Pathology of Lymph Nodes and Spleen Flashcards

1
Q

Common cause of acute cervical lymphadenitis?

A

Microbial infections of the teeth or tonsils

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2
Q

What is the structure of the white pulp follicles?

A

Artery with an eccentric collar of T lymphocytes (periarteriolar lymphatic sheath).

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3
Q

What are the four functions of the spleen?

A

1) Phagocytosis of blood cells and particulate matter
2) Antibody production
3) Haematopoiesis
4) Sequestration of formed blood elements

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4
Q

Where does pitting of RBCs occur?

A

In splenic macrophages

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5
Q

What is pitting of RBCs?

A

Excision of inclusions in RBCs by splenic M0 e.g.

  • Heinz bodies
  • Howell-Jolly bodies
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6
Q

How do T lymphocytes in the spleen recognise antigens and trigger production of antibodies?

A

Dendritic cells in the periarterial lymphatic sheath trap antigens and present them to T lymphocytes –> interact with B cells at edges of white pulp follicles –> generate antibody secreting plasma cells.

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7
Q

What is the role of the spleen in haematopoiesis?

A
  • Generally ceases pre birth
  • Can reactivate in severe anemia
  • Prominent site of extra medullary haemopoiesis in myeloproliferative disorders (e.g. CML)
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8
Q

Effect of spleen in sequestration of formed blood elements?

A
  • Usually only 30-40mL RBCs
  • 30-40% platelets
  • With splenomegaly, sequestered volume greatly increases: can induce thrombo-/leuko-cytopenia
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9
Q

What is the clinical manifestation of splenic insufficiency (i.e.post splenectomy / auto-infarction)?

A

Increased susceptibility to sepsis causes by encapsulated bacteria e.g.

  • pneumococcus
  • meningococcus
  • H. influenzae.
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10
Q

Symptoms of splenomegaly?

A
  • Dragging sensation LUQ

- Compression of stomach -> discomfort after eating

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11
Q

What characterises hypersplenism?

A

-Leukopenia
-Thrombocytopenia
-Anemia
(alone or in combination) ?due to increased sequestration of formed blood elements > M0 phagocytosis.

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12
Q

Morphology of long standing congestive splenomegaly?

A
  • Large spleen (1-5kg)
  • Organ firm
  • Capsule thick and fibrous
  • Red pulp congested initially, becomes increasingly fibrotic and cellular
  • Deposition of collagen in BM of sinusoids
  • Slowing of blood flow from cords > sinusoids prolongs exposure of cells to M0 > hypersplenism
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13
Q

Cause of splenic infarcts?

A

Occlusion of splenic artery or its branches.

-common site of emboli (usually from heart)

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14
Q

Morphology of splenic infarcts?

A

-Pale, wedge shaped, subcapsular infarcts
-overlying capsule often covered with fibrin
-heals by scarring
If septic: + suppurative necrosis.

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15
Q

What are spleniculi?

A
  • Accessory spleens
  • Present in 20-35% post mortems
  • Small, spherical structures histologically and functionally identical to N spleen
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16
Q

When are spleniculi clinically significant?

A

-Signficant in haematologic disorders e.g. hereditary spherocytosis, immune thrombocytopenic purpura.
Splenectomy is treatment: failure to remove spleniculi may negate this.

17
Q

Cause of spontaneous splenic rupture without trauma?

A

Minor physical insult to a spleen made fragile by condition e.g. :
-infectious mono
-malaria
-typhoid fever
-lymphoid neoplasms
Cause rapid splenic enlargement, thin capsule susceptible to rupture.