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56 Cards in this Set
- Front
- Back
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WHAT ARE FIVE TYPES OF CONNECTIVE TISSUE?
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LOOSE
DENSE FIBROUS ELASTIC RETICULAR ADIPOSE |
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WHERE ARE LOOSE CONNECTIVE TISSUES FOUND?
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SURROUNDING NERVES, BLOOD VESSELS, BETWEEN MUSCLES, AND UNDER SKIN
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WHERE ARE DENSE FIBROUS CONNECTIVE TISSUES LOCATED?
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TENDONS, LIGAMENTS, HEART VALVES, SCLERA OF THE EYE, DEEP SKIN LAYERS
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WHERE ARE ELASTIC CONNECTIVE TISSUES LOCATED?
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LARGE ARTERIES, LOWER RESPIRATORY TRACT, BETWEEN VERTEBRA
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WHERE ARE RETICULAR CONNECTIVE TISSUES LOCATED?
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LYMPH NODES, LIVER, SPLEEN, THYMUS, AND BONE MARROW
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WHERE ARE ADIPOSE CONNECTIVE TISSUES LOCATED?
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HYPODERMIS, SURFACE OF THE HEART, OMENTUM, AROUND KIDNEYS, BACK OF EYEBALLS, SURROUNDING JOINTS
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WHAT IS THE MAIN STRUCTURE OF LOOSE CONNECTIVE TISSUE?
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MAINLY FIBROBLASTS WITH LESSER AMOUNTS OF COLLAGEN AND ELASTIN CELLS
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WHAT IS THE MAIN FUNCTION OF LOOSE CONNECTIVE TISSUE?
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BINDS ORGANS, HOLDS TISSUE FLUIDS, DIFFUSION
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WHAT IS THE MAIN STRUCTURE OF DENSE FIBROUS CONNECTIVE TISSUE?
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DENSELY-PACKED COLLAGEN FIBERS
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WHAT IS THE MAIN FUNCTION OF DENSE FIBROUS CONNECTIVE TISSUE?
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PROVIDES STRONG, FLEXIBLE SUPPORT
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WHAT IS THE STRUCTURE OF ELASTIC CONNECTIVE TISSUES?
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MAINLY IRREGULARLY ARRANGED ELASTIC FIBERS
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WHAT IS THE MAIN FUNCTION OF ELASTIC CONNECTIVE TISSUES?
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SUPPORTS, PROVIDES FRAMEWORK
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WHAT IS THE STRUCTURE OF RETICULAR CONNECTIVE TISSUES?
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RETICULAR FIBERS FORMING SUPPORTIVE NETWORK
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WHAT IS THE MAIN FUNCTION OF RETICULAR CONNECTIVE TISSUES?
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STORES, PHAGOCYTIC
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WHAT IS THE STRUCTURE OF ADIPOSE CONNECTIVE TISSUES?
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ADIPOSE CELLS
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WHAT IS THE MAIN FUNCTION OF ADIPOSE TISSUES?
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PROTECTS, FAT, INSULATES
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WHAT THREE THINGS ARE ALL MSENCHYMES COMPOSED OF?
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CELLS
FIBERS GROUND CELLS |
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WHAT ARE THE MAIN FUNCTIONS OF BLOOD?
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Homeostasis
O2 transport Body temp pH Fights infection |
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WHERE IS MOST OF THE BLOOD MADE?
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IN THE SKULL, RIBS AND STERNUM
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WHAT CELLS ARRISE FROM PLEURIPOTENTIAL STEM CELLS IN THE BONE MARROW?
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RBC'S
LYMPHOCYTES MONOCYTES GRANULOCYTES MAGAKARYOCYTES |
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WHAT ARE LYMPHOCYTES INVOLVED IN?
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MEMORY IMMUNITY
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WHAT DO MONOCYTES BECOME?
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MACROPHAGES
(ENF OF INFLAMMATORY RESPONSE) |
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WHAT ARE GRANULOCYTES?
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CONTAIN GRANUOLES
NEUTROPHILS ARE A TYPE OF GRANULOCYTE (EARLY STAGE OF INFLAMMATION AND INFECTION) |
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WHAT DIFFERENTIATES MEGAKARYOCYTES FROM THE OTHER CELLS THAT ARRISE FROM MARROW?
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MEGAKARYOCYTES DON'T LEAVE THE BONE MARROW. LITTLE PIECES EXTRUDE THROUGH THE BONE AND BUD OFF INTO PLATELETS
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HOW MANY KINDS OF TOLL RECEPTORS ARE THERE?
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11
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WHAT DOES TOLL 4 RECOGNIZE?
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A PIECE OF THE CELL WALL ON GRAM NEGATIVE CALLED LPS, LIPOPOLYSACHARIDE OR ENDOTOXIN
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WHAT DOES TOLL 9 RECOGNIZE?
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CERTAIN DNA IN BACTERIA
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WHAT DOES TOLL 8 RECOGNIZE?
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CERTAIN RNA IN BACTERIA
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WHAT ARE THE STEPS IN CLOT FORMATION?
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Platelet plug - a loose collection of platelets that cover the damaged area
Blood clotting occurs via coagulation factors Fibrin is activated from Fibrinogen Proteases when activated Perform limited proteolysis Fibrinogen (no activity) Make a couple of specific clips Remainder is Fibrin Fibrin interacts with other fibrin - crosslink - form a fibrin molecule Wrap around the platelets mechanically to withstand the force of the blood flow (Make it strong) |
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INFLAMMATORY MEDIATOR
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Responsible for one or more steps in the inflammatory response
Get repair materials to the wound site Routes blood flow to the wound site Allows materials to leak out from the venule |
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SYMPTOMS OF INFLAMMATION
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HEAT
REDNESS SWELLING PAIN LOSS OF FUNCTIONS |
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CHEMOTAXIS
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INFLAMMATORY CELLS MOVE IN RESPONSE TO CHEMICAL STIMULUS
EXAMPLES: ENDOTOXIN, COMPLEMENT PEPTIDE C5a, fMLP(TERMINAL TRIPEPTIDE ON BACTERIAL CELL), LEUKOTRIENE B4 CELLS EXPRESS RECEPTORS TO CHEMICAL STIMULI (WBCs) CELLS MOVE ALONG THE CONCENTRATION GRADIENT OF THE CHEMOTACTIC STIMULUS |
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HOW DOES AN ATTRACTED LEUCOCYTE MOVE TOWARD fMLP AT THE INFLAMMATION SITE?
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THE LEUKOCYTE HAS fMLP RECEPTORS THAT BIND THE fMLP AND MOVE IN THE DIRECTION OF THE GREATEST CONCENTRATION OF fMLP AS THE fMLP RECEPTORS UPREGULATE NEAR THE SITE OF BINDING
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RANK CHEMOTACTIC AGENTS IN ORDER FROM STRONGEST TO WEAKEST
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ENDOTOXIN>INTERLEUKIN-1>C5a>fMLP>TNFalpha>LTB4
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MOVEMENT OF CELLS TO THE INJURED AREA
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ROLLING - MOVEMENT TO THE AREA
ACTIVATION - ADHESION - Neutrophils have Selectins which bind to selective receptors called adhesions which allows cell/cell adhesion TRANSMIGRATION-moves through the gap b/t endothelial cells |
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ACTIONS OF NEUTROPHILS
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RECRUITMENT
PHAGOCYTOSIS REPIRATORY BURST CYTOKINE SECRETION |
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PHAGOCYTOSIS
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MACROPHAGES & NEUTROPHILS OCCASIONALLY RECOGNISE BACTERIA OR EXTRANEOUS FOREIGN MATERIAL
USUALLY, MICROORGANISMS MUST BE COATED WITH OPSININS BEFORE INFLAMMATORY CELLS RECOGNIZE THEM INFLAMMATORY CELLS HAVE RECEPTORS FOR THE OPSONINS -->RECOGNITION & PHAGOCYTOSIS |
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OPSININS
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Fc FRAGMENT OF IMMUNOGLOBULIN G (IgG) - NATURALLY -OCCURING ANTIBODY TO INGESTED PARTICLES
COMPLEMENT FRAGMENT C3b |
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STAGES OF PHAGOCYTOSIS
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RECOGNITION AND ATTACHEMENT
ENGULFMENT KILLING AND DEGREDATION |
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PROCESS FOR THE FORMATION OF OXYGEN RADICALS
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THE NADPH OXIDASE ENZYME IS COMPOSED OF A NUMBER OF DIFFERENT SUBUNITS
SUBUNITS COME TOGETHER AND BECOME AN ACTIVATED NADPH MOLECULE ACTIVATED NADPH OXIDASE CONVERTS O2 MOLECULES TO SUPEROXIDE ION O2- A SECOND ENZYME, SUPEROXIDE DISMUTASE CONVERTS THE SUPEROXIDE TO HYDROGEN PEROXIDE PEROXIDASE ENZYMES AND IRON FURTHUR CONVERT THE HYDROGEN PEROXIDE TO HYPOCHLORITE IONS AND HYDROXYL RADICALS O2 and H2O2 are very weak antibacterial agents So, OH or Ocl radicals are generated Bacteria have no defences against these latter two |
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TRUE OR FALSE
NADPH oxidase deficiency makes an individual more succeptable to bacterial infection |
TRUE
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_________ ARE ONLY PRESENT DURING INFLAMMATORY RESPONSE
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NEUTROPHILS
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______________ ARE PRESENT EVERYWHERE ALL THE TIME
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MACROPHAGES
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MONOCYTE
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CIRCULATING DORMANT MACROPHAGE
MACROPHAGES CAN ONLY FUNCTION IN THE TISSUE NOT IN THE BLOOD |
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ACTIONS OF ACTIVATED MACROPHAGE IN TISSUE INJURY
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TOXIC OXYGEN METABOLITES
PROTEASES NEUTROPHIL CHEMOTACTIC FACTORS COAGULATION FACTORS A.A. METABOLITES NITRIC OXIDE |
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ACTIONS OF ACTIVATED MACROPHAGE IN FIBROSIS
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GROWTH FACTORS (PDGF, FGF, TGFbeta)
FIBROGENIC CYTOKINES ANGIOGENESIS FACTORS (FGF) "REMODELING" COLLAGENASES |
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CHEMICAL MEDIATORS
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HUNDREDS
FOUND IN TEH BLOOD MADE IN THE LIVER AND WBCs MAY BE MADE IN THE ACTIVE STATE BUT ARE SEQUESTERED IN GRANUOLES(HISTAMINE, 5HT, LYSOSOMAL ENZYMES) MAY BE MADE AND STORED IN INACTIVE STATE(PROSTAGLANDINS, LTs, PAFs, ACTIVATED O2s, NITRIC OXIDE, CYTOKINES ALL ARE SHORT-LIVED START AND STOP INFLAMMATORY PROCESS QUICKLY FOR EACH MEDIATOR THERE IS AT LEAST ONE INHIBITOR |
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ACTIVATED HAGEMAN FACTOR
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ACTIVATES BRADYKININ WHICH CAUSES INCREASED VASCULAR PERMEABILITY
ACTIVATES PLASMIN WHICH BREAKS DOWN FIBRIN AND PROMOTES CHEMOTAXIS ACTIVATES FIBRIN FOR CLOTTING |
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COMPLEMENT AND COMPLEMENT COMPONENTS
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COMPLEMENT IS A SERIES OF 20 PROTEINS MADE IN THE LIVER
ALWAYS PRESENT IN THE PLASMA IN THE INACTIVE FORM COMPLEMENT COMPONENTS ARE INACTIVE UNTIL CLEAVED COMPONENT IS CLEAVED BY UPSTREAM MOLECULE LARGE FRAGMENT AQUIRES ENZYME ACTIVITY SMALL FRAGMENT IS ACTIVE AS ANAPHYLATOXIN UNTIL FRAGMENT(s) BLOCKED BY AN INHIBITOR |
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WHAT ARE THE FUNCTIONS OF OPSANIN, PHAGOCYTOSIS, AND MAC?
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As a result of the activation of complement proteins, many proteins activated with many different functions
Three to know: 1. Opsanin 2. Phagocytosis 3. MAC C3a - C3 activated works as a opsinin - coats bacteria for recognition C3b - active in phogocytosis - puts a hole in the bacterial wall - MAC membrane attack complex |
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HISTAMINE
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Histamine increases vascular permeability
Observable phenomenon Bradykinin and histamine do the same thing Need both so that you can still respond in the absence of one or the other When you have an infection and you want vascular permeability mast cells release histamine Over release of histamine - too much stimulation blocked airways etc A little is good - a lot is bad |
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EICOSANOIDS
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20-CARBON PHOSPHOLIPIDS
NEWLY-FORMED MEDIATORS COMPRISE PROSTAGLANDINS, THOMBOXANES, & LEUKOTRIENS DERIVED FROM NEUTROPHILS & MACROPHAGES IN INFLAMMATION Come from cell mebrane phosphlipids Phospholipases - arachidonic acid to make Eicosenoids Steroids inhibit Cyclooxygenase (COX) - NSAIDS work here, ASA, etc ASA irreverable inhibit and inactivate COX enzyme The rest are reversable COX 2 is only expressed during inflammation(was believed) but other effects were found Asthma drugs Lipoxygenase pathways - inhibit LTs |
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PLATELET ACTIVATING FACTOR (PAF)
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NEWLY-FORMED MEDIATOR
DERIVED FROM A VARIETY OF CELL TYPES CAN DO ALMOST ANYTHING IN THE INFLAMMATORY PROCESS |
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CYTOKINES
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MOST ARE SIMPLE POLYPEPTIDES OR GLYCOPROTEINS (MW<30KD)
PRODUCTION IS REGULATED BY INDUCING STIMULI AT THE LEVEL OF TRANSCRIPTION AND TRANSLATION (CONSTITUTIVE EXPRESSING IS UNCOMMON) PRODUCTION IS TRANSIENT AND ACTION RADIUS IS SHORT ACT BY BINDING TO HIGH-AFFINITY CELL-SURFACE RECEPTORS ACTIONS ATTRIBUTED TO ALTERED GENE EXPRESSION IN TARGET CELLS HORMONE WHICH ACTIVATES THE CELL |
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AN EXAMPLE OF CYTOKINES STIMULATING A MEMBRANE BOUND RECEPTOR
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Cytokines stimulate Janus Kinase,membrane bound receptor, Janus Kinase becomes phosphoralated which then binds to and activates STAT,transcription activator,
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Other important thinks to keep in mind with regards to inflammation
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Transudate - initial liquid and proteins that move into the wound area
Exudate - when the cells move into the wound area Diapedesis - move from blood into wounded area All is to kill bacteria and wound repair Important concepts - amplification - movement of receptors towards the invading bacteria Cascade- when you have a series of proteolysis reactions - activation of one - catalyses the activation of others All mediators have an inhibitor and are short lived to control inflammation Pre-cursors always there in inactive forms Sequestration - active but hidden Overlapping functions Mediators make cell move or secrete |
