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GERR Physiology > Renal regulation of ECF osmolarity and volume > Flashcards

Renal regulation of ECF osmolarity and volume Flashcards

1
Q

Why is ECF osmolarity strictly controlled

A
  • to guard against changes in ICF composition
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2
Q

ECF loss results in what

A

increase in osmolarity = cells shrink

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3
Q

ECF gain results in what

A

decrease in osmolarity = cells swell

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4
Q

Describe what regulates ECF osmolarity and volume ( 5 )

A 
1- ADH 
2- Aldosterone 
3- RAAS 
4- Atrial natriuretic peptide 
5- Thirst
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5
Q

Explain the mechanism by which ADH is secreted with Hypertonic ECF ( <280 )

A
  • osmoreceptor neurons in hypothalamus have aquaporin channels that allow water to exit cell when ECF is hypertonic
  • shrinking of osmoreceptor neurons opens stretch sensitive channels
  • calcium and sodium enters causing depolarisation
  • action potential passes down to supra optic and paraventricular neurons
  • ADH is released from posterior pituitary
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6
Q

What are the effects of ADH secretion

A
  • increased water reabsorption at DCT and collecting duct
  • ADH inserts aquaporin channels into walls of DCT and Collecting duct to allow water back into blood
  • dilutes plasma
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7
Q

Explain the mechanism by which ADH is secreted with Hypotonic ECF ( >280 )

A
  • aquaporin channels allow water to enter cell by osmosis
  • osmoreceptors expand causing stretch channels to be inactivated
  • decrease in Ca and NA result in no depolarization and no action potential
  • no signal is sent for ADH release
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8
Q

What are the effects of no ADH secretion

A
  • no reabsorption of water at DCT and CD
  • ECF osmolarity increases
  • dilute urine
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9
Q

Explain the mechanism by which ADH is secreted due to Blood pressure increase

A
  • Baroreceptors in carotid sinus and aortic arch sense stretch of blood vessel wall
  • baroreceptors activate with every heart beat and cause Ca and Na to enter and depolarize the nerve cell
  • signal sent up to hypothalamus
  • Inhibiting Supra optic and Paraventricular release of ADH
  • decrease water reabsorption = decrease BP
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10
Q

Explain the mechanism by which ADH is secreted due to Blood pressure decrease

A
  • signals sent to hypothalamus from baroreceptors are reduced
  • ADH release is increased by supra optic and paraventricular
  • increasing water reabsorption = increase BP
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11
Q

Explain the mechanism by which Aldosterone is secreted to hyperkalaemia

A
  • mineralocorticoids are released by zona glomerulosa
  • K is reabsorbed in PCT, Asc Loop, DCT and CD
  • triggers aldosterone which increases expression of Na K pump in DCT and CD
  • increasing Na reabsorption and K secretion
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12
Q

What causes release of aldosterone ( 4 )

A

1- increase of K in plasma
2- Increase of ACTH, AngII
3- decrease of plasma PH
4- decrease of atrial stretch , BP

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13
Q

Explain the result of Aldosterone on ECF

A

-increase of sodium reabsorption = increase of water reabsorption and K secretion to urine

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14
Q

What are the results of Hyperaldosteronism

A
  • Hypertension and Hypokalemia
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15
Q

How is Hyperaldosteronism treated

A
  • treated by surgery or aldosterone antagonist
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16
Q

What are the causes of Hypoaldosteronism

A

1- primary, secondary , tertiary adrenal insufficiency
2- congenital adrenal hyperplasia
3- medications

17
Q

What are the results of Hypoaldosteronism

A
  • Hyperkalaemia : palpitations , muscle pain , abnormal heart rhythm , cardiac arrest
18
Q

What is isolated hypoaldosteronism

A
  • reduced production of aldosterone without corresponding changes in cortisol
19
Q

What is used to differentiate between the causes of hypoaldesteronism in patient

A
  • ACTH release is stimulated
  • if low aldosterone release then primary hypoaldestornism
  • if large aldosterone release then secondary hypoaldosteronism
20
Q

Explain the mechanism by which RAAS is activated due to reduced ECF osmolarity and the result

A
  • Na reabsorption is reduced in DCT
  • detected by kidney to cause renin release
  • renin enters blood stream causing Angiotensinogen to convert to AngI
  • Ang I becomes AngII
  • AngII acts on adrenal cortex to cause aldosterone release
  • increasing Na reabsorption
  • increases water reabsorption
21
Q

Where else does AngII act on other than adrenal cortex

A
  • acts on brain to stimulate ADH secretion
  • increases water reabsorption
  • increase BV= increase BP & CO
22
Q

What three things activate RAAS

A
  • decrease in ECF osmolarity
  • increase in SNS
  • decrease in Blood pressure
23
Q

What happens when ECF osmolarity is low and we want an increase in Na reabsorption to increase osmolarity but not an increase in water which would dilute the ECF

A
  • Hypothalamus will override the effects of AngII on ADH release
  • decrease ADH release = reduce water reabsorption
24
Q

What happens due to reduced Na reabsorption to the Juxta-glomerular cells

A
  • PGE2 is activated in juxtaglomerular cells

- results in renin production from them

25
Q

What happens due to Sympathetic activity to the Juxta-glomerular cells

A
  • increases cAMP

- results in renin production

26
Q

What happens when blood pressure increases is detected in afferent arteriole

A
  • stretch sensitive channels on Juxta-glomerular cells are activated
  • decrease cAMP
  • stop renin production
27
Q

Explain the mechanism by which Atrial Natriuretic Peptide is secreted due to increase in BV and the result

A
  • ANP is released by atrial myocytes in response to atrial distension
  • ANP inhibits renin release
  • decreases circulating AngII and aldosterone ( natriuresis and diuresis )
  • ANP improves GFR = Diuresis
  • reduces BV = reduce BP
  • ANP also causes vasodilation = decrease in BP
28
Q

Explain the mechanism by which RAAS is activated due to Sympathetic activity and decrease Blood pressure and the result

A
  • renin enters blood stream causing Angiotensinogen to convert to AngI
  • Ang I becomes AngII
  • AngII acts on adrenal cortex to cause aldosterone release
  • AngII also acts to release ADH which results in increase of water reabsorption
  • increasing Na reabsorption
  • increases water reabsorption
  • increases BV= increase BP & CO
29
Q

What is the purpose of Natriuretic peptides

A
  • natural counter-regulatory system for RAAS

- useful for hypertension and CHF treatment because it maintains K levels in body

30
Q

Explain the mechanism by which Thirst is activated by high ECF

A
  • ECF osmolarity increase activates thirst sensors
  • increases water consumption
  • normalises osmolarity
31
Q

How is the thirst mechanism separate from ADH ( 3 reasons )

A

1- Thirst is anticipated ( ex: when you eat )
2- thirst is rapidly suppressed after drinking even if what has driven the thirst is still there
3- threshold for thirst activation is higher than ADH

32
Q

Where are thirst sensors

A
  • suggested to be anterior cingulate cortex in brain
33
Q

What activates thirst sensors ( 3 )

A

1- High ECF osmolarity
2- Bria input ( food )
3- input from body ( dry mouth, hypovalemia )

34
Q

How do kidney’s know what and how much to eliminate (4 steps ) and what Is the result

A

1- imbalance in BV/BP or osmolarity produces a stimulus
2- stretch sensors or Na transporters are activated
3- signals are sent to control centres ( hypothalamus , JG apparatus , heart )
4- Effectors released ( renin , aldosterone, ADH release )
5- Natriuresis, Diuresis , water consumption response

35
Q

What’s the homeostatic mechanism of decrease in ECF osmolarity and decrease in Na ( hint : macula dense )

A
  • Na transporters are activated
  • signals sent to Macula Densa
  • Increase renin production
  • increase Na and H20 reabsorption
36
Q

Which of these treatments for hypertension are working to RAS or Kidneys

1- Diuertics 
2- Calcium channel blockers 
3- ACE inhibitors 
4- AngII receptor antagonist 
5- Beta-adrenergic receptor antagonist 
6- Vasodilators 
7- Renin inhibitors 
8- Aldosterone receptor antagonist 
9- Alpha2 adrenergic receptor
A

1- effect on kidney
2- major effect directly on blood vessels
3- doesn’t allow AngII activation by renin
4- effect kidney
5- affect SNS on renin release
6- major effect directly on blood vessels
7- effect kidney
8- effect kidney
9 -major effect directly on blood vessels

GERR Physiology (18 decks)

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