Chapter 16 Micro

jennraq2u's version from 2015-10-17 02:34


Question Answer
innate immunitydefenses present @birth;skin/membranes/fever/inflammation/anti-micro subst
adaptive immunity (slower response)specific response 2 specific micr-O breached innate immunity defenses
toll-like receptors (TLRs) (activates innate)recognizes pathogens/activates immune response against those pathogens
PAMP (pathogen associated molecular patterns)molecules present on pathogens and not self
cytokinesproteins regulate the intensity/duration of immune responses
dermisskin's inner thicker poriton; made of connective tissue
epidermisouter/thinner pt/tighlty packed epithelial cells/dead top layer has keratin
mucous membranesepithelial layer/underlying connective tissue layer; secret mucous(1st Line of D
mucusglycoprotein r/t goblet cells; Prevents tracks from drying out;
lacrimal appartuscontinous draining of tears=keeps micr-O from settling; dilutes irritants
saliva (antibody Immunoglobin A)dilutes micr-O surface of teeth/mouth ; prevents colonization of Micro-O
ciliamove synchronously=propel dust/micr-O upward to throat away from GI/Resp
ciliiary escalatorcouging/sneezing speed up rate of 1 2 3 cm/hr;
epiglotttiscovers larynx r/t swallowing; prevents micro-o entering lower resp tract
lysozyme (breaks peptiglycan in cell wall)enzyme breaks down gram-(+) cellwalls & to a lesser extent gram(-)
vaginal secretionslactic acid; ph inhibits micr-O growth& same for cervical mucus too
normal microbiotaprevent overgrowth;alter ph O2 avaliability; make harmful things 4 pathogens
Granulocyteslarge graules visible under light microscope after staining (3kinds=NBE)
neutrophilsstain pale lilac; 2-5lobes;INTIAL stage of infection; highly phagocytic/motile
basophilsblue/purple stain; release histamine & substances r/t inflamation/ALLErgic
Eosinophilsstain red/orange; produce toxic proteins; discharge peroxide ions to kill invade
Agranulocytesgranules NOT visible; (3Kinds=monyctes, dendritic cells, & lymphoctyes)
monocytesNOT actively phagocytic until leave blood & mature into Macrophages
macrophagesphagocytic cell; mature monocyte
dendrtiic cells (phagocytizes)mostly @ eperdermis of skin/MM/thymus/lymph nodes; iniate adaptive immuni
lymphoctyesnatural killer cells/ T Cells / & B Cells
Natural Killer (NK) cellsattack celsl w/ abnormal or unusual plasma membrane proteins; vesicles/toxic
perforininserts in plasma membrane @ target cell=channels in membrane=cytolysis
granzymesprotein-digesting enzymes induce apoptosis/self-destruction
phagocytescells perform phagocytosis collectively;WBCs or derivatives of WBCs
fixed macrophages (histiocytes)already live in certain pt of body; dont have to arrive; Liver/lungs/etc
free(wandering) macrophagesroam tissues & gather @ site of infection
Intial Phase of INfectionGraunlocytes (neutrophils dominate site of infection)
As Infection ProgressesMacrophages domoinate(=increased # of monocytes r/t differential WBC count
chemotaxischemical attraction of phagocyts 2 micr-O
adherence attachment of phagocyts plasma membrane 2 surface of micr-O/foreign mater
opsonizationcoating process promotes attacthment of micr-O 2 phagocyte
ingestionplasma membrane extends (projections) psudopods that engulf micr-O
inflammationr/t 4 S/S(redness/pain/heat/swelling & soemtimes 5th=loss of function)
Function Inflammation1)Destroy/remove Micr-o 2)limit/walling off injurious agent 3)repair/replace tissue damaged
acute phase proteinsinduce local & systemic responses r/t inflammation
Increased Permeabilitygood stuff from blood gets to pass thru walls of BV to inured area for help
histaminevasodilation;present in many cells, like MAST in connective tissue, basophils & platelets;
kininscause vasodilation; @plasma; help w/ chemostaxis by attracting Neutropils to injury area
prostaglandinsreleased by damged cells; help phagocytes move thru capillary walls
leukotrinesmade by MAST cells; help attach phagocytes to pathogens
abscesslocalized accumulation of puss r/t boils & pustules
marginationphagocytes stick to entothlium of BV
chillshivering as body temp RISES!
crisisbody temp is falling
complement systemnot adpatable & doesn't change over lifetime=innate immune system(kills via cytolysis*inflammation*phagocytoisis/prevent damage 2 tissues
classic pathwayanti-b bind to antigens(microbes) =1)Antiboides attach to antigens(2)Activated C1 activates C2etc(3)C2a&C4b=activate C3(cytolysis/inflammation/opsonization)
Alternative PathwayNO anti-B! Activated by contact b/t proteins&pathogen=C3+FactorB/D/P*C3splits into fragments=C3a=inflammation&C3bcytolysis/opsoinzation
Lectin Pathwaymannose-binding lectin binds 2 mannose on surface of microbe=enhances phagocytosis/activates complement
lectinsproteins that bind to carbs on a CELL not ANTi-b
interferoninterfere w/ viral (x); not virus specific=used for diff't virusesa
antiviral proteins (AVP)disrupt various stages of viral (X)
antimicrobial peptidesbroad spectrum agisnt pathogens all kinds; inhbit cell wall/forming pores/destroying DNA/RNA. Made from ribosoes