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126 Cards in this Set
- Front
- Back
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INFLAMMATION IS
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A RESPONSE OF THE BODY TO INJURY WHICH INVOLVES NEURAL, VASCULAR, CHEMICAL, AND CELLULAR PROCESSES
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INFLAMMATION
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INITIATES REPAIR
PART OF INNATE IMMUNITY (MAY WORK IN CONCERT WITH IMMUNOLOGIC REACTIONS) MUST BE REGULATED (NOT OCCUR SPONTANEOUSLY; NOT EXCESSIVELY DAMAGE TISSUE; CAN CAUSE CONSIDERABLE HARM; NECROSIS OF NORMAL TISSUE; HEALING BY FIBROSIS; TURN OFF WHEN JOB IS DONE) |
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INFLAMMATION INVOLVES
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BLOOD LEUKOCYTES
PLASMA PROTEINS AND OTHER MEDIATORS ENDOTHELIUM CONNECTIVE TISSUE CELLS EXTRACELLULAR MATRIX PROBABLY OTHER THINGS WE DON’T KNOW ABOUT YET! |
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INFLAMMATION -REDUNDANT SYSTEM-
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ONE MEDIATOR - MULTIPLE EFFECTS
DIFFERENT MEDIATORS – SAME EFFECT MEDIATORS AMPLIFY RESPONSE BY STIMULATING OTHER MEDIATORS MANY MEDIATORS HAVE YET TO BE DISCOVERED |
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INFLAMMATION -FIVE STEPS (5 R’s)-
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RECOGNITION OF INJURIOUS AGENT
RECRUITMENT OF LEUKOCYTES REMOVAL OF INJURIOUS AGENT REGULATION OF RESPONSE RESOLUTION (REPAIR) |
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INFLAMMATION -CARDINAL CLINICAL SIGNS-
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REDNESS (RUBOR)
SWELLING (TUMOR) HEAT (CALOR) PAIN (DOLOR) LOSS OF FUNCTION (FUNCTIO LAESA) |
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ACUTE INFLAMMATION -PURPOSE-
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ELIMINATE PATHOLOGIC INSULT
REMOVE INJURED TISSUE INITIATE REPAIR |
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ACUTE INFLAMMATION -GENERAL FEATURES-
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RAPID RESPONSE TO INJURY
LASTS FEW MINUTES… FEW DAYS STEREOTYPED RESPONSE (REGARDLESS OF TYPE OF INJURY) INTENSITY EQUALS DEGREE OF INJURY MAY HAVE LOCAL AND SYSTEMIC EFFECTS MAY HARM HOST (FOREIGN AGENTS MAY PERSIST; EXCESSIVE TISSUE DAMAGE MAY OCCUR) DESIGNED TO: DELIVER LEUKOCYTES AND PLASMA PROTEINS, TO THE SITE OF INJURY, TO CLEAR INVADERS AND NECROTIC TISSUE |
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ACUTE INFLAMMATION -STIMULI-
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INFECTIONS (BACTERIA, VIRUSES, FUNGI; MOST COMMON CAUSE)
TRAUMA (PHYSICAL, CHEMICAL, THERMAL) TISSUE NECROSIS (ISCHEMIA) FOREIGN BODIES IMMUNE REACTIONS (HYPERSENSITIVITY REACTIONS; CAN BE SERIOUS) |
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ACUTE INFLAMMATION -STEPS-
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VASCULAR EVENTS
CELLULAR EVENTS |
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ACUTE INFLAMMATION -VASCULAR EVENTS-
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LOCAL VASOCONSTRICTION
VASCULAR DILATATION INCREASED PERMEABILITY LYMPHATIC RESPONSE |
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ACUTE INFLAMMATION -LOCAL VASOCONSTRICTION-
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NEUROGENIC REFLEX TO INJURY
TRANSIENT - RESOLVES WITHIN SECONDS TO MINUTES |
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ACUTE INFLAMMATION -VASCULAR DILATATION-
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INCREASED BLOOD FLOW (ENGORGEMENT OF CAPILLARY BEDS)
ACCOUNTS FOR REDNESS (ERYTHEMA, HYPEREMIA) ACCOUNTS FOR HEAT POSTCAPILLARY VENULE CAUSES STASIS AND SLOWING OF BLOOD (ALLOWS LEUKOCYTES TO MARGINATE) VASOACTIVE MEDIATORS FROM CELLS AND PLASMA |
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ACUTE INFLAMMATION -INCREASED VASCULAR PERMEABILITY-
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↑ INTRAVASCULAR PRESSURE
EXTRAVASCULAR LEAKAGE OF FLUID LOW-PROTEIN TRANSUDATE (WATERY EDEMA FLUID) COLLECTS IN INTERSTITIUM ACCOUNTS FOR SWELLING |
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ENDOTHELIAL CELL CONTRACTION
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INCREASED VASCULAR PERMEABILITY MECHANISMS
MAJOR CAUSE HISTAMINE, BRADYKININ, LEUKOTRIENES IMMEDIATE TRANSIENT RESPONSE (10-15 MIN) CYTOSKELETON CHANGES 4-6 HRS LATER POSTCAPILLARY VENULE |
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ENDOTHELIAL INJURY
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INCREASED VASCULAR PERMEABILITY MECHANISMS
DIRECT INJURY: SEVERE INJURIES (BURNS, INFECTIONS); ENDOTHELIAL CELL NECROSIS/DETACHMENT; IMMEDIATE SUSTAINED RESPONSE (HRS TO DAYS); VENULES, CAPILLARIES, AND ARTERIOLES LEUKOCYTE-MEDIATED: TOXIC MEDIATORS FROM MARGINATED CELLS |
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INCREASED TRANSCYTOSIS
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INCREASED VASCULAR PERMEABILITY MECHANISMS
CHANNELS FORMED BY FUSION OF INTRACELLULAR VESICLES |
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LEAKAGE OF NEW BLOOD VESSELS
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INCREASED VASCULAR PERMEABILITY MECHANISMS
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ACUTE INFLAMMATION -RESPONSE OF LYMPHATIC VESSELS-
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TRANSPORT INJURIOUS AGENT TO LYMPH NODES
LYMPHANGITIS (INF OF LYMPHATIC VESSELS) LYMPHADENITIS (INF OF LYMPH NODES) |
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ACUTE INFLAMMATION -CELLULAR EVENTS-
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LEUKOCYTE RECRUITMENT
LEUKOCYTE ACTIVATION LEUKOCYTE-INDUCED TISSUE INJURY DEFECTS IN LEUKOCYTE FUNCTION |
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HALLMARK CELL OF ACUTE INFLAMMATORY
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POLYMORPHONUCLEAR LEUKOCYTE (PMN OR NEUTROPHIL)
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ACUTE INFLAMMATION -LEUKOCYTE RECRUITMENT-
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MARGINATION
ROLLING ADHESION TRANSMIGRATION CHEMOTAXIS |
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ACUTE INFLAMMATION -MARGINATION-
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PMN’S NORMALLY TRAVEL IN THE CENTER OF THE VESSEL (DUE TO PHYSICS OF LAMINAR FLOW)
STASIS CAUSES PMN’S TO SETTLE TOWARDS THE VESSEL WALL (RBC’S ASSUME CENTER OF FLOW; PMN’S GO TO PERIPHERY OF FLOW) |
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ACUTE INFLAMMATION -ROLLING-
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PMN’S TUMBLE ALONG ENDOTHELIUM
MEDIATORS UPREGULATE SELECTINS (MOVE FROM INTRACELLULAR WEIBEL-PALADE BODIES TO CELL SURFACE; FACILITATE LEUKOCYTE BINDING ONLY AT SITE OF INFLAMMATION PROMOTED BY CYTOKINES (TNF, IL-1) TRANSIENT STICKING TO ENDOTHELIUM (SIALYL-LEWIS X BINDS TO SELECTINS) |
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LEUKOCYTE BINDING AT SITE OF INFLAMMATION
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E-SELECTIN ON ENDOTHELIUM
P-SELECTIN ON ENDOTHELIUM, PLATELETS, AND LEUKOCYTES L-SELECTIN ON LEUKOCYTES |
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SIALYL-LEWIS X BODIES
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CARBYHYDRATE
ON CELL WALLS BLOOD GROUP AG CELL-TO-CELL RECOGNITION MEDIATES ADHESION DEFECT CAUSES IMMUNODEFICIENCY |
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ACUTE INFLAMMATION -ADHESION-
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LEUKOCYTES ADHERE TO ENDOTHELIUM (AKA PAVEMENTING)
MEDIATED BY INTEGRINS ON LEUKOCYTES (ACTIVATED BY CHEMOKINES; BIND TO PROTEOGLYCAN LIGANDS ON ENDOTHELIUM) |
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ACUTE INFLAMMATION -TRANSMIGRATION-
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SQUEEZE THROUGH ENDOTHELIAL INTERCELLULAR JUNCTIONS (AKA DIAPEDESIS)
MAINLY IN VENULES MEDIATED BY PLATELET CELL ADHESION MOLECULES (PCAM) FOCAL DEGRADATION OF BASEMENT BY COLLAGENASES |
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ACUTE INFLAMMATION -CHEMOTAXIS-
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PMN’S FOLLOW CHEMICAL GRADIENT
CHEMICAL SUBSTANCES AT INJURY SITE INDUCE MOVEMENT OF LEUKOCYTES |
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CHEMOTAXIS -CHEMICAL SUBSTANCES-
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BACTERIAL PEPTIDES
CYTOKINES (CHEMOKINES) COMPLEMENT SYSTEM COMPONENTS (C5a) ARACHIDONIC ACID PRODUCTS (LEUKOTRIENE B4) |
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CHEMOTAXIS -MOVEMENT OF LEUKOCYTES-
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G-PROTEIN MEDIATED SIGNALS
↑ CYTOSOLIC CALCIUM ASSEMBLY OF CYTOSKELETON CONTRACTILE ELEMENTS FORMATION OF PSEUDOPODS DIRECTED BY CHEMOTAXIC CHEMICAL GRADIENT |
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NEUTROPHILS
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DOMINATE IN FIRST 6-24 HRS
MOST NUMEROUS RAPID RESPONSE TO CHEMOKINES FIRMLY ATTACH TO ENDOTHELIUM SHORT LIVED (DIE BY APOPTOSIS IN 24-48 HRS) |
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MONOCYTES
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TYPE OF LEUKOCYTE
DOMINATE IN 24-48 HRS PERIOD |
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CHEMOTAXIS -TYPES OF LEUKOCYTES-
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SOME INFECTIONS CONTINUE TO RECRUIT NEUTROPHILS
VIRAL INFECTIONS ATTRACT LYMPHOCYTES EOSINOPHILS DOMINATE IN HYPERSENSITIVITY REACTIONS |
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LEUKOCYTE ACTIVATION -STIMULI-
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MICROBES: TOLL-LIKE RECEPTORS (DETECT ENDOTOXIN); G-PROTEIN RECEPTORS (DETECT BACTERIAL PEPTIDES)
NECROTIC CELLS OTHER MEDIATORS |
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LEUKOCYTE ACTIVATION -RESULTS-
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PHAGOCYTOSIS OF PARTICLES
KILLING OF PHAGOCYTIZED PARTICLES DEGRADATION OF DEAD MICROBES PRODUCTION OF MEDIATORS TO AMPLIFY INFLAMMATION |
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PHAGOCYTOSIS RECOGNITION AND ATTACHMENT
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LEUKOCYTE BINDS TO CELL SURFACE RECEPTORS
ENHANCED BY OPSONIZATION FACILITATES RAPID PHAGOCYTOSIS TRIGGERS ENGULFMENT TYPES: IgG ANTIBODIES; PRODUCTS OF PROTEIN C3 (C3b); COLLECTINS (CARBOHYDRATE-BINDING LECTINS IN PLASMA) |
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PHAGOCYTOSIS ENGULFMENT
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PSEUDOPODS EXTEND AROUND PARTICLE
PHAGOCYTIC VACUOLE (PHAGOSOME) FORMS VACUOLE FUSES WITH LYSOSOME (PHAGOLYSOSOME) |
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OXIDATIVE BURST
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PHAGOCYTOSIS -KILLING PHAGOCYTIZED MATERIALS-
TRIGGERED BY PHAGOCYTOSIS PRODUCTION OF ROS (H2O2…) FREE RADICALS DESTROY MICROBES |
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AZUROPHILIC GRANULES
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PHAGOCYTOSIS -KILLING PHAGOCYTIZED MATERIALS-
CONTAIN MYELOPEROXIDASE HALOGENATION PROCESS |
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OTHER PHAGOCYTOSIS MECHANISMS
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BACTERIAL PERMEABILITY INCREASING PROTEIN
LYSOZYME MAJOR BASIC PROTEIN DEFENSINS |
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LEUKOCYTE ACTIVATION -RESULTS-
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DEGRADATION OF DEAD MICROBES (LYSOSOMAL ACID HYDROLYSIS; ELASTASE)
AMPLIFICATION OF INFLAMMATION (ARACHIDONIC ACID METABOLITES; CYTOKINES) |
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LEUKOCYTE-INDUCED INJURY: INJURY TO NORMAL CELLS
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DOES NOT DISTINGUISH BETWEEN HOST AND OFFENDER
SAME MECHANISMS INVOLVED LYSOSOMAL ENZYMES SECRETED DUE TO: OPEN PHAGOCYTIC VACUOLE TO OUTSIDE; UNDIGESTIBLE MATERIALS (“FRUSTRATED” PHAGOCYTOSIS); PHAGOCYTOSIS OF MATERIALS THAT DAMAGE LYSOSOMAL MEMBRANES (URATE CRYSTALS) |
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LEUKOCYTE-INDUCED INJURY: EXAMPLES
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“BY-STANDER” CELLS: MAJOR SOURCE OF INJURY; CHRONIC INFECTIONS (TB)
ATTEMPT TO CLEAR DAMAGES/DEAD TISSUE: PROLONGES AND EXACERBATES INJURY; REPERFUSION INJURY AFTER MI INAPPROPRIATE INFLAMMATORY RESPONSE: AUTOIMMUNE DISEASES; ALLERGIC DISEASES |
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DEFECTS IN LEUKOCYTE FUNCTION
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SERIOUS, LIFE-THREATENING
LEAD TO RECURRENT INFECTIONS CAUSES: BONE MARROW SUPPRESSION (CHEMOTHERAPY & IRRADIATION); METABOLIC DISEASES (DIABETES MELLITUS); GENETIC DEFECTS |
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LEUKOCYTE ADHESION DEFICIENCY (LAD)
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GENETIC DEFECTS IN LEUKOCYTE FUNCTION
DEFECT IN LEUKOCYTE ADHESION DEFECTIVE INTEGRINS DEFECTIVE PHAGOCYTOSIS |
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MICROBICIDAL INACTIVITY
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GENETIC DEFECTS IN LEUKOCYTE FUNCTION
CHRONIC GRANULOMATOUS DISEASES PHAGOSOME OXIDASE DEFICIENCY MICROBES NOT KILLED MACROPHAGES ACCUMULATE IN GRANULOMAS |
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CHEDIAK-HIGASHI SYNDROME
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GENETIC DEFECTS IN LEUKOCYTE FUNCTION
IMPAIRED TRAFFICKING OF ORGANELLES PHAGOSOME FAILS TO FUSE WITH LYSOSOME IMPAIRED FUNCTION OF CYTOTOXIC T-CELLS SEVERE IMMUNIDEFICIENCY |
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ACUTE INFLAMMATION -CHEMICAL MEDIATION-
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COMPLEX PROCESS
MANY KNOWN MEDIATORS MANY UNKNOWN MEDIATORS KNOWLEDGE USED TO PHARMACOLOGICALLY ALTER PROCESS (ANTI-INFLAMMATORY DRUGS; INFLAMMATORY-INDUCING DRUGS) SOME PRODUCED BY INF CELLS (IN CYTOPLASMIC GRANULES; SECRETED AFTER CELL ACTIVATION) SOME CIRCULATE SYSTEMICALLY (MOST MADE BY LIVER; IN INACTIVE FORM; ACTIVATED AT INF SITE BY PROTEOLYTIC CLEAVAGE) MOST BIND TO RECEPTORS ON TARGET CELLS (MAY HAVE ONE OR SEVERAL TARGETS; MAY HAVE DIFFERENT EFFECT WITH DIFFERENT TARGETS) TARGET CELLS MAY RELEASE SECONDARY EFFECTOR MEDIATORS (SOME HAVE SIMILAR EFFECTS AND AMPLIFY PROCESS; SOME HAVE OPPOSING EFFECTS TO REGULATE PROCESS) ACTIONS TIGHTLY REGULATED (DECAY RAPIDLY; INACTIVATED BY ENZYMES; ELIMINATED BY SCAVENGER MOLECULES; SOME ARE INHIBITED) |
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ACUTE INFLAMMATION -CELL-DERIVED MEDIATORS-
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VASOACTIVE AMINES
ARACHIDONIC ACID METABOLITES PLATELET-ACTIVATING FACTOR CYTOKINES REACTIVE OXYGEN SPECIES (ROS) NITRIC OXIDE LEUKOCYTE LYSOSOMAL ENZYMES NEUROPEPTIDES |
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ACUTE INFLAMMATION -VASOACTIVE AMINES-
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HISTAMINE FROM MAST CELLS
SEROTONIN FROM PLATELETS |
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ACUTE INFLAMMATION -HISTAMINE-
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MAINLY FROM MAST CELLS (ALSO EOSINOPHILS & PLATELETS)
INACTIVATED BY HISTAMINASE COUNTERACTED BY ANTIHISTAMINIC DRUGS |
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HISTAMINE STIMULI FOR RELEASE
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PHYSICAL INJURY
IMMUNE REACTIONS - BINDING OF IgE TO Fc RECEPTORS ANAPHYLATOXINS - C3a AND C5a FRAGMENTS LEUKOCYTE-DERIVED HISTAMINE RELEASING PROTEIN S NEUROPEPTIDES - SUBSTANCE P CERTAIN CYTOKINES – IL-1 AND IL-8 |
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HISTAMINE FUNCTIONS
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ARTERIAL DILATION
INCREASED VASCULAR PERMEABILITY (IMMEDIATE PHASE; ENDOTHELIAL CONTRACTION; CREATION OF INTERENDOTHELIAL GAPS) |
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ANTIHISTAMINICS
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DIPHENHYDRAMINE
BENADRYL® H1 RECEPTOR ANTAGONIST |
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ACUTE INFLAMMATION -SEROTONIN-
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5-HYDROXYTRYPTAMINE
RELEASED FROM PLATELETS (PLATELET DENSE GRANULES) RELEASED DURING PLATELET AGGREGATION SAME ACTIONS AS HISTAMINE (VASCULAR DILATION; ↑ VASCULAR PERMEABILITY) |
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ACUTE INFLAMMATION -ARACHIDONIC ACID METABOLITES-
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EICASANOIDS
SHORT-ACTING HORMONES MEDIATE EVERY STEP OF INF INHIBITING AGENTS ↓ INF LEUKOCYTES, MAST CELLS, ENDOTHELIAL CELLS, PLATELETS |
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ACUTE INFLAMMATION ARACHIDONIC ACID PATHWAYS
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CYCLOOXYGENASE PATHWAY (PROSTAGLANDINS; THROMBOXANE A2)
LIPOOXYGENASE PATHWAY (LEUKOTRIENES; LIPOXINS) |
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ACUTE INFLAMMATION -PLATELET ACTIVATING FACTOR-
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PHOSPHOLIPID MEDIATORS
LEUKOCYTES AND PLATELETS BROAD SPECTRUM OF EFFECTS VASODILATION AND ↑ PERMEABILITY ALSO LEUKOCYTE ADHESION, CHEMOTAXIS |
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ACUTE INFLAMMATION -CYTOKINES-
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POLYPEPTIDE MEDIATORS
ACTIVATED MACROPHAGES INFLAMMATION AND IMMUNITY SYSTEMIC ACUTE-PHASE RXN TYPES: BRADYKININ, INTERLEUKINS, TUMOR NECROSIS FACTOR, CHEMOKINES |
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ACUTE INFLAMMATION -BRADYKININ-
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VASCULAR DILATION
INCREASED VASCULAR PERMEABILITY PAIN |
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ACUTE INFLAMMATION -INTERLEUKINS AND TNF-
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ACT ON LEUKOCYTES
MEDIATE CELL COMMUNICATION ACTIVATES ENDOTHELIUM (BIND LEUKOCYTES) SYSTEMIC ACUTE PHASE RXN (FEVER) ACTIVATE FIBROBLASTS STIMULATE MORE CYTOKINES |
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ACUTE INFLAMMATION -CHEMOKINES-
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CHEMOATTRACTION FOR LEUKOCYTES
DIFFERENT CHEMOKINES ATTRACT DIFFERENT CELLS LEUKOCYTE ACTIVATION |
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ACUTE INFLAMMATION -REACTIVE OXYGEN SPECIES-
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CAUSE TISSUE INJURY
AMPLIFY CASCADE OF MEDIATORS |
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ACUTE INFLAMMATION -NITRIC OXIDE-
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INDUCED BY CYTOKINES
CAUSES VASODILATION |
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ACUTE INFLAMMATION -LEUKOCYTE LYSOSOMAL ENZYMES-
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PROTEASES (ELASTASE; COLLAGENASE)
INACTIVATED BY ANTIPROTEASES (IN SERUM AND TISSUE FLUIDS; α1-ANTITRYPSIN INHIBITS ELASTASE; DEFICIENCY SUSTAINS INF IE EMPHYSEMA) |
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ACUTE INFLAMMATION -NEUROPEPTIDES-
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SUBSTANCE P
TRANSMITS PAIN SIGNALS MODULATES VASCULAR PERMEABILITY IMPORTANT IN LUNGS AND GIT |
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ACUTE INFLAMMATION -PLASMA-PROTEIN DERIVED MEDIATORS-
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COMPLEMENT
KININS COAGULATION SYSTEM |
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ACUTE INFLAMMATION -COMPLEMENT- PLASMA PROTEINS (C1-C9)
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ACTIVE C3 IS CRITICAL STEP
CLASSIC PATHWAY ALTERNATIVE PATHWAY LECTIN PATHWAY |
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ACUTE INFLAMMATION -COMPLEMENT- EFFECTS
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FORMATION OF MEMBRANE ATTACK COMPLEX (C3a AND C5a: ANAPHYLACTOXINS; CAUSE MAST CELLS TO RELEASE HISTAMINE; ACTIVATE LIPOXYGENASE PATHWAY)
LEUKOCYTE ACTIVATION, ADHESION, CHEMOSTAXIS PHAGOCYTOSIS – OPSONIZATION C3b |
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ACUTE INFLAMMATION -COMPLEMENT- INHIBITION
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PLASMA REGULATORY PROTEINS
PREVENTS DAMAGE TO NORMAL CELLS INAPPROPRIATE/EXCESSIVE ACTIVATION SERIOUS |
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ACUTE INFLAMMATION -KININS-
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BRADYKININ (ACTIVATE HAGEMAN FACTOR)
VASCULAR DILATION INCREASED PERMEABILITY PAIN |
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ACUTE INFLAMMATION -COAGULATION SYSTEM-
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THROMBIN MOST IMPORTANT
ACTIVATES ENDOTHELIUM (ENHANCES ADHESION) GENERATES FIBRINOPEPTIDES (↑ VASCULAR PERMEABILITY; LEUKOCYTE CHEMOTAXIS) |
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ACUTE INFLAMMATION -TERMINATION-
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LOSS OF CHEMICAL MEDIATORS (NEUTRALIZATION; DECAY; DEGRADATION)
VASCULAR PERMEABILITY RETURNS TO NORMAL LEUKOCYTE ACTIVITY CEASES INHIBITORY MEDIATORS (FROM LEUKOCYTES) REMOVAL OF DEBRIS (LYMPHATIC DRAINAGE; MACROPHAGE PHAGOCYTOSIS) |
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ACUTE INFLAMMATION -OUTCOMES-
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DEPENDS ON: NATURE & INTENSITY OF INFLAMMATION; SITE AND TISSUE INVOLVED; ABILITY OF HOST TO RESPOND
GENERALLY ONE OF THE FOLLOWING: RESOLUTION; PROGRESSION TO CHRONIC INF; SCARRING OR FIBROSIS |
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ACUTE INFLAMMATION -RESOLUTION-
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TISSUE RESTORED TO NORMAL STATE
MILD, SHORT-LIVED INJURY MINIMAL TISSUE DAMAGE LABILE OR STABLE TISSUE |
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ACUTE INFLAMMATION -PROGRESS TO CHRONIC INFLAMMATION-
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OFFENDING AGENT NOT REMOVED
MAY START AS CHRONIC INF MAY LEAD TO RESOLUTION, OR LEAD TO SCARRING |
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ACUTE INFLAMMATION -SCARRING-
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HEALING WITH COLLAGEN (FIBROSIS)
AFTER SEVERE INJURY, OR STABLE OR PERMANENT TISSUES FIBRINOUS EXUDATES, ABSCESSES |
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CHRONIC INFLAMMATION -GENERAL FEATURES-
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PROLONGED DURATION (WEEKS… MONTHS… YEARS)
SIMULTANEOUS (INFLAMMATION; HEALING; TISSUE INJURY) |
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CHRONIC INFLAMMATION -CHARACTERISTICS-
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MONONUCLEAR CELLS INFILTRATION (MACROPHAGES; LYMPHOCYTES; PLASMA CELLS)
TISSUE DESTRUCTION REPAIR (ANGIOGENESIS; FIBROSIS) |
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PROGRESSION OF ACUTE INF
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CHRONIC INFLAMMATION -STIMULIS-
INJURY NOT RESOLVES PERSISTENCE OF INJURIOUS AGENT INTERFERENCE WITH HEALING |
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PERSISTENT INFECTIONS
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CHRONIC INFLAMMATION -STIMULIS-
MICROBES DIFFICULT TO ERADICATE MYCOBACTERIA, TREPONEMA CERTAIN VIRUSES AND FUNGI T-LYMPHOCYTE-MEDIATED RESPONSE |
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IMMUNE-RELATED DISEASES
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CHRONIC INFLAMMATION -STIMULIS-
HYPERSENSITIVITY DISEASES AUTOIMMUNE DISEASES SELF-PERPETUATING REACTIONS |
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PROLONGED EXPOSURE TO TOXIC AGENTS
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CHRONIC INFLAMMATION -STIMULIS-
NONDEGRADABLE MATERIALS (SILICA) |
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CHRONIC INFLAMMATION -CELLS-
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MACROPHAGES
LYMPHOCYTES PLASMA CELLS EOSINOPHILS MAST CELLS NEUTROPHILS |
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CHRONIC INFLAMMATION -MACROPHAGES-
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DOMINANT CELL OF CHRONIC INF
DERIVED FROM BLOOD MONOCYTES |
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CHRONIC INFLAMMATION -MACROPHAGES- TYPES
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CONNECTIVE TISSUE MACROPHAGES
KUPFFER CELLS OF LIVER SINUS HISTIOCYTES OF SPLEEN/NODES MICROGLIAL CELLS OF CNS ALVEOLAR MACROPHAGES OF LUNGS |
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CHRONIC INFLAMMATION -MACROPHAGES- FUNCTIONS
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FILTER PARTICULATE MATTER (FOREIGN DEBRIS, MICROBES, DEAD CELLS)
ANTI-PRESENTING CELLS |
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CHRONIC INFLAMMATION -MACROPHAGE LIFE CYCLE-
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CIRCULATING MONOCYTE (1-2 DAYS; ADHERENT MONOCYTE; EMIGRATING MONOCYTE)
TISSUE MACROPHAGE (ENLARGE; ↑ PHAGOCYTIC ACTIVITY; ↑ LIFE SPAN) ACTIVATED MACROPHAGE (ENLARGE AGAIN; ↑ LYSOSOMAL ENZYMES; ↑ KILLING CAPACITY) |
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CHRONIC INFLAMMATION -MACROPHAGE MORPHOLOGY-
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LARGE, FLAT, PINK
SIMILAR TO EPITHELIAL CELLS (EPITHELOID CELLS) MAY FUSE TO FORM “GIANT CELLS” (FOREIGN BODY; LANGERHANS - TB; TOUTON – XANTHOGRANULOMA) |
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CHRONIC INFLAMMATION -MACROPHAGE ACTIVATION-
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BACTERIAL ENDOTOXINS
CYTOKINES ACUTE INF MEDIATORS EXTRACELLULAR MATRIX PROTEINS (FIBRONECTIN) |
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CHRONIC INFLAMMATION -MACROPHAGE PRODUCTS-
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PROTEASES: PLASMINOGEN ACTIVATOR (AMPLIFIES INFLAMMATION)
ROS AND NO ARACHIDONIC ACID METABOLITES CYTOKINES (IL, TNF, GROWTH FACTORS) |
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CHRONIC INFLAMMATION -MACROPHAGE RESOLUTION-
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DIE
WANDER OFF INTO LYMPHATICS MAY ACCUMULATE (STEADY RELEASE OF CHEMOKINES; GRANULOMATOUS INFLAMMATION) |
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CHRONIC INFLAMMATION -LYMPHOCYTES-
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RESPOND TO: SPECIFIC IMMUNE STIMULI; NON-IMMUNE STIMULI (TISSUE NECROSIS)
BOTH T AND B CELLS MECHANISM OF ATTRACTION (ADHESION MOLECULES AND CYTOKINES; ANTIGEN PRESENTATION) |
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CHRONIC INFLAMMATION -PLASMA CELLS-
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FROM ACTIVATED B LYMPHOCYTES
PRODUCE ANTIBODIES AGAINST PERSISTENT ANTIGENS |
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CHRONIC INFLAMMATION -EOSINOPHILS-
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PARASITIC INFECTIONS
BASIC PROTEIN TOXIC TO PARASITES ALLERGIES FUNCTION SIMILAR TO NEUTROPHILS |
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CHRONIC INFLAMMATION -OTHER CELLS-
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MAST CELLS (MOST IMPORTANT IN ACUTE INF)
NEUTROPHILS (PERSISTENT MICROBES OR NECROTIC TISSUE) |
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GRANULOMATOUS INFLAMMATION
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DISTINCTIVE FORM OF CHRONIC INF
AGGREGATES OF ACTIVATES MACROPHAGES “WALLS OFF” OFFENDING AGENT DOES NOT ERADICATE AGENT MAY TERMINATE IN FIBROSIS (WITH ORGAN DYSFUNCTION) |
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GRANULOMATOUS INFLAMMATION -STIMULI-
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CERTAIN MICROBES: TUBERCULOSIS, LEPROSY, SYPHILIS, CAT SCRATCH FEVER, SARCOIDOSIS, CROHN’S DISEASE, FUNGI
INERT FOREIGN BODIES: FOREIGN BODY GRANULOMAS |
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GRANULOMATOUS INFLAMMATION -MICROSCOPIC APPEARANCE-
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SPHERICAL LESIONS (MAY COALESE TOGETHER)
CENTRAL ZONE OF NECROSIS (NOT IN ALL CASES IE NON-CASEATING GRANULOMAS; CASEOUS NECROSIS IN TB; AMORPHOUS CELL DEBRIS; DUE TO HYPOXIA AND FREE-RADICAL INJURY) THICK LAYER OF MACROPHAGES (LARGE, ACTIVATED CELLS WITH PINK CYTOPLASM; MAY PACK TOGETHER AND BECOME EPITHELOID; MAY FORM MULTINUCLEATED GIANT CELLS) THIN LAYER OF LYMPHOCYTES (SECRETING CYTOKINES TO ACTIVATE MACROPHAGES) OUTER LAYER OF FIBROSIS (INCREASES AS GRANULOMA AGES; MAY IMPAIR FUNCTION) |
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INFLAMMATION -CLASSIFICATION-
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DURATION
LOCATION TYPE OF EDEMA MORPHOLOGY |
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INFLAMMATION -CLASSIFICATION BY DURATION-
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ACUTE: EDEMA, STIMULATION OF PLATELETS, PRESENCE OF PMN’S
CHRONIC: LYMPHOYTES, PLASMA CELLS, MACROPHAGES |
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INFLAMMATION -CLASSIFICATION BY LOCATION-
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ADD –ITIS TO TISSUE TYPE: APPENDICITIS, GINGIVITIS
EXCEPTIONS: PNEUMONIA |
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EDEMA IS
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ACCUMULATION OF FLUID IN THE EXTRACELLULAR COMPARTMENT AND INTERSTITIAL TISSUES
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INFLAMMATION -CLASSIFICATION BY TYPE OF EDEMA-
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EFFUSION: EDEMA IN A BODY CAVITY
TRANSUDATE: NON-INFLAMMATORY (LOW PROTEIN; LOW SPECIFIC GRAVITY) EXUDATE: INFLAMMATORY (HIGH PROTEIN; HIGH SPECIFIC GRAVITY) |
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INFLAMMATION -PATTERNS OF EXUDATION-
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SEROUS
SUPPURATIVE (PURULENT) FIBRINOUS SEROSANGUINOUS CATARRHAL |
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SEROUS EXUDATE
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MILD INJURY
WATERY, LOW PROTEIN FLIUD (TRANSUDATE; CHIEFLY SERUM) YELLOW/STRAWBERRY COLORED BLISTER – FRICTIONAL, BURN, VIRAL EFFUSIONS ARE OFTEN SEROUS MAY BECOME PURULENT WITH SECONDARY INFECTION |
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SUPPURATIVE EXUDATE
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PURULENT INFLAMMATION
COMMONLY CALLED PUS COMPOSED OF PMN’S AND NECROTIC DEBRIS PYOGENIC INFECTIONS (STAPH, STREP; ABSCESSES: LOCALIZED; CELLULITIS: DIFFUSE) LEAD TO SCARRING |
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ABSCESSES
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SUPPURATIVE EXUDATE
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CELLULITIS
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SUPPURATIVE EXUDATE
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FIBRINOUS EXUDATE
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MORE SEVERE INJURIES
GREAT VASCULAR PERMEABILITY (FIBINOGEN ESCAPES AND POLYMERIZES INTO FIBRIN) OFTEN INVOLVES BODY CAVITIES: MENINGITIS (MENINGITIS); PERICARDIUM (FIBRINOUS PERICARDITIS, RHEUMATIC FEVER); PLEURA (PLEURITIS) |
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SEROSANGUINOUS EXUDATE
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SEROUS EXUDATE WITH RBC’s
BLOOD BLISTER |
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CATARRHAL EXUDATE
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CONTAINS MUCOUS
COMMON COLD |
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INFLAMMATION -CLASSIFICATION BY MORPHOLOGY-
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ABSCESS
CELLULITIS ULCERATIVE PSEUDOMEMBRANEOUS |
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ABSCESS
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LOCALIZED ACCUMULATION OF SUPPURATIVE EXUDATE
PUS = DEAD AND LIVE NEUTROPHILS + NECROTIC DEBRIS |
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CELLULITIS
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DIFFUSE, ILL-DEFINED, SPREADING PURULENT INFECTION
RED AND HOT HYALURONIDASE, ETC FROM BACTERIA |
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ULCERATIVE
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NECROSIS OF SURFACE TISSUES
LOSS OF SURFACE EPITHELIUM COVERED WITH INFLAMED NECROTIC TISSUE (GRANUMATION TISSUE AND FIBROSIS) SKIN, MOUTH, STOMACH, INTESTINES, GU TRACT SYPHILITIC CHANCRE, PEPTIC ULCER |
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PSEUDOMEMBRANOUS
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SIMILAR TO ULCERATIVE BUT NOT AS DEEP
SUPERICIAL EXUDATE OF: FIBRIN, PMN’S, NECROTIC DEBRIS USUALLY COVERS AN ULCER DIPHTHERIAL PHARYNGITIS, ULCERATIVE COLITIS, PEMPHIGUS |
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INFLAMMATION -SYSTEMIC MANIFESTATIONS-
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FEVER
ELEVATED PLASMA PROTEINS LEUKOCYTOSIS SEPSIS OTHER CHANGES: CARDIOVASCULAR CHANGES, ANOREXIA, SOMNOLENCE, MALAISE, CACHEXIA |
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INFLAMMATION -FEVER-
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ELEVATION OF BODY TEMPERATURE USUALLY 1-4º C
USUALLY OCCURS WITH INFECTION MAY HELP WARD OFF INFECTION PYROGENS CYCLOOXYGENASE INHIBITORS: NASIDS (ASPIRIN) INHIBIT IL-1 |
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INFLAMMATION -FEVER- PYROGENS
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EXOGENOUS (LIPOPOLYSACCHARIDES FROM BACTERIA)
STIMULATE CYTOKINE SECRETION (ENDOGENOUS PYROGENS) IL-1, IL-6, TNF- ↑ CYCLOOXYGENASE… ARACHIDONIC ACID…PROSTAGLANDINS (RELEASE NEUROTRANSMITTERS IN HYPOTHALAMUS; ALTERS “THERMOSTAT” TO HIGHER TEMPERATURE) |
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INFLAMMATION ↑ PLASMA PROTEINS
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CYTOKINES STIMULATE HEPATOCYTES
“ACUTE PHASE” PROTEINS: C-REACTIVE PROTEIN; FIBRINOGEN (BINDS RBC’S, ↑ SED RATE); SERUM AMYLOID A PROTEIN ACT AS OPSONINS, FIX COMPLEMENT… USEFUL LAB TESTS CRP USED TO DX MI |
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INFLAMMATION -LEUKOCYTOSIS-
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INCREASE IN CIRCULATING LEUKOCYTES (MAY INCREASE 3-20 FOLD; LEUKEMOID REACTION)
ESPECIALLY WITH BACTERIAL INFECTIONS ACCELERATED RELEASE FROM MARROW (MEDIATES BY CYTOKINES IE IL-1, TNF; COLONY STIMULATING FACTORS) NEUTROPHILIA IS THE HALLMARK OF ACUTE INFLAMMATION (“SHIFT TO THE LEFT” INDICATES BACTERIAL INFECTION) LYMPHOCYTES INCREASE IN VIRAL INFECTIONS EOSINOPHILIA WITH PARASITIC AND ALLERGIES PARADOXICAL LEUKOPENIA MAY OCCUR (DECREASED WBC COUNT; CYTOKINE-INDUCED SEQUESTERING OF LEUKOCYTES IN NODES; TYPHOID, RICKETTSIA, SOME VIRUSES & PARASITES) |
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INFLAMMATION -SEPSIS-
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SEVERE BACTERIAL INFECTIONS
LARGE VOLUME OF LPS (MASSIVE CYTOKINE PRODUCTION) SEPTIC SHOCK (DIC, HYPOGLYCEMIA, HYPOTENSION) |
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INFLAMMATION -OTHER SYSTEMIC CHANGES-
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ANOREXIA (TNF-MEDIATED APPETITE SUPPRESSION)
SOMNOLENCE (CYTOKINE ACTION ON CNS) MALAISE (CYTOKINE ACTION ON CNS) CACHEXIA (WASTING SYNDROME) |
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INFLAMMATION CARDIOVASCULAR CHANGES
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↑ HEART RATE
↑ BLOOD PRESSURE ↓ SWEATING CHILLS (PRECEPTION OF BEING COLD) RIGORS (SHIVERING) REDIRECTED BLOOD FLOW TO DEEP TISSUES RELATED TO FEVER |
