pH-regulation Flashcards Preview

Renal exam 1 > pH-regulation > Flashcards

Flashcards in pH-regulation Deck (33):

what are the non-volatile compounds from diet?

sulfuric acid and phosphoric acid


how to keep pH constant

[HCO3-]/PCO2 constant


Cause of respiratory acidosis, where is it located on graph

increase PCO2
point on normal buffer slope below 7.4


Cause of respiratory alkalosis, where is it located on graph

decreased PCO2

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

Na/H+ 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

proximal tubule


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+?

pH 4.4

[H+]=0.4 mmol/L


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

40 torr


normal Lab value for arterial pH

pH 7.35-7.45


normal Lab value for bicarbonate

calculated or measured: 24mmol/L


normal Lab value for Urinary titratable acid

0-20 mmol/day

up to 40 mmol/day in acidosis--can be much higher in ketoacidosis or other condt


normal Lab value for urinary ammonium ion

20-40 mEq/day

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

8-12 mEq/L

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?

hemoglobin buffer

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?

what happens?

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


compensation for metabolic alkalosis

decrease ventilation, decrease HCO3- reabsorption, active HCO3- sectretion by B-type intercalating cells