Bile, Chole., Gallstones; Pancreatitis

Front 1

Two functions of bile

Back 1

1) Exocrine secretion - normal digestion

2) Excretion of metabolic waste

Front 2

detergents that solubilize lipids in bile and in the gut

Back 2

Bile salts

Front 3

What gives bile its color?

Back 3

Bilirubin, derived from heme breakdown

Front 4

Major route of cholesterol degradation in the human body

Back 4

Bile acid synthesis by liver

Front 5

Amphiphilic: defn

Back 5

Having both a polar and nonpolar portion. this is what makes bile salts good detergents.

Front 6

Micelle: defn

Back 6

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

Front 7

What is the biliary canaliculus?

Back 7

Channel running between adjacent hepatocytes where bile is formed.

Front 8

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

Back 8

secretin

Front 9

What does the gallbladder do?

Back 9

Removes sodium, chloride, and water from bile, leaving organic components. Effectively it concentrates bile and makes it more effective

Front 10

T/F Concentrated bile is hyperosmolar

Back 10

F. Micelles are not osmotically active.

Front 11

When is CCK released?

Back 11

When protein or fat from food enters the duodenum.

Front 12

WHat does CCK do?

Back 12

Causes the gallbladder to contract and sphincter of Oddi to relax, emptying bile into the gut.

Front 13

What happens to conjugated bile salts?

Back 13

Normally they dont get absorbed in the jejunum or duodenum but stay in intestinal lumen where they carry out detergent function

Front 14

What is the enterohepatic circulation?

Back 14

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.

Front 15

What happens to the small (5%) amount of bile salts that reaches the colon?

Back 15

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

Front 16

What does "conjugated" mean?

Back 16

The bile salts carboxylic group is amidated (conjugated) to taurine or glycine

Front 17

T/F Deoxycholic and lithocholic acids are toxic and may play a role in pathogenesis of gallstones or even cancer

Back 17

T

Front 18

What is acholic stool and why does it occur?

Back 18

When bile duct is completely obsturcted, bilirubin can't reach the colon. Stools lose brown color and become chalky gray.

Front 19

What causes the brown color of stool?

Back 19

When bilirubin reaches the colon it is acted on by intestinal bacteria --> brown color

Front 20

What causes upregulation of bile salt synthesis?

Back 20

When bile salts fail to return to liver/are deficient in gut

Front 21

What happens to LDL when bile salt synthesis is upregulated?

Back 21

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.

Front 22

What is cholestasis?

Back 22

Condition in which bile formation is impaired and bile components (bilirubin, bile salts, cholesterol) accumulate in blood.

Front 23

Cholelithiasis: defn

Back 23

Gallstone disease

Front 24

Cholecytolithiasis

Back 24

Gallstones in gallbladder

Front 25

Choledocholithiasis

Back 25

Gallstones in bile ducts

Front 26

What is cholecystectomy?

Back 26

Surgery that cures gallstones by removing gallbladder

Front 27

What are most gallstones made of?

Back 27

cholesterol monohydrate

Front 28

What is the typical gallstone patient?

Back 28

Five Fs:

Fat, Fair, Fertile, Female, Forty

Front 29

What is the cause of black pigment stones with calcium bilirubinate?

Back 29

Theyre due to increased heme turnover, from chronic hemolytic disease, cirrhosis, hypersplenism.

Front 30

What is the cause of brown pigment stones?

Back 30

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.

Front 31

Where are brown pigment stones common?

Back 31

rice growing areas of Asia, due to strictures caused by infection with liver flukes

Front 32

Stricture: defn

Back 32

narrowing, stenosis

Front 33

What is the pathophysiology of gallstones?

Back 33

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.

Front 34

How do estrogens affect formation of gallstones?

Back 34

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.

Front 35

What are the 4 stages of gallstone formation?

Back 35

1) Lithogenic state
2) Asymptomatic gallstones
3) Symptomatic gallstones
4) Complicated gallstones

Front 36

What are symptoms of gallstones?

Back 36

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

Front 37

Characteristics of biliary colic

Back 37

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.

Front 38

What are acute complicatiosn of gallstones?

Back 38

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.

Front 39

What happens if gallstones escape into the common bile duct?

Back 39

May produce obstructive jaundice with elevation of liver enzymes.

Front 40

How to distinguish choledocholithiasis from biliary obstruction from cancer or pancreas?

Back 40

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.

Front 41

The bile duct and pancreatic duct both empty into the duodenum through the channel _________

Back 41

ampulla of Vater

Front 42

What happens if a stone passing through the ampulla transiently obstructs pancreatic secretory flow?

Back 42

Can trigger acute pancreatitis

Front 43

What happens in acute cholecystitis?

Back 43

Obstruction of gallbladder causes inflammation and ischemia over a few hours.

Can result in gallbladder gangrene and perforation

Front 44

What happens in ascending cholangitis?

Back 44

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

Front 45

What is Charcot's triad?

Back 45

RUQ pain

Fever

Jaundice

Front 46

Treatment for ascending cholangitis

Back 46

Antibiotics

Intervention to take out stone

Front 47

What is chronic cholecystitis?

Back 47

Gallstones in gallbladder over time produce chronic inflammation and fibrotic.

Normal function of gallbladder is lost.

Front 48

In what settings does gallbladder cancer usually occur?

Back 48

Usually from chonic cholecystitis

Front 49

T/F Gallstones are visible on xrays

Back 49

F. It depends on the type of stone

Front 50

Which gallstones are radiolucent and opaque on xray?

Back 50

Lucent: Cholesterol (most common)

Opaque: pigment stones that contain Calcium.

Front 51

Best way to dx gallstones

Back 51

ultrasound

Front 52

What is HIDA radionuclide gallbladder scanning and what is it useful for?

Back 52

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.

Front 53

What is cholangiography?

Back 53

imaging of bile ducts.

Front 54

What is life like without a gallbladder?

Back 54

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.

Front 55

What is ursodeoxycholic acid?

Back 55

A bile salt found in bears that dissolves gallbladder stones.

Gradually leaches cholesterol and dissolves stones

Front 56

How to prevent gallstone formation in high risk patients?

Back 56

Giving ursodeoxycholic acid

Front 57

Who are high risk patients for gallstone formation?

Back 57

Those undergoing rapid weight loss (25% will form cholesterol gallstones in 4 months)

Front 58

Lifetime risk of gallstones

Back 58

Prevalence: 25%
Surgery: 10%

Front 59

Four E’s of biliary colic

Back 59

1) Epigastric
2) Episodic
3) Extremely painful
4) Extended (>30 minutes)

Front 60

Which enzymes from the pancreas are secreted in the active form? inactive?

Back 60

Active: those for FAT and CARBOHYDRATE digestion (lipase, amylase)

Inactive: Proteases and phospholipases

Front 61

Most of the pancreas output is _________

Back 61

proteases (70%)

Front 62

Converts trypsinogen --> trypsin

Back 62

enterokinase

Front 63

Where is enterokinase located?

Back 63

intestinal brush border

Front 64

Pancreatic ducts secrete _______ while acini secrete ______

Back 64

bicarb; enzymes

Front 65

what increases pancreatic secretion?

Back 65

Neural stimulation (vagus n, enteropancreatic cholinergic neurons); Hormonal (secretin and CCK) stimuli

Front 66

How is pancreatic secretion inhibited?

Back 66

By a negative fb loop.

The presence of activated trypsin, chymotrypsin, and elastase in duodenum --> decrease in CCK ---> decrease in pancreatic secretions

Front 67

Defn of acute pancreatitis

Back 67

Acute inflam process arising in exocrine pancreas presenting with abdominal pain, and associated with elevated pancreatic enzymes in blood and urine.

Front 68

Pathogenesis of pancreatitis

Back 68

Inactive pancreatic enzymes become activated and start digesting the pancreas

Front 69

What is the change in calcium in the blood with pancreatitis and why?

Back 69

HYPOcalcemia.

Several factors cause it including hypoalbuminemia, calcium complexing with released fatty acids in the peripancreatic region, and inhibition of parathormone release.

Front 70

Most common causes of acute pancreatitis

Back 70

Alcohol

Gallstones


Trauma/surgery

Certain drugs

Infection


Idiopathic in 30%

Front 71

Common clinical manifestations of pancreatitis

Back 71

Abdominal pain, vomiting, jaundice, fever, tachycardia, cyanosis, respiratory distress with severe attacks.

Front 72

Phlegmon: defn

Back 72

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.

Front 73

How is pancreatitis diagnosed?

Back 73

Elevated serum amylase/lipase in patient with suggestive clinical findings

Front 74

Which of serum amylase or lipase is more specific and sensitive to pancreatitis dx?

Back 74

lipase. amylase is associated with other disease states.

Front 75

What is treatment of acute pancreatitis?

Back 75

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

Front 76

Chronic pancreatitis: defn

Back 76

recurrent/persistent abdominal pain and / or evidence of pancreatic insufficiency (steatorrhea or diabetes).

Continuing inflam. process of the pancreas with irreversible morphologic changes.

Front 77

Etiology of chronic pancreatitis

Back 77

Majority have alcohol-related disease

Cystic fibrosis - association

30% are idiopathic

Hereditary - mutations in trypsin gene.

Ductal obstruction

Front 78

Common clinical presentations of chronic pancreatitis

Back 78

Pain (most common)

steatorrhea

diabetes (type 1)

Extrahepatic biliary obstruction - due to fibrosis of head of pancreas

Front 79

pancreatic pseudocyst: defn

Back 79

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

Front 80

How to dx chronic pancreatitis

Back 80

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

Front 81

What is the Secretin/CCK stimulation test?

Back 81

80% sensitive, 90% specific test for pancreatic function

Front 82

What is treatment of chronic pancreatitis aimed at?

Back 82

1) Pain relief

2) Treatment of steatorrhea

3) Treatment of diabetes

Front 83

What is autoimmune pancreatitis?

Back 83

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

Front 84

hereditary pancreatitis due to a mutation in __________

Back 84

trypsinogen

Front 85

Grey Turner's sign: defn

Back 85

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

Front 86

What is teh relationship between Adult Respiratory Distress Syndrome (ARDS) and pancreatitis?

Back 86

Can occur with severe pancreatitis. More common in setting of hyperlipidemia.

Cytokine mediated.

Front 87

What is a method of detecting pancreatic necrosis in pancreatitis?

Back 87

CT with contrast

Front 88

What are some early indicators that the pancreatitis is severe?

Back 88

tachycardia
tachypnea
hypotension
hypoxemia
hemoconcentration (decr in blood fluid)
oliguria
encephalopathy

Front 89

Naso-gastric Suction: what is it used for in pancreatitis?

Back 89

Persistent vomiting, obstruction

Front 90

When do pseudocysts occur following pancreatitis?

Back 90

>4 weeks

Front 91

What is steatorrhea?

Back 91

Visible fat/oil droplets in stool.Increased volume, light color, foul odor.

Front 92

What is the cause of pain in pancreatitis?

Back 92

Pancreatic duct obstruction with increased pressure.

Ischemia

Pseudocyst

Front 93

Pathogenesis of steatorrhea

Back 93

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.

Front 94

Magnetic resonance cholangiopancreatography (MRCP): what is it?

Back 94

MR tool to visualize biliary and pancreatic ducts in a non-invasive manner. Use to determine if gallstones are blocking.

Front 95

What are the most sensitive structural diagnostic tests for pancreatitis?

Back 95

MR cholangiopancreatography ; endoscopic retrograde cholangiopancreatography ; Endoscopic ultrasound (EUS)

Front 96

What is the Double Lumen Tube Test? How performed? What are downsides?

Back 96

Determines volume and composition (specifically bicarb) of duodenal fluid

Downsides: unpleasant, time-consuming

Front 97

How to manage exocrine insufficiency with diet?

Back 97

Modify fat intake

Medium chain triglycerides

Enzyme replacement therapy

Take vitamins, especially fat soluble

Front 98

What is the theoretical basis for enzyme replacement therapy?

Back 98

Lack of proteases from pancreas causes increase in CCK release which exacerbates pain. Exogenous proteases degrading CCK decreases pain.

Front 99

T/F The risk of pancreatic cancer is increased with chronic pancreatitis

Back 99

T