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My2 renal > Physiology 6: endocrine control of body volume > Flashcards

Physiology 6: endocrine control of body volume Flashcards

1
Q

what is the osmolarity osmolarity of the filtrate when it reaches the distal convoluted tubule

A

100 mosmol/l (hypotonic)

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2
Q

what is the osmolarity of the cortex vs the medulla

A

cortex isotonic and osmolarity increases towards the centre and becomes very hypertonic

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3
Q

where do distal tubules empty into

A

collecting ducts

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4
Q

what happens to urea in the distal tubule

A

becomes concentrated as low permeability

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5
Q

what is reabsorbed in the early distal tubule

A

NaKCl co-transport and reabsorption

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6
Q

what is reabsorbed and secreted in the late distal tubule

A

Ca reabsorption, Na and K reabsorption, H+ secretion

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7
Q

what happens in the early collecting duct

A

similar to late distal tubule

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8
Q

what happens in the late collecting duct

A

water permeable depending on ADH levels

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9
Q

what affect does ADH have on kidneys

A

increases water reabsorption

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10
Q

what type of peptide and hormone is ADH

A

octapeptide - neurohormone

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11
Q

where is ADH synthesised

A

supraoptic and paraventricular nuclei in the HYPOTHALAMUS

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12
Q

where is ADH stored

A

posterior pituitary

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13
Q

how does dehydration trigger ADH release

A

increased plasma osmolarity is detected by hypothalamic osmoreceptors which triggers an AP to release ADH

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14
Q

how does decreased atrial pressure trigger ADH release

A

stretch receptors in the left atrium detect low pressure and cause AP to release ADH

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15
Q

what is the Half life of ADH

A

10-15 minutes

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16
Q

what part of the nephron does ADH affect and how does it work

A

distal tubule/ collecting duct - uses ATP to insert water channels (aquaporins) into the lumen membrane

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17
Q

what affect does nicotine have on ADH levels

A

stimulates ADH release

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18
Q

what affect does alcohol have on ADH levels

A

inhibits ADH release

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19
Q

what affect does high levels of ADH have on urine and vice versa

A

high ADH = high water permeability = hypertonic urine / low ADH = low water permeability = hypotonic urine

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20
Q

what is central diabetes insipidus

A

damage to hypothalamus/ pituitary where ADH is not released

21
Q

what is nephrogenic diabetes insipidus

A

kidneys to not respond to ADH

22
Q

what are the symptoms of diabetes insipidus

A

large volumes of dilute urine + constant thirst

23
Q

what is the treatment for diabetes insipidus

A

nephrogenic: thiazide diuretics / central: ADH replacement

24
Q

what effect does aldosterone have on the kidneys

A

causes Na reabsorption and H/K secretion

25
Q

where is aldosterone secreted

A

adrenal cortex

26
Q

what can cause aldosterone to be released (3)

A

increased K in blood, decreased Na in blood, RAAS system

27
Q

where is K normally reabsorbed and how much is reabsorbed

A

proximal tubule - 90%

28
Q

what happens to K in the distal tubule when no aldosterone is released

A

rest is reabsorbed and no K is excreted in the urine

29
Q

how does increased [K]plasma directly stimulate aldosterone release

A

stimulates the adrenal cortex to secrete aldosterone

30
Q

how does decreased [Na]plasma indirectly stimulate aldosterone release

A

from the juxtogolmerular apparatus causing renin release

31
Q

what do the kidneys release renin in response to (3)

A

decreased NaCl / decreased ECF volume / decreased arterial BP

32
Q

what does renin do

A

converts angiotensinogen (liver) –> angiotensin I

33
Q

what does ACE do (lungs)

A

convert angiotensin I –> angiotensin II

34
Q

what does angiotensin II do

A

causes the release of aldosterone from the adrenal cortex

35
Q

what cells release renin

A

granular cells in the juxtaglomerular apparatus

36
Q

what 3 ways can renin be released by the kidneys

A

1) reduced pressure in afferent arteriole 2) macula densa senses reduced NaCl 3) increased sympathetic activity (from decreased BP detected by baroreceptors)

37
Q

what can an increased in the RAAS system causes

A

hypertension, fluid retention and congestive heart failure (and hypokalaemia)

38
Q

how can an overactive RAAS system be treated

A

low salt diet, loop diuretics and ACEi

39
Q

what effects does atrial natriuretic hormone (ANP) have on the kidneys

A

decreased Na reabsorption

40
Q

where is ANP produced and stored

A

produced in heart and stored in atrial muscle cells

41
Q

when is ANP released

A

when atrial muscle cells are stretched due to increased plasma volume (BP)

42
Q

how does ANP cause plasma volume decrease in the kidneys

A

by reducing Na reabsorption which causes diuresis which causes decreased plasma volume

43
Q

what effects does ANP have on the whole body to decrease BP (4)

A

reduced Na reabsorption / reduced renin production / vasodilation / reduced sympathetic activity

44
Q

what effects does Parathyroid hormone have on the kidneys

A

increased Ca reabsorption and decreased phosphate reabsorption

45
Q

what happens to filtrate (urine) once it leaves the kidneys

A

traveled down ureters by peristalsis to bladder for temporary storage and then micturition

46
Q

what happens in the first stage of micturition - the micturition reflex

A

bladder can hold 250-400ml of urine before stretch receptors initiate micturition and cause involuntary bladder contraction and opening of internal and external urethral sphincter (parasympathetics)

47
Q

what happens in the second stage of micturition - voluntary control.

A

deliberate tightening of external sphincter and pelvic diaphragm

48
Q

what is water diuresis

A

increased urine flow but no increased solute excretion

49
Q

what is osmotic diuresis

A

increased urine flow and increased solutes (usually Na) in urine

My2 renal (27 decks)

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