Endocrine Case Histories - Case 8

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.)