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116 Cards in this Set
- Front
- Back
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name 6 nephritic syn
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Poststrep, RPGN, MPGN, Goodpasteur, IgA, Alport
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name 5 nephrotic syn
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mem, minimal change, FSGS, DM, Lupus
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Potter sequence
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bilateral renal agenesis leading to hypoplastic lung, defect in extremities. present oligohydramnios
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oligohydramnios: mech?
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unable to renally excrete amniotic fluid swallowed by fetus
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hyperhydramnios seen with
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duo atresia (or tracheo-eso fistula
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renal ectopia
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MC pelvic kidney
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increase incidence UTI
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in women bc shorter urethra, and increased in pregnancy
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vesicoureteral reflux, role UTI
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reflux from bladder into ureter--can cause spread of UTI to kidneys
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cystitis characteristics, labs
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pyuria, hematuria, but no urinary WBC
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difference UTI and acute pyelonephritis
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acute pyelo=acute infxn of renal parenchyma, has pathognomoninc white cell casts with F, incr WBC, and flank pain
(UTI-freq, dysuria, pyuria**, bacteriuria, +/-hematuria) |
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def bacteruria
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>10^5 org per mm urine
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key causes AIN
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penicillin derv (methicillin), NSAIDs, diuretics
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natural course AIN
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should resolve on cessation of Rx
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def renal papillary necrosis, what 3 assoc?
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ischemic necrosis of tips of renal papillae
MC DM (infxn w vascular dz), abuse phenacetin w ASA and analgesics, rarely acute pyelo |
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ATN natural course
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reversible, should resolve within 2 wks (necrotic tubular cells replaced)
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initial phase ATN, beware of
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oliguric phase, increasing K (beware of arrhyth, pts most likely to die in this stage)--must make sure its not prerenal oliguria
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oliguria
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-initial phase ATN
-prerenal -postrenal obstruct |
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ATN pathophysio/mech, assoc w 3 conditions
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ppt by renal ischaemia, ie hypotension, shock
assoc w gram neg sepsis, trauma, hemorrhage |
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ATN main causes 3
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renal ischaemia (shock), myoglobinuria, toxins
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toxicities cause ATN
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direct injury to prox tub:
mercuric Cl, gentamicin, ethylene glycol |
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results ethylene glycol ingestion
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ATN, renal oxalosis w intratubular oxalate deposits
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fanconi syndrome, def/problem
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hereditary or acquired impaired resorption glu, aa, phosphate, HCO3
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MC acute renal failure
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ATN
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fanconi syndrome-clinical presentation
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glycosuia, hyperphosphaturia, hypophosphatemia, aminoaciduria, systemic acidosis
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hartnup dz-problem and manifestations
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genetically impaired reabsorption of Tryp, causes pellagra (B3 defic)
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how diagnose chronic pyelo
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histology-coarse, asymm corticomed scarring and deformity renal pelvis and calices
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histol of chronic pyelo
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coarse, asymm corticomed scarring and deformity renal pelvis and calices, interstitial fibrosis, tubular atrophy which can contain eosinophillic proteinaceous casts (thyroidization of kidney)
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acute pyelo is damage where (cortex? glom? tubules?)
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cortex, sparing glomeruli/vessels
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cause chronic pyelo, progression dz
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usu chronic UT obstruction and repeated acute inflamm
leads to renal HTN, ESRD |
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diffuse cortical necrosis, def
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acute, generalized infarction of both cortices sparing the medulla
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diffuse cortical necrosis-mech
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vasospasm and DIC
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diffuse cortical necrosis-assoc w
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obstretric cxns (abruptio placentae, preeclampsia), septic shock
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nephrocalcinosis, def, assoc
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diffuse dep of Ca due to hyperCa: hyperPTH, milk alkali, hyperphosphate 2/2 RF
Note: this can be both a cause and effect of RF |
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urolithiasis: main types general character
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1. Ca (80%)
2. Al/Mg/P (struvite)-urease + infxn, radioopaque 3. uric acid-radiolucent 4. cystine-radiolucent |
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types Ca kidney stones, assoc dz
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Caoxalate or CaP or both.
causes hyperCa: hyperPTH, cancer, inc vitD, milk-alkali synd |
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T/F: Ca kidney stones tend to recur
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T
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Struvite stone charac
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2nd MC, radioopaque, staghorn calculi
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complication struvite stone
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staghorn calculi can become nidus for UTI
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struvite assoc w which infxns
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urease positive (Proteus, Staph)
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struvite grow in urine of what pH
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alkaline
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uric kidney stones assoc
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hyperuricemia, incl gout, high cell turnover in leuk/MPD
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T/F Cystine stones almost always assoc cystinuria
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T (or genetically determined aminoaciduria)
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cxns assoc w APKD, or problems assov w APKD
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-berry aneury
-secondary polycythemia (hi renin,HTN) -cysts in liver and other organs -MVP (?) |
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clinical presentation APKD
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HTN, hematuria, palpable renal masses
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describe genetics APKD, when present
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AD 90% mutat in APKD1 on chrom 16, MC genetic disorder of kidney presents age 15-30 although defect present from birth
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where are cysts in APKD? bilateral?
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bilateral in renal parenchyma
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IPKD, (infantile polycys kid dz) genetics, present
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AR, cysts are evident at birth, dies shortly after
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acquired cystic dz assoc w
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long-term dialysis, increased chance RCC
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path of aquired cystic dz
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multiple cysts w glomerular and tubular atrophy and scarring
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lab characteristics uremia
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acidosis (from accum sulfates, phosphates)
hyperK, hypoCa, anemia, HTN (very hi renin) |
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how does kidney fxn progress in uremia (early and late)
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initially unable to concentrate urine, later unable to dilute
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clinical present uremia
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anorexia, N/V, neuro (AMS to convulsion/coma), bleeding, accum of urochrome in skin, fibrinous pericarditis
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nonrenal causes azotemia (2 general)
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pre-renal, post-renal obstruct (must be bilateral)
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how does gram - sepsis result in pre-renal azotemia
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marked vasodilation leads to peripheral pooling blood, less RBF
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key lab characteristics pre-renal cause ARF
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hi urine osmo (>500), relatively low urine Na (<10) FENa<1%, BUN/Cr>20
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lab characteristics post-renal cause ARF
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very hi urine Na (>40) with urine osmo <350, FENa >4%, (BUN/Cr >15)
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lab character intrinsic renal cause ARF
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key-epithelial/granular casts
labs: urine osm<350, urineNa>20, FENa>2%, BUN/Cr<15 |
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def ARF
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abrupt decline renal fxn with incr Cr and BUN (over span several days)
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kidney retains ___ in pre-renal ARF
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both Na and H2O
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main causes chronic renal failure
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HTN, DM
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consequences RF (8)
(think hormone, metabolic, and systemic) |
anemia (no EPO), renal osteodystrophy (no vitD), metab acidosis (decr acid sxn and decr gen HCO3), hyperK, uremic encephalolpathy, Na/H2O overload (leads to CHF, pul edema), chronic pyelonephritis, HTN
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T/F chronic pyelonephritis is a cxn of RF
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T
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T/F pul edema can be seen with RF
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T (H2O and Na overload causes CHF, pul edema)
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hormonal related problems due to RF
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anemia (no EPO), and renal osteodystrophy (no activ vitD)
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"classic" triad presentation RCC, "commonly"
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flank pain, palpable mass, hematuria
commonly: fever |
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clinical present RCC other than renal
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polycythemia (incr EPO)
hyperCa (para neo PTH), also ACTH, prolactin |
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RCC originates
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renal tubules, starting in poles (often superior)
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risk factors RCC
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smoking, long-term dialysis (via acquired cystic kidney dz)
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RCC spread
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hematogenous (often early), via IVC
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histol RCC cells
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polygonal clear cells
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RCC assoc with what genetic? which chromo?
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VHL, deletion chrom 3
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Wilms tumor, genetics, age present
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WT1 deletion short arm chrom 11 (tumor suppressor), present 2-4 (MC renal cancer of childhood)
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WAGR syndrome
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Wilms' tumor, Aniridia, GU malform, Retardation
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how wilms tumor present
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huge palpable flank mass, hemihypertrophy
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Beckwith Wiedermann, descrip, genetics
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macroglossia, oragnomegaly, neonatal hypogly, embryonal tumors, deletion WT2
**genomic imprinting, abnl alleles always from mom |
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risk factors TCC
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PeeSAC: phenacetin, smoking, aniline (or benzidine), cyclophosphamide
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T/F EtOH a risk factor for TCC
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F
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natural process TCC: mech spread, tx
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local extension, removed but tends to recur
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SCC UT malignancy seen with
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Schisto or chronic bac infxn
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compensation in metab alkalosis
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for every incr 1 HCO3, incr 0.7PCO2
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compensat in acute respir acidosis for incr 10PCO2
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incr 1 HCO3 for every incr 10 PCO2
(chronic it's 3.5 for every 10) |
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respir alkalsos compensat for decrease 10PCO2
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for every decr 10PCO2:
acute= decr 2 HCO3 chronic=decr 5 HCO3 |
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clinical Nephrotic
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proteinuria, hypoalbuminemia->edema, hyperlipid
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histol min change dz
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LM: normal
IF: none EM: fusion epithelial foot processes |
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min change-in who? when? tx?
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usu young children, responds well to steroids
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FSGS histol
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LM: segmental sclerosis and hyalinosis of capially tufts of deep juxtameduallry glom
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FSGS similar to,
worse in pts |
similar to minimal change but older pts
worse in HIV |
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membranous GN epidemio
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one of main primary causes of nephrotic seen in teens, young adults.
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clinical present mem GN
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nephrotic syn with azotemia
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histol mem GN
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LM: thickened capillary
IF: subepithelial IC (granular IF) EM: spike and dome |
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assoc/cxns of mem GN
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-10% of SLE have this
-cause renal vein thrombosis |
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DM kidney damage
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nephrotic
EM/LM: incr GM thickness (earliest change EM) increased mesangial in either diffuse or nodular way |
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Kimmelstiel-Wilson nodules
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seen in nodular DM nephropathy
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renal dz assoc with RA, plasmoid dzs
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renal amyloidosis-subendo and mesangial amyloid deposits
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renal amyloidosis causes what type kidney damage
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nephrotic syndrome
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histol of 5 stages of SLE kidney damage
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1-nothing observable
2=mesangial, little protein and little hematuria, not very clin significant 3=focal prolifer, involves <1/2 glom 4=diff prolifer, most severe 5=membranous (exactly same as mem) |
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describe Diffuse Prolifer SLE kidney dz and histol
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both nephrotic and nephritic presentation, involves almost all glomeruli
LM: wire loop abnormalities from IC deposits IF: subendo IC EM: endothelial cell prolifer |
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clinical charact of nephritic syn
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oliguria, azotemia, HTN, hematuria (some red cell casts)
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causes renal nephritic syn
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1) Post strep (usu GAS)
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labs on post strep GN
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low C3, hi ASO
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T/F Post-strep GN is a result of moderate inflamm rxn
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F, result of intense inflamm rxn, almost all glom in both kidneys
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gross specimen: changes in post-Step GN
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punctate hemorr on surface both kidneys,
enlarged, swollen, hyper cellular bloodless glommerli |
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LM, EM histol post strep GN
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IF: lumpy bumpy, subepithelial
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RPGN
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nephritic
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post-strep
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nephritic
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membranous-type of GN?
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nephrotic
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histol RPGN and types (3)
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all kinds: LM: crescentic
1) 10% Goopasteure: IF: linear (anti glom BM) 2) 50% post strep (IC) 3) pauci immune (no IC, but ANCA+) |
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nomenclature RPGN types
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ANCA-neg forms:
RPGN I=anti G BM RPGN II=IC RPGNIII=ANCA + |
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goodpasteur present, type pts
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anti BM Abs (both alveolar and glomerular), hemorrhagic pneumonitis (pneu w hemoptysis), + nephritic syn
seen in med mid 20's |
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Alport syndrome, descrip and genetics
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hereditary nephritis (ESRD by 30) w nerve deafness, lens dislocation and cataracts.
mutat in alpha5 col IV |
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histol of Alport syn nephritis
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irregular G BM thickening with foci of splitting of lamina densa
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most common cause adult and child nephrotic
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adult=mem GN
child=min change |
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Berger's dz, descrip
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IgA nephropathy, mild dz often post infxs
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IgA nephropathy histol
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IF/EM: mesangial deposits IgA
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slow progression to RF, v fast
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slow=MPGN
fast=RPGN/crescentic |
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main clinical differences nephritic v nephrotic
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nephritic=hematuria, HTN,
nephrotic=proteinuria, edema |
