PPOM 2 Block 3 OMK

Which translocation is associated with acute promyelocytic leukemia?

t(15;17)

What causes hypertension and edema in nephritic syndrome?

Decreased glomerular filtration causes sodium and water retention.

How should antibiotics be selected for urinary tract infections in long-term care residents?

Use urine culture and susceptibility results to select narrow-spectrum antibiotics.

What urinary obstruction complication warrants hospital admission?

Pyelonephritis with ureteral obstruction.

What additional symptoms warrant hospitalization in a nonpregnant patient with urinary tract infection?

Severe pain requiring parenteral medication or urinary retention.

What symptoms suggest acute bacterial prostatitis?

Fever, chills, dysuria, urinary frequency, urgency, and perineal pain.

Which Enterococcus species commonly cause urinary tract infections?

Enterococcus faecalis and Enterococcus faecium.

What alternative antibiotic is listed for acute bacterial prostatitis?

Trimethoprim-sulfamethoxazole, guided by susceptibility testing.

What complications of acute pyelonephritis are associated with diabetes?

Renal papillary necrosis and emphysematous pyelonephritis.

What symptoms suggest urethritis rather than cystitis?

Dysuria and urethral discharge without urinary frequency or urgency.

What preventive measures are listed for recurrent cystitis?

Cranberry juice and prophylactic antibiotics.

Which infections involve the lower urinary tract?

Cystitis, urethritis, and prostatitis.

Which organism is most commonly associated with malakoplakia?

Defective macrophage phagolysosomal function.

What causes a urachal cyst?

Persistence of the central urachal canal with obliteration of both ends.

Which embryologic structure gives rise to the ureteric bud?

Mesonephric (Wolffian) duct.

What is the most common cause of hydronephrosis in infants and children?

Ureteropelvic junction obstruction.

What causes congenital ureteropelvic junction obstruction?

Abnormal smooth muscle organization or excessive collagen deposition.

What extrinsic abnormality can cause ureteropelvic junction obstruction?

Compression by an abnormal renal blood vessel.

What is the hallmark of ureteritis follicularis?

Subepithelial lymphocyte aggregates causing mucosal elevations.

What is the hallmark of ureteritis cystica?

Cystic spaces within urothelial nests in the lamina propria.

What are common intrinsic causes of ureteral obstruction?

Calculi, tumors, strictures, and blood clots.

What medications are associated with sclerosing retroperitoneal fibrosis?

Ergot derivatives and beta-adrenergic blockers.

What is the characteristic benign tumor-like lesion of the ureter?

Fibroepithelial polyp.

What is the hallmark histologic finding of urethral condyloma?

Koilocytosis associated with human papillomavirus.

What causes hematuria in nephritic syndrome?

Inflammatory injury to glomerular capillary walls.

What are the hallmark findings of nephritic syndrome?

Hematuria, red blood cell casts, oliguria, hypertension, edema, and mild proteinuria.

What causes azotemia in nephritic syndrome?

Decreased glomerular filtration increases blood urea nitrogen and creatinine.

What abnormal immunoglobulin causes immunoglobulin A nephropathy?

Galactose-deficient immunoglobulin A1.

Which vasculitis is associated with immunoglobulin A nephropathy?

Immunoglobulin A vasculitis (Henoch–Schönlein purpura).

What is the light microscopy finding in immunoglobulin A nephropathy?

Mesangial expansion and cell proliferation.

What is the main management of poststreptococcal glomerulonephritis?

Supportive treatment of hypertension, edema, and volume overload.

What is the electron microscopy finding in poststreptococcal glomerulonephritis?

Subepithelial electron-dense humps

What is the immunofluorescence pattern in poststreptococcal glomerulonephritis?

Granular immunoglobulin G and complement component 3 (starry sky)

What is the light microscopy finding in poststreptococcal glomerulonephritis?

Diffuse glomerular hypercellularity with neutrophil infiltration.

What is the hallmark pathology of rapidly progressive glomerulonephritis?

Crescent formation in Bowman's space.

What forms glomerular crescents?

Fibrin, parietal epithelial cells, monocytes, and macrophages.

What are the three immunofluorescence patterns of rapidly progressive glomerulonephritis?

Linear, granular, and pauci-immune (minimal or absent staining).

What forms glomerular crescents?

Fibrin, parietal epithelial cells, monocytes, and macrophages.

Which antibody is associated with microscopic polyangiitis?

Anti-myeloperoxidase antibodies (perinuclear antineutrophil cytoplasmic antibodies).

What are the classic findings of granulomatosis with polyangiitis?

Recurrent sinusitis, saddle-nose deformity, pulmonary disease, and glomerulonephritis.

What renal biopsy pattern occurs in granulomatosis with polyangiitis?

Pauci-immune crescentic glomerulonephritis.

Which lupus nephritis class causes nephrotic syndrome?

Class V (membranous nephropathy).

What complement findings occur in lupus nephritis?

Decreased complement components 3 and 4.

What is the classification of lupus nephritis from Classes I through VI?

Minimal mesangial, mesangial proliferative, focal proliferative, diffuse proliferative, membranous, advanced sclerosing.

Which lupus nephritis classes show wire-loop lesions?

Classes III and IV.

What causes wire-loop lesions in proliferative lupus nephritis?

Subendothelial immune complex deposits.

Which lupus nephritis class shows advanced global sclerosis?

Class VI.

What is the characteristic electron microscopy finding in Alport syndrome?

Basket-weave splitting and lamination of the glomerular basement membrane.

What is the characteristic finding in thin basement membrane disease?

Diffuse basement membrane thinning with familial hematuria and usually normal renal function.

What is the gross appearance of benign nephrosclerosis?

Shrunken kidneys with finely granular cortical surfaces.

How does benign nephrosclerosis cause renal injury?

Luminal narrowing → chronic ischemia → glomerulosclerosis and tubular atrophy.

How is renal function affected in uncomplicated benign nephrosclerosis?

Usually minimally affected; renal disease progresses slowly.

What increases the severity of benign nephrosclerosis?

Hypertension, diabetes, advanced age, and African ancestry.

What is the hallmark histopathologic finding of malignant nephrosclerosis?

Hyperplastic arteriolosclerosis → concentric onion-skin lesions.

What additional vascular lesion occurs in malignant nephrosclerosis?

Fibrinoid necrosis of small renal arteries.

What causes fibrinoid necrosis in malignant nephrosclerosis?

Endothelial injury → fibrinogen leakage and deposition in vessel walls.

Why should blood pressure not be lowered too rapidly during hypertensive emergency?

Rapid reduction can cause inadequate perfusion of vital organs, especially the brain.

What three major conditions cause thrombotic microangiopathy in this lecture?

Malignant hypertension, hemolytic uremic syndrome, and thrombotic thrombocytopenic purpura.

What causes microangiopathic hemolytic anemia?

Microvascular thrombi shear red blood cells → schistocytes.

What other organism can cause Shiga toxin-associated hemolytic uremic syndrome?

Shigella dysenteriae serotype 1.

What is the characteristic renal histopathology of typical hemolytic uremic syndrome?

Glomerular capillary thrombi and mesangial matrix disruption.

Which complement protein deficiency is strongly associated with atypical hemolytic uremic syndrome?

Complement factor H deficiency.

What other complement regulatory proteins may be abnormal in atypical hemolytic uremic syndrome?

Complement factor I and CD46.

What is the characteristic histopathology of chronic atypical hemolytic uremic syndrome?

Glomerular basement membrane splitting or reduplication.

What causes atypical hemolytic uremic syndrome?

Complement regulatory protein abnormalities → uncontrolled complement activation.

What is the classic pentad of thrombotic thrombocytopenic purpura?

Fever, neurological symptoms, hemolytic anemia, thrombocytopenia, and renal failure.

What is the normal function of ADAMTS13?

Cleaves large von Willebrand factor multimers to limit platelet aggregation.

What treatment removes pathogenic autoantibodies in thrombotic thrombocytopenic purpura?

Plasma exchange with replacement plasma.

Which clinical manifestation is more prominent in thrombotic thrombocytopenic purpura than hemolytic uremic syndrome?

Neurological abnormalities.

What gross renal finding may occur in severe thrombotic microangiopathies?

Diffuse cortical necrosis involving the cortex and columns of Bertin.

What is the second most common cause of renal artery stenosis?

Fibromuscular dysplasia, especially in young women.

What hormone increases in unilateral renal artery stenosis?

Renin → activation of the renin-angiotensin-aldosterone system.

Which kidney develops more severe hypertensive arteriolosclerosis in unilateral renal artery stenosis?

The contralateral, nonischemic kidney.

What are the histopathologic findings of chronic renal ischemic atrophy?

Crowded sclerotic glomeruli, atrophic tubules, and interstitial fibrosis.

Which arterial layer is commonly thickened in renal fibromuscular dysplasia?

Tunica media → fibrous thickening and luminal stenosis.

What is the most common cause of renal infarction?

Emboli, commonly from left-sided cardiac mural thrombi.

What type of necrosis occurs in renal infarction?

Coagulative necrosis.

What is the characteristic gross appearance of renal infarction?

Pale, wedge-shaped lesion with the base toward the cortex and apex toward the medulla.

Why are renal infarcts usually pale?

Kidneys have limited collateral circulation.

What histopathologic finding characterizes renal atheroembolic disease?

Cholesterol clefts within renal arteries.

What procedures can precipitate renal atheroembolic disease?

Abdominal aortic surgery or aortography.

Why does sickle cell disease preferentially injure the renal medulla?

The medulla's hypoxic, hypertonic environment promotes red blood cell sickling.

What are the major renal manifestations of sickle cell nephropathy?

Hematuria, impaired urinary concentrating ability, and papillary necrosis.

What conditions can cause ischemic acute tubular injury?

Hypovolemic shock, microscopic polyangiitis, hemolytic uremic syndrome, and thrombotic thrombocytopenic purpura.

What endogenous substances cause toxic acute tubular injury?

Myoglobin, hemoglobin, monoclonal light chains, bile, and bilirubin.

What endogenous substances cause toxic acute tubular injury?

Myoglobin, hemoglobin, monoclonal light chains, bile, and bilirubin.

How does ischemia alter tubular epithelial cell polarity?

Redistribution of sodium-potassium ATPase disrupts normal ion transport.

How does loss of tubular cell polarity decrease glomerular filtration rate?

Increased distal sodium delivery → Vasoconstriction → Decreased filtration.

How do cytokines contribute to acute tubular injury?

Injured tubular cells release cytokines that recruit leukocytes and worsen inflammation.

What is tubular back-leak in acute tubular injury?

Patchy necrosis with intervening preserved tubular segments.

What is the characteristic pattern of toxic acute tubular injury?

Extensive necrosis, especially involving proximal convoluted tubules.

What are the characteristic histologic findings of acute tubular injury?

Tubular epithelial necrosis, sloughing, dilation, and intratubular casts.

What pigment casts can appear in acute tubular injury?

Brownish-pink casts containing pigments derived from myoglobin or hemoglobin.

What distinguishes grade 1 from grade 2 vesicoureteral reflux?

Grade 1 involves only the ureter; grade 2 also reaches the renal pelvis without dilation.

What distinguishes grade 3 vesicoureteral reflux?

Mild dilation of the ureter and renal collecting system.

What distinguishes grade 4 vesicoureteral reflux?

Moderate dilation, ureteral tortuosity, and blunted renal fornices with preserved papillae.

What distinguishes grade 5 vesicoureteral reflux?

Severe dilation and tortuosity with loss of renal fornices and papillary impressions.

What is the difference between complete and incomplete ureteral duplication?

Complete = two separate ureters; incomplete = two ureters join before entering the bladder.