Flashcards Internal Medicine EOR: Renal / Genitourinary (2026) (Smarty PANCE) | Quizlet

What are Acid-Base Disorders?

A group of conditions characterized by abnormal blood pH resulting from primary disturbances in respiratory (PCO2) or metabolic (HCO3-) parameters, classified as acidosis or alkalosis.

What is the normal range for arterial pH, PaCO2, and HCO3-?

pH 7.35-7.45, PaCO2 35-45 mmHg, HCO3- 22-26 mEq/L.

How do you calculate the anion gap and what is normal?

Anion gap = Na - (Cl + HCO3); normal is 8-12 mEq/L.

What are the causes of high anion gap metabolic acidosis (mnemonic MUDPILES)?

Methanol, Uremia, DKA, Propylene glycol, Iron/INH, Lactic acidosis, Ethylene glycol, Salicylates.

What are common causes of normal anion gap (hyperchloremic) metabolic acidosis?

Diarrhea, renal tubular acidosis, carbonic anhydrase inhibitors, and excessive normal saline administration.

What is Winter's formula and what does it assess?

Expected PaCO2 = (1.5 x HCO3) + 8 +/- 2; assesses appropriate respiratory compensation for metabolic acidosis.

How do you determine respiratory vs metabolic primary disorder?

If pH and PaCO2 move in opposite directions, the disorder is respiratory; if they move in the same direction, it is metabolic.

What is Hyperkalemia?

An elevated serum potassium level greater than 5.0-5.5 mEq/L that can cause life-threatening cardiac arrhythmias.

What are the classic ECG changes of hyperkalemia in order of progression?

Peaked T waves, then widened QRS and prolonged PR, then loss of P waves, then sine wave pattern and ventricular fibrillation/asystole.

What is the first-line treatment to stabilize the cardiac membrane in hyperkalemia?

IV calcium gluconate (or calcium chloride); it does not lower potassium but protects the myocardium.

What treatments temporarily shift potassium intracellularly?

Insulin with glucose, beta-2 agonists (albuterol), and sodium bicarbonate (if acidotic).

What treatments actually remove potassium from the body?

Loop diuretics, potassium binders (patiromer, sodium zirconium cyclosilicate), and hemodialysis.

What are common causes of hyperkalemia?

Renal failure, ACE inhibitors/ARBs, potassium-sparing diuretics, tissue breakdown (rhabdomyolysis, hemolysis), Addison disease, and acidosis.

What is pseudohyperkalemia?

A falsely elevated potassium caused by hemolysis during venipuncture, prolonged tourniquet use, or marked thrombocytosis/leukocytosis.

What is Hypokalemia?

A low serum potassium level less than 3.5 mEq/L that can cause muscle weakness, arrhythmias, and ECG changes.

What are the characteristic ECG findings of hypokalemia?

Flattened T waves, ST depression, and prominent U waves; severe cases risk torsades de pointes.

What are common causes of hypokalemia?

GI losses (vomiting, diarrhea), diuretics, hyperaldosteronism, hypomagnesemia, and intracellular shift (insulin, beta-agonists, alkalosis).

Why must magnesium be corrected in refractory hypokalemia?

Hypomagnesemia promotes renal potassium wasting, making hypokalemia resistant to replacement until magnesium is repleted.

What are the clinical features of hypokalemia?

Muscle weakness, cramps, fatigue, ileus/constipation, and in severe cases paralysis and cardiac arrhythmias.

What is the general approach to potassium replacement in hypokalemia?

Oral potassium for mild-moderate cases; IV potassium (no faster than 10-20 mEq/hr) for severe or symptomatic cases, with cardiac monitoring.

What is Hypernatremia?

An elevated serum sodium greater than 145 mEq/L, reflecting a water deficit relative to sodium and causing hypertonicity.

What is the predominant symptom category of hypernatremia?

Neurologic symptoms from cellular dehydration: lethargy, irritability, weakness, seizures, and coma.

What are common causes of hypernatremia?

Inadequate water intake, diabetes insipidus, osmotic diuresis, GI water losses, and excessive sodium intake.

Why must hypernatremia be corrected slowly?

Rapid correction can cause cerebral edema; sodium should be lowered no more than about 10-12 mEq/L per 24 hours.

How do you differentiate central from nephrogenic diabetes insipidus?

Administer desmopressin (DDAVP): central DI responds with increased urine osmolality, nephrogenic DI does not respond.

What fluid is used to correct hypernatremia in a hypovolemic patient?

Isotonic saline first to restore volume, then hypotonic fluids (D5W or 0.45% saline) to correct the free water deficit.

What is Hyponatremia?

A serum sodium less than 135 mEq/L, the most common electrolyte disorder, classified by volume status and serum osmolality.

What is the first step in evaluating hyponatremia?

Measure serum osmolality to classify as hypotonic, isotonic, or hypertonic hyponatremia.

What are causes of hypovolemic hypotonic hyponatremia?

GI losses, diuretics (especially thiazides), and third spacing, with renal or extrarenal sodium loss.

What characterizes SIADH?

Euvolemic hyponatremia with low serum osmolality, inappropriately concentrated urine (urine osm >100), elevated urine sodium, and normal thyroid/adrenal function.

What is the danger of correcting hyponatremia too quickly?

Osmotic demyelination syndrome (central pontine myelinolysis); limit correction to about 6-8 mEq/L per 24 hours.

What is the treatment for severe symptomatic hyponatremia with seizures?

Hypertonic (3%) saline to raise sodium acutely and control symptoms.

What is Hypercalcemia?

An elevated serum calcium level that produces neurologic, GI, renal, and cardiac manifestations, often summarized as "stones, bones, groans, and psychiatric overtones."

What are the two most common causes of hypercalcemia?

Primary hyperparathyroidism (outpatient) and malignancy (inpatient/hospitalized).

What are the clinical manifestations of hypercalcemia?

Kidney stones, bone pain, abdominal pain/constipation, polyuria, fatigue, confusion, and depression.

What ECG change is associated with hypercalcemia?

Shortened QT interval.

What is the initial treatment of severe hypercalcemia?

Aggressive IV isotonic saline hydration, followed by calcitonin and bisphosphonates (e.g., zoledronic acid) for sustained lowering.

How does PTH level help differentiate causes of hypercalcemia?

Elevated or high-normal PTH suggests primary hyperparathyroidism; suppressed PTH suggests malignancy or vitamin D excess.

What is Hypocalcemia?

A low serum calcium level causing neuromuscular irritability, tetany, and characteristic physical exam and ECG findings.

What are the classic physical exam signs of hypocalcemia?

Chvostek sign (facial twitch on tapping facial nerve) and Trousseau sign (carpal spasm with BP cuff inflation).

What ECG change is associated with hypocalcemia?

Prolonged QT interval, which can predispose to arrhythmias.

What are common causes of hypocalcemia?

Hypoparathyroidism (often post-thyroidectomy), vitamin D deficiency, chronic kidney disease, hypomagnesemia, and pancreatitis.

What is the treatment for symptomatic hypocalcemia?

IV calcium gluconate for acute symptoms; oral calcium and vitamin D for chronic management.

Why must you check magnesium in hypocalcemia?

Hypomagnesemia impairs PTH secretion and action, causing hypocalcemia refractory to calcium replacement until magnesium is corrected.

What are Magnesium / Phosphate Disorders?

Electrolyte abnormalities involving magnesium or phosphate that disrupt neuromuscular, cardiac, and metabolic function and often coexist with other electrolyte derangements.

What are the clinical features of hypomagnesemia?

Neuromuscular irritability (tremor, tetany), arrhythmias including torsades de pointes, and refractory hypokalemia/hypocalcemia.

What are common causes of hypomagnesemia?

Alcohol use disorder, diarrhea, diuretics, proton pump inhibitors, and poor intake/malnutrition.

What causes hypermagnesemia and how does it present?

Most often renal failure (often with magnesium-containing antacids/laxatives); presents with decreased reflexes, hypotension, respiratory depression, and cardiac arrest in severe cases.

What are causes and features of hypophosphatemia?

Refeeding syndrome, alcohol use disorder, and DKA treatment; presents with muscle weakness, rhabdomyolysis, and respiratory failure when severe.

What causes hyperphosphatemia?

Chronic kidney disease (most common), tumor lysis syndrome, and rhabdomyolysis; can precipitate with calcium causing hypocalcemia.

What is Cystitis (Urinary Tract Infection, UTI)?

An infection of the bladder, most commonly bacterial, presenting with lower urinary tract symptoms.

What is the most common causative organism of uncomplicated cystitis?

Escherichia coli (responsible for roughly 80% of cases).

What are the classic symptoms of cystitis?

Dysuria, urinary frequency, urgency, and suprapubic discomfort, typically without fever or flank pain.

What urinalysis findings support a diagnosis of cystitis?

Positive leukocyte esterase, positive nitrites, pyuria, and possibly hematuria; culture confirms the organism.

What is first-line treatment for uncomplicated cystitis?

Nitrofurantoin, trimethoprim-sulfamethoxazole, or fosfomycin, depending on local resistance patterns.

What defines a complicated UTI?

A UTI in the setting of structural/functional abnormality, pregnancy, indwelling catheter, immunocompromise, or in males.

How is asymptomatic bacteriuria managed, and what are the exceptions?

Generally not treated, except in pregnant patients and those undergoing urologic procedures.

What is Prostatitis?

Inflammation or infection of the prostate gland, which may be acute bacterial, chronic bacterial, chronic pelvic pain syndrome, or asymptomatic inflammatory.

What are the symptoms of acute bacterial prostatitis?

Fever, chills, dysuria, pelvic/perineal pain, and an exquisitely tender, boggy, warm prostate on exam.

Why should vigorous prostate massage be avoided in acute bacterial prostatitis?

It can precipitate bacteremia and sepsis.

What are the most common causative organisms of bacterial prostatitis?

Gram-negative organisms, especially E. coli, and in younger sexually active men consider N. gonorrhoeae and C. trachomatis.

What is the treatment for acute bacterial prostatitis?

Fluoroquinolones or trimethoprim-sulfamethoxazole for an extended course (often 4-6 weeks).

How does chronic bacterial prostatitis present?

Recurrent UTIs with the same organism, pelvic discomfort, and variable urinary symptoms, often with few systemic signs.

What is Pyelonephritis?

An infection of the renal parenchyma and collecting system, typically ascending from the lower urinary tract.

What is the classic clinical triad of acute pyelonephritis?

Fever, flank pain (costovertebral angle tenderness), and nausea/vomiting, often with lower urinary tract symptoms.

What is the most common causative organism of pyelonephritis?

Escherichia coli.

What urinalysis finding is suggestive of pyelonephritis rather than cystitis?

White blood cell casts indicate renal parenchymal involvement.

When is hospitalization indicated for pyelonephritis?

Sepsis, inability to tolerate oral intake, pregnancy, hemodynamic instability, or failure of outpatient therapy.

What imaging is indicated when pyelonephritis does not improve with treatment?

CT of the abdomen/pelvis to evaluate for abscess, obstruction, or emphysematous pyelonephritis.

What is Renal Cell Carcinoma?

The most common primary malignant tumor of the kidney, arising from the renal tubular epithelium.

What is the classic triad of renal cell carcinoma and how often is it present?

Flank pain, hematuria, and a palpable abdominal mass; the full triad is present in only about 10% of cases.

What are major risk factors for renal cell carcinoma?

Smoking, obesity, hypertension, acquired cystic kidney disease from dialysis, and von Hippel-Lindau disease.

What paraneoplastic syndromes are associated with renal cell carcinoma?

Polycythemia (erythropoietin), hypercalcemia (PTHrP), and hypertension (renin).

What is the imaging study of choice for renal cell carcinoma?

CT scan of the abdomen with and without contrast.

What is the primary treatment for localized renal cell carcinoma?

Surgical resection (partial or radical nephrectomy), as it is generally resistant to conventional chemotherapy and radiation.

What is Bladder Cancer?

A malignancy of the bladder, most commonly urothelial (transitional cell) carcinoma, classically presenting with painless hematuria.

What is the most common presenting symptom of bladder cancer?

Painless gross hematuria.

What are the major risk factors for bladder cancer?

Cigarette smoking (most important), occupational exposure to aromatic amines, and cyclophosphamide; Schistosoma haematobium is linked to squamous cell type.

What is the diagnostic study of choice for bladder cancer?

Cystoscopy with biopsy; urine cytology can be supportive.

What is the most common histologic type of bladder cancer in the United States?

Urothelial (transitional cell) carcinoma.

How is non-muscle-invasive bladder cancer commonly treated?

Transurethral resection of the bladder tumor (TURBT), often followed by intravesical therapy such as BCG.

What is Prostate Cancer?

A malignancy of the prostate gland, most commonly adenocarcinoma, and the most common non-cutaneous cancer in men.

Where does prostate cancer most commonly arise within the gland?

The peripheral zone of the prostate.

How does prostate cancer typically present?

Often asymptomatic and detected by elevated PSA or abnormal digital rectal exam; advanced disease may cause bone pain from metastases.

What digital rectal exam finding suggests prostate cancer?

A hard, irregular, or nodular prostate.

How is the diagnosis of prostate cancer confirmed?

Transrectal ultrasound-guided prostate biopsy, with grading by the Gleason score.

Where does prostate cancer characteristically metastasize?

Bone, classically producing osteoblastic (sclerotic) lesions.

What is Benign Prostatic Hyperplasia (BPH)?

A non-malignant enlargement of the prostate gland that commonly causes lower urinary tract symptoms in older men.

In which zone of the prostate does BPH typically occur?

The transition (periurethral) zone.

What are the typical symptoms of BPH?

Obstructive and irritative voiding symptoms: hesitancy, weak stream, incomplete emptying, nocturia, frequency, and urgency.

What are the first-line medications for BPH and how do they work?

Alpha-blockers (e.g., tamsulosin) relax smooth muscle for rapid symptom relief; 5-alpha-reductase inhibitors (e.g., finasteride) shrink the prostate over months.

What medications can acutely worsen BPH symptoms or precipitate urinary retention?

Anticholinergics and sympathomimetics (e.g., decongestants).

What is the definitive surgical treatment for refractory BPH?

Transurethral resection of the prostate (TURP).

What is Urolithiasis / Nephrolithiasis?

The formation of stones within the urinary tract, causing pain, hematuria, and potential obstruction.

What is the most common type of kidney stone?

Calcium oxalate stones.

What is the classic presentation of nephrolithiasis?

Sudden severe colicky flank pain radiating to the groin, with hematuria, nausea, and an inability to find a comfortable position.

What is the imaging study of choice for diagnosing kidney stones?

Non-contrast helical CT of the abdomen and pelvis.

What size stones are likely to pass spontaneously?

Stones less than 5 mm typically pass spontaneously; those larger than 10 mm often require intervention.

Which stone type is radiolucent on plain film and associated with acidic urine?

Uric acid stones.

Which stone type is associated with urease-producing organisms (Proteus) and staghorn calculi?

Struvite (magnesium ammonium phosphate) stones.