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Nur 270 Exam 3
Diabetes Mellitus
| Question | Answer |
|---|---|
| What are the 3 types of cells in the pancreas? | Alpha, Beta, Delta |
| Alpha Cells secrete... | Glucagon, and are located in the peripheral portion of the islet |
| Beta Cells secrete.... | Insulin & Mylin, and are located in the central portion of the islet |
| Delta Cells secrete | Gastrin & Somatostatin |
| Insulin is secreted in response to | elevated blood glucose levels |
| 2 Problems associated with DM | Chronic Insulin Dependency (Type I) Insulin Resistance (Type II) |
| What does insulin Do? | -Blood Glucose levels +uptake & use of glucose by adipose and muscle cells + phosphorylation of glucose by liver +lipogenesis +Amino Acid incorporation into proteins |
| Why do we need insulin? | -transport of glucose, amino acid, potassium, & phosphorous across the membrane -to activate enzymes that promote metabolism -fixed receptor model-combines with receptor on cell |
| Insulin Deficit causes | -hypoglycemia +increased fat metabolism -protein synthesis |
| If insulin is present... | glucose intake is excess of caloric need is stored as glycogen in liver, and muscle or fat , when it is absent or not used. |
| If insulin is deficit there is decreased.... | -transport of glucose across the cell membrane -glycogenesis & excess glucose remains in the blood |
| If insulin is deficit there is increased... | -glycolysis: glycogen stores are reduced and liver glucose added to blood -glucogenesis and more liver glucose is added to the blood |
| What happens to the brain when there is an insulin deficit? | Brain cells are not insulin dependent & must have a constant supply of glucose. -the brain can get glucose out of the blood without insulin |
| What happens to the metabolism when there is an insulin deficit? | fatigue, weakness, and weight loss |
| If a person is hypoglycemic what happens? | They could go into a coma |
| What is hyperosmolarity? | Excess sugar in the blood |
| Glycosuria and osmotic diuresis occurs when... | -Blood Glucose conc. exceeds renal threshold |
| Glycosuria causes.... | -Sugar detected in urine -lrg amts. of water, electrolytes, and calories may be lost -polyphagia |
| Osmotic diuresis causes... | -fluid shifts from intracellular to extracellular resulting in a deficit -body tries to dilute sugar & throws all intracellular water into the blood |
| Glycagon | -counter regulatory hormone to insulin -promotes use of stored fuels during fasting |
| Glycogenolysis | breakdown of glycogen |
| Glyconeogenesis | Creation of glucose |
| Ketogenesis | Creation of Ketones |
| Lipolysis | breakdown of fat-->results in weight loss |
| Diabetes Risk Factors | -Obesity -Family Hx -Race (AA, Latin, Asian, N. Americans) -HTN -Triglycerides -Hx of Fast Glucose btwn 110 & 125 -Delivery of a bby > 9lbs |
| Diabetes Screening | -@ least q yr beginning at age 45 (A1C) -@ risk ethnic groups (AA, Latin, Asian, N. Americans) -Bp > 140/90 -Hx of impaired glucose tolerance -Delivered bby > 9lbs -Obesity: > 120% of desired weight -DM in 1st degree relative -HDL (good) < 35 -Tri |
| Type I Diabetes Facts | -beta cells -pancreatic failure -needs insulin replacement |
| Type II Diabetes Facts | -Insulin Resistance -Deficit -Have some pancreas function -These pts take pills |
| Diabetes #1s | -#1 cause of non-traumatic amputations -#1 reason for dialysis -#1 cause of blindness in US (diabetic retinopathy) |
| Type I DM info | -Affects 5-10% of all diabetics -Juvenile onset -Ketosis prone (DKA) -Rapid onset -Viral mediated (abnormal immune response) -Mostly thin at Dx |
| Type I: Patho | -Cellular destruction, IgG antibodies -Viral disease or inherited and combined with environment factors -destruction associated with hla-dr3 or hla-dr4 -lack of insulin, excess glucagon |
| Type I Signs and Symptoms | -polyuria -polydypsia -polyphagia -hyperglycemia -weight loss -weakness -ketosis-->DKA-->Coma (Ketones pickle the brain causing coma) |
| Type 2: DM Info | -Affects 90-95% of all diabetics -adult onsdet, ketosis resistent -usually >40 -Genetic or obesity induced -no islet cell antibodies -40% will eventually need insulin |
| Type 2: Patho | -genetic susceptibility unmasked by environmental factors -pancreas may produce too little insulin -body can't use insulin that's produced -resistance -decreased weight -decreased # of beta cells -normal ration of alpha to beta cells |
| Insulin Resistance | Glucose can't move from blood into cells and builds up in the blood |
| The body's insulin responses include.... | -normal: peak at zero then levels out -Type 2: no significant spike then levels out |
| Type 1.5 Diabetes | -Form of Type 1 -affects people over 30 -produce islet cell antibodies & Glutamic acid decarboylases antibodies that destroy insulin producing cells -may respond to diet, exercise, and oral agents -over time insulin production drops and insulin needed |
| Type 1.5 Diabetes continued | -lower lipid & total cholesterol levels -less HTN -Less Insulin resistance than Type 2 -Hepatitis -drug induced toxicity |
| Diabetes Blood Tests | -Glycosylated hbg (A1C <6.5) -3 hr glucose tolerance test -self monitoring of blood glucose -Fastic blood sugar < 100 -2 hr after meal <180 |
| A1C test | -if blood sugar is elevated, glucose attaches to hbg for life of the red blood cell (60 to 90 days) -Shows pattern of blood glucose levels over 2-3 months -normal values 5-6% -Prediabetes 6-6.5% -Diabetes > 6.5% |
| Normal Glucose Values | Fasting < 100 After meal <180 A1C <6 |
| Diabetes Diagnosis Criteria | -Fasting BS > 126 -Random BS > 200 -Polyuria -Polydipsia -Polyphagia -Glucose Tolerance Test > 200 after drinking beverage with 75g of carbs -A1C > 6.3 |
| Diabetes Management | -Reducing A1C by 1% to reduce (eye problems, nerve damage, & kidney problems (25%)) -Controlled HTN: BP < 130/80 -Controlled Lipids: LDL, HDL, triglycerides -Exercise -Weight Control -Minimize risk factors -medications -prevent complications |
| DIabetes Goals | -Blood glucose: individual goals -Fasting 80 to 120 -after meal <180 -A1C < 6.5% -HS BS 100-140 -Urine: negative ketones (if BS > 250) -Avoid hypoglycemia |
| Blood sugar and the Elderly | Keep it higher than lower to prevent falls |
| To Avoiding Complications | -BP < 130/80 -LDLs < 130 -HDLs > 35 -Daily aspirin for prophylaxis -Statins every day to reduce risk of coronary artery disease |
| What can a diabetic do to avoid kidney disease? | Take an Ace Inhibitor (prils) Slows decline in GFR protect kidneys |
| Adverse reaction of Ace Inhibitors | Dry Cough Angioedemia |
| What can be used instead of ace inhibitors to protect the kidneys? | Calcium Channel Blockers |
| Monitoring pts with Diabetes | -quarterly dr. visits -A1C 3 to 6 months -Lipids annually -Urinalysis, micoralbumin yearly -yearly dilated eye exam |
| How does exercise help diabetic patients? | -need for insulin and other meds +insulin sensitivity in muslces enhances fibrinolysis -platelet adhesiveness -progression from IGT to Type 2 -BS by + uptake of glucose by body muscles regular exercise 20 to 45 minute aerobics 3x week if bs <100 ea |
| Weight | -80 to 90% of TYpe 2 are overweight -establish ideal body weight -Overweight: loss of 10 to 20 lbs |
| Diet | -medical nutrition therapy -keep glucose, lipids, & weight as close to normal as possible -1600, 1800 cal ADA diet -Carb Counting: (60g limit meals, 30g limit snacks) |
| Oral Drug Therapy | -If A1C > 8, start lifestyle changes -Avoid clinical inertia |
| What are some Insulin Stimulators (squeeze pancreas)? | sulfonylureas -glimipride -glipizide -glyburide -meglitimide |
| What are some Insulin sensitizers? | Thiazolidinediones (actos) |
| What are some liver blockers? | Biguanide (metformin) DPP4s: "gliptins" (keeps BS down without side effects of sulfa-drugs) |
| Sulfonylureas | -stimulating pancreas to release insulin -hypoglycemia most common side effect -First generation no longer used -2nd generation: (-ide)1/2 hr ac |
| Biguanides | 1st drug of choice (metformin) used alone or in combo. --suppresses glucose production in liver -increases tissue sensitivity to insulin -doesn't stimulate insulin secreation (no hypoglycemia) -Enhances weight loss -GI Upset, diarrhea, take with mea |
| Meglitinides | -Helps pancrease make more insulin -Take w/ meals -Very expensive -Causes gas -Nateglinide (starlix) -Repaglinide (prandin) |
| Alpha-glucosidase inhibitors | -Take with 1st bite of food -work in digestive tract -excreted by kidneys -blocks action of enzyme that breaks down carbs -no hypoglycemia -SE: flatuence -Acarbose (precose) & miglitol (glyset) |
| Thiazolidinediones (TZDs) | -decrease insulin resistence -wt gain -swelling (may indicate CHF) -may preserve beta cell function -class effect + CHF -risk of osteoporosis in post menopausal women -Avandia (rosiglitazone) (off market) |
| Dipeptidyl peptidase-4 (DPP IV) inhibitors | -latest class -reduces blood glucose -"Gliptins" -inhibits degredation of GLP-1 -doses based on creatinine clearance -once daily w/ or w/o meal -no hypoglycemia -no GI SE with metformin |
| Combo Drugs | -Glycovance (glyburide & Metoformin) -Metaglip (glipizide & Metformin) -Janumet (Januvia & Metformin) |
| Combo Treatment | -insulin +sulfonylurea -insulin + Metformin -insulin + alpha-glycosidase inhibitor -insulin + thiazolidinedione minimizes cost |
| Injectable Meds | Amylin analog: pramlintide (symlin) Incretin mimetics: exenatide (Byetta) Incretin mimetics: liraglitude (Victoza) Insulin |
| Insulins | All are hypoglycemics Differ in a) speed of onset b) time of peak action c) duration |
| Types of insulin | Rapid, Short, intermediate, & long-acting Basal: controls fasting blood sugar (once per day) Bolus: controls meal time insulin |
| Rapid Insulin | Onset: < 15 min Peak: 0.5 to 1.5 hrs Duration: 4 to 6 houris Out of system after meal is digested Ex. Lispro (Humalog), Aspart (Novolog) |
| Short Insulin | Onset: 30 to 60 minutes (already finished meal) Peak: 2 to 4 hours (meal had digested) Duration: 6 to 8 hours (risk for hypoglycemia before nxt meal) Ex. Novolin R, Humulin R, regular insulin |
| Intermediate Insulin (bid insulins) | Onset: 1 to 4 hours Peak: 6 to 12 hours Duration 12 to 18 hours these are being phased out Ex. NpH, Novolin, Humalin |
| Long acting Insulin | Onset: 6 to 14 hours Peak: many small peaks Duration: 18 to 36 hours Ex. Glargine (Lantas), Detemir (Levemir) |
| Mixed Insulin (bid dosing) | Novolin 70/30=Novolin & Regular Humalin 70/30=Humalin & Regular Novolog 70/30=Novolog 12 hr & Novolog Short acting Humalog 75/25=Humalog 12 hour & Humalog Short Acting Humalog 50/50=Humalog 12 hour & Humalog short acting |
| Insulin strength | u-100 or 100 units/ml (most common) u-500 or 500 units/ml |
| How is insulin made? | Past: beef and pork pancreata Now: all human or analog insulin (human insulin being phased out) |
| Can log insulins be mixed? Ex. Humalog + Novolog | No. Lantas, Levemir, Novolog, and humalog cannot be mixed with each other. However you can mix Humalog long acting, with humalog short acting |
| What are the rules of injecting insulin? | -store syringes at room temp. -Don't clean needle with etoh -store open insulin and pens at room temp -warm cold insulin -store pre-filled syringes with needle up -Draw up regular then nph -Rotate injection sites |
| What are the preferred insulin injection sites? | Abdomen (fastest absorption) Arms thighs Buttocks |
| IV Insulin | ICU: infusions/drips: Regular -Regular is cheaper and consistent with no peaks In 2006: IV approved -Aspart (recombinant) -Human insulin (recombinant)-Novolog & Novolin-R |
| Insulin Problems | -allergic reac. (not w/human) -Lipodystrophy-irreg. absorption -Lipoatrophy < of sq fat, dimpling -lipohyperthrophy-dev. of fibrofatty masses -insulin edema -insulin resistence- requires > 200 u for more than 2 d w/ no infection. Tx. Diff combo of in |
| Insulin Pens | -Virtually Painless -3 indicators to verify accuracy of dose (visual, aud, tactile)--safer -lacks stigma of needle, better adherence -> cost, shorter storage life 7 to 30 d -don't carry with needle attached -Ex. Novolog, Humalog, Levemir, Lantis, Aph |
| Insulin pumps are good for... | -pts who have fluctuating BS levels despite diet & insulin (A1C >7) -pregnant women |
| What are drawbacks of insulin pumps? | -infection at the site -catheter clogging -insulin loss for loose connection |
| Insulin pumps are not good for... | -pts who don't comply with standard diet, insulin, or self monitoring -pts who miss scheduled appointments -those who can't recognize hypoglycemia -pts w/ microvascular diabetic complications |
| Continuous glucose monitoring systems | -several on the market -sensor implanted under skin in abd, changed q3d -con't glucose readings sent from transmitter to monitor clipped on belt -waterproof -costs $1000, sensor $35 |
| Complications of DM | -hypoglycemia -insulin shock (coma) -Lipodystrophies -Hyperglycemia -DKA -HHNK |
| Characteristics of hypoglycemia | -BS < 70 -too little food, too much med -tremors, weakness, cold, clammy, unconscious sudden onset -Treatment: 15gm carbs prn, retest BS, repeat q 15 min |
| Characteristics of Hyperglycemia | -BS >350 -too much food, too little med, infection -polyuria, polydypsia, polyphagia -blurred vision, dry skin, slow onset -Treatment: insulin |
| Hypoglycemia | -may not proceed from mild to severe -Beta Blockers (-olol) may mask adrenergic s/s of low BS - >1/2 episodes occur at night |
| Risk factors of hypoglycemia | -Insulin -wt loss -onset of menses -intense exercise -etoh -drugs -low cal meal |
| Which factors differentiate DKA from HHNKS | -Level of hyperglycemia -amt of ketones produced -potassium levels -amt of vol. depletion -dosage of insulin needed |
| Mild hypoglycemia | -adrenergic & cholinergic s/s -sweating, tremor, pallor -tachycardia, palpitations, anxiety, weakness, hunger, cold, clammy, paresthesia -Treatment: 15gm of carbs |
| Moderate Hypoglycemia | -neuroglycopenia, impaired function of the brain & CNS -H/A, irritability, confusion, behavior change, drowsy -decreased concentration, blurred vision -Treatment: 15gm carbs |
| Severe Hypoglycemia | -Neuroglycopia: unable to swallow -disoriented, unresponsive, stupor, sz, coma -Treatment: glucogon 1 mg sc/IM -IV-50% Dextrose: check BS 15min |
| What do fast acting carbs do (15gm)? | -Raise BS within 15 min |
| Examples of 15 gm carbs | -4-6 oz OJ -3 glucose tabs -4-6 oz reg. soda -piece of fruit -8 oz milk -2 T raisins -3-4 packets of sugar -1 tube glucose gel -1 tube cake icing |
| Characteristics of HHNK | -Usually Type 2 -BS >1000 -Azotemia, hct + plasma osmolarity +pH >7.45 +bicarb >15 +BUN & creatinine |
| S/s of HHNK | Dehydration hypotension - CVP dry mucus membranes -skin turgor neurologic impairment seizures confusion tremor hallucinations coma |
| Characteristics of DKA | Usually Type 1 BS >500 but <1000 +Plasma osmolarity -pH < 7.3 -Bicarb <15 +BUN hyperkalemia (initially) |
| S/s of DKA | dehydration (thirst) hypotension tachycardia dry skin dry mucus membranes Kussmaul respirations Acetone breath (fruity) polyuria nocturia visual disturbances |
| Treatment for HHNKS | FLUIDS insulin to a lesser degree assess for & treat cause monitor neuro and cv status |
| Treatment for DKA | INSULIN fluids to a lesser degree D5NS if BS <250 correct BG first then lytes monitor K levels if pH <7 may give bicarb |
| Etiology of HHNKS | Type 2 diabetes concurrent illness elderly & institutionalized drugs, enteral feedings, peritoneal dialysis mortality up to 70% Preventive ED: call provider if 2 consecutive BS > 300, tired w/o cause, frequent urination |
| Etiology of DKA | Type 1 diabetic young pt missed or reduced insulin dose stress, growth spurts, pregnancy, infection, surgery meds-thiazie, phenytoin, glucocorticoids, sympathomimetics |
| DKA Pathology | -stimulates counterreg. hormones, causes incr. in BS severe circulating insulin ineffective -can't burn glucose w/o insulin-->fat metab.-->Inc. ketones-->overloads metabolic sys. & resp. buffering begins -glucose in urine, diuresis-->dehyd & lyte imbal. |
| Macrovascular complications | -atherosclerotic changes -cerebrovascular disease -coronary artery disease -renal artery stenosis -peripherovascular disease |
| Microvascular complications | -neuropathies retinopathies nephropathies |
| Retinopathy | -DM leading cause of blindness -Types: Background & proliferative -vision not affected w/ background -can become blind w/proliferative -Type 1: visit opthamologist w/in 5 yr of dx & yrly therafter -Type 2: examined @ dx & yearly |
| Nephropathy | -proteinuria 1st sign -low protein diet -ace inhibitors, calcium antagonist decreased protein excretion -diabetic nephrology is the number one leading dx of new dialysis |
| Autonomic neuropathy | -affects cardiovascular, GI, & urogenital -GI: gastroparesis--stomach empties slowly, fills up quickly, bloated, retain food for 12 hrs, BS fluctuates -RX: frequent sm. meals, low fat & fiber, reglan |
| Peripheral neuropathy | -numbness, tingling, burning pain in fet -sy usually initially worse @ nite -relieved by walking progressing to constant w/ greater intensity |
| Peripheral Vascular Disease | -DM #1 cause of amputations in US -aggravated by activity -relieved by rest -cold, loss of hair -shiny skin, toenail hypertrophy, decreased pulses, pallor on elevation, prolonged cap refill |
| Diabetic food care | -never barefoot, well fitting shoes, clean stockings -don't self treat corns, ingrown toenails, etc. -avoid smoking (decr. circul.) & cold exposure -check temp of h20 before bathing -don't use heating pad or hot h20 bottles -don't cross legs when sit |
| What is Regranex? | -topical gel -stimulates collagen growth |
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cmunchaquita04
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