Exocrine Pancreas, Gallbladder, and Liver Flashcards
Annular Pancreas
Developmental malformation where the pancreas forms a ring and obstructs the duodenum
Acute Pancreatitis
pathophysiology and causes
- Inflammation and hemmorhage of the pancrease due to premature activation of TRYPSIN which activates other enzymes still in the pancreas and results in autodigestion
- Get liquefactive and hemmorhagic necrosis of pancreas and fat necrosis of the peripancreatic fat
- Usually due to alcohol (stimulates contraction of sphincter of oddi) and gallstones (block ampulla)
- See in trauma (automobil accident in buckled child), hypercalcemia (activates enzymes), hyperlipidemia, drugs, scorpion stings, mumps, rupture of posterior duodenal ulcer
Acute Pancreatitis clinical features and complications
Epigastric pain that radiates to the BACK
Nausea and vommitting
Periumbilical and flank hemmorhage
elevated serum LIPASE and amylase
Hypocalcemia (Ca2+ consumed during saponification in fat necrosis)
Complications include
1) Shock
2) Pancreatic Pseudocyst = fibrous tissue arround liquefactive necrosis. presents as palpable abdominal mass persistently elevated amylase. Rupture can release enzymes into abdominal cavity and cause hemmorhage
3) Pancreatic Abscess = usually due to E Coli. Get ab pain, fever, and persistenly elevated serum amylase
4) DIC and ARDS (enzymes in blood and can reach the lung)
Chronic Pancreatitis
Fibrosis of pancreatic parenchyma usually due to reccurent bouts of pancreatitis in alcoholics and CF (thick secretions)
Clinical features
1) Epigastric pain that RADIATES to the BACK
2) Pancreatic Insufficiency = malabsorption, steatorrhea, and deficiency of fat soluable vitamins
3) Dystrophic Calcification of parenchyma presents as “chain of lakes” due to dilation of pancreatic ducts
4) Can cause secondary DM if there is destruction of islets
5) Increased risk for pancreatic carcinoma
Pancreatic Carcinoma
Adenocarcinoma arising from the DUCTS usually seen in elderly
Risk factors = smoking and chronic pancreatitis
Clinical features
1) Epigastric abdominal pain and weight loss
2) Obstructive jaundice with PALE STOOLS and PALPABALE GALLBLADDER if tumor is in HEAD of pancreas
3) Can get secondary DM if tumor is in body or tail
4) Migratory thrombophlebitis = trousseau sign = swelling, erythema, and tenderness in extremities
Serum tumor marker is CA 19-9
Need to do whipple procedure = en bloc removal of head and neck of pancreas, proximal duodenum, and gallbladder
1 year survival <10%
Biliary Atresia
Failure to form or early destruction of extrahepatic biliary tree
Leads to biliary obstruction in first 3 months of life
Presents with jaundice (conjugated bilirubin) that progresses to cirrhosis
Cholelithiasis
Gallstones = solid round stones in the gallbladder
Due to precipitation of cholesterol or bilirubin in bile
arise when
1) supersaturation of of cholesterol or bilirubin
2) decreased phopsholipids or bile acids that normally increase the solubility of cholesterol and bilirubin
-colestyramine is a lipid lowering drug that binds bile acids
3) stasis
Usually asymptomatic but complications include biliary colic, acute/chronic cholecystitis, ascending cholangitis, gallstone illeus, gallbladder cancer
Cholesterol Stones
yellow
radiolucent usually
Risk factors
1) 40s to 50s
2) estrogen (female gender, obesity, multiple pregnancies, and oral contraceptives) = icreases HMGCoaA reductase activity leading to increased cholesterol synthesis. Also increases lipoprotein receptors on hepatocytes increasing cholesterol uptake
3) clofibrate = lipid lowering drug that increases HMGCoaA reductase activity leading to increased cholesterol synthesis. Also decreased conversion of cholesterol to bile acids
4) Native American ethnicity
5) Chrohn Disease = affects terminal illeum where bile salts and acids are normally taken up
6) Cirrhosis = decreased production of bile salts by hepatocytes
Bilirubin Stones
Black
Radiopaque
Risk Factors include
1) Extravascular hemolysis = increased unconjugated bilirubin in bile
2) Biliary tract infection by E. coli
3) Biliary tract infection by Ascaris lumbricoides = roundowrm that infects biliary tree
4) Biliary tract infection by Clonorchis sinensis = liver fluke in CHina, Korea, and Vietnam that infects biliary tree (also increases risk of gallstones, cholangitis, and cholangiosarcoma)
biliary colic
Waxing and waning right upper quadrant pain as the gallbladder contracts against a stone lodged in the cystic duct (relieved if stone passes)
If stone is lodged in the common bile duct then can get acute pancreatitis or obstructive jaundice
acute cholecystitis
Acute inflammation of the gallbladder wall
impacted stone in cystic duct results in dilation with pressure ischemia and bacterial overgrowth and inflammation
Present with right upper quadrant pain that RADIATES TO R SCAPULA, fever, nausea, vomiting, increased WBC and serum alkaline phosphatase
Risk of rupture if untreated
chronic cholecystitis
Chronic inflammation of the gallbladder due to chemical irritation of longstanding cholelithiasis
see rokitansky-aschoff sinus = herniation of gallbladder mucoa into muscular wall
presents with vague upper right quadrant pain, especially after eating
Porcelain gall bladder is late complication = shrunken, hard, fibrosis, dystrophic calcification
INCREASED risk for CARCINOMA
treatment = cholecystectomy
ascending cholangitis
bacterial infection of the bile ducts with enteric gram negative bacteria
Presents as jaundice , ab pain, and spsis (fever and hcills)
gallstone illeus
Cholecystitis causes fistula between gallbladder and small bowel allowing stones to pass directly into small bowel and obstruct them
gallbladder carcinoma
Adenocarcinoma arising from GLANDULAR EPITHELIUM that lines the gallbladder wall
Gallstones are major risk factor (especially if get porcelain gallbladder)
presents as cholecystitis in ELDERLY women (this is unusual cus cholecystitis typically presents in 40s-50s)
Jaundice
Yellow discoloration of the skin
earliest sign is scleral icterus (yellowing sclera)
Due to increased serum bilirubin usually >2.5mg/dL when have messed up bilirubin metabolism
Normal Bilirubin metabolism
1) RBS are consumed by macrophages of reticuloendothelial system
2) Protoporphyrin is converted into UnConjugated Bilirubin (UCB)
3) Albumin carries UCB to liver
4) Uridine Glucuonyl Transferase (UGT) in hepatocytes conjugates the bilirubin (CB)
5) CB is transferred to bile canniculi by a protein to form protein
6) Bile is stored in the gallbladder
7) Bile is released into duodenum to aid in digestion
8) Intestinal flora convert CB to urobilinogen
9) Urobilinogen is oxidized to stercobilin (makes poop brown) and urobilin (partially reabsorbed into blood and filtered by kidney to make urine yellow)
- Note UCB is not water soluable and therefore not present in urine
Extravascular Hemolysis or Inneffective Erythropoiesis
Extremely high levels of UCB overwhelm the conjugating ability of the liver
get increased serum UCB giving rise to jaundice
Clinically get dark urine due to increased urine urobilinogen
Increased risk of pigmented bilirubin gallstones due to excess bilirubin being made
Physiologic jaundice of the newborn
Newborn liver has transiently low Uridine Glucuonyl Transferase activity and so can’t conjugate the normal amount of UCB that is presented to it.
UCB builds up so see increase in teh serum and get jaundice
UCB is FAT SOLUABLE and can deposit in the BASAL GANGLIA (kerinicterus) leading to neuro deficitis or death
treat with phototherapy that somehow makes UCB water soluable and able to excrete in urine
Gilbert Syndrome
Auto recessive Mildly low Uridine Glucuonyl Transferase activity. During times of stress/infection get increased UCB and liver cant keep up so person becomes jaundiced whenever they are physiologically challneged by something but otherwise are healthy
Crigler-Najjar Syndrome
Absence of Uridine Glucuonyl Transferase leads to elevated UCB in serum leading to jaundice. Get deposition in fat of basal ganglia resulting in kernicterus and typically fatal early in life
Dubin-Johnson Syndrome
+
Rotor syndrome
Auto recessive Deficiency of bilirubin canicular TRANSPORT PROTEIN.
Get increased CB in serum and present with a very DARK LIVER.
Rotor syndrome is similar but lack dark liver
Biliary Tract Obstruction
gallstones, pancreatic carcinoma, cholangiocarcinoma, parasites, and liver fluke (clonorchis sinensis).
Get increased serum CB, decreased urine urobilinogen and increased alkaline phosphatase
Dark urine due to bilirubinuria and pale stool
pruritis due to increased bile acids in plasma
Hypercholesterolemia with xanthomas
Steatorrhea with malabsoprtion of fat soluable vitamins
Viral Hepatitis as it relates to Jaundice
Inflamation disrups hepatocytes and smill bile ductules
Increase in bot hserum UCB and CB
Dark urine due to increased bilirubinuria
Urine urobilinogen is normal or decreased (less CB being delivered to duodenum and more in blood)