Diabetes and Endocrine System - Vocabulary Flashcards
Overview of Diabetes
Diabetes is a group of diseases characterized by abnormalities in fat, carbohydrate, and protein metabolism that lead to hyperglycemia and can cause microvascular changes and neuropathic complications.
Increasing frequency in the US is linked to obesity and diet; lifestyle and cultural factors influence prevalence and management.
Education and ongoing management are essential for prevention of complications, especially in patients with cardiac disease, hypertension, or other comorbidities.
Pathophysiology and Mechanisms
Mechanisms (general): defects in secretion of insulin and/or insulin action, after metabolism of carbohydrates, fats, and proteins.
Type 1 diabetes: autoimmune destruction of pancreatic beta cells leading to absolute insulin deficiency.
Type 2 diabetes: insulin resistance with progressive insulin deficiency (impaired secretion and/or insulin resistance; may involve β-cell burnout over time).
Other specific types: genetic defects of beta cell function, genetic defects in insulin action, disease of the pancreas (e.g., cystic fibrosis), or drug-induced/organ transplant–related diabetes (e.g., steroids).
Gestational diabetes: occurs during pregnancy; increases risk of developing diabetes later in life.
Organ transplant and steroids can induce hyperglycemia or diabetes due to glucocorticoid effects on glucose metabolism.
Typical presentation varies; undiagnosed adults may present with few symptoms but hyperglycemia is detected via testing.
Classic Clinical Presentation and Signs
Three hallmark symptoms (polys):
Polyuria (frequent urination)
Polydipsia (excessive thirst)
Polyphagia (increased hunger)
The trio is often referred to as the three polys.
Other symptoms/signs: fatigue, weight loss, blurred vision, infections, slow wound healing.
In late hyperglycemia or poorly controlled diabetes, patients may report fatigue, blurred vision, and weight loss due to poor glucose utilization and dehydration.
Diagnostic and Monitoring Measures
Finger-stick glucose testing in acute settings; immediate reading helps triage.
Critical thresholds observed in practice (example values from the transcript):
Critical high: reading above 600 (for some monitors).
Critical low: reading below 60.
Laboratory tests commonly used:
CBC and CMP for general assessment and electrolyte status.
Fasting blood glucose thresholds mentioned: normal below 100\%? (clarification needed). In the discussion, fasting glucose under 100 mg/dL is described as normal; values around 101 mg/dL are noted as borderline; above 120 mg/dL is not normal.
Hemoglobin A1c (HbA1c) measures average blood glucose over about 3\text{ months}.
Normal HbA1c is described as below 5.6\%. An HbA1c of 8.9\% indicates poor control and a need for treatment adjustment.
Home monitoring and data sharing:
Patients may use home glucose monitoring devices; some systems allow clinicians to read data remotely.
Regular follow-up labs include fasting glucose and HbA1c to assess control over time.
Goals and Interpretation of Key Numbers
Fasting blood glucose goals in the discussion:
Target: below 100 \text{ mg/dL} (normal range).
Borderline/acceptable reading: around 101\ \text{mg/dL}.
Not normal: above 120 \text{ mg/dL}.
HbA1c goals and interpretation:
HbA1c reflects average glucose over about 3 months.
A reduction of HbA1c by about 1\% is typical with effective therapy such as metformin, depending on baseline values.
An HbA1c of 8.9\% indicates suboptimal control and a need for therapy adjustment.
Pharmacologic Treatments (Overview)
Medication classes are chosen based on where the patient’s metabolic defect lies (insulin deficiency vs insulin resistance) and severity.
Goals include lowering blood glucose, minimizing hypoglycemia, and improving long-term outcomes; therapy often involves lifestyle changes plus pharmacotherapy.
Metformin (Biguanide) – First-line for Type 2 Diabetes (as discussed)
Mechanism: decreases hepatic glucose production via reduced gluconeogenesis and glycogenolysis; enhances insulin-mediated glucose uptake in peripheral tissues (e.g., muscle); overall reduces hyperglycemia.
Efficacy: lowers HbA1c by about 1\% on average.
Benefits: generally not associated with weight gain; may cause weight loss of 2-3\text{ kg} in some patients.
Safety and tolerability: not associated with hypoglycemia when used alone; GI side effects (nausea, diarrhea, abdominal discomfort) and metallic taste; vitamin B12 malabsorption may occur and require monitoring/supplementation.
Dosing and titration: start low and go slow; typical titration is +500\text{ mg every 2 weeks}; the majority of glucose-lowering effect is achieved around 1500\text{ mg/day} with little additional benefit above that dose.
Renal considerations: eliminated by the kidneys; renal function should be assessed before starting and periodically thereafter (renal clearance calculations).
Contraindications/risks: generally avoided in significant renal impairment, hepatic impairment, heart failure in some contexts, alcohol use disorder, and other hypoxic states due to risk of lactic acidosis.
Drug interactions: alcohol may increase risk of hypoglycemia; interactions with other antidiabetic agents exist but are limited.
Special notes from evidence: a Cochrane review (3,347 studies, >70,000 subjects) found no overall increase in lactic acidosis with metformin vs other therapies, though high-risk groups require careful consideration.
Practical tips: take with meals to reduce GI side effects; monitor B12; assess renal function periodically.
Sulfonylureas – Insulin Secretagogues
Mechanism: close ATP-sensitive potassium channels in pancreatic beta cells, leading to cell depolarization, calcium influx, and increased insulin secretion.
Generations:
First generation: e.g., tolbutamide.
Second generation: e.g., glipizide (glipizide is still widely used).
Third generation: newer agents (examples discussed include glipizide; the note suggests third-generation options exist).
Role in therapy: often used in combination with metformin; can reduce HbA1c by up to about 0.5-1.0\% in some regimens.
Key drawback: higher risk of hypoglycemia compared to other agents.
Real-world mechanism explanation (from transcript): in type 2 diabetes, impaired ATP-sensitive K+ channel closure reduces insulin secretion; sulfonylureas help close these channels to restore insulin release.
Incretin-Based Therapies and GLP-1 Pathway
Incretins: hormones released by the gut in response to meals that enhance insulin secretion and suppress glucagon, contributing to better postprandial glucose control.
GLP-1 (glucagon-like peptide-1):
Increases insulin secretion and suppresses glucagon when nutrients are present in the gut.
Slows gastric emptying, producing a more gradual rise in glucose after meals.
Suppresses appetite, aiding weight management.
DPP-4 inhibitors (gliptins):
Mechanism: inhibit DPP-4 enzyme, which degrades GLP-1, thereby prolonging endogenous incretin action.
Example: Januvia (sitagliptin).
GLP-1 receptor agonists (GLP-1 mimetics):
Examples discussed include exenatide (BYETTA), injected subcutaneously, typically before meals; dosing can be twice daily.
They mimic GLP-1 action but are resistant to DPP-4 degradation.
Summary of role: incretin-based therapies help lower glucose with potential weight loss benefits and a lower risk of hypoglycemia compared to secretagogues when used alone.
SGLT2 Inhibitors and Other Oral Agents
SGLT2 inhibitors (incretin-independent glucose lowering): block renal glucose reabsorption in the proximal tubule, promoting glucosuria and reducing plasma glucose.
Examples discussed include Jardiance (empagliflozin) and Steglatro (ertugliflozin).
They provide cardiovascular and renal benefits in many patients, though not all patients are eligible due to kidney function and other factors.
Insulin Therapy – Types and Use
Indications: required for Type 1 diabetes and often added for Type 2 diabetes when other meds do not achieve control.
Types of insulin:
Rapid-acting insulins: Lispro, Aspart (often used around meals or as part of a bolus regimen).
Long-acting insulins: Glargine (Lantus), Detemir; used for basal coverage (usually given at night or once daily).
Mixed insulins: e.g., 70/30 mixtures (70% Intermediate-acting to cover basal plus 30% rapid-acting for meals).
Typical regimen considerations: insulin regimens are often tailored based on patient needs, with combinations of basal and bolus insulin or premixed regimens.
Goal: achieve blood glucose control while avoiding hypoglycemia; monitor regularly and adjust dosing as needed.
Hypoglycemia: Recognition and Emergency Management
Early signs/symptoms: shakiness, sweating (diaphoresis), confusion, dizziness, hunger, irritability.
Management for awake patients: provide fast-acting carbohydrates (e.g., orange juice or oral glucose) and recheck glucose after 15 minutes; repeat if still low; avoid giving by mouth if patient is unconscious or at risk of choking.
Management for unconscious or unable to swallow: administer glucagon (emergency kit) or, if IV access is available, IV dextrose (e.g., dextrose 50% solution) can be given; call emergency services (EMS) if there is any concern about the patient’s ability to maintain airway or consciousness.
Practical tips: have quick source of glucose available; educate patients to recognize early hypoglycemia and to carry fast-acting carbs; ensure caregivers know when and how to administer glucagon.
Patient Education, Adherence, and Lifestyle Counseling
Education is a key role for nurses and physicians: diet, exercise, and medication adherence significantly impact outcomes.
Barriers to adherence discussed:
Cost/insurance access and affordability.
Access to pharmacies and medication availability.
Side effects leading to reluctance to take meds.
Preference for home remedies or alternative therapies in some cultures.
Importance of follow-up and monitoring:
Regular monitoring of fasting glucose, HbA1c, lipids, and renal/hepatic function as appropriate.
Reassessing medications based on lifestyle, weight, and comorbidities.
Education on proper insulin administration techniques and safe storage.
Lifestyle factors:
Diet: emphasis on balanced diet; discussion of low-carbohydrate/low-sugar approaches as part of glucose control.
Exercise: planning activity around insulin dosing and meals to avoid hypoglycemia.
Weight management: addressing obesity and its role in Type 2 diabetes risk and control.
Cultural and personal factors: varying beliefs about medications and therapies; need for culturally sensitive education and shared decision-making.
Diabetes Subtypes and Key Distinctions (Recap)
Type 1 diabetes:
Autoimmune beta-cell destruction; absolute insulin deficiency; often younger individuals.
Type 2 diabetes:
Insulin resistance with progressive deficiency; often older individuals; strongly linked to obesity and lifestyle.
Gestational diabetes:
Occurs during pregnancy; increases risk of type 2 diabetes later in life for the mother and child.
Other specified types:
Genetic defects of beta-cell function, insulin action; pancreatic disease (e.g., CF); drug/therapy-induced diabetes (e.g., steroids, transplant-related).
Practical Takeaways for Exam Preparation
Be able to distinguish type 1 vs type 2 diabetes in terms of pathophysiology and typical patient demographics.
Recognize the classic triad of diabetes symptoms: polyuria, polydipsia, polyphagia, plus fatigue, weight loss, and blurred vision.
Understand the purpose, mechanism, and typical side effects of major drug classes: metformin, sulfonylureas, GLP-1 mimetics, DPP-4 inhibitors, SGLT2 inhibitors, and insulin (rapid-acting, long-acting, and mixed regimens).
Know the key monitoring metrics: fasting glucose targets, HbA1c targets, and the use of home glucose monitoring data to guide therapy adjustments.
Be prepared to discuss hypoglycemia management steps and the importance of timely education and follow-up for medication adherence and lifestyle changes.
Understand how comorbidities (hypertension, hyperlipidemia, obesity) interact with diabetes management and why integrated care is critical.
Appreciate the broader context: the social determinants of health affecting diabetes care (insurance, access to healthy foods, cultural beliefs about medications).
Quick References (LaTeX-formatted for study notes)
Fasting blood glucose goals described: <100\ \text{mg/dL (normal)}, \approx 101\ \text{mg/dL (acceptable)}, >120\ \text{mg/dL (not normal)}
HbA1c: measures average glucose over \approx 3\text{ months}; normal HbA1c described as <5.6\%; typical HbA1c reduction with metformin: \approx -1\%
Metformin dosing guidance: start at low dose, titrate by +500\ \text{mg every 2 weeks}; most effect around 1500\ \text{mg/day}; monitor renal function due to renal clearance; avoid in significant renal/hepatic impairment; lactic acidosis risk discussed with comorbid conditions
Insulin regimens: rapid-acting (Lispro/Aspart), long-acting (Glargine/Lantus, Detemir), mixed (e.g., 70/30)); basal-bolus strategy common in Type 1 and many Type 2 cases
Hypoglycemia management: if awake—provide fast-acting carbohydrate (e.g., orange juice or oral glucose); if unconscious—glucagon or IV dextrose with EMS activation; avoid oral intake if risk of airway compromise
Incretin-based therapies:
DPP-4 inhibitors (e.g., Januvia) prolong endogenous GLP-1 activity
GLP-1 receptor agonists (e.g., exenatide) mimic GLP-1 action
SGLT2 inhibitors (e.g., Jardiance, Steglatro) promote glucosuria and reduce plasma glucose