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):
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:
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 :
- 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:
- 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)
* 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)
- Multiple ulcer disease
- Gastric hypersecretion
- Islet cell tumour
Malignant 60%
&
benign40%
3.MEN (1, 2A, 2B)