Introduction To Renal Physiology || Live Streaming скачать в хорошем качестве

Introduction To Renal Physiology || Live Streaming

📌𝗙𝗼𝗿 𝗡𝗼𝘁𝗲𝘀 𝗢𝗳 𝗧𝗵𝗶𝘀 𝗦𝗲𝘀𝘀𝗶𝗼𝗻 𝗝𝗼𝗶𝗻 𝗺𝘆 𝗧𝗲𝗹𝗲𝗴𝗿𝗮𝗺 𝗰𝗵𝗮𝗻𝗻𝗲𝗹 𝗵𝗲𝗿𝗲:-​ https://telegram.me/bhanuprakashdr​ 📌 𝐅𝐨𝐥𝐥𝐨𝐰 𝐨𝐧 𝐈𝐧𝐬𝐭𝐚𝐠𝐫𝐚𝐦:-   / drgbhanuprakash   📌𝗦𝘂𝗯𝘀𝗰𝗿𝗶𝗯𝗲 𝗧𝗼 𝗠𝘆 𝗠𝗮𝗶𝗹𝗶𝗻𝗴 𝗟𝗶𝘀𝘁:- https://linktr.ee/DrGBhanuprakash Renal Physiology - Part 2:-    • Renal Physiology - Part 2 || Live Streaming   Renal Physiology - Part 3:-    • Renal Physiology - Part 3 || Live Streaming   Introduction To Renal Physiology The renal system consists of the kidney, ureters, and the urethra. The overall function of the system filters approximately 200 liters of fluid a day from renal blood flow which allows for toxins, metabolic waste products, and excess ion to be excreted while keeping essential substances in the blood. The kidney regulates plasma osmolarity by modulating the amount of water, solutes, and electrolytes in the blood. It ensures long term acid-base balance and also produces erythropoietin which stimulates the production of red blood cell. It also produces renin for blood pressure regulation and carries out the conversion of vitamin D to its active form. Glomerular filtration is the initial process of urine production. It is a passive process in which hydrostatic pressure pushes fluid and solute through a membrane with no energy requirement. The filtration membrane has three layers: fenestrated endothelium of the glomerular capillaries which allows blood components except the cells to pass through; basement membrane, which is a negatively charged physical barrier that prevents proteins from permeating; and foot processes of podocytes of the glomerular capsule that creates more selective filtration. The outward and inward force from the capillaries determines how much water and solutes cross the filtration membrane. Hydrostatic pressure from the glomerular capillaries is the major filtration force with a pressure of 55mmHg. The other potential filtration force is the capsular space colloid osmotic pressure, but it is zero because proteins are not usually present within the capsular space. Then the capsular space hydrostatic pressure and the colloid osmotic pressure in glomerular capillaries negate the filtration force from the hydrostatic pressure in the glomerular capillaries, creating a net filtration pressure which plays a big role in the glomerular filtration rate (GFR). GFR is the volume of fluid filtered in a minute, and it depends on the net filtration pressure, the total available surface area for filtration, and filtration membrane permeability. The normal GFR is between 120 to 125ml/min. It is regulated intrinsically and extrinsically to maintain the GFR. The intrinsic control function by adjusting its own resistance to blood flow via a myogenic mechanism and a tubuloglomerular feedback mechanism. The myogenic mechanism maintains the GFR by constricting the afferent arteriole when the vascular smooth muscle stretches due to high blood pressure. It dilates the vascular smooth muscle when pressure is low within the afferent arteriole allowing more blood to flow through. Then the tubuloglomerular feedback mechanism function to maintain the GFR by sensing the amount of NaCl within the tubule. Macula densa cells sense NaCl around the ascending limb of the nephron loop.[5] When blood pressure is high, the GFR will also be high; this decreases the time needed for sodium reabsorption, and therefore sodium concentration is high in the tubule. The macula densa cell senses it and releases the vasoconstrictor chemicals which constricts the afferent arteriole and reduces blood flow. Then when the pressure is low, Na gets reabsorbed more causing its concentration in the tubule to be low, and macula densa do not release vasoconstricting molecules. The extrinsic control maintains the GFR and also maintains the systemic blood pressure via the sympathetic nervous system and the renin-angiotensin-aldosterone mechanism. When the volume of fluid in the extracellular decreases excessively, norepinephrine and epinephrine get released and causing vasoconstriction leading to a decrease in blood flow to the kidney and the level of GFR. Also, the renin-angiotensin-aldosterone axis gets activated by three means when the blood pressure drops. The first is the activation of the beta-1 adrenergic receptor, which causes the release of renin from the granular cells of the kidney. The second mechanism is the macula densa cells which sense low NaCl concentration during decreased blood flow to the kidney and trigger the granular cells to release renin. The third mechanism is the stretch receptor around the granular cells senses decreased tension during decreased blood flow to the kidney and also triggers the release of renin, therefore, regulating the glomerular filtration