How is the pancreas related to the small intestine?
The terminal part of the main pancreatic duct is confluent with the common bile duct . . .
Enters lumen of duodenum, called papilla of Vater.
Compare and contrast the features of the exocrine portion and the endocrine portion of the pancreas.
List the main secretory products of the pancreas.
Amylase - digestion of starch
lipase - digestion of lipis
peptidases - digestion of proteins
Controlled by vagus nerve and CCK and secretin.
List the main causes of acute pancreatitis.
Acute . . . response to tissue necrosis caused by digestive enzymes. Recall enzymes remain as proenzymes until they enter the duodenum. Premature activation >> AUTODIGESTION
1. bile stones
Correlate the pathologic findings in acute pancreatitis with the clinical features of this disease.
Leakage of digestive enzymes in abdominal cavity >> peritoneal irritation
- sudden onset
- abdominal pain, N, V
- peritonoeal rigidity
- Labs: leukocytosis, elevated amylase and lipase (will show 24-72 hrs after attack)
What are the most common complications of acute pancreatitis?
spilling of digestive enzymes >> peritonitis
destruction of parenchyma >> pseudocysts
necrotic parenchyma >> infection/abscess
acute >> chronic pancreatitis
destruction of tissue >> pancreatic insufficiency, diabetes
What is chronic pancreatitis, and how does this disease present clinically?
= irregular fibrosis replacing portions of normal pancreatic parenchyma (progressive and irreversible)
will see marked fibrosis, scattered foci of chronic inflammation replacing acini, calcifications
pain: entrapment of nerves (celiac plexus), stenosis of duodenum >> impeding passage of food
exocrine insufficiency: malabsorption, steatorrhea
endocrine insufficiency: >70% have DM
How common are tumors of the pancreas?
> 95% are adenocarcinomas, solid, and derived from pancreatic ducts
4th major cause of cancer related deaths
< 50: M>F, 3:1
> 50: M = F
Compare adenocarcinoma of the pancreas with tumors of the endocrine pancreas.
adenocarcinoma = epithelial lesion originating from ducts
60% located at head of pancreas (contains most ducts)
varying amounts of differentiation
courvoisier's sign >> dilated palpable GB
Trousseau's syndrome >> migratory phelbitis
islet cell tumors = develop from any of the four cell types
insulinomas (beta cell)
measure 1-3 cm
hyperinsulinemia: syncopy, sweating
gastrinomas from developmentally pluripotetent stem cells
have zollinger-ellison syndrome: intractable peptic ulcer
How common is diabetes mellitus?
Common, 1-2% worldwide
Two most common forms = type 1 (5-10%) and type 2 (90-95%)
Classify diabetes mellitus according to the pathogenesis of this disease.
An absolute deficiency of insulin: lack of beta cells, destruction
A relative deficiency: demand exceeds supply
Interference with insulin binding to target tissues: faulty receptors, antibodies
Compare and contrast type 1 and type 2 diabetes mellitus.
Type 1: Type 2
Age of onset <30, >30
speed of onset sudden, gradual
body build normal, obese
family hx <20%, 60%
twin concordance low, hi
antibodies to islet cells positive, neg
histology of islets loss of beta cells, normal (hyalinized)
serum insulin level low, normal
treatment insulin, diet or oral agents
Explain the pathogenesis of hyperglycemia in diabetes mellitus.
decreased insulin >> increased glyogenolysis
Explain the pathogenesis of diabetic ketoacidosis.
Anaerobic glycolysis is used for energy production, resulting in the formation of excess amount of lactic acid. >> lactic acidosis. Inadequate utilization of fats and reduced lipogenesis lead to the accumulation of free fatty acids, which are oxidized to ketones >> ketoacidosis.
Explain how the cardiovascular, renal, ocular, and neurologic complications of diabetes mellitus develop.
cardiac: atherosclerosis develops in the aorta and branches
renal: microangiopathy, widened mesangial areas, ischemia, infection >> glomerulosclerosis, pyelonephritis, papillary necrosis
ocular: vascular changes, opacities (deposition of sorbitol and fructose), microinfarcts, hemorrhage
neurologic: most due to microangiopathy >> widespread focal eschemia, also depostion of sorbitol and fructose in axons and myelin sheaths
What is the pathogenesis of polydipsia, polyphagia, and polyuria in diabetes mellitus?
excessive loss of water >> polydypsia
abnormal utilization of carbs/prot/fats creates negative energy balance >> polyphagia