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60 Cards in this Set
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define: azotemia & uremia |
azotemia: acute retention of nitrogenous wastes
uremia: symptomatic renal failure (azotemia) (pt needs dialysis) |
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define: oliguria & anuria |
oliguria: Urine output <400-500 ml/day
anuria: 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? |
(140-age) x weight (kg)/ serum Cr x 72.
you can use it for chronic kidney disease bc the renal function is steady. |
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what two serum lab values are used to evaluate Acute Kidney Injury (AKI)? what else is used? |
seum lab values: BUN and creatinine (cr is used to define acute kidney injury)
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what are the 3 categories of acute kidney injury? |
Pre-renal |
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what are the 4 main phases of urinary elimination of nitrogenous waste?
what category of acute kidney injury matches each phase? |
1) delivery to the glomerular capillaries via an adequate renal blood flow (pre-renal azotemia) |
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what is the MC cause of acute kidney injury? |
acute tubular necrosis (ATN) |
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what are the 3 etiologies of pre-renal azotemia? |
1. volume depletion: low intake, diarrhea, vomiting, NG tube suction, hemorrhage, burns
2. decreased effective arterial blood volume: CHF, liver dz w/ ascites, nephrotic syndrome, sepsis, 3rd spacing
3. alteration in intra-renal hemodynamics: primary renal vasoconstriction- hepatorenal syndrome or hypercalcemia, drug induced- NSAIDS & ACEI/ARB |
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how do NSAIDs induce AKI?
ACE I? |
NSAIDs: inhibit Prostaglandins --> constricts the afferent arteriole & worsens GFR.
--> 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? |
hx |
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what are the 5 etiologies of intrinsic AKI? |
1. acute tubular necrosis- MC, ischemia, sepsis, or nephrotoxins
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what 5 conditions can cause ischemi acute tubular necrosis? |
1. prolonged pre-renal azotemia |
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what 4 conditions can cause septic acute tubular necrosis? |
1. systemic hypotension |
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what are the 2 conditions that can cause nephrotoxic acute tubular necrosis? |
Drug induced (radiocontrast dye- very common, aminoglycosides, amphotericin B, cisplatin, acetaminophen)
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what would the labs show in a pt w/ ATN? |
BUN/Cr ration <10:1
*Serum Cr does NOT return to normal after fluid repletion (differentiates ATN from pre-renal disease where Cr would return to baseline) |
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what causes acute interstitial nephritis?
What is the classic clinical triad associated with it? |
AKI d/t lymphocytic infiltration of the interstitium |
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what is the MC cause of acute interstitial nephritis?
what infections and systemic illnesses can cause acute interstitial nephritis? |
MC= drugs (71%)
infection: bacterial, viral, tb
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what are the 3 steps for an acute interstitial nephritis evaluation? |
hx: involving a preceding illness or drug exposure |
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what are the 3 indications for a renal biopsy of a pt w/ acute interstitial nephritis? |
-uncertainty of diagnosis |
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what is the tx of acute interstitial nephritis? |
discontinue offending drug, tx underlying infection, tx systemic illness (^remove cause)
*steroid therapy in those pts who do not respond to conservative measures. Taper once serum Cr returns to baseline |
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what 5 conditions or group of conditions fall under the category of acute glomerulonephritis? |
- postinfectious (post-streptococcal or endocarditis- associated) |
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what are the four steps for acute glomerulonephritis evaluation? |
- analysis of urine sediment (dysmorphic RBC's, RBC casts) |
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what 6 conditions cause hypocomplementemia in glomerular dz? |
postinfectious GN |
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what five vascular syndromes cause acute kidney injury? |
-renal artery thromboembolism |
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what 2 conditions cause intratubular obstruction that can lead to acute kidney injury? |
- intratubular crystal deposition
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what four conditions can cause in intrinsic upper tract obstruction leading to postrenal acute kidney injury?
extrinisc? |
intrinsic: -nephrolithiasis
extrinsic: -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? |
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? |
- post void residual bladder volume: >100 ml c/w voiding dysfunction |
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how do you tx a lower tract obstruction?
upper tract? |
lower: bladder catheter |
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what are the tubular defects associated w/ obstructive nephropathy? |
-impaired concentrating ability |
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what are the six risk factors for contrast nephropathy that leads to ATN (w/i 48 hrs of contrast)? |
- underlying renal failure |
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what are the 3 ways used to prevent contrast nephropathy? |
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? |
Renal failure |
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what are the 9 causes of rhabdomyolysis? |
Trauma or compression |
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how do you tx rhabdomyolysis? |
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? |
d/t accumulation and storage in the proximal tubular cells which induces damage. |
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what are the 5 renal manifestations of hypercalcemia? |
-direct renal vasoconstriction |
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in ambulatory pts, what is the etiology of hypercalcemia?
How about in hospitalized pts? |
ambulatory: primary hyperparathyroidism |
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how do you tx hypercalcemia? |
-isotonic saline (for volume deficiency)
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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? |
Atheroembolic renal dz Pathognomonic: biconvex cholesterol clefts. |
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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? |
cyclophosphamide and steroids
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pt presents which hemoptysis and kidney failure. You draw blood and find Anti-GBM ab in serum. Renal biopsy shows linear deposition of IgG along the glomerular capillaries. Dx, tx, what are the circulating Abs directed against? |
Dx: Rapidly progressive crescentic glomerulonephritis---- Goodpasture's syndrome
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what are the 3 hep C associated renal diseases? and how do you tx them? |
-Mixed cryglobulinemia |
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what are the 3 types of lupus nephritis that require tx? WHat is the tx? |
severe focal proliferation cyclophosphamide and steroids (mycophenolate may be more efficacious than cyclophosphamide) |
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what are the 5 indications for dialysis? |
uremic syndrome |
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What are the associated signs and sxs of uremic syndrome? |
signs: pericardial friction rub or pericardial effusion, tremors, asterixis (flapping tremor or liver flap), myoclonus, wrist or foot drop, seizures, and bleeding tendency (diathesis) |
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what is winter's formula?
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respiratory compensation for a metabolic acidosis |
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what is the pathophysiology of hepatorenal syndrome? |
-portal HTN |
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pt presents in your ICU which rapidly progressive renal failure. The pt is oliguric and anuric. Dx |
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 |
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 |
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how do you tx hepatorenal syndrome? |
midodrine (selective alpha 1 agonist--- systemic vasoconstriction) |
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what are the 5 components of tumor lysis syndrome? |
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? |
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? |
Prevent: allopurinol rasburicase, hemodialysis if oligoanuric (removes uric acid), and CRRT (continuous renal replacement therapy)-- preferred in hyperphosphatemic renal failure, 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? |
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? |
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? |
proximal RTA intracellular crystal formation--> impaired proximal tubular function. |
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what are the 5 features associated w/ TTP-HUS? |
-microangiopathic hemolytic anemia* |
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what are the causes of TTP-HUS?
Tx? |
MC- idiopathic
Tx: plasma exchange |