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Lymph Node, Lymphadenitis part 2

Posted July 29, 2016. Pathology

Lymphadenitis

This is the inflammation of the lymph nodes. This can be classified into the following types :

1. Acute Lymphadenitis:

  • · Specific
  • · Non-specific

2. Chronic Lymphadenitis:

  • · Specific
  • · Non-Specific

Acute Lymphadenitis (Specific). This may be :

  1. Localized e.g. Regional Lymph Node in appendicitis and tonsillitis extremities infection.
  2.  Generalized e.g In Viraemia, Bacteraemia (More common in children) 

Acute Lymphadenitis (Non-Specific)

Acute lymphadenitis may be due to the Common Organism like Staph, which leads to localized abscess. Streptococci leads to cellulites.

Other causes are Typhoid bacilli.

Acute Suppurative Lymphadenitis

sign and symptoms are :

  1. Lymph nodes are tender and hot.
  2. Microscopically there are mainly polys in the germinal centers.
  3. Pyogenic Bacteria present in the germinal center and this are may undergo necrosis.
  4. Histiocytes may contains Particulate of bacteria.
  5. Ultimately there is resolution.

 Result of acute lymphadenitis

  1. Resolution. 
  2. Abscess and draining sinuses formation.
  3. Scarring.

Chronic Lymphadenitis (Non-specific) classified into:

  1. B-Cell Hyperplasia (Follicular hyperplasia)
  2. T-Cell or Paracortical Hyperplasia
  3. Sinus Histiocytosis.

 B-Cell Hyperplasia (Hyperplastic lymphadenitis)

This is  due to infections by Microbes.

Causes of B-cell hyperplasia:

  1. Secondary Syphilis
  2. Toxoplasmosis
  3. Rheumatoid Arthritis
  4. AIDS.

Microscopic appearance of B-cell hyperplasia:

  1. Germinal centers are enlarged.
  2. Enlarged Lymph node and with presence of various stages of “Blast” transform.

D/D of B-cell hyperplasia from Follicular Lymph node:

  1. Blast cells and histiocytes  in Germinal center.
  2. There is Phagocytic activity
  3. There is presence of polys, monocytes, and eosinophils in parafollicular area.
  4. Mitosis in germinal center are seen.
  5. There is Variation in Nodule Size.
  6. Monomorphic cells in NHL.
Findings B-Hyperplasia Follicular lymphoma
Blast cells and histiocytes in germinal center present Not prominent
Phagocytic activity present not seen
Presence of polys, monocytes, eosinophils present monotonous population
Mitosis in germinal center  present usually absent
Size of nodule variable uniform

Paracortical Hyperplasia (T-cell Hyperplasia)

There is predominantly hyperplasia of T cells. The T-Cell change may encroach B-cell area.

Signs and symptoms:

  1. Skin rashes and enlarged lymph nodes.
  2. There is Fever and enlarged Liver and Spleen.
  3. Patient may have Painful Joints.

Causes:

  1. Drugs
  2. Dilantin Na
  3. S.Pox Vaccination
  4. Immunological disorder

Microscopic appearance:

  1. There is proliferation of T-Lymphocytes and  Immunoblastic cells.
  2. ay see polys, eosinophils and macrophages.
  3. Hypertrophy of sinusoids and vascular endothelial cells seen , this is  also called Pseudolymphomatous Pattern.

Sinus Histiocytosis (Sinus Hyperplasia)

  1. There is distension and prominics of Lymph sinusoids.
  2. This is  Seen in lymph node draining Carcinoma of Breast.
  3. When present in carcinoma of breast is sign of favorable prognosis.

Chronically  increased Lymph nodes are not tender and their common site is axilla and inguinal area.

Specific Chronic Lymphadenitis

May be seen in –

  1. Tuberculosis.
  2. Brucellosis.
  3. L.venereum.
  4. Sarcoidosis
  5. Histoplasmosis
Findings Tuberculosis Sarcoidosis
Granuloma soft hard
Mantoux test positive negative
Kveim test negative positive
AFB stain positive negative

Noncaseating granuloma may be seen in:

  1. Some patients with Hodgkin's disease.
  2. Crohn’s disease.
  3. Syphilis.

Immunoblastic Lymphadenitis

This condition also called Angioimmunoblastic lymphadenopathy.

It resemble clinically like Hodgkin disease and needs to differentiate histologically from it.

Signs and symptoms

  1. There may be fever.
  2. Patient may have sweating.
  3. There are skin rashes.
  4. There is generalized enlargement of the lymph nodes.
  5. There is enlarged liver and spleen.
  6. patient may history of autoimmune disease.
  7. Sometime may see autoimmune hemolytic anemia.
  8. There is polyclonal hypergammaglobulinemia.

Microscopic appearance

  1. There are small arborizing blood vessels with prominent endothelial cells.
  2. There are numerous immunoblastic cells and plasma cells.
  3. There is deposition of eosinophilic PAS positive material.
  4. There are occasional epithelial cells.

Outcome of the disease

  1. The patient may have a aplastic anemia.
  2. The patient may develop Lymphoma.
  3. Bone marrow show Lennert's lymphoma (in 70% ) of the cases.

Angiofollicular Hyperplasia 

This is also called Castleman's disease, Giant lymph node hyperplasia and Benign giant lymphoma.

Its etiology is unknown.

Signs and symptoms

  1. Usually there is presentation of mediastinal mass.
  2. There is fatigue, night sweating, nausea and weight loss. 
  3. There may be anemia and fever.
  4. there may be flu like symptoms.
  5. There is enlargement of the lymph nodes.
  6. There is hyperglobulinemia.

Microscopic appearance

There are following variant of this condition:

  1. Hyaline- vascular type
  2. Plasma cell type
  3. Mixed type 
  4. Plasmablastic type

Differential diagnosis

  • In case of mediastinal mass needs to differentiate from lymphoma.
  • From Kaposi sarcoma.

Lymphangiopathic Histiocytosis

This is also called Rosai-Dorfman disease. Also called as sinus histiocytosis with massive lymphadenopathy.

This is chronic disease and unknown etiology.

Age: This is mainly seen in children and young adults.

Signs and symptoms

  1. There is massive increase in the size of lymph nodes.
  2. There may be fever.

Microscopic appearance

  1. There is Increase in histiocytes in sinusoids.
  2. Occasional Mononuclear giant cells are seen.
  3. Follicular centers are absent.
  4. Increase plasma cells seen in the medullary cards.
  5. Capsular and Pericapsular inflammation and fibrosis are common.

Outcome

  1. This may subside.
  2. In some cases may lead to death.

Dermatopathic Lymphadenopathy

It is also called lipo melanotic Reticulosis.

This is seen in chronic inflammation or destructive (Exfoliative) lesion of the skin.

Microscope appearance:

  1. It is characterized by widened pale staining paracortical area  (T-lymphocyte Zone).
  2. There are Foamy, vacuolated macrophages.
  3. Some of the macrophage contains melanin and hemosiderin.
  4. There is Increase in Eosinophils, plasma  cells and immunoblastic cells.

Necrotizing Lymphadenitis

  1. This is Seen in:
    1. Lupus erythematosus.
    2. Bubonic Plagues.
    3. Infectious Mononucleosis.
    4. Anthrax.
    5. Typhoid.
    6. Dilantin sodium  hypersensitivity.

Microscope appearance:

  1. There is Extensive Haemorrhage.
  2. There is necrosis.
  3. This are is surrounded by the histiocytes.

Lymphadenopathy due to AIDS

Characterized by:

  1. Marked follicular hyperplasia.
  2. Infiltration of follicles by small Lymphocytes.
  3. There are  Foci of intra-follicular haemorrhage “follicle lysis”.
  4. Focal perisinusoidal or monocytoid B-cell hyperplasia.

There is High incidence of:

  1. B-cell Lymphoma.
  2. Hodgkin disease.
  3. Kaposi sarcoma.

Kikuchi Disease

  1. It is also called as Histiocytic Necrotizing Lymphadenopathy.
  2. There is unknown etiology.
  3. It is more common in young females.
  4. Histology: There is  Paracortical Necrosis surrounded by histiocytes.

Idiopathic infraction of Lymph Node

It is seen in Patient with pyrexia of unknown origin (PUO).

                                           Causes of Enlargement of Lymph Node

The causes of enlargement of the lymph node is classified as follows:

1. Localized or generalized

2. Acute:

  •  Specific
  •  Non-specific

3. Chronic:

  •  Specific
  •  Non-specific

4. Tumors:

  • Primary
  • Secondary

5. Pseudolymphomatous  conditions:

  • Follicular Hyperplasia.
  • Post vaccinal

Causes of enlargement of the lymph nodes

  1. Lymphangiopathic histiocytosis (Rosai- Dorfman disease).
  2. Angiofollicular hyperplasia (Castleman’s disease, benign giant lymphoma).
  3. Immunoblastic lymphadenopathy (Lennert’s Lymphoma).
  4. Dermatopathic Lymphadenopathy.
  5. Necrotizing lymphadenopathy.
  6. AID- lymphadenopathy.
  7. Kikuchi disease.
  8. Idiopathic infarction of Lymph Node.
  9. Cat- scratch disease.


Lymph node Structure Part 1

Posted July 27, 2016. Pathology

Lymph node 

Lymph Node are part of the reticuloendothelial system.

Reticuloendothelial SystemReticuloendothelial System is a term used by Aschoff and Kiyono with criteria of:

1.      Phagocytic activity.

2.      Staining with vital dyes.

3.      Juxtaposition to reticulum of connective tissues and lining cells of Blood vessels.

Components of Reticuloendothelial System are :

1.     Intravascular: 

  • ·       Monocytes
  • ·        Endothelial cells (Kupffer cells)
  • ·        Lymph node sinuses
  • ·        Splenic sinuses
  • ·        Adrenal Capillaries

2.      Extravascular:

  • ·        Reticulum cells
  • ·        Histiocytes and macrophages (of Connective tissues)

Lymphoid Tissue

Lymphoid tissue is present throughout the body, calculated that in a man there are about 1300g of lymphoid tissue. Lymph node contains about 100g and bone marrow about 70g.

Lymphoid tissue divided into :

Central components which includes: 

  •    Appendix
  •    Peyer's patches
  •    Thymus  
  •   Tonsils

Peripheral component includes:   

  • Lymph nodes
  • Spleen

 

 This diagram shows different parts of the Lymph node

Sinusoids are lined by the endothelial cells and in between there are flat Littoral cells.

Flat Littoral Cells has the following properties:

·        Can proliferate

·        Can Hypertrophy

·        Phagocytosis (House cleaning, functions of lymph node)

·        May detach and become free phagocytes in lymphoid  sinuses and lead to sinus histiocytosis or sinus Catarrh of German authors.

Histology:

Lymph node consists of :

  • Medulla.
  • Cortex.
  • Peripheral sinus.
  • Cortical area.
  • Deep paracortical area.
  • Sinusoides.
  • Medullary cards.
  • Afferent and efferent vessels

 

Lymph node showing detail of structure 

Primary Follicle when activated, it transform into  ---- Secondary Follicle.

Germinal center contains following cells :

  • Lymphocytes.
  • Lymphoblasts.
  • Histiocytes.
  • Mitosis.

                                                        T- Lymphocytes 

T-Lymphocytes converted into à Convoluted T-Cells, this transform into T-  Immunoblastic cells, ------->T-Lymphoblast ------> T-Prolymphocytes -------->T-Lymphocytes.

Functions of lymphocytes:

  1.       Formation of Lymphocytes as B and T lymphocytes which takes part in the immunity.
  2.        Production of Ab takes place by B- lymphocytes.
  3.        Filtration of Lymph removes  Particulate matter like Bacteria, Virus, cellular debris, anthracotic pigments and cancer cells.
  4.        Phagocytosis by these lymphocytes.
  5.       They have important role  Role in Inflammation and Infection:

Lymph Node are labile.  Relatively larger at birth,  Modified by stress, adrenal gland , thyroid hormones and  immune response.

·        Biopsy of Lymph Node used for:

  1.   Bacterial Examination where one can do culture and sensitivity(C/S).
  2.   Cytologic imprint for the better differentiation of the cells.
  3.  Histological Examination can differentiate inflammation, metastatic tumor infiltrate, or primary tumor like lymphomas .

Electron microscopy may be done on biopsy material:

  •   Immunophenotyping.
  •  Chromosomal studies.
  •  Gene Rearrangement Analysis.
  •  DNA Ploidy studies

Indications for Lymph Node Biopsy:

  1.  To make a diagnoses in case of Persistent enlargement of the lymph nodes
  2.   To make diagnosis in a patient with PUO, weight loss and enlarged lymph nodes.
  3.    To confirm diagnoses already suspected on other grounds.
  4.     To assess in the extent of spread of known malignant diseases.
  5.       To monitor the progress of disease in patient with malignant lymph nodes.

Precaution for lymph node biopsy:

  1.      Inguinal lymph nodes wherever these are enlarged should be avoided. Take biopsy from other group.
  2.      Always take biopsy from the larger lymph node.
  3.      Axillary and cervical lymph nodes are more representative.
  4.      Superficial small lymph node may slow non-specific hyperplasia whereas deeper node in the same group may show diagnostic feature.
  • Lymph  node with normal picture shows:             
  •   Narrow peripheral sinus.
  •    Sinusoids are not prominent.
  •    Macrophages are not prominent.
  • There are   Small ill-defined germinal centers.
  • There are   Sparse Lymphocytes in Reticular framework.  
  • The   Size is  Small.

Activation of Lymph Node in Acute Disease:

  1. There is increase in the size of lymph node.   
  2. There is dilatation of the sinusoidal  Sinuses.
  3. The  Sinusoids are prominent.
  4. The   Macrophages are increased in number.
  5. There is increased number of   Polys and Necrosis.
  6. The germinal centers are prominent  with increased number of mitosis.

Activation of Lymph Node in Chronic Disease

  1. There is increase in the size of lymph node.
  2. There is increase number of plasma cells and eosinophils.
  3. Also can see above changes seen in acute diseases.

 


Lecture on Ulcerative Colitis and Crohn's Disease

Posted Nov. 3, 2014. Pathology

Ulcerative Colitis  is an inflammatory bowel disease (IBD) that affects the large intestine (colon and rectum). Ulcerative colitis affects the only the large intestine.

Crohn’s disease is inflammatory bowel disease. While Crohn’s can affect any part of the gastrointestinal (GI) tract from mouth to anus, 

Ulcerative colitis is considered to be the autoimmune disease. This is due to inflammation caused by the immune system and mainly occurs in the large intestine.

Following are the signs and symptoms of Ulcerative colitis.

  1. Diarrhea, often with blood or pus
  2. Abdominal pain and cramping
  3. Rectal pain
  4. Rectal bleeding , there is  passing small amount of blood with stool
  5. Urgency to defecate
  6. Inability to defecate despite urgency
  7. Weight loss
  8. Fatigue
  9. Fever
  10. In children, failure to grow

Crohn's disease cause is unknown.Diet and stress were suspected, but now doctors know that these factors may aggravate but don't cause Crohn's disease. A number of factors, such as heredity and a malfunctioning immune system, likely play a role in its development.

Following are the main signs ans symptoms of the active Crohn's disease.

  1. Diarrhea with cramps.
  2. Fever and fatigue.
  3. Abdominal pain and cramping.
  4. Blood seen in the stools.
  5. Mouth ulcers.
  6. There is decrease in the appetite.
  7. There is weight loss.
  8. There is involvement of the perianal area.
Comparison table

Pathologic findings

              Ulcerative colitis                 Crohn's disease                                
Location
   
Ileum                       --                                      ++
Rectum                      ++                    + --
Skip lesion                      --                    +
Continuous involvement of colon                      ++

                  --

Involvement of Ileum

                     --                      ++
Gross appearance
                                    
Broad based ulcers                    ++                      --
Strictures                  + --                     ++
Fissures                   + --                     ++
Fistulas                  + --                     ++
Cobblestone appearance (mucosa)                  --                     ++
Pseudopolyp                  ++                     --
Microscopic appearance
   
Crypt abscess                  ++                       --
Granuloma formation                 --                    ++
Lymphoid aggregates                 --                     ++
Fibrosis of the wall                 --                     ++
Transmural involvement                  --                      ++
 
 


Lecture on Hepatitis B Virus

Posted Feb. 18, 2014. Pathology

Hepatitis B virus also called as serum hepatitis virus.

  • This is hepatotropic virus because it proliferate in the liver.
  • Hemophilic patient with multiple transfusions serum reacted with serum of Australian patient ,so this is called as Australia antigen

Epidemiology

  1. Long incubation period
    1. Asymptomatic period is from 4 to 26 weeks.
    2. Average time is 1.5 to 2 months.
  2. Acute disease
    1. This may last for weeks to months.

HBV causes hepatitis in

  1. Human .
  2. Woodchucks and ducks.
  3. Ground and tree squirrel.

HBV can cause

  1. chronic hepatitis.
  2. Scarring of liver leading to cirrhosis.
  3. Liver failure.
  4. Liver cancer.
  5. Ultimately leads to death.
  1. Mode of Spread of the disease
    1. Parental mode like blood, blood products, and needle pricks.
    2. It can spread by through semen and saliva.
    3. Vertical transmission can occur through mothers.
    4. Dialysis patients are at higher risk.
    5. Health workers are also high risk group.
    6. In 1/3 of the cases source is unknown.
    7. Drug addicts are also high risk group.

Source of spread

  1. Blood and blood products.
  2. Body fluids :
    1. Semen.
    2. Vaginal secretions.
    3. Saliva.
    4. Open sore .
    5. Breast milk.
  1. Virus present in
    1. It is present in the last days of incubation period in the blood.
    2. It is present in acute and chronic stages of disease.
    3. This is present in physiologic and pathologic fluids except feces.

Infectivity of various materials

  1. Blood is ++++.
  2. Body fluids are + to +++.
  3. Stool is negative.

Infective hepatocytes can :

  • Synthesize and secrete massive amount of HBS which appears in cells and serum.
  • This may occur with or without replication of infectious viron.

rong>Who poses more risk

  1. Health workers and dialysis patients are more at risk.

Structure of HB virus

  • This is DNA virus.
  • Complete virus particle is called Dane particle and it is 42 nm in diameter.
  • On E/M Virus particle consists of :
    • Sphere 20 nm D.
    • Tubules 20 × 100 nm.
    • Dane particle which consists of DNA + coat proteins.
    • Sphere and tubules are excessive proteins and these are surface antigens HBs proteins.
    • These sphere and tubules (HBs Ag) are not infective.
  • HBV genome is double stranded DNA.
  • HBV antigens are :
    • HBs antigen.
    • HBc antigen
    • HBe antigen.
  • HBV antibodies are :
    • Anti-HBs.
    • Anti-HBc
    • Ant-HBe
  • There are few Dane particles in the serum as compared to surface antigen HBs.

Outcome of HBV infection

  1. There may be asymptomatic carrier who are without obvious disease.
  2. Patient may have acute hepatitis.
  3. Patient may go into chronic stage as chronic hepatitis.
    1. Chronic hepatitis may be non-progressive.
    2. Chronic hepatitis may be progressive with development of cirrhosis.
  4. Patient may develop fulminant hepatitis with massive necrosis.

Chronic Carrier

  • Following is the criteria to label patient as Carrier.
    1. These patient has no signs and symptoms.
    2. Liver function tests are normal.
    3. HBs antigen is positive.
    4. These patients has increased risk for liver cell carcinoma. This risk may be be 273 times

Post exposure prophylaxis

  1. If there is percutaneous prick then give hepatitis B immunoglobulin (HBIG) 0.06 ml/kg IM or 5 ml as single dose.
  2. Can give vaccine 1.0 ml within 7 days.
  3. Vaccine alone may be of value in poor patients (A.J.Med.1989).

Perinatal exposure

  1. Give HBIG 0.5 ml IM within 12 hours of exposure.


Sexual exposure

  1. Give 0.06 ml/ kg or 5 ml IM within 14 days of contact.

Risk and prevention in pregnant mothers

  1. If mother is HBs positive then infectivity for newborn is 40 %.
  2. If mother is HBs positive and HBe positive then infectivity for new born is 85 to 95 %.
  3. If newborn given vaccine or HBIG after 7 days then it has no value.
  4. So HBIG + vaccine should be given to newborn within 2 to 12 hours. Maximum can be delayed up to 48 to 72 hours.

Diagnosis and various panel for various conditions of HBV infection

  1. Screening panel consists of :
    1. HBs Ag.
    2. Anti-HBs.
    3. This is panel is used for :
      1. Blood donors.
      2. Perinatal.
      3. Dialysis centers.
  2. HBV monitoring panel consists of :
    1. HBs Ag.
    2. HBe Ag.
    3. Anti-HBe Abs
    4. This panel is used for :
      1. Patients with HBV infection.
      2. Define degree of infectivity.
      3. Potential for chronic hepatitis.
      4. When there is seroconversion from HBe-Ag to HBe- Abs is good prognostic factor.