Acid-Base Homeostasis (16) Flashcards

1
Q

Acid production

A

Total CO2 25mol/day

Unmetabolised acids 50 mmol/day (urine, sulphuric acid, phosphoric acid)

Plasma [H+] 40nmol/L

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2
Q

Buffering systems

A

Hb, bicarbonate, phosphate, proteins, ammonia, organic acids

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3
Q

pH

A

[H+]

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4
Q

Normal pH

A

7.45-7.35

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5
Q

Normal [H+]

A

35-45 nmol/L

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6
Q

[H+]

A

low - alkolotic, high-acidotic

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7
Q

Henderson-Hasselbalch equation

A

H+ + HCO3- H2CO3 CO2 + H2O

pH = pK + log ([HCO3-]/[pCO2] x a)

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8
Q

[H+] homeostasis requires

A

Balance between H+ production and regeneration of HCO3-

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9
Q

Sites of acid-base metabolism

A

Lungs, kidney, GI tract, liver

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10
Q

Tissue gas exchange

A

CO2 non-polar, easily pass into RBC, if acidify RBC changes shape and releases O2 > lungs

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11
Q

RBC equation

A

H+Hb+O2 > HbO2 > H+ + HCO3 (CO2/Cl-)

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12
Q

When does haemoglobin dissociated curve shift right?

A
Right shift
Increased
2,3 diPG
H+ acidosis
Temperature
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13
Q

Kidney

A
  • Bicarbonate is lost (active Na+/H+ pump)
  • Regeneration of bicarbonate in renal tubule
  • Distal tubercle under aldosterone control - regulates salt and water (Na+ secreted, K+ absorbed)
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14
Q

GI

A

Stomach secretes [H+], pancreatic juice [HCO3-]

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15
Q

Liver

A

Dominant site of lactate metabolism, only site of urea synthesis

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16
Q

Severe liver failure

A

Metabolic alkalosis, NH4+ toxicity

NH4+ + oxo-glutamate X>X glutamine
NH4+ + CO2 X>X urea and H+

17
Q

Compensatory mechanisms

A

Respiratory, renal bicarbonate regeneration, hepatic shift between urea synthesis and ammonia excretion

18
Q

Normal [H+]

A

36-44 nmol/L

19
Q

Normal Na+

A

132-144 mmol/L

20
Q

Normal K+

A

3.5-5.5 mmol/L

21
Q

Normal Cl-

A

98-108 mmol/L

22
Q

Normal HCO3-

A

21-28 mmol/L

23
Q

Normal urea

A
24
Q

Normal creatine

A
25
Q

Metabolic acidosis

A

Increased H+ formation, acid ingestion, reduced renal H+ excretion, loss of bicarbonate (High H+, low CO2, high O2)

26
Q

Metabolic alkalosis

A

Generation of bicarbonate by gastric mucosa, renal generation of HCO3- in hypokalaemia, administration of bicarbonate
(Low H+, high CO2, low pO2)

27
Q

Consequences of metabolic alkalosis

A

K+ > cells and urine
PO4 > cells
Respiratory suppression

28
Q

Respiratory acidosis

A

CO2 retention due to - inadequate ventilation and perfusion, parenchymal lung disease
(High H+, High CO2, Low pO2)

29
Q

Respiratory alkalosis

A

Increased CO2 excretion - hyperventilation

Low H+, Low pCO2, High pO2

30
Q

Causes of increased H+ formation

A

Ketoacidosis, diabetic, alcoholic, lactic acidosis, poisoning, inherited organic acidoses

31
Q

Diabetic keto-acidosis

A

Hyperglycaemia, osmotic diuresis > pre-renal uraemia, hyperketonaemia, increase FFA
(all lead to acidosis)

32
Q

Lactic acidosis

A

Shock or metabolic and toxic causes

33
Q

Normal lactic acid levels

A

0.9-1.7 mmol/L

34
Q

Acidosis in an alcoholic

A

NAD+ depletion (thiamine), thiamine deficiency (PDH co-factor), enhanced glycolysis for ATP formation, leto-acids (B-HBD) secondary to counter-regulatory hormones, profuse vomiting

35
Q

In alkalosis

A

Increased glycolysis, reduced O2 delivery due to shift in O2 dissociation curve, lactate induced vasoconstriction, impaired mitochondrial respiration

36
Q

O2 debt in alkalosis due to

A

Further anaerobic lactate production, hyperventilation

37
Q

reduced H+ excretion

A

Renal tubular acidosis, generalised renal failure

38
Q

Renal failure

A

Reduced volume of nephrons, increased bicarbonate loss, reduced NH4+ excretion, NH4+ to liver for urea and H+ synthesis, only fraction of NH4+ derived from glutamine (normal approx 100%)