ch 3 exam 1

leukocytosis

increase wbc

leukopenia

decreased WBC

causes of inflammation

immune response to infectious microorganisms

trauma

surgery

caustic chemicals

extremes of heat and cold

ischemic damage to body tissues

acute inflammation: onset, local and systemic signs, cellular infiltrate, tissue injury and fibrosis

fast, prominent, neutrophils, mat have extensive damage, limited fibrosis

chronic inflammation: onset, local and systemic signs, cellular infiltrate, tissue injury and fibrosis

slow, may be subtle, macrophages and lymphocytes, severe fibrosis and progressive inflammation

phases of acute inflammation

vascular phase: momentary vasoconstriction followed rapidly by vasodilation, increased vascular permeability

cellular phase: delivery of neutrophills MAT

Cellular phase MAT

Margination-WBC line up against inner wall of blood vessel

Adhesion- WBC adhere to endothelial cells of blood vessel wall

Transmigration- WBC change shape and squeeze though junctions between the endothelial cells to reach site of injury

hisamine

released from mast cells, earliest and strongest, vasodilation and increased capillary permeability

leukotrienes

airway smooth muscle contraction, vascular permeability, recruits neutrophils and eosinophils

cytokines

secreted from leukocytes, chemical messengers, premote fever and recruits immune cells

inflammatory phase

immediate, 3-5 days, vasodilation, recruits neutrophils, then macrophages

proliferative phase

around 3-5 days later for 2-3 weeks, granulation tissue formation, fibroblast activity, epithelialization, regulated by growth factors and cytokines

remodeling phase

collagen remodeling, tensile strength increases, blood supply decreases, scar formation

impaired wound healing by

malnutrition, impaired blood flow and O2 delivery, impaired inflammatory and immune responses, infection, wound separation, foreign bodies, age

viruses

DNR/RNA and protein coat, smallest, needs host to replicate, antivirals slow replication (influenza, common cold, HIV, measles)

Bacteria

cell w/o nucleus, gram +-, common on surfaces, antibiotics kill or slow down bacterial reproduction (strep, sinus & lung infections)

fungi

unicellular or multicellular contain membrane bound nucleus, infect body surfaces/ openings, antifungals destroy cell wall (athletes foot and yeast infection)

modes of transportation

inhalation, oral ingestion, dermal penetration, direct contact

antigen

substance that triggers an immune response

antobody

protein made by b cells, recognise, tage, and neutralize antigens

primary lymphoid organs

Bone marrow and thymus

peripheral or secondary lymphoid system

stores immune system cells, process antigens and promote interaction with mature immune cells

Colony Stimulating Factors CSFs

proteins that stimulate the bone marrow to make more blood cells

cytokines

small proteins that act as chemical messengers between immune cells

chemokines

guide immune cells during infection or injury

IgD

found on B lymphocytes, needed for maturation of T cells

Dosn’t activate immune system

Directs differentiation of B cells into plasma cells

IgE

allergic and hypersensitivity reactions

IgM

forms natural antibodies; prominent in early immune responses

presence indicates current infection

first antibody made by fetus

IgG

displays antiviral, antitoxin, and antibacterial properties, most abundant, able to cross placenta and provides passive immunity to fetus

IgA

protects mucous membranes, present in colostrum to protect infant from GI infections

Innate Immunity

Bodys first line of defense, natural and non-specific. Born with it, begins early nad rapid

Adaptive Immunity

acquired and particular, second line of defense, specific and has memory, usually delayed

Innate Immune Cells

granulocytes and monocytes

Tissue: mast cells, macrophages, dendritic cells (antigen presenting cells)

Antigen presenting cells

capture, process, and present an antigen to T-cell lymphocytes linking the innate immune system with adaptive

Dendritic