G: Electrolytes

Question 1

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Answer 1

A: K+ is important for regulating intracellular pH / [DNA&Protein synthesis] / RMP / and cardiac&muscular activity. Wide fluctuations from dietary K+ intake WILL NOT change [K+ concentration] in cells or [EXTRAcellular Fluid] = stays pretty constant. There are 2 mechanisms maintaining [K+ homeostasis/ Intake=Output(GI & urinary)]

1. ECF K+ mechanisms
2. adjustment of RENAL K+ Excretion to match dietary K+ intake.

B: When [K+ INtake] > [K+ output] = HYPERkalemia = [+ positive K+ balance]

C: Buffering K+ load is CRUCIAL to preventing life-threatening HYPERkalemia / hypOkalemia

Question 2

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Answer 2

A: Although [K+ amount] in body is determined by Kidneys, Plasma Hormones like [Insulin/Epi/Aldosterone] all move K+ INTO cells–> [DEC Plasma K+]. Decreasing these hormones will increase plasma K+.
A2:
ºInsulin IS MOST important [K+ uptake hormone]= shifts K+ into cells postprandial
ºEpi acting on [BETA 2 RECEPTORS]—> K+ UPTAKE INTO CELLS
º[Aldosterone] simulates [Na/K ATPase pump] which INC K+ SeCretion—> INC urinary K+ EXCRETION
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B: [Plasma K+], Aldosterone and ADH regulate [Renal K+ Excretion]. [Bodily Na/K ATPase pump] can [DEC Plasma K+] when stimulated by high amounts of extracellular K+
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C: Epi acting on [alpha 1 receptors] during exercise–> K+ release out of cells–> [INC Plasma K+]

*[Cell Lysis (surgery/burns)] and *[HyperosmoLality (cells shrink & become too concentrated in K+ so K+ leaves into plasma] —-> INC [Plasma K+].

Question 3

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Answer 3

A: Normally K+ is 85% ReAbsorbed and only 15% of it is Excreted Renally. K+ Diet changes can alter this.
ºDEC dietary K+ —> INC K+ ReAbsorption = 99%
and
ºINC dietary K+(eating too much K+) —-> INC K+ SeCretion and EXCRETION = 80% = “K+ spilling” but this takes hours
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B: K+ SeCretion INTO the [DCT and CD] is regulated by 3 things:
1) [Na/K ATPase pump]
2) [Tubular cell to Lumen electrochemical gradient] = -40 mV
3) [K+ permeability of (Apical Lumen) membrane]

C: K+ SeCretion can also be altered by
1. Hormones: [Glucocorticoids INC K+ SC indirectly by INC GFR] & Aldosterone

2A. [Tubular Fluid Flow] (Diuresis vs. ANTIdiuresis) displays Opposing Effects of ADH On K+ Secretion.

2B: [Diuresis/ INC DCT Fluid Flow] –>INC K+ Secretion & DEC ADH –> DEC Tubular negativity–>ultimately DEC K+ secretion or K+ is maintained
{it is exact opposite for ANTIdiuresis}

Question 4

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Answer 4

A: EXCRETION of K+ depends on rate and direction of K+ transport by DCT and CD. During [DEC Dietary K+ Intake/Depletion] only 1% of Filtered Load K+ is Excreted (vs. normally 15-80% is Excreted).

C: [CHRONIC metabolic acidosis] has long-term effect after days. It uses a [K+/H+ exchanger] which moves [K+ OUT OF Tubule] and H+ in—> [INC Plasma K+].

2. These INC Plasma K+ will activate aldosterone system—>[INC K+ permeability of apical DCT/CD] AND thus returns [INC K+ SeCretion & Excretion]

Question 5

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Answer 5

“All Monkeys Like Hot Sex”! –>
[Acetazolamide/PCT]

[Mannitol/(descending LOH)]

[Lasix/ (Ascending THICK LOH)]

[HCTZ/DCT]

[Sparing Diuretics/CD]

A: [K+ WASTING Diuretics]
ºLASIX/FUROSEMIDE
ºACETAZOLAMIDE
ºMANNITOL

Question 6

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Answer 6

“All Monkeys Like Hot Sex”! –>
[Acetazolamide/PCT]

[Mannitol/(descending LOH)]

[Lasix/ (Ascending THICK LOH)]

[HCTZ/DCT]

[SAT Sparing Diuretics/CD]

A: [K+ Sparing Diuretics :-) ]

• spironolactone
• amiloride
• triamterene

Question 7

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Answer 7

A: [Multivalent ions Ca+ and inorganic phosphate (Pi)]. Normally, Renal EXCRETION of [Ca+ & Pi] are balanced by GI Absorption / [Bone Resorption] / [INC Renal tubular ReAbsorption INC]

B: Pi is an important buffer in cells, plasma and urine.

C: During pregnancy, [GI Absorption] actually EXCEEDS [Renal excretion] and [Ca+ & Pi] accumulate in newly formed fetal tissue/bone!

E: 99% of body Ca+ is stored in bone as [Calcium phosphate].{ 0.9%=ICF and 0.1%= ECF }. [Plasma Ca+ is 50% FREE floating ionized] / 45% protein bound / 5% complexed]
ºAcidosis—> INC [Free Floating ionized Ca+] = HYPERcalcemia

º alkalosis—> decreases [Free Floating ionized Ca+] Ca+ by binding them to albumins = hypOcalcemia

Question 8

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Answer 8

A:1) INC [calciTRiol/vitamin D3 metabolite] —> [INC Renal Absorption of Ca+]—-> [DEC Ca+ EXCRETION].
and
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B: DEC [Plasma Ca+]–> INC PTH—>
1. [INC ReAbsorption of Ca+ by Kidneys]
2. INC calciTRiol —> INC [Bone resorption]
………..BOTH—> [INC Plasma Ca+]

D: INC [Plasma Ca+] –> INC Calcitonin–> [INC (Ca+ Bone Deposition) AND [Ca+ & Pi Excretion] = “Calcitonin saves the day from too much Ca+ & Pi and DECREASES [Plasma Ca+ & Pi]!”

E: 99% of Filtered Ca+ is ReAbsorbed really and this occurs by both ACTIVE and passive mechanisms along nephron transcellular and PARAcellular pathways. Pumps like the [Ca+ATPase] and [3Na/1Ca ANTIporter] are used

F: Calcitonin is made in the Thyroid

Question 9

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Answer 9

A: 86% of body {Pi} is stored in bone as [Calcium phosphate].{ 14%=ICF and [almost nothing in ECF] }. [Plasma Pi is 10% protein bound. [NET {Pi} intake = 500 mg/day]

B: PTH–> [INC Plasma Pi & Ca+ from bone resorption] BUT also [INC Pi EXCRETION specifically lol]

C: INC [calciTRiol/vitamin D3 metabolite] —> INC Bone resorption AND [DEC {Pi} EXCRETION]

D: [“Spill-Over” effect] = [Plasma phosphate] concentration is very close in amount to [Renal Plasma Threshold] for phosphate –>means Kidneys prevent [Plasma phosphate] from getting too high!

E: PTH is weird monkey when it comes to {Pi}! It works with [calciTRiol in the blood to [INC plasma {Pi}] BUT works with

[Calcitonin in Kidneys to [DEC Plasma Pi]

Question 10

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Answer 10

1. [0.9% NaCl Saline = 308 mOsm/L]

2.

Question 11

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Answer 11

A2: [Pancreatic Diabetes Mellitus]–> DKA–> INC H+ and therefore [DEC Cl- AND (HCO3 as it buffers H+)]—-> INC Anion Gap
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a3: vomiting—> DEC H+—> [INC HCO3] BUT also [DEC Cl-]
—> [Anion Gap STAYS CONSTANT]