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See Lawsons & the RCPA manual

  • Thyroid - diffuse enlargement 'goitre'
    • Nodular enlargement
  • Immune e.g. hashimoto's thyroiditis, Graves
  • Inflammatory - thyroiditis
  • Tumours
    • Malignant: papillary, medullary, follicular
    • Benign: follicular adenoma with no vascular involvement
  • Hyperthyroidism symptoms
    • Muscle wasting
    • Fine hair
    • Exophthalmus
    • Goiter
    • Sweating
    • Tachycardia, high output failure
    • Weight loss
    • Oligomenorrhea
    • Tremor
  • Look for: lid retraction (due to levator palpebrae superioris); warm, flushed (increased bloodflow, peripheral vasodilation), sweaty palms
    • Lid retraction = sympathomimetic effects of thyroxine = most typically seen in hyperthyroidism (any cause), because there are many causes of hyperthyroidism, and Graves is only one of them. (E.g. tumour of pituitary, secondary hyperthyroidism, thyroxine tablets)
  • Tremor, chorea, myopathy
  • Increased rate of osteoporosis
  • Bruit over thyroid occurs in hyperthyroidism

Both cases:

  • Family history - autoimmune diseases go in families
  • Medications - can cause hyper/hypothyroidism. Include naturopathy. Some people buy thyroid hormone to try to lose weight.

Case one

  • Think about anxiety
  • Investigations
    • Thyroid tests: TSH is the first of the hormones to become elevated (inverse logarithmic relationship between TSH and T3/T4)
    • Antithyroid antibodies; TSHR-Ab in Graves
    • Lump: ultrasound, then FNAB and biopsy
  • Treatment - start with medications first, then try surgery
  • Normal thyroid histo
    • Follicular arrangement
    • Colloid filled spaces surrounded by epithelial cells = a follicle
    • Epithelial cells are cuboidal
    • Colloid is pink
    • Parafollicular (C) cells and fine CT are between follicles
    • This is an endocrine gland, so there are lots of blood vessels
    • Thyroid gland is surrounded by a fine CT capsule
  • Abnormal slide
    • Section shows thyroid tissue
    • Architecture - abnormal; not many visible colloid spaces; reduced colloid content
    • The follicles are irregular in size and shape.
    • Follicular cells are larger, chromatin in nuclei is opened, nuclei are bigger, cytoplasm is bigger. Cells look more active.
    • Some of the cells are now columnar
    • Cells are heaped up in some areas - the architecture is "papillary"
    • TSHR-Abs are causing cells to be whipped to work (antibodies drive the process; it's not real TSH). Thyroid stimulating immunoglobulin
    • Scalloped edges to follicle because follicles are gobbling up the colloid to secrete it very rapidly
    • This is hyperplasia
    • Lymphocytes in thyroid
    • Hyperaemia - increased blood supply to thyroid - lots of little blood vessels
      • Therefore bruits
  • Neoplasia of thyroid gland - rely on whether it goes through the capsule of the gland (because the cells look benign)

Case two

  • Think about depression
  • Talks very slowly with hypothyroidism
  • Goitre assessment: From behind, press hard, and then get her to drink water - thyroid gland goes up and down
  • Hashimoto's - autoimmune that destroys the thyroid tissue
    • TSH elevated therefore
  • TSH is pushing thyroid, but it's not responding
  • Section
    • Lymphocyte clusters with germinal centres - lymphoid follicles (tertiary lymphoid tissue)
    • This is an autoimmune disease where the immune system reacts against thyroid antigens on thyroid itself. Damage --> depletion of thyroid tissue.
    • The lymphoid tissue is making antibodies
    • CD8+ T cells are attacking the gland
  • Cytologic change in
    • Larger cells
    • Pink, plump, granular
      • Hurthle cells: because of accumulation of mitochondria in the cytoplasm
    • Colloid lake - large amount of colloid, pulled away from edges
    • Increase in CT, a lot of collagen laid down in gland
    • Chronic inflammation has simultaneous injury and repair/fibrosis. Gland can end up becoming a useless scar.

Case three

  • Lymph node: capsule, subcapsular sinus, cortex (lymphocytes: B in follicle, and T are between the follicles), medulla (plasma cells, macrophages)
  • Causes of lymphadenopathy
    • Antigen stimulation (reactive hyperplasia) - HIV, hep B, IE, SLE
    • Inflammation (lymphadenitis - infection of the lymph node) - e.g. TB
    • Metastatic
    • Primary - lymphomas (Hodgkin or non Hodgkin)
  • Examination
    • Warm, tender, mobile - infection
    • Fixed, stone hard - malignancy with invasion; desmoplasia
    • Rubbery LN - Hodgkin
  • Put specimens in formalin normally, but not lymph nodes.
    • Would kill bacteria
    • Needs to come up fresh and fast
    • Lymph tissue is triaged, a sample is taken for MCS, and take samples for cytogenetics, flow cytometry
  • Patterns: follicular, interfollicular, sinusoidal, mixed, necrotising, granulomatous
    • follicular
    • interfollicular - viral infections, vaccinations
    • sinusoids - surgical drainage, macroscopic debris etc
    • granuloma - sarcoidosis, TB
    • See AEB/Lectures/Lymphadenopathy
  • Slide - we see secondary lymphoid follicles. Prominent follicular hyperplasia. Prominent follicular sinuses. Loss of cortical architecture.
    • his slide

shows reactive lymphadenopathy with increased macrophages (histiocytes) within medullary sinuses. There are three general causes of lymphadenopathy (and note that lymph node disease always needs histological proof). o Antigenic stimulation causing reactive lymphadenopathy and follicular hyperplasia (often due to bacterial infection). o Lymphadenitis due to infection. It can be localised or generalised.  Local: often indicates a bacterial cause like extrapulmonary TB.  Systemic: may also indicate infection but also autoimmunity. o Tumours, either metastases or primary tumours (lymphomas).

Case four

  • Travel history, sexual history
  • Need to elicit more from her history, such as sputum production, coughing, weight loss, contacts, anyone else who has had it, what she has been doing and sexual history.
    • Profession e.g. needle stick injury
    • rheumatoid arthritis? joint disease?
    • feel the liver - hepatitis? look for jaundice too
  • Characterise the lymphadenopathy: is it generalised or local, their texture and any hint of splenomegaly.
  • Investigations include: FBC (looking at WCs and their appearance), blood microscopy/blood film, CXR, blood culture, serology (EBV, CMV, HIV), FNAB (but more useful in metastatic disease), excisional biopsy (gold standard, but always requires fresh tissue) where they can process it through flow cytometry to look for WCCs. LFTs and UEC if concerned about hepatitis. Mantoux test.
  • FNAB/excision biopsy to see cytology and histology.
  • Send lymph node
  • Lymphomas refer to the malignant proliferation of lymphocytes which accumulate in lymph nodes, causing lymphadenopathy. They are most common in young adults and the elderly (bimodal distribution), with a M:F ratio of 2:1.
  • Specimen four (nodular sclerosing Hodgkin’s lymphoma): This is the most common type of Hodgkin’s lymphoma, characterised by its grossly abnormal size, connective tissue between nodules, background lymphocytes, Reed-Sternberg cells (which have pale cytoplasm, are binucleated, have eosinophilic nucleoli, and some of which look like lacunar cells).
    • Low power: thick collagen bands separating the whole organ into LARGE nodules
    • High power: not follicles, just SMALL nodules of cells have Reed Sternberg cells (large) with big red nucleoli
      • Owl-eyes: mirror-image nuclei (2 nuclei next to each other)
      • The RS cells sit in a little space called a lacune
    • This is not a follicular appearance, because there aren't real follicles, they're nodules
    • Thickened capsules
    • Lymphocytes, eosinophils, neutrophils
    • Dark squished cells = mummified cells. Other variants are popcorn cells and lacunar cells. = Reed Sternberg cells
    • Lymphoma is a primary malignancy of a lymph node
  • Nodular sclerosing is the commonest type (esp. in young people). Has a good prognosis.
  • Prognosis depends on lymphoma staging (Ann-Arbor staging).
    • I: Single group of lymph nodes affected.
    • II: Two separate chains, but on the same side of the diaphragm.
      • IIa: no constitutional symptoms; IIb: constitutional symptoms.
    • III: Two or more separate chains but on different sides of the diaphragm.
    • IV: Outside lymphatic tissue. e.g. spleen, other organs
  • Also will be useful to do a whole body CT and PET scan.
  • Read wikipedia: Ann-Arbor staging
  • need a whole lymph node to diagnose lymphoma because you need architecture

Case

  • 47 year old male with 9 week history of worsening lethargy and 5kg of weight loss. On examination, he was pale, there were a few bruises on his arms and legs. He had hepatosplenomegaly and generalised lymphadenopathy (bad generalised disease). His FBC revealed low Hb, low RCC, decreased PCV, low platelets (thrombocytopenia) and an increased ESR.
    • Possibly abnormal bone marrow - something is replacing his bone marrow. We get a sample of soft tissue from the presacral area (it's pushing out of bone marrow)
    • Pancytopenia correlates with bruising history
  • This is a type of non-Hodgkin's lymphoma. Based on lineage (B or T cells) - then follicular, nonfollicular or diffuse, then we go into the lineage in detail (based on how differentiated the cells are).
  • A bone marrow aspirate and trephine biopsy showed infilitration of the marrow by diffuse large B-cell lymphoma (a high grade NHL). This was confirmed by excision biopsy of a pre- sacral mass. Histology shows, via immunohistochemistry (immunoperoxidase) for the CD20 cell surface marker (present on B lymphocytes). The patient was treated with chemotherapy but the patient died after relapsing into a coma.
  • Specimen five (diffuse large B-cell lymphoma): This slide shows a soft tissue mass showing abnormal B cells infilitrating the lymph node but not forming its normal architectural features. These cells show the cytological features of malignancy, including mitotic figures, high N:C ratio, prominent nucleoli and chromatin, hyperchromasia.
    • It's a dog's breakfast - poorly differentiated tumour, hard to tell what it is. Rely on other tests to help us = immunoperoxidase test: add a colour tag for surface antigens. The antibodies will tag the cell and make it coloured. Normally do a large panel (for not only lymphomas, but also carcinomas etc). Tissue to flow cytometry tells us the breakdown of cell percentage in different types. Also do cytogenetics for lineage etc.

Look at images of disease

  • 2 cases:
    • Hodgkin lymphoma: enlargement of lymph nodes, contiguous pattern, no extranodal
    • Non Hodgkin Lymphoma: Mass of tissue engulfing a kidney - a lot of extracapsular stuff