Treatment for Type I DM

    Cards (34)

    • What is the main treatment for DM type I?
      Exogenous insulin
    • What is insulin?
      Insulin is a peptide hormone produced in the pancreas within the beta cells of islets of Langerhans
    • What is the composition of insulin?
      Two peptide chains (A & B) connected by sulfide bonds
    • What does basal insulin secretion indicate?
      • Administered to mimic basal insulin production
      • Only subcutaneous administration
      • Once or twice daily
    • What does bolus insulin level indicate?
      • Administered to mimic the prandial release of insulin
      • Subcutaneous or intravenous administration
      • Rapidly lowers blood glucose
      • Administered 3 times per day 20-30 mins prior to a meal
    • What is the mechanism of insulin synthesis?
      Insulin gene transcription and translation in the rER of pancreatic β-cellspreproinsulin (precursor protein)
      Signal proteases remove the signal peptide of preproinsulin → proinsulin
      Protein folding and formation of one disulfide bridge in the α-chain and two disulfide bridges between the α-chain and β-chain
      Proinsulin is transported to the Golgi apparatuspackaged in membrane-bound secretory granules with proprotein convertases
      Proinsulin is cleaved by proteasesmature insulin and C-peptide
      Secretion of insulin and C-peptide via exocytosis
    • What is the mechanism of action of insulin?
      Enzyme-linked receptors
      Secretion pathway
      • Stimulated by an increase in blood glucose
      • Glucose enters the pancreatic B-cells via GLUT2 transporters & is metabolized to generated ATP
      • Intracellular ATP binds & blocks ATP-sensitive K+channels, increasing the intracellular K+ conc. & raising membrane potential (depolarization occurs)
      • Voltage gated Ca2+ channels opens & Ca2+ enters the pancreatic B-cells
      • Increased intracellular Ca2+ triggers the fusion of insulin-containing secretory granules to the cell membrane
      • Exocytosis of insulin into the bloodstream
    • What are the target organs of insulin?
      • Liver
      • Adipose tissue
      • Muscles
    • What are the effects of insulin from the lowering blood glucose POV?
      • Facilitates glucose uptake by peripheral tissues
      • Stimulates glycogenesis
      • Inhibits glycogenolysis
    • What are the effects of insulin from the fat-sparing effect?
      • Promotes lipogenesis
      • Inhibits lipolysis
    • What are the effects of insulin from the anabolic effect POV?
      • Stimulates amino acids by tissue
      • Increases protein synthesis
      • Inhibits proteolysis
    • What are the type of insulin preparations?
      Human insulins
      • Humulin R-short acting
      • Isophane (NPH,Protamine) & Lente (Zinc)-Intermediate acting
      Insulin analogues
      • Lispro-Ultrashort acting
      • Glargine-Long acting
      Mixed insulins
    • What are the characteristics of human insulins?
      • Have the same amino acid sequence
      • Produced by human recombinant DNA tehnology with genetically altered E.Coli strains
    • What are the benefits of human insulins comapred to animal insulins?
      • Less allergic reactions
      • Less insulin resistance
      • Less local adverse drug reactions at the site of injections
    • What are the characteristics of insulin analogues?
      • Genetic engineered altered insulin
      • Has modified pharmacokinetics but performs the same pharmacodynamic effect
    • What are the characteristics of insulin Lispro?
      • Rapid acting
      • Due to the amino acid sequence at position 28 & 29 in the B-chain
    • What are the characteristics of insulin Glargine?
      • Long acting
      • Has no peak plasma conc. due to precipitation at the injection site
      • Precipitates due to solubility in differrent pH levels 7 & depot formation at subcutaneous tissue
      • Has slower onset & prolonged effect
    • Insulin preparations
    • Graph form of insulin preparations
    • When is insulin included part of the treatment?
      • Type I DM
      • Type II DM when it is not controlled by any oral anti-diabetic drugs
      • Complications like DKA
      • Pregnancy
    • What are the sites of insulin injections?
      • Upper outer arm
      • Belly (Below the belly button)
      • Upper outer thighs
      • Buttocks
    • Why must be the injection sites for insulin be rotated?
      To avoid lipodystrophy
    • What are the types of insulin delivery systems?
      • Syringe
      • Pen
      • Pump
      • Intranasal insulin
    • What are the advantages of using an insulin pen?
      • More convenient
      • More accurate dosage
      • Less painful
    • What are the advantages of insulin pump?
      • Used for continuous subcutaneous insulin infusion therapy
      • Mimics both basal & bolus insulin releases
      • Decreases the risk of hypoglycemia
    • What are the adverse effects of insulin?
      • Hypoglycemia
      • Lipodystrophy at injection sites
      • Allergy
      • Insulin resistance
    • What is meant by liposdystrophy?
      Repeated insulin injections at the same spot causing atrophy of subcutaneous fatty tissue at the site of injection due to local immune reaction
    • How to prevent lipodystrophy?
      Rotate the site of insulin injections
    • What are the two types of hyperglycemic emergencies?
      • Diabetic ketoacidosis (DKA)
      • Hyperglycemic hyperosmolar state (HHS)
    • What are the characteristics of DKA?
      • Absolute insulin defieciency resulting in severe hyperglycemia, ketone body production & systemic acidosis
      • Develops over hours to 1-2 days
      • Most common in type I DM
      • Plasma glucose >250mg/dL
      • ArterialpH <7.3
      • Bicarbonate <15 mEq/L
      • Moderate ketonuria
      • Anion gap >12mEq/L
    • What are the characteristics of HHS?
      • Severe relative insulin deficiency resulting in profound hyperglycemia & hyperosmolality and no significant ketone production/acidosis
      • Develops over days to weeks
      • Most common in type II DM
      • Higher mortality rate
      • Plasma glucose >600 mg/dL
      • Arterial pH >7.3
      • Bicarbonate >15mEq/L
      • Minimal ketonuria
      • Serum osmolality >320 mosm/L
    • What is the pathophysiology of potassium loss?
      • Due to acidosis
      • Extracellular accumulation of H+ ions
      • Leads to shift of K+ from intracellular to extracellular space
      • Most K+ is lost in urine due to osmotic diuresis
      • Leading to loss of fluids & electrolytes
      • Dehydration activates RAA axis
      • All which leads to hypokalemia
    • What is the key component of hyperglycemic ketoacidosis?
      • Hyperglycemia
      • Glycosuria
      • Ketonuria
      • Acidosis
      • Low intracellular K+
      • Fluid & electrolyte imbalance
    • What are the recommended treatment for hyprglycemic ketoacidosis?
      • Correct fluid imbalance with normal saline
      • Correct serum potassium
      • Subcutaneous rapid/Short acting IV insulin
      • Bicarbonate - Extreme acidosis
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