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Flashcards in deck_1649855 Deck (79):
1

How do the kidneys control plasma volume?

• Filtering and variably recovering salts

2

How do the kidneys control plasma osmolarity?

• Filtering and variably recovering water

3

How do the kidneys variably control plasma pH?

• Filtering and variably recovering hydrogen carbonate and active secretion of hydrogen ions

4

What is normal pH range?

• 7.38 - 7.42

5

When does alkalaemia occur?

>7.42

6

When does acidaemia occur?

7

What is normal conc of H+?

37-43 nmol/l

8

Outline what occurs in alkalaemia

• Lowers solubility of Ca2+ salts, free Ca2+ binds to proteins. Results in hypocalcaemia ○ Increases excitability of nerves • Paraesthesia • Tetany

9

What is % mortality at pH 7.55?

45%

10

What is % mortality at pH 7.65?

80%

11

Outline what occurs in acidaemia

• Hyperkalaemia (heart arrythmias and arrest) • Affects many enzymes ○ Reduces cardiac and skeletal muscle contractility ○ Reduced glycolysis in many tissues ○ Reduced hepatic function • Effects severe under 7.1 • Life threatening below pH 7.0

12

How much HCO3- is required for accurate pH maintenance?

• 20x as much HCO3- as there is CO2 • pH = pK + log (HCO3-/pCO2 x 0.23) • Log 20 (20x higher) = 1.3 • pK - 6.1 + 1.3 = 7.4

13

What is CO2 determined by?

• Controlled by chemoreceptors • Disturbed by respiratory disease

14

What is HCO3- conc determined by?

• Controlled by kidneyDisturbed by metabolic and renal disease

15

What is HCO3- largely created by?

• Red blood cells

16

What is respiratory acidaemia (acidosis)?

• Hypoventilation leads to hypercapnia • Hypercapnia causes plasma pH to fall • Less than 20x amount of HCO3- • pH

17

What is respiratory alkalaemia (alkalosis)?

• Hyperventilation leads to hypocapnia • Fall in pCO2 causes pH to rise • More than 20x amount of HCO3- than CO2

18

What is normal pH?

7.38 - 7.42

19

What is normal HCO3-

• 22 - 29 mmol/l

20

What is normal pO2?

• 9.8 - 14.2 kPa

21

What is normal pCO2?

• 4.2 - 6.0 kPa

22

How is pH corrected in respiratory alkalosis/acidosis?

• Central chemoreceptors normally control pCO2 within tight limits • Peripheral chemoreceptors enable changes in respiration driven by changes in plasma pH • This is CORRECTION - Changing the factor at hand

23

How is pH compensated in respiratory acidosis/alkalosis

• changes in pCO2 compensated by changes in HCO3- • Kidney control HCO3- • Respiratory acidosis is compensated by kidneys increasing HCO3- • Respiratory alkalosis is compensated by kidneys decreasing HCO3-

24

What is metabolic acidosis?

• Tissues produce acid (or acid in blood - amino acids) • H+ reacts with HCO3-, leading to fall in pHMetabolic acidosis

25

How is metabolic acidosis compensated (acidosis means alteration in buffer base!)?

• Compensated by changes in ventilation ○ Peripheral chemoreceptors increase ventilation ○ This lowers pCO2Restores pH towards normal

26

What is metabolic alkalosis caused by?

• Plasma HCO3- rises (after vomiting for instance) • Plasma pH rises • Metabolic alkalosis

27

How is metabolic alkalosis compensated?

• Partially compensated by decreased ventilation

28

How are respiratory changes in pH changed? (use correct terminology)

• Compensated by kidney • Corrected by breathing

29

How are metabolic changes in pH modified? (use correct terminology)

• Compensated by breathing (changing factor than other directly changes) • Corrected by kidney

30

What is produced in metabolic acidosis?

• H+ ions which react with HCO3- to produce CO2 in venous blood • CO2 breathed out, proportionally reducing HCO3-

31

Why can metabolic alkalosis only be partially compensated?

• Because can only slightly reduce respiratory to increase CO2 • At risk of hypoxia

32

How much HCO3- filtered per day?

• 4500 mmol

33

How can HCO3- be increased?

• Recover all filtered HCO3-Make new

34

Give two ways in which kidneys synthesise HCO3-

• Amino acidsCO2

35

How do the kidneys make new HCO3- from CO2?

• Kidneys produce a lot of CO2 • Combined with water to produced H2CO3- • H+ excreted into water, HCO3- into blood

36

How do the kidneys make new HCO3- from amino acids?

• Glutamine • Produces NH4- to enter urine, HCO3- excreted into blood

37

Where is HCO3- recovered in kidney?

• 80-90% in PCT • Remainder in thick ascending limb of loop of henle

38

How is HCO3- recovered in PCT of kidney?

• H+ exported from cell into lumen via Na-H antiporter ○ Up conc grad ○ Energy from movement of Na+ down Conc grad (Na/K+ ATPase on basolateral membrane • H+ reacts with HCO3- in lumen, making CO2 + H20 • CO2 enters cell, reacts with H20 to make HCO3- • HCO3- exported with K+ into ECG

39

How is HCO3- created from amino acids in the PCT?

• Glutamine broken down to produced ○ A-ketoglutarate (HCO3-) ○ Ammonium (NH4+) ○ HCO3- into ECF ○ NH4+ into lumen

40

What does HCO3- reabsorption look like in PCT?

• DRAW IT NOW

41

What has happened to HCO3- by the time of the DCT?

Has almost all been filtered and recovered

42

How is HCO3- recovered in distal tubule cells?

• CO2 produced and combined with H20 to make H2CO3- • Na+ gradient insufficient to drive H+ secretion • H+ actively transported out of cell via H+ ATPase and H+/K+ antiporter • H+ bound to HPO42- + H+ -> H2PO4- in lumen

43

What happens to K+ when cells export H+?

• K+ is absorbed into blood

44

Why may you end up absorbing a large amount of K+?

• If a large amount of HCO3- needs to be reabsorbed due to respiratory acidosis, large amount of K+ will be reabsorbed with it. May cause hyperkalaemia

45

What is minimum urine pH

4.5

46

What is a titratable acid?

• One which can freely gain H+ ions in an acid/base reaction

47

How is H+ buffered in urine?

• HP04 2- -> H2PO4- • NH3 -> NH4+(ammonia -> ammonium)

48

What is daily acid secretion?

• 50-100mmol H+

49

How is H+ excretion controlled?

• pH detected by intracellular pH of tubular cells • Change in rate of HCO3- export to ECF produced by changes in ECF (H+ automatically excreted)

50

How is respiratory acidosis associated with K+?

• Causes hyperkalaemia • HCO3- being generated, H+ being expelledK+ taken in in exchange for H+

51

How is metabolic alkalosis associated with hypokalaemia?

• Hypokalaemia

52

How does hyperkalaemia cause metabolic acidosis?

• As K+ rises, kidneys ability to reabsorb and create HCO3- reduced. • Hyper kalaemia makes intracellular pH alkaline, favouring HCO3- excretion

53

How does hypokalaemia cause metabolic alkalosis?

• Hypokalaemia makes intracellular pH acidic, favouring H+ excretion and HCO3- recovery

54

Draw activities of DCT

NOW

55

Give 4 cellular responses to acidosis

• Enhanced H+/Na+ exchange ○ Full recovery of all filtered HCO3- ○ Enhanced ammonium production in PCT ○ Increased activity of H+ ATPase in distal tubule ○ Increased activity of H+ ATP-ase from tubular cells to ECF

56

What is metabolic acidosis due to?

• Fall in HCO3- • A gain in H+

57

What is metabolic alkalosis due to?

• Due to rise in HCO3- • A fall in H+

58

Give an outline of metabolic acidosis

• Acids produced metabolically • Produced from H+ and an anion (lactate, ketones) • H+ reacts with HCO3-, producing CO2 which is breathed outSome HCO3- replaced by anion from acid

59

What happens to HCO3- after vomiting?

• Large increase in HCO3- and as replacement H+ produced • Kidneys cannot excrete HCO3- as they are trying to compensate for dehydration • HCO3- and Na+ recovery is favoured to increase osmolarity of plasma and cause osmotic movement of water • Metabolic alkalosis ensues

60

How can you treat metabolic alkalosis after vomiting?

• Rehydration • Post rehydration HCO3- will be excreted quickly

61

Why does HCO3- increase after persistent vomiting?

• H+ decreased in stomach • More H+ produced, releases HCO3- into blood • Hypokalaemia ensues

62

Why does hypokalaemia occur as a result of vomiting?

• H+ secretion in kidney stops, so does K+ reabsorption (Antiporter, intercalated cells)

63

Why do side effects of vomiting include hypokalaemia?>

• H+ secretion in kidney stops, so does K+ reabsorption • More K+ lost in urine • Hypokalaemia

64

Give three causes of metabolic acidosis

• Excess metabolic production of acids • Acids are ingested (amino acids) • Problem with the renal excretion of acid

65

What is the anion gap?

• Indicates whether an HCO3- has been replaced with something other than Cl-

66

How is the anion gap calculated?

• Difference between (Na+ + K+) and (Cl- + HCO3-)

67

What is the normal value of the anion gao?

• 10-15 mmol/l

68

When is the anion gap increased?

• If anions from metabolic acid has replaced plasma HCO3-

69

hen can renal problems reduce HCO3- without increasing the anion gap?

If HCO3- replaced with Cl-

70

Give four causes of an increased anion gap metabolic acidosis

• Lactate • Ketoacids • Toxic alcohols • Aspirin

71

What is renal correction of low pH?

• Fall in tubular cell intra-cellular pH stimulates acid secretion and HCO3- recovery, thus raising plasma HCO3-

72

How can metabolic alkalosis occur?

• HCO3- increases after persistent vomiting • Should be very easy to correct

73

What is the issue with a HCO3- infusion?

• Excreted in kidney immediately

74

Why does vomiting compromise ability to excrete HCO3-?

• Vomiting also causes dehydration • Volume depletion. Capacity to lose HCO3- is less, because high rates of recovery favour HCO3- recovery and H+ secretion

75

How do you treat metabolic alkalosis?

• Rehydrate

76

What is a dangerous effect of metabolic acidosis?

• Hyperkalaemia ○ K+ moves out of cells, in order to control intracellular pH More K+ reabsorbed in distal nephron, as a result of H+ excretio

77

What is a dangerous effect of metabolic alkalosis?

• Hypokalaemia ○ K+ moves into cellsLess K+ reabsorption (less H+ excreted in distal nephron

78

How does hypokalaemia cause metabolic alkalosis?

• Make intracellular pH of tubule cells acidic ○ Favours H+ excretion and HCO3- recovery ○ Therefore metabolic alkalosis occurs

79

How does hyperkalaemia cause metabolic acidosis?

• Makes intracellular pH alkaline ○ Favours HCO3- excretion ○ Therefore metabolic acidosis