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Disease of Major Organs > Acid base > Flashcards

Acid base Flashcards

1
Q

Why are buffers required in the human body?

A

We are net producers of acid so the buffers are required for net neutrality

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2
Q

What happens when a patient acid base is unbalanced?

A

acidaemic (H+>45nmol/L – pH<7.35)

alkalaemic (H+<35nmol/L – pH>7.45).

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3
Q

Define buffer and name the ones of the body

A

Buffering systems describe systems that resist changes in pH when an acid or base is added to ensure H+ ions are transported and excreted without causing damage to physiological processes. The main buffer systems are haemoglobin, phosphate, ammonia, plasma proteins, bicarbonate.

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4
Q

Describe the buffering actions of bicarbonate

A

This is the most important buffer. Here the bicarb is the base and CO2 is the acid. Bicarbonate mops up free H+ to form carbonic acid. Carbonic acid readily dissociates to H2O and CO2. CO2 can be lost via breathing

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5
Q

Phosphate as a buffer

A

This buffering occurs using a buffering pair monohydrogen phosphate and dihydrogen phosphate. It mainly acts in the urine

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6
Q

Ammonia as buffer

A

Similar to phosphate this buffer is via the buffering pair ammonia and ammonium ion. Ammonia is an active buffer in the urine providing a route of nitrogen excretion without generating H+

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7
Q

Describe haemoglobin as a buffer

A

Buffer system used to buffer CO2 in the blood. Here CO2 is reduced, produces bicarb, and a HHb. The buffering is best described using the bohr effect and Haldane effect. Basically increase in CO2 in the blood cause blood pH to decrease.

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8
Q

Proteins as a buffering system

A

Buffering of plasma proteins are dependent on the R-groups and side chains. These give either weakly acidic or basic characterisitcs. Basic groups act as buffers to accept H+. The most abundant buffer is albumin.

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9
Q

Goal of the lungs in terms of acid base

A

Gaseous exchange between blood and air is facilitated by the lungs to excrete CO2 and increase O2 - thus maintaining an acid base balance

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10
Q

What is the perfusion rate in a healthy individual?

A

In a healthy person the blood pCO2 remains constant as the rate of elimination is equal to the rate of production

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11
Q

How can perfusion be analysed? and what needs to be noted?

A

Blood gas analyser.

  • Need to note what type of blood sample was collected e.g. arterial, venous, and capillary samples
  • because there are differential partial pressures of O2 and CO2
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12
Q

What is the haemoglobin binding affinity to oxygen affected by?

A

affinity of haemoglobin to oxygen is affected by temperature, H+ and 2-3 DPG concentrations.

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13
Q

In what conditions will heamoglobin binding affinity be reduced?

A

Increased temperatures, hypoxia & anaemia, increased 2-3DPG, and increased hydrogen ion concentrations

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14
Q

What is respiratory compensation? How does it work in alkalaemia and acidaemia?

A

Ventilation is altered by the brainstem respiratory centres to aid in metabolic acid-base disturbances to bring pH to its physiological state.

  • In acidaemia- increasing respiratory rate to excrete more CO2
  • In alkalaemia- reduction of respiratory rate to decrease the CO2 output
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15
Q

What are the acid base functions of the kidney?

A

Major regulator of the acid-base balance by excreting H+ ions, reabsorb bicarbonate and regenerate bicarbonate

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16
Q

The kidney aims to acidify urine by secreting bicarbonate into the filtrate. True or false

A

Aims to acidify urine without excreting bicarbonate

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17
Q

How is bicarbonate regenerated in the DCT?

A

The regeneration of bicarbonate occurs in the intercalated cells where carbonic anhydrase combines water and CO2 to make carbonic acid. The carbonic acid dissociates to bicarb and H+. The bicarb enters the blood using a bicarb-Na+ co-transporter

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18
Q

How is the secreted H+ in the DCT excreted?

A

H+ is secreted by an Na+-H+ antitransporter. H+ in the lumen combines with monohydrogen phosphate, which is excreted as dihydrogen phosphate.

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19
Q

How is bicarbonate reabsorbed in the proximal tubule?

A

The tubular cells secrete H+ into the lumen using a Na+-H+ antitransporter. H+ combines with the free bicarbonate to make carbonic acid. Carbonic acid is broken down by carbonic anhydrase to water and CO2. Water and CO2 is freely absorbed into the tubular cells, where this process can occur but in reverse. H+ is regenerated to furhter assist reabsorbing more bicarbonate

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20
Q

Describe the hormonal actions that can induce homeostasis of the acid base.

A

ALdosterone act to regulate Na reabsorption. It causes reabsorption of Na+ in exchange for excretion of K+ and H+ into the filtrate.

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21
Q

What is the main difference between renal and pulmonary compensation?

A

Compared to pulmonary compensation, which occurs quickly, the renal compensation occurs over days to regulate to the plasma pH

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22
Q

How does the kidney adapt in disturb acid base balances?

A
  • In acidosis the kidneys will act to increase the bicarbonate concentration by maximising bicarbonate reabsorption and regeneration, resulting in net excretion of H+
  • Alkalaemia the renal compensation acts to decrease the regeneration of bicarbonate in the kidneys.
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23
Q

How does the livers function affect acid base balance?

A

It is a dominant site for lactate metabolims and the only site for urea synthesis (waste of ammonia metabolism).

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24
Q

How does high ammonia concentrations affect the body?

A

Hyperammonaemia can cause tachypnoea and lead to respiratory alkalosis

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25
Q

What is lactic acidosis?

A

Results from increased prodiction (anaerobic glycolysis) or decreased condsumtpion (liver disease)

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26
Q

Causes of lactic acidosis.

A

Type A - tissue hypoxia

  • shock
  • cardiovascular insufficiency
  • hypovolaemia
  • profound anaemia

Type B- tissue oxygenation normal

  • Disease: DM, liver failure, renal failure, seizures
  • Toxins: alcohols, CO, salicylates/paracetamol
  • Congenital enzyme defects

D-lactic acidosis

  • D-isomer produced by bacteria in the GI
  • Short bowel syndrome with bacterial overgrowth
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27
Q

Clinical manifistations of lactic acidosis.

A
  • metabolic acidosis
  • high anion gap
  • high urate concentration
  • increased white blood cell count (sepsis)
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28
Q

What blood sample is used in blood gas analysers?

A

Heparinised whole blood with no air bubbles

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29
Q

What do the blood gas analysers measure?

A 
Electrolytes
- Na, K, Cl, ionised Ca
Co-oximetry
- total Hb, O2 sat, oxy-Hb, CO-Hb
Metabolite
- glucose and lactate
Calculates parameters
- base excess, standard bicarbonate, anion gap, total CO2

pH and gases
- pH, PO2, PCO2

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30
Q

What measurement methods are available in blood gas analysers?

A

There are three methods of measurement: potentiometric, amperometric, spectrophotometry

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31
Q

How can we approximate bicarbonate in the blood?

A

Total CO2 has been shown to be able to approximate the amount of bicarbonate in the blood.
- A decrease in total CO2 indicates respiratory alkalosis/metabolic acidosis

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32
Q

Following a pH test what measure should follow?

A

Measure of pCO2 to determien the metabolic and pulmonary state

33
Q

Match the following.

  1. PCO2>6.0kPa
  2. PCO2<4.7kPa

A. Metabolic acidosis
B. Respiratory acidosis
C. Metabolic alkalosis
D. Respiratory alkalosis

A
  1. BC

2. AD

34
Q

How is the standard bicarbonate used in asssessing acid base disturbances?

A

Assessed by measuring bicarb at physiological conditions. This removes the respiratory contribution so an abnormal standard bicarbonate is indicative of metabolic contribution to acid-based disturbances

35
Q

Match the following

  1. Low standard bicarbonate
  2. High standard bicarbonate
  3. Normal standard bicarbonate

A. Respiratory disturbance
B. Metabolic alkalosis
C. Metabolic acidosis

A

1 C
2B
3A

36
Q

What does base excess measure?

A

Describe the metabolic component of an acid-base disturbance independently of changes in CO2. The measure is the amount of strong acid/base needed to titrate 1L of whole blood to physiological pH at pCO2 of 5.33kPa and a temp of 37.

37
Q

True or false: A highly negative BE indicates metabolic alkalosis

A

False.
Highly negative BE = metabolic acidosis, highly positive BE= metabolic alkalosis

Normal range: -2.3->2.3mmol/L

38
Q

What does the anion gap measure?

A

Calculating the difference between sum of measured cations and anions.

AG=(Na+K)-(Cl+HCO3)

39
Q

Describe an absent anion gap

A

Occurs with increase in unmeasured cations, hypoalbuminaemia, bromide toxicity or nitrates

40
Q

What does a low or negatice anion gap indicate?

A

A low or negative gap is observed when hyperchloremia is caused by high levels of cations, monoclonal IgG gammopathy, or hypocalcaemia

41
Q

What are the biochemical features of metabolic acidosis?

A

Biochemical characterisation of decreases bicarbonate, decreased pH, N/D PCO2 and increased PO2

42
Q

What causes the hyperventilation in metabolic acidosis?

A

pulmonary compensation

43
Q

State the causes of metabolic acidosis with examples

A 
Increased acid formation 
- lactic acidosis, diabetic ketoacidosis
Gain of acid
- IV, infusion of ammonia chloride
Loss of base
- Gi loss, renal loss
Decreasd acid secretion
- Uraemic acidosis, RTA
44
Q

How is metabolic acidosis first investigated?

A

pH to establish acidosis. pCO2 to determine origin (PCO2<4.7kPa for metabolic acidosis)

45
Q

How is the anion gap utilised in metabolic acidosis investigation?

A

To determine if there is normal anion or non-anion gap metabolic acidosis.

46
Q

How does the non-gap (normal anion gap) metabolic acidosis form?

A

Occurs when there is a loss of bicarbonate, but it is replaced by Cl- causing a normal anion gap

47
Q

What causes non-gap (normal anion gap) metabolic acidosis

A

GI losses

  • diarrhoea
  • intestinal fisulae
  • pancreatitis

Renal tubular acidosis

Other:

  • renal insufficiency
  • recovery from ketoacidosis
  • carbonic anhydrase inhibitors (acetozalmide)
48
Q

In what cases should RTA be suspected?

A

When there is normal anion gap, no GI losses, and hypercholaraemic metabolic acidosis

49
Q

Match the following

  1. Type I
  2. Type II
  3. Type IV

A. Urine pH>5.5
B. Urine pH<5.5

A

1A
2B
3B

50
Q

Match the following

  1. DCT
  2. PCT
  3. Hypoaldosteronism

A. RTA Type IV
B. RTA Type II
C. RTA Type I

A

1C
2B
3A

51
Q

Describe RTA type I

A

Inability to secrete H+ in the DCT, thus, not acidifying urine.
Biochemical features urine pH>5.5, hypokalaemia, hypercalciuria, nephrocalcinosis, renal calculi

52
Q

What is a positive test for RTA I?

A

It can be investigated using a urine acidification test, where a urine of pH<5.5 following acid load is a positive test.

53
Q

Describe RTA type II

A

a genetic disease, is characterised by the decreased ability to reabsorb filtered products, but since DCT is normal the urine acidification is normal.
Biochemical features: urine pH<5.5, hypokalaemia, osteomalacia and calciruia without stone formation – urinary glucose, phosphate and urate may be increased with aminoaciduria and hypercitrateuira in Fanconi

54
Q

What is a positive test for RTA II?

A

Abnormal high fractional excretion of bicarbonate when its at 20mmol/L

55
Q

Describe RTA type IV

A 
Adrenal failure (hypoaldosteronism) or hyporeninaemics which results in sodium wasting and decreased H+ and K+ excretion by ATPases in DCT. 
- Acidification normal though

Biochemical features: urine pH<5.5, hyperkalaemia and sodium wasting

56
Q

What is a positive test for RTA IV?

A

Renin/aldosterone measure

57
Q

What is the basis for respiratory acidosis?

A

Failure of ventilating CO2 resulting in its accumulation

58
Q

Biochemical features of respiratory acidosis?

A

Increased pCO2- hypercapnia
Decreased pH
Decreased ratio HCO3/PCO2 (this causes change to pH)

59
Q

What causes respiratory acidosis?

A

CNS depression
- anaesthetics, narcotics, opiates

CNS disease
- trauma, stroke, MI

neurological diseaes
- spinal cord lesions, Guillan Barre syndrome)

60
Q

Group the defects to respiratory function

A

Mechanical - myasthenic syndrome, myopathies, thoracic trauma

Pulmonary disease - COPD or obstructive defects

61
Q

What systemic effects does metabolic acidosis have?

A

Negative inotropic effects on CVS
- arteriolar vasodilation, constriction of peripheral veins

Bohr shift to the right
- Increased oxygen availability at tissues

CNS
- unconciousness

Hyperkalaemia
- moves from ICF to ECF due to decreased renal excretion

62
Q

What is the bodys biochemical approach to metabolic acidosis?

A

Buffers
- HCO3- will act to try and mop up the acute increase in H+.

Respiratory compensation

  • Greatest effect, rapid, reaches optimum 12-24hrs
  • Chemoreceptors cause hyperventilation
  • but this is self-limiting as hyperventilation results in the generation of CO2

Renal compensation

  • present but insignificant
  • increase H+ excretion, regeneration of HCO3- via inhibited urea production, increased renal gluconeogenesis and Na+-H+ exchange
63
Q

How do you treat metabolic acidosis?

A

First treat underlying cause.

- Alkali administration: IV sodium bicarbonate

64
Q

What are the systemic effects of pulmonary acidosis?

A

Systemic effects

hypoxaemia, neurological (hypercapnia), effects of acidosis (Bohr shift, hyperkalaemia)

65
Q

What is the biological response to respiratory acidosis?

A

Buffering
- Primarily haemoglobin

Respiratory compensation
- Hyperventilation stimulated, but underlying cause prevents adequate response

Renal (2-5 days) compensation

  • most effective
  • increasing bicarbonate reabsorption, excrete phosphate as H2PO4-, increase urinary ammonium and increase the Na+-H+ exchange
66
Q

Describe management of pulmonary acidosis.

A

Treat underlying cause, maintain arterial PO2 (avoid hypoxic stimulus of respiration), avoid rapid correction of PCO2, and the use of bronchodilators.

67
Q

Biochemical features of metabolic alkalosis

A

Decrease in H+ (pH increase)
Increase in bicarb
Slight increase in pCO2
Decrease in K+

68
Q

Describe the development of alkalosis using GI loss of different electrolytes.

A

Loss of H+ simple

  • Loss of Cl- will stimulate the kidney to retain HCO3- causing a metabolic alkalosis state
  • GI loss in Na+ or K+ the kidney will respond by retaining Na+/K+ at the expense of excreting H+, thus lowering the H+ concentration
69
Q

How can Cl be used in categorising metabolic acidosis?

A

The causes can be divided based on urine Cl- to determine saline responsiveness.

70
Q

What are saline responsive causes?

A

saline responsive (urine Cl- < 20mmol/L) causes are gastrointestinal (vomiting, gastric drainage), exogenous alkali administration (citrate in transfusions, sodium bicarbonate), or diuretics.

71
Q

What are saline unresponsive causes?

A

Saline unresponsive (urine Cl->20mmol/L) causes can be associated with hypertension (mineralocorticoid excess) (primary hyperaldosteronisms, Cushing’s syndrome), or others such as barters, Gitelmans or refeeding syndrome.

72
Q

Systemic effects of metabolic alkalosis

A 
Impaired O2 delivery
K depletion - sustains alkalissi and manifest as muscle weakness
Neuromuscular hyperexcitibility (acute)
73
Q

Biological response to metabolic alkalosis

A

Pulmonary

  • Decreased stimulation of chemoreceptors - self-limiting as increased pCO2 stimulates ventilation
  • Hypoxic stimulus overrides decrease in H+ stimulus in the respiratory centre

Renal

  • Exacerbates the alkalosis by reabsorbing HCO3 due to decreased GFR
  • The potassium deficiency has the same effect through the activation of mineralocorticoids actively excreting H+ to take up K+ and Na+.
74
Q

How is metabolic alkalosis managed?

A

Treat underlying cause and the factors that exacerbate alkalosis.

  • volume expansion if saline responsive
  • potassium and magnesium replacement
  • if hyperaldosteronism then give spironolactone or amiloride

NOTE: saline to un-responsive will cause sodium excess.

75
Q

Biochemical features of respiratory alkalosis

A

increase in pH, decrease in PCO2, N/D HCO3-, decreased K+ & phosphate

76
Q

What is respiratory alkalosis caused by?

A

Involve hyperventilation
Pulmonary causes
- pneumonia, pulmonary oedema, lung fibrosis, asthma

Non-pulmonary stimulation of the respiratory centre

  • cortical influences
  • drugs (salicylates, catecholamines)
  • endogenous compounds (hepatic failure, toxins, pregnancy)
  • CNS lesions (meningitis, SAH)
  • hypoxia (high altitude)
77
Q

Manifestations of pulmonary alkalosis

A
  • Acute hypocapnia decreases cerebral blood flow causing light headedness and confusion
  • perioral and peripheral parasthesia or cardiovascular effects (high HR, tightening chest, angina)
  • Mild hypokalaemia and hypophosphataemia
78
Q

Treatment of pulmonary alkalosis

A

Treat underlying cause

Disease of Major Organs (14 decks)

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