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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
What happens to NH4+ and HCO3- that are produced during acidemia?
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
What system is important for storing NH3 in medullary interstitium?
Formation of new bicarbonate
27
What is the major method for neutralizing acid in urine?
NH3 produced during formation of new bicarbonate Thereby increasing H secretion
28
What limits H+ secretion into the lumen of the CT by the ATPases? What fixes this?
H+ gradient between the plasma and the tubule lumen Titratable buffers (phosphate and ammonia) allow more hydrogen ions to be excreted See figure
29
What is the major titratable acid ?
NH3 produced in glutamine metabolism in proximal tubule Allows renal excretion of an increased acid load
30
What hormone stimulates H secretion?
Aldosterone See figure
31
Net Acid Excretion (NAE) =
NAE = (UNH4V + UTAV) – UHCO3V ``` U = urine V = urine volume per unit of time ```
32
UNH4V
urine ammonium excretion most important, ammonia to ammonium allows excretion of large amounts
33
UNTAV
titratable acid excretion - eg phosphate useful but limited
34
UHCO3V
bicarbonate excretion important in recycling bicarbonate
35
Types of renal tubular acidosis
Inappropriate response by kidney Type 1 - distal nephron Type 2 - proximal type Type 4 - hypoaltosteronism
36
Type 1 RTA
distal nephron (late nephron segments) unable to excrete acid load due to failure to secrete H into lumen
37
Type 2 RTA
proximal type reduced ability to reabsorb bicarbonate
38
Type 4 RTA
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
How the kidney regulate acid/base in long term?
Proximal tubule Collecting tubules
40
Proximal tubule regulation of acid/base in long term?
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
Collecting tubules regulation of acid/base in long term?
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
Expected compensatory responses during acidosis and alkalosis
See figure
43
Anion gap caculation
Na+ – (HCO3- + Cl-)
44
What is the normal anion gap in a healthy person?
11 mEq/L
45
What does an increased anion gap indicate about metabolic acidosis?
Increased acid production (lactic acidosis, ketoacidosis - diabetes, starvation, alcohol related) Increased acid ingestion (methanol, ethylene glycol, aspirin, propylene glycol)
46
What does no change in anion gap indicate about metabolic acidosis?
loss of bicarbonate (diarrhea-intestinal loss, type 2 RTA-proximal tubule) Decreased renal acid secretion (type 1 RT - distal, type 4 RTA -hypoaldosteronism)
47
What happens when there is metabolic acidosis due to gain of acid
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
Why doesn't the anion gap change when there is metabolic acidosis due to loss of HCO3-?
hyperchloremic metabolic acidosis lost HCO3- replaced by Cl- Na+ – (HCO3- + Cl-) remains unchanged

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