The Immune System

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The Immune System by Mind Map: The Immune System

1. Parts 1 and 2 Immunity

1.1. "immunis" or exempt

1.2. Function of immune system is to protect from invasion by infectious organisms, toxic agents, and abnormal cells (cancer)

1.2.1. Recognizes "self" from "non-self" through a process known as

1.2.1.1. Tolerance

1.2.2. Defends the body against non-self

1.2.3. Mounts an appropriate response to neutralize or eliminate the invader/foreign substance (effector function)

1.2.4. Remember (memory response)

1.2.5. Consequences

1.2.5.1. Desirable

1.2.5.1.1. Natural resistance

1.2.5.1.2. Recovery

1.2.5.1.3. Acquired resistance

1.2.5.2. Undesirable

1.2.5.2.1. Allergy

1.2.5.2.2. Rejection of transplant

1.2.5.2.3. Autoimmune disorder

1.3. Factors affecting immunity

1.3.1. Aging

1.3.1.1. Changes/mutations occur that affect/confuse/overwhelm the immune systems

1.3.1.1.1. Cancer

1.3.1.1.2. Autoimmune diseases

1.3.1.2. Changes in innate immunity:

1.3.1.2.1. Thinning of skin

1.3.1.2.2. Decreased acidity of GI tract

1.3.1.2.3. Decreased pulmonary function and air exchange

1.3.1.2.4. Less acidic urine/urine retention

1.3.1.2.5. Decreased functional capacity

1.3.1.2.6. Decreased NK cells

1.3.1.3. Changes in acquired immunity:

1.3.1.3.1. Thymus gland atrophy

1.3.1.3.2. Decreased numbers of T cells

1.3.1.3.3. Decreased antibody response to antigenic challenge

1.3.1.3.4. Increased genetic mutation

1.3.1.3.5. Poor nutrition

1.3.1.3.6. Chronic disease

1.3.2. Nutrition status

1.3.2.1. Calories

1.3.2.2. Protein

1.3.2.3. Vitamins and minerals

1.3.2.4. Alcoholism

1.3.3. Environmental and toxic exposures

1.3.3.1. Can overwhelm immune response or trigger genetic response leading to autoimmune reactions

1.3.4. Trauma

1.3.4.1. Stress on body systems and disruption of protective barriers depress immune function

1.3.5. Burns

1.3.5.1. Breakdown of innate immune systems

1.3.6. Sleep disturbances and psychosocial stress

1.3.7. Underlying disease

1.3.7.1. Cancer, diabetes mellitus, HIV/AIDS

1.3.8. Medications

1.3.8.1. Glucocorticoids and immunosuppressants

1.3.9. Iatrogenic factors

1.3.9.1. Catheters

1.3.9.2. Tubes

1.3.9.3. External fixation devices

1.3.9.4. Prosthetic joints

1.4. Cells and non-cellular components

1.4.1. Antigens

1.4.1.1. Any substance (usually foreign) that binds specifically to an antibody or a T-cell receptor

1.4.1.1.1. Typically recognized as non-self

1.4.1.1.2. Macromolecules such as:

1.4.1.2. Immunogen

1.4.1.2.1. An antigen capable of inducing an immune response from the adaptive immune system

1.4.1.2.2. Epitope/Antigenic Determinant

1.4.2. Antibodies

1.4.2.1. Specific glycoproteins called immunoglobulins, secreted by plasma cells

1.4.2.1.1. Membrane-bound receptors on the surface of naive B cells

1.4.2.1.2. Adult levels attained by age 16

1.4.2.2. Types:

1.4.2.2.1. IgM

1.4.2.2.2. IgG

1.4.2.2.3. IgA

1.4.2.2.4. IgD

1.4.2.2.5. IgE

1.4.2.3. Regions:

1.4.2.3.1. Antigen binding (Fab)

1.4.2.3.2. Fragment Crystallizable (Fc)

1.4.2.4. Participate in:

1.4.2.4.1. Specific binding to epitopes of specific antigens

1.4.2.4.2. Direct the attack against the antigen or cells bearing it

1.4.2.4.3. Complement fixation

1.4.2.4.4. Placental transfer

1.4.2.5. Antibody response

1.4.2.5.1. Primary

1.4.2.5.2. Secondary (anamestic)

1.4.2.6. 4 mechanisms of action:

1.4.2.6.1. Agglutination

1.4.2.6.2. Precipitation

1.4.2.6.3. Neutralization

1.4.2.6.4. Lysis

1.4.3. Complement

1.4.3.1. System of circulating proteins activated by antibody-antigen reaction

1.4.3.1.1. Soluble mediators (effectors) of the innate (natural) immune system

1.4.3.1.2. Important effector of humoral immunity

1.4.3.2. Activated compliment system:

1.4.3.2.1. Reactive site on antibody interacts with complement proteins

1.4.3.2.2. Initiates a cascade

1.4.3.2.3. Stimulates phagocytosis (opsonization)

1.4.3.2.4. Causes rupture of cell membranes by membrane attack complexes (MAC)

1.4.3.2.5. Enhances inflammatory response

1.4.3.2.6. Complement components are cleaved into fragments during activation

1.4.3.3. Functions

1.4.3.3.1. Lysis

1.4.3.3.2. Opsonization

1.4.3.3.3. Activation of inflammatory response

1.4.3.3.4. Immune clearance

1.4.3.4. Nomenclature

1.4.3.4.1. Complement (C) is divided into numbered components, which are then divided into lettered subunits (C1q, C1r, C1s)

1.4.3.4.2. Complement fragments formed by enzymatic reactions are labelled as well (C3a, C3b)

1.4.3.5. Pathways

1.4.3.5.1. Classical

1.4.3.5.2. Alternative

1.4.3.5.3. Both pathways end with a different form of C5 convertase, both of which will produce the same result

1.4.3.5.4. Membrane Attack Complex (MAC)

1.4.4. Leukocytes

1.4.4.1. White blood cells

1.4.4.2. Participate/regulate immune responses

1.4.4.3. Types:

1.4.4.3.1. Granulocytes (65%)

1.4.4.3.2. Monocytes (5%)

1.4.4.3.3. Lymphocytes (30%)

1.4.5. Lymphocytes

1.4.6. Cytokines

1.5. 3 arms

1.5.1. Host barriers

1.5.1.1. Anatomic/External

1.5.1.1.1. Intact skin

1.5.1.1.2. Mucous membranes

1.5.1.2. Physiologic/Internal

1.5.1.2.1. Normal body temperature

1.5.1.2.2. pH of body fluids

1.5.1.2.3. Oxygen tension

1.5.1.2.4. Soluble factors

1.5.2. Natural immunity

1.5.2.1. Innate or inborn resistance

1.5.2.2. Triggered when:

1.5.2.2.1. Organism has penetrated the first line of defense

1.5.2.3. Types

1.5.2.3.1. Active

1.5.2.3.2. Passive

1.5.2.4. Components

1.5.2.4.1. Cellular

1.5.2.4.2. Humoral

1.5.2.5. Cardinal features

1.5.2.5.1. Non-specific

1.5.2.5.2. Responds to foreign microbes only

1.5.2.5.3. Response occurs within hours of initial infection

1.5.3. Adaptive immunity

1.5.3.1. Allows the body to recognize, remember, and respond to an antigen (specific stimulus)

1.5.3.1.1. Is NOT independent of innate immunity

1.5.3.1.2. Operates under MHC restriction (self vs non-self)

1.5.3.2. Triggered when:

1.5.3.2.1. A foreign molecule has invaded the body

1.5.3.2.2. The 1st and 2nd line of defense has been compromised

1.5.3.3. Types

1.5.3.3.1. Active

1.5.3.3.2. Passive

1.5.3.4. Components

1.5.3.4.1. Cellular

1.5.3.4.2. Humoral (extracellular pathogens)

1.5.3.5. Cardinal features

1.5.3.5.1. Specificity

1.5.3.5.2. Diversity

1.5.3.5.3. Memory

1.5.3.5.4. Specialization

1.5.3.5.5. Self-limitation

1.5.3.5.6. Non-reactivity to self

1.5.3.6. Additional aspects

1.5.3.6.1. Recognition of antigen

1.5.3.6.2. Generation of lymphocyte specificity and diversity

1.5.3.6.3. Role of the MHC (Major Histocompatibility Complex)

1.5.3.6.4. Processing and presentation of antigens

1.5.3.6.5. Clonal selection of lymphocytes

1.5.3.6.6. Activation of T helper cells

1.5.3.6.7. Generation of the humoral and cell-mediated responses

1.5.4. Comparison of Natural and Adaptive Immunity

1.5.4.1. Natural

1.5.4.1.1. Same intensity on repeated exposure

1.5.4.1.2. No memory

1.5.4.1.3. PMNs, Macrophages, Monos, Eos, NKs

1.5.4.1.4. Complement, interferons, lysosomal, enzymes, acute phase proteins

1.5.4.2. Adaptive

1.5.4.2.1. More rapid and intense on repeated exposure

1.5.4.2.2. Memory

1.5.4.2.3. T and B lymphocytes

1.5.4.2.4. Cytokines, antibodies

1.6. Mammalian Immunologic Development

1.6.1. Origin and development of blood cells

1.6.1.1. Hematopoiesis

1.6.1.1.1. Formation and development of blood cells

1.6.1.1.2. Stem cells

1.6.2. Primary lymphoid organs

1.6.2.1. Functions:

1.6.2.1.1. Provide the appropriate micro-environment for continued:

1.6.2.2. Organs:

1.6.2.2.1. Bone marrow

1.6.2.2.2. Thymus

1.6.3. Secondary lymphoid organs

1.6.3.1. Functions:

1.6.3.1.1. Trap/process antigens from defined tissues or vascular spaces

1.6.3.1.2. Provide site where mature lymphocytes can interact with antigens

1.6.3.1.3. Unique microenvironment for the initiation and development of immune responses

1.6.3.2. Organs:

1.6.3.2.1. Lymph nodes

1.6.3.2.2. Spleen

1.6.3.2.3. Mucosal/gut-associated lymphoid tissue

1.6.3.2.4. Thoracic duct

1.6.3.2.5. Bronchus-associated lymphoid tissues

1.6.3.2.6. Blood

1.7. Stimulation/control of immune response

1.7.1. T helper cells (major regulator)

1.7.2. Multiple chemical mediators:

1.7.2.1. Produced and released macrophages and T cells

1.7.2.1.1. Autocrine and paracrine activity

1.7.2.2. Cytokines

1.7.2.2.1. Interleukins, interleukin-1 (ILs, IL-1)

1.7.2.2.2. Tumor necrosis factor (TNF)

1.7.2.2.3. Granulocyte and monocyte colony-stimulating factors (GM-CSF)

1.7.2.2.4. Interferon

1.7.2.3. Prostaglandins

1.7.2.4. Leukotrienes

1.7.2.5. Complement system

1.8. Immunology

1.8.1. Molecules, cells, organs, and systems responsible for the recognitions and disposal of foreign material

1.8.2. How body components respond and interact

1.8.3. The desirable and undesirable consequences of immune interactions

1.8.4. The ways in which the immune system can be advantageously modified

2. Part 3 Cell Injury

2.1. Most pathological processes start with injuries to cells which results in disruption of homeostasis

2.2. Mechanism of injury

2.2.1. Ischemia/hypoxia

2.2.1.1. Restriction in blood supply to tissues and deprivation of adequate oxygen to the body region, respectively

2.2.2. Infectious agents

2.2.3. Immune reactions

2.2.4. Genetic factors

2.2.5. Nutritional factors

2.2.6. Physical factors

2.2.7. Chemical (endogenous or exogenous) factors

2.2.8. Age

2.3. Consequences of cell injury

2.3.1. Pathologies cause injury to cells which make up tissues and organs

2.3.1.1. Dysfunctional cells lead to impaired organ function

2.3.2. Cell injury occurs if cell's adaptive capacity is exceeded (cannot maintain homeostasis)

2.3.2.1. Reversible injury (cell able to regain homeostasis)

2.3.2.2. Irreversible injury causes cell death (necrosis)

2.3.2.2.1. Damage to nucleus, mitochondria, and cell membrane

2.3.3. Repair and regeneration may or may not restore original tissue or function

2.3.3.1. Normal function tissue vs. scar tissue

2.4. Cellular adaptation to cell injury

2.4.1. As cells encounter frequent phsyiologic stress or pathologic insult, they undergo adaptation

2.4.1.1. Allows cells to function in an altered environment

2.4.2. Examples of adaptation

2.4.2.1. Exercise

2.4.2.1.1. Beneficial adaptation in muscle structure and function in response to progressive overload

2.4.2.2. Smoking

2.4.2.2.1. Detrimental adaptation in epithelium of upper respiratory tract in response to chronic exposure to smoke

2.4.3. Types of cellular adaptation

2.4.3.1. Atrophy

2.4.3.1.1. Reduction in cell size

2.4.3.2. Hypertrophy

2.4.3.2.1. Increase in cell size

2.4.3.3. Hyperplasia

2.4.3.3.1. Increase in the number of cells

2.4.3.4. Dysplasia

2.4.3.4.1. Increase in cell numbers with altered morphology

2.4.3.5. Metaplasia

2.4.3.5.1. Complete change in morphology

2.4.3.6. Neoplasia

2.4.3.6.1. Hyperplasia with no discernible cause

2.4.4. Biochemical mechanisms

2.4.4.1. Ischemia

2.4.4.1.1. Blood flow or oxygen supply below minimum to maintain cell homeostasis and metabolic function

2.4.4.1.2. O2 needed for energy production

2.4.4.1.3. Results in intracellular accumulation of ions and fluids

2.4.4.1.4. Mitochondria dysfunction

2.4.4.1.5. Lysosome release

2.4.4.1.6. Cellular necrosis

2.4.4.2. Cellular necrosis

2.4.4.2.1. After cell death, lysosomes release digestive enzymes

2.4.4.2.2. Necrotic cells often release markers

2.4.4.2.3. Removal of necrotic tissue is necessary for normal healing (purpose of inflammatory response)

2.4.5. Healing

2.4.5.1. Historically

2.4.5.1.1. Incorrect approach to wound healing

2.4.5.2. Current treatment strategy

2.4.5.2.1. Refrain from interfering with the acute aspect of inflammation

2.4.5.2.2. As stated earlier:

2.4.5.3. Phases

2.4.5.3.1. Hemostasis and degeneration

2.4.5.3.2. Inflammation

2.4.5.3.3. Proliferation and migration

2.4.5.3.4. Remodeling and maturation

2.4.5.4. Ideally, healing process...

2.4.5.4.1. Allows for full restoration (regeneration) of original structure and function

2.4.5.4.2. Influenced by:

2.4.5.5. If injury is severe...

2.4.5.5.1. Full restoration is not possible

2.4.5.5.2. Nonfunctional connective tissue replaces normal cells/tissue with firbrosis and scar tissue

3. Part 4 Illness

3.1. Infectious Diseases

3.1.1. Normal flora

3.1.1.1. Describes microorganisms that are frequently found on or in the bodies of healthy individuals

3.1.1.2. Skin

3.1.1.2.1. Propionibacterium acnes

3.1.1.2.2. Micrococcus

3.1.1.2.3. Staphylococcus spp.

3.1.1.2.4. Diphtheroids are common

3.1.1.3. Mouth

3.1.1.3.1. Streptococcus spp. (most common)

3.1.1.3.2. Staphylococcus

3.1.1.3.3. Peptrostreptococcus

3.1.1.3.4. Other anaerobes

3.1.1.4. Respiratory tract

3.1.1.4.1. Beyond the oropharynx

3.1.1.4.2. Nose and nasopharynx

3.1.1.4.3. During community outbreaks:

3.1.1.5. Gastrointestinal tract

3.1.1.5.1. Most microorganisms are destroyed by the stomach

3.1.1.5.2. Most common:

3.1.1.5.3. Antibiotics can alter the normal flora of the GI, allowing superinfections to occur:

3.1.1.6. Genitourinary tract

3.1.1.6.1. Otermost segment of urethra

3.1.1.6.2. Colonized by skin organisms

3.1.1.6.3. Vagina

3.1.2. Definitions

3.1.2.1. Infection

3.1.2.1.1. When a microorganism invades a host and multiplies enough to disrupt normal function by causing signs and symptoms

3.1.2.2. Pathogenicity

3.1.2.2.1. Ability of an organism to cause disease

3.1.2.3. Transmission/route of entry

3.1.2.3.1. Passing of a communicable disease from an infected individual to another

3.1.2.4. Incubation period

3.1.2.4.1. Time immediately before the onset of acute disease (1 to 2 days)

3.1.2.5. Latency period

3.1.2.5.1. Organism is dormant or inactive in the host

3.1.2.6. Confirm whether the patient has an active infection or immunity

3.1.2.6.1. Acute phase

3.1.2.6.2. Convalescence phase

3.1.2.6.3. Convalescent titers

3.1.3. Caused by:

3.1.3.1. Opportunists

3.1.3.1.1. Organisms of the normal flora that do not normally cause infection but do so if the homeostatic condition of the host changes

3.1.3.2. Infectious agents

3.1.3.2.1. Organisms that invade and replicate in their host and can be transmitted causing a communicable disease

3.1.3.2.2. Induce a pathogenic response

3.1.4. Chain of transmission

3.1.4.1. Contact

3.1.4.1.1. Skin to skin, mucous membranes

3.1.4.1.2. Indirect contact

3.1.4.2. Airborne

3.1.4.2.1. Microorganisms

3.1.4.2.2. Propelled from respiratory tract

3.1.4.3. Droplets

3.1.4.3.1. Particles contained in respiratory droplets

3.1.4.4. Vehicle

3.1.4.4.1. Microorganisms transmitted through contaminated source

3.1.4.5. Vector borne

3.1.4.5.1. Intermediate animal

3.1.5. Bacteria

3.1.5.1. Single-cell prokaryotic microorganisms with cell walls

3.1.5.2. Lack a distinct nucleus

3.1.5.2.1. DNA is not confined to a nuclear compartment

3.1.5.3. Classified according to

3.1.5.3.1. Cell structure/shape

3.1.5.3.2. Staining characteristics

3.1.5.3.3. Motility

3.1.5.3.4. Growth medium/metabolism

3.1.5.4. Infections you may come in contact with:

3.1.5.4.1. Staphylococcal

3.1.5.4.2. Streptococcal

3.1.5.4.3. Pseudomonas aeruginosa

3.1.5.4.4. Borrelia burgdorferi

3.1.5.4.5. Clostridium difficile

3.1.5.4.6. Haemophilus influenza

3.1.5.5. Common infections acquired during hospitalization:

3.1.5.5.1. Urinary tract (Foley catheters)

3.1.5.5.2. Blood stream (IV catheters, surgical wounds)

3.1.5.5.3. Pneumonia (ventilators, impaired consciousness, poor pulmonary hygiene)

3.1.5.5.4. Gastrointestinal (antibiotics kill normal flora)

3.1.6. Virus

3.1.6.1. Collection of nucleic acid (either DNA or RNA) surrounded by a protein shell (capsid)

3.1.6.2. Do not have machinery to replicate

3.1.6.2.1. Must infect cells and hijack cellular mechanisms of the host's cells to replicate

3.1.6.3. Classified according to

3.1.6.3.1. Size

3.1.6.3.2. Shape

3.1.6.3.3. Means of transmission

3.1.6.3.4. Type of genetic material

3.1.6.4. Infections you may come in contact with:

3.1.6.4.1. Hepatitis A, B, C, D, E, and non-ABCDE

3.1.6.4.2. Secondary Hepatitis

3.1.6.4.3. Influenza

3.1.6.4.4. HIV

3.1.6.4.5. Hemorrhagic viruses

3.1.7. Fungi

3.1.7.1. Single or multicellular, filamentous organisms

3.1.7.1.1. Possess hyphae-filamentous outgrowths

3.1.7.1.2. Surrounded by cell wall

3.1.7.1.3. Nonmotile

3.1.7.1.4. Reproduce by division and budding

3.1.7.1.5. Yeasts and molds

3.1.7.2. Mycoses

3.1.7.2.1. Diseases caused by fungi

3.1.7.2.2. Usually on skin or mucous membranes

3.1.7.2.3. Signs and symptoms

3.1.7.2.4. Prevention

3.1.7.2.5. Treatment

3.1.8. Parasites (Protozoa and helminths)

3.1.8.1. Protozoa

3.1.8.1.1. Single cell organisms with a cell membrane

3.1.8.2. Helminths

3.1.8.2.1. Parasitic worms

3.2. Immunodeficiencies

3.2.1. Failure of the immune system due to a deficiency in immune components or function

3.2.2. Types

3.2.2.1. Primary

3.2.2.1.1. Genetic or developmental defect

3.2.2.2. Secondary

3.2.2.2.1. Acquired

3.3. Hypersensitivity reactions

3.3.1. Types

3.3.1.1. I. Anaphylactic

3.3.1.1.1. Occurs within minutes of contact with an antigen

3.3.1.1.2. IgE-mediated

3.3.1.1.3. Non-parasitic allergens

3.3.1.1.4. Anaphylatoxins

3.3.1.2. II. Cytotoxic

3.3.1.2.1. IgG or IgM mediated

3.3.1.2.2. Transfusion/transplantation reaction

3.3.1.2.3. Autoimmune hemolytic anemia

3.3.1.3. III. Immune complex

3.3.1.3.1. Ag-Ab complexes are deposited on tissues causing inflammation or tissue damage

3.3.1.3.2. Arthus reactions, most autoimmune diseases

3.3.1.4. IV. Cell-mediated

3.3.1.4.1. Delayed

3.3.1.4.2. CD4+ and CD8+ T cells activate macrophages and inflammatory cells, inducing tissue injury

3.3.1.4.3. Direct killing of target cells by CD4+ and CD8+ cells

3.4. Autoimmune disorders

3.4.1. Conditions in which immunological destruction of the body's own tissues and damage to body organs results from the presence of autoantibodies or auto-reactive cells

3.4.2. Immune mechanisms are directed against self-antigens

3.4.2.1. Body fails to distinguish self from non-self (loss of tolerance)

3.4.2.2. Attacks skin, joints, heart, lungs, eyes, blood vessels

3.4.3. Etiology

3.4.3.1. Genetically inherited

3.4.3.2. More common in females

3.4.3.3. Autoantibodies increase with age

3.4.3.4. Foreign antigens that are similar to self antigens can induce the production of antibodies that recognized self-antigens

3.4.4. Pathogenesis

3.4.4.1. Cell-mediated and humoral immune responses against "normal" tissues

3.4.4.2. Damages affected tissues

3.4.4.3. Types:

3.4.4.3.1. Organ-specific (diabetes)

3.4.4.3.2. Systemic (SLE)

3.4.5. Clinical manifestations depend upon organ affected

3.4.6. Medical management

3.4.6.1. Diagnosis (difficult)

3.4.6.1.1. Autoantibodies detected

3.4.6.2. Treatment

3.4.6.2.1. Relieve symptoms

3.4.6.2.2. Minimize tissue damage

3.4.6.2.3. Immunosuppression

3.4.6.2.4. Gene therapy?

3.4.7. Systematic Lupus Erythematosus

3.4.7.1. Chronic inflammatory autoimmune disorder

3.4.7.2. Widespread immune activity, can affect any cell, tissue, or organ of body

3.4.7.3. More common in young women (15-40 yrs)

3.4.7.3.1. Strong genetic susceptibility

3.4.7.3.2. More common in African Americans (3x)

3.4.7.4. Multiple possible triggers

3.4.7.4.1. Infection (EBV)

3.4.7.4.2. Stress

3.4.7.4.3. Pregnancy

3.4.7.4.4. Drugs

3.4.7.5. Pathogenesis

3.4.7.5.1. Body produces autoantibodies, specifically antinuclear (ANAs) and anti-DNA antibodies

3.4.7.5.2. Deposition of antigen-antibody complexes in various tissues (generalized autoimmunity)

3.4.7.5.3. Activates immune and inflammatory response resulting in tissue damage by white blood cells, cytokines, and compliment

3.4.7.6. Clinical manifestations

3.4.7.6.1. Cutaneous

3.4.7.6.2. Musculoskeletal

3.4.7.6.3. Cardiopulmonary

3.4.7.6.4. CNS

3.4.7.6.5. Blood and blood vessels

3.4.7.7. Diagnosis

3.4.7.7.1. Difficult, multiple criteria must be met (4 of 11)

3.4.7.8. Treatment

3.4.7.8.1. NSAIDs for pain and inflammation

3.4.7.8.2. Methotrexate

3.4.7.8.3. Immunomodulating drugs

3.4.7.8.4. Glucocorticoids

3.4.7.9. Important considerations for PT

3.4.7.9.1. Fatigue, weakness, poor conditioning (adjust workload and exercise prescription)

3.4.7.9.2. Skin care and appropriate precautions with modalities

3.4.7.9.3. Joint involvement (similar precautions as for RA)

3.4.7.9.4. Medication side effects, particularly glucocorticoids

3.4.8. Other autoimmune diseases

3.4.8.1. Polyarteritis nodosa

3.4.8.1.1. Small to medium blood vessels

3.4.8.2. Polymyalgia rheumatica

3.4.8.2.1. Large muscle groups

3.4.8.3. Rheumatoid arthritis

3.4.8.3.1. Synovial joints

3.4.8.4. Sarcoidosis

3.4.8.4.1. Lungs, lymph nodes, eyes

3.4.8.5. Scleroderma

3.4.8.5.1. Fibrosis of skin, intestines, lungs

3.4.8.6. Sjogren's syndrome

3.4.8.6.1. Tear and salivary glands (exocrine glands), joints

3.4.8.7. Chronic fatigue syndrome and fibromyalgia syndrome

3.5. Organ transplantation

3.5.1. Act of transferring cells, tissues, or organs from one site to another

3.5.2. Immune system is the most formidable barrier to transplantation

3.5.2.1. Immune system recognized transplanted tissue/organ as foreign and mounts an immune response

3.5.2.1.1. Type IV cell mediated reaction

3.5.2.2. Immunosuppressive drugs allowed phenomenal growth in the number of successful transplants

3.5.2.3. Key is appropriate tissue matching

3.5.2.3.1. Match HLA cell-surface antigens (self-antigens)

3.5.2.3.2. Major Histocompatibility Complex (MHC)

3.5.2.4. Types of transplants:

3.5.2.4.1. Autograft

3.5.2.4.2. Isograft

3.5.2.4.3. Allograft

3.5.2.4.4. Xenograft

3.5.2.5. Preventing rejections

3.5.2.5.1. Donor testing/tissue typing

3.5.2.5.2. Biochemical markers

3.5.2.5.3. General immunosuppressive therapy

3.5.2.6. Important considerations for PT

3.5.2.6.1. Exercise

3.5.2.6.2. Specific exercise and rehabilitation recommendations depend on organ transplanted

3.5.2.6.3. Stay alert for signs of rejection