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Renal System > Loop of Henle, Distal Tubule and Collecting Duct > Flashcards

Loop of Henle, Distal Tubule and Collecting Duct Flashcards

1
Q

What are the 2 key functionally distinct components of the Loop of Henle?

A
  1. Descending Limb (cortex –> medulla)

2. Thick Ascending Limb (medulla –> cortex)

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2
Q

What is the key function of the thick ascending limb?

A

To create a hyperosmolar interstitial space in the medulla to drive water loss from the descending limb and cortical collecting duct

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3
Q

What is the descending limb permeable to?

A

Water, not NaCl

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4
Q

Does water leave or enter the descending limb?

A

Leave the filtrate because of osmotic force

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5
Q

What happens to the water once it has left the descending limb?

A

Gets removed by the vasa recta

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6
Q

What is the permeability of the thick ascending limb (TAL)?

A

permeable to NaCl, impermeable to water

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7
Q

What does TAL do?

A

Actively transports Na+ into the medullary interstitium, and other ions follow (e.g. Cl-)

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8
Q

What is the osmotic pressure difference between the luminal side and interstitial side called?

A

Transverse gradient

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9
Q

What is the transverse gradient?

A

200mOsm/kg H2O

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10
Q

What is the primary active transport process in the TAL?

A

Na+/K+-ATPase on the basal cell membrane

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11
Q

What transporter is used by the TAL to move ions into the cell?

A

NKCC2 (Na+K+2Cl- transporter) on the apical membrane

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12
Q

What is the systematic name of the gene for NKCC2?

A

SLC12A1

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13
Q

What type of transporter is NKCC2?

A

Cation coupled chloride transporter

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14
Q

What is K+ recycling important for?

A

To ensure that the NKCC2 transporter can maintain its role of transporting large quantities of Na+ and Cl-
Na+ conc is much higher, so K+ needs to be recycled

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15
Q

What drugs inhibit the transporter NKCC2?

A

Loop diuretics

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16
Q

Examples of loop diuretics?

A

Furosemide, bumetanide, piretanide

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17
Q

What are the uses of furosemide?

A

cardiac failure, renal failure

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18
Q

What are the side effects of furosemide?

A

K+ loss (& subsequent hypokalaemia)
Hypovolaemia
Mild metabolic alkalosis
Los of Mg2+ and Ca2+

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19
Q

What is the permeability of the thin ascending limb?

A

Impermeable to water, permeable to Na+ so allows Na+ to passively move out into th emedullary interstitial fluid

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20
Q

What is Bartter’s syndrome?

A

Impairment of the transport processes in TAL

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21
Q

What transporter is used for Na+ absorption in the distal tubule?

A

Na+-Cl- transporter

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22
Q

What drugs block Na+ absorption in the distal tubule?

A

Thiazides and thiazide-like drugs

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23
Q

Examples of thiazides?

A

bendroflumethiazide, hydrochlorothiazide

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24
Q

Examples of thiazide-like drugs?

A

indapamide

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25
Q

What are the uses of thiazides and thiazide-like drugs?

A

antihypertensive

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26
Q

What are the side-effects of thiazides and thiazide-like drugs?

A

Increased uric acid
Hyperglycaemia
Hyponatraemia

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27
Q

What is the permeability of the collecting tube?

A

impermeable to urea and NaCl, sodium permeability controlled by ENaC, water permeability is regulated by ADH

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28
Q

What channel is used for water entry into the cell?

29
Q

What channel is used for water entry into interstitial space?

30
Q

What effect does aldosterone have on the channels in the collecting tubule?

A

Aldosterone stimulates synthesis of ENaC, K+ channels and Na+/K+-ATPase

31
Q

What is aldosterone important for?

A

K+ output regulation, Na+ & water retention

32
Q

What drug blocks the effect of aldosterone?

A

Spironolactone

33
Q

What are the uses of spironolactone

A

heart failure (K+ sparing diuretic)

34
Q

What are the side effects of spironolactone?

A

Gynaecomastia, menstrual disorders, testicular atrophy, hyperkalaemia

35
Q

Where does ADH have an effect on urea permeability?

A

Medullary collecting duct, but NOT cortical collecting tubule

36
Q

Which parts of the nephron are urea permeable?

A

Loop of Henle, medullary collecting duct

37
Q

What happens to urea in the medullary collecting duct?

A

Urea moves out due to increased urea concentration

38
Q

What effect does ADH have on urea permeability?

39
Q

How does ADH increase urea permeability?

A

increase the expression of UT-A1 (urea transporter A1)

40
Q

What does the urea in the medullary interstitial fluid do?

A

Increase the osmotic pressure in the medulla, and aids water reabsorption in the medulla

41
Q

What transporter is used for urea reabsorption in the loop of Henle?

42
Q

Where is ADH synthesised?

A

Hypothalamus

43
Q

Where is ADH released from?

A

The terminals of the hypothalamic neurones found within the posterior pituitary

44
Q

Where does ADH act in?

A

distal tubule and collecting tubule

45
Q

How does ADH affect urine concentration?

A

Increases water permeability by increasing AQP2

46
Q

How does ADH affect osmolality in the nephron?

A

High osmolality i.e. concentrated urine

47
Q

What happens to the osmolality in the nephron with no ADH?

48
Q

What happens to the osmolality in the nephron with maximum ADH?

49
Q

What happens to the flow rate in the nephron with no ADH?

50
Q

What happens to the flow rate in the nephron with maximum ADH?

51
Q

What is the normal urine volume?

52
Q

What is the urine volume with absence of ADH?

53
Q

Where is aldosterone synthesised?

A

Zona glomerulosa of the adrenal gland

54
Q

What happens with urea production in the presence of selective protein starvation?

A

Urea production low, so the kidney has a lower capacity to concentrate urine

55
Q

What urea transporter is regulated by ADH?

56
Q

What adaptation enables medullary cells to survive in high osmolarity?

A

Accumulation of organic osmolytes within the cells

57
Q

What are examples of organic osmolytes in the medullary cells?

A

Sorbitol, inositol, glycerophosphorylcholine, bwetaine

58
Q

What is Diabetes Insipidus?

A

Loss of ADH secretion or a low in sensitivity of the kidney to ADH

59
Q

What are the consequences of diabetes insipidus?

A

Unable to produce concentrated urine, leading to polyuria (with low osmolality), dehydration, hypovolaemia
This would cause polydipsia (drinking too much)
If fluid intake inadequate, they become hypernatraemic

60
Q

What are the two forms of diabetes insipidus?

A

Central and Nephrogenic

61
Q

What are the causes of central diabetes insipidus?

A

head injury, tumours, infection

62
Q

What is an example of an ADH analogue?

A

Desmopressin

63
Q

How can central diabetes insipidus be managed?

A

Give desmopressin

Thiazide diuretics

64
Q

What are the causes of nephrogenic diabetes insipidus?

A

Toxicity (e.g. Lithium), Hypercalcaemia, genetic (mutations in either V2 or AQP2)

65
Q

Treatments for nephrogenic diabetes insipidus?

A

NOT wit desmopressin
Thiazide diuretic
Low salt diet

66
Q

What does SIADH stand for?

A

Syndromes in Inappropriate ADH

67
Q

What are symptoms of SIADH related to?

A

Inappropriately high ADH

68
Q

What is a common cause of SIADH?

A

Head injury

69
Q

What are the treatments for SIADH?

A

Fluid restrction, give urea

Renal System (6 decks)

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