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Questions and Answers
What is the primary mediator responsible for causing blood vessel smooth muscle relaxation and increased vascular permeability?
What is the primary mediator responsible for causing blood vessel smooth muscle relaxation and increased vascular permeability?
Which of the following is NOT a role of histamine in immediate hypersensitivity reactions?
Which of the following is NOT a role of histamine in immediate hypersensitivity reactions?
What type of hypersensitivity reaction is characterized as immediate?
What type of hypersensitivity reaction is characterized as immediate?
Which lipid mediator is known as the most potent vasoactive and spasmogenic agent?
Which lipid mediator is known as the most potent vasoactive and spasmogenic agent?
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Which mediator is responsible for platelet aggregation and the release of histamine?
Which mediator is responsible for platelet aggregation and the release of histamine?
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What is the role of cytokines such as TNF and IL-1 in immediate hypersensitivity reactions?
What is the role of cytokines such as TNF and IL-1 in immediate hypersensitivity reactions?
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Which of the following mediators is responsible for tissue damage during immediate hypersensitivity reactions?
Which of the following mediators is responsible for tissue damage during immediate hypersensitivity reactions?
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What is one of the primary effects of prostaglandin D2 in immediate hypersensitivity reactions?
What is one of the primary effects of prostaglandin D2 in immediate hypersensitivity reactions?
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Which bodily fluids can transmit HIV when concentrated enough?
Which bodily fluids can transmit HIV when concentrated enough?
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What is a primary mode of HIV transmission?
What is a primary mode of HIV transmission?
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What is a hallmark feature of AIDS?
What is a hallmark feature of AIDS?
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During which phase of HIV infection may a person show no symptoms?
During which phase of HIV infection may a person show no symptoms?
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What type of infections are commonly associated with clinical manifestation of AIDS?
What type of infections are commonly associated with clinical manifestation of AIDS?
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What is one of the increased risks associated with HIV transmission?
What is one of the increased risks associated with HIV transmission?
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Which immune cells does HIV primarily infect?
Which immune cells does HIV primarily infect?
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Which of the following is not considered a clinical feature of AIDS?
Which of the following is not considered a clinical feature of AIDS?
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What does hypersensitivity refer to in the context of immune responses?
What does hypersensitivity refer to in the context of immune responses?
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Which type of hypersensitivity reaction is characterized as 'immediate'?
Which type of hypersensitivity reaction is characterized as 'immediate'?
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What underlies the immediate reaction in Type I hypersensitivity?
What underlies the immediate reaction in Type I hypersensitivity?
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Which allergenic condition correlates with Type I hypersensitivity?
Which allergenic condition correlates with Type I hypersensitivity?
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What is a defining feature of the late-phase reaction in Type I hypersensitivity?
What is a defining feature of the late-phase reaction in Type I hypersensitivity?
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What is typically released from mast cells during a Type I hypersensitivity reaction?
What is typically released from mast cells during a Type I hypersensitivity reaction?
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What is the main consequence of hypersensitivity disorders?
What is the main consequence of hypersensitivity disorders?
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Which immunoglobulin is primarily involved in immediate hypersensitivity reactions?
Which immunoglobulin is primarily involved in immediate hypersensitivity reactions?
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What type of hypersensitivity reaction is associated with Systemic Lupus Erythematosus (SLE)?
What type of hypersensitivity reaction is associated with Systemic Lupus Erythematosus (SLE)?
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Which of the following is a characteristic clinical manifestation of SLE?
Which of the following is a characteristic clinical manifestation of SLE?
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What role do autoantibodies play in SLE?
What role do autoantibodies play in SLE?
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What is a common systemic manifestation experienced by patients with SLE?
What is a common systemic manifestation experienced by patients with SLE?
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Which of the following organs can be affected by the immunological processes in SLE?
Which of the following organs can be affected by the immunological processes in SLE?
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How are B cells involved in the pathogenesis of SLE?
How are B cells involved in the pathogenesis of SLE?
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What triggers the autoimmune response in Systemic Lupus Erythematosus?
What triggers the autoimmune response in Systemic Lupus Erythematosus?
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Which types of antibodies are commonly found in individuals with SLE?
Which types of antibodies are commonly found in individuals with SLE?
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What occurs during the early period after primary HIV infection?
What occurs during the early period after primary HIV infection?
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When does the cytotoxic T lymphocyte (CTL) response to HIV become detectable?
When does the cytotoxic T lymphocyte (CTL) response to HIV become detectable?
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What happens to the CD4+ T-cell count during the period of clinical latency?
What happens to the CD4+ T-cell count during the period of clinical latency?
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At what time does the humoral immune response to HIV peak?
At what time does the humoral immune response to HIV peak?
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What is a substantial risk when the CD4+ T-cell count drops below a critical level?
What is a substantial risk when the CD4+ T-cell count drops below a critical level?
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Which specific T-cell responses expand significantly during the initial weeks following HIV infection?
Which specific T-cell responses expand significantly during the initial weeks following HIV infection?
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What is not a known feature of the clinical course of HIV infection?
What is not a known feature of the clinical course of HIV infection?
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What is the risk associated with a decreased CD4+ T-cell count?
What is the risk associated with a decreased CD4+ T-cell count?
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Study Notes
Epidemiology of AIDS
- HIV present in blood, semen, saliva, vaginal secretions, and breast milk at a concentration sufficient for transmission.
- Entry must be through injection or contact with a tear or lesion in the skin or mucous membranes.
- Primary transmission routes: sexual contact and intravenous drug use.
- HIV can also be transmitted across the placenta and through breast milk.
- Increased risk of HIV transmission for intravenous drug users, individuals with multiple sexual partners, and those engaging in unprotected sex.
HIV to AIDS progression
- HIV infects CD4 helper T lymphocytes, dendritic cells, and macrophages.
- Antibody production occurs after infection, but these antibodies cannot destroy all viral cells.
- Hallmark of AIDS: Loss of cell-mediated and humoral immunity due to the depletion of CD4 TH1 lymphocytes.
Clinical Features of AIDS
- Clinical latency initially characterized by the absence of symptoms.
- Clinical manifestations can include: fever, weight loss, diarrhea, generalized lymphadenopathy, multiple opportunistic infections, neurological disease, and secondary neoplasms.
Type I, Immediate Hypersensitivity Reaction
- Occurs within seconds to minutes.
- Also known as allergy.
- IgE-mediated response that triggers the release of inflammatory mediators from sensitized mast cells.
- Examples include food allergy, hay fever (allergic Rhinitis), and anaphylaxis.
- Two stages of response:
- Immediate (early-phase) reaction: Lasts about 1 hour. Sensitized mast cells binding the antigen leads to degranulation and release of preformed mediators. Causes vasodilation and nonvascular smooth muscle contraction.
- Late-phase reaction: Occurs 2-24 hours after exposure. Caused by the recruitment of eosinophils and the release of cytokines and membrane phospholipids from mast cells. Similar symptoms to the early phase, but last longer.
Type I, Immediate Hypersensitivity Reaction - Mast Cell Mediators
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Preformed (primary) mediators:
- Vasoactive amines: Most important is histamine. Causes vasodilation and increased vascular permeability (edema, hives). Other effects include smooth muscle spasm (bronchospasm) and increased mucus secretion (nasal, bronchial, and gastric glands).
- Enzymes: Proteases, acid hydrolases. Cause tissue damage, production of kinins and complement.
- Proteoglycans: Package and store amines.
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Lipid mediators:
- Leukotrients: Most potent vasoactive and spasmogenic agent known. Increases vascular permeability and bronchial smooth muscle spasm.
- Prostaglandin D2: Produced by the cyclooxygenase pathway. Causes intense bronchospasm and increased mucus secretion.
- Platelet-activating factor (PAF): Causes platelet aggregation, histamine release, bronchospasm, increased vascular permeability, and vasodilation. Chemotactic for neutrophils and eosinophils.
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Cytokines:
- TNF, IL-1, chemokines. Promote leukocyte recruitment.
Systemic Lupus Erythematosus (SLE)
- Autoimmune response; Type III hypersensitivity reaction (antigen-antibody complex-mediated).
- Chronic disease caused by a persistent antigen.
- Antigen-antibody binding stimulates inflammation and complex deposition in various organs.
- Antigens: Components of self cells (cell membrane, cytoplasm, nucleus).
- Antibodies: Produced by activated B cells. Includes autoantibodies like antinuclear antibodies (ANA), antiphospholipid, and anticytoplasmic antibodies.
- Activation of T cells contributes to inflammation and permanent organ damage.
Systemic Lupus Erythematosus (SLE) - Pathogenesis and Clinical Expression
- Pathogenesis: Progressive deposition and inflammation caused by immune complex deposits in the skin, joints, kidneys, vessels, heart, and CNS.
- Tissue injury: Refer to type III hypersensitivity reaction.
- Clinical expression: Progressive renal and vascular disease, positive antinuclear antibodies (ANA).
- Local manifestations: Skin, musculoskeletal, pulmonary, and kidney involvement. Characteristic facial rash across the nose and cheeks ("butterfly rash"). Arthritis, glomerulonephritis, etc.
- Systemic manifestations: Fatigue, pleural effusion, pericardial effusion.
Clinical Course of HIV Infection
- Early period after primary infection: Dissemination of the virus, development of an immune response to HIV, and often an acute viral syndrome.
- Clinical latency: Viral replication continues, and the CD4+ T-cell count gradually decreases until it reaches a critical level, increasing the risk of AIDS-associated diseases.
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Immune response to HIV infection:
- Cytotoxic T lymphocyte (CTL) response: Detectable within 2-3 weeks of initial infection, peaking at 9-12 weeks. Significant expansion of virus-specific CD8+ T-cell clones occurs during this period, with up to 10% of a patient's CTLs potentially being HIV-specific at 12 weeks.
- Humoral immune response: Peaks around 12 weeks.
Manifestations of HIV Infection and AIDS
- Manifestations of HIV infection and AIDS include opportunistic infections, malignancies, neurological disorders, and wasting syndrome.
Content Overview
- Review of immunity
- Diseases of the immune system:
- Hypersensitivity:
- Type I (Immediate)
- Type II (Antibody-mediated)
- Type III (Immune complex-mediated)
- Type IV (Cell-mediated)
- Autoimmune:
- Systemic Lupus Erythematosus (SLE)
- Rejection of Tissue Transplants
- Immunodeficiency syndromes:
- Acquired Immunodeficiency Diseases (AIDS)
- Hypersensitivity:
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Description
This quiz covers the epidemiology of AIDS, including transmission routes, risk factors, and the progression from HIV to AIDS. It also addresses the clinical features and the immune system's response to the virus, focusing on CD4 lymphocytes and the hallmark symptoms of AIDS.