Week 7 · Genitourinary Disorders II — Interactive Reading Report

Orientation

How to read this week

Week 6 was the kidney as a filter — infection, injury, failure, and the chemistry it controls. Week 7 is the plumbing on either side of that filter: the artery that feeds it and the tube that drains it. One organizing idea runs through all five topics — obstruction.

Half one

The upper tract — perfusion & stones

Renal artery stenosis — the artery that feeds the kidney
Nephrolithiasis — the stone that blocks the ureter

Diagnostic currency: a pressure gradient, a stone size, and a urine pH. The question is whether perfusion and drainage are intact.

Half two

The lower tract — outlet, prostate & trauma

Bladder dysfunction and acute urinary retention
Benign prostatic hyperplasia
Penile shaft fracture

Diagnostic currency: a postvoid residual, a French catheter size, and a digital rectal examination. The question is whether the patient can void.

The thread that ties all five together

In every one of these disorders the injury is mechanical and the danger is delay — a renal artery narrowed past 70%, a ureter plugged by a stone larger than 10 mm, a bladder outlet closed by a hyperplastic prostate, a urethra torn and unrecognized, a tunica albuginea ruptured and left unrepaired. Find the obstruction, size it, and relieve it before the organ on the other side gives out.

Your reading map

The three assigned chapters — and the two topics that ride with them
Ch.	Title	What it actually contains
45	Renal Artery Stenosis	Definition and ischemic nephropathy · renin–angiotensin pathophysiology · fibromuscular dysplasia vs. atherosclerosis · the ten circumstances that should make you consider RAS · Doppler US, CTA, MRA and the DSA gold standard · the hemodynamic criteria for a significant stenosis · ACEI/ARB first-line therapy · PTRA, stenting and surgical reconstruction · geriatric considerations Langley & Talley
46	Nephrolithiasis	Stone composition and the 80% calcium rule · supersaturation, inhibitors and the dietary drivers · seven stone types by urine pH and mechanism · colicky flank pain and where the stone is by where the pain goes · noncontrast helical CT vs. ultrasound · analgesia, medical expulsive therapy and hydration · ureteroscopy and percutaneous nephrolithotomy · recurrence prevention by stone type Couture
44	Benign Prostatic Hyperplasia	Hyperplasia of the prostate after 50 · age-related incidence · irritative vs. obstructive symptoms · DRE findings and what raises malignancy suspicion · PSA and the IPSS · α₁-blockers, 5ARIs, antimuscarinics and PDE5 inhibitors · TURP, TUIP and open prostatectomy · gerontological considerations Roberg
—	Bladder Dysfunction & Acute Urinary Retention	From the lecture deck, not the assigned chapters. Etiology by category · chronic vs. acute retention · postvoid residual · the catheter decompression ladder · the trauma exception · postobstructive diuresis week7_GU.pptx
—	Penile Shaft Fracture	From the lecture deck, not the assigned chapters. Rupture of the corpus cavernosum and tunica albuginea · the 25–30% urethral injury rate · popping sound and detumescence · retrograde urethrography before catheterization · early surgical repair week7_GU.pptx

Where the deck and the chapter disagree — answer from the chapter

The assigned chapters and Dr. Gantioque's slides differ on several numbers. The practice questions cite the chapters, so the chapter value is the one to answer with. The differences are flagged inside each section below rather than silently averaged.

RAS and age at hypertension onset — Ch. 45 says younger than 30 or older than 55; the slides say younger than 20 or older than 50.
Fibromuscular dysplasia — Ch. 45 says ages 25–50, about 90% women; the slides say ages 30–40.
RAS etiology — the slides list obesity and omit tobacco; Ch. 45 lists tobacco use and does not list obesity.
Stone epidemiology — Ch. 46 says 11% lifetime risk and onset in the 30s; the slides say 6–12% and peak incidence at 40–60 years.
BPH incidence over 80 — Ch. 44 says more than 80%; the slides say more than 90%.

The numbers worth carrying in

<10% / >90%

FMD vs. atherosclerosis in RAS

Fibromuscular dysplasia accounts for under 10% of RAS; atherosclerosis for more than 90%.

10–40%

of refractory hypertension is RAS

Against less than 1% of patients with mild hypertension.

80%

of kidney stones are calcium

Calcium oxalate more often than calcium phosphate. Uric acid is only about 5%.

>200 mL

Postvoid residual is abnormal

The single number that defines retention on the bladder scan.

Chapter 45 · Renal Artery Stenosis · Langley & Talley

Renal Artery Stenosis

Renal artery stenosis is a stenosis or narrowing in the lumen of the renal arteries — a progressive disease in which vascular supply is reduced and perfusion to the kidney leads to gradual loss of renal function through ischemia and eventual death of the organ. When the stenosis is hemodynamically significant, the resulting fall in GFR is called ischemic nephropathy.

Definition

Two terms, one disease

RAS — a stenosis or narrowing in the lumen of the renal arteries.
Ischemic nephropathy — the decreased GFR that results from a hemodynamically significant stenosis.

RAS is the major cause of renovascular hypertension, may account for 1–10% of the 50 million people in the United States with hypertension, and is recognized as an important cause of chronic renal insufficiency and end-stage renal disease.

Pathophysiology

The two-kidney trap

Reduced blood flow triggers release of renin and angiotensin II.
Renin initiates the cascade that produces hypertension that can be very severe and very difficult to control.
The stenotic kidney atrophies — this is ischemic nephropathy.
The other kidney is damaged by that same hypertension: hypertensive nephrosclerosis, with progressive scarring and loss of filtering function.
Compensatory contralateral hypertrophy may temporarily maintain renal function — which is why the disease stays silent.

Why unilateral disease still ends in kidney failure

Only one artery is narrow, yet both kidneys are at risk. The stenotic kidney shrinks from ischemia while the nonstenotic kidney is scarred by the hypertension the stenosis itself provoked. Compensatory hypertrophy of the healthy kidney hides the loss until it can no longer keep up. Unilateral and bilateral RAS can both ultimately lead to chronic kidney disease.

Etiology — the ten causes

Vascular

Structural

Atherosclerosis
Fibromuscular dysplasia
Dissection
Renal artery coarctation
Renal artery aneurysm

Inflammatory & embolic

Acquired

Vasculitis — e.g., Takayasu arteritis
Thromboembolic disease
Radiation injury

External

Compressive & behavioral

Extrinsic compression
Tobacco use

The slides list obesity here and omit tobacco; the chapter does the reverse.

How often RAS is the answer — by blood pressure phenotype

RAS is rare in ordinary hypertension and common in the hypertension that will not behave. Hover a band for the source phrasing.

Uncommon — look elsewhere first Common enough to work up A recognized cause of advanced disease

Types of RAS — the two headline entities

Fibromuscular dysplasia vs. atherosclerosis
Feature	Fibromuscular dysplasia	Atherosclerosis
Share of RAS	< 10% of cases	> 90% of all cases — most RAS is atherosclerotic
Mechanism	An abnormality in the lining of the renal artery; fibrous tissue forms, narrowing and stenosing the vessel	Buildup of cholesterol deposits, or plaque, in the lining of the arteries
Who	Ages 25–50, mostly women (90%) versus men — though men tend to have more aggressive forms The slides say ages 30–40 and "almost exclusively women." Ch. 45 is the value to answer with.	Men older than 45 and women older than 55
Risk factors	Familial tendency is possible, but recent studies indicate fewer than 8% of patients had a family member with the condition	Hypertension · high cholesterol · insulin resistance and/or diabetes · overweight or obesity · smoking · lack of physical activity · poor diet high in fat, cholesterol, sodium and sugar · family history of early heart disease
Preferred treatment	PTRA first; reserve surgery for complications of PTRA or recurrent stenosis after initial PTRA	Lifestyle + medical therapy first; revascularization for the criteria below

Signs and symptoms

RAS is usually asymptomatic until the stenosis is severe and impairing renal function. Symptoms of a significant decrease in renal function include increase or decrease in urination, edema, shortness of breath, drowsiness, generalized itching, dry skin, discolored skin, headaches, weight loss and/or appetite loss, nausea and/or vomiting, sleep problems, muscle cramping, and trouble concentrating.

The ten circumstances that should make you consider RAS

Onset of hypertension (usually sudden) at younger than 30 years or older than 55 years of age
Hypertension that was well controlled has become difficult to treat — despite three or more different BP control medications
Malignant, accelerated, or resistant hypertension
No family history of hypertension
Unexplained heart failure or "flash" pulmonary edema
Asymmetric (differently sized and shaped) kidneys on ultrasound
Epigastric or renal artery bruits on auscultation or ultrasound
Atherosclerotic disease of the aorta or peripheral arteries
A decline in estimated GFR by > 30% from baseline after initiation of an ACEI or an ARB
Metabolic acidosis

Laboratory and diagnostics

General laboratory

BUN, serum creatinine, potassium

BUN and SCr are elevated only once significant ischemia has occurred — a normal creatinine does not exclude RAS.
Hypokalemia occurs from activation of the renin–angiotensin system in response to decreased blood flow to the kidney.
Metabolic acidosis accompanies it.

The classic trap

Hypo-, not hyper-

RAS produces hypokalemia and metabolic acidosis — not hyperkalemia, and not metabolic alkalosis. The stenotic kidney behaves like a kidney losing salt and potassium under aldosterone drive, not like a failing kidney retaining potassium.

Imaging and pressure measurement — in the order you reach for them
Test	What it gives you	The catch
Doppler ultrasound	Initial diagnostic screening. Sensitivity 85%, specificity 92%.	Results are highly dependent on patient habitus, cooperation, and the skill of the technician. If the stenosis is critical (> 70%) on Doppler or MRI, an invasive diagnostic test may be required.
CT angiography (CTA)	Noninvasive; allows 3D viewing of vessels. May be used when MRA is contraindicated.	Less specific than MRA. Risk of contrast-induced nephropathy, and it requires more contrast medium than renal angiography.
MR angiography (MRA)	Functional assessment of blood flow to the kidneys and of kidney function.	Turbulent flow can give false positives. Uses gadolinium — must be avoided in moderate- or end-stage renal failure. Cannot be used with many implanted devices, including previous renal stents — so it cannot evaluate in-stent restenosis.
Intra-arterial DSA	The definitive diagnostic test and current gold standard. Renal artery pressure is measured during catheterization and used to guide treatment if PTRA is warranted.	Invasive; contrast-induced nephropathy risk — though the volume can be controlled, and CO₂ subtraction angiography can replace contrast dye.

What counts as a significant stenosis

Visual measurement of 50–70% stenosis is deemed significant — and may require intervention — when one of the following is present:

A resting translesional mean pressure gradient of ≥ 10 mmHg
A hyperemic peak systolic pressure gradient of ≥ 20 mmHg
Or a renal flow reserve ≤ 0.8

The most direct measure of the hemodynamic or functional significance of a stenosis is the differential pressure across the stenosis.

Tests no longer recommended

Captopril renal scintigraphy and the captopril test — ACC/AHA guidelines no longer recommend these for diagnosing RAS, though they may still be used to guide revascularization decisions when determining hemodynamic severity.
Renal vein renin sampling and peripheral renal levels — not generally recommended, due to low specificity and sensitivity.

Treatment

Lifestyle

Reduce atherosclerotic risk

Exercise
Healthy body weight
Healthy diet — limit fat, cholesterol, sodium, and sugar
Smoking cessation

Medical

The cornerstone

ACE inhibitors, ARBs, RAAS blockade — first line
Statins (lipid-lowering agents)
Antiplatelet therapy — e.g., aspirin

Optimize glycemic, BP, and cholesterol management to current evidence-based guidelines. Goal BP < 130/80 mmHg.

Before you start an ACEI or ARB in RAS

Further decline in GFR may occur in patients with RAS — these agents can cause acute renal failure.
Start all medications at lower doses and titrate up only after evaluating response.
Patients starting renin–angiotensin blockade should have their BP, kidney function, and electrolytes checked within 2 weeks of starting the medication.
Many individuals require two or more medications; in addition to an ACEI or ARB, a diuretic, β-blocker, or calcium channel blocker may be needed.
Minoxidil is reserved for patients unresponsive to all other agents — referral to a hypertension specialist is prudent.

ACE inhibitors for renal artery stenosis
Agent	Usual dose / frequency
benazepril (Lotensin)	10–40 mg daily
captopril (Capoten)	12.5–100 mg BID or TID
enalapril (Vasotec)	5–40 mg daily or BID
fosinopril (Monopril)	10–40 mg daily
lisinopril (Zestril)	5–40 mg daily
moexipril (Univasc)	7.5–30 mg daily
perindopril (Aceon)	4–8 mg daily
quinapril (Accupril)	10–80 mg daily
ramipril (Altace)	2.5–20 mg daily
trandolapril (Mavik)	1–4 mg daily

Angiotensin II receptor blockers for renal artery stenosis
Agent	Usual dose / frequency
azilsartan (Edarbi)	40–80 mg daily
candesartan (Atacand)	8–32 mg daily
eprosartan mesylate (Teveten)	400–800 mg daily or BID
irbesartan (Avapro)	75–300 mg daily
losartan (Cozaar)	25–100 mg daily
olmesartan (Benicar)	20–40 mg daily
telmisartan (Micardis)	20–80 mg daily
valsartan (Diovan)	40–320 mg daily or BID

Table 45.1 — the ladder as the chapter writes it
Line	What it contains
First line	Medications + lifestyle. Primary options: captopril or enalapril or valsartan or losartan Secondary options: HCTZ or furosemide or atenolol or amlodipine or nifedipine or prazosin Tertiary options: clonidine or hydralazine or methyldopa or minoxidil Plus antiplatelet: aspirin or clopidogrel Plus statin: atorvastatin or fluvastatin or lovastatin or rosuvastatin or simvastatin
Second line	Renal artery stenting + continuing medical management, plus post-stent clopidogrel.
Third line	Surgical reconstruction of the renal arteries.

Revascularization

When the AHA says to restore blood flow

Revascularization is recommended when the renal artery is reduced by more than 70% of its diameter, or when there is 50–70% stenosis with a significant hemodynamic gradient across the stenosis, along with:

Uncontrolled hypertension on three agents, one of which is a diuretic
Ischemic neuropathy
Or exacerbation of other cardiac disorders, to include unstable angina or CHF

The slides put the threshold differently — revascularization is not generally attempted if less than 50% of the artery is stenosed.

Minimally invasive

Catheter-based

PTRA — risks include renal artery dissection, rupture, thrombosis, and embolism
PTRA with stent placement
Thrombolysis in the event of acute thrombosis

Associated risks overall include hemorrhage and contrast-induced nephropathy.

Surgical

For complex disease only

Recommended for complex renal artery stenosis only — recent studies do not show improved outcomes compared with medical management
Treat RAS from fibromuscular dysplasia with PTRA first; reserve surgery for PTRA complications or recurrent stenosis after initial PTRA
Renal artery bypass / reconstruction — largely replaced by PTRA due to complications
Endarterectomy

Other considerations worth remembering

All patients with atherosclerotic RAS should be assessed for coronary artery disease.
Most patients should receive an ACEI or an ARB and a statin — the statin not only reduces cardiac risk but may induce regression of RAS.
A key feature of treating atherosclerotic RAS is reducing serum lipids and cholesterol, which contribute to atherosclerosis in the renal artery and in the kidney itself.

Geriatric considerations

Consider RAS in older adults when the onset of hypertension was diagnosed at age > 55 years.
Hypertension caused by RAS further increases the risk of coronary artery disease and stroke — patients should be screened for such disease.
Weigh risk versus benefit for medical and/or surgical management.
Management should be individualized and aim to control BP with fewer medications so as to minimize adverse effects; the choice of ACEI or ARB and the dosage may differ based on individual kidney function.

Chapter 46 · Nephrolithiasis · Couture

Nephrolithiasis

Nephrolithiasis is a condition in which one or more stones are present in the pelvis, in the calyces of the kidney, or in the ureter. Calculi may be composed of calcium oxalate or calcium phosphate — the two most common compositions — or of uric acid, struvite, or cystine.

~11%

lifetime risk in the United States

The chapter's figure, and increasing. The slides say 6–12%. Greater in men than women.

30s

usual age of onset

The slides put peak incidence later, between 40 and 60 years.

~50%

recur within 10 years

The slides break it down further: 40% at 5 years, 75% at 20 years.

90%

of urinary calculi are radiopaque

Which is why a plain film still finds most of them — but not all.

Etiology and risk factors

Urine chemistry

Formation and inhibition

Supersaturation of urine with stone-forming salts
Decreased or absent stone inhibitors — citrate, magnesium, and pyrophosphate
Low citrate levels
Decreased renal acid excretion, a precursor of uric acid, leads to hyperuricosuria and decreases calcium oxalate solubility

Dietary drivers

What goes in

Low fluid intake
High sodium intake — sodium excretion pulls calcium excretion, and mobilizes calcium from bone
High animal protein intake
High fructose intake
Low dietary calcium intake — can cause oxalate levels to rise
Overload of calcium supplement intake
Foods high in oxalate — nuts, chocolate, dark green leafy vegetables, rhubarb, beets, okra

Host factors

Who forms stones

Gender and age; family history; genetic predisposition — males have increased genetic predisposition
Geography and dehydration, which occurs more frequently in hot, arid environments
Life stress; immobility; sleeping position — a correlation exists between sleep posture and unilateral renal stone formation
Preexisting conditions: primary hyperparathyroidism, obesity, diabetes, gout, cardiovascular disease
Postsurgical: small bowel resection, gastric bypass, colectomy
Urinary tract infections; oxidative stress — stone formation is linked to production of reactive oxygen species, and oxidative stress is linked to idiopathic calcium oxalate nephrolithiasis

Drugs associated with stone formation

Triamterene (Dyrenium) · steroids · vitamin D supplements · carbonic anhydrase inhibitors · indinavir (Crixivan), a protease inhibitor · colchicine · chemotherapy agents.

What the stone is made of

Calcium dominates so heavily that "kidney stone" and "calcium stone" are nearly the same statement. Hover a bar for the detail.

Calcium oxalate / phosphate Uric acid Infection- and hereditary-related

The seven stone types — and the urine pH that gives them away

Stone type by mechanism, pH clue, and treatment
Type	Mechanism and clue	Treatment
Hypercalciuric calcium — absorptive types I, II, III	Increased absorption of calcium at the level of the small bowel (jejunum). Type I is independent of calcium intake — urine calcium is increased on a regular or even a low-calcium diet. Type II is diet-dependent — dramatically decreasing dietary calcium may decrease hypercalciuria. Type III results from a renal phosphate leak that causes increased vitamin D synthesis and increased small bowel absorption of calcium.	Focused on decreasing bowel absorption of calcium.
Hypercalciuric calcium — resorptive	Because of hyperparathyroidism; hypercalcemia, hypophosphatemia, and elevated levels of parathyroid hormone are present.	Surgical resection of the adenoma cures the disease and the stones.
Hypercalciuric calcium — renal leak	Renal tubules are unable to reabsorb filtered calcium efficiently, and hypercalciuria occurs.	Thiazides are effective as long-term therapy.
Hyperuricosuric calcium	Caused by dietary excess or uric acid metabolic defects. In contrast to those with uric acid calculi, these patients maintain a urinary pH > 5.5.	Directed at the uricosuria.
Hyperoxaluric calcium	Due to primary intestinal disorders; patients usually have a history of chronic diarrhea, often with inflammatory bowel disease or steatorrhea. Calcium is unavailable to bind oxalate, which is then freely and rapidly absorbed.	Increased fluid intake must be emphasized.
Hypocitraturic calcium	May result from chronic diarrhea, type I renal tubular acidosis, or chronic or aggressive thiazide diuretic treatment; may also be idiopathic. Citrate binds calcium in solution, decreasing available calcium for stone formation.	Potassium citrate 20 mEq TID with meals.
Uric acid	Frequently have urinary pH lower than 5.5. The chapter also states the average urinary pH is 5.85 in the same sentence — an internal contradiction, flagged rather than resolved.	Increasing the pH to levels higher than 6.5 can dramatically increase solubility and dissolve large stones.
Struvite	Magnesium–ammonium–phosphate stones. Commonly seen in women with recurrent urinary tract infections; most stones are large and cause obstruction and bleeding. Radiodense. Urinary pH is high (> 7–7.5). Caused by urease-producing organisms — Proteus sp., Haemophilus sp., Klebsiella sp., and Ureaplasma urealyticum.	Requires eradicating the infection with antibiotics plus intervention. Stones are soft and amenable to percutaneous nephrolithotomy or extracorporeal shock wave lithotripsy.
Cystine	Result of abnormal excretion of cystine, ornithine, lysine, and arginine. Cystine is the only amino acid that becomes insoluble in urine. Difficult to manage.	Tiopronin, penicillamine, or potassium citrate; alkalinize the urine to pH > 7.5 and < 8.

The urine pH map — which stone forms where

Urine pH is the cheapest clue to stone type. Acid urine favors uric acid; alkaline urine favors struvite. Hover each zone.

Uric acid — acid urine Calcium with uricosuria Struvite — infection, alkaline urine Cystine treatment target

One chapter sentence to read carefully

Chapter 46 states that "high urine pH level is the main risk factor for calcium oxalate and calcium phosphate." That sits awkwardly beside the rest of the chapter, which assigns alkaline urine to struvite and acid urine to uric acid. Treat the pH associations in the table above as the ones the exam will use, and know that high pH is the classic driver of struvite and calcium phosphate stones.

Clinical manifestations

The pain

Where the stone is, by where it hurts

Acute flank pain, colic-like — sudden onset of severe pain in the costovertebral angle, flank, and/or lateral abdomen
Colicky or constant — the patient cannot find a comfortable position; pain is not relieved by position
If flank pain increases in intensity and radiates downward to the groin, the stone has passed to the lower third of the ureter
Frequency, urgency, and dysuria suggest the stone is in the portion of the ureter within the bladder wall
Oliguria and acute renal failure may occur when both collecting systems are obstructed by stones

Everything else

Accompanying findings

Testicular pain
Nausea and vomiting; diaphoresis
Costovertebral angle tenderness
Hematuria
History of prior stone formation

On examination, vital signs matter: fever suggests an occult infection, and hypotension with an altered mental status suggests urosepsis. The abdominal exam is usually benign — tenderness to palpation, rebound, or guarding suggests a more serious intra-abdominal process. Palpate the abdominal aorta for tenderness or pulsatile enlargement suggestive of aneurysm.

Hematuria — present, absent, and unrelated to severity

Microscopic hematuria in more than 80% of patients
Gross hematuria in about one third
Absent urinary blood in 10–30%
The amount of hematuria does not correlate with the degree of urinary obstruction.

Laboratory and imaging

Diagnostic studies for suspected nephrolithiasis
Study	Performance and what it shows	Limitations
Noncontrast helical CT	The test of choice and gold standard radiographic test. Detects calculi as small as 1 mm. Sensitivity 95%, specificity 98%, accuracy 97%. Directly visualizes hydroureter, hydronephrosis, and ureteral edema. Performed rapidly, requires no IV contrast, and detects other nonurologic causes — including AAA.	Does not evaluate flow or renal function. Has replaced IVP.
Renal ultrasound	No radiation. Can be used as the initial test versus CT. Twinkling signal and shadow measurements improve detection and sizing. Hydronephrosis detection: sensitivity 85–94%, specificity 100%.	Less sensitive to detecting stones. May miss stones < 5 mm. May miss obstruction in the early phase of renal colic. Provides anatomic information only. No increase in adverse outcomes versus CT.
KUB radiograph	Reveals opaque calculi. Distinguishes calcium-bearing (radiopaque) from noncalcium stones; assists in locating radiopaque stones and excluding other pathology in nonpregnant patients.	Cannot distinguish a radiopaque stone from a phlebolith or bowel contents. Oblique films assist in localizing suspicious calcifications.
Pyelogram (excretory or retrograde)	Permits the exact definition of stones and reveals the presence or absence of obstruction.	IVP establishes the diagnosis in 95% and demonstrates severity of obstruction, but helical CT has replaced it as the test of choice.
Laboratory	Urinalysis reveals blood; WBC and bacteria suggest infection. CBC — WBC > 15,000 suggests concomitant infection. Urine culture. Serum chemistries should include calcium, electrolytes, phosphate, and uric acid. Electrolytes, glucose, BUN, creatinine. Pregnancy test when suggestive.	A 24-hour urine collection for calcium, uric acid, phosphate, oxalate, and citrate excretion is generally reserved for those with recurrent stones.

Pregnancy

Every effort should be made to minimize ionizing radiation exposure to the fetus.
Ultrasound is the imaging modality of choice in pregnancy.
Avoid NSAIDs in pregnancy, particularly in the third trimester.
Diagnostic procedures and surgery: ureteroscopy, shock-wave lithotripsy, percutaneous nephrolithotomy.

How well each study actually performs

Sensitivity and specificity for the renal and stone studies named in this week's material. Hover a bar for the source.

Sensitivity Specificity

Management

The first order of business is analgesia

Provide adequate analgesia as soon as the diagnosis is suspected on clinical and laboratory findings — a rapid dipstick urine test for blood, positive in conjunction with clinical findings, is sufficient to begin analgesic therapy. Randomized trials note parenteral NSAIDs are as effective as narcotics for renal colic, and a combination of IV NSAIDs and opioids decreases ED stay and provides better pain control than either alone.

Medications for renal colic
Agent	Dose	Notes
Ketorolac (Toradol)	30–60 mg IM or 30 mg IV	Alone or with opiates. Reduce to 30 mg IM or 15 mg IV if > 65 years or < 50 kg. Avoid in renal dysfunction — parenteral NSAIDs may lower kidney blood flow and glomerular filtration.
Morphine sulfate	2–10 mg IM/IV/SC q2–6h PRN	May redose more frequently if needed.
Hydromorphone (Dilaudid)	1–4 mg IM/IV/SC q4–6h PRN	Reduce dose in opiate-naive patients.
Hydrocodone / acetaminophen	Combination analgesic	May be necessary when pain is unrelieved by NSAIDs.
Hydroxyzine (Vistaril)	25–50 mg IM (not IV) q4–6h	Adjunct.
Ondansetron (Zofran)	4 mg IM/IV, not to exceed 8 mg/dose IV	Antiemetic. Alternatives include prochlorperazine, droperidol, hydroxyzine.

The opioid trap in stone patients

Patients with nephrolithiasis are at risk for long-term opioid dependence.
Patients with a history of nephrolithiasis were found to take more narcotics than those with no history of stones.
Alternate pain management strategies must be assessed to prevent opioid overuse and dependence.

Hasten passage

Hydration and medical expulsive therapy

Induce high urine flow with oral intake of at least 2–3 L of fluids per 24 hours to ensure a urine output of at least 2 L per day.
The slides add an IV route: 1 L of normal saline over 30–60 minutes, then 200–500 mL/h; bolus volume-compromised patients in 500 mL increments until urine output is adequate.
Medical expulsive therapy for urethral stones up to 10 mm that are eligible for observation — antispasmodics relax ureteral smooth muscle and have been shown to hasten stone passage by 5–7 days.

Medical expulsive therapy

The agents

α-blockers — doxazosin (Cardura) 4 mg PO daily; tamsulosin (Flomax) 0.4 mg PO daily; alfuzosin (Uroxatral) 10 mg PO daily
Calcium channel blockers — nifedipine (Procardia XL) 30 mg PO daily

The slides state these are most efficacious for stones < 5 mm and that tamsulosin and nifedipine are equally effective; the chapter offers medical expulsive therapy for stones up to 10 mm eligible for observation. Tamsulosin is prescribed on discharge at 0.4 mg PO daily for 4 weeks.

Stone size decides the plan

The single measurement that separates "drink and wait" from "operating room." Hover each zone.

Interventions for stones larger than 10 mm

Ureteroscopy — scope through ureter, bladder, and kidney; a basket breaks up stones; a stent may be inserted to keep the ureter patent
Percutaneous nephrolithotomy — surgery to remove the stone via a small tube
Percutaneous nephrolithotripsy — soundwaves or laser break up the stone and the pieces are vacuumed out
Laparoscopic techniques
Open surgery
Newer options named in the chapter: ultrasonic propulsion, which allows noninvasive stone dislodgement and mobilization in an awake patient, and burst wave lithotripsy, a promising ultrasound technology for transcutaneous stone fragmentation.

Prevention after the stone is gone

After removal, the goal is stone prevention. The recurrence rate is approximately 20–50%. Regular medical prophylaxis may effectively prevent recurrence in patients with a history of recurrence, calcium oxalate dihydrate stones, hypercalciuria, or hyperuricuria — but cost effectiveness, patient compliance, and gastrointestinal upset may limit patient acceptability and clinical use.

Management of kidney stones
Type	Dietary modifications	Treatment and rationale
All	Adequate fluid intake — make sure the patient has > 2 L of fluids per 24 hours. Promote a low-glycemic diet, a healthy diet, and exercise.	Higher fluid intake can decrease the risk of kidney stones.
Hypercalciuria, calcium oxalate (Type I)	Avoid foods high in salt — canned or processed foods, cheese, pickles, dried meats; do not add salt to food. Reduce animal protein (meat, eggs). Calcium supplements if not getting enough calcium through diet. Avoid foods high in oxalate — beans, spinach, rhubarb, chocolate, wheat, nuts, berries.	Thiazide diuretics: hydrochlorothiazide 25–50 mg PO daily — increases the urinary excretion of calcium (limited long-term use, < 5 years). Potassium citrate 10–20 mEq PO TID with meals — raises the citrate and pH of urine. Calcium citrate 250–500 mg PO TID with meals — raises the citrate and pH of urine and binds urinary oxalate; increases bone density by 1%/year.
Hypercalciuria, calcium oxalate (Type II)	No specific medical therapy is available.
Renal hypercalciuria	HCTZs — effective as long-term therapy.
Hypocitraturia	Potassium citrate supplements 20 mEq TID with meals.
Calcium phosphate	Avoid foods high in salt. Reduce animal protein. Calcium supplements if not getting enough calcium through diet. Reduce phosphate intake — decrease intake of dairy products, legumes, chocolate, and nuts by about one third.	Cranberry juice: at least 16 oz per day — acidifies urine.
Uric acid stones	Decrease protein intake. Purine dietary restrictions — limit animal protein (red meat, fish, shellfish). Reduce or eliminate alcohol intake.	Allopurinol 300 mg PO daily (adjust dose for renal dysfunction; doses > 300 mg should be divided and given BID) — decreases uric acid in the blood and urine. Potassium citrate 10–20 mEq PO TID with meals — raises the citrate and pH of urine.
Cystine stones	Increase fluid intake. Decrease methionine (sulfur) intake. Avoid dairy products, eggs, legumes, greens.	Tiopronin (Thiola) 800 mg/day PO in 3 divided doses, or penicillamine (Cuprimine) 2 g PO daily (range 1–4 g/day), or α-mercaptopropionylglycine (tiopronin) — decreases cystine in the urine. Potassium citrate 10–20 mEq PO TID with meals — alkalinize the urine to pH > 7.5 and < 8; lowers cystine concentrations and prevents formation of cystine calculi in the urine.
Struvite stones	Avoid supplemental magnesium.	Antibiotics — eliminates infection. Acetohydroxamic acid (Lithostat) 15 mg/kg/day PO TID; max 1.5 g/day — an effective urease inhibitor but poorly tolerated because of GI adverse effects. Tiopronin 800 mg/day PO TID at least 1 hour before or 2 hours after meals. Consider surgical intervention, especially for stones > 10 mm or if there is evidence of ongoing obstruction or infection.

Differential diagnosis worth ruling out

Dissecting or rupturing AAA · pyelonephritis · papillary necrosis (sickle cell disease, NSAID analgesic abuse, diabetes, or infection) · renal infarction (vascular dissection or arterial embolus) · ectopic pregnancy · ovarian cyst or torsion · appendicitis · intestinal obstruction · biliary tract disease · musculoskeletal strain · lower lobe pneumonia · malingering or narcotic dependence, which is a diagnosis of exclusion.

Lecture deck · Bladder Dysfunction

Bladder Dysfunction & Acute Urinary Retention

Acute urinary retention is the sudden inability to void spontaneously. It occurs most frequently in men older than 60 years, and the single most testable fact about it is that the most common cause of AUR in the emergency department is benign prostatic hyperplasia.

Source note

This topic and the penile fracture section that follows come from Dr. Gantioque's week7_GU.pptx, not from the three assigned chapters. They are on the deck's topic list and in your Week 7 practice-question set, so they are exam material — but they are not in Chapters 44, 45, or 46.

Acute versus chronic — the one distinction to hold on to

Acute retention is painful: lower abdominal or suprapubic discomfort, with a patient who may appear restless or in distress. Chronic urinary retention is usually painless — the bladder simply never empties, and the patient may present with overflow incontinence or a palpable bladder instead of pain.

Etiology — the differential by category

The list is not exhaustive, and the categories overlap: obstruction can be anatomic, neurologic, or pharmacologic.

Filter by cause

Anatomic

Urethral

Tumor
Pelvic masses
Prolapse of pelvic organs
Foreign body
Calculus
Urethritis
Stricture
Meatal stenosis — can also be seen in females
Hematoma
Vulvar edema after vaginal delivery

Anatomic

Prostate gland

Benign prostatic hypertrophy — the most common ED cause
Carcinoma
Prostatitis
Contracture of the bladder neck
Prostatic infarction

Anatomic

Penis

Phimosis
Paraphimosis
Meatal stenosis
Foreign-body constriction

Neurologic

Motor / paralytic & sensory / paralytic

Motor or paralytic: spinal shock; spinal cord syndromes
Sensory or paralytic: diabetes; multiple sclerosis; spinal cord syndromes

A neurologic cause is a cannot-miss: evaluate for spinal cord compression.

Pharmacologic

Drugs

Antihistamines
Anticholinergics
Antispasmodics
Tricyclic antidepressants
α-Adrenergic stimulators
Narcotics
NSAIDs

Take a thorough drug history including over-the-counter medications, especially if no other clear reason for the retention emerges.

History, examination, and workup

History

What to ask

History of urinary retention, BPH, or prostate cancer
History of other cancer; history of radiation treatment
History of pelvic trauma
Signs or symptoms of infection, including an abscess
Signs or symptoms of calculus
Any neurologic symptoms; back pain
History of or current IV drug abuse
A complete list of all medications

Physical

What to examine

Vital signs — any evidence of infection? Shock?
Abdominal examination
Rectal examination
Genitourinary examination; consider a pelvic examination in all women
Thorough neurologic examination if appropriate
In the trauma patient, evaluate for evidence of urethral injury

Because there are so many causes, the workup is selective

A thorough history and physical examination are imperative and will determine further workup. Beyond that:

Basic chemistry to assess renal function only if concerned for acute renal insufficiency — this usually does not occur in AUR.
No benefit to a PSA test in the ED — it is usually elevated in the setting of AUR anyway.
Urinalysis only if indicated on history or examination.
Abdominal or pelvic ultrasound, or CT abdomen/pelvis, if concerned for mass, malignancy, abscess, bladder calculi, or another anatomic etiologic agent.
Neuro or spinal imaging if there is concern for an acute neurologic process.

>200 mL

Postvoid residual is abnormal

Obtained as a diagnostic procedure. More than 200 mL is usually considered abnormal.

>60 yr

the age AUR favors

It occurs most frequently in men older than 60 years.

2–3 hr

observe after decompression

To make sure a postobstructive diuresis does not cause clinical deterioration.

Decompression — the ladder, in order

The first therapeutic move is prompt bladder decompression, and the catheter you choose depends on what you know about the urethra. Walk the ladder in this order.

Urethral catheterization ladder for acute urinary retention
Step	Attempt	When to choose it
1	14–18F urinary catheter	The default first attempt for everyone.
2	Downsize to 10–12F	If unable to pass a 14–18F catheter and there is a history of prior transurethral procedure or known stricture.
3	20–22F with a coudé tip	In men with no prior instrumentation in whom a catheter will not pass. The coudé tip lets you steer past an enlarged median lobe.
4	Suprapubic aspiration (temporizing) or suprapubic catheter	If a catheter still cannot be passed. Suprapubic aspiration is a temporizing measure; suprapubic catheter placement is definitive.

The trauma exception — do not catheterize yet

Defer catheterization in the trauma patient suspected of having a urethral injury until a retrograde urethrogram has been done. The findings that should stop your hand are:

Gross hematuria
High-riding prostate on rectal examination
Blood at the meatus

Passing a catheter through a torn urethra converts a partial injury into a complete one.

After decompression

Watch for

Postobstructive diuresis

Rapid decompression following catheter placement may result in transient gross hematuria — rarely clinically significant.
Postobstructive diuresis can be a complication of AUR in the catheterized patient.
There are no randomized trials comparing rapid and intermittent bladder decompression.
It is generally now felt that rapid bladder decompression is safe provided supportive care is available if hypotension develops.
It is probably best to observe for 2–3 hours after decompression.

The post-decompression checklist

Drain the bladder and monitor urine output.
Place a leg catheter bag before discharge if the catheter is to remain indwelling, and educate the patient and family on catheter care.
Start patients with BPH on an α-blocker.
Consider stopping any medication that may be contributing to the AUR.
Treat constipation if appropriate.
Address any life-threatening presentation first.

Prophylactic antibiotics are not indicated

Although commonly used, prophylactic antibiotics are not indicated for patients with an indwelling urinary catheter and no evidence of infection.

Medications for the retention patient with BPH
Agent	Dose
Prazosin HCl (Minipress)	Initially 1 mg PO BID to TID, slowly increase to 20 mg/day in divided doses
Tamsulosin (Flomax)	0.4 mg PO once daily after the same meal; may increase to 0.8 mg PO once daily
Alfuzosin (Uroxatral)	10 mg PO daily after the same meal each day
Terazosin (Hytrin)	Start 1 mg PO at bedtime; maximum 20 mg/day

Admission criteria

Who stays

Significant postobstructive diuresis requiring IV fluids or pressors
Sepsis
Obstruction related to spinal cord compression
Consider admission in a patient with obstruction due to malignancy or mass
Any process requiring acute urologic or surgical intervention

Discharge & follow-up

Who goes home

Most patients can be discharged.
Most patients will need follow-up for ongoing evaluation and management of AUR as well as catheter management.

Pearls and pitfalls: carefully evaluate for evidence of a mass or malignancy as the cause; carefully evaluate for evidence of spinal cord compression; take a thorough drug history including over-the-counter medications.

Chapter 44 · Benign Prostatic Hyperplasia · Roberg

Benign Prostatic Hyperplasia

The prostate weighs on average 20 g in normal 21- to 30-year-old men. Benign prostatic hyperplasia is the enlargement of the prostate gland, commonly seen in men older than 50 years — a progressive condition that can obstruct the urethra and interfere with urine flow. It is a hyperplastic process resulting from an increase in cell numbers, not simply enlargement of existing cells.

BPH incidence is age, almost nothing else

The proportion of men with BPH climbs with each decade after 50. Hover a bar for the exact figures and the deck-versus-chapter difference.

Fourth–fifth decade Sixth decade Beyond 80 — the majority of men

Cause

What is known — and not

The exact cause is unknown.
The condition may be a response of the prostate gland to androgen hormones over time.
Dietary fat and alcohol consumption may play a role.

Race

Risk differs by group

Black men are more likely than white men to have larger prostate volume and more symptoms.
Asian men are less likely than white and Black men to have BPH.

Geriatric anatomy

What the prostate does with age

By the fourth decade, stromal fibrous elements and glandular tissue hypertrophy, stimulated by dihydrotestosterone — the active androgen within the prostate. Hyperplastic nodules enlarge, ultimately leading to urethral obstruction.

Clinical manifestations

Irritative

Consequence of bladder dysfunction

Frequency
Dysuria
Urgency
Nocturia
Incontinence

Obstructive

Consequence of the outlet

Hesitancy
Straining
Starting and stopping
Dribbling
Retention
Decreased force and caliber of stream
Sensation of incomplete bladder emptying
Double voiding — urinating a second time within 2 hours

The digital rectal examination — and one rule that gets tested

On DRE, the prostate may be enlarged.
Size does not correlate with severity of symptoms or with the degree of obstruction. A small prostate can obstruct severely; a large one may not.
The prostate should feel smooth and rubbery.
Focal enlargement, nodularity, or extreme hardness may represent malignancy — further investigation is indicated with transrectal ultrasound and biopsy.
A palpable bladder is consistent with urinary retention.

Laboratory findings and testing

Workup for suspected BPH
Test	What it tells you
Urinalysis	Assess for blood, leukocytes, bacteria, protein, or glucose. Pyuria suggests infection. Hematuria may be a sign of malignancy.
Urine culture	To rule out UTI if irritative symptoms are present and to exclude infectious causes; usually performed if the initial urinalysis indicates an abnormality.
BUN / creatinine	To assess for renal insufficiency.
Prostate-specific antigen	Considered optional, yet most practitioners include it in the initial evaluation. 4–10 ng/mL suggests a risk of approximately 25%. Above 10 ng/mL suggests a risk of more than 50%. Below 4 ng/mL does not guarantee that the patient does not have cancer. Because an overlap exists between levels seen in BPH and in prostate cancer, its use is controversial. Other causes of an elevated PSA: prostate cancer, bacterial prostatitis, UTI.
Transrectal ultrasound	Useful for helping to determine bladder and prostate size; indicated with a palpable nodule or an elevated PSA.
Endoscopy of the lower urinary tract	May be indicated in patients scheduled for invasive treatment, or in whom a foreign body or malignancy is suspected. Also indicated with a history of STI, prolonged catheterization, or trauma.
Urine cytology	Used to screen for bladder cancer; useful in men with hematuria and irritative symptoms.
Other testing	Flow rate · post-void residual urine · pressure-flow studies · urodynamic studies.

Symptom scoring — the IPSS / AUA-SI

The severity of BPH can be determined with the International Prostate Symptom Score (IPSS) / American Urological Association Symptom Index (AUA-SI), plus a disease-specific quality-of-life question. It is a useful way to assess symptoms over time in a quantitative way. The seven questions concern: incomplete emptying · frequency · intermittency · urgency · weak stream · straining · nocturia.

Management

Mild symptoms

Watchful waiting and lifestyle

The patient may recover spontaneously over time — "watchful waiting."
Nightly fluid restriction
Timed bladder voiding
Regular physical activity
Treatment of constipation
Avoiding irritative foods
Avoiding alcohol and caffeine
Avoid medication that can worsen symptoms.

Mild to moderate

α-Blockers — the preferred agents

α-Blockers relax muscle fibers in the prostate gland and capsule and in the internal urethral sphincter, thereby facilitating emptying of the bladder. Some have an effect on blood pressure. Hypotension and dizziness are the most commonly reported adverse effects.

Medications that make BPH worse — two mechanisms

Decongestants, diuretics, and other sympathomimetics act on α receptors to enhance prostate muscle tone, which increases dynamic obstruction.
Anticholinergics (antihistamines), bowel antispasmodics, tricyclic antidepressants, opiates, and antipsychotics decrease bladder muscle contraction, thus increasing urine retention.

A medication review is mandatory whenever a previously stable patient suddenly worsens — including over-the-counter decongestants and antihistamines.

Alpha blockers for BPH
Agent	Dose	Notes
Terazosin (Hytrin)	1 mg at bedtime, increasing up to 10 mg at bedtime as necessary or tolerated	α₁ blockade. The slides give a maximum of 20 mg/day.
Prazosin (Minipress)	1–5 mg PO BID	α₁ blockade.
Doxazosin (Cardura)	1–8 mg daily	α₁ blockade.
Tamsulosin (Flomax)	0.4 or 0.8 mg daily	α₁ blockade — the slides note it has fewer adverse effects.
Alfuzosin (Uroxatral)	10 mg once daily	α₁ blockade.
Silodosin (Rapaflo)	8 mg once daily with a meal	α₁ blockade.
Phenoxybenzamine	5–10 mg twice daily	Named in the slides only — α₁ and α₂ blockade.

Hormonal manipulation — 5-alpha reductase inhibitors

Finasteride (Proscar) 5 mg/day — blocks the conversion of testosterone to dihydrotestosterone; works on the epithelial component of the prostate, resulting in reduction in the size of the gland and improvement in symptoms. Six months of therapy is required for maximal effect.
Dutasteride (Avodart) 0.5 mg once a day.
Estrogens, antiandrogens, or gonadotropin-releasing hormone may be used, but only if finasteride is not tolerated because of adverse effects.

Muscarinic receptor antagonists — anticholinergics

Indicated when a patient has bothersome irritative voiding symptoms despite treatment with an alpha₁-adrenergic antagonist. Typically added sequentially to an established alpha₁-adrenergic antagonist regimen.

Tolterodine (Detrol / Detrol LA) — 1–2 mg BID; Detrol LA 2–4 mg daily
Fesoterodine (Toviaz) — 4–8 mg daily

Phosphodiesterase 5 inhibitors

Tadalafil (Cialis) 5 mg daily — for patients with BPH and erectile dysfunction, or those with lower urinary tract symptoms that are not responsive to an alpha-adrenergic antagonist.

Combination therapy

Dutasteride-tamsulosin (Jalyn) 0.5 mg / 0.4 mg daily.
The benefit of combination therapy with any alpha₁-adrenergic antagonist and any 5ARI is well established.
May be considered in symptomatic patients who do not respond to an adequate trial of monotherapy, or in symptomatic patients at high risk of BPH complications.

Phytotherapy

Uses of plants or plant extracts have not been evaluated by the FDA or any regulatory agency for safety and efficacy. Popular extracts include saw palmetto berry; bark of Pygeum africanum; roots of Echinacea purpurea and Hypoxis rooperi; pollen extract; leaves of the trembling poplar; rye; common or stinging nettle; and pumpkin/squash. Herbal remedies are sold as "dietary supplements," with no requirement for proof of efficacy or safety prior to marketing.

Surgery — when symptoms are significant

Procedures for BPH
Procedure	What to know
Transurethral resection of the prostate (TURP)	Low mortality (0.23%) but moderate morbidity (18%). Should bring about improvement in the signs and symptoms of BPH. Repeat resection is needed in fewer than 10% of cases. Retrograde ejaculation may occur after the procedure. Uncommon complications: bladder neck contracture · bleeding · TUR syndrome (irrigating fluid absorbed in large quantities through veins that are cut open) · urethral stricture disease · incontinence · impotence. The slides give a mortality of 1%; the chapter says 0.23%.
Open simple prostatectomy	Reserved for patients with a very large prostate, accompanying bladder stones, bladder diverticula, or who cannot be positioned for transurethral surgery.
Transurethral incision of the prostate (TUIP)	No tissue is resected. Antegrade ejaculation is usually maintained. Can usually be performed as an outpatient procedure. May benefit patients with BPH associated with a smaller prostate gland, especially younger men.

Options that offer promise but carry few long-term data

Laser therapy — potassium-titanyl-phosphate (KTP) and holmium lasers are widely used to cut and/or remove the prostate; transurethral laser-induced prostatectomy (TULIP) is performed under transrectal ultrasound guidance. Advantages: minimal blood loss and fluid absorption; rare TUR syndrome; can treat patients on anticoagulation therapy; outpatient therapy. Disadvantages: lack of tissue for pathologic evaluation; longer postoperative catheterization time; more frequent irritative voiding complaints; expense of laser fibers and generators.
Transurethral microwave therapy (TUMT) — microwave hyperthermia delivered via transurethral catheter or transrectal route; associated with significant prostate swelling needing a urinary catheter until the swelling subsides. In terms of efficacy it places between medical therapy and TURP. The 2018 AUA guideline states TUMT may be offered, but patients need to be informed it has higher surgical retreatment rates than TURP.
Transurethral needle ablation (TUNA) — interstitial radiofrequency needles pierce the prostatic urethral mucosa and heat tissue, producing coagulative necrosis. Improvement in voiding has been reported, but the 2018 AUA guideline does not recommend TUNA for the treatment of BPH.
High-intensity ultrasound energy therapy — heat vaporization of tissue creates a cavity in the prostatic urethra; may be delivered rectally or outside the body; urinary retention is common with its use.
Radiofrequency-generated water thermotherapy — turns sterile water into vapor or steam delivered directly into the obstructive prostate tissue.
Prostatic artery embolization — an incidental discovery that results in improved BPH symptoms; yet to be established as a treatment option and considered experimental.
Urethral stents — for patients who are not candidates for standard surgery; can be performed under local anesthesia and are preferred to chronic catheterization or suprapubic cystostomy.

Gerontological considerations

Physiologic changes

Kidney, bladder, prostate, sexual function

Diminished kidney mass, blood flow, and GFR — 10% per decade after age 30. The kidneys are the primary route of elimination of most drugs and their metabolites.
Assessment of eGFR or creatinine clearance is often required to adjust drug therapy; determine renal function using the Cockcroft-Gault equation.
Normal creatinine clearance: males younger than 40 years 107–139 mL/min; females younger than 40 years 87–107 mL/min. Values decrease by about 6.5 mL/min for every 10 years after age 20.
Reduced bladder elasticity, muscle tone, and capacity
Increased postvoid residual and nocturnal urine production
Decreased testosterone leads to an increased estrogen-to-androgen ratio; decreased sperm motility; increased incidence of gynecomastia
Slowed arousal and increased time to achieve erection; erection less firm and shorter lasting; delayed ejaculation and decreased forcefulness; longer interval to subsequent erection

Clinical implications

How to take the history

Many men are overly sensitive about complaints of the male genitourinary system and are often not inclined to initiate discussion or seek help — take an active role in screening with an approach that is open, trustworthy, and nonjudgmental.
Sexual function remains important to many men, even at 80 years and older. Lack of an available partner, poor health, erectile dysfunction, medication adverse effects, and lack of desire are the main reasons men do not continue to have sex. Acute and chronic alcohol use can lead to impotence.
Nocturia is reported in 66% of patients over 65 years, due to impaired ability to concentrate urine and reduced bladder capacity or BPH — a frequent cause of insomnia.
The digital rectal exam is almost universally dreaded by men — provide privacy and allow for dignity.
In men diagnosed with BPH, periodic evaluation for prostate cancer must continue.
A man may decline treatment for BPH because of fear of erectile dysfunction.

Possible findings in the older adult — decreased drug clearance

Decreased drug clearance increases the risk of: adverse drug reactions · nephrotoxicity · renal complications · volume/fluid overload (especially in heart failure patients) · hyponatremia and dehydration (especially in patients taking thiazide diuretics) · hypernatremia (especially in patients with fever) · hyperkalemia (especially in patients taking potassium-sparing diuretics) · metabolic acidosis · urinary urgency · incontinence · UTIs · polyuria at night · falls.

Lecture deck · Penile Shaft Fracture

Penile Shaft Fracture

A penile fracture is the traumatic rupture of the corpus cavernosum and the encompassing tunica albuginea. It may involve the corpus spongiosum and the urethra. Hematoma formation occurs at the rupture site, and the injury is usually unilateral and transverse, with the most common fracture site the proximal shaft of the penis.

Source note

Like the bladder dysfunction section, this topic comes from the week7_GU.pptx lecture deck rather than the three assigned chapters. It is on the deck's topic list and in the Week 7 practice-question set.

25–30%

have an associated urethral injury

The injury may be partial or complete — which is why the urethrogram comes before the catheter.

Proximal

shaft is the most common site

Usually unilateral and transverse, with the hematoma at the rupture site.

Delay

is the major cause of morbidity

Penile fracture is not a rare occurrence — and it is mainly a clinical diagnosis.

Mechanism

Why an erection makes it vulnerable

During erection, pressure within the corpus cavernosum is maximal, close to arterial pressure, increasing the volume in each corpus to maximum, which thins the tunica albuginea, making it susceptible to rupture.

Penile erection stretches the spongiosum to the limit, which limits movement vertically while allowing lateral movements; this forms a bend at the base of the penis, making it vulnerable to lateral swing and rupture of the corpus cavernosum.

Causes

Blunt trauma to the erect penis

Sexual intercourse
Manipulation
Fall on the erect penis
Entanglement in clothing
Taghaandan — the Middle Eastern practice of forcefully bending the erect penis to cause detumescence

Predisposing factors

Peyronie disease
Urethritis in the past
Surgical procedure on the corpus cavernosum, or trauma to the corpus cavernosum resulting in weak scar tissue

Signs and symptoms

History

What the patient reports

A loud popping or crunching sound heard at the time of injury
Immediate detumescence
Severe penile pain
Deviation of the penis away from the side of injury
Penile swelling and ecchymosis
Blood at the urethral meatus if there is a urethral injury
Dysuria, inability to void, or an increase in the size of the swelling with voiding, due to extravasation of urine

Interviews to complete

The questions that date the injury

Cause of the injury
Sudden painful sensation in the erect penis during sexual intercourse or soon after, with loss of erection
Blood at the urethral meatus after intercourse
Problems with poor erections after the injury if presentation is delayed
Penile deviation with erection
Urinary retention or weak urinary stream

Physical examination — and the finding that changes the plan

Swelling and blue-black discoloration at the base of the penis, usually on one side
Ecchymosis may also involve the scrotum
Penis flaccid and edematous with angulation away from the side of the tear
A defect in the penile shaft may be palpable at the site of the tear
Blood at the tip of the penis or frank hematuria suggests an associated urethral injury
Urethrocavernous or urethrocutaneous fistulas may be present as late complications of a penile fracture

Workup

Essential workup and diagnostic testing
Study	Why
Urinalysis	To evaluate urethral trauma — may have frank blood or microscopic hematuria.
PT / PTT	If the patient is on Coumadin or has a history of a bleeding disorder.
Retrograde urethrography	Recommended in all cases of suspected urethral trauma. Should be done with low pressure during injection, and before urethral catheterization.
Cavernosography, MRI, ultrasonography	May be needed to confirm the diagnosis and site of the tear. Ultrasonography may also be done to confirm a suspected tear.
Diagnostic exploration	Recommended when cavernosography is negative but clinical suspicion of a fracture is high.

The sequencing rule

Retrograde urethrography comes before urethral catheterization. Catheterize only after urethral trauma has been excluded. Then:

Urologic evaluation and early surgical treatment are essential to prevent complications such as erectile dysfunction, impotence, penile deformity, and urethral stricture. All patients with a suspected or definite diagnosis must have early urologic evaluation.

Treatment

Local measures only

What ice and a tongue blade actually do

Ice packs to the penis; splinting of the penis with a tongue blade — these are local hemorrhage control, nothing more.
Prophylactic antibiotic use is unnecessary.
ED treatment is directed toward reducing hemorrhage and preventing further complications.

Definitive

Surgery, and where the patient goes

Combined efforts of provider and urologist are aimed toward restoration of normal shape of the penis and sexual and urinary functions.
All patients with penile fracture must be hospitalized for prompt surgery.
If immediate urologic consultation and treatment are unavailable, the patient may be transferred to a suitable hospital after initial stabilization and transfer criteria have been met.
Follow up with a urologist to ensure adequate repair and return to normal sexual and urinary function.

Pearls and pitfalls

Penile fracture is not a rare occurrence.
Coitus and penile manipulation are the most common causes.
Delay in seeking treatment is the major cause of morbidity.
It is mainly a clinical diagnosis — cavernosography, MRI, and ultrasound may be used to confirm it.
Early surgical repair is important.

Coverage check

Where Week 6 ends and Week 7 begins

Week 6 was Genitourinary Disorders I and Week 7 is Genitourinary Disorders II, so it is fair to ask whether the two overlap. They do not: Week 6 taught the kidney's frameworks, and Week 7 teaches the lesions that break them. Nothing in the five Week 7 topics is taught as a topic in Week 6, and nothing from Week 6 is re-taught here.

Which week owns which topic
Topic	Taught in	Where it comes up the other week
UTI, CAUTI, cystitis, urethritis, prostatitis	Week 6 · Ch. 42	Urethritis is listed as a cause of acute urinary retention; prostatitis and bladder neck contracture are prostatic causes of AUR.
Pyelonephritis & urosepsis	Week 6 · Ch. 42	Sepsis is an admission criterion for AUR, and hypotension with altered mental status in a stone patient suggests urosepsis.
Glomerulonephritis & nephrotic syndrome	Week 6 · Ch. 42	No overlap with Week 7.
AKI — prerenal, intrarenal, postrenal; acute tubular necrosis	Week 6 · Ch. 43	Week 6 named calculi, tumors, urethral strictures, and BPH as the mechanical causes of postrenal AKI. Week 7 teaches those lesions in full — the framework stays in Week 6.
CKD staging, renal replacement therapy, drug dosing in renal impairment	Week 6 · Ch. 43	RAS and unrecognized obstruction both end in chronic kidney disease if missed; the geriatric drug-clearance material in Ch. 44 assumes the Week 6 dosing rules.
Sodium, potassium, calcium, magnesium, phosphorus	Week 6 · Ch. 78	RAS produces hypokalemia and metabolic acidosis. The older-adult risk list in Ch. 44 is a list of the very imbalances Week 6 taught.
Acid–base disorders	Week 6 · Ch. 78	Metabolic acidosis is one of the ten circumstances that should make you consider RAS.
Intravenous fluid management	Week 6 · Ch. 78	Stone hydration and postobstructive diuresis after catheter decompression are both fluid problems.
Renal artery stenosis	Week 7 · Ch. 45	Week 6 mentions it only in passing, as a secondary cause of metabolic acidosis and as a line in a perfusion list.
Nephrolithiasis	Week 7 · Ch. 46	Week 6 mentions "calculi" only as a cause of obstruction and as a reason to image.
Benign prostatic hyperplasia	Week 7 · Ch. 44	Week 6 mentions BPH only inside the postrenal AKI cause list and a one-line caution about sympathomimetics.
Bladder dysfunction & acute urinary retention	Week 7 · lecture deck	Not covered in Week 6 at all.
Penile shaft fracture	Week 7 · lecture deck	Not covered in Week 6 at all.

The three places the two weeks actually touch

Bridge 1

Obstruction → postrenal AKI

Week 6 gave you the AKI framework and its urine-output and creatinine criteria. Week 7 hands you the obstructing lesions: a stone, a hyperplastic prostate, a urethral stricture. When both collecting systems are obstructed by stones, oliguria and acute renal failure follow — that sentence in Ch. 46 is Week 6 and Week 7 meeting.

Bridge 2

Ischemia → ischemic nephropathy

Week 6 listed renal artery stenosis as a cause of metabolic acidosis and as a perfusion problem. Week 7 is where that entity lives: reduced flow, renin release, hypertension, and a kidney that atrophies while the other one is scarred by the pressure.

Bridge 3

UTI → struvite stone

Week 6 taught the UTI and named the urease-producing organisms. Week 7 is where they do their damage: Proteus, Klebsiella, Haemophilus, and Ureaplasma split urea, push urine pH above 7–7.5, and grow a magnesium–ammonium–phosphate stone.

Bottom line on coverage

No topic is taught twice. The five Week 7 topics are new; the Week 6 topics stay in Week 6.
Nothing falls in the gap. The cross-references happen deliberately: RAS is taught as "fibromuscular dysplasia or atherosclerosis," not re-taught as "a cause of CKD."
There is no Chapter 27-style duplication here. Chapters 44, 45, and 46 are assigned only in Week 7.
When a question asks about AKI staging or CKD management, it is a Week 6 question. When it asks about a pressure gradient, a stone size, a postvoid residual, or a French catheter, it is a Week 7 question.

For Study

What to lock in

Five topics, five currencies: a pressure gradient, a stone size, a urine pH, a postvoid residual, and a urethrogram. Each card below is a number or rule that changes what you do next.

Split it

The two types of RAS

Fibromuscular dysplasia < 10% — fibrous tissue in the vessel lining, ages 25–50, about 90% women. Atherosclerosis > 90% — men older than 45 and women older than 55, with hypertension, high cholesterol, insulin resistance or diabetes, smoking, and inactivity.

Suspect it

When RAS is the answer

Sudden hypertension at < 30 or > 55 years; previously controlled hypertension now resistant on three or more agents; malignant, accelerated, or resistant hypertension; no family history; flash pulmonary edema; an epigastric bruit; asymmetric kidneys on ultrasound; and an eGFR fall of more than 30% after starting an ACEI or ARB.

Get the direction right

RAS electrolytes

Hypokalemia and metabolic acidosis from renin–angiotensin activation. Not hyperkalemia, not alkalosis. BUN and creatinine rise only after significant ischemia, so a normal creatinine proves nothing.

Name the gold standard

Intra-arterial DSA

The definitive test. 50–70% stenosis counts as significant when there is a resting translesional mean gradient ≥ 10 mmHg, a hyperemic peak systolic gradient ≥ 20 mmHg, or a renal flow reserve ≤ 0.8.

Treat it

ACEI or ARB first

Plus a statin and antiplatelet therapy, lifestyle change, and a BP goal of < 130/80 mmHg. Start low, titrate up, and recheck BP, kidney function, and electrolytes within 2 weeks. Minoxidil is reserved for the unresponsive.

Revascularize it

The AHA threshold

> 70% of the diameter, or 50–70% with a significant gradient, plus uncontrolled hypertension on three agents one of which is a diuretic, ischemic neuropathy, or unstable angina or CHF. Statins may induce regression of RAS.

Composition

The 80% calcium rule

80% of renal calculi are calcium, with calcium oxalate more common than calcium phosphate. Uric acid is about 5%. 90% of urinary calculi are radiopaque.

Read the pH

Struvite vs. uric acid

Struvite — urine pH > 7–7.5, driven by urease-splitting organisms; treat the infection. Uric acid — urine pH < 5.5; raise it above 6.5 to dissolve the stone.

Image it

CT, except in pregnancy

Noncontrast helical CT is the test of choice — finds stones to 1 mm, sensitivity 95%, specificity 98%, no contrast, and it also finds an AAA. Ultrasound is the modality of choice in pregnancy; avoid NSAIDs, especially in the third trimester.

Dose it

Ketorolac

30–60 mg IM or 30 mg IV, alone or with an opioid — the combination beats either alone. Reduce to 30 mg IM or 15 mg IV if older than 65 years or under 50 kg. Avoid in renal dysfunction.

Flush it

2–3 L to pass a stone

Oral intake of at least 2–3 L per 24 hours, targeting a urine output of at least 2 L per day. Medical expulsive therapy with an α-blocker or nifedipine hastens passage by 5–7 days.

Measure it

The postvoid residual

AUR is the sudden inability to void spontaneously, most frequent in men older than 60, and the most common ED cause is BPH. A postvoid residual greater than 200 mL is usually considered abnormal.

Walk the ladder

Catheter sizes in order

14–18F first → 10–12F if there is a prior transurethral procedure or known stricture → 20–22F coudé in a man with no prior instrumentation → suprapubic aspiration or catheter.

Stop

The trauma exception

Defer catheterization for gross hematuria, a high-riding prostate, or blood at the meatus until a retrograde urethrogram is done. The same rule governs penile fracture: urethrography before catheterization.

Remember

Prostate size proves nothing

DRE size does not correlate with symptom severity or degree of obstruction. A 5ARI needs 6 months for maximal effect. Focal enlargement, nodularity, or extreme hardness suggests malignancy — go to TRUS and biopsy.

Self-Check

Rapid-fire review

19 questions covering all five topics and all three chapters. Answer out loud first, then reveal.

Define renal artery stenosis and ischemic nephropathy.

RAS is a stenosis or narrowing in the lumen of the renal arteries. Ischemic nephropathy is the decreased GFR that results from a hemodynamically significant stenosis. RAS is a progressive disease in which vascular supply is reduced and perfusion to the kidney leads to gradual loss of renal function due to ischemia and eventual death of the organ.

Which type of RAS accounts for fewer than 10% of cases, and who typically gets it?

Fibromuscular dysplasia — less than 10% of RAS, due to an abnormality in the lining of the renal artery in which fibrous tissue forms and narrows the vessel. It occurs in ages 25–50 years and mostly in women (90%), although men tend to have more aggressive forms. Fewer than 8% of patients had a family member with the condition. Atherosclerosis accounts for more than 90% of cases and is typically seen in men older than 45 and women older than 55.

Which change in kidney function after starting an ACEI or ARB should make you consider RAS?

A decline in estimated GFR by more than 30% from baseline renal function after initiation of an ACEI or an ARB. That is one of the ten circumstances in which RAS should be considered — alongside sudden hypertension at younger than 30 or older than 55 years, previously controlled hypertension that has become difficult to treat despite three or more agents, malignant or accelerated or resistant hypertension, no family history of hypertension, unexplained heart failure or "flash" pulmonary edema, asymmetric kidneys on ultrasound, epigastric or renal artery bruits, atherosclerotic disease of the aorta or peripheral arteries, and metabolic acidosis.

What two electrolyte and acid–base abnormalities does RAS produce — and what does it not produce?

Hypokalemia occurs from activation of the renin–angiotensin system in response to decreased blood flow to the kidney, and metabolic acidosis is one of the circumstances that should prompt consideration of RAS. It does not produce hyperkalemia or metabolic alkalosis. Note also that BUN and serum creatinine are elevated only once significant ischemia has occurred.

What is the definitive diagnostic test for RAS, and what makes a 50–70% stenosis "significant"?

Intra-arterial digital subtraction angiography — currently the gold standard. A visual stenosis measurement of 50–70% with one of the following is deemed significant and may require intervention: a resting translesional mean pressure gradient of ≥ 10 mmHg; a hyperemic peak systolic pressure gradient of ≥ 20 mmHg; or a renal flow reserve ≤ 0.8. The most direct measure of hemodynamic significance is the differential pressure across the stenosis.

Which two RAS tests are no longer recommended?

Captopril renal scintigraphy and the captopril test — ACC/AHA guidelines no longer recommend them for diagnosing RAS, although they may still be used to guide revascularization decisions when determining hemodynamic severity. Renal vein renin sampling and peripheral renal levels are not generally recommended due to low specificity and sensitivity.

What is first-line drug therapy in RAS, what is the BP goal, and when do you recheck labs?

ACE inhibitors or ARBs are considered first-line treatment, combined with a statin and antiplatelet therapy such as aspirin, on a foundation of lifestyle change. The recommended BP goal is < 130/80 mmHg. Start all medications at lower doses and titrate up after evaluating response. Because these agents can cause acute renal failure and further decline in GFR in RAS, patients should have their BP, kidney function, and electrolytes checked within 2 weeks of starting medication. Many individuals require two or more medications to reach goal.

When does the AHA recommend revascularization for RAS?

When the renal artery is reduced by more than 70% of its diameter, or when there is 50–70% stenosis with a significant hemodynamic gradient across the stenosis, along with: uncontrolled hypertension on three agents, one of which is a diuretic; ischemic neuropathy; or exacerbation of other cardiac disorders, to include unstable angina or CHF. Risks include hemorrhage and contrast-induced nephropathy. For fibromuscular dysplasia, treat with PTRA first and reserve surgery for PTRA complications or recurrent stenosis.

What percentage of renal calculi are calcium, and which calcium salt is more common?

Calcium stones constitute 80% of renal calculi, and calcium oxalate is more common than calcium phosphate. Uric acid is next at about 5%, followed by struvite and cystine. 90% of urinary calculi are radiopaque.

Which stone type forms at a urine pH greater than 7–7.5, which organisms cause it, and how is it treated?

Struvite — magnesium–ammonium–phosphate stones. They are commonly seen in women with recurrent urinary tract infections, most are large and cause obstruction and bleeding, they are radiodense, and the urinary pH is high (> 7–7.5). They are caused by urease-producing organisms — Proteus sp., Haemophilus sp., Klebsiella sp., and Ureaplasma urealyticum. Treatment requires eradicating the infection with antibiotics plus interventional techniques; the stones are soft and amenable to percutaneous nephrolithotomy or extracorporeal shock wave lithotripsy. Medical options include acetohydroxamic acid, an effective but poorly tolerated urease inhibitor, and surgery is considered for stones > 10 mm or ongoing obstruction or infection.

A patient has uric acid calculi. What urine pH do you expect, and what is the treatment target?

Uric acid calculi are frequently associated with urinary pH levels lower than 5.5. Increasing the pH to levels higher than 6.5 can dramatically increase solubility and dissolve large stones. Treatment also includes allopurinol 300 mg PO daily (adjust for renal dysfunction; doses > 300 mg divided BID) and potassium citrate 10–20 mEq PO TID with meals, plus reduced protein, purine restriction, and reduced or eliminated alcohol.

What is the test of choice for nephrolithiasis, and what is the imaging modality of choice in pregnancy?

Noncontrast helical abdomen/pelvis CT is the gold standard radiographic test — it detects calculi as small as 1 mm, has sensitivity 95%, specificity 98%, and accuracy 97%, requires no IV contrast, and can detect other nonurologic causes such as an AAA. In pregnancy, every effort should be made to minimize ionizing radiation to the fetus, and ultrasound is the imaging modality of choice — hydronephrosis sensitivity 85–94%, specificity 100%, though it may miss stones smaller than 5 mm.

Give the ketorolac dose for renal colic, and the reduced dose.

Ketorolac 30–60 mg IM or 30 mg IV, alone or with opiates. Reduce the dose to 30 mg IM or 15 mg IV if the patient is older than 65 years or weighs less than 50 kg. Parenteral NSAIDs are as effective as narcotics for renal colic, and combining IV NSAIDs with opioids decreases ED stay and provides better pain control than either alone. Avoid NSAIDs in patients with renal dysfunction, as parenteral NSAIDs may lower kidney blood flow and glomerular filtration.

How much fluid do you give to hasten stone passage?

Induce high urine flow with oral intake of at least 2–3 L of fluids per 24 hours to ensure a urine output of at least 2 L per day. The slides add an IV route: 1 L of normal saline infused over 30–60 minutes followed by 200–500 mL/h, bolusing volume-compromised patients in 500 mL increments until urine output is adequate. Medical expulsive therapy — an α-blocker (doxazosin 4 mg, tamsulosin 0.4 mg, or alfuzosin 10 mg daily) or nifedipine 30 mg daily — has been shown to hasten stone passage by 5–7 days.

Define acute urinary retention, name the most common ED cause, and state the abnormal postvoid residual.

AUR is the sudden inability to void spontaneously. It occurs most frequently in men older than 60 years, and the most common cause of AUR in the emergency department is benign prostatic hyperplasia. A postvoid residual greater than 200 mL is usually considered abnormal. Acute retention is painful — lower abdominal or suprapubic discomfort with a restless or distressed patient — whereas chronic urinary retention is usually painless.

Give the catheter decompression ladder for AUR, and state the trauma exception.

Step 1: try a 14–18F urinary catheter. Step 2: if unable to pass it and there is a history of a prior transurethral procedure or known stricture, downsize to a 10–12F. Step 3: in men with no prior instrumentation in whom a catheter will not pass, consider a 20–22F catheter with a coudé tip. Step 4: if a catheter still cannot be passed, suprapubic aspiration as a temporizing measure or placement of a suprapubic catheter. Trauma exception: defer catheterization in the trauma patient suspected of urethral injury — gross hematuria, a high-riding prostate on rectal examination, or blood at the meatus — until a retrograde urethrogram has been done.

In BPH, does prostate size on DRE correlate with symptoms? What findings suggest malignancy, and how long does a 5ARI take to work?

Size does not correlate with severity of symptoms or with degree of obstruction. The prostate should feel smooth and rubbery. Focal enlargement, nodularity, or extreme hardness may represent malignancy, and further investigation is indicated with transrectal ultrasound and biopsy. A 5-alpha reductase inhibitor such as finasteride 5 mg/day or dutasteride 0.5 mg/day works on the epithelial component by blocking conversion of testosterone to dihydrotestosterone — and six months of therapy is required for maximal effect.

Describe the two mechanisms by which medications worsen BPH.

First, decongestants, diuretics, and other sympathomimetics act on α receptors to enhance prostate muscle tone, which increases dynamic obstruction. Second, anticholinergics (antihistamines), bowel antispasmodics, tricyclic antidepressants, opiates, and antipsychotics decrease bladder muscle contraction, thus increasing urine retention. This is why a medication review — including over-the-counter products — is mandatory when a previously stable patient suddenly worsens.

In penile shaft fracture: what ruptures, what is the most common site, what percentage have a urethral injury, and what must precede catheterization?

The corpus cavernosum and the encompassing tunica albuginea rupture; the injury may involve the corpus spongiosum and urethra. The injury is usually unilateral and transverse, and the most common fracture site is the proximal shaft of the penis. 25–30% have an associated urethral injury, which may be partial or complete. Retrograde urethrography is recommended in all cases of suspected urethral trauma — performed with low pressure during injection and before urethral catheterization. Prophylactic antibiotics are unnecessary. All patients must be hospitalized for prompt surgery, because early surgical repair prevents erectile dysfunction, impotence, penile deformity, and urethral stricture.

References

Sources

The three assigned chapters for Week 7, plus the lecture deck that supplies the two additional topics.

Assigned chapters

Langley, K. J., & Talley, M. H. (2021). Renal artery stenosis. In Practice considerations for adult-gerontology acute care nurse practitioners (3rd ed., Chapter 45, pp. 684–692). Los Angeles, CA: Barkley & Associates.

Couture, M. (2021). Nephrolithiasis. In Practice considerations for adult-gerontology acute care nurse practitioners (3rd ed., Chapter 46, pp. 693–703). Los Angeles, CA: Barkley & Associates.

Roberg, J. J. (2021). Benign prostatic hyperplasia. In Practice considerations for adult-gerontology acute care nurse practitioners (3rd ed., Chapter 44, pp. 673–683). Los Angeles, CA: Barkley & Associates.

Lecture material

Gantioque, R. (2026). Genitourinary disorders II [PowerPoint slides]. NURS 5163, School of Nursing, California State University, Los Angeles. week7_GU.pptx, 56 slides. Source of the bladder dysfunction / acute urinary retention and penile shaft fracture sections.

N5301 Week 07 — October 5 — Genitourinary Disorders [Course reading]. (2026). California State University, Los Angeles, School of Nursing.

Selected sources cited in the reading

Bavishi, C., de Leeuw, P., & Messerli, F. (2016). Atherosclerotic renal artery stenosis and hypertension: Pragmatism, pitfalls, and perspectives. The American Journal of Medicine, 129(6), 635.e5–635.e14.

Murphy, T. P., Cooper, C. J., Pencina, K. M., D'Agostino, R., Massaro, J., Cutlip, D. E., . . . Tuttle, K. R. (2016). Relationship of albuminuria and renal artery stent outcomes: Results from the Cardiovascular Outcomes with Renal Artery Lesions (CORAL) randomized clinical trial. Hypertension, 68(5), 1145.

Smith-Bindman, R., Aubin, C., Bailitz, J., Bengiamin, R. N., Camargo, C. A., Corbo, J., . . . Cummings, S. R. (2014). Ultrasonography versus computed tomography for suspected nephrolithiasis. The New England Journal of Medicine, 371(12), 1100–1110.

Pearle, M. S., Goldfarb, D. S., Assimos, D. G., Curhan, G., Denu-Ciocca, C. J., Matlaga, B. R., . . . American Urological Association. (2014). Medical management of kidney stones: AUA guideline. The Journal of Urology, 192(2), 316–324.

Foster, H. E., Barry, M. J., Gandhi, M. C., Kaplan, S. A., Kohler, T. S., Lerner, L. B., . . . McVary, K. T. (2019). Benign prostatic hyperplasia: Surgical management of benign prostatic hyperplasia / lower urinary tract symptoms. Linthicum, MD: American Urological Association.

McVary, K. T., Roehrborn, C. G., Alvins, A. L., Barry, M. J., Bruskewitz, R. C., Donnell, R. F., . . . Wei, J. T. (2011). Update on AUA guideline on the management of benign prostatic hyperplasia. The Journal of Urology, 185(5), 1793–1803.

Week 7 · Genitourinary Disorders II — built from N5301 Week 07 - Oct 5 - Genitourinary Disorders.pdf (Chapters 45, 46, and 44) and week7_GU.pptx. Every dose, threshold, and duration above was checked back against those sources, and the places where the deck and the chapters disagree are flagged in the section where they occur rather than silently reconciled. Single self-contained HTML file: fully offline, no login, no external dependencies. Press Cmd+P to print with every section expanded.

Study material — verify before clinical use.