Acid-Base Balance, Electrolytes, and Renal Pathophysiology Review

A comprehensive set of flashcards covering acid-base disorders, electrolytes, urine findings, and renal diseases as presented in the lecture notes.

What is the normal pH range used in this lecture, and how are values outside it categorized?

Normal pH is 7.35–7.45; pH < 7.35 is acidic and pH > 7.45 is alkalotic.

What is the normal PaCO2 range and how do deviations relate to acid-base status?

Normal PaCO2 is 35–45 mmHg; PaCO2 < 35 is alkalotic (respiratory alkalosis tendency) and PaCO2 > 45 is acidotic (respiratory acidosis tendency).

How should bicarbonate (HCO3-) be interpreted in acid-base disorders, and what do low vs high HCO3- indicate?

HCO3- acts as a base; low HCO3- indicates metabolic acidosis; high HCO3- indicates metabolic alkalosis.

What mnemonic describes the relationship between CO2 and pH in respiratory vs metabolic disorders?

ROAM: Respiratory (CO2) opposite to pH, Metabolic (HCO3-) equal to pH.

What is the normal anion gap and how is it used in metabolic acidosis?

Anion gap normal range is 8–16 mEq/L. Elevated AG suggests generation of new acid (e.g., ketoacidosis, lactic acidosis); normal AG suggests bicarbonate loss.

What does Mud PILES stand for in metabolic acidosis evaluation?

Methanol, Uremia, Diabetic ketoacidosis, Paraldehyde, Isoniazid, Lactic acidosis, Ethylene glycol, Salicylates, Starvation.

What is the typical normal range for the anion gap, and what indicates an abnormal gap?

Normal 8–16 mEq/L; >16 indicates elevated anion gap; <8 is not typically useful.

If pH is 7.30 and PaCO2 is 37 mmHg with HCO3- of 20 mEq/L, what is the acid-base disorder?

Metabolic acidosis (low pH and low HCO3- with near-normal PaCO2).

What ABG pattern indicates metabolic acidosis?

Low pH with low HCO3- (PaCO2 may be normal or show partial compensation).

What ABG pattern indicates metabolic alkalosis?

High pH with high HCO3- (PaCO2 may be elevated if there is respiratory compensation).

What ABG pattern indicates respiratory acidosis?

Low pH with high PaCO2.

What ABG pattern indicates respiratory alkalosis?

High pH with low PaCO2.

What is hyponatremia, and what are common presenting symptoms?

Na < 135 mEq/L; symptoms include headache, nausea/vomiting, lethargy, disorientation, seizures, and possible coma.

What is the target sodium range to avoid osmotic demyelination when treating hyponatremia?

Goal is to correct toward 125–130 mEq/L slowly to prevent osmotic demyelination.

What causes hypernatremia and how can it present clinically?

Na > 145 mEq/L; causes include dehydration and water loss (central or nephrogenic DI); symptoms include thirst and weakness.

How should hypernatremia be managed based on volume status?

Hypovolemic: isotonic saline; Euvolemic: free water or 5% dextrose; Hypervolemic: 5% dextose IV with loop diuretics; dialysis if needed.

What defines hypokalemia and what are common presentations?

K+ < 3.5 mEq/L; causes include diuretics, GI losses, adrenal disorders; symptoms include muscle weakness, cramps, arrhythmias; EKG shows flattened/inverted T waves.

What conditions can cause potassium to be resistant to therapy, and what is a key related electrolyte interaction?

Hypomagnesemia can cause potassium to be resistant to replacement; Mg must be corrected as needed.

What defines hyperkalemia and what are common causes and ECG findings?

K+ > 5 mEq/L; causes include CKD, Addison disease, ACE inhibitors/ARBs, potassium-sparing diuretics, beta blockers; EKG may show peaked T waves.

What is the treatment approach for hyperkalemia?

Temporary measures: insulin with glucose, bicarbonate, and albuterol; then loop diuretics; consider dialysis for severe cases.

What is hypomagnesemia and its common causes and symptoms?

Mg < 1.8 mg/dL; due to diuretics, laxatives, diarrhea; symptoms include tremors, nystagmus, arrhythmias; treat with oral Mg for chronic and IV MgSO4 for symptomatic.

What is hypermagnesemia and its typical consequences and management?

Mg > 2.5 mg/dL; due to CKD or excess magnesium intake; causes decreased DTRs, hypotension, bradycardia; management includes stopping Mg, calcium chloride IV, possible dialysis.

What is the hallmark urine finding in acute tubular necrosis (ATN)?

Muddy brown granular casts in urine.

What FE Na values distinguish prerenal, intrinsic, and postrenal AKI?

FE Na < 1% = prerenal; 1–

What is the most common intrinsic AKI cause and its typical presentation?

Acute tubular necrosis (ATN) >80–85% of intrinsic AKI; often due to ischemia/shock or nephrotoxins; muddy brown casts and low urine osmolality.

What are common features of renal cell carcinoma and its risk factors?

Hematuria is common; flank pain, abdominal mass; smoking is a major risk factor; imaging shows a solid renal mass; 2–3% of cancers.

What is Wilms tumor and its typical demographic and presentation?

Nephroblastoma; most common abdominal malignancy in children under 5; presents as an abdominal mass, may have hypertension and pain; ultrasound then CT; good prognosis with chemo.

How is chronic kidney disease defined and diagnosed?

CKD defined as GFR

What are key management strategies to slow CKD progression?

Blood pressure control (ACE inhibitors/ARBs if proteinuric), A1c control, LDL <100, stop smoking, weight management, avoid nephrotoxins; dialysis or transplant when needed.

What is renal artery stenosis and how is it diagnosed and treated?

Resistant hypertension with possible bruit; diagnosed by Doppler ultrasound showing resistance index; treated by addressing underlying cause, possibly angioplasty with/without stenting.

What is polycystic kidney disease (PKD) and its typical associations and management?

Inherited disease with cyst formation; HTN, hematuria, proteinuria; liver cysts; associated with MVP; managed with BP control; may require dialysis or transplant.

What is the ultimate goal of CKD management if transplant is not an option?

Conservative care, symptom management, advanced care planning, and palliative care.