Immunology intro

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Understanding the human immune system. Includes discussions about Allergy, Rheumatology and Non-infectious skin diseases (acne and psoriasis)

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  • These invaders include viruses, bacteria, protozoa or even larger parasites. In addition, we develop immune responses against our own proteins (and other molecules) in autoimmunity and against our own aberrant cells in tumor immunity.
  • Our first line of defense against foreign organisms are barrier tissues such as the skin that stop the entry of organism into our bodies.If, however, these barrier layers are penetrated, the body contains cells that respond rapidly to the presence of the invader. (READ SLIDE)Immediate challenge also comes from soluble molecules that deprive the invading organism of essential nutrients (such as iron) and from certain molecules that are found on the surfaces of epithelia, in secretions (such as tears and saliva) and in the blood stream. This form of immunity is the innate or non-specific immune system that is continually ready to respond to invasion.
  • In the specific immune system, we see the production of antibodies (soluble proteins that bind to foreign antigens) and cell-mediated responses in which specific cells recognize foreign pathogens and destroy them.READ SLIDEThe response to a second round of infection is often more rapid than to the primary infection because of the activation of memory B and T cells.
  • Innate immune system is our first line of defense against invading organisms Adaptive immune system acts as a second line of defense and also affords protection against re-exposure to the same pathogen.
  • Each of the major subdivisions of the immune system has both cellular and humoral components by which they carry out their protective function (Figure 1). In addition, the innate immune system also has anatomical features that function as barriers to infection. Although these two arms of the immune system have distinct functions, there is interplay between these systems (i.e., components of the innate immune system influence the adaptive immune system and vice versa). Although the innate and adaptive immune systems both function to protect against invading organisms, they differ in a number of ways. The adaptive immune system requires some time to react to an invading organism, whereas the innate immune system includes defenses that, for the most part, are constitutively present and ready to be mobilized upon infection. Second, the adaptive immune system is antigen specific and reacts only with the organism that induced the response. In contrast, the innate system is not antigen specific and reacts equally well to a variety of organisms. Finally, the adaptive immune system demonstrates immunological memory. It “remembers” that it has encountered an invading organism and reacts more rapidly on subsequent exposure to the same organism. In contrast, the innate immune system does not demonstrate immunological memory.
  • All cells of the immune system have their origin in the bone marrow and they include myeloid (neutrophils, basophils, eosinpophils, macrophages and dendritic cells) and lymphoid (B lymphocyte, T lymphocyte and Natural Killer) cells (Figure 2), which differentiate along distinct pathways (Figure 3). The myeloid progenitor (stem) cell in the bone marrow gives rise to erythrocytes, platelets, neutrophils, monocytes/macrophages and dendritic cells whereas the lymphoid progenitor (stem) cell gives rise to the NK, T cells and B cells. For T cell development the precursor T cells must migrate to the thymus where they undergo differentiation into two distinct types of T cells, the CD4+ T helper cell and the CD8+ pre-cytotoxic T cell. Two types of T helper cells are produced in the thymus the TH1 cells, which help the CD8+ pre-cytotoxic cells to differentiate into cytotoxic T cells, and TH2 cells, which help B cells, differentiate into plasma cells, which secrete antibodies.
  • The main function of the immune system is self/non-self discriminationREAD SLIDE Since pathogens may replicate intracellularly (viruses and some bacteria and parasites) or extracellularly (most bacteria, fungi and parasites), different components of the immune system have evolved to protect against these different types of pathogens.
  • Although the immune system, for the most part, has beneficial effects, there can be detrimental effects as well. READ SLIDEDuring inflammation, which is the response to an invading organism, there may be local discomfort and collateral damage to healthy tissue as a result of the toxic products produced by the immune response. In addition, in some cases the immune response can be directed toward self tissues resulting in autoimmune disease.
  • Among the mechanical anatomical barriers are the skin and internal epithelial layers, the movement of the intestines and the oscillation of broncho-pulmonary cilia. Associated with these protective surfaces are chemical and biological agents.
  • The epithelial surfaces form a physical barrier that is very impermeable to most infectious agents. Skin….READ SLIDE The desquamation of skin epithelium also helps remove bacteria and other infectious agents that have adhered to the epithelial surfaces
  • The anatomical barriers are very effective in preventing colonization of tissues by microorganisms. However, when there is damage to tissues the anatomical barriers are breached and infection may occur. Once infectious agents have penetrated tissues, another innate defense mechanism comes into play, namely acute inflammation.READ SLIDE
  • OPSONIZATION - The process by which bacteria are altered in such a manner that they are more readily and more efficiently engulfed by phagocytes.
  • Depending on the severity of the tissue injury, the coagulation system may or may not be activated.READ SLIDECHEMOTAXIS - A response of motile cells or organisms in which the direction of movement is affected by the gradient of a diffusible substance. Differs from chemokinesis in that the gradient alters probability of motion in one direction only, rather than rate or frequency of random motion.
  • These cells are the main line of defense in the non-specific immune system
  • PMNs are motile phagocytic cells that have lobed nuclei. They can be identified by their characteristic nucleus or by an antigen present on the cell surface called CD66. They contain two kinds of granules the contents of which are involved in the antimicrobial properties of these cells.READ SLIDE
  • Unlike PMNs they do not contain granules but they have numerous lysosomes which have contents similar to the PNM granules.
  • DIAPEDESIS –CHEMOTAXIS -
  • The immune system normally protects the body against harmful substances, such as bacteria and viruses. It also reacts to foreign substances called allergens, which are generally harmless and in most people do not cause a problem.But in a person with allergies, the immune response is oversensitive. When it recognizes an allergen, the immune system launches a response. Chemicals such as histamines are released. These chemicals cause allergy symptoms.
  • INSECT VENOM: Bedbug bite; Bee sting; Bites - insects, bees, and spiders; Black widow spider bite; Brown recluse bite; Flea bite; Honey bee or hornet sting; Lice bites; Mite bite; Scorpion bite; Spider bite; Wasp sting; Yellow jacket sting
  • CERTAIN MEDICINES MAY CAUSE AN INCREASE IN EOSINOPHILS:Amphetamines (appetite suppressants)Certain laxatives containing psylliumCertain antibioticsInterferonTranquilizers
  • Eosinophils become active when you have certain allergic diseases, infections, and other medical conditions.
  • CUSHING’S DISEASE - Cushing’s disease is a condition in which the pituitary gland releases too much adrenocorticotropic hormone (ACTH). The pituitary gland is an organ of the endocrine system.Cushing's disease is a form of Cushing syndrome.CausesCushing's disease is caused by a tumor or excess growth (hyperplasia) of the pituitary gland. This gland is located at the base of the brain.People with Cushing's disease have too much ACTH. ACTH stimulates the production and release of cortisol, a stress hormone. Too much ACTH means too much cortisol.Cortisol is normally released during stressful situations. It controls the body's use of carbohydrates, fats, and proteins and also helps reduce the immune system's response to swelling (inflammation).NORMAL EOSINOPHIL WBC COUNT: Less than 350 cells per microliter (cells/mcL).
  • This reduces the amount of air that can pass by.
  • In sensitive people, asthma symptoms can be triggered by breathing in allergy-causing substances (called allergens or triggers).
  • ASA-INDUCED ASTHMA ATTACKS ACCOUNTS ONLY TO 2.7%ALTERNATIVE TO ASA ARE THE COXIBS (COX – 2 INHIBITORS) such as CELECOXIB ( but ADR’s include heart attacks and stroke)
  • Most people with asthma have attacks separated by symptom-free periods. Some people have long-term shortness of breath with episodes of increased shortness of breath. Either wheezing or a cough may be the main symptom.Asthma attacks can last for minutes to days, and can become dangerous if the airflow is severely restricted.
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  • Blood gases is a measurement of how much oxygen and carbon dioxide is in your blood. It also determines the acidity (pH) of your blood.
  • There is no special preparation. If you are on oxygen therapy, the oxygen concentration must remain constant for 20 minutes before the test.How the Test Will FeelYou may feel brief cramping or throbbing at the puncture site.
  • Spirometry is frequently used to evaluate lung function in people with obstructive or restrictive lung diseases such as asthma or cystic fibrosis.PEAK FLOW MEASUREMENTS – a peak flow of 50% to 80% - shows moderate asthma attack. Below 50% shows severe asthma attack.
  • CORTICOSTEROIDS – PREVENT AIRWAYS FROM SWELLING LA BETA AGONISTS – RELAX THE MUSCLES OF THE AIRWAYS
  • They also can be used just before exercising to help prevent asthma symptoms that are caused by exercise.Tell your doctor if you are using quick-relief medicines twice a week or more to control your asthma symptoms. Your asthma may not be under control, and your doctor may need to change your dose of daily control drugs.
  • Smoking outside the house is not enough. Family members and visitors who smoke outside carry smoke residue inside on their clothes and hair -- this can trigger asthma symptoms.
  • There are several ways to do a skin biopsy. Most procedures can be easily done in outpatient medical offices or your doctor's office.Which procedure you have depends the location, size, and type of lump or sore. You will receive some type of numbing medicine (anesthetic) before any type of skin biopsy.Punch biopsies are most often used for deeper skin spots or sores. Your doctor removes a small round piece of skin (usually the size of a pencil eraser) using a sharp, hollow instrument. If a large sample is taken, the area may be closed with stitches.An excisional biopsy is done to remove the entire lesion. A numbing medicine is injected into the area. Then the entire lump, spot, or sore is removed, going as deep as needed to get the whole area. The area is closed with stitches. Pressure is applied to the area to stop any bleeding. If a large area is biopsied, a skin graft or flap of normal skin may be used to replace the skin that was removed.An incisional biopsy takes a piece of a larger growth for examination. The area is injected with a numbing medicine. A piece of the growth is cut and sent to the lab for examination. You may have stitches, if needed. The rest of the growth can be treated after the diagnosis is made.our doctor may order a skin biopsy if you have signs or symptoms of:Chronic or acute skin rashesNoncancerous (benign) growthsSkin cancerOther skin conditionsRisks may include:InfectionScar (keloids)You will bleed slightly during the procedure. Te
  • SCRAPE METHODINCISIO METHODPUNCH METHOD
  • Cartilage normally protects a joint, allowing it to move smoothly. Cartilage also absorbs shock when pressure is placed on the joint, such as when you walk. Without the normal amount of cartilage, the bones rub together, causing pain, swelling (inflammation), and stiffness.
  • Rheumatoid arthritis is different from osteoarthritis, the common arthritis that often comes with older age. RA can affect body parts besides joints, such as your eyes, mouth and lungs. RA is an autoimmune disease, which means the arthritis results from your immune system attacking your body's own tissues.
  • Muscles that have been damaged by some rheumatic diseases release certain enzymes into the blood, and these enzymes can be detected through blood tests.
  • Osteoarthritis (also sometimes referred to as “degenerative joint disease” or “degenerative arthritis”)
  • Over time, joints may lose their range of motion and may become deformed.
  • Osteoarthritis is a chronic disease of the joint cartilage and bone, often thought to result from "wear and tear" on a joint, although there are other causes such as congenital defects, trauma and metabolic disorders. Joints appear larger, are stiff and painful and usually feel worse the more they are used throughout the day.
  • You'll likely be diagnosed with rheumatic fever if you meet two major criteria, or one major and two minor criteria, and have signs that you've had a previous strep infection.
  • An increased ESR rate may be due to some infections, including:Body-wide (systemic) infectionBone infectionsInfection of the heart or heart valvesRheumatic feverSevere skin infections, such as erysipelasTuberculosis
  • Stress does not cause acne, but can make it worse.
  • Acne develops when an oily substance that lubricates your hair and skin (sebum) plugs the hair follicles. Bacteria can trigger inflammation and infection.
  • These lines show up when blood vessels under the skin get larger. This area of the skin may be somewhat swollen, warm, and red
  • Researchers funded in part by the National Institute of Arthritis and Musculoskeletal and Skin Diseases December 2007 research.
  • RETINOIDS etc. - They work by promoting cell turnover and preventing plugging of the hair follicles. A number of topical antibiotics also are available. They work by killing excess skin bacteria.
  • USE OR ORAL CONTRACEPTIVESThe most serious potential complication is a slightly increased risk of heart disease, high blood pressure and blood clots.
  • hey may cause temporary, severe redness, scaling and blistering, and long-term discoloration of the skin.
  • . The word guttate is from the Latin word meaning "drop."
  • Guttate psoriasis often comes on quite suddenly. A variety of conditions can bring on an attack of guttate psoriasis, including upper respiratory infections, streptococcal throat infections (strep throat), tonsillitis, stress, injury to the skin and the administration of certain drugs including antimalarials and beta-blockers.
  • . It can be more troublesome in overweight people and those with deep skin folds.
  • ay be localized to certain areas of the body, such as the hands and feet, or covering most of the body. It begins with the reddening of the skin followed by formation of pustules and scaling.
  • People experiencing the symptoms of erythrodermic psoriasis flare should go see a doctor immediately. Erythrodermic psoriasis causes protein and fluid loss that can lead to severe illness. The condition may also bring on infection, pneumonia and congestive heart failure. People with severe cases of this condition often require hospitalization.
  • SKIN INJURY due to vaccinations, sunburns and scratches can triggerKOEBNER PHENOMENON – MINOR SKIN TRAUMAS SUCH AS SCRAPED KNEES, GARDEN SCRAPES AND BUG BITEShe Koebner phenomenon is named after Dr. Heinrich Koebner, a German dermatologist who noticed the phenomenon in the 19th century. A slight scratch won't cause koebnerization, but a cut or bite that damages the dermis (the layer of skin below the surface) may begin to show lesions.
  • Topical treatments—medications applied to the skin—are usually the first line of defense in treating psoriasis. Topicals slow down or normalize excessive cell reproduction and reduce the inflammation associated with psoriasis.
  • UVB and UVA TREATMENTS - Present in natural sunlight, UVB is an effective treatment for psoriasis. UVB penetrates the skin and slows the growth of affected skin cells. Psoralen is a light sensitizing medicationDuring UVB treatment, your psoriasis may worsen temporarily before improving. The skin may redden and itch from exposure to the UVB light. To avoid further irritation, the amount of UVB administered may need to be reduced. Occasionally, temporary flares occur with low-level doses of UVB. These reactions tend to resolve with continued treatment.
  • Remember to wear sunscreen on areas of your skin unaffected by psoriasis.
  • They are usually used for individuals with moderate to severe psoriasis and psoriatic arthritis. Systemic medications are also used in those who are not responsive or are unable to take topical medications or UV light therapy
  • Interleukins-12/23 are also cytokines which are thought to promote the inflammation associated with psoriasis.
  • Immunology intro

    1. 1. IMMUNOLOGY:A BACKGROUND Reported by: MA. LOURDES L. MOJARES, R. Ph. CEU Graduate School Ph. D. in Pharmacy
    2. 2. IMMUNOLOGY: DEFINITIONStudy of;1. the protection of the humanbody from foreignmacromolecules or invadingorganisms.2 responses of the human bodyto them.
    3. 3. OUR FIRST LINE OF DEFENSE:These cells include; 1. macrophages 2. neutrophils that engulf foreign organisms and kill them without the need for antibodies.
    4. 4. OUR SECOND LINE OF DEFENSE: The specific or adaptive immune systemWhich may take days to respondto a primary invasion (that isinfection by an organism that hasnot hitherto been seen).
    5. 5. THE IMMUNE SYSTEM1. Innate or Non-specific Immune System1. Adaptive or Specific Immune System
    6. 6. OVERVIEW OF THE IMMUNESYSTEM
    7. 7. DEVELOPMENT OF THE CELLS OFTHE IMMUNE SYSTEM
    8. 8. CELLS OF THE IMMUNE SYSTEM
    9. 9. MAIN FUNCTION OF THE IMMUNESYSTEMThe ability to distinguish between self and non-self is necessary to protect the organism from invading pathogens and to eliminate modified or altered cells (e.g. malignant cells).
    10. 10. MAIN FUNCTION OF THE IMMUNESYSTEM It is important to remember that infection with an organism does not necessarily mean diseases, since the immune system in most cases will be able to eliminate the infection before disease occurs.
    11. 11. CAUSES OF A DISEASE:When the bolus of infection ishigh.The virulence of the microrganismis great.When immunity is compromised.
    12. 12. NON – SPECIFIC SPECIFICIMMUNITY IMMUNITYResponse is antigen- Response is antigen-dependent dependentThere is immediate There is lag time betweenmaximal response exposure and maximal responseNon-antigen specific Antigen - specificExposure results in no Exposure results inimmunologic memory immunologic memory
    13. 13. INNATE / NON-SPECIFICIMMUNITYThe elements of the innate(non-specific) immune systeminclude; 1. anatomical barriers 2. secretory molecules 3. cellular components
    14. 14. ANATOMICAL BARRIERS TOINFECTIONS1. MECHANICAL FACTORSThe skin acts as our first line of defense against invading organisms. Movement due to cilia or peristalsis helps to keep air passages and the gastrointestinal tract free from microorganisms.
    15. 15. ANATOMICAL BARRIERS TOINFECTIONS1. MECHANICAL FACTORSThe flushing action of tears and saliva helps prevent infection of the eyes and mouth. The trapping effect of mucus that lines the respiratory and gastrointestinal tract helps protect the lungs and digestive systems from infection.
    16. 16. ANATOMICAL BARRIERS TOINFECTIONS2. CHEMICAL FACTORSFatty acids in sweat inhibit the growth of bacteria.Lysozyme and phospholipase found in tears, saliva and nasal secretions can breakdown the cell wall of bacteria and destabilize bacterial membranes.
    17. 17. ANATOMICAL BARRIERS TOINFECTIONS2. CHEMICAL FACTORSThe low pH of sweat and gastric secretions prevents growth of bacteria.Defensins (low MW proteins) found in the lung and gastrointestinal tract have antimicrobial activity.
    18. 18. ANATOMICAL BARRIERS TOINFECTIONS3. BIOLOGICAL FACTORSThe normal flora of the skin and in the gastrointestinal tract can prevent the colonization of pathogenic bacteria by; 1. secreting toxic substances 2. competing with pathogenic bacteria for nutrients or attachment to cell surfaces.
    19. 19. HUMORAL BARRIERS TOINFECTIONSHumoral factors play an important role in inflammation, which is characterized by edema and the recruitment of phagocytic cells. These humoral factors are found in serum or they are formed at the site of infection.
    20. 20. HUMORAL BARRIERS TOINFECTIONS1. Complement System The complement system is the major humoral non-specific defense mechanism.
    21. 21. HUMORAL BARRIERS TOINFECTIONS1. Complement System Once activated complement can lead to; a. increased vascular permeabilityb. recruitment of phagocytic cells, c. lysisd. opsonization of bacteria
    22. 22. HUMORAL BARRIERS TOINFECTIONS2. Coagulation System Some products of the coagulation because of their ability to; a. increase vascular permeability b. act as chemotactic agents for phagocytic cells.
    23. 23. HUMORAL BARRIERS TOINFECTIONS2. Coagulation System In addition, some of the products of the coagulation system are directly antimicrobial. For example, beta-lysin, a protein produced by platelets during coagulation can lyse many Gram positive bacteria by acting as a cationic detergent.
    24. 24. HUMORAL BARRIERS TOINFECTIONS2. Lactoferrin and TransferrinBy binding iron, an essential nutrient for bacteria, these proteins limit bacterial growth.
    25. 25. HUMORAL BARRIERS TOINFECTIONS3. InterferonsInterferons are proteins that can limit virus replication in cells.4. LysozymeLysozyme breaks down the cell wall of the bacteria.
    26. 26. HUMORAL BARRIERS TOINFECTIONS5. Interleukin – 1Il-1 induces fever and the production of acute phase proteins, some of which are antimicrobial because they can opsonize bacteria.
    27. 27. PHYSICO-CHEMICAL BARRIERS TO INFECTIONSSYSTEM / ORGAN ACTIVE COMPONENT EFFECTOR MECHANISMSKIN SQUAMOUS CELLS / DESQUAMATION SWEAT FLUSHING ORGANIC ACIDSGI TRACT COLUMNAR CELLS PERISTALSIS LOW pH BILE ACID FLUSHING THIOCYANATELUNGS TRACHEAL CILIA MUCOSCIALARY ELEVATOR SURFACTANTNASOPHARYNX MUCUS, SALIVA, FLUSHINGAND EYE TEARS LYSOZYME
    28. 28. PHYSICO-CHEMICAL BARRIERS TO INFECTIONSSYSTEM / ORGAN ACTIVE COMPONENT EFFECTOR MECHANISMCIRCULATION PHAGOCYTIC CELLS PHAGOCYTOSISAND ANDLYPHOID ORGANS INTRACELLULAR KILLING NK CELLS DIRECT AND AND K CELLS ANTIBODY DEPENDENT CYTOLYSIS LAK IL – 2 ACTIVATED CYTOLYSIS
    29. 29. PHYSICO-CHEMICAL BARRIERS TO INFECTIONSSYSTEM / ACTIVE COMPONENT EFFECTOR MECHANISMORGANSERUM LACTOFERRIN IRON BINDING AND TRANSFERRIN INTERFERONS ANTIVIRAL PROTEINS TNF - ALPHA ANTIVIRAL, PHAGOCYTE ACTIVATION
    30. 30. PHYSICO-CHEMICAL BARRIERS TO INFECTIONSSYSTEM / ORGAN ACTIVE COMPONENT EFFECTOR MECHANISMSERUM LYSOZYME PEPTIDOGLYCAN HYDROLYSIS FIBRONECTIN OPSONIZATION AND PHAGOCYTOSIS COMPLEMENT OPZONIZATION, ENHANCED PHAGOCYTOSIS, INFLAMMATION
    31. 31. CELLULAR BARRIERS TOINFECTIONSPart of the inflammatory response is the recruitment of polymorphonucleareosinophile s and macrophages to sites of infection.
    32. 32. CELLULAR BARRIERS TOINFECTIONS1. NeutrophilsPolymorphonuclear cells are recruited to the site of infection where they phagocytose invading organisms and kill them intracellularly. In addition, PMNs contribute to collateral tissue damage that occurs during inflammation.
    33. 33. CELLULAR BARRIERS TOINFECTIONS2. Macrophages and Newly Recruited Monocytes Differentiate into macrophages, also function in phagocytosis and intracellular killing of microorganisms.
    34. 34. CELLULAR BARRIERS TO INFECTIONS3. Natural Killers (NK)andLymphokine Activated Killer (LAK) cellsNK and LAK cells can nonspecifically kill virus infected and tumor cells. These cells are not part of the inflammatory response but they are important in nonspecific immunity to viral infections and tumor surveillance.
    35. 35. NK CELLS AND ITS ACTIVATION
    36. 36. CELLULAR BARRIERS TOINFECTIONS4. Eosinophils They have proteins in granules that are effective in killing certain parasites.
    37. 37. KILLER (K) CELLSKiller(K) cells are not a morphologically distinct type of cell.Rather a K cell is any cell that mediates antibody-dependent cellular cytotoxicity (ADCC).
    38. 38. KILLER (K) CELLSInADCC antibody acts as a link to bring the K cell and the target cell together to allow killing to occur.K cells have on their surface an Fc receptor for antibody and thus they can recognize, bind and kill target cells coated with antibody.
    39. 39. KILLER (K) CELLSKillercells which have Fc receptors include NK, LAK, and macrophages which have an Fc receptor for IgG antibodies and eosinophils which have an Fc receptor for IgE antibodies.
    40. 40. KILLING OF OPSONIZEDTARGET BY THE K CELL
    41. 41. PHAGOCYTOSIS AND INTRACELLULAR KILLINGA. PHAGOCYTIC CELLS1. Neutrophiles / Polymorphonuclear (PMN) Cells1.1 primary or azurophilic granules, which are abundant in young newly formed PMNs, contain cationic proteins and defensins that can kill bacteria, proteolytic enzymes like elastase, and cathepsin G to breakdown proteins, lysozyme to break down bacterial cell walls, and characteristically, myeloperoxidase, which is involved in the generation of bacteriocidal compounds.
    42. 42. PHAGOCYTOSIS AND INTRACELLULAR KILLINGA. PHAGOCYTIC CELLS1. Neutrophiles / Polymorphonuclear (PMN) Cells 1. 2 secondary or specific granule These contain lysozyme, NADPH oxidase components, which are involved in the generation of toxic oxygen products, and characteristically lactoferrin, an iron chelating protein and B12- binding protein.
    43. 43. PHAGOCYTOSIS AND INTRACELLULAR KILLINGA. PHAGOCYTIC CELLS2. Monocytes / MacrophagesMacrophages are phagocytic cells that have a characteristic kidney-shaped nucleus. They can be identified morphologically or by the presence of the CD14 cell surface marker.
    44. 44. OXYGEN –INDEPENDENT MECHANISMSOF INTRACELLULAR KILLINGEFFECTOR FUNCTIONMOLECULECationic Proteins Damage to microbial(including cathepsin) membranesLysozyme Splits mucopeptide in the bacterial cell wallLactoferrin Deprives proliferating bacteria of ironProteolytic and Digestion of killedHydrolytic Enzymes organisms
    45. 45. RESPONSE OF PHAGOCYTES TOINFECTION Circulating PMNs and monocytes respond to danger (SOS) signals generated at the site of an infection. SOS signals include; 1. N-formyl-methionine containing peptides released by bacteria 2. clotting system peptides 3. complement products 4. cytokines released from tissue macrophages that have encountered bacteria in tissue
    46. 46. RESPONSE OF PHAGOCYTES TOINFECTIONSome of the SOS signals stimulateendothelial cells near the site of theinfection to express cell adhesionmolecules such as;1. ICAM-12. selectinswhich bind to components on the surfaceof phagocytic cells and cause thephagocytes to adhere to the endothelium.
    47. 47. RESPONSE OF PHAGOCYTES TOINFECTIONVasodilators produced at the site of infection cause the junctions between endothelial cells to loosen and the phagocytes then cross the endothelial barrier by “squeezing” between the endothelial cells in a process called “DIAPEDESIS.”
    48. 48. CHEMOTACTIC RESPONSE TOINFLAMMATORY STIMULUS
    49. 49. RESPONSE OF PHAGOCYTES TOINFECTIONOnce in the tissue spaces some of the SOS signals attract phagocytes to the infection site by chemotaxis (movement toward an increasing chemical gradient).
    50. 50. RESPONSE OF PHAGOCYTES TOINFECTIONThe SOS signals also activate the phagocytes, which results in;1. increased phagocytosis2. intracellular killing of the invadingorganisms.
    51. 51. DISEASES OF THE IMMUNE SYSTEMALLERGIES:Asthma (Bronchial, Exercise Induced)Dermatitis (Contact and Atopic)Arthritis (Rheumatoid and Reactive)
    52. 52. ALLERGY: DEFINITIONAn immune response or reaction to substances that are usually not harmful.Allergies are pretty common. Both genes and environment play a role.
    53. 53. COMMON ALLERGENS: Drugs Dust Food Insect venom Mold Pet and other animal dander Pollen
    54. 54. RARE ALLERGENS: Hot or Cold Temperatures SunlightFriction (clothing/garters, rubbing or stroking theskin)
    55. 55. ALLERGY: SYMPTOMSAllergens that one breathes 1. stuffy nose 2. itchy nose and throat 3. mucus production 4. cough 5. wheezing
    56. 56. ALLERGY: SYMPTOMSAllergens that touch the eyes 1. itchy 2. watery 3. red 4. swollen
    57. 57. ALLERGY: SYMPTOMSAllergens that one gets from foods eaten / drugs taken. 1. nausea and vomiting 2. abdominal pain 3. cramps 4. diarrhea 5. life-threatening reaction
    58. 58. ALLERGY TESTING: Complete Blood Count (CBC)Eosinophil WBC CountAn absolute eosinophil count is ablood test that measures thenumber of white blood cells calledeosinophils.
    59. 59. ALLERGY TESTING:Eosinophil WBC Count This test may help diagnose:1. Acute hypereosinophilic syndrome (a rare but sometimes fatal leukemia-like condition)2. An allergic reaction (can also reveal how severe the reaction is)3. Early stages of Cushings disease4. Infection by a parasite
    60. 60. ABNORMALLY HIGHEOSINOPHIL WBC COUNT: Asthma Autoimmune diseases Eczema Hay fever Leukemia
    61. 61. ABNORMALLY LOWEOSINOPHIL WBC COUNT:CAUSES Alcohol intoxication Over production of certain steroids in the body (such as cortisol)
    62. 62. ALLERGY: TREATMENTAnaphylaxis - treated with epinephrine Avoid exposure to ―triggers‖Anthihistamines
    63. 63. ALLERGY: TREATMENTDecongestants – used with caution in patients with; 1. hypertension 2. heart problems, 3. prostate enlargement
    64. 64. ALLERGY: TREATMENTLeukotriene inhibitors such as Zafirlukast (Accolate) and (Monteleukast) Singulair. For treatment of indoor and outdoor allergies and asthma.
    65. 65. ALLERGY: TREATMENT Allergy Shots or Immunotherapy
    66. 66. ALLERGY: PROGNOSIS Most allergies can be easily treated with medication. Some children may outgrow an allergy, especially food allergies. However, once a substance has triggered an allergic reaction, it usually continues to affect the person.
    67. 67. ALLERGY: PROGNOSIS Allergyshots / Immunology are most effective when used to treat people with hay fever symptoms and severe insect sting allergies. Theyare not used to treat food allergies because of the danger of a severe reaction.
    68. 68. ALLERGY: PROGNOSIS Allergy shots may need years of treatment, but they work in most cases. However, they may cause uncomfortable side effects; hives and rash Anaphylaxis (life-threatening allergic reaction) Breathing problems and discomfort during the allergic reaction Drowsiness and other side effects of medicines
    69. 69. ALLERGY: PREVENTIONBreastfeeding babies for 4 to 6 months. Hygiene Hypothesis Involves exposure of an infant to ―allergens‖ during the first year of life.
    70. 70. ALLERGY: SYMPTOMSAllergens that touch the skin 1. rash 2. hives 3. itching 4. peeling
    71. 71. DISEASES OF THEIMMUNE SYSTEMASTHMA:BRONCHIALEXERCISE -INDUCED
    72. 72. ASTHMA: DEFINITIONA disorder that causes theairways of the lungs to swelland narrow, leading to;1. wheezing2. shortness of breath3. chest tightness4. coughing
    73. 73. ASTHMA: CAUSES Inflammation in the airways.When an asthma attackoccurs, the musclessurrounding the airwaysbecome tight and the lining ofthe air passages swells.
    74. 74. PATHOLOGY OF ASTHMA
    75. 75. ASTHMA TRIGGERS: Animals (pet hair or dander) Dust Changes in weather (most often cold weather) Chemicals in the air or in food Exercise Mold and Pollen Respiratory infections, such as the common cold Strong emotions (stress) Tobacco smoke
    76. 76. ASTHMA DRUG TRIGGERS:AspirinNSAIDs These drugs act as a deregulator of leukotrienes.Leukotrienes are substances in the body that cause inflammation and many of the symptoms in asthma.
    77. 77. ASTHMA: SYMPTOMSCough with or without sputum (phlegm) productionPulling in of the skin between the ribs when breathing (intercostal retractions)Shortness of breath that gets worse with exercise or activity
    78. 78. ASTHMA: SYMPTOMS Wheezing, which: Comes in episodes with symptom-free periods in between May be worse at night or in early morning May go away on its own Gets better when using drugs that open the airways (bronchodilators) Gets worse when breathing in cold air Gets worse with exercise Gets worse with heartburn (reflux) Usually begins suddenly
    79. 79. ASTHMA: EMERGENCY SYMPTOMS Bluish color to the lips and face Decreased level of alertness, such as severe drowsiness or confusion, during an asthma attack Extreme difficulty breathing Rapid pulse Severe anxiety due to shortness of breath Sweating
    80. 80. ASTHMA: OTHER SYMPTOMS THAT MAYOCCUR Abnormal breathing pattern -- breathing out takes more than twice as long as breathing in Breathing temporarily stops Chest pain Tightness in the chest
    81. 81. ASTHMA:EXAMINATIONS AND TESTS Skin Prick Test Placing a small amount of substances that may be causing your symptoms on the skin, most often on the forearm, upper arm, or back. Then, the skin is pricked so the allergen goes under the skins surface.
    82. 82. ASTHMA:EXAMINATIONS AND TESTS Skin Prick Test Thehealth care provider closely watches the skin for swelling and redness or other signs of a reaction. Results are usually seen within 15-20 minutes. Several allergens can be tested at the same time.
    83. 83. ASTHMA:EXAMINATIONS AND TESTS Intradermal Skin Test: Injecting a small amount of allergen into the skin. Then the health care provider watches for a reaction at the site. This test is more likely to be used to find out if you are allergic to something specific, such as bee venom or penicillin
    84. 84. ASTHMA:EXAMINATIONS AND TESTS Patch Testing Used to diagnose the cause of skin reactions that occur after the substance touches the skin. Possible allergens are taped to the skin for 48 hours. The health care provider will look at the area in 72 - 96 hours.
    85. 85. ASTHMA:EXAMINATIONS AND TESTS ArterialBlood Gas Performed by collecting a sample of blood through a needle from an artery. The test is used to 1. evaluate respiratory diseases and conditions that affect the lungs, 2. to determine the effectiveness of oxygen therapy.
    86. 86. ASTHMA:EXAMINATIONS AND TESTS Arterial Blood Gas 3. The acid-base component of the test also gives information on how well the kidneys are functioning.
    87. 87. ASTHMA:EXAMINATIONS AND TESTS Blood Tests Measure; 1. eosinophil count (a type of white blood cell) 2. IgE (a type of immune system protein called an immunoglobulin)
    88. 88. ASTHMA:EXAMINATIONS AND TESTS Chest X-Rays Lung Function Tests (by Spirometry) Painless study of air volume and flow rate within the lungs. Peak Flow Measurements
    89. 89. SPIROMETRY:
    90. 90. ASTHMA: GOALS OF TREATMENTControl swelling of the airways.Stay away from the substance triggers.
    91. 91. KINDS OF MEDICATION INTREATING ASTHMAControl drugs to PREVENT attacksQuick-relief (rescue) drugs for use DURING attacks
    92. 92. LONG-TERM CONTROL DRUGSFOR ASTHMA Inhaled  Leokotriene Modifiers Corticosteroids (Singulair, Accolate) LA – beta agonist  Cromolyn Sodium (Intal) Inhalers  Nedocromil Sodium Omalizumab (Xolair) (Tilade) Combination Therapy  Alternate Names (Combination of all fours)
    93. 93. QUICK RELIEF (RESCUE)DRUGS for ASTHMAThese work fast to control asthma symptoms.You take them when you are coughing, wheezing,having trouble breathing, or having an asthmaattack. Short-Acting Bronchodilators (Proventil, Ventolin,Xopenex) Oral Steroids (Corticosteroids)
    94. 94. ASTHMA: PROGNOSIS There is no cure for asthma, although symptoms sometimes improve over time.With proper self management and medical treatment, most people with asthma can lead normal lives.
    95. 95. ASTHMA ACTION PLAN:A plan for taking asthma medications when your condition is stable.A list of asthma triggers and how to avoid them.How to recognize when your asthma is getting worse, and when to call your doctor or nurse
    96. 96. ASTHMA:POSSIBLE COMPLICATIONS Death Decreased ability to exercise and take part in other activities Lack of sleep due to nighttime symptoms Permanent changes in the function of the lungs Persistent cough Trouble breathing that requires breathing assistance (ventilator)
    97. 97. ASTHMA: PREVENTIONCover bedding with "allergy- proof" casings to reduce exposure to dust mites.Remove carpets from bedrooms and vacuum regularly.Use only unscented detergents and cleaning materials in the home.
    98. 98. ASTHMA: PREVENTIONKeep humidity levels low and fix leaks to reduce the growth of organisms such as mold.Keep the house clean and keep food in containers and out of bedrooms -- this helps reduce the possibility of cockroaches, which can trigger asthma attacks in some people.
    99. 99. ASTHMA: PREVENTION If a person is allergic to an animal that cannot be removed from the home, the animal should be kept out of the bedroom.Place filtering material over the heating outlets to trap animal dander.
    100. 100. ASTHMA: PREVENTIONEliminate tobacco smoke from the home.This is the single most importantthing a family can do to help achild with asthma.
    101. 101. DISEASESOF THEIMMUNE SYSTEM CONTACT DERMATITIS ALLERGIC TYPE IRRITANT TYPE
    102. 102. CONTACT DERMATITIS:DEFINITION A condition in which the skin becomes red, sore, or inflamed after direct contact with a substance.Two kinds of contact dermatitis: 1. irritant dermatitis 2. allergic dermatitis
    103. 103. IRRITANT CONTACTDERMATITIS:The most common type.Its caused by contact with acids, alkaline materials such as soaps, detergents, fabric softeners, solvents, or other chemicals.The reaction usually looks like a burn.
    104. 104. IRRITANTS INCLUDE:CementHairdyesLong-term exposure to wet diapersPesticides or weed killersRubber glovesShampoos
    105. 105. ALLERGIC CONTACTDERMATITIS: DEFINITIONThis is caused by exposure to a substance or material to which one have become; 1. extra sensitive 2. allergic
    106. 106. COMMON ALLERGENS: Adhesives, including  Balsam of Peru (used those used for false in many personal eyelashes or toupees products and cosmetics, as well as in many foods and Antibiotics such as drinks) neomycin rubbed on the surface of the skin  Fabrics and clothing
    107. 107. COMMON ALLERGENS: Fragrances in  Nickel or other metals perfumes, cosmetics, (found in jewelry, soaps, and watch straps, metal moisturizers zips, bra hooks, buttons, pocketknives, lipstick Nail polish, hair dyes, holders, and powder and permanent wave compacts) solutions
    108. 108. COMMON ALLERGENS: Poison ivy, poison oak, poison sumac, and other plants Rubber or latex gloves or shoes Coal Tar Products, Sulfa Ointments, Shaving Lotions, Sun Screens, Lime Oil ( due to photosensitivity) Air-borne allergens (Ragweed, Insecticides)
    109. 109. POISON IVY NICKELRASH ERYTHEMA
    110. 110. CONTACT DERMATITIS:SYMPTOMS ALLERGIC DERMATITIS  IRRITANT1. Itching DERMATITIS 1. Burning and Pain2. Red, Streaky, Patchy Rash 2. Dry, red, rough skin3. Warm and Tender Skin 3. Cuts and Fissures on Hands4. Scaly, Crusty, Raw and Thickened Skin
    111. 111. LABORATORY EXAMS ANDTESTS: DERMATITISAllergy Testing / Skin Patch Testing It determine which allergen is causing the reaction. Patch testing is used for certain patients who have long-term, repeated contact dermatitis.
    112. 112. LABORATORY EXAMS ANDTESTS: DERMATITISAllergy Testing / Skin Patch Testing It requires three office visits and must be done by a health care provider with the experience and skill to interpret the results correctly.
    113. 113. LABORATORY EXAMS ANDTESTS: DERMATITISSkin Lesion BiopsyThe removal of a piece of skin to diagnose or rule out an illness. Shave biopsy Punch biopsyExcisional biopsyIncisional biopsy
    114. 114. SKIN LESION BIOPSY: PROCEDURES
    115. 115. LABORATORY EXAMS ANDTESTS: DERMATITISSkin or Nail CultureA laboratory test to look for andidentify germs that causeproblems with the skin or nails.It is called a mucosal culture if thesample involves the mucousmembranes.
    116. 116. LABORATORY EXAMS ANDTESTS: DERMATITISSkin or Nail CultureThis test may be done to diagnose the cause of: 1. A fungus infection of the skin, finger or toenail 2. A skin rash or sore that appears to be infected 3. A skin ulcer that is not healing
    117. 117. DERMATITIS: TREATMENT Washing with lots of water to remove any traces of the irritant that may remain on the skin. Avoid further exposure to known irritants or allergens. In some cases, the best treatment is to do nothing to the area. Emollients or moisturizers help keep the skin moist, and also help skin repair itself. They protect the skin from becoming inflamed again. They are a key part of preventing and treating contact dermatitis.
    118. 118. DERMATITIS: TREATMENT Corticosteroid ointments and creams – reduce inflammation Tacrolimus ointment or Pimecrolimus cream Corticosteroid pills or shots Wet Dressings / Antipruritic lotions
    119. 119. DERMATITIS: PROGNOSISContact dermatitis usually clears up without complications in 2 or 3 weeks. However, it may return if the substance or material that caused it cannot be found or avoided.
    120. 120. DERMATITIS: PROGNOSISThere may be a need to change your job or job habits if the disorder is caused by occupational exposure.
    121. 121. RHEUMATOLOGYRheumatoid ArthritisOsteoarthritisGoutRheumatic Fever
    122. 122. RHEUMATOLOGY: DEFINITION Deals with the diagnosis and therapy of rheumatic diseases. Deals mainly with clinical problems involving joints, soft tissues, autoimmune diseases, vasculitis, and heritable connective tissue disorders.
    123. 123. RHEUMATISM: DEFINITIONA non-specific term used to describe any painful disorder affecting the loco-motor system including joints, muscles, connective tissues, soft tissues around the joints and bones
    124. 124. RHEUMATISM: DEFINITIONAlso used to describe rheumatic fever affecting heart valves. Rheumatoid arthritisAlkylosingspondylitis Gout Systemic LE
    125. 125. ARTHRITIS: DEFINITION Inflammation of one or more joints. A joint is the area where two bones meet. There are over 100 different types of arthritis.
    126. 126. ARTHRITIS: CAUSESBreakdown of cartilage Joint inflammation, due to; 1. autoimmune disease (the bodys immune system mistakenly attacks healthy tissue) 2. Broken bone 3. General "wear and tear" on jointsInfection, usually by bacteria or virus
    127. 127. ARTHRITIS: SYMPTOMS Joint pain Joint swelling Reduced ability to move the joint Redness of the skin around a joint Stiffness, especially in the morning Warmth around a join
    128. 128. ARTHRITIS: NON-PHARMACOLOGICAL TREATMENT GOAL: to reduce pain, improve function, and prevent further joint damage.The underlying cause cannot usually be cured.
    129. 129. ARTHRITIS: NON-PHARMACOLOGICAL TREATMENTLIFESTYLE CHANGESLifestyle changes are thepreferred treatment forosteoarthritis and other types ofjoint inflammation. Diet and Exercise
    130. 130. ARTHRITIS: NON-PHARMACOLOGICAL TREATMENT Exercise programs may include:Low-impact aerobic activity (also called endurance exercise)Range of motion exercises for flexibilityStrength training for muscle tone
    131. 131. ARTHRITIS: NON-PHARMACOLOGICAL TREATMENTPhysical Therapy:1 Heat or ice compress2. Splints or orthotics to supportjoints and help improve theirposition; this is often needed forrheumatoid arthritis3. Water therapy / Hydrotherapy4. Massage
    132. 132. ARTHRITIS: NON-PHARMACOLOGICAL TREATMENT 8 to 10 hours of sleep Avoid staying in one position for too long. Avoid positions or movements that place extra stress on your sore joints. Meditation, Yoga, Tai-chi Eat your fruits and vegetables
    133. 133. ARTHRITIS: NON-PHARMACOLOGICAL TREATMENTEat foods rich in omega-3 fatty acids, such as cold water fish (salmon, mackerel, and herring), flaxseed, rapeseed (canola) oil, soybeans, soybean oil, pumpkin seeds, and walnuts.
    134. 134. ARTHRITIS: NON-PHARMACOLOGICAL TREATMENT Change your home to make activities easier. Example, install grab bars in the shower, the tub, and near the toilet. Lose the excess weight. Apply capsaicin liniment over painful joints.
    135. 135. ARTHRITIS: -PHARMACOLOGICALTREATMENTAcetaminophen is usually triedfirst. Take up to 4 grams a day (twoarthritis-strength every 8 hours).Do not take more than therecommended dose or take the drugalong with a lot of alcohol. Doing somay damage your your liver.
    136. 136. ARTHRITIS: -PHARMACOLOGICALTREATMENT Aspirin, Ibuprofen, or Naproxen are nonsteroidal anti-inflammatory drugs (NSAIDs)Potential side effects include heartattack, stroke, stomachulcers, bleeding from the digestivetract, and kidney damage.
    137. 137. ARTHRITIS: -PHARMACOLOGICALTREATMENTBiologics are used for 5. rituximab (Rituxan) the treatment of  6. golimumab autoimmune arthritis. (Simponi)1. etanercept (Enbrel)  7. certolizumab2. infliximab (Cimzia) (Remicade)  8. tocilizumab3. adalimumab (Actemra) (Humira)4. abatacept (Orencia)
    138. 138. ARTHRITIS:-PHARMACOLOGICALTREATMENT Corticosteroids ("steroids") help reduce inflammation. They may be injected into painful joints or given by mouth. Disease-modifyinganti-rheumatic drugs (DMARDs) are used to treat autoimmune arthritis.
    139. 139. ARTHRITIS:-PHARMACOLOGICALTREATMENT DMARD’s include; 1. methotrexate 2. gold salts 3. penicillamine 4. sulfasalazine 5. hydroxychloroquine
    140. 140. ARTHRITIS:-PHARMACOLOGICALTREATMENTImmunosuppressants such as azathioprine or cyclophosphamide are used to treat patients with rheumatoid arthritis when other medications have not worked.
    141. 141. ARTHRITIS:SURGICAL TREATMENT Arthroplasty to rebuild the joint
    142. 142. ARTHRITIS:SURGICAL TREATMENT Joint Replacement such as, total knee joint replacement.
    143. 143. ARTHRITIS: PROGNOSISA few arthritis-related disorders can be completely cured with proper treatment.Most forms of arthritis however are long-term (chronic) conditions.
    144. 144. ARTHRITIS: PROGNOSIS Complications of arthritis include:Long-term (chronic) painDisabilityDifficulty performing daily activities
    145. 145. ARTHRITIS: PREVENTIONEarly diagnosis and treatment can help prevent joint damage. If you have a family history of arthritis, tell your doctor, even if you do not have joint pain.Avoiding excessive, repeated motions may help protect against osteoarthritis.
    146. 146. RHEUMATOID ARTHRITIS Or RA, is a form of arthritis that causes pain, swelling, stiffness and loss of function in the joints. It can affect any joint but is common in the wrist and fingers. More women than men get rheumatoid arthritis. It often starts between ages 25 and 55.
    147. 147. LABORATORY EXAMS andTESTS: ARTHRITIS Antinuclear antibody (ANA) Commonly found in the blood of people who have lupus, ANAs (abnormal antibodies directed against the cells’ nuclei) can also suggest the presence of polymyositis, scleroderma, Sjogren’s syndrome, mixed connective tissue disease or rheumatoid arthritis.
    148. 148. LABORATORY EXAMS andTESTS: ARTHRITIS Antinuclear antibody (ANA) Tests to detect specific subsets of these antibodies can be used to confirm the diagnosis of a particular disease or form of arthritis.
    149. 149. LABORATORY EXAMS andTESTS: ARTHRITIS Rheumatoid factor (RF) Designed to detect and measure the level of an antibody that acts against the blood component gamma globulin. This test is often positive in people with rheumatoid arthritis.
    150. 150. LABORATORY EXAMS andTESTS: ARTHRITIS Uric acid Measurement By measuring the level of uric acid in the blood, this test helps doctors diagnose gout, a condition that occurs when excess uric acid crystallizes and forms deposits in the joints and other tissues, causing inflammation and severe pain.
    151. 151. LABORATORY EXAMS andTESTS: ARTHRITIS HLA tissue typing This test, which detects the presence of certain genetic markers in the blood, can often confirm a diagnosis of ankylosingspondylitis (a disease involving inflammation of the spine and sacroiliac joint) or Reiter’s syndrome (a disease involving inflammation of the urethra, eyes and joints).
    152. 152. LABORATORY EXAMS andTESTS: ARTHRITIS HLA tissue typing The genetic marker HLA-B27 is almost always present in people with either of these diseases.
    153. 153. LABORATORY EXAMS andTESTS: ARTHRITIS Erythrocyte sedimentation rate Also called ESR or ―sed rate,‖ this test measures how fast red blood cells cling together, fall and settle (like sediment) in the bottom of a glass tube over the course of an hour. The higher the rate, the greater the amount of inflammation.
    154. 154. LABORATORY EXAMS andTESTS: ARTHRITIS Lyme Serology This test detects an immune response to the infectious agent that causes Lyme disease and thus can be used to confirm a diagnosis of the disease.
    155. 155. LABORATORY EXAMS andTESTS: ARTHRITIS Skin Biopsy Taking small samples of skin and examining them under a microscope can help doctors diagnose forms of arthritis that involve the skin, such as lupus, vasculitis (inflammation of the blood vessels) and psoriatic arthritis.
    156. 156. LABORATORY EXAMS andTESTS: ARTHRITIS Muscle biopsy By going a little deeper into the tissue than with the skin biopsy, the surgeon can take a sample of muscle to be examined for signs of damage to the muscle fibers. Findings can confirm a diagnosis of polymyositis or vasculitis.
    157. 157. LABORATORY EXAMS andTESTS: ARTHRITIS Joint fluid tests In this procedure, which is similar to drawing blood, the doctor inserts a needle into a joint space and removes fluid. An examination of the fluid may reveal uric acid crystals, confirming a diagnosis of gout or bacteria, suggesting that the joint inflammation is caused by infection.
    158. 158. LABORATORY EXAMS andTESTS: ARTHRITIS Muscle Enzymes Test ( CPK, Aldolase) Such tests can measure the amount of muscle damaged as well as how effective medication has been in reducing the inflammation that caused the muscle damage.
    159. 159. RHEUMATOID ARTHRITIS An autoimmune disease in which the bodys immune system attacks itself. The pattern of joints affected is usually symmetrical, involves the hands and other joints and is worse in the morning.
    160. 160. RHEUMATOID ARTHRITIS Rheumatoid arthritis is also a systemic disease, involving other body organs, whereas osteoarthritis is limited to the joints. Overtime, both forms of arthritis can be crippling.
    161. 161. RHEUMATOID ARTHRITIS:CAUSES Causeof RA is unknown. It is an autoimmune disease, which means the bodys immune system mistakenly attacks healthy tissue. RA can occur at any age, but is more common in middle age. Women get RA more often than men.
    162. 162. RHEUMATOID ARTHRITIS:CAUSES Infection, genes, and hormone changes may be linked to the disease.
    163. 163. RHEUMATOID ARTHRITIS:SYMPTOMS1. Morning stiffness, which lastsmore than 1 hour, is common.Joints may feel warm, tender, andstiff when not used for an hour.2. Joint pain is often felt on thesame joint on both sides of thebody.
    164. 164. RHEUMATOID ARTHRITIS:SYMPTOMS 3. Chest pain when taking a breath (pleurisy) 4. Dry eyes and mouth (Sjogren syndrome) 5. Eye burning, itching, and discharge 6. Nodules under the skin (usually a sign of more severe disease) 7. Numbness, tingling, or burning in the hands and feet 8. Sleep difficulties
    165. 165. RHEUMATOID ARTHRITIS:TREATMENT RA usually requires lifelong treatment, including medications, physical therapy, exercise, education, and possibly surgery. Early, aggressive treatment for RA can delay joint destruction.
    166. 166. OSTEOARTHRITIS: DEFINITION Associated with the aging process and can affect any joint. The cartilage of the affected joint is gradually worn down, eventually causing bone to rub against bone. Bony spurs develop on the unprotected bones causing pain and inflammation.
    167. 167. OSTEOARTHRITIS: DEFINITION
    168. 168. OSTEOARTHRITIS: HANDS
    169. 169. OSTEOARTHRITIS: CAUSES Aging.The water content of the cartilage increases and the protein makeup of cartilage degenerates. Repetitive use of the joints over the years causes damage to the cartilage that leads to joint pain and swelling.
    170. 170. OSTEOARTHRITIS: CAUSES Heredity. The genetic basic cause of this condition.
    171. 171. OSTEOARTHRITIS: RISK FACTORS Older age Sex Bone deformities Joint injuries Obesity Sedentary lifestyles Diseases, like diabetes, hypothyroidism, gout, Paget’s disease Certain occupations
    172. 172. OSTEOARTHRITIS: SYMPTOMS Pain Tenderness Stiffness Loss of flexibility Grating sensation Bone spurs
    173. 173. GOUT: DEFINITION It can cause an attack of sudden burning pain, stiffness, and swelling in a joint, usually a big toe.These attacks can happen over and over unless gout is treated.
    174. 174. GOUT: DEFINITIONOver time, they can harm the joints, tendons, and other tissues.Gout is most common in men.
    175. 175. GOUT: CAUSES AND RISK FACTORS High levels of uric acid in the blood, which crytallize in the joints. Overweight High alcohol consumption Diet rich in fish and meat (due to purine content) Diuretics
    176. 176. GOUT: THE THREE STAGES Stage One: High Blood Acid levelsThe uric acid level in the blood may be higher than normal, but there are no symptoms of gout. High uric acid in the blood (hyperuricemia) may never progress beyond this stage, and symptoms of gout may never develop. Some people may have kidney stones before having their first attack of gout.
    177. 177. GOUT: THE THREE STAGES Stage Two: Episodes of acute gouty arthritis separated by periods without symptoms.This stage is also called intercritical or interval gout. Uric acid crystals begin to form in the joint fluid, usually in one joint-most commonly the big toe-and the body often responds with a sudden inflammatory reaction: a gout attack.
    178. 178. GOUT: THE THREE STAGES Stage Two: Episodes of acute gouty arthritis separated by periods without symptoms.Although the big toe is the most common site for a gout attack, gout may develop in other joints, including the knee, ankle, and joints in the foot, wrist, and fingers. After the gout attack is over, the affected joint and surrounding tissues feel normal within days until the next attack, which often occurs within 2 years
    179. 179. GOUT: THE THREE STAGES Stage Two: Episodes of acute gouty arthritis separated by periods without symptoms.For many people this period becomes progressively shorter as attacks occur more often. Later attacks may be more severe, last longer, and involve more than one joint.
    180. 180. GOUT: THE THREE STAGES Stage Three: Chronic Tophaceous GoutIf gout symptoms have occurred off and on without treatment for several years, they may become ongoing (chronic) and frequently affect more than one joint. There may no longer be periods of time between attacks.
    181. 181. GOUT: THE THREE STAGES Stage Three: Chronic Tophaceous Gout By this time, enough uric acid crystals have accumulated in the body to form gritty nodules called tophi. When located just under the surface of the skin, these deposits are usually firm and movable. The overlying skin may be thin and red. Tophi that are very near the skin may appear cream-colored or yellow.
    182. 182. GOUT: THE THREE STAGES Stage Three: Chronic Tophaceous Gout At first, tophi are usually found on or near the elbow, over the fingers and toes, or on the outer edge of the ear.
    183. 183. GOUT: THE THREE STAGES Stage Three: Chronic Tophaceous Gout Progressive crippling and destruction of cartilage and bone is possible.This stage of gout is uncommon because ofadvances in the early treatment of gout.
    184. 184. GOUT: NON-PHARMACOLOGICALMANAGEMENT Eat moderate amounts of a healthy mix of foods. Avoid regular daily intake of meat, seafood, and alcohol (especially beer). Drink plenty of water and other fluids.
    185. 185. RHEUMATIC FEVER: DEFINITION An inflammatory disease that may develop after an infection with group A Streptococcus bacteria (such as strep throat or scarlet fever). The disease can affect the heart, joints, skin, and brain.
    186. 186. RHEUMATIC FEVER: CAUSES,INCIDENCE, RISK FACTORS Common worldwide and is responsible for many cases of damaged heart valves.Rheumatic fever mainly affects children ages 5 -15, and occurs approximately 14-28 days after strep throat or scarlet fever.
    187. 187. RHEUMATIC FEVER: SYMPTOMS Abdominal pain Fever Heart (cardiac) problems, which may not have symptoms, or may result in shortness of breath and chest pain Joint pain, arthritis (mainly in the knees, elbows, ankles, and wrists) Joint swelling; redness or warmth
    188. 188. RHEUMATIC FEVER: SYMPTOMS Nosebleeds (epistaxis) Skin nodules Skin rash (erythemamarginatum)1. Skin eruption on the trunk andupper part of the arms or legs2. Eruptions that look ring-shaped orsnake-like
    189. 189. RHEUMATIC FEVER: SYMPTOMS Sydenham chorea (emotional instability, muscle weakness and quick, uncoordinated jerky movements that mainly affect the face, feet, and hands)
    190. 190. RHEUMATIC FEVER: MAJORCRITERIAS FOR DIAGNOSIS1. Arthritis in several large joints (polyarthritis)2. Heart inflammation (carditis)3. Nodules under the skin (subcutaneous skin nodules)4. Rapid, jerky movements (chorea, Sydenham chorea)5. Skin rash (erythemamarginatum)
    191. 191. RHEUMATIC FEVER: MINORCRITERIAS FOR DIAGNOSIS6. Fever7. High ESR8. Joint pain9. Abnormal EKG
    192. 192. RHEUMATIC FEVER: LABORATORYEXAMS AND TESTSBlood test for recurrent strep infection (such as an ASO test)Antistreptolysin O (ASO) titer is a blood test to measure antibodies against streptolysin O, a substance produced by group A Streptococcus bacteria. Complete blood count Electrocardiogram Sedimentation rate (ESR)
    193. 193. RHEUMATIC FEVER: LABORATORYEXAMS AND TESTS Sedimentation rate (ESR)Normal ValuesAdults (Westergren method):Men under 50 years old: less than 15 mm/hrMen over 50 years old: less than 20 mm/hrWomen under 50 years old: less than 20 mm/hrWomen over 50 years old: less than 30 mm/hr
    194. 194. RHEUMATIC FEVER: LABORATORYEXAMS AND TESTSChildren (Westergren method):Newborn: 0 to 2 mm/hrNewborn to puberty: 3 to 13 mm/hr
    195. 195. RHEUMATIC FEVER: TREATMENT Low doses of antibiotics (such as penicillin, sulfadiazine, or erythromycin) over the long term to prevent strep throat from returning. Anti-inflammatory (Aspirin or Corticosteroids)
    196. 196. RHEUMATIC FEVER: PROGNOSIS If rheumatic fever returns, the doctor may recommend the patient take low-dose antibiotics continually, especially during the first 3 -5 years after the first episode of the disease. Heart complications may be severe, particularly if the heart valves are involved.
    197. 197. RHEUMATIC FEVER:COMPLICATIONS Arrhythmias Damage to heart valves (in particular, mitral stenosis and aortic stenosis) Endocarditis Heart failure Pericarditis Sydenham chorea
    198. 198. RHEUMATIC FEVER: PREVENTIONThe most important way to prevent rheumatic fever is by getting quick treatment for strep throat and scarlet fever.
    199. 199. NON-INFECTIOUSTOPICALDISEASESACNE(VULGARIS, CYSTIC, ROSACEA)PSORIASIS
    200. 200. SKIN ANATOMY:
    201. 201. ACNE: DEFINITION Common skin disease that causes pimples. Pimples form when hair follicles under the skin clog up. Most pimples form on the face, neck, back, chest and shoulders. Anyone can get acne, but it is common in teenagers and young adults. It is not serious, but it can cause scars.
    202. 202. ACNE: BODY PARTS AFFECTEDAcne typically appears on your face, neck, chest, back and shoulders, which are the areas of the skin with the largest number of functional oil glands.
    203. 203. ACNE: CAUSESHormonal changes (during puberty and pregnancy.Overproduction of sebum / oilIrregular shedding of dead skin cells resulting in irritation of the hair follicles of skinBuildup of bacteria
    204. 204. ACNE: HOW IT DEVELOPS
    205. 205. ACNE: FACTORS THAT WORSENS IT HormonesAndrogens are hormones thatincrease in boys and girls duringpuberty and cause the sebaceousglands to enlarge and make moresebum.Hormonal changes related topregnancy and the use of oralcontraceptives can also affectsebum production.
    206. 206. ACNE: FACTORS THAT WORSENS IT Certain medications Drugs containing; 1. corticosteroids 2. androgens 3. lithium are known to cause acne.
    207. 207. ACNE: FACTORS THAT WORSENS IT Diet Studies indicate that certain dietary factors, including dairy products and carbohydrate-rich foods — such as bread, bagels and chips, which increase blood sugar — may trigger acne.
    208. 208. ACNE: DIFFERENT FORMS NON-INFLAMMATORY LESIONS1. Comedones (Whiteheads andBlackheads)Created when the openings of hairfollicles become clogged and blockedwith oil secretions, dead skin cellsand sometimes bacteria.
    209. 209. ACNE: DIFFERENT FORMS NON-INFLAMMATORY LESIONS1. Comedones (Whiteheads andBlackheads)When comedones are open at the skinsurface, theyre called blackheadsbecause of the dark appearance of theplugs in the hair follicles.
    210. 210. ACNE: DIFFERENT FORMS NON-INFLAMMATORY LESIONS1. Comedones (Whiteheads andBlackheads)When comedones are closed, theyrecalled whiteheads — slightly raised,skin-colored bumps.
    211. 211. ACNE: DIFFERENT FORMS INFLAMMATORY LESIONS 1. Papules - small raised bumps that signal inflammation or infection in the hair follicles. Papules may be red and tender.
    212. 212. ACNE: DIFFERENT FORMS INFLAMMATORY LESIONS2. Pustules (pimples) - are red, tenderbumps with white pus at their tips.
    213. 213. ACNE: DIFFERENT FORMS INFLAMMATORY LESIONS3. Nodules - are large, solid, painfullumps beneath the surface of the skin.Theyre formed by the buildup ofsecretions deep within hair follicles.
    214. 214. ACNE: DIFFERENT FORMS INFLAMMATORY LESIONS 4. Cysts - painful, pus-filled lumps beneath the surface of the skin. These boil-like infections can cause scars.
    215. 215. ACNE ROSACEA: DEFINITIONA long-term disease that affects the skin and sometimes the eyes.It causes redness and pimples.Rosaceais most common in women and people with fair skin. It usually starts between age 30 and 60.
    216. 216. ACNE ROSACEA: SYMPTOMS Frequent redness (flushing) of the face. Most redness is at the center of the face (forehead, nose, cheeks, and chin). A burning feeling and slight swelling. Small red lines under the skin.
    217. 217. ACNE ROSACEA: SYMPTOMS Constant redness along with bumps on the skin. Sometimes the bumps have pus inside (pimples), but not always. Solid bumps on the skin may later become painful. Inflamed eyes/eyelids. Swollen, red, large bumpy nose.
    218. 218. ACNE ROSACEA: SYMPTOMS Thicker skin. The skin on the forehead, chin, cheeks, or other areas can become thicker because of rosacea.
    219. 219. ACNE ROSACEA: CAUSES When blood vessels expand tooeasily, causing flushing.People who blush a lot may be morelikely to get rosacea. Hereditary
    220. 220. ACNE ROSACEA: CAUSES Patients’skin with rosacea were to have high levels of cathelicidins, peptides with antimicrobial and pro- inflammatory properties that protect the skin against infection.
    221. 221. ACNE ROSACEA: CAUSES Levelsof stratum corneumtryptic enzyme or SCTE — the enzyme responsible for cleaving the inactive cathelicidins into their active form — were also elevated in people with the disease. A flaw in the immune system contributes to this disease.
    222. 222. ACNE ROSACEA: FACTORS THATMAKE IT WORSE Heat (including hot baths) Heavy exercise Sunlight Winds Very cold temperatures Hot or spicy foods and drinks Drinking alcohol Menopause Emotional stress Long-term use of steroids on the face
    223. 223. ACNE ROSACEA: TREATMENTAdapalene Cream or Gel (Differin)A moderator of differentiation of follicular epithelial cells, keratinization, and inflammatory processes.It has both exfoliating and anti- inflammatory effects.
    224. 224. ACNE ROSACEA: TREATMENT Electro surgery and Laser surgeryImproves skin appearance withless scarring.
    225. 225. ACNE ROSACEA: TREATMENT Scraping off the excess skin tissue from a swollen, bumpy nose.Application of green-tinted foundation or make-up to conceal the skin redness.
    226. 226. ACNE: RISK FACTORS Teenagers Women and girls, two to seven days before their periods Pregnant women People using certain medications, including those containing corticosteroids, androgens or lithium
    227. 227. ACNE: RISK FACTORS Direct skin contact with greasy or oily substances, or to certain cosmetics applied directly to the skin A family history of acne Friction or pressure on the skin caused by various items, such as telephones or cellphones, helmets, tight collars and backpacks
    228. 228. ACNE: NON-PHARMACOLOGICALTREATMENTS Wash problem areas with a gentle cleanser. Avoid irritants (greasy cosmetics, oily hairstyling products, oil-based sunscreens) Keep hair away from your face Avoid tight-fitting clothes Don’t prick or squeeze!
    229. 229. ACNE: PHARMACOLOGICALTREATMENTS OTC topical medications containing salicylic acid, benzoyl peroxide, sulfur, resorcinol. Prescription medications such as retinoids, adapalene, tazarotene
    230. 230. ACNE: PHARMACOLOGICALTREATMENTS Antibiotics – for moderate to severe acne. Isotretinoin – for deep, cystic acne. Oral Contraceptives -a combination of norgestimate and ethinylestradiol (Ortho Tri-Cyclen, Previfem), can improve acne in women.
    231. 231. ACNE: COSMETIC / SURGICALTREATMENTS Laser / Light TherapyLaser treatment – damages the oilglands, to produce lesser oil.Light therapy – targets the bacteriathat causes acne inflammation
    232. 232. ACNE: COSMETIC / SURGICALTREATMENTS Chemical Peels / Microdermabrasion Lessen the appearance of fine lines, sun damage and minor facial scars — are most effective when used in combination with other acne treatments.
    233. 233. ACNE: COSMETIC / SURGICALTREATMENTS Acne Scar Treatment 1. Dermabrasion 2. Microdermabrasion (such as Diamond Peeling) 3. Soft Tissue (Collagen) Fillers 4. Chemical Peels 5. RadioFrequency Treatments 6. Skin Surgery ( by Punch Excision)
    234. 234. ACNE: PREVENTION Wash acne-prone areas only twice a day. Avoid heavy make-up / foundation. Wear loose-fitting clothes. Shower after excersizing or after doing strenous work.
    235. 235. PSORIASIS
    236. 236. PSORIASIS: DEFINITIONA skin disease that causes scaling and inflammation (pain, swelling, heat, and redness). Skincells grow deep in the skin and slowly rise to the surface.
    237. 237. PSORIASIS: DEFINITION Thisprocess is called cell turnover, and it takes about a month. Withpsoriasis, it can happen in just a few days because the cells rise too fast and pile up on the surface.
    238. 238. PSORIASIS: DEFINITIONA chronic, autoimmune disease that appears on the skin. Itoccurs when the immune system sends out faulty signals that speed up the growth cycle of skin cells. Psoriasis is not contagious.
    239. 239. PSORIASIS: FIVE TYPES Plaque Psoriasis (psoriasis vulgaris)The most prevalent form of the disease. About 80 percent of those who have psoriasis have this type.It is characterized by raised, inflamed, red lesions covered by a silvery white scale. It is typically found on the elbows, knees, scalp and lower back.
    240. 240. PSORIASIS: FIVE TYPES Plaque Psoriasis (psoriasis vulgaris)
    241. 241. PSORIASIS: FIVE TYPES Guttate PsoriasisAform of psoriasis that often starts in childhood or young adulthood. This form of psoriasis appears as small, red, individual spots on the skin.Guttatelesions usually appear on the trunk and limbs. These spots are not usually as thick as plaque lesions.
    242. 242. PSORIASIS: FIVE TYPES Guttate Psoriasis
    243. 243. PSORIASIS: FIVE TYPES Inverse PsoriasisFound in the armpits, groin, under the breasts, and in other skin folds around the genitals and the buttocks.This type of psoriasis appears as bright- red lesions that are smooth and shiny. Inverse psoriasis is subject to irritation from rubbing and sweating because of its location in skin folds and tender areas.
    244. 244. PSORIASIS: FIVE TYPES Inverse Psoriasis
    245. 245. PSORIASIS: FIVE TYPES Pustular Psoriasis Primarily seen in adults, pustular psoriasis is characterized by white blisters of noninfectious pus (consisting of white blood cells) surrounded by red skin.
    246. 246. PSORIASIS: FIVE TYPES Pustular Psoriasis Triggers include irritating topical agents, overexposure to UV light, pregnancy, systemic steroids, infections, stress and sudden withdrawal of systemic medications or potent topical steroids.
    247. 247. PSORIASIS: FIVE TYPES Erythrodermic Psoriasis An inflammatory form of psoriasis that affects most of the body surface. It may occur in association with von Zumbuschpustular psoriasis. The reddening and shedding of the skin are often accompanied by severe itching and pain, heart rate increase, and fluctuating body temperature.
    248. 248. PSORIASIS: FIVE TYPES Erythrodermic PsoriasisTriggers include; a. abrupt withdrawal of a systemic psoriasis treatment including cortisoneb. allergic reaction to a drug resulting in the Koebnerresponsec. severe sunburnd. infectione. medications such as lithium, anti-malarial drugsf. strong coal tar products.
    249. 249. PSORIASIS: FIVE TYPES Erythrodermic Psoriasis
    250. 250. PSORIASIS: CAUSES Stress Injury / Trauma to skin – Koeb- ner phenomenon Medications, such as;lithiumantimalarialsinderalquinidineindomethacin
    251. 251. PSORIASIS: PHARMACOLOGICALTREATMENT Corticosteroids – most frequent Anthralin,synthetic Vitamin D3, and Vitamin A are also used in prescription topical treatments to control psoriasis lesions. OTC topicals containing salicylic acid and coal tar.
    252. 252. PSORIASIS: PHARMACOLOGICALTREATMENT Phototherapy / Light Therapy with PsoralenIt involves exposing the skin toultraviolet light on a regular basisand under medical supervision. Consistency is the key for thesuccess of this treatment.
    253. 253. PSORIASIS: PHARMACOLOGICALTREATMENT Sunlight Start with five to 10 minutes of noontime sun daily. Gradually increase exposure time by 30 seconds if the skin tolerates it.To get the most from the sun, all affected areas should receive equal and adequate exposure.
    254. 254. PSORIASIS: PHARMACOLOGICALTREATMENT Laser treatments 1. Excimer Laser – FDA approved for chronic, localized psoriasis plaques.
    255. 255. PSORIASIS: PHARMACOLOGICALTREATMENT Laser treatments 2. Pulsed Laser - uses a dye and different wavelength of light than the excimer laser or other UVB-based treatments, pulsed dye lasers destroy the tiny blood vessels that contribute to the formation of psoriasis lesions.
    256. 256. PSORIASIS: PHARMACOLOGICALTREATMENT Traditional Systemic MedicationsAcitretin (Psoriatane)CyclosporinMethotrexate Off-lablesystemics (hydroxyurea, isotretinoins, sulfasalazine, 6-thioguanine, mycophenolatemofetil)
    257. 257. PSORIASIS: PHARMACOLOGICALTREATMENTBiologics – moderate to severepsoriasis1. T-cell blockers – Amevive (Alefacept),Raptiva (Efalizumab)2. Tumor necrosis factor-alpha (TNF-alpha) blockers - Enbrel (etanercept),Humira (adalimumab), Remicade(infliximab) and Simponi (golimumab)
    258. 258. PSORIASIS: PHARMACOLOGICALTREATMENT Biologics – moderate to severe psoriasis 3. Interleukin 12/23Stelara(ustekinumab) works by selectively targeting the cytokines interleukin-12 (IL12) and interleukin 23 (IL23).
    259. 259. PSORIASIS: NON -PHARMACOLOGICAL TREATMENTA. Lifestyle changes 1. diet – avoid gluten (wheat and red meat) and fatty acids. 2. take fish oil supplements EAT WELL….LOSE WEIGHT 3. Anti-inflammatory Diet Heart-Healthy Diet
    260. 260. PSORIASIS: NON -PHARMACOLOGICAL TREATMENTB. Mind –Body medicine 1. meditation 2. cognitive behavioral therapy
    261. 261. PSORIASIS: NON -PHARMACOLOGICAL TREATMENTC. Whole Medical Systems 1. TCM - acupunture 2. Ayurveda - Yoga 3. Naturopathy 4. Homeopathy

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