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Flashcards in Renal Deck (148):
1

horseshoe kidney

most common ceongenital, abnormally in lower abdomen (gets stuck on IMA), conjoined at lower pole

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renal agenesis

can be uni or B/L

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unilateral renal agenesis

hypertrophy of existing kidney, hyperfiltration inc. risk of renal failure in life,

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B/L renal agenesis

oligohydraminos leading to lung hypoplasia, flat face with low set ears, dev. defects of extremities (Potter Sequence); incompatible with life

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dysplastic kidney

non-inheritaed, congenital malformation of renal parenchyma chatacterized by cysts and abnormal tissue especially cartilage; usually unilaterial

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if dysplastic kidney is kidney then what needs to be done

must distinguish it from PKD

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Polycystic Kidney Disease (PKD) characterisitcs

inherited, B/L enlarged kidneys with cysts in renal cortex and medulla,

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Autosomal recessive PKD (Juvenile form) characteristics

presents in infants, worsening renal failure, HTN, potter sequence may be seen, assoc. with congenital hepatic fibrosis (which will show as portal HTN) and hepatic cysts

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Autosomal dominant PKD (Adult, ADult)

presents in young adults, HTN, hematuria, worsening renal failure, due to mutations in APKD1 or APKD2, assoc with berry aneurysm (cause of deaths), hepatic cysts, mitral valve prolapse, pt will have inc. renin causing the HTN

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family Hx of deaths from intracrainial bleeds from aneuryms and renal disease?

think possibly of autosomal dominant PKD

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Medullary systic kidney disease

inherited (autosomal dominant) defect, cysts in medullary collecting ducts, parenchymal fibrosis causing a shrunken kidneys, worsening renal failure

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Acute renal failure is characterized as

azotemia often with oliguria

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types of acute renal failure

prerenal, postrenal, intrarenal azotemia

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pre-renal acute renal failure

dec. blood flow to the kidney; LABS: dec. GFR, azotemia, oliguria, BUN/Cr > 15 (why? low BF causues renin-aldos sequence leading to inc. Na thus inc. H20 thus inc. BUN reabsorption with Cr excretion not chaning), tubulues activity intact

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post-renal acute renal failure

dec. outflow, back P in kidney that lowers GFR; decreased GFR, azotemia, oliguria,

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intral renal acute renal failure

within kidney is a blockage

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early stage of post renal azotemia

inc. back pressure leads to inc. BUN resorpt to increaces BUN: Cr ration, tubular fxn will be intact

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long standing obstruction of post renal azotemia

now decreased resorpt of BUN causing BUN:Cr to decrease, decreased reabsorption of sodium, inability to concentrate urine....long standing blockage starts to damage tubules

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Intrarenal acute renal failure subtypes

ATN, Acute interstitial nephritis, renal papillary necrosis

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Acute tubular necrosis

injury and necrosis of tubular epi. cells, necrotic cells plug tubules causing obstruction and lowering GFR, brown granular casts seen in urine; decrased reabsort of BUN (BUN:Cr <15), decreased reabsort of Na, cant concentrate urine

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most common cause of ARF

ATN

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etiologies of ATN

ischemia and nephrotoxic

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Ischemic ATN

decreased blood supply causing necrosis of tubules, often preceded by prerenal azotemia, prox tubule and medullary segment of thick ascending limb particularly susceptible

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Nephrotoxic ATN

toxic agent causes it, prox tubule is susceptible

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Nephrotoxic ATN causes

aminoglycosides, heavy metals, myoglobinuria, ethylene glycol (cause oxalate crystals in urine), radiocontrast dye, urate

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Clinical features of ATN

oliguria with brown granular casts, elevated BUN and creatinine, hyperkalemia with metabolic acidosis

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oliguria from ATN can last how long

2-3 weeks

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Acute interstitial nephritis

drug induced hypersensitivity rxn, causes include NSAIDs, PCN, diuretics

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presentation of acute interstitial nephritis

oliguria, fever, rash days to weeks after starting drug, Eosinophils seen in urine, resolves with drug cessation, can progress to renal papillary necrosis

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renal papillary necrosis

necrosis of the renal papillae

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presentation of renal papillary necrosis

gross hematuria, flank pain

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renal papillary necrosis causes

chronic analgesic use, diabetes mellitus, sickle cell traint or disease, severe acute pyelonephritis

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Nephrotic syndrome def

proteinuria (>3.5 g/day); hypoalbuminemia (cause edema), hypogammaglobulinemia (inc risk of infection), hypercoaguable state (lose ATIII), hyperlipidemia and hypercholesterolemia

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Nephrotic Syndromes

minimal change disease, FSGS, Membranous nephropathy, membranoproliferative glomerulonephritis, diabetes mellitus cause, Systemic amyloidosis

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minimal change disease

most common nephrotic in children, usually idiopathic, may be assoc with hodgkin lymphoma

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Most common nephrotic syndrome in children

minimal change disease

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minimal change disease pathogenesis

effacement of the foot processes, due to cytokines

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MCD histology

normal glomeruli on HnE stain, effacement of processes on EM, no Ig complex deposits (negative IF)

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MCD proteinuria characterisitc

selective; loss of albumin but not Ig

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MCD Tx

steroids

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Focal segmental glomerular sclerosis

most common cause of nephrotic syndrome in hispanics and african americans, usually idiopathic; may be assoc. with HIV, heroin use, sickle cell disease

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most common cause of nephrotic syndrome in Hispanics and African Americans

FSGS

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FSGS histology

focal and segmental sclerosis on HnE, effacement of foot process on EM, negative IF

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what does focal refer to

only 1 glomeruli or small number of them

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what does segmental mean

only portion of the affected glomeruli is affected

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if MCD does not respond of steroids and progress it becomes what

FSGS

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FSGS respnce to steroids

poor response and progresses to chronic renal failure

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membranous nephropathy

usually idiopathic; assoc. with Hep B, Hep C, SOlid tumors, SLE, Drugs...most common cause of nephrotic in caucasian adults

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most common nephrotic syndrome in caucasian adults

membranous nephropathy

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membranous nephropathy histology

thick glomerular basement membrane on HnE, granular IF, sub-epi deposits with spike and dome appearance on EM

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nephrotic syndrome assoc with SLE

membranous nephropathy

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if the membrane in glomeruli is thickened then...

its membranous nepohropahty or membranoproliferative due to the Ig depot

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membranous nephropathy pathogenesis

the Ig deposits sub-endothelial and then the podocyte lays down more basement membrane leading to the spike and done appearance

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membranoproliferative glomerular nephritis (MPGN)

thick capillary membraines on HnE, often with tram track appearance, granular IF

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MPGN pathogensis

Ig deposits, mesangium proliferates thru the deposit to create tram track

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MPGN subtypes

Type I: subendothelial, Type II: intramembranous

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TYpe I MPGN

subendothelial, assoc. with HBV, HCV; mor eoften with tram track look

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Type II MPGN

intramembranous; assoc. with C3 nephritic factor (an auto antibody that stabalized C3 convertase)

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MPGN causes nephrotic or nephritic?

can cause either or BOTH

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membranous and MPGN distribution in glomeruli

membranous type = right under podocytes (epithelial), MPGN I = under endothelial, MPGN = intramembrane

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Nephrotic syndrome caused by DM

high glucose cauises non-enzyme glycosylation of vascular basement membrane resulting in hyaline arteriolosclerosis, efferent artiole more affected than afferent leadin to inc. glomerular pressure

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DM nephrotic syndrome pathogenesis

the NEG cuases back pressure leading to sclerosis of the glomerulus,

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Tx to slow the DM neptjrotic syndrome progression

ACE inhibitor due to angiotensin II acts on efferent vessel

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Kimmelstiel-wilson noldules

seen in the DM nephrotic syndrome from the sclerosis and is patho-neumonic

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Systemic Amyloidosis

kidney most common involved, amyloid deposits in mesangium resulting in nephrotic syndrome, apple green birefringence under polarized light

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Nephritic syndrome

limited proteinuria, oliguria, azotemia, salt retention with periorbital edema and HTN, RBC casts and dysmorphic RBC in urine...glomerular inflammation and bleeding

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Bx of nephritic syndomr glomeruli

hypercellular, inflamed glomeruli; immune complex deposition activates complement, C5a is a chemoattractant for neutros

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nephritic syndrome subtypes

Post. Strept. glomerular nephritis, RPGN, IgA nephropathy, Alport syndrome

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PSGN

nephritic syndrome that arises after group A Beta hemolytic strep infection of skin or pharynx

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more often PSGN strept need what virulence factor?

M protein, defines it as a nephritic strain

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PSGN presentation

2-3 weeks after infection, hematuria (coca cola urine), oliguria, HTN, periorbital edema, more often seen in children but adults can be affected

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PSGN histology

hypercellular, inflames glomeruli on HnE, Ig deposition (granular IF), subepithelial humps on EM

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PSGN Tx

supportive due to the deposits go to sub-epi layer and then eventually disappear; children rarely progress to renal failure; adults could dev. RPGN

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RPGN

nephritic syndrome that progresses to renal failure in weeks to months

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RPGN Bx

crescents in bowens space and the cresencts are made of fibrin and macrophages

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RPGN IF subtypes

linear = Goodpasture syndrome; granular = PSGN, diffuse proliferative glomerularnephritis; Negative IF = wegener granulomatosis, polyangiitis, churg strauss syndrome

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Goodpasture syndrome

Ab againts collagen in glomerular and alveolar basement membranse; presents as hematuria hemoptysis, classically young adult males

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SLE most common type of renal disease

diffuse proliferative golerulonephroitis type, SLE usuallly causes this instead of the nephrotic one mentioned, granular immune complex deposition

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after a negative IF (pauci immune) then

ANCA test is performed; c-ANCA = wegeners granulomatosis (kidney disease is RPGN along with lung invokvement and nasopharynx involvement); p-ANCA is microscopic polyangiitis or churg strauss....to distinguish CS has granulomatous inflammation, eosinophils, asthma

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IgA nephropathy

mose common nephropathy world wide, IgA depot in mesangium

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IgA nephropathy presentation

episodic gross or microscope hematuria with RBC casts following usually a mucosal infection; granular IF; may slowly progress to renal failure

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ALport syndrome

inheritated defect in type IV collagen; most commonly X-linked; results in thinning and splitting of glomerular basement membrane

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ALport syndrome presentation

isolated hematuria, sensory hearing loss, ocular disturbances

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UTI usually caused by

ascending infections

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cystitis

bladder inflammation; presents with dysuria, urinary frequency, urinary urgency, supra-pubic pain; systemic signs are usually absent

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risk factors for UTI

sexual intercourse, urinary stasis, catheters

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Labs for cystitis

UA: cloudy urine with >WBC
Dipstick: + leukocyte esterase and nitrites
CUlture >100,000 CFU

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etiologies of cystits

E. COli (80%), staph. saprophyticus (young sexually active women), kleb. pneumoniae, proteus mirabilis (alkaline urine), enterococcus faecalis

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sterile pyuria

pyuria with - urine culture; suggests urethritis from chlamydia, trachomatis, neisseria gonorrhoeae

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pyelonephritis

kidney infection; usually ascending infection

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pyelonephritis inc. risk factor

vesicoureteral reflux

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pyelonephritis presentation

fever, flank pain, WBC casts, leukocytosis along with the Sx of cystitis ( dysuria, urinary frequency, urinary urgency, supra-pubic pain)

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pyelonephritis etiologies

E. COli (90%), klebsiella species, enterococcus faecalis

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Chronic pyelonephritis

interstiail fibrosis and atrophy of tubules due to multiple bouts of acute form; due to vesicoureteral reflux (children) or obstruction

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chronic pyelonephritis Bx

cortical scarring with blunted calyces; if scarring at upper and lower poles then it is characteristic for vesicoureteral reflux

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chronic pyelonephritis histology

thyroidization of kidney (atrophic tubules contain eosinophilic peoteinaceous material reminiscent of thyroid follicles)

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chronic pyelopnephritis UA

waxy casts seen

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nepholithiasis

urinary solute as a stone; risk factors include high conc. of solute in urinary filtrae and low urine volume

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nephrolitiasis presentation

colicky pain with hematuria and unilateral flank tenderness; stone will pass in hours or else sugery may be required

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calcium oxalate or calcium phosphate stones

most common seen in adults

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causes of Ca-oxalate or Ca-Pi stones

idiopathic calciuria; hypercalcemia causes must be ruled out; may be seen in crohns

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Tx of Ca-oxalate or Ca-Pi stones

thiazides (Ca sparring diuretucs)

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ammonium, Mg, Pi

2nd most common type

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ammonium, Mg, Pi causes

infection with urease + organisms (proteus vulgaris, klebsiella); alkaline the urine causing stone; stag horn stones; usually requires surgery

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ammonium, Mg, Pi stone Tx

staghorn stones thus need surgery, Ab for the offending agent

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Uric acid stones

3rd most common; radiolucent

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Uric stone causes

risks: hot, arid climate, low urine volume, acidic pH; stones seen in gout pt, hyperuricemia or myeloproliferative disorders inc. risk

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uric stone Tx

HYDRATION AND ALKALIZATION OF URINE; allopurinaol can help in gout pt

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cysteine stones

rare, more commonly in children

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cysteine stones causes

cysteinuria (due to genetic defect in tubles)

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cysteine stone Tx

may form stag horns, hydration and alkalization of urine

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end sdtage kidney failure

result from glomerular, tubular, inflammatory, vascularf insults to kidney; most common causes HTN, DM, glomerular disease

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Uremia

azotemia; nausea, anorexia, pericarditis, platelet dysfxn, encepalopathy with asterixis, urea deposition in skin

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clinical features seen in end stage kidney failure

Uremia, salt/water retention (with resultant HTN), hyperkalemia with metabolic acidosis, anemia, hypocalcemia, renal osteodystrophy (damage to bone due to failure; components osteitis fibrosa cystica, osteomalacia, osteoporosis)

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renal peritubular interstitial cells

secrete EPO

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osteitis fibrosa cystica

hypocalcemia...PTH rise....resportion of calcium from bone leading to cysts and fibrosis

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osteomalacia

cannout mineralize the osteoid created

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end stage renal failure Tx

kidneys shrink and due to dialysis they create cysts, increased risk for renal cell carcinoma (pt on dialysis)

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Angiomyolipoma

hamartoma comprised of BV, Smooth Muscle, Adipose tissue; increased frequency in tuberous sclerosis

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Renal cell carcinoma

malignant epithelial tumor arising kidney tubules

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renal cell carcinoma presentation

classic triad: hematuria, palpable mass, flank pain; other Sx: fever, lbs loss, paraneoplastic syndrome (EPO, renin, PTHrP, ACTH)

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renal cell carcinoma extra things

rarely may present with left sided varicocele (only occurs on LEFT side including only L-kidney)

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most common cell variant for renal cell carcinoma

cells with clear cytoplasm

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renal cell carcinoma pathogenesis

loss of VHL tumor suppressor; causes increse inculin growth factor-1, inc. HIF transcription factor that increase VEGF, PDGF

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sporadic pathway of RCC

single tumor, upper pole, adult smoker, assoc. with VHL loss

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hereditary pathway of RCC

younger, multiple and B/L, assoc. with VHL loss

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Von Hippel-Lindau disease

autosomal dom disorder assoc. with inactivation of VHL; increases risk for hemangioblastoma of cerebellum and RCC

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RCC loves to go where..

renal vein

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Wilms tumor

most common to arise in children (avg age is 3), malignant renal tumor comprised of blastema (primitive cells for kidney dev.), primitive glomeruli, tubules, stromal cells

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Wilms tumor presentation

large, unilateral flank mass, hematuria, HTN

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Wilms tumor gene mutation

WT1

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WAGR syndrome

WIlms tumor, Aniridia, Genital abnormalities, Retardation

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Beckwith-Wiedemann syndrome

Wilms tumor, neonatal hypoglycemia, muscular hemihypertrophy, organomegaly (including tongue)

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urothelial carcinoma

malignant tumor from urothelial lining of renal pelvis, ureter, bladder, urethra

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most common type of lower urinary tract cancer

urothelial carcinoma; usually arise in bladder

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number 1 major risk factor for urothelial carcinoma

cigarettes because of the polycyclic aromatic hydrocarbons

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risk factors for urothelial carcinoma

smoking, naphthylamine, azo dyes (coloring including hair), long term cyclophosamide or phenacetin use

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urothelial carcinoma presentation

usually older adults with painless hematuria

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2 pathways for causation of urothelial carcinoma

flat and papillary; papillary growth being a vascularized growth with epi cells (progress from LG to HG then INVADES); flat pathyway is a flat lesion that starts has HG and then invades ,assoc. with earl;y p53 mutations

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urothelial carcinoma are often multifocal and recur due to

the entire urothelial field are exposed to the carfinogens so eventually they are all cancerous or become cancerous

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squamous cell carcinoma

malignant proliferation of squamous cells; usually involves bladder; arises in a background of squamous metaplasia

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squamnous cell carcinoma risk factors

chronic cystitis, schistosoma hematobium (middle eastern usually), long standing nephrolithiasis

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urothelial cells become what during irriation

becomes squamous metaplasia and then allows for squamous cell carcinomas

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adenocarcinoma

malignant proliferation of glands, usually involve bladder

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adenocarcinoma arise frm

urachal remnant, cystitis glandularis, exstrophy

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urachal remnant

from a tube that drains bladder to yolk sac and has glands in it, thus allow for production of adenocarfcinoma; the adenocarcinoma will be at dome of bladder

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cystits glandularis

chronic inflammation leading to a columnar metaplasia to allow for creation of adenocarcinoma of bladder

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exstrophy

congenital defect to form caudal portion of bladder wall and anterior abdom wall