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242 Cards in this Set
- Front
- Back
first decade, edema, HTN, oliguria, hematuria ( cola colored) , azotemia, mild proteinuria goes away
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acute prolif glom nephritis
acute post infectious, acute post strep -may not go away in adults |
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a form of APGN w marked hypercellularity, leukocyte infiltration, sub ep hump and neutrophil in llumen, granular deposits of igg, igm, c3 in mesangium (subep humps)
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diffuse prolif glomerulonephritis-
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what is the hallmark of FSGS
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ep cell foot process effacement and detachment
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what is the mutation in FSGS
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NPHS1- on chrom 19q13- for nephrin which controls glom perm
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dz that have nephrotic synd and FSGS are due to what mutation
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a mutation of the slit diaphragm which could be NPHS1, podocin or actinin 4, and TRpC6
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what is the most common cause of nephrotic syn
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FSGS-occurs in sev dz settings and is always a marker for bad prog w progression of renal dz
-20% will get malignant FSGS-dead in 2y |
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how does FSGS differ from min change
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1. high hematuria,htn and dec gfr
2. poor response to cs tx 3, non sective proteinuria 4.signif progress to chronic kidney dz |
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HIV FSGS is called
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collapsing FSGS
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what are the three mesangial dzs
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iga, mpgn I, mpgn II
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what is the most common glom nephritis
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iga nephropathy- two types are HS purpura and berger
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what is hematuria in iga nephropathy coincident with
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significant infxn at body site
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iga nephropathy has true mixed__ and __
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hematuria and proteinuria
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in iga neph, recurrent episodes of __ occur without progression of renal dz
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hematuria
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what are three main histo changes in MPGN
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1. alter glom BM
2. prolif of glom cells ( mostly in mesangium) 3. leukocyte infilt |
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the most common presentation of MPGN is
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combo hematuria and proteinuria
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what is another name for MPGN II
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dense deposit disease
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what infection is assoc with MPGN I
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hep c
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what is histo important in MPGN I
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subendo deposits
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50 percent MPGN progess to __ __ __ in 1 yr
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chronic renal failurew
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what does mpgn I usu present as
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nephrotic synd w mild hematuria
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what is secondary mpgn I assoc with
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chronic antigenemia- adults
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mpgn I occurs in pt with
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hep c, chronic immune complex dz, endocarditis, malignancies
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what age group is mpgn II
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children
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what is dom clinical finding in mpgn Ii
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hematuria and 50 percent have nephritic synd
-mpgn II - more dismal prognosis |
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what is the histo of mpgn II
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intramembranous dense depostis in glom BM, ratty and irreg, lipid deposits
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What is the mech behin MPGN II
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alternative complement pathway is always turned on, so there is too much complement- c3nef(nephric factor) is an igg autoantibody actives the path
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most primary glom dz progess to __ __
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chronic glomnephritis
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what do you see in histo of chronic glomneph
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trichrom stain shows replacement of almost all glomeruli
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what are main diseases that lean to CG
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PSGN, cresenteric, FSGS. MPGN II
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what do you see on histo of mpgn
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Mesangial cell proliferation
Increased mesangial matrix (black with silver stain). Basement membrane thickening and focal splitting, Accentuation lobular architecture Influx PMNs |
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in both types of mpgn what does mesangial matrix do to the BM
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dissects or splits it
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the MDRD equation takes into account the patients:
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age, female or black
bc in renal disease age gender and race are most imp |
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why does gfr decrease with age
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Global glomerulosclerosis consequent to “normal” aging- there is a loss of cortex and ischemia
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what are the three biggest risk factors for CKD
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obesity, age and HTN
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which laboratory tests below may be used to indicate kidney
damage for staging patients in stages 1 or 2? |
urine albumin or kidney biopsy
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what does obesity due in the MDRD equation
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obesity results in an underestimation
of the estimated GFR. |
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besides obesity what is the other problem with the MDRD equation
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In a patient with a risk factor for CKD (obesity) but no apparent signs
of kidney damage, serum creatinine will not be sensitive enough to reveal a decrease in GFR corresponding with early CKD; therefore his GFR may be relatively overestimated. |
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Which of the listed pathophysiologic mechanisms is the etiology of isolated nephrotic range proteinuria?
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Diffuse injury to the glomerular basement membranes throughout both kidneys
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Idiopathic membranous glomerulopathy is an immune-mediated disorder with localization of immune complexes in which location and pattern within the glomerulus?
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subep diffuse
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Large epidemiologic studies have demonstrated an apparent
increase in the prevalence of CKD Stage 3 over the last 2 decades from 5% to 8%. What factor of those below may contribute to these findings? |
agining of us pop
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The most accurate serum test currently available for the assessment of patients with early CKD is:
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cystatin c
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what are the cutoff for Bp that indicated HTN
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140 and 90
Pre-disease hypertension:120-139 mmHg systolic; 80-89 mmHg diastolic. |
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ost likely cause of Nephrotic Syndrome with a history of progressive isolated proteinuria?
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membranous glomerulopathy idiopathic
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what differentiates FSGS causing nephrotic synd and idiopathic membranous cause of nephrotic synd
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FSGS occurs in Hispanic and African-American patients with onset in the 3rd and 4th decades in contrast to Membranous which has a later onset and occurs in Caucasian males.
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Which clinical course is most likely for patients with Nephrotic Syndrome (NS) caused by Idiopathic Membranous Glomerulopathy?
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Insidious onset progressive proteinuria that evolves to NS; 50% patients develop remission of NS; 1/3 of patients progress to end-stage renal disease.
high insidence of remission if untreated |
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heymann deposits___
immune complex deposits__ anti GMB deposits__ |
subep (cationic)
subendo (anionic) GBM |
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what are two small vessel renal vasc dz
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benign nephrosclerosis
malignant htn |
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what is a large vessel renal vasc dz
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renal a sclerosis
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what are two thrombotic microangiopathies
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HUS and TTP
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what are the effects of benign nephosclerosis
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multifocal ischemia of parenchyma supplied by sclerotic vessels
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what are three causes of BNS
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increasing age, HTN, DM
medial and intimal thickening ( interloblar and aff arterioles) and hyaline deposition in arterioles |
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BNS is not assoc with __ __ with the exceptions of af amer, severe HTN, DM
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renal insufficency
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what is malig htn superimposed on usually
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benign htn, seconday htn, or CKD
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what are the effects of malig htn
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ischemic kidneys, elevated renin, self perpetuating cycle of damage, arterio and nephrosclerosis, bleeding
necrosis leads to arteriosclerosis |
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what causes a flea bitten kidney
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malig htn
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increase diastolic above 130, papiledema, encephalopathy, renal faiure, early sx due to inc intracranial p
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malig htn
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__ __ __ is a potentially curable form of htn
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renal artery stenosis
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what is the lesion in renal a stenosis
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atheromatous plaque at origin of renal a. also fibromuscular dysplasia..can have it in one or both kidneys ( one big one small ( other one inc gfr and inc htn and >glomsclerosis)
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what are the clinical effects of thrombotic microangiopathies
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thromb in caps and arterioles, microangipathic hemolytic anemia, thrombocytopenia>>lead to vasc obstruction, vasoconstriction and ischemia
|
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HUS clinical features
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after intestinal infxn, sudden onset of bleeding,oliguria, anemia, NEURO CHANGE, HTN!
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cortical necrosis, arteriole thrombosis, glom change, intima and media hyperplasia
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HUS
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what are the pentad of TTP ( thrombotic thrombocytopenia purpura) features
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fever, neuro change, hemolytic anemia, thrombocytopenia, renal failure in 50%
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what is the gene affected in ttp
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ADAMTS13
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what are the two types of hereditary nephritis
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alport synd and thin BM dz- both have asymptomatic hematuria
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what is another name for thin BM or alport disease
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benign familial hematuria
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what percentage of alport pt get renal failure
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all of them
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what is the inheritance pattern of alport
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x linked where men get full dz and there is also AD and AR where men and women can both get full dz
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what is appearance of alport on EM
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moth eaten
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what is the majority of inheritance in thin bm dz
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most heterozygous and carriers
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what is the end result of thin bm
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rnal fxn is normal and rare progression to end stage, they have hematuria and proteinuria
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what are some secondary nephrotic diseases
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DM, SLE, hep C, HIV nephropathy
|
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what are some acute nephritic diseases
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SLE, bacterial endocarditis, goodpastures, HS, IGA neph
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what are the two main processes assoc with diabetic nephropathy
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metabolic: glycosolation-thicken BM and tubules inc mesangial matrix sclerosis
hemodynamic: nodular glom sclerosis( keimellsteil wilson) -arterioscler (hyaline) and papillary necrosis -hy |
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what are the three changes that are seen with nephosclerosis in a kidney with long term diabetes
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diffuse granular transformatio
thinning of renal cortex irreg cortical depressions secondary to pyelonephritis |
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what is the marker for the extent of diabetic neph--when is it irreversible
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degree of proteinuria
> 300 albumin/cr/d (acr) is macroalbuminuria and diab glom scler no tx intervention only renal failure |
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what is the histo appearance of diffuse prolif lupus nephritis
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subendo immune deposits that correspond with wire loops, increase cellularity, increase glom size, glom appears stuffed into bowmans with a dec in urinary space
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class i minimal mesangial lupus neph histo changes
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IF mesangial immune deposits but glomeruli are normal by light microscopy.
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class II mesangial lupus neph histo change
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— Light microscopy reveals mesangial hypercellularity or mesangial matrix expansion.
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what is seen in urine and what is clinical effect of mesangial lupus neph
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Urine: At most mild proteinuria or mild microscopic hematuria
Clinical: Generally associated with an excellent renal prognosis |
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what is seen in urine and what is the clinical effect of focal prolif lupus neph class III
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Urine: Hematuria (microscopic) without (or minimal) proteinuria Clinical: Death directly attributable to renal disease or advanced renal failure within 5 years occurs in < 5% of patients
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what is seen in urine and what is the clincal efffect of diffuse prolif lupus neph class IV
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Urine: Nephritic Syndrome or visible hematuria; mild proteinuria
Clinical: 50% respond to immunosuppressive therapy. No response or recurrence occurs in ~50%. 1/3 progress to end-stage renal disease |
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what is seen in urine and what is the clinical effect of membranous lupus neph class V
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Urine: Patients typically present with Nephrotic Syndrome; may occasionally show microscopic hematuria if they have associated proliferative component
Clinical: Most patients maintain a normal plasma creatinine for five years or more with no progression of renal disease |
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what is char of advanced sclerosing lupus neph class VI
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Characterized global sclerosis in greater than 90% of glomeruli; represents advanced stage lupus nephritis Classes III, IV & V ; end-stage renal disease
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fpln- histo
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necrotizing lesions, subendo dep=wire loops
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dfln histo
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mesangial and cap subendo deposits
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membranous lupus neph histo
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thickening of glom cap wall, meangial expansion and hypercellularity, Subepithelial immune deposits (D) are characteristic of any form of membranous nephropathy, but the intraendothelial tubuloreticular structures (arrow) strongly suggest underlying lupus
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in all classes of lupus nephritis the deposits are __ but in membranous they are__
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subendo
subepithelial and subendo |
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mesangial gn__
fpgn__ diffuse prolif gn__ membranous gn__ |
1.mesangial
2.mes and subendo 3. mes and subendo more than focal 4. subendo and subepi and mes |
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what is the most common cause of acute renal failure
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acute kidney injury
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what are the two common causes of acute kidney injury
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ischemia and direct injury to the tubule
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what tubules have a high rish for ischemia and injury
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PCT- by high demands
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what phase of aki is this: pregressive azotemia and oliguria
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initiating phase 24-36 hrs
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what phase of aki is this: oliguria, high azotemia, metab acidosis, hyperkalemia, transient
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maintenance phase
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what phase of aki is this: polyuria, hypokalemia, decreasing azotemia
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recovery phase
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what is aki prog related to
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underlying cause- 95 percent get better but burn and sepsis have worse prog
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what are the common bacterias in UTI
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gram neg- ecoli, enterobacterm proteus, klebsiella
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what are most UTIs caused by
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ascending cystitis
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what is most vesicoureteral reflux caused by
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partial or absent intravesical ureter
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Wheres is most inflam in acute pyelonephritis
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cortex and medulla
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what are the three complications of acute pyelonephritis
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papillary necrosis, pyenephrosis, perinephritic abcess
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what is analgesic nephropathy
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chronic renal dz caused by chronic massive dose of phenactin and one other analgesic- usu aspirin)-first seen in switzerland
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what path changes are seen in analgesic neph
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papillary necrosis in medulla and then cortical tubulointersitial nephritis
gross: red brown necrotic papilla sloughed into calyx |
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what is a severe sx of RPGN
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oliguria -death in weeks to months
blood in urine HTN, edema, mailaise weak, nausea rapidly rising azotemia |
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what are the three dx criteria for RPGN
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1. decline in renal fxn 50% loss or greater
2. rapid decline in <3 mo 3. renal biopsy finding of crescents |
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what are the tx for RPGN
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CS, immunosuppressants, some will need dialysis and transplant
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who gets RPGN
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55 yo and caucasions
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what are the three mech of RPGN-to cause severe glom injury
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anti gbm, immune complex mediated cresenteric, pauci immune type
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what is seen in histo of crescentic GN
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collapsed compacted glom tufts, crescent shaped mass, dense inflitrates of Macrophages and leukocytes. obliteration of urinary space, fibrin strands, *wrinkling of gbm
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where is the goodpasteure ag
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in the alpha3 chain of collagen type IV
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what is the tx for goodpasteure
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plasmaphoresis to rmeove pathogenic circulating abs also immunosuppression
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what three diseases are included under type II immune complex deposition RPGN
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iga neph, acute prolif gn , lupus nephritis
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what is seen on histo of type ii immune complex RPGN
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cell prolif w/in glom tuft and crescent formation, granular immune complex depos
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what is the tx for type II RPGN
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tx underlying prob
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what Ab do most pt with type III RPGN have
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anti neutrophil cytoplasmic abs (ANCAs)
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what is the most common benign renal neoplasm
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renal papillary adeonoma
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what are the three main benign renal neoplasms
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renal pap adenoma, angiomyolipoma, oncocytoma
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what are the two main malignant renal tumors
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renal cell carcinoma, urothelial carcinoma
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what kind of tumore is a renal fibroma or hamartoma
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renal nmedullary interstitial cell tumore
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what are three stomal or mesenchymal tumors
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lipoma, leiomyoma, angioma
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what are the two benign renal tumors that are not small
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oncomyocytoma, angiomyocytoma
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how big are renal papillary adenomas
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less than one cm-- now if a neoplasma is adeonoma like and is bigger than that it is called a low grade RCC
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what is the path of renal pap adenoma
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cortical discrete, yellow-gray, small, multiple
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What is common between low grade rcc and renal pap adenoma
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trisomy 7, 17, acidophil cytoplasm, papillae, thin fibrovascular cores
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where do renal oncocytomas arise from- what is their main role
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type a intercalated cells of the renal cortex CDs, involved in acid base homeostasis
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what is the chromosomal aleration in oncocytoma- what can it be confused with
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10q dele, RON proto oncogene
ddx needs to be estab between RCC chromophobe |
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what is this path: mohangony brown, well circumscribed neoplasm, with a stellate scar, may be very large >10cm
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oncocytoma
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what is this: abundant acidophilic granular cytoplasma, alveaolar nesting or solid pattern. EM- shows packed w mitochondria
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oncocytoma
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__ neoplasma has a strong assoc with tuberous sclerosis
what gene losss is it assoc with |
angiomyolipoma
loss of TSC 1 or TSC 2 tumor suppressor gene |
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what neoplasm is this: first presenting sign may be hemorrhage or shock- due to rupture and masive retroperitoneal hemorrhage
|
renal angiomyolipoma
|
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what is an important dx clue for angiomyolipoma
|
intimate relat of perivasc epiteloid sm mus cells (PECs) of the tumor with large vessel
|
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what tumor is this: young adult with severe HTN due to excessive renin secretion- histo resembles hemangiopericytoma and glomus tumores
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juxtaglomerular cell tumor
|
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how common is RCC
|
it is unusual compared to the other organ tumors but of the renal tumors it is the most common
|
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who gets rcc
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men 6th to 8th decade
|
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what are risk factors for rcc
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cig smoke, dm, estrogen, CRD
occurs mosly sporadic but 4 % is AD |
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what are ther hereditary RCC types
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1. von hippel landau- most common
2. hereditary clear cell carc 3. hered pap carc |
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what is the most common rcc
|
clear cell
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is clear cell rcc sporadic or inherited
|
mostly sporadic but the inherited type has a chrom 3 short arm dele--VHL tumor supressor dele
|
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what genes are assoc with pap carcinoma
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chrom 7,17, 16 Y met , prcc oncogenes
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what tumor is this: pale espinophilic cytoplasm, nuclear halo, good prognosis, from type b intercalated cells of renal cortex, looks like oncocytoma
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chromophobe renal carcinoma
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what malignant rcc's have worst prog
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collecting (bellini) duct carcinoma, - medullary location
and sarcomatoid and medullary carcinoma |
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what is the clinical triad of rcc
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hematuria, costovertebral pain, palpable flank mass
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what are the presenting sx of rcc usu assoc with
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metastasis
|
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what is the prog of rcc with and without met
|
overall 45% 5 y survival, but 75 % without met and 15 % with met
|
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of the rcc classify prog as better, avg and worse
|
pap and chromophobe= better
clear= avg worse= sarcomatoid and medullary |
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what is the mode of spread of most rcc
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hematogenous
|
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if rcc penetrates gerots fascia- what stage are you
|
iv
|
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what tumor is this: ywllowish, one pole of kidney, well circ, inades IVC, combo of cystic and solid, varigated, can get into renal vein
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RCC
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what tumor is this:sim to oncocytoma, see mitochon.some clear cells. granular cytoplasm, perinuclear clear halo, solid pattern of growth
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chromophobe
|
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what is another name for clear cell
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hypernephroma
|
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why is it called clear cell
|
bc there is glycogen and lipid which looks clear- looks sim to normal adrenal
|
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what is this tumor: entrap glomerulus, diffuse pattern of growth, pink in cyto
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clear cell
|
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what tumor is this: made of spindle cells. sim mesenchymal tumore
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sarcomatoid
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what tumor is this: in pt with sickle cell dz, poorly differentiated, heavily infiltrated with neutrophils
|
renal medullary carcinoma
|
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where do clear cell tumors come from
|
PCT
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where do pap rcc come from
|
DCT
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where do tubular or spindle rcc come from
|
LOH or CD
|
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where do oncocytoma and chromophobe rcc come from
|
intercalated cell of cortex
|
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where do CD carcinoma or medullary carcinomas come from
|
CD of medulla
|
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what tumor is this: originate from urothelium of renal prelvis, hematuria, small, flank pain, hydronephrosis, infiltrate wall of pelvis and calyces
|
urothelial( transitional cc) of renal pelvis
|
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what is this: child, large abdominal mass, palpable, hematuria, htn
|
wilms tumor
|
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what is a group one wilms tumor
|
WAGR assoc with chrom 11 and WNT1 mut or loss
|
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what is group two wilms
|
denys-dash synd- gonadal and retinal tumors assoc with WNT1
|
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what is group 3 wilms
|
beckwith windmann synd- assoc with WNT 2
|
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what tumor is this: small, well circ. areas of necrosis, lower pole, nephrogenic rests( precursor for b/l) tumors, atypical nec. p53, hyperchrom nuc
|
wilms- small round cell tumor of childhood
|
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what is the favorable triphasic histology
|
mimics normal kidney with three cell types: 1. blastemal 2. epithelial 3. stromal (spindle)...no signif anaplasia
|
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what is anaplasia assoc with
|
p53 mutation and chemo resistance
|
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how do you get most diverticula
|
aquired from urethral obstruction
ie prostae enlarged |
|
what do diverticula predispose pt to
|
infxn, vesicoureteral refluz if impinge on ureter, carcinomas that will be more advanced due to thin wall
|
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what can happen to exposed mucosa of bladder exstrophy
|
can undergo metaplasia and get infected, also pt is incr risk for adenocarincoma
tx w surgery |
|
what is the prog for grades I-III vesicoureteral reflux
|
it will disappear child given antibiotics daily
|
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what is a urachal cyst
|
ant to bladder, midline. heterogenous, causes pain, and fever- carcinomas may arise from them . closed at umbilicus. cyst can get infected
|
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what are the three most common causes of acute cystitis
|
1. ecoli 2 . proteus 3. klebsiella 4. enterobacter
also radiation can cause it |
|
what is the path of cystitis
|
hyperemia and exudate. non specific acute inflam
|
|
who gets hemorrhagic cystitis
|
pt on antitumor drugs such as cyclophosphamide
also adenovirus pt |
|
what is the diff between chronic cystitis and acute cystitis
|
chronic- mononuclear cells and acute- pmns
|
|
follicular cystitis is not necess assoc with
|
infxn
|
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what are sx of cystitis and what is tx
|
freq, lower abdominal pain localized over bladder or suprapubic. dysuria,
tx: hospitalization and antibiotics |
|
what is the main sx assoc with interstitial cystitis
|
chronic pelvic pain- recurring, suprapubic, freq urgency, hematuria dysuria, ****with out evidence of bact infxn- some say only psychos have it
|
|
what are some cytoscopic sx of chronic cystitis
|
punctate hem, glomerulations, fissure, mast cells, transmural fibrosis, HUNNER's ulcers!
|
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what is this: peculiar pattern of bladder inflam, 3-4 cm in diam, soft yellow plaques , foamy macrophages, giant cells, enlarged lysosomes called michaelis gutmann bodies, related to chronic bact infxn,
|
malakoplakia
|
|
who gets makaloplakia
|
immunosupressed transplant pt
|
|
what is this: inflam conditon resulting from irritation to the bladder from indwelling catherters, extensive submucosal edema- raises ep
|
polypoid cystitis
|
|
not a neoplastic mass, benign reactive process that occurs in the urothelium, caused by chronic irritation from a stone or previous surgery, causes metaplasia of urothelium>devel pap and tubular growths
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nephrogenic adenoma
|
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what layer are nephrogenic adenomas in
|
the lamina propria- they spare the muscularis
|
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what are sx of NA
|
irritative voiding and hematuria
|
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who is most likely to get NA
|
men age 26-80, that have had repeat biopsies for urthelial carcinoma
|
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what are the cytoscopic findings of NA
|
multiple polypoid or single papillary . cystic, or polypoid growths lined by cuboidal ep, it can occur at diverticula or at sites of previous surgery- definitive dx can only be made at biopsy
|
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what is this: caused by irrriation, causes metaplasia of urothelium, forms buds that grow down into lamina propria- buds can become cystic deposits or fill with mucin
|
cystits cystitca and cystitis glandularis
|
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CC arises when the urothelial cells int he center of solid clusters of __ __ undergo degenerative changes- these are large cysts
|
brunns nests
|
|
intestinal CG is a risk factor for bladder ___
|
adenocarcinoma
|
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what sx are assoc w CC and CG
|
those sx of irritation, freq, dysuria, urgency, hematuria
|
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what is seen on path of CC and CG
|
cobblestone appearance with a focal polypoid mass
|
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what is keratinizing sqaumous metaplasia of bladder a risk factor for
|
devel of carcinoma, bladder contracture
|
|
sq metaplasia of bladder can occur secondary to
|
chronic cystits. schistosomiasis, diverticulum, non functioning bladder
|
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sq cell carcinoma of bladder are mostly just __ variants
|
transitional cell carc
|
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what are the sq cell carcinoma of bladder
|
mixed carcinoma, adenocarincoma, small cell carcinoma
|
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what kind of neoplasms make up 90 percent of bladder neoplasia
|
urothelial tumors
|
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what are the benign nonep bladder tumors
|
leimyoma, lipoma, fibroma, neurofibroma
|
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what are the two malignant nonep bladder tumors
|
rhabdomyosarcoma
|
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what tumor has a cambium layer of clusters of tumor cells present beneath ep- results in nevoid appearance
|
rhabdomyosarcoma
|
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what is a malignant non ep tumor that is part of a systemic dz
|
primary malignant lymphoma
in assoc with chronic cystitis |
|
who is at the highest risk for urothelial cell carcinomas
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white males..industrial, cig smokers, exposure to aryamines, schistomes, long term analgesics, long term exposure to cyclophoshamide or radiation
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what chrom are assoc with urotheliam carcinoma
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chrom 9 monosomy or dele ( for more superficial tumors), also chrom 17 deled ( for invasive), CIS is assoc with p53
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what is usu the only clincal finding with urothelial cell carcinoma
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painless hematuria
** frequently multiple tumors at initial dx |
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what is the tx for noninvasive TCC
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transurethral resection or intravesical therapy
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what is tx for invasive tcc
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segmental cystectomy, radical cystectomy, immunotherapy
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what is the most common malig bladder cancer
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papillary carcinoma non invasive
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flat lesions cause discomfort but papillary lesions cause__
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hematuria
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what are some benign changes in bladder urothelium- flat
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hyperplasia, reacive atypia, atypia of unknown signif-->
none of these have increase risk of malignancy |
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what are some premalig changes in bladder- flat
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dysplasia and cis
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what are some high risk changes for devel of invasive carcinoma
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dysplasia, CIS
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what bladder lesion is this: benign, no atypia, low recurrence, fibrovasc core, small, extends from surface, lined with normal ep
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papilloma
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what bladder lesion is this: younger males, trigone region, low recurrencem raised bump, covered with normal ep, prolif into lamina propria, ep growing down
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inverted papilloma
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what bladder lesion is this: moderate recurrence, thickened ep covering pap porjections, minimal cellular atypia
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pap urothelial neoplasia of low malig potential
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what bladder lesion is this: most common of papilllary tumors, high recurrence rate, very thick epm scattered hyperchomatic nuc, mitosis
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pap carcinoma- low grade tcc
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what bladder lesion is this: high recurrence rate, severe cytologic atypia, hyperchromatic nuc, huge nuc, multifocal
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pap carcinoma high grade tcc
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both low and high grade pap carcinoma do not invade as much as
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flat CIS
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what bladder lesion is this: nodular, fills lumen, hemorrhagic. tan, full thickness, ulceration and necrosis, yellow areas
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high grade pap carcinoma
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__ is critical for prognosis
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stage
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cytology for urothelial neoplasia has high specificty for___ and low sensitivity for __ and __
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high grade
hg and lg |
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what is it important to rule out when you think that you have an adenocarcinoma of the bladder
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that it is not a Met from another place
- in bladder it is in the dome cells ( urachal remnants -also seen in relation to chronic inflam w intestinal metaplasia |
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what does red and clear urine indicate
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free hb and myoglobin
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what can you do with a midstream urine catch
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microscopy and culture
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what is a sterile suprapubic aspiration of urine used for
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to eval for lower UTI- best technique for getting culture bladder urine for <1 yo
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dilute urine can give misleading __ results
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negative
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bacterial overgrowth produces__ urine
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alkaline
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what is the ref range for urine specific gravity
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1.020 and 1.028
dont use dipstick to test this |
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should there ever be positive glucose on a dipstick
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no must find explaination
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dipstick is highly sensitive for blood but low___
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specificity
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dipstick esterase is more __ than __
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sensitive than specifiv
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dipstick nitrite is more__than __
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specific than senstive
but both esterase and nitrite lack sensitivty |
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what holds RBC casts together
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tamm horsefall
- this means the prob is in the kidneys |
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what is the common matrix of hyaline casts
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tamm horsefal protein- secreted by renal tubule
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what is the avg urine protein conc
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5mg/dl
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where does all protein in urine come from
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hemorrhage from mucosa or penetrating the GBM
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what do you have to do if you want plasma from drawn blood
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give anticoag- to prevent clotting
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what are the alpha and beta globulins
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specialized and diverse proteins
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isolated porteinuria is always assoc with
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renal origin
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albumin has a high sensitivity of glom perm because it is
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small and anionic
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what is almost always the cause of proteinuria
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glomerular dz--- tubularintersitial dz and overflow hardly ever happens bc its mild and not really detected by dipstick
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dipstick is not accurate in assessing the ___ of proteinuria
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severity
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in order to know the severity of proteinuria you need to order
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24 hr quantative urine, pcr and acr
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