Chapter 8 - Renal Physiology

Question 1

4 Kidney Functions

Answer 1

1. Production of erythropoietin for stimulating RBC synthesis
2. Activation of Vitamin D
3. Production of glucose via gluconeogenesis
4. Regulation of BP, blood volume, and extracellular fluid concentration

Question 2

Overall Kidney Pathway/Function

Answer 2

Blood comes in from renal artery, is filtered and leaves through renal vein, waste products from blood leave through urine via ureters (one in each kidney), goes to urinary bladder for excretion through urethra

They are 0.5% of body weight, use up 6% of oxygen and receive 25% of cardiac output

Question 3

Nephron Location

Answer 3

Functional unit of kidney, renal vascular system interfaced with renal tubular system

Renal tubular system starts in cortex and receives fluid of filtration from vascular system, then extends from cortex into inner medulla, loops back into cortex then back to medullar and into renal pelvis

Question 4

Glomerulus and Bowman’s Capsule (interface)

Answer 4

Glomerulus is a network of porous capillaries with pores in endothelial cells and large gaps between cells, it is enveloped by Bowman’s capsule

Interface between glomerulus and Bowman’s capsule is highly permeable to all small molecules (except proteins) and blood pressure in glomerular capillaries drives filtration of fluid from glomerular capillary into Bowman’s capsule

Question 5

Glomerular Filtrate and Rate

Answer 5

Identical to plasma except with no proteins

Rate - 180L/day but urine flow is just 2L/day because the vast majority of glomerular filtrate is reabsorbed by renal tubular system

Question 6

Juxtamedullary Nephron and Cortical Nephron

Answer 6

Juxtamedullary nephrons have long loop of Henle that extends into renal medulla

Cortical nephron has a short one situated mostly in the renal cortex

Question 7

Filtration Pathway

Answer 7

Glomerulus-Bowman’s Filtration Unit (renal corpuscle) –> Proximal convoluted tube (reabsorbs 60% of filtrated without changing fluid osmolarity via parallel reabsorption) –> descending limb of Loop of Henle –> ascending limb of Loop of Henle (produced osmotic gradient in renal interstitium) –> renal cortex area –> distal convoluted tubule (diluting segment) –> medullary conduction duct

Question 8

Renal Plasma Flow distribution

Answer 8

Blood enters glomerulus from renal artery

20% goes to Bowman’s capsule by glomerular filtration and 80% enters peritubular capillaries

Question 9

Loop of Henle

Answer 9

Produced osmotic gradient in renal interstitial (from 300mOsM–>1,200mOsM) to renal medulla

Question 10

Medullary Conducting Duct

Answer 10

Last segment of nephron, produces concentrated urine during dehydration by allowing fluid in collecting duct to equilibrate with the high osmolarity renal medulla

Question 11

Distal Convoluted Tubule Function

Answer 11

After loop of Henle - lowers tubular fluid osmolarity (lower than 100 mOsM) by reabsorbing Na+ from tubular fluid to peritubular capillaries

Question 12

3 Fundamental Processes in a Nephron

Answer 12

1. Glomerular Filtration - Loading fluid from glomerular capillary into renal tubular system for processing
2. Tubular Reabsorption - Returning good stuff (e.g. glucose) from renal tubular system to peritubular capillary
3. Tubular Secretion - Dumping additional Waste (e.g. H+) from peritubular capillary into renal tubular system for excretion

Question 13

Hydrostatic Pressure for Glomerular Filtration (and equation)

Answer 13

Glomerular capillary blood pressure (Pgc) is higher than Bowman’s capsule fluid pressure (Pbc) - resulting in a net hydrostatic pressure for glomerular filtration

Net Hydrostatic Pressure for Glomerular Filtration = Pgc -Pbc

Question 14

Protein Osmotic Pressure (and equation)

Answer 14

Protein osmotic pressure in glomerular capillary blood (πgb) is higher than in Bowman’s capsule fluid (πbc) - resulting in net protein osmotic pressure against glomerular filtration

Net Protein Osmotic Pressure Against Glomerular Filtration = πgc - πbc

Question 15

Glomerular Filtration Pressure (equation) and Information

Answer 15

Glomerular Filtration Pressure = Pgc - Pbc - πgc + πbc

Pgc is normally the largest term and primary driving pressure (πgc is usually second largest), the other two are relatively small because tubular fluid flows freely to the renal pelvis and proteins are normally not filtered into the Bowman’s capsule

Hydrostatic pressure favors fluid filtration and protein osmotic pressure favors fluid absorption

Question 16

Afferent and Efferent Arterioles

Answer 16

Afferent and efferent arterioles differential regulates glomerular filtration rate and renal plasma flow

Blood goes from renal artery –> afferent arteriole –> glomerular capillaries (and either into the Bowman’s capsule for glomerular filtration or) –> efferent arteriole –> peritubular capillaries (can now go to Bowman’s capsule or continue on, also collects from Bowman’s capsule) –> renal vein

Glomerular capillary BP and glomerular filtration rate are dependent on vascular resistances of afferent and efferent arterioles because glomerular capillary is situated between the arterioles

Afferent arteriole controls BP drop from renal artery to glomerular capillary, vasoconstriction of arteriole decreases glomerular filtration pressure and filtration rate because an increase in the resistance of the arteriole increases the BP drop from the renal artery to the glomerular capillary

Efferent arteriole controls BP drop from glomerular capsular to peritubular capillary, vasoconstriction of the arteriole increases glomerular filtration pressure and filtration rate because increase in resistance decreases pressure drop from glomerular capillary to the peritubular capullar

Question 17

RBF and GFR

Answer 17

Changes in renal blood flow do no necessarily follow changes in glomerular filtration rate - sympathetic stimulation decreases both but efferent arteriole vasoconstriction (induced by angiotensin II) increases filtration rate but decreases renal blood flow

GFR is an important criterion in the classification of kidney disease

Question 18

Renal Reabsorption

Answer 18

Process of transporting a molecule by renal tubular cells from glomerular filtrate in the renal tubular system to peritubular capillaries, decreasing the excretion of the molecule

Question 19

Renal Excretion

Answer 19

Process of transporting a molecule by renal tubular cells from the peritubular capillaries into the renal tubular system, increasing the excretion of a molecule

Question 20

Excretion Magnitude (and equation)

Answer 20

Glomerular filtration is the common first step for excretion of all molecules but actual excretion magnitude is determined by relative magnitudes of renal absorption and secretion

Excretion = Filtration - Reabsorption + Secretion

Question 21

Creatinine Excretion

Answer 21

Determined by glomerular filtration only because it is neither reabsorbed nor secreted by renal tubular cells

Question 22

Glucose Excretion

Answer 22

Usually zero because glucose is completely reabsorbed from glomerular filtrate in the tubular system to the peritubular capillaries

Na+/glucose transporter (SGLT2) in luminal membrane of proximal tubular call, once high concentration inside cell the glucose carrier (GLUT2) in basolateral membrane facilitates diffusion down concentration gradient from inside cell to interstitial where it diffuses into peritubular capillary network (Na+/K+ pump transports Na+ out of cell into interstitium)

Question 23

PAH Excretion

Answer 23

Diagnostic agent for renal function - determined by renal plasma flow because PAH enters renal tubular system by glomerular filtration and is also secreted almost completely from peritubular capillaries into the renal tubular system

Question 24

Proximal Convoluted Tubule and Transporters

Answer 24

First renal segment after Bowman’s capsule, major site of renal reabsorption (more than 60% here)

There is the lumen of the proximal tubule, then the proximal convoluted tubule cell, then the interstitial space, and then the bloodstream

Major functions: isosmotic fluid reabsorption, reabsorption of organic anions (ex. glucose, AAs), acid-base regulation (ex. reabsorption of HCO3- and secretion of H+ and NH4+)

Transporters on the luminal side of proximal tubular cells are Na+-coupled transporters for driving reabsorption of molecules against their concentration gradients (co-transport, Na+ and molecule (like phosphate) transported in together, then Na+ removed from cell by the K+/Na+ pump and molecule moves down gradient and out of cell onto basolateral side)

Basolateral side diffuses into peritubular capillary

Question 25

Glucose Levels in Urine/Diabetes (and equation)

Answer 25

Glucose should not be in urine of healthy patients because plasma [glucose] is below threshold for complete reabsorption of glucose from glomerular filtrate (should be 5mM on average and 9mM after a meal)

The threshold (11mM) is when all binding sites of glucose transporters are saturated and renal tubular transport reaches maximum transport rate

In patients with diabetes, it can exceed the threshold for complete glucose reabsorption and some glucose will be excreted into the urine, high concentration of glucose is toxic to organ systems so in patients with diabetes, pharmacological blockers of the Na+-glucose cotransporter is used to block renal reabsorption of glucose and increase its excretion in urine

Rate of Urinary Glucose Excretion = Glomerular Filtration Rate x [plasma glucose] - Max Transport Rate

Question 26

Osmolarity in Proximal Tubule

Answer 26

Osmolarity of fluid leaving proximal tubule is isosmotic relative to osmolarity of plasma because high water permeability of proximal tubule allows water reabsorption to follow solute reabsorption

Question 27

Loop of Henle Pathway and Basic Function

Answer 27

Loop of Henle is tubular segment following proximal convoluted tubule that extends from cortex to medulla and then loops back to the cortex

Its job is to generate an osmotic gradient in the renal interstitium via countercurrent multiplication

Renal medulla is high osmolarity and cortex is low osmolarity

Question 28

Countercurrent Multiplication

Answer 28

Countercurrent - opposite direction of fluid flow in the ascending and descending limbs of the Loop of Henle

Multiplication - amplification of the Na+ pumping effect of each segment of the loops to generate a large overall osmotic gradient in the renal interstitium - each segment of the loop is capable of generating approximately 200mOsM gradient between the renal tubular fluid and the renal interstitium (overall osmotic gradient ranges from 300mOsM in renal cortex to 1,200 mOsM in the renal medulla)

Question 29

Ascending and Descending Limb Features

Answer 29

Descending limb has low Na+ pumping activity and high H2O permeability, ascending has high Na+ pumping activity and low H2O permeability

Descending limb has a lot of aquaporin channels for high water permeability which causes tubular fluid of descending limb to reach osmolarity of renal interstitium (goes from 300-1,200 mOsM at the bottom)

Ascending limb has a lot of Na+ pumping activity to create a local osmotic gradient that is approximately 200mOsM higher in the renal interstitium than tubular fluid in the ascending limb (goes from 1,200-100mOsM at the top)

The countercurrent fluid flow transfers fluid of high osmolarity from the descending limb to the ascending limb for further concentration

Question 30

Explanation of creation of concentration gradient in Loop of Henle

Answer 30

The whole loop is filled at 300mOsM, Na+ pump in the ascending limb pumps Na+ out to make that part all 200 mOsM and the interstitium becomes 400mOsM. By diffusion and water permeability the descending limb is all 400 mOsM too.

Countercurrent flow pushes new 300mOsM solution into the descending limb (top part is 300mOsM, bottom is 400mOsM) and the ascending moves up (top part is 200mOsm bottom part is 400 mOsM).

The ascending limb pumps out Na+ again so it ranges from 300mOsM at the bottom to 100 mOsM at the top (and the interstitium ranges from 500 at bottom to 300 at top, this equilibrates with the descending making it in the same range)

This continues until the descending limb is increasing by 100 mOsM each step and the ascending limb is increasing by each step

Question 31

Urea

Answer 31

Urea transport contributes to the production of concentrated urine and the generation of osmotic gradient in the renal interstitium

Product of protein metabolism, contributes to high osmolarity in renal medulla (it is concentrated in the renal medulla which then drives the transported of urea by facilitated diffusion into the bottom portion of the loop of Henle)

Accumulates in renal medulla as a result of water reabsorption which causes it to become concentrated passively in the tubular fluid along the renal tubular system, and it leaves the renal tubular system at the medullary collecting duct and reenters at the bottom of the loop of Henle because urea transporters are enriched at this location

Question 32

Regulation of ECF Osmolarity (and equation) and ADH

Answer 32

Maintenance of normal plasma osmolarity is essential because cell volume is determined by ECF osmolarity (low osmolarity causes cell swelling, very dangerous for brain, and high osmolarity causes cell shrinkage)

Osmoreceptors in hypothalamus detect increase in plasma osmolarity and stimulate release of ADH/vasopressin into circulation from posterior pituitary, reaches kidneys and causes the kidneys to increase water absorption and urine osmolarity (conserving water for restoring ECF osmolarity), concentration of ADH in plasma is directly (and linearly) related to urine osmolarity - ADH also stimulates thirst for drinking water (to restore normal plasma osmolarity)

High ECF Osmolarity –> increase in ADH/VP in blood (via hypothalamus) –> increased renal reabsorption of water

Question 33

ADH/VP Deficiency

Answer 33

Not capable of producing concentrated urine, tend to produce a lot of urine with low osmolarity (called diabetes insipidus) - can be caused by genetic deficiencies in vasopressin receptor and aquaporin

Question 34

ADH/VP Mechanism

Answer 34

ADH/VP increases renal reabsorption of water by increasing water permeability of the collecting duct (allowing equilibration of fluid osmolarity in collecting duct with high osmolarity in the renal medulla)

This is done by ADH/VP binding to a GPCR that is coupled by Gs to adenylate cyclase that catalyzes generation of cAMP from ATP. cAMP activates signaling pathways that stimulate synthesis of aquaporin water channels, the package of those channels in membrane vesicles, and the fusion of aquaporin containing vesicles with the cell membrane (causing equilibration with cells in the collecting duct where osmolarity is at 1,200mOsM)

Question 35

ECF Volume Regulation

Answer 35

ECF volume regulation is done via the renin-angiotensin-aldosterone system

In response to low renal perfusion (bc of low ECF volume), the kidney secretes renin (proteolytic enzyme) into circulation after low Na+ levels are sensed by juxtaglomerular apparatus (macula densa cells sense Na+ levels through distal tubule), this causes the juxtaglomerular cells to relate renin, it catalyzes conversion of angiotensinogen (a precursor synthesized by liver) to angiotensinogen I, which is then converted to angiotensin II by angiotensin-converting enzymes on endothelial cells in the pulmonary and renal circulation

Angiotensin II stimulates release of aldoestrone, a steroid hormone by adrenal cortical cells into circulation, this increases Na+ reabsorption in the distal tubule, connecting tubule, and cortical collecting duct by stimulating expression of Na+ channels on luminal side and Na+/K+-ATPase on basolateral side of tubular epithelial cells, this conserves Na+ and water for restoring normal plasma volume

Low ECF volume –> renin release from kidney via juxtaglomerular apparatus which senses low Na+ levels –> renin catalyzes angiotensinogen (from liver) –> angiotensin I –> angiotensin II (by angiotensinogen-coverting enzymes on endothelial cells in pulmonary and renal circulation) –> release of aldosterone by adrenal cortical cells –> increased Na+ reabsorption in tubule, conserving Na+ and water for restoring ECF volume

Question 36

All Effects of Angiotensin II

Answer 36

1. Release of aldosterone by adrenal cortical cells
2. Stimulates arteriolar vasoconstriction in systemic circulation (increases peripheral resistance and arterial BP)
3. Stimulates efferent arteriolar vasoconstriction in kidney, causing increase in glomerular filtration rate
4. Stimulates sympathetic nervous system (increasing cardiac output and BP)
5. Increases secretion of ADH by posterior pituitary leading to increase in renal water reabsorption (increasing plasma volume)

Question 37

Renin-Angiotensin-Aldosterone System and Problems

Answer 37

It acts as negative feedback mechanism for maintaining normal blood volume and BP, overactivity of the system can cause abnormal increase in blood volume and hypertension, can be treated with inhibitors of the renin-angiotensin-aldosterone system (ex. angiotensin-converting enzyme inhibitor, aldosterone receptor antagonist, etc. for the treatment of hypertension)

Question 38

Regulation of ECF [Ca2+]

Answer 38

1. Vitamin D is hydroxylated in the liver and kidney
2. Parathyroid hormone and Vitamin D enhance renal Ca2+ reabsorption by stimulating protein expression of Ca2+ transporters in renal tubular epithelial cells

Important for all organ systems - cardiac muscle contraction and NT release are all dependent on Ca2+ influx from ECF into cytoplasm through calcium channels in cell membrane

Plasma Ca2+ is filtered into the renal tubular system by glomerular filtration, more than 80% of filtered Ca2+ is reabsorbed passively in the proximal tubule and ascending limb of loop of Henle via the ca2+ concentration gradient produced by Na+ and water reabsorption

15-20% of filtered Ca2+ is reabsorbed by tubular cells in distal tubule under regulation by parathyroid hormone and Vitamin D (this happens by Ca2+ entering luminal side of tubular cell via calcium channels and leaving via the basolateral side through Na+/Ca2+ exchange and Ca2+-ATPase)

Parathyroid hormone, Vitamin D, and estrogen enhance renal Ca2+ reabsorption by stimulating the expression of Ca2+ transporters in the tubular epithelial cells

Question 39

Regulation of ECF pH (and equations)

Answer 39

Need to keep ECF within 6.8-7.7 (normal is 7.4) via respiratory and renal control of CO2/bicarbonate buffer system

CO2 + H2O H2CO3 H+ + HCO3-

pH = pK + log([HCO3-]/[aPCO2]) (Henderson Hasselbalch equation)

The HH equation predicts the extracellular pH and is determined by the HCO3 to PCO2 ratio, respiratory system regulates extracellular pH by regulating PCO2 in ECF and kidneys regulate pH by regulating [HCO3] in the ECF

HCO3- can be lost from the ECF by glomerular filtration of HCO3- from plasma into renal tubular system and neutralization of HCO3- by H+ produced from protein and fat metabolism - kidneys capture HCO3- in glomerular filtrate completely by tubular reabsorption

HCO3- in urine is normally zero, kidneys excrete H+ by tubular secretion of H+ and ammonium (NH4+)

Question 40

Tubular Reabsorption of Bicarbonate (and inhibitors)

Answer 40

Bicarbonate is filtered from the plasma into the renal tubular system by glomerular filtration but is completely reabsorbed back into circulation by renal tubular cells (80% of filtered HCO3- is reabsorbed by proximal tubule, and 20% is reabsorbed by ascending limb of loop of Henle, distal convoluted tubule and collecting duct)

Tubular epithelial cells reabsorb filtered HCO3- indirectly - inside tubular cell, carbonic anhydrase converts H2O and CO2 to H+ and HCO3-, H+ then goes from a tubular cell into tubular lumen by Na+/H+ exchange and H+-ATPase at luminal membrane for neutralization of luminal HCO3- to form H2CO3, which is converted back to CO2 and H2O on the luminal membrane

Luminal CO2 then enters tubular cell and blood via diffusion and HCO3- is transported from a tubular cell into ECF and circulation via Na+/HCO3- cotransport and HCO3-/Cl- exchange at the basolateral membrane

Carbonic anhydrase is critical for renal HCO3- reabsorption, inhibitors of it can be used to increase HCO3- excretion to treat respiratory alkalosis caused by hyperventilation at high altitudes (hyperventilation is necessary for blood oxygenation at high altitudes but suppresses the respiratory center and the inhibitor helps normalize the ratio of CO2 to HCO3- and the pH of ECF)

Question 41

Renal Excretion of Titratable Acid

Answer 41

Renal excretion of H+ production from protein and fat metabolism is necessary to prevent the H+ from neutralizing extracellular HCO3-, mechanism is similar to HCO3- reabsorption but excreted H+ is buffered by phosphate in the urine

Carbonic anhydrase inside tubular cell catalyzes conversion of CO2 and H2O to H+ and HCO3-, H+ is then transported actively from a tubular cell into luminal fluid by H+-ATPase at the luminal membrane and HCO3- is transported into circulation by the HCO2-/Cl- exchange at the basolateral membrane

H+ is buffered mostly by phosphate causing a modest decrease in pH (so urine can range from pH 5-8 depending on diet, Western diet is more acidic)

Amount of H+ captured by buffer in urine is known as “titratable acid” because it can be determined by titrating the urine back to 7.4

Question 42

Renal Excretion of Ammonium (and equation)

Answer 42

Excretion of ammonium (NH4+) contributed to 50% of total renal excretion of H+ - count it and titratable acid for total renal acid excretion

Renal tubular cells produce HCO3- and NH4+ from glutamine (HCO3- is transported from a tubular cell to the circulation via Na+/HCO3- cotransport in the basolateral membrane and NH4+ is excreted into tubular fluid through channels and Na+/NH4+ exchange at luminal membrane

NH4+ is in equilibrium with ammonia (NH3) and H+ inside tubular cells and in tubular fluid and at pH 7.4 98% is at NH4+

Question 43

Mechanisms for Production of Concentrated Urine

Answer 43

1. Generation of osmotic gradient in Renal Interstitium
2. ADH increases water permeability of collecting duct to enable the diffusion of water from collecting duct to the renal interstitium

Question 44

Mechanisms for the Production of Dilute Urine

Answer 44

1. Reduction of tubular fluid osmolarity by Na+ pumping
2. In absence of vasopressin (ADH), water channels are removed from collecting duct membrane causing the tubular fluid to remain hypo osmotic as it passes through the collecting duct

Question 45

Hypertension and Sympathetic Nervous System / Kidney

Answer 45

The sympathetic nervous system stimulates renin release by kidneys and kidneys stimulate activity of sympathetic nervous system via angiotensin II activity

Sympathetic nervous system causes vasoconstriction leading to hypertension

Angiotensin II induces vasoconstriction aldosterone induced Na+ and water retention, causing hypertension

Question 46

Respiratory and Metabolic Relation to pH and Issues

Answer 46

Hypoventilation causes an increase in CO2 and respiratory acidosis

Hyperventilation causes a decrease in CO2 and respiratory alkalosis

A Decrease in HCO3- and therefore more acid production is metabolic acidosis

An increase in HCO3- and therefore more bicarbonate production is metabolic alkalosis

Question 47

Regulation of Acid-Base by the Kidneys

Answer 47

1. Tubular reabsorption of HCO3-
2. Tubular secretion of H+ as titratable acid
3. Tubular excretion of NH4+

Question 48

Renal Clearance (and equations)

Answer 48

Renal clearance is a measure of the kidney’s rate of clearing plasma of a given molecule (X) by urinary excretion

Clearance of X (in volume/time) = [X in urine] x Urine Flow (volume/time) / [X in plasma]
C=UV/P
Clearance of X = Rate of Urinary Secretion of X / [X in plasma]

Question 49

Substances that are Filtered Only (and equations)

Answer 49

For substances that are filtered only - clearance equals glomerular filtration rate (ex. creatinine, inulin)

Creatinine (product of muscle metabolism) is filtered into the renal tubular system by glomerular filtration but is neither reabsorbed nor secreted by tubular cells so the rate of urinary excretion of creatine equals the rate of entry of creatine into the renal tubular system by GFR

Rate of Urinary Excretion of Creatinine = [creatinine in plasma] x GFR

Clearance of Creatinine = GFR

Can understand by recognizing that GFR is the flow of plasma into the renal tubular system that can be cleaned of creatinine, estimated GFR based on creatinine clearance is an important indicator of kidney function and kidney disease diagnosis - can do this boy collecting blood for measuring creatine concentration in blood and collecting urine and measuring creatine concentration in urine, high creatinine concentration is urine is indicator of kidney failure

Question 50

Substances that are Filtered and Reabsorbed (equations/relations)

Answer 50

For substances that are filtered and reabsorbed clearance is lower than glomerular filtration rate (GFR), (ex. Na+)

When a substance X is filtered into renal tubular system by glomerular filtration and then reabsorbed by tubular cells, the rate of urinary excretion is less than the rate of delivery of the substance carried by glomerular filtration

Rate of Urinary Excretion of X

Question 51

Substances that are Filtered and Secreted (equations/relations)

Answer 51

For substances that are filtered and secreted, clearance is higher than GFR (ex. PAH, a diagnostic agent for assessing renal perfusion, its clearance approximates renal plasma flow since kidneys clear PAH almost completely from the plasma that enters the renal circulation)

20% of renal plasma flow is filtered into renal tubular system and the other 80% go to peritubular capillaries where substances can be secreted into renal tubular system for secretion, when substance X is filtered into renal tubular system via glomerular filtration and also secreted by tubular cells, the rate of urinary excretion is higher than the rate of delivery of the substance carried by glomerular filtration

Rate of Urinary Excretion of X > [X in plasma] x GFR
Clearance of X > GFR

Question 52

Summary of Clearance of a Substance

Answer 52

Clearance can range from zero to renal plasma flow (max)

Clearance = GFR for filtration only
Clearance GFR for filtration + secretion

Question 53

Urine Storage and Release

Answer 53

Urine produced by kidneys is stored in the urinary bladder and periodically released through the urethra during urination

Micturition center in brain stem regulates urine storage (continence) and urination (micturition) or the lower urinary tract by regulating parasympathetic, sympathetic, and somatic outputs in response to mechanosensory input from urinary bladder wall

Question 54

3 Structures of lower urinary tract

Answer 54

Three muscular structures of lower urinary tract - urinary bladder, bladder outlet, and external urethral spinster are regulated by 3 branches of the nervous system

Question 55

Continence Phase

Answer 55

During continence phase (when urinary bladder is not fully filled) mechanosensory input to the micturition center is low because mechanical stretch of urinary bladder is low and the micturition center inhibits parasympathetic output and stimulates sympathetic and somatic outputs to lower urinary tract

Inhibition of parasympathetic output to detrusor smooth muscle cells causes relaxation of bladder wall for accommodating continued filling of the urinary bladder with urine and stimulation of sympathetic output to smooth muscle cells of internal urethral sphincter and somatic output to skeletal muscle cells of external urethral sphincter causes contraction of these two sphincters to prevent leakage of urine during continence phase

Question 56

Bladder Muscle Anatomy and Innervation

Answer 56

Detrusor muscle of bladder wall (smooth muscle) is stimulated by the pelvic nerve of the parasympathetic nervous system

Internal Urethral sphincter (smooth muscle) is stimulated by the hypogastric nerve of the sympathetic nervous system

External Urethral Sphincter (skeletal muscle) is stimulated by the pedestal nerve of the somatic nervous system

Question 57

Micturition Phase

Answer 57

Opposite of continence phase - when the urinary bladder is fully filled the mechanosensory input to the micturition center is high because mechanical stretch of the urinary bladder wall is high - therefore the micturition center stimulates parasympathetic output and inhibits sympathetic and somatic outputs to the lower urinary tract

The stimulation of parasympathetic output to detrusor smooth muscle cells causes contraction of bladder wall and build up of pressure inside urinary bladder, inhibition of sympathetic output to smooth muscle cells of internal sphincter and somatic output to skeletal muscle cells of the external sphincter causes relaxation of these two sphincters for urinary flow during micturition phase

Question 58

Overactive bladder syndrome

Answer 58

characterized by increase in urgency for urination, can treat with muscarinic receptor antagonists to block the stimulating effect of parasympathetic nervous system on detrusor smooth muscle cells in the bladder wall - can also target sensory pathway from urinary bladder to micturition center

Question 59

Chronic Kidney Failure

Answer 59

Kidney failure is characterized by diminished GFR, increased urinary excretion of protein, or both

Can lead to accumulation of waste products and excess volume in the extracellular fluid which can lead to failure of multiple organ systems (ex. abnormally high K+ can lead to abnormalities in membrane potentials and cardiac arrhythmia)

Question 60

Dialysis

Answer 60

Dialysis systems are used for removing waste products from ECF in patients with kidney failure - it is a diffusional exchange of waste products between ECF and dialysate through a membrane system that is selectively permeable to small molecules but is impermeable to proteins and cells

Question 61

Peritoneal Dialysis

Answer 61

Clean dialysate is infused into the abdominal cavity via a catheter. the peritoneum lining the abdominal cavity consists of a monolayer of mesothelial cells facing the abdominal cavity and a capillary network underneath the mesothelial layer - the peritoneum serves as a membrane system for diffusional exchange between the dialysate and the ECF

After 4-6 hours of equilibration, the dialysate is drained from the abdominal cavity using a drain bag for disposal, can be performed at home and is done 4 times each day

Question 62

Hemodialysis

Answer 62

Blood is pumped out of patient’s circulation via an artery into a membrane dialyzer for diffusional exchange with dialysate, cleaned blood leaving the membrane dialyzer is pumped back into patients circulation via a vein

The dialyzer membrane is engineered to be permeable to small molecules but impermeable to proteins and cells and the dialysate is continuously refreshed with clean dialysate by a separate pump

Takes place in a clinical center, lasts 3-5 hours and is 3 times per week

Question 63

Kidney Transplant

Answer 63

Transplant health kidney from donor to recipient, donor kidney’s renal artery and renal vein are connected to recipient’s artery and vein the abdominal cavity, donor kidneys ureter is connected to recipients urinary bladder

Recipients failed kidneys are usually left in place unless they cause infection or hypertension in the patient

Question 64

Diuretics

Answer 64

They lower plasma volume by inhibiting Na+ reabsorption