Kidney- the basics first

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  • Created by: Sarah
  • Created on: 14-05-17 09:02
where do thiazide diuretics act?
early DT
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what transporter does thiazide diuretics affect?
NCC
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what are the 2 main differences between bartters and gitelmans?
1) Bartters- thick ascending limb, affects CLCK, bartinin, ROMK NKCC2, hypercalcuria (too high ca) 2) Gitelmans- affects NCC, early DT, hypocalciuria (too low)
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what are the side effects of thiazide diuretics like?
gitelmans
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what does the loop of henle reabsorb?
H2O, Ca, Mg, Na+Cl
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what proteins are on a proximal tubule cell?
NHE3, SGLT1+SGLT2, NapiII
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what happens to a NapiII KO?
bone dev bad- small bones and less dense, have hypokalemia
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how many mutations in SLGT1+2 is there?
21
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what 2 cell types are in the late DT and CD?
1)principal 2) intercalated
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what channels/transporters does the principle cell hav?
EnaC, ROMK, AQP2, AP3, AQP4, Kir2.3
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What does the principal cell absorb?
Na and H2o
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What does the principle cell secrete?
K+ (ROMK) and H+
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what does channel does Liddles syndrome affect?
Enac (in principle cell
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what can hyperaldosteronism be caused by?
in EnaC or mineralcorticoid rec
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principle cell diseases?
diabetes insipidus, hypoaldosteronism, liddle syndrome
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what is the diuretic for the cortical collecting duct?
amiloride
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what does amiloride block?
EnaC
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what does the collecting duct have a low permeability to?
sodium
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when is the collecting duct permeable to urea and water?
presence of vasopressin
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what is theorder and percenrages of sdium reabsorption?
PT (70%) 20% Loop and 9% DT+CD
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what is the point of reg by aldosterone for sodium uptake in the kidney?
DT + CD
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how much Na should be in your urine?
1%
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where is reg of water uptake in the kidney? by what?
DT and CD, vasopressin
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how much water and Na reabsorbed by PT?
70%
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how much of the water we filter do we reabsorb?
99%
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where is most K+ reabsorbed in the kidney?
80% PT (20% loop)
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secretion of H+ by what?
PT, prncipal and alpha IC
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where is bicarbonate reabsorbed?
PT, principal and alpha IC
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where is Vasopressin made?
neurosecretory cells in the hypothalamus
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where is vasopressin released?
posterior pituitary
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pathway of vasopressin?
down the axons of neurosecretory cells (down pituitary stork), stored at nerve terminals until ap releases
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what is osmalility?
how concenrated solution is, high osmalitlity- lots of ions
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what does vasopressin maintain?
body fluid osmalality
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why is importnat to maintain osmalality?
make cells swells up
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main action of vasopressin?
to keep water
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what osmaliltity is low what will this do to Vasopressin?
inhibits vasopressin, don't reabsorb water so become more concentrated again
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what do osmoreceptors detect?
changes in osmalality of plasma
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how much does the osmalality have to change the osmoreceptors?
3mosmol/kg h2o
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where are osmoreceptors found?
cell body of supra-optic and paraventricular nucelus in hypothalamus
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under normal conditions is vasopressin released?
yes
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activation of osmoreceptors in the hypothalamus (paraventricular nucleus+ supra-optic) gives a feeling of what?
thirst
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what increases the release of vasopressin?
ingest solute (eg salt), you are water deficient, high osmalality, stressed+drugs- nicotine, 3-4 methylendioxymethamphetamine (ecstasy)
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what does ecstasy do?
you can't get rid of any water so your brain swells up, take up too much water because of vasopressin
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what inhibits vasopressin release?
decreased osmalility, excessive fluid ingestion (drink loads of water), drugs- alcohol
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what does alcohol inhibit?
vasopressin
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what happens when you drink alcohol?
inhibits release of vasopressin, less water absorbed, excreting water in urine -> dehydration
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what happens to plasma vasopressin as plasma osmalility goes up?
vasopressin goes up
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normal plasma osmalilty?
290 mosm/kgh2o
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what happens if your osmalility is really low?
completely inhibit vasopressin
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as vasopressin goes up what happens to urine osmalitily?
urine osmalility goes up as becomes more concentrated, excrete less water
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rate limiting step for how much water you reabsorb?
AQP2- in the principal cell in the late DT and CD
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what is the vasopressin rec on the basoltaeral m of which cell?
V2 on principal cell
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activation of the v2 rec intiates what?
a signalling cascade -> activates protein kinase A (enzyme add phosphate adds it to proteins) -> phosphorylates pros on vesicles causes them to go fuse with membrane -> AQP2 on M of vesicle
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what is the effect of more AP2 channels from vasopressin?
fall in body osmalility and reabsorb more water
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how much water can vasopressin make you reabsorb?
23L a day!
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what are the symptoms of diabetes insipdus?
copious amounts of dilute urine (lose water 23L a day!))
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2 kinds of diabetes inspidus?
central diabetes or nephrogenic
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what is the problem in central Diabetes insipidus?
no release of vasopressin
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can you treat central diabetes insipidus?
yes with a nasal spray DDAVP (argenine vasopressin)
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what is the problem with nephrogenic diabetes insipidus
no response to vasopressin, probs with V2 rec, mutations in AQP2 gene
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where is aldosterone released from?
zona glomerulsa- part of the adrenal gland
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what is aldosterone?
mineracorticoid (reg of mineral content of the body)
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when is aldosterone released (3 things)?
1) plasma K+ (-0.1mM) , decrease in sodium minor conc maintained by osmoregulation 3) fall in ECF volume- via renin angiotensin
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concentration of sodium regulated by what
Vasopressin
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what does aldoserone act on?
acts on DT and CD
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what cells does aldosterone act on?
principal and intercalated cells
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what does aldosteronemake principal cells do?
reabsorption of sodium which drives reabsorption of water
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what does aldosterone make alpha IC cells od?
increased secretion of K+ and H+
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so aldosterone does with the triggers, what are the triggers?
1) fall in Na + H2o 3) increase in K+
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how does it fit with the triggers?
reabsorbs more Na and H2O when fall, secretes K+ when it goes high
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what happens to aldosterone?
steroid hormone, diffuses into principal cell, binds to cytosolic mineralcorticoid receptor, initiates process where aldosterone-rec complex moves to nucleus, stimulates rna transcription+ pro syn
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what pathway does aldosterone go by?
genomic pathway
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what proteins are made from aldosterone?
H+ and K+secretion pros, Na reabsorption proteins, more ROMK, ENaC, Sodium-po ATPase, sodium-hydrogen exchangers
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net effect of aldosterone?
increase plasma content, increase ECF volume, palsma K+ decreases, decrease H+
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what is content? aldosterone regs Na content!
how many mmols in your whole body
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what does aldosterone coordiante with?
renin-angiotensin system
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what is liddle syndrome symptoms?
hypertension (really really high bp),
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what is liddles syndrome caused by?
excess sodium reabsorption by ENac even tho aldosterone low, mutation in ENaC get in M cell struggles to pull them out by endocytosis can't happen
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main points of liddles?
way too many ENaC -> reabsorbing loads of sodium -> water follows -> ecf vol increases -> high bp
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what are the symptoms of hypoaldosteronism?
excreting salt (sodium+Cl) but high aldosterone so should be absorbing more Na, lose sodium even tho high aldosterone
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whats the cause of hyperaldosteronism?
no response to aldosterone, mutation in mineralcorticoid rec, loads of aldosterone not a lot of ENac-> not absorbing sodium so hypotension
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what does the renin angiotensin system regulate?
body fluid volume, plasma Na+K
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where is renin released from?
juxtaglomerular apparatus, granular cells in the wall of the afferent arteriole
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juxtaglomerular apparatus
early DT is passing very close to its own glomerulus, specialised maccula densa cells
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what does maccula densa cells look at?
flow rate of tubular fluid
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what doe the maccula densa cells affect if tubular rate is not right?
afferent arteriole
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why are they called granular cells in the afferent arteriole?
granules in them of renin
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when do granular cells in the afferent arteriole release renin?
chemical sigs by maccula densa or sympa nerve fibres release
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what happens when renins released into plasma?
initiates renin-angiotensin system
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what happens in the renin-angiotensin cascade?
fall in ECF vol -> impacts of tubular flow rate and sympa NS -> graunular cells release renin-> renin converts Angiotensinogen to angiontensin 1 -> antiogentin 1 to angitensin 2 by ACE
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active component of renin-agiotensin?
angiotensin 2
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where is majority of Angiotensin 1 -> angiotensin 2 by ACE made?
in the lungs as occurs in the most capillarie density (angiotensin 2 made in capillaries)
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Angiotesin 2 has 2 actions what?
1) stimulates zona glomerulsa to stimulate aldosterone (higher plasma Na +ECFvol) potent vasoconstriction- brings bp up
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what can ACE inhibitors be used for?
reduce bp, less aldosterone and less vasoconstriction
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your body will maintain volume or body osmolality if it has to dcide?
willmantain ECF vol at expense of osmolality everytime as volume impacts on bp
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ingest of salt what happens with vol osmalility?
absorb Na+Cl, sodium plasma goesup, increase in osmalility impacts VP syst, got osmotic gradient pulls water out of cells into ICF,
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whats the prob
increase in osmalility of plasma from increased Na wants to release vasopressin but will have more water ECF vol will get even higher,
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ingesting salt (Na)increases ECF vol inhibits aldosterone does what?
loss of water, lose Na, red ECF volume
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why is there no problem between vasopressin and aldosterone?
vasopressin system is reset
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why is aldosterone more important than vasopressin?
stimulates ECF vol, sodium content and blood pressure
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what happens to vasopressin levels if you have a volume expansion?
release of Vasopressin is released so aldosterone reg can predominant
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what happens if you are volume depleted?
can enhance vasopressin works with aldosterone brings ECF vol back to normal
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can upreg and down reg vasopressin depending on what?
ECF vol of body
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