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Life Maintenance > Acid-base balance > Flashcards

Acid-base balance Flashcards

1
Q

What is the normal serum pH of the body?

A

7.35-7.45

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2
Q

How does pH relate to [H+]?

A

pH = -log10 [H+]

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3
Q

What are the main sources of acid in the body?

A

OXPHOS (CO2)

Metabolism of dietary proteins (non-volatile acids, H2SO4 and HCl)

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4
Q

What are the main mechanisms governing serum pH?

A

ICF and ECF buffering systems
Respiratory system
Kidney

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5
Q

What is a buffer?

A

A solution that minimises changes in [H+] ie. pH

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6
Q

Which buffer systems are present in the ICF and ECF?

A

bicarbonate system
phosphate system
protein buffers (e.g. Hb)

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7
Q

What is the relationship between pK and pH?

A

when pH=pK

[acid] = [base]

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8
Q

What is pK?

A

equilibrium constant

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9
Q

When is a buffer most successful?

A

1 pH either side of its pK

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10
Q

What is the Henderson-Hasselbach equation?

A

CO2 + H2O-> H2CO3

-> H(+) + HCO3(-)

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11
Q

What is the relative molar ratio between HCO3- and CO2?

A

20 HCO3- : 1 CO2

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12
Q

Which buffer is the more suited (in terms of pK) to the blood pH?

A

phosphate buffer

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13
Q

Why is bicarbonate buffer system more readily used in the body?

A

CO2 and HCO3- the two critical components of the buffer are independently regulated and replenished

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14
Q

What is the pK of the bicarbonate buffer system?

A

pK = 6.1

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15
Q

How do the kidneys work in acid-base control?

A

excretion of H+ in tubular fluid
Reabsorption/secretion of HCO3-
ammonia, phosphate and bicarbonate buffer systems at play within tubular fluid

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16
Q

How is bicarbonate handled by the kidney?

A

HCO3- cons reabsorbed from the PCT

AND kidney generates new bicarb. which is released at a controlled rate

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17
Q

How do thiazide diuretics work?

A

Inhibition of carbonic anhydrase (dependent on h+ influx from Na+H+ ATPase pump)

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18
Q

Where does de novo synthesis of HCO3- occur?

A

in the PCT

For every 1xbicarb reabsorbed from the tubular fluid, one is returned to the blood

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19
Q

How much bicarbonate is reabsorbed at the PCT?

A

85-90%

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20
Q

Where does acid-balance occur in the nephron?

A

In the intercalated cells of the late DCT and collecting duct

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21
Q

What is the composition of the fluid in the DCT?

A

[HCO3-] is low

H+ reacts with other buffers

22
Q

What is the role of the H+-ATPase pump in the DCT?

A

It pumps H+ against its concentration gradient into the tubule (secretion)

23
Q

Which cells is the Cl - HCO3- exchanger predominantly found in?

A

intercalated cells

24
Q

How does the phosphate buffer system work in the kidney?

A

H+ ions are mopped up by HPO4(2-) to make H2PO4(-)
H2PO4(-) is then excreted in urine
This occurs in the tubular lumen (extracellular to the intercalated cells)

25
Q

The H+-ATPase pump which pumps out H+ ions from intercalated cells into the tubular lumen is sensitive to which RAAS hormone?

A

Aldosterone

26
Q

What is the pK of the phosphate buffer system?

A

6.8

27
Q

What is the breakdown reaction of glutamine in the kidney?

A

glutamine -> a-ketoglutarate + NH3

28
Q

Which enzyme catalyses the breakdown of glutamine?

A

Glutaminase

29
Q

How is ammonia excreted from the body?

A

urinary excretion
As ammonium salts
e.g. NH4+

30
Q

What are the main ways by which acid-base balance is achieved by the kidney?

A
  1. reabsorption of bicarbonate
  2. acidification of phosphate
  3. Ammonia secretion
31
Q

What are the 3 mechanisms by which plasma pH is corrected?

A
  1. intra- and extra-cellular buffering
  2. Respiratory compensation of pCO2 (in ECF)
  3. Renal adjustment of [bicarbonate] (in ECF)
32
Q

What are pH changes in plasma called? What types are there?

A

Acidosis: pH<7.4
Alkalosis: pH>7.4

Respiratory or Metabolic
Defined depending on the causative event, initiating disturbance

33
Q

What is the caveat with compensation for acid-balance disturbance?

A

Perfect compensation is not possible

UNLESS you are actively correcting the underlying cause as well

34
Q

How does the kidney detect changes in pH balance?

A

Some candidate molecular pH sensors: GRP4, ErbB1/2 kinases, bicarbonate-stimulated adenylate cyclase (sAC)
But no one master pH sensor

35
Q

What is the role of the respiratory system in acid-base balance?

A

chemosensitive centre in medulla of brainstem - regulates respiration
monitors CO2 levels as indirect measure of pH in CSF and therefore plasma
(Indirect because H+ cannot cross BBB)

36
Q

Where are the peripheral chemoreceptors located?

A

Aortic arch

Carotid bodies

37
Q

What happens when medullary chemoreceptors detect a reduction in CSF pH?

A

Increased respiration rate
(compensatory hyperventilation)
-> hypocapnia (as more CO2 is breathed off)
-> normal plasma pH is restored

38
Q

What are common causes of metabolic acidosis?

A

severe sepsis: lactate
DKA: ketone bodies such as 3-hydroxybutyrate
Diarrhoea: loss of bicarbonate from GI tract

39
Q

What is the chemical pathology underlying metabolic acidosis?

A

increased [H+]
OR
reduced [HCO3-]
in ECF

40
Q

What equations connects [H=], [HCO3-] and pH?

A

pH = pK + log([HCO3-]/[H+])

41
Q

What is the main function of compensation in acid-base balance?

A

returns dysregulated ECF pH to within normal range

42
Q

What are the main mechanisms that are employed to correct acid-base imbalance?

A

kidney: increased H+ and NH4+ secretion, increased neobicarbonate synthesis and reabsorption

Lung: change in respiratory rate to modulate pCO2

ICF+ECF buffering: HCO3- used up to mop up excess H+
H+ may remain high after this

43
Q

What are the main causes of metabolic alkalosis?

A

excessive diuretic use:
chronic loss of electrolytes (e.g. Cl-, Na+, K+) -> causes increased H+ secretion

Vomiting: loss of H+ from GI tract

Ingestion of alkaline antacids

Hypokalaemia

44
Q

What are common causes of respiratory acidosis? What are the compensatory mechanisms?

A

causes:
emphysema, asthma, COPD

compensation:
increased plasma HCO3-
acidic urine -> increased H+ excretion

45
Q

What are common causes of respiratory alkalosis? What are the compensatory mechanisms?

A

causes:
hyperventilation

compensation:
reduced plasma HCO3-
alkaline urine -> increased HCO3- excretion and reduced H+ secretion
reduced pCO2 loss mediated by reduced respiratory drive

46
Q

How are pH, [H+] and [HCO3-] affected in the different types of acid-base imbalance?

A

respiratory acidosis:
reduced pH
increased pCO2
increased HCO3-

respiratory alkalosis:
increased pH
reduced pCO2
normal or reduced HCO3-

metabolic acidosis:
reduced pH
normal pCO2
reduced HCO3-

Metabolic alkalosis:
increased pH
normal CO2
increased HCO3-

47
Q

What is simple acid-base disorder?

A

results from a single primary disturbance

WITH normal physiological compensation

48
Q

What is mixed acid-base disorder?

A

Occurs in seriously unwell patients
2 or more primary disorders of pH imbalance occurs simultaneously
Net affect may be additive = extreme alteration to pH
e.g. metabolic acidosis + resp. acidosis
or may have opposing effects causing no net difference in pH
e.g. metabolic acidosis + respiratory alkalosis

49
Q

What is the Siggaard-Andersen in vivo nomogram?

A

Diagram which predicts behaviour of whole body during pH imbalance and acid-base disturbance
PLUS body’s response to therapeutic intervention

50
Q

What is an anion gap in acidosis?

A

High anion gap metabolic acidosis is a form of mixed acid-base balance disorder

high anion gap is when > 12mEq/L
(measure of serum ion concentrations)

Typically caused by excess acid production in body. Can also be caused by MeOH ingestion or aspirin OD

51
Q

What are the causes of high anion-gap metabolic acidosis?

A 
Carbon monoxide, cyanide, congenital HF
Aminoglycosides
Theophylline, toluene (glue)
Methanol
Uraemia
DKA, alcoholic KA, Starvation KA
Paracetamol OD, phenformin, paraldehyde
Iron, Isoniazid, inborn errors of metabolism 
Lactic acidosis
EtOH, ethylene glycol 
Salicyclates/Aspirin
52
Q

What is Isoniazid?

A

Antibiotic
used in Tx of TB
Often used in combo with rifampicin, pyrazinamide and streptomycin or ethambutol for active TB

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