6. ADISSONS DISEASE
DEFINITION:
Inadequate secretion of ATCH
from pitutary gland results
adrenal in sufficiency . Primary
adrenal insufficiency results
from idiopathic atropy or
destruction of adrenal glands
by autoimmune process.
7. ETIOLOGY AND RISK FACTORS
• Tuberculosis (TB) :TB is an infection which
usually affects the lungs. In some cases the
infection can spread to, and gradually
destroy, the adrenals
• Other infections can sometimes affect
both adrenals.
• Cancers of other parts of the body can
spread and destroy the adrenals.
• Rare hereditary conditions.
• adrenalectomy
• Auto immune diseases: auto-immune
diseases the immune system makes
antibodies against part or parts of the
body. In auto-immune Addison's disease,
you make antibodies which attach to cells
in the adrenal cortex
8. CLINICAL MANIFESTATION
• General weakness and becoming easily tired.
• Darkened areas of skin ('pigmentation').
• Blood pressure is low and falls further when
you stand which can make you dizzy.
• Being off your food and weight loss.
• Feeling sick and vomiting from time to time.
• Abdominal pains which may come and go.
• Diarrhoea or constipation which may come and
go.
• Cramps and pains in muscles.
• Craving for salt, or salty foods and drinks.
• Menstrual periods in women may become
irregular, or stop.
10. TREATMENT
• Cortisol replacement
• You need steroid medication to replace the cortisol
which you no longer make. This is usually with a
medicine called hydrocortisone which is very similar to
cortisol. The amount is usually about 15-25 mg each
day. Some people need more than this, and others less.
The daily amount is broken up into two or three doses
each day with a higher dose taken in the morning than
in the evening. For example, you may be advised to
take 15 mg in the morning and 10 mg early evening.
11. • Replacing aldosterone
Fludrocortisone is a substitute medicine for
aldosterone. This helps to regulate blood
pressure and blood salt level. You may also be
advised to take extra salt each day.
• Addisonian crisis
• This is a medical emergency. You will be given
hydrocortisone injections, a 'drip' of fluid to bring
up your blood pressure, and may need intensive
care until the crisis is over. then need to continue
taking hydrocortisone medication
12. CUSHING SYNDROME
• DEFINITION:. Cushing's syndrome develops
when the level of a glucocorticoid in your
body is too high over a long period of time.
Too much glucocorticoid can occur from an
exogenous or endogenous source
13. ETIOLOGY
• Adrenal hyperplasia - which means there is
increased number and growth of the cells in
the adrenal glands. These cells then make too
much cortisol. There are various different
types of adrenal hyperplasia.
• A benign (noncancerous) tumour of an
adrenal gland.
• A malignant (cancerous) tumour of an adrenal
gland
14. SIGNS AND SYMPTOMS
• Obesity -
• Facial puffiness, and the face often looks redder
than usual.
• Diabetes.
• Facial hair in women.
• High blood pressure.
• Muscle weakness.
• Thin skin which bruises easily.
• Purple/pink stretch marks
• Tiredness.
• Aches and pains - particularly backache.
• Mood swings - such as being more irritable,
depressed, or anxious than usual.
• Lack of sex drive (libido).
• Periods may become irregular, or stop, in
women.
• Osteoporosis . You may fracture a bone more
easily than usual.
• Oedema around the ankles.
16. TREATMENT
• Radiotherapy to the pituitary gland can destroy the pituitary
adenoma. This has a good chance of success, but may take months
or years to take effect. Medication (see below) may be needed until
the radiation treatment takes effect. Also, the radiotherapy may
damage the normal pituitary cells, and may cause low levels of
other hormones made by the pituitary gland. However,
replacement hormone therapy can usually be taken if this occurs.
• Surgery to remove both adrenal glands is an option. This stops your
body making any cortisol (and other hormones) from your adrenal
glands. You will need lifelong replacement therapy of certain
hormones. However, the adenoma will remain in the pituitary and
continue to produce high levels of ACTH which can cause problems
in some cases.
• Medication to block the production or effects of cortisol may work.
There are several medicines which can be tried with various levels
of success.
19. DIAGNOSTIC TESTS
• Abdominal CT scan
• Adrenal biopsy
• Catecholamines blood test
• Glucose test
• Metanephrine blood test
• MIBG scintiscan
• MRI of abdomen
• Urine catecholamines
20. TREATMENT
• Treatment involves removing the tumor with surgery. It
is important to stabilize blood pressure and pulse with
medication before surgery. close monitoring of vital
signs.
• After surgery, it is necessary to continually monitor all
vital signs in an intensive care unit. When the tumor
cannot be surgically removed, medication is needed to
manage it. This usually requires a combination of
medications to control the effects of the excessive
hormones. Radiation therapy and chemotherapy have
not been effective in curing this kind of tumor.
21. NURSING MANAGEMENT
• Risk for injury related to weakness
• Risk for infection related to altered protein
metabolism
• Self care deficit related to fatigue and muscle
wasting
• Altered body image related to tunical obesity
22. Corticotropin-Releasing Factor Test in Normal Subjects and
Patients with Hypothalamic-Pituitary-Adrenal Disorders*
• Corticotropin-releasing factor (CRF) tests were performed in normal subjects and
patients with hypothalamicpituitary-adrenal disorders. In normal subjects, after iv
administation of 500 μg synthetic ovine CRF, plasma ACTH rose significantly to
approximately 3.6 times the basal level at 30–60 min and cortisol reached a peak
of 2.3 times the basal level at 60–90 min, whereas aldosterone peaked at 1.6 times
the basal level at 60 min. Injection of 100 μg CRF in normal subjects also caused a
significant increase in plasma ACTH and cortisol levels but only a slight increase in
aldosterone. However, the total hormone released and their peak levels were
lower than those elicited by the 500-μg dosage. In patients with Cushing’s disease,
although the basal and peak levels of plasma ACTH and cortisol induced by
administration of CRF were variable, the ratios of increase for the two hormones
elicited by CRF were lower than those in normal subjects, especially for cortisol. In
patients with Cushing’s syndrome due to an adrenal adenoma, basal levels of
ACTH were markedly suppressed and plasma ACTH and cortisol did not rise after
CRF. In patients with isolated ACTH deficiency or Sheehan’s syndrome the basal
level of plasma ACTH was less than 5 pg/ml and no change in plasma ACTH
occurred after injection of CRF. In patients with Nelson’s syndrome or Addison’s
disease the basal levels of ACTH were extremely elevated but infusion of CRF
increased plasma ACTH to even higher levels.
