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Neph

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Question
Answer
3 categories of ARF, what's MC?   prerenal (MC), renal, postrenal (least common)  
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biggest risk ARF   infxn  
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T/F urine output is decrsd in ARF   F, can be oliguric, anuric, nonoliguric  
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key lab values use to difft pre-renal v ATN (renal) causes of ARF   [Pre-renal value always listed 1st, then ATN] U_osmol: >500 v >350; U_Na: <20 v >40; FE_Na: <1% v >1%; BUN:serum_Cr : >20 v <20  
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how urine sediment is difft bw pre-renal and renal ARF   pre-renal: hyaline casts, ATN: granular casts w epithelial cells  
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proteinuria (3/4+) suggests pre-renal or renal ARF?   renal ARF (specifically glomerular)  
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Causes ATN: MC, other causes   MC=ischemia, other: Abs ie aminoglycosides, radiocontrast, NSAID esp in CHF, mscl damage, hemoglobulinuria, MM Ig chains, chemo Rx  
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2 main causes of ARF due to renal dzs   1) ATN, 2) glomerular  
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causes of postrenal ARF   MC=BPH, also stones (but would need to be bilateral)  
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RBC casts suggests what ARF etiology   glomerular  
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WBC casts suggests what ARF etiology   acute interstitial nephritis or pyelonephritis  
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fatty casts suggests what ARF etiology   nephrotic syndome (glomerular cause ARF)  
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key causes of prerenal ARF   anything hypovolemia, incl decrsd CO and systemic vasodilate (ie sepsis)  
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if renal perfusion is already compromised, what Rx can ppt ARF   NSAIDs, ACEI, cyclosporin  
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metabolic changes seen in ARF   metabolic acidosis w incrsd anion gap, hi K and P, low Ca and Na + uremia  
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at what level correct acidosis w bicarb   <16  
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when start dialysis for ARF   symptomatic uremia, intractable acidemia, hyperK, or vol overload  
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causes of CRF    
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cut offs for severity of CRF   (all in GFR) mild=70-120; mod=30-70; severe=<30; ESRD=<10  
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at what pt does uremia usu become symptomatic   BUN>60  
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what level of Serum Cr is considered chronic renal insuffic; what does that term mean?   1.5-3 [kidneys are irrev compromised, but not failed]  
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clinica features of CRF by organ system (HTN, GI, CNS, Heme, Lytes, hormone, ID)   HTN=decrsd GFR->aldos,incrsd BP;GI=uremia->N/V;CNS=lethargy,periph neuro,hyerreflexia;Heme=normocyt anemia(low EPO),uremia inihibits plts(bldg);Lytes=hi P->low vit D, low Ca++->incrsd PTH;hormone: lo testost,amenorrhea,hi prolactin;ID=uremia inhib immune  
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summary of lytes in CRF   hi K, Mg, P and metabolic acidosis  
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define renal osteodystrophy   bone pain, fractures from incrsd P leading to low Ca++ and 2ry hyperparathyroidism  
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Tx CRF: diet, Rx   Diet: low protein, K, Mg, P (and low Na if CHF, HTN, oliguria); Rx: ACEI to decrs proteinuria and progression to ESRD, BP control w ACEI +/- diuretics, Rx control of glycemia  
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Tx CRF: lytes, heme   Lytes: hyperP: Ca++ citrate which binds P, prevent 2ry hyperparathyroid by Ca++ and vitD, for acidosis give bicarb; heme: give EPO  
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in ARF which diuretic give   furosemide, if pul edema or oliguric  
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absolute indications for dialysis   AEIOU, A=acidosis, E=electrolytes (hi K), I=intoxications, O=overload (hypervol), U=uremia  
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which intoxications use dialysis for   MELA=MetOH, ethylene glycol, Li, aspirin  
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what symptoms of uremia, which symptom is absolute indication for dialysis?   N/V, CNS: changes in mental status, seizures, **absolute indication=uremic pericarditis  
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Access options for hemodialysis   1) central catheter to subclavian, 2) A-V fistula, best for permanent access, needs time to mature, listen for bruits to make sure open, 3) implantable graft **Note: blood must be heparinized  
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what deficit of renal failure can't be corrected w dialysis   renal synthesis of EPO and vit D  
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complications/limitations of hemodialysis   hypotension; CNS: hyposmol of ECF wrt brain causes N/V, headache; heparin complications; vascular access infxn; amyloidosis b2 microglobulin in bones and joints  
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complications/limitations of peritoneal dialysis   hi glu soln leads to hyperglycemia, incrsd triglycerides; fluid maintained at waist; abd/inguinal hernia; peritonitis risk  
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what dialysis membrane is used in peritoneal dialysis   the peritoneum  
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proteinuria defined by lab value? Nephrotic level of proteinuria?   proteinuria= >150mg/d; nephrotic level= >3.5g/d  
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key features of nephrotic syn   proteinuria >3.5g/d, hypoalbumin, hyperlipid, edema, hypecoag (losing anti-coag), infxn (losing Ig)  
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3 categories of proteinuria   1) glomerular (more protein loss than other categories), 2) tubular, 3) other (UTI, fever, heavy exertion/stress, CHF, preg, orthostatic)  
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tx nephrotic syndrome (general, not etiology specific)   1) underlying dz (can incl steroids for some glomerul), 2)ACEI decrs albumin loss, esstl for DM w HTN, 3) diuretics for edema, 4) limit protein intake, 5) tx incrsd chol, 6) vaccine flu and PNA  
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key features of nephritic syn   hematuria, HTN, incrsd BUN (can also see edema and proteinuria (but not in range of nephrotic))  
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MC cause of nephritic syndrome   Post Strep  
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which glomerular dzs have tx   min change=steroids, FSGS ? Combo--not clear effective, HIV nephropathy=prednisone, ACEI, HAART  
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MC causes of nephrotic in kids, adults   kids=min change; adults=membranous, then FSGS, then membranoprolifer  
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FSGS nephrotic or nephritic?   nephrotic, but often hematuria and HTN are present  
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which glomerul dz shows thickening of capillary walls   membranous  
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what dz: asx mild hematuria/proteinuria that becomes gross hematuria after URI or exercise   IgA (bergers)  
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hematuria w hi freq hearing loss   Alports (hereditary nephritis), complete picture includes: hematuria, pyuria, proteinuria + hi freq hearing loss w/o deafness  
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which glomerular dz assoc w HepC and cryoglobulinemia   Membranoprolifer  
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characteristics, tx of Post Strep GN   10-14d after infxn, nephritic but also see proteinuria, edema and low complement; usu children, usu self-limited [tx anti-HTN, loop diuretics]  
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which vascular dzs can cause GN, how difft   Wegeners, Goodpasteurs, PAN (+ Scleroderma): Goodpasteurs usu see hemoptysis first; Wegeners has nasal involvement/bldg; PAN has no pul component  
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tx Wegeners GN? Goodpasteur GN?   both steroids and cyclophosphamide  
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MC cause acute interstitial nephritis? In children other causes?   MC=Rx, but can be after infxn esp in children (ie Strep, Legionella), + sarcoid  
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key features acute interstitial nephritis   ARF, rash, fever, eosinophilia (so seeing eosinophils in urine suggests dx)--note can't always difft from ATN w/o bx but usu don't need bx  
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how are acute and chronic interstitial nephritis difft   chronic doesn't have hypersensitivity component w eos; a progressive fibrosis/scarring process [+/- pap necrosis  
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MC cause of pap necrosis? How dx?   MC=overuse OTC painkillers, (also DM, sickle cell, EtOH, UTI/UTO); dx=excretory urogram  
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how can analgesic nephropathy present   either interstitial nephritis or pap necrosis and ARF or CRF  
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cxns of pap nerosis   sloughed pap can obstruct ureter  
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name 5 tubulointerstitial dzs   1) acute/chronic interstitial nephritis, 2) renal pap necrosis, 3) renal tub acidosis, 4) hatnup syndrome, 5) fanconis  
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describe acid-base state of 3 renal tubular acidosis (RTA) dzs   RTA1&2=low K, hi Cl, non AG metab acid w alk urine; RTA4=hi K, non AG met acidosis w acidic urine  
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cxns of ea RTA   RTA1=renal stones, rickets/osteomalacia; RTA2&4=no stones  
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name defect in ea RTA   RTA1=can't secrete H+ in distal tub; RTA2=can't reabsorb HCO3 in prox tub; RTA4=hypoaldost, distal tb decrsd Na absorb and Na, K sxn  
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tx of RTA1, 2   RTA1=bicarb to prevent stones, P to help acid sxn; RTA2=no bicarb (would just be excreted), Na restriction  
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describe defect and clinical pic of Hartnup syn   defect: AR aa transporter can't transport Tryp, causing nicotinamide defic; clinical like pellagra dermatitis, diarrhea, + ataxia, psych dz [ dementia in pellagra]  
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tx Hartnup syndrome   suppl nicotinamide if symptomatic  
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describe defect, clinical pic of Fanconis   prox tub has defective transport of numerous substances; has proteinuria, polyuria, dehydration, RTA2, low K; urine contains hi glu, P, and Ca++  
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clinical cxns of Fanconis   low P leads to rickets, impaired growth, osteomalacia, and path fx bones  
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tx Fanconis   P, K, alkali, salt, hydration  
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what lab value suggests myoglobulinuria or rhabdomyolysis   very high CPK value  
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key features of adult polycystic kidney dz   hematuria, abd pain, abd mass, HTN, berry aneurysms, cysts in other organs, MVP, colon diverticuli, abd/inguinal hernias  
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dx, tx adult polycystic kid dz   dx: US, tx: none (50% ESRD, course variable)  
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define medullary sponge kidney   cystic dilation of collecting ducts, thgt assoc w hyperparathyroid and parathyroid carcinoma  
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dx, presentation, tx medullary sponge kidney   dx: IVP; presentation: hematuria, UTI, stones; tx:none [stone prevention, tx UTIs]  
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define, tx of simple renal cyst   common (1/2 pts>50), no tx (Asx)  
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name 4 renal vascular dzs   1) renal artery stenosis, 2) renal vein thrombosis, 3) HTN nephrosclerosis, 4) sickle cell nephropathy  
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2 types of renal artery stenosis, seen in which pts   1) atheroscl, 2/3, see in older men w hi chol and smoking; 2) fibromuscular dyspl  
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3 clinical features suggesting renal artery stenosis   1) sudden onset of HTN w/o fam hx, 2) refractory HTN, 3) abd bruit  
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dx of renal artery stenosis (3)   1) renal arteriogram w contrast if no RF, 2) MRA if RF, 3) captopril renal scintigram scan if nml renal fxn  
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tx renal arter stenosis   revascul w percut translum angio (PRTA), success fibromusc>athero; surgery if PRTA is not successful  
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can see renal vein thrombosis w   nephrotic syn, preg, OCP  
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2 types o f HTN nephrosclerosis and pts   1) benign, thicken of arterioles in long-standing HTN; 2) malignant: rapid decrs renal fxn and incrs HTN in AA men; grtly incrsd BP (papilloedema, cardiac decomp, CNS); rapid incrs Cr, proteinuria, RBC/WBC +/- nephrotic +/- microangiopathic hemo anemia  
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describe sickle cell nephropathy presentation, progression, tx   nephrotic, often pap necrosis incrsd UTI, if tubules damaged can't concentrate urine leading to dehydration and more sickle events; ACEI can help  
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risk factors for stones, incl MC, dzs, Rx, ID   MC=low fluid intake; dzs=RTA1, hyperparathyroid, gout, Crohns; Rx=loop, acetazolamide (carbonic anhydrase), antacids, chemo; male; ID=UTI w urease org [PESK=Proteus, Enterobac, Serratia, Kleb]  
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types of stones, which seen in radiography, and which most common   1) Ca++ (MC)=can see, 2) uric=can't see, 3) struvite (ammonium Mg PO4)=can see; 4) cystine=can't see  
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bipyramidal or biconcave oval stone on radiograph=what type?   Ca++  
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flat sq plate kidney stone=what type? See on radiograph?   uric, can't see on plain radiograph  
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rectangular prism kidney stone=what type? See on radio?   struvite, can see  
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hexagon kidney stone=what type? See on radiograph?   cystine, can't see on plain radiograph  
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what incrses risk of uric acid kidney stones   gout, chemo of leuk and lymph  
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what incrses risk of Ca++ kidney stones   inrs Ca++=hyperparathyroid, sarcoid, cancer, vitD; incrs oxaloate=steatorrhea, B6 defic, Crohns  
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what incrs risk of struvite stones   alk urine, UTI w urease bug PESK =proteus, enterobac, serratia, klebsiella  
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tx/prevention Ca++ stones   limit Ca++ intake, thiazide diuretic [for all stones: hydration, pain manage]  
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tx/prevention cystine stones   limit protein, allopurinol [for all stones: hydration, pain manage]  
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if urine acidic w stones, what type? Alk?   acid think uric acid stone, alk think struvite  
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pyuria w stones, think what type   struvite (UTI w urease bug)  
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when admit pt w kidney stone   if cant control pain w oral meds, renal colic + UTI +/- F, stone >1cm which isn't likely to pass spontaneously  
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2 procedures for stones won't pass   1) extracorpeal shock wave lithotripsy (breaks up stones 0.5-2cm), 2) percut nphrolithotomy (>2cm)  
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UTO: clinical presentation of upper UTO v lower   upper UTO=renal colic; lower UTO=urination  
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causes of upper UTO   intrinsic renal=kidney stones, sloughed papillae, blood clots, tumor; extrinsic=preg, tumors, AAA  
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causes of lower UTO   BPH, prostate cancer, bladder cancer  
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dx of UTO (3)   renal US, IVP (but not in preg, CRF), voiding cystourethrography can be used for lower UTO  
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Prostate cancer: MC type, risk factors   95% adeno; risk: ***age, AA, high fat diet, fam Hx, herbicides/pesticides  
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progression of prostate cancer and when presents   starts periphery, moves centrally, then obstructive but by this time often mets (can present bone pain, ie lower back)  
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dx prostate cancer   1) DRE (dig rectal exam): abnml -> TRUS (transrectal US) w bx regardless of PSA; 2) PSA>10 or velocity>0.75/yr -> TRUS w bx  
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what can incrs PSA other than cancer   BPH, age, prostatitis, needle bx, prostate massage (but not DRE)  
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stages of prostate cancer   A=nonpalp, confined to prostate, B=pap nodule, confined to prostate, C=beyond capsule w/o met, D=mets  
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tx for difft stages prostate cancer   1) localized to prostate (A, B)=radical prostatectomy (old asx men <10yr survival might leave),2) local invasive=radiation and androgen deprivation; 3) mets=decrs testosterone (remove testes, anti-androgen, leut hormone rel hormone agonist (Leuprolide))  
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classic triad of renal cell carcinoma presentation   (only 10%) hematuria, flank pain, abd mass  
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what dz has autosomal dominant transmission at risk renal cell carcinoma   VHL (but only 2% of RCC, most are sporadic cancers)  
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risks for renal cell carcinoma (5)   smoking, phenacetin analgesics, adult polycystic kidney dz, VHL, Hg&cadmium exposure  
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dx renal cell carcinoma   renal US, f/u CT for staging  
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tx renal cell carcinoma   radical nephrectomy, incl Gerota's fascia  
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MC genitourinary cancer   bladder cancer  
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MC type of bladder cancer   transitional cell (90%)  
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tx bladder cancer   local excision, but likely to recur  
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risks for bladder cancer   smoking, aniline and azo dyes, radiation, coffee, sweeteners, cyclophosphamide  
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how does bladder cancer nmlly present   hematuria (r/o infxn)  
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dx bladder cancer   cytoscopy+bx; CXR and CT for staging  
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staging of bladder cancer and treatments   0=mucosa (intravesicular chemo), A=lamina propria (transurethral resxn, but recur so rept cytoscopy), B=mscl invasion (radical cystectomy+LN dsxn, urinary diversion), C=perivascular fat (same tx as B), D=mets to LN, other sites (cystectomy and chemo)  
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types of germ cell testicular cancers   seminoma (MC, slow growth, late invasion, radiosensitive), nonseminomas usu containing 2 of: embryonal, choriocarcinoma, teratoma, yolk sac  
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qualities of embryonal testicular cancer; germ cell? Seminoma?   germ cell nonseminoma; hemorr/necrosis, mets abd lymph&lungs early, incrsd AFP  
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qualities of choriocarcinoma testicular cancer; germ cell? Seminoma?   germ cell nonseminoma; most aggressive, usu met by time dx, but rare; incrsd bHCG (but also seen in other testic cancers)  
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qualties of seminoma? Germ cell?   germ cell; MC, slow growth, late invasion, radiosensitive  
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qualities of teratoma? Germ cell? Seminoma?   germ cell, nonseminoma; rarely met  
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qualities of yolk sac testic cancer? Germ cell? Seminoma?   germ cell, nonseminoma; usu in young boys  
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name non germ cell testicular cancers   Leydig (sxn hormones causing precocious puberty or gynecomastia, if met poor px), Sertoli (usu benign)  
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which more common: germ cell or non germ cell testic cancers   germ cell (95%) and of those MC is seminoma  
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staging of testicular cancer   A=testicle/cord, B=retroperitoneal LN spread below diaphragm, C=distant mets  
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difftl for testicular cancer   varicocele (dilated veins in testicle), testicular torsion, spermatocele (testic cyst), hydrocele (fluid in testis)  
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incrsd risk testic cancer   cryptorchidism (even if surgical repair), Klinefelter  
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incrsd AFP in testicular cancer indicates   embyronal germ cell nonseminoma  
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risk penile cancer, age peaks   risk: circumcision may protect, HSV, HPV18; peak age 60  
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MC etiologies for epidimytis   in kids/old: E Coli, in young adult=Chlamydia or gonorrh  
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how difft testicular torsion and epidimytis   testicular torsion is sudden, testicle elevated in scrotum, no F, usu appears in adolescent  
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