RENAL 08: HORMONAL REGULATION OF BODY SALTS Flashcards

1
Q

diuretics that block thick ascending limb of loop of henle lead to what effect on water?

A

Water wasting

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2
Q

What are the conditions for Na balance?

A

Na intake must exactly equal Na excretion

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3
Q

What is a positive sodium balance indicating

A

you have etra sodium retained in volume, so you epand ECF because body holds onto water (hyperosmotic), this expands the blood volume and increases arterial pressure as well as leads to an increase in body weight due to edema

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4
Q

What is a negative sodium balance indicating

A

You have a decrease of sodium intake, and therefore a reduction in ECF (hyposmotic), so you have a volume contraction. Because blood volume is decreasing, this decreases arterial pressure and body weight

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5
Q

What is ECV

A

Effective circulating volume; potion of ECF that is in the vascular system and effectively perfusing tisues

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6
Q

Volume receptors on afferent side of circulation

A

Cardiac atria (will release ANP); intrathoracic veins

This is because of the relationship of salt and volume

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7
Q

Afferent pressure sensors

A

Aortic and carotid baroreceptors (will communicate to brain if shit is going down); afferent arteriole also has an internal baroreceptor

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8
Q

Afferent receptors in kidney specifically

A

Pressure sensors in macula densa will determine if you’ve got too much tubular fluid

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9
Q

Efferent sensors - neurohumoral

A

RAAS
SNS/Catecholamines
ANP/BNP
Prostaglandins

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10
Q

Efferent hemodynamic forces effect on kidney salt excretion

A

GFR effects, peritubular forces will either increase or decrease based on what is required

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11
Q

Renal SnS activity leads to what?

A

Vasoconstrition of afferent arterioles - increased proximal tubule Na reabsorption.
Therefore-decrease GFR but what does go through you absorb more Na from.

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12
Q

Tubuloglomerular feedback

A

Macula densa senses flow and salt content in lumen - this is going to feed back to glomerulus to tell it what to do. if flow and Na are high, this causes contraction of afferent arteriole to decrease GFR. If there is low flow and low salt, prostaglandins and NO will be released to increase filration in the glomerulus.

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13
Q

Reinin is produced by what

A

Cells in the juxtaglomerular apparatus

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14
Q

When is renin secreted?

A

In situations of low sodium

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15
Q

If you have a high salt diet what does your renin secretion look like?

A

It’s low

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16
Q

How do we control renin production (3)

A
  1. SNS nerve activation (NE) - innervate afferent arterioles - activates b1 receptors and produce renin in juxtaglomerular cells
  2. Low pressure on afferent arteriole - intrarenal baroreeptors within juxtaglomerular cells will sense this and produce renin so we hold onto more water
  3. Macula densa - release of ATP causes reduced renin secretionof JG cells - prostaglaindins cause increased renin release from JG cells
17
Q

RAAS system

A

Renin –> Ang I –> ACE makes Ang II-

ANG II and ang III will stimulate aldosterone release from adrenal cortex (under ACTH presence), leaing to a dcrease of Na and H20 secretion. Ang II will also cause for ADH to be released from posterior pituitary

18
Q
ADH affects (salt/water)
Aldosterone affects (salt/water)
A

Water

salt

19
Q

What does aldosterone do

A

Affects late distalt ubule and collecting duct, inserts more NKA and also increases activity

20
Q

Is aldosterone potassium saving or wasting

A

wasting

21
Q

Is aldosterone sodium wasting or saving

A

Saving

22
Q

ANP is released from where

A

Atria (as well as ventricles but mostly atria)

23
Q

ANP is released when

A

when you have a volume overload and stretch is sensed

24
Q

What is the job of ANP

A

Salt wasting

25
Q

How does ANP affect the kidney

A

Affects vasculature similar to ang II , but also affects tubules. Unlike ang II however it has a dual effect:

  1. DILATION of afferent arteriole (causes a net increase in GFR
  2. Suppress renin, aldosterone, and decrese sodium reabsorption
26
Q

Other natriuretic proteins

A

BNP

Urodilatin

27
Q

What is a major cause of edema

A

increase in capillary hydrostatic pressure and decrease in oncotic pressure

28
Q

how do we treat edema

A

diuretics