exam 2 Flashcards by britt rank

Type of immunity that:

Non-specific general Immediate response
No immunological memory
broad range

Innate Immunity

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type of immunity that:

Specific to antigen
Lag time from exposure to response
Immunological memory after exposure

Adaptive Immunity

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Natural barriers and the inflammatory response

Innate resistance

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Skin and mucous membranes

First line

Natural barriers:

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Inflammation is the ____ line of defense

second

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Adaptive (acquired) immunity is the ____ line of defense

third

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Synthesize and secrete substances to trap or destroy microorganisms

Antimicrobial peptides
Normal microbiome

Biochemical barriers
(first line of defense)

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Cellular and chemical components
Nonspecific
Rapidly initiated

Inflammatory response

second line of defense

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Clinical Indications:

Generalized malaise
Fever
Pain often localized to the inflamed area
Rapid pulse rate

Acute Inflammatory Response

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Lab Values:

Increased neutrophil count in peripheral blood
Increased erythrocyte sedimentation rate
Increased acute phase proteins in blood

Acute Inflammatory Response

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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)

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Can destroy pathogens directly

Activates or collaborates with every other component of the inflammatory response

Complement system

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Pathway that:

Antibody and antigens

Classical

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Pathway that:

Mannose-containing bacterial carbohydrates

Lectin:

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Pathway that:

Gram-negative bacterial and fungal cell wall polysaccharides (pathogen surfaces)

Alternative:

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Humoral
Pattern Receptors
Compliment
Enzymes
Cytokines

Cellular
Phagocytes
Natural Killer Cells

Innate Immunity

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Humoral
Antibodies
Cytokines

Cellular
T cells
B cells

Adaptive Immunity

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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

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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

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Inflammation Cellular Mediators that:

Mast cells
Granulocytes (neutrophils, eosinophils, basophils)
Monocytes and macrophages
Natural killer (NK) cells and lymphocytes
Cellular fragments (platelets)

Cellular mediators

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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

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Inflammation Cellular Mediators that:

Regulate innate or adaptive resistance by affecting other neighboring cells.

Are either proinflammatory or antiinflammatory.

Chemokines or cytokines

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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:

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Cytokines that:

Are produced primarily by macrophages and lymphocytes in response to a microorganisms or stimulation by other products of inflammation.

Interleukins (ILs)

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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

1. Cell is destroyed by antibodies and complement. 2. Cell destruction occurs through phagocytosis. 3. Neutrophils release granules. 4. Antibody-dependent cell-mediated cytotoxicity is present. 5. 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