🎧 New: AI-Generated Podcasts Turn your study notes into engaging audio conversations. Learn more

Juxtaglomerular Apparatus and AKI Overview
24 Questions
0 Views

Juxtaglomerular Apparatus and AKI Overview

Created by
@SufficientPentagon

Podcast Beta

Play an AI-generated podcast conversation about this lesson

Questions and Answers

What is the primary function of juxtaglomerular cells?

  • To synthesize and store erythropoietin.
  • To regulate sodium absorption.
  • To promote vasodilation of the efferent arteriole.
  • To synthesize and store renin. (correct)
  • What role does the Macula Densa play in kidney function?

  • It senses decreased NaCl levels. (correct)
  • It senses decreased blood pressure.
  • It synthesizes renin directly.
  • It causes vasodilation of the afferent arteriole.
  • How do ACE inhibitors contribute to prerenal acute kidney injury (AKI)?

  • By decreasing levels of angiotensin II. (correct)
  • By increasing renal blood flow.
  • By promoting vasodilation of the efferent arteriole.
  • By causing constriction of the afferent arteriole.
  • Which of the following conditions can lead to prerenal AKI?

    <p>Volume depletion due to severe burns.</p> Signup and view all the answers

    What is the effect of NSAIDs on the kidneys?

    <p>They block prostaglandins that dilate the afferent arteriole.</p> Signup and view all the answers

    Which nephrotoxic drug is known to interfere with the protective mechanism of prostaglandins?

    <p>Indomethacin.</p> Signup and view all the answers

    What condition is primarily associated with postrenal acute kidney injury (AKI)?

    <p>Prostatic hypertrophy.</p> Signup and view all the answers

    What metabolic condition is a characteristic feature of Chronic Kidney Disease?

    <p>Metabolic acidosis.</p> Signup and view all the answers

    What is the consequence of low levels of angiotensin II on the afferent and efferent arterioles?

    <p>Decreases glomerular filtration rate</p> Signup and view all the answers

    Which component of the juxtaglomerular apparatus is responsible for synthesizing and storing renin?

    <p>Juxtaglomerular cells</p> Signup and view all the answers

    What is the primary mechanism through which NSAIDs cause prerenal acute kidney injury?

    <p>Inhibition of prostaglandins that dilate the afferent arteriole</p> Signup and view all the answers

    Which of the following conditions is classified under intrarenal acute kidney injury?

    <p>Acute tubular necrosis</p> Signup and view all the answers

    What role do mesangial cells play in kidney function?

    <p>Form connections for selective vasoconstriction/vasodilation</p> Signup and view all the answers

    Which of the following drugs is known as a renin inhibitor?

    <p>Aliskiren</p> Signup and view all the answers

    What is a common consequence of prolonged ischemia in the kidneys?

    <p>Acute tubular necrosis</p> Signup and view all the answers

    Which two conditions are the most common causes of chronic kidney disease?

    <p>Diabetes mellitus and hypertension</p> Signup and view all the answers

    What is one way that mesangial cells contribute to kidney function?

    <p>They allow for selective vasoconstriction and vasodilation of arterioles.</p> Signup and view all the answers

    What is a potential cause of prerenal acute kidney injury due to medication use?

    <p>Inhibition of prostaglandins by NSAIDs.</p> Signup and view all the answers

    Which consequence is likely when angiotensin II levels are low?

    <p>Dilation of the efferent arteriole resulting in decreased GFR.</p> Signup and view all the answers

    How do nephrotoxic drugs like calcineurin inhibitors affect kidney health?

    <p>They cause damage to the glomeruli and renal tubules.</p> Signup and view all the answers

    Which condition is categorized as postrenal acute kidney injury?

    <p>Prostatic hypertrophy causing urinary obstruction.</p> Signup and view all the answers

    What is a likely consequence of prolonged ischemia in the kidney?

    <p>Development of acute tubular necrosis.</p> Signup and view all the answers

    What paracrine factor is involved in regulating renal hemodynamics at the juxtaglomerular apparatus?

    <p>Adenosine.</p> Signup and view all the answers

    What is a common complication of chronic kidney disease?

    <p>Fluid retention and hypertension.</p> Signup and view all the answers

    Study Notes

    Juxtaglomerular Apparatus

    • Juxtaglomerular cells located in the afferent arteriole are responsible for synthesizing and storing renin.
    • Renin release is triggered by stimuli like low blood flow.
    • Macula densa cells in the distal convoluted tubule (DCT) detect decreased sodium chloride (NaCl).
    • Mesangial cells utilize actin and microtubules to create connections, allowing for selective vasoconstriction/vasodilation of the afferent and efferent arterioles.
    • Mesangial cell contraction plays a role in this modulation of blood vessel diameter.
    • Macula densa cells release paracrine factors like adenosine and ATP, influencing nearby juxtaglomerular cells and mesangial cells to regulate renin secretion and hemodynamics of the afferent arteriole.

    Renin Inhibition

    • Aliskiren is the only known renin inhibitor.

    Acute Kidney Injury (AKI)

    • Prerenal AKI is characterized by a decrease in blood flow to the kidneys, often caused by:
      • Volume depletion: Hemorrhage, severe burns, diarrhea, emesis.
      • Cardiovascular disease: Heart failure, acute coronary syndrome.
      • Medications: NSAIDs, ARBs, ACE inhibitors, diuretics.
    • ACE inhibitors and ARBs can cause prerenal AKI by reducing angiotensin II levels, which normally constricts the efferent arteriole. This dilation of the efferent arteriole leads to reduced glomerular filtration rate (GFR).
    • NSAIDs can cause prerenal AKI by blocking prostaglandins, which normally dilate the afferent arteriole, resulting in decreased GFR.
    • Intrarenal AKI involves direct damage to the kidney itself:
      • Damaged Glomerulus: Glomerulonephritis.
      • Damaged Tubular Cells: Acute tubular necrosis.
    • Intrarenal AKI can be caused by:
      • Prolonged ischemia (lack of blood flow).
      • Toxic substances: Drugs, x-ray contrast dye.
    • Nephrotoxic drugs can contribute to intrarenal AKI:
      • NSAIDs: Especially indomethacin, interfere with prostaglandin's protective mechanisms.
      • Antibiotics: Amphotericin B, aminoglycosides, vancomycin.
      • Calcineurin inhibitors: Tacrolimus, cyclosporine.
      • Antivirals: Acyclovir.
    • Postrenal AKI is caused by obstruction of urine flow:
      • Prostatic hypertrophy.
      • Pelvic masses.
      • Nephrolithiasis (kidney stones).

    Chronic Kidney Disease (CKD)

    • Hypertension and diabetes mellitus are the two most common causes of CKD.
    • Metabolic acidosis is a common complication of CKD.
    • Secondary hyperparathyroidism is a complication of CKD.

    Juxtaglomerular Apparatus

    • Contains 3 components: juxtaglomerular cells, macula densa, and mesangial cells
    • Juxtaglomerular cells secrete renin in response to low blood flow
    • Macula densa sense decreased sodium chloride (NaCl) concentrations
    • Mesangial cells contract to cause vasoconstriction or vasodilation of afferent and efferent arterioles

    Macula Densa Cells

    • Release paracrine factors adenosine and ATP
    • These factors regulate renin secretion, and the hemodynamics of the afferent arteriole

    Aliskiren

    • Only renin inhibitor

    Acute Kidney Injury (AKI)

    • Prerenal AKI: occurs before kidney injury.
      • Volume depletion
        • Hemorrhage, severe burns, diarrhea, emesis
      • Cardiovascular disease
        • Heart failure, acute coronary syndrome
      • Medications
        • NSAIDs, ARBs, ACE inhibitors, diuretics
    • Intrarenal AKI: occurs within the kidneys
      • Damaged glomerulus (e.g. glomerulonephritis)
      • Damaged tubular cells (e.g. acute tubular necrosis)
      • Prolonged ischemia
      • Toxic substances (drugs, x-ray contrast dye)
    • Postrenal AKI: occurs after the kidneys
      • Prostatic hypertrophy, pelvic masses, nephrolithiasis

    ACE Inhibitors and ARBs

    • Angiotensin II constricts the efferent arteriole, increasing the glomerular filtration rate (GFR)
    • Low levels of angiotensin II cause the efferent arteriole to dilate, decreasing the GFR

    NSAIDs

    • Block prostaglandins, which dilate the afferent arteriole
    • Decrease the GFR

    Nephrotoxic Drugs

    • NSAIDs, especially indomethacin, interfere with prostaglandins' protective mechanism
    • Antibiotics: Amphotericin B, aminoglycosides, vancomycin
    • Calcineurin inhibitors: Tacrolimus and cyclosporine
    • Antivirals: Acyclovir

    Chronic Kidney Disease (CKD)

    • Most common causes: hypertension and diabetes mellitus
    • Metabolic acidosis can occur
    • Secondary hyperparathyroidism can occur

    Juxtaglomerular Apparatus

    • Composed of three parts: juxtaglomerular cells, macula densa, and mesangial cells
    • Juxtaglomerular cells in the afferent arteriole synthesize and store renin, released in response to low blood flow
    • Macula densa in the distal convoluted tubule senses decreased NaCl levels
    • Mesangial cells connect via actin and microtubules, contracting to constrict or dilate the afferent and efferent arterioles
    • Macula densa cells release paracrine factors like adenosine and ATP
    • These factors regulate renin secretion and hemodynamics of the afferent arteriole

    Renin Inhibitor

    • Aliskiren is the only renin inhibitor

    Acute Kidney Injury (AKI)

    • Classified into three types: prerenal, intrarenal, and postrenal

    Prerenal AKI

    • Caused by decreased blood flow to the kidneys
    • Common causes: volume depletion, cardiovascular disease, medications (NSAIDS, ARBs, ACE inhibitors, diuretics)

    How ACE Inhibitors and ARBs Cause Prerenal AKI

    • Angiotensin II constricts the efferent arteriole, increasing glomerular filtration rate (GFR)
    • Low angiotensin II levels lead to efferent arteriole dilation, decreasing GFR

    How NSAIDs Cause Prerenal AKI

    • NSAIDs block the production of prostaglandins, which normally dilate the afferent arteriole, decreasing GFR

    Intrarenal AKI

    • Caused by damage within the kidneys
    • Common causes: glomerular damage (glomerulonephritis), tubular cell damage (acute tubular necrosis)

    Intrarenal AKI Causes

    • Prolonged ischemia (lack of blood flow)
    • Toxic substances (drugs, x-ray contrast dye)

    Nephrotoxic Drugs

    • Can cause intrarenal AKI
    • Examples: NSAIDs (especially indomethacin), antibiotics (amphotericin B, aminoglycosides, vancomycin), calcineurin inhibitors (tacrolimus, cyclosporine), antivirals (acyclovir)

    Postrenal AKI

    • Caused by obstruction of urine flow
    • Common causes: prostatic hypertrophy, pelvic masses, nephrolithiasis (kidney stones)

    Chronic Kidney Disease (CKD)

    • Most commonly caused by hypertension and diabetes mellitus

    CKD Complications

    • Metabolic acidosis
    • Secondary hyperparathyroidism

    Studying That Suits You

    Use AI to generate personalized quizzes and flashcards to suit your learning preferences.

    Quiz Team

    Related Documents

    Kidney Pathology and RAAS PDF

    Description

    This quiz covers key aspects of the juxtaglomerular apparatus, including the roles of juxtaglomerular cells, macula densa, and mesangial cells in regulating blood flow and renin secretion. It also touches on acute kidney injury (AKI) and the impact of prerenal causes. Test your understanding of these important renal concepts!

    More Quizzes Like This

    Use Quizgecko on...
    Browser
    Browser