Diabetes Pancreas is responsible for insulin levelsAlpha cells- Produce glucagon - Stimulates breakdown of glycogen in liver (glycogenolysis)- Stimulated formation of carbohydrates in liver- Stimulates breakdown of lipids- Secretion is regulated by blood sugar levels - Low sugar levels= alpha release glucagonBeta cells- Secrete insulin – helps glucose to move across the cell membrane,  blood glucose levels- Secretion is regulated by blood glucose level- High gluc=beta release insulinDelta cells- Produces somatostatin – inhibits the production of glucagon and insulin- Balances Alpha and Beta cell functionType I- IDDM- Autoimmune disease- beta cell destruction- Often leads to absolute insulin dependency- Affects 10% of people with DM- Develops most often in children and young adults- Strongly inherited - Environmental factors can be the trigger – chemical toxin found in smoked meat- Viruses that trigger autoimmune response- Islet antibodies (presence can diagnose pre-clinical DM)- Obesity is a factor but less so than with type 2- Symptoms appear after 80% of beta cells destroyed Type II- NIDDM- Most common – affects 90% of people with DM- Usually diagnosed after age 40, but seeing in younger & younger people- Associated with older age, obesity, family history of DM, previous gestational DM, physical inactivity, certain ethnic populations- Hereditary traits- mostly with identical twins- Obesity is a major risk factor – 88% are obese (20% over ideal weight)- Impaired liver/muscle tissue sensitivity to insulin- Impaired insulin secretion - NO beta cell destruction (chronic high glucose make beta cells less efficient)Gestational DM- Glucose intolerance first diagnosed during pregnancy- Affects about 5% of DM population- Symptoms generally disappear after termination of pregnancyDM1. Insulin is needed in a prescribed amount for glucose to get into cells- unlocks the door2. Nerve, intestine, kidney don’t need insulin to use glucose3. Low glucose levels stimulate the release of stored glucose4. High glucose levels stimulate pancreas to release more insulin5. Decreased glucose utilizationa. Nerve, intestine and kidney cells don’t need insulin to transport glucose into their cellsb. Skeletal and fat cells doc. Ingested glucose can’t be transported into cells, so plasma levels rised. Liver can’t store glucose as glycogen without adequate insuline. So blood glucose levels continue to risef. Glucose appears in urineg. Glucose is osmotic diuretich. Dehydration appears- osmotic diuresis6. Increased fat mobilizationa. Muscle are crying for glucose so fat stores are broken downb. Ketones are formed as a byproduct of fat metabolism, and produce hydrogen ionsc. Measured in urine, smelled on breathd. Acid/base balance disturbed- metabolic acidosise. Lipid breakdown increases lipid levelsf. Leads to arteriosclerosis 7. Increased protein utilizationa. Amino acids (building blocks of protein) are converted to glucose in the liver – further elevating glucose levels- leads to protein breakdownb. Insulin is needed to build proteinc. Type 1 diabetics often appear emaciated due to constant protein breakdown.Symptoms- Cardinal signs- Polyuria, Polydipsia (from dehydration) Polyphagia (protein breakdown)- Weight loss (Water loss, less muscle mass, protein breakdown)- Blurred vision (blood vessels clogging- not feeding retina)- Pruritis, vaginitis (bacterial and fungal infections- great food available)- Weakness, fatigue, dizziness (K loss, postural  B/P from fluid loss)- Asymptomatic (type 2) (Body adapts to slow changes, for a while)- Slow healing wounds, dark patches (acanthosis nigricans)Ranges- Fasting blood sugar- <100 norm/ 100-125 pre/ >126 DIABETES- Glucose tolerance- <140 norm/ 140-199 pre/ >200 DIABETES- GTT should return to normal in 2 hoursSulfonylureas- Diabeta, Glucotrol, Amaryl, Micronase- Stimulate beta cells to secrete insulin- Mild diuretic- Take 1-2 times per day before meals- Used for Type 2Biguanides- Metformin (Glucophage)- Makes muscle cells more sensitive to insulin- Decreases glucose produced by liver- Decreases LDL’s and triglycerides- Decreases amount of insulin needed in type 2- Take 1-3 times per dayAlpha Gluc Inhibitor- Acarbose (Precose), Glycet- Delays digestion of complex carbohydrates, so glucose levels peak later after meals- Take with every meal- Used in type 2 DMMeglitinides- Prandin, Starlix- Stimulates beta to secrete insulin- Take 30 before each meal- Used for type 2Thiazolidinediones- Dangerous- Avandia (restricted use, heart damage), Actose (linked to bladder cancer), Resulin (liver damage)- Increases insulin action at receptors in liver and peripheral tissue (to store more glucose in liver)CHRONIC COMPLICATIONSMacrovascular (larger vessels)- CAD, cerebrovascular disease, hypertension, peripheral vascular disease- Occur years before symptoms of DM even appear- Tight glucose control minimizes thisRetinopathy- Caused by lack of oxygen from occluded vesselsNephropathy- Damage to smaller blood vessels- No symptoms early- Late symptoms- swelling, proteinuria, renal failure- Checking urine protein is importantNeuropathic complications- MOST COMMON PROBLEM- Numbness, tingling, painCycle of foot wound1. Neuropathy2. Minor trauma3. Ulceration4. Poor healing5. Gangrene - Smooth, shiny, red skin, with a small digital ulcer, and a ‘Terry’s nail’ (pale, with a distal band of reddish-brown color) due to chronic renal failure. This combination is highly suspicious of diabetic