Pancreas Flashcards

1
Q

How is the pancreas related to the small intestine?

A

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

Enters lumen of duodenum, called papilla of Vater.

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2
Q

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

A
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3
Q

List the main secretory products of the pancreas.

A

Amylase - digestion of starch

lipase - digestion of lipis

peptidases - digestion of proteins

insulin

glucagon

Controlled by vagus nerve and CCK and secretin.

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4
Q

List the main causes of acute pancreatitis.

A

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
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5
Q

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

A

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)
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6
Q

What are the most common complications of acute pancreatitis?

A

spilling of digestive enzymes >> peritonitis

destruction of parenchyma >> pseudocysts

necrotic parenchyma >> infection/abscess

acute >> chronic pancreatitis

destruction of tissue >> pancreatic insufficiency, diabetes

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7
Q

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

A

= 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

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8
Q

How common are tumors of the pancreas?

A

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

4th major cause of cancer related deaths

< 50: M>F, 3:1

> 50: M = F

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9
Q

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

A

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

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10
Q

How common is diabetes mellitus?

A

Common, 1-2% worldwide

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

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11
Q

Classify diabetes mellitus according to the pathogenesis of this disease.

A

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

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12
Q

Compare and contrast type 1 and type 2 diabetes mellitus.

A

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

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13
Q

Explain the pathogenesis of hyperglycemia in diabetes mellitus.

A

decreased insulin >> increased glyogenolysis

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14
Q

Explain the pathogenesis of diabetic ketoacidosis.

A

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.

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15
Q

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

A

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

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16
Q

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

A

excessive loss of water >> polydypsia

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