CV Biophysics & Kidney Flashcards

Question

Capillary Starling Forces: Capillary Filtration Coefficient (Kf) | How do we use this to determine filtration rate?

Answer 1

-Secondary to all other capillary starling forces -Related to capillary permeability and surface area (the more surface area we have, the more area for movement) Filtration Rate = Kf (NFP) Normal Kf is 12.5

Answer 2

-If capillaries are crushed from some sort of trauma, the plasma proteins leak out into the interstial space causing significant swelling -Crush injury, sepsis or severe acidosis, a condition where cells are dying/ imploding in an unplanned manner

Answer 3

-Responsible for absorbing extra fluid and dumping it back into the top of the thorax, allowing it to be reabsorbed back into the cardiovascular system -In a healthy person, the lymphatic system can increase it's rate of work by 20-40x in terms of managing extra fluid -After an injury where cell walls are damaged, the lymphatic system can absorb some of the extra fluid in the interstitial space but it is not specialied to pick up extra proteins. -The lymphatic system typically increases its rate of action with increased muscle movement. If someone is immobile and in a hospital bed, the lymphatic system is not going to be able to do it's job effectively

Answer 4

Albumin: 4.5g/dl --> 21.8 mmHg Globulins: 2.5g/dL --> 6.0mmHg Fibrinogen: 0.3g/dL --> 0.2mmHg

Answer 5

Via a one-way valve system that relies on our skeletal muscles compressing and relaxing against the lymphatic system Without movement, fluid will accumulate in the legs and we are more prone to blood clots in the lower extremities.

Answer 6

Forces that favor filtration: 30mmHg -3mmHg 8mmHg Forces that oppose filtration: 28mmHg NFP = Pcap - Pisf - Plasma Oncotic Pressure + Interstitial Oncotic Pressure Gives us a NFP of 13mmHg Favors filtration

Answer 7

Forces that favor filtration: 10mmHg -3mmHg 8mmHg Oppose Filtration: 28mmHg NFP = Pcap - Pisf - Plasma Oncotic Pressure + Interstitial Oncotic Pressure NFP: -7mmHg, favors reabsorption Plasma oncotic pressure is the opposing pressure in both venous and arteriole ends

Answer 8

17.3mmHg Capillaries get larger as we move from the arteriole end to the venous end If we use this number in our NFP equation, we end up with an average NFP of 0.3mmHg throughout each capillary

Answer 9

The smaller the molecular weight, the more likely the membrane is permeable to that substane. The exception for NaCl is the BBB.

Answer 10

-Renal artery pressure if ~100mmHg -Blood encounters vascular resistance when traveling through the kidney, and by the time it reaches the renal vein, the pressure is around 0mmHg -Energy/ATP is removed from the blood as it moves through resistance, causing a decrease in pressure as it continues to encounter resistance

Answer 11

-First set of capillaries in the kidneys -Afferent arteriole is immediately upstream to the glomerular capillaries--> very important in determining how much pressure the glomerular capillaries have -The pressure in the glomerular capillaries determines the glomerular filtration rate -Normal pressure in the glomerular capillaries is around 60mmHg. This high pressure is used to push fluid out of the capillaries at a rate of about 125ml/min

Answer 12

-Plasma oncotic pressure is 28mmHg at the beginning of the glomerular capillaries -As we move through the glomerular capillary, the plasma oncotic pressure increases ( 28mmHg --> 32mmHg-->36mmHg) due to the fact that the glomerulus is filtering fluid, but the amount of colloids remains the same

Answer 13

-If blood flow is too low, the afferent arteriole will relax to increase blood flow to the glomerulus -Increasing renal blood flow increases GFR -If renal blood flow is too high, the afferent arteriole constricts to reduce overperfusion -Decreasing renal blood flow decreases GFR Autoregulation typically occurs between 50mmHg and 150mmHg. The afferent arteriole is able to regulate RBF fairly well if BP is too high, but RBF and GFR starts to steeply drop off well before 50mmHg. If someone has had chronic HTN, the afferent arteriole will not be able to relax as well

Answer 14

Ptubule- 18mmHg -The fluid from filtration fills the PCT until it reaches a P of 18mmHg --> empties into ureters and bladder to be excreted or leaves the PCT --> renal interstitium --> reabsorbed PT capillaries The body can physically pump things into the tubule (secretion). Leaves the PT capillaries --> renal interstitium --> P tubule Ex: Toxins, K+, Na+ Oncotic pressure in the tubule should be 0mmHg because in a healthy person, we are not filtering protein

Answer 15

We need to compare against the numbers in the PCT NFP = Pcap - Pisf - Plasma oncotic + Isf Oncotic Take the Pcap from the glomerular capillar; 60mmHg Use the Ptubule in place of Pisf; 18mmHg Take the median plasma oncotic number from glomerular capillary Isf Oncotic = PCT oncotic; 0mmHg 60mmHg-18mmHg-32mmHg= NFP of 10mmHg

Answer 16

-Primary function is to regulate GFR -If the efferent arteriole constricts, it will increase renal blood pressure in the glomerulus, causing an increase in GFR -If the efferent arteriole relaxes, it will decrease renal blood pressure in the glomerulus, causing a decrease in GFR -Higher vascular resistance in this arteriole than in the afferent -Pressure at the end of the efferent arteriole is 18mmHg

Answer 17

-Where the majority (99%) of our reabsorption takes place, so we should assume our NFP will favor that Pcap: 13mmHg Pisf: 6mmHg Plasma Oncotic: 36mmHg --> 32mmHg --> 28mmHg Oncotic Isf: 15mmHg (due to proteins in the renal intersitium) NFP= Pcap - Pisf - Plasma Onc. + Onc. isf = -10mmHg OR NRP is 10mmHg -Fluid that was filtered into the PCT will exit through or in between the cells lining the wall of the PCT, travel through the renal intersitium, and become reabsorbed at the PT capillaries in order to be returned to the CV system

Answer 18

-Proteins -Ions -Electrolytes -Large energy compounds -Intermediary place between blood vessels and tubules

Answer 19

Efferent arteriole constriction or relaxation determines how much fluid is being filtered -The more fluid we filter (higher filtration fraction), the higher the osmotic pressure will be on the efferent end -The less fluid we filter (lower filtration fraction), the lower the osmotic pressure will be on the efferent end This represents the change in osmotic pressure that we see along the glomerular capillary

Answer 20

GFR/ RPF (Renal Plasma Flow)= FF RBF = ~1100ml/min (~22% of CO) If your HCT is 0.4, that means the remaing 60% of RBF is plasma RPF= 660ml/min 125ml/min/660ml/min = 19%

Answer 21

-Increase in afferent arteriole resistance decreases Pcap in glomerulus --> Decreasing GFR--> Decreasing renal blood flow -Decrease in afferent arteriole resistance causes an increase in Pcap --> Increase in GFR -->increase in renal blood flow -Increase in efferent arteriole resistance causes and increase in Pcap in glomerulus --> increase in GFR --> decrease in renal blood flow -Decrease in efferent arteriole resistance causes a decrease in Pcap --> decrease in GFR --> Increase in renal blood flow

Answer 22

Normal UOP should be 1ml/min -Increase in RBF --> Increase GFR --> Increase UOP --> Decreased BP -Decrease in RBF --> Decrease in GFR --> Decrease in UOP --> Increased BP Renal system favors fluid excretion and decreased pressures. It autoregulates better at a high pressure

Answer 23

A) Filtration Only: Happens when we don't have any specialized transporters designed to retain or reabsorb whatever is being filtered B) Filtration, Partial Reabsorption: Na+ is a good example. We typically eat more Na+ that we need. Reabsorb what we need, filter the rest C) Filtration w/ complete reabsorption: Glucose in a non-diabetic patient. If glucose is present in the urine, BG is way too high or there is an issue with the transport system. D) Filtration w/ secretion: A small portion of this was filtered, and the remainder of this was secreted. Paraminohippuric acid (PAH); a diagnostic compound that gives us an idea of what the renal blood flow is. The higher the amount of PAH removed, the better the RBF The lower the amount of PAH removed, the lower the RBF is

Answer 24

1. Fenestrations: Specialized openings in the renal glomerular endothelium that allow the cell to be more permeable 2. Epithelium/ Epithelial Cells: Specialized to provide support to the glomerular capillary bed. Pressure is high in the glomerulus, so this is important 3. Baesment Membrane: Thick layer of connective tissue that is littered with negative charges in order to prevent other negatively charged particles from exiting through the slit pores (proteins) 4. Endothelium 5. Podocytes: What makes up the epithelium and provides structural support under the high pressure system in the glomerulus. Keeps the glomerular capillary from swelling due to chronic HTN (tries to). If you have chronic HTN and the pressure at the renal artery is 200mmHg instead of 100mmHg, this significantly increases the pressure within the glomerulus 6. Slit Pores: "Foot processes" that are openings between podocytes.

Answer 25

1. Polycationic dextran: The charge on the sugar compound is positive, so the filtration rate will be higher 2. Polyanionic dextran: The negative charged will be repelled by the basement membrane of the glomerulus, so it's filterability is reduced If the compound is larger, it's less filterable If the compound is smaller, it's more filterable

Answer 26

-Long term regulator of BP: If someone has chronic HTN, their kidneys are not functioning properly -Long term pH regulator: Produces HCO3- in response to excess protons, and the kidney also decides how much HCO3- to reabsorb -Long term RBC/Hct regulator: O2 sensors deep inside the medullary portions of the kidney. If O2 levels are low, the kidneys release EPO--> increases the number of RBCs in circulation by stimulating the bone marrow.

Answer 27

-Long term electrolyte regulator: Filtration & reabsorption of electroyltes -Long term vit. D regulator: Vit. D is activated at the kidney -Long term serum glucose regulator: Filtration & reabsorption of glucose. If there is excess glucose, kidney will typically reabsorb until it reaches the maxmimum amount that the kidney can reabsorb. If glucose is absurdly high, glucose will be filtered out

Answer 28

-Some drug clearance usually via secretion -Long term metabolic waste removal: Nitrogenous compounds such as uric acid -Osmolarity: Can decide how much water and NaCl to reabsorb independent of each other. Usually managed by ADH

Answer 29

Renal artery --> Segmental arteries --> interlobar arteries --> arcuate arteries --> interlobular arteries --> afferent arterioles -> Glomerular capillaries --> Efferent Arteriole--> peritubular capillaries These are all located behind the PT capillaries: --> Interlobular veins --> Arcuate veins --> Interlobar veins --> Segmental veins --> Renal veins Arteries split into smaller arteries Veins converge into larger veins

Answer 30

1. Arcuate Artery 2. Arcuate Vein 3. Afferent Arteriole 4. JG apparatus 5. Efferent Arteriole 6. Glomerulus 7. Bowman's Capsule 8. Proximal Tubule 9. Cortical collecting tubule 10. Collecting Duct 11. Loop of Henle 12. Peritubular Capillaries 13. Distal Tubule

Answer 31

90-95% of our nephrons are very superficial and are located in the cortex -PT capillaries and renal vessels are in the outer medulla 5-10% of our nephrons are deep medullary nephrons -Unequal number of descending and ascending PT capillaries here. -Called descending and ascending Vasa Recta -We have more ascending vasa recta than descending; causing the velocity of blood flow to slow as it ascends. This is important in maintaining a normal level of solutes in the deep interstitium; if the blood flow was too fast, it would "wash out" the solutes traveling through the renal interstitium -Receive a limited supply of blood, so if BP is low, the deep medullary PT capillaries will be the most sensitive to those changes

Answer 32

1. R. Adrenal Gland 2. L. Adrenal Gland 3. Gastric surface of L kidney 4. Splenic surface 5. Pancreatic surface 6. Descending colic (colon) surface 7. Duodenal surface 8. R colic flexure surface (colon) 9. Hepatic Surface Cancer in these other organs are likely to spread to the "surface" of the kidney that it touches

Answer 33

Have the ability to obstruct the ureter, allowing metabolic waste products to build up on that side of the body in the kidney and creating more work

Answer 34

-Mix of SNS or PNS -Pudendal nerve originates on spinal nerves S2, S3, S4 -Controls emptying of the bladder and bowels, and responsible for erections in men -Why removal of the prostate can be risky, concern for cutting the pudendal nerve

Answer 35

1. Proximal convoluted tubule 2. Afferent & Efferent Arterioles 3. Straight Proximal tubule 4. Descending Thin Loop of Henle 5. Ascending thin Loop of Henle 6. Thick ascending limb of Loop of Henle 7. Macula Densa (Located in the TAL Loop of Henle) 8. Glomerulus 9. Bowman's Capsule 10. Distal convoluted tubule 11. Cortical Collecting Duct 12. Medullar Collecting Duct -Outer MCD and Inner MCD 13. Papillary Duct

Answer 36

-TAL of Loop of Henle -Sits on top of the afferent and efferent arterioles entering the glomerulus -Measures flow through the kidney. -When flow is low, renin is released -Increased Renin leads to increased Angiotensin II --> constricts the efferent arteriole, occluding outflow--> increases Pg -Flow is too high --> decreased amounts of Renin released --> decreased Angiotensin II --> relaxation of the efferent arteriole

Answer 37

-Quantity of plasma that is cleared of a substance per time (mL/minute) -Cx = Clearance (mL/minute) -V = Urine Flow rate (~1ml/min) -Ux = Urine concentration (mg/ml) -Px = Plasma concentration (mg/ml) Cx = V * Ux/ Px

Answer 38

In a healthy individual, we should be filtering 125ml/min We usually reabsorb 124ml/min UOP = 1ml/min -If there is no impediment to filtration, the concentration in the glomerulus should match the concentration in the PCT. -If the compound is completely reabsorbed (glucose), the concentration at the end of the PCT will be very, very low -This means that our renal clearance would be very low- we are not clearing the plasma of this compound

Answer 39

-Inulin is small enough to be freely filtered -Inulin is not reabsorbed at all; however, plasma is still be reabsorbed into the PT capillaries at a rate of 124ml/min -Concentration in the early PCT should be the same as plasma concentration -As it moves through the nephron, the concentration of Inulin will increase significantly (plasma being reabsorbed, but the inulin remains) --> eventually the entire amount of Inulin will be concentrated in the 1ml/min of urine -Renal clearance will be very high- we've cleared plasma at a rate of 124ml/min -Dilution of whatever Inulin remains in the PT capillaries will take place as the plasma is reabsorbed. Meaning that the concentration of inulin in the renal vein will be significantly lower than the concentration in the renal artery

Answer 40

1 dL= 100ml If filtering 125ml/min, urine concentration would be 1.25mg/ml Plasma concentration is 1mg/100ml Cx= V * Ux/Px (1ml/min * 1.25mg/ml)/1mg/100ml Cx = 125ml/min Gold standard for determining GFR- clearance of Inulin

Answer 41

Excretion Rate = V * Ux Mg/min mmol/min mEq/min

Answer 42

GFR x Px mg/min mmol/min mEq/min

Answer 43

Filtered Load- Excretion Rate (GFR * Px) - (V * Ux) mg/min mmol/min mEq/min

Answer 44

Excretion Rate - Filtered Load (V * Ux) - (GFR * Px)

Answer 45

-PAH is filerted into the PCT and secreted from the PT capillaries into the PCT -Clearance rate is very high, and will be equivalent to whatever the renal plasma flow is *** Use the clearance rate of PAH to determine the renal plasma flow ***

Answer 46

Chronic HTN- Increases the pressure upstream from the AA and will also increase pressure in the glomerular capillary despite the constriction of the AA in order to prevent Increased pressure in the glomerular capillary causes an icrease in GFR, but not an increase in reabsorption rate; therefore, without proper autoregulation of the kidney, a patient with HTN would be dumping urine. On a day-to-day basis when we have normal fluctuations in our BP, our kidneys can autoregulate well. Chronic HTN will ultimately cause an issue with our autoregulation

Answer 47

A decrease in pressure in the glomerular capillary means that our GFR will be decreased --> we are not filtering appropriately Because there is a lower filtration rate, the fluid will be moving slower, spending more time in the tubule, which means it has a higher chance of being reabsorbed Reabsorption depends on time. More time spent in the PCT, higher chance of being reabsorbed

Answer 48

-Creatinine is freely filtered, but not reabsorbed. The further along the tubule we go, the higher the concentration of creatinine becomes because water continues to be absorbed but creatinine is not -All glucose reabsorption happens at the PCT. Concentration should be the same as plasma glucose once it's filtered, but should completely be reabsorbed steeply decreasing the glucose concentration throughout the remained of the tubule -Same for AA ^ -Na+ concentration is fairly consistent throughout the proximal tubule because as Na+ is being absorbed, water is also being absorbed -Cl- tends to become slightly more concentrated than Na+ as we move through the proximal tubule. In the second half of the proximal tubule, Cl- is most concentrated, and this favors reabsorption

Answer 49

-Macula Densa is looking at how many Na+ pass the sensor per unit/time -Normal GFR & reabsorption in the PCT, macula densa will not need to make any adjustments -High GFR, but normal reasborption --> a higher quantity of NaCL will make it to the macula densa. Macula Densa will then reduce renin -Low GFR, but normal reabsorption rate --> lower quantity of NaCl observed at the macula densa. Will increase renin release -Normal GFR, but drug is given to increase reabsoprtion at the PCT --> macula densa will observe a lower amount of NaCl and release renin even though GFR is normal. ACE Inhibitor or ARB should help here

Answer 50

Renin released by the JG cells in kidney --> angiotensinogen is converted into angiotensin I --> ACE (found in large amounts in the lungs) converts ATI to AT II --> efferent arterioles are constricted --> Aldosterone signals to increase NaCl and water absorption in the PCT Secondary affect is that the afferent arterioles dilate, increasing RBF to this area, further increasing Pg. Happens possibly from NO- still trying to work out details Renin is the rate-limiting step

Answer 51

-All filtered glucose should be reabsorbed in the PCT. -The SGLT transporter brings 1 Na+ from the tubular lumen down it's concentration gradient, into the tubular cells, and 1 glucose with it -What happens if glucose is too high? Hyperfiltration of glucose causes increased reabsorption of Na+. This causes increased renin release by the macula densa, increasing GFR. This increases the workload on the nephron and can destroy nephrons if hyperglycemia is chronically uncontrolled -Because glucose is being packed into the tubular cells, the GLUT transporter on the basolateral side does not need ATP. Glucose moves down its concentration gradient

Answer 52

-Small, filtered easily, and the body reabsorbs 100% of the AA that are filtered -Sodium/Amino Acid transporter works the same way that the SGLT transporter does. 1 Na+ moves across it's concentration gradient from the tubular lumen into the tubular cells, bringing one AA with it -Hyperfiltration of AA is the same as glucose. -AA are passively allowed out of the basolateral side of the cell in the same way as glucose

Answer 53

S1 Segment (Early PCT): -90% of glucose transportation is done here by the SGLT2 transporters (second isoform of SGLT) -Low affinity 1 Na+, 1 glucose -GLUT-2 transporter is on the basolateral side S2 & S3 (Later PCT): -SGLT-1 Transporters on apical side (~10% of glucose transportation) -High Affinity - 2 Na+, 1 glucose; takes more effort to pump glucose into the cell from a fairly dilute concentration in the PCT - GLUT-1 transporter on basolateral

Answer 54

-Filtered load of glucose depends on GFR and plasma concentration of glucose -Vertical axis is showing glucose filtered load, reabsorption, or excretion -Horizontal axis is showing up plasma glucose concentration -Threshold (Graph shows 200, Schmidt says <200mg/dL); the point where the PCT can no longer reabsorb 100% of the glucose, and some glucose will start to be excreted. As BG increases, excretion rate also increases -Transport maximum is ~ 300mg/dL; at this point, there will be a rapid increase in the amount of glucose excrese

Answer 55

Afferent arteriole

Answer 56

-Main effect: When Ang II binds to the AT I receptor, the speed of the Na+/K+/ATPase pump increases 1. Causing an increase in Na+ leaving the cell--> causing an increase in the concentration gradient --> Na+ will flow in faster at the NHE exchanger 2. Speeds the rate of reabsorption for HCO3- via the Na+/HCO3- cotransporter (secondary active transporter) -HCO3- drives this pump, not Na+ Located in the PCT

Answer 57

-Paracellular reabsorptionm (passive) originates at the tight junction of the apical membrane of the tubular lumen. This pathway goes between cells 1. Cl- is reabsorbed this way --> moves into the renal interstitium because of the electrical gradient created by Na+ 2. Water also moves this way 3. Areas of the kidney that are impermeable to water (Thin Ascending Loop) will have very tight junctions and will lack aquaporins -Transcellular reabsorption happens via a transporter or channel within the cell wall 1. Water moves through aquaporins via the transcellular route. Follows solute traveling to the renal interstitium via osmosis

Answer 58

-Bulk flow: Happens at the area of the tubule where filtration is very heavy, and reabsorption is also very heavy. NFP at the glomerular capillaries is about 10mmHg, and NRP at the peritubular capillaries is also 10mmHg -When discussing bulk flow in regards to filtration and reabsorption, it takes place at the PCT -Urea, a metabolic waste product, is somewhere stored within the renal interstitium and is used to help reabsorb water via osmosis -Brush border on the apical side of the proximal tubule cells; increases the surface area of the cells lining the apical border of the tubule by ~20x. This allows for a large amount of the cell to be exposed to the fluid in the proximal tubule as well as a large area for the kidney to place transporters

Answer 59

Vrm in the tubular cells is -70mV Vrm in the tubular lumen is -3mV (due to a combination of K+, Na+ and Cl-)

Answer 60

-Proteins are negatively charged, large, and typically not filtered -We do have ~some~ proteins that filtered; 1.8g/day in a completely healthy person. The brush border along the tubular cells "collect" proteins occasionally -1.7g of protein is reabsorbed via endocytosis/pinocytosis. The PCT cell will engulf the protein, convert them into amino acids, and reabsorb them in the PCT. This process only takes in the PCT -100mg excreted in the urine. This amount should not make urine cloudy

Answer 61

NHE: A form of secretion; secreting H+ ions at the PCT. This exchanger is also the primary reabsorption process for Na+ in the PCT -H+ secreted into PCT, combines with HCO3- to form H2CO3 -Carbonic anhydrase dissociates H2CO3 into H2O and CO2 -H2O is easily reabsorbed via osmosis. CO2 easily diffuses across the membrane -Carbonic anhydrase can be: 1. Tethered to the cell wall 2. Floating freely in the proximal tubule 3. Inside of the tubular cell -Carbonic anhydrase then drives the reaction in the opposite direction once in the cell; CO2 + H2O = H2CO3 -Dissociates again into H+, HCO3- -H+ is secreted into tubule, joins with HCO3-, or combines with NH4 (buffer for the urine) -HCO3- is reabsorbed into the renal interstitium --> PT capillaries

Answer 62

-NHE would not cycle as fast -Significantly less Na+ reabsorbed --> less water retained --> volume loss -HCO3- would be not reabsorbed due to no C.A, HCO3- lost in the urine resulting in acidosis

Answer 63

-Glutamine produced in the liver can be converted into two different compounds in the PCT: 1. HCO3- 2. NH4+ 1 Glutamine is turned into 1 glucose --> turned into 2HCO3- or into 2NH4+ The NH4+/ Na+ secretes NH4+ out into the tubular lumen, where H+ can attach to be excreted through the urine This is another method for the body to buffer our blood by getting rid of extra protons. Liver failure means the person will not be able to produce glutamine as effectively

Answer 64

-NaHPO4- is a urinary buffer in addition to NH4+ and HCO3-

Answer 65

-Ca++ is reabsorbed in multiple areas of the tubule -Follows both pathways of reabsorption; 1. Paracellular: Ca++ is "dragged" along with water and other solutes via the paracellular route. If the reabsorption rate in the PCT increases for any reason, thats typically means that the reabsorption rate of Ca++ will also increase 2. Transcellular: -Ca++ channel on the apical side that allows Ca++ into the tubular cells (concentration gradient) -Ca++ ATPase pump that directly pumps Ca++ out into the renal interstitium -Ca++/Na+ exchanger (3 Na+ in, 1 Ca++ out) Ca++ filtration heavily depends on acid/base balance. If Ca++ is bound to albumin (or something else that's negatively charged), it's not going to be filtered

Answer 66

-Parathyroid gland located on the sides of the thyroid gland; monitors level of Ca++ in the extracellular fluid which should mirror our plasma Ca++ -When Ca++ levels are low, PTH is released and does: 1. PTH encourages vitamin D3 activation --> increases the amount of dietary Ca++ that we absorb 2. Influences Ca++ reabsorption system in the kidney via increased number of Ca++ channels 3. Increased Ca++ release from bones by increasing number of osteoclasts --> break down the bone (hardened Ca++ and phosphate) --> release Ca++ -Risk of osteoporosis 4. Decreased activity of osteoblasts The opposite is true if Ca++ levels are high

Answer 67

-ACh -Choline -Creatinine -Dopamine -Epinephrine -Histamine -5-HT -Norepi

Answer 68

-Atropine -Isoprel -Morphine -Procaine -Quinine -Tetraethylammonium (TEA)

Answer 69

-Bile Salts -Hippurates -Oxalate -Prostaglandins -Urate

Answer 70

-Acetazolamide -Chlorothiazide -Furosemide -PCN -- needs to be given with hippurate -Salicylates -Sulfonamides -PAH

Answer 71

Cation Secretion: H+ Dependent antiporters bring one H+ ion into the cell in exchange for secreting a cation into the tubule Anion Secretion: This pathway uses an intermediary called alpha-ketogluterate (a-kb). A transport system brings 3 Na+ with each 1 a-kb into the tubular cell. The increased concentration of a-kb in the tubular cells causes organic anions to be secreted into the tubular cells from the renal interstitium. Once in the tubular cell, the organic anion is secreted into the tubular lumen via a facilitated transporter If two compounds are using the same transporter system, we can increase the levels of the one we do not want to keep around so that the transporter system secretes the compound in higher concentration

Answer 72

-Tubular fluid moves through the descending thin loop of henle deeper into the kidney where the renal interstitium becomes more concentrated. -Water should continue to be reabsorbed as we move deeper into the tubule provided that that portion of the tubule is permeable to water -Impermeable to ions - ~20% of our water is reabsorbed here

Answer 73

-The more superficial the fluid travels, the more dilute the renal interstitium becomes -Impermeable to water -NaCl ATPase transporter; reabsorbs Na+ and Cl- -Does this in relatively small amounts

Answer 74

-Relatively impermeable to water -Important area for cationic electrolyte reabsorption (Mg++ & Ca++ > Na+, K+) ~25% reabsorption here -There are K+ leak channels here that allow K+ to move down it's concentration gradient and out into the tubular lumen and into the renal interstitium -There is enough K+ leaking out into the lumen that the Vrm in the tubular lumen here is +8mV -The +8mV charge is what drive the paracellular reabsorption of Ca++ and Mg++ -NHE is here, acid/base balance takes place here as well -Na+, 2Cl-, K+ transporter pushes 1 Na+, 2Cl-, and 1 K+ into the tubular cell -The ion reabsorption that takes place here plays a very major role in the concentration of the renal interstitium. The ions reabsorbed here tend to settle in the deeper parts of the renal interstitium, contributing to the high osmolarity

Answer 75

-Shut down the Na+,2Cl,K+ ion transporter at the thick ascending loop of henle -Withouth the action of that pump, ultimately leads to a less concentrated renal interstitium -Significantly decreases our ability to reabsorb water; increased water excreted -Na+ is then reabsorbed at the distal convoluted tubule, causing an increase in K+ secretion

Answer 76

-Deepest part of the renal interstitium has an osmolarity of ~1200 mOsm/ml. This is the most concentrated that our renal interstitium can be. This is an example of a kidney that is conserving water -Urine osmolarity should also be 1200. -The limitation to concentrate our urine depends on how concentrated our renal interstitium is -Our urine osmolarity should reflect what the osmolarity is in the deepest part of the renal interstitium- the collecting duct

Answer 77

-Another area of the tubule where PTH can influence Ca++ reabsorption -PTH can increase the number of Ca++ channels we have on the luminar side of the cell allowing Ca++ into the tubular cell -This will also increase the amount of Ca++ pumps on the basolateral side of the cell to increase reabsorption into the renal interstitium. Ca++ ATPase and Ca++/Na++ (primary) exchanger are typically found together -Simple reabsorption of Na+ and Cl- also takes place here. NaCl transporter on the apical side takes in 1 Na+ and 1 Cl-

Answer 78

Inhibit the simple Na+/Cl- transporter in the distal tubule -By blocking the Na+/Cl- transporter, we are decreasing the amount of Na+ entering from the tubular lumen. -This will cause an increase in the rate of the Na+/Ca++ exchanger --> pushing more Ca++ into the renal interstitium for reabsorption -Sometimes prescribed for patients with osteoporosis -Need to be mindful of additional Ca++ intake in non-osteoporosis patients -Useful in patients who have recurrent kidney stones; reducing the amount of Ca++ in the urine reduces the risk of it crystalizing

Answer 79

-Sensitive to both ADH and aldosterone -When thinking of principal cells- think K+ regulation -Work via aldosterone receptors found inside the cell -Aldosterone is a cholesterol derivative and has no problem making it through the cell wall -This system is designed to mimic the actions of the Na+/K+/ATPase pump. Speeds up the pump cycling rate, increases the amount of Na+ and K+ channels on the apical side -Increases the amount of K+ secretion by increasing number of K+ channels --> More k+ leaving the cell --> more K+ brought in via the Na/K/ATPase pump from the renal interstitium -Increases the rate of Na+ reabsorption by increasing the amount of Na+ that leaks in through the ENaC Na+ channel --> pumped out into the renal interstitium via Na+/K+/ATPase pump

Answer 80

State of the cell wall during differnt phases of K+ excretion -ROMK Channel: Renal Outer Medullary K+ Channel -BK Channel: Big K+ channels. Secondary to ROMK Low excretion state: -ROMK is sequestered (inside the cell, inactive) -Bk is closed Normal excretion state: -ROMK moves to cell wall (aldo mediated), opens -BK is closed High excretion state: -ROMK is open -BK is open (aldo mediated)

Answer 81

Na+ channel blocking diuretics (decreases Na+ absorption); block the ENaC channel --> indirectly slowing down the Na/K/ATPase cycling --> reducing the amount of K+ secreted -Amiloride -Trimaterene Aldosterone antagonists: Inhibit the aldosterone receptor --> decreases the speed of the Na/K/ATPase pump --> leading to decreased Na+ reabsorption and K+ secretion

Answer 82

-If Na+ reabsorption is blocked higher in the tubule, this mean that there will be a larger amount of Na+ arriving at the principle cells of the distal tubule -More Na+ leaks in through the ENaC channels --> more Na+ is pumped into the renal interstitium by the Na/K/ATPase pump -This means that more K+ will need to be secreted in order to keep up with the increased rate of Na+ reabsorption here Anything that increases that amount of Na+ being reabsorbed at the principal cells will indirectly result in a higher rate of K+ secretion

Answer 83

-Most superficial layer of the adrenal gland is the Zona Glomerulosa; aldosterone is secreted here -Zona fasciculata is the next deeper portion -Zona reticularis is deep to the fasciculata -Cortisol and androgens are produced here; androstenedione, small amount of estrogen (fasciculata for estrogen) -Medulla is the deepest -Catecholamines are produced here. Epi/Norepi in a 4:1 ratio

Answer 84

-The zona glomerulosa is sensitive to K+ levels. If K+ is high, more aldoesterone is release --> Causes an increase of Na+ at the principal cells and indirectly increasing K+ secretion If K+ is low, less aldosterone is secreted AT1 receptors are also found in the zona glomerulosa ANG II binds to the AT I receptors, and more aldosterone is secreted from the zona glomerulosa -Aldosterone synthase is present in the zona glomerulosa

Answer 85

-Cholesterol derivitive -Glucocorticoid responsible for glucose management -Looks exactly like aldosterone, so if we have an extra amount of cortisol being made, it can interact with aldosterone receptors in the principal cells and drive blood pressure up -Enzyme 11Beta-Hydroxy-steroid-dehydrogenase degrades or destroys cortisol within the principal cell so that it does not interact with the aldosterone receptors. -Real licorice is an inhibitor. Typically used as a flavoring in tobacco

Answer 86

-Handle acid/base regulation -Sensitive to ADH -Type A intercalated cells secrete H+ 1. H+ ATPase pump uses ATP to secrete H+ into the distal tubular lumen. Very high H+ concentrating capacity 2. H+/K+/ATPase: Secretes H+ into the distal tubule in exchange for K+ -Type B intercalated cells reabsorb H+ and secrete HCO3- 1. All we need to know is that there is a way to secrete HCO3-

Answer 87

-Both intercalated & principal cells are sensitive to ADH -V2 receptors, found in the late distal tubule and collecting duct, bind ADH -ADH binds to V2 --> activates protein kinase A --> phosphorylates aquaporin channel vesicles (AQP-2) ---> move to the apical side of the cell wall --> increase H2O entry from the tubular lumen -AQP 3, 4 on the basolateral side; non-ADH dependent and always present If we need to conserve water, ADH is increased If we need to secrete water, ADH is decreased The only signaling compound that can control water reabsorption separate from salt reabsorption

Answer 88

Nephrogenic DI: -A problem at the level of the kidney that inhibits response to vasopressin. Lithium can induce Ex: Problem with Protein Kinase A- unable to cause phosphorylation of the AQP-2 channels Central DI: Problem secreting vasopression In either form, urine becomes very, very dilute because we are reabsorbing electrolytes but not reabsorbing water. Osmolarity can be diluted to ~ 50mOsm/ml

Answer 89

Factors that control ADH: -Osmoreceptors: Sense osmolarity changes -Baroreceptors: Blood pressure in high pressure side of circulation -Blood volume sensors in the large veins & atria Sensors send this information to two nuclei in the hypothalamus. Both nuclei send ADH to the posterior pituitary gland --> enters blood stream here 1. Osmoreceptors 2. Paraventricular nuclei- Located on the sides of the third ventricle. 1/6th of ADH production 3. Posterior pituitary/ neurohypophysis 4. Anterior lobe/ adenohypophysis 5. Supraoptic nuclei- Located above the eye, in front of the hypothalamus. Gives us 5/6th of our ADH production

Answer 90

Nuclei!!!!!

Answer 91

-A cell is in an isotonic solution; volume of cell will not change -Cell is in a hypotonic solution; water will move into cell until the osmolarity of the cell equals the osmolarity of the solution -This would cause a reduction of ADH released from the posterior pituitary -Swelling of the osmoreceptor causes a reduction in action potentials sent to the ADH production areas (supraoptic & paraventricular nuclei) -Cell is in a hypertonic solution; water will leave the cell until the osmolarity of the cell equals the osmolarity of the solution -This would cause an increase in ADH released from the posterior pituitary -Shrinkage of the osmoreceptor causes an increase in the firing rate of action potentials Electrolytes responsible for osmolarity are typically Na and Cl

Answer 92

-PCT does not have any major shifts from normal osmolarity of ~300. H2O is reabsorbed along with NaCl -Environment changes in the Loop of Henle; in the deep parts of the kidney there is a lot of protein, urea, electrolytes in the renal interstitium. Water leaves the descending thin loop of henle, electrolytes do not. -Ascending Thin Loop is impermeable to water- NaCl is being reabsorbed, loop is becoming more and more dilute. -Thick ascending loop & the early distal convoluted tubule are the diluting segment -Osmolarity beyond the early distal tubule is completely dependant upon ADH -

Answer 93

-Small and freely filterable -ADH plays a role in the osmolarity of the Loop of Henle by dictating urea reabsorption in this area -Small amount reabsorbed at the PCT by being dragged along with H2O -When there is a large amount of circulating ADH, there is an increased number of AQP-2 channels along with Urea transporters in the cell wall of the collecting duct. This causes an increase in osmolarity in the medulla of the kidney which also effects parts of the loop of henle -Urea transporters are UT- A1 and UT-A3

Answer 94

Decrease thirst: Reduction in plasma osmolarity Increase in blood volume Increased BP Decreased Ang II Gastric Distention Increase thirst: Increase in plasma osmolarity Decreased blood volume Decreased BP Increased Ang II Dryness of mouth

Answer 95

Decrease ADH: Decreased plasma osmolarity, Increased BV & BP ETOH Haldol Increase ADH: Increased plasma osmolarity, decreased BV & BP Hypoxia Nausea Morphine Nicotine

Answer 96

-Drinking 1L of fluid should have a minor effect on our plasma osmolarity as long as we have a functioning ADH system -Urine flow rate will begin to increase until plasma osmolarity has been restored to normal -Urine osmolarity will be very dilute Normal urine osmo should be about ~600mOsm/ml

Answer 97

This area of the nephron becomes diluted down to about 100mOsm/ml -No matter how much ADH is present, this area of the tubule will become diluted -This segment of the nephron is at the end of the thick ascending loop of henle/early distal convoluted tubule

Answer 98

-Very dilute, means we are not conserving water -Conditions that would cause this? -Low ADH: -High plasma volume -High BP -Low plasma osmolarity -ETOH -Haldol

Answer 99

-Water conservation -High ADH -Low plasma volume -Low BP -High plasma osmolarity -Nicotine, morphine -Hypoxia, nausea

Answer 100

This graph shows up the concentration changes of different compounds throughout the nephron Why is PAH so much more concentrated than creatinine? Because it is being filtered AND secreted

Answer 101

-Diuresis- Di refers to both salt and water -An increase in fluid excretion happens when taking diuretics -This fluid typically comes from our ECF -Plasma volume: 1/5th of ECF -Interstitial fluid volume: 4/5ths of ECF When exposed to the drug for the first time, patient will dump a lot of fluid. ECF volume decreases. The initial dose of the diuretic will keep this condition maintained- patient will not continue dumping additional fluid off In this graph, about 1L of ECF fluid is removed. That would mean: -1/5th is coming from the plasma volume (~200ml) - 4/5ths is coming from the interstitial volume (~800ml) -The body will typically find away to compensate against a medication that solely relaxes blood vessels (alpha-1 blocker). Can help short-term -Diuretics are able to maintain the change chronically

Answer 102

-Extra Na+ intake should match Na+ output in a person with healthy kidneys -Chronically high circulating Ang II: Our BP will increase significantly with increased Na+ & water intake -Conditions that can cause this: Renal artery stenosis, CKD -Ang II blockade: Will probably also have low aldosterone. Causes a difficulty in retaining Na+, meaning it will very difficult to manage low BP in a patient like this -ACE Inhibitors and ARBS -Somebody with a horrificly unhealthy diet. Taking in a ton of salt everyday--> the body will decrease Ang II levels because we need to decrease Na+ reabsorption significantly

Answer 103

-Renal Artery Stenosis in one kidney--> blood pressure behind that stenosis will be low. -This will cause a low Pg --> reduced GFR --> meaning a lower amount of NaCl will make it to the macula densa--> renin will be released in response to the low GFR at this kidney --> Circulating Ang II will be released --> Constriction at the efferent arteriole --> increased GFR --> Increased aldo leading to Na and H2O reabsorption in an attempt to bring up BP. Both kidneys will be conserving water due to Aldo & Ang II The healthy kidney will reduce the amount of renin that it's releasing; however, the renin output from the stenosed kidney will overcome that. This can cause permanent damage to the healthy kidney - on the receiving end of high Pg, high GFR, chronically Tx: Stent Ace inhibitors Renin Inhibitors ARB (-tan) Remove affected kidney

Answer 104

-Taste bud is an electrically excitable cell with K+ and Na+ channels (no Cl-) -Increasing the amount of Na+ surrounding the taste bud, the taste bud becomes more excitable --> allowing us to taste our the ingredients in our food more easily Table salt is NaCl-, and typically Cl- is inibitory, but because we don't have any Cl- channels on our taste buds the Cl- doesn't have any affect

Answer 105

Increased Na+ in diet will cause an increase in H2O retention Increase in Na+ in diet --> increased Na+ in plasma --> increased Na+ in glomerular filtrate --> Increased Na+ at the macula densa --> decrease in Aldo & Ang II Increased Na+ in plasma also leads to increase in blood volume --> increased MAP --> Increased Pg --> Increased GFR --> Increased Na+ at macula densa --> decreased aldo & ang II

Answer 106

-This graph shows that if our kidney's are functioning normally, we should have minimal fluctuations in MAP when taking in excess Na+ -Essential HTN: Set-point for MAP is wrong. Higher than normal. Salt-sensitive vs nonsalt-sensitive -Nonsalt-sensitive: Tends to handle excess salt intake slightly better than salt-sensitive HTN -Salt-sensitive HTN: Renal vascular HTN, renal stenosis, anything that involves overexpression of the RAA system -Effects african-americans, some of the asian population -African-africans tend not to be effected by this -African-american population affected by salt-sensitive HTN have a low renin form of HTN; which is the opposite of what we would expect to see considering high renin would help us get rid of excess Na ACE inhibitors are useful even though there isn't much to inhibit

Answer 107

Osmotic diuretics: Mannitol Excess glucose Excess vitamin C Basically anything that causes the tubule to have more "stuff" in it, it will make it harder for water to be reabsorbed from that environment

Answer 108

ARBS: Effect contriction of the efferent arteriole. AT-I receptor dependent process; if the AT-I receptor is blocked, less Na+ reabsorption will happen in the PCT ACE Inhibitors: Inhibit Ang I from converting to Ang II; cannot bind to AT-I, less Na+ reabsorption in the PCT

Answer 109

Creatinine Clearance: Px: 1mg/dL Filtered Load: 1.25dL/min Secretion (don't really need to worry about this): 0.15mg/min Adds up to 1.4mg/min excretion rate Excretion rate must equal production rate Typically have 2million nephrons. If we instantaneously lose half of our nephrons via unilateral nephrectomy: Filtered load becomes: 0.625dL/min (62.5ml/min) Px will initially be 1mg/dL We are filtering and excreting half of what we normally do. Plasma concentration of creatinine will begin to rise up until to the point that excretion rate and production rate are now equal again. Px will need to double in order for our excretion rate to match our production rate

Answer 110

-As long as the remaining kidney is healthy, overtime we will see physiologic hypertrophy of the kidney. The remaining kidney will be able to increase it's GFR and increase it's workload without destroying itself in the process -Remaining kidney is able to increase it's GFR by about 50%

Answer 111

Normal Kidneys: 2 million nephrons Each nephron filters about 62.5 nl/min UOP: 1ml/min Unhealthy loss of nephrons: GFR is slightly higher than what would we would expect because of pathologic hypertrophy The volume excreted per nephron here is the damaging workload

Answer 112

TBW: 2/3rds of fluid is ICF TBW: 1/3rd of fluid is ECF Normal osmolarity is 300mOsm/ml- no corrections need to be made here A. Adding Isotonic NaCl: Graph shifts to the right --> meaning ECF is increased, but no reason for NaCl to enter the cells B. Add Hypertonic NaCl: Increase osmolarity. Decreasing ICF fluid and increasing ECF in order to balance osmolarity C. Adding hypotonic NaCl: Decrease osmolarity, but increase volume in ECF and ICF in order to balance osmolarity