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Case Study 8
Endocrine Case Histories - Case 8
A 21-year-old noncompliant female with a history of type I (insulin-dependent) diabetes mellitus
was found in a coma. Her blood glucose was high, as well as her urine glucose, urine ketones,
and serum ketones. Her serum bicarbonate was < 12 mEq/L. Her respiration was exaggerated
and his breath had an acetone odor. Her blood pressure was 90/60 and his pulse weak and rapid
(120).
Endocrine
Diabetes Mellitus
Answers:
1. Noncompliant is the failure or refusal to comply (as in the taking of prescribed
medication).
2. This person is experiencing ketoacidosis as suggested by the acetone odor on his
breath due to elevated fatty acid metabolism. This indicates that there was not enough
insulin to allow the blood glucose to get into the cells, so the cells shifted to their second
preferred fuel (fats) for metabolism, thus dumping keto acids, causing the acetone
breath odor.
3. The serum bicarbonate is low due to the buffering of the keto acids by the bicarbonate
ions.
4. This is an example of metabolic acidosis.
5. Dyspnea is caused by the acidosis, which stimulates the respiratory center, producing
the rapid, deep respiration known as Kussmaul breathing (as described by Kussmaul).
Hypotension is caused by fluid loss from an osmotic diuresis (glucose loss in the urine).
Tachycardia is a reflex response in an attempt to overcome the hypotension.
6. This person needs a rapid-acting insulin and IV fluids in the form of 0.9% sodium
chloride (plus bicarbonate if the blood pH is <7.1 and the serum bicarbonate is <10
mEq/L). (There are approximately seven forms of insulin currently available in the United
States with different rates of onset, effectiveness, and duration of action. They are
generally classified into rapid-, intermediate-, and long-acting insulins.)
Case Study 15
A 30-year-old male 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; anemia (hematocrit 27); enlarged heart (upon radiological
exam); constipation, and hypothermia. Plasma concentrations of total and free T4 and T3 follow:
Free
Radioimmunoassay (RIA) of peripheral blood indicated elevated TSH levels. A TSH stimulation
test did not increase the output of thyroid hormones from the thyroid gland.
Endocrine
Primary Hypothyroidism
Answers:
1. The endocrine organ involved is the thyroid gland.
2. This is a primary disorder since the TSH stimulation test did not increase the output of
thyroid hormones from the thyroid gland. Circulating TSH levels are useful in making the
diagnosis. TSH would be very high in primary hypothyroidism due to the lack of
feedback inhibition on the pituitary. TSH would be very low in secondary hypothyroidism
due to the absence of TSH from the pituitary. Circulating levels of TRH would be helpful
but not necessary.
3. The feedback loop involves the following: TRH from the hypothalamus stimulates the
release of TSH from the anterior pituitary, which in turn should stimulate the thyroid
gland to relapse T4 and T3. With low circulating levels of thyroid hormones, the negative
feedback will cause an elevation in TSH output. Even with the elevated TSH, the thyroid
gland is unresponsive and does not increase the hormonal output.
4. Defects could be present in the uptake of iodide into the thyroid gland; the conversion of
iodide to iodine; the iodination of the tyrosine molecule; the coupling of MITs and DITs or
DITs with DITs; or the release of the hormones from the thyroglobulin molecules. There
may also be a deficiency of TSH receptors on the thyroid gland itself.
5. There may be a palpable goiter since there is an elevated circulating level of TSH due to
the negative feedback stimulus from low circulating levels of thyroid hormones. This
chronic TSH stimulation may cause hypertrophy of the gland, thus causing a goiter.
(Goiter may also be present in secondary hypothyroidism or in the euthyroid state.)
6. Suitable treatment for this individual would be replacement thyroid hormone therapy.
Synthetic preparations of T4 (L-thyroxine), 150-200 µg/day, may be given orally. (T3
should not be used alone for long-term replacement because its rapid turnover requires
that it be taken several times each day.)