Renal Exam 3 OH.pdf

● ● Exam 3 Study Guide-Renal 50 questions - 75 min ○ ~10 questions/lecture (a little more CKD but otherwise pretty equal) ○ 3 short answer – captain obvious things (no guarantee but potentials here) ■ Causes of prerenal, intrarenal, obstruction AKI? – pre/intra = nephrotoxic agents ■ What electrol...

● ● Exam 3 Study Guide-Renal 50 questions - 75 min ○ ~10 questions/lecture (a little more CKD but otherwise pretty equal) ○ 3 short answer – captain obvious things (no guarantee but potentials here) ■ Causes of prerenal, intrarenal, obstruction AKI? – pre/intra = nephrotoxic agents ■ What electrolytes are we concerned about? ■ What kind of casts would we see depending on type/location? ■ List 3 nephrotoxic agents sold OTC → NSAIDs (Aspirin, Ibuprofen), PPIs ○ Will be given reference ranges for ABG/BMP/etc to calculate acid base parameters REAL OH Notes form 7/17 at the bottom: Chronic Kidney Disease ● Major high points: how to use the result to factor in when you are diagnosing and staging CKD ● Who is most affected?/Who are we screening? ○ DMII (annually), HTN, PCKD, CVD, family hx ○ PCKD-Polycystic Kidney Dz: MC genetic kidney condition (Alex loves it) ■ Uncontrolled growth of cysts leads to kidney failure ■ Asymptomatic till 30-40, family hx – autosomal dominant! ■ Dx: If any family hx – urine spot microalbumin, K+ levels, renal US ■ Sx: Chronic hematuria, frequent UTI, flank pain, HTN, cysts elsewhere ■ Tx: Early intervention, ACEI, control BP, low Na diet, avoid nephrotoxins ● What test? ○ SCr – diagnostic – will rise fairly slowly so helps with tracking progress ○ GFR – staging – tells us additional info on blood flow/filtration in kidney (<60) ○ Urine albumin/creatinine ratio – prognostic indicator – tells us how sick within their class ■ Albumin–how much protein is spilling into urine. At a certain criteria→CKD ● First indicator of CKD ● How much protein spilling in 24hrs, most sensitive indicator → hard to test so instead we estimate the average protein lost in 24hrs using creatinine/albumin ratio → urine spot microalbumin test ○ Monitor serum electrolytes: K+ ○ Renal US: small kidneys (hallmark of CKD), cysts, stone or structural abnormality ● Presentation: Most commonly asymptomatic w/ RFs (Once pt is symptomatic → already severe) ● Ex Case: 65 yo with DMII presents to clinic for follow up on elevated SCr, reference range then and now, GFR now, suspect CKD (with chart) ○ Question: what stage he has and what relevance of proteinuria is? Better or worse prognosis? Would you send to nephrology? ● ● How to prevent progression – know this is a progressive condition and irreversible ○ ○ ● ● Goal: Slow the progression (preserve kidney fx) and prevent end-stage disease Screen HR pts, treat comorbid conditions, refer to nephrology early, when to start dialysis ■ ACEi/ARB, glucose control, statins, avoid nephrotoxin, low Na/K/phosphorus diet ○ Nephrotoxins: NSAIDs, contrast, lithium, acyclovir/valacyclovir ○ Stop ACEi/ARB if: acute renal failure, hyperkalemia, hypovolemia, GFR <15 (likely not a specific question bc she said everyone will be different deciding this) ○ Regain function: Some GFR back if acute problem but generally will decrease over time–slowly in healthy pt and quick in sick ○ Refer for dialysis when ESRD–GFR <15, or emergent status (hyperkalemia, PE, severe metabolic acidosis, fluid overload, neuro sx (neuropathy, sz), critically ill pt) End-stage (<15) ○ Tx: dialysis and renal replacement ○ Types–hemodialysis, peritoneal dialysis, continuous renal replacement therapy ○ Replacement–younger, healthy pt, no comorbidities, PCKD (most common reason) Complications of CKD (not mentioned in OH but hella slides on it) – almost all organ systems ○ Reduced kidney fx: ↓GFR, ↑BUN, ↑SCr, electrolyte imbalance ○ Cardio-renal syndrome: untreated HTN causes CKD and CKD worsens HTN ○ Hyperkalemia, pericardial effusion, anemia of chronic dz (↓Epo), neurologic sx, neuropathy, mineral/bone disorders, derm sx, immune consequences, hyperphosphatemia, thyroid probs, insulin/glucose metabolism, low estrogen/testosterone, pregnancy complications Acute Kidney Injury (Focus on big picture) – what category is it in and why does that matter? ● Who is most at risk? Hospitalized, 65+, HTN, CKD, liver failure, heart disease (CHF), COPD, DM ● Pt pres: Acutely ill and often hospitalized (maybe sepsis, maybe pre-renal injury) ○ Urine output – Ins and outs = how much fluid is going in and how much is going out ■ Oliguria – relatively late finding (parameters given), helps dx ○ Patient decline, confusion, bloody urine, edema, drug reaction, purpura ● What constitutes acute renal injury aka definition? ○ Rapid/dramatic Rise SCr relative to kidney not being able to do its job (↓GFR) ○ Nml: Filter, reabsorb, secrete → excrete ○ AKI: Filtration→rapid ↓GFR, Reabsorption→↓reabsorption of electrolytes, H2O, Secretion →impaired secretion of toxins from vasa recta to tubule, Excretion→blocked & backs up ○ Think – Loop and proximal tubule – what should be there/what shouldn’t ■ Sodium, chloride, potassium, water, electrolytes, toxins ■ NSAIDS HARM THE KIDNEY – definitely a question ○ REVERSIBLE if we treat the underlying problem (differentiates from CKD) ● How fast does it develop? (if someone has a different answer pop it in) ○ Sudden: 1-7 days & Persistent >24hrs ● Diagnosis ○ SCr: gold standard for ID AKI ■ Need another to compare → rapid rise is the definition → >1.5x baseline SCr ■ amount/rate of rise will tell us if they have or are heading towards an acute injury (will be given reference range) ○ SCr, GFR (helps w/ dx), K+ = 3 labs of diagnosis ○ UA will tell us if there’s proteinuria or hematuria and urine output can help (not required) ○ BUN–more sensitive to metabolic activity, hydration status ■ ● High but SCr normal→ratio favors BUN→check if pt is hydrated/find other cause // if not → hydrate the pt and will balance ■ BUN is much more transient, if super high = uremic syndrome (SICK) Categories of acute renal injury (based on the functions of the kidney) ○ Pre-renal – most common ■ Not enough blood for whatever reason → low BP in glomerulus → less filtering ● Kidneys are working fine! Often reversible if you can restore BF! ■ Low BP = low hydrostatic pressure → Creatinine isn’t pushed out (rise in SCr) ■ Causes: Hypovolemia (v/d), decomp CHF (not enough fluid in vasculature to get to kidneys), Liver failure, near-sepsis, bleeding, anaphylaxis (fluid can’t get where needed), NSAIDs (afferent constriction) or ACEI/ARBs (efferent dilation) ■ What will we see in the rest of the patient? ● Difficulty managing fluids, electrolytes, toxins ● Elevated BUN (Azotemia), build up of toxins, elevated K – risk of arrhythmias, fluid overload, low Na ● SOB, swollen, hyponatremia (where sodium goes water goes) ● Fractional excretion of Na is low → losing the sodium earlier (normal if pre-renal because nephrons are working) ■ Tx: restore BF & BV, restore CO, fluids/electrolytes, treat underlying causes ■ Case: Pt brought in to ED vomiting, diarrhea, ALOC ● What kind of AKI? Pre-renal ○ Intrarenal (parenchymal) ■ 2 Main Causes: prerenal, immune-related (or postrenal from Hydronephrosis) ■ Not receiving blood flow (pre-renal issue) → low filtration → kidney can’t get nutrients it needs or rid of waste → begins to necrose/fail ■ 4 categories of causes: Glomerulonephritis, Tubular, Interstitial, Vascular ■ Fractional excretion of urine is higher here – oliguria ■ Acute Glomerulonephritis (aka “Nephritic Syndrome” – common in kids; strep) ● Inflamed, ineffective basement membrane → things get through ○ RBCs & protein (less than -otic), RBC casts, WBC casts (if infx) ○ ^ causes anemia & hypoalbuminemia ● Causes: immune problem → current infx or abnormal/autoimmune, endocarditis, Lupus-adults (SLE), SICK kid ● Children & Adolescents – Post-strep (can cause nephritic/nephrotic) ○ IgA nephropathy (Berger’s) vs. IgA Henoch-Schonlein Purpura ■ Berger’s: IgA deposition in glomerulus (only affects kidney) ■ Henoch: systemic IgA → palpable purpura (vasculitis) & arthritis ● Adults ○ Goodpasture Syndrome → autoimmune kidneys AND lungs ■ Hematuria & Hemoptysis; needs plasmapheresis ● Classic triad = Edema (everywhere), Hematuria, HTN (ehh like you dgaf) ● Labs: UA cola/rust-colored urine, sub-nephrotic proteinuria (< 300mg), Azotemia (Creatinine > 1.2; BUN > 20mg) ● Tx: treat the Triad of things wrong with the pt (and antibiotics if infx) ○ Edema & fluid overload → loop diuretics ○ HTN → salt/fluid restriction, loops, antihypertensives ○ Inflammation → Corticosteroids ● Electrolyte problems, toxins build up, Na/K imbalance, fluid overload Acute Tubular Necrosis (ATN) – MCC in hospitalized pts; pre-renal cause ● Causes: sepsis, meds, contrast, rhabdo, prolonged prerenal AKI ● Fractional Excretion of Na+ is high (>3%) ● RF: hospitalized/sick, Diabetes, CV disease, underlying CKD ● Pt pres: HTN, oliguria, edema (check for sacral!), n/v, ALOC ● Labs: ↓ GFR, ↑ SCr, Hyperkalemia, Muddy brown casts (necrotic cells) ● Tx: treat underlying cause, manage fluids & electrolytes ■ Acute Interstitial Nephritis (AIN) ● Causes: ATN, nephrotoxins, pyelonephritis, immune-mediated (SLE) ● Classic Triad → Fever, Maculo Rash, Eosinophilia = Hypersensitivity rxn ○ Often in the setting of a systemic drug eruption ■ Vascular ● Causes: anything that affects macro/microvasculature (vasculitis, atherosclerosis, DM, malignant HTN, etc.) → ischemia → AKI ● Tx: treat underlying cause & reperfusion of kidney ■ Different casts associated w/ location of damage (sign something is wrong in tube) ● Red cell casts – glomerulonephritis or vasculitis ● White cell casts – acute interstitial nephritis ● Fatty casts – nephrotic syndrome or minimal change disease ● Muddy brown casts – acute tubular necrosis ○ Postrenal – easy, there's a blockage (calyces to urethra) ■ Kidney is fine, pee can’t get out, backup to kidney → hydronephrosis (moneyy) ● Kidney pressure is increasing → squishes tissue → ischemic ■ Backup causes increased hydrostatic pressure in Bowman’s so we start filtering in the wrong/opposite direction → INTO the glomerulus ■ MCC = BPH, 2nd cause = kidney stones (must be BILATERAL for AKI) ■ Pt presentation: anuria ■ NOT always AKI, just causes hydronephrosis – BOTH w/ blockage = AKI ■ Dx: kidney US → helical CT (CT is more info, definitive dx) ● Rise in SCr tells us AKI, US confirms hydronephrosis (diagnostic) ■ Tx: restore urine flow/remove the blockage ● stones commonly in vesicoureteral junction ■ Case: Pt presents, cannot pee, what are we going to order? What kind of AKI is the cause? Renal US (showing hydronephrosis) and post-renal Indications for Dialysis (AEIOU): Acidosis, Electrolyte disturbance, Intoxication w/ nephrotoxins, Overload (fluid), Uremic complications (pericarditis, platelet dysfx/bleeding) Prevention: ID risks, monitor fluid/electrolyte status, monitor renal function (BUN, SCr, GFR), remove and avoid nephrotoxins What are the complications? → Kidney Failure? ■ ● ● ● Acid-Base ● Use pt scenario and lab findings to determine: pH – 7.40 CO2 – 40 HCO3- -- 24 ○ LOW pH, HIGH CO2 = RESPIRATORY ACIDOSIS ○ HIGH pH, LOW CO2 = RESPIRATORY ALKALOSIS ○ HIGH pH, HIGH HCO3- = METABOLIC ALKALOSIS ○ LOW pH, LOW HCO3- = METABOLIC ACIDOSIS ● Questions of Evaluation: FOCUS ON #1, 2, +/- 3 ○ 1. Acidosis or Alkalosis? (check pH) ○ 2. Respiratory or Metabolic? CO2 and pH moving in the same or opposite directions? ■ SaMe direction = Metabolic; Opposite direction = Respiratory (idk helps me…) ○ 3. Who’s just trying to compensate? (check pH, CO2 and HCO3-) ○ 4. Is there an anion gap? (automatic metabolic acidosis if AG >20) NOT ON EXAM ○ 5. If a metabolic acidosis exists, is it “pure” or “mixed” disorder? – (likely not on exam!) Nephrotic vs Nephritic Syndrome ● Nephrotic vs Nephritic ○ Nephritic = inflammation & small loss of protein ○ Nephrotic = gross loss of protein (>3.5g/24hrs) ■ Bowman’s capsule problem ■ RBC in urine = filtration system is not working ● Hematuria – caused by Bowman's capsule = nephritic ○ Bladder cancer until ID otherwise ○ Glomerulus or urinary system (renal pelvis, ureter, bladder, urethra) ○ Check vasculature and check for injury in urinary system ○ Pt history → sx of infx, UTI or STI, painful/painless, change in flow, hx kidney disease, recent travel (parasitic – Schistosomiasis), TB ■ Painful = infx, stones, trauma, autosomal dominant polycystic kidney disease ■ Painless = bladder cancer (older male, smoker, occupational exposures) ● Mining, rubber workers, mechanics, painters, railroad & truckers ○ PE: is it infection, stone, renal parenchymal disease, or CANCER? (CA details @ end) ● ● ● ■ Infection → fever, suprapubic tenderness, CVA tenderness ■ Stone → acute flank/abd pain, Pacing, +/- CVA tenderness ○ Labs: UA, dip, microscopy, culture w/ sensitivity, sent home with screen to catch stone ○ Dx image: US bladder & renal scan (+/- Helical CT, IV Pyelogram) ○ Refer: Urology (cancer), Nephrology (nephritis), Gynecology (females)/UroGyn Proteinuria – happening at the layers ○ Spot microalbumin on ALL pts w/ CVD, HTN, DVT, Diabetes, fam hx of Kidney disease ■ Early & sensitive indicator of renal damage ■ Can be benign → if positive, repeat the test each visit! Persistent = go looking! ○ 3 filtering layers: Capillary endothelium → Basement membrane → Podocytes ■ Podocytes broken = no BM→ lose oncotic pressure and protein “pours out” ■ No longer outflow in bowman's capsule – hypoalbuminemia → Blood flow problem ■ No protein in blood → lost oncotic pressure everywhere so fluid starts leaking out = 3rd spacing = interstitial oedema → everywhere the skin is thin (Anasarca) such as eyes & scrotum → Nephrotic level protein loss ○ Causes: Benign (fever, acute illness, exercise, dehydration, stress, inflammation) ■ Pathologic = CKD, Glomerular, Tubular, Multiple Myeloma, Rhabdo) Nephrotic Syndrome (>3.5g protein in urine) ○ Massive proteinuria leading to hypoalbuminemia, hyperlipidemia & oedema ■ HLD because liver is trying hard to make proteins (glycoproteins) ○ Sx: sick, fatigued, foamy urine, edema everywhere, rapid weight gain, +/- Xanthelasma ○ Lab: UA (confirm proteinuria), SCr & GFR, serum albumin, lipid panel, HIV/Hep B&C ○ Primary Causes of Nephrotic Syndrome ■ Minimal Change Disease (little kid nephropathy) – peak 2-6yo, most idiopathic ● Responds well to corticosteroids ● Patho = ↑ permeability in all 3 layers ● Minimal change = GFR/SCr normal; thinning of podocyte foot processes ● Anasarca → huge edema all over especially eyes/face & scrotum ○ SWOLLEN UP CHILD! ● Do not give diuretics!! Depleted intravascular volume is too severe ■ Focal Segmental Glomerulosclerosis (MCC in adults) ● Caused by destruction of all 3 filtration layers, but segmented… ○ Due to infx, nephrotoxic drugs, DM, HTN, CVD, Lupus ● S/S of nephrotic syndrome with addition of HTN ● Hyaline & Waxy casts ● Ultimately leads to ESRD if unresponsive to therapy (corticosteroids) ○ Causes: DM, HIV, Lupus, Hep B/C, NSAIDs, Amyloidosis, Preeclampsia, HTN, CVD, MM Management of Nephrotic Syndrome ○ Maintain negative sodium balance (low salt diet) bc Na causes kidney to retain fluid, but it won’t stay in the intravascular space→ will just flow out into interstitial space and ↑ swelling! ○ Increase dietary protein intake (IV albumin doesn’t work) ○ Loop diuretics(better if ↓GFR) ↓fluid intravascularly so interstitial fluid moves→vasculature ○ ACEI (reduce proteinuria & renal protective), Corticosteroids, Statins Male GU (not really touched on in OH so quick overview–key ones = BPH and Prostatitis) ● Lower UTI ○ ● ● ● ● ● ● ● ● ● ● Symptoms ■ Storage–nocturia(hallmark of early BPH), frequency, urgency, incontinence ■ Voiding–hesitancy(second hallmark^), intermittency, slow/splitting/spraying stream, straining, terminal dribble, dysuria(NOT BPH) ■ Post-void–feeling of incomplete emptying, post-void dribble ○ Dx: H&P, PE +DRE, urine dip, culture & sensitivity (infection?), microscopy (renal prob?), cytology, urethral cultures, PSA, prostate US, testicular US, CT BPH – prostate >20g, MC benign tumor in men (age related) ○ Complications: urinary retention, recurrent UTI, bladder calculi, hematuria, bladder instability, renal impairment ○ Management: lifestyle/fluid management (avoid irritants–caffeine, etoh), drugs (alpha blockers–osins, 5alpha reductase inhibitors–Finasteride), refer to urology ■ Consider Transurethral Resection of Prostate (TURP) Prostatitis (know the 4 categories) ○ Chronic prostatitis/chronic pelvic pain syndrome – 3+ mo of pain, urinary sx similar to BPH ○ Acute bacterial prostatitis – SICK patient (fever, chills, + urinary sx) → hospital!! ○ Chronic bacterial prostatitis – similar to ^ + painful ejaculation and insidious onset ○ Asymptomatic inflammatory prostatitis – not discussed ○ Dx: urine dip, urine culture & sensitivity, urine testing, GC/CT testing, blood culture Urethritis – (#1 cause - chlamydia), urinary sx, inflammation of urethra w/o infection, urine dip clean ○ Tx: fluids, analgesic, void after intercourse, tx chlamydia(if present) +/- referral if sx persist Phimosis – Inability to retract foreskin, normally newborns, paraphimosis = emergency Balanitis – inflammation of glans penis (MCC = C. albicans so look for diabetes or skin infection) ○ Sx: pain, itching, ulcerations/rash, odor, edema, erythema, discharge, dysuria ○ Tx: hygiene, topical antifungal/antibiotic/steroid, oral antiviral, referral/circumcision Epididymitis/Orchitis (Transitioning to testicular problems) ○ <35: MCC–STI (GC/CT), diffuse scrotal pain, +/- edema, lower UTI sx ○ 35+: same sx, often w/ BPH, CC–e coli, pseudomonas, ureaplasma, mycoplasma ○ Dx: UA, culture, CT/CT test, urethral swab, mumps serology → Tx accordingly ○ w/ fever → rule out Fournier’s gangrene (necrotizing fasciitis of perineum)–surg emergency Testicular Torsion – emergency, normally younger, post-trauma or spontaneous → ischemia Varicocele – dilation of pampiniform plexus of spermatic veins (bag of worms), usually L side ○ Sx: Asymptomatic, dull achy scrotal pain, worse w/ standing, atrophy of testicle → ↓fertility ○ Tx: most don’t require intervention, can offer surgical ligation or embolization Hydrocele – collection of fluid, transillumination helps w/ dx → scrotal US, usually resolve Cryptorchidism – testes not palpable after 4mo of age ○ Consequences: infertility, inguinal hernia, torsion, testicular cancer GU Cancers (not really touched on in OH so quick overview) ● Prostate cancer – most common malignancy in men (only 3% mortality) ○ Sx: early–asymptomatic // advanced–urinary retention, bone pain, anemia, WL, fatigue ○ Screening: PSA (start ~age 45, every 2yrs or annually if HR) & DRE ■ MCC of elevated PSA: BPH, prostatitis, prostate cancer ■ Also: surg/catheter, excessive bike riding, anal sex ● ● ● ● ● ● ● ● ■ Normal PSA: no true value given, normally <3.5ISH ■ PSA + DRE → transrectal US → prostate biopsy (gold standard of dx) ○ Staging: just know the Gleason score is used (score 6-10 & grade 1-5) Testicular cancer – most common malignancy men 15-35yr ○ RF: cryptorchidism, family hx, tumors, cancers elsewhere, down syndrome/klinefelter ○ Pt pres: painless mass, firm, ontender, not transilluminate, testicular swelling ○ Dx: scrotum US, tumor markers – AFP, b-hCG, LDH ○ Tx: radical inguinal orchiectomy, assess the retroperitoneal lymph nodes (+/- removal) Renal cell carcinoma – 60s, male 2x, cigarette smoking-big RF, normally found on other CT/US ○ “Too Late Triad” – flank pain, hematuria, palpable mass (aka once sx it has progressed) Bladder cancer – male 3x, cigarette smoking-60% of cases, mean age dx 65yo, work hazards ○ Sx: Hematuria (85-90%), urinary frequency/urgency, palpable masses–late finding ○ Dx: CT urogram or MRI, confirmed by cystoscopy and biopsy via transurethral resection ○ Tx: cystectomy, chemo, BCG (bacillus calmette-guerin) ■ just remember → refer to urology/uro-oncology OH NOTES for this section: Case: Urinary voiding symptoms male 70s – reasons ○ Ex: BPH or infectious ○ Ex: PSA is 150 (aka hella high) → think prostate cancer Who is at risk of bladder cancer ○ Male 3:1, mean age 65, cigarette smoking, exposure to industrial dyes/solvents Why do we care about frank blood and clots in urine? → bladder cancer (till proven otherwise) ○ RF: smoker, industrial hazards Case: Urgent care bloody urine with clots now when peeing nothing there anymore ○ Dx: Bladder Cancer → Refer to urology for scope and biopsy ○ ○ ○ ○ ○ ○ REAL exam review: def questions right here Patient has hematuria → what are the things we need to know about the pt to decide what is wrong ■ Older male – bladder cancer ■ Female or young male – pain? post-viral? Neither? Assume glomerulus involved Prostatitis – know the difference between chronic and acute ■ Acute–very sick pt, reason why (manipulation-biopsy, contaminated, etc) E.coli ● Remember prostate by rectum→e coli Renal carcinoma ■ Too late triad: hematuria, flank pain, palpable mass ● Others: night sweats, weight loss, other constitutional sx ■ Dx: definitive–biopsy the tissue, first–CT scan Stage CKD using chart What medications are used to tx CKD ■ ACE/ARBs, ● Know a lot about what ACE/ARBs do ● Lower BP, renal protective properties, short circuits RAS system Acid-Base – given numbers ■ ID what type of problem it is, use her formula ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ Which kind of kidney disease causes hyperlipidemia? Kids ■ Nephrotic syndrome ■ anasarka When is the PSA a problem? SUPER obvious ■ General practice – over 4 or rising quickly → refer to urology ■ What else to do? DRE → the two help with dx, can have one without the other ■ Low UT sx → PSA, DRE Pt in ED super sick – understand characteristics that will tell us what kind of AKI it is ■ Swollen–nephrotic ■ Post-strep–glomerulonephritis ■ Kid–minimal change disease (cant see it easily) ■ Diabetes, HTN, sulfa medication for prostatitis → intrarenal interstitium ■ Vomiting, diarrhea, blood loss – prerenal Obstructive uropathy – older male, older ■ Causes: Stone, prostate problem, bladder tumor ■ Pt pres: Pacing, pain ■ Dx: US–bilateral hydronephrosis, labs–elevated SCr Casts–come from nephron, know location based on description ■ RBC casts–glomerulus (key one, rest are above) Know drugs for management of BPH and fx ■ alpha blockers–osins ● Helps with urinary sx, opens everything up-dilation ■ 5alpha reductase inhibitors–Finasteride ● Tx the cause, stops prostate from getting bigger ■ Rarely use antimuscarinics–causes urinary retention, only use for detrusor instability (bladder contracting at abnml times–incontinence) Testicular problems ■ Young men, esp hx of crypto ■ Painless mass → testicular US (solid mass) → uro-oncology Varicocele – very common, young men ■ normally left, bag of worms ■ Mild sx, achy dull pain, worse w/ sex, worse w/ standing ■ Normally self limiting, bad → testicular atrophy & infertility Hydrocele – little kids ■ Tunica vaginalis ■ Transilluminates ■ Tx: normally self-limiting otherwise testicular atrophy (drain it) Testicular torsion ■ Severe pain, congenital problem or trauma/infection ■ Tx: emergent w/in 12 hrs or testicular atrophy Blood clots in urine → bladder cancer until proven otherwise Hella protein in urine → Nephrotic syndrome ■ MCC: minimal change disease Prostate cancer, imaging → MRI ■ If negative – basically rules out prostate cancer! Very sensitive test ■ Definitive dx: biopsy PCKD – Polycystic Kidney Disease ■ Frequent UTI, hematuria, family hx ■ Tx: control their blood pressure, renal replacement ○ ○ ○ ○ OTC nephrotoxins ■ NSAIDS, PPIs Acute tubular necrosis – brown muddy urine Nephrotic syndromes – foamy urine Stop ACEi → if have prerenal AKI → absolute CI → TAKE THEM OFF