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Diabetes and Endocrinology Review (Key Concepts)

Diabetes: Type 1 vs Type 2

  • Type 1 diabetes (T1D)

    • Autoimmune destruction of pancreatic beta cells leading to insulin deficiency; usually presents in childhood or young adults.

    • Classic presentation: polyuria, polydipsia, weight loss; may progress rapidly to metabolic decompensation and DKA (diabetic ketoacidosis).

    • honeymoon period: after diagnosis there can be a brief window where residual insulin is still produced; insulin requirements can change quickly in the weeks following diagnosis.

    • Treatment: lifelong insulin; insulin therapy has evolved to pumps and basal-bolus regimens (basal insulin like glargine; bolus rapid-acting insulin like lispro/aspart). Self-management is critical (carb counting, activity, illness management).

    • Education about microvascular and macrovascular complications remains essential.

  • Type 2 diabetes (T2D)

    • Predominantly due to insulin resistance with relative insulin deficiency and glucagon dysregulation; accounts for >90% of diabetes cases in adults.

    • Usually has insidious onset; many individuals are asymptomatic at diagnosis, making screening crucial.

    • Pathophysiology features include insulin resistance, relative insulin deficiency, and glucagon dysregulation contributing to hyperglycemia.

    • Management emphasizes lifestyle changes, weight management, and a stepped pharmacologic approach; cardiovascular risk management is central because of high ASCVD risk.

  • Shared themes across types

    • Both types have risks of microvascular (retinopathy, nephropathy, neuropathy) and macrovascular (ASCVD: CHD, stroke, PAD) complications if not controlled.

    • Nonpharmacologic care (diet, exercise, weight loss, self-management education) is foundational for both types.

    • Screening vs diagnosis: asymptomatic screening vs diagnostic testing when symptoms are present.

Diagnostic thresholds and screening for Type 2 diabetes

  • Diagnostic criteria (any one of the following confirms diabetes):

    • A1c \ge 6.5\%

    • FPG \ge 126 \text{mg/dL}

    • 2\text{ hr }PG \ge 200 \text{mg/dL} during an oral glucose tolerance test

    • Random plasma glucose \ge 200 \text{mg/dL} with classic hyperglycemia symptoms

  • Important notes about testing

    • A1c reflects average glucose over the past ~90\text{ days} due to RBC turnover (~90 days).

    • If the patient is not fasting, a fasting glucose criterion may not apply; repeat or use A1c for management decisions.

    • A1c is the preferred test for monitoring treatment response and progression (gold standard in many guidelines).

  • Prediabetes and screening guidelines (ADA/Task Force context)

    • Prediabetes: 5.7\% < A1c < 6.4\%

    • Screen adults aged 35-70 with BMI in overweight/obese category; other adults start screening at age 45 if BMI is not overweight/obese.

    • If prediabetes present (A1c 5.7\% \le A1c \le 6.4\%), screen annually.

    • Women with prior gestational diabetes should be screened every 3 years regardless of age.

  • Special cases and screening concepts

    • Screening is appropriate for asymptomatic individuals; diagnostic testing is used when symptoms are present.

    • In symptomatic patients, diabetes is diagnosed with one of the above thresholds, not just screening tests.

Nonpharmacologic management and goals (baseline for all patients)

  • Lifestyle and education

    • Medical nutrition therapy (dietitian referral, individualized eating plan).

    • Physical activity: aim for at least 150 \text{minutes of moderate-to-vigorous activity per week}; can be broken into shorter bouts (e.g., 5-10 minutes multiple times per day) and increased gradually.

    • Weight management: goal to reduce body weight by 5\% \text{to} \ 10\% in overweight/obese patients to improve glycemic control and comorbidities.

    • Self-management support is critical; address barriers (cost, access to healthy foods, physical activity, adherence).

  • Education on risk and prevention

    • Stigma around Type 2 diabetes exists; genetic factors contribute to risk.

    • Emphasize that diabetes risk is not solely about lifestyle; genetics and metabolism play roles.

  • Monitoring and preventive care (ABCD-like framework from ADA resources)

    • A: A1c trajectory and goals; monitor at intervals (typical follow-up every 3 months until goal and then every 3–6 months). Discuss trends and actionable changes.

    • B: Blood pressure control (target commonly < 130/80\, mmHg for diabetics at risk).

    • C: Lipids management and cardiovascular risk reduction.

    • D: Diet and exercise; weight management strategies; nutrition counseling.

    • E: Eyes – annual dilated eye exam for retinopathy.

    • F: Feet – foot exams at every visit; educate on foot care and daily self-checks.

    • G: GFR and proteinuria – screen microalbuminuria; earlier urinary protein abnormalities can precede GFR decline.

    • H: Health maintenance – smoking cessation, vaccines, and general wellness.

    • I: Immunizations – ensure age-appropriate vaccines.

    • T: Dental exams – dental health considerations for overall health in diabetes.

  • Glycemic targets and considerations

    • General target: A1c \lt 7\% for many nonpregnant adults; some patients may have a target of \lt 8\% if risk of hypoglycemia or other factors warrents.

    • If hypoglycemia risk is high or patient-specific factors dictate, an higher goal (e.g., <8%) may be appropriate.

Pharmacologic therapy for Type 2 diabetes: categories, mechanisms, pros/cons

  • Metformin (first-line)

    • Class: Biguanide; mechanism: ↓ hepatic glucose production (gluconeogenesis).

    • Advantages: no hypoglycemia risk, weight neutral or weight loss potential, long track record, cost-effective (including generic immediate-release options).

    • Disadvantages/limits: GI side effects (gas, cramping, diarrhea); B12 deficiency with long-term use; lactic acidosis risk in select settings; contraindicated if eGFR < 30 mL/min/1.73m^2.

    • Special notes: also recommended for prediabetes in many guidelines.

  • SGLT2 inhibitors (GLUT-2 kidney reabsorption inhibitors)

    • Mechanism: block renal glucose reabsorption → glucosuria; mild diuretic effect.

    • Advantages: no hypoglycemia risk; potential weight loss; CV risk reduction signals with certain agents (e.g., canagliflozin, empagliflozin); modest BP reduction.

    • Disadvantages/risks: higher cost; risk of genital mycotic infections; volume depletion/hypotension; rare risk of DKA with euglycemia; possible fracture risk with some agents (e.g., canagliflozin); may increase LDL cholesterol.

    • Notable caveat: monitor kidney function and LDL levels; avoid in advanced CKD where eGFR too low.

  • GLP-1 receptor agonists (injectables, “Cadillac” options)

    • Mechanism: incretin mimetics that increase glucose-dependent insulin secretion, suppress glucagon, slow gastric emptying, and promote satiety/weight loss.

    • Advantages: no intrinsic hypoglycemia risk when used alone; weight loss; some agents improve cardiovascular risk markers.

    • Disadvantages/risks: high cost; GI side effects (nausea, vomiting, diarrhea) especially at initiation; most are injectable (though there are oral formulations for some agents in development; refrigeration requirements vary); theoretical but not yet clearly established risk of pancreatitis and thyroid C-cell tumors in animal data.

    • Practical notes: often used when weight loss is desirable or CV risk reduction is a goal; many are expensive; patient preference for injections matters.

  • DPP-4 inhibitors (gliptins)

    • Mechanism: increase incretin levels, thereby enhancing glucose-dependent insulin secretion and decreasing glucagon release.

    • Advantages: oral agents; low risk of hypoglycemia; well tolerated.

    • Disadvantages/risks: higher cost than metformin; potential risk of pancreatitis; possible joint pains reported.

  • Thiazolidinediones (glitazones)

    • Mechanism: improve insulin sensitivity in peripheral tissues.

    • Advantages: no direct hypoglycemia risk; can be useful in certain insulin-resistant patients.

    • Disadvantages/risks: multiple safety concerns including edema/heart failure risk, weight gain, fracture risk, potential bladder cancer risk, and increased LDL in some patients; not frequently used in practice today.

  • Sulfonylureas (2nd-generation commonly used agents: glipizide, glyburide historically; modern choices prefer glipizide)

    • Mechanism: stimulate pancreatic beta cells to secrete more insulin.

    • Advantages: effective and inexpensive; familiar to clinicians.

    • Disadvantages/risks: hypoglycemia risk; weight gain; less favorable cardiovascular risk profile compared to some newer agents; generally used as second-line after metformin when cost is a concern or when other agents are not tolerated.

  • Insulin therapy (essential for many patients with T2D, especially long-standing disease or poor response to oral agents)

    • Mechanism: substitutes or supplements endogenous insulin; various compounds range from rapid-acting to long-acting; overall potent glucose disposal and suppression of hepatic glucose production.

    • Types and common uses:

    • Rapid-acting: Lispro, Aspart (before meals for mealtime coverage).

    • Short-acting: Regular insulin (short-acting; often used in older regimens or IV in hospital settings).

    • Intermediate-acting: NPH (neutral protamine Hagedorn).

    • Long-acting/Basal: Glargine (Lantus) and others; used for overnight basal coverage; often started as once-daily dosing.

    • Initiation and escalation considerations:

    • Initiation is typically considered when metformin and lifestyle are insufficient to achieve A1c goals or in cases of severe hyperglycemia, ketosis, or in the inpatient/ER setting.

    • In many patients, we begin with basal insulin (e.g., glargine) and adjust dose to achieve fasting glucose goals; may add mealtime rapid-acting insulin if postprandial glucose remains high.

    • Pros/cons:

    • Pros: potent, flexible, can achieve near-normal glycemia; reduces microvascular complications with long-term use.

    • Cons: risk of hypoglycemia, weight gain; regimen complexity and patient burden (frequent injections, glucose monitoring).

  • Practical guidelines for initiating therapy (algorithmic sense)

    • Step 1 (new diagnosis of T2D): begin with metformin and lifestyle modification unless contraindicated (eGFR < 30 mL/min/1.73m^2).

    • Step 2 (3 months later, at follow-up): if A1c remains above goal (often 7%), add a second agent (could be a second oral agent or a GLP-1 RA/SGLT2 depending on comorbidities and cost); consider patient preferences and CV/renal status.

    • Step 3 (consider cardiovascular/renal status): for patients with ASCVD, CKD, heart failure, prefer SGLT2 inhibitor or GLP-1 RA with proven CV benefit where appropriate.

    • Step 4 (insulin): initiate when metformin plus another agent fails to achieve goals or when there is significant hyperglycemia at presentation (e.g., FBG > 250 mg/dL, random > 300 mg/dL, A1c > 9% with symptoms or long-standing diabetes).

    • When starting insulin in Type 2 diabetes: begin with basal insulin (e.g., glargine) once daily; may add preprandial insulin if needed to control postprandial spikes and adjust per carb intake and glucose monitoring.

  • Hypoglycemia risk and weight considerations

    • Sulfonylureas and insulin have the highest risk of hypoglycemia; some agents (GLP-1 RAs, SGLT2 inhibitors) have lower hypoglycemia risk when used as monotherapy.

    • Weight gain is more common with insulin and sulfonylureas; GLP-1 RAs and SGLT2 inhibitors can promote weight loss or be weight-neutral.

  • Hyperosmolar Hyperglycemic State (HHS)

    • A severe hyperglycemic emergency characterized by very high glucose without significant ketoacidosis; symptoms include extreme thirst, polyuria, visual changes, confusion.

    • Management: aggressive IV fluids, electrolyte correction, and insulin as needed; addressed in hospital settings.

  • Take-home on pharmacology and decision-making

    • Medication choices should be individualized based on cost, weight effects, hypoglycemia risk, cardiovascular/renal comorbidities, and patient preferences.

    • When cardiovascular risk or CKD is a concern, prefer SGLT2 inhibitors or GLP-1 RAs with CV benefit when appropriate.

    • When cost is a major factor or in newly diagnosed patients, metformin remains a cornerstone and often the first-line therapy.

    • Always check for contraindications and interactions (e.g., renal function with metformin; pancreatitis risk with GLP-1 RAs and DPP-4 inhibitors; volume status with SGLT2s).

  • Quick reference: medication class comparison at a glance

    • Hypoglycemia risk: Sulfonylureas, Insulin (high) > DPP-4 inhibitors, SGLT2 inhibitors (low-to-moderate) > GLP-1 RAs (low-to-moderate).

    • Weight effects: Metformin (weight neutral or loss), SGLT2 inhibitors (weight loss), GLP-1 RAs (weight loss), Sulfonylureas and Insulin (weight gain).

    • Cardiovascular impact: SGLT2 inhibitors and some GLP-1 RAs show CV benefits; others vary by agent.

    • Cost considerations: GLP-1 RAs and SGLT2 inhibitors tend to be expensive; older agents (metformin, sulfonylureas) are cheaper.

Complications and preventive care in diabetes

  • Macrovascular (large vessels)

    • Coronary artery disease, cerebrovascular disease, peripheral artery disease.

    • Aggressive risk factor management reduces progression (glycemia, BP, lipids).

  • Microvascular (small vessels)

    • Retinopathy, nephropathy, neuropathy.

    • Regular screening and early intervention are crucial; laser therapy or anti-VEGF for retinopathy; ACE inhibitors/ARBs for nephropathy; neuropathy screening and foot care.

  • Preventive care recommendations (practical points)

    • Annual dilated eye exam to screen for retinopathy.

    • Regular foot examinations and patient education for foot care; daily self-inspection.

    • Blood pressure management with a target around 130/80 \text{mmHg} when applicable.

    • Lipids management and cardiovascular risk reduction; antiplatelet therapy (e.g., aspirin) in selected individuals; statin therapy per risk and guidelines.

    • Vaccinations and general health maintenance.

  • Metabolic considerations and bariatric/metabolic surgery

    • Consider metabolic surgery for BMI > 40 or BMI 35-39.9 with significant comorbidity and poor weight loss response; patient eligibility depends on surgical candidacy and comorbidities.

Triglycerides and hypertriglyceridemia

  • Definitions and targets

    • Normal triglycerides: <150 \text{mg/dL}

    • Very high triglycerides: >500 \text{mg/dL} increases pancreatitis risk and complicates LDL calculation on lipid panels.

  • Management approaches

    • Dietary and lifestyle changes (therapeutic lifestyle changes).

    • Omega-3 fatty acids/fish oils for triglyceride reduction.

    • If triglycerides are primarily genetic (isolated hypertriglyceridemia) and lifestyle changes are insufficient: consider fibrates; niacin is less favored due to side effects.

  • Lipid panel caveats

    • When triglycerides are very high, LDL is not reliably calculated from the standard panel; order a direct LDL measurement if needed.

Pituitary, thyroid, parathyroid, adrenal, and related endocrine topics

  • Pituitary gland overview

    • Posterior pituitary hormones: vasopressin (antidiuretic hormone, ADH) and oxytocin.

    • Anterior pituitary hormones: growth hormone (GH), prolactin, TSH, LH, FSH, ACTH.

  • Pituitary adenomas

    • Usually benign; common age range for presentation is 35-60 years.

    • Mass effect can cause visual field defects (classically bitemporal hemianopia from optic chiasm compression).

    • Prolactinomas: Most common functional pituitary adenoma; hyperprolactinemia leads to galactorrhea, amenorrhea in women, and in men erectile dysfunction; treatment with dopamine agonists (e.g., bromocriptine, cabergoline).

    • Acromegaly (GH-secreting): occurs in adults after epiphyseal closure; features include enlarged hands/feet, prognathism, macroglossia, sleep apnea, diabetes risk; GH not suppressed by oral glucose tolerance test is a key diagnostic clue; treatment often surgical, sometimes medical therapy.

    • Gigantism: GH excess before epiphyseal closure (in children) causing tall stature.

    • Dwarfism: many etiologies; achondroplasia is the most common; careful notes about GH use in individuals with disproportionate growth.

  • Growth hormone considerations

    • GH therapy is contraindicated or used with caution in certain settings (e.g., certain occupations or conditions) due to potential for disproportionate growth; clinical decision-making should be individualized.

  • Diabetes insipidus and SIADH

    • Diabetes insipidus (DI): Central DI (↓ ADH secretion) vs Nephrogenic DI (kidneys unresponsive to ADH).

    • Central DI: treat with desmopressin (DDAVP) and manage fluids; causes include idiopathic, trauma, pituitary surgery, hypoxic injury, infection.

    • Nephrogenic DI: treat with fluid management and salt restriction; thiazide diuretics and indomethacin can help by promoting a degree of volume depletion and enhancing concentrating ability.

    • Syndrome of Inappropriate Antidiuretic Hormone (SIADH): excessive ADH leading to hyponatremia; causes include CNS disturbances, pulmonary disease (e.g., pneumonia), malignancies (notably small cell lung cancer), and certain meds; management is fluid restriction and treating the underlying cause.

  • Thyroid disorders

    • Hyperthyroidism overview: Graves’ disease is a common autoimmune cause; clinical features include weight loss, heat intolerance, anxiety, tremor, tachycardia; exophthalmos and pretibial myxedema are characteristic of Graves’ disease.

    • Diagnostic clues: low TSH with high free T4 (and possibly T3); thyroid autoantibodies; radioactive iodine uptake; thyroid ultrasound with nodules.

    • Treatment options: antithyroid drugs (methimazole or propylthiouracil), radioactive iodine therapy, and surgery; beta-blockers for symptomatic control.

    • Subacute thyroiditis (de Quervain): post-viral thyroiditis with anterior neck pain; elevated T4/T3 with suppressed TSH; NSAIDs for pain; steroids if needed; beta-blockers for symptoms.

    • Hypothyroidism overview: primary hypothyroidism (most commonly Hashimoto’s thyroiditis); central hypothyroidism (hypothalamic/pituitary causes) is rarer.

    • Primary hypothyroidism: high TSH with low T4; treatment with levothyroxine and monitoring of TSH.

    • Central hypothyroidism: low/normal TSH with low T4; treat with thyroid hormone replacement.

    • Thyroid nodules and cancer risk assessment: suspicious features include age < 30, history of neck irradiation, hard fixed nodules, cervical lymphadenopathy, vocal cord paralysis; ultrasound features suggestive of cancer include microcalcifications, hypoechoic texture, irregular margins; FNA biopsy guided by ultrasound is key when suspicious.

    • Thyroid cancers: most common types are papillary (~85%), follicular (~12%), and anaplastic (<3%); medullary thyroid cancer is another type; primary cancers metastasize from breast, colon, kidney, melanomas to the thyroid.

    • Management of thyroid cancer: surgical resection is primary therapy; post-op radioiodine therapy may be used; long-term follow-up with thyroid hormone replacement (T4).

  • Osteoporosis and osteopenia

    • Osteopenia: bone mineral density (BMD) T-score between -1.0 \text{and} \-2.5.

    • Osteoporosis: T-score ≤ -2.5 or a history of fragility fracture or a high FRAX 10-year fracture risk.

    • Prevention and treatment: adequate calcium and vitamin D; weight-bearing exercise; smoking cessation; fall prevention.

    • Calcium and vitamin D supplementation: calcium ~ 1200 \text{mg/day}; vitamin D ~ 800\-1000 \text{IU/day} (intake varies by age and guideline).

    • First-line therapy: oral bisphosphonates (e.g., alendronate) with contraindications including esophageal disorders or inability to stay upright for 60 minutes after taking the medication; advanced CKD (eGFR < 30) also cautions use.

    • Second-line/alternative therapies: IV agents for high fracture risk or intolerance to oral agents; anabolic agents may be considered in very high-risk patients.

    • Monitoring: repeat DEXA every 1–2 years after starting therapy, then every 2–5 years once stable.

  • Vitamin D deficiency

    • Definition: vitamin D level < 20 \text{ng/mL}.

    • Etiology: often secondary to hypocalcemia or vitamin D deficiency; fortified foods and supplements help; sources include fatty fish, fortified dairy products, and sunlight exposure in moderation.

    • Population recommendations: general adults 600–800 IU/day; higher risk groups or older adults (>70) commonly advised to take 800–1000 IU/day depending on guidelines.

  • Parathyroid disorders

    • Primary hyperparathyroidism: usually due to a single parathyroid adenoma; symptoms may be subtle or mass-related; classic mnemonic includes bones, stones, abdominal groans, psychiatric moans, fatigue. Diagnosis: hypercalcemia with elevated intact PTH; treatment: parathyroidectomy if symptomatic or with complications (e.g., kidney stones, bone disease).

    • Secondary hyperparathyroidism: most commonly due to chronic kidney disease; may also result from inadequate calcium intake/absorption.

    • Tertiary hyperparathyroidism: autonomous PTH secretion after long-standing secondary hyperparathyroidism.

    • Hypoparathyroidism (post-surgical or other etiologies): low calcium with low PTH; symptoms include perioral numbness, paresthesias, carpal/torque spasms (Chvostek’s sign and Trousseau’s sign); treatment includes calcium and vitamin D supplementation and correction of hypomagnesemia if present.

  • Adrenal disorders

    • Cushing’s syndrome vs Cushing’s disease

    • Cushing’s syndrome: hypercortisolism from any cause; includes exogenous (steroid meds) and endogenous etiologies (ACTH-dependent and ACTH-independent).

    • Endogenous Cushing’s disease: ACTH-dependent, most often due to a pituitary ACTH-secreting adenoma; ectopic ACTH production is another ACTH-dependent cause; ACTH-independent causes include adrenal adenomas/carcinomas.

    • Diagnosis involves 24-hour urinary free cortisol, late-night salivary cortisol, or overnight dexamethasone suppression test; ACTH measurement to distinguish pituitary vs non-pituitary sources.

    • Treatment depends on etiology (withdraw steroids if exogenous; pituitary adenoma resection for Cushing’s disease; ectopic ACTH source removal if present).

    • Adrenal insufficiency (primary Addison’s disease vs secondary/tertiary)

    • Primary adrenal insufficiency: autoimmune adrenalitis is common; skin hyperpigmentation can occur due to high ACTH; hyponatremia and hyperkalemia may be present; diagnosis via serum cortisol and ACTH; confirm with ACTH stimulation test showing subnormal cortisol response.

    • Secondary/tertiary adrenal insufficiency: due to pituitary/hypothalamic dysfunction; less hyperpigmentation; diagnosis with low/normal ACTH and low cortisol.

    • Treatment: glucocorticoid replacement (± mineralocorticoid replacement if needed).

  • Pheochromocytoma

    • Catecholamine-secreting tumor of the adrenal medulla; classic triad and sustained hypertension; diagnosis via plasma free metanephrines or 24-hour urine metanephrines/catecholamines; imaging (CT/MRI) of abdomen/pelvis to locate tumor.

    • Preoperative management: alpha-blockade first to control hypertension, then beta-blockade; surgical resection is treatment of choice.

  • Multiple endocrine neoplasias (MEN)

    • MEN1: the three P’s – pituitary, parathyroid, and pancreas (and/or pancreatic neuroendocrine tumors).

    • MEN2A: medullary thyroid carcinoma, pheochromocytoma, and primary hyperparathyroidism.

    • MEN2B: medullary thyroid carcinoma, mucosal neuromas; does not typically involve primary hyperparathyroidism.

  • Male hypogonadism and testosterone therapy considerations

    • Primary hypogonadism: testicular failure; high LH/FSH with low testosterone.

    • Secondary hypogonadism: pituitary/hypothalamic dysfunction; low testosterone with low/normal LH/FSH.

    • Testosterone therapy: absolute contraindications include history of breast cancer, significant polycythemia (hematocrit > 54\%), and prostate cancer; PSA thresholds and urology evaluation recommended if elevated.

    • Symptoms of hypogonadism: loss of body hair, sexual dysfunction, hot flashes, fatigue; not routinely screened unless symptoms are present.

  • Practical exam and study tips from the lecture

    • Read the vignette fully; all details can be pertinent to selecting the correct management or identifying contraindications.

    • For thyroid and pituitary topics, remember the pattern of posterior vs anterior hormones and the typical mass-effects (e.g., bitemporal hemianopia with pituitary adenomas).

    • For diabetes pharmacology, be prepared to discuss mechanism, hypoglycemia risk, weight effects, cardiovascular risks, and cost considerations when selecting therapy.

    • Use the common exam questions to practice: how to distinguish DKA from HHS (DKA—metabolic acidosis; HHS—marked hyperglycemia without ketoacidosis), how to interpret TSH/T4 for thyroid disorders, and how to approach management with insulin initiation when A1c is very high or in acute settings.

Quick takeaways for exam questions

  • Diagnostic criteria you must memorize:

    • A1c \ge 6.5\% or FPG \ge 126 \text{mg/dL} or 2hOGTT \ge 200 \text{mg/dL} or symptomatic hyperglycemia with random glucose \ge 200 \text{mg/dL}.

  • Treatment goals commonly used in boards:

    • A1c \lt 7\% (with some patients allowed up to 8\% depending on risk of hypoglycemia and comorbidities).

  • First-line pharmacotherapy for T2D:

    • Metformin (unless contraindicated by renal function, e.g., eGFR < 30 \text{mL/min/1.73 m^2}).

  • When to start insulin in T2D:

    • In patients with severe hyperglycemia, ketosis or weight loss (e.g., fasting glucose > 250 \text{mg/dL} or random glucose > 300 \text{mg/dL} or A1c > 9\%) or after failure of two oral agents.

  • Complications you must screen for and manage:

    • Microvascular: retinopathy, nephropathy (proteinuria/motility), neuropathy (foot exams).

    • Macrovascular: CHD, stroke, PAD; aggressive risk factor modification is essential.

  • Key hormonal topics you should know:

    • Posterior pituitary hormones: ADH and oxytocin.

    • Prolactinoma: treat with dopamine agonists; MRI for pituitary; check for galactorrhea and menstrual changes.

    • Acromegaly/gigantism: GH secretion and glucose intolerance; oral glucose suppression test findings; treat with surgical resection when feasible.

    • Pheochromocytoma: alpha- then beta-blockade before surgery; confirm with metanephrines and localize with imaging.

    • Hyper- and hypothyroidism: classic TSH-T4 patterns and management strategies; thyroid nodules with FNA guidelines.

If you’d like, I can convert this into a compact, exam-ready cheat sheet with color-coded sections for quick reference during a test. Also tell me if you want only the diabetes portion or the full endocrine scope included, and I can adjust the depth accordingly.