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84 Cards in this Set
- Front
- Back
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define: azotemia
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acute retention of nitrogenous wastes
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define: uremia
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symptomatic renal failure (symptomatic azotemia)
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define: oliguria
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Urine output <400-500 ml/day
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define: anuria
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Urine output <50-100 ml/day
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what is the cockcroft-gault formula? what can't you use this formula for? why?
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(140-age) x weight (kg)/ serum Cr x 72.
Can't use it for acute renal failure bc the renal function is not in a steady state. you can use it for chronic kidney disease bc the renal function is steady. |
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what 5 conditions are associated w/ an elevated BUN and preserved GFR?
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upper GI bleeding
hypercatabolic state and increased tissue breakdown steroids increased protein intake tetracycline antibiotics |
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what two serum lab values are used to evaluate AKI? what else is used?
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seum lab values: BUN and creatinine (cr is used to define acute kidney injury)
other: GFR |
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what medications are associated w/ an elevated Cr and preserved GFR?
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Trimethoprime and cimetidine (bc they inhibit proximal tubular secretion of cr which increases serum cr levels though GFR is unaffected
and substances that interfere w/ the cr assay: cefoxitin, flucytosine, and acetoacetate |
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what are the 3 categories of acute kidney injury?
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Pre-renal
intrinsic renal post-renal |
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what are the four main phases involved in the urinary elimination of nitrogenous waste? what category of acute kidney injury matches each of the four phases?
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1) delivery to the glomerular capillaries via an adequate renal blood flow (pre-renal azotemia)
2) formation of plasma UF containing BUN and Cr (intrinsic azotemia) 3) normal tubular handling of the UF in its passage through the nephron into the collecting system (intrinsic azotemia) 4) excretion through a nonobstructed urinary tract (post renal azotemia) |
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what is the most common cause of acute kidney injury?
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acute tubular necrosis
approx- 45% |
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what are the 3 etiologies of pre-renal azotemia?
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volume depletion, decreased effective arterial blood volume, alteration in intra-renal hemodynamics
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what are the six ways that pre-renal azotemia can come about d/t volume depletion?
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deficient fluid intake
diarrhea vomiting NG tube suction hemorrhage burns |
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what are the five ways that pre-renal azotemia can come about d/t decreased effective arterial blood volume?
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CHF
liver disease w/ ascites nephrotic syndrome sepsis third spacing |
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what are the two ways that pre-renal azotemia can come about d/t alteration in intra-renal hemodynamics?
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1) primary renal vasoconstriction (hepatorenal syndrome, hypercalcemia)
2) drug-induced (NSAIDs and ACEI/ARB) |
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how do NSAIDs induce AKI? ACE I?
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NSAIDs: PGs maintain GFR by maintaining afferent arteriole dilatation, inhibition of PG production constricts the afferent arteriole and worsens GFR.
ACEI: angiotensin II maintains GFR by efferent arteriole constriction which maintains intraglomerular pressure. Inhibition of angiotensin II dilates the efferent arteriole leading to dec back-pressure and worsening GFR. |
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what are the 3 steps for pre-renal azotemia evaluation?
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hx
PE: skin turgor, dry mucous membranes, JG veins, orthostatics Labs: FENA <1% (only reliable in oliguria)--> (UNa x PCr/ PNa x UCr) x 100, BUN/Cr ratio>20, hemoconcentration (elevated Hb and Hct) |
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what are the five etiologies of intrinsic AKI?
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acute tubular necrosis- MC
acute interstitial nephritis acute glomerulonephritis acute vascular syndromes intratubular obstruction |
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what are the 3 types of acute tubular necrosis?
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ischemic
septic nephrotoxic |
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what 5 conditions can cause ischemi acute tubular necrosis?
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prolonged pre-renal azotemia
hypotension hypovolemic shock Cardiac arrest cardiopulmonary bypass |
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what four conditions can cause septic acute tubular necrosis?
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systemic hypotension
direct renal vasoconstriction release of cytokines (TNF) activation of neutrophils by endotoxin |
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what are the 2 conditions that can cause nephrotoxic acute tubular necrosis?
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Drug induced (radiocontrast dye- very common, aminoglycosides, amphotericin B, cisplatin, acetaminophen)
pigment nephropathy (hemoglobin and myoglobin- mc : rhabdo) |
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what would the labs show in a pt w/ ATN?
BUN/Cr ratio? FENA? urine sediment? |
BUN/Cr ration <10:1
FENA >2% (not seen in contrast nephropathy or rhabdomyolysis) Urine sediment would show tubular epithelial cells and granular casts (muddy brown) |
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what causes acute interstitial nephritis? What is the classic clinical triad associated with it?
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AKI d/t lymphocytic infiltration of the interstitium
clinical triad: fever+ rash+ eosinophilia (only found in 10%) |
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what is the MC cause of acute interstitial nephritis?
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drugs- 71%
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what infections and systemic illnesses can cause interstitial nephritis?
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infection: bacterial, viral, tb
systemic: sarcoid, sjogren's and TINU (tubulointerstitial nephritis and uveitis) |
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what infections and systemic illnesses can cause interstitial nephritis?
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infection: bacterial, viral, tb
systemic: sarcoid, sjogren's and TINU (tubulointerstitial nephritis and uveitis) |
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what are the 3 steps for an acute interstitial nephritis evaluation?
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hx: involving a preceding illness or drug exposure
PE: fever, rash Lab data: eosinophilia, eosinophiluria, and analysis of urine sediment- WBC's or WBC casts in the absence of a urine infection. |
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what are the 3 steps for an acute interstitial nephritis evaluation?
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hx: involving a preceding illness or drug exposure
PE: fever, rash Lab data: eosinophilia, eosinophiluria, and analysis of urine sediment- WBC's or WBC casts in the absence of a urine infection. |
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what are the 3 indications for a renal biopsy of a pt w/ acute interstitial nephritis?
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-uncertainty of diagnosis
-advanced renal failure -lack of recovery once drug is discontinued |
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what are the 3 indications for a renal biopsy of a pt w/ acute interstitial nephritis?
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-uncertainty of diagnosis
-advanced renal failure -lack of recovery once drug is discontinued |
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what is the tx of acute interstitial nephritis tx?
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discontinue offending drug, tx underlying infection, tx systemic illness and steroid therapy in those pts who do not respond to conservative measures.
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what is the tx of acute interstitial nephritis tx?
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discontinue offending drug, tx underlying infection, tx systemic illness and steroid therapy in those pts who do not respond to conservative measures.
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when do you begin gradual tapering of acute interstitial nephritis tx?
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once serum Cr has returned to baseline.
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when do you begin gradual tapering of acute interstitial nephritis tx?
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once serum Cr has returned to baseline.
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what 5 conditions or group of conditions fall under the category of acute glomerulonephritis?
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- postinfectious (post-streptococcal or endocarditis- associated)
- systemic vasculitis (ANCA-associated such as wegner's granulomatosis and microscopic polyangiitis) and mixed cryglobulinemia. - Goodpasture's syndrome - Lupus nephritis - Rapidly progressive GN (crescentic GN) |
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what are the four steps for acute glomerulonephritis evaluation?
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- analysis of urine sediment (dysmorphic RBC's, RBC casts)
- variable degree of proteinuria - serologies (ANA, complement, hepatitis panel ANCA, anti-GBM, ASO titers, RPR) - renal biopsy for definitive diagnosis*** |
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what 6 conditions cause hypocomplementemia in glomerular dz?
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postinfectious GN
lupus nephritis membranoproliferative GN mixed cryoglobinemia atheroembolic renal dz thrombotic thrombocytopenic purpura (last two are non-immune complex mediated renal dzes) |
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what five syndromes cause acute kidney injury?
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-renal artery thromboembolism
-renal vein thrombosis -renal artery dissection -atheroembolic renal dz -thrombotic microangiopathies (HUS-TTP, scleroderma renal crisis and malignant HTN) |
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what 2 conditions cause intratubular obstruction that can lead to acute kidney injury?
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- intratubular crystal deposition
* tumor lysis syndrome (acute uric acid nephropathy) * Ethylene glycol toxicity (calcium oxalate deposition) * Medication-associated (acyclovir and indinavir) - intratubular protein deposition * multiple myeloma (filtered light chains--> cast nephropathy) |
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what four conditions can cause in intrinsic upper tract obstruction leading to postrenal acute kidney injury?
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-nephrolithiasis
-papillary necrosis -blood clot -transitional cell cancer |
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what 4 conditions can cause an extrinsic upper tract obstruction that may lead to post renal AKI?
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-retroperitoneal or pelvic malignancy
-retroperitoneal fibrosis -endometriosis -AAA |
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what are the 7 conditions that can cause a lower tract obstruction that may lead to post renal AKI?
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BPH, prostate CA, transitional cell CA, urethral stricture, bladder stones, blood clot, neurogenic bladder
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what are the 2 steps for evaluating a postrenal AKI?
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- post void residual bladder volume: >100 ml c/w voiding dysfunction
- radiologic studies: *Ultrasound (everyone gets a renal ultrasound) and CT scan are most commonly used by our guest speaker... other scans: Nuclear medicine (used as a tie breaker if you don't know what is going on), retrograde pyelography and antegrade nephrostograms. |
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how do you tx a lower tract obstruction? upper tract?
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lower: bladder catheter
upper: ureteral stents and/or percutaneous nephrostomies (straight into the bladder and drain the bladder from there) |
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what 6 things does functional recovery from hydronephrosis depend on?
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1) duration
2) severity 3) pt age 4) condition of contralateral kidney 5) degree of hydration 6) presence of infection |
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what are the tubular defects associated w/ obstructive nephropathy?
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-impaired concentrating ability
-impaired sodium reabsorption -type 1 RTA (renal tubular acidosis): hyperkalemic acidosis d/t diminished distal hydrogen and potassium secretion |
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When does ATN occur d/t contrast nephropathy? what are the 2 theories about the Mech of injury?
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w/n first 48 hours after IV contrast administration;
1) renal vasoconstriction results in medullary hypoxia 2) direct cytotoxic effects of contrast agents |
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what are the six risk factors for contrast nephropathy?
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- underlying renal failure
- DM nephropathy - heart failure or other cause of reduced renal perfusion (hypovolemia) - multiple myeloma - high total dose of contrast - high osmolality ionic agents |
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what are the 3 ways used to prevent contrast nephropathy?
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low or iso-osmolal nonionic agents
isotonic saline (pre and post procedure) acetylcysteine (harmless and inexpensive) |
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what are the clinical manifestations of rhabdomyolysis?
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Renal failure
Muscle pain and weakness Elevated CK (creatine kinase) level Myoglobinuria U/A: +blood but no RBC’s Hyperkalemia and hyperphosphatemia Hypocalcemia Hyperuricemia Elevated transaminases (ALT and AST) |
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what are the 9 causes of rhabdomyolysis?
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Trauma or compression
Drugs and toxins Extreme exertion Seizures Alcoholism Malignant hyperthermia Neuroleptic malignant syndrome Electrolyte abnormalities Myopathies |
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what 5 drugs can cause rhabdomyolysis?
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hyperlipidemic agents (stains and fibrates)
colchicine cocaine heroin and opioid analgesics alcohol |
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how do you tx rhabdomyolysis?
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isotonic saline (incr urine flow to protect kidney tubules from myoglobinuric damage)
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how do aminoglycosides cause nephrotoxicity? When does this usually occur? Once discontinuing the drug, how long does renal recovery take?
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d/t accumulation and storage in the proximal tubular cells which induces damage.
AKI usually occurs after 5-7 days of therapy. 3 weeks. |
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what are the 5 renal manifestations of hypercalcemia?
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-direct renal vasoconstriction
-volume contraction -chronic hypercalcemic nephropathy (nephrocalcinosis) -nephrolithiasis -nephrogenic diabetes insipidus |
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in ambulatory pts, what is the etiology of hypercalcemia? How about in hospitalized pts?
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ambulatory: primary hyperparathyroidism
hospitalized: malignancy |
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how do you tx hypercalcemia?
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-isotonic saline
-loop diuretics -calcitonin -bisphosphonates (zolendronate over pamidronate) |
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Pt presents to your office after mitral valve replacement surgery. He has cyanotic digits, livedo reticularis and his kidneys are failing. dx: and what is the pathognomic sign for this disease?
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Atheroembolic renal dz
Pathognomonic: biconvex cholesterol clefts. Can also have Ischemic bowel, eosinophilia, eosinophiluria and hypocomplementemia. |
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how do you tx the ANCA positive vasculitis? Which ANCA positive vasculitis involves the respiratory tract? which one causes pauci-immune glomerulonephritis?
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cyclophosphamide and steroids
Respiratory tract: Wegener's granulomatosis pauci-immune glomerulonephritis: Microscopic polyangiitis. |
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pt presents which hemoptysis and kidney failure. You draw blood and find Anti-GBM ab in serum. Renal biopsy shows liner deposition of IgG along the glomerular capillaries. Dx, tx, name type of HSN, and what are the circulating Abs directed against?
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Dx: Rapidly progressive crescentic glomerulonephritis---- Goodpasture's syndrome
tx: plasmapheresis combined w/ cyclophosphamide and steroids HSN: 2 Circulating abs are directed against the alpha 3 chain of type 4 collagen found in the alveolar and glomerular basement membranes. |
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what are the 3 hep C associated renal diseases? and how do you tx them?
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-Mixed cryglobulinemia
-membranoproliferative glomerulonephritis -membraneous nephropathy Tx: aimed against Hep C virus. If CrCl> 50 (give pegylated interferon alpha and ribavirin), if CrCl <50 (give nonpegylated interferon alpha) |
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what are the 3 types of lupus nephritis that require tx? WHat is the tx?
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severe focal proliferation
diffuse proliferative membranous tx: cyclophosphamide and steroids (mycophenolate may be more efficacious than cyclophosphamide) |
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what are the 5 indications for dialysis?
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uremic syndrome
uncontrollable hyperkalemia severe metabolic acidosis refractory fluid overload severe renal failure (BUN > 100 or Cr>10) |
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define uremic syndrome. What are the associated sxs?
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sxs and signs which result from the toxic effects of elevated levels of nitrogenous and other wastes in the blood
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What are the associated signs and sxs of uremic syndrome?
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signs: pericardial friction rub or pericardial effusion, tremors, asterixis (flapping tremor or liver flap), myoclonus, wrist or foot drop, seizures, and bleeding tendency (diathesis)
sxs: N/V, poor appetite, fatigue/lethargy, pruritis and altered mentation |
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what is winter's formula?
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respiratory compensation for a metabolic acidosis
PCO2= 1.5 x (HCO3) + 8 (+/-2) eg: HCO3= 20, expected PCO2= 36-40 |
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what are the 3 therapeutic modalities of dialysis?
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intermittent hemodialysis, peritoneal dialysis, and slow continuous therapies
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what is a vascath? how long can they stay in?
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a temporary dual lumen (venous and arterial ports) used for acute dialysis.
Femoral vascath- can remain for 3 days to 1 wk internal jugular vascath- can remain for 2-3 weeks. |
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what is the permcath? how long can it remain? WHat are the two forms of permanent accesses in chronic dialysis patients?
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Permcath: longer dialysis catheter which is tunneled subQ. Can remain for weeks to months and has less risk of infection
permanent accesses: Arteriovenous fistula (AVF) and arteriovenous graft (AVG) |
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what is the pathophysiology of hepatorenal syndrome?
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-portal HTN
-splanchnic vasodilatation -arterial underfilling and systemic vasodilatation - hepatorenal reflex- stim of vasoconstrictor systems -renal vasoconstriction |
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pt presents in your ICU which rapidly progressive renal failure. The pt is oliguric and anuric. Dx
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Hepatorenal syndrome type I, median survival 2 weeks
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pt presents in your ICU which slowly progressive and indolent renal failure over months. His ascites is resistant to diuretics. Dx
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type II hepatorenal syndrome
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what is the criteria for hepatorenal syndrome?
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-acute/chronic liver dz w/ portal HTN
-low GFR -r/o other causes - lack of renal improvement despite diuretic withdrawal and volume expansion -oliguria -urine Na <10 mEq/L -proteinuria <500 mg/day |
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how do you tx hepatorenal syndrome?
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midodrine (selective alpha 1 agonist--- systemic vasoconstriction)
octreotide (somatostatin analog, inhibitor of endogenous vasodilator release) albumin and vasopressin liver transplant in appropriate candidates |
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what are the 5 components of tumor lysis syndrome?
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hyperuricemia, hyperphosphatemia, hyperkalemia, hypocalcemia and AKI
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when do you usually see tumor lysis syndrome? when do you usually see AKI associated w/ these circumstances?
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in lymphomas and leukemias both spontaneously (AKI d/t acute uric acid nephropathy w/ a lack of hyperphosphatemia) and post-chemotherapy (AKI d/t severe hyperphosphatemia)
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what are the 3 ways you can prevent tumor lysis syndrome in your pt? How do you tx tumor lysis syndrome?
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allopurinol
rasburicase 0.9 NS IVF hydration to maintain a high urine output tx: IVF hydration and diuretics (to wash out obstructing uric acid crystals), rasburicase, hemodialysis if oligoanuric (removes uric acid), and CRRT (continuous renal replacement therapy)-- preferred in hyperphosphatemic renal failure. The CRRT will avoid the rebound hyperphosphatemia seen w/ intermittent hemodialysis. |
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what is the most common renal diagnosis in pts w/ multiple myeloma? what does it cause?
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Cast nephropathy- binding of Tamm-Horsfall mucoprotein (normally synthesized in the TAL of loop of henle) causing direct tubular injury w/ intratubular cast formation and obstruction
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what is the difference between AL amyloidosis assoc w/ multiple myeloma and light chain deposition disease?
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In AL Amyloidosis--> Light chain fragments form Congo red Positive B-pleated fibrils, in LCDD they do not form fibrils and their deposits are congo red negative.
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what are the three signs of fanconi syndrome? what is fanconi syndrome d/ t?
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proximal RTA
phosphate wasting hypouricemia d/t: reabsorption of filtered light chain in proximal tubules. That accumulation in proximal cells w/ subsequent intracellular crystal formation leads to impaired proximal tubular function. |
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what are the 5 features associated w/ TTP-HUS?
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-microangiopathic hemolytic anemia*
-thrombocytopenia* - AKI - neurologic abnormalities - fever |
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what are the causes of TTP-HUS?
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MC- idiopathic
shiga-toxin producing E. coli Drugs: quinine, ticlid, cyclosporine, mitomycin pregnancy/ post partum HIV sepsis postcardiac bypass |
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how do you tx TTP-HUS?
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plasma exchange (high mortality rate associated if not treated)
sterois |
