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Y2S1 > PHYS Renal Tubular Mechanisms & Fluid Osmolarity & Electrolytes - Week 10 > Flashcards

PHYS Renal Tubular Mechanisms & Fluid Osmolarity & Electrolytes - Week 10 Flashcards

1
Q

Describe pathway of paracellular tubular reabsorption.

A

Via tight junctions.

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2
Q

Describe pathway of transcellular tubular reabsorption.

A

Apical or luminal membrane -> cytosol of luminal cell -> exists via basolateral membrane -> interstitium -> endothelial membrane of capillary -> plasma.

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3
Q

In which tubular segment is the greatest percentage of Na+ and H2O reabsorbed?

A

PCT.

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4
Q

What is the transport max? What happens to excess?

A

Transport maximum - for most substances that are actively reabsorbed, there is a limit to the rate that the solute can be transported (back into the peritubular capillaries) – due to saturation of available carrier proteins and or leakage back into the lumen (gradient-limited systems) -> excess excreted via urine.

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5
Q

The filtration rate of glucose is proportional to

A

Plasma glucose concentration, until Tm (transport max) is reached - often considered a sign of glucosuria.

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6
Q

Glucosuria cause. Clinical sign of what condition?

A

Tm glucose reached - due to increased BGL & GFR. Clinical sign of DM.

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7
Q

Reduced afferent flow has what affect on PGC & GFR?

A

Afferent arteriole constricted -> reduced blood flow -> reduced PGC -> reduced GFR.

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8
Q

Reduced efferent flow has what affect on PGC & GFR?

A

Efferent arteriole constricted -> increased PGC -> increased GFR.

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9
Q

Increased efferent flow has what affect on PGC & GFR?

A

Efferent arteriole dilated -> reduced PGC -> reduced GFR.

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10
Q

Increased afferent flow has what affect on PGC & GFR?

A

Afferent arteriole dilated -> increased PGC -> increased GFR.

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11
Q

What is the relationship btw increased GFR & reabsorption?

A

High GFR -> inadequate reabsorption -> loss of substances via urine.

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12
Q

What is the relationship btw decreased GFR & reabsorption?

A

Low GFR -> increased reabsorption -> wastes not excreted.

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13
Q

Small changes in GFR correspond to: small OR large changes in the volume of filtrate that must be processed?

A

Large (e.g., 10% increased in GFR = 18L more filtrate which must be processed).

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14
Q

If an increase in hydrostatic pressure occurs, how does the afferent arteriole respond?

A

An increase in hydrostatic pressure against the afferent arteriole walls-> activation of stretch receptors -> initiate vasoconstriction to return GFR to normal -> via opening calcium channels in the vascular smooth muscle cell membrane -> calcium and vascular smooth muscle cell contraction -> vasoconstriction of the afferent arteriole -> reducing GFR to normal range.

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15
Q

Myogenic mechanism vs tubuloglomerular feedback as intrinsic mechanisms involved in autoregulation of GFR & BP.

A
  • Myogenic mechanism – constriction/dilation of renal arterioles (via Laplace’s law) to maintain relatively constant GFR level in response to changes in BP as detected by smooth muscle cell receptors (responsible for dilation/constriction of arterioles).
  • Tubuloglomerular feedback – constriction/dilation of renal arterioles due to changes in concentration of filtered load of sodium & waste products as detected by macula densa cells (see below).
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16
Q

Macula densa response to increased GFR.

A

GFR increased -> flow through tubule increases -> increased luminal NaCl concentration in filtrate -> macula densa cells sense increase/decrease in renal flow rate -> release adenosine which acts on cells of afferent arteriole -> constriction -> resistance increases -> hydrostatic pressure increase -> GFR decreases.
(& macula densa cells also secrete renin which acts on cells of efferent arteriole -> dilation).

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17
Q

Is RBF, GFR, urine flow autoregulated?

A

RBF & GFR is autoregulated via intrinsic mechanisms, however urine flow is not.

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18
Q

What is pressure natriuresis?

A

Increased renal perfusion pressure leads to a decrease in tubular reabsorption of sodium and an increased sodium excretion. The set point of blood pressure is the point at which pressure natriuresis and extracellular fluid volume are in equilibrium.

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19
Q

Main inputs of Na+ from the body.

A

Food.

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20
Q

Main outputs of Na+ from the body.

A

Sweat, urine, faeces.

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21
Q

Pathway of increased NaCl intake on CVS pressure

A

High NaCl intake -> increased osmolarity of ICF & ECF -> increased ECF & reduced ICF (cells shrink) -> increased CVS pressures (as CVS is a closed system).

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22
Q

Natriuresis means

A

Excretion of Na+ via urine.

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23
Q

What receptors detect changes in total body concentrations of Na+?

A

CVS stretch-sensitive receptors & baroreceptors as well as renal sensors (e.g., macula densa) will detect changes in Na+ concentrations.

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24
Q

If MAP has a sustained decrease, then what is the effect on Na+ & H2O excretion via urine?

A

Reduced.

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25
Q

If MAP has a sustained increase, then what is the effect on Na+ & H2O excretion via urine?

A

Increased.

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26
Q

Tubular Na+ reabsorption is controlled by what hormone.

A

Aldosterone.

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27
Q

From where is aldosterone secreted?

A

Zona glomerulosa cells of adrenal glands.

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28
Q

Na+ movement across descending tubule.

A

Impermeable.

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29
Q

Aldosterone function & effect on late distal tubule & collecting duct cells.

A

Aldosterone travels from suprarenal glands via bloodstream -> peritubular capillaries -> diffuses across basolateral cell membrane into late distal tubule or collecting duct -> binds to mineralcorticoid receptor in the cytoplasm -> travels to nucleus -> modulates transcription & translation -> increases Na+ transporting proteins.

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30
Q

BP, Na+ plasma concentration, K+ plasma concentration in Addison’s disease vs aldosteronism.

A

Addison’s - low BP, low Na+, high K+
Aldosteronism - high BP, high Na+, low K+.

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31
Q

RAS system affect on sympathetic activity.

A

Increased.

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32
Q

RAS system affect on Na+, K+, water movement.

A

Na+ reabsorption. K+ excretion. H2O retention.

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33
Q

RAS system affect on blood vessel diameter & BP.

A

Vasoconstriction. Increased BP.

34
Q

RAS system affect on ADH secretion & water movement.

A

Secretion from pituitary gland increased -> water absorption.

35
Q

RAS system affect on juxtaglomerular apparatus perfusion.

A

Increased.

36
Q

What triggers increase in RAS?

A

Decreased renal perfusion/drop in BP.

37
Q

What is the effect of the RAS system on Na+ reabsorption & excretion?

A

Increased Na+ tubular reabsorption. Decreased Na+ urinary excretion.

38
Q

What is the rate-limiting step of RAS?

A

Plasma concentration of renin.

39
Q

Where is renin synthesised, stored & released from?

A

Granular cells in the juxtaglomerular region of the afferent renal arteriole.

40
Q

What 3 factors trigger the synthesis, storage and release of renin?

A
  1. Drop in renal arterial pressure as detected by intrarenal baroreceptors.
  2. Decrease in luminal Na+ passing through the macula densa.
  3. Increase in renal sympathetic nerve activity.
41
Q

Decreased in plasma volume has what affect on juxtaglomerular cell stretch & renin secretion.

A

Reduced plasma volume -> reduced renal arterial pressure -> reduced stretch of juxtaglomerular cells -> reduced Ca2+ release -> increased renin secretion.

42
Q

Increase in plasma volume has what affect on juxtaglomerular cell stretch & renin secretion.

A

Increased plasma volume -> increased renal arterial pressure -> increased stretch of juxtaglomerular cells -> increased Ca2+ release -> decreased renin secretion.

43
Q

Increased luminal Na+ passing through the macula densa has what affect on renin secretion?

A

Decreased renin secretion.

44
Q

Decreased luminal Na+ passing through the macula densa has what affect on renin secretion?

A

Increased renin secretion.

45
Q

Decreased plasma volume/BP has what affect on renin secretion as mediated by RSNA?

A

Increased activation of RSNA -> increased activation of juxtaglomerular B-receptors -> increased renin secretion.

46
Q

Increased plasma volume/BP has what affect on renin secretion as mediated by RSNA?

A

Decreased activation of RSNA -> decreased activation of juxtaglomerular B-receptors -> decreased renin secretion.

47
Q

ANP agonist will have what affect. Expand. Explain MOA.

A

Reduced BP. Atrial natriuretic peptide. Acts acutely to reduce plasma volume by increased renal excretion of salt & water, vasodilating, increased vascular prmeability.

48
Q

Total body water is what proportion of body mass in men & women.

A
  1. 50%.
49
Q

Amount of water present in each of the body fluid compartments.

A
  • ICF (2/3) = fluid within cells
  • ECF (1/3) = fluid outside cells – serum (1/4), interstitial fluid (3/4), lymph & transcellular fluid (e.g., CSF).
50
Q

How does interstitial fluid enter plasma?

A

Via capillary membrane or lymphatics.

51
Q

How does intracellular fluid enter interstitial fluid compartment?

A

Via cell membrane.

52
Q

Define osmolarity.

A

Osmolarity = concentration of solution expressed as the total number of solute particles/osmoles per litre (takes into account all solute concentrations, not just the concentrations of those solutes that cannot diffuse).

53
Q

Define molarity.

A

Molarity = number of moles dissolved in a litre of solution.

54
Q

1 mole of glucose has an osmolarity of ___ osmoles?

A

1.

55
Q

1 mole of NaCl has an osmolarity of ___ osmoles?

A

2.

56
Q

1 mole of MgCl2 has an osmolarity of ___ osmoles?

A

3.

57
Q

In what fluid compartment is the greatest concentration of K+, protein, Na+ present?

A

K+ highest in cell/intracellular fluid.
Na+ highest in interstitial fluid & blood.
Protein highest in cell & blood.

58
Q

Increase or decrease in water input will cause what impact on cells?

A

Swelling/shrinking - however it takes >10min for water to diffuse from interstitial fluids/plasma into cells.

59
Q

Order outputs of H2O from the body by greatest to smallest percentage.

A

Urine (60%), insensible loss via skin & lungs (28%), sweat (8%), faeces (4%).

60
Q

Define polyuria

A

> 2.5L urine output/day.

61
Q

Define oligouria.

A

<400ml urine output/day.

62
Q

Changes in plasma osmolarity trigger changes in what receptors? What is the consequent pathway?

A

Hypothalamic osmoreceptors. Osmoreceptors located @ paraventricular & supraoptic nuclei detect change in plasma osmolarity -> Hering bodies nearby synthesise & secrete ADH/arginine vasopressin released by posterior pituitary nerve roots.

63
Q

Where are osmoreceptors located?

A

Paraventricular & supraoptic nuclei within the hypothalamus (which is attached to the pituitary gland, hence ‘hypothalamic osmoreceptors’).

64
Q

How much ADH is secreted at normal, low & high plasma osmolarities (=, <, > 290mOsmol/L)? How is this controlled?

A

Small amount. Very little. Large amount. Change in solute concentration -> swelling/shrinking of osmoreceptors -> decreased/increasing firing rates -> decreased/increased ADH secretion.

65
Q

What is the affect of ADH on the late distal tubule & collecting duct cells? Pathway.

A

Increased H2O permeability.
ADH in peritubular capillaries diffuses across endothelial cells of capillary and bind to vasopressin/V-type receptors on cell membrane of late distal tubule OR collecting duct cells -> triggers pathway -> causes aquaporins, normally residing in cellular cytosol, to insert into membrane of lumen -> increases H2O uptake and diffusion into peritubular capillaries.

66
Q

What is water diuresis? What is it used for/what is its effect?

A

Water diuresis is an increase in urinary water output with little to no change in solute excretion. Excess water in the plasma dilutes plasma, making the plasma hypoosmotic. Hence this process of removing excess water from the body (i.e., water diuresis), correct plasma hypo-osmolarity.

67
Q

Osmolarity of the cortex and medulla compared to the blood?

A

The renal cortex is iso-osmolar with blood whilst the renal medulla increases in osmolarity from the corticomedullary junction to the renal papilla.

68
Q

Why is a hyperosmotic gradient needed in the most distal parts of the nephron?

A

Key to reuptake of water in the collecting duct.

69
Q

Osmolarity of tubular fluid compared to plasma @ Bowman’s space, beginning of the loop of Henle, at the loop of Henle, end of the loop of Henle, ascending tubule, collecting duct?

A

Iso-osmotic, iso-osmotic, hyperosmotic, hyperosmotic, depends.

70
Q

What is the renal counter-current exchange mechanism? What is it used for in the kidneys?

A

A counter-current mechanism is a system where fluid flows in opposite directions through adjacent tubes.Thismechanism is used to concentrate urine in the kidneys.

71
Q

3 x aspects of the renal counter-current exchange mechanism. State what is responsible for completing/actioning each of these stages.

A
  1. Create gradient (via tubular mechanisms in the loop of Henle)
  2. Maintain gradient (via vasa recta)
  3. Utilise the gradient (via the collecting duct under the influence of ADH).
72
Q

Under what condition is the collecting duct impermeable to water

A

Absence of ADH.

73
Q

ADH causes what action in collecting duct cells.

A

Insertion of aquaporins into the luminal membranes.

74
Q

What medication may result in reduced medullary concentration gradients?

A

Loop diuretics (e.g., frusemide).

75
Q

State whether intracellular fluid has a high or low concentration of Na+ & K+. Do the same for ECF.

A

Low. High. Opposite for ECF.

76
Q

What separates the intracellular from the interstitial fluid from each other?

A

Cell membrane.

77
Q

What separates interstitial fluid from the plasma?

A

Capillary membrane.

78
Q

What is the stimulus for increased aldosterone secretion?

A

Increased plasma/blood angiotensin II concentration.

79
Q

In the presence of aldosterone, most of the reabsorption of Na+ occurs where?

A

PCT. As aldosterone blocks Na+ transporter synthesis & CD/DTs.

80
Q

Excretion of a particular solute (e.g., NaCl) =

A

Net glomerular filtration rate - net tubular reabsorption.

Y2S1 (72 decks)

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