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Med-Surg Ch 20

Diabetes Mellitus

Pancreas A&P Located behind stomach, between spleen and duodenum Exocrine (Lipase, Amylase) Endocrine (Insulin) Alpha Cells (Glucagon, released when below 70) Beta Cells (Insulin) Delta Cells (Inhibit production of insulin, Maintains homeostasis)
Fasting Blood Glucose (FBG or FBS) 70-110 mg/dL NPO 8 hours, water allowed Series over 125 = diabetic Can be altered to a false positive by corticosteroids and diuretics
Oral Glucose Tolerance Test (OGTT) 2hours <139-normal 140-199:impaired 200-diabetes mellitus 30, 60, 120 min. (blood and urine) May get dizzy or sick, may stop test
Glycosylated Hemoglobin (HbA1C) 4-5.9% normal 7% or < = well controlled diabetes 8% or > = poor control Measures Hgb for past 3 months
Pancreas MRI & CT Scan Looking to tumors
Age Related Changes in Pancreas Decreased ability to metabolize glucose Delayed release of insulin Decreased sensitivity to circulating insulin
Diabetes Mellitus Quick Facts 6thleading cause of death in America Leading cause of end stage renal disease (ESRD) Most frequent cause of blindness and amputations Affects ~23.6 million, 1.6 million new cases dx/year Over $174 billion spent for care in 2002
4 Types of Diabetes DM 1 DM 2 Gestational DM Other (Drug induced and Infection)
Diabetes Type 1 (Stats and Triggers) 5-10% of diabetes Children/adolescents (avg age 10-15) Genetic predisposition Environmental triggers: Viral infections (measles, mumps, coxsackievirus); Chemical Toxins (smoked and cured meats) Acute illness: 80-90% of cells are destroyed. > in infec
Diabetes Type 1 Pathophysiology Autoimmune/Idiopathic (no know cause) Beta cells destroyed (insulin not produced to unlock cell door to accept glucose); Alpha cells produce excess glucagon (glucose can’t get in cell to be used, excess build up)
Type 1 Diabetes Manifestations Polyuria (> urine) Polydipsia (> thirst) Glycosuria (glucose in urine) Polyphagia (> hunger) Anorexia, malaise, fatigue Blurred vision (lenses swell) Diabetic ketoacidosis: Body thinks not enough glucose in blood, breaks down fats and muscle for ene
Type 2 Diabetes Most common age: middle-older adult Insulin present but tissues resistant. (key to cell does not fit) (Obesity, inactivity, illnesses, meds, age) Sufficient insulin to prevent DKA Gradual onset; delayed diagnosis (1/2 dsagnosis already have complicatio
Type 2 Diabetes Risk Factors Family Hx Obesity Physical inactivity Race/ethnicity: African-American, Hispanic, Native or Alaskan American/Asian Female Hx HTN (> 130/85) HDL cholesterol (<35 mg/dL) Triglyceride level (>250 mg/dL) Metabolic syndrome Anti-platelet + treat hyper
Metabolic Syndrome Places patient at risk for Coronary Artery Disease Combination of factors noted: Abdominal obesity, Hyperlipidemia, HTN, Insulin resistance, Increased tendency toward clotting and inflammation (elevated C-reactive protein)
Manifestations of Type 2 Diabetes Hyperglycemia Polyuria (excessive urination) Polydipsia (excessive hunger) Blurred vision Fatigue Paresthesias (numbness) Skin infections HTN Recurrent Infections
Why increased Diabetes in Elderly Baby Boomers (> 50+; Type 1s living longer, medical advancement) Normal physiologic changes with aging: Lost thirst mechanism, < hungar, tired, visual changes, excess sugar confusion blamed on delusion/dementia, polyuria > comorbidities Polypharmacy
Recognizing Diabetes in Elderly Indicators: Orthostatic hypotension, Periodontal disease, Infections, Stroke, Gastroparesis, Impotence, Neuropathy, Confusion, Glaucoma Longer recovery periods after surgery, illness Increases potential for complications from illness or treatment
Diabetes Diagnostics Manifestations + Random (or casual) plasma glucose >200 mg/dL Fasting Plasma Glucose >126 mg/dL OGTT: 2 hr. plasma glucose >200 mg/dL
Who to test for Diabetes? Age 45+ BMI >25 Clients with risk factors: HTN, Ethinsity, Over 50, Obesity, Problems with lipids (metabolic syndrom), Female reproduction
Blood MGT Tests Fasting Blood Glucose (normal 70-110) Hemoglobin A1C Can dx DM: >6.5% Elevated if 7-9% Poor control at >9% Glycemic goals are age-related.
Urine MGT Tests Urine Testing: Glucose, Ketones (protein breakdown) Urine albumin (U/A): possible nephropathy, need a creatine clearance for “albumin to creatine ratio” Microalbumin; earliest indicator of nephropathy, usually followed by macroalbuminuria
Lipid MGT Tests Cholesterol Levels LDL<100 mg/dL (ADA recommends <70) HDL>45 mg/dL (Women: >50) Triglycerides<150 mg/dL
Self-Monitoring Blood Glucose Levels Type 1: 3-4/day (on insulin only) Type 2: enough to reach goals > BGM when ill, pregnant, change meds BGM affected by: Hematocrit (High=false low, Low=false high), Medications, Supplies (dry/cool, matching codes, exp), blood vol, Gout
Goal of Diabetes Treatment Maintain glycemic control Prevent complications
Diabetes Diet Treatment Maintain as near normal glucose as possible Optimum serum lipid levels Low-fat diet Attain or maintain optimum weight Low-carb diet Eat complex carb rather than simple
Exercise Treatment of Diabetes Increases uptake of glucose by cells Decreases cholesterol/triglycerides May need cardiac screening before beginning
Rapid-acting Insulin Humalog, Novolog (SubQ) Onset 10-15 min Peak 1-1.5 hour Duration 1-1.5 hour
Short-acting Insulin Regular “R” (IM, SubQ, IV) Onset ½-1hour Peak 2-3 hours Duration 4-6hours
Intermediate Insulin NPH, Lente, Levemir Onset 1 ½-2 hours Peak 6-8 hours Duration 12-16 hours
Long-acting Insulin Lantus, (cannot mix) Onset Not defined Peak None Duration 24+hours
Combination Insulin Humulinor Novolin 50/50, 70/30 Onset 30 min Peak 4-8 hours Duration 24 hours
Factors influencing insulin absorption Injection site: Abdomen is fastest, Deltoid, Thigh, Buttocks is slowest Speed of absorption Fastest: abdomen Rotate to prevent lipohypertrophyand lipoatrophy Rotate within ONE site
Hypoglycemic Agents: Sulfonylureas Glimepiride(Amaryl) Glipizide(Glucotrol) Glyburide(Diabeta) Tolbutamide(Orinase) Stimulate pancreas to secrete more insulin Increase sensitivity in peripheral tissues Side effects: Hypoglycemia, Weight gain, GI symptoms
Hypoglycemic Agents: Biguanides Metformin (Glucophage) Reduces FBG and postprandial (after meals) hyperglycemia < glucose production Makes insulin more effective Use with diet and lifestyle changes Cannot take 2 days pre or post contrast testing
Hypoglycemic Agents: Alpha-glucoside inhibitors Acarbose (Precose) Slows carb digestion and delay glucose absorption Take immediately before a meal SE: flatulence, diarrhea, abdominal discomfort. Hypoglycemia is NOT a side effect!
Hypoglycemic Agents: D-Phenylalanine Nateglinide (Starlix) Stimulate insulin secretion after meals Take shortly before meals Side effects: Hypoglycemia, Weight gain
Hypoglycemic Agents: IncretinMimetics Exematide(Byetta) Sub Q Signals pancreas to make right amount of insulin after meals < rate of glucose entering blood < conversion of glycogen to glucose Injected 30 min-2hrs before meals with 30+ Carbs Don’t take after meals or more often than 12 h
Hypoglycemic Agents: DPP-4 Inhibitors Sitagliptin (Januvia) Decrease liver release of glucose Increase insulin secretion Side effects: Headache, Nasopharyngitis, UTI Diet and exercise modifications
Medication Considerations Monitor close, 7 days Diet/exercise Avoid when lactating or pregnant Increase stress(trauma, surgery, etc) may discontinue and use insulin Avoid ETOH Interferes with birth control ASA therapy (aspirin) is wanted in CAD SE: GI bleed, ulcers, liver d
Diabetic Diet Consistent Carbohydrate Diabetes Meal Plan ADA Diabetic Exchange List (Divides foods into carbs, fats, protein, etc.) Diet Plan for T1 Diabetes: Based on insulin regiment Diet Plan for T2 Diabetes: Balance meals and snacks “No Concentrated Sweets”
Dietary Considerations No Alcohol Non-nutritive sweeteners: Sweet & Low, Nutrasweet, Sunnette, Splenda Nutritive sweeteners: sorbitol, fructose, xylitol “sugar-free” and “dietetic” on labels
Diabetic Sick Day Rules Increase BG monitoring to every 4 hours Test urine for ketones when BG >240 Continue insulin and oral meds Hydrate Call PCP: Persistent N/V, diarrhea; Moderate or large ketones; Persistent hyperglycemia; Fever for >24 hours
Diabetic Exercise/Footwear/Inspection Neuropathy, file/no clip/cut straight, buy afternoon, leather/canvas, no tight/loose Toes, mirror, no barefoot, no cross legs, WHITE cloth. No temp extremes or exercise during poor BGM T1 (> risk for hypo/hyperglycemia) T2 (may < meds, < cadiac risks)
Special considerations for young Continue sports with precautions May require diet/insulin modifications Start slow, extend activity over prolonged time May need carbohydrate drink one hour into activity Monitor BGL Snack available after exercise May need to adjust insulin prior to
Complications of Diabetes Hypo/hyperglycemia Diabetic Ketoacidosis (DKA) Hyperosmolic Hyperglycemic State (HHS) Multiple Chronic Complications
Manifestation of Hyperglycemia Polydipsia Polyuria Polyphagia Decreased energy Malaise and fatigue Blurred vision Dry, itchy skin Headache HTN
Hyperglycemia Symptoms Major complications: DKA and HHS Dawn Phenomenon (4-8 am) SomogyiPhenomenon (Low at time, then high later, with no known reason; Can become insulin resistant for 2-24 hrs)
Diabetic Ketoacidosis (DKA) Breakdown of fats and proteins Liver produces ketones (metabolic acidosis) Bicarbs (buffering mechanism shot) Fluid/electrolyte imbalance Occurs with increased energy needs Increased exercise Emotional stress Forgot to take insulin, sick, infection
Manifestations of DKA Dehydration Warm/dry skin, poor turgor Soft eyeballs, Dry mucous membranes Weak, Malaise Rapid, weak pulse Hypotension K+ and Glucoseare reciprocal N/V, Ketonebreath “fruity”, Lethargy, Coma, Abd pain Kussmaul's respirations (deep rapid hyperventi
DKA Diagnostics Blood glucose (250 or ^) Blood pH (below 7.35) Bicarb (low) Ketones present in blood Ketones and glucose present in urine Electrolyte abnormalities (massive fluid loss) Na+, K+, Cl- (low)
DKA Treatment Immediate medical attention Frequent Blood Glucose monitoring Insulin (more than likely it’s R, IV) Restore fluid and electrolyte balance Monitor cardiac rhythm (Low potassium, sodium, etc.) Treat underlying condition (Infection? Forgot insulin?)
Hyperosmolar Hyperglycemic State (HHS) T2 diabetes potential complication Life-threatening—High mortality rate Slow onset (over about 1-14 days)
Hyperosmolar Hyperglycemic State (HHS) Triggers Infection therapeutic agent acute/chronic illness
Hyperosmolar Hyperglycemic State (HHS) Manifestations Plasma osmolarity(>340mOsm/L.) Stealing the fluid from everyone else Blood glucose severely (>600-2000) Normal <110 Neurological Dehydration No acidosis (difference in HHS and DKA)
Hyperosmolar Hyperglycemic State (HHS) Treatment May require: artificial ventilation and nasogastricsuction Correct fluid and electrolyte imbalances (isotonic fluids, K+replacement) Regular insulin until glucose decreases below 250 mg/dL Treat underlying condition
Hypoglycemia AKA “low blood sugar” or “insulin shock” Blood Glucose: <45-60mg/dL Mismatch between insulin intake/needs Can result in death Causes: Alcohol, Drugs, Physical Activity, Lack of Carbohydrates
Hypoglycemia Manifestations Hunger Nausea Anxiety Pale, cool skin Sweating Shakiness Irritability Tachycardia Hypotension Headache Difficulty thinking/concentrating Change in emotions Slurred speech Blurred vision Decreased LOC Seizures/Coma
Treatment of Mild Hypoglycemia 15g CHO: 3 glucose tabs, ½ cup fruit juice or regular soda, 5 lifesaver candies, 3 tsp of honey, 3 large marshmallows DO NOT add sugar to fruit juice 15/15 rule Wait 15 and repeat if necessary Hypoglycemic episodes >2-3x/wk need diabetes MGT plan adju
Treatment of Severe Hypoglycemia Hospitalization if: Blood glucose < 50, Coma, seizures, altered behavior, no one to remain with client for 12 hours after treatment, caused by sulfonylurea drug If alert administer 15 g CHO If altered LOC, Parenteralglucose or glucagon
Macrocirculation of Diabetes Atherosclerosis CAD HTN Stroke
Microcirculation of Diabetes Perpherial Vascular Disease Intermittent claudication (pain with activity, goes away with rests) Occlusions/Thrombosis Ulcerations (Infection, Gangrene = amputation) Diabetic Retinopathy Cataracts Diabetic Nephropathy (loves the heart and kidneys)
Peripheral Neuropathies Bilateral sensory disorders (Paresthesias, numbness/tingling, Pain-burning, shooting, aching, cold feet, Impaired sensations) Single nerve (Palsy of 3rdCranial nerve, Radiculopathy, Femoral neuropathy, Entrapment or compression of nerve)
Visceral Neuropathies Sweating dysfunction Abnormal pupillary function Cardiovascular dysfunction Gastroparesis Genitourinary dysfunction (Bladder, Sexual function)
Diabetes increases susceptibility to infection Bladder/kidney infections Skin, nails, and mucous membranes prone to tuberculosis Osteomyelitis (bone infection, feet) Risk factors (Sensory deficits lead to unknown trauma, vascular/neurological impairments, hyperglycemia altered neutrophil function)
Diabetes Periodontal Disease If occurs progresses more rapidly Microangiopathy (gingivitis and periodonitis) Diabetes doesn’t cause it, but can increase progression
Diabetic Foot Complications Angiopathy, neuropathy, infection High risk for amputations Unrecognized foot trauma Daily foot care Use proper fitting shoes Have professional foot/nail care Clean with white washcloth! Buying and wearing shoes Care of toenails
Created by: nimeggs