Term
| Definition: Acute Kidney Injury |
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Definition
| -abrupt, sustained reductionin GFR caused by renal dz resulting in azotemia (often characterized by red/absent urine pdn) |
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Term
| What are the major syndromes in urology (5)? |
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Definition
-acute kidney injry (AKI)
-chronic kidney dz (CKD)
-glomerular dz
-UTI
-urolithiasis |
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Term
| How do you ID an azotemia on lab data? |
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Definition
| -high BUN + high Creatinine + low urine spec gravity |
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Term
| How do you ID a prerenal azotemia on lab data? |
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Definition
| -high BUN + high creatinine + normal urine SG |
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Term
| How do you ID a postrenal azotemia on lab data? |
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Definition
-UT obstruction: no urination + distended bladder
-Bladder rupture: creatinine in abdominal effusion is 2X blood levels |
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Term
| Which lab value do we use to assess kidney FUNCTION? |
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Definition
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Term
| Is creatinine insensitive or sensitive early in renal failure? HOw is this clinically used? |
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Definition
-insensitive
-incrimental changes in either directions shows change in kidney function |
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Term
| Why is it so important to distinguish b/n AKI and CKD? |
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Definition
| -AKI has better prognosis due to ability to regen |
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Term
| What are the possible outcomes of ARF? |
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Definition
-remaining healthy tissue hypertrophies to compensate
-affected tissue regenerates |
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Term
| What decides whether or not the tissue affected by ARF can regenerate? |
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Definition
| -if BM is intact then it can regen |
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Term
| What are the two mechanisms behind ARF? Which is more likely to spare the BM and thus more likely to regen? |
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Definition
-neprotoxin: more likely to spare BM
-ischemic insult |
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Term
| How are lab results different b/n ARF and CKD? |
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Definition
-ARF: numbers change over time + more dramatic electrolyte abnormalities + normal PCV
-CKD: numbers are bad but really stay the same + electrolytes are around normal b/c has had time to compensate + low PCV |
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Term
| What is the big point about AKI? |
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Definition
| -with AKI there is the potential for recovery of renal function BUT there is also ongoing, active losses and it is more volatile situation |
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Term
| What historical findings do we see for AKI and CKD? |
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Definition
-AKI: anuria, oliguria, short duration of illness, exposure to nephrotoxins
-CKD: PU/PD, prior evidence |
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Term
| How does BCS change b/n AKI and CKD? |
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Definition
-AKI: good BCS
-CKD: poor BCS, poor haircoat |
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Term
| Describe the gross appearance of the kidneys b/n AKI and CKD? |
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Definition
-AKI: enlarged, painful
-CKD: small, shrunken |
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Term
| Describe the difference of severity of dz b/n AKI and CKD. |
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Definition
-AKI: profound for deg of dysfunction
-CKD: mild for deg of dysfunction |
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Term
| Describe the azotemia seen with AKI and CKD. |
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Definition
-AKI: rapidly progressive
-CKD: stable over time |
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Term
| What do we see on urine sediment with AKI and CKD? |
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Definition
-AKI: casts, active sediment
-CKD: benign |
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Term
| What do we see on abdominal rads with AKI and CKD? |
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Definition
-AKI: enlarged
-CKD: small, shrunken, and rarely deminerlization of bone in young, growing animals |
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Term
| Approximately what percentage of CO goes to the kidneys? |
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Definition
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Term
| Why do nephrotoxins cause so much damage? |
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Definition
| -high delivery of blood to the kidneys due to high vascularity thus nephrotoxins have a lot of contact w/ epi cells |
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Term
| Where in the kidney is the majority of concentration gradient? |
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Definition
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Term
| Which major group of antibiotics are nephrotoxic? |
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Definition
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Term
| Which therapeutic agents are known for being nephrotoxic? |
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Definition
-Aminoglycosides: acute tubular necrosis
-NSAIDs: paling of medullary cavity |
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Term
| Which non-therapeutic agents are known for being nephrotoxic? |
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Definition
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Term
| True or False: The less metabolically active the cell, the less it can handle being without oxygen etc. |
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Definition
| -FALSE, the more metabolically active the cell the less it can handle being wihtout oxygen etc |
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Term
| True or False: If you kill the blood flow to one part of the nephron, the entire thing does b/c it acts as a functional unit. |
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Definition
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Term
| What is the purpose behind the selective constriction of the afferent and efferent arterioles? |
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Definition
| -work to regulate BP going to the kidney to prevent damage to the glomerulus |
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Term
| What substances control the selective constriction of the afferent and efferent arterioles? |
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Definition
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Term
| What are some infectious diseases that cause AKI? |
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Definition
-pyelonephritis
-Leptospirosis: zoonotic!
-Lyme dz: eastern US
-Babesiosis
-FIP |
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Term
| What are some common causes of hypercalcemia seen w/ AKI? |
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Definition
-Malignancy (lymphoma)
-rodenticides |
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Term
| What is a common cause of AKI in male cats? |
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Definition
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Term
| What are the 3 phases of AKI? |
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Definition
-Initiation: time of exposure to development of azotemia
-Maintenance (1-3w): renal lesions are established, azotemia present
-Recovery (ww-mm): repair of tubules, compensation |
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Term
| Which stage of AKI is the best time to treat? |
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Definition
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Term
| What are the two major requirements for catching AKI in the initiation phase? |
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Definition
-clinical suspicion of an at-risk patient
-appropriate monitoring |
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Term
| Which patients are considered at-risk for AKI? |
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Definition
-patients receiving nephrotoxic drugs
-dehydration, hypotension, sepsis, anesthesia: potential for poor renal perfusion
-older patients
-severe systemic dz: pancreatitis, peritonitis, sepsis, Addison's |
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Term
| What do we monitor for poor renal perfusion? |
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Definition
-hydration status!!!
-BW
-BP
-pulse character
-urine output
-drugs that interfere with autoregulation: NSAIDs |
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Term
| What do we see on UA with AKI? |
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Definition
-Glucosuria w/out hyperglycemia: indicates tubular injury
-proteinuria: tubular injury
-urine sediment: casts (most specific) |
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