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CBIO 2210 week 11 notes

by: Elise Weidner

CBIO 2210 week 11 notes CBIO2210

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Elise Weidner

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notes from lecture 3/29/16
Anatomy and Physiology II
Rob Nichols
Class Notes
Anatomy II
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This 4 page Class Notes was uploaded by Elise Weidner on Wednesday March 30, 2016. The Class Notes belongs to CBIO2210 at University of Georgia taught by Rob Nichols in Spring 2016. Since its upload, it has received 21 views. For similar materials see Anatomy and Physiology II in Anatomy at University of Georgia.

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Date Created: 03/30/16
CBIO2210 Notes 3/29/16 Mechanisms of Urine Formation 2 main events (filtration and reabsorption/secretion) 1. Glomerular filtration 2. Tubular reabsorption a. Returns all glucose and amino acids to the plasma (keeps from losing nutrients) b. returns 99% of water, salt, and other components (keeps from dehydrating) 3. Tubular secretion a. reverse of reabsorption: selective addition of plasma components to urine Glomerular Filtration  Passive, mechanical process driven by hydrostatic pressure o Like straining pasta o Hydrostatic pressure is the pressure of the blood trapped inside the tube (like hose with holes in it with water spraying out)  The glomerulus is a very efficient filter because: (high pressure and high surface area) o its filtration membrane is very permeable and has a large surface area o glomerular blood pressure is higher (60 mm Hg) than other capillaries (~ 35 mm Hg)  Molecules >3 nm are not filtered (e.g., plasma proteins) and function to maintain a colloid osmotic pressure in the plasma o Protein should not be able to get through Glomerular Filtration Rate (GFR)  GFR = volume of filtrate formed by the kidneys in one minute o normal ranges:  120-125 ml/min for males  105-110 ml/min for females  These numbers mean filtration process is good/ healthy  What factors affect and control this amount of filtrate? o total surface area available for filtration (decreases with diseases such as glomerulonephritis) o permeability of the filtration membrane (size or charge of filtration slit diaphragms, size of podocyte foot processes) o most significant = net filtration pressure  Blood hydrostatic pressure-colloid osmotic pressure-capsular pressure=net filtration pressure  COP (caused by albumin in plasma) and CP(pressure that fluid in capsule has-why kidneys have to keep the BP up) both try to draw the fluid back in  Albumin made in liver and people with liver issues are very susceptible to low albumin levels so they will lose excess fluid (can look like kidney disease, but not) Regulation of GFR  GFR is tightly controlled by mechanisms both within the kidney and without  Intrinsic controls (aka, “renal autoregulation”) o kidney itself regulates (increase or decrease) GFR despite changes in systemic BP o even with fluctuations of MAP between 80-180 mm Hg, the GFR can be kept constant  Extrinsic controls o nervous and endocrine mechanisms that maintain systemic BP, indirectly affecting GFR o remember relationship: BP ➙ NFP ➙ GFR Intrinsic Controls  Myogenic mechanism o vascular smooth muscle has a tendency to contract when stretched (JG = smooth wrapped around afferent arteriole-keeps too much high pressure blood from entering) o ⇧ BP ➙ stretch of afferent arterioles ➙ constriction of arterioles ➙ restricting blood flow into glomerulus (⇩ GFR)  protects glomerular vessels from damaging effects of high BP o ⇩ BP ➙ less stretch ➙ dilation of afferent arterioles ➙ increased blood flow into glomerulus (⇧ GFR)  maintains GFR (even when exercising) by keeping NFP in normal range even with a reduction of systemic BP o (don’t need to know other two bullets) Extrinsic Controls  When blood losses are so significant and intrinsic mechanisms are not adequate to maintain GFR, sympathetic hormones (Epi/NE) are released o cause constriction of afferent arterioles  recall that this is actually as systemic response to stress (i.e., stress increases BP)  its function is to save your life in the event of significant blood loss (shock) o inhibit filtration (reduce plasma fluid loss) o macula densa cells (of JGA) detect changes in filtrate that they interpret as a decreased GFR o MD cells of JGA stimulate granular cells to release renin (not a hormone, it is an enzyme/ catalyst that raises blood pressure)  Renin is the first reaction in a chain reaction. It only catalyzes one thing o Turns Angiotensin (come from liver, constricts arteries) into Angiotensin I (doesn’t do much) o The enzyme Angiotensin Converting Enzyme from lungs converts Angiotensin I to Angiotensin II which is the active form which causes 5 things that raise BP Tubular Reabsorption  The kidneys filter the body’s entire plasma volume about 60 times / day (approx. every 22 minutes). o GFR = 120 mL/min = 7,200 mL/hour o In other words, your entire plasma volume would be filtered out of your kidneys in less than 30 minutes if not for reabsorption (transport of molecules from filtrate to blood).  Reabsorption may be active or passive.  65% of reabsorption takes place in the PCT  Use a sodium gradient for energy instead of glucose (like wheel in mill) (always less sodium in cytoplasm o Where sodium goes, water follows  Know #4 on chart o Aquaporins-Aqua channels  Allow water to be drawn back in  #2 and #3 pulls glucose and nutrients into blood (this is why should not be glucose in urine) o Keeps you from starving  Reabsorption Rates:  Any solutes that are actively reabsorbed require transport proteins in the membrane of the tubule cells. o the number of transporters for a particular solute indicates the importance of that solute to the body (i.e., high number of glucose and amino acid transporters vs. no urea transporters) o there is a transport max (Tm) determined by the number of transport proteins for a substance  hyperglycemia (glucose in urine because too much glucose in blood)➙ glycosuria


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