Physiology 5 + 6 Flashcards

1
Q

What is the composition of water in the body?

A

Total = 42L
intracellular fluid = 28L
Extracellular = 14L (3L in plasma, 11L in interstitial fluid)

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2
Q

How does the kidney maintain extracellular fluid?

A

By controlling sodium levels. Water follows sodium.

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3
Q

How is the extracellular fluid levels measured?

A

By the baroreceptors:
low pressure - atrial
High pressure - carotid and aortic arch

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4
Q

What happens during vomiting?

A

You lose water and salt - become hypovolaemic.

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5
Q

What happens during hypovolaemia?

A

The low and high pressure barrow receptors reduce firing rate - this reduces inhibition on the hypothalamus - this increases ADH.
Also increases sympathetic vasoconstriction.
increases renin production.

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6
Q

What does an increase in ADH do to increase ECF?

A

It acts on the collecting duct - increases water permeability to reabsorb more water and concentrate the urine.

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7
Q

What is a possible complication of increased ADH during hypovolaemia?

A

we are only reabsorbing water at the collecting duct, so we might become hyposmotic.

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8
Q

What does sympathetic vasoconstriction achieve during hypovolaemia?

A

causes vasoconstriction of all blood vessels, to increase blood pressure. Also causes vasoconstriction of afferent arteriole in particular (which maintains GFR as the efferent arteriole is constricted).

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9
Q

What does the release of renin achieve during hypovolaemia?

A

Renin increases angiotensin II.

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10
Q

What does angiotensin II achieve during hypovolaemia?

A

It causes constriction of the efferent arteriole - this reduces the hydrostatic pressure in the proximal tubule - and since theres less water, oncotic pressure is higher - this causes increased NaCl reabsorption at the proximal tubule and water.

It causes release of aldosterone from the adrenal gland - this increases sodium chloride and water reabsorption at distal tubule.

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11
Q

What are the effects of angiotensin II on the hypothalamus?

A

The cause increased release and production of ADH.

They increase thirst and salt appetite.

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12
Q

What are the steps in RAAS?

A

Liver produces angiotensinogen
juxtaglomerular cells secrete renin
this converts angiotensinogen into angiotensin I
angiotensin convertinge enzyme converts angiotensin in into angiotensin II.

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13
Q

What is the rate limiting step in RAAS?

A

The release of renin.

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14
Q

What stimulates renin release?

A

Paracrine activity from the macula dense - causing secretion of renin from the juxtaglomerular cells.
Macula densa - decreased blood flow past or increased sodium chloride.

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15
Q

What inhibits renin release?

A

Angiotensin II

ADH

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16
Q

In hypovolaemia, is volume or osmolarity most important?

A

Volume - to maintain perfusion to the brain. In normal blood volume, the osmolarity has control over ADH.

17
Q

How does the macula dense control GFR?

A

The macula dense has a porcine effect on the afferent arterioles - it measures the blood flow - to constrict or dilate the afferent arterioles accordingly.

18
Q

What are the actions of angiotensin II?

A

Stimulates aldosterone - NaCl reabsorption at distal tubule.
ADH release from hypothalamus - increased H2O reabsorption from collecting duct.
Hypothalamus - increased thirst and salt
Sympathetic activity - increased vasoconstriction (at afferent arteriole to maintain GFR)
vasoconstriction of efferent arteriole - to reduce hydrostatic pressure at proximal tubules - to increase NaCl reabsorption at proximal tubules

19
Q

What is the main action of aldosterone?

A

Increases reabsorption of sodium (and chloride)

increases secretion of potassium

20
Q

What is ANP?

A

Atrial natriuretic peptide - secreted from the cardiac atria.

21
Q

What triggers a release in ANP?

A

Increased ECF - stretching the atria due to an increased blood pressure.

22
Q

What is the function of ANP?

A

It increases sodium secretion, but has NO EFFECT on potassium.

23
Q

What is aldosterone escape?

A

This is when theres too much production of aldosterone, causing too much sodium retention leading to a massive increase in ECF and blood pressure. To counteract this and to allow the sodium to escape, the cardiac atria secretes ANP - this allows the sodium and fluid to escape, decreasing the fluid volume.

24
Q

What is one side effect of aldosterone escape and hyperaldosteronism?

A

Hypokalaemia - ANP doesn’t reverse the increased secretion of potassium which occurs due to aldosterone.

25
Q

What happens to glucose during diabetes?

A

Theres too much glucose, it exceeds the Tm value, so the excess remains in the filtrate and is excreted in the urine.

26
Q

What does glucose in the tubule do to sodium and water?

A

The glucose creates an osmotic effect on the water, meaning more water is retained in the tubule and less is reabsorbed into the blood.
The increase in water dilutes the sodium - meaning sodiums concentration gradient is weaker and less sodium is reabsorbed.

27
Q

What is the effect of less sodium being reabsorbed on glucose reabsorption?

A

Reduced sodium reabsorption causes reduced glucose reabsorption - because glucose uses a paired transporter with sodium to go against its own gradient and enter the cell.

28
Q

How much urine does a diabetic patient produce?

A

6-8L per day of isotonic urine

29
Q

what is a hyperglycaemic coma?

A

When there’s too much glucose which has caused increased water excretion, leading to hypovolaemia and reduced perfusion to the brain.

30
Q

What is hypoglycaemic coma?

A

When theres too little glucose delivered to the brain.

31
Q

What is a side effect of loop diuretics?

A

Hypokalaemia (because they can inhibit transporters Na_Cl-K - which reduces the reabsorption of potassium along with sodium and chloride).