S6 L2 AKI Flashcards
Recap of Antihypertensive Drug Classes
- A, A, A, B, C, D
AKI:
- Can eGFR be used to measure AKI?
eGFR -
This is not reliable to use in an AKI, as AKI is a sudden change in creatinine levels, GFR assumes creatinine is stable
Defining AKI:
- What is it?
- How is it measured?
- Associated with…
- Is it reversible?
Staging AKI:
- 2 ways
Staging:
- Creatinine
- Urine output
- Stage 1, 2, 3 - Creatinine values
- Stage 1, 2, 3 - Urine Output values
What happens if get different stages for each?
Does everyone who comes into hospital with AKI need fluid?
Stage according to the MOST SEVERE classification outcome
Does everyone who comes into hospital with AKI need fluid?
Nope, not everyone
Diagnstic approach:
- 3 types of AKI
Pre-Renal AKI:
- 7 cause of this and explain them
Sepsis (leads to shock) - bacterial endotoxins in blood stream will cause profound vasodilation, reduce total peripheral resistance, leading to hypodiffusion of the kidney (although sepsis causes hypodiffusion, haven’t lost actual volume of blood)
Hypo-volaemia (leads to shock) - loss of circulating volume
Shock - catastrophic fall In blood pressure, leads to hypoperfusion, e.g. anaphylaxis, mechanical shock, cardiogenic shock
Renal artery stenosis - e.g. atheroma will cause hypoperfusion of the kidney
Congestive cardiac failure (CCF) - poor cardiac output, leads to hypoperfusion of kidney (25% of cardiac output goes to the kidney)
NSAIDs - Impair the mechanisms of renal autoregulation so can predispose to prerenal AKI, this through - kidneys respond to prostaglandins which cause vasodilation and improve renal blood
flow, NSAIDs inhibit prostaglandins synthesis, so effectively get vasoconstriction within the glomerular, so reduces renal blood flow
ACEi - Impair the mechanisms of renal autoregulation so can predispose to prerenal AKI, does this through: Angiotensin II preferential vasoconstricts the efferent arteriole, ACE inhibit angiotensin II, allow more bloood to escape the glomerulus, so less time and less blood in the glomerulus…
Intrinsic Renal AKI:
- 4 cause of this and explain them
• Acute tubular necrosis (ATN): ischeamia (can be caused by any prerenal cause that continues), rhabdomyolysis (muscle break down leads to release of myoglobin, myoglobin can damage the kidney), drug toxicity (e.g. Gentamicin) and toxins.
Break down the words: Acute means sudden, tubular is the cells that are affected, necrosis means death
• Acute interstitial nephritis: interstial space talking about here, rather than the tubules, inflammation and oedema of interstitum (due to drugs e.g. ACEi (can cause pre and intrinsic renal), infections, hypercalcemia, multiple myeloma)
• Glomerular disease: acute glomerulonephritis, rapidly progressive glomerulonephritis
• Vascular disease: vasculitis (inflammation of blood vessels in the glomerulus), malignant hypertension, thrombotic microangiopathies
Post-Renal AKI:
- 4 cause of this and explain them
Fluid Assessment
- How to do a Fluid Assessment
Complications of AKI
- 4 types and explain
Investigations of AKI:
- 4 main and explain them
Biochemical Changes Following AKI
- List them
What is Hydronephrosis and Hydroureter?
- What are these?
• Hydronephrosis - condition where one or both of the kidneys become stretched or swollen due to build up within them, specially in the calyces
• Hydroureter - abnormal enlargement of the ureter caused by any blockages hat prevents urine from draining into the bladder
CT scan showing hydronephritis
Management of AKI
- Each type (3 types of AKI)
Treat underlying cause
Best thing is to prevent an AKI!
What is Nephrostomy?
