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

Endocrine, Renal, and Genitourinary Systems syllabus — full chapter and topic list

Expand any chapter to see its topics and sub-topics. This is the whole examinable outline for Endocrine, Renal, and Genitourinary Systems in Physician Assistant National Certifying Examination (PANCE), not a summary of it.

1. 1

   Diabetes and Glucose Disorders

   4 topics

   • Type 1 and type 2 diabetes mellitus
     • Diagnostic criteria and A1c targets
     • Pharmacologic management and insulin
   • Diabetic ketoacidosis and hyperosmolar hyperglycemic state
   • Hypoglycemia
   • Diabetic complications
2. 2

   Thyroid, Adrenal, and Pituitary Disorders

   4 topics

   • Hypothyroidism and hyperthyroidism
     • Thyroid storm and myxedema coma
   • Thyroid nodules and cancer
   • Adrenal disorders
     • Cushing syndrome and Addison disease
   • Pituitary disorders and diabetes insipidus
3. 3

   Calcium, Bone, and Reproductive Endocrinology

   3 topics

   • Hyperparathyroidism and hypoparathyroidism
   • Calcium and phosphate homeostasis
   • PCOS and reproductive hormone disorders
4. 4

   Renal and Acid-Base Disorders

   4 topics

   • Acute kidney injury
     • Prerenal, intrinsic, postrenal classification
   • Chronic kidney disease
   • Glomerular and tubulointerstitial disease
   • Fluid, electrolyte, and acid-base disturbances
     • Sodium and potassium disorders
     • Metabolic and respiratory acid-base interpretation
5. 5

   Genitourinary and Male Reproductive Disorders

   5 topics

   • Urinary tract infection and pyelonephritis
   • Nephrolithiasis
   • Benign prostatic hyperplasia and prostatitis
   • Testicular and prostate cancer
     • Testicular torsion and acute scrotum
   • Erectile dysfunction and hematuria workup

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

19 of 51 cards from the Endocrine, Renal, and Genitourinary Systems deck — real questions with worked answers.

1. What are the diagnostic glycemic thresholds for diabetes mellitus (any one criterion, confirmed)?

   Fasting plasma glucose $\geq 126$ mg/dL; 2-hour OGTT glucose $\geq 200$ mg/dL; HbA1c $\geq 6.5\%$; or random glucose $\geq 200$ mg/dL with classic symptoms. Prediabetes: FPG $100$–$125$, A1c $5.7$–$6.4\%$.

2. Contrast the pathophysiology of type 1 vs type 2 diabetes mellitus.

   Type 1: autoimmune T-cell destruction of pancreatic $\beta$-cells $\to$ absolute insulin deficiency (anti-GAD, anti-islet antibodies; prone to DKA). Type 2: peripheral insulin resistance plus progressive $\beta$-cell dysfunction $\to$ relative insulin deficiency (obesity-associated, often asymptomatic).

3. What is the first-line pharmacologic agent for type 2 diabetes and its main contraindication?

   Metformin (a biguanide that decreases hepatic gluconeogenesis and improves insulin sensitivity). Avoid when eGFR $< 30$ mL/min/1.73 m$^{2}$ due to lactic acidosis risk; hold around iodinated contrast.

4. What laboratory triad defines diabetic ketoacidosis (DKA)?

   Hyperglycemia (glucose usually $> 250$ mg/dL), anion-gap metabolic acidosis (pH $< 7.3$, $\ce{HCO3-} < 18$ mEq/L), and ketonemia/ketonuria ($\beta$-hydroxybutyrate elevated).

5. How does hyperosmolar hyperglycemic state (HHS) differ from DKA?

   HHS: glucose often $> 600$ mg/dL, serum osmolality $> 320$ mOsm/kg, minimal/no ketosis, pH $> 7.3$, $\ce{HCO3-} > 18$. Profound dehydration and altered mental status; typically type 2 DM. DKA is more acute with marked acidosis and ketones.

6. Outline the core management sequence for DKA.

   1) IV isotonic fluids ($\ce{0.9\% NaCl}$); 2) IV insulin infusion; 3) replace potassium (start when $\ce{K+} < 5.3$ and urinating—total body K is depleted); 4) correct precipitant. Add dextrose when glucose $\approx 200$ mg/dL while continuing insulin to clear ketones.

7. Why must potassium be monitored closely during DKA treatment?

   Total body potassium is depleted despite normal/high serum K (acidosis shifts $\ce{K+}$ out of cells). Insulin and fluids drive $\ce{K+}$ intracellularly, causing potentially fatal hypokalemia. Hold insulin if $\ce{K+} < 3.3$ mEq/L until repleted.

8. State Whipple's triad for hypoglycemia.

   (1) Symptoms consistent with hypoglycemia, (2) a low measured plasma glucose ($< 70$ mg/dL, often $< 55$), and (3) resolution of symptoms after glucose is raised.

9. Distinguish neurogenic (autonomic) from neuroglycopenic symptoms of hypoglycemia.

   Neurogenic/autonomic: tremor, palpitations, sweating, anxiety, hunger (early, adrenergic). Neuroglycopenic: confusion, slurred speech, seizures, coma (from CNS glucose deprivation, later/more severe).

10. What is the treatment of severe hypoglycemia in an unconscious patient without IV access?

    Intramuscular or subcutaneous glucagon $1$ mg. If IV access available, give $\ce{D50}$ (25 g dextrose). Conscious patients: 15–20 g fast-acting oral carbohydrate, recheck in 15 minutes (rule of 15).

11. List the major microvascular complications of diabetes.

    Retinopathy (leading cause of new adult blindness), nephropathy (leading cause of ESRD—earliest sign microalbuminuria), and peripheral/autonomic neuropathy (stocking-glove sensory loss, gastroparesis).

12. Which medication class is renoprotective in diabetic nephropathy and why?

    ACE inhibitors or ARBs—they reduce intraglomerular pressure by dilating the efferent arteriole, decreasing albuminuria and slowing progression. SGLT2 inhibitors also provide cardiorenal protection.

13. What are the standard glycemic and screening targets for most adults with diabetes?

    HbA1c $< 7\%$ for most; BP $< 130/80$ mmHg; annual dilated eye exam, foot exam, and urine albumin-to-creatinine ratio; statin therapy for cardiovascular risk reduction.

14. What are the classic lab findings and most common cause of primary hypothyroidism?

    Elevated TSH with low free $T_4$. Most common cause: Hashimoto's (chronic autoimmune) thyroiditis with anti-TPO antibodies. Symptoms: fatigue, cold intolerance, weight gain, constipation, bradycardia.

15. What is the most common cause of hyperthyroidism and its distinguishing features?

    Graves' disease—TSH receptor stimulating antibodies. Low TSH, high free $T_4$; unique findings: diffuse goiter with bruit, exophthalmos/orbitopathy, and pretibial myxedema; diffuse uptake on radioactive iodine scan.

16. How are first-line antithyroid drugs chosen, and which is preferred in pregnancy?

    Methimazole is generally first-line (more potent, once daily). Propylthiouracil (PTU) is preferred in the first trimester of pregnancy and thyroid storm (blocks peripheral $T_4\to T_3$). Both inhibit thyroid peroxidase.

17. Define myxedema coma and thyroid storm.

    Myxedema coma: severe decompensated hypothyroidism—hypothermia, bradycardia, altered mentation, hyponatremia. Thyroid storm: life-threatening thyrotoxicosis—fever, tachyarrhythmia, agitation; treat with beta-blocker, PTU, iodine (after PTU), and glucocorticoids.

18. What features of a thyroid nodule raise suspicion for malignancy on ultrasound?

    Hypoechoic, microcalcifications, irregular/infiltrative margins, taller-than-wide shape, and increased intranodular vascularity. A cold (non-functioning) nodule on scintigraphy also warrants fine-needle aspiration biopsy.

19. Name the most common thyroid cancer and the one associated with MEN2 / calcitonin.

    Papillary carcinoma is most common (excellent prognosis, spreads via lymphatics, Psammoma bodies). Medullary carcinoma arises from parafollicular C cells, secretes calcitonin, and is linked to MEN2 (RET mutation).

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