Physiology 6 Flashcards
the tubular fluid leaving the loop of henle is hypo or hyper osmotic to plasma?
hypo-osmotic
- 100 mosmol/L
describe fluid entering the collecting duct from the distal tubule?
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which parts of the nephron are found in the cortex/medulla?
in cortex - glomerulus - proximal tubula - distal tubule - top of collecting duct medulla = loop of henle
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hormones only affect cells of which part of the nephron?
distal tubule and collecting duct
- no effect on cells making up proximal tubule or loop of henle
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what regulates ion and water balance in the distal tubule and collecting duct?
hormones
- ADH = water reabsorption
- aldosterone = Na+ reabsorption, K+/K+ secretion
atrial natriuretic hormone = reduced Na+ reabsorption
PTH = Ca2+ reabsorption, reduced phosphate reabsorption
main regulator of salt balance?
aldosterone
osmolarity of fluid in distal tubule?
100
distal tubule is very permeable to water and urea, true or false?
false
low permeability due to tight junctions between cells
- therefore …………….
describe the early part of the distal tubule
triple co-transporter present (Na+, K+, 2Cl-)
= NaCl reabsorption
describe the late segment of the distal tubule
Ca2+ reabsorption
H+ secretion
Na+ and K+ reabsorption (basal state)
collecting duct
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collecting duct
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what is ADH?
octapeptide neurohormone synthesises by the supraoptic and paraventricular nuclei in the hypothalamus
how is ADH synthesises and transported and released?
synthesised by supraoptic and paraventricular nuclei in the hypothalamus
transported down nerve axon towards terminal in posterior pituitary where is is stored in granules
released into the blood by posterior pituitary when action potentials down the nerve axons lead to Ca2+ dependant exocytosis
half life of ADH?
10-15 mins
how does ADH work?
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what stimulates/inhibits release of ADH?
dehydration causing increase in plasma osmolarity = increases release = high permeability = hypertonic urine
very hydrated causing lower plasma osmolarity = reduced release = low permeability = hypotonic urine
how does ADH affect the collecting duct?
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// lots of ADH
corticointerstitial fluid osmolarity = 300
fluid entering distal tubule = osmolarity = 100
= osmotic gradient
ADH allows expression of aquaporins in distal tubule so water can flow down concentration gradient from tubular fluid into corticointerstitial fluid
//lots of ADH?
corticomedullary concentration gradient continues
fluid entering collecting duct = 300, where medullary interstitial fluid = 600 so water flows out
this continues down duct until fluid leaves collecting duct into renal pelvis
how is this different in presence of minimal ADH?
osmotic gradient still present between fluid entering distal tubule and corticointerstitial fluid (100 vs 300)
however lack of ADH means no aquaporins expressed so no pathway for water to move down this gradient
= no movement/reabsorption of water
= large volume of dilute urine produced
how does plasma concentration of ADH affect amount of solute (salts) excreted in urine?
Has no affect
only affects water balance so can influence relative osmolarity but actual amount of salt excreted stays the same
how does water deficit lead to ADH release?
increased plasma osmolarity > detected by osmoreceptors in hypothalamus > stimulates hypothalamic neurones
or in severe fluid loss
- reduced ECF volume > significant decrease in MAP > detected by stretch receptors in left atrium > stimulates hypothalamic neurones > increased ADH production
2 types of diabetes insipidus?
central - cant produce/secrete ADH
nephrogenic - able to produce and secrete ADH but its not acting on target cells
features of diabetes insipidus?
large volumes of dilate urine (up to 20L per day)
how is diabetes insipidus managed?
ADH replacement
feed-forward control of ADH?
stimulation of stretch receptors in upper GI tract exerts feed-forward inhibition of ADH
how does smoking/alcohol affect ADH release?
nicotine = stimulates release alcohol = inhibits release
major site for reabsorption in the nephron?
proximal tubule (2/3 of salt reabsorption and a fair bit of water absorption too)
what is aldosterone and what does it do?
steroid hormone secreted by adrenal cortex which stimulates Na+ reabsorption and K+ secretion
when is aldosterone secreted?
in response to rising [K+] or falling [Na+] in the blood
or
activation of the RAAS system
what would happen without aldosterone?
continuous secretion of Na+
= depletion of blood volume etc
how does aldosterone affect K+?
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where is renin secreted from and what does it do?
secreted from granular cells in juxtaglomerular apparatus
cleaves angiotensinogen to angiotensin 1
what happens to angiotensin 1?
converted to angiotensin 2 by ACE (secreted by lungs)
angiotensin 2 acts on adrenal cortex to secrete aldosterone
what does angiotensin 2 do?
stimulates ADH release
causes thirst
arteriolar vasoconstriction
3 control mechanisms of renin release from granular cells in JGA?
reduced pressure in afferent arteriole (pressure receptors) = increased renin release
reduced salt sensed by macula densa cells = increased renin release
increased stimulation of granular cells by sympathetic nervous system = increased renin release
how does aldosterone affect Na+ reabsorption?
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how is RAAS involved in heart failure fluid retention?
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what is ANP?
atrial natiuretic peptide
stored in atrial muscle cells and released when these cells are mechanically stretched due to an increase in circulating volume
ANP promotes excretion of Na+ and diuresis, thus decreasing plasma volume
also exerts effects on the cardiovascular system to lower blood pressure
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describe the process of micturition
urine formed in the kidneys and propelled by peristalsis through ureters to the bladder to temporary storage
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