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Renal I Final > Lecture 5: Acid/Base Balance > Flashcards

Lecture 5: Acid/Base Balance Flashcards

1
Q

Acid produced from cellular metabolism is eliminated via the lungs in form of CO2, what is a product of the dissociation and what kind of acid is this?

A
  • Carbonic acid
  • Volatile acid
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2
Q

Acid produced from metabolism of protein and eliminated by the kidney is what kind of acid?

A
  • Fixed acid
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3
Q

Calculation of pH

A

pH = log (1/H+)

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4
Q

What is the first line of defense against pH shift?

A

Chemical buffer system

1) HCO3- buffer
2) Phosphate buffer
3) Protein buffer

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5
Q

What is the second line of defense against pH shift?

A

Physiological buffers

1) Respiratory mechanism (CO2 excretion)
2) Renal mechanism (H+ secretion)

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6
Q

What is the biggest source of acid on a daily base?

A

Production of CO2 during aerobic respiration

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7
Q

CO2 from aerobic respiration combines with what molecules to form, and then dissociate into?

A

CO2 + H2O –>H2CO3 –> HCO3- + H+

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8
Q

What is the additional component of the bicarbonate buffer system, molecule involved, and where does it occur?

A

NaHCO3 in ECF

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9
Q

What does NaHCO3 ionize to?

A

Almost completely to HCO3- and NA+

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10
Q

What makes up the phosphate buffer system; when does each act?

A
  • NaH2PO4 (acid) which donates H+ when the [H+] falls
  • NaHPO4 (base) that can accept a free H+ when the [H+] rises
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11
Q

Where is phosphate significantly concentrated in the kidney?

A

The tubules, thereby increasing the buffering power of the phosphate system

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12
Q

What are the protein buffers in ICF and ECF?

A

ECF - albumin

ICF - hemoglobin

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13
Q

Which AA makes these proteins effective buffers, why?

A

Histidine - can bind or release H+

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14
Q

What is the role of hemoglobin as a buffer in the blood?

A
  • Hb buffers the H+ generated from metabolically produced CO2 in transit between the tissues and the lungs.
  • Venous blood is only slightly more acidic than arterial blood despite the large volumes of H+ generating CO2 carried in venous blood
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15
Q

What is the primary ECF buffer against noncarbonic acid charges?

A

H2CO3:HCO3- buffer system

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16
Q

What is the primary ICF buffer; that also buffers ECF?

A

Protein buffer system

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17
Q

We only measure the ECF pH clinically while managing patients, but is the ICF pH important; which is more efficient?

A
  • Intracellular pH affects cell function
  • Intracellular buffer system is more active and efficient in managing major pH changes
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18
Q

What is the most important buffer against carbonic acid changes and the most important urinary buffer?

A

Carbonic acid changes = Hemoglobin buffer

Urinary buffer = Phosphate buffer system

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19
Q

What is the calculation for pH when given HCO3- and PCO2?

A

pH = 6.1 + log ((HCO3-)/(0.03 x PCO2))

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20
Q

If asked to solved for [HCO3-], what is the rearranged equation?

A

[HCO3-] = 10^(pH-6.1) x 0.03 x PCO2

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21
Q

If asked to solve for PCO2, what is the rearranged equation?

A

PCO2 = ((HCO3-)/(10^(pH-6.1) x 0.03))

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22
Q

Why does faster, deeper breathing cause pH to rise?

A

More CO2 eliminated from lungs, which means less H2CO3 is formed, which means less H+ (higher pH)

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23
Q

Which physiologic buffer system responds quickest and which is needed for long term adjustments?

A

Respiratory = quickest (within minutes) by chemoreceptors sending pH

Renal system = long term adjustments (take 24 hour before kicking in)

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24
Q

How are the kidneys able to regulate pH?

A

Kindeys can produce HCO3- to replenish lost supplies

  • When blood is acidic, kidneys reabsorb HCO3- and excrete H+
  • When blood is alkaline, kidneys excrete HCO3- and retain H+
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25
Q

What is acidemia vs. alkalemia and what is the only value needed for measurement?

A

Acidemia indicated an acid pH (less than 7.35)

Alkalemia indicates an alkaline pH (greater than 7.45)

* Only refer to the pH of blood so this is the only value you need!

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26
Q

Respiratory acidosis; what values?

A
  • Result of abnormal CO2 retention arising from hypoventilation
  • pH <7.35 and a PaCO2 above 45 mmHg. HCO3- is normal
27
Q

Respiratory alkalosis; what values?

A
  • Lungs eliminating too much CO2
  • pH > 7.45 and a PaCO2 below 35 mmHg. HCO3- is normal
28
Q

Metabolic acidosis causes, values?

A
  • Inability of the kidneys to excrete normal amounts of acid or a loss of base
  • HCO3- <22 mEq/L and pH below 7.35, PCO2 is normal
29
Q

Metabolic alkalosis causes, values?

A
  • Loss of stomach acid, excess loss of Na+ or K+, renal loss of H+, or gain of base
  • HCO3- >26 mEq/L and a pH >7.45, PaCO2 is normal
30
Q

Normal range for pH, PaCO2, and HCO3- *KNOW THEM*

What is the mnemoic for determing the cause???

A

pH = 7.35 -7.45

PaCO2 = 35-45

HCO3- = 22-26

ROME = Respiratory Opposite Metabolic Equal

31
Q

How to determine if complete or partial compensation?

A

Partial = pH not in normal range and opposite direction of HCO3- and PCO2

* If pH is acidotic and PCO2 is high you know its respiratory acidosis. If the HCO3- is not within the normal range you know you have respiratory acidosis w/ partial metabolic compensation

Complete = pH in normal range and opposite direction of HCO3- and PCO2

32
Q

Label A-F in this diagram

A

A) Acute respiratory acidosis

B) Chronic respiratory acidosis

C) Metabolic alkalosis

D) Metabolic acidosis

E) Chronic respiratory alkalosis

F) Acute respiratory alkalosis

33
Q

How would you interpret this?

A

Metabolic acidosis w/ partial respiratory compensation

34
Q

Kidneys excreting acidic urine or basic urine reduces the amount in which compartment?

A

ECF

35
Q

What occurs if more H+ is secreted in the tubular lumen than HCO3- that is filtered?

A

Net loss of acid from the ECF

36
Q

What happens if more HCO3- is filtered than H+ is secreted?

A

There will be a net loss of base

37
Q

Large numbers of HCO3- and H+ enter the tubular lumen how?

A
  • Large amounts of HCO3- are filtered continuously
  • Large numbers of H+ are secreted into the tubular lumen by tubular epithelial cells
38
Q

What is the major mechanisms by which the kidneys maintain pH; what 2 steps are involved?

A

Regulation of serum bicarbonate concentration by promoting bicarbonate reabsorption and H+ excretion in the urine.

1) Proximal tubule reabsorb majority of HCO3- filtered from the blood, then…
2) Distal tubular secretion of H+ ions occurs

39
Q

If the PCT reabsorbs all of the bicarbonate what occurs to H+; what cells involved in what part of nephron?

A

The late DCT intercalated cells will secrete more H+, and the HCO3- will be left behind in the body

40
Q

If you are in alkalosis what will the PCT do and the late DCT?

A

PCT will not reabsorb all the HCO3-, and late DCT has nothing to do with alkalosis, just acidosis

41
Q

Why is there a net gain of HCO3- in the kidney?

A

Since H+ has a new buffer (NH3 or phosphate), and the H+ is secreted, leaving behind the HCO3-

42
Q

Intercalated cells are inolved in?

A

FIne regulation of acid-base balance

43
Q

2 types of intercalated cells; which is most abundant?

A

Type A (most abundant): H+-secreting, HCO3-reabsorbing, K+-reabsorbing cells

Type B: HCO3-secreting, H+-reabsorbing, K+ secreting cells, oppostie actions of type A

44
Q

How do Type A intercalated cells function; what 2 pumps?

A

They actively secrete H+ into tubilar lumen via 2 types of primary active transport mechanisms: H+ ATPase pumps and H+-K+ ATPase pumps

*Important for helping us when we are acidotic

45
Q

In contrast to Type A cells, where are the pumps for Type B cells and what are they?

A

Active H+-ATPase pumps and H+-K+-ATPase pumps are located at the basolateral membrane and the Cl2-HCO3 antiporters are located at the luminal membrane

46
Q

In the intercalated cells of the dital tubule, a H/CL co-transport is involved with secretion of?

A

H+

47
Q

What does the formationof the H+ inside the cell provide?

A

A gradient for the secretion of more H+ into the lumen to complex with and reabsorb more HCO3-

48
Q

Why is the distal pathway a major site for creating an acidic urine pH 4.5

A

Accounts for only 5% of secreted H+, but the H+ gradient it can form is 900x!

49
Q

What are the 2 main urinary buffers; which is the major?

A
  1. Phosphate buffer (major buffer)
  2. Ammonia buffer
50
Q

The concentration of phosphate in the urine depends on (aka what is the rate limiting step)?

A

Amount of dietary intake and the amount filtered and later reabsorbed in the proximal tubules

51
Q

What is the phosphate buffer rxn?

A

H+ + HPO4 —> H2PO4-

52
Q

The phosphate that is filtered is in what forms; what happens to the phosphate as it moves through the PCT?

A

20% H2PO4

80% HPO4

As H+ secretion decreases the pH in the PCT, up to 50% of the phosphate in the lumen goes to the H2PO4 form.

53
Q

Luminal Na+ is reabsorbed in exchange for, and what does the Na+ leave with?

A

Na+ is reabsorbed in exchange for H+ and the Na+ exits together with the HCO3- formed in the cell, across the basolateral membrane

54
Q

What is the amount of HCO3 generated for each H+ secreted due to what?

A

One HCO3- is generated for each H+ secreted due to titration of the phosphate from the mono- to the di-protonated form. Diprotonated phsophates (H2PO4 is excreted)

55
Q

What is the most abundandnt naturally occuring AA that provides an unending substrate for renal ammoniagenesis?

A

Glutamine

56
Q

Where is glutamine absorbed from and what is it converted to; what else is produced by this rxn?

A

Proximal tubule cells absorb glutamine from peritubular capillaries and convert glutamine into ammonium (NH4) and alpha-ketoglutarate; this rxn also generates 2 HCO3- ions, which are returned to systemic circulation

57
Q

What happens to the NH4 produced from glutamine?

A

Transported across the apical membrane via NHE, and is eventually eliminated in the urine

58
Q

What is the sum of the NH4+ excretion and the titratable acids excreted (in mEq/L) minus the HCO3- (mEq) that might escape in urine called?

A

NET ACID EXCRETION

59
Q

How does RAAS play a role in acid-base of the kidneys?

A
  • Primary role is the aldosterone on the distal tubule and collecting duct to stimulate Na+ reabsorption by principal cells
  • Stimulates intercalated cells in these segments to secrete H+, this effect is both direct and indirect.
60
Q

Explain the direct and indirect effect of aldosterone on acid-base maintenacne?

A
  • Stimulating Na+ reabsorption by principal cells hyperpolarizes the transepithelial voltage
  • Change in transepithelial voltage facilitates the secretion of H+ by the intercalated cells (type A) = indirect effect
  • Aldosterone (and angiotensin II) acts directly on intercalated cells to stimulate H+ secretion via the H+ ATPase
61
Q

Calculation for Anion Gap

A

AG = [Na+] - ([Cl-] + [HCO3])

62
Q

What constitutes a high anion gap metabolic acidosis; what does this mean?

A

Range of 30 mEq/L or more = high anion gap acidosis is virtually always present regardless of what the pH and the [HCO3-] are

63
Q

What is a increases anion gap called; and what causes it?

A

Normochloremia

  • Diabetes mellitus (ketoacidosis)
  • Lactic acidosis
  • Chronic renal failure
  • Aspirin poisoning
  • Methanol poisoning
  • Ethylene glycol poisoning
  • Starvation
64
Q

What is normal anion gap called metabolic acidosis called; what causes it?

A

Hyperchloremic

  • Diarrhea
  • Renal tubular acidosis
  • Carbonic ahydrase inhibitors
  • Addison’s disease

Renal I Final (6 decks)

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