6. Control of Acid Base and Potassium Concentration Flashcards
(102 cards)
1
Q
What is the normal range of plasma pH?
A
7.38-7.46
2
Q
What is the normal range of plasma [H+]?
A
37-43mmol/L
3
Q
Where are the results of acidaemia severe?
A
When pH drops below 7.1
4
Q
When are the results of acidaemia life threatening?
A
When pH drops below 7.0
5
Q
What are the results of acidaemia?
A
Reduced enzyme function, reduced cardiac and skeletal muscle contractility, reduced glycolysis, reduced hepatic function, increased plasma potassium.
6
Q
What is the effect of alkalaemia?
A
Reduced solubility of calcium salts, free Ca2+ leaves the ECF, binding to bone and proteins, so hypocalcaemia and increased excitability of nerves.
7
Q
What happens with pH >7.45?
A
Paresthesia, and tetany - uncontrolled muscle contractions.
8
Q
What is the mortality risk with pH > 7.55?
A
45%
9
Q
What is the mortality risk with pH > 7.65?
A
80%
10
Q
How are major changes in pH from small [H+] changes prevented?
A
With buffering of H+ ions.
11
Q
What is the important buffering system of H+?
A
Carbon dioxide/ hydrogen carbonate system.
12
Q
What determines the extent of the H+ reaction with CO2 in buffering?
A
The ratio of pCO2 of the plasma to [HCO3-].
13
Q
What organ controls pCO2 of the plasma?
A
The lungs.
14
Q
What organ controls [HCO3-] of the plasma?
A
The kidneys.
15
Q
What is the normal ratio of pCO2:[HCO3-]?
A
20:1.
16
Q
How can pH be calculated from pCO2 and [HCO3-]?
A
pH = 6.1 + log ([HCO3-]/(pCO2 x 0.23)).
17
Q
What is the mechanism of respiratory alkalaemia?
A
Hyperventilation leads to hypocapnia so the ratio is altered, more H+ is buffered, and pH rises.
18
Q
What is the mechanism of respiratory acidaemia?
A
Hypoventilation leads to hypercapnia so the ratio is altered, less H+ are buffered, and the pH decreases.
19
Q
Generally, how is respiratory acidaemia or alkalaemia compensated for?
A
Changes in [HCO3-] by the kidney from variable excretion and production.
20
Q
How is respiratory acidaemia compensated for?
A
If pCO2 rises, [HCO3-] rises proportionally to restore pH as the kidneys excrete less and produce more.
21
Q
How is respiratory alkalaemia compensated for?
A
If pCO2 falls, [HCO3-] falls proportionally to restore pH as the kidneys excrete more and produce less.
22
Q
What is the mechanism behind metabolic acidosis?
A
Metabolically produced H+ ions react with HCO3- to make CO2 in the venous blood. The CO2 is breathed out through the lungs and there is a proportional reduction of [HCO3-]. This alters the ratio, less H+ is buffered, and pH decreases.
23
Q
What is the mechanism behind metabolic alkalosis?
A
If plasma [HCO3-] rises, e.g. from persistent vomiting, the ratio will be faltered, relatively more H+ is buffered, and pH increases.
24
Q
What can cause a metabolic increase in [HCO3-]?
A
Persistent vomiting.
25
Generally, how is metabolic acidosis or alkalosis compensated for?
pCO2 is altered by the lungs to balance the ratio and restore pH. Changes in plasma pH drive changes in pCO2 by the peripheral chemoreceptors.
26
How is metabolic acidosis compensated for?
If [HCO3-] falls, pCO2 is lowered proportionally by increasing ventilation.
27
How is metabolic alkalosis partially compensated for?
If [HCO3-] rises, pCO2 is slightly raised by reducing ventilation to a point.
28
What will the following arterial blood gas results be for respiratory acidaemia: pH, pCO2, [HCO3-], pO2?
pH low, pCO2 high, [HCO3-] normal, pO2 low.
29
What will the following arterial blood gas results be for partially/fully compensated respiratory acidaemia: pH, pCO2, [HCO3-], pO2?
pH low or normal, pCO2 high, [HCO3-] high, pO2 low.
30
What will the following arterial blood gas results be for respiratory alkalaemia: pH, pCO2, [HCO3-], pO2?
pH high, pCO2 low, [HCO3-] normal, pO2 normal or high.
31
What will the following arterial blood gas results be for partially/fully compensated respiratory alkalaemia: pH, pCO2, [HCO3-], pO2?
pH high or normal, pCO2 low, [HCO3-] low, pO2 high.
32
What will the following arterial blood gas results be for metabolic acidosis: pH, pCO2, [HCO3-], pO2, anion gap?
pH low, pCO2 normal, [HCO3-] low, pO2 normal, anion gap high.
33
What will the following arterial blood gas results be for partially/fully compensated metabolic acidosis: pH, pCO2, [HCO3-], pO2, anion gap?
pH low or normal, pCO2 low, [HCO3-] low, pO2 high or normal, anion gap high.
34
What will the following arterial blood gas results be for metabolic alkalosis: pH, pCO2, [HCO3-], pO2?
pH high, pCO2 normal, [HCO3-] high, pO2 normal.
35
What will the following arterial blood gas results be for partially/fully compensated alkalosis: pH, pCO2, [HCO3-], pO2?
pH high or normal, pCO2 high, [HCO3-] high, pO2 low or normal.
36
Where is a large fraction of HCO3- reabsorbed?
In the proximal convoluted tubule.
37
How is HCO3- reabsorbed in the PCT?
3Na2KATPase sets up a Na+ concentration gradient in PCT cells, H+ ions are pumped out of the apical membrane up their concentration gradient in exchange for the inward movement of Na+ down its concentration gradient. The H+ reacts with the filtered HCO3- to produce CO2 which enters the cell and reacts with water to produce H+ ions. The H+ is exported, recreating HCO3-, which crosses the basolateral membrane to enter the plasma.
38
Where is filtered HCO3- reabsorbed in the kidney?
80-90% in the PCT, up to 15% in the thick ascending limb of the loop of Henle.
39
How is H+ excreted in the distal convoluted tubule?
H+ is pumped across the apical membrane by H+-ATPase.
40
Why does H+ need to be actively transported in excretion in the distal convoluted tubule?
Because most HCO3- as been recovered and the Na+ gradient is insufficient to drive H+ secretion.
41
What happens to K+ when H+ is exported in the distal convoluted tubule?
K+ is absorbed into the blood.
42
How is blood pH linked to K+?
As H+ is exported, K+ is absorbed in the blood. So lots of H+ exported, means lots of K+ absorbed.
43
What is the minimum pH of the urine?
4.5
44
How is H+ buffered in the urine?
There is no HCO3-, so instead it is buffered by phosphate. The rest of H+ in the urine is attached to ammonia as ammonium.
45
What is meant by phosphate being a titratable acid?
It can freely gain H+ ions in an acid/base reaction.
46
What K+ level is metabolic acidosis associated with?
Hyperkalaemia.
47
Why is metabolic acidosis associated with hyperkalaemia?
As [K+] rises, the kidney's ability to reabsorb and create HCO3- is reduced. Hyperkalaemia makes intracellular pH alkaline, favouring HCO3- excretion.
48
How is metabolic alkalosis associated with hypokalaemia?
Hypokalaemia makes intracellular pH acidic so favours H+ excretion and HCO3- recovery.
49
Why does [HCO3-] increase after persistent vomiting?
The kidneys try to compensate for the dehydration, so can't excrete HCO3-. This means HCO3- and Na+ recovery is favoured to increase osmolarity of the plasma to increase movement of water in.
50
How does the body respond to [HCO3-] increases after persistent vomiting?
It stops actively secreting H+, as this would worsen metabolic alkalosis.
51
What is the effect of H+ stopping secretion on K+ reabsorption?
It stops K+ reabsorption.
52
When does metabolic acidosis occur?
If there is excess metabolic production of acids, acids are ingested, HCO3- is lost, or there is a problem with the renal excretion of acid.
53
What is the anion gap?
The difference between the sum of the measured concentrations of Na+ and K+ and the sum of the measured concentrations of Cl- and HCO3-.
54
When does the anion gap increase?
When HCP3- is replaced in the plasma by another anion not included in the calculation, e.g. with excess acid production.
55
Why does metabolic acidosis from renal excretion of H+ not result in an anion gap change?
The [HCO3-] is changed directly without replacement by an unmeasured ion, so the gap doesn't change.
56
What is the plasma [K+] range?
3.5-5.3mmol/L
57
Why is high [K+] inside the cell essential?
Maintains cell volume, regulated intracellular pH, controls cell-enzyme function, DNA/protein synthesis, cell growth.
58
Why is low [K+] outside the cell necessary?
To maintain the steep K+ ion gradient responsible for the membrane potential of excitable and non-excitable cells.
59
How does increased ECF [K+] affect the cell membrane?
It depolarises the cell membrane.
60
How does reduced ECF [K+] affect the cell membrane.
It hyperpolarises the cell membrane.
61
What metabolic disturbance result from extremely low extracellular [K+]?
Inability of the kidney to form concentrated urine, a tendency to develop metabolic alkalosis, large enhancement of renal ammonium excretion.
62
What homeostatic mechanism keep the ECF [K+] tightly controlled?
External and internal balance.
63
Which cells secrete K+ in the DCT and collecting duct?
Principal cells.
64
How is K+ secretion powered in the DCT and collecting duct?
It is a passive process driven by the electro-chemical gradient for K+ between the principal cell and the lumen.
65
Through which channel is Na+ reabsorbed in the DCT and collecting duct?
ENaC.
66
What tubular factors affect K+ secretion by principal cell?
Aldosterone, ECF [K+], acid base status.
67
Which luminal factors affect K+ secretion by principal cells?
Increased distal tubular flow rate means more K+ loss, increased Na+ delivery to distal tubule means more K+ loss.
68
How does aldosterone affect the channels in the basolateral and apical membranes?
Basolateral - increased transcription of Na-K-ATPase.
| Apical - increases transcription of ENaC and K+ channels.
69
What is the overall result of aldosterone on K+ excretion?
Increases it.
70
How does [K+] affect aldosterone secretion?
Increased K+ stimulates aldosterone secretion.
71
How does acidaemia affect secretion of K+?
It decreases [K+] in principal cells and therefore decreases secretion.
72
How does alkalaemia affect secretion of K+?
It increased [K+] in principal cells and therefore increases secretion.
73
How is K+ absorbed in the DCT and collecting duct via intercalated cells?
In an active process that is mediated by H+-K+-ATPase in the apical membrane.
74
What is the external balance of K+?
It regulates the total body K+ content which depends on dietary intake and excretion. It controls K+ long-term by varying excretion.
75
What is the internal balance of K+?
It regulates K+ movement between ECF and ICF in moment to moment control.
76
How does internal balance respond to increased ECF/plasma [K+]?
Need to move K+ into ICF so more Na-K-ATPase active.
77
How does internal balance response to decreased ECF/plasma [K+]?
Need to move K+ into ECF so more K+ channels active.
78
How does insulin cause K+ to move intracellularly?
K+ in splanchnic blood stimulates insulin secretion from the pancreas. Insulin increases the amount of Na-K-ATPase so there is uptake of K+.
79
How do catecholamines (B2 agonists) cause K+ to move intracellularly?
B2 adrenoceptors stimulate Na-K-ATPase. Exercise and trauma increases K+ exit from the cells and increased catecholamine help offset ECF [K+] rise.
80
How does aldosterone cause K+ to move intracellularly?
It is a steroid hormone that increases transcription of Na-K-ATPase in the basolateral membrane and ENaC/K+ channels in the apical membrane. This gives increased K+ excretion.
81
How does exercise cause K+ to move extracellularly?
Skeletal muscle contraction releases K+, the increase is proportional to the intensity of the exercise. Uptake of K+ by non-contracting tissues prevents hyperkalaemia.
82
How does cell lysis cause K+ to move extracellularly?
K+ is released from the ICF to the ECF in cell lysis.
83
What can cause cell lysis?
Trauma to skeletal muscle, intravascular haemolysis, and cancer chemotherapy.
84
How does plasma hyperosmolarity cause K+ to move extracellularly?
Increased plasma osmolarity causes water to move from ICF to ECF by osmosis. [K+] increases in ICF and then K+ moves down gradient.
85
How does hypokalaemia affect cardiac cells?
It hyperpolarises them so more fast Na+ channels are available in active form and the heart is more excitable.
86
How does hyperkalaemia affect cardiac cells?
It depolarises them as more fast Na+ channels stay inactive and the heart is less excitable.
87
What are the external balance problems that cause hypokalaemia?
Inadequate intake, excessive loss - diarrhoea/ vomiting, diuretic drugs/ osmotic diuresis, high aldosterone.
88
What are the internal balance problems that cause hypokalaemia?
Shift of potassium ECF -> ICF from alkalosis.
89
What are the GI clinical features of hypokalaemia?
Neuromuscular dysfunction so paralytic ileus.
90
What are the skeletal muscle clinical features of hypokalemia?
Neuromuscular dysfunction so muscle weakness.
91
What are the renal clinical features of hypokalaemia?
Dysfunction of collecting duct cells so unresponsive to ADH and nephrogenic diabetes.
92
How is hypokalaemia treated?
Treat cause, K+ replacement either IV or oral, if from high aldosterone - K+ sparing diuretics (block aldosterone), K+ sparing (amiloride), and aldosterone antagonists (spironolactone).
93
What are the ECG changes of hypokalaemia?
ST depression, shallow T wave, and prominent U wave.
94
What are the external balance problems causing hyperkalaemia?
Inadequate renal excretion, acute kidney injury, chronic kidney injury, reduced mineralocorticoid effect (drugs which reduce aldosterone action, adrenal insufficiency).
95
What are the internal balance problems causing hyperkalamia?
Shifts of K+ from ICF -> ECF from acidaemia and cell lysis.
96
What are the GI clinical features of hyperkalaemia?
Neuromuscular dysfunction so paralytic ileus.
97
What are the ECG changes with serum [K+] of 6.5-7mmol/L?
Tall, peaked T waves.
98
What are the ECG changes with serum [K+] of 8mmol/L?
Prolonged PR interval, tall T waves, ST segment depression.
99
What are the ECF changes with serum [K+] of 9mmol/L?
Widened QRS interval.
100
What are the ECF changes with serum [K+] of 10mmol/L?
Ventricular fibrillation.
101
What are the emergency treatments of hyperkalaemia?
Reduce K+ effect on heart with IV calcium gluconate, shift K+ into ICF via IV glucose and insulin, dialysis.
102
What are the longer term treatments of hyperkalaemia?
Remove excess K+ wit dialysis or oral K+ binding resins to bind K+ in the gut, reduce intake, and treat cause.
