GI USMLE Flashcards
baby vomits milk when fed and has a gastric air bubble. What kind of fistula is present?
blind esophagus w/ lower segment of esophagus attached to trachea
After a stressful life event, 30 y/o female has diarrhea and blood per rectum; intestinal bx shows transmural inflammation. what is thedx
crohn’s dz
young man presents w/ mental deterioration and tremors. he has brown pigmentation in a ring around the periphery of his cornea and altered LFTs. What tx should he receive?
penicillamine for wilson’s dz
20y/o male presents w/ idiopathic hyprbilirubinemia. what is the most common cause?
Gilberts dz
Given the embrionic gut region, give the aa that supplies it and the sxs supplied:
Foregut
Celiac aa
stomach to prox duodenum, liver, gallbladder, pancreas
Given the embrionic gut region, give the aa that supplies it and the sxs supplied:
midgut
SMA
distal duodenum to prox 2/3 of transverse colon
Given the embrionic gut region, give the aa that supplies it and the sxs supplied:
hndgut
IMA
distal 1/3 of transvere colon to upper portion of the rectum
Stoach recieves main blood supply from branches of this ________
celiac trunk
because of portal-systemic anastomoses blockage of 1 vv can result in congestion of blood in an alternate route. Given the backup what type of pathology would you see.
L gastric →azygous
What is this a common complication with?
esophageal varicies
Portal HTN
mneu: varices of GUT, BUTT, and CAPUT are commonly seen with portal hypertension
because of portal-systemic anastomoses blockage of 1 aa can result in congestion of blood in an alternate route. Given the backup what type of pathology would you see.
Superior →inferior rectal
What is this a common complication with?
external hemorrhoids
mneu: varices of GUT, BUTT, and CAPUT are commonly seen with portal hypertension
because of portal-systemic anastomoses blockage of 1 vv can result in congestion of blood in an alternate route. Given the backup what type of pathology would you see.
Paraumbilical →inferior epigastric
What is this a common complication with?
caput medusae at naval
mneu: varices of GUT, BUTT, and CAPUT are commonly seen with portal hypertension
because of portal-systemic anastomoses blockage of 1 artery can result in congestion of blood in an alternate route. What two places do the the retroperitonal vv usually back up to?
renal and paravertebral vv
layers of gut wall (inside to outside)[pic.p.264]
1) mucosa
2) submucosa
3) muscularis externa
4) serosa/adventita
mucosal layer consists of these three layers (give fxs as well)
epithelium (absorption) lamina propria (support) muscularis mucosa (mucosal motility
Submucosa includes this nerve plexus that controls these fxs
Submucosal (Meissner’s)
controls Secretions, blood flow, and absorption
Muscularis externa includes this nerve plexus that controls these fxs
Myenteric nerve plexis (Auerbach’s)
controls mobility
Muscularis externa has these two layers of mm
outer longitudinal layer
inner circular layer
This enteric nerve plexus coordinates MOTILITY along the entire gut wall. It contains cell bbodies of some parasympathetic terminal effector neurons. It is located between inner and outer layers (longitudinal and circular) smooth mm in the GI tract wall
Myenteric (Auerbach’s) plexus
This enteric nerve plexus regulates local SECRETIONS, blood flow, and absorption. It contains cell bodies of some parasympathetc terminal effector neurons. It is located between the mucosal and inner layer of smooth mm in the GI tract wall.
Submucosal (Meissner’s) plexus
These glands secrete alkaline mucus to neutrolize acid contents entering the duodenum from the stomach. They are located in the duodenal submucosa.
brunners glands
these are the only GI submucosal glands
brunner’s glands
hypertrophy of Brunner’s glands is seen in what dz
Peptic Ulcer dz
Unencapsulated lymphoid tissue found in lamina propria and submucosa of the small intestine
Peyer’s patch
Peyer’s patches are covered by a single layer of cuboidal enterocytes with specialized _____ cells intersperced.
M cells
Are their goblet cells in peyer’s patches
no
______ take up antigen.
M cells.
Stimulated _____ leave Peyer’s patch and travel through lyph and blood to lamina propria of the intestine, where they differentiate into __________.
M cells
IgA-secreting plasma cells
_____ receives protective secretory component and is then transported across epithelium to gut to deal with intraluminal Ag
IgA
Irregular “capillaries” with fenestrated endothelium (pores 100-200 nm in diameter). No basement membrane. Allows macromolecules of plasma full access to basal surface of hepatocytes through perisinusoidal space (space of Disse)
Sinusoids of liver
line formed where hindgut meets ectoderm
pectinate line
Above pectinate line or below pectinate line:
internal hemorrhoids (not painful)
above pectinate line
Above pectinate line or below pectinate line:
external hemorrhoids (painful)
below pectinate line
Above pectinate line gets _________ innervation (visceral or somatic innervation)
Viscral
internal hemorrhoids receive ________ innervation
visceral
arterial supply of above the pectinate line is from the _________
superior rectal artery (branch of IMA)
venous drainage of above the pectinate line is to the _________ to the IMV to the portal system
supierior rectal vein
cancer associated with above pectinate line is _________
adenocarcinoma
Below pectinate line is innervated via ________ innervation
somatic
external hemorrhoids recieve _______ innervation and are therefore quite painful
somatic
cancer associated with below pectinate line
squamous cell carcinoma
arterial supply to below pectinate line
inferior rectal aa (branch of internal pudendal aa)
venous drainage of below pectinate line is to _______ to internal pudendal vv to internal iliac vv to IVC
inferior rectal vv
lateral to medial in the femoral triangle
which of these sxs lie inside the femoral sheath
femoral nn, aa, vv, empty space and lymphatics (deep inguinal LNs
all except femoral nn lie in the sheath
mneu: N-(AVEL)
what sxs make up the femoral triangle
1) sartorius mm
2) inguinal ligament
3) adductor longus mm
this drug class consists of Cimetidine, rantidine, famotidine, nizatidine
H2 blockers
these drugs reversibly block histamine H2 receptors leading to decreased H+ secretion by parietal cells
H2 blockers (tidines)
these drugs are used for peptic ulcer, gastritis, mild esophageal reflux
H2 blockers (tidines)
This drug is a potent inhibitor of P-450; it also has an antiadrogenic effect and decreased renal excretion of cratinine. Other H2 blockers are relatively free fo these effects
Cimetidine
these drugs include omeprazole, lansoprazole
protone pump inhibitors (prazoles)
these drugs work by irreversibly inhibiting H+/K+ATPase in stomach parietal cells
protone pump inhibitors (prazoles)
These drugs are used for peptic ulcers, gastritis, esophageal reflux, and zollinger-ellison syndrome
protone pump inhibitors (prazoles)
these drugs work by binding to the ulcer base, providing physical protection, and allowing HCO3- secretion to reestablish pH gradient to the mucus layer
Bismuth, sucralfate
these drugs are used to help in ulcer healing and traveler’s diarrhea
Bismuth, sucralfate
triple therapy of H. pylori ucers includes
1) metronidazole
2) bismuth
3) amoxicillin (or tetracycline)
this drug is a PGE1 analog that increases production and secretion of gastric mucous barrier, and decreases acid production
misoprostol
this drug is used clinically to prevent NSAID-induced peptic ulcers, maintain a patent ductus arteriosus, and to induce labor
misoprostol
toxicity of this drug includes diarrhea. It is contraindicated in women of childbearing potential (abortifacient)
misoprostol
drugs of these this class includes pirenzepine & propantheline
muscarinic antagonist
these drugs act by blocking M1 receptors on Enterochromaffin-like (ECL) cells (decreasing histamine secretion) and M3 receptors on parietal cells (decreased H+ secertion)
Muscarinic antagoinists
these drugs are clinically indicated only for peptic ulcer
muscarinic antagonist
these drugs toxicieite include bradycardia, dry mouth, difficulty focusing eyes
muscarinic antagonist
this drug is a monoclonal antibody to TNF-alpha, a proinflammatory cytokine
infliximab
this drug is used for Crohn’s dz & rheumatoid arthritis
infliximab
this drug for crohns dz and arthritis has toxicities that include respiratory infection, fever, hypotension
infliximab
These drugs act with a combination of sulfapyridine (antibacterial) and mesalamine (anti-inflammatory) which is activated by colonic bacteria.
sulfasalazine
this drug is used clinically for ulcerative colitis & crohn’s dz
sulfasalazine
the toxicities of this drug include malaise, nausea, sulfonamide toxicity, reversible oligospermia
sulfasalazine
This drug is a 5-HT3 antagonist.
Ondansetron
this drug is used to control vomiting postoperatively and in patients undergoing cancer chemotherapy
ondansetron
you will not vomit with ONDANSetron, so you can go ON DANCing.
toxicities of this antiemetic include headache and constipation
ondansetron
overuse of these drugs can affect absorption, bioavaiability, or urinary excretion of other drugs by altering gastric and urinary pH or by delaying gastric emptying
antacid
Antacids:
Primary SEs of Aluminum hydroxide
constipation and hypophosphetemia
mneu: aluMINIMUM amount of feces
Antacids:
Primary SEs of magnesium hydroxide
diarrhea
mneu: Mg- Must Go to the bathroom
Antacids:
Primary SEs of calcium carbonate
hypercalcemia and rebound acid increase
all antacids can cause _______
hypokalemia
This is a very aggressive CA, prognosis averages 6 mo. or less, usually already metastasized at presentation.
panceratic adenocarcinoma
pancreatic adenocarcinomas are more common in the pancreatic ______(head or tail)
head–obstuctive jaundice
this often presents with:
1) abd pain radiating to back
2) weight loss (due to malabsorption & anorexia)
3) migratory thrombophlebitis (trousseau’s syndrome)
4) obstructive jaundice w/ palpable gallbladder (courvoisier’s sign)
pancreatic adenocarcinoma
this is caused by activation of pancreatic enzymes leading to autodigestion
acute pancreatitis
causes of acute pancreatitis
Gallstones Ethanol Trauma Steroids Mumps Auutoimmune dz Scorpion sting Hypercalcemia/Hyperlipidemai Drugs (e.g., sufla drugs)
mneu: GET SMASHeD
this can cause fatal pancreatitis
ddI (videx)
what is the clinical presentaton of acute pancreatitis
pt presents w/ epigastric abdominal pain raiating to back with anerexia and nausia
what 2 labs will be elevated in acute pancratitis
amylase, lipase
amylase and lipase which has the higher specificity
lipase
acute pancreatitis can lead to (give 3)
DIC, ARDS, diffuse fat necrosis, hypocalcemia, pseudocyst formation, hemorrhage, and infection
chronic calcifying pancreatitis is strongly associated with _______
alcoholism
chronic obstructive pancreatitis is stongly associated with ______
gallstones
these form when solubizing bile acids and lecithin are overwhelmed by increased cholesterol and/or bilirubin
gallstones
risk factors for gallstones
1) fat
2) female
3) fertile
4) forty
3 types of gallstones
1) cholesterol stones
2) mixed stones
3) pigment stones
these stones are radioluscent with 10-20% opacity due to calcifications. They are associated with obesity, Crohn’s dz, cystic fibrosis, advanced age, clofibrate, estrogens, multiparity, rapid weight loss, and Native American origin
Cholesterol stones
these stones are the most common type. They are radioluscent and they have both cholesterol and pigment components.
mixed stones
these stones are radiopaque. They are seen in pts w/ chronic RBC hemolysis, alcoholic cirrhosis, advanced age, and biliary infection.
pigment stones
how do you dx gallstones
US
how do you tx gallstones
cholecystectomy
rare, often fatal childhood hepatoencephalopathy. Findings include fatty liver (microvesicular fatty change), hypoglycemia, and coma. It is associated with viral infection (especially VZV and infuenza B) and salysylates; thus, aspirin is no longer recommended for children (use acetaminophen, with caution)
Reye’s syndrome
Most common primary malignant tumor of the liver in adults.
hepatocellular carcinoma (hepatoma)
this CA is associated with hepatitis B & C, Wilson’s dz, hemochromatosis, alpha 1 antitripsin deficiency, alcoholic cirrhosis, and carcinogins (e.g., aflatoxin B1)
hepatocellular carcinoma.
this CA can present with tender hepatomegaly, ascites, polycythemia, and hypoglycemia
hepatocellular carcinoma
hepatocellular carcinoma, like renal cell carcinoma, is commonly spread via this method of dissemination
hematogenous
HCC shows elevated serum _________ level
alpha fetaprotien
HCC may lead to this syndrome ______.
Budd-Chiari syndrome
intrahepatic, autoimmune disorder characterized by severe obstructive jaundice, statorrhea, pruritis, hypercholesterolemia (xanthoma).
labs show: ↑alk phos, ↑ serum mitochondrial Ab
primary billiary cirrhosis
this disorder is due to extrahepatic biliary obstruction. Increased pressure in intrahepatic ducts leading to injury/fibrosis. Often complicated by ascending cholangitis (bacterial infection), bile statis, and “bile lakes.”
labs show: ↑alk phos & ↑conjugated bilirubin
secondary biliary cirrhosis
both intra- and extrahepatic. Inflamation and fibrosis of bile ducts leads to alternating strictures and dilation with “beading” on ERCP.
Primary sclerosing cholangitis
Primary sclerosing cholangitis us assiciated with ________
ulcerative colitis
Primary sclerosing cholangitis can lead to _______
secondary biliary cirrhosis
charcot’s triad of cholangitis
1) jaundice
2) fever
3) RUQ pain
mildly ↓ UDP-glucuronyl transferase. Asymptomatic but unconjugated bilirubin is elevated without overt hemolysis. Associated with stress
Gilbert syndrome
Absent UDP-glucuronyl transferase. Presents early in life; pts die within a few years.
Crigler-Najjar syndrome, type I
Findings include: juandice, kernicterus (bilirubin deposition in brain), ↑ unconjugated bilirubin.
Crigler-Najjar syndrome, type I
treatment of Crigler-Najjar syndrome, type I
plasmapheresis and phototherapy
Crigler-Najjar type I is a severe dz. Type II is less severe and responds to _______
phenobarbital
this d/o is due to conjugated hyperbilirubinemia due to defective liver excretion. Grossly black liver. Benign.
Dubin-Johnson syndrome.
this syndrome is similar to Dubin-Johnson syndrome but even milder and does not cause black liver.
Rotor’s syndrome
normally, liver cells convert unconjugated (indirect) bilirubin into _________ bilirubin
conjugated (direct)
_______ is water soluble and can be excreted into urine
Direct bilirubin
The liver converts some of the direct bilirubin into bile to be converted by gut bacteria to ________
urobilogen
Some urobilogen is _______
reabsorbed.
Some urobilinogen is also formed directly from ________
heme metabolism
Give the jaundice type:
conjugated/unconjucated hyperbilirubinemia
↑ urine bilirubin
nml/↓ urine urobilinogen
hepatocellular jaundice
Give the jaundice type:
conjugated hyperbilirubinemia
↑ urine bilirubin
↓ urine urobilinogen
obstructive jaundice
Give the jaundice type:
unconjucated hyperbilirubinemia
no urine bilirubin
↑ urine urobilinogen
hemolytic jaundice
deposition of hemosiderin (iron)
hemosiderosis
dz caused by iron deposition
hemochromatosis
classic triad of hemochromatosis
1) micronodular cirrhosis
2) pancreatic fibrosis
3) skin pitmentation
