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Lecture  Day 2

Lecture Day 2



Immunology sec D ADDU

Immunology sec D ADDU



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    Lecture  Day 2 Lecture Day 2 Presentation Transcript

    • Lecture Day 2
    • PneumocystisCarinii Pneumonia
      Most common opportunistic infection,80%
      ommonly found in the lungs of healthy people, but being a source of opportunistic infection it can cause a lung infection in people with a weakened immune system
      P. carinii, Pneumocystisjirovecii is a fungus and invades within pulmonary alveoli and forms consolidation in parenchyma
      the disease attacks the interstitial, fibrous tissue of the lungs, with marked thickening of the alveolar septa and alveoli and leading to significant hypoxia
    • Sx: nonproductive cough
      fever, chills, SOB, dyspnea,
      weight loss and night sweats
      Tx: trimethoprim-sulfamethomexazole, pentamidine and steroids
    • Mycobacterium Avium Complex
      Also, M. intracellulare, , M. scrofulaceum are acid fast bacilli cause respiratory tract infection and increase mortality rates
      Sx:include fever, fatigue, and weight loss
      Tx: Clarithromycin/Azithromycin, Anti-tuberculosis medication
    • Wasting Syndrome
      Profound, involuntary weight loss exceeding 10% of baseline body weight and chronic diarrhea for more than 30 days, intermittent fever
      May be due to hypermetabolic state, anorexia, diarrhea, malnutrition, GI malabsorption, low food intake
      Symptomatic,diet, control of diarrhea
    • Kaposi’s sarcoma
      Most common HIV-related malignancy
      Involves endothelial layers of blood and lymphatic vessels
      First noted by Dr. Moritz Kaposi in 1872, a tumor caused by Human herpesvirus 8
      Sx: may range from localized cutaneous symptoms to disseminated disease which may appear brownish pink to deep purple
      Treatment: palliative, HAART
    • Cryptococcus Neoformans
      Fungal infection that causes meningitis, and symptoms of fever, headache,malaise and stiff neck
      Tx: Amphotericin B, fluconazole
    • Post exposure prophylaxis
      a course of antiretroviral drugs which is thought to reduce the risk of seroconversion after events with high risk of exposure to HIV
      To be most effective, treatment should begin within an hour of possible infection, and no longer than 72 hours post-exposure. Prophylactic treatment for HIV typically lasts four weeks
    • Needle stick Injuries and aids
      CDC guidelines generally recommend a PEP protocol with 3 or more antiviral drugs, when it is known that the donor was HIV positive
      PEP drugs for prevention of HIV infection are given for 4 weeks and may include nucleoside reverse transcriptase inhibitors (NRTIs), nucleotide reverse transcriptase inhibitors (NtRTIs), nonnucleoside reverse transcriptase inhibitors (NNRTIs), protease inhibitors (PIs), and a single fusion inhibitor.
      Regardless whether PEP is instituted, follow-up of exposed individuals includes counseling and HIV testing by enzyme immunoassay to monitor for a possible seroconversion for at least 6 months after exposure. Such tests are done at baseline, 6 weeks, 12 weeks, and 6 months, and/or longer.
      There is currently no publicly available vaccine for HIV or cure for HIV or AIDS
      "highly active antiretroviral therapy“(HAART)
      Drugs that inhibit the reverse transcriptase prevent it from copying the RNA into DNA
      Drugs called protease inhibitors prevent the viral protease from trimming down the large proteins made late during infection
    • Allergy- an inappropriate response of the immune system to normally harmless substances
      Atopy- refers to allergic reactions by the actions of IgE antibodies and a genetic predisposition to allergic conditions.
      Mast cells- also called basophils, are trigerred by IgEs to release chemical mediators to produce allergic reactions
      T cells- secrete substances called lymphokines that encourage cell growth, activation, destroys target cells, and stimulate macrophages
    • Antigens are divided into 2 groups:
      Complete protein antigens-stimulate complete humoral response eg. Animal dander, pollen, horse serum
      Low molecular weight substances- eg. haptens
    • Primary mediators
      found in mast cells
      Histamine- causes erythema, localized edema, pruritus, contraction of bronchial muscle,dilation of small venules and constriction of large ones.
    • Prostaglandins- are composed of unsaturated fatty acids, produce smooth muscle contraction, vasodilation and increased capillary permeability.
    • 2. Secondary mediators
      a. Leukotrienes- released by mast cells that initiate inflammatory response, cause smooth muscle contraction,bronchial constriction and mucus secretion on the pathways.
      b. Bradykinin- polypeptide that causes increase vascular permeability, vasodilation, hypotension, and smooth muscle contraction and stimulates nerve cell fibers
      c. Serotonin- released during platelet aggregation causing contraction of bronchial smooth muscle
      Is a reflection of excessive or aberrant immune response
      It does not usually occur with first exposure to an allergen, but with re-exposure after sensitization in a predisposed individual
    • TYPES of hypersensitivities
      Type I/ Anaphylactic
      Characterized by edema in tissues , larynx and hypotension
      It is immediate and mediated by IgE antibodies
      Example:asthma, urticaria,allergic rhinitis,
    • Type II/ Cytotoxic
      Occurs when the system mistakenly identifies a normal constituent of the body as foreign
      Involves binding of IgG and IgM antibodies resulting to destruction of cells
      Example: myasthenia gravis, idiopathic thrombocytopenic purpura, hemolytic anemia
    • Type III/Immune Complex
      Involves immune complexes formed when antigens bind to antibodies
      Example: Systemic Lupus Erythematosus, Rheumatoid arthritis
    • Type IV/Delayed type
      Also called cellular hypersensitivity, occurs 24-72 hours after exposure to an allergen
      Example: contact dermatitis, mantoux test, transplant rejection
    • Allergic Rhinitis
      Also called hay fever, pollinosis
      Sensitization begins with exposure and on re-exposure the nasal mucosa reacts followed by edema formation and leukocyte infiltration
      Sx: nasal congestion, watery nasal discharge, sneezing,nasal itching
      Mgt: Avoid allergens, antihistamine, adrenergics, mast cell stabilizers, corticosteroids
    • Contact Dermatitis
      Or dermatitis venenata, a type IV hypersensitivity
      Acute or chronic skin inflammation that results from direct skin contact with chemicals or allergens
      80% are due to excessive exposure to irritants
      Sx: itching, burning, erythema, vesicles, edema, followed by weeping crusting , drying and peeling of the skin
    • Atopic Dermatitis
      A type I hypersensitivity, affects mostly children
      Sx: pruritus and hyperirritability of the skin
      Chronic with remission and exacerbation
      Mgt: wearing cotton fabrics, using mild detergent, avoiding allergens, moisturizer,
    • Food Allergy
      IgE mediated hypersensitivity
      Most common: seafood, legumes, nuts, egg, milk and chocolate
      SX: urticaria, wheezing, cough, laryngeal edema, swelling of lips, tongue, abdominal pain, cramps, vomiting, diarrhea
      Mgt: elimination of allergen, H1 and H2 blockers, antihistamine, corticosteroids
    • Serum sickness
      A type III hypersensitivity, traditionally results from administration of antisera of animal sources
      Sx: usually begin 6-10 days after administration includes: inflammation of injection site, lymphadenopathy, tender joints, peripheral neuritis, vasculitis
      Mgt: Antihistamines and corticosteroids
    • Latex Allergy
      Reaction to natural rubber proteins derived from the rubber tree (Heveabrasiliensis) found in Africa and Southeast Asia.
      Implicated with rhinitis, conjunctivitis and contact dermatitis
      Prevention:nonpowdered, low-protein latex and nonlatex gloves.