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126 Cards in this Set

  • Front
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INFLAMMATION IS
A RESPONSE OF THE BODY TO INJURY WHICH INVOLVES NEURAL, VASCULAR, CHEMICAL, AND CELLULAR PROCESSES
INFLAMMATION
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)
INFLAMMATION INVOLVES
BLOOD LEUKOCYTES

PLASMA PROTEINS AND OTHER MEDIATORS

ENDOTHELIUM

CONNECTIVE TISSUE CELLS

EXTRACELLULAR MATRIX

PROBABLY OTHER THINGS WE DON’T KNOW ABOUT YET!
INFLAMMATION -REDUNDANT SYSTEM-
ONE MEDIATOR - MULTIPLE EFFECTS

DIFFERENT MEDIATORS – SAME EFFECT

MEDIATORS AMPLIFY RESPONSE BY STIMULATING OTHER MEDIATORS

MANY MEDIATORS HAVE YET TO BE DISCOVERED
INFLAMMATION -FIVE STEPS (5 R’s)-
RECOGNITION OF INJURIOUS AGENT

RECRUITMENT OF LEUKOCYTES

REMOVAL OF INJURIOUS AGENT

REGULATION OF RESPONSE

RESOLUTION (REPAIR)
INFLAMMATION -CARDINAL CLINICAL SIGNS-
REDNESS (RUBOR)

SWELLING (TUMOR)

HEAT (CALOR)

PAIN (DOLOR)

LOSS OF FUNCTION (FUNCTIO LAESA)
ACUTE INFLAMMATION -PURPOSE-
ELIMINATE PATHOLOGIC INSULT

REMOVE INJURED TISSUE

INITIATE REPAIR
ACUTE INFLAMMATION -GENERAL FEATURES-
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
ACUTE INFLAMMATION -STIMULI-
INFECTIONS (BACTERIA, VIRUSES, FUNGI; MOST COMMON CAUSE)

TRAUMA (PHYSICAL, CHEMICAL, THERMAL)

TISSUE NECROSIS (ISCHEMIA)

FOREIGN BODIES

IMMUNE REACTIONS (HYPERSENSITIVITY REACTIONS; CAN BE SERIOUS)
ACUTE INFLAMMATION -STEPS-
VASCULAR EVENTS

CELLULAR EVENTS
ACUTE INFLAMMATION -VASCULAR EVENTS-
LOCAL VASOCONSTRICTION

VASCULAR DILATATION

INCREASED PERMEABILITY

LYMPHATIC RESPONSE
ACUTE INFLAMMATION -LOCAL VASOCONSTRICTION-
NEUROGENIC REFLEX TO INJURY

TRANSIENT - RESOLVES WITHIN SECONDS TO MINUTES
ACUTE INFLAMMATION -VASCULAR DILATATION-
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
ACUTE INFLAMMATION -INCREASED VASCULAR PERMEABILITY-
↑ INTRAVASCULAR PRESSURE

EXTRAVASCULAR LEAKAGE OF FLUID

LOW-PROTEIN TRANSUDATE (WATERY EDEMA FLUID)

COLLECTS IN INTERSTITIUM

ACCOUNTS FOR SWELLING
ENDOTHELIAL CELL CONTRACTION
INCREASED VASCULAR PERMEABILITY MECHANISMS

MAJOR CAUSE

HISTAMINE, BRADYKININ, LEUKOTRIENES

IMMEDIATE TRANSIENT RESPONSE (10-15 MIN)

CYTOSKELETON CHANGES 4-6 HRS LATER

POSTCAPILLARY VENULE
ENDOTHELIAL INJURY
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
INCREASED TRANSCYTOSIS
INCREASED VASCULAR PERMEABILITY MECHANISMS

CHANNELS FORMED BY FUSION OF INTRACELLULAR VESICLES
LEAKAGE OF NEW BLOOD VESSELS
INCREASED VASCULAR PERMEABILITY MECHANISMS
ACUTE INFLAMMATION -RESPONSE OF LYMPHATIC VESSELS-
TRANSPORT INJURIOUS AGENT TO LYMPH NODES

LYMPHANGITIS (INF OF LYMPHATIC VESSELS)

LYMPHADENITIS (INF OF LYMPH NODES)
ACUTE INFLAMMATION -CELLULAR EVENTS-
LEUKOCYTE RECRUITMENT

LEUKOCYTE ACTIVATION

LEUKOCYTE-INDUCED TISSUE INJURY

DEFECTS IN LEUKOCYTE FUNCTION
HALLMARK CELL OF ACUTE INFLAMMATORY
POLYMORPHONUCLEAR LEUKOCYTE (PMN OR NEUTROPHIL)
ACUTE INFLAMMATION -LEUKOCYTE RECRUITMENT-
MARGINATION

ROLLING

ADHESION

TRANSMIGRATION

CHEMOTAXIS
ACUTE INFLAMMATION -MARGINATION-
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)
ACUTE INFLAMMATION -ROLLING-
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)
LEUKOCYTE BINDING AT SITE OF INFLAMMATION
E-SELECTIN ON ENDOTHELIUM

P-SELECTIN ON ENDOTHELIUM, PLATELETS, AND LEUKOCYTES

L-SELECTIN ON LEUKOCYTES
SIALYL-LEWIS X BODIES
CARBYHYDRATE

ON CELL WALLS

BLOOD GROUP AG

CELL-TO-CELL RECOGNITION

MEDIATES ADHESION

DEFECT CAUSES IMMUNODEFICIENCY
ACUTE INFLAMMATION -ADHESION-
LEUKOCYTES ADHERE TO ENDOTHELIUM (AKA PAVEMENTING)

MEDIATED BY INTEGRINS ON LEUKOCYTES (ACTIVATED BY CHEMOKINES; BIND TO PROTEOGLYCAN LIGANDS ON ENDOTHELIUM)
ACUTE INFLAMMATION -TRANSMIGRATION-
SQUEEZE THROUGH ENDOTHELIAL INTERCELLULAR JUNCTIONS (AKA DIAPEDESIS)

MAINLY IN VENULES

MEDIATED BY PLATELET CELL ADHESION MOLECULES (PCAM)

FOCAL DEGRADATION OF BASEMENT BY COLLAGENASES
ACUTE INFLAMMATION -CHEMOTAXIS-
PMN’S FOLLOW CHEMICAL GRADIENT

CHEMICAL SUBSTANCES AT INJURY SITE

INDUCE MOVEMENT OF LEUKOCYTES
CHEMOTAXIS -CHEMICAL SUBSTANCES-
BACTERIAL PEPTIDES

CYTOKINES (CHEMOKINES)

COMPLEMENT SYSTEM COMPONENTS (C5a)

ARACHIDONIC ACID PRODUCTS (LEUKOTRIENE B4)
CHEMOTAXIS -MOVEMENT OF LEUKOCYTES-
G-PROTEIN MEDIATED SIGNALS

↑ CYTOSOLIC CALCIUM

ASSEMBLY OF CYTOSKELETON CONTRACTILE ELEMENTS

FORMATION OF PSEUDOPODS

DIRECTED BY CHEMOTAXIC CHEMICAL GRADIENT
NEUTROPHILS
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)
MONOCYTES
TYPE OF LEUKOCYTE

DOMINATE IN 24-48 HRS PERIOD
CHEMOTAXIS -TYPES OF LEUKOCYTES-
SOME INFECTIONS CONTINUE TO RECRUIT NEUTROPHILS

VIRAL INFECTIONS ATTRACT LYMPHOCYTES

EOSINOPHILS DOMINATE IN HYPERSENSITIVITY REACTIONS
LEUKOCYTE ACTIVATION -STIMULI-
MICROBES: TOLL-LIKE RECEPTORS (DETECT ENDOTOXIN); G-PROTEIN RECEPTORS (DETECT BACTERIAL PEPTIDES)

NECROTIC CELLS

OTHER MEDIATORS
LEUKOCYTE ACTIVATION -RESULTS-
PHAGOCYTOSIS OF PARTICLES

KILLING OF PHAGOCYTIZED PARTICLES

DEGRADATION OF DEAD MICROBES

PRODUCTION OF MEDIATORS TO AMPLIFY INFLAMMATION
PHAGOCYTOSIS RECOGNITION AND ATTACHMENT
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)
PHAGOCYTOSIS ENGULFMENT
PSEUDOPODS EXTEND AROUND PARTICLE

PHAGOCYTIC VACUOLE (PHAGOSOME) FORMS

VACUOLE FUSES WITH LYSOSOME (PHAGOLYSOSOME)
OXIDATIVE BURST
PHAGOCYTOSIS -KILLING PHAGOCYTIZED MATERIALS-

TRIGGERED BY PHAGOCYTOSIS

PRODUCTION OF ROS (H2O2…)

FREE RADICALS DESTROY MICROBES
AZUROPHILIC GRANULES
PHAGOCYTOSIS -KILLING PHAGOCYTIZED MATERIALS-

CONTAIN MYELOPEROXIDASE

HALOGENATION PROCESS
OTHER PHAGOCYTOSIS MECHANISMS
BACTERIAL PERMEABILITY INCREASING PROTEIN

LYSOZYME

MAJOR BASIC PROTEIN

DEFENSINS
LEUKOCYTE ACTIVATION -RESULTS-
DEGRADATION OF DEAD MICROBES (LYSOSOMAL ACID HYDROLYSIS; ELASTASE)

AMPLIFICATION OF INFLAMMATION (ARACHIDONIC ACID METABOLITES; CYTOKINES)
LEUKOCYTE-INDUCED INJURY: INJURY TO NORMAL CELLS
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)
LEUKOCYTE-INDUCED INJURY: EXAMPLES
“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
DEFECTS IN LEUKOCYTE FUNCTION
SERIOUS, LIFE-THREATENING

LEAD TO RECURRENT INFECTIONS

CAUSES: BONE MARROW SUPPRESSION (CHEMOTHERAPY & IRRADIATION); METABOLIC DISEASES (DIABETES MELLITUS); GENETIC DEFECTS
LEUKOCYTE ADHESION DEFICIENCY (LAD)
GENETIC DEFECTS IN LEUKOCYTE FUNCTION

DEFECT IN LEUKOCYTE ADHESION

DEFECTIVE INTEGRINS

DEFECTIVE PHAGOCYTOSIS
MICROBICIDAL INACTIVITY
GENETIC DEFECTS IN LEUKOCYTE FUNCTION

CHRONIC GRANULOMATOUS DISEASES

PHAGOSOME OXIDASE DEFICIENCY

MICROBES NOT KILLED

MACROPHAGES ACCUMULATE IN GRANULOMAS
CHEDIAK-HIGASHI SYNDROME
GENETIC DEFECTS IN LEUKOCYTE FUNCTION

IMPAIRED TRAFFICKING OF ORGANELLES

PHAGOSOME FAILS TO FUSE WITH LYSOSOME

IMPAIRED FUNCTION OF CYTOTOXIC T-CELLS

SEVERE IMMUNIDEFICIENCY
ACUTE INFLAMMATION -CHEMICAL MEDIATION-
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)
ACUTE INFLAMMATION -CELL-DERIVED MEDIATORS-
VASOACTIVE AMINES

ARACHIDONIC ACID METABOLITES

PLATELET-ACTIVATING FACTOR

CYTOKINES

REACTIVE OXYGEN SPECIES (ROS)

NITRIC OXIDE

LEUKOCYTE LYSOSOMAL ENZYMES

NEUROPEPTIDES
ACUTE INFLAMMATION -VASOACTIVE AMINES-
HISTAMINE FROM MAST CELLS

SEROTONIN FROM PLATELETS
ACUTE INFLAMMATION -HISTAMINE-
MAINLY FROM MAST CELLS (ALSO EOSINOPHILS & PLATELETS)

INACTIVATED BY HISTAMINASE

COUNTERACTED BY ANTIHISTAMINIC DRUGS
HISTAMINE STIMULI FOR RELEASE
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
HISTAMINE FUNCTIONS
ARTERIAL DILATION

INCREASED VASCULAR PERMEABILITY (IMMEDIATE PHASE; ENDOTHELIAL CONTRACTION; CREATION OF INTERENDOTHELIAL GAPS)
ANTIHISTAMINICS
DIPHENHYDRAMINE

BENADRYL®

H1 RECEPTOR ANTAGONIST
ACUTE INFLAMMATION -SEROTONIN-
5-HYDROXYTRYPTAMINE

RELEASED FROM PLATELETS (PLATELET DENSE GRANULES)

RELEASED DURING PLATELET AGGREGATION

SAME ACTIONS AS HISTAMINE (VASCULAR DILATION; ↑ VASCULAR PERMEABILITY)
ACUTE INFLAMMATION -ARACHIDONIC ACID METABOLITES-
EICASANOIDS

SHORT-ACTING HORMONES

MEDIATE EVERY STEP OF INF

INHIBITING AGENTS ↓ INF

LEUKOCYTES, MAST CELLS, ENDOTHELIAL CELLS, PLATELETS
ACUTE INFLAMMATION ARACHIDONIC ACID PATHWAYS
CYCLOOXYGENASE PATHWAY (PROSTAGLANDINS; THROMBOXANE A2)

LIPOOXYGENASE PATHWAY (LEUKOTRIENES; LIPOXINS)
ACUTE INFLAMMATION -PLATELET ACTIVATING FACTOR-
PHOSPHOLIPID MEDIATORS

LEUKOCYTES AND PLATELETS

BROAD SPECTRUM OF EFFECTS

VASODILATION AND ↑ PERMEABILITY

ALSO LEUKOCYTE ADHESION, CHEMOTAXIS
ACUTE INFLAMMATION -CYTOKINES-
POLYPEPTIDE MEDIATORS

ACTIVATED MACROPHAGES

INFLAMMATION AND IMMUNITY

SYSTEMIC ACUTE-PHASE RXN

TYPES: BRADYKININ, INTERLEUKINS, TUMOR NECROSIS FACTOR, CHEMOKINES
ACUTE INFLAMMATION -BRADYKININ-
VASCULAR DILATION

INCREASED VASCULAR PERMEABILITY

PAIN
ACUTE INFLAMMATION -INTERLEUKINS AND TNF-
ACT ON LEUKOCYTES

MEDIATE CELL COMMUNICATION

ACTIVATES ENDOTHELIUM (BIND LEUKOCYTES)

SYSTEMIC ACUTE PHASE RXN (FEVER)

ACTIVATE FIBROBLASTS

STIMULATE MORE CYTOKINES
ACUTE INFLAMMATION -CHEMOKINES-
CHEMOATTRACTION FOR LEUKOCYTES

DIFFERENT CHEMOKINES ATTRACT DIFFERENT CELLS

LEUKOCYTE ACTIVATION
ACUTE INFLAMMATION -REACTIVE OXYGEN SPECIES-
CAUSE TISSUE INJURY

AMPLIFY CASCADE OF MEDIATORS
ACUTE INFLAMMATION -NITRIC OXIDE-
INDUCED BY CYTOKINES

CAUSES VASODILATION
ACUTE INFLAMMATION -LEUKOCYTE LYSOSOMAL ENZYMES-
PROTEASES (ELASTASE; COLLAGENASE)

INACTIVATED BY ANTIPROTEASES (IN SERUM AND TISSUE FLUIDS; α1-ANTITRYPSIN INHIBITS ELASTASE; DEFICIENCY SUSTAINS INF IE EMPHYSEMA)
ACUTE INFLAMMATION -NEUROPEPTIDES-
SUBSTANCE P

TRANSMITS PAIN SIGNALS

MODULATES VASCULAR PERMEABILITY

IMPORTANT IN LUNGS AND GIT
ACUTE INFLAMMATION -PLASMA-PROTEIN DERIVED MEDIATORS-
COMPLEMENT

KININS

COAGULATION SYSTEM
ACUTE INFLAMMATION -COMPLEMENT- PLASMA PROTEINS (C1-C9)
ACTIVE C3 IS CRITICAL STEP

CLASSIC PATHWAY

ALTERNATIVE PATHWAY

LECTIN PATHWAY
ACUTE INFLAMMATION -COMPLEMENT- EFFECTS
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
ACUTE INFLAMMATION -COMPLEMENT- INHIBITION
PLASMA REGULATORY PROTEINS

PREVENTS DAMAGE TO NORMAL CELLS

INAPPROPRIATE/EXCESSIVE ACTIVATION SERIOUS
ACUTE INFLAMMATION -KININS-
BRADYKININ (ACTIVATE HAGEMAN FACTOR)

VASCULAR DILATION

INCREASED PERMEABILITY
PAIN
ACUTE INFLAMMATION -COAGULATION SYSTEM-
THROMBIN MOST IMPORTANT

ACTIVATES ENDOTHELIUM (ENHANCES ADHESION)

GENERATES FIBRINOPEPTIDES (↑ VASCULAR PERMEABILITY; LEUKOCYTE CHEMOTAXIS)
ACUTE INFLAMMATION -TERMINATION-
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)
ACUTE INFLAMMATION -OUTCOMES-
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
ACUTE INFLAMMATION -RESOLUTION-
TISSUE RESTORED TO NORMAL STATE

MILD, SHORT-LIVED INJURY

MINIMAL TISSUE DAMAGE

LABILE OR STABLE TISSUE
ACUTE INFLAMMATION -PROGRESS TO CHRONIC INFLAMMATION-
OFFENDING AGENT NOT REMOVED

MAY START AS CHRONIC INF

MAY LEAD TO RESOLUTION, OR LEAD TO SCARRING
ACUTE INFLAMMATION -SCARRING-
HEALING WITH COLLAGEN (FIBROSIS)

AFTER SEVERE INJURY, OR

STABLE OR PERMANENT TISSUES

FIBRINOUS EXUDATES, ABSCESSES
CHRONIC INFLAMMATION -GENERAL FEATURES-
PROLONGED DURATION (WEEKS… MONTHS… YEARS)

SIMULTANEOUS (INFLAMMATION; HEALING; TISSUE INJURY)
CHRONIC INFLAMMATION -CHARACTERISTICS-
MONONUCLEAR CELLS INFILTRATION (MACROPHAGES; LYMPHOCYTES; PLASMA CELLS)

TISSUE DESTRUCTION

REPAIR (ANGIOGENESIS; FIBROSIS)
PROGRESSION OF ACUTE INF
CHRONIC INFLAMMATION -STIMULIS-

INJURY NOT RESOLVES

PERSISTENCE OF INJURIOUS AGENT

INTERFERENCE WITH HEALING
PERSISTENT INFECTIONS
CHRONIC INFLAMMATION -STIMULIS-

MICROBES DIFFICULT TO ERADICATE

MYCOBACTERIA, TREPONEMA

CERTAIN VIRUSES AND FUNGI

T-LYMPHOCYTE-MEDIATED RESPONSE
IMMUNE-RELATED DISEASES
CHRONIC INFLAMMATION -STIMULIS-

HYPERSENSITIVITY DISEASES

AUTOIMMUNE DISEASES

SELF-PERPETUATING REACTIONS
PROLONGED EXPOSURE TO TOXIC AGENTS
CHRONIC INFLAMMATION -STIMULIS-

NONDEGRADABLE MATERIALS (SILICA)
CHRONIC INFLAMMATION -CELLS-
MACROPHAGES

LYMPHOCYTES

PLASMA CELLS

EOSINOPHILS

MAST CELLS

NEUTROPHILS
CHRONIC INFLAMMATION -MACROPHAGES-
DOMINANT CELL OF CHRONIC INF

DERIVED FROM BLOOD MONOCYTES
CHRONIC INFLAMMATION -MACROPHAGES- TYPES
CONNECTIVE TISSUE MACROPHAGES

KUPFFER CELLS OF LIVER

SINUS HISTIOCYTES OF SPLEEN/NODES

MICROGLIAL CELLS OF CNS

ALVEOLAR MACROPHAGES OF LUNGS
CHRONIC INFLAMMATION -MACROPHAGES- FUNCTIONS
FILTER PARTICULATE MATTER (FOREIGN DEBRIS, MICROBES, DEAD CELLS)

ANTI-PRESENTING CELLS
CHRONIC INFLAMMATION -MACROPHAGE LIFE CYCLE-
CIRCULATING MONOCYTE (1-2 DAYS; ADHERENT MONOCYTE; EMIGRATING MONOCYTE)

TISSUE MACROPHAGE (ENLARGE; ↑ PHAGOCYTIC ACTIVITY; ↑ LIFE SPAN)

ACTIVATED MACROPHAGE (ENLARGE AGAIN; ↑ LYSOSOMAL ENZYMES; ↑ KILLING CAPACITY)
CHRONIC INFLAMMATION -MACROPHAGE MORPHOLOGY-
LARGE, FLAT, PINK

SIMILAR TO EPITHELIAL CELLS (EPITHELOID CELLS)

MAY FUSE TO FORM “GIANT CELLS” (FOREIGN BODY; LANGERHANS - TB; TOUTON – XANTHOGRANULOMA)
CHRONIC INFLAMMATION -MACROPHAGE ACTIVATION-
BACTERIAL ENDOTOXINS

CYTOKINES

ACUTE INF MEDIATORS

EXTRACELLULAR MATRIX PROTEINS (FIBRONECTIN)
CHRONIC INFLAMMATION -MACROPHAGE PRODUCTS-
PROTEASES: PLASMINOGEN ACTIVATOR (AMPLIFIES INFLAMMATION)

ROS AND NO

ARACHIDONIC ACID METABOLITES

CYTOKINES (IL, TNF, GROWTH FACTORS)
CHRONIC INFLAMMATION -MACROPHAGE RESOLUTION-
DIE

WANDER OFF INTO LYMPHATICS

MAY ACCUMULATE (STEADY RELEASE OF CHEMOKINES; GRANULOMATOUS INFLAMMATION)
CHRONIC INFLAMMATION -LYMPHOCYTES-
RESPOND TO: SPECIFIC IMMUNE STIMULI; NON-IMMUNE STIMULI (TISSUE NECROSIS)

BOTH T AND B CELLS

MECHANISM OF ATTRACTION (ADHESION MOLECULES AND CYTOKINES; ANTIGEN PRESENTATION)
CHRONIC INFLAMMATION -PLASMA CELLS-
FROM ACTIVATED B LYMPHOCYTES

PRODUCE ANTIBODIES AGAINST PERSISTENT ANTIGENS
CHRONIC INFLAMMATION -EOSINOPHILS-
PARASITIC INFECTIONS

BASIC PROTEIN TOXIC TO PARASITES

ALLERGIES

FUNCTION SIMILAR TO NEUTROPHILS
CHRONIC INFLAMMATION -OTHER CELLS-
MAST CELLS (MOST IMPORTANT IN ACUTE INF)

NEUTROPHILS (PERSISTENT MICROBES OR NECROTIC TISSUE)
GRANULOMATOUS INFLAMMATION
DISTINCTIVE FORM OF CHRONIC INF

AGGREGATES OF ACTIVATES MACROPHAGES

“WALLS OFF” OFFENDING AGENT

DOES NOT ERADICATE AGENT

MAY TERMINATE IN FIBROSIS (WITH ORGAN DYSFUNCTION)
GRANULOMATOUS INFLAMMATION -STIMULI-
CERTAIN MICROBES: TUBERCULOSIS, LEPROSY, SYPHILIS, CAT SCRATCH FEVER, SARCOIDOSIS, CROHN’S DISEASE, FUNGI

INERT FOREIGN BODIES: FOREIGN BODY GRANULOMAS
GRANULOMATOUS INFLAMMATION -MICROSCOPIC APPEARANCE-
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)
INFLAMMATION -CLASSIFICATION-
DURATION

LOCATION

TYPE OF EDEMA

MORPHOLOGY
INFLAMMATION -CLASSIFICATION BY DURATION-
ACUTE: EDEMA, STIMULATION OF PLATELETS, PRESENCE OF PMN’S

CHRONIC: LYMPHOYTES, PLASMA CELLS, MACROPHAGES
INFLAMMATION -CLASSIFICATION BY LOCATION-
ADD –ITIS TO TISSUE TYPE: APPENDICITIS, GINGIVITIS

EXCEPTIONS: PNEUMONIA
EDEMA IS
ACCUMULATION OF FLUID IN THE EXTRACELLULAR COMPARTMENT AND INTERSTITIAL TISSUES
INFLAMMATION -CLASSIFICATION BY TYPE OF EDEMA-
EFFUSION: EDEMA IN A BODY CAVITY

TRANSUDATE: NON-INFLAMMATORY (LOW PROTEIN; LOW SPECIFIC GRAVITY)

EXUDATE: INFLAMMATORY (HIGH PROTEIN; HIGH SPECIFIC GRAVITY)
INFLAMMATION -PATTERNS OF EXUDATION-
SEROUS

SUPPURATIVE (PURULENT)

FIBRINOUS

SEROSANGUINOUS

CATARRHAL
SEROUS EXUDATE
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
SUPPURATIVE EXUDATE
PURULENT INFLAMMATION

COMMONLY CALLED PUS

COMPOSED OF PMN’S AND NECROTIC DEBRIS

PYOGENIC INFECTIONS (STAPH, STREP; ABSCESSES: LOCALIZED; CELLULITIS: DIFFUSE)

LEAD TO SCARRING
ABSCESSES
SUPPURATIVE EXUDATE
CELLULITIS
SUPPURATIVE EXUDATE
FIBRINOUS EXUDATE
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)
SEROSANGUINOUS EXUDATE
SEROUS EXUDATE WITH RBC’s

BLOOD BLISTER
CATARRHAL EXUDATE
CONTAINS MUCOUS

COMMON COLD
INFLAMMATION -CLASSIFICATION BY MORPHOLOGY-
ABSCESS

CELLULITIS

ULCERATIVE

PSEUDOMEMBRANEOUS
ABSCESS
LOCALIZED ACCUMULATION OF SUPPURATIVE EXUDATE

PUS = DEAD AND LIVE NEUTROPHILS + NECROTIC DEBRIS
CELLULITIS
DIFFUSE, ILL-DEFINED, SPREADING PURULENT INFECTION

RED AND HOT

HYALURONIDASE, ETC FROM BACTERIA
ULCERATIVE
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
PSEUDOMEMBRANOUS
SIMILAR TO ULCERATIVE BUT NOT AS DEEP

SUPERICIAL EXUDATE OF: FIBRIN, PMN’S, NECROTIC DEBRIS

USUALLY COVERS AN ULCER

DIPHTHERIAL PHARYNGITIS, ULCERATIVE COLITIS, PEMPHIGUS
INFLAMMATION -SYSTEMIC MANIFESTATIONS-
FEVER

ELEVATED PLASMA PROTEINS

LEUKOCYTOSIS

SEPSIS

OTHER CHANGES: CARDIOVASCULAR CHANGES, ANOREXIA, SOMNOLENCE, MALAISE, CACHEXIA
INFLAMMATION -FEVER-
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
INFLAMMATION -FEVER- PYROGENS
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)
INFLAMMATION ↑ PLASMA PROTEINS
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
INFLAMMATION -LEUKOCYTOSIS-
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)
INFLAMMATION -SEPSIS-
SEVERE BACTERIAL INFECTIONS

LARGE VOLUME OF LPS (MASSIVE CYTOKINE PRODUCTION)

SEPTIC SHOCK (DIC, HYPOGLYCEMIA, HYPOTENSION)
INFLAMMATION -OTHER SYSTEMIC CHANGES-
ANOREXIA (TNF-MEDIATED APPETITE SUPPRESSION)

SOMNOLENCE (CYTOKINE ACTION ON CNS)

MALAISE (CYTOKINE ACTION ON CNS)

CACHEXIA (WASTING SYNDROME)
INFLAMMATION CARDIOVASCULAR CHANGES
↑ HEART RATE

↑ BLOOD PRESSURE

↓ SWEATING

CHILLS (PRECEPTION OF BEING COLD)

RIGORS (SHIVERING)

REDIRECTED BLOOD FLOW TO DEEP TISSUES

RELATED TO FEVER