Immunity/Inflammation/Infection

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Purpose of Immune Response

To prevent infection of the injured tissue

First line of defense

Innate resistance
natural or native immunity
natural barriers (physical, mechanical, and biochemical)
Inflammation

Second line of defense

Inflammation
activated to protect the body from further injury, prevent infection of the injured tissue, and promote healing

Third line of defense

Adaptive (acquired) immunity
acquired or specific immunity
induced in a relatively slower and more specific process
involves memory, creating a more rapid response for next exposure to the same microorganism

Innate Immunity

Includes
Physical barriers
Mechanical barriers
Biochemical barriers
Inflammation

Physical barriers

Skin
Lining of hollow organs (eg: stomach)
Membrane sheets (genitourinary tract)
protection from pathogens
epithelial cells and other linings
sloughed off with dead skin
trapped and moved by cilia (coughing, sneezing)

Biochemical barriers

substances secreted to trap/ destroy pathogens
Mucus
Perspiration: lysozyme attack the cell walls of gm.pos. bacteria
Saliva (lysozyme)
Tears (lysozyme)
Ear wax (cerumen)
Glands in skin secrete antibacterial/antifungal lactic acid/fatty acids

sebaceous glands

in skin
secrete fatty acids and lactic acid
kill bacteria and fungi

antimicrobial peptides

toxic to certain bacteria, fungi, and viruses

Normal Bacterial Flora

NON PATHOGENIC
Do not cause disease
Help digest food in GI tract
Intestine helps digest fatty acids and other substances while preventing colonization with disease causers

Antibiotic

treatment can disturb the natural flora, leading to an overgrowth of:
Candida (yeast): yeast vaginitis common in women
Clostridium Difficile (bacteria)

Inflammation

Caused by a variety of materials, including infection, mechanical damage, ischemia, nutrient deprivation, temperature extremes, radiation, etc.
blood vessels dilate, increasing blood flow to the area
vascular permeability increases
Usually has local manifestations
- Redness
- Heat
- Swelling
- Pain
- Loss of Function

Inflammatory process

1) Bacteria and other pathogens enter wound
2) Platelets from blood release blood clotting proteins at would site
3) Mast cells secrete factors that mediate VASODILATION, vascular constriction,
4) Delivery of blood, plasma, & cells to injured area increases
5) Neutrophils secrete factors that kill and degrade pathogens
6) Neutrophils and macrophages remove pathogens by phagocytosis
7) Macrophages secrete hormones called cytokines that attract immune system cells to the site and activate cells involved in tissue repair
8) Inflammatory response continues until the foreign material is eliminated and the wound is repaired

Vascular response

Blood vessel dilation, increased vascular permeability and leakage, white blood cell adherence to the inner walls of the vessels and migration through the vessels
Occurs at site of tissue injury (localized reaction to contrast with immune response which is generalized)
Depends on activity of cellular and chemical components
Nonspecific: tissues respond the same way regardless of cause of injury - hypoxia, cut, infection etc.

Redness and Heat

occurs due to blood vessel dilation (increased circulation)

Swelling

occurs due to increased vascular permeability and leakage of fluid out of the vessel

Serous Fluid and Pus

occurs due to white blood cell migration through vessel to injury. WBCs (leukocytes) instructed to do so by CHEMOTACTIC FACTOR

Mast Cell

important to inflammatory process
Bags of cellular granules outside blood vessels
Activated by stimuli: tissue injury, chemical toxins, immunologic disturbances, after activation of toll-like receptors by viruses or bacteria
Granules break down and their chemical components are released and become active immediately
release histmaine, chemotactic factors (neurtrophils, eosinophils) & prostagladins

Mast cell degranulation

chemotactic factors are released
- neutrophils & eosinophils
histamine is released
prostaglandins are released

Histamine

Released post mast cell activation
Causes temporary, rapid vasoconstriction in large vessels and dilation in small vessels
Enhances vascular permeability
Two types of histamine receptors: H1 and H2.
Activation of H1's promotes inflammation, while activation of H2 receptors discourages inflammation

prostaglandins

platelet-activating factor
increase vasopermeability, vasodilation, platelet aggregation, neutrophil chemotaxis, and pain

Plasma protein systems

contain inactive enzymes (proenzymes)
responsible for:
Protein systems
Complement system
Coagulation system
Kinin system

Complement system

Can destroy pathogens directly
Activates or collaborates with every other component of the inflammatory response

1) opsonization of bacteria
2) chemo-attraction of leukocytes
3) induction of mast cell degranulation (anaphylatoxins)
4) formation of an attack complex that lyses cells by disrupting their outer membranes

Coagulation (clotting) system

Forms a fibrinous meshwork at an injured or inflamed site
Prevents the spread of infection
Keeps microorganisms and foreign bodies at the site of greatest inflammatory cell activity
Forms a clot that stops bleeding
Provides a framework for repair and healing
contains fibrin (an insoluble protein)

Kinin system

Functions to activate and assist inflammatory cells
Primary kinin is bradykinin
Causes dilation of blood vessels, pain, smooth muscle contraction, vascular permeability, and leukocyte chemotaxis

Phagocytosis

A cell ingests and disposes of foreign material, including bacteria, through phagocytosis

1) Phagocyte recognizes and binds to the target
2) Engulphment (endocytosis) of the target
3) Fusion of the phagocytic vacuole (phagosome) with the lysosome of the phagocyte
4) Destruction of the target by lysosomal enzymes

Phagocytes

live in the blood stream, and must exit into the tissues once inflammatory response has been activated
ingest bacteria, dead cells, and cellular debris
remove them from the area

Steps of phagocytosis

Margination: become more sticky, adhere
Diapedesis: emigration through to tissues
Opsonization: adherence to target
Engulfment : ingestion or endocytosis
Phagosome formation
Fusion with lysosomal granules
Destruction of the target

Neutrophils

Polymorphonuclear neutrophils (PMNs)
Predominate in early inflammatory responses
Ingest bacteria, dead cells, and cellular debris
Cells are short lived and become a component of the purulent exudate
first at site of injury

Monocytes

produced in the bone marrow, enter the circulation, and migrate to the inflammatory site, where they develop into macrophages

Macrophages

typically arrive at the inflammatory site 24 hours or later after neutrophils
release mediators and cytokines, allowing for prolonged inflammation

cytokines

intracellular chemical messengers
produced by macrophages
released during inflammation
increase adhesion molecules on endothelial cell membranes
cause chemotaxis and activation of neutrophils, macrophages, and eosinophils

Eosinophils

Mildly phagocytic
Defense against parasites and regulation of vascular mediators
contains granules with basic proteins

Natural killer (NK) cells

recognize and eliminate cells infected with viruses and some function in eliminating cancer cells

Platelets

Activation results in degranulation and interaction with components of the coagulation system

Opsonins

Fragments generated during complement activation
Adhere to surface of pathogenic microorganisms
Give phagocytes signal to destroy microorganism
usually instruct neutrophils and macrophages to destroy via phagocytosis

Interleukins

Cytokines produced primarily by macrophages and lymphocytes in response to a pathogen or stimulation by other products of inflammation

Interferon

Protects against viral infections
Produced and released by virally infected host cells in response to viral double-stranded RNA

Tumor necrosis factor-alpha

Secreted by macrophages
Induces fever by acting as an endogenous pyrogen
Increases synthesis of inflammatory serum proteins
Causes muscle wasting (cachexia) and intravascular thrombosis

chronic inflammation

Two weeks or longer
Sometimes preceded by an unsuccessful acute response
Large amounts of neutrophils degranulation and die
Leads to pus formation, purulent discharge and sometimes incomplete wound healing
Dense infiltration of lymphocytes and macrophages
If macrophages can't ward off infection, then a granuloma may form (encapsulated mass)

Systemic response to inflammation

Fever, Leukocytosis & pain

Fever

Induced by cytokines
Induced by endogenous pyrogens
Both act on the hypothalamus - raise temperature

Leukocytosis

Circulating leukocytes increase (mostly neutrophils).
Causes a "left shift" - more immature leuks than mature

Pain

Caused by kinins (eg: bradykinin) and prostaglandins at the site of injury (active in the inflammatory process)

Dysfunctional wound healing

Some part of the process was abnormal
Abnormalities in the inflammatory process, insufficient or excessive repair or re-infection
physiologic states : eg: diabetes, hypoxia

Keloid scar

Raised and extends beyond original wound boundaries. Often after surgery/piercing

Hypertrophic Scar

Remains within original boundaries but excessive tissue build up. Tends to regress over time.

Contracture

Results in deformity. Eg: scar tissue over a joint. Commonly seen with serious burns.

Dehiscense

Wound pulls apart at the suture line. Usually 5-12 days after suturing.

Innate (natural) Immunity

Inflammation

Active Immunity

Produced by an individual in response to an antigen or after immunization

Adaptive (Acquired) Immunity

Affords long-term protection
Also called "immune response"
Slow acting, specific and long lived.

Passive Acquired Immuity

Does not involve the host's immune response at all
Occurs when antibodies or T lymphocytes are transferred from a donor to recipient (eg: mother to child in utero or clinical immunotherapy)
temporary - last as long as the donated immune cells do

Immune response

involves antibodies (Humoral) and T-Cells (Cellular)

Antibody

protect individuals from infection
circulates in the blood and binds to antigens on infectious agent cells (bacteria/viruses)
Kills or triggers a response within the vicinity that leads to death of the bacteria/virus

T cells

triggered by an immune response
Develop into a variety of types of cells that react directly with antigen on surface of bacteria/viruses
Some of the resulting cells instruct other cells to secrete cytokines to kill the bacteria/viruses
Cytotoxic T Cells (Tc cells) attack and kill targets directly

Immune globulins

Prepared from individuals who've had the infection (eg: rabies)

Antigens

Molecules that react with antibodies or antigen receptors on B and T cells. Can also be immunogens. often combined with "adjuvants" in vaccines also present in allergens, and lead to the responses we call allergic reactions

Immunogenic antigens

immunogens
INDUCE an immune response
produce antibodies and T cells

Epitope

precise area of the molecule recognized
matches with the paratope (antigen binding site) on the antibody

Adjuvants

substances that boost the immune response producing activity

Immunogens

produce an immune response leading to activation of T cells

antibody titer

used to check a person's immunity to certain viruses. Since some antibodies don't circulate in blood, this assessment cannot always be done.

Cytotoxic T Lymphocytes

Instruct cells to self destroy (apoptosis) (tumour cells, viruses)

T lymphocytes

T cells that produce cytokines that activate macrophages (phagocytosis)

Regulatory T Lymphocytes

(Treg Cells): Produced in response to antigen recognition. Control/limit the immune response to protect the host's healthy cells.

Allergy

Deleterious effects of hypersensitivity to environmental (exogenous) antigens

Autoimmunity

Disturbance in the immunologic tolerance of self-antigens (antigen in the body that does not elicit an immune response)

Alloimmunity

Immune reaction to tissues of ANOTHER INDIVIDUAL
Disturbance in the immunologic tolerance of self - antigens (body usually controls and limits these).
Antibodies against their own antigens.
Damages host tissues.
Basis for many clinical disorders (lupus, rheumatoid arthritis)

Systemic lupus erythematosus (SLE)

Chronic multisystem inflammatory disease
Autoantibodies against:
Nucleic acids, erythrocytes, coagulation proteins, phospholipids, lymphocytes, platelets, etc.

type 1 hypersensitivity reaction

IgE-mediated reaction
Principally involves mast cells
Caused by foods, drugs, pollens, dust, molds, bees, etc.
S&S include itching, edema, hypotension, bronchospasms (esp. with asthma) conjunctivitis, rhinitis, urticaria (hives) & dysrhythmias
Ex: allergic rhinitis

allergic rhinitis

Type 1 IgE mediated reaction
allergic reaction that occurs when the immune system overreacts to substances that have been inhaled
seasonally caused by an allergic reaction to pollen spores
caused by ragweed, fungus, grass, tree pollen, pet danders, etc.

type 2 hypersensitivity reaction

Tissue-specific reaction
Mediated by IgG and IgM
Principally involves macrophages in tissues
Generally reactions against a specific cell or tissue
Occurs with graves disease, autoimmune hemolytic anemia, etc.
Often caused by drugs

HIV

infects and destroys helper T cells necessary for the development of plasma cells and cytotoxic T cells
suppress the immune response against itself & creates a generalized immune deficiency by suppressing the development of immune responses against other pathogens and microorganisms. LEADS TO AIDS!!!
a blood-borne pathogen. Most common route of transmission is through heterosexual activity. It is also a retrovirus, containing genetic information in the form of RNA rather than DNA
The presence of circulating antibody against the HIV indicates infection by the virus, although most people asymptomatic
Although the person may appear asymptomatic, the virus is actively proliferating in lymph nodes

coagulation cascade

intrinsic pathway: Hageman factor circulates in its inactive form in the blood. the intrinsic clotting pathway is activated when it contains injured endothelium
extrinsic pathway: endothelial cells and macrophages are damaged, releasing tissue thromboplastin

tissue regeneration

Restoration of the original structure and physiologic function
Occurs with healthy cells that remain after tissue has been destroyed
Begin to proliferate by mitosis to replace the lost cells

tissue repair

Takes place if fibrin persists in the wound
Regeneration is not possible
Replacement of destroyed tissue with scar tissue
Scar tissue is not able to perform the physiologic functions of the destroyed tissue

primary intention

wounds heal after there has been minimal tissue loss, such as after a clean surgical incision
process of collagen synthesis

secondary intention

occurs in wounds with significant tissue loss
left open and closes naturally

fibroblasts

migrate to the site of inflammation to begin the process of tissue repair
synthesize collagen and fibrin
form a matrix for replacement of tissue cells or scar tissue

B lymphocytes

B cells
produce antibodies that enter blood and react with antigens

T lymphocytes

T cells
attack the antigen directly

allergens

antigens that induce an allergic response

immunoglobulin

Molecules known to have specificity for several antigens
Characterized by antigenic, structural, and functional differences
IgG, IgM, IgA, IgD, IgE

IgM

largest of immunoglobulins

IgE

spacial class of antibody that protects the individual from infection with large parasites
produced against relatively harmless environmental antigens
causes allergies such as allergic rhinitis
designed to initiate an inflammatory response
attracts eosinophils to the site of a parasitic infection

hypersensitivity

an altered immunologic response to an antigen
results in disease or damage to the individual cell
immediate: within minutes to hours
delayed: several hours. reaches max. severity days later

anaphylaxis

most rapid and sever immediate hypersensitivity reaction

non immunologic urticaria

hives that occur as a result of exposure to cold temperatures, emotional stress, meds, etc.

atopic

individual genetically predisposed to developing allergies

tolerance

State of immunologic control of that the individual does not make a detrimental immune response against their own cells and tissues

blood group antigens

RBC surface antigens which can be target of alloimmune reactions

type 3

immune complex mediated hypersensitivity reaction
no organ specific reactions

type 4

cell-mediated hypersensitivity reactions

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