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60 Cards in this Set
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Type I RTA |
DCT cannot secrete H+ to acidify urine. K+ builds up and is excreted in urine Very low bicarb Low K Bilateral kidney stones Low Ca (may cause rickets) High urine pH + UNC Patient with Sjogrens or RA |
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Type II RTA |
Proximal tubule excreting too much bicarb Fanconi Syndrome Low HCO3 (not as low at Type I) Low K Low urine pH No kidney stones Can be caused by acetylzolamine (carbonic anhydrase inhibitor) |
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Type IV RTA |
Distal tubules fails to excrete H/K Commonly aldo deficiency or resistance Hyperkalemia Diabetics Tx: fludrocortisone |
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pre-renal failure |
decrease in blood flow to the kidney Increases aldo, incerasse Na and H2O reabsorption, greatly increases BUN flow into the blood. BUN:Cr > 15, low UNa, low FeNa, high Uosm |
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Post-renal failure |
decrease in outflow Back pressure from obstruction cause BUN to leak back into the blood BUN:Cr>15, high UNa, high FeNa, low Uosm Anuria and hydronephrosis |
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Intrarenal failure |
Problem within the kidney BUN can't be reabsorbed BUN:Cr<15, high UNa, high FeNa, low Uosm Diuretics can obscure these values |
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Acute Tubular Necrosis |
Kidney attack Necrosis of tubular epithelial cells plug tubules and create obstruction Decreased GFR and brown muddy casts BUN"Cr<15, Uosm low, high UNa |
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Brown granular casts are seen in |
Acute tubular necrosis |
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Ischemic tubular necrosis |
decrease in blood supply leading to necrosis PT and thick ascending limb are the most susceptible |
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Nephrotoxic tubular necrosis |
Toxic agents cause necrosis PT most susceptible May cause hyperkalemia |
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Toxic agents that can cause tubular necrosis |
Aminoglycosides, heavy metals, myoglobinuria, ethylene glycol, contract dye, urate |
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Phases of Acute Tubular necrosis |
1. Injury 2. Maintenance phase: increase BUN:Cr, hyperkalemia, metabolic acidosis, oliguria 3. Recovery: polyuria, hypokalemia |
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Acute interstitial nephritis |
drug induced hypersensitivity reaction of interstitial and tubules Can be caused by NSAIDs, penicillin, diuretics, and Bactrim Oliguria, fever, rash days to weeks after starting drug Eosinophils in the urine May progress to renal papillary necrosis |
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Renal papillary necrosis |
sloughing of renal papillae leads to gross hematuria and flank pain May be triggered by infection or immune stimulus Associated with: DM, acute pyelonephritis, acetaminophen use, sickle cell |
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Nephrotic syndrome |
Massive proteinuria (>3.5g/day) Hypoalbuminemia (causes edema) Hypogammaglobulinemia (infections) Hypercoagulable state (loss of ATIII) Hyperlipidemia (increased liver activity to try and make more albumin) |
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Minimal change disease |
Nephrotic most common in children thinning of foot processes on EM leads to a decrease in the negative charge of the basement membrane Loss of albumin but not immunoglobulin (no immune complex deposition) May follow URI or allergic reaction associated with Hodgken's lymphoma (cytokines damage podocytes) Tx: steroids |
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focal segmental glomerulosclerosis |
nephrotic Collagen deposition in the glomeruli. Only effects some glomeruli Thinning of foot processes on EM, sclerosis on LM No immune complexes Common in hispanics and AA Associated with HIV, sickle cell, and heroin use Tx: doesn't respond well to steroids |
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membranous nephropathy |
Nephrotic Immune complex deposition leads to thickening of glomerular membrane Common in white adults Associated with Hep B & C, solid tumors, SLE, or drugs Spike and dome on EM Granular on IF Tx: poor response to steroids |
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Membranoproliferative glomerulonephritis Type I |
Nephritic or nephrotic immune complex deposition under endothelial cells. Seen with Hep B and C Tram track appearance on IF |
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Membranoproliferative glomerulonephritis Type II |
Nephritic or nephrotic Immune complex deposits within basement membrane Associated with C3 nephritic factor (stabilizes C3 and over activates compliment) Causes hypocomplement serum levels Tram track on IF |
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Diabetic glomerulonephropathy |
Nephrotic Nonenzymatic glycosylation of basement membrane leads to hyaline arteriolosclerosis and thickening Efferent arteriol is more effected, leading to increased GF pressure Formation of Kimmelstiel Wilson nodules |
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Amyloidosis |
Amyloid deposits in the kidney kidney most effected Apple green birefringence with congo red stain Associated with multiple myeloma, TB, and RA |
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nephritic syndrome |
Glomerular inflammation and bleeding limited proteinuria (<3.5 g/day) oliguria and azotemia salt retention causing periorbital edema and HT RBC casts in urine Decrease GFR, Increase BUN:Cr |
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Post strep glomerulnephritis |
Nephritic Nephritogenic strains carry M protein 2-3 weeks post infection: cola colored urine, periorbial and peripheral edema and HT Crescent seen around glomeruli, made of fibrin and macrophages EM: subepithelial humps IF: granular |
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IgA nephropathy (Bergers) |
Nephritic IgA complex deposition in mesangium Compliment activated via alternative and lecithin pathway Common in children Occurs days after URI and GI infection Seen with Henoch Schonlein purport Hematuria and RBC casts in urine |
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Alport syndrome |
Nephritic Inherited defect in Type IV collagen, commonly x-linked Results in thinning and splitting of the basememnt membrane Presents as hematuria, hearing loss, and ocular problems |
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Rapidly progressing GN Type I |
Linear IF pattern Crescents on LM Anti-basement membrane antibodies Ex: Goodpastures-antibodies to type IV collagen |
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Rapidly progressing GN Type II |
Granular IF Crescents on LM Immune complex deposition Ex: Post strep GN progression and SLE |
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Rapidly progressing GN Type III |
Negative IF Pauci-immune c-anca or p-anca positive Ex: vasculitis |
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Diffuse proliferative GN |
Type IV Lupus nephritis Proteinuria, hematuria, decreased GFR Immune deposits of IgG and C3 LM: Wire looping Severe, can progress to ESRD |
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Cystitis |
Bladder infection Urinalysis: >10WBCs dipstick: + leukocyte esterase and nitrites (gram -) culture: >100,000 colonies Dysuria, frequency, urgency, suprapubic pain |
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Sterile pyuria |
pyuria with negative urine culture Suggests urethritis due to chlamydia or gonorrhea |
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Pyelonephritis |
kidney infection, usually ascending affects mostly the cortex, sparing the glomeruli Risk increases with vesicoureteral reflect Fever, flank pain, WBC casts, leukocytosis |
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Chronic pyelonephritis |
interstitial fibrosis and atrophy of the tubules due to multiple infections tubules contain eosinophilic casts resembling tyroid tissue |
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Nephrolithiasis |
Precipitation of urinary solute as a stone Risk factors: increased solute concentration an decreased urine volume |
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Calcium oxalate/phosphate stones |
most common. Cause: idiopathic, hypercalciuria, Chron's, ethylene glycol, too much Vit C *Increased Ca in urine, but normal in blood Tx: Ca sparing diuretic |
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Ammonium Mg Phosphate stone |
Strive stone 2nd most common Causes: infection (proteus, klebsiella) Urine will be alkaline Can form stag horn calculi which needs surgical removal |
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Uric acid stones |
Radiolucent (not seen on Xray) Causes: gout, hyperuricemia (leukemia) Risk factors: dehydration Tx: hydration and alkalization of urine with KHCO3 |
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Cystine stones |
rare, seen in children Causes: decreases reabsorption of cysteine. May form stag horn calculi Tx: hydration and alkalization of urine |
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Symptoms of uremia |
Nausea, anorexia, pericarditis, platelet dysfuntion, encaphalopathy, urea crystal deposition |
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End stage kidney failure |
Common causes: HT, DM, glomerular disease Cx: salt and H2O retention with HT Hyperkalemia with metabolic acidosis Anemia Hypocalcemia and high phosphate Dyslipidemia Renal osteodystrophy Tx: dialysis or transplant |
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Renal osteodystrophy |
Low Ca, high phosphate, and failure of Vit D hydroxylation lead to secondary hyperparathyroidism Ca is reabsorbed from the body causing bone thinning |
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Hyperkalemia |
Result: peaked T waves, wide QRS, torsades Causes: acidosis decreased insulin digoxin beta blockets cell lysis hyperosmolar state kidney disease Type IV RTA |
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Hypokalemia |
Result: u waves, flat t waves, arrhythmias, muscle weakness causes: high insulin beta adrenergic stimulation alkalosis GI loss, vomiting, diarrhea, diuretics Type I and II RTA Hypomagnesemia |
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Hypercalcemia |
Symptoms: stones bone pain abdominal pain, nausea, constipation anxiety, AMS Causes: increased bone resorption hyperpatathyroidism malignancy increase Vit D high calcium carbonate intake |
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Hypocalcemia |
Signs: seizures, tetany Causes: hypoparathyroid renal failure pancreatitis low Mg |
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Hyperphosphatemia |
Mostly asymptomatic, symptoms are from decreased Ca Causes: tumor lysis syndrome rhabdomyolysis phosphate laxatives kidney disease hypoparathyroid |
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Hypophosphatemia |
Symptoms: weakness form ATP depletion Causes: hyperparathyroid antacids DKA refeeding syndrome in alcoholics Fanconi syndrome |
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Hypermagnesemia |
Symptoms: decreased reflexes, paralysis Bradycardia, hypotension, lethargy Causes: renal insufficiency |
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Hypomagnesemia |
Symptoms: tetany, tremor, lethargic Can cause hypokalemia and hypocalcemia Causes: GI loss, diarrhea pancreatitis renal loss, diuretics omeprazol foscarnet |
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Hyponatremia |
Brain swells, causing malaise, stupor, coma Causes: decreased fluid to kidney ineffective kidneys too much ADH Psycogenic polydipsia |
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central pontine myelinolysis |
overly rapid correction of hyponaremia causes demyelination of central pontine axons at the base of the pons Loss of corticospinal and corticobulbar tracts leading to quadriplegia |
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Hypernatremia |
Brain thinks causing irritability, stupor, coma Causes: water loss Diabetes insipidus |
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Horseshoe kidney
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kidneys conjoined at lower pole. Located in lower abdomen Most common |
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Renal agenesis unilateral |
Absence of one kidney Leads to hypertrophy of single kidney |
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Renal agenesis bilateral |
Oligohydramnios Also have lung hypoplasia, flat face, low set ears (Potter sequence) Not compatible with life |
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Dysplastic kidney |
congenital malformation of renal parenchyma with cysts and cartilege. No renal tissue and absent ureter. Noninherited. usually unilateral |
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Polycystic kidney disease recessive |
Inherited Bilateral enlarged kidneys with cysts in cortex and medulla Presents in infants with HT, renal failure, Potter sequence, hepatic fibrosis, and hepatic cysts (portal HT) |
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Polycystic kidney disease dominant |
Inherited Bilateral enlarged kidneys with cysts in cortex and medulla Presents in young adults with HT, hematuria and renal failure APKD1 or 2 mutation Associated with berry aneurysm, hepatic cysts, and mitral valve prolapse *FH of sudden death |
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Medullary cystic kidney disease |
Inherited Cysts in collecting ducts. Parenchymal fibrosis leads to shrunken kidney and renal failure. |
