1. Chapter 13 Disorders of the Pancreas
The Nature of Disease: Pathophysiology for the Health Professions, 2nd ed. Thomas H. McConnell

2. NORMAL PANCREATIC PHYSIOLOGY
The exocrine pancreas excretes digestive juice into the intestine.
Protease secreted as inactive enzyme (zymogen)
Lipase and amylase secreted as active enzyme
The endocrine pancreas excretes hormones into blood.
Alpha cells: glucagon. Functional opposite of insulin, stimulates liver glycogen >> glucose. Raises blood glucose
Beta cells: insulin. Opens cell membrane to glucose. Lowers blood glucose
Delta cells: somatostatin. Inhibits glycogen formation and insulin secretion. Raises blood glucose
PP cells: pancreatic polypeptide, acts on stomach to stimulate juices and slow intestinal motility

3. Figure 13.1 The pancreas and its anatomic relationships
Figure 13.1 The pancreas and its anatomic relationships. Cross-section of the upper abdomen. View from inferior to pancreas, looking superiorly

4. Figure 13.2 Anatomic detail of the pancreas

5. Figure 13.3 Glucose, glycogen, insulin, and glucagon metabolism
Figure 13.3 Glucose, glycogen, insulin and glucagon metabolism. Insulin promotes lower blood glucose by increasing peripheral cell glucose
uptake. Glucagon promotes higher blood glucose by stimulating glycogen breakdown into glucose and glucose synthesis from amino acids.
(Adapted with permission from McConnell TH, Hull KL. Human Form Human Function: Essentials of Anatomy & Physiology. Baltimore (MD): Wolters
Kluwer Health; 2011.)

6. PANCREATITIS Acute pancreatitis causes reversible injury.
Chronic alcohol abuse causes 2/3 of cases.
Half of patients have gallstones.
Chronic pancreatitis is associated with irreversible pancreatic injury.
Repeated bouts of acute pancreatitis
5% of patients with stones develop pancreatitis.

7. Figure 13.4 The pathogenesis of acute pancreatitis
Acinar injury or duct obstruction releases enzymes
into tissue, where the enzymes digest fat and
blood vessels.

8. Figure 13.5 Acute pancreatitis
Figure 13.5 Acute pancreatitis. Dissection of esophagus, stomach,
duodenum, gallbladder, and pancreas. The gallbladder is full of
gallstones, and the surface of the pancreas is covered with an acute
inflammatory exudate. Gallstones are an important cause of pancreatitis.

9. Figure 13.6 Acute hemorrhagic pancreatitis
Figure 13.6 Acute hemorrhagic pancreatitis. Multiple crosssections
of the pancreas. Pancreatic injury or duct obstruction
releases enzymes that digest fat and blood vessels, causing local
hemorrhage.

10. Figure 13.7 The consequences of pancreatitis
Figure 13.7 The consequences of pancreatitis. The consequences
of acute and chronic pancreatitis are compared.

11. Figure 13.8 Gross anatomy of chronic pancreatitis
Figure 13.8 Gross anatomy of chronic pancreatitis. The pancreas
is abnormally pale, dense, and fibrotic, and the pancreatic duct is
dilated from chronic obstruction. The white marker indicates the
opening of the pancreatic duct into the duodenum where a pancreatic
stone (removed) obstructed the lumen.

12. Figure 13.9 Complications of chronic pancreatitis

13. DIABETES Diabetes mellitus is not a single disease entity.
Euglycemia, prediabetes, diabetes
Type I diabetes is an autoimmune disease.
10% of cases, less genetic influence, normal peripheral cell insulin sensitivity, rapid teen onset, decreased beta cells, low blood insulin, not obese, difficult glucose control, ketoacidosis common
Type II diabetes is a multifactorial disease.
90% of cases, more genetic influence, decreased peripheral cell insulin sensitivity, slow adult onset, obese, normal beta cells, normal to high blood insulin, glucose control easier, ketoacidosis uncommon
Other causes: pregnancy, steroid Rx

14. DIABETES—(cont.)
The complications of diabetes are mainly caused by hyperglycemia.
Glycoproteins >> accelerate atherosclerosis, cause diabetic microangiopathy, retinal and kidney disease
The diagnosis of diabetes should be made according to established criteria.
Treatment of diabetes depends on calorie and insulin management.

15. Figure 13.10 Comparison of age distribution in Type I and Type II diabetes
diabetes. The figure shows the age at onset and relative numbers of
new cases of both types of diabetes. Type II diabetes appears much
later and is much more common than Type I.

16. Table 13.1 Diabetes Types I/II Compared

17. Figure 13.11 The pathogenesis of Type I diabetes
Figure The pathogenesis of Type I diabetes. Type I diabetes
is caused by autoimmune destruction of beta cells, which is induced
by some type of environmental insult in genetically susceptible
people.

18. Figure 13.12 The pathogenesis of Type II diabetes
Figure The pathogenesis of Type II diabetes. The primary
mechanisms are peripheral tissue resistance to the effect of insulin,
beta-cell inadequacy, and strong genetic susceptibility.

19. Figure 13.13 Metabolic derangements in diabetes
Figure Metabolic derangements in diabetes. Insulin deficiency
prevents tissue metabolism of glucose and liver storage of glucose as
glycogen; hyperglycemia is the result. Instead of glucose, tissues burn fat,
which produces a large amount of acid. Excess glucose spills into urine and
carries water with it; dehydration is the result. Either severe dehydration or
excessive amounts of acid can cause diabetic coma.

20. Figure 13.14 Long-term complications of diabetes

21. Figure 13.15 Diabetic nephrosclerosis
Figure Diabetic nephrosclerosis. A. Normal kidney. B. Diabetic
nephrosclerosis. Note the small size of the diseased kidney.

22. Figure 13.16 Diabetic retinopathy
Figure Diabetic retinopathy. Funduscopy of the right eye.

23. PANCREATIC NEOPLASMS Cystic neoplasms are uncommon and usually benign.
Pancreatic carcinoma is common and lethal.
Islet cell tumors are usually benign and functional.

24. Figure 13.17 Pancreatic carcinoma
Figure Pancreatic carcinoma. This example is in the tail of the
gland; most occur in the head.

25. Figure 13.18 Complications of carcinoma of the pancreas