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Urinary System > Session 6 > Flashcards

Session 6 Flashcards

1
Q

Where are osmoreceptors which control plasma osmolarity located?

A

Within the Organum Vasculosum of the Lamina Terminalis.

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2
Q

Which regulatory pathways do osmoreceptors send signals to?

A

ADH pathway and thirst pathway.

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3
Q

Under what conditions is ADH released in response to osmoreceptor stimulation?

A

Water loss which is sensed by increased osmolarity and decreased ECV.

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4
Q

When is thirst activaterd by osmoreceptors?

A

When the body is at around 10% dehydration.

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5
Q

Why is central diabetes insipidus caused?

A

Low plasma ADH levels.

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6
Q

How is central diabetes insipidus managed?

A

ADH injections or ADH nasal sprays.

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7
Q

What conditions can result in central diabetes insipidus?

A

Damage to hypothalamus or pituitary gland; brain injury; basal skull fracture; tumours; sarcoidosis/TB; aneurysm; encephalitis/meningitis; Langerhans cell histiocytosis.

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8
Q

Why is nephrogenic diabetes insipidus caused?

A

Acquired insensitivity of the kidneys to ADH.

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9
Q

How is nephrogenic diabetes insipidus treated?

A

Treat the underlying cause of the condition and then add thiazide and amiloride diuretics if needed.

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10
Q

What is SIADH?

A

Syndrome of inappropriate ADH secretion.

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11
Q

Why is SIADH caused?

A

Due to excessive release of ADH from the posterior pituitary gland or another source.

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12
Q

What does SIADH cause?

A

Dilutional hyponatraemia as plasma sodium levels are lowered and total body fluid is increased.

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13
Q

What effect does decreased plasma osmolarity have on ADH levels?

A

Reduces them.

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14
Q

What effect does reduced ADH levels have on the kidneys?

A

Less expression of aquaporins on the basolateral membrane of the late DCT and CD so limited water uptake and large amounts of hyposmotic urine are lost: diuresis.

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15
Q

What effect does increased ADH levels have on the distal nephrons in the kidney?

A

More aquaporin channels are inserted into the basolateral membrane of the late DCT and CD.

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16
Q

How is the medullary gradient of the kidneys created?

A

Uses the action of the TAL of the LH: it is impermeable to water but actively transports NaCl from the tubule so osmolarity in the tubule decreases and sodium concentration in the interstitium increases to form a gradient.

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17
Q

How is a vertical osmotic gradient created in the interstitial fluid of the medulla of the kidneys?

A

Sodium, chloride and urea diffuse from the hypertonic interstitium into the vasa recta; osmolarity of blood increases to maximum at bottom of the loop; ascending blood has a higher solute content than the interstitium so water enters the blood; causes creation of an osmotic gradient.

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18
Q

What is an effective osmole?

A

A solute which doesn’t readily move across membranes so is effective at exerting an osmotic force on the membrane.

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19
Q

What is an ineffective osmole?

A

A substance which can move freely across a membrane so isn’t effective at exerting a force on the membrane; they have little or no effect on plasma osmolarity in the body.

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20
Q

Is urea an effective or ineffective osmole? Why?

A

Effective in the kidneys as is hydrophilic so wont readily permeate lipid bilayers; ineffective in other parts of the body as urea transporters are present to facilitate urea diffusion.

21
Q

How is urea recycled in the kidneys?

A

Reabsorbed in the MCD; diffuses from the interstitium back into the loop of Henle.

22
Q

How does ADH alter urea recycling?

A

Increased ADH increases fractional excretion of urea so urea recycling increases.

23
Q

Why is urea recycled?

A

To regulate urine osmolarity.

24
Q

What diuretics act on the proximal tubule of the kidney nephrons?

A

Carbonic anhydrase inhibitors and osmotic diuretics.

25
Q

What diuretics act on the loop of Henle of the kidney nephrons?

A

Loop diuretics.

26
Q

Which diuretics act on the distal convoluted tubule of the kidney nephrons?

A

Thiazide diuretics.

27
Q

Which diuretics act on the collecting ducts of the kidney nephrons?

A

Potassium sparing diuretics and aldosterone antagonists.

28
Q

Give an example of a carbonic anhydrase inhibitor.

A

Acetazolamide.

29
Q

Give an example of a loop diuretic.

A

Furosemide, bumetanide.

30
Q

GIve an example of a thiazide diuretic.

A

Metalozone, indapamide.

31
Q

Give an example of a potassium sparing diuretic.

A

Amiloride.

32
Q

Give an example of an aldosterone antagonist.

A

Spironolactone.

33
Q

How do loop diuretics act?

A

Inhibit the Na-K-2Cl symporters in the loop of Henle.

34
Q

How do thiazide diuretics act?

A

Inhibit the Na-Cl symporters in the early distal convoluted tubule.

35
Q

How do potassium sparing diuretics act?

A

Inhibit renal sodium channels in the late distal tubule and collecting ducts.

36
Q

How do aldosterone antagonists act?

A

Competitively bind to aldosterone receptors on principal cells in the late distal tubule collecting ducts to inhibit them.

37
Q

How do osmotic diuretics act?

A

Diffuse into the nephron and increase osmolarity of the urine to cause increased sodium and water loss.

38
Q

How do carbonic anhydrase diuretics act?

A

Inhibit carbonic anhydrase enzyme to interfere with sodium and bicarbonate resorption in the proximal tubule.

39
Q

Why are loop diuretics very potent?

A

A lot of sodium is normally resorbed in the LH so inhibition of this can have large effects on urine osmolarity.

40
Q

How do loop diuretics enter kidney nephrons?

A

Via the PCT along the organic anion pathway.

41
Q

How are loop diuretics used clinically?

A

In heart failure to reduce preload and afterload; IV in acute pulmonary oedema for rapid action; for fluid retention and oedema in nephrotic syndrome, renal failure and liver cirrhosis; in hypercalcaemia as impairs calcium resorption in the LH.

42
Q

Why are thiazide diuretics ineffective in renal failure?

A

Less potent than loop diuretics as little sodium is reabsorbed normally in the DCT.

43
Q

Why are thiazide diuretics useful in patients with osteoporosis?

A

They reduce calcium loss in urine.

44
Q

How may diuretics cause hyperkalaemia?

A

Some have a potassium sparing effect (those acting in the late DCT and CD) so cause more potassium to be reabsorbed, particularly important if patients are on ACEI or potassium supplements or are really impaired.

45
Q

How are aldosterone antagonists useful clinically?

A

In treating primary aldosteronism; preferred drug in ascites and oedema treatment in cirrhosis; used with loop diuretics for heart failure; used in uncontrolled hypertension.

46
Q

How may carbonic anhydrase inhibitors cause metabolic acidosis?

A

Cause more bicarbonate to be lost in urine.

47
Q

How are carbonic anhydrase inhibitors useful clinically?

A

In glaucoma treatment to reduce formation of aqueous humour in the eyes.

48
Q

How are osmotic diuretics useful clinically?

A

In treating cerebral oedema.

Urinary System (11 decks)

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