Central chemoreceptors Flashcards Preview

Physioloogy and pharmacology > Central chemoreceptors > Flashcards

Flashcards in Central chemoreceptors Deck (19)
Loading flashcards...

What is the main activator of the central chemoreceptors

Hypercapnia - Increased CO2 levels


Where are the central chemoreceptors found

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


What pCO2 is required in order to double ventilation



What happens if arterial pCO2 increases?

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


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

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


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

Acid activated - serotonin
Acid inhibited - GABA


What responses are seen as a result of respiratory acidosis

Both peripheral and central chemoreceptor action
Peripheral is faster, As pO2 falls the response to pCO2 is enhanced


What response is seen as a result of metabolic acidosis

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


What are the renal mechanisms of action

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


Where does HCO3 handling take place

90% in the proximal tubule
10% in the distal tubule


How does HCO3- get reabsorbed at the proximal cell

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


How is urine acidification achieved

Filtered Na2HPO4 loses a Na ion to the Na/H exchanger
Gains an H from the exchanger to form NaH2PO4


Why is ammonia production important in urine acidification

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


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

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


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

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


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

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


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

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


What is an additive mixed dissorder

Both same type of pH change - Life threatening


Give three mixed disorder examples

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