4. INTRODUCTION
The pancreas is about 6 inches long
and sits across the back of the
abdomen, behind the stomach in the
upper left abdomen. The head of the
pancreas is on the right side of the
abdomen and is connected to the
duodenum (the first section of the
small intestine) through a small tube
called the pancreatic duct. The
narrow end of the pancreas, called the
tail, extends to the left side of the
body.
5. Functions of the Pancreas
Exocrine Function:
The pancreas contains exocrine glands that
produce enzymes important to digestion. These
enzymes include TRYPSIN and CHYMOTRYPSIN
proteins; AMYLASE carbohydrates; and LIPASE
to break down fats.
Endocrine Function:
The endocrine component of the pancreas
consists of islet cells (islets of Langerhans)
that create and release
important hormones directly into the
bloodstream.
6. ISLET OF LANGERHANS
HUMAN PANCREAS CONTAIN ABOUT ONE TO
TWO MILLIONS ISLETS CELL
THERE ARE FOUR TYPE OF ISLETS OF
LANGERHANS
Alpha-cells or α-cells SECRETE GLUCAGON
Beta cells (β cells) SECRET INSULIN
Delta cells (δ-cells or D cells) SECRETE
SOMATOSTATIN
F CELLS OR PP CELLS SECRETE PANCREATIC
POLYPEPTIDE
7. INSULIN
SOURCE OF SECRETION
BETA CELLS OF ISLETS OF LANGERHANS
CHEMISTRY ANDHALF LIFE
IT IS A POLYPEPTIDE WITH 51 AMINO ACIDS BIOLOGICAL
HALF LIFE IS 5 MINUTES
the time required for the body to eliminate half of an
administered dose of any substance by regular physiological
processes
SYNTHESIS
IT IS SYNTHESISED IN ROUGH ENDOPLASMIC
RETICULUM OF BETA CELLS.
PREPROINSULIN PROINSULIN INSULIN
8. METABOLISM
IT IS DEGRADED IN LIVER AND KIDNEY BY CELLULAR ENZYME
CALLED INSULIN PROTEASE.
ACTION OF INSULIN
ON CARBOHYDRATE METABOLISM
IT IS THE ONLY ANTI DIABETIC HORMONE SECRETED IN
BODY ,I.E. IT REDUCES BLOOD GLUCOSE LEVEL BY
FOLLOWING ACTION
--INCREASE THE TRANSPORT AND UPTAKE OF GLUCOSE BY
CELLS:
INSULIN FASCILITATESTHE TRANSPORT OF GLUCOSE FROM
BLOOD INTO THE CELLS BY INCREASING THE PERMEABILITY
OF CELL MEMBRANE TO GLUCOSE. GLUCOSE IS
TRANSPORTED IN CELLS BY THE HELP OF GLUCOSE
TRANSPORTERS ( GLUT).
GLUT 4 IS INSULIN SENSITIVE AND IS LOCATED IN
CYTOPLASMIC VESICLES.
9. WHEN INSULIN RECEPTOR COMPLEX IS
FORMED IN THE MEMBRANE OF CELL
THE GLUT4 ARE ATTRACTED TOWARDS
THE MEMBRANE AND GLUT4 IS
RELEASED INTO THE MEMBRANE. NOW
IT STARTS TRANSPORTING GLUCOSE
MOLECULE FROM EXTRACELLULAR
FLUID INTO CELLS.
CELLS WHERE GLUCOSE IS METABOLISED
( LIVER, MUSCLE, AND ADIPOSE TISSUE )
WHERE NOT METABOLISED ( BRAIN
EXCEPT HYPOTHALAMUS, RENAL
TUBULES, MUCOUS MEMBRANE OF
INTESTINE, RBCs.
10. 1. PROMOTES PHERIPHERAL UTILIZATION
OF GLUCOSE
2. PROMOTES STORAGE OF GLUCOSE-
GLYCOGENESIS STORAGE OF GLUCOSE
INTO GLYCOGEN IN MUSCLES AND
LIVER
3. INHIBTS GLYCOGENOLYSIS.
BREAKDOWN OF GLYCOGEN INTO
GLUCOSE
4. INHIBITS GLUCONEOGENSIS:
FORMATION OF GLUCOSE FROM
PROTEINS BY INHIBITING THE
RELEASE OF AMINO ACIDS.
11. ON PROTEIN MTABOLISM
IT INCREASE THE SYNTHESIS OF FATTY ACIDS
AND STORAGE OF PROTEIN AND INHIBITS THE
CELLULAR UTILIZATION OF PROTEINS BY:
INCREASES THE PERMEABILTY OF CELL
MEMBRANE FOR AMINO ACID
PREVENT PROTEIN CATABOLISM
ON FAT METABOLISM
INSULIN STIMULATE THE SYNTHESIS OF FAT
AND STORAGE OF FAT
13. APPLIED PHYSIOLOGY
DEVELOPS DUE TODEFICIENCY OF HORMONE
INSULIN
TYPES
a) TYPE 1 DIEBETS MELLITUS: DUE TO DEFICIENCY
OF INSULIN DUE TO DESTRUCTION OF BETA
CELLS OF ISLETS F LANGERHANS. USUALLY
DEVELOPS BEFORE 40 YEARS OF AGE.
CAUSE ; VIRAL INFECTION, CONGENITAL
DISORDER,
AUTOIMMUNE DISEASE
b) TYPE 2 DIABETS MELLITUS : DUE TO INSULIN
RESISTANCE
CAUSE : GENETIC DISORDER, LIFE STYLE , STRESS.
14. SIGN AND SYMPTOMS OF
DIABETES MELLITUS
1. INCREASED BLOOD GLUCOSE LEVEL(NORMAL
80-100mg/dl) fasting
2. Loss of glucose in urine ( glucosuria)
3. Polyuria and polydipsia:
4. Polyphagia : intake of excessive food
5. Acetone BREATHING
6. KUSSMAUL BREATHING: INCREASE RATE
AND DEPTH OF RESPIRATION
7. COMA
16. DIAGNOSTIC TEST
FASTING BLOOD GLUCOSE LEVEL
POSTPRANDIAL BLOOD GLUCOSE
GLUCOSE TOLERANCE TEST
GLYCOSYLATED HEMOGLOBIN
17. GLUCAGON
SOURCE OF SECRETION:
ALPHA CELLS OF ISLET OF LANGERHANS
CHEMISTRY AND HALF LIFE:
IT IS A POLYPEPTIDE CONTAIN 29 AMINO ACIDS.
HALF LIFE IS 3 TO 6 MINUTES.
METABOLISM:
ABOUT 30% DEGRADED IN LIVER AND 20% IN
KIDNEY. 50 % DEGREDED IN BLOOD BY
ENZYME SERINE AND CYSTEINE PROTEASES.
18. ACTION OF GLUCAGON
ON CARBOHYDRATE:
IT INCREASES THE BLOOD GLUCOSE LEVEL
BY INCRESING GLYCOGENOLYSIS
BY INCREASING GLUCONEOGENESIS
ON PROTEIN METABOLISM:
INCREASES THE TRANSPORT OF AMINO ACIDS
INTO LIVER CELLS.
ON FAT METABOLISM:
IT SHOWS LIPOLYTIC AND KETOGENIC ACTIONS.
KETOGENIC MEANS FORMATION OF KETONE
BODIES.
19. REGULATION OF GLUCAGON
SECRETION
ROLE OF BLOOD GLUCOSE LEVEL :
DECREASE IN BLOOD GLUCOSE LEVEL INCREASES THE
SECRETION
ROLE OF AMINO ACID LEVEL
INCREASE IN AMINO ACID INCREASE THE SECRETION
WHICH IN TURN INCREASE THE CONVERSION OF AMINO
ACID INTO GLUCOSE.
ROLE OF OTHER FACTOR
EXERCISE
STRESS
GASTRIN INCRESES THE SECRETION
CHOLECYSTOKININ
CORTISOL
21. SOMATOSTATIN
SECRETED FROM
HYPOTHALAMUS
D CELLS OF ISLETS OF LANGERHANS
D CELLS IN STOMACH AND UPPER PART OF SMALL
INTESTINE
CHEMISTRY & HALF LIFE:
IT IS A POLYPEPTIDE. AND HAVE HALF LIFE OF 2 TO 4
MIN.
METABOLISM:
DEGRADED IN LIVER
22. ACTION OF SOMATOSTATIN
INHIBIT BOTH GLUCAGON AND INSULIN
DECREASES THE MOTILITY OF STOMACH,
DUODENUM AND GALLBLADDER.
REDUCES SECRETION OF GASTRIC HORMONE
IT INHIBIT SECRETION OF GROWTH HORMONE
AND TSH FROM ANTERIOR PITUITARY.
THUS KNOWN AS
GROWTH HORMONE INHIBITORY HORMONE(
GHIH)