exam 2 Flashcards
Type of immunity that:
Non-specific general Immediate response
No immunological memory
broad range
Innate Immunity
type of immunity that:
Specific to antigen
Lag time from exposure to response
Immunological memory after exposure
Adaptive Immunity
Natural barriers and the inflammatory response
Innate resistance
Skin and mucous membranes
First line
Natural barriers:
Inflammation is the ____ line of defense
second
Adaptive (acquired) immunity is the ____ line of defense
third
Synthesize and secrete substances to trap or destroy microorganisms
Antimicrobial peptides
Normal microbiome
Biochemical barriers (first line of defense)
Cellular and chemical components
Nonspecific
Rapidly initiated
Inflammatory response
second line of defense
Clinical Indications:
Generalized malaise
Fever
Pain often localized to the inflamed area
Rapid pulse rate
Acute Inflammatory Response
Lab Values:
Increased neutrophil count in peripheral blood
Increased erythrocyte sedimentation rate
Increased acute phase proteins in blood
Acute Inflammatory Response
Protein systems that provide a biochemical barrier against invading pathogens are the:
(3 types of plasma protein systems)
Complement system
Clotting system
Kinin system
(Plasma Protein Systems)
Can destroy pathogens directly
Activates or collaborates with every other component of the inflammatory response
Complement system
Pathway that:
Antibody and antigens
Classical
Pathway that:
Mannose-containing bacterial carbohydrates
Lectin:
Pathway that:
Gram-negative bacterial and fungal cell wall polysaccharides (pathogen surfaces)
Alternative:
Humoral Pattern Receptors Compliment Enzymes Cytokines
Cellular
Phagocytes
Natural Killer Cells
Innate Immunity
Humoral
Antibodies
Cytokines
Cellular
T cells
B cells
Adaptive Immunity
PLasma protein system where:
Forms a fibrinous mesh at an injured or inflamed site
Prevents the spread of infection.
Keeps microorganisms and foreign bodies at the site of inflammation for removal.
Forms a clot that stops the bleeding.
Provides a framework for repair and healing
clotting
Plasma protein system where:
Functions to activate and assist inflammatory cells.
Causes dilation of blood vessels, pain, smooth muscle contraction, vascular permeability, and leukocyte chemotaxis.
Kinin
Inflammation Cellular Mediators that:
Mast cells
Granulocytes (neutrophils, eosinophils, basophils)
Monocytes and macrophages
Natural killer (NK) cells and lymphocytes
Cellular fragments (platelets)
Cellular mediators
Inflammation Cellular Mediators that:
Are responsible for vascular changes.
Modulate the localization and activities of other inflammatory cells.
Include histamine, chemotactic factors, leukotrienes, prostaglandins, and the platelet-activating factor.
Biochemical mediators
Inflammation Cellular Mediators that:
Regulate innate or adaptive resistance by affecting other neighboring cells.
Are either proinflammatory or antiinflammatory.
Chemokines or cytokines
Inflammation Cellular Mediators that:
The same molecule may have a large variety of different biologic activities, depending on the particular target cell to which it binds.
Are either synergistic or antagonistic.
Include interleukins, interferons, and tumor necrosis factor (TNF).
Actions are pleiotropic:
Cytokines that:
Are produced primarily by macrophages and lymphocytes in response to a microorganisms or stimulation by other products of inflammation.
Interleukins (ILs)
Cytokines that:
Protect against viral infections
Interferons (INFs)
Cytokines that:
Produces local and systemic effects
TNF-α
Cytokines that:
pro inflammatory that causes fevers
IL1
Cytokines that:
pro inflammatory that help with healing
IL6
Are cellular bags of granules located in loose connective tissues close to blood vessels.
(Skin, digestive lining, and respiratory tract)
Mast Cells
how are mast cells activated?
Physical injury, chemical agents, immunologic processes, and TLRs
Mast cells release chemicals in what two ways?
Degranulation
Synthesis of lipid-derived chemical mediators
Predominate in early inflammatory responses.
Ingest bacteria, dead cells, and cellular debris.
Are short lived and become components of the purulent exudate (pus).
Neutrophils
Phagocytes
Primary roles:
Removal of debris in sterile lesions
Phagocytosis of bacteria in nonsterile lesions
Neutrophils
Phagocytes
Provide the defense against parasites and regulate vascular mediators.
Help control vascular effects of inflammation.
primary defense against parasites
Eosinophils
Phagocytes
Are similar to but are not mast cells.
Are an important source for cytokine IL-4.
Are associated with allergies and asthma.
Their role is uncertain.
Basophils
Phagocytes
Is the process by which a cell ingests and disposes of foreign material.
Phagocytosis
6 steps of Phagocytosis
Opsonization Recognition Engulfment Phagosome formation Fusion with lysosomal granules Destruction of the target
Are susceptible to bacterial infections.
Have transiently depressed inflammatory and immune function.
neonates
End-products of adaptive immunity:
T and B cells
Lymphocytes:
End-products of adaptive immunity:
Immunoglobulins (Ig)
Antibodies:
Each individual T or B cell specifically recognizes only one particular_______
antigen.
Primary lymphoid organs:
Is the _____ for T cells
_____ for B cells.
Is the thymus for T cells
bone marrow for B cells.
B cell receptors (BCRs) on their _______
cell membrane
types of T cells
Cytotoxic T-cells
Helper T-cells
Memory T-cells
contains surface protein CD8
destroys viral infections
distroys tumor cells
Cytotoxic T-cells
contains CD4
Helper T-cells
Antibodies or T cells are produced after either
a natural exposure to an antigen or after immunization.
Is long lived
Active Immunity—Active Acquired Immunity
Preformed antibodies or T lymphocytes are transferred from a donor to a recipient.
Occurs naturally or artificially.
Is temporary or short lived.
Passive Immunity—Passive Acquired Immunity
Is a molecule that can react with antibodies or receptors on B and T cells.
Is mostly protein but can be other molecules as well.
Sites for binding to antibodies and lymphocytes
Antigen
An antigen that can trigger an immune response
Immunogenic antigen
Antigen’s binding site:
antigenic determinant (epitope)
Antibody or lymphocyte’s binding site:
Antigen-binding site (paratope)
Is also called immunoglobulin (Ig).
Is produced by plasma cells.
Antibody
Antibody that:
Most of protective activity against infection
Crosses the placenta
IgG
Antibody that:
Most of protective activity in body secretions
IgA
Antibody that:
Mediator of many common allergic responses
Defends against parasitic infections
IgE
Antibody that:
Functions as one type of B-cell antigen receptor
IgD
Antibody that:
First antibody produced during the initial, or primary, response to an antigen
IgM
Protects against infection.
antibody
type of antibody that
Inactivates or blocks the binding of an antigen to a receptor.
Neutralization: (direct)
type of antibody that
: Clumps insoluble particles in suspension.
Agglutination (direct)
type of antibody that
Makes a soluble antigen into an insoluble precipitate.
Precipitation:
Is an exaggerated response against an environmental antigen.
Allergy:
Is a misdirected response against the host’s own cells.
Autoimmunity
Is directed against beneficial foreign tissues (e.g., transfusions, transplants)
Alloimmunity:
Immunity is insufficient to protect the host.
Immunodeficiency:
Hypersensitivity where:
IgE mediated
Type I
Hypersensitivity where:
• Tissue-specific reactions
Type II
Hypersensitivity where:
• Immune complex mediated
Type III
Hypersensitivity where:
- Cell mediated
- Delayed
Type IV
Develops in minutes after exposure. Itching Erythema Headaches Contraction of respiratory bronchioles Laryngeal edema Vomiting, abdominal cramps, diarrhea Vascular collapse
Anaphylaxis
Bronchial constriction
Edema
Vasodilation
Manifestations from H1
Type I Hypersensitivity
Increases gastric secretions
Decreases the release of
histamine from mast cells
and basophils
Manifestations from H2
Type I Hypersensitivity
5 steps in Type II Hypersensitivity
- Cell is destroyed by antibodies and complement.
- Cell destruction occurs through phagocytosis.
- Neutrophils release granules.
- Antibody-dependent cell-mediated cytotoxicity is present.
- Causes target cell malfunction
Is characterized by a variety of symptoms.
Periods of remission or exacerbation occur.
Examples Serum sickness Arthritis reaction—Rheumatoid Arthus reaction Systemic Lupus
Type III Hypersensitivity Immune Complex Disease
Is mediated by T lymphocytes or is cell mediated.
Destruction of the tissue is usually caused by direct killing by toxins from cytotoxic T (Tc) cells
Helper T (Th) 1 and Th 17 cells produce cytokines that recruit phagocytes, especially macrophages.
Type IV Hypersensitivity
Is a breakdown of tolerance during which the body’s immune system begins to recognize self-antigens as foreign.
Autoimmunity
Individual’s immune system reacting against antigens on the tissues of other members of the same species
Alloimmunity
Clinical manifestations:
Arthralgias or arthritis Vasculitis and rash Renal disease Hematologic changes, especially anemia Cardiovascular disease
Systemic lupus erythematosus (SLE
5 SLE treatment’s
Corticosteroids Hydroxyhloroquin Nonsteroidal anti-inflammatory drugs Disease modifying anti-rheumatic drugs Immunosuppressive ddrugs
Exist in reservoirs (contaminated soil, contaminated water, breast milk), animals, or another human.
Infectious microorganisms:
Is the period from initial exposure to the onset of the first symptoms; could last from hours to years
Incubation
The occurrence of initial symptoms are often very mild with feelings of discomfort and tiredness.
Prodromal
Invasion is farther and affects other body tissues.
Invasion
Recovery occurs and symptoms decline, or the disease is fatal, or has a period of latency.
Convalescence
Manifestations include:
Fatigue, malaise, weakness, loss of concentration, generalized aching, and loss of appetite.
Infectious Disease
Is the hallmark of infection.
Body temperature is regulated at a higher level than normal.
Fever
Diseases with relatively high, but constant, rates of infection in a particular population
Endemic
Number of new infections in a particular population that greatly exceeds the number usually observed
Epidemic
An epidemic that spreads over a large area such as a continent or worldwide
Pandemic
Enzymes released during growth
Damages cell membranes, activates second messengers, and inhibits protein synthesis.
Exotoxins
Contained in cell walls of gram-negative bacteria and released during lysis of bacteria
Is called pyrogenic bacteria because they activate inflammation and produce fever
Endotoxins:
Alter surface molecules that express antigens.
Resistant
Produce toxins and extracellular enzymes to destroy phagocytic cells.
Bacterial Infections
Coat the crystalline fragment (Fc) portion of an individual’s antibody, preventing complement activation or phagocytosis.
Bacterial Infections
Degrade immune cells.
Bind and neutralize antibodies.
Evade complement.
Cause immune suppression.
Bacterial Infections
Systemic infection is usually from immunosuppression.
Fungal Infections
Adapt to the host environment.
Wide temperature variations, low oxygen, alkaline pH
Fungal Infections
Suppress the immune defenses.
Fungal Infections
Some fungi survive ________ by replicating in the phagosome or inhibiting lysosomal enzymes.
phagocytosis
______ encapsulate, alter antigen expression, and stimulate immunosuppressive cytokines to resist phagocytosis.
Fungi
Is the most common fungal infection.
Candida albicans:
Resides in skin, gastrointestinal tract, mouth, and vagina.
Local defense mechanisms and microbiome produce antifungal agents.
Candida albicans
Survive intracellularly Coat themselves Gene switch Antigenic variation Degrade IgG and IgA Neutralize antibodies Tissue damage from infestation and toxins
Parasitic and ProtozoanInfections
Are rarely transmitted from human to human; are transmitted mainly through vectors.
Parasitic and ProtozoanInfections
Intracellular parasites
Viruses
Life cycle: Completely intracellular
Attaches or binds to the host cell via protein receptors.
Penetrates the host cell.
Viral Infection and Injury
Releases genetic information into the host cytoplasm.
RNA viruses enter the host nucleus.
Produce messenger RNA (mRNA) (new viral material).
May produce provirus DNA (retroviruses, HIV).
DNA viruses enter the host nucleus.
May integrate into the host DNA; may make mRNA.
Viral Infection and Injury
Harmful effects:
Inhibition of DNA, RNA, or protein synthesis
Disruption of lysosomal membranes
Promotion of cell apoptosis
Fusion of adjacent cells (giant cells)
Transformation into cancer cells
Alteration of antigenic properties (immune attacks normal cells)
Viral Infection and Injury
Depletes the body’s T helper (Th) cells.
Is susceptible to life-threatening infections and cancer.
Acquired immunodeficiency syndrome (AIDS) is caused by the virus, HIV.
Stores genetic material on two copies of RNA rather than the usual dsDNA.
Carries an enzyme, reverse transcriptase, that creates a dsDNA version of the virus.
RNA virus (retrovirus)
gp120 protein binds to the CD4 molecule found primarily on the surface of Th cells
Typically cause a significant decrease of Th.
Reverses CD4:CD8 ratio.
HIV structure
CXCR4 and CCR5
CXCR4 prefer T cells and form syncytium.
CCR5 prefer macrophages and do not form syncytium.
Co-receptors
Clinical manifestations:
Serologically negative, serologically positive but asymptomatic, early stages of HIV, or AIDS
Window period: Infectious but asymptomatic
Fatigue, headache, muscle aches, fever
May be asymptomatic for years
Acquired Immunodeficiency Syndrome
Diagnosis:
Uses various clinical conditions and laboratory tests
Atypical or opportunistic infections and/or cancer
CD4+ T-cell numbers are at or below 200 cells/µL
Acquired Immunodeficiency Syndrome
Treatment: Antiretroviral therapy (ART)
Three or more drugs: Usually two drugs target reverse transcriptase (inhibits reverse transcriptase) and one is from a different class of drugs.
Acquired Immunodeficiency Syndrome
can results in reactions such as disturbances of cognition, emotion, and behavior that can adversely affect well-being
Stress
Nearly of all illness and disease can be attributed to stress
70%
Three stages of General Adaptation Syndrome
Alarm stage
Stage of resistance or adaptation
Stage of exhaustion
Glucocorticoids from the adrenal cortex in response to adrenocorticotropic hormone (ACTH) from the pituitary gland
Major Stress Hormones
Balances the sympathetic nervous system
Influences the adaptation or maladaptation to stress
Parasympathetic System
Adaptive physiologic response to stressful events
Allostasis
Long-term or chronic exaggerated responses to stress
Can lead to disease
Chronic or Disregulated Allostasis
