extracellular fluid control and regulation (renal) Flashcards

1
Q
Which hormone(s) increases the permeability of the collecting ducts by inserting aquaporins?
A Adrenaline
B Aldosterone
C Renin
D Vasopressin

I don’t get the relationship between osmolality and blood volume

A

OPTION D - ADH/vasopressin

binds to v2 receptors on basal membrane.
to increase AQP-2 expression on luminal membrane. This increases the permeability of the cell. allows water reabsorption back into circulation

has an antidiuretic effect allowing more water reabsorption so there is more concentrated urine

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2
Q
Which substrate binds to receptors in the medullary collecting duct to increase sodium excretion?
Aldosterone	
Atrial Naturetic Peptide	
Renin	
Vasopressin
A

but id argue its ANP - literally naturesis
and helps to reduce the BP

cos renin is an enzyme and will eventually increase sodium reabsorb

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3
Q

Which of these statements accurately describes metabolic water?
A There is no difference between metabolic water and ingested water.
B Metabolic water is formed when organic food molecules are aerobically catabolized.
C Metabolic water is formed when inorganic food molecules are anaerobically catabolized.
D None of the above

A

OPTION B

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4
Q

Which statement accurately describes the Proximal Tubule?
A The PT is the region on the nephron where maximum reabsorption takes place.
B The PT is responsible for water reabsorption.
C The PT is heavily involved in counter current multiplication.
D The main role of PT is maximum water reabsorption.

A

OPTION A
around 65%-70% of glomerular filtrate us slevtively reabsorbed here and goes back to blood
it has lots of microvilli to do this and special pumps, cotransporters and mitch!

> option d is descending limb of HEnle

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5
Q

where are oxytocin nd ADH prodcued

A

the posterior pituitary

Endocrine neurons have cell bodies located in the SON and PVN

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6
Q

what is renal clearance

A

how quickly a susbtance is removed from plasma and extrected by the kidney in urine
high clearance = quick removal!

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7
Q

what 3 cells are present in the glomerulus to enable ultrafiltration

A

capiilary endothelium
basement membrane
bowmans capsule epithelium // podocyres
» large molecules and proteins cannot pass so at the efferent arteriole there is low blood waterpotential so water reabsorbs

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8
Q

What is the effect of ADH on urine?
A More ADH, the more dilute urine
B More ADH, the more concentrated urine
C No effect on urine

A

OPTION - concentrated urine

ADH binds to v2 receptors on basolateral membrane. stimulates AQP2 antiporters tp be expressed the DCT and CD enabling water reabsorbption -> increase in ECF/blood volume, increase in BP

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9
Q

true or false: the hypothalamus and pituitary are involved in production of aldosterone (mineralcorticoid)

A

fALSE¬
SNS allows renin release (due to low BP lowECF, high osmolarity as less water , )
stimulates RAAS (Renin angiotensin aldosterone system),

Angiotensin II stimulates the production of aldosterone in the adrenal cortex z. Glomerulosa

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10
Q
Which region of the nephron is impermeable to water?
A descending limb
B collecting sucts
C proximal tubule
D ascending limb
E glomerulus
A

ascending limb - has lots of tight junction so impermeable to water

complete opposite to descending limb

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11
Q

what are the gernael effects of too much ECF and too littlw ECF

A

too much = pressure naturesis and pressure diuresis. can put strain on kidney and maybe lead to failure/rupture of vessels/ haemmorge .. conditions assoicated with high BP,oedema

too little = rate of excretion of water and electrolytes is slow.. low BP

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12
Q

why does an increase in ECF indirectly affect the peripheral vacalr resistance

A

increasing ECF will increse BP as the blood volume increases, so will the end diastolic volume and the stroke volume – increase in cardiac output and BP

I guess to compensate
this increase in BP can result in vasoconstriction of blood vessels/ smaller radius which increases Total periphery resistance

as radius of vessel decresea, resistance increaes

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13
Q

what is the ECF

A

made up of water and osomolytes, mainly sodium so regulation excretion of sodium and osomoregulation is the way to go to cotnrol ECF

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14
Q

how much does the kidney process

A

to maintain a GFR of 120ml/min, kindey uses 25% of cardiac output so the pressure has to be kept at 120/80mmHg to maintain blood flow to kidney

kidney filters 180L/day and only 1% of this is excreted so we do be reabsorbing 99% of this!!

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15
Q
which of these component(s) are completely reabsorbed by kidney?
A water
B sodium
C bicarbonate
D urea
E glucose
A

glucose and bicarb fully reasborpbed back into blood
> if there is glucose in urine indicates high sugar levels, possible diabetes
> if there is bicarb, usually excrete bicarb ions

the others are partially reabsorbed but can be excreted and are present in urine

> > quite rarely do we get substance that is fully excreted in the urine like toxins like aminohippuricacid

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16
Q

describe what triggers the release of renin

A
  1. low BP or high plasma osmolarity sensed by SMuscleCells of afferent arteiole and will signal the JXG cells to release renin from their granules
  2. sympathetic innervation can stimulate renin release
  3. macular densa cells have osmoreceptors of DCT can detect the increase in plasma osmolarity (as fluid volume is decreased) again stimulating relase of renin
17
Q

how does renin and ACE compare?

A

renin has a longer half life of 30-60 mins whilst ACE is only a few minutes
> therefore ANG2 can be synthesised whilst renin is still in circulation

ACE is secreted from the lungs, renin secreted from the kidneys

18
Q

describe the actions of RAAS // end results

A

renin released in repsonse to low BP so aim to Increase BP
> vasoconstict
> inrease GFR
> increase water and elecrtolyte retention throgh stmualtion of ADH and aldosterone (sodium retain)
> increase sympathetic tone, increase CO

19
Q

how does the osmolarity of the nephron change?

A

as we move down from the cortex to the medulla, the osmolarity increases
this helps with water absorption as the water will move from a high osmo to a low osmo

so water leaves the tubule and enters interstitial space

20
Q

describe the coutercurrent mechanism (And potential issue)

A
  1. the ascending limb is impermeable to water
    it will actively transport electrolytes/sodium into the Interstitial space (thick part), lowering the water potential of it and thin part is permeable to salt so can passively reabsorb salt here
  2. the descending tube is permeable to water so water enters interstitial space via osmosis.
    this then lowers the water potential of the tubule as we move down the limb and increases the osmolarity/solute conc along the tubule.
  3. the filtrate leaves ascending limb and enters the collecting duct
  4. repeat this process as now we can afford to pump more electrolytes from the ascedning limb

variable permeability of the limbs allows this counter current mechanism to occur!
> conc. urine is the result but too concentrated urine can result in kideny stone foration

21
Q

osmosis

A

moving from a high to a low water potential

22
Q

what is function of aldosterone? how does it do this?

A

upregulates expression of ENaC, ROuterMedulK on the luminal membrane of DCT
and increase Na/K pump on basal membrane
= sodium reabsorb + potassium excrte
works synegistically with ADH on the DCT to increase sodium reabsorption into blood and potassium excretion

23
Q

how can ENaC be regulated?

A

upregulated expression in presecnes of aldosterone.

inhibited by action of Atrial natuiretic peptide and also the drug amiloride (diuretic)

24
Q

how can the SNS be stimulated with response to a drop in ECF/ BP

A

baroreceptors and osmoreceptors detect these changes and snese the low GFR and slow renal blood flow
can trigger vasoconstriction and activate sympathetic
neurons that stimulate renin production by juxtaglomerular cells.

Overall, they serve to reduce blood flow to the kidneys
and while boosting the reabsorption of salt and water, together helping redirect blood to more critical organs and stem loss of extracellular volume.
> but then this would trigger the release of renin surely
> also constrict of efferent ateriole would increase the GFR

25
Q

where are renal baroreceptors located?

A

the afferent arteriole - JXG
the macula densa cells - DCT
> threshold of 80mmHg and below will see an increase in renin secretion

both specialized smooth muscle cells that can detect changes in BP as they have mechanosensitive ion channels

macula densa cells are senstive to low chloride and will release renin if just under 60mM of chloride

26
Q

how do ACE inhibotors work. what would they treat?

A

ACE have Zn+ and H+ in the carboxy terminal regions which make up the active site of the enzyme
inhibitor binds to the Zinc+ and will then block this action , inigibing thte enzyme
> competitive inhibition of enxyme

will help to treat hypertension as the ang2 cannot be synthesised so cannot perform its actions to raise the blood pressure

27
Q

how does an increase in ECF increase the BP?

A

MAKES USE OF barorecptors
> heart barorecprtos will affect the cardiac output and indirectly affect the TPR
> renal barorecptors will alter fluid and electrolyte balance
alter sympathetic tone

incease BV, EDV, SV, CO, BP

28
Q

how would kidney stenoisis/ renal cirrosis contribute to the pathophysiology of control of ECF?

A

stenosis = slowing of blood flow
1. reduced GFR, reduced BP
2, stimulates RAAS to increase the BP which is then uncontrolled as the issue of renal damage is not resolved

so there is an increase in na+h20 retained = hypertesnion

29
Q

what stimulates ADH release from the pituitary?

A

ADH RELEASED IN RESPONSE TO
> there is a high plasma osmolarity (high salt conc
> due to a low blood volume=low BP
hard to find a pure osmotic stimulus