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90 Cards in this Set
- Front
- Back
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extraneous effect caused by a vaccine
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adverse reaction
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"side effect"
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adverse reaction
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any event following a vaccination
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adverse event
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may not be a true adverse reaction
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adverse event
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common with inactivated vaccines
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local adverse reactions
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usually mild and self-limited
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local adverse reactions
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systemic adverse reactions are
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nonspecific
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peripheral myopathy with complete body weakness; rapid or gradual associated with some vaccines
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guillain-barre syndrome
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very rare adverse reaction which can be minimized by screening
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allergy
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used to kill bacteria and prevent contamination of vaccines
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thimerisol
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encephalopathy following pertussis vaccine is a
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permanent contraindication
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severe allergy to prior dose of vaccine or component is a
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permanent contraindication
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severe illness; contraindication or precaution when giving live and inactivated vaccines
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precaution for BOTH
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dose of corticosteroids which lead to immunosuppression
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> or equal to 20 mg per day or 2 mg / kg per day
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when you should get a flu vaccine following tx with transplant
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after 6 months and then annually
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Locally Activates vascular endothelium
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IL-1
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Increases adhesion of macrophages
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IL-1
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Allows macrophages & PMNs to leave blood and
enter infected tissue |
IL-1
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Locally Activates lymphocytes
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IL-1
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Systemically promotes fever and IL-6
production |
IL-1
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Locally lymphocyte activation and antibody
production |
IL-6
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B-cell growth and differentiation
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IL-6
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Proliferation of thymocytes and peripheral T-cells
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IL-6
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Augments NK-cell activity
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IL-6
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Only local effects
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IL-8 and IL-12
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Chemotactic factor for PMNs
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IL-8
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Increases access of effector cells
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IL-8
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Activates PMNs
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IL-8
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Activates NK cells
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IL-12
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Induces the differentiation of CD4 T cells
into TH1 cells |
IL-12
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are critical in the control of
parasitic infections |
T cells
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crucial in eradicating
parasitic infection |
TH1 cells and cytokines
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in unicellular parasitic infections IL-12 is produced by
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phagocytic cells
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in unicellular parasitic infections IFN-γ is produced by __
under the induction of IL-12 |
NK cells and T cells
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in unicellular parasitic infections Macrophages are activated by
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IFN-γ
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For intracellular protozoan (unicellular)
infections __ is the primary cytokine controlling the resolution of the infection |
IFN-γ
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TH2 cells and cytokines driving
eosinophils, mast cells and IgE are crucial in eradicating the infection from the GI tract |
multicellular helminth infections
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In Multicellular (Helminth) Infections IL-4 production is induced by
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the helminth
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In Multicellular (Helminth) Infections __ drives TH2 cell proliferation and
maturation of B cells and production of IgE and IgG4 |
IL-4
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In Multicellular (Helminth) Infections IL-5 production causes an increase in
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eosinophil production
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In Multicellular (Helminth) Infections IL-4, 9 and 3 cause an increase in
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mast cells
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In parasitic disease is a potent negative
regulator of both TH1 and TH2 |
IL-10
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Prevents an overwhelming inflammatory
response thus preventing tissue damage and possible death |
IL-10
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Down regulates IL-5 and IFN-γ
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IL-10
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Transforming Growth Factor β
(TGF- β) is produced by |
activated macrophages and
T cells |
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Decrease TNF-α production and
inflammation |
TGF- β
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Act synergistically with IL-10 to inhibit
macrophage effector functions |
TGF- β
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Along with IL-10 helps maintain a
balance between protection and disease |
TGF- β
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Exact role not known
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IgE and Eosinophils
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In vitro parasite specific IgE and
eosinophils can kill certain parasites by |
ADCC
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Most important cell in the response to
parasitic infections |
activated macrophages
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is the main mechanism by
which the parasites are killed by activated macrophages |
Nitric oxide
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stimulate the production
of nitric oxide and IL-10 and TGF-β inhibit nitric oxide production |
TNF-α and INF-γ
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– Malaria
– Toxoplamosis – Trypanosoma |
Infections in which CD8 are important
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are the most effective of the
phagocytes at killing fungi |
Neutrophils
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are much less
potent than neutrophils or activated macrophages at killing fungi |
Inactivated macrophages
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can kill fungi either directly (rare)
or indirectly after activation to produce cytokines such as TNF-α and IFN-γ |
NK cells
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Released from NK cells, CD8 cells, and
CD4 TH1 cells |
IFN-γ
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Promotes the activation of macrophages
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IFN-γ
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Promotes the differentiation of naïve CD4
cells into TH1 cells |
IFN-γ
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Prevents the differentiation of naïve CD4
cells into TH2 cells |
IFN-γ
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is crucial to
the control and resolution of systemic fungal infections |
CD4 T-cell mediated immunity
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cause skin, nail, and hair
infections only |
Dermatophytes
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topical disease only, never
systemic disease |
Dermatophytes
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TH1 response or delayed hypersensitivity
response is most important with |
immunity to dermatophytes
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with immunity to dermatophytes __ results in chronic disease and little
inflammation |
TH2 response or type I hypersensitivity
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with immunity to dermatophytes __ limits the disease and has a greater
inflammatory response |
TH1 response or DT hypersensitivity
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Bacteria with a large
quantity of __ on its surface evade complement in the absence of antibodies |
sialic
acids |
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Streptococcus pyogenes and
Staphylococcus aureus evade complement when |
Ab are not present
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Have long half-lives in tissue
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macrophages
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Most abundant of the WBCs
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pmns
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Normally not present in tissues but are attracted
into infected tissue by cytokines released from phagocytosing macrophages and chemotactic factors released by complement activation |
pmns
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Become the dominant phagocytic cell at the site
of infection |
pmns
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initiate the inflammatory
response when infection is the cause |
Macrophages
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Mucosal secretions contain __ in greatest
quantity |
IgA
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They prevent viral replication within
infected cells and its spread into uninfected cells |
Interferon α& β in virally-infected cells
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Activate NK cells to kill virus-infected cells
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Interferon α& β in virally-infected cells
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Increase MHC class I expression
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Interferon α& β in virally-infected cells
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Consist of physical barriers, complement,
acute-phase proteins, phagocytic cells, NK cells, interferon α& β |
innate response
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can bind to surface
antigens on the virus preventing binding to the host cell |
Specific antibodies
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can bind the viral antigen on the host cell surface,
activate complement and result is cell lysis |
Ab
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can bind the viral antigen on the host cell surface,
activate ADCC by activating NK cells and result in cell death by apoptosis |
Ab
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Starts with activation of T-cells in draining
lymphoid tissue |
acquired immune response
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influence the
differentiation of CD4 cells during the adaptive immune response |
Cytokines released by cells during the
innate immune response |
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is produced primarily by dendritic
cells and macrophages and drive the differentiation to TH1 cells |
IL-12
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IL-12 and INF-γ prevent the development of
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TH2 cells
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promote activation of B-cells
and the differentiation of CD4 cells into TH2 cells |
IL-4 and IL-6
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IL-4 prevents the differentiation of CD4
cells into |
TH1 cells
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It takes days for activated effector Tcells
to emigrate to the site of infection |
5-6
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Major envelope glycoprotein
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gp-160
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