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Presented By :
Dr Sangeeta Sunil Bhujbal
Lecturer
College Of Nursing,
B.J.Govt.Medical .College
Sassoon General Hospital.
Pune.(Maharashtra)
Diabetes mellitus is a group of
metabolic diseases characterized by
increased level of glucose in the
blood resulting from defects in
insulin, secretion , insulin action or
both.
(ADA)
CLASSIFICATION
1. Type-I-IDDM.
2. Type II-NIDDM.
3. Gestational Diabetes.
4. DM associated with other
condition or syndrome.
 Type-I-IDDM –
Inadequate amount of insulin are produced
by pancreas resulting in insulin deficiency &
so patient need for insulin injection to control
the blood.
 Type-II-(NIDDM)
Result from decrease in the sensitivity of
the cell to insulin & a decrease in amount in
amount of insulin produced.
 Gestation-DM –
Person have onset of glucose abnormality
during pregnancy.
ETIOLOGY
1) Type-I
A) Genetic factors- people do not inherit type I
diabetes itself, they inherit a genetic
predisposition for tendency towards developing
Type-I diabetes.
B) Immunological factor- In Type-I diabetes there
is evidence of an auto immune response. This is
an abnormal in body, responding to these tissues
as if they are foreign auto antibodies against
itself cells & against endogenous ( Internal
insulin)
C) Environmental factors- certain viruses or
toxins may precipitate the auto immune process
that leads to beta cell destruction.
ETIOLOGY
2.Type-II Diabetes
A) Age- ( Insulin resistance) tends to occur age
over 65 years.)
B) Obesity.
C) Family History.
D) Ethnic Group- Which are more susceptible
than blacks.
ANATOMY & PHYSIOLOGY
Type-I Pathophysiology
Due to food eaten cannot be
stored but instead remains in
the blood stain
Post pradeal (after
medication) Hyperglycemia
Due to unchecked
production by the liver
Fasting hyper Glycemia
Deficiency in production of insulin by pancreatic
beta cells
In addition the breakdown of fat occurs , resulting in
an increased production of ketone bodies. Excess
ketone resulting ketoacidosis (DKA)
Type-II Pathophysiology
Impaired insulin
secretion
Gastrointestinal
absorption of
glucose
Increased basel
hepatic glucose
production
Decreased insulin
stimulated
glucose uptake.
Hyperglycemia
Assessing the patient with
Diabetes
1) History –
 Symptoms related to the diagnose of
DM
 Results of blood glucose monitoring
 Status symptoms & management of
chronic complications of DM
 Use of tobacco alcohol
 Life style cultural psychological &
economic factors that may affect DM
treatment.
Physical Examination
 Blood pressure (seating, Standing)
 Body Mass Index (Weight/ Height in cm x 100)
 Fundo scopic examination
 Foot examination
 Skin examination
 Neurological examination
 Oral examination
Diagnostic Evaluation
1. Fasting plasma glucose level-above 140 mg/dl or
Random Plasma glucose level over 200 mg/dl
2. Glucose tolerance Test
3. HgbA1 (A1C)
4. Test for microalbuminurea
5. Serum creatinine level
6. Urine analysis
7. Electrocardiogram
Signs & Symptoms
Three Ps
1) Polyurea ( Increased urination)
2) Plydispsia ( Increased thirst)
3) Polyphagia( Increased appetite)
Other S/S
 Glycosuria
 Electrolyte loss
 Fatigue & weakness
 Tingling or numbness in handsor feet.
 Skin lesion or wound that are slow to
heal.
 Dry Skin
 Recurrent infection.
If diabetic Ketoacidosis
 Sudden weight loss
 Nausea
 Vomiting
 Abdominal pain
 Fruit order of breath
 Hypertension
 Even comma or death.
Medical Treatment
Agent Starting
Dose
Max.
Dose
Duration of
action
Freq. Metabolism
First Generation
1)Tolbutamide 0.5 mg 2-3 gm 6-12 hrs 1-3 days By liver to inactive
product
2)Tolazamide 100 mg 1.0 gm 12-24 hrs 1-2 days By liver to active &
inactive products
requiring renal route
3)Acetohexami
de
250 mg 1.5 gm 12-18 hrs 1-2 days Same tolazamide
4)Chloropropa
mide
100-250
mg
0.5gm 50 hrs 1 /day Approx 70% by liver to
less active product by
renal route imperative
Second Generation- Biguonides
1) Glyburide 2.5-
5.0mg
20 mg 10-20 hrs 1-2/days By liver to mostly insert
product
2) Glipizide 2.5-5.0
mg
40 mg 12-24 hrs 1-2 days By liver to insert
products
Types of Insulin
Action Preparation Appea
rance
Action in
Hours
Onset Peak Duration
Short Insulin injection Regular
Insulin
Clear ½-1 2-4 6-8
Insulin, Zinc suspension,
semilente Insulin
Cloudy ½-1 2-8 8-16
Intermedi
ate
Isophane Insulin suspension,
NPH Insulin
Cloudy 1-2 6-12 18-26
Insulin, Zinc suspension,
Ente Insulin
Cloudy 1-3 6-12 18-26
Long Protamine zinc insulin ,
suspension protamine, Zinc
Insulin
Cloudy 4-6 18-24 28-36
Extended Insulin Zinc
suspension, Ultrotente Insulin
Cloudy 4-6 14-24 36
Premixed 70% NPH, 30% Regular Cloudy ½ 2-12 18-26
Complications
A) Acute Complications-
1) Hypoglycemia
2) Hyperglycemia may lead to
* Diabetic ketoacodosis in type-I DM
* Hyperosmolar, non ketotic syndrome
in
Type-II Diabetes
B) Chronic Complications-
1) Macrovasclar Disease
a) Coronary artery disease
b) Cerebro vascular disease
c) Peripheral vascular disease
2) Micro vascular Disease
a) Retinopathy
b) Nephropathy
c) Neuropathy
Management of DM
Diet
Exercise
Monitoring
Meditation
Education
Diabetes
Management
Nutritional
Elements
Quantity
Calories Ideal Weight x 28
Cal/ Kg
Carbohydrate 45% to 60%
Protein 0.8gm/Kg of body
weight
Fat
1)Polyunsatu
rated fat
2)Saturated
fat
3)Cholesterol
60% to 8%
10%
< 300 mg/ day
Fibre 40 gm/ day
Sodium <= 3000mg/day
EXERCISE
I) Benefits of Exercise
 Improve Insulin Insensitivity
 Lower blood glucose during & after exercise
 Improves lipid profile
 Improves some hypertension
 Increase energy expenditure
 Promotes cardiovascular fitness
 Increased strength & flexibility
 Improves sense of well being.
Exercise Type-Aerobic
III) Monitoring
 Self monitoring of blood glucose
 Urine glucose
 Urine testing for ketones.
Health Education
 Teach the client to identify clinical
manifestations & how to manage
hypoglycemia.
 How to check of insulin reaction
 Tell patient avoid excessive exercise
 Take food soon after insulin, do not delay.
 Teach the client about diet & insulin dose.
 Explain the patient to carry Identification
card & sugar.
 Explain about the prevention of long term
complications of diabetes & develop
positive self concept & a feeling of control.
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Ppt presentation on diabetes mellitus

  • 1. Presented By : Dr Sangeeta Sunil Bhujbal Lecturer College Of Nursing, B.J.Govt.Medical .College Sassoon General Hospital. Pune.(Maharashtra)
  • 2. Diabetes mellitus is a group of metabolic diseases characterized by increased level of glucose in the blood resulting from defects in insulin, secretion , insulin action or both. (ADA)
  • 3. CLASSIFICATION 1. Type-I-IDDM. 2. Type II-NIDDM. 3. Gestational Diabetes. 4. DM associated with other condition or syndrome.
  • 4.  Type-I-IDDM – Inadequate amount of insulin are produced by pancreas resulting in insulin deficiency & so patient need for insulin injection to control the blood.  Type-II-(NIDDM) Result from decrease in the sensitivity of the cell to insulin & a decrease in amount in amount of insulin produced.  Gestation-DM – Person have onset of glucose abnormality during pregnancy.
  • 5. ETIOLOGY 1) Type-I A) Genetic factors- people do not inherit type I diabetes itself, they inherit a genetic predisposition for tendency towards developing Type-I diabetes. B) Immunological factor- In Type-I diabetes there is evidence of an auto immune response. This is an abnormal in body, responding to these tissues as if they are foreign auto antibodies against itself cells & against endogenous ( Internal insulin) C) Environmental factors- certain viruses or toxins may precipitate the auto immune process that leads to beta cell destruction.
  • 6. ETIOLOGY 2.Type-II Diabetes A) Age- ( Insulin resistance) tends to occur age over 65 years.) B) Obesity. C) Family History. D) Ethnic Group- Which are more susceptible than blacks.
  • 8. Type-I Pathophysiology Due to food eaten cannot be stored but instead remains in the blood stain Post pradeal (after medication) Hyperglycemia Due to unchecked production by the liver Fasting hyper Glycemia Deficiency in production of insulin by pancreatic beta cells In addition the breakdown of fat occurs , resulting in an increased production of ketone bodies. Excess ketone resulting ketoacidosis (DKA)
  • 9. Type-II Pathophysiology Impaired insulin secretion Gastrointestinal absorption of glucose Increased basel hepatic glucose production Decreased insulin stimulated glucose uptake. Hyperglycemia
  • 10. Assessing the patient with Diabetes 1) History –  Symptoms related to the diagnose of DM  Results of blood glucose monitoring  Status symptoms & management of chronic complications of DM  Use of tobacco alcohol  Life style cultural psychological & economic factors that may affect DM treatment.
  • 11. Physical Examination  Blood pressure (seating, Standing)  Body Mass Index (Weight/ Height in cm x 100)  Fundo scopic examination  Foot examination  Skin examination  Neurological examination  Oral examination
  • 12. Diagnostic Evaluation 1. Fasting plasma glucose level-above 140 mg/dl or Random Plasma glucose level over 200 mg/dl 2. Glucose tolerance Test 3. HgbA1 (A1C) 4. Test for microalbuminurea 5. Serum creatinine level 6. Urine analysis 7. Electrocardiogram
  • 13. Signs & Symptoms Three Ps 1) Polyurea ( Increased urination) 2) Plydispsia ( Increased thirst) 3) Polyphagia( Increased appetite) Other S/S  Glycosuria  Electrolyte loss  Fatigue & weakness  Tingling or numbness in handsor feet.  Skin lesion or wound that are slow to heal.  Dry Skin  Recurrent infection. If diabetic Ketoacidosis  Sudden weight loss  Nausea  Vomiting  Abdominal pain  Fruit order of breath  Hypertension  Even comma or death.
  • 14. Medical Treatment Agent Starting Dose Max. Dose Duration of action Freq. Metabolism First Generation 1)Tolbutamide 0.5 mg 2-3 gm 6-12 hrs 1-3 days By liver to inactive product 2)Tolazamide 100 mg 1.0 gm 12-24 hrs 1-2 days By liver to active & inactive products requiring renal route 3)Acetohexami de 250 mg 1.5 gm 12-18 hrs 1-2 days Same tolazamide 4)Chloropropa mide 100-250 mg 0.5gm 50 hrs 1 /day Approx 70% by liver to less active product by renal route imperative Second Generation- Biguonides 1) Glyburide 2.5- 5.0mg 20 mg 10-20 hrs 1-2/days By liver to mostly insert product 2) Glipizide 2.5-5.0 mg 40 mg 12-24 hrs 1-2 days By liver to insert products
  • 15. Types of Insulin Action Preparation Appea rance Action in Hours Onset Peak Duration Short Insulin injection Regular Insulin Clear ½-1 2-4 6-8 Insulin, Zinc suspension, semilente Insulin Cloudy ½-1 2-8 8-16 Intermedi ate Isophane Insulin suspension, NPH Insulin Cloudy 1-2 6-12 18-26 Insulin, Zinc suspension, Ente Insulin Cloudy 1-3 6-12 18-26 Long Protamine zinc insulin , suspension protamine, Zinc Insulin Cloudy 4-6 18-24 28-36 Extended Insulin Zinc suspension, Ultrotente Insulin Cloudy 4-6 14-24 36 Premixed 70% NPH, 30% Regular Cloudy ½ 2-12 18-26
  • 16. Complications A) Acute Complications- 1) Hypoglycemia 2) Hyperglycemia may lead to * Diabetic ketoacodosis in type-I DM * Hyperosmolar, non ketotic syndrome in Type-II Diabetes B) Chronic Complications- 1) Macrovasclar Disease a) Coronary artery disease b) Cerebro vascular disease c) Peripheral vascular disease 2) Micro vascular Disease a) Retinopathy b) Nephropathy c) Neuropathy
  • 18. Nutritional Elements Quantity Calories Ideal Weight x 28 Cal/ Kg Carbohydrate 45% to 60% Protein 0.8gm/Kg of body weight Fat 1)Polyunsatu rated fat 2)Saturated fat 3)Cholesterol 60% to 8% 10% < 300 mg/ day Fibre 40 gm/ day Sodium <= 3000mg/day
  • 19. EXERCISE I) Benefits of Exercise  Improve Insulin Insensitivity  Lower blood glucose during & after exercise  Improves lipid profile  Improves some hypertension  Increase energy expenditure  Promotes cardiovascular fitness  Increased strength & flexibility  Improves sense of well being. Exercise Type-Aerobic III) Monitoring  Self monitoring of blood glucose  Urine glucose  Urine testing for ketones.
  • 20. Health Education  Teach the client to identify clinical manifestations & how to manage hypoglycemia.  How to check of insulin reaction  Tell patient avoid excessive exercise  Take food soon after insulin, do not delay.  Teach the client about diet & insulin dose.  Explain the patient to carry Identification card & sugar.  Explain about the prevention of long term complications of diabetes & develop positive self concept & a feeling of control.