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Block 2 > Acid Base Regulation > Flashcards

Acid Base Regulation Flashcards

1
Q

Define acid. Give an example.

A

Any chemical that can donate H+ (proton) e.g. HCL -> H+ + Cl-

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2
Q

Define base. Give an example.

A

Any chemical that can accept H+ e.g. NaOH -> Na+ + OH- which allows OH-+ H+ -> H2O

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3
Q

What is the difference between a strong and weak acid? Give examples.

A

Strong acid: completely dissociates in water releasing large amounts of H+ e.g. HCl -> H+ + Cl

Weak acids: incompletely dissociates in water + reaches equilibrium with its conjugate base forming a buffer pair that responds to changes in [H+] by reversibly binding H+ e.g. H2CO3 H+ + HCO3-

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4
Q

How do you measure acidity (pH scale)?

A

[H+] in mol/L but because there is a wide range of these values, you should take the negative logarithm to base 10 [H+] = pH range between 1-14

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5
Q

What is the relationship between pH and H+ concentration?

A

Inverse relationship where a 1 unit pH change is equivalent to a 10-fold increase in [H+] - as [H+] increases, pH decreases

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6
Q

What is the average pH of blood?

A

7.4 (7.36-7.44) = [H+] between 36-44 nanomoles/litre

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7
Q

Survival for short periods is possible at pH values ranging between?

A

6.8-8.0

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8
Q

Why is the regulation of H+ concentration more complex and tightly regulated than for other ions?

A

H+ is small + charged thus affecting protein function:

  • Alters protein activity especially enzymes; body wide effect where many physiological processes sensitive to small change in [H+]
  • Alters binding of other ions e.g. low [H+] increases Ca2+ binding to albumin
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9
Q

What processes are usually sufficient to maintain ion concentration?

A

Balance of intake, production + excretion to maintain homeostasis (kidney has a role)

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10
Q

What is acid-base regulation?

A

Control of [H+]

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11
Q

Why is it a bad thing if ion binding is altered in the body?

A

The body will think that the levels are different to what they are + try to correct this

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12
Q

What are the 2 sources of H+ in the body?

A
  1. Volatile acids (more easily vapourised)

2. Non-volatile (fixed/non-respiratory acids)

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13
Q

What is a volatile acid?

A

An acid that can leave solution + enter the atmosphere via lung excretion

H+ generated from aerobic metabolism + CO2 production by tissues (H2CO3)

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14
Q

What is a non-volatile acid?

A

Organics acids (H+) e.g. lactic or keto acids formed in certain circumstances from other metabolic processes + excreted by the kidneys

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15
Q

What are the 3 main mechanisms to maintain H+ concentration and thus, minimise changes in pH?

A
  1. Buffer systems: rapid chemical reaction that minimises sudden changes in pH (unable to change overall body H+)
  2. Lungs: RAPIDLY adjust excretion of CO2
  3. Kidneys: SLOWLY adjust urine excretion of H+ altering body HCO3- levels
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16
Q

Why are buffer systems only a good short-term mechanism to maintain pH?

A

They mop up H+ but cannot excrete it out of body so make pH appear maintained short-term but eventually will run out of ways to mop H+ up

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17
Q

What is a buffer? How does they work?

A

Any substance that reversibly binds H+ i.e. weak acid

Buffer + H+ HBuffer

So if H+ added, buffer binds it to form Hbuffer removing H+ however, if H+ removed, Hbuffer releases H+ adding H+

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18
Q

What are the 3 main buffer systems in the body?

A
  1. Bicarbonate (most important in EC): HCO3- + H+ H2CO3
  2. Phosphate (IC + urine): HPO42- + H+ H2PO4-
  3. Protein (mainly IC): Pr- + H+ HPr
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19
Q

What are the 3 types of protein buffer systems?

A
  1. Hb (RBC)
  2. AA (proteins)
  3. Plasma protein (albumin)
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20
Q

Explain the bicarbonate buffer system.

A

H+ + HCO3- (kidneys) H2CO3 (carbonic anhydrase/dehydratase) H2O + CO2 (lungs)

Connects the lungs control of [CO2] to kidneys control of [HCO3-] in acid-base balance -> shows how systems can compensate for each other

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21
Q

What is the Henderson-Hasselbalch (H-H) equation? What does it allow us to work out?

A

pH = pK + log10[HCO3-]/[CO2]

pK = constant
[HCO3-] = from kidneys
[CO2] = from lungs - measured from pCO2

Allows us to calculate pH based on measurements of [HCO3-] + [CO2] ratio (2 concentrations easily measured in arterial blood)

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22
Q

In arterial blood, what should ratio of HCO3- and CO2 concentration be roughly?

A

20:1

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23
Q

What are the 2 ways the body maintains pH?

A
  1. Functional ability of lungs to maintain [CO2] i.e. rapid response (mins-hrs) alters CO2 elimination via change in ventilation to restore pH
  2. Functional ability of kidneys to maintain [HCO3-] i.e. slow response (hrs-days) alters HCO3- production + H+ excretion to restore pH
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24
Q

pH is dependent on the __ of HCO3- and CO2 concentrations not the ___.

A 
Ratio
Amounts (i.e. do not have be identical in concentration)
25
Q

How can HCO3- and CO2 concentration change in order to decrease or increase pH?

A

Decreased pH: Increased [CO2] or decreased [HCO3-] or both

Increased pH: Decreased [CO2] or increased [HCO3-] or both

26
Q

How can the kidneys control acid-base balance and therefore, pH?

A

Control ECF pH via 2 mechanisms (both rely on kidneys ability to secrete H+):

  1. Excretion of H+ (non-volatile acid production) in urine -> urine usually acidic (+ production of new HCO3- in turn)
  2. Reabsorption of filtered HCO3- to avoid reduction in [HCO3-]

H+ loss = HCO3- gain

27
Q

Is there normally HCO3- in the urine? Why?

A

No

Because then less would be available to bind H+ in plasma, adding H+ to plasma and decreasing plasma pH

28
Q

How much of the filtered HCO3- must be reabsorbed and where does this occur?

A

Must reabsorb 100%

Majority of reabsorption occurs in proximal convoluted tubule (small amount in late distal + collecting tubules)

29
Q

How is HCO3- reabsorbed from the tubular lumen of the kidneys?

A
  1. HCO3- converted to H2CO3 (using secreted H+) + then CO2 + H2O (cannot be reabsorbed directly)
  2. CO2 + H2O transported into tubular cells + converted back to H2CO3 via carbonic anhydrase
  3. H2CO3 dissociates back into HCO3- + H+ -> H+ stays in cell to be secreted again whilst HCO3- co-transported with Na+

= no net gain/loss of H+ or HCO3- = no change in acid-base status despite H+ secretion as its just cycling round + reclaiming HCO3- that was already in blood

30
Q

How is H+ secreted in the kidneys? Where does this occur?

A

Uses H+/K+ ATPase transporters in type A intercalating cells to pump H+ into tubular lumen = generates 800-fold H+ gradient + a min urine pH of 4.5

Late distal + cortical collecting tubules

31
Q

Why are buffers needed in the urine?

A

Comfort

Allow sufficient H+ to be excreted in urine to secrete all 70-100mmol of non-volatile H+

To stop H+/K+ ATPase switching off (stops working when there is high [H+])

32
Q

What are the 2 main urinary buffers?

A
  1. Phosphate

2. Ammonia

33
Q

Why is it important to generate new HCO3- in the kidneys?

A

Some is consumed buffering non-volatile acids produced each day but it needs to return to blood so H+ can bind it instead of H+ increasing + pH decreasing

34
Q

How does the urinary phosphate buffer work?

A

Filtered phosphate has 2 forms that create a buffer pair in tubular fluid: monoprotic (HPO42-)+ diprotic (H2PO4)

Excess of HPO42- can pick up excess secreted H+ in lumen excreting it in urine -> leads to HCO3- production which passes into blood

HPO42- + H+ H2PO4-

35
Q

In terms of the urinary phosphate buffer, what does H+ combine with when excreted? What process occurs at the same time?

A

NaHPO4-

HCO3- passes into interstitial fluid

36
Q

How does the urinary ammonia buffer work?

A

Ammonia + ammonium form a buffer pair:

NH3 + H+ NH4+

NH3 secreted mainly in collecting duct + picks up excess secreted H+ excreting it in urine as NH4+ (in turn HCO3- is produced + goes into interstitial fluid then blood)

37
Q

How is ammonium (NH4+) synthesized? What then happens to it?

A

From glutamine via glutaminase in PCT cells

Broken down to glutamate + then α-ketoglutarate

38
Q

How is the urinary ammonia buffer regulated?

A

Responds to body’s acid-base status -> decrease in pH stimulates renal glutamine metabolism leading to increased H+ excretion (+ vice versa)

39
Q

Why are renal responses to pH slower than in the lungs?

A

Because the kidneys response requires protein synthesis + breakdown

40
Q

What 4 factors stimulate H+ secretion in the kidneys?

A
  1. Increased pCO2 in ECF
  2. Decreased pH of ECF
  3. Increased aldosterone
  4. Hypokalaemia
41
Q

Define acidosis.

A

Any process that results in blood becoming more acidic than normal i.e. lower pH via addition if acid/loss of alkali

Can have respiratory or metabolic causes

42
Q

Define alkalosis.

A

Any process that results in blood becoming more alkaline than normal i.e. higher pH via addition of alkali/loss of acid

Can have respiratory or metabolic causes

43
Q

What will happen if a disease alters the ratio of HCO3- concentration to CO2 concentration?

A

Change in pH i.e. acidosis or alkalosis (signify underlying disease)

44
Q

What is a metabolic problem?

A

Primary problem affecting [HCO3-]

45
Q

What is a respiratory problem?

A

Primary problem affecting CO2 excretion

46
Q

What is compensation?

A

When a change in either [HCO3-] or [CO2] is compensated by via the other parameter changing in order to minimise the change in pH attempting to restore it back to normal

47
Q

If a disease is compensated for, what will you see in terms of HCO3- and CO2 concentration?

A

Both [HCO3-] AND [CO2] will lie outside normal ranges in same direction i.e. both will be raised/lowered

48
Q

What can cause a respiratory acidosis?

A

Any disorder affecting lungs, chest wall, nerves, muscles or CNS leading to inappropriate reduction in ventilation thus, increasing [CO2]

49
Q

What can cause a respiratory alkalosis?

A

Any disorder leading to inappropriate increase in ventilation e.g. anxiety + hyperventilation or high altitude leading to decreasing [CO2]

50
Q

What can cause a metabolic acidosis?

A

Addition of exogenous acid e.g. methanol or endogenous acid e.g. lactic/keto acids

Failure of H+ secretion e.g. decreased kidney function

Loss of HCO3- e.g. severe prolonged diarrhoea

-> decreasing [HCO3-]

51
Q

What can help narrow the underlying differential diagnosis of a metabolic acidosis?

A

Anion gap

52
Q

What can cause a metabolic alkalosis?

A

Addition of alkali

Excess loss of H+ e.g. severe prolonged vomiting

Excess aldosterone e.g. due to dehydration - stimulates H+ secretion in distal tubule

-> increased [HCO3-]

53
Q

How can you treat metabolic acid-base disorders?

A
  1. Treat + correct underlying problem whenever possible most importantly
  2. Use substances to neutralise acid or base OCCASIONALLY e.g. sodium bicarbonate to treat acidosis or ammonium chloride for alkalosis
54
Q

How should you interpret acid-base changes?

A
  1. Look at pH
  2. Look at [HCO3-] + pCO2
  3. Look for compensation evidence
55
Q

What does it mean if HCO3- + CO2 concentration are both out of range but in OPPOSITE directions?

A

Mixed metabolic and respiratory disorder

56
Q

What will a blood gas show in a respiratory acidosis? What if its compensated for?

A

Increased pCO2

Compensation: increased pCO2 + increased [HCO3-]

57
Q

What will a blood gas show in a respiratory alkalosis? What if its compensated for?

A

Decreased pCO2

Compensation: decreased pCO2 + decreased [HCO3-]

58
Q

What will a blood gas show in a metabolic acidosis? What if its compensated for?

A

Decreased [HCO3-]

Compensation: decreased [HCO3-] + decreased pCO2

59
Q

What will a blood gas show in a metabolic alkalosis? What if its compensated for?

A

Increased [HCO3-]

Compensation: increased [HCO3-] and increased pCO2

Block 2 (45 decks)

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