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level: Level 1

Questions and Answers List

level questions: Level 1

Question	Answer
Clinical manifestations: proteinuria, hypoalbuminemia, general edema, hypercholesterolemia and lipidura	nephrotic syndrome
most common cause of nephrotic syndrome in children's from 2-6 years of age.	minimal change disease
Biopsy: Light microscopy: No abnormalities Immunofluorescence: Negative Electron microscopy: Foot process enfacement	Minimal Change disease
Most common Renal disease in adults.	focal segmental glomerulosclerosis
Clinical pathophysiology syndrome: -Podocyte injury and depletion -Glomerular segmental scarring (sclerosis)	focal segmental glomerulosclerosis
Biopsy: light microscopy-sclerotic segments and segmental deposition of the proteins in capillary (hyalinosis) Electronic microscopy-foot process Immunoflourescent: IgM & C3	focal segmental glomerulosclerosis
20-30% is in Caucasian adults, during 4-5 decades of life most common in men. Light microscopy: capillary walls appear thickened Biopsy: Immunofluorescence: IgG & C3	membranous nephropathy
Reduction of GFR, Non - nephrotic proteinuria, edema, hypertension, RBC cast, Azotemia, oliguria and hematuria.	nephritic syndrome
Appears after 1-4 weeks after Streptococcal infection (A-B hemolytic Strepotococci). Most common in children's of 6-10 years	poststreptococcal glomerulonephritis
Biopsy: Light microscopy: Diffuse glomerular hypercellularity and infiltrations of polymorphonuclear leukocytes, monocytes and macrophages Immunofluorescence: IgG C3 and IgM Electron microscopy: sub-epithelial deposits "Humps"	poststreptococcal glomerulonephritis
Malaise, fever, oliguria and hematuria (weeks later after trot infection)	post strep glomerulonephritis symptoms
Rapid progressive loss of renal function. Biopsy: Crescentic glomerulonephritis	rapidly progressive glomerulonephritis
Caused by a deposition of IgA immune complex in the glomerular mesangium. Frequent in Asian and American Indian population. Biopsy: it can range from morphological normal to mesangial and proliferative and crescentic Dark immune IgA complex depositions	IgA nephropathy
10% of the people are born with malformations of the urinary system, it can be in early development of later( hydronephrosis and nephron loss can occur)	Congenital Urinary Tract obstruction
Solitary kidney enlarges as a compensatory hypertrophy and it can develop some glomerular sclerosis.	Agenesis of the kidney
Failure of the kidney develop a normal size	hypoplasia
Kidney lies above the pelvic brim or within the pelvis.	Ectopic kidney
Fusion of the upper or lower pole of the kidney and it continues across the midline anterior to the great vessels	horseshoe kidney
Formation of stones by supersaturation of: -magnesium ammonium phosphate -calcium oxalate and phosphate -uric acid -cysteine	Urolithiasis
Clinical manifestation: pain in the back, change in urine output, no alleviating factos, hypertension. Risk factos: dietary( animal proteins, oxalate, sodium, sucrose or fructose) Non dietary( race, obesity, lack of water, medications)	Urolithiasis
Pain is abrupt and intensities over time , gross hematuria, urinary frequency, nausea, vomitting can occur. Physical findings: costovertebral angel tenderness	Ureteal colic
Highest sensitivity and specificity for kidney diagnosis	ct scan
Detects opaque calcareous or cysteine stone	KUB
Detects hydronephrosis and hydroureter	Ultrasound
Causes: Ischemia and Nephrotoxic Etiology: patients with severe trauma, cardiac surgery, severe burn, sepsis Morphology: vacuolization loss of brush borders, cast obstruction, flattened simplified tubulars epithellium	acute tubular injury/ necrosis
Involves inflammatory injuries of the tubules and azotemia. Causes: analgesic nephropathy Etiology: most commonly detected in women of six and seventh decades of life . Clinical presentation: impaired ability to concentrate urine, salt waisting, low ability to excrete acids and defects on reabsorption	Tubulointerstitial disease
Etiology: caused by gram negative bacilli (E. Colli) or in immunocompromised people: Polyomavirus cytomegalovirus and Adenovirus. *Because of urethral catheterization or other instrumentation)	Pyelonephritis
Morphology: patchy interstitial suppurative inflammation and intratubular aggregates of neutrophils Clinical manifestation: sudden onset at the costovertebral angle, fever, malaise, dysuria, frequency Labs: WBC cast	acute pyelonephritis
Morphology and radiographic: irregular scared, bilateral and asymmetrical contracted kidney significant bacteriuria Clinical features: back pain, pyuria, bacteriuria, flank tenderness	chronic pyelonephritis
Small tumors (<.5cm) Appears pale yellow, discrete well circumscribed nodules	Renal Papillary ademona
Consist of vessels, smith muscle, and fat originating from perivascular epithelioid cells Loss of futon mutations in TSCS and TSC2 Spontaneous hemorrhages	angiomyolipoma
Large eosiphilic cells, may achieve a large size 12 cm	oncocytoma
Morphology: arise most commonly in the poles of the kidney. bright yellow-gray spherical masses. Clinical features: costovertebral pain, hematuria and palpable mass. Also the general symptoms are shown Can occur metastasis	renal cell carcinoma
most common renal malignancy in children Clinical manifestation: flank mass, hematuria, abdominal pain and fever	wilms tumor
Epidemiology: more common in men of 50-80 years old, in urban nations Risk factors: cigarette smoking, industrial exposure to aryl amines, schistosomes haematobium infection, long use of analgesics, radiation or heavy long term exposure to cyclophosphamide. Clinical manifestation: Painless hematuria , dysuria, urgency Morphology: Hematogenous dissemination to liver, lungs, and bone marrow	Bladder cancer