Download printable version of the five cases here

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?
13. Why would it be unnecessary to treat Hazel with supplemental EPI?
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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
Urinalysis
Fasting blood glucose 93 mg/dL
(normal is 65-100 mg/dL)
Urine osmolarity <200 mOsm/L
(much more dilute than normal)
Serum sodium 145 mmol/L
(normal is 135-145 mmol/L)
Urine volume 15 L/day
(normal is 2-3 liters/day)
Serum potassium 2.8 mEq/L
(normal is 3.5-5 mmol/L)
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 selfadminister 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?
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?
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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? 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 (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?
Case 5
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?