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Dr. Chavan P.R.
Pharm D
 Diabetes mellitus (DM) is a group of
metabolic disorders characterized by
hyperglycemia and abnormalities in
carbohydrate, fat, and protein metabolism.
 It results from defects in insulin secretion,
insulin sensitivity, or both.
 Chronic microvascular, macrovascular, and
neuropathic complications may ensue.
 Type 1 DM
 Type 2 DM
 Gestational DM
 LADA (Latent autoimmune diabetes in
adults )
 MODY (Maturity Onset Diabetes of the Young)
 Other
 Type 1 DM accounts for 5% to 10% of all
diabetes cases.
 It generally develops in childhood or early
adulthood and results from immune
mediated destruction of pancreatic β -cells,
resulting in an absolute deficiency of insulin.
 There is a long preclinical period (up to 9 to
13 years) marked by the presence of immune
markers when β -cell destruction is thought
to occur.
 Hyperglycemia - 80% to 90% of β cells
destruction.
 “honeymoon” phase
 autoimmunity - unknown,
 but the process is mediated by macrophages
and T lymphocytes with circulating
autoantibodies to various β -cell antigens
(e.g., islet cell antibody, insulin antibodies).
 Type 2 DM - 90% of DM cases and is usually
characterized by the presence of both insulin
resistance and relative insulin deficiency.
 Insulin resistance is manifested by increased
lipolysis and free fatty acid production,
increased hepatic glucose production, and
decreased skeletal muscle uptake of glucose.
 β -Cell dysfunction is progressive and
contributes to worsening blood glucose
control over time.
 Type 2 DM occurs when a diabetogenic
lifestyle (excessive calories, inadequate
exercise, and obesity) is superimposed upon
a susceptible genotype.
 Endocrine disorders (e.g., Acromegaly, cushing’s
syndrome),
 Gestational diabetes mellitus (GDM),
 Diseases of the exocrine pancreas
(e.g., Pancreatitis), and
 Medications (e.g., Glucocorticoids, pentamidine,
niacin, and α interferon). Infections- (e.g. CMV)
 Uncommon forms of immune mediated DM –(e.g.
Stiff man syndrome)
 Other genetic syndromes (e.g. Down’s syndrome,
turner’s syndrome)
 Impaired fasting glucose and impaired
glucose tolerance are terms used to describe
patients whose plasma glucose levels are
higher than normal but not diagnostic of DM
 These disorders are risk factors for
developing DM and cardiovascular disease
and are associated with the insulin-resistance
syndrome.
 Microvascular complications include
 retinopathy,
 neuropathy, and
 nephropathy.
 Macrovascular complications include
 coronary heart disease,
 stroke, and
 peripheral vascular disease.
 Individuals with type 1 DM are often
 thin and are prone to develop diabetic
ketoacidosis if insulin is withheld or under
conditions of severe stress with an excess of
insulin counterregulatory hormones.
 Between 20% and 40% of patients present
with diabetic ketoacidosis after several days
of polyuria, polydipsia, polyphagia, and
weight loss.
 TYPE 2 DIABETES MELLITUS
 Patients with type 2 DM are often
asymptomatic and may be diagnosed
secondary to unrelated blood testing.
 presence of complications - DM for several
years.
 Lethargy, polyuria, nocturia, and polydipsia
 significant weight loss is less common.
 Screening for type 2 DM - every 3 years in all
adults beginning at the age of 45.
 Testing should be considered at an earlier
age and more frequently in individuals with
risk factors (e.g., family history of DM,
obesity, signs of insulin resistance).
 • The recommended screening test is a
fasting plasma glucose (FPG).
 Normal FPG < 100 mg/dL (5.6 mmol/L).
 Impaired FPG - 100 to 125 mg/dL (5.6 to 6.9
mmol/L).
 Impaired glucose tolerance is diagnosed
when the 2-hour postload sample of the oral
glucose tolerance test is between 140 and
199 mg per dL (7.8 to 11.0 mmol/L). •
 Pregnant women should undergo risk
assessment for GDM at their first prenatal
visit and proceed with glucose testing if at
high risk (e.g., positive family history,
personal history of GDM, marked obesity, or
member of a high-risk ethnic group).
 Criteria for the Diagnosis of Diabetes Mellitus
 Symptoms + plasma glucose concentration
≥200 mg/dL (11.1 mmol/L) or
 Fastingc plasma glucose ≥126 mg/dL (7.0
mmol/L) or
 2-Hour postload glucose ≥200 mg/dL (11.1
mmol/L) during an OGTT
Biochemical Index ADA ACE and
AACE
Hemoglobin A1C <7% ≤6.5%
Preprandial plasma
glucose
90–130 mg/dL
(5.0–7.2 mmol/L)
<110 mg/
(6.1 mmol/L) dL
Postprandial plasma
glucose
<180 mg/dLb
(<10 mmol/L)
<140 mg/dL
(<7.8 mmol/L)
 The goals of therapy in DM are
 To ameliorate symptoms of hyperglycemia,
 Reduce the onset and progression of
microvascular and macrovascular
complications,
 Reduce mortality, and
 Improve quality of life.
 Desirable plasma glucose and glycosylated
hemoglobin (A1c)
Diabetes (2)

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Diabetes (2)

  • 2.  Diabetes mellitus (DM) is a group of metabolic disorders characterized by hyperglycemia and abnormalities in carbohydrate, fat, and protein metabolism.  It results from defects in insulin secretion, insulin sensitivity, or both.  Chronic microvascular, macrovascular, and neuropathic complications may ensue.
  • 3.  Type 1 DM  Type 2 DM  Gestational DM  LADA (Latent autoimmune diabetes in adults )  MODY (Maturity Onset Diabetes of the Young)  Other
  • 4.
  • 5.  Type 1 DM accounts for 5% to 10% of all diabetes cases.  It generally develops in childhood or early adulthood and results from immune mediated destruction of pancreatic β -cells, resulting in an absolute deficiency of insulin.  There is a long preclinical period (up to 9 to 13 years) marked by the presence of immune markers when β -cell destruction is thought to occur.
  • 6.  Hyperglycemia - 80% to 90% of β cells destruction.  “honeymoon” phase  autoimmunity - unknown,  but the process is mediated by macrophages and T lymphocytes with circulating autoantibodies to various β -cell antigens (e.g., islet cell antibody, insulin antibodies).
  • 7.  Type 2 DM - 90% of DM cases and is usually characterized by the presence of both insulin resistance and relative insulin deficiency.  Insulin resistance is manifested by increased lipolysis and free fatty acid production, increased hepatic glucose production, and decreased skeletal muscle uptake of glucose.
  • 8.  β -Cell dysfunction is progressive and contributes to worsening blood glucose control over time.  Type 2 DM occurs when a diabetogenic lifestyle (excessive calories, inadequate exercise, and obesity) is superimposed upon a susceptible genotype.
  • 9.  Endocrine disorders (e.g., Acromegaly, cushing’s syndrome),  Gestational diabetes mellitus (GDM),  Diseases of the exocrine pancreas (e.g., Pancreatitis), and  Medications (e.g., Glucocorticoids, pentamidine, niacin, and α interferon). Infections- (e.g. CMV)  Uncommon forms of immune mediated DM –(e.g. Stiff man syndrome)  Other genetic syndromes (e.g. Down’s syndrome, turner’s syndrome)
  • 10.  Impaired fasting glucose and impaired glucose tolerance are terms used to describe patients whose plasma glucose levels are higher than normal but not diagnostic of DM  These disorders are risk factors for developing DM and cardiovascular disease and are associated with the insulin-resistance syndrome.
  • 11.  Microvascular complications include  retinopathy,  neuropathy, and  nephropathy.  Macrovascular complications include  coronary heart disease,  stroke, and  peripheral vascular disease.
  • 12.  Individuals with type 1 DM are often  thin and are prone to develop diabetic ketoacidosis if insulin is withheld or under conditions of severe stress with an excess of insulin counterregulatory hormones.  Between 20% and 40% of patients present with diabetic ketoacidosis after several days of polyuria, polydipsia, polyphagia, and weight loss.
  • 13.  TYPE 2 DIABETES MELLITUS  Patients with type 2 DM are often asymptomatic and may be diagnosed secondary to unrelated blood testing.  presence of complications - DM for several years.  Lethargy, polyuria, nocturia, and polydipsia  significant weight loss is less common.
  • 14.
  • 15.  Screening for type 2 DM - every 3 years in all adults beginning at the age of 45.  Testing should be considered at an earlier age and more frequently in individuals with risk factors (e.g., family history of DM, obesity, signs of insulin resistance).
  • 16.  • The recommended screening test is a fasting plasma glucose (FPG).  Normal FPG < 100 mg/dL (5.6 mmol/L).  Impaired FPG - 100 to 125 mg/dL (5.6 to 6.9 mmol/L).  Impaired glucose tolerance is diagnosed when the 2-hour postload sample of the oral glucose tolerance test is between 140 and 199 mg per dL (7.8 to 11.0 mmol/L). •
  • 17.  Pregnant women should undergo risk assessment for GDM at their first prenatal visit and proceed with glucose testing if at high risk (e.g., positive family history, personal history of GDM, marked obesity, or member of a high-risk ethnic group).
  • 18.  Criteria for the Diagnosis of Diabetes Mellitus  Symptoms + plasma glucose concentration ≥200 mg/dL (11.1 mmol/L) or  Fastingc plasma glucose ≥126 mg/dL (7.0 mmol/L) or  2-Hour postload glucose ≥200 mg/dL (11.1 mmol/L) during an OGTT
  • 19. Biochemical Index ADA ACE and AACE Hemoglobin A1C <7% ≤6.5% Preprandial plasma glucose 90–130 mg/dL (5.0–7.2 mmol/L) <110 mg/ (6.1 mmol/L) dL Postprandial plasma glucose <180 mg/dLb (<10 mmol/L) <140 mg/dL (<7.8 mmol/L)
  • 20.  The goals of therapy in DM are  To ameliorate symptoms of hyperglycemia,  Reduce the onset and progression of microvascular and macrovascular complications,  Reduce mortality, and  Improve quality of life.  Desirable plasma glucose and glycosylated hemoglobin (A1c)