Pancreas

Question 1

How is the pancreas related to the small intestine?

Answer 1

The terminal part of the main pancreatic duct is confluent with the common bile duct . . .

Enters lumen of duodenum, called papilla of Vater.

Question 2

Compare and contrast the features of the exocrine portion and the endocrine portion of the pancreas.

Question 3

List the main secretory products of the pancreas.

Answer 3

Amylase - digestion of starch

lipase - digestion of lipis

peptidases - digestion of proteins

insulin

glucagon

Controlled by vagus nerve and CCK and secretin.

Question 4

List the main causes of acute pancreatitis.

Answer 4

Acute . . . response to tissue necrosis caused by digestive enzymes. Recall enzymes remain as proenzymes until they enter the duodenum. Premature activation >> AUTODIGESTION

Causes:

1. bile stones
2. Alcohol
3. overeating
4. Viruses
5. Drugs
6. trauma/surgery

Question 5

Correlate the pathologic findings in acute pancreatitis with the clinical features of this disease.

Answer 5

Leakage of digestive enzymes in abdominal cavity >> peritoneal irritation

- sudden onset

- abdominal pain, N, V

-distress, sweating

- syncope/shock

- peritonoeal rigidity

• Labs: leukocytosis, elevated amylase and lipase (will show 24-72 hrs after attack)

Question 6

What are the most common complications of acute pancreatitis?

Answer 6

spilling of digestive enzymes >> peritonitis

destruction of parenchyma >> pseudocysts

necrotic parenchyma >> infection/abscess

acute >> chronic pancreatitis

destruction of tissue >> pancreatic insufficiency, diabetes

Question 7

What is chronic pancreatitis, and how does this disease present clinically?

Answer 7

= 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

Question 8

How common are tumors of the pancreas?

Answer 8

> 95% are adenocarcinomas, solid, and derived from pancreatic ducts

4th major cause of cancer related deaths

< 50: M>F, 3:1

> 50: M = F

Question 9

Compare adenocarcinoma of the pancreas with tumors of the endocrine pancreas.

Answer 9

adenocarcinoma = epithelial lesion originating from ducts

60% located at head of pancreas (contains most ducts)

varying amounts of differentiation

varying symptoms

• 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

Question 10

How common is diabetes mellitus?

Answer 10

Common, 1-2% worldwide

Two most common forms = type 1 (5-10%) and type 2 (90-95%)

Question 11

Classify diabetes mellitus according to the pathogenesis of this disease.

Answer 11

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

Question 12

Compare and contrast type 1 and type 2 diabetes mellitus.

Answer 12

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

Question 13

Explain the pathogenesis of hyperglycemia in diabetes mellitus.

Answer 13

decreased insulin >> increased glyogenolysis

Question 14

Explain the pathogenesis of diabetic ketoacidosis.

Answer 14

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.

Question 15

Explain how the cardiovascular, renal, ocular, and neurologic complications of diabetes mellitus develop.

Answer 15

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

Question 16

What is the pathogenesis of polydipsia, polyphagia, and polyuria in diabetes mellitus?

Answer 16

excessive loss of water >> polydypsia

abnormal utilization of carbs/prot/fats creates negative energy balance >> polyphagia