Step 2 Gu

Front 1

Most Common Neprhopathy of Hodgkin's Lymphoma:

Back 1

Minimal Change Dz;-- responds to corticosteroids

Front 2

Most Common Nephropathy of Carcinoma

Back 2

membranous Nephropathy

Front 3

Most common adult nephropathy:

Back 3

membranous glomerulonephritis. Diffuse thickening, EM: subepithelial deposits

Front 4

Defining feature of minimal change dz:

Back 4

foot process effacement only visible on EM
selective loss of Albumin not globulins due to loss of anion charge

Front 5

MCC nephrotic sro in children

Back 5

Hodgkins lymphoma
responds to steroids

Front 6

DM pt has nephropathy with azotemia & proteinuria: course of action

Back 6

DM pt has nephropathy with azotemia & proteinuria: course of action
--> intensive BP control
all else can help other aspects, but BP control is most importnat
NB: intensive glycmeic control reduces occurance & progression of microproteinuria, but not effective in controlling proteinuria

Front 7

Palpable mass through abdomen near kidneys

Back 7

Adrenal masses are almost never palpable. if you can papate something you're palpating kidney.

Front 8

suspected penile fx
dx, tx

Back 8

--> Retrograde urethrogram for urethral competance + immediate surgical exploration

Front 9

Determining the Source of Blood in Hematuria

Back 9

Early in Stream: Urethral
End of Stream: Bladder or Prostate
Whole Stream: Ureters or Kidneys
Clotting rules out nephrotic sro

Front 10

Types of Kidney Damage Associated with HIV:

Back 10

MCC: focal & segmental glomerulosclerosis aka HIV-related nephropathy < proteinuria
others: membranous glomerulonephritis
mesnagioproliferative glomerulonephritis
diffuse proliferative glomerulonephritis

Front 11

calcium oxalate crystals
in urine sediment

Back 11

frequent finding in urinary sediment, not suggestive unless flank pain

Front 12

Renal Manifestation of Hepatitis B:

Back 12

Membranous Glomerulonephritis from deposition of HBeAg into glomeruli

Front 13

Pt with suspected kidney Stone:
course of action

Back 13

Non-contrast CT
NSAIDS > Narcotics
Stones <5 mm can be passed with fluid >2L/d
Refer to uroloogy for anuriak urosepsis or ARF

Front 14

radioopaque hexagonal stonaes

Back 14

Cystinuria: dibasic amino acid transporter failure
radioopaque hexagonal stonaes
urinary cyanide nitropruside test is positive to confirm

Front 15

suspected urethral injury

Back 15

--> Retrograde urethrogram to assess extent and location
most urethral injuries are treated with suprapubic catheter & urinary diversion while thigns heal and then whatever's left (strictures) are taken care of aftewrwards

Front 16

most common kidney stones:

Back 16

calcium oxalate - envelope shaped; many malabsoprtive causes this, including diarrhea (unabsorbed FA's bind Ca2+ which would normally bind oxalate and prevent its absoprtion)
cqalcium phosphate stones: hyperparathyroidism or renal tubular acidosis

Front 17

struvitestones

Back 17

UTI

Front 18

cysteine sotnes

Back 18

inborn metz error

Front 19

uric stones

Back 19

increased cell turnover + dehydration

Front 20

ADPKC manifestations:

Back 20

Renal Cysts, Barry Aneurysm, Hepatic Cysts, Valvular Heart Dz (Prolapse, Regurg), Colonic Diverticula, Abdominal Wall & Inguinal Hernia

Front 21

complications of nephrotic sro:

Back 21

protein malnutrition
iron resistant iron deficiency anemia (transferrin loss)
vitD deficiency (loss of binding protein)
hypothyroid (loss of thyroid binding globulin)
increased susceptibility to infx

Front 22

Kidney stones in Crohns pts:

Back 22

hyperoxaluria
fat malabsoprtion --> hyperoxaluria. obtained from diet, normal product of metzm;
normally ca2+ binds oxalate in gut & prevents absorption
with fat malabbsorption, ca2+ bound by fat, not axalate --> unbound oxalate enters bloodstream
excess (unabsorbed) bile salts --> damage mucosa --> increased oxalate absorption

Front 23

Best dietary advice for decreasing renal calculi:

Back 23

1. at least 2L fluid/day 2. restrict protein & oxalate 3. decrease sodium 4. Increase dietary calcium (limiting calcium paradoxically increases stone formation)

Front 24

Diabetic kidneys damage patter

Back 24

nodular glomerulosclerosis

Front 25

Drugs with Renal crystal deposition

Back 25

: uricemia, indinavir, acyclovir & sulfonamide

Front 26

Earliest Renal Abnormality in Diabetics

Back 26

Glomerular Hyperfiltration, usually detectable immediatly on Dx of Diabetes
--> intraglomerular hyptersion --> progressive glomerular damage
The effectiveness of ACEI's is in their ability to reduce intraglomerular hypertension

Front 27

acyclovir can crystalize in renal tubules
prevent by

Back 27

aggresive IV hydration

Front 28

BPH + elevated Cr
course of action

Back 28

Abd US for hydronephrosis
+ hydronephrosis --> intermittent catheterization until surgical fix

Front 29

segment of bladder most likely to rupture

Back 29

dome of bladder has developmental hiatus form urachus

Front 30

MCC Epididymitits:

Back 30

Younger Pts: Chlamydia & Gonorrhea
Older Pts (Non-sexual = 2/2 UTI organisms) = GNRs = E coli > Psuedomonoas

Front 31

Nephrotic Sros not 2/2 a systemic dz:

Back 31

MInimal change dz (childen)
Membranous
Focal Segmental Glomerulosclerosis: Obesity, heroin,IV, African Americans

Front 32

Contrast induced nephropathy
course of action

Back 32

worry about it if baseline Cr >1/5 and/or diabtetic
if so, US if possible, else non-ionic contrast agents, adequate IV hydration & acetylcystine

Front 33

Bladder Cancer Screening

Back 33

There is none. No good predictive tool.

Front 34

membranoproliferative glomerulonephritis type 2

Back 34

"dense deposit dz"
C3 depsoition, IgG antibodies vs C3 convertase (aka C3 nephritic factor) --> persistent complement activation & renal damage

Front 35

Nephrotic Sro --> Severe Pain + Gross Hematuria

Back 35

=Renal Vein Thrombosis from lost ATIII
MCC: membranous Glomerulonephritis

Front 36

Oliguria, BUN/Cr ratio > 20 --> first step:

Back 36

check the foley for clog -- then fluid challenge.

Front 37

FENa in renal vs pre-renal dz

Back 37

Prerenal Azotemia FE-Na <1, intrinsic renal disease FE-Na >1;

Front 38

simple renal cyst

Back 38

common in pts over 50, benign, no sx, found incidentally
make sure it does not have any of the following:
1. multilocular mass, 2 thickened/irregular walls, 3 thicken septae within mass, or 4 contrast enhancement

Front 39

acute prostatitis symptoms, what next?

Back 39

mid-stream urine catch for cx;
don't need prostatic fluid, and over vigorous massage would cause bactermia;

Front 40

coffin lid crystals

Back 40

= struvite from urease orgganisms (say it in a dracula voice)

Front 41

renal Transplatn pt with oliguria

Back 41

radioisotope scan, MRI, renal US, Bx
ureteral obstruction, cyclosporin tox, acute rejexn, vascular obstrx, ATN, etc

Front 42

young black man with painless hematuria:

Back 42

sickle cell trait believed 2/2 papillary necrosis

Front 43

Renal care for SLE

Back 43

All pts with new onset SLE need a kidney bx to establish type of renal involvement to determien treatment; could be anywhere from mild to rapidly progressive;

Front 44

Ureteral Colic: KUB non diagnostic, stones on CT

Back 44

1 uric acid stones, 2 Ca2+ stones <3mm, 3 non stones (blood clot, tumor)

Front 45

tx: uric acid stones

Back 45

acutely: alkalinze the urine with K citrate or K HCO3 to >6.5 to dissolve stone
chronic: low purine diet, allopurinol

Front 46

Risk factors for membranous nephropathy:

Back 46

Hep B, Hep C, malaria, syphilis

Front 47

Unilateral Varicocele
course of action

Back 47

does not resolve when recumbant --> suspect underlying RCC
Abdominal CT

Front 48

Casts: WBC, Fatty, Waxy

Back 48

WBC casts = interstitial or pyelonephritis
Fatty casts = nephrotic sro
Broad casts/Waxy Casts = Chronic renal failure

Front 49

Findings of ATN:

Back 49

Urins Osmolality 300-350, but never <300, Urine Na >20, FE Na >2%

Front 50

Renal Tubular Acidoses:

Back 50

Suspect when Non-Anion Gap Acidosis
Type 1: Defective Hydrogen secretion; genetic in children; else amphotericin or multiple myeloma; Acidotic & Hypokalemic; Nephrolithiases
Rx: Oral HCO3
Type 2: Decreased HCO3 resporption in proximal tubule; Fanconi sro, many causes, carbonic anhydrase most common
Rx: thirazides produce vlume deplestion raises threshold for HCO3 resoprtion
Type 4: damaged JG apparatus --> no RAAS --> Na/K exchange defect in distal tubule;
hyperkalemic, hyperchloremic; obstructive, dysplastic multicystic kidneys, or renal dz

Front 51

Best Dx Test: Kidney Stones

Back 51

Non Constrast Abdominal CT

Front 52

allopurinol mechanism

Back 52

prevents production (XO inhibitor)

Front 53

Dig is cleared by the:

Back 53

Kidney

Front 54

Analgesic nephropathy

Back 54

= papillary necoris + tublointerstital nephritis (nephrotic)
complixns: premature aging, atherosclerosis, & Urinary Tract CA

Front 55

Nephrotic Syndrome Complications:

Back 55

1. Hypercoagulability from loss of AT3 protein
2. Alteration in lipid metzm: esp increased LDL & decreased HDL
--> High risk for stroke/MI/ischemia
Renal veins most succeptible to hypercoagulability

Front 56

Most Common Complixn of Veiscoureteral Reflux

Back 56

--> Renal Scarring