Control of Plasma pH Flashcards

1
Q

State the normal plasma pH range

A

7.35-7.45

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2
Q

Compare Acidaemia and Acidosis

Is Acidaemia or Alkalaemia more dangerous?

A

Acidaemia is low blood pH due to acidosis

Alkalaemia is more dangerous

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3
Q

How does Alkalaemia affect Ca and nerves?

A
  • Reduces solubility of Ca salts, so free Ca2+ leaves ECF and binds to bone and proteins-> Hypocalcaemia
  • This makes nerves more excitable-> Parasthesia and Tetany (Uncontrolled muscle contractions)
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4
Q

What is the mortality rate if pH is above;

  • 7.55
  • 7.65
A
  • pH>7.55 mortality: 45%

- pH>7.65 mortality: 80%

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5
Q

How does Acidaemia affect K+ movement?

When are effects of Acidaemia seen? When is it life threatening?

A
  • Affects enzyme function, leading to K+ movement out of cells-> Hyperkalaemia
  • Effects seen below pH 7.1
  • Life threatening below pH 7.0
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6
Q

The ECF [H+] is very low so small amounts of acid would change pH dramatically. This is buffered by H+ binding to various sites

What is the most important ECF buffer for H+?

A

The CO2/ HCO3 system

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7
Q

Compare Respiratory Acidaemia and Alkalaemia

How are they compensated really?

A
  • Acidaemia: Rises in pCO2
  • Renal compensation: Increased HCO3
  • Alkalmaemia: Falls in pCO2
  • Renal compensation: Decreased HCO3
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8
Q

Compare Metabolic Acidosis and Alkalosis

How are they compensated by the respiratory system?

A
  • Acidosis: Decreased HCO3
  • Respiratory compensation: Reduced pCO2 (hyperventilation)
  • Alkalosis: Increased HCO3
  • Respiratory compensation: Increased pCO2 (hypoventilation)
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9
Q

Why is Respiratory compensation of metabolic alkalosis limited?

A

Hypoventialtion is limited as it can cause hypoxaemia

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10
Q

If acid is produced metabolically, recovery of l filtered HCO3 will be insufficient to restore plasma [HCO3].

How does the kidney compensate?

A
  • Kidney makes HCO3 (normally only made in RBCs)
  • The byproduct of this, H+, must be excreted into urine
  • To prevent a damaging urinary acidity, the H+ must be buffered by other filtered substances or by buffers made in the kidney
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11
Q

How much HCO3 is reabsorbed in;

  • PCT
  • TAL
  • DCT, via Intercalated cells
A

PCT: 80-90%
TAL: Up to 15%
DCT, Intercalated cells: Remaining

(Overall, 100% of HCO3 is reabsorbed)

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12
Q

Describe HCO3 reabsorption in CD Intercalated cells

A
  • H-ATPase on AM pumps H+ out (Na gradient too low to use NHE)
  • CO2 enters cell and reacts with water-> H2CO3 which dissociates into H+ and HCO3-
  • New HCO3- ions enter blood via HCO3-Cl Antiport on BM
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14
Q

Compare H+ buffering systems in PCT and DCT

A

PCT;
- NH3 from Glutamine diffuses into lumen and combines with H+-> NH4+

DCT;
- H+ pumped out via H-ATPase into lumen and combines with Monobasic phosphate (HPO4 2-)-> H2PO4-

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15
Q

Describe how HCO3 is created in PCT (and also some in DCT)

A
  • Glutamine broken down into NH4+ and Alpha-ketoglutarate
  • NH4+ dissociates into NH3 and H+, NH3 diffuses into lumen and binds to H+ to reform NH4+ (in lumen)
  • Alpha-ketoglutate breaks down into 2 HCO3 ions, which enter blood via Na-HCO3 symport on BM
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16
Q

How does ECF pH affect secretion of acid by kidney?

Why is this done?

A

Fall in pH-> Increased acid secretion into lumen

To prevent HCO3 depletion (Used to neutralise pH)

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17
Q

Why does acidosis cause Hyperkalaemia?

A
  • More H+ enters cell from ECF, so more K+ enters ECF from cell
  • Less K+ excreted in distal nephron

(In alkalosis, less K+ enters ECF and more is excreted)

18
Q

Why does Hyperkalaemia cause acidosis?

A
  • Tubular cells more alkaline, as H+ moves out of cells and K+ moves in
  • To counter alkaline, HCO3 excreted in blood
19
Q

What are 4 causes of metabolic acidosis

A
  • Excess acid production metabolically (Lactic)
  • Acid ingestion
  • Impaired renal acc excretion
  • HCO3 loss
20
Q

If excess acid is produced metabolically, what replaces HCO3 in plasma?

A

The associated anion

This influences the anion gap

21
Q

What is the Anion gap? (Normally 8-14mM)

How does anion gap change when HCO3 is replaced by an anion not included in the calculation group?

A

Difference between combined sum of [K] and [Na] and combined sum of [Cl] and [HCO3]

Anion gap increases when HCO3 replaced (Renal acidosis doesn’t change anion gap as Cl replaces HCO3)

22
Q

What does the anion gap represent?

A

ECF level of unmeasured ions

23
Q

How do we differentiate between ;

  • Renal compensation of respiratory alkalosis
  • Respiratory compensation of metabolic acidosis
A

Anion gap will be increased in metabolic acidosis

24
Q

Explain the effect of Ethylene Glycol on the Anion Gap if ingested

What are the 2 substances this chemical is found in?

A
  • Increases anion gap
  • Due to acids produced by its metabolism
  • Engine coolants
  • Anti freeze

(Can be ingested as suicide attempt/ accident)

25
Q

List 4 signs/ symptoms of Ethylene Glycol ingestion

A

CNS related;

  • Slurred speech
  • Confusion
  • Stupor
  • May be misdiagnosed with alcohol intoxication
26
Q

What are 2 diagnostic clues of Ethylene Glycol ingestion

A
  • Anion gap acidosis

- Oxalate crystals in urine with renal failure

29
Q

Monobasic phopshate (HPO4 2-) is a H+ buffer in urine.

When does it become more effective?

A

Gets more effective as urine pH falls (Urine [H+] increases)