USMLE Step 3 (Fach) / Endocrinology (Lektion)

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• Myxedema coma Myxedema coma is an extremely rare condition caused by decompensation of an existing thyroid hormone deficiency and can be triggered by infections, surgery, and trauma. Myxedema coma is a potentially life-threatening condition and, if left untreated, is fatal in ∼ 40% of cases. Clinical presentation:- Cardinal symptoms: impaired mental status, hypothermia, and concurrent myxedema- Hypoventilation with hypercapnia- Hypotension (possibly shock) and bradycardia Treatment:- IV combination of T4 and T3 (plus IV hydrocortisone in some cases)  - Patients should be treated and monitored in an ICU.
• Myxedema coma Myxedema coma is an extremely rare condition caused by decompensation of an existing thyroid hormone deficiency and can be triggered by infections, surgery, and trauma. Myxedema coma is a potentially life-threatening condition and, if left untreated, is fatal in ∼ 40% of cases. Clinical presentation:- Cardinal symptoms: impaired mental status, hypothermia, and concurrent myxedema- Hypoventilation with hypercapnia- Hypotension (possibly shock) and bradycardia Treatment:- IV combination of T4 and T3 (plus IV hydrocortisone in some cases)  - Patients should be treated and monitored in an ICU.
• Hypocalcemia – Management - Calcium supplementation:→ IV calcium (1-2 g calcium gluconate in 50 mL of 5% dextrose infused over 10–20 mins): indicated in severely symptomatic patients (e.g., tetany, seizures), those with a prolonged QT interval, and asymptomatic patients with an acute decrease in serum corrected calcium to ≤ 7.5 mg/dL (≤ 1.9 mmol/L) → Oral calcium: indicated in patients with mild neuromuscular irritability (e.g., paresthesias), and those with serum corrected calcium > 7.5 mg/dL (> 1.9 mmol/L) - Vitamin D supplementation: indicated in hypocalcemia caused by hypoparathyroidism or vitamin D deficiency - For patients taking loop diuretics, medication change to thiazides   - Magnesium supplementation: indicated in hypocalcemia caused by hypomagnesemia
• Osteoporosis Demographics: higher incidence in individuals of Asian, Hispanic and northern European ancestry than in black populations Type I (postmenopausal osteoporosis): postmenopausal women Secondary osteoporosis:- Drug-induced/iatrogenic: especially after systemic long-term therapy with corticosteroids (e.g., in patients with autoimmune disease)- Other: Long-term therapy with proton-pump inhibitors, anti-epileptic drugs, aromatase inhibitors- Endocrine/metabolic: hypercortisolism, hypogonadism, hyperthyroidism, hyperparathyroidism, renal disease- Immobilization- Alcohol abuse Risk factors:- Cigarette smoking- Family history of osteoporosis- Malnutrition, malabsorption- Low body weight Lifestyle measures- Avoid alcohol and nicotine- Sufficient intake of calcium and vitamin D  - Physical activity with strength and balance training  - Avoid or minimize glucocorticoids Medical therapy:- Indication→ History of fragility fractures→ T-scores ≤ -2.5→ T-score between -1 and -2.5 with severely increased risk of fracture- 1st-line treatment: bisphosphonates (alendronate, risedronate); inhibit osteoclasts and therefore bone resorption- Teriparatide (parathyroid hormone analog): alternative for severe osteoporosis (T-score ≤ -3.5) or for patients with contraindications to bisphosphonates  - Raloxifene (selective estrogen receptor modulator, SERM) for patients with contraindications to bisphosphonates or those who also require breast cancer prophylaxis (but increases the risk of thromboembolism)  - Denosumab (monoclonal antibody against RANKL): for patients with impaired renal function, or no success with bisphosphonates  
• Cushing syndrome Primary hypercortisolism (ACTH-independent Cushing's syndrome)Secondary hypercortisolism:- Pituitary ACTH production (Cushing disease)- Ectopic ACTH production Clinical features:- Skin→ Thin, easily bruisable skin with stretch marks (classically purple abdominal striae) and/or ecchymoses→ Delayed wound healing→ Flushing of the face→ Hirsutism→ Acne→ If secondary hypercortisolism: often hyperpigmentation (darkening of the skin due to an overproduction of melanin), especially in areas that are not normally exposed to the sun (e.g., palm creases, oral cavity)- Neuropsychological: lethargy, depression, sleep disturbance, psychosis- Musculoskeletal:→ Osteopenia, osteoporosis, pathological fractures, avascular necrosis of the femoral head  → Muscle atrophy/weakness  - Endocrine and metabolic: → Diabetes mellitus→ Dyslipidemia  → Weight gain characterized by central obesity, moon facies, and a buffalo hump  → ♂: decreased libido→ ♀: decreased libido, virilization, and/or irregular menstrual cycles  - Secondary hypertension (∼ 90% of cases)  - Increased susceptibility to infections- Peptic ulcer disease- Cataracts  Diagnostics:- Hypernatremia, hypokalemia, metabolic alkalosis  - Hyperglycemia- Hyperlipidemia (hypercholesterolemia and hypertriglyceridemia)- Leukocytosis (predominantly neutrophilic), eosinopenia, thrombocytosis  1. Any one of the following can be used as an initial screening test:- ↑ 24-hour urine cortisol  - ↑ early morning serum cortisol levels following a low-dose dexamethasone suppression test  - ↑ midnight salivary cortisol- ↑ midnight serum cortisol2. Serum ACTH levels- Low (< 5 pg/mL): suspect primary hypercortisolism (adrenal adenoma, carcinoma)- Normal or elevated (> 20 pg/mL): suspect secondary hypercortisolism3. If secondary hypercortisolism is suspected:- High-dose dexamethasone suppression test  → Adequate suppression of cortisol levels to less than 50% of baseline: Cushing's disease→ No suppression: ectopic ACTH production- CRH stimulation test:→ ACTH and cortisol levels increase further: Cushing's disease→ No increase in ACTH or cortisol levels: ectopic ACTH production - If primary hypercortisolism is suspected: CT and/or MRI of the abdomen for adrenal tumors- If Cushing's disease is suspected: CT and/or MRI of the skull - If ectopic ACTH production is suspected: chest x-ray and/or CT, abdominal CT Treatment:- Exogenous Cushing's syndrome: Consider lowering the dose of glucocorticoids/consider the use of alternatives to glucocorticoids (e.g., azathioprine)- Endogenous Cushing's syndrome: → Inoperable disease: Drugs to suppress cortisol synthesis: metyrapone, mitotane, ketoconazole→ Operable disease: surgical therapy is the treatment of choice
• Nelson syndrome (or post adrenalectomy syndrome) Can occur after bilateral adrenalectomy in patients with a previously undiscovered pituitary adenoma   Pathophysiology: bilateral adrenalectomy → no endogenous cortisol production → no negative feedback from cortisol on hypothalamus → increased CRH production → uncontrolled enlargement of preexisting ACTH-secreting pituitary adenoma → increased secretion of ACTH and melanocyte-stimulating hormone  → symptoms of pituitary adenoma and ↑ MSH Clinical features: headaches, bitemporal hemianopia, cutaneous hyperpigmentation Diagnostics: high levels of beta-MSH and ACTH; pituitary adenoma on MRI confirms diagnosis Treatment: pituitary radiation therapy or surgery
• Nelson syndrome (or post adrenalectomy syndrome) Can occur after bilateral adrenalectomy in patients with a previously undiscovered pituitary adenoma   Pathophysiology: bilateral adrenalectomy → no endogenous cortisol production → no negative feedback from cortisol on hypothalamus → increased CRH production → uncontrolled enlargement of preexisting ACTH-secreting pituitary adenoma → increased secretion of ACTH and melanocyte-stimulating hormone  → symptoms of pituitary adenoma and ↑ MSH Clinical features: headaches, bitemporal hemianopia, cutaneous hyperpigmentation Diagnostics: high levels of beta-MSH and ACTH; pituitary adenoma on MRI confirms diagnosis Treatment: pituitary radiation therapy or surgery
• Adrenal insufficiency Diagnostics:- Serum electrolytes: Hyponatremia, hyperkalemia, normal anion gap metabolic acidosis, mild hypercalcemia (in up to one-third of cases)- Hypoglycemia  - ↑ Serum creatinine and BUN as a result of hypovolemia- Complete blood count: eosinophilia Diagnosis:1. Morning serum cortisol levels: < 3 μg/dL (< 80 nmol/L) confirms adrenal insufficiency.  2. Confirmatory test- ACTH stimulation test (cosyntropin test): measurement of serum cortisol before and 30 minutes after administration of exogenous ACTH (e.g., cosyntropin)→ Failure of cortisol to rise > 20 μg/dL after ACTH administration confirms primary adrenal insufficiency)→ In secondary/tertiary adrenal insufficiency: exogenous ACTH → ↑ cortisol (usually a rise in cortisol > 20 μg/dL)  OR - Metyrapone stimulation test→ Metyrapone inhibits 11β hydroxylase → impaired conversion of 11-deoxycortisol to cortisol (last step of cortisol synthesis)→ Adrenal insufficiency is diagnosed if the 11-deoxycortisol level does not exceed 70 ng/mL and the cortisol level is < 5 μg/dL.  → Physiological response: metyrapone → ↓ cortisol synthesis → ↑ CRH and ↑ ACTH (negative feedback) → ↑ adrenal steroidogenesis → ↑ 11-deoxycortisol and ↑ cortisol→ In primary adrenal insufficiency: metyrapone → ↓ cortisol synthesis → ↑ in CRH/ACTH → no increase in adrenal steroid production → ↓ 11-deoxycortisol and ↓ cortisol→ In secondary/tertiary adrenal insufficiency: metyrapone → ↓ cortisol → ↓ CRH/ACTH → no increase in adrenal steroidogenesis → ↓ 11-deoxycortisol and ↓ cortisol Treatment:- Glucocorticoid replacement: Hydrocortisone: administered in 2–3 doses daily    - Mineralocorticoid replacement: Fludrocortisone  - Loss of libido can be treated with dehydroepiandrosterone (DHEA).  Secondary and tertiary adrenal insufficiency: Only glucocorticoid replacement is necessary
• Adrenal crisis (Addisonian crisis) Acute, severe glucocorticoid deficiency that requires immediate emergency treatment. Causes:- Stress (e.g., infection, trauma, surgery) in a patient with underlying adrenal insufficiency- Sudden discontinuation of glucocorticoids after prolonged glucocorticoid therapy- Bilateral adrenal hemorrhage or infarction (e.g., Waterhouse-Friderichsen syndrome)- Pituitary apoplexy   Clinical features:- Hypotension, shock- Impaired consciousness, coma- Fever- Vomiting, diarrhea- Severe abdominal pain (which resembles peritonitis)- Hypoglycemia, hyponatremia, hyperkalemia, and metabolic acidosis Therapy:- Administration of high doses of hydrocortisone: 100 mg IV every 8 hours- Alternatively: dexamethasone 4 mg IV every 12 hours- Does not interfere with testing, as opposed to hydrocortisone - Fluid resuscitation with normal saline to treat hypotension and hyponatremia- Correct hypoglycemia with 50% dextrose- Intensive care monitoring
• Hyperalosteronism Clinical features:- Hypertension- Features of hypokalemia  → Fatigue→ Muscle weakness, cramping→ Headaches→ Polyuria and polydipsia  → Palpitations→ Constipation- Lack of significant edema (explained by aldosterone escape) - Paresthesia in severe cases due to metabolic alkalosis   Diagnostics:1. Plasma aldosterone concentration to plasma renin activity (PAC/PRA ratio; aldosterone-to-renin ratio, or ARR)- ↑ PAC (> 15 ng/dL or 416 pmol/L) and ↓ PRA- ↑ PAC/PRA ratio (ratio > 20)2. Confirmatory test- Oral sodium loading test- Saline infusion test- Fludrocortisone suppression test - Imaging: → Adrenal CT→ Adrenal venous sampling Treatment:- Bilateral adrenal hyperplasia: Aldosterone receptor antagonists (epleronone, spironolactone)- Unilateral autonomous aldosterone secretion (adenoma, unilateral hyperplasia, carcinoma): Surgery
• Multiple endocrine neoplasia (MEN) Multiple endocrine neoplasia (MEN) is a term used to describe three autosomal dominant syndromes. MEN 1:- Genetics: Altered menin protein expression- Primary hyperparathyroidism (∼ 90% of cases)- Endocrine pancreatic tumors (∼ 50-80% of cases) such as gastrinoma (most common) - Pituitary adenoma (∼ 30-50% of cases): most commonly prolactinoma- Carcinoid tumors (∼ 10-15% of cases)- Management:→ Parathyroidectomy→ Excision of pancreatic tumor→ Transsphenoidal surgery for excision of pituitary adenoma MEN 2:- Altered expression of the RET proto-oncogene → elevated tyrosine kinase activity- Medullary thyroid carcinoma (95-100% of cases)- Pheochromocytoma (∼ 40% of cases)- MEN 2A: Primary hyperparathyroidism (∼ 20-30% of cases)- MEN 2B: Multiple neurinomas (mucosal neuromas, intestinal ganglioneuromatosis), Marfanoid habitus (> 95%)- Management:→ Thyroidectomy including cervical lymph nodes→ Pheochromocytoma should first be ruled out (e.g., measuring urine metanephrines) or treated before undergoing surgery  → If pheochromocytoma: adrenalectomy→ If hyperparathyroidism: parathyroidectomy
• Pheochromocytoma Age range: 3rd-5th decades of life Etiology:- Localization:∼ 90% adrenal medulla (physiologically activated by acetylcholine)  ∼ 10% extra-adrenal in the sympathetic ganglia  ∼ 10% at multiple locations- The majority of pheochromocytomas are benign, unilateral, catecholamine-producing tumors. - Rarely, pheochromocytomas also produce other hormones such as EPO.- 25% of pheochromocytomas are hereditary. - Associations include:→ Multiple endocrine neoplasia type 2 (MEN 2A, MEN 2B)→ Neurofibromatosis type 1 (NF1)→ Von Hippel-Lindau (VHL) disease“10 percent rule”: Roughly 10% of pheochromocytomas are extra-adrenal, multiple, bilateral, malignant, pediatric cases, not associated with hypertension, or show calcifications on imaging! Clinical features:- Episodic hypertension (or persistent hypertension in some cases)  - Paroxysmal→ Throbbing headache→ Diaphoresis→ Heart palpitations and tachycardia→ Pallor  → Abdominal pain and nausea→ Anxiety- Weight loss due to increased basal metabolism- Hyperglycemia- If EPO is secreted, signs of polycythemiaHypertensive crises can be triggered by palpation of the tumor on abdominal exam! Diagnostics:- Best initial test: metanephrines (metabolites of catecholamines) in plasma (high sensitivity)- Confirmatory test: metanephrines and catecholamines in 24-hour urine (high specificity)- 24-hour ambulatory blood pressure monitoring  - Adrenal/abdominal CT or MRI (after positive biochemistry tests to localize tumor) Treatment:1. First, a non-selective alpha blocker is given: phenoxybenzamine blocks alpha-1 and alpha-2 adrenoceptors equally and irreversibly.2. After sufficient alpha-adrenergic blockade, a beta blocker may be started for additional blood pressure control and control of tachyarrhythmias.- Treatment of choice: laparoscopic tumor resection (adrenalectomy): "No-touch" technique  
• Thiazolidinediones (glitazones, insulin sensitizers) Active agents:- Pioglitazone- Rosiglitazone Mechanism of action: activation of the transcription factor PPARγ (peroxisome proliferator-activated receptor of gamma type) → ↑ transcription of genes involved in glucose and lipid metabolism → ↑ levels of adipokines such as adiponectin → ↑ storage of triglycerides and subsequent reduction of products of lipid metabolism (e.g., free fatty acids) that enhance insulin resistance → glucose utilization is increased and hepatic glucose production reduced Indications: may be considered as a monotherapy in patients with severe renal failure and/or contraindications for insulin therapy Clinical characteristics:- Glycemic efficacy: lowers HbA1c by 1% in 3 months- Favorable effect on lipid metabolism: ↓ triglyceride, ↓ LDL, ↑ HDL- No risk of hypoglycemia Important side effects:- Fluid retention and edema- Weight gain- Increased risk of heart failure- Increased risk of bone fractures (osteoporosis!) Contraindications:- Congestive heart failure (NYHA III or IV)- Liver failure- Pioglitazone: history of bladder cancer or active bladder cancer; macrohematuria of unknown origin
• Delayed puberty in boys Etiology:- Primary hypogonadism, e.g., Klinefelter syndrome- Secondary hypogonadism:→ Constitutional, chronic illness, malnutrition→ Hypothyroidism, hyperprolactinemia→ Kallmann syndrome→ Craniopharyngioma Clinical features:- Absent testicular enlargement by age 14- Delayed growth spurt Initial workup:1. Bone age radiograph (> 1 year → further workup)2. FSH, LH, testosterone, TSH, prolactin
• Biguanides (metformin) Mechanism of action: enhances the effect of insulin- Reduction in insulin resistance via modification of glucose metabolic pathwaysInhibits mitochondrial glycerophosphate dehydrogenase (mGPD)- Decreases hepatic gluconeogenesis and intestinal glucose absorption- Increases peripheral insulin sensitivity Indications: drug of choice in all patients with type 2 diabetes   Clinical characteristics:- Glycemic efficacy: lowers HbA1c by 1.2–2% over 3 months- Weight loss or weight stabilization- No risk of hypoglycemia- Beneficial effect on dyslipidemia- Studies show metformin reduces the risk of macroangiopathic complications in diabetic patients.  - Cost-effective Metformin-associated lactic acidosis  - Incidence: ∼ 8 cases/100,000 patient years- Clinical features: frequently nonspecific→ Gastrointestinal prodromal symptoms: nausea, vomiting, diarrhea, abdominal pain→ Severe symptoms: muscle cramps, hyperventilation, apathy, disorientation, coma- High-risk groups: Elderly individuals, Patients with cardiac or renal insufficiency- Diagnostics:→ Arterial blood gas (ABG): metabolic acidosis and anion gap→ ↑ Serum lactate- Treatment: discontinue metformin and treat acidosis - Gastrointestinal complaints are common: nausea, diarrhea, flatulence  - Vitamin B12 deficiency  - Metallic taste in the mouth (dysgeusia) Contraindications:- Renal failure (if creatinine clearance < 30 mL/min)- Severe liver failure  - Intravenous iodinated contrast medium  - Pause metformin prior to surgery- Chronic pancreatitis, starvation ketosis, ketoacidosis, sepsis  - Heart failure (NYHA III and IV), respiratory failure, shock, sepsis  - Alcoholism- Important interactions: sulfonylureas  Metformin treatment must be paused prior to the administration of a contrast medium or scheduled surgery to reduce the risk of lactic acidosis!
• Subclinical hypothyroidism Clinical features:- Elevated TSH - Normal free T4- Mild symptoms may or may not be present Indications for treatment:- TSH ≥ 10 µU/mL- TSH 7-9.9 µU/mL→ Age < 70: Treat→ Age ≥ 70: Treat if convincing hypothyroid symptoms- TSH upper limit of normal-6.9 µU/mL→ Age < 70: Treat if convincing hypothyroid symptoms, enlarging goiter, or elevated anti-TPO titer→ Age ≥ 70: Do not treat (possible harm) Complications:- Recurrent miscarriages- Severe preeclampsia- Preterm birth, low birth weight- Placental abruption- Anti-thyroid peroxidase (anti-TPO) antibodies are associated with increased risk for pregnancy loss
• Subclinical hyperthyroidism Clinical characteristics:- Suppressed TSH- Normal thyroid hormone levels- Hyperthyroid symptoms may or may not be present Causes:- Exogenous thyroid hormone- Graves disease- Nodular thyroid disease Indications for treatment:- TSH persistently < 0.1 µU/mL- TSH 0.1-0.5 µU/mL plus additional risk factors:→ Age ≥ 65→ Heart disease→ Osteoporosis→ Nodular thyroid disease
• McCune-Albright syndrome Clinical triad:1. Polyostotic fibrous dysplasia2. Cafe-au-lait spots  3. Hormonal abnormalities: Peripheral precocious puberty- Due to elevated estrogens produced by ovarian cysts
• Linagliptine Dipeptidyl peptidase-4 inhibitor Clinical characteristics:- Glycemic efficacy: lowers HbA1c by 0.5-0.75% over 3 months- No risk of hypoglycemia unless insulin and/or insulinotropic drugs are used simultaneously Important side effects:- Gastrointestinal complaints: diarrhea, constipation (milder than in GLP-1 agonist exposure)- Nasopharyngitis and upper respiratory tract infection- Arthralgia- Headaches, dizziness- Urinary infections (mild) - Increased risk of pancreatitis- Acute renal failure  
• Sitagliptin Dipeptidyl peptidase-4 inhibitor Clinical characteristics:- Glycemic efficacy: lowers HbA1c by 0.5-0.75% over 3 months- No risk of hypoglycemia unless insulin and/or insulinotropic drugs are used simultaneously Important side effects:- Gastrointestinal complaints: diarrhea, constipation (milder than in GLP-1 agonist exposure)- Nasopharyngitis and upper respiratory tract infection- Arthralgia- Headaches, dizziness- Urinary infections (mild) - Increased risk of pancreatitis- Acute renal failure  
• Liraglutide Glucagon-like peptide-1 receptor agonist Clinical characteristics:- Glycemic efficacy: lowers HbA1c by 0.5-1.5% over 3 months- Subcutaneous injection- Weight loss- No risk of hypoglycemia Side effects:- Gastrointestinal complaints (particularly impaired gastric emptying!)  - Increased risk of pancreatitis and potentially pancreatic cancer
• Exenatide Glucagon-like peptide-1 receptor agonist Clinical characteristics:- Glycemic efficacy: lowers HbA1c by 0.5-1.5% over 3 months- Subcutaneous injection- Weight loss- No risk of hypoglycemia Side effects:- Gastrointestinal complaints (particularly impaired gastric emptying!)  - Increased risk of pancreatitis and potentially pancreatic cancer
• Glipizide Short-acting sulfonylurea Important side effects:- Life-threatening hypoglycemia  - Increased risk in patients with renal failure - Weight gain- Hematological changes: granulocytopenia, hemolytic anemia- Allergic skin reactions- Alcohol intolerance  - Compared to metformin, sulfonylureas are associated with more cardiovascular (macrovascular) complications.
• Glyburide Long-acting sulfonylurea Important side effects:- Life-threatening hypoglycemia  - Increased risk in patients with renal failure - Weight gain- Hematological changes: granulocytopenia, hemolytic anemia- Allergic skin reactions- Alcohol intolerance  - Compared to metformin, sulfonylureas are associated with more cardiovascular (macrovascular) complications.
• Dapagliflozine SGLT-2 inhibitor Clinical characteristics- Glycemic efficacy: lowers HbA1c by 0.6% over 3 months- Promotes weight loss- Reduces blood pressure Important side effects:- Urinary tract infections, genital infections (vulvovaginitis, balanitis)- Dehydration as a result of polyuria- Severe diabetic ketoacidosis Contraindications:- Chronic kidney disease  - Recurrent urinary tract infections (e.g., in patients with anatomical or functional anomalies of the urinary tract)
• Empagliflozine SGLT-2 inhibitor Clinical characteristics- Glycemic efficacy: lowers HbA1c by 0.6% over 3 months- Promotes weight loss- Reduces blood pressure Important side effects:- Urinary tract infections, genital infections (vulvovaginitis, balanitis)- Dehydration as a result of polyuria- Severe diabetic ketoacidosis Contraindications:- Chronic kidney disease  - Recurrent urinary tract infections (e.g., in patients with anatomical or functional anomalies of the urinary tract)
• Effects of combined estrogen/progesterone menopausal hormone therapy Beneficial:- Menopausal symptoms (e.g., hot flashes, vaginal atrophy)- Bone mass/fractures- Colon cancer- Type 2 diabetes mellitus- All-cause mortality (age < 60) Detrimental:- Venous thromboembolism- Breast cancer- Coronary heart disease (age ≥ 60)- Stroke- Gall bladder disease
• Management of DKA IV fluids:- Rapid infusion of 0.9% normal saline- Add dextrose 5% when serum glucose is ≤ 200 mg/dL Insulin:- Start continuous IV insulin infusion (hold if K+ < 3.3 mEq/L)- Switch to SQ (basal bolus) insulin for the following: able to eat, glucose < 200 mg/dL, anion gap < 12 mEq/L & serum HCO3 ≥ 15 mEq/L- Overlap SQ & IV insulin by 1-2 hours Potassium:- Add IV K+ if serum K+ < 5.3 mEq/L (hold if ≥ 5.3 mEq/L)- Nearly all patients' K+ depleted, even with hyperkalemia Bicarbonate: Consider for patients with pH ≤ 6.9 Phosphate:- Consider for phosphte < 1.0 mg/dL, cardiac dysfunction, or respiratory depression- Monitor serum calcium frequently
• Surgical complications of adrenalectomy for pheochromocytoma Hypertensive crisis:- Mechanism: ↑ Catecholamine release due to endotracheal intubation & adrenal gland manipulation, ↑ Serum norepinephrine with larger tumors (> 4 cm diameter)- Treatment: Intravenous nitroprusside, phentolamine, or nicardipine Hypotension:- Mechanism: ↓ Catecholamines after tumor removal, persistent alpha blockade from preoperative long-acting alpha blocker (e.g., phenoxybenzamine)- Treatment: Normal saline bolus, pressors if unresponsive Hypoglycemia: - Mechanism: ↑ Insulin secretion following tumor removal (catecholamines suppress insulin secretion)- Treatment: Intravenous dextrose infusion Cardiac tachyarrhythmias:- Mechanism: ↑ Catecholamine release from adrenal gland handling- Treatment: Intravenous lidocaine or esmolol
• Indications for statin therapy in the prevention of ASCVD Secondary prevention in established ASCVD:- Acute coronary syndrome- Stable angina- Arterial revascularization- Stroke, TIA, PAD→ Age ≤ 75: High-intensity statin→ Age > 75: Moderate-intensity statin LDL ≥ 190 mg/dL → High-intensity statin Age ≥ 40 with diabetes mellitus- 10-year ASCVD risk ≥ 20% → High-intensity statin- 10-year ASCVD risk < 20% → Moderate-intensity statin Estimated 10-year ASCVD risk > 7.5-10% → Moderate- to high-intensity statin
• Vitamin D deficiency Risk factors:- Institutionalized (e.g., nursing homes)- Dark skin- Decreased sun exposure- Obesity- Osteoporosis- Malabsorption- Advanced age- Chronic kidney disease Clinical features:- Usually asymptomatic- Low bone density- Fracture- Osteomalacia: Bone pain, muscle weakness Diagnosis:- Deficiency: Serum 25(OH)D < 20 ng/mL- Insufficiency: Serum 25(OH)D 20-30 ng/mL Initial treatment:- Cholecalciferol (vitamin D3) 50,000 IU/week for 8 weeks to achieve 25(OH)D > 30 ng/mLMaintenance:- Normal intestinal absorption 1500-2000 IU/day- Malabsorption 3000-6000 IU/day
• TSH-secreting pituitary adenoma Clinical features:- Thyrotoxicosis- Diffuse goiter- Possible mass effect symptoms (e.g., headache, visual field defects) Laboratory findings:- Elevated TSH- Elevated T3 & T4- Elevated alpha subunit (85% of patients)- Elevation of other pituitary hormones MRI: Pituitary mass Additional test:- Minimal or no suppression of TSH by exogenous thyroxine- Elevated sex hormone-binding globulin- Normal thyroid hormone receptor beta gene Treatment:- Somatostatin analogs- Transsphenoidal surgery
• Screening tests for diabetes mellitus Hemoglobin A1c:- Preferred test in non-fasting state- ≥ 6.5 = diabetes mellitus- 5.7-6.4% = increased risk- < 5.7 = normal Fasting blood glucose:- ≥ 126 mg/dL = diabetes mellitus- 100-125 = increased risk- < 100 mg/dL = normal Random glucose levels:- ≥ 200 mg/dL = diabetes mellitus- 140-199 mg/dL = increased risk- < 140 mg/dL = normal Oral glucose tolerance test:- Most sensitive test- 75-g glucose load with glucose testing for 2 hours- ≥ 200 mg/dL = diabetes mellitus- 140-199 mg/dL = increased risk- < 140 mg/dL = normal Testing may be repeated in cases of discordant or equivocal results. If a patient is asymptomatic, a positive test should be reconfirmed with the same test on a different day.
• Conditions that alter TBG concentration Increased TBG:- Estrogens (e.g., pregnancy, OCPs, HRT) & estrogenic medications (e.g., tamoxifen)- Acute hepatitis Decreased TBG:- Androgenic hormones- High-dose glucocorticoids/hypercortisolism- Hypoproteinemia (e.g., nephrotic syndrome, starvation)- Chronic liver disease
• Gestational diabetes mellitus First and second trimester (the first 24 weeks of pregnancy): the diagnosis of diabetes mellitus and gestational diabetes is confirmed with two independent measurements ≥ 126 mg/dL and 92-125 mg/dL respectively   Third trimester (at 24–28 weeks):- Recommended in all pregnancies!- Initial screening: 50-g, one-hour oral glucose challenge testblood glucose level should be < 135 mg/dl- Confirmation test: 100-g, three-hour oral glucose tolerance test (oGTT)blood glucose level should be < 140 mg/dl Target blood glucose levels:- Fasting ≤ 95 mg/dL- 1-hour postprandial ≤ 140 mg/dL- 2-hour postprandial ≤ 120 mg/dL Treatment:- First-line: Dietary modifications- Second-line: Insulin, metformin
• Primary hyperparathyroidism – Treatment Surgical:- Indications→ Symptomatic patients→ Asymptomatic patients who meet at least one of the following criteria:→ Age < 50 years→ Serum calcium level more than 1 mg/dL higher than the normal upper limit→ Impaired renal function (eGFR < 60 mL/min)→ Increased calcium excretion (> 400 mg/day) in combination with an increased risk for nephrolithiasis→ Evidence of nephrolithiasis or nephrocalcinosis via imaging→ Reduced bone mineral density (T-score < -2.5 at lumbar spine, total hip, femoral neck, or distal third of the radius, or preexisting asymptomatic vertebral fracture)- The procedure depends on the pathology:→ Solitary adenoma: remove only the respective gland (parathyroidectomy)→ Hyperplasia: remove all four glands (total parathyroidectomy)  → Carcinoma: resection of tumor, ipsilateral thyroid lobe, and enlarged lymph nodes Nonsurgical: in symptomatic patients who are not able to undergo surgery or asymptomatic patients who do not meet the criteria for surgical therapy→ Calcimimetics (e.g., cinacalcet)  → In patients with osteoporosis: bisphosphonates→ Avoid lithium and thiazide diuretics.
• Thyroid effects of amiodarone Decreased T4-T3 conversion: ↑ T4, ↓ T3, Normal/↑ TSH- Treatment: None needed Inhibition of thyroid hormone synthesis: ↑ TSH, ↓ T4- Treatment: Levothyroxine AIT type 1 (iodine-induced increase in thyroid hormone synthesis): ↓ TSH, ↑ T3 & T4- ↓ RAIU- Increased vascularity on ultrasound- Treatment: Antithyroid drugs AIT type 2 (destructive thyroiditis): ↓ TSH, ↑ T3 & T4- Undetectable RAIU- Decreased vascularity on ultrasound- Treatment: Glucocorticoids
• Levothyroxine replacement therapy for hypothyroidism Initial dose- Standard dose: 75-125 mcg/day- Elderly, heart disease: 25-50 mcg/day Dose adjustments- Increase dose every 6 weeks until TSH is within normal range Maintenance therapy- Monitor TSH every 6-12 months Conditions requiring higher doses- Malabsorption (eg, celiac disease)- Drugs that interfere with absorption (eg, iron, calcium)- Drugs that increase thyroxine metabolism (eg, phenytoin, carbamazepine, rifampin)- Other: obesity, pregnancy, overt proteinuria
• Pseudohypoparathyroidism Pseudohypoparathyroidism type 1A: end-organ (i.e., bones and kidneys) resistance to parathyroid hormone (PTH) despite sufficient PTH synthesis due to a defective Gs protein alpha subunit Inheritance: autosomal dominant; gene defect inherited from the mother (imprinting) Clinical features- Persistent hypocalcemia despite increased levels of PTH- Features of Albright hereditary osteodystrophy→ Short stature, round face, as well as metacarpal and metatarsal shortening (shortened fourth and fifth digits)→ Intellectual disability (oligophrenia)→ Additionally signs of hypoparathyroidism: hypocalcemia, tetany, cerebral seizures, intracranial calcifications, and tooth anomalies Pseudopseudohypoparathyroidism: extremely rare condition that mimics PHP type 1a but without end-organ resistance to PTH- Inheritance: defective Gs protein alpha subunit is inherited from the father- Clinical features: normal calcium and PTH, features of Albright hereditary osteodystrophy Laboratory findings:- Pseudohypoparathyroidism type 1a: ↑ PTH, ↓ calcitriol, ↓ calcium, ↑ phosphate- Pseudopseudohypoparathyroidism: normal PTH, calcitriol, calcium, and phosphate

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