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Urinary System > Session 4 > Flashcards

Session 4 Flashcards

1
Q

Define effective circulating volume of blood.

A

The volume of arterial blood effectively perfusing tissues.

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2
Q

Where in the kidneys is most sodium filtered?

A

2/3rds in the proximal tubule; 1/4th in the ascending thick and thin limb of the loop of Henle; the rest in the DCT and CD.

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3
Q

WHat effect does an increase in renal artery BP have?

A

Number of Na-H antiporters decreases; Na-K-ATPase activity decreases; more sodium and water are excreted and ECV decreases.

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4
Q

What transporters act to reabsorbed sodium in the PCT?

A

Na-H antiporter; Na-glucose symporter; Na-AA co-transporter; Na-Pi transporter.

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5
Q

Describe the histological appearance of the PCT.

A

Many mitochondria in cells, Star shaped lumen, brush border on cells.

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6
Q

What transporters allow sodium resorption in the loop of Henle?

A

Na-K-2Cl symporter.

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7
Q

What transporters allow resorption of sodium in the early distal tubule?

A

Na-Cl symporter.

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8
Q

What transporters allow sodium resorption in the late distal tubule and collecting duct?

A

ENaC.

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9
Q

Which substances are completely reabsorbed in the PCT?

A

Glucose, amino acids and lactate.

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10
Q

Describe resorption in S1 of the PCT.

A

3Na-2K-ATPase transporter and NaHCo3 co-transporter on the basolateral membrane.
NHE, Na-glucose co-transporter, Na-AA co-transporter, Na-Pi co-transporter and aquaporins present on the apical membrane.

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11
Q

Describe S2 and S3 of the PCT.

A

3Na-2K-ATPase and NHE on the basolateral membrane.
NHE and aquaporins on the apical membrane.
Chloride may move transcellularly coupled to Na-K-ATPase or paracellularly.

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12
Q

What is the function of glomerulotubular balance?

A

Autoregulation of GFR: blunts sodium excretion in response to GFR changes.

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13
Q

Describe the histological appearance of the loop of Henle.

A

Cells are thin and have no brush border, very few mitochondria as no active transport.

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14
Q

Describe the movement of water in the loop of Henle.

A

Moves via osmosis in a countercurrent exchange: concentration gradient exists from the cortex to the inside of the medulla which drives water movement from the tubule into the blood; tubule becomes hypertonic by the bottom of the loop of Henle which allows passive transport of ions from the tubule to be driven.

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15
Q

Describe the movement of ions in the loop of Henle.

A

Little/no movement of ions in the descending limb; only passive movement in the thin ascending limb driven by the concentration gradient created by water movement; active transport begins in the thick ascending limb.

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16
Q

Describe ion transport in the thick ascending limb of a nephron.

A

NKCC2 and ROMK on the apical membrane allow resorption of Na and Cl; K diffuses back into the tubule via ROMK to power the NKCC2 transporter.

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17
Q

Why is the thick ascending limb of a nephron sensitive to hypoxia?

A

It has a high energy demand due to the amount of active transport occurring in NKCC2.

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18
Q

Describe the appearance of the distal tubule histologically.

A

Nuclei of cells are usually apical, large tubular lumen.

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19
Q

Describe sodium reabsorption in the early distal tubule of a nephron.

A

Moves across the apical membrane via NCC transporters. Moves across the basolateral membrane via 3Na-2K-ATPase. Chloride follows the sodium to maintain electroneutrality.

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20
Q

Where in a kidney nephron do thiazide diuretics act?

A

On NCC transporters on the apical membrane in the distal tubule.

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21
Q

How do thiazides achieve their diuretic function?

A

The block NCC channels in the distal tubule of the nephron so sodium isn’t reabsorbed and therefore more urine is produced.

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22
Q

Describe sodium reabsorption in the late distal tubule of the kidney nephron.

A

Sodium moves across the apical membrane via NCC and ENaC. Sodium moves across the basolateral membrane via 3Na-2K-ATPase. Chloride follows sodium to maintain electroneutrality.

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23
Q

Where do amiloride diuretics act?

A

On ENaC on the apical membrane of the late distal tubule of the kidney nephron.

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24
Q

How do amilorides achieve their diuretic function?

A

They block ENaC on the apical membrane of the late distal tubule so sodium isn’t reabsorbed and therefore more urine is produced.

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25
Q

What effect does handling of tubular secretions in the distal tubule of the nephron have on the secretion’s osmolarity?

A

Makes the secretion more hypo-osmotic as it is further diluted by the removal of ions; mainly sodium and chloride.

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26
Q

Where is the majority of calcium reabsorbed in the kidney nephron?

A

The distal convoluted tubule.

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27
Q

Describe calcium reabsorption in the kidney.

A

Mainly occurs in the DCT. Most calcium is bound by proteins so isnt filtered from the blood. When calcium enters the tubule cells it is immediately bound by calbindin and shuttled to the basolateral cell membrane where it enters the blood via NCX.

28
Q

What substances regulate calcium reuptake in the kidneys?

A

PTH and vitamin D.

29
Q

What is the function of principal cells in the collecting ducts of the kidney?

A

To reabsorb sodium ions via ENaC.

30
Q

How is water resorbed in the collecting ducts of the kidneys?

A

Via aquaporins (mainly aquaporin 2); process is dependent on ADH action.

31
Q

How does ADH affect water resorption in the collecting ducts of the kidneys?

A

ADH activates aquaporin 2 channels in the principal cells of the kidney collecting ducts. When aqp2 channels are activated, water can leave the collecting ducts and concentrate urine.

32
Q

What is the function of A-IC cells in the kidney collecting ducts?

A

Reabsorb chloride ions and secrete hydrogen ions.

33
Q

What is the function of B-IC cells in the kidney collecting ducts?

A

Reabsorb chloride ions and secrete bicarbonate ions.

34
Q

How is blood pressure regulated in the short-term?

A

Via the baroreceptor reflex.

35
Q

How is blood pressure regulated in the medium and long term?

A

Via neurohormonal responses which are directed to controlling sodium balance and extracellular fluid volume. E.g. RAAS, SNS, ADH and ANP.

36
Q

Where is renin produced?

A

In granular cells within the juxtaglomerular apparatus of the kidneys.

37
Q

What stimulates renin release?

A

Reduced NaCl delivery to the distal tubules, reduced perfusion in the kidneys, SNS stimulation to the juxtaglomerular apparatus, stimulation by prostaglandins and NO (usually released due to reduced NaCl delivery).

38
Q

What is the function of renin?

A

Converts angiotensinogen to angiotensin I.

39
Q

What is the function of ACE?

A

Converts ang I to ang II.

40
Q

What is the function of ang II?

A

In the kidney: vasoconstriction of afferent and efferent arterioles; increased sodium resorption in the PCT by stimulating the NHE.
In arterioles: vasoconstriction.
In the SNS: increased NA release.
In the adrenal cortex: aldosterone release activation ENaC and apical K channels and increasing basolateral Na-K-ATPase activity in the kidneys.
In the hypothalamus: increased ADH release; increased thirst.

41
Q

What breaks down bradykinin?

A

Kininase enzymes, in particular ACE.

42
Q

What is the function of bradykinin?

A

Vasodilator, may also mediate the dry cough people on ACE-inhibitors get.

43
Q

What effect does increased SNS tone have on the kidneys?

A

Reduces renal blood flow by causing arteriolar vasoconstriction so GFR and sodium excretion are reduced.
NHE and Na-K-ATPase are activated in the PCT.
Renin release is stimulated.

44
Q

What causes ADH release?

A

Increases in plasma osmolality or severe hypovolaemia.

45
Q

Where in the kidney does ADH act?

A

ON the thick ascending limb of the nephron to stimulate apical NKCC co-transporters.

46
Q

What effect do atrial natriuretic peptides have on the kidneys?

A

Cause vasodilation of the afferent arteriole; inhibit sodium resorption in the nephron.

47
Q

What causes ANP release?

A

Stretch in atrial myocytes caused by increased blood pressure.

48
Q

Where is ANP synthesised and stored?

A

Within atrial myocytes.

49
Q

What is the function of prostaglandins?

A

Vasodilators; also act locally to enhance GFR and reduce sodium resorption on PGE2 receptors.

50
Q

Why is prostaglandin release important when ang II levels are raised?

A

Prostaglandins act as a buffer to excessive vasoconstriction produced by SNS and RAAS so helps to maintain renal blood flow and GFR in the presence of vasoconstrictors.

51
Q

What is the function of NSAIDs?

A

Inhibit cyclo-oxygenase pathway involved in prostaglandin formation.

52
Q

Why should patients with renal failure be taken off NSAIDs?

A

When renal perfusion is low they can further decrease GFR by preventing prostaglandin formation so can lead to acute renal failure in patients with renal pathologies.

53
Q

How is dopamine formed?

A

Formed locally in the kidney from circulating L-DOPA.

54
Q

What is the function of dopamine in the kidney?

A

Causes vasodilation and increased renal blood flow; inhibits NHE and Na-K-ATPase in the principal cells of the PCT and TAL to reduce NaCl resorption.

55
Q

What us hypertension?

A

A sustained increase in blood pressure over 140/90.

56
Q

What is primary hypertension?

A

Sustained increase in blood pressure with an unknown cause.

57
Q

What is secondary hypertension?

A

A sustained increase in blood pressure with a defined cause.

58
Q

How is secondary hypertension treated?

A

By treating the primary cause of the hypertension, not the hypertension itself.

59
Q

How might renovascular disease cause hypertension?

A

Renal artery stenosis causes reduced perfusion to the kidney so renin production increases and RAAS is activated, this causes vasoconstriction and sodium retention at the other kidney so BP increases.

60
Q

How might renal parenchymal disease cause hypertension?

A

Early disease causes a loss of vasodilator substances. Late stage disease causes sodium and water retention due to inadequate GFR so volume-dependent hypertension results.

61
Q

How might Conn’s syndrome cause hypertension?

A

Causes increased aldosterone secretion leading to hypokalaemia and hypertension.

62
Q

What is Conn’s syndrome?

A

An aldosterone secreting adenoma.

63
Q

How might Cushing’s syndrome cause hypertension?

A

Causes excess cortisol production which acts on aldosterone receptors to cause sodium and water retention, leading to hypertension.

64
Q

What is phaeochromocytoma?

A

A tumour of the adrenal medulla which secretes catecholamines (adrenaline and NA).

65
Q

How is primary hypertension treated?

A

Targeting the RAAS system with ACE-inhibitors or ang II receptor antagonists; using vasodilators such as L-type calcium channel blockers; using diuretics such as thiazide or amiloride diuretics; using beta-blockers (only used in conjunction with other treatments); non-pharmacologically via exercise, diet, lifestyle, etc.

Urinary System (11 decks)

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