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Ch 2 Patho
Body Defenses
| Question | Answer |
|---|---|
| Stress | .universal experience of human existence that can negatively affect the body's homeostasis.<p> .Can contribute directly to the development/exacerbation of a disease.<p> .Can contribute to - behaviors(smoking/drugs)<p> .Can arise from +(weddings/vacatio |
| Hans Selye | .described body changes associated with stress in the 1930's.<p> .Noted that body responded to stimuli, or stressor with a series of non-specific events. |
| general adaption syndrome (GAS) | .A cluster of systemic manifestations as a result of modifying in an attempt to cope with a stressor.<P> .Factors include natural reserve, time, genetics, age, gender, health status, nutrition, sleep-wake cycles, hardiness, & psychosocial factors. |
| general adaption syndrome (GAS) 3 steps | 1. Alarm<br> 2. Resistance<br> 3. Exhaustion<br> |
| (GAS) step 1: Alarm stage | .generalized stimulation of the sympathetic nervous system resulting in the release of catecholamines and cortisol, or the fight-or-flight response. |
| (GAS) step 2: Resistance | .body chooses the most effective and advantageous defense<p> .fight/flight symptoms disappear<p> .Body will adapt/alter to attempt to become desensitized(meditation/relaxation)<p> . |
| (GAS) step 3: Exhaustion | .initiated if stressor is prolonged or overwhelms the body.<p> .Body becomes depleted and damage may appear as homeostasis cannot be maintained.<p> .Disease or death results<p> .anxiety, depression, headaches, insomnia, infections, cardiovascular disea |
| Local Adaptation Syndrome | .confines the damage of the stressor to 1 location .ex:local tissue trauma |
| Stress factors | .genetics,age,gender,life experiences,dietary status,& social support<p> .coping strategies(physical activity,sleep,diet)<p> .maladaptive(smoking,alcohol,drugs,eating) |
| Immune system | .protects the body against microorganisms(bacteria,viruses,fungi,protozoans,prions)& removes damaged cells & destroys cancer cells<p> .ability to respond to a foreign agent or antigen |
| 1st line of defense | .Non-specific<p> .Most prominent(skin & mucous membranes)<p> .skin is acidic that inhibits bacterial growth<p> .Hydrochloric acid in stomach destroys bacteria. .Tears & saliva: Lysozyme, destroys bacterial cell walls |
| 2nd line of defense | 1. inflammatory response<p> 2. pyrogens<p> 3. interferons<p> 4. complement proteins |
| Inflammatory response | .erythema(redness),edema(swelling),heat,& pain<p> .triggered by mediators (mast cells:histamine;vasodilation & prostagladins;pain receptors) .arterioles limit bleeding & extent<p> .know the process of <b>(NOTES) |
| Pyrogens | .Molecules released by macrophages that have been exposed to bacteria.<p> .Travel to hypothalamus & ^ body temp.Not good for bacteria.Spleen & Liver remove iron from blood .Fever increases metabolism(^ healing&phagocytosis)<p> .over 105 denatures prote |
| Interferons<p> <b>BOOK figure 2-5 | .Def:proteins released from cells infected by viruses<p> .Bind to noninfected<p> .triggers synthesis of enzymes that inhibit viral replication<p> .viruses cannot replicate in uninfected .Interferon production is dying cells attempt to protect other ce |
| Complement proteins | .involves blood plasma proteins that enhance action of antibodies<p> .5 form membrane-attack complex in bacteria<p> .water makes cell swell,burst<p> .Stimulate vasodilation<p> .permeability of vessels<p> .chemical attractants<p> .bind to microbes<p> |
| 3rd line of defense | .Body's own immune system<p> .players in the recognition of the antigens that make it through the first 2 layers of immunity are T cells and B cells. .Circulate through body fluid & lymphoid tissue(tonsils,lymph nodes,spleen,intestinal lymphoid tissue) |
| T cells (cellular immunity) | .produced in the bone marrow<p> .matures in the thymus (named T cell)<p> .2 types:regulator and effector<p> .Work to protect against virus & cancer<p> .responsible for hypersensitivity & transplant rejection |
| regulator cells (T cells) | .include helper T cells & suppressor T cells<p> .Helper T cell-activates B cells to produce antibodies<p> .Suppressor T cells-turns antibody production off |
| effector (T cells) | .Killer cells/cytotoxic cells(destroy antigens)<p> .destroys cells infected with viruses by releasing lymphokines that destroy cell walls. |
| B cells (humoral immunity) | .Mature in bone marrow<p> .memory or immunoglobulin-secreting(antibody)cells .Eliminate bacteria,neutralize toxins,prevent viral reinfection,immediate inflammatory response .B cell activates & multiplies into antibody-producing or memory cell |
| memory cell (B cell) | .aids quick response to subsequent exposures to an antigen because memory cells recall the antigen as foreign, and antibody production is rapid |
| acquired immunity | Results from subsequent exposure to an antigen because memory cells recall the antigen as foreign, and antibody production is rapid. .<b>BOOK Table 2-3 |
| Active acquired immunity | Process gained by actively having an antigen through invasion or vaccination. In active immunity, a person makes his or her own antibodies, and protection is usually long term. |
| Altered Immune Response | Malfunctions may include exaggeration (hyper sensitivity), misdirection(autoimmune), or diminution(immunodeficiency) |
| Hypersensitivity | inflated or inappropriate response to an antigen. The result is inflammation and destruction of tissue. May be immediate or delayed. .<b>NOTES for different types .BOOK p40 Table 2-2 |
| Allogenic transplant | Tissue is used from the same species of similar tissue type but is not identical |
| Syngenic transplant | Use tissue from the identical twin of the host |
| Autologous transplant | the host and donor are the same person<p> .storing his/her own blood prior to surgery |
| Hyperacute tissue rejections | .Occurs 3 days after transplant<p> .systemic inflammatory reaction<p> .tissue becomes permanently necrotic<p> |
| Acute tissue rejection | .Most common and treatable type of rejection<p> .between 4 days and 3 months following the transplant<p> .cell mediated & result in lyses or necrosis<p> .inflammatory response at the graft site<p> |
| Chronic tissue rejection | .4 months to a year after the transplant<p> .Most likely due to antibody-mediated immune response<p> .Antibodies & complements deposit in the transplanted tissue vessel walls, resulting in decreased blood flow and ischemia |
| Autoimmune disorders | .normal defenses become self destructive<p> .Theory:viral,genetic,medicinal,hormonal,environmental<p> .More women than men<p> .Periods of exacerbation(worsening)&remission(easing)<p> .Ex:SLE,rheumetoid arthritis,Guillain-Barre syndrome |
| Immunodeficiency | A diminished or absent immune response that increases susceptibility to infections<p> .May be primary(reflecting a defect with the immune system) or secondary(reflecting an underlying disease or factor that is suppressing the immune system)<p> |
| Immunodeficiency (continued) | Most common forms are caused by viral infections or iatrogenic reactions to therapeutic drugs (ex:corticosteroids and chemotherapy) |
| Primary deficits | Involve basic developmental failures, many resulting from genetic or congenital abnormalities(ex:hypogammaglobulinemia) |
| Secondary or acquired immunodeficiency | Loss of immune function because of a specific cause. May include infection, splenectomy, malnurition, hepatic disease, drug therapy, or stress. |
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