PRESENTATION ON

SUBMITTED TO: MRS BABITA KUMARI PRESENTED BY: MS.KIRAN

ASSISTANT PROFESSOR M.Sc. NURSING II YEAR
ACN BARU SAHIB ACN BARU SAHIB
UNIVERSAL SYMBOL FOR DIABETES
MELLITUS
 CONTENTS:

• Introduction
• Definition
• Risk factors and causes
• Sign and symptoms
• Types
• Pathophysiology
• Diagnostic evaluation
• Complications
• Treatment
 INTRODUCTION

Diabetes mellitus (DM), is a group of metabolic diseases in which there

are high blood sugar levels(hyperglycaemia) over a prolonged period.

 Symptoms of high blood sugar include frequent urination, increased

thirst, and increased hunger. Diabetes is due to either the pancreas not
producing enough insulin or the cells of the body not responding
properly to the insulin produced.
 DEFINITION

Diabetes is a group of metabolic diseases characterized by

hyperglycaemia resulting from defects in insulin secretion, insulin
action, or both.
 EPIDEMIOLOGY

Globally
382 million people had diabetes in 2013.
By 2035, this number will rise to 592 million.
In India
65.1 million people had diabetes in 2013 .
By 2035, this number will increase by 70.6%.
 ANATOMY OF PANCREAS

The adult pancreas is a transversely oriented retroperitoneal organ

extending from the "C " loop of the duodenum to the hilum of the
spleen.
EXOCRINE secretion :Pancreatic juice enzymes promote the
digestion of carbohydrates, proteins and fats.
ENDOCRINE secretion :Insulin and glucagon- enter portal vein
– transported directly to the liver – regulate metabolism of
carbohydrates, proteins and fats.
 RISK FACTORS

NON-MODIFIABLE:
Age: 45 or more
Race : African American, Asian American.
Familial history : a parent, or siblings with diabetes.
 MODIFIABLE:

Pre diabetes
Heart and blood disease
Hypertension
Low HDL cholesterol and high triglycerides
Obesity
 Polycystic ovary syndrome
Physical inactivity
 CLASSIFICATION

Classification by American diabetic association 2009 :

Type 1 diabetes
Type 2 diabetes
Gestational diabetes mellitus (GDM)
 TYPE 1 DM

Juvenile / IDDM(5 to 10%)

Autoimmune destruction of pancreatic beta cells.
 Individual has an absolute insulin deficiency and no longer
produces insulin.
Such patients are absolutely dependent on exogenously
administered insulin for survival.
 TYPE 2 DIABETES MELLITUS

Most common type.

Comprises 90 to 95% of DM cases.
Most type 2 DM patients are overweight, and most are
diagnosed as adults.
Approximately half of the patients are unaware of their disease.
 THE UNDERLYING PATHOPHYSIOLOGIC DEFECT IN TYPE
2 DM IS CHARACTERIZED BY THE FOLLOWING THREE
DISORDERS:

1.Peripheral resistance to insulin, especially in muscle cells.

2. Increased production of glucose by the liver.
3. Insulin secretary defect of the beta cells .
• Obesity contributes greatly to insulin resistance.
• Insulin resistance generally decreases with weight loss.
 COMPONENTS OF DM-II

• Insulin Resistance
• B-cell Dysfunction
 CLINICAL PRESENTATION

Patients can be asymptomatic

• Polyuria.
• Polydipsia.
• Polyphagia.
• Fatigue.
• Weight loss.
• Most patients are discovered while performing urine glucose screening.
 DIAGNOSTIC EVALUATION

Fasting Plasma Glucose

Oral Glucose Tolerance Test (OGTT)
 Glycosylated Haemoglobin (HbA1c)
 Urinalysis presence of:
• Glycosuria
• Ketone bodies
ADDITIONAL INVESTIGATIONS:
Lipid profile
Fundoscopic examination
LFT
Urine analysis
ECG
Test to assess other complications
MANAGEMENT OF DM
Dietary treatment should aim at:

Ensuring weight control.

Providing nutritional requirements.
 Allowing good glycaemic control with blood glucose levels as close
to normal as possible.
Correcting any associated blood lipid abnormalities.
EXERCISE

Physical activity promotes weight reduction and improves

insulin sensitivity, thus lowering blood glucose levels.
People should, however, be educated about the potential risk of
hypoglycaemia and how to avoid it.
Avoid trauma to extremities.
Patients who have BS >200mg/dl and who have urine ketones should
not begin exercise until urine tests are NEGATIVE.
 Use of proper footwear.
Avoid exercise in extreme heat or cold.
Have snacks after the exercise , to avoid post exercise hypoglycaemia.
 ORAL ANTI-DIABETIC AGENTS

There are currently four classes of oral anti-diabetic agents:

• Sulfonylureas (gliclazide, glimepiride, glipizide, glyburide)
• Meglitinides (nateglinide, repaglinide)
• Biguanides (metformin)
• Thiazolidinediones (pioglitazone, rosiglitazone)
• Alpha Glucosidase inhibitors (miglitol, voglibose, acarbose)
 INSULIN THERAPY

Short-term use:
Acute illness, surgery, stress and emergencies
Insulin may be used as initial therapy in type 2 diabetes
Severe metabolic decompensation (diabetic ketoacidosis,
hyperosmolar nonketotic coma, lactic acidosis, severe
hypertriglyceridemia).
 INSULIN THERAPY

Long-term use:
If targets have not been reached after optimal dose of
combination therapy, consider change to multi-dose insulin
therapy.
 ROUTES OF ADMINISTRATION

Subcutaneous for long term regular use

Intravenous infusion in acute conditions- diabetes Ketoacidosis,
Perioperative period.
 Intraperitoneal – Peritoneal dialysis patients
Inhaled insulin- experimental
COMPLICATIONS OF INSULIN THERAPY
1.Hypoglycaemia
2.Lipodystrophy
3.Systemic allergic reactions
4.Insulin resistance
 COMPLICATIONS OF DIABETES
MELLITUS
Acute complications:
I. Diabetic ketoacidosis
II. Hypoglycaemia
III. Diabetic nonketotic hyperosmolar coma
 DIABETIC KETOACIDOSIS
• Serious condition occur due to complication of Diabetes Mellitus.
• Carry significant risk of death and morbidity especially if treatment
is delayed.
• Occurs due to shortage of insulin in response to body switches to
burn the fatty acids and produce ketones and that can cause
ketoacidosis symptoms and complications.
CLINICAL FEATURES
• Nausea/Vomiting.
• Polydipsia.
• Polyuria/Oliguria.
• Abdominal pain
• Hyperventilation/ Fruity breath.
• Tachycardia.
• Hypotension.
• Mental status changes.
• Coma.
• Kussmaul’s breathing.
 MANAGEMENT

PRINCIPLES OF TREATMENT:-
1. Careful management of fluid deficits.
2. Correction of acidosis & hyperglycaemia via Insulin administration.
3. Correction of electrolyte imbalances.
4. Treatment of underlying causes.
5. Monitoring of complications of treatment.
Chronic complications:
Retinopathy
Nephropathy
Neuropathy
Diabetic Foot
Cardio-vascular
Peripheral Vascular Disease.
 NURSING MANAGEMENT

Obtain history :
• Current problems and General health history
Family history
• Has the patient experienced polyuria, polydipsia, polyphagia, and any other
symptoms?
• Number of years since diagnosis of DM?
• Symptoms of complications?
PHYSICAL EXAMINATION:
General: Recent wt. loss or gain, fatigue, anxiety
Skin: lesion, infections, dehydration,
Eyes: changes in vision, “floaters, halos, cataracts…
Cardiovascular: orthostatic hypotension, claudication
GI: diarrhoea, increased hunger and thirst
GU: polyurea, nocturia  Neurologic: numbness, and tingling of extremities
IMBALANCED NUTRITION : MORE THAN BODY REQUIREMENT
RELATED TO INTAKE OF EXCESS OF ACTIVITY EXPENDITURES

1. Assess the current timings and content of meals

2. Advise patient on the importance of an individualized meal plan in
meeting weight loss goals.
3. Explain the importance of exercise in maintain / reducing body
weight.
4. Assist the patient to establish goals for weekly weight loss and
incentives to assist in achieving them.
RISK FOR INJURY ( HYPOGLYCAEMIA) RELATED TO
EFFECTS OF INSULIN, INABILITY TO EAT

1.Closely monitor blood glucose levels to detect hypoglycaemia. Instruct

the patient in the importance of accuracy in insulin preparation and meal
timings to avoid hypoglycaemia.
2.Treat hypoglycaemia promptly with 15 to 20 gm of fast acting
carbohydrates.
3. Encourage patients to carry sugar candy all times.
4. Encourage patient to wear identification bracelet.
DEFICIT KNOWLEDGE RELATED TO USE OF ORAL
HYPOGLYCAEMIC AGENTS

1.Assess level of knowledge of disease and ability to care self.

2. Assess adherence to diet therapy, monitoring procedures,
medication, treatment, and exercise regimen.
3.Assess for signs for hyperglycaemia or hypoglycaemia.
4.Perform skin and extremity assessment for peripheral
neuropathy or any injury in feet and lower extremities.
RISK FOR IMPAIRED SKIN INTEGRITY RELATED TO
DECREASED SENSATION AND CIRCULATION TO LOWER
EXTREMITIES.

1.Assess feet and legs for skin temperature sensation, soft tissue injures,
corn, dryness, hammer toe.
2.Maintain skin integrity by protecting feet from break down.
3.Use heel protectors, special mattresses, foot cradles for patient on bed rest.
4.Avoid Appling drying agent to skin. (alcohol)
5.Apply moisturizers to maintain suppleness and prevent cracking and
fissures. Instruct patient in foot care guidelines
 CONCLUSION

Type 2 diabetes is a “life style” disease, characterized by

hyperglycaemia resulting from defects in insulin secretion, insulin
action, or both. Caring for diabetes can also help prevent other
health problems over the years.
 BIBLIOGRAPHY
Brunner & Suddhart’s. “Textbook of medical-surgical nursing”. 11 th
edition published by Elsevier,

Smeltzer CS. Bare B. Brunner & Suddarth’s Textbook of Medical

Surgical Nursing. 10th ed. Philadelphia (PA): Lippincott Publishers;
2006.

Chintamani. Lewis’s Medical Surgical Nursing. 7 thed. New Delhi:

Elsevier limited; 2010.

Black M Joyce. Types. Treatment and Fracture Healing. Medical

Surgical Nursing.7th edition.
 ASSIGNMENT

• SOMOGYI EFFECT?????

• DAWN EFFECT?????