Diabetes Mellitus

1. Diabetes Mellitus
Tanseer Ahmed
R.N, Dipcard, Post RN, MSN.
Senior Lecturer
Liaquat National College of
Nursing

2.  Review the anatomy & Physiology of pancreas.
 Define Diabetes Mellitus
 Define classification of Diabetes.
 Briefly explain Type 1 diabetes, its pathophysiology, causes and sign
and symptoms.
 Briefly explain Type 2 diabetes, its pathophysiology, causes and sign
and symptoms.
 Explain diagnostic test to detect Diabetes.
 Describe treatment of Diabetes.
 List down complications of Diabetes.
 Describe collaborative care of Diabetes.
 Insulin (Structure , Function & Types)
Objectives

3. Pancreatic Anatomy
 Gland with both exocrine and endocrine functions
 15-25 cm long
 60-100 g
 Location: retro-peritoneum, 2nd lumbar vertebral level
 Extends in an oblique, transverse position
 Parts of pancreas: head, neck, body and tail

4. Pancreatic Hormones, Insulin and Glucagon, Regulate
Metabolism

5. Production of Pancreatic Hormones by Three Cell Types
 Alpha cells produce glucagon.
 Beta cells produce insulin.
 Delta cells produce somatostatin.

6. Islet of Langerhans Cross-section
 Three cell types are present, A
(glucagon secretion), B (Insulin
secretion) and D (Somatostatin
secretion)
 A and D cells are located around the
perimeter while B cells are located in
the interior
 Venous return containing insulin flows
by the A cells on its way out of the
islets

7. Definition:-
 Diabetes mellitus is a group of metabolic disease characterized by
elevated levels of glucose in the blood(hyperglycemia)resulting
from defects in insulin secretion ,insulin action or both.
 Diabetes mellitus is a chronic ,lifelong condition that affects your
body’s ability to use the energy found in the food.

8. Classification of Diabetes Mellitus
 Type 1 diabetes mellitus
 Type 2 diabetes mellitus

9. Type 1 Diabetes Mellitus
 Type 1 diabetes also called insulin-
dependent diabetes.
 This type of diabetes is characterized by loss
of insulin-producing beta cells in islets of the
Langerhans in the pancreas.
 It used to be called juvenile-onset diabetes,
because it often begins in childhood.
 It may be caused by a genetic predisposition.
 It could also be the result of faulty beta cells
in the pancreas that normally produce
insulin.

10. Pathophysiology
 Type 1 diabetes occurs as a result of the body's immune system
attacking the insulin producing beta cells of the pancreas,
although it is not clear why this happens. A lack of insulin in
the blood means inadequate amounts of glucose are taken up
by cells of the body to provide energy for cellular functions.
Consequently, glucose remains in the blood leading to a high
blood sugar level.

11. What is insulin and how does it work?
 Insulin is the principal hormone that regulates uptake of glucose
from the blood into most cells (primarily muscle and fat cells, but
not central nervous system cells).
 Therefore deficiency of insulin or the insensitivity of its receptors
plays a central role in all forms of diabetes mellitus.
 Most of the carbohydrates in food are converted within a few hours
to the monosaccharide glucose, the principal carbohydrate found in
blood and used by the body as fuel.
 Insulin is released into the blood by beta cells (β-cells), found in the
Islets of Langerhans in the pancreas, in response to rising levels of
blood glucose, typically after eating.

12. Cont.….
 Insulin is used by about two-thirds of the body's cells to absorb
glucose from the blood for use as fuel, for conversion to other needed
molecules, or for storage.
 Insulin is also the principal control signal for conversion of glucose to
glycogen for internal storage in liver and muscle cells.
 Lowered glucose levels result both in the reduced release of insulin
from the beta cells.
 If the amount of insulin available is insufficient, if cells respond
poorly to the effects of insulin (insulin insensitivity or resistance),
there can be persistent high levels of blood glucose, poor protein
synthesis, and other metabolic derangements, such as acidosis.

13. Causes
 Viral infection - Some research has suggested that the immune
system is activated in response to viral infection. As the immune cells
are activated against the virus particles, they are also activated against
the beta cells of the pancreas. Viruses that have been implicated in the
causation of type 1 diabetes include rubella viruses.
 Genetic tendency - Type 1 diabetes seems to run in families which
suggests a genetic basis to the pathology of the condition. Some HLA
(Human Leukocyte antigen) genotypes are known to raise the risk of
developing type 1 diabetes.
 Lack of vitamin D:-There is thought that lack of vitamin D in the
first year of a child's life may raise the risk of type 1 diabetes
developing.

14. Cont.…..
 Development of antibodies - Some researchers have suggested that
the development of antibodies against proteins in cow's milk may
also lead to the development of antibodies that attack the beta cells of
the pancreas. The presence of antibodies against pancreatic beta cells
is seen in a subtype of type 1 diabetes mellitus.
 Certain drugs and chemicals may also play a role in
the development of type 1 diabetes by destroying the pancreatic beta
cells. These include chemicals such as pyrinuron (Vacor, N-3-
pyridylmethyl-N'-p-nitrophenyl urea) which is used as a rat poison
and is no longer used in the USA. An anticancer and antibiotic agent
called streptozotocin used to treat pancreatic cancer also destroys the
pancreatic beta cells.

15. Sign and symptoms of DM 1
 Kussmaul breathing
 Abdominal pain
 Nausea vomiting
 Polydipsia
 Polyuria
 Polyphagia

16. Type 2 Diabetes Mellitus
 By far the most common form of diabetes is type 2 diabetes,
accounting for 95% of diabetes cases in adults.
 It used to be called as adult onset diabetes or non-insulin
dependent diabetes.

17. Pathophysiology:-
 DM 2 is due to insulin resistance or reduce insulin sensitivity,
combined with relatively reduced insulin secretion, which in cases
become absolute. The defective responsiveness of body to insulin
almost certainly involves in the insulin receptor in cell membrane.
 The pancreas usually produce some insulin.
 Type 2 diabetes is caused by either inadequate production of the
hormone insulin or a lack of response to insulin by various cells of
the body.

18.  Insulin resistance refers to when cells of the body such as the
muscle, liver and fat cells fail to respond to insulin, even when
levels are high. In fat cells, triglycerides are instead broken down to
produce free fatty acids for energy; muscle cells are deprived of an
energy source and liver cells fail to build up glycogen stores.
 This also leads to an overall rise in the level of glucose in the blood.
Glycogen stores become markedly reduced and there is less glucose
available for release when it may be needed. Obesity and lack of
physical activity are thought to be major causes of insulin resistance.

19. Normal regulation of blood sugar
 Glucose is an important source of energy in the body. It is mainly
obtained from carbohydrates in the diet which are broken down into
glucose for the various cells of the body to utilize. The liver is also
able to manufacture glucose from its glycogen stores.
 In a healthy person, a rise in blood sugar after a meal triggers the
pancreatic beta cells to release the hormone insulin. Insulin, in turn,
stimulates cells to take up the glucose from the blood. When blood
glucose levels fall, during exercise for example, insulin levels also
decline.

20.  As well as insulin stimulating the uptake of glucose from the
blood by body cells, it also induces the:
 Conversion of glucose to pyruvate (glycolysis) to release free
energy.
 Conversion of excess glucose to glycogen for storage in the liver
(glycogenesis).
 Uptake and synthesis of amino acids, proteins, and fat

21. Causes
 Weight
 Fat distribution
 Sedentary life styles
 Race
 Family history
 Age(more than 45)
 Pre diabetes
 Polycystic ovary syndrome
 Body mass index higher than 25
 Removal of pancreas

22. Sign and symptoms
Initial symptoms:-
 Polyuria
 Polydipsia
 Polyphagia
 Unintended weight loss
 Irritability and other mood changes
 Fatigue and weakness

23.  Blurred vision
 Vaginal yeast infection in female/Balanitis(inflammation of penis)
 Tingling or numbness in hands or feet
 Fatigue
 Nausea vomiting

24. Later sign symptoms
 Perspiration
 Irritability
 Wound not heal easily
 Trembling
 Confusion

25. Differences between type-1 and type-2 Diabetes
Mellitus
 Type 1
 Young age
 Normal BMI, not obese
 No immediate family history
 Short duration of symptoms (weeks)
 Can present with diabetic coma
(diabetic ketoacidosis)
 Insulin required
 Type 2
 Middle aged, elderly
 Usually overweight/obese
 Family history usual
 Symptoms may be present for
months/years
 Do not present with diabetic coma
 Insulin not necessarily required
 Previous diabetes in pregnancy

26. Diagnosis.
 The diagnosis of type 1 diabetes and many cases of type 2, is
usually prompted by recent-onset symptoms of excessive
urination (polyuria) and excessive thirst (polydipsia), and often
accompanied by weight loss.
 The diagnosis of other types of diabetes is usually made in other
ways. These include ordinary health screening; detection of
hyperglycemia during other medical investigations;
 Diabetes mellitus is characterized by recurrent or persistent
hyperglycemia, and is diagnosed by demonstrating any one of the
following

27. Diagnostic test
 Glycated hemoglobin (A1C) test :-An A1C level of 6.5 percent or
higher on two separate tests indicates that you have diabetes. An A1C
between 5.7 and 6.4 percent indicates prediabetes. Below 5.7 is
considered normal.
 Random blood sugar test:-a random blood sugar level of 200
milligrams per deciliter (mg/dL) ,11.1 millimoles per liter (mmol/L) or
higher suggests diabetes.
 Fasting blood sugar test:-A fasting blood sugar level from 100 to 125
mg/dL (5.6 to 6.9 mmol/L) is considered prediabetes. If it's 126 mg/dL (7
mmol/L) or higher on two separate tests, you have diabetes.
 Oral glucose tolerance test:-A blood sugar level less than 140 mg/dL
(7.8 mmol/L) is normal. A reading of more than 200 mg/dL (11.1
mmol/L) after two hours indicates diabetes. A reading between 140 and
199 mg/dL (7.8 mmol/L and 11.0 mmol/L) indicates prediabetes.

29. Complications
 Heart and blood vessel disease
 Nerve damage(neuropathy)
 Kidney damage(nephropathy)
 Eye damage(Retinopathy)
 Diabetic foot
 Hearing impairment
 Itching
 Hypoglycemia
 Ketoacidosis

30. Acute complications
Diabetic ketoacidosis
Hyperglycemia hyperosmolar state
Hypoglycemia

31. Chronic complications
 Chronic complications-------------Vascular Disease
Vascular Disease
 Microvascular And Macrovascular
 Diabetic Neuropathy
 Diabetic Nephropathy
 Diabetic Retinopathy
 Diabetic Cardiomyopathy
 Diabetic Angiopathy

32. Diabetes Mellitus
 Goals of diabetes management:
Reduce symptoms
Promote well-being
Prevent acute complications
Delay onset and progression of long-term complications
ay onset and progression of long-term complications

33. Diabetes Mellitus
Collaborative Care
 Patient teaching
 Nutritional therapy
 Drug therapy
 Exercise
 Self-monitoring of blood glucose

34. Nutritional Therapy
 Within the context of an overall healthy eating
plan, a person with diabetes can eat the same
foods as a person without diabetes
 Overall goal of nutritional therapy
Assist people to make changes in nutrition
and exercise habits that will lead to
improved metabolic control
 Food composition
Meal plan developed with dietitian
Nutritionally balanced
Does not prohibit the consumption of any
one type of food.

35. Exercise
Essential part of diabetes management
Increases insulin sensitivity
Lowers blood glucose levels
Decreases insulin resistance
Take small carbohydrate snacks Q 30 min during exercise to
prevent hypoglycemia
Exercise after meals
Exercise plans should be individualized
Monitor blood glucose levels before, during, and after exercise

36. Monitoring Blood Glucose
 Self-monitoring of blood glucose (SMBG)
Allows self-management decisions regarding diet, exercise, and
medication
Important for detecting episodic hyperglycemia and
hypoglycemia
Patient education is crucial

37. Structure of Insulin
 Insulin is a polypeptide hormone, composed of two chains (A and B)
 BOTH chains are derived from proinsulin, a prohormone.
 The two chains are joined by disulfide bonds.

38. Roles of Insulin
 Acts on tissues (especially liver, skeletal muscle, adipose) to increase
uptake of glucose and amino acids.
- without insulin, most tissues do not take in glucose and amino
acids well (except brain).
 Increases glycogen production (glucose storage) in the liver and
muscle.
 Stimulates lipid synthesis from free fatty acids and triglycerides in
adipose tissue.
 Also stimulates potassium uptake by cells (role in potassium
homeostasis).

39. The commonly used types of insulin are:
 1. Rapid-acting types are presently insulin analogues, such as the insulin
analogues aspart or lispro. these begin to work within 5 to 15 minutes and
are active for 3 to 4 hours

40.  2. Short-acting, such as regular insulin – starts working within 30 minutes
and is active about 5 to 8 hours
 A mixture of NPH and regular insulin – starts working in 30 minutes and
is active 16 to 24 hours. There are several variations with different
proportions of the mixed insulins

41.  3. Intermediate-acting, such as NPH (Neutral Protamine Hagedorn) –
starts working in 1 to 3 hours and is active 16 to 24 hours
 Insulin glargine and Insulin detemir – both insulin analogues which start
working within 1 to 2 hours and continue to be active, without major
peaks or dips, for about 24 hours, although this varies in many individuals.

42. Long Acting
 4. Long-acting, such as ultralente insulin – starts working in 4 to 6 hours,
and is active well beyond 32 hours

43. References:-
 http://www.mayoclinic.org/diseases-conditions/diabetes/basics/tests-
diagnosis/con
 http://www.news-medical.net/health/Diabetes-Mellitus-Type-1-
Pathophysiology.aspx
 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3486979/