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Case 0
(Your textbook will prove particularly useful in this case.)
A 50-year-old male (Horace C.) had a total thyroidectomy followed by thyroid hormone-replacement
therapy. Thirty-six hours later he developed laryngeal spasms, a mild tetany, and cramps in the muscles
of the hands and arms. The following tests were performed:
Plasma calcium 7.0 mg/dL (normal is 9.0-10.5 mg/dL)
Plasma phosphorus 5.0 mg/dL (normal is 2.4- 4.1 mg/dL)
Plasma chloride 99 mEq/L (normal is 97-110 mEg/L)
1. Of the plasma electrolytes, which is most seriously disturbed?
2. What hormone(s) regulate plasma calcium?
3. What gland is the source of those hormone(s)?
4. What has happened to those glands in Horace?
5. What endocrine disorder is present in Horace? Could this have been avoided?
6. What caused Horace's tetany and laryngeal spasms?
As a follow-up, calcium gluconate and vitamin D (calcitriol) were given orally each day and the tetany
and laryngeal spasms were alleviated.
7. During the treatment phase, what is the purpose of vitamin D administration with supplemental
calcium?
8. Diagram the negative feedback loop for the hormone(s) involved and be sure to identify the effectors
and the hormone that acts on each effector.
9. Is hormone replacement therapy necessary for Horace or could his case be managed by supplements
and vitamins?
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Case 1
Hazel C. a 30-year-old female demonstrated a subtle onset of the following symptoms: dull facial
expression; droopy eyelids; puffiness of the face and periorbital swelling; sparse, dry hair; dry, scaly skin;
evidence of intellectual impairment; lethargy; a change of personality; bradycardia (60 b/min); a blood
pressure of 90/70; constipation, and hypothermia. The patient does not complain of pain.
Plasma concentrations of total and free T4 and T3 follow:
T4
T3
Total
3 ug/dL (normal is 4-12 ug/dL)
0.14 ng/dL (normal is 75-195 ng/dL)
Free
0.6 ng/dL
0.01 ng/dL
A blood sample indicated elevated TSH levels.
A TSH stimulation test did not increase the output of thyroid hormones from the thyroid gland.
A biopsy of Hazel's thyroid revealed large numbers of lymphocytes in her thyroid gland.
1. How do Hazel's levels of T3 and T4 compare to normal?
2. What do Hazel's elevated levels of TSH reveal about the function of her anterior pituitary? about her
thyroid glands?
3. What is a TSH stimulation test and how are the results interpreted?
4. Name the endocrine disorder in this case.
5. Is this a primary or secondary disorder? How is this determined?
6. Diagram the feedback loop involved.
7. What is a palpable goiter and would you expect to find a palpable goiter in this case? Explain your
answer.
8. Why does Hazel have a lower-than-normal body temperature?
9. What is the most likely explanation for the bradycardia and low blood pressure in Hazel C?
10. If a person has bradycardia and hypotension, which of the following hormones would most
immediately restore heart rate and blood pressure to normal: TH or EPI? Would you recommend that
hormone for Hazel C?
11. Describe a suitable treatment for Hazel. Would this treatment require injections or capsules?
12. Is this treatment expected to return blood pressure and heart rate to normal? Why or why not?
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13. Why would it be unnecessary to treat Hazel with supplemental EPI?
Case 2
Thomas L. a 28-year-old male, complained of abrupt polydipsia (excessive thirst) and polyuria (excessive
urine volume) . Blood and urine analyses provided the following results:
Blood Tests
Fasting blood glucose 93 mg/dL (normal is 65-100 mg/dL)
Serum sodium 145 mmol/L
(normal is 135-145 mmol/L)
Serum potassium 2.8 mEq/L
(normal is 3.5-5 mmol/L)
Urinalysis
Urine osmolarity <200 mOsm/L (much more dilute than normal)
Urine volume 15 L/day
(normal is 2-3 liters/day)
Urine glucose 0
(normal is 0)
Water deprivation and hypertonic saline infusion did not cause a significant reduction in the polyuria nor
did the urine become more concentrated.
Complete water-deprivation resulted in a urine osmolarity 225 mOsm/L.
Following administration of exogenous ADH , there was a significant concentration of the urine and a
decrease in urinary output.
1. Is Thomas hypoglycemic?
2. To maintain a steady state how much water must Thomas drink per day?
3a. Why was a water deprivation and hypertonic saline infusion ordered?
3b. How would a normal healthy person respond to these tests? Think of how urine volume and
concentration would be affected.
4. Why did the water deprivation and hypertonic saline infusion not result in a concentrated urine?
5. Are Thomas's kidneys capable of responding to ADH? What is the evidence?
6. What is the name of this endocrine disorder?
7. Is there a defective endocrine gland? If so, which is it?
8. Thomas L. was given a nasal spray containing a synthetic substance to self-administer to treat this
condition. What compound was in the nasal spray?
9. Why was this compound given as a nasal spray? Why not have Thomas consume it in tablet form?
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10. Diagram the hypothalamic-pituitary-target organ pathway for this individual and indicate the normal
and pathophysiological conditions involved.
11. The symptoms appeared abruptly. What could have been the cause of this endocrine disorder?
What question would you like to ask Thomas that would help you determine the cause of the abrupt
onset?
11. What is the long-term prognosis for Thomas L? Must he take the nasal spray for the rest of his life?
Why or why not?
Case 3
Oscar T. a 45-year-old male from the Midwest presented with the following symptoms during February:
weakness, fatigue, orthostatic hypotension, weight loss, dehydration, and decreased cold tolerance. His
blood chemistry values follow:
Serum sodium 128 mEq/L (normal = 135-146 mEg/L)
Serum potassium 6.3 mEq/L (normal = 3.5-5 mEq/L)
Fasting blood glucose 65 mg/dL (normal = 65-100 mg/dL)
Hematology tests resulted in the following values:
Hematocrit 50% (normal is 42-52%); Leukocytes 5000/cu mm (normal is 4300-10800/ cu mm)
Oscar also noticed increased pigmentation (tanning) of both exposed and nonexposed portions of the
body and back. A plasma cortisol determination indicated a low cortisol level. Following administration
of ACTH, plasma cortisol did not rise significantly after sixty and ninety minutes. Endogenous circulating
levels of ACTH were later determined to be significantly elevated.
1. What is orthostatic hypotension?
2. What hormone from which organ is most likely involved with Oscar's serum electrolyte imbalance?
3. Is Oscar anemic? Which of the test results answers this question?
4. Does Oscar have an infection? Which of the test results answers this question?
5. Which hormone is most likely associated with the symptoms of weaknesss, fatigue, weight loss and
decreased cold tolerance?
6a. What endocrine organ is the site of the malfunction?
6b. What hormones are normally secreted from this gland?
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6c. Is more than one hormone deficient in Oscar?
7. How is it possible for Oscar's plasma glucose to be within the normal range?
7. What is the name of this disorder?
8. In a normal person, how would plasma cortisol levels be affected following administration of ACTH?
What do Oscar's ACTH test results imply?
9. Is this a primary or secondary disturbance? Explain your answer.
10. Why is Oscar's endogenous circulating level of ACTH significantly elevated?
11a. What is the cause of Oscar's hyperpigmentation?
11b. How is hyperpigmentation related to his high levels of ACTH?
12. What type of replacement therapy would be required for Oscar? Will the replacement of one
hormone suffice to treat all his symptoms?
13. Diagram the feedback loops for this endocrine disorder.
14. What is the long-term outlook for Oscar? Might one expect Oscar's abnormal pigmentation to
resolve once his treatment has begun? Explain.
Case 4
Julian, a 21-year-old male, demonstrated the following:
Poor muscle development; High-pitched voice; microphallis; eunuchoidism; anosmia; tall stature (6'7")
Upon further questioning, it was found that Julian was born with a cleft palate, only one kidney and
cryptorchidism.
A blood sample revealed low serum levels of FSH, LH and Testosterone.
1. Define microphallis, eunuchodism, anosmia and cryptorchidism.
2. What secondary sex characteristics is Julian lacking?
3. Name the endocrine disorder (be specific) in this case. Is this a primary or secondary disorder?
4. Diagram the feedback loop involved.
5. Why is Julian suffering from anosmia?
6. How can Julian's tall stature be explained?
7. Can his condition be treated? If so, how?
8. Will he be able to father children if left untreated? Why or why not?
9. Is this disorder genetic? If so, which chromosome is affected? Is this always the case?