Week two required Flashcards
Include AKI in a differential diagnosis based on various signs and symptoms
Recognize signs like anorexia, fatigue, nausea, vomiting, pruritus, seizures, and dyspnea. Also, evaluate lab results for ↑ Serum Creatinine and ↓ in urine output.
Recognize AKI quickly and efficiently based on lab work and urine output
AKI is typically recognized by an increase in serum creatinine and a decrease in urine output, with KDIGO stages providing a guideline for severity.
Stage the degree of AKI based on established baseline creatinine
Stage 1: ↑ x 1.5–1.9 or ↑ 0.3 mg/dl; Stage 2: ↑ x 2.0–2.9; Stage 3: ↑ x 3 or ↑ Cr > 4.0 mg/dl or need for dialysis.
Recite the etiology of AKI (prerenal, postrenal, intrinsic) from most common to least common
Prerenal: ↓ Renal perfusion; Postrenal: Obstruction; Intrinsic: AIN, GN, ATN.
Formulate a differential using initial lab work as well as physical exam and history to assist in patient care on rounds
Use lab work (BUN:Cr ratio, Urine osmolality, FeNa) and history (volume loss, medications, comorbid conditions) to guide diagnosis.
Provide a stepwise approach to workup and diagnosis to avoid unnecessary/costly workups
1) Review H&P and hospital records. 2) Analyze lab results and urine output. 3) Consider renal ultrasound and further tests if needed.
Recognize possible warning signs of ‘zebras’ when considering the etiology of AKI
Zebras include rare causes like glomerulonephritis, vasculitis, or drug-induced nephropathy, requiring a high index of suspicion.
Recommend treatment for AKI based on the etiology
Prerenal: Restore perfusion; Postrenal: Relieve obstruction; Intrinsic: Treat underlying cause, support renal function.
Recognize and recite the indications for emergent dialysis
Emergent dialysis is indicated for severe acidosis, hyperkalemia, toxin ingestion, volume overload, and uremia.
Recommend strategies to help prevent AKI
Prevent hypotension, avoid nephrotoxic drugs, ensure adequate hydration, and monitor renal function in at-risk patients.
Epidemiology of AKI
2-3 cases per 1000 persons; 7% of hospitalized patients; 2/3 of ICU patients; Typically because of sepsis; 2/3 of AKI cases resolve within 7 days; Mortality: 25-80%.
Definition of AKI
↓ Kidney function within 48 hours, ↑ Serum Creatinine, ↓ in urine output, and Need for Renal Replacement Therapy (RRT).
KDIGO Stages of AKI
Stage 1: ↑ x 1.5–1.9 OR ↑ 0.3 mg/dl, <0.5 ml/kg/h x 6–12hrs; Stage 2: ↑ x 2.0–2.9, <0.5 ml/kg/h x 12 hrs; Stage 3: ↑ x 3 OR ↑ Cr > 4.0 mg/dl, need for dialysis, or <35 GFR.
Symptoms of AKI
Nonspecific symptoms: Anorexia, Fatigue, Change in mentation, Nausea & vomiting, Pruritus, Seizures, Dyspnea.
Signs of AKI
Asterixis, Myoclonus, Pericardial rub, Edema, Lung Rales, ↓ Urine output (Oliguria: < 400 cc per day; Anuria: <100cc per day).
Prerenal AKI: Epidemiology
Accounts for 70% of community-acquired AKI and 40% of hospital-acquired AKI.
Prerenal AKI: Etiology
Systemic Volume Depletion, ↓ Mean Arterial Pressure, Isolated ↓ Renal Perfusion, Medications (e.g., ACE/ARB, NSAIDs).
Prerenal AKI: Treatment
Stop nephrotoxic medications, ensure adequate blood pressure (MAP > 65 mmHg), and maintain normal urine output with intravenous fluids.
Postrenal AKI: Epidemiology
Accounts for 17% of community-acquired AKI.
Postrenal AKI: Etiology
Extrarenal obstruction: BPH, Neurogenic bladder, Retroperitoneal fibrosis, Cancer. Intrarenal obstruction: Stones, Crystals, Clots, Tumors.
Postrenal AKI: Treatment
Relieve obstruction and hydrate if needed.
Intrinsic AKI: Classification
Glomerular (GN), Interstitial (AIN), Tubular (ATN), Vascular causes (e.g., renal vein thrombosis, malignant hypertension).
Acute Tubular Necrosis (ATN): Epidemiology
85% of intrinsic disease is ATN; 50% ischemic, 35% toxic.
ATN: Pathology
Tubular necrosis occurs due to decreased blood flow or direct toxic effect, leading to cast formation and tubule obstruction.
ATN: Treatment
Supportive care: maintain euvolemic state, remove nephrotoxic agents, monitor drug levels, and prevent contrast nephropathy.
AIN: Common Causes
Medications (e.g., NSAIDs, antibiotics), infections (e.g., EBV, CMV), autoimmune diseases (e.g., SLE), neoplasms.
AIN: Diagnosis
Eosinophilia on CBC, sterile pyuria, WBC casts, and possible proteinuria and hematuria.
Glomerulonephritis: Key Facts
Accounts for 5% of intrinsic causes of AKI; presents with proteinuria, hematuria, and nephrotic/nephritic syndromes.
Emergent Hemodialysis Indications
Acidosis, Electrolyte abnormalities (hyperkalemia), Ingestion of toxins, Fluid overload, Uremia.
Identify the signs and symptoms of potassium disorders
Hypokalemia: Weakness, fatigue, muscle cramps. Hyperkalemia: Weakness, paralysis, arrhythmias.
Recite the major components of the differential diagnosis of hypokalemia and hyperkalemia
Hypokalemia: GI loss, renal loss, transcellular shift. Hyperkalemia: Renal failure, acidosis, medication effects.
Consistently provide treatment for hypokalemia by the most appropriate route and dosage of potassium
For every 10mEq of potassium given, serum K+ rises by ~0.1mEq/L. Oral route preferred, IV for severe cases.
Quickly provide treatment for hyperkalemia under various clinical conditions
Membrane stabilization: Calcium gluconate. Cellular shift: Insulin + Dextrose, β2-agonists. Potassium elimination: Sodium polystyrene, Furosemide.
Recite and identify the electrocardiographic changes of hypo and hyperkalemia
Hypokalemia: U-wave, flattened T-waves, ST depression. Hyperkalemia: Peaked T-waves, widened QRS, sine wave.
Quickly correct serum calcium levels based on serum albumin levels
Corrected Ca = (4 – Albumin) x 0.8 + Serum Calcium. Used to determine true calcium levels.
Explain hormonal regulation of calcium and connect this to forming a differential diagnosis for calcium and phosphorus abnormalities
PTH increases serum calcium and decreases phosphorus. Calcitriol increases both calcium and phosphorus. Calcitonin decreases both.
Provide a workup to narrow down your differential diagnosis of hypercalcemia and hypocalcemia
Hypercalcemia: Check PTH, PTHrP, 25(OH)D, 1,25(OH)2D. Hypocalcemia: Check PTH, magnesium, phosphorus, vitamin D levels.
Recite the treatment for hypercalcemia while factoring in the severity of disease
Mild: Hydration. Moderate: Hydration + Bisphosphonates. Severe: Hydration + Bisphosphonates + Calcitonin.
Apply the signs and symptoms of electrolyte disturbances to differential diagnosis of common presentations
Hypercalcemia: Stones, bones, groans, psychiatric overtones. Hypocalcemia: Tetany, seizures, QT prolongation.
Identify EKG changes as they relate to electrolyte disturbances
Hypocalcemia: QT prolongation. Hypercalcemia: Shortened QT. Hypokalemia: U-wave. Hyperkalemia: Peaked T-wave.
Consistently suggest approximate dosage of electrolyte replacement and route of administration in routine electrolyte deficiencies
Hypokalemia: 10-20 mEq potassium chloride orally. Hypocalcemia: 1-2 g calcium carbonate orally. Hypomagnesemia: 2 g magnesium sulfate IV.
Function and regulation of potassium
Maintains cellular voltage gradient, critical for action potential in cardiac, neuromuscular, and gastric tissues. Regulated by Na-K-ATPase, acid-base balance, and renal excretion.
Etiology of hypokalemia
Decreased intake, transcellular shift (alkalosis, β2-agonists), GI loss (diarrhea), renal loss (diuretics, RTA).
Etiology of hyperkalemia
Increased intake (rare), transcellular shift (acidosis, insulin deficiency), decreased renal excretion (CKD, hypoaldosteronism).
Treatment of hypokalemia
Replace potassium: 10 mEq raises serum K+ by ~0.1mEq/L. Oral preferred, IV for severe cases. Monitor EKG and potassium levels.
Treatment of hyperkalemia
Membrane stabilization: Calcium gluconate. Cellular shift: Insulin + Dextrose, β2-agonists. Elimination: Sodium polystyrene, Furosemide, hemodialysis.
Function and regulation of calcium
Bone mineralization, muscle contraction, neurotransmitter release. Regulated by PTH, calcitriol, and calcitonin.
Etiology of hypercalcemia
Most commonly due to malignancy or hyperparathyroidism. Other causes include granulomatous diseases, immobility, and certain medications.
Etiology of hypocalcemia
Hypoparathyroidism, vitamin D deficiency, cell lysis, hypomagnesemia, pancreatitis, transfusion, respiratory alkalosis.
Signs and symptoms of hypercalcemia
Neurological: Fatigue, confusion, coma. Renal: Nephrolithiasis, DI, AKI. GI: Nausea, vomiting, constipation. Cardiovascular: Short QT, arrhythmias.
Signs and symptoms of hypocalcemia
Neuromuscular: Tetany, seizures, Chvostek’s sign, Trousseau’s sign. Cardiovascular: QT prolongation, hypotension.
Function and regulation of phosphorus
Energy transfer (ATP), bone mineralization, cell membrane integrity, enzyme function. Regulated by dietary intake, PTH, and kidney excretion.
Etiology of hyperphosphatemia
Increased GI absorption (laxatives, vitamin D toxicity), decreased renal excretion (CKD), intracellular release (tumor lysis, rhabdomyolysis).
Etiology of hypophosphatemia
Decreased GI absorption (malnutrition, antacids), increased renal excretion (diuretics, RTA), intracellular shift (refeeding syndrome, respiratory alkalosis).
Signs and symptoms of hyperphosphatemia
Asymptomatic unless calcium-phosphate precipitates occur, leading to soft tissue calcification, arrhythmias, pruritus.
Signs and symptoms of hypophosphatemia
Weakness, respiratory failure, rhabdomyolysis, impaired platelet and WBC function, seizures.
Function and regulation of magnesium
Enzyme cofactor, maintains cardiovascular and neuromuscular function, RNA/DNA synthesis. Regulated by dietary intake and kidney excretion.
Etiology of hypermagnesemia
Renal failure, tissue breakdown (sepsis, rhabdomyolysis), iatrogenic (magnesium-containing medications).
Etiology of hypomagnesemia
Diabetes mellitus, alcoholism, diuretic use, GI loss (malabsorption, diarrhea), endocrine disorders.
Signs and symptoms of hypermagnesemia
Paresthesia, paralysis, respiratory depression, bradycardia, hypotension.
Signs and symptoms of hypomagnesemia
Neurological: Tremors, seizures. Cardiovascular: QT prolongation, Torsades de pointes. Electrolyte abnormalities: Hypokalemia, hypocalcemia.
