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MSC: Disease of major orgns > Acid Base Homeostasis > Flashcards

Acid Base Homeostasis Flashcards

1
Q

How is the Plasma H+ maintained?

A

The maintenance of plasma [H+] in the face of enormous turnover depends very heavily on buffers, and excretion of CO2 and nitrogenous waste

  • H+ ions are produced in mmol quantities, yet must be kept at nmol concentrations by BUFFERS
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2
Q

What is Plasma H+?

A

40 nmol/L

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3
Q

What are the acids Produced in the body?

A
  • Carbon dioxide: Produced by Tissue respiration, Excreted by lungs
  • Lactate: Produced in Glycolysis, Excreted by Gluconeogenesis
  • Fatty acids: Produced by Lipolysis, Excrted by Re-esterification and oxidation
  • Ketoacids: Produced by Ketogenesis, Excreted by Oxidation
  • H+ generated from urea synthesis: Produced by Ureagenesis. Excreted by Oxidation of amino acids
  • Sulphuric acid: Produced by Metabolism of Met and Cys, Excreted by Renal excretion
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4
Q

Why must H+ levels be kept low?

A

Plasma [H+] is low and cannot be allowed to rise or fall appreciably because H+ ions bind avidly to proteins, changing their conformation and therefore their actions

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5
Q

What is a Buffer?

A

A buffer is a solution which resists change in pH when an acid or base is added

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6
Q

What are buffering systems?

A
  • Bicarbonate
  • Phosphate
  • Ammonia
  • Haemoglobin
  • Proteins
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7
Q

What are acids and bases?

A
  • Acids are H+ donors. Strong acids readily donate H+
  • Bases are H+ acceptors. Strong bases readily accept H+
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8
Q

What is pH?

A

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

pH = -log10[H+]

pH scale was devised to cope with the wide range of H+ concentrations encountered in chemistry

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9
Q

What is considered to devaitions of H+?

A
  • If [H+] >45 nmol/L (pH <7.35), the patient is acidaemic
  • If [H+] <35 nmol/L (pH >7.45), the patient is alkalaemic
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10
Q

What is Ka and pKa?

A
  • Ka = acid dissociation constant
  • pKa = negative logarithm of Ka

pKa = -log10Ka

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11
Q

How are pH and pKa related

A

pKa = pH when half of the acid has dissociated (i.e. when acid and conjugate base are in equal proportions so [base]/[acid] = 1)

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12
Q

What is the Henderson-Hasselbalch Equation?

A

pH = pKa + log10(base/acid)

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13
Q

What is Ka?

A

Ka = [H+][A-] / [HA]

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14
Q

How is the equilibrium equation involving Carbon dioxide and Bicarbonate written?

A

[H+] + HCO3- ⇌ H2CO3 ⇌ CO2 + H2O

  • CO2 acting as an acid: When dissolved in plasma, CO2 becomes an acid (carbonic acid; H2CO3), which readily dissociates to release [H+].
  • [HCO3-] acting as a base: [HCO3-] accepts a proton to form carbonic acid, which is converted to CO2 for excretion in the lungs
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15
Q

Which enzyme catalyses the equation for carbonic acid?

A

Carbonic anhydrase

  • Found in high concentrations in RBCs and in the renal tubules – catalyses reaction both ways (formation of CO2 and H2O from carbonic acid [proximal tubule], and formation of carbonic acid from CO2 and H2O [RBCs])
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16
Q

pH = 6.1 + log10( [HCO3-] / pCO2 x α)

  • pCO2 = partial pressure of CO2 (kPa)
  • α = solubility constant (0.225 for CO2)
A
17
Q

What is pH propotional to?

A

pH is proportional to [HCO3-] / pCO2

​Blood pH depends not on absolute amounts of CO2 or HCO3-, but on the ratio of the two

18
Q

Describe the Bicarbonate buffering system

A
  • Bicarbonate (HCO3-) acts as a buffer, “mopping up” H+ ions
  • However, it cannot buffer CO2, because of the above equation (buffering by bicarbonate would only result in the production of more CO2)
  • Equilibration of CO2 therefore requires non-bicarbonate buffers (e.g. Hb, proteins – see later)
19
Q

Describe the Phosphate buffering system

A
  • Monohydrogen phosphate and dihydrogen phosphate form a buffer pair:

[HPO4]2- + H+ ⇌ H2PO4-

  • Concentrations of these anions are too low in plasma to make an appreciable difference, but they are important buffers in urine
20
Q

Describe the Ammonia Buffering system

A
  • Ammonia and ammonium ions form a buffer pair:

[NH3] + [H+] ⇌ [NH4]+

  • Vast majority of ammonia in the body is already in ammonium ([NH4]+) form, but NH3 is an important buffer in urine so provides a route for nitrogen excretion that does not result in the generation of H+
  • Urea cycle results in generation of H+
21
Q

How does Haemogobin provide a buffer?

A

Principal non-bicarbonate buffer - important for buffering CO2

  • Reduction of CO2
  • Production of HCO3-
  • Formation of HHb
22
Q

Describe the Protein buffering system

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

23
Q

Which organs are involved in Acid-Base metabolism?

A
  • Liver
  • Lungs
  • Kidneys
  • GI Tract
24
Q

How is Acid-Base regulated through the lungs?

A
  • Gaseous exchange between the blood and the air, facilitated by alveoli in the lungs to excrete CO2
  • Respiratory control mechanisms are extremely sensitive to pCO2 – respiratory rate can increase or decrease depending on pCO2
  • In a healthy person, the rate of elimination is equal to the rate of production, so that blood pCO2 remains constant
25
Q

How does Pulmonary Gash exchange take place?

A
  • Inhale oxygen-rich air with low CO2 content
  • As blood travels around the body, the oxygen is used by the tissues, and CO2 is produced
  • CO2 is excreted when the blood is returned to the lungs, and more oxygen is taken on board
  • As a result, different partial pressures of O2 and CO2 are expected in different sample types (arterial vs. venous vs. capillary)
26
Q

What does the oxyhaemoglobbin dissociation curve describe?

A

Describes relationship between pO2 and %O2 saturation:

  • ↑ pO2, O2 binds to Hb
  • ↓ pO2, O2 is released from oxyHb
27
Q

When does the Oxyhaemoglobin Dissociation curve shift to the right?

A

Curve shifts to the right. This means Hb has reduced affinity for O2. Higher pO2 required to maintain saturation when:

  • Body temperature increases
  • Patient is hypoxic or anaemic
  • [H+] increases (Bohr effect)
28
Q

How does the respiratory system compensate for Acidaemia?

A
  • Respiratory compensation involves increasing the respiratory rate
  • This increases the amount of CO2 blown off in expired air, and reduces the pCO2 in the blood
29
Q

How does the respiratory system compensate for Alkalaemia?

A
  • Respiratory compensation involves reducing the respiratory rate
  • This decreases the amount of CO2 blown off in expired air, and increases the pCO2 in the blood
30
Q

How does the kidney participate in Acid-Base balance?

A
  • Excretion of H+ ions (distal tubule)
  • Reabsorption of bicarbonate (proximal tubule)
  • Regeneration of bicarbonate (distal tubule)
  • Creates acidic urine containing almost no bicarbonate
31
Q

How is Bicarbonate regenerated in the Kidneys?

A
  • H2CO3 generated from CO2 and H2O under action of carbonic anhydrase. This dissociates into H+ and HCO3-
  • H+ actively secreted into glomerular filtrate in exchange for Na+ (4), where H+ ions are excreted as dihydrogen phosphate (H2PO4-) (1)
  • HCO3- and Na+ ions pumped into plasma
  • Continued formation of H+ in renal tubular cells is accompanied by stoichiometric generation of bicarbonate so excretion of H+ results in regeneration of bicarbonate so maintains buffering capacity
32
Q

How is Bicarbonate reabsorbed?

A
  • Bicarbonate present in filtrate accepts a proton to form H2CO3 which forms CO2 and H2O
  • CO2 diffuses into tubular cell, where it generates H2CO3, which then dissociates to form HCO3- and H+
  • The bicarbonate formed in the cell is pumped into the plasma (along with Na+ for charge balance)
  • H+ ions secreted into glomerular filtrate in exchange for Na+ (4)
33
Q

What is the mineralcorticoid action in the kidney and how is it involed in acid base regulation?

A
  • Excretion of potassium and hydrogen ions in the distal tubule, with concomitant reabsorption of sodium ions
  • Under the control of aldosterone
  • ↑ Aldosterone leads to ↑ sodium reabsorption and potassium/hydrogen ion excretion
34
Q

How do the kidneys compensate for Acidaemia?

A
  • Renal compensation involves increasing the bicarbonate concentration
  • This is achieved by maximising bicarbonate reabsorption and regeneration in the kidney
35
Q

How do the kidneys compensate for Alkalaemia?

A
  • Renal compensation involves reducing the bicarbonate concentration
  • This is achieved by reducing the regeneration of bicarbonate in the kidney
36
Q

How is Acid-Base regulated in the GI tract?

A
  • H+ secreted into stomach as HCl
  • Bicarbonate secreted by pancreas into duodenum à needed to neutralise acid from stomach (contents of intestines are rich in bicarbonate)
37
Q

How is Acid-Base regulated in the liver?

A
  • Dominant site of lactate metabolism (Cori cycle). Increased production (e.g. anaerobic glycolysis) or decreased consumption (e.g. liver disease) lactate can causes Lactic Acidosis
  • Only site of urea synthesis (waste product of ammonia metabolism). High concentrations of ammonia (hyperammonaemia) can cause tachypnoea, and lead to a respiratory alkalosis
38
Q

What causes lactic acidosis?

A

Type A – tissue hypoxia

  • Shock (septic and cardiogenic)
  • Cardiovascular insufficiency
  • Hypovolaemia
  • Profound anaemia
  • Asphyxia

Type B – tissue oxygenation normal

  • Disease: DM, liver failure, renal failure, seizures
  • Toxins: alcohols, CO, salicylates / paracetamol
  • Congenital enzyme defects (e.g. pyruvate dehydrogenase deficiency)

D-lactic acidosis

  • D-isomer produced by bacteria within GI tract
  • Short bowel syndrome and bacterial overgrowth
39
Q

What are clinical laboratory indications of Lactic Acidosis?

A
  • Metabolic acidosis
  • High anion gap (presence of lactate anions)
  • High urate concentration (lactate competes with urate for renal tubular excretion)
  • IncreasedWBC (sepsis)

MSC: Disease of major orgns (23 decks)

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