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PANCREAS

- Anatomy and
Histology
- Normal Physiology of
the Endocrine Pancreas
PANCREAS- Anatomy

A soft, lobulated organ that


stretches obliquely across
the posterior abdominal
wall in the epigastric
region.
It is situated behind the
stomach and extends from
the duodenum to the
spleen
ANATOMY- Type of Gland

Soft, fleshy organ with little connective tissue


Endocrine
Islet of Langerhans
Produces the hormones insulin and glucagon
Exocrine
Produces secretion that contains enzymes capable of
hydrolyzing CHON, fats and CHO
ANATOMY- Parts and their Relations

HEAD- the broad, right extremity. It lies within the


curve of the duodenum
Uncinate process- a prolongation of the left and caudal
borders of the head
Anterior Surface- most of the right side separated from the
tranverse colon by the areolar tissue; lower part of the
surface below the transverse colon is covered by
peritoneum; it is in contact with coils of the small intestines
Posterior Surface- it is in contact with IVC, common bile
duct, renal veins, rt crud of diaphragm and aorta
ANATOMY- Parts and their Relations

NECK
A constricted portion to the left of the head
Above,it adjoins the pylorus
Behind, it is related to the origin of the portal vein
and gastroduodenal artery
TAIL
Left extrimity extending to the surface of spleen,
in splenorenal ligament
ANATOMY- Parts and their Relations

BODY
Anterior surface- it is separated from the stomach by the
omental bursa
Posterior Surface- non-peritoneal, related to the aorta, splenic
vein, left kidney and vessels;origin of superior mesenteric artery
and crura of diaphragm
Inferior Surface- related to duodenal flexure, coils of jejunum
and left colic flexure
Anterior Border- layers of transverse mesocolon diverge along
this
Superior Border- related to celiac artery with hepatic artery to
right and splenic artery to left
ANATOMY- Parts and their Relations
ANATOMY- Ducts

Major- Duct of Wirsung


It extends toward right, reaches neck of pancreas where it
turns caudally and dorsally and comes in contact with the
common bile duct forming the Ampulla of Vater
Pass obliquely through the wall of the descending
duodenum and open through a common orifice into its
lumen
Accessory- Duct of Santorini
Drains part of the head and enters the duodenum above the
major duct
ANATOMY- Blood Supply

Arteries
Numerous small branches from the splenic artery
Retroduodenal branch of gastroduodenal artery
Superior pancreaticoduodenal from gastroduodenal
artery
Inferior panceaticoduodenal artery from the superior
mesenteric artery
Veins
Drain into both the splenic and superior mesenteric
veins
HISTOLOGY (Endocrine Pancreas)

Islets of Langerhans
It is formed by relatively
small aggregations of
cells
They are scattered
throughout the gland
but are somewhat more
numerous in the tail
than in the body than
the head of the gland
HISTOLOGY (Endocrine Pancreas)

Each islet is composed of


2- 3 thousand cells that
are arranged in
anastomosing cords and
plates
They are demarcated
from the surrounding
acinar tissue by a thin
layer of reticular fibers that
extend inward to form a
delicate investment
around the capillaries
HISTOLOGY (Endocrine Pancreas)

Principal Types of Cells


CELLS- Glucagon
Located mainly at the
periphery of the islet; few
are scattered along the
capillaries in its interior
CELLS- Insulin
It is the predominant cell
type in the islet; it
occupies it center and
makes up 60% of its
mass
HISTOLOGY (Endocrine Pancreas)
Cells
Secretes Somatostatin
F Cells
Secretes pancreatic polypeptide
They are widely scattered
Few in number and may occur
among the acini as well as in the
islet
***distinctive features that permit
identification
- differences in size,
density, internal structure of
secretory granules
HISTOLOGY (Endocrine Pancreas)

Type of Islet Cell Product Action


(25%) Glucagon Regulation of
metabolism of CHO,
CHON, and fats
(60%) Insulin Regulation of
metabolism of CHO,
CHON, and fats

Somatostatin Regulation of islet cell


secretion
F Pancreatic Polypeptide Slows absorption of
food
HISTOLOGY (Endocrine Pancreas)

Interactions between hormones


Somatostatin

(-) (+) (-) (-)

Insulin Glucagon Pancreatic


polypeptide
(-)
HISTOPHYSIOLOGY

GLUCOSE
It is the major product of CHO digestion in the
alimentary tract
It is utilized as an energy source in cell metabolism
throughout the body and is controlled by hormones
secreted by the principal cell types
Insulin
A polypeptide consisting of a chain of 21 amino
acids (- chain) and a chain of 30 amino acids (-
chain) linked together by 2 disulfide bridges.
HISTOPHYSIOLOGY-
Insulin Synthesis

Preproinsulin
Synthesized in RER of
cell
Proinsulin
Result of folding which is
facilitated by C peptide
Measurement of C peptide
by radioimmunoassay
provides index of cell fxn
in patients receiving
exogenous insulin
HISTOPHYSIOLOGY-
Insulin Synthesis

Insulin
Action of proteases on
proinsulin forms insulin
Insulin is packed in
Golgi apparatus and
expelled by exocytosis
via fenestrations of
capillary endothelium
into the blood stream
HISTOPHYSIOLOGY

Other two major peptide hormones


Glucagon
Produced by the cells
It is secreted in response to a fall in blood glucose
concentration
It acts mainly upon the hepatic cells, increasing the
degradation of glycogen to release glucose into the
blood
It is also capable of increasing gluconeogenesis by the
hepatic cells when glycogen is depleted
HISTOPHYSIOLOGY

Somatostatin
It is secreted by the cells
A small polypeptide of only 14 amino acids
Its secretion is stimulated by the post prandial increase
in blood glucose, amino acids of fatty acids
It decrease the rate of secretion of both insulin and
glucagon
It diminish motility of the stomach, small intestine and
gall bladder
It is also produced by cells in the hypothalamus where it
serves to reduce the secretion of growth hormone by the
somatotrophs of the anterior pituitary
Comparison of Insulin with Glucagon
Features Insulin Glucagon
Effects Glucose transport: insulin facilitates glucose entry Stimulates release of glucose
into cells by increasing # of glucose transporters in into bloodstream
cell membrane
Anabolic Catabolic
Hormone of energy storage Energy release
Glycogenesis, antigluconeogenic, antilipolytic, Glycogenolytic,
antiketotic gluconeogenesis, lipolytic,
ketogenic
Stimulates uptake of amino acids, FFA, ketones Stimulates release of amino
and K into cells acids, FFA and ketones into
bloodstream
Stimulates synthesis of glycogen, CHON and lipids Stimulates glycogen, CHON
and lipid degradation
Excess causes hypoglycemia Excess worsens DM
Deficiency causes DM Deficiency causes
hypoglycemia
Comparison of Insulin with Glucagon

Feature Insulin Glucagon


Stimulators Glucose Hypoglycemia, amino
acids
Glucagon, secretin, CCK, gastric CCK, gastrin, cortisol
inhibitory peptide
adrenergic stimulation adrenergic stimulation
Exercise, infection, stress
Inhibitors Glucagon, epinephrine, GH, cortisol Insulin, Somatostatin,
Secretin
Hypoglycemia Glucose, FFA
adrenergic stimulation adrenergic stimulation
K depletion, hypoaldosteronism, thiazide
diuretics
EXOCRINE GLAND

Consist of compound acinous gland made up of


many small lobules bound by loose connective
tissue
Acini
Round or slightly elongated
Consist of 40-50 pyramidal cell
EXOCRINE GLAND

Acinar cells
Strongly basophilic high conc. of ribonucleoproteins
Apical cytoplasm is filled w/ large # of secretory
vesicles/granules
Vesicles containing the precursors of the pancreatic digestive
enzymes (zymogen granules)
Lower portion is crowded w/ closely spaced parallel
cisternae of granular ER
Duct System

Centroacinar cells
Low cuboidal or squamous cells lining the duct extend
a short distance into the acinus
Unique for pancreas
Identified by their pale staining in histologic staining;
low density and paucity in EM
Centroacinar are continuous w/ the lining
epithelium of intercalated ducts that drains
acinus
Duct System

Interlobular ducts are lined w/ low columnar


epithelium containing occasional goblet cells
Smaller ducts are active in transporting water
and bicarbonate ions into the lumen
Interlobular ducts join the main pancreatic ducts
Blood Vessels, Lymphatics and
Nerves

Arterial supply splenic and


pancreaticoduodenal arteries
Venous drainage corresponding veins drains
to the portal veins
Lymph drainage drain into the celiac and
superior mesenteric lymph nodes
Nerve supply symphathetic and
parasymphathetic vagus nerve fibers
Diabetes Mellitus
-Definition
- Signs and Symptoms
Diabetes Mellitus

It is a syndrome of impaired carbohydrate,fat,


and protein metabolism caused by either lack of
insulin secretion or decreased sensitivity of the
tissues to insulin
Type I diabetes (IDDM)- caused by lack of insulin
secretion.
Type II diabetes (NIDDM)- caused by decreased
sensitivity of target tissues to the metabolic effect of
insulin (insulin resistance)
Diabetes Mellitus

The basic effect of insulin lack or insulin


resistance on glucose metabolism is to prevent
the efficient uptake and utilization of glucose by
most cells of the body(except those of the brain)
Blood glucose concentration increases
Cell utilization of glucose falls increasingly lower
Utilization of fats and proteins increases
Diabetes Mellitus - Types

Feature Type 1 (IDDM) Type 2 (NIDDM)


Age of Onset Usually < 40 Usually >40
Insulin Requirement Always Not in early stage
Involves Obesity No Yes
Autoimmune Yes No
Destruction of cells in
Pancreatic Islet
Involves Insulin No Yes
Resistance
Ketosis as Yes Rarely
Complication
Diabetes Mellitus- Metabolic
Changes; Signs and Symptoms

Metabolic Changes Signs and Symptoms


Reduced entry of glucose and amino acids Significant hyperglycemia,
into peripheral tissues and increased including during fasting and
liberation of glucose into circulation from the postprandial states
liver
Intracellular glucose deficiency forces energy Weight loss
requirements to be met by increasing
catabolism of fat
-Hypersecretion of glucagon and -Body enters starvation state
glucocorticoids increases amino acid supply -Serum albumin decreases
for gluconeogenesis
-Accelerated CHON catabolism and
decreased CHON synthesis causes CHON
depletion
Diabetes Mellitus- Metabolic
Changes; Signs and Symptoms
Metabolic Changes Signs and Symptoms
Circulating FFAs are increased as a Ketosis ( excess acetyl coenzyme A
result of insulin inhibition of lipase production of acetoacetate, acetone and
hypersecretion of glucagon hydroxybutyrate o be formed in liver and
enter circulation)
-Excess EC glucose causes Hyperosmolar plasma, leading to total
hyperosmolality of blood body depletion of K and Na and severe
-Hyperosmolality of blood causes metabolic or lactic acidosis
renal capacity for glucose -Glycosuria and osmotic diuresis causing
reabsorption to be exceeded polyuria
-Resultant dehydration leading to
polydipsia
-Polyphagia occurs in attempt to cover
glucose loss, leading to further mobilization
of CHON and fat stores and weight loss

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