Pharmacotherapy in Diabetes Mellitus

PHARMACOTHERAPY IN
DIABETES MELLITUS
PREPARED BY:
Dipendra Khadka
B. Pharmacy 3rd Year
Roll no: 10
CONTENTS
 Introduction to Diabetes Mellitus
 Classification of DM
 Comparison between Type I and Type II diabetes
 Pathogenesis
 Clinical features
 Complications
 Laboratory Investigation
 Goals
 Management of DM
Treatment for Type I DM
Treatment for Type II DM
• Oral Hypoglycaemic Drugs (OHD)
khadkadipendra2015@gmail.com 10/13/2020 2
DIABETES MELLITUS (DM)
 Isa clinical syndrome characterized by
hyperglycemia due to absolute or deficiency of
insulin.
 According to WHO, DM is a heterogeneous
metabolic disorder characterized by common

features of chronic hyperglycemia with
disturbance of carbohydrate, fat and protein
metabolism.
CLASSIFICATION OF DM
According to American Diabetes Association
(ADA):
i. Type I Diabetes Mellitus : Insulin
dependent diabetes mellitus (IDDM)
ii. Type II Diabetes Mellitus: Non- Insulin
dependent diabetes mellitus (NIDDM)
iii. Gestational Diabetes
iv. Diabetes due to other causes.
◦ Eg: Genetic defect, Medication induced
COMPARISON BETWEEN TYPE I AND
TYPE II DIABETES
S.N VARIABLES TYPE I TYPE II
1. Age of onset Usually occurs in Frequently over age of 35
children or young adults
2. Nutritional status at Frequently Usually presence of Obesity

time of onset Undernourished
3. Prevalence 5 to 10% of diagnosed 90 to 95% of diagnosed diabetes

diabetes
4. Genetic Moderate Very strong

Pre-disposition
5. Defect or Deficiency β- cells are destroyed, Inability of β- cells to produce
eliminating the appropriate quantities of insulin,
production of insulin insulin resistance, other defect.
5
PATHOGENESIS
Depending upon etiology of DM,
hyperglycemia is due to:
Reduced insulin secretion
Decreased glucose by the body
Increased glucose production
CLINICAL FEATURES
 Weight loss
 Dryness of mouth and throat
 Polyuria
 Polydipsia
 Polyphagia
 Fatigue
COMPLICATIONS
 Retinopathy
 Nephropathy
 Neuropathy
 Myocardial infraction
 Ketoacidosis -Type I
 Hyperglycemia Osmolar Non- Ketotic
Coma- Type II
LABORATORY INVESTIGATION
1. Urine analysis: Urine test for glucose,
ketone bodies.
2. Blood analysis for:
 Fasting Plasma glucose
 Glucose Tolerance test
 Random Plasma glucose
3. Glucosylated haemoglobin
4. Blood lipid profile
5. Renal function
GOALS
Goals of THERAPY IN DIABETES MELLITUS
are directed toward attaining
Normoglycemia, reducing the onset and
progression of retinopathy, nephropathy,
and neuropathy complications, intensive
therapy for associated cardiovascular risk
factors, and improving quality and
quantity of life.
MANAGEMENT OF DM
 Discipline in life style, sleeping, walking,
exercise etc..
 Restricted diet i.e. sugar, sweet
 Drugs- Oral Hypoglycemic Drug or Insulin
TREATMENT FOR TYPE I-DM
 The goal in administering Insulin to Type I
diabetes is to control hyperglycemia, avoid
ketoacidosis and maintain acceptable levels of
glycosylated haemoglobin.
 Continuous subcutaneous insulin infusion-
also called the insulin pump which is another

method of insulin delivery.
TREATMENT FOR TYPE II-DM
 Currently,
Six classes of oral agents are
approved for the treatment of Type II DM
Oral
Hypoglycaemic
Drugs (OHD)
SULFONYLUREAS
1. First Generation: Carbutamide,

Tolbutamide, Chlorpropamide.
2. Second Generation: Glyburide, Glipizide,
Glyclazide, Glibornuride
MOA
 The primary MOA of Sulfonylureas is to stimulate
the release of insulin.
Sulfonylureas interact with receptor of pancreatic β- cells
Block ATP-sensitive potassium channel
Leads the opening of voltage sensitive Ca- channel
Produce infux of Ca
Results in β-cells production of insulin

BIGUANIDES- Metformin, Phenformin
 Metformin enhances insulin sensitivity of both
hepatic and peripheral tissue. It is therefore
considered as insulin sensitizer.
 Metformin has approximately 50% to 60% oral
bioavailability
Low lipid solubility
Volume of distribution that approx body water
 Phenformin was removed from the marked in
the 1970’s because of an association with lactic
acidosis.
α-GLUCOSIDASE INHIBITORS
 α-Glucosidase inhibitors competitively inhibit
enzymes (i.e maltase, isomaltase, sucrase,
and glucoamylase) in the small intestine,
delaying the breakdown of sucrose and
complex carbohydrates.
THIAZOLIDINEDIONES
 TZDs work by binding to the peroxisome
proliferator-activated receptor-γ (PPAR-γ),
which are primarily located on fat cells and
vascular cells.
 TZDs enhance insulin sensitivity at muscle,
liver, and fat tissues indirectly. TZDs cause

preadipocytes to differentiate into mature fat
cells in subcutaneous fat stores.
GLINIDES- Meglitinide, Repaglinide, Nateglinide
 Theyare prandile insulin releaser that

stimulate the rapid insulin secretion.
DPP -IV (Dipeptidyl Peptidase-IV) Inhibitors
 Suppress the degradation of a variety of

bioactive peptides, including glucagon-like
peptide-1.
 DPP-IV inhibitors partially reduce the
inappropriately elevated glucagon and

stimulate glucose-dependent insulin
secretion.
 A combination of sitagliptin and metformin
was approved in 2007 and also indicated to

improve glycemic.
REFERENCES
 Inzucchi SE. Oral Antihyperglycemic Therapy
for Type 2 Diabetes Scientific Review. The
Journal of the American Medical Association
2002;287:360-372.
 DeWitt DE., Hirsch IB. Outpatient Insulin
Therapy in Type 1 and Type 2 Diabetes

Mellitus. The Journal of the American Medical
Association 2003;289(17)
 https://drive.google.com/file/d/0Bz7qbN2P
wThAY3dkZk9FSXhESFU/edit?pli=1
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PHARMACOTHERAPY IN

metabolic disorder characterized by common

2. Nutritional status at Frequently Usually presence of Obesity

3. Prevalence 5 to 10% of diagnosed 90 to 95% of diagnosed diabetes

4. Genetic Moderate Very strong

also called the insulin pump which is another

1. First Generation: Carbutamide,

the release of insulin.

Sulfonylureas interact with receptor of pancreatic β- cells

Block ATP-sensitive potassium channel

Leads the opening of voltage sensitive Ca- channel

Results in β-cells production of insulin

liver, and fat tissues indirectly. TZDs cause

 Theyare prandile insulin releaser that

 Suppress the degradation of a variety of

inappropriately elevated glucagon and

was approved in 2007 and also indicated to

Therapy in Type 1 and Type 2 Diabetes

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