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urinary system > tubular fucntion 2 > Flashcards

tubular fucntion 2 Flashcards

1
Q

describe the renin-angiotensin system

A

liver produce angiotensinogen
JGA produce renin - renin convert angiotensinogen to Ang1
angiotensin converting enzyme convert ang1 to ang2
ang2 -> aldosterone

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2
Q

where is ang2 produced

A

lung

ACE there because large endothelial surface

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3
Q

where is aldosterone produced

A

medulla of the adrenal cortex

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4
Q

effect of ang 2

A

vasoconstriction - increase Bp

increase Na uptake - increase water reabsorption - increase ECF - increase BP

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5
Q

effect of aldosterone

A

increase Na and water retention

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6
Q

what is aldosterone

A

steroid hormone

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7
Q

what stimulates the production of aldosterone

A

released in response to ang2
decrease in bp - baroreceptors
decreased osmolarity of the ultrafiltrate

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8
Q

action of aldosterone

A

increase Na reabsorption - control 35g/na a day
increased K secretion
increased H ion secretion
acts on principle cells of collecting duct
increae expression of apical Na channel
increasse formation of Na-K ATPase pumps

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9
Q

MECHANISM of aldosterone

A

diffuse into cells
bind to steroid hormone receptor in cytoplasm
heat shock proteins bound to receptor
they are released when aldosterone binds
aldosterone receptors dimerises
acts as a TF

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10
Q

things transcribed because of aldosterone

A

TF
regulatory proteins
transport machinery

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11
Q

regulatory proteins action

A

open Na channels on apical membranes

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12
Q

describe hypoaldosteronism

A

reabsorption of Na in distal nephron reduced
increased urinary loss
ECF vol falls and there is increased renin, ang2 and ADH
cause: low BP -> dizziness, salt craving, palpitations

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13
Q

describe hyperaldosteronism

A

reabsorption in the distal tubule increased
reduced urinary loss
ECF increase = hypertension
reduced renin, ang 2 and ADH
increased ANP and BNP
causes: high bp, muscle weakness, polyuria and thirst

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14
Q

how does hyperaldosteronism cause thirst and polyuria

A

high osmolarity
therefore thirsty to increase osmolarity
drink more
urinate more

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15
Q

Liddle’s syndrome

A 
inherited disease of high BP 
mutation in aldosterone activated na channel
always on 
always reabsorb too much na 
= water retention = hypertension
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16
Q

low pressure baroreceptors

A

heart - atria and RV

17
Q

High pressure baroreceptors

A

vasculature system - pul vasculature, carotid sinus, aortic arch, JGA
after LV and before capillaries

18
Q

action of low pressure system

A

response to low pressure: signal through afferent fibres to brainstem - sump activity -ADH
response to high pressure - atrial stretch - ANP, BNP

19
Q

action of high pressure baroreceptors

A

only to low pressure
signal through afferent fibre to brainstem - sump activity -ADH
JGA cells - renin released

20
Q

what stimulates ANP

A

made in RA

in response to atrial stretch

21
Q

action of ANP

A

vasodilation
inhibit Na reabsorption in PCT and collecting ducts
inhibit renin and aldoseterone
reduce BP

22
Q

concentrations of k

A

main intracellular ion
150mmol/l in
3-5mmol/l out

23
Q

effect of K

A

extracellular
high - depolarise mem - AP - heart arrhythmia
low - heart arrhythmia

24
Q

action regarding K after a meal

A

increase plasma K

tissue uptake stimulated by insulin, aldosterone and adrenaline

25
Q

immediate response to dietary K

A

controlled by Na K ATPase
easy to accommodate in whole system
on every cell
K doesn’t rise

26
Q

fraction of K reaching each point in the nephron

A

descending limb - 30%
DCT - 10%
collecting duct - 1-80%

27
Q

what is K secretion stimulated by

A

plasma K
aldosterone
tubular flow rate
plasma pH

28
Q

potassium secretion

A

into cell by na k pump
leak out through k channel
rehulated by membrane potential - if outside more -ve it moves out

29
Q

how does aldosterone affect K

A

DCT and collecting duct
stimulate Na and K channels and Na K ATPase
also stimulate K channel on luminal side

30
Q

tubular flow and K

A

stim K secretion
cells in collecting tubules - cilia
flow increase - activate PDK1
increase ca conc - increase K channels

31
Q

Hypokalemia

A

susceptible if on diuretics - increased tubular flow, surreptitious vomiting - not taking enough in, diarrhoea - excrete through faeces, genetics - Gitelman’s syndrome - mutation in Na Cl transporter in distal nephron - increassed K excretion

32
Q

hyperkalaemia

A

common
response to K sparing anti-diuretics
ACE inhibitors
elderly

urinary system (9 decks)

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