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Flashcards in Q & A Physiology Deck (20)
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1
Q

How does water get made to move?

A

Under pressure

2
Q

What are the 2 different types of pressure?

A

Hydrostatic pressure and osmotic pressure

3
Q

Why do vasa recta get a lower hydrostatic pressure?

A

Because a lot of hydrostatic pressure is lost at the glomerulus

4
Q

What drives GFR?

A

Hydrostatic pressure which is controlled by afferent and efferent arteriole diameter.

Osmotic pressure controlled by transport of solutes to set up an osmotic gradient and selective water-proofing (aquaporins and ADH)

5
Q

What does glomerular filtration result in?

A

blood that does not contain any cells, protein complexes, and >50 kDa proteins

6
Q

What does GFR depend on?

A

Permeability of membrane

Surface area of membrane

Filtration pressure

7
Q

What determines filtration pressure?

A

Glomerular blood hydrostatic pressure drives filtration out of the glomerulus and osmotic pressure back into the glomerulus

8
Q

How is glucose transport done into the cells from the lumen during reabsorption?

A

Glucose concentration within cell is kept high by co-transporting glucose with sodium into the cell and then opening glucose transporters on the other side to go down the concentration gradient that was created. Most of this happens in the PCT

9
Q

How do we sense BP?

A
Stretch receptors (barorececeptors that sense stretch decrease and stimulate noradrenaline release)
Atrial mechanoreceptors which sense increase in stretch and release ANP
Afferent arteriole stretch (sense myogenic autoregulation)

Osmolarity
(Osmoreceptors sense increase in osmolarity of blood and release ADH)

Kidney function (tubuloglomerular feedback)

10
Q

What do mesangial (macula densa) cells produce?

A

Nitric Oxide

11
Q

How is GFR maintained?

A

Myogenic autoregulation (works well both ways)

AtII (complex; it constricts both arterioles to maintain GFR)

12
Q

What does ANP do?

A

Dilates Aff and constricts Eff to produce more GFR

Tubuloglomerular feedback (movement through kidney is too slow means low BP which interpreted as low salt at DCT and so Afferent arteriole is dilated increasing GFR.

13
Q

How does the sympathetic NS affect GFR?

A

It constricts AA and decreases GFR dramatically

14
Q

How does reabsorption get increased?

A

RAAS (AtII and aldosterone increase Na reabsorption and water follows increasing BP)

ADH opens up CD/CT aquaporins causing water to be reabsorbed

15
Q

How does reabsorption get decreased?

A

ANP Blocks Na+ reabsorption and water follows

16
Q

What happens when there is high amounts of aldosterone?

A

Potassium is leached

17
Q

Where is most AtII activity taking place?

A

At the afferent arteriole and the Proximal Convoluted Tubule.

AtII does affect DCT but not as much as PCT. Aldosterone does most of the work.

18
Q

What is NorAdrenaline’s effect on the Afferent arteriole?

A

Dramatic constriction

19
Q

Why can AtII act as a dipsogen?

A

It can pass the blood brain barrier through leaky tight junctions and interact with the receptors

20
Q

Why does AtII constrict afferent arteriole?

A

MAP is increased all around the body so it is a compensatory mechanism