[PHYSIO] GI/Renal 2023/24 Flashcards
- Glucose absorption from the intestinal lumen is enhanced by which of the following substance?
a. magnesium
b. potassium
c. amino acid
d. sodium
(d) sodium.
Rationale:
Glucose absorption from the intestinal lumen is primarily facilitated through a process known as sodium-dependent glucose transport. This process involves the sodium-glucose linked transporter (SGLT1) located on the apical membrane of enterocytes in the small intestine.
Here’s how it works:
- Sodium Gradient: The sodium-potassium ATPase pump on the basolateral membrane of enterocytes actively transports sodium ions out of the cell and potassium ions into the cell. This creates a low intracellular sodium concentration.
- Sodium-Glucose Co-Transport: The SGLT1 transporter uses the sodium gradient to transport glucose against its concentration gradient from the intestinal lumen into the enterocyte. As sodium ions move down their concentration gradient into the cell, glucose is co-transported along with them.
- Facilitated Diffusion: Once inside the enterocyte, glucose exits the cell across the basolateral membrane via facilitated diffusion through the GLUT2 transporter into the bloodstream.
This mechanism ensures efficient absorption of glucose from the diet, making sodium a crucial factor in the process.
Magnesium, potassium, and amino acids do not play a direct role in the co-transport of glucose in this manner. While they have other important physiological roles, they do not enhance glucose absorption from the intestinal lumen as sodium does.
- Absorption of glucose involves:
A. sodium-glucose transport protein-1 (SGLT-1) in the apical membrane and glucose transporter-2 (GLUT-2) in the basolateral membrane
B. SGLT-1 in the apical membrane and GLUT-5 in the basolateral membrane
C. GLUT-5 in the apical membrane and GLUT-2 in the basolateral membrane
D. GLUT-2 in the apical membrane and SGLT-1 in the basolateral membrane
(a) sodium-glucose transport protein-1 (SGLT-1) in the apical membrane and glucose transporter-2 (GLUT-2) in the basolateral membrane.
Rationale:
- SGLT-1 in the Apical Membrane: The sodium-glucose linked transporter 1 (SGLT-1) is located in the apical membrane of enterocytes in the small intestine. This transporter uses the sodium gradient created by the sodium-potassium ATPase pump to co-transport glucose and sodium into the cell from the intestinal lumen. This process is essential for the active absorption of glucose.
- GLUT-2 in the Basolateral Membrane: Once inside the enterocyte, glucose needs to be transported into the bloodstream. This is achieved through facilitated diffusion using the glucose transporter 2 (GLUT-2), which is located in the basolateral membrane. GLUT-2 allows glucose to exit the enterocyte and enter the interstitial fluid, from where it can diffuse into the capillaries and be carried away by the bloodstream.
This dual mechanism ensures efficient and regulated absorption of glucose from the diet, maintaining proper blood glucose levels. The other options do not correctly pair the transport proteins involved in glucose absorption:
- Option B: GLUT-5 is involved in fructose transport, not glucose.
- Option C: GLUT-5 is in the apical membrane for fructose absorption.
- Option D: GLUT-2 is correctly placed in the basolateral membrane, but SGLT-1 is the transporter in the apical membrane for glucose absorption, not the basolateral membrane.
- A patient with tuberculosis undergoes removal of a big and long mass in his ileum. Which of the following will not be absorbed properly?
a. sodium
b. dipeptides
c. vitamin B12
d. calcium
(c) vitamin B12.
Rationale:
The ileum is the final part of the small intestine and is specifically responsible for the absorption of certain crucial nutrients, including vitamin B12 and bile salts.
- Vitamin B12: The absorption of vitamin B12 occurs in the terminal ileum. It requires intrinsic factor (a glycoprotein produced by the stomach) to be bound to it. The intrinsic factor-vitamin B12 complex is recognized by specific receptors in the ileum, facilitating its absorption. Removal of the ileum or significant damage to it can lead to malabsorption of vitamin B12, resulting in deficiencies such as pernicious anemia.
- Sodium: Sodium is absorbed throughout the small intestine and colon. The absorption is not specific to the ileum and thus would not be significantly impacted by the removal of a portion of the ileum.
- Dipeptides: Dipeptides and other small peptides are absorbed mainly in the duodenum and jejunum, where they are broken down into amino acids by peptidases on the brush border of enterocytes.
- Calcium: Calcium absorption primarily occurs in the duodenum and jejunum and is regulated by vitamin D. While the ileum can also absorb calcium, its removal would not have as significant an impact on calcium absorption as it would on vitamin B12 absorption.
Therefore, the removal of a large section of the ileum would specifically impair the absorption of vitamin B12.
- During normal salivary secretion, the tonicity of the salivary secretion in the oral cavity becomes:
A. hypotonic
B. hypertonic
C. isotonic
D. acidic
(a) hypotonic.
Rationale:
Saliva is initially isotonic when it is secreted by the acinar cells of the salivary glands. However, as it passes through the ductal system, its composition changes due to the reabsorption of sodium and chloride ions and the secretion of potassium and bicarbonate ions. This process reduces the osmolarity of the saliva, making it hypotonic by the time it reaches the oral cavity.
During normal salivary secretion:
- Isotonic secretion: Saliva starts as isotonic in the acini of the salivary glands.
- Modification in ducts: As saliva moves through the ducts, it undergoes modification. Sodium and chloride ions are reabsorbed, and potassium and bicarbonate ions are secreted.
- Final composition: The final saliva that is released into the oral cavity is hypotonic because more sodium and chloride ions are reabsorbed than potassium and bicarbonate ions are secreted.
This hypotonic nature of saliva helps to maintain the oral mucosa’s hydration and plays a role in the initial digestion of food and oral hygiene.
- The hormone that stimulates the parietal cells to secrete hydrochloric acid:
a. cholecystokinin
b. secretin
c. histamine
d. Motilin
(c) histamine.
Rationale:
Histamine is one of the key regulators of hydrochloric acid (HCl) secretion in the stomach. It stimulates the parietal cells to secrete HCl through the following mechanism:
- Histamine Release: Histamine is released by enterochromaffin-like (ECL) cells in the stomach.
- Receptor Binding: Histamine binds to H2 receptors on the parietal cells.
- Acid Secretion: This binding activates the parietal cells to secrete hydrochloric acid into the stomach lumen.
Other hormones mentioned:
- Cholecystokinin (a): This hormone is primarily involved in stimulating the digestion of fat and protein by causing the gallbladder to contract and release bile, and by stimulating the release of digestive enzymes from the pancreas. It does not directly stimulate acid secretion by parietal cells.
- Secretin (b): This hormone stimulates the pancreas to secrete bicarbonate-rich fluid, which neutralizes the acidic chyme entering the duodenum from the stomach. Secretin actually inhibits gastric acid secretion.
- Motilin (d): This hormone stimulates gastric and intestinal motility but does not directly affect the secretion of hydrochloric acid by parietal cells.
Therefore, histamine is the hormone that directly stimulates the parietal cells to secrete hydrochloric acid.
- When the pH of the stomach lumen falls below 3, the antrum of the stomach releases a peptide that acts locally to inhibit gastrin release. The peptide is:
a. enterogastrone
b. gastric inhibitory peptide (GIP)
c. secretin
d. somatostatin
(d) somatostatin.
Rationale:
Somatostatin is a peptide hormone that is released by D cells in the antrum of the stomach. It plays a critical role in the regulation of gastric acid secretion by inhibiting the release of gastrin.
When the pH of the stomach lumen falls below 3, the acidic environment stimulates the release of somatostatin. Somatostatin then acts locally to inhibit the secretion of gastrin by G cells. Gastrin is a hormone that stimulates the secretion of hydrochloric acid by parietal cells. By inhibiting gastrin, somatostatin helps to reduce further acid secretion and maintain the pH balance in the stomach.
Other options:
- Enterogastrone (a): This is a general term for hormones that inhibit gastric functions, but it is not a specific hormone.
- Gastric inhibitory peptide (GIP) (b): GIP is mainly involved in inhibiting gastric motility and stimulating insulin release, not directly inhibiting gastrin.
- Secretin (c): Secretin primarily stimulates the pancreas to release bicarbonate to neutralize the acid in the duodenum and inhibits gastric acid secretion indirectly, but it is not released in response to low pH in the stomach antrum.
Therefore, somatostatin is the peptide that directly inhibits gastrin release when the pH of the stomach lumen falls below 3.
- One of the following is TRUE about the migrating myoelectric complex (MMC):
A. It is similar to small intestinal pendular movements.
B. It occurs between meals and during fasting.
C. Its most intense phase is phase I.
D. It involves only movement, never secretions in the small intestine.
(b) It occurs between meals and during fasting.
Rationale:
The migrating myoelectric complex (MMC) is a pattern of electromechanical activity observed in the gastrointestinal (GI) tract during fasting. It serves to clear residual food, secretions, and debris from the stomach and small intestine in preparation for the next meal.
- Between meals and fasting: The MMC typically occurs between meals and during fasting periods, ensuring the GI tract is clean and empty for the next meal. This process prevents bacterial overgrowth and keeps the small intestine ready for the next intake of food.
Explanation of other options:
- (A) Similar to small intestinal pendular movements: Pendular movements are mixing movements that occur during digestion to mix chyme with digestive juices, whereas MMC is a series of contractions that occur during fasting.
- (C) Its most intense phase is phase I: The MMC has four phases. Phase III is the most intense phase, characterized by strong, rhythmic contractions that sweep through the intestine. Phase I is a quiescent period with no contractions.
- (D) Only movement, never secretions: While the MMC primarily involves motility, it also includes secretions. During the MMC, there are periods of increased secretion, particularly in phase III, which helps to clear out the intestinal lumen.
Therefore, the statement that is true about the MMC is that it occurs between meals and during fasting.
- When one swallows:
A. the lower esophageal sphincter contracts.
B. secondary peristalsis in the esophagus is always initiated by the voluntary act of swallowing.
C. pressure at the lower esophageal sphincter falls.
D. smooth muscle is the first to contract as peristalsis starts in the uppermost portion of the esophageal body.
(c) pressure at the lower esophageal sphincter falls.
Rationale:
When one swallows, the following physiological events occur:
- Relaxation of the Lower Esophageal Sphincter (LES): Swallowing initiates a series of coordinated muscle contractions known as peristalsis. One of the key events during swallowing is the relaxation of the lower esophageal sphincter (LES), which reduces the pressure at this sphincter. This relaxation allows the bolus of food to pass from the esophagus into the stomach. After the food passes, the LES contracts again to prevent the reflux of gastric contents back into the esophagus.
Explanation of other options:
- (A) The lower esophageal sphincter contracts: During swallowing, the LES actually relaxes to allow the passage of food into the stomach. It contracts after the food has passed to prevent reflux.
- (B) Secondary peristalsis in the esophagus is always initiated by the voluntary act of swallowing: Secondary peristalsis is initiated by the presence of residual food in the esophagus, not by the act of swallowing. It helps clear any remaining food that did not pass with the primary peristaltic wave.
- (D) Smooth muscle is the first to contract as peristalsis starts in the uppermost portion of the esophageal body: The upper third of the esophagus is composed of skeletal muscle, which is the first to contract during swallowing. The smooth muscle of the lower two-thirds of the esophagus contracts later as the peristaltic wave moves down.
Therefore, the correct statement about what happens when one swallows is that the pressure at the lower esophageal sphincter falls, allowing the bolus to pass into the stomach.
- Secondary esophageal peristalsis is stimulated by:
a. sleep
b. swallowing
c. esophageal distension
d. anesthesia
(c) esophageal distension.
Rationale:
Secondary esophageal peristalsis is a reflexive response to esophageal distension, which can occur when a bolus of food or liquid is stuck or moves slowly through the esophagus. This type of peristalsis is not initiated by the act of swallowing but is triggered by the presence of the bolus itself stretching the esophagus.
- Esophageal distension: When the esophagus is distended by residual food or other materials, mechanoreceptors in the esophageal wall are activated. This triggers a reflexive peristaltic wave (secondary peristalsis) to clear the esophagus of the obstruction.
Explanation of other options:
- (a) Sleep: Sleep does not directly stimulate secondary peristalsis.
- (b) Swallowing: Swallowing initiates primary peristalsis, not secondary peristalsis. Secondary peristalsis is specifically in response to esophageal distension.
- (d) Anesthesia: Anesthesia generally depresses reflexes, including peristaltic movements, rather than stimulating secondary peristalsis.
Therefore, esophageal distension is the stimulus for secondary esophageal peristalsis.
- Which of the following gastric secretion is responsible for protein digestion?
A. pepsin
B. pancreatic proteases
C. ptyalin
D. hydrochloric acid
(a) pepsin.
Rationale:
Pepsin is an enzyme secreted by the chief cells of the stomach in the form of its inactive precursor, pepsinogen. When pepsinogen is exposed to the acidic environment of the stomach (due to hydrochloric acid), it is converted into its active form, pepsin. Pepsin is responsible for breaking down proteins into smaller peptides, which is a crucial step in protein digestion.
Explanation of other options:
- (b) Pancreatic proteases: While pancreatic proteases (such as trypsin, chymotrypsin, and carboxypeptidase) are also involved in protein digestion, they are not gastric secretions. They are secreted by the pancreas into the small intestine.
- (c) Ptyalin: Also known as salivary amylase, ptyalin is an enzyme secreted in the saliva that begins the digestion of starches into maltose and dextrin. It is not involved in protein digestion.
- (d) Hydrochloric acid: Hydrochloric acid, secreted by the parietal cells of the stomach, creates an acidic environment which is necessary for the conversion of pepsinogen to pepsin and for the overall digestive process. However, it does not directly digest proteins; it provides the conditions for pepsin to function.
Therefore, pepsin is the specific gastric secretion responsible for protein digestion.
- Which of the following hormones tends to stimulate pancreatic secretion that is rich in bicarbonate?
a. somatostatin
b. secretin
c. CCK
d. gastrin
(b) secretin.
Rationale:
Secretin is a hormone released by the S cells of the duodenum in response to the presence of acidic chyme entering the small intestine from the stomach. The primary function of secretin is to stimulate the pancreas to secrete a bicarbonate-rich fluid. This bicarbonate helps to neutralize the acidic chyme, creating a more favorable pH environment for the action of digestive enzymes in the small intestine.
Explanation of other options:
- (a) Somatostatin: Somatostatin inhibits the secretion of several hormones and enzymes, including those from the pancreas, but it is not specifically involved in stimulating bicarbonate secretion.
- (c) CCK (Cholecystokinin): CCK stimulates the pancreas to release digestive enzymes and the gallbladder to release bile, but it does not primarily stimulate the secretion of bicarbonate.
- (d) Gastrin: Gastrin primarily stimulates the secretion of hydrochloric acid from the stomach’s parietal cells and has a minor role in stimulating pancreatic enzyme secretion, but it is not involved in the secretion of bicarbonate.
Therefore, secretin is the hormone that stimulates the pancreatic secretion that is rich in bicarbonate.
- Gastric emptying is:
A. accelerated by the presence of acid in the duodenum
B. faster for liquids than for solid particles
C. slower for isotonic liquids than for hypertonic liquids
D. increased as the caloric content of the nutrients in the duodenum increases
(b) faster for liquids than for solid particles.
Rationale:
Gastric emptying refers to the process by which the contents of the stomach are moved into the duodenum. Several factors influence the rate of gastric emptying, and the type of ingested material plays a significant role.
Explanation of other options:
(a) Accelerated by the presence of acid in the duodenum: The presence of acid in the duodenum actually slows down gastric emptying. This is part of a feedback mechanism to ensure that the acidic chyme is neutralized by bicarbonate secreted by the pancreas and bile before more chyme enters the duodenum.
(c) Slower for isotonic liquids than for hypertonic liquids: Isotonic liquids empty faster than hypertonic liquids. Hypertonic solutions slow gastric emptying because they draw water into the stomach to dilute the hypertonic solution, delaying the emptying process.
(d) Increased as the caloric content of the nutrients in the duodenum increases: The presence of high caloric content, particularly fats, in the duodenum slows down gastric emptying. This ensures proper digestion and absorption of nutrients by giving the intestine more time to process the chyme.
- Which of the following decreases gastric emptying?
a. cholecystokinin
b. very fatty chyme from the stomach
c. highly osmotic chyme from the stomach
d. All
(d) All.
Rationale:
Several factors can decrease gastric emptying, and all the options listed in the question contribute to slowing down this process:
- (a) Cholecystokinin (CCK): This hormone is released by the small intestine in response to the presence of fats and proteins. CCK slows down gastric emptying to allow more time for the digestion and absorption of nutrients in the small intestine.
- (c) Highly osmotic chyme from the stomach: Hyperosmotic solutions in the stomach slow down gastric emptying. This is because the body needs time to adjust the osmolarity of the chyme to a level that is suitable for the small intestine, preventing potential damage from highly concentrated substances.
- (b) Very fatty chyme from the stomach: Fats are one of the main factors that slow gastric emptying. The presence of fats in the stomach and duodenum triggers the release of hormones like CCK, which slow down the movement of chyme into the small intestine to allow sufficient time for digestion and emulsification of fats.
Therefore, all of these factors (CCK, highly osmotic chyme, and very fatty chyme) contribute to decreasing the rate of gastric emptying.
The following are effects of activation of the RAAS EXCEPT:
A. increased renal medullary blood flow
B. increased renal vascular resistance
C. stimulation of the zona glomerulosa
D. contraction of vascular smooth muscle
(a) increased renal medullary blood flow.
Rationale:
The renin-angiotensin-aldosterone system (RAAS) is a hormone system that regulates blood pressure and fluid balance. The activation of RAAS typically leads to several physiological effects, including:
- Increased renal vascular resistance: Angiotensin II, a key component of RAAS, causes vasoconstriction of the efferent arterioles in the kidneys, which increases renal vascular resistance and helps to maintain glomerular filtration rate (GFR) despite decreased renal perfusion.
- Stimulation of the zona glomerulosa: Angiotensin II stimulates the adrenal cortex, specifically the zona glomerulosa, to secrete aldosterone. Aldosterone increases sodium and water reabsorption in the kidneys, contributing to increased blood volume and blood pressure.
- Contraction of vascular smooth muscle: Angiotensin II causes widespread vasoconstriction by acting on vascular smooth muscle, increasing systemic vascular resistance and thereby raising blood pressure.
Increased renal medullary blood flow is not a typical effect of RAAS activation. In fact, the vasoconstrictive effects of angiotensin II tend to reduce blood flow in certain renal areas, including the medulla, to prioritize maintaining GFR. Thus, the effect of increased renal medullary blood flow is inconsistent with the typical actions of RAAS activation.
The highest percentage of glomerular filtrate reabsorption occurs in:
a. Bowman’s capsule
b. proximal tubule
c. thick ascending limb of loop of Henle
d. distal tubule
(b) proximal tubule.
Rationale:
The proximal tubule is the site where the highest percentage of glomerular filtrate reabsorption occurs. Approximately 65-70% of the filtered load of water, sodium, chloride, potassium, bicarbonate, and other solutes is reabsorbed here. The proximal tubule is highly efficient in reabsorbing most of the essential nutrients, electrolytes, and water back into the bloodstream.
Explanation of other options:
- (a) Bowman’s capsule: This is the site of filtration, not reabsorption. The filtrate is formed here from the blood but no reabsorption occurs in Bowman’s capsule.
- (c) Thick ascending limb of loop of Henle: This segment reabsorbs significant amounts of sodium, potassium, and chloride, but it does not reabsorb as much as the proximal tubule.
- (d) Distal tubule: The distal tubule reabsorbs a smaller percentage of the filtrate compared to the proximal tubule. It plays a role in fine-tuning the reabsorption of ions and water, influenced by hormones such as aldosterone and antidiuretic hormone (ADH).
Therefore, the proximal tubule is the primary site of reabsorption in the nephron, handling the bulk of the filtrate reabsorption.
According to the tubuloglomerular feedback theory, an increase in the flow of tubular fluid to the macula densa will result in:
A. a decrease in the glomerular filtration rate
B. an increase in renal blood flow
C. an increase in renin secretion
D. an increase in proximal tubule solute and water reabsorption
(a) a decrease in the glomerular filtration rate.
Rationale:
The tubuloglomerular feedback mechanism involves the macula densa cells, which are part of the juxtaglomerular apparatus in the kidney. These cells sense the flow rate and sodium chloride concentration of the tubular fluid in the distal tubule. When there is an increase in the flow of tubular fluid to the macula densa, the following occurs:
- Detection by Macula Densa: The macula densa detects the increased flow rate and/or elevated sodium chloride concentration.
- Signal Transmission: The macula densa sends signals to the afferent arteriole.
- Constriction of Afferent Arteriole: These signals cause the afferent arteriole to constrict, reducing blood flow into the glomerulus.
- Reduction in GFR: The decreased blood flow results in a reduction in the glomerular filtration rate (GFR), thereby decreasing the amount of filtrate formed.
Explanation of other options:
- (b) An increase in renal blood flow: Tubuloglomerular feedback typically results in decreased renal blood flow due to the constriction of the afferent arteriole.
- (c) An increase in renin secretion: Increased tubular flow detected by the macula densa actually inhibits renin secretion, which is contrary to the answer choice.
- (d) An increase in proximal tubule solute and water reabsorption: Tubuloglomerular feedback primarily affects the GFR and does not directly influence reabsorption processes in the proximal tubule.
Thus, an increase in the flow of tubular fluid to the macula densa results in a decrease in the glomerular filtration rate as part of the tubuloglomerular feedback mechanism.
Which of the following is responsible for setting up the hyperosmolarity of the renal medulla?
A. Na/H antiport in proximal convoluted tubule
B. differential permeability of the descending and ascending limbs of loop of Henle
C. secretion of urea
D. maximal reabsorption of ions in the proximal convoluted tubule
(b) differential permeability of the descending and ascending limbs of the loop of Henle.
Rationale:
The hyperosmolarity of the renal medulla is primarily established by the countercurrent multiplication mechanism, which relies on the differential permeability of the descending and ascending limbs of the loop of Henle.
- Descending Limb: This limb is permeable to water but not to solutes. As the filtrate descends, water is reabsorbed into the medullary interstitium, which is increasingly hyperosmotic, causing the filtrate to become more concentrated.
- Ascending Limb: This limb is impermeable to water but actively reabsorbs sodium, potassium, and chloride ions into the interstitium. This active transport of solutes without water creates a hypoosmotic filtrate while increasing the osmolarity of the medullary interstitium.
This countercurrent mechanism creates and maintains a gradient of increasing osmolarity in the medulla, which is crucial for the kidney’s ability to concentrate urine.
Explanation of other options:
- (a) Na+-H+ antiport in proximal convoluted tubule: While important for acid-base balance and sodium reabsorption, this mechanism does not establish the hyperosmolarity of the renal medulla.
- (c) Secretion of urea: Urea contributes to the osmotic gradient in the medulla, but it is not the primary mechanism for setting up the hyperosmolarity. Urea recycling in the inner medulla enhances the gradient but works in conjunction with the loop of Henle’s differential permeability.
- (d) Maximal reabsorption of ions in the proximal convoluted tubule: While the proximal tubule reabsorbs a significant amount of solutes and water, it does not contribute directly to the medullary osmotic gradient, as its function is more focused on bulk reabsorption.
Thus, the differential permeability of the descending and ascending limbs of the loop of Henle is the key factor responsible for setting up the hyperosmolarity of the renal medulla.
The independence of renal blood flow from mean systemic arterial pressure is termed:
a. glomerulo-tubular balance
b. distal tubulo-glomerular feedback
c. autoregulation
d. pressure diuresis
(c) autoregulation.
Rationale:
Autoregulation refers to the kidney’s ability to maintain a relatively constant renal blood flow (RBF) and glomerular filtration rate (GFR) despite changes in mean systemic arterial pressure. This is achieved through two main mechanisms:
- Myogenic Mechanism: When there is an increase in blood pressure, the afferent arterioles constrict to prevent an increase in GFR. Conversely, when there is a decrease in blood pressure, the afferent arterioles dilate to maintain GFR.
- Tubuloglomerular Feedback: The macula densa cells of the juxtaglomerular apparatus sense changes in the flow and sodium chloride concentration in the distal tubule. Based on these changes, the afferent arterioles either constrict or dilate to stabilize GFR.
Explanation of other options:
- (a) Glomerulo-tubular balance: This refers to the matching of reabsorption rates in the proximal tubule to the rate of filtration. It is a mechanism to balance the filtration and reabsorption processes, not directly related to maintaining RBF independent of systemic pressure.
- (b) Distal tubulo-glomerulo feedback: While similar to tubuloglomerular feedback, this term is not commonly used. Tubuloglomerular feedback is a component of autoregulation.
- (d) Pressure diuresis: This is the process by which increased blood pressure leads to increased urine production. It is a broader systemic response to increased blood pressure and is not specific to the intrinsic ability of the kidneys to regulate their own blood flow and GFR.
Therefore, the independence of renal blood flow from mean systemic arterial pressure is termed autoregulation.
The urine volume flow rate times the urine concentration of a substance is equal to its rate of:
a. net tubular secretion
b. net tubular reabsorption
c. excretion
d. filtration
(b) excretion.
Rationale:
The rate of excretion of a substance in the urine can be calculated by multiplying the urine flow rate (V) by the urine concentration of the substance (U(_x)). This relationship is represented by the formula:
[ \text{Rate of excretion} = V \times U_x ]
where:
- ( V ) is the urine volume flow rate (usually in mL/min)
- ( U_x ) is the concentration of the substance in the urine (usually in mg/mL or mmol/L)
This formula gives the amount of the substance excreted in the urine per unit of time.
Explanation of other options:
- (a) Net tubular secretion: This refers to the movement of substances from the peritubular capillaries into the tubular fluid, but it is not directly calculated by multiplying urine flow rate by urine concentration.
- (c) Net tubular reabsorption: This refers to the movement of substances from the tubular fluid back into the peritubular capillaries. The calculation of net reabsorption involves comparing the amount filtered at the glomerulus to the amount excreted in the urine, not directly from urine concentration and flow rate.
- (d) Filtration: The filtration rate of a substance is usually described by the glomerular filtration rate (GFR) multiplied by the plasma concentration of the substance (P(_x)). It is not directly given by the product of urine flow rate and urine concentration.
Therefore, the urine volume flow rate times the urine concentration of a substance is equal to its rate of excretion.
Constriction of the renal afferent glomerular arterioles tends to ____ glomerular capillary hydrostatic pressure and _______ renal blood flow.
a. decrease, increase
b. increase, decrease
c. increase, increase
d. decrease, decrease
(d) decrease, decrease.
Rationale:
Constriction of the renal afferent arterioles reduces the blood flow into the glomerulus. This leads to:
- Decreased glomerular capillary hydrostatic pressure: With less blood entering the glomerulus due to afferent arteriole constriction, the pressure within the glomerular capillaries decreases. This results in a lower glomerular filtration rate (GFR).
- Decreased renal blood flow: Constriction of the afferent arterioles directly reduces the overall blood flow to the kidneys, further decreasing the amount of blood available for filtration and perfusion of the renal tissues.
Therefore, the constriction of the renal afferent arterioles results in both a decrease in glomerular capillary hydrostatic pressure and a decrease in renal blood flow.
Which of the following structures is a barrier to the filtration of proteins across the glomerulus?
a. capillary endothelial cells
b. basement membrane
c. parietal epithelial cells
d. mesangial cells
(b) basement membrane.
Rationale:
The glomerular filtration barrier consists of three layers:
1. Capillary Endothelial Cells: These cells have fenestrations (pores) that allow most substances in the blood to pass through but not large proteins.
2. Basement Membrane: This layer is the primary barrier to protein filtration. It contains a meshwork of negatively charged proteins and glycoproteins that repel negatively charged molecules, such as plasma proteins, preventing their passage.
3. Podocytes (Visceral Epithelial Cells): These cells have foot processes that create slit diaphragms, providing an additional barrier to the passage of proteins and large molecules.
Explanation of other options:
- (a) Capillary Endothelial Cells: While they form part of the filtration barrier, their fenestrations do not provide significant resistance to the passage of proteins compared to the basement membrane.
- (c) Parietal Epithelial Cells: These cells line Bowman’s capsule and are not directly involved in the filtration barrier.
- (d) Mesangial Cells: These cells provide structural support and secrete extracellular matrix, but they are not a part of the filtration barrier preventing protein passage.
Therefore, the basement membrane is the primary barrier to the filtration of proteins across the glomerulus.
Because of autoregulation by the myogenic theory mechanism, an increase in the renal perfusion pressure will lead to:
A. a reduction in the intravascular hydrostatic pressure
B. a decrease in the afferent arteriolar wall tension
C. a decrease in the transmural pressure in the afferent arteriole
D. an increase in the afferent arteriolar radius followed by afferent arteriolar vasoconstriction
(d) an increase in the afferent arteriolar radius followed by afferent arteriolar vasoconstriction.
Rationale:
The myogenic mechanism is a form of autoregulation that helps maintain stable renal blood flow and glomerular filtration rate (GFR) despite changes in systemic blood pressure. Here’s how it works:
- Initial Increase in Perfusion Pressure: When there is an increase in renal perfusion pressure, the walls of the afferent arterioles initially stretch.
- Myogenic Response: This stretch is detected by the smooth muscle cells in the arteriolar walls. In response to the increased tension, these muscle cells contract, leading to vasoconstriction of the afferent arteriole.
- Resulting Effect: The vasoconstriction reduces the diameter of the afferent arteriole, which helps to reduce the renal blood flow back to a more stable level, thereby maintaining a relatively constant GFR.
Explanation of other options:
- (a) A reduction in the intravascular hydrostatic pressure: The intravascular hydrostatic pressure would initially increase with increased perfusion pressure before autoregulatory mechanisms take effect to counteract this.
- (b) A decrease in the afferent arteriolar wall tension: There is actually an initial increase in wall tension due to the stretch caused by increased perfusion pressure.
- (c) A decrease in the transmural pressure in the afferent arteriole: Transmural pressure (the difference between intravascular and extravascular pressure) initially increases due to increased perfusion pressure, not decreases.
Therefore, an increase in the afferent arteriolar radius followed by afferent arteriolar vasoconstriction is the correct answer, as it describes the initial stretching and subsequent myogenic response leading to vasoconstriction.
This is the first step in urine formation
A. Tubular reabsorption
B. Glomerular filtration
C. Tubular secretion
D. Tubular filtration
B. Glomerular filtration
Rationale: The first step in urine formation is glomerular filtration, where blood plasma is filtered in the glomeruli of the kidneys to form the filtrate that will eventually become urine.
Which of the following events occur when GFR is high?
A. Increased NaCl reabsorption in PCT
B. Uptake of NaCl by the macula densa
C. Afferent arteriolar dilation due to increased ATP and adenosine
D. Renin release is high
B. Uptake of NaCl by the macula densa
Rationale: When GFR is high, there is increased delivery of NaCl to the distal tubule, where the macula densa cells detect the high NaCl concentration and initiate tubuloglomerular feedback to decrease GFR.
