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Liver Anatomy

Posted June 22, 2017. Pathology Pathology - Liver


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The liver develops In the third week of gestation from foregut (primitive duodenum) which develops from endodermal cells. Also, gallbladder and hepatocytes develop from the endodermal cells.

Connective tissue and sinusoids develop from mesenchymal cells.                                                                     

Intrahepatic bile duct development complete at a 3rd month and bile secretion also start by that time.


The liver is the main organ to store iron and is the site for hematopoiesis. Hematopoiesis stops in two months after birth but may be found in occasional foci in the liver. In premature baby these foci are abundant. The weight of the liver in full term baby is 75 to 180g.Umbilical Vein is the main source of blood supply in fetus after delivery it atrophies and gets round ligament. Liver grows slower than other structures in adult liver weighs 1200 to1500 g (1350G)⅕ of the total body weight (2.5% of total body weight)

The weight of the liver in full term baby is 75 to 180 g. Umbilical Vein is the main source of blood supply in fetus after delivery it atrophies and gets round ligament. Liver grows slower than other structures in adult liver weighs 1200 to1500 g (1350G)⅕ of the total body weight (2.5% of total body weight)

Umbilical Vein is the main source of blood supply in fetus after delivery, it atrophies and transforms into round ligament.  Liver grows slower than other structures in adult liver weighs 1200 to1500 g (1350G)⅕ of the total body weight (2.5% of total body weight)

The Liver grows slower than other structures. in adult liver weighs 1200 to1500 g (average 1350G) and is 1/5 Th of the total body weight (2.5% of total body weight).


     The liver is divided by a falciform ligament into right and left lobes.The right lobe is divided into quadrate lobe (inferior surface) and caudate lobe ( posterior surface).The upper border extends to the 5th intercostal space.

     The liver is covered by thin fibrous capsule called Glisson capsule.The gallbladder is under the right lobe. The Porta hepatis is a deep fissure in the inferior surface of the liver through which all the neurovascular structures( except hepatic veins ) and hepatic ducts enter or leave the liver.It contains the right and left hepatic ducts, right and left branches of the hepatic artery and portal vein. The left lobe is six times smaller than the right lobe. 


In the porta hepatis, the hepatic artery is anterior, bile duct also anterior and the portal vein is posterior.


Teres ligament developed from an inferior umbilical vein. Ligamentum venosum developed from posterior ductus venosus. The lower edge of the liver is unusual to be 1 to 3 cm below the costal margin.

    The connective tissue surrounds all blood vessels and ducts to finest radicals to join inner aspect of Glisson capsule.

 Liver Blood supply

    Hepatic artery carries 600 ml of blood per minute while portal vein 900 ml of blood per minutes. Hepatic artery supplies 30 to 40 % of oxygen while portal vein supplies 50 to 60% oxygen. The pressure in the hepatic artery is 90 mm of Hg and in the portal vein is 8 to 10 mm of Hg.


   The portal vein has a high level of oxygen content equal to 80% saturation. Mixing of the portal vein and hepatic artery blood leads to drop in the arterial pressure.


These vessels enter into sinusoids and all sinusoids drain blood to central veins. All central veins give rise to right and left hepatic veins Which continue to inferior vena cava.


 Biliary Tract

      From the liver left and right duct joins to form the common hepatic duct.The common hepatic duct is joined by the cystic duct from the gallbladder.They give rise to common bile duct the diameter of the duct is .5 to 1.5cm.The common bile duct is joined by the pancreatic duct and they open to the ampulla of water in the duodenum, the ampulla of water is controlled by sphincter of Oddi which is Spiral valve, is a fold of mucosa.




Lymph Node REAL Classification of Lymphoid Neoplasm

Posted Sept. 5, 2016. Pathology Pathology - Lymph node

REAL classification is Revised European – American classification of lymphoid neoplasm.

It includes :

  1. Lymphocytic leukemia
  2. Non – Hodgkin’s lymphoma
  3. Plasma cell tumors.

REAL classification is into 4 broad categories based on the immunophenotype.

  1. Precursor B – cell neoplasm (Neoplasm of mature B – lymphocytes).
  2. Peripheral B – lymphocyte neoplasm (Neoplasm of mature B – lymphocytes).
  3. Precursor T – lymphocyte neoplasm (Neoplasm of immature T – lymphocyte).
  4. Peripheral T – lymphocyte neoplasm (Neoplasm of mature T – lymphocyte)

Precursor B – lymphocyte = Precursor B – cell lymphoblastic leukemia/lymphoma.

Precursor T – lymphocyte = Precursor T – cell lymphoblastic leukemia/lymphoma.

Peripheral B – lymphocyte gives rise to:

  1. Chronic lymphocytic leukemia / small lymphocytic lymphoma.
  2. Lymphoplasmacytic lymphoma.
  3. Mantle cell lymphoma.
  4. Follicular lymphoma.
  5. Marginal zone lymphoma.
  6. Hairy cell leukemia.
  7. Plasmacytoma/plasma cell myeloma.
  8. Diffuse large cell (B) lymphoma.
  9. Burkitt’s lymphoma.

Peripheral T – cell and NK –  neoplasm give rise to:

  1. T cell chronic lymphocytic leukemia.
  2. Large granular lymphocytic leukemia.
  3. Angioimmunoblastic T – Cell lymphoma.
  4. Angiocentric lymphoma (NK – T – cell lymphoma).
  5. Intestinal T – cell lymphoma.
  6. Adult T – cell leukemia/lymphoma.
  7. Anaplastic large cell lymphoma.


Lymphoma, Clinical differences in Non Hodgkin's and Hodgkin's lymphoma

Posted Sept. 4, 2016. Pathology Pathology - Lymph node

Non-Hodgkin’s and Hodgkin’s lymphoma can be differentiated and is shown in the tabulated form.

Sign and Symptom Non-Hodgkin’s lymphoma  Hodgkin’s lymphoma
Age  Common at extreme of age Peak at 18 to 38 years. rare at puberty
General condition Often effected Usually excellent
Pruritus usually absent mostly common
Fever Rare in early stage May be present in early stage
Lesion in respiratory and GIT Common Rare
Lymph Nodes  Often symmetrical Often unilateral
Cervical lymph nodes Often bilateral and upper group Often unilateral and lower group
Contiguous spread Rare Common
Response to radiation Immediate Delayed
Epitrochlear lymph nodes  Maybe positive Practically never
Sternal lymph node Practically never Sometimes positive
Leukemic phase May be seen Absent
Extranodal involvement Common Uncommon


Spleen Tumors

Posted Sept. 4, 2016. Pathology Pathology - Lymph node

Tumors of the spleen may be benign and malignant.

Benign tumors :

  1. Benign cyst of Echinococcus.
  2. Mesothelium lined inclusion cyst.
  3. The false cyst which has no lining and this may be encapsulated hematoma.
  4. Rarely may be a hemangioma.

Malignant tumors:

Primaries are Non-Hodgkin’ lymphoma (NHL) and Hodgkin’s lymphoma (HD)>.

Secondary involvement is by the NHL and HD.



Spleen, Hypersplenism , Splenomegaly

Posted Sept. 3, 2016. Pathology Pathology - Lymph node

Hypersplenism is characterized by a triad of :

  1. Splenomegaly
  2. There is a decreased number of RBCs, WBCs, Platelets or combination of these three elements.
  3. Above deficiency of the cells can be corrected by splenectomy.

Mechanism of hypersplenism:

  1. This is uncertain but there are postulates.
  2. This may be due to increased sequestration.
  3. This may be due to lysis of the cells by macrophagic cells.


Etiological classification

1. Infections: There is enlargement of the spleen in acute pyogenic infection. In septicemia, the spleen is enlarged and called septic spleen.

While non-pyogenic bacteria are Tuberculosis, Typhoid, Brucellosis, and Sarcoidosis.


B = Brucellosis       E = Echinococcus      S = Syphilis and Subacute bacterial endocarditis         T 4 = T.B, Typhoid, Toxoplasmosis and Trypanosomiasis

C = CMvirus M = Malaria   H = Histoplasmosis           K = Kala-azar  I = Infectious mononucleosis.

2. Circulatory disturbance: Persistent or chronic venous congestion leads to congestive splenomegaly. This is due to the portal or splenic vein hypertension.

  • Right heart causes are a chronic congestive failure, Rarely the weight is more than 500 gram.
  • Cirrhosis will lead to increased portal vein pressure due to fibrosis. Massive enlargement 1000 to 5000 grams.
  • Portal vein or splenic vein thrombosis may be seen in pylephlebitis or in carcinoma of stomach and pancreas.

3. Storage diseases: This  may be due to :

  1. Amyloidosis and it gives rise to Sago's spleen.
  2. Lipid storage diseases are Familial hyperlipidemia like: 
    1. Deficiency of alpha-lipoprotein.
    2.  Poorly controlled diabetes.
    3. Hypothyroidism.
    4. Prolonged obstructive jaundice.

Hereditary causes are :

  • Gaucher's disease.
  • Niemann Pick disease.
  • Glycogen storage disease.

4. Neoplasm :

  1. Primary causes are rare benign tumors like Fibroma, Osteoma, Chondroma, and cyst.
  2. Primary malignant tumors are Non-Hodgkin's lymphoma and Hodgkin's lymphoma.
  3. Secondary tumors are lymphomas and rarely carcinoma and sarcoma.

5. Blood disorders :

  1. Primary causes lead to anemia, thrombocytopenia, and leucopenia.
  2. Secondary causes are hemolytic anemia, Idiopathic thrombocytopenia (ITP), leukemia and lymphoma infiltrate, chronic marrow failure like myeloid metaplasia.

6. Immunological conditions like Rheumatoid arthritis and systemic lupus erythematosus (SLE).

7. Splenic infarct in early-stage leads enlargement of the spleen. Later on, fibrosis may bring it back to normal size.

Causes are :

  1. Occlusion of a major splenic artery or branch due to emboli from the heart.
  2. Septic infarct in infective endocarditis.
  3. The Less common cause is local thrombosis in myeloproliferative disorders and sickle cell anemia.


Spleen Part 1

Posted Sept. 2, 2016. Pathology


  1. Its weight is 150 grams and measuring 12×7×3 cms.
  2. It has thin capsules which consists of connective tissues.
  3. There are no smooth muscles in the capsules. So spleen has no contractile function.
  4. There are grey specks areas  called splenic or malpighian follicles. This is called white pulp.
  5. While mononuclear phagocytic system and sinusoid is called Red pulp.
  6. There are two circuits of circulation :
  7. Open circuit is slow. There are thin sinusoids called cords of Billroth. These are part of Red pulp. These splenic cords consists of net work of macrophagic cells and this functional and physical filter.
  8. Closed circuit is fast. It has afferent artery converting into vein.

Functions of spleen

  1. Filtration : 1/120 RBC dies every day. This death takes place in 50% in the spleen.
  2. Culling : This destruction and removal of abnormal RBCs and antibody coated cells.
  3. Pitting : This is removal of inclusion like siderotic granules, Heinz bodies, and Howell Jowel bodies.
  4. Phagocytosis : Other particulate material like bacteria, viruses, carcinoma cells, macromolecule of Gaucher's and Niemann Pick disease are removed by phagocytosis.
  5. Major secondary organ : In immune system it's role is both in humoral and cellular immunity.
  6. Source of lymphoid cells : There may be extramedullary hematopoiesis, called myeloid metaplasia.
  7. Storage site : It stores platelets 30 to 40%. In case of enlargement of spleen, this may reach to 80 to 90%.
    1. There are 30 to 40 ml of RBCs and it increases in case of splenomegaly.


Work-up of Lymphoma case

Posted Sept. 2, 2016. Pathology

1. Blood work up includes:

    • Total leucocytes (TLC).
    • Differential leucocyte count (DLC).
    • Hemoglobin
    • Erythrocyte sedimentation rate (ESR)
    • Platelet count.

2 Bipedal lymphangiogram. This is done for iliac and para aortic lymph nodes.

3. Staging laparotomy : Laparoscopy can be done for  splenectomy, liver biopsy, abdominal lymph nodes and bone marrow biopsy.

4.Clinical Examination : Do careful examination of lymph node, spleen, liver and etc.

5. Biochemical tests are needed are Liver function test (LFT) and lactate dehydrogenase (LDH).

6. Ultrasonography , CT scan and MRI are advised for further work up.

7. Advised liver and spleen scan.


25% positive in nonpalpable spleen by the pathologist.

50% negative in palpable spleen by the pathologist.

Bone Marrow

9 to 29% may show in the form of aggregates or diffuse infiltrate.