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APP > Acid-base balance > Flashcards

Acid-base balance Flashcards

1
Q

What is normal plasma pH?

A

7.35-7.45

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2
Q

How are acids produced?

A

In the course of metabolism

  • e.g. oxidation of carbohydrates, most amino acids produces CO2
  • lactic acids during anaerobic glycolysis
  • metabolism of AAs (sulfur-containing cysteine = H2SO4)
  • alkali lost in faese
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3
Q

What different levels is acid-base balance regulated at?

A
  1. buffering systems within extracellular (and to a certain extent intracellular) fluids
  2. lungs
  3. kidneys
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4
Q

Which is the first level of acid-base regulation to respond to a change in pH?

A

Chemical buffer systems - act within seconds

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5
Q

What do buffers do?

A

Bind H+

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6
Q

Why are intracellular buffers important? Give examples

A

Since changes in extracellular pH cause changes in intracellular pH (largely because CO2 can rapidly diffuse across cell membranes), intracellular buffers are needed – important examples are haemoglobin, other proteins, and phosphates

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7
Q

What is the most powerful extracellular buffer?

A

Bicarbonate buffer system

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8
Q

Describe bicarb buffer system using an equation

A

H2O + CO2 → H2CO3 → H+ + HCO3-

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9
Q

Give the equation for the equilibrium coefficient for the bicarb buffer equation

A

K = [H+][HCO3-]/[CO2]

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10
Q

What can we derive from K = [H+][HCO3-]/[CO2]?

A

Henderson Hasselbalch equation, where 6.1 = the pK and 0.03 = the solubility of CO2 in the blood

pH = 6.1 + log{[HCO3-]/(0.03 x pCO2)}

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11
Q

What does the Henderson Hasselbalch equation show us?

A

the ratio between [HCO3-] and pCO2 determines the plasma pH

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12
Q

Describe the mechanism underlying the bicarbonate buffer system

A

When acid is added to the blood (i.e. the H+ concentration increases), the HCO3- accepts H+, forming carbonic acid, which is then converted into H2O and CO2 (catalysed by carbonic anhydrase). The CO2 is eliminated through the lungs, and so the [HCO3-]/pCO2 ratio has been brought back towards normal

Conversely, when the H+ concentration decreases, the carbonic acid dissociates to supply H+. The ventilation rate will then decrease, retaining CO2 and attempting to normalise the [HCO3-]/pCO2 ratio.

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13
Q

What is the second line of defence for changes in plasma pH?

A

Lungs

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14
Q

How can the lungs affect ph?

A

alter ventilation rate to increase/decrease. CO2 removal in acidosis/alkalosis respectively

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15
Q

What detects changes pCO2 and pH? What do these do?

A

Peripheral and central chemoreceptors

Input to the respiratory centre (response in 3-12 minutes)

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16
Q

Describe peripheral chemoreceptors

A

carotid bodies (changes in blood oxygen and CO2, pH) and aortic bodies (CO2 and O2), stimulate respiratory centre in medulla which sends nervous impulses to the external intercostals and the diaphragm via the intercostal nerve and the phrenic nerve to incease breathing rate and the volume of lungs durng inhalation

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17
Q

Describe central chemoreceptors

A

located on the ventrolateral surface of the medulla and detect changes of pH of the CSF - pH and CO2

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18
Q

On what time frame do the kidneys act to respond to a change in pH?

A

Hours - days

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19
Q

How much acid must be secreted to reabsorb HCO3-?

A

4390mEq

to recover 4320mEq passively filtered and 70mEq to buffer net acid production

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20
Q

How much HCO3- reabsorbed in the PCT?

A

~80%

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21
Q

Describe HCO3- reabsorption in PCT

A

See OneNote for diagram

  • mainly driven by Na gradient → Na/H anti porter and H+/ATPase
  • Can leave via NBCe1
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22
Q

Where does regeneration of HCO3- to replace the 70mEq that neutralises the daily non-volatile acid load occur?

A

Mainly in the CD

23
Q

Draw a diagram of HCO3- reabsorption in the collecting duct

A

OneNote

  • type A intercalated cells
  • H+ secreted across the membrane via V-type H+-ATPases and HKA (H+/K+echange)
24
Q

Draw a diagram of HCO3- secretion in the CD

A

OneNote

25
Q

What happens when H+ is secreted into the tubular fluid?

A

Combines with urinary buffers:

phosphate or ammonia

26
Q

When is HCO3- secretion possible? What is this mediated by?

A

Alkalosis

Type B intercalated cells

27
Q

What is an additional important mechanism by which the kidney contribute to the maintenance of acid-base balance?

A

Through synthesis and excretion of ammonium ions

Ammoniagenesis occurs mainly in the PCT - generated ammonium secreted and HCO3- allow to re-enter the bloodstream

Produced through metabolism of glutamine
Glutamine → glutamic acid (glutaminase)
Glutamic acid → α-ketoglutarate (glutamate dehydrogenase)
Each step yields a molecule of NH4+ and HCO3-
HCO3- leaves basolaterally
NH4+ leaves cell, substituting for H+ in the Na+/H+ antiporter

Much of the secreted NH4+ from the PCT is reabsorbed in the TALH, substituting for K+ in NKCC2 (as well as the +ve transepithelial voltage means that there is paracellular absorption of NH4+)
The NH4+ reabsorbed by the TALH accumulates in the medullary interstitium. From there it is secrered into the tubular fluid by the collecting duct
NH3 which diffuses into the collecting duct through Rh glycoproteins from medullary interstitium becomes trapped as it is protonated in the acidic tubular fluid (increased diffusion trapping as pH falls luminally). This leads to the excretion of the NH4+.
Important as should the NH4+ instead be reabsorbed, it is neutralised to produce urea (consuming HCO3-) in the process, meaning it doesn’t result in the net excretion of acid

28
Q

What does the Henderson-Hasselbalch model not account for?

A

the intake and output of all substances that can affect [H+]

29
Q

What is an alternative to the Henderson-Hasselbalch model? Describe it.

A

Stewart model

based upon three ‘independent’ variables that determine pH: the strong ion difference (SID), the total weak acids ([ATot]) and pCO2

30
Q

What are strong ions?

A

hose that fully dissociate in plasma, including sodium, potassium, and chloride, thus the SID can be calculated by subtracting the sum of all the strong anions from the sum of all the strong cations:

SID ≈ [Na+] + [K+] – [Cl-]

31
Q

What is the SID approximately equal to?

A

Because SID is dependent on plasma electrolyte concentration, it is largely controlled by the kidneys, and under normal physiological conditions is approximately equal to 40mEq/L

32
Q

Describe conc of weak acid from Stewart model

A

[ATot] is the concentration of weak acid, composed in the plasma mainly of albumin and phosphate
It can therefore be defined as the total protein in the blood and as such, the liver and haematopoietic system are crucial in its control

33
Q

What is pCO2 controlled by?

A

Lungs

34
Q

What can we model acid-base disturbances using?

A

Davenport diagrams

35
Q

How may deviations from normal pH on a Davenport diagram be compensated for?

A

Respiratory deviations are compensated for by renal mechanisms, whereby plasma [HCO3-] is either increased or decreased (in acidosis or alkalosis respectively), which helps to return plasma pH to normal

Comparatively, the compensatory response for metabolic deviations is mediated by alterations in the rate of ventilation, thereby increasing or reducing pCO2 to bring about a change in plasma pH of the opposite nature

36
Q

Draw a Davenport diagram

A

OneNote

37
Q

Draw the table expected changes mediated by acid-base disturbances

A

OneNote

38
Q

What us metabolic acidosis caused by?

A

Low [HCO3-]

39
Q

What may cause metabolic acidosis?

A 
1- Hyperkalaemia 
2 - Intense exercise 
3 - Diarrhoea → loss of HCO3-
4- Diabetic ketoacidosis
5 - Renal tubular acidosis → where the kidney fails to either reabsorb or regenerate HCO3-
40
Q

How does the body compensate for metabolic acidosis? Give example of this

A

Respiratory compensation

Characteristic Kussmaul breathing n DKA -hyperventilation

41
Q

What could be used to neutralise metabolic acidosis?

A
  • sodium bicarbonate
42
Q

What is respiratory acidosis characterised by?

A

Characterised by high pCO2 and a compensatory high [HCO3-]

43
Q

What may cause respiratory acidosis?

A
  • Reduced ventilation (e.g. kyphoscoliosis)
  • Opoid analgesics or damage to respiratory centre
  • COPD or asthma
44
Q

Treatment of respiratory acidosis

A

mechanical ventilation, however it may be possible to treat the cause of the disturbance – for example the administration of salbutamol (a β2-agonist, hence bronchodilator) to asthmatics.

45
Q

how may the body increase [HCO3-] to compensate for respiratory acidosis?

A

Upregulation of ammonia genesis (increasing formation of NH3 buffer)
Increased expression of apical H+/K+ ATPase in type A intercalated cels in order to increase H+ secretion and thus increase HCO3- reabsorption

46
Q

What is metabolic alkalosis characterised by?

A

Elevated [HCO3-]

47
Q

What may cause metabolic alkalosis?

A
  • vomiting (loss of HCl)
  • hyperaldosteroism or Conns (upregulation of Na+/K+ ATPase, ENac, increase Na+ reabsorption and K= excretion → hypokalaemia → H+ secreted in order to attempt to take up K+)
  • diuretics
48
Q

Describe the compensation that occurs with metabolic alkalosis?

A

Respiratory

Central chemoreceptors detect increased pH and cause a decreased ventilatory drive → hypoventilation
This raises levels of pCO2 in the body, which is used to form the carbonic acid intermediate, thus decreasing pH
This hypoventilation however may cause hypoxia, which would stimulate the peripheral chemoRs to increase ventilatory drive, nullifying any effects of the alkalaemia on ventilatory drive
This is thought to account for the variability in patients’ pCO2 levels in respiratory alkalosis
This is important clinically as patients presenting with hypoxaemia and hypercapnia may be incorrectly diagnosed with respiratory failure, with the underlying respiratory alkalosis going undetected

49
Q

Treatment of metabolic alkalosis

A

oral ammonium chloride

50
Q

What is respiratory alkalosis characterised by?

A

low pCO2

51
Q

What is respiratory alkalosis caused by?

A

hyperventilation – can occur due to anxiety (in which there is increased respiratory drive) or ascent to high altitude, as hypoxia stimulates peripheral chemoRs which increase ventilatory drive as a result
This causes more CO2 to be “blown off”, decreasing [H+] of the plasma

52
Q

How may compensation for respiratory alkalosis occur?

A

Long-term compensation can occur in the kidneys through the activation of B-type intercalated cells, which have the reverse orientation to type A intercalated cells, and so secrete HCO3- and retina H+, causing elevated levels of [HCO3-]

53
Q

What may be used for the treatment of respiratory alkalosis

A

carbonic anhydrase inhibitors (e.g. acetazolamide), are often used in the treatment of altitude sickness. These inhibit the uptake of HCO3- in the kidney, thereby helping to correct alkalosis.

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