Volume Disorders

Question 1

Signs/Symptoms of Vol Depletion

Answer 1

• Dec IV fluid –> hypotension/dizziness, low JVP, reflex tachy AND dec renal flow and thus dec GFR
• Dec IT fluid –> poor skin turgor (tenting of skin) and dry mucous membranes

Question 2

Bartter Syndrome

Answer 2

VOL DEPLETION

• Loss of function of Na-K-2Cl, ROMK or basolateral Cl- channels
• Present w/ low EC vol or low BP, reflex elev in renin/angio II and low potassium
• **Looks same as tx w/ loop diuretic

Question 3

Gitelman Syndrome

Answer 3

VOL DEPLETION

• Loss of function of Na-Cl co transporter in early distal tubule
• Present w/ low EC vol or low BP, reflex elev in renin/angio II, low potassium and hypocalciuria
• **Looks same as tx w/ thiazide diuretic

Question 4

Pseudohypoaldosteronism Type 1

Answer 4

VOL DEPLETION

• Loss of function in ENaC or mineralocorticoid receptor –> collecting tubule does not respond to aldosterone
• Present w/ vol depletion, low BP, hyperkalemia despite high aldosterone in blood

Question 5

How does heart failure lead to vol overload?

Answer 5

• Vol overload primarily due to dec CO –> dec in “effective circulating volume” (the blood flow that kidney gets from heart) –> kidney sense low flow –> RAAS –> retain water and Na
• So these is vol overload yet dec filling of renal arterial bed (which act RAAS)

Question 6

What are the 3 ways liver failure can lead to vol overload?

Answer 6

1- Can be due to splanchnic vasodilation/dec systemic resistance –> less “effective circulating volume” –> RAAS

2- Can be inc hepatic sinusoidal pressure –> edema in sinusoids (ascites in R CHF)

3- Can be hypoalbuminemia –> dec oncotic pressure in cap –> edema

Question 7

How does nephrotic syndrome lead to vol overload?

Answer 7

Glomerular protein leakage/ protein lost in urine –> hypoalbuminemia –> dec oncotic pressure –> edema

Question 8

How does end stage renal failure lead to vol overload?

Answer 8

Vol overload primarily due to Na/water retention which inc hydrostatic pressure –> edema

Question 9

Syndrome of Apparent Mineralocorticoid Excess

Answer 9

• Problem w/ OSHD which normally convert cortisol (active) –> cortisone (inactive)
• Now more cortisol which can activate mineralocorticoid receptor (MR) –> inappropriate MR signaling –> chronic Na reabsorption –> hypertension, hypokalemia, low aldosterone

Question 10

Liddle’s Syndrome

Answer 10

• Gain of function (overactivity) in ENaC

- Present w/ HTN, low renin and low aldosterone, hypokalemia

Question 11

Gordon’s Syndrome

Answer 11

• Overactive NaCl co-transporter and inhibition of ROMK

- Present w/ severe HTN and hyperkalemia