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APHY 201 Exam 4c
Ch. 17 Physiology of the Kidneys (Renal)
| Question | Answer |
|---|---|
| What are the 5 primary functions of the kidneys regarding the body's extracellular fluid environment? | The kidneys regulate blood plasma volume, wastes, electrolytes, and pH, and they secrete erythropoietin along with the liver. |
| What are the most common compositions of kidney stones? | About 80% are calcium stones, but others can be made of magnesium ammonium phosphate or uric acid. |
| What are 3 primary treatment options for kidney stones? | Treatments include medications, lithotripsy to shatter the stones with shock waves, and surgery. |
| What muscle lines the wall of the urinary bladder and what structures connect its cells? | The detrusor muscle lines the bladder wall, and its smooth muscle cells are connected by gap junctions. |
| How is the detrusor muscle innervated? (SNS or PSNS; ACh or NE/E, what type of receptors) | It is innervated by parasympathetic neurons that release acetylcholine onto muscarinic ACh receptors. |
| What types of muscle compose the 2 sphincters surrounding the urethra? | The internal urethral sphincter is made of smooth muscle, and the external urethral sphincter is made of skeletal muscle. |
| What is the reflex where stretch receptors in the bladder signal the spinal cord to inhibit parasympathetic nerves to the detrusor muscle and stimulate somatic motor neurons to the external urethral sphincter, preventing involuntary emptying? | the guarding reflex |
| (colored) How does stretch of the bladder initiate the voiding reflex? What structures are involved? How are SNS and PSNS involved? | Stretch information passes to the micturition center of the pons, causing parasympathetic neurons to rhythmically contract the detrusor muscles while inhibiting sympathetic innervation to relax the internal urethral sphincter. |
| What occurs when increased abdominal pressure causes urine leakage because the pelvic floor no longer provides adequate support to the urethra, often due to childbirth or aging? | stress urinary incontinence in women |
| What is a frequent cause of urinary incontinence in men? | In men, urinary incontinence frequently occurs as a result of treatments for prostate cancer. |
| What are 3 hallmark symptoms of an overactive bladder? | It involves uncontrolled contractions of the detrusor muscle that produce a great urge to urinate, frequent urinations, and the leakage of a large volume of urine. |
| How is urinary incontinence diagnosed using urodynamic testing? | It is diagnosed via cystometric tests where bladder pressure and compliance are measured as the bladder is filled with warm water and the subject indicates when the urge to urinate appears. |
| (starred) What is the pathway of blood through the renal blood vessels? | renal artery to segmental arteries, interlobar arteries, arcuate arteries, interlobular arteries, afferent arterioles, glomerulus, efferent arterioles, peritubular capillaries, interlobular veins, arcuate veins, interlobar veins, and renal vein. |
| What is the pathway of fluid through the nephron tubules? | Filtrate passes from the glomerular capsule into the proximal convoluted tubule, down and up the loop of Henle, into the distal convoluted tubule, and finally into the collecting duct where it drains into a minor calyx as urine. |
| What are the differences between juxtamedullary and cortical nephrons? | Juxtamedullary nephrons sit closer to the corticomedullary junction, have longer loops of Henle, and are better at making concentrated urine, while cortical nephrons sit more superficially in the cortex and have shorter loops. |
| What is the incurable congenital disorder where kidneys are enlarged by hundreds to thousands of fluid-filled cysts forming in nephron segments, with the autosomal dominant form affecting roughly 1 in 1,000 people? | Polycystic Kidney Disease (PKD) |
| What 2 general structures make up the renal corpuscle? | The renal corpuscle is composed of the glomerular capillaries and the surrounding glomerular (Bowman’s) capsule. |
| What structure of the glomerulus filters blood? Their large pores allow water and solutes to leave while blocking blood cells, and surrounding charges discourage plasma proteins from passing through. | fenestrated capillaries |
| What are the 3 layers of the filtration membrane that filtrate must pass through? | Filtrate must pass through the capillary fenestrae, the glomerular basement membrane, and the visceral layer of the glomerular capsule composed of podocytes with foot processes. |
| What are prevented from entering the urine by slit diaphragms between podocyte foot processes, and any small amounts that filter out are almost entirely reabsorbed in the proximal convoluted tubule by active receptor-mediated endocytosis? | almost all proteins, though a little albumin makes it through |
| What 3 forces interact to produce the net filtration pressure of about 10mmHg in the glomerular capsule? | The net filtration pressure is produced by an interaction between the hydrostatic pressure of the blood, colloid osmotic pressure, and capsular pressure. |
| What is the normal Glomerular Filtration Rate (GFR) and how fast does it process the body's blood? | The normal GFR is 115 to 125 ml per minute (180 L/day), meaning the total blood volume is filtered every 40 minutes. |
| (important) What 3 main systems control the adjustment of glomerular blood pressure and GFR? | GFR is controlled by extrinsic sympathetic control, intrinsic renal autoregulation, and hormonal mechanisms involving renin and angiotensin. |
| How does the sympathetic nervous system regulate GFR during a fight-or-flight reaction or strenuous exercise? | It triggers vasoconstriction of the afferent arterioles to decrease urine formation, which compensates for drops in blood pressure and redirects blood flow to the heart, brain, and skeletal muscles. |
| How does the myogenic mechanism of renal autoregulation maintain a constant GFR? | Smooth muscle cells in the afferent arterioles sense stretching from rising blood pressure and reflexively contract to decrease excess blood flow, or relax when blood pressure falls to increase flow. |
| How does tubuloglomerular feedback regulate GFR when tubule fluid flows too quickly? | Macula densa cells monitor tubule fluid; if it becomes too salty, they secrete ATP (converted to adenosine) that stimulates juxtaglomerular cells to constrict the afferent arteriole, slowing the flow and normalizing sodium concentration. |
| What are the potential effects of abnormal Glomerular Filtration Rates? (if it's higher or lower) | If GFR increases, dehydration and electrolyte depletion can occur from high urine output; if GFR decreases, wastes are reabsorbed, potentially causing azotemia. |
| What is the systemic blood pressure range over which renal autoregulation of GFR is stable? | Renal autoregulation can stabilize GFR for a MAP blood pressure range of 70 to 180 mmHg, but it cannot compensate for extreme fluctuations. |
| (process question) How does Angiotensin II maintain waste filtration when systemic blood pressure decreases? | It constricts the efferent arterioles more than the afferent arterioles, which increases glomerular blood pressure to maintain GFR despite decreased systemic blood pressure. |
| How does Angiotensin II work to increase blood volume and systemic blood pressure? (3 things) | It enhances NaCl and water reabsorption by lowering peritubular capillary pressure, directly stimulating the proximal convoluted tubule, and stimulating the secretion of aldosterone and ADH. |
| What is the minimum volume of urine in mL that must be excreted to rid the body of wastes, and what is this called? | A minimum of 400 mL must be excreted, which is known as obligatory water loss. |
| What percent of unregulated water reabsorption occurs in the nephrons? (2 structures are responsible) | 85% of reabsorption occurs in the proximal tubules (65%) and the descending loop of Henle (20%). |
| What is the osmolality of filtrate in the glomerular capsule compared to blood plasma? | It is iso-osmotic to blood plasma, at approximately 300 mOsm. |
| How does the active transport of sodium in the proximal tubule drive water reabsorption? what is the term for the driving force of the water? | Sodium is actively pumped out of the filtrate into the peritubular blood, setting up what's called a concentration gradient that drives the osmosis of water. |
| How do cells of the proximal tubules maintain a lower sodium concentration than the filtrate? | They maintain lower concentration due to Na+/K+ pumps on their basal side and a generally low permeability to sodium. |
| How does the active transport of sodium affect chloride in the proximal tubule? | Pumping sodium into the interstitial space attracts negative chloride ions out of the filtrate via electrostatic attraction. |
| What hormone regulates the absorption of the final 15% of water later in the nephron? | It is absorbed under the control of anti-diuretic hormone (ADH). |
| Which portion of the loop of Henle sets up the concentration gradient for the osmosis of water? | The ascending portion of the loop of Henle |
| How do the permeabilities of salt and water differ in the ASCENDING limb of the loop of Henle? | Salt is pumped out ascending limb, but walls are impermeable to water. Na+ moves down its gradient from filtrate into tubule cells; Cl- and K+ 2° transport by Na+-K+-2Cl- cotransport. Na+ is pumped out, Cl- follows, and K+ diffuses back into filtrate |
| What effect does the ascending limb have on the surrounding interstitial fluid and the tubular fluid? (what part is hypertonic and what is hypotonic) | It makes the interstitial fluid increasingly solute-concentrated (hypertonic) and the tubular fluid increasingly dilute (hypotonic) as it ascends. |
| What is the permeability of the descending limb of the loop of Henle? | It is not permeable to salt, but it is highly permeable to water. |
| (process question) How does the countercurrent multiplier mechanism operate between the two limbs of the loop of Henle? | It operates as a positive feedback mechanism: salt removed by the ascending limb concentrates the interstitial fluid, which draws more water out of the descending limb, thereby making the fluid entering the ascending limb even saltier. |
| What role do the vasa recta play in the countercurrent system? | These specialized blood vessels take in salts in their descending portion and lose them in the ascending portion, which keeps salts trapped in the interstitial space while removing reabsorbed water. |
| (process question) How does urea contribute to the countercurrent system in the kidneys? | Urea is transported out of the collecting duct and diffuses back into the ascending limb, helping to increase the osmolarity of the deep medulla to reach a maximum concentration of 1200 mOsm. |
| In the proximal tubule, is there active transport of a solute involved, and is water passively transported? | Na+ is actively transported, and water is passively transported. |
| In the descending limb of the nephron loop, is there active transport of a solute involved, and is water passively transported? | There is no active transport, but water is passively transported. |
| In the thin segment of the ascending limb, is there active transport of a solute involved, and is water passively transported? | There is no active transport, and no passive water transport. |
| In the thick segment of the ascending limb, is there active transport of a solute involved, and is water passively transported? | Na+ is actively transported, but no water is passively transported. |
| In the distal tubule, is there active transport of a solute involved, and is water passively transported? | Na+ is actively transported, and no water is passively transported except in the last part of the tubule that is permeable to water. |
| In the collecting duct, what largely determines the passive transport of water? | It depends on the presence of ADH-induced aquaporins. |
| (hello question) What happens when ADH binds to receptors on the collecting duct cells? | It triggers cAMP and protein kinase, causing vesicles containing aquaporin channels to fuse to the plasma membrane and allow water to exit via osmosis. |
| Where is Anti-Diuretic Hormone (ADH) produced, stored, and released? | ADH is produced by neurons in the hypothalamus and is stored and released from the posterior pituitary gland. |
| How does the body regulate ADH when blood osmolality increases due to dehydration? (what receptor, does ADH go up or down, and does urine volume go up or down) | Osmoreceptors in the hypothalamus react, ADH secretion is increased, and urine volume decreases. |
| How does the body regulate ADH when blood osmolality decreases due to water uptake? (what receptor, does ADH go up or down, and does urine volume go up or down) | Osmoreceptors in the hypothalamus react, ADH secretion is decreased, and urine volume increases. |
| How do stretch receptors in the left atrium influence ADH secretion when blood volume goes up? (what receptor, does ADH go up or down, and does urine volume go up or down) | They react to the stretch, causing ADH secretion to decrease and urine volume to increase. |
| How do stretch receptors in the left atrium influence ADH secretion when blood volume goes down? (what receptor, does ADH go up or down, and does urine volume go up or down) | They react to the drop in volume, causing ADH secretion to increase and urine volume to decrease. |
| What are the 2-3 characteristic signs of diabetes insipidus? | It is characterized by polyuria (large urine volume), excessive thirst/polydipsia (drinking many fluids), and hypotonic, dilute urine under 300 mOsm. note that polyphagia is related not to diabetes insipidus but mellitus |
| What is the difference between central and nephrogenic diabetes insipidus? | Central diabetes insipidus is caused by inadequate ADH secretion, whereas nephrogenic diabetes insipidus is the kidneys' inability to respond to ADH. |
| What are common causes of nephrogenic diabetes insipidus? | It can be caused by genetic defects in aquaporin channels or ADH receptors, or acquired from drug therapy such as lithium. |
| What 3 processes are involved in renal clearance to remove excess ions and wastes from the blood? | Renal clearance involves filtration, reabsorption (which decreases clearance), and secretion (which increases clearance). |
| How is the excretion rate calculated and what does it measure (abbreviation)? | The excretion rate is calculated as (filtration rate + secretion rate) - reabsorption rate, and it is used to measure the glomerular filtration rate (GFR). |
| What are the membrane carriers that transport foreign molecules like drugs into the tubules for excretion? | They are called organic anion transporters (OATs) or organic cation transporters (OCTs). |
| Why do OATs and OCTs overlap in function and potentially interfere with therapeutic drugs? | These carriers are polyspecific and can transport many different molecules very rapidly. |
| What is inulin and why is it a great indicator of glomerular filtration rate? | Inulin is a plant polysaccharide that is an excellent indicator of GFR because it is filtered but not reabsorbed or secreted, meaning all filtered inulin is excreted in the urine. |
| What is the formula for calculating GFR using inulin? | The formula is GFR = (V × U) / P, where V is the rate of urine formation, U is inulin concentration in the urine, and P is inulin concentration in the plasma. |
| How is renal plasma clearance defined? | It is the volume of plasma from which a substance is completely removed by the kidneys in one minute. |
| (repeated question) What is the average Glomerular Filtration Rate (GFR)? | The average GFR is 120 mL/min. |
| How does a substance's renal clearance compare to GFR if it can be reabsorbed? | If a substance is reabsorbed, its clearance is less than the GFR. |
| How does a substance's renal clearance compare to GFR if it is filtered and secreted? | If a substance is filtered and secreted, its clearance will be greater than the GFR. |
| Why is the clearance of urea less than the average GFR? | The clearance of urea is 75 mL/min, which is less than the average GFR because some urea is reabsorbed. |
| (process question) Why is creatinine's renal plasma clearance slightly greater than the true GFR? | Creatinine is filtered and not reabsorbed, but it is slightly secreted by the tubules. |
| How is creatinine used in practice to assess kidney function without an IV of inulin? (plus 3 factors) | Creatinine’s plasma concentration, along with a person’s age, sex, and weight, is used in equations to calculate an estimated GFR (eGFR). |
| What does a blood urea nitrogen (BUN) test measure? | It measures the ratio of the plasma concentrations of urea to creatinine to provide additional information about kidney health. |
| What happens to a substance during filtration and how does it affect clearance? | The substance enters the glomerular ultrafiltrate, and some or all of it may enter the urine and be cleared from the blood. |
| What happens during reabsorption and how does it affect the clearance rate? | A substance is transported from the filtrate back into the blood, which decreases the clearance rate to less than the GFR. |
| What happens during secretion and how does it affect renal plasma clearance? | A substance is transported from peritubular blood into the filtrate, causing its renal plasma clearance to be greater than the GFR. |
| What is the renal clearance rate of a substance that is not filtered, such as proteins? | Its renal clearance rate is zero. |
| What is the renal clearance rate of a substance that is filtered but neither reabsorbed nor secreted, such as inulin? | Its renal clearance rate is equal to the GFR (115-125 mL/min). |
| What is the renal clearance rate of a substance that is filtered and partially reabsorbed, such as urea? | Its renal clearance rate is less than the GFR. |
| What is the renal clearance rate of a substance that is filtered and completely reabsorbed, such as glucose? | Its renal clearance rate is zero. |
| What is the renal clearance rate of a substance that is filtered and secreted, such as PAH? | Its renal clearance is greater than the GFR, up to the total plasma flow rate of about 625 mL/min. |
| Why is para-aminohippuric acid (PAH) injected to measure total renal blood flow? | PAH is completely cleared in a single pass (20% filtered and 80% secreted), so its clearance of about 625 mL/min indicates total renal blood flow. |
| Where and how is glucose completely reabsorbed in the kidneys? | Glucose is completely reabsorbed in the proximal convoluted tubule via secondary active transport with sodium, facilitated diffusion, and simple diffusion. |
| what is the transport maximum for glucose/Na+ cotransporters? | Tm is 375 mg/min |
| What happens when glucose in the filtrate exceeds the transport maximum (Tm) of 375 mg/min? | The glucose will not be completely reabsorbed because all of the carriers are saturated and in use. |
| What is glycosuria and what condition does it indicate? | Glycosuria is when extra glucose spills over into the urine, and it is a sign of diabetes mellitus. |
| Why does glucose begin to spill into the urine at a plasma concentration of 180-200 mg/dL, which is below the average transport maximum? | Some nephrons apparently have a lower transport maximum (Tm) than the average. |
| How does extra glucose in the blood affect water reabsorption? | Extra glucose results in decreased water reabsorption from the filtrate, leading to possible dehydration. |
| How do kidneys maintain electrolyte and acid-base balance in the body? | The kidneys match the excretion of electrolytes (Na+, K+, Cl−, bicarbonate, phosphate) to their ingestion. |
| Why is the control of sodium (Na+) and potassium (K+) levels important? what do they regulate? | Na+ control regulates blood pressure and volume, while K+ control is vital for healthy skeletal and cardiac muscle activity. |
| What hormone plays a major role in both Na+ and K+ balance? | Aldosterone, known as the "salt-retaining hormone," controls the additional reabsorption of Na+ and secretion of K+. |
| How much of the filtered Na+ and K+ is reabsorbed early in the nephron without regulation? | About 90% of filtered Na+ and K+ is reabsorbed early in the nephron. |
| Where in the nephron does aldosterone control the regulated reabsorption of Na+ and secretion of K+? (2 substructures named) | Aldosterone controls this in the distal tubule and collecting duct. |
| What is the aldosterone-independent response to an increase in blood K+? | An increase in blood K+ directly triggers an increase in K+ channels in the cortical collecting duct, which are removed when K+ levels drop. |
| What is the aldosterone-dependent response to an increase in blood K+? | High K+ triggers the adrenal cortex to release aldosterone, which increases K+ secretion in the distal tubule and collecting duct. |
| What 3 factors drive extra potassium secretion when sodium absorption is increased? | It is driven by the potential difference created by Na+ reabsorption, renin secretion by the juxtaglomerular apparatus, and increased tubule flow rates bending primary cilia to activate K+ channels. |
| What directly and indirectly stimulates the secretion of aldosterone? | A rise in blood K+ directly stimulates the adrenal cortex, while a fall in blood Na+ indirectly stimulates it via the renin-angiotensin-aldosterone system. |
| Where is the juxtaglomerular apparatus located? | It is located where the afferent arteriole comes into contact with the distal tubule or the ascending limb of the loop of Henle. |
| What is the pathway of the renin-angiotensin-aldosterone system when plasma Na+ drops? | Granular cells secrete renin, which converts angiotensinogen to angiotensin I, ACE converts it to angiotensin II, and angiotensin II stimulates the adrenal cortex to make aldosterone. |
| What are the 3 main effects of aldosterone stimulated by angiotensin II? | It promotes Na+ reabsorption from the cortical collecting duct, increases blood volume and pressure, and promotes K+ secretion. |
| How do low salt levels lead to the secretion of renin? | Low salt levels inhibit ADH secretion, reducing blood volume, which is detected by granular cell baroreceptors that then secrete renin. |
| What is the macula densa and what is its role in glomerular filtration? | It is part of the distal tubule/ascending limb that acts as a sensor for tubuloglomerular feedback to regulate the glomerular filtration rate via negative feedback. |
| How does the macula densa respond to increased Na+ and water in the filtrate? | It sends an ATP/adenosine signal to constrict the afferent arteriole to limit filtration, and inhibits renin production to decrease Na+ reabsorption. |
| What stimulates the release of Atrial Natriuretic Peptide (ANP) and what are its 3 functions? | Increased blood volume stretches the atria to release ANP, which stimulates the kidneys to excrete more salt, excrete more water, and decrease blood volume and pressure. |
| What is B-type natriuretic peptide (BNP) and why is it measured clinically? | BNP is a hormone released by the heart's ventricles in response to increased volume and pressure, and its levels are measured to help diagnose congestive heart failure. |
| How are renin, angiotensin II, and aldosterone affected by a decrease in blood volume? | Their secretion and production all increase because low blood volume stimulates renal baroreceptors to release renin. |
| How do rising potassium levels affect the regulation of renin and aldosterone? | Rising K+ has no effect on renin or angiotensin II, but directly stimulates the adrenal cortex to increase aldosterone secretion. |
| What effect does increased sympathetic nerve activity have on renin and aldosterone? | It increases renin, angiotensin II, and aldosterone secretion through the constriction of afferent arterioles and direct stimulation of renin release. |
| (starred) How does acidosis lead to "secondary" hyperkalemia? | H+ diffuses into body cells and drives K+ out into the extracellular fluid, which causes hyperkalemia and can lead to CNS depression. |
| (starred) How does alkalosis lead to "secondary" hypokalemia? | H+ diffuses out of body cells and K+ diffuses in to maintain charge balance, which depolarizes cell membranes and overstimulates muscles, causing spasms. |
| (starred) How does the reabsorption of Na+ relate to the secretion of K+ and H+? | Reabsorption of Na+ stimulates the secretion of K+ and H+ due to electrostatic attraction, and K+ and H+ compete for secretion via antiport pumps. |
| (starred) How does primary hyperkalemia lead to acidosis? | Hyperkalemia stimulates the secretion of K+ and inhibits the secretion of H+, which leaves excess acid in the blood. |
| How do the kidneys maintain a normal blood pH of 5 to 7? | The kidneys maintain blood pH by reabsorbing bicarbonate and secreting H+, which makes the resulting urine acidic. |
| Which structure uses Na+/H+ pumps in the apical surface of its cells to regulate acid-base balance? | The proximal convoluted tubule uses secondary active transport Na+/H+ pumps to pull Na+ into the cells and kick H+ out into the tubular fluid. |
| How is bicarbonate reabsorbed if it cannot cross the apical cell membrane of the proximal convoluted tubule? | It binds with H+ to form carbonic acid, is converted to CO2 and H2O by carbonic anhydrase to enter the cell, and is then converted back into bicarbonate. |
| Which pumps are primarily responsible for acidifying the urine in the distal convoluted tubule? | The primary active transport H+ (ATPase) pumps in the distal convoluted tubule are responsible for increasing H+ secretion. |
| How do the kidneys compensate for respiratory alkalosis? | Less H+ is available to transport bicarbonate, so less bicarbonate is reabsorbed, and the extra bicarbonate secretion makes the blood more acidic. |
| How do the kidneys compensate for respiratory acidosis? | The proximal tubule metabolizes glutamine into ammonia and new bicarbonate, which enters the blood to neutralize acid while the ammonia buffers H+ in the urine. |
| Why must urine be buffered and what is its limiting pH? | Nephrons cannot produce urine more acidic than a pH of 4.5, so buffers are needed to tie up loose H+ to allow for increased H+ secretion. |
| What two substances act as buffers in the urine to increase H+ secretion? | Phosphates, which enter via filtration, and ammonia, which comes from the deamination of amino acids, act as urinary buffers. |
| (starred) what are the 5 diuretic categories? | loop diuretics, thiazides, carbonic anhydrase inhibitors, osmotic diuretics, potassium-sparing diuretics |
| (starred) what is the mechanism of action and major site of action for loop diuretics? | inhibits sodium transport at the thick segments of ascending limbs |
| (starred) what is the mechanism of action and major site of action for thiazides? | inhibits sodium transport at the last part of ascending limb and first part of distal tubule |
| (starred) what is the mechanism of action and major site of action for CAH inhibitors? | inhibits reabsorption of bicarbonate at the proximal tubule |
| (starred) what is the mechanism of action and major site of action for osmotic diuretics? | reduces osmotic reabsorption of water by reducing osmotic gradient at the last part of distal tubule and cortical collecting duct |
| (starred) what is the mechanism of action and major site of action for potassium-sparing diuretics? (split) | can inhibit action of aldosterone or inhibit Na+ reabsorption and K+ secretion; in the last part of distal tubule and cortical collecting duct |
| What are diuretics used for clinically? | Diuretics are used clinically to decrease high blood pressure and relieve edema by increasing urine volume and decreasing blood volume. |
| How do loop diuretics like Lasix work? | Loop diuretics are the most powerful diuretics and inhibit up to 25% of water reabsorption by inhibiting salt transport out of the ascending loop of Henle. |
| How do thiazide diuretics work? | Thiazide diuretics inhibit salt transport in the distal tubule and can inhibit up to 8% of water reabsorption. |
| What is the function of carbonic anhydrase inhibitors as diuretics? | They are weaker diuretics that inhibit water reabsorption when bicarbonate is reabsorbed and also promote the excretion of bicarbonate. |
| How do osmotic diuretics like Mannitol reduce water reabsorption? | Osmotic diuretics reduce water reabsorption by adding extra solutes to the filtrate, a mechanism that can also happen as a side effect of diabetes mellitus when extra glucose is present. |
| How do potassium-sparing diuretics function? | They act as aldosterone receptor antagonists to block the reabsorption of sodium and the secretion of potassium. |
| What conditions can PAH and inulin clearance tests diagnose? | These renal function tests can diagnose nephritis or renal insufficiency. |
| What does microalbuminuria signify? | Microalbuminuria is an above-normal urinary albumin excretion rate that signifies renal damage due to hypertension or diabetes. |
| What is proteinuria? | Proteinuria is the overexcretion of proteins, which is typically seen in nephrotic syndrome. |
| What defines acute renal failure? | It is a short-term loss of the kidneys' ability to regulate blood volume, pH, and solute concentrations over a period of hours or days. |
| What usually causes acute renal failure? | It is usually due to decreased blood flow through the kidneys caused by atherosclerosis of renal arteries, inflammation of renal tubules, or the use of certain drugs like NSAIDs. |
| What causes glomerulonephritis? | It is an autoimmune disease with antibodies produced in response to a streptococcus infection, leading to inflammation of the glomerulus. |
| How does glomerulonephritis lead to edema? | The disease destroys many glomeruli and makes others more permeable to proteins, and the loss of proteins from the blood reduces blood osmotic pressure, causing fluid accumulation. |
| What is renal insufficiency and what can cause it? | Renal insufficiency is any reduction in renal activity and can be caused by glomerulonephritis, diabetes, atherosclerosis, or kidney stones. |
| What are the potential complications of renal insufficiency? | It can lead to high blood pressure, high blood K+ and H+, and uremia (urea in the blood). |
| What is the purpose of hemodialysis? | Hemodialysis acts as an artificial kidney to cleanse the blood of wastes as it passes through dialysis fluid, typically requiring three sessions a week for several hours per session. |
| How does continuous ambulatory peritoneal dialysis (CAPD) work? | In CAPD, dialysis fluid is introduced into the abdominal cavity where wastes pass out of abdominal blood vessels into the fluid, which is then pumped out. |
| What are the drawbacks of CAPD compared to hemodialysis? | CAPD is not as effective as hemodialysis and carries a risk of infection. |
| (bolded) what do the capillary fenestrae filter? | They allow blood plasma, water, and small solutes to pass through while preventing large cells (-cytes) from escaping the blood. Proteins can get past these |
| (bolded) what does the glomerular basement filter? | It traps large structures like blood cells and large proteins inside the blood. It filters by using two main rules: size and electrical charge. It allows water, ions, and small molecules (like glucose) to pass through to make urine |
| (bolded) what does the visceral layer of the glomerular capsule filter? | stops almost all protein in the plasma from entering the filtrate |
| (bolded) a protein defect where causes proteinuria? | at the slit diaphragms of the renal corpuscle |
| what is the protein-free fluid forced from blood into Bowman's capsule during the first step of urine formation? | glomerular ultrafiltrate |
| what are the 2 intrinsic ways GFR is regulated? | myogenic; tubuloglomerular feedback |
| true or false, decrease in urine formation helps compensate for drop in central blood pressure | true |
| when the SNS is in control of the GFR, it increases or decreases blood volume? | increases by not making so much urine |
| if systemic BP rises and constricts the afferent arteriole, what does the efferent do? | dilates to protect filtration slits |
| if systemic BP falls and dilates afferent arteriole, what does the efferent do? | constricts to enhance filtration |
| angiotensin II constricts the ______ arterioles more than than the ______ arterioles | efferent more than the afferent--the net effect is to increase glomerular BP in the face of decreased systemic BP. this effect also enhances the reabsorption of NaCl and water from nephron |
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