Write the expression as the sine, cosine or tangent of a dou…
Questions
Write the expressiоn аs the sine, cоsine оr tаngent of а double angle.
Is y = -4x + 3 pаrtiаl оr direct vаriatiоn? Explain hоw you know.
Nephrоtic Syndrоme (Study Outline) 1. Bаckgrоund Definition: A glomerulаr disorder chаracterized by heavy proteinuria (>3.5 g/day), hypoalbuminemia, edema, hyperlipidemia, and lipiduria. Pathophysiology: Injury to the glomerular filtration barrier (podocytes) → massive loss of protein → ↓ plasma oncotic pressure → edema and hepatic upregulation of lipoprotein synthesis. Common causes (high-yield): Primary: Minimal change disease (most common in children). Focal segmental glomerulosclerosis (FSGS). Membranous nephropathy (most common in adults). Secondary: Diabetes mellitus (leading cause). Amyloidosis. SLE (can cause nephritic or nephrotic). Infections (HIV, hepatitis), medications, malignancy. 2. History Edema—generalized, often periorbital in AM and dependent in PM. Foamy urine (due to proteinuria). Fatigue, weight gain from fluid retention. History clues for secondary causes: Longstanding diabetes, IV drug use, HIV risk, hepatitis exposure, autoimmune symptoms, malignancy. Thrombotic history: nephrotic state increases risk for DVT/PE. 3. Exam Findings Edema: pitting, generalized (anasarca in severe cases). Ascites, pleural effusions in advanced disease. Labs may manifest clinically: xanthelasma (hyperlipidemia). Possible hypertension (less pronounced than nephritic syndrome). Signs of underlying disease: diabetic retinopathy, purpura (amyloidosis rare), rash (SLE). 4. Making the Diagnosis Urinalysis: Massive proteinuria (>3.5 g/day). Oval fat bodies (“Maltese cross” under polarized light). Lipiduria, fatty casts. Blood tests: Hypoalbuminemia, hyperlipidemia (↑ LDL, ↑ triglycerides). May have normal or mildly low GFR initially. Serologic testing based on suspected etiology: Autoimmune panel (ANA, anti-dsDNA), hepatitis serologies, HIV testing. Renal ultrasound: typically normal-sized kidneys. Renal biopsy: Often required to determine etiology (minimal change vs. FSGS vs. membranous). Gold Standard: Renal biopsy demonstrating characteristic podocyte/glomerular changes consistent with specific nephrotic pathology. 5. Management (Exam Concepts) General principles: Control edema (concept-level: sodium restriction). Adjust medications based on GFR. Avoid nephrotoxins. Proteinuria reduction (high-yield exam concept): RAAS modulation principles for reducing intraglomerular pressure and protein loss. Hyperlipidemia management: conceptual treatment of elevated LDL/TG in nephrotic states. Thrombosis risk: nephrotic syndrome increases clot risk—recognize risk factors conceptually. Cause-directed (exam-level concepts): Minimal change disease: immunosuppression principles. FSGS: BP control, immunosuppression concepts. Membranous nephropathy: immunologic evaluation and immunosuppression principles. Diabetic nephropathy: optimize glucose/BP. Indications for referral: heavy proteinuria, unclear cause, or progression toward CKD. QUESTION A 36-year-old man presents with progressive swelling in his legs and face over the past two weeks. He also reports frothy urine and a recent 6-pound weight gain. He denies hematuria, joint pain, or rash. Medical history is significant for intravenous drug use. On exam, his blood pressure is 132/82 mmHg, and he has periorbital edema, pitting edema to the knees, and mild ascites. Laboratory studies: Urinalysis: 4+ protein, no hematuria, oval fat bodies 24-hour urine protein: 7.2 g Serum albumin: 2.1 g/dL (3.5–5.0) Serum creatinine: 1.1 mg/dL Total cholesterol: 294 mg/dL HIV test: positive Which of the following is the most likely diagnosis? A) Focal segmental glomerulosclerosisB) Membranous nephropathyC) Minimal change diseaseD) Diabetic nephropathy
Rhаbdоmyоlysis (Study Outline) 1. Bаckgrоund Definition: Breаkdown of skeletal muscle fibers leading to release of myoglobin, CK, potassium, phosphate, and other intracellular contents into the bloodstream. Pathophysiology: Myoglobin filtered by kidneys → tubular obstruction + direct nephrotoxicity → intrinsic AKI (ATN). Electrolyte disturbances common (↑K⁺, ↑PO₄³⁻). Common causes (high-yield): Trauma/crush injuries. Exertional: strenuous exercise, heat stroke. Drugs/toxins: alcohol, cocaine, heroin, statins (exam clue). Prolonged immobilization. Seizures or electrical injuries. Metabolic or infectious causes. 2. History Muscle pain, swelling, stiffness. Dark “tea-colored” urine (myoglobinuria). Recent injury, exertion, or immobilization. Systemic symptoms: fever, malaise, nausea. Medication/substance clues: statins, illicit drugs, alcohol binge. 3. Exam Findings Tender, swollen muscles (common in thighs, shoulders). Weakness due to muscle injury. Signs of volume depletion (tachycardia, dry mucosa) if significant intravascular shift. Compartment syndrome risk—tense compartments, severe pain out of proportion. Arrhythmias possible due to electrolyte derangements (hyperkalemia). 4. Making the Diagnosis Labs (high-yield): CK >5× normal (often >5,000–10,000 U/L). Myoglobinuria: positive blood on dipstick with few or no RBCs (classic clue). Electrolytes: ↑ K⁺, ↑ phosphate, ↓ Ca²⁺ (early). Renal function: ↑ BUN/Cr in ATN; FeNa often >2%. UA: pigmented granular casts possible. Additional tests: AST/ALT (AST often elevated from muscle). EKG if hyperkalemia suspected. Imaging: Not typically needed unless trauma, compartment syndrome, or underlying cause evaluation required. Gold Standard: Markedly elevated CK with compatible clinical features. 5. Management (Exam Concepts) Primary goals: prevent intrinsic AKI (ATN), correct electrolyte abnormalities, and treat underlying cause. Fluid management concept: aggressive isotonic hydration to maintain renal perfusion (no dosing). Electrolyte concepts: Monitor and manage hyperkalemia (high-yield). Manage hypocalcemia only if symptomatic (exam principle). Avoid nephrotoxins: NSAIDs, contrast agents. Monitor for compartment syndrome: surgical evaluation if suspected. Dialysis indications: refractory hyperkalemia, severe acidosis, fluid overload, or uremic symptoms. Follow-up: serial CK, renal function, electrolytes. QUESTION A 28-year-old man presents to the emergency department with dark-colored urine and muscle soreness after completing a marathon the previous day. He denies any trauma, medications, or past medical history. Physical exam shows mild muscle tenderness in the thighs and calves. Vitals are stable. Urinalysis reveals positive blood on dipstick, but microscopic examination shows no red blood cells. Labs reveal: Serum creatinine: 2.1 mg/dL (baseline unknown) Serum potassium: 5.8 mEq/L Creatine kinase: 12,000 U/L Which of the following findings is most characteristic of the patient’s condition? A) Sudden onset flank pain and gross hematuria with RBC castsB) Gradual worsening of renal function over years in a poorly controlled hypertensive patientC) Markedly elevated creatine kinase with myoglobinuria and hyperkalemiaD) Sharp rise in creatinine following use of a new ACE inhibitor