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Acid-Base Balance, Electrolytes, and Renal Pathophysiology Review

pH and acid-base basics

  • Normal ranges used in this lecture:
    • pH: pH_{normal}=7.35\text{ to }7.45
    • PaCO₂: pCO_2\in[35,45]\ \text{mmHg}
    • PO₂: pO_2\in[80,100]\ \text{mmHg}
    • HCO₃⁻: [HCO_3^-]\in[22,28]\ \text{mEq/L}
  • Interpretive thresholds:
    • If pH < 7.35 → acidotic; if pH > 7.45 → alkalotic
    • CO₂ as an acid (respiratory): too much CO₂ → respiratory acidosis; too little CO₂ → respiratory alkalosis
    • Bicarb (HCO₃⁻) as a base (metabolic): too little base or too much acid → metabolic acidosis; too much base or loss of acid → metabolic alkalosis
  • Anion gap and its use (not always shown here but essential):
    • Normal range for anion gap: AG\in[8,16]\ \text{mEq/L}
    • Formula (lab-based, often with or without K⁺):
    • AG = [Na^+] - ([Cl^-] + [HCO_3^-])
    • Normal anion gap acidosis vs elevated anion gap acidosis helps distinguish loss of bicarbonate (normal AG) from generation of organic acids (elevated AG)
  • Conceptual relationships:
    • Metabolic processes: [HCO_3^-] and pH move in the same direction (both decrease in metabolic acidosis, both increase in metabolic alkalosis)
    • Respiratory processes: pH and CO₂ move in opposite directions (increased CO₂ lowers pH → acidosis; decreased CO₂ raises pH → alkalosis)
  • Visual mnemonic (ROAM):
    • Respiratory: the relationships are opposite between CO₂ and pH
    • Metabolic: the relationships are in the same direction between bicarbonate and pH
  • Quick ABG interpretation approach (boards-style thinking): starting from the pH, decide if acidotic or alkalotic, then predict what CO₂ or HCO₃⁻ would look like for a respiratory vs metabolic process, then verify with the numbers you’re given
  • Example scenario (DKA in ED):
    • In metabolic acidosis from DKA, expect low pH and low HCO₃⁻ with compensatory respiratory changes (low PaCO₂ from hyperventilation)
  • Practical ABG interpretation example (from the transcript):
    • Given pH = 7.3, normal CO₂ around 37, low HCO₃⁻ = 20 → metabolic acidosis (not a metabolic alkalosis or respiratory acidosis)

Acid-base problem-solving framework and example thought process

  • Stepwise thought process when evaluating ABG data:
    • 1) Look at the pH and categorize as normal, acidic, or alkalotic
    • 2) If acidic, decide whether this is respiratory (CO₂ should be high) or metabolic (HCO₃⁻ should be low); if alkalotic, decide the opposite
    • 3) Check the accompanying CO₂ and HCO₃⁻ values to confirm the source (respiratory vs metabolic)
    • 4) Consider compensation or mixed disorders if numbers don’t fit a single primary process
  • Board-vignette example from the lecture:
    • pH = 7.3 (acidic)
    • CO₂ = 37 (normal)
    • HCO₃⁻ = 20 (low)
    • Interpretation: metabolic acidosis (low bicarbonate with acidemia); CO₂ not elevated, so not primary respiratory acidosis; compensation would be respiratory (blowing off CO₂), but in this example CO₂ is normal, suggesting an inadequately compensated metabolic acidosis or a mixed picture

Anion gap and the mud-piles differential

  • Anion gap utility:
    • Helps classify metabolic acidosis into either normal anion gap (hyperchloremic) or elevated anion gap
  • Normal anion gap metabolic acidosis causes (loss of bicarbonate or failure to generate bicarbonate):
    • GI bicarbonate loss (diarrhea, pancreatic fistula), renal tubular acidosis, ureteral diversion
  • Elevated anion gap metabolic acidosis causes (generation of new acid):
    • Ketoacidosis (diabetic, alcoholic, starvation), lactic acidosis, toxin ingestions (ethylene glycol, methanol, salicylates), renal failure
  • Mud Piles mnemonic (for metabolic acidosis etiologies):
    • Methanol
    • Uremia
    • Diabetic ketoacidosis (DKA)
    • Propylene glycol / Paraldehyde (… depending on mnemonic variant)
    • Isoniazid or Iron (ingestions)
    • Lactic acidosis
    • Ethylene glycol
    • Salicylates
    • Starvation
  • Practical use:
    • If AG elevated (e.g., AG ≈ 18) → suggests generation of new acid (e.g., lactic acidosis, ketoacidosis)
    • If AG normal (e.g., AG ≈ 10) → bicarbonate loss (e.g., GI loss)

Interpreting ABGs and acid-base disorders in clinical context

  • Respiratory acidosis pathology:
    • Hypoventilation leading to CO₂ retention (high PaCO₂)
    • Examples: poor ventilation due to hotdog airway obstruction, severe COPD, morbid obesity, neuromuscular disease; asthmatics can have one or the other depending on the phase
  • Respiratory alkalosis pathology:
    • Hyperventilation with excessive CO₂ loss (low PaCO₂)
    • Examples: high-altitude sickness, pulmonary embolism, aspirin overdose, iatrogenic hyperventilation (bagging too fast, ventilator settings)
  • Metabolic acidosis pathology:
    • Low bicarbonate or increased non-volatile acids; often associated with DKA, lactic acidosis, renal failure, toxin ingestions
  • Metabolic alkalosis pathology:
    • Increased bicarbonate usually due to loss of acid (vomiting, gastric suctioning) or diuretic use; rare cases of bicarbonate administration

Sodium (Na⁺) disorders

  • Hyponatremia: Na⁺ < 135 mEq/L
    • Reflects excess water retention and volume status changes; causes include SIADH, CHF, cirrhosis, nephrotic syndrome, psychogenic polydipsia, small cell carcinoma, certain meds (SSRIs/SNRIs)
    • Clinical: headache, nausea/vomiting, lethargy, confusion, seizures, coma
    • Treatment goal: restrict water intake and correct sodium gradually; target around 125\le [Na^+]\le 130\ \text{mEq/L} to reduce risk of osmotic demyelination
  • Hypernatremia: Na⁺ > 145 mEq/L
    • Reflects water loss or decreased water intake; management depends on volume status
    • Hypovolemic: isotonic saline (normal saline)
    • Euvolemic: 5% dextrose IV or oral water intake
    • Hypervolemic: 5% dextrose IV with loop diuretics; may require dialysis in severe cases

Potassium (K⁺) disorders

  • Hypokalemia: K⁺ < 3.5 mEq/L
    • Causes: meds, GI losses (diarrhea, vomiting), adrenal disorders (hyperaldosteronism), renal losses
    • Presentation: muscle weakness, cramps, arrhythmias, ileus; metabolic alkalosis tendency
    • EKG: flattened/inverted T waves
    • Magnesium status matters: hypomagnesemia causes K⁺ resistance to therapy; ensure Mg²⁺ assessment and correction
    • Replacement: oral preferred if possible; IV if severe
  • Hyperkalemia: K⁺ > 5 mEq/L
    • Causes: ACE inhibitors/ARBs, potassium-sparing diuretics, CKD, adrenal insufficiency (Addison), insulin deficiency/diabetes with acidosis
    • Presentation: muscle weakness, possible paralysis, ileus, conduction abnormalities
    • EKG: peaked T waves (and other changes as it worsens)
    • Immediate treatment to move K⁺ into cells: 50 mEq dextrose with 10 units regular insulin, bicarbonate, and/or inhaled albuterol (short-term)
    • Additional measures: loop diuretics, non-dialysis removal if possible; many cases require dialysis in severe hyperkalemia

Magnesium (Mg²⁺) and calcium interplay

  • Hypomagnesemia: Mg²⁺ < 1.8 mg/dL
    • Causes: diuretic overuse, laxative abuse, diarrhea; chronic causes include pregnancy, bariatric surgery, alcohol use disorder, malnutrition
    • Presentation: tremors, nystagmus, weakness, lethargy, arrhythmias; may accompany hypocalcemia and hypokalemia
    • Treatment:
    • Chronic: oral magnesium oxide
    • Symptomatic or severe: IV magnesium sulfate
    • Associated electrolyte corrections (Ca²⁺, K⁺) as needed
  • Hypermagnesemia: Mg²⁺ > 2.5 mg/dL
    • Causes: CKD, ESRD, excessive magnesium intake
    • Presentation: decreased DTRs, confusion, hypotension, bradycardia, arrhythmias; can cause hypocalcemia
    • Treatment: discontinue exogenous magnesium; IV calcium chloride; dialysis if severe or unable to excrete magnesium
  • Calcium-magnesium interplay:
    • Hypermagnesemia can suppress parathyroid hormone (PTH) and lower serum calcium
    • Hypomagnesemia can impair PTH response to calcium and cause hypocalcemia due to decreased bone responsiveness
    • Note: Both high and low Mg²⁺ can result in hypocalcemia via different mechanisms

Kidney function tests and urinary findings (urine microscopy slide overview)

  • Use slide as a study aid for pattern recognition:
    • Nephrotic syndrome: prominent proteinuria
    • Glomerulonephritis: red cell casts and hematuria
    • Acute cystitis: mostly white cells
    • Pyelonephritis: white cell casts; pyuria; bacteriuria
    • Acute interstitial nephritis: white cell casts with eosinophils (eosinophiluria)
    • Acute tubular necrosis (ATN): granular casts (muddy brown casts); low urine specific gravity (less concentrated, e.g., SG < 1.01)
  • Imaging and follow-up concepts:
    • Distinct image patterns and casts help differentiate conditions; labs and clinical context are essential for vignette-based exams

Kidney stones (urolithiasis)

  • Types (most common and notable):
    • Calcium oxalate and calcium phosphate stones (most common)
    • Struvite stones associated with infection (more common in elderly)
    • Uric acid stones are radiolucent on plain x-ray
    • Cystine stones are genetic and relatively rare
  • Risk factors:
    • High sodium diet, high protein, high oxalate/purine diets
    • Dehydration and heat exposure
  • Presentation: colicky flank/back pain that moves with stone progression; pain may radiate to the groin; nausea/vomiting; gross or microscopic hematuria
  • Diagnosis: non-contrast spiral CT is the standard imaging test
  • Management:
    • Most stones ≤5–6 mm pass spontaneously
    • Stones >5–6 mm may require ureteral stent placement or lithotripsy
    • Diet modification and increased fluid intake to prevent recurrence

Pyelonephritis and renal infections

  • Pyelonephritis: ascending infection from lower urinary tract to kidney
    • Common organisms: Escherichia coli is the most frequent; others include Proteus, Klebsiella, Pseudomonas, Staphylococcus aureus, etc.
    • Clinical features: fever, rigors, nausea/vomiting, CVA tenderness, hematuria possible; dysuria and urinary frequency may be present
    • Lab findings: pyuria, bacteriuria, white cell casts; CBC with leukocytosis; blood cultures if septic
    • Imaging and evaluation:
    • Renal ultrasound or CT if obstruction suspected
    • Treatment approach:
    • Stable patients: outpatient management with oral antibiotics (e.g., fluoroquinolones such as ciprofloxacin or levofloxacin, or Bactrim if tolerable)
    • Unstable or resistance concerns: initial IV broad-spectrum antibiotics (e.g., ceftriaxone) followed by oral step-down when feasible
  • Horseshoe kidney:
    • Often incidental; increased risk of obstruction or infection when symptomatic
    • Monitoring with renal ultrasound, BP checks, and urinalyses; prophylactic antibiotics may be needed in severe cases

Renal tumors and pediatric renal cancers

  • Renal cell carcinoma (RCC):
    • Accounts for about 2\%\text{ to }3\% of all adult cancers
    • Male > female; smoking a major risk factor
    • Classic presentation: hematuria (≈60%), flank pain or abdominal mass (≈30%)
    • Imaging: CT abdomen/pelvis to evaluate extent and metastasis; about 20\%\text{ to }30\% present with metastatic disease at diagnosis
  • Wilms tumor (nephroblastoma):
    • Most common abdominal malignancy in children
    • ~5% of pediatric cancers; typically presents before age 5 (most before age 10)
    • Associated anomalies: horseshoe kidney, cryptorchidism, hypospadias, duplications of collecting system
    • Presentation: palpable abdominal mass, abdominal pain, hypertension, hematuria
    • Imaging: ultrasound first, then CT to evaluate for metastasis (lung)
    • Management: nephrectomy and chemotherapy; prognosis generally favorable in many cases

Acute kidney injury (AKI) and progression to chronic kidney disease (CKD)

  • Acute kidney injury (AKI): rapid loss of kidney function over hours to days
    • Often reversible but can be permanent
    • Characterized by a rapid rise in serum creatinine
    • Common etiologies: prerenal, intrinsic renal, postrenal
    • Diagnostic tool: fractional excretion of sodium (FENa) helps differentiate prerenal from intrinsic/postrenal causes
  • Fractional excretion of sodium (FENa):
    • Interpretation thresholds:
    • FENa < 1%: prerenal etiology (volume depletion, CHF, renal hypoperfusion, sepsis, contrast nephropathy)
    • 1% ≤ FENa < 4%: intrinsic renal injury (acute tubular necrosis, acute interstitial nephritis, glomerulonephritis)
    • FENa ≥ 4%: postrenal/obstructive process
  • Intrinsic renal injury (main causes):
    • Acute tubular necrosis (ATN): ~80–85% of intrinsic AKI
    • Common etiologies: shock/ischemia; infections; toxins (contrast dye, nephrotoxic meds like certain antibiotics, NSAIDs in excess, aminoglycosides, amphotericin)
    • Urine findings: muddy brown granular casts; urine is typically poorly concentrated (SG < 1.01)
    • Electrolytes: hyperkalemia, hyperphosphatemia
    • Acute interstitial nephritis (AIN): ~10–15%
    • Common drugs: NSAIDs, penicillins, sulfa drugs, cephalosporins, phenytoin, rifampin; allergic/inflammatory diseases (lupus, sarcoidosis)
    • Clinical: fever, rash, arthralgias; eosinophilia; eosinophiluria
    • Urine: pyuria with eosinophils, white cell casts
    • Management: remove offending agent; steroids if persistent; possible dialysis
    • Glomerulonephritis: ~5%
  • Other renal syndromes:
    • Acute post-streptococcal glomerulonephritis: common in children; occurs 1–3 weeks after strep pharyngitis or skin infection; presents with hypertension, edema, hematuria, and proteinuria; ASO titer may be used if strep infection not documented; renal ultrasound and sometimes biopsy; steroids may be considered in some cases
  • Rhabdomyolysis-associated AKI:
    • Mechanism: myoglobin release from muscle breakdown (often due to trauma, severe exertion, heat illness, statin use, drugs)
    • Classic signs: severe myalgias, weakness, tea/cola-colored urine; dipstick may show blood but microscopy shows few or no red cells (myoglobinuria)
    • Management: aggressive IV hydration; prognosis depends on extent of kidney injury
  • Nephrotoxic exposures and AKI risk factors:
    • IV radiographic contrast, NSAIDs, certain antibiotics, rhabdomyolysis, sepsis, dehydration

Acute kidney injury complications and treatment in detail

  • Acute interstitial nephritis and glomerulonephritis management nuances:
    • AIN often requires removing the offending agent and may need steroids; dialysis in severe cases
    • Glomerulonephritis management depends on etiology and severity; steroids or immunosuppressants may be used in some cases
  • Nephrotic vs nephritic presentations (brief recap):
    • Nephrotic: heavy proteinuria, hypoalbuminemia, edema, hyperlipidemia; risk of thrombosis; diuretic and ACE inhibitor strategies
    • Nephritic: hematuria with red blood cell casts, varying degrees of proteinuria, hypertension, and edema
  • Multiple myeloma and CRAB criteria (protein deposition diseases):
    • CRAB: Calcium elevation, Renal insufficiency, Anemia, Bone lesions
    • Presence of Bence Jones proteins (light chains) in urine; management by oncology with dialysis if renal failure; diagnostic biopsy may be required

Chronic kidney disease (CKD) and related conditions

  • CKD definition and diagnostic criteria:
    • Kidney disease lasting >3 months with either a
    • decreased GFR < 60 mL/min, or
    • markers of kidney damage such as albuminuria (>30 mg/day)
    • Albuminuria can precede a drop in GFR (early marker)
  • Common CKD etiologies:
    • Diabetes mellitus, hypertension, vascular diseases, nephrotoxic medications, glomerulonephritis, prior AKI, trauma
  • End-stage kidney disease (ESKD) manifestations:
    • Fatigue, malaise, sleep disturbances, headaches, anorexia, metallic taste, hiccups, nausea, pruritus
    • Cachexia, weight loss, altered mental status, foamy urine, pericardial rub
  • CKD management goals and strategies:
    • Blood pressure control and glycemic control (A1c targets in diabetics)
    • LDL cholesterol target: < 100 mg/dL
    • Smoking cessation and weight management
    • Avoid nephrotoxic agents (e.g., NSAIDs)
    • Use ACE inhibitors or ARBs in patients with diabetes and/or proteinuria to slow progression
    • Conservative care while awaiting transplant; palliative care and advance care planning if transplant not an option
  • Renal artery stenosis (RAS) as a CKD cause:
    • Common in patients with resistant hypertension; consider RAS in patients with poorly controlled BP
    • Diagnostic approach: Doppler ultrasound to assess renal resistance index
    • Treatment: address underlying cause; angioplasty with or without stenting as needed
  • Polycystic kidney disease (PKD):
    • Prevalence: about 1 in 1000 people
    • Inheritance: autosomal dominant
    • Increases risk of hypertension, hematuria, proteinuria, and progressive kidney failure; cysts may also appear in liver, spleen, and pancreas
    • Associated features: mitral valve prolapse, kidney stones, UTIs, berry aneurysms in Circle of Willis
    • Management: aggressive BP control slows progression; eventual transplant or dialysis; imaging with ultrasound and MRI/CT as needed

Pediatric renal tumors and special conditions

  • Wilms tumor (nephroblastoma): discussed above under tumors; emphasis on pediatric presentation and prognosis

Self-care and clinician wellness reminder

  • The lecturer emphasizes self-care as essential for sustaining study and clinical work:
    • Regular breaks, social connection, hobbies, and rest
    • Small daily routines (e.g., quiet mornings) help prevent burnout
    • Balancing study with activities like reading, walking, travel, and time with friends
    • Acknowledge that long-term well-being supports better patient care

Quick reference and closing notes

  • Remember key normal values and thresholds:
    • pH{normal}=7.35\text{ to }7.45\,,\ pqCO2=35\text{ to }45\,mmHg\,,\,[HCO_3^-]=22\text{ to }28\,\text{mEq/L}
    • AG:\in[8,16]\,\text{mEq/L}
    • Na⁺: hyponatremia < 135 mEq/L; hypernatremia > 145 mEq/L; target 125–130 mEq/L for correction
    • K⁺:
    • Mg²⁺:
    • CKD criteria: GFR < 60 mL/min/1.73m² or albuminuria > 30 mg/day
  • The educational ethos throughout emphasizes pattern recognition, careful analysis of ABG, and integration of clinical context, labs, and imaging for proper diagnosis and management
  • Always tailor treatment to patient context: stability, comorbidities, and organ function, and involve nephrology early in AKI/CKD cases