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17 Cards in this Set
- Front
- Back
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Acute Interstitial (Hypersensitivity) Nephritis
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ARF with interstitial inflammatory cells
Causes: idiopathic (no Ephils), drugs, infections, etc. Drug causes include: NSAIDs, Methicillin, Anti-biotics, Diuretics Mechanism is ALLERGIC Acute deterioration of renal function (improves on cessation of drug use) Treatment is supportive Stop drug --> usually fully reversible |
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Chronic Interstitial Nephritis
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CRF with mixed infiltrate in interstitium
Tubular atrophy and fibrosis Mechanism is Physical/Chemical or Ischemic Main causes: drugs (NSAIDs, lithium), UTO, stones, PCKD Asymmetrically scarred, shrunken kidneys Remove inciting agent Support renal failure |
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Acute Pyelonephritis
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Usually due to bacterial infection
Ascending infections affect pelvis Hematogenous infections affect cortex Presents as fever, chills, flank pain Predisposed: pregnant women, diabetics, catheters Ascending --> E. Coli; Hematogenous --> Staph Aureus Acute inflammatory infiltrate of tubules Treatment is anti-biotics |
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Chronic Pyelonephritis
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Infections secondary to vesicuretereal reflux
Small kidneys with coarse scars, dilated papillae, atrophy Non-specific interstitial infiltrate Tubular atrophy with "THYROIDIZATION" Fibrosis, Glomerulosclerosis Treatment is support and treatment of hypertension Prophylactic anti-biotics to prevent UTIs |
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Acute Tubular Necrosis
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Most common cause of ARF
ARF secondary to tubular damage Causes: ischemic, POST-TRANSPLANT, toxic, obstructive Phases: oliguric, diuretic, regenerative Histo -- Prox. tubular epithelial cell degeneration, interstitial edema Mitotic activity in regenerative phase Treatment is supportive 30% return to normal renal function Poor prognostic factors: severe oliguria |
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Papillary Necrosis
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Predisposed: analgesic use (PHENACETIN), diabetics, sickle cell pts.
Histo -- acute inflammation in papillae, with necrosis |
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Urolithiasis
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5% of women; 10% of men
40 - 70% recur 50% symptomatic within 5 yrs. SEVERE PAIN Etiology: idiopathic (75%), Infection (15%), Hypercalciuria |
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Autosomal Dominant Polycystic Kidney Disease (ADPKD)
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Very large cystic kidneys
NO dysplasia ALL portions of neprhon involved (bilateral) Declining renal function --> 50% ESRD Cysts also in liver, spleen, and pancreas (do NOT affect function) MV prolapse (25%), Cerebral aneurysms (10-20% [15% of deaths]) PKD 1, 2, 3 encode polycystins (85%, 15%, <1%) Effect cell-cell and cell-matrix interactions |
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Autosomal Recessive Polycystic Kidney Disease (ARPKD)
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Large, SMOOTH kidneys
Narrow cysts perpendicular to capsule Involves COLLECTING DUCTS Often fatal @ birth or postnatally Pancreatic and hepatic cysts (DO affect function) PKHD1 gene encodes fibrocystin |
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Dialysis Related Cysts
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75% after 5 yrs on dialysis
Form stones --> hematuria RCC in 5-10% BOTH cortical and medullary |
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Benign Simple Cystic Disease
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Translucent cysts on surface of cortex
NO clinical significance 50% once older than 50 |
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Multicystic Renal Dysplasia
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Usually UNILATERAL
Multiple cysts of variable size Misshapen kidney Most common cause of abdominal mass in newborns |
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Acute Cellular Rejection
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Most common form
Usually within first 3 months (can occur any time) Presents with rising creatinine and fever Histo -- tubulitis, interstitial inflammation Treat wih increased immunosuppression Can have a vascular component |
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Acute Humoral Rejection
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Affects capillaries
Can use fluorescent Abs to C4d to diagnose Also, increased donor-specific Abs Rarely, severe with necrotizing arteritis |
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Chronic Allograft Nephropathy
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Most frequent cause of graft loss today
Creatinine SLOWLY rises Non-specific tubular atrophy, interstitial inflammation, glomerular sclerosis |
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Calcineurin-Inhibitor Toxicity
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Causes NODULAR HYALINIZATION of arterioles
Also, causes changes identical to chronic rejection |
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Recurrent disease in grafts
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Type II MPGN (100%)
Diabetic GN (>90%) IgA Nephropathy (40-60%) FSGN (35%) Loss of graft is rare in all of them EXCEPT for FSGN (10-30%) |
