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Question 1

Sodium is reabsorbed in 3 ways:

Answer 1

Na+ channel
Co-transport
Exchange

Question 2

Function of C.A. inhibitors (+ downstream effects)

Side effect?

Answer 2

Inhibit intracellular C.A. –> decrease H+ secretion for HCO3 reabsorption –> decreased Na exchange –> diuresis

Acidosis (decreased HCO3 reabsorption)

Question 3

Function of loop diuretics

Side effects?

Answer 3

Inhibit NaKCl2 –> doesn’t draw water out of descending limb –> diuresis

Doesn’t build intracellular K+, so no leakage back into lumen, so no positive lumen, so no Mg/Ca reabsorption

Excretion of H2O, Na, K, Mg, Ca, Cl
Hypomagnesemia, hypocalcemia

Question 4

Function of thiazides

Side effect?

Answer 4

Inhibit Na/Cl cotransporter –> Na+ excretion –> diuresis

Low intracellular Na+ causes basolateral exchange for Ca++, encouraging apical calcium intake

Question 5

How do loop diuretics and thiazides affect body pH?

Answer 5

Alkalosis

Loss of water = more H+ mopped up by bicarbonate

Question 6

3 main mechanisms of aldosterone

KNOW THESE

Answer 6

Increase Na+ channels

Increase H+ ATPase

Increase Na/K ATPase

Question 7

Results of aldosterone antagonists

Answer 7

Inhibit Na reabsorption

Inhibited H+ secretion

Inhibited K+ secretion

Hyperkalemia, acidosis

Question 8

When looking at an ABG, specifically pH and HCO3 (acid-base problem), how do you know if it’s respiratory or metabolic?

Answer 8

Same direction = metabolic

Opposite directions = respiratory

Question 9

Equation for calculating blood osmolality

Answer 9

2[Na] + Glc/18 + BUN/2.8

Question 10

In ANY azotemia, will creatinine increase or decrease?

Answer 10

Increase

Question 11

In ANY azotemia, will BUN increase or decrease?

Answer 11

Increase

Just depends on how much compared to creatinine

Question 12

In renal azotemia, why is FENa >2%?

Answer 12

Lost ability to reabsorb Na+ somehow

Question 13

In pre-renal azotemia, why is FENa

Answer 13

Not as much Na+ is getting to the nephron