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PHGY 210 > Renal (K+ and H+) > Flashcards

Renal (K+ and H+) Flashcards

1
Q

What is the important of the potassium ion in the body?

A

K+ = most abundant INTRACELLULAR ion
98% in intracellular fluid, 2% in extracellular fluid

K+ concentration in extracellular fluid → excitable tissues (nerve and muscle, including cardiac muscles)

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2
Q

What are the resting membrane potentials of the excitable tissues related to ?

A

Directly related to relative intacellular and extracellular K concentrations

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3
Q

What concentrations of K+ are considered to be Hyperkalemia and Hypokalemia?
What do these concentration cause?

A

Hyperkalemia = high extracellular concentration > 5 mEq/L

Hypokalemia = low extracellular concentration < 3.5 mEq/L
*Very narrow range

Both cause abnormal rhythms of the heart and abnormalities of skeletal muscle contractions

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4
Q

REVIEW SLIDE 4!

A
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5
Q

How is potassium balance maintained?
(Intake and Excretion)

A

By Dietary Intake!!
Orange juice, banana, watermelon, pinapple, nuts, potatoes, tomatoes

Excretions = 90% excreted into urine + 10% excreted into faces

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6
Q

How does renal regulation of potassium work?

A
  • K is filtered freely at glomerulus (just a bit, not so much)
  • Normally, tubules reabsorb most of the filtered K, so very little is secreted
  • But K+ can be secreted at the cortical collecting ducts (can go seen in urine even if almost all reabsorbed)

*Changes in K excretion due to changes in K+ secretion in the CCD (come in the DCT)
*net reabsorption normally around 86% (15-99%)

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7
Q

How is K+ secretion in the CCD done (pump level)?

A

Coupled with Na+ reabsorption
Counter-transport

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8
Q

Which 2 factors regulate K secretion?

A
  1. Dietary intake of potassium
  2. Aldosterone
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9
Q

What is the process of regulation of K+ secretion by dietary intake and aldosterone?

A

↑ K+ intake → ↑ Plasma K+ → In the Adrenal Cortex: ↑ Aldosterone secretion → ↑ Plasma aldosterone → In the CCD: ↑ K+ secretion → ↑ K+ excretion

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10
Q

How can the renin-aldosterone system impact the excretion of K+ and Na+?

A

Na+ and K+ go opposit ways!!!

↓ Plasma volume → ↑ Plasma Angiotensin II → In the Adrenal Cortex: ↑ Aldosterone secretion → ↑ Plasma aldosterone → In the CCD: ↑ K+ secretion → ↑ K+ excretion + ↑ Na+ reabsorption → ↓ Na excretion

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11
Q

What is Hyperaldosteronism?

A

When adrenal hormone aldosterone is released in excess

Most common cause: adenoma (tumor-like) of adrenal gland → produces aldosterone autonomously

Increased fluid volume, hypertension (bc increases reabsorption of Na+), hypokalemia
Renin is suppressed
Metabolic alkalosis is often seen as well

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12
Q

What is the physiological concentration of H+?

A

pH of about 7.4 (tightly controlled between 7.35 - 7.45)
H+ concentration = 40 nmol/L

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13
Q

Which reaction is used to control H+ concentration in the body?

A

Carbonic anhydrase:
CO2 + H2O ←→ H2CO3 ←→ HCO3- + H+

*When body gains a bicarbonate ion = body losing 1 H+

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14
Q

What are different sources of H+ gain for the body?

A
  • Generation of H+ from CO2 (if too much CO2)
  • Production of nonvolatile acids from the metabolism fo protein and other organic molecules
  • loss of bicarbonate in diarrhea or other nongastric GI fluids
  • loss of bicarbonate in urine
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15
Q

What are different sources of H+ loss for the body?

A
  • Utilization of H+ in the metabolism of various organic anions
  • loss of H+ in vomitus (only way to lose H+ from the GIT)
  • in the urine (physiological or pathological)
  • Hyperventilation (loss of CO2 favours the reversed reaction which utilizes H+)
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16
Q

Which are the most important nonvolatile acids?

A

Phosphoric acid
Sulfuric acid
Lactic acid

*Average net production = 40-80 mmmol of H+/day (rate of use ot these acids)

17
Q

What is a buffer?
Which are the major extracellular and intracellular buffers?

A

Any substance that can reversibly bind H+ ions
H+ + buffer ←→ Buffer

Helps maintaining the concentration of H+ ions in a tight range

pH = -log [H+]

Extracellular buffer: CO2 and HCO3-
Intracellular buffer: phosphates and proteins

*Buffering NOT eliminate H+ ions from body, keeps them locked

18
Q

Which systems are responsible for H+ balance?

A

Respiratory system (controls CO2)
Kidneys (control HCO3-)

They work together to minimize change in pH

19
Q

What are the 2 possibilities for renal control of pH via HCO3- control?

A

Low H+ concentration (high pH: alkalosis) → Kidneys excrete HCO3-

High H+ concentration (low pH: acidosis) → Kidneys produce new HCO3- and add to plasma

20
Q

What does the HCO3- reabsorption look like in the kidneys?

A

80% in the Proximal tubule
15% in Thick ascending limb
5% in CCD
0% excreted except in case of alkalosis

21
Q

How is addition of new HCO3- to plasma achieved?
In case of acidosis

A
  1. H+ secretion and excretion on nonbicarbonate buffers (ex: phosphates)
  2. by glutamine metabolism with NH4+ excretion

*Both can be viewed as H+ excretion by the kidney
Kidneys normally contribute enough new HCO3- to plasma to compensate the 40-80 mmol/day generated by use of nonvolatile acids

22
Q

What is the process of reabsorption of HCO3-?

A

*Not that H2O and CO2 are available everywhere

In the tubular epithelial cells:
1. CO2 + H2O → H2CO3 → HCO3- + H+ (Carbonic Anhydrase)
2. HCO3- reabsorbed to interstitial fluid
3. H+ goes into tubular lumen by H+/K+-ATPase and Na+/H+ anti-porter where it is coupled with HCO3-
In thubular lumen: HCO3- + H+ → H2CO3 →CO2 + H2O (reversed rxn)

23
Q

What is the process by which new HCO3- added to plasma in case of need by H+ secretion and excretion on nonbicarbonate buffers (ex: phosphates)?

A

*Only after all HCO3- has been reabsorbed and no longer is available in the lumen

24
Q

What is the process by which new HCO3- added to plasma in case of need by H+ secretion and excretion on nonbicarbonate buffers (ex: phosphates)?

A

*Only after all HCO3- has been reabsorbed and no longer is available in the lumen

In the tubular epithelial cells:
1. CO2 + H2O → H2CO3 → HCO3- + H+ (Carbonic Anhydrase)
2. HCO3- reabsorbed to interstitial fluid
3. H+ goes into tubular lumen by H+/K+-ATPase and Na+/H+ anti-porter where it is coupled with HCO3- (Up to there, same as HCO3- reabsorption)
4. In tubular lumen:
HPO4 2- (filtered) Acting as buffer + H+ → (H2PO4) - → excreted

25
Q

What is the process by which new HCO3- added to plasma in case of need by glutamine metabolism with NH4+ excretion ?

A

*Mainly in the proximal tubule
H+ excretion bound to NH3

  1. Glutamine from interstitial fluid and from tubular lumen (by Na+ cotransport) enters tubular epithelial cells
  2. In tubular epithelial cells: Glutamine → HCO3- + NH4+
  3. HCO3- is reabsorbed
  4. NH4+ goes into tubular lumen by counter-transport with Na+
  5. NH4+ is excreted
26
Q

What is the primary cause of Alkalosis and Acidosis?

A

Respiratory alkalosis and acidosis

All other causes are classified as metabolic alkalosis and acidosis

27
Q

What is does the renal response to acidosis look like?

A
  1. Sufficient H+ are secreted to reabsorb all filtered HCO3-
  2. Body still has too much H+ so kidneys have to produce more HCO3- by different ways such as HPO4 2-
  3. Tubular glutamine metabolism and NH4+ excretion increased (new HCO3- in plasma)

Net result: More new HCO3- in plasma compensates for acidosis + urine highly acidic (lowest attainable pH = 4.4)

28
Q

What is does the renal response to alkalosis look like?

A
  1. Significatn HCO3- excreted in urine
  2. Little to no H+ secretion on non-HCO3- urinary buffers
  3. Tubular glutamine metabolism and NH4+ excretion ↓ so little or no new HCO3- added to plasma

Net result: Plasma HCO3- decrease + highly alkaline urine (pH > 7.4)

29
Q

REVIEW SLIDE 6 OF H+ lecture

A
30
Q

What are clinical examples of Respiratory and Metabolic acidosis and alkalosis?

A

Respiratory acidosis: too much CO2 ex: respiratory failure with CO2 retention

Respiratory alkalosis: not enough CO2, ex: hyperventilation

Metabolic acidosis: diarrhea (loss of HCO3-), renal failure (accumulation of inorganic acids) *when excess of H+ not caused by CO2

Metabolic alkalosis: too much HCO3- base, vomiting (loss of H+), hyperaldosteronism (increase H+ secretion in DCT and CCD)

31
Q

What are diuretics?

A

Drugs used clinically to increase the volume of urine excreted

Act on tubules to inhibit reabsorption of Na, along with chloride and/or bicarbonate → increase excretion of these ions
H2O excrtion increases too

32
Q

What are loop diuretics?
Give an example

A

Acts on thick ascending limb of the loop of Henle
Inhibits cotransport (reabsorption) of Na+, Cl- and K+ (Na+-K+-2Cl-cotransporter)
*One of the most commonly used diuretics
ex: furosemide

33
Q

What are Potassium-sparing diuretics?
Give an example

A

Inhibit Na reabsorption and K+ secretion in the CCD (diffusion across tubular lumen-CCD epithelial cells)
Unlike other diuretics, plasma concentration of K+ does not decrease
*Used for hypokalemic patients

Blocks action of aldosterone or blocks epithelial Na+ channel in CCD (aldosterone-regulated) (aldosterone usually upregulates these pumps)

ex: amiloride, spironolactone

34
Q

What are clinical uses of diuretics?

A
  • Renal retention of salt and H2O (edema)

ex: congestive heart failure (lowering cardiac output) bc water in the lungs

ex: hypertension caused by renal retention

35
Q

What are common features of kidney diseases or failures?

A
  • Proteinuria (protein in urine) → problem at level of GFR
  • Accumulation of waste products in blood (ex: urea, creatinine, phosphate, sulfate)
  • High K+ concentration in blood
  • Metabolic acidosis (accumulation of phosphate, sulfate, etc.)
  • Anemia (decrease secretion of erythropoietin)
  • Decrease secretion of 1,25-VitamineD → hypocalcemia
36
Q

What are treatments for kidney failures?

A

When 90% nephrons start working, can’t sustain life → need renal replacement therapy

Renal replacement therapy options:
1. Hemodialysis
2. Peritoneal dialysis
3. Kidney transplantation

37
Q

What is Hemodialysis?

A

A form of renal replacement therapy, you connect to a machine and filter the blood
4h, 3x/week

38
Q

What is Peritoneal dialysis?

A

A form of renal replacement therapy
Lining of patient’s own abdominal cavity (peritoneum) used as dialysis membrane

Fluid injected into cavity via tube inserted through abdominal wall → Solutes diffuses into fluid from person’s blood → Fluid changes several times/day
*Don’t have to go to hospital

39
Q

What is the major problem with kidney transplantation?

A

The shortage of donors
(Donors can function quite normally with one kidney though)

PHGY 210 (7 decks)

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