4.2 Diuretics and Kidney Diseases

<p>The thick ascending limb of the loop of Henle. (D)</p> Signup and view all the answers

<p>Decrease the osmolarity in the medullary interstitium. (A)</p> Signup and view all the answers

<p>Sodium, two chloride, one potassium cotransporter. (D)</p> Signup and view all the answers

<p>Increased osmotic pressure in the tubule, preventing water reabsorption. (B)</p> Signup and view all the answers

<p>Reduces the kidneys' ability to concentrate urine by decreasing renal medullary osmolarity. (B)</p> Signup and view all the answers

<p>Precipitation of antigen-antibody complexes in glomerular membranes (A)</p> Signup and view all the answers

<p>Nephrotic syndrome (D)</p> Signup and view all the answers

<p>Creatinine excretion decreases, leading to accumulation (D)</p> Signup and view all the answers

<p>Rapid flow of fluid through the collecting ducts and loop of Henle. (B)</p> Signup and view all the answers

<p>Fecal contamination ascending from the lower urinary tract (C)</p> Signup and view all the answers

<p>Loss of more than 75% of nephrons (A)</p> Signup and view all the answers

<p>Greatly decreased tubular reabsorption and increased excretion. (C)</p> Signup and view all the answers

<p>It primarily affects the renal medulla (B)</p> Signup and view all the answers

<p>Glomerular filtration (B)</p> Signup and view all the answers

<p>Rapid flushing of the fluid and high solute concentration in the tubules. (A)</p> Signup and view all the answers

<p>Thiazide diuretics (A)</p> Signup and view all the answers

<p>Proximal tubule (A)</p> Signup and view all the answers

<p>Antagonizing mineralocorticoid receptors (A)</p> Signup and view all the answers

<p>Aldosterone stimulates the sodium potassium ATPase pump creating a concentration gradient for reabsorption (B)</p> Signup and view all the answers

<p>They decrease potassium excretion (A)</p> Signup and view all the answers

<p>Acute kidney injury (A)</p> Signup and view all the answers

<p>Pre-renal AKI (C)</p> Signup and view all the answers

<p>Decreased blood flow to the kidneys (B)</p> Signup and view all the answers

<p>Kidney stones (B)</p> Signup and view all the answers

<p>Accumulation of water and solutes (C)</p> Signup and view all the answers

<p>To maintain a gradient for sodium reabsorption (D)</p> Signup and view all the answers

<p>act on the early distal tubules (C)</p> Signup and view all the answers

<p>Decreases potassium excretion (C)</p> Signup and view all the answers

<p>It decreases sodium reabsorption (B)</p> Signup and view all the answers

<p>Increased bicarbonate loss in urine (A)</p> Signup and view all the answers

<p>Decreased sodium reabsorption needs, reducing energy demand. (A)</p> Signup and view all the answers

<p>Insoluble immune complexes trapped in glomerular capillaries. (B)</p> Signup and view all the answers

<p>Severe ischemia and/or toxins destroying epithelial cells. (A)</p> Signup and view all the answers

<p>It prevents proper urine flow, leading to backpressure and injury. (B)</p> Signup and view all the answers

<p>Retention of potassium which can be fatal. (B)</p> Signup and view all the answers

<p>Adaptive changes in surviving nephrons causing further injury. (B)</p> Signup and view all the answers

<p>A need for dialysis or a kidney transplant. (B)</p> Signup and view all the answers

<p>Atherosclerosis of larger renal arteries. (C)</p> Signup and view all the answers

<p>Unilateral injury when one kidney can compensate. (B)</p> Signup and view all the answers

<p>Through sclerotic lesions of smaller renal vessels. (A)</p> Signup and view all the answers

<p>Edema and hypertension. (A)</p> Signup and view all the answers

<p>The number of functional nephrons decreases with age. (C)</p> Signup and view all the answers

<p>Obesity. (D)</p> Signup and view all the answers

<p>To lower arterial pressure and glomerular hydrostatic pressure. (C)</p> Signup and view all the answers

<p>The epithelial cells will be destroyed. (D)</p> Signup and view all the answers

Diuretics increase urine output by reducing sodium reabsorption in the renal tubules. This leads to increased osmotic pressure and water excretion.

The body compensates for fluid loss caused by diuretics. This eventually brings urine output back to normal, even if blood pressure and extracellular fluid volume decrease.

Increased osmotic pressure in the renal tubules drives water excretion. This can be caused by high levels of certain solutes, like glucose in diabetes.

Loop diuretics, like furosemide, block a specific transporter in the thick ascending limb of the loop of Henle. This inhibits sodium, chloride, and potassium reabsorption, elevating osmotic pressure in the tubules.

Loop diuretics disrupt the counter-current multiplier system by decreasing medullary osmolarity. This impairs the kidneys' ability to concentrate or dilute urine.

Glucose levels exceeding the reabsorptive capacity of the tubules lead to excess glucose acting as an osmotic diuretic, increasing urine output.

The kidneys regulate the volume and composition of urine based on the body's needs, adjusting water and solute reabsorption.

A decrease in extracellular fluid volume triggers compensatory mechanisms to restore balance. Diuretics initially cause fluid loss, but then the body adapts.

A type of diuretic that blocks the sodium chloride cotransporter in the early distal tubules, limiting sodium reabsorption and increasing urine output.

A type of diuretic that inhibits carbonic anhydrase, an enzyme crucial for bicarbonate reabsorption in the proximal tubules.

Refers to diuretics that promote potassium retention by blocking the action of aldosterone, reducing potassium secretion in the collecting tubules.

A type of diuretic that blocks aldosterone receptors in the collecting tubules, reducing sodium reabsorption and potassium secretion.

A pump located in the basal outer membrane of principal cells in the late distal tubule and collecting tubules, responsible for maintaining a low intracellular sodium concentration.

A type of diuretic that directly blocks sodium channels in the luminal membrane of collecting tubules, reducing sodium reabsorption and potassium secretion.

A sudden loss of kidney function that occurs over a few days, often due to decreased blood supply to the kidneys.

A type of AKI caused by decreased blood flow to the kidneys, often due to conditions like heart failure or low blood pressure.

A type of AKI caused by damage to the kidneys themselves, affecting blood vessels or tubules.

A type of AKI caused by obstruction of the urinary tract, often due to kidney stones.

The normal blood flow received by the kidneys, about 20-25% of the cardiac output.

The rate at which fluid is filtered from the blood into the glomerulus.

Decreased urine output, often a symptom of kidney dysfunction.

The accumulation of water and solutes in the body, often a consequence of decreased kidney function.

The kidneys are resilient to reduced blood flow because they scale down sodium reabsorption, decreasing energy and oxygen demand.

As renal blood flow and GFR drop, the kidneys use less energy. Only a minimal amount of oxygen is needed to keep the cells alive.

Prolonged reduced renal blood flow can cause hypoxia, damage, and potentially death to kidney cells.

Intrarenal acute kidney injury is caused by problems originating within the kidneys themselves, leading to a sudden decrease in function.

A type of intrarenal acute kidney injury where an abnormal immune response damages the glomeruli, often triggered by an infection.

Tubular necrosis occurs when the epithelial lining of the tubules is destroyed, often due to ischemia or toxins.

Severe ischemia (lack of blood flow) to the kidneys, often caused by shock, can trigger tubular necrosis.

Poisons, toxins, and certain medications can also damage tubular epithelial cells, causing tubular necrosis.

Obstruction in the lower urinary tract, even if only affecting one kidney, can cause acute kidney injury.

Chronic kidney disease is characterized by long-term kidney damage or decreased function for at least three months.

Damage to a large number of nephrons causes adaptive changes like increased blood flow and GFR in the remaining nephrons.

The progressive nature of CKD can lead to further injury and potentially kidney failure, requiring dialysis or transplant.

Lowering blood pressure and reducing pressure within the glomeruli helps slow CKD's progression.

Diabetes and hypertension are the leading causes of end-stage renal disease, with obesity being a major risk factor.

Chronic glomerulonephritis is a slow and progressive kidney disease characterized by inflammation and damage to the glomerular capillary loops, leading to eventual irreversible renal failure.

Interstitial nephritis is a kidney condition characterized by inflammation and damage to the renal interstitium, the space between the renal tubules. It can be caused by various factors, including infections, drugs, and toxins, and can lead to nephron destruction.

Paolonephritis is a specific type of interstitial nephritis caused by bacterial infection, usually E. coli, which enters the kidneys via the urinary tract.

Nephrotic syndrome is characterized by excessive protein loss in the urine, often accompanied by other kidney abnormalities. It can be caused by various factors, including glomerulonephritis, amyloidosis, and minimal change nephrotic syndrome.

The body can compensate for kidney damage by increasing the workload on remaining healthy nephrons. However, as more nephrons are destroyed, this compensatory ability decreases, leading to fluid and solute retention, ultimately causing kidney failure.

As the number of functioning nephrons decreases, the waste products of metabolism, such as urea and creatinine, accumulate in the blood, leading to a rise in their plasma concentration.

The GFR (Glomerular Filtration Rate) is a measure of kidney function. It reflects the volume of blood filtered by the kidneys per unit time. As nephrons are damaged, the GFR decreases, leading to reduced waste excretion and accumulation of waste products in the blood.

Some substances, like phosphate and hydrogen, can be maintained within normal ranges even with moderate reduction in GFR. However, their concentration rises, but not proportionally to the GFR decline, due to increased secretion into the tubular lumen.

The kidneys' ability to dilute or concentrate urine depends on the flow rate through the renal tubules. When nephrons are damaged, high flow rates in the remaining nephrons impair both diluting and concentrating mechanisms, leading to imbalances in urine composition.

When the number of functioning nephrons is reduced significantly, the remaining nephrons must work harder to excrete the same amount of fluid and solutes. This increased workload can impact their ability to concentrate or dilute urine.