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module 104 - theme 3 > regulation of homeostasis via the kidney > Flashcards

regulation of homeostasis via the kidney Flashcards

1
Q

what is fluid balance?

A

the amount of water gained by the body each day equals the amount lost

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2
Q

what is electrolyte balance?

A

the ion gain each days equals ion loss

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3
Q

what is acid-base balance?

A

H+ gain is offset by H+ loss

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4
Q

what do acids do?

A

release H+ into solution

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5
Q

what do bases do?

A

remove H+ from solution

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6
Q

what are the 2 groupings of acids and bases?

A

strong or weak

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7
Q

what do buffers do?

A
  • resist changes in pH
  • when H+ added, buffer removes it
  • when H+ removed, buffer replaces it
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8
Q

what are the 3 types of bugger systems?

A
  • carbonic acid/bicarbonate
  • protein
  • phosphate
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9
Q

what is the optimal pH window?

A

7.2-7.4

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10
Q

what happens when the lungs excrete a large amount of CO2?

A
  • potential acid is formed by metabolism

- CO2 reacts with water to form carbonic anhydrase

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11
Q

what must the kidneys do to maintain acid-base balance?

A
  • excrete non-volatile acids produced form normal metabolism

- reabsorb virtually all filtered HCO3-

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12
Q

what does HCO3- do?

A

acts as a physiological buffer

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13
Q

what is the average blood pH?

A

7.4

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14
Q

what is the average urine pH?

A

6.0

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15
Q

what is the average concentration of HCO3- in the blood?

A

24mM

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16
Q

wha is the average partial pressure of CO2 in the blood?

A

40mmHg

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17
Q

what happens when the partial pressure of CO2 increases?

A

pH decreases

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18
Q

what happens when the partial pressure of CO2 decreases?

A

pH increases

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19
Q

what detects the changes in pH levels?

A

peripheral chemoreceptors

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20
Q

what happens to adjust respiration rates?

A

the peripheral chemoreceptors act on respiration centres in the brain

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21
Q

how does renal tubular acidosis occur?

A

when there is insufficient reabsorption of HCO3- and H+ secretion

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22
Q

what happens if pH or ECF falls?

A

acidaemia

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23
Q

what needs to happen to reverse acidaemia?

A
  • more secretion of H+ into filtrate

- reabsorption of HCO3- back into ECF

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24
Q

when is secretion of H+ inhibited?

A

when urine pH falls below 4.5

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25
Q

what happens if pH or ECF increases?

A

alkalaemia

26
Q

what needs to happen to reverse alkalemia?

A
  • secretion of H+ into filtrate

- reabsorption of HCO3- declines extracellular

27
Q

what is acidosis?

A

when the pH of body fluids falls below 7.35

28
Q

what is alkalosis?

A

when the pH of body fluids goes above 7.45

29
Q

how do you reverse acidosis?

A
  • get rid of H+ out of the body
  • excrete H+ via the lungs as CO2 and in the kidneys as H+
  • generate more buffer (HCO3-) in the kidneys
30
Q

how do you reverse alkalosis?

A
  • increase H+ levels in the body
  • reduce excretion of CO2 via the lungs
  • increase excretion of HCO3- buffer via kidneys
  • increase generation of H+ via kidneys
31
Q

what causes respiratory acidosis?

A
  • caused by inadequate ventilation

- can be acute or chronic

32
Q

what causes metabolic acidosis?

A
  • results from all conditions other than respiratory that decrease pH
  • always chronic
33
Q

how can you gain H+?

A
  • CO2 in blood (combines with H2O to form carbonic acid)
  • non-volatile acids from metabolism
  • loss of HCO3- in diarrhoea or non-gastric GI fluis
  • loss of HCO3- in urine
34
Q

how do you treat metabolic acidosis?

A
  • give IV isotonic HCO3-

- give IV lactate solution

35
Q

how do you treat respiratory acidosis?

A
  • restore ventilation
  • treat underlying dysfunction or disease
  • give IV lactate solution
36
Q

what causes respiratory alkalosis?

A
  • caused by hyperventilation

- can be acute or chronic

37
Q

what causes metabolic alkalosis?

A
  • results from all other conditions other than respiratory that increase pH
  • always chronic
38
Q

how ca you suffer a loss of H+?

A
  • use of H+ in metabolism of organic ions
  • loss of H+ in vomit
  • loss of H+ in urine
  • hyperventilation
39
Q

how do you treat metabolic alkalosis?

A
  • give electrolytes to replace those lost
  • give IV Cl- containing solution
  • treat underlying disorder
40
Q

how do you treat respiratory alkalosis?

A
  • treat underlying cause
  • breathe into paper bag
  • give IV Cl- containing solution
41
Q

what are some causes of respiratory acidosis?

A
  • reduced elimination of CO2 from the body fluids
  • asphyxia
  • hypoventilation
  • advanced asthma
  • severe emphysema
42
Q

what are some causes of metabolic acidosis?

A
  • elimination of large amounts of HCO3- resulting from mucous secretion
  • direct reduction of the body fluid pH as acid is absorbed
  • production of large amounts of fatty acids and other acidic metabolites such as ketone bodies (untreated diabetes mellitus)
  • inadequate oxygen delivery to tissue resulting in anaerobic respiration and lactic acid build up
43
Q

what are some causes of respiratory alkalosis?

A
  • reduced CO2 levels in the extracellular fluid
  • decreases atmospheric pressure reduces oxygen levels, which stimulates the chemoreceptor reflux causing hyperventilation
44
Q

what are some causes of metabolic alkalosis?

A
  • elimination of H+ and reabsorption of HCO3- in the stomach or kidney
  • ingestion of alkaline substances
45
Q

how does ADH work?

A
  • interacts with V2 receptors on the basolateral surface of principal cells in the collecting duct
  • results in increased permeability of collecting duct to H2O by insertion of aquaporin-2 water channels on apical surface
  • maximal ADH leads to production of low amounts of concentrated urine
46
Q

how is volume regulated by ADH?

A
  • ADH released in response to changes in plasma osmolarity and effective circulating volume
  • these changes are detected by osmoreceptors and baroreceptors
47
Q

what happens in dehydration?

A
  • increased plasma osmolarity stimulates osmoreceptors in the hypothalamus which trigger ADH release
  • more water reabsorbed from collecting ducts in kidney back into circulation leading to increased ECV
  • increased osmolarity also stimulates a second group of osmorecetpors in the hypothalamus which triggers thirst
  • promotes water intake which enters circulation which also increases ECV
48
Q

how does urea play a part in the countercurrent multiplication?

A
  • active transport of NaCl contributes 600-1000mOsm
  • urea is freely filtered at glomerulus
  • some reabsorption in proximal tubule, but LOH and distal tubule relatively impermeable to urea
  • urea can diffuse out of collecting drug into medulla down its concentration gradient
  • this adds to the osmolarity of medullary interstitium
49
Q

what are the 2 main types of central vascular sensors?

A
  • low pressure blood volume receptors

- high pressure arterial stretch receptors

50
Q

where are the low pressure blood volume receptors found?

A
  • large systemic veins
  • cardiac atria
  • pulmonary vasculature
51
Q

where are the high pressure arterial stretch receptors found?

A
  • carotid sinus
  • aortic arch
  • renal afferent arteriole
52
Q

what is the feedback control of ECV mediated by?

A

baroreceptor stimulation

53
Q

what are the 4 parallel effector pathways that act on the kidney?

A

1) RAAS
2) sympathetic nervous system
3) ADH release
4) ANP release

54
Q

what are the 3 ways that decreased ECV stimulates Reni release?

A

1) decreased renal perfusion pressure detected in the afferent arteriole the ‘renal baroreceptor’
2) decreased Na+ concentration in the distal tubule detected by the macula densa cells the ‘renal Na+ sensor’
3) decreased sympathetic BP also triggers effects of the sympathetic nervous system supplying the JGA

55
Q

what are the 3 actions of AngII that increase ECV?

A

1) enhances tubular Na+ transport in the kidney: promotes Na+ and water reabsorption from tubule
2) stimulation of aldosterone release from adrenal cortex: more Na+ and water is reabsorbed from distal tubule/collecting duct
3) acts on hypothalamus to stimulate thirst and ADH release into circulation: water intake adds to ECV and ADH increases water reabsorption from the collecting duct

56
Q

what is a long term effect of AngII?

A

causes renal hypertrophy so more protein synthesis of Na+ transporters and channels

57
Q

what are the 3 actions of aldosterone that increase ECV?

A

1) stimulates Na+ reabsorption in the distal tubule and collecting duct
2) aldosterone also exerts indirect negative feedback on the RAAS by increasing ECV and lowering plasma K+ concentrations
3) important in conserving Na+ and water but also important in preventing large variation in plasma K+ levels

58
Q

what is the RAAS volume regulation pathway?

A

1) decreased ECV
2) detected by renal baroreceptors and renal Na+ sensors
3) activation of the RAAS
4) AngII and aldosterone
5) reduced Na+ excretion by the kidney and increased renal Na+ reabsorption
6) increased ECV

59
Q

what is the ANS volume regulation pathway?

A

1) decreased ECV
2) detected by peripheral baroreceptors
3) signals to hypothalamus in brain
4) activation of the ANS
5) direct effets on renal haemodynamics and activation of RAAS
6) reduced Na+ excretion by the kidney and increased renal Na+ reabsorption
7) increased ECV

60
Q

what are the 2 ADH volume regulation pathways?

A

FIRST ONE

1) decreased ECV
2) detected by peripheral baroreceptors
3) signals to hypothalamus in brain
4) release of ADH into circulation
5) increased water reabsorption in the kidney
6) increased ECV

SECOND ONE

1) decreased ECV = increased plasma osmolarity
2) detected by osmoreceptors in hypothalamus
3) release of ADH into circulation
4) increased water reabsorption in kidney
5) increased ECV

61
Q

how does ANP work?

A
  • designed to lower ECV
  • atrial myocytes synthesise and store ANP
  • increased ECV causes atrial stretch which leads to ANP release into circulation
  • ANP promotes natriuresis
  • also causes renal vasodilation so increased blood flow leads to increased GFR so more Na+ excreted
  • more Na+ reaches the macula densa so rent release by JGA is reduced: reduces the effects of AngII
62
Q

what is the overall effect of ANP?

A

inhibits actions of renin and opposes effects of AngII

module 104 - theme 3 (13 decks)

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