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adv. patho > exam 2 > Flashcards

exam 2 Flashcards

1
Q

Type of immunity that:

Non-specific general Immediate response
No immunological memory
broad range

A

Innate Immunity

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2
Q

type of immunity that:

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

A

Adaptive Immunity

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3
Q

Natural barriers and the inflammatory response

A

Innate resistance

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4
Q

Skin and mucous membranes

A

First line

Natural barriers:

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5
Q

Inflammation is the ____ line of defense

A

second

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6
Q

Adaptive (acquired) immunity is the ____ line of defense

A

third

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7
Q

Synthesize and secrete substances to trap or destroy microorganisms

Antimicrobial peptides
Normal microbiome

A 
Biochemical barriers
(first line of defense)
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8
Q

Cellular and chemical components
Nonspecific
Rapidly initiated

A

Inflammatory response

second line of defense

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9
Q

Clinical Indications:

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

A

Acute Inflammatory Response

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10
Q

Lab Values:

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

A

Acute Inflammatory Response

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11
Q

Protein systems that provide a biochemical barrier against invading pathogens are the:

(3 types of plasma protein systems)

A

Complement system
Clotting system
Kinin system

(Plasma Protein Systems)

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12
Q

Can destroy pathogens directly

Activates or collaborates with every other component of the inflammatory response

A

Complement system

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13
Q

Pathway that:

Antibody and antigens

A

Classical

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14
Q

Pathway that:

Mannose-containing bacterial carbohydrates

A

Lectin:

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15
Q

Pathway that:

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

A

Alternative:

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16
Q 
Humoral
Pattern Receptors
Compliment
Enzymes
Cytokines

Cellular
Phagocytes
Natural Killer Cells

A

Innate Immunity

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17
Q

Humoral
Antibodies
Cytokines

Cellular
T cells
B cells

A

Adaptive Immunity

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18
Q

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

A

clotting

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19
Q

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.

A

Kinin

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20
Q

Inflammation Cellular Mediators that:

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

A

Cellular mediators

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21
Q

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.

A

Biochemical mediators

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22
Q

Inflammation Cellular Mediators that:

Regulate innate or adaptive resistance by affecting other neighboring cells.

Are either proinflammatory or antiinflammatory.

A

Chemokines or cytokines

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23
Q

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).

A

Actions are pleiotropic:

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24
Q

Cytokines that:

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

A

Interleukins (ILs)

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25
Q

Cytokines that:

Protect against viral infections

A

Interferons (INFs)

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26
Q

Cytokines that:

Produces local and systemic effects

A

TNF-α

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27
Q

Cytokines that:

pro inflammatory that causes fevers

A

IL1

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28
Q

Cytokines that:

pro inflammatory that help with healing

A

IL6

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29
Q

Are cellular bags of granules located in loose connective tissues close to blood vessels.

(Skin, digestive lining, and respiratory tract)

A

Mast Cells

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30
Q

how are mast cells activated?

A

Physical injury, chemical agents, immunologic processes, and TLRs

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31
Q

Mast cells release chemicals in what two ways?

A

Degranulation

Synthesis of lipid-derived chemical mediators

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32
Q

Predominate in early inflammatory responses.

Ingest bacteria, dead cells, and cellular debris.

Are short lived and become components of the purulent exudate (pus).

A

Neutrophils

Phagocytes

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33
Q

Primary roles:

Removal of debris in sterile lesions
Phagocytosis of bacteria in nonsterile lesions

A

Neutrophils

Phagocytes

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34
Q

Provide the defense against parasites and regulate vascular mediators.

Help control vascular effects of inflammation.

primary defense against parasites

A

Eosinophils

Phagocytes

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35
Q

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.

A

Basophils

Phagocytes

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36
Q

Is the process by which a cell ingests and disposes of foreign material.

A

Phagocytosis

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37
Q

6 steps of Phagocytosis

A 
Opsonization
Recognition
Engulfment 
Phagosome formation
Fusion with lysosomal granules
Destruction of the target
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38
Q

Are susceptible to bacterial infections.

Have transiently depressed inflammatory and immune function.

A

neonates

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39
Q

End-products of adaptive immunity:

T and B cells

A

Lymphocytes:

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40
Q

End-products of adaptive immunity:

Immunoglobulins (Ig)

A

Antibodies:

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41
Q

Each individual T or B cell specifically recognizes only one particular_______

A

antigen.

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42
Q

Primary lymphoid organs:

Is the _____ for T cells
_____ for B cells.

A

Is the thymus for T cells

bone marrow for B cells.

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43
Q

B cell receptors (BCRs) on their _______

A

cell membrane

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44
Q

types of T cells

A

Cytotoxic T-cells
Helper T-cells
Memory T-cells

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45
Q

contains surface protein CD8
destroys viral infections
distroys tumor cells

A

Cytotoxic T-cells

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46
Q

contains CD4

A

Helper T-cells

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47
Q

Antibodies or T cells are produced after either
a natural exposure to an antigen or after immunization.

Is long lived

A

Active Immunity—Active Acquired Immunity

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48
Q

Preformed antibodies or T lymphocytes are transferred from a donor to a recipient.

Occurs naturally or artificially.

Is temporary or short lived.

A

Passive Immunity—Passive Acquired Immunity

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49
Q

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

A

Antigen

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50
Q

An antigen that can trigger an immune response

A

Immunogenic antigen

51
Q

Antigen’s binding site:

A

antigenic determinant (epitope)

52
Q

Antibody or lymphocyte’s binding site:

A

Antigen-binding site (paratope)

53
Q

Is also called immunoglobulin (Ig).

Is produced by plasma cells.

A

Antibody

54
Q

Antibody that:

Most of protective activity against infection

Crosses the placenta

A

IgG

55
Q

Antibody that:

Most of protective activity in body secretions

A

IgA

56
Q

Antibody that:

Mediator of many common allergic responses

Defends against parasitic infections

A

IgE

57
Q

Antibody that:

Functions as one type of B-cell antigen receptor

A

IgD

58
Q

Antibody that:

First antibody produced during the initial, or primary, response to an antigen

A

IgM

59
Q

Protects against infection.

A

antibody

60
Q

type of antibody that

Inactivates or blocks the binding of an antigen to a receptor.

A

Neutralization: (direct)

61
Q

type of antibody that

: Clumps insoluble particles in suspension.

A

Agglutination (direct)

62
Q

type of antibody that

Makes a soluble antigen into an insoluble precipitate.

A

Precipitation:

63
Q

Is an exaggerated response against an environmental antigen.

A

Allergy:

64
Q

Is a misdirected response against the host’s own cells.

A

Autoimmunity

65
Q

Is directed against beneficial foreign tissues (e.g., transfusions, transplants)

A

Alloimmunity:

66
Q

Immunity is insufficient to protect the host.

A

Immunodeficiency:

67
Q

Hypersensitivity where:

IgE mediated

A

Type I

68
Q

Hypersensitivity where:

• Tissue-specific reactions

A

Type II

69
Q

Hypersensitivity where:

• Immune complex mediated

A

Type III

70
Q

Hypersensitivity where:

  • Cell mediated
  • Delayed
A

Type IV

71
Q 
Develops in minutes after exposure.
 Itching
 Erythema
 Headaches
 Contraction of respiratory bronchioles
 Laryngeal edema 
 Vomiting, abdominal cramps, diarrhea
 Vascular collapse
A

Anaphylaxis

72
Q

 Bronchial constriction
 Edema
 Vasodilation

A

Manifestations from H1

Type I Hypersensitivity

73
Q

Increases gastric secretions

Decreases the release of
histamine from mast cells
and basophils

A

Manifestations from H2

Type I Hypersensitivity

74
Q

5 steps in Type II Hypersensitivity

A
  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
75
Q

Is characterized by a variety of symptoms.

Periods of remission or exacerbation occur.

Examples
Serum sickness
Arthritis reaction—Rheumatoid 
Arthus reaction
Systemic Lupus
A

Type III Hypersensitivity Immune Complex Disease

76
Q

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.

A

Type IV Hypersensitivity

77
Q

Is a breakdown of tolerance during which the body’s immune system begins to recognize self-antigens as foreign.

A

Autoimmunity

78
Q

Individual’s immune system reacting against antigens on the tissues of other members of the same species

A

Alloimmunity

79
Q

Clinical manifestations:

Arthralgias or arthritis 
Vasculitis and rash 
Renal disease 
Hematologic changes, especially anemia
Cardiovascular disease
A

Systemic lupus erythematosus (SLE

80
Q

5 SLE treatment’s

A 
Corticosteroids
Hydroxyhloroquin
Nonsteroidal anti-inflammatory drugs
Disease modifying anti-rheumatic drugs
Immunosuppressive ddrugs
81
Q

Exist in reservoirs (contaminated soil, contaminated water, breast milk), animals, or another human.

A

Infectious microorganisms:

82
Q

Is the period from initial exposure to the onset of the first symptoms; could last from hours to years

A

Incubation

83
Q

The occurrence of initial symptoms are often very mild with feelings of discomfort and tiredness.

A

Prodromal

84
Q

Invasion is farther and affects other body tissues.

A

Invasion

85
Q

Recovery occurs and symptoms decline, or the disease is fatal, or has a period of latency.

A

Convalescence

86
Q

Manifestations include:

Fatigue, malaise, weakness, loss of concentration, generalized aching, and loss of appetite.

A

Infectious Disease

87
Q

Is the hallmark of infection.

Body temperature is regulated at a higher level than normal.

A

Fever

88
Q

Diseases with relatively high, but constant, rates of infection in a particular population

A

Endemic

89
Q

Number of new infections in a particular population that greatly exceeds the number usually observed

A

Epidemic

90
Q

An epidemic that spreads over a large area such as a continent or worldwide

A

Pandemic

91
Q

Enzymes released during growth

Damages cell membranes, activates second messengers, and inhibits protein synthesis.

A

Exotoxins

92
Q

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

A

Endotoxins:

93
Q

Alter surface molecules that express antigens.

A

Resistant

94
Q

Produce toxins and extracellular enzymes to destroy phagocytic cells.

A

Bacterial Infections

95
Q

Coat the crystalline fragment (Fc) portion of an individual’s antibody, preventing complement activation or phagocytosis.

A

Bacterial Infections

96
Q

Degrade immune cells.
Bind and neutralize antibodies.
Evade complement.
Cause immune suppression.

A

Bacterial Infections

97
Q

Systemic infection is usually from immunosuppression.

A

Fungal Infections

98
Q

Adapt to the host environment.

Wide temperature variations, low oxygen, alkaline pH

A

Fungal Infections

99
Q

Suppress the immune defenses.

A

Fungal Infections

100
Q

Some fungi survive ________ by replicating in the phagosome or inhibiting lysosomal enzymes.

A

phagocytosis

101
Q

______ encapsulate, alter antigen expression, and stimulate immunosuppressive cytokines to resist phagocytosis.

A

Fungi

102
Q

Is the most common fungal infection.

A

Candida albicans:

103
Q

Resides in skin, gastrointestinal tract, mouth, and vagina.

Local defense mechanisms and microbiome produce antifungal agents.

A

Candida albicans

104
Q 
Survive intracellularly
Coat themselves
Gene switch
Antigenic variation
Degrade IgG and IgA
Neutralize antibodies 	
Tissue damage from infestation and toxins
A

Parasitic and ProtozoanInfections

105
Q

Are rarely transmitted from human to human; are transmitted mainly through vectors.

A

Parasitic and ProtozoanInfections

106
Q

Intracellular parasites

A

Viruses

107
Q

Life cycle: Completely intracellular

Attaches or binds to the host cell via protein receptors.

Penetrates the host cell.

A

Viral Infection and Injury

108
Q

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.

A

Viral Infection and Injury

109
Q

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)

A

Viral Infection and Injury

110
Q

Depletes the body’s T helper (Th) cells.

Is susceptible to life-threatening infections and cancer.

A

Acquired immunodeficiency syndrome (AIDS) is caused by the virus, HIV.

111
Q

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.

A

RNA virus (retrovirus)

112
Q

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.

A

HIV structure

113
Q

CXCR4 and CCR5
CXCR4 prefer T cells and form syncytium.
CCR5 prefer macrophages and do not form syncytium.

A

Co-receptors

114
Q

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

A

Acquired Immunodeficiency Syndrome

115
Q

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

A

Acquired Immunodeficiency Syndrome

116
Q

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.

A

Acquired Immunodeficiency Syndrome

117
Q

can results in reactions such as disturbances of cognition, emotion, and behavior that can adversely affect well-being

A

Stress

118
Q

Nearly of all illness and disease can be attributed to stress

A

70%

119
Q

Three stages of General Adaptation Syndrome

A

Alarm stage

Stage of resistance or adaptation

Stage of exhaustion

120
Q

Glucocorticoids from the adrenal cortex in response to adrenocorticotropic hormone (ACTH) from the pituitary gland

A

Major Stress Hormones

121
Q

Balances the sympathetic nervous system

Influences the adaptation or maladaptation to stress

A

Parasympathetic System

122
Q

Adaptive physiologic response to stressful events

A

Allostasis

123
Q

Long-term or chronic exaggerated responses to stress

Can lead to disease

A

Chronic or Disregulated Allostasis

adv. patho (10 decks)

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