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Pathophysiology > Unit 1 - Chapter 7 - Immunity > Flashcards

Unit 1 - Chapter 7 - Immunity Flashcards

1
Q

what is the immune system reponsible for

A

body defenses

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2
Q

what are nonspecific responses (defenses)

A

phagocytosis and inflammation

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3
Q

what are some examples of specific responses (defenses)

A

production of specific antibodies against foreign substances

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4
Q

what are the 4 components of the immune systems

A
  • lmymphoid structure
  • immune cells
  • tissues
  • chemical mediators
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5
Q

what are some examples of lymphoid structures

A

-lymoh nodes
- spleen
- tonsils
- intestinal lymphois tissue
- lymphatic circulation

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6
Q

what are some examples of immune cells

A
  • lymphocytes
  • macrophagues
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7
Q

what are examples of tissues

A
  • bone marrow
  • thymus
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8
Q

what are examples of chemical mediators

A

histamine and interleukins

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9
Q

what are antigens and what are examples of cell suface antigens

A
  • usually exogenous substances
  • proteins, polysaccharides, glycoproteins
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10
Q

expand on self antigens

A
    • HLA proteins label cells of the individual.
  • Immune system ignores self-cells.
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11
Q

expand on non-self antigens

A
  • Immune system recognizes specific nonself antigens as
    foreign.
  • Development of a specific response to that particular antigen
  • Memory cells produced to respond quickly to antigen
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12
Q

expand on macrophages

A

 Initiation of immune response
 Develop from monocytes
 Part of the mononuclear phagocytotic system
 Engulf foreign material
 Display antigens of foreign material
 Secrete chemicals (monokines, interleukins)
 Present throughout the body

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13
Q

expand on T lymphocytes

A
  • From bone marrow stem cells
  • Further differentiation in thymus
  • Cell-mediated immunity
  • Cytotoxic T killer cells
  • Helper T cells
  • Memory T cells
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14
Q

expand on B lymphocytes

A
  • Responsible for production of antibodies
  • Humoral immunity
  • Mature in bone marrow (Proceed to spleen and lymphoid tissue)
  • Plasma cells (Produce antibodies)
  • B memory cells (Can quickly form clone of plasma cells)
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15
Q

what is humoral immunity

A

antibodies are produced to protect the body

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16
Q

what is cell-mediated immunity

A

lymphocytes are programmed to attack nonself cells to protect the body

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17
Q

where is igG found

A

Most common in blood

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18
Q

when is igM first to increase

A

First to increase in immune response

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19
Q

where is igA found

A

In secretions
* Tears
* Saliva and mucous membranes
* Colostrum

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20
Q

expand on igE

A

 Allergic response
 Causes release of histamine and other chemicals
 Results in inflammation

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21
Q

expand on igD

A

 Attached to B cells
 Activates B cells

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22
Q

expand on antigens

A
  • foreign substance
  • microbes
  • component of cell that stimulates immune response
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23
Q

expand on antibodies

A
  • specific protein produces in humoral response to bind with antigen
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24
Q

expand on autoantibodies

A

antibodies against self antigen
- attacks bodies own tissues

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25
Q

expand on thymus

A

-gland located in the mediastinum
- site of maturation and proliferation of T lymphocytes

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26
Q

expand on hymphatic tissue and organs

A
  • contain many lymphocytes
  • filter body fluids
  • remove foreign matter
  • immune response
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27
Q

expand on bone marrow

A
  • source of stem cells, leukocytes and maturation of B lymphocytes
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28
Q

expand on neutrophils

A

white blood cells for phagocytosis, nonspecific defense, active in inflammatory process

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29
Q

expand on basophils

A
  • white blood cells
  • bing igE
  • release histamine
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30
Q

expand on eosinophils

A
  • white blood cells
  • paticipate in allergic responses and defense against parasites
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31
Q

expand on monocytes

A
  • white blood cells
  • migrate from the blood into tissues to become macrophagues
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32
Q

expand on macrophages

A
  • phagocytosis
  • process and present antigens to lymphocytes for the immune response
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33
Q

expand on mast cells

A
  • release chemical mediators such as histamine in connective tissue
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34
Q

expand on b lymphocytes

A
  • humoral immunity activated cells that becomes an antibody producing plasma cell or a B memory cell
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35
Q

expand on plasma cells

A
  • develop from B lymphocytes to produce and secrete specific antibodies
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36
Q

expand on T lymphocytes

A
  • white blood cells
  • cell mediated immunity
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37
Q

expand on cytotoxic or killer T cells

A
  • destroy antigens, cancer cells and virus infected cells
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38
Q

expand on memory T cells

A
  • remember antigen and quickly stimulate immune response on reexposure
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39
Q

expand on helper T cells

A
  • active B and T cells
  • control or limit specific immune response
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40
Q

expand on natural killer lymphocytes

A
  • destroy foreign cells, virus infected cells and cancer cells
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41
Q

expand on complements

A

group of inactive proteins in the circulation that, when activated, stimulate the release of other chemical mediators, promoting inflammation, chemotaxis and phagocytosis

42
Q

expand on histamine

A

released from mast cells and basophils, particulary in allergic reactions, causes vasodilation and increased vascular permeability or edema, also contraction of bronchiolar smooth mucles and pruritus

43
Q

expand on kinins (bradykinin)

A

cause vasodilation, increased permeability (edema) and pain

44
Q

expand on prostaglandins

A

group of lipids with varying effects, some cause inflammation, vasodilation and increased permeability and pain

45
Q

expand on leukotrienes

A

group of lipids, derived from mast cells and basophils, which cause contraction of bronchiolar smooth muscle and have a role in development of inflammation

46
Q

expand on cytokines (messengers)

A
  • produced by macrophagues and activated T lymphocytes
  • stimulate activation and proliferation of B and T cells
  • communication between cells
  • involved in fever, inflammation and keukocyosis
47
Q

expand on tumor necrosis factor

A

a cytokine active in the inflammatory and immune responses
- stimulates fever and chemotaxis
- mediator of tissue wasting
- stimulates T cells
- mediator in septic shock
- stimulates necrosis in some tumors

48
Q

expand on chemotactic factors

A

attract phagocytes to areas of inflammation

49
Q

expand on complement system

A
  • activated during immune reactions with igG or igM
  • group of inactive proteins circulating in blood
  • causes cell damage and further inflammation when activated
50
Q

expand on chemical mediatora and their functions

A
  • involved in inflammation and immune reactions
  • functions are signaling and causing cellular damage
51
Q

expand on titer (titre) diagnostic tests

A

measures levels of serum immunoglobulins

52
Q

expand on indirect coombs test - diagnostic tests

A

detects rh blood incompatibility

53
Q

expand on elisa diagnostic tests

A
  • detects hiv antibodies
  • used for a number of other diseases
54
Q

expand on mhc typing diagnostic tests

A
  • tissue matching before transplantation procedures
55
Q

expand on natural immunity

A

species specific

56
Q

expand on innate immunity

A
  • gene specific
  • related to ethnicity
57
Q

expand on the primary response of immunity

A
  • first exposure to antigen
  • 1 to 2 weeks before antibody titer reaches efficacy
58
Q

expand on the secondary response of immunity

A
  • repeat exposure to the same antigen
  • more rapid response, with efficacy in 1 to 3 days
59
Q

expand on active natural immunity

A

 Natural exposure to antigen
 Development of antibodies

60
Q

expand on active artifical immuity

A

 Antigen purposefully introduced to body
 Stimulation of antibody production
 Immunization
 Booster immunization

61
Q

expand on passive natural immunity

A

 IgG transferred from mother to fetus:
* Across placenta
* Through breast milk
 Protection of infant for the first few months of life or until weaned

62
Q

expand on passive artifical immunity

A

 Injection of antibodies
 Short-term protection

63
Q

explain the mechanism of natural active acquired immunity and provide an example

A
  • pathogens enter body and cause illness; antibodies form in host
  • ex) person has chickenpox once
64
Q

explain the mechanism of artificial active acquired immunity and provide an example

A
  • vaccine is injected into person; no illness results, but antibodies form
  • ex) person has measels vaccine and gains immunity
65
Q

explain the mechanism of natural passive acquired immunity and provide an example

A
  • antibodies passed direvtly from mother to child to povide temporary protection
  • ex) placental passage during pregnancy or ingestion of breast milk
66
Q

explain the mechanism of artifical passive aquired immunity and povide an example

A
  • antibodies injected into person to provide temporary protection or minimize severity of infection
  • ex) gammagloubin if recent exposure to microbe
67
Q

what are the outcomes of infectious diseases

A
  • some occurence has declines where vaccination rates are high
  • search for additional vaccines continuous
68
Q

what is the difference between emerging and re-emerging infectious diseases

A
  • emerging infectious diseases are newly identifies in a population
  • re-emerging infectious diseases were previously under control
69
Q

expand on bioterrorism

A

 Biological agents used to attack civilians and/or
military personal
 May use altered antigenic forms of common
viruses or bacteria
 Widespread impact on population due to a lack
of vaccines

70
Q

expand on hyperacute organ transplant rejection

A

occurs immediately after transplantation

71
Q

expand on acute organ transplant rejection

A

develops after several weeks

72
Q

expand on chronic organ transplant rejection

A

occurs after months or years

73
Q

expand on immunosuppression techniques when it comes to organ transplantation

A
  • reduces immune response
  • prevents rejection
74
Q

expand on drug treatment when it comes to organ transplantation

A
  • careful dosing to prevent kidney damage
  • many drugs in clinical trials
75
Q

expand on common allergic reactions

A
  • caused by allergen
  • skin rashes
  • hay fever
76
Q

expand on causative mechanism allergic reactions

A
  • exposure to allergen
  • development of igEs
  • mast cells
77
Q

what are sign affects of type 1 hypersensitivity allergic reactions

A
  • hay fever (allergic rhinitis, nasal mucosa)
  • food allergies (digestive tract mucosa)
  • atopic dermatitis/eczema
  • asthma (bronchial mucosa)
78
Q

expand on anaphylaxis

A
  • severe, life threatening
  • systemic hypersensitivity reaction
  • decreased blood pressure caused by release of histamine
  • airway obstruction
  • severe hypoxia
79
Q

what can anaphylaxis be caused by

A
  • latex materials
  • insect stings
  • nuts or shellfish
    0 various drugs
80
Q

what are signs and symptoms of anaphylactic shock

A
  • itching/tingling (especially in oral cavity)
  • coughing
  • difficulty breathing
  • weakness
  • dizziness or fainting
  • edema
  • hives
81
Q

what is the first thing you should do if you experience or witness anaphylaxis

A
  • administer epipen
  • call 911
82
Q

how is anaphylaxis treated in emergency departments

A
  • epinephrine
  • glucocoticoids
  • antihistimines
  • oxygen
  • stabilize blood pressure
83
Q

expand on type 2 cytotoxic hypersensitivity

A
  • anitigen is present on cell membrance (may be normal body component or exogenous)
  • circulating igGs react with antigen (destruction by phagocytosis or cytolytic enzymes)
84
Q

expand on type 3 immune complex hypersensitivity

A
  • antigen combines with antibody (forms immune complexes, deposited in tissue and activation of complement system)
  • process causes inflammation and tissue destruction
85
Q

expand on type 4 cell mediatedof delayed hypersensitivity

A
  • delayed response by sensitized T lymphocytes
  • release of lymohokines
  • inflammatory response
  • destruction of the antigen
86
Q

expand on autoimmune disorders

A
  • development of antibodies against own cells or tissues
  • autoantibodies are antibodies formed against self antigens loss of tolerence
  • disorder can affect single organs or tissues or can be generalized
87
Q

expand on systemic lupus erthematosus (SLE)

A
  • chronic inflammatory disease
  • affects a number of organ systems
  • characteristic facial rash “butterfly rash”
  • affects primarily young women
  • incidence is higher in african americans, asians, hispanics and native americans
88
Q

what are the signs and symptoms of systemic lupus erthematosus (SLE)

A
  • arthralgia, fatigue, malaise
  • cardiovascular problems
  • polyuria
89
Q

what is the treatment for systemic lupus erthematosus (SLE)

A
  • treated by a rheumatologist
  • glucocorticoid
  • nonsteroidal antiinflammatory drug
90
Q

where are the common manifestations of systemic lupus erthematosus (SLE)

A

joints, skin, kidneys, lungs, heart, blood bessels, central nervous system and bone marrow

91
Q

expand on immunodeficiency

A
  • partial or total loss of one or more immune system components
  • increased risk of infection and cancer
    predisposition to the development of opportunistic infections is caused by normal flora
  • prophylactic antimicrobial drugs may be used prior to invasive procedures
92
Q

expand on primary immunodeficiencies

A

basic developmental failure somewhere in the system

93
Q

expand on secondary or acquired immunodeficiencies

A
  • loss of the immune response from specific causes
  • can occur at any time during the life span
94
Q

expand on acquired immunodeficiency syndrome (aids)

A
  • chronic infectious disease caused by the human immunodeficiency virus (hiv)
  • hiv destroys helper T cells
  • loss of immune responses
  • increased susceptibility to secondary infections and cancer
  • prolonged latent period
  • development may be suppresed by antivirals
95
Q

expand on the history of aids

A
  • first case recognized in 1979; hiv identified in 1984
  • evidence of earlier sporadic cases
  • now considered to be a pandemic
  • occurs in men and women
96
Q

expand on the agent

A
  • human immunodeficiency virus
  • retrovirus
  • hiv-1 (major cause of aids in us and europe)
  • hiv-2 (major cause of aids in central africa)
97
Q

how does hiv gets transmitted

A

blood
semen
vaginal fluids

98
Q

expand on hiv diagnostic tests

A
  • presence of hiv infection
  • blood test for hiv antibodies
  • three stage process
99
Q

what are the generalized effects of hiv

A
  • lymphadenopathy
  • fatigue and weakness
  • headache
  • arthralgia
  • gastrointestinal effects primarily due to opportunistic infections
  • aids dementia
100
Q

expand on secondary infections relating to aids

A
  • primary cause of death
  • frequently multiple more extensive and severe than usual
  • drug treatment often ineffective
  • lungs
  • cold sores
  • candida
  • tuberculosis
101
Q

expand on cancer correlation with aids

A
  • increased incidence of all cancers
  • unusual cancers are often markers for aids (kaposi sarcoms, non-hodgkin lymphoma)
102
Q

expand on the treatments of aids

A
  • non nucleoside reverse transcriptase inhibitors
  • nucleoside reverse transcriptase inhibitors
  • protease inhibitors
  • fusion inhibitors

Pathophysiology (9 decks)

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