SM 196: Na Balance Flashcards

1
Q

What is the body’s response to a rapid increase in Na intake?

A

Positive Na Balance occurs as it takes days for excretion to rise to level of intake. Higher ECF osmolality = more thirst = gain of water weight to achieve isoosmotic balance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Na balance is the key controller of ____.

A

ECF Volume Regulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the sensors for Volume regulation? What are the effectors for volume regulation?

A

Sensors: Volume receptors, baroreceptors, macula densa
Effectors: RAAS, SNS, TGF - help regulate renal Na Clearance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the physiologic responses to Volume Depletion?

A
  1. Thorax volume sensors stimulated
  2. Increased Renal SNS = Renin release from granular cells in wall of AA + more PT Na transport through Na/H exchanger
  3. Less stretch = less ANP release = more active Na channels in medullary CD = more Na reabsorption
  4. Low renal blood flow + low GFR = more Ang II EA VC = more GFR = more filtration = high Pi,ptc = more driving force for Na reabsorption (Glom Tub Balance)
  5. Less NaCl to macula densa = renin release (Ang II) + less TGF from adenosine = AA VD = raises GFR
  6. Ang II = EA VC (more GFR) + more PT Na reabsorption through Na/H exchanger + more aldosterone secretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Glucocorticoid-Remediable Aldosteronism vs. Apparent Mineralocorticoid Excess

A

GRA: AD, early onset HTN, suppressible by GCs
caused by 2-enzymes crossed over synthesized together = Aldo produced when ACTH stimulated = too much Na reabsorption

AME: AR, due to mutation in enzyme than inactivates cortisol, causes too much cortisol = bombards aldo receptor = mimicks aldo effects
Low blood aldo level, but high Na reabsorption
Tx: receptor blockers (ARBs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Liddle Syndrome vs. Pseudohypoaldosteronism I

A

LS: AD HTN, activating mutations in ENaC = more Na reabsorption (tx with ENaC blockers)

PHAI: loss of fx in ENaC = high aldo levels but HYPOTENSION

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Bartter’s Syndrome vs. Gitelman’s Syndrome

A

BS: loss of fx mutation in NKCC2, ROMK, Cl basal channel, or Barttin in TAL = less Na reabsorption
Differentiate from overdiuresis b/c urine Cl is high

GS: loss of fx mutation in NCCT in DCT - causes more Ca Reabsorption and less Na Reabsorption = hypokalemic alkalosis, mimicks chronic thiazide diuresis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly