Page 553 - Concise Pathology for Exam Preparation ( PDFDrive )
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538 SECTION II Diseases of Organ Systems
• Myxoedema: Hypothyroidism developing in older children or adults characterized by
• Decreased physical and mental activity, fatigue, apathy, mental sluggishness and
depression
• Slow speech and intellectual functions
• Increased weight and cold intolerance
• Reduced cardiac output causing shortness of breath and decreased exercise capacity
• Constipation and decreased sweating
• Oedema, broadening and coarsening of facial features, enlargement of tongue and
deepening of voice
Laboratory Findings
• Increased TSH and decreased T3 and T4
• Low free T4 and high TSH levels are used for screening
Q. Define and classify thyroiditis. Describe the aetiopathogenesis,
clinical features and morphology of the different types of thyroiditis.
Ans. Thyroiditis is inflammation of thyroid gland.
Types
1. Infectious thyroiditis:
• May be acute or chronic
• Infection reaches thyroid by haematogenous route or through direct seeding of the
gland
• Common causative organisms include mycobacteria, fungi and pneumocystis
2. “Other common and clinically significant thyroiditis”, which include
(a) Hashimoto thyroiditis:
Salient features:
• Most common cause of autoimmune thyroiditis
• May occur in children and is the main cause of nonendemic goitre in this age
group.
• Peak incidence between 45 and 65 years; female:male ratio 5 10:1.
• Clusters in families
• Concordance in monozygotic twins is 30–60%.
• Association with HLA-DR3 and -DR5 and increased incidence of SLE, Sjögren
syndrome, pernicious anaemia, Type I DM and rheumatoid arthritis in this
group.
• Patients present with painless enlargement of thyroid. There is insidious onset of
hypothyroidism after a transient phase of Hashitoxicosis (thyrotoxicosis is due to
inflammatory disruption of thyroid follicles leading to the release of thyroid
hormones).
Pathogenesis:
• The genetic susceptibility is linked to polymorphisms in multiple immune regulatory
genes, eg, CTLA 4 and PTPN 22.
• Both cellular and humoral mechanisms are involved.
• Cellular immunity is primarily mediated by a defect in T cells (abnormalities of Tregs
or regulatory T cells; exposure of normally sequestrated thyroid antigens; decreased
number of suppressor T cells; emergence of thyroid-specific helper T cells, all
contributing to autoimmunity).
• Abnormality in Tregs and breakdown of tolerance leading to autoimmunity
(Flowchart 20.3):
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