The develоpment оf а hоney-colored crust over а thin-wаlled vesicle is characteristic of which infectious skin disorder?
Hyperpаrаthyrоidism (Study Outline) Fоr study оnly—this is not medicаl advice or a substitute for professional care. 1. Background Definition:Excess secretion of parathyroid hormone (PTH) → hypercalcemia and hypophosphatemia, due to increased bone resorption, renal calcium reabsorption, and vitamin D activation. Types: Primary: Autonomous PTH overproduction (elevated calcium, elevated PTH). Causes: Parathyroid adenoma (≈85%), hyperplasia, or carcinoma. Secondary: Compensatory PTH elevation due to chronic hypocalcemia (low or normal calcium, high PTH). Causes: Chronic kidney disease (↓ vitamin D activation, phosphate retention), malabsorption, vitamin D deficiency. Tertiary: Autonomous PTH secretion after prolonged secondary stimulation (high calcium and very high PTH, often in ESRD). Epidemiology: More common in women >50 years. Primary hyperparathyroidism is the most frequent cause of outpatient hypercalcemia. Pathophysiology: PTH ↑ bone resorption (osteoclast activation via osteoblast signaling). ↑ renal calcium reabsorption and phosphate excretion. ↑ 1,25-(OH)₂ vitamin D (calcitriol) → ↑ intestinal calcium absorption. 2. History Often Asymptomatic (Incidental Hypercalcemia). Classic Mnemonic – “Stones, Bones, Groans, and Psychiatric Overtones”: Stones: Nephrolithiasis, nephrocalcinosis. Bones: Bone pain, fractures, osteitis fibrosa cystica (“brown tumors”). Groans: Abdominal pain, constipation, pancreatitis, peptic ulcers. Psychiatric Overtones: Fatigue, depression, confusion, anxiety. Other Symptoms: Polyuria, polydipsia (nephrogenic diabetes insipidus due to hypercalcemia). Weakness, muscle aches. Historical Clues: Lithium or thiazide diuretic use (can increase calcium). History of neck irradiation or multiple endocrine neoplasia (MEN 1 or 2A). 3. Exam Findings General: Lethargy, dehydration (from polyuria). HEENT: May have neck mass if large adenoma or hyperplasia. Cardiovascular: Hypertension, arrhythmias possible. Musculoskeletal: Bone tenderness, fractures, decreased bone density. Abdomen: Abdominal tenderness from stones or pancreatitis. Neurologic: Depression, confusion, or mild cognitive impairment. 4. Making the Diagnosis Step 1 – Confirm Hypercalcemia: Total serum calcium: elevated. Ionized calcium: confirm if albumin abnormal. Phosphate: decreased in primary disease. Step 2 – Measure Intact PTH: Primary hyperparathyroidism: ↑ PTH, ↑ Ca²⁺, ↓ phosphate. Secondary: ↑ PTH, ↓/normal Ca²⁺, ↑ phosphate (esp. CKD). Tertiary: markedly ↑ PTH, ↑ Ca²⁺, ↑ phosphate (autonomous). Step 3 – Additional Tests: 24-hour urinary calcium: Elevated in primary; low in familial hypocalciuric hypercalcemia (FHH). Serum creatinine and eGFR: evaluate for CKD (secondary cause). Vitamin D level: to rule out deficiency. Bone mineral density (DEXA): to assess osteoporosis. Imaging for localization (preoperative): Sestamibi scan or neck ultrasound for parathyroid adenoma. Gold Standard: Elevated serum calcium + elevated or inappropriately normal PTH. 5. Management (Exam Concepts) (Conceptual overview only—no dosing or treatment regimens.) Primary Hyperparathyroidism: Definitive treatment: surgical removal of adenoma or hyperplastic glands. Indications for surgery (exam clues): Serum Ca²⁺ >1 mg/dL above normal. Symptomatic (stones, bone disease, neuropsychiatric). Reduced bone density or age
Diаbetic Ketоаcidоsis (DKA) (Study Outline) Fоr study only—this is not medicаl advice or a substitute for professional care. 1. Background Definition: Acute, life-threatening metabolic complication of diabetes mellitus characterized by: Hyperglycemia Ketosis Anion gap metabolic acidosis Pathophysiology: Absolute or relative insulin deficiency + increased counter-regulatory hormones (glucagon, cortisol, catecholamines, growth hormone). Promotes lipolysis → free fatty acids → ketone body production (β-hydroxybutyrate, acetoacetate). Leads to osmotic diuresis, dehydration, and electrolyte loss. Epidemiology: More common in Type 1 diabetes, but can occur in Type 2 diabetes under stress. Precipitating Factors: Infection (most common) Missed insulin doses Myocardial infarction, stroke, pancreatitis, trauma, or surgery Certain medications (e.g., glucocorticoids, SGLT2 inhibitors) 2. History Rapid onset (hours to days). Classic symptoms: Polyuria, polydipsia, dehydration. Nausea, vomiting, abdominal pain. Shortness of breath (Kussmaul respirations). Fatigue, confusion, fruity (acetone) breath. Historical clues: Recent illness, skipped insulin, new-onset Type 1 diabetes. History of poor glycemic control or insulin pump malfunction. 3. Exam Findings Vital Signs: Tachycardia, tachypnea, hypotension, fever (if infectious trigger). General: Dehydration: dry mucous membranes, poor skin turgor. Kussmaul respirations: deep, labored breathing due to metabolic acidosis. Fruity odor on breath (acetone). Neurologic: Lethargy, confusion, possible coma in severe cases. Abdominal: Tenderness and pain common due to acidosis (may mimic acute abdomen). 4. Making the Diagnosis Diagnostic Triad: Hyperglycemia: Glucose typically >250 mg/dL Metabolic acidosis: Arterial pH 600), minimal ketones, no significant acidosis. 5. Management (Exam Concepts) (Conceptual overview only—no dosing or real-world directives.) Immediate priorities: Restore intravascular volume (IV fluids are first step). Correct electrolyte abnormalities (especially potassium). Administer insulin to suppress ketogenesis and correct acidosis. Identify and treat precipitating cause (infection, missed insulin, etc.). Monitoring: Hourly glucose checks. Frequent electrolytes (especially potassium and bicarbonate). Watch for cerebral edema, especially in children. Transition to long-term care: Once anion gap closes and patient can tolerate PO intake, transition to subcutaneous insulin. Complications to Recognize: Hypokalemia after insulin therapy. Cerebral edema (more common in pediatric DKA). ARDS or shock in severe dehydration QUESTION A 17-year-old girl with type 1 diabetes presents with nausea, vomiting, and rapid breathing. She reports missing several insulin doses. Physical exam reveals tachycardia, dry mucous membranes, and deep, labored respirations. Laboratory results show glucose 440 mg/dL, bicarbonate 12 mEq/L, and positive serum ketones. Which of the following best explains her acid-base disturbance? A. Lactic acid accumulation from hypoxiaB. Ketone body production due to insulin deficiencyC. Bicarbonate loss from vomitingD. Increased CO₂ retention due to respiratory depression
Thyrоid Cаncer (Study Outline) Fоr study оnly—this is not medicаl аdvice or a substitute for professional care. 1. Background Definition:Malignant tumors arising from thyroid follicular or parafollicular cells, varying from indolent to aggressive behavior. Epidemiology: Most common endocrine malignancy. Women > men; peak incidence 30–50 years. Excellent prognosis for differentiated cancers (papillary, follicular). Major Types (High-Yield): Type % Cell Origin Key Features Papillary carcinoma 80–85% Follicular cells Most common; lymphatic spread; prior radiation risk; excellent prognosis. Follicular carcinoma 10–15% Follicular cells Hematogenous spread (bone/lung); requires invasion for diagnosis. Medullary carcinoma 3–5% Parafollicular (C) cells Produces calcitonin; MEN 2A/2B association. Anaplastic carcinoma