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1. Khyber Medical University
• Subject: Adult Health Nursing
• Topics: Diabetes Mellitus
• Prepared by: Awal Sher Khan

2. Objectives
• At the end of this presentation the students will be
able to:
• Review of anatomy and physiology of endocrine
pancreases.
• Discuss classification of diabetes mellitus.
• Discuss etiology, pathophysiology, and clinical
manifestations of type-I and type-II DM.
• Identify differences between type-I and type-II DM.
• Describes complications of diabetes mellitus.

3. Objectives cont…
• Discuss medical diagnosis and medical
management for diabetes.
• Make nursing diagnosis and nursing
interventions for diabetes.

4. Anatomy & physiology of endocrine
pancreas
• The pancreas is a gland organ in the digestive and
endocrine system. It is both an endocrine gland
producing several important hormones, including
insulin, glucagon, and somatostatin, as well as an
exocrine gland, secreting pancreatic juice containing
digestive enzymes that pass to the small intestine.
• The part of the pancreas with endocrine function is
made up of approximately a million cell clusters
called islets of Langerhans.

5. Cont….
• There are four main cell
types in the islets. They
are classified by their
secretion: α cells
secrete glucagon, β cells
secrete insulin, δ cells
secrete somatostatin,
and PP cells secrete
pancreatic polypeptide.

7. Diabetes mellitus
• Diabetes mellitus, describes a group of metabolic
diseases in which the person has high blood
glucose (blood sugar), either because insulin
production is inadequate or because the body's
cells do not respond properly to insulin or both.
• Patients with high blood sugar will typically
experience Polyuria (frequent urination), they
will become increasingly thirsty (Polydipsia) and
hungry (Polyphagia).

8. Classification of diabetes
There are three types of diabetes:
1) Type 1 Diabetes:
• The body does not produce insulin. Some
people may refer to this type as insulin-
dependent diabetes, juvenile diabetes,
or early-onset diabetes.
• People usually develop type 1 diabetes
before their 40th year, often in early
adulthood or teenage years.

9. Cont…
• 2) Type 2 Diabetes:
• The body does not produce enough insulin for
proper function, or the cells in the body do
not react to insulin (insulin resistance).
• Approximately 90% of all cases of diabetes
worldwide are of this type

10. Cont…
3) Gestational diabetes
• This type affects females during pregnancy.
Some women have very high levels of glucose
in their blood, and their bodies are unable to
produce enough insulin to transport all of the
glucose into their cells, resulting in
progressively rising levels of glucose

11. Type-I
• Etiology
• Diabetes type 1 is induced by one or more of the
following:
• Genetics
• Environmental
• Virus
• Autoimmune

12. Signs and symptoms
The classical symptoms of type 1 diabetes include:
• Polyuria (frequent urination).
• Polydipsia (increased thirst).
• Polyphagia (increased hunger).
• Fatigue.
• weight loss.

13. Pathophysiology
• The pathophysiology of type 1 DM is basically a
destruction of beta cells in the pancreas, regardless
of which risk factors or causative entities have been
present.
• Individual risk factors can have separate
pathophysiological processes to, in turn, cause this
beta cell destruction.

14. Cont…
• Still, a process that appears to be common to most
risk factors is an autoimmune response towards beta
cells, involving an expansion of autoreactive CD4+
and CD8+ T helper cells, autoantibody-producing B
cells and activation of the innate immune system.

15. Type-II
• Diabetes mellitus type 2 – formerly non-insulin-
dependent diabetes mellitus (NIDDM) or adult-onset
diabetes – is a metabolic disorder that is
characterized by high blood glucose in the context of
insulin resistance and relative insulin deficiency.
• Etiology:
• Genetic factors
• Ethnic origin
• Being overweight or obese
• Age

16. Signs and symptoms
The classic symptoms of diabetes are
• Polyuria (frequent urination),
• Polydipsia (increased thirst),
• Polyphagia (increased hunger), and weight loss.
• Blurred vision
• Itchiness
• Peripheral neuropathy
• Recurrent vaginal infections
• Fatigue

17. Pathophysiology
• Type 2 diabetes is due to insufficient insulin
production from beta cells in the setting of insulin
resistance.
• Insulin resistance, which is the inability of cells to
respond adequately to normal levels of insulin,
occurs primarily within the muscles, liver and fat
tissue.
• In the liver, insulin normally suppresses glucose
release. However in the setting of insulin resistance,
the liver inappropriately releases glucose into the
blood.

18. Difference between type-I and
type-II

19. Diagnosis
• A fasting blood glucose test:
• (no food or liquids other than water) for eight hours.
• A normal fasting blood glucose level is less than 100
mg/dl.
• A diagnosis of diabetes is made if blood glucose
reading is 126 mg/dl or higher after two consecutive
blood tests.
• (In 1997, the American Diabetes Association lowered
the level at which diabetes is diagnosed to 126 mg/dl
from 140 mg/dl.)

20. Cont…
• A "random" blood glucose test taken at any
time.
• A diagnosis of diabetes is made if blood
glucose reading is 200 mg/dl or higher and
symptoms of disease such as fatigue,
excessive urination, excessive thirst or
unplanned weight loss.

21. Cont...
Glucose tolerance test :
• The test measure the body’s ability to store glucose
by removing it from blood.
• After fasting overnight,75g concentrated sugar-
water solution is given at selected intervals (hourly, 2
hourly or 3 hourly)
• Blood glucose is tested over several hours.
• In a person without diabetes, glucose levels returns
to normal in 2-3 hours.
• Diabetes is diagnosed if blood glucose levels are 200
mg/dl or higher.

22. Management
• Management of type 2 diabetes focuses on:
– lifestyle interventions,
– lowering other cardiovascular risk factors
– maintaining blood glucose levels in the normal range.
– Self-monitoring of blood glucose
• Lifestyle
• Exercise program
• A diabetic diet that promotes weight loss is important.
• Culturally appropriate education may help people with type 2
diabetes control their blood sugar levels

23. Conti…
Medications
• There are two categories of antidiabetic
agents:
• Oral medications (sulfonylureas, biguanides,
a-Glucosidase Inhibitors and
Thiazolidinediones.
• Injectable insulin. IDDM requires treatment
with insulin. Most types of insulin are
available in 100 u/1ml

24. GLUCOSE
ABSORPTION
GLUCOSE
PRODUCTION
Metformin
Thiazolidinediones
MUSCLE
PERIPHERAL
GLUCOSE UPTAKE
Thiazolidinediones
Metformin
PANCREAS
INSULIN SECRETION
Sulfonylureas: Glyburide, Gliclazide, Glimepiride
Non-SU Secretagogues: Repaglinide, Nateglinide
ADIPOSE
TISSUE
LIVER
Alpha-glucosidase inhibitors
INTESTINE
Action Sites of oral hypoglycemic
agents

25. Macrovascular Microvascular
Stroke
Heart disease and
hypertension
2-4 X increased risk
Foot problems
Diabetic eye disease
(retinopathy and cataracts)
Renal disease
Peripheral Neuropathy
Peripheral
vascular disease
Diabetes: Complications
Complications
Erectile Dysfunction

26. Complications
• Diabetes doubles the risk of cardiovascular disease
(angina and myocardial infarction), stroke and
peripheral vascular disease.
• Diabetes also causes "microvascular“ complications
such as damage to the small blood vessels.
• Diabetic retinopathy, which affects blood vessel
formation in the retina of the eye, can lead to visual
symptoms, reduced vision, and potentially blindness.

27. Cont….
• Diabetic nephropathy, the impact of diabetes on the
kidneys, can lead to scarring changes in the kidney
tissue, loss of small or progressively larger amounts
of protein in the urine, and eventually chronic kidney
disease requiring dialysis.
• Diabetic neuropathy is the impact of diabetes on the
nervous system, most commonly causing numbness,
tingling and pain in the feet and also increasing the
risk of skin damage due to altered sensation.
• Diabetic foot ulcers that can be difficult to treat and
occasionally require amputation.

28. Conti…
• Diabetic Ketoacidosis in type 1DM due to lack
of insulin mobilization of fatty acids from
adipose tissue.
• Fatty acids levels ketone production by
the liver, characterized by blood sugar
(>250mg/dl), pH(<7.3) bicarbonate(<15mEq/L)
and presence of ketones in the urine.

29. Nursing diagnosis
• Imbalanced Nutrition Less Than Body Requirements
related to reduction of carbohydrate metabolism
due to insulin deficiency, inadequate intake due to
nausea and vomiting.
• Fluid Volume Deficit related to polyuria, decreased
fluid intake.
• Impaired Skin Integrity related to decreased sensory
sensation, impaired circulation, decreased
activity /mobilization, lack of knowledge of skin care.

30. Cont….
• Activity Intolerance related to weakness due to
decreased energy production.
• High risk of injury associated with decreased
sensation sensory (visual), weakness, and
hypoglycemia.
• Stress and anxiety related to disease.

31. Nursing interventions
• Administer insulin or an oral antidiabetic drug as
prescribed.
• Treat hypoglycemic reactions promptly by giving
carbohydrates in the form of fruit juice, hard candy,
honey or I.V. dextrose.
• Provide skin care, especially to the feet and legs.
• Assist the patient to develop coping strategies.
• Keep accurate records of vital signs, weight, fluid
intake, urine output, and caloric intake.

32. Cont…
• Monitor diabetic effects on the cardiovascular,
peripheral vascular, and nervous systems.
• Observe for signs of urinary tract and monitor the
patient’s urine for protein, an early sign of
nephropathy.
• Recommend regular ophthalmologic examinations.
• Teach the patient how to care for his feet.
• Teach the patient and the family how to monitor the
patient’s diet.

33. References
• "Diabetes Blue Circle Symbol". International Diabetes
Federation. 17 March 2006.
• Shoback, edited by David G. Gardner, Dolores
(2011).Greenspan's basic & clinical
endocrinology (9th ed.). New York: McGraw-Hill
Medical. pp. Chapter 17.
• http://www.npr.org/blogs/health/2012/06/21/1555
05445/how-to-spot-a-neglected-tropical-disease
• Williams textbook of endocrinology (12th ed.).
Philadelphia: Elsevier/Saunders. pp. 1371–1435.