Central chemoreceptors Flashcards

1
Q

What is the main activator of the central chemoreceptors

A

Hypercapnia - Increased CO2 levels

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2
Q

Where are the central chemoreceptors found

A

Brain parenchyma

In the bathed extracellular fluid - separated from the blood by the blood brain barrier

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3
Q

What pCO2 is required in order to double ventilation

A

40-45mmHg

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4
Q

What happens if arterial pCO2 increases?

A

Brain exctracellular fluid pCO2 increases - causes a pH fall and stimulation of the central chemoreceptors

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5
Q

Why is a larger fall in pH seen in the blood vessel

A

Poor ion permeability - less non-bicarb buffering power (fewer proteins) so larger fall

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6
Q

What 2 neuronal populations are found on the ventrolateral medulla and other brainstem nuclei

A

Acid activated - serotonin

Acid inhibited - GABA

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7
Q

What responses are seen as a result of respiratory acidosis

A

Both peripheral and central chemoreceptor action

Peripheral is faster, As pO2 falls the response to pCO2 is enhanced

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8
Q

What response is seen as a result of metabolic acidosis

A

Severe response - hyperventilating (Kussmaul breathing)
Large reduction in pCO2 - peripheral acute response (short term)
Central - longer term role

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9
Q

What are the renal mechanisms of action

A

Long term regulation
3 mechanisms - HCO3 handling
Urine acidification
Ammonia synthesis

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10
Q

Where does HCO3 handling take place

A

90% in the proximal tubule

10% in the distal tubule

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11
Q

How does HCO3- get reabsorbed at the proximal cell

A

Binds to H+ secreted by the Na/H to form H2CO3 - carbonic anhydrase to form CO2 and H2O - enters the cell - intracellular carbonic anhydrase to remake H2CO3 - Dissociates into HCO3- reabsorbed and H+ is recycled

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12
Q

How is urine acidification achieved

A

Filtered Na2HPO4 loses a Na ion to the Na/H exchanger

Gains an H from the exchanger to form NaH2PO4

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13
Q

Why is ammonia production important in urine acidification

A

Ammonia produced in Krebs cycle - Glutamine - alpha keto-glutarate
Gains an H+ and becomes impermeable to the cell membrane so stays in the renal fluid and is excreted in urine

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14
Q

What is the renal compensation for respiratory acidosis CO2 elimination is low (lung disease)

A

Secretion of H+ increased
Increased reabsorption of HCO3-
Rise in pH but further rise in HCO3-

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15
Q

What is the renal compensation for respiratory alkalosis (Increased CO2 elimination) - Hyperventilating

A

Reduced secretion of H+
Reduced reabsorption of HCO3-
Fall in pH but further drop in HCO3-

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16
Q

What respiratory compensation is there for metabolic acidosis (Ingestion of acid, Loss of alkaline, Diarrhoea)

A

Increase respiratory rate
Reduced arterial pCO2
increased pH and drop in pCO2
Renal correction too: Increased secretion of H+, Increased reabsorption of HCO3-

17
Q

What is the respiratory compensation of metabolic alkalosis (loss of acid/vomiting)

A

Reduced respiratory rate
Increased arterial pCO2
Reduced pH and rise in pCO2

18
Q

What is an additive mixed dissorder

A

Both same type of pH change - Life threatening

19
Q

Give three mixed disorder examples

A
  1. Alcoholics - met acidosis (alc breakdown) met alkalosis (Vomiting)
  2. Asthma - resp acidosis and lactic acidosis due to lack of O2
  3. COPD patients treated with diuretics - resp acidosis and met alkalosis