in how many flash card cloze format you need to cover  this lecture . answer in number .
the lecture :
Graves' Disease
Clinical Triad:
Hyperthyroidism with diffuse gland enlargement.
Infiltrative ophthalmopathy (exophthalmos).
Localized dermopathy (pretibial myxedema, seen in a minority of patients).
Pathogenesis:
Autoimmune disorder where antibodies stimulate the TSH receptor.
The most important antibody is Thyroid Stimulating Immunoglobulin (TSI).
Genetic factors are significant (30–40% concordance in identical twins).
Ophthalmopathy (Exophthalmos):
Caused by:
Infiltration of T cells in the retro-orbital space.
Swelling of extraocular muscles.
Accumulation of glycosaminoglycans (e.g., hyaluronic acid).
Increased fat cells.
Morphology:
Thyroid gland: Enlarged due to hyperplasia of follicular epithelial cells.
Follicular epithelium: Crowded, forming small papillae.
Colloid: Pale with scalloped margins.
Lymphoid infiltrates: Predominantly T cells with germinal centers.
Types of Thyroiditis
1. Acute Thyroiditis
Bacterial infection (e.g., Staphylococcus, Streptococcus).
Radiation injury.
2. Subacute Thyroiditis
Granulomatous (de Quervain): Viral origin, associated with infections like coxsackievirus, mumps, etc.
Subacute Lymphocytic: Often postpartum; presents with mild hyperthyroidism.
3. Chronic Thyroiditis
Hashimoto’s Thyroiditis: Autoimmune destruction leading to hypothyroidism.
Riedel’s Thyroiditis: Rare, marked by fibrosis.
Hashimoto Thyroiditis
Most common cause of hypothyroidism in iodine-sufficient areas.
Age: Typically 45-65 years, with a female predominance (10:1 to 20:1).
Autoantibodies: Target thyroglobulin and thyroid peroxidase.
Pathogenesis:
Breakdown in self-tolerance to thyroid antigens.
Cell death by:
CD8+ T cells (cytotoxic T-cell-mediated cell death).
Cytokines (e.g., IFN-γ).
Antibody-dependent cytotoxicity.
Morphology:
Thyroid: Diffusely enlarged with intact capsule.
Parenchyma: Dense lymphocytic infiltrate with germinal centers.
Hürthle cells: Present, indicating metaplasia in response to injury.
Subacute (Painless) Lymphocytic Thyroiditis
Clinical presentation: Mild hyperthyroidism, sometimes with goitrous enlargement.
Morphology: Lymphocytic infiltrates with germinal centers, without fibrosis or Hürthle cell metaplasia (unlike Hashimoto's).
Granulomatous (De Quervain) Thyroiditis
Triggered by viral infections and has a seasonal incidence (peaking in summer).
Clinical features: Painful enlargement of the thyroid, often after a respiratory infection.
Histology: Patchy inflammation with giant cells surrounding disrupted follicles.
Hypothyroidism
Causes:
Primary Hypothyroidism:

Genetic defects (e.g., PAX8, FOXE1, TSH receptor mutations).
Postablative (e.g., surgery, radiation).
Autoimmune (Hashimoto’s).
Iodine deficiency.
Drug-induced (e.g., lithium).
Congenital biosynthetic defect (dyshormonogenetic goiter).
Secondary (Central) Hypothyroidism:

Pituitary or hypothalamic failure.
Cretinism
Hypothyroidism in infants or children.
Causes:
Developmental anomalies (e.g., thyroid agenesis).
Genetic defects in hormone synthesis.
Endemic iodine deficiency.
Fetal exposure to antithyroid drugs.
Clinical Features:
Severe mental retardation.
Short stature, coarse facial features, protruding tongue, and umbilical hernia.
Myxedema
Hypothyroidism in older children or adults.
Causes:
Ablation of the thyroid.
Autoimmune thyroiditis.
Goiter (endemic or sporadic).
Hypothalamic-pituitary lesions.
Prolonged antithyroid drug use.
Thyroid cancer.
Mild developmental anomalies.