Unit 1 - Chapter 7 - Immunity Flashcards
1
Q
what is the immune system reponsible for
A
body defenses
2
Q
what are nonspecific responses (defenses)
A
phagocytosis and inflammation
3
Q
what are some examples of specific responses (defenses)
A
production of specific antibodies against foreign substances
4
Q
what are the 4 components of the immune systems
A
- lmymphoid structure
- immune cells
- tissues
- chemical mediators
5
Q
what are some examples of lymphoid structures
A
-lymoh nodes
- spleen
- tonsils
- intestinal lymphois tissue
- lymphatic circulation
6
Q
what are some examples of immune cells
A
- lymphocytes
- macrophagues
7
Q
what are examples of tissues
A
- bone marrow
- thymus
8
Q
what are examples of chemical mediators
A
histamine and interleukins
9
Q
what are antigens and what are examples of cell suface antigens
A
- usually exogenous substances
- proteins, polysaccharides, glycoproteins
10
Q
expand on self antigens
A
- HLA proteins label cells of the individual.
- Immune system ignores self-cells.
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
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
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
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)
15
Q
what is humoral immunity
A
antibodies are produced to protect the body
16
Q
what is cell-mediated immunity
A
lymphocytes are programmed to attack nonself cells to protect the body
17
Q
where is igG found
A
Most common in blood
18
Q
when is igM first to increase
A
First to increase in immune response
19
Q
where is igA found
A
In secretions
* Tears
* Saliva and mucous membranes
* Colostrum
20
Q
expand on igE
A
Allergic response
Causes release of histamine and other chemicals
Results in inflammation
21
Q
expand on igD
A
Attached to B cells
Activates B cells
22
Q
expand on antigens
A
- foreign substance
- microbes
- component of cell that stimulates immune response
23
Q
expand on antibodies
A
- specific protein produces in humoral response to bind with antigen
24
Q
expand on autoantibodies
A
antibodies against self antigen
- attacks bodies own tissues
25
expand on thymus
-gland located in the mediastinum
- site of maturation and proliferation of T lymphocytes
26
expand on hymphatic tissue and organs
- contain many lymphocytes
- filter body fluids
- remove foreign matter
- immune response
27
expand on bone marrow
- source of stem cells, leukocytes and maturation of B lymphocytes
28
expand on neutrophils
white blood cells for phagocytosis, nonspecific defense, active in inflammatory process
29
expand on basophils
- white blood cells
- bing igE
- release histamine
30
expand on eosinophils
- white blood cells
- paticipate in allergic responses and defense against parasites
31
expand on monocytes
- white blood cells
- migrate from the blood into tissues to become macrophagues
32
expand on macrophages
- phagocytosis
- process and present antigens to lymphocytes for the immune response
33
expand on mast cells
- release chemical mediators such as histamine in connective tissue
34
expand on b lymphocytes
- humoral immunity activated cells that becomes an antibody producing plasma cell or a B memory cell
35
expand on plasma cells
- develop from B lymphocytes to produce and secrete specific antibodies
36
expand on T lymphocytes
- white blood cells
- cell mediated immunity
37
expand on cytotoxic or killer T cells
- destroy antigens, cancer cells and virus infected cells
38
expand on memory T cells
- remember antigen and quickly stimulate immune response on reexposure
39
expand on helper T cells
- active B and T cells
- control or limit specific immune response
40
expand on natural killer lymphocytes
- destroy foreign cells, virus infected cells and cancer cells
41
expand on complements
group of inactive proteins in the circulation that, when activated, stimulate the release of other chemical mediators, promoting inflammation, chemotaxis and phagocytosis
42
expand on histamine
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
expand on kinins (bradykinin)
cause vasodilation, increased permeability (edema) and pain
44
expand on prostaglandins
group of lipids with varying effects, some cause inflammation, vasodilation and increased permeability and pain
45
expand on leukotrienes
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
expand on cytokines (messengers)
- 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
expand on tumor necrosis factor
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
expand on chemotactic factors
attract phagocytes to areas of inflammation
49
expand on complement system
- activated during immune reactions with igG or igM
- group of inactive proteins circulating in blood
- causes cell damage and further inflammation when activated
50
expand on chemical mediatora and their functions
- involved in inflammation and immune reactions
- functions are signaling and causing cellular damage
51
expand on titer (titre) diagnostic tests
measures levels of serum immunoglobulins
52
expand on indirect coombs test - diagnostic tests
detects rh blood incompatibility
53
expand on elisa diagnostic tests
- detects hiv antibodies
- used for a number of other diseases
54
expand on mhc typing diagnostic tests
- tissue matching before transplantation procedures
55
expand on natural immunity
species specific
56
expand on innate immunity
- gene specific
- related to ethnicity
57
expand on the primary response of immunity
- first exposure to antigen
- 1 to 2 weeks before antibody titer reaches efficacy
58
expand on the secondary response of immunity
- repeat exposure to the same antigen
- more rapid response, with efficacy in 1 to 3 days
59
expand on active natural immunity
Natural exposure to antigen
Development of antibodies
60
expand on active artifical immuity
Antigen purposefully introduced to body
Stimulation of antibody production
Immunization
Booster immunization
61
expand on passive natural immunity
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
expand on passive artifical immunity
Injection of antibodies
Short-term protection
63
explain the mechanism of natural active acquired immunity and provide an example
- pathogens enter body and cause illness; antibodies form in host
- ex) person has chickenpox once
64
explain the mechanism of artificial active acquired immunity and provide an example
- vaccine is injected into person; no illness results, but antibodies form
- ex) person has measels vaccine and gains immunity
65
explain the mechanism of natural passive acquired immunity and provide an example
- antibodies passed direvtly from mother to child to povide temporary protection
- ex) placental passage during pregnancy or ingestion of breast milk
66
explain the mechanism of artifical passive aquired immunity and povide an example
- antibodies injected into person to provide temporary protection or minimize severity of infection
- ex) gammagloubin if recent exposure to microbe
67
what are the outcomes of infectious diseases
- some occurence has declines where vaccination rates are high
- search for additional vaccines continuous
68
what is the difference between emerging and re-emerging infectious diseases
- emerging infectious diseases are newly identifies in a population
- re-emerging infectious diseases were previously under control
69
expand on bioterrorism
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
expand on hyperacute organ transplant rejection
occurs immediately after transplantation
71
expand on acute organ transplant rejection
develops after several weeks
72
expand on chronic organ transplant rejection
occurs after months or years
73
expand on immunosuppression techniques when it comes to organ transplantation
- reduces immune response
- prevents rejection
74
expand on drug treatment when it comes to organ transplantation
- careful dosing to prevent kidney damage
- many drugs in clinical trials
75
expand on common allergic reactions
- caused by allergen
- skin rashes
- hay fever
76
expand on causative mechanism allergic reactions
- exposure to allergen
- development of igEs
- mast cells
77
what are sign affects of type 1 hypersensitivity allergic reactions
- hay fever (allergic rhinitis, nasal mucosa)
- food allergies (digestive tract mucosa)
- atopic dermatitis/eczema
- asthma (bronchial mucosa)
78
expand on anaphylaxis
- severe, life threatening
- systemic hypersensitivity reaction
- decreased blood pressure caused by release of histamine
- airway obstruction
- severe hypoxia
79
what can anaphylaxis be caused by
- latex materials
- insect stings
- nuts or shellfish
0 various drugs
80
what are signs and symptoms of anaphylactic shock
- itching/tingling (especially in oral cavity)
- coughing
- difficulty breathing
- weakness
- dizziness or fainting
- edema
- hives
81
what is the first thing you should do if you experience or witness anaphylaxis
- administer epipen
- call 911
82
how is anaphylaxis treated in emergency departments
- epinephrine
- glucocoticoids
- antihistimines
- oxygen
- stabilize blood pressure
83
expand on type 2 cytotoxic hypersensitivity
- 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
expand on type 3 immune complex hypersensitivity
- antigen combines with antibody (forms immune complexes, deposited in tissue and activation of complement system)
- process causes inflammation and tissue destruction
85
expand on type 4 cell mediatedof delayed hypersensitivity
- delayed response by sensitized T lymphocytes
- release of lymohokines
- inflammatory response
- destruction of the antigen
86
expand on autoimmune disorders
- 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
expand on systemic lupus erthematosus (SLE)
- 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
what are the signs and symptoms of systemic lupus erthematosus (SLE)
- arthralgia, fatigue, malaise
- cardiovascular problems
- polyuria
89
what is the treatment for systemic lupus erthematosus (SLE)
- treated by a rheumatologist
- glucocorticoid
- nonsteroidal antiinflammatory drug
90
where are the common manifestations of systemic lupus erthematosus (SLE)
joints, skin, kidneys, lungs, heart, blood bessels, central nervous system and bone marrow
91
expand on immunodeficiency
- 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
expand on primary immunodeficiencies
basic developmental failure somewhere in the system
93
expand on secondary or acquired immunodeficiencies
- loss of the immune response from specific causes
- can occur at any time during the life span
94
expand on acquired immunodeficiency syndrome (aids)
- 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
expand on the history of aids
- 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
expand on the agent
- human immunodeficiency virus
- retrovirus
- hiv-1 (major cause of aids in us and europe)
- hiv-2 (major cause of aids in central africa)
97
how does hiv gets transmitted
blood
semen
vaginal fluids
98
expand on hiv diagnostic tests
- presence of hiv infection
- blood test for hiv antibodies
- three stage process
99
what are the generalized effects of hiv
- lymphadenopathy
- fatigue and weakness
- headache
- arthralgia
- gastrointestinal effects primarily due to opportunistic infections
- aids dementia
100
expand on secondary infections relating to aids
- primary cause of death
- frequently multiple more extensive and severe than usual
- drug treatment often ineffective
- lungs
- cold sores
- candida
- tuberculosis
101
expand on cancer correlation with aids
- increased incidence of all cancers
- unusual cancers are often markers for aids (kaposi sarcoms, non-hodgkin lymphoma)
102
expand on the treatments of aids
- non nucleoside reverse transcriptase inhibitors
- nucleoside reverse transcriptase inhibitors
- protease inhibitors
- fusion inhibitors
