Renal System 4 Flashcards

1
Q

What are the fluid dynamics like in water?

A

Rapidly equilibriates throughout ICF and ECF, decreases osmolarity

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2
Q

What is the fluid dynamic like in an isotonic solution?

A

It will remain in the ECF, and has no effect on plasma osmolarity

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3
Q

Where is the precursor to ADH made and stored?

A

Made in the hypothalamus and stored in vesicles in the posterior pituitary

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4
Q

What do osmoreceptors in the hypothalamus sense?

A

Increase in Na+ concentration

Increase in osmolarity

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5
Q

When is ADH released into the bloodstream?

A

When a signal is sent to the posterior pituitary

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6
Q

What do osmoreceptors have?

A

Stretch-inhibited cation channels

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7
Q

What can cause cells to shrink?

A

The hypertonic stimulus action channels opening

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8
Q

What triggers action potentials?

A

Na+ entering the cells

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9
Q

What has a linear relationship?

A

Plasma ADH and Plasma osmolarity

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10
Q

Is thirst or ADH more sensitive to regulate?

A

ADH

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11
Q

What can also increase ADH release?

A

A decrease in blood pressure/blood volume

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12
Q

Is there negative feedback in ADH release?

A

Yes, there’s a return to homeostasis when a response brings plasma osmolarity back to normal

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13
Q

What is ADH good at maintaining?

A

Water balance

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14
Q

What is the renin-angiotensin-aldosterone system important in?

A

Maintaining sodium balance and blood pressure regulation

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15
Q

What happens in the juxtaglomerular apparatus?

A

Macula densa cells respond to a decrease in NaCl content by increasing prostaglandins, granular cells in the afferent arteriole release renin and a decrease in pressure in afferent arteriole also acts on the juxtaglomerula cells cause the release of renin

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16
Q

What is the juxtaglomerular apparatus?

A

Where the distal convoluted tubule touches the glomerulus

17
Q

What triggers the release of renin from granular (juxtaglomerular) cells?

A

Low NaCl concentration in the distal tubule (depleted Na)
Decreased perfusion pressure (by granular cells themselves)
Increased sympathetic activity (eg baroreceptors)

18
Q

Examples of triggers for renin release?

A

Low blood pressure
Low blood volume
Low Na content

19
Q

What converts angiotensinogen to angiotensin 1?

A

Renin (released from JG cells in the kidneys) and is the rate limiting step

20
Q

What converts angiotensin 1 to angiotensin 2?

A

Angiotensin converting enzyme (ACE)- in lungs

21
Q

What are the key properties of angiotensin 2?

A

Increases aldosterone release
Vasoconstriction
Increases sodium and water reabsorption in proximal and distal convoluted tubules
Stimulates thirst and salt intake, release of ADH

22
Q

Where/why is aldosterone released?

A

Released from adrenal cortex in response to angiotensin 2

23
Q

What does aldosterone do?

A

It acts on distal tubule and collecting ducts to increase transcription of Na/K+ ATPase pumps thus increasing Na+ reabsorption and K+ excretion, and water reabsorption also increases via osmosis resulting in Na+ and water retention

24
Q

What does the negative feedback from homeostatic plasma levels of Na and K inhibit?

A

Adrenal cortex

25
Q

What does salt increase?

A

Osmolarity

26
Q

What do ACE (angiotensin-converting enzyme) inhibitors reduce?

A

Angiotensin 2

27
Q

What maintains water and salt balance independent of each other?

A

ADH maintains water balance, RAA (renin-angiotensin-aldosterone system) maintains salt balance

28
Q

What is fluid loss/haemorrhage and what does it affect?

A

Isosmotic, affects renin-angiotensin system and antidiuretic hormone

29
Q

How are hormones released?

A

In an hour to hour basis

30
Q

When is RAAS activated?

A

After a number of minutes