Anatomy of Pancreas


According to Gray's Anatomy Textbook

The pancreas  is a compound racemose  friable gland, analogous in its structures to the salivary glands, though softer and less compactly arranged than those organs. Its secretion, the pancreatic juice, carried by the pancreatic duct to the duodenum, is an important digestive fluid. In addition the pancreas has an important internal secretion, probably elaborated by the cells of Langerhans, which is taken up by the blood stream and is concerned with sugar metabolism. It is long and irregularly prismatic in shape; its right extremity, being broad, is called the head, and is connected to the main portion of the organ, or body, by a slight constriction, the neck; while its left extremity gradually tapers to form the tail. It is situated transversely across the posterior wall of the abdomen, at the back of the epigastric and left hypochondriac regions. Its length varies from 12.5 to 15 cm., and its weight from 60 to 100 gm.

 Relations.—The Head (caput pancreatis) is flattened from before backward, and is lodged within the curve of the duodenum. Its upper border is overlapped by the superior part of the duodenum and its lower overlaps the horizontal part; its right and left borders overlap in front, and insinuate themselves behind, the descending and ascending parts of the duodenum respectively. The angle of junction of the lower and left lateral borders forms a prolongation, termed the uncinate process. In the groove between the duodenum and the right lateral and lower borders in front are the anastomosing superior and inferior pancreaticoduodenal arteries; the common bile duct descends behind, close to the right border, to its termination in the descending part of the duodenum.   2 Anterior Surface.—The greater part of the right half of this surface is in contact with the transverse colon, only areolar tissue intervening. From its upper part the neck springs, its right limit being marked by a groove for the gastroduodenal artery. 

The lower part of the right half, below the transverse colon, is covered by peritoneum continuous with the inferior layer of the transverse mesocolon, and is in contact with the coils of the small intestine. The superior mesenteric artery passes down in front of the left half across the uncinate process; the superior mesenteric vein runs upward on the right side of the artery and, behind the neck, joins with the lienal vein to form the portal vein.   3 
Posterior Surface.—The posterior surface is in relation with the inferior vena cava, the common bile duct, the renal veins, the right crus of the diaphragm, and the aorta.   4  The Neck springs from the right upper portion of the front of the head. It is about 2.5 cm. long, and is directed at first upward and forward, and then upward and to the left to join the body; it is somewhat flattened from above downward and backward. Its antero-superior surface supports the pylorus; its postero-inferior surface is in relation with the commencement of the portal vein; on the right it is grooved by the gastroduodenal artery.   5  The Body (corpus pancreatis) is somewhat prismatic in shape, and has three surfaces: anterior, posterior, and inferior.   6  The anterior surface (facies anterior) is somewhat concave; and is directed forward and upward: it is covered by the postero-inferior surface of the stomach which rests upon it, the two organs being separated by the omental bursa. Where it joins the neck there is a well-marked prominence, the tuber omentale, which abuts against the posterior surface of the lesser omentum.   7  The posterior surface (facies posterior) is devoid of peritoneum, and is in contact with the aorta, the lienal vein, the left kidney and its vessels, the left suprarenal gland, the origin of the superior mesenteric artery, and the crura of the diaphragm.   8  The inferior surface (facies inferior) is narrow on the right but broader on the left, and is covered by peritoneum; it lies upon the duodenojejunal flexure and on some coils of the jejunum; its left extremity rests on the left colic flexure.   9  The superior border (margo superior) is blunt and flat to the right; narrow and sharp to the left, near the tail. It commences on the right in the omental tuberosity, and is in relation with the celiac artery, from which the hepatic artery courses to the right just above the gland, while the lienal artery runs toward the left in a groove along this border.   10  The anterior border (margo anterior) separates the anterior from the inferior surface, and along this border the two layers of the transverse mesocolon diverge from one another; one passing upward over the anterior surface, the other backward over the inferior surface.   11  The inferior border (margo inferior) separates the posterior from the inferior surface; the superior mesenteric vessels emerge under its right extremity.   12  The Tail (cauda pancreatis) is narrow; it extends to the left as far as the lower part of the gastric surface of the spleen, lying in the phrenicolienal ligament, and it is in contact with the left colic flexure.   13  Birmingham described the body of the pancreas as projecting forward as a prominent ridge into the abdominal cavity and forming part of a shelf on which the stomach lies. “The portion of the pancreas to the left of the middle line has a very considerable antero-posterior thickness; as a result the anterior surface is of considerable extent; it looks strongly upward, and forms a large and important part of the shelf. As the pancreas extends to the left toward the spleen it crosses the upper part of the kidney, and is so moulded on to it that the top of the kidney forms an extension inward and backward of the upper surface of the pancreas and extends the bed in this direction. On the other hand, the extremity of the pancreas comes in contact with the spleen in such a way that the plane of its upper surface runs with little interruption upward and backward into the concave gastric surface of the spleen, which completes the bed behind and to the left, and, running upward, forms a partial cap for the wide end of the stomach

The Pancreatic Duct (ductus pancreaticus [Wirsungi]; duct of Wirsung) extends transversely from left to right through the substance of the pancreas (Fig. 1100). It commences by the junction of the small ducts of the lobules situated in the tail of the pancreas, and, running from left to right through the body, it receives the ducts of the various lobules composing the gland. Considerably augmented in size, it reaches the neck, and turning downward, backward, and to the right, it comes into relation with the common bile duct, which lies to its right side; leaving the head of the gland, it passes very obliquely through the mucous and muscular coats of the duodenum, and ends by an orifice common to it and the common bile duct upon the summit of the duodenal papilla, situated at the medial side of the descending portion of the duodenum, 7.5 to 10 cm. below the pylorus. The pancreatic duct, near the duodenum, is about the size of an ordinary quill. Sometimes the pancreatic duct and the common bile duct open separately into the duodenum. Frequently there is an additional duct, which is given off from the pancreatic duct in the neck of the pancreas and opens into the duodenum about 2.5 cm. above the duodenal papilla. It receives the ducts from the lower part of the head, and is known as the accessory pancreatic duct (duct of Santorini).   15 Development 
The pancreas is developed in two parts, a dorsal and a ventral. The former arises as a diverticulum from the dorsal aspect of the duodenum a short distance above the hepatic diverticulum, and, growing upward and backward into the dorsal mesogastrium, forms a part of the head and uncinate process and the whole of the body and tail of the pancreas. The ventral part appears in the form of a diverticulum from the primitive bile-duct and forms the remainder of the head and uncinate process of the pancreas. The duct of the dorsal part (accessory pancreatic duct) therefore opens independently into the duodenum, while that of the ventral part (pancreatic duct) opens with the common bile-duct. About the sixth week the two parts of the pancreas meet and fuse and a communication is established between their ducts. After this has occurred the terminal part of the accessory duct, i. e., the part between the duodenum and the point of meeting of the two ducts, undergoes little or no enlargement, while the pancreatic duct increases in size and forms the main duct of the gland. The opening of the accessory duct into the duodenum is sometimes obliterated, and even when it remains patent it is probable that the whole of the pancreatic secretion is conveyed through the pancreatic duct

At first the pancreas is directed upward and backward between the two layers of the dorsal mesogastrium, which give to it a complete peritoneal investment, and its surfaces look to the right and left. With the change in the position of the stomach the dorsal mesogastrium is drawn downward and to the left, and the right side of the pancreas is directed backward and the left forward . 

The right surface becomes applied to the posterior abdominal wall, and the peritoneum which covered it undergoes absorption  and thus, in the adult, the gland appears to lie behind the peritoneal cavity.   17 Structure —In structure, the pancreas resembles the salivary glands. It differs from them, however, in certain particulars, and is looser and softer in its texture. It is not enclosed in a distinct capsule, but is surrounded by areolar tissue, which dips into its interior, and connects together the various lobules of which it is composed. Each lobule, like the lobules of the salivary glands, consists of one of the ultimate ramifications of the main duct, ending in a number of cecal pouches or alveoli, which are tubular and somewhat convoluted. The minute ducts connected with the alveoli are narrow and lined with flattened cells. The alveoli are almost completely filled with secreting cells, so that scarcely any lumen is visible. In some animals spindle-shaped cells occupy the center of the alveolus and are known as the centroacinar cells of Langerhans. These are prolongations of the terminal ducts. The true secreting cells which line the wall of the alveolus are very characteristic. 

They are columnar in shape and present two zones: an outer one, clear and finely striated next the basement membrane, and an inner granular one next the lumen. In hardened specimens the outer zone stains deeply with various dyes, whereas the inner zone stains slightly. During activity the granular zone gradually diminishes in size, and when exhausted is only seen as a small area next to the lumen. During the resting stages it gradually increases until it forms nearly three-fourths of the cell. In some of the secreting cells of the pancreas is a spherical mass, staining more easily than the rest of the cell; this is termed the paranucleus, and is believed to be an extension from the nucleus. The connective tissue between the alveoli presents in certain parts collections of cells, which are termed interalveolar cell islets (islands of Langerhans). The cells of these stain lightly with hematoxylin or carmine, and are more or less polyhedral in shape, forming a net-work in which ramify many capillaries. There are two main types of cell in the islets, distinguished as A-cells and B-cells according to the special staining reactions of the granules they contain. The cell islets have been supposed to produce the internal secretion of the pancreas which is necessary for carbohydrate metabolism, but numerous researches have so far failed to elucidate their real function
The walls of the pancreatic duct are thin, consisting of two coats, an external fibrous and an internal mucous; the latter is smooth, and furnished near its termination with a few scattered follicles.   19 Vessels and Nerves.—The arteries of the pancreas are derived from the lienal, and the pancreaticoduodenal branches of the hepatic and superior mesenteric. Its veins open into the lienal and superior mesenteric veins. Its lymphatics are described on page 711. Its nerves are filaments from the lienal plexus

Sites Of Insulin Injections,Where To Inject?

Insulin for routine treatment is given subcutaneously by
intermittent injections or by continuous infusion. Insulin can
be injected subcutaneously almost anywhere if there is enough flesh. 

The best site is the front of the thigh. The lower
abdominal wall, buttocks, and upper arms may also be used.
Patients who want to wear sleeveless clothes should normally
avoid using the arms in case unsightly marks or fat hypertrophy
should appear; some may then prefer to confine injections to
the lower abdomen.
It is important to vary the injection sites from day to day,
using for example, each thigh alternately over as wide an area as possible. 

Absorption of insulin varies from one site to
another, being most rapid from the abdominal site, and less
rapid from the arms and least from the legs. 

If there are any difficulties with “control” it is advisable to use one area
consistently—for example, the thigh.
In diabetic emergencies soluble insulin is given
intravenously, or occasionally intramuscularly

When A Type1 Diabetes Should Use Insulin?

Indications for insulin in Type 2 diabetes
Approximately 6% of non-obese and 2% of obese Type 2
diabetic patients need to start insulin each year. 

Predicting the
need for insulin is difficult: those of lean body mass, especially
in the presence of islet cell antibodies, are at greatest risk.

Whether to give insulin to Type 2 diabetic patients is one of
the most important yet difficult decisions to be made in treating
these patients. Failure to give insulin to some patients results in
protracted and needless malaise if not actual danger.

On the other hand, giving insulin inappropriately can cause needless
problems, notably from hypoglycaemia and weight gain.

ndications for giving insulin to Type 2 diabetic patients
who are inadequately controlled despite adherence to their
recommended diet and oral hypoglycaemic agents are as

• Continuing weight loss (even if this is insidious), and
persistent symptoms, or both. Insulin treatment in these
patients almost always results in a substantial improvement in

• A non-obese patient without symptoms whose weight is stable
and who is conscientious with existing medication. Diabetic
control will usually improve, and about half of the patients
will enjoy an improvement in well-being.

• An obese patient without symptoms whose weight is stable
presents an even more difficult problem. 

The correct management is to ensure that they are taking their
medication, together with intensification of diet, but
sometimes insulin may be needed simply to improve control
of diabetes in order to reduce long-term complications
during the following decade or more. 

A reduction of HbA1C of approximately 2% together with weight gain of around
5-7 kg can be expected.

Unfortunately improvement in glycaemic control is not always achieved

Patient choice is important here, and some prefer not to take insulin after all
explanations have been presented. Reluctant patients can be

Types Of Diabetes

Types of diabetes:-

1-Type 1 diabetes (previously insulin dependent diabetes) is:

due to B-cell destruction, usually leading to absolute insulin
deficiency). It can be immune mediated or idiopathic.

2-Type 2 diabetes (previously non-insulin dependent

 ranges from those with predominant insulin
resistance associated with relative insulin deficiency, to those
with a predominantly insulin secretory defect with insulin

Type 1 and Type 2 diabetes are the commonest forms of
primary diabetes mellitus. The division is important both
clinically in assessing the need for treatment, and also in
understanding the causes of diabetes which are entirely
different in the two groups.
Type 1 diabetes
Type 1 diabetes is due to destruction of B-cells in the
pancreatic islets of Langerhans with resulting loss of insulin

A combination of environmental and genetic
factors that trigger an autoimmune attack on the B-cells is
responsible, occurring in genetically susceptible individuals.
Thus, among monozygotic identical twins only about one-third
of the pairs are concordant for diabetes in contrast to the
situation in Type 2 diabetes where almost all pairs are

The process of islet destruction probably begins
very early in life and is known to start several years before the
clinical onset of diabetes.

HLA status

The major histocompatibility complex antigens are adjuncts
to several types of immunological activity. Ninety percent of
Type 1 diabetic patients show either DR3 or DR4, or both
together, while DR2 is protective against diabetes.
Autoantibodies and cellular immunity
Islet cell antibodies are present at diagnosis in most Type 1
diabetic patients and gradually decline and disappear during
the following years. 

Antibodies to specific proteins have more
recently been identified: these include antibodies to glutamic
acid decarboxylase (GAD, a 64-kDa antigen); and even closer
association is found in the presence of antibodies to tyrosine
phosphatase (37 kDa, IA-2). 

The presence in a non-diabetic
individual of three or more antibodies (islet cell antibodies,
anti-GAD antibodies, anti-IA-2 antibodies, anti-insulin
autoantibodies) indicates an 88% chance of developing
diabetes within 10 years.
The presence of insulinitis at the onset of Type 1 diabetes
represents the role of inflammatory cells (for example, cytotoxic
T cells and macrophages) in B-cell destruction.

also produce cytokines leading to activation of lymphocytes
known to be present at the onset of Type 1 diabetes.
Attempts have been made to prevent the onset of Type 1
diabetes. Immune suppression can to some extent preserve islet
function, but permanent remissions are not normally achieved
and the treatment is in any case too dangerous for routine use

The use of nicotinamide to prevent diabetes by altering
macrophage function has not proved to be of benefit. Giving
insulin itself may conserve islet function; the results of trials
are awaited.
Associated autoimmune disorders
The incidence of coeliac disease, Addison’s disease,
hypothyroidism, and pernicious anaemia are increased in
Type 1 diabetic patients, and appear to occur especially in
those with persisting islet cell antibodies.
Risks of inheriting diabetes
A child of a mother with Type 1 diabetes has an increased risk
of developing the same type of diabetes, amounting to
1-2% by 25 years; the risk is about three times greater if the
father has this disease. If both parents have the disease the risk
is further increased and genetic counselling should be sought
by these rare couples.

Type 2 diabetes
There are numerous causes of Type 2 diabetes, which is now
known to include a wide range of disorders with differing
progression and outlook. 

The underlying mechanism is due
either to diminished insulin secretion—that is, an islet defect,
associated with increased peripheral resistance to the action of
insulin resulting in decreased peripheral glucose uptake, or
increased hepatic glucose output. Probably as many as 98% of
Type 2 diabetic patients are “idiopathic”—that is, no specific
causative defect has been identified. 

Whether decreasing insulin
secretion or increasing insulin resistance occurs first is still
uncertain, but the sequence of events may vary in different
Obesity is the commonest cause of insulin
resistance. Other rare insulin resistant states are shown in
the table.
Some adults (especially those not overweight) over 25 years
of age who appear to present with Type 2 diabetes may have
latent autoimmune diabetes of adulthood (LADA) and become
insulin dependent. Autoantibodies are often present in this
group of patients.
Type 2 diabetes is a slowly progressive disease: insulin
secretion declines over several decades, resulting in an
insidious deterioration of glycaemic control which becomes
increasingly difficult to achieve.

The Full List Of Diabetes Treatments

The Full Treatment List for Diabetes

At this time, there is no cure for diabetes, but with careful, medically monitored management, diabetes can be successfully managed, minimizing complications and allowing people with diabetes to live a normal active life. 

Treatment of all types of diabetes includes regular monitoring of blood sugar levels, following a well-balanced healthy diet and regular aerobic exercise program recommended by your health care provider. It is also important not to smoke and to follow your health care provider's advice on preventing, monitoring, and treating any coexisting medical conditions, such as hypertension and high cholesterol.

Type 1 diabetes is always managed with injected insulin
A new treatment that may be an option for some people with type 1 diabetes is pancreatic islet transplantation
This experimental surgery transplants insulin-producing beta cells from a donor into the pancreas of a person with type 1 diabetes.

Type 2 diabetes is often managed with oral antidiabetic drugs, such as glipizide, glyburide, and metformin.
Pregnant women with gestational diabetes may be treated with glyburide, and some people with type 2 diabetes or gestational diabetes may need insulin injections.
The list of treatments mentioned in various sources for Diabetes includes the following list. 
Always seek professional medical advice about any treatment or change in treatment plans.

* Diet changes
* Weight loss
* Exercise - with care and under medical advice; take extra care if using diabetes pills or insulin.
* Diabetes control - ongoing monitoring and control of diabetic blood sugar levels:
          o Diabetic blood sugar control
          o Self monitored blood glucose testing
          o Finger-prick blood glucose tests
          o Urine glucose testing
          o Urine ketone testing
* Diabetes treatment strategies
o Diet changes - usually part of any diabetes treatment plan
o Lifestyle changes only - i.e. the use of diet, exercise and weight loss only without medications.
o Diabetic blood sugar control - this is an important aspect of all diabetes treatment plans
o Diabetes pills
o Insulin
o Diabetes pills and insulin combined
o Brief insulin use then diabetes pills only - a "hit early" research strategy to normalize blood sugars quickly with insulin and then stop insulin after a few weeks; mainly for Type 2 diabetes
o Diabetes pills during honeymoon phase then insulin later - for early-stage treatment strategy for newly diagnosed Type 1 diabetes
o Regular checkups for diabetes complications
o Treatment of any diabetes complications
  o Checkups for associated conditions of diabetes
  * Diabetes pills - i.e. diabetes medications; mostly for Type 2 diabetes rather than Type 1 diabetes
     o Sulphonylureas
     o Metformin
* Combined diabetes pills and insulin
          o Bedtime insulin daytime sulphonylureas (BIDS) - a combination of insulin and diabetes pills
  * Insulin - and there are various types of insulin:
          1-Very rapid acting insulin
          2- Short-acting insulin
          3- Long-acting insulin
          4- Animal insulin
          5- Insulin combinations
1- Very rapid acting insulins - usually acting within less than 30 minutes and not lasting long
          o Insulin lispro
          o Humalog
2- Short-acting insulins - usually acting within 30 minutes and lasting a few hours only
          o Regular insulin
          o Humulin R
          o Novolin R
          o Rapidact insulin
  3- Long-acting insulins - usually acting for 12 to 24 hours
          o NPH insulins
          o Lente insulins
          o Ultra-lente insulins
4- Animal insulin - rarely used in modern days
          o Beef insulin
          o Pork insulin
5- Insulin combinations
          o Combined insulin R and insulin NPH
6- Insulin delivery devices
          o Insulin syringes
          o Insulin pens
          o Insulin automatic injectors
          o Insulin pumps
          o Insulin jet injectors
* Diabetes complication prevention treatments - there are numerous products claimed, often dubiously, to prevent diabetes complications; some such possibilities are:
o Vitamin E - some studies have shown some small benefits.
o Vitamin C - some studies have shown some small benefits.
o Antioxidants - because Vitamin C and Vitamin E are antioxidants.
o Low-dose aspirin - the preventive benefits against heart disease may be worthwhile in preventing diabetic heart disease
 o Chromium - in our opinion probably of dubious benefit.
* Potassium - possibly used for treatment of potassium deficiency
* Vitamin A - to prevent vitamin A deficiency
* Zinc - possibly used for treatment of related zinc deficiency
* ACE inhibitors - good evidence that they provide renovascular protection in both hypertensive and non-hypertensive diabetic patients
* Statins - recommended in patients with and LDL> 3.4 for prevention of cardiovascular disease
* Diabetes pills - i.e. diabetes medications; mostly for Type 2 diabetes rather than Type 1 diabetes
o Sulphonylureas
          o Metformin
          o Acarbose
          o Repaglinide
          o Thiazoldediones