Pathology 1 - Block 1 - Part 2

davidwurbel7's version from 2016-04-12 18:54


Question Answer
Increase in temperature of an areaCalor
Swelling in an areaTumor
Pain in an areaDolor
Redness in an areaRubor
Calor, Tumor, Dolor, Rubor and loss of function are indication of thisInflammation
Following transient vasoconstriction, this is induced primarily by histamine and Nitric oxideVasodialation
This is the hallmark of Acute InflammationIncreased Vascular Permeability
Adherent leukocytes damage endothelium by release of oxygen free radicalsLeukocyte Mediated Injury
The source of inflammation using histamine and serotoninMast Cells
Elimination of microbes and dead tissue; source of cytokines and play a role in immune responseMacrophages
The source of inflammation using nitric oxide and cytokinesEndothelium Cells
Elimination of microbes and dead tissuePMN
(Insert 14-17)
Question Answer
Increased blood flow (vasodilation), Increased permeability, Endothelial cells activation (adhesion), Migration of leukocytes (PMNs) from vessels. Activation of leukocyes. Migration in tissues to injury siteAcute Inflammation
These cytokines are associated with inflammationTNF and IL-1
Anything that upsets the homeostasis of an area of the bodyInflammation
Toll-like receptors (TLRs) and Inflammasome that recognize common molecules are examples of thesePattern Recognition Receptors
These can be located on Membrane, Endosomes or CytosolTLR
Multiprotein cytoplasmic complex that recognizes dead cell products, Uric acid, ATP Crystals and Microbial productsInflammasome
Objective is to increase blood flow to inflamed site and to increase permeability of vessels which allows easy access of plasma, proteins, cellsVascular Changes
The release of Histamine and nitric oxide results in this in the blood vesselArteriolar Vasodilation
PMN lining the wall of the blood vesselMargination
Protein / cellular rich fluid into tissuesExudate
Fluid moving into tissues that is does not contain proteinTransudate
Histamine, Bradykinin, and Leukotrienes produce this in post capillary venulesContraction
This occurs in venules, and pulmonary capillaries and is associated in late stage inflammation and can be remain for hoursLeukocytes-Mediated Vascular Injury
Receptors on PMNs bind sugars (lectin)Sialyl-Lewis X
Histamine and thrombin induce this selectin to form on the surface of the endotheliumE-Selectin
P-Selectins translocate from this in endothelial cellWiebel Palade Body
Intercellular cell adhesion molecule 1 (ICAM-1) binds to thisLFA-1
Vascular cell adhesion molecule 1 (VCAM-1) binds to thisVFA-1
Facilitate transport through ECPECAM-1
Locomotion orientated along a chemical gradientChemotaxis
Chemoattractants binds to this surface receptor that will cause a release in intracellular calcium that polymerizes actin7 Transmembrane G-protein-coupled receptors (GPCRs)
Rapid responders Short lived 6 – 24 hoursPMNs
Derived from circulating monocytes Longer survival 24 – 48 hoursMacrophages
In an infection with this organism, PMNs persist for several daysPseudomonas Infections
In an infection with these, Lymphocytes are the early respondersViral Infections
In this type of reaction, Eosinophils are the prominent respondersHypersensitivity Reactions
ROS is generated by the enzymeNADPH Oxidase
NADPH oxidase oxidizes NADPH, and in the process also converts molecular oxygen to superoxide results in release of energyRespiratory Burst
NADPH oxidase oxidizes NADPH, and in the process also converts molecular oxygen to superoxide results in release of energy: respiratory burst. Superoxide dismutase converts superoxide to hydrogen peroxide. Hydrogen peroxide combines with myeloperoxidase and chloride ion to form hypochlorous free radicals (HOCL)Oxygen Dependent Mechanism
Killing of microbes by action of substances within leukocyte granulesOxygen Independent Mechanism
Oxygen Independent Mechanism produces myeloperoxidase (MPO) lysozyme, defensins, acid hydrolyases, elastaseAzurophilic Granules (primary)
Oxygen Independent Mechanism collagenase, gelatinase lactoferrin, plasminogen activator, major basic protein (seen in eosinophils)Secondary/Specific Granules
β2 chain defect in Integrins. Cant bind ICAM-1LAD-1
Sialyl-Lewis X absent. Cant bind to E or P selectinLAD-2
Mutation in LYST ((lysosomal regulator trafficking) gene. Neutropenia, Defective degranulation, Delayed killing. Giant granules. Impaired organelle fusion. Involve also Platelets, nerves, malanocytes, lymphocytesChediak-Higashi Syndrome
X- linked recessive disorder, defect in gene encoding for NADPH oxidase. Deficiency of NADPH oxidase in neutrophils and macrophages results in decreased production of super oxide and absence of ‘respiratory burstChronic Granulomatous Disease
This screening test is negative in CGDNitroblue Tetrazolium (NBT) Test

Chemical Mediators of Inflammation

Question Answer
Hyperemia, edema, PMN incursion are histological markers of this with necrosis / causative agents may be present depending on the infectious agentAcute Inflammation
Low protein content in edema fluid. Endothelial cells intact is the characteristic of this inflammation. Fluid accumulates in various sites (effusions) Pleura, Peritoneum, Pericardium, SkinSerous Inflammation
High molecular weight proteins present. Endothelium permeableFibrinous Inflammation
Pus - Edema fluid, PMNs, Necrotic debris, Organisms present due to bacterial infection (Pyogenic organisms) that forms an abscessSuppurative (purulent) Inflammation
Loss of lining membrane due to necrosis. Inflammatory insult local. Resolution requires growth of new epithelium from marginsUlcerative (Necrosis) Inflammation
Severe inflammatory response. Causing necrosis of capillary walls. Bleeding into tissuesHemorrhagic Inflammation
Histamine and serotonin are example of this type of chemical mediatorsPreformed Mediators
Prostaglandins, Leukotrienes, platelet-activating factors, ROS, and nitric oxide are examples of this type of chemical mediatorsDe Novo Mediators
Located in mast cells especially adjacent to vessels, circulating basophils and platelets. Actions includes arteriolar dilation. Increases permeability of venules. “Immediate transient” effectHistamine
Pre-formed in Platelets, Neural cells, enterochromaffin cells. Regulates intestinal motility. Neurotransmitter. Released when platelets aggregate. Induces vasoconstriction during clottingSerotoin
Eicosanoids are derived from 20-carbon fatty acids - Prostaglandins, Leukotrienes and LipoxinsArachadonic Acid Metabolites
Found in Platelets. Produced by Thromboxane synthesase. Causes platelet aggregation ++,VasoconstrictorTXA2
Found in ECs. Produced by Prostacycline synthesase. Causes inhibition of platelet aggregationPGI2
Found in Mast cells (also E and F)/ Causes vasodilationPGD2
PMNs produces 5-HPETE through this pathwayLipoxygenase Pathway
5-HPETE is converted into 5-HETE which is this for PMNsChemokine
Platelet use 12 lipoxygenase to produce this which acts as an inhibitory to PMN activityLipoxins
Produced in response to inflammation. Constitutively present in most tissues. PGs serve local functions Fluid/electrolyte balance in kidneys and cytoprotection in GITCOX-1
Produced in response to inflammation. Not present in most tissues. Do not inhibit protective COX activityCOX-2
Produced by Platelets, monocytes. PMNs, Basophils, Endothelial cells. Phospholipid derivative by Membrane Phospholipase A2Platelet Activating Factor (PAF)
Platelet activation via G protein-coupled receptor. Enhances degranulation. Vasoconstriction, Bronchconstriction. Vasodilation, increased permeability 100 – 1000 X Histamine effectPlatelet Activating Factor (PAF)
Enhances PMN attachment to Endothelial cells through integrin mechanism. Enhances chemotaxis. Increases PMN oxidative burst. Enhances PMN degranulationPlatelet Activating Factor (PAF)
Produced by many cell types. Act on many cell types. Polypeptides. Bind to receptors on target cells. Examples of the Inflammatory types are TNF, IL1, IL6Cytokines
TNF, IL1, IL6, Chemokines are present inAcute Inflammation
IFN-g IL-12 are present inChronic inflammation
This cytokine is lymphocyte derived and recruits PMNsIL-17
Endothelial activation. Gene transcription -> adhesion molecules. Synthesis of other mediators - Chemokines, Eicosanoids, Pro – thrombogenic. Activates tissue fibroblastsIL-1
Small proteins (8 – 10kD). Chemoattractants for leukocytes. Different chemokines attract specific leukocytes. Activate leukocytes (PMN Integrins). Control cell location in lymphoid tissue (T, B)Chemokines
Extracellular release from PMNs -> H2O2, OH-, O2-, HOCl, + NO. Low level secretion. Stimulate endothelial cells Chemokine release (IL8), Adhesion molecule expression, Cytokine productionOxygen-Derived Free Radicals (ODFRs)
Ceruloplasmin, Transferrin, SOD (superoxide Dysmutase), Catalase, Gluthathione peroxidase are examples of theseAntioxidants
Short half life acts locally. Type 1 in neurons and acts as a neurotransmitter. Type 2 is inducible and acts as a killing agent. Type 3 in ECs causes smooth muscle relaxation in vessels, vasodilation and antagonizes platelet activationNitric Oxide
(Insert 105-109)
Question Answer
This is present in the lung and GIT especially. Pain. BP regulation. Endocrine stimulation. Increase vascular permeabilitySubstance P
This is the most abundant protein in plasmaAlbumin
This is the second most abundant protein in plasmaIgG
Exposure to collagen activates thisCoagulation System
The first step of the coagulation system is thisFactor XII
Dilation of blood vessels Vascular permeability ++, Smooth muscle contraction and Pain. Inactivated rapidly by KininaseBradykinin
Factor XII + HMWK -> Bradykinin is this systemKinin System
This can be found in urine which is evidence that the fibrinolytic system has been activatedFibrin-Split Products
Short half life of components and breakdown of components and antagonists of mediators are factors that make up thisAnti-Inflammatory Mechanisms

Chronic Inflammation

Question Answer
May arise from preceding acute inflammation due to a persisting agent or outside interference with healingChronic Inflammation
(Insert Macrophage)
Question Answer
Mobilized by infections, necrosis. T and B into tissues in chronic inflammationLymphocytes
B cell derived following antigen stimulation. Produce antibodiesPlasma Cells
IgE responses to parasites and allergies. Granules contain MBP (Major basic protein)Eosinophil
Sentinel cells – widespread distribution. Release histamines, AA metabolites producing vascular changes. Have IgE receptors that bind native IgE. Predispose to allergic reactionsMast Cells
Macrophages surround injurious agent. Wall it off from body. Fibroblasts come in and lay down collagen which is a better wallGranulomatous Inflammation
This macrophage is involved in the inflammatory responseClassical Macrophage M1
This macrophage is involved in the repair responseAlternate Macrophage M2
Transformed Macrophages. Pale pink granular cytoplasm. Indistinct cell boundaries. Resemble epithelial cellsEpithelioid Cell
Fused epithelioid cells with 20+ nuclei 40 μm diameterGiant Cell
Giant cell in which the nuclei are organized near membrane of the cellLanghans type Giant Cell
Giant cell in which the nuclei are congregated near the center of the cellForeign body type Giant Cell
Central area of caseous necrosis. Surrounded by epithelioid cells/ giant cells. Lymphocytes around periphery. Fibroblasts lay down collagenTuberculosis Granuloma
Central necrosis in granuloma. Cheese like consistency. Stains pinkCaseous Necrosis
Associated with Sarcoidosis. Usually extensive tissue involvement. Associated with hypercalcemia. The etiology unknown and heals by fibrosis which leads to organ damageNon-Caseous Granulomas
Fever. Acute phase protein production. Leukocytosis. Cardiovascular response. Decreased sweating. Rigors/ chills that could lead to Septic shockAcute Phase Response
IL-6, IL1, TNF ++synthesis by liver of CRP, Fibrinogen and SAA protein. Production is increased 100 to 1000 foldAcute Phase Proteins
Increase to 15- 20K. TNF, IL-1 release of PMNs from marrow. Shift to left. Colony Stimulating Factor secretion which Increased BM production of precursorsLeukocytosis
Viral infectionsLymphocytosis
Allergy, Parasitic infectionsEosinophilia
Typhoid fever, some viruses, Rickettsia. Overwhelming infections and cancerLeukopenia
Physiologic adjustment to infection. Redirection of blood from skin. Reduction in heat loss. Rigors, chillsCVS, Sweating, Rigors/ chills
Clotting cascade at an inappropriate time within the blood vessels throughout the bodyDisseminated Intravascular Coagulation (DIC)
This acute phase protein can act as an opsoninCRP
CRP Fibrinogen and SAA are these types of proteinsAcute Phase Proteins
The prostaglandin that has pyrogenic propertiesPGE2
Chronic production of SAA proteins can lead to thisAmyloid
The clinical importance of this acute phase protein is necrosis associated with acute inflammation (bacterial infections, example acute osteomyelitis), as a marker for increased risk of myocardial infarction (MI) and the monitoring Rheumatoid arthritisC- reactive protein (CPR)
This is characterized by greater than 10% of band forms or earlier forms in the bloodShift to the Left
This is characterized by an absolute increase in lymphocytes. Can be seen in viral infections, mumps, infectious mononucleosisLymphocytosis