Case Study Analysis: SLE, Glomerulonephritis, and Graves' Disease

This document presents an analysis of two case studies. The first case focuses on Systemic Lupus Erythematosus (SLE), detailing its immunological basis, the significance of antinuclear antibodies, the causes of glomerulonephritis, vasculitis, and skin rash. It categorizes the hypersensitivity reactions involved and explains the mechanism of action of prednisolone in treating the symptoms. Additionally, it discusses the biochemical mechanism of action of aspirin, the macromolecules affected, and potential side effects. The second case study centers on Graves' Disease, examining its immunological basis, the causes of thyrotoxicosis and hyperthyroidism, and the classification of hypersensitivity reactions. It emphasizes the importance of ruling out toxic multinodular goitre and describes the biochemical pathway involved in thyroid hormone synthesis. The analysis incorporates references to support the understanding of the diseases.

Case study -1
1. Explain the immunological basis of her disease condition and the
significance of her elevated levels of antinuclear antibodies (ANA).
The patient is suffering from SLE (Systemic Lupus Erythematosus). It is an
autoimmune disease. It is relapsing, remitting multisystem in nature. The
disease acts against the nucleus of the own cell body and causes inflammation
and organ damage. There is a production of antinuclear antibodies . These
antigens from an antibody –nuclear antigen immune complex. This deposits in
tissues causing inflammation and tissue injury. There is an increase in cell
death and there is a defective clearance of the dead cell material.
There is inappropriate activation of B lymphocytes. T cells in SLE Patients also
show abnormal signalling and secretion of cytokinines , which causes
inflammation.
The disease is characterised by production of self-destructive antibody. These
antibodies target the nucleus . Hence called as an antinuclear antibody. The
levels of these are on a higher side in SLE.
2. Explain as to what caused her glomerular nephritis, vasculitis and bilateral
skin rash.
In SLE the bilateral skin rash occurs due to acute cutaneous lupus. This causes a
rash on the sun exposed area. The bilateral skin rash is the best-known
example of the effect of SLE on skin.
Glomerular nephritis occurs during the flare of the disease. The cell damage is
extensive. Hence it is necessary to keep a check on the routine urine analysis.
Nephritis develops very late.
Vasculitis mainly develops due to complex interplay among the immune cells,
endothelial cells , auto antibodies which are deposited in cell and the immune
complex deposition. All these factors cause vasculitis.
3. How would you categorise the type of hypersensitivity reactions causing the
above disease?

SLE is known as an autoimmune chronic inflammatory condition. It is type III
hypersensitivity response. Patients with SLE have B cells activation with mainly
immature B cells are in dominance.
4. Explain how prednisolone helped to treat the symptoms.
The above-mentioned medicine Prednisolone is a steroid. It prevents the
release of antibodies which deposit in cells to cause inflammation. Hence in
case of SLE, it is utilised to reduce the inflammation. It makes the life of the
patient better.
5. Explain the biochemical mechanism of action of aspirin in its interaction with
cyclooxygenase. Which class of macromolecules are affected by this
interaction (inhibition) and state briefly a major side effect that may develop as
a result of extensive aspirin therapy?
There are two types of cyclooxygenase. COX-1 and COX-2. Aspirin works on
both of them. These COX produce prostaglandins which act as pro-
inflammatory. Aspirin acts on COX-2 and modifies it to produce lipoxins. This
acts as anti-inflammatory.
4-benzenesulfonamide 5 is the macromolecule involved in this interaction
Aspirin has many common and rare side effects. The common side effects
include excessive acid secretion from stomach, nausea, stomach cramps. Due
to extensive use of aspirin, there can be symptoms like rupture of stomach
walls, bleeding intestine walls, decrease blood platelets, brain haemorrhage,
seizures etc.
Case study -2
1. Discuss the immunological basis of the disease.
Graves Disease is an autoimmune disorder which is characterised by the
infiltration of immune effectors cells and thyroid antigen-specific T cells into
the thyroid stimulating hormone receptor in the tissues. Example- orbits
causing exophthalmos. Also, the antibodies produced activate thyroid

stimulating hormone receptor leading to overproduction of thyroid. It also
causes thyroid hyperplasia.
2. What is the cause of thyrotoxicosis and hyperthyroidism?
Graves Disease is the most common cause of thyrotoxicosis. Graves Disease is
autoimmune in nature. Due to this antibodies are produced which stimulate
the thyroid gland to produce excessive of thyroid hormone causing
thyrotoxicosis . Hyperthyroidism is also caused due to the same factor.
3. How would you categorise the hypersensitivity reactions causing the
disease?
It is a type II hypersensitivity reaction . In this, the antibodies produced as a
result of person’s immune system response to bind to own antigen on the own
cell surface. This causes a B cell response.
4. Discuss the significance of ruling out toxic multinodular goitre in arriving at a
differential diagnosis.
Toxic nodular goitre is mainly caused by iodine deficiency. Once its presence is
ruled out , we can be convinced that patient does not have an iodine
deficiency. In multinodular goitre the T4 is low. In our case T4 is high. Hence
once toxic multinodular goitre is ruled out and we were able to reach a
differential diagnosis.
5. Describe the biochemical pathway or steps involved in the synthesis of
thyroid hormone.
Biochemical pathway in synthesis of thyroid hormone
Iodine Transport-Iodide is actively transported from the blood. It reaches the
follicular lumen.
Thyroglobulin synthesis- This is a protein which has a large number of tyrosine
amino acids. This goes on to become individual thyroid molecules. Then
thyroglobulin after getting synthesised in follicular epithelium cell is then
secreted into follicular lumen.
Thyroid Peroxidase-It first generated I2 by oxidising I- . Then the I2 is
organised. Singly and doubly bond iodinated species of tyrosine is formed.

These are Monoiodotyrosine( MIT) and Diiodotyrosine(DIT). Then Thyroid
Peroxidase combines with MIT and DIT which reduces to generate T3 AND T4.
T3 and T4 are transported in circulation.
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