Lymph Nodes and the Spleen

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Lymph Nodes

Normal Anatomy of lymph node (Figure 15-1 Robbins, p. 645)

• Small bean-shaped structure less than 2 cm in length

• Soft in consistency

• Connective tissue capsule around the outside is perforated by afferent lymphatics

• Lymphatic fluid

o Afferent lymphatics ( peripheral subcapsular sinus ( sinuses in the lymph node (medullary sinuses) ( hilus ( efferent lymphatics

o The sinuses within the lymph node are lined by histiocytes which are cells that phagocytize, process, and present antigens to either T cells or B cells.

• T cells: paracortical areas toward the outside of the lymph node that surround the follicles

• B cells: follicles

o Mantle zone: contains virginal or memory B cells

▪ Located on the outside of the follicle

▪ Thicker on one side than the other

o Transformed lymphocytes on the inside of the follicle

• Lymph nodes also have a blood supply.

• Medullary area – predominately plasma cells

o Located in the middle of the lymph node

o Transformed lymphocytes become plasma cells and migrate to this area where they sit around blood vessels and secrete immunoglobulins into the circulation

Slide: Photomicrograph of a lymph node with fatty soft tissue surrounding it. Parts identified include: capsule, subcapsular sinus, paracortical region, follicle, mantle zone

Slide: Immunohistochemical stain of B-lymphocytes. Mantle zone and germinal center areas are seen.

Slide: A lymph node stained for T lymphocytes. Paracortical areas surrounding the lymphoid follicles are seen.

Reactive changes in lymph nodes

• Nonspecific lymphadenitis

o Acute form: (often occurs with bacterial infection)

▪ Lymph node enlargement mostly due to follicular hyperplasia

▪ Active germinal centers

▪ Mitotic figures within the follicular centers

▪ Tingible body macrophages: antigen processing macrophages that have moved from the sinuses to the follicular centers to present antigens to the B cells

• Contain particulate debris

• May be focally necrotic with abscess formation (Acute necrotizing lymphadenitis)

▪ Neutrophils in sinuses and around the follicles

▪ Endothelial cells lining the sinuses may hypertrophy and become more prominent than usual.

▪ Affected lymph nodes are swollen, tender, and may be warm to the touch from increased vascular blood flow (overlying skin is often hyperemic)

▪ Sometimes there are draining sinuses from lymph nodes to the skin surface in cases of supportive necrosis

▪ Etiology

• Bacterial infection

• Foreign body reactions from wounds or IV drug users

• Mesenteric adenitis: enlarged lymph nodes in the mesentery draining the GI tract

o Mimics acute appendicitis

• Generalized lymphadenopathy: occurs with viremia or septicemia

• Localized infection usually just involves the local lymph nodes

• Different reaction patterns in lymph nodes

o Nonstimulated follicles are primary follicles and don’t have germinal centers

o Stimulus activating B cells ( hyperplasia of B cell areas (follicles) with formation of germinal centers that are mitotically active and contain tingible body macrophages

o Stimulus activating T cells (viral infections) ( enlargement of the lymph nodes due to expansion of paracortical areas

o Long standing chronic infections ( enlargement of the medullary area from an increase in plasma cells (produced from the activated germinal centers)

o Chronic inflammation (especially lymph nodes draining cancer) ( hyperplasia of the histiocytes in the sinusoids

o Typically there is a combination of reactive patterns in each lymph node

• Chronic forms of nonspecific lymphadenitis

o Can lead to follicular hyperplasia (antigenic stimulation of B lymphocytes)

o Mostly from chronic bacterial infections, but also can be caused by rheumatoid arthritis, syphilis and AIDS

Slide: Section of lymph node with prominent follicular hyperplasia. The mantle zone has one side is thicker than the other. The germinal center with large pale staining cells and small dark staining cells is extremely mitotically active. The large clear areas are the tingible body macrophages.

Slide: Closer view of the germinal center. Tingible body macrophages with debris can be seen, and there are a lot of mitotic figures within the germinal center. This is hard to differentiate from follicular lymphoma. But, with a lymphoma you won’t see tingible body macrophages and the lymphoid cells in the background will be homogenous instead of heterogeneous.

Slide: Lymph node with suppuration and abscess formation. It is full of neutrophils and necrotic debris.

Other chronic reactions in lymph nodes:

• Paracortical (interfollicular) hyperplasia

o Antigenic stimulation of T lymphocytes

o Etiologies

▪ Viral infections (herpes zoster and EBV- infectious mononucleosis)

▪ Drug reactions: dilantin

▪ Vaccination reactions

▪ Skin diseases: dermatopathic lymphadenopathy (melanin pigment in the lymph node)

Slide: Enlarged lymph node from a person taking Dilantin. It is hard to see the germinal centers because of hyperplasia of the T cells in the interfollicular areas.

Slide: T cell hyperplasia. Transformed T lymphocytes are very heterogeneous.

• Mixed follicular and paracortical hyperplasia (Somewhat specific for certain conditions)

o Toxoplasmosis: involves the cervical lymph nodes which have aggregates of epithelioid histiocytes within the interfollicular/paracortical areas

o Kawasaki’s disease (a.k.a. Mucocutaneous lymph node syndrome)

▪ Disease in children; etiology unknown

▪ Children develop conjunctivitis, erythema of the oral mucosa, erythematous desquamative rash of the palms and soles (like Rocky Mountain Spotted Fever), cervical lymph node enlargement

▪ Lymph nodes exhibit microthrombi and multiple areas of necrosis

▪ Inflammation and infarction of the coronary vessels may lead to myocardial infarction

o Sinus histiocytosis

▪ Distension and prominence of lymphatic sinusoids with proliferation of histiocytes

▪ Frequently encountered in regional nodes draining a site of cancer

o Granulomatous inflammation

▪ Granuloma: collection of histiocytes

▪ Caseating granuloma: Tuberculosis and brucellosis

• Necrosis in center

▪ Non-caseating granuloma: fungi, sarcoidosis

▪ Stellate granulomas – star like

• Cat scratch disease, lymphogranuloma venereum, tularemia

Slide: Sinus histiocytosis. Subcapsular sinus full of pink histiocytes. Prominence of sinusoids are also apparent.

Slide: Caseating granuloma

Slide: Coccidiomycosis (non-caseating granuloma). You can see large spheroids with multiple fungi surrounded by epithelioid histiocytes, a response to fungal infections.

Slide: Stellate granuloma

The Spleen

• Function

o The spleen filters the blood.

• Splenomegaly – important to identify because it may give a clue to the underlying hematological disorder

o The patient feels a dragging sensation in the left upper quadrant

o Early satiety after eating (spleen pressures the stomach)

o Exaggeration of storage function of the spleen

o Sequestration syndrome leading to peripheral cytopenias due to the hypersplenism

o Can be corrected with a splenectomy; but not performed very often because the spleen aids in the prevention of blood-borne infections

o Causes:

▪ Infections

▪ Congestive states related to portal hypertension (hyperemia of spleen)

▪ Lymphohematogenous disorders like leukemias and lymphomas

▪ Immunological inflammatory conditions: SLE, other autoimmune disorders

▪ Metabolic storage diseases (refer to table in book for a list of these)

• Splenic Architecture (Figure 15-38, p. 687)

o The spleen has a fibrous capsule, a single artery and a single vein

o Blood vessels separate along the periarterial or lymphoid sheath

▪ This sheath is a group of lymphocytes that surround the blood vessels. Antigenic substances in the bloodstream are then exposed to these lymphocytes.

o Red pulp: splenic cord and venous sinuses

o White pulp: splenic lymphoid nodules

Slide: Illustration of spleen. Arterial blood supply comes through the hilus through the periarterial lymphoid sheath, then through the sinusoids within the spleen. The red blood cells are forced to go through fenestrations in the splenic cords to enter venous circulations. Damaged red blood cells are removed by cells of the reticuloendothelial system.

Slide: Normal spleen. The red purple stain shows the red pulp, and the little white dots are the white pulp.

• Nonspecific Acute Splenitis

o Splenic enlargement occurs as a nonspecific reaction to any blood-borne infection

o Grossly, the spleen is soft, and the red pulp (splenic cords and sinusoids) is congested

o Increase in neutrophils with abscess formation

o There may be foci of necrosis

• Congestive splenomegaly

o Chronic venous congestion can lead to splenic enlargement, capsular and parenchymal fibrosis, and hemorrhage.

o Etiology

▪ Systemic (central) venous congestion from right sided heart failure or cor pulmonale following left-sided failure

▪ Hepatic cirrhosis: portal hypertension may lead to massive splenomegaly

▪ Obstruction of the extrahepatic portal vein or splenic vein may be associated with intrahepatic obstructive disease, vascular inflammation or neoplasms.

• Splenic infarcts

o Most commonly due to occlusion of the splenic artery or one of its branches within the spleen

o The splenic artery is the only artery that supplies the spleen

o Etiology

▪ Thromboemoblic disease – typically bland (not infected)

▪ Sickle cell anemia – more multifocal; can progress to destruction of the entire spleen

▪ Infective endocarditis (chronic infection of the heart valves)

Slide: Infarct of spleen. The spleen shows a white area because blood supply has been cut off.

• Splenic neoplasms

o Primary splenic neoplasms are rare. Most are secondary (metastasis from elsewhere).

o Lymphomas, leukemias, and metastatic carcinomas can show up because the spleen tries to filter out the neoplastic elements in the blood

o Rare primary neoplasms: fibromas, osteomas, chondromas, lymphangiomas, hemangiomas

▪ Usually findings at autopsy, because they don’t create any significant pathology themselves

• Congenital anomalies of the spleen

o Hypoplasia: abnormally small

o Asplenia: total absence of the spleen

▪ Rare

▪ Usually associated with other congenital anomalies like situs inversus and cardiac malformations

▪ Patients have problems with septicemia

o Accessory spleens: very common

▪ Significant when therapeutic removal of all splenic tissues may be beneficial, as in hereditary spherocytosis, thrombocytopenic purpura and some causes of hypersplenism

▪ May occur as a natural phenomenon, or with minor trauma causing seeding of the spleen throughout the peritoneum

▪ Radionucleotide scans can be performed to identify all splenic tissues in the body so they can be removed.

• Splenic rupture

o Especially in automobile accidents – Wear your seatbelt!! Hitting the steering wheel can rupture the spleen leading to massive intraperitoneal hemorrhage and death.

o Spontaneous rupture in patients with splenomegaly

▪ Be careful during palpation because enlarged spleens can be very fragile.

▪ Occurs with infectious mononucleosis which is especially susceptible to minor trauma

▪ Also occurs with malaria, typhoid fever, leukemia, acute splenitis

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