Lymphatic System
Lymphatic System
• IMMUNITY/DEFENSE
-Fluids from all capillary beds are
filtered
-Immune cells stand ready to respond
to foreign cells or chemicals
encountered
-Lymph nodes filter the lymph
Microorganisms and other foreign
substances are filtered:
• Has openings; take note of the
-from LYMPH: by LYMPH NODES
overlapping arrangement of the simple
-from BLOOD: by SPLEEN
squamous epithelium cells
• Collecting ducts: (Right & Thoracic)
-Right Lymphatic Duct – receives lymph from R arm,
R side of head and thorax; empties into Right
= subclavian vein
- the lymphatic vessels from the upper right limb and
right half of the head, neck and chest:
= forms & enters to the Right Lymphatic Duct;
= empties to the Right Subclavian Vein
LYMPHATIC VESSELS
LYMPH NODE
• Lymph nodes - only organs that filter lymph
(whereas, the spleen filters the blood)
• Fewer efferent vessels, slows flow through node
• Capsule – dense connective tissue that TONSIL
surrounds/envelopes each lymph node
-looks like an orange peel
- gives off trabeculae, divides node into compartments
containing stroma (reticular CT) and parenchyma
(lymphocytes and APCs) subdivided into cortex
(lymphatic nodules) and medulla (NOT INCLUDED SA LEC)
• Trabeculae – subdivide lymph nodes into
compartments containing lymphatic tissues and
sinuses
-Looks like the wedges in an orange
- has afferent vessels: Afferent lymphatic vessels
flow into a lymph node and carry unfiltered lymph
fluid (whereas, Efferent lymphatic vessels flow out
of a lymph node and carry filtered lymph fluid)
• Lymphatic tissue- (inside trabeculae;
compartments of lymph nodes) consists of
lymphocytes and other cells that can form
aggregations of tissue
• Lymphatic sinuses – spaces between lymphatic
tissue; contain macrophages on a network of fibers 5
• Covered by epithelium
3 SUPERFICIAL AGGREGATIONS OF LYMPH NODES • Pathogens get into tonsillar crypts and
*superficial, since it is on the top; can be touched and encounter lymphocytes
-invading pathogens: for example, there is a
felt when there’s an infection or
bacteria which tries to invade the body, it will
LYMPHADENOPATHY* go to the tonsillar crypt, then will meet with
lymphocytes, where they will be attacked
1. INGUINAL NODES (HITA OR THIGH PART)
2. AXILLARY NODES
3. CERVICAL NODES
L OCATION OF TONSILS HISTOLOGY OF THYMUS
(diff types of tonsils: )
• Palatine tonsils
- a.k.a. “tonsils” since it is the one visible when
one has tonsillitis
- pair at posterior margin of oral cavity
- most often infected
- stays behind tonsillar pillars
Grading of tonsillitis:
-GRADE 1: if it goes beyond the tonsillar pillar
-GRADE 2: reaches/midway the uvula (ngala-ngala) -each lobe of the thymus is surrounded by a thin
-GRADE 3: touches the uvula connective tissue: CAPSULE
-GRADE 4: kisses the uvula (tonsils touch each other) - TRABECULAE: forms the capsule and divides it into lobes
-occurs due to bacterial infection -lymphocytes are numerous and form cortex,
- if experiencing tonsillitis more than 6 times a year, which are dark-staining areas: CORTEX
doctor will recommend it to be removes, since more
complications can happen SPLEEN
• Lingual tonsils -graveyard of dead RBCs
- pair at root of tongue - filters the blood
- easily detects the infections or antigens /
• Pharyngeal tonsil (adenoid)
invading pathogens easily
- single tonsil on wall of pharynx
- is sometimes removed under T and A • Parenchyma appears in fresh specimens as:
-TNA: Tonsillectomy and Adenoidectomy - red pulp: sinuses filled with erythrocytes
- “-ectomy: removal” - white pulp: lymphocytes, macrophages;
- Tonsillectomy: removal of tonsils surrounds small branches of splenic artery
- Adenoidectomy: removal of adenoids Functions:
- blood production in fetus
THYMUS - blood reservoir (receptacle /vessel of blood); so
that in times of emergency, such as hemorrhage,
the spleen would contract, and would release the
blood stored there, as an additional blood supply)
- RBC disposal (has a life span: 120 days to live)
-if RBCs die, they go to the spleen
- immune reactions: spleen filters blood, quick to detect
antigens
THYMUS
• Capsule gives off trabeculae, divides parenchyma into
lobules of cortex and medulla
• Reticular epithelial cells
- form blood thymus barrier in cortex
• isolates developing T lymphocytes from foreign antigens, so
that it will mature
• site for maturation of T cells (para di maattack han bad orgs.)
-secretes hormones (thymopoietin, thymulin and thymosins)
• to promote development and action of T lymphocytes in
combating against infection
• Very large in fetus; after age 14 begins involution
- thymus continues to increase in size til the 1st year of birth
- remains on the same size as the person grows older
- at age 60, the thymus starts to decrease in size (obvious)
- in elderly (by 40 years of age) mostly fatty and fibrous
tissue; replaced by adipose tissue
PHAGOCYTIC CELLS
• Phagocytosis- the ingestion
(eating up/cell eating) and
destruction of particles by cells
called phagocytes
a. Neutrophils
b. Macrophages
NEUTROPHILS
• Phagocytize bacteria
• Create a killing zone
-degranulation
* lysosomes discharge into tissue
fluid
• FIRST cell to enter infected tissues
from the blood in large numbers (the
first one to respond, wherein they kill
and eat the bacteria)
• After eating and engulfing the
INTERFERONS bacteria, neutrophils often DIE after
phagocytizing a single microorganism
• Secreted by certain cells invaded by viruses and will form PUS (nana made up of:
-generalized protection debris, dead tissues, dead bacteria
-diffuse to neighboring cells and stimulate them to and neutrophils)
produce antiviral proteins • Neutrophils die to save one from
-activate natural killer cells and macrophages infection (manifested in NANA/PUS)
*destroy infected host cells (extra)
*stimulate destruction of cancer cells -respiratory burst
• Proteins secreted by the body, to protect itself from *toxic chemicals are created
viral infections (O2.-, H2O2, HClO)
• Specifically, these are the ones giving the
body protection against viral infections & MONOCYTES
viruses • Circulating precursors to macrophages
• Interferons don’t protect the cells that (before macrophages form, there are
produce them. It is NOT self-serving. Rather, it monocytes as precursors)
will bind to the surface of the neighboring cell • Specialized macrophages found in specific
where they stimulate to produce antiviral localities
proteins. -dendritic cells (found in)
• The antiviral proteins are the ones which * epidermis, oral mucosa, esophagus,
inhibit viral reproduction by preventing the vagina, and lymphatic organs -they are
production of a new viral nuclei and proteins strategically placed on areas which will
• Some interferons play a role in the activation serve as point of entry of microorganisms
of immune cells such as macrophages and - microglia (CNS)
natural killer cells. - alveolar macrophages (lungs)
- hepatic macrophages (liver)
*a.k.a Kupffer cells
MACROPHAGES LYMPHOCYTES
• “macro“ means BIG; capable of eating up larger • Circulating blood contains
particles • 80% T cells (the ones that mature sa thymus)
• Monocytes that leave the blood, enter tissues and • 15% B cells (B lymphocytes)
enlarge about FIVEFOLD (& become a macrophage) • 5% NK cells (natural killer cells)
• Monocytes and macrophages form the mononuclear NATURAL KILLER CELLS
phagocytic system • Type of lymphocyte produced in the red
• “mono” since they’re phagocytes with a single, bone marrow
unlobed nucleus • Recognize classes of cells such as tumor cells
• Found in the CNS (microglia), lungs (dust cells), or virus infected cells in general
liver (Kupffer cells) • Do not exhibit a memory response, only
• Appear in the infected tissues after neutrophils and capable of recognizing whether cells are
are responsible for the cleanup of dead neutrophils tumor cells, virus infected cells (viruses need
and other cellular debris (After the attack and death a cell for it to survive, replicate and
of neutrophils, macrophages/mononuclear reproduce) (so a virus on a table is not yet
phagocytic system will appear later on and are functional, unless it attaches to a human
responsible for cleaning up the warzone; nauurhi cell/other cells)
pag-ulpot)
IMMUNE SURVEILLANCE
• Found in potential entry of microorganisms:
• NK cells
-beneath the skin, mucous membranes, around
-destroy bacteria, transplanted cells, cells
blood and lymphatic vessels
infected by viruses, and cancer cells
* release perforins and granzymes
CELLS OF INFLAMMATION
• Basophils INFLAMMATION (not that bad)
• Eosinophils • Defensive response to tissue injury
• Lymphocytes 1. limits spread of pathogens, then destroys them
(if nahubag, may nacircle ha gilid han
BASOPHILS hubag/circumscribe; so that the lymphocytes,
• Derived from the red bone marrow leukocytes & other cells will go as an aid and kill
• Aid mobility and action of WBCs by release of: it & not escape)
2. removes debris
- histamine (vasodilator) 3. initiates tissue repair
*pinapadako an vessels so that WBCs can enter+move
• Cytokines
• ↑ blood flow to infected tissue - small proteins regulate inflammation
• Increased blood flow to infected tissue is and immunity; include:
IMPORTANT so that the “soldiers of the body” or *interferons, interleukins, tumor necrosis
(WBCs) leukocytes as well as lymphocytes will be Factor (TNF), and chemotactic factors
easily transported to the infected area
• Suffix “-itis” denotes inflammation of specific
- heparin (anticoagulant) organs
• prevents immobilization of phagocytes • (appendicitis – appendix; bronchitis – bronchiole;
• allows the phagocytes to flow glossitis – tongue; prostatitis – prostate;
cystitis - bladder )
EOSINOPHILS • Cardinal signs
• Produces in the red bone marrow 1. Redness (erythema) caused by hyperemia
• Phagocytize antigen-antibody complexes *↑ blood flow = hyperemia
• A.K.A “immune complex” *there is redness due to the increased blood
• Antigen + Antibody = Immune Complex flow on the area, so that WBCs, other soldiers
• An invading pathogen ginkaon han antibody & defenses can enter
*blood contains nutrients & oxygen necessary
• Eats up the antigen-antibody complex
for tissue repair (in times of damage)
• Also part in cleaning up the warzone
*“Rubor” in Latin = redness
• Antiparasitic effects (in times when one has a _______________________________________________________________________________________________
• Eosinophils also reduces the inflammatory response, 4. Pain caused by inflammatory chemicals
since basophils, mast cells and histamine promote (bradykinin, prostaglandins) secreted by
inflammation in order to combat the body against damaged cells, pressure on nerves (due to
protection. TOO MUCH OF SOMETHING IS BAD swelling, it compresses nerve endings = pain)
• Eosinophils control excessive inflammation *”Dolor” in Latin = “pain”
___________________________________________________________________________________________________________________________
5. Loss of function
* “Functio Laesa” in Latin = loss of function
*if your hand is inflamed, you won’t be able to use it
THREE MAJOR PROCESSES OF INFLAMMATION CONTAINMENT AND DESTRUCTION OF PATHOGENS
1. Mobilization of body defenses
(pagsulong han body defenses to the area of injury) • Fibrinogen now in tissue clots, helps in trapping
pathogens (circumscribe/make fence)
2. Containment and destruction of pathogens • Heparin prevents clotting at the site of injury
(masulong through the blood during increased blood -needed since pathogens are in a fluid pocket,
flow; tumor will circumscribe to avoid microorganisms surrounded by a clot, and it allows blood to flow
from escaping; para maattack han mga soldiers) • Chemotaxis
3. Tissue clean-up and repair -leukocytes are attracted to chemotactic
(some of it after inflammation, some have none) chemicals
• Neutrophils are quickest to respond
TYPES OF INFLAMMATION -phagocytosis
-respiratory burst
a. LOCAL INFLAMMATION – confined to a specific area -secrete cytokines for recruitment of
of the body macrophages and neutrophils
-inflammation in the arm, leg -macrophages and T cells secrete colony-
b. SYSTEMIC INFLAMMATION – generally distributed stimulating factor to stimulate leukopoiesis
throughout the body
TISSUE CLEANUP
3 ADDITIONAL FEATURES IN SYSTEMIC
• Monocytes the primary agents of cleanup
INFLAMMATION:
arrive in 8 to 12 hours, become macrophages
1. Red bone marrow produces & releases large -after the war/attack, 8-12 hours later, monocytes
numbers of neutrophils, which promote will arrive to clean up the area and become
phagocytosis macrophages
2. Pyrogens, chemicals released by microorganism, • Edema ↓ venous flow (decreased blood flow),
neutrophils, and other cells, stimulate fever ↑ lymphatic flow (increased lymphatic flow) that
production (pyrogenic material) favors removal of bacteria and debris
3. Decreased blood volume can cause shock and -after inflammation, there will be edema so
death decreased redness and heat
-Increase of lymphatic flow helps in removing the
MOBILIZATION OF DEFENSES
dead bacteria and dead debris
• Kinins, histamine, and leukotrienes are secreted by
• Formation of pus
damaged cells, basophils and mast cells
- mixture of tissue fluid, cellular debris, dying
-stimulate vasodilation that leads to hyperemia
neutrophils and microbes
(increased blood flow)
*causes redness and heat TISSUE REPAIR
* ↑ local metabolic rate (increased consumption of • Blood platelets and endothelial cells in
energy), promotes cell multiplication and healing injured area secrete a cytokine, PDGF, that
*dilute toxins, provides O2, nutrients, waste stimulates fibroblasts to multiply and
removal (to repair tissues that have been damaged) synthesize collagen
- stimulates ↑ permeability of blood capillaries • Facilitated by hyperemia that provides
*allows blood cells, plasma proteins (antibodies, materials needed and heat that increases
complement proteins, fibrinogen) into tissue metabolism
*clotting sequesters bacteria, forms scaffold for -hyperemia is important since it helps in carrying the
tissue repair defenses and RBCs which carry oxygen and nutrients
to the area of injury
• Fibrin clot may provide a scaffold for
Repair (scaffold – forming)
• Pain limits use of body part allowing for
Repair (inflammation has pain due to the
compression of nerve endings and release of some
chemicals; it also functions for us to not move the
area, since if masakit it area, we won’t keep on
moving it; less movement = faster healing; like repair
ha kalsada, di anay pinapagamit para mafix)
FEVER
• Is not an illness per se (per se = itself), which explains
why some doctor’s don’t prescribe medications agad 2. CELL-MEDIATED IMMUNITY
• Defense mechanism; does more good than harm - a type of immune response due to T lymphocyte
-promotes interferon activity activity
-accelerating metabolic rate and tissue repair -Cytotoxic T cells which attack and destroy invading
-inhibiting pathogen reproduction antigens through the release of chemical compounds
• A cytokine, interleukin 1, called a pyrogen on the antigen membrane (ex: injection of a toxin)
-pyrogens cause fever
-secreted by macrophages, stimulates anterior 3. AUTOIMMUNITY
hypothalamus to secrete PGE which resets body -results from the inability of the body to distinguish
thermostat higher cell from non-cell, causing an immune system to
> 40°C may cause delirium carry out immune response against the normal cells
43°C - 46°C may cause coma-death -Self-destruction (own cells kill own cells)
-not that good since it can lead to autoimmune disease
• Stages of fever:
• onset, stadium, defervescence
• Antigens are substances that stimulate adaptive
immune responses
1. FOREIGN ANTIGENS – introduced from the
outside of the body
2. SELF ANTIGENS – molecules produced by the
person’s body that stimulate an immune response
• Autoimmune disease
-results when self-antigens stimulate unwanted
destruction of normal tissue
TYPES OF IMMUNITY:
1.Humoral Immunity
-is created by an antibody production of B lymphocyte
involvement
a. Primary Response
-the first time that the antigen enters the body, it is
identified by T lymphocytes
-there will be B cell differentiation
-growth will begin
-in 6 days, immunoglobulin M antibodies can already be
measured in the bloodstream IgA – protects person from infection; important in the respiratory
-by day 10, production of immunoglobulin G, which tract, genital tract and urinary system; breast milk is rich in
helps in combating against infection begins, which immunoglobulin A, which is good for babies and adds protection;
would last for several weeks passed from the mother to the baby through breast milk
b. Secondary Response
- second time of entry of the microorganism IgD - also functions as antigen binding receptors of B cells
- thus, the body can produce antibodies immediately due
to the memory cells from previous encounter IgE – Eosinophil levels are high during parasitic activities sa body
c. Complement Activation
IgG - is passed to the fetus via the placenta to the baby; initially, a
- composed of 20 different proteins; usually non-
fetus once born has an immature immune system, so IgG from the
functional molecules until activated by an antigen-antibody
mother can help through the placenta
contact, it will begin a cascade of reaction; one complement
will activate the other, then so on & so forth
IgM – the first to be produced and is made at the fetus
-cascade of response: there is increased vascular
by 5 months of age
permeability, smooth muscle contraction, chemotaxis,
phagocytosis, etc.
• T lymphocytes PASSIVE AND ACTIVE IMMUNITY HAVE (4) FOUR TYPES:
-account for 70-80% of blood lymphocytes • NATURAL
-responsible for cell-mediated immunity -natural active, natural passive
-produced in bone marrow, but mature sa thymus gland -natural: natural happening or event in the body
THREE (3) SUBTYPES OF T LYMPHOCYTES: NATURAL ACTIVE IMMUNITY:
1. CYTOTOXIC (Killer) T cells – bind to surface of antigen and *Natural = involuntary action of body, natural la
directly destroys cell membrane and phagocytize *Active = body develops antibodies as it encounters a virus
2. HELPER T cells (CD4) – stimulate B lymphocytes to divide *has memory cells so that next time, if the virus is encountered
and mature into plasma cells & begin secreting Ig by the body, antibodies will already be available and be easily
(immunoglobulin); help in Ig formation activated due to previous encounter
-Helper T cells (CD4) stimulate B lymphocytes Ex: previous exposure to an antigen; like experience
- B lymphocytes help form immunoglobulin/antibodies of chicken pox
-In patients with HIV/AIDS, the CD4 cells are directly NATURAL PASSIVE IMMUNITY:
attacked by the virus *Natural = happens in a natural course
-Thus, they lack CD4 cells, thus also lack B lymphocytes, and *Passive = body receives antibodies
thus lack immunoglobulin/ antibodies; if lacking antibodies, *only temporary
then one will be prone to infection, even a simple infection *usually after 2 months, it wears off; explains why
can be full-blown; person becomes babies need to be immunized/vaccinated at once
*“IMMUNOCOMPROMISED” = immune system is not Ex: Transfer of IgG (immunoglobulin G) from the mother to
functioning properly the fetus via the placenta; IgA (immunoglobulin A) from the
-No one dies of HIV/AIDS per se, but they die due to mother to the baby via the breast milk, since babies still
complications like infection; immunocompromised people have weak immune systems, and need great protection (to
must avoid crowded places, limit interactions for them to some diseases)
not be prone to infections and diseases
3. SUPPRESSOR T cells – decrease (controls) production of
immune globulin against specific antigen • ARTIFICIAL
-artificial active, artificial passive
ACTIVATION & MULTIPLICATION OF LYMPHOCYTES -artificial: synthetic or gintutuyo na happening
1.Antigen Recognition -actins are done for the body to produce antibodies
*B-cell receptors *and each receptor would artificially or synthetically
*T-cell receptors bind to a SPECIFIC antigen* ARTIFICIAL ACTIVE IMMUNITY
note that ANTIGENS are the INVADING MICROORGANISMS *Artificial = intended an way, not acquired naturally
-B-cell and T-cell receptors will receive and bind to antigens, *Active = body produces antibodies
and will recognize them for body defenses to occur
Ex: Immunizations; BCG (Bacille Calmette-Guerin) for
*Major Histocompatibility Complex (MHC) tuberculosis against mycobacterium tuberculosis; live or
-molecules, glycoproteins that have binding sites to antigen not, attenuated (weakened) bacteria is given to produce
-bind to antigen receptors: B-cell and T-cell receptors and antibodies, not antibodies per se, so that when the virus
stimulate them is encountered again, the body can recognize it and
-acts as a serving tray for antigens prepare antibodies due to memory cells
-Helper T cells will come to the rescue
-Suppressor T cells will control ARTIFICIAL PASSIVE IMMUNITY
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*Artificial = artificially-prepared through injections
*Costimulation – cytokines (needed to achieve costimulation) *Passive = toxoids/antibodies are received
-costimulation by a second signal is required; can be achieved Ex: injections for tetanus toxoid and (ATS) Anti-
through cytokines, which are proteins or peptides secreted by tetanus Serum; body only receives them & NOT forms
one cell as a regulator of neighboring cells them
LYMPHOCYTE PROLIFERATION
DIFFERENCE OF PASSIVE AND ACTIVE IMMUNITY:
• Interleukin 2 receptors and interleukin are produces
• Interleukin 2 binds to the receptors and stimulate the • ACTIVE IMMUNITY– body forms & develops antibodies
helper T cells to divide • PASSIVE IIMUNITY – body receives antibodies