What is Addison’s
disease
Addison's disease (also known
as chronic
adrenal insufficiency,
hypocortisolism or
hypocorticism) is a rare
endocrine disorder in which the
adrenal gland does not produce
enough steroid hormones (
glucocorticoids and often
mineralocorticoids). It may
develop in children, adults or
some species of animals, and
may occur as the result of many
underlying causes.
Cause Symptoms
•Adrenal dysgenesis
-All causes in this category are -Low blood pressure that falls further
genetic, and generally very when standing
rare -have darkening (hyperpigmentation)
of the skin, including areas not
•Impaired steroidogenesis exposed to the sun
-To form cortisol, the adrenal
gland requires cholesterol, -conditions that often occur together
which is then converted with Addison's: goiter and vitiligo
biochemically into steroid
hormones. Interruptions in the
delivery of cholesterol include
Smith-Lemli-Opitz syndrome
and abetalipoproteinemia
• Sign and Test
• The short test compares
blood cortisol levels
before and after 250
micrograms of
tetracosactide (IM/IV) is
given. If, one hour later,
plasma cortisol exceeds
170 nmol/L and has risen
by at least 330 nmol/L to
at least 690 nmol/L,
adrenal failure is
excluded.
• The long test uses 1 mg
tetracosactide (IM).
Blood is taken 1, 4, 8,
and 24 hours later.
Normal plasma cortisol
level should reach 1000
nmol/L by 4 hours. In
primary Addison's
disease, the cortisol level
is reduced at all stages
whereas in secondary
corticoadrenal
insufficiency, a delayed
but normal response is
seen.
Treatment
Treatment for Addison's
disease involves replacing the
missing cortisol, usually in the
form of hydrocortisone tablets,
in a dosing regimen that mimics
the physiological
concentrations of cortisol.
Alternatively one quarter as
much prednisolone may be
used for equal glucocorticoid
effect as hydrocortisone.
Treatment must usually be
continued for life. In addition,
many patients require
fludrocortisone as replacement
for the missing aldosterone.
Caution must be exercised
when the person with Addison's
disease becomes unwell, has
surgery or becomes pregnant.
Medication may need to be
increased during times of
stress, infection, or injury.
• What is Agromegaly?
• a syndrome that results when
the pituitary gland produces
excess growth hormone
(hGH) after epiphyseal plate
closure at puberty. A number
of disorders may increase the
pituitary's GH output,
although most commonly it
involves a GH producing
tumor called
pituitary adenoma, derived
from a distinct type of cell
Cause
-Pituitary adenoma
the overproduction of growth
hormones is caused by a
benign tumor of the pituitary
gland, called an adenoma
-Other tumors
In a few patients, acromegaly
is caused not by pituitary
tumors but by tumors of the
pancreas, lungs, and
adrenal glands
- Human Growth Hormone
abuse
The misuse of human growth
hormone for bodybuilding and
'bulking up' .
Symptom
-Facial aspect of a patient with
acromegaly. The nose is widened and
thickened, the cheekbones are
obvious, the forehead bulges, the lips
are thick and the facial lines are
marked. The forehead and overlying
skin is thickened, sometimes leading
to frontal bossing.
-As compared with the hand of a
typical person (left), the hand of a
patient with acromegaly (right) is
enlarged, the fingers are widened,
thickened and stubby, and the soft
tissue is thickened.
-Mandibular overgrowth leads to
prognathism, maxillary widening,
teeth separation and jaw
malocclusion
• Sign and test Treatment
-Surgery
• Frequent blood -radiotherapy
sampling with serum
-somatostatin analogues
GH measurement
shows that in normal -and dopamine agonists act at the
subjects (left panel) level of the pituitary adenoma
GH can fluctuate
between undetectable
levels (most of the
time) and peaks of up
to 30 μg/l (90 mIU/l),
owing to the episodic
nature of GH
secretion, while in
patients with
acromegaly (an
example is given on
right panel), GH
hypersecretion is
continuous and GH
never returns to

undetectable levels .
• What is
Hyperthyroidism?
• Hyperthyroidism is the
term for overactive tissue
within the thyroid gland,
resulting in overproduction
and thus an excess of
circulating free thyroid
hormones: thyroxine (T4),
triiodothyronine (T3), or
both. Thyroid hormone is
important at a cellular
level, affecting nearly
every type of tissue in the
body
Cause
-Graves' disease (the most
common etiology with 70-80%)
-Toxic thyroid adenoma
-Toxic multinodular goitre
Symptoms
-include weight loss (often accompanied
by an increased appetite),
-anxiety
-intolerance to heat
-fatigue
-hair loss
-weakness, hyperactivity, irritability,
apathy, depression, polyuria, polydipsia,
delirium, tremor, pretibial myxedema,
and sweating.
• Sign and Test Treatment
• A diagnosis may be
suspected on history and -Temporary medical
physical examination, and therapy
is confirmed with blood
tests. -Surgery
• Measuring the level of
thyroid-stimulating hormone
(TSH) in the blood is
usually all that is required.
A low TSH indicates that
the pituitary gland is being
inhibited by increased
levels of T4 and/or T3 in the
blood, and is therefore a
reliable marker of
hyperthyroidism. Rarely, a
low TSH indicates primary
failure of the pituitary, or
temporary inhibition of the
pituitary due to another
illness (euthyroid sick
syndrome) and so checking
the T4 and T3 is still
clinically useful.
• Measuring specific
antibodies, such as anti-
TSH-receptor antibodies in
Graves' disease, or anti-
thyroid-peroxidase in
Hashimoto's thyroiditis—a
common cause of
HYPOthyroidism—may also
contribute to the diagnosis.
• What is Cushing Cause
Syndroms? Symptoms
- is a hormone * In pituitary Cushing's, a
(endocrine) disorder benign pituitary adenoma -rapid weight gain
caused by high secretes ACTH. This is also -thinning of the skin (which causes
levels of cortisol known as Cushing's disease and
(hypercortisolism) in easy bruising and dryness,
is responsible for 65% of
the blood. This can endogenous Cushing's particularly the hands)
be caused by taking syndrome
glucocorticoid -the growth of fat pads along the
drugs, or by tumors * In adrenal Cushing's, collar bone and on the back of the
that produce cortisol neck
or excess cortisol is produced
adrenocorticotropic by adrenal gland tumors, -excess sweating
hormone (ACTH).[1] hyperplastic adrenal glands,
Cushing's disease or adrenal glands with
refers to one
specific cause, a nodular adrenal hyperplasia
non-cancerous
tumor (adenoma) in tumors outside the normal
the pituitary gland pituitary-adrenal system can
that produces large produce ACTH that affects
amounts of ACTH, the adrenal glands. This
which in turn
elevates cortisol. It final etiology is called
can usually be ectopic or paraneoplastic
cured by surgery. Cushing's syndrome and is
seen in diseases like small
cell lung cancer
• Sign and test
• When Cushing's syndrome is
suspected, either a dexamethasone
suppression test (administration of
dexamethasone and frequent
determination of cortisol and ACTH
level), or a 24-hour urinary
measurement for cortisol offer equal
detection rates.[5] Dexamethasone is a
glucocorticoid and simulates the effects
of cortisol, including negative feedback
on the pituitary gland. When
dexamethasone is administered and a
blood sample is tested, high cortisol
would be indicative of Cushing's
syndrome because there is an ectopic
source of cortisol or ACTH (eg: adrenal
adenoma) that is not inhibited by the
dexamethasone. A novel approach,
recently cleared by the US FDA, is
sampling cortisol in saliva over 24 hours,
which may be equally sensitive, as late
night levels of salivary cortisol are high
in Cushingoid patients. Other pituitary
hormone levels may need to be
ascertained. Performing a physical
examination to determine any visual
field defect may be necessary if a
pituitary lesion is suspected, which may
compress the optic chiasm causing
typical bitemporal hemianopia.
•
When any of these tests are positive,
CT scanning of the adrenal gland and
MRI of the pituitary gland are performed
to detect the presence of any adrenal or
pituitary adenomas or incidentalomas
(the incidental discovery of harmless
lesions). Scintigraphy of the adrenal
gland with iodocholesterol scan is
occasionally necessary. Very rarely,
determining the cortisol levels in various
veins in the body by venous
catheterization, working towards the
pituitary (petrosal sinus sampling) is
necessary.
Treatment
- most patients are effectively treated by
carefully tapering off (and eventually
stopping) the medication that causes the
symptoms.
If an adrenal adenoma is identified it may be
removed by surgery. An ACTH-secreting
corticotrophic pituitary adenoma should be
removed after diagnosis. Regardless of the
adenoma's location, most patients will require
steroid replacement postoperatively at least in
the interim as long-term suppression of
pituitary ACTH and normal adrenal tissue
does not recover immediately. Clearly, if both
adrenals are removed, replacement with
hydrocortisone or prednisolone is imperative.
In those patients not suitable for or unwilling
to undergo surgery, several drugs have been
found to inhibit cortisol synthesis (e.g.
ketoconazole, metyrapone) but they are of
limited efficacy.
Removal of the adrenals in the absence of a
known tumor is occasionally performed to
eliminate the production of excess cortisol. In
some occasions, this removes negative
feedback from a previously occult pituitary
adenoma, which starts growing rapidly and
produces extreme levels of ACTH, leading to
hyperpigmentation. This clinical situation is
known as Nelson's syndrome