Physician Assistant National Certifying Examination (PANCE) Endocrine, Renal, and Genitourinary Systems Syllabus

What screening tests are used for Cushing's syndrome?

Late-night salivary cortisol, 24-hour urinary free cortisol, and the 1 mg overnight low-dose dexamethasone suppression test. A high ACTH-dependent source (pituitary adenoma) is the most common cause (Cushing disease).

Describe the lab pattern and confirmatory test for primary hyperaldosteronism (Conn syndrome).

Hypertension with hypokalemia and metabolic alkalosis; elevated aldosterone with suppressed renin (high aldosterone-to-renin ratio). Confirm with saline suppression/oral salt loading showing non-suppressible aldosterone.

What is the classic triad of pheochromocytoma and the diagnostic test?

Episodic Headache, Palpitations, and diaphoresis (Sweating) with paroxysmal hypertension. Diagnose with plasma free or 24-hour urinary fractionated metanephrines. Treat with alpha-blockade (phenoxybenzamine) before beta-blockade.

How do you interpret the cosyntropin (ACTH) stimulation test for adrenal insufficiency?

Give synthetic ACTH; an inadequate cortisol rise confirms adrenal insufficiency. Pair with baseline ACTH: high ACTH = primary (adrenal); low/normal ACTH = secondary (pituitary/hypothalamic).

What is the cause and presentation of central diabetes insipidus, and how is it confirmed?

Deficient ADH (vasopressin) secretion $\to$ polyuria with dilute urine and hypernatremia. Water deprivation test fails to concentrate urine, but urine osmolality rises after desmopressin (DDAVP)—distinguishing it from nephrogenic DI (no response).

Differentiate SIADH from diabetes insipidus by sodium and urine findings.

SIADH: excess ADH $\to$ euvolemic hyponatremia, concentrated urine (high urine osmolality and urine $\ce{Na+}$), low serum osmolality. DI: ADH deficiency/resistance $\to$ hypernatremia with inappropriately dilute (low osmolality) urine and polyuria.

What hormone excess characterizes acromegaly, and what is the best screening test?

Growth hormone excess (usually a pituitary somatotroph adenoma) acting via IGF-1. Screen with serum IGF-1; confirm with failure of GH suppression during an oral glucose tolerance test. Features: enlarged hands/jaw, frontal bossing.

What are the symptoms and treatment of a prolactinoma?

Hyperprolactinemia $\to$ galactorrhea, amenorrhea/infertility, decreased libido, and (if large) bitemporal hemianopsia. First-line treatment is a dopamine agonist (cabergoline or bromocriptine), not surgery, for most.

Compare primary, secondary, and tertiary hyperparathyroidism.

Primary: autonomous PTH (usually adenoma) $\to$ high Ca, low phosphate. Secondary: low Ca (e.g., CKD/vitamin D deficiency) $\to$ high PTH, low/normal Ca. Tertiary: autonomous PTH after prolonged secondary stimulation $\to$ high PTH and high Ca.

What is the most common cause of primary hyperparathyroidism and its classic symptom mnemonic?

A single parathyroid adenoma. Hypercalcemia presents as 'stones, bones, abdominal groans, and psychiatric overtones'—nephrolithiasis, bone pain/osteoporosis, constipation/pancreatitis, and depression/confusion.

What lab pattern and symptoms characterize hypoparathyroidism?

Low PTH $\to$ hypocalcemia and hyperphosphatemia. Neuromuscular irritability: perioral tingling, tetany, Chvostek sign (facial twitch) and Trousseau sign (carpal spasm with BP cuff), prolonged $QT$ interval. Often post-thyroidectomy.

How is the corrected calcium calculated for a hypoalbuminemic patient?

$$\text{Corrected Ca} = \text{measured Ca} + 0.8 \times (4.0 - \text{albumin})$$ where albumin is in g/dL. Each 1 g/dL drop in albumin lowers total calcium by $\approx 0.8$ mg/dL without changing ionized (active) calcium.

Describe the hormonal regulation of calcium by PTH and vitamin D.

PTH raises serum Ca by stimulating bone resorption, renal Ca reabsorption, renal phosphate excretion, and activation of vitamin D (1-$\alpha$-hydroxylase). Active vitamin D (calcitriol) increases intestinal Ca and phosphate absorption. Calcitonin lowers Ca.

What are the Rotterdam criteria for diagnosing PCOS?

At least 2 of 3: (1) oligo-/anovulation, (2) clinical or biochemical hyperandrogenism (hirsutism, acne, elevated testosterone), (3) polycystic ovaries on ultrasound. Diagnosis of exclusion; associated with insulin resistance and elevated LH:FSH ratio.

What are first-line treatments for PCOS based on the patient's goal?

Not seeking pregnancy: combined oral contraceptives (regulate cycles, reduce androgens) plus lifestyle/metformin for insulin resistance. Seeking pregnancy: letrozole (preferred over clomiphene) for ovulation induction.

How is acute kidney injury staged/defined by the KDIGO creatinine and urine criteria?

AKI: rise in serum creatinine $\geq 0.3$ mg/dL within 48 h, or $\geq 1.5\times$ baseline within 7 days, or urine output $< 0.5$ mL/kg/h for $\geq 6$ h. Stages 1–3 by magnitude of creatinine rise and oliguria duration.

Use the FeNa to differentiate prerenal from intrinsic (ATN) acute kidney injury.

$$FeNa = \frac{U_{Na} \times P_{Cr}}{P_{Na} \times U_{Cr}} \times 100\%$$ Prerenal: $FeNa < 1\%$ (and BUN:Cr $> 20:1$), urine concentrated. ATN/intrinsic: $FeNa > 2\%$, with muddy brown granular casts and isosthenuria.

List the three categories of AKI etiology with an example of each.

Prerenal (hypoperfusion: hypovolemia, heart failure, NSAIDs). Intrinsic/renal (ATN from ischemia or nephrotoxins, AIN, glomerulonephritis). Postrenal (obstruction: BPH, stones, tumor causing bilateral hydronephrosis).

What defines chronic kidney disease and how is it staged?

CKD: kidney damage or eGFR $< 60$ mL/min/1.73 m$^{2}$ for $\geq 3$ months. Staged G1 ($\geq 90$) to G5 ($< 15$, kidney failure) by eGFR, plus albuminuria categories A1–A3. Leading causes: diabetes and hypertension.

What metabolic and hematologic complications accompany advanced CKD?

Anemia (decreased erythropoietin), renal osteodystrophy (low vitamin D, hyperphosphatemia, secondary hyperparathyroidism), hyperkalemia, metabolic acidosis, fluid overload/hypertension, and uremia. Treat with phosphate binders, ESAs, and vitamin D analogs.

Contrast nephritic and nephrotic syndromes.

Nephritic: hematuria with RBC casts, hypertension, mild–moderate proteinuria, oliguria (inflammatory, e.g., post-streptococcal GN, IgA nephropathy). Nephrotic: proteinuria $> 3.5$ g/day, hypoalbuminemia, edema, hyperlipidemia (e.g., minimal change, FSGS, membranous).

What is the classic presentation of post-streptococcal glomerulonephritis?

A child 1–3 weeks after group A strep pharyngitis or impetigo develops cola-colored (hematuria) urine, edema, and hypertension. Labs: low complement ($\downarrow C3$), elevated ASO/anti-DNase B titers. Usually self-limited.

Which glomerular disease is most common worldwide and its hallmark?

IgA nephropathy (Berger disease)—episodic gross hematuria occurring concurrently with or within days of an upper respiratory infection (synpharyngitic). Mesangial IgA deposits on biopsy; normal complement levels.

What is the most common cause of nephrotic syndrome in children and its treatment?

Minimal change disease—effacement of podocyte foot processes on electron microscopy with normal light microscopy. Highly responsive to corticosteroids; often follows infection or immunization.

Distinguish acute tubular necrosis from acute interstitial nephritis.

ATN: tubular injury from ischemia or nephrotoxins (aminoglycosides, contrast) $\to$ muddy brown granular casts. AIN: allergic/immune reaction (NSAIDs, beta-lactams, PPIs) $\to$ fever, rash, eosinophilia, and white cell casts/eosinophiluria.

How do you calculate and interpret the serum anion gap?

$$AG = \ce{Na+} - (\ce{Cl-} + \ce{HCO3-})$$ Normal $\approx 8$–$12$ mEq/L. High-gap acidosis causes (MUDPILES): Methanol, Uremia, DKA, Propylene glycol, Isoniazid, Lactic acidosis, Ethylene glycol, Salicylates.

Use Winter's formula to assess respiratory compensation in metabolic acidosis.

$$P_{CO_2} = 1.5 \times [\ce{HCO3-}] + 8 \pm 2$$ If the measured $P_{CO_2}$ is higher than predicted, there is a concomitant respiratory acidosis; if lower, a concomitant respiratory alkalosis.

How is hyponatremia classified and a key cause of each volume status given?

By volume status: Hypovolemic (GI/renal losses, diuretics), Euvolemic (SIADH, hypothyroidism, adrenal insufficiency), and Hypervolemic (CHF, cirrhosis, nephrotic syndrome). Correct slowly ($< 8$ mEq/L per 24 h) to avoid osmotic demyelination.

What ECG changes and emergency treatment characterize severe hyperkalemia?

ECG: peaked T waves $\to$ widened QRS, loss of P waves, sine wave. Emergency: IV calcium gluconate (stabilizes myocardium), then insulin + dextrose and albuterol (shift K intracellularly), followed by removal (loop diuretics, dialysis, GI binders).

What organism and findings define uncomplicated cystitis versus pyelonephritis?

Most common organism: $E.\ coli$. Cystitis: dysuria, frequency, urgency, suprapubic pain (no fever). Pyelonephritis: fever, flank pain/CVA tenderness, nausea, plus white cell casts in urine. First-line cystitis therapy: nitrofurantoin or TMP-SMX.

What is the composition and characteristic feature of the most common kidney stone, and how are stones prevented?

Calcium oxalate stones are most common—radiopaque, envelope-shaped crystals. Prevention: increase fluid intake, reduce sodium, normal dietary calcium, and thiazide diuretics (decrease urinary calcium). Struvite stones form staghorn calculi with urease-producing organisms (Proteus).