1. DAY 1 IMMUNOLOGY LECTURE BACHELOR OF SCIENCE IN NURSING Ateneo de davao University
2. OBJECTIVES Review the inflammatory process Review the anatomy and physiology of the immune system Understand the different types of immune response Enumerate the different stages of immune response Learn about the different types of primary immunodeficiencies
4. Inflammation the complex biological response of vascular tissues to harmful stimuli, such as pathogens, damaged cells, or irritants. It is a protective attempt by the organism to remove the injurious stimuli as well as initiate the healing process for the tissue
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6. As soon as the tissue is ruptured, the damaged cells release chemicals such as histamine, which serve as alarm signals. The chemicals released activate numerous defense mechanisms in the body. Histamine forces nearby blood vessels to dilate and to allow more diffusion by becoming leakier. Due to this, blood flow to the affected area increases, and the plasma of the blood seeps into the interstitial fluid of the damaged tissues.
7. Other chemicals that are released attract phagocytes and other leukocytes to the affected area. These leukocytes squeeze out of the blood vessels into the interstitial fluid and tissue spaces. This increase in blood flow, blood plasma, and white blood cells causes the redness, heat, and swelling that are normally found in inflammation. The leukocytes that have been attracted to the area engulf the bacteria, and any dead body cells damaged by the pathogens or by the injury. This may result in the death of the leukocytes, as well, and their remains are also digested. Pus found at the site of infection consists mainly of white blood cells and blood plasma
12. WHITE BLOOD CELLS Also called LEUKOCYTES are cells of the immune system defending the body against both infectious disease and foreign materials Generally divided into 2 types: Granulocytes and agranulocytes
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15. a.Basophils- capable of engulfing invaders and secreting histamine b. Eosinophils- dispose of cellular debris and involved in allergic and parasitic reactions. c.Neutrophils- involved in inflammatory process and phagocytosis
16. d. Monocytes- migrate to tissues to become macrophages, and serves as antigen presenting cell e.Lymphocytes- may become B and T lymphocytes to defend against invaders
17. Lymphoid Tissues 1.Spleen, which is composed of red and white pulp that acts like a filter where red blood cells are destroyed It synthesizes antibodies in its white pulp and removes, from blood and lymph node circulation, antibody-coated bacteria along with antibody-coated blood cells It also contains in its reserve, half of the body's monocytes
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19. Lymph nodes, which are connected to lymph channels & capillaries remove foreign material from the lymph before it enters the blood stream.
20. 3. Tonsils & adenoids, contain immune cells that defend the body’s mucosal surfaces.
21. Immunity the body’s specific protective response to an invading agent. Has 2 general types: 1. Natural 2. Acquired
22. 1.Natural immunity nonspecific immunity- present at birth “self versus non-self” Ex. physical and chemical barriers and white blood cell action
23. 2. Acquired immunity develops after birth, usually after prior exposure to an antigen has 2 types: 1.Active acquired-defenses are developed by the own person’s body 2.Passive acquired- temporary immunity transmitted from another source.
24. Active or Passive? Immunity to tetanus Answer: active Immunity on the first 6 months of life Answer: passive
27. Antibodies Are also called immunoglobulins They arise from a plasma cell which arose also from B-lymphocytes Some actions of antibodies include: Agglutination Opsonization Release of vasoactive substances Phagocytosis
37. 2. Humoral Responsealso called antibody response,begins with B lymphocytes becoming plasma cells that produce antibodies which combine to disable the invader
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39. 3. Cellular Response Involves T lymphocytes that turn into special cytotoxic cells that attack pathogens. T cells arise from stem cells that migrated to the thymus gland
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42. 3. Supressor T cells- decrease B-cell production4. memory T cells- are responsible for recognizing antigens from previous exposure
45. A. Recognition Stagethe body recognizes the invaders as foreign by using lymph nodes and lymphocytes as surveillance
46. B. Proliferation Stagethe circulating lymphocyte returns to the nearest lymph node with the antigenic message and the lymph node in turn stimulates its resident B and T lymphocytes to enlarge and divide.
47. c. response stageinitiation of humoral and cellular response forming the t cells.d.effector stageresults to the total destruction of the microbes or neutralization of toxins.
48. WHITE BLOOD CELL COUNT Normal WBC count : 5000-10,000 cells/mm3 Leukocytosis Leukopenia
49. Bone marrow biopsy-the removal of soft tissue from inside bone for study- commonly taken from the hip bone, check for bleeding problems- patient may feel sharp pain
51. Phagocytic Dysfunction 1.Hyperimmunoglobinemia E /Job’s Syndrome Hyper IgE syndrome (HIES) no known cause Sx: recurrent staphylococcal infections, unusual eczema-like skin rashes, severe lung infections very high concentrations of the serum antibody IgE skeletal abnormalities such as fractures scoliosis and dental problems such as retention of deciduous teeth
52. no existing cure, only symptomatic IV gamma globulin Source: www.jobsyndrome.com
53. Chronic Granulomatous Disease pt. has no inflammatory response. Sx: increased incidence of bacterial, fungal & viral infectioncold abscess, mouth ulcers, stomatitis8 or more ear infections in a year Management: Early Diagnosis is essentialGranulocyte transfusionAntibiotic therapy
54. B-cell deficiencies Aggamaglobulinemia/Bruton’s Disease Sex-linked Males are mostly affected Results from lack of differentiation form B-cell precursors into mature B-cells No plasma cells are formed leading to complete lack of antibody production
55. Symptoms:Pyogenic infection starting 5-6 months of age frequent ear and sinus infections, pneumonia, and gastroenteritis. Certain viruses, such as hepatitis and polio viruses, can also pose a threat. Children with XLA grow slowly, have small tonsils and lymph nodes, and may develop chronic skin infections
56. Hypogammaglobulinemia Results from lack of differentiation of some B cells into plasma cellsalso called common variable immunodeficiency, etiology is unknown. Symptoms:pernicious anemia high susceptibility to infection Management:Intravenous immunoglobulinAntibioticsVitamin B12 injection
57. T-cell deficiencies DiGeorge syndrome/thymichypoplasia Velo-Cardio-Facial syndrome, DiGeorge Syndrome, Shprintzen syndrome, conotruncal anomaly face syndrome, Congenital ThymicAplasia, Strong Syndrome, Thymichypoplasia, and DiGeorge anomaly Congenital in origin, thymus fails to develop normally due to deletion of chromosome 22 Sx: hypoparathyroidism, which results in hypocalcemia hypoplastic thymus or absent thymus, which results in problems in the immune system
59. Management: There is no cure, the key is to identify each of the associated features and manage each using the best available treatments Management of hypocalcemia Antibiotics Thymus transplantation, cardiac surgery
60. COMBINED T-CELL & B-CELL DEFICIENCIES Ataxia-Telangectasia Also called Boder-Sedgwick syndrome or Louis–Bar syndrome a rare, neurodegenerative, inherited disease that affects many parts of the body and causes severe disability. Ataxia refers to poor coordination and telangiectasia to small dilated blood vessels, both of which are hallmarks of the disease. It affects the cerebellum and also weakens the immune system in about 70% of the cases, leading to respiratory disorders
61. about half the people with A-T have immune problems. These usually take the form of repeated colds and runny noses Treatment is symptomatic and supportive. Physical and occupational therapy may help maintain flexibility. Gamma-globulin injections may be given to help supplement a weakened immune system. High-dose vitamin regimens may also be used. Antibiotics are used to treat infections,low doses of chemotherapy to reduce the risk of cancer but this is controversial.
64. AIDS is pandemic In 2007, it was estimated that 33.2 million people lived with the disease worldwide, and that AIDS killed an estimated 2.1 million people, including 330,000 children.
65. History Scientists identified a type of chimpanzee in West Africa as the source of HIV infection in humans. The virus most likely jumped to humans when humans hunted these chimpanzees for meat and came into contact with their infected blood. Over several years, the virus slowly spread across Africa and later into other parts of the world
66. AIDS was first reported June 5, 1981, when the U.S. Centers for Disease Control (CDC) recorded a cluster of Pneumocystiscarinii in five homosexual men in Los Angeles
67. AIDS Acquired immune deficiency syndrome or acquired immunodeficiency syndrome (AIDS) is a disease of the human immune system caused by the human immunodeficiency virus or HIV
68. HIV HIV is a retrovirus that primarily infects vital organs of the human immune system such as CD4+ T cells , macrophages HIV belongs to the group retroviruses that carry their genetic material in RNA
69. WHAT IS A RETROVIRUS? A retrovirus is an RNA virus that is replicated in a host cell via the enzyme reverse transcriptase to produce DNA from its RNA genome The DNA is then incorporated into the host's genome by an integrase enzyme. The virus thereafter replicates as part of the host cell's DNA.
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71. Transmission involve anal, vaginal or oral sex, blood transfusion, contaminated hypodermic needles, exchange between mother and baby during pregnancy, childbirth, breastfeeding or other exposure to one of the above bodily fluids.
72. STAGES OF HIV DISEASE 1.Primary Infection/Acute HIV Syndrome, Stage I From period of infection to development of antibodies and intense viral replication Sx: none to severe flu-like symptoms
73. Criteria for Stage I During the first stage of HIV, an individual generally has flu like symptoms which last for a week or two. WHO provides the following criteria for placing a patient in this stage: Asymptomatic Persistent generalized lymphadenopathy
74. 2. HIV asymptomatic/Category A/stage II More than 500 CD4 cells In stage II, many people are completely asymptomatic, but others demonstrate a number of physical symptoms that healthcare providers can use to stage the patient. WHO criteria for this stage include the following: Moderate unexplained weight loss Recurring respiratory tract infections Herpes Zoster (shingles) Angular cheilitis (lesions at the corner of the mouth) Recurring oral ulceration Papularpruritic eruptions (skin rash possibly related to insect bites) Seborrhoeic dermatitis (a skin disorder that causes scaly, itchy, flaky skin) Fungal nail infections.
75. HIV symptomatic/ Category B/stage iii Consists of symptomatic conditions not listed in category C Criteria for Stage III In stage III, HIV patients begin to exhibit more serious symptoms. This is also when opportunistic infections begin to take advantage of the weakened immune system. WHO criteria for placing a patient in this stage include the following:
76. Unexplained severe weight loss Unexplained chronic diarrhea lasting for longer than one month Unexplained persistent fever, either intermittent or constant Persistant oral candidiasis (yeast infection of the mouth) Oral hairy leukoplakia (a white patch on the side of the tongue with a hairy appearance) Pulmonary tuberculosis
77. Severe bacterial infections (for example, pneumonia, meningitis, and empyema) Acute necrotizing ulcerative stomatitis (inflammation of the stomach mucous lining), gingivitis (inflammation of the gums), or periodontitis (inflammation of the tissue that supports the teeth) Unexplained anemia), neutropenia, and/or chronic thrombocytopenia
78. AIDS category C/stage IV Less than 200 CD4 cells Criteria for Stage IV (AIDS) In stage IV, a patient is considered to have progressed from HIV to AIDS. This stage is characterized by more severe symptoms and an even greater number of opportunistic infections. WHO criteria for this stage include the following:
79. HIV wasting syndrome Pneumocystis pneumonia (pneumonia caused by a yeast-like fungus) Recurrent severe bacterial pneumonia Chronic herpes simplex infection Esophageal candidiasis (yeast-like infection of the esophagus) Extrapulmonary tuberculosis Kaposi sarcoma (a tumor caused by human herpesvirus 8) Cytomegalovirus infection (an infection caused by human herpesvirus 5) Central nervous system toxoplasmosis (a parasite affecting the central nervous system, including brain) HIV encephalopathy (a brain disorder) Extrapulmonarycryptococcosis including meningitis
80. Disseminated non-tuberculousmycrobacteria infection Progressive multifocal leukoencephalopathy (the reactivation of a common virus in the central nervous system) Chronic cryptosporidiosis (a parasitic disease) Chronic isosporiasis (a parasitic intestinal disease) Disseminated mycosis (a fungus that causes infection) Recurrent septicemia (also known as blood poisoning) Lymphoma (cerebral or B cell non-Hodgkin) Invasive cervical carcinoma Atypical disseminated leishmaniasis (a parasite transmitted by the sand fly) Symptomatic HIV-associated nephropathy or HIV-associated cardiomyopathy.
81. DIAGNOSIS HIV antibody test Once infected the body usually responds by producing antibodies 3 to 12 weeks / “window period” EIA or Enzyme Immunoassay or ELISA Identifies antibodies directed against HIV