CASE 8 Flashcards
Buffers
- can bind H3O+
- blunt any change in pH
- carbonate buffer (hemoglobin) -> catalyzed by carbonic anhydrase
- phosphate buffer
- protein buffer
chloric shift
- HCO3- can leave the red blood cell
- Chlorine can move into the cell
- co2 + H20 –> H2CO3 –> HCO3- + H3O+ (reversible)
phosphate buffer
- made up of hydrogen phosphate ion, HPO42- and a dihydrogen phosphate ion H2PO4-
- urinary buffer
- its concentration progressively increases as fluid is resorbed within the tubule.
- H2PO4- –> H3O+ + HPO42-
Protein buffer
- largest buffer pool in body
- zwitterions, can react with themselves
- amphoteric, function as acid and base
- contain many ionizable groups which can release or bind H+
- albumin and plasma globulins are major extracellular protein buffers
isohydric principle
- all buffers work together, all buffers are in equilibrium at the same H+
Chemical buffering
- first line of defense of blood pH
- minimizes change in pH but does not remove acid or base from the body
Respiratory response
- second line of defense of blood pH
- breathing removes CO2 as fast as its produced
- large loads of acid stimulate breathing –> removes Co2 from body and lowers H2CO3 in arterial blood, reducing acidic shift in blood pH.
- regulated by chemoreceptors: carotid (pCO2, pO2 and pH) and medullary chemoreceptors (pCO2 and pO2)
Renal response
- third line of defense of blood pH
- remove excess H+
- H+ are excreted in combination with urinary buffers
- at the same time, kidney adds HCO3- to the ECF to replace HCO3- used to buffer strong acids .
- excrete anions (phosphate, chloride and sulfate) that are liberated from strong acids
- affect blood pH more slowly than other buffering mechanisms in body
renal mechanisms for regulating acid-base balance
- reabsorbing/creating HCO3-
- excreting HCO3-, losing a HCO3- generates more H+ and gaining HCO3- decreases H+ levels
to absorb HCO3- the kidney has to secrete H+
NHE (Na+ H+ exchanger)
- tubule cells can pass HCO3- generated within them into the peritubular capillary blood
- HCO3- leaves the cell either accompanied by Na+ or in exchange for Cl-.
- H+ is actively secreted mostly by a Na+ H+ antiporter (NHE), but also by H+ ATPase
- for each HCO3- that dissapears, a HCO3- generated within the tubule cells enters the blood
body must produce ‘new’ HCO3-
- phosphate buffer system: Type A intercalated cells secrete H+ actively via H+ ATPase pump and via K+H+antiporter. Secreted H+ combines with HPO4 2- to form H2PO4- which flows out of the urine.
- Ammonium ions produced by glutamine metabolism in PCT cells, NH4+ are weak acids and donate few H+ at physiological pH. For each glutamine metabolized, two NH4+ and two HCO3- result.
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Distal nephron
- principal cells: reabsorb sodium and water and secrete potassium
- Intercalated:
- A cells: secrete H+ and reabsorb HCO3- (acidosis)
- B cells: secrete HCO3- and reabsorb H+ (alkalosis)
Phosphate/ammonia buffer
because the urine has to have a minimun pH of 4.5 not too much H+ can be excreted from the filtrate. Therefore, the H+ uses the buffers in the tubular fluid which are mainly phosphate and ammonia. When there is an excess of H+, the kidney does not only reabsorb HCO3- but also generates new HCO3-
Henderson-hasselbach equation
- determine pH of a buffer
Ph = Pka + log [conjugated base] / [acid]
Acidosis
- low pH causes denaturation
- coma
- impaired organ function. Blood becomes sluggish and exhausted. Oxygen levels within your body decrease, further impairing organ function
- respiratory failure
- shock or death
- respiratory rate goes up in order to get back to normal PCO2