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Test 1- Bouma

Stress, Ischemia, Inflamm., Immunity, Infection

TermDefinition
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