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;
99 Cards in this Set
- Front
- Back
Two functions of bile
|
1) Exocrine secretion - normal digestion
2) Excretion of metabolic waste |
|
detergents that solubilize lipids in bile and in the gut
|
Bile salts
|
|
What gives bile its color?
|
Bilirubin, derived from heme breakdown
|
|
Major route of cholesterol degradation in the human body
|
Bile acid synthesis by liver
|
|
Amphiphilic: defn
|
Having both a polar and nonpolar portion. this is what makes bile salts good detergents.
|
|
Micelle: defn
|
Nonpolar parts on inside away from water, polar parts in contact with water.
Lipids that are normally insoluble are dissolved into the nonpolar core of bile salt micelle |
|
What is the biliary canaliculus?
|
Channel running between adjacent hepatocytes where bile is formed.
|
|
acid entering duodenum from stomach causes release of the hormone _____ which stimulates bicarb secretion, the main mech by which gastric acid is neutralized in duodenum
|
secretin
|
|
What does the gallbladder do?
|
Removes sodium, chloride, and water from bile, leaving organic components. Effectively it concentrates bile and makes it more effective
|
|
T/F Concentrated bile is hyperosmolar
|
F. Micelles are not osmotically active.
|
|
When is CCK released?
|
When protein or fat from food enters the duodenum.
|
|
WHat does CCK do?
|
Causes the gallbladder to contract and sphincter of Oddi to relax, emptying bile into the gut.
|
|
What happens to conjugated bile salts?
|
Normally they dont get absorbed in the jejunum or duodenum but stay in intestinal lumen where they carry out detergent function
|
|
What is the enterohepatic circulation?
|
Process by which conjugated bile salts are reabsorbed, return to liver in portal blood partly bound to albumin, and taken up by hepatocytse and immediately secreted back into bile.
|
|
What happens to the small (5%) amount of bile salts that reaches the colon?
|
Anaerobic bacteria deconjugate the bile salt and it becomes secondary bile salts, which can be passively reabsorbed from colon, taken up by liver, and made into bile salts
|
|
What does "conjugated" mean?
|
The bile salts carboxylic group is amidated (conjugated) to taurine or glycine
|
|
T/F Deoxycholic and lithocholic acids are toxic and may play a role in pathogenesis of gallstones or even cancer
|
T
|
|
What is acholic stool and why does it occur?
|
When bile duct is completely obsturcted, bilirubin can't reach the colon. Stools lose brown color and become chalky gray.
|
|
What causes the brown color of stool?
|
When bilirubin reaches the colon it is acted on by intestinal bacteria --> brown color
|
|
What causes upregulation of bile salt synthesis?
|
When bile salts fail to return to liver/are deficient in gut
|
|
What happens to LDL when bile salt synthesis is upregulated?
|
Liver cholesterol is used up making the bile salts, then the liver takes up LDL to replace the cholesterol it's using, and serum LDL cholesterol falls.
|
|
What is cholestasis?
|
Condition in which bile formation is impaired and bile components (bilirubin, bile salts, cholesterol) accumulate in blood.
|
|
Cholelithiasis: defn
|
Gallstone disease
|
|
Cholecytolithiasis
|
Gallstones in gallbladder
|
|
Choledocholithiasis
|
Gallstones in bile ducts
|
|
What is cholecystectomy?
|
Surgery that cures gallstones by removing gallbladder
|
|
What are most gallstones made of?
|
cholesterol monohydrate
|
|
What is the typical gallstone patient?
|
Five Fs:
Fat, Fair, Fertile, Female, Forty |
|
What is the cause of black pigment stones with calcium bilirubinate?
|
Theyre due to increased heme turnover, from chronic hemolytic disease, cirrhosis, hypersplenism.
|
|
What is the cause of brown pigment stones?
|
They contain calcium salts of fatty acids and bilirubin.
Formed when there's a biliary stricture where stasis allows chronic bacterial colonization of bile. Bacterial esterases act on conjugated bilirubin and phospholipid to release free bilirubin and fatty acids that precipitate calcium. Form within bile ducts. |
|
Where are brown pigment stones common?
|
rice growing areas of Asia, due to strictures caused by infection with liver flukes
|
|
Stricture: defn
|
narrowing, stenosis
|
|
What is the pathophysiology of gallstones?
|
Bile becomes supersaturated, which depends on the amount of a solute secreted into bile at level of canaliculus and degree to which it's concentrated.
Nucleation occurs in supersaturated bile, leading to crystal precipitation. Mucus traps crystals, forming biliary "sludge" Stasis allows aggregation and fusion of crystals into macroscopic stones. |
|
How do estrogens affect formation of gallstones?
|
Estrogens in women increase cholesterol content of bile relative to bile salts and phospholipid.
This causes bile to become supersaturated with cholesterol when it's concentrated. |
|
What are the 4 stages of gallstone formation?
|
1) Lithogenic state
2) Asymptomatic gallstones 3) Symptomatic gallstones 4) Complicated gallstones |
|
What are symptoms of gallstones?
|
biliary colic - thought to result when stones or sludge transiently obstruct flow of file, raising pressure or increasing wall tension.
Recurrent episodes likely to occur. Indications for cholecystectomy |
|
Characteristics of biliary colic
|
Continuous, epigastric and/or right upper quadrant, typically lasts for >30 minutes.
Sometimes very severe. NOT pain that occurs routinely or predictably from a fatty meal. These are more likely GERD or IBS. |
|
What are acute complicatiosn of gallstones?
|
If gallstone is impcated in the cystic duct for more than a few hours, the gallbladder becomes ischemic and inflamed, leading to bacterial overgrowth - acute cholecystitis.
|
|
What happens if gallstones escape into the common bile duct?
|
May produce obstructive jaundice with elevation of liver enzymes.
|
|
How to distinguish choledocholithiasis from biliary obstruction from cancer or pancreas?
|
In cancer, the obstruction is usually painless and steadily progrsesive. In choledocholithiasis , it's usually accompanied by biliary colic symptoms and jaundice tends to fluctuate.
|
|
The bile duct and pancreatic duct both empty into the duodenum through the channel _________
|
ampulla of Vater
|
|
What happens if a stone passing through the ampulla transiently obstructs pancreatic secretory flow?
|
Can trigger acute pancreatitis
|
|
What happens in acute cholecystitis?
|
Obstruction of gallbladder causes inflammation and ischemia over a few hours.
Can result in gallbladder gangrene and perforation |
|
What happens in ascending cholangitis?
|
Persistent impaction of stone in common bile duct causes dilation --> pyogenic infection with gram negative bacteria.
Leads to Charcot's triad of RUQ pain, fever, and jaundive |
|
What is Charcot's triad?
|
RUQ pain
Fever Jaundice |
|
Treatment for ascending cholangitis
|
Antibiotics
Intervention to take out stone |
|
What is chronic cholecystitis?
|
Gallstones in gallbladder over time produce chronic inflammation and fibrotic.
Normal function of gallbladder is lost. |
|
In what settings does gallbladder cancer usually occur?
|
Usually from chonic cholecystitis
|
|
T/F Gallstones are visible on xrays
|
F. It depends on the type of stone
|
|
Which gallstones are radiolucent and opaque on xray?
|
Lucent: Cholesterol (most common)
Opaque: pigment stones that contain Calcium. |
|
Best way to dx gallstones
|
ultrasound
|
|
What is HIDA radionuclide gallbladder scanning and what is it useful for?
|
When acute cholecystitis is suspected.
Liver takes up HIDA and normally should be seen to enter gallbladder and bile duct and duodenum. If not seen, this supports a dx of acute cholecystitis. |
|
What is cholangiography?
|
imaging of bile ducts.
|
|
What is life like without a gallbladder?
|
Bile salts circulate continuously. About 5--10% of people develop diarrhea due to increased bile salt reaching the colon. This responds to bile-acid binding resins.
|
|
What is ursodeoxycholic acid?
|
A bile salt found in bears that dissolves gallbladder stones.
Gradually leaches cholesterol and dissolves stones |
|
How to prevent gallstone formation in high risk patients?
|
Giving ursodeoxycholic acid
|
|
Who are high risk patients for gallstone formation?
|
Those undergoing rapid weight loss (25% will form cholesterol gallstones in 4 months)
|
|
Lifetime risk of gallstones
|
Prevalence: 25%
Surgery: 10% |
|
Four E’s of biliary colic
|
1) Epigastric
2) Episodic 3) Extremely painful 4) Extended (>30 minutes) |
|
Which enzymes from the pancreas are secreted in the active form? inactive?
|
Active: those for FAT and CARBOHYDRATE digestion (lipase, amylase)
Inactive: Proteases and phospholipases |
|
Most of the pancreas output is _________
|
proteases (70%)
|
|
Converts trypsinogen --> trypsin
|
enterokinase
|
|
Where is enterokinase located?
|
intestinal brush border
|
|
Pancreatic ducts secrete _______ while acini secrete ______
|
bicarb; enzymes
|
|
what increases pancreatic secretion?
|
Neural stimulation (vagus n, enteropancreatic cholinergic neurons); Hormonal (secretin and CCK) stimuli
|
|
How is pancreatic secretion inhibited?
|
By a negative fb loop.
The presence of activated trypsin, chymotrypsin, and elastase in duodenum --> decrease in CCK ---> decrease in pancreatic secretions |
|
Defn of acute pancreatitis
|
Acute inflam process arising in exocrine pancreas presenting with abdominal pain, and associated with elevated pancreatic enzymes in blood and urine.
|
|
Pathogenesis of pancreatitis
|
Inactive pancreatic enzymes become activated and start digesting the pancreas
|
|
What is the change in calcium in the blood with pancreatitis and why?
|
HYPOcalcemia.
Several factors cause it including hypoalbuminemia, calcium complexing with released fatty acids in the peripancreatic region, and inhibition of parathormone release. |
|
Most common causes of acute pancreatitis
|
Alcohol
Gallstones Trauma/surgery Certain drugs Infection Idiopathic in 30% |
|
Common clinical manifestations of pancreatitis
|
Abdominal pain, vomiting, jaundice, fever, tachycardia, cyanosis, respiratory distress with severe attacks.
|
|
Phlegmon: defn
|
spreading diffuse inflammatory process with formation of suppurative/purulent exudate or pus. This is the result of acute purulent inflammation which is due to bacterial infection.
|
|
How is pancreatitis diagnosed?
|
Elevated serum amylase/lipase in patient with suggestive clinical findings
|
|
Which of serum amylase or lipase is more specific and sensitive to pancreatitis dx?
|
lipase. amylase is associated with other disease states.
|
|
What is treatment of acute pancreatitis?
|
Supportive, based on severity of disease.
1) Rehydration 2) No oral intake 3) Adequate pain control 4) Nasogastric suction if vomiting or signs of an intestinal ileus 5) Close monitoring of serum electrolyte status 6) Respiratory support if evidence of impending respiratory distress 7) Replacement of blood 8) Parenteral nutrition for severe, prolonged attack 9) Abx if underlying infection |
|
Chronic pancreatitis: defn
|
recurrent/persistent abdominal pain and / or evidence of pancreatic insufficiency (steatorrhea or diabetes).
Continuing inflam. process of the pancreas with irreversible morphologic changes. |
|
Etiology of chronic pancreatitis
|
Majority have alcohol-related disease
Cystic fibrosis - association 30% are idiopathic Hereditary - mutations in trypsin gene. Ductal obstruction |
|
Common clinical presentations of chronic pancreatitis
|
Pain (most common)
steatorrhea diabetes (type 1) Extrahepatic biliary obstruction - due to fibrosis of head of pancreas |
|
pancreatic pseudocyst: defn
|
a circumscribed collection of fluid rich in pancreatic enzymes, blood, and necrotic tissue, typically located in the lesser sac of the abdomen.
Usually a complication of chronic pancreatitis |
|
How to dx chronic pancreatitis
|
Clinical history and confirmed by tests which define structure
a) plain xray (will see calcifications) b) ultrasound (ductal dilatation - non specific) c) CT scan of abdomen d) MRCP (ductal imaging) e) ERCP (ductal ectasia, narrowing) f) endoscopic ultrasound |
|
What is the Secretin/CCK stimulation test?
|
80% sensitive, 90% specific test for pancreatic function
|
|
What is treatment of chronic pancreatitis aimed at?
|
1) Pain relief
2) Treatment of steatorrhea 3) Treatment of diabetes |
|
What is autoimmune pancreatitis?
|
Rare disease. See mild recurrent pancreatitis, biliary and pancreatis duct strictures resembling primary sclerosing cholangitis, pancreatic mass.
On histology, see extensive lymphoblastic infiltrate and dense fibrosis. Treatment is glucocorticoids |
|
hereditary pancreatitis due to a mutation in __________
|
trypsinogen
|
|
Grey Turner's sign: defn
|
bruising of the flanks.
This sign takes 24–48 hours. It can predict a severe attack of acute pancreatitis. Sign of retroperitoneal hemorrhage. methemalbumin formed from digested blood tracks subcutaneously around the abdomen from the inflamed pancreas |
|
What is teh relationship between Adult Respiratory Distress Syndrome (ARDS) and pancreatitis?
|
Can occur with severe pancreatitis. More common in setting of hyperlipidemia.
Cytokine mediated. |
|
What is a method of detecting pancreatic necrosis in pancreatitis?
|
CT with contrast
|
|
What are some early indicators that the pancreatitis is severe?
|
tachycardia
tachypnea hypotension hypoxemia hemoconcentration (decr in blood fluid) oliguria encephalopathy |
|
Naso-gastric Suction: what is it used for in pancreatitis?
|
Persistent vomiting, obstruction
|
|
When do pseudocysts occur following pancreatitis?
|
>4 weeks
|
|
What is steatorrhea?
|
Visible fat/oil droplets in stool.Increased volume, light color, foul odor.
|
|
What is the cause of pain in pancreatitis?
|
Pancreatic duct obstruction with increased pressure.
Ischemia Pseudocyst |
|
Pathogenesis of steatorrhea
|
Decreased concetrations of lipase and colipase.
Decrease in duodenal pH. (pancreatic lipase is not active at pH <4.5) Also see precipitation of bile salts. |
|
Magnetic resonance cholangiopancreatography (MRCP): what is it?
|
MR tool to visualize biliary and pancreatic ducts in a non-invasive manner. Use to determine if gallstones are blocking.
|
|
What are the most sensitive structural diagnostic tests for pancreatitis?
|
MR cholangiopancreatography ; endoscopic retrograde cholangiopancreatography ; Endoscopic ultrasound (EUS)
|
|
What is the Double Lumen Tube Test? How performed? What are downsides?
|
Determines volume and composition (specifically bicarb) of duodenal fluid
Downsides: unpleasant, time-consuming |
|
How to manage exocrine insufficiency with diet?
|
Modify fat intake
Medium chain triglycerides Enzyme replacement therapy Take vitamins, especially fat soluble |
|
What is the theoretical basis for enzyme replacement therapy?
|
Lack of proteases from pancreas causes increase in CCK release which exacerbates pain. Exogenous proteases degrading CCK decreases pain.
|
|
T/F The risk of pancreatic cancer is increased with chronic pancreatitis
|
T
|