Physiology (6-8) Flashcards

(96 cards)

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
Where is aldosterone secreted from?
Adrenal cortex
26
When is aldosterone secreted?
In response to: - Increased [K+]p - Decreased [Na+]p Activation of RAAS
27
If aldosterone is absent, how much K+ is present in the urine?
None
28
How does decreased [Na+]p result in aldosterone secretion?
Indirectly via the juxtaglomerular apparatus
29
Where is renin produced and what does it do?
Kidneys: | - Converts Angiotensinogen -> Angiotensin I
30
Where is ACE produced and what does it do?
Lungs: | - Converts Angiotensin I -> Angiotensin II
31
What effects does Angiotensin II have?
Increases adrenal cortex secretion of Aldosterone | Increases thirst
32
What can the juxtaglomerular granular cells release and when do they secrete it?
Renin: - When afferent arteriole BP drops - When macula dense senses decreases [Na+]DCT - Increased SNS activity due to reduced BP
33
How does fluid retention arise in CHF?
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
34
Where is ANP produced and stored?
Produced by heart | Stored in atrial muscle cells
35
When is ANP released?
When atrial muscle cells are stretched due to increased plasma volume
36
What effects does ANP have?
Increases Na+ excretion Diuresis Reduces BP via CVS affects (All reduce plasma volume and hence BP)
37
How does ANP reduced BP via the SNS?
Inhibits SNS: - Reduces CO - Reduces peripheral resistance
38
What effect does ANP have on afferent arterioles in the kidney?
1. Smooth muscle contraction inhibited 2. Vasodilation 3. Increased GFR 4. More Na+ and water filtered 5. Increased excretion of Na+ and water
39
How can micturition be voluntarily controlled?
Tightening of: - External urethral sphincter - Pelvic diaphragm
40
What happens when bladder stretch receptors are activated?
Bladder contracts | Urethral sphincters open
41
How much urine can the bladder hold before the stretch receptors are activated?
250-400ml of urine
42
What part of the brain controls the voluntary inhibition of the micturition reflex?
Cerebral cortex
43
What branch of the ANS controls the micturition reflex?
PNS
44
What causes the maximum ADH secretion?
Increased ECF osmolarity AND decreased ECF volume
45
What is the pH of arterial blood?
7.45
46
What is the pH of venous blood?
7.35
47
How can pH be calculated?
pH = log(1/[H+])
48
How can acidosis arise via the CNS?
CNS depression
49
How can alkalosis arise via the CNS?
Overexcitability of peripheral nervous sytem and the CNS later
50
What are the three sources of H+ in the body?
Carbonic acid formation Inorganic acid formation during nutrient breakdown Organic acids from metabolism
51
What do buffer systems consist of?
One substance to yield H+ if [H+] decreases -> HA | One substance to bind H+ if [H+] increases -> A-
52
What happens to HA H+ + A- if H+ is added to the system?
Equilibrium shifts left: - A- mops up excess H+ -> Increased [HA] Results in increased [HA] and decreased [A-]
53
What happens to HA H+ + A- if a base is added to the system?
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
What is Ka?
The dissociation constant for acids
55
How can Ka be calculated?
Ka = ([H+] x [A-]) / [HA]
56
How is pKa calculated?
pKa = -log(Ka)
57
How can [H+] be calculated from the equation from Ka?
[H+] = (Ka x [HA]) / [A-]
58
How can pH be calculated from pKa? What is the name for his equation?
pH = pKa + log([A-] / [HA]) | Henderson-Hasselbach equation
59
What is the most important physiological buffer equation?
CO₂ + H₂O ⇌ H₂CO₃ ⇌ H⁺ + HCO₃⁻ ^ Carbonic Anhydrase
60
How can the pH of a solution of H₂CO₃ be calculated?
pH = pKa + log([HCO₃⁻] / [H₂CO₃)
61
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)
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
What effect do the kidneys have on [bicarbonate]?
1. Variable reabsorption of filtered bicarbonate 2. Kidneys can add 'new' bicarbonate to the blood: - [HCO₃⁻]renal vein > [HCO₃⁻]renal artery
63
If no bicarbonate was reabsorbed, how much HCl would this be equivalent to adding to the body?
4L
64
Describe the unorthodox reabsorption of HCO₃⁻
1. HCO₃⁻ disappears in tubule to make H₂CO₃ | 2. Reappears in ISF from H₂CO₃
65
What happens if [HCO₃⁻]tubular fluid is low?
H+ combines with the next most powerful buffer -> PO₄³⁻
66
What is the process by which more HCO₃⁻ is made if [HCO₃⁻]tubular fluid decreases?
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
How does PO₄³⁻ aid in increasing [HCO₃⁻]i?
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
How can we measure the amount if titratable acid?
Measure amount of strong base (NaOH) that needs added to urine to get the pH = 7.4
69
What is the max amount of titratable acid that can be made every day and what implication does this have?
~40mmol/L | This means the max amount of 'new' HCO₃⁻ that can be made is ~40mmol/L
70
What is the normal ammonium excretion?
~20mmol/day
71
During acidosis, what can the ammonium excretion rise to?
500-600mmol/day
72
Approximately 4300mmol/day of bicarbonate is reabsorbed every day, what implication does this have?
~4300mmol/day H+ must be secreted
73
How much phosphoric acid is produced per day and what implication on H+ does this have?
20mmol of phosphoric acid produced per day so 20mmol of H+ must be secreted
74
How much ammonium is produced per day and what implication on H+ does this have?
40mmol of ammonium produced per day so 40mmol of H+ must be secreted
75
How can the total H+ secretion be calculated?
``` Bicarbonate reabsorption (4300mmol/day) TA (Phosphoric acid) excretion (20mmol.day) Ammonium excretion (40mmol/day) ``` Total = 4360mmol/day H+ secreted
76
How can the total H+ excretion be calculated?
``` TA (Phosphoric acid) excretion (20mmol.day) Ammonium excretion (40mmol/day) ``` Total = 60mmol/day H+ excreted = 60mmol/day 'new' bicarbonate made per day
77
What three conditions need met for a person to be of normal acid-base status?
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
What is the primary priority is the normal acid-base balance is disrupted?
Restore pH to 7.4 - This is compensation - Restored irrespective of what happens to - > [HCO₃⁻]p - > Paco₂
79
What conditions must be met for an acid-base disturbance to be corrected?
Restoration (to normal) of: - pH - [HCO₃⁻]p - Paco₂
80
What is the name of the diagram that an ABG can be plotted on?
Davenport diagram
81
What is respiratory acidosis?
Carbon dioxide retention
82
What can cause respiratory acidosis?
COPD Airway restriction (Asthma or Tumour) Chest injuries Respiratory depression
83
What criteria need to be met for uncompensated respiratory acidosis?
pH 45mmHg
84
What is the main way that respiratory acidosis can be compensated?
Via increased H+ excretion in the kidneys
85
What causes respiratory alkalosis?
Reduction in inspired PO2 at altitude: 1. Hypoxia stimulates peripheral chemoceptors 2. Hyperventilation -> Reduces Paco₂
86
What else can cause hyperventilation and therefore result in respiratory alkalosis?
Fever Brainstem damage Hysteria
87
What criteria need to be met for uncompensated respiratory alkalosis?
pH >7.45 | Paco₂
88
How do the kidneys compensate for respiratory alkalosis?
Reduces H+ secretion which increases HCO₃⁻ excretion
89
What can cause a metabolic acidosis?
``` Ingestion of: - Acids - Acid producing food Excessive H+ production: - Lactic acid during exercise - DKA Excessive loss of base: - Diarrhoea -> HCO₃⁻ lost ```
90
What criteria need to be met for uncompensated metabolic acidosis?
pH
91
What causes a reduced [HCO₃⁻]p in metabolic acidosis?
Buffers excess H+ | HCO₃⁻ loss
92
How does respiratory compensation aim to fix metabolic acidosis?
Reduced pH -> Peripheral chemoceptors -> Carbon dioxide blown off
93
How is metabolic acidosis corrected?
Reduced filtered HCO₃⁻ therefore it is all readily reabsorbed Increased H+ secretion: - Increases TA + ammonium production -> Increases production of 'new' HCO₃⁻
94
What can cause metabolic alkalosis?
``` Vomiting -> HCl loss Ingestion of: - Alkali (eg NaHCO₃ in antacids) - Alkali producing food Aldosterone hypersecretion: - Increased Na+/H+ exchange -> Acid secretion ```
95
How is metabolic alkalosis compensated?
Increased pH -> Reduced ventilation -> Increased Paco₂ Increased [H+]p -> Decreased pH [HCO₃⁻]p rises more
96
How is metabolic alkalosis corrected?
Increases filtration of HCO₃⁻ -> Reduced HCO₃⁻ reabsorption -> Increased HCO₃⁻ excretion (alkaline urine) No TA or ammonium generated