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Nur 270 Exam 3

Diabetes Mellitus

QuestionAnswer
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
Created by: cmunchaquita04