• HOW DOES IT TIE IN TO THE CARDIOVASCULAR SYSTEM?
• CIRCULATES BODY FLUIDS BACK TO THE BLOOD
• WHAT WOULD HAPPEN IF IT DIDN’T?
LYMPHATIC CAPILLARIES
• HOW DO THEY DIFFER FROM BLOOD CAPILLARIES?• PARALLEL BLOOD CAPILLARIES• SIMILAR STRUCTURE• MORE FLUID EXITS CAPILLARIES ON ARTERIOLE
SIDE THAN REABSORBED ON VENULE SIDE• INTERSTITIAL FLUID ENTERS= LYMPH• CELLS OVERLAP, AREN’T ATTACHED SO PROTIENS
AND OTHER MATERIAL ENTERS WHEN PRESSURE INCREASES
• FUNCTION OF LACTEALS?• GO TO LYMPHATIC VESSELS
• HYDROSTATIC PRESSURE FORCES LYMPH IN
• PROTEIN ATTACHMENT FIBERS ?
• HOW DOES LYMPH FLOW THROUGH THE VESSELS?– LIKE VEINS:
• SKELETAL MUSCLE CONTRACTION• CONTRACTION OF RESPIRATORY MUSCLES• CONTRACTION OF SMOOTH MUSCLE IN
LYMPH VESSELS• VALVES
LYMPHATIC TRUNKS
• LYMPHATIC VESSELS DRAIN INTO LYMPHATIC TRUNKS• NAMED FOR REGIONS THEY DRAIN• JOIN THE COLLECTING TRUNKS:
• THORACIC DUCT– LARGER AND LONGER– FROM ABDOMINAL REGION TO LEFT SUBCLAVIAN
VEIN– DRAINS INTESTINAL, LUMBAR, INTERCOSTAL
TRUNKS, LEFT SUBCLAVIAN, LEFT JUGULAR, & LEFT BRONCHOMEDIASTINAL TRUNKS
• RIGHT LYMPHATIC DUCT– RIGHT THORAX TO RIGHT SUBCLAVIAN VEIN
• TO PLASMA
LYMPH FLOW
• FLUID MOVEMENT FROM CAPILLARIES TO INTERSTITIAL FLUID TO LYMPH IS USUALLY BALANCED
• OBSTRUCTION OF FLOW LEADS TO ?– EDEMA
LYMPH NODES
• USUALLY AFTER LYMPH VESSELS
• ~1IN; BEAN SHAPED; HILUM; CAPSULE FORMS; LYMPH NODULES/FOLLICLES
• AFFERENT LYMPH VESSELS ENTER AT VARIOUS AREAS ALONG CAPSULE
• EFFERENT VESSLES EXIT AT HILUM
LYMPH NODULES
• CONTAIN B LYMPHOCYTES AND MACROPHAGES TO FIGHT INVADING PATHOGENS WHY IN LYMPH NODES?
• SOME LYMPH NODULES ARE ASSOCIATED WITH OTHER SYSTEMS:– TONSILS– PEYER’S PATCHES: M CELLS (MICROFOLD) PICK UP
ATIGENS FROM LUMEN OF SMALL INTESTINE AND BY TANSCYTOSIS 9VESSICLE MEDIATED) TRANSFER IT TO OTHER DENDRITIC CELLS AND T LYMPHOCYTES
• LYMPH SINUSES PROVIDE PATHWAY FOR LYMPH TO CIRCULATE
LYMPH NODE
Structure of the lymph node. 1. Afferent lymphatic vessel 2. Sinus 3. Nodule 4. Capsule 5. Medulla 6. Valve to prevent backflow 7. Efferent lymphatic vessel.
en.wikipedia.org
LOCATIONS OF LYMPH NODES
• CERVICAL
• AXILLARY
• SUPRATROCHLEAR: MEDIAL SIDE OF ELBOW
• INGUINAL
• PELVIC
• ABDOMINAL
• THORACIC
THYMUS• BILOBED; CAPSULE; MEDIASTINUM;
ANTERIOR TO AORTIC ARCH; POSTERIOR TO STERNUM;TO PERICARDIUM
• SHRINKS WITH AGE; ADIPOSE AND CONNECTIVE TISSUE FILLS IN
• CONNECTIVE TISSUE FROM CAPSULE FORMS LOBULES
• LOBULES CONTAIN LYMPHOCYTES (MARROW) MATURE INTO T LYMPHOCYTES DUE TO HORMONES THYMOSINS SECRETED BY EPITHELIAL CELLS OF THYMUS
SPLEEN
• LARGEST LYMPHATIC ORGAN
• UPPER LEFT ABDOMEN; INFERIOR TO DIAPHRAGM; ANTERIOR TO STOMACH
• STRUCTURE SIMILAR TO LYMPH NODES; HILUM FOR BLOOD VESSELS AND NERVES;
• VENOUS SINUSES FILLED WITH BLOOD
PULP
• WHITE PULP
– TINY ISLANDS; SPLENIC NODULES PACKED WITH LYMPHOCYTES
• RED PULP
– REST OF LOBULES; SURROUND VENOUS SINUSES; CONTAINS RBCs, LYMPHOCYTES AND MACROPHAGES
• CAPILLARIES OF RED PULP PERMEABLE: ALLOW RBCs TO PASS AND DAMAGED RBCs RUPTURE AND MACROPHAGES REMOVE DEBRIES
• MACROPHAGES DESTROY PATHOGENS
• LYMPHOCYTES DEFEND AGAINST INFECTIONS
• SPLEEN FILTERS BLOOD
http://www.google.com/imgres?imgurl=http://img338.imageshack.us/img338/6852/bitencaca8qz.jpg&imgrefurl=http://
BODY DEFENSES
• PATHOGENS: – BACTERIA; PROTOZOA; FUNGI; – VIRUSES
• INFECTION DOESN’T ALWAYS HAVE SYMPTOMS
• INNATE/NONSPECIFIC DEFENSES
• ADAPTIVE/ SPECIFIC DEFENSES
INNATE DEFENSES
• SPECIES RESISTANCE
• MECHANCIAL BARRIERS
• CHEMICAL BARRIERS
• NATURAL KILLER CELLS
• INFLAMMATION
• PHAGOCYTOSIS
• FEVER
SPECIES RESISTANCE
• A SPECIES CAN’T GET CERTAIN DISEASES ?– DON’T HAVE THE RECEPTORS; OR DON’T
HAVE CORRECT TEMPERATURE OR CHEMICAL ENVIRONMENT;
FIRST LINE OF DEFENSE MECHANICAL BARRIERS
• SKIN– SLOUGHS OFF REMOVING BACTERIA
• MUCOUS MEMBRANES– CILLIATED EPITHELIUM
• HAIRS TRAP INFECTIOUS AGENTS
• SWEAT, MUCUS, TEARS, SALIVA, AND URINE WASH AWAY PATHOGENS
SECOND LINE OF DEFENSE
• CHEMICAL BARRIERS
• ENZYMESGASTRIC
– JUICE: PEPSIN & HCl
– TEARS: LYSOSOMES
– HCl
– SALT
– INTERFERRONS
• HORMONELIKE PEPTIDES PRODUCED BY LYMPJHOCYTES OR FIBROBLASTS VS. VIRUSES AND TUMOR CELLS
• HELP TO BLOCK THE REPRODUCTION OF VIRUSES
• STIMULATE PHAGOCYTES AND OTHER CELLS TO RESIST INFECTION AND HINDER THE GROWTH OF TUMORS
• DEFENSINS– PEPTIDES MADE BY GRANULOCYTES OF
INTESTINAL EPITHELIUM– GENES ACTIVATED BY SOME ANTIGENS OR
VIRUSES FORM DEFENSINS– SOME MAKE HOLES IN CELL WALLS AND
MEMBRANES
• COLLECTINS– PROTEINS VS. BACTERIA, VIRUSES AND
YEASTS– ATTACK THE DIFFERENT SUGARS ON
PATHOGEN MEMBRANES MAKING IT MORE EASILY PHAGOCYTIZED
• COMPLEMENT SYSTEM:– GROUP OF PROTEINS IN FLUIDS REACT
AS A CASCADE– BY ONE OF 2 PATHWAYS
• CLASSICAL– ATTACHES TO ANTIBODY ATTACHED TO AN
ANTIGEN
• ALTERNATE– EXPOSURE TO ANTIGENS WITHOUT ANTIBODIES
– STIMULATES INFLAMMATION ATTRACTS AND ENHANCES PHAGOCYTES
INFLAMMATION
• REDNESS, SWELLING, HEAT AND PAIN– HOW?
• DUE TO PATHOGENS (MAINLY); HEAT, UV, ACIDS, BASES
• WHITE BLOOD CELLS INCREASE:– FIRST ?– MONOCYTES BECOME MACROPHAGES– PUS ?
• EXUDATE: WITH CLOTTING FACTORS RELEASE FIBRIN
• FIBROBLASTS WALL OFF AREA TO INHIBIT SPREAD OF PATHOGENS/TOXINS
PHAGOCYTOSIS
• MOSTLY NEUTROPHILS AND MONOCYTES DIFFERENCE?
• CHEMOTAXIS ?
• MONOCYTES MACROPHAGES: FREE OR FIXED ?
• MONONUCLEAR PHAGOCYTIC SYSTEM/RETICULOENDOTHELIAL SYSTEM
FEVER
• BODY TEMP CONTROLLED BY ?• SO WHAT CHANGES TO ALLOW FEVER?• VIRAL OR BACTERIAL INFECTION CAUSES
LYMPHOCYTES TO RELEASE INTERLEUKIN 1/ ENDOGENOUS PYROGEN RAISES SET POINT
• HIGHER TEMP CUASES LIVER AND SPLEEN TO HOLD IRON SO BACTERIA AND FUNGI CAN’T GROW
• PHAGOCYTES ARE MORE ACTIVE ?
ADAPTIVE DEFENSE (SPECIFIC)
• THIRD LINE OF DEFENSE: IMMUNITY– A RESISTANCE TO SPECIFIC PATHOGENS
OR TOXINS AND OTHER BY-PRODUCTS
• MUST DETERMINE SELF AND NON-SELF ANTIGENS
ANTIGENS
• PROTEINS, POLYSACCHARIDES, GLYCOPROTIENS, OR GLYCOLIPIDS
• BEFORE BIRTH SELF ANTIGENS ARE RECOGNIZED• LARGE AND COMPLEX CAUSE MORE RESPONSE• HAPTENS
– SMALL MOLECULE THAT MAY CAUSE A RESPONSE WHEN COMBINED WITH A LARGER COMPOUND
• DRUGS, DUST, DANDER, CHEMICALS
LYMPHOCYTE PRODUCTION
• DURING FETAL DEVELOPMENT UNSPECIALIZED LYMPHOCYTES RELEASED TO BLOOD
• HALF GO TO THYMUS AND THYMOSINS MATURE THE T LYMPHOCYTES
• MOST OF LYMPHOCYTES IN BLOOD• REST MATURE IN MARROW B LYMPHOCYTES• BOTH FOUND IN LYMPH NODES, SPLEEN, INTESTINAL
LINING• BOTH ARE CLONED FROM ORIGINAL VARIETY CELL; EACH
ONE HAS A ANTIGEN RECEPTOR SO ONLY RESPONDS TO A SPECIFIC ANTIGEN
• B CELLS PRODUCE ANTIBODIES; T CELLS INTERACT DIRECTLY
T CELL RESPONSE
• ACTIVATED BY ANTIGEN-PRESENTING CELL LIKE SOME MACROPHAGES AND B CELLS
• PHAGOCYTE DIGESTS BACTERIA ?, SOME OF ANTIGEN TRAVELS OUT TO MAJOR HISTOCAMPATABILITY COMPLEX (MHC) (HUMAN LEUKOCYTE ANTIGENS/HLA)
• FOUND ON ALL CELL MEMBRANES BUT RBCs (CLASS I) OR ON SURFACE OF ANTIGEN-PRESENTING CELLS, THYMUS CELLS AND ACTIVATED T CELLS (CLASS II)
• MHC ANTIGENS HELP T CELLS RECOGNIZE FOREIGN ANTIGENS• CELLULAR IMMUNE RESPONSE:
– ACTIVATED T CELLS REACT DIRECTLY WITH ANTIGEN PRESENTING CELL
• T CELLS ALSO SECRETE POLYPEPTIDES: CYTOKINES:– INTERLEUKIN 1: ACTIVATES T CELLS; STIMULATES THEM TO
RELEASE CYTOKINES– INTERLEUKIN 2: T CELL PROLIFERATION; STIMULATES T
CELLS TO RELEASE CYTOKINES– CFSs STIMULATE BONE MARROW TO PRODUCE
LYMPHOCYTES; CAUSE B CELLS TO GROW AND MATURE; ACTIVATE MACROPHAGES
– INTERFERONS– TUMOR NECROSIS FACTOR: STOPS TUMOR GROWTH,
CAUSES FEVER; STIMULATES LYMPHOCYTE DIFFERENTIATION; RELEASES GROWTH FACTORS
– ALSO RELEASE TOXINS TO KILL ANTIGEN BEARING CELLS, AND GROWTH INHIBITING FACTORS
CYTOTOXIC T CELL
• RECOGNIZES ANTIGENS OF CANCEROUS CELLS OR VIRALLY INFECTED CELLS
• ACTIVATED BY CYTOKINES FROM HELPER T CELL
• THEY CLONE: PROLIFERATE
• BIND TO ANTIGEN BEARING CELL AND RELEASE PERFORIN
MEMORY T CELLS
• FROM CD8 T CELLS (CYTOTOXIC) • FOR FUTURE PROTECTION• CD8 T CELL CONTAQCTS ANTIGEN
BEARING CELL IT FORMS A DUMBELL SHAPE– DIVIDES: ONE CELL BECOMES ACTIVE
CYTOTOXIC CELL OTHER SIDE BECOMES A MEMORY T CELL
• DURING SECOND INFECTION THIS CELL DIVIDES INTO CYTOTOXIC CELLS
B CELLSHUMONAL RESPONSE
• USUALLY ACTIVATED BY HELPER T CELL BUT SOME ARE DIRECTLY ACTIVATED (ANTIGEN)
• WHEN B CELL ATTACHES TO ANTIGEN HELPER T CELL RELEASES CYTOKINES– STIMULATE PROLIFERATION OF B CELL– ATTRACT MACROPHAGES AND
LEUKOCYTES• SOME OF THE B CELLS BECOME MEMORY
CELLS
• SOME BECOME PLASMA CELLS– PRODUCE ANTIBODIES/
IMMUNOGLOBULINS– HAVE A LOT OF GA– 2,000 ANTIBODIES/MINUTE– CAN ONLY PRODUCE ONE TYPE OF
ANTIBODY– POLYCLONAL RESPONSE: MORE THAN
ONE ANTIGEN ?
• T CELLS CAN RELEASE CYTOKINES TO INHIBIT B CELL FUNCTION
ANTIBODIES
• GAMMA GLOBULINS• SOLUBLE, GLOBULAR PROTIENS• 4 AMINO ACID CHAINS- DISULFIDE BONDS• 2 IDENTICAL LIGHT CHAINS AND 2
IDENTICAL HEAVY CHAINS• 5 DIFFERENT HEAVY CHAINS= 5 DIFFERENT
ANTIBODIES• SPECIFIC SHAPE GIVES PHYSIOLOGY• VARIABLE REGIONS FIT ANTIGEN
• ANTIGEN BINDING SITE FORMS AROUND ANTIGEN AND IDIOTYPES IS PART THAT BINDS
• REST IS CONSTANT REGION: BINDS TO CELL SRUCTURES OR CHEMICALS
IMMUNOGLOBULINS
• IgG: – 80%; PLASMA AND TISSUE FLUID; VS.
BACTERIA, VIRUSES AND TOXINS; ACTIVATES COMPLEMENT; ANTI-Rh
• IgA: – 13%; EXOCRINE SECRETIONS: BREAST
MILK, TEARS, NASAL FLUID, GASTRIC JUICE, INTESTINAL JUICE, BILE, URINE; VS. BACTERIA AND VIRUSES
• IgM: – 6%; IN PLASMA; VS. FOOD, BACTERIA;
ACTIVATES COMPLEMENT; ANTI-A/ANTI-B;
• IgD: – <1%; ON SURFACES OF MOST B CELLS,
ESPECIALLY INFANTS; ANTIGEN RECEPTOR WHICH ACTIVATES B CELLS;
• IgE: – <1%; EXOCRINE SECRETIONS LIKE IgA;
PROMOTES INFLAMMATION AND ALLERGIC REACTIONS;
DIRECT ATTACK
• ANTIBODIES ANTIGEN = AGGLUTINATION OR PRECIPITATION– PHAGOCYTES GET THEM EASIER– NEUTRALIZE TOXIC PART
COMPLEMENT ACTIVATION
• IgG OR IgM + ANTIGENS EXPOSED REACTIVE SITES ON CONSTANT REGION = ACTIVATION OF COMPLEMENT PROTEINS WHICH CAUSE:– OPSONIZATION: COATING ANTIGEN-
ANTIBODY COMPLEX– MORE EASILY PHAGOCYTIZED– CHEMOTAXIS– CLUMPING– LYSIS OF MEMBRANES
INFLAMMATION
• IgE USUALLY ATTACHED TO MAST CELLS
• ANTIGENS BIND AND STIMULATE MAST CELL TO RELEASE HISTAMINE
• VASODILATION AND EDEMA
IMMUNE RESPONSE
• PRIMARY RESPONSE– PLASMA CELLS RELEASES IgM, THEN IgG– TAKES HOURS TO DAYS, LASTS WEEKS– BUT: GET DISEASE– FORM MEMORY CELLS
• SECONDARY RESPONSE– MEMORY CELLS ACTIVATED, PRODUCE IgG– FOLLICULAR DENDRITIC CELLS STIMULATE
MEMORY CELLS
TYPES OF IMMUNITY
• ACTIVE VS. PASSIVE• NATURALLY ACQUIRED ACTIVE IMMUNITY
– DISEASE
• ARTIFICIALLY ACQUIRED ACTIVE IMMUNITY– VACCINE; SUBUNIT VACCINE
– HERD IMMUNITY• ARTIFICIALLY ACQUIRED PASSIVE IMMUNITY
– ANTISERUM; ANTITOXIN
• NATURALLY ACQUIRED PASSIVE IMMUNITY– IgG THROUGH BLOOD; NURSING
ALLERGIES
• ALLERGEN• TYPES
– IMMEDIATE REACTION/ANAPHALACTIC: TYPE I
• INHERITED: OVERPRODUCE IgE; • PRIMARY RESPONSE ACTIVATES B CELLS• SECONDARY: QUICK RELEASE OF HISTAMINE,
PROSTAGLANDIN D, LEUKOTRIENES• SEVERE INFLAMMATION• MAY NEED EPINEPHRINE OR DIE IN 5 MINUTES
• ANTIBODY-DEPENDENT CYTOTOXIC REACTIONS: TYPE II– TAKE 1-3 HOURS– SPECIFIC CELL BINDS ALLERGEN
PHAGOCYTOSIS AND COMPLEMENT MEDIATED LYSIS
– WRONG BLOOD TRANSFUSION• IMMUNE COMPLEX REACTIONS: TYPE III
– TAKES 1-3 HOURS– PHAGOCYTOSIS AND COMPLEMENT CAN’T
CLEAR ANTIGEN-ANTIBODY COMPLEXES– MAY BLOCK SMALL VESSELS AND CAUSE
DAMAGE– AUTOIMMUNITY
• DELAYED-REACTION ALLERGY: TYPE IV– COULD AFFECT ANYONE– REPEATED EXPOSURE TO CHEMICALS– EVENTUALLY STIMULATES T CELLS – T CELLS AND PHAGOCYTES RELEASE
CHEMICALS THAT CAUSE DERMATITIS– USUALLY TAKES 48 HOURS
TISSUE REJECTION• MAY RECOGNIZE ANTIGENS AS FOREIGN
– THE MORE DIFFERENT THE ANTIGENS ARE: MORE SEVERE RESPONSE
– ANTIGEN MATCH– TYPES OF TRANSPLANT TISSUE
• ISOGRAFT: IDENTICAL TWIN• AUTOGRAFT: SAME PERSON• ALLOGRAFT: ANOTHER PERSON• XENOGRAFT: DIFFERENT SPECIES
• GRAFT-VERSUS-HOST DISEASE: TISSUE MAY PRODUCE CHEMICALS THAT HARM RECIPIENT
• MAY USE IMMUNOSUPRESSIVE DRUGS PROB? (BEFORE)
AUTOIMMUNITY
• CAN’T TELL SELF VS. NONSELF• AUTOANTIBODIES AND CYTOTOXIC T CELLS ATTACK
BODY’S TISSUES • CAUSES: NOT SURE
– VIRUS COAT WITH HUMAN PROTEIN– T CELLS DON’T LEARN SELF ANTIGENS IN THYMUS– NONSELF TOO CLOSE TO A SELF– FETAL CELLS CIRCULATING IN WOMAN
TRIGGERED SOMEHOW TO STIMULATE ANTIBODIES: MICROCHIMERISM
– SCLERODERMA
LIFE SPAN CHANGES• THYMUS SHRINKS• 70: IMMUNE SYSTEM AT 25%• MORE SUSCEPTIBLE TO CANCER AND DISEASES
LIKE INFLUENZA• T CELL NUMBER DECREASES SLIGHTLY, B CELL
DOESN’T• ANTIBODY RESPONSE SLOWS: VACCINES ?• IgA, IgG INCREASE %; IgD, IgE DECREASE; MORE
AUTOANTIBODIES• HAVE TO BE CAREFUL WITH IMMUNOSUPRESSIVE
TREATMENTS