Regulation of ECF volume Flashcards

1
Q

What is the TBW distribution determined by?

A

number of osmotically active particles in each component

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2
Q

What are the major ECF osmoles?

A

sodium and chloride

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3
Q

What is the major ICF osmole?

A

potassium salts

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4
Q

What are the 2 parts of the ECF?

A

plasma and ISF

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5
Q

fraction distribution of water between ICF and ECF

A

ECF - 1/3

ICF -2/3

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6
Q

What happens as a result of changes in sodium content of the ECF?

A

changes in ECF volume which leads to affects on volume of blood perfusing tissues and effective circulating volume and blood pressure

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7
Q

What is sodium regulation dependent on? (hint: what receptors?)

A

high and low pressure baroreceptors

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8
Q

If excessive salt and water is lost what happens to blood pressure? explain

A

decrease PV, decrease venous pressure, venous return, atrial pressure, EDD, SV, CO and bp

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9
Q

If there is salt and water loss what do high pressure baroreceptors do?

A

increase sympathetic VC therefore increasing TPR and bloo dpressure

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10
Q

sympathetic vasoconstriction effects on kidney

A

renal artery constriction and renin increase

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11
Q

What does renin do?

A

cleaves angiotensinogen to angiotensin 1

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12
Q

angiotensin 2 - how does it increase bp?

A

increase sodium and water reabsorption at proximal tubule

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13
Q

What does aldosterone do to increase bp?

A

increase distal tube reabsorption of sodium and water

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14
Q

How is the changes in proximal tubule sodium reabsorption after vomiting achieved?

A

changes in rate of uptake by peritubular capillaries determined by oncotic pressure

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15
Q

Why is the oncotic pressure and hence sodium reabsorption increased after vomiting?

A

sodium and water = wet stuff = lost

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16
Q

How much of sodium and water can be reabsorbed at proximal tubule after vomiting?

A

75%

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17
Q

Why is GFR unaffected after vomiting? When would it be affected?

A

autoregulation - constriction of afferent arteriole and angiotensin 2 constriction on efferent
considerable decrease in mean blood pressure

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18
Q

What regulates distal tubule sodium reabsorption?

A

aldosterone

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19
Q

How is aldosterone secretion controlled?

A

reflexes involving kidney themselves

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20
Q

What are juxtaglomerular cells?

A

large epithelial cells of afferent arteriole before it enters the glomerulus with plentiful granules

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21
Q

What is the macula densa?

A

closely associated loop of distal tubule

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22
Q

JG cells + macula densa =?

A

juxtaglomerular apparatus

23
Q

Where is renin produced? in response to..

A

juxtaglomerular cells

drop in bp

24
Q

What converts angiotensin 1 –> angiotensin 2?

A

ACE

25
Q

Explain the 4 was in which angiotensin 2 increases bp

A

adrenal cortex to produce aldosterone which increases sodium rebabsorption
arteriolar vasoconstriction
medulla oblongata control centre
Hypothalamus –> ADH and thirst

26
Q

Where is the enzyme ACE found?

A

throughout vascular endothelium

greatest proportion in pulmonary circuit

27
Q

How does angiotensin 2 stimulate aldosterone production?

A

stimulates aldosterone secreting cells in the zona glomerulosa of the adrenal cortex

28
Q

Where does aldosterone travel to and what is its effect?

A

in blood to kidney

increase distal tubule sodium reabsorption

29
Q

What is the rate limiting step of sodium reabsorption (angiotensin 2 pathway)

A

renin release as angiotensinogen is always present

30
Q

List the 5 things which controls renin release

A

P in afferent arteriole at JG cells decreases
increased sympathetic nerve activity by beta 1 effect
inversely proportional to sodium delivery at macula densa
angiotensin 2 feedback to inhibit renin
ADH inhibits renin release

31
Q

How do JG cells increase renin release?

A

“renal baroreceptors”

less distension –> more renin

32
Q

What is meant by the JG cells renin pathway being an intrinsic property?

A

occur even if denervated

33
Q

Is GFR increases explain how it is decreased eg tight control

A

increased GFR means more fluid in proximal tubule and flow past the macula densa increases which sends paracrine signals to the JG cells to produce renin. afferent arteriole constricts, resistance increases, hydrostatic pressure decreases and GFR decreases

34
Q

Is osmolarity or ECF volume more important to restore first in an emergency?

A

volume

35
Q

What is normally the main determinant of ADH?

A

osmolarity

36
Q

What should you do in the case of large salt and water loss and why?

A

infuse or drink saline

lose salt and water - replace salt and water

37
Q

Aldosterone and ANP - which increases sodium reabsorption and which increases sodium excretion?

A

Aldosterone - reabsorption

ANP - excretion

38
Q

Why would weight gain occur if someone was given aldosterone?

A

sodium and water retention

39
Q

After a few days of aldosterone administration what happens?

A

spontaneous diuresis due to volume expansion and potassium loss
ANP over-rides aldosterone

40
Q

Is someone with conns depleted of sodium or potassium?

A

potassium

41
Q

What secretes ANP and when?

A

atrial cells

expansion of ECF volume

42
Q

What does ANP cause?

A

natriuresis - loss of sodium and water in urine

43
Q

If blood glucose is uncontrolled in diabetes what happens to glucose in proximal tubule?

A

persists as exceeded TM

44
Q

What does glucose excess in proximal tubule result in?

A

water retention in tubule which dilutes contents

45
Q

Why is sodium reabsorption decreased in hyperglycaemia? Knock on effect of this?

A

concentration gradient decreased as sodium in lumen diluted

glucose shares symport - not reabsorbed

46
Q

In hyperglycaemia why is the fluid not as concentrated in descending limb?

A

sodium and glucose exert osmotic efflux on water to retain it

47
Q

Why is sodium reabsorption in distal tubule decreased in hyperglycaemia?

A

macula densa senses large volume in distal tubule

renin is suppressed

48
Q

Why is ADH ability to conserve water abolished in hyperglycaemia? Why is it stimulated in the first place?

A

interstitial gradient wrecked

losing a lot of fluid - ADH stimulated via baroreceptors as change in volume not osmolarity (osmoreceptors)

49
Q

Cause of hyperglycaemic coma

A

inadequate blood flow to brain - severe salt and water depletion causing thirst and hypotension

50
Q

Cause of hypoglycaemic coma

A

inadequate glucose to brain

51
Q

Why is hyperglycaemia diabetes problem not self limiting?

A

liver still producing glucose

52
Q

What is also transported with sodium and chloride in the loop of henle? importance?

A

potassium

loop diuretics can cause potassium wasting

53
Q

How is energy supplied to the Na/K/Cl transport in ascending loop of henle?

A

Na/KATPase as the co-transporter is passive