Acid Base Balance Flashcards

(109 cards)

1
Q

Why is ECF pH regulation so important?

A

H+ is very reactive, changes in pH cause changes in metabolic reactions

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2
Q

What is the normal blood pH?

A

7.4

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3
Q

Which ions contribute to pH?

A

FREE H+

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4
Q

What is the typical concentration of free H+?

A

40x10^-9

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5
Q

What are the sources of acid?

A

Respiratory Acid Metabolic acid

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6
Q

How is respiratory acid produced?

A

CO2 + H2O = H2CO3 = H+ + HCO3-

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7
Q

Why is carbonic acid not normally a net contributor to acid levels?

A

Usually ↑acid = ↑ventilation

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8
Q

What are the sources of metabolic acid?

A

Inorganic acids Organic acids

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9
Q

What are the sources of inorganic acids?

A

S-containing amino acids (H2SO4) Phospholipids (Phosphoric acids)

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10
Q

What are the sources of organic acids?

A

Fatty acids Lactic acids

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11
Q

What is the normal daily net gain of acid?

A

50-100mmoles H+/day

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12
Q

What is the source of alkali?

A

Oxidation of organic anions i.e citrate

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13
Q

Carbonic acid dissociates into what?

A

H+ + HCO3-

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14
Q

What is the role of buffers?

A

Minimise pH changes when H+ ions are removed

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15
Q

What is the Henderson-Hasselbalch equation?

A

pH defined in ratio of acid to base pH = pK + log([A-]/[HA])

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16
Q

What is the most important extracellular buffer?

A

Bicarbonate buffer system

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17
Q

What is the pK of bicarbonate?

A

6.1

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18
Q

What is the ratio of bicarbonate to carbonic acid in normal blood pH?

A

20:1

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19
Q

The quantity of H2CO3 depends on what?

A

CO2 in plasma Solubility/partial pressure of CO2

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20
Q

What is the normal [HCO3-] in man?

A

24mmoles/L (22-26)

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21
Q

What is the normal pCO2 in man?

A

40mmHg (36-44)

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22
Q

Why does the increased levels of H2O and CO2 due to carbonic acid dissociation not cause equilibrium and increased H+?

A

The CO2 is exhaled

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23
Q

What is the net effect of respiratory compensation of increased acid?

A

The dissociation is driven to the right and more able to act as a buffer

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24
Q

Decreased [H+] will lead to what?

A

Decreased ventilation, increased CO2

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25
[HCO3-] is regulated where?
Renal system
26
PCO2 is regulated where?
Respiratory system
27
What are the ECF buffers?
HCO3- Plasma proteins Dibasic phosphate
28
How do plasma proteins buffer acid?
Pr- + H+ = HPr
29
How does Dibasic phosphate buffer acid?
HPO42- + H+ « H2PO4- (monobasic phosphate)
30
What are the primary intracellular buffers?
Proteins Organic/inorganic phosphates Haemoglobin
31
How is movement of H+ kept electrochemically neutral?
Exchange for K+ Or Accompany with Cl-
32
How does acidosis cause ventricular fibrillation?
Movement of K+ out of cells causes Hyperkalemia Depolarisation of excitable dissues --\> VFib
33
Where is the additional store of acid buffer?
Bone
34
How does chronic renal failure lead to bone wasting?
The additional store of carbonate (bones) is broken down to free it
35
Acidosis leads to what change in the blood?
Hyperkalemia
36
Where is metabolic acid buffered?
43% in plasma 57% in cells
37
Where is respiratory acid buffered?
97% in cells (Hb and plasma proteins)
38
How does the kidney regulate [HCO3-]?
Reabsorption of HCO3- Generation of new HCO3-
39
Where is new HCO3- generated?
Kidneys
40
Secretion of H+ from tubule cells is coupled with what?
Passive Na+ reabsorption
41
What is the mechanism for HCO3- reabsorption?
H+ filtered out (Na+ reabsorbed) H+ and HCO3- forms H2O + CO2 in presence of carbionic anhydrase on luminal membrane CO2 taken up and form back into H+ and HCO3- in presence of carbionic anhydrase HCO3- passes back into the peritubular capillaries with Na+
42
What enzyme assists with HCO3- dissociation?
Carbonic anhydrase
43
What is the source of secreted H+?
H+ released by the dissociation of H2CO3
44
Where does the bulk of HCO3- reabsorption take place?
Proximal tubule (\>90%)
45
Where is carbonic anhydrase located?
All tubule cells Luminal membrane of tubule
46
How much H+ is excreted in HCO3- reabsorption?
None
47
What would be the result of failure to reabsorb intestinal bicarbonate?
Metabolic Acidosis
48
What are the minimum and maximum pH of urine in humans?
4.5-5 (minimum) 8 (maximum)
49
What are the acid buffers in urine?
Dibasic phosphate Uric acid Creatinine
50
What is titratable acidity?
The amount of NaOH needed to titrate urine pH back to 7.4 for a 24hr urine sample
51
What is the indirect source of new HCO3-?
CO2 in blood
52
How does blood CO2 form new HCO3-?
CO2 enters tubule cells, combines with H2O = carbonic acid This yields H+ and (new) HCO3- Passes into capillaries with Na+ | (in presence of carbonic anhydrase)
53
Formation of new HCO3- takes place where? Why?
Distal tubule Phosphate ions become highly concentrated here (exhausted Tm mechanism)
54
What is the fate of produced when the distal tubule produces HCO3-?
Exchanged for Na+ (Na2HPO4) Bound to phosphate (HPO42-) Excreted as H2PO4-
55
What is the source of CO2 for production of new bicarbonate?
Blood (dependent on PCO2)
56
Why is [PO4] high in the distal tubule?
Because what isnt absorbed in the proximal tubule is concentrated in the loop of Henle
57
What is the purpose of ammonium excretion?
Adaptive response to acid loads Generated HCO3- and H+
58
What is the solubility of ammonia?
Lipid soluble
59
Why is Ammonium used for responding to acid loads?
Because Ammonium is NOT lipid soluble
60
Where is ammonia produced in the body?
Deamination of amino acids - glutamine
61
How is Ammonia produced?
Deamination of glutamine by renal glutaminase within renal tubule cells
62
What is the mechanism of H+ secretion via ammonium?
NH3 passes into tubule Combines with H+ to form NH4+ NH4+ + Cl- = NH4Cl NH4Cl is excreted
63
What is the source of secreted CO2 in ammonium excretion?
CO2 from the blood (reforms H+ and HCO3-)
64
How does ammonium enter the proximal tubule?
Presence of NH4+/Na+ exchangers in the proximal tubule
65
Glutamine reductase acting on glutamine forms what?
Glutamate
66
How does ammonium enter the tubule in the distal tubule?
Passive flow of lipid soluble NH3 into the tubule
67
Where is the ammonium/sodium antitransporter located?
Brush border membrane of the proximal tubule
68
Renal glutaminase is dependent on what?
pH pH↓ = ↑glutaminase activity Leading to greated NH4+ excretion
69
How long does it take for the kidney to respond to increased acid loads by ammonium excretion? Why?
4-5 days Slow rate of increased protein (glutamine) synthesis
70
How much H+ is lost per day via ammonium excretion?
30-50mmoles | (up to 250 in severe acidosis)
71
What are the main mechanisms of renal H+ excretion?
Ammonium Phosphate Bicarbonate
72
What are the causes of acute respiratory acidosis?
Obstruction of airways Drugs which depress medullary centres (Barbiturates, opiates)
73
What are the causes of chronic respiratory acidosis?
Chronic lung disease: Bronchitis, emphysema, asthma
74
What change in [HCO3-] is seen in chronic respiratory acidosis?
Increased bicarbonate
75
Renal compensation only serves to correct what?
pH level of blood - not the disturbance
76
What are the causes of acute respiratory alkalosis?
Hyperventilation Aspirin First ascent to altitude
77
What are the cause of chronic respiratory alkalosis?
Long term high altitude PO2 \<60mmHg
78
How does bicarbonate respond to high pH?
Decreased [HCO3-]
79
What is the net effect in urine in a ↓PCO2?
Less HCO3- reabsorption, leading to HCO3- excretion
80
What is metabolic acidosis?
Decreased [HCO3-]
81
What are the causes of metabolic acidosis?
Increased H+ production: Diabetic ketoacidosis, lactic acidosis Failure to excrete normal dietary load of H+ in renal failure Loss of HCO3- in diarrhoea
82
Increased ventilation due to metabolic acidosis presents how?
Kussmaul breathing
83
Kussmaul breathing is a sign of what?
Arterial pH \<7 Renal failure Diabetic ketoacidosis
84
How is blood pH defined?
[HCO3-]/PCO2
85
What are the responses to increased metabolic H+ in the body?
Immediate: ECF/ICF buffering Minutes: Respiratory compensation Hours/days: Generation of HCO3-, stimulation of renal glutaminase
86
What is metabolic alkalosis?
↑[HCO3-] causing increased PCO2 to protect the pH
87
What are the causes of metabolic alkalosis?
H+ loss due to vomiting Renal H+ due to aldosterone excess, liquorice Excess HCO3- administration in impaired renal function Massive blood transfusions (8+ units)
88
How do massive blood transfusions lead to metabolic alkalosis?
Blood banks add citrate to prevent coagulation - converted to HCO3-
89
How does excess HCO3- lead to alkalosis?
Filtered load of HCO3- exceeds secreted H+ needed to reabsorb it
90
How does respiratory compensation cause a delay in renal correction of metabolic acidosis?
In order to protect pH, ventilation decreases to blow off less CO2 and increase acidity But blowing off CO2 means the kidney can't use the H+ to reabsorb the excess HCO3-
91
What is the primary disturbance in respiratory acidosis?
Increased PCO2
92
What is the primary disturbance in respiratory alkalosis?
Decreased PCO2
93
What is the primary disturbance in metabolic acidosis?
Decreased [HCO3-]
94
What is the primary disturbance in metabolic alkalosis?
Increased [HCO3-]
95
An increase in pH is caused by what?
Increased HCO3- Or Decreased PCO2
96
A decrease in pH is caused by what?
Decreased HCO3- Or Increased PCO2
97
How do pH changes relative to PCO2 differ in chronic vs acute respiratory acidosis?
Chronic acidosis - increase in PCO2 has a smaller decrease in pH Acute acidosis - increase in PCO2 has a larger decrease in pH
98
Why do PCO2 changes cause smaller changes in blood pH in chronic acidosis?
Because after 4-5 days, NH3 production will have increased and is able to act as a buffer
99
How does haemorrhage cause lactic acidosis?
Loss of blood = ↓perfusion of tissues = ↓Aerobic respiration = Lactic acid production
100
How does severe acidosis lead to kyperkalemia?
H+ ions are buffered intracellularly in exchange for K+ ions
101
How would a patient in severe acidosis leading to hyperkalemia be treated?
Insulin (uptake of K+) Calcium resonium (exchange Ca2+ for K+) Ca gluconate (decrease heart excitability)
102
When managing severe acidosis, what levels should be monitored?
ph, HCO3-, etc POTASSIUM (risk of hypokalemia)
103
How would severe vomiting affect acid/base levels?
Loss of NaCl/H2O --\> hypovolaemia Loss of HCl --\> metabolic alkalosis
104
How would vomiting causing hypovolaemia worsen the metabolic alkalosis?
Hypovolemia would stimulate aldosterone production Aldosterone would cause distal tubule exchange of Na+ for H+, leading to further loss of H+ Additional loss of K+
105
How does excess liquorice affect the acid/base balance?
Contains glycyrrhizic acid, acts like aldosterone Causes more H+ secretion leading to metabolic alkalosis
106
What is the anion gap?
Difference between sum of principal cations (Na+, K+) and principal anions (Cl-, HCO3-)
107
What is a normal anion gap?
16mmoles/L (14-18)
108
How does acidosis due to loss of bicarbonate affect the anion gap?
No change in anion gap, loss of HCO3- is compensated by increasing Cl-
109
How does acidosis due to lactic/diabetic acidosis affect the anion gap?
Reduction in bicarbonate made up for with lactate, acetoacetate, B-OH butyrate So anion gap