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CRR > H+J. Lecture 28+29 Regulation of acid-base balance > Flashcards

H+J. Lecture 28+29 Regulation of acid-base balance Flashcards

1
Q

do acids accept or yield protons?

A

yield

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2
Q

do bases accept or yield protons?

A

accept

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3
Q

do strong acids/bases dissociate more or less in solution compared to weak acids/bases?

A

dissociate more

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4
Q

do strong or weak acids liberate more protons?

A

strong

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5
Q

do strong or weak acids buffer more protons?

A

weak

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6
Q

what is the equation for the dissociation constant?

A

(proton conc x conjugate base conc)/ (conc of undissociated acid)

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7
Q

what is the equation for pH?

A

-log10[H+]

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8
Q

what happens to [H+] as pH goes down/more acidic?

A

it increases

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9
Q

what is the [H+] in ECF?

A

around 4 x 10-8 M

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10
Q

what is the pH of arterial blood?

A

around 7.45

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11
Q

what is the pH of venous blood?

A

around 7.35

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12
Q

what is the pH range compatible with life?

A

6.8-8.0

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13
Q

what happens outside the pH range of 6.8-8.0?

A

death

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14
Q

what is pH less than 7.35 called?

A

acidosis

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15
Q

what is pH more than 7.45 called?

A

alkalosis

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16
Q

what 3 things can small changed in pH affect?

A

Nerve excitability
Enzyme activity
K+ homeostasis

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17
Q

what affects does acidosis have on CNS activity?

A

decreases it

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18
Q

what can acidosis lead to?

A

disorientation, coma, death

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19
Q

what affects does alkalosis have on CNS activity?

A

increases it

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20
Q

what can alkalosis lead to?

A

pins/needles, muscle twitch, death

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21
Q

what are enzymes?

A

proteins that are made from AAs

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22
Q

what are AA R-groups?

A

titratable side-chains

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23
Q

why is R-group charge vital?

A

to correct folding

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24
Q

why is the 3D shape of enzymes vital?

A

for functioning

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25
Q

are proton handling and K+ secretion linked?

A

yes

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26
Q

what effect does acidosis have on secretion of H+?

A

increases it

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27
Q

what does an increase in secretion of H+ result in?

A

decrease secretion of K+

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28
Q

what does a decrease secretion of K+ lead to?

A

hyperkalaemia

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29
Q

what does hyperkalaemia cause?

A

depolarisation of excitable cells

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30
Q

what are the 2 sources of acids and bases?

A

food and metabolism

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31
Q

how are proteins a source of acids?

A

contain phosphorus and sulphur, converted to phosphoric and sulphuric acid (strong acids)

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32
Q

what does fruit digestion yield?

A

release of bases

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33
Q

what is released from fat metabolism?

A

fatty acids

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34
Q

what type of acids are fatty acids?

A

Weak acids, yield protons

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35
Q

what is produced from anaerobic glycolysis?

A

lactic acids

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36
Q

what type of acid lactic acid?

A

Weak acid, yields protons

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37
Q

what is CO2 from respiring cells hydrated to form?

A

carbonic acid

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38
Q

is carbonic acid a strong or weak acid?

A

weak

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39
Q

what is the formation of carbonic acid catalysed by?

A

carbonic anhydrase

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40
Q

is the formation of carbonic acid reversible?

A

yes, at the lungs

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41
Q

what produces vast quantities of carbonic acid?

A

respiring cells

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42
Q

what are the 3 mechanisms of maintaining acid-base balance?

A

Blood buffers
Respiratory compensation
Renal compensation

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43
Q

how long do blood buffers take to work?

A

seconds

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44
Q

how long does respiratory compensation take to work?

A

minutes

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45
Q

how long does renal compensation take to work?

A

hours to days

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46
Q

what is a buffer?

A

weak acid or base

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47
Q

can buffers absorb protons?

A

yes

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48
Q

is blood buffering effective?

A

yes, very effective

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49
Q

what is the main blood buffer?

A

bicarbonate

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50
Q

is H2CO3 difficult to measure?

A

yes, very difficult to measure

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51
Q

what does the relationship of CO2 and H2CO3 in solution depends on?

A

partial pressure (Pco2) and its solubility

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52
Q

what is the equations for pK?

A

-log10K

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53
Q

what is the Henderson-Hasselbalch equation?

A

pH = pK + log10([HCO3-] /alphaPco2)

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54
Q

what does blood pH depend on?

A

HCO3- and CO2 concentration

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55
Q

what can be altered to regulate pH?

A

CO2

HCO3-

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56
Q

how is CO2 regulated?

A

by the lungs

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57
Q

how is HCO3- regulated?

A

by the kidneys

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58
Q

how can conditions be diagnosed clinically?

A

by measuring H-H equation parameters

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59
Q

what effect does respiratory acidosis have on CO2?

A

increases it

60
Q

what affect does increased CO2 have on bicarbonate?

A

increases it

61
Q

what affect does increased bicarbonate have on H+?

A

increases it

62
Q

what affect does increased H+ have on pH?

A

decreases it

63
Q

what effect does respiratory alkalosis have on CO2?

A

decreases it

64
Q

what affect does decreased CO2 have on bicarbonate?

A

decreases it

65
Q

what affect does decreased bicarbonate have on H+?

A

decreases it

66
Q

what affect does decreased H+ have on pH?

A

increases it

67
Q

what affect does metabolic acidosis have on pH and bicarbonate?

A

add acid, decreases them

68
Q

what affect does metabolic alkalosis have on pH and bicarbonate?

A

add base, increases them

69
Q

what are the 3 other buffering systems, apart from bicarbonate?

A

Haemoglobin
Plasma proteins
Phosphate

70
Q

what does haemoglobin buffer metabolically to produce?

A

CO2

71
Q

what are the H+ mopped up by?

A

reduced haemoglobin (Hb)

72
Q

what happens to Hb after O2 delivery to cells?

A

it is reduced

73
Q

is O2 low or high in the lungs?

A

high

74
Q

what does high O2 in the lungs do?

A

liberates CO2, removing the excess acid

75
Q

In ECF, what is made possible by proteins

A

small amount of buffering

76
Q

what are proteins composed of

A

AAs which contain acidic and basic R groups and are amphoteric

77
Q

are carboxyl R groups strong or weak acids or bases

A

weak acids

78
Q

Amino R groups strong or weak acids or bases

A

weak bases

79
Q

why do phosphate play a minor role in ECF

A

due to relatively low concentration

80
Q

when is phosphate a good urinary buffer and why

A

under normal conditions as there is little reabsorption

81
Q

what is the Henderson-Hasselbalch equation

A

pH = pK + log10([HCO3-]/αPco2)

82
Q

what does the Henderson-Hasselbalch equation predicts in Respiratory compensation

A

predicts that if the pH decreases then it is likely that the Pco2 will be increased

83
Q

is the CO2 solubility (α) high or low in Henderson-Hasselbalch equation

A

low (0.03)

84
Q

what is increased Pco2 detected by

A

Central chemoreceptors

Peripheral chemoreceptors

85
Q

where are Central chemoreceptors located

A

brainstem

86
Q

where are Peripheral chemoreceptors located

A

aortic arch

87
Q

what happens if the pH drops

A

CO2 is increased

88
Q

what detects a pH decrease

A

Detected by brainstem/peripheral chemoreceptors

89
Q

what occurs if the pH drops and CO2 is increased

A

Causes increased ventilation to blow off CO2

90
Q

when ventilation occurs to blow off CO2, what then happens

A

increases blood pH

negative feedback

91
Q

what does the Henderson-Hasselbalch equation predicts in Renal Compensation

A

predicts that if the pH decreases then it is likely that bicarbonate will be decreased

92
Q

how can the kidney compensate by

A

by regulating bicarbonate reabsorption and proton secretion

93
Q

what is Renal Compensation more efficient at

A

restoring pH balance

94
Q

For every bicarbonate absorbed how many H+ secreted into urine

A

1

95
Q

In respiratory compensation, how is pH regulated

A

by change in CO2

96
Q

how happens to Plasma [H+] in acidosis Renal Compensation

A

Plasma [H+] is increased

97
Q

why is less HCO3- filtered in acidosis Renal Compensation

A

filtered as it is buffering the increased H+

98
Q

why does urine becomes more acidic in acidosis Renal Compensation

A

Renal H+ secretion increases

99
Q

how happens to Plasma [H+] in alkalosis Renal Compensation

A

Plasma [H+] decreases

100
Q

why is less HCO3- filtered in alkalosis Renal Compensation

A

as it is less required for buffering

101
Q

why is not all HCO3- reabsorbed in alkalosis Renal Compensation

A

because H+ availability is rate limiting

102
Q

what happens to urine in alkalosis Renal Compensation

A

urine becomes more alkaline

103
Q

what must be maintained

to acidify urine during acidosis

A

gradient for H+ secretion

104
Q

what helps to maintain the gradient of H+

A

If H+ is mopped up by buffers in urine

105
Q

what is secreted H+ buffered by

A

Phosphate and Ammonia

106
Q

what happens too Phosphate In acidosis

A

capacity is exceeded

107
Q

what does ammonia + proton make

A

ammonium ion

108
Q

where is ammonia secreted

A

in the kidney

109
Q

is ammonia weak/strong acid/base?

A

Weak base

110
Q

what is Ammonia produced from

A

glutamine metabolism

111
Q

when is Production of Ammonia up-regulated

A

during acidosis

112
Q

what does Ammonia in collecting ducts do

A

mops up urinary H+ during acidosis

113
Q

what does an acid-base disturbance affects

A

pH, Pco2 and/or [HCO3-]

at least 2 out of 3 of them

114
Q

when does Compensation comes into play in an acid-base disturbance

A

immediately

115
Q

what does Compensation correct in an acid-base disturbance

A

Corrects pH change only

116
Q

what is sacrificed in Compensation in an acid-base disturbance

A

Pco2 and HCO3- sacrificed to restore pH

117
Q

what does Correction correct in an acid-base disturbance

A

Complete restoration of pH, Pco2 and HCO3-

118
Q

4 types of of acid-base balance disorder

A

Respiratory acidosis
Respiratory alkalosis
Metabolic acidosis
Metabolic alkalosis

119
Q

what is a change in pH that has a respiratory cause associated with

A

abnormal Pco2

120
Q

what does an abnormal Pco2 gives rise to

A

gives rise to a change in carbonic acid-derived H+

121
Q

what is a change in pH that has a metabolic cause associated with

A

altered [HCO3-] as a result of the participation of HCO3- in buffering abnormal [H+]

122
Q

Respiratory Acidosis cause

A

Retention of CO2 (hypoventilation)

123
Q

Respiratory Acidosis uncompensated result

A

pH decreases, HCO3- increases

124
Q

Respiratory Acidosis compensated result

A

Increased reabsorption of HCO3-
Secretion of ammonium
HCO3- remains elevated

125
Q

Acute intracellular buffering in Respiratory Acidosis time course

A

seconds or minutes

126
Q

Chronic renal compensation in Respiratory Acidosis time course

A

days

127
Q

3 Clinical causes of Respiratory Acidosis

A

Drug-induced depression of respiratory centres
Pulmonary oedema
Emphysema

128
Q

Respiratory Alkalosis cause

A

Loss of CO2 (hyperventilation)

129
Q

Respiratory Alkalosis uncompensated result

A

pH increases, HCO3- decreases

130
Q

Respiratory Alkalosis compensated result

A

Decreased reabsorption of HCO3-

Decreased secretion of ammonium

HCO3- remains depressed

131
Q

Acute intracellular buffering in Respiratory Alkalosis time course

A

seconds or minutes

132
Q

Chronic renal compensation in Respiratory Alkalosis time course

A

days

133
Q

4 Clinical causes of Respiratory Alkalosis

A

Anxiety, fear
Pain
Aspirin poisoning
High altitude

134
Q

Metabolic Acidosis cause

A

Loss of HCO3- or addition of H+ to plasma

135
Q

Metabolic Acidosis Uncompensated result

A

pH decreases, HCO3- decreases

136
Q

Metabolic Acidosis compensated result

A

Respiratory compensation (increased ventilation) partially restores pH

Renal compensation completes the restoration of pH by increasing reabsorption of HCO3-

137
Q

Acute respiratory of Metabolic Acidosis Time course

A

seconds or minutes

138
Q

Chronic renal compensation of Metabolic Acidosis Time course

A

days

139
Q

4 Clinical causes of Metabolic Acidosis

A

Diabetic keto-acidosis (abnormal fat metabolism)

Diarrhoea (loss of HCO3-)

Heavy exercise (addition of lactic acid)

Renal failure (reduced secretion of protons)

140
Q

Metabolic Alkalosis cause

A

Addition of HCO3- or loss of H+ from plasma

141
Q

Metabolic Alkalosis Uncompensated result:

A

pH increases, HCO3- increases

142
Q

Metabolic Alkalosis compensated result

A

Respiratory compensation (increased ventilation) partially restores pH (C)

Renal compensation completes the restoration of pH by decreasing reabsorption of HCO3-

143
Q

Acute respiratory in Metabolic Alkalosis Time course

A

seconds and minutes

144
Q

Chronic renal compensation in Metabolic Alkalosis Time course

A

days

145
Q

2 Clinical causes of Metabolic Alkalosis

A

Ingestion of antacids

Vomiting (loss of HCl)

146
Q

what is respiratory compensation response limited by

A

hypoxaemia which counteracts response via chemoreceptors

147
Q

what is the most effective at causing compensation

A

the renal response of in metabolic alkalosis

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