Pancreas: Has both exocrine(food digestion) and endocrine function.

Insulin: Moves glucose from blood across cell membrane into cells. Once in blood is rapidly bound to receptor sites on muscle and fat cells, or is destroyed by liver and kidneys. Released within minutes of eating, peaks in 30 minutes, return to baseline 2-3hrs. Glucagon: Stimulates breakdown of glycogen in liver to increase blood glucose levels. Produced by alpha cells of islets of Langerhan's. Glycogenolysis: Breakdown of liver glycogen Gluconeogenesis: Formation of glucose from fats and proteins(can lead to ketosis in Type 1 DM). Somatostatin: Produced by delta cells of I of L. Neurotransmiter inhibits production of both insulin and glucagon. Insulin antagonists: Cortisol, Growth hormone Epinephrine Growth hormone inhibiting hormone Diabetes Mellitus: disorder of hyperglycemia resulting from absent or insufficient insulin supplies or poor utilization of insulin available or both which leads to abnormal fat, carb, and protein metabolism Diagnostic Screening for DM Fasting blood glucose >126mg/dL, or, Random glucose >200mg/dL, or, 2 hr. postload glucose > 200mg/dL during OGTT (oral glucose tolerance test) Impaired Fasting Glucose (IFG) (pre-diabetes) if FBG >100mg/dL but < 126mg/dL Normal Fasting Glucose = 100 mg/dL A1c: values above 7-9% considered elevated. Urine glucose and ketone levels: Not as accurate, but patients could have ketones in urine and glucose in urine. Albuminuria: Used with creatinine clearance test to determine early nephropathy. Cholesterol: HDL>45 LDL<100 Triglycerides<150 SMBG: self monitoring blood glucose Types of DM Type 1 (5-10%) of total cases. Autoimmune disease(90%) Destruction of beta cells of islets of Langerhans. This begins with insulinitis(chronic inflammatory process in response of destruction of beta cells), May also be idiopathic(10%). Genetic predisposition with an environmental trigger. Viral(mumps, rubella, coxsackievirus B4). Chemical toxin(found in smoked and cured meat). Clinical manifestations: Occur when 90% of beta cells are destroyed. Hyperglycemia: Elevated glucose in blood Ketosis: Accumlation of ketones in blood from breakdown of Fats and Proteins. Glucosuria: glucose in urine Polydipsia: excess thirst Polyuria: excess urination Polyphagia: excess hunger Exogenous insulin: insulin from source outside of ones body. Type 1 patients have to have this. Weight loss despite food intake Extreme fatigue

Pruritis (itching) and vaginal itching blurred vision, tingling, numbness, pain in legs/arms, and slow-healing skin infections. Type 2: (90-95% of total cases)(usually manifest in middle age or older)(Heredity plays a role in transmission into), insulin resistance (cant bind with receptor sites). Hyperglycemia occurs even though there is plenty of endogenous insulin. The pancreas then works harder to produce even more. In type 2, there is no ketosis. Risk factors: Heredity: Parents or siblings Obesity: Physical inactivity: Race: Hypertension: Gestational diabetes: Metabolic syndrome: (occurs in 50% of adults over 50) Cluster of manifestations: Hypertension, elevated C-reactive protein, abdominal obesity, and fasting BG above 110. These combine to increase risk of type 2 dm. Clinical manifestations: Hyperglycemia not as severe as type 1 Polyuria Polydipsea NOT polyphagia Vaginal itching blurred vision, tingling, numbness, pain in legs/arms, and slowhealing skin infections. Complications of DM Hyperglycemia: Hot and dry sugar is high Dawn phenomenon: rise of BG between 4am and 8am Somogyi phenomenon: Hypoglycemia at night with rebound morning levels of hyperglycemic. Diabetic ketoacidosis: Type 1 DM. Fat stores break down. Oxidation of fatty acids causes increased ketone levels in blood. During chemical reaction during formation of ketones, bicarbonate is lossed, and buffering does not occur, resulting in acidosis. Causes: or missed insulin dose; illness/infection; undiagnosed/untreated DM (may be initial manifestation of DM) DX findings:Glucose 300-1,000 mg/dL, low bicarb, low pH, BUN, Cr, Hct & Hgb Manifestations: dehydration, electrolyte loss, metabolic acidosis, BG >250, ketones in urine, 3P's, blurred vision, weakness, headache, hypotension (from polyuria), anorexia, N/V, abdominal pain, fruity (acetone) breath, Kussmaul resps (blowing off CO2-acidosis), Depression of CNS, can lead to coma and death. Must have medical attention immediately. Stress increases risk: Stress can be illness, infection or omitting insulin doses. 4 metabolic problems: Hyperosmolarity Metabolic acidosis Extracellular volume depletion from osmotic diuresis Electrolyte imbalances

Medical treatment of DKA:(p. 996) 1.admin. O2 & rehydration with 0.9% NS at rapid rate till BP/urine output in normal range; then add IV Regular insulin & monitor K+ 2. BG ~ 250 mg/dL, change to D5W to prevent hypotension & cerebral edema; admin. K+ 3. Monitor BG hourly; monitor cardiac rhythms and K+ level q 2-4 hours 4. Post-event: educate to avoid repeat episodes Hyperosmolar hyperglycemic state(Type 2): insulin resistance, acute/chronic illness, meds that exacerbate hyperglycemia (ex. Thiazide diuretics), Osmolarity of 340 or greater, hyperglycemia, 3Ps, neurologic changes (often 1stsign), hypotension, profound dehydration, but acidosis/ketosis is MISSING TX: Life threatening, fluid replacement: correct electrolyte imbalances; insulin admin; cardiac monitoring for hyper/hypokalemia (K+); safety measures due to impaired sensorium; strict I&O, will stop insulin tx at BG 250 since ketosis is not present in this condition. Most common precipitating factor is infection. ** Because of delay in tx, hyperglycemia, dehydration, hyperosmolarity more severe! Mortality 10-40% See table 18-3, p. 993 (NCCLEB) Hypoglycemic(insulin shock): Primary due to mismatch in insulin administration. Too little food; excessive physical activity TIRED: Tachycardia, irritability, restless, excessive hunger, diaphoresis/depression. Cold and clammy needs candy. TX: 15g fast-acting concentrated source of carbohydrates; retest in 15 mins; snack of protein/starch unless regular meal is due (the 15/15 rule)=3 glucose tablets, half cup of fruit juice or regular soda (DO NOT add sugar), 8 oz. skim milk, 5 Life Savers candy, 3 tsp. sugar or 3 large marshmallows Altered consciousness: Glucagon 1 mg SQ, IM, or IV followed by oral carb; (can cause N/V if person unconscious when given) Acute care setting 25-50% concentration of Dextrose given 10mL/1 minute IVP; follow with IV infusion of D5W. ** most rapid method to BG Chronic complications of DM Macrovascular disease: atherosclerosis causes abnormalities in platelets, RBCs, clotting factors, changes in arterial walls thicken, sclerose and occlude. Doubles risk of CAD, cerebral vascular and peripheral vascular disease. Manifestations = pulses, Intermittent claudication(pain In butt, thigh, calf when walking) Microvascular disease :Small vessel disease affecting arterioles, venules, capillaries Characterized by thickening of the capillary basement membrane. Affects eyes, kidneys, nervous system, and peripheral circulation Retinopathy: Progressive deterioration of the small vessels in retina. Leading cause of blindness in US After 10 yrs, 50% of all DM and 90% of poorly controlled glucose have some level of retinopathy 3 stages: 1.Tiny red dots in retina, yellow lipid deposits, macular edema,

microaneurysmsdistorted vision 2.Multiple hemorrhages on retina, white fluffy lesions; increased destruction or vessels 3.Body develops new abnormal vessels. Vessels fragile and bleed easily which prevent light from entering. See red/black spots or lines. Risk for retinal detachment. Neuropathy: Proteinuria HTN Edema Renal insufficiency & failure Occurs with Type I and Type 2 1stsign = proteinuria Preventive regimen of ACE Inhibitor + ARB (angio-tensinII receptor blocker) Lo-protein lo-sodium diet) Nephropathy: Peripheral (sensorimotor): affects distal portion of the nerves, esp. in LEs anifestations:paresthesia,numbness, proprioception M Management: analgesics, tricyclicantidepressants, anti-seizure meds, TENS unit to block pain impulses Autonomic: affects nearly every organ Cardiacfixed tachycardia, postural hypotension, Silent MI/ischemia GI delayed gastric emptying (gastroparesis), bloating, N/V, constipation or night diarrhea Renalurinary retention, neurogenicbladder Endocrine-Hypoglycemic unawareness Repro-Male impotence, libido ,vaginitis Why Cells are Damaged in Long-term DM 1. accumulation of by-products from glucose metabolism such as sorbitol which damages nerves (dont we use this in gum?) 2. abnormal glucose molecules in basement membrane of certain cells 3. derangement of RBC fx that leads to oxygen in tissues Diabetes Management Monitor Glucose Levels (self-monitoring) Adjust diet Utilize pharmacological agents Adhere to exercise regimen Avoid Hypoglycemia/Hyperglycemia episodes Avoid long term systemic complications-retinopathy, nephropathy, and neuropathy Early detection&action Assess long-term control -GlycosylatedHemoglobin-HgbA1C;Ideal = 7% or less ******GOAL = Normal blood glucose levels with minimal complications

TXS: Pharmacologic therapies: Prefilled pins= refrig 30 days; Vials= room temp 4wks Types of insulin Name Onset Peak Duration Rapid Lispro,Aspart,Gluilisine 15min 1-1.5hr 3-4hr Short Regular(Novilin-R,Humulin-r) 30-60 2-3 4-6 Intermed NPH Humulin 2 6-8 12-16 Long acting Lantus 2 16-20 24+

Hypoglycemic agents: Type 2. Prevent breakdown of glycogen. Increase insulin production. Increase glucose uptake by cells. Sick Day management: Monitor BG 4xday, test urine for ketone if BG>240, continue insulin, sip 812oz fluid per hour. Giving easily digested liquid or soft food if solid food not tolerated. Notify provider if unable to eat for 24hr or vomiting and diarrhea for 6hrs. Surgery: transplant of pancreas or beta cells. Investigative stage.