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28 Cards in this Set

  • Front
  • Back
Actions of Insulin
Increase glucose uptake into cells, Promotes formation of glycogen, decreases gluconeogenesis, stimulates fat deposition and inhibits lipolysis, Storage of AA ans protein
Acute problems of Diabetes?
From Hyperglycemia: diabetic Ketoacidosis, non-ketotic hyperosmolar state
Long-Term complications of Hyperglycemia?
Retinopathy, Neuropathy, Nephropathy, Vasculopathy: CVD, peripheral VD, stroke
Classic presentation of type-1 Diabetes mellitus?
Pplyuria, polydypsia, polyphagia.
Ketoacidosis, enuresis(bed wetting), growth retardation, fasting hyperglycemia
Diabetic Ketoacidosis
Confusion, Lethargy, dehydration, tachypnia, Kussmal respirations, fruity breath
Etiology of Type-1 Diabetes Mellitus?
Familial, HLA associated
Diagnosis of Type-1 Diabetes Mellitus?
1 symptoms
2 causal plasma glucose > 200
3 FPG > 126
4 2 HR PG > 200 after oral glucose tolerance test
Etiology of Type-2 Diabetes Mellitus?
Very strong genetic component, not HLA mediated, strong association with obesity
Insulin Resistant Syndrome?
Hyperlipidemia, increased triglycerides, decreased HDL, increased LDL, Hypertension, increase PAI1: deacreased fibrinolysis, increase risce of CV moridity, obesity, no ketoacidosis
Maturing onset diabetes of the young: Chromosomal mutation. Looks like Type 2 but at younger age
Threatment of Type-2 Diabetes Mellitus?
Diet, exercise, weight lose, pharmacology
Screening for Diabetes Mellitus?
Type 1 not recomended
Type 2: every three years after 45, younger if obese, primary relative with DM, high risk ethnic group...
Impaired fasting glucose
FPG = 100-126
Impaired glucose tolerance
Post-prandial plasma glucose = 140-200
Non-ketotic Hyperosmolar State (NKHS)?
Hyperglycemia, hyperosmolarity, osmotic diuresis, mental status changes, seizures, coma
Seen in Type-2 especially in elderly
Treat with fluid replacement
Cells in Islets of Langerhans and what they secrete?
Beta: Insulin
Alpha: Glucagon
delta: Somatastatin
PP: polypeptide
Enterochromaffin: Serotonin
Preproinsulin Cleaved to form?
Insulin and C-peptide(used as a marker for endogenous insulin formation)
How does Glucose stimulates release of Insulin?
Glucose enters GLUT-2, turned to ATP which blocks K+ channel, Membrane depolarizes, Opens Calcium channel, calcium influx causes insulin release and synthesis
How does insulin cause its effects?
Insulin binds Tyrosine Kinase receptor, activate PI-3K pathway , increase GLUT-4 expression, synth of lipids, pts, glycogen
Insulin binds Tyrosine Kinase receptor, activates MAPKinase pathway, cell growth and prolifeation
Obesity linked to Diabetes?
Central Worse than gluteal and subcutaneous, FFA and TGI inhibit signalling, Cytokines from fat: leptin, resistin, adiponectin
Mitochondrial Diabetes?
Maternally inherited, Cannot make ATP and need ATP for insulin synthesis, rare
causes of Type-1 diabetes(Beta cell destrubtion)?
insulitis: CD4 and CD8 cells
Cytokines produced locally
Auto-AB against islet cels or insulin
Amyloid(Type 2)
Macrovescicular Complications of Diabetes?
Accelerated Athersclerosis: MI, Renal artery athero, hypertension, gangrene of lower extremities
Hyaline arteriosclerosis:HTN
Microvescicular Complications of Diabetes-retinopathy?
Retina, new vescels form on disk and retina and hemorrhage and cause vitrious death.
Microvescicular Complications of Diabetes-Nephropathy?
Renal vascular lesions,
Glomerular lesions: capillary basement thickeninf, mesangial sclerosis, nodular glomerulosclerosis (Kimmelstiel-wilson lesion)
Microvescicular Complications of Diabetes-Peripheral neuropathy?
Axial, autonomic, weakness, functional disability, predisposed to ulcers, infection, gangrene
Beta cell, solitary, 90% benign,
Triad: glucose <50, CNS symptomes, attacks with fasts or exercise.
Found in Parncreas, duodenum, peripancreatic tissue.
Cause Zollinger-ellison syndrome:multiple peptic ulcers, usually invasion or mets