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CRRAB 2 > Acid/Base > Flashcards

Acid/Base Flashcards

1
Q

What reaction does Carbonic Anhydrase catalyze?

A

CO2 + H2O H2CO3 H+ +HCO3-

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2
Q

Besides bicarb, what are the other buffers?

A

hemoglobin, PO4-, Albumin

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3
Q

What is a primary side effect of chronic acidosis?

A

Osteopenia, due to bicarb resorption from bone

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4
Q

What is Kussmaul breathing and why does it happen?

A

Kussmaul breathing is slow, deep, labored, breaths. It happens because in acidosis there is a rise in H+ ions which drives the CA equation towards H2O and CO2. Kussmaul breathing is how the body blows off the extra CO2 that is produced.

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5
Q

What happens at pH 7.2 and below?

A

Decrease in cardiac contractility.

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6
Q

Besides Kussmaul breathing and HCO3 resorption from bone, what other effects does acidosis have on the body? [2]

A

Increased circulating cathecolamine levels

Stimulates protein catabolism –> negative nitrogen balance. Become profoundly malnourished very quickly.

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7
Q

What happens to breathing in an alkalosis?

A

hypoventilation leading to an increase in CO2

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8
Q

What happens to oxygen and energy production in alkalosis? [2]

A

The oxygen dissociation curve is shifted to the left thereby decreasing oxygen delivery to the tissues.

Lactate production increases.

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9
Q

How do we produce volatile acids?

A

By metabolizing the carbohydrates and fats we eat.

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10
Q

How do we deal with volatile acids?

A

We break them down to CO2 and H2O and excrete them via the lungs

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11
Q

How do we produce and excrete non-volatile acids?

A

By metabolizing ingested proteins. These are generally sulfur containing acids or hydrochloric acid.

We produce 50-100mEq/day that must be excreted by the kidneys. Lungs can’t metabolize.

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12
Q

What group of people have a very very high level of non-volatile acids to deal with?

A

Body builders, paleo diet

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13
Q

Given that non-volatile acids are absorbed in the GI tract, how does the body balance acid there?

A

H+ is excreted on the apical side and HCO3- is extruded on the basolateral side of the gasc.

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14
Q

Why doesn’t the acid/balance in the GI tract change the pH of the body?

A

H+ is dumped into the lumen and HCO3- is taken up into the serum in the

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15
Q

What must the kidney do prevent chronic acidosis (normal function)? [2] Which type(s) of acid does this apply to?

A
  1. reabsorb every single bicarb in the proximal tubule
  2. Have a way to excrete acid into the urine and reabsorb more bicarb than was consumed.

Trick Question: Both volatile and non-volatile acids. Both consume bicarb to buffer acid

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16
Q

Can the kidneys bind the H+ to bicarb to excrete into urine?

A

No because it would use up all the bicarb silly.

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17
Q

So then what does the kidney make to carry h+ in the urine? Where is it made?

A

Ammonium. It’s made in the proximal tubule.

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18
Q

Do proximal tubule cell sense pH?

A

Yes (through a variety of means)

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19
Q

How does H+ get out of the cell in the proximal tubule?

A

anti-porter with Sodium

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20
Q

How does ammonium get out of the proximal tubule cell?

A

antiporter with sodium

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21
Q

What the bicarb/ammonium reaction for the proximal tubule

A

NH4+ alpha ketoglutarate 2HCO3

each glutamine creates an NH4 and 2 HCO3s

22
Q

What enzyme catalyzes the production of bicarb in the proximal tubule? What reaction does it catalyze?

A

glutaminase. Glutamine –> a ketoglutarate

23
Q

How is ammonium/bicarb reaction regulated?

A

by the amount of glutaminase in the cell. When pH decreases, glutaminase is upregulated. lower pH also upregulates Carbonic anhydrase (need to get rid of h+ sl also drive h+/Na antiporter

24
Q

How is ammonium balanced with its conjugate base? what is the pK?

A

NH4+ NH3+ + H(+)

ammonium ammonia and hydrogen ion

pK = 9

25
Q

What organ can regulate ammonium?

A

liver

26
Q

How does liver regulated ammonium?

A

NH4 + 2HCO3 –> urea + CO2+ 3H2

27
Q

Given the liver’s regulation system how do we keep the ammonium in balance?

A

the ammonium made in the proximal tubule of the kidney, stays in the kidney

28
Q

How is extracellular pH signaled through intracellularly? [2]

A

If metabolic acidosis: drop in HCO3 improves the gradient for the basolateral exchangers (NA/HCO3 symporter)

If respiratory process: increased CO2 diffuses across the cell and lowers the pH

29
Q

What do intracellular pH signalling pathways in proximal tubule trigger?

A

transporters on proximal tubule become upregulated and glutaminase becomes activated

30
Q

What is ammonium recycling?

A

It is where ammonium is reabsorbed in the thick ascending limb (NKCC2 channel) (replaced by k+) and dumped into the interstitium where it disassociates to (NH3 + H). Crosses basolateral side of collecting ducts and goes back in to lumen where it absorbs H+ ion. Given the acidity of collecting duct, the NH4 is unable to cross back over into the cell. Some of it goes back to the proximal tubules. [NH3] concentration in interstitium is high.

prevents ammonium from entering circulation where it would be taken up by liver and consume bicarb.

31
Q

What are the non-bicarb bases and what ratio of hydrogen do they carry in the urine?

A

NH4 2/3

H2PO4 1/3

32
Q

How does phosphorus get into the urine?

A

filtration

33
Q

What channels are in the a intercalated cell?

A

Apical
K+/H+ (out) antiporter
h+ ATPase

Basolateral
k/cl symporter (out)
HCO3 (out)/Cl anitporter
K+ and Cl- leakage channels

34
Q

What transporters are in b intercalated cell?

A

Apical
Cl in/ HCO3 out

basolateral
H ATPase
Cl leakage channel

35
Q

What causes respiratory ventilation?

A

primary rise in pCO2 due to lack of ventilation (drug induced or pulmonary issues)

36
Q

What changes occur in blood chemistry in respiratory acidosis? what is the equivalency?

A

increase in h+, increase in HCO3

10mmHG rise in CO2 ~ 1 mEq rise in HCO3

37
Q

How does the body buffer resp. acidosis?

A

Ammonium excretion in proximal tubule and HCO3 resorb in a intercalated cell

38
Q

What causes loss of Bicarb in metabolic acidosis? What corresponding change is made and why?

A

lost in GI tract: diarrhea, fistulas, etc.

Equation is shifted toward H+ and HCO3 so [H+} increses

39
Q

What causes initial rise in h+ in metabolic acidosis? What corresponding change is made, why?

A

Metabolism of lactate, ketones, renal failure, aspirin toxicity, methanol, ethylene glycol.

Equation shifts to the left, toward CO2 and H2o which causes loss of bicarb

40
Q

What is renal tubular acidosis?

A

loss of H+ and HCO3 in tubule (different dx if proximal versus distal etc.)

41
Q

What happens to PCO2 in metabolic acidosis?

A

PCO2 goes down via stimulated alveolar ventilation –> kussmaul breathing

42
Q

How does kidney respond to metabolic acidosis?

A

create bicard through glutamine pathway in proximal tubule. this only stabilizes you, doesn’t fix problem

43
Q

What creates anion gap and what is the normal number

A

albumin creates anion gap and 10 is normal

44
Q

how does non-anion gap acidosis work?

A

HCl + NaHCO3 –> NaCl + H2 CO3 –> CO2 + H2O

Lost HCO3- but gained Cl- so anion gap doesnt change

45
Q

How does anion gap acidosis work?

A

H (A-) + Na HCO3 –> NaA + H2CO3 –> CO2 + H2O

A- is some negative that isn’t measured such as a toxin.

so burned up bicarb with no measured ion to replace it

46
Q

What AG number is abnormal i.e. diagnosable

A

AG > 20 some type of anion gap metabolic acidosis

47
Q

What causes respiratory alkalosis?

A

decrease in oxygen. High altitude, hyperventilation, CHF, PE, asthma in kids

48
Q

What happens chemically in respiratory alkalosis?

A

due to decreased CO2, equation shifts to the left.

In acute cases, h+ will be released from intracellular buffers such as hemoglobin and esp. phosphorus.

Downregulates enzymes because you don’t want to be making ammonium in proximal tubule anymore

systemic ammomium goes to kidney where it is metabolized with 2 HCO3 consumed in the process. Helps balance alkalosis

49
Q

What causes metabolic alkalosis?

A

Must have inciting event and something that maintains it. Rare.

50
Q

What causes rise in bicarb in metabolic alkalosis?

A

usually impairment in renal excretion such as volume depletion.

51
Q

What causes loss of hydrogen in metabolic alkalosis?

A

NG suction, vomiting

52
Q

How does loss of gastric H+ secretions lead to increased bicarb?

A

Gastric: h+ out, bicarb in

Pancreas: bicarb out, h+ in

in NG suction H+ ions never reach pancreas so it is not triggered, as a result you just lose h+

CRRAB 2 (12 decks)

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