Acute Kidney Injury Quiz

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Questions and Answers

What is a potential consequence of prolonged prerenal acute kidney injury?

Chronic kidney disease

Glomerulosclerosis

Acute Tubular Necrosis (ATN) (correct)

Nephrotoxic damage

Which medication class inhibits renal prostaglandin production and thereby affects renal vasodilation?

Calcium channel blockers

Beta-blockers

NSAIDs (correct)

ACE inhibitors

What type of injury does prerenal acute kidney injury primarily involve?

Renal hypoperfusion (correct)

Glomerular damage

Tubular necrosis

Parenchymal damage

Which of the following is NOT a common cause of intrinsic acute kidney injury?

Long-standing hypertension Signup and view all the answers

Which condition can lead to acute tubular necrosis (ATN) due to ischemic injury?

Prerenal AKI Signup and view all the answers

What is the most common cause of intrinsic AKI?

Acute Tubular Necrosis (ATN) Signup and view all the answers

What characterizes the transition from prerenal AKI to ATN in terms of kidney damage?

Irreversible tubular damage Signup and view all the answers

Which category of nephrotoxins includes substances such as heavy metals and X-ray contrast media?

Exogenous nephrotoxins Signup and view all the answers

What is the mechanism responsible for decreased glomerular filtration rate (GFR) in post-renal AKI?

Underperfusion of glomeruli Signup and view all the answers

Which of the following factors can contribute to structural obstruction in post-renal AKI?

Kidney stones Signup and view all the answers

What is the purpose of renal replacement therapy in the context of acute kidney injury?

To remove waste products and correct electrolyte imbalances Signup and view all the answers

Which of the following statements about the timing of dialysis in AKI is accurate?

There is still debate regarding the appropriate timing to initiate dialysis. Signup and view all the answers

What common principle is critical in the management of individuals at risk for AKI?

Optimization of hemodynamics Signup and view all the answers

Which factor is likely NOT a cause of post-renal AKI?

Dehydration Signup and view all the answers

How does acute kidney injury (AKI) impact long-term health outcomes?

It is associated with an increased risk of long-term complications. Signup and view all the answers

What is the effect of angiotensin II in the pathophysiology of post-renal AKI?

It leads to intrarenal vasoconstriction. Signup and view all the answers

What characterizes acute kidney injury (AKI)?

Sudden impairment of kidney function Signup and view all the answers

Which of the following statements about pre-renal AKI is true?

It is characterized by renal hypoperfusion. Signup and view all the answers

Which category of AKI is associated with intrinsic kidney damage?

Intrinsic renal AKI Signup and view all the answers

What is a common clinical presentation of AKI?

Peripheral and pulmonary edema Signup and view all the answers

Which factor is NOT a typical cause of pre-renal AKI?

Obstructive uropathy Signup and view all the answers

What is the effect of renal vasoconstriction in pre-renal AKI?

Helps maintain normal glomerular filtration rate Signup and view all the answers

What is a typical metabolic feature of AKI?

Retention of nitrogenous waste products Signup and view all the answers

Which laboratory test is relevant in diagnosing AKI?

Serum creatinine concentration Signup and view all the answers

What characterizes the management principles of AKI?

Management focuses on addressing the underlying cause Signup and view all the answers

A decreased glomerular filtration rate (GFR) can lead to which of the following?

Retention of electrolytes and metabolic waste Signup and view all the answers

Which of the following could be a clinical feature of hyperkalemia in AKI?

Bradycardia Signup and view all the answers

How is acute tubular necrosis (ATN) classified in relation to AKI?

As an intrinsic renal cause of AKI Signup and view all the answers

Which mediator is involved in the compensatory response to renal hypoperfusion?

Prostaglandins Signup and view all the answers

In the case of systemic hypotension, what typically occurs related to GFR?

Renal autoregulation fails below a certain BP Signup and view all the answers

Study Notes

Acute Kidney Injury (AKI)

Sudden impairment of kidney function resulting in the retention of waste products.
Characterized by increased serum urea and creatinine, often with decreased urine volume.
It's a clinical syndrome with multiple causes leading to a rapid reduction in kidney function.
The failure to maintain fluid, electrolyte and acid-base homeostasis.

Acute vs Chronic Kidney Injury

Acute kidney injury involves a rapid loss of kidney function (hours to days) that is potentially reversible.
Chronic kidney injury is a progressive loss of kidney function over months to years, usually irreversible.

Clinical Presentation of AKI

Highly variable, ranging from asymptomatic with transient laboratory changes to severe and rapidly fatal derangements in volume regulation, electrolytes, and acid-base composition of the plasma.

Metabolic Features of AKI & Clinical Features

Retention of Nitrogenous Waste Products: Increased urea and creatinine leading to nausea, vomiting, hiccups, altered consciousness, and gastrointestinal bleeding.
Retention of Water: Hyponatremia leading to peripheral and pulmonary edema, ascites, and pleural effusion.
Retention of Potassium: Hyperkalemia causing typical ECG changes (peaked T waves, flattened P waves, QRS depression, widened QRS complex), muscle weakness, paralysis, and cardiac arrest.
Retention of Acid: Metabolic acidosis leading to Kussmaul breathing.

Etiology and Pathophysiology of AKI

Divided into three categories: Pre-renal, Intrinsic, and Post-renal.
Pre-Renal: Functional impairment due to decreased renal blood flow (ischemia), lack of structural renal damage, and rapid reversibility if the underlying cause is managed.
Intrinsic: Intrinsic kidney damage affecting glomeruli, tubules, interstitium, vasculature, or parenchyma.
Post-Renal: Obstruction to extra-renal collecting system.

Pre-Renal AKI

Most common form of AKI.
Characterized by circulatory insufficiency, renal hypoperfusion, preservation of normal tubular function, and rapid reversibility.
Causes: Hypovolemia (haemorrhage, GIT fluid loss, diuresis, burns), decreased cardiac output (cardiogenic shock, massive pulmonary embolus, cardiac tamponade), hypotension (sepsis), and drugs (vasodilators, ACE inhibitors).
Pathophysiology: Normal GFR is maintained by relative resistance of afferent and efferent renal arterioles, mild hypovolemia triggers compensatory changes like renal vasoconstriction and salt and water reabsorption.
Mediators of Response: Renin-Angiotensin-Aldosterone System, Norepinephrine, Vasopressin, and Intrarenal prostaglandins.
Risk Factors: Atherosclerosis, long-standing hypertension, and older age.
Drugs Affecting Response: NSAIDs inhibit renal prostaglandin production, limiting renal afferent vasodilation, ACE inhibitors and ARBs limit renal efferent vasoconstriction.
Prolonged periods of Pre-Renal AKI can lead to ischemic injury (acute tubular necrosis).

Intrinsic Renal AKI

Most Common Causes: Renal ischemia (tubular injury/ATN), and nephrotoxins (endogenous and exogenous).
Other Causes: Glomerulonephritis, vascular disease, severe hypertension, systemic diseases affecting the kidney, infiltrative disorders.

Intrinsic Renal AKI: Pathophysiology

Prerenal kidney injury and ischemia-associated AKI are a continuum of manifestations of renal hypoperfusion.

Acute Tubular Necrosis (ATN)

Most common cause of AKI, accounting for 45% of cases.
Often triggered by ischemia.
Loss of integrity of tight junctions leading to back leakage of glomerular filtrate.
Potentially reversible.

Post-Renal AKI

Urine flow is blocked leading to increased hydrostatic pressure and interference with glomerular filtration.
Prolonged obstruction can lead to secondary renal tubular damage.
Causes: Functional or structural derangements anywhere from the renal pelvis to the tip of the urethra.
Pathophysiology: Hemodynamic alterations triggered by an abrupt increase in intratubular pressures, initial afferent arteriolar dilation followed by intrarenal vasoconstriction.

Treatment of AKI

Varies according to the underlying cause.
Common Principles: Optimization of hemodynamics, correction of fluid and electrolyte imbalances, discontinuation of nephrotoxic medications, dose adjustment of medications, avoidance of complications, treat underlying infections, and provision of renal replacement therapy.

Dialysis

Indicated when medical management fails to control volume overload, severe hyperkalemia, severe acidosis, some toxic ingestions, and severe complications of uremia.
Principle: Semi-permeable membrane surrounded by a dialysate bath.

Prognosis/Disease Course

AKI is associated with an increased risk of mortality, longer length of stay, and increased costs.
Prerenal AKI generally carries a better prognosis than intrinsic AKI.
Prognosis varies from complete recovery to progressive CKD (ESRD).

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Description

Test your knowledge about Acute Kidney Injury (AKI) and its clinical features. This quiz covers the definitions, differences between acute and chronic kidney injury, and the metabolic implications of AKI. Explore the symptoms, causes, and diagnostic markers associated with this critical condition.