Autoimmune disorders of pituitary gland

1. DEPARTMENT OF ZOOLOGY
Dr.Harisingh Gour University Sagar
(A central University)

2. Autoimmune disorders of
pituitary gland
Submitted to
Dr.Payal
Mahobia
Asst.Prof.
Department of
zoology
Submitted by
Lekhan singh
lodhi

4. Autoimmune disorders of pituitary
gland
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Autoimmune diseases are patho-physiological states that result from a
loss of self-tolerance and the consequent immune destruction of host
tissues.
Autoimmunity is mediated by a variety of molecular and cellular events,
and responses. The development of an autoimmune disease is a very
complex process in which recognition of self-antigens by lymphocytes is
centrally involved in pathologic organ damage.
Autoimmune disease are defined as diseases in which immune responses
to specific self-antigens contribute to the ongoing tissue damage that
occurs in that disease

6. Autoimmune disorders of pituitary
gland
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Autoimmune diseases may be either tissue-specific (e.g., thyroid, β-
cells of the pancreas), where unique tissue-specific antigens are
targeted, or may be more systemic, in which multiple tissues are
affected, and a variety of apparently ubiquitously expressed
autoantigens are target.
Autoimmunity is not set off by a single cause and is triggered by a
variety of agents and molecular and cellular pathways and events.
Several elements and mechanisms underlying autoimmune responses
have been identified.
However, even if a given AD were to be initiated primarily by a single
trigger, other events and regulating mechanisms come into play,
thereby adding complexity to the process.

8. Examples of selected human autoimmune diseases.

9. Mechanism Underlying Autoimmune
Disorders
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The vast majority of AD stem from abnormalities in the mechanisms of
peripheral tolerance that fine-tune the repertoires of mature T and B
peripheral lymphocytes.
The mere presence of autoreactive lymphocytes in an individual’s
repertoire is not enough to trigger AD: it only predisposes that individual
to developing AD. For AD to develop, a stimulus that activates the
autoreactive cells must be present, and mechanisms designed to
regulate autoreactive lymphocyte responses must fail.
We will now discuss several mechanisms, some of which remain
controversial, that are believed to contribute to the development of AD
in susceptible individuals.

10. Fig. Mechanisms of autoimmunity.
-Release of Sequestered Antigens
-Molecular mimicry

11. Hashimoto's thyroiditis disease
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Hashimoto's thyroiditis disease : Sometimes the production of thyroxine
hormone is very less in thyroid gland.
The drug use to cure this disease sometimes act as antigens like
substances.
Therefore to counter this,antibodies are formed in the body ,which along
with toxic substances also destroy the thyroid gland,thus it is also know as
autoimmune disease on suicide of thyroid gland.
It was first described by the Japanese physician Hakaru Hashimoto in
1912.

12. Signs and symptoms of Hashimoto's
thyroiditis
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The most common symptoms include the following: fatigue, weight
gain, pale or puffy face, feeling cold, joint and muscle pain, constipation,
dry and thinning hair, heavy menstrual flow or irregular periods,
depression, panic disorder, a slowed heart rate, and problems getting
pregnant and maintaining pregnancy.
Hashimoto’s disease is about seven times more common in women
than in men.
Physiologically, antibodies against thyroid peroxidase (TPO) (also called
TPOAb) and/or thyroglobulin cause gradual destruction of follicles in the
thyroid gland. Accordingly, the disease can be detected clinically by
looking for these antibodies in the blood. It is also characterized by
invasion of the thyroid tissue by leukocytes, mainly T-lymphocytes.

13. The thyroid of someone with Hashimoto's thyroiditis as seen with a microscope at low
magnifiaton
-Histological seen as secondary lymphoid follicles (germinal centers, not to be confused with
the normally present colloid-filled follicles that constitute the thyroid). Atrophy of the colloid
bodies is lined by Hurtle cells, cells with intensely eosinophilic, granular cytoplasm, a
metaplasia from the normal cuboidal cells that constitute the lining of the thyroid follicles.

14. Pathophysiology
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Various auto-antibodies may be present against thyroid peroxidase,
thyroglobulin and TSH receptors, although a small percentage of
patients may have none of these antibodies present.
antibody-dependent cell-mediated cytotoxicity is a substantial factor
behind the apoptotic fall-out of Hashimoto's thyroiditis. Activation of
cytotoxic T-lymphocytes (CD8+ T-cells) in response to cell-mediated
immune response affected by helper T-lymphocytes (CD4+ T-cells) is
central to thyrocyte destruction.
As is characteristic of type IV hypersensitivities, recruitment of
macrophages is another effect of the helper T-lymphocyte activation,
with Th1 axis lymphocytes producing inflammatory cytokines within
thyroid tissue to further macrophage activation and migration into the
thyroid gland for direct effect.

15. Diagnosis
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Diagnosis is usually made by detecting elevated levels of anti-thyroid
peroxidase antibodies (TPOAb) in the serum, but seronegative (without
circulating autoantibodies) thyroiditis is also possible.
Given the relatively non-specific symptoms of initial hypothyroidism,
Hashimoto's thyroiditis is often misdiagnosed as depression,
cyclothymia, PMS, chronic fatigue syndrome, fibromyalgia and, less
frequently, as erectile dysfunction or an anxiety disorder.
On gross examination, there is often presentation of a hard goitre that
is not painful to the touch;
other symptoms seen with hypothyroidism, such as periorbital
myxedema, depend on the current state of progression of the response,
especially given the usually gradual development of clinically relevant
hypothyroidism.

16. Treatment
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Managing hormone levels
Hypothyroidism caused by Hashimoto's thyroiditis is treated with thyroid
hormone replacement agents such as levothyroxine, triiodothyronine or
desiccated thyroid extract.
A tablet taken once a day generally keeps the thyroid hormone levels
normal.
In most cases, the treatment needs to be taken for the rest of the patient's
life.
In the event that hypothyroidism is caused by Hashimoto's thyroiditis, it is
recommended that the TSH levels be kept under 3.0.

17. Addison’s disease
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Addison’s disease, the common term for primary adrenal insufficiency,
occurs when the adrenal glands are damaged and cannot produce enough
of the adrenal hormone cortisol.
The adrenal hormone aldosterone may also be lacking.
Adrenal hormones, such as cortisol and aldosterone, play key roles in the
functioning of the human body, such as regulating blood pressure;
metabolism, the way the body uses digested food for energy; and the
body’s response to stress.
In addition, the body uses the adrenal hormone dehydroepiandrosterone
(DHEA) to make androgens and estrogens, the male and female sex
hormones.

19. Signs and symptoms
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The signs and symptoms include
fatigue; lightheadedness upon standing or difficulty standing
, muscle weakness, fever, weight loss, anxiety, nausea, vomiting, diarrhea,
headache, sweating, changes in mood or personality, and joint and muscle
pains.
Some patients have cravings for salt or salty foods due to the loss of
sodium through their urine.
Hyperpigmentation of the skin may be seen, particularly when the patient
lives in a sunny area, as well as darkening of the palmar crease, sites of
friction, recent scars, the vermilion border of the lips, and genital skin.
Low blood pressure with or without orthostatic hypotension (blood
pressure that decreases with standing)
Characteristic symptoms are:Hypoglycemia,Confusion, psychosis, slurred
speech,Hypercalcemia,

20. Fig.-Classic darkening of the skin due to increased pigment as seen
in Addison's disease

21. Causes
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Causes of adrenal insufficiency can be categorized by the mechanism
through which they cause the adrenal glands to produce insufficient cortisol.
These are adrenal dysgenesis (the gland has not formed adequately during
development), impaired steroidogenesis (the gland is present but is
biochemically unable to produce cortisol) or adrenal destruction (disease
processes leading to glandular damage).
Adrenal destruction Autoimmune adrenalitis is the most common cause of
Addison's disease in the industrialized world. Autoimmune destruction of
the adrenal cortex is caused by an immune reaction against the enzyme 21-
hydroxylase (a phenomenon first described in 1992).
impaired steroidogenesis To form cortisol, the adrenal gland requires
cholesterol, which is then converted biochemically into steroid hormones.
Interruptions in the delivery of cholesterol include Smith-Lemli-Opitz
syndrome and abetalipoproteinemia.

22. Diagnosis
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Addison's disease is generally diagnosed by blood tests, urine tests, and
medical imaging.
In suspected cases of Addison's disease, demonstration of low adrenal
hormone levels even after appropriate stimulation (called the ACTH
stimulation test) with synthetic pituitary ACTH hormone tetracosactide is
needed for the diagnosis.
Other tests may be performed to distinguish between various causes of
hypoadrenalism, including renin and adrenocorticotropic hormone levels, as
well as medical imaging - usually in the form of ultrasound, computed
tomography or magnetic resonance imaging.

23. Treatment
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Adrenal insufficiency is treated by replacing, or substituting, the hormones
that the adrenal glands are not making. The dose of each medication is
adjusted to meet the needs of the patient.
Cortisol is replaced with a corticosteroid, such as hydrocortisone,
prednisone, or dexamethasone, taken orally one to three times each day,
depending on which medication is chosen.
f aldosterone is also deficient, it is replaced with oral doses of a
mineralocorticoid hormone, called fludrocortisone acetate (Florinef), taken
once or twice daily.
During adrenal crisis, low blood pressure, low blood glucose, low blood
sodium, and high blood levels of potassium can be life threatening.
Standard therapy involves immediate IV injections of corticosteroids and
large volumes of IV saline solution with dextrose, a type of sugar. This
treatment usually brings rapid improvement.

24. THANK YOU