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EMS > Theme 4: Disorders of Metabolism - Part 1 > Flashcards

Theme 4: Disorders of Metabolism - Part 1 Flashcards

1
Q

In a titration apparatus, what is put in the burette and what is put in the flask?

A
  • burette contains the base

- the flask contains the acid with a suitable indicator

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2
Q

Why is the maintenance of [H+] so important?

A
  • changes in [H+] can affect the surface charge and physical conformation of proteins, changing their function
  • the gradient of [H+] between the inner and outer mitochondrial membrane drives oxidative phosphorylation so the body won’t be able to produce ATP
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3
Q

Where do we remove H+ ions?

A
  1. Lungs - excretion of CO2 in expired air

2. Kidney - excretion of H+ in urine

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4
Q

What is the concentration of H+ in the plasma?

A

40 mol/L

-H+ ions are produced in mmol quantities, yet must be kept at nmol concentrations

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5
Q

Where do our H+ ions come from?

A
  1. Glucose (incomplete metabolism)
    Glucose —> 2 lactate + 2H+
  2. Triglycerides (incomplete metabolism - ketogenesis)
  3. Amino acid metabolism (urea genesis)
    -metabolism of neutral amino acids results in the generation of H+
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6
Q

What are acid and bases also known as?

A

Acids - H+ donors

Bases - H+ acceptors

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7
Q

What is pH and how do you calculate it?

A

Negative logarithm of the hydrogen ion concentration (mol/L)

pH = -log10[H+]

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8
Q

Why is the pH scale used rather than [H+]?

A

logs make the wide range of H+ concentrations more manageable

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9
Q

If a patient is acidotic, what does this mean?

A

[H+] > 45nmol/L

pH < 7.35

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10
Q

If a patient is alkalaemic, what does this mean?

A

[H+] < 35 nmol/L

pH > 7.45

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11
Q

What is Ka and how do you calculate pKa?

A

Ka - acid dissociation constant

pKa = -log10Ka

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12
Q

What does it mean if there is a high Ka?

A

high Ka = greater the dissociation = stronger acid

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13
Q

What is the Henderson-hasselbalch equation?

A

pH = pKa + log10 [[base]/[acid]]

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14
Q

How does CO2 act as an acid?

A

when dissolved in plasma, CO2 becomes an acid (carbonic acid; H2CO3) which readily dissociates to release H+

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15
Q

how does HCO3- act as a base?

A

HCO3- accepts a proton to form carbonic acid, which is converted to CO2 for excretion in the lungs

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16
Q

How can you convert partial pressure of CO2 into a concentration?

A

x by a

alpHa is the solubility constant

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17
Q

What is a buffer?

A

A buffer is a solution which resists change in pH when an acid or base is added
Buffering ensures H+ ions are transported and excreted safely without affecting physiological processes

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18
Q

Name 5 buffers in the body

A
  • bicarbonate
  • haemoglobin
  • phosphate
  • ammonia
  • proteins
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19
Q

Why does equilibrium of CO2 require a non-bicarbonate buffer?

A

because buffering CO2 by bicarbonate would only result in the production of more CO2

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20
Q

Describe haemoglobin as a buffer

A
  • principle non-bicarbonate buffer - important for buffering CO2
  • reduction of CO2
  • production of HCO3
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21
Q

Describe phosphate as a buffer

A

-Monohydrogen phosphate and dihydrogen phosphate from a buffer pair:
HPO42- + H+ —> H2PO4-
-important buffer in urine, where phosphate is present at a much higher concentration

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22
Q

Describe ammonia as a buffer

A

-Ammonia and ammonium ions form a buffer pair:
NH3+H+ —> NH4+
-Vast majority of ammonia in the body is already in ammonium form, limiting its buffering capacity
-Most important role in urinary ammonium excretion is providing a route for ammonium disposal that does not result in the generation of H+

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23
Q

Describe proteins as a buffer

A
  • Proteins contain weakly acidic and basic groups due to their amino acid composition, and can therefore accept and donate H+ ions to some extent
  • Albumin is the predominant plasma protein, and is the main protein buffer in this compartment (it has a net negative charge, so can “mop up” H+ ions)
  • bone proteins also play a role in buffering
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24
Q

Describe the relationship between Hb saturation and pO2

A
  • sigmoid relationship

- pO2 can decrease significantly before saturation is affected

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25
Q

When would the curve shift to the right?

A
  1. If body temp increases
  2. If patient is hypoxic or anaemic (increase in 2,3-DPG)
  3. [H+] increases - Bohr effect
    Hb then has a reduced affinity for O2 and O2 is more available to the tissues
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26
Q

Why does an increase in 2,3-DPG shift the curve to the right?

A

2,3-DPG binds to haemoglobin and rearranges it to the T state, which decreases its affinity for O2

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27
Q

Explain the 3 acid-base processes in the kidney?

Why are they important?

A
  1. Excretion of H+ (distal tubule)
  2. Reabsorption of bicarbonate (proximal tubule)
  3. Regeneration of bicarbonate (distal tubule)
    These functions create acidic urine containing almost no bicarbonate
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28
Q

How do we reabsorb bicarbonate?

A

-bicarbonate cannot be directly reabsorbed, as luminal membranes are impermeable to it
- so we rely on CO2 to diffuse
see process acid base lecture part 1

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29
Q

What is the function of carbonic anhydrase in renal bicarbonate reabsorption?

A

H2CO3 generated from CO2 and H2O under action of carbonic anhydrase –> H2CO3 formed dissociates into H+ and HCO3-

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30
Q

How do we maintain buffering capacity in renal tubular cells?

A

Continued formation of H+ in the renal tubular cells is accompanied by stoichiometric generation of bicarbonate —> excretion of H+ results in bicarbonate generation

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31
Q

What does aldosterone do in the kidney?

A

-increase aldosterone leads to increase sodium reabsorption and potassium /hydrogen ion excretion in the distal tubule

32
Q

In what ways do we consume or produce H+ in the kidneys?

A
  • CO2 production from complete oxidation of carbohydrates and fats
  • metabolism of lactate, ketones and amino acids (consumption of H+)
  • metabolism of NH4+ to urea via the urea cycle (producer of H+
  • production of plasma proteins e.g albumin (buffering)
33
Q

What is hyperammoniaemia in liver failure?

A
  • in liver failure, liver is unable to perform urea cycle, which normally converts toxic ammonia to urea for excretion in urine
  • ammonia stimulates the respiratory centre, causing the patient to hyperventilate and blow off CO2 —> leads to increase in blood pH —> respiratory alkalosis
  • metabolic alkalosis can also arise as a result of reduced production of H+
34
Q

How do we determine the acid-base status of a patient

A

Blood gas machine:

  1. pH
  2. gases
    - pCO2, pO2
  3. metabolites
    - glucose
    - lactate
  4. electrolytes
    - sodium, potassium, chloride, calcium
  5. co-oximetry
    - total Hb, O2 saturation, OxyHb, COHb, MetHb
35
Q

How can you ensure samples for blood gas analysis are going to be accurate?

A

Samples must be:

  • well-mixed, heparinised whole blood with no air bubbles (air bubbles can affect pO2, can increase pH and can decrease pCO2)
  • analysed immediately (in-vitro glycolysis can cause a time dependent decrease in pO2 and increase in pCO2)
  • Not sent via pneumatic tube system (rapid deceleration of sample can affect pO2 and pCO2 if air bubbles present)
36
Q

What are the two main types of samples you can obtain?

A
  1. arterial blood (much more painful to obtain)

2. venous blood

37
Q

What is the principle feature of respiratory acidosis?

A

increase in pCO2

lungs can’t get rid of enough CO2 to maintain acid-base homeostasis

38
Q

What is the principle feature of respiratory alkalosis?

A

decrease in pCO2

lungs get rid of too much CO2

39
Q

What is the principle feature of metabolic acidosis?

A

decrease in HCO3-

low bicarb because it is being used up buffering excess hydrogen ions

40
Q

What is the principle feature of metabolic alkalosis?

A

increase in HCO3-

41
Q

What is the pH range for acidosis?

A

pH < 7.35

42
Q

What is the pH range for alkalosis?

A

pH > 7.45

43
Q

How do you work out if the alkalosis/ acidosis is respiratory or metabolic?

A

look at the pCO2
Acidosis:
-increase pCO2 = respiratory
-normal pCO2 (or decrease CO2 if there is compensation) = metabolic
Alkalosis:
-decrease pCO2 = respiratory
-normal pCO2 (or increase pCO2 if there is compensation) = metabolic

44
Q

What is compensation?

A
  • secondary changes in bicarbonate and pCO2 to correct for the primary disorder
  • changes in bicarb concentration (brought about by renal regeneration) can compensate for respiratory disorders - slow
  • changes in pCO2 (respiratory rate) can occur to compensate for metabolic disorders - fast
  • compensatory mechanisms aim to restore a neutral pH
  • but full compensation rarely occurs, and overcompensation never occurs
45
Q

How would we compensate for respiratory alkalosis?

A

decrease HCO3-

46
Q

How would we compensate for metabolic acidosis?

A

decrease pCO2

47
Q

What are the two ways of measuring bicarb?

A
  1. Bicarb (main lab) (22-29 mmol/L)
    - approximation of bicarb, calculated in part from CO2
  2. Bicarb (standard) (22-26 mmol/L)
    - Removes respiratory contribution so an abnormal standard bicarb tells us there is a metabolic component to the disorder
    - uses Henderson-hesselbalch equation to calculate bicarb from pH and “corrected” pCO2
48
Q

What is:

  1. Base Excess
  2. Anion Gap
A
  1. Base excess (-2.3 to +2.3 mmol/L)
    - amount of acid or alkali to titrate blood pH to 7.4
    - normal base excess = purely respiratory disorder
    - tells us if there is a metabolic component to the disorder
  2. Anion gap (8-16 mmol/L)
    - difference between the sum of measured anions and cations
    - anion gap = ([Na+] + [K+]) - ([Cl-] + [HCO3-])
    - increased anion gap indicates that there are significant amounts for “unmeasured” anions e.g ketones, lactate, salicylate, proteins etc
    - can be useful in determining the cause of a metabolic acidosis
49
Q

What are the biological features of metabolic acidosis?

A
  • decrease pH
  • increase [H+]
  • decrease CO2
  • decrease HCO3-
  • increase pO2
50
Q

What are the signs and symptoms of metabolic acidosis?

A
  • nausea, vomiting and anorexia frequently present
  • subjective sense of dyspnoea caused by stimulation of the respiratory centre
  • deep laboured breathing pattern, known as Kussmaul breathing, seen in severe acidosis
  • other symptoms caused by underlying disorder
51
Q

What are the causes of metabolic acidosis?

A
  1. Increased acid formation (caused by increased anion gap metabolic acidosis)
    - ketoacidosis (diabetic, alcoholic or starvation)
    - lactic acidosis
    - poisoning (salicylate, toxic alcohols)
  2. Acid ingestion
  3. Decreased acid excretion
    - uraemia, RTA type 1 (distal)
  4. Loss of bicarb
    - GI: diarrhoea/fistula- intestinal fluid v rich in bicarb
    - RTA type 2 (proximal)
    - carbonic anhydrase inhibitors e.g acetazolamide
52
Q

What is the physiological response to metabolic acidosis?

A

Buffering:
-acute increase [H+] resisted by bicarb buffering, causing decrease HCO3
-protein buffering important in chronic acidosis
Compensation:
-respiratory: respiratory centre stimulated —> hyperventilation (blows off CO2, but self-limiting as generates additional co2)
-renal (urine H+ excretion maximised, increased rate of regeneration of bicarb)

53
Q

How do we treat metabolic acidosis?

A

IV sodium bicarb

  • usually only given if pH < 7.00
  • caution: rapid correction impairs O2 delivery, rebound alkalosis possible
54
Q

What are the chemical features of metabolic alkalosis?

A
  • increase pH
  • decrease [H+]
  • increase/N pCO2
  • increase HCO3-
  • decrease O2
55
Q

What are the signs and symptoms of metabolic alkalosis?

A
  • usually related to underlying disorder
  • more severe alkalosis increases protein binding of Ca2+, leading to hypocalcaemia —> causes headache, lethargy, and neuromuscular excitability, sometimes with delirium, tetany and seizures
  • lowers threshold for arrhythmias
56
Q

What are the causes of metabolic alkalosis?

A
  1. Loss of H+
    - vomiting (gastric secretions full of HCl)
  2. Administration of bicarbonate
  3. Potassium depletion
57
Q

Why can hypokalaemia cause a metabolic alkalosis?

A
  • kidneys: excretion of H+ favoured in order to spare K+ at aldosterone controlled renal transporter
  • cells: K+ ions are transported out of the RBCs to increase plasma concentration –> H+ ions move into cells to maintain electroneutrality. This leads to a decrease in plasma [H+]
58
Q

What is the physiological response of metabolic alkalosis?

A
  • buffering: release of H+ from buffers
  • compensation: respiratory - reduced respiratory rate to retain CO2
  • renal:
  • decrease GRF leads to inappropriately high bicarb reabsorption
  • potassium deficiency contributes to persistence of alkalosis
59
Q

How do we treat metabolic alkalosis?

A
  • treat underlying cause

- treat factors that sustain alkalosis e.g replace potassium

60
Q

How do we treat respiratory acidosis?

A
  • decrease pH
  • increase [H+]
  • increase pCO2
  • increase/N HCO3-
  • decrease pO2
61
Q

What are the signs and symptoms of respiratory acidosis?

A
  • usually related to underlying disorder

- some patients may complain of dyspnoea

62
Q

What are the two causes of respiratory acidosis?

A
  1. Defective control of respiration
    - CNS depression - anaesthetics, sedatives, narcotics
    - CNS disease - trauma, haemorrhage, infarction, tumour
    - neurological disease - spinal cord lesions, Guillain-barre
  2. Defective respiratory function
    - mechanical - myopathies, pneumothorax, pleural effusion
    - pulmonary disease - COPD, severe asthma, impaired perfusion
63
Q

What is the physiological response of respiratory acidosis?

A
  1. Buffering - limited buffering by haemoglobin
  2. Compensation
    - metabolic compensation tends to be slow
    - respiratory: increase pCO2 stimulate respiratory centre
    - renal: max bicarb reabsorption, increase in urinary NH4+, almost all phosphate excreted as H2PO4-
64
Q

How do we treat respiratory acidosis?

A
  • treat underlying cause
  • maintain adequate arterial pO2, but avoid loss of hypoxic stimulus to respiration
  • avoid rapid correction of pCO2 (risk of alkalosis due to persistence of compensation)
65
Q

What are the signs of respiratory alkalosis?

A
  • increase pH
  • decrease [H+]
  • decrease pCO2
  • decrease/N HCO3-
  • increase pO2
66
Q

What are the symptoms of respiratory alkalosis?

A
  • Usually related to underlying disorder
  • principle feature is decreased pCO2
  • More severe alkalosis increases protein binding of Ca2+, leading to hypocalcaemia –> causes headache, lethargy and neuromuscular excitability, delirium, tetany and seizures
67
Q

What are the causes of respiratory alkalosis?

A

increase in respiratory rate or volume or both

  1. Central:
    - head injury
    - stroke
    - hyperventilation
    - drugs
    - sepsis
    - chronic liver disease
  2. Pulmonary
    - pulmonary embolism
    - pneumonia
    - asthma
    - pulmonary oedema
  3. iatrogenic
    - excessive mechanical ventilation
68
Q

What is the physiological response of respiratory alkalosis?

A
  1. buffering: release of H+ from non-bicarbonate buffers
  2. compensation:
    - respiratory: inhibitory effect of decreased pCO2 overwhelmed by primary cause
    - renal: decreased renal regeneration of bicarb (CO2 is substrate, therefore CO2 is preserved)
69
Q

What are mixed disorders?

A
  • two or more primary acid base disorders presenting in the same patient
  • can be either additive or counterbalancing
70
Q

How would respiratory failure come about from two additive disorders?

A

Respiratory acidosis (increase pCO2) and metabolic acidosis (increase lactic acid)

71
Q

How would vomiting and CCF failure come about from two additive disorders?

A

metabolic alkalosis (loss of H+) and respiratory alkalosis (increase respiratory rate)

72
Q

What would salicylate poisoning cause?

A
  • counterbalancing

- metabolic acidosis and respiratory alkalosis (increase respiratory rate)

73
Q

What would vomiting and renal failure cause?

A
  • counterbalancing

- metabolic alkalosis (loss of H+) and metabolic acidosis (decrease renal H+ excretion)

74
Q

How can vomiting cause hypokalaemia?

A
  • gastric fluid is not very rich in potassium, but it is very rich in H+ ions
  • loss of H+ ions from vomiting causes potassium depletion by:
    1. kidneys: excretion of K+ favoured in order to spare H+ ions at aldosterone-controlled renal transporter
    2. cells: H+ ions are transported out of the RBCs to increase plasma concentration - K+ moves into cells to maintain electroneutrality - this leads to a decrease in plasma [K+]
75
Q

What happens to calcium levels in acidosis?

A

as H+ binds to albumin to reduce plasma [H+], Ca2+ must be released, resulting in hypercalcaemia

76
Q

What happens to calcium level in alkalosis?

A

as H+ is released from albumin to increase plasma [H+], Ca2+ must bind to albumin

77
Q

How do you know if compensation is full or partial?

A

if the pH has not returned to normal, compensation is partial

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