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Flashcards in Pancreas Deck (16):
1

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.

2

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

3

List the main secretory products of the pancreas.

Amylase - digestion of starch

lipase - digestion of lipis

peptidases - digestion of proteins

insulin

glucagon

Controlled by vagus nerve and CCK and secretin.

4

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

Causes:

1. bile stones

2. Alcohol

3. overeating

4. Viruses

5. Drugs

6. trauma/surgery

 

5

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

-distress, sweating

- syncope/shock

- peritonoeal rigidity

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

6

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

7

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

 

8

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

9

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

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

10

How common is diabetes mellitus?

Common, 1-2% worldwide

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

11

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

12

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

13

Explain the pathogenesis of hyperglycemia in diabetes mellitus.

decreased insulin >> increased glyogenolysis

 

14

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.

15

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

16

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