Hyperthyroidism….

Management…
A. Propylthiouracil /PTU/
and methimazole…
Indications to use
Antithyroid drugs
include
1. Graves’ disease in
young patients
2. Hyperthyroidism during
pregnancy
3. The need to achieve
euthyroid state before
surgery or radiation
• B. Iodine
 It also decreases the
vascularity of the thyroid
gland, making surgery
safer and easier
• The administration of
iodine in large doses
rapidly inhibits synthesis of
T3 and
C. Beta adrenergic blockers
Beta adrenergic blockers are used f
sympathetic relief
increased beta adrenergic receptor stimulation
caused by excess thyroid hormone
_ropranolol: administered with other anti-
thyroid agents and rapidly provides
symptomatic relief
_Atenolol :is the preferred beta adrenergic
blocker for use in hyperthyroidism patient with
asthma or heart disease
 avoid high fiber diets

 Postoperative
complications include:
 Hypothyroidism
 Damage to or in advertent
removal of parathyroid
glands causing
hypoparathyroidism and
hypocalcaemia,
hemorrhage, injury to the
recurrent or superior
laryngeal nerve, thyrotoxic
crisis and infection
A high calorie diet (4000 to
5000cal/day)
Hypoparathyroidism
Causes
 Iatrogenic: The most
common cause and this may
include: Accidental removal
 of the parathyroid glands or
damage to the vascular supply
of the gland during neck
surgery
 E.g.: Thyroidectomy, neck
surgery, Radiation
therapy
 Autoimmune disease
 Genetics
 Idiopathic
 high serum calcium levels
can cause hypotension,
serious cardiac
dysrhythmias, or cardiac
arrest

 Vitamin D is used in
chronic and resistant
hypocalcaemia to enhance
intestinal calcium
absorption
Primary hyperparathyroidism-is due to an
increased secretion of PTH leading to disorders
of calcium, phosphate, and bone metabolism
The most common cause is benign
tumor/adenoma/in the parathyroid hormone
Secondary hyperparathyroidism-appears
due to compensatory response to conditions
that induce or cause hypocalcaemia, the main
stimulus of PTH secretion
E.g. vitamin D deficiencies, malabsorption, chronic
kidney disease, and hyperphosphatemia
Tertiary hyperparathyroidism-occurs when
there is hyperplasia of the parathyroid glands
and loss of negative feed back from circulating
calcium
levels
Complications
Renal failure
Pancreatitis
Cardiac changes
Long bone, rib and vertebral
fracture
 Criteria for surgery
includes:
 Serum calcium levels grater
than 12 mg/dl
 Hypercalciuria (greater than
400mg/day
 Markedly reduced bone
mineral density
 Overt symptoms-E.g.:
neuromuscular effects,
nephrolithiasis or those
under the age of 50
Calcimimetic agents- are a class of
drugs that increase the sensitivity of
the calcium receptor on the
parathyroid gland
 Bisphosphonates-
inhibit osteoclastic
bone resorption and
rapidly normalize serum
calcium level
 Oral phosphate-used to
inhibit the calcium
absorbing effects of
vitamin D in the
intestine
 1. Cushing
Clinical manifestations syndrome…
 Weight gain—the most common feature results
from the accumulation of adipose tissue in the
trunk and cervical spine area/Buffalo hump/,
face/moon face
 Transient weight gain- from sodium and water
retention may
 be present
 Hyperglycemia-occurs because of glucose
intolerance
 and increased gluconeogenesis by the liver
Menstrual disorders and hirsutism in women
and gynecomastia

Menstrual disorders and hirsutism in women

and gynecomastia and impotence in men are
seen more commonly in adrenal carcinomas
 1. Cushing syndrome…
Clinical manifestations…
 Muscle wasting following catabolic effects
of cortisol on peripheral tissue which
leads to muscle weakness, especially in
the extremities
 Mood disturbances (irritability, anxiety,
euphoria), insomnia, irrationality, and
occasionally psychosis may occur
 Hypernatremia and hypokalemia
 Hyperpigmentation of the skin
 Osteoporosis with subsequent pathologic
fracture
 Mineralocorticoid excess may cause
hypertension
secondary to fluid retention where as adrenal
androgen excess may cause severe acne,
virilization in women, and feminization in
men
 Urine cortisol levels beyond the
normal range of 80-120 mcg in 24
hours in adult indicates Cushing
syndrome
If Cushing syndrome has
developed during the course
of prolonged administration
of corticosteroids one or more
of the following alternatives
are used:
Gradual discontinuance of corticosteroid
therapy
Reduction of corticosteroid dose-gradual
tapering of the corticosteroids
• Addison’s disease
Etiology
 Autoimmune or idiopathic
 atrophy
 Infection
 Tuberculosis and histoplasmosis
are the most common infections
that destroy adrenal gland tissue
 Surgical removal of both adrenal
glands
 Inadequate secretion of ACTH
 from the pituitary gland
 Therapeutic use of
corticosteroids is the most
common cause of adrenocortical
insufficiency
 Clinical manifestations
Emaciation
Dark pigmentation of the skin
Hypotension, and low blood glucose levels
Hyponatremia, and hyperkalemia . Why?????

In severe cases the disturbance of sodium

and potassium metabolism may be marked by
depletion of sodium and water and severe,
chronic dehydration
Mental status changes such as depression,
emotional lability, apathy, and confusion are
present in 60% to 80% of patients

Addisonian crisis is a life threatening medical

emergency requiring aggressive management
 Hyperaldosteronism
 Is characterized by excessive aldosterone
secretion
 The main effects of aldosterone are
sodium retention, potassium and
hydrogen ion excretion

 Primary hyperaldosternoism-is most

commonly caused by a small solitary
adrenocortical adenoma
 hypertension are caused by
primary hyperaldosternoism
 Secondary hyperaldosternoism-occurs in
response to a non adrenal cause of
elevated aldosterone levels such as renal
artery stenosis, rennin-secreting tumors,
and chronic kidney disease
 Hyperaldosteronism should be suspected
in all hypertension patients with
hypokalemia who are not being treated
with diuretics
 The preferred treatment
of primary
hyperaldosternoism is
surgical removal of the
adenoma
 The preferred treatment
of secondary
hyperaldosternoism is
treating the etiology
accordingly.