Physiology-Acid Base Balance Flashcards
In what sequence do the body’s acid-base defenses normally get rid of excess H+ in the body?
First the bicarbonate buffer grabs H+, second the lungs help via expiration of CO2 and finally the kidneys generate new bicarbonate and secrete H+ bound as ammonia and phosphate in the urine.
Use the Hendersen-Hasselbach equation to show how the kidney and the lung can both cause acidosis (respiratory acidosis & metabolic acidosis).
The lung can increase PCO2 by decrease expiration. This will cause a decrease in the pH as seen below. The kidney can increase HCO3 excretion, which will also decrease pH as seen below.
The pKa of bicarbonate is 6.1, but the physiological pH is 7.4. How is bicarbonate such a good buffer in a system with a pH so far from its pKa?
The pKa of 6.1 is measured in a closed system. However, in our bodies the system is open and we can continually exhale CO2 from our bodies.
What portion of buffering power in the blood is represented by bicarbonate?
2/3 is bicarbonate and 1/3 non-bicarbonate.
Where in this diagram would you find respiratory acidosis and alkalosis? Metabolic acidosis and alkalosis?
Respiratory acidosis = low pH and high CO2. Metabolic acidosis = low pH and low CO2. Respiratory alkalosis = high pH and low CO2. Metabolic alkalosis = high pH and high CO2.
What would happen to a blood pH of 7.4 in response to increasing PCO2 if non-bicarbonate buffer concentration was unlimited? What if it was 0?
Unlimited = no change in pH. 0 non-bicarbonate buffer = new blood pH of 7.1 instead of 7.2 as seen below.
You have an old patient with emphysema in your clinic. Blood work reveals that the patient is in respiratory acidosis. How do the kidneys function to return this patient back to a healthy physiological pH?
By making more bicarbonate and secreting more acid, the pH will raise back to 7.4ish.
How do the lungs function to recover from metabolic alkalosis?
Metabolic alkalosis happens when HCO3 levels are high. The lungs increase PCO2 and return the pH back to normal.
HCO3 doesn’t just get willy nilly reabsorbed in the kidney anywhere it wants. What does HCO3 reabsorption depend on?
H+ secreting via either the Na+/H+ exchange pump or the H+ATPase. Once H+ is in the lumen, it finds bicarbonate and forms carbonic acid. Carbonic anhydrase then converts the carbonic acid to water and CO2 which can be reabsorbed into the PCT epithelium. Inside the cell, carbonic anhydrase converts H2O and CO2 back to HCO3 and it exits via the (3)HCO3-Na exchanger.
Where is most bicarbonate reabsorbed in the kidney?
PCT
How is bicarbonate reabsorbed in the collecting duct?
It occurs in the intercalated cells. It is the exact same as the PCT except the lumen exchanger is a K+/H+ exchange pump instead of a Na+/H+ exchange pump. The basal exchanger is a Cl/HCO3 exchange pump.
How do the intercalated cells of the collecting duct adjust to alkalosis?
In beta-intercalated cells, the HCO3/Cl exchanger switches from the blood side to the lumen side.
How do the cells in the nephron compensate for acidosis with bicarbonate?
This is different from normal bicarbonate reabsorption because carbonic acid is not reabsorbed and the H+ is secreted where it binds phosphate and leaves in the urine.
How do the cells in the nephron compensate for acidosis with H+ handling?
Ammonia produced from protein metabolism can bind up H+ and be secreted as NH4+ in the PCT. As NH4+ moves down the loop of Henle, it is taken out of the tubule and into the interstitium where it generates an osmotic gradient for water retention. It is then taken back up by the cells of the collecting duct and moved back into the tubule so it can be excreted in the urine. Additionally, new bicarbonate is released from protein metabolism.
How does NH4+ get into the proximal convoluted tubule?
Diffusion of gaseous NH3 and then it combines with H+ to make NH4+ or passage of liquid NH4+ through a Na+ exchange pump.
How much H+ do we typically excrete in a day? How is that H+ distributed? How do these values differ in acidosis and alkalosis?
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The kidney excretes about 70mmol H+/day. How much “new” HCO3 is created by the kidney each day?
70mmol. Any formation of acid = loss of HCO3 which must be produced again by the kidney.
You are in the field working as a doctor and one of your patients is acidotic. You don’t have any lactated Ringer solution, what food can you give this patient?
Oranges. The citrate in oranges is metabolized to form bicarbonate and will alkalize the blood.
How would you expect plasma bicarbonate to change in a patient with COPD?
Respiratory acidosis. Due to decreased ventilation they will have an increased PCO2. This causes a decreased plasma pH. The kidney responds by increasing HCO3 production to bind up acid and raise the pH.
How would you expect plasma bicarbonate to change in a patient having a panic attack?
Respiratory alkalosis. Due to increased ventilation they will have a decreased PCO2. This causes an increase in plasma pH. The kidney responds by decreasing HCO3 reabsorption and decrease new HCO3 production to increase free acid and lower the pH.
How would you expect plasma bicarbonate to change in a patient with diabetic ketoacidosis?
Metabolic acidosis. Due to low plasma bicarbonate levels, plasma pH will decrease. The lungs respond by decreasing PCO2 and increasing the pH.
How would you expect plasma bicarbonate to change in a patient who has experienced excessive vomiting recently?
Metabolic alkalosis. Due to high plasma bicarbonate levels, plasma pH will increase. The lungs respond by increasing PCO2 and decreasing the pH.
How do you know what type of acid-base problem this patient has?
Increased levels of HCO3 = renal compensation for acidosis. Decreased levels of HCO3 = renal compensation for alkalosis.
What happens to urea metabolism when a patient is acidotic?
It is increased and NH3 from protein metabolism grabs H+ and is excreted in the urine.
What two factors govern the regulation of hydrogen ion release from glomerular tubules?
PCO2 and local pH. (increased H+ secretion is a result of increased PCO2 or decreased pH).
What regulatory mechanisms take place at the proximal tubule of the nephron in response to acidosis? What about on the distal end?
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How do you determine acid-base status of a patient in the clinic?
pH [7.4], HCO3 [24 mEq/L] and PCO2 [40 mmHg]
A patient comes to the ED while having an asthma attack. You get her stabilized and run some labs: pH 7.25, PCO2 62mmHg, HCO3 26 mEq/L. What is the acid-base state of this patient?
The patient has acute respiratory acidosis with beginnings go renal compensation.
A patient comes to the ED while having a COPD exacerbation. Labs show a pH of 7.35, PCO2 of 60mmHg and HCO3 32 mEq/L. What is the acid-base state of this patient?
This patient has chronic respiratory acidosis with renal compensation.
A patient comes to the ED. She has type I diabetes and has not had her insulin shot today. Labs reveal pH 7.29, PCO2 26mmHg and HCO3 12 mEq/L. What is the acid-base state of this patient?
This patient has metabolic acidosis with renal compensation.
A patient comes to the ED. He has been vomiting all day. Labs reveal pH 7.5, PCO2 48mmHg and HCO3 47 mEq/L. What is the acid-base state of this patient?
This patient has metabolic alkalosis with respiratory compensation.
A patient comes to the ED. She is a diabetic and hasn’t taken her insulin in a few days. Labs reveal pH 7.31, PCO2 30 mmHg and HCO3 16 mEq/L. What is the acid-base state of this patient?
This patient has metabolic acidosis with respiratory compensation.
A patient presents to the ED with abnormal acid-base labs that do not show appropriate compensatory response for alkalosis or acidosis. What should you suspect in this patient?
Presence of two or more underlying causes creating a mixed acid-base disorder.
A 55 year old male presents to the ED with sever diarrhea. History only reveals tobacco us. Labs reveal a pH of 7.15, PCO2 of 50 mmHg and HCO3 of 7 mEq/L. What is the acid-base status of this patient?
Note that the patient has acidosis, but the bicarbonate is not coming up and the PCO2 is not coming down. This indicates a mixed acidosis with a metabolic component (loss of HCO3 in diarrhea) and failure of respiratory compensation (emphysema from tobacco use).
How can ingestion of a large quantity of aspirin cause a mixed acid-base disorder? How will labs present in these patients?
Salicylic acid = metabolic acidosis. Aspirin stimulates hyperventilation = respiratory alkalosis. The patient may have a normal pH with abnormal PCO2 and HCO3 levels.
What are the clinical causes of metabolic acidosis?
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What are the clinical causes of metabolic alkalosis?
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What lab value is used to distinguish between different types of metabolic acidosis? What does it measure?
Anion gap [12]. [Na+]-[HCO3-]-[Cl-]. It is essentially measuring the gap between the cation (Na) and the anions (Cl & HCO3). The gap will increase as the amount of unmeasured anions increase. The gap will decrease as the amount of unmeasured anions decreases.
How might the anion gap present in patients with diabetes? What other conditions may present in this way?
With diabetes you have increased organic acids (ketoacids) and will cause a decrease in Cl. This will cause an increased anion gap. “MUDPILES”: Methanol, Uremia, Diabetes, Propylene glycol, Infection, Lactic acidosis, Ethylene glycol, Salicylates
What types of metabolic acidosis will present with a normal anion gap?
Diarrhea and renal tubular acidosis.
How do you differentiate between acute and chronic respiratory acidosis and alkalosis?
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You see a body builder in clinic and he tells you that he is not feeling well lately. History reveals that he has been overusing diuretics to get into a particular weight loss. How might this affect the acid-base status of this patient?
Extensive use of diuretics causes increased plasma aldosterone and potassium depletion. Both of these things cause H+ secretion at the distal tubule, increased HCO3 reabsorption and will cause metabolic alkalosis.
