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Flashcards in pH-regulation Deck (33):
1

what are the non-volatile compounds from diet?

sulfuric acid and phosphoric acid

2

how to keep pH constant

[HCO3-]/PCO2 constant

3

Cause of respiratory acidosis, where is it located on graph

hypoventilation
increase PCO2
point on normal buffer slope below 7.4

4

Cause of respiratory alkalosis, where is it located on graph

hyperventilation
decreased PCO2

point on normal buffer slope above pH 7.4

5

Cause of metabolic acidosis, where is it located on graph

loss of HCO3-
point on 40 torr isobar below ph7.4

6

metabolic alkalosis, where is it located on graph

increased HCO3- concentration
point on 40 torr above 7.4

7

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

8

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

9

where is majority of bicarbonate reabsorbed

proximal tubule

10

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

11

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

12

what is the limiting urine pH? H+?

pH 4.4

[H+]=0.4 mmol/L

13

for every H2PO4 excreted in urine, what happens?

1 H+ eliminated

1 HCO3- in blood

14

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)

15

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

16

how does NH4 contribute to severe acidosis

NH4+ production contributes up to 250 mmol/day of new bicarbonate to blood

17

normal Lab value for Arterial PCO2

40 torr

18

normal Lab value for arterial pH

pH 7.35-7.45

19

normal Lab value for bicarbonate

calculated or measured: 24mmol/L

20

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

21

normal Lab value for urinary ammonium ion

20-40 mEq/day

up to 250 mEq/day an acidosis

22

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

23

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

24

what happens in acute vs chronic respiratory acidosis

[HCO3-] slighly increased and remains on normal buffer slope=acute

chronic:
-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)

25

acute respiratory alkalosis? causes?

decreased PCO2--> pH of blood increased


causes: fear, anxiety, trauma,, salicylate intoxication

~0.2 mmol/L decrease [HCO3-]

26

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

27

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

28

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

29

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

30

what limits H+ to be excreted as H2PO4

amt of HPO4 in filtrate, requirement of body to retain phosphate (~75% filtrered phosphate reabsorbed)

31

what is the rate of H+ secretion dependent on?

pH-->activate s Na+/H antiporter and H+/ATPase

32

causes of acute vs chronic respiratory acidosis

acute: severe asthma, pneumonia, aspiration of foreign object, drugs that cause respiratory depression

chronic: emphysema, chronic bronchitis

33

compensation for metabolic alkalosis

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