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46 Cards in this Set
- Front
- Back
Important GI ligaments--
Falciform Hepatoduodenal Gastrohepatic Gastrosplenic Splenorenal |
F: liver to anterior abdominal wall; ligamentum teres
H: liver to duodenum; carries portal triad (hepatic a., portal v., common bile duct) GH: liver to lesser curvature of stomach; contains gastric arteries GS: greater curvature of stomach to spleen; contains short gastric aa. S: spleen to posterior abdominal wall; contains splenic a. & v. |
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Layers of gut wall
Basal electric rhythm: stomach, duodenum, ileum |
"MSMS"
Mucosa Submucosa--includes submucosal nerves (Meissner); control secretions Muscularis externa--includes myenteric nerves (Auerbach); controls motility Serosa Stomach--3 waves/min Duodenum 12 waves/min Ileum 8 waves/min |
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GI histology--
Esophagus Stomach Duodenum Jejunum Ileum Colon |
E: nonkeratinized stratified squamous epithelium
S: gastric glands D: villi, brunner glands (submucosal, secrete bicarb) J: plicae circulares I: peyer patches (lymphoid aggregates); largest portion of goblet cells in small intestine C: no villi, numerous goblet cells |
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Common abdominal aorta branches
Celiac trunk Bifurcation of abdominal aorta Renal arteries |
C: T12
B: bi"four"cation--L4 R: L1--"only need one" kidney |
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Anal fissure
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"Pain while Pooping"--tear in anal mucosa below pectinate line; commonly in posterior area as this area is poorly perfused
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Liver anatomy--
Zone 1 Zone 3 |
**Z1: periportal--**first affected by viral hepatitis
**Z3: pericentral vein (centrilobular)--affected first by ischemia, contains P-450 system (sensitive to toxins; **site of acetaminophen toxicity), **site of alcoholic hepatitis |
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Indirect versus Direct hernias
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"MDs don't LIe"--medial~direct; lateral~indirect
I: IN the scrotum, INternal inguinal ring, INfants; due to failure of processus vaginalis to close (can form hydrocele); covered by all 3 layers of spermatic fascia Lateral to inferior epigastric aa. D: typically older men, only passes thru external inguinal ring-->only have external spermatic fascia Medial to inferior epigastric aa. |
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GI regulatory substances--
CCK Gastrin Motilin |
CCK: duodenum/jejunum; inc gallbladder contraction, sphincter of Oddi relaxation, and potentiates pancreatic secretion; regulated by FA's and AA's
G: antrum of stomach; inc gastric H+ secretion and growth of gastric mucosa; regulated by stomach distention, alkalinization, AA's, peptides, vagal stimulation M: small intestine; produces migrating motor complexes (MMCs), inc in fasting state; **erythromycin is motilin receptor agonist** |
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GI regulatory substances--
Secretin Somatostatin Vasoactive intestinal peptide (VIP) |
Se: duodenum; increase pancreatic HCO3- secretion; regulated by acid and FAs in lumen of duodenum
So: pancreatic islets & GI mucosa; inhibitory hormone; shuts down GI tract V: inc intestinal water and electrolyte excretion, relaxes sphincters *VIPoma: islet cell pancreatic tumor-->watery diarrhea, hypokalemia, achlorhydria |
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Gastric parietal cell--
Vagal stimulation Gastrin Histamine |
V: stimulates both parietal and G cells to potentiate acid secretion
G: stimulated by vagus n. (GRP not ACh-->atropine does not block gastrin stimulation); directly stimulates parietal cell and also stimulates ECL cell (most important mechanism) H: ECL cells secrete histamine to directly stimulate acid secretion via H+/K+ ATPase |
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Vitamin absorption
Bile acids Folate Iron Vitamin B12 |
"Iron Fist, Bro"
Iron: duodenum Folate: jejunum B12: ileum, along w/bile; requires intrinsic factor from parietal cells |
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Bilirubin
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Product of heme metabolism (M0's); removed from blood by liver, conjugated w/glucuronate, excreted in bile
Direct--conjugated w/glucuronic acid-->water soluble Indirect--unconjugated; water insoluble |
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Salivary gland tumors--
Pleomorphic adenoma Warthin tumor Mucoepidermoid carcinoma |
Pleomorphic: benign, painless, mobile mass; biphasic--cartilage (chondromyxoid stroma) and epithelium; **high rate of recurrence
WARthin: lymphocytes and germinal centers; need these components for war Mucoepidermoid: malignant; mucinous & squamous cells |
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Esophageal cancer--
Adenocarcinoma Squamous cell |
Present w/progressive dysphagia (first solids, then liquids); Worldwide squamous more common, in US adenocarcinoma is.
A: lower 1/3 of esophagus; Risk factors: achalasia, barret, cigarettes, obesity, GERD S: upper 2/3; Risk factors: hot liquids, alcohol, tobacco, smoked foods (nitrosamines), diverticula |
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Acute gastritis (erosive)
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AKA acute stress ulcers; disruption of mucosal barrier leading to inflammation
Due to stress, NSAIDs, alcohol as well as: burns (curling ulcer--dec plasma volume->sloughing of gastric mucosa) brain injury (cushing ulcer--inc vagal stimulation->H+ production) **"Burned by curling iron" or "Cushioned by brain" **Erosions do not fully extend thru the muscularis mucosa |
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Chronic gastritis (nonerosive)--
Type A Type B |
A: Autoimmune; autoabs to parietal cells-->dec H+ and dec intrinsic factor (pernicious anemia); typically seen in "first" part of stomach
B: due to H. pylori Bacteria; commonly seen in antrum; inc risk of gastric adenocarcinoma & MALT lymphoma |
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Stomach cancer--
Intestinal Diffuse *3 most common mets of gastric Ca* |
Almost always adenocarcinoma, aggressive, **acanthosis nigricans**
I: associated w/ H. pylori, nitrosamines, tobacco; commonly on lesser curvature of stomach D: NOT associated w/H. pylori; "signet ring cells"--nucleus pushed off to side due to mucin Common mets: Virchow node--left supraclavicular node Krukenberg--bilateral mets to ovaries; signet ring cells Sister Mary Joseph--subcutaneous periumbilical nodule |
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Peptic ulcer disease
Gastric Duodenal |
G: pain greater w/meals; inc risk of carcinoma; possibly due to NSAIDs
D: pain decreases w/meals; 100% association w/H. pylori infxn; may be due to zollinger-ellison syndrome (tx-remove tumor); can see hypertrophy of brunner glands; no association w/risk of carcinoma Best long-term tx is to eradicate H. pylori infxn *antrum (prepylorus) most commonly colonized area* H. pylori decreases somatostatin secreting cells-->increased acid secretion-->ulcers |
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Abetalipoproteinemia
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Dec synthesis of apolipoprotein B-->inability to generate chylomicrons
Presents early in childhood w/failure to thrive, steatorrhea, night blindness (dec fat-soluble vitamin absorption) |
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Crohn disease
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"A fat granny in a sting bikini and an old crone skipping down a cobblestone path away from the train wreck"
Creeping fat Granulomas--TH1 String sign Skip lesions Cobblestone mucosa Transmural inflammation-->fistulas Rectal sparing ***Ileum always involved-->impaired bile acid absorption->fat malabsorption->lipids binds Ca-->increased oxalate and oxalate kidney stones |
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Ulcerative colitis
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ULLCCCERS
Ulcers Large intestine, Lead pipe appearance Continuous, CRC, Crypt abscesses Extends proximally Red diarrhea Sclerosing cholangitis |
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False versus True diverticuli
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F: only mucosa and submucosa outpouch; occurs where vasa recta perforate muscularis externa, commonly in sigmoid colon; due to inc intraluminal pressure and dec dietary fiber
i.e. Zenker--dysphagia, halitosis *may cause colovesical fistula--pneumaturia* T: all 3 gut wall layers outpouch; i.e. meckel--persistence of vitelline duct; may see ectopic gastric mucosa/pancreatic tissue T |
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Colonic polyps--
Adenomatous Juvenile Hamartomatous |
A: inc size, inc epithelial dysplasia, villous histology-->inc malignancy risk; may cause lower GI bleed or secretory diarrhea; precancerous
J: <5yo; if single->no malignant potential; juvenile polyposis syndrome--multiple juvenile polyps-->inc risk of adenocarcinoma H: Peutz-Jeghers--AD, multiple nonmalignant hamartomas thru out GI tract, hyperpigmented (freckled) mouth/lips/hands |
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CRC Genetics--
Familial adenomatous polyposis Gardner syndrome Turcot syndrome Hereditary nonpolyposis CRC |
FAP: AD, mutation of APC; 100% progress to CRC-->prophylactic colon resection; rectum always involved
G: FAP + osseous and soft tissue tumors T: FAP + malignant CNS tumor; turcot=turban HNPCC/lynch: AD, mutation of DNA mismatch repair genes; proximal colon always involved |
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CRC--
Presentation Dx Pathogenesis (2 methods) |
P: most often in rectosigmoid, association w/S. bovis
Right side: iron deficiency anemia, bleeding, exophytic mass Left side: obstruction (napkin-ring lesion), colicky pain D: Iron deficiency anemia in males >50 and postmenopausal females raises suspicion Pa: 1-microsatellite instability~DNA mismatch repair gene mutations 2-APC/b-catenin (small polyp)-->k-RAS (polyp grows)-->p53, DCC mutations "AK-53" |
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Cirrhosis and Portal HTN
Sx's due to liver cell failure -inc NH3 -inc estrogen -dec protein synthesis (albumin) |
C: diffuse fibrosis and nodular regeneration
inc NH3: hepatic encephalopathy, fetor hepaticus inc estrogen: spider nevi, gynecomastia, testicular atrophy dec protein: ankle edema, bleeding tendency |
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Serum markers of liver/pancrease--
Alkaline phosphatase (ALP) Aminotransferases (AST, ALT) Amylase Ceruloplasmin g-glutamyl transpeptidase (GGT) Lipase |
ALP: obstructive hepatobiliary disease, HCC, bone disease
ALT>AST--viral hepatitis AST>ALT--alcoholic hepatitis-"make a toAST w/alcohol" Amylase: acute pancreatitis Cerulo: dec in wilson GGT: more specific than ALP for biliary/liver disease Lipase: acute pancreatitis |
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Alcoholic liver disease--
Hepatic steatosis Alcoholic hepatitis Alcoholic cirrhosis |
HS: reversible change of macrovesicular fatty deposits; reversed w/alcohol cessation
Alcohol-->inc NADH-->dec b-oxidation of FFA & dec gluconeogenesis AH: affect centrilobular region first; swollen, necrotic hepatocytes; mallory bodies (eosinophilic inclusions) **acetaldehyde mediates damage** AST>ALT AC: irreversible, shrunken |
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Non-alcoholic fatty liver disease
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NAFLD (NASH): ALT>AST; insulin resistance common
Fatty infiltration of hepatocytes-->cellular ballooning and eventual necrosis May cause cirrhosis and HCC Independent of alcohol use |
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Hepatic encephalopathy
Define Triggers |
cirrhosis-->decreased NH3 metabolism-->neuropsych dysfxn
T: Inc NH3--dietary protein, GI bleed, constipation Dec NH3--renal failure, diuretics, post-TIPS T: lactulose (acidifies GI to generation NH4+) |
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HCC--
Risk factors Findings Presentation |
RF: HBV, HCV, wilson, hemochromatosis, a1-antitrypsin deficiency, alcoholic cirrhosis, carcinogens (aflatoxin->p53 mutation)
Spread hematogenously; elevated AFP P: jaundice, tender hepatomegaly, ascites, anorexia *Most common hepatic malignancy is mets from another site, not HCC*-->multiple nodules |
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Other liver tumors--
Cavernous hemangioma Hepatic adenoma Angiosarcoma |
CH: most common, benign; biopsy contraindicated due to risk of hemorrhage
HA: benign, related to oral contraceptive or anabolic steroid use A: malignant tumor; due to exposure to arsenic and vinyl chloride |
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Hereditary hyperbilirubinemias--
Gilbert syndrome Crigler-Najjar syndrome Dubin-Johnson syndrome Rotor syndrome |
UGT--conjugation enzyme (UDP-glucuronosyltransferase)
GS: low UGT; jaundice during stress, otherwise a-sx CN (sounds evil): absent UGT; kernicterus, fatal DJ: deficiency of CB canalicular transport (ATP-dependent process); black liver, benign R: milder DJ, no black liver |
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Wilson disease--
Cause Findings Tx |
Inadequate hepatic copper excretion (bile)-->copper accumulation-->produces free radicals->tissue damage
F: dec ceruloplasmin, corneal deposits (kayser-fleischer rings), **basal ganglia degeneration (parkinsonian Sx's), dementia, dyskinesia Tx: penicillamine or trientine; AR inheritence |
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Hemochromatosis
Findings Etiology: primary, secondary Tx |
Cirrhosis, "Bronze diabetes"
Primary: AR mutation of protein on basolateral surface of intestinal cells that regulates tranferrin/iron complex-->excessive uptake due to lack of regulation Secondary: chronic transfusion Tx: phlebotomy *menstruation slows progression as iron is lost during bleeding |
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Biliary tract diseases--
Primary biliary cirrhosis Primary sclerosing cholangitis |
PBS: autoimmune rxn-->lymphocytic infiltrate + granulomas-->destruction of intralobular bile ducts; serum mitochondrial abs (IgM) and other autoimmune conditions
pts present: pruritis, jaundice, dark urine; may see xanthelasma formation (inc cholesterol) labs: inc CB, inc ALP PSC: concentric "onion skin" bile duct fibrosis-->alternating strictures and dilation w/beading on ERCP; Same pt presentation, and same labs **Associated w/ulcerative colitis; +p-anca** |
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Gallstones--
Risk factors Types |
RFs (4 F's): Fertile, Fat, Forty, Female
Inc cholesterol, dec bile salt or biliary stasis==> inc risk of gallstone Cholesterol stones: estrogen tx (stimulates HMG-CoA reductase activity-->**inc cholesterol synthesis), rapid weight loss, fibrate & bile resin tx **Pigment stones** Black--radiopaque, chronic hemolysis Brown--radiolucent, infxn Associated w/biliary infxns of E. coli or flukes Infxn-->release of b-glucuronidase by injured hepatocytes & bacteria-->inc UCB in bile **opioid analgesics and alcohol can cause contraction of sphincter of oddi-->biliary colic |
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Pancreatitis--
Acute pseudocyst Chronic |
A: often due to alcohol, gallstones, trauma
Elevated amylase & lipase (higher specificity) Can lead to DIC, ARDS, hypocalcemia P: persistently elevated amylase; lined by granulation tissue, not epithelium; filled with fluid rich w/enzymes and debris C: alcohol abuse most common cause, CF in kids; often calcifications present (chains of lakes) Can lead to pancreatic insufficiency->steatorrhea, fat-soluble vitamin deficiencies; increased risk for pancreatic adenocarcinoma |
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Pancreatic adenocarcinoma--
Origin Marker Risk factors Co-presentation Tx |
O: arises from pancreatic ducts (glandular)
M: CA-19-9 RF: *smoking*, chronic pancreatitis, age >50 Co: Obstructive jaundice w/palpable nontender gallbladder (courvoisier sign--tumor in head of pancreas) Migratory thrombophlebitis--redness & tenderness on palpation of extremities; essentially superficial venous thrombosis (trousseau syndrome) Secondary DM if tumor in body or tail Tx: whipple procedure--remove head/neck of pancreas, proximal duodenum, & gall bladder |
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H2 blockers--
Mechanism Toxicity |
CimetiDINE, ranitiDINE, ~dine
M: reversible block of H2 receptors-->decreased H+ secretion by parietal cells T: Cimetidine is potent P450 inhibitor, also causes gynecomastia/impotence |
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PPI's--
Mechanism Toxicity |
Omeprazole, ~"prazole"
M: irreversibly inhibit H+/K+ ATPase in stomach parietal cells T: increased risk of C. diff; may see hypergastrinemia; decreased Mg2+ with long-term use |
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Bismuth, Sucralfate
Mechanism; Use Misoprostol Mechanism; Use Octreotide Use |
B,S: bind to ulcer base, providing physical protection-->allows HCO3 to establish mucous layer
M: PGE analog; inc production of mucous barrier Prevents NSAID-induced ulcers; also ripens cervix O: acute variceal bleeds, acromegaly, VIPoma, carcinoid tumor |
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Antacid use--
Aluminum hydroxide Magnesium hydroxide |
AlOH: Alu"minimum" amount of feces--constipation
also hypophosphatemia, proximal weakness Mg: "Must Go to the bathroom"--diarrhea also cardiac arrest (prolong QT), htn |
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Osmotic laxatives--
Magnesium hydroxide, magnesium citrate, polyethylene glycol, lactulose Mechanism Use |
M: provide osmotic load to draw water out
U: constipation Lactulose used in hepatic encephalopathy to excrete NH4+ |
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Infliximab
Sulfasalazine |
I: anti-TNF; crohn disease, ulcerative colitis, RA, ankylosing spondylitis, psoriasis
S: combination of sulfa (abx) & aspirin (ASA); activated by colonic bacteria may cause sulfonamide toxicity |
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Odansetron, Alosetron
Metoclopramide |
O: 5-HT3 antagonist, also decreases vagal stimulation
controls vomiting postop & after CTX may cause HA M: D2 receptor antagonist (prokinetic); increases motility and LES tone **used in gastroparesis and antiemetic** *can cause parkinsonian effects** |