Kidney- the basics first
0.0 / 5
- Created by: Sarah
- Created on: 14-05-17 09:02
where do thiazide diuretics act?
early DT
1 of 103
what transporter does thiazide diuretics affect?
NCC
2 of 103
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)
3 of 103
what are the side effects of thiazide diuretics like?
gitelmans
4 of 103
what does the loop of henle reabsorb?
H2O, Ca, Mg, Na+Cl
5 of 103
what proteins are on a proximal tubule cell?
NHE3, SGLT1+SGLT2, NapiII
6 of 103
what happens to a NapiII KO?
bone dev bad- small bones and less dense, have hypokalemia
7 of 103
how many mutations in SLGT1+2 is there?
21
8 of 103
what 2 cell types are in the late DT and CD?
1)principal 2) intercalated
9 of 103
what channels/transporters does the principle cell hav?
EnaC, ROMK, AQP2, AP3, AQP4, Kir2.3
10 of 103
What does the principal cell absorb?
Na and H2o
11 of 103
What does the principle cell secrete?
K+ (ROMK) and H+
12 of 103
what does channel does Liddles syndrome affect?
Enac (in principle cell
13 of 103
what can hyperaldosteronism be caused by?
in EnaC or mineralcorticoid rec
14 of 103
principle cell diseases?
diabetes insipidus, hypoaldosteronism, liddle syndrome
15 of 103
what is the diuretic for the cortical collecting duct?
amiloride
16 of 103
what does amiloride block?
EnaC
17 of 103
what does the collecting duct have a low permeability to?
sodium
18 of 103
when is the collecting duct permeable to urea and water?
presence of vasopressin
19 of 103
what is theorder and percenrages of sdium reabsorption?
PT (70%) 20% Loop and 9% DT+CD
20 of 103
what is the point of reg by aldosterone for sodium uptake in the kidney?
DT + CD
21 of 103
how much Na should be in your urine?
1%
22 of 103
where is reg of water uptake in the kidney? by what?
DT and CD, vasopressin
23 of 103
how much water and Na reabsorbed by PT?
70%
24 of 103
how much of the water we filter do we reabsorb?
99%
25 of 103
where is most K+ reabsorbed in the kidney?
80% PT (20% loop)
26 of 103
secretion of H+ by what?
PT, prncipal and alpha IC
27 of 103
where is bicarbonate reabsorbed?
PT, principal and alpha IC
28 of 103
where is Vasopressin made?
neurosecretory cells in the hypothalamus
29 of 103
where is vasopressin released?
posterior pituitary
30 of 103
pathway of vasopressin?
down the axons of neurosecretory cells (down pituitary stork), stored at nerve terminals until ap releases
31 of 103
what is osmalility?
how concenrated solution is, high osmalitlity- lots of ions
32 of 103
what does vasopressin maintain?
body fluid osmalality
33 of 103
why is importnat to maintain osmalality?
make cells swells up
34 of 103
main action of vasopressin?
to keep water
35 of 103
what osmaliltity is low what will this do to Vasopressin?
inhibits vasopressin, don't reabsorb water so become more concentrated again
36 of 103
what do osmoreceptors detect?
changes in osmalality of plasma
37 of 103
how much does the osmalality have to change the osmoreceptors?
3mosmol/kg h2o
38 of 103
where are osmoreceptors found?
cell body of supra-optic and paraventricular nucelus in hypothalamus
39 of 103
under normal conditions is vasopressin released?
yes
40 of 103
activation of osmoreceptors in the hypothalamus (paraventricular nucleus+ supra-optic) gives a feeling of what?
thirst
41 of 103
what increases the release of vasopressin?
ingest solute (eg salt), you are water deficient, high osmalality, stressed+drugs- nicotine, 3-4 methylendioxymethamphetamine (ecstasy)
42 of 103
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
43 of 103
what inhibits vasopressin release?
decreased osmalility, excessive fluid ingestion (drink loads of water), drugs- alcohol
44 of 103
what does alcohol inhibit?
vasopressin
45 of 103
what happens when you drink alcohol?
inhibits release of vasopressin, less water absorbed, excreting water in urine -> dehydration
46 of 103
what happens to plasma vasopressin as plasma osmalility goes up?
vasopressin goes up
47 of 103
normal plasma osmalilty?
290 mosm/kgh2o
48 of 103
what happens if your osmalility is really low?
completely inhibit vasopressin
49 of 103
as vasopressin goes up what happens to urine osmalitily?
urine osmalility goes up as becomes more concentrated, excrete less water
50 of 103
rate limiting step for how much water you reabsorb?
AQP2- in the principal cell in the late DT and CD
51 of 103
what is the vasopressin rec on the basoltaeral m of which cell?
V2 on principal cell
52 of 103
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
53 of 103
what is the effect of more AP2 channels from vasopressin?
fall in body osmalility and reabsorb more water
54 of 103
how much water can vasopressin make you reabsorb?
23L a day!
55 of 103
what are the symptoms of diabetes insipdus?
copious amounts of dilute urine (lose water 23L a day!))
56 of 103
2 kinds of diabetes inspidus?
central diabetes or nephrogenic
57 of 103
what is the problem in central Diabetes insipidus?
no release of vasopressin
58 of 103
can you treat central diabetes insipidus?
yes with a nasal spray DDAVP (argenine vasopressin)
59 of 103
what is the problem with nephrogenic diabetes insipidus
no response to vasopressin, probs with V2 rec, mutations in AQP2 gene
60 of 103
where is aldosterone released from?
zona glomerulsa- part of the adrenal gland
61 of 103
what is aldosterone?
mineracorticoid (reg of mineral content of the body)
62 of 103
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
63 of 103
concentration of sodium regulated by what
Vasopressin
64 of 103
what does aldoserone act on?
acts on DT and CD
65 of 103
what cells does aldosterone act on?
principal and intercalated cells
66 of 103
what does aldosteronemake principal cells do?
reabsorption of sodium which drives reabsorption of water
67 of 103
what does aldosterone make alpha IC cells od?
increased secretion of K+ and H+
68 of 103
so aldosterone does with the triggers, what are the triggers?
1) fall in Na + H2o 3) increase in K+
69 of 103
how does it fit with the triggers?
reabsorbs more Na and H2O when fall, secretes K+ when it goes high
70 of 103
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
71 of 103
what pathway does aldosterone go by?
genomic pathway
72 of 103
what proteins are made from aldosterone?
H+ and K+secretion pros, Na reabsorption proteins, more ROMK, ENaC, Sodium-po ATPase, sodium-hydrogen exchangers
73 of 103
net effect of aldosterone?
increase plasma content, increase ECF volume, palsma K+ decreases, decrease H+
74 of 103
what is content? aldosterone regs Na content!
how many mmols in your whole body
75 of 103
what does aldosterone coordiante with?
renin-angiotensin system
76 of 103
what is liddle syndrome symptoms?
hypertension (really really high bp),
77 of 103
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
78 of 103
main points of liddles?
way too many ENaC -> reabsorbing loads of sodium -> water follows -> ecf vol increases -> high bp
79 of 103
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
80 of 103
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
81 of 103
what does the renin angiotensin system regulate?
body fluid volume, plasma Na+K
82 of 103
where is renin released from?
juxtaglomerular apparatus, granular cells in the wall of the afferent arteriole
83 of 103
juxtaglomerular apparatus
early DT is passing very close to its own glomerulus, specialised maccula densa cells
84 of 103
what does maccula densa cells look at?
flow rate of tubular fluid
85 of 103
what doe the maccula densa cells affect if tubular rate is not right?
afferent arteriole
86 of 103
why are they called granular cells in the afferent arteriole?
granules in them of renin
87 of 103
when do granular cells in the afferent arteriole release renin?
chemical sigs by maccula densa or sympa nerve fibres release
88 of 103
what happens when renins released into plasma?
initiates renin-angiotensin system
89 of 103
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
90 of 103
active component of renin-agiotensin?
angiotensin 2
91 of 103
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)
92 of 103
Angiotesin 2 has 2 actions what?
1) stimulates zona glomerulsa to stimulate aldosterone (higher plasma Na +ECFvol) potent vasoconstriction- brings bp up
93 of 103
what can ACE inhibitors be used for?
reduce bp, less aldosterone and less vasoconstriction
94 of 103
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
95 of 103
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,
96 of 103
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,
97 of 103
ingesting salt (Na)increases ECF vol inhibits aldosterone does what?
loss of water, lose Na, red ECF volume
98 of 103
why is there no problem between vasopressin and aldosterone?
vasopressin system is reset
99 of 103
why is aldosterone more important than vasopressin?
stimulates ECF vol, sodium content and blood pressure
100 of 103
what happens to vasopressin levels if you have a volume expansion?
release of Vasopressin is released so aldosterone reg can predominant
101 of 103
what happens if you are volume depleted?
can enhance vasopressin works with aldosterone brings ECF vol back to normal
102 of 103
can upreg and down reg vasopressin depending on what?
ECF vol of body
103 of 103
Other cards in this set
Card 2
Front
what transporter does thiazide diuretics affect?
Back
NCC
Card 3
Front
what are the 2 main differences between bartters and gitelmans?
Back
Card 4
Front
what are the side effects of thiazide diuretics like?
Back
Card 5
Front
what does the loop of henle reabsorb?
Back
Similar Biology resources:
0.0 / 5
0.0 / 5
0.0 / 5
0.0 / 5
0.0 / 5
0.0 / 5
0.0 / 5
0.0 / 5
0.0 / 5
Comments
No comments have yet been made