Sie sind auf Seite 1von 12

BLOOD HEMATOCRIT CLOTTING PROTEINS LEUKOCYTES (WBC)

- “river of life” - “blood fraction”; percentage - Help stem blood loss when blood - Contains nuclei and organelles
- Transports everything that must 45% --- RBC vessel is injured - Form protective, movable army
be carried 1%< --- WBC, Platelets that helps defend body against
- Only fluid tissue in the body 55% --- Plasma ANTIBODIES damage by bacteria, viruses,
- Help protect body from parasites, and tumor cells
COMPONENTS OF BLOOD PHYSICAL CHARACTERISTICS AND pathogens - Able to slip into and out of blood
FORMED ELEMENTS VOLUME vessels (diapedesis: leaping
- Living blood cells suspended in • Blood proteins ↓, liver is across)
the plasma BLOOD stimulated to produce proteins
- CONSISTENCY: sticky, opaque • Blood becomes too acid CIRCULATORY SYSTEM
PLASMA fluid which is heavier than water; (acidosis) or too basic (alkalosis), - Means of transportation to areas
- Nonliving fluid matrix 5x thicker respiratory & urinary systems of the bodies where their service
- COLOR: color varies to scarlet restore it to its normal, slightly is needed for inflammatory or
• Collagen & Elastic Fibers- (oxy-rich) to dull red or purple alkaline pH range immune response
absent from blood (oxy-poor) • Plasma distributes body heat, by-
• Dissolved protein- visible; - TASTE: metallic, salty taste; product of cellular metabolism POSITIVE CHEMOTAXIS
turned to fibrin strand during slightly alkaline (pH between 7.35 - Capability of locating areas of
blood clotting and 7.45) B. FORMED ELEMENTS tissue damage and infection in
• Sample Blood (separated)- plasma - TEMPERATURE: 38°C or 100.4°F; (1) ERYTHROCYTES (RBC) the body by responding to
on top, formed elements at higher than body temp. (friction - Ferry oxygen to all cells of the certain chemicals that diffused
bottom produced as blood flows through body from damaged cells
vessels) - Anucleate (lack nucleus)
ERYTHROCYTES (RBC) - 8% of body weight; 5-6 L or 6 - “bags” of hemoglobin molecules AMOEBOID MOTION
- Reddish “pellet” at bottom of quarts –volume in healthy adults - Lack mitochondria; makes - Form flowing cytoplasmic
tube energy through anaerobic extensions that help move them
- Formed elements that function A. PLASMA mechanism along
in oxygen transport - 90% water; liquid part of blood - Small flexible cell; biconcave disc - Action made by WBC by moving
- 45% of the total blood sample - Dissolved substances: nutrients, - Outnumbers WBC by about 1,000 through spaces once they have
salts, respiratory gases, to 1; major factor contributing to “caught the scent”
BUFFY COAT hormones, plasma proteins, blood viscosity
- Thin, whitish layer at the waste, products of cell LEUKOCYTOSIS
junction between RBC and metabolism HEMOGLOBIN (Hb) - Refers to a total WBC count
plasma ---iron-bearing protein that above 11,000 cells/mm3
- Contains: WBC, platelets PLASMA PROTEINS transports most of oxygen that is - Indicates that a bacterial or viral
- Most abundant solutes carried by blood. infection is stewing in the body
LEUKOCYTES (WBC) - Made most by LIVER ---the more Hb a RBC contain,
- Act in various ways to protect the the more oxygen can be carried. LEUKOPENIA
body ALBUMIN - Abnormally low WBC count
- Acts as a carrier to shuttle certain (2) LEUKOCYTES (WBC) - Caused by certain drugs
PLATELET molecules through circulation - Crucial for body defense
- Cell fragments that help stop - Important blood buffer - 4,800-10,800 WBCs/mm3 of
bleeding - Contributes to osmotic pressure blood
2 MAJOR GROUPS OF WBCs (a) LYMPHOCYTES Myeloid tissue in adults is found → When enough hemoglobin has
I. GRANULOCYTES • Have large, dark purple nucleus in: Axial Skeleton, Pectoral & been accumulated, nucleus and
- Granule containing WBCs that occupies most of the cell Pelvic Girdle, Proximal Epiphyses organelles are ejected
- Have lobed nuclei volume of humerus and femur → Cell collapses inward
• Slightly larger than RBC → Result is reticulocyte (young
(a) NEUTROPHILS • Tend to take up residence in HEMOCYTOBLAST RBC) because it contains rER
• Most numerous WBC lymphatic tissues (tonsils) where - Resides in red bone marrow → Reticulocyte enters bloodstream
• Have multilobed nucleus they play an important role in - Stem cell where all formed to transport oxygen
• Have very fine granules that immune response elements arise from → 2 days of release, it ejects
respond to both acidic and basic • Second most numerous WBC in - Forms 2 types of descendants: remaining ER and become RBC
stains blood (a) LYMPHOID STEM CELL → Entire developmental process
• Avid phagocytes at sites of acute • Produces lymphocytes from hemocytoblast to mature
infection (b) MONOCYTES and myeloid stem cell RBC takes 3-5 days
• Particularly partial to: bacteria • Largest of the WBCs (b) MYELOID STEM CELL
and fungi which they kill during • Have abundant cytoplasm and • Can produce all other ERYTHROPOIETIN
respiratory burst distinctive U or kidney-shaped classes of formed - Hormone that controls the rate
nucleus elements of RBC production
(b) EOSINOPHILS • When it migrates into tissues, - Kidney plays a major role in
• Have blue-red nucleus (earmuffs) the change into macrophages FORMATION OF RBC producing this hormone.
and brick-red cytoplasmic with huge appetite → As they age, RBC becomes rigid - When blood oxygen level begins
granules MACROPHAGES- important in ad falls apart in 100-120 days to decline, kidneys step up their
• Increases rapidly during fighting chronic infections → Remains are eliminated by release of erythropoietin which
infections by parasitic worms phagocytes (spleen, liver, other targets the BONE MARROW,
ingested in foods “Never Let Monkeys Eat Bananas” body tissues) prodding it into "high gear" to
• They gather around and release → RBC components are salvaged turn out more RBCs.
enzymes from cytoplasmic (3) PLATELETS → Iron is bound to protein as
granules onto parasite’s surface, - Fragments of bizarre ferritin • Number of RBC in blood is
digesting it away multinucleate cells → Balance of heme group is determined by the ability of the
(MEGAKARYOCYTES), which degraded to bilirubin, secreted available RBCs to transport enough
(c) BASOPHILS pinch off thousands of anucleate into intestine by liver cells oxygen.
• Rarest WBC platelet “pieces” that quickly seal → Becomes brown pigment called
• Have large histamine-containing themselves off from the stercobilin that leaves body in FORMATION OF WBC &
granules that stains dark blue. surrounding fluids feces PLATELETS
HISTAMINE- inflammatory - Appear dark staining, irregularly → Globin is broken down to amino
chemical that makes blood shaped bodies acid, released in circulation COLONY STIMULATING FACTORS
vessels leaky & attracts other - Normal platelet count: 300,000 → Lost blood cells are replaced (CSFs) & INTERLEUKINS
WBC to inflamed sites. cells/mm3 more or less continuously by - Prompted red bone marrow to
division of hemocytoblast in red turn out leukocytes
HEMATOPOIESIS (BLOOD CELL bone marrow. - enhance the ability of mature
AGRANULOCYTES FORMATION) → RBC divide many times and leukocytes to protect the body
Lack visible cytoplasmic granules - Occurs in red bone marrow or begin synthesizing huge amount
Nuclei are closer to norm myeloid tissue. of hemoglobin
THROMBOPOIETIN • Platelets release chemicals BLOOD GROUPS & TRANSFUSIONS RH BLOOD GROUPS
- accelerates the production of that enhace the vascular ANTIGEN - Named because one of eight Rh
platelets from megakaryocytes spasms and attract more - Substance that the body antigens (agglutinogen D) was
platelets. recognizes as foreign originally identified in Rhesus
BONE MARROW BIOPSY • As more platelets pile up, - It stimulates immune system to monkeys
- provides cells for a microscopic platelet plug forms. mount defense against it
examination ANTIBODIES → Anti-Rh antibodies aren’t
- a special needle is used to - COAGULATION EVENTS - “recognizers” automatically formed by Rh-
withdraw a small sample of red OCCUR. - Present in plasma that attach individuals.
marrow from one of the flat • Injured tissues are releasing RBCs bearing surface antigens → If an Rh- receives Rh+ blood,
bones TISSUE FACTOR (TF), which different from those on the immune system becomes
interacts with PLATELET patient’s RBCs. sensitized and begins producing
HEMOSTASIS FACTOR 3 (PF3) anti Rh+ antibodies against
- stopping the bleeding - PF3- a phospholipid that AGGLUTINATION foreign blood type.
- fast and localized response, coats surfaces of the platelets - Phenomenon where the binding
involves many substances • The combination interacts of antibodies causes foreign RBCs HEMOLYSIS
normally present in the plasma, with clotting factors and to clump - Rupture of RBCs
released by platelets and injured calcium ions (Ca2+) which is - Leads to clogging of small blood - Doesn’t occur in an Rh- person
tissue cells. essential in CLOTTING vessels throughout the body with first transfusion of Rh+
PROCESS, to form an blood because it takes time to
PHASES OF HEMOSTASIS ACTIVATOR that leads to AGGLUTINOGENS react and start making
formation of THROMBIN. - Sometimes called to the RBC antibodies.
(1) VASCULAR SPASMS OCCUR. • THROMBIN joins soluble antigens that promotes clumping
FIBRINOGEN proteins into RhoGAM
VASOCONSTRICTION- immediate long, hairlike molecules if AGGLUTININS - Immune serum that prevents
response to blood vessel injury, insoluble FIBRIN. - Antibodies that bind sensitization and subsequent
decreasinf blood loss until clotting • FIBRIN forms a meshwork agglutinogens together immune response.
occur. that traps RBCs and forms - Treatment in the 28th week of
Other causes: basis of clot. ABO BLOOD GROUPS pregnancy and again shortly after
• DIRECT INJURY to smooth muscle • Within an hour, clot begins - Based on which of two antigens, giving birth
cells to retract, squeezing that type A or B does a person
• stimulation of LOCAL PAIN SERUM (plasma minus inherits HEMOLYTIC DISEASE OF THE
RECEPTORS clotting proteins) from the - Antibodies form during infancy NEWBORN
• release of SEROTONIN by platelets mass & pulling ruptured against ABO antigens not present - Condition where the RBCs of the
edges of blood vessel closer on own RBCs baby is destroyed (due to
(2) PLATELET PLUG FORMS. together. antibodies that crossed the
• Platelets are repelled by BLOOD TYPE ANTIGEN placenta)
intact endothelium BLOOD CLOTS WITHIN 3-6 MINS. Type A A antigen - The baby is ANEMIC, HYPOXIC,
• When underlying Once CLOTTING CASCADE started, Type B B antigen & CYANOTIC (skin takes on blue
COLLAGEN FIBERS are triggering factors are inactivated to Type AB A & B antigen cast)
exposed, platelets become prevent widespread clotting. Type O No antigen
STICKY and clings to
damaged site.
DEVELOPMENTAL ASPECTS WASTE PRODUCTS OF METABOLISM (urea, - occur chiefly in dark-skinned - thrombus that breaks away from
uric acid)
→ Sites of blood cell formation: people living in malaria belt of the vessel wall and floats freely in
RESPIRATORY GASES (O2 and CO2)
Fetal liver and spleen HORMONES (steroids, thyroid hormone: Africa the bloodstream
→ 7th month: Fetus’s red bone carried by plasma proteins)
marrow- chief site of SICKLE CELL TRAIT (SCT) → CEREBRAL EMBOLUS causes
hematopoiesis - carrying just one sickling gene STROKE (brain tissue dies)
→ Day 28: embryonic blood cells - don’t display symptoms but can → Undesirable clotting may be
FORMED ELEMENTS 45% pass on the sickling gene to
are circulating in newly formed caused by anything that
CELL TYPE NUMBER FUNCTIONS
blood vessels (per mm3)
offspring endothelium of blood vessel
→ FETAL HEMOGLOBIN (HbF): Erythrocytes 4-6 Transport oxygen which encourages clinging of
- differs from hemoglobin (RBC) million & carbon dioxide POLYCYTHEMIA platelets
formed AFTER birth Leukocytes 4,800- Defense & - excessive or abnormal increase in
(WBC) 10,800 immunity the number of RBC
- has greater ability to pick up Basophil
THROMBOCYTOPENIA
oxygen Eosinophil - result from marrow cancer - Results from insufficient number
→ After birth: Fetal blood cells are Neutrophil (polycythemia vera) of circulating platelets
Lymphocyte - Arise from conditions that
replaced by RBCs that contain
Monocyte SECONDARY POLYCYTHEMIA
hemoglobin A (HbA) SUPPRESSES BONE MARROW
Platelets 250,000- Blood Clotting
→ Jaundiced: PHYSIOLOGIC 400,000 - a normal physiologic response to (bone marrow cancer, radiation,
JAUNDICE; Situation where fetal living in high altitude certain drugs)
RBCs are destroyed fast that
immature liver can’t get rid the HOMEOSTATIC IMBALANCE LEUKEMIA PETECHIAE
body hemoglobin breakdown - bone marrow becomes cancerous - Small purplish blotches
products fast enough LEUKOPENIA - huge number of WBC turned out - Resembles rash on skin
- Abnormally low WBC count - excessive production of abnormal
PLASMA 55% - Caused by certain drugs WBC → Vit K deficient- Vit K supplement
CONSTITUENT MAJOR FUNCTION → Liver function is impaired- blood
WATER -90% of volume; solvent THROMBUS
ANEMIA transfusion
-absorbs heat
- A decrease in the oxygen- - clot that develops and lersist in
SALT
(ELECTROLYTES) carrying ability of blood an unbroken vessel HEMOPHILIA
Sodium -Osmotic balance CAUSE: - Applies to several hereditary
Potassium -pH buffering PULMONARY THROMBOSIS
Calcium -regulation of membrane → Lower-than-normal number bleeding disorder
of RBC - blockage forms in blood vessels - Result from lack of factors
Magnesium permeability
serving the lungs needed for clotting
Chloride → Abnormal/ deficient
Bicarbonate - consequences may be DEATH of - Bleeding occurs, hemophiliacs
hemoglobin content in RBC
PLASMA lung tissue and fatal hypoxia are given transfusion of fresh
PROTEINS
Albumin -Osmotic balance, pH SICKLE CELL ANEMIA (SCA) plasma or injections of purified
HYPOXIA clotting factor
buffering - body doesn’t form normal
Fibrinogen -Clotting of blood - inadequate oxygen delivery to
hemoglobin
Globulins -Defense (antibodies); body tissues AIDS
Lipid transport - Abnormal hemoglobin is formed
SUBSTANCE TRANSPORTED BY BLOOD - becomes spiky and sharp when - Acquired immune deficiency
EMBOLUS syndrome
oxygen is unloaded or oxygen
NUTRIENTS (glucose, fatty acids, amino acids, content in blood decreases below - Condition of depressed
vitamins) immunity
normal
LYMPHATIC SYSTEM & BODY - impairs ability of cells to make LYMPHATIC COLLECTING VESSELS substance in the lymph before it is
DEFENSES exchanges with interstitial fluid - larger lymphatic vessels returned to the blood
and ultimately the blood
LYMPHATIC SYSTEM (a) LYMPH is transported from • LYMPHOCYTES: responds to
- Consist of two semi-independent LYMPH LYMPH CAPILLARIES through foreign substances in lymphatic
parts: - clear water; Interstitial fluid LYMPHATIC COLLECTING stream
(1) meandering network of VESSELS, until it returns to the - vary in size but mostly they are
LYMPHATIC VESSELS LYMPH CAPILLARIES VENOUS SYSTEM through two KIDNEY-SHAPED, 1cm long, &
- transport fluids that escaped - Weave between tissue cells & large ducts in thoracic region. "buried" in the connective tissue
from blood back to blood capillaries in the loose surrounding it
cardiovascular system connective tissues of body RIGHT LYMPHATIC DUCT - Each node is surrounded by a
(2) various LYMPHOID TISSUES - absorbs leaked fluid; permeable - drains lymph from RIGHT ARM fibrous CAPSULE from which
AND ORGANS and RIGHT SIDE of HEAD and TRABECULAE (connective tissue
- houses PHAGOCYTIC CELLS & MINIVALVES THORAX strands) extend inward to divide
LYMPHOCYTES, which play - flaplike; act as one-way swinging the node into a number of
essential roles in body defense doors LARGE THORACIC DUCT compartments
and resistance to disease - formed by the edges of - receives lymph from rest of the - INTERNAL FRAMEWORK:
- low-pressure, pumpless system endothelial cells with their walls body network of soft reticular
loosely overlap one another connective tissue ("cellular
LYMPHATIC VESSELS - anchored by fine collagen fibers (b) BOTH DUCTS empty lymph into bleachers")
- as blood circulates through body, to surrounding structure SUBCLAVIAN VEIN on their own - provides place for continually
the nutrients, wastes, & gases are - GAPE OPEN: fluid pressure is side of body. changing population of
exchanged between BLOOD & HIGHER IN INTERSTITIAL lymphocytes to "sit" as they
INTERSTITIAL FLUID SPACE (allows fluid to enter • Lymph is transported by: monitor lymphatic stream.
- FUNCTION: to form elaborate lymphatic capillary) (1) Milking action of skeletal muscles
drainage system that licks up (2) Pressure changes in thorax during LYMPHOCYTES
excess interstitial fluid and • PRESSURE IS HIGHER INSIDE breathing - arise at the ted bone marrow but
return it to the blood. LYMPHATIC VESSELS: (3) Smooth muscles in the walls of migrates to lymph nodes & other
- also called LYMPHATICS; forms Endothelial cell flaps are forced larger lymphatic contracts lymphatic organs
one-way system, & lymph flows together, preventing lymph from RHYTHMICALLY, helping to "pump"
only TOWARDS the HEART leaking back out & forcing it lymph along. CORTEX
- thin walled, larger ones have along the vessel - outer part of the node
valves. LYMPH NODES - contains FOLLICLES (collection
Proteins, Cell Debris, Bacteria, - helps protect body by of lymphocytes) which have
Viruses: prevented from entering REMOVING FOREIGN GERMINAL CENTERS (dark-
INTERSTITIAL FLUID: includes fluid BLOOD CAPILLARIES, but enters MATERIAL & by PRODUCING staining centers)
that remains behind in tissue spaces; LYMPHATIC CAPILLARIES LYMPHOCYTES
3L daily (especially inflamed areas) - clusters along lymphatic vessels GERMINAL CENTERS
and filters lymph that is - enlarges when B CELLS are
EDEMA • WBC can also travel in lymph transported towards the heart. generating PLASMA CELLS
- swelling; fluid that accumulates - CONTAINS: (daughter cells)
in the tissues • MACROPHAGES: engulfs &
destroys bacteria, viruses, and foreign
PLASMA CELLS (3) Destroy WORN-OUT RBC & - LOCATION: proximal large INNATE DEFENSE SYSTEM
- releases ANTIBODIES return some of their breakdown intestine - NONSPECIFIC DEFENSE
products to LIVER. - FUNCTION: their macrophages SYSTEM
T-CELLS (4) Platelet Storage capture and destroy harmful - responds immediately to protect
- lymphocytes "in transit" (5) Blood Reservoir bacteria, preventing them from body
- made up of the rest of the (6) For fetus: important penetrating the intestinal wall - generally PREVENTING THE
cortical cells hematopoietic site; Adult: production ENTRY & SPREAD OF
- circulates continuously between of lymphocyte MUCOSA-ASSOCIATED LYMPHOID MICROORGANISMS in the body
BLOOD, LYMPH NODES, TISSUE (MALT)
LYMPHATIC STREAM, B. THYMUS - collection of small lymphoid Includes: Intact Skin & Mucous
performing its SURVEILLANCE - DESCRIPTION: lymphoid mass tissues Membrane, Inflammatory
ROLE. - LOCATION: anterior - Includes: Peyer's Patches, Response, Number of Proteins
mediastinum overlying the heart Appendix, Tonsils produced by Body Cells
MEDULLARY CORDS - FUNCTION: functions at peak - acts as SENTINEL
- inward extensions of cortical level only during youth - protect upper respiratory & ADAPTIVE DEFENSE SYSTEM
tissue digestive tracts from constant - SPECIFIC DEFENSE SYSTEM
- contains both B & T Cells C. TONSILS attacks of foreign matter entering - fights invaders that gets passed
- DESCRIPTION: small masses of those cavities the innate defense by mounting
• Phagocytic macrophages are lymphoid tissue an attack against one or more
located at CENTRAL MEDULLA - LOCATION: deep to the mucosa BODY DEFENSES particular foreign substance
of the LYMPH NODE. surrounding the pharynx (throat) - needs to be sensitized by initial
• LYMPH enters the CONVEX - FUNCTION: trap & remove IMMUNE SYSTEM (functional exposure to an antigen (foreign
SIDE (LYMPH NODE) via bacteria or other foreign system) substance) before it can protect
AFFERENT LYMPHATIC pathogens entering throat - Structure: variety of molecule body against invader.
VESSELS -- flows through # of that INHABITS LYMPHOID - it "remembers" which invaders it
SINUSES (space) -- exits from the TONSILITIS TISSUES & ORGANS and has fought
node at HILUM (indented - tonsils are congested with CIRCULATES IN BODY FLUID.
region) via EFFERENT bacteria and becomes swollen, IMMUNE SYSTEM PROTECTS:
LYMPHATIC VESSELS. red, and sore Most Important Immune Cells: a) DIRECTLY: cell attack
Lymphocytes, Dendritic Cells, b) INDIRECTLY: releasing
OTHER LYMPHOID ORGANS D. PEYER’S PATCHES Macrophages (both innate & adaptive mobilizing chemicals &
A. SPLEEN - DESCRIPTION: Resembles mechanism) protective antibody molecules
- DESCRIPTION: soft organ tonsils
- LOCATION: left side of abdominal - LOCATION: wall of distal small TWO TYPES OF DEFENSE IMMUNITY
cavity, beneath diaphragm, curls intestine MECHANISMS: - highly specific resistance to disease
around the anterolateral aspect of - FUNCTION: their macrophages (Makes up the immune system)
stomach. capture and destroy harmful 1) INNATE DEFENSE INNATE BODY DEFENSES
- FUNCTION: bacteria, preventing them from MECHANISM - Refers to mechanical barriers that
(1) Filters and cleanses BLOOD of penetrating the intestinal wall 2) ADAPTIVE DEFENSE cover body surfaces and to the cells
bacteria, viruses & debris MECHANISM and chemicals that act on initial
(2) Provides site for LYMPHOCYTE (E) APPENDIX battle-fronts to protect body from
PROLIFERATION & IMMUNE - DESCRIPTION: Tube-like pathogens (harmful microorganism)
SURVEILLANCE offshoot
SURFACE MEMBRANE BARRIER NK CELLS concentration of signaling Other protective events occurring at
- roam the body in blood and molecules) inflamed site:
FIRST LINE OF DEFENSE includes: lymph -- Dilation of blood vessels • CLOTTING PROTEINS are
SKIN & MUCOUS MEMBRANE - -unique group of aggressive increase blood flow in the area, activated & begin to WALL OFF
SKIN lymphocytes that can lyse (burst) accounting for redness amd heat damaged area with fibrin to
- Keratinized epidermis is a strong & kill cancer cells, virus-infected observed. prevent spread of harmful agents
physical barrier body cell, other non-specific -- Increased permeability allows to neighboring tissue.
- MUCOUS MEMBRANE targets well before the adaptive fluid to leak from blood into • FIBRIN MESH forms scaffolding
- provides mechanical barrier arm of immune system is listed tissue spaces, causes LOCAL for permanent repair.
- lines all body cavities open to to fight. EDEMA, which activates pain
exterior - recognizes certain sugars on the receptors in area (Local heat increases metabolic rate
- produces variety of protective "intruder's" surface -- If the swollen, painful area is a of tissue cells, speeding up defense
secretion: - attack target cell's membrane & JOINT, its function is impaired. actions & repair process)
• acidic pH of skin secretion release lytic chemicals called -- LIMITATION OF JOINT
(acid mantle) -- inhibits PERFORIN & GRANZYMES MOVEMENT (fifth cardinal sign
bacterial growth; SEBUM (enzymes) which degrades target of inflammation) ANTIMICROBIAL PROTEINS
contains chemicals that is cell contents. - enhance the innate defenses
toxic to bacteria; vaginal - releases powerful inflammatory ONCE INFLAMMATORY PROCESS either by ATTACKING
secretions (very acidic) response HAS BEGUN: MICROORGANISMS DIRECTLY
• Sticky mucus -- traps 1) NEUTROPHILS enter blood from or by HINDERING THEIR
microorganisms that enter INFLAMMATORY RESPONSE bone marrow & roll along blood ABILITY TO REPRODUCE
DIGESTIVE & - Response triggered when body vessel walls - most important of these are
RESPIRATORY passageways tissue is injured 2) Point where CHEMICAL COMPLEMENT and
• Stomach Mucosa -- secretes SIGNALS is at its STRONGEST, INTERFERON.
gastric juice containing HCl FOUR COMMON INDICATORS they FLATTEN OUT and
& protein-digesting enzymes (Cardinal Signs) OF ACUTE SQUEEZE through CAPILLARY COMPLEMENT
• Saliva & Lacrimal Secretion -- INFLAMMATION WALLS (DIAPEDESIS) - refers to a group of at least 20
contains LYSOZYME 1) REDNESS 3) NEUTROPHILS gather at the site plasma proteins that circulate in
2) HEAT of tissue injury, after an hour, the blood in an inactive state
INTERNAL DEFENSES: CELLS & 3) PAIN they devour any foreign material • If complement becomes
CHEMICALS 4) SWELLING (edema) present attached or fixed to foreign
--- Monocytes follows cells, or mismatched RBC, it
SECOND LINE OF DEFENSE INFLAMMATORY PROCESS Neutrophils into inflamed area. is activated & becomes a
- uses enormous number of cells & - begins with: Chemical "alarm" MAJOR FACTOR in FIGHT
chemicals - When cells are damaged, they MONOCYTES AGAINST FOREIGN CELLS.
- rely on the destructive powers of release HISTAMINE and KININS - fairly poor phagocytes
cells called PHAGOCYTES and • Causes Blood Vessels in area to - within 12 after entering the COMPLEMENT FIXATION
NATURAL KILLER CELLS (NK DILATE tissue- it becomes - Occurs when complement
CELLS) • Make Capillaries LEAKY MACROPHAGES with insatiable proteins bind to certain sugars or
• Attracts PHAGOCYTES & WBC appetites. proteins on foreign cell's surface.
(POSITIVE CHEMOTAXIS: cells
are moving toward high
RESULT OF COMPLEMENT - systemic response to invading OVERLAPPING ARMS OF RULE: small molecules aren't
FIXATION microorganism ADAPTIVE DEFENSE SYSTEM ANTIGENIC. But when linked to own
1) Formation of Membrane Attack 1) HUMORAL IMMUNITY proteins, immune system might
Complexes (MAC) HYPOTHALAMUS (ANTIBODY-MEDIATED) attack.
- produces holes or pores in the - regulates body temperature - provided by antibodies (immune
foreign cell's surface. - body's thermostat proteins) present in the body's HAPTEN
2) Pores allows water to rush in the humor. - INCOMPLETE ANTIGEN;
cell PYROGENS 2) CELLULAR IMMUNITY (CELL- troublesome small molecules
3) Causing it to burst or lyse. - Chemicals secreted by WBC and MEDIATED)
macrophages exposed to foreign - Lymphocytes defends body CELLS OF ADAPTIVE DEFENSE
• Activated complement: amplifies cells or substance in the body SYSTEM: OVERVIEW
inflammatory response CELLULAR TARGETS of CELLULAR
• Some molecules released during ADAPTIVE BODY DEFENSE ARMS: Crucial cells of adaptive system:
activation process: - body's third line of defense; • Virus-infected cell • LYMPHOCYTES
VASODILATORS & specific defense system • Cancer cell - originate from
CHEMOTAXIS CHEMICALS - stalks & eliminates with nearly • Cells of foreign grafts HEMOCYTOBLAST in red bone
(attract neutrophils and equal precision almost any type marrow.
macrophages into region) of pathogen Lymphocytes acts against target: - immature (naive) lymphocytes
- functional system that recognizes • DIRECTLY: Lysing antigen released from marrow are
OPSONIZATION antigens and acts to inactivate or • INDIRECTLY: releasing IDENTICAL.
- cause cell membrane of foreign destroy them. chemicals that enhance - "Identity" depends on where in
cells to become STICKY so they inflammatory response or the body it becomes
are easier to phagocytize IMMUNE RESPONSE activate immune cells IMMUNOCOMPETENT (capable
- increased internal nonspecific of responding to specific antigen
CASCADE defense and provides protection CELLS INVOLVED IN IMMUNE by BINDING to it with
- particular sequence that must carefully targeted against RESPONSES ANTIGEN-SPECIFIC
activate complement proteins SPECIFIC antigen. ANTIGEN RECEPTORS)
- insures that complement is not - substance capable of provoking
accidentally activated. IMMUNOLOGY: study of immunity an immune response Major Lymphocytes:
- not normally present in our (a) B LYMPHOCYTES (B CELLS)
INTERFERON IMPORTANT ASPECTS OF bodies; NONSELF. - produce antibodies & oversee
- molecules that diffuse to nearby ADAPTIVE DEFENSE • PROTEINS: provoke HUMORAL IMMUNITY
cells and bind their membrane 1) It is ANTIGEN SPECIFIC (act strongest response - target SPECIFIC extracellular
receptors against particular pathogen) • ANTIGENIC: Pollar grains & antigens
- the binding stimulates the 2) It is SYSTEMIC (not restricted to microorganism (bacteria, - develop immunocompetence in
synthesis of proteins that initial infection site) fungi, virus) -- their surface BONE MARROW
interfere with ability to multiply 3) It has MEMORY (recognizes and bear such foreign molecules (b) T LYMPHOCYTES (T CELLS)
of viruses within healthy cells mounts stronger attacks on - don't produce antibodies &
encountered pathogen) SELF-ANTIGENS constitute CELL-MEDIATED
FEVER - don't trigger own immune defense
- abnormally high body response - can recognize & eliminate
temperature - strongly antigenic to other SPECIFIC virus-infected or
people tumor cells
- Arise from lymphocytes that → When they present antigens, CLONAL SELECTION ACTIVE & PASSIVE HUMORAL
migrate to THYMUS (where they DENDRITIC CELLS & - Lymphocytes begins to grow and IMMUNITY
undergo maturation for 2-3 days) MACROPHAGES activate T multiplies rapidly to form army
- Only maturing T Cells with CELLS. of cells exactly like its self ACTIVE IMMUNITY
SHARPEST ABILITY to identify → ACTIVATED T CELLS release - produces ANTIBODIES when B
FOREIGN antigens survive. chemicals that prod CLONES Cells encounter antigens
- MATURE T CELLS circulate MACROPHAGES to become - resulting family of identical cells - May be: NATURALLY
continuously throughout the ACTIVATED. descended from SAME ancestor ACQUIRED (bacterial & viral
body → ACTIVATED MACROPHAGES cell infection; which develop signs &
become true "killers" that are symptoms of disease and suffer a
Once lymphocyte is insatiable phagocytes and secrete CLONE FORMATION little) or ARTIFICIALLY
IMMUNOCOMPETENT, it will be BACTERICIDAL CHEMICALS. - primary humoral response to ACQUIRED (through vaccines:
able to react to ONE DISTINCT antigen contains pathogens that are dead
ANTIGEN. THIRD ANTIGEN CAPTURE AND or attenuated/weakened)
DELIVERY SYSTEM: Migration of PLASMA CELLS
• ANTIGEN-PRESENTING CELLS dendritic cells to secondary lymphoid - Descendants of most cell clone Benefits from VACCINES:
- do not respond to specific organs. members 1) Spare SIGNS & SYMPTOMS
antigen - produce same highly specific 2) Weakened antigens are still able
- activates lymphocytes DENDRITIC CELLS: antibodies (2,000 molecules per to stimulate antibody production
- major role is to ENGULF - efficient antigen catcher (due to second) & promote immunological
antigens, PRESENT fragments long, wispy extension) - this flurry of activity lasts only memory
where T Cells can recognize - once they ENGULF antigens for 4-5 days; then plasma cells
them. (phagocytosis), they ENTER begins to die BOOSTER SHOTS
nearby lymphatics to get to - Intensify immune response at
MAJOR CELLS ACTING AS APCs: lymphoid organ where they will MEMORY CELLS later meetings with same antigen
Dendritic Cells, Macrophages, B present antigens to T Cells - B cell clone members that don't
Lymphocytes - most effective antigen become plasma cells HERD IMMUNITY
- key link between innate and - long lived; capable of responding - phenomenon which population
(1) DENDRITIC CELLS adaptive immune response to same antigen of people are generally protected
- present in connective tissues and - responsible for because most of a given
epidermis (also called HUMORAL (ANTIBODY- IMMUNOLOGICAL MEMORY population is immune to a
LANGERHANS CELLS) MEDIATED) IMMUNE RESPONSE disease or infection
- body's frontiers, act as MOBILE • B Cells (immunocompetent, SECONDARY HUMORAL
SENTINELS immature) is stimulated to RESPONSES PASSIVE IMMUNITY
(2) MACROPHAGES complete development: when - Later immune responses, - antibodies are obtained from
- Widely distributed at ANTIGEN binds with its produced much faster, more SERUM of an immune human or
LYMPHOID ORGANS and SURFACE RECEPTORS. prolonged, more effective than animal donor.
CONNECTIVE TISSUES • Binding activate lymphocytes to primary response. - B cells are not challenged,
- Act as PHAGOCYTES in innate "switch on" & undergo CLONAL immunological response doesn't
defense system SELECTION. occur, temporary protection end
- tend to remain fixed in lymphoid when it degrades in the body
organs - is conferred NATURALLY on
fetus: Mother's antibodies cross
placenta and enter fetal - formed in response to huge IMMUNOGLOBULIN CLASSES 4. Opsonization
circulation, after birth, number of different antigens Class Location Biological Function 5. Precipitation
IgM -Attached to -Fixes complement
breastfeeding. B CELL
- Cross linking reaction
- is conferred ARTIFICIALLY: ANTIBODIES: BASIC STRUCTURE - Free in - Antigen-antibody complex are so
Person receives immune serum • Consist of FOUR PLASMA large that they become insoluble
or GAMMA GLOBULIN POLYPEPTIDE CHAINS IgA PLASMA -Bathes & protects and settle out of solution
(monomer), mucosal surfaces
(Donated antibodies) linked by DISULFIDE SECRETIONS
(sulfur-to-sulfur) BONDS (dimer) CELLULAR (CELL MEDIATED)
GAMMA GLOBULIN • TWO of four chains are IgD Always -receptor of IMMUNE RESPONSE
- Commonly administered after IDENTICAL: HEAVY attached to B immunocompetent MAIN DIFFERENCE:
CELL B cell
exposure to hepatitis. CHAINS --B cells SECRETES antibody
-important in
- provides immediate protection, • TWO other chains are also activation of B cell “weapons” whereas T cells FIGHT
but effect is short lived (2-3 IDENTICAL but only HALF IgG Abundant in -MAIN ANTIBODY antibody directly.
weeks) as long as heavy chains: PLASMA, 75- of both primary & --IMMUNOCOMPETENT T cells are
- Other IMMUNE SERA are used LIGHT CHAINS 85% of secondary response activated to form a clone by binding
circulating -crosses placenta
to treat: • Y-SHAPED antibodies -provides PASSIVE with “recognized” antigen
• poisonous snake bites • Each of four chains had IMMUNITY to fetus --T CELLS aren’t able to bind with
(antivenom) VARIABLE (V) REGION at -Fixes complement FREE antigens
• botulism one end, CONSTANT (C) IgE Secreted by -binds to MAST --Antigens must be “presented” by a
PLASMA CELLS &
• rabies REGION at another end. CELLS in BASOPHILS macrophages & double recognition
• tetanus (antitoxin) skin, -triggers release of occur.
ANTIGEN-BINDING SITE mucosae of HISTAMINE
MONOCLONAL ANTIBODIES - formed by variable regions of gastrointestin -allergic responses 2 TYPES OF THAT ARE INVOLVED
al &
- are descendants of a single cell heavy & light chains; uniquely respiratory IN ACTIVATION PROCESS
and pure antibody preparations shaped to "fit" specific antigen tract, tonsils (1) HELPER T CELL
that exhibits specificity for only (2) CYTOTOXIC T CELL
one antigen. "STEM" or CONSTANT REGION OF ANTIBODY FUNCTION
- being used for early cancer ANTIBODY Ways of Inactivating Antibodies ANTIGEN PRESENTATION
diagnosis, pregnancy, hepatitis, - determines type of antibody 1. Complement Fixation - Known to be essential for
and rabies formed COMPLEMENT activation and clonal section of T
- how antibody class carry out its --chief antibody ammunition cells.
ANTIBODIES immune roles in the body used against cellular antigens
- Also referred to as - determines the cell types or 2. Neutralization CYTOKININE
IMMUNOGLOBULINS (Igs) chemicals with which antibody - Antibodies bind to specific sites - Chemicals released by
- constitute the gamma globulin can bind on bacterial exotoxins (toxic macrophages and dendritic cells
part of blood proteins chemicals secreted by bacteria) - Plays important roles in immune
- -soluble proteins secreted & ANTIBODY CLASSES or on viruses that cause cell response
activated by B cells or by plasma Major Ig Classes: MADGE injury.
cell offspring in response to Antibodies IgD, IgG, IgE: Y-shaped 3. Agglutination CYTOTOXIC T CELLS
antigen Antibody IgA: occur in both - Clumping of foreign cells - Specialize in killing virus-
- capable of binding specifically monomer and dimer (two linked - Occurs when mismatched blood infected, cancer, or foreign graft
with that antigen monomer) forms is transfused and is the basis of cells directly.
Antibody IgM: pentamers test used for blood typing.
One way a cytotoxic T (3) ALLOGRAFTS 1ST MONTH OF EMBRYONIC ALLERGIES
cell accomplishes killing virus is by: - Tissue grafts taken from person DEVELOPMENT: STEM CELLS - Also called HYPERSENSITIVITY
1. Binding tightly to a foreign cell other than identical twin originate in SPLEEN & LIVER - Abnormally vigorous immune
2. Releasing toxic chemicals called (4) XENOGRAFTS responses which immune system
PERFORIN and GRANZYMES - Tissue grafts harvested from LATER: BONE MARROW becomes cause TISSUE DAMAGE as it
from its granules different animal species. predominant source of stem cells fights off perceived “threat”
3. PERFORIN enters foreign cell’s (Hemocytoblast)
plasma membrane (delivering Ideal donor organs/tissues: ALLERGEN (allo=altered;
lethal hit). Pores appear in target AUTOGRAFT & ISOGRAFT In late fetal life/ shortly after birth: erg=reaction)
cell’s membrane young lymphocytes develop SELF- --used to distinguish this type of
4. Granzymes enter and kill foreign IMMUNOSUPPRESSIVE THERAPY TOLERANCE & antigen from producing normal
cells - received by patient after surgery IMMUNOCOMPETENCE in immune response.
5. Cytotoxic cell then detaches and to prevent rejection "programming organs" (THYMUS & TYPES OF ALLERGIES
seeks other foreign prey to - includes: CORTICOSTEROIDS BONE MARROW) 1. Reaction where cells are LYSED
attack. (suppress inflammation), 2. Inflammation due to ANTIGEN-
ANTIPROLIFERATIVE DRUGS, NERVOUS SYSTEM ANTIBODY COMPLEXES
HELPER T CELLS RADIATION (X-RAY) THERAPY, - help to control the activity of the (glomerulonephritis)
- Act as “director” or “managers” of & IMMUNOSUPPRESSOR immune response.
adaptive immune response DRUGS. IMMEDIATE HYPERSENSITIVITY
- Once activated, they circulate - Also called acute hypersensitivity
through the body, recruiting DEVELOPMENTAL ASPECTS HOMEOSTATIC IMBALANCE - Most common type of
other cells to fight the invaders. hypersensitivity
5TH WEEK: Lymphatic vessels & Large numbers of bacteria and virus
REGULATORY T CELLS main clusters of Lymph Nodes are trapped in the nodes: Nodes ANAPHYLACTIC SHOCK
- formerly called suppressor T cell become INFLAMED, SWOLLEN, & - Body-wide, systemic, acute
- released chemicals that suppress Before birth: lymphoid organs are TENDER TO TOUCH. allergy response
activity of both T and B cells poorly developed (except thymus and - Occurs when allergen directly
- vital for winding down & spleen) LYMPH NODES: can be secondary enters blood and circulates
stopping immune response cancer site rapidly through body
- prevents uncontrolled or After birth: they become heavily
unnecessary immune system populated by lymphocytes as PUS DELAYED HYPERSENSITIVITY
activity immune system begins to function - Mixture of dead or dying - Mediated mainly by special
neutrophils, broken down tissue subgroup of helper T cell,
ORGAN TRANSPLANTS & ELEPHANTIASIS cells, living and dead pathogens cytotoxic T cell, & macrophages
REJECTION - tropical disease which lymphatics - If inflammatory mechanism fails take much longer to appear than
4 MAJOR TYPES OF TRANSPLANT become clogged with parasitic to fully clear the area of debris, any acute reactions produced by
(1) AUTOGRAFTS worms sac of pus becomes walled off antibodies
- Tissue grafts transplanted in the forming ABSCESS. - Chemicals mediating this
SAME PERSON EDEMA: result when Lymphatic reaction: CYTOKINES (released
(2) ISOGRAFTS vessels are blocked, or removed PENICILLIN REACTION by activated T cells.)
- Tissue grafts donated by - Binding of penicillin to blood
genetically identical person proteins
(identical twin)
ALLERGIC CONTACT DERMATITIS SYSTEMIC LUPUS AIDS
- Most familiar delayed ERYTHEMATOSUS (SLE) - Acquired immune deficiency
hypersensitivity reaction - Systemic disease that occurs syndrome
- Follows skin contact with poison mainly in young women & - Currently most important & most
ivy, some heavy metals & certain particularly affects kidneys, devastating of acquired
cosmetic and deodorant heart, lungs, and immunodeficiency
chemicals. - Cripples immune system by
GLOMERULONEPHRITIS interfering with activity of helper
MANTOUX & TINE TEST - Severe impairment of kidney T cells
- Skin test for detecting function due to acute
tuberculosis, depend on delayed inflammation
hypersensitivity reactions.
Trigger normal state of self-tolerance
AUTOIMMUNE DISEASES break down:
- Body produces antibodies and → New self-antigens appear.
sensitized T cells that attack and “hidden” antigens are found in
damage its own tissues sperm cell, eye lens, and certain
proteins in thyroid gland.
MOST COMMON: → Foreign antigens resemble
self-antigens.
RHEUMATOID ARTHRITIS Streptococcus bacteria are
- Systematically destroys joints known to cross-react with heart
antigens
MYASTHENIA GRAVIS
- Impairs communication between RHEUMATIC HEART FEVER
nerves and skeletal muscles - Age-old disease
- Causes damage to both heart
MULTIPLE SCLEROSIS muscle and valves, as well as
- Destroys the white matter joint and kidneys.
(myelin sheaths) of brain and
spinal cord IMMUNODEFICIENCIES
- Include both congenital and
GRAVE’S DISEASE acquired conditions in which
- Thyroid gland produces excessive production or function of
amounts of thyroxine in response immune cells or complement is
to autoantibodies that mimic abnormal.
TSH
SEVERE COMBINED
TYPE 1 DIABETES MELLITUS IMMUNODEFICIENCY (SCID)
- Destroys pancreatic beta cells, - Most devastating congenital
resulting in deficient production condition
of insulin - There is a marked deficit of both
B and T cells.