This document provides information on diabetes mellitus, including its definition, types, pathophysiology, diagnosis, treatment, complications, and nursing interventions. It defines diabetes as a disorder of carbohydrate metabolism resulting from impaired insulin production, action, or both. The three main types are described as type 1 diabetes (insulin dependent), type 2 diabetes (non-insulin dependent), and gestational diabetes. Risk factors, symptoms, diagnostic tests, and treatment options are outlined for each type. Potential acute and chronic complications of diabetes are also reviewed.

1. DIABETES MELLITUS

2. OBJECTIVES
At the end of presentation the learner's would be able to;
Define diabetes mellitus.
Difference between type l, type ll and gestational
diabetes mellitus.
Describe the Pathophysiology of type l and type ll
diabetes mellitus.
Discuss the diagnosis of diabetes mellitus.
Explain the treatment and prevention of diabetes
mellitus.
Enlist the complication of diabetes mellitus.

3. DIABETES MELLITUS
Diabetes mellitus is a disorder of
carbohydrate metabolism characterized by
high level of blood glucose resulting from
impaired ability to produce insulin, insulin
action or both.

4. TYPES OF DIABETES MELLITUS
There are three main types of diabetes mellitus;
1. Type l diabetes or insulin dependant diabetes
2. Type ll diabetes or non insulin dependant diabetes
3. Gestational diabetes

5. TYPE I DIABETES MELLITUS
 Type I diabetes also known as juvenile or
insulin-dependant diabetes. It is an
autoimmune condition in which the pancrease
produce little or no insulin due to body
attacking its own pancrease with antibodies and
destroy the beta cell.
 Age mostly occur 4 to 7 years and 10 to 14
years.

6. PATHOPHYSIOLOGY
Type l diabetic is idiopathic and autoimmune
Organ-specific deficit may induce an autoimmune
attack on beta cell s. this attack, in turn, causes an
inflammatory response in the pancrease called
insulitis.
Islet cell antibodies may be present long before
symptoms become apparent. These immune markers
also precede evidence of beta cell deficiency.
Autoantibodies against insulin have also been noted.
By the time the disease become apparent, 80% of the
beta cells are gone.

7. CAUSES OF TYPE I DIABETES
The exact cause is unknown.
Genetic predisposition
Faulty beta cells in the pancrease
Exposure to virus and other environmental factor
RISK FACTORS
Genetic
Family history
Geography
Age mostly 4 to 14 years

8. SIGN AND SYMPTOMS
Polydipsia or Increase thirst
Polyuria or Frequent urination
Polyphagia or Extreme hunger
Weight loss
Blurred vision
Fatigue and weakness
Irritability and mood change

9. TREATMENT AND PREVENTION
One of the best treatment of type I diabetes is insulin;
1. short acting – insulin ( Humulin R)
2. Long acting insulin (novolog, flexpen, fiasp).
3. Intermediate –acting –insulin ( Humulin-n)
4. Long-acting insulin ( lantus, levemir)
 According to researcher Type I diabetes is not
preventable right now but can be prevented by taking
good care of your body –maintaining healthy diet and
staying physically fit and active.

10. TYPE II DIABETES
Type ll diabetes also known as adult-onset diabetes or
non- insulin dependant diabetes characterized by high
blood glucose level, insulin resistance and lack of
insulin.
In type ll diabetes the beta cell of the pancrease
produce insulin but the body is unable to use it
effectively because the cell of the body are resistance
to the action of insulin.

11. PATHOPHYSIOLOGY

12. RISK FACTORS
MODIFIABLE RISK
FACTORS
Obesity
Sedentary life style
Hypertension
Stress factors
Smoking
NON MODIFIABLE RISK
FACTORS
Ethnicity
Family history of type ll
diabetes
Age
Gender
History of gestational
diabetes
inflammation

13. SIGN AND SYMPTOMS
Polydipsia or increase thirst
Polyuria or increase urination
Polyphagia or extreme hunger
Weight loss
Slow-healing sores
Areas of darkened skin, usually in the arms
and neck.

14. TREATMENT
1. Metformin (BIGUANIDES- Glucophage) should be
the first line drug for managing type ll diabetes.
2. Insulin and sulfonylureas (Glipizide-Glucotrol,
glyburide-Diabeta, Glimepiride-Amaryl) should be
second line.
3. Thiazolidinediones (Piogiltazones-Actos) should be
third line drug for managing type ll diabetes.

15. Gestational diabetes
Gestational diabetes develop s during pregnancy.
Gestational diabetes is caused when the insulin
receptor do not function properly.
This is likely due to pregnancy related factor such as
the presence of human placental lactogen that
interference with susceptible insulin receptor.
Mostly detected at 24 to 28 weeks of pregnancy.
Gestational diabetes goes away after birth but
increase risk of developing type 2 DM for mother and
children.

16. RISK FACTORS AND
SYMPTOMS
RISK FACTORS
1. Body mass index more than
30/kg/m2
2. Previous gestational diabetes
3. Family history of diabetes
4. Previous baby weight 4.5kg
or more
5. Sedentary life style
6. History of smoking
SIGN AND SYMPTOMS
1. Drinking a lot or
polydipsia
2. Urination more than usual
3. Infection in bladder,
vagina and skin
4. The tummy looks bigger
5. Nausea
6. Vomiting
7. Fatigue

17. DIAGNOSTIC EVALUATION
Diabetes can be diagnosed in any of the following
ways;
1. History
2. Physical examination
3. Labs test

18. LABS DIAGNOSIS
1. FBS (Fasting blood sugar) greater than or equal to
126 mg/dl.
2. RBS (Random blood sugar) greater than or equal to
200mg/dl
3. OGTT (Oral glucose tolerance test) more than or
equal to 200 mg/dl, on the 2hours sample.
4. HBA1C (Glycated Hemoglobin A1C) 6..1 to 7 target
range for diabetes.

19. HISTORY
1. Have you had increase thirst, increase urination and
fatigue?
2. How long have the symptoms been present?
3. Have you had an increase in appetite?
4. Have you lost weight lately?
5. Is there a family history of diabetes?
6. What other medical condition do you have?
7. What are medicine are you currently taking?
8. Have you been ill recently?
9. Has growth and development progressed normally ( if
the person is child)?

20. PHYSICAL EXAMINATION
Assess skin for dehydration, infection and poor wound
healing.
Numbness and tingling of the extremities, tremor,
twitching, drowsiness, lethargy and crying.
Eyes; blurred vision, retinopathy, cataract, glaucoma.
Cardiovascular; weak pulse, orthostatic hypotension,
tachycardia, ECG changes.
Respiratory ; breathing pattern, characteristics of
metabolic acidosis
Gastrointestinal; nausea, vomiting, abdominal bloating
and diarrhea.
Genitourinary; nocturia, and polyuria.
Nutrition level; check weight and body mass index(BMI)

21. complication
ACUTE
COMPLICATION
CHRONIC
COMPLICATIION
1. Hypoglycemia
2. Diabetic ketoacidosis
(DKK)
3. Hyperosmolar
hyperglycemic
nonketotic
syndrome(HHNS)
Macrovascular-(atherosclerosis
plaque)
1. Coronary arteries- MI
2. Cerebral arteries- stroke
3. Peripheral vessels- ulcer,
amputation, infection
Microvascular (capillary
damage)
1. Retinopathy
2. Neuropathy
3. Nephropathy

22. Nursing intervention
1. Monitor patient's FBS, RBS and HBA1C.
2. Assess for sign of hyperglycemia such as polyphagia,
polyuria, polydipsia, blurred vision.
3. Assess for sign of hypoglycemia such as anxiety, tremor and
slurring of speech, dizziness, diaphrosis.
4. Assess feet for pulses, temperature , sensation and instruct the
patient to avoid heating pads and always to wear shoes when
walking.
5. Teach the patient about role of exercise in diabetes.
6. Teach patient about an importance of proper meal and
adequate calorie intake.
7. Teach the patient about disease process and problem
associated with disease.
8. Teach the patient how to administered insulin properly.

23. REFFRENCES
1.Pathophysiology made incredible easy
book 2nd edition.
2.American diabetes association guideline.