Physiology Lab
1.
2.
3.
If the H+ concentration of a blood sample is
40 × 10−9 Eq/L, what is the pH of the blood?
A weak acid, HA, dissociates in solution into
H+ and the conjugate base, A−. If the pK of
this weak acid is 4.5, will the concentration of
HA or A− be higher at a pH of 7.4? How
much higher will it be?
For the three sets of information shown in
Table 4–3, calculate the missing values.
4. A man with chronic obstructive pulmonary
disease is hypoventilating. The
hypoventilation caused him to retain CO2 and
to increase his arterial Pco2 to 70 mm Hg
(much higher than the normal value of 40 mm
Hg). If his arterial HCO3- concentration is
normal (24 mEq/L), what is his arterial pH? Is
this value compatible with life? What value of
arterial HCO3- would make his arterial pH
7.4?
5. Figure below shows a titration curve for a
hypothetical buffer, a weak acid.
What is the approximate pK of this buffer? At a pH of 7.4, which is the
predominant form of the buffer, HA or A−?

Mr. Tony is a 66-year-old long-distance truck driver.
Ten years ago, he was diagnosed with focal
segmental glomerulosclerosis (a glomerular disease
that causes nephrotic syndrome). Because he is
constantly on the road, Roger found it difficult to
have periodic check-ups. Recently, however, his
symptoms were alarming—he had gained weight, his
face and legs were swollen, and his pants no longer
buttoned around the waist. Since these are signs that
his physician had warned him about, he called in sick
and made an appointment for a check-up. On
physical examination, the physician noted periorbital
edema, pitting edema of his extremities, ascites, and
an S3 gallop. Plasma and 24-hr urine values are
shown in Table below
The physician ordered a strict low-Na+ diet and prescribed a loop diuretic,
furosemide. After a few days, Roger called in to report that the furosemide
wasn’t working—“nothing’s happening, doc.” The physician increased the
dosage of furosemide and prescribed a second diuretic, spironolactone, to be
taken at the same time.
1.
As a consequence of long-standing focal segmental
glomerulosclerosis, Roger developed nephrotic syndrome, a
clinical complex characterized, first and foremost, by
proteinuria. Why was Roger excreting large amounts of protein
in his urine?
2. Why did Roger have hypoalbuminemia, and what is the expected
effect on plasma oncotic pressure?
3. What mechanism can you propose for his hyperlipidemia? For his
lipiduria?
4. Roger had generalized edema, caused in part by his
hypoalbuminemia. How does hypoalbuminemia lead to
generalized edema?
5. An additional cause of Roger’s edema was retention of Na+ and
water by his kidneys. Propose a mechanism for increased Na+ and
water reabsorption in nephrotic syndrome and explain how this
increase would contribute to edema.
6. What is the meaning of his S3 gallop?
6. The presence of generalized edema is associated
with increased total body Na+ content. If Roger’s
total body Na+ content was increased, why did he
have a normal plasma Na+ concentration?
8. Why did Roger’s physician place him on a low
Na+ diet?
9. Roger needed to receive a diuretic in order to
increase his Na+ and water excretion. Why was the
initial dosage of furosemide ineffective? What was
the rationale for increasing the dosage?
10. Why was spironolactone added to his treatment?