Diabetes and Thyroid Dysfunction Medium Quiz

Differentiating Type I and Type II Diabetes

• Type 1 diabetes onset usually occurs in childhood or adolescence.
• Type 2 diabetes can start at any age, but typically after 40, and is occurring more frequently in younger individuals.
• Type 1 is an autoimmune condition where the body's immune system attacks and destroys insulin-producing beta cells, leading to an absolute insulin deficiency.
• Type 2 is characterized by insulin resistance and a relative insulin deficiency, where the body doesn't produce enough or cells don't respond properly.

Treatments for Type I and Type II Diabetes

• Type 1 diabetes is primarily treated with insulin therapy because the body cannot produce insulin.
• Type 2 treatment starts with lifestyle changes and oral medications, potentially progressing to injectable medications.
• Rapid-acting insulin like insulin lispro or aspart controls blood sugar spikes when taken before meals.
• Short-acting insulin, or regular insulin, is taken 30-60 minutes before meals.
• Intermediate-acting insulin, NPH insulin, covers insulin needs for about half a day or overnight.
• Long-acting insulin like insulin glargine or detemir provides a steady insulin level throughout the day.
• Ultra-long-acting insulin like insulin degludec lasts for over 24 hours.
• Amylinomimetics like Pramlintide control blood sugar levels after meals.
• Metformin decreases glucose production in the liver and improves insulin sensitivity.
• Sulfonylureas like glipizide and glyburide stimulate the pancreas to release more insulin.
• Meglitinides like repaglinide stimulate insulin release faster than sulfonylureas.
• Thiazolidinediones like pioglitazone improve insulin sensitivity.
• DPP-4 inhibitors like sitagliptin increase insulin release and decrease glucagon levels.
• SGLT2 inhibitors like canagliflozin help the kidneys remove glucose from the bloodstream.
• GLP-1 receptor agonists like liraglutide increase insulin secretion and decrease appetite.
• Insulin may be required if other medications are insufficient for controlling blood sugar levels.

A1C Values in Diabetes

• Glycosylated hemoglobin (Hemoglobin A1C) measures average blood sugar levels over the past 2-3 months.
• Normal A1C is below 5.7%.
• Prediabetes ranges from 5.7% to 6.4%.
• An A1C of 6.5% or higher indicates diabetes.
• A less stringent A1C goal greater than 7% may be more appropriate for some Type 2 diabetics.
• The general A1C target for most adults with diabetes is less than 7%.
• Less stringent targets of 7-8% A1C may be suitable for older adults, those with severe hypoglycemia history, or comorbidities.
• More stringent targets A1C less than 6.5% may be considered for younger, healthier people at low hypoglycemia risk.
• A1C values above the goal of 7% may require treatment adjustments, including meds and lifestyle changes.
• Significantly high A1C values of 8% or above suggest poor control and indicate need for more intensive interventions.
• Primary goals of treating T1DM or T2DM are managing blood glucose levels and preventing long-term complications.
• Proper diet and physical activity form the base of diabetes management.

Insulin Function

• Insulin helps cells in muscles, fat, and the liver absorb glucose from the bloodstream; the glucose is then utilized for energy or stored.
• By promoting glucose uptake, insulin lowers blood sugar levels, preventing hyperglycemia.
• Insulin stimulates the conversion of glucose into glycogen in the liver and muscles, known as glycogenesis.
• Insulin suppresses glucose production in the liver from non-carbohydrate sources like amino acids and fats, also known as gluconeogenesis.
• Insulin promotes excess glucose storage as fat in adipose tissues and inhibits fat breakdown, helping to maintain energy balance.
• Insulin facilitates amino acid uptake into cells, promoting protein synthesis and muscle growth.

Initiating Insulin in Type II Diabetes

• Insulin initiation is recommended when A1C remains above target, usually 7%, despite optimal oral medications and/or GLP-1 receptor agonists use.
• Insulin is needed when a patient's fasting blood glucose levels are consistently above 130 mg/dL.
• It is recommended with severe hyperglycemia, if a patient's A1C is greater than 10% or blood glucose levels are consistently above 300 mg/dL.
• The presence of hyperglycemia symptoms like polyuria, polydipsia, weight loss, or evidence of catabolism require insulin.
• Acute illness, hospitalization, or surgery, may require insulin to manage blood glucose levels.
• A basal insulin regimen typically starts with 0.1-0.2 units/kg per day or 10 units per day.
• The dose should be titrated every 2-3 days based on fasting blood glucose levels, aiming for 80-130 mg/dL.
• A basal-bolus regimen includes long-acting insulin like insulin glargine or detemir for a steady level throughout the day.
• Bolus insulin involves rapid-acting insulin like insulin lispro or aspart before meals to control postprandial glucose spikes.
• Premixed insulin combines intermediate-acting and rapid-acting insulin in one injection, taken before breakfast and dinner.
• Monitoring and adjustment involve self-monitoring of blood glucose levels to appropriately adjust insulin doses.
• Regular follow-ups with healthcare providers are essential to review blood glucose logs and adjust insulin doses.
• Patient education includes proper injection technique training, rotating injection sites to avoid lipodystrophy.
• Educate patients on hypoglycemia management, recognizing and managing hypoglycemia, including carrying fast-acting carbohydrates.

ADA Algorithm for Type II Diabetes

• Initial management emphasizes lifestyle modifications, including a balanced diet rich in vegetables, fruits, whole grains, and lean proteins.
• Physical activity should consist of at least 150 minutes of moderate-intensity aerobic activity per week.
• The goal for weight management should be a 5-10% reduction in body weight for overweight or obese individuals.
• Metformin is the recommended initial pharmacologic treatment unless contraindicated.
• Additional medications beyond lifestyle modifications and metformin are considered based on patient factors if glycemic targets aren't met.
• GLP-1 receptor agonists like liraglutide or semaglutide and SGLT2 inhibitors like empagliflozin or canagliflozin are used for atherosclerotic cardiovascular disease (ASCVD) or high risk.
• SGLT2 inhibitors are preferred for heart failure (HF) or chronic kidney disease (CKD) due to their benefits in reducing heart failure and slowing CKD progression.
• DPP-4 inhibitors like sitagliptin, GLP-1 receptor agonists like exenatide, SGLT2 inhibitors like dapagliflozin, and thiazolidinediones like pioglitazone are used to minimize hypoglycemia.
• GLP-1 receptor agonists like liraglutide and SGLT2 inhibitors like canagliflozin help with weight management.
• Cost should be considered with sulfonylureas like glipizide and thiazolidinediones like pioglitazone.
• For insulin therapy, basal insulin is initiated if A1C remains above target despite dual/triple therapy.
• Basal-bolus regimens should be considered for patients with severe hyperglycemia or those not achieving targets with basal insulin alone.

Continued Care for Type II Diabetes

• Regular monitoring involves frequent blood glucose monitoring and A1C testing every 3-6 months.
• Adjustments should modify treatment based on glucose levels, A1C results, and patient preferences.
• Comprehensive care includes cardiovascular risk management, addressing hypertension, dyslipidemia, and smoking cessation, as well as diabetes self-management education (DSME).

Oral Antidiabetic Agents and Their Mechanisms

• First and second generation sulfonylureas, biguanides, alpha-glucosidase inhibitors, thiazolidinediones, meglitinides, and incrins are oral antidiabetic agents.
• Fixed combinations of oral antidiabetic drugs also qualify.
• Examples of first and second generation sulfonylureas include glibenclamide (glyburide), glipizide, and glimepiride.
• These drugs stimulate the pancreas to release more insulin by binding to sulfonylurea receptors on pancreatic β-cells, causing closure of ATP-sensitive potassium channels, leading to cell depolarization, calcium influx, and subsequent insulin release.
• Biguanides like metformin inhibit hepatic glucose production (gluconeogenesis), reducing liver glucose production.
• Metformin enhances insulin sensitivity in peripheral tissues like muscle and fat, increasing glucose uptake, and may improve lipid profiles.
• Alpha-glucosidase inhibitors like acarbose and miglitol inhibit the enzyme alpha-glucosidase, responsible for breaking down complex carbohydrates into simpler sugars in the small intestine.
• These drugs delay carbohydrate absorption by inhibiting alpha-glucosidase, preventing rapid blood glucose spikes after meals.
• Thiazolidinediones (TZDs) like pioglitazone and rosiglitazone activate peroxisome proliferator-activated receptor-gamma (PPAR-y) in the liver, muscle, and fat tissues, leading to increased insulin sensitivity.
• TZDs help in the redistribution of fat, reducing lipotoxicity andimproving insulin action, without directly affecting insulin secretion.
• Meglitinides like repaglinide and nateglinide stimulate insulin secretion from the pancreas, similar to sulfonylureas.
• They bind to different sites on the sulfonylurea receptor, work similarly by closing ATP-sensitive potassium channels in pancreatic β-cells.
• These drugs have a faster onset and shorter duration than sulfonylureas, effectively controlling postprandial glucose spikes.
• Incretins include GLP-1 receptor agonists like exenatide and liraglutide, mimic the action of the incretin hormone GLP-1, which is released in response to meals.
• GLP-1 increases insulin secretion in a glucose-dependent manner, suppresses glucagon release, and slows gastric emptying, reducing appetite and lowering blood glucose levels.
• DPP-4 inhibitors like sitagliptin and saxagliptin prevent the breakdown of endogenous GLP-1 by inhibiting the DPP-4 enzyme.
• DPP-4 prolongs the action of GLP-1 and enhances insulin secretion in a glucose-dependent manner.
• The fixed combination drug Glyburide/Metformin (Glucovance) includes a sulfonylurea (glyburide) and a biguanide (metformin).
• Glyburide stimulates insulin secretion from the pancreas and Metformin reduces hepatic glucose production and improves insulin sensitivity.

Summary of Oral Antidiabetic Agents

• Sulfonylureas stimulate insulin secretion from the pancreas, lowering blood glucose.
• Biguanides reduce hepatic glucose production and improve insulin sensitivity, lowering blood glucose.
• Alpha-glucosidase inhibitors prevent carbohydrate breakdown and absorption, stabilizing postprandial blood glucose levels.
• Thiazolidinediones (TZDs) improve insulin sensitivity in liver, muscle, and fat cells, lowering blood glucose.
• Meglitinides stimulate insulin secretion, lowering blood glucose after meals.
• Incretins enhance insulin secretion and inhibit glucagon release, for the reduction of blood glucose .
• A fixed combination of glyburide and metformin enhances insulin secretion and improves insulin sensitivity, reducing liver glucose production.

Side Effects of Oral Antidiabetic Drugs

• Sulfonylureas can lead to hypoglycemia, weight gain, gastrointestinal disturbances, allergic reactions, hematological issues, and potential cardiovascular risks.
• Metformin can commonly cause gastrointestinal distress and rarely causes lactic acidosis, or vitamin B12 deficiency.
• Alpha-glucosidase inhibitors can cause flatulence, diarrhea, and abdominal pain.
• Thiazolidinediones (TZDs) can cause fluid retention, edema, heart failure, fractures, hepatic toxicity, and bladder cancer.
• Meglitinides can cause hypoglycemia and weight gain with possible gastrointestinal discomfort and allergic reactions.
• Incretins can lead to gastrointestinal issues, pancreatitis, injection site reactions, and potential thyroid cancer.
• Fixed combination drugs like glyburide/metformin can cause hypoglycemia, gastrointestinal issues, the rare serious side effect of lactic acidosis and weight gain from sulfonylureas.

Risks and Contraindications

• Sulfonylureas' major side effect is hypoglycemia; intensifying drugs include nonsteroidal anti-inflammatory drugs (NSAIDs), sulfonamide antibiotics, alcohol, and cimetidine drugs.
• Beta blockers can suppress insulin release to diminish the benefits of sulfonylureas.
• Monitor Kidney function for Metformin - risk of lactic acidosis, especially in patients with renal impairment.
• Metformin is often the first-line treatment for type 2 diabetes since it helps lower glucose production in the liver.
• Risk of hypoglycemia from from glimepiride and glipizide, especially in elderly patients or those with renal impairment.
• Take glimepiride and glipizide with meals to reduce the risk of low blood sugar.
• Repaglinide and Nateglinide pose a hypoglycemia risk similar to sulfonylureas.
• Repaglinide and Nateglinide are short-acting and taken before meals to help control postprandial blood glucose levels.
• Pioglitazone and rosiglitazone cause cause or exacerbate heart failure so monitor for fluid retention.
• Take acarbose and miglitol with the first bite of each meal to slow carbohydrate absorption.
• Sitagliptin and saxagliptin pose risk pancreatitis monitor for symptoms like severe abdominal pain.
• Canagliflozin and dapagliflozin increase the risk of urinary tract infections and genital infections, so kidney function must be monitored.

Hypothyroidism

• Signs and symptoms depend on disease severity.
• Face is pale, puffy, and expressionless.
• Skin is cold and dry, hair is course and brittle, and hair loss occurs.
• Heart rate and temperature are lowered.
• Patients complain of lethargy, fatigue, and cold intolerance.
• Mentation may be impaired, deepened voice.
• Females experience heavy menses.

Myxedema vs Cretinism

• Myxedema is an advanced hypothyroidism in adults while Cretinism is a congenital hypothyroidism.
• Fatigue, weight gain, dry skin, hair loss, swelling of face and limbs are signs of Myxedema.
• Stunted growth, intellectual disability, delayed development, and physical abnormalities are signs of Cretinism.
• Myxedema is caused by autoimmune thyroiditis, thyroid surgery, or severe iodine deficiency that develops later in life.
• Cretinism is genetic defects or iodine deficiency during pregnancy and is present at birth or early infancy.
• Physical signs of Myxedema include a puffy face and mental sluggishness.
• Physical signs of Cretinism include a puffy face, protruding tongue, wide neck, large abdomen, and short stature.
• Myxedema coma is life-threatening.
• Cretinism can lead to severe cognitive impairment and growth abnormalities if untreated.
• An effective treatment for is Thyroid hormone replacement therapy.

Hypothyroidism in Pregnant Women

• Implications for NPs begins with Early Detection and Management - screen thyroid function early, especially in women with risk factors.
• Thyroid Hormone Replacement - adjust levothyroxine doses and regularly monitor TSH and free T4.
• Continuous montitoring with frequent follow ups that can provide better outcomes
• NPs can provide clear instructions on medication use with Early aducation.

Pediatric Hypothyroidism

• NPs should ensure newborn screening for hypothyroidism is performed and follow up on abnormal results appropriately.
• Initiate levothyroxine treatment as soon as hypothyroidism is diagnosed and adjust doses based on regular monitoring of TSH and free T4 levels.
• Regular monitoring of growth and developmental milestones.
• Nps should provide comprehensive education and make the risks and benefits clear.

Labs in Hypothyroidism

• Total T4 (mcg/dL) Normal -4.5-12.5 Hypothyroid - Under 4.5, Hyperthyroid- Over 12.5
• Free T4 (ng/dL) Normal -0.9-2, Hypothyroid - Under 0.9, Hyperthyroid- Over 2
• Total T3 (ng/dL) Normal -80-220, Hypothyroid - Under 80, Hyperthyroid- Over 220
• Free T3 (pg/dL) Normal -230-620, Hypothyroid - Under 230, Hyperthyroid- Over 620
• TSH (microunits/mL) Normal -0.3-6, Hypothyroid - Over 6, Hyperthyroid- Under 0.3
• Treat with Levothyroxine; start with a starting dose around 1.6 mcg/kg/day (adjusted based on age, weight, and comorbidities).
• If TSH < 7 mIU/L but no symptoms? Just monitor.
• A TSH > 7 mIU/L or symptoms? Consider a low dose of Levothyroxine (25–50 mcg/day).
• If a patient is Pregnancy or planning pregnancy? Treat even with mild TSH elevation to avoid complications.

Key Things to Know

• Hypothyroidism may require lifelong medication.
• Start low - check TSH and free T4 6-8 weeks after starting or adjusting dose, then every 6-12 months..
• Check for Under-treatment (fatigue, weight gain) and over-treatment (palpitations).
• Dose needs often increase with pregnancy.
• Elderly patient requires lower dose- Dose by weight/age.
• Know signs of hypo- and hyperthyroidism & adhere to medicaton schedules.
• Cardiovascular risk factors for older patients.

Drugs for Hypothyroidism that Patients Should Avoid

• Reduce Levothyroxine - H2 receptor blockers, proton pump inhibitors, cholestyramine.
• Take drugs 4 hours apart.
• Use carbamazepine, Rifampin or Phenytoin to accelerate Levo.
• Can cause bone loss.
• Can result in nervousness, irritability, restlessness, headache etc.
• May induce Adrenal crisis, if adrenal insufficiency is unrecognized and untreated before starting thyroid therapy.
• **There meds are accelerate metabolism of levothyroxine and can thereby reduse its effects. An increase in levothyroxine dosage may be needed.
• It may Intensify effects of Warfarin.. Reduce dosage if needed..
• Exercise caution when catecholamines and levothyroxine are used together.