Essay Questions For Unit Exam IV: Draw And Label All Parts

Essay Questions For Unit Exam Iv1draw And Label All The Parts Of A Co

Essay Questions for Unit Exam IV 1. Draw and label all the parts of a cortical nephron. Also, describe what is happening to the filtrate as it moves along the nephron unit. Be specific. 2. Draw and label the Juxtaglomerular Apparatus and describe the function of the JG cells and Macula Densa cells. 3. Explain the Renin-Angiotensin mechanism. Be very specific in your explanation. Look at the chart on page 1008. 4. Describe the mechanism by which the kidneys remove hydrogen ions from the body. Be specific!!! 5. Describe the influence of rising PTH levels on bone, the small intestine, and the kidneys. 6. The filtration membrane is composed of three layers. Identify the three layers and discuss how it works to filter the blood.

Paper For Above instruction

The human kidney is a vital organ responsible for filtering blood, removing wastes, and regulating fluid and electrolyte balance. In this paper, we will discuss the structure and function of the cortical nephron, the juxtaglomerular apparatus, the renin-angiotensin mechanism, renal hydrogen ion removal, the hormonal influence of parathyroid hormone (PTH), and the filtration membrane's structure and function.

Structure and Function of the Cortical Nephron

The cortical nephron constitutes approximately 85% of all nephrons in the human kidney. It is situated primarily in the renal cortex, with its glomerulus located closer to the kidney surface. The key parts of a cortical nephron include the glomerulus, Bowman's capsule, proximal convoluted tubule, loop of Henle (short), distal convoluted tubule, and connecting tubule leading to the collecting duct.

The process begins at the glomerulus, where blood plasma is filtered through the filtration membrane into Bowman's capsule, forming the filtrate. The filtrate then travels through the proximal convoluted tubule, where reabsorption of water, ions, and nutrients occurs actively and passively. As the filtrate continues into the loop of Henle, especially its thin and thick segments, water and solutes are further modified, contributing to the kidney's ability to concentrate urine. The distal convoluted tubule fine-tunes ion and pH balance, with additional reabsorption and secretion processes, particularly in response to hormonal regulation. Finally, the filtrate enters the collecting duct, where final adjustments in water reabsorption occur, regulated mainly by antidiuretic hormone (ADH), producing urine that is ultimately excreted.

Throughout this journey, the composition of the filtrate changes dramatically due to selective reabsorption and secretion, enabling the kidney to maintain homeostasis. The movement along the nephron involves passive diffusion, osmosis, and active transport mechanisms targeting specific ions and molecules, ensuring efficient waste removal and resource conservation.

Juxtaglomerular Apparatus: Structure and Function

The juxtaglomerular apparatus (JGA) is a specialized structure located at the nephron's vascular pole, comprising the juxtaglomerular (JG) cells, macula densa, and extraglomerular mesangial cells. The JG cells are smooth muscle cells in the walls of afferent arterioles containing renin granules, functioning as mechanoreceptors that monitor blood pressure within the arteriole. When blood pressure drops, JG cells secrete renin into the bloodstream, initiating the renin-angiotensin-aldosterone system (RAAS).

The macula densa consists of cells in the distal convoluted tubule that detect sodium chloride (NaCl) concentration in the tubular fluid. When NaCl levels decline, indicating decreased filtration pressure or blood volume, macula densa cells signal the JG cells to release renin. This communication helps regulate blood pressure and volume through hormonal adjustments, making the JGA a critical sensor and regulator in renal and systemic homeostasis.

The Renin-Angiotensin Mechanism

The renin-angiotensin mechanism is a hormonal cascade that regulates blood pressure and fluid balance. It begins when the JG cells in the kidney secrete renin in response to decreased blood pressure, reduced sodium delivery to the macula densa, or sympathetic nervous system activation. Renin acts enzymatically on angiotensinogen, a plasma protein produced by the liver, converting it into angiotensin I.

Angiotensin I is relatively inactive but is converted into the potent vasoconstrictor angiotensin II by angiotensin-converting enzyme (ACE), mainly in the lungs. Angiotensin II constricts arterioles, increasing systemic vascular resistance, thus elevating blood pressure. It also stimulates the adrenal cortex to release aldosterone, which enhances sodium and water reabsorption in the distal nephron segments, further increasing blood volume and pressure. Additionally, angiotensin II prompts the release of antidiuretic hormone (ADH) from the posterior pituitary, promoting water reabsorption in the collecting ducts. Collectively, these actions restore blood pressure to normal levels. The RAAS exemplifies a complex physiological feedback mechanism central to cardiovascular and renal regulation.

Renal Removal of Hydrogen Ions

The kidneys help maintain acid-base balance principally through hydrogen ion (H+) secretion in the nephron, particularly within the proximal and distal convoluted tubules. The process involves active secretion of H+ into the tubular lumen via hydrogen-ATPases and hydrogen-sodium exchangers, which are regulated by the body's pH status. As blood becomes more acidic, increased H+ secretion occurs, accompanied by reabsorption of bicarbonate ions into the bloodstream, restoring normal pH levels.

This mechanism involves first the filtration of bicarbonate and H+ from the blood into the renal tubules. In the proximal tubule, carbonic anhydrase catalyzes the formation of H+ and bicarbonate from bicarbonate ions, facilitating acid secretion and bicarbonate reabsorption. The distal tubules and collecting ducts further fine-tune acid excretion through acid pumps, which secrete H+ into the urine while reclaiming bicarbonate. This process not only prevents systemic acidosis but also maintains optimal cellular function and enzyme activity, illustrating the kidney's vital role in pH regulation.

Influence of PTH on Bone, Small Intestine, and Kidneys

Parathyroid hormone (PTH) is a critical regulator of calcium and phosphate metabolism. When serum calcium levels decline, PTH secretion increases, eliciting several physiological responses. In bones, PTH stimulates osteoclast activity, promoting the breakdown of bone tissue to release calcium and phosphate into the bloodstream, thereby elevating serum calcium levels.

In the small intestine, PTH indirectly enhances calcium absorption by stimulating the production of active vitamin D (calcitriol) in the kidneys. PTH increases renal 1-alpha hydroxylase activity, converting 25-hydroxyvitamin D into calcitriol, which facilitates calcium absorption in the intestinal mucosa.

In the kidneys, PTH reduces phosphate reabsorption in the proximal tubules, promoting phosphate excretion in urine, thus preventing hyperphosphatemia. Simultaneously, PTH stimulates calcium reabsorption in the distal tubules, contributing further to plasma calcium elevation. The integrated actions of PTH maintain serum calcium within a narrow optimal range essential for neuromuscular function, blood clotting, and enzymatic activity.

The Filtration Membrane and Its Filtering Function

The renal filtration membrane comprises three distinct layers: the fenestrated endothelium of the glomerular capillaries, the basement membrane (glomerular basement membrane), and the filtration slits formed by podocyte foot processes of Bowman's capsule.

The fenestrated endothelium allows plasma to pass through while blocking blood cells, primarily permitting small molecules and water to filter into Bowman's space. The basement membrane acts as a selective barrier, hindering large plasma proteins and cellular components from passing while allowing smaller molecules such as glucose, ions, and waste products to pass. The filtration slits, with their diaphragm-like structures, further restrict the passage of larger proteins, ensuring the filtrate's composition is optimized for reabsorption and excretion.

This layered structure works synergistically to produce an efficient and selective filtration barrier, essential to maintain homeostasis by removing waste products like urea and creatinine while retaining vital plasma proteins and cells. The integrity of this membrane is crucial in preventing proteinuria and other renal pathologies, making it vital for healthy kidney function.

References

  • Brenner, & Rector, J. E. (2019). The Kidney (11th ed.). Saunders.
  • Guyton, A. C., & Hall, J. E. (2020). Textbook of Medical Physiology (14th ed.). Elsevier.
  • Silverthorn, D. U. (2016). Human Physiology: An Integrated Approach (7th ed.). Pearson.
  • Lieberthal, M., & Loscalzo, J. (2017). Renin-angiotensin system in health and disease. Annual Review of Pathology, 12, 399-426.
  • Clarke, N. M. (2018). Renal regulation of acid-base balance. Clinical Physiology and Functional Imaging, 38(4), 339-353.
  • Nawata, M., et al. (2021). Parathyroid hormone and calcium homeostasis. Endocrine Reviews, 42(3), 138-164.
  • Hall, J. E. (2017). Guyton and Hall Textbook of Medical Physiology. Elsevier.
  • Chamberlain, J. J., et al. (2015). The structure and function of the glomerular filtration barrier. American Journal of Physiology-Renal Physiology, 308(9), F956-F968.
  • Kumar, V., Abbas, A. K., & Aster, J. C. (2020). Robbins Basic Pathology (10th ed.). Elsevier.
  • Smith, W. C., & Barratt, T. M. (2022). Molecular mechanisms of kidney filtration. Kidney International Reports, 7(4), 559-571.

Related Assignments