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Med Phys > Lecture 6: Renal > Flashcards

Lecture 6: Renal Flashcards

1
Q

What does the kidney regulate?

A

Water/electrolyte balance
Fluid/osmolality
Arterial BP
Acid-base Balance
Erythrocyte production
Hormone secretion, metabolism, and excretion

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2
Q

How does the kidney regulate our electrolytes/water?

A

Excretion of metabolic products
Excretion/retention of water/electrolytes

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3
Q

How does the kidney regulate blood pressure?

A

Excreting/retaining water/sodium
Renin and angiotensin II

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4
Q

How does the kidney regulate our acid-base balance?

A

Excreting acids and/or bicarb

Note:
Think metabolic acidosis/alkalosis

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5
Q

How does our kidney regulate our RBC production?

A

It can secrete erythropoeitin when we are hypoxic.

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6
Q

Where is the hilum found in a kidney and what is it?

A

It is found on the medial side of each kidney, and it is the indented region that contains the renal artery/vein, lymphatics, nerves, and ureter.

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7
Q

What are the 3 main layers/sections of the kidney?

A

Superficial to deep:
Outer cortex
Inner Medulla
Renal pelvis

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8
Q

What structure is found in the medulla of the kidneys?

A

Renal pyramids, about 8-10, which terminate in the papilla.

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9
Q

What are the extensions of the renal pelvis?

A

Major calices, which have minor calices.

A minor calyx connects to a renal pyramid.
A major calyx connects multiple minor calices.

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10
Q

What is the basic unit of the kidney?

A

Nephrons, about 1 million per kidney.

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11
Q

About how much blood does our kidney get?

A

22% of our entire CO
1100 mL/min

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12
Q

How does arterial blood supply branch off in the kidney?

A

Starts with the:
Renal artery
Segmental arteries
InterLOBAR arteries
Arcuate arteries
InterLOBULAR arteries

Note: Lobules are smaller than lobes, so they are the last branching.

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13
Q

How does the blood supply of a single nephron work?

A

Arcuate arteries give off interlobular arteries, which have tiny branches called afferent arterioles. These afferent arterioles go to glomeruli and leave via efferent arterioles.

Peritubular capillaries are found along the loops, and are connecting the veins and arteries.

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14
Q

What are the two capillary beds of a nephron?

A

Glomerular capillaries
Peritubular capillaries

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15
Q

What kind of pressure does a glomerular capillary have?

A

High hydrostatic pressure, which encourages rapid fluid FILTRATION.

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16
Q

What kind of pressure does a peritubular capillary have?

A

Low hydrostatic pressure, which encourages rapid fluid REABSORPTION.

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17
Q

What separates the glomerular capillary from the peritubular capillary?

A

EFFERENT arterioles.

Note:
E for exit. Exiting the glomerulus.

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18
Q

How do the kidneys control the hydrostatic pressures of both capillary beds?

A

By adjusting afferent and efferent arteriole pressures.

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19
Q

What is the average pressure of a glomerular capillary?

A

60 mm Hg (high hydrostatic pressure)

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20
Q

What structure encases a glomerulus?

A

Bowman’s Capsule.

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21
Q

Describe fluid as it leaves the glomerulus.

A

Fluid will be filtered out of the glomerular capsule, going into the surrounding Bowman’s capsule and then into the PCT.

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22
Q

What parts of the loop of Henle are thin? thick?

A

The descending and lower loop is thin.
Once it is halfway up ascending, it becomes thicker.

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23
Q

Where do I find the macula densa?

A

End of the thick ASCENDING limb, which is essentially next to Bowman’s capsule again.

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24
Q

Name the parts of the nephron, beginning at the glomerulus.

A

Glomerulus (Cortex)
Bowman’s capsule (Cortex)
Proximal Tubule (Cortex)
Descending thin loop of Henle (Medulla)
Ascending thin loop of Henle (Medulla)
Ascending thick loop of Henle (Medulla)
Distal tubule (Cortex)
Connecting tubule (Cortex)
Cortical collecting duct (Cortex)
Medullary collecting tubule (Medulla)
Medullary collecting duct (Medulla)

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25
Q

What key differences define a cortical nephron?

A

Glomeruli in outer cortex.
Loops of Henle are short, they barely get into the medulla.
Their vascular structure is composed of peritubular capillaries surrounding the entire structure.

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26
Q

What key differences define a juxtamedullary nephron?

A

Their glomeruli are very close to the outer medullary zone.
Loops of Henle are very long, dipping deep into the medulla.
Their peritubular capillaries are very long, known as vasa recta.

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27
Q

What are afferent arterioles branches off of?

A

InterLOBULAR arteries.

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28
Q

What 4 processes are involved in concentrating urine?

A

Filtration
Reabsorption
Secretion
Excretion

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29
Q

Where does filtration occur?

A

Glomerular capillaries, which go into Bowman’s capsule.

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30
Q

What is reabsorption?

A

Water and solutes going back into the BLOOD.

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31
Q

What is secretion?

A

Peritubular capillaries sending substances into the tubules (aka the urine)

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32
Q

What is excretion?

A

Excretion = Filtration - Reabsorption + Secretion.

Note:
Reabsorption is the only thing that takes stuff OUT of the tubules.

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33
Q

What substance in our body is solely filtered?

A

Creatinine.

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34
Q

What substances in our body are filtrated and/or reabsorbed?

A

Electrolytes

Note:
They get reabsorbed, but NOT completely.

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35
Q

What substances in our body get filtered but not excreted?

A

Amino acids and glucose.

Note: They get reabsorbed completely.

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36
Q

What substances are freely filtered and secreted?

A

Organic acids and bases

Note:
Stuff that should be renally cleared ASAP.
0 Reabsorption.

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37
Q

What are the end products of metabolism that we suck at reabsorbing?

A

Urea
Creatinine
Uric acid

Note:
AKA everything we find in large concentrations in our urine.

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38
Q

If a substance has poor reabsorption, would I expect a high or low excretion rate?

A

High.

Note:
Poor reabsorption means we are bad at getting it BACK INTO the body.

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39
Q

What is the main role of secretion?

A

Determining how many H+ and K+ we excrete in our urine.

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40
Q

What electrolytes have high reabsorption rates?

A

Sodium, Chloride, and Bicarb.

Note:
This is why we see LOW amts of these in our urine.

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41
Q

Name some substances we filter in large amts, but are reabsorbed completely.

A

Glucose and amino acids.

Note:
In a normal urine sample, we should not see any glucose or AAs in it.

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42
Q

What does High GFR imply?

A

Rapid removal of waste. We can filter our body fluid faster and more times a day.

Note:
We filter our 3L of plasma 60 times a day.
GFR = 180L/day.

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43
Q

What substance are glomerular capillaries IMPERMEABLE to?

A

Proteins!

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44
Q

What is glomerular filtrate composed of?

A

Should be identical to plasma concentration EXCEPT:

No proteins
No RBCs
Low calcium & fatty acids (protein bound)

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45
Q

What forces contribute to GFR?

A

Hydrostatic forces
Colloid osmotic forces
Capillary filtration coefficient

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46
Q

What is the capillary filtration coefficient determined by?

A

It is the product of how permeable the capillary membrane is and the surface area available for filtration.

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47
Q

What is special about glomerular capillary membranes?

A

It has 3 layers.
Each layer is negatively charged, which repels proteins.
Each layer is thicker but more permeable, depending on a substances charge and size.

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48
Q

What are the 3 layers of the filtration barrier?

A

Endothelium, made of fenestrations and negative charges to repel proteins.

Basement membrane, a meshwork of collagen that has large fenestrations for water and small solutes.

Epithelial cells (Podocytes), lining the outer surface of the glomerulus. They have foot-like processes separated by slit pores (gaps), which filtrate can move through)

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49
Q

What substances are freely filtered?

A

Freely filtered means filtered as much as water.

Water, sodium, glucose, and inulin.

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50
Q

What substances are not freely filtered?

A

Myoglobin, Albumin (extremely poor filterability)

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51
Q

What is filterability of a solute related to?

A

It is inversely proportional to its size.

AKA the bigger the solute, the WORSE the filterability.

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52
Q

How do I determine the net filtration pressure?

A

It is the sum of hydrostatic pressure and colloid osmotic forces.

Net filtration pressure (10 mm Hg) = Glomerular hydrostatic pressure (60 mm Hg) - Bowman’s capsule pressure (18 mm Hg) - Glomerular colloid osmotic pressure (32 mm Hg)

Note:
Glomerular hydrostatic is pushing fluid out of the glomerulus.

Bowman’s capsule surrounds a glomerulus, so its hydrostatic pressure pushes fluid back into the glomerulus.

Colloid osmotic means the protein’s pull on water, so the albumin is drawing water back into the glomerulus.

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53
Q

What does AT2 do to glomerular arterioles and therefore glomerular pressure?

A

Constriction of BOTH afferent and efferent arterioles. It constricts efferent arterioles more though.

This increases pressure within the glomerulus, which increases GFR (it is increasing hydrostatic pressure).

Note:
ACEI cause dilation of efferent arterioles, which is why they drop your GFR and can lead to possible acute renal failure.

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54
Q

What does an increase in the filtration coefficient do to GFR?

A

Increases GFR.

Note:
Filtration coefficient is Kf.

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55
Q

How does kidney disease affect Kf?

A

It lowers it via two ways:

Lowering number of functional glomerular capillaries (aka lower surface area)

Increases membrane thickness. (Uncontrolled HTN or DM)

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56
Q

What does an increase in Bowman’s capsule hydrostatic pressure do to GFR?

A

It decreases it.

GFR is going out of the glomerulus, but because Bowman’s capsule surrounds the glomerulus, its hydrostatic pressure pushes stuff back in.

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57
Q

What is a common cause of increased Bowman’s capsule pressure?

A

Obstruction of the urinary tract via stones (calcium or uric acid)

This causes drops in GFR, and can damage/destroy the kidney eventually.

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58
Q

What does a greater rate of blood flow into the glomerulus do to GFR?

A

Increases GFR.

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59
Q

What 3 pressures can affect glomerular hydrostatic pressure?

A

Arterial BP
Afferent arteriole pressure
Efferent arteriole pressure

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60
Q

What does increased arterial BP do to GFR?

A

Increases it, because it increases glomerular hydrostatic pressure.

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61
Q

What does increased afferent arteriole resistance do to GFR?

A

Decreases it, because it reduces glomerular hydrostatic pressure.

Note:
I think of it as less fluid going in, so there is less fluid to push against the edges.

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62
Q

What does increased efferent arteriole resistance do to GFR?

A

Increases it, because it increases glomerular hydrostatic pressure.

Note:
If it gets too high, renal blood flow is reduced, which will actually cause a lowered GFR.

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63
Q

What is renal arterial pressure usually the same as?

A

Systemic arterial pressure.

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64
Q

Where do I find the most resistance in the kidney’s arteries?

A

Interlobular arteries
Afferent arterioles
Efferent arterioles

(aka the 3 smallest arteries)

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65
Q

What systems control efferent arteriole resistance?

A

SNS
Hormones
Local, internal renal control mechanisms.

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66
Q

Does a change in systemic arterial pressure greatly affect renal blood flow?

A

No. The kidneys generally auto-regulate themselves to maintain pressure and GFR between 80-170 mm Hg.

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67
Q

What does strong SNS stimulation do to the kidney and arterioles?

A

Constriction of renal arterioles, decreasing blood flow and GFR.

Note:
Requires STRONG SNS stimulation.
When SNS is activated, you generally don’t pee, so kidney function must decrease.

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68
Q

What 3 hormones affect renal blood flow and what is their effect?

A

NE, epi, and endothelin.

Constriction of renal blood vessels, decreasing blood flow and therefore GFR. (only happens under extreme conditions like massive hemorrhaging)

Note:
Endothelin is released by damaged vascular endothelial cells, not well-understood.

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69
Q

What does AT2 do?

A

Constriction of all kidney arterioles EXCEPT pre-glomerular ones, aka afferent arterioles.

Efferent arterioles are highly sensitive to it, so they will constrict heavily. This reduces renal blood flow a little, but it can increase glomerular hydrostatic pressure a lot and therefore GFR.

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70
Q

Why don’t afferent arterioles get affected by AT2?

A

Lack of receptors
Nitric oxide and prostaglandins also prevent its constriction.

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71
Q

When does AT2 generally get activated?

A

Low arterial BP
Volume depletion

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72
Q

How does AT2 affect renal blood flow?

A

Decreases flow to peritubular capillaries, causing us to reabsorb more Na and water to restore our BP.

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73
Q

What does an increase in glomerular colloid osmotic pressure do to GFR? What can cause it?

A

Decreases it.

Caused by decreased renal blood flow, or increased plasma proteins.

74
Q

What can decrease the filtration coefficient? What does it do to GFR?

A

Decreases it.

Caused by renal disease, DM, and uncontrolled HTN.

75
Q

What can decrease efferent arteriolar resistance? What does it do to GFR?

A

Anything that blocks the formation of AT2.

Caused by ACEI, renin inhibitors, ARBs.

76
Q

What is tubuloglomerular feedback?

A

The kidneys have their own feedback mechanism to autoregulate their GFR.

It determines the [NaCl] at the macula densa and renal arteriolar resistance.

This is to prevent large fluctuations in renal excretion.

77
Q

What are the two feedback mechanisms?

A

Afferent arteriolar feedback mechanisms
Efferent arteriolar feedback mechanisms

78
Q

What are the two components that affect feedback?

A

Within the juxtaglomerular apparatus (JGA), we have the macula densa in the distal tubule, as well as the juxtaglomerular cells within the walls of both arterioles.

79
Q

What happens if the macula densa detects a low [NaCl] in the tubule?

A

It will dilate AFFERENT arterioles and increase the release of renin.

Note:
Decreasing GFR causes increased sodium chloride reabsorption earlier in the tubule.

80
Q

Where is renin stored?

A

In the kidneys, specifically in the juxtaglomerular cells found in both afferent and efferent arterioles.

81
Q

What are the two ways the macula densa raises GFR?

A

Dilation of afferent arterioles to raise glomerular hydrostatic pressure and therefore GFR.

Increase renin release, which leads to increased AT2 acting on AT2 receptors and constricting efferent arterioles to raise glomerular hydrostatic pressure and therefore GFR.

82
Q

If I have high NaCl reabsorption in the PCT, would I expect low or high NaCl in the macula densa?

A

Low.

The macula densa is found at the DCT, so all the reabsorption happened upstream of it.

83
Q

What renal issues can an ACE inhibitor cause?

A

Renal artery stenosis
Decreased GFR
Sudden/acute renal failure.

84
Q

What is the main determinant of final urinary excretion rates?

A

Tubular reabsorption.

85
Q

What is glomerular filtration similar to in renal excretion?

A

Tubular secretion.

86
Q

What process in renal excretion is highly selective?

A

Tubular reabsorption.

It completely reabsorbs glucose, and highly reabsorbs Na, Cl, and bicarb.

87
Q

What process in renal excretion is relatively non-selective?

A

Glomerular filtration.

88
Q

What substances are poorly reabsorbed?

A

Urea and creatinine, hence why we measure BUN and creatinine to approximate GFR.

Note:
They are highly excreted.

89
Q

What ion is the least reabsorbed?

A

Potassium.
Has about an 88% reabsorption rate.

90
Q

What ion is the most absorbed?

A

Bicarb, 99.9%.

91
Q

What substance do we have to filter the most of?

A

Sodium!

92
Q

What two things does a solute have to pass to get reabsorbed into blood?

A

First, it passes across the tubular epithelial cells into the renal interstitial fluid.

Second, it passes across the peritubular capillary membrane into the bloodstream.

93
Q

What are the two ways a solute can pass into the renal interstitial fluid?

A

Water and solutes: transcellular (across the cell’s mebrane)

Paracellular: in between two cell junctions (like an alley between two buildings)

94
Q

How does a solute/water pass through the peritubular capillary membrane?

A

Bulk flow, or ultrafiltration.

Note:
Mediated by hydrostatic and colloid osmotic forces.

95
Q

Define active transport for tubular reabsorption.

A

Against an electrochemical gradient, requiring ATP.

This is known as PRIMARY active transport.

96
Q

Define secondary active transport for tubular reabsorption.

A

Same as active transport, except the solute is attached to the energy source indirectly.

An example would be glucose!

97
Q

What kind of junctions are found between tubular epithelial cells?

A

Tight junctions.

98
Q

What type of junction does paracellular transport go through?

A

Tight junctions.

99
Q

What are the 4 primary active transporters of the kidney?

A

Na-K ATPase
H ATPase
H-K ATPase
Ca ATPase

100
Q

Where do I find an ATPase?

A

It is bound to the membrane.

101
Q

What does active transporting of sodium into the bloodstream from tubular epithelial cells cause?

A

A concentration gradient favoring the flow of sodium into the tubular epithelial cells from the TUBULAR lumen.

102
Q

What does secondary active transport require?

A

Indirect energy source, which commonly occurs as 2 substances interacting with a carrier molecule to move across a cell membrane.

103
Q

What substances use secondary active transport?

A

Glucose and amino acids.

104
Q

What transporters does secondary active transport use?

A

SGLT2 and SGLT1 (aka sodium-glucose co transporters)

They can combine with a sodium ion and an amino acid/glucose.

105
Q

Where does secondary active transport occur?

A

Occurs going from the tubular lumen to the tubular cells in the PCT.

Afterwards, glucose and amino acids can diffuse across the peritubular capillary membrane.

106
Q

What medication can inhibit secondary active transport?

A

Invokana, which inhibits SGLT transporters.

107
Q

How much of our glucose is reabsorbed in the PCT?

A

100%

90% in the early PCT by SGLT2
10% in the later PCT by SGLT1.

108
Q

Why is glucose considered secondary active transport?

A

It is reabsorbed against a gradient, and sodium is technically the primary active transport.

109
Q

Which SGLT does much of our glucose reabsorption?

A

SGLT2, in the early PCT.

110
Q

What does the reabsorption of sodium in allow us to excrete in the PCT?

A

Hydrogen ions via the sodium-hydrogen exchanger. (NHE).

Na-H Exchanger.

111
Q

Where do I find the NHE (sodium hydrogen exchanger)?

A

Brush border of the luminal membrane, aka the side facing the tubular lumen.

Note:
He calls this counter transport.

112
Q

How do we achieve a transport maximum?

A

When all transporters are occupied/saturated.

Specifically, this means that tubular load exceeds the capacity of carrier proteins and enzymes involved in transporting.

113
Q

If I achieve my transport maximum, how are filtration, reabsorption, and excretion affected for glucose?

A

Once maxed, my filtered load and excretion of glucose will rise linearly.

My reabsorption will plateau once transport max is reached. It cannot increase more.

114
Q

What is the transport maximum for kidneys to reabsorb glucose?

A

375 mg/min.

115
Q

What is the average plasma glucose threshold concentration and what will happen if I surpass it?

A

It is around 200 mg/dl.

If I exceed that much glucose in my plasma, my urine will start to have glucose in it as the filtered load increases.

116
Q

What kind of substances are not affected by a transport maximum?

A

Passively absorbed substances.

Note:
They don’t need transporters.

117
Q

What determines how fast a passively reabsorbed substance is reabsorbed?

A

Electrochemical gradient for diffusion.
Permeability of the membrane.
Time that the fluid remains in the tubule.

118
Q

What is the name of the relationship for passive diffusion in the kidneys?

A

Gradient-time transport.

The greater the gradient or the longer the fluid remains in the tubule, the greater the rate of diffusion.

119
Q

Is sodium actively transported or passively diffused? Why is it unique?

A

It is actively transported, but behaves like a passive diffusion. Because of this, sodium reabsorption is dependent more on its concentration and how long it remains in the tubules.

Note: Our ATPase activity is so high that we cannot get to the transport maximum.

120
Q

What happens to sodium reabsorption if we have a high concentration of it in the tubular lumen?

A

Increased reabsorption.

121
Q

What happens to sodium reabsorption if we have a slow tubular flow rate?

A

Increased reabsorption.

AKA the macula densa/BP response.

122
Q

How do we rebsorb water?

A

Osmosis.

Note:
It will follow the solutes that we actively transport.

123
Q

When is water permeability highest in the nephron?

A

PCT, the tight junctions are highly permeable to water.

124
Q

When is water permeability low in the nephron?

A

Loop of Henle and DCT.

Note:
We can increase water permeability in the collecting duct and DCT via ADH.

125
Q

What is reabsorbed in the PCT?

A

65% of the filtered load that contains sodium and water and chloride (less)

126
Q

How does the PCT achieve high reabsoprtion?

A

It has a lot of active transporters and energy.
It has an extensive brush border, which means increased surface area.
It has a lot of protein carriers and lots of co-transporters and counter-transporters.

127
Q

What two substances increase in tubular concentration in the PCT?

A

Urea and Creatinine.

Note:
Tubular concentration is what we will eventually urinate.
These are the two substance we want to get rid of.

128
Q

BONUS: What diuretic works on the PCT?

A

Carbonic anhydrase inhibitors.

129
Q

What part of the loop of Henle is still permeable to water?

A

Descending loop, which does another 20% of water filtration.

130
Q

What does the descending loop of Henle do?

A

Moderately permeable to most solutes, such as urea and sodium.

Simple diffusion of substances through its wall.

131
Q

What part of the loop of Henle is IMpermeable to water?

A

The ascending segment, both thin and thick.

132
Q

What is different about the thin segment of the ascending loop of Henle?

A

It has lower absorptive capacity.

133
Q

What happens in the thick ascending loop of Henle?

A

High metabolic activity combined with thick epithelial cells.

Allows of active reabsorption of 25% of Na, Cl, and K.

Also can reabsorb Ca, bicarb, and Mg.

134
Q

What is the one substance secreted into the tubular lumen in the ascending loop of Henle?

A

H+ ions.

135
Q

Bonus: What diuretic affects the ascending loop of Henle?

A

Loop diuretics, inhibition of Na/2Cl/K pump.

136
Q

BONUS: What diuretic works on the PCT?

A

Carbonic anhydrase inhibitors.

137
Q

What do the thick epithelial cells do in the ascending loop of Henle?

A

They have ATPase sodium potassium pumps that move sodium to the renal interstitial fluid and potassium into the tubular cell.

This allows sodium to move from the tubular fluid into the cell.

138
Q

What 3 loop diuretics did Dr. Shephard mention in his lecture that act on the thick ascending limb of the loop of Henle?

A

Furosemide (Lasix)
Ethacrynic acid (Edecrin)
Bumetanide (Bumex)

139
Q

What does blocking of the sodium-chloride-potassium cotransporter do to our urinary concentrations?

A

Raises urine output of sodium, chloride, and potassium.
Raises output of other electrolytes, as well as water.
It essentially decreases the ability of the kidney to CONCENTRATE urine.

140
Q

Which part of the distal tubule is the macula densa?

A

First portion.

141
Q

What happens in the second segment of the distal tubule?

A

Reabsorption of many ions, but IMPERMEABLE to water and urea.

It is often known as the diluting segment because it is diluting the tubular fluid.

142
Q

BONUS: what diuretic works on the early part of the DCT?

A

Thiazide diuretics, which inhibit the sodium-chloride co-transporter.

143
Q

What happens in the first segment of the DCT?

A

Reabsorption of 5% of the filtered load of NaCl.
NaCl cotransporter reabsorbs NaCl from the tubular lumen.

Na-K ATPase kicks sodium out of the renal epithelial cell into the renal interstitial fluid.

144
Q

What two cell types can I find in the late DCT and cortical collecting tubule?

A

Principal cells
Intercalated cells

145
Q

What do principal cells do?

A

They reabsorb sodium & water from the tubular fluid.
They secrete potassium INTO the tubular fluid.

146
Q

What do intercalated cells do?

A

Reabsorb potassium from the tubular fluid and secrete hydrogen ions INTO the tubular fluid.
Reabsorb bicarb.

147
Q

Which cells do the potassium-sparing diuretics work on?

A

Principal cells, since they are the ones that secrete potassium into the tubular fluid.

148
Q

What is the main role of the medullary collecting duct?

A

Final site for processing urine.
It determines the final output of water and solutes.

Note:
Reabsorbs < 10% of filtered water and sodium.

149
Q

What are the special characteristics of the medullary collecting duct?

A

ADH affects it.
High ADH causes high water reabsorption and therefore low urine volume. It will concentrate all the solutes.

Permeable to urea.
Secretes hydrogen ions into the lumen against a concentration gradient to maintain acid-base balance. (also absorbs bicarb)

150
Q

If I reabsorb more water than solute, what would happen to my tubular fluid concentration ratio?

A

It would rise above 1.

151
Q

What two substances are often used in GFR testing?

A

PAH and Inulin.

152
Q

If I reabsorb more of a solute than water, what would I expect the concentration ratio to be?

A

Less than 1.

153
Q

If GFR is increased, is tubular reabsorption increased or decreased?

A

Increased automatically. This is to prevent DCT overload.

154
Q

What are the two forces at work within the peritubular capillary?

A

Peritubular hydrostatic pressure pushes solutes OUT of the peritubular capillary. (Pc)
Peritubular colloid osmotic pressure draws solutes INTO THE PERITUBULAR CAPILLARY (pi c)

155
Q

What is the effect of aldosterone? Where does it have its effect?

A

Principal cells of the cortical collecting tubule.

Increase sodium reabsorption, while simultaneously increasing potassium excretion.

It stimulates the Na-K ATPase pump found on the basolateral side of the cortical collecting tubule membrane. (AKA the side that faces the faces the renal interstitial fluid and peritubular capillary.)

156
Q

What happens to our plasma osmolarity if we drink excess water?

A

With functional kidneys, barely anything should happen.

157
Q

How do we maintain our plasma osmolarity if we drink excess water?

A

We have to increase our ability to dilute filtrate by reabsorbing solutes at a greater proportion than water.

158
Q

What tonicity does tubular fluid start out as?

A

Isotonic, aka equal parts solute and water.

159
Q

What happens to water as we go down the descending loop of Henle?

A

Reabsorption, and the tubular fluid reaches equilibrium with the medulla, which is hypertonic.

160
Q

What happens to water as we go up the ascending loop of Henle?

A

It stays in the tubular fluid, but we reabsorb lots of Na/Cl/K.

161
Q

What kind of tonicity is tubular fluid entering the DCT?

A

Hypotonic (we just took most of the electrolytes out without reabsorbing water)

162
Q

What should happen to urine as it enters the DCT and collecting ducts without ADH?

A

We reabsorb even more NaCl, so the tubular fluid osmolarity drops even more.

163
Q

How do we lose water from the body?

A

Lungs
GI tract
Skin
Kidneys

164
Q

If we have a water deficit, what do our kidneys do?

A

Concentrate urine, reabsorbing water.

165
Q

What is a high urine specific gravity indicative of?

A

Concentrated urine. Solutes are heavier than water.

166
Q

What two conditions are required for us to concentrate urine?

A

Lots of ADH (reabsorption of water, which concentrates urine)

Hyperosmotic medulla (which draws water out of the descending loop of Henle)

167
Q

What is the countercurrent mechanism needed for?

A

To generate the hyperosmotic medullary interstitium, which surrounds the tubular fluid as it descends into the medulla during the descending loop of Henle.

168
Q

What 4 processes produce the countercurrent mechanism?

A
  1. Active transport of Na and co-transport of K, Cl, and other ions OUT of the thick ascending loop of Henle, into the medullary interstitium.
  2. Active transport of ions from collecting ducts into medullary interstitium.
  3. Facilitated diffusion of urea from inner medullary collecting ducts into medullar interstitium.
  4. Diffusion of only a little water from the medullary tubules into the medullary interstitium.
169
Q

What is the main function of the loop of Henle?

A

Trapping solutes in the medullary interstitium.

170
Q

What is unique about the thick ascending limb of the loop of Henle in terms of reabsorption?

A

It is completely impermeable to water, NaCl and Urea diffusion. ADH also cannot affect it.

It actively transport large amounts of NaCl.

171
Q

What are the only two parts of the nephron impermeable to water reabsorption even in the presence of ADH?

A

The ascending loop of Henle. (thin and thick)

172
Q

What part of the nephron has 0 NaCl active transport?

A

Both the thin ascending and thin descending loops. They are both naturally permeable to NaCl.

173
Q

What is the only part of the nephron that is permeable to urea?

A

Inner medullary collecting duct, but only in the presence of ADH.

174
Q

What are the 6 steps that produce the hyperosmotic medullary?

A
  1. Loop begins with 300 mOsm, the same mOsm leaving the PCT.
  2. Ion pump of thick ascending reduces mOsm inside the tubule to 200.
  3. The descending loop and interstitial fluid reaches equilibrium via osmosis leaving the descending limb going into the medullary.
  4. More fluid flows into the descending loop from the PCT, pushing the hyperosmotic fluid in the descending loop to the ascending loop.
  5. More ions are pumped into the medullary interstitium from the ascending loop, increasing medullary mOsm to 500.
  6. Repeat steps 4-6. Essentially, more solutes get pumped into the medullary interstitium at the ascending loop. Water can’t leave the ascending loop, so the medullary interstitium increases in mOsm steadily.
175
Q

Is the tubular fluid high in mOsm or low as it enters the DCT?

A

It should be low, around 100 mOsm. Most of the solutes are sent into the medullary interstitium to concentrate it.

176
Q

What is cortical collecting tubule reabsorption heavily dependent on?

A

The Plasma [] of ADH.

Without ADH, it cannot reabsorb water. It will only reabsorb solutes and dilute the urine.

177
Q

How much does urea contribute to the hyperosmotic renal medullary interstitium?

A

40%

178
Q

Why is urea passively reabsorbed in the tubule?

A

It helps to trap it in the renal medulla, maintaining the hyperosmolarity.

179
Q

What happens to my urea if ADH is high?

A

I would expect high reabsorption of urea.

180
Q

How does the vasa recta affect the hyperosmolarity of the renal medulla?

A

Because medullary blood flow is low, it can minimize solute loss.

Initially, the descending limb forces water out of the capillaries and solutes into the capillaries.

However, because it is also U shaped, water can flow back into the ascending limb of the vasa recta, and solutes will consequently flow back out into the medullary interstitium.

181
Q

Describe the effects of a water deficit on osmolarity and ADH.

A

Water deficit leads to…

Increased extracellular osmolarity

Increased ADH secretion

Increased Plasma ADH

Increased water permeability in DCT and collecting ducts.

Increased water reabsorption

Decreased water excreted.

Negative feedback loop. Once we restore water balance, it will inhibit ADH secretion.

Med Phys (11 decks)

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