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DSE 1, Endocrinology, SEM 5
Vijaygarh Jyotish Ray College
Presented By
Pranab Karmakar
Nilanjana Mondal
Tousif Khan
2 February 2021
PANCREATIC DISEASES
 Location
The pancreas is located behind the stomach in the upper left abdomen. It lies in close proximity to the
Duodenum.
 Morphology
i. It is an elongated organ, light tan or yellowish colour.
ii. It is lobulated, compound , acinar gland, with a very thin
capsule and septa.
iii. Long duct system.
iv. Exocrine part is major with very many serous acini and some
ducts.
v. Endocrine part is minor. Many clusters of cells – islets of
Langerhans.
vi. Islets of Langerhans contains different cells like Alpha cell, Beta
cell, Delta cell, F cell.
 Hormones
The endocrine part of the pancreas secretes different hormones like Insulin, Glucagon, Somatostatin and
Pancreatic polypeptide.
2
PANCREASE
3
 SECRETION
Insulin is released by the Beta cells in the islets of Langerhans of Pancreas.
 ABOUT
I. Human insulin is composed of 51 amino acids, and has a molecular
mass of 5808 Da. The molecular formula of human insulin is
C257H383N65O77S6. It is a combination of two peptide chains (dimer)
named an A-chain and a B-chain, which are linked together by
two disulfide bonds. The A-chain is composed of 21 amino acids, while
the B-chain consists of 30 residues.
II. Insulin is encoded by the INS gene, which is located on Chromosome
11p15.5.
III. The main function of Insulin in human is to decrease blood glucose level.
 DISEASES
Due to the abnormal quantity of insulin production in human causes several
diseases. Like
• Hypo secretion – Diabetes mellitus (Type I)
• Hyper secretion - Hyperinsulinemia
Human insulin chain A (grey)
and chain B (green)
INSULIN
DIABETES MELLITUS (Type I)
Hyposecretion
 HISTORY
Diabetes has been affecting lives for thousands of years. Ancient Indians (400–500 A.D.)
were well aware of the condition, and had even identified two types of the condition.
They tested for diabetes — which they called “honey urine” — by determining if ants were
attracted to a person’s urine. “Diabetes” is a Greek word means “to go through”. In
1926, Edward Albert Sharpey-Schafer announced that the pancreas of a patient with
diabetes was unable to produce what he termed “insulin,” a chemical the body uses to
break down sugar.
Edward Albert Sharpey-Schafer
 ETIOLOGY
In type 1 diabetes mellitus (previously called juvenile-onset or insulin-dependent), insulin production is absent
because of autoimmune pancreatic beta-cell destruction possibly triggered by an environmental exposure in
genetically susceptible people. Destruction progresses sub-clinically over months or years until beta-cell mass
decreases to the point that insulin concentrations are no longer adequate to control plasma glucose levels. The
pathogenesis of the autoimmune beta-cell destruction involves incompletely understood interactions between
auto-antigens, and environmental factors.
Although type 1 diabetes can appear at any age, it appears at two noticeable peaks. The first
peak occurs in children between 4 and 7 years old, and the second is in children between 10 and 14 years old.
 It is thought that Auto-antigens proteins (glutamic acid decarboxylase, insulin, proinsulin etc) are exposed or
released during normal beta-cell turnover or beta-cell injury, activating primarily a T cell‒mediated immune
response resulting in beta-cell destruction.
5
 Several viruses (including coxsackievirus, rubella virus, and retroviruses) may directly infect and destroy beta
cells, or they may cause beta-cell destruction indirectly by stimulating an immune response or other
mechanism.
 Diet may also be a factor. Exposure of infants to dairy products (especially cow’s milk and the milk protein
beta casein), high nitrates in drinking water, and low vitamin D consumption have been linked to increased risk
of type 1 diabetes. Early (< 4 months) or late (> 7 months) exposure to gluten and cereals increases islet cell
autoantibody production.
6
SYMPTOMS
Diabetes initially might not cause any symptoms. It can sometimes be caught early with a routine blood test
before a person develops symptoms. When diabetes does cause symptoms, they may include:
 excessive urination containing glucose called Glycosuria.
 excessive thirst, leading to drinking a lot of fluid
 weight loss.
 People with diabetes also have an increased susceptibility to infections.
 If the blood sugar level gets too high then several complications occur, such as confused thinking, weakness,
nausea, vomiting, and even seizures and coma. This situation is called hyperosmolar syndrome.
EFFECTS
7
 Retinopathy
Tiny blood vessels in the retina can become damaged by high blood
sugar. The damage can block blood flow to the retina, or can lead to
bleeding into the retina. Both reduce the retina's ability to see light.
 Neuropathy
This is another term for nerve damage. The most common type is
peripheral neuropathy, which affects nerves in the feet and hands. The
nerves to the legs are damaged first, causing pain and numbness in the
feet. This can advance to cause symptoms in the legs and hands.
Damage to the nerves that control digestion, sexual function, and
urination can also occur.
 Nephropathy
This refers to damage to the kidneys. This complication is more likely if
blood sugars remain elevated and high blood pressure is not treated
aggressively.
 Atherosclerosis
Atherosclerosis is fat buildup in the artery walls. This can impair blood
flow to all parts of the body.
8
DIAGNOSIS
 Fasting plasma glucose (FPG) test
A blood sample is taken in the morning after patient fast overnight. A normal fasting blood sugar level is
between 70 and 100 mg/dL. Diabetes is diagnosed if the fasting blood sugar level is 126 mg/dL or higher.
 Oral glucose tolerance test (OGTT)
Blood sugar is measured two hours after drink a liquid containing 75 grams of glucose. Diabetes is
diagnosed if the blood sugar level is 200 mg/dL or higher.
 Random blood glucose test
A blood sugar of 200 mg/dL or greater at any time of day, combined with symptoms of diabetes, is
sufficient to make the diagnosis.
 Hemoglobin A1c (glycohemoglobin)
This test measures your average blood glucose level over the prior two to three months. Diabetes is
diagnosed if the hemoglobin A1c level is 6.5% or higher.
9
TREATMENT
 Anyone who has type 1 diabetes needs lifelong insulin therapy.
Types of insulin are many and include:
Short-acting (regular) insulin - Humulin R and Novolin R
Rapid-acting insulin - insulin glulisine (Apidra), insulin lispro (Humalog)
Intermediate-acting (NPH) insulin - insulin glargine (Lantus, Toujeo Solostar)
Long-acting insulin - insulin NPH (Novolin N, Humulin N)
 Artificial - In September 2016, the Food and Drug Administration
approved the first artificial pancreas for people with type 1 diabetes
who are age 14 and older. The implanted device links a continuous
glucose monitor, which checks blood sugar levels every five minutes,
to an insulin pump. The device automatically delivers the correct
amount of insulin when the monitor indicates it's needed.
 Physical Exercise - Aim for at least 150 minutes of aerobic exercise a week, with no more than two days
without any exercise. The goal for children is at least an hour of activity a day.
 Healthy diet - it's important to center your diet on nutritious, low-fat, high-fiber foods such as Fruits,
Vegetables, Whole grains.
10
PREVENTION
There are no preventive method right now.
HYPERINSULINEMIA
Hypersecretion
 HISTORY
In the beginning of 1954 McQuarrie saw that in the family seventh young child suffered
irreparable brain damage from severe hypoglycemia. Another four were examples of
severe spontaneous hypoglycemia in infants who were victims of delayed diagnosis and
inadequate early therapy. Then he said that it would be due to the mutation of
Hexokinase 1 gene. Then in 1960 Berson & Yalow J. Clin. Invest. discovered
Hyperinsulinemia in Leucine Sensitive Idiopathic Hypoglycemia of Infancy.
McQuarrie
12
Berson & Yalow J. Clin. Invest
Hyperinsulinemia is a condition where the blood insulin level is higher than what is considered normal in
people without diabetes. Although hyperinsulinemia is not diabetes, the condition is often associated with
type 2 diabetes. People with hyperinsulinemia have difficulty maintaining a normal blood sugar level, which
means the pancreas has to produce increasing amounts of insulin in order to control it. There are several
causes for this condition.
 Diabetes mellitus (type II) - The typical cause of hyperinsulinemia is insulin resistance. Insulin resistance is
what happens whe body doesn’t respond correctly to insulin. This incorrect response causes body to need
the pancreas to produce more insulin.
 Less common causes of this condition are insulinoma. Insulinoma is a rare tumor of the pancreas cells
that produce insulin.
 Nesidioblastosis is when the pancreas produces too many cells that make insulin.
 Hyperinsulinemia may also develop after having gastric bypass surgery. The theory is that the cells have
become too large and active for the body, but the body has changed significantly after the bypass.
 People may be more susceptible to developing hyperinsulinemia from insulin resistance due to a family
history or genetic predisposition.
 ETIOLOGY
13
SYMPTOMS
Hyperinsulinemia may not have any noticeable symptoms. However, some possible symptoms
may include:
sugar cravings
unusual weight gain
frequent hunger
excessive hunger
issues with concentration
anxiety or feelings of panic
lack of focus or ambition
extreme tiredness
hypoglycemia, or low blood sugar
Symptoms in infants and young children may include:
difficulty feeding
extreme irritability
lethargy or no energy
14
EFFECTS
Hyperinsulinemia can cause low blood sugar. Low blood sugar can cause several serious
complications. These complications may include:
seizures
coma
cognitive function issues (especially in young children)
Higher triglyceride levels
High uric acid
Hardening of the arteries (artherosclerosis)
Weight gain
Hypertension
Type 2 diabetes
15
DIAGNOSIS
16
Diagnosis can be made by checking fasting and post parandial insulin levels either with
normal meal or with 100 g of oral glucose.
TREATMENT
 Medication - medication may be prescribed to maintain a normal blood sugar level.
Some of the drugs that may be prescribed are described below.
Insulin secretion inhibiting agents - diazoxide (Rx), octreotide (Rx), nifedipine (Rx)
Dextrose and glucose release stimulators - dextrose (Rx), glucagon
Drugs that inhibit the insulin effect - somatropin (Rx), Hydrocortisone (Hydrocortone, Cortef)
 Exercise - Aerobic and resistance training are beneficial exercises for hyperinsulinemia. However, a
person should discuss their exercise plans with their doctor.
 Diet - Diets that focus on glycemic control are beneficial when treating hyperinsulinemia. A diet low in
simple carbohydrates can help people regulate glucose levels.
17
REFERENCES
1. en.wikipedia.org/wiki/Type_2_diabetes
2. www.health.harvard.edu/a_to_z/type-2-diabetes-mellitus-a-to-z
3. emedicine.medscape.com/article/921258-medication
4. www.diabetes.co.uk/hyperinsulinemia.html
5. en.wikipedia.org/wiki/Hyperinsulinemia
6. www.healthline.com/health/hyperinsulinemia
7. www.ncbi.nlm.nih.gov/pmc/articles/PMC6735759/
8. www.google.co.in/imghp?hl=en&tab=ri&ogbl
9. www.ncbi.nlm.nih.gov/books/NBK513253/
18
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Pancreatic diseases

  • 1. DSE 1, Endocrinology, SEM 5 Vijaygarh Jyotish Ray College Presented By Pranab Karmakar Nilanjana Mondal Tousif Khan 2 February 2021 PANCREATIC DISEASES
  • 2.  Location The pancreas is located behind the stomach in the upper left abdomen. It lies in close proximity to the Duodenum.  Morphology i. It is an elongated organ, light tan or yellowish colour. ii. It is lobulated, compound , acinar gland, with a very thin capsule and septa. iii. Long duct system. iv. Exocrine part is major with very many serous acini and some ducts. v. Endocrine part is minor. Many clusters of cells – islets of Langerhans. vi. Islets of Langerhans contains different cells like Alpha cell, Beta cell, Delta cell, F cell.  Hormones The endocrine part of the pancreas secretes different hormones like Insulin, Glucagon, Somatostatin and Pancreatic polypeptide. 2 PANCREASE
  • 3. 3  SECRETION Insulin is released by the Beta cells in the islets of Langerhans of Pancreas.  ABOUT I. Human insulin is composed of 51 amino acids, and has a molecular mass of 5808 Da. The molecular formula of human insulin is C257H383N65O77S6. It is a combination of two peptide chains (dimer) named an A-chain and a B-chain, which are linked together by two disulfide bonds. The A-chain is composed of 21 amino acids, while the B-chain consists of 30 residues. II. Insulin is encoded by the INS gene, which is located on Chromosome 11p15.5. III. The main function of Insulin in human is to decrease blood glucose level.  DISEASES Due to the abnormal quantity of insulin production in human causes several diseases. Like • Hypo secretion – Diabetes mellitus (Type I) • Hyper secretion - Hyperinsulinemia Human insulin chain A (grey) and chain B (green) INSULIN
  • 4. DIABETES MELLITUS (Type I) Hyposecretion
  • 5.  HISTORY Diabetes has been affecting lives for thousands of years. Ancient Indians (400–500 A.D.) were well aware of the condition, and had even identified two types of the condition. They tested for diabetes — which they called “honey urine” — by determining if ants were attracted to a person’s urine. “Diabetes” is a Greek word means “to go through”. In 1926, Edward Albert Sharpey-Schafer announced that the pancreas of a patient with diabetes was unable to produce what he termed “insulin,” a chemical the body uses to break down sugar. Edward Albert Sharpey-Schafer  ETIOLOGY In type 1 diabetes mellitus (previously called juvenile-onset or insulin-dependent), insulin production is absent because of autoimmune pancreatic beta-cell destruction possibly triggered by an environmental exposure in genetically susceptible people. Destruction progresses sub-clinically over months or years until beta-cell mass decreases to the point that insulin concentrations are no longer adequate to control plasma glucose levels. The pathogenesis of the autoimmune beta-cell destruction involves incompletely understood interactions between auto-antigens, and environmental factors. Although type 1 diabetes can appear at any age, it appears at two noticeable peaks. The first peak occurs in children between 4 and 7 years old, and the second is in children between 10 and 14 years old.  It is thought that Auto-antigens proteins (glutamic acid decarboxylase, insulin, proinsulin etc) are exposed or released during normal beta-cell turnover or beta-cell injury, activating primarily a T cell‒mediated immune response resulting in beta-cell destruction. 5
  • 6.  Several viruses (including coxsackievirus, rubella virus, and retroviruses) may directly infect and destroy beta cells, or they may cause beta-cell destruction indirectly by stimulating an immune response or other mechanism.  Diet may also be a factor. Exposure of infants to dairy products (especially cow’s milk and the milk protein beta casein), high nitrates in drinking water, and low vitamin D consumption have been linked to increased risk of type 1 diabetes. Early (< 4 months) or late (> 7 months) exposure to gluten and cereals increases islet cell autoantibody production. 6
  • 7. SYMPTOMS Diabetes initially might not cause any symptoms. It can sometimes be caught early with a routine blood test before a person develops symptoms. When diabetes does cause symptoms, they may include:  excessive urination containing glucose called Glycosuria.  excessive thirst, leading to drinking a lot of fluid  weight loss.  People with diabetes also have an increased susceptibility to infections.  If the blood sugar level gets too high then several complications occur, such as confused thinking, weakness, nausea, vomiting, and even seizures and coma. This situation is called hyperosmolar syndrome. EFFECTS 7  Retinopathy Tiny blood vessels in the retina can become damaged by high blood sugar. The damage can block blood flow to the retina, or can lead to bleeding into the retina. Both reduce the retina's ability to see light.
  • 8.  Neuropathy This is another term for nerve damage. The most common type is peripheral neuropathy, which affects nerves in the feet and hands. The nerves to the legs are damaged first, causing pain and numbness in the feet. This can advance to cause symptoms in the legs and hands. Damage to the nerves that control digestion, sexual function, and urination can also occur.  Nephropathy This refers to damage to the kidneys. This complication is more likely if blood sugars remain elevated and high blood pressure is not treated aggressively.  Atherosclerosis Atherosclerosis is fat buildup in the artery walls. This can impair blood flow to all parts of the body. 8
  • 9. DIAGNOSIS  Fasting plasma glucose (FPG) test A blood sample is taken in the morning after patient fast overnight. A normal fasting blood sugar level is between 70 and 100 mg/dL. Diabetes is diagnosed if the fasting blood sugar level is 126 mg/dL or higher.  Oral glucose tolerance test (OGTT) Blood sugar is measured two hours after drink a liquid containing 75 grams of glucose. Diabetes is diagnosed if the blood sugar level is 200 mg/dL or higher.  Random blood glucose test A blood sugar of 200 mg/dL or greater at any time of day, combined with symptoms of diabetes, is sufficient to make the diagnosis.  Hemoglobin A1c (glycohemoglobin) This test measures your average blood glucose level over the prior two to three months. Diabetes is diagnosed if the hemoglobin A1c level is 6.5% or higher. 9
  • 10. TREATMENT  Anyone who has type 1 diabetes needs lifelong insulin therapy. Types of insulin are many and include: Short-acting (regular) insulin - Humulin R and Novolin R Rapid-acting insulin - insulin glulisine (Apidra), insulin lispro (Humalog) Intermediate-acting (NPH) insulin - insulin glargine (Lantus, Toujeo Solostar) Long-acting insulin - insulin NPH (Novolin N, Humulin N)  Artificial - In September 2016, the Food and Drug Administration approved the first artificial pancreas for people with type 1 diabetes who are age 14 and older. The implanted device links a continuous glucose monitor, which checks blood sugar levels every five minutes, to an insulin pump. The device automatically delivers the correct amount of insulin when the monitor indicates it's needed.  Physical Exercise - Aim for at least 150 minutes of aerobic exercise a week, with no more than two days without any exercise. The goal for children is at least an hour of activity a day.  Healthy diet - it's important to center your diet on nutritious, low-fat, high-fiber foods such as Fruits, Vegetables, Whole grains. 10 PREVENTION There are no preventive method right now.
  • 12.  HISTORY In the beginning of 1954 McQuarrie saw that in the family seventh young child suffered irreparable brain damage from severe hypoglycemia. Another four were examples of severe spontaneous hypoglycemia in infants who were victims of delayed diagnosis and inadequate early therapy. Then he said that it would be due to the mutation of Hexokinase 1 gene. Then in 1960 Berson & Yalow J. Clin. Invest. discovered Hyperinsulinemia in Leucine Sensitive Idiopathic Hypoglycemia of Infancy. McQuarrie 12 Berson & Yalow J. Clin. Invest
  • 13. Hyperinsulinemia is a condition where the blood insulin level is higher than what is considered normal in people without diabetes. Although hyperinsulinemia is not diabetes, the condition is often associated with type 2 diabetes. People with hyperinsulinemia have difficulty maintaining a normal blood sugar level, which means the pancreas has to produce increasing amounts of insulin in order to control it. There are several causes for this condition.  Diabetes mellitus (type II) - The typical cause of hyperinsulinemia is insulin resistance. Insulin resistance is what happens whe body doesn’t respond correctly to insulin. This incorrect response causes body to need the pancreas to produce more insulin.  Less common causes of this condition are insulinoma. Insulinoma is a rare tumor of the pancreas cells that produce insulin.  Nesidioblastosis is when the pancreas produces too many cells that make insulin.  Hyperinsulinemia may also develop after having gastric bypass surgery. The theory is that the cells have become too large and active for the body, but the body has changed significantly after the bypass.  People may be more susceptible to developing hyperinsulinemia from insulin resistance due to a family history or genetic predisposition.  ETIOLOGY 13
  • 14. SYMPTOMS Hyperinsulinemia may not have any noticeable symptoms. However, some possible symptoms may include: sugar cravings unusual weight gain frequent hunger excessive hunger issues with concentration anxiety or feelings of panic lack of focus or ambition extreme tiredness hypoglycemia, or low blood sugar Symptoms in infants and young children may include: difficulty feeding extreme irritability lethargy or no energy 14
  • 15. EFFECTS Hyperinsulinemia can cause low blood sugar. Low blood sugar can cause several serious complications. These complications may include: seizures coma cognitive function issues (especially in young children) Higher triglyceride levels High uric acid Hardening of the arteries (artherosclerosis) Weight gain Hypertension Type 2 diabetes 15
  • 16. DIAGNOSIS 16 Diagnosis can be made by checking fasting and post parandial insulin levels either with normal meal or with 100 g of oral glucose.
  • 17. TREATMENT  Medication - medication may be prescribed to maintain a normal blood sugar level. Some of the drugs that may be prescribed are described below. Insulin secretion inhibiting agents - diazoxide (Rx), octreotide (Rx), nifedipine (Rx) Dextrose and glucose release stimulators - dextrose (Rx), glucagon Drugs that inhibit the insulin effect - somatropin (Rx), Hydrocortisone (Hydrocortone, Cortef)  Exercise - Aerobic and resistance training are beneficial exercises for hyperinsulinemia. However, a person should discuss their exercise plans with their doctor.  Diet - Diets that focus on glycemic control are beneficial when treating hyperinsulinemia. A diet low in simple carbohydrates can help people regulate glucose levels. 17
  • 18. REFERENCES 1. en.wikipedia.org/wiki/Type_2_diabetes 2. www.health.harvard.edu/a_to_z/type-2-diabetes-mellitus-a-to-z 3. emedicine.medscape.com/article/921258-medication 4. www.diabetes.co.uk/hyperinsulinemia.html 5. en.wikipedia.org/wiki/Hyperinsulinemia 6. www.healthline.com/health/hyperinsulinemia 7. www.ncbi.nlm.nih.gov/pmc/articles/PMC6735759/ 8. www.google.co.in/imghp?hl=en&tab=ri&ogbl 9. www.ncbi.nlm.nih.gov/books/NBK513253/ 18
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