Diabetes Mellitus (Type 1 & 2) - PDF

Diabetes Mellitus (DM)  Syndrome of  Disorder of carbohydrate, fat, and protein metabolism  Hyperglycemia resulting from deficits in insulin secretion, insulin action, or a combination of both  Two distinct types: type 1 and type 2  Type 1 (Insulin depend...

Diabetes Mellitus (DM)  Syndrome of  Disorder of carbohydrate, fat, and protein metabolism  Hyperglycemia resulting from deficits in insulin secretion, insulin action, or a combination of both  Two distinct types: type 1 and type 2  Type 1 (Insulin dependent, IDDM, Juvenile onset)  Type 2 (Non insulin dependent NIDDM, Adult onset) DM Epidemiology  Impaired fasting glucose (IFG) and impaired glucose tolerance (IGT) are used to describe  Fasting glucose between 100 and 125 mg/dL  2-hour post-glucose load blood glucose 140 to 199 mg/dL  DM is the most common endocrine disorder  Affecting 25.8 million people in the United States  Complications  Cardiovascular and peripheral vascular disease, decreased immune system functioning, renal failure, and retinopathy  Diabetic nephropathy is now the leading cause of end-stage renal disease  DM also is the leading cause of acquired blindness in the United States Diagnostic Testing  Pre-Diabetes  Fasting BG 100-125 mg/dl  2-hour plasma glucose (75 gm glucose load) 140-199 mg/dl  HbA1c 5.7% – 6.4% DM Type 1  Severe insulin deficiency (body can’t make enough insulin)  Resulting from beta-cell destruction and producing hyperglycemia (genetic abnormality)  Lack of insulin alters lipid, carbohydrate, and protein metabolism  Complications: Diabetic ketoacidosis (DKA), hyperosmolar hyperglycemic syndrome (HHS)  Life-threatening sequelae of hyperglycemia DM Type 1: Epidemiology  Occurs in approximately 1 in 800,000 Americans  10% of all cases of diabetes  1.5 to 2 times more common in whites  60% of patients are under age 18 years  Correlates with differential expression of human leukocyte antigen (HLA) haplotypes  Latent autoimmune diabetes of adults (LADA)—nonpediatric patients  Two forms  Immune-mediated DM (90%): autoimmune destruction of the beta cells  Idiopathic DM: no known cause and has no evidence of autoimmunity  Inherited: need for insulin replacement therapy is variable DM Type 1: Pathophysiology  Reduction or absence of functioning beta cells- insulin absence  Absence of C-peptides  Begins with a genetic susceptibility—mapped to the HLA region on chromosome HLA-DR3 & HLA-DR4  Some triggering mechanism (e.g., viral infection or other environmental factor)  Stimulates an inflammatory response  Initiates autoimmune infiltration of the pancreatic beta cells DM Type 1: Clinical Presentation (subjective)  Subjective  Manifestation of symptoms varies  Classic symptoms of type 1 DM are polydipsia, polyuria, polyphagia, anorexia, and weight loss  Additional symptoms  Nocturnalenuresis, visual changes, weakness, fatigue, nausea, abdominal pain  May present with repeated infections, decreased wound healing, or infections that are uncommon DM Type 1: Clinical Presentation (objective)  Objective  Weight loss despite normal or increased appetite (polyphagia)  Reduced muscle mass  Ketones (byproduct) in urine due to body fat-burning  Signs of dehydration: poor skin turgor and dry mucous membranes  Neurological: diabetic retinopathy, third cranial nerve palsy, or the sixth (abducens) and fourth (trochlear) cranial nerves can also be affected in cranial neuropathy DM Diagnostic Testing  Initial testing  In office  Casual (random) plasma glucose measurement  Urine should be tested for ketones  Current recommendation for the diagnosis of diabetes  Symptoms of diabetes (e.g., polyuria, polydipsia, weight loss) plus a casual (random) plasma glucose level of 200 mg/dL or higher  OR fasting plasma glucose level of 125 mg/dL or higher  OR a 2-hour plasma glucose of 199 mg/dL or higher during an oral glucose tolerance test (OGTT) with a 75-g glucose load (not for routine use)  These criteria should be confirmed by repeat testing on a different day except in the case of unequivocal hyperglycemia with acute metabolic decompensation DM Diagnostic Testing  Subsequent testing  A1C  Mean plasma glucose concentration over the preceding 2 to 3 months  Documenting the degree of glycemic control  ADA recommends that the treatment goal should be a A1C below 6.0% Older population: 6.0%-7.0%  Fasting lipid profile urinalysis, microalbuminuria, thyroid function tests, and serum creatinine if protein is present Hypoglycemia  Management of hypoglycemia  Plasma glucose less than 70 mg/dL is diagnostic  Can occur for a variety of reasons  Excessive exogenous insulin  Missed meals or inadequate food intake  Exerciseabundance, alcohol ingestion, drug interactions, and a decrease in liver or kidney function  Signs and symptoms  Diaphoresis, tachycardia, hunger, shakiness, altered mentation (ranging from inability to concentrate to coma), slurred speech, and seizure, headache  Will start like this (easily recognizable) Hypoglycemia - Treatment  Goal: normalize the plasma glucose promptly  Accomplished by the ingestion of 15 g of carbohydrate  Blood glucose should be checked 15 minutes after treatment  Additional carbohydrate should be given if the blood glucose results remain less than 60 mg/dL  For severe hypoglycemia and if the patient is unconscious or unable to swallow, 1 mg of glucagon SQ or D5W IVP can be given DM Type 1: Management  Requires ongoing health care and education to prevent acute and chronic complications  Complex and lifelong management  ADA recommends a team approach  Treatment program requires  Insulin regimens  Frequent self-monitoring of blood glucose (SMBG): ACHS sugars  Medical nutrition therapy (MNT)  Regular exercise  Continuing education in the prevention and treatment of complications  Periodic assessment of treatment goals DM Type 1: Management (cont’d)  Insulin therapy  Initial goal: normalize blood glucose  Plasma glucose levels at 80 to 120 mg/dL before meals  Plasma glucose levels of 100 to 140 mg/dL at bedtime  A1C below 7%  New-onset type 1 diabetic often presents in crisis and requires hospitalization – Covered by endocrinologist  Intensive insulin regimens  Does increase the chance of hypoglycemic episodes (the tighter you control sugar, the more normalized you control it, the easier the chance for hypoglycemia)  Doses of regular insulin before meals with an evening dose of neutral protamine Hagedorn (NPH). Now more on long acting insulin and supplemented with regular insulin  Requires diligent and frequent blood glucose monitoring Insulin calculation  Insulin start – 0.5 units/kg/day (2/3 in am & 1/3 in pm)  BG > 140 mg/dl before evening meal – add 2-5 units every 3 days  Once afternoon is check fasting – if elevated, give 2/3 before breakfast & 1/3 before dinner  After afternoon & fasting are regulated -> work on late morning to keep due  Decreased sensitivity at night to counter regulatory hormones d/t growth hormone spike  Hypoglycemia at 3 am  Sugar elevated throughout (hormones release) night-> high at 7 am  Sugar becomes elevated at 7  Treatment am  Increase evening dose of  Treatment insulin  Reduce/omit bedtime dose  Levemir – shorter acting than Lantus (benefits to take long acing insulin earlier)  Give long acting earlier DM Type 1: Management SBGM  Self-monitoring of blood glucose (SMBG)  Plasma venous glucose measurements are within 15% of the results of whole blood capillary test results  Used to evaluate the effectiveness of the insulin regimen, medical nutrition therapy, and exercise  It is the most useful mechanism to maintain glucose levels as close to normal as possible  Optimal monitoring for patients with type 1 DM is 3 to 4 times a day—before each meal and before bedtime (ACHS) DM Type 1: Management (diet)  Diet  Meal planning or medical nutritional therapy (MNT) done with collaborative team  May require substantial lifestyle changes  Goals of nutritional therapy  Maintain normal blood glucose level  Prevent hypoglycemia  Maintain normal serum lipid levels  Attain or maintain reasonable body weight  Promote healthy eating patterns  Diet  Carbs 55-60%  Fiber 25 gm/1000 cal  Fat 25-35%  Protein 15-20%  Type 1  3 meals/day with 3 snacks  Counting Carbs  Type 2  Meals 5 hours apart DM Type 1: Management (exercise)  Exercise  Before beginning an exercise program  Screeningfor the presence of macrovascular and microvascular complications  Coronary artery disease (CAD), peripheral arterial disease, retinopathy, nephropathy, and peripheral or autonomic neuropathy  No exercise limitation as long as glycemic control is good and there is no evidence of complications DM Type 1: Management (exercise cont’d)  Exercise (cont’d)  Exercise can exacerbate hyperglycemia or hypoglycemia  Check blood glucose before, every 30 to 60 minutes during, and after exercise  Avoid exercise if the fasting glucose is more than 250 mg/dL and ketosis is present or if the glucose level is more than 300 mg/dL, regardless of whether ketosis is present.  Consume additional carbohydrate if the glucose is less than 100 mg/dL and as needed to avoid hypoglycemia.  Identify when changes in insulin or food are necessary  Individualized to patient’s interest, lifestyle, physical condition, and motivation  Include 150 minutes/week of moderate to intense aerobic activity  Muscle-strengthening exercises can also be added DM Type 1: Complications  Retinopathy, nephropathy, and neuropathy  Significantly reduced when HbA1C levels are maintained below 7%  HbA1c determination should be performed at least twice a year in patients with good control and quarterly in patients whose therapy has changed or who are not meeting glycemic goals  Comprehensive foot exam and a funduscopic exam  Referral to a specialist for the following complications may be indicated  Retinopathy, hyperlipidemia, nephropathy, hypertension, macrovascular disease, and neuropathy Ketoacidosis: DKA  Elevated glucose -> increased osmolality -> dehydration  14% of all hospital admissions  Type 1 & Type 2 with 90% Beta cell function loss  See with pumps (clogged or malfunctioned), insulin omission, illness  Subjective  3 Ps (polyuria, polydipsia, polyphagia), N&V, Sunken eyes & poor turgor (dehydration), hyperkalemia  Labs  Glucose >250 mg/dl; PH 5.0 mEq/L Ketoacidosis - Management  Insulin  Loading 0.1-0.15 units/kg Reg IV - then continuous IV drip 0.1 units/kg/hr  If plasma glucose doesn’t fall by 10% w/in 1st hour – give second loading dose  When plasma glucose is 200 –decrease IV to 0.05 units/kg/hr  Maintain D5W & 0.45 NS to maintain BG 200 until ketosis is resolved  Once acidosis is corrected – SQ insulin  Sodium Bicarbonate  Rarely needed  50-100 mEeq/liter of hypotonic saline if pH is < 7.0 mol/L Diabetes Mellitus Type 2  Group of heterogeneous forms characterized by insufficient circulating endogenous insulin, resistance to insulin action, and an inadequate compensatory insulin secretion response  Fifth leading cause of death in the United States  Contributes to many other diseases, particularly heart disease, which is the leading cause of death  Reduces life expectancy because of complications DM Type 2: Epidemiology and Causes  Prevalence of type 2 DM in United States is 6.6%  Often asymptomatic in its early stages  Chronic hyperglycemia associated with long-term damage and dysfunction of various organs  Risk factors  First-degree relative with type 2 DM  Disproportionate number of African Americans, Hispanic Americans, Native Americans, Asian Americans, and Pacific Islanders have diabetes  Increases with age  History of gestational DM  Pharmacological agents associated with iatrogenic hyperglycemia: glucocorticoids, hormonal therapies, immunosuppressants, nicotinic acid, protease inhibitors, atypical antipsychotic agents, antihypertensives  Distinct linkage between CAD, hyperlipidemia, obesity, and DM DM Type 2: Pathophysiology  Two physiological abnormalities  Insulin resistance: inherited feature associated with acquired traits of obesity and aging  Impaired insulin secretion: still some circulating insulin  Hyperinsulinemia fails to keep pace—hyperglycemia  Decline in beta-cell function overtime  Impaired insulin secretion occurs in response to a glycemic load  Potential defect in the conversion of proinsulin to insulin or the premature, dysregulated secretion of proinsulin  Serum levels of amylin decrease with insulin  DM Type 2: Pathophysiology (cont’d)  Insulin resistance worsens  Manifesting first as postprandial hyperglycemia (couple hours after meals, levels wont return to normal as quick as someone without T2D)  Eventually as fasting hyperglycemia  Obesity contributes to peripheral insulin resistance  Sympathetic tone and cardiac contractility are increased by hyperinsulinemia  Triad of  disturbed glucose metabolism  hypertension (>140/90 mm Hg),  dyslipidemia with obesity is referred to as insulin resistance syndrome, syndrome X, obesity dyslipidemia syndrome, or the metabolic syndrome DM Type 2: Clinical Presentation  Asymptomatic individuals diagnosed during a routine physical examination or during treatment for another condition  Subjective  Onset is insidious  Present with pruritus or neuropathic complaints such as numbness and tingling  Increased urination, nocturia, thirst, or polydipsia  Present with infection, especially candidiasis  Symptoms of type 1 and type 2 DM are basically the same  Objective  Often obese, signs of comorbid diseases are possible DM Type 2: Diagnostic Testing  Initial testing  Office setting  Random capillary glucose measurement  Resultof 200 mg/dL or more should be evaluated by screening for blood glucose with whole blood  Itis important to consider that certain drugs, including glucocorticoids, furosemide (Lasix), thiazides, phenytoin (Dilantin), estrogen-containing products, beta-blockers, and nicotinic acid can produce hyperglycemia  Ifthe random plasma glucose level is elevated, the urine should be tested for ketones DM Type 2: Diagnostic Reasoning (cont’d)  Four ways to diagnose diabetes  A1C ≥6.5% on 2 occasions  Symptoms of DM plus random plasma glucose concentration ≥200 mg/dL on 2 occasions  Fasting plasma glucose ≥126 mg/dL on 2 occasions  Fasting is defined as no caloric intake for at least 9 hours  Two-hour post-load glucose ≥200 mg/dL during an oral glucose tolerance test on 2 occasions  The test should be performed using a glucose load containing the equivalent of 75 g of anhydrous glucose dissolved in water  This test is not recommended for routine clinical use or in pregnancy DM Type 2: Management  Chronic illness that requires ongoing health care and education to prevent acute and chronic complications  Frequent SMBG  Medical nutritional therapy with weight reduction when indicated  Use of oral glucose-lowering agents and/or insulin  Regular exercise  Continuing education in the prevention and treatment of complications  Periodic assessment of treatment goals  DM Type 2: Management (cont’d)  Exercise  Before beginning an exercise program  Screening for the presence of macrovascular and microvascular complications that may be worsened by exercise  Exercise can cause hypoglycemia  Check blood glucose before and after exercise.  Avoid exercise if the fasting glucose is more than 250 mg/dL and ketosis is present  Avoid exercise if the glucose level is more than 300 mg/dL, regardless of whether ketosis is present  Consume additional carbohydrate if the glucose is less than 100 mg/dL and as needed to avoid hypoglycemia  Exercise prescription should be individualized DM Type 2: Management (cont’d)  Subsequent management  Fasting plasma glucose measurements are less than 200 mg/dL (as close to 120 as possible)  Presenting symptoms are not severe  Dietand exercise should be initiated to control hyperglycemia  Frequent follow-up during the trial period (e.g. 180 blood sugar, since < 200, give three months, or HgbA1C is in 7%, want three months to bring it down, or fasting > 300, put on oral agent during 3-month trial)  Symptomatic patients and patients with marked hyperglycemia (fasting plasma glucose 300 mg/dL or more) will show significant improvement in both with initiation of an oral agent DM Type 2: Hyperosmolar Hyperglycemic Non-Ketosis Syndrome (HHS)  Profound dehydration from prolonged hyperglycemia  Associated with a high mortality rate (30-50%)  Seen in older adults with an infection  Undiagnosed DM may develop into this condition because of prolonged hyperglycemia without treatment  Symptoms  Severe hyperglycemia (more than 600 mg/dL)  Plasma or serum hyperosmolality (more than 340 mOsm)  Profound dehydration Hyperosmolar Hyperglycemic Non-Ketosis Syndrome (HHS)  Subjective / Objective  Disorientation, lethargy, seizure, stupor, coma, dehydration S&S, polyuria, hypotension, tachycardia  Labs  BG > 600 -1000; elev serum osmolarity (>310 mOsm/L); elev BUN & Cr, Na; pH & anion gap normal; C-peptides present = some insulin is being made to prevent ketosis Hyperosmolar Hyperglycemic Non-Ketosis Syndrome (HHS) - Management  Critical Care – invasive  Fluid replacement – isotonic until hemodynamically stable  If not hypotensive or once serum Na is 145 mEq/L hypotonic solutions used to hydrate (0.45 NS)  Fluids 4-6 L in first 8-10 hrs  Overall 6-10 L  Monitor for complications of fluid; cardiac failure, cerebral edema, seizure (especially in elderly) Hyperosmolar Hyperglycemic Non-Ketosis Syndrome (HHS) - Management  Insulin  Loading 0.1-0.15 units/kg Reg IV - then continuous IV drip 0.1 units/kg/hr  If PG doesn’t fall by 10% w/in 1st hour – give second loading dose  When PG is 200 –decrease IV to 0.05 units/kg/hr  Maintain D5W & 0.45 NS to maintain BG 200 until metabolic imbalance is resolved  Continue monitoring Electrolytes (Na, K, HCO3, Cl, Phosphorous) prn  Cardiac monitoring for dysrhythmias - K DM Type 2: Management - Pharmacological  Pharmacological therapy  Required when dietary modification and exercise do not result in blood glucose control  Should always be considered an adjunct therapy to diet and exercise and not as a substitute  Oral medication is initiated when 3 months of nutritional therapy and exercise have not achieved and maintained fasting plasma glucose levels