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BMS242 - Phys/Pharm of Cells > Renal Physiology > Flashcards

Renal Physiology Flashcards

1
Q

On average how much glomerular filtrate is produced per day?

A

180L

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2
Q

If the blood plasma volume is roughly 2.8L how many times per day is it filtered?

A

180/2.8 = 63

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3
Q

What percentage of the plasma leaves the blood and is filtered in the kidneys?

A

20%

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4
Q

What are the three layers of the filtration barrier?

A

Cap endothelium, basement membrane and podocytes

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5
Q

Which layer of the filtration barrier contributes the most filtration of the plasma?

A

Basement membrane

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6
Q

Which layer of the filtration barrier restricts the efflux of large proteins and blood cells?

A

Cap endothelium

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7
Q

What is the other name for the epithelial layer of the filtration barrier and what is its main role?

A

Podocytes - mainteneance of structure of the barrier and the phagocytosis of FBs

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8
Q

What is the name given to the gaps between the cells in the endothelial layer of the filtration barrier that the filtrate moves through?

A

Circular fenestrations

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9
Q

What are the main constituents of the basement membrane?

A

Glycoproteins - collagen, laminin and fibronectin

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10
Q

What polarity of molecule is given preferential efflux through the basement membrane?

A

Positvely charges

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11
Q

What are the three determinants of filtration of a substance?

A

Size shape charge

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12
Q

What is the name of the projections from the cell body of the podocytes?

A

Trabeculae

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13
Q

Explain how the pedicels interact to add an additional layer of filtration in the glomerulus?

A

Pedicels interdigitate to create slit pores in which filtrate can pass through

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14
Q

What is meant by a substance that is freely filtered in the glomerulus?

A

It can pass freely between the blood plasma and tubular fluid. Conc of both substances will be the same and two compartments willl have a F/P of 1

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15
Q

What is the relationship between the filtrate/plasma ratio and the amount of filtration?

A

The lower the F/P - less likley to be filtered

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16
Q

Molecules up to a molecular weight of 70kDa are freely filtered, T or F?

A

F - moleucles up to 10KDA freely filtered above 70 kDa arent filtered at all

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17
Q

Why can Cl- and HCO3-ions pass freely through the filtration barrier despite being negatively charged?

A

Because they have a tiny mass

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18
Q

What is meant by the filtration constant, Kf?

A

The perm of the filtration barrier

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19
Q

GFR is proportional to the forces that favour filtration minus the forces that oppose filtration, T or F?

A

T

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20
Q

What is the equation for GFR?

A

Kf((P cap + Π bc ) - (P bc + Π cap ))

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21
Q

What is the symbol for oncotic pressure?

A

Π

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22
Q

What is the average value of capillary hydrostatic pressure in the glomerulus?

A

60 mmHg

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23
Q

Why is there a small drop in capillary hydrostatic pressure across the length of the afferent arteriole in the glomerulus?

A

Due to movement of water out of the capillary into the tubular fluid

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24
Q

What is the approximate value of the hydrostatic pressure of the tubular fluid?

A

20 mmHg

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25
Q

Why doesn’t the pressure of the tubular fluid increase?

A

Because fluid moving through the nephron so pressure is maintained

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26
Q

What is the value of the oncotic pressure in the capillary and why does it increase over the length of the vessel?

A

30 mmHg - increases due to the loss of fluid over the vessel but the retention of protein leading to an increase in its concentration and thus an increase in osmolality

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27
Q

What is the rough value for the net filtration pressure in the glomerulus?

A

10 mmHg

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28
Q

There is always a positive driving force for fluid efflux across the length of the capillaries and thus a movement of fluid out of the vessels, T or F?

A

T

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29
Q

What is the approximate rate of filtration in a single nephron? Use this value to estimate the number of nephrons in the kidney?

A

50nl min-1 125x10-3/50x10-9 = 2.5x106 – 2.5 million

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30
Q

What is meant by the nephron autoregulation range?

A

The autoregulation range is a range of arterial BPs in which the kidney can maintain a steady renal blood flow, cap P and GFR

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31
Q

How do the glomeruli maintain constant RBF, Pcap and GFR despite changes in atrial blood pressure?

A

Regulation of diameter of the afferent arterioles

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32
Q

Vasoconstriction of the afferent arterioles causes a decrease in renal blood flow, capillary hydrostatic pressure thus decreasing GFR, T or F?

A

T

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33
Q

What happens as a result of vasodilation of the afferent arteriole?

A

Vasodilation causes increase RBF to the glomerulus and this increasing the hydrostatic pressure and GFR

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34
Q

How does the kidney respond to an increase in arterial blood pressure?

A

An increase in P(art) leads to inc in P(cap) and GFD. Vasoconstriction in the afferent artiole - decreases RBF and hydrostatic pressure to maintain the GFR

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35
Q

How does the kidney respond to a decrease in arterial blood pressure?

A

A decrease in P(A) leads to dec in P(cap) and GFR. To prevent this vasodilation occurs in afferent arteriole. Increasing renal blood flow and hydrostatic pressure to help maintain GFR

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36
Q

Explain the myogenic theory of kidney autoregulation?

A

Myogenic theory sates that autoreg of afferent arteriole diameter is inherrent prop of the capillary smooth muscle. Increase in P(A) results in activation of strech receptors in the smooth muscles of the walls causing vasoconstirction to prevent an increase in GFR

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37
Q

Explain the tubuloglomerular theory of kidney autoregulation?

A

Due to closeness of distal tubule to glomerulus. Increase in GFR and RBF detected by macula densa cells of the JGA. Cells of the JGA release vasoconstrictory facotrs to minimise any increase in RBF, hydrostatic pressure and GFR

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38
Q

It is now believed that the tubuloglomerular theory is solely responsible for autoregulation in the nephron, T or F?

A

F - combination of tubuloglomerular and myogenic theory

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39
Q

What is the minimum amount of urine produced in a day?

A

300 mls

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40
Q

What is the maximum amount of urine produced in a day?

A

23 L

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41
Q

What is the result of the differences in osmolarity between the tubular and interstitial fluid?

A

Water movement

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42
Q

What are the two structures of the nephron that contribute to the countercurrent multiplier?

A

LoH and CD

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43
Q

What is meant by the term osmolality?

A

Conc of substance timed by the number of ions it dissociates into in solution

44
Q

Describe the movement of water and ions across the ascending limb of the Loop of Henle and the effect this has on the osmolality of the interstitial and tubular fluid?

A

In the ascending limb - net loss of Na and Cl from tubular fluid into IF - Decreasing the osmolality of the tubular fluid and increasing the osmolality of the interstitial fluid. The ascending limb in impermabel to water so there is no movement

45
Q

What is the net result of the gradients set up by the ascending limb of the Loop of Henle?

A

Sets up a driving force for water reabsoportion from the descending limb

46
Q

The descending limb is permeable to Na+ and K+, T or F?

A

F- impermable

47
Q

What happens in the collecting duct of the nephron and what is the effect of this on tubular fluid osmolality?

A

bular fluid into the intersitial fluid leading to an increase in tubuar fluid osmolality

48
Q

Describe the osmotic gradients that exist in the nephron.

A

There is a transverse osmotic gradient between the ascending and descending limbs of the Loop of Henle with the descending limb having a higher osmolality. This drives water entry into the tubular fluid in the descending limb. There is then also a vertical osmotic gradient present in both ascending and descending limbs with the tip of the Loop of Henle having the highest osmolality that decreases as it heads up towards the cortex.

49
Q

The osmolality increases up the descending limb of the Loop of Henle, T or F?

A

F - decreases

50
Q

The osmolality increases down the length of the descending limb of the Loop of Henle, T or F?

A

T

51
Q

Where is water first reabsorbed in the nephron?

A

Thin descending limb of the LoH

52
Q

What channel is present in the thin descending limb that mediates water uptake from the tubular fluid?

A

AQP1

53
Q

What is the result of knocking out the gene responsible for water uptake in the thin descending limb?

A

Problems with urine concentration

54
Q

The thin ascending limb is permeable to H2O, T or F?

A

F - impermeable

55
Q

As well as Na+ and Cl-, the thin ascending limb is permeable to urea, T or F?

A

T

56
Q

Which side of the cell membrane faces the tubular fluid in the nephron?

A

Apical

57
Q

Which side of the cell membrane

A

Basolateral

58
Q

Describe the role of the Na+/K+ATPase and the K+ Channel in the thick ascending limb cells?

A

3NaO 2KI - sets up low IC Na – Basolateral K channels allows K to move back out of the cell

59
Q

What is the role of NKCC2 in the thick ascending limb cells?

A

Brings in Na, K and 2Cl at the apical membrane

60
Q

Why and how is K+ recycled across the membrane of cells in the thick ascending limb?

A

K needs to recycle of apical membrane of the cells in the TAL as there isnt enough tubular K to maintain NKCC2 - so K in through NKCC2 moves back into the tubular fluid through apical ROMK

61
Q

What is the fate of the Cl- ions brought into the cells in the thick ascending limb?

A

Cl in through NKCC2 moves through basolateral Cl channel CLCK regulated by Barttin

62
Q

What is Bartters syndrome and how is it caused?

A

Disease of the TAL - inap solute handling –> Results in the excretion of excessive ammounts of NaCl and polyuria and hypokalameia - loss of function in NKCC2, ROMK, Barttin or CLCK

63
Q

Which cells/region of the nephron is responsible for the mediation and regulation of water reabsorption?

A

Principal cells in the collecting duct

64
Q

Explain what is happening at the apical membrane of the principal cells?

A

ENaC brings Na+ ions into the cell down their concentration gradient set up by the Na+/K+ATPase. ROMK allows for the movement of K+ brought into the cell by the Na+/K+ATPase to move into the tubular fluid. AQP2 mediates water uptake from the tubular fluid into the cel

65
Q

Explain what is happening at the basolateral membrane of the principal cells?

A

The Na+/K+ATPase transports Na+ out and K+ creating a low intracellular [Na+]. Kir2.3 allows K+ brought in by the ATPase to move back out into the interstitial fluid meanwhile water brought in at the apical membrane moves out into the tissues through AQP3 and 4.

66
Q

What is diabetes insipidus and how is it caused?

A

DI disease of collecting duct - excretion of large volumes of insipid urine. Polyuria and polydipsia. Mutations in gene of AQP2 or AVP R

67
Q

Urea plays a role in the reabsorption of water from the tubular fluid, T or F? ­

A

T

68
Q

What percentage of the interstitial fluid osmolality is contributed by the presence of urea?

A

50%

69
Q

Explain how urea is transported in the collecting duct?

A

W/ AVP urea transporters are stimulated alsong with water out into the interstitiaal fluid

70
Q

What are the transporters in the collecting duct responsible for urea movement and how do they act?

A

Apical UT-A1 brings urea into the cell from tubular fluid which then leaves through UT-A3

71
Q

What are the implications of knocking out urea transporters present in the collecting duct?

A

UT-A1 and A3 knockouts have a loss of urea transportation in the collecting duct. This results in a reduced urine concentration when the mice are exposed freely to water. In water deprived situations the knockouts exhibit no significant change in urine concentration despite the wild type showing a massive increase.

72
Q

What are the vasa recta?

A

Specialised blood vessels that enteer the medulla and run alongside the LoH exiting the medulla at the cortex at the same level that they entered

73
Q

What happens to the blood plasma as it moves down the vasa recta?

A

Ca, Cl and CO(NH2)2 move into the plasma as the osmolality of the surrounding tissue fluid is much greater. This meands that water movs out of the plasma

74
Q

As the blood plasma moves up the ascending limb of the vasa recta water enters and Na+, Cl- and CO(NH2)2 move into the tissue fluid, T or F?

A

T

75
Q

What type of inheritance pattern is seen in Liddle’s syndrome?

A

Autodominant

76
Q

List some of the characteristic symptoms of Liddle’s syndrome?

A

Na and water retention, resulting in inc ECFV and hypertension. Secondary effects include high K secretion and thus hypokalaemia as well as metabolic alkalosis due to increase H secretion

77
Q

Why are renin and aldosterone levels low in patients with Liddle’s syndrome?

A

Body decrease the levels of aldosterone and renin to try to decrease the ECFV and decrease Na reabsorption

78
Q

Which cells in which part of the nephron are effected in patients with Liddle’s syndrome?

A

Principal cells in the collecting duct

79
Q

What is the name of the channel that mediates the reabsorption of Na+ from the tubular fluid?

A

Epithelial Na channel (ENaC)

80
Q

The cells in the nephron that mediate Na+ reabsorption are said to control the regulation of Na+ concentration in the body, T or F?

A

F - principal cells regulate Na content and not concentration

81
Q

Describe the structure of the channel in the principal cells that mediates Na+ reabsorption?

A

ENaC consists of three subunits; α, β and γ. These are said to be present in a 1:1:1 ratio

82
Q

Each subunit of the ENaC gene is encoded by a different exon, T or F?

A

F - sep gene for each S/U

83
Q

In which subunits of the ENaC channel are Liddle’s syndrome mutations found?

A

Beta and gamma

84
Q

Where abouts in the ENaC subunit do Liddle’s syndrome mutations often occur?

A

C term

85
Q

What is the significance of where the Liddle’s syndrome mutations occur in the subunit and its effect on the overall ENaC function?

A

The carboxyl terminus of the β and γ subunits contain proline rich motifs that are truncated or deleted in Liddle’s mutations. These motifs are a signalling region that directs the endocytosis of the ENaC channel from the membrane. These mutations in these regions results in a decreased degree of endocytosis and thus an increased ENaC presence in the membrane resulting in greater Na+ currents and reabsorption from the apical membrane of the principal cells

86
Q

What is the effect of Liddle’s mutations on the Na+ currents generated in the principal cells, two effects?

A

Increase N of ENAC and inc P0 increasing Na currents

87
Q

What is the effect of increased Na+ reabsorption on water and K+ handling by the cell as a result of Liddle’s mutations?

A

Due to increase Na+ reabsorption there is also increased water reuptake through AQP2. In addition, increase Na+ reabsorption causes an increase in K+ secretion from the apical membrane by ROMK and thus causing a drop in extracellular K+ levels known as hypokalaemia

88
Q

What is the name of the other cell type in the collecting duct other than the principal cells?

A

Intercallated cells

89
Q

What is meant by the transepithelial potential?

A

Potential acorss an epithelial cell layer given by sum of apical and basolateral Vms

90
Q

What is the effect of increased Na+ reabsorption on the transepithelial potential in the nephron?

A

Increase in reab or + charge. Creates a greater transepithelial potential due to greater negative charge in the tubular fluid

91
Q

What is the result of changes in the transepithelial potential on H+ secretion from the principal cells and how can this account for one of the secondary effects of Liddle’s syndrome?

A

The increased transepithelial potential provides a greater driving force for H+ secretion from the α intercalated cells in the collecting duct by the H+/K+ exchanger. A greater secretion and thus excretion of protons from the cells accounts for the increase pH and metabolic alkalosis seen in Liddle’s patients

92
Q

What happens in the collecting duct in response to an increase in blood pressure in normal individuals?

A

There will be a decrease in the secretion of renin along with aldosterone from the posterior pituitary gland. This will lead to decreased production of ENaC and increased endocytosis from the apical membrane thus causing a decrease in Na+ reabsorption and thus water too. This will act to reduce blood pressure to normal levels

93
Q

What happens at the level of the principal cells in response to an increase in blood pressure in patients with Liddle’s syndrome?

A

Aldosterone and renin levels are already depleted due to the compensatory response to increased Na+ reabsorption through the ENaC channels. In addition, the ENaC channels aren’t being effectively removed from the membrane of the principal cells and thus the hypertension persists

94
Q

Liddle’s syndrome mutations are gain of function mutations, T or F?

A

T - gain of function

95
Q

Name a suitable treatment for Liddle’s syndrome and how it works?

A

K+ sparing diuretics such as amiloride are an effective treatment for Liddle’s syndrome. Amiloride acts by inhibiting the ENaC channel and thus preventing Na+ uptake from the tubular fluid. This leads to a decrease in water reuptake also and thus a decrease in blood pressure. As Na+ absorption is decreased, so too is K+ secretion thus helping K+ concentration to increase to normal levels

96
Q

What is spironolactone and how does it act?

A

Spironolactone is a mineralocorticoid antagonist that binds to the receptor that aldosterone does and prevents it from binding. This helps to prevent the insertion of AQP2 into the apical membrane of the principal cells and thus prevents water reabsorption

97
Q

Recall the mechanism of vasopressin’s action?

A

Vasopressin is made in the hypothalamus and travels along the neurosecretory cells down the hypothalamic-hypophyseal axis to the posterior pituitary gland where it is secreted into the blood. Once in the kidney vasopressin binds to the AVP2 receptor on the basolateral membrane of the principal cells. Activation of this receptor results in the activation of adenylate cyclase and the increased activity of protein kinase A. PKA phosphorylates AQP2 channels within vesicles below the apical membrane of the principal cells. Phosphorylation of the these channels leads to vesicle shuttling and AQP2 insertion into the apical membrane of the principal cells and subsequent water reabsorption.

98
Q

What is diabetes insipidus and how is it caused?

A

Diabetes insipidus is a disease characterised by an increased urine flow rate with large volumes of dilute urine. It is associated with mutations in the gene for AQP2 or the AVP2R

99
Q

What are the symptoms of diabetes insipidus?

A

Polyuria and a compensatory polydipsia

100
Q

What are the different types of diabetes insipidus and how do they differ?

A

Central DI – due to impaired AVP production. Nephrogenic DI – due to impaired effect of AVP and a defect at the level of the kidney that prevents its ability to respond. Primary polydipsia – induced by the ingestion of a massive volume of water that leads to the suppression of vasopressin production and release and can cause the excretion of too much water in the urine. Gestational DI – caused by overactivity of placental enzymes that lead to the breakdown of maternal AVP in some pregnant women

101
Q

What are the two ways in which diabetes insipidus can be obtained?

A

Congenital and acquired

102
Q

How can central diabetes insipidus be acquired?

A

Damage to the pituitary gland as a result of trauma, infection or surgery

103
Q

How can central diabetes insipidus be congenital?

A

Neurohypophyseal DI – caused by a mutation in the AVP gene that impacts its transport from the hypothalamus to the posterior pituitary gland

104
Q

How can nephrogenic diabetes insipidus be acquired?

A

Interference with AVP by lithium (used for treating bipolar disorder), antibiotics, antifungals, antineoplastic drugs. Additionally, hypokalaemia and hypocalciuria as well as acute and chronic renal failure can cause nephrogenic diabetes insipidus

105
Q

How can nephrogenic diabetes insipidus be congenital?

A

Due to mutations in the AVP2R or AQP2 genes. AVP2R mutations tend to be X-linked and account for the majority of congenital nephrogenic DI. In contrast mutations in AQP2 channels that are dominant tend to impact the trafficking of the protein to the membrane whereas the recessive mutations impact its function

106
Q

How can central DI be treated?

A

Administration of vasopressin in the form of a desmopressin nasal spray. As the kidneys can still respond to AVP this increases urine osmolality and alleviates the symptoms

107
Q

How can nephrogenic DI be treated?

A

The treatment of nephrogenic DI is extremely tricky as the body no longer responds to AVP. Modulatory drugs can help to refold misfolded conformations of the AQP2 channel along with pharmacological chaperones. Other treatments include cGMP and cAMP pathway agonists and statins.

BMS242 - Phys/Pharm of Cells (3 decks)

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