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Test 1- Bouma
Stress, Ischemia, Inflamm., Immunity, Infection
| Term | Definition |
|---|---|
| Naturopathy | spirit guide and heal us |
| Allopathy | scientific knowledge, understand what is impacting body and what body is doing in response, DOES NOT DEAL WITH EVERYTHING |
| Homeostasis | "Balance", steady-like state |
| Stress | Altered balance |
| Cannon | linked physiological and psychological stress |
| Hans Selye | PHYSICAL, injected estrogen in rats, inc. size in adrenal cortex, inc. gastric ulcers, dec. atrophy thymus gland and lymphoid, GAS |
| Benson | identified concept of a stressor and stress response |
| Endogenous | INSIDE the body, tumor, allergy, defect, could turn on signals and pathways that are not needed at the right time, give false signals, cause stress on the rest of body |
| Exogenous | OUTSIDE the body, noises, nasty smell, cold, heat, worries, |
| Interactional | within person and environment |
| appraisal | what person perceives |
| past | experience, past history |
| magnitude and duration | size and consequences |
| coping potential | how you deal |
| noxious stressor | irritating to indiv., pneumonia, bee sting |
| pleasant stimuli | can be stressor, tickling, wedding |
| anticipatory stress response | PSYCHOLOGICAL, anticipation generates response ahead of disruption |
| GAS | general adaptation syndrome |
| alarm | fight or flight |
| action | resistance or adaptation |
| exhaustion | body gets to a point where it won't respond anymore, feedback shut off or decompensation occurs |
| HPA Axis | hypothalamus secretes CRH binds to pituitary, pituitary secretes ACTH binds to adrenal, adrenal releases glucocorticoid hormones that help enhance immunity during ACUTE stress and repress immunity during CHRONIC stress |
| Stage 1 | alarm stage |
| Stage 2 | resistance or adaptation |
| Stage 3 | exhaustion |
| Immune responses regulated by | macrophages, dendritic cells, NK cells |
| Th1 | PRO-inflamm, promote cellular immunity to protect the body from intracellular antigens, respond immediately |
| Th2 | ANTI-inflamm, produce antibodies that protect the body from extracellular antigens, respond later and deal with infection later |
| microenvironment | infection is inside the body |
| mast blood cell | WBC comes in to destroy and then eat them |
| psycho | consciousness |
| endocrine | brain and spinal cord |
| Th2 shift | dec. in Th1 and inc. in Th2 |
| cellular adaptation | REVERSIBLE structural or functional response, sublethal |
| cellular injury | CANNOT return to homeostasis, lethal |
| causes of cellular injury | hypoxia, chemicals, infection, mechanical pressure, physical agents, genetic errors |
| hypertrophy | inc. in size of cell |
| hyperplasia | inc. in # of cells |
| atrophy | dec. in cell size |
| metaplasia | reversible replacement of one mature cell type for another |
| dysplasia | inc. in number of cells of NOT the same cells as before |
| hypoxic injury | #1 cause of all cell injury, dec. oxygen in air, dec. RBC, dec. hemoglobin efficacy |
| ischemia | dec. blood supply, #1 cause of hypoxia |
| anoxia | total lack of oxygen |
| reperfusion injury | cut off of blood flow |
| necrosis (infarction) | cellular dissolution due to cellular death |
| apoptosis | death of single cells |
| coagulative necrosis | change from gelatinous to firm and opaque state Ex: kidneys, heart, adrenal glands |
| liquefactive necrosis | soft and liquefied, fluid filled cysts EX: brain tissue, fatty tissue |
| caseous necrosis | hard case on outside surrounding partial liquid inside EX: TV in lungs |
| fat necrosis | breakdown fats to create soaps with calcium and sodium Ex: pancreas, breasts, abdom organs |
| gangrenous necrosis | lg areas of tissue death due to hypoxic injury, NOT true cell death |
| somatic death | entire organism |
| local cell injury | hand injury |
| systemic cell injury | hand injury that became infected and microorganism multiplied in blood stream causing septicemia |
| first line of defense | innate, physical/ chemical barriers |
| second line of defense | inflamm |
| third line of defense | adaptive (acquired) |
| physical barrier examples | skin, mucous secretions from linings of GI, GU, and respiratory tracts, vomiting, coughing and sneezing |
| chemical barrier examples | saliva, tears. ear wax, sweat, mucus, normal bacterial flora |
| Cardinal symptoms of inflamm | redness, swelling, pain, loss of funct, heat |
| what can cause inflam | infection, extreme temp, radiation, ischemia, |
| what happens in body that causes inflamm symptoms | blood vessels constrict while capillary beds dilate, vascular permeability |
| goals of inflamm | limit and control the inflamm process, prevent and limit infection and further damage, initiate adaptive immune response, initiate healing |
| 3 plasma protein systems | complement, coagulation, kinin |
| outcome of the complement system | leukocyte migration |
| Complement system NEEDS what | C3 to release histamine and so the opsonin can slime and cause phagocytosis |
| clotting system | forms fibrinous meshwork at site to keep microorganisms at site, prevents spread of infection, forms clot |
| kinin system | dilation of blood vessels, PAIN, vascular permeability, leukocyte chemotaxis |
| what does kinin system make | bradykinin which makes prostaglandins and together they cause PAIN |
| cytokines | conductors of inflamm (IL, TNF, INF, chemokines) |
| chemotaxis | movement of cells to the point of bacteria or infection |
| phagocytosis | engulf bacteria |
| angiogenesis | redevelopment of cells |
| Interleukins | produced by macrophages, help create a fever |
| interferon | protects against viral infection |
| Tumor necrosis factor | induces fever, causes cachexia and intravascular thrombosis with cancer pts |
| chemokines | attract bacteria/ leukocytes to site |
| mast cells | contain histamine/ chemotaxis, cellular bags in loose connective tissue hanging out waiting to attack |
| histamine causes what | most vascular effects, making the wall more porous |
| what is attracted to histamine release | neutrophils |
| Histamine1 receptor | proinflamm, constricts |
| Histamine2 receptor | anti-inflamm, induces secretion of gastric acid |
| prostaglandins | induce pain |
| margination | neutrophils line up against walls and wait to find gap to squeeze through to go and fight bacteria, PAVEMENTING |
| platelets | made in bone marrow and component of blood, help with clotting |
| neutrophils | first responders, ingest bacteria, dead cells, and cellular debris |
| monocyte/macrophages | monocytes produced in bone marrow and migrate to inflamm site and then become macrophages, there within 24 hrs |
| eosinophils | fight against parasite |
| dendritic cells | call other adaptive immunity to come, interact with T lymphocutes |
| diapedesis | emigration of cells through the endothelial junction |
| phagocytosis steps | adherence, engulfment, phagosome formation, fusion with ysosomal granules, destruction of the target |
| acute inflamm | isolates to its own area, fever |
| serous exudate | watery exudate, early inflamm |
| fibrinous exudate | thick, more advanced inflamm |
| purulent exudate | pus, bacterial infection |
| hemorrhagic exudate | blood, indicates bleeding |
| leukocytosis | inc number of leukocytes, WBC count is high |
| chronic inflamm | lasting longer than 2 wks, too much bacteria and can't fight it off, acute inflamm couldn't get job done, granuloma formation, |
| who have depresses inflamm and immune function | neonates |
| what phagocyte is not capable of efficient chemotaxis in peds | netrophils |
| what ages do the immune system start to fade | older adults |
| adaptive (acquired) immunity | slow responders, have memory, destruction of infection resistant to inflamm |
| lymphocytes | primary cells for adaptive immunity, WBC |
| what immunity attack and create antibodies so next time they see the organism they know it | adaptive |
| active immunity | exposed to an antigen, immunization |
| passive immunity | given someone else's antibodies, IgG infusion, baby gets from mother |
| humoral immunity | b cell lymphocytes, produce antibodies or immunoglobulins that incapacitate antigen |
| cellular immunity | t cell lymphocytes, attack antigens directly |
| immunocompetent | capable of binding with a specific antigen |
| primary response- I got eM | IgM- will go up and then down |
| secondary/chronic response | IgG- goes up later and stays up |
| what react to antigens | antibodies |
| IgG | most abundant, most protective, transported across placenta |
| IgA1 | found in blood |
| IgA2 | body secretions, saliva, sweat, fluid in lungs |
| IgM | first produced, first antibody to infection, largest, synthesized during fetal life |
| IgD | low concentrate in the bloodI |
| IgE | EMERGENCY, allergic/ hypersensitivity reaction, protects against lg parasites, attracts eosinophils, mast cell degranulation- release histamine |
| what are direct antibody reactions | neutralization (bacteria can't move), agglutination (clump together), precipitation (stick together) |
| what are indirect antibody reactions | inflamm, phagocytosis, complement |
| true/false: both t and b cells have memory cells | true |
| Th | HELP respond to antigen |
| CD4 reacts with what class | MHC class II |
| Tc (cytotoxic)/ NK | destroy cancer/ virus cells |
| CD8 reacts with what class | MHC class II |
| Treg (regulatory) | turn on and off other t cells |
| how long do maternal antibodies provide protection | 5-6 months |
| fetus antibodies | good IgM, bad IgG, IgA responds |
| what ages are more likely to get cancer bc of the less amount of cytotoxic cells | older adults |
| symbiosis | benefits only human, no harm to the microorganism |
| mutualism | benefits the human and the microorganism |
| commensalism | benefits the microorganism, no harm to the human |
| pathogenicity | benefits he microorganism, harms the human |
| communicability | ability to spread from one indic. to others and cause disease |
| immunogenicity | ability of pathogens to induce an immune response |
| bacteria | produce surface coats that inhibit phagocytosis and toxins |
| viruses | have to be in cell to replicate |
| Exotoxins | break apart plasma cell membrane |
| endotoxins | when release= BAD bc of fever that comes with |
| bacteremia | NOT GROWING, in wound |
| septicemia | GROWING, throughout whole body, lead to septic shock |
| single cell fungal microorganism | yeast |
| multi- cell fungal microorganim | mold |
| pathogenicity | adapt to host environment, low OX and moist environment, |
| mycoses | diseases caused by fungi |
| dermatophytes | fungi that invade the skin, hair, or nails |
| what type of infection is opportunistic | fungal |
| parasitic | unicellular protozoa to lg worms |
| bacteriocidal | kills |
| bacteriostatic | stops from growing |
| primary immunodeficiency | genetic |
| second immunodeficiency | acquired- HIV |
| Hallmark sign for immunodeficiency | severe, unusual, recurrent infections |
| 5 primary immune deficiencies | b lymphocyte, t lymphocyte, combined t and b, complement, phagocyte |
| hypersensitivity | exaggerated response to something in environment |
| immediate hypersensitivity reaction | so much of a reaction go into shock |
| delayed hypersensitivity reaction | after awhile final get a reaction/rash |
| allergy | reaction of immune system to some antigen in environment |
| autoimmunity | breakdown of tolerance, disturbance in immunologic system to fighting against self |
| alloimmunity | transfusion, transplant |
| Type 1 hypersensitivity | IgG mediated- ALLERGIC REACTION |
| type 2 hypersensitivity | tissue specific |
| type 3 hypersensitivity | immune complex-mediate reactions |
| type 4 hypersensitivity | cell mediated |
| anaphylaxis | acute, sudden, rapidly progressive hives and respiratory distress |
| universal donor | type o |
| universal recipient | type ab |
| graft rejection- hyperacute | first week or when getting it |
| graft rejection- acute | first 100 days |
| graft rejection- chronic | always at risk |
Created by:
mls02744
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