Renal Physiology Practice Questions

Q: Deficiency of vasopressin results in:

Inability of the kidney to concentrate urine. ***Inability of the kidney to concentrate urine*** - Vasopressin, also known as **Antidiuretic Hormone (ADH)**, acts on the renal collecting ducts to increase water reabsorption. - A deficiency in vasopressin means the kidneys cannot reabsorb water effectively, leading to the production of large volumes of dilute urine, which is an inability to concentrate urine. *Increased water loss* - While there is **increased water loss** from the body due to a lack of reabsorption, this is a consequence of the primary physiological defect, which is the kidney's inability to concentrate urine. - The direct effect of vasopressin deficiency is on the kidney's concentrating mechanism. *Increased urine output* - **Increased urine output**, or polyuria, is a clinical manifestation of the kidney's inability to concentrate urine due to vasopressin deficiency. - It describes the symptom rather than the underlying physiological impairment at the renal tubules. *Hyponatremia* - **Hyponatremia** (low sodium) typically occurs with an excess of ADH (like in SIADH), leading to water retention and dilutional hyponatremia. - In vasopressin deficiency (diabetes insipidus), patients are more prone to **hypernatremia** due to excessive water loss.

Q: All of the following are true about the action of ADH, except:

Increased secretion when plasma osmolality is low. ***Increased secretion when plasma osmolality is low*** - **Antidiuretic hormone (ADH)** secretion is *inhibited* when plasma osmolality is low. - ADH is secreted to conserve water and *increase* plasma osmolality when it is too high, or plasma volume is too low. - Normal osmolality range is 280-290 mOsm/kg; ADH secretion increases above this threshold. *Acts on collecting ducts and increases water permeability* - This statement is true; ADH binds to **V2 receptors** on the principal cells of the collecting ducts. - This binding leads to the insertion of **aquaporin-2 channels** into the apical membrane, increasing water reabsorption. *Secreted by neurosecretion from posterior pituitary* - This statement is true; ADH is synthesized in the **hypothalamus** (supraoptic and paraventricular nuclei) and transported down nerve axons. - It is then stored in and released from the **posterior pituitary gland**, a process known as neurosecretion. *Post-operative increase in secretion* - This statement is true; surgical stress, pain, and common postoperative medications (e.g., narcotics) can stimulate ADH release. - This can lead to **hyponatremia** and fluid retention in the postoperative period due to excessive free water reabsorption.

Q: What does aquaporin deficiency cause?

Nephrogenic diabetes insipidus. ***Nephrogenic diabetes insipidus*** - Aquaporins, specifically **aquaporin-2**, are crucial for **water reabsorption** in the renal collecting ducts in response to ADH. - A deficiency or dysfunction of aquaporins leads to the kidneys being unable to concentrate urine, resulting in **excessive dilute urine production** and **polydipsia**, characteristic of nephrogenic diabetes insipidus. *Liddle syndrome* - This is an **autosomal dominant** disorder caused by a **gain-of-function mutation** in the **epithelial sodium channel (ENaC)**, leading to increased sodium reabsorption and hypertension. - It does not involve aquaporin deficiency but rather an overactive sodium channel. *Bartter syndrome* - Characterized by mutations in the **Na-K-2Cl cotransporter (NKCC2)** in the thick ascending limb of the loop of Henle, leading to impaired reabsorption of sodium, potassium, and chloride. - It results in **hypokalemia**, **metabolic alkalosis**, and **hypotension**, and is not directly caused by aquaporin deficiency. *Gitelman syndrome* - Caused by mutations in the **thiazide-sensitive Na–Cl cotransporter (NCC)** in the distal convoluted tubule, impairing sodium and chloride reabsorption. - It presents with symptoms similar to thiazide diuretic use, including **hypokalemia**, **hypomagnesemia**, and **metabolic alkalosis**, and is distinct from aquaporin-related disorders.

Q: Calculate net filtration pressure with the following data: PGC = 42 mm Hg, πGC = 12 mm Hg, PBC = 16 mm Hg. Assume that no proteins were filtered.

14 mm Hg. ***14 mm Hg*** - The **net filtration pressure (NFP)** is calculated using the formula: **NFP = (PGC - PBC) - πGC**. - Plugging in the given values: (42 mmHg - 16 mmHg) - 12 mmHg = 26 mmHg - 12 mmHg = **14 mmHg**. *28 mm Hg* - This answer likely results from an incorrect application of the NFP formula, such as adding the oncotic pressure instead of subtracting it, or miscalculating the difference between hydrostatic pressures. - For example, if both hydrostatic and oncotic pressures were added (42 + 12 + 16), it would yield a much higher number, or if the subtraction was done incorrectly. *Data not sufficient* - All necessary variables for calculating the NFP are provided: **glomerular hydrostatic pressure (PGC)**, **glomerular oncotic pressure (πGC)**, and **Bowman's capsule hydrostatic pressure (PBC)**. - The assumption that "no proteins were filtered" simplifies the calculation, confirming that sufficient data is available. *34 mm Hg* - This result would occur if the oncotic pressure in Bowman's capsule (πBC) was incorrectly considered, or if a different formulation of the NFP calculation was used. - Given that **πBC is assumed to be zero** (as no proteins are filtered into Bowman's capsule), any calculation that leads to 34 mmHg is likely based on an error in applying the formula, such as adding **πGC** instead of subtracting it from the hydrostatic pressure difference.

Q: GFR is increased by all except?

Renal stone in ureter. ***Renal stone in ureter*** - A renal stone in the ureter causes **post-renal obstruction**, leading to a buildup of pressure in the Bowman's capsule, which in turn **reduces GFR**. - **Obstruction** impedes urine outflow, thereby increasing **hydrostatic pressure** in the tubular system and opposing filtration. *Efferent arteriole constriction* - **Constriction of the efferent arteriole** increases the **hydrostatic pressure** within the glomerulus, which promotes an increase in GFR. - This constriction retains blood in the glomerulus, thereby increasing the **filtration pressure**. *Increased renal blood flow* - An **increase in renal blood flow** elevates the **glomerular hydrostatic pressure** and increases the amount of plasma available for filtration, leading to an **increased GFR**. - A higher flow rate also helps to maintain a more constant **glomerular capillary oncotic pressure**, preventing early filtration equilibrium. *Decreased oncotic pressure* - **Decreased oncotic pressure** in the glomerular capillaries (e.g., due to hypoproteinemia) reduces the osmotic force opposing filtration. - This reduction in opposing force allows for a net increase in the **filtration pressure**, thereby **increasing GFR**.

Q: Which of the following is not an effect of efferent arteriole constriction:

Decreased GFR. ***Decreased GFR*** - **Efferent arteriole constriction** typically *increases* GFR, not decreases it - Constriction raises **glomerular hydrostatic pressure** (PGC) by increasing resistance to outflow, which *enhances* the driving force for filtration - The initial and predominant effect is an **increase in GFR**, making "Decreased GFR" NOT a typical effect - Only with *severe* prolonged constriction might GFR eventually fall due to markedly reduced renal blood flow and extreme protein concentration *Increased glomerular hydrostatic pressure* - This IS an effect of efferent arteriole constriction - Constriction increases resistance to blood leaving the glomerulus, causing blood to "back up" and **raising hydrostatic pressure** in glomerular capillaries - This elevated pressure directly increases the filtration force *Decreased blood flow in peritubular vessels* - This IS an effect of efferent arteriole constriction - Blood exits the glomerulus through the efferent arteriole to reach peritubular capillaries - Constriction restricts this outflow, resulting in **reduced blood flow** to downstream peritubular vessels *Increased oncotic pressure in peritubular vessels* - This IS an effect of efferent arteriole constriction - As filtration increases due to higher glomerular pressure, plasma proteins (which cannot be filtered) become more concentrated in the blood - This concentrated blood flows into peritubular capillaries, resulting in **elevated oncotic pressure** that favors reabsorption

Q: Which of the following is the diluting segment of kidney?

Ascending thick loop of Henle. ***Ascending thick loop of Henle*** - The **thick ascending limb of the loop of Henle** is known as the *diluting segment* because it actively reabsorbs **solutes (Na+, K+, Cl-)** but is impermeable to **water**. - This action leads to a decrease in the osmolality of the tubular fluid, effectively *diluting* it entering the distal tubule. *Collecting duct* - The collecting duct is primarily involved in **water reabsorption** under the influence of **ADH**, which can concentrate the urine. - While it can reabsorb some solutes, its main role is to regulate **final urine concentration**. *Descending loop of Henle* - The descending loop of Henle is highly permeable to **water** but relatively impermeable to **solutes**. - As water leaves this segment, the tubular fluid becomes more **concentrated**, not diluted. *PCT* - The **proximal convoluted tubule (PCT)** reabsorbs a large percentage of both **water and solutes** in an isotonic manner. - Although it reduces the volume of filtrate, it does not significantly change its **osmolality** (i.e., it doesn't dilute the fluid).

Q: True about countercurrent multiplier system in the kidney except:

Involves collecting duct. ***Involves collecting duct*** - The **collecting duct** is *not* part of the countercurrent *multiplier* system but rather the countercurrent *exchange* system, - The collecting duct is the target of **ADH** where fine-tuning of water reabsorption occurs, influenced by the medullary osmotic gradient generated by the multiplier. *Occurs in Loop of Henle* - The **Loop of Henle**, specifically the ascending and descending limbs, is the anatomical site where the **countercurrent multiplier** system operates. - This structure's unique hairpin turn and differing permeabilities are crucial for establishing the osmotic gradient. *Requires NaCl transport* - Active transport of **NaCl** in the thick ascending limb of the Loop of Henle is the *driving force* for the countercurrent multiplication process. - This reabsorption of solutes without water permeability creates the initial osmotic gradient. *Creates hyperosmotic medulla* - The primary function of the **countercurrent multiplier** system is to establish and maintain a **hyperosmotic medullary interstitium**. - This high osmolarity is essential for subsequent water reabsorption from the collecting ducts, allowing for the concentration of urine.

Q: Where is the main site of sodium reabsorption in the nephron?

Proximal tubule. ***Proximal tubule*** - The **proximal tubule** reabsorbs approximately **65-70% of filtered sodium**, making it the primary site of sodium reabsorption. - This high rate of reabsorption is crucial for maintaining overall **fluid and electrolyte balance**. *Collecting duct* - The **collecting duct** reabsorbs a smaller, regulated amount of sodium, typically **2-5%**, under hormonal control by **aldosterone**. - Its main roles include **fine-tuning** water and electrolyte balance. *Loop of Henle* - The **loop of Henle** reabsorbs approximately **25%** of filtered sodium, primarily in its **thick ascending limb**. - Its main function is to create a **medullary osmotic gradient** for concentrated urine. *Distal tubule* - The **distal tubule** reabsorbs about **5%** of filtered sodium, which is also influenced by hormones like **aldosterone**. - It plays a role in **acid-base balance** and diluting or concentrating urine.

Q: A 40-year-old woman with chronic kidney disease presents with hyperkalemia. Which of the following represents the immediate effect of hyperkalemia on membrane physiology?

Depolarization of resting membrane potential. ***Depolarization of resting membrane potential*** - Hyperkalemia leads to an increase in extracellular potassium, which **decreases the transmembrane potassium gradient**. - This shifts the **resting membrane potential (RMP) toward zero (less negative)**, representing **depolarization** of the cell membrane. - This is the **immediate and direct effect** of elevated extracellular potassium on all excitable cells, based on the **Nernst equation for potassium**. *Prolonged action potential duration* - Hyperkalemia typically **shortens the action potential duration** in most excitable cells, not prolongs it. - This is primarily due to the increased potassium conductance, which hastens **repolarization**. *Decreased skeletal muscle contractility* - While this is a **clinical consequence** of hyperkalemia, it is a **secondary effect** resulting from persistent depolarization. - The initial membrane depolarization eventually leads to **sodium channel inactivation**, causing muscle weakness. - This is not the immediate membrane effect but rather a downstream consequence. *Decreased cardiac excitability* - This is also a **clinical consequence** of severe or prolonged hyperkalemia, not the immediate membrane effect. - The initial depolarization eventually leads to **persistent sodium channel inactivation**, depressing myocardial excitability and conduction. - This manifests as **bradycardia, widened QRS complexes, and potentially asystole**.

Question 1

Deficiency of vasopressin results in:

Accepted Answer

Inability of the kidney to concentrate urine

Answer

Increased water loss

Answer

Increased urine output

Answer

Hyponatremia

Question 2

All of the following are true about the action of ADH, except:

Accepted Answer

Increased secretion when plasma osmolality is low

Answer

Acts on collecting ducts and increases water permeability

Answer

Secreted by neurosecretion from posterior pituitary

Answer

Post-operative increase in secretion

Question 3

What does aquaporin deficiency cause?

Accepted Answer

Nephrogenic diabetes insipidus

Answer

Liddle syndrome

Answer

Bartter syndrome

Answer

Gitelman syndrome

Question 4

Calculate net filtration pressure with the following data: PGC = 42 mm Hg, πGC = 12 mm Hg, PBC = 16 mm Hg. Assume that no proteins were filtered.

Accepted Answer

14 mm Hg

Answer

28 mm Hg

Answer

Data not sufficient

Answer

34 mm Hg

Question 5

GFR is increased by all except?

Accepted Answer

Renal stone in ureter

Answer

Efferent arteriole constriction

Answer

Increased renal blood flow

Answer

Decreased oncotic pressure

Question 6

Which of the following is not an effect of efferent arteriole constriction:

Accepted Answer

Decreased GFR

Answer

Increased glomerular hydrostatic pressure

Answer

Decreased blood flow in peritubular vessels

Answer

Increased oncotic pressure in peritubular vessels

Question 7

Which of the following is the diluting segment of kidney?

Accepted Answer

Ascending thick loop of Henle

Answer

Collecting duct

Answer

Descending loop of Henle

Answer

PCT

Question 8

True about countercurrent multiplier system in the kidney except:

Accepted Answer

Involves collecting duct

Answer

Occurs in Loop of Henle

Answer

Requires NaCl transport

Answer

Creates hyperosmotic medulla

Question 9

Where is the main site of sodium reabsorption in the nephron?

Accepted Answer

Proximal tubule

Answer

Collecting duct

Answer

Loop of Henle

Answer

Distal tubule

Question 10

A 40-year-old woman with chronic kidney disease presents with hyperkalemia. Which of the following represents the immediate effect of hyperkalemia on membrane physiology?

Accepted Answer

Depolarization of resting membrane potential

Answer

Prolonged action potential duration

Answer

Decreased skeletal muscle contractility

Answer

Decreased cardiac excitability

Renal Physiology — MCQs

Renal Physiology — MCQs

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