T1DM.pdf

T YPE 1 DIABETES A N DY R O G E R S , PA - C PERFORMANCE MEDICINE OBJECTIVES T1D Overview T1D Pathophysiology, Etiology, and Epidemiology T1D Presentation, Signs, and Symptoms T1D Diagnosis and Treatment Insulin Overview Management of Hypoglycemia and Hyperglycemia T1D Comp...

T YPE 1 DIABETES A N DY R O G E R S , PA - C PERFORMANCE MEDICINE OBJECTIVES T1D Overview T1D Pathophysiology, Etiology, and Epidemiology T1D Presentation, Signs, and Symptoms T1D Diagnosis and Treatment Insulin Overview Management of Hypoglycemia and Hyperglycemia T1D Complications Device Demonstrations T1D OVERVIEW PAT H O P H Y S I O L O G Y, E T I O L O G Y, EPIDEMIOLOGY T1D AT A GLANCE Pathophysiology: autoimmune destruction of beta cells Etiology: genetic predisposition + environmental trigger Prevalence: 1.25 million Americans w/ T1D – Only 5-10% of all diabetes Incidence: 21% increase in incidence b/t 2001-2009 Lab Diagnostics: Clinical, FPG, RPG, A1C, C-Peptide, Antibodies Treatment Gold Standard: Insulin via MDI or CI + SMBG or CGM PANCE Blueprint: Endocrinology 6% T1D PATHOPHYSIOLOGY Genetic predisposition (HLA-DQ, HLA-DR)* & environmental agent induce a complex, almost individualized, autoimmune destruction of pancreatic β cells Pancreatic specimens, taken from tissue samples at onset of symptoms, have shown signs of a chronic inflammatory state of its endocrine portions, as evidenced by inflammatory markers.1 Anatomical changes of the pancreas (i.e. decrease in size and weight) also provide clues to the Progressive inflammatory autoimmune process ensues – Evidenced by pancreatic tissue specimens & serological markers at onset of symptoms show the presence of autoantibodies T1D ETIOLOGY Coxsackie virus Cow’s milk – Historical autopsy evidence, dating as far – Early introduction of cow’s milk has been back as the 1970’s, taken from children with shown to produce a humoral response, onset of T1D diagnosis in diabetic complete with diabetogenic antigens, that ketoacidosis (DKA) revealed the isolation of trigger an inflammatory autoimmune the Coxsackie Virus B4 from the islet cells of response. the pancreas. – The potential mechanism of action, though Vitamin D Deficiency not fully realized, may involve increased gut permeability through gut flor modification – Trends show an overwhelming incidence and with the early introduction of complex prevalence of T1D in areas with significantly proteins. less sun exposure. – Theorists would say inadequate activation of the immunologic cascade derived from inadequate levels of vitamin D leaves pancreatic β cells more susceptible to autoimmune attack. T1D EPIDEMIOLOGY “Type 1 diabetes can be diagnosed at any age and in people of every race, shape and size.” – Dr. Peters and Dr. Wood Peak incidence in 5-7 y.o. and puberty Equal among male and female Highest incidence in Finland (overwhelmingly) – 65 new cases per 100,000 children aged < 20 per year while Sweden, at 2nd, comes in at 30 per 100,000 T1D PRESENTATION S I G N S A N D S Y M P TO M S CLINICAL SCENARIO 9 year old boy presents with polyuria, polydipsia, and unintentional wt loss despite increase in appetite x 3-6 mo. Mother confirms hx and admits to a subtle change in mood and energy, and a worsening over the past couple of weeks. Mother is convinced this is the flu and asks for a flu test. Flu Test negative (-). RPG = 450 mg/dL: A1C = 9%; GADA, IAA, & IA-2A = pending SIGNS AND S Y M P TO M S T1D DIAGNOSTICS DIAGNOSTIC CRITERIA Diagnostic Test (+) Results A1c > 6.5% (measured in 3 mo increments to reflect RBC life) Fasting plasma glucose (FPG) > 126 mg/dL (no caloric intake for at least 8 hr) Random plasma glucose (RPG) > 200 mg/dL Antibodies + for > 1 (Insulin autoantibodies IAA, Glutamic acid decarboxylase autoantibodies GADA, Zinc transporter-8 autoantibodies ZnT8A, islet cell cytoplasmic autoantibodies ICA, etc.) C-Peptide < 0.2 nmol/L Hyperglycemia in the presence of antibodies C-Peptide levels determine the level of endogenous insulin levels/activity or disease progression T1D MONITORING C H E C K YO U R B L O O D G L U C O S E  Self Monitoring of Blood Glucose GLUCOSE – What? Using a small blood sample via M O N I TO R I N G finger prick to test serum glucose levels – Why? Test glucose to see how if insulin SMBG = doses are keeping patients in target – What is target? 80-120 mg/dL Self Monitoring of – When to check? Blood Glucose 3 to 4 times daily With 50 strips per bottle, this means about 150 per month – Brands? One Touch, Freestyle, Contour, Accu-Check  Continuous Glucose Monitoring – What? A sensor with an electrode placed GLUCOSE SQ measures the glucose in the interstitial M O N I TO R I N G fluid with readings every 5 min – Why? CGM = Pro’s: More readings and more trends, less Continuous finger sticks, alarms for low’s/high’s Con’s: Expense, +/- delay in BG’s in real time Glucose – How often to change? ~ 10 days Monitoring depending on brand – How to write? Easiest to have patient fill out contact form on company’s website for coverage info – Brands? Dexcom, Medtronic, Freestyle  GLYCEMIC GOALS A1c < 7% ↓ microvascular complications, and, if implemented soon after dx, is assoc with reduction in macrovascular ds. – Patients with T1D are usually seen every 3-6 months depending on A1c and change in treatment* A1c 80 mg/dL Glucagon injection for severe hypoglycemia – “Mini” Gluc protocol** “QUICK” CARBS What? A simple carb that is readily available to get in the bloodstream Who? – 4 oz. juice or regular soda – 1 juice box – 4 glucose tabs – 1 gummy pack – 1 glucose gel pack – 1 tablespoon honey or sugar When? Now. Get the sugar in NOW. Common mistakes? – Too much too quickly means you’ll have rebound hyperglycemia – A “slow” carb before a “quick” carb That quick carb won’t absorb and it’ll take longer for the BG to come up i.e. chocolate milk before juice ANOTHER QUESTION FOR THE GROUP 15 yo F with T1D presents to your urgent care for what you suspect is acute sinusitis x 1 wk. She admits to feeling fatigued with a HA, sore throat, productive cough, and just feeling all together terrible. Her BG’s have been running a little higher d/t her illness. Her CBC comes back with an elevated white count but strep is negative.You want to give her an abx to make her feel better but she tells you her friend came the other day and got a shot of something that made her feel better really quickly. What is this injection her friend most likely got? Do we give it to her? Why or why not? HYPERGLYCEMIA High Blood Glucose > 150 mg/dL Signs/Symptoms – Polyuria, polydipsia, polyphagia, blurry vision, fatigue – Think of the undiagnosed T1D patient Causes – Miscalculation of insulin dose, missing a dose/non-compliance, stress, illness, age/hormones Treatment – Correction Factor (CF)* = 1800/TDD Then (BG – target)/CF for number of units given for correction dose i.e. BG is 250 and with a goal of 150 and I weigh 144 lbs, how much insulin to give? – Wait 1-2 hours before giving another dose and do not give full dose Remember DOA for rapid acting insulin is 4 hrs What do we check when BG’s > 250 mg/dL? What can you always do to help BG’s come down? I N PAT I E N T H Y P E R G LY C E M I A SETTING Example of order set for inpatient setting for treatment of hyperglycemia. Ere on the side of caution to prevent hypoglycemia. Time and fluids will be your biggest friend. DKA Diabetic Ketoacidosis, in laymen's terms is the blood turning acidic d/t dehydration and high blood glucose, creating a harmful environment for the body – Dehydration + increased blood glucose – insulin (a counter-regulatory hormone) = accumulation of free fatty acids (β-hydroxybutyric acid and acetoacetic acid) which then dissociate to hydrogen ions that bind to bicarb = decreased bicarb and increased anion gap Signs/Symptoms: – Fruity breath/odor*, Kussmaul’s respirations,** weakness, n/v, abdominal pain, weakness/fatigue, extreme dehydration Causes: – Pump malfunction/occlusion, non-compliance, comorbidities, sickness, undiagnosed T1D Treatment: – Fluids (1L of 0.9% NS per hour initially) + insulin drip (0.1 U/kg/hr) +/- potassium – Replace with bicarb?*** OTHER “T1D” MEDICATIONS AMYLIN Symlin© (Pramlintide) What? (MOA) Synthetic Amylin, a hormone produced by pancreatic ß-cells Why? (Indication) Adjunctive therapy to insulin for post-prandial glucose control How? (ROA) Injectable pen device, Starting Dose of 15 mcg (up to 120 mcg) with each meal of at least 30g carbs or 250 calories Where? Not used in the US a lot, more so in Europe Oh no! (AE/SE’s) – Severe hypoglycemia (Consider mealtime insulin dosing adjustment) – Nausea, vomiting, stomach upset OTHER “T1D” MEDICATIONS S G LT1/ 2 I N HIBITOR S Farxiga© (Dapagliflozin), Jardiance© (Empagliflozin), Zynquista© (Sotagliflozin)* What? (MOA) SGLT1 inhibitor, which inhibits the reabsorption of glucose in the kidneys Why? (Indication) Adjunctive therapy to insulin for A1C and FPG/RPG reduction How? (ROA) 1 pill PO daily in different dosage forms Where? Not approved yet, but used off-label Oh no! (AE/SE’s) – Hypotension, Acute Kidney Injury, DKA in the Type 1 Diabetes Population** – Yeast Infections, Acute pharyngitis, changes in urinary habits INSULIN FOR SPECIAL POPULATIONS Insulin Resistant – Think of the obese patient requiring more than 200 units daily or more than 100 units per dose – Use insulin with higher potency/concentration (i.e. Humalin R U-500 vial, Tresiba U-200 pen) Pregnancy – Tighter control is needed to prevent pre/postnatal complications – General goals = FPG’s < 90 mg/dL, PPG’s 300 mg/d or >200 μg/min) confirmed on at least 2 occasions 3-6 months apart – progressive decline in GFR – ↑arterial BP Treatment: – Yearly measurement of creatinine, urinary albumin excretion, K – Consider ACE/ARB – Insulin dose adjustments based on GFR & refer to nephrology if GFR < 30  Stocking-and-glove distribution in distal extremities – loss of balance, especially with the eyes closed, & N E U R O PAT H Y painless injuries due to loss of sensation Test with pinprick, vibration tuning fork, 10-g monofilament, & ankle reflexes All pts should be screened for distal symmetric polyneuropathy (DPN) at dx of type 2 and 5 yrs after dx of type 1 and at least yearly thereafter Prevention & regular foot exams are best, but some medications may help sensation: – Pregabalin (Lyrica) – Gabapentin (Neurontin) – TCAs (amitryptilline, nortryptilline, imipramine) – Topical lidocaine or capsaicin can help Neuropathy + poor perfusion (due to atherosclerosis/PAD) → non-healing foot ulcers, amputations – Refer to wound care or podiatry! CHECK YOUR PT’S FEET! ON THE RISE NEW INSULIN & T1D DELAY 2023 Advanced Technologies and Treatments for Diabetes (ATTD) Conference in Berlin shared information on two new Once Weekly Insulins in studies: – Icodec (Novo Nordisk, ½ life 7-8 days) and Efsitora (Lilly, ½ life 17 days) – Demonstrating promise with less hypoglycemia & more TIR – Studied in Type 2 diabetes Teplizumab is FDA approved for delay of T1D Onset – First of its kind with more in the pipeline from other companies – From ProventionBio & Sanofi, Expensive for full course of treatment – Delays onset for about 2 years – Must be in “Stage 2” or detectable antibody positive without seroconversion to T1D Studying T2DM medications for T1DM – Metformin and GLP-1 Agonists Reduces insulin requirements & decreases hepatic glucose production WRAP-UP Every T1D needs: – T1D Medical Alert ID – Insulin (basal and bolus) through some sort of delivery device – Needles to deliver the insulin +/- skin adhesive for pumps – Blood glucose monitoring through some sort of device +/- testing strips (which are expensive), lacets for the meter, skin adhesives for CGM’s – UTD Glucagon Injection (expires each year) – Supplies for low’s on hand – Alcohol preps All this on top of quarterly visits that include A1C and neuro/podiatry checks, yearly funduscopic exams, health plans to attend school, extra supplies should pump sites fail or insulin degrades in the hot car, or extra insulin for when BG’s go out of control… A N DY R O G E R S , PA - C PERFORMANCE MEDICINE A N DY @ P E R F O R M A N C E M E D I C I N E. N E T THANK YOU!