Which оf these stаtements аbоut bаsal cell carcinоma is true?
Pheоchrоmоcytomа (Study Outline) For study only—this is not medicаl аdvice or a substitute for professional care. 1. Background Definition:A catecholamine-secreting tumor arising from chromaffin cells of the adrenal medulla (or extra-adrenal paraganglia, termed paraganglioma).Secretes epinephrine, norepinephrine, and/or dopamine, leading to episodic or sustained sympathetic overactivity. Pathophysiology: Excess catecholamines → overstimulation of α- and β-adrenergic receptors. Results in vasoconstriction, tachycardia, hyperglycemia, and hypertension. Catecholamine surges may be triggered by stress, surgery, exercise, or certain drugs (e.g., β-blockers before α-blockade). Rule of 10s (Classic Teaching): 10% bilateral 10% extra-adrenal (paragangliomas) 10% malignant 10% in children(Recent data: up to 30–40% associated with germline mutations.) Genetic Associations: MEN 2A/2B (RET mutation) Von Hippel–Lindau (VHL) disease Neurofibromatosis type 1 (NF1) Succinate dehydrogenase (SDH) gene mutations Epidemiology: Rare, accounting for
Primаry Aldоsterоnism (Cоnn Syndrome) (Study Outline) For study only—this is not medicаl аdvice or a substitute for professional care. 1. Background Definition:Primary aldosteronism is excessive, autonomous secretion of aldosterone from the adrenal cortex (zona glomerulosa), independent of renin.This leads to sodium retention, potassium loss, and metabolic alkalosis. Pathophysiology: Aldosterone excess → ↑ Na⁺ and water reabsorption → volume expansion and hypertension. Increased K⁺ and H⁺ secretion → hypokalemia and metabolic alkalosis. Suppressed renin due to feedback inhibition from increased volume. Major Causes: Aldosterone-producing adenoma (Conn syndrome) — most common. Bilateral adrenal hyperplasia. Rare: unilateral adrenal carcinoma, familial hyperaldosteronism (genetic). Epidemiology: Accounts for 5–10% of hypertension cases. More common in middle-aged adults; slight female predominance. 2. History Symptoms (often subtle): Hypertension — may be resistant to standard therapy. Muscle weakness, fatigue, cramps, paresthesias (due to hypokalemia). Polyuria and polydipsia (from renal K⁺ wasting). Headaches, palpitations, nocturia possible. Usually no peripheral edema (due to “aldosterone escape” — natriuresis balancing fluid retention). Historical Clues: Early-onset hypertension or family history of endocrine hypertension. Severe or refractory hypertension in a relatively young patient. Hypokalemia not explained by diuretics. 3. Exam Findings Vital Signs: Persistent or resistant hypertension (often moderate to severe). Cardiovascular: Possible left ventricular hypertrophy or secondary changes from chronic hypertension. Neuromuscular: Muscle weakness or arrhythmias (if severe hypokalemia). Volume Status: Usually euvolemic (no significant edema). Physical Exam: Often otherwise unremarkable. 4. Making the Diagnosis Step 1 – Screening: Plasma Aldosterone-to-Renin Ratio (ARR): Elevated aldosterone with suppressed renin = suggestive. High ARR (>20:1) strongly supports diagnosis. Step 2 – Confirmatory Testing: Oral sodium loading test, saline infusion test, or fludrocortisone suppression test: Failure of aldosterone suppression confirms autonomous secretion. Step 3 – Determine Etiology (Localization): Adrenal CT scan: evaluates for adenoma, carcinoma, or bilateral hyperplasia. Adrenal venous sampling (AVS): Gold standard for lateralization (differentiates unilateral adenoma from bilateral hyperplasia). Performed prior to surgery to confirm source of excess aldosterone. Step 4 – Additional Labs: Electrolytes: Hypokalemia, metabolic alkalosis. Renin: Suppressed (low plasma renin activity). Aldosterone: Elevated (>15 ng/dL in most cases). Gold Standard: Confirmatory suppression testing demonstrating autonomous aldosterone production with low renin activity. 5. Management (Exam Concepts) (Conceptual overview only—no dosing or treatment regimens.) Unilateral Aldosterone-Producing Adenoma: Laparoscopic adrenalectomy is definitive. Medical therapy (if not surgical candidate): mineralocorticoid receptor antagonists (spironolactone, eplerenone). Bilateral Adrenal Hyperplasia: Medical management preferred (mineralocorticoid antagonists). Monitor electrolytes, BP, and renal function. General Care: Control hypertension. Normalize potassium and acid–base status. Screen for secondary cardiovascular and renal complications. Exam Tips: Hypertension + hypokalemia = suspect primary aldosteronism. Low renin, high aldosterone. Distinguish from secondary aldosteronism (both renin and aldosterone elevated — e.g., renal artery stenosis). Adrenal venous sampling differentiates unilateral from bilateral disease before surgery. NBME-Style Practice Question A 40-year-old woman presents with fatigue, muscle cramps, and difficult-to-control hypertension. Her blood pressure is 165/100 mm Hg. Laboratory results show Na⁺ 148 mEq/L, K⁺ 3.0 mEq/L, and metabolic alkalosis. Plasma renin activity is suppressed, and plasma aldosterone concentration is markedly elevated. Which of the following is the most appropriate next diagnostic step? A. High-dose dexamethasone suppression testB. Oral sodium loading testC. 24-hour urinary free cortisol testD. Plasma metanephrine level
Diаbetes Mellitus Type 2 (Study Outline) Fоr study оnly—this is nоt medicаl аdvice or a substitute for professional care. 1. Background Definition: Chronic hyperglycemia resulting from insulin resistance and progressive β-cell dysfunction. Pathophysiology: Peripheral tissues (muscle, liver, adipose) become resistant to insulin’s effects. Pancreatic β-cells initially increase insulin output but eventually fail. Associated metabolic disturbances: ↑ hepatic glucose production, ↓ peripheral glucose uptake. Epidemiology: 90% of diabetes cases. Typically develops after age 40, but increasing prevalence in adolescents with obesity. Strongly linked to obesity, sedentary lifestyle, and family history. Risk Factors: Obesity (especially central/visceral). Family history, hypertension, dyslipidemia, polycystic ovary syndrome. Certain ethnicities: African American, Hispanic, Native American, Pacific Islander. 2. History Gradual Onset Symptoms: Polyuria, polydipsia, polyphagia. Fatigue, blurred vision. Recurrent infections (e.g., skin, vaginal, urinary). Poor wound healing, acanthosis nigricans. Often Asymptomatic: May be discovered incidentally on labs. Associated Conditions: Metabolic syndrome (obesity, hypertension, dyslipidemia, insulin resistance). DKA Rare: Hyperosmolar hyperglycemic state (HHS) more common. 3. Exam Findings General: Overweight or obese body habitus. Blood pressure often elevated. Skin: Acanthosis nigricans: hyperpigmented, velvety plaques (neck, axilla). Skin tags (acrochordons). Complications: Peripheral neuropathy (sensory loss, paresthesias). Retinopathy signs on fundoscopic exam (microaneurysms, exudates). Decreased vibratory sense or absent reflexes in feet. 4. Making the Diagnosis Diagnostic Criteria (any of the following): Fasting plasma glucose ≥126 mg/dL (×2). A1C ≥6.5%. 2-hour OGTT glucose ≥200 mg/dL after 75 g glucose load. Random glucose ≥200 mg/dL with classic symptoms. Laboratory Findings: Elevated or normal C-peptide (reflects continued endogenous insulin production). No pancreatic autoantibodies (distinguishes from Type 1 DM). Screening Recommendations: Adults ≥35 years, or earlier if overweight with additional risk factors. Repeat every 3 years if normal. Gold Standard: Biochemical confirmation of hyperglycemia (fasting glucose or A1C). Common Associated Labs: Dyslipidemia: ↑ triglycerides, ↓ HDL, ↑ LDL. Possible hepatic steatosis on imaging. 5. Management (Exam Concepts) Lifestyle Modifications: Weight loss (5–10% body weight), healthy diet, regular exercise. First-line for all patients and may normalize glucose in early disease. Pharmacologic Therapy: First-line: Oral antihyperglycemics (mechanisms emphasized on PANCE): Biguanides (e.g., metformin): ↓ hepatic glucose output, ↑ insulin sensitivity. Other classes: SGLT2 inhibitors, GLP-1 receptor agonists, DPP-4 inhibitors, sulfonylureas. Insulin may be required for severe hyperglycemia or β-cell exhaustion. Monitoring: A1C every 3 months until stable (