Session 4- Control of body fluid volume and osmolality Flashcards

1
Q

what is renin

A

an enzyme that is synthesized and stpred in JGA in the kidney

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2
Q

what stimulates renin release

A

LOW BP

increased sympathetic innervation
-granular cells of the JGA are innervated by sympathetic system, resulting in an increase in renin release
fall in wall tension of afferent arteiole

Decreased Na+ to the macula densa

-if less NaCl reaches the macula densa, the macula densa is stimulated to release prostaglandins which act on granular cells causing renin release

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3
Q

how does the RAAS system work

A

angiotensiogen-> angiotensin I via renin
angiotensin I -> angiotensin II VIA ACE
angiotensin II-> aldosterone

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4
Q

action of angiotensin II

A

directly vasoconstricts efferent arteioles within the glomerulus which increases GFR

stimulates the zona glomerulosa of the adrenal cortex to release aldosterone

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5
Q

action of aldosterone

A

directly increases Na+ reabsorption from the DCT
releases ADH
stimulate thrist

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6
Q

where does prostaglandin synthesis occur

A

cortex
medulla
collecting duct epithelial cells

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7
Q

what do prostaglandins do

A

vasodilators

renin release

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8
Q

what stimulates prostaglandin release

A

a decrease in effective circulating volume of Na+

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9
Q

action of ANP

A

inhibit Na+/K+/ATPase and close Na+ channels of the collecting ducts and DCT reducing Na+ reabsorption. Thus, Na+ and water excretion by the kidney is increased

vasodilate afferent arterioles, thereby increasing GFR

inhibit aldosterone release

inhibit ADH release

decrease renin release

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10
Q

how do starling forces affect the reabsorption of sodium if blood pressure increases

A

if BP increases, there is more blood voluem meaning the hydrostatic pressure of the peritubular capillaries increases and the oncotic pressure decreases which causes water reabsorption to decrease in the PCT

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11
Q

in the PCT how is the intial BP rise diminished

A

reduced number of Na-H antiporters and reduced Na- K ATPase activity in proximal tubule

this causes reduction in sodium resorption in proximal tubule

reduction in water resorption

ECF volume decreased

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12
Q

what is pressure natriuresis

A

increased sodium excretion

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13
Q

what is pressure diuresis

A

increased water excretion

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14
Q

how does congestive heart failure affetc the kidneys

A

CO falls and heart fsils to perfuse kidneys adequately

hypoperfusoon results in Na+ and water retention by the kidneys leading to oedema

renal hypoperfusion following a fall in CO is sense by the kidneys as hypovolaemia

this results in compensation by retaining NaCl and water to increase circulating fluid volume - RAAS

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15
Q

how does cardiac failure affect the lungs

A

this increase in pulmonary venous pressure results in transudation from the capillaries in the lungs and in pulmonary oedema

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16
Q

what is hypervolaemia

A

excess of fluid

17
Q

how does hypertension affect teh kidneys

A

arteriosclerosis of the major renal arteries

hyalinization of the small vessels with intimal thickening

this can lead to chronic renal damage and a reduction in the size of the kidneys

18
Q

renal causes of secondary hypertension

A

most diseases of the kidney cause-
impaired Na+ and water excretion, increases blood volume
stimulation of renin release

renal artery stenosis also causes reduced perfusion of the kidney and therefore excessive activation of the RAAS

19
Q

what senses changes in osmolarity in the brain

A

hypothalmic osmoreceptors located in the organum vasculature of the lamina terminalis- OVLT located in brain

20
Q

Where is ADH produced

A

the supraoptic nucleus of the hypothalamus then transported to the posterior pituitary

21
Q

what triggers ADH release

A

increase in plasma osmolality

22
Q

ADH effect

A

reduced water excretion
blood vessel vasoconstriction

it binds to V2 receptors on the basal membrane

  • G protein coupled receptors when activated cause fusion of inactive aquaporin 2 vesicles with the luminal membrane
  • creates ac channel through with water can pass
  • passive flow of water
23
Q

what is diabetes insipidus

A

too little ADH

inability to reabsorb water from the distal part of the nephron due to failure of secretion or action of ADH

24
Q

symptoms of diabetes insipidus

A

polyuria
polydipsia
low urine osmolality

25
Q

cental diabetes insipidus

A

impaired ADH synthesis or secretion by the hypothalamus- damage to hypothalamus or pituitary

  • brain injury
  • sarcoidosis
  • tumour
  • aneurysm
  • some forms of encaphalitis or meningitis
26
Q

how do we treat central diabetes insipidus

A

administrating ADH

27
Q

nephrogenic diabetes insipidus

A

acquired insensitivity of the kidney to ADH

water is inadequately reabsorbed from the collecting ducts so a large quantity of urine is produced

28
Q

what is SIADH

A

syndrome of inappropriate antidiuretic hormone secretion

excessive release of ADH from the PP gland or another source

chracterized by dilutional hyponatraemia