Cabs Unit 4 Renal A&p Questions

Front 1

Where do the kidneys lie?

Back 1

Retroperitoneal, both kidneys underlie floating ribs 11 and 12. The right kidney is more inferior- about 1 finger above the iliac crest

Front 2

Which 3 places do kidney stones collect?

Back 2

Ureteropelvic junction, where it crosses the pelvic brim at the external iliac vessels, where it enters the bladder (called waldeyer’s sheath)

Front 3

Pain from the kidney can be referred to areas on the skin- which dermatomes are often involved?

Back 3

T11 to L2. The umbilicis is T10, so inferior to this area

Front 4

The kidney is surrounded by two layers of fact- what are these layers?

Back 4

Perirenal- the fat adjacent and Pararenal- the fat further out

Front 5

What can a kink in the ureter cause (i.e. from starvation)?

Back 5

Hydronephrosis

Front 6

Is the renal vein anterior or posterior to the renal artery at the renal hilum?

Back 6

Vein is anterior, artery is posterior

Front 7

What are the areas of the kidney from external to medial?

Back 7

Outer layer: cortex (find glomeruli, prox and distal conv tubules), Middle: medullary part (pyramids contain primarily collecting ducts and loops of Henle), tip of pyramid is papilla where the ducts drain to a minor calyx. These minor calyces unite to form major calyces, which drain into the renal pelvis.

Front 8

What is the main muscle found within the bladder wall?

Back 8

Detrussor muscle

Front 9

How is the bladder innervated?

Back 9

Sympathetic: Relaxation of the detrussor muscle and constriction of the internal urethral sphincter; Parasympathetic: Contraction of the detrussor muscle and relaxation of the internal sphincter; Pudendal (somatic) innervates the external urethral sphincter

Front 10

Why is it hard to potty train before the age of 3?

Back 10

No control over the pudendal muscle which innervates the external urethral sphincter

Front 11

What are the major renal functions?

Back 11

Fluid/electrolyte balance, acid-base balance, remove waste (urea, uric acid and creatinine), hormone secretion (erythropoeitin and Vit D3) and metabolizing drugs/excreting drugs

Front 12

What is a renal corpuscle?

Back 12

The glomerulus and Bowman's capsule

Front 13

What is the function of the macula densa?

Back 13

A juxtoglomerular apparatus that senses the amount of solute within the tubule. Senses concentration of Na+ and Cl-. If amount of solute is low- sensed as an indication that glomerular filtration may be low or renal blood flow may be low. It then stimulates granular cells (juxtaglomerular) to secrete renin which increase pressures and increase glomerular filtration.

Front 14

What is the overall function of the distal convoluted tubule?

Back 14

Fine tunes absorption and secretion of ions

Front 15

Where does ADH act?

Back 15

Collecting duct

Front 16

What part of the segments of the nephron is most important for determining if urine is concentrated or dilute?

Back 16

Collecting duct

Front 17

How are the afferent and efferent arterioles affected by angiotensin II?

Back 17

Angiotensin II has a greater affect on efferent than afferent which can increase glomerular filtration. I.e. lets renal plasma enter (despite vasoconstriction) but since the efferent is MORE constricted, it is held in the glomerulus longer for filtration.

Front 18

What comprises the glomerulus?

Back 18

Tufts of fenestrated capillaries with protein membrane windows through which solute can pass easily and water. An endothelial layer of cells surrounds the glomerulus

Front 19

Where is urine collected in the renal corpuscle?

Back 19

In Bowman's space- space between Bowman's capsule and the glomerulus

Front 20

What structures are found on the visceral layer of the glomerulus?

Back 20

Contains cells called podacyte cells (foot cells), which have little foot processes called pedicells. These foot process are not connected together and therefore, have slit pores. This allows solute and water to pass throughthe fenestrated endothelium into the Bowman’s space

Front 21

What is the basement membrane?

Back 21

A negatively charged glycoprotein gel found between the visceral epithelial tissue and the fenestrated endothelium. Holds together these two layers (fenestrated endothelium of the glomerulus and the visceral epithelium of Bowman's capsule)

Front 22

Which cells hold together the glomerulus?

Back 22

Mesangial cells

Front 23

What are the structures from internal to external of the renal corpuscle?

Back 23

Capillary lumen, fenestrated endothelium, basement membrane, visceral epithelial layer (contains pedicells and podocytes), Bowman's space, Parietal epithelial layer

Front 24

How is the basement membrane comprised?

Back 24

Central dense section called the lamina densa (where glycoproteins are tightly compacted), Lamina rara interna (deep to the fenestrated endothelium) and the lamina rara externa (underneath the visceral epithelium)

Front 25

What is the infectious significance of the basement membrane?

Back 25

Many of the glomerulonephritities accompany many systemic disease. Many of the diseases are consequence of immune complex deposition forming in situ in the basement membrane. This triggers the glomerulonephritis. Whether it is post infectious glomerulonephritis- post streptococcal- or membranoproliferative associated with HIV, Hep B or SLE.

Front 26

What is the rule of thumb for differentiating between nephrotic vs nephritic syndrome?

Back 26

Subendothelial (lamina rara interna)- precipitates nephritic syndrome- which is more inflamatory response with white cells/red cells present in urine; Subepithelial (lamina rara externa)- deposits of immune complexes- nephrotic syndrome- characterized by proteinuria (>3.5 grams) lost in the urine per day

Front 27

Nephrotic or nephritic: Protein in urine

Back 27

Nephrotic

Front 28

Nephrotic or nephritic: WBC/RBC in urine

Back 28

Nephritic

Front 29

Nephrotic or nephritic: subendothelial layer (lamina rara interna)

Back 29

Nephritic

Front 30

Nephrotic or nephritic: subepithelial layer (lamina rara externa)

Back 30

Nephrotic

Front 31

What is the #1 cause of nephrotic syndrome in adults?

Back 31

Membranous glomerulopathy (immune complex)

Front 32

What is the #1 cause of nephrotic syndrome in children?

Back 32

Minimal change disease- idiopathic

Front 33

Nephritic can lead to nephrotic: TRUE or FALSE

Back 33

TRUE

Front 34

Which glomerulonephropathy involves less than 50% of the glomeruli on light microscopy?

Back 34

Focal

Front 35

Which glomerulonephropathy involves greater than 50% of the glomeruli on light microscopy?

Back 35

Diffuse

Front 36

Which glomerulonephropathy involves only part of the glomerular tuft (usually in a focal manner)?

Back 36

Segmental

Front 37

Which glomerulonephropathy involves the entire glomerular tuft; can be seen with either focal or diffuse disease?

Back 37

Global

Front 38

Which glomerulonephropathy involves thickening of the glomerular capillary wall, with distinctive basement membrane "spikes"?

Back 38

Membranous

Front 39

Which glomerulonephropathy involves an increased number of cells in the glomerulus?

Back 39

Proliferative

Front 40

Which glomerulonephropathy involves both thickening of the glomerular capillary wall and distinctive double contours or "tram tracks" as well as proliferative changes?

Back 40

Membranoproliferative

Front 41

Which glomerulonephropathy involves an accumulation of cells within Bowman's space?

Back 41

Crescent- often associated with more severe disease

Front 42

Which glomerulonephropathy is segmenal or global capillary collapse or closure of the capillary lumens?

Back 42

Glomerulosclerosis

Front 43

Which glomerulonephropathy involves any condition associated with inflammation of the glomerular tuft?

Back 43

Glomerulonephritis

Front 44

How does membranoproliferative glomerulonephritis lead to chronic kidney disease?

Back 44

Loss of filtration surface area, while at the same time, because of immune response, there is damage to the filtration membrane (big holes). Small surface area and big holes leads to proteins escaping through. This may damage the negatively charged basement membrane. The charge was initially repulsing albumin. Albumin can then sneak through. This leads to proteinuria. There is also oliguria because less urine is produced by the reduced surface area for filtration. Within the urine, however, there will be casts, RBC, WBC, proteins, etc

Front 45

What is the functions of kidney filtration?

Back 45

The blood is filtered by nephron. Each nephron begins in a renal corpuscle. Cells, proteins, and other large molecules are filtered out of the glomerulus by a process of ultrafiltration, leaving an ultrafiltrate to enter Bowman's space. Filtration is driven by Starling forces. The ultrafiltrate is passed through the proximal convoluted tubule, the loop of Henle, the distal convoluted tubule, and a series of collecting ducts to form urine.

Front 46

What is the function of reabsorption?

Back 46

Tubular reabsorption is the process by which solutes and water are removed from the tubular fluid and transported back into the blood. Reabsorption is a two-step process beginning with the active or passive extraction of substances from the tubule fluid into the renal interstitium and then the transport of these substances from the interstitium into the bloodstream. These transport processes are driven by Starling forces, diffusion, and active transport.

Front 47

What is the function of renal secretion?

Back 47

Tubular secretion is the transfer of materials from peritubular capillaries to renal tubular lumen. Tubular secretion is caused mainly by active transport. Usually only a few substances are secreted. These substances are present in great excess, or are natural poisons.

Front 48

Why is the basement membrane negatively charged?

Back 48

Cations that are larger can pass through whereas anions cannot not (even if they are smaller). This is because of the electric (-) charge; one of the reasons that albumin cannot pass through.

Front 49

What is capillary hydrostatic pressure?

Back 49

The pushing force that pushes fluid out of the capillary into Bowman’s space

Front 50

What is the hydrostatic pressure of Bowman's space?

Back 50

The pressure pushing fluid from Bowman's space into the capillary – analagous to interstitial hydrostatic pressure

Front 51

What is the capillary osmotic pressure (COP)?

Back 51

Related to the solute found within the capillary: includes largely, albumin: pushes it into the capillary

Front 52

How is the glomerulus different than any other capillary bed?

Back 52

All across the glomerulus there is net filtration pushing fluid into the bowman’s space; whereas in a normal capillary: filtration occurs at the arteriole end and absorption at the venule end

Front 53

Do changes in blood pressure alter filtration?

Back 53

No (under normal circumstances)- Filtration is constant between MAP of 80-180 mm Hg; glomerular filtration ceases at <45-50mm Hg (in cases of shock); MAP= diastolic + 1/3 pulse pressure

Front 54

How does the kidney use renal autoregulation of blood flow to maintain constant filtration rates?

Back 54

Macula densa senses the amount of solute within the distal tubule; When there is increased blood flow, increased pressure and increased filtration, the amount of solute increases within the nephron. This is sensed by macula densa, which feeds back to the afferent arteriole to constrict and decrease the filtration. Prevents excessive loss if you have elevated pressures; if pressure drops, the RAAS system kicks in to increase blood volume

Front 55

Which factors affect glomerular hydrostatic pressure?

Back 55

Hormone and sympathetic affects; Shock (cardiogenic or hemorrhagic- sympathetic affects)

Front 56

Why should people with renal disease not be given NSAIDS?

Back 56

NSAIDs will inhibit the vasodilatory affect of prostaglandins on epithelial tissue, which will in turn inhibit blood flow to the kidney

Front 57

How do the hormonal and sympathetic effects affect glomerular hydrostatic pressure?

Back 57

Regulation of the diameter of the afferent and efferent arterioles (angiotensin II), vasoconstriction (sympathetic response: epi, norepi, ADH or thromboxane-a prostaglandin), vasodilation (ANP, histamine, NO, prostacyclin), afferent arteriole dilation (increased flow, PGC and GFR), efferent arteriole dilation (increased blood flow, decreased PGC and decreased GFR)

Front 58

Which factors affect Bowman's capsule hydrostatic pressure?

Back 58

Factors that increase pressure in Bowman's space and thus decrease GFR: postrenal (downstream obstruction) such as nephro or ureterolithiasis or BPH --> leads to a buildup of urine within the kidney, which can increase Bowman's hydrostatic pressure. Leads to acute renal failure; if the pressure builds up large enough in Bowman's space, it can equalize with the glomerular hydrostatic pressure and can lead to no fluid filtering through the glomerulus.

Front 59

What does a decrease in capillary osmotic pressure lead to?

Back 59

An increase in GFR

Front 60

How can you dilute capillary osmotic pressure?

Back 60

Normal saline infusion

Front 61

How is GFR measured?

Back 61

Renal clearance- volume of plasma in which a substance is completely removed per time *usually minutes

Front 62

What is the GFR formula?

Back 62

(U*V)/P; where U= urine concentration, V=urine flow rate (amount/min), P= plasma concentration

Front 63

What is the gold standard for GFR?

Back 63

Inulin clearance- a substance that is filtered, but not secreted or absorbed. Must be injected because inulin is not produced endogenously

Front 64

Where is creatinine derived from?

Back 64

Creatine phosphate- muscle; backup source for ATP

Front 65

How is plasma creatinine related to GFR?

Back 65

Inversely, 1/2 GFR= 2x creatinine; a doubling of creatinine equals a 50% drop in the GFR

Front 66

What are the 3 categorical causes of acute renal failure?

Back 66

Prerenal, intrinsic and postrenal (obstruction)

Front 67

A decrease in blood volume; heart disease, shock, decreased blood volume are examples of which type of renal failure?

Back 67

Prerenal

Front 68

A tubular, glomerular or vascular defect are which type of acute renal failure?

Back 68

Intrinsic

Front 69

An obstruction is which type of renal failure?

Back 69

Postrenal

Front 70

What is an example of ischemic renal failure?

Back 70

Hemolytic uremic syndrome- chronic renal failure usually associated with uremia

Front 71

Are the first two stages of kidney failure symptomatic or asymptomatic?

Back 71

Asymptomatic

Front 72

At what GFR rate is there renal insufficiency and development of azotemia?

Back 72

When GFR drops below 50

Front 73

Renal failure is associated with what range of GFR?

Back 73

5-20 mL/min

Front 74

ESRD is associated with what GFR rate?

Back 74

Less than 5mL/min

Front 75

What does 'fluid 3rd space' reference?

Back 75

When fluid is pushed into the intersitial space due instead of capillaries (due to large holes within the glomerulus); baroreceptors interpret a decrease in pressure --> RAAS system kicks in and adds to the problem --> ascites or anasarca

Front 76

What are symptoms of uremia?

Back 76

Uremic frost, GI upset, asterixis, encephalopathy

Front 77

Which type of anemia is associated with CKD?

Back 77

Normocytic, normochromic anemia; anemia of chronic disease

Front 78

How is acid/base balance altered with CKD?

Back 78

Decreased filtration of hydrogen and amonium- buildup of hydrogen

Front 79

How is vitamin D synthesis altered with CKD?

Back 79

Vitamin D is no longer activated (final step is within the kidney); leads to no calcitriol, less calcium; hypocalcemia can lead to a seconday hyperparathyroidism

Front 80

What are burr cells?

Back 80

Part of the findings in chronic renal failure; they are spikes on the red blood cell surface created by uremia

Front 81

How are electrolytes altered in uremia?

Back 81

Hyponatremia, hyperphosphatemia, hypocalcemia, hyperuricemia…how do you get hyponatremia if you are not excreting out? More water is being retained and absorbed than sodium so relative amounts are off. Produces dilutional hyponatremia in the plasma

Front 82

What is the number 1 cause of chronic kidney disease in the US?

Back 82

Diabetes

Front 83

What is the critical point where there is insufficient nephrons to support healthy kidney function?

Back 83

Typically when only 1/4 of the total bilateral renal mass is left.

Front 84

What are the events that describe chronic renal disease in the musculoskeletal system after the kidneys are only at 1/4 bilateral mass remaining?

Back 84

One of the early findings in decreased GFR is hyperphosphatemia due to decreased phosphate excretion --> either binds serum calcium directly (decreased serum free calcium) or inhibits vitamin D synthesis activation in the kidney- decreased vit D absorption. End result is hypocalcemia. Hypocalcemia and elevated hyperphosphate trigger secondary hyperparathyroidism --> triggers release of Ca from bone and bone resorption --> produces osteomalacia and osteitis fibrosa

Front 85

Is a low protein diet renal protective or harmful to GFR?

Back 85

Reducing intake of protein slowed reduction of GFR by about 75%- one way to treat renal disease!

Front 86

Which renal calculation is used to differentiat between prerenal and intrinsic causes of renal failure?

Back 86

"Fractional excretion" = excretion rate/filtered load; Typically 99% of sodium that is filtered is reabsorbed (lose little in the urine). When we have prerenal failure- there is decreased volume entering the kidney- activates RAAS. Causes more sodium to be reabsorbed from the nephron. The fractional excretion becomes LESS than 1% as more sodium than normal is being reabsorbed. If it is greater than 2%, than it is probably an issue with reabsorption in the tubules

Front 87

Where is most of sodium (and really everything else filtered) reabsorbed within the nephron?

Back 87

70% of sodium is reabsorbed in the proximal tubule (nearly 100% of glucose is also absorbed here); then thick ascending limb at 25%, distal 5%, collecting duct 3% with a final excretion of <1% in the end

Front 88

Where do loop diuretics act to inhibit sodium reabsorption?

Back 88

Thick ascending limb

Front 89

Where do thiazide diuretics act?

Back 89

Distal convoluted tubule

Front 90

Which drug is a more potent diuretic?

Back 90

Loops- block more sodium reabsorption

Front 91

Why is hypokalemia a result of diuretics?

Back 91

Not only because there is no reabsorption of K , but also by maintaining sodium there are HIGH flow rates which promotes K secretion

Front 92

What occurs for the proximale tubule transport?

Back 92

Main location for ion and other filtered products to be reabsorbed. Na+ gradient creates energy for cotransport of H20 and solutes, all filtered glucose and amino acids are reabsorbed here, largest amount of Na+, K+, Ca++, Cl- and HCO3-. The Na+:Glucose transport for H+ exchange (hydrogen is secreted out for the exchange of sodium coming back in

Front 93

What are the two main concepts of glucose transport?

Back 93

1: When glucose appears in the urine, it is referred to as glucose threshold (onset of glucosuria) 2: When all of the glucose carriers are saturated- reached the transport maximum; anything beyond will spill into the urine

Front 94

What is the glucose threshold?

Back 94

When there is around 240mg/dL of glucose in the plasma. Any glucose above this level will start to show in the urine

Front 95

What is splay?

Back 95

The amount of glucose that is excreted beyond 240mg/dL that can be variable. The kidney can still reabsorb some glucose at this point. Once it reaches the threshold maximum, however ALL additional excreted

Front 96

What are the parts of the loop of henle?

Back 96

Descending thin limb, ascending thin limb, thick ascending limb

Front 97

What is the descending thin limb permeable to?

Back 97

Permeable to water, some salt

Front 98

what is the ascending thin limb permeable to?

Back 98

Permeable to salt; NOT water

Front 99

Is the end of the loop of henle more hypoosmotic or hyperosmotic?

Back 99

Hypoosmotic- goes from 300 where it enters to 100 where it ends (more solute than water is reabsorbed)

Front 100

What steps occur in the loop of henle?

Back 100

Filtrate enters, goes from 300 milliosmoles up to 1200 milliosmoles (loses water in the descending thin limb- more concentrated)

Front 101

What is the function of the thick ascending limb?

Back 101

Diluting segment! Dilutes the filtrate from 300 where it enters to 100 where it ends (more solute than water is reabsorbed)

Front 102

What is the function of the distal nephron tubular transport- includes distal convoluted tubule and the collecting duct?

Back 102

Fine tunes solute and water transport to create potentially large differences in ion concentrations and osmolality between urine and plasma

Front 103

How does the distal nephron tubular transport work?

Back 103

Reabsorbs 9% filtered Na, 19% H20; Aldosterone effects: Increased Na+ reabsorption, K+ and H+ secretion (large influence); AVP/ADH secretion: Increase water reabsorption

Front 104

Where is aldosterone secreted from?

Back 104

Adrenal cortex

Front 105

Under which conditions is aldosterone secreted?

Back 105

Decreased blood volume and blood pressure to the kidney or a high potassium diet

Front 106

What are the affects of aldosterone?

Back 106

Principle cell found within the distal convoluted tubule and collecting duct; Affects include: increasing the activity and number of Na/K atpase pumps, increases a pore called epithelial sodium channel on the luminal side for sodium to be reabsorbed from filtrate back into the blood, increases potassium channels, increases the activity and number of potassium/hydrogen ion exchanger

Front 107

What is the net effect of aldosterone on the distal tubule and collecting duct?

Back 107

Will increase sodium reabsorption, increase potassium secretion, increase hydrogen ion secretion

Front 108

How does AVP/ADH increase water reabsorption?

Back 108

As a hormone- stimulates the synthesis of aquaporin 2 channels within the collecting duct and distal convoluted tubule. Increase of reabsorption of water causes increased urine concentration. ADH also increases urea reabsorption from the medullary portion of the collecting duct. This adds to the gradient to increase the milliosmole gradient. Also activates the sodium, k, 2cl- pump on the loop of henle. ADH helps to increase osmolarity of the interstitial space around the nephron- pump out more solute in the loop of henle (increases osmolarity), increases urea reabsorption (increases osmolarity), increases water reabsorption (also increases since plasma osmolarity is high) --> produce a concentrated urine. If you are well hydrated, ADH is not secreted.

Front 109

Is ADH secreted in a well hydrated person?

Back 109

No

Front 110

What is the main contraindication for a thiazide diuretic?

Back 110

Hyponatremia! Can exacerbate this significantly (moreso than loops)

Front 111

How would an ACE inhibitor produce hyperkalemia?

Back 111

By blocking aldosterone secretion

Front 112

What accounts for most of urinary K+?

Back 112

Secretion in the collecting duct

Front 113

What are the K+ sparing diuretics?

Back 113

Block aldosterone receptors: spironolactone; Block Na+ channels on epithelial cells in the distal nephron tubule: Triamterene

Front 114

What determines urine osmolality?

Back 114

Concentrated or dilute urine requires a medullary osmotic gradient created by "countercurrent multiplier" effect of the loop of henle and is maintained by "countercurrent exchange" effect of the Vasa Recta; regulated by AVP

Front 115

What is a countercurrent mechanism?

Back 115

One example is: panpiniform plexus- in which heat from artery is taken by the vein in the opposite direction--heat of the arteriole blood diffuses to the venous and back to the body

Front 116

What is created in the loop of henle through countercurrent mechanisms?

Back 116

The corticomedullary/corticopapillary gradient. If the loop of henle is diseased- cannot concentrate urine

Front 117

Which waste product is also important for maintaining the corticomedullary concentration gradient?

Back 117

Urea

Front 118

How does countercurrent exchange work in the vasa recta?

Back 118

Blood has to flow through the vasa recta to supply nutrients and O2 while also removing CO2. In order to flow through and not dilute the gradient, must flow through this loop in a countercurrent exchange mechanism through the vasa recta. So, you have the loop of henle and surrounding it is a capillary loop called vasa recta. As the capillary descends into the more concentrated region, it loses water and picks up solute- concentration within the blood capillary equilibrates with the interstitial space osmolality and therefore it doesn’t dilute medullary gradient or drop off more water.

Front 119

How is concentrated urine formed?

Back 119

The initial condition is hyperosmolar plasma (275-290) --> stimulates AVP/ADH --> AVO increases collecting duct permeability through increased luminal membrane water channels (aquaporin 2) --> Urine osmolality is then 1200 mosm/L vs plasma of 285-300 mosm/L --> end result is conservation of 1-1.5 L of body H2O/day

Front 120

How is dilute urine formed?

Back 120

The initial condition is hypoosmolar --> AVP secretion is inhibited --> collecting ducts remain impermeable to H2O --> medullary gradient is diluted --> urine is hyposmolar at 50-75 mosm/L

Front 121

What are the steps for creating low osmolality urine (diluted)?

Back 121

Drink plenty of water --> reduced ADH secretion for posterior pituitary --> Decreased water permeability of principle cells --> decreased water reabsorption --> Decreased urine osmolarity and increased urine volume

Front 122

What are the steps for creating high osmolality urine (concentrated)?

Back 122

Deprived of water --> stimulates osmoreceptors in anterior hypothalamus --> increased ADH secretion from posterior pituitary --> Increased water permeability in principle cells --> increased water reabsorption --> increased urine osmolality and decreased urine volume (concentrated!)

Front 123

What occurs in the proximal convoluted tubule?

Back 123

Reabsorb Na and water. Osmotic and CAI work here. Most of Na absorbed here. Early: HCO3- Late: Cl-

Front 124

What occurs in the thin descending limb?

Back 124

Permeable to both salts and water. Water moves out of the lumen into the blood, solutes move in to the lumen out of the blood. Becomes hyperosmotic

Front 125

What occurs in the thin ascending limb?

Back 125

Permeable to NaCl but impermeable to water; solutes move OUT, water stays IN. Tubular fluid becomes progessively hypoosmotic as it flows up the ascending limb

Front 126

What occurs in the thick ascending limb?

Back 126

Reabsorbs a significant amount of Na by active mechanisms. Normally absorbs 25% of Na. Contains the Na,K,2Cl cotransporter (3 ion cotransporter). There is net reabsorption of Na, K and Cl in the thick ascending limb. Loop diuretics work here. Impermeable to water. NaCl is reabsorbed but not water along with it. This is considered a diluting segment

Front 127

What does impermeable to water mean?

Back 127

Impermeable to water means that water cannot leave the lumen!

Front 128

What is the terminal nephron?

Back 128

The distal tubule and collecting duct: referred to as the terminal nephron

Front 129

What occurs in the early distal tubule?

Back 129

Early distal tubule is impermeable to water. Reabsorbs solute and leaves water behind in the lumen. This dilutes tubular fluid.- Sometimes called cortical diluting segment. Often already somewhat dilute due to the thick ascending limb already diluting (compared to the blood)-->further dilutes!

Front 130

What occurs in the late distal tubule and collecting duct?

Back 130

Comprised of two cells: Principle: involved in Na reabsorption and K secretion and water reabsorption. Alpha-intercalated cells: K reabsorption and H+ secretion. Na+ diffuses down its gradient through the NaK exchange pumps. Thus causing secretion of K and reabsorption of Na. In patients who take loops or thiazides- this is why there is hypokalemia because there is significant exchange of K for Na to reabsorb the Na that is being lost. These are late "fine adjustments". Water reabsorption is variable and controlled by ADH- secreted by the posterior lobe of the pituitary gland . When ADH levels are high, the water permeability of the principal cells is high and water is reabsorbed with NaCl

Front 131

Functions of aldosterone:

Back 131

Steroid hormone that acts directly on the principle cells to increase Na reabsorption. (in exchange for K secretion). Increases K secretion; Functions: induces the synthesis of more luminal membrane Na channel, increases the quantity of NaK atpase, also increases the number of K channels in the luminal membrane which coordinates with increased driving force to increase K secretion

Front 132

What are loop diuretics?

Back 132

Organic acids that attach to the Cl- binding site of the NaK2CL transporter and inhibit the cotransporter. At maximal dosages, loop diuretics completely inhibit NaCl reabsorption in the thick ascending limb and caan cause excretion of as much as 25% of the filtered Na

Front 133

What are thiazide diuretics?

Back 133

Organic acids that bind to the Cl site of othe NaCl cotransporter in the early distal tubule and prevent it from cycling, thus inhibiting NaCL reabsorption in the early distal tubule.

Front 134

What are k-sparing diuretics?

Back 134

used in the late distal tubule. Some inhibit aldosterone secretion and others block the Na-K exchanger channels.

Front 135

What happens with diabetes insipidus?

Back 135

Central: The posterior pituitary is unable to secrete ADH in response to an osmotic stimulus. ADH levels are low or zero and the entire distal tubule and collecting ducts are impermeable to water- WATER stays IN the lumen and CANNOT leave. This makes for very dilute urine. Nephrogenic: Defect in the response of the kidneys to ADH. Secretion from the posterior pituitary is normal. Defect in the receptor and principle cells are unresponsive to ADH