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38 Cards in this Set
- Front
- Back
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Effect of sympathetic stimulation on GFR |
Low level discharge reduces RBF but not GFR High discharge reduces both RBF and GFR Sympathetic tone also causes contraction of mesangial cells |
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What effects renin release? |
Intrarenal baroreceptors Macula densa (releases prostaglandin I2-->Renin secretion) Renal sympathetic nerves (Direct: beta 1 receptors in macula densa stimulate renin secretion; indirect: constriction of afferent arterioles which reduces stretch of granular cells which stimulates renin; reduced GFR makes macula densa stimulate release) |
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Effects of Angiotensin II |
Systemic vasoconstriction Mesangial cell contraction, lowers GFR Aldosterone secretion Thirst Sodium reabsorption in proximal tubule ADH secretion |
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Filtration equation |
Plasma conc x GFR |
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Excretion equation |
Urinary conc x urinary flow |
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Fractional excretion |
Mass excreted/unit time _________________________ Mass filtered/unit time in tubular dysfunction, can't reabsorb so will be very high |
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GFR equation (inulin) |
Urinary conc x Urinary flow / Plasma conc |
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Causes of proteinuria |
Problems with overflow (low level proteinuria) Problems with tubules (mid-level) Problems with glomerulus (over 3.5g proteinuria) |
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2 quantitative measures of proteinuria |
24 urine collection Spot urine:creatinine ratio (like measuring protein per GFR) |
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Criteria for nephrotic syndrome |
Proteinuria more than 3.5g/24 hr At least one of: hypoalbuminemia, edema, hyperlipidemia, hypercoagulable state |
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5 nephrotic conditions |
Minimal Change Disease Focal Segmental Glomerulonephritis Membranous nephropathy Diabetes mellitus Amyloidosis |
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FSGS |
More common in African Americans Correlated with hypertension Segmental sclerosis with hyalination, negative immunofluorescence, tubule serving sclerotic glomerulus may atrophy leading to interstitial necrosis Immunosuppressive therapies High risk of recurrence in transplants |
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Membranous nephropathy |
Severe nephrotic syndrome High correlation with hypercoagulability and PE Most common idiopathic nephrotic syndrome in whites Immunosuppressive therapies Can be caused by lupus, hep B or C or syphilis Light microscopy: thickening of GBM Capillary walls thickened, spikes on outer side of capillaries No endocapillary proliferation Spikes and holes with black stain Immunofluorescence: Fine granular loop staying with IgG and C3 Electron microscopy: Spikes on silver stain |
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Diabetic nephropathy |
Light microscopy: Glomerulomegaly Diffuse glomerulosclerosis, increase in mesangial matrix Interstitial fibrosis No immunofluorescence Electron microscopy: Thickening of GBM Mesangial widening Some foot process effacement |
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Amyloidosis |
Rare cause of nephrotic syndrome Massive proteinuria Collection of amorphous mateiral in glomeruli, mesangium with nodular mesangial expansion Can also be in tubular basement membrane, interstitium and vessels Congo red stain confirms diagnosis Immunofluorescence: If light chain amyloid, then light chain positive Electron: Randomly oriented fibrils Usually related to underlying lymphoproliferative neoplasm |
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3 factors that control aldosterone release |
Increased plasma K+ Decreased plasma Na+ Angiotensin II |
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3 pathways that stimulate renin release |
Stimulation of baroreceptors Decreased wall tension of afferent arteriole Macula densa senses decreased filtration |
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3 effects of ANP |
Increases GFR via relaxing mesangial cells and dilating afferent arterioles Inhibiting Na+ reabsorption in collecting ducts Inhibiting renin, aldosterone and ADH release |
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Fractional excretion of sodium |
(Urine Na/serum Na) / (urine Cr/serum Cr) Cr normalizes for concentration of urine Low FENa of less than <1% shows an expected retention of sodium in pre-renal ARF Higher FENa is consistent with post-renal and renal ARF ONLY CAN BE USED IN OLIGURIC PATIENTS |
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Muddy brown casts |
Mean ATN!!! |
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IgA Nephropathy |
Common in central America Glomerulonephritic syndrome Prognosis: slowly progressive hypertension, eventual ESRD No treatment Light microscopy: Proliferation of mesangial cells, crescents Immunofluorescence: IgA and C3 deposits Electron: Large msangial electron dense deposits |
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Post-infectious glomerulonephritis |
Most often in children Gross hematuria Previous strep infection Low C3 and C4 levels, positive ASO Light: Enlarged glomeruli with endocappilary proliferation Neutrophils, swollen cells Cellular crescents may be seen Immunofluorescence: Granular positivity for IgG and C3 along capillary loops Electron microscopy: Large humps between GBM and pododyctes |
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Membranoproliferative glomerulonephritis |
Nephrotic and nephritic presentation C3 and C4 low Immunosuppressive therapy for treatment Poor prognosis Diffuse thickening of cpillary loops, increased mesangial cells and matrix Silver stain shows double contours of BM showing "tram track" Immunofluorescence: C3 in mesangial and capillary loop pattern Electron: Mesangium enlarged by excess matrix Deposits present between GBM and endothelial cells Hep-C correlation |
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3 non-systemic nephritic diseases |
Membranoproliferative IgA nephropathy Post-infectious glomerulonephritis |
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Lupus nephritis |
Low complement, positive ANA Three light microscopy presentations: Mesangial proliferation, endocapillary proliferation or GBM thickening ("membranous). Can show necrotizing crescents. Immunofluoresence: Positive in all five markers Electron: Mesangial deposits, subendothelial deposits or subepithelial deposits |
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Pauci-immune nephritis |
Serologies: ANCA Treatment: immunosuppression Poor prognosis Light microscopy: crescents/necrotizing lesions Unaffected glomeruli look normal Immunofluorescence: NONE Electron: Absence of electron-dense immune deposits |
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Anti-GBM disease |
Rapid rise in serum-creatinine and RBC casts, severe renal failure Anti-GBM antibodies present Light: diffuse cellular crescent formation and necrotizing lesions Ruptured GBMs Immunoflourescence: Linear IgG positivity in GBM Electron microscopy: no immune deposits |
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Formula for plasma osmolality |
2 x [Na] + [BUN]/2.8 + [glucose]/18 |
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2 Causes of hyper-osmolar hyponatremia |
Diabetes mellitus Hypertonic mannitol infusions |
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Two causes of hypovolemic hyponatremia |
Non-renal volume loss (low UNa) Renal volume loss (high UNa) from diuretics |
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Two causes of euvolemic hyponatremia |
Low Uosm - > primary polidypsia Normal Uosm - > SIADH (increased volume triggers sodium loss via ANP and aldosterone blockage), hypothyroidism |
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Hypervolemic hyponatremia |
Low UNa --> CHF, Cirrhosis, Nephrotic SYndrome High UNa-->Renal failure, no capacity to make dilute urine, makes isotonic urine |
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Max rate of increasing serum Na levels |
.5 mEq/L per hour, max 12 mEq/L per day |
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Causes of hypernatremia |
Urinary losses of hypotonic fluid (diabetes insipidus, osmotic diuresis, intrinsic renal disease GI losses without accompanying thirst Other loss of hyptonic fluid without thirst Administration fo hypertonic saline Hypthalamic lesions affecting thirst center ONLY REALLY OCCURS WHEN THERE IS VOLUME LOSS WITHOUT THIRST REFLEX |
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Best diuretic for hypercalcemia |
Furosemide |
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Best diuretic for chronic renal calcium stone formation |
Thiazide diuretics Increase calcium reabsorption (opposite of loop diuretics) |
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ADH effects on receptors |
V2 receptors increase adenyly cyclase, cAMP and aquaporin insertion V1 receptors cause vasoconstriction |
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MUDPILERS |
Methanol Uremia Diabetic |
