1. ENDOCRINE PANCREAS

3.  Diabetes Mellitus  Islet Cell tumors

4. INTRODUCTION  One million islets of Langerhans  Several types of cells “Immunohistochemistery” ß (beta)->70% insulin А (alpha)->20% glucagons D (delta)->5-10% somatostatin P.P Cell-> 1-2% pancreatic polypeptide Other rare cells: - D1 cells - VIP ( vasoactive intestinal polypeptide ) - Enterochromaffin cells - 5 HT-(serotonin)

5.  Each type of pancreatic islet cells may give mainly benign tumour -> (ADENOMA) called Islet cell tumours: Insulinoma Glucagonoma Somatostatinoma VIPomaCarcinoid tumours Gastrinoma Multiple Endocrine Neoplasia(MEN)

8. DIABETES MELLITUS

9. DEFINITION  Diabetes Mellitus is a chronic disorder of carbohydrate, fat, and protein metabolism.  In which there is impaired glucose utilization due to defective or deficient insulin secretory response inducing hyperglycemia

10. CLASSIFICATION  Primary (idiopathic) Diabetes Mellitus Type-1 (Insulin Dependent Diabetes Mellitus)  Type-1A (immune mediated)  Type-1B (idiopathic) Type-2 (Non-insulin Dependent Diabetes Mellitus)  * Non-obese NIDDM  * Obese NIDDM  * Maturity onset diabetes of the young (MOD)  * Gestational DM

11.  Secondary Diabetes Mellitus:  - Chronic pancreatitis  - Post pancreatectomy  - Hormonal tumours (acromegaly, Cushing’s ---)  - Drugs (corticosteroids)  - Haemochromatosis  - Genetic disorders e.g. lipodystrophy  - Gestational DM

12. Primary Diabetes Mellitus is by far the most common in our countery and worldwide. Type 1 and type2 have different pathogenetic and metabolic characeristics. Simillar long term comlications occur in both types.

13.  MODY (maturity-onset DM of the Young): Young Rare Linked to chrom. 7 & 20 Autosomal dominant Mild hyperglycemia

14.  ACUTE METABOLIC COMPLICATIONS:

15. Diabetic Ketoacidosis coma: In Type I Diabetes Mellitus Due to severe insulin deficiency with increase glucagons. Decrease insulin  lipolysis  free fatty acids  Increase Glucagon  oxidation of FFA in liver  Ketoacidosis  Coma

16. Non ketotic Hyperosmolar Coma: In Type II DM (NIDDM) Elderly Uncontroled DM Sustained hyperglycemic diuresis  Severe dehydration  coma Lack of symptoms (nausea, vomiting and respiratory difficulties)  Delay the seeking of medical attention.  Hypoglycemia Coma

17. Morphology & Late Complications  Depends on : - Duration - Metabolic control - Genetic factors

18.  Microangiopathy: Thickening of basement membrane PAS + Advanced glycosylation end product. - Renal Glomeruli  ( (nephropathy - Retina  ( (retinopathy - Nerves  (neuropathy)

19.  Atherosclerosis: - Myocardial infarction - Cerebral stroke. - Aortic aneurysm. - Gangrene of lower extremities

21.  Neuropathy: - Symmetric peripheral neuropathy. - Sexual impotence. -Bowel and bladder dysfunction.

22. Diabetic Nephropathy  Glomerular involvement : 1. Diffuse glomerulosclerosis. 2. Nodular glomerulosclerosis “ KimmelStiel – Wilson lesion ”  Nephrotic Syndrome  Arteriolosclerosis:  Pyelonephritis (acute & chronic) * Necrotizing papillitis.

23. Diabetic Ocular complications:  - Retinopathy : Non – proliferative retinopathy ( hemorrhage, oedema, exudates microaneurysms and microangiopathy) Proliferative retinopathy Neovascularization and fibrosis  blindness (macula )  - Vitrous hemorrhage.  - Cataract formation.  - Glaucoma *Diabetes Mellitus are more susceptible to infection.

25. ISLET CELL TUMOURS  Rare  Adult  Multiple / solitary  May be functional  Mainly benign / can be malignant

26. ISLET CELL TUMOURS Three Syndromes: 1.Hyperinsulinism & hypoglycemia : (insulinoma) of Beta cells solitary adenomas multiple Can be malignant

27. ISLET CELL TUMOURS 2.Zollinger – Ellison Syndrome (Gastrinoma) - Multiple ulcer disease - Gastric hypersecretion - Islet cell tumour Malignant 60%& benign40% 3.MEN (1, 2A, 2B)