Term
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Definition
pH = -log[H]
pH = log(1/[H]) |
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Term
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Definition
pH = pKa + log([A]/[HA])
Note: pH = pKa when [A] = [HA] |
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Term
| How are buffers affected when the pKa and pH are similar/different? |
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Definition
When the pKa and pH are at similar values, the buffer is more effective. Vice versa, as they get further apart. When they are far apart, the addition of acid such as HCl will change the pH considerably.
Note: buffers are most effective when pH is within 1.5 units of pK |
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Term
| If urine pH is around 4.5, what is the pK concentration that is most effective for buffering? |
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Definition
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Term
| How do changes in pH affect the body? |
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Definition
| Proteins are especially vulnerable to changes in pH b/c the charge can alter the three dimensional structure. |
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Term
| What are some non-bicarb buffers? Which one is the most important? |
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Definition
1. Hemoglobin - most important
-Buffering capacity comes from protonation and deprotonation of histidine
2. Plasma Proteins
-albumin has highest buffering capacity
3. Phosphate -phosphoric acid |
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Term
| How is PCO2 converted to [CO2]? (in terms of pH) |
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Definition
pH = 6.1 + log[HCO3]/.03PCO2
Solubility of CO2 is .03 mM/mmHg |
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Term
| How does the buffering capacity of an open vs. closed system compare? |
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Definition
| An open system buffering capacity is much higher at pH 7.4 than at 6.1. If the system were closed, the final pH would be much higher (lower buffering capacity). |
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Term
| Which buffer is more prominent intracellular vs. extracellular? |
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Definition
Intracellular - Protein is most important
Extracellular - Bicarb is most important |
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Term
| What is the isohydric principle? Why is it significant? What is normally assessed to show this? |
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Definition
All buffers in a homogenous sol'n are in equilibrium with the same [H]
Important because the total acid-base status can be assessed by knowing the status of one of the buffers.
Bicarb is the one normally assessed. |
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Term
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Definition
| H produced by respiration. All gets blown off as CO2. |
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Term
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Definition
Protein and amino acid axidation produces strong non-volatile acids including H2SO4 from methionine, cysteine, and cystine.
These acids do not circulate as free acids, but instead are consumed by bicarb.
This buffering yields Na and consumes bicarb. |
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Term
| What is the role of the kidney in regulating acid in the blood? |
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Definition
| To remove acid salts, and replenish bicarb lost in the buffering reaction. |
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Term
| What is the net acid load equal to and why is it significant? |
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Definition
| It is equal to the amount of non-volatile acid production. It is significant b/c the kidneys must excrete an amount equal to it in order to regulate acid/base balance. |
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Term
| What is titratable acid? How is it measured? |
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Definition
It is the amount of H that is excreted combined with urinary buffers such as phosphate, creatinine and other bases.
It is measured as the amount of strong base (NaOH) required to bring the urine pH back to the pH of blood (7.4) |
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Term
| What is the largest component of titratable acid? |
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Definition
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Term
| How do NH4+ excretion and bicarb relate? |
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Definition
| For every NH4+ excreted, one bicarb is returned to the ECF |
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Term
| How is Net Acid Excretion (NAE) measured? |
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Definition
Titratable acid excretion + NH4 excretion - HCO3 lost in the urine
Note: HCO3 is not typically lost in very large amounts, so it is normally negligible in the above equation |
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Term
| Where in the nephron is the majority of bicarb reabsorbed? |
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Definition
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Term
| What is the cellular mechanism for bicarb reabsorption? |
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Definition
H is pumped into the tubular fluid via 2 mechanisms:
1. Na - H antiporter
2. H ATPase
When H is in the tubular fluid, it combines with HCO3 to for H2CO3. CA then converts this to CO2 and H2O, which are readily absorbed by the apical membrane.
In the cell, CA forms H2CO3, which then forms H and HCO3
Most of the HCO3 exits the basolateral membrane via the Na - HCO3 symporter. Some HCO3 exits via the Cl - HCO3 antiporter. |
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Term
| What happens to the intercalated cells when the pH decreases? |
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Definition
| They insert more H-ATPase pumps into the apical membrane allowing more H to be pumped into the tubular fluid |
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Term
| What are 2 ways in which HCO3 is restored in the body via the kidney? |
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Definition
1. Formation of titratable acid - H+ is secreted and combines with urinary bufffers (phosphate, creatinine). H+ secretion results in excretion of H+ with a buffer, and HCO3- is added back into the blood.
2. Ammonium production - When glutamine is metabolized, NH4+ is produced. NH4+ is excreted with the acid anion (e.g. SO4-2) and returns NaHCO3 to the plasma.
NH4 is not excreted, but rather enters the systemic circulation where it titrates HCO3. Each molecule NH4 excreted results in a molecule of new HCO3 added to the plasma |
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Term
| What happens to NH4 during acidosis and alkalosis? |
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Definition
Acidosis - enzymes responsible for glutamine metabolism are stimulated. More enzyme results in more NH4 formation, and more HCO3 formation. Tends to increase pH.
Alkalosis - Glutamine metabolism is reduced, resulting in less HCO3 formation. |
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Term
| Respiratory acidosis? Primary event? Secondary event? |
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Definition
Primary - Increased PCO2
Secondary (compensatory) - Increase in plasma HCO3 |
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Term
| How long does the renal response take for compensation to respiratory acidosis? What are the actions that occur? |
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Definition
The response can take up to 24 hours.
Consists of H+ excretion and HCO3 reabsorption and formation |
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Term
| Respiratory alkalosis. Primary event? Secondary? |
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Definition
Primary - Decreased PCO2
Secondary - Decrease in plasma [HCO3] via decreased H+ excretion in the kidney and decreased HCO3 absorption. |
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Term
| Metabolic acidosis. Primary event? Secondary event? |
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Definition
Primary - Decreased plasma [HCO3]
Secondary - Decrease in PCO2 from hyperventilation |
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Term
| Causes of metabolic acidosis |
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Definition
1. An increase in H+ from endogenous sources
lactic acidosis
ketoacidosis
2. Increase in H+ from exogenous sources
ingestion of methanol or ethylene glycol
ingestion of salicylates
3. Decreased H+ from the kidney
4. Loss of bicarb from the GI tract |
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Term
| How is the Anion gap calculated? |
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Definition
| Difference b/t Na and (HCO3 and Cl-) |
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Term
| What's the normal range for the anion gap? |
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Definition
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Term
| How can metabolic acidosis occur in the absence of an increased anion gap? |
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Definition
| Diarrhea. B/c HCO3 is lost from the body, one would think this would change the anion gap. However, as HCO3 goes down, Cl- absorption goes up. |
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Term
| How does excessive vomiting cause metabolic alkalosis? |
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Definition
Loss of HCl from vomiting causes an increase in [HCO3]. Normally, the kidneys would excrete HCO3, but in persistent vomiting, the urine is sometimes acidic and renal HCO3 reabsorption is enhanced. The high [HCO3] is paradoxically maintained.
Excessive vomiting causes a loss of extracellular fluid volume. Decrease in arterial BP activates mechanisms that reduce Na excretion. GFR is decreaed. Leads to higher H+ secretion. More HCO3 is added to blood and more HCO3 is reabsorbed from the tubular fluid. |
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Term
| What is the respiratory compensation for metabolic acidosis? |
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Definition
| 1.2mmHg drop in PCO2 per 1 mEq/L in HCO3 |
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Term
| What is the Renal compensation for respiratory acidosis? |
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Definition
| 3.5 mEq/L increase in HCO3 per 10mmHg increase in PCO2 |
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Term
| What is the respiratory compensation for metabolic alkalosis? |
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Definition
| 0.7 mmHg increase PCO2 per 1 mEq/L increase in HCO3 |
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Term
| What is the renal compensation for respiratory alkalosis? |
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Definition
| 5 mEq/L decrease in HCO3 per 10 mmHg drop in PCO2 |
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