Kidney usmle

7/23/2019 Kidney usmle

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www.natures.irMore Free USMLE , MCCEE ,MCQe and AMQ Flashcards

What is the most commoncause of TIN (Tubulointerstitial

nephritis)?APN (Acute pyelonephritis)

APN (Acute pyelonephritis) is

most common in male/female?

APN is

female>male

What is the most commoncause of APN?

E. Coli

VUR (Vesicoureteral reflux) = ?urine refluxes into the ureters during

micturition

What is the most commonmechanism for upper/lower

UTIs in females?Ascending infection

Findings in APN and NOT lowerUTIs?

Pain in fever, flankWBC casts in urine
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Causes of CPN (Chronicpyeonephritis)?

VUR (Vesicoureteral reflux) in younggirls,

chronic hydronephrosis

CPN (Chronic pyeonephritis) =?

cortical scars overlie blunt calyces;visible with IVP

CPN (Chronic pyeonephritis)

microscopic findings?

glomerular scarring; tubular atrophy

("thyroidization")

Reflux nephropathy causeswhat?

causes hypertenstion in children

what are causes of druginduced TIN = ?

methicillin, NSAIDs, rifampin,sulfonamides

Pathogenesis of drug inducedTIN?

abrupt onset fever, oliguria, rash

Analgesic nephropathypathogenesis = ?

acetaminophen + aspirin; renalpapillary necrosis


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Renal papillary necrosiscomplications?

"ring defect" on IVP from sloughing ofpapilla

Prevention of uratenephropathy?

allopurinol before aggresive cancertherapy

Chronic Pb poisoning

pathogenesis?

proximal tubules with nuclear acid-

fast inclusions

BJ (Bence Jones) proteinuria =?

casts with foreign body giant cellreaction

CRF (Chronic Renal Failure)Hematologic findings = ?

normocytic anemia; qualitativeplatelet defect

Renal osteodystrophy is due to?due to secondary HPTH

(hyperparathyroidism), osteomalacia,osteoporosis

CRFcardiovascular findings?

hypertention, pericarditis, CHF,atherosclerosis


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CRF (chronic renal failure)causes?

anion gap metabolic acidosis; serum phosphorus/ potassium;

serum calcium

increased Cystatin C is anindicator of ?

biomarker of kidney function

CRF

urinalysis findings?

Free water clearance in CRF is zero

Waxy/broad casts

BNS (benign nephrosclerosis)kidney of essential hypertension

is due to what?hyaline arteriolosclerosis

Malignant hypertensionmost common cause?

pre-existing BNS (Benignnephrosclerosis)

Malignant hypertensionclinical findings?

blood pressure 210/120 mm Hg,encephalopathy, renal failure

Malignant hypertensioninital treatment?

IV nitroprusside (intravenous sodium)


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Renal infarctionmost common causes?

embolization

Renal infarctionindication?

sudden flank pain and hematuria

Sickle cell trait/ disease

clinical presentations?

hematuria,loss of concentration,

renal papillary necrosisAPN; pyeonephritis

Diffuse cortical necrosis = ?anuria followed by ARF in pregnant

woman

What is the most commoncause of upper urinary tract

obstruction?Hydronephrosis

What is the most commoncause of upper urinary tract

obstruction?Renal stone

What is the most commonmetabolic abnormality causing

calcium stones?

Hypercalciuria


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______ increase reabsorptionof calcium out of urine?

Thiazides increase reabsorption ofcalcium out of urine

What is the most commoncause of renal stones?

calcium oxalate; calcium phosphate

Struvite stone = ?(Manesium ammonium phosphate)MAP; urease producers; alkaline

urine pH

Renal stoneclinical findings?

ipsilateral colicky pain in flankradiating to groin; hematuria

diagnosis of Plain film? 80% stones radiopaque

Diagnosis of Spiral CT?is the best overall sensitivity and

specificity; expensive

Diagnosis usage of ultrasoundin renal stones?

detects hydronephrosis, not stone


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What is done for stoneprevention?

hydration is very important

Rx for calcium stones? hydrochlorothiazide

Angiomyolipoma is associated

with?

hamartoma associated with tuberous

sclerosis

Renal cell carcinomaappearance?

yellow tumor with renal vein invasion

Renal cell carcinoma derivesfrom what?

proximal tubule cell

what is the most cause of Renalcell carcinoma?

smoking

Renal cell carcinomainvades____?

renal vein poor prognosis


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Clinical findings of renal cellcarcinoma?

hematuria, flank pain, abdominalmass

Renal cell carcinomalab findings?

ectopic secretion EPO and PTH-related peptide

what is the most common cause

of TCC renal pelvis?smoking

what is the most common causeof renal tumor in children?

Wilms' tumor

Wilms' tumor in children = ?with unilateral flank mass and

hypertention

Wilms' tumor is due to? hypertension due to renin secretion

what happens to vitamin D inRenal function?

Second hydroxylatioin of vitamin D: 1--hydroxylase in proximal tubule


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what is the most common upperurinary tract cause of hematuria

Renal stone

Iwhat is the most commoncause of lower urinary tract

hematuriainfection

what is the most commonnoninfectious cause of lower

urinary tract hematuriatransitional cell carcinoma bladder

what is the most common causeof microscopic hematuria in

adult malesBenign prostatic hyperplasia

What drugs most commonlycauses hematuria?

anticoagulants

Persistent proteinuria usuallyindicates ___?

indicates intrinsic renal disease

how does Serum blood ureanitrogen (BUN) relate to extra

renal loss(eg. skin)?

Urea: some extrarenal loss (eg. skin)with high serum concentration


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What is the most commoncause of increased serum

BUN?congestive heart failure

What is the end-product ofcreatine metabolism?

Creatinine

what happens to Creatinine in

the kidneys?

Creatinine is filtered in the kidneys;

not reabsorbed or secreted

what do Creatine supplementseffect the level of serum

creatinine? serum creatinine

what does Azotemia do toserum BUN level and

creatinine?

serum BUN and creatinine

what happens to the urea in theproximal tubule

Urea: filtered; partly reabsorbed

what is the cause of Prerenalazotemia?

cardiac output, GFR; ratio > 15


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Renal azotemia is caused by ?details?

-parenchymal damage to teh kidneys-intrinsic renal disease; extrarenal

loss of urea; ratio 15

cause of postrenal azotemia?obstruction behind kidneys;

initially ration > 15; 15 if obstruction persists

Nephrotoxic drugs in elderly: =

?

adjust dose and interval for normal

in CCr (Creatinine clearance)

CCr dosage in relation to age normally decreases with age

what are causes of IncreasedCCr ?

normal pregnancyearly diabetic glomerulopathy

what is the gold standard to testrenal disease?

Urinalysis

how ischemic is the renalmedulla?

the renal medulla is relativelyischemic


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in afferent arterioles whatcontrols blood flow

Renal PGE(sub)2 : vasodilationafferent arteriole

in efferent arterioles whatcontrols blood flow?

ATII (vasoconstrictor)

GBM (glomerular basementmembrane); what determines

the protein filtration?the size and charge

Albumin negative charge, whatis it repelled by?

repelled by negatively charged GBM(glomerular basement membrane)

what is a sign of nephroticsyndrome?

Fusion of the podocytes

proliferation of parietal epithelialcells causes?

"cresents"

what type of kidney isassociated with Turner's

syndrome?

horseshoe kidney


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what is the most common typeof cystic disease in children?

renal dysplasia

linear IF(Immunofluorescence);what is the linear pattern?

anti-GBM disease(Goodpasture syndrome)

Granular pattern indicates = ?immunocomplex type of

glomerulonephritis

how does EM (Electronmicroscopy) detect sites of IC(immunocomplex) deposition?

immunocomplex deposits areelectron-dense

what is the most commonmechanism causingglomerulonephritis?

Immunocomplexes

in what process doImmunocomplexes attract

neutrophils

activate complement C5aproduced attracts neutrophils

Nephritic syndrome = ? neutrophil-related injury to glomeruli


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does pitting edema distinguishnephritic from nephrotic

syndrome?

Pitting edema: does NOT distinguishnephritic from nephrotic syndrome

Nephritic syndromeclinical and lab findings= ?

moderate proteinuria; dysmorphicRBCs, RBC casts

Nephrotic syndrome; injury is

due to ?

cytonkine injury to podocytes; loss of

negative charge on GBM

Nephrotic syndromelab findings?

proteinuria > 3.5g/24 hours; fattycasts

which has less glomerularinlammation

Nephrotic or nephritic syndrome?

Nephrotic has less glomerularinlammation than nephritic syndrome

What is the most common typeof chronic renal failure in US?

Diabetic glomerulopathyType 1 > type 2 diabetes

what is the most common causeof diabetic glomerulopathy?

poor glycemic control


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Pathogenesis of diabeticglomerulopathy?

NEG (Nonenzymatic glycosylation) ofthe GMB (glomerular basement

membrane): vessel/tubularpermeability to protein

Osmotic damagewhat happens to sorbitol?

sorbitol (it is osmotically active)

Hyaline arteriolosclerosis ofefferent arteriole

how does it cause injury? GFR producing hyperfiltration injury

Microangiopathy in diabeticglomerulopathy

increase or decrease ?` deposition type IV collagen

what is the first lab sign ofdiabetic glomerulopathy?

Microalbuminuria

ACE inhibitor/ receptor blockersshow the progression of what in

diabetes?

shows the slow progression ofnephropathy in type 1/type 2 diabetes

Alport's syndrome?hereditary nephritis, sensorineural

hearing loss, ocular defects


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thin basement membranedisease?

persistent hematuria

what is the most common causeof chronic glomerulonephritis?

Rapidly progressiveglomerulonephritis (RPGN)

what is the most common cause

of ARF (Acute renal failure)?ATN (Acute tubular necrosis)

what is the most common causeof ischemic ATN?

Prerenal azotemia

what is the key cast of ATN(Acute tubular necrosis)?

Renal tubular cell cast

what is the most common causeof nephrotoxic ATN(Acute

tubular necrosis) ?Amioglycosides

ATN (Acute tubular necrosis)lab findings?

-renal tubular cell casts-BUN: creatinine ratio 15;

hyperkalemia, metabolic acidosis


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Focal glomerulonephritisDescription?

Only a few glomeruli are abnormal

Diffuse glomerulonephritisDescription?

All glomeruli are abnormal

Proliferative glomerulonephritis

Description?>100 nuclei in affected glomeruli

Membranous glomerulopathyDescription?

Thick GBM, no proliferative change

Membranoproliferativeglomerulonephritis

Description?Thick GBM, hypercellular glomeruli

Focal segmentalglomerulosclerosis

Description?

Fibrosis involving only a segment ofthe involved glomerulus

Crescentic glomerulonephritisDescription?

Proliferation of parietal epithelial cellsaround glomerulus


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Primary glomerular diseaseDescription?

Involves only glomeruli and no othertarget organs (eg., minimal change

disease)

Secondary glomerular diseaseDescription?

Involves glomeruli and other targetorgans (eg., SLE)

type of proteinuria:Functional

definition?

Protein < 2 g/24hr

Not associated with renal disease

type of proteinuria:Overflow

definition?

Protein loss is variableLMW proteinuria

Amount filtered >tubular reabsorption

type of proteinuria:Glomerular

definition?

Nephritic syndrome: protein > 150mg/24hr,

but 3.5

g/24hr

type of proteinuria:

Tubular

definition?

Protein < 2 g/24hr

Defect in proximal tubulereabsorption of LMW proteins (eg.

amino acids at normal filtered loads)

Increased Serum BUN

Causes? (5)

Decreased cardiac output,Increased protein intake,

Increased tissue catabolism,

Acute glomerulonephritis,Acute or chronic renal failure,Postrenal disease


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Decreased Serum BUN

Causes? (3)

Increased plasma volume,Decreased urea synthesis,Decreased protein intake

Causes of Increased CCr?Normal pregnancy,

Early diabetic glomerulopathy

Causes of Decreased CCr?Elderly people,

Acute and chronic renal disease

Type II MPGN

nephrotic or nephritic?Nephrotic


nephrotic or nephritic?

Nephrotic

Diffuse proliferative

glomerulonephritis (SLE)


Nephritic

Diffuse membranousglomerulopathy


Nephrotic


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IgA glomerulopathy (Berger'sdisease)


Nephritic

Rapidly progressive crescenticglomerulonephritis


Nephritic

Type I MPGN


Post-streptococcalglomerulonephritis


Nephritic

Minimal change disease


Prerenal azotemia:

FENa%,BUN:Cr,

UNa,UOsm,

urinalysis

Prerenal azotemia:

FENa% 15UNa 500urinalysis: Normal sediment or

hyaline

Acute glomerulonephritis:FENa%,BUN:Cr,

UNa,UOsm,

urinalysis

Acute glomerulonephritis:FENa% 15UNa 500urinalysis: RBC casts, hematuria


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Acute tubular necrosis:FENa%,BUN:Cr,

UNa,UOsm,

urinalysis

Acute tubular necrosis:FENa% >2BUN:Cr 15

UNa >40UOsm 2BUN:Cr 15

UNa >40UOsm 150mg but less than

3,500mg/24hours

Damage to GBM; nonselectiveproteinuria with loss of albumin and

globulins

Nephrotic Syndrome>3,500mg of protein/24hours

Selective Proteinuria with only theloss of albumin


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What is the normal BUN? 7-18mg/dl

T/F Urea is partly reabsorbed inthe PCT?

True

What is the BUN dependent

upon?

GFR, Protein intake or break down,

Proximal tubule reabsorption

Most common cause ofincreased serum BUN

CHF (decrease GFR)

What is the normal Creatinine? (0.6-1.2)

Where does on get creatinine? End product of Creatine in muscle

Creatinine is filtered in thekidney but not....

reabsorbed or secreted


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What should the BUN/Cr ratiobe?

Less than 15

Azotemia Increase in BUN/Cr in the serum

How does one break Azotemia

up?Prerenal, Renal, Postrenal

Name 2 pathologies that willcause Prerenal azotemia?

Blood loss, CHF

Why does BUN go up morethan Cr during Prerenal

Azotemia?

First the urea is being made quickerthan the creatinine, but also the ureacan be reabsorbed while the Cr can

not.

What is the BUN:Cr level withsomeone with CHF/Blood loss?

>15

normal BUN:Cr is


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What is the BUN:Cr ratio withsomeone with a renal disease?

15

Name some examples of PostRenal Azotemia?

Prostate hyperplasia, Blockage ofureters by stones/cancer

Oval Fat Bodies Nephrotic Syndrome

RBC cast Nephritic type of Glomerulonephritis

WBC cast Acute Pyelonephritis


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Waxy Cast Sign of chronic renal Failure

fusion of the podocytes? sign of Nephrotic syndrome

Focal Glomerulonephritis? Only a few Glomeruli are abnormal

Diffuse Glomerulophritis All glomeruli are abnormal

Proliferative Glomerulonephritis >100 nuclei in affected glomeruli

Membranous Glomerulopathy Thick GBM, no proliferative change

membranoproliferativeGlomerulopathy

Thick GBM, Hypercellular glomeruli


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Focal Segmentalglomerulosclerosis?

Fibrosis involving only a segment ofthe involved glomerulus

Crescentric Glomerulonephritis?Proliferation of parietal epithelial cells

around glomerulus

Primary glomerular diseaseInvolves only glomeruli no other

organ (ex minimal change Disease)

Secondary Glomerular disease?Involves glomeruli and other target

organs (ex. SLE)

Fatty cast with maltesecrossses?

Nephrotic Syndrome

total body water is what percentof body weight?

~60%

Na is major component of whatcompartment?

ECF


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K is component of which?(major)

ICF

calculate pOsm2(serumNa)+serumglucose/18+serum

blood urea nitrogen/2.8=275-295

Can urea diffuse freely? yes

does water shift with changes inurea?

No

hyponatremia shift water inwhat direction?

into the cell (into ICF)

what does TBNa+ stand for? total body Na

decreased TBNa signals what? sign of volume depletion


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dry mucous membranes,decrease skin turgor, drop inBP, increase in pulse from

sitting to supine (positive tilttest)

signs of volume depletion

increased TBNa may producewhat>

ascites, effusions

so if the interstitum has too much Na,then water from the capillary will be

pulled out and heldd there

becuase of gravity, it will move to thefeet

if you have no starling forcechanges, can you have pitting

edema?

no, not likely to occur withoutchanges in starling

Isotonic loss of fluid, what are

the TBNA, TBW?will there be signs of

dehydration?

TBNa is low, so is TBW, but serum

Na and POsm are normal.YES

Can pitting edemas be seen ininfusion of saline?

yes, if excessive infusion of isotonicsolution

Hyponatremia has what affecton POsm?

decrease


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water shift to what comp. inhyponatremia?

shift into the ICF

what are some examples ofrenal Na loss?

loop diuretics, addisons disease, 21-hydroxylase deficiency

isotonic loss, give an examplediarrhea, ECF contracted, normal ICF

volume, normal POsm and serum Na

isotonic gain, example:isotonic saline infusion, see other

card, leads to an increase in the ECFvolume

Gain of waterdecrease POsm, Na, expanded ECF,

expanded ICFexample: SIADH

hypertonic loss of Nadecrease in POsm, Na, contracted

ECF, expanded ICF

hypotonic gain of Na

decrease in Posm, Na, expandedICF, expanded ECF

ex. right sided heart failure, cirrhosis,nephrotic syndrome


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in ptting edema states, whatendocrine changes are there

that cause the state?

release of catecholamines, renin-angiotensin-aldosterone, stimulate

release of ADH, increased retentionof Na, changes the starling forces,

the Na containing fluid is redirected tothe interstitum and causes ptting

hypotonic loss of Nastate the POsm, Na, ECF, ICF,

example

increase in POsm, NaECF is contractICF is contract

osmotic diuresis--glucose, sweating,infant diarrhea

insensible water loss--fever, ordiabetes insipidus

increased POsm, Na

ECF expanded, ICF contractedwater is going to flow from cells to theoutside where the water was lost

hypertonic gain of Naincreased POsm,ECF expansionICF contraction

hyperglycemia

increases POsm, NaECF contractionICF contraction

ex. ketoacidosis,we will get a hypotonic loss of waterand Na (osmodiuresis)--leading to

volume depletion

aldosterone mediated control ofwhat channels where?

Na/K/Cl channelslocated in the distal and collecting

ductNa is exchanged for K, and if K is not

present, it will exchange for Hloss of H will cause a increase in

reabsorption of HCO3 in the blood


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Hypokalemia has what affect oninsulin?

INHIBITS SECRETION OF INSULIN

hyperkalemia has what affecton insulin?

INCREASE PRODUCTION

aldosterone affects...K and H in the late distal and CT

resorption of K by the H/K/ATPase

arterial pHalkalosis causes H to move outof the cells and K will into the

cell, causing

hypokalemia

acidosis will shift H... into the cell, K out, and hyperkalemia

loop and thiazide have whataffect on K?

hypokalemia

renal failure leads to whatchange in K?

hyperkalemiawhich can lead to arrythemias

peaked T waves


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Resp acidosis is defined asPaCO2 is high, pH is low, and HCO3

is risingcompensated by renal

if serum bicarb is over 30, thenwe know it is acute or chronic?

renal compensation for chronic respacidosis

U waves are a sign of? hypokalemia

CNS respiratory center--stim/depression causes what?

depression: resp acidosisstim: resp alkalosis

upper airwaysobstruction--get acidosis

rib fracture: hyperventilation from pain

lungsCOPD, CF: acidosis

restrictive airway: alkalosisothers: PE, mild bronchial asthma

define resp. alkalosis PaCO2


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increased anion gap metabolicacidosis

the anions of acid replace the bicarbHCO3 loss is now countered by

anions of the acid

Adult polycystic kidney disease

Asymptomatic until middle age. Renal

insuficiency, hematuria, hypertension.Abdominal masses and flank pain.Renal failure. Associated with liver

cysts, berry aneurysms, mitralprolapse.

Nephritic syndrome Hematuria, hypertension, azotemia,oliguria, proteinuria 3.5g/day,

hypoalbuminemia, generalizededema, hyperlipidemia

Acute poststreptococalglomerulonephritis light

microscopy

Hypercellular glomeruli withneutrophils, red cell casts in renal

tubules

Acute poststreptococalglomerulonephritis

immunofluorescence

Granular deposits of IgG, IgM and C3throughout the glomerulus

Acute poststreptococoal

glomerulonephritis electronmicroscopy

subepithelial humps immune complex

deposits


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Pathogenesis of Goodpasturesyndrome

anti-GBM antibodies damage kidneysand lungs. Antigen is collagen type IV

Clinical presentation ofGoodpasture syndrome

nephritic syndrome with hemoptysis.Most will develop RPGN

Goodpasture syndrome electron

microscopyGBM disruption

Goodpasture syndromeimmunofluorescence

Smooth and linear pattern of IgG andC3 in the GBM

Causes of RPGNGoodpasture, poststreptococal, SLE,

Wegner

RPGN light microscopyCrescent formation in Bowman's

space (macrophages, fibrin parietalendothelial cells)

RPGN immunofluorescencegranular or linear deposits of Ig and

complement


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RPGN electron microscopy GBM disruption and discontinuity

IgA nephropathy (Bergerdisease)

Most common cause of GN. Nephriticsyndrome with recurrent hematuria.Associated with celiac sprue and

Henoch-Schonlein purpura

IgA nephropathy light

microscopyMesangial proliferation

IgA nephropathyimmunofluorescence

Mesangial deposits of IgA and C3

IgA nephropathy electronmicroscopy

Mesangial immune complex deposits

MPGN clinical features

Nephiritic or nephrotic. Decreased

C3. C3 nephritic factor antibodyactivates C3 convertase with

degradation of C3

MPGN light microscopyMesangial rpoliferation with BM

thickening and tram tracking (splitting

of basemant membrane)


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MPGN immunofluorescenceGranular pattern of C3 often with IgG

C1q and C4

MPGN electron microscopysubendothelial and mesangial

immune complex deposits

Alport syndrome

X-linked defect in type 4 collagencharacterized ny nephritis, hearingloss and ocular abnormalities. EM:

alternating thickening and thinning ofBM

Membranous GN etiology85% idiopathic, penicillamine, HBV,

HCV, SLE, DM

Membranous GN lighmicroscopy

Diffuse membrane-like thickening ofcapillary walls, baseman membrane

projection spikes

Membranous GNimmunofluorescence

Granular and linear pattern of IgGand C3

Membranous GN EMSubepithelial deposits, effacement of

podocyte foot processes


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Minimal change diseaseNephrotic syndrome in children 2-6years. EM: effacement of epithelialfoot processes. Rx.: corticosteroids

Focal segmentalglomerulosclerosis light

microscopy

Focal segmental sclerosis andhyalinization of glomeruli

Focal segmental

glomerulosclerosis IF

IgM and C3 deposits in sclerotic

segments

Mention all nephritic syndromepathologies

Poststreptococal, Goodpasture, IgAnephropathy, RPGN, MPGN, Alport

Mention all nephrotic syndromepathologies

MGN, minimal changee disease, focalsegmental glomerulonephritis

Features of chronicglomerulonephritis

Renal failure, uremia, anemia,

proteinuria, hypertension, azotemia,reduction of GFR, hypocalcemia (novitamin D), hyperphosphatemia.

Hyalinization of glomeruli, fibrosis,atrophy and lymphocytes

Features of acute tubular

necrosis

Reversible injury. Oliguria, increased

BUN and creatinine, metabolicacidosis and hyperkalemia


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Causes of ischemic acutetubular necrosis

hemorrhage, severe renalvasoconstriction, hypotension,

dehydration, shock

Causes of nephrotoxic acutetubular necrosis

polymyxin, methicillin, gentamicin,sulfonamides

Clinical features of acute

pyelonephritis

E. coli, proteus, kleibsiella,enterobacter. Fever, chills, dysuria,

frequency, urgency, costovertebralangle tenderness, pyuria, WBC casts

Types of renal calculi

Calcium oxalate (75%), struvite(asoociated with urea-splitting

bacteria - proteus), uric acid (gout,leukimia, acid urine)

Clinical features of renal calculiUnilateral colic pain, hematuria,

obstruction, infection. Calcium stonesare raddiopaque.

Clinical features of renal cellcarcinoma

Cigarette smoke is risk factor.Hematuria, palpable mass and flank

pain

Renal cell carcinomaparaneoplastic syndromes

Polycythemia (EPO), hypertension(renin), Cushing syndrome


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Wilms tumor

Mutations in WT-1 and WT-2suppressor genes. WAGR syndrome

- Wilm's tumor, aniridia, genitalanomalies, mental retardation

In order for secondhydroxylation of vitamin D to

occur, what enzyme isrequired?

1-alpha-hydroxylase in proximaltubule

What is the most commonupper urinary tract cause of

hematuria?Renal stone

What is the most commoncause of lower urinary tract

hematuria?Infection

What is the most commonnoninfectious cause of lower

urinary tract hematuria?Transitional cell carcinoma bladder

What is the most commoncause of microscopic hematuria

in adult males?BPH

What is the most commondrugs causing hematuria?

Anticoagulants


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What does persistentproteinuria usually indicate?

intrinsic renal disease

What is the most commoncause of increased serum

BUN?CHF

What is end-product of creatine

metabolism?Creatinine

Why is creatinine an excellentmetabolite for renal clearance

testing?Filtered; not reabsorbed or secreted

What does creatinesupplements increase?

serum creatinine

What is increase in serum BUNand creatinine called?

Azotemia

What is filtered, but partlyreabsorbed?

Urea


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What are key findings inprerenal azotemia?

- decreased Cardiac Output- decreased GFR

- ratio > 15

What are key findings in renalazotemia?

- intrinsic renal disease- extrarenal loss of urea

- ratio 15

- If obstruction persists,


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What vasodilates afferentarteriole?

Renal PGE2

What vasoconstricts efferentarteriole?

ATII

What determines protein

filtration?

GBM's- size

- charge

_____ has a negative charge; itis repelled by negatively

charged GBM.Albumin

Fusion of podocytes is a sign of:

nephrotic syndrome

What are crescents?proliferations of parietal epithelial

cells

Horseshoe kidney is associatedwith:

Turner's Syndrome


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What is the most commoncystic disease in children?

Renal dysplasia

Linear ImmunoFluorescenceindicates:

anti-GBM disease (GoodpastureSyndrome)

Granular pattern on

Immunofluorescence indicates:

immunocomplex type of

glomerulonephritis

Under an Electron microscope,immunocomplex deposits are

_____electron-dense

What is the most commonmechanism causingglomerulonephritis?

immunocomplex

What does immunocomplexesdo?

1. activate complement2. C5a produced

3. attract neutrophils

Nephritic syndrome is a _____-related injury to glomeruli

neutrophil


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Does pitting edema distinguishnephritic from nephrotic

syndrome?NO

What are features of nephriticsyndrome?

- moderate proteinuria (3.5- fatty casts

Which syndrome has lessglomerular inflammation?

Nephrotic syndrome

Diabetic glomerulopathy is morecommon in type ___ diabetes

type 1 diabetes

What is the most commoncause of diabetic

glomerulopathy?

poor glycemic control


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In nonenzymatic glycosylation,there is a _______ to protein

high vessel/tubular permeability

There is increase in what inosmotic damage to glomerular

capillary endothelial cells?sorbitol

What does hyalinearteriolosclerosis of efferent

arteriole increase?GFR, producing hyperfiltration injury

What increases inmicroangiopathy?

deposition type IV collagen

What is the first sign of diabeticglomerulopathy?

microalbuminuria

What slows progression ofnephropathy in type 1/type 2

diabetes?ACE inhibitor/receptor blockers

What are features of Alport'ssyndrome?

- hereditary nephritis- sensorineural hearing loss

- ocular defects


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What occurs in thin basementmembrane disease?

persistant hematuria

What is the most commoncause of chronic

glomerulonephritis?

Rapidly progressiveglomerulonephritis (RPGN)

What is the most common

cause of Acute Renal failure?Acute Tubular Necrosis (ATN)

What is the most common typeof Acute Tubular Necrosis

(ATN)?Ischemic Acute Tubular Necrosis

What is the most commoncause of ischemic ATN?

prerenal azotemia

What cast is seen in ATN? Renal tubular cell cast

What is the most commoncause of nephrotoxic ATN?

aminoglycosides


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What are features of ATN?- BUN:Cr ratio


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What are causes of ChronicPyelonephritis (CPN)?

- VUR in young girls- chronic hydronephrosis

What is visible with IVP inCPN?

cortical scars that overlie bluntcalyces

What are features of CPN?- glomerular scarring

- tubular atrophy (thyroidization)

What is a cause of hypertensionin children?

Reflux nephropathy

What are acute drug-inducedTIN?

- methicillin- NSAID- rifampin

- sulfonamides

What are features of acutedrug-induced TIN?

- abrupt onset fever- oliguria

- rash

Analgesic nephropathy occursfrom chornic use of _____

acetaminophen + aspirin (causesrenal papillary necrosis)


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What is visibly seen on IVP ofRenal Papillary necrosis?

'ring defect' from sloughing of papilla

How do you prevent uratenephropathy?

allopurinol BEFORE aggressivecancer therapy

What are features of Chronic

lead poisoning?

proximal tubules with nuclear acid-

fast inclusions

What casts does Bence JonesProtein produce?

tubular casts with foreign body giantcell reaction

What anemia does ChronicRenal Failure produce?

normocytic anemia (qualitativeplatelet defect)

Chronic Renal Faiure producesrenal osteodystrophy due to?

- secondary HPTH- osteomalacia- osteoporosis

What does Chronic renal failureproduce?

- hypertension- pericarditis

- CHF- atherosclerosis


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What are features of CRF?- high anion gap metabolic acidosis- high serum phosphorus/potassium

- low serum calcium

What is a biomarker of kidneyfunction?

Cystatin C

What is free water clearance in

CRF?zero

What casts are sign of CRF? waxy casts

___ is kidney of essentialhypertension, due to hyaline

arteriolosclerosis.Benign nephrosclerosis

What is the most commoncause of malignant

hypertension?pre-existing Benign Nephrosclerosis

What are features of malignanthypertension?

- >210/120 mm Hg- encephalopathy

- renal failure


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what is initial treatment formalignant hypertension?

nitroprusside

What is the most commoncause of renal infarction?

emboli

What are features of renal

infarction?

- hematuria

- flank pain

What are features of sickle cellnephropathy?

- loss concentration- hematuria

- renal papillary necrosis- APN

What are features of diffusecortical necrosis?

- anuria followed by ARF in pregnantwomen

What is the most commoncomplication of upper urinary

tract obstruction?hydronephrosis

What is the most commoncause o fupper urinary tract

obstruction?

Renal stone


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What is the most commonmetabolic abnormality causing

calcium stones?hypercalciuria

What increases reabsorption ofcalcium out of urine?

thiazides

What is the most common renal

stone?calcium oxalate

What are renal stones?- calcium oxalate

- calcium phosphate

What are struvite stones?

- Magnesium ammonium phosphate(MAP)

- urease producers- alkaline urine pH

What are features of renalstones?

- ipsilateral colicky pain in flankradiating to the groin

- hematuria

In plain film, 80% stones are____

radioplaque


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What is the best overallsensitivity and specificity in

renal stones?spiral CT

What detects hydronephrosis,not stones?

ultrasound

What is very important to

prevent stones?hydration

What is the Rx for calciumstones?

hydrochlorothiazide

What is hamartoma associatedwith tuberous sclerosis?

Angiomyolipoma

_____ is a yellow tumor withrenal vein invasion

Renal cell carcinoma

Renal cell carcinoma derivesfrom ____ cell

proximal tubule cell


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What is the msot commoncause of renal cell carcinoma?

smoking

Renal cell carcinoma invades___

renal vein

What is the triad for renal cell

carcinoma?

- hematuria- flank pain

- abdominal mass

Renal cell carcinoma hasectopic secretion of:

- EPO- PTH-related peptide

What is the most commoncause of transitional cell

carcinoma (TCC)?smoking

What is the msot commonprimary renal tumor in children?

Wilm's tumor

What are features of Wilm'stumor?

- child with unilateral flank mass- hypertension


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Wilm's tumor causeshypertension how?

Hypertension due to renin secretion

First sign tubule cell dysfunction inability to concentrate urine

Fixed specific gravitychronic renal failure; cannot

concentrate or dilute urine

Negative urine bilirubin + traceurobilinogen

normal urine

Positive urine bilirubin, absenturobilinogen

obstructive jaundice

Positive urine bilirubin +increased urobilinogen

hepatitis

Negative urine bilirubin +increased urobilinogen

extravascular hemolytic anemia


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Positive urine nitrite + positiveurine leukocyte esterase

urinary tract infection

Sterile pyuriapositive urine leukocyte esterase but

negative standard culture; TB, C.trachomatis

Prerenal azotemia BUN and creatinine; renal blood

flow (e.g. heart failure, hypovolemia)

Renal azotemia BUN and creatinine due to intrinsicrenal disease (acute tubular necrosis)

Postrenal azotemia BUN and creatinine due to

obstruction to urine flow

Serum BUN:creatinine ratio15:1 (prerenal

or postrenal azotemia)

BUN 80 mg/dL:creatinine 8mg/dL

ratio 10/1 - renal failure


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BUN 80 mg/dL:creatinine 2mg/dL

ratio 40/1 - prerenal azotemia orpostrenal azotemia

Creatinine clearance measures GFR

Proteinuria important sign of renal dysfunction

RBC casts nephritic type of glomerulonephritis

WBC castsacute pyelonephritis, acutetubulointerstitial nephritis

Fatty casts with Maltesecrosses

nephrotic syndrome

Hyaline castsnormal unless associated with

proteinuria


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Renal tubular cell casts acute tubular necrosis

Waxy or broad casts chronic renal failure

Cystinuria hexagonal crystals

Horseshoe kidney Turners syndrome; lower poles fused

Renal dysplasiaMC childhood cystic disease;

abnormal development; flank mass

Maternal oligohydramniosfetal juvenile polycystic kidney

disease; Potters facies in newborn

Adult polycystic kidney diseaseAD; hypertension MC sign; cerebral

berry aneurysms


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Visceral epithelial cells synthesize basement membrane

Glomerular BMnegative charge due to heparan

sulfate

Nephritic syndromeoliguria; RBC casts; hypertension;

mild to moderate proteinuria

Nephrotic syndromeproteinuria >3.5 g/day; ascites andpitting edema; fatty casts; fusion of

podocytes

Immunofluorescencelinear (anti-glomerular BM

antibodies); granular (IC deposition)

IgA GNMC GN; usually nephritic; episodichematuria; mesangial IC (lgA-anti-

IgA) deposits

Post-streptococcal GNnephritic; subepithelial deposits;skin/pharyngeal infections; anti-

DNAase B


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SLE type IV GNnephritic; subendothelial deposits;

anti-DNA antibodies

Crescentic GNcrescents from parietal cell

proliferation; worst GN;Goodpastures, Wegeners

Goodpasturesnephritic; anti-BM antibodies

(glomerular + pulmonary capillary);crescentic GN

S/Syoung male with hemoptysisprogressing to renal failure

Minimal change disease (lipoidnephrosis)

MCC childhood nephrotic syndrome

Lipoid nephrosispodocyte fusion; loss of negative

charge in glomerular BM


nephrotic syndrome; AIDS and IVheroin abuse


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Membranous GNMCC adult nephrotic syndrome;

subepithelial deposits;epimembranous spikes

Causes membranous GN HBV, ACE inhibitors, cancer

Type I MPGNnephrotic; subepithelial deposits;

HCV association; tram tracks

Type II MPGNnephrotic; C3 nephritic factor;

intramembranous ICs (dense depositdisease)

DM nodular glomerulosclerosis microalbuminuria first sign

DM glomerulosclerosisnodules with collagen in mesangium;hyaline arteriolosclerosis of arterioles

ACE inhibitorsinhibit angiotensin II vasoconstriction

of efferent arterioles


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Alports syndromeXD hereditary nephritis withsensorineural hearing loss

Ischemic ATNprerenal azotemia MCC; renal tubularcell casts; BUN:creatinine ratio


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Chronic pyelonephritisU-shaped scars overlying blunt

calyces

Drug-induced tubulointerstitialnephritis

type I/IV reaction; e.g., penicillin

S/SARF, fever, rash, eosinophilia,

eosinophiluria, WBC casts

Analgesic nephropathyaspirin plus acetaminophen; renalpapillary necrosis; IVP with ring

defect

Myeloma kidneyBJ protein produces foreign body

reaction in tubules

Urate nephropathyprevent by giving allopurinol prior to

chemotherapy

CRFfixed specific gravity; BUN:creatinine


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Renal osteodystrophy CRFhypovitaminosis D (no 1--

hydroxylase); produces osteomalacia

Renal osteodystrophy CRF osteoporosis from metabolic acidosis

Renal osteodystrophy CRFsecondary HPTH with increased

osteoclastic activity

S/S CRFpericarditis, prolonged bleeding time,

normocytic anemia, pathologicfractures

Benign nephrosclerosiskidney of hypertension; shrunken

kidneys due to hyalinearteriolosclerosis

Malignant hypertensionrenal failure; encephalopathy; BP>210/120 mm Hg; IV nitroprusside

Renal findingsnecrotizing arteriolitis; flea bitten

kidney; hyperplastic arteriolosclerosis


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Renal infarctionpale infarcts; hematuria; common in

polyarteritis nodosa

Hydronephrosisrenal stone MCC; atrophy of

cortex/medulla; postrenal azotemia

Renal stonesmost contain calcium (calcium

oxalate/phosphate); hypercalciuriaMC risk factor

S/Scolicky pain radiating into groin,

hematuria; x-ray usually shows stone

Staghorn calculusdue to urease producing organisms

(Proteus); alkaline urine pH; ammoniasmell

Angiomyolipomahamartoma; associated with tuberous

sclerosis

Renal cell carcinomasmoking MCC; invasion renal

vein/vena cava; lung, bone mets;

yellow colored


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S/Sflank mass, hematuria; ectopichormones (EPO, PTH relatedpeptide), left-sided varicocele

Renal pelvis transitional cellcarcinoma

smoking MCC, phenacetin, anilinedyes, cyclophosphamide

Wilms tumorhypertension, unilateral abdominal

mass in child;aniridia/hemihypertrophy in AD types

Urine draining from umbilicus persistent urachus

Retroperitoneal fibrosis produces hydronephrosis

Bladder extrophy abdominal wall defect + epispadias

Bladder diverticulamost commonly due to prostatic

hyperplasia with urethral obstruction


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Acute cystitisE. coli; females > males; no fever,

flank pain, or WBC casts

Bladder transitional cellcarcinoma

smoking MCC, aniline dyes,cyclophosphamide; papillary

S/S hematuria; hydronephrosis

Bladder adenocarcinomarisk factors persistent urachus,

extrophy

Bladder squamous cellcarcinoma

Schistosoma hematobium infection

Hypospadiasventral opening on penis due tofailure closure of urethral folds

Epispadiasdorsal opening on penis due to defect

in genital tubercle


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Peyronies diseasepainful curvature penis due to

fibromatosis

Priapism persistent/painful erection; HbSS

Squamous cell carcinoma penisHPV and lack of circumcision most

important risk factors

Cryptorchidismundescended testis; risk for

seminoma applies to cryptorchidtestis and normal testis

Orchitismumps usually unilateral (infertility

uncommon)

Epididymitis35 - E. coli, P. aeruginosa

S/Sscrotal pain relieved by elevation of

scrotum (Prehns sign)


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Varicoceleleft-sided scrotal mass; spermatic

vein drains into left renal vein;infertility common

Varicocelemay be due to invasion of left renal

vein by renal cell carcinoma

Hydrocelepersistent tunica vaginalis; scrotum

transilluminates

Torsion of testicletesticle high in canal; absent

cremasteric reflex

Testicular cancerunilateral painless mass that does not

transilluminate

Risk factorscryptorchid testis, Klinefelters,

testicular feminization

SeminomaMC cancer; radiosensitive; large cells

with lymphoid infiltrate; small

percentage have hCG


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Spermatocytic variant >65 yrs of age

Embryonal carcinomahemorrhage/necrosis; hematogenousspread before lymphatic; AFP, hCG

Yolk sac tumor MC testicular cancer in boys; AFP

Choriocarcinomamost aggressive testicle cancer;

hCG

Teratomamore often benign in children than

adult

Teratocarcinoma teratoma + embryonal carcinoma

Malignant lymphomaMC type in elderly; metastasis not

primary cancer


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ProstateDHT derived stimulation embryo;periurethral area - hyperplasia;

peripheral area - cancer

Prostatitisperineal pain, fever; WBCs at end of

voiding

Benign prostatic hyperplasiaDHT/estrogen-mediated;

glandular/smooth muscle hyperplasia

S/Sall men develop; urethral obstructionMC (hesitancy, dribbling, nocturia),

hematuria, dysuria Rx

Prostate cancerDHT-mediated; palpable with rectal

exam; osteoblastic metastasis ( AP)

PSAsensitive but not specific for prostate

cancer; in hyperplasia

Right Scrotal Varicocele

Rgiht testicular vein into the venacava blockd due to retroperitoneal

fibrosis...most common complicationis hydronephrosis though


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Exstrophy of the bladderassicated with what?

Epispadisis as well asADENOCARCINOMA of bladder due

to glandular metaplasia

MCC of bladderadenocarcinoma

Urachal cyst remnants*** urine toumbililicus

MC uropathogen

E coli - UTA, acute cystis#2 is satph saprophyticus in young

womenAdenovirus causes hemorrhagic

cystics in kids

Lab finiiding in pyuria

10 WBC/HPF, bacteriria hemauria,LEUKOCYTE ESETASE and

NITRITE positive** forenterobacteriace nonoxidase10^5*** gold standard for dx

culture may be negative in chylamdia

asymptomatic bacteruriapregnancy, elderly women, diabetes

mellitus

Sterile pyuria

+LEstease-nitrite-Renal Tb

-ChlamydiaAcute tubulointerstitial nephritis**


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Bladder cancer

TCC by far most common- multifocaland reccur

-smoking, aniline dyeCyclophosphamide

Schistasoma hematobium (morecommonly SCC)

-might have RBC antigens good signSigns - DYSURIA, microscopic

hmaturia, painless

MC Cancer in urethra SCC

Phimosiscan't retract foreskin

can't be aquired by inflammatoryscarring due to balanoposthitis

Bowen disase

Leukoplakia of penile shaf - recuros

for SCCASSOCIATION WITH VISCERAL

CANCER**

Ddx - EQ- HOV mucosal glans andpreuce -> SCC

SCC of penis - inguinal and iliacnodes**

Cyrptorchidism

Seminoma causing 5xMajority stuck in inguinal which relies

on androgen-due to arrest in gem cell maturation


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Epididymitis

hematogenous, LYMPHCYTIC

INFILTRATE***Ddx embroynal - hematgons ->lymphatic bulky with necrosisYolk sac - AFP schiller duval

Chordo- hCG ->GYNECOMASTIA***

poor pxTeratoma - ALL MALIGNANT MAY

HAVE IMATURE FOCUS due o SCCLymphoma -MCC ni older than 60

Leydig -gynecomastica - seritoli lookslike smeinferous tubul

Prostatis

Caused by E coli, pseudomonas and

klebsiella**Lowerback pain dysuria feverHave to get a fractionatd sample and

milk out last part for DxChronic - abacterial


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BPH

Se trbecular bladder from backpressure

-DHT mediator and estrogenHyeprlasia of gland and stroma intrsinitional and periurethral zone

Stromal hyperplasai-> obsctruction

Hard to start and stop urnePSA elevated

Posternal azotemia-> ARF

Prostatic cancer pathogenesi

DHT dependent - polymorphisms ofAR thought to be ome sensitive

-develops in peripheral zone so youpalpate with DRE

-hard gritt firm apperance90% 15 year survival with Rx

Signs of malignacy of porstatecancer

PERINEURAL INVASIONBV, capsule etc

Sx - obstructive uropathy, bony met'svia the batson plexus (also seen in

breast) connects pelvis to the

veretrabral plexus, alk phos elevationHIGH PSA over 10 more specific forcancer than elevation

Paget histologyadenocarcinoma in epithelial not

dermal layer-PAS + unlike melanoma

Prognostic value of scamouscells in endometrial cancer

none unless cancerous then itsbaaad

PCOS pathophys

LH-> androgen-> estrogen->positive

LH feedback negative FSH noovulation and follicular degeneration

with no FSH causing the cysticchanges


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Sudden onst of pain 6 weeksafter lat period

Ectopic pregnancy -> shock,bleleding adnexal mass

Dx with beta hcg

MCC ovarian mass in youngwomen

folicular cyst with fluid accumulation,rupture with pain Dx ultrasound

OCP decrease risk of what? endometrial and ovarian cancer

Palpable ovarian mass? Cancer

Endeometrial hyperplasia and100% superficial squamous

cells on pap smearEstrogen secreting tumor

CA125

SURFACE DERIVED TUMORS

ONLYSerous - fallopian tube looking

bilateral psammoma bodies

Wolfian remnant gartner duct cyst


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Bladder looking ovarian tumor Brenner=bladder

Diamniotic monochorionic Identical Twin

Monochorionic monoamniotic Identical Twin maybe siamese

Diamniotic fraternal or identical

Precocious Puberty in a boyMCC

Midline hemartoma, girls it'sidiopathic

parinuaud's syndromeSC compression etc -> paralysis of

upwards gaze

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