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Year 2 - Renal (DP) > Physiology (6-8) > Flashcards

Physiology (6-8) Flashcards

1
Q

What is the tonicity of the tubular fluid entering the DCT compared to blood?

A

hypo-osmotic (~100mosmol/L)

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2
Q

What is the collecting duct bathed in?

A

Progressively increasing [ISF]:

- 300 -> 1200mosmol/L

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3
Q

What percentage of filtered ions are reabsorbed before the DCT?

A

> 95%

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4
Q

What is the residual load of NaCl that reaches the DCT?

A

~700-1000nmol/day

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5
Q

Why is the residual load of NaCl in the DCT important?

A

Salt balance

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6
Q

What effect does ADH have on the regulation of water and ion balance?

A

Increases water reabsorption

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7
Q

What effect does Aldosterone have on the regulation of water and ion balance?

A

Increases Na+ reabsorption

Increases H+ and K+ excretion

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8
Q

What effect does Atrial Natriuretic hormone have on the regulation of water and ion balance?

A

Reduces Na+ reabsorption

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9
Q

What effect does PTH have on the regulation of water and ion balance?

A

Increases calcium reabsorption

Decreases phosphate reabsorption

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10
Q

What does the DCT have a low permeability to?

A

Water

Urea

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11
Q

What happens in the early segment of the DCT?

A

NaCl reabsorption via the Triple-transporter

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12
Q

Which of the following does not happen in the late segment of the DCT:

  • Calcium reabsorption
  • H+ secretion
  • Na+ reabsorption
  • K+ reabsorption
  • Phosphate secretion
A

Phsophate secretion

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13
Q

What is the early collecting duct similar to?

A

Late DCT

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14
Q

What is the permeability of the late collecting duct?

A

Low ion permeability

High water permeability

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15
Q

Where is ADH (an octopeptide) synthesised and from what?

A

Supraoptic nuclei and Paraventricular nuclei in the hypothalamus

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16
Q

Where is ADH stored?

A

In granules in the posterior pituitary

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17
Q

What is the approximate half life of ADH in the plasma?

A

10-15 minutes

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18
Q

How does ADH increase water reabsorption?

A
  1. Binds to an Arginine Vasopressin Receptor 2 (V2)
  2. ATP -> cAMP
  3. cAMP causes increased transcription and insertion of aquaporins in the lumenal/apical membrane
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19
Q

In high [ADH]p, what is urine like?

A

Hypertonic (Up to 1400mosmol/L)

Low volume

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20
Q

In low [ADH]p, what is urine like?

A

Hypotonic urine (

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21
Q

What is the dominant factor controling thirst and ADH secretion?

A

Increased osmolarity activating hypothalamic osmoreceptors

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22
Q

When are left atrial volume receptors important in water balance?

A

In large plasma volume or BP changes

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23
Q

What causes left atrial volume receptors to encourage ADH release?

A

Very low plasma volume
OR
Hugh drop in BP

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24
Q

Apart from increasing water reabsorption, how else does ADH increase BP?

A

Causes peripheral vasoconstriction -> BP rises

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25
Q

Where is aldosterone secreted from?

A

Adrenal cortex

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26
Q

When is aldosterone secreted?

A

In response to:
- Increased [K+]p
- Decreased [Na+]p
Activation of RAAS

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27
Q

If aldosterone is absent, how much K+ is present in the urine?

A

None

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28
Q

How does decreased [Na+]p result in aldosterone secretion?

A

Indirectly via the juxtaglomerular apparatus

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29
Q

Where is renin produced and what does it do?

A

Kidneys:

- Converts Angiotensinogen -> Angiotensin I

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30
Q

Where is ACE produced and what does it do?

A

Lungs:

- Converts Angiotensin I -> Angiotensin II

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31
Q

What effects does Angiotensin II have?

A

Increases adrenal cortex secretion of Aldosterone

Increases thirst

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32
Q

What can the juxtaglomerular granular cells release and when do they secrete it?

A

Renin:

 - When afferent arteriole BP drops
 - When macula dense senses decreases [Na+]DCT
 - Increased SNS activity due to reduced BP
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33
Q

How does fluid retention arise in CHF?

A
  1. Failing heart
  2. Decreased CO and SV
  3. Decreased BP
  4. Activation of RAAS
  5. Increased Na+ and water retention
  6. Fluid overload
  7. Further heart failure
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34
Q

Where is ANP produced and stored?

A

Produced by heart

Stored in atrial muscle cells

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35
Q

When is ANP released?

A

When atrial muscle cells are stretched due to increased plasma volume

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36
Q

What effects does ANP have?

A

Increases Na+ excretion
Diuresis
Reduces BP via CVS affects
(All reduce plasma volume and hence BP)

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37
Q

How does ANP reduced BP via the SNS?

A

Inhibits SNS:

 - Reduces CO
 - Reduces peripheral resistance
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38
Q

What effect does ANP have on afferent arterioles in the kidney?

A
  1. Smooth muscle contraction inhibited
  2. Vasodilation
  3. Increased GFR
  4. More Na+ and water filtered
  5. Increased excretion of Na+ and water
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39
Q

How can micturition be voluntarily controlled?

A

Tightening of:

 - External urethral sphincter
 - Pelvic diaphragm
40
Q

What happens when bladder stretch receptors are activated?

A

Bladder contracts

Urethral sphincters open

41
Q

How much urine can the bladder hold before the stretch receptors are activated?

A

250-400ml of urine

42
Q

What part of the brain controls the voluntary inhibition of the micturition reflex?

A

Cerebral cortex

43
Q

What branch of the ANS controls the micturition reflex?

A

PNS

44
Q

What causes the maximum ADH secretion?

A

Increased ECF osmolarity AND decreased ECF volume

45
Q

What is the pH of arterial blood?

A

7.45

46
Q

What is the pH of venous blood?

A

7.35

47
Q

How can pH be calculated?

A

pH = log(1/[H+])

48
Q

How can acidosis arise via the CNS?

A

CNS depression

49
Q

How can alkalosis arise via the CNS?

A

Overexcitability of peripheral nervous sytem and the CNS later

50
Q

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

A

Carbonic acid formation
Inorganic acid formation during nutrient breakdown
Organic acids from metabolism

51
Q

What do buffer systems consist of?

A

One substance to yield H+ if [H+] decreases -> HA

One substance to bind H+ if [H+] increases -> A-

52
Q

What happens to HA H+ + A- if H+ is added to the system?

A

Equilibrium shifts left:
- A- mops up excess H+ -> Increased [HA]
Results in increased [HA] and decreased [A-]

53
Q

What happens to HA H+ + A- if a base is added to the system?

A

Equilibrium shifts right:
- Base has added OH-
-> H+ mops up OH- to form water
- [H+] decreases -> Increased HA dissociation
Results in decreased [HA] and increased [A-]

54
Q

What is Ka?

A

The dissociation constant for acids

55
Q

How can Ka be calculated?

A

Ka = ([H+] x [A-]) / [HA]

56
Q

How is pKa calculated?

A

pKa = -log(Ka)

57
Q

How can [H+] be calculated from the equation from Ka?

A

[H+] = (Ka x [HA]) / [A-]

58
Q

How can pH be calculated from pKa? What is the name for his equation?

A

pH = pKa + log([A-] / [HA])

Henderson-Hasselbach equation

59
Q

What is the most important physiological buffer equation?

A

CO₂ + H₂O ⇌ H₂CO₃ ⇌ H⁺ + HCO₃⁻
^
Carbonic Anhydrase

60
Q

How can the pH of a solution of H₂CO₃ be calculated?

A

pH = pKa + log([HCO₃⁻] / [H₂CO₃)

61
Q

Given the pKa of a solution of H₂CO₃ is 6.1 and H₂CO₃ is a function of Pco₂ (with the arterial Pco₂ = 40mmHg and the solubility constant of CO₂ = 0.03mmol/mmHg/L) calculate the pH of a solution of H₂CO₃ when [HCO₃⁻] = 24mmol/L (normal [HCO₃⁻]p)

A

pH = 6.1 + log([HCO₃⁻] / Pco₂ x solubility constant of CO₂)
Therefore
pH = 6.1 + log(24mmol/L / 40 x 0.03) = 7.4

62
Q

What effect do the kidneys have on [bicarbonate]?

A
  1. Variable reabsorption of filtered bicarbonate
  2. Kidneys can add ‘new’ bicarbonate to the blood:
    • [HCO₃⁻]renal vein > [HCO₃⁻]renal artery
63
Q

If no bicarbonate was reabsorbed, how much HCl would this be equivalent to adding to the body?

A

4L

64
Q

Describe the unorthodox reabsorption of HCO₃⁻

A
  1. HCO₃⁻ disappears in tubule to make H₂CO₃

2. Reappears in ISF from H₂CO₃

65
Q

What happens if [HCO₃⁻]tubular fluid is low?

A

H+ combines with the next most powerful buffer -> PO₄³⁻

66
Q

What is the process by which more HCO₃⁻ is made if [HCO₃⁻]tubular fluid decreases?

A
  1. [HCO₃⁻] falls
  2. More H+ secreted
  3. [H+]i falls
  4. H₂CO₃ ⇌ H⁺ + HCO₃⁻ shifts right to replace lost H+
  5. HCO₃⁻ also made
  6. [HCO₃⁻]i rises
67
Q

How does PO₄³⁻ aid in increasing [HCO₃⁻]i?

A
  1. HPO₄²⁻ ⇌ PO₄³⁻ + H+ moves right
  2. H+ secreted into lumen
  3. [H+]i falls
  4. H₂CO₃ ⇌ H⁺ + HCO₃⁻ shifts right to replace lost H+
  5. HCO₃⁻ also made
  6. [HCO₃⁻]i rises
68
Q

How can we measure the amount if titratable acid?

A

Measure amount of strong base (NaOH) that needs added to urine to get the pH = 7.4

69
Q

What is the max amount of titratable acid that can be made every day and what implication does this have?

A

~40mmol/L

This means the max amount of ‘new’ HCO₃⁻ that can be made is ~40mmol/L

70
Q

What is the normal ammonium excretion?

A

~20mmol/day

71
Q

During acidosis, what can the ammonium excretion rise to?

A

500-600mmol/day

72
Q

Approximately 4300mmol/day of bicarbonate is reabsorbed every day, what implication does this have?

A

~4300mmol/day H+ must be secreted

73
Q

How much phosphoric acid is produced per day and what implication on H+ does this have?

A

20mmol of phosphoric acid produced per day so 20mmol of H+ must be secreted

74
Q

How much ammonium is produced per day and what implication on H+ does this have?

A

40mmol of ammonium produced per day so 40mmol of H+ must be secreted

75
Q

How can the total H+ secretion be calculated?

A 
Bicarbonate reabsorption (4300mmol/day)
TA (Phosphoric acid) excretion (20mmol.day)
Ammonium excretion (40mmol/day)

Total = 4360mmol/day H+ secreted

76
Q

How can the total H+ excretion be calculated?

A 
TA (Phosphoric acid) excretion (20mmol.day)
Ammonium excretion (40mmol/day)

Total = 60mmol/day H+ excreted = 60mmol/day ‘new’ bicarbonate made per day

77
Q

What three conditions need met for a person to be of normal acid-base status?

A
  1. Plasma pH close to 7.4 (7.35 - 7.45)
  2. [HCO₃⁻]p close to 25mmol/L (23 - 27)
  3. Paco₂ close to 40mmHg (35-45) (4.5 - 6.0 kPa)
78
Q

What is the primary priority is the normal acid-base balance is disrupted?

A

Restore pH to 7.4

 - This is compensation
 - Restored irrespective of what happens to
           - > [HCO₃⁻]p
           - > Paco₂
79
Q

What conditions must be met for an acid-base disturbance to be corrected?

A

Restoration (to normal) of:

 - pH
 - [HCO₃⁻]p
 - Paco₂
80
Q

What is the name of the diagram that an ABG can be plotted on?

A

Davenport diagram

81
Q

What is respiratory acidosis?

A

Carbon dioxide retention

82
Q

What can cause respiratory acidosis?

A

COPD
Airway restriction (Asthma or Tumour)
Chest injuries
Respiratory depression

83
Q

What criteria need to be met for uncompensated respiratory acidosis?

A

pH 45mmHg

84
Q

What is the main way that respiratory acidosis can be compensated?

A

Via increased H+ excretion in the kidneys

85
Q

What causes respiratory alkalosis?

A

Reduction in inspired PO2 at altitude:

 1. Hypoxia stimulates peripheral chemoceptors
 2. Hyperventilation -> Reduces Paco₂
86
Q

What else can cause hyperventilation and therefore result in respiratory alkalosis?

A

Fever
Brainstem damage
Hysteria

87
Q

What criteria need to be met for uncompensated respiratory alkalosis?

A

pH >7.45

Paco₂

88
Q

How do the kidneys compensate for respiratory alkalosis?

A

Reduces H+ secretion which increases HCO₃⁻ excretion

89
Q

What can cause a metabolic acidosis?

A 
Ingestion of:
     - Acids
     - Acid producing food
Excessive H+ production:
     - Lactic acid during exercise
     - DKA
Excessive loss of base:
     - Diarrhoea -> HCO₃⁻ lost
90
Q

What criteria need to be met for uncompensated metabolic acidosis?

A

pH

91
Q

What causes a reduced [HCO₃⁻]p in metabolic acidosis?

A

Buffers excess H+

HCO₃⁻ loss

92
Q

How does respiratory compensation aim to fix metabolic acidosis?

A

Reduced pH -> Peripheral chemoceptors -> Carbon dioxide blown off

93
Q

How is metabolic acidosis corrected?

A

Reduced filtered HCO₃⁻ therefore it is all readily reabsorbed
Increased H+ secretion:
- Increases TA + ammonium production
-> Increases production of ‘new’ HCO₃⁻

94
Q

What can cause metabolic alkalosis?

A 
Vomiting -> HCl loss
Ingestion of:
     - Alkali (eg NaHCO₃ in antacids)
     - Alkali producing food
Aldosterone hypersecretion:
     - Increased Na+/H+ exchange -> Acid secretion
95
Q

How is metabolic alkalosis compensated?

A

Increased pH -> Reduced ventilation -> Increased Paco₂
Increased [H+]p -> Decreased pH
[HCO₃⁻]p rises more

96
Q

How is metabolic alkalosis corrected?

A

Increases filtration of HCO₃⁻ -> Reduced HCO₃⁻ reabsorption -> Increased HCO₃⁻ excretion (alkaline urine)
No TA or ammonium generated

Year 2 - Renal (DP) (15 decks)

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