DIABETES MELLITUS
LAKSHMI E
M PHARM
PHARMACY PRACTICE
DIABETES MELLITUS
 Diabetes mellitus is a chronic disorder of
carbohydrate, protein and fat metabolism resulting
from insulin deficiency or abnormality in the use of
insulin
 It results from defects in insulin secretion, insulin
sensitivity, or both.
DIAGNOSIS
 Fasting blood glucose level
≥126 mg/dl
 Casual blood glucose level
≥ 200 mg/dl
 oral glucose tolerance test
75g
 Glycated haemoglobin
5.7-6.4 (prediabetes)
Types
 Type 1 Diabetes Mellitus
 Type 2 Diabetes Mellitus
 Gestational Diabetes
 Other types:
 LADA (Latent Autoimmune Diabetes in
Adults)
 MODY (maturity-onset diabetes of youth)
Secondary Diabetes Mellitus
TYPE 1 Diabetes Mellitus
 Was previously called insulin-dependent diabetes
mellitus (IDDM) or juvenile-onset diabetes.
 Type 1 diabetes develops when the body’s immune system
destroys pancreatic beta cells, the only cells in the body
that make the hormone insulin that regulates blood
glucose.
 This form of diabetes usually strikes children and young
adults, although disease onset can occur at any age.
 Type 1 diabetes may account for 5% to 10% of all
diagnosed cases of diabetes.
 Risk factors for type 1 diabetes may include autoimmune,
genetic, and environmental factors.
TYPE 2 DM
 Was previously called non-insulin-dependent
diabetes mellitus (NIDDM) or adult-onset diabetes.
 Type 2 diabetes may account for about 90% to 95% of
all diagnosed cases of diabetes.
 It usually begins as insulin resistance, a disorder in
which the cells do not use insulin properly. As the
need for insulin rises, the pancreas gradually loses its
ability to produce insulin.
cont….
 Type 2 diabetes is associated with older age, obesity,
family history of diabetes, history of gestational
diabetes, impaired glucose metabolism, physical
inactivity, and race/ethnicity.
 Type 2 diabetes is increasingly being diagnosed in
children and adolescents.
Type 1 & Type 2
Gestational diabetes
 A form of glucose intolerance that is diagnosed in
some women during pregnancy.
 During pregnancy, gestational diabetes requires
treatment to normalize maternal blood glucose levels
to avoid complications in the infant.
 After pregnancy, 5% to 10% of women with
gestational diabetes are found to have type 2 diabetes.
 Women who have had gestational diabetes have a
20% to 50% chance of developing diabetes in the next
5-10 years.
Other types of DM
 Other specific types of diabetes result from specific
genetic conditions (such as maturity-onset diabetes of
youth), surgery, drugs, malnutrition, infections, and
other illnesses.
 Such types of diabetes may account for 1% to 5% of all
diagnosed cases of diabetes.
 LADA (Latent Autoimmune Diabetes in
Adults)
 MODY (maturity-onset diabetes of youth)
Secondary Diabetes Mellitus
LADA Latent Autoimmune Diabetes in Adults (LADA) is a form of
autoimmune (type 1 diabetes) which is diagnosed in
individuals who are older than the usual age of onset of type 1
diabetes.
 About 80% of adults apparently with recently diagnosed Type
2 diabetes but with GAD auto-antibodies (i.e. LADA)
progress to insulin requirement within 6 years.
 The potential value of identifying this group at high risk of
progression to insulin dependence includes:
 the avoidance of using metformin treatment
 the early introduction of insulin therapy
MODY (maturity-onset diabetes of youth)
 MODY – Maturity Onset Diabetes of the Young
 MODY is a monogenic form of diabetes with an
autosomal dominant mode of inheritance:
 Mutations in any one of several transcription factors or in
the enzyme glucokinase lead to insufficient insulin release
from pancreatic ß-cells, causing MODY.
 Different subtypes of MODY are identified based on the
mutated gene.
 Originally, diagnosis of MODY was based on presence of
non-ketotic hyperglycemia in adolescents or young
adults in conjunction with a family history of diabetes.
Secondary DM
Secondary causes of Diabetes mellitus include:
 Acromegaly,
 Cushing syndrome,
 Thyrotoxicosis,
 Pheochromocytoma
 Chronic pancreatitis,
 Cancer
Drug induced hyperglycemia:
 Atypical Antipsychotics - Alter receptor binding characteristics,
leading to increased insulin resistance.
 Beta-blockers - Inhibit insulin secretion.
 Calcium Channel Blockers - Inhibits secretion of insulin by
interfering with cytosolic calcium release.
 Corticosteroids - Cause peripheral insulin resistance and
gluconeogensis.
 Fluoroquinolones - Inhibits insulin secretion by blocking ATP
sensitive potassium channels.
 Naicin - They cause increased insulin resistance due to increased
free fatty acid mobilization.
 Phenothiazines - Inhibit insulin secretion.
 Protease Inhibitors - Inhibit the conversion of proinsulin to insulin.
 Thiazide Diuretics - Inhibit insulin secretion due to hypokalemia.
They also cause increased insulin resistance due to increased free
fatty acid mobilization
Complications
EPIDEMIOLOGY
 Globally, an estimated 422 millon adults are living with
diabetes mellitus, according to the latest 2016 data
from WHO.
 Increases in the overall diabetes prevalence rates
largely reflect an increase risk factors for type 2,
notably greater longevity and being overweight or
obese.
ETIOLOGY
 Chronic hyperglycaemia with disturbances of
carbohydrate
 Fat and protein metabolism resulting from defects in
insulin secretion
 Insulin action
 The effects of diabetes mellitus include long–term
damage, dysfunction and failure of various organs.
Physical inactivity and weight gain leads
to diabetes mellitus.
Signs & Symptoms
Increased thirst (polydipsia)
Frequent urination (polyuria)
Hunger (polyphagia)
Fatigue
Blurred vision
Numbness or tingling in the feet or hands
Unexplained weight loss
Increase blood sugar/glucose level
Management
 Dietary management:
Don’t skip meals
Measure food accurately, do not estimate
Less added fat, fewer fatty foods and low
cholesterol.
Advise use of complex carbohydrates to help
stabilize blood sugar. Meal should include
more fibre and starch and fewer simple or
refined sugars.
Avoid concentrated sweets, high in sugar
(jellies, jams, cakes, ice creams)
cont….
 If taking insulin, eat extra food before periods of
vigorous exercise.
 Keep weight at normal level, obese diabetics should be
on a strict weight control program and should lose
weight.
Treatment algorithm
Diabetes mellitus presentation

Diabetes mellitus presentation

  • 1.
    DIABETES MELLITUS LAKSHMI E MPHARM PHARMACY PRACTICE
  • 2.
    DIABETES MELLITUS  Diabetesmellitus is a chronic disorder of carbohydrate, protein and fat metabolism resulting from insulin deficiency or abnormality in the use of insulin  It results from defects in insulin secretion, insulin sensitivity, or both.
  • 3.
    DIAGNOSIS  Fasting bloodglucose level ≥126 mg/dl  Casual blood glucose level ≥ 200 mg/dl  oral glucose tolerance test 75g  Glycated haemoglobin 5.7-6.4 (prediabetes)
  • 7.
    Types  Type 1Diabetes Mellitus  Type 2 Diabetes Mellitus  Gestational Diabetes  Other types:  LADA (Latent Autoimmune Diabetes in Adults)  MODY (maturity-onset diabetes of youth) Secondary Diabetes Mellitus
  • 8.
    TYPE 1 DiabetesMellitus  Was previously called insulin-dependent diabetes mellitus (IDDM) or juvenile-onset diabetes.  Type 1 diabetes develops when the body’s immune system destroys pancreatic beta cells, the only cells in the body that make the hormone insulin that regulates blood glucose.  This form of diabetes usually strikes children and young adults, although disease onset can occur at any age.  Type 1 diabetes may account for 5% to 10% of all diagnosed cases of diabetes.  Risk factors for type 1 diabetes may include autoimmune, genetic, and environmental factors.
  • 9.
    TYPE 2 DM Was previously called non-insulin-dependent diabetes mellitus (NIDDM) or adult-onset diabetes.  Type 2 diabetes may account for about 90% to 95% of all diagnosed cases of diabetes.  It usually begins as insulin resistance, a disorder in which the cells do not use insulin properly. As the need for insulin rises, the pancreas gradually loses its ability to produce insulin.
  • 10.
    cont….  Type 2diabetes is associated with older age, obesity, family history of diabetes, history of gestational diabetes, impaired glucose metabolism, physical inactivity, and race/ethnicity.  Type 2 diabetes is increasingly being diagnosed in children and adolescents.
  • 11.
    Type 1 &Type 2
  • 13.
    Gestational diabetes  Aform of glucose intolerance that is diagnosed in some women during pregnancy.  During pregnancy, gestational diabetes requires treatment to normalize maternal blood glucose levels to avoid complications in the infant.  After pregnancy, 5% to 10% of women with gestational diabetes are found to have type 2 diabetes.  Women who have had gestational diabetes have a 20% to 50% chance of developing diabetes in the next 5-10 years.
  • 14.
    Other types ofDM  Other specific types of diabetes result from specific genetic conditions (such as maturity-onset diabetes of youth), surgery, drugs, malnutrition, infections, and other illnesses.  Such types of diabetes may account for 1% to 5% of all diagnosed cases of diabetes.  LADA (Latent Autoimmune Diabetes in Adults)  MODY (maturity-onset diabetes of youth) Secondary Diabetes Mellitus
  • 15.
    LADA Latent AutoimmuneDiabetes in Adults (LADA) is a form of autoimmune (type 1 diabetes) which is diagnosed in individuals who are older than the usual age of onset of type 1 diabetes.  About 80% of adults apparently with recently diagnosed Type 2 diabetes but with GAD auto-antibodies (i.e. LADA) progress to insulin requirement within 6 years.  The potential value of identifying this group at high risk of progression to insulin dependence includes:  the avoidance of using metformin treatment  the early introduction of insulin therapy
  • 16.
    MODY (maturity-onset diabetesof youth)  MODY – Maturity Onset Diabetes of the Young  MODY is a monogenic form of diabetes with an autosomal dominant mode of inheritance:  Mutations in any one of several transcription factors or in the enzyme glucokinase lead to insufficient insulin release from pancreatic ß-cells, causing MODY.  Different subtypes of MODY are identified based on the mutated gene.  Originally, diagnosis of MODY was based on presence of non-ketotic hyperglycemia in adolescents or young adults in conjunction with a family history of diabetes.
  • 17.
    Secondary DM Secondary causesof Diabetes mellitus include:  Acromegaly,  Cushing syndrome,  Thyrotoxicosis,  Pheochromocytoma  Chronic pancreatitis,  Cancer
  • 18.
    Drug induced hyperglycemia: Atypical Antipsychotics - Alter receptor binding characteristics, leading to increased insulin resistance.  Beta-blockers - Inhibit insulin secretion.  Calcium Channel Blockers - Inhibits secretion of insulin by interfering with cytosolic calcium release.  Corticosteroids - Cause peripheral insulin resistance and gluconeogensis.  Fluoroquinolones - Inhibits insulin secretion by blocking ATP sensitive potassium channels.  Naicin - They cause increased insulin resistance due to increased free fatty acid mobilization.  Phenothiazines - Inhibit insulin secretion.  Protease Inhibitors - Inhibit the conversion of proinsulin to insulin.  Thiazide Diuretics - Inhibit insulin secretion due to hypokalemia. They also cause increased insulin resistance due to increased free fatty acid mobilization
  • 19.
  • 21.
    EPIDEMIOLOGY  Globally, anestimated 422 millon adults are living with diabetes mellitus, according to the latest 2016 data from WHO.  Increases in the overall diabetes prevalence rates largely reflect an increase risk factors for type 2, notably greater longevity and being overweight or obese.
  • 22.
    ETIOLOGY  Chronic hyperglycaemiawith disturbances of carbohydrate  Fat and protein metabolism resulting from defects in insulin secretion  Insulin action  The effects of diabetes mellitus include long–term damage, dysfunction and failure of various organs.
  • 23.
    Physical inactivity andweight gain leads to diabetes mellitus.
  • 25.
    Signs & Symptoms Increasedthirst (polydipsia) Frequent urination (polyuria) Hunger (polyphagia) Fatigue Blurred vision Numbness or tingling in the feet or hands Unexplained weight loss Increase blood sugar/glucose level
  • 26.
    Management  Dietary management: Don’tskip meals Measure food accurately, do not estimate Less added fat, fewer fatty foods and low cholesterol. Advise use of complex carbohydrates to help stabilize blood sugar. Meal should include more fibre and starch and fewer simple or refined sugars. Avoid concentrated sweets, high in sugar (jellies, jams, cakes, ice creams)
  • 27.
    cont….  If takinginsulin, eat extra food before periods of vigorous exercise.  Keep weight at normal level, obese diabetics should be on a strict weight control program and should lose weight.
  • 41.