Acid base

Question 1

true or false:

nl H+ and pH signify normal acid base status

Answer 1

nope

Question 2

true or false:

the H+ and pH is determined by the ratio of the two determinants of acidity and not either variable individually

Answer 2

true

Question 3

H+ ion balance involves 3 factors

Answer 3

1. hydrogen ion input
2. body buffering
3. acid excretion by the kidney

Question 4

the average daily american diet generates approximately _____ hydrogen ion input

Answer 4

1 mEq/kg

Question 5

in alkalemia, H+ is _______ in exchange for K+ and can lead to

Answer 5

externalized

and can lead to hypokalemia

Question 6

in acedemia, H+ is _____ into the intracellular compartment in an electron-neutral exchange for K+ leading to

Answer 6

redistributed

and can lead to hyperkalemia

Question 7

bicarbonate reabsorption and net acid excretion are accomplished by

Answer 7

tubular secretion of H+ into the luminal fluid across the nephron

Question 8

where is bicarb reabsorption

Answer 8

PCT

Question 9

hydrogen ion secretion by the

Answer 9

CT

Question 10

max. urinary acidification

Answer 10

pH 4.5

Question 11

Daily H loads are buffered by

Answer 11

bicarb and tritratable acid

Question 12

About 50% of the daily endogenous acid load is buffered by extracellular ________, with the remainder buffered by other extracellular and intracellular proton acceptors, and bone.

Answer 12

bicarbonate

Question 13

true or false:

.

9. NAE = TA (titratable acid) excretion + NH4+ excretion – residual HCO3- excretion. Under steady-state conditions, NAE (new HCO3- generation) = Endogenous acid load.
10. There are four cardinal acid-base disorders: Metabolic disorders (metabolic acidosis and metabolic alkalosis) are initiated by a change in plasma [HCO3-], whereas respiratory disorders (respiratory acidosis and respiratory alkalosis) are initiated by a change in PaCO2. The primary change in either plasma [HCO3-] or PaCO2 elicits in vivo a secondary response in the other component that tends to minimize the change in acidity.
11. A simple acid-base disorder comprises the primary (initiating) abnormality in plasma [HCO3-] or PaCO2 coupled with the appropriate secondary response in the other component. Absence of an appropriate secondary response denotes the co-existence of an additional acid-base disorder. The simultaneous presence of two or more simple acid-base disorders defines a mixed acid-base disorder.

Respiratory Acid-Base

1. Respiratory acidosis is the acid-base disorder initiated by an increase in PaCO2 (hypercapnia). Most cases of respiratory acidosis reflect a decrease in alveolar ventilation. The increased PaCO2 is accompanied by a secondary increase in plasma [HCO3-] that attenuates the impact of hypercapnia on systemic acidity. Thus, simple respiratory acidosis is characterized by hypercapnia, acidemia, and a secondary increase in plasma [HCO3-].
2. The adaptive increase in plasma [HCO3-] characteristic of respiratory acidosis occurs in two phases: acute and chronic.
3. Acute adaptation originates exclusively from acidic titration of the body’s nonbicarbonate buffers. It is completed within 5-10 min from onset of hypercapnia. On average, plasma [HCO3-] increases by about 0.1 mEq/L for each mm Hg acute increment in PaCO2. The compensation equations are printed (and will be given to you during the exam) on the “Useful Formulas” page in the back of the syllabus.
4. Chronic adaptation originates from upregulation of renal acidification mechanisms that results in 1) a transient increase in urinary net acid excretion (mostly a rise in ammonium excretion) that generates the new HCO3- for body fluids; and 2) a persistent increase in the rate of renal bicarbonate reabsorption that maintains the increased plasma [HCO3-]. It requires 3-5 days of sustained hypercapnia for completion. On average, plasma [HCO3-] increases by about 0.35 mEq/L for each mm Hg chronic increment in PaCO2.
5. Failure of the [HCO3-] to increase by the expected amount represents an independent metabolic acid-base disturbance, and a mixed acid-base disorder. A [HCO3-] above expected represents a concomitant metabolic alkalosis, and a [HCO3-] below expected represents a concomitant metabolic acidosis.
6. Respiratory alkalosis is the acid-base disorder initiated by a reduction in PaCO2 (hypocapnia). Most cases of respiratory alkalosis reflect an increase in alveolar ventilation. The reduced PaCO2 is accompanied by a secondary decrease in plasma [HCO3-] that attenuates the impact of hypocapnia on systemic acidity. Thus, simple respiratory alkalosis is characterized by hypocapnia, alkalemia, and a secondary decrease in plasma [HCO3-].
7. The adaptive decrease in plasma [HCO3-] characteristic of respiratory alkalosis occurs in two phases: acute and chronic.
8. Acute adaptation originates exclusively from alkaline titration of the body’s nonbicarbonate buffers. It is completed within 5-10 min from onset of hypocapnia. On average, plasma [HCO3-] decreases by about 0.2 mEq/L for each mm Hg acute reduction in PaCO2.
9. Chronic adaptation originates from downregulation of renal acidification mechanisms that results in 1) a transient decrease in urinary net acid excretion (mostly a fall in ammonium excretion and an early component of increased HCO3- excretion) that reduces the body’s HCO3- stores; and 2) a persistent decrease in the rate of renal bicarbonate reabsorption that maintains the decreased plasma [HCO3-]. It requires 2-3 days of sustained hypocapnia for completion. On average, plasma [HCO3-] decreases by about 0.4 mEq/L for each mm Hg chronic decrement in PaCO2.
10. Failure of the [HCO3-] to decrease by the expected amount represents an independent metabolic acid-base disturbance, and a mixed acid-base disorder. A [HCO3-] above expected represents a concomitant metabolic alkalosis, and a [HCO3-] below expected represents a concomitant metabolic acidosis.

Tomorrow we will complete the Acid-Base section of the Physiology/Pathophysiology Unit. This will include lectures on Metabolic Acidosis and Metabolic Alkalosis. This material is difficult, but we have 2 small groups next week devoted to working on this material.

Keep up the great work, and please keep your questions coming. We will have our first review session tomorrow at 1PM in Jaharis on the physiology material covered to this point. This will be interactive with PollEverywhere questions. I think it will be fun, and I hope you can make it. I will then be having Office Hours tomorrow at 2PM in MedEd 316 – come by and let’s rap Renal. I’m happy to clarify any material.

Finally, I’d like to remind those in small group 9 (Reaves/Kumar/Gordon) that the session on 8/23 has been moved from MedEd 507 to MedEd 312.

All the best,

Scott J. Gilbert, MD
Course Director, From Health to Disease
Section Leader, Renal Course
Tufts University School of Medicine
800 Washington St, Box 391
Boston, MA 02111
617-636-9425 (office)
617-636-8329 (fax)
sgilbert@tuftsmedicalcenter.org

Answer 13

true