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121 Cards in this Set

  • Front
  • Back
First Line of Defense

*General
*Physical Barriers: Skin, lining of the mucosa, tears, sebaceous glands etc.
*Known as Innate Immunity: They are in place prior to an encounter with an infectious agent and provide rapid protection.
Second Line of Defense

*General
*Inflammation: A process involving multiple cell types and other factors that are intended to help the body eliminate the initial cause of cellular injury and remove damaged tissue.
*Known as Innate Immunity: They are in place prior to an encounter with an infectious agent and provide rapid protection. In place when we are born.
Third Line of Defense

*General
*Adaptive or Acquired Immunity: Responds less rapidly than innate immunity, but is more effective and specific to the offending pathogen
*Learned Immunity
*Antibodies and Vaccines
First Line of Defense

*Detailed 1
*Skin: Protects our body against all different types of pathogens. Any compromise to skin integrity can allow pathogens to enter much more easily.
*Lining of the GI, GU and Resp. Tract: The mucosa contains microbial molecules that can kill a wide range of pathogens.
*Coughing and sneezing are responses to try and eliminate a pathogen that the body recognizes.
First Line of Defense:

*Detailed 2
*Mucous is thick and sticky that's primary goal is to trap foreign substances and organisms. It contains enzymes that are harmful to pathogens, which makes it a physical and biochemical barrier.
*Cilia catch and push foreign substances and pathogens out of the body
*Biochemical Barriers: Contain substances that help to kill pathogens and prevent other foreign substances from entering the body.
First Line of Defense:

*Detailed 3
*Normal Flora of the body helps to prevent infection in the GI, skin and vagina by preventing other types of more opportunistic infections from taking hold.
*Antibiotics can be harmful bc it can kill the normal flora of the gut causing clostridium difficle to take over and cause major GI distress.
Second Line of Defense:

*Detailed
*Inflammatory Response: Normally occurs due to invasion of foreign objects or if the body perceives something as harmful, such as an allergy.
*Inflammation Causes: Infection, mechanical damage, ischemia, nutrient deprivation, temperature extremes, radiation etc.
*Local Manifestations: Occurs in the inflammatory process.
*Warmth, Edema (Swelling), Erythema (Redness), Pain or Organ Dysfunction.
Inflammation
*Purpose:
*Prevent and limit infections and further damage.
*Interact with components of the adaptive immune system.
*Prepare the area of injury for healing.
*Limit and control the inflammatory process
*The body limits further damage to the body by signaling the immune system to activate. This may take a day, so the inflammatory response is the first responder to the injury site.
Inflammation Cont.
*Inflammatory process attempts to prepare the area for healing by helping to remove debris from the dead cells, killing pathogens and producing cellular signals to begin tissue growth.
*Finally the inflammatory response attempts to control itself by creating self limiting signals to prevent over-responsiveness.
Inflammatory Process:

*5 Outcomes: Vasodilation
1. Vasodilation: (Redness/Heat) Earliest manifestation of inflammation response. Caused by nitrous oxide and histamine release. It allows more inflammatory and immune cells to come to the injury site. Increases the temp of the site, to make more pathogens unable to survive.
Inflammatory Process:

*5 Outcomes: Vascular Permeability
2. Vascular Permeability: (Edema) Signaled by histamine, leukotienes, bradykinin, and protaglandins. Allows neutrophils to get to the site of injury and allows fluid to leak into the tissue at the site of injury. The fluid helps to dilute the toxins released by the pathogen and to dilute the pathogen in general.

*First it allows neutrophils to come to the injury site, and later on it allows macrophages to enter the area and destroy the bacteria through pagocytosis.
Inflammatory Process:

*5 Outcomes: Cellular Infiltration:
3. Cellular Infiltration: (Pus) Made up of a protein rich fluid and dead neutrophils or other cells that have been killed by the invading pathogen or foreign objects. Or it can be made up of pathogens that were killed by the macrophages or neutrophils.
Inflammatory Process:

*5 Outcomes: Thrombosis
4. Thrombosis: (Clots) Form in order to prevent the spread of infection or foreign objects, stops bleeding and provides a framework for repair and healing. The primary substance of clots is Fibrin.
Inflammatory Process:

*5 Outcomes: Stimulation of Nerve Endings
5. Stimulation of Nerve Endings: (Pain) Bradykinin signals a pain response, which is the body's conscious notification system that something is wrong,
Inflmmatory Process:

*Eosinophils and Leukocytes Roles
*Eosinophils help to prevent inflammation from spreading to non damaged areas

*Leukocytes (WBC) release super oxide free radicals in response to contact with microbes or other cells. These free radials combine with nitrous oxide to further elicit the inflammatory process.
Mast Cell Degranualation
*Mast cells are the most important activator of the inflammatory response.

*Mast cells are found in the outer surfaces of the body, and in the lining of connective tissue, BV and respiratory tract

*Degranulation: An immediate response to foreign pathogens or objects
Process of Mast Cell Degranulation:

*2 possible outcomes
1. Histamine is Released
Or
2. Chemotactic Factors Occur
Process of Mast Cell Degranulation:

1. Histamine is Released
*When histamine is released, there is a rapid constriction of the smooth muscle, and dilation of the postcapillary venules. This causes an increase in blood flow to the microcirculation.
*Also causes increased vascular permeability.
Process of Mast Cell Degranulation:

2. Chemotactic Factors
*Chemotactic factors will diffuse from a site of inflammation forming a gradient and causing the directional movement (Chemotaxis) of cells toward the inflammation.
*Chemotaxic factors cause neutrophils and eosinophils to move towards the inflammation
Mast Cell Synthesis:
*Activated mast cells begin new synthesis of other mediators of inflammation such as Leukotrienes, Protaglandins and Platelet Activating Factor.
*Leukotrienes: Produce histamine like affects except are used in later stages of the inflammatory process bc they stimulate slower and have prolonged affects
Mast Cell Synthesis Contd
*Prostaglandins: Cause increased permeability, neutrophil chemotaxis and pain by directly effecting the nerves.
*Platelet Activating Factors: Causes same effect of leukotrienes, but also activates platelets to help in clotting.
Plasma Systems:

1.Complement System
*Activated components of the complement system can destroy pathogens directly and collaborate with all other parts of the inflammatory response.
*C3 and C5 are activated and form 3 subunits:
1. Opsonins: Makes bacteria susceptible to phagocytosis
2. Chemotactic Factos: Cause neutrophils and eosnophils to move towards inflamed site
Plasma System:

1.Complement System Contd
3. Anaphylatoxins: Molecules that induce a rapid degranulation of mast cells, thus increasing inflammation.
*Component Group C5b-C9: Attaches to the cell wall of the gram negative bacteria and creates pores, which allow fluids and ions to enter the pathogen and causes cell lysis.
Plasma Systems:

2. Clotting System (Coagulating)
*A group of plasma proteins that form a fibrinious mesh work at an injured or inflamed site.
*This forms a clot which stops the bleeding, traps the infectious organism and prevents spreading, keeps microorganisms at the site of greatest inflammatory cell activity and provides a framework for future repair and healing.
Plasma System:

2. Clotting System (Coagulation) Contd.
*Main substance in the fibrinous mesh is Fibrin, an insoluble protein produced by the coagulation cascade
*Fibrinopeptides (FP): 2 low molecular weight peptides are released when fibrinogen is activated to produce fibrin.
*Process:
Factor X- Thrombin- Fibrinogin-Fibrin or FP
Plasma Systems:

3.Kinin System
*Interacts with the coagulating system
*Bradykinin: Final product of the kinin system. It causes dilation of BV, acts with prostaglandins to induce pain, causes smooth muscle to contract, and increase vascular permeability.
*Bradykinin induces smooth muscle contraction slower then histamine and is more important in the later stages of the inflammation response.
Process of Phagocytosis:
*Phagocytosis is the process by which a cell ingests and disposes of foreign material
*Neutrophils and Macrophages are the two most important phagocytes
*Pavementing: The process of leukocytes (WBC) attaching to the endothelium (Wall of BV) and slowly moving through the wall of the BV, known as Diapedesis.
*Once the WBC are in the tissue, they are attracted to the inflammatory site by chemotactic factors from degranulation.
Process of Phagocytosis Contd:
*Then the neutrophil, machrophage or monocyte will attempt to phagocytize the pathogen.
*This process is much easier if opsonisation occurs.
*The pathogen is then broken down inside of the phagocytic cell bc there is H2O2 or O2 in the phagocyte.
*Vasodilation helps move the lining of BV apart, which allows WBC to squeeze thru more easily.
Cellular Components of Inflammation:

1.Neutrophil
*Predominant phagocyte in early inflammation response, 6-12 hrs after injury

*Severe inflammatory factors rapidly attract them.

*Becomes part of the pus bc they do not divide and are sensitive to acidic environments

*Leukocytes
Cellular Components of Inflammation:

2.Monocyte/Macrophage
*Monocyte: Immature WBC
*Macrophage: Mature Tissue Cell
*They are the largest normal blood cells, and produced in the marrow
*Macrophages are more active then monocytic precursors.
*Enter the site 24hrs or later, replacing the neutrophils.
*TB, typhoid fever, listeriosis and brucellosis are all resistant to macrophages
Cellular Components of Inflammation:

3.Eosinophil
*Mildly phagocytic

*Serves as primary defense against parasites

*Helps to regulate vascular mediators released from mast cells, which helps to prevent excessive inflammation.
Cellular Components of Inflammation:

4.Natural Killers
*Recognizes and eliminates cells infected with viruses and abnormal host cells... such as cancer
Cellular Components of Inflammation:

5.Platelet
*Activated by collagen, thromvin, platelet activating factor (PAF)

*Interact with components of the coagulation cascade to stop bleeding.

*Degranulates to release serotonin which preforms similar to histamine.
Cellular Products:

*Cytokines
*Secreted by cells to either be pro-inflammatory or anti-inflammatory
Cytokines:

1.Interleukins
*Produced by macrophages and lymphocytes after recognition of a pathogen
*Causes systematic reaction like fever, growth of blood vessels or down regulation, which is the prevention of the inflammatory response from getting too over powered.
Cytokines:

1.Interleukines Contd
*Increased BV allows from more O2 and nutrients to be delievered to the injury site.
*Can be hijacked in cancer, meaning blood cells will be brought to the cancer, which will cause the cancer cells to grow more.
Cytokines:

2.Interferons
*Activates acquired immune system
*Protect against viral infections and intracellular parasites
*Increases microbiocidal (destruction of microbes) activity of macrophages
*Development of acquired immune response against viral antigens
*Also helps activate T-Helper Cells
Cytokines:

3.TNF-α
*Tumor Necrosis Factor- Alpha
*Macrophages secrete this in response to recognition of foreign materials by Toll-like receptors
*Mast Cells also play are role
Cytokines:

3.TNF-α Contd
*Induces fever, causes increased inflammation related serum protein creation in the liver, muscle wasting, intravascular thrombosis (blood clot within a BV) in a severe infection and cancer
*Activated with recognition of foreign objects
Chemokines:
*Small proteins that induce/create leukocyte chemotaxis
Exudative Fluids (Wound Fluids)

1. Serous Exudate
*Watery exudate
*Indicated early inflammation

*Ex: Fluid in a blister
Exudative Fluids (Wound Fluids)

2. Fibrinous Exudate
*Thich, clotted exudate
*Indicates a more advanced inflammation
*Can also be seen as scabbing of a wound

*Ex: Lungs of an individual with pneumonia
Exudative Fluids (Wound Fluids)

3. Purulent Exudate
*Pus
*Indicates a bacterial infection
*Characterized by cysts and abscesses
Exudative Fluids (Wound Fluids)

4. Hemorrhagic (Sanguinous) Exudate
*Exudate contains blood
*Filled with erythrocytes
Exudative Fluids (Wound Fluids):

*Serusanguinous
*Mixture of serous and sanguinous exudate
Systematic Manifestation:

1.Fever
*Fever occurs due to the inflammation from Interleukin and TNF Cytokines
Systematic Manifestation:

2.Increased Concentration of Plasma Proteins
*There will be an increase in the number of plasma proteins produced by the liver, such as fibrogen, C-reactive protein, and serum amyloid A protein.
*Increased production is stimulated by cytokines.
Systematic Manifestation:

3.Skeletal Muscle Catabolism
*Occurs bc skeletal muscle has a high metabolism and thus requires a lot of energy.
*By reducing this energy requirement, the body can focus its energy on fighting the illness.
Systematic Manifestation:

4.Lab Findings
*Increase # of WBC
*Increase # of Band Cells (Immature WBC)
*Increase # of Neutrophils
*This is known as Left Shift
Systematic Manifestation:

5.Increased Erythrocyte Sedimentation Rate (ESR)
*A general, non specific measure of inflammation
Chronic Inflammation:
*Inflammation that last more then 2 weeks

*Can occur without having acute inflammation first
Causes of Chronic Inflammation:

1. High Lipid and Wax Content
1. Some organisims have a high lipid and wax content, making phagocytosis ineffective. Therefore, the bacteria can live inside the machrophage for long periods of time causing chronic inflammation
Ex: TB bacteria
Causes of Chronic Inflammation:

2. Toxins, Chemicals, or Foreign Bodies
2. Some bacteria may release toxins that cannot be eliminated from the body, causing chronic inflammation.
Ex: Asbestosis and Silicosis
*Other potential foreign bodies can include dissolving sutures, or surgical instruments that are left inside the wound.
*Can Lead to cancer
Effects of Chronic Inflammation:
*Can lead to fibrosis and necrosis of the tissue
*Can increase the rate/risk of Arteriosclerosis, which can eventually lead to problems such as stroke and heart attack
*Can also cause cancer, as free radicals can be released by macrophage and can DNA mutations.
Methods of Wound Healing:

1. Primary Intention
*The wound is approximated (Close together), and thus can heal from the sides of the wound.
*Using this method there is little, or no, scar tissue
*This type of healing can also occur if a wider wound is sutured
Methods of Wound Healing:

2. Secondary Intention
*The wound is wider, and granulation tissue must come up from the base of the wound
*This process takes much longer, the scarring is much greater and may need more medical help in order to heal bc of drainage, complexity and infection
3 Phases of Wound Healing:

1. Inflammation
*This is discussed in the past few index cards

*In general its the process of a fibrous clot created to protect the wound (Scabbing)
3 Phases of Wound Healing:

2.Reconstruction or Proliferative Phase
*Begins within 2-3 days of healing
*Fibroblasts synthesize and secrets collagen, growth factors and other elements needed for healing
*Fibroblast, and vascular endothelial serve as foundation for scar tissue at the site
*After granulation tissue grows to the surface, epithelial cells form at the edge of the wound and slowly come together to close the wound
3 Phases of Wound Healing:

3.Maturation or Remodeling Phase
*Begins 3 weeks after injury, and can last up to 6 months or longer
*Scar tissue underlying the epithelial cells are remodeled
*Most wounds do not regain their tensile strength and thus are more easily injured in the future
*Scar tissue maintains integrity but not the functional properties of endothelial cells
Dysfunctions During Inflammatory Response:

1. Hemorrhage
*Pooling of blood in the area

*This delays the healing process bc these cells must be cleared before repair
Dysfunctions During Inflammatory Response:

2.Fibrous Adhesion
*Excessive fibrin formation

*Could be problematic since they could causes sticking of tissues together
Dysfunctions During Inflammatory Response:

3.Excessive Scar Formation
*Excessive scar formation at the site of injury
Dysfunctions During Inflammatory Response:

4.Wound Sepsis
*Severe infection of the wound that enters the bloodstream
Dysfunctions During Inflammatory Response:

5.Hypovolemia
*If someone is dehydrated, there is less ability to produce plasma for healing
*Also reduces blow flow to the area
Dysfunctions During Inflammatory Response:

6.Hypoproteinemia
*Abnormal deficiency of protein in the blood
*Protein is required to heal wounds, thus if this occurs, the healing process will slow or stop.
*This is why sick patients often have trouble with wound healing bc of inadequate nutrition
Dysfunctional Wound Healing during Reconstructive Phase:

1. Keloids
*Excessive collagen formation
*They are benign tumors, caused by excess production of scar tissue
*More likely in the African American population and tends to have genetic basis
*Not harmful on their own, however they can become infected and cause ulcerations
*High likelihood of it coming back, even if surgically removed
Dysfunctional Wound Healing during Reconstructive Phase:

2.Hypertrophic Scar
*Does not extend beyond boundaries of the wound but is raised.
*Generally recedes over time
*It is not harmful and generally does not have any side effects
Dysfunctional Wound Healing during Epithelialization Phase:

1.Dehiscene
*Reopening of a closed wound
*Usually occurs 5-12 days after suturing
*Suture tension can occur due to wound infection, sepsis, or obesity
Dysfunctional Wound Healing during Epithelialization Phase:

2.Evisceration
*Protrusion of an organ from a dehisced wound
Pediatrics and Inflammation Response:
*They have transiently depressed inflammatory and immune function
*Neutrophils are not capable of efficient chemotaxis
*Neonates express complement deficiency
*Younger children are at a greater risk of infection bc of their decreased inflammatory response.
Elderly and Inflammation Response:
*Inflammation is less visible bc of lower fevers and lower WBC spikes
*Impaired inflammation is likely a result of chronic illness, such as diabetes of heart disease
*Chronic medication intake decreases the inflammatory response
Elderly and Inflammation Response Contd:
*Healing response is diminished due to loss of the regenerative ability in the skin
*First sign might be delirium
*2 most common infections are UTI and Pneumonia
Active Immunity:
*Acquired immunity, gained after birth
*Produced by the individual after either natural exposure or vaccination
Passive Immunity:
*Aquired immuniity, gained after birth
*Does not invovled the individual at all
*Occurs when antibodies or T cells are passed from donor to reciepient
Ex: Mother to Baby via placenta or breast milk
Ex: When Immune Globulin Serum (Antibodies) are injected into an individual
Lymphocytes:

T Cells
*Attacks the antigen directly
*Produced in stem cells and mature in thymus
*Function in the peripheral (Surface) tissue and produce cell mediated immunity
*Aides in antibody production
Types of T Cells:

1.Helper T Cell
*Activates other WBC, including maturation of B cells, activates cytotoxic T cells and macrophages
*Also known as CD4 cells
HIV:

*Affects CD4 cells
*Virus enters through exchange
of bodily fluids (sexual intercourse, IV drug use, blood transfusion).
*The body will have flu like symptoms during acute
infection just after the pathogen has been passed to the person.
*Within 4-7 weeks at most, the person will seroconvert, meaning they will show as HIV+ on an antibody test
HIV Infection:
*The body has difficulty attacking CD4 cells infected with HIV because it does not display any antigens
on the surface of the cell.
*Therefore Natural Killer
Cells and other inflammatory and immune cells cannot remove the virus from the body.
*HIV is a reverse transcriptase virus
*It replicates using the CD4 cells machinery, then once filled with the virus, the cell will lyse and the virus will spread further.
HIV Lab Tests
*Viral Load: >25000 is very high.
*With medication, the load can become non-detectable
*CD4 Cells: Normally between 800-1000 body can still provoke a substantial immune response when
>500.
*When less than 500, patient becomes at risk for opportunistic infections
*A non-detectable viral load and CD4 count >500 shows the disease is in control.
Potential Diseases for HIV Patients
*Specific to decreased immune infection:
*Thrush
*PCP Pneumonia
*Kaposi’s Sarcoma (type of cancer)
*Other opportunistic infections
Types of T Cells:

2.Cytotoxic T Cells
*Destroys virally infected cells
Types of T Cells:

3.Memory T Cells
*Remembers antigens and if seen again, they can expand quickly
Ex: With pathogens and cancer
Types of T Cells:

4.Regulatory T Cells
*Prevents autoimmune attacks
Types of T Cells:

5.Natural Killers
*Kills viruses
Lymphocytes:

B Cells
*Produce the antibodies that enter the bloodstream to react with antigen
*Engluf the antigen and thru a complicated process, multiply, and mature into plasma cells that produce antibodies.
*During maturation some cells multiply into memory B cells, then they are stored away and if that antigen is found again, the body can more quickly response to the pathogen
Naive B Cells
*Express IgD and IgM in their membranes that serve as receptors for antibodies but do not secrete antibodies
Cell Mediated Response:

1.T Cell Receptor Complex
*Requires antigen in an MHC, a specific manor on the target cell for antibody to attach to antigen
Major Histocompatibiliy Complex (MHC)
*On cell surface of all cells except RBC
*These identify the cells to the immune system as "self" so the body does not attack
*Transplant rejection occurs bc the MHC of the donor is slightly different then the recipient
*Antibodies identify irregularities, due to pathogens, in the MHC and attach to the part of the cell
Cell Mediated Response:

2.Cytotoxic T Lymphocytes
*Destruction of tumor cells, and viruses
Cell Mediated Response:

3.Natural Killer Cells
*Similar to T cells, but lack antigen specific receptors
*Kill viruses
*Responds to interferon's and cytokines
*Causes Apoptosis
Antibodies-Humoral Immunity:

*General Info
*Anitbodies are also called immunoglobulins
*Produced by plasma cells (B cells)
*5 Class of antibodies which is characterized by antigenic, structural and functional differences
*Recognizes MHC
Antibodies-Humoral Immunity:

*Direct Effects
*A membrane attack complex is activated, assisting the antibody to attack and kill the cell directly
*Can block the pathogen from attaching to or entering cells
*Can neutralize toxins released by bacteria so it does not affect the cell
Antibodies-Humoral Immunity:

*Indirect Effects
*Neutrophils, monocytes, macrophages and eosinophils are signaled to phagocytize the cell
*Also can recognize viral antigens on the surface of a cell, thus signaling phagocytosis
*Also osponizes the bacteria, making it more susceptible to phagocytosis
Antibody Function:

1.IgE
*Parasites
*Allergies
Antibody Function:

2.IgA
*IgA1: In the blood
*IgA2: In secretions such as breast milk, sweat etc.
*Prevents invasions through mucosal membranes
*Acts as most protective agent against infection
Antibody Function:

3.IgM
*Initial response antibody
*Antibodies responsible for blood types (ABO)
Antibody Function:

4.IgD
*Antigen receptor on early B cells, need for B cell maturation
Antibody Function:

5.IgG
*Antiviral, antitoxin and antibacterial purposes
*Secondary response
*Only Ig that passes through the placenta
Antibody Function:

*Monoclonal Antibodies
*An immune response with only one specific antibody
*Uses for developing extremely specific and sensitive lab test
Ex: Home pregnancy test
*Also used as therapies for some illnesses
Ex: Rheumatoid Arthritis
*If it ends in "imab" or "umab", usually its monoclonal
Most immune responses are ployclonal
Aging and Immune Function
*Decreased T cell activity
*Thymic size is 15% of its max size
*Decreased production of specific antibodies
*Increase in circulation antigen-antibody complexes
*Increase in circulation autoantibodies
*Decrease in circulation memory B cells
*This all leads to a decreased inflammatory and immune response, making them more susceptible to infection and cancer
Hypersensitive Reactions:

*General
*An inappropriate or exaggerated response of immune system

*Individualized
Hypersensitive Reactions:

*3 types
1. Allergy: Deleterious effects of hypersensitivity to enviormental antigens
2.Autoimmune: Disturbance in the immunologic tolerance of self antigens
3.Alloimmune: Immune reaction to tissues of another individual
*Could be immediate or delayed
Allergic and Hypersensitive Reactions:

1. Type I
*IgE Mediated
*Signs and symptoms are due to mast cell degranulation
*Causes an immediate reactions
Ex: Beet sting, asthma, anaphylaxis
*Biggest problem is with gas exchange
Allergic and Hypersensitive Reactions:

1. Type I Manifestations
*Itching *Urticaria (Hives) *Conjuctivitis *Rhinitis (Nasal Congestion) *Hypotension *Bronchospasm *Dysrrhythmias (Abnormal rhythm)
*GI cramps and malabsorbtion
Allergic and Hypertensive Reactions:

2. Type II
*Specific cell or tissues are the target of an immune response
Allergic and Hypertensive Reactions:

2. Type II: 5 Mechanisms
1.Cell is destroyed by antibodies and complement
2.Cell destruction by phagocytosis
3.Soluble antigen may enter the circulation and deposit on tissues
4.Antibody dependent, cell mediated cytotoxicity
5.Causes target cell malfunction
Allergic and Hypertensive Reactions:

2. Type II (Cytotoxic)
*IgG and IgM mediated
*Example is mismatched blood transfusion
*Example is Graves Disease, which is an autoimmune disease, attacking the thyroid, causing overproduction of thyroid stimulating hormone
Blood Types:
*Type AB: Have A and B antigen, but no antibodies... Can receive any blood type, known as the Universal Recipient
*Type O: No antigens, but they have antibody A and antibody B... Can give blood to anyone, known as the Universal Donor
*Type O can only receive type O blood
Rhesus Compatibility (Rh)
*Positive/Negative associated with blood type
*Rh+ means the person has the Rh antigen
*Rh+ individual can receive blood from anyone, but Rh- can only receive from an Rh- donor
*AB+ is universal recipient and O- is universal donor
Allergic and Hypertensive Reactions:

2. Type III (Immune Complex)
*Involves the generation of the complement cascade
*Found in blood or body fluids
Hypersensitive Reactions:

3. Type III (Immune Complex)- Serum Sickness
*Reaction caused by the formation of immune complexes in the blood.
*Induced by antibiotics, food or insect venom
*Manifestations: Focal tissue, damage and edema, rash and swelling
*Self Limiting
*Treatment is to remove the sensitizing antigen
Hypersensitive Reactions:

3. Type III (Immune Complex)- Systematic Lupus Erythematosus
*Chronic inflammatory condition that can affect any organ in the body
*Linked to heredity, hormonal, immunologic and environmental
*Characterized by the formation of antigen-antibody complexes and very common in those with autoimmune diseases
Hypersensitive Reactions:

4. Type IV
*Does not involve antibodies, and therefore is also call cell-mediated
*Cytotoxic T Lymphocytes or Cytokine producing Th1 cells attack the body.
*This is delayed hypersensitivity, and make take 2-3 days to develop
Hypersensitive Reactions:

4. Type IV Examples
*Rheumatoid Arthritis: Complement cascade attack the synovial joints, causing pain and destruction of tissue
*Diabetes Mellitus 1: Body attacks beta cells in the pancreas
*Multiple Sclerosis: Body attacks the myelin sheath that helps with nerve conduction
Hypersensitive Reactions:

4. Type IV Examples Contd.
*Contact Dermatitis: Causes itching
*Crohn's Disease
*Transplant Rejection (Acute Graft): Attacks transplanted tissue or organ
Immune Deficiencies:
*Failure to immune mechanisms of self defense
*Primary (Congenital) Immunodeficiency: Caused by a genetic degecy
*Secondary (Acquired) Immunodeficiency: Caused by another illness or medication.
*Ex: Chemotherapy, HIV, Chronic Illnesses or immunosupressive drugs
Autoimmune Disease
*The body is attacking itself
*Systematic Lupus Erythematosus: Random inflammation throughout the body
*Guillain Barre Syndrome: Effects periperal N.S. and nerves are demyleinated
*RA: Attacks synovial joints primarily, leading to cartilage destruction and joint stiffness
*Graves Disease: Autoantibodies stimulate the TSH receptor cuasing TSH production and thryoid growth
*Diabetes Mellitus 1
Alloimmune Disease:
*Attacks non-self tissue that may be beneficial to the body
*Transfusion Rejection
*Transplant Rejection
*Fetomaternal Alloimmune Throbocytopenia: The fetus expresses different antigens that the mother does not have
Phase of Infection:
1. Pathogen Enters
2. Pathogen Incubates (Maintained for growth)
3. Then there is potential for inflammatory system to fight off the pathogen before it expands, and the person will not have any signs or symptoms
Phase of Infection Contd:
4. The inflammatory was not effective in destroying the pathogen so it reaches Prodromal Phase: Subclinical illness, disease present but few symptoms
5.Next it enters the Clinical Stage, which shows an overt infection with noticeable symptoms and changes in lab tests
Phase of Infection Cond:
6. Individual can then enter into 3 different paths:
A. Convalescence/Recovery: Infection is contained and treated
B. Chronic Infection: Such as TB, HIV
C. Overwhelming Infection: Usually the bacteria enters the bloodstream (Septicemia). If not treated, the pathogen will overtake the body and organs will start to shut down and high risk of death.