Wednesday, April 15 Lecture

Wednesday’s lecture covered the last topic of the cardiovascular system (how fetal blood circulation differs from that of an adult, and the changes in a fetal heart after birth) as well as part of the lymphatic and immune system.  Lymph fluid is created from the blood plasma that leaks out of blood capillaries into tissues to become interstitial fluid.  The lymph moves through capillaries (which are single layers of simple squamous epithelium and fenestrated for the movement of small particles) then into lymphatic vessels (which are larger in size).  The lymph is filtered through lymph nodes that lie along lymph vessels.  There are three major clusters of lymph nodes in the cervical, axillary, and inguinal regions (where pathogens can more easily enter the body).  The lymph is then dumped into the venous blood via the thoracic and lymphatic ducts through the left and right subclavian veins, respectively. 

Lymph nodes house attacking “units” for the immune system.  Just under the outer capsule, the subcapsular sinus is filled with lymph fluid and contains resident macrophages, which are APC’s or antigen-presenting cells.  They identify self from non-self cells in order to determine an immune response.  Self proteins contain MHC-1, or a major histocompatibility complex (which is also used to determine tissue compatibility in organ donations).  MHC-II’s are released when a macrophage, B-cell, or eosinophil undergoes phagocytocis.  Transient macrophages move throughout the lymph fluid and are specialized in determining if anything is foreign.

There are specific steps that occur in response to the invasion of a foreign cell:

1)      Chemotaxis—chemicals are released the attract WBC’s (especially macrophages) to the damaged tissue.  (example: prostaglandins, histamine, bradykinin, collectively known as chemokines that induce vasodilation)

2)      Adhesion—margination is when ICAM’s, or intercellular adhesion molecules, are formed on a WBC, and pavementing is the tethering of the matching ICAM’s to the vessel wall to slow down the WBC and allow it to move out of the blood vessel.

3)      Diapedesis—WBC’s move through the blood vessel wall and extend “arms” to create a pseudopod.  They then ingest the microbe and fuse with other pseudopods to make a phagosome.  The phagosome fuses with already present lysosomes to create a phagolysosome in which oxygen free radicals destroy the microbe.

Lastly, we covered the topic of complement protein activation, the activation sequence to activate a MAC (membrane attack complex) and the by-products that become potent vasodilators.

 

One topic that was peculiar to me was the drainage of lymph fluid into the venous blood.  The right lymphatic duct drains lymph from the upper right quadrant of the body into the right subclavian vein and the thoracic duct is responsible for the remaining 75 % of the lymph fluid.  I wonder what the anatomical significance of this unbalance is.  I thought it could be because of vital organs that lie in the 75 % of the body drained by the thoracic duct.  Although there would be more lymph fluid that could be “infiltrated by a microbe,” there would also be more WBC’s available to attack the pathogens.  The right lymphatic duct doesn’t seem to be as important, considering that the only vital organ it drains is the right half of the brain.  In fact, some individuals do not even have a right lymphatic duct and instead the lymph fluid is drained directly into the veins of the neck.  I could not find a valid explanation for the disparity between the two draining ducts so if anyone has any information it would be appreciated!