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141 Cards in this Set
- Front
- Back
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ancient emerging agents
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schistosomiasis
tuberculosis |
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unrecognized emerging agents
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Helicobacter pylori
gastritis HBV HCV legionnaires |
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entirely new agents
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HIV lyme
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result of immunosuppression
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CMV pneumonia
Kaposi's sarcoma P. jiroveci |
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introduced to a new area
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West Nile
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driven by antibodies
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CA(community-acquired) MRSA
XDR(extremely drug resistant) tuberculosis |
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List the Category A agents of Bioterrorism
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Anthrax: Bacilis anthracis
Botulism: Clostridium botulinum toxin Plague: Yersinia pestis Smallpox: Variola major/Variola minor viruses Tularemia: Francisella tularensis Viral hemorrhagic fever: filoviruses, S Am. HF arenaviruses, African arenavirus (Lassa fever), Nairovirus (Bunyavirus) |
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Why are they Category A?
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Major Public Health Impact***
Social impact Surveillance and action plan required pose a danger as bioweapons easily produced easily distributed likely to cause great morbidity and/or mortality |
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Path of influenza
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infection--> skin,throat,lungs,intestine,urinary tract --> local replication (influenza, diphtheria, shigella dysentery, ascending pyelonephritis)
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Path of malaria
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infection-->skin,throat,lungs,intestine,urinary tract --> lymph node (via lymph vessel)--> bloodstream --> dissemination (dengue, malaria, typhus)
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Path of hepatitis
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infection-->skin, throat, lungs, intestine, urinary tract --> lymph node via lymph vessel--> bloodstream --> LIVER (hepatitis and yellow fever)
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Path of hematogenous pyelonephritis
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infection --> skin, throat, lungs, intestine, urinary tract --> lymph node via lymph vessel --> bloodstream --> kidney (hematogenous pyelonephritis)
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routes of entry for agents
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1. skin: access to deeper tissues and bloodstream
2. Respiratory tract: mucous membrane: living microbes, contaminated food/water, toxins produced by microbes growing on food urogenital tract: STDs and UTIs |
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Horizontal transmission
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direct contact with human, animal, insect or Fomite
airborne fecal-oral sexual parenteral: blood/body fluids |
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Vertical transmission
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mom to child
prior to birth, after birth (during breastfeeding) |
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major mech microbes evade Host response
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1. modulation of surface structure to avoid recognition
2. inhibit phagocytosis 3. escape phagosome 4. inhibit phagosome-lysosome fusion 5. modulate signal transduction, gene expression, cell death 6. inhibit antigen presentation 7. hide from immune surveillance: viral latency 8. viral cytokines or soluble receptor homologue |
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listeria monocytogenes selectively targets
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placental tissue
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several respiratory viruses cause more severe disease in
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male infants
some dimorphic fungi have predilection for males over females |
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pneumococcal pneumonia causes what kind of inflammatory response?
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suppurative inflammation w/ PMNs
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secondary syphilis in dermis causes what kind of inflammatory response?
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mononuclear inflammation-lymphocytes
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TB causes what kind of inflammatory response?
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granulomatous inflammation
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herpes blister in mucosa (Detachment of epithelial cells) what kind of inflammatory response?
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cytopathic-cytoproliferative response
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what causes necrotizing response?
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glomerular necrosis due to anti-neutrophil cytoplasmic auto-ab ANCA
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schistosoma haematobium causes what kind of immune response?
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calcified eggs and scarring
chronic inflammation and scarring |
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5 different ways by which microorganisms can be detected
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1. direct visualization
2. detection of microbial antigen 3. clues produced by host response to specific microorganisms 4. detection of nucleotide sequences 5. isolation of org in culture |
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agents for newborn meningitis
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Grp B strep (S. galactiae)
Listeria monocytogenes E. coli Herpes simplex 1/2 |
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agents for infant meningitis
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Neisseria meningitidis
Strep peumoniae enteroviruses** |
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agents for children meningitis
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N meningitidis
S. penumoniae enteroviruses (echo, coxsackie, entero) |
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agents for young adults meningitis
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N meningitidis, HSV2
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agents for mature adults meningitis
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S. pneumoniae
West Nile HSV1 |
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agents for old adults meningitis
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S. pneumoniae
Listeria monocytogenes West Nile |
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LRI newborn
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Chlamydia trachomatis
RSV |
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LRI infants
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H. influenzae
S. pneumoniae RSV parainfluenzae viruses metapneumovirus |
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LRI children
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Haemophilus influenzae
S. pneumoniae parainfluenza viruses metapneumoviruses |
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LRI young adult
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mycoplasma penumoniae
chlamydophila penumoniae adenovirus |
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LRI mature adult
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chlamydophila penumoniae
S. penumoniae Legionella Influenzae virus |
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LRI older adults
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H. influenzae
S. penumoniae influenza RSV |
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acute inflammation can be due to
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infections
tissue necrosis (ischemica, trauma physical or chemical injury), foreign bodies: splinters, dirt, sutures, medical devices immune reactions |
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effects of acute inflammation
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-increased blood flow
-protein leakage --> edema -PMN emigration |
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describe mvmt of plasma proteins and cells
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INCREASED hydrostatic pressure:
DECREASED colloid osmotic pressure Inflammation |
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increased hydrostatic pressure
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venous outflow obstruction (congestive heart failure)
transudate** decreased protein, decreased specific gravity, NO cells |
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decreased colloid osmotic pressure
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decreased protein synthesis (liver disease)
increased protein loss (kidney disease) |
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inflammation
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1-vasodilation
2-stasis 3-EXUDATE: increased interendothelial spaces increased protein, increased specific gravity cellular debris |
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vascular flow and caliber changes in acute inflammation
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vasodilation
stasis mvmt of leukocytes into tissue |
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vasodilation
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increased BF
induced histamine and NO heat and redness (erythema) increased permeability outpouring of protein-rich fluid --> edema |
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stasis
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loss of fluid and increased vessel size
RBCs concentrate in small vessels, increased blood viscosity, vascular congestion, local redness |
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increased vascular permeability
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1-retraction of endothelial cells:
2-endothelial injury 3-leukocyte mediated vascular injury 4-increased trancytosis |
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retraction of endothelial cells
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mainly in venules
histamine NO other mediators rapid and short-lived (min) |
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endothelial injury
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arterioles, caps, venules
burnes, microbial toxins rapid, hrs to days |
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leukocyte mediated vascular injury
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venules and pulm capillaries
assoc with late stages of inflammation long-lived hrs |
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increased transcytosis
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venules
VEGF-induced |
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recruitment of leukocytes VIA what processes? from capillaries to surrounding tissue
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changes in vessels lumen lead to leukocyte extravasation:
margination rolling adhesion transmigration chemotaxis |
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molecules involved in recruitment
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P-selectin: rolling
E-selectin: rolling and adhesion Gly-Cam-1, CD34: rolling ICAM-1 adhesion, arrest, transmigration VCAM-1 adhesion |
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leukocyte-induced injury
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collateral damage from normal defense reaction against microbes
inflammatory response is inappropriately directed against host tissues (autoimmune) host reacts excessively against usually harmless substances (allergies) |
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defects in leukocyte function: acquired
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bone marrow suppression: production of leukocytes
diabetes, malignancy sepsis, chronic dialysis --> adhesion and chemotaxis leukemia, anemia, sepsis, diabetes, malnutrition: phagocytosis and microbicidal activity |
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genetic defects in leukocyte function
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leukocyte adhesion deficiency: leukocyte adhesion
LAD2: leukocyte adhesion: def in fucosyl transferase chronic granulomatous disease: oxidative burst x-linked or autosomal MPO disease: Microbial killing, defective MPO-H2O2 system Chediak-Higashi: function affecting protein involved in lysosomal membrane traffic |
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termination signals of acute inflammation
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mediators have short half-life
produced in bursts stop signals triggered as inflammatory stimulus is removed anti-inflammatory lipoxins: generated by arachidonic acid pathway secretion of transforming gf-beta, TGF-beta, IL-10: counteracts each other stopping TH1 and TH2 lipid resolvins and protectins cholinergic discharge -inhibit TNG synthesis in macs |
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histamine released in response to
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physical injury
IgE Ab bound to mast cells binding allergins anaphylatoxins (C3a, C5a) histamine releasing protein from WBC neuropeptides IL-1, IL-8 |
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serotonin
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released from platelets/neuroendocrine cells on GI tract in response to:
platelet aggregation in contact with collagen and thombin, ADP, Ag:Ab complexes |
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arachidonic acid metabolites are derived from
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dietary AA or from conversion of linoleic acid
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AA is esterified by
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membrane phosphlipases
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cyclooxygenases and lipoxygenases produce AA-derived mediators together known as
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eicosanoid: bind to Gprotein coupled receptors and mediate almost every step of inflammation
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PAF platelet activating factor
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causes platelet aggregation
elaborated by platelets, basophils, mast cells, PMN, macs endothelial cells (secreted or cell-bound) vasoconstriction and bronchoconstriction low levels, VASODILATION AND VASO PERMEABILITY ACTIVITY MUCH GREATER than histamine leukocyte adhesion, chemotaxis, degranulation, oxidative burst |
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Eicosanoids: inflammatory actions
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1. vasodilation
2. vasoconstrction 3. increased vascular permeability 4. chemotaxis, leukocytes adhesion |
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eicosanoids that cause vasodilation
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PGI2 (prostacycline)
PGE1,2 PGD2 |
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eicosanoids that cause vasoconstriction
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Thomboxane
leukotrienes C4, D4, E4 |
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eicosanids that Increases Vascular permeability
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leukotrienes, C4, D4, E4
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eicosanoids that mediate chemotaxis, leukocyte adhesion
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leukotrienes, B4, HETE
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cycooxygenase, prostaglandins, thomboxanes are produced by
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mast
macs endothelial vascular and systemic functions COX-1 (constitutive),2 (inducible) |
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lipoxygenase leukotrienes
lipoxins |
leukotrienes are secreted by leukocytes
lipoxins generated by meutrophils and platelets in sequence inverse relationship btwn production of lipoxin and leukotrienes R |
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ROS derived from
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NADPH oxidase system
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NO synthesized from
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Arg by
eNOS nNOS iNOS |
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NO Causes
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vascular SM relaxation and vasodilation
decrease leukocyte adhesion KILL MICROBE in macs: NO + O2*- --> OH* + NO2 |
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source of TNF
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macs
mast T cells |
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action of TNF
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increase endothelial adhesion
secretion of other cytokines systemic effects |
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actions of IL-1
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similar to TNG
greater role in FEVER |
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source of IL-1
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macs
endothelial epithelial |
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source of IL-6
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macs and other cells
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action of IL-6
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acute phase response (systemic)
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chemokines
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macs
endothelial T cells mast |
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principal actions of chemokines
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recruit leukocytes to site of inflammation
migration of cells to normal tissues |
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cytokines of chronic inflammation
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IL-12
INF gamma IL-17 |
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cytokines/chemokines of acute inflammation
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TNF
IL-1,6 chemokines |
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source of IL-12
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DC and macs
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source of INF gamma
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T cells and NK cells
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source of IL17
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T cells
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IL-12 action
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increased production of INFgamma
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INF-gamma action
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activation of macrophages
increased killing |
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IL-17 action
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recruit neutrophils and monocytes
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local actions of TNF and IL-1
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vascular endothelium: increased expression of leukocyte adhesion molecules
increased procoagulant, decreased anticoagulant leukocytes: activation and production of cytokines fibroblast proliferation: increased collagen synthesis (repair) |
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systemic actions of TNF and IL-1
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fever
leukocyte increased acute phase protein decrease appetite and increased sleep systemic manifestations of inflammation |
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roles of plasma-protein derived mediators of inflammatory responses
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1. complement: anaphylatoxins and antimicrobial functions
2. kinins: increased vascular permeability (bradykinin = pain) 3. clotting factors: contain microbes, isolate injury, prevent bleeding |
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source of IL-12
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DC and macs
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agents of acute inflammation
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injury
infarction bacterial infection toxins trauma |
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source of INF gamma
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T cells and NK cells
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source of IL17
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T cells
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IL-12 action
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increased production of INFgamma
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INF-gamma action
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activation of macrophages
increased killing |
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IL-17 action
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recruit neutrophils and monocytes
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local actions of TNF and IL-1
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vascular endothelium: increased expression of leukocyte adhesion molecules
increased procoagulant, decreased anticoagulant leukocytes: activation and production of cytokines fibroblast proliferation: increased collagen synthesis (repair) |
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systemic actions of TNF and IL-1
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fever
leukocyte increased acute phase protein decrease appetite and increased sleep systemic manifestations of inflammation |
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roles of plasma-protein derived mediators of inflammatory responses
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1. complement: anaphylatoxins and antimicrobial functions
2. kinins: increased vascular permeability (bradykinin = pain) 3. clotting factors: contain microbes, isolate injury, prevent bleeding |
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agents of acute inflammation
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injury
infarction bacterial infection toxins trauma |
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agents of chronic inflammation
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viral infections
chronic infections persistent injury autoimmune disorders |
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morphologic patterns of acute inflammation
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1-serous
2-fibrous 3-suppurative 4-ulcers |
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serous
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thin fluid from plasma secretions of mesothelial cells lining body cavities (effusions)
blisters |
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fibrinous
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formation and depositiong of fibrin in EC space, meninges, pericardium pleura
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suppurative
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localized collection of PURULENT inflammation (PMN, liquefactive necrosis, edem fluid)
associated with pyogenic bacteria |
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ulcers
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local excavation of surface of organs or tissue produced by sloughing of inflamed necrotic tissue
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processes leading to chronic inflammation
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1-inflammation of prolonged duration: active inflammation
tissue destruction attempts at repair may follow acute inflammation may begin INSIDIOUSLY: low grade smoldering often asx response |
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morphologic features of chronic inflammation
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infiltration of mononuclear cells: macs, lymphocytes, plasma cells
tissue destruction induced by persistent offending agent OR inflammatory cells (parenchymal destruction) attempts at healing by connective tissue replacement of damaged tissues -proliferation of small BVs (angiogenesis) -fibrosis |
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leukocyte-induced injury CHRONIC
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arthritis: lymphocytes, macrophages, Ab?
asthma: eosinphils IgE atherosclerosis: macs and lymphocytes chronic transplant rejection: lymphocytes and cytokines pulmonary fibrosis: macs and fibroblasts |
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what cells?
may assume configuration of lymphoid organs long-standing rheumatoid arthritis |
Plasma cells
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what cells? major basic protein
toxic to parasites |
eosinophils
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what cells?
hypersensitivity Type I secrete many cytokines: pro- and anti-inflammatory |
Mast cells
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foreign granuloma
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foreign body visualized in center of granuloma
epitheloid and giant cells form around foreign body **no specific inflammatory or immune response |
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immune granuloma
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insoluble particles often microbes at heart
epitheloid and giant cells form periphery around granuloma **immune cells present involves macs, T cell interactions prototype: TB central caseating necrosis |
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microscopic aggregation of epitheloid macs surrounded by a collar of MONONUCLEAR LEUKOCYTES
lymphocytes, few plasma cells become ENCASE in fibroblasts and connective tissue |
granuloma
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GIANT cells
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fused epitheloid macs
peripheral: langhans-type giant cell haphazard: foreign body-type giant cell |
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what is this?
caseating granuloma activated epitheloid mac giant cells central necrosis ACID FAST BACILLI |
TB mycobacterium tuberculosis
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ACID FAST BACILLI in macs
noncaseating granuloma |
leprosy M leprae
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rounded or stellate granuloma including granular debris and PMNs
giant cells are rare |
Cat scratch disease
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wall of histiocytes
plasma cell infiltrate central necrosis |
Syphilis T pallidum
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immune reaction to intestinal bacteria and self-antigen occasional noncaseating granuloma
dense chronic inflammatory infiltrate |
Crohn disease
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unknown/noninfectious noncaseating granulomas
many macs |
sarcoidosis
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exogenous - silica
endogenous substances (atherosclerosis -lipids) |
prolonged exposure to toxic substances
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rheumatoid arthritis
systemic lupus erythematosus |
autoimmune reactions
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what is the main different between acute and chronic?
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besides early and late onset
fluid exudation in acute NO fluid exudate in chronic PMN in acute with minimal lasting damage monocytes, macs, lymphocytes, vessel proliferation, scarring fibrosis in chronic |
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what are the beneficial effects of inflammation?
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contain and isolate injury
destroy microbes inactivate toxins prepare for healing lifesaving |
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what are the harmful effects of inflammation?
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relentlessly progressive hypersensitivity reaction
autoimmune responses can be lifethreatening |
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acute phase response
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FEVER
acute phase proteins: c-reactive protein, fibrinogen, serum amyloid A, erythrocyte sedimentation rate rises, IL-6, IL-1, TNF sleep decreased appetite malaise increased pulse and BP rigors (shivering) chills (search for warmth) |
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leukocytosis
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15,000-20,000 cells/ul
bacterial infections neutrophilia viral lymphocytosis paraiste eosinophilia leukopenia = decreased WBC count overwhelming infection in debilitated pt --> leukopenia |
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left shift
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release from bone marrow younger and younger neutrophilic precursors
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leukemoid reaction
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40-100,000 cells
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infections in which fever is primary manigestation
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acute inflammation associated with human/environmental sources:
adenovirus, EBV, CMV, primary HIV, staph, listeria, salmonella, paratyphi strep that causes subacute endocarditis assoc w/ animals: coxiella, leptospira, brucella granulomatous infections mycobacterium TB, histplasma capsulatum drug fever: cytokine therapy malignancies esp dangerous: fever in neutrophenic pts nocosomial onset of fever (resistant microbes) |
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systemic effects of inflammation
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acute phase
sepsis septic shock liver damage: hepatic failure lung damage: adult respiratory distress |
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large amount of bacteria, LPS, toxins in blood
extremely high levels of cytokine production |
sepsis
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disseminated intravascular coagulation
hypoglycemia NO-induced heart failure and loss of perfusion |
septic shock
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consequences of defective inflammation
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increased susceptibility to infections
delayed healing of wounds and tissue damage |
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consequences of excessive inflammation
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allergies
autoimmune disease alzheimer's atherosclerosis ischemic heart disease |
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prolonged inflammation and fibrosis
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chronic infections
metabolic diseases |
