Diabetes mellitus is a group of metabolic diseases characterized by hyperglycemia resulting from defects in insulin secretion, insulin action. Diabetes mellitus Hyperglycemia metabolism health Health

1. Diabetes Mellitus
Chetan Sharma
Pharm.D Scholar

2. What is Diabetes?
Diabetes mellitus is a group of metabolic
diseases characterized by hyperglycemia
resulting from defects in insulin secretion,
insulin action, or both. The chronic
hyperglycemia of diabetes is associated with
long-term damage, dysfunction, and failure of
various organs, especially the eyes, kidneys,
nerves, heart, and blood vessels.
● Metabolic disease
● Hyperglycemia
● Defect in insulin secretion
or insulin action , maybe
both

3. Diabetes Mellitus :
Type 1 and Type 2
● Type 1 diabetes is a chronic illness
characterized by the body’s inability to produce
insulin due to the autoimmune destruction of
the beta cells in the pancreas. Although onset
frequently occurs in childhood, the disease can
also develop in adults.
● Type 2 diabetes mellitus consists of an array of
dysfunctions characterized by hyperglycemia
and resulting from the combination of
resistance to insulin action, inadequate insulin
secretion, and excessive or inappropriate
glucagon secretion. Poorly controlled type 2
diabetes is associated with an array of
microvascular, macrovascular, and neuropathic
complications.
Type 1
● Chronic Illness
● Inability to produce insulin
due to autoimmune
destruction of beta Cells
● Usually in children but can
also occur in adults
Type 2
● Insulin Level Disbalance
● Muscle Resistance to insulin

4. CLASSICAL
SYMPTOMS OF DM
The 3 Ps of Diabetes :
● Polyuria
condition where the body urinates more than usual and
passes excessive or abnormally large amounts of urine
each time you urinate.
● Polyphagia
medical term for excessive or extreme hunger.
● Polydipsia
medical name for the feeling of extreme thirstiness.
● Weight loss
● Extreme Urination
● Extreme Hunger
● Extreme Thirst
● Loss of Weight

5. Diagnostic
Symptoms
Type 1 :
● Polyphagia
● Polyuria
● Polydipsia
● Unexplained weight loss
● Fatigue
● Blurred vision
● Nausea
● Diabetic Ketoacidosis (DKA)
Type 2 :
● All the same with Type 1 except DKA**
● Lower Extremity Paresthesia *
● Yeast infection (eg. Balanitis in men)
**DKA in type 2 patients is rare and less severe but can occur.
*Paresthesia refers to the numbness or tingling feeling in the
arm or legs . It can happen unexpectedly.
Diabetic ketoacidosis (DKA) is an
acute, major, life-threatening
complication of diabetes characterized
by hyperglycemia, ketoacidosis, and
ketonuria.

6. Diagnostic Tests Type 1 :
● A fasting plasma glucose (FPG) level ≥126
mg/dL (7.0 mmol/L), or
● A 2-hour plasma glucose level ≥200 mg/dL
(11.1 mmol/L) during a 75-g oral glucose
tolerance test (OGTT), or
● A random plasma glucose ≥200 mg/dL (11.1
mmol/L) in a patient with classic symptoms of
hyperglycemia or hyperglycemic crisis
Type 2 :
● Whether a hemoglobin A1c (HbA1c) level of
6.5% or higher should be a primary diagnostic
criterion or an optional criterion remains a point
of controversy.
● And The Same Test as Type 1
The main Difference with Type 1 and
Type 2 is that there is DKA present in
patients with Type 1 DM and it usually is
diagnosed in children .

7. Type 1 DM Etiology
Type 1A DM results from autoimmune
destruction of the beta cells of the pancreas
and involves both genetic predisposition
and an environmental component.
● No insulin Secretion
● Alteration of metabolism of
carbohydrates, Amino Acids and Fats
● Reduction in Glucose Metabolism
● Increase in Amino acid and Fat
Utilization Leading to Hyperglycemia
Rarer Condition than Type 2 DM.

8. Pathophysiology of Type 1 DM

9. Type 2 DM Etiology
The etiology of type 2 diabetes mellitus
appears to involve complex interactions
between environmental and genetic factors.
Presumably, the disease develops when a
diabetogenic lifestyle (ie, excessive caloric
intake, inadequate caloric expenditure,
obesity) is superimposed on a susceptible
genotype.
● Insulin Resistance
● Beta Cells Dysfunction
Obesity, Lifestyle and Diet takes a
huge responsibility for developing
type 2 DM .
Genetic factors also contribute
though.

10. Pathophysiology of Type 2 DM

11. Gestational
Diabetes
● Patients with gestational DM have onset or
discovery of glucose intolerance during
pregnancy.
● From 20 weeks onward, insulin resistance is
usually noted primarily in the skeletal muscles.
● However, sensitivity of adipose tissue to insulin
is unchanged.
● The goals of blood glucose control during
pregnancy are rigorous. Optimally pre-meal
glucose should be less than 100 mg/dL (5.5
mmol/L) and post-meal value not exceeding
130 mg/dL (7.2 mmol/L).
● It resolves after postpartum.
● Approximately, 50% who develop gestational
diabetes develop type-II later in life.

12. Treatment
Diet and Exercise
The treatment for DM is a combination of Nutritional
therapy, Exercise and Pharmacotherapy.
The nutrition should have carbohydrates, fats and
protein intake in the correct amount.
The caloric intake should be around 30Kcal/kg .
● Carbohydrate = 55% ~ 60% of total caloric
intake
● Fats = <30% of total caloric intake and for
overweight/obese patients should not exceed
<15% of total caloric intake.
● Proteins = 10% ~ 20% of total caloric intake

13. Treatment
Pharmacotherapy
The pharmacotherapy treatment of diabetes depends upon
the type of diabetes. The treatment of type 1 diabetes and
gestational diabetes is insulin. Type 1 diabetes requires
lifelong insulin replacement.
● Rapid acting insulin: The rapid acting insulin
preparations are regular insulin, insulin lispro and
insulin aspart.
● Intermediate acting insulin: The intermediate acting
insulin are NPH (isophane ) and lente insulin.
● Long acting insulin: The long acting insulins are
basal insulins. The two insulins available are insulin
glargine and insulin detremir.
Insulin delivery: The insulin is delivered in the
subcutaneous space by using insulin syringes or insulin
pens. The sites for injection are the anterior abdominal
wall, thighs ,buttocks and arms are the preferred sites for
subcutaneous injection. The initial insulin dosage is 0.5-1
unit /kg in patients of Type 1 diabetes.

14. Treatment
Oral Drug Therapy
Sulphonylureas : The sulphonylureas stimulate insulin
secretion by the beta cell of pancreas. They also
decrease hepatic glucose production; may improve
insulin sensitivity at the receptor. They include:
● Glimepiride (Tablet size 1 mg, 2 mg ,4 mg) daily
dose 1-6 mg once a day
● Glipizide (5 mg, 10 mg) daily dose 2.5-20 mg in
2-doses
● Glibenclamide (1.25 mg 2.5 mg 5 mg) daily
dose 2.5-20 in 1-2 daily dose
● Gliclazide (40, 80 mg) daily dose is 40-240 mg
in two doses
Biguanides : Metformin is a biguanide that has insulin
sensitizing properties. It may be used as monotherapy
or in combination with other classes of agents or
insulin.

15. Treatment
Oral Drug Therapy
Thiazolidinediones: They enhance tissue sensitivity to
insulin in muscle through activation of intracellular
receptors.They require the presence of insulin for
action. These drugs cause increase in weight and
increase of subcutaneous fat. They are
contraindicated in people with congestive heart failure
and liver disease. They require monitoring of the liver
enzymes every 6 months. These drugs can be used as
monotherapy or in combination with sulfonylureas and
metformin.
● Rosiglitazone (2-8 mg daily)
● Pioglitazone ( 15-30 mg daily)

16. Treatment
A Hb1Ac Test Above 6.5% is
indicative of DM.
Depending upon patient :
● Glycemic Control
● Insulin Therapy
● Diet and Exercise plan

17. Treatment

18. References ● Type 1 Diabetes Mellitus
https://emedicine.medscape.com/article/117739-
overview#a1
● Type 2 Diabetes Mellitus
https://emedicine.medscape.com/article/117853-
overview#a1
● National health mission guidelines
https://www.nhm.gov.in/images/pdf/guidelines/nrhm
-guidelines/stg/diabetes-mellitus.pdf