Urinary System Past Paper (PDF)

 Two Questions in Two Minutes Anatomy of the kidneys Gross Anatomy Microanatomy The Process of Urine Formation Glomerular Filtration Tubular Reabsorption and Secretion The Renin Angiotensin Aldosterone System Regulation of Glomerular Filtration Intrinsic Control...

 Two Questions in Two Minutes Anatomy of the kidneys Gross Anatomy Microanatomy The Process of Urine Formation Glomerular Filtration Tubular Reabsorption and Secretion The Renin Angiotensin Aldosterone System Regulation of Glomerular Filtration Intrinsic Control More Questions!  The Cardiovascular System - 19% of assessment The Respiratory System - 17% of assessment The Digestive System - 16% of assessment The Urinary System - 14% of assessment The Reproductive System - 17% of assessment The Immune System - 17% of assessment The primary structure found within the medulla is the ________. a.loop of Henle b.minor calyces c.portal system d.ureter The right kidney is slightly lower because ________. a.it is displaced by the liver b.it is displaced by the heart c.it is slightly smaller d.it needs protection of the lower ribs The primary structure found within the medulla is the ________. a.loop of Henle b.minor calyces c.portal system d.ureter The right kidney is slightly lower because ________. a.it is displaced by the liver b.it is displaced by the heart c.it is slightly smaller d.it needs protection of the lower ribs Location, location, location… Liver pointing this way. Posterior View Transverse Plane The kidneys lie on either side of the spine (about T12 to L3) in the retroperitoneal space between the parietal peritoneum and the posterior abdominal wall.  Renal hilum (collective term for this recessed area where nerves, blood vessels, and the ureter passes) Renal calyces (singular: calyx): are conduits to the renal pelvis. Collecting ducts of pyramids empty into minor calyces. 4-5 minor calyces form a single major calyx.         Now we have our glomerular filtrate!   Apical Side Basal Side (facing lumen) H2O Peritubular capillary H2O Na+ Glucose In the lumen of the PCT, HCO 3– combines with hydrogen ions to form carbonic acid (H2CO 3). This is enzymatically catalyzed into CO 2 and water, which diffuse across the apical membrane into the cell.    Regulation of Reabsorption and Secretion DON’T PANIC! It’s easy to get overwhelmed, but remember what the RAAS system ultimately does: Regulates blood pressure by controlling fluid and electrolyte balance. Blood pressure falls RAAS Flow Chart (you’re dehydrated) (slightly less panic inducing) Increase in blood pressure Kidneys release renin Renin cleaves Vasoconstriction angiotensinogen to create angiotensin I Release of Reabsorption of Aldosterone sodium and water ACE cleaves angiotensin I to create angiotensin Reabsorption of Release of ADH II water  ▪ The Actors ▪ The Audience(Targets) ▪ Adrenal ▪ Kidneys ▪ Renin Glands (which become a producer of aldosterone) ▪ Angiotensin Converting ▪ Lungs Enzyme ▪ Blood (ACE) Vessels ▪ Angiotensinogen performing as: ▪ Liver ▪ Pituitary Gland ▪ Angiotensin I (which becomes a producer of ADH) ▪ Angiotensin II  The Renin-Angiotensin-Aldosterone System (RAAS) RENIN ▪ The kidneys produce renin in response to a decrease in renal perfusion (a drop in blood pressure). ▪ Basically, the macula densa is like an old Jedi master. ▪ Specifically, macula densa stimulates the juxtaglomerular cells (found near the nephrons’ glomeruli) release renin, and the renin goes into circulation. SO DO I!   ▪ The liver produces the precursor protein Angiotensinogen which is freely circulating in the blood. Angiotensinogen RENIN Angiotensin I ▪ When the enzyme renin encounters angiotensinogen, it converts it into angiotensin I  ACE is produced in the lungs but binds to the surfaces of endothelial cells in the afferent arterioles and glomerulus. It enzymatically converts inactive angiotensin I into active angiotensin II. Angiotensin I Angiotensin Converting Enzyme (ACE) Angiotensin II  Blood pressure RAAS Flow Chart falls (slightly less panic inducing) Increase in blood pressure You are Kidneys release here renin Renin cleaves Vasoconstriction angiotensinogen to create angiotensin I Release of Reabsorption of Aldosterone sodium and water ACE cleaves angiotensin I to Reabsorption of create angiotensin II Release of ADH water  ▪ Adrenal Glands release aldosterone (a mineralocorticoid) that causes the kidneys to reabsorb Na+ and water. ▪ Aldosterone is often called the “salt-retaining hormone.” Angiotensin II ▪ Blood Vessels constrict ▪ Pituitary Gland releases vasopressin also known as (ADH), which increases the amount of water absorbed from the kidneys’ collecting ducts. The net effect: water (and Na+) is reabsorbed, blood pressure increases!  4-ish steps? (Trying to simplify things here) 1. Renin (released from the JGA in the kidneys) converts angiotensinogen (produced in the liver) into angiotensin I. 2. Angiotensin Converting Enzyme (produced in the lungs) converts Angiotensin I into the active Angiotensin II. 3. Angiotensin II exerts its effects on: 1. Blood vessels (causing vasoconstriction) 2. The Adrenal Glands (causing release of aldosterone) 3. The Pituitary Gland (causing release of vasopressin) 4. Aldosterone increases reabsorption of Na+ and water from the kidneys, and vasopressin also increases reabsorption of water    Stimulus: An increase in mean arterial blood pressure (MABP) leads to increased renal blood pressure and an increase in GFR. Receptor: Stretch receptors in the walls of the afferent arterioles are activated above the normal level. Control Center: Elevated activation of the stretch receptors leads to a depolarization of the smooth muscle cells forming part of the wall of the afferent arterioles. Effector: The smooth muscle cells undergo reflex contraction, causing vasoconstriction of the afferent arterioles. Response: Vasoconstriction of the afferent arterioles reduces the rate of blood flow into the glomeruli. This reduces downstream glomerular pressure, and thus prevents downstream glomerular blood pressure from rising. As a result, GFR returns to its optimal value. Essentially, the reverse happens when there is a drop in blood pressure  Tubuloglomerular autoregulation, also known as tubuloglomerular feedback, involves specialized osmoreceptor cells of the macula densa.  Stimulus: Anything that leads to an increase in GFR acts as a stimulus, because if GFR is increased, then tubular filtrate passes through the renal tubules too quickly. This means that the renal tubule is not able to reabsorb sufficient levels of Na+, Cl-, or water. Receptor: Macula densa cells are thought to detect changes in the composition of the tubular filtrate, in the final region of the ascending limb of the loop of Henle (to which they lie adjacent), in particular, concentrations of Na+, Cl-, and water.  Control Center and Effectors: The macula densa cells respond to increased concentrations of Na+, Cl-, and water by inhibiting the release of the effector nitric oxide (NO) from nearby cells in the juxtaglomerular apparatus. As NO causes vasodilation, a reduction in NO leads to vasoconstriction in the afferent arteriole. Response: Vasoconstriction of the afferent arterioles reduces the rate of blood flow into the glomeruli, and returns GFR to its optimal value. This forms a negative feedback loop, with the response leading to a reduction in the stimulus. Tubuloglomerular autoregulation