Flashcards in Week 9 - Acute Kidney injury Deck (55)
How is GFR measured?
-Measure in serum creatinine
Why is AKI treated as a medical emergency?
-Delayed treatment leads to irreversible renal failure
What are the three groups of causes of AKI?
What type of injury cause pre-renal failure?
-Anything which causes volume depletion to the kidney eg heart failure, cirrhosis
What type of diseases cause intrinsic renal AKI?
-Any kind of necrosis or ischaemia which affects the parenchyma eg glomerulonephritis, Acute Tubular Necrosis
What type of injury causes post-renal AKI?
-Anything which obstructs the urinary tract eg stones, prostate hyperplasia
What is the major cause of AKI?
-Acute tubular necrosis
Describe the pathophysiology of pre-renal AKI
-Reduced renal blood flow reduces GFR
-There is no cellular damage so kidneys work hard to restors bloodflow and avidly resorb salt and water
Does pre-renal AKI respond to fluid resuscitation?
Describe urine production in pre-renal AKI
-Little and concentrated because reabsorbing fluid
Why is hypertension significant in pre-renal AKI?
-Blood pressure may seem adequate however the patient may normally have high BP so their current BP is low and the person is at risk of pre-renal AKI
Describe autoregulation in pre-renal AKI
-Reduced renal perfusion causes vasodilation of afferent arteriole to increase renal blood flow
-Vasoconstriction of efferent arteriole to increase renal blood pressure
-Attempts to maintain GFR
Why does AKI occur in pre-renal states?
-Autoregulation becomes overwhelmed and cannot maintain GFR
At what pressures is autoregulation able to work?
Name 2 drugs which can override autoregulation and explain why?
-NSAIDs -> inhibit prostaglandin production -> inadequate vasodilation of afferent arteriole
-ACE inhibitor -> inhibits angiotensin II which acts as a vasoconstrictor of efferent arteriole
What develops from pre-renal AKI if the underlying cause is not treated?
-Acute tubular necrosis
What are the major causes of acute tubular necrosis?
What is acute tubular necrosis?
-Injury to proximal tubular cells which results in inability to resorb salts and water efficiently or expel excess water
Does ATN respond to fluid resuscitation?
-Sometimes but high risk of fluid overload
Is AKI reversible?
When does mortality significantly increase in AKI?
-If dialysis is required
Describe the pathophysiology of ischaemic necrosis
-The PCT is the most susceptible area to hypoxia as it has the higest O2 demand
-Any cause of hypoxia to the cells results in injury and the cells can no longer function
Describe the urine produced in ATN
-Often copious and dilute
Describe the pathophysiology of toxin ATN
-Nephrotoxins damage epithelial cells lining tubules and cause shedding into lumen
-ATN is much more likely to occur if there is reduced perfusion and presence of a nephrotoxin
Name some endogenous nephrotoxins
-Myoglobin, bilirubin, urate
NAme some exogenous nephrotoxins?
-drugs eg gentamycin, NSAIDs
What is rhabdomyolysis and why can it cause AKI?
-Muscle necrosis, often due to crush injuries, causes release of myoglobin
-Myoglobin is filtered at the glomerulus and is toxic to tubule and may cause obstruction -> causes AKI
What is characteristic of rhabdomyolysis?
-Produces black urine
What is acute glomerulonephritis?
-Immune diseases which affect the kidney
-Can by primary and only affect the kidneys or secondary as part of a systemic process