I, Shivlal Yadav, am deeply grateful to all those who have provided me with
the support and guidance necessary to complete this project on
“Autoimmune Disorder.”
First and foremost, I would like to express my sincere thanks to my Biology
teacher, Mrs Shikha Ma’am , for their invaluable guidance, encouragement,
and insights throughout the course of this project. Their expertise and
constructive feedback have been instrumental in shaping my understanding
of this important topic.
I would also like to thanks to my Principal Mrs. Neelam Shukla for giving us
the opportunity to work on this project.
Additionally, I would like to acknowledge the support of my classmates and
friends who have contributed their ideas and feedback, helping me to refine
my work. Their camaraderie and encouragement have been a great source of
motivation
Shivlal Yadav
XII-A3
Memory-based acquired immunity evolved in higher
vertebrates based on the ability to differentiate foreign
organisms (e.g., pathogens) from selfcells. While we still
do not understand the basis of this, two corollaries of
this ability have to be understood. One, higher
vertebrates can distinguish foreign molecules as well as
foreign organisms.
Most of the experimental immunology deals with this
aspect. Two, sometimes, due to genetic and other
unknown reasons, the body attacks self-cells. This
results in damage to the body and is called “auto-
immune disease/disorder.”
Rheumatoid arthritis which affects many people in
our society is an common auto-immune disease.
Rheumatoid Arthritis (RA) is a chronic autoimmune disorder characterized by
inflammation of the synovial membrane (the lining of the joints), which can lead to
joint damage and deformity. Here are some key aspects of Rheumatoid Arthritis:
1. Autoimmune Nature: In RA, the body's immune system mistakenly attacks its
own tissues, primarily targeting the synovium, the membrane that lines the joints.
This autoimmune response leads to inflammation, swelling, and pain in the affected
joints.
2. Symptoms: Common symptoms of RA include joint pain, stiffness, and swelling,
particularly in the hands, wrists, feet, and knees. The stiffness is often more
pronounced in the morning or after periods of inactivity. RA can also cause fatigue,
fever, and weight loss.
3. Joint Damage: Over time, the persistent inflammation in RA can damage
cartilage, bones, and ligaments within the joint. This can result in joint deformity,
loss of function, and disability.
4. Systemic Effects: While RA primarily affects the joints, it can also have systemic
effects, potentially impacting other organs and systems in the body, such as the
skin, eyes, lungs, heart, and blood vessels.
5. Risk Factors: The exact cause of RA is not fully understood, but a combination of
genetic, environmental, and hormonal factors likely plays a role. Women are more
commonly affected than men, and the risk of RA increases with age.
6. Diagnosis: Diagnosis of RA typically involves a combination of medical history,
physical examination, blood tests (such as rheumatoid factor and anti-cyclic
citrullinated peptide antibodies), and imaging studies (such as X-rays and MRI).
7. Treatment: While there is no cure for RA, treatments aim to reduce
inflammation, alleviate symptoms, slow joint damage, and improve quality of life.
Medications commonly used to manage RA include nonsteroidal anti-inflammatory
drugs (NSAIDs), disease-modifying antirheumatic drugs (DMARDs), corticosteroids,
and biologic agents. Physical therapy, occupational therapy, and lifestyle
modifications can also be beneficial.
“Rheumatoid Arthritis is a complex and potentially debilitating condition that
requires ongoing medical management and support from healthcare professionals.”
Graves' disease is an autoimmune disorder that leads to hyperthyroidism, or
overactivity of the thyroid gland. Here are the key points about Graves' disease:
1. Autoimmune Nature: In Graves' disease, the immune system produces antibodies
known as thyroid-stimulating immunoglobulins (TSIs) that bind to the thyroid-
stimulating hormone (TSH) receptors on the thyroid gland. This stimulates the thyroid
to produce excess thyroid hormones (thyroxine or T4 and triiodothyronine or T3).
2. Symptoms: The overproduction of thyroid hormones leads to a variety of symptoms,
including:
- Rapid heartbeat (tachycardia)
- Weight loss despite normal or increased appetite
- Nervousness and irritability
- Tremors in the hands or fingers
- Increased sensitivity to heat
- Sweating
- Changes in menstrual cycles
- Increased frequency of bowel movements
- Bulging eyes (exophthalmos), a condition specifically associated with Graves'
ophthalmopathy
3. Causes: The exact cause of Graves' disease is unknown, but it involves a
combination of genetic and environmental factors. It is more common in women and
often occurs before the age of 40.
4. Diagnosis: Diagnosis of Graves' disease is based on clinical symptoms, blood tests that
measure levels of thyroid hormones (T3 and T4) and thyroid-stimulating hormone
(TSH), and the presence of TSIs. Imaging studies such as thyroid scans can also be used.
5. Treatment: Treatment options for Graves' disease aim to reduce the production of
thyroid hormones and alleviate symptoms. These include:
- Antithyroid medications (such as methimazole or propylthiouracil) to reduce
thyroid hormone production
- Radioactive iodine therapy to destroy overactive thyroid cells
- Beta-blockers to manage symptoms such as rapid heart rate and tremors
- Surgery (thyroidectomy) to remove part or all of the thyroid gland, typically
reserved for cases where other treatments are not suitable or effective
“Graves' disease is the most common cause of hyperthyroidism and requires careful
management by healthcare professionals to control thyroid hormone levels and manage
symptoms effectively.”
Myasthenia Gravis (MG) is a chronic autoimmune neuromuscular disorder characterized
by weakness and rapid fatigue of voluntary muscles. Here are the key points about
Myasthenia Gravis:
1. Autoimmune Nature: In Myasthenia Gravis, the immune system produces antibodies
that block or destroy many of the muscle receptor sites for acetylcholine, a
neurotransmitter essential for muscle contraction. This interference reduces the
muscle's ability to respond to nerve signals, leading to muscle weakness.
2. Symptoms: The hallmark of MG is muscle weakness that worsens with activity and
improves with rest. Common symptoms include:
- Drooping of one or both eyelids (ptosis)
- Blurred or double vision (diplopia) due to weakness of the muscles that control eye
movements
- Difficulty swallowing (dysphagia)
- Shortness of breath
- Impaired speech (dysarthria)
- Weakness in the arms, hands, fingers, legs, and neck
3. Affected Muscles: MG primarily affects voluntary muscles, particularly those that
control eye and eyelid movement, facial expression, chewing, swallowing, and speaking.
In severe cases, muscles that control breathing and neck and limb movements can also
be involved.
4. Diagnosis: Diagnosis of Myasthenia Gravis involves a combination of clinical evaluation,
antibody blood tests (such as the anti-acetylcholine receptor antibody test),
electrophysiological studies (such as repetitive nerve stimulation and single-fiber
electromyography), and imaging studies to check for thymus abnormalities (like a
thymoma).
5. Treatment: While there is no cure for MG, treatments can help manage symptoms
and improve muscle function. These treatments include:
- Medications that improve communication between nerves and muscles (such as
acetylcholinesterase inhibitors like pyridostigmine)
- Immunosuppressive drugs (such as corticosteroids, azathioprine, or mycophenolate
mofetil) to reduce the immune response
- Surgical removal of the thymus gland (thymectomy), which can reduce symptoms
in some patients, especially those with a thymoma
“Myasthenia Gravis is a serious condition that requires careful and ongoing medical
management to control symptoms and prevent complications.”
