• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/91

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

91 Cards in this Set

  • Front
  • Back
What does the falciform ligament connect and what is in it?
Connects the liver to the anterior abdominal wall and contains the ligamentum teres. It is a derivative of the fetal umbilical vein.
What does the hepatoduodenal ligament connect and what is in it?
It connects the liver to the duodenum and it contains the portal triad (hepatic artery, portal vein, common bile duct). It may be compressed between the thumb and index finger placed in omental foramen to control bleeding. It connects the greater and lesser sacs.
What does the gastrohepatic ligament connect and what is in it?
It connects the liver to the lesser curvature of the stomach and contains the gastric arteries. It separates the right greater and lesser sacs and may be cut during surgery to access the lesser sac.
What does the gastrocolic ligament connect and what is in it?
It separates the greater curvature of the stomach and the colon. It contains the gastroepiploic arteries and is part of the greater omentum.
What does the gastrosplenic ligament connect and what is in it?
It connects the greater curvature of the stomach to the spleen and contains the short gastric arteries. It separates the left greater and lesser sacs.
What is the splenorenal ligament connect and what is in it?
It connects the spleen to the posterior abdominal wall and contains the splenic artery and vein.
Internal thoracic/mammary (subclavian) arteries anastomose with?
Superior epigastric (internal thoracic) and inferior epigastric arteries (external iliac)
Superior pancreaticoduodenal (celiac trunk) anastomoses with?
Inferior pancreaticoduodenal artery (SMA)
Middle colic artery anastomoses with (SMA)?
Left colic artery (IMA)
Superior rectal artery (IMA) anastomoses with?
Middle rectal artery (internal iliac)
What do tumors of the head of the pancreas block?
The common bile duct
What is a sliding hiatal hernia?
The GE junction is displaced and the stomach herniates through the esophageal hiatus of the diaphragm. There is an "hourglass stomach"
What is a paraesophageal hernia?
The GE junction is normal and the cardia moves into the thorax.
What is an indirect inguinal hernia?
The bowel enters the internal (deep) inguinal ring lateral to the inferior epigastric artery, then the external inguinal ring (superficial), then INTO the scrotum. Due to failure of processus vaginalis to close (can form hydrocele). It follows the path of descent of the testes and is covered by spermatic fascia.
What is a direct inguinal hernia?
The bowel goes through the inguinal triangle (medial to the inferior epigastric artery) then through the external (superficial) inguinal ring only. It occurs in older men and is NOT covered by internal spermatic fascia.
What is a femoral hernia?
The bowel protrudes below the inguinal ligament through the femoral canal below and lateral to the pubic tubercle. Occurs in women and is the leading cause of bowel incarceration.
Why are Brunner's glands important?
They are the only GI submucosal glands. They are located in the duodenum and are hypertrophied in peptic ulcer disease (secrete alkaline mucus).
What causes Achalasia?
Loss of Auerbach's plexus (myenteric). Loss of inhibitory NO secretion. There is high LES opening pressure and uncoordinated peristalsis, resulting in progressive dysphagia for solids and liquids.
What is the difference between tropical sprue and Celiac disease?
Tropical sprue occurs at all levels of the small bowel whereas celiac sprue primarily occurs in the proximal small bowel (jejunum- folate deficiency).
What are the symptoms of Whipple's disease?
Arthralgias, cardiac and neurologic symptoms; PAS-positive macrophages in the lamina propria of the intestine
What are the features of disaccharidase deficiency?
Normal appearing villi, osmotic diarrhea (stool osmolar gap increases), stool pH decreases, and increased H+ in the breath because the abundance of excess lactose allows bacterial overgrowth.
What are the features of abetalipoproteinemia?
Patients cannot generate chylomicrons so there is decreased secretion of cholesterol and VLDL into the blood stream and fat accumulation in enterocytes. Patients present early with ataxia, night blindness, and acanthocytosos. Treat with vitamin E!
What are causes of acute gastritis? (erosive)
Stress, NSAIDs, alcohol, uremia, burns (Curling's ulcer due to decreased plasma volume and sloughing of the gastric mucosa), and brain injury (Cushing's ulcer due to increased vagal stimulation, which stimulates acid production)

Erosions means they don't penetrate the muscularis mucosa
What are the causes of chronic gastritis?
It can be autoimmune characterized by autoantibodies to parietal cells, pernicious anemia, and anchlorydria (fundus/body) OR can be caused by H. pylori (antrum), which has an increased risk of MALT lymphoma!
What causes Merckel's diverticulum and what are its symptoms?
MC congenital abnormality of the GI tract. It is due to persistence of the vitelline duct or yolk stalk. It can contain ectopic acid-secreting gastric mucosa and/or pancreatic tissue. It can lead to bleeding, intusussception, volvulus, or obstruction near the terminal ileum.
DX: Pertechnetate!!!!!!
What is Hirschsprung's disease?
Lack of ganglion cells/enteric nervous plexuses (Auerbach's and Meissner's) due to failure of neural crest cell migration. This presents as chronic constipation early in life and congenital megacolon. Failure to pass meconium. There is a constricted aganglionic part and a dilated portion proximal to that. Involves the rectum!
What is Hirschsprung's disease associated with?
Downs syndrome!
What causes duodenal atresia?
Failure of recanalization of the small bowel. Leads to early bilous vomiting with proximal stomach dilation and a "double bubble"
What GI problems is Downs syndrome associated with?
Hirschsprung disease, celiac disease, annular pancreas, and duodenal atresia!!!!
What is angiodysplasia?
Tortuous dilation of blood vessels, mostly in the cecum, terminal ileum, and ascending colon, that leads to bleeding. More common in older patients.
What is Peutz-Jeghers syndrome?
AD syndrome featuring multiple nonmalignant hamartomas throughout the GI tract, along with hyperpigmented mouth (inside of cheek), lips, hands, and genitalia. Associated with increased risk of visceral malignancy.
What is Gardner's syndrome?
FAP + osseous and soft tissue tumors, retinal hyperplasia
What is Turcot's syndrome?
FAP + malignant CNS tumor
What segments of the GI tract do FAP and HNPCC always involve?
FAP- rectum
HNPCC (macrosatellite instability)- proximal colon
What are the symptoms of distal CRC?
Obstruction, colicky pain, hematochezia (left-sided)
What are the symptoms of proximal CRC?
Dull pain, Fe-deficiency anemia, fatigue
What is the APC/beta-catenin pathway?
Loss of APC gene (progress from normal to at risk- decreased intracellular adhesion and proliferation). K-RAS mutation (at risk to adenoma- unregulated intracellular signal transduction). Loss of p53 (adenoma to carcinoma- increased tumorigenesis)
When do carcinoid tumors produce symptoms?
When they metastasize or occur OUTSIDE the GI tract (the liver metabolizes 5-HT)
What features are used to diagnose carcinoids?
Dense core bodies on EM, produce 5-HIAA. Treat with octreotide!
What are the effects of portal hypertension?
Esophageal varices (hematemesis, melena)
Peptic ulcer (melena)
Splenomegaly
Caput medusae, ascites
Portal hypertensive gastropathy
Hemorrhoids
What are causes of micronodular cirrhosis?
Alcohol, hemochromatosis, Wilson's disease (all metabolic causes)
What are causes of macronodular cirrhosis?
Postinfectious (viral), drug-induced; increased risk of HCC
What type of trait is AAT?
Codominant
What are the features of cholestasis (obstructed bile flow)?
Increased conjugated bilirubin, increased cholesterol, increased alkaline phosphatase, malabsorption of fat-soluble vitamins
What is PBC?
Autoimmune destruction of small and medium-sized intrahepatic bile ducts (granulomas); increased serum anti-mitochondrial antibodies; usually occurs in older women with other autoimmune disorders.
What is PSC?
Progressive fibrosis and destruction of extrahepatic and large intrahepatic bile ducts (onion skin). There is beading of the contrast medium. Associated with IBD (UC). Hypergammaglobinemia (IgM) and can lead to secondary biliary cirrhosis
What can cause secondary biliary cirrhosis?
Extrahepatic biliary obstruction: Gallstone, biliary stricture, chronic pancreatits, carcinoma of the pancreatic head. All increase pressure in the intrahepatic ducts, leading to injury/fibrosis affecting both intrahepatic and extrahepatic bile ducts.
What are the causes of acute pancreatitis?
Gallstones, Ethanol, Trauma, Steroids, Mumps, Autoimmune disease, Scorpion sting, Hypercalcemia/hyperlipidemia, ERCP, Drugs
What are the effects of chronic pancreatitis?
Malabsorption of fat-soluble vitamins, stearorrhea, DM
What are the effects of acute pancreatitis?
ARDS, DIC, diffuse fat necrosis, hypocalcemia, pseudocyst formation (contains granulation tissue and fibrosis), hemorrhage, infection, multiorgan failure
What is the portal-systemic anastomosis at the esophagus?
Left gastric vein to the esophageal veins
What is the portal-systemic anastomosis at the umbilicus?
Paraumbilical veins with the superificial and inferior epigastric veins
What is the portal-systemic anastomosis at the rectum?
Superior rectal vein with the middle and inferior rectal veins
What supplies the area above the pectinate line?
Superior rectal artery (IMA); venous drainage is to the superior rectal vein ---> inferior mesenteric vein ---> portal system
What supplies the area below the pectinate line?
Inferior rectal artery (Pudendal artery). Venous drainage is to the inferior rectal vein ----> internal pudendal vein ----> internal iliac vein ----> IVC
What is the order of salivary glands from most mucinous to most serous?
Sublingual, submandibular, parotid
What is the RLS in carbohydrate digestion?
Producing monosaccharides from oligosaccharides (oligosaccharide hydrolases) at the brush border of the intestine.
How are glucose, galactose, and fructose taken up by the intestine?
Glucose/galactose- SGLT1 (Na-dep)
Fructose- GLUT-5

all transported to blood via GLUT2
What is the form of bilirubin that is excreted in the feces?
Stercobilin- gives stool its color; gut bacteria excrete conjugated bilirubin from the liver in bile.
What form of bilirubin is excreted in the urine?
Urobilin- gives urine its color
What is a pleomorphic adenoma?
Benign salivary gland tumor, MC, occurs in the parotid in middle aged women, high rate of recurrence, but removable
What is Warthin's tumor?
Heterotopic salivary gland tissue trapped in a lymph node; seen in old men and smokers
What is the MCC malignant salivary gland tumor?
Mucoepidermoid carcinoma
What are causes of secondary achalasia?
Chagas' disease, Scleroderma (the E in CREST). These are due to low pressure proximal to the LES
What is associated with gastric carcinoma?
Achlorydria, chronic gastritis, type A blood, dietary nitrosamines
Where does stomach cancer metastasize?
Early on to node and liver; later to bilateral ovaries (Krukenberg) and subcutaneous periumbilical (Sister Mary Joseph)
What is linitis plastica?
When stomach cancer is diffusely infiltrative and causes the stomach to look thickened, rigid, and leathery
What are the features of gastric ulcers?
70% H. pylori, also NSAID, pain is greater with meals. Due to decreased mucosal protection against gastric acid.
What are the features of duodenal ulcers?
100% from H. pylori, pain decreases with meals, due to increased gastric acid secretion or decreased mucosal protection. Hypertrophy of Brunner's glands!!
What are the complications of peptic ulcer disease?
1. Bleeding
2. Perforation- acute peritonitis with pneumoperitoneum
3. Penetration into pancreas
4. Obstruction
What are the complications of Crohn's disease?
Affects the terminal ileum usually so B12 deficiency, gallstones from decreased bile absorption, kidney stones from decreased oxalate binding; also strictures, fistulas, perianal disease
What are the extraintestinal manifestations of Crohn's disease?
Migratory polyarthritis, erythema nodosum, ankylosing spondylitis, uveitis, immunologic disorders
What are the imaging appearances of Crohn's and UC respectively?
Crohns- String sign due to creeping fat and bowel wall thickening
UC- Lead pipe due to loss of haustra
What is the MCC of appendicitis in kids? adults?
Kids- lymphoid hyperplasia following viral infection.
Adults- obstruction, fecolith
Where do most diverticula occur?
Where the vasa recta perforate the muscularis mucosa. Most are false and don't have a full muscularis mucosa. Most in sigmoid colon.
What is a complication of diverticulitis?
Bright red rectal bleeding, colovesical fistula (fistula with bladder that shows up as air in the urine- pneumaturia), perforation (peritonitis), abscess formation, bowel stenosis.
Where is the MC location of Zenker's diverticulum?
Junction of the pharynx and esophagus due to cricopharyngeal muscle dysfunction.
Where does volvulus MC occur?
At the cecum and sigmoid colon where there is redundant mesentery. Usually in elderly
What is Budd-Chiari syndrome?
Occlusion of the IVC or hepatic veins with centrilobular congestion and necrosis, leading to congestive liver disease (Nutmeg liver). There is NO JVD and patients may have visible abdominal and back veins.

Classical triad of abdominal pain, ascites and hepatomegaly

Associated with hypercoagulable states, polycythemia vera, pregnancy, and HCC
What are the sources of urobilinogen?
-Gut bacteria convert direct bilirubin in bile to urobilinogen.
-Some comes from heme metablism (this is why there is still some urine urobilinogen in hemolytic anemia jaundice)
What can cause cholesterol gallstones?
Increased cholesterol (obesity, Crohns disease, cystic fibrosis, age), decreased bile salts, gallbladder stasis (decreased CCK, increased SST); also clofibrates, estrogens, multiparity, rapid weight loss, Native americans. ONLY form in the gallbladder.

-These are radiolucent, but 20% have calcifications that may be seen
What can cause pigment stones?
Radio-opaque
-Chronic hemolysis, alcoholic cirrhosis, age, biliary infection (beta-glucuronidase release from bacteria produces black pigment stones, bacterial phospholipases hydrolyze biliary phospholipids to produce brown pigment stones). They can fom in the lumen of the CBD as well as in the gallbladder.
What is biliary colic?
Obstruction of the CBD by gallstones causes bile duct contraction, which causes pain; in DM no pain. Patients present with localized epigastric or RUQ pain that occurs after a meal, increases in intensity, and remains steady for 1-4 hours.
What happens if a gallstone obstructs the ileocecal valve?
Gallstone ileus- see air in biliary tree; fistula between gallbladder and small intestine!
What can cause cholecystitis?
Gallstones (chemical irritation and inflammation due to stones in the GB causes mucus layer to be obstructed and exposed to bile detergents. This leads to more inflammation and hypomotility, causing ischemia). Also rarely ischemia (PAN) and infection (CMV). If the bile duct becomes involved (ascending cholangitis- increased ALP).

RUQ pain. Murphy's sign- inspiratory arrest on deep palpation due to pain
What level of the spinal cord are the celiac trunk, SMA, and IMA?
Celiac trunk- T12
SMA- L1
IMA- L3
What are the inclusions seen in AAT?
Misfolded gene product that has accumulated in the hepatocellular ER.
What are the labs seen in hemolytic causes of jaundice?
-Increased serum unconjugated bilirubin
-Absent urine bilirubin (unconjugated bilirubin is insoluble)
-Increased urine urobilinogen (comes from the metabolism of heme)
What are the labs seen in hepatocellular (hepatitis, alcoholic liver disease, hepatotoxicity, PBC- bile cannot be excreted from the liver or cannot be metabolized) jaundice?
-Increased serum conjugated/unconjugated bilirubin
-Increased urine bilirubin
-Normal/decreased urine urobilinogen
What are the labs seen in obstructive (gallstones, pancreatic cancer, etc- bile cannot get to the gut) jaundice?
-Increased serum conjugated bilirubin
-Increased urine bilirubin
-Decreased urine urobilinogen (bile cannot access the gut so it can't be converted to urobilinogen). This also leads to pale stools.
What are signs of pancreatic cancer?
1. Abdominal pain radiation to back
2. Weight loss (malabsorption)
3. Migratory thrombophlebetis- redness and tenderness on palpation of extremities (Trousseau's syndrome)
4. Obstructive jaundice with a palpable gallbladder (Courvoisier's sign)