GI Flashcards
Foregut
Pharynx → duodenum
Midgut
Duodenum → 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 degree counterclockwise
Defect rostral fold closure
Sternal defects
Defect lateral fold closure
Omphalocele, gastroschisis
Defect caudal fold closure
Bladder exstrophy
Duodenal atresia
- Failure to recanalize
- Dilation of the stomach and proximal duodenum (“double bubble” on x-ray)
- Associated with Down syndrome
Jejunal and ileal atresia
- Disruption of mesenteric vessels
- Ischemic necrosis
- Segmental resorption (bowel discontinuity or “apple peel”)
Hypertrophic pyloric stenosis is associated with exposure to
Macrolides
Hypertrophic pyloric stenosis is associated with what type of alkalosis
Results in hypokalemic and hypochloremic metabolic alkalosis (secondary to vomiting of gastric acid and subsequent volume contraction)
Annular pancreas
Ventral pancreatic bud abnormally encircles 2nd part of the duodenum. Forms a ring of pancreatic tissue that may cause duodena narrowing and nonbilious 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
Embryology of spleen
Arises in mesentery of stomach (hence is mesodermal) but has foregut supply (celiac trunk → splenic artery)
Retroperitoneal structures
Include GI structures that lack a mesentery and non-GI structures. Injuries to retroperitoneal structures can cause blood or gas accumulation in the retroperitoneal space.
- Suprarenal (adrenal) glands
- Aorta and IVC
- Duodenum (2nd through 4th parts)
- Pancreas (except tail)
- Ureters
- Colon (descending and ascending)
- Kidneys
- Esophagus (thoracic portion)
- Rectum (partially)
“SAD PUCKER”
Superior mesenteric artery syndrome
Characterized by intermittent intestinal obstruction symptoms (primarily postprandial pain) when transverse (3rd) portion of duodenum is compressed between the SMA and aorta. Typically occurs in conditions associated with diminished mesenteric fat (eg low body weight/malnutrition)
Branches of celiac trunk
Common hepatic, splenic, and left gastric
Kupffer cells
Specialized macrophages that form the lining of sinusoids
Hepatic stellate (Ito) cells
Located in space of Disse and store vitamin A when quiescent and produce extracellular matrix when activated.
Zone I
- Periportal zone
- Affected 1st by viral hepatitis
- Ingested toxins (eg cocaine)
Zone II
- Intermediate zone
- Yellow fever
Zone III
- Pericentral vein (centrilobular) zone
- Affected 1st by ischemia
- Contains cytochrome P450 system
- Most sensitive to metabolic toxins
- Site of alcoholic hepatitis
Painless jaundice
Usually caused by tumors that arise in the head of pancreas (usually ductal adenocarcinoma) that can cause obstruction of the common bile duct
Layers of spermatic cord and their derivatives
- Internal spermatic fascia (transversalis fascia)
- Cremasteric muscle and fascia (internal oblique)
- External spermatic fascia (external oblique)
“ICE tie”
Carbohydrate absorption
- Only monosaccharides (glucose, galactose, fructose) are absorbed by enterocytes
- Glucose and galactose are taken up by SGLT1 (Na+ dependent)
- Fructose is taken up by facilitated diffusion by GLUT-5
- All are transported to blood by GLUT-2
- D-xylose absorption test: distinguishes GI mucosal damage from other causes of malabsorption
Where is iron absorbed
Duodenum
Where is folate absorbed
Small bowel, therefore clinically relevant in patients with small bowel disease or after resection.
Where is B12 absorbed
Terminal ileum along with bile salts, requires intrinsic factor
Pleomorphic adenoma
- Salivary gland tumor
- Benign mixed tumor
- Most common salivary gland tumor
- Composed of chondromyxoid stroma and epithelium and recurs if incompletely excise or ruptured intraoperatively
Mucoepidermoid carcinoma
- Salivary gland tumor
- Most common malignant tumor
- Has mucinous and squamous components
Warthin tumor
- Salivary gland tumor
- Papillary cystadenoma lymphomatosum
- Benign cystic tumor with germinal centers
Sclerodermal esophageal dysmotility
Esophageal smooth muscle atrophy → ↓ LES pressure and dysmotility → acid reflux and dysphagia → stricture, Barret esophagus, and aspiration. Part of CREST syndrome.
Eosinophilic esophagitis
Infiltration of eosinophils in the esophagus often in atopic patients. Food allergens → dysphagia, food impaction. Esophageal rings and linear furrows often seen on endoscopy. Unresponsive to GERD therapy.
How do burns cause acute gastritis
Burns (Curling ulcers) → hypovolemia → mucosal ischemia
“Burned by the Curling iron”
How does brain injury cause acute gastritis
Brain injury (Cushing injury) → ↑ vagal stimulation → ↑ ACh → ↑ H+ production
“Always Cushion the brain”
Mentrier disease
Gastric hyperplasia of the mucosa → hypertrophied rugae (looking like brain gyri), excess mucus production with resultant protein loss and parietal cell atrophy with ↓ acid production. PRECANCEROUS.
Complication of ulcers
Hemorrhage, obstruction, perforation
HEMORRHAGE: gastric, duodenal (posterior > anterior); most common complication; ruptured gastric ulcer on the lesser curvature of the stomach → bleeding from the LEFT GASTRIC ARTERY; an ulcer on the posterior wall of the duodenum → bleeding from the GASTRODUODENAL ARTERY
OBSTRUCTION: pyloric channel, duodenal
PERFORATION: duodenal (anterior > posterior); may see free air under diaphragm with referred pain to the shoulder via phrenic nerve
Pathological findings of celiac disease
- Villous atrophy (blunting)
- Crypt hyperplasia
- Intraepithelial lyphocytosis
Pathological findings of lactose intolerance
Normal appearing villi except with secondary to injury at tips of villi (eg viral enteritis)
Location of celiac disease vs tropical sprue
CELIAC DISEASE: ↓ mucosal absorption primarily affects distal duodenum and/or proximal jejunum
TROPICAL SPRUE: ↓ mucosal absorption affecting duodenum and jejunum but can involve ileum with time (associated withe megaloblastic anemia due to folate deficiency and later B12 deficiency)
Microscopic morphology of Crohn disease vs ulcerative colitis
CROHN DISEASE: noncaseating granulomas and lymphoid aggregates
ULCERATIVE COLITIS: crypt abscesses and ulcers, bleeding, no granulomas
Cause of Zenker diverticulum
Esophageal dysmotility causes herniation of the mucosal tissue at Killian triangle between the thyropharyngeal and cricopharyngeal parts of the interior pharyngeal constrictor
Meckels diverticulum is a persistence of what
Vitelline duct
Malrotation
Anomaly of midgut rotation during fetal development → IMPROPER POSITIONING OF BOWEL, formation of fibrous bands (Ladd bands). Can lead to volvulus, duodenal obstruction.
Volvulus is the twisting of a portion of bowel around its
Mesentery.
Acute mesenteric ischemia
Critical blockage of intestinal blood flow (often embolic occlusion of SMA) → small bowel necrosis → abdominal pain out of proportion to physical findings. May see red “currant jelly” stools.
Chronic mesenteric ischemia
“Intestinal angina”: atherosclerosis of celiac artery, SMA or IMA → intestinal hypoperfusion → postprandial epigastric pain → food aversion and weight loss
Angiodysplasia
Tortuous dilation of vessels → hematochezia. Most often found in cecum, terminal ileum, ascending colon. More common in older patients. Confirmed by angiography.
Ileus
Intestinal hypomotility without obstruction → constipation and ↓ flatus; distended/tympanic abdomen with ↓ bowel sounds. Associated with abdominal surgeries, opiates, hypokalemia, sepsis. Treatment: bowel rest, electrolyte correction, cholinergic drugs (stimulate motility)
Hyperplastic colonic polyp
Non-neoplastic. Generally smaller and majority located in rectosigmoid area.
Hamartomatous colonic polyp
Generally non-neoplastic; solitary lesions do not have a significant risk of malignant transformation. Growths of normal colonic tissue with distorted architecture. Associated with Peutz-Jeghers syndrome and juvenile polyposis.
Adenomatous colonic polyp
Neoplastic, via chromosomal instability pathway with mutations in APC and KRAS. Tubular histology has less malignant potential than villous; tubulovillous has intermediate malignant potential. Usually asymptomatic, may present with occult bleeding.
Serrated colonic polyp
Premalignant, via CpG hypermethylatin phenotype pathway with microsatellite and mutations in BRAF. “Saw tooth” pattern of cysts on biopsy. Up to 20% of cases sporadic CRC.
Familial adenomatous polyposis
- AD mutation of APC tumor suppressor gene on chromosome 5q
- 2-hit hypothesis
- Thousands of polyps arise staring after puberty
- Pancolonic
- Always involves the rectum
- Prophylactic colectomy or else 100% progress to CRC
Gardner syndrome
FAP + osseous and soft tissue tumors, congenital hypertrophy of retinal pigment epithelium, impacted/supernumerary teeth.
Turcot syndrome
FAP + malignant CNS tumor.
Juvenile polyposis syndrome
AD syndrome in children (
Peutz-Jeghers syndrome
AD syndrome featuring numerous hamartomas throughout GI tract, along with hyperpigmented mouth, lips, hands, genitalia. Associated with ↑ risk of breast and GI cancers (eg colorectal, stomach, small bowel, pancretic)
Non-alcoholic fatty liver disease
- Metabolic syndrome (insulin resistance)
- Obesity → fatty infiltration of hepatocytes → cellular “ballooning” and eventual necrosis
- May cause cirrhosis and HCC
- Independent of alcohol use
- ALT > AST
Hepatic encephalopathy
- Cirrhosis → portosystemic shunts → ↓ NH3 metabolism → neuropsychiatric dysfunction
- Spectrum from disorientation/asterixis (mild) to difficult arousal or coma (severe
- Triggers include ↑ NH3 production and absorption (due to dietary protein, GI bleed, constipation, infection) or ↓ NH3 removal (due to renal failure, diuretics, bypassed hepatic blood flow post-TIPS)
- TREATMENT: lactulose (↑ NH4+ generation) and rifamixin or neomycin (↓ NH4+ producing gut bacteria)
Pathology of primary sclerosing cholangitis
Unknown cause of concentric “onion skin” bile duct fibrosis → alternating strictures and dilation with “beading” of intra and extra hepatic bile ducts on ERCP, magnetic resonance cholangiopancreatography.
Pathology of primary biliary cirrhosis
Autoimmune reaction → lymphocytic infiltrate + granulomas → destruction of intralobular bile ducts
Pathology of secondary biliary cirrhosis
Extrahepatic biliary obstruction → ↑ pressure in intrahepatic ducts → injury/fibrosis and bile stasis
Cholesterol stones are associated with
- Obestity
- Crohn disease
- Advanced age
- Estrogen therapy
- Multiparity
- Rapid weight loss
- Native American origin
Pigment stones are associated with
- Crohn disease
- Chronic hemolysis
- Alcoholic cirrhosis
- Advanced age
- Biliary infections
- Total parenteral nutrition (TPN)
Cholecystitis via primary infection occurs by which organism
CMV
Causes of acute pancreatitis
- Idiopathic
- Gallstones
- Ethanol
- Trauma
- Steroids
- Mumps
- Autoimmune disease
- Scorpion sting
- Hypercalcemia/Hypertriglyceridemia
“I GET SMASHED”
Complications of acute pancreatitis
- Pseudocyst (lined by granulation tissue, not epithelium)
- Necrosis
- Hemorrhage
- Infection
- Organ failure (ARDS, shock, renal failure)
- Hypocalcemia (precipitation of Ca2+ soaps)
What is Courvoisier’s sign
Obstructive jaundice with palpable, nontender gallbladder. Associated with pancreatic adenocarcinoma.
Pancreatic adenocarcinoma is associated with what tumor marker
CA 19-9 but also CEA (less specific)
Conditions developed above and below pectinate/dentate line
Above pectinate line → internal hemorrhoids, adenocarcinoma
Below pectinate line → external hemorrhoids, anal fissures, squamous cell carcinoma
Compare the arterial supply above and below the pectinate line
Above the pectinate line → superior rectal artery (branch of IMA)
Below the pectinate line → inferior rectal artery (branch of inferior pudendal artery)
Compare the venous supply above and below the pectinate line
Above the pectinate line: superior rectal vein → inferior mesenteric vein → portal system
Below the pectinate line: inferior rectal vein → internal pudendal vein → inferior iliac vein → common iliac vein → IVC
Compare lymphatic drainage above and below the pectinate line
Above the pectinate line → internal iliac lymph nodes
Below the pectinate line → superficial inguinal nodes
Internal hemorrhoids
Receive visceral innervation and are therefore not painful
External hemorrhoids
Receive somatic innervation (inferior rectal branch of pudendal nerve) and are therefore painful if thrombosed
Anal fissure
- Tear in the anal mucosa below the Pectinate line
- Pain while Pooping
- Blood on the toilet Paper
- Located Posteriorly because this area is Poorly Perfused
- Associated with low fiber diets and constipation
