Diabetes Mellitus Presentation PDF

Diabetes Mellitus Elizabeth Sendlak PA-C, MPAS Objectives Define the diagnostic criteria for diabetes Describe the significance of impaired fasting glucose and metabolic syndrome List risk factors for diabetes Explain the pathogenesis of diabetes types 1 and 2 State life...

Diabetes Mellitus Elizabeth Sendlak PA-C, MPAS Objectives Define the diagnostic criteria for diabetes Describe the significance of impaired fasting glucose and metabolic syndrome List risk factors for diabetes Explain the pathogenesis of diabetes types 1 and 2 State lifestyle modifications for prevention of diabetes type 2 Define current screening guidelines for diabetes Explain microvascular and macrovascular complications associated with diabetes Identify comorbid conditions associated with diabetes and appropriate medical modifications State the components of an out-patient diabetic exam List appropriate health maintenance recommendations for a diabetic patient Objectives Identify types of neuropathy associated with diabetes and the appropriate treatment options available State possible infectious complications associated with diabetes Describe diabetic retinopathy findings and the appropriate screening and prevention methods Describe findings seen with diabetic renal disease and role of microalbumin monitoring Describe findings of diabetic foot infections and the associated complications Describe treatment options available for diabetes including lifestyle modifications and medications Explain use of glucometer and continuous glucose monitors in the monitoring of home blood glucose levels List symptoms associated with hypoglycemia Describe treatment of hypoglycemia Explain Somogyi effect and Dawn Phenomenon State screening guidelines for gestational diabetes Define the diagnostic criteria for gestational diabetes List treatment options for gestational diabetes Identify complications associated with gestational diabetes in the mother and infant Diabetes Mellitus Syndrome of disordered metabolism and inappropriate hyperglycemia May be d/t deficiency of insulin secretion OR combination of insulin resistance and inadequate insulin secretion Over 37 million people in the US diagnosed with DM (10.5% of the population) 5-10% due to Type 1, remainder with Type 2 Diabetes Mellitus  Can be Primary or Secondary  May be temporary in some cases depending on cause  Primary etiologies:  Type 2 Diabetes (most common)  Type 1 Diabetes  Gestational  Malnutrition-related (rare – beta cell dysfunction, blood sugar imbalances) Diabetes Mellitus  Secondary etiologies:  Pancreatic disease  Pancreatitis, malignancy  Other endocrine disorders  Cushing’s, acromegaly, pheochromocytoma, glucagonoma  Medications  Corticosteroids, diuretics, beta-blockers, niacin  Genetic disorders  Cystic Fibrosis Diabetes Mellitus  Serum glucose is major energy source for all tissues  Especially brain, muscles, RBCs  Glucose metabolism occurs through glycogenolysis (breakdown of glycogen) and gluconeogenesis (synthesis of new CHO from non-CHO source) Diabetes Mellitus  Insulin is the key regulator of serum glucose concentration  Synthesized in beta-cells of islets in pancreas as a precursor, then cleaved into its active form and a C-peptide residual  Normally, a basal amount of insulin is produced and secreted, along with a bolus response to a glucose load in the serum Diabetes Mellitus  Glucagon acts in the liver to promote gluconeogenesis and glycogenolysis  Incretins (GLP-1 Proteins) = hormone that inhibits glucagon secretion and stimulates insulin secretion during meals (impt in many new meds!)  Epinephrine works on receptors in the liver to effect same changes as glucagon  Also works on alpha-2 receptors of beta cells to inhibit insulin release  Induces symptoms of hypoglycemia (tremor, sweating, anxiety)  Cortisol and Growth Hormone inhibit glucose utilization by promoting gluconeogenesis and inhibiting glucose uptake in tissues (raise serum glc when needed, ie stressful situations) DM Diagnostic Criteria  Hemoglobin A1C 6.5% or higher  Fasting plasma glucose 126 mg/dL or higher after 8hr fast  Random (casual) plasma glucose > 200mg/dL with classic symptoms  Polydipsia, polyuria, polyphagia, unexplained weight loss, fatigue  2 hour plasma glucose level 200mg/dL or greater after a glucose load (OGTT)  Test should be repeated to confirm diagnosis DM Diagnostic Criteria Diabetes.org DM Signs/Symptoms  Classic “3-P’s”  Polyuria, polydipsia, polyphagia  Can be more common in Type 1 DM  Weight loss  More common in Type 1 DM  Dehydration  Altered mental status  Blurred vision  Fungal and/or bacterial infections  Polyneuropathy  Most patients have NO symptoms and are found on screening tests  This is the goal, to diagnosis before complications occur! Type 1 Diabetes Mellitus  Due to autoimmune destruction of pancreatic islet beta cells  Rate of destruction is variable  Progression from Stage 1 (autoantibodies present but normal glucose tolerance)  Stage 2 (autoantibodies with glucose intolerance)  Stage 3 (symptomatic disease)  Most common in children/young adults  Can occur at any age  Insulin is absent  Plasma glucagon is elevated, however beta cells unable to respond to stimulus to produce insulin  Exogenous insulin is required to prevent ketosis and reduce blood glucose Type 1 Diabetes Mellitus  Typically due to anti-islet cell antibodies  Some cases due to autoantibodies against glutamic acid decarboxylase (GAD)  This is impt for testing (can check GAD AB)  Latent form of Type 1 DM exists  LADA (Latent Autoimmune Diabetes of Adults)  Often confused in adults with Type 2 DM  Slowly leads to insulin deficiency with evidence of autoimmune islet cell destruction Type 1 Diabetes Mellitus  Evaluation of autoantibodies can be helpful to differentiate Type 1 vs Type 2 if diagnosis unclear  Can also be used to screen family members of patient with Type 1 DM  Autoantibodies presence can precede onset of disease by 5 years or more  New medication aims to slow this progression (Tzield)  Anti-islet cell antibodies, insulin autoantibodies, glutamate decarboxylase (GAD) antibodies, and insulinoma-related antigen-2 are all highly sensitive (approx. 80%), and highly specific (approx. 99%) for Type 1 DM Type 1 Diabetes Mellitus  Risks a/w Type 1 DM:  Can develop Diabetic Ketoacidosis (DKA)  Can also see same chronic complications as seen in Type 2 DM (will discuss)  Higher rate of other autoimmune disorders  Since Type 1 is due to severe insulin deficiency  therapy must be replacement of insulin  Medications that stimulate insulin production or activity are not effective Type 1 Diabetes Mellitus  Diabetic Ketoacidosis  Emergency situation!  Can affect Type 1 and Type 2 diabetics  However much greater risk in Type 1 d/t severe insulin deficiency  Can be precipitated by inadequate insulin (new dx, compliance)  Also can be associated with infection (UTI, pneumonia), or vascular issue (MI, CVA) Type 1 Diabetes Mellitus  Lack of insulin leads to accumulation of ketones in the serum  lowering of pH  Insulin deficiency  glycogenolysis, gluconeogenesis, lipolysis  Ketones are a product of fat breakdown to form glucose  Lack of insulin  ketone accumulation  acidosis  High serum glucose causes osmotic diuresis  dehydration, electrolyte loss, worsening of acidosis Type 1 Diabetes Mellitus  DKA diagnostic criteria  Serum glucose > 250mg/dL  Arterial pH ≤ 7.30  HCO3 ≤ 18mmol/L  Anion gap > 10  Urine/serum ketones positive Type 1 Diabetes Mellitus  DKA Signs/Symptoms  Vomiting (from acidosis)  Thirst  Polyuria  Weight loss (from dehydration)  Abdominal pain  Tachycardia, dry skin/mucous membranes, hypotension  Kussmaul breathing (hyperventilation from metabolic acidosis)  Acetone smell to breath and urine (juicy fruit)  Confusion and coma Type 1 Diabetes Mellitus  DKA Work-up  Serum electrolytes, ketones  CBC and blood cultures (signs of infection that may have triggered DKA)  Blood gas to assess acid-base status and severity  Urinalysis (infection), urine ketones  EKG (peaked T waves with hyperkalemia, or other arrhythmia)  CRX (evaluate for infection or CHF)  CT/MRI of head if altered mental status (cerebral edema can occur with fluid shifts)  Consider abdominal US/imaging to evaluate for infectious source if needed Type 1 Diabetes Mellitus  DKA Treatment  Restore hydration with normal saline (monitor electrolytes closely)  Replace insulin with IV insulin (monitor glucose closely)  Replace electrolytes  Especially potassium as can continue to drop once insulin infused and acidosis starts to correct  Restore acid-base balance (IV fluids and insulin will remove ketones)  Determine cause of DKA – must treat precipitating factor!  ? Non-compliance with treatment, infection, MI Type 1 Diabetes Mellitus  DKA complications  Altered mental status (monitor for cerebral edema)  Hypotension (pre-renal from dehydration)  Hypothermia (rapid IV fluid replacement)  DVT (acidosis can cause hypercoagulability)  Hypoglycemia, hypokalemia  CHF  ICU setting typically required if:  Altered mental status, severe acidosis (pH 160 if no RFs for CV disease (>130 if + RFs) in children  Thyroid screening and Celiac disease screening annually Type 1 Diabetes Mellitus  Second most frequent chronic childhood illness (asthma #1)  Critical to educate parents and child about disease state, diet, insulin, screenings required for end-organ damage  Can be very difficult time during adolescence Diabetes Mellitus - Other  MODY (maturity-onset diabetes of the young)  Genetic defects with beta cell dysfunction (genetic disorder)  Neither Type 1 or Type 2  Autosomal dominant  Often times characterized as the “young and skinny” type 2 DM  Insulin resistance not typically present  Islet function typically preserved for at least 3-5 years after onset Type 2 Diabetes Mellitus  Incidence increases with age  Age of onset typically > 40  Associated with obesity  Increased caloric intake and decreased caloric expenditure  Strong genetic link  Ask about FHx!  90% concordance in identical twins; 15-25% for non-identical siblings  Endogenous insulin is present (normal or increased)  Insulin resistance almost always present Type 2 DM Pathogenesis  Insulin resistance  Cells become less responsive to insulin  Impaired insulin secretion from the pancreas  Can see loss of beta cells over time  High insulin levels commonly seen in most people with diabetes, especially early on   Dyslipidemia  Hypercoagulability  Atherosclerosis  Further weight gain/obesity (insulin acts as a growth hormone) Impaired Fasting Glucose  Prediabetes  Impaired fasting glucose between 100-125mg/dL  Impaired glucose tolerance  Glucose level measured 2hrs after 75mg glucose oral load  140-199mg/dL  Hgb A1C 5.7-6.4%  Without significant change/weight loss, high rate of conversion into frank DM Type 2  Educate patient on l/s modifications for prevention into DM  Impaired glucose tolerance is the biggest predictor of cardiovascular risk Type 2 DM Risk Factors  Family history  Low birth weight, low weight at 12mo of age  Male gender  Age > 45yo  Ethnicity: Hispanic, Native-American, African-American, Asian-American, Pacific Islanders  H/o gestational diabetes  HTN  Dyslipidemia  PCOS, acanthosis nigricans (a/w insulin resistance)  Obesity (abdominal circumference)  Sedentary lifestyle  Western diet  Stress Acanthosis nigricans – velvety, dark discoloration of skin in body folds/creases Metabolic Syndrome  Cluster of conditions that occur together, increasing the risk for diabetes and cardiovascular disease  Involves 3 or more of the following:  Central (abdominal) obesity as measured by waist circumference  Men > 40 inches, women > 35 inches  Fasting triglycerides ≥ 150mg/dL (or under tx for this)  HDL cholesterol  Men < 40, women < 50  BP ≥ 130/85 (or under tx for this)  Fasting glucose ≥ 100mg/dL Obesity  Can be primary or secondary etiologies (Cushing’s, hypothyroid)  Measures used to diagnose obesity  BMI = kg/m2  Waist circumference (measured midway between lowest rib and iliac crest while standing)  Ghrelin and leptin are 2 feedback mediators on appetite  Current area of interest for research and development on role of these in weight loss medications Obesity  BMI  18.5-24.9 = healthy weight  25-29.9 = overweight  30-34.9 = obese (Class 1)  35-39.9 = severe obesity (Class 2)  40+ = profound obesity (Class 3) Type 2 DM Prevention  Consume a healthy, balanced diet  Fruits, vegetables, fiber, protein  Limit foods high in sugar (soda, white breads, baked goods)  Low fat (especially saturated) diet  Aerobic exercise  150 min of moderate exercise per week  Weight loss/maintaining healthy weight  5% weight loss associated with 74% reduction in risk of developing diabetes  Smoking cessation Type 2 DM Screening  Consider in all patients every 3 years starting at age 45  Some guidelines recommend annually for all adults  Consider earlier screening (30yo) and more frequently if:  BMI 25+ and acanthosis nigricans  Sedentary  1st degree relative with DM  High-risk ethnicity  H/o gestation DM or delivery of > 9lb infant  H/o impaired fasting glucose  HTN  HDL < 36mg/dL or triglycerides > 249  PCOS  H/o vascular disease Type 2 DM  Hyperosmolar Nonketotic (HONK) Hyperglycemia State  Typically found in Type 2 DM, however, can occur in Type 1  Severe hyperglycemia  diuresis due to high osmotic load through nephrons  severe dehydration  Presence of insulin prevents ketosis  However, insulin present at insufficient levels Type 2 DM  HONK diagnostic criteria  Plasma glucose > 600mg/dL  Arterial pH > 7.30  Serum HCO3 > 15  Anion gap can be variable  Urine/serum ketones absent (or minimal)  Serum osmolality > 320mOsm/kg Type 2 DM  HONK presentation  Altered mental status/coma  Severe dehydration  Stroke/MI/Acute lower extremity arterial insufficiency  Arterial thrombosis due to pro-inflammatory effect of extreme hyperglycemia (hyperviscosity and glycosylated proteins) Type 2 DM  HONK Treatment  Fluid replacement with normal saline  Cautious, slow infusion of insulin  Frequent monitoring of serum osmolality, glucose, and electrolytes  Anticoagulation  Must monitor for signs of cerebral edema and thrombotic complications Type 2 DM Treatment  L/S modifications  Diet, exercise, weight loss, self monitoring/screening, reduction of other RFs (HTN, lipids)  Medications (oral, injectables, insulin)  Typical progression is:  L/s modifications  l/s mods + oral medications  l/s mods + oral meds + insulin  In some cases, may progress right to insulin management depending on severity Type 2 DM Treatment  Diet  Avoid refined sugars  < 30% of calories should be from fat  At least 15%+ should come from protein  Remainder is from “healthy” carbohydrates  Whole grains, fruits, vegetables, legumes, low-fat dairy  Total calories per day depends on BMI  If ideal weight  1800cal/day  If overweight  caloric restriction based on weight loss of 1kg/wk  Refer to RD/diabetic educator! Type 2 DM Treatment  Glycemic index = measures how foods affect blood sugar levels  Area under the curve of blood glucose values elicited by a carbohydrate containing food item divided by the same measure of an equivalent amount of pure glucose  How fast and how high does a certain food make a person’s blood glucose rise?  Working principle behind Atkin’s and South Beach diets  Utilizing a low glycemic index diet to elicit normal glucose levels and low GI foods also tend to inhibit appetite DM Treatment  Carbohydrate counting:  Educate patients on how to estimate the grams of carbohydrate (or the GI) of food items  Especially useful for insulin-dependent patients (Type 1 or Type 2)  Typically taught by a registered dietician/diabetic educator  Prescribing a diet to your patients:  Lifelong changes only – avoid crash diets  Slow weight loss  Limit alcohol consumption DM Treatment  Exercise  At least 150 minutes per week of moderate exercise (50-70% max HR)  Resistance exercises for all muscle groups  Build up slowly in sedentary patients!  Caution with potential for hypoglycemia during exercise  Especially if Type 1 DM  CHO (20-40g) prior to and during exercise  May need to reduce insulin dose if intense exercise planned DM Treatment  Self-monitoring/screening  Examine feet daily  Annual eye exam  Weight, BP, lipid screening/monitoring  Stay UTD with vaccinations (flu, pneumonia, hep B series)  Glucometer/CGM DM Treatment  Optimal glucose control  Fasting 80-139 mg/dL  2-hr post-prandial 130-180 mg/dL  Pregnancy guidelines stricter (ADA, ACOG)  Fasting 60-99 mg/dL (also before meals)  Peak 1-2hr post-prandial 100-129 mg/dL  Very tight control – can be at risk for hypoglycemia! DM Treatment  Glucose monitoring  Can be performed with glucometer via fingerstick  Newer monitoring uses Continuous Glucose Monitors  10 day (Dexcom) to 14 day (Libre) subcutaneous interstitial glucose sensor worn which then downloads to smartphone app or reader device  Have alarms to alert patient of low or high BS  Most insurances cover if on daily insulin injection DM Treatment DM Treatment Type 2 DM Treatment  Combination therapy is very common  Many options, important to practice shared decision making  Patient preference (PO vs injectable)  How many times/day  Cost  Not a static condition – requires continual monitoring of treatment success  Initiating a medication does not mean l/s modifications no longer needed!  Side effect and organ damage monitoring should be performed routinely Type 2 DM Treatment  Oral medications  Metformin  Sulfonylureas  Meglitinides  Alpha-glucosidase inhibitors  Thiazolidinediones  DPP-4 inhibitors  Incretin memetics  SGLT-2 inhibitors Type 2 DM Treatment  Metformin  Very common initial medication  Used in monotherapy and combination with many other meds  Decreases gluconeogenesis, glycogenolysis, and oxidation of fatty acids in the liver  Facilitates insulin binding to receptors on insulin target tissues  Does NOT cause hypoglycemia  Common side effects are GI upset, mainly diarrhea (temporary)  Lessened by taking with food and slowly titrate up dose  Risk of lactic acidosis  Avoid if hepatic or renal failure  Need to hold dose x 48hrs after IV contrast administration  Hold x 48hrs for surgical procedures Type 2 DM Treatment  Sulfonylureas  Works on beta islet cells to increase insulin production  Works well if islet cells are functional  Risk of hypoglycemia!  Caution in the elderly Type 2 DM Treatment  Meglitinides  Work on same receptors as sulfonylureas, but much shorter half-life  Given just before meals to control post-prandial rise in glucose  Not commonly used (expensive and inconvenient)  Also risk of hypoglycemia! Type 2 DM Treatment  Alpha-glucosidase inhibitors  Block the enzyme responsible for breakdown of sucrose  glucose and fructose  Decreases absorption of monosaccharides  If patient is taking this medication along with other medications that can cause hypoglycemia (ie. Sulfonylurea, insulin), they must carry oral glucose preparation  This medication will block the absorption of sucrose and other disaccharides Type 2 DM Treatment  Thiazolidinediones (TZDs)  Act intracellularly to enhance insulin receptor activity  increased insulin sensitivity  Must monitor LFTs  Original medication caused rare but severe hepatic failure  Most common side effect is fluid retention  Caution if CHF Type 2 DM Treatment  Dipeptidyl peptidase IV (DPP-4) Inhibitors  DPP-4 is a gut enzyme that degrades glucagon-like peptide-1 (GLP-1)  GLP-1 is released by intestinal mucosal cells in response to glucose, which then mediates the release of insulin  GLP-1 is deficient in Type 2 DM (? May be dysfunctional in Type 1)  Oral, once daily medication, however not as great of impact on A1C compared to GLP-1 Type 2 DM Treatment  Incretin Mimetics  Synthetic analogue to GLP-1  Significant effect on A1C  Desirable side effect of weight loss  Slows gastric emptying  can cause n/v  Most are injectables  Oral version = Rybelsus (semaglutide)  Tirzepatide (Mounjaro) – GLP-1 and GIP (glucose-dependent insulinotropic peptide)  Newest, with even greater A1C/weight loss effects  Some have other desirable effects for reduction in cardiovascular disease  Branded under alternative names for weight loss Type 2 DM Treatment  Sodium-glucose Co-transporter 2 (SGLT-2) inhibitors  Block reabsorption of glucose in the renal tubules  Causes increased urination  Can cause UTIs and yeast infections  Some also found to reduce risk of heart disease  Can be used for heart disease w/o diagnosis of DM  Also have shown benefit of slowing progression of renal disease Type 2 DM Treatment  Amylin analogues  Pramlinitide (Symlin)  stimulates amylin activity  Amylin = hormone secreted by pancreatic islet cells that follows insulin secretion  Acts to slow gastric emptying and decrease release of glucagon (reduces hepatic gluconeogenesis)  Only approved for use in conjunction with insulin therapy  Also only available as injectable DM Treatment  Insulin  Originally derived from pork/beef sources, now made by recombinant technology = recombinant human insulin  C-peptide is removed which leads to less allergic reactions  Available in IV, SQ and inhaled forms DM Treatment  Inhaled insulin  Affreza  Cannot be used if asthma, COPD or smoking within the past 6 months DM Treatment  For Type 2 DM, typically start with basal insulin if needed  Once daily injection  Add in bolus or “mealtime” insulin if suboptimal control  Improved control with CHO counting and appropriate bolus dose PRIOR to meal  Can also use “sliding scale”  Type 1 DM requires insulin  can be through injections (basal + bolus) or insulin pump Type 2 DM Treatment  Sliding Scale  Reactive approach to blood glucose levels  Suboptimal control typically achieved Insulin Therapy  Overuse of a single site can lead to abnormal fat deposition or atrophy  decreased absorption of the insulin  Must rotate sites  Accidental blood vessel or intradermal injection can affect onset of action time Insulin Pumps  Designed for use by highly motivated patients  Typically used in Type 1 DM, but occasionally used in Type 2  Requires frequent monitoring of glucose levels  Requires a moderate degree of knowledge/training on:  I:C ratios  CHO counting/estimation  Correction factors for pre-prandial glucose  Comfortableness with pump and supplies  Awareness of complications and responses  Provides an infusion of pre-set basal rate short-acting insulin (amounts can vary through-out the day)  Operator then can set pre-meal boluses Insulin Pumps  “artificial pancreas”  Bluetooth interface with CGM and the pump  CGM senses interstitial glucose (9-15min delay from blood glucose)  Insulin administration adjusted based on glucose measurement Treatment Overview  Type 1 DM  Insulin is absolute requirement  Type 2 DM  Shared decision making, tailor therapy to each individual patient  Basic algorithms Lipid Guidelines  Lipids should be screened at least every 5 years  Typically done more often  All patients with DM aged 40-75 are recommended (ACC/AHA) to be on at least a moderate dose of a statin medication  Reduces LDL 30-50% from baseline  High dose statin recommended if 10 year CVD event risk is > 10%  ACSVD calculator Blood Pressure Guidelines  JNC 8 Recommendations  Reduce BP to < 140/90 for all patients with diabetes  Some guidelines recommend 135/85; < 130/80 if high risk for CV disease  Recommends preferential use of ACE-I/ARB, followed by CCBs for optimal BP control ACCORD Trial  Large multi-centered trial that revealed contradictory information  Tight control of DM (A1C 30%, consider additional management strategies prior to discontinuing ACE/ARB Diabetes During Pregnancy  Critical to identify at risk mothers because 2 patients are affected by maternal diabetes!  Pre-existing diabetes with the following complications presents serious issues/complications if mother were to become pregnant:  Evidence of ischemic heart disease  Advanced nephropathy  Advanced retinopathy  Severe, symptomatic autonomic neuropathy Diabetes During Pregnancy  Screen for diabetes during pregnancy with 50g oral glucose tolerance test  Typically completed at 24-28 weeks  High risk patients are also screened at first prenatal visit (FBS, A1C)  FHx, obese, previous glucosuria  If positive  then check 100g test  Mother is typically asymptomatic when diagnosis does not precede pregnancy Diabetes During Pregnancy  Overt diabetes is diagnosed if at first prenatal visit:  Fasting plasma glucose ≥ 126mg/dL  Hgb A1C ≥ 6.5%  Random plasma glucose ≥ 200mg/dL  Gestational Diabetes diagnosed if at ANY time:  Fasting plasma glucose 95-125mg/dL  Hgb A1C 5.7-6.4%  OR if positive on 1hr or 3hr oral glucose tolerance test (24-28wks gestation) Diabetes During Pregnancy  Maternal risks:  Fetal risks:  Metabolic derangements  Congenital malformations (DKA, HONK) (not GDM)  Cardiac defects  Progression of  Spina bifida/sacral agenesis microvascular complications  Stillbirth  Retinopathy, nephropathy  SIDS  UTIs  Neonatal complications  Pre-eclampsia  Respiratorydistress syndrome, neonatal jaundice,  Higher rate of c-sections hypoglycemia  Adult onset of diabetes Diabetes During Pregnancy  Risks to infant of a diabetic mother:  Macrosomia (larger than avg size)  Respiratory Distress Syndrome  Cardiac defects  Great vessel anomalies (transposition of great arteries, tetralogy of Fallot, truncus arteriosis)  Septal defects  Skeletal defects  Caudal regression syndrome (sacral agenesis)  Cleft palate/lip  Genitourinary defects  Renal agenesis  Ureteral duplication  Hypoglycemia, hypocalcemia, hypomagnesemia, polycythemia, jaundice  Transient heart enlargement (resolves after birth) Diabetes During Pregnancy  Unlike pre-existing diabetes, gestational diabetes is not associated with increased risks of congenital malformations  Roughly 50% of women with gestational diabetes will go on to eventually develop Type 2 DM Diabetes During Pregnancy  Treatment  Gestational DM often responds to diet alone  Insulin is preferred if needed, as it does not cross the placenta  Approximately 1/3 of women will require insulin  Metformin and sulfonylureas can be used, but with caution because they do cross the placenta Diabetes During Pregnancy  Pre-existing diabetes:  Counsel mom about the risks  Optimize glucose control and A1C PRIOR to conception when feasible  Close glucose monitoring  DKA can be lethal to fetus (almost 50% mortality); hypoglycemia not as harmful to the fetus  Insulin requirements increase during 2nd and 3rd trimesters  Screen for retinopathy and nephropathy more frequently  Advise mom on smoking cessation  Control BP and screen for pre-eclampsia  Recommend folic acid supplement  C-section recommended if suspect macrosomia Diabetes in the Elderly  Multiple factors must be considered in treatment of DM in our elderly patients  If co-morbid depression and/or dementia, can create additional barriers to treatment/goals  May have associated poor vision, decreased dexterity  Monitor for drug-drug interactions  Slower metabolism of medications  Poor diet  Inability to exercise  Hypoglycemia can be dangerous!  Must set realistic goals Surgery in Patient with Diabetes  According to AHA/ACC guidelines, DM is an intermediate clinical predictor of perioperative cardiopulmonary complications  Optimize glucose control, electrolytes and BP prior  If patient is treated with insulin  standard to cut dose in half prior to surgery if NPO (night prior for long acting insulin) Hypoglycemia  Most commonly due to complication of insulin therapy  Can also result from sulfonylureas and other oral medications  Typically defined as glucose < 60mg/dL  Below 50, start to see impairment in cognitive function  Reduced level of consciousness can start at 40  Coma and/or seizure below 30  Greatest risk seen:  Before meals  Nocturnal  Alcohol use  Exertion Hypoglycemia  Symptoms  Sweating  Shaking  Tachycardia  Hunger  Dizziness, clumsiness  Irritability, decreased concentration  Numbness/tingling  Blurred vision  Slurred speech  Seizures/LOC Hypoglycemia  Symptoms of hypoglycemia can also be elicited by normalizing blood sugar in poorly-controlled diabetes  Hypoglycemia unawareness:  In patients with long-standing diabetes, can see blunted or absent physiological counterregulatory hormone release  Do not feel typical s/sx of hypoglycemia  This can be accelerated with tight glucose control if multiple/frequent mild hypoglycemia events occur Hypoglycemia  Somogyi Effect  Nocturnal hypoglycemia from too high of a dose of insulin given at night (peak action will then be around 2-4am)  Counterregulatory hormones (cortisol) are at their lowest point at this time  Results in high morning glucose levels  Counterregulatory hormones eventually respond to hypoglycemia and “overshoot”  Differs from Dawn Phenomenon, which is a high fasting morning glucose level from normal cortisol release around 6am  Check glucose level at 2-3am in order to differentiate Hypoglycemia  Treatment  Give glucose/simple sugars  Juice, milk, soda, hard candies, jellybeans  IV dextrose  Glucagon (IM or intranasally)  Relaxation of tight control for several weeks my facilitate return of hypoglycemia awareness