flashcard 8

(50 cards)

1
Q

What is the functional unit of the kidney, and what are its three main components?

A

The nephron, consisting of the renal corpuscle (glomerulus + Bowman’s capsule), the renal tubule (proximal tubule, loop of Henle, distal tubule), and the collecting duct.

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2
Q

How do cortical nephrons differ from juxtamedullary nephrons in structure and function?

A

Cortical nephrons have shorter loops of Henle that dip only slightly into the medulla, mainly carrying out filtration and bulk reabsorption. Juxtamedullary nephrons have long loops extending deep into the medulla, critical for generating and maintaining medullary concentration gradients.

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3
Q

What is the initial process that occurs in the renal corpuscle?

A

Glomerular filtration, where plasma is forced through the fenestrated capillaries of the glomerulus into Bowman’s space, creating filtrate.

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4
Q

Approximately what percentage of plasma entering the afferent arteriole is filtered into Bowman’s capsule?

A

Around 20% of plasma is filtered into Bowman’s capsule; the remaining 80% continues through the efferent arteriole to peritubular capillaries.

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5
Q

What prevents large proteins and blood cells from entering the filtrate during glomerular filtration?

A

The size- and charge-selective filtration barrier (fenestrated endothelium, basement membrane, and podocyte slit diaphragms) excludes large proteins (e.g., albumin) and cells, allowing only small molecules to pass.

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6
Q

What three pressures determine net filtration pressure in the glomerulus?

A

Glomerular capillary hydrostatic pressure (favors filtration), Bowman’s capsule hydrostatic pressure (opposes filtration), and glomerular capillary colloid osmotic pressure (opposes filtration).

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7
Q

How does constriction of the afferent arteriole affect glomerular filtration rate (GFR)?

A

Constricting the afferent arteriole reduces blood flow into the glomerulus, lowering glomerular hydrostatic pressure and decreasing GFR.

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8
Q

What is the effect of constricting the efferent arteriole on GFR?

A

Constricting the efferent arteriole increases hydrostatic pressure in the glomerulus, thereby increasing GFR (up to a limit before backpressure rises too much).

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9
Q

What is tubular reabsorption, and where does most of it occur?

A

Tubular reabsorption is the movement of filtered substances (water, electrolytes, nutrients) from filtrate back into peritubular capillaries. About 65–70% of filtered fluid is reabsorbed in the proximal convoluted tubule.

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10
Q

How does the permeability of the descending limb of the loop of Henle differ from that of the ascending limb?

A

The descending limb is permeable to water but not to solutes, causing the filtrate to become more concentrated as water is reabsorbed. The ascending limb is impermeable to water but actively reabsorbs Na⁺, K⁺, and Cl⁻, diluting the filtrate.

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11
Q

What mechanism creates and maintains the medullary osmotic gradient?

A

The countercurrent multiplier system: the loop of Henle’s descending limb loses water, concentrating filtrate; the thick ascending limb actively pumps out ions without water, diluting filtrate; vasa recta capillaries preserve the gradient by countercurrent exchange.

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12
Q

How is final urine osmolarity determined in the collecting duct?

A

By variable reabsorption of water and solutes under hormonal control (mainly ADH and aldosterone), in response to the body’s hydration status, which adjusts permeability of collecting duct water channels.

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13
Q

What hormone increases the water permeability of the collecting duct, and where is it produced?

A

Antidiuretic hormone (ADH or vasopressin), produced by the hypothalamus and released from the posterior pituitary, increases aquaporin insertion in the collecting duct, promoting water reabsorption.

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14
Q

What triggers aldosterone release, and what is its primary renal effect?

A

Aldosterone is released from the adrenal cortex in response to angiotensin II or high plasma K⁺. It increases Na⁺ reabsorption and K⁺ secretion in the distal tubule and collecting duct, indirectly promoting water retention.

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15
Q

What is the macula densa, and how does it contribute to tubuloglomerular feedback?

A

The macula densa is a specialized group of cells in the distal tubule that senses NaCl concentration. If NaCl delivery is high, they release paracrine signals causing afferent arteriole constriction to reduce GFR; if NaCl is low, they cause dilation to increase GFR.

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16
Q

Explain the myogenic mechanism of GFR autoregulation.

A

When systemic blood pressure rises, the afferent arteriole stretches and reflexively constricts (myogenic response) to maintain constant blood flow and GFR. If pressure falls, the arteriole dilates to preserve GFR.

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17
Q

Why is GFR normally maintained relatively constant despite fluctuations in systemic blood pressure?

A

Autoregulation via the myogenic response and tubuloglomerular feedback ensures stable GFR by adjusting afferent/efferent arteriole tone, preventing large swings in filtration.

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18
Q

How is GFR clinically estimated using inulin clearance?

A

Inulin is freely filtered, not reabsorbed, secreted, or metabolized. By measuring plasma inulin concentration, urine inulin concentration, and urine flow rate, GFR = ([Inulin]_urine × Urine flow) ÷ [Inulin]_plasma.

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19
Q

Why is creatinine clearance used as an endogenous estimate of GFR?

A

Creatinine is produced at a fairly constant rate by muscle metabolism, freely filtered, not reabsorbed, and minimally secreted. Measuring its plasma and urine concentrations gives an approximate GFR without requiring infusion.

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20
Q

What are limitations of using creatinine clearance to estimate GFR?

A

Approximately 7–10% of creatinine is secreted in the proximal tubule (overestimating GFR), and factors such as age, muscle mass, diet, exercise, and certain medications (e.g., trimethoprim, cimetidine) can alter serum creatinine independently of GFR.

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21
Q

What is the typical normal GFR in a young healthy adult, and how does it change with age?

A

Normal GFR is about 120–125 mL/min. GFR declines gradually with age (e.g., by 1 mL/min per year after age 40), so elderly individuals often have lower ‘normal’ GFR.

22
Q

How do clinicians classify stages of chronic kidney disease (CKD) based on estimated GFR?

A

CKD stages are defined as: Stage 1 (GFR ≥90 with kidney damage), Stage 2 (60–89), Stage 3a (45–59), Stage 3b (30–44), Stage 4 (15–29), Stage 5 (<15, kidney failure).

23
Q

What major functions, beyond filtration, do the kidneys perform to maintain homeostasis?

A

Control of blood composition (fluid/electrolyte balance), regulation of blood volume and pressure, endocrine functions (erythropoietin and calcitriol production), acid-base balance, and excretion of metabolic wastes (urea, uric acid, creatinine).

24
Q

How do the kidneys contribute to acid-base balance through bicarbonate reabsorption?

A

In proximal tubule cells, filtered HCO₃⁻ combines with secreted H⁺ to form CO₂ + H₂O (via carbonic anhydrase). CO₂ diffuses into cells, is reconverted to HCO₃⁻, which is reabsorbed with Na⁺, while H⁺ is secreted back into lumen.

25
What role does renal ammoniagenesis (glutamine metabolism) play in acid excretion?
Glutamine is metabolized in proximal tubule cells to produce NH₄⁺ and HCO₃⁻. NH₄⁺ is secreted into filtrate (excreting acid), while HCO₃⁻ enters peritubular capillaries (replenishing blood buffer).
26
How can the kidneys compensate for metabolic acidosis?
By increasing H⁺ secretion and NH₄⁺ excretion, reabsorbing more HCO₃⁻, and generating new HCO₃⁻ via glutamine metabolism, thus restoring blood pH toward normal.
27
What is the countercurrent exchange mechanism in the vasa recta?
Blood in the vasa recta flows opposite to filtrate in the loop of Henle. As blood descends into the medulla, it picks up solutes and loses water; as it ascends, it loses solutes and gains water. This preserves the medullary osmotic gradient.
28
How do the kidneys regulate blood pressure through the renin–angiotensin–aldosterone system (RAAS)?
Juxtaglomerular cells release renin in response to low renal perfusion. Renin converts angiotensinogen to angiotensin I, which is converted to angiotensin II (a vasoconstrictor) by ACE. Angiotensin II stimulates aldosterone release, increasing Na⁺/water reabsorption and raising blood pressure.
29
What stimuli trigger renin release from juxtaglomerular cells?
Decreased stretch of afferent arteriole (low renal perfusion pressure), reduced NaCl delivery to macula densa, and sympathetic β₁-adrenergic stimulation.
30
Through which mechanism does angiotensin II directly increase GFR in early hypovolemia?
At low to moderate levels, angiotensin II preferentially constricts efferent arterioles (more than afferent), increasing glomerular capillary pressure and helping maintain GFR despite reduced renal perfusion.
31
What hormones do the kidneys produce that affect erythropoiesis and calcium homeostasis?
Erythropoietin (EPO) from peritubular interstitial cells stimulates red blood cell production in bone marrow. Calcitriol (active vitamin D) produced by 1α-hydroxylase in proximal tubule cells enhances intestinal Ca²⁺ absorption.
32
How does decreased renal function lead to anemia?
Impaired kidneys produce less erythropoietin, resulting in reduced stimulation of erythrocyte production, causing anemia in chronic kidney disease.
33
In the proximal tubule, what transporter exchanges Na⁺ for H⁺, and why is this important?
The Na⁺/H⁺ exchanger (NHE) secretes H⁺ into filtrate in exchange for Na⁺ reabsorption. This process is vital for reclaiming filtered bicarbonate and regulating acid-base balance.
34
Describe how loop diuretics affect the countercurrent multiplier and medullary gradient.
Loop diuretics (e.g., furosemide) inhibit Na⁺-K⁺-2Cl⁻ cotransporters in the thick ascending limb, preventing ion reabsorption that normally dilutes the ascending limb. This disrupts the medullary gradient, reducing water reabsorption in the collecting duct and causing diuresis.
35
What is the significance of the filtration coefficient (Kf) in GFR?
Kf reflects the total surface area and permeability of glomerular capillaries. Changes in Kf (e.g., due to glomerular damage reducing surface area) directly decrease GFR.
36
How do prostaglandins influence GFR and renal blood flow?
Prostaglandins (e.g., PGE₂, PGI₂) dilate afferent arterioles, increasing renal blood flow and GFR. They counteract excessive vasoconstriction from sympathetic stimulation or angiotensin II.
37
Why might NSAIDs impair renal function in susceptible individuals?
NSAIDs inhibit cyclooxygenase enzymes, reducing prostaglandin synthesis. Without prostaglandin-mediated afferent arteriole dilation, GFR may drop, especially under conditions dependent on prostaglandins (e.g., dehydration, heart failure).
38
What laboratory values change in acute kidney injury regarding BUN and creatinine?
In acute kidney injury, both blood urea nitrogen (BUN) and serum creatinine rise due to reduced GFR. The BUN:creatinine ratio may help distinguish pre-renal (ratio >20:1) from intrinsic renal (ratio ~10–15:1) causes.
39
How does the kidney participate in potassium homeostasis?
The distal tubule and collecting duct secrete K⁺ via principal cells under the influence of aldosterone (increases Na⁺ reabsorption and K⁺ secretion). This maintains plasma K⁺ within a narrow range.
40
What is the renal handling of glucose under normal conditions, and what happens in uncontrolled diabetes mellitus?
Normally, nearly all filtered glucose is reabsorbed in the proximal tubule via sodium–glucose cotransporters. In diabetes, plasma glucose may exceed the transport maximum (Tm) of these transporters, resulting in glycosuria.
41
Define renal plasma flow (RPF) and how it differs from GFR.
RPF is the volume of plasma delivered to the kidneys per unit time. GFR is the volume of plasma filtered by glomeruli per unit time. Approximately 20% of RPF is filtered, so GFR ≈ 0.2 × RPF.
42
What marker (exogenous or endogenous) is used to measure RPF, and how?
Para-aminohippuric acid (PAH) clearance approximates RPF because PAH is freely filtered and actively secreted by proximal tubule cells, so nearly all PAH entering the kidney is excreted. RPF ≈ PAH clearance.
43
How does sympathetic nervous system activation affect renal function during acute hemorrhage?
Sympathetic activation constricts afferent arterioles (via α₁-adrenergic receptors), reducing RPF and GFR to conserve blood volume. It also stimulates renin release, activating RAAS to retain Na⁺ and water.
44
What is renal autoregulation, and why is it clinically important?
Renal autoregulation maintains relatively constant renal blood flow and GFR over a range of mean arterial pressures (≈80–180 mm Hg) via myogenic and tubuloglomerular feedback mechanisms. It protects glomeruli from pressure fluctuations.
45
How is phosphate homeostasis influenced by the kidney?
The proximal tubule reabsorbs filtered phosphate via sodium–phosphate cotransporters. Parathyroid hormone inhibits phosphate reabsorption, increasing phosphate excretion, thereby balancing plasma phosphate levels.
46
What is renal autoregulation?
Renal autoregulation maintains relatively constant renal blood flow and GFR over a range of mean arterial pressures (≈80–180 mm Hg) via myogenic and tubuloglomerular feedback mechanisms. It protects glomeruli from pressure fluctuations.
47
What changes in renal handling of calcium occur under PTH influence?
PTH increases distal tubule calcium reabsorption while reducing phosphate reabsorption in the proximal tubule. It also stimulates 1α-hydroxylase to increase calcitriol production, enhancing intestinal Ca²⁺ absorption.
48
Why is urine osmolality an important clinical measurement?
Urine osmolality reflects the kidney’s ability to concentrate or dilute urine. High osmolality indicates water conservation (e.g., dehydration or high ADH), and low osmolality indicates water excretion (e.g., overhydration or low ADH).
49
What is the significance of the clearance equation?
This equation calculates the volume of plasma from which substance S is completely cleared per unit time. For inulin or creatinine, it approximates GFR; for PAH, it approximates RPF.
50
How does diabetic nephropathy initially affect GFR, and what is the long-term consequence?
Early diabetic nephropathy causes hyperfiltration (increased GFR) due to glomerular hypertension. Over time, damage to glomeruli and basement membranes leads to declining GFR and progressive kidney failure.