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What begins once the renal reserve is lost?
Renal insufficiency
What portion of nephron function loss is defined by renal insufficiency?
> 2/3 (66%)
T/F: Renal insufficiency appears outwardly normal and has a loss of urine concentrating ability and capacity to compensate for stresses.
True!
What process does this shift to once azotemia is evident?
How much nephron function loss is this defined by?
Renal failure
> 3/4 (75%)
What is the injury to renal parenchyma +/- decreased kidney function?
Acute kidney injury
T/F: Acute kidney injury can be community or hospital acquired.
True!
Acute kidney injury is graded I-V from least to most severe based on blood levels of —-.
Creatinine
What is defined by increased serum creatinine and BUN and indicates a decreased GFR?
Azotemia
T/F: If you have azotemia, you know there is intrinsic renal disease.
False! Azotemia does NOT always mean intrinsic renal disease.
What do we call the manifestation of physical signs associated with renal failure or azotemia?
Uremia
Name FIVE of the clinical signs that contribute to uremic SYNDROME.
1. Anemia
2. Gastroenteritis
3. Acidosis
4. Osteodystrophy
5. Encephalopathy
6. Coagulopathy
What is the difference between anuria, oliguria, and polyuria?
Anuria: no urine production
Oliguria: < 0.3 ml/kg/hr (for >6 hour time period)
Polyuria: >2 ml/kg/hr
T/F: All azotemic patients are in renal failure, but not all patients with renal failure are azotemic.
False! Patients with renal failure are ALWAYS azotemic, but NOT all azotemic patients are in renal failure.
What are the THREE classifications to localize azotemia and how are they defined?
Prenal: concentrated USG
Renal: isosthenuric USG (1.008-1.012)
Post-renal: physical exam and diagnostics
In prerenal azotemia, concentrated urine in a dog would be greater than —— in dogs and —- in cats.
>1.030
>1.035
What THREE things hemodynamically mediate decreased GFR in pre-renal azotemia?
1. Decreased renal blood flow
2. Decreased perfusion pressure
3. Increased renal vascular resistance
What are the TWO hallmarks of pre-renal azotemia?
Mild azotemia and increased USG
What azotemia is intrinsic and involves damage to any section of kidney?
Renal
What are the TWO major differentials for a post-renal azotemia?
Outflow obstruction and urinary tract rupture
T/F: Outflow obstruction increases hydrostatic pressure and dissipates ultrafiltration pressure within glomerular capillaries. Urinary rupture involves reabsorption of filtrates.
True!
What are the FOUR phases of AKI in order?
Induction -> extension -> maintenance -> recovery
Describe the timeline for induction, extension, maintenance, and recovery as AKI progresses.
Induction: minutes/hours
Extension: hours/days
Maintenance: days/weeks
Recovery: weeks/months
What phase of AKI involves the evolving of parenchymal injury, where the tubular epithelium undergoes sublethal injury?
Induction
The intervention in what AKI phase prevents severe injury?
Induction
What phase of AKI involves alterations in renal perfusion, continued hypoxia, secondary inflammation, and ongoing epithelial injury?
Extension
What THREE clinical signs manifest during the extension phase of AKI?
1. Progressive decreased GFR
2. Loss of urine concentration
3. Development oliguria/azotemia
What phase of AKI is defined by irreversible epithelial damage after a critical amount of damage?
Maintenance
What THREE clinical signs manifest during the maintenance phase of AKI?
1. Altered regional blood flow
2. Urine volume decreased
3. Complications of uremia
T/F: Elimination of factors alter existing damage/rate of recovery in the maintenance phase of AKI.
False! Elimination of factors do NOT alter existing damage/rate of recovery.
What phase of AKI involves the regeneration and repair of renal tissue to restore renal function?
Recovery
What TWO clinical signs are associated with the recovery phase of AKI?
Increased urine output and progressive resolution azotemia
T/F: Increased urine production does not always correspond to an improved GFR.
True!
What is the physiologic response to the recovery phase of AKI?
Diuresis
In the recovery phase, renal injury induces ———- production and alters —————-. Repair factors contribute to —-.
Growth factor
Gene expression
Fibrosis
What are FOUR reasons kidneys are uniquely susceptible to injury?
1. 25% bloodflow each cardiac cycle
2. 90% cortex, 10% medulla circulation
3. Tubules concentrate certain drugs/toxins
4. Subclinical kidney disease difficult to distinguish
What are the THREE main functions of the kidney?
1. Maintain water balance
2. Excrete waste products
3. Endocrine (Renin, EPO, vitamin D, Ca2+)
What THREE systemic effects occur in acute kidney injury?
1. GI (vomiting, anorexia, halitosis, oral ulcers, diarrhea)
2. CNS (mental dullness, seizures)
3. Respiratory (acute pneumonitis)
You are presented a patient who has normal BCS and hair coat. There is recent onset of clinical signs like anorexia, V/D, and lethargy. On oral exam, you notice uremic halitosis and ulcers. There is renal pain and the kidneys feel enlarged. The patent is oliguric or polyuric and has severe signs for degree of azotemia.
Is this acute kidney injury or chronic kidney disease?
Acute kidney disease
You are presented a patient with poor BCS and hair coat. There is a history of gradual weight loss and loosening clinical signs. There is no renal pain and the kidneys feel small on palpation. It has a nonregenerative anemia and is polyuric. There are mild signs for degree of azotemia.
Is this acute kidney injury or chronic kidney disease?
Chronic kidney disease
Name at least TWO metabolic causes of acute kidney injury.
Hypercalcemia, ischemia, renal tubular acidosis (Fanconi's)
Name at least TWO neoplastic causes of acute kidney injury.
Renal carcinoma, renal lymphoma, nephroblastoma, transitional cell carcinoma, hermangiosarcoma, metastasis
Name at least TWO bacterial infectious causes of acute kidney injury.
1. Pyelonephritis
2. Leptospirosis
Name at least TWO viral infectious causes of acute kidney injury.
1. FIP
2. FeLV
Name at least TWO fungal infectious causes of acute kidney injury.
Histo, blasto, coccidiodes
Name at least TWO rickettsial infectious causes of acute kidney injury.
RMSF, Ehrlichiosis
Name ONE protozoal infectious cause of acute kidney injury.
Leishmania
Name TWO parasitic infectious causes of acute kidney injury.
D. Renale, Larval migrans
Name TWO inflammatory causes of acute kidney injury.
Glomerulonephritis, amyloidosis
Name TWO traumatic causes of acute kidney injury.
Renal avulsion, renal hemorrhage
Name at least THREE toxic causes of acute kidney injury.
Ethylene glycol, lily, grape/raisin, hypercalcemia, antimicrobials, antifungals, antivirals, chemotherapy drugs, etc.
What is a vascular cause of acute kidney injury?
Thromboembolism (renal infarct)
What is the baseline diagnostic plan in acute kidney injury?
CBC/Chem/UA -> UPC -> Blood pressure and ocular exam -> Urine culture -> Lepto PCR/titers -> abdominal radiographs/ultrasounds
Name THREE additional testing options you can do.
Contrast studies, appropriate infectious/vector testing, FNA, fractional excretions/osmolalities, GFR study, renal biopsy
What is the prognosis of lepto?
Fair/good (wth appropriate treatment early enough)
What is the prognosis of ethylene glycol or if DIC?
Grave
Acute kidney injury is more difficult to treat with concurrent —————.
Heart disease
What are the THREE most likely causes of death during initial AKI management?
1. Hyperkalemia
2. Metabolic acidosis
3. Severe azotemia
What is the next major cause of death associated with vigorous fluid therapy?
Overhydration and pulmonary edema
What is the overall prognostic breakdown of AKI?
50% die or euthanized
20% return to normal creatinine levels
30% survive with chronic renal failure
What is the prognosis with oliguria?
Grave (likely die or euthanized)
T/F: Non-oliguria does not guarantee survival, and dogs and cats may survive with severe oliguric ARF and may return with renal function and urine production following several months of hemodialysis.
True!
Animals with anuria cannot survive without —-.
Dialysis