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44 Cards in this Set
- Front
- Back
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Hypersensitivity
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• Excessive or inappropriate activation of the immune response
• The body is damaged by the immune response, rather than by the antigen (often called allergen) • Four types of hypersensitivities • Types I, II, and III are all immediate hypersensitivities; they develop within about a half hour or sooner. Our own response can cause problems within the body as well Caused by endogenous (present on the membrane of body cells) and exogenous (adsorbed on the membrane surface) antigens |
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Type I Hypersensitivity
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• Commonly called “allergic reactions”
• IgE mediated • Systemic or anaphylactic reactions • Common allergens: - Plant pollens - House dust mites - Animal dander - Foods - Chemicals i.e. penicillin Allergic reactions - IgE mediated Ex. Peanut butter - type 1 hypersensitivity *it’s important to know examples and the mechanism of how it all work |
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Type I Hypersensitivity - Local or atopic reactions
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• Local or atopic reactions (genetic)
– Rhinitis (hay fever) – Food allergies – Bronchial asthma – Hives – Atopic dermatitis (eczema) Atopic: reactions that usually occur when the antigen is confined to a particular site by virtue of exposure. This includes environmental allergins. Immediate hypersensitivity disorders tend to be inherited. |
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Type I Hypersensitivity - Central cells involved?
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Central cells: T helper cells (Th2) and mast cells/basophils.
Type 1 plays a protective role in the control of parasitic infections. |
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Type I Hypersensitivity - Mechanism Info
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Il-3 Il-4, Il-5 = cytokines
The antibodies are attached to the mast cells: sensitization (degranulation) The antigen binds to cell associated IgE --> a number of outcomes occur Two phases: primary (vasodilation and smooth muscle contraction; within 5-30 min from exposure) and secondary (more intense infiltration + chronic inflammation; within 2 - 8 hours from exposure) |
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Kinds of mediators? - Hypersensitivity 1
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• Histamine
– Potent vasodilator, increases permeability of capillaries and venules, causes smooth muscles to contract and bronchial constriction • Acetylcholine – Produces bronchial smooth muscle contraction, dilation of small blood vessels • Kinins i.e. bradykinin – Potent inflammatory peptides – Produce vasodilation and smooth muscle contraction Require enzymatic modification Primary reaction mediated by: mast cell degranulation and release of these mediators (on left). Secondary reaction medicated by: lipid mediators and immune response cytokines. |
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Primary reaction - Hypersensitivity 1
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Primary reaction mediated by: mast cell degranulation and release of these mediators (on left).
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Secondary reaction - Hypersensitivity 1
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Secondary reaction medicated by: lipid mediators and immune response cytokines.
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Is the following statement true or false:
When mast cells degranulate, histamine is released. |
True
Histamine is one of the first chemical mediators released during the inflammatory response as a result of mast cell degranulation.Mast cell stabilizers (used to treat asthma) prevent the histamine from being released; antihistamines (used to treat allergies) compete with histamine for receptor sites, lessening the inflammatory response. |
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Allergy Shots
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• Small amounts of antigen administered and
concentrations gradually increased • Increases production of IgG • IgG binds to the allergen before it binds to IgE, reducing tissue damage IgG is a competitive inhibitor against IgE, which stops the sensitisation process |
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Anaphylaxis
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• Life-threatening systemic response to inflammatory mediators
released in type I hypersensitivity • Activation of mast cells bound to IgE throughout the body – Histamine, acetylcholine, kinins, leukotrienes, and prostaglandins all cause vasodilation • What will happen when arterioles vasodilate throughout the body? – Acetylcholine, kinins, leukotrienes, and prostaglandins all can cause bronchoconstriction • What will happen when the bronchioles constrict? Systemic and life threatening extreme allergic response Vasodilatation. = decrease in blood pressure (hypotension) which can lead to shock Genetics plays a large role in being this severely allergic Bronchioles constrict = restricts the passage of air |
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Sequence of vascular events in anaphylactic shock
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Release of histamine
Blood vessels dilate and leak plasma Blood pressure falls Venous return to heart impaired Cardiac output inadequate Circulation drastically reduced Volume of blood that is ejected from the heart on a per beat basis therefore reduced cardiac output = reduced circulation flow |
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Why is an Epipen important?
Alpha receptors found on walls of blood vessels. Role? Beta receptors found on the heart and lungs. Role ? |
Epi pen = adrenaline/epinephrine is inside. Activates the alpha and beta receptors. Alpha cells of blood vessels: constrict the blood vessels which will increase the pressure of the system and increase venous return, increases blood circulation as a whole. Beta cells of the heart and lungs, relaxes the smooth muscles in the bronchioles to help facilitate breathing and the passage of
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Where are the alpha receptors found?
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blood vessels
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Where are the beta receptors found?
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heart and lungs
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Type II Hypersensitivity
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• Cytotoxic
• IgG or IgM antibodies attack antigens on cell surfaces or in connective tissues causing destruction Type 2 = ONLY IgG and IgM (no IgE are present) – Usually involves antigens on red or white blood cells – Transfusion reactions – Rh disease (rhesus isoimmunisation) – Drug reactions |
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What are the three subsections of Type II Hypersensitivity?
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Complement- and Antibody-Mediated Cell Destruction
Complement- and Antibody-Mediated Inflammation Antibody - Mediated Cellular Dysfunction |
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Complement- and Antibody-Mediated Cell Destruction:
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Complement-mediated cell
destruction • Cells are coated with molecules that make them attractive to phagocytes OR due to formation of membrane attack proteins that disrupt the integrity of the cell membrane and cause cell lysis ADCC • Cells coated with IgG are killed by effector cells that bind to their target by their receptors for IgG, cell lysis then occurs ADCC: antibody-dependent cell-mediated cytotoxicity (does not require complement) Activating a complement system in response to the antigens that are present in the blood system Cell destruction is the general mechanism: ADCC and complement mediated cell destruction Examples: mismatched blood transfusions, hemolytic disease of newborn, drug reactions |
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Mechanisms of Type II Hypersensitivity
Complement- and Antibody-Mediated Inflammation: |
1. Antibodies deposited in
extracellular tissue 2. Complement system is activated 3. Neutrophils and monocytes are recruited/activated 4. Leukocytes release injurious substances that result in inflammation/tissue damage e.g. vascular rejection of organ grafts Injury results from inflammation rather than phagocytosis or lysis. |
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Mechanisms of Type II Hypersensitivity
Antibody - Mediated Cellular Dysfunction: |
1. Antibodies bind to target cell
receptors 2. Leads to a change in cell function e.g. Graves disease (TSH), myasthenia gravis (Ach) Antibodies bind to specific target cell receptors and changes the cell function (no cell death). |
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Why is type O blood considered the universal donor?
a. It has both A and B antigens on the RBC. b. It has neither A or B antigens on the RBC. c. It has no antibodies in the plasma. d. It has A and B antibodies in the plasma. |
b. It has neither A or B antigens on the RBC.
Antigens are the components that elicit an immune response (type II hypersensitivity reaction). Type O blood has no antigens on the RBC, so anyone can receive it because there is nothing to stimulate production of antibodies against it. The fact that type O blood has both A and B antibodies has nothing to do with creating the antigen-antibody response. |
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Type III Hypersensitivity: Complex-Mediated Disorders
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1. Free-floating antigen + antibody
--> circulating immune complex 2. Immune complexes deposit on walls of blood vessels 3. Complement activation of IgG or IgMantibodies 4. Neutrophils and inflammatory cells are recruited 5. Blood vessels are damaged E.g. Autoimmune vasculitis (Lupus), Glomerulonephritis, Serum sickness (systemic), arthus reaction (local) Antigen and antibody combining and forming a complex leading to the recruitment of inflammatory signals Systemic Immune Complex Disorders: serum sickness (temporary damage if acute, ie. penicillin) Local Immune Complex Reactions: localized tissue necrosis caused by immune complexes |
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Type IV Hypersensitivity
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Cell-mediated: sensitized T cells attack antigen
• Two types of type IV hypersensitivity reactions: 1. Direct cell-mediated cytotoxicity • Viral reactions 2. Delayed-type hypersensitivity • Tuberculin test • Allergic contact dermatitis • Hypersensitivity pneumonitis Auto immune = abnormal or excessive response |
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Mechanisms of Type IV Hypersensitivity - Direct
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Direct cell-mediated cytotoxicity
- CD8+ cytotoxic T lymphocytes directly kill antigen-bearing target cells with class I MHC molecules Antigen is broken up into smaller pieces and activated the CD4+ cell. --> CD8* = cytotoxicity CTLs cannot distinguish between cytopathic and noncytopathic viruses, therefore they kill virtually all infected cells regardless of whether the infection is harmful. Ex. some versions of hepatitis. |
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Mechanisms of Type IV Hypersensitivity - Delayed
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Delayed-Type Hypersensitivity
Disorders - Exposure to an antigen results in activation of a T-cell–mediated immune response, which is slow to develop (delayed). 1. Th1 cells are activated and secrete cytokines 2. Cytokines cause activation of macrophages, lymphocytes, fibroblasts, and inflammatory cells (24-72 hrs to synthesize these effector molecules) Slow to develop because there are more steps in the process. Activate T helper cells -->activate cytokines which then stimulate other cells = results in delayed response |
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Type IV Hypersensitivity Example
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Example: Poison Ivy
The first exposure to poison ivy, there will be no reaction. However, T cells may become sensitized to it. On the next exposure, the typical rash and irritation appear, caused by T-cell secretion of cytokines (toxic substances) that damage the tissues where the ivy oil has been absorbed. This is an example of a delayed response - seeing the rash hours after you are exposed You normally only have one type of response occur - direct OR delayed, depending on the exposure. Bee sting = direct, immediate swelling / delayed, second sting = anaphylactic shock |
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Autoimmune Diseases
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• Normally, immune response recognizes the difference
between the individual’s own tissues and those of invaders (tolerance). • In autoimmunity, this self-tolerance breaks down and immune system destroys body’s own tissue – Immune system attacks self-antigens • Autoimmune diseases occur when individuals develop antibodies to their own tissues or self-antigens. |
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Is the following statement true or false:
Patients who suffer from autoimmune disease have hypoactive immune systems. |
False
In autoimmune diseases, the immune system is hyperactive—it attacks self-antigens and destroys its own body tissues. |
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Immunodeficiency - Primary
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• Primary
– B-cell deficiencies – Immunologic deficiencies – T-cell deficiencies – Combined immunodeficiencies |
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Immunodeficiency - Secondary
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AIDS
Secondary/Acquired – AIDS |
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Human Immunodeficiency Virus - Transmission
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• Transmitted by body fluids
– Sexual contact (most frequent mode) – Breast milk – Blood-to-blood contact • Contaminated needles • Transfusions • During pregnancy or birth When the cell count is <200 you get the AIDS illness, meaning you are at the end of your spectrum. |
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Human Immunodeficiency Virus - Info
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• Retrovirus: carries its genetic info in RNA rather than
DNA • Primary target cell: CD4+ cells/helper T cells • Viral replication within CD4+ cells AIDS = suffer from the low Helper T cell count |
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HIV Virion
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• HIV virion is spherical and
contains electron-dense core • Surrounded by a lipid enveloped • Contains capsid protein p24 • Most deadly detected antigen • Target for antibodies used in screening for HIV Being a retrovirus makes HIV very dangerous |
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HIV Infects a Cell
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1. Virus binds to CD4+ T cell and surface
molecules i.e. chemokine receptors (critical for infection process) (attachment phase) 2. Uncoating of the virus, contents of viral core enter the host cell 3. DNA synthesis: reverse transcriptase makes a copy of viral RNA, and then in reverse makes a complementary DNA strand (cDNA) 4. cDNA enters nucleus and becomes part of CD4+, inserted into cell’s original DNA 5. Transcription of viral DNA to form mRNA – virus may remain non transcribed/dormant within infected cells for months or years 6. Translation of the viral mRNA, ribosomal RNA uses instructions in mRNA to create a polypeptide 7. Cleavage – protease enzyme cuts polypeptide chain into the individual core proteins that will make new viruses 8. Core protein migrates to cell membrane where they acquire lipid membrane that buds off cell membrane > cell death |
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HIV Infects a Cell #2
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There may be a delay when it infects a resting cells until something else stimulates the action for it to start the lytic phase.
Important: although HIV can infect resting cells, the initiation of transcription and viral replication occurs only when the infected cell is activated by exposure to antigens or cytokines |
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Course of HIV Infection
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• Primary infection phase
– Signs of systemic infection: occurs 1-4 days after exposure, duration of 7-10 days – Immune system responds and antibodies against HIV appear (1-6 months) • Latent period phase – Virus is replicating, TH cell count gradually falls – May last 10–11 years or longer • Overt AIDS phase – TH cell count <200 cells/mL or AIDS-defining illness |
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How long is the primary Infection phase of HIV?
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• Primary infection phase
– Signs of systemic infection: occurs 1-4 days after exposure, duration of 7-10 days – Immune system responds and antibodies against HIV appear (1-6 months) Can appear that you have the common cold after having been exposed for a few days (initial reaction to the virus). |
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How long is the latent period phase of HIV?
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• Latent period phase
– Virus is replicating, TH cell count gradually falls – May last 10–11 years or longer |
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Signs and Symptoms of HIV Infection - Initial:
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Initial HIV Infection:
HIV + Fever Headache Fatigue Enlarged lymph nodes |
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Signs and Symptoms of HIV Infection - Asymptomatic:
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HIV+
Lack of energy Weight loss Frequent fever and sweats Persistent and frequent yeast infection Persistent skin rashes or flaky skin Short-term memory loss Mouth, genital, or anal herpes sores Mouth and genital herpes sores are a give-away that you probably have HIV+, it normally is seen at the ends of the asymptomatic period. |
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Signs and Symptoms of HIV Infection - AIDS:
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HIV +
Fever One of AIDS indicator diseases Cough and shortness of breath Seizures and lack of coordination Difficult or painful swallowing Confusion and forgetfulness Vision loss Nausea Coma Extreme fatigue |
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AIDS-Associated Illnesses
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• Opportunistic infections
– Respiratory – Gastrointestinal – Nervous system • AIDS dementia complex • Malignancies • Wasting syndrome |
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Treatment for AIDS
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• Genetic makeup of the AIDS virus varies from strain to strain.
• HIV tends to mutate frequently, which adds to the difficulty of producing a vaccine. • No cure for AIDS. • Combination medications have stopped HIV replication to such an extent that the viral load becomes undetectable in some individuals. • Examples: nucleotide analogs and protease inhibitors • AZT (zidovudine) and several others are nucleotide analogs to stop viral DNA production. • Protease inhibitors stop the assembly of viruses. A common cocktail contains two analogs such as AZT and 3TC (lamivudine, Epivir) plus a protease inhibitor Medications are very expensive, cause side effects, and the regimen of pill taking throughout the day is very demanding. • If the drugs are not taken as prescribed or if the therapy is stopped, resistance or relapse may occur. • The sooner drug therapy begins after infection, the better the chances are that the immune system will not be destroyed by HIV. |
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Treatment for AIDS
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• Examples: nucleotide analogs and protease inhibitors
• AZT (zidovudine) and several others are nucleotide analogs to stop viral DNA production. • Protease inhibitors stop the assembly of viruses. A common cocktail contains two analogs such as AZT and 3TC (lamivudine, Epivir) plus a protease inhibitor Medications are very expensive, cause side effects, and the regimen of pill taking throughout the day is very demanding. • If the drugs are not taken as prescribed or if the therapy is stopped, resistance or relapse may occur. • The sooner drug therapy begins after infection, the better the chances are that the immune system will not be destroyed by HIV. |
