SPLEEN STRUCTURE
FUNCTIONS
PRESENTOR: DR.HARSHA PG1
MODERATOR: DR PRANATHI(SR)
SPLEEN
• Spleen is reticuloendothelial organ ,that has its embryologic origin in
dorsal mesogastrium about 5weeks gestation .
• Adult location :in left upper quadrant attached to stomach via
gastrolineal ligament and to kidney by lienorenal ligament.
• It is largest lymphoid organ.
• It is encapsulated organ.
LOCATION
• It is a wedge shaped organ
lying mainly in the left
hypochondrium and partly in
the epigastrium
• It is wedged between the
fundus of the stomach and
diaphragm
• Tetrahedral in shape
SPLEEN:
HISTOLOGY
• In cut section, spleen looks like a
red sea with white spots in it.
• Composed of –
• Red pulp = 75%
• White pulp = 25%
RED PULP
• The red pulp is primarily involved in:
• • Filtering the blood
• • Recycling old or damaged red blood cells (RBCs)
• • Storing platelets
• • Acting as a blood reservoir (in some animals)
RED PULP
• The red pulp consists of:
• 1. Splenic Sinusoids:
• • Blood-filled channels lined by specialized endothelial cells (stave
cells).
• • These sinusoids allow selective passage of healthy blood cells,
while old or damaged ones are trapped.
• 2. Splenic Cords (Cords of Billroth):
• • Located between sinusoids.
• • Made of reticular connective tissue rich in macrophages,
monocytes, plasma cells, and blood cells (RBCs, platelets, etc.).
• • Macrophages here phagocytose old or abnormal RBCs and
pathogens.
WHITE PULP
• Composed of lymphoid tissue (similar to lymph nodes).
• • Involved in the production and activation of lymphocytes
(especially B and T cells).
• • Acts like a filter for pathogens in the blood.
WHITE PULP
• White pulp is organized around central arteries and has three main components:
• 1. Periarteriolar Lymphoid Sheath (PALS):
• • Cylindrical sheath of T lymphocytes surrounding the central artery.
• • Site of T-cell activation.
• 2. Lymphoid Follicles (Malpighian corpuscles):
• • Found adjacent to PALS.
• • Rich in B lymphocytes.
• • Can develop germinal centers when activated (e.g., during infection) → site
of B-cell proliferation and antibody production.
• 3. Marginal Zone:
• • Lies between white and red pulp.
• • Contains antigen-presenting cells (e.g., dendritic cells, macrophages).
• • Important for trapping antigens and initiating immune responses.
BLOOD SUPPLY
• Blood supply : SPLENIC ARTERY
• Venous drainage : SPLENIC VEIN
• Nerve supply : It has only sympathetic supply(Vasomotor)
• Lymphatic supply : via SUBCAPSULAR LYMPHATIC PLEXUS into
SPLENIC HILAR LYMPH NODES and finally into CELIAC NODES
FUNCTIONS
• Maintanence of quality control over erythrocytes in red pulp by
removal of senescent and defective red blood cells.
• Synthesis of antibodies in white pulp.
• Removal of antibody coated bacteria and antibody coated blood cells
from circulation.
• Spleen is in portal circulation.
• Blood flows into spleen at rate of 150ml/min through splenic
artery ,ultimately ramifies into central arterioles.
• Some blood goes from arterioles to capillaries and then to splenic
veins and out of spleen.
• Majority of the blood from central arterioles flows into macrophages
lined sinuses and cords.
• Blood entering sinuses reenters the circulation through the splenic
venules.
• To return to circulation ,blood cells in cords must squeeze through
slits in cord lining to enter the sinuses that lead to venules.
• Old and damaged erythrocytes are less deformable and are retained
in cords ,where they are destroyed and their components recycled.
• Red cell inclusions such as parasites,nuclear residua(Howell-jolly
bodies) or denatured hemoglobin( Heinz bodies) are pinched off in
process of passing through the slits a process called Pitting.
• Culling of dead and damaged cells and pitting of cells with inclusions
appear to occur without delay .
• Because the blood transit time through the spleen is only slightly
slower than in other organs.
ADAPTIVE FUNCTIONS OF SPLEEN:
• 1)Clearance of bacteria and particulates from blood.
• 2)Generation of immune responses to certain pathogens.
• 3)Generation of cellular components of blood (extramedullary
hematopoiesis)
• Normal human Spleen contains approximately 1/3rd
of the total body
platelets and significant number of marginated neutrophils.
APPROACH TO SPLENOMEGALY:
• Heavy sensation in LUQ.
• Massive splenomegaly causes early satiety.
• Pain may result in acute swelling of spleen with stretching of capsule.
• SUBACUTE BACTERILA ENDOCARDITIS can present with severe LUQ
and pleuritic chest pain may accompany thromboembolic occlusion of
splenic blood flow.
• PALPABLE SPLEEN is major physical sign suggesting enlargement of
spleen.
• Normal spleen1) weighs <250 gms
• 2)decreases in size with age
• 3)lies within rib cage,
• 4)maximum cephalocaudal diameter of13cm by USG
SPLENOMEGALY:
• 1)Enlargement due to increased demand for splenic function.
• 2)Enlargement due to abnormal splenic or portal blood flow.
• 3)Infiltration of spleen.
• 4)Infiltration.
CLASSIFICATION OF SPLENOMEGALY
• Mild - Spleen palpable but not extending below the umbilicus
• Moderate - Extends below the umbilicus but not to pelvis
• Massive - Extends into pelvis or across midline
SPLENOMEGALY GROUPED CAUSES
MASSIVE SPLENOMEGALY:
TROPICAL SPLENOMEGALY
• Also known as HYPER REACTIVE MALARIAL SPLENOMEGALY.
• One of the leading causes of splenomegaly in malaria endemic areas.
• PATHOLOGY:
• 1) Aberrant immune response to chronic antigenic
stimulationexcessive production of immunoglobulins especially of
IgM TYPEthese Ig aggregate to form macroglobulins i.e high
molecular weight immune complexes.
DIAGNOSTIC CRITERIA:
• MAJOR CRITERIA:
• 1)Persistent gross splenomegaly extending more than 10 cm below
costal margin without any apparent cause.
• 2)Elevated anti malarial antibody titre ,IGM>2SD above the mean
value
• 3)Favourable response to long term malaria prophylaxis.
MINOR CRITERIA:
• Hepatic sinusoidal lymphocytosis.
• normal cellular or humoral response to other antigenic stimulus
• Hypersplenism
• Lymphocyte proliferation
• occurrence in family and tribes.
CLINICAL FEATURES
• Abdominal swelling
• Dragging sensation in abdomen
• Acute left sided abd pain secondary to splenic infarction.
• Increased susceptibility to infections
• Bleeding manifestations
• ON PHYSICAL EXAMINATIONmassive splenomegaly often extending
across the midline to right side of abdomen or downward into RIF
LAB FINDINGS
• Pancytopenia especially anemia.
• Reticulocytosis.
• Thin and thick smear examined under geimsa stain.
• Increased bilirubin
• Sinusoidal lymphocytosis on liver biopsy.
MANAGEMENT
• Enlarged spleen regresses over period of months with effective
antimalarial prophylaxis.
• Drugs like chloroquine,mefloquine.
• FOLLOWING ARE NOT INDICATED:
• Splenectomy
• Splenic irradiation
• Antimitotic therapy
CONGENITAL ANOMALIES OF SPLEEN
1. ASPLENIA – Congenital absence of spleen
• - Autosomal recessive condition
• 2. POLYSPLENIA/ ACCESSORY SPLEEN
• 3. WANDERING SPLEEN – The ligaments of spleen may be abnormally
long or too wide or may be absent which provides great mobility to
spleen
HYPERSPLENISM VS SPLENOMEGALY
POST SPLENECTOMY VACCINATION
THANK YOU

Spleen structure and function,anatomy ppt

  • 1.
  • 2.
    SPLEEN • Spleen isreticuloendothelial organ ,that has its embryologic origin in dorsal mesogastrium about 5weeks gestation . • Adult location :in left upper quadrant attached to stomach via gastrolineal ligament and to kidney by lienorenal ligament. • It is largest lymphoid organ. • It is encapsulated organ.
  • 3.
    LOCATION • It isa wedge shaped organ lying mainly in the left hypochondrium and partly in the epigastrium • It is wedged between the fundus of the stomach and diaphragm • Tetrahedral in shape
  • 4.
  • 5.
    HISTOLOGY • In cutsection, spleen looks like a red sea with white spots in it. • Composed of – • Red pulp = 75% • White pulp = 25%
  • 6.
    RED PULP • Thered pulp is primarily involved in: • • Filtering the blood • • Recycling old or damaged red blood cells (RBCs) • • Storing platelets • • Acting as a blood reservoir (in some animals)
  • 7.
    RED PULP • Thered pulp consists of: • 1. Splenic Sinusoids: • • Blood-filled channels lined by specialized endothelial cells (stave cells). • • These sinusoids allow selective passage of healthy blood cells, while old or damaged ones are trapped. • 2. Splenic Cords (Cords of Billroth): • • Located between sinusoids. • • Made of reticular connective tissue rich in macrophages, monocytes, plasma cells, and blood cells (RBCs, platelets, etc.). • • Macrophages here phagocytose old or abnormal RBCs and pathogens.
  • 8.
    WHITE PULP • Composedof lymphoid tissue (similar to lymph nodes). • • Involved in the production and activation of lymphocytes (especially B and T cells). • • Acts like a filter for pathogens in the blood.
  • 9.
    WHITE PULP • Whitepulp is organized around central arteries and has three main components: • 1. Periarteriolar Lymphoid Sheath (PALS): • • Cylindrical sheath of T lymphocytes surrounding the central artery. • • Site of T-cell activation. • 2. Lymphoid Follicles (Malpighian corpuscles): • • Found adjacent to PALS. • • Rich in B lymphocytes. • • Can develop germinal centers when activated (e.g., during infection) → site of B-cell proliferation and antibody production. • 3. Marginal Zone: • • Lies between white and red pulp. • • Contains antigen-presenting cells (e.g., dendritic cells, macrophages). • • Important for trapping antigens and initiating immune responses.
  • 10.
    BLOOD SUPPLY • Bloodsupply : SPLENIC ARTERY • Venous drainage : SPLENIC VEIN • Nerve supply : It has only sympathetic supply(Vasomotor) • Lymphatic supply : via SUBCAPSULAR LYMPHATIC PLEXUS into SPLENIC HILAR LYMPH NODES and finally into CELIAC NODES
  • 12.
    FUNCTIONS • Maintanence ofquality control over erythrocytes in red pulp by removal of senescent and defective red blood cells. • Synthesis of antibodies in white pulp. • Removal of antibody coated bacteria and antibody coated blood cells from circulation. • Spleen is in portal circulation. • Blood flows into spleen at rate of 150ml/min through splenic artery ,ultimately ramifies into central arterioles. • Some blood goes from arterioles to capillaries and then to splenic veins and out of spleen.
  • 13.
    • Majority ofthe blood from central arterioles flows into macrophages lined sinuses and cords. • Blood entering sinuses reenters the circulation through the splenic venules. • To return to circulation ,blood cells in cords must squeeze through slits in cord lining to enter the sinuses that lead to venules. • Old and damaged erythrocytes are less deformable and are retained in cords ,where they are destroyed and their components recycled.
  • 15.
    • Red cellinclusions such as parasites,nuclear residua(Howell-jolly bodies) or denatured hemoglobin( Heinz bodies) are pinched off in process of passing through the slits a process called Pitting. • Culling of dead and damaged cells and pitting of cells with inclusions appear to occur without delay . • Because the blood transit time through the spleen is only slightly slower than in other organs.
  • 16.
    ADAPTIVE FUNCTIONS OFSPLEEN: • 1)Clearance of bacteria and particulates from blood. • 2)Generation of immune responses to certain pathogens. • 3)Generation of cellular components of blood (extramedullary hematopoiesis) • Normal human Spleen contains approximately 1/3rd of the total body platelets and significant number of marginated neutrophils.
  • 17.
    APPROACH TO SPLENOMEGALY: •Heavy sensation in LUQ. • Massive splenomegaly causes early satiety. • Pain may result in acute swelling of spleen with stretching of capsule. • SUBACUTE BACTERILA ENDOCARDITIS can present with severe LUQ and pleuritic chest pain may accompany thromboembolic occlusion of splenic blood flow.
  • 18.
    • PALPABLE SPLEENis major physical sign suggesting enlargement of spleen. • Normal spleen1) weighs <250 gms • 2)decreases in size with age • 3)lies within rib cage, • 4)maximum cephalocaudal diameter of13cm by USG
  • 20.
    SPLENOMEGALY: • 1)Enlargement dueto increased demand for splenic function. • 2)Enlargement due to abnormal splenic or portal blood flow. • 3)Infiltration of spleen. • 4)Infiltration.
  • 21.
    CLASSIFICATION OF SPLENOMEGALY •Mild - Spleen palpable but not extending below the umbilicus • Moderate - Extends below the umbilicus but not to pelvis • Massive - Extends into pelvis or across midline
  • 23.
  • 24.
  • 25.
    TROPICAL SPLENOMEGALY • Alsoknown as HYPER REACTIVE MALARIAL SPLENOMEGALY. • One of the leading causes of splenomegaly in malaria endemic areas. • PATHOLOGY: • 1) Aberrant immune response to chronic antigenic stimulationexcessive production of immunoglobulins especially of IgM TYPEthese Ig aggregate to form macroglobulins i.e high molecular weight immune complexes.
  • 26.
    DIAGNOSTIC CRITERIA: • MAJORCRITERIA: • 1)Persistent gross splenomegaly extending more than 10 cm below costal margin without any apparent cause. • 2)Elevated anti malarial antibody titre ,IGM>2SD above the mean value • 3)Favourable response to long term malaria prophylaxis.
  • 27.
    MINOR CRITERIA: • Hepaticsinusoidal lymphocytosis. • normal cellular or humoral response to other antigenic stimulus • Hypersplenism • Lymphocyte proliferation • occurrence in family and tribes.
  • 28.
    CLINICAL FEATURES • Abdominalswelling • Dragging sensation in abdomen • Acute left sided abd pain secondary to splenic infarction. • Increased susceptibility to infections • Bleeding manifestations • ON PHYSICAL EXAMINATIONmassive splenomegaly often extending across the midline to right side of abdomen or downward into RIF
  • 29.
    LAB FINDINGS • Pancytopeniaespecially anemia. • Reticulocytosis. • Thin and thick smear examined under geimsa stain. • Increased bilirubin • Sinusoidal lymphocytosis on liver biopsy.
  • 30.
    MANAGEMENT • Enlarged spleenregresses over period of months with effective antimalarial prophylaxis. • Drugs like chloroquine,mefloquine. • FOLLOWING ARE NOT INDICATED: • Splenectomy • Splenic irradiation • Antimitotic therapy
  • 31.
    CONGENITAL ANOMALIES OFSPLEEN 1. ASPLENIA – Congenital absence of spleen • - Autosomal recessive condition • 2. POLYSPLENIA/ ACCESSORY SPLEEN • 3. WANDERING SPLEEN – The ligaments of spleen may be abnormally long or too wide or may be absent which provides great mobility to spleen
  • 33.
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  • 35.