Flashcards in pH-regulation Deck (33):
what are the non-volatile compounds from diet?
sulfuric acid and phosphoric acid
how to keep pH constant
Cause of respiratory acidosis, where is it located on graph
point on normal buffer slope below 7.4
Cause of respiratory alkalosis, where is it located on graph
point on normal buffer slope above pH 7.4
Cause of metabolic acidosis, where is it located on graph
loss of HCO3-
point on 40 torr isobar below ph7.4
metabolic alkalosis, where is it located on graph
increased HCO3- concentration
point on 40 torr above 7.4
H+ excretion in proximal tubule
what does H+ excretion depend on in proximal tubule
Na/K+ ATPase pump on basolateral membrane generates the Na electrochemical gradient, which will drive efflux of protons via H+/Na+ exchanger
H+ excretion in collecting tubule? what stimulates it? what causes recycling of ATPase back to cytoplasm?
ONLYactive H+ATPase pump directly into lumen
stimulated by low pH
high pH-stimulates recycling
where is majority of bicarbonate reabsorbed
whats the difference between bicarbonate reabsorption from proximal tubule and collecting duct
prox: uses Na transporter to transport HCO3= into blood
collecting duct: HCO3 via Cl- antiporter
what actively secretes bicarbonate? when does this usually occur?
Type B intercalated cells at collecting tubule--> reverse polarity of membrane transporter
Usually occur during chronic alkalosis
what is the limiting urine pH? H+?
for every H2PO4 excreted in urine, what happens?
1 H+ eliminated
1 HCO3- in blood
what does titratable acid measure? how do you determine it?
what other weak acids can contribute to the titratable acid? when do those acids occur?
measure of H+ excreted in urine as undissociated weak acid: H2PO4 most abundant
with 24 hr urine collection: measure amt of NaOH required to back-titrate urine pH to 7.4
Beta-hydroxybutyric acid (during ketoacidosis)
lactic acid (during lactic acidosis)
how is H+ excreted as NH4+? what does NH4+ respond to?
due to glutaminase -->end result of alpha-ketoglutarate + NH4+
Net effect: excretion of proton in lumen and addition of NEW MOLECULES(2) of HCO3-to blood
NH4+ excretion increases rapidly in response to increased urine acidity
how does NH4 contribute to severe acidosis
NH4+ production contributes up to 250 mmol/day of new bicarbonate to blood
normal Lab value for Arterial PCO2
normal Lab value for arterial pH
normal Lab value for bicarbonate
calculated or measured: 24mmol/L
normal Lab value for Urinary titratable acid
up to 40 mmol/day in acidosis--can be much higher in ketoacidosis or other condt
normal Lab value for urinary ammonium ion
up to 250 mEq/day an acidosis
normal Lab value for anion gap?
how does large anion gap occur
what does large anion gap indicate
large anion gap:
-production or ingestion of fixed acid
-accumulation of anions
large anion gap=metabolic acidosis
what is the main buffer for acute respiratory acidosis? how much bicarbonate is increased?
0.1 mmol/L increase in [HCO3-/per torr
what happens in acute vs chronic respiratory acidosis
[HCO3-] slighly increased and remains on normal buffer slope=acute
-increase H+-->stimulate H+ excretion
-all filtered HCO3- reabsorbed
-increased excretion of H2PO4 and NH4-->new HCO3 to plasma
~0.35mmol increase in HCO3- instead of 0.1mmol (acute)
acute respiratory alkalosis? causes?
decreased PCO2--> pH of blood increased
causes: fear, anxiety, trauma,, salicylate intoxication
~0.2 mmol/L decrease [HCO3-]
causes of chronic respiratory alkalosis?
mechanical hyperventilation, many cardiopulmonary disorder
-increase in pH decrease secretion of H+ by renal tubular cells --lack of H+ secretion prevents complete absorption of HCO3- ---> HCO3- lost in urine
-B type intercalated cells of collecting tubule--actively secrete HCO3- into filtrate
high anion gap metabolic acidosis
increase acid load-->
-HCO3- consumed by buffering rxn
-anions accumulate in ECF
rapid respiratory response: hyperventilation decreases PCO2 and increases pH
Renal response: reabsorption of all HCO3-, increased titratable acid and ammonia excretion
Hyperchloremic (non-gap) metaboilc acidosis
-GI or renal loss of HCO3- -->kidney retain NaCl to maintain extracellular volume-->net exchange of HCO3- for Cl- --> sum remains constant--> no Anion gap
where are type B intercalated cells located? function?
in the collecting tubule, so its the Cl/HCO3 antiporter switches with H+/ATPase
actively secretes bicarbonate into tubular lumen
what limits H+ to be excreted as H2PO4
amt of HPO4 in filtrate, requirement of body to retain phosphate (~75% filtrered phosphate reabsorbed)
what is the rate of H+ secretion dependent on?
pH-->activate s Na+/H antiporter and H+/ATPase
causes of acute vs chronic respiratory acidosis
acute: severe asthma, pneumonia, aspiration of foreign object, drugs that cause respiratory depression
chronic: emphysema, chronic bronchitis