Homeostasis and pH Flashcards

1
Q

How is the body a net producer of acid?

A
  • The Krebs cycle produces CO2 – volatile acids
  • Metabolism of many foodstuffs produces H+ that consumes bicarbonate – non-volatile acids, such as phosphoric and lactic acids.
  • Majority of gut segments secrete bicarbonate into the lumen and hence protons into blood.
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2
Q

What affects the acid-base balance in the body?

A

Disease
Diet
Poisoning

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3
Q

What is PaCO2 directly proportional to?

A

Rate of CO2 consumption / Alveolar ventilation rate

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4
Q

What does increased and decreased PaCO2 indicate?

A

Increased PaCO2 indicates hypoventilation

Decreased PaCO2 indicates hyperventilation

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5
Q

Describe acid-base regulation at the kidney.

A
  • A fall in bicarbonate stimulates an increase in net acid excretion by the kidney
  • Long term compensatory adjustments – hours to days
  • Absorbs or excretes acids and bases, produces HCO3- to replenish that lost in buffering
  • If blood is acidic, the kidneys reabsorb HCO3- and excrete H+
  • If blood is alkaline, the kidneys excrete HCOs- and retain H+
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6
Q

Name the 4 simple acid-base disorders.

A

Metabolic acidosis
Metabolic alkalosis
Respiratory acidosis
Respiratory alkalosis

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7
Q

What is acidaemia/alkalaemia?

A

Blood pH is less than 7.35 or greater than 7.45. too much or too little acid or base in blood.

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8
Q

What are respiratory and metabolic disturbances indicated by?

A

Respiratory is indicated by blood PaCO2.

Metabolic is indicated by blood bicarbonate.

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9
Q

What are the normal pH, bicarbonate and CO2 values?

A

pH = 7.4
Bicarbonate = 24 mmol/l
CO2 = 40 mmHg

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10
Q

What is metabolic acidosis the result of?

A

Metabolic acidosis is the most common disorder. Resulting from an increase of acid or by excess loss of bicarbonate.

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11
Q

What are the most common causes of metabolic acidosis?

A
  • Endogenous sources of acids e.g. uremia (uremic acids)
  • Exogenous sources of acids e.g. ethylene glycol toxicity (glycolic acid)
  • Ketosis (keto acids)
  • Lacticacidemia (lactic acid)
  • Aspirin toxicity (acetylsalicylic acid)
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12
Q

What are the 2 causes of metabolic alkalosis?

A
  • GI or urinary H+ loss through vomiting or via the urinary tract
  • Base gain is a less common mechanism
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13
Q

What are the symptoms and treatments of metabolic alkalosis due to GI/urinary H+ loss?

A
  • Vomiting (most common)
  • Renal losses as compensation for primary respiratory acidosis
  • Loop/thiazide diuretics
  • Hyperaldosteronism
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14
Q

What are the treatments of metabolic alkalosis due to base gain?

A
  • Administration of sodium bicarbonate to treat metabolic acidosis
  • Administration of organic ions which are metabolized to HCO3 - (e. citrate in blood transfusions)
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15
Q

What are the causes of respiratory acidosis?

A

Hypoventilation or decreased gas exchange due to:

  • Severe pulmonary diseases e.g. respiratory obstruction
  • Neuromuscular disorders that impair the mechanics of breathing
  • Drugs that decrease respiratory rate (general anaesthetics, opiates)
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16
Q

What are the causes of respiratory alkalosis?

A

Hyperventilation

  • Hypoxaemia, such as congestive heart failure, hypotension, anaemia
  • Altitude – most obviously in man
17
Q

What is involved in chronic respiratory disorders?

A
  • Mismatch between PCO2 and pH, in fact pH can be relatively normal
  • Both HCO3 and PCO2 are increased (see arrows), movement in same direction is compensatory; bicarbonate tells us it is not acute respiratory acidosis here
  • Compensatory processes at kidney
18
Q

What are the interpretative steps to determine acid-base disorders and arterial blood gas?

A
  1. Check PO2
  2. Check pH – trend to acidosis or alkalosis?
  3. Look at PCO2 vs pH. Do they match?
  4. Look at bicarbonate. Is that normal?
  5. What is the compensation, if any?
  6. Check signs
  7. Identify disorder
19
Q

Summarise metabolic acidosis in terms of pH, H+ concentration, primary effect and secondary effect.

A

Decreased pH
Increased H+
Decreased HCO3-
Decreased PCO2

20
Q

Summarise metabolic alkalosis in terms of pH, H+ concentration, primary effect and secondary effect.

A

Increased pH
Decreased H+
Increased HCO3-
Increased PCO2

21
Q

Summarise respiratory acidosis in terms of pH, H+ concentration, primary effect and secondary effect.

A

Decreased pH
Increased H+
Increased PCO2
Increased HCO3-

22
Q

Summarise respiratory alkalosis in terms of pH, H+ concentration, primary effect and secondary effect.

A

Increased pH
Decreased H+
Decreased PCO2
Decreased HCO3-

23
Q

What is the mechanism of anaesthetic induced acidosis?

A
  1. Anaesthesia depresses ventilation, (maybe tissue hypoxia so increased lactic acid)
  2. Increased CO2 concentration. Detected by chemoreceptors.
  3. Increased H+ concentration
  4. Respiratory and metabolic acidosis
  5. Detected by kidneys
24
Q

What is the mechanism of altitude induced respiratory alkalosis?

A
  1. Primary increased ventilation
  2. Decreased CO2 concentration
  3. Decreased H+ and HCO3- concentrations due to equilibrium
  4. Chemoreceptors unable to decrease ventilation. Renal response.
  5. At altitude, ventilation driven by hypoxia not PaCO2 so PaCO2 stays low.
25
Q

What is the mechanism of vomiting induced metabolic alkalosis?

A
  1. Primary loss of H+ so decreased H+ concentration
  2. Increased HCO3- concentration
  3. Metabolic alkalosis
  4. Renal response and chemoreceptors decrease ventilation rate
  5. Increased CO2 to increase H+ concentration. (Regulated by chemoreceptors to decrease and increase CO2)
26
Q

What is the mechanism of diarrhoea induced metabolic acidosis?

A
  1. Primary loss of HCO3- so decreased HCO3- concentration
  2. Increased H+ concentration
  3. Metabolic acidosis
  4. Renal response and chemoreceptors increase ventilation rate
  5. Decreased CO2 to increase HCO3- concentration
27
Q

Why is diarrhoea induced metabolic acidosis more complicated?

A
  1. Loss of water
  2. Loss of extracellular Na+, K+, Cl- and HCO3-
  3. Cardiovascular responses
  4. Hormonal responses – such as renin, angiotensin, aldosterone