Week two required Flashcards

1
Q

Include AKI in a differential diagnosis based on various signs and symptoms

A

Recognize signs like anorexia, fatigue, nausea, vomiting, pruritus, seizures, and dyspnea. Also, evaluate lab results for ↑ Serum Creatinine and ↓ in urine output.

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2
Q

Recognize AKI quickly and efficiently based on lab work and urine output

A

AKI is typically recognized by an increase in serum creatinine and a decrease in urine output, with KDIGO stages providing a guideline for severity.

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3
Q

Stage the degree of AKI based on established baseline creatinine

A

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.

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4
Q

Recite the etiology of AKI (prerenal, postrenal, intrinsic) from most common to least common

A

Prerenal: ↓ Renal perfusion; Postrenal: Obstruction; Intrinsic: AIN, GN, ATN.

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5
Q

Formulate a differential using initial lab work as well as physical exam and history to assist in patient care on rounds

A

Use lab work (BUN:Cr ratio, Urine osmolality, FeNa) and history (volume loss, medications, comorbid conditions) to guide diagnosis.

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6
Q

Provide a stepwise approach to workup and diagnosis to avoid unnecessary/costly workups

A

1) Review H&P and hospital records. 2) Analyze lab results and urine output. 3) Consider renal ultrasound and further tests if needed.

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7
Q

Recognize possible warning signs of ‘zebras’ when considering the etiology of AKI

A

Zebras include rare causes like glomerulonephritis, vasculitis, or drug-induced nephropathy, requiring a high index of suspicion.

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8
Q

Recommend treatment for AKI based on the etiology

A

Prerenal: Restore perfusion; Postrenal: Relieve obstruction; Intrinsic: Treat underlying cause, support renal function.

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9
Q

Recognize and recite the indications for emergent dialysis

A

Emergent dialysis is indicated for severe acidosis, hyperkalemia, toxin ingestion, volume overload, and uremia.

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10
Q

Recommend strategies to help prevent AKI

A

Prevent hypotension, avoid nephrotoxic drugs, ensure adequate hydration, and monitor renal function in at-risk patients.

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11
Q

Epidemiology of AKI

A

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%.

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12
Q

Definition of AKI

A

↓ Kidney function within 48 hours, ↑ Serum Creatinine, ↓ in urine output, and Need for Renal Replacement Therapy (RRT).

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13
Q

KDIGO Stages of AKI

A

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.

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14
Q

Symptoms of AKI

A

Nonspecific symptoms: Anorexia, Fatigue, Change in mentation, Nausea & vomiting, Pruritus, Seizures, Dyspnea.

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15
Q

Signs of AKI

A

Asterixis, Myoclonus, Pericardial rub, Edema, Lung Rales, ↓ Urine output (Oliguria: < 400 cc per day; Anuria: <100cc per day).

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16
Q

Prerenal AKI: Epidemiology

A

Accounts for 70% of community-acquired AKI and 40% of hospital-acquired AKI.

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17
Q

Prerenal AKI: Etiology

A

Systemic Volume Depletion, ↓ Mean Arterial Pressure, Isolated ↓ Renal Perfusion, Medications (e.g., ACE/ARB, NSAIDs).

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18
Q

Prerenal AKI: Treatment

A

Stop nephrotoxic medications, ensure adequate blood pressure (MAP > 65 mmHg), and maintain normal urine output with intravenous fluids.

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19
Q

Postrenal AKI: Epidemiology

A

Accounts for 17% of community-acquired AKI.

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20
Q

Postrenal AKI: Etiology

A

Extrarenal obstruction: BPH, Neurogenic bladder, Retroperitoneal fibrosis, Cancer. Intrarenal obstruction: Stones, Crystals, Clots, Tumors.

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21
Q

Postrenal AKI: Treatment

A

Relieve obstruction and hydrate if needed.

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22
Q

Intrinsic AKI: Classification

A

Glomerular (GN), Interstitial (AIN), Tubular (ATN), Vascular causes (e.g., renal vein thrombosis, malignant hypertension).

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23
Q

Acute Tubular Necrosis (ATN): Epidemiology

A

85% of intrinsic disease is ATN; 50% ischemic, 35% toxic.

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24
Q

ATN: Pathology

A

Tubular necrosis occurs due to decreased blood flow or direct toxic effect, leading to cast formation and tubule obstruction.

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25
Q

ATN: Treatment

A

Supportive care: maintain euvolemic state, remove nephrotoxic agents, monitor drug levels, and prevent contrast nephropathy.

26
Q

AIN: Common Causes

A

Medications (e.g., NSAIDs, antibiotics), infections (e.g., EBV, CMV), autoimmune diseases (e.g., SLE), neoplasms.

27
Q

AIN: Diagnosis

A

Eosinophilia on CBC, sterile pyuria, WBC casts, and possible proteinuria and hematuria.

28
Q

Glomerulonephritis: Key Facts

A

Accounts for 5% of intrinsic causes of AKI; presents with proteinuria, hematuria, and nephrotic/nephritic syndromes.

29
Q

Emergent Hemodialysis Indications

A

Acidosis, Electrolyte abnormalities (hyperkalemia), Ingestion of toxins, Fluid overload, Uremia.

30
Q

Identify the signs and symptoms of potassium disorders

A

Hypokalemia: Weakness, fatigue, muscle cramps. Hyperkalemia: Weakness, paralysis, arrhythmias.

31
Q

Recite the major components of the differential diagnosis of hypokalemia and hyperkalemia

A

Hypokalemia: GI loss, renal loss, transcellular shift. Hyperkalemia: Renal failure, acidosis, medication effects.

32
Q

Consistently provide treatment for hypokalemia by the most appropriate route and dosage of potassium

A

For every 10mEq of potassium given, serum K+ rises by ~0.1mEq/L. Oral route preferred, IV for severe cases.

33
Q

Quickly provide treatment for hyperkalemia under various clinical conditions

A

Membrane stabilization: Calcium gluconate. Cellular shift: Insulin + Dextrose, β2-agonists. Potassium elimination: Sodium polystyrene, Furosemide.

34
Q

Recite and identify the electrocardiographic changes of hypo and hyperkalemia

A

Hypokalemia: U-wave, flattened T-waves, ST depression. Hyperkalemia: Peaked T-waves, widened QRS, sine wave.

35
Q

Quickly correct serum calcium levels based on serum albumin levels

A

Corrected Ca = (4 – Albumin) x 0.8 + Serum Calcium. Used to determine true calcium levels.

36
Q

Explain hormonal regulation of calcium and connect this to forming a differential diagnosis for calcium and phosphorus abnormalities

A

PTH increases serum calcium and decreases phosphorus. Calcitriol increases both calcium and phosphorus. Calcitonin decreases both.

37
Q

Provide a workup to narrow down your differential diagnosis of hypercalcemia and hypocalcemia

A

Hypercalcemia: Check PTH, PTHrP, 25(OH)D, 1,25(OH)2D. Hypocalcemia: Check PTH, magnesium, phosphorus, vitamin D levels.

38
Q

Recite the treatment for hypercalcemia while factoring in the severity of disease

A

Mild: Hydration. Moderate: Hydration + Bisphosphonates. Severe: Hydration + Bisphosphonates + Calcitonin.

39
Q

Apply the signs and symptoms of electrolyte disturbances to differential diagnosis of common presentations

A

Hypercalcemia: Stones, bones, groans, psychiatric overtones. Hypocalcemia: Tetany, seizures, QT prolongation.

40
Q

Identify EKG changes as they relate to electrolyte disturbances

A

Hypocalcemia: QT prolongation. Hypercalcemia: Shortened QT. Hypokalemia: U-wave. Hyperkalemia: Peaked T-wave.

41
Q

Consistently suggest approximate dosage of electrolyte replacement and route of administration in routine electrolyte deficiencies

A

Hypokalemia: 10-20 mEq potassium chloride orally. Hypocalcemia: 1-2 g calcium carbonate orally. Hypomagnesemia: 2 g magnesium sulfate IV.

42
Q

Function and regulation of potassium

A

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.

43
Q

Etiology of hypokalemia

A

Decreased intake, transcellular shift (alkalosis, β2-agonists), GI loss (diarrhea), renal loss (diuretics, RTA).

44
Q

Etiology of hyperkalemia

A

Increased intake (rare), transcellular shift (acidosis, insulin deficiency), decreased renal excretion (CKD, hypoaldosteronism).

45
Q

Treatment of hypokalemia

A

Replace potassium: 10 mEq raises serum K+ by ~0.1mEq/L. Oral preferred, IV for severe cases. Monitor EKG and potassium levels.

46
Q

Treatment of hyperkalemia

A

Membrane stabilization: Calcium gluconate. Cellular shift: Insulin + Dextrose, β2-agonists. Elimination: Sodium polystyrene, Furosemide, hemodialysis.

47
Q

Function and regulation of calcium

A

Bone mineralization, muscle contraction, neurotransmitter release. Regulated by PTH, calcitriol, and calcitonin.

48
Q

Etiology of hypercalcemia

A

Most commonly due to malignancy or hyperparathyroidism. Other causes include granulomatous diseases, immobility, and certain medications.

49
Q

Etiology of hypocalcemia

A

Hypoparathyroidism, vitamin D deficiency, cell lysis, hypomagnesemia, pancreatitis, transfusion, respiratory alkalosis.

50
Q

Signs and symptoms of hypercalcemia

A

Neurological: Fatigue, confusion, coma. Renal: Nephrolithiasis, DI, AKI. GI: Nausea, vomiting, constipation. Cardiovascular: Short QT, arrhythmias.

51
Q

Signs and symptoms of hypocalcemia

A

Neuromuscular: Tetany, seizures, Chvostek’s sign, Trousseau’s sign. Cardiovascular: QT prolongation, hypotension.

52
Q

Function and regulation of phosphorus

A

Energy transfer (ATP), bone mineralization, cell membrane integrity, enzyme function. Regulated by dietary intake, PTH, and kidney excretion.

53
Q

Etiology of hyperphosphatemia

A

Increased GI absorption (laxatives, vitamin D toxicity), decreased renal excretion (CKD), intracellular release (tumor lysis, rhabdomyolysis).

54
Q

Etiology of hypophosphatemia

A

Decreased GI absorption (malnutrition, antacids), increased renal excretion (diuretics, RTA), intracellular shift (refeeding syndrome, respiratory alkalosis).

55
Q

Signs and symptoms of hyperphosphatemia

A

Asymptomatic unless calcium-phosphate precipitates occur, leading to soft tissue calcification, arrhythmias, pruritus.

56
Q

Signs and symptoms of hypophosphatemia

A

Weakness, respiratory failure, rhabdomyolysis, impaired platelet and WBC function, seizures.

57
Q

Function and regulation of magnesium

A

Enzyme cofactor, maintains cardiovascular and neuromuscular function, RNA/DNA synthesis. Regulated by dietary intake and kidney excretion.

58
Q

Etiology of hypermagnesemia

A

Renal failure, tissue breakdown (sepsis, rhabdomyolysis), iatrogenic (magnesium-containing medications).

59
Q

Etiology of hypomagnesemia

A

Diabetes mellitus, alcoholism, diuretic use, GI loss (malabsorption, diarrhea), endocrine disorders.

60
Q

Signs and symptoms of hypermagnesemia

A

Paresthesia, paralysis, respiratory depression, bradycardia, hypotension.

61
Q

Signs and symptoms of hypomagnesemia

A

Neurological: Tremors, seizures. Cardiovascular: QT prolongation, Torsades de pointes. Electrolyte abnormalities: Hypokalemia, hypocalcemia.