ENDOCRINE PANCREAS

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Transcript ENDOCRINE PANCREAS

ENDOCRINE
PANCREAS
 Diabetes Mellitus
 Islet Cell tumors
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)
 Each type of pancreatic islet cells may
give mainly benign tumour ->
(ADENOMA) called Islet cell tumours:
Insulinoma
Glucagonoma Somatostatinoma
VIPoma
Carcinoid tumours
Gastrinoma

Multiple Endocrine Neoplasia
(MEN)
DIABETES MELLITUS
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
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
 Secondary Diabetes Mellitus:
- Chronic pancreatitis
- Post pancreatectomy
- Hormonal tumours (acromegaly,
Cushing’s ---)
- Drugs (corticosteroids)
- Haemochromatosis
- Genetic disorders e.g. lipodystrophy
- Gestational DM

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.
 MODY (maturity-onset DM of the
Young):
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Young
Rare
Linked to chrom. 7 & 20
Autosomal dominant
Mild hyperglycemia
 ACUTE METABOLIC
COMPLICATIONS:
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
Non ketotic Hyperosmolar
Coma:


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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
Morphology & Late
Complications
 Depends on :

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
- Duration
- Metabolic control
- Genetic factors
 Microangiopathy:
Thickening of basement membrane PAS +
Advanced glycosylation end product .
 - Renal Glomeruli () nephropathy
 - Retina ( ) retinopathy
 - Nerves (neuropathy)
 Atherosclerosis:




-
Myocardial infarction
Cerebral stroke .
Aortic aneurysm .
Gangrene of lower extremities
 Neuropathy:
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- Symmetric peripheral neuropathy .
- Sexual impotence .
- Bowel and bladder dysfunction.
Diabetic Nephropathy
Glomerular involvement :

1.
2.
Diffuse glomerulosclerosis .
Nodular glomerulosclerosis
“ KimmelStiel – Wilson lesion ”
 Nephrotic Syndrome
Arteriolosclerosis:
Pyelonephritis (acute & chronic)

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* Necrotizing papillitis .
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.
ISLET CELL TUMOURS
 Rare
 Adult
 Multiple / solitary
 May be functional
 Mainly benign / can be malignant
ISLET CELL TUMOURS
Three Syndromes:
1. Hyperinsulinism & hypoglycemia :




)insulinoma) of Beta cells
solitary adenomas
multiple
Can be malignant
ISLET CELL TUMOURS
2. Zollinger – Ellison Syndrome
(Gastrinoma)
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- Multiple ulcer disease
- Gastric hypersecretion
- Islet cell tumour
Malignant 60%
&
benign40%
3.MEN (1, 2A, 2B)