Spleen and Thymus Pathology
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Direct answer
The spleen filters and immunologically surveys blood, so it enlarges by congestion (portal hypertension), work hypertrophy (haemolysis), infiltration (leukaemia, lymphoma, storage disease) or infection — and in India the tropical causes, malaria, visceral leishmaniasis and hyperreactive malarial splenomegaly, sit beside the universal ones. Its removal or functional loss trades cytopenias for infection risk with encapsulated organisms, which is why vaccination precedes splenectomy. The thymus educates T lymphocytes and gives up thymoma — an epithelial neoplasm crowded with immature T cells — whose clinical fame rests on its myasthenia gravis association and whose behaviour is defined by capsular invasion rather than cellular atypia.
What you must remember
- Indian big-spleen causes: malaria (including hyperreactive malarial splenomegaly), visceral leishmaniasis (kala-azar), portal hypertension, chronic myeloid leukaemia and myelofibrosis, haemolytic anaemia and lymphoma.
- Hypersplenism quartet: splenomegaly, pancytopenia, hypercellular marrow, and correction after splenectomy — all four needed for the term.
- Hyposplenism markers: Howell-Jolly bodies and target cells on the smear (sickle cell autosplenectomy, coeliac disease, post-splenectomy).
- Overwhelming post-splenectomy infection (OPSI): encapsulated organisms — pneumococcus, Haemophilus influenzae type b, meningococcus; vaccinate before elective splenectomy and counsel about fever.
- Splenic emergencies: delayed rupture after blunt trauma (Kehr's sign — left shoulder tip pain) and wedge infarcts in haemoglobinopathies and endocarditis.
- Thymoma essentials: WHO types A, AB, B1-B3 based on epithelial cell shape and lymphocyte ratio; behaviour follows Masaoka staging of capsular and adjacent-structure invasion.
- Myasthenia link: roughly a third of thymoma patients develop myasthenia gravis, and about 10-15 per cent of myasthenia patients harbour a thymoma — the percentages FMGE expects.
Massive splenomegaly in an Indian clinic
A 30-year-old from an endemic district reports three months of low-grade fever, weight loss and a spleen descending 12 centimetres below the costal margin with mild pancytopenia. The differential runs in a fixed order: malaria parasites on smear (or antigen test), rK39 serology for visceral leishmaniasis with marrow evidence of LD bodies, then a blood picture for chronic myeloid leukaemia — huge spleen with leucocytosis and basophilia — and myelofibrosis with a dry tap and teardrop cells. Each step is cheap and sequential, and treatment diverges completely: antimalarials, liposomal amphotericin or miltefosine, a tyrosine kinase inhibitor, or supportive transplant planning. The teaching point is that in this geography the infection usually wins the argument, but you never announce kala-azar without looking at the marrow or the serology that proves it.
Where students slip
Candidates call any enlarged spleen with low counts "hypersplenism", forgetting the quartet demands hypercellular marrow and correctability — a marrow aspirate belongs in the workup. The OPSI question usually fails on timing: vaccines are given before elective splenectomy (pneumococcal, Hib, meningococcal, plus influenza annually), not after emergency removal. In thymoma questions, students grade malignancy by histology; in reality B-type thymomas look bland yet recur by local invasion, so Masaoka stage — capsular integrity first — is what predicts outcome, a distinction examiners probe directly.
Frequently asked questions
What are the four criteria for hypersplenism?
Splenomegaly, peripheral cytopenias, a hypercellular marrow, and restoration of blood counts after splenectomy.
Which organisms cause OPSI?
Encapsulated bacteria — Streptococcus pneumoniae above all, plus Haemophilus influenzae type b and Neisseria meningitidis — hence vaccination before splenectomy.
What do Howell-Jolly bodies indicate?
Functional hyposplenism or asplenia, as in sickle cell autosplenectomy or surgical removal, with consequent infection vulnerability.
What is the relationship between thymoma and myasthenia gravis?
Roughly a third of thymoma patients develop myasthenia, and about 10-15 per cent of myasthenia patients have a thymoma; thymic follicular hyperplasia accounts for many of the rest.
What governs prognosis in thymoma?
Masaoka staging of capsular and mediastinal invasion, more than the WHO histological subtype.