE
Hernia
protrusion of peritoneum through an opening- usually a site of weakness
Diaphragmatic hernia
abdominal structures enter thorax
- may occur infants due to defective pleuroperitoneal membrane
Hiatal hernia
common hernia in which stomach herniates upward through esophageal hiatus of diaphragm
Sliding hiatal hernia
most common. GE junction displaced upwards. “Hourglas stomach”
Paraesophageal hernia
GE juction is normal. FUNDUS protrudes into thorax
Indirect hernia
goes through INTERNAL inguinal ring, external inguinal ring, and INTO scrotum.
- Enters internal inguinal ring LATERAL to inferior epigastric artery
Cause of indirect inguinal hernia in infants
Due to failure of processus vaginalis to close (can form hydrocele). Much more common in males
Direct inguinal hernia
protrudes through inguinal (Hasselbach’s triangle. Bulges directly rhough abdominal wall MEDIAL to inferior epigastric artery. Goes through ONLY the external (superficial) inguinal canal.
- Covered by external spermatic fascia. Usually in oldern man
Mneumonic for Indirect/Direct Inguinal Hernias
MDs don’t LIe
- Medial to inferior epigatric - Direct
- Lateral to inferior epigastric -Indirect
Femoral hernia
protrudes BELOW inguinal ligament through femoral canal and lateral to pubic tubercle. More common in women.
Most common cause of bowel incarceration
Femoral hernia
Hasselbach’s Triangle
Inguinal Triangle
- Inferior epigatric vessels
- Lateral border of rectus abdominus
- Inguinal ligament
Gastrin
- found in G cells (antrum of stomach)
- increases gastric H+ secretion
- increases growth of gastric mucosa
- increases gastric motility
Gastrin regulation
- INCREASED by stomach distention/alkanization, amino acids, peptides, vagal stimulation
- DECREASED by stomach pH < 1.5
Associations w/ gastrin
HIGHLY elevated in Zollinger-Ellision syndrome
- Increased by chronic PPI use
- Phenylalanine and tryptophan are potent stimulators
Cholecystokinin
- made by I cells (duodenum, jejunum)
- increase pancreatic secretion
- increase gall bladder contraction
- DECREASES gastric emptying
- DECREASE sphincter of Oddi relaxation
Cholecystokinin regulation
- increased by fatty acids, amino acids
Cholecystokinin Notes
Cholecystokinin acts on neuronal muscarininc pathways to cause pancreatic secretions
Secretin
S cells (duodenum)
- increase pancreatic HCO3 secretion
- decrease gastric acid secretion
- increases bile secretion
Secretin regulation
Increased by fatty acids in lumen of duodenum
- Increased HCO3 neutralizes gastric acid in duodenum allowing pancreatic enzymes to function
Somatosatin
secreted by D cells (pancreatic islets, GI mucosa)
- decreases gastric acid and pepsinogen secretion
- decreases pancreatic and small intestine fluid secretion
- decreases gallbladder contraction
- decreases insulin and glucagon release
Somatostatin regulaton
- increased by acid
- decreased by vagal stimulation
- inhibitory hormone.
- Antigrowth hromone effects (inhibits digestion and absorption of substances needed for growth)
Glucose-dependent insulinotropic peptide
K cells (duodenum, jejunum) Exocrine: decreases gastric H secretion Endocrine: increases insulin release
Glucose-dependent insulinotropic peptide: regulation
increased by fatty acids, amino acids, oral glucose
- Also known as GIP
- An oral glucose load is used more rapidly than IV due to GIP
Vasoactive intestinal polypeptide (VIP)
Parasympathetic ganglia in sphincters, gallbladder, small intestine
- Increases water and electrolyte secretion
- Increases relaxation of intestinal smooth muscle and sphincters
VIP Regulation
- Increased y distention of vagal stimulation
- Decreased by adrenergic input
VIPoma
- non alpha, non-B islet pancreatic tumor that secretes VIP.
Associated with WHDA syndrome -
Watery Diarrhea, Hypokalemia, and Achlorydia
Nitric Oxide
Increases smooth muscle relaxation, including lower esophageal sphincter
NO and its implication in achalasia
Loss of NO secretion is implicated in lower esophageal tone in achalasia
Motilin
- found in small intestine
- produce migrating motor complexes
Motilin regulation
- increased in fasting state
- motilin receptor agonists (such as erythromycin) are used to stimulate intestinal peristalsis
Intrinsic factor
- found in parietal cells (stomach)
- Vitamin B12 - binding porein (required for B12 uptake to terminal ileum)
Autoimmune destruction of parietal cells
Chronic gastritis and pernicious anemia
Gastric acid
- secreted by parietal cells (stomach)
- decrease stomach pH
Gastric acid regulation
- Increased by histamine, ACh, gastrin
- Decreased by somatostatin, GIP, prostaglandin, secretin
Gastrinoma
gastrin-secreting tumor that causes continuous high levels of acid secretion
Pepsin
- found in chief cells (stomach)
- protein degestin
Pepsin regulation
increased by vagal stimulation, local acid
Inactive pepsinogen –> pepsin by H+
HCO3
- made by mucosal cells (stomach, duodenum, salivary glands, pancreas) and Brunner’s glands (duodenum)
- neutralizes aics
HCO3 regulation
Increased by pancreatic and biliary secretion with secretiin
- HCO3 is trapped in mucus that covers the gatric epithelium
Saliva
secretion from parotid, submandibular, and sublingual glands is stimulated by SYMPATHETIC and PARASYMPATHETIC acitivity.
Amylase digests starch, Bicarb neutralizes bacterial acids, Mucins lubricate food
Normally hypotonic because of absorption but more isotonic with higher flow rates
Discuss atropine and parietal cells
Atropine blocks vagal stimulation of parietal cells. Vagal stimulation of G cells (secretes gastrin) is unaffected because uses GRP as neurotransmitter not ACh
Gastrin increases acid secretion through its effect on which cells
ECL cells (which lead to histamine release) rather than through direct effect on parietal cells
Brunner’s glands
located in duodenal submucosa. Secretes alkaline mucus. Hypetrophy seen in peptic ulcer disease
Nature of pancreatic secretions
Isotonic fluid
low flow –> high Cl-
High flow –> High Bicarb
Alpha-amylase
Pancreatic secretion. Digests starch.
*Secreted in active form
Lipase, Phospholipase A, colipase
Pancreatic secretions. Aids in fat digestion.
Pancreatic proteases
- Digests proteins
- Includes trypsin, chemotrypsin, elastase, carboxypeptidases
Trypsinogen
Converted to active enzyme trypsin –> activation of other pro-enzymes and creation of more trypsinogen (positive feedback loop)
Enterokinase/ Enteropeptidase
converts trypsinogen to trypsin
- secreted from duodenal mucosa
Salivary amylase
Starts carbohydrate digestion. Hydolyzes alpha 1,4 linkages to yield disaccarides (maltose and alpha limit dextrins)
Pancreatic amylase
Highest concentration in duodenal lumen, hydrolyzes starch to oligosaccharides and disaccharides
Oligosaccharide hydrolases
At intestinal brush border.
RATE LIMITING STEP in carbohydrate digesti, produce monosaccharide from oligo-disaccharides
Monosaccharide absorption
- Only monosaccharides (glucose, galactose, fructorse) are absorbed by enterocytes. All are transported to blood by GLUT-4
Glucose and galactose absorption
Taken by SGLT1 (Na+ dependent)
Fructose absorption
Facilitated diffusion by GLUT-5.
D-xylose absorption test
Distinguishes GI mucosal damage from other causes of malasborption
Fe absoprtion
absorbed as Fe2+ in DUODENUM
Folate absorption
Absorped in jejunum
B12 absorption
absorbed in terminal ileum, along with bile acids, requires intrinsic factor
Peyer’s patches
unencapsulated lymphoid tissue found in lamina proproa and submucosa of ileum. Contains specialized M cells that take up antigen
Discuss B cells and Peyer’s Patches
B cells stimulated by germinal centers of Peyer’s patches differentiate in to Ig-A secreting plasma cells, which ultimately reside in lamina propria.
IgA receives protective secretory component and is then transported across epithelium to deal with intraluminal antigen
Bile Composition
composed of bile salts (bile acids conjugated to glycine/taurine, making them water soluble), phospholipids, cholesterol, bilirubin, water, and ions.
Bile Function
Digestion and absorption of lipids and fat soluble vitamins. Cholesterol excretion (body's only means of eliminating cholesterol) Antimicrobial activity (via membrane disruption)
Enzyme that catalyze bile formation
Cholesterol 7-alpha hydroxylase catalyzes rate limiting step.
Bilirubin
product of heme metabolism. Bilirubin is removed from by liver, conjugated wth glucuronate, and excreted in bile
Direct bilrubin
Made in liver
- conjugated in glucuronic acid; water soluble
Indirect bilirubin
Unconjugated - water insoluble
- made from breakdown of heme
Trace Heme break down
- RBCs lyse
- Heme breaks down to form unconjugated bilirubin (water insoluble)
- Albumin- complexes w/ unconjugated bilirubin for transport to liver
- UDP-glucoronsyl transferase in liver conjugates bilirubin to make direct bilirubin
- Direct bilirubin is secreted into gut and broken down by gut bacteria to become urobillinogen
Discuss pathway of urobillinogen
Product of gut bacteria breakdown of direct billirubin.
- 80% of urobillinogen is excreted into feces
- 20% of urobillinogen is absorted into gut - small fraction is excreted in kidney as urobilin (gives pee its color)
- majority of absorbed urobillinogen is recirculated in the enterohepatic circulation