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46 Cards in this Set
- Front
- Back
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Osmotic nephrosis
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Reversible renal tubular injury (within 6 hours)
Hydropic change (distention of phagolysosomes) Most often following agents to induce osmotic diuresis (manitol, sucrose, dextrans) radiocontrast, IVIg |
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Types of acute tubular necrosis
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Ischemic and toxic
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What part of the kidney is most susceptible to acute tubular necrosis?
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PCT
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Route of pyelonephritis
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Ascending - 95%
predisposing conditions are those that retard urinary drainage vesicourethral sphincter incompentence Hematogenous |
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Serious complications of pyelonephritis
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Papillary necrosis
Pyonephrosis Perinephric abscess |
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Tubulointerstitial nephritis signs/symptoms
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Fever
Eosinophilia Renal tubular fnc abnormalities Oliguric acute renal failure |
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Tubulointerstitial nephritis pathogenesis
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IgE and cell-mediated immune response against
Tubular cells or tubular basement membrane |
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Analgesic abuse nephropathy
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Cause of papillary necrosis, tubulointerstitial nephritis
Increased risk for urothelial carcinomas |
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Cast nephropathy
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Sequelae of plasma cell dyscrasias
Brittle casts of Bence Jones proteins in tubules Surrounded by inflammation Associated with tubular injury |
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Hypokalemia nephropathy
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Coarse vacuolar change in tubules
Reversible |
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Hyaline droplet change in renal tubules
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Reversible
Sign of protein reabsorption |
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Acute tubular necrosis
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Injury to tubular epithelium results in acute renal failure
Not necessarily necrosis Common cause of ARF |
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Ischemic acute tubular necrosis
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Inadequate end organ perfusion
Usually in setting of hypotension and shock Usually reversible AKA vasomotor nephropathy |
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Why are the tubules vulnerable to injury?
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Toxic
Large surface area for renal absorption of potential toxins Active transport systems that can be used by toxins Concentrating capacity for toxins Ischemic Medulla receives only a small portion of total renal blood flow |
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Pathophysiology of changes in acute tubular necrosis leading to acute renal failure
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Vasoconstriction 2/2 activation of RAA system because of decreased sodium reabsorption
Tubules obstructed by casts leading to increased tubular pressure Leak of filtrate through tubular epi/BM into interstitium Toxins may direct effect on filtration by glomerular capillary wall damage |
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Ischemic acute tubular necrosis pathology
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Swollen kidney
Pale cortex, congested medulla Usually effects the straight portion of the proximal tubule and ascending thick limb of Henle Somewhat patchy Simplification of PCT (loss of brush border, dilation, flattening) Single cell necrosis exposing BM Granular/hylanine casts Interstitial edema Regenerative changes |
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Nephrotoxic acute tubular necrosis
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Extensive distribution
Confluent necrosis Usually involved PCT and DCT |
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Acute tubular necrosis pathology
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Pigmented granular and eosinophilic casts prominent
Epithelial regeneration: flattened cells, mitotic figures |
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Tubulointerstitial nephritis
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Group of inflammatory diseases that primarily involve tubules and interstitium
Diverse causes Glomeruli involved only late |
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Clinical signs of tubular dysfunction
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Impaired concentration of urine
polyuria, nocturia Salt wasting Metabolic acidosis -diminished ability to excrete acids Defects in secretion or reabsorption |
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Pyelonephritis cause
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>85% caused by grame negs bacilli
E. coli, Proteus, Klebsiella, Enterobacter (bowel flora) |
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Who gets pyelonephritis from hematogenous route?
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Urethral obstruction
Debilitated patients Immunosuppresed More likely when bug is not bowel flora |
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Acute pyelonephritis increased risk
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Urinary obstruction
Instrumentation Vesicoureteral reflux Scarring from previous disease Pregnancy Female Diabetes Immunodeficiency |
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Pathology of acute pyelonephritis
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Discrete focal abscesses, wedge-shaped coalescent suppuration, yellow-white microabscesses
Patchy interstitial suppurative inflammation and tubular necrosis Damage often greatest at poles |
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Chronic pyelonephritis
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Pelvic/calyceal damage
Obstructive or reflex Irregular granular scarring, usually asymmetric Coarse, broad-based, U-shaped, cortico-medullary scar overlying a dilated/blunted/deformed calyx Often effects poles |
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Acute drug-induced interstitial nephritis
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Most common drug injury to kidney
Onset 15 days after exposure Immunologic damage-- as drug is secreted it binds to component of tubule, making it immunogenic IgE and cell-mediated response |
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Clinical presentation of acute drug-induced interstitial nephritis
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Fever
Eosinophilia Skin rash Renal fnc abnormalities Oliguria 50% of patients |
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Pathology of drug induced interstitial nephritis
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Interstital inflammation and edema
Eosinophils prominent Can have granulomas Tubular necrosis and regeneration |
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Analgesic abuse nephropathy
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Associated with phenacetin compounds in large quantities over time
(acetaminophen, NSAIDs) Direct nephrotoxicity on medullary cells (covalent binding and oxidative damage) Also vascular changes -- ischemia Papillary necrosis then tubulointerstital nephritis |
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Pathology in analgesic abuse nephropathy
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Various stages of
Necrosis Calcification Sloughing Fragmentation |
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Urate nephropathy
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Acute uric acid nephropathy
Chronic urate (gouty) nephropathy Nephrolithiasis |
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Cause of renal dysfunction in multiple myeloma
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Bence Jones proteinuria
--directly toxic to epi cells --In acidic conditions, combine with Tamm-Horsfall protein to form tubular casts, with subsequent obstruction and peritubular inflammation |
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Acute renal failure signs
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Acute drop in GFR
Oliguria/anuria (<400ml/24hrs) Elevated BUN/creatinine |
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General causes of acute renal failure
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Prerenal
Post renal Intrarenal Glomerular, vascular Interstital, tubular |
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Drugs causing Fanconi syndrome
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Degraded tetracycline
Lead Bismuth Via direction cytotoxicity to proximal tubule |
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Drugs that cause acute tubular necrosis
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Many
Antibiotics frequently Gentamicin, kanamycin, neomycin Colistimethate Polymixin B cephaloridine Ampotericine B Rifampin Mercury, gold, chromium Carbon tetrachloride Glycerols |
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Drugs that damage glomerulus via hypersensitivity
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Penicillamine
Procanimide Hydralazine Probenacid Trimethdione Gold Hydrocarbons Mercurical diuretics |
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Drugs that cause renal tubular acidosis
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via direct cytotoxicity to distal tubule
Amphotericin B Vit D toxicity Lithium |
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Drugs that cause acute interstitial nephritis
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Hypersensitivity effect on the interstitum
Methicillin Penicillin G Rifampin Phenindione Thiazides Phenylbutazone Cimetidine |
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Drugs that cause chronic interstitial nephritis, papillary necrosis
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Phenacetin
Aspirin Paracetol Via cytotoxicity and ischemia |
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Tubulointerstitial diseases
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Pyelonephritis
Interstitial nephritis |
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Pathogenic sequence of ascending pyelonephritis
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Colonization of distal urethral and introitus
Introduction into bladder (F>M, outflow obstruction) Incompetence in vesicourethral orafice |
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Why are the poles more effected in pyelonephritis?
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Papillae are different
Compound papillae at poles Concave Allow bacteria to enter ducts and tubules |
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Acute vs chronic tubulointerstitial nephritis
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Chronic = presence of fibrosis
Its always a lymphocytic infiltrate |
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Cellular infiltrate in tubulointerstitial nephritis
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Mostly T help cells
Macrophages Notable eosinophils |
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Acute uric acid nephropathy
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Precipitation of uric acid crystals primarily in collecting duct
Leads to obstruction and ARF Cancer patients after chemo Acid pH in tubules increases |
