6. Renal Control of Acid-Base Flashcards

(29 cards)

1
Q

What are fixed acids?

A

non-carbonic acids generated metabolically like sulfuric and phosphoric acids
Initially neutralized by buffers in body fluids and ultimately excreted in urine

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2
Q

What are the metabolic sources of H?

A

oxidative metabolism of CO2
Fixed: glycolysis (lactic acid), incomplete FA oxidation (ketones), Protein, nucleic acid, phospholipid metabolism (sulfuric, phosphoric, hydrochloric acids)

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3
Q

What is the primary buffer system?

A

bicarb/CO2 buffer

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4
Q

What are the ECF buffer systems?

A

bicarb/CO2
inorganic phosphate (HPO4)
Plasma proteins

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5
Q

What are the ICF buffers?

A
Cell proteins (hemoglobin)
Organic phosphates (ATP, 2,3 DPG)
Bicarb/CO2
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6
Q

What is the Henderson-Hasselbalch equation?

A

pH = pK + log [A-]/[HA]

A- = HCO3
HA = CO2 or CO2 = (0.03*PCO2)
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7
Q

What are volatile acids?

A

Produced by metabolic processes that can be expired by respiratory tract
Carbonic acid system

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8
Q

What is the renal response to excess acid?

A

all of filtered HCO3 is reabsorbed and additional H is secreted into lumen, excreted primarily as ammonium

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9
Q

What is the renal response to excess base?

A

Incomplete reabsorption of filtered HCO3
Decreased H secretion
secretion of HCO3 in collecting duct

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10
Q

Most H is excreted in combination with urinary buffers. What are the two types?

A

Titratable acid: conjugated bases of metabolic acids accept H in lumen (phosphate, creatinine, urate)

Ammonia: generated by tubular epithelium

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11
Q

H excretion = ?

A

urinary excretion of titratable acid + ammonium - HCO3

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12
Q

HCO3 excretion is equivalent to adding ___ to body fluids

A

acids

*for each mEq of HCO3 lost, a free H is left behind

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13
Q

Where is a major site for the formation of ammonia ?

A

Proximal tubule when glutamine is converted to ammonia

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14
Q

What do alpha - intercalated cells secreted?

A

H by H ATPase pump

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15
Q

What do beta - intercalated cells secrete?

A

HCO3 to eliminate excess base

HCO3/Cl exchanger

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16
Q

The activity of H-ATPase in the alpha-intercalated cells are directly stimulated by what?

17
Q

acid base status of hyperaldosterone patient

A

alkalosis

and hypokalemic

18
Q

Most of the H secreted by the proximal tubule is used to do what?

A

reabsorb filtered HCO3 so luminal pH falls only slightly in this segment

19
Q

Why must all of the filtered HCO3 needs to be reclaimed in normal individuals?

A

because excretion of HCO3 has same effects as gaining H; excretion of even small fraction of filtered HCO3 would acidify body fluids

20
Q

How does HCO3 get across the membrane?

A

it temporarily is converted to CO2

21
Q

80% of the filtered HCO3 is reabsorbed in PT, what is this ultimately dependent on?

22
Q

If there is an excess amount of HCO3 in the plasma, what is preventing the bicarb from being reabsorbed?

A

it is a saturable process and the antiporters are filled

23
Q

what is the most important buffer converted to titratable acid?

A

filtered HPO4

24
Q

What is the process of excretion of H as ammonium in the proximal tubule?

A

glutamine in the cells is converted to 2 ammonium. This is converted to ammonia so that it can freely pass through the membrane to the tubular fluid. The Na/H exchanger pushes H out into the tubular fluid and joins NH3 and is excreted as ammonium. Also 2 bicarbs are produced by glutamine oxidation

25
What are the factors controlling renal H secretion?
``` intracellular pH Plasma PCO2 CA activity Na reabsorption (angiotensin/aldosterone) Extracellular [K] aldosterone ```
26
What is hyperchloremic acidosis?
when metabolic acidosis occurs and anion gap is unchanged due to loss of HCO3 is matched by gain of Cl
27
What is normochloremic acidosis?
It is a high anion gap that occurs in metabolic acidosis due to HCO3 being replaced by unmeasured anion (lactate, ketoacidosis, poisoning)
28
What are some causes of anion gap?
``` E. Elm Park ethanol ethylene glycol lactic acid methanol paraldehyde aspirin renal failure ketone bodies or MUDPILES ```
29
What is MUDPILES?
``` methanol uremia diabetic ketoacidosis, starvation or alcoholic ketoacidosis paraldehyde iron lactic acidosis ethylene glycol salicylate ```