CASE STUDY DISCUSSIONS*() W^dad\nd[Y^hZVhZ
She was investigated for diabetes insipidus with a fluid deprivation test. At
the end of the test, her plasma osmolality was still high with a low urine
osmolality suggesting diabetes insipidus as she has failed to conserve water
during water deprivation. However, she responded to desmopressin by
producing a more concentrated urine, suggesting a deficiency of ADH rather
than renal insensitivity to ADH. It is most likely that Sarah is suffering from
cranial diabetes insipidus.DISCUSSION OF CASE STUDY 7.2
Ian has subclinical or compensated hypothyroidism, that is, he is at a
higher risk of developing clinical hypothyroidism. Indeed, some patients
with subclinical or compensated hypothyroidism show clinical features
of hypothyroidism. An increased release of TSH is required to stimulate
the release of thyroid hormones from a deteriorating thyroid gland. Ian’s
condition should be reviewed every few months and antibodies against his
thyroid gland should be measured to detect whether there is an autoimmune
cause.DISCUSSION OF CASE STUDY 7.3
Amelia has hyponatremia with hyperkalemia. This indicates deficiency of
mineralocorticoids that is typical of Addison’s disease. The clinical features
are also consistent with Addison’s disease and Amelia has presented with an
adrenal crisis. Amelia is dehydrated and this explains the high serum urea
caused by a low glomerular filtration rate. She should be treated by correcting
her fluid balance and then placing her on a steroid regimen that includes
hydrocortisone and fludrocortisone.DISCUSSION OF CASE STUDY 7.4
Jaclyn is a type 1 diabetic and presented with diabetic ketoacidosis (DKA), a
medical emergency. This has probably occurred because Jaclyn has failed to
take her insulin therapy although it may be that it has been precipitated by
infections or even excessive stress. An overview of DKA is provided inFigure
7.25. The patient should be treated immediately. This will include infusions
of isotonic saline to restore blood volume, insulin infusions to reduce
hyperglycemia, K+ supplements to replace lost K+ and possibly hydrogen
carbonate infusions to alleviate the severe acidosis present in this case.DISCUSSION OF CASE STUDY 7.5
Rachel’s symptoms indicate a possible PCOS. The moderate increase in
testosterone combined with a raised LH and typical clinical findings are
strongly supportive of this diagnosis. The pathogenesis of this condition is
unknown. Normal ovaries synthesize androgens, such as testosterone and
androstenedione. In PCOS their secretion increases and in the liver and
adipose tissue they are converted to estrogens that inhibit release of FSH
and prevent ovulation. Luteinizing hormone release is stimulated and in turn
stimulates further release of androgens leading to hirsutism.CHAPTER 8
DISCUSSION OF CASE STUDY 8.1
Ted has acute renal failure as a result of his accident. This acute renal failure
may have been caused by release of myoglobin from crushed muscles together
with loss of blood. This explains the high serum concentration of urea and its
osmolality. The hyperkalemia is a result of renal failure but possibly also due