Body Fluids And GFR Flashcards by K C

Which starling force primarily drives glomerular filtration?

Glomerular hydrostatic pressure

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1️⃣ Q: What is the equation for calculating GFR?

GFR = (PGC - PBS - πGC + πBS) x Kf

Where:
• PGC = Glomerular capillary hydrostatic pressure (favors filtration)
• PBS = Hydrostatic pressure in Bowman’s space (opposes filtration)
• πGC = Oncotic pressure in glomerular capillaries (opposes filtration)
• πBS = Oncotic pressure in Bowman’s space (usually zero)
• Kf = Filtration coefficient

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What two factors determine the filtration coefficient (Kf)?

Permeability (μ) of the glomerular membrane
1. Surface area available for filtration

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What is the effect of afferent arteriolar constriction on GFR?

• ↓ Glomerular capillary hydrostatic pressure (PGC)
• ↓ Renal plasma flow (RPF)
• ↓ GFR

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A patient has increased oncotic pressure (πGC) in glomerular capillaries. What effect does this have on GFR?

A) Increase GFR
B) Decrease GFR
C) No effect on GFR
D) Increase renal plasma flow (RPF)

✅ Decrease GFR

Higher oncotic pressure in capillaries means more force opposes filtration, leading to a reduced GFR

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In response to low GFR, what is the kidney’s autoregulatory response?

A) Afferent arteriole constriction
B) Efferent arteriole dilation
C) Afferent arteriole dilation & Efferent arteriole constriction
D) No change in vascular resistance

✅ Afferent arteriole dilation & Efferent arteriole constriction

– Dilation of the afferent arteriole increases renal blood flow, and efferent arteriole constriction maintains glomerular pressure.

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Which pressure drives glomerular filtration the most?

A) Hydrostatic pressure in Bowman’s space (PBS)
B) Oncotic pressure in Bowman’s space (πBS)
C) Glomerular capillary hydrostatic pressure (PGC)
D) Oncotic pressure in glomerular capillaries (πGC)

✅ Glomerular capillary hydrostatic pressure (PGC)

– PGC is the major force that favors filtration.

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How does proteinuria (nephrotic syndrome) affect GFR?

• ↓ Plasma oncotic pressure (πGC) → Less opposition to filtration → Initially ↑ GFR
• Chronic damage leads to ↓ GFR over time

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What happens to GFR in urinary tract obstruction (e.g., kidney stone)?

• ↑ Hydrostatic pressure in Bowman’s space (PBS) → Opposes filtration → ↓ GFR

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What is the primary mechanism for glucose reabsorption in the proximal tubule? 

Secondary active transport via sodium-glucose cotransporters (SGLT1/SGLT2). This process uses the sodium gradient created by the Na-K-ATPase pump to move glucose against its concentration gradient, ensuring nearly 100% reabsorption under normal conditions.

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What percentage of the filtered Na⁺ load is reabsorbed in the ascending limb of the loop of Henle? 

25%. The thick ascending limb reabsorbs about 25% of the filtered Na⁺ load via the Na-2Cl-K cotransporter, contributing to the medullary concentration gradient.

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Which ion is regulated by both reabsorption and secretion in the distal nephron depending on intake? 

K⁺ (Potassium). K⁺ regulation varies with intake: 2% excreted at low intake, 10-20% at normal intake, and net secretion up to 150% at high intake, influenced by aldosterone.

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What is the main role of the Na-K-ATPase pump in tubular cells? 

To maintain a low intracellular Na⁺ concentration and a negative membrane potential (-70 mV). It pumps 3 Na⁺ out and 2 K⁺ into the cell, driving secondary active transport processes.

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How do SGLT2 inhibitors like empagliflozin work? 

They prevent glucose reabsorption in the proximal tubule by blocking SGLT2, leading to increased urinary glucose excretion. This helps manage diabetes but may increase UTI risk due to high urine glucose.

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What process reabsorbs small proteins and macromolecules in the proximal tubule?

Pinocytosis. This active transport mechanism involves the luminal membrane forming vesicles to engulf macromolecules, which are then hydrolyzed into amino acids, requiring ATP.

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What happens when the tubular load exceeds the transport maximum? 

Urinary excretion of the substance begins. When the nephron’s reabsorption capacity is saturated, excess substance is excreted in urine, e.g., glucose in hyperglycemia.

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Which hormone regulates water reabsorption in the late distal tubule and collecting duct? 

Antidiuretic hormone (ADH). ADH increases water permeability via aquaporin channels, allowing water to follow osmotic gradients based on hydration status.

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What is the role of urea recirculation in the renal medulla? 

It contributes to the hyperosmolarity of the medulla and concentrated urine formation. Urea, trapped by recirculation between the collecting duct and loop of Henle, enhances medullary osmolarity with ADH influence.

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What is the primary mechanism for NaCl reabsorption in the second half of the proximal tubule?

Na-H and Cl-anion exchangers with paracellular solvent drag. This process leverages high Cl⁻ concentration and solvent drag to reabsorb NaCl efficiently.

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What is the equation for urinary excretion in the renal tubules? 

Urinary excretion = glomerular filtration - tubular reabsorption + tubular secretion. This formula summarizes the balance of filtration, reabsorption, and secretion in urine formation.

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Why is reabsorption more significant than secretion in urine formation?
 

Reabsorption reclaims most filtered substances (e.g., 67% of Na⁺ in the proximal tubule), while secretion plays a smaller role, mainly adjusting K⁺ and H⁺ levels.

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What drives transport from the interstitial fluid to the peritubular capillaries? 

Bulk flow mediated by hydrostatic and colloid osmotic forces. These forces move reabsorbed solutes and water from the interstitium into the capillaries.

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What percentage of the glomerular filtrate is reabsorbed in the proximal tubule?

67%. The proximal tubule reabsorbs 67% of water, Na⁺, Cl⁻, K⁺, and all glucose, amino acids, and proteins, maintaining osmolality.

Which part of the nephron has a high permeability to urea under the influence of ADH?

• Answer: Medullary collecting duct

•	Key Takeaway: ADH upregulates specific urea transporters (UTA1, UTA3) in the medullary collecting duct, increasing urea permeability and aiding in urine concentration.

A substance is filtered but neither reabsorbed nor secreted by the renal tubules. What does its clearance measure?

• Answer: Glomerular Filtration Rate (GFR) • Key Takeaway: Clearance of such a substance (like inulin) equals GFR because all that is filtered is excreted unchanged.

When the macula densa detects elevated NaCl in the distal tubule, how does it adjust renal blood flow?

It releases ATP causing afferent arteriole constriction and reduces GFR. ## Footnote The tubuloglomerular feedback mechanism helps regulate GFR by adjusting arteriolar tone based on distal sodium concentration.

Which portion of the renal tubule is impermeable to water under normal physiological conditions but reabsorbs large amounts of solute?

Thick ascending limb of Henle’s loop ## Footnote The Na⁺-K⁺-2Cl⁻ cotransporter actively reabsorbs solutes here, generating a dilute tubular fluid because the segment is water-impermeable.

What happens to GFR if there is selective constriction of the efferent arteriole?

GFR increases initially (due to increased glomerular capillary pressure) but can fall if constriction is severe. ## Footnote Mild to moderate efferent arteriolar constriction raises P_GC and thus GFR. Severe constriction reduces renal blood flow and eventually lowers GFR.

How does hypoalbuminemia (e.g., from liver disease) affect GFR?

Increases GFR (↓ plasma oncotic pressure in glomerular capillaries). ## Footnote Lower oncotic pressure offers less opposition to filtration, raising net filtration pressure.

In the proximal tubule, which transport mechanism primarily drives glucose reabsorption?

Secondary active transport via Na⁺-dependent cotransport (SGLT). ## Footnote A low intracellular Na⁺ concentration (maintained by the basolateral Na⁺/K⁺ ATPase) creates a gradient driving glucose uptake from tubular fluid.

Why does blocking the Na⁺-H⁺ exchanger in the proximal tubule reduce ammonium (NH₄⁺) excretion?

Less H⁺ is secreted into the lumen to combine with NH₃, reducing NH₄⁺ formation and excretion. ## Footnote NH₄⁺ excretion depends on sufficient proton secretion into the tubular lumen.

If the filtrate in the distal tubule has low NaCl concentration, what is the juxtaglomerular (JG) apparatus’ primary response?

Increase renin release → formation of angiotensin II → primarily constricts efferent arteriole → supports GFR. ## Footnote Tubuloglomerular feedback ensures adequate GFR through hormonal and local signals.

In volume expansion, which hormonal change most effectively reduces proximal tubule sodium reabsorption?

Decreased angiotensin II levels. ## Footnote Angiotensin II powerfully stimulates Na⁺ reabsorption in the proximal tubule. Lower levels lead to less reabsorption.

In hypovolemia, what is the primary response of juxtaglomerular (JG) cells in the kidney?

Release renin into circulation → activates RAAS → restores BP and volume.

Which organ is most sensitive to hypoperfusion due to its lack of energy reserves?

Brain — needs continuous oxygen and glucose; quickly affected by ischemia.

What are the two key mechanisms of renal autoregulation?

Myogenic mechanism and tubuloglomerular feedback — they maintain stable GFR and RBF across a range of BPs.

During hypovolemia with reduced urine output, which hormone most significantly reduces urine flow rate?

ADH (vasopressin) — increases water reabsorption in the collecting duct.

A trauma patient in ICU develops hypernatremia and high urine output. What is the likely status of ADH?

Low or absent ADH — indicates central diabetes insipidus due to hypothalamic/posterior pituitary damage.

What effect does ADH have on the late distal tubule and collecting duct?

Inserts aquaporin-2 into the luminal membrane, increasing water reabsorption.

How does free water clearance change in the presence of high ADH?

It becomes negative — water is reabsorbed without solutes, concentrating urine.

What distinguishes psychogenic polydipsia from diabetes insipidus during a water deprivation test?

In psychogenic polydipsia, urine osmolality increases as ADH acts normally. In DI, urine stays dilute.

What is the primary barrier preventing protein (e.g., albumin) filtration in the glomerulus?

The negatively charged components of the filtration barrier (basement membrane + slit diaphragm) repel negatively charged plasma proteins.

A defect in the NKCC2 transporter (e.g., Bartter syndrome) would most likely lead to which electrolyte disturbances?

Hypokalemia and hypocalcemia ## Footnote Due to impaired K⁺ recycling and loss of positive luminal voltage → ↓ Ca²⁺ and Mg²⁺ paracellular reabsorption.

What intrinsic renal mechanism helps maintain GFR despite changes in systemic blood pressure?

The myogenic reflex — afferent arterioles constrict or dilate in response to changes in pressure to stabilize GFR.

Which renal cells are primarily responsible for K⁺ reabsorption during potassium depletion?

Type A intercalated cells in the collecting duct, via the H⁺/K⁺ ATPase on the apical membrane.

How does aldosterone increase K⁺ secretion in the nephron?

Aldosterone: • ↑ ENaC (Na⁺ entry) • ↑ Na⁺/K⁺ ATPase (K⁺ uptake into cell) • ↑ ROMK channels (K⁺ secretion into lumen)

What is the main mechanism of Ca²⁺ reabsorption in the proximal tubule and thick ascending limb?

Passive paracellular reabsorption, driven by solvent drag and positive luminal voltage.

Why does volume contraction decrease urinary calcium excretion?

Volume contraction → ↑ Na⁺ and water reabsorption → Ca²⁺ follows via solvent drag → ↓ urinary Ca²⁺

How is Ca²⁺ reabsorbed in the distal tubule, and what regulates it?

Active transcellular transport, stimulated by PTH, and functionally independent of Na⁺ transport.

What is the mechanism of ion trapping in the urine?

Drugs become ionized in certain urine pH environments (acidic or alkaline). • Ionized = not reabsorbed → trapped in urine • This enhances renal excretion of weak acids or bases

What is the correct definition of clearance in pharmacokinetics?

Clearance is the volume of plasma completely cleared of drug per unit time, not the amount of drug in urine.

Why do weak bases accumulate in breast milk?

Because milk is slightly acidic, weak bases become ionized → cannot diffuse back → they are trapped in milk.

Flashcard Q: How is HCO₃⁻ reabsorbed in the kidney, and why is this process impaired during alkalosis?

A: • HCO₃⁻ is not directly reabsorbed; it must first react with secreted H⁺ in the tubular lumen • This forms H₂CO₃, which breaks into CO₂ + H₂O • CO₂ diffuses into the tubular cell, is reconverted into HCO₃⁻, and that new HCO₃⁻ is transported into the blood • In alkalosis, low CO₂ → low H⁺ secretion → less HCO₃⁻ reabsorbed → more is lost in urine → alkalosis is corrected