immune diseases

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immune diseases

  1. 1. Prepared by: Mae Michelle F. Aguilar RN Advance Pathophysiology USI-Graduate School MAN-MS
  2. 2. HYPERSENSITIVITY DISORDERS • The excessive or inappropriate activation of the immune system. • Disorders caused by the immune responses are collectively referred to as hypersensitivity reactions.
  3. 3. TYPE 1 IMMEDIATE HYPERSENSITIVITY
  4. 4. • IgE mediated, occurs rapidly within minuites of antigen challenge. • Referred to as allergic reactions and the antigens causing the response as allergens.
  5. 5. •CD4+ helper T cells of the TH2 type and Mast Cells or basophils.
  6. 6. • CD4+ T cell of TH2 cells differentiate in response to allergens and helminthes (intestinal parasites). • Cytokines of TH2 stimulate differentiation of B cells into IgE producing plasma cells, acts as growth factor for mast cells and recruit and activate eosinophils
  7. 7. • MAST CELLS are tissue cells while BASOPHILS are blood cells. • Distributed throughout connective tissue, beneath the skin and mucous membranes of the respiratory tract, GIT, GUT and adjacent to blood and vessles.
  8. 8. • With subsequent exposure, the sensitizing allergen binds to the cell associated IgE • Degranulation of sensitized mast cells occur (Release of their performed mediators)
  9. 9. Initial or Early Response • 5 to 30 mins of exposure to antigen and subsides within 60 mins. • Mediators: Histamine, Acetylcholine, enzymes such as trypsin and chymase that lead to generation of kinins • Vasodilation, vascular damage, smooth muscle spasms
  10. 10. Secondary or Late Phase • 2 to 8 hours later and lasts for several days. • Results from lipid mediators and cytokines involved in the inflammatory response. • Mast cell membrane phospholipids which broken down to form Archidonic Acid where leukotrienes and prostaglandins are synthesized.
  11. 11. • Similar effects with histamine and acetylcholine though effects are delayed and prolonged by comparison. • Mast cells also produce cytokines and chemotactic factors that attract eosinophils and leukocytes to the site of allergen contact.
  12. 12. • Responses: Mucosal edema, Mucus secretion, Leukocyte infiltration, Epithelial damage, bronchospasm.
  13. 13. Clinical Effects: • Systemic anaphylactic shock occurs with the activation of mast cells in the vascular system. • Local or atopic reactions occur if confined to a particular site by virtue of exposure.
  14. 14. Source: Robbins PATHOLOGIC BASIS OF DISEASE 6th ed
  15. 15. ALLERGIC DISORDERS
  16. 16. ANAPHYLAXIS • Systemic, life-threatening hypersensitivity reaction characterized by vasodilation. • Fall in blood pressure, airway constriction, vascular swelling, obstruction of upper airway ANAPHYLACTIC SHOCK
  17. 17. • MILD SYSTEMIC REACTIONS – Peripheral tingling – Sensation of warmth – Fullness of mouth and throat – Nasal congestion – Periorbital swelling – Pruritus – Sneezing – Tearing of the eyes
  18. 18. • MODERATE SYSTEMIC REACTIONS – Flushing – Warmth – Anxiety – Itching in addition to above symptoms – Dyspnea, coughing, wheezing, bronchospasm, edema of airways.
  19. 19. • SEVERE SYSTEMIC REACTIONS – Bronchospasm – Laryngeal edema – Severe dyspnea – Cyanosis – Hypotension – Dysphagia – Abdominal Cramping – Vomiting – Diarrhea – Seizure – Cardiac arrest and coma
  20. 20. Common medications that cause anaphylaxis • Antibiotics (Penicillin and sulfa antibiotics) • Allopurinol • Radio contrast agents • Anesthetic agents (lidocaine, procaine) • Vaccines • Hormones • Aspirin • NSAIDs
  21. 21. Prevention • Avoidance of potential allergens • Screening for allergies • Wear medical alert bracelets • Desensitization • Carry an Emergency Kit (EpiPen)
  22. 22. Medical Management • CPR • Oxygen • Epinephrine • Intravenous infusion (NSS), volume expanders and vassopressors • Antihistamines and corticosteroids to treat urticaria and angioedema • Aminophylline and corticosteroids
  23. 23. NURSING MANAGEMENT • Assess the airway, breathing pattern and other vital signs. • Emergency measures ( intubation, administration of emergency medications, insertion of intravenous lines, fluid administration, oxygen administration) • Health Teaching!
  24. 24. ALLERGIC RHINITIS • Inflammation of the nasal mucosa. • hay fever; chronic allergic rhinitis, pollinosis • Most common form of respiratory allergy. • Often occurs with other conditions such as allergic conjunctivitis, sinusitis and asthma.
  25. 25. • Induced by airborne pollen or molds. • Histamine is the major mediator of allergic reactions in the nasal mucosa. • Upon inhalation or ingestion of the antigen, nasal mucosa reacts by slowing the ciliary action, edema formation and leukocyte (eosinophils) infiltration.
  26. 26. • Complications may result to allergic asthma, chronic nasal obstruction, chronic otitis media with hearing loss, anosomia (absence of the sense of smell)
  27. 27. Assessment and Diagnostic Findings • Nasal smears • Peripheral blood counts • Total serum IgE • Epicutaneos and intradermal screening • RAST • Food elimination and challenge • Nasal provocation test
  28. 28. Medical Management AVOIDANCE THERAPY PHARMACOLOGIC THERAPY GOAL: RELIEF from symptoms!
  29. 29. PHARMACOLOGIC THERAPY • Antihistamines – H1 receptor antagonist (H1 blockers) – H1 blockers selectively bind to H1 receptors preventing actions of histamines at these sites – Oral antihistamines – limited to certain patients with hay fever, vasomotor rhinitis, urticaria (hives) and mild asthma –Major side effect : SEDATION
  30. 30. • Nervousness, tremors, dizziness, dry mouth, palpitations, anorexia, nausea and vomiting. • Contraindicated: Third trimester of pregnancy, nursing mothers and newborns, in children and elderly people and in patients with conditions that can be aggravated by muscarinic blockage.
  31. 31. • 2nd generation or non-sedating H1 receptor antagonists – Does not cross the blood brain barrier and do not bind to the cholinergic, serotonin, or alpha- adrenergic receptors. – Binds to the peripheral nervous system H1 receptors causing less sedation.
  32. 32. • Sedating – Ethanolamine : Diphenhydramine (Benadryl) •MAJOR SIDE EFFECTS NURSING IMPLICATIONS: •drowsiness, and confusion Teach patient to avoid alcohol, driving or engaging in hazardous activities •dry mouth, nausea, vomiting Sucking on hard candy or ice chips for relief of dry mouth, •Photosensitivity Encourage use of sunscreen and hat while outdoors •urinary retention Assess for urinary retention, monitor urinary output
  33. 33. • Non-Sedating –Loratadine (Claritin) –Cetirizine (Zyrtec)
  34. 34. • ADRENERGIC AGENTS – Vasoconstrictors of mucosal vessels, are used topically (nasal and ophthalmic) in addition to the oral route. – Drops or spray has fewer side effects, however used for a few days to avoid rebound congestion. • Xylometazoline hydrochloride
  35. 35. • MAST CELL STABILIZERS – Intranasal cromolyn sodium (Nasalcrom) – A spray that acts by stabilizing the mast cell membrane thus reducing histamine and other mediators of the allergic response. – Used prophilactically before exposure to allergens. – Benefits may take a week or so to occur.
  36. 36. • CORTICOSTEROIDS – For more severe cases that cannot be controlled by conventional medications. – Dexamethasone, budesonide, fluticasone, beclomethasone. – Anti-inflammatory – Suppress host defenses so they must be used with caution for patients with tuberculosis, untreated bacterial infections of the lungs.
  37. 37. • Side Effects: Fluid retention, weight gain, hypertension, gastric irritation, glucose intolerance, and adrenal suppression.
  38. 38. • IMMUNOTHERAPY – Used to treat IgE mediated diseases by injections of allergen extracts. – Patient is at risk for general and potentially fatal, anaphylaxis
  39. 39. NURSING INTERVENTIONS • Improving Breathing Pattern • Promoting understanding of allergy control • Coping with a chronic disorder • Monitor and manage potential complications.
  40. 40. ATOPIC DERMATITIS • Family history is common. • Highest incidence in infants and children
  41. 41. • Significant elevations of serum IgE and peripheral eosinophilia. • Pruritus and hyperirritability of the skin. • Large amounts of histamine in the skin. • Chronic condition with remissions and exacerbations. • Tendency to recur with remission from adolescence to age 20
  42. 42. DERMATITIS MEDICAMENTOSA (DRUG REACTIONS) • Skin rashes induced by the internal administration of certain medications. • Common causes are cephalosporins, includin g ampicillin, semi synthetic penicillins, and barbiturates.
  43. 43. FOOD ALLERGIES • Primary target of food allergy may be the skin, the gastrointestinal tract or the respiratory system. • Occur at any age but manifests during childhood.
  44. 44. LATEX ALLERGY • Allergic reaction to natural rubber proteins.
  45. 45. TYPE II ANTIBODY- MEDIATED HYPERSENSITIVITY
  46. 46. • Type II (Cytotoxic) hypersensitivity are mediated by IgG and IgM antibodies directed against target antigens on the surface of cells or other tissue components. • Complement-mediated or antibody-mediated cytotoxicity • Antigens are endogenous or exogenous
  47. 47. Source: Robbins PATHOLOGIC BASIS OF DISEASE 6th ed.
  48. 48. 1.Transfusion reactions 2.Erythroblastosis fetalis 3.Autoimmune hemolytic anemia, agranulocytosis, thrombocytopenia – (+) antibodies vs own blood cells 4.Pemphigus vulgaris – Ab’s vs. desmosomes 5.Drug reactions
  49. 49. BLOOD TRANSFUSION REACTION • Cells from an incompatible donor react with autochthonous antibody of the host.
  50. 50. Nursing Interventions when complications occurs in Blood transfusion • If blood transfusion reaction occurs. STOP THE TRANSFUSION. • Start IV line (0.9% NaCl) • Place the client in fowler’s position if with SOB and administer O2 therapy. • The nurse remains with the client, observing signs and symptoms and monitoring vital signs as often as every 5 minutes. • Notify the physician immediately. • The nurse prepares to administer emergency drugs such as antihistamines, vasopressor, fluids, and steroids as per physician’s order or protocol. • Obtain a urine specimen and send to the laboratory to determine presence of hemoglobin as a result of RBC hemolysis. • Blood container, tubing, attached label, and transfusion record are saved and returned to the laboratory for analysis.
  51. 51. ERYTHROBLASTOSIS FETALIS • Antigenic difference between mother and fetus and antibodies from the mother cross the placenta and cause destruction of fetal blood cells.
  52. 52. Antibody-Dependent Cell-Mediated Cytotoxicity (ADCC) • due to NK activity  non-sensitized cells with Fc receptors • Ab + Ag  activation of NK cells  bind to Fc fragment of IgG  cell lysis without phagocytosis • Destruction of targets too large to be phagocytosed (parasites, tumor cells) + graft rejection
  53. 53. Antibody-Dependent Cell-Mediated Cytotoxicity (ADCC) Source: Robbins PATHOLOGIC BASIS OF DISEASE 6th ed.
  54. 54. Antibody-Mediated Cellular Dysfunction 1.Myasthenia gravis – acetylcholine receptors 2.Goodpasture’s syndrome – type IV collagen 3.Pernicious anemia – intrinsic factor 4.Acute rheumatic fever – antibodies vs. Streptococcal antigens cross-react with heart
  55. 55. • Antibodies directed against cell surface receptors  impair or deregulate function Source: Robbins PATHOLOGIC BASIS OF DISEASE 6th ed.
  56. 56. MYASTHENIA GRAVIS • a type of autoimmune disorder, a neuromuscular disease that usually results to muscle weakness and fatigue primarily in the face. This makes the muscles get tired and weakened more easily than what is normal.
  57. 57. TYPE III (IMMUNE COMPLEX MEDIATED) HYPERSENSITIVITY
  58. 58. Immune Complex Mediated • Formation of immune complexes in circulation  deposit in various tissues  trigger classical pathway of complement activation • Produce damage as they localize within blood vessel walls or when trapped in filtering structures (e.g. renal glomeruli)
  59. 59. Source: Robbins PATHOLOGIC BASIS OF DISEASE 6th ed.
  60. 60. Source: Robbins PATHOLOGIC BASIS OF DISEASE 6th ed.
  61. 61. Source: Robbins PATHOLOGIC BASIS OF DISEASE 6th ed.
  62. 62. ANTIGEN CLINICAL MANIFESTATION EXOGENOUS Infectious agents: Bacteria: Y. enterocolitica Streptococci T. pallidum Viruses: Hep. B, CMV Parasites: Plasmodium Schistosoma Fungi: Actinomycetes Arthritis GN, Infective endocarditis Glomerulonephritis Polyarteritis nodosa Glomerulonephritis Farmer’s lung ENDOGENOUS Nuclear antigens Immunoglobulins Tumor antigens SLE Rheumatoid arthritis Glomerulonephritis Antigens Associated with Immune Complex Disorders
  63. 63. SERUM SICKNESS • Patient forms antibodies to xenogeneic Ig administered during passive immune therapy regimens ARTHUS REACTION • Seen when boosters are administered to individuals who already possess high antibody titers to vaccine molecules • Localized area to tissue necrosis  edema, hemorrhage, ulceration • Develop over a few hours
  64. 64. TYPE IV (CELL-MEDIATED) HYPERSENSITIVITY
  65. 65. • Initiated by sensitized T lymphocytes • Principal pattern of immunologic response to intracellular microbiologic agents (particularly Mycobacterium tuberculosis) as well as viruses, fungi, protozoa & parasites
  66. 66. Delayed-type hypersensitivity • Mediated by CD4 T cells • 1st exposure to Ag  CD4 T cells + class II MHC  differentiation of naïve CD4 T cells to TH1 cells  release of IL-12, IFN- , IL-2, TNF & lymphotoxin • Tuberculin skin test, contact dermatitis, granulomatous inflammation
  67. 67. Tuberculin Test
  68. 68. CONTACT DERMATITIS • (Dermatitis venenata) Acute or Chronic skin inflammation that results from direct skin contact with other chemicals or allergens
  69. 69. P o i s o n I v y
  70. 70. Treatment • Avoidance of offending material • Burrow’s solution or cool water compress • Systemic Corticosteroids (Prednisone) • Topical Corticosteroids • Oral antihistamines • Hydrophilic cream or petrolatum • Antibiotics for infection
  71. 71. T Cell-Mediated Cytotoxicity • Mediated by CD8+ T cells • Sensitized CD8+ T cells kill antigen- bearing target cells • Graft rejection, virus infections, tumor immunity
  72. 72. • Two mechanisms: a)Perforin-granzyme-dependent killing  cause perforation of plasma membrane b)Fas-FasL-dependent killing  activation of apoptosis
  73. 73. TRANSPLANT REJECTION • One of the goals of present day immunologic research is successful transplantation of tissues in humans without immunologic rejection.
  74. 74. Mechanisms in Graft Rejection • Antigens responsible for rejection in humans are those of the Major Histocompatibility antigen (HLA) system • T cell-Mediated Reactions and Antibody-mediated reactions
  75. 75. T cell mediated Reactions • Activation of the CD8 CTLsand delayed hypersensitivity reactions triggered by activated CD4 helper cells seem to be involved.
  76. 76. Increasing Graft Survival • Immunosuppressive Therapy – Azathiprine, steroids, cyclosporine, antilymphocyte globulins, monoclonal anti-T cell antibodies – Cyclosporine suppresses T cells mediated immunity by inhibiting activation of cytokine genes, in particular, the gene for IL 2.
  77. 77. AUTOIMMUNE DISEASES
  78. 78. • Caused by the breakdown in the ability of the immune system to differentiate between self and non self.
  79. 79. • The ability of the immune system to differentiate self from non-self is called SELF TOLERANCE. • Maintained through central and peripheral mechanisms that delete auto reactive B or T cells or suppress or inactivate immune responses that would be destructive to host tissues.
  80. 80. • Defects on these mechanisms could impair self-tolerance and predispose one to autoimmune disorders.
  81. 81. Mechanisms of Autoimmune Disease • Genetic Susceptibility – Increase incidence and severity of autoimmune diseases is shown in familial clustering of several autoimmune diseases and the observation that a certain inherited HLA genotypes occur more frequently with a variety of autoimmune disorders.
  82. 82. – 90% of people with Ankylosing Spondylitis carry the HLA-B27 antigen – Rheumatoid Arthritis (HLA-DR4) – SLE (HLA-DR3)
  83. 83. • Environmental Factors – Breakdown of T cell Anergy – Release of Sequestered Antigens – Molecular Mimicry – Superantigens
  84. 84. RHEUMATOID ARTHRITIS • The autoimmune reaction primarily occurs in the synovial tissue.
  85. 85. Presentation of antigen to T cells T and B cell proliferation. Angiogenesis in synovial lining Neutrophil accumulation in synovial fluid. Cell proliferation. No cartilage invasion. Synovitis. Early pannus invasion. Chondrocyte activation. Degredation of cartilage by proteinase Subchondral bone erosion Pannus invation of cartilage. Chondrocyte proliferation. Laxity of ligaments Swelling of small joints, pain, stiffness, fatigue Warm, swollen, effusions, pain, poss. Rheumatoid nodules, decreased motion Increase in severity of signs and symptoms Joint instability, contractures, decreased ROM, systemic complications
  86. 86. Treatment • Medications that treat pain and inflammation. – Aspirin – NSAIDs – Corticosteroids – DMARDs (disease modifying anti rheumatic drugs)
  87. 87. LUPUS • condition characterized by chronic inflammation of body tissues caused by autoimmune disease • abnormal antibodies produced in blood  target tissues within own body rather than foreign infectious agents • antibodies & accompanying cells of inflammation can involve tissues anywhere in the body  has potential to affect a variety of areas of the body
  88. 88. • can cause disease of the skin, heart, lungs, kidneys, joints, and/or nervous system • only the skin involved  discoid lupus • internal organs involved  SLE
  89. 89. • shape  referred to as the "butterfly rash" of SLE • painless, does not itch • worsened by exposure to sunlight (photosensitivity)
  90. 90. • no permanent cure for SLE • goal of treatment - to relieve symptoms & protect organs by decreasing inflammation and/or the level of autoimmune activity in the body • mild symptoms - need no treatment or only intermittent courses of antiinflammatory medications • serious illness (damage to internal organ) - require high doses of corticosteroids with other medications that suppress the body's immune system
  91. 91. • NSAIDs • Topical corticosteroid creams • Anti-Malarials to treat joint pain, skin rashes, mouth ulcers, fatigue and fever • Systemic corticosteroids • Cytotoxic therapy to treat diffuse proliferative Glomerulonephritis • Immunosuppressive • Methotrexate (anti inflammatory and immunosuppressive.)
  92. 92. IMMUNODEFICIENCY DISORDERS
  93. 93. BITS OF HISTORY HIV came from a similar virus found in chimpanzees - SIV. HIV probably entered the United States around 1970 CDC in 1981 noticed unusual clusters of Kaposi’s sarcoma in gay men in NY and San Francisco, which led to the disease to be called GRID (Gay Related Immune Deficiency). By 1982 the disease was apparent in heterosexuals and was renamed AIDS (Acquired Immune Deficiency). 1984- Scientists(Dr. Luc Montagnier, Dr. Robert Gallo) identify HIV (initially called LAV or HTLV-III) as the cause of AIDS 1987- AZT is the first drug approved for treating AIDS
  94. 94. AIDS HIV STATISTICS • DOH Current report
  95. 95. Who is at risk? The following are behaviors that increase chances of getting HIV: • Injecting drugs or steroids or shared equipment (such as needles, syringes, works) with others • Unprotected vaginal, anal, or oral sex, multiple partners, or anonymous partners • Diagnosed with or treated for hepatitis, tuberculosis (TB), or a sexually transmitted disease (STD) • Had unprotected sex with someone who could answer yes to any of the criteria as listed above.
  96. 96. HIV LIFE CYCLE • Binding- HIV searches for cells that have CD4 surface receptors. Main target is the T4-lymphocyte. The T4-cell is responsible for warning your immune system that there are invaders in the system. • Reverse Transcription- Makes a DNA copy of the virus’s RNA. Can be blocked by Nucleoside Reverse Transcriptase Inhibitors (NRTIs) and Non- Nucleoside Reverse Transcriptase Inhibitors (NNRTIs) • Integration-The HIV DNA is then carried to the cell’s nucleus. When the cell makes new proteins, it accidentally makes new HIVs. Integration can be blocked by integrase inhibitors, a new class of drugs that are in the earliest stage of research.
  97. 97. • Transcription-Once HIV’s genetic material is inside the cell’s nucleus, it directs the cell to produce new HIV. The strands of viral DNA nucleus separate and special enzymes create messenger RNA (mRNA). This can be blocked by antisense antiviral or transcription inhibitors (Tis) new classes of drugs that are in the earliest of research. • Translation-The mRNA carries instructions for making new viral proteins from the nucleus. • Viral Assembly and Maturation-The virus becomes an infection and each infected cell can produce lots of new viruses. Viral assembly can be blocked by Protease Inhibitors (PIs).
  98. 98. • Helper T-Cells (also called T4 or CD4)- help other cells destroy infective organisms. • Suppressor T-Cells (also called T8 or CD8)-suppress the activity of other lymphocytes so they don’t destroy normal tissue. • Killer T-Cells (also called cytotoxic T lymphocytes, or CTLs, and are another kind of T8 or CD8 cell)- recognize and destroy abnormal or infected cells. CD4/T-CELLS
  99. 99. How long after exposure? • It can take some time for the immune system to produce enough antibodies for the antibody test to detect, and this time period can vary from person to person. This time period is commonly referred to as the “window period.” • Most people will develop detectable antibodies within 2 to 8 weeks (the average is 25 days). Even so, there is a chance that some individuals will take longer to develop detectable antibodies. • Therefore, if the initial negative HIV test was conducted within the first 3 months after possible exposure, repeat testing should be considered >3 months after the exposure occurred to account for the possibility of a false-negative result. Ninety- seven percent of persons will develop antibodies in the first 3 months following the time of their infection. In very rare cases, it can take up to 6 months to develop antibodies to HIV.
  100. 100. TESTING FOR THE VIRUS • EIA (enzyme immunoassay) used on blood drawn from a vein, is the most common screening test used to look for antibodies to HIV. A positive (reactive) EIA must be used with a follow-up (confirmatory) test such as the Western blot to make a positive diagnosis. There are EIA tests that use other body fluids to look for antibodies to HIV. These include: Oral Fluid Tests – use oral fluid (not saliva) that is collected from the mouth using a special collection device. This is an EIA antibody test similar to the standard blood EIA test. A follow-up confirmatory Western Blot uses the same oral fluid sample. Urine Tests – use urine instead of blood. The sensitivity and specificity (accuracy) are somewhat less than that of the blood and oral fluid tests. This is also an EIA antibody test similar to blood EIA tests and requires a follow-up confirmatory Western Blot using the same urine sample.
  101. 101. • Rapid Tests: A rapid test is a screening test that produces very quick results, in approximately 20 minutes. Rapid tests use blood from a vein or from a finger stick, or oral fluid to look for the presence of antibodies to HIV. As is true for all screening tests, a reactive rapid HIV test result must be confirmed with a follow-up confirmatory test before a final diagnosis of infection can be made. • Home Testing Kits The testing procedure involves pricking a finger with a special device, placing drops of blood on a specially treated card, and then mailing the card in to be tested at a licensed laboratory. Customers are given an identification number to use when phoning in for the results. All individuals receiving a positive test result are provided referrals for a follow-up confirmatory test, as well as information and resources on treatment and support services. • RNA Tests RNA tests look for genetic material of the virus and can be used in screening the blood supply and for detection of very early infection rare cases when antibody tests are unable to detect antibodies to HIV.
  102. 102. Modes of transmission Sexual contact Homosexuals (MSM), & Heterosexuals Parenteral transmission IVDA, Hemophiliacs, accidental needle sticks Vertical transmission From mother to child during delivery (MTCT)
  103. 103. • HIV stands for human immunodeficiency virus. This is the virus that causes AIDS. HIV is different from most other viruses because it attacks the immune system. The immune system gives our bodies the ability to fight infections. HIV finds and destroys a type of white blood cell (T cells or CD4 cells) that the immune system must have to fight disease.
  104. 104. Symptoms of HIV HIV can cause any symptoms of illness, since infections can occur throughout the body. Special symptoms relating to HIV infection include: • Diarrhea • Fatigue • Fever • Frequent vaginal yeast infections • Headache • Mouth sores, including candidal infection • Muscular stiffness or aching • Rash of various types, including seborrheic dermatitis • Sore throat • Swollen lymph glands
  105. 105. AIDS • AIDS stands for acquired immunodeficiency syndrome. AIDS is the final stage of HIV infection. It can take years for a person infected with HIV, even without treatment, to reach this stage. Having AIDS means that the virus has weakened the immune system to the point at which the body has a difficult time fighting infections. When someone has one or more of these infections and a low number of T cells, he or she has AIDS.
  106. 106. Symptoms of AIDS • The following is a list of AIDS-related infections and cancers that people with AIDS acquire as their CD4 count decreases. Previously, having AIDS was defined as having HIV infection and getting one of these additional diseases. Now it is additionally defined as a CD4 count below 200, even without an opportunistic infection. Many other illnesses and corresponding symptoms may develop in addition to those listed here.
  107. 107. Absolute CD4 Count • Normal Values- in a healthy adult, a normal CD4 count can vary a great deal but is typically 600-1200 cells per cubic millimeter of blood • Between 600 and 350 – in an HIV+ person, this range is considered “very good”. HIV medications are typically not indicated. • Between 350-200-the immune system is weakened and therefore the HIV+ person may be at increased risk for infection and illness. May start taking HIV medications. • Less than 200 – The immune system is severely weakened and the HIV+ person is at much greater risk of opportunistic infections. HIV medications and prophylactic antibiotics will be prescribed to help prevent illnesses and infections. The patient be classified as having AIDS.
  108. 108. CD4 count below 200 cells/ml • Pneumocystis carinii pneumonia, "PCP pneumonia," now called Pneumocystic jiroveci pneumonia • Candida esophagitis -- painful yeast infection of the esophagus • Bacillary angiomatosis -- Skin lesions caused by a bacteria called Bartonella, which is usually acquired from cat scratches
  109. 109. CD4 count below 100 cells/ml • Cryptococcal meningitis -- infection of the lining of the brain by a yeast • AIDS dementia -- worsening and slowing of mental function, caused by HIV itself • Toxoplasmosis encephalitis -- infection of the brain by a parasite, which is frequently found in cat feces; causes discrete lesions in the brain • Progressive multifocal leukoencephalopathy -- a viral disease of the brain caused by a virus (called the JC virus) that results in a severe decline in cognitive and motor functions • Wasting syndrome -- extreme weight loss and loss of appetite, caused by HIV • Cryptosporidium diarrhea -- Extreme diarrhea caused by one of several related parasites
  110. 110. Asymptomatic HIV • Asymptomatic HIV infection is a phase of chronic infection with human immunodeficiency virus (HIV) during which there are no symptoms of HIV infection. • The length of this phase varies from person to person. It depends on how quickly the HIV virus is copying itself and the genetic differences that affect the way the immune system handles the virus. • Some people can go 10 years or longer without symptoms, while others may have symptoms and worsening immune function within a few years after the original infection. • People with asymptomatic infection can progress to symptomatic HIV infection and develop opportunistic infections associated with HIV. In addition, pregnant women with asymptomatic HIV infection can still transmit HIV to their fetus. • People who are asymptomatic but who have CD4 lymphocyte counts of less than 200 should be on therapy.
  111. 111. HIV-Type 2 • Persons infected with HIV-2, immunodeficiency seems to develop more slowly and to be milder. Compared with persons infected with HIV-1, those with HIV-2 are less infectious early in the course of infection. • Both HIV-1 and HIV-2 have the same modes of transmission and are associated with similar opportunistic infections and AIDS. • As the disease advances, HIV-2 infectiousness seems to increase; however, compared with HIV-1, the duration of this increased infectiousness is shorter. HIV-1 and HIV-2 also differ in geographic patterns of infection; the United States has few reported cases. • HIV-2 is highly concentrated in West Africa countries such as Senegal, Nigeria, Ghana, and the Ivory Coast. HIV-2 also spreads to other parts of the world but predominantly to those countries having strong ties to West Africa.

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