Term
| where does inflammation occur, why, what does it involve, what regulates it |
|
Definition
vascularized CT responds to noxious stimuli. involves plasma, circulating cells, vessels and CT
mediated by chemicals from plasma and cells |
|
|
Term
| what are causes of inflammation (6) |
|
Definition
toxins from microbes of enivornment physical factors like heat or trauma microbes necrotic tissue foreign bodies immune response: hypersensitive, autoimmune, immune complex |
|
|
Term
| what are the function os fhte 1ummune response (4) |
|
Definition
protect healthy tissue by localising the isolating injured tissue inactivate toxins made by humoral factors and enzymes destories or limits growth of infectous agents prepares area for wound healing |
|
|
Term
| what are the down sides to inflammation, give an example (4) |
|
Definition
organ damage: myocarditis
excessive scar formation: keloids, contractures
fistula formation: chrons disease
infiltration and inflammation of healthy tissue: glomerulonephritis, arthritis, allergic reactions |
|
|
Term
| what are the reaction of vessels to infammation (7) |
|
Definition
accumulation of fluid leukocyte recruitment rubor: erythema calor: heat tumor: swelling dolor: pain loss of function: function laesa |
|
|
Term
| what is the time length of chronic vs acute inflammation |
|
Definition
chronic is days to years acute is minutes to days |
|
|
Term
| what are the 2 main characteristics of chronic and accute inflammation |
|
Definition
chronice: vascular perforationa and scaring, lymphocytes and macrophages
acute: fluid and plasm aprotein edudates neutrophillic leukocyte accumulation |
|
|
Term
| what is the general MOA of acute inflammation |
|
Definition
Vasoactive mediators (histamine from mast cells, leukotrienes) cause endothelial contraction
Contraction (vasodilation) opens space between cells allowing substances through that are bigger than normal and increases blood flow
This immediate transient response lasts for 15-30 min
Neutrophils arrive and recruit macrophages via cytokines (or endothelium changes)
Macrophages sustain the inflammation and vessel contraction
New vessel formation persists until intracellular junctions form |
|
|
Term
|
Definition
| fluid filled tumor/swelling due to new vessels because they are leaky and allow the plasma out. Could spread sutures apart. |
|
|
Term
| what are normal changes for a vessel |
|
Definition
| hydrostatic pressure and colloid osmotic pressure are in check not allowing protein leakage |
|
|
Term
| transudate: what is it, what qualifies it, what are the results of it |
|
Definition
o Fluid with low protein concentration and specific gravity of <1.012 o Secondary to hydrostatic imbalance o Fluid leaks from vessels into ECF due to: Decreased protein synthesis decreases colloid osmotic pressure. Increased hydrostatic pressure due to venous outflow obstruction |
|
|
Term
| edudate; what is it a sign on, what qualifies it, what is the reuslt of it |
|
Definition
o Big sign of inflammation o Inflammatory extravascular fluid has a high protein concentration, cellular debris, and specific gravity >1.020 o Secondary to alteration of vascular permeability o Fluid and proteins leak out due to: Vasodilation and stasis due to inflammation. Increased endothelial spaces due to inflammation |
|
|
Term
| edema: what is it, where does it come from, what activates it |
|
Definition
Big sign of inflammation
Inflammatory extravascular fluid has a high protein concentration, cellular debris, and specific gravity >1.020
Secondary to alteration of vascular permeability
Fluid and proteins leak out due to
Vasodilation and stasis due to inflammation
Increased endothelial spaces due to inflammation |
|
|
Term
|
Definition
o Vasodilation in arterioles then capillary beds o Slowing of circulation secondary to increased permeability of microvasculature resulting in outpour of protein into ECF o Stasis allowing leukocytes to stick to endothelium and migrate across vessel wall into interstitial tissue |
|
|
Term
|
Definition
| • Purulent inflammatory exudate rich in leukocytes, debris of dead cells and microbes |
|
|
Term
| what is rolling, adhesion, and transmigration dependent on |
|
Definition
|
|
Term
| why do neutrophils come first to an inflammatory site |
|
Definition
| rolling, adhesion, and transmigration are required on the arriving cell. neutrophils dont have to do this |
|
|
Term
| selectin: what is it, where is it, what locations, what types |
|
Definition
o Sugars on cells that bind sialylated forms of oligosaccharides o Stored on weibel-palade bodies. Histamine stimulates movement to cell border to be used.
endoderm E-selectin, P selecting platelets P selectin leukocytes L sekectin |
|
|
Term
| what are endothelial adhesion molecules, what do they do |
|
Definition
o Act as ligans for integrins like CAMs (on surface of cells) o Immunoglobin family o Major protein mediating transmigration (PECAM-1) o Help WBC bind other cells |
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|
Term
| integrans: what ate they, where are they, how are they acivated, where do they go |
|
Definition
o Transmembrane glycoproteins o Mostly on WBC with its ligand on the endothelium o They are always on WBC surface and not sequestered but don’t have a high binding affinity unless activated by histamine or thrombin o Bind ligands on endothelial cells, other leukocytes, and ECM |
|
|
Term
| what does rolling adhesion |
|
Definition
| neutrophils, monocytes, eosinophils, lymphocytes |
|
|
Term
| transmigration: aka, function, MOA |
|
Definition
•Adhesion molecules help WBC get between cells. proteases (ex: collagenases) secreted to digest the basement membrane and let the cell get through
diapedisis |
|
|
Term
| activation of rolling or transmigration by leukocytes |
|
Definition
• Leukocytes respond with oxidative burse to… o Destroy invading microbes o Degranulate to release digestive enzymes that help clear dead tissue and microbes o Elaborate arachidonic acid metabolites to recruit other cells involved in inflammation repair |
|
|
Term
| what is the most common type of activation in transmigration, exmples too |
|
Definition
o G-protein signals the release of Ca from the cell stores signaling Arachadonic acid Degranulation Opsin release serum proteins that bind targets for phagocytosis • IgG can also serve as this tag |
|
|
Term
| what helps phagocyte recognize particles, what is it made of, give examples |
|
Definition
opsonin, serum protein Ig Fc region, C3b fragment of complement, collectins bind microbe wall sugar |
|
|
Term
| how do phagocytes kills stuff |
|
Definition
A. vacuole with microbe (phagosome) fills with lysosomal granules B. oxidative burse stimulated via NADPH oxidase C. NADPH oxidase converts oxygen to superoxide D. superoxide converts to hydrogen peroxide E. hydrogen peroxide converts to a hydroxyl radical F. asurophilic granules of neutrophils myeloperoxidase uses halides (Cl ) to make hypochlororous radical (bleach) G. HOCl- does most microbe killing |
|
|
Term
| what are other ways of killing other than phagocytes |
|
Definition
o Neutrophil extracellular traps (NETs): chromatin and anti-microbial granule proteins o Bactericidial permeability increasing protein: activates phospholipase o Lysosome: decrades bacteria oligosaccharides o Major basic protein: in eosinophils, kills invasive parasites o Defensins: forms pores in microbial membranes |
|
|
Term
| resident cells: functions, what are they |
|
Definition
initiate acute inflammation
mast cells and macriphages |
|
|
Term
| mast cells, what to they react to, what do they do |
|
Definition
o React to physical trauma, complement products, microbes, neuropeptides o Release histamine, leukotrienes, enzymes, cytokines (TNF, IL-1, chemokines) |
|
|
Term
| macrophages what do the recognize what do they do |
|
Definition
| o Recognize microbes and secrete cytokines causing inflammation |
|
|
Term
| how is the inflammatry response terminated |
|
Definition
| Due to short half-life of chemical mediators of inflammation and switch to production of anti-inflammatory mediators |
|
|
Term
| where do cell derived mediators come from |
|
Definition
o Locally made by cells at inflammation site From platelets, neutrophils, monocytes, macrophages, mast cells o Derived from circulating inactive precursors Made in the liver Ex: complement, kinins |
|
|
Term
| how are cell derived mediators produced |
|
Definition
o Sequestered in intracellular granules and stored until used Ex: histamine in mas cell granules o Made upon request Ex: prostaglandins, cytokines |
|
|
Term
| how do cell derived mediators work |
|
Definition
o Can act on one or a few cell types with different actions in each cell o Can have direct enzymatic or toxic activity without required binding to receptor first |
|
|
Term
| how are cell derived mediators regulated |
|
Definition
| o Quickly decay, are inactivated by enzymes, are eliminated, or are inhibited |
|
|
Term
| what are the vasoactive amines |
|
Definition
cell derived mediators histamine and serotonin |
|
|
Term
| where is histamine made, what does it do |
|
Definition
o Made resident mast cells (and basophils and platelets which circulate)
vasodilation and permeability increase Venular endothelial contraction and formation of interendothelial gaps |
|
|
Term
| what is histamine activated and inactivated by |
|
Definition
Physical injury, trauma, or heat Immune reactions binding IgE to Fc receptor on mast cell C3a and C5a anaphylatoxins Leukocyte derived histamine releasing proteins Neuropeptides (substance P) Cytokines IL1 and IL8 Physical injury, trauma, or heat Immune reactions binding IgE to Fc receptor on mast cell C3a and C5a anaphylatoxins Leukocyte derived histamine releasing proteins Neuropeptides (substance P) Cytokines IL1 and IL8
Inactivated by histaminase |
|
|
Term
| where is serotonin made what does it do |
|
Definition
o In platelet granules released during aggregation Induces vasoconstriction during clotting (notes say vasodilation and increased permeability) o Made in some neurons and enterochromaffin cells Neurotransmitter that regulates intestinal motility |
|
|
Term
| ecosanoids: what are they, what do they do, where do they come from, how are they regulated |
|
Definition
o AA metabolite cell mediators o Initiate and inhibit inflammation o Increases synthesis at sites of inflammation o Released from leukocytes, mast cells, endothelial cells, and platelets o Decay spontaneously or are enzymatically destroyed |
|
|
Term
| explain the process of ecosanoid formation up until the splitting point |
|
Definition
• Phospholipases are activated by physical, chemical, or inflammatory mediator stimuli o Inhibited by steroids • Phospholipases release membrane phospholipid arachadonic acid (derived from linoleic acid) • Arachadonic acid is converted to o Cyclooxygenase and 5-lipooxygenase |
|
|
Term
| explain the path of cycloogygenase until its three terminal pathways and their functions |
|
Definition
Cyclooxygenase is converted to prostaglandin G2 then prostaglandin H2 Prostaglandin H2 is turned into different products • Prostacyclin GI2 via prostacyclin synthase in endothelial cells o Vasodilation, inhibits platelet aggregation • Thromboxane A2 via thromboxane synthase in platelets o vasoconstriction, platelet aggregation • Prostacyclin GD2 + GE2 in mast cells (notes say macrophages, endothelium, and platelets) o vasodilation, increase vascular permeability, pain, fever |
|
|
Term
| explain the pathway of lipooxygenase until its terminal products and their functions |
|
Definition
Is converted to 5-HPETE in leukocytes which is converted to • 12-lipooxygenase which is converted to o Lipotoxin A4 +B4 in platelets and neutrophils inhibit neutrophil adhesion and chemotaxis platelets need neutrophils to do final activation • Leukotriene A4 which is converted to o Leukotriene B4 in neutrophils causes chemotaxis to recruit neutrophils o Leukotriene C4-E4 in mast cells bronchospasm, increased vascular permeability, vasoconstriction |
|
|
Term
| where is platelet activating factor made, how |
|
Definition
• generated from membrane phospholipids of neutrophils, monocytes, basophils, endothelial cells, and platelets • phospholipase A2 releases PAF from the membrane |
|
|
Term
| what does platelet activating factor do |
|
Definition
o Platelet activation o causes bronchioconstriction (more than histamine) o vascular effects low levels: vasodilation, increased permeability high levels: vasoconstriction, bronchoconstriction o stimulates synthesis of other mediators o enhances leukocyte adhesion, chemotaxis, leukocyte degranulation, and respiratory burst |
|
|
Term
| what cytokines are major players in acute inflammation |
|
Definition
| TNF, IL-1, IL-6, IL-17, chemokines |
|
|
Term
| what cytokines are major players in chronic inflammation |
|
Definition
|
|
Term
| INF and IL1: what stimulates production, what makes them |
|
Definition
o Produced by activated macrophages, mast cells, endothelial cells o Secreted via stimulation by microbial products, immune complexes IL-1 is also released from the imflammasome (see above) |
|
|
Term
| enothelial effects of TNF and IL-1 |
|
Definition
• Leukocyte adherence • Prostaglandin GI2 synthesis • Coagulation activation, anticoagulant decrease (via TNF) • IL-1, IL-8, IL-6, PDGF increase |
|
|
Term
| systemic effects of TNF and IL-1, include any helper mediators too |
|
Definition
• Fever, lethargy, decreased appetite (IL-1, IL-6, TNF) • Increased acute phase protein in liver (IL-1, IL-6) • Hemodynamic effects: shock • decreased BP (TNF) • Cachexia: metabolic wasting • Neutrophilia • Insulin release in skeletal muscle (TNF, IL-1) |
|
|
Term
| fibroblast affects of IL-1 |
|
Definition
• Proliferation • Collagenase and collagen increase • Protease increase • PGE synthesis |
|
|
Term
| leukocyte effects of TNF and IL1 |
|
Definition
• Activation (TNF, IL-1) • stimulate marrow precursors to produce more leukocytes to replace the ones consumed in inflammation (TNF, IL-1, IL-6) • Stimulate expression of adhesion molecules on endothelial cells • Increase IL-6 and IL-6 |
|
|
Term
| how do chemokines work, what types are there |
|
Definition
Bind to G protein receptor (CXCr4 or CCR5) on target cell
CXC and CC |
|
|
Term
| CXC: what does it act on, what makes it, what stimuli |
|
Definition
• Act mostly on neutrophils • Produced by macrophages, endothelial cells, mast cells, and fibroblasts in response to IL-1 and TNF |
|
|
Term
| CC chemokine: 3 functions and their MOA |
|
Definition
• Monocyte chemoattractant o Include monocyte chemoattractant protein-1 and macrophage inflammatory protein-1a • Memory CD4 chemo attractant o RANTES: Regulated on activation normal T cell expressed and secreted • Eosinophil chemoattractant o Via eotaxin |
|
|
Term
| functions of both types of chemokines |
|
Definition
Chemoattractants for leukocytes Activate leukocytes Control development of T vs B lymphocytes in nodes and spleen |
|
|
Term
| what enzymes makes ROS, where, what stimuli |
|
Definition
• made with NADPH oxidase (phagocyte oxidase) in lysosome • released from neutrophils and macrophages via stimulifrom microbes, immune complexes, cytokines |
|
|
Term
| what are the functions of high and low levels of ROS |
|
Definition
o Low levels: increase chemokine, cytokine, adhesion molecule expression o High levels: injury Endothelial damage via thrombosis and increased permeability Protease activation and antiprotease activation breaks down ECM Direct cell injury |
|
|
Term
| what are the functions of NO |
|
Definition
o Regulates neurotransmitter release and blood flow in CNS o Used in macrophages as (microbocidal) cytotoxic agent o Relaxes smooth muscle in endothelial cells causing vasodilation o Antagonize platelet adhesion, aggregation, and degranulation o Reduce leukocyte recruitment |
|
|
Term
|
Definition
| o Made on demant from L-arginine + O2 + NADPH + nitric oxide synthase (NOS) |
|
|
Term
| function of complement C1-9 |
|
Definition
o Activated by proteolysis o Cause MAC attack: lysis of microbe |
|
|
Term
| C3 is activated by three pathways, explain them |
|
Definition
Classic complement pathway: triggered when C1 encounters antigen-antibody complex Alternate plathway: triggered when bacterial product encounters properdin and Factors B and D Lectin pathway: triggered when plasma lectin binds to mannose on microbe which starts the classic pathway |
|
|
Term
| once activated, C3 goes to microbe surface then what |
|
Definition
C3 convertase which cleaves it into C3a and C3b C5 convertase which cleaves it into C5a and C5b |
|
|
Term
| vascular effects of complements |
|
Definition
(C3a and C5a) • Induce mast cells to release histamine increasing permeability with vasodilation • Can cause symptoms like anaphylaxis • C5a activates lipooxygenase pathway which makes more inflammatory mediators |
|
|
Term
| laukocyte effects of complements |
|
Definition
(C5a, C3a, C4a) • Activate leukocytes • Increase adhesion to endothelium • Chemoattractant to neutrophils, monocytes, eosinophils, and basophils |
|
|
Term
| phagocyte effects of complements |
|
Definition
| • C3b acts as opsonin which makes phagocytosis easier for neutrophils and macrophages |
|
|
Term
| MAC effects of complements |
|
Definition
(C9) • Needs C6-8 to activate it • Kills bacteria by making pores and disrupting osmotic balance |
|
|
Term
| hageman factor: where is it made, what does it do |
|
Definition
o Made in liver and circulates inactive until it finds collagen, BM, or activated platelets o Initiates kinin system and clotting system, fibrinolytic system, complement system |
|
|
Term
|
Definition
Bradykinin is formed from its precursor (HMW kininogen) Bradykinin causes increased vascular permeability, arteriolar dilation, bronchial contraction Kallikerin is intermediate is made and activates Hageman factor to create a loop Bradykinin is degraded by kinases quickly |
|
|
Term
| explain the clotting system |
|
Definition
Thrombin • cleaves fibrinogen which makes fibrin clots • binds to platelets, endothelial cells and enhances leukocyte adhesion • generates fibrinopeptides during fibrinogen cleavage that increase vascular permeability • cleaves C5 to C5a
Factor Xa • causes increased vascular permeability and leukocyte emigration |
|
|
Term
| explain the fibrinolytic system |
|
Definition
Plasminogen activator is released from endothelium, leukocytes and tissues Activated by kallikerin Cleaves fibrin and lyses clots Cleaves C3 into C3a causing vasodilation and increase permeavility |
|
|
Term
| what are the antiinflammatory cell mediators. what do they do |
|
Definition
• Lipoxins: see arachidonic derived mediators • IL-10: down regulate response of macrophages • TGF-B: helps in fibrosis tissue repair after inflammation |
|
|
Term
| what cells or molecules are involved in acute respiratory distress syndrom |
|
Definition
|
|
Term
| what cells or molecules are involved in acute transplant rejection |
|
Definition
| lymphocytes, andibodies, complement |
|
|
Term
| what cells or molecules are involved in asthma |
|
Definition
|
|
Term
| what cells or molecules are involved in glomerulnopheritis |
|
Definition
| antibodies, complement, neutrophils, monocytes |
|
|
Term
| what cells or molecules are involved in septic shock |
|
Definition
|
|
Term
| what cells or molecules are involved in athlerosclerosis |
|
Definition
| macrophages and lymphocytes |
|
|
Term
| what cells or molecules are involved in primary fibrosis |
|
Definition
| macrophages and fibroblasts |
|
|
Term
| what cells or molecules are involved in chronic transplate rejection |
|
Definition
| lymphocytes, macrophages, cytokines |
|
|
Term
| what cells or molecules are involved in RA |
|
Definition
| lymphocytes, macrophages, antibodies |
|
|
Term
| chrnic inflammation: length, three characteristics |
|
Definition
• Infiltration with mononuclear cells o macrophages, lymphocytes, plasma cells • Tissue destruction o Due to inflammatory products • Repair o new vessel proliferation (angiogenesis) o fibrosis |
|
|
Term
| what does chronic inflammation happen |
|
Definition
persistant infection immune mediated inflammatory diseases prolonged exposure to toxic agents |
|
|
Term
| give examples of persistant infections that cause chronic inflammation |
|
Definition
o Mycobacterium tuberculosis, treponema pallidum (syphilis), some viruses and fungi o T lymphocyte mediated delayed type hypersensitivity |
|
|
Term
| give examples of immune inflammatory disease that cause chronic inflammation |
|
Definition
o Autoimmune reactions Rheumatoid arthritis, IBS, psoriasis o Allergic diseases Bronchial asthma Mixed acute and chronic symptoms |
|
|
Term
| what is the dominant cell of chronic inflammation |
|
Definition
|
|
Term
| what is the mononuclear phagocyte / reticular endothelial system |
|
Definition
Macrophages usually hang out in CT of spleen, liver, and lymphnodes There are also some around the tissues to clean up particulates and kill microbes |
|
|
Term
| explain macrophage production |
|
Definition
Come from precursors in marrow that release monocytes into blood Arrive at site of injury in 24-48 hours and mature into macrophages |
|
|
Term
| how are macrophages classically activated, what do they do |
|
Definition
• Stimulated by endotoxin, T cell signals, INF-γ, particulates • Production of products for microbe digestion o lysosomal enzymes, NO, ROS • Secrete eicosanoids, cytokines and complements to stimulate inflammation • Display T antigens to T cells and respond to their signsls |
|
|
Term
| how are macrophages alternativly activated what do they do |
|
Definition
• Stimulated by InF-γ, IL-4, IL-3, T cells, mast cells, and eosinophils • Secrete growth factors for angiogenesis • Activate fibroblasts to stimulate collage synthesis • Classic activation can turn into alternate later |
|
|
Term
| how do lymphocytes sustain chronic inflammation |
|
Definition
Macrophages display antigens stimulate T cell T cell produces INF-γ to activate macrophage |
|
|
Term
| what are plasma cells, what do they do |
|
Definition
o Terminally differentiated T cells o Produce antibodies against antigens in inflammatory site |
|
|
Term
| eosinophils: location, function |
|
Definition
o Usually around parasitic infections or IgE mediated allergic reactions o Travel on adhesion molecules and towards eotaxn chemokines o Granules have major basic protein Charged cationic protein Parasite toxin Causes epithelial cell necrosis |
|
|
Term
| mast cells: location, function |
|
Definition
o Distributed in CT o Participate in acute and chronic inflammatory response o Produce inflammatory cytokines o Has IgE antibody for environmental antigens when IgE encouters mast cell it releases histamine and causes acute inflammation too much of this can cause anaphylactic shock |
|
|
Term
| what are the morphological patterns of inflammation |
|
Definition
| serous, fibrinous, suppurative, ulceration, granulomatous |
|
|
Term
| serous inflammation: characterized by, develops intp, morphology |
|
Definition
• Serous cavity is filled with protein poor • from either serum or mesothelial cell secretions
• increased vascular permeability
• skin blister |
|
|
Term
| fibrinous inflammation: characterized by, develops intp, morphology |
|
Definition
• fibrin can be seen in the ECF • seen on meningies, pericardium, and pleura
• greater vascular permeability that allows fibrinogen to escape
• fibrinous pericarditis • may lead to dangerous adhesions that restrict organ function |
|
|
Term
| suppurative inflammation: characterized by, develops intp, morphology |
|
Definition
• large amounts of purulent exudate (pus) containing neutrophils, necrotic cells, and edema fluid • abscess = focal collection of pus
• pyogenic organisms (e.g., S. aureus)
• skin abscess • scaring in the future |
|
|
Term
| ulcerative inflammation: characterized by, develops intp, morphology, example |
|
Definition
• epithelial surface becomes necrotic and eroded
• sloughing of necrosed and inflammatory tissue near the surface
• peptic ulcer • stasis ulcers (diabetics) |
|
|
Term
| granulomatous inflammation: characterized by, develops intp, example |
|
Definition
• aggregates of activated macrophages that assume an epithelioid appearance (are flat like squamous cells) • macrophages may fuse to form multinucleate giant cells
• persistent T-cell response to microbes and foreign bodies (attempting to “wall off” invader)
• persistent T-cell response to microbes and foreign bodies (attempting to “wall off” invader) |
|
|
Term
| what cytokines have a role in the acute phase reaction, what is their role |
|
Definition
TNF and IL-1 have similar functions
IL-6 stimulates hepatic synthesis of plasma proteins |
|
|
Term
| explain how a fever is produced |
|
Definition
o Bacterial products (like LPS layer) release IL-1 and TNF (endogenous pyrogens) o IL-1 and TNF increase cyclooxygenases which convert AA into prostaglandins o PGE2 stimulates neurotransmitters that increase the temp set point in the hypothalamus o Fever helps fight off the organisms |
|
|
Term
| what are the acute phase proteins, what are the released by, from where |
|
Definition
IL-6 in hepatocytes
o C-Reactive protein o Fibrinogen o Serum amyloid A |
|
|
Term
| c reactive protein: function, interpertation |
|
Definition
Measure of inflammation Marker for necrosis and disease activity Elevation indicates increased risk for MI or stroke |
|
|
Term
| fibrinogen: function, interpertation |
|
Definition
Increased during inflammation Binds to RBC and causes them to stack (rouleaux) and sediment Basis of erythrocyte sedimentation rate lab test (higher in women) |
|
|
Term
| serum amyloid A: function, staining |
|
Definition
Replaces apolipoprotein to help target lipids to macrophages for energy source Stained with congo red. Shows green in polarized light |
|
|
Term
| what are normal, infectous, and super nigh WBC counts |
|
Definition
Normal 4,000 – 11,000 cells/uL Normal infection levels 15,000 – 20,000 cells/mL Extraordinary levels 40,000 – 100,000 cells/mL |
|
|
Term
| what is a super high WBC count called, why |
|
Definition
| • Leukemoid reactions: levels of leukocytes seen in leukemia because the cancer is WBC reproducing at high rates |
|
|
Term
| what are the causes of leukocytosis/neutropenia |
|
Definition
Accelerated release of cells (due to cytokines and increased colony stimulating factors (CSFs)) from the marrow post-mitotic pool Increased lymphocytes are associated with viral infections Increased neutrophils are associated with bacterial infection and acute inflammation |
|
|
Term
| what does shift left mean |
|
Definition
| presence of immature cells |
|
|
Term
| what is the concern about immature leukocytes in the blood |
|
Definition
Asurophilic granules arise when these immature leukocytes mature in the bood Dhole bodies: Blue cytoplasmic inclusions that are remnents of the ER |
|
|
Term
|
Definition
o Can come from drug therapy Catecholamines, lithium, corticosteroids Inhibit adhesion molecules and release of neutrophils from migrating pools |
|
|
Term
|
Definition
| o Associated with type I and II hypersensitivity (allergic reaction, asthma) and parasite infections |
|
|
Term
| leukopenia: definition, cause |
|
Definition
o Decrease in WBC o Associated with some viral infections, typhoid fever, rickettsiae, some protozoa |
|
|
Term
| what are other symptoms of acute phase reaction |
|
Definition
o Increase HR and BP o Decreased swelling o Shivering, Rigors, chills o Anorexia, malaise o Sepsis |
|
|