This document provides an overview of diabetes mellitus (DM), including: 1) It defines DM as a metabolic disorder characterized by chronic hyperglycemia resulting from defects in insulin secretion or action. 2) It classifies the main types of DM as type 1, type 2, and gestational diabetes and discusses their characteristics. 3) It discusses the etiology, pathophysiology, clinical manifestations, diagnosis, and management of type 1 and type 2 DM.

1. DIABETES MELLITUS
Prepared By
Asghar Khan

2. Objectives
At the end of this presentation the students will be able to
 Review anatomy & physiology of pancreas
 Define different disorders of pancreas
 Discuss epidemiology of diabetes mellitus (DM).
 Briefly discuss the classification of DM.
 Discuss etiology, pathophysiology, and clinical
manifestation of Type 1 & Type 2 DM.
 Identify main differences between type 1& type 2
DM
 Identify pathogenesis and manifestation of the acute
and chronic complications of DM.

3. A & P of Pancreas
 Pale grey gland weighing about 60 grams. It is
about 12 to 15 cm long.
 Situated transversely in the epigastric and left
hypochondriac regions.
 Consists of a broad head, a body and a narrow
tail.
 Head lies in the curve of the duodenum, the
body behind the stomach
 Tail lies in front of the left kidney and just
reaches the spleen.

5. The Exocrine Pancreas
 Consists of a large number of lobules made up of small alveoli,
the walls of which consist of secretory cells.
 Each lobule is drained by a tiny duct and these unite eventually
to form the pancreatic duct, which extends the whole length of
the gland and opens into the duodenum.
 Just before entering the duodenum the pancreatic duct joins the
common bile duct to form the hepatopancreatic ampulla.
 The duodenal opening of the ampulla is controlled by the
hepatopancreatic sphincter (of Oddi).
 The function of the exocrine pancreas is to produce pancreatic
juice containing enzymes that digest carbohydrates, proteins
and fats

6. The Endocrine Pancreas
 Distributed throughout the gland are groups of specialized
cells called the pancreatic islets (of Langerhans).
 The islets have no ducts so the hormones diffuse directly
into the blood.
 The endocrine pancreas consists of about 1-2 million
microscopic units, the islets of Langerhans. That account
1% of the pancreas.
 The four most important cell types are;
 A (alpha)
 B (beta)
 D (delta)
 PP (Pancreatic polypeptide)

8.  B cells constitute 70% of islet cell population and secrete
insulin, that lowers blood glucose level.
 A cells account for 20% and secretes glucagon, that raises
blood glucose level
 D cells make up 5-10% and contain somatostatin, that
suppresses the release of insulin and glucagon.
 PP cells constitute 1-2% and secrete a hormone of
unknown function pancreatic polypeptide

9. Effects of Insulin on Metabolism
Carbohydrate metabolism
 Insulin increases glucose transport into skeletal muscle
and adipose tissue.
  Glycogen synthesis (Insulin increases glycogen
synthesis, i.e. extra glucose in the liver, skeletal muscle
and adipose tissue is converted into glycogen and stored
there).
  Glycogenolysis (Insulin decrease the breakdown of
stored glycogen into glucose)
  Gluconeogenesis (Insulin also decreases the formation
of glucose from other substances such as amino acid,
lactic acid and glycerol)

10. Effects of Insulin on Metabolism
Lipid Metabolism
  Lipogenesis and  lipolysis (Insulin also facilitates
triglyceride synthesis from glucose in fat cells and inhibits
the intracellular breakdown of stored triglycerides)
 Protein Metabolism
  Protein synthesis (Insulin also inhibits protein
breakdown and increases protein synthesis by increasing
the active transport of amino acids into body cells)

11. Effects of Glucagon on Metabolism
Carbohydrate Metabolism
 Stimulation of Glycogenolysis: (Glucagon initiates
glycogenolysis or the breakdown of liver glycogen as
a means of raising blood glucose)
 Inhibition of glycogen synthesis: ( Glucagon inhibits
the formation of glycogen from glucose)
 Stimulation of gluconeogenesis: (Glucagon also
increases the transport of amino acids into the liver
and stimulates their conversion into glucose, a process
called gluconeogenesis)

12. Effects of Glucagon on Metabolism
Lipid Metabolism
 Stimulation of lipolysis (Enhances lipolysis in
adipose tissue, liberating fatty acids and glycerol for
use in gluconeogenesis )
 Stimulation of ketogenesis
 Inhibition of triglyceride synthesis
Protein Metabolism
 Stimulation of proteolysis (Increases breakdown of
proteins into amino acids for use in gluconeogenesis)
 Increases transport of amino acids into hepatic
cells

13. Counter-Regulatory Hormones
 Other hormones that can affect blood glucose
include the catecholamines, growth hormone,
and the glucocorticoids.
 These hormones, along with glucagon, are
sometimes called counter-regulatory
hormones because they counteract the storage
functions of insulin in regulating blood glucose
levels during periods of fasting, exercise, and
other situations.

14. Epinephrine.
 From adrenal medulla helps to maintain blood glucose
levels during periods of stress.
 Has the potent effect of causing glycogenolysis in the
liver, thus increasing glucose level into the blood.
 Inhibits insulin release from the beta cells thus
decreases the movement of glucose into muscle cells.
 Increasing the breakdown of muscle glycogen
stores.

15.  Epinephrine also has a direct lipolytic effect on
adipose cells, thereby increasing the mobilization of
fatty acids for use as an energy source.
 The blood glucose–elevating effect of epinephrine is
also an important homeostatic mechanism during
periods of hypoglycemia.

16. Growth Hormone
 Has many metabolic effects.
 Increases protein synthesis in all cells of the body,
 Mobilizes fatty acids from adipose tissue,
 Antagonizes the effects of insulin.
 The most important physiologic effect of growth hormone
is stimulation of longitudinal growth by increasing the
formation of new bone and cartilage.
 The secretion of growth hormone is normally inhibited by
insulin.

17.  During periods of fasting, when both blood glucose
levels and insulin secretion fall, growth hormone
levels increase.
 Exercise such as running and cycling, and various
stresses, including anesthesia, fever, and trauma,
increase growth hormone levels.
 Chronic hypersecretion of growth hormone, as occurs
in acromegaly, can lead to glucose intolerance and the
development of DM.
 The production of growth hormone is pulsatile and
circulating levels increase during childhood, peak at
uberty, and decrease with aging.

18. Glucocorticoid Hormones
 synthesized in the adrenal cortex along with other
corticosteroid hormones, are critical to survival during
periods of fasting and starvation.
 They stimulate gluconeogenesis by the liver,
producing an increase in hepatic glucose production.
 Glucocorticoids also modulate the immune response,
exerting an overall anti-inflammatory response.
 Synthetic use of glucocorticoids, such as prednisone,
are a common treatment for inflammatory diseases
with a subsequent impact on blood glucose levels.

19. Diabetes Mellitus (DM)
 The term diabetes mellitus describes a metabolic
disorder of multiple etiology, characterized by chronic
hyperglycemia with disturbances of carbohydrate, fat
and protein metabolism resulting from an imbalance
b/w insulin availability and insulin need.
OR
 Diabetes mellitus is a group of metabolic diseases
characterized by elevated levels of glucose in the
blood (hyperglycemia) resulting from defects in
insulin secretion, insulin action, or both (American
Diabetes Association [ADA],

20. Diabetes Mellitus (DM)
 Insulin, a hormone produced by the pancreas, controls
the level of glucose in the blood by regulating the
production and storage of glucose.
 In the diabetic state, the cells may stop responding to
insulin or the pancreas may stop producing insulin
entirely.
 The effects of diabetes mellitus include long-term
damage, dysfunction and failure associated with
microvascular, macrovascular, and metabolic
complications of various organs.

21. Prevalence of DM
 It is top 5 of the most significant diseases in the
developed world.
 In 2012 according to the WHO, at least 271 million
people world wide suffered from DM.
 According to ADA 26.8 million with DM, 6.2 million
people undiagnosed and about 41 million would be
considered pre-diabetic in USA.
 Its incidences are increasing rapidly and it is estimated
that by the year 2030 this number will be doubled.
 The current prevalence of type 2 diabetes mellitus in
 Pakistan is 11.77%.

22. Classification According To Categories
There are several different types of diabetes mellitus.
 Type 1 Diabetes Mellitus - formerly known as
insulin-dependent diabetes mellitus (IDDM),
childhood diabetes, or juvenile-onset diabetes.
 Type 2 Diabetes Mellitus - previously known as
adult-onset diabetes, maturity-onset diabetes, or non-
insulin dependent diabetes mellitus (NIDDM)

23.  Gestational Diabetes. It develops during pregnancy
and may improve or disappear after delivery, involves
a combination of inadequate insulin secretion and
responsiveness, resembling type 2 diabetes in several
respects.
 Other specific types. Formerly known as secondary
diabetes, describes diabetes that is associated with
certain other conditions and syndromes.

24. Stages of Glucose Intolerance
 Prediabetes and diabetes
 The categories of Impaired Glucose Tolerance
(IGT) and Impaired Fasting Plasma Glucose
(IFG) refers to metabolic stages intermediate
b/w normal glucose homeostasis and diabetes,
and are labeled together as prediabetes.
 Prediabetes is associated with increased risk for
atherosclerosis, heart diseases and progress to
type 2 DM.

26. Diagnosis of DM
 In order to determine whether or not a patient has pre-
diabetes or diabetes, health care providers conduct
 A Fasting Plasma Glucose Test (FPG) or an Oral Glucose
Tolerance Test (OGTT) or HbA1C . Either test can be
used to diagnose pre-diabetes or diabetes.

27. HBA1C ≥ 6.5 %

28.  FPG test, A fasting blood glucose level between 110 and
126 mg/dl signals pre-diabetes.
 A person with a fasting blood glucose level of 126 mg/dl
or higher has diabetes.
 In the OGT test, a person's blood glucose level is
measured after a fast and two hours after drinking a
glucose-rich beverage.
 If the two-hour blood glucose level is between 140 and
200mg/dl, the person tested, has pre-diabetes.
 If the two-hour blood glucose level is at 200 mg/dl or
higher, the person, tested has diabetes

29. Glycated Hemoglobin Testing
 Glycated hemoglobin, also referred to as
glycohemoglobin, glycosylated hemoglobin, HbA1c,
or A1C is a term used to describe hemoglobin into
which glucose has been incorporated.
 It is recommended that persons with diabetes lower
their A1C to 7.0% or even achieve a normal glycemic
level of less than 6.0%.
 The level of A1C present in the blood provides an
index of blood glucose levels over the previous 6 to
12 weeks.

30. Other Tests For DM
Capillary Blood Tests
This test is used for self
Monitoring of blood
glucose. The drop of
capillary blood is placed
on or absorbed by reagent
strip, and glucose levels
are determined
electronically using a
glucose meter.

31. Other Tests For DM
 Urine Test:
 When blood glucose reaches 180-200 mg/100ml,the
kidney begin to excrete glucose into the urine. (renal
threshold).
 The level of glucose in urine depends on many factors and
therefore not routinely recommended in recent practice.
 Urine Acetone:
 The presence of acetone in the urine is called Ketonuria.
Ketonuria is a sign that a diabetes is out of control. Clients
are often told to test for urinary ketones if their blood
glucose level exceeds 240mg/dl.

32. Type 1 DM
 Type 1 diabetes is characterized by loss of the insulin-
producing beta cells of the islets of Langerhans of the
pancreas leading to absolute lack of insulin
 About 10% of all people with DM have type 1
disease.
 Most people with Type1 DM develop the disease
before age 30.
 “Less common and more severe condition”.
 subdivided into two
 Types—type 1A immune-mediated diabetes and type
1B idiopathic (non–immune-related) diabetes.

33. Etiology
 It is thought that combined genetic, immunologic and
possibly environmental (e.g. viral) factors contribute
to beta-cell destruction.
 Genetic
 The genetic tendency has been found in people with
certain HLA (human leukocyte antigen) types i.e.
DR3 or DR4).
 Approximately 3% to 4% of children develop type 1
diabetes when a parent has the disease.

34. Auto-Immunity
 This is an abnormal response in which antibodies are
directed against normal tissues of the body,
responding to these tissues as if they are foreign.
 Autoantibodies against islet cells and against
endogenous (internal) insulin have been detected in
people at the time of diagnosis and even several years
before the development of clinical signs of type 1
diabetes.
 Islet cells antibodies act against beta cells and destroy
these cells.

35. Environmental Factors
 Viruses like Rubella, Mumps and Measles may play role
in causing type 1 diabetes.
 They trigger autoimmune process in genetically
susceptible individuals.

36. Pathophysiology
The destruction of the beta cells results in absolute lack of
insulin production.
Unchecked glucose production by the liver leads to fasting
hyperglycemia.
glucose derived from food cannot be stored in the liver but
remains in the bloodstream and contributes to postprandial
(after meals) hyperglycemia
Breakdown of stored glucose (glycogenolysis) and
production of new glucose from amino acids and other
substrates (gluconeogenesis) occur in an uncontrolled way
and contribute further to hyperglycemia.

37.  If the concentration of glucose in the blood
exceeds usually 180 to 200 mg/dl, the glucose
then appears in the urine (glucosuria).
 Fat break-down occurs as an alternate fuel for
energy, resulting in an increased production of
ketone bodies, which are the byproducts of fat
breakdown and causing diabetic keto-acidosis
(DKA).

38. Type 2 Diabetes Mellitus (T2DM)
 T2DM is a syndrome in which hyperglycemia is
caused by the combination of insulin resistance
(inability of the peripheral tissues to respond to
insulin), insulin deficiency (a derangement in insulin
secretion with relative to glucose load) and relative
insulin deficiency.

39. Etiology:
 Genetic factor:
 Insulin secretion and action may be altered by many
genes (not yet identified)
 Environmental factor:
 Obesity,
 Aging, sedentary life style,
 diet etc

40.  People with upper body obesity (central obesity) are
at great risk for developing T2DM and metabolic
disturbances than person with lower body obesity.
 Fat tissue particularly abdominal fat, is known to
become increasingly resistant to the action of insulin.
 Unexercised muscle tissue also becomes insulin
resistant.

41. Pathophysiology
 Normally, insulin binds to special receptors on cell
surfaces leading to glucose uptake and glucose
metabolism.
 In type 2 diabetes, due to insulin resistance and impaired
insulin secretion glucose uptake is diminished and also
glucose released by the liver is increased leading to
hyperglycemia.
 Increased amount of insulin must be secreted to maintain
the glucose level at a normal or slightly elevated level but
the beta cells cannot fulfill the increased demand for
insulin, the glucose level rises, and type 2 diabetes
develops.

42. Insulin resistance in early stage of T2DM
B cells increase insulin production to compensate
And maintain blood glucose level
(hyperinsulinemia)
In late stage if insulin resistance persists, B cells
either due to genetic defect, fat toxicity or
exhaustion begin to fail resulting in
hyperglycemia

43.  Despite the impaired insulin secretion, there is enough
insulin present to prevent the breakdown of fat and the
accompanying production of ketone bodies.
 Therefore, DKA (diabetic ketoacidosis) does not
typically occur in type 2 diabetes.
 Uncontrolled type 2 diabetes may, however, lead to
another acute problem, HHNS (Hyperosmolar
Hyperglycemic Nonketotic Syndrome)

44. Clinical Manifestation of DM
 Hyperglycemia & glycosuria
 Polyphagia, polyuria and polydipsia
 Weight loss ( common in Type 1 DM)
 Ketoacidosis ( common in Type 1 DM)
 Blurred vision
 Fatigue and weakness
 Numbness and paresthesias (tingling sensation)
 Skin lesions and other skin infections
 Poor wound healing
 Candidal infection (pruritus & vulvovaginitis)

45. Comparison of Type 1 and Type 2 DM
Features
Age Of Onset
Type of onset
Usual body wt
Family history
Monozygotic
twin
HLA
associations
Islet lesions
Beta cell mass
Circulating
insulin level
Treatment
Type 1 DM
Usually 20 Yrs
Abrupt
Normal or loss
<20%
50% concordant
+
Early-inflammation
Late—atrophy and fibrosis
Markedly reduced
Markedly reduced
Insulin absolutely required
Type 2 DM
Usually 30 yeas of age
Gradual
Overweight
>60%
90% concordant
No
Late Fibrosis
Normal or slightly reduced
Elevated or normal
Not needed initially

46. Acute Complications Of DM
The three major acute complication of DM are;
 Diabetic Ketoacidosis
 Hyperosmolar Hyperglycemic State
 Hypoglycemia

47. Diabetic Ketoacidosis (DKA)
The three major metabolic derangements in DKA are
 Hyperglycemia, (blood glucose levels >250 mg dL [13.8
mmol/L])
 ketosis, [ketonemia and moderate Ketonuria] and
 Metabolic acidosis. (low serum bicarbonate (<15 mEq/L [15
mmol/L]), and low pH <7.3).

48. Mechanism
DKA most commonly occurs in a person with type 1
diabetes,
Lack of insulin leads to mobilization of fatty acids from
adipose tissue because of the unsuppressed adipose cell
lipase activity that breaks down triglycerides into fatty
acids and glycerol.
The increase in fatty acid levels leads to ketone
production by the liver.
It can occur at the onset of the disease, often before the
disease has been diagnosed.

50. Clinical Manifestations
 Dehydration caused by hyperglycemia
 Warm, dry skin, dry mucous membrane
 Abdominal pain and tenderness may be experienced
without abdominal disease.
 Tachycardia, hypotension, acute weight loss
 Anorexia, nausea & vomiting
 Odor of ketones on the breath
 Depression of the CNS and coma
 Compensatory rapid , deep respiration (Kussmaul
respiration- is a deep and labored breathing pattern often
associated with severe metabolic acidosis to wash out
CO2)

51. Treatment
 The goals in treating DKA are to improve circulatory
volume and tissue perfusion, decrease blood glucose,
correct the acidosis, and correct electrolyte imbalances.
 intravenous fluid and electrolyte replacement solutions.
 An initial loading dose of regular insulin is often given
intravenously, followed by continuous low-dose infusion.
 May be necessary to add potassium to the intravenous
infusion.
 The most common complications from overtreatment of
DKA are hypoglycemia and hypokalemia.

52. Hyperosmolar Hyperglycemic State
 HHS is characterized by hyperglycemia (blood glucose
 >600 mg/dL [33.3 mmol/L]), hyperosmolarity (plasma
osmolarity >320 mOsm/L) and dehydration, the absence
of ketoacidosis, and depression of the sensorium.
 HHS may occur in various conditions, including type 2
diabetes, acute pancreatitis, severe infection, myocardial
infarction, and treatment with oral or parenteral nutrition
solutions.
 It is seen most frequently in people with type 2 diabetes.

53. Pathogenesis
 A partial or relative insulin deficiency may initiate the
syndrome by reducing glucose utilization while inducing
hyperglucagonemia and increasing hepatic glucose output.
 With massive glycosuria, obligatory water loss occurs.
 Dehydration is usually more severe than DKA.
 As the plasma volume contracts, renal insufficiency develops
and the resultant limitation of renal glucose losses leads to
increasingly higher blood glucose levels and severity of the
hyperosmolar state.
 In hyperosmolar states, the increased serum osmolarity has the
effect of pulling water out of body cells, including brain cells.
 The condition may be complicated by thromboembolic events
arising because of the high serum osmolality.

54. Clinical Manifestations and Treatment
 Weakness, dehydration, polyuria, neurologic signs and
symptoms, and excessive thirst.
 Neurologic signs including hemiparesis, seizures, and
coma can occur.
 HHS requires correction of dehydration, hyperglycemia,
electrolyte imbalance, and frequent patient monitoring.
 The treatment of HHS requires judicious medical
observation and care as water moves back into brain cells,
posing a threat of cerebral edema.
 Extensive potassium losses that also have occurred during
the diuretic phase of the disorder require correction.

55. Hypoglycemia
Hypoglycemia is generally defined as cognitive impairment
with a blood glucose concentration of less than 60 mg/dL.
It occurs most commonly in people treated with insulin
injections, prolonged hypoglycemia can also result from
some oral hypoglycemic agents.

56. Etiology and Pathogenesis
Error in insulin dose, failure to eat, increased exercise,
decreased insulin need after removal of a stress situation,
medication changes, and a change in insulin injection
site.
Alcohol decreases liver gluconeogenesis, and people with
diabetes need to be cautioned about its potential for causing
hypoglycemia, especially if it is consumed in large amounts
or on an empty stomach

57. Clinical Manifestations
 Headache,
 Difficulty in problem solving,
 Disturbed or altered behavior, coma, and seizures may
occur.
 Anxiety,
 Tachycardia,
 Sweating, and
 Constriction of the skin vessels (i.e., the skin is cool
and clammy).

58. Treatment.
 Immediate administration of 15 to 20 g of glucose in a
concentrated carbohydrate source.
 It is important not to overtreat hypoglycemia and
cause hyperglycemia.
 This is supported by testing the blood glucose 15
minutes following the ingestion of glucose, and if
necessary, repeating the 15-g concentrated
carbohydrate (15/15 rule).
 Glucagon may be given intramuscularly or
subcutaneously.

59. Somogyi Effect
 The Somogyi effect describes a cycle of insulin-induced
Posthypoglycemic episodes.
 Insulin-induced hypoglycemia produces a compensatory
increase in blood levels of catecholamines, glucagon,
cortisol, and growth hormone.
 These counter-regulatory hormones cause blood glucose
to become elevated.

60. Dawn Phenomenon
 The dawn phenomenon is characterized by increased
levels of fasting blood glucose or insulin requirements, or
both, between 5 and 9 am without antecedent
hypoglycemia (as opposed to the Somogyi).
 It occurs in people with type 1 or type 2 diabetes.
 Attributed to an increased rate of insulin clearance,
decreased insulin sensitivity, or both.

61. Chronic Complications
 Microvascular Complications
1. Neuropathies
2. Disorders of Gastrointestinal Motility
3. Nephropathies
4. Retinopathies
 Macrovascular Complications
1. Coronary artery disease,
2. Cerebrovascular disease, and
3. Peripheral vascular disease (Diabetic Foot)

62. Neuropathies
Thickening of the walls of the nutrient vessels that supply
the nerve, leading to the assumption that vessel ischemia
plays a major role in the development of these neural
changes.
Segmental demyelination process that affects the Schwann
cell. This demyelination process is accompanied by a
slowing of nerve conduction.

63. Disorders of Gastrointestinal Motility
The symptoms vary in severity and include constipation,
diarrhea and fecal incontinence, nausea and vomiting, and
upper abdominal discomfort referred to as dyspepsia.
Gastroparesis (delayed emptying of stomach) is commonly
seen in persons with diabetes. The disorder is characterized
by complaints of epigastric discomfort, nausea, postprandial
vomiting, bloating, and early satiety.
Pathogenesis of these disorders is poorly understood,
neuropathy and metabolic abnormalities secondary to
hyperglycemia are thought to play an important role

64. Nephropathies
Affects people with both type 1 and type 2 diabetes. The
term diabetic nephropathy is used to describe the
combination of lesions that often occur concurrently in the
diabetic kidney.
Nodular glomerulosclerosis is a form of glomerulosclerosis
that involves the development of nodular lesions in the
glomerular capillaries of the kidneys, causing impaired
blood flow with progressive loss of kidney function and,
eventually, renal failure.

65. Retinopathies
Diabetic retinopathy is characterized by abnormal
retinal vascular permeability, microaneurysm formation,
neovascularization and associated hemorrhage, scarring,
and retinal detachment.

66. Macrovascular Complications
Diabetic macrovascular complications result from changes
in the medium to large blood vessels.
Blood vessel walls thicken, sclerose, and become occluded
by plaque that adheres to the vessel walls. Eventually, blood
flow is blocked.
1. Coronary artery disease,
2. Cerebrovascular disease, and
3. Peripheral vascular disease (Diabetic Foot)

67. Diabetic Foot Ulcers
 Foot problems are common among people with diabetes
and may become severe enough to cause ulceration,
infection, and, eventually, the need for amputation.
 In people with diabetes, lesions of the feet represent the
effects of neuropathy and vascular insufficiency.
 People with sensory neuropathies have impaired pain
sensation and are often unaware of the constant trauma to
the feet caused by poorly fitting shoes, improper weight
bearing, hard objects or pebbles in the shoes, or infections
such as athlete’s foot

68. Prevention
 Wear shoes that have been fitted correctly
 Inspect feet daily for blisters, open sores, and fungal
infection (e.g., athlete’s foot) between the toes.
 If their eyesight is poor, a family member should do
this for them.
 Smoking should be avoided because it causes
vasoconstriction and contributes to vascular disease.
 Because cold produces vasoconstriction, appropriate
foot coverings should be used to keep the feet warm
and dry.

69.  Toenails should be cut straight across to prevent
ingrown toenails.
 The toenails are often thickened and deformed,
requiring the services of a podiatrist.
 Self-treatment of foot problems in this population,
such as difficult toe nails, calluses, and other issues,
should be strongly discouraged.

70. Dietary Management of DM
 For all patients with diabetes, the meal plan must consider
the patient’s food preferences, lifestyle, usual eating times,
and ethnic and cultural background.
 A thorough assessment of the patient’s need for weight
loss, gain, or maintenance is also undertaken
 In most instances, the person with type 2 diabetes requires
weight reduction.
 The priority for a young patient with type 1 diabetes,
should be a diet with enough calories to maintain normal
growth and development.

71.  Currently, the American Dietetic Association recommend
that 50% to 60% of calories should be derived from
carbohydrates, 20% to 30% from fat, and the remaining
10% to 20% from protein.
 The latest nutrition guidelines recommend that all
carbohydrates be eaten in moderation to avoid high
postprandial blood glucose levels.
 The use of fiber in diabetic diet is recommended.
 This type of diet plays a role in lowering total
cholesterol and low-density lipoprotein cholesterol in
the blood.

72.  Combining starchy foods with protein- and fat-containing
foods tends to slow their absorption and lower the
glycemic response.
 In general, eating foods that are raw and whole results in a
lower glycemic response than eating chopped, puréed, or
cooked foods.
 Eating whole fruit instead of drinking juice decreases the
glycemic response because fiber in the fruit slows
absorption.

73. Exercise
 Exercise lowers the blood glucose level by increasing the
uptake of glucose by body muscles and by improving insulin
utilization.
 It also improves circulation and muscle tone.
 Resistance (strength) training, such as weight lifting, can
increase lean muscle mass, thereby increasing the resting
metabolic rate.
 These effects are useful in diabetes in relation to losing weight,
easing stress, and maintaining a feeling of well-being.
 Exercise also alters blood lipid levels, increasing levels of
high-density lipoproteins and decreasing total cholesterol and
triglyceride levels. This is especially important to the person
with diabetes because of the increased risk of cardiovascular
disease

74.  Patients who have blood glucose levels exceeding 250
mg/dL and who have ketones in their urine should not
begin exercising until the urine tests negative for ketones
and the blood glucose level is closer to normal.
 The patient who requires insulin should be taught to eat a
15-g carbohydrate snack (a fruit exchange) or a snack of
complex carbohydrate with a protein before engaging in
moderate exercise, to prevent unexpected hypoglycemia

75. Medical Management of DM
Oral Antidiabetic Agents:
 Oral antidiabetic agents are indicated for patients who
have type 2 diabetes that cannot be treated by diet and
exercise alone
 Contraindicated during pregnancy.
 Classified into five classes on the basis of their action
namely:
1. Sulfonylureas
2. Biguanides
3. Alpha Glucosidase Inhibitors
4. Thiazolidinediones
5. Meglitinides

76. Sulfonylureas
The sulfonylureas can be divided into first and second-
generation categories.
 First Generation: Acetohexamide, chlorpropamide
 Second Generation: Glipizide, glyburide, glimepiride
Action
 Directly stimulating the pancreas to secrete insulin.
 Improves insulin action at the cellular level and may also
directly decrease glucose production by the liver.
Side effects
 Most commonly GI symptoms and dermatologic reactions.
 Hypoglycemia when excessive dose is used or when the
patient omits or delays meals, reduces food intake, or increases
activity.

77. Biguanides
Action
 The biguanides e.g. Metformin (Glucophage) increases the
use of glucose by muscle and fat cells, decreases hepatic
glucose production, and decreases intestinal absorption of
glucose..
Side effects
 Lactic acidosis is a potential and serious complication of
biguanide therapy
Contraindications
 Renal impairment (serum creatinine level more than 1.4).
 Hold Metformin for 2 days before any diagnostic testing
that may require use of a contrast agent.

78. Alpha Glucosidase Inhibitors
 They include acarbonose
Action
 They work by delaying the absorption of glucose in
the intestinal system
 They can be used alone with dietary treatment as
monotherapy or in combination with sulfonylureas,
thiazolidinediones, or meglitinides
Side effects
 Hypoglycemia may occur when used in
combination
 Diarrhea and flatulence.

79. Thiazolidinedions
Rosiglitizone and pioglitozone are categorized as
thiazolidinediones
Action
 Thiazolidinediones enhance insulin action at the
receptor site and decrease production of glucose by
the liver.
Side effects
 These medications may affect liver function
 Thiazolidinediones can cause resumption of
ovulation in perimenopausal an ovulatory women,
making pregnancy a possibility.

80. Meglitinides
This class includes Repaglinide
Action
 Lowers the blood glucose level by stimulating insulin
release from the pancreatic beta cells.
 Also indicated for use in combination with metformin
Side effects
 The principal side effect of repaglinide is hypo-glycemia;
however, this side effect is less severe and frequent than
for a sulfonylurea

81. Insulin
Parenteral insulin is obtained from pork and beef
pancreas.
 Indicated for type 1 DM patients
 It was introduced in 1983.
 The concentration of insulin is 100 units/ml.

82. Types of Insulin
There are several standard types of insulin:
 Rapid acting.
 Short acting
 Intermediate acting.
 Long acting.
 Combinations

83. Rapid acting Insulin
Examples: Lispro (Humalog)
Appearance: a clear liquid solution like water.
Action of Lispro= 5-15 min.
 The hypoglycemic drug of choice for diabetics
experiencing acute or chronic diabetic emergencies,
e.g., DKA, HNKC (Hyperosmolar Non Ketotic
Coma) etc.
 Lispro acts faster than regular insulin, thus it must not
be administered greater than >5 min before meals.
 Route= SC.

84. Short Acting Insulin
Example: Regular insulin (Humulin-R).
 Appearance: a clear liquid solution like water.
 Onset of action = 30min-1hr.
 Humulin-R is the only insulin preparation that
can be given IV.
 Regular insulin is given 30 min. before meals.
 Regular Insulin routes: SC, IV

85. Intermediate Acting Insulin
Examples: Neutral Protamine Hagedorn (NPH),
Humulin N, Lente, Humulin L.
NPH and Humulin-N contains protamine, a protein that
prolongs the action of insulin.
Lente and Humulin L contains Zinc that also prolongs
the action of insulin.
The onset of action:1-2 hrs.
Duration of action:18-24 hrs.
Route= SC

86. Long acting Insulin
Examples: Humulin Ultralente, Lantus (an insulin
glargine).
Long acting insulin absorb slower than other insulin b/c
of its large crystals, which dissolve slowly and prolongs
the action.
Onset of action: 4-8 hrs and lasts for 24-36 hrs.
Lantus is an analogue of human insulin
It is administered once daily HS.
With Lantus, clients c/o pain at injection site.
Available with ―Optipen or insulin pen.
Route= SC.

87. Combination Insulin
They are commercially premixed.
 Examples: Humulin 70/30, Humulin 50/50,
Humalog 75/25.

88. Insulin
Side-effects: Hypoglycemic reaction, confusion,
agitation, tremors, headache, weakness, lethargy,
fatigue, urticaria, redness, irritation or swelling at
insulin injection site, tachycardia, palpitation,
rebound Hyperglycemia (Somogyi effect),
lipodystrophy, shock.
Contraindications:
Hypersensitivity to beef, pork, zinc, protamine insulin.

89. Nursing Management
Patient education:
 Knowledge about nutrition,
 Medication effects and side effects
 Exercise, disease progression, prevention strategies
 Blood glucose monitoring techniques
 Medication adjustment

90. Nursing Diagnoses
Major nursing diagnoses may include the following:
 Risk for fluid volume deficit related to polyuria and
dehydration
 Fluid and electrolyte imbalance related to fluid loss
or shifts
 Deficient knowledge about diabetes self-care skills
or information
 Anxiety related to loss of control, fear of inability
to manage diabetes, misinformation related to
diabetes, fear of diabetes complications

91. Teaching Survival Skills
Simple pathophysiology
a. Basic definition of diabetes (having a high blood
glucose level)
b. Normal blood glucose ranges and target blood
glucose levels.
c. Effect of insulin and exercise (decrease glucose)
d. Effect of food and stress, including illness and
infections (increase glucose)
e. Basic treatment approaches

92. Treatment modalities
 a. Administration of insulin and oral antidiabetes
medications
 b. Diet information (food groups, timing of meals)
 c. Monitoring of blood glucose and ketones
Recognition, treatment, and prevention of acute
complications
 a. Hypoglycemia
 b. Hyperglycemia

93. Teaching Preventive Measures
 Foot care
 Eye care
 General hygiene (e.g. skin care, oral hygiene)
 Risk factor management (e.g. control of blood
pressure and blood lipid levels, and normalizing blood
glucose levels)

94. Patients With Diabetes Who Are
Undergoing Surgery
 During periods of physiologic stress, such as surgery, blood
glucose levels tend to increase, because levels of stress
hormones (epinephrine, norepinephrine, glucagon, cortisol, and
growth hormone) increase.
 Frequent blood glucose monitoring is essential throughout
the preoperative and postoperative periods.
 The use of IV insulin and dextrose has become widespread.
 Monitor for cardiovascular complications because of the
increased prevalence of atherosclerosis, wound infections, and
skin breakdown.
 Maintaining adequate nutrition and blood glucose control
promote wound healing.

95. Nothing by Mouth
 IV dextrose may be administered to provide calories
and to avoid hypoglycemia.
 Even without food, glucose levels may increase as a
result of hepatic glucose production, especially in
patients with type 1 diabetes and lean patients with
type 2 diabetes.
 Furthermore, in type 1 diabetes, elimination of the
insulin dose may lead to the development of DKA.
 Administration of insulin to patients with type 1
diabetes who are NPO is an important nursing action.

96. Reference
Carol. P. M. (2000) Pathophysiology concepts of altered
health states. Philidelphia: J. B. Lippincot.