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Physiology > Lecture 6: Acid/Base > Flashcards

Lecture 6: Acid/Base Flashcards

1
Q

pH =

A

pH = log[H+] -1

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2
Q

What is a basic pH? Lethal? What happens at this pH?

A

pH > 7.6 considered basic (low H+). Over 8 is lethal.

over excitability of peripheral then central nervous systems

muscle twitching / spasms (respiratory impairment)

CNS actions - convulsions

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3
Q

What is acidic pH? What happens at this pH? lethal?

A

pH < 7.2 considered acidic (high H+). Lower than 6.8 is lethal

depression of CNS

disorientation

coma

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4
Q

What is normal blood pH?

A

7.4 (slightly basic)

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5
Q

What is the major source of volatile acids?

A

oxidative metabolism of carbohydrates and triglycerides

Metabolism produces CO2, which is converted to carbonic acid (H2CO3) and back to CO2 for excretion by the lungs.

CO2 + H2O H2CO3 H+ + HCO3-

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6
Q

What catalyzes the CO2 + H2O H2CO3 H+ + HCO3- reaction?

A

carbonic anhydrase (CA)

Reversible

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7
Q

What types of oxidative metabolism do not produce carbon dioxide?

A

hypoxia (lactic acid) oxidation

fat oxidation in diabetes mellitus (ketoacids)

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8
Q

What are non-volatile acids?

A

Acids produced in the body from sources other than CO2

For example, with diets high in protein, there is a net production of acids

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9
Q

Where are non-volatile acids excreted?

A

Not broken down to CO2

Not excreted by the lungs

Excreted by the kidneys

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10
Q

What are other means of losing acids and bases?

A

Vomit - H+ loss

diarrhea - HCO3- loss

urine - HCO3- loss

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11
Q

What is the relationship between pH, CO2 and HCO3- ?

A

Henderson Hasselbalch Equation

pH α concentration of HCO3-/dissolved CO2

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12
Q

What do buffers in the blood and tissue do?

A

Acutely prevent large shifts in pH

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13
Q

What are the buffers in the blood?

A
  1. Plasma - bicarbonate buffers (account for 75% of plasma buffering), plasma proteins, phosphate buffers
  2. Erythrocytes - bicarbonate buffers, hemoglobin
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14
Q

What are the buffers in the tissue?

A
  1. Skeletal muscle - contains large % of total body HCO3-
  2. Bone - large store of calcium carbonate, main source for neutralizing non-carbonic acid, chronic metabolic acidosis (e.g. lactic acidosis, ketoacidosis)
    is associated with bone deterioration
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15
Q

Respiration in A/B balance

A

eliminates CO2 from the blood and shifts the equilibrium away from H2CO3 (and vice versa).

incr RR -> dear CO2 -> incr pH

decr RR -> incr CO2 -> dear pH

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16
Q

What happens during hyperventilation?

A

we lose CO2 and plasma CO2 goes down

The equation is driven to the left and plasma H+ decreases

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17
Q

What happens during hypoventilation?

A

we retain CO2 and plasma CO2 goes up

The equation is driven to the right and plasma H+ increases

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18
Q

What does long term pH control require?

A

long-term pH control requires the kidney

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19
Q

What are the three renal mechanisms for responding to pH changes?

A
  1. bicarbonate reabsorption (in the proximal tubule)
  2. formation of new bicarbonate and ammonium (from glutamate) - ammonium (NH4) stored as ammonia (NH3) in the medullary
    interstitum
  3. active secretion of hydrogen ions, titratable acids (ammonia/phosphate) and aldosterone production
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20
Q

Where does bicarbonate reabsorption occur primarily?

A

Proximal tubule (85%)

Some reabsorption in collecting ducts (15%)

21
Q

How is bicarbonate reabsorption accomplished?

A

bicarbonate in the filtrate is broken down and reformed
in the cell for reabsorption

See figure

22
Q

What would happen to bicarbonate excretion and plasma pH if carbonic anhydrase was not working (blocked?)

A

loss of HCO3 in the urine

consequently, plasma pH would decrease

23
Q

What would happen to bicarbonate excretion and plasma pH if the Na:H exchange was not working

A

loss of HCO3 in the urine

consequently, plasma pH would decrease

24
Q

What is glutamine converted to during acidemia? Where?

A

NH4+ and HCO3- (formation of new bicarbonate)

in proximal tubule

25
Q

What happens to NH4+ and HCO3- that are produced during acidemia?

A

the bicarbonate is reabsorbed (not excreted)

the NH4+ is secreted into the tubule lumen (but not excreted) -

reabsorbed in loop of Henle (uses Na:Cl:K transporter) into the medullary intersitium

converted to NH3 (ammonia) + H

NH3 stored for when kidney needs to excrete large amounts of H (but note - H not excreted either)

this process is “neutral” - HCO3- + H are added to the body

See figure

26
Q

What system is important for storing NH3 in medullary interstitium?

A

Formation of new bicarbonate

27
Q

What is the major method for neutralizing acid in urine?

A

NH3 produced during formation of new bicarbonate

Thereby increasing H secretion

28
Q

What limits H+ secretion into the lumen of the CT by the ATPases? What fixes this?

A

H+ gradient between the plasma and the tubule lumen

Titratable buffers (phosphate and ammonia) allow more hydrogen ions to be excreted

See figure

29
Q

What is the major titratable acid ?

A

NH3 produced in glutamine metabolism in proximal tubule

Allows renal excretion of an increased acid load

30
Q

What hormone stimulates H secretion?

A

Aldosterone

See figure

31
Q

Net Acid Excretion (NAE) =

A

NAE = (UNH4V + UTAV) – UHCO3V

U = urine
V = urine volume per unit of time
32
Q

UNH4V

A

urine ammonium excretion

most important, ammonia to ammonium allows excretion of large amounts

33
Q

UNTAV

A

titratable acid excretion - eg phosphate

useful but limited

34
Q

UHCO3V

A

bicarbonate excretion

important in recycling bicarbonate

35
Q

Types of renal tubular acidosis

A

Inappropriate response by kidney

Type 1 - distal nephron

Type 2 - proximal type

Type 4 - hypoaltosteronism

36
Q

Type 1 RTA

A

distal nephron (late nephron segments)

unable to excrete acid load

due to failure to secrete H into lumen

37
Q

Type 2 RTA

A

proximal type

reduced ability to reabsorb bicarbonate

38
Q

Type 4 RTA

A

hypoaldosteronism

aldosterone deficiency or action

adrenal gland fails to secrete aldosterone (most often cause)

decreased ability to secrete H (so titratable acids can’t work)

39
Q

How the kidney regulate acid/base in long term?

A

Proximal tubule

Collecting tubules

40
Q

Proximal tubule regulation of acid/base in long term?

A

increase or decrease in bicarbonate reabsorption

increase or decrease in glutamine conversion to HCO3 + NH4 - HCO3 reabsorbed, NH4 converted to NH3 and stored in medullary interstitium next
to collecting tubules(H not excreted)

41
Q

Collecting tubules regulation of acid/base in long term?

A

increase or decrease active H secretion (into tubule lumen)

increase or decrease active H secretion due to aldosterone

increase or decrease in titratable acids

NH3 diffusion from medullary interstitum to tubule lumen - binds free H

42
Q

Expected compensatory responses during acidosis and alkalosis

A

See figure

43
Q

Anion gap caculation

A

Na+ – (HCO3- + Cl-)

44
Q

What is the normal anion gap in a healthy person?

A

11 mEq/L

45
Q

What does an increased anion gap indicate about metabolic acidosis?

A

Increased acid production (lactic acidosis, ketoacidosis - diabetes, starvation, alcohol related)

Increased acid ingestion (methanol, ethylene glycol, aspirin, propylene glycol)

46
Q

What does no change in anion gap indicate about metabolic acidosis?

A

loss of bicarbonate (diarrhea-intestinal loss, type 2 RTA-proximal tubule)

Decreased renal acid secretion (type 1 RT - distal, type 4 RTA -hypoaldosteronism)

47
Q

What happens when there is metabolic acidosis due to gain of acid

A

Na : HCO3
Na:Cl
Na : ??? - represents normal 11 mEg/L of an unmeasured anion
Na : ???? - ???? represents unmeasured acid (ingested or produced)

the added acid associated with sodium - increases gap

48
Q

Why doesn’t the anion gap change when there is metabolic acidosis due to loss of HCO3-?

A

hyperchloremic metabolic acidosis

lost HCO3- replaced by Cl-

Na+ – (HCO3- + Cl-) remains unchanged

Physiology (19 decks)

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