ACID BASE BALANCE Flashcards

(35 cards)

1
Q

non-volatile (fixed) acid

A

acids that are normally produced during normal metabolic processes in the body or excreted
- cannot be eliminated by ventilation via the lungs

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2
Q

examples of nonvolatile acids

A

lactic acid, sulfuric and phosphoric acids, keto acids, uremic acids

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3
Q

sources of nonvolatile acids

A

anaerobic glycolysis (lactic acid), fatty acid oxidation (ketone production), amino acid metabolism, nucleic acid oxidation, fecal base loss

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4
Q

T or F: CO2 is a nonvolatile acid

A

FALSE

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5
Q

volatility

A

describes how easily a substance will vaporize

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6
Q

which source of acid is produced in greater amounts in the body?

A

nonvolatile
- nonvolatile ~50-100mmoles/day
- volatile 15-20 mmoles/day (want this to be low)

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7
Q

normal concentration of bicarb in the blood?

A

24 mM

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8
Q

role of the kidney in acid-base balance

A

1- prevent bicarb loss (by reabsorbing ALL bicarb that is freely filtered and replenishing bicarb that was consumed from buffering fixed H+)
2- excrete acid equal to nonvolatile acid production (~50-100mEq/day)

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9
Q

How is bicarb reabsorbed at the PT?

A

NHE at the proximal tubule reabsorbs Na+ and exchanges for H+ to the ECF
- the H+ binds bicarb –> carbonic acid and carbonic anhydrase converts to CO2 and H2O which can freely enter the cell
- carbonic anhydrase in the cell converts CO2 and H2O to bicarb
- bicarb is shuttled into the blood by a NBCe1 transporter on the BASOLATERAL membrane

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10
Q

NBCe1 transporter

A

Na+/HCO3- cotransporter 1
- transporter on the BASOLATERAL membrane of tubular cell that shuttles bicarb back into the blood from the kidney

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11
Q

what affect does angiotensin 2 have on the NHE at the proximal tubule?

A

upregulates the NHE at the proximal tubule to further regulate acid/bicarb balance

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12
Q

where does most bicarb get reabsorbed and why?

A

at the proximal tubule (~80% bicarb reabsorption)

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13
Q

how much bicarb is reabsorbed at the TAL and DT?

A

10% and 6% respectively

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14
Q

alpha intercalated cell

A

cell of the collecting duct that secretes acid and reabsorbs bicarb to maintain acid-base homeostasis
- secretes H+ into the filtrate where buffers (HPO3- and NH3) are present to titrate and form titratable acids in the urine before excretion

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15
Q

intercalated beta cell

A

cell of the collecting duct that is typically only active during periods of alkalosis
(i.e vomiting)
- secretes bicarb
- has Pendrin transporter to move bicarb into the tubular fluid and returns H+ back into the blood to restore pH

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16
Q

2 major buffers of the kidney

A

phosphate and ammonium

17
Q

titratable acid

A

acid that can pick up free H+ of the acid load

18
Q

Phosphate as a urinary buffer

A

titrates free H+ in the filtrate after alpha intercalated cell secretes it
- 1/3 of the acid load

19
Q

Ammonia as a urinary buffer

A

titrates free H+ in the filtrate after alpha intercalated cell secretes it
- 2/3 of the acid load

20
Q

why are urinary buffers critical?

A

prevents the urine from being too acidic, which would compromise the ability of the kidneys to function
- without buffers, free H+ would be traveling through the kidneys

21
Q

what is the source of ammonia used to titrate acid in urine?

A

metabolism of glutamine

22
Q

where is NH3/NH4+ reabsorbed and secreted?

A

reabsorbed in TAL and secreted in CD
- H+ is also secreted at CD –> NH4+ excreted in urine

23
Q

How does the kidney respond to acid loads?

A

1- reabsorbs ALL bicarb
2- increases H+ excretion in form of titratable acids
3- produces more NH4+
- these are done via enzyme synthesis, transporter regulation etc

24
Q

what is the minimum pH of urine?

A

4.5; kidneys can only excrete nanomolars of acid without causing kidney damage
- the kidneys excrete 50-100mEq of acid/day in the form of titratable acids which would not be possible without buffering the H+ with nonvolatile acids

25
acidemia
decreased blood pH - high H+ concentration
26
alkalemia
increased blood pH - high bicarb concentration
27
acidosis
physiologic condition that acts to increase H+ concentration - gain of acid and/or loss of buffer - example: diarrhea
28
alkalosis
physiologic condition that acts to decrease H+ concentration - gain of buffer and/or loss of acid - example: vomiting
29
in what scenario is buffering sufficient to restore pH?
acute acidosis - bicarb in the ECF acts in seconds-mins - proteins and phosphates in the ICF act in hrs
30
in what scenario is renal compensation required to restore pH?
chronic acidosis
31
respiratory acid-base disorders
reflect changes in pCO2 - example: COPD --> respiratory acidosis - drugs and CNS disorders --> resp alkalosis
32
metabolic acid-base disorders
reflect changes in bicarb - diarrhea, renal failure, ingesting Aspirin --> metabolic acidosis - vomiting--> metabolic alkalosis
33
T or F: pH is dependent on the ratio of bicarb and pCO2
TRUE
34
how to resolve metabolic acidosis? (base deficit)
decrease pCO2 which would decrease H+ concentration
35
how to resolve metabolic alkalosis?
increase pCO2 to increase H+ concentration