Acid base balance Flashcards

1
Q

How do you calculate pH?

A

-log10[H+]

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2
Q

What is the broad pH range for fluids in the body?

A

6.8 - 8.0

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3
Q

What is the normal pH range for plasma?

A

7.35 - 7.45

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4
Q

What can changes in plasma pH affect? (3)

A
  • Excitability of muscles and nerves
  • Enzyme activity
  • K+ levels
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5
Q

What happens to K+ levels during acidosis?

A
  • K+ released from cells in exchange for H+
  • Hyperkalaemia
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6
Q

What happens to K+ levels during alkalosis?

A
  • H+ released from cells in exchange for K+
  • Hypokalaemia
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7
Q

What is the net excess of H+ ions from diet/metabolism?

A

70 mmol/day

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8
Q

What 3 systems are involved in pH regulation?

A
  • Blood and tissue buffers
  • Respiration
  • Renal
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9
Q

Where are buffers present in the body? (4)

A
  • Blood
  • Extracellular fluid
  • Intracellular fluid
  • Urine
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10
Q

What are examples of buffers? (4)

A
  • Haemoglobin
  • HCO3-
  • Inorganic phosphate
  • Weak acids/bases on proteins
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11
Q

What is the carbonic acid/bicarbonate equilibrium reaction?

A

CO2 + H2O ⇌ H2CO3 ⇌ H+ + HCO3-

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12
Q

What is H2CO3?

A

Carbonic acid

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13
Q

What is the Henderson - Hasselbalch equation?

A

pH = pK + log [HCO3-]/[H2CO3]
- H2CO3 ~ CO2 so usually divided by [CO2] instead of H2CO3

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14
Q

What is pK at 37°C?

A

6.1

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15
Q

What is normal pH?

A

7.4

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16
Q

What does acidosis mean?

A

Fall in pH

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17
Q

What does alkalosis mean?

A

Rise in pH

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18
Q

What is respiratory acidosis?

A

A problem with the lungs causes an increase in CO2 which reduces pH

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19
Q

What is hypercapnia?

A

Too much CO2

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20
Q

Which 3 conditions cause an increase in ventilation?

A
  • Hypoxia
  • Hypercapnia
  • Acidosis
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21
Q

What are the 2 types of chemoreceptors?

A
  • Peripheral
  • Central
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22
Q

What are the peripheral chemoreceptors? (2)

A

Carotid and aortic bodies

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23
Q

Which nerves do the carotid and aortic bodies signal via? (3)

A
  • Sinus nerve
  • Vagus nerve
  • Glossopharyngeal nerve
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24
Q

What is the main stimulus for the peripheral chemoreceptors?

A

Hypoxia

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25
Q

What is the main cell type in the peripheral chemoreceptors?

A

Glomus cell

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26
Q

What is the role of glomus cells?

A

Neuronal - fire action potentials

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27
Q

What are the 2 cell types in the carotid bodies?

A
  • Glomus cells
  • Type II cells
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28
Q

What is the role of type II cells?

A

Supporting cells

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29
Q

What is cranial nerve IX?

A
  • Cranial nerve 9
  • Glossopharyngeal nerve
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30
Q

Which divisions of the nervous system innervate the peripheral chemoreceptors?

A

Sympathetic and parasympathetic

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31
Q

What are BK K+ channels activated by?

A

Ca2+

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32
Q

What state are the BK K+ channels of the glomus cells in during normal oxygen conditions?

A

Open

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33
Q

What happens in the glomus cells when there is low O2/high CO2/low pH? (4)

A
  • BK K+ channels inhibited
  • Causes depolarisation, action potential fires
  • Causes voltage gated Ca2+ channels to open = increased intracellular Ca2+
  • Neurotransmitter released
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34
Q

What conditions trigger the glomus cells to fire action potentials? (3)

A
  • Low oxygen (hypoxia)
  • High carbon dioxide (hypercapnia)
  • Low pH
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35
Q

Which neurotransmitters are released by glomus cells? (6)

A
  • Acetylcholine
  • Dopamine
  • Noradrenaline
  • 5-HT
  • Substance P
  • ANP
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36
Q

What causes the glomus cells to be more sensitive to changes in PO2? (2)

A
  • Hypercapnia
  • Low pH
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37
Q

What causes the glomus cells to be less sensitive to changes in PO2? (2)

A
  • Low CO2
  • High pH
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38
Q

What affects the glomus cells’ sensitivity to PCO2?

A

pH

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39
Q

What drives breathing under normal conditions?

A

Central chemoreceptors

40
Q

What is the main stimulus for the central chemoreceptors?

A

Hypercapnia

41
Q

Where are the central chemoreceptors located?

A
  • Brain parenchyma
42
Q

What are the central chemoreceptors surrounded by?

A

BECF (brain extracellular fluid)

43
Q

How are central chemoreceptors separated from arterial blood?

A

Blood brain barrier

44
Q

What are the features of the blood brain barrier? (2)

A
  • Poor ion permeability (i.e. H+ and HCO3-)
  • High CO2 permeability
45
Q

Why does a small change in CO2 cause a big pH change in the BECF?

A

BECF doesn’t have many buffers

46
Q

How does BECF cope with long term large changes in pH?

A

Can transport HCO3- from the blood into the BECF

47
Q

Which kind of disorder changes the pH of BECF more?

A

Respiratory disorders

48
Q

Why are central chemoreceptors less affected by metabolic disorders than respiratory?

A

Metabolic disorders could involve increases in H+ and the blood brain barrier has a low permeability to ions but a high permeability to CO2

49
Q

Which brainstem nuclei contain central chemoreceptor neurons?

A

Ventrolateral medulla and other brainstem nuclei

50
Q

What are the 2 neuronal types of central chemoreceptors?

A
  • Acid activated (serotonin)
  • Acid inhibited (GABA)
51
Q

What is Kussmaul breathing?

A

Sever hyperventilation associated with metabolic acidosis

52
Q

What are the 3 renal mechanisms involved in long-term acid base balance?

A
  • HCO3- handling (reabsorption)
  • Urine acidification
  • Ammonia synthesis
53
Q

Where in the nephron is HCO3- reabsorbed? (2)

A
  • 90% proximal tubule
  • 10% distal tubule
54
Q

How is HCO3- reabsorbed in the proximal tubule cells? (6)

A
  • H+ secreted across the apical membrane
  • H+ bind with HCO3- in the filtrate to form H2CO3
  • H2CO3 broken into H2O and CO2 by carbonic anhydrase on the apical membrane
  • H2O and CO2 diffuse into the cell and recombine into H2CO3 via carbonic anhydrase
  • H2CO3 dissociates into H+ and HCO3-
  • HCO3- absorbed across the basolateral membrane via Na+ cotransporter
55
Q

Which proteins are present in the basolateral membrane of proximal tubule cells? (3)

A
  • Na+/K+ ATPase
  • K+ channel
  • HCO3-/Na+ cotransporter
56
Q

What is the purpose of the Na+/K+ ATPase on the basolateral membrane of proximal tubule cells? (2)

A
  • Sets a negative membrane potential and sets up an electrochemical gradient for Na+ to enter the cell on the apical membrane
  • Pumps 3 Na+ out of the cell and 2 K+ in
57
Q

Which proteins are present in the apical membrane of proximal tubule cells? (1)

A

Na+/H+ exchanger

58
Q

What is base conservation? (2)

A
  • 25% acidification of the urine
  • 75% ammonia synthesis
59
Q

What is urine acidification?

A

Alkaline salts in the urine are converted to acid salts in order to allow the body to excrete H+ without lowering the pH of the urine too much

60
Q

What is the process of urine acidification involving alkaline phosphate? (3)

A
  • Na2HPO (alkaline phosphate) becomes NaHPO4-, the Na+ is absorbed across the apical membrane
  • H+ is secreted across apical membrane and binds to NaHPO4- to form NaH2PO4 (replaces Na+)
  • NaH2PO4 (acid phosphate) is excreted in the urine
61
Q

What is the formula for alkaline phosphate?

A

Na2HPO

62
Q

What is the formula for acid phosphate?

A

NaH2PO4

63
Q

What is NH3?

A

Ammonia

64
Q

How is ammonia produced?

A

The metabolism of glutamine in the kidneys releases NH3 and H+

65
Q

What is the product of glutamine metabolism?

A

Alpha keto-glutarate

66
Q

What is NH4+?

A

Ammonium

67
Q

Is ammonia permeable or impermeable?

A

Permeable

68
Q

Is ammonium permeable or impermeable?

A

Impermeable

69
Q

How is ammonia excreted?

A
  • NH3 from glutamine metabolism diffuses into the tubular fluid
  • H+ is secreted across the apical membrane
  • H+ binds with NH3 to form NH4+ which is impermeable so is excreted in the urine
70
Q

What is diffusion trapping?

A
  • NH3 and H+ diffuse out of the renal cells and combine to form NH4+ which is impermeable and therefore trapped outside of the cells to be excreted
  • NH3 acts as a buffer as it binds to H+ which removes them from the body without lowering the pH of the urine too much
71
Q

How do the kidneys respond to acidosis? (4)

A
  • Upregulation of H+ excretion
  • No change in HCO3- handling (100% absorption)
  • pH of urine decreases
  • Causes plasma pH to increase back to normal
72
Q

How do the kidneys respond to alkalosis? (4)

A
  • Downregulation of H+ excretion
  • Potential upregulation of HCO3- excretion
  • pH of urine increases
  • Causes plasma pH to decrease back to normal
73
Q

What are the 2 types of acid base disorders?

A
  • Respiratory acidosis/alkalosis
  • Metabolic acidosis/alkalosis
74
Q

What causes respiratory acidosis?

A

Increase in CO2 due to changes in lung function

75
Q

What causes respiratory alkalosis?

A

Decrease in CO2 due to changes in lung function

76
Q

What causes metabolic acidosis?

A

Increase in acid/decrease in base

77
Q

What causes metabolic alkalosis?

A

Decrease in acid/increase in base

78
Q

Which lung conditions can cause respiratory acidosis? (2)

A
  • Emphysema
  • Chronic bronchitis
79
Q

What changes in the buffer system are caused by respiratory acidosis? (2)

A
  • Increase in CO2 causes equilibrium to shift to the right so more H+ and HCO3- are produced
  • This results in increase PCO2, increased HCO3- and low pH
80
Q

What is the renal compensation for respiratory acidosis? (3)

A
  • Increased H+ secretion
  • Increased reabsorption of HCO3- (more been made)
  • pH increases closer to normal at the expense of HCO3- levels being high
81
Q

What changes in the buffer system are caused by respiratory alkalosis? (2)

A
  • Decrease in CO2 causes equilibrium to shift to the left so H+ and HCO3- are used up
  • This results in low PCO2, low HCO3- and high pH
82
Q

What is the renal compensation for respiratory alkalosis? (3)

A
  • Decreased H+ secretion
  • Potential secretion of HCO3- (severe cases)
  • pH drops closer to normal at the expense of low HCO3- levels
83
Q

What diseases can cause metabolic acidosis? (3)

A
  • Diarrhoea (loss of alkaline fluid)
  • Cholera (diarrhoea)
  • Diabetic ketoacidosis (generation of excess acid)
84
Q

What changes in the buffer system are caused by metabolic acidosis? (2)

A
  • Excess H+ bind with HCO3- forming H2CO3, H2O, CO2
  • This results in low pH, low HCO3- and normal PCO2
85
Q

What is the respiratory compensation for metabolic acidosis? (1)

A

Increased respiratory rate to decrease PCO2 (stimulation of chemoreceptors)

86
Q

What is the renal compensation for metabolic acidosis? (2)

A
  • Increased H+ secretion
  • Increased reabsorption of new HCO3- (no change seen in HCO3- levels)
87
Q

What changes in the buffer system are caused by metabolic alkalosis? (2)

A
  • Loss of H+ causes equilibrium to shift to the right which generates H+ and more HCO3-
  • This results in high HCO3-, high pH and normal PCO2
88
Q

What issues can cause metabolic alkalosis? (2)

A
  • Ingestion of alkaline fluid
  • Vomiting (loss of acid)
89
Q

What is the respiratory compensation for metabolic alkalosis? (2)

A
  • Decreased respiratory rate to increase PCO2 (inhibition of chemoreceptors)
  • More PCO2 causes more H+ and HCO3- to be made which bring pH down closer to normal
90
Q

When is a mixed disorder life threatening?

A

When they are both of the same type e.g. respiratory and metabolic acidosis

91
Q

When is a mixed disorder mild?

A

When they are of opposite types

92
Q

What mixed disorder does an alcoholic patient have?

A
  • Metabolic acidosis (breakdown of alcohol)
  • Metabolic alkalosis (vomiting)
  • Mild because they are opposite types
93
Q

What mixed disorder does an asthma attack cause?

A
  • Respiratory acidosis (can’t excrete CO2)
  • Lactic (metabolic) acidosis (lack of O2)
  • Life threatening because they are both acidosis
94
Q

What mixed disorder do COPD patients who are treated with diuretics have?

A
  • Respiratory acidosis (COPD, can’t get rid of CO2)
  • Metabolic alkalosis (diuretics cause excretion of H+)
  • Mild because they are opposite types
95
Q

What mixed disorder does salicylate poisoning cause?

A
  • Metabolic acidosis (ingested salicylic acid)
  • Respiratory alkalosis (aspirin stimulates respiratory centre)
  • Mild because they are opposite types
96
Q

What is salicylate?

A

Aspirin (salicylic acid)