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Renal Flashcards

1
Q

Nephrotic Syndrome vs. Nephritic Syndrome

A

Nephrotic Syndrome

  • Heavy proteinuria (>3.5g)
  • Hypoalbuminemia
  • Edema
  • Hyperlipidemia & lipiduria
  • Normal complement levels
  • Oval fat bodies
  • Free fat droplets
  • Few cellular elements
  • Fatty casts

. Nephritic Syndrome

  • Variable proteinuria (<3.5g)
  • Hypertension
  • Hematuria
  • Red Cell Casts/Granular casts
  • White Blood Cells
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2
Q

Minimal Change Disease

A
  • ETIOLOGY: most common in children
  • Idiopathic- Associated with Hodgkin’s lymphoma or renal cell carcinoma
  • PATHOGENESIS: primary target is glomerular epithelial cells (podocytes)
  • Injury results in increased glomerular permeability and proteinuira
  • Unclear but maybe circulating “glomerular permeability factors”
  • No immune complex depositon, non inflammatory injury
  • MORPHOLOGY: foot process effacement, detachment of epithelial cells / basement membrane (seen only on EM)
  • SYMPTOMS: selectiveproteinuriaàspecifically hypoalbuminemia
  • Periorbital, pedal edema
  • Normal blood pressure
  • Bland urine sediment
  • DIAGNOSIS: low albumin, normal creatinine
  • Urine: proteinuria, bland urine sediment
  • Physical exam: Normal BP, Edema (perioribital, pedal)
  • LM- normal, IF- no immunoglobuilin deposit.
  • TREATMENT: steroidtherapy (8 weeks)
  • Frequent relapse when stopping steroids (1/3 of them)
  • Renal failure & mortality rates are low although somewhat higher in adults than children
  • Pts die of complications of NS or therapy
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3
Q

Focal Segmental Glomerulosclerosis (FSGS)

  • Focal (some glomeruli are affected bit not others)
  • Segmental (affecting only a segment of each glomerulus)
  • Glomerulo(of glomeruli)
  • Sclerosis: scarring
A
  • ETIOLOGY: African American adults
  • Primary: idiopathic
  • Secondary to: HIV, morbid obesity, heroin, chronic reflux nephropathy, malignancies (lymphoma)
  • Anything that causes a reduction in renal mass will result in compensatory hyperfiltrationin remaining glomeruli leading injury pattern
  • Glomerulonephritis
  • Renal ablation nephropathy (partial nephrectomy)
  • Congenital unilateral renal agenesis or aplasia
  • PATHOGENESIS:
  • Secondary: reduction in renal mass due to disease→ →compensatory hyperfiltration → intraglomerular HTN →hyperfiltration injury → sclerosis
  • MORPHOLOGY: patchy fusion of foot processes and effacement
  • SYMPTOMS: insidious onset of asymptomatic proteinuria
  • Hypertension and renal insufficiency
  • Foamy urine
  • Progression to nephroticsyndrome with massive proteinuria & microscopic hematuria
  • Degree of proteinuria is an important prognostic indicator
  • Anasarca(generalized edema)
  • ESRD by 5-20 years
  • DIAGNOSIS: LM (FSGS), IF (negative or IgM& C3 deposits), EM (patchy fusion of the foot processes and effacement
  • TREATMENT: no response to steroids

•

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4
Q

Membranous Nephropathy

A
  • ASSOCIATIONS: idiopathic, endogenous antigens (DNA “SLE”/ tumors) SLE, Hepatitis B, Syphilis, Malaria, Penicillamine, Gold, mercury, Captopril,
  • Present with nephrotic syndrome, microscopic hematuria, HTN, renal insufficiency (late), renal vein thombosis
  • PATHOGENESIS: deposition of immune complexes in sub-epithelial zone or the deposition of circulating ICs
  • Resembles membranous nephropathy to experimental animal disease (HeymannNephritis)
  • Ag-Ab reaction →complement activation → C5b-C9 insertion into podocyte membrane→ detachment of podocyte → GFM damage → increased permeability
  • MORPHOLOGY: diffuse thickening of the GBM
  • IF: Deposits of IgG and C3 along basement membrane
  • EM: Growth of new GBM over depositions → spikes/domes
  • SYMPTOMS: nephrotic syndrome, renal failure
  • Renal HTN, microscopic hematuria
  • Loss of antithrombin3 → hypercoagulablestate → DVT, PE , and renal vein thrombosis
  • LM: diffuse thickening of the GBM with little increase in cellularity
  • IF: fine granular deposits of IgG, C3 along with basement membrane – subepithelial
  • EM: subepithelial immune complex deposits and proliferation & growth of new GBM “spikes” formation
  • Poor prognosis:male, >50, >10gm proteinuria
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5
Q

Diabetic Nephropathy

A
  • ETIOLOGY: systemic hyperglycemia damages glomerulus and arterioles
  • Leading cause of ESRD in USA
  • PATHOGENESIS:
  • Glycosylation, increased TGF-b →matrix formation → mesangium expansion
  • Increased type IV collagen, increased fibronectin, decreased proteoglycan heparin sulfate → thickening GBM
  • Hyperfiltration+ increased glomerular capillary pressure + glomerular hypertrophy → hypertrophy
  • Earliest lesion: expansion of mesangial matrix and thickening of GBM
  • Later lesions: diffuse global glomerulosclerosis with diffuse increase in mesangial matrix & diffuse thickening of GBM
  • MORPHOLOGY: Kimmelstiel-Wilson nodules contains lipids and fibrin (plasma proteins)
  • Ischemia causes tubular atrophy and interstitial fibrosis
  • Hyaline arteriolosclerosis
  • SYMPTOMS: initially hyperglycemia→ hyperfiltration, increased GFR
  • 7-13 years: microalbuminuria(30-300mg/24hr), incipient nephropathy
  • 10-20 years: macroalbuminuria(>300/24h), overt nephropathy
  • Progressive proteinuria, HTN, decline in GFR (12 ml/min/year)
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6
Q

Amyloidosis

A
  • ETIOLOGY: no immune or inflammatory response elicited by amyloid fibrils
  • AL (Primary): light chain produced by abnormal plasma cell clone (multiple myeloma)
  • AA (Secondary): amyloid precursor protein, apolipoprotein produced by liver during chronic inflammation
  • Rheumatoid arthritis, Behcetsyndrome, Crhonsdisease, osteomyelitis, TB, renal cell carcinoma, hodgkin’sdisease
  • B-pleated sheets: Organized fibrillary aggregates resistant to removal
  • PATHOGENESIS: organ damage/dysfunction due to infiltration by amyloid fibrilsand replacement of normal organ architecture (no inflammation)
  • MORPHOLOGY: nodular hyaline material within mesangium and capillary lumens
  • SYMPTOMS: Bence-Jones proteinuria, edema, nephroticsyndrome (proteinuria)
  • Poor prognosis → COD due to end-organ failure
  • Heart: CM/CHF, arrythmias, heart block
  • GI: hepatomegaly, malabsorption, bleeding
  • Neuro: ischemic stroke, neuropathy, orthostatic hypotension
  • Skin: easy bruising, purpura
  • DIAGNOSIS: biopsy of organ involved→ Congo Red Stain (kidney, skin, heart, liver)
  • Polarizable apple green bifringence
  • LM:nodular, amorphous hyaline material in the mesangium & capillary loops, with resultant narrowing or closing of capillary lumens
  • EM: subendothelial & mesangial fibrils
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7
Q

IgA Nephropathy
AKA Berger’s Disease, Mesangioproliferative Glomerulonephritis

A
  • ETIOLOGY: most common type of glomerulonephritis, generally a prolonged benign course
  • IgA Nephropathy→20-30 years old (Asians and Caucasians)
  • Henoch-SchonleinPurpura (HSP) → children
  • PATHOGENESIS: production of IgA immune-complexes (mucosal)
  • MORPHOLOGY: segmental areas of increased mesangial matrix and hypercellularity
  • Mesangial and subendothelial deposits of IgA and C3
  • SYMPTOMS: hematuria worsens during URI or GI infections(gross hematuria), persistent microscopic hematuria between these episodes
  • Non nephrotic range Proteinuria <3.5gm/day
  • Normal C3/C4
  • COMPLICATION: RPGN (nephritic → nephrotic) can progress to ESRD
  • Type 2 Rapidly Progressing GN
  • LM: segmental areas of increased mesangial matrix & hypercellularity
  • IF: mesangial and subendothelia ldeposits of IgA& C3 (+/- IgG, IgM)
  • EM: Mesangial and subendothelial deposits
  • ASSOCIATIONS:
  • Hepatic cirrhosis, gluten enteropathy, HIV, Minimal Change Disease, Ankylosing Spondylitis,Wegener’s small cell Carcinoma
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8
Q

Post-Streptococcal Glomerulonephritis (PSGN)

A
  • ETIOLOGY: 10 days following pharyngitis or 3 weeks following impetigo
  • Children 6-10 years old
  • PATHOGENESIS: infection with B-hemolytic streptococci
  • MORPHOLOGY: subendothelial deposition of immune complexes
  • Initially Hypercellular glomeruli (PMNs + monocytes)→ deposits cleared accounting for resolution of hematuria and renal failure
  • LATER: EM:Subepithelial humps→ responsible for epithelial cell damage and proteinuria, IC deposits cleared slowly (separated from circulation by GBM) limiting their clearance
  • LM: Diffuse proliferation of mesangium, endothelium, epithelial cells. Closure of capillary loops due to proliferation & swelling of endothelial cells & leukocyte infiltration
  • IF:Deposits of IgG and C3 i nmesangium& along capillary walls
  • EM: election dense deposits in sub epithelial space “humps”
  • SYMPTOMS: abrupt onset of nephritic syndrome (proteinuria >2gm)
  • Low levels of complement
  • Children: spontaneous recovery, renal failure in <1% (10-40 years after)
  • Some may develop renal insufficiency as long as 10-40 years after the initial illness
  • COMPLICATIONS:
  • Some glomeruli irreversibly damaged → compensatory hyperfiltration
  • Chronic increase in capillary pressure → glomerulo sclerosis→ FSGS
  • DIAGNOSIS: increased anti-streptolysin O or increased anti-DNAase B with low complement
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9
Q

Membranoproliferative
Glomerulonephritis (MPGN)

A
  • ETIOLOGY: thickening of GBM, mesangial proliferation, and infiltration of inflammatory cells
  • 3 major types → all have same histology
  • Differentiated via EM and IF
  • Presents before age 30
  • PATHOGENESIS:
  • Type I: subendothelial deposits (C3 + IgG + C4)
  • Classical Pathway
  • Lupus, Hepatitis B/C, Endocarditis, cryoglobulinemia, parasitic infection
  • Type II: deposition of unknown dense material along GBM
  • Alternative pathway (decreased C3 due to C3 nephritic factor that stabilizes C3bBb) (C3 + BM+ IgG, C1q, C4 absent)
  • Type III: subendothelial, mesangial, subepithelial deposits (C3 +/- IgG)
  • MORPHOLOGY:
  • Histology: mesangial expansion and hypercellularity with thickening of capillary loops to duplicated GBM → tram track appearance
  • SYMPTOMS: presents before 30 years old
  • 1) Hematuria or proteinuria
  • 2) Acute nephritic syndrome (hematuria, HTN, edema)
  • 3) Recurrent episodes of gross hematuria
  • 4) Insidious onset of edema and nephrotic syndrome
  • Progresses to ESRD in 10-15 years

•

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10
Q
A
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11
Q

Rapidly Progressive Glomerulonephritis (RPGN)

A
  • ETIOLOGY: “Cresentic Glomerulonephritis”
  • MORPHOLOGY: characterized by proliferative GN with prominent “crescent” formation in 30-70% of glomeruli and +/- segmental necrosis
  • (parietal cells)
  • Cellular→ Fibrocellular→ Fibrous
  • SYMPTOMS: 75% die or are placed on dialysis within 2 years
  • Severe oliguria
  • Severe glomerular injury:
  • Proteinuria (non-nephrotic), hematuria, RBC cast, HTN, Edema, oliguria
  • Histosame regardless of cause
  • DIAGNOSIS:
  • Immunofluorescence
  • Linear Staining: Type I RPGN → Anti-GBM Disease→ Goodpasture’s, idiopathic
  • Granular Staining: Type II RPGN → Immune Complex Disease → SLE, IgA, Post-Infectious,henochschonlein, idipathic
  • No Staining: Type III RPGN → Pauci-Immune→ Wegner’s, Microscopic PAN, Churg-Strauss
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12
Q

Alport Syndrome

A
  • ETIOLOGY: defects in collagen IV synthesis (bm)
  • X-linked(80%)
  • M > F, 5-20 years old
  • PATHOGENESIS: COL4A4 & COL4A5 genes used to make BM
  • MORPHOLOGY: basket-weaveappearance (alternating thick/thin of lamina densa)
  • IF is negative for alpha 3,4,5 collagen
  • EM: thin basement membrane with splitting and lamination
  • SYMPTOMS:
  • Nephritis (hematuria, proteinuria, renal failure)
  • Nerve deafness
  • Eye disorders → cataracts(juvenile form)
  • Normal complement levels
  • INVESTIGATIONS: biopsy, immunostain,
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13
Q

Benign Hypertensive Nephrosclerosis

A
  • ETIOLOGY: long standing history of hypertension, asymptomatic
  • Young, black males
  • PATHOGENESIS:
  • Hypertension→ medial/intimal thickening → afferent arteriole luminal narrowing→ hyaline arteriosclerosis via leakage of plasma proteins to tunica media
  • MORPHOLOGY:
  • Vascular: medial and intimal thickening
  • Hyaline arteriolosclerosis (due to extravasation of plasma proteins through injured endothelium)
  • Glomerular: global sclerosis(ischemic injury).. leading to nephron loss
  • Grainy leather
  • Leading to nephron loss
  • FSGS (adaptive injury), compensatory hyperfiltration due to nephron loss
  • Tubules: tubular atrophy, interstitial fibrosis (ischemic mediated)
  • SYMPTOMS: mild proteinuria (<1g/day)
  • Normal or slightly reduced GFR
  • No microscopic hematuria
  • Slow progressive elevation in serum creatinine
  • Risk Factors for ESRD: blacks,diabetes, HTN
  • DIAGNOSIS: bland urine sediment
  • LVH, retinopathy, stroke
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14
Q

Malignancy Hypertensive Nephrosclerosis

A
  • ETIOLOGY: renal disease associated with >180/120 mmHg
  • Young black males
  • PATHOGENESIS: develops in patients with pre-existing essential hypertension, secondary hypertension (pheochromocytoma, primary hyperaldosteronism)
  • MORPHOLOGY: petechial hemorrhages on cortical surfaces
  • Necrotizing arteriolitis& intravascular thrombosis
  • Onion-skin lesion
  • SYMPTOMS: look for end organ damage
  • Malignant HTN Crisis: renal failure + other organ involvement developing over hours or days
  • Hematuria, headache, encephalopathy, acute MI, aortic dissection, blurry vision
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15
Q

Hemolytic Uremic Syndrome (HUS)
Thrombotic Thrombocytopenic Purpura (TTP)

A
  • ETIOLOGY: disorders characterized by abnormal platelet aggregation
  • HUS: seen in children→ following EHEC inflammatory diarrhea (0157:H7)
  • TTP: associated with SLE, HIV
  • PATHOGENESIS: thrombosis in small vessels results in mechanical injury to circulating RBCs → microangiopathichemolytic anemia
  • Lead to ischemic injury to target organs: kidney, brain, heart
  • HUS:
  • Associatedw/ viral, Salmonella, or Shigella infection
  • Induced by quinine, gemcitabine, cyclosporine, OCP
  • SYMPTOMS
  • HUS: more severe renal failure, less CNS involvement
  • TTP: renal failure less severe, more CNS involvement
  • DIAGNOSIS: Microangiopathic hemolytic anemia; schistocytes in peripheral blood smear
  • Thrombocytopenia, acute renal failure, macroangiopathic hemolytic anemia, neurological abnormalities: headache, confusion, seizure, stroke, fever
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16
Q

Renal Artery Stenosis (RAS)

A
  • ETIOLOGY: narrowing of one or both renal arteries
  • 75-90% due to occlusion by atheromatous plaque
  • Takayasu’s arteritis, aortic/renal dissection
  • SYMPTOMS: flank or epigastric bruit, acute renal failure
  • Sudden onset of uncontrolled HTN in previously well-controlled patient
  • Flash pulmonary edema with normal LV function
  • Accelerated or malignant HTN
  • Ischemic Nephropathy: diffuse ischemic atrophy, no arteriosclerosis within kidney due to stenotic renal artery but hypertensive arteriosclerosis in contra-lateral kidney, arterioles protected from transmission of high pressure due to stenoticrenal artery
  • DIAGNOSIS: asymmetrical kidney size
  • Renal arteriogram (gold standard)
  • Renal artery doppleràmeasures renal:aortavelocities (>3.5 ratio = RAS)
  • TREATMENT: angioplasty and stent
  • Uncontrolledhypertention
  • Declining renal function (elevated CR)
  • Recurrent pulmonary edema
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17
Q

Acute Tubular Necrosis (ATN)

A
  • ETIOLOGY: acute injury to renal tubules, causing necrosis.. Acute renal failure
  • PATHOGENESIS: toxic vs ischemic
  • Toxic: exogenous (aminoglycosides) or endogenous (hemoglobinuria, myoglobinuria)
  • Ischemic: hypotension, vasodilatory infection (septic shock), hemorrhagic shock, hypovolemic shock
  • SYMPTOMS: hypotension, oliguria/anuria, uremia(pericardial rub)
  • Elevated creatinine & BUN
  • Anemia(decreased EPO)
  • Metabolic acidosis
  • Initiation Phase (36 hours): acute decrease in GFR, rapid increase in creatinine & BUN
  • Maintenance Phase (3 weeks): plateau of creatinine/BUN, oliguria, uremia, acidosis, hyperkalemia
  • Recovery Phase: tubular function restored, increasing GFR, increase urine volume, gradual decrease in creatinine& BUN
  • DIAGNOSIS: muddy brown granular casts, epithelial cell casts, proteinuria
    1. Ischemic insult- hypotension, vasodilaroty, hemorrhagic shock: GI bleeding, Hypovolemic shock: vomiting, diarrhea
    1. Nephrotoxic insult
  • Exogenous- Aminoglycosides, contrast media “CT/cardiac cath”
  • Endogenous-Hemoglobinuria, myroglobinura
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18
Q

Tubulointerstitial Nephritis

A
  • ETIOLOGY: characterized by interstitial inflammation, edema, fibrosis, but normal glomeruli
  • PATHOGENESIS:
  • Acute: antibiotics (allergic reaction 2 weeks after starting), infection, idiopathic, sarcoidosis
  • Drugs (antibiotics)
  • Infections
  • Idiopathic
  • sarcoidosis
  • Chronic: pyelonephritis (infection), analgesic abuse (ASA, Tylenol), urate nephropathy
  • SYMPTOMS:
  • Impaired urinary concentration (polyuria, nocturia)
  • Salt wasting (hyponatremia)
  • Metabolic acidosis (decreased ability to excrete acid
  • No significant proteinuria or hematuria
  • DIAGNOSIS: confirmation by renal biopsy
  • if AIN → eosinophils, WBC casts, high K, low HCO3
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19
Q

Acute Drug Induced Interstitial Nephritis (AIN)

A
  • PATHOGENESIS: Onset usually two weeks after starting medication
  • Penicillin (antibiotics),cephalosporin, NSAIDS, sulfonamides, ciprofloxacin
  • SYMPTOMS: Allergic-typereaction (interstitial infiltration)
  • 2 weeks after start of medication (first exposure)
  • 3-5 days of second exposure
  • Fever, rash, eosinophilia, ARF/oliguria
  • DIAGNOSIS: Eosinophils, sterile pyuria, WBC casts, proteinuria
  • Confirmation by renal biopsy
  • Increased BUN and creatinine
  • Tubular dysfunction: High K, low HCO3
  • Urine microscopy:
  • Eosinophils, sterile pyuria, WBC casts, proteinuria
  • Blood Test:
  • increased BUN & Creatinine, Increased eosinophil count, Tubular dysfunction: high K, low HCO3
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20
Q

Acute Pyelonephritis

A
  • PATHOGENESIS: most commonly due to E. Coli
  • Spares glomerulus → normal GFR
  • Bloodstream: seeding of kidney from distant source (bacterial endocarditis, septicemia, TB)
  • MAJOR: Ascending Infection:short urethra, foleycatheter, intercourse (women), BPH, catheterization, urine stasis (men) → vesiculourete ralreflux = retrograde
  • SYMPTOMS: fever, dysuria, flank pain, nausea/vomiting, Costovertebral angle tenderness
  • Complications: papillary necrosis, pyonephrosis, perinephric abscess (3 P’s)
  • DIAGNOSIS: elevated BUN/creatinine, WBC (neutrophil) casts, pyuria
21
Q

Chronic Pyelonephritis

A
  • ETIOLOGY: recurrent or persistent renal infection
  • Progressive renal scarring
  • Chronic tubulointerstitial nephritis
  • ESRD
  • Pt with anatomical abnormalities
  • PATHOGENESIS:
  • Chronic Obstructive Pyelonephritis: posterior urethral valves, kidney stones
  • Reflux Nephropathy: vesicoureteral reflux (most common)
  • MORPHOLOGY:
  • Reflux: silent onset.. Pt presents late, renal insufficiency and hypertension, proteinuria(worse with FSGS).
  • VUR-selective scarring and calyx dilation at poles
  • Obstructive: diffuse dilation and scarring of calyxes
  • Microscopic: tubular atrophy, chronic interstitial inflammation, fibrosis in cortex and medulla
  • SYMPTOMS:
  • Reflux pyelonephritis is silent until later in disease
  • Renal insufficiency
  • Hypertension
  • Can progress to FSGS

•

22
Q

Papillary Necrosis + Chronic Analgesic Abuse

A
  • ETIOLOGY: papillary damage due to direct toxic effect
  • Phenacetin
  • ASA
  • Caffeine
  • Acetaminophen
  • Codeine
  • PATHOGENESIS: Interstitial inflammation→ compresses medullary vasculature → ischemia and papillary necrosis
  • SYMPTOMS: excretion of necrotic papilla
  • Gross hematuria
  • Pyelonephritis
  • Renal colic (ureter obstruction)
  • Progressive renal failure
  • Urothelial carcinoma (rare)
23
Q

Obstructive Uropathy

A
  • ETIOLOGY: obstruction at any level of the urinary tract from urethra to renal pelvis
  • PATHOGENESIS:
  • BPH
  • Bladder cancer
  • Kidney stone
  • Papillarynecrosis
  • Retroperitone aladenopathy
  • MORPHOLOGY: dilationof renal pelvis and calyces → unable to excrete due to obstruction
  • High pressure in pelvis is transmitted through collecting tubules into renal cortex… causing atrophy
  • SYMPTOMS: hydronephrosis
  • Irreversible damage and renal failure if not relieved by 2-3 weeks
24
Q

Renal Stones: Nephrolithiasis / Urolithiasis

A
  • ETIOLOGY: men > women, 20-30 years old, idiopathic or specific disease (gout, cystinuria, hyperoxaluria)
  • PATHOGENESIS:
  • Calcium containing (75%)→ calcium oxalate, calcium phosphate
  • Struvite (10-15%) à(Mg/Ammonium phosphate), high PH
  • Uric Acid- radiolucent (5%)
  • Cystine- radiolucent (1-2%)
  • SYMPTOMS: silent if they remain in renal pelvis
  • Symptomatic if stone passes into ureters
  • Renal colic: abrupt onset of flank pain radiating to groin
  • Gross or microscopic hematuria (ulceration of urothelium)
  • Superimposed UTI (due to urinary stasis)
  • Hydronephrosis(due to obstruction of ureter)
  • TREATMENT: IV antibiotic, surgery
  • PREVENTION: increased fluid intake, alkalization of urine (increase solubility of uric acid), low sodium diet (Na reabsorbed in PCT with Ca2+)
25
Q

Autosomal Dominant Polycystic Kidney Disease (ADPKD)

A
  • ETIOLOGY: multiple fluid filled cysts in different tubules leading to increased kidney size
  • PKD1 gene chromosome 16 (85-90%),
  • PKD2 gene (10-15%)
  • Later onset of cysts
  • Fewer & smaller cysts
  • Slower progression
  • Later age of ESRD
  • 80% over 30 years old
  • PATHOGENESIS: mutations in polycystin1,2 or fibrocystin
  • Growth of cysts leads to
  • Compression & destruction of normal adjacent parenchyma
  • Glomeruli are overperfused
  • But small number of nephrons involved and no evidence of FSGS
  • Defects in cell-cell and cell-matrix interactions
  • Abnormal ECM + Cell proliferation + fluid secretion = CYST
  • MORPHOLOGY: arteriolar sclerosis with interstitial fibrosis
  • Bilateral cysts
  • SYMPTOMS: asymptomatic until 4thdecade
  • Hypertension (cysts compress renal vessels = increased RAAS)
  • Hematuria (rupture of cysts in collecting system)
  • Flank pain (stretching of renal capsule)
  • Nephrolithiasis (>50% uric stones)
  • Renal Failure: compression/destruction of normal parenchyma and overperfusion (few glomeruli involved)
  • Hepatic cysts, Berry aneurysms, pancreatic cysts, cardiac valve disease, colonic diverticulosis

•

26
Q

Autosomal Recessive Polycystic Kidney Disease (Childhood)

A
  • ETIOLOGY: PKHD1(fibrocystin) chromosome 6p21-23
  • MORPHOLOGY: smaller cysts arising from the collecting ducts
  • SYMPTOMS: enlarged, cystic kidneys at birth
  • Potter’s Sequence: flat face, low set ears, pulmonary hypoplasia, oligohydramnios (due to renal agenesis)
  • Hepatic fibrosis → childhood cirrhosis
28
Q

Angiomyolipoma

A
  • ETIOLOGY: sporadic, 45 years old,benign rarely malignant
  • MORPHOLOGY: triphasic(muscle, fat, vessels)
  • SYMPTOMS: involves lymph nodes, spleen, renal vein
  • Flank pain
  • Hematuria
  • Retroperitoneal hemorrhage
29
Q

Renal Cell Carcinoma

A
  • ETIOLOGY: tumor of renal tubular epithelial cells
  • Von-Hippel-Lindau(VHL) tumor suppressor gene mutation is halted àincrease IGF-1
  • Hereditary papillary RCCa(multiple, bilateral, younger age group)
  • Most common cancer of the kidney (90%)
  • Males > females, 6thdecade of life
  • Clear cell- VHL is halted
  • Papillary- MEN1 unregulated
  • MORPHOLOGY: clear cells containing fats/lipids (stain Oil Red O / Sudan Black)
  • SYMPTOMS:
  • Painless hematuria, Flank pain, Palpable mass
  • Paraneoplastic syndromes:
  • Polycythemia (EPO), Hypertension (Renin), Hypercalcemia (PTH), Cushing’s (ACTH)
  • Leukamoid Reaction, Amyloidosis
  • DIAGNOSIS: renal ultrasound, CT scan, biopsy
  • GRADE, nuclear Grade (Fuhrman) (1-4)
  • STAGING:
  • Stage I: confined to kidney
  • Stage II: perirenalfat
  • Stage III: lymph node & IVC
  • Stage IV: adjacent organs + metastasis
31
Q

Wilms Tumor

A
  • ETIOLOGY: commonest solid tumor in children
  • <6 years (90%)
  • 2 tumor suppressor genes on chromosome 11 short arm
  • Mutation in WT-1 and WT-2 tumor suppressor genes
  • MORPHOLOGY: single, well-circumscribed, encapsulated grey/white
  • Triphasic (blastema, stroma, epithelial)
  • Anaplasia
  • Palpable abdominal mass, abdominal pain, tumor compresses renal vessels
32
Q

Diverticula

A
  • ETIOLOGY: pouch-like eversion or evagination of the bladder wall
  • Congenital: due to defect in development of the muscle wall
  • Acquired: due to increased intravesicalpressure secondary to obstruction of urine outflow (BPH)
  • COMPLICATIONS:
  • Urine stasis→ infection or stone formation
  • Carcinomas
33
Q

Exstrophy

A

•Tied umbilical cord above hyperemic mucosa of the everted bladder

34
Q

Urachus

A
  • ETIOLOGY: persisting connection between bladder and umbilicus
  • MORPHOLOGY:
  • Patent: connects directly to external abdominal wall
  • Cyst: subepigastricsinus
35
Q

Cystitis

A
  • ETIOLOGY: usually secondary to infection
  • Bacteria- E Coli, proteus, klebsiella, enterobacter
  • Fungus- Candida
  • Parasites-Schistosomahematobium
  • Or Iatrogenic- chemotherapy, radiation (hemorrhagic cystitis)
  • RISK FACTORS:
  • Females(short urethra)
  • Diabetes mellitus
  • Instrumentation(catheter,cytoscopy)
  • Bladder outlet obstruction (male-prostate hyperplasia)
  • Bladder calculi
  • SYMPTOMS: urinary frequency, dysuria (burning), suprapubicpain, microhematuria
  • CHRONIC INTERSTITIAL CYSTITIS
  • Middle aged female
  • Clinically :suprapubic pain, frequency/urgency, nocturia/hematuria
  • Cystoscopic examination: Edema, hemorrhage, ulceration
  • Chronic inflammation, mast cells

•

37
Q

Urothelial (Bladder) Carcinoma

A
  • ETIOLOGY: M > F, 50-80 years old
  • p53, Rb, p16, FGFR3
  • RISK FACTORS:
  • Smoking
  • Drugs: analgesic abuse, cyclophosphamide
  • Chemicals: napthylamine, rubber products
  • Infections: Schistosomiasis(Squamous cell)
  • MORPHOLOGY: fibrovascularcore
  • Papillary(75%):exophytic, superficial invasion, low grade, better prognosis
  • Projects into lumen of bladder and causes obstructive symptoms
  • Flat: non invasice(carninomain situ) or deeply invasive at diagnosis, high grade tumor, metastasis
  • SYMPTOMS: painless hematuria, dysuria, urgency/frequency, flank pain
  • Hydronephrosis
  • TREATMENT: total urothelial resection (TUR)
  • STAGE: depth of invasion of bladder wall, nodal metastases, distant metastases
  • GRADE: based on architecture and cytology
  • Low grade
  • High grade
  • PROGNOSIS: depth of invasion, nodal metastases, architecture
38
Q

Prostatitis

A
  • SYMPTOMS:
  • Dysuria (frequency, urgency)
  • Lower back/pelvic/genital pain
  • Fever, chills, leukocytosis
  • Loss of sex drive
  • Painful erection/ejaculation
  • DIAGNOSIS: DRE→enlarged tender prostate
39
Q

Benign Prostate Hyperplasia (BPH)

A
  • ETIOLOGY: non-neoplastic, not pre-malignant
  • Older age when testosteronelevels are low
  • PATHOGENESIS: periurethral and central zones
  • Testosterone→ (5a-reductase) → DHT → transcription of growth factor
  • SYMPTOMS: 10% symptomatic
  • Urethral compression → difficulty stopping/starting
  • Frequency / dribbling
  • Nocturia, dysuria
  • Urine retention → inability to complete void bladder → hydronephrosis/infections/stones
  • TREATMENT: Transurethral resection (TURP)
  • Treatment with testosterone doesn’t aggravate BPH
  • Possible role of estrogen- increased receptors for DHT on prostatic cells
  • 5a-reductase inhibitors (Fenastiride)
  • TURP
40
Q

Prostate Carcinoma

A
  • ETIOLOGY: most common cancer in males in USA
  • HPC1 or RNASEL gene
  • RISK FACTORS:
  • Age (>65 years old)
  • Race: African American, Caribbean
  • High fat diet
  • Family history
  • Hereditary prostate cancer gene (HPC1) (RNASEL)
  • SYMPTOMS: asymptomatic at early stages
  • Hematuria
  • Late stage/metastasis- bone pain usually Back pain with metastasis through Batson’s Venous Plexus
  • Dysuria
  • Weightloss
  • Nodular hyperplasia: dyuria, weak interrupted urine flow
  • SCREENING: PSA screening, DRE (nodular prostate), Transurethral ultrasound,biposies(6-12 multiple areas)
41
Q

Cryptorchidism

A
  • ETIOLOGY: failure of a testis to descend completely into its normal position within the scrotum
  • Hormonal dysfunction
  • mechanical
  • More common on right side
  • Premature birth (30%)
  • MORPHOLOGY: relative hyperplasia ofinterstitium
  • Nonfunctional Sertoli cells (decreased inhibin, increased FSH)
  • Hyalinization of basement membrane of seminiferous tubules
  • COMPLICATIONS:
  • Germ cell tumors, intra abdominal
  • Infertility
  • TREATMENT: surgical
  • Orchiopexy(before 2 years): to prevent infertility
  • Orchiopexy(before 5 years): to prevent tumors

•

42
Q

Testicular Torsion

A
  • ETIOLOGY: twisting of spermatic cord
  • PATHOGENESIS: obstruction of venous drainage àcongestion
  • SYMPTOMS: red infarction
43
Q

Testicular Tumors

A
  • Teratomas& Yolk Sac: infants / children
  • Mixed Germ Cell Tumor: 15-30 years old
  • Increased AFP and b-HCG
  • Seminoma: 30-50 years old
  • Lymphomas: 60 years old <
  • EPIDEMIOLOGY
  • Isochromosomei(12p)
  • Cryptorchidism
  • Testicular dysgenesis →Klinefelter’ssyndrome
  • SYMPTOMS:
  • Unilateral mass
  • Heaviness in scrotum
  • Hydrocele
  • Breast enlargement
  • Testicular pain
44
Q

Testicular Tumors: Germ Cell Tumors

A
  • SEMINOMA(30%) →middle-aged, pure pattern (surgery/radio)
  • Sheets of cells (fried egg) + lymphocytic infiltrate
  • Increased LDH
  • No necrosis or hemorrhage but still malignant
  • Spread through lymph (good prognosis)
  • NON-SEMINOMA (worse prognosis) (surgery/chemo)
  • Teratoma: children (benign) / adults (malignant)
  • Choriocarcinoma(serum b-hCG)
  • Yolk Sac (serum AFP + alpha-1-antitrypsin + Schiller-Duval Bodies)
  • Embryonal carcinoma
  • Mixed germ cell Tumor (60%)→ seminoma + non-seminoma
  • 3rd decade of life
  • Ill defined hemorrhagic mass, cystic, solid
  • Spread through blood and lymph (good prog)
45
Q

Phimosis / Paraphimosis

A
  • Phimosis: the orifice of the prepuce is too small to permit normal retraction
  • Due to: development anomalies or infection and scarring of the preputial ring
  • Paraphimosis: when a phimotic prepuce is forcibly retracted over the glans penis causing marked constriction and swelling
46
Q

Penile Squamous Cell Carcinoma

A
  • ETIOLOGY: rare in Jews & Muslims (protective effects of circumcision)
  • 40-70 years old
  • PATHOGENESIS:
  • Carcinogens in smegma
  • HPV 16/18
  • Cigarette smoking
  • Bowen’s Disease (solitary plaque on shaft of penis)
  • SYMPTOMS: slow growing, locally invasive tumors

•

47
Q

Scrotal Lesions

A
  • Hematocele: blood in tunica vaginalis (trauma)
  • Hydrocele: accumulation of fluid in the scrotum
  • Chylocele: accumulation of lymph in the tunica
  • Varicocele: dilation of congested blood vessels in the spermatic cord
  • Spermatocele: dilation of epididymis with semen

Pathology (3 decks)

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