Diabetes mellitus yashwant kumar.
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Diabetes Mellitus TYPE 1
BY
YASHWANT KUMAR
GROUP -8.
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Diabetes Mellitus ¨ The disease is characterized by an absolute
deficiency of insulin caused by an autoimmune attack on the β cells of the pancreas.
¨ About 10% of the ten million diabetics in USA has type 1 diabetes, only (2/3)is diagnosed.
¨ Complication: stroke, heart attack, kidney disease, eye disease and nerve damage.
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Diabetes – Insulin(synthesis, storage, secretion)
¨ insulin mRNA is translated as a single chain precursor called preproinsulin
¨ removal of signal peptide during insertion into the endoplasmic reticulum generates proinsulin
¨ Produced within the pancreas by β cells islets of Langerhans
¨ Within the endoplasmic reticulum, proinsulin is exposed to several specific endopeptidases which excise the C peptide, thereby generating the mature form of insulin
¨ Stored as β granules
Zn
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Diabetes – Insulin(Biochemical Role)
-Tyrosine Kinase receptors are the locks in which the insulin key fits- Involved in signal transduction(insulin hormone being 1st messenger)
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ALTERED CHO METABOLISM
Insulin
Glucose Utilization +
Glycogenolysis
Hyperglycemia
Glucosuria¯ (osmotic diuresis)
¯ Polyuria*(and electrolyte imbalance)
Polydipsia*
* Hallmark symptoms of diabetes
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ALTERED PROTEIN METABOLISM
Insulin
Protein Catabolism
Gluconeogenesis(amino acids glucose)
Hyperglycemia
Weight Loss and Fatigue
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ALTERED FAT METABOLISM
Insulin
Lipolysis
Free fatty acids + ketones
Acidosis + Weight Loss
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Type 1 Diabetes MellitusType 1 Diabetes Mellitus
¨ Formerly known as “juvenile onset” or “insulin dependent” diabetes
¨ Most often occurs in people under 30 years of age
¨ Peak onset between ages 11 and 13
¨ Formerly known as “juvenile onset” or “insulin dependent” diabetes
¨ Most often occurs in people under 30 years of age
¨ Peak onset between ages 11 and 13
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Type 1 Diabetes Mellitus
Etiology and Pathophysiology
Type 1 Diabetes Mellitus
Etiology and Pathophysiology
¨ Progressive destruction of pancreatic cells
¨ Auto antibodies cause a reduction of 80% to 90% of normal cell function before manifestations occur
¨ Progressive destruction of pancreatic cells
¨ Auto antibodies cause a reduction of 80% to 90% of normal cell function before manifestations occur
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Type 1 Diabetes Mellitus
Etiology and Pathophysiology
Type 1 Diabetes Mellitus
Etiology and Pathophysiology
¨ Causes:–Genetic predisposition–Exposure to a virus
¨ Causes:–Genetic predisposition–Exposure to a virus
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Type 1 Diabetes Mellitus
Onset of Disease
Type 1 Diabetes Mellitus
Onset of Disease
¨ Manifestations develop when the pancreas can no longer produce insulin–Rapid onset of symptoms–Present at ER with impending
or actual ketoacidosis
¨ Manifestations develop when the pancreas can no longer produce insulin–Rapid onset of symptoms–Present at ER with impending
or actual ketoacidosis
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Type 1 Diabetes Mellitus
Onset of Disease
Type 1 Diabetes Mellitus
Onset of Disease
¨ Weight loss¨ Polydipsia (excessive thirst)¨ Polyuria (frequent urination)¨ Polyphagia (excessive hunger)¨ Weakness and fatigue¨ Ketoacidosis
¨ Weight loss¨ Polydipsia (excessive thirst)¨ Polyuria (frequent urination)¨ Polyphagia (excessive hunger)¨ Weakness and fatigue¨ Ketoacidosis
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Type 1 Diabetes Mellitus
Onset of Disease
Type 1 Diabetes Mellitus
Onset of Disease
¨ Diabetic ketoacidosis (DKA)–Life-threatening complication of Type 1 DM–Occurs in the absence of insulin–Results in metabolic acidosis
¨ Diabetic ketoacidosis (DKA)–Life-threatening complication of Type 1 DM–Occurs in the absence of insulin–Results in metabolic acidosis
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Clinical ManifestationsType 1 Diabetes MellitusClinical ManifestationsType 1 Diabetes Mellitus
¨ Polyuria¨ Polydipsia¨ Polyphagia¨ Weight loss
¨ Polyuria¨ Polydipsia¨ Polyphagia¨ Weight loss
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DIFFERENCE
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Type 1 Diabetes Mellitus Diagnostic Studies¨ Fasting plasma glucose level 7 mmol/L
¨ Random plasma glucose level 11.1 mmol/L plus symptoms
¨ mmol/L 2 hr post challenge
¨ Hemoglobin A1C test (glycosylated Hgb)– Reflects amount of glucose attached to Hgb over life of RBC– Indicates overall glucose control over previous 90 – 120 days
¨ Impaired Glucose Tolerance Test – patient is “challenged” with glucose load. Patient should be able to maintain normal BG. Diabetes if BG > 11.1
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Diabetes MellitusDrug Therapy: Insulin
¨ Exogenous insulin:
–Required for all patient with type 1 DM.
¨ Types of insulin–Human insulin
• Most widely used type of insulin• Cost-effective• Likelihood of allergic reaction
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Diabetes MellitusDrug Therapy: Insulin
– Insulins differ in regard to onset, peak action, and duration
–Different types of insulin may be used for combination therapy
– Rapid-acting: Lispro– *Short-acting: Regular– *Intermediate-acting: NPH or Lente– Long-acting: Ultralente, Lantus
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Injection Sites
Fig. 47-5
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Diabetes MellitusDrug Therapy: Insulin¨ Insulin delivery methods
– Ordinary SQ injection– Insulin pen
• preloaded with insulin; “dial” the dose– Insulin pump
• Continuous “basal” infusion. At mealtime, user programs to deliver “bolus” infusion that correlates with amount of CHOs ingested. Allows tight control and greater flexibility with meals and activity
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Diabetes MellitusDrug Therapy: Insulin¨ Insulin delivery methods
– Intensive insulin therapy• Multiple daily injects and frequent SMBG
¨ Problems with insulin therapy– Hypoglycemia (BS < 3.9 mmol/L)
• Due to too much insulin in relation to glucose availability
– Allergic reactions • Local inflammatory reaction– Lipodystrophy
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Diabetes MellitusNutritional Therapy¨ Exercise
–Essential part of diabetes management– Increases insulin sensitivity–Lowers blood glucose levels–Decreases insulin resistance
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Diabetes MellitusPancreas Transplantation¨ Used for patients with type 1 DM who
have end-stage renal disease and who have had or plan to have a kidney transplant
¨ Eliminates the need for exogenous insulin
¨ Can also eliminate hypoglycemia and hyperglycemia
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Diabetes – Oral Medications
¨ Sulfonylureas¨ Biguanides¨ Sulfonylureas and biguanide combination
drugs¨ Thiazolidinediones¨ Alpha-glycosidase inhibitors¨ Meglitinides
6 Classes :
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Thank You