Flashcards in GI Deck (144):
pharynx to duodenum
duodenum to proximal 2/3 of transverse colon
distal 1/3 of transverse colon to anal canal above pectinate line
rostral fold closure fail ->
lateral fold closure fail ->
caudal fold closure fail ->
6th week: midgut herniates through umbilical ring. 10th week: returns to abdominal cavity + rotates around SMA
derived from foregut. ventral pancreatic buds contribute to uncinate process and main pancreatic duct. dorsal pancreatic bud becomes body, tail, isthmus, and accessory duct. both buds contribute to pancreatic head.
ventral pancreatic bud abnormally encircles 2nd part of duodenum
ventral and dorsal parts fail to fuse at 8 wks. common. usually w/o Sx, but can -> chronic abd. pain and/or pancreatitis.
arises in mesentery of stomach (= mesodermal). supplied by foregut (celiac) artery
where's the portal triad?
in the hepatoduodenal ligament
connects liver to ant. abd. wall. containes ligamentum teres hepatis (from fetal umbilical vein). derived from ventral mesentery
connects liver to duodenum. contains portal triad. pringle maneuver: compress by pinching, hold in omental foramen to control bleeding (hole between greater + lesser sacs)
connects liver to lesser curvature. contains gastric arteries. separates greater and lesser sacs on the right. cut during surgery to access lesser sac.
connects greater curvature w/transverse colon. contains castroepiploic arteries. part of greater omentum.
connects greater curvature and spleen. contains short gastrics, L gastroepiploic vessels. separates greater + lesser sacs on the left.
connects spleen to posterior abd. wall. contains splenic artery and vein, tail of pancreas
level of celiac
level of SMA
L1 (same as L renal)
level of IMA
level of aorta bifircation
occurs when 3rd part of duodenum (transverse) is entrapped between SMA and aorta -> intestinal obstruction
portosystemic anastamosis: esophagus
L gastric esophageal
portosystemic anastamosis: umbilicus
paraumbilical small epigastric veins of ant. abd. wall
portosystemic anastamosis: rectum
superior rectal middle and inferior rectal
above pectinate line
internal hemorrhoids (not painful cause they have visceral innervation), adenocarcinoma. supplied by superior rectal artery (from IMA). drained by superior rectal vein -> inf. mesenteric vein -> portal system. lymph drainage -> internal iliac nodes
below pectinate line
external hemorrhoids (somatic innervation from inf. rectal from pudendal -> painful). supplied by inf. rectal artery (from internal pudendal. drained by inf. rectal vein -> internal pudendal -> internal iliac -> common iliac -> IVC. lymph -> superficial inguinal nodes.
tear in anal mucosa below Pectinate line. Pain while Popping; blood on toilet Paper. located Posterior since this area = Poorly Perfused
hepatocyte surface orientation
apical faces bile canaliculi. basolateral faces sinusoids.
liver zone I
periportal zone: affected 1st by viral hepatitis and ingested toxins (e.g. cocaine).
liver zone II
intermediate zone: yellow fever
liver zone III
pericentral vein (centrilobular) zone: affected 1st by ischemia. contains cytochrome P-450 system. most sensitive to metabolic toxins. site of EtOH hepatitis.
fascial tube 3-4cm below inguinal ligament. contains femoral vein, artery, and canal (deep inguinal nodes) but not femoral nerve.
indirect inguinal hernia
goes through internal (deep) inguinal ring, external (superficial) inguinal ring, and into the scrotum. enters internal inguinal ring lateral to inferior epigastrics. occurs in infants 2/2 processus vaginalis failing to close -> hydrocele. covered by all 3 layers of fascia.
direct inguinal hernia
protrudes through inguinal (hesselbach) triangle. bulges directly through abd wall medial to inf. epigastrics. goes through external (superficial) inguinal ring only. covered by external spermatic fascia. older men. MDs don't LIe: Medial to inf. epigastric arte
indirect vs. direct mnemonic
MDs don't LIe: Medial to inf. epigastric artery = Direct. Lateral to inf. epigastric artery = Indirect
protrudes below inguinal ligament through femoral canal below and lateral to pubic tubercle. leading cause of bowel incarceration.
superolateral: inf. epigastrics
inferolateral: inguinal ligament
medial: lateral border of rectus abdominis
made by G cells in stomach antrum and duodenum. action: inc. gastric acid, inc. growth of gastric mucosa, inc. gastric motility. reg: +: stomach distention/alkalinization, AAs, peptides, vagal stim. -: pH <1.5. inc. w/H. pylori and chronic PPI use.
made by D cells in pancreatic islets and GI mucosa. action: dec. gastric acid, pepsinogen, pancreatic and small intestine fluid secretion, gallbladder contraction, insulin and glucagon release. reg: +: acid. -: vagal stimulation
made by I cells in duodenum, jejunum. actions: inc. pancreatic secretion, gallbladder contraction, sphincter of Oddi relaxation. dec. gastric emptying. reg: +: FAs, AAs. acts on neural muscarinic pathways to cause pancreatic secretion.
made by S cells in duodenum. actions: inc. pancreatic bicarb secretion, bile secretion. dec. gastric acid secretion. reg: +: acid, FAs in duodenum lumen. inc. bicarb neutralizes gastric acid, allowing pancreatic enzymes to fxn.
made by K cells in duodenum, jejunum. action: exocrine: dec. gastric H secretion. endocrine: inc. insulin release. reg: +: FAs, AAs, oral glucose. the reason why oral glucose -> more insulin than IV glucose
made in small intestine. actions: produces migrating motor complexes (MMCs). reg: +: fasting state. receptor agonists (e.g. erythromycin) used to stimulate intestinal peristalsis
made by parasympathetic ganglia in sphincters, gallbladder, small intestine. actions: inc. intestinal water and electrolyte secretion, inc. relaxation of intestinal smooth muscle and sphincters. reg: +: distention, vagal stim. -: adrenergic input.
actions: inc. smooth muscle relaxation, including LES. loss of NO secretion implicated in inc. LES tone of achalasia
made by parietal cells in stomach. actions: vit B12 binding protein
made by chief cells in stomach. action: protein digestion. reg: +: vagal stim, local acid. pepsinogen -> pepsin in presence of acid
Na/glucose or galactose cotransporters
transports all monosaccharides to blood
D-xylose absorption test
distinguishes GI mucosal damage from other causes of malabsorption.
as Fe2+ in duodenum
digestion and absorption of lipids and ADEK
cholesterol excretion (only way!)
antimicrobial activity (via membrane disruption)
candida: white pseudomembranes
HSV-1: punched-out ulcers
CMV: linear ulcers
triad: dysphagia, Fe-def. anemia, esophageal webs. may be associated w/glossitis. inc. risk of squamous cell CA.
happens w/burns. dec. plasma volume -> sloughing of gastric mucosa (can't sweep away excess acid). "burned by a curling iron"
happens w/brain injury. inc. ICP -> inc. vagal stimulation -> inc. ACh -> inc. acid production. "always cushion the brain"
type A chronic gastritis
in fundus/body. Autoimmune d/o characterized by AutoAbs (side effect, not cause) to parietal cells (-> atrophy), pernicious Anemia, and Achlorhydria (-> G cell hyperplasia). T-cell mediated: type IV HSR. predisposes to adenoCA by -> intestinal metaplasia
type B chronic gastritis
antrum. most common type. caused by H pylori Bacteria. inc. risk of MALT lymphoma.
gastric hyperplasia of mucosa -> hypertrophied rugae, excess mucus production w/resultant protein loss and parietal cell atrophy w/dec. acid production. precancerous. rugae of stomach are so hypertrophied that they look like brain gyri.
intestinal gastric adenoCA
associated w/H pylori, dietary nitrosamines, tobacco, achlorhydria, chronic gastritis. commonly on lesser curvature. looks like ulcer w/heaped up margins. blood type A association. sister mary joseph nodule = subQ periumbilical met.
diffuse gastric adenoCA
not associated w/H pylori. signet ring cells (= mucin-filled cells w/peripheral nuclei). stomach wall grossly thickened + leathery (linitis plastica <- inflammation). krukenberg tumor: b/l ovarian mets produce lots of mucin.
lesser stomach curvature -> L gastric bleed
posterior duodenum -> gastroduodenal bleed
similar to celiacs but responds to Abx. j + i > d (unlike celiac)
infxn w/tropheryma whipplea (GP), PAS+, foamy macrophages in intestinal lamina propria, mesenteric nodes. foamy whipped cream in a CAN: Cardiac Sx, Arthralgias, Neuro Sx. older men. macrophages can accumulate, compress lacteals -> steatorrhea, fat malabsorption.
noncaseating granulomas and lymphoid aggregates (Th1 mediated)
crypt abscesses and ulcers, bleeding, no granulomas (Th2 mediated)
extraintestinal manifestations: crohns
strictures (string sign), fistulas (can -> UTIs), perianal dz, AK, pyoderma gangrenosum, aphthous ulcers, uveitis, Ca oxalate stones (inc. absorption w/inflam)
extraintestinal manifestations: UC
pyoderma gangrenosum, erythema nodosum, PSC, AK, aphthous ulcers, uveitis. p-ANCA.
steroids, AZA, Abx (e.g. cipro, flagyl), infliximab, adalimumab. quit smoking
5-aminosalicylic preps (e.g. mesalaine), 6-mercaptopurine, infliximab, colectomy. smoking helps.
false. herniation of mucosal tissue at killina traingle between thyropharyngeal and cricopharyngeal parts of inf. pharyngeal constrictor.
mutation associated w/hirschsprung dz
acquired malformation of mucosal and submucosal capillaries from inc. tension. tortuous dilation of vessels -> hematochezia. usually cecum, can be terminal ileum, ascending colon. old people. confirmed by angiography.
atherosclerosis of SMA. pain after eating -> wt. loss. occurs at watershed areas.
non-neoplastic. generally smaller and majority located in rectosigmoid (L-side).
non-neoplastic, solitary. distorted architecture but otherwise normal tissue. associated w/peutz-jegher + juvenile polyposis.
neoplastic via chromosomal instability pathway w/mutations in APC and KRAS. tubular histology = less malignant than villous. ASA = protective.
premalignant, via CpG hypermethylation phenotype pathway w/microsatellite instability and BRAF mutations. "saw-tooth" pattern of crypts on Bx. up to 20% of sporadic CRC
inc. risk if polyps are:
>2cm, sessile (flat), villous histologically
AD APC (tumor suppressor) mutation on chromosome 5q. 2 hit hypothesis. 100% progression to CRC w/o resection. pancolonic, always involves rectum.
FAP + osseous and soft tissue tumors, congenital hypertrophy of retinal pigment epithelium, impacted/supernumerary teeth.
FAP + malignant CNS tumor (think turcot = turban)
AD. numerous hamartomas throughout GI + hyperpigmented mouth, lips, hands, genitalia. associated w/risk of colorectal, breast, stomach, small bowel, and pancreatic CA
AD. children, typically <5yrs old. numerous hamartomatous polyps in colon, stomach, small bowel. inc. risk of CRC. solitary rectal polyp = common: can prolapse + bleed
previously HNPCC. AD of DNA mismatch repair genes w/subsequent microsatellite instability. 80% -> CRC. proximal colon (R-side) = always involved. associated w/endometrial, ovarian, and skin CA. can be identified w/3-2-1 rule: 3 relatives w/lynch across 2 generations, 1 Dx younger than age 50.
CRC location & presentation
rectosigmoid > ascending > descending. ascending: exophytic mass, Fe def. anemia, wt. loss. descending: infiltrating mass, partial obstruction, colicky pain, hematochezia. can p/w strep bovis bacteremia.
microsatellite instability pathway
~15%. DNA mismatch repair gene mutations -> sporadic and lynch syndrome. mutations accumulate, but no defined morphologic correlates. R-side more common
chromosomal instability. 85%. normal colon (+ loss of APC gene) -> colon at risk (+ KRAS mutation) -> adenoma (+ loss of p53, DCC) -> CA. L-side more common.
produce TGF-beta -> fibrosis (in cirrhosis). lie beneath endothelial cells that line sinusoids
= alk phos. Dx of cholestatic and obstructive hepatobiliary dz, HCC, infiltrative d/os, bone dz.
viral hep (ALT>AST), EtOH hep (AST>ALT)
acute pancreatitis, mumps
dec. in wilson dz
= gamma-glutamyl transpeptidase. inc. in various liver and biliary dz but NOT in bone dz. associated w/EtOH.
most specific for acute pancreatitis
findings of reye syndrome
mitochondrial abnormalities, fatty liver, hypoglycemia, vomiting, coma. associated w/ASA Tx of flu B, VZV. MoA: ASA metabolites -> beta-oxidation by reversible inhibition of mitochondrial enzymes.
alcoholic hepatitis histo
swollen and necrotic hepatocytes w/neutrophilic infiltration. mallory bodies = intracytoplasmic eosinophilic inclusions of damaged keratin filaments.
causes of inc. NH3 production and/or absorption
dietary protein, GI bleed, constipation, infection
causes of dec. NH3 removal
bypassed hepatic blood flow, renal failure, diuretics
inc. NH4 generation
spread of HCC
hematogenous, often through renal vein (-> budd-chiari)
common, benign liver tumor. age 30-50. Bx: dont! b/c of hemorrhage risk
rare, benign tumor, often OCP- or anabolic steroid-related. may regress spontaneously or rupture (-> pain, shock).
malignant endothelial tumor associated with exposure to arsenic, vinyl chloride
hepatic vein thrombosis/compression -> centrilobular congestive liver dz (hepatomegaly, varices, pain, -> liver failure). no JVD. associated w/hypercoagulation, PV, postpartum, HCC. can -> nutmeg liver
alpha1-antitrypsin def. (in liver)
misfolded protein aggregates in hepatocellular ER -> cirrhosis w/PAS + globules in liver. codominant trait.
indirect hyperbili causes
hemolysis (overwhelms conjugation), physiologic (low UGT activity), crigler-najjar (no UGT), gilberts (AR, low UGT)
general causes of direct hyperbili
obstruction, biliary tract dz, excretion defect
causes of obstructive jaundice
gallstones, cholangiocarcinoma, pancreatic or liver CA, liver fluke
bili excretion defects
dubin-johnson (AR, dev. b. canilicular transport protein -> dark liver, no Sx), rotor syndrome (similar w/normal appearing liver)
what determines urine urobilinogen levels?
how much conjugated bili gets into the duodenum
why is urine dark in obstructive jaundice?
conjugated bili is water soluble
why is urine dark in hemolytic jaundice?
it is eventually conjugated, excreted into GI tract, and processed into/excreted as urobilinogen
mildly dec. UDP-glucuronosyltransferase conjugation and impaired bilirubin uptake. bilirubin inc. w/fasting + stress. very common, not worrisome
absent UDP-glucuronosyltransferase. type 1 presents early, death in 1st few yrs. jaundice, kernicterus. Tx: plasmapharesis + phototherapy. type 2: less severe, phenobarbital -> inc. liver enzyme synthesis
conjugated hyperbili due to defective excretion. black liver. benign
like dubin-johnson but even milder and liver appears normal.
Cs! low Ceruloplasmin, Cirrhosis, Corneal deposits, Cu accumulation, CA (HCC). AR, chromosome 13: ATP7B gene (hepatocyte ATP cotransporter excretion of Cu into bile). other Sx: hemolytic anemia, basal ganglia degeneration, asterixis, dementia, dysarthria. Tx: chelation w/penicillamine/trientine, oral zinc
hemosiderosis: Fe (hemosiderin) deposition stains prussian blue (distinguishes from lipofuschin). triad: micronodular cirrhosis, DM, skin pigmentation = bronze diabetes. -> HF, testicular atrophy, inc. HCC risk. AR (primary) or 2/2 chronic infusion Tx. inc. ferrition, inc. Fe, dec. TIBC -> inc. transferrin saturation. H63D or C282Y mutation on HFE gene. association w/HLA-A3. slower progression in women. Tx: repeat phleb, chelation (has "fer" in names)
secondary biliary cirrhosis
extrahepatic obstruction (stones, strictures, pancreatic CA) -> inc. intrahepatic pressure -> injury/fibrosis + bile stasis. may be complicated by ascending cholangitis
autoimmune (middle-aged women) -> lymphocytic infiltration + granulomas -> destruction of intralobular bile ducts (-> obstructive jaundice). anti-mitochondrial Ab (including IgM).
young men w/IBD. concentric "onion skin" bile duct fibrosis -> alternating strictures and dilation w/beading of intra- and extra-hepatic bile ducts on ERCP, MRCP. hypergammaglobulinemia (IgM). p-ANCA. can -> secondary biliary cirrhosis, cholangioCA
calcified 2/2 chronic cholecystitis. Tx: phrophylactic chole (high risk of CA)
weird causes of acute pancreatitis
steroids, mumps, autoimmune, hyperCa, drugs (sulfa, MRTIs, protease inhibitors), scorpion sting.
complications of acute pancreatitis
DIC, ARDS, diffuse fat necrosis, hypoCa, pseudocyst, hemorrhage, infxn, multiorgan failure
redness + TTP. associated w/pancreatic CA = trousseau syndrome.
palpable, nontender gallbladder
courvousier sign = associated w/pancreatic CA (w/obstructive jaundice)
reversible H2 blocker. potent P450 inhibitor. antiandrogenic effects. crosses BBB (-> confusion, dizziness, h/a) and placenta. dec. renal Cr excretion
side effects of PPIs
inc. risk of c. diff, pna. dec. serum Mg w/long term us
bind to ulcer base (physical protection) and allows HCO3- secretion to reestablish pH gradient in mucus layer.
PGE1 analog -> inc. production/secretion of gastric mucus + dec. acid secretion. tox: diarrhea.
long-acting somatostatin analog. inhibits actions of splanchnic vasoconstriction hormones. Tx: variceal bleeds, acromegaly, VIPoma, carcinoid tumors. tox: N, cramps, steatorrhea
antacid side effect
aluminum hydroxide side effects
aluminimum amount of feces + hypophosphatemia, prox muscle weakness, osteodystrophy, seizures
Ca carbonate SE
hyperCa, rebound acid inc. can chelate and dec. effectiveness of other drugs (e.g. tetracycline)
Mg hydroxide SE
diarrhea, hyporeflexia, hypotension, cardiac arrest.
combination of sulfapyridine (Abx) + 5-aminosalicylic acid (anti-inflam). activated by colonic bacteria. Tx: UC, crohns. SE: nalaise, N, sulfonamide tox, reversible oligospermia
Mg hydroxide, Mg citrate, polyethylene glycol, lactulose
5-HT3 antagonist; dec. vagal stim. powerful, central-acting antiemetic. tox: h/a, constipation, QT prolongation
D2 antagonist. inc. resting tone, contractility, LES tone, motility. does not influence colon transport time. Tx: DM and postsurgery gastroparesis, antiemetic. tox: parkinsonian Sx, TD, reslessness, drowsiness, fatigue, depression, diarrhea. drug-drug w/digoxin and DM meds.