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54 Cards in this Set
- Front
- Back
Bradykinin
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Vascular permeability, smooth muscle contraction, pain
Hageman factor contacting collagen and BM to protect from injury |
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Complement C5a
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Neutrophil chemoattractant
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Histamine
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Increased vascular permeability, mucous secretion
Released upon IgE binding |
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IL-1
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Mediate systemic effects of fever, metabolic wasting, hypotension
Produced by macrophages |
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Phospholipase C
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Catalyzes release of arachidonic acid from phospholipid
Generated from platelet activation |
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Platelet-activating factor
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Vascular permeability, neutrophil aggregation, platelet activation
From most cells in vascular system |
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Tumor necrosis factor alpha
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Mediate systemic effects of fever, metabolic wasting, hypotension. SHOCK, endothelium activation, leukocyte recruitment and vascular leak
Produced by macrophages |
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Myeloperoxidase
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Converts hydrogen peroxide to HOCl- which destroys phagocytosed organisms
Stored in azurophilic granules of neutrophils |
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Leukotriene B4
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Neutrophil chemoattractant
From lipoxygenase pathway of arachidonic acid metabolism |
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Selectins
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Rolling action for neutrophils (P and E selectin on endothelial cells, L-selectin on neutrophils)
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Integrins
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Firm adhesion between neutrophils and endothelial cells
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Complement C3b
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Facilitates phagocytosis
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NADPH oxidase
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Microbicidal activity in oxidative burst
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IFN-gamma
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Potent macrophage stimulator, Inhibits Th2 cells to promote cellular immunity
TFNalpha from macropahges induces granulomas |
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Thromboxane A2
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Vasoconstriction
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NO
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Vasodilation and inhibits platelet activation (endothelium) or kill organisms (macrophages)
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Leukotriene E4
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Vasoconstriction
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TGF-beta
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Fibroblast chemotaxis and collagen production stimulation. Inhibit collagen degredation
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Fibronectin
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Extracellular matrix protein which interacts with integrins
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Platelet derived growth factor
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migration and proliferation of fibroblasts, smooth muscle cells and platelets
From endothelium, macrophages, smooth muscle cells, platelets |
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Endostatin
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inhibits angiogenesis
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Vascular endothelial growth factor
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promotes angiogenesis
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Epidermal growth factor
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epithelial cell and fibroblast proliferation
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ADP
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Induces platelet aggregation
In platelet dense bodies |
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Fibrinogen
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Binds GPIIb/IIIa receptor to crosslink platelets
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Von Willibrand factor
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Promote platelet aggregation and activation
Links to exposed extracellular matrix and platelets after injury. Released from endothelium or platelet granules |
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Thrombomodulin
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Binds thrombin and inhibits coagulation by activating protein C
On intact endothelium |
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LPS
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From many bacteria, induces IL-1 and TNF release and can lead to shock (VIA PROTEIN A)
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Toxic shock syndrome toxin-1
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Superantigen released by staphylococcal organisms
T lymphocyte activator |
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Prostacyclin
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Vasodilator, inhibits platelet activation
Limits thrombus formation to area of injury |
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Apoptosis characteristics; Extrinsic vs Intrinsic
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Cell shrinkage, basophilia (pyknosis) and nuclear shrinking, membrane blebbing, nuclear fragmentation (karyorrhexis) = irreversible, and fading (karyolysis) and formation of apoptotic bodies
NO inflammation Extrinsic - Fas ligand binds CD95, or Killer T cell releases perforin and granzyme B FAS ligand defects implicated in clonal deletion of T cells, may have SLE role Intrinsic - embryogenesis, hormone, atrophy or insults lead to increased Bax (pro-apoptosis) and less Bcl-2 (anti); mitochondria permeability up, Cytochrome c release Converge to activate caspases and cell death |
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Necrosis Types
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Coagulative - SOLID organs (ex heart, liver, kidney)
Liquefactive - brain, abscess, pleural effusion Caseous - TB, fungi Fatty - pancreas (saponification with hypocalcemia) Fibrinoid - vessels Gangrenous - dry (ischemic coagulative) or wet (with bacteria). Limbs and GI tract |
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Reversible and Irreversible cell injury
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Reversible - Low ATP, Swelling (Na/K Pump dysfunction), chromatin clumping, fatty change, ribosomal detachment
Irreversible - Nuclear pyknosis, karyolysis, karyorrhexis, Ca++ influx (caspases), membrane damage, lysosomal rupture, cyt C release |
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Main watershed areas
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Splenic flexure; ACA/MCA overlap
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Red vs pale infarcts
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Red - loose tissue with collaterals (liver, lungs, intestine) or reperfusion (free radicals)
Pale - solid tissue with single blood supply (heart, kidney, spleen) |
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Shock types
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Hypo-volemic/cardiogenic - low output failure, high TPR, cold, clammy
Septic - high output failure, low TPR, dilated arterioles, high return, HOT |
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Acute vs chronic inflammation players
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Acute - PMN, eosinophil, Abx mediate - rapid
Chronic - mononuclear cell mediate, persistent destruction and repair, vessel proliferation, fibrosis |
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WBC Extravasation
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Rolling - Sialyl Lewis X binds E and P selectin
Tight binding - Integrin binds ICAM-1 Diapedesis - PECAM Migration - attracted by C5a, IL-8, LTB4, Kallikrein (CILK) |
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Wound healing phases
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Inflammatory - platelets, PMNs, macrophages form clot, vessel permeability and PMN migration, debris cleared in 2 days
Proliferative - Fibroblasts, myofibroblasts, endothelial cells and keratinocytes. Granulation tissue, collagen, clot dissolution and wound contraction Remodeling - 1 week - fibroblasts, Type III collagen replaced by Type I |
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Transudate vs Exudate
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Transudate - hypocellular, protein poor, SG <1.1012, Due to high pressure, low oncotic pressure, Na+ retained
Exudate - Cellular, protein rich, SG >1.020, due to lymphatic obstruction or inflammation |
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Amyloidosis Proteins
a) AL b) AA c) Transthyretin c) Amylin d) ACAL e) B-amyloid f) B2 microglobulin |
a) AL - multiple myeloma bence jones proteins
b) AA - acute phase reactants (inflammation) c) Transthyretin - Senile cardiac c) Amylin - DM II d) ACAL - Calcitonin, medullary thyroid cancer e) B-amyloid - Alzheimers f) B2 microglobulin - dialysis associated |
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Cachexia mediators
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Loss of weight, muscle atrophy, fatigue of chronic disease
Mediated by TNFa, IFN gamma, IL-6 |
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Associated neoplasm: Down Syndrome
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ALL, AML
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Associated neoplasm: Plummer-Vinson syndrome
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atrophic glossitis, esophageal webs, anemia - IRON DEF
Squamous cell carcinoma of esophagus |
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Associated neoplasm: Paget's disease
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Cement pattern
Secondary osteosarcoma and fibrosarcoma |
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Associated neoplasm: AIDS
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lymphomas and Kaposi sarcoma
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Body Lymphatic Drainage
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Upper limbs, lateral breast - Axillary nodes
Stomach - Celiac nodes Duodenum, jejunum - superior mesenteric Sigmoid Colon - Colic or inferior mesenteric Rectum above pectinate line - internal iliac Anal canal below pectinate line - superficial inguinal Testes - superficial and deep plexuses to para-aortic Scrotum - superficial inguinal Thigh (superficial) - superficial inguinal Lateral side of dorsum of foot, posterior calf - popliteal Right lymphatic duct only right arm and right half of head, rest is thoracic duct |
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IL-10
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Promotes humoral response. Inhibits Th1 cells in favor of Th2
Reduces inflammation |
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IL-4
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Promotes B cell activation and IgE class switch
From Th2 cells |
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IL-5
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Promotes B cell activation and IgA class switch
From Th2 cells |
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IL-8
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Activates neutrophils to come to inflamed area
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Anti inflammatory cytokines
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IL-10
TGF-beta Produced by regulatory T-cells |
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Interferon mechanism
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Puts cells in antiviral state
IFNa and B - inhibit viral protein synthesis IFNgamma - promote MHC I and II expression, Activates NK cells and macrophages |
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IL-12, absence
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Promotes cellular response
Shift to Th1 immunity, activates Th1 cells, IFN gamma production, macrophage, NK and CD8 T cell production Absence - delayed hypersensitivity or cytotoxicity against intracellular. High mycobacterium infections. Give IFNgamma |