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CPR > Renal Physiology > Flashcards

Renal Physiology Flashcards

1
Q

What’s the marker for total body water?

A

antipyrine

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2
Q

Marker for ECF?

A

Inulin, sucrose

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3
Q

Marker for plasma volume?

A

Evans blue dye and RISA (radio-iodinated human serum albumin)

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4
Q

An example of hypotonic expansion?

A

Giving pure water to someone intravenously. The expansion refers to volume expansion of extracellular fluid. The ICF also expands; the ECF was made hypotonic relative to the ICF.

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5
Q

Example of hypertonic expansion?

A

Administering hyper-concentrated fluid intravenously. ECF volume is expanded, ECF is made hypertonic, and ICF volume contracts.

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6
Q

Example of isotonic expansion and contraction?

A

Blood transfusion and hemorrhage, respectfully

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7
Q

Example of hypertonic contraction?

A

Sweating or too much ADH; gives of primarily water from ECF, making ECF volume deplete and ECF becomes hypertonic. ICF then moves to ECF.

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8
Q

Example of hypotonic contraction?

A

Not sure of a good realistic example, but theoretically peeing off super-concentrated urine would leave the ECF volume-depleted and hypotonic. Fluid from ECF would then move to ICF.

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9
Q

Considering the Starling forces, where does pressure primarily affect fluid movement between plasma and interstitial fluid, and where does oncotic pressure primarily act?

A

Hydrostatic Pressure at arteriolar end, oncotic pressure at venule end

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10
Q

How are amino acids and glucose reabsorbed?

A

In the proximal tubule by secondary active transport coupled to Na

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11
Q

What portion of the kidney is under the most regulation/variability?

A

Distal tubule

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12
Q

What’s Tm?

A

other than a way to teach pokemon new moves, it’s also the limit of tubular reabsorption. For example, when blood glucose levels get too high, the flow of glucose through the proximal tubule is higher than Tm(glucose) and glucose is excreted in the urine

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13
Q

How much of the fluid from the glomerular arterioles flow into Bowman’s space?

A

most of the fluid

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14
Q

What’s splay?

A

It refers to how Tm doesn’t occur at an exact, sharp point of solute concentration. Instead, variability in the performance of nephrons causes different neprhons to have different individual Tm’s, which causes filtration to exceed reabsorption at different concentrations. It causes the filtration/reabsorption curve intersection to be rounded instead of sharp (splaying).

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15
Q

What do minimal, mean, and maximum threshold refer to?

A

The minimum is the first concentration at which a solute isn’t fully reabsorbed. Max is when maximum reabsorption occurs. Mean is the middle of the two

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16
Q

What’s reabsorbed in the proximal tubule?

A

Amino acids, citrate, potassium, glucose, bicarbonate, phosphate

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17
Q

Example of competitive reabsorption?

A

Glucose, fructose, xylose, and galactose are all absorbed by the same transport protein. If Glucose concentration meets Tm(glucose) then none of the other sugars can be reabsorbed

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18
Q

What solutes are normally reabsorbed isotonically?

A

Na, Cl, and HCO3-

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19
Q

How does creatinine clearance differ from GFR?

A

Creatinine clearance is usually a good estimate of GFR under normal conditions. However, in a patient with tubular disease or AKI, with low GFR, creatinine clearance over-estimates GFR

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20
Q

What approximates renal plasma flow? And what’s the significance of renal plasma flow?

A

PAH (para-aminohippurate) clearnce, when PAH is administered in low doses, can be used to calculate renal plasma flow. RPF=U(PAH)xV/(renal arterial plasma concentration of PAH – renal venule plasma conc of PAH). Instead, clearance of PAH is just divided by 0.9 to approximate RPF; the resulting value is called effective RPF. renal plasma flow can be used to calculate renal blood flow; RBF=RPF/(1-hematocrit)

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21
Q

What’s filtration fraction?

A

It’s GFR/RPF. The fraction of RPF that is filtered into Bowman’s capsule.

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22
Q

What do the macula densa cells sense?

A

NaCl concentration. When GFR is reduced, filtrate flow rate through the loop of Henle is reduced, and NaCl reabsorption is thus increased there. This would cause a decrease in [NaCl] at the macula densa

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23
Q

Which arteriole does AT2 primarily act upon?

A

The efferent arteriole. This constricts it, which increases the upstream glomerular pressure. Ultimately maintains GFR while reduced RBF.

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24
Q

What activates macula densa cells, and what do they do in response?

A

Activated by low [NaCl] and they cause dilation of the afferent arteriole (through unknown mechanism) and constriction of the efferent arteriole (through AT2) to increase GFR

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25
Q

How do the JG cells increase AT2 levels?

A

They secrete renin, which is the enzyme that readily converts angiotensinogen to AT1, and then angiotensin converting enzyme (ACE) converts AT1 to AT2

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26
Q

How does the stretch of afferent arterioles affect renin secretion?

A

decreased BP/volume decreases afferent arteriole stretch which leads to renin secretion.

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27
Q

Where does hormonal control of Na and water reabsorption take place?

A

At the distal tubule

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28
Q

Wher does primary active transport of Na occur in the renal tubules?

A

at Na/K ATPase pumps on the basolateral side of the epithelium

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29
Q

What are the major Na transporters of the various parts of the renal tubule?

A

In the proximal tubule it’s the Na/H countertransporter and the Na/Phosphate cotransporter, in the loop of Henle it’s the Na/K/2Cl transporter, in the distal convoluted tubule it’s the thiazide-sensitive Na/Cl cotransporter, and in the collecting duct it’s the ENaC ion channel

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30
Q

Where are the aquaporins?

A

Aquaporin 1 is in the proximal tubule apical and basolateral membranes, aquaporins 2 is in the collecting duct luminal membrane, and 3 and 4 are in the collecting duct basolateral membranes

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31
Q

Which aquaporin is reg’d by ADH?

A

aquaporin 2

32
Q

what does apical mean?

A

the same as luminal

33
Q

What protein do loop diuretics act on, and what are some examples of them?

A

the NKCC (Na/K/Cl cotransporter), eg furosemide, bumetadine

34
Q

What sodium transport proteins does AT2 act upon?

A

it increases the Na/H exchanger at the apical membrane (increases its functionality)

35
Q

What tubular transport proteins does ADH act upon?

A

it increases the abundance of NKCC, ENaC, and aquaporin 2

36
Q

What tubular transport proteins does aldosterone act upon?

A

It increases the expression of Na/Cl cotransporter and ENaC

also increases ROMK1 which leads to increased K excretion

37
Q

Where does iso-osmotic reabsorption occur?

A

In the proximal tubules

38
Q

Where is ADH secreted from?

A

The posterior pituitary

39
Q

What’s the difference between water diuresis and osmotic diuresis?

A

Water diuresis is when there’s low ADH/aquaporin 2 and water is excreted in excess of solute. Osmotic diuresis is when excess urine is a result of excess solute excretion (eg, diabetes mellititus and glycosuria)

40
Q

What leads to ADH release?

A

barorecoptor firing, which responds to blood pressure

hypothalmic osmoreceptor firing

41
Q

How do baroreceptors affect GFR?

A

baroreceptors fire when BP is high and act as negative feedback to the baroreflex

high BP causes alpha adrenergic effect of affernt arteriole vasoconstriction to reduce GFR. (Remember, baroreceptor firing also causes ADH release)

42
Q

What’s myogenic feedback?

A

the process of renal arterioles responding to increased blood pressure by constricting (within normal BP fluctuation)

43
Q

what’s glomerulotubular feedback?

A

the macula densa sensing low NaCl (which means low GFR) and responding with renin to increase GFR

44
Q

Where is aldosterone secreted from?

A

the zona glomerulosa of the adrenal cortex

45
Q

What does aldosterone stimulate?

A

reabsorption of sodium at the distal tubule and collecting duct

46
Q

What stimulates release of aldosterone?

A

angiotensin 2 and high [K] which both act on the zona glomerulosa

47
Q

What type of hormone is aldosterone?

A

a mineralocorticoid (steroid)

48
Q

Where is ACE found in the highest concentration?

A

the lungs

49
Q

What prompts renin secretion?

A

sympathetic nerves to the nephron (which were activated from systemc baroreceptors), intrarenal baroreceptors, and macula densa (fires on low NaCl concentration, resulting from low GFR and the resultant increase in Na reabsorption)

50
Q

What;s ANF?

A

Atrial Natriuretic Factor, secreted by atria when it fills too much (high blood volume, hypertension). Inhibits reabsorption of Na and increases GFR, and decreases renin release

51
Q

Do cardiovascular baroreceptors fire more or less often as blood pressure increases?

A

More often

52
Q

How does CV baroreceptors affect ADH secretion?

A

when they fire less often with decreased volume, ADH secretion is stimulated (ADH secretion is also stimulated by AT2)

53
Q

Where are osmoreceptors and what do they do?

A

they’re in the hypothalamus, and they fire more often as blood osmolarity increases. Their firing stimulates ADH secretion

54
Q

What stimulates ADH secretion?

A

AT2, CV baroreceptors, and hypothalmic osmoreceptors

55
Q

What increases thirst?

A

CV baroreceptors, hypothalamus osmoreceptors, AT2

56
Q

What are the effects of lowering and raising the intercellular potassium concentration?

A

lowering–depolarizes cells, causes spasms and possibly arrythmias

raising–hyperpolarizes, skeletal muscle weakness, arrythmias

57
Q

What does potassium experience in a nephron, and to what degree?

A

Reabsorption in the proximal tubule and loop of Henle–pretty constant

secretion in coritical collecting duct–regulation of potassium

58
Q

What hormone affects K secretion, and how?

A

Aldosterone increases K secretion by increasing basal Na/K ATPase in epithelia of cortical collecting duct, which raises intracellular K and thus K secretion. Plasma K levels affect aldosterone secretion directly by receptors at the zona glomerulosa

remember–aldosterone also increases Na reabsorption

59
Q

What’s a ROMK channel?

A

It stands for Rat Outer Medullar K+ channel. They’re in the collecting tubules and in the thick ascending limb (TAL) of the loop of Henle. in the TAL they allow K to be recycled and used in the NKCC channel, and in the collecting duct they allow K to be secreted.

ROMK1 is in the coolecting duct (cortical and outer) and does K secretion, ROMK2 and ROMK3 are in the TAL and DCT and do K recycling

60
Q

What are the cell types of the connecting tubule and cortical collecting duct?

A

principal cells account for 75% of the cells here, and they do K secretion and Na reabsorption and water reabsorption

intercalated cells comprise the reamining 25%. they do acid-base balance. alpha intercalated cells secret H+ and reabsorb bicarb, while beta IC’s secrete bicarb and reabsorb acid

61
Q

what transporter proteins are in the CCD?

A

aquaporin 2, ENaC, ROMK1, and the stuff from IC alpha and beta cells

62
Q

Which IC cell type has twhich transporter proteins on which surface?

A

Type alpha IC’s have H+ ATPase on the apical membrane and CL/HCO3 exchanger on basal membranes to secrete H+ and reabsorb bicarb

type B has the same transporters but on reverse surfaces to secrete bicarb and reabsorb H+

63
Q

Considering the CCD and OMCD, which IC is more common where?

A

beta in CCD, alpha in OMCD

64
Q

CCD has what types of cells?

A

CD cells with ROMK1 and ENaC and aquaporin 2, IC-alpha and IC-beta

65
Q

OMCD has what types of cells?

A

CD cells with ROMK-1 and ENaC and aquaporin 2, IC-alpha cells

66
Q

IMCD has what type of cells?

A

mostly inter-medullary CD cells, which have ENaC but don’t do a lot of Na reabsorption, and H/Cl exchangers to secrete H

67
Q

What does hypo/hypercalcemia cause?

A

hypocalcemic tetanic skeletal muscle contraction and arrythmias, respectively

68
Q

What’s PTH’s effect on calcium levels?

A

increases calcium levels by resorbing bone, increasing VitD to absorb more Ca from bone, and decrease Ca excretion in kidney by increasing tubular reabsorption

69
Q

Where is Ca reabsorbed?

A

In the PCT, loop of Henle, and DCT in order of most to least reabsorption

control occurs in the late distal tubule by PTH

70
Q

Where is phosphate reabsorbed, and what controls it?

A

normally 85% is reabsorbed and 15% excreted. Most reabsorption takes place in the PCT and the rest in the DCT

PTH regulates it; increased PTH increases plasma Ca and Pi, and it also decreases the Tm_reabsorption of Pi, which causes Pi flow to surpass Tm

This causes increased Pi excretion by decreasing reabsorption

71
Q

Where is Magnesium reabsorbed?

A

mainly in the loop of Henle via tight junction gaps

control is exerted mainly in the collecting ducts

72
Q

What are the 3 main ways the kidneys affect pH?

A

H secretion, bicarb reabsorption, and formation of new bicarb

73
Q

How is H secreted?

A

It occurs primarily in the PCT, where epithelia have basolateral carbonic anhydrase to turn CO2 and H2O into bicarb and H, and the H is then secreted by secondary active transport in exchange for Na reabsorption

In the CCD and OMCD, alpha ICs do primary active secretion of H

74
Q

How is bicarb reabsorbed?

A

It isn’t directly reabsorbed. Instead, H that is secreted from the epithelia combines with bicarb to make CO2 and H20. the CO2 passively diffuses into the epithelium, where carbonic anhydrase turns it into H and bicarb. The H is then secreted again, and the bicarb moves through a tranport channel on the basolateral side

75
Q

How does the kidney correct alkalemia and acidemia?

A

whichever is excess (H or bicarb) is excreted (because bicarb reabsorption and H secretion are coupled, whichever’s in excess cannot be retained)

76
Q

describe the phosphate buffer

A

it’s between HPO4(-2) and H2PO4(-1). H can’t just be secreted freely or else it would lower the pH of urine too much, so it needs to be coupled to an anion buffer system. It combines with HPO4(-2) and allows NaHCO3 to reabsorb into the ECF

77
Q

ammonia buffer?

A

NH3 is constantly synthed by epithelial cells and secreted; it combines with H to form ammonium and is excreted with Cl

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