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325 Cards in this Set
- Front
- Back
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Phosphoinositide-3-kinase/AKT
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physiologic cardiomyocyte hypertrophy
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Pathologic cardiomyocytehypertrophy
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g-protein pathway
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Concentric heart hypertrophy
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pressure overload, HTN, Valve stenosis
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Eccentric heart hypertrophy
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volume overload
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Estrogen hyperplasia
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endometrium/abnormal bleeding
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DHT
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Prostate hyperplasia
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marrow hyperplasia
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erythropoeitin
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Adrenal/thyroid hyperplasia
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ACTH, TSH (pituitary)
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cause of hyperthyroidism or chushings
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increased cortisol, thyroid hyperplasia
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E6, E7
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HPV genes, inhibit cell cycle inhibitors
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Charcot-marie tooth atrophy
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myelin defect sensory and motor neurons
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Werding Hoffman/ SMA
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Hereditary loss of motor neuron atrophy
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senile brain atrophy
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atrohphy from chronic escmeia
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Marasmus
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Severe protein/cal manutrition/ Lipofuscin
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cachexia
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severe MM wasting UB pathway associated with chronic inflammation
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columnar to squamous metaplasia
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respiratory passages of smoker/inhalant
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cuboid to squamous metaplasia
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blocked ducts of glands
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trasnitional to squamous
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urinary bladder chronic inflammation
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barrett metaplasia
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glandular metaplasia. squamous epi to columnar. CAN be dystrophic eventually
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Myositis ossificans
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bone laide wher tissue has been (dystrophic calcification)
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chromatin clumping
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pyknosis- reversible cell infuryl
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nuclear disollution
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irreversible cell injury
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mitochondrial swelling
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mitochondrial dysfunction
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ATGs
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Genes that control autophagy- activated by starvatino
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2 necrosis methods
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autolysis or emigrated leukocytes
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necrosis morphology
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eosinophilic, motheaten, calcified dead cells, nuclear changes
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Karyolysis, phyknosis, Karrerhexis
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fading, Clumping/shrinking ( happens with decreased pH), fragmentation of pyknoit nucleus
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Coagulative necrosis
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MI, hypoxia, white, solid, cell outlines, cleared via phagocytosis, general organ necrosis.
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liquefactive necrosis
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CNS, Abcesses
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Gangrene
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Surgical term, Wet= infection on necrosis
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caseous necrosis
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TB, Micoses, Granuloma, white cheese, fragment cells, amorphous , dystrophic calcification (can see on x-ray)
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Fat necrosis
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trauma, pancreatitis, Ca saponification- hard spots
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decreased atp pathway
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decreased Na pump actvity- Increase water/Na, K efflux,- hydropic change,
Ca pump fails- increased cytoplasmic ca Ribosomes detach- decreased apoprotein- steatosis decreased glycogen- increased anaerobic glycolysis- decreased pH- pyknosis |
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Mitochondrial damage pathway
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permeable transition pore opens- lossof proton gradient for oxphos- decreased ATP (decreased atp pathway)
Cytochrome C released- activates caspases and apoptosis pathway |
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Cyanide poisoning
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poison cytochrom oxidase- decrease atp- (atp pathway)
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calcium homeostasis loss pathway
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increase permeability- cyt C or caspase activation- apoptosis,
Ca is 2nd messenger for PLA2 activation as well as Proteas,ATPase PM disruption- decreased atp- decreased na/k echange- swelling |
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OH- sources
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uv/xrays on H20 and the Fenton Reaction
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NO* sources
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Metabolites in monocytes/ neutrophils
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02 sources
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neutrophil oxidative burst
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CCL4/ CYP450 pathway
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breakdown ER membrane- polysomes detach- decreased protein, increased lipid (steatosis)
-releasee lipid peroxidation products fro SER (02*) PM damage- increase Na/Ca leads to hydropic change- massive increase in Ca Mito damage- cell death |
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Acetamenophen poison
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Acet- CYP450= NAPQI (toxin), CHS reduces, too much of this and you get massive cell necrosis
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Radicals pathological effects
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1- lipid membrane peroxidation- neccrosis/ cyt C apoptosis
2-Oxidtion/midificatio of proteins- P53 Apoptosis 3- DNA lesions- apoptosis/malignancy |
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Ceruloplasmin
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binds to cu to keep it from being toxic
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Catalase
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in peroxisome- breaks h202 (peroxide)
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SOD
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in moto/cytosol converts superoxide to H202
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GSH i
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in mito, converts hydroxyl to h2o2, which is broken down to H2o, and O2
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Consequences of ROS damage
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1- Mitochondria can't make ATP
2PM damage- leaks 3 Lysosome M loss- acid hydrolyses leak out |
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Causes of reperfusion damage
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1- increases ROS/RNS
2- increased PMNs (ROS) by cytokines from ischemic tissue 3- activation of compliment |
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Perfusion injury pathogenesis
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mito shock, Increased ROS, Increased Ca, Rapid PH change, inflammation- disrupts mito pore, causes hypercontracture- death
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Rxn to misfolded proteins
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increased chaperones
activate UB degredation decreased protein synthesis, activate caspases- apoptosis |
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amyloid
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misfolded protein outside of cell causes cell damage
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3 shock consequences
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decreased perfusion- hypoxia- decreased ATP
acidemia- pyknosis, lysis |
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Cardiomyocyte shock
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Pump failure, infarct, myocarditis, arrythmeas
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Obstructive shock
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Blockage return to L atria,
Tamponade, Tension pneumothorax |
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Hypovolemic shock/hemmorhagic
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>20% blood loss
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Distribution shock
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Anaphylactic- IgE/Eiosinophils
Neurogenic- loss of vessel tone- decreased perfusion |
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increased catecholamines
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vasodilation- cool,clammy, blue, rapid HR
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Non-progressive shock
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Neurohumoral maintenance of CO
NE @ alpha 1- vaso constriction increased HR/BP |
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Progressive Shock
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Renal insufficiency- endothelial damage, hypoxia, organfailure, blood pooling, decreased CO
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Irreversible shock w/cytokines
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membrane rupture- lysozyme leak,
Vasodilators, Increase permeability IL1/6, NO, PAF, ROS |
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CNS shock damage
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Ischemia Necrosis
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Lungs shock damage
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diffuse alveolar damage
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heart/gut shock damage
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coagulative necrosis, hemorrhage
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Suprarenal shock damage
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lipid depletion
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kidney shock damage
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acute tubular necrosis
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Liver shock damage
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steatosis
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Periphery shock damage
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DIC
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C3a, C5a
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Complement cytokine for vasodilation, inflammation
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C3b
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complement cytokine for opsonization, phagocytosis
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cytotoxic XII
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increased thrombosis/ischemia/dic
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IL10, sTNFR
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Anti-inflammatory cytokines with PMN activation
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cytokines from neutrophil for Macrophage activation
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TNF/IL1
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TNF/IL1 cytokines:
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IL1,6; NO, PAF, ROS-
Vasodilation, Increased permeability, decreased perfusion |
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Sepsis/Complement activates endothelium- cytokines:
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C3a, C3b, C5a, XII, monocyte, neutrophil activation
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Apoptotic cell histology
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single round cell, intensely eiosinophilic w/ dense pyknotic nucleus (if in liver: viral hep)
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FasL/LipaseA
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control apoptosis pathway
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Autophagy
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eat self for Energy
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Apoptosis
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energy dependent, no inflammatory response, breaks into particles, neighbors eat
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bax activation mech.
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ROS, RAD- increased misfolded proteins- increased P53, bax activates
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SIRS
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sepsis: crazy immune response- VasoD, decreaed Perfusion
CO maintained, Increased edema, pooling |
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acute endothelial damage
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coagulation pathway
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3 apoptosis regulators
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mitochondrial intrinsic pathway9
extrinsic death signal8 cytotoxic t-lymphocyte- apoptosis |
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Intrinsic mitochondrial pathway Apoptosis
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GF regulated, bax activation- open mito channel- cytC enters cytoplasm- bind PAF1- activate caspase 9- activate DNAse (DNA ladder)- phosphatidylserine expressed and found with annexin staining receptor
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aPAF1
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mitochondrial intrinsic cell death pathway
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DNA ladder
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mitochondrial intrinsic cell death pathway
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Extrinsic death signal Receptor 8
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TNF, FAS activate death domain on adapter proteins- activate executioner caspases
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fasL
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T lymphocyte receptor in death domain of extrinsic eath signal
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TNF anti apoptotic pathway
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TNF-NFKB- stimulate BCL2 production- anti apoptosis
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cytotoxic t-lymphocyte apoptosis
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immune response (fas-fasL)- perforin- insert granzye B- activate caspase 9 cascade
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Anti-apoptosis signals
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NFKB, IAPs, FLIP, BCL2
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NFKB
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proinflammatory response w/ IL2, upregulates BCL (apoptosis)
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Epstein Barr Virus
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Blocked NFKB (wich upregulates bcl) or BCL-1 with are pro-apoptotic
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Block? in apoptosis to cause tumors?
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P53 and/or bcl-1/NFKB
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BCL-1 vs BCL2
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BCL-2 anti apoptosis
BLC-2 pro-apoptosis |
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4 causes of liver steatosis
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increased fat synthsis, production (DM, obesity, steatosis)
decreased acceptor synthesis (ribosomes detach) CCL4/malnutrition decreased mito oxiation- decreased ATP (anoxia, shock, Heart failure) Multiple mitochondrial/chromosomal defects: EtOH |
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Hyaline change
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proetein accumulation, glossy pink
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Intracellular hyaline
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Resorption of protien in proteinurea
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exracellular hyaaline
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Arterioles/amyloids protein aggregate
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Causes of amyloid
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Proteinurea- resorption
Defective transport/secretion- alpha antitrypsin, ER accumulation, cytoskeletal proteinsl |
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a-1-antitrypsin
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blocks proteinase/collagenase
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Gylocogen accumulation disorder morphology
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DM/Storage problem
Clear vacuoles in the hne PAS positive Kidney/liver, beta islets of langerhans, myocardium |
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Lipofuscin
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product of rad/injury to the membranes of cell. granule dark brown. insoluble bodies from lipid peroxidation of subellular membranes.
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Brown atrophy
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Marsamus/ heart, liver in individuals with dibiliitating disease. brown grains of lipofuscin in polses of muclie
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Tyrosinase
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converts tirosine to melanin
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hemosiderin
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aggregate of hgb w/ fe2+ stains with prussian blue, caused by Fe overload.
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hemosiderosis
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Fe deposits in parencymal cells, no organ damage
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heterchromatosis
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huge fe deposition with organ damage
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bilirubin
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hg derivative w/o fe- causes jaundace
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Kernicterus
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accumulation of bilirubin in brain of newborn
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Dystrophic calcification
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myositis ossificans. @ nucleus causes decreased cell function, normal serum calcium deposits into non-viable tissue. stains deep purple
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metastaticc calcification
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hypercalcemia/hyperphosphatemia
deposits in organs that lose acid (lungs, pulmonary veins, gastric mucosa) Nephrocalcinosis |
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causes of hypercalcemia
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primary hyperthyroidism (Increased pth)
bone Cancer crazy vit D in serum |
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hyperphosphatemia
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renal failure- metastatic calcification
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characteristics of acute inflammation
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increased diameter, increased flow
protein/leukocyte leukocyte emigration, activation, accumulation to eliminate offending agents |
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Pus
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neutrophils, cell debris, microbes
Purulent exudate- edema fluid |
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Fast/Short edema
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Retraction of endothelial cells;
histamine, vasoconstriction |
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Fast/long edema
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damage to endothelium; burns, toxins
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late inflammation/ long
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leukocyte mediated edema (IL1,IL6, TNF)
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Increased transcytosis edema
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VEGF
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Selectins
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Rolling
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Integrins
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Adhesion
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PELAM, CD31
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expressed by TNF, IL1 gene; adhesion molecule that facilitates leukocyte migration
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Leukotriene B4
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Chemotoaxis from metabolism of AA that brings leukocytes into tissue
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Collagenase
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Secreted by leukocytes to get through endothelial basement membrane
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Early 24/ late 72 inflammation
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24- leukocyte neutrophils
72- monocyte macrophages |
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Leukocyte surface receptor
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microbial product TLR, G Protein coupled, Opsonin, cytokine receptor
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Leukocyte TLR
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toll-like-receptor: microbial product receptor- associated cellular kinases stimulate productio of microcidal substances and cytokines
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leukocyte g-proein coupled receptor
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PMN, macrophages: N-formylmethionine (bacterial protein)
activation-migration-respiratory burst |
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leukocyte opsonin receptor
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Ab receptor, complement protein, lectin
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IGg, C36
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Leukocyte opsonin (lectins)
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Leukocyte Fc or C3b
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Phagocytosis + cell activation
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major macrophage activator
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IFN gamma
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Leukocyte cytokine receptor
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responde to molecule/cytokine (IFN gamma)
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Leukocyte pahgocytosis 3 steps
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recognition, engulfment, killing
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Leukocyte phagocytosis receptor
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mannose receptor, opsonin receptor, scavenger receptor
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Leukocyte engulfment pathway
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surround w/pseudopod- PM pinches off- phagosome- fise w/lysosome- phagolysozome- granule deposits into phagolysozome
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Leukocyte killing methods
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ROS via burst or MPO, RNS w/ PMNs, macrophages
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Most effective PMN bacteriocide
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ROS-> H2O+MPO+Halide
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LAD
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leukocyte disiease deficient in integrins/selectins
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CGD
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leukocyte disease deficient oxidative burst in leukocyte
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MPO deficiency
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decreased killing efficiency in leukocytes
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chediak-higashi
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decreased leukocyte function due to cytoskeletal dysfunction
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Cycloxegyynase products
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PGs
Thomboxane |
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Lipoxygenase/5HPETE products
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5HETE, Leukotriene B4
Leukotriene CDE Lipoxin |
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Vasodilators
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PGs (w/pain)
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Vasoconstrictors
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Thromboxane, LT CDE
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increased vascular permeability
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LT CDE
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Chemotaxin, Leukocyte Adhesion
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Leukotriene B4, HETE
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Histamine
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in mast cells: VD, increased permeability
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Seratonin
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in platelets, acts like histamine
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NO
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from endothelial cell, macrophages, neurons in brain
VasoD, microcidal |
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TNF/IL1
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Produced by activated macrophages
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IFNgamma a
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activates macrophages to produce IL1/TNF
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Expression of endothelial adhesion molecules
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TNF
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IL1
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similar to TNF / role in fever in brain
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responsible for fever
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IL1/ PgE2
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Pain
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PGs, Kinins
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TNF/IL effect on vasculature
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Increased leukocyte adhesion molecules, Prod IL1/Chemokines
decrease anti-coagulant increased coagulant |
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TNF/IL effect on leukocyte
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activation/production of IL1,6
inflammation |
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TNF/IL1 effect on fibroblasts
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proliferation, collage synthesis,
activate collagenases, proteinases, PGE synthesis Leads to repair |
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compliment derived inflammation mediators
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C3a, C5a
C3b MAC |
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Mac complex
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lysis of molecule/ cell
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Bradykinin
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from kinins, increase vascular permeability, increased pain, increased sm M contraction or dilation
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thrombin/Fibrin
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proteases activated in coagulation- inflammation protein
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3 acute inflammation actions
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resolution,
healing goes chronic |
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3 major chronic inflammation outcomes
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infiltrage w/ mononuclear cells
tissue destruction repair by angiogenesis/ fibrosis |
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Chronic cell
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monocyte macrophage
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Chronic inflammation mononuclear cells
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B/T lymphocytes
Plasma cells (Abs) macrophages |
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Fc receptor for IgE
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on Mast cells
release mediators (degranulation) |
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Eiosinophils
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Chronic inflamation
Mediated by IGe, Parasitic infection |
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MBP
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Protein in Eiosinophil granule
Toxic to parasites, lyse cells |
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Eiosiniphelia
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parasitic infection
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osteomyelitis
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neutrophils presist for many months in chronic inflammation
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granulomatous
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having a lot of granulomas
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granuloma predominant cell
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activated macrophage w/ epetheliod appearance
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caseating granuloma
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TB
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TB
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caseating granuloma, macrophages round w/ fibroblast, langerhans giant cells, center is amorphoous w/ acid fast bacili (bacteria)
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leprosy
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Acid fast bacili-- noncaseating
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Syphillis
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gumma from chanchre in genitalia
cell structure- plasma cell infiltrate |
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cat-scratch fever
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lymp node in neck, granuloma
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Sarcoidosis
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non-caseating granuloma w/ increased macrophages
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Older Granuloma
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rim of fibroblast + CT
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amny nuclei arranged peripherally
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langerhans[type giant cell
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foreign body type giant cell
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many neuclei haphazardly arranged
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miliary patter in lung
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scattered white patches
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histo; non-caseating
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long, nuclei, epitheiiod cells w/ pink cytoplasm
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foreign body granuloma
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inert foreign body
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immune granuloma
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agent incites cell-mediated response
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Blue granuloma stain w/ acid-fast bacili
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TB
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Serous inflammation
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thin fluid from serous or mesothellial cells effusion
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fibrinous inflammatino
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sever injury: large molecule pass vascular barrier- amorphous coagulant
resolution: finbrinous or scarring lack of macrophages or neutrophils |
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supparative inflammation
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large amounts of purulent exudate
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pyogenic organism
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staphylococcus- PUS
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Suppurative abcess
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focal, confined, center necrotic (liquefactive), rim of neutrophils/repair
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ulceration mechanism
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defect of surface of organ or tissue produced by the shedding of inflammatory necrotic tissue
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bronchiopheumonia
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consolidated abscess pneumonia
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fibrinous inflammaiton microscope
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some macrophages w/ lots of fibers. Pink
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peritonitis
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ruptured colon- fibrinous inflammatioon
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serosanginous effusion
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w/ rRBCs, NOT exudate, transudate w/RBCs
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2nd line of defense
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lymphatics w/MPS system, leukocytes, cell debris
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lymphangitis
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lymphatics/vessels secondarily inflamed
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lymphadenitis
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drainage lymph nodes are inflamed, hyperpasia of lymph follicles/
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Overwhelmed lymph nodes
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can lead to bacteremia
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systemic cytokines for acute phase rxn
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NF, IL1, IL6
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effects of systemic cytokines for acute phase reaction
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fever, leukocytosis, acute phase protein synthesis, sepsis
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brain cytokines systemic effect
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TNF, IL-1, fever
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Liver cytokine effect
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IL-1, IL6- acute phase protein synthesis this is where acute phase proteins come from
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bone marrow cytokine/effect
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IL-1 IL-6, TNFa, leukocyte production
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pyrogens
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fever inducers
exo-bacterka endo- Il-1 TNFa |
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Pyrogen mechanism
|
increased prostaglandin synthesis in hypothalamus (block cox by nsaid)
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CRP
|
liver acute phase inflammation protein
Opsonin- complement MI marker |
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SAA
|
Serum amyloid A- inflammation acute phase protein, opsonin
|
|
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Erythrocyte sedimentation rate test
|
acute phase fibrinogen binds erythrocytes- fall out of serum faster
|
|
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endotoxic shock
|
gram negative bacteria... right?
|
|
|
normal blood leukocyte level
leukocytosis leukoid reaction |
4-10
15-20k 40-100k |
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inflammation leukocytosis
|
intial- storage dump from marrow
prolonged- CSF- stimulates bone marrow precursors |
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CSF
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colony stimulating factor, stimulate bone marrow precursor
|
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Neutrophilia
|
bacterial infection
|
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lymphocyteoma
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viral infection (mono)
|
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eosinophelia
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parasites, hay fever, asthma
|
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lymphopenia
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typhoid fever, decrease number of white cells.
Can be bad in pt with decreased immune response |
|
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sepsis mechanism
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increase organism LPS- major TNFa, IL1 production- DIC, hypoglycemia, hoptensic shock
|
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4 sources of excessive inflammation
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allergies, autoimmune disease, non-autoimmune disease
porolonged infetion/fibrosis- chronic infection or metabolic disorder |
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left shifft
|
immiture leukocytes
being pumped out too soon |
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injury to cells only=
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regernetation: proliferation of the cells within the matrix
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complete regeneration
|
renewing tissues continuously cycling labile cells
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compensatory growth
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hyperplasia: quiescent stabile cells (G0) stimulated- rapid divisinos
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injury to cell and matrix
|
repair:
wound- scar chronic inflammaiton- fibrosis |
|
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permenant cell repair
|
neurons and caridomyocites havve left the cell cycle
only leads to scarring |
|
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CNS repair
|
replaced with glial cells
|
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Sk MM repair
|
satellite cells can do some regeneration
|
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Cardiac MM repair
|
Scarring
|
|
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Restriction points of cell division
|
g1/s and g2/m
|
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CDKI
|
cdk inhibitors (cyklins,CDK)
control complex that regulates restriction point of cell division |
|
|
P53 in cell cycle
|
can lead to senescence of cycle
a cell cycle inhibiting gene trasncription factor |
|
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EGF/TGFa
|
EGF family- stimulate cell division
binds to EGFr Grows stuff |
|
|
ERB B1
|
main EGF receptor, target for potential cancer therapy
|
|
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ERB B2
|
therapy target in current breast cancer tx
|
|
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HGF
|
recepter is cMET- involved in tumors
|
|
|
VEGF
|
Receptor is VEGFr2- promotes angiogenesis/granulation
|
|
|
VEGF transcription factor
|
HIF, Cytokines, hypoxia
|
|
|
FGF
|
fibroblast growth factor- angiogenesis
develompental of sk M wound repair, hematopoisis |
|
|
TGFb
|
fibroblast/ sm m signal fibrinogenesis, fibrosis
can inhibit growth- lack of receptor- uncontrolled growth anti-inflammatory, stabilize angiogenesis |
|
|
ligand receptor binding :
Intrinsic kinase activity |
uses GF
P13-map Kinase, IP3 pathway |
|
|
ligand binding receptor w/o intrinsic kinase activity
|
cytokines- recruit kinases: JAK STAT
|
|
|
Jak2
|
target for leukemia- cene coding for new blood cell production
|
|
|
ligand binding receptor: G protein coupled
|
CAMP- transcription
retinopathy, hyperparathyroidism |
|
|
ligand binding receptor:steroid hormone
|
recetor in nucleus
|
|
|
c-MYC, c-JUN
|
growth promoting genes
transcription factors |
|
|
oncogenes
|
defective protooncogenes- help cancer grow
|
|
|
integrins
|
signal b/t ECM/BM
can relay information to the inside of the cell |
|
|
ECM fibrous structural proteins
|
collagen/elastin: tensile strenght and recoil
|
|
|
ECM adhesive glycoproteins
|
fibronectin/laminin: connect elements in ECM
|
|
|
PG Hyaluranon
|
reslilience and lubrication
Hyaluranon binds lots of h2O osteoarthritis |
|
|
Type IV collagen
|
In BM
|
|
|
BM contains:
|
type ive collagen (laminin/proteoglycans)
highly organized epithelial, endothelial, sm M cells |
|
|
CM interstitial matrix
|
fibrillar collagen (CDE), elastin, Pg, hyaluranon
|
|
|
Scurvy collagen
|
fibrillar
all the other types |
|
|
Erhlos danlos, osteogenesis imperfecta
|
Type IV non-fibrillar
|
|
|
Marfan's
|
defective in elasti tissues
elastin, fibrillin, elastic fibers |
|
|
Proteinases in angiogensis
|
remodel invading tissues
|
|
|
endostatin
|
released by proteases- inhibits angeogenesis
|
|
|
four classes of cell-adhesion proteins
|
Ig, CAMS,
Cadherens, Integrins selectins |
|
|
cadherins/integrins
|
linc cell surface with cytoskeleton through binding acting/ intrinsic fibers
|
|
|
immediate wound repair
|
blood clot, fibrin
|
|
|
24hr wound repair
|
neutrophils, leukocytes
|
|
|
24-48 hr wound repair
|
epithelial regeneratin
|
|
|
day 3-7 wound repair
|
granulation, epithelial growth
|
|
|
2nd week wound repair
|
collagen, fibroblast, blanching (decreased vessels)
|
|
|
end of 1st mo wound repair
|
scar of CT covered by epithelium
in histo: still has bvs- don't let that throw you off |
|
|
most important in angiogenesis
|
VEGF, VEGFr
|
|
|
antigenesis pathway
|
precursurs from bone marrow-> MMPs degrade BM -> Cells migrate-> proliferate and mature
|
|
|
Notch pathway
|
Modulate vasculature, prevent excessive angiogenesis
|
|
|
5 CT repair steps
|
inflammation,
new bvs fibroblasts migrate proliferate deposit ECM scar, maturation, reoganization |
|
|
wound healing: blood clot
|
coagulation pathway> scaffold>
in 24hours neutrophils |
|
|
wound healing granular tissue formation
|
24-72hours fibroblasts and endothelial cells
48hours- epitheiol cells deposit BM |
|
|
Hallmark of tissue repair
|
granulation
(bs, fibroblasts, edema) |
|
|
wound healling collagen deposition
|
48-96 hours macrophages replace neutrophils and deposit ECM
|
|
|
wound healing scar formatino
|
wk 2- blanching- pale, avascular, fibroblasts w/ dense collagen
end of 1st month- CT covered by intact epidermis |
|
|
wound healing: wound contraction
|
secondary intent large wounds, myofibroblastscontract, increased ECM production
|
|
|
wound healing: CT remodeling
|
collagenise, gelatinase, stromylase, bound MMPs (adams)
|
|
|
ADAMS
|
membrane bound MMPs (Ct Remodeling)
|
|
|
TIMPs
|
tissue inhibitor factor of MMPs- inhibit collagenase
|
|
|
Recovery of strength
|
1st wk 10%
plateau 70-80 |
|
|
Wound healing four systemic factors
|
nutritino (vit c, proteins
metabolic states (DM) circulation (DM, atherosclerosis) Hormones |
|
|
glucocorticoids and wound healing
|
corticosteroids inhibit mediators at AA path that start healing/inflammation and collagen synthsis
|
|
|
wound healing local factors
|
mechanical- ab pressure
size, locatio, type, foreign body |
|
|
foreign body repair
|
repair w/ granulation but surrounded by granuloma
|
|
|
keloid
|
excess type III collagen, hypertrop[hic fiberblast secretions past the scar boundaries that doesn't regresss
|
|
|
excessive fibroblasts
|
desmoids
fibromatosis |
|
|
proud flesh
|
excess granulation tissue
|
|
|
hypertrophic scar
|
doesn't spread past the eges of the lesion
type I collagen Myofibroblasts |
|
|
Fibrosis
|
TGFb (fibroblast signal)
excess collagen/ ECM |
|
|
Osteopontin
|
probmots fibrosis
Block this and you have decreased granulation base and scarring |
|
|
Fibrosis of Chronic disease
|
cirrhosis, chronic pancreatitis, pulmonary fibrosis
|
|
|
pluripotent SC
|
endo/meso/ecto
|
|
|
blastocyst ES cells
|
pluripotent
|
|
|
somatic adult SCells
|
restricted capacity in niches
|
|
|
transdifferentiation
|
change in differntiation of a cell
|
|
|
developmental plasticity
|
can differentiate to diverse lineages
|
|
|
pt induced pluripotent=
|
embryonic SC
|
|
|
Marrow HSCs
|
all blood cells
found in cord blood, marrow, peripheral blood (marker cd34) |
|
|
Stromal cells
|
multipotent> stroma, not blood
|
|
|
oval cells
|
liver SC hepatocytes, biliary clls
|
|
|
Brain SC
|
neuronal SC- target for parkinsons/alzheimers
|
|
|
Hallmar for chronic inflammation
|
monocytes
|
|
|
best opsonin for phagocytosis
|
C3b
|
|
|
IFNgamma
|
macrophge ctivating signal from CD4 lymphocytes
|
|
|
PLC
|
IP3- Ca pathway, CAMP
|
|
|
abcess is chronic but inside
|
is acute- ly
|
|
|
Von Willebrand
|
inhbited platelet adherence
|
|
|
P+ selectins
|
Rolling
|
|
|
Hallmark of acute inflammation
|
edema/leukocytes
|
|
|
Creatine Kinase
|
cell destruction, MI signal
|
|
|
Post necrosis
|
scar is formed
|
|
|
acidophil body
|
viral infection in liver
apoptosis in skin |
|
|
fibrinectin
|
ECM protein
|
|
|
RAS/RAF
|
mapKinase
GF signaled |
|
|
Endonuclease
|
chops DNA in apoptosis
|
|
|
BCL-2
|
anti-apoptosis
keeps mitochondrial gate closed |
|
|
Aspirin has a significant effect on
|
platelet funciton
not hepatocyte poison |
|
|
Intracellular Ca stored in
|
ER, mitochondria
|
|
|
NO synthase
|
argenine to RNS in macrophages
|
|
|
Sirtuin
|
Calorie restriction leads to long life
|
|
|
phosphatidyl serine vs inositide
|
serine- apoptosis
inositide- physiologic cardiomyocyte hypertrophy |
