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113 Cards in this Set
- Front
- Back
which kidney is used for donor transplantation
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left kidney because it has a longer renal vein
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this structure passes under uterine artery and ductus deferens
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ureters
*water under the bridge |
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how are plasma volume and extracellular volume measured respectively
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plasma volume - radiolalbeled abmunim
ECV - inulin |
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60-40-20 rule
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60% body weight is water
40% ICF 20% ECF *1/4 of 20% is plasma and 3/4 is interstitium |
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what is lost during nephrotic syndrome resulting in albuminuria, generalized edema, and hyperlipidemia
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charge barrier of BM
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what gives the BM its negative charge
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heparan sulfate
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calculate renal clearance of a substance (x)
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Cx = (Ux)(V)/Px
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what substance can be used to calculate GFR because it is freely filtered and is neither reabsorbed nor secreted
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inulin
GFR = U(inulin) x V/P(inulin) |
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what substance can be used to estimate effective renal plasma flow because it is both free filtered and actively secreted
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PAH
All PAH entering the kidney is excreted |
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ERPF underestimates true RPF by about 10%
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**
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calculate RBF using RPF and HCT
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RBF = RPF/(1-HCT)
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calculate Filtration Fraction (FF)
normal value |
FF = GFR/RPF
normal FF = 20% |
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calculate filtered load of a substance
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GFR x plasma concentration
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what drug would inhibit efferent arteriole constriction and therefore decrease FF
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ACE inhibitor
ATN II constricts efferent arteriole |
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what happens to the RPF, GFR, and FF when efferent arteriole is constricted
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RPF decreases
GFR increases FF increases |
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what does increased/decreased plasma protein concentration do to the GFR and FF
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increased protein- decreased GFR and FF
decreased protein - increase GFR and FF |
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at what plasma glucose does glucosuria begin and when are all transporters fully saturated in PCT
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plasma glucose 160-200 - glucosuria begins
plasma glucose 350 - all transporters are fully saturated |
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deficiency of the neutral amino acid (tryptophan) transporter in the PCT resulting in pellagra
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Hartnup's disease
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this hormone inhibits Na/phosphate cotransport increasing phosphate excretion
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PTH
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this part of the kidney induces the paracellular reabsorption of Mg and Ca
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ascending loop of Henle
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this part of the renal tubule is impermeable to water and therefore makes urine less concentrated
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ascending loop of Henle
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this is the concentrating segment of the kidney making urine hypertonic
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descending loop of Henle
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this is the diluting part of the renal tubule making urine hypotonic
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early distal convoluted tubule
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this hormone increases Ca/Na exchange and therefore increaes Ca reabsorption in DCT
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PTH
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this hormone leads to insertion of Na channels in collect tubule
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Aldosterone
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this segment of the kidney has isotonic absorption
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PCT
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affects baroreceptor function and limits reflex bradycardia which normally accompanies pressor effects
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ATN II
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release in response to increased volume, relaxes vascular smooth muscle via cGMP causing increased GFR and decreased renin
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ANP
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responds to increased osmolarity and decreased volume
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ADH
*volume takes precedence over osmolarity |
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functions of ATN II
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1. vasoconstriction - increased BP and FF (efferent arteriole)
2. upregulates aldosterone 3. upregulates ADH 4. increases PCT Na/H activity 5. stimulates thirst |
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secrete renin in response to decreased renal blood pressure or stimulation of B1 receptor
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JG cells
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two parts of juxtaglomerular apparatus
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JG cells - modified smooth muscle of afferent arteriole that secrete renin
macula densa - Na sensor in the DCT |
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released in response to hypoxia from endothelial cells of peritubular capillaries
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erythropoietin
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two functions of PTH on the kidney
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1. directly increases renal calcium reabsorption
2. indirectly stimulates PCT to make 1,25-OH Vit. D |
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can cause acute renal failure by inhibiting production of prostaglandins
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NSAIDs
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secreted in response to increased atrial pressure
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ANP
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secreted in response to decreased serum calcium or Vit. D, or increased serum phosphate
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PTH
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where is ACE found
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lung
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secreted in response to decreased blood volume or increased plasma K
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aldosterone
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6 things that cause hyperkalemia (potassium shift out of cells)
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1. insulin deficiency (decreased Na/K ATPase)
2. B-antagonists (decreased Na/K ATPase) 3. acidosis 4. hyperosmolarity 5. digitalis 6. cell lysis |
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4 things that cause hypokalemia (postassium shift into cells)
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1. Insulin
2. B-agonists 3. Alkalosis 4. hypo-osmolarity |
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associated with U waves on ECG and flattened T waves
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hypokalemia
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associated with peaked T waves and wide QRS complex on ECG
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hyperkalemia
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associated with tetany
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hypocalcemia
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associated with neuromuscular irritability and arrhythmias
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hypomagnesia
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shortcut for respiratory compensation in response to metabolic acidosis
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PCO2 increases by 0.7 mmHg for every 1 mEq/L increase in HCO3
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causes of anion gap metabolic acidosis
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KUSMALE:
ketoacidosis uremia salicylates methanol acetominophen lactic acidosis ethylene glycol |
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causes of non-anion gap metabolic acidosis
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diarrhea
renal tubular acidosis hyperchloremia |
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causes of metabolic alkalosis
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vomiting
antacids hyperaldosteronism |
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defect distally in collecting tubules ability to excrete H
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type 1 RTA
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RTA associated with hypokalemia and risk for calcium kidney stones
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type 1 RTA
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proximal defect in PCT ability to reabsorb HCO3, associated with hypokalemia and hypophosphatemic rickets
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type 2 RTA
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hypoaldosteronism due to lack of collecting tubule response to aldosterone, associated with hyperkalemia and inhibition of ammonium excretion in PCT
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type 4 RTA
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what are granular (muddy brown) casts associated with
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acute tubular necrosis
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what are WBC casts associated with
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tubulointerstitial inflammation
acute pyelonephritis transplant rejection |
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what are RBC casts associated with
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glomerulonephritis
ischemia malignant HTN |
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two conditions associated with hematuria but no casts
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bladder cancer
kidney stones |
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associated with pyuria but no casts
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acute cystitis
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an inflammatory process involving the glomeruli resulting in hematuria and RBC casts in urine
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nephritic syndrome
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enlarged and hypercellular glomeruli with subepithelial immune complex humps
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acute poststreptococcal glomerulonephritis
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what do the crescents consist of in RPGN
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fibrin, C3b, parietal cells, monocytes, and macrophages
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3 diseases associated with RPGN
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1. goodpasture syndrome (anti-GBM)
2. Wegener's granulomatosis (c-ANCA) 3. microscopic polyangiitis (p-ANCA) |
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type II hypersensitivity reaction involving GBM (with linear staining) and alveolar BM
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Goodpasture syndrome
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most common cause of death in SLE
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diffuse proliferative glomerulonephritis
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associated with wire looping of capillaries and subendothelial anti-DNA immune complexes
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diffuse proliferative glomerulonephritis due to SLE
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associated with IgA IC deposits in the mesangium
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Berger's disease (IgA glomerulopathy)
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mutation in type IV collagen resulting in split basement membrane
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Alport's syndrome
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X-linked dominant disorder associated with nerve disorder, ocular disorder, deafness, and split BM
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Alport's syndrome
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presence with massive proteinuria, hyperlipidemia, fatty casts, edema; associated with thromboembolisma and increased risk of infection
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nephrotic syndrome
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most common form of adult nephrotic syndrome
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diffuse membranous glomerulopathy
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associated with diffuse capillary and GBM thickening with spiked and dome appearance with supepithelial deposits
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diffuse membranous glomerulopathy
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normal glomeruli with foot process effacement; selective loss of albumin due to GBM polyanion loss
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minimal change disease
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what treatment does minimal change disease response to
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corticosteroids
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cause of congo red stain with apple-green birefringence nephrotic syndrome
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amyloidosis due to chronic conditions such as MM, TB, RA
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nonenzymatic glycosylation of GBM and efferent arteriole leading to mesangial expansion and nodular sclerosis
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diabetic glomerulonephropathy
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most common glomerular disease in HIV patients
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focal segmental glomerulsclerosis
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this glomerular disease can present as either nephritic or nephrotic and has "tram-track" appearance
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membranoproliferative glomerulonephritis
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differentiate type 1 and 2 membranoproliferative glomerulonephritis
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type 1 - GBM splitting caused by mesangial growth
type 2 - dense deposits |
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what are type 1 and 2 membranoproliferative glomerulonephritis associated with
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type 1 - HBV and HCV
type 2 - C3 nephritic factor |
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glomerular disease associated with smooth linear pattern on immunofluorescence
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Goodpasture's syndrome
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associated with lump bumpy pattern on immunofluorescence
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acute postreptococcal glomerulonephritis
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prevention of kidney stones
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fluid intake
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what can lead to hypercalcemia resulting in kidney stones
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increased PTH from parathyroid
cancer |
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what two things can lead to oxalate crystals forming kidney stones
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ethylene glycol
vitamin C |
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what is the only kidney stone that is radiolucent (cannot seen in x-ray)
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uric acid
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kidney stone caused by infection of urease-positive bug
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ammonium magnesium phosphate
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what type of kidney stone can form staghorn calculi
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ammonium magnesium phosphate
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kidney stone seen in gout or increased cell turnover such as leukemia
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uric acid
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hexagonal kidney stone that can be treated with alkalinization of urine
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cystine stone
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renal malignancy associated with von Hippel-lindau syndrome and gene deletion in chromosome 3
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renal cell carcinoma
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where does renal cell carcinoma metastasize to
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lung and bone
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4 hormones associated with the paraneoplastic syndrome or renal cell carcinoma
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EPO
ACTH PTHrP prolactin |
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childhood renal malignancy associated with deletion of tumor suppressor gene WT1 on chromosome 11
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wilms' tumor
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most common tumor of urinary tract system
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transition cell carcinoma
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what does painless hematuria suggest
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bladder cancer
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4 potential causes of bladder cancer
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phenacetin
smoking aniline dyes cyclophsophamide |
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what is classic of pyelonephritis
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WBC casts in urine with fever and CVA tenderness
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associated with tubules containing eosinophilic casts (thyroidization of kidney)
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chronic pyelonephritis
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infection affecting cortex of kidney with relative sparing of glomeruli/vessels
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acute
*chronic has both corticomedullary scarring and blunted calyx |
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associated with fever, rash, hematuria, and CVA tenderness 1-2 weeks after drug administration
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drug-induced interstitial nephritis
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drugs associated with drug-induced interstitial nephritis
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NSAIDs
penicillin derivatives sulfonamides rifampin |
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most common cause of acute renal failure in hospital
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acute tubular necrosis
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4 things associated with renal papillary necrosis
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1. diabetes mellitus
2. acute pyelonephritis 3. chronic phenacetin use (acetominophen is phenatcetin derivative) 4. sickle cell anemia |
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prerenal azotemia
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due to decreased renal blood flow so urea is retained by kidney to conserve volume; BUN/creatinine ratio increases
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intrinsic renal azotemia
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generally due to acute tubular necrosis that is either ischemic or toxic; BUN/creatinine ratio decreases because BUN cannot be reabsorbed
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postrenal azotemia
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due to outflow obstruction, develops only with bilateral obstruction
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causes of postrenal azotemia
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stones
BPH neoplasia congenital anomalies |
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associated with volume overload, hyperkalemia, metabolic acidosis, anemia, secondary hyperparathyroidism due to phosphate retention, dyslipidemia (increased triglycerides)
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renal failure
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autosomal-dominant kidney mutation associated with berry aneurysms and mitral valve prolapse
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Adult PKD
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autosomal-recessive kidney mutation associated with Potter's sequence
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Infantile PKD
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small kidneys associated dilated cortical collecting ducts that sometimes leads to fibrosis and progressive renal insufficiency
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medullary cystic disease
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can result in cortical and medullary cysts
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dialysis
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where are simple kidney cysts found
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cortex
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