10-Endocrine Pancreas

Endocrine Pancreas
Dr. Isam Eldin Mohamed Abd Alla

ENDOCRINE PANCREAS
BY :- NOURA ABUBAKR BATCH(4)

duc
ts
& islets
ves 2%
sel
s
18
%
exocrine pancreas
80%
60-70% 20 % 10%
B-cells A-cells D-cells
F-
cells
Endocrine cells in islets of Langerhans
Are scattered throughout the pancreas
but more plenty in the tail
• A – cells secrete Glucagon
• B – cells secrete Insulin.
• D– cells secrete Somatostatin.
• F – cells secrete Pancreatic polypeptide.
Insulin:
Is a peptide hormone made of A & B chains
Synthesis of insulin:
• Synthesized as pre-proinsulin (insulin,
signal peptide & connecting C- peptide)
• Signal peptide is removed as it enters the
endoplasmic reticulum.
The remainder (proinsulin) is then folded &
stored in granules (vesicles) in Golgi
apparatus,
Folding is facilitated by the connecting
peptide (C peptide), which connect the A
and B chains,
• C peptide level can be measured by
radioimmunoassay as an index of B cell
function in patients receiving exogenous
insulin.
Mechanism of insulin action
• Physiologic effects of Insulin:
1. Stimulates entry of glucose into the cells
of the muscles, adipose tissues via GLUT4 &
Liver.
NOTE Brain, placenta, RBCs, enerocytes &
renal tubular cells are not dependent on
Insulin for glucose entry.
2. Stimulates entry of amino acids &
Potassium ions into the cells.
3. Stimulates glucose utilization (glycolysis)
4. Stimulates storage of excess glucose as
glycogen in the liver & muscles,.
5. Stimulates proteins synthesis & inhibit
catabolism → growth.
6. Stimulates removal of cholesterol & fatty
acids from the circulating lipoproteins in
the blood.
7. Stimulates fats synthesis from glucose
metabolite Acetyl Co-A & facilitates lipids
storage.
Regulation of insulin secretion:
• Stimulators of insulin secretion:
↑ of circulating glucose level
(hyperglycaemia), the main stimulus.
↑ of circulating amino & keto-acids level.
 Parasympathetic vagal fibers to the pancreas.
↑ intracellular cyclic AMP Via Gulcagon
 Gulcagon Which ↑ the circulating glucose
level & intracellular cyclic AMP.
 Oral hypoglycaemic drugs such as
Sulfonylurea.
Insulin secretion
Inhibitors of insulin secretion:
Hypoglycaemia.
Hypokalaemia (K+ depletion).
Sympathetic nervous system via α
adrenergic receptors.
Potassium channels openers (Diazoxide)
Thiazide diuretics by causing K+ depletion
damage of pancreatic cells. .
Diabetes mellitus (DM):
• Is a chronic disorder of carbohydrates,
lipids & proteins metabolism, the main
characteristic of which is persistent
hyperglycaemia.
• (Fasting plasma glucose level above
125mg/dL, or Random plasma glucose
level above 200mg/dL+ clinical
symptoms).
• Normal Fasting plasma glucose level = 70
Type of diabetes:
1 .Type 1 DM (insulin dependent diabetes
mellitus IDDM).
• Occurs before age of 40years mainly in
children (juvenile DM).
• Is due to insulin deficiency caused by
autoimmune destruction of the pancreatic
B cells after infections mainly viral
infection.
• Treatment depends on insulin.
2. Type 2 DM (Non insulin dependent
diabetes mellitus NIDDM :
Occurs after the age of
40 years.
• Is due to tissue resistance to insulin
action or defective insulin secretion.
• Obesity is one of the causes of this
resistance,
• . This type is more related to genetics
(inheritance) than type 1.
• Pathophysiology of DM:
• ↓glucose entry & utilization by the cells→
hyperglycaemia & plasma hyperosmolality that
stimulates the thirst center to ↑ drinking of
water (polydipsia). Hyperglycaemia with plasma
glucose level above 180mgldL→ ↑the glucose
filtration in the kidneys to a degree that
saturate glucose transporter for renal glucose
reabsorption → Appearance of considerable
amount of glucose in the urine (Glycosuria).
• ↓ glucose reabsorption → ↓ renal water
reabsorption by osmotic drag → ↑rate of
urination (Polyuria) → dehydration
hypovolaemia which also stimulates the
thirst center causing polydipsia.
• ↓glucose utilization → ↑action of
lipolytic hormones (glucagon, T3, T4, cortisol,
catechoamines, & growth
hormone to cause lipolysis &mobilization
of fatty acids as alternative source of
• loss of body weight mainly in type 1
.Oxidation of fatty acids generates large
amount of Acetyl CoA above the capacity
of citric acid cycle, leading to formation of
ketone bodies (Acetoacetic acid,β
Hydroxybutyric acid & Acetone)→
ketoacidosis
• DKA → stimulation of chemoreceptors &
respiratory center causing increase in
respiratory rate & depth (Hyperventilation
or Kussmaul breathing)in which acetone
can be smelled in the patient breath.
• Coma can result from three causes in DM:
• 1. Hyperosmolality.
• 2.Acidosis.
• 3. Hypoperfusion caused by
hypovolaemia & atherosclerosis.
Symptoms & signs of Diabetes:
• Glycosuria.
• Polyuria ( Frequent urination).
• Polydipssia
• Polyphagia.
• Weight loss.
• Hyperventilation.
• Defective sensations.
• Dealyed wound healing.
• Symptoms of Angina pectoris.

10-Endocrine Pancreas

Uploaded by

Copyright:

Available Formats

10-Endocrine Pancreas

Uploaded by

Document Information

Original Title

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

10-Endocrine Pancreas

Uploaded by

Copyright:

Available Formats

Endocrine Pancreas

Dr. Isam Eldin Mohamed Abd Alla

BY :- NOURA ABUBAKR BATCH(4)

You might also like