immuno_mod2_ms1

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soren101
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immuno_mod2_ms1
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2011-07-26 12:27:27
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immunology ms1 mod2
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immunology mod2 ms1
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  1. DESCRIBE THE 3 PHASES OF HOST DEFENCE
    INNATE IMMUNITY (IMMEDIATE: 0-4 HRS). INVOLVES COMPLEMENT

    EARLY INDUCED (EARLY: 4HRS TO 4DAYS). INVOLVES PHAGOCYTOSIS

    ADAPTIVE (LATE: 4+ DAYS). INVOLVES T & B CELLS AND CLONAL EXPANSION
  2. HERPES SIMPLEX
    INNATE IMMEDIATE PHASE

    LATENCY (HIDING)

    INVADE SENSORY NEURONS WHICH EXPRESS RELATIVELEY LOW LEVELS OF MHC, THUS AVOID CTLs

    OTHER HIDING PATHOGEN IS HIV
  3. HIV
    IMMEDIATE INNATE PHASE

    HIDING

    INSERT INTO HOST DNA (PRIMARILY T LYMPHS AND MACROPHAGES)

    OTHER HIDING PATHOGEN IS HERPES SIMPLEX

    ALSO DECREASES MHC I AND B-2 MICROGLOBULIN TRANSCRIPTION

    BLOCKS TAP AND INCREASES MHC I TURNOVER THROUGH ENDOCYTOSIS

    LITTLE IMPACT ON HLA-C&E FOR PROTECTION AGAINST NK CELLS
  4. LIPOPOLYSACCARIDE (LPS) AND LIPOTEICHOIC ACID (LTA)
    2 POTENT COMPLEMENT ACTIVATORS

    GRAM-NEGATIVE LPS AND GRAM POSITIVE LTA

    BACTERIA HAVE EVOLVED SEVERAL MECHANISMS FOR AVOIDING ACTIVATION OF COMPLEMENT BY LPS AND LTA
  5. SALMONELLA AND E. COLI
    IMMEDIATE INNATE PHASE

    BLOCK COMPLEMENT (C3b)

    O-ANTIGENS COMPOSED OF LONG CHAIN POLYSACCHARIDES CREATING A THICK WALL OF "SMOOTH STRAINS"

    NEISSERIA GONORRHEAE AND STREP PYROGENES ALSO BLOCK COMPLEMENT

    DOWNSIDE IS LONG POLYSACCHARIDE CHAINS ARE HIGHLY IMMUNOGENIC

    SALMONELLA ALSO RESISTANT TO LYSOSOMAL DAMAGE (EARLY INDUCIBLE PHASE) PhoQ-PhoP
  6. NEISSERIA GONORRHEAE (IMMEDIATE INNATE)
    IMMEDIATE INNATE PHASE

    BLOCK COMPLEMENT

    SIALIC ACID IS ASSOCIATED WITH OLIGOSACCHARIDES OF HOST AND INHIBITS COMPLEMENT

    N. GONORRHEAE ATTACHES SIALIC ACID TO LPS (NOW LIPOOLIGOSACCARIDE (LOS))

    SALMONELLA, E. COLI, AND STREP PYROGENES ALSO BLOCK COMPLEMENT

    N. GONORRHEA ALSO SHOWS ANTIGENIC DIVERSITY IN LATE PHASE
  7. STREP PYROGENES (IMMEDIATE)
    BLOCKS COMPLEMENT AND PHAGOCYTOSIS

    PROTEIN M BINDS HOST FACTOR H WHICH DESTROYS C3b

    C3b INVOLVED IN OPSONIZATION AND ALSO PART OF C5 CONVERTASE THAT FORMS MAC

    SALMONELLA, E. COLI, AND N. GONORRHEAE ALSO BLOCK COMPLEMENT

    PHAGO CHEMOTAXIS IN EARLY INDUCED PHASE
  8. HOST REGULATORS OF COMPLEMENT (6)
    FACTOR H: COENZYME ALONG WITH FACTOR I THAT INHIBITS C3b BY ACTIVATING ENZYME THAT CLEAVES. ALSO INACTIVATES ALTERNATE PATHWAY BY DISSOCIATING Bb FROM THE C3bBb COMPLEX

    C4bBb: COFACTOR IN CLEAVAGE OF C4b BY FACTOR I, INHIBITING FROM INTERACTING WITH C2a IN FORMING C3 CONVERTASE

    COMLEMENT RECEPTOR TYPE 1 (CR1) AND MEMBRANE COFACTOR PROTEIN (MCP): BOTH COFACTORS FOR FACTOR I CLEAVAGE OF C4b AND C3b

    DECAY ACCELERATING FACTOR (DAF): BINDS C3 CONVERTASE IN BOTH CLASSICAL AND ALT PATHWAYS CAUSING DISASSOCIATION OF CONVERTASE COMPLEX

    CD59: INVIBITS MAC FORMATION BY INTERFERING WITH DEPOSITION OF C9 MOLECULES
  9. STAPH. AUREUS (BARRIER)
    EARLY INDUCIBLE

    PROTECTIVE BARRIER

    GENERATES WALL OF FIBRIN THAT STOPS LEUKOCYTES. PRODUCES COAGULASE WHICH ACTIVATES PROTHROMBIN --> THROMBIN --> FIBRINOGEN --> FIBRIN

    PRODUCES STAPHYLOKINASE WHICH DIGESTS FIBRIN SO STAPH AUREUS CAN ESCAPE

    STREP PNEUMONIAE ALSO MAKES BARRIER

    STAPH AUREUSCAN CAN RESIST LYSOSOMAL DAMAGE IN EARLY INDICIBLE PHASE AND MISDIRECT IMMUNE RESPONSE AND INTERFERE IN Ab FUNCTION IN LATE PHASE
  10. STREP PNEUMONIAE (EARLY INDUCIBLE)
    EARLY INDUCED PHASE

    PROTECTIVE BARRIER

    CAN MAKE 90 DIFFERENT POLYSACCHARIDES THAT MAKE THICK SLIMY WALL "CAPSULE" THAT INHIBITS PHAGOCYTOSIS

    POLYSACCHARIDES ARE IMMUNOGENIC AND WILL EVENTUALLY STIMULATE OPSONINS

    BASIS OF RECENTLY DEVELOPED PNEUM VACCINES

    STAPH AUREUS ALSO MAKE BARRIERS

    STREP PNEUM ALSO SHOWS ANTIGEN DIVERSITY IN LATE PHASE
  11. STREP PYOGENES (EARLY INDUCED)
    PHAGOCYTE CHEMOTAXIS

    PRODUCES C5a PEPTIDASE THAT CLEAVES POTENT LEUKOCYTE CHEMOATTRACTANT C5a

    C5a AND C3a ARE ANAPHYLOTOXINS WHICH ATTRACT LEUKOCYTES AND INCREASE VASCULAR PERMEABILITY

    INHIBITS COMPLEMENT IN IMMEDIATE INNATE PHASE
  12. PANTON-VALENTINE LEUKOCIDIN (PVL) IN STAPH AUREUS
    EARLY INDUCIBLE PHASE

    KILLING PHAGOCYTES

    PVL IS PORE-FORMING CYTOTOXIN ASSOCIATED WITH INCREASED VIRULENCE

    PRESENT IN MAJORITY OF COMMUNITY-ASSOCIATED MRSA (CA-MRSA)

    YERSINIA PESTIS ALSO PHAGOCYTE KILLER

    STAPH AUREUS ALSO USES PROTECTIVE BARRIER IN EARLY INDUCIBLE STAGE
  13. YERSINIA PESTIS
    EARLY INDUCIBLE PHASE

    KILLING PHAGOCYTES

    YERSINIA OUTER PROTEINS (YOPs) B/D FORMS PORES IN CELL MEMBRANES OF HOST MACROPHAGES AND LINKED TO CELL LYSIS

    YOP J INJECTED INTO CYTOPLASM OF HOST CELLS VIA TYPE III (NEEDLE) SECRETION SYSTEM. YOP J INTERFERES WITH SIGNALING PATHWAYS REQUIRED FOR VARIOUS PHAGOCYTIC ACTIVITIES, ACTIVATION OF CYTOKINE GENES, AND CAN TRIGGER APOPTOSIS

    PVL IN STAPH AUREUS ALSO A PHAGOCYTE KILLER
  14. LEGIONELLA PNEUMOPHILIA
    EARLY INDUCIBLE PHASE

    INHIBITS PHAGO/LYSOSOME FUSION

    CREATES ABNORMAL ENDOSOME IN ALVEOLAR MACROPHAGES

    ERROR IN SIGNALING BETWEEN C3 ON BACTERIAL SURFACE BINDS AND RECEPTORS CR1 AND CR3 ON PHAG CELL CAUSES ABNORMAL COILING OF PSEUDOPOD AROUND BACTERIUM
  15. MYCOBACTERIUM TUBERCULOSIS
    EARLY INDUCIBLE PHASE

    RESISTANCE TO LYSOSOMAL DAMAGE - HYDROPHOBIC SHIELD

    SOME INHIBITION OF PHAGO/LYSOSOMAL FUSION

    THICK WAXY HYDROPHOBIC CELL WALL COMPONENTS, MAINLY MYCOLIC ACIDS, PREVENT DEGRADATION

    CAN FORM GRANULOMAS

    BACILLUS ANTHRACIS, SALMONELLA, AND STAPH AUREUS ALSO HAVE RESISTANCE
  16. BACILLUS ANTHRACIS
    EARLY INDUCIBLE PHASE

    RESISTANCE TO LYSOSOMAL DAMAGE

    UNNATURAL ISOMERIC D-CONFIGURATION OF POLY D-GLUTAMATE CAPSULE NOT RECOGNIZED BY CONVENTIONAL PROTEASES OF THE LYSOSOMES

    MYCO TUBERCULOSIS, SALMONELLA, AND STAPH AUREUS ALSO RESIST LYSOSOMAL DAMAGE
  17. SALMONELLA (EARLY INDECIBLE PHASE)
    RESISTANCE TO LYSOSOMAL DAMAGE - ALTERED SUSEPTIBILITY TO ANTI MICROBIAL PEPTIDES

    GENETIC SENSING SYSTEM PhoP-PhoQ REGULON

    PhoQ SENSES PHAGO/LYSO FUSION BY PRESENCE OF CATIONIC ANTI-MICROBIAL PEPTIDES (DEFENSINS) AND DROP IN Mg++. CATIONIC ANTI-MICROBIAL PEPTIDES BIND IONICALLY TO NEGATIVE PHOS GROUPS OF LPSs RESULTING IN PORE FORMATION ON BACTERIA

    PhoP TRANSCRIPTIONAL ACTIVATOR FOR MULTIPLE GENES (30+) THAT INTERFERE WITH VARIOUS DESTRUCTIVE PROCESSES IN PHAGOCYTES, INCLUDING THE CHANGE OF LPSs THAT PREVENT IT FROM BEING TARGETED BY ANTI-MICROBIAL PEPTIDES, REDUCED CYTOKINE RESPONSES, AND DECREASED ANTIGEN PRESENTATION.

    MYCO TUBERCULOSIS, BACILLUS ANTHRACIS, AND STAPH AUREUS ALSO HAVE RESISTANCE TO LYSOSOMAL DAMAGE

    SALMONELLA ALSO INHIBITS COMPLEMENT PATHWAY (IMMEDIATE INNATE PHASE)
  18. STAPH AUREUS (LYSOSOMAL RESISTANCE)
    EARLY INDUCIBLE PHASE

    RESISTANCE TO LYSOSOMAL DAMAGE - INHIBITION OF O2 DEPENDENT KILLING

    CATALASE BREAKS DOWN RESPIRATORY BURST PRODUCT, H2O2, INTO WATER AND OXYGEN

    MYCO TUBERCULOSIS, BACILLUS ANTHRACIS, AND SALMONELLA ALSO RESISTANT TO LYSOSOMAL DAMAGE

    STAPH AUREUS ALSO HAS PROTECTIVE BARRIER IN EARLY INDUCIBLE PHASE AND CAN MISDIRECT IMMUNE RESPONSES AND INTERFERE WITH Ab FUNCTION IN LATE PHASE
  19. LISTERIA MONOCYTOGENES
    EARLY INDUCIBLE PHASE

    ESCAPE FROM LYSOSOME

    PORE-FORMING HEMOLYSIN (LISTERIOLYSIN O) AND 2 FORMS OF PHOSPHOLIPASE C

    ONCE LYSED FROM LYSOSOME, INTERACTS WITH HOST ACTIN CYTOSKELETAL SYSTEM USING ACTIN-BASED MOTILITY AND ESCAPES INTO ADJACENT CELLS

    INDUCES OWN MOVEMENT THROUGH ACTIN POLYMERIZATION WHICH PROTECTS FROM Ab AND EXTRACELLULAR ENVIRONMENT
  20. STAPH AUREUS (IMMUNE RESPONSE)
    LATE PHASE

    MISDIRECTING IMMUNE RESPONSE - DEPLETION OF ANTIGEN-SPECIFIC T CELLS

    PRODUCES SUPERANTIGENS THAT ACTIVATE LARGE # OF T CELLS WITH PRO-INFLAMMATORY CAPABILITIES (TH1 & TH17). ALSO IL-2, IFN-g, IL-1, AND TNF-a

    RESPONSES ARE POLYCLONAL AND INVOLVE 20-40% OF ALL CD4+ T CELLS LEADING TO TOXIC SHOCK SYNDROME

    MAY DRIVE T CELL ARM OF IMMUNE RESPONSE TO PARALYSIS (DEPLETION)

    MYCO LEPRAE ALSO MISDIRECTS IMMUNE RESPONSES

    STAPH AUREUS HAS PROTECTIVE BARRIER AND RESISTANCE TO LYSOSOMAL DAMAGE (EARLY INDUCIBLE)
  21. MYCOBACTERIUM LEPRAE
    LATE PHASE

    MISDIRECTING IMMUNE RESPONSE - SKEWING TH1 TH2 BALANCE

    2 FORMS: LEPROMATOUS LEPROSY ASSOCIATED WITH FULMINATE SYSTEMIC SPREAD FO PATHOGEN. HIGH TH2 BUT NO TH1, ABSENCE OF CELL-MEDIATED IMMUNITY WHICH IS NEEDED.

    TUBERCULOID LEPROSY ASSOCIATED WITH RESTRICTED SPREAD AND PROMINEMT CELL-MEDIATED IMMUNITY (HIGH TH1). GRANULOMAS AND NORMAL Ab SERUM LEVELS
  22. TREPONEMA PALLIDUM
    LATE PHASE

    HOST-PARASITE MIMICRY

    AGENT OF SYPHILIS BINDS TO HOST FIBRONECTIN RECEPTORS, OF WHICH THERE ARE MANY

    FIBRONECTIN SERVES AS BRIDGE THAT ALLOWS PATHOGEN TO BIND AND COLONIZE HOST TISSUES

    COATED IN FIBRONECTIN ALSO CLOAKS TREPONEMA PALLIDUM FROM HOST IMMUNE SYSTEM
  23. STAPH AUREUS (ANTIBODY FUNCTION)
    LATE PHASE

    INTERFERENCE OF Ab FUNCTION - NEUTRALIZATION OF OPSONIZING Ab

    STAPH PROTEIN A (SPA) BINDS TO IgG THROUGH ITS Fc REGION WHICH CAUSES IT TO LOSE OPSONIZING CAPABILITY

    NEISSERIA MENINGITIS ALSO INTERFERES IN Ab FUNCTION

    AUREUS ALSO HAS BARRIER AND LYSOSOMAL RESISTANCE IN EARLY INDUCIBLE PHASE AND MISDIRECTING IMMUNE RESPONSE IN LATE PHASE
  24. NEISSERIA MENINGITIS
    LATE PHASE

    INTERFERES IN Ab FUNCTION - IgA PROTEASE

    FRAGMENTS OF IgA THAT REMAIN CONTINUE TO BIND TO PATHOGEN AND BLOCK COMPLEMENT ACTIVATING IgG Ab FROM BINDING

    STAPH AUREUS ALSO INTERFERES IN Ab FUNCTION
  25. STREP PNEUMONIAE (LATE)
    LATE PHASE

    ANTIGEN DIVERSITY

    EACH STRAIN (90+) CARRIES SLIGHTLY DIFFERENT POLYSACCHARIDE ANTIGENS IN THEIR CAPSULES. IMMUNITY TO ONE STRAIN STILL LEAVES INDIVIDUALS UNPROTECTED AGAINST OTHER STRAINS (SEROTYPES)

    INFLUENZA, T. BRUCEI, N. GONORRHEA ALSO SHOW ANTIGENIC VARIATION
  26. INFLUENZA VIRUS
    LATE PHASE

    ANTIGENIC DIVERSITY - RNA

    ANTIGENIC DRIFT = EPIDEMIC. POINT MUTATIONS (ESPECIALLY IN HEMAGGLUTININ AND NEURAMINIDASE) CAUSE EPITOPE CHANGES LEADING TO DIMINISHED ABILITY OF PREVIOUSLY EXISTING Ab TO RECOGNIZE VIRUS

    ANTIGENIC SHIFT = PANDEMIC. REASSORTMENT OF GENOMIC SEGMENTS USUALLY FROM DIFFERENT SPECIES (PIGS, BIRDS)

    STREP PNEUM, T. BRUCEI, AND N. GONORRHEA ALSO SHOW ANTIGENIC DIVERSITY
  27. TRYPANOSOMA BRUCEI
    LATE PHASE

    ANTIGENIC VARIATION - GENE REARRANGEMENT

    AFRICAN SLEEPING SICKNESS

    UNIQUE EXPRESSION SITE ONLY ALLOWS ONE VARIABLE SURFACE GLYCOPROTEIN (VSG) TO BE EXRESSED AT A TIME.

    GENE CONVERSION SWITCHES OUT VSG IN EXPRESSION SITE WITH NEW ONE, CAUSING WAVES OF ANTIGENICALLY DISTINCT TRYPANOSOMES AND CYCLICAL NATURE OF THE DISEASE

    STREP PNEUM, INFLUENZA, AND N. GONORRHEA ALSO HAS ANTIGENIC DIVERSITY
  28. NEISSERIA GONORRHEA
    LATE PHASE

    ANTIGENIC VARIATION

    PILUS STRUCTURE ALLOWS BINDING TO HOST EPITHELIAL CELLS

    NUMEROUS VARIATIONS OF PROTEIN PILIN BUT ONLY ONE EXPRESSED AT A TIME, SO ABLE TO EVADE BY CHANGING SURFACE ANTIGENS

    STREP PNEUM, T. BRUCEI, INFLUENZA ALSO SHOW ANTIGENIC DIVERSITY

    N. GONORRHEA ALSO BLOCKS COMPLEMENT IN IMMEDIATE INNATE PHASE
  29. CYTOMEGALOVIRUS (CMV)
    DECREASED EXPRESSION OF MHC CLASS I

    BLOCKS TAP

    INCREASED TURNOVER OF MHC VIA ENDOCYTOSIS

    HEAVY CHAIN MIMICRY COMPETES FOR B-2 MICROGLOBULIN

    BLOCKS HLA-A,B,C BUT NOT E WHICH PROTECTS AGAINST NK CELLS

    HIV & ADENOVIRUS ALSO DECREASE MHC
  30. ADENOVIRUS
    DECREASED EXPRESSION OF MCH CLASS I

    PREVENTS TAP ASSOCIATION WITH TAPSIN

    HIV AND CMV ALSO DECREASE MCH
  31. STRATEGIES FOR EVADING IMMEDIATE INNATE PHASE
    HIDING (INSIDE T LYMPHS AND MACROs) HIV

    LATENCY (HERPES)

    INHIBIT COMPLEMENT- BARRIERS (LONG CHAIN POLYSACCHARIDES), SIALIC ACID, M PROTEIN
  32. STRATAGIES FOR EVADING EARLY INDUCIBLE PHASE
    EVADING PHAGOCYTOSIS - COAGULASE, POLYSACCHARIDE CAPSULE

    PHAGOCYTE CHEMOTAXIS (C5a PEPTIDASE)

    KILLING PHAGOCYTES (PORE-FORMING, APOPTOSIS)

    INHIBIT LYSOSOME FUSION (ENDOSOME ABNORMALITY)

    RESISTANCE TO LYSOSOMAL DAMAGE (HYDROPHOBIC SHIELD, D-CONFIGURATION, CATIONIC LYSO ANTI-MICRO, BREAKDOWN OF H2O2

    ESCAPE PHAGOSOME
  33. STRATAGIES FOR EVADING LATE PHASE
    MISDIRECTION OF IMMUNE RESPONSE (DEPLETION, SKEWING TH1 TH2 BALANCE)

    HOST MIMICRY (FIBRONECTIN)

    INTERFERENCE WITH Ab FUNCTION (NEUTRALIZATION, IgA PROTEASE)

    ANTIGENIC VARIATION (SEROTYPES, ANTIGENIC DRIFT/SHIFT, GENE REARRANGEMENT)

    DECREASED EXPRESSION OF MHC
  34. HYPERSENSITIVITY
    HYPERSENSITIVITY = ALLERGY = EXAGGERATED MANIFESTATION OF NORMAL IMMUNE RESPONSE THAT:

    1) EXCEED HEALTHY LIMITS OF INTENSITY AND/OR

    2) DIRECTED AT TISSUES PARTICULARLY SENSITIVE TO PRODUCTS OF SUCH RESPONSIVENESS

    INDIVIDUALS WITH PREDISPOSITION FOR ALLERGY ARE ATOPIC
  35. ALLERGEN
    ANTIGEN (HARMLESS IN MOST INDIVIDUALS) THAT STIMULATES ALLERGIC RESPONSES IN ATOPICS

    ESP (IgE ASSOCIATED ALLERGY)
  36. IMMUNE RESPONSE VS. IMMUNE REACTION
    HYPERSENSITIVETY DISEASES REQUIRE SENSITIZATION INVOLVING AN IMMUNE RESPONSE THAT PRODUCES POTENTIALLY HARMFULL SOLUABLE OR CELLULAR FACTORS

    PATHOLOGY WHEN THESE FACTORS COMBINE WITH AND ELICIT DAMAGE TO HOST TISSUES (IMMUNE REACTIONS)
  37. SENSITIZATION VS. ELICITATION
    HYPERSENSITIVITY DISEASES REQUIRE INITIAL SENSITIZING EXPOSURE TO ALLERGEN, FOLLOWED BY EXPOSURES TO ALLERGEN THAT ELICIT SYMPTOMS

    IN SOME CASES, SENSITIZATION PHASE MAY BE COMPLETED BEFORE ALLERGEN IS CLEARED FROM BODY, ALLOWING ELICITATION TO BEGIN DURING INITIAL ALLERGEN EXPOSURE
  38. TYPE 1 HS
    IMMEDIATE

    Ag-SPECIFIC IgE Ab

    IgE-FIXED MAST CELLS, BASOPHILS, AND EOSINOPHILS DEGRANULATE TO RELEASE ACTIVE AGENTS

    INITIAL EXPOSURE GENERALLY COMES BY WAY OF TRANSMUCOSAL PRESENTATION OF Ag THAT PROMOTES TH2 RESPONSE, FOLLOWED BY B-CELL ACTIVATION

    Ab CAN ENTER ORAL OR RESP ROUTES AND ARE USUALLY SMALL SOLUABLE MOLECULES

    IL-4 BY TH2 CELLS PROMOTE SELECTIVE SWITCHING TO IgE

    Ag-SPECIFIC IgE BINDS VIA Fc REGION (TAIL DOWN) TO MAST CELLS, BASOPHILS, EOSINOPHILS THAT EXPRESS Fc-EPSILON-R1 FOUND IN MUCOSAL AND EPITHELIAL TISSUES.

    Ab-SPECIFIC IgE MAY REMAIN ASSOCIATED FOR YEARS

    • ex:
    • RHINITIS
    • ASTHMA
    • VENOM REACTIONS
    • FOOD ALLERGIES
    • DRUG ALLERGIES
    • URTICARIA (HIVES)
    • ANAPHYLACTIV SHOCK
  39. ELICITATION OF TYPE 1 HS
    CROSSLINKING OF Ag-SPECIFIC IgE PREVIOUSLY FIXED TO MAST CELLS AND OBSERVED WITHIN MINUTES OF EXPOSURE

    REACTIONS VARY WITH INTENSITY DEPENDING ON DOSE AND ROUTE OF ALLERGEN EXPOSURE

    SYMPTOMS RANGE FROM MINOR LOCALIZED IRRITATIONS (RHINITIS) TO SERIOUS LOCALIZED REACTIONS (ASTHMA) TO LIFE-THREATENING SYSTEMIC CIRCULATORY COLLAPSE (ANAPHYLACTIC SHOCK)

    IMMEDIATE RESPONSE ACCOMPANIED BY SLOW (HOURS) ADDITIONAL WAVES OF IgE RESPONSES AND INFLAMMATORY ACTIVITIES (LATE-PHASE RESPONSE)
  40. DEGRANULATION
    TYPE 1 HS

    • CAUSES VASCULAR PERMEABILITY, INC BLOOD FLOW, DEC BLOOD PRESSURE, INC MUCOUS SECRETIONS, AND SMOOTH
    • MUSCLE CONTRACTIONS

    BRIDGING OF IgE TRIGGERS INFLUX OF Ca++ INTO CELL RESULTING IN 1) DEC cAMP THAT INITIATES MEMBRANE DESTABILIZAITON FOR GRANUAL RELEASE 2) MEMBRANE LIPID TURNOVER, VIA ARCHIDONIC ACID, LEUKOTRIENES AND PROSTAGLANDINS

    RELEASED PRODUCTS CIRCULATING AT SIGNIFICANT LEVELS WITHIN MINUTES

    • EXAMPLES:
    • HISTAMINES - INC VASC PERM AND LOCAL BLOOD FLOW
    • LEUKOTRIENES & PROSTAGLANDINS - SMOOTH MUSCLE CONTRACTION, INC VASC PERM AND MUCOUS SEC
    • CHEMOKINES - ATTRACT LEUKOCYTES
    • ENZYMES - BREAK DOWN TISSUE MATRIX PROTEINS
    • CYTOKINES - INC INFLAMMATORY ACTIVITIES, INC TH2 RESPONSE, INC GROWTH AND ACTIVITIES OF EOSINOPHILS
  41. TYPE 1 HS SITES OF REACTIVITY
    • SKIN:
    • LOCALIZED WHEAL-AND-FLARE REACTIONS OBSERVED FOLLOWING LOCAL INTRACUTANEOUS EXPOSURE TO ALLERGEN (ex INSECT BITE). SKIN TESTS FOR Ag-SPECIFIC IgE HYPERSENSE MIMIC AND MEASURE THIS LOCLAIZED REACTION. URTICARIA (HIVES) IS MORE DISSEMINATED, OFTEN ASSOCIATED WITH ALLERGEN INGESTION AND MIGRATION TO SKIN

    • GUT:
    • CRAMPING, VOMITING, DIARRHEA DIE TO SMOOTH MUSCLE CONTRACTION. IF ALLERGEN FOUND SYSTEMICALLY, URTICARIA AND/OR ANAJPHYLAXIS CAN OCCUR

    • LUNGS:
    • ALLERGIC RHINITIS ASSOCIATED WITH NASOPHARYNX AND UPPER AIRWAY. MORE SERIOUS REACTIONS OCCUR FOLLOWING ACTIVATION OF MAST CELLS OR THE SUBMUCOSA OF LOWER AIRWAYS RESULTING IN ASTHMA

    • SYSTEMIC:
    • SIGNIFICANT EXPOSURE CAN RESULT IN CATASTROPHIC WIDESPREAD INCREASES IN VASC PERM, DEC IN BLOOD PRESSURE, AND SMOOTH MUSCLE CONTRACTION THAT CONSTRICTS AIRWAYS (WHILE SURROUNDING TISSUES SWELL DUE TO ABNORMAL SHIFTS IN FLUIDS. SYSTEMIC ANAPHYLAXIS
  42. TREATMENTS FOR TYPE 1 HS
    AVOIDANCE

    DESENSITIZATION - GIVING MULTIPLE, VERY SMALL THEN ESCALATING DOSES OF ALLERGEN WHICH SHIFT IgE TO IgG. EFFECTIVENESS HIGHLY VARIABLE, IMPERMINANT, AND MAY RESULT IN ANAPHYLAXIS

    INHIBITION OF MEDIATOR RELEASE - INHIBIT CALCIUM INFLUX OR RAISE LEVELS OF cAMP

    INHIBITION OF MEDIATOR EFFECTS: REVERSE TARGET TISSUE ACTIVITIES CAUSED BY MEDIATORS. EPINEPHRINE PROMOTES REFORMING OF ENDOTHELIAL TIGHT JUNCTIONS, RELAXATION OF SMOOTH MUSCLE, AND STIMULATION OF HEART. BRONCHODIALATORS AND ANTIHISTAMINES (H-RECEPTOR ANTAGONISTS. INFLAMMATORY ACTIVITIES, ESP LATE PHASE RESPONSES, CAN BE TREATED WITH ADMIN OF CORTICOSTEROIDS
  43. TYPE II HS SENSITIZATION
    CYTOTOXIC ANTIBODY

    PRODUCTION OF SPECIFIC Ab REACTIVE WITH EXTRINSIC (FOREIGN) Ag OR REACTIVE WITH INTRINSIC Ag PRODUCED BY TARGET TISSUE.


    Ag STICKS NONSPECIFICALLY TO TISSUE & ABSORBED

    INCOMPLLETE NEGATIVE SELECTION OF B CELLS SPECIFIC FOR SELF
  44. TYPE II HS ELICITATION
    ONSET AND SEVERITY VARIES BASED ON KINETICS AND EXACT CHARACTERISTICS (eg SPECIFICITY, AFFINITY, ISOTYPE) OF Ab PRODUCED

    SYMPTOMS CAUSED BY BINDING OF Ab (USUALLY IgG) SPECIFICALLY TO Ag-COATED HOST CELLS, FOLLOWED BY DIRECT LYSIS DUE TO COMPLEMENT ACTIVATION AND FURTHER AGGRAVATED RELEASE OF COMPLEMENT CASCADE (ANAPHLATOXINS C3a, C5a). FcR BEARING AND CR BEARING LEUKOCYTES ALSO RECRUITED TO AREA.

    SMOOTH LAYER OF Ab/COMPLEMENT COATING TISSUE UNLIKE RANDOM COATING OF TYPE III
  45. HEMOLYTIC DISEASE OF NEWBORN
    TYPE II HS

    Rh- MOM HAS Rh+ BABY. BIRTH CAUSES SENSITIZATION OF MOM TO Rh+ BLOOD. IF 2ND BABY IS Rh+, MOM'S Ab (IgG) ATTACK FETAL HEMOGLOBIN CAUSING SEVERE FETAL ANEMIA.

    GIVE RhoGam
  46. GOODPASTURE'S SYNDROME
    TYPE II HS

    AUTOIMMUNE DISORDER WHERE Ab BINDS TO BASEMENT MEMBRANES OF RENAL GLOMERULI (SOMETIMES PULMINARY ALVEOLI).

    SPECIFIC FOR ALPH-3 CHAIN OF TYPE IV COLLAGEN.

    TRIGGERS COMPLEMENT CASCADE, ACTIVATION OF MONOCYTES & NEUTROPHILS VIA Fc RECEPTORS
  47. TYPE III HS SENSITIZATION AND ELICITATION
    IMMUNE COMPLEX DISEASE

    INITIAL Ag EXPOSURE RESULTS IN ACTIVATION OF Ag-SPECIFIC B CELLS.

    SPECIFIC IgG Ab REACT WITH Ag THAT IS TYPICALLY SOLUABLE AND FREELY CIRCULATING

    MANY MOLECULES OF Ab BIND TO MANY MOLECULES OF Ag, FORMING CROSSLINKS RESULTING IN LARGE INSOLUABLE Ag-Ab COMPLEXES.

    FcR+ AND CR+ PHAGOCYTES CANNOT HANDLE, CAUSING DEPOSITION IN/ON FILTERING ORGANS SUCH AS KIDNEYS OR AREAS RICH IN CAPILLARY BEDS SUCH AS LUNGS
  48. ARTHUS REACTION
    TYPE III HS

    INJECTION OF Ag ATTRACTS CIRCULATING IgG, FORMING IMMUNE COMPLEXES, ACTIVATING COMPLEMENT CASCADE, ATTRACTING PHAGOCYTIC CELLS (C5a), AND RESULTING IN LOCAL INFLAMMATORY RESPONSE

    SERUM SICKNESS AND ADMIN OF LARGE DOSES OF DRUGS CAUSE Ag-Ab COMPLEXES
  49. TYPE IV HS SENSITIZATION
    DELAYED TYPE (DTH)

    ACTIVATION OF CD4+ TH1/17 CELLS

    OCCURS OVER 10-14 DAYS WHEN SMALL Ag ASSOCIATES COVALENTLY WITH HOST MEMBRANE PROTEINS.

    CD4+ ACTIVATED AGAINST Ag SUBSEQUENTLY FOCUS EFFECTOR ACTIVITIES ON HOST TISSUE TO WHICH Ag IS ATTACHED

    Ag TAKEN INTO CELLS EVENTUALLY PRESENTED BY MHC I AND THEN RECOGNIZED BY CD8+ CELLS LEADING TO RELEASE OF INFLAMMATORY CYTOKINES AND LYSING OF HOST TISSUES
  50. TYPE IV HS ELICITATION
    EXAGERATED FORM OF CELL-MEDIATED IMMUNITY (INTRACELLULAR)

    Ag TAKEN INTO CELLS THEN PRESENTED BY MHC 1 ACTIVATES CD4+ AND CD8+ CELLS.

    CYTOKINES INCLUDING CHEMOKINES, IFN-GAMMA, TNF-ALPHA & BETA, AND IL-3/GM-CSF RELEASED. RARELY SEE ANTIBODIES (TH2 EXTRACELLULAR)

    INFLUX OF CELLS CAUSES EDEMA AND INDURATION (FIRM TO THE TOUCH) DUE TO HIGH DENSITY CELL. TYPE I SWELLING IS SOFT TO THE TOUCH DUE TO INFLAMMATION CAUSED BY FLUID.
  51. 3 VARIANTS OF TYPE IV HS (DTH)
    NOT MUTUALLY EXCLUSIVE

    CONTACT HS - EPIDERMAL REACTION WITH LANGERHANS' CELL MOSTLY PRESENTING Ag TO T CELLS. INFILTRATING T CELLS MOSTLY CD4+. OCCURS WITHIN 24-48 HRS OF EXPOSURE. DO NOT CONFUSE WITH SYMPTOMS RESULTING FROM NON-IMMUNOGENIC TISSUE-DAMAGING IRRITANTS.

    TUBERCULIN HS - INTRADERMAL REACTION MOSTLY BY MACROPHAGES AS Ag PRESENTERS. MONOCYTES MAKE UP 80-90% INFILTRATE WITH CD4+ OUTNUMBERING CD8+ 2-TO-1. OCCURS WITHIN 24-48 HOURS. CLASSIC ex TUBERCULIN SKIN TESTING

    GRANULOMATOUS HS - CAN PROGESS FROM TUBERCULIN HS AND OCCURS SLOWLY (21-28 DAYS). PERSISTANCE OF DIFFICULT-TO-DEGRADE Ag WITHIN MACROPHAGES, INCLUDING INTRACELLULAR PATHOGENS. INORGANIC MATERIALS CAN STIMULATE, BUT DISTINGUISH DUE TO LACK OF LYMPHOCYTES. GRANULOMA FORMATION MAINLY DUE TO RECRUITMENT, PROLIF, AND ACTIVATION OF TH1 LYMPHS AT SITE OF RESPONSE. T CELLS FORM "CUFF" AROUND FUSED MACROPHAGES CALLED MULTI-NUC GIANT CELLS. EPIITHELIOID CELLS ALSO RECRUITED (RARE MACROPHAGE SECRETES TNF-ALPHA). PHYSICAL DAMAGE TO TISSUE DUE TO HIGH DENSITY CELLULAR CONTENT AND FIBROSIS OBSERVED DUE TO INC COLLAGEN SYNTH.
  52. LEUKOCYTE ADHESION DEFICIENCY
    IMMUNODEFICIENCY

    DEFECTIVE INTEGRIN (CD18)

    AFFECT ABILITY OF LEUKS TO MOVE FROM BLOOD TO SITE OF INFECTION
  53. CHRONIC GRANULOMATOUS DISEASE
    IMMUNODIFICIENCY

    DEFECTIVE SUPEROXIDE PRODUCTION AFFECTING ABILITY OF PHAGS TO DESTROY INGESTED BACTERIA

    INABILITY TO REDUCE NITROBLUE TETRAZOLIUM DYE (TEST)

    O2 + NADPH OXIDASE --> SUPEROXIDE (O2-)
  54. PERCENTAGE OF IMMUNODEDICIENCY DISEASES
    COMPLEMENT ~2-4%

    PHAG ~15%

    • B CELL ~50%
    • NORM CIRCULATING B CELLS ~20-30%

    T CELL ~30-40%
  55. ANTIBODY VS. CELL-MEDIATED IMMUNODEFICIENCY
    • ANTIBODY:
    • FREQUENT EXTRA-CELLULAR INFECTIONS

    REDUCED SERUM Ab LEVELS; PARTICULAR ISOTYPE LEVELS

    REDUCED CIRCULATING B CELLS; SURFACE Ig+ CELLS (NORM 20-30% OF LYMPHS)

    REDUCED FUNCTIONAL B CELLS (TEST WILL STAPH PROTEIN A)

    • CELL-MEDIATED:
    • FREQUENT VIRAL, FUNGAL, AND INTRACELLULAR INFECTION

    REDUCED CIRCULATING T CELLS (CD3, 4, 8)

    REDUCED FUNCTIONAL T CELLS (TEST PHYTOHEMAGGLUTININ PHA)

    NEGATIVE SKIN TEST Ag ASSOCIATED WITH MICROORGANISMS COMMONLY FOUND IN ENVIR
  56. SCID
    FAMILY OF IMMUNODEFICIENCY DISORDERS (DEFECTIVE EARLY PROGENITOR CELLS

    MAY FOLLOW AUTOSOMAL OR SEX LINKED PATTERS

    EITHER COMPLETE ABSENCE OF T&B CELLS, OR SOME B CELLS PRESENT BUT DYSFUNCTIONAL DUE TO NO CD4 CELLS

    ~50% OF AUTOSOMAL DUE TO LACK OF ADA OR PURINE NUCLEOSIDE PHOSPHORYLASE (PNP)

    BARE-LEUKOCYTE SYND: CLASS I OR II MHC MOLECULES CAUSE IMPAIRED DEVELOPMENT OR IMPAIRED ACTIVATION OF SUBSETS OF T CELLS (ex VARIANT CLASS I INVOLVES MUTATED TAP GENES, CAN'T PRESENT TO CD8+)

    RAG DEFICIENCY

    X-LINKED: DEFICIENT CYTOKINE RECEPTORS (IL2, 4, 7, 9, 15). IL7 IMPORTANT FOR EARLY PROGENITOR DEV
  57. AGAMMAGLOBULINEMIAS
    IMMUNODEFICIENCY: B CELLS MISSING OR DYSFUNCTIONAL

    MAY BE ALL B CELLS OR PARTICULAR ISOTYPE

    MAY BE INDIRECT CAUSED BY FAULTY CD4+

    X-LINKED CONGENITAL: BRUTON'S, DEFECTIVE TYROSINE KINASE (btk) FOR V-DJ JOINING. PRE B CELLS MAY BE PRESENT BUT SUBSEQUENT MATURATION DEFECTIVE. YOUNG BOYS

    COMMON VARIABLE IMMUNODEFICIENCY (CVI): LOOKS LIKE BRUTONS BUT IN OLDER PATIENTS. EQUAL M/F SO AUTOSOMAL.

    SELECTIVE IgA MOST COMMON

    X-LINKED HYPER IgM SYNDROME: DEFECTIVE CD40 LIGAND ON ACTIVATED T CELLS, SO CANNOT INITIATE B CELL ISOTYPE SWITCHING (LYMPH NODES LACK GERMINAL CENTERS)

    ACTIVATION INDUCED CYTIDINE DEAMINASE DEFICIENCY (AID): B CELLS WITH DEFECTIVE CLASS SWITCHING AND AFFINITY MATURATION
  58. DiGEORGE'S SYNDROME
    IMMUNODEFICIENCY: CELL-MEDIATED

    CONGENITAL THYMIC DYSPLASIA (PHARENGIAL ARCHES)

    THYMUS, PARATHYROID, AORTIC ARCH, OTHER UPPER-CHEST TISSUES, DYSMORPHIC FACESE

    PRE T CELLS PRESENT AND CAN BE INDUCED TO MATURATION (THERAPUTIC)

    B CELLS PRESENT BUT VARIABLE FUNCTION DUE TO ABSENCE OF FUNCTIONAL T CELLS
  59. MUCOCUTANEOUS CANDIDAISIS
    CELL MEDIATED IMMUNODEFICIENCY

    SELECTIVE DYSFUNTION ASSOCIATED WITH CANDIDA (YEAST) INFECTIONS

    OTHER T CELL FUNCTIONS NORMAL
  60. AIDS
    CELL MEDIATED IMMUNODEFICIENCY

    HIV USES CD4+ RECEPTORS TO ENTER CELLS (Gp120 BINDS TO CD4+ RECEPTOR)

    CERTAIN CHEMOKINE RECEPTORS ACT AS CORECEPTORS (CCR5 ON T & MACRO, CXCR4 ON T ONLY)

    DECREASED CD4+ (TH1,17,2), DEND CELLS, MACROPHAGES. EFFECTS BOTH ADAPTIVE & NON-ADAPTIVE

    KAPOSI'S SARCOMA: INCREASED CANCER INCIDENCE

    • NORM CD4 ~1200ul
    • ASYMPTOMATIC HIV ~800ul
    • AS OPPOR INFECTIONS BEGIN <500ul
    • FULL-BLOWN AIDS <200ul
  61. PROBLEMS WITH T CELL CENTRAL TOLERANCE
    CERTAIN SELF PEPTIDES MAY NOT BE AVAILABLE IN THYMUS FOR NEGATIVE SELECTION

    • MHC MAY NOT PRESENT CERTAIN PEPTIDES EFFECTIVELY FOR NEGATIVE SELECTION
    • DEPENDS ON EXACTLY WHICH MHC ALLELS AN INDIVIDUAL CARRIES

    RELATIVE RISK: PROBABILITY FOR PARTICULAR AUTOIMMUNE DISEASE IN CERTAIN INDIVIDUALS DEPENDING ON CONSTELLATION OF MHC ALLELS

    EPITOPE SPREADING: CRYPTIC EPITOPES -- SELF-Ag PRESENTED AT TOO LOW OF CONCENTRATIONS TO COMPLETELY ELIMINATE REACTIVITY, AND MAY BECOME PROMINENT LATER IN THE RESPONSE
  62. PROBLEMS WITH PERIPHERAL T CELL TOLERANCE
    SEQUESTERED SELF-Ag IN IMMUNOLOGICALLY PRIVILEGED SITES ARE RELEASED INTO PERIPHERY

    INAPPROPRIATE EXPRESSION OF CLASS II MHC WILL INCREASE THE PROBABILITY OF AUTOIMMUNE T CELL RESPONSIVENESS IN TH1,17, AND 2

    INAPPROPRIATE EXPRESSION OF CO-STIM MOLECULES (B7, CD80/86) WILL NOT CAUSE ANERGY/APOPTOSIS IN CTLs

    DYSFUNCTIONAL T-REG MAY DISTURB BALANCE OF CYTOKINES ALLOWING IMMUNOREGULATORY DYSFUNCTIONS AND EXPRESSION OF PATHOLOGICAL SELF-REACTIVITIES
  63. PROBLEMS WITH B CELL CENTRAL TOLERANCE
    LIMITED EXPOSURE TO SELF Ag IN MARROW

    SOMATIC MUTATIONS IN B CELLS ACTVATED TO FOREIGN Ag MAY CAUSE EXPRESSION OF RECEPTORS FOR Ag WITH NEW REACTIVITIES AGAINST SELF

    ANTIGEN MIMICRY: SIMILARITY BETWEEN FOREIGN Ag AND SELF THAT ALLOWS IMMUNE CROSS REACTIVITY (ex RHEUMATIC FEVER/HEART DISEASE
  64. PROBLEMS WITH B CELL PERIPHERAL TOLERANCE
    SELF Ag SEQUESTERING (ex CNS AND EYE LENS)

    SPLIT TOLERANCE (2 CELL TYPES NEEDED FOR ACTIVATION) INEFFECTIVE DUE TO 1) ACTIVAGTION OF ANERGIC T CELLS OR 2) BYPASS OF T CELLS DUE TO MITOGENS/ADJUVANTS (NONSPECIFIC T-INDUCER INDEPENDENT) OR PHYSICAL LINKAGE OF FOREIGN Ag TO SELF Ag (NONSPECIFIC T-INDUCER DEPENDENT) CAUSING ACTIVATION OF DORMANT SELF-REACTIVE B CELLS

    NEO-EPITOPES CREATED AS RESULT OF PARTIAL DEGRADATION OF SELF Ag DURING INJURY OR TRAUMA. SELF Ag DEFORMED AND POSSESSES FOREIGN CHARACTER
  65. ADCC
    INVOLVED IN AUTOIMMUNITY

    Ab-DEPENDENT CELL-MEDIATED CYTOTOXICITY

    Fc RECEPTOR BEARING KILLER CELLS (K/NK CELLS) AND CR BEARING PHAGOS ATTACK CELLS BOUND BY SPECIFIC Ab
  66. AUTOIMMUNITY ANTI-RECEPTOR DISEASES
    GRAVE'S DISEASE: THYROID STIM HORMONE RECEPTOR AGONIST. stimulating thyroid hormone synthesis and secretion, and thyroid growth (causing a diffusely enlarged goiter). The resulting state of hyperthyroidism can cause a dramatic constellation of neuropsychological and physical signs and symptoms, which can severely compromise the patients’ ability to maintain jobs and relationships

    MYASTHENIA GRAVIS - ACh RECEPTOR AGONIST

    INSULIN-DEPENDENT DIABETES MELLITUS - PANCREATIC BETA CELLS. EXCESSIVE TIREDNESS, INCREASED THIRST, POLYURIA, WEIGHT LOSS
  67. MULTIPLE SCLEROSIS
    AUTOIMMUNE

    INDUCTIVE EFFECT UNKNOWN

    MIXED Ab AND CELL-MEDIATED RESPONSES PROBABLY INVOLVING TYPE II & IV HS
  68. RHEUMATOID ARTHRITIS
    AUTOIMMUNE

    MIXED Ab AND CMI EFFECTORS INVOLVING TYPE III & IV HS

    PROMINENT IMMUNE COMPLEX IN JOINTS

    ABNORMAL IgG PRODUCED IN SYNOVIUM, AND Ab RESPONSE IS INITIATED AGAINST ABNORMAL IgG (REFERRED TO AS RHEUMATOID FACTOR RF)

    COMPLEMENT THEN STARTS DESTROYING HOST TISSUE
  69. SYSTEMIC LUPUS ERYTHEMATOSUS
    AUTOIMMUNE

    SYSTEMIC, PROMINENT ANA+/DNA REACTIVE Ab AND HEMATOPOIETIC/LYMPHOPOIETIC CELL Ab

    GREATER INCIDENCE IN WOMEN OF CHILD-BEARING YEARS (SEX HORMONE INFLUENCES)

    RASH, SERUM COMPLEMENT DEPLETION, KIDNEY DISEASE, LE CELLS

    ATTACK ERYTHS, PLATELETS, COAGULANTS, LYMPHS, NEUTS, NEURO, DNA, IgG
  70. GOODPASTURE'S SYNDROME
    AUTOIMMUNE

    TYPE II HS AGAINST COLLOGEN TYPE IV OF BM OF RENAL GLOMERULI, AND LESSER EXTENT PULMONARY ALVEOLI
  71. GUILLIAN-BARRE SYNDROME
    AUTOIMMUNE

    ACUTE IDIOPATHIC POLYNEURITIS

    PERIPHERAL NERVE DEMYLINATION
  72. HASHIMOTO'S DISEASE
    AUTOIMMUNE DISEASE

    HYPOTHYROIDISM

    ANTI-THYROGLOBULIN; ANTI-THYROID EPITHELIUM
  73. ADDISON'S DISEASE
    AUTOIMMUNE

    ADRENAL GLANDS

    ANTI-ADRENAL CELL MEMBRANES; LYMPH/MONO CORTICAL INFILTRATION
  74. SJOGREN'S SYNDROME
    AUTOIMMUNE

    SALIVARY GLANDS

    GLANDULAR INFLAMMATION
  75. THROMBOCYTOPENIAS
    AUTOIMMUNE

    PLATELETS OR MEGAKARYOCYTES

    PLATELET DESTRUCTION/ ABNORMAL BLEEDING
  76. CHRONIC ATROPHIC GASTRITIS; PERNICIOUS ANEMIA
    GASTRIC MUCOSA

    LOSS OF GASTRIC SECRETORY FUNCTION

    FAILURE OF B12 ABSORPTION DUE TO LOSS OF INTRINSIC FACTOR PRODUCING CELLS (PARIETAL CELLS IN STOMACH)

    water soluble vitamin with a key role in the normal functioning of the brain and nervous system, and for the formation of blood.
  77. CROHN'S DISEASE
    AUTOIMMUNE

    INTESTINAL GRANULOMATOUS DISEASE

    MUCOSAL MEMBRANE OF TERMINAL ILEUM

    MUCOSAL ULCERATION; OBSTRUCTIVE GRANULOMA
  78. RHEUMATIC FEVER
    AUTOIMMUNE

    HEART

    MYOCARDITIS; SCARRING OF HEART VALVES
  79. PEMPHIGUS VULGARIS
    AUTOIMMUNE

    EPIDERMIS

    BLISTERING OF SKIN
  80. RHEUMATOID ARTHRITIS
    AUTOIMMUNE

    INITIALLY JOINTS

    SPREAD TO CARTILAGE AND NEIGHBORING BONE AND MUSCLE

    IMMUNE COMPLEX DISEASE IN SYNOVIUM, RF AGAINST IgG PROMINENT

    INFLAMMATORY CELLS NOTED
  81. TRANSPLANTATION DEFINITIONS
    SYNGENEIC - IDENTICAL TWINS

    ALLOGENEIC - DIFFERING GENETICS BETWEEN MEMBERS OF SAME SPECIES

    XENOGENEIC - MAJOR GENETIC DIFFERENCES BETWEEN DIFFERENT SPECIES

    AUTOGRAFT - TISSUE GRAFTED BACK INTO ORIGINAL DONOR

    ISOGRAFT - TISSUE GRAFTED BETWEEN SYNGENEIC INDIVIDUALS
  82. 3 PHASES INVOLVED IN ALLOGRAFT REJECTION
    RECOGNITION PHASE - APCs TAKE UP GRAFT Ag AND PRESENT. Ag REACTIVE LYMPHS ACTIVATED, AND VASCULARIZATION HELPS ACTIVATE CIRCULATING LYMPHS. EARLY RESPONSE MAINLY BY CD4+ CELLS

    PROLIFERATION AND DIFFERENTIATION PHASE - CD4+ CELLS & MACROPHAGS MEDIATE T & B CELLS. EFFECTOR T CELLS LEAVE LYMPH NODE AND REACH GRAFT THROUGH BLOOD

    DESTRUCTIVE PHASE - CTLs PRIMARY FORCE IN GRAFT REJECTION. CYTOLYSIS INVOLVES BINDING, MOVING CYTOPLASMIC GRANULES (CONTAIN PERFORIN) AND GRANZYMES ADJACENT TO TARGET CELL. ACTIVATED B CELLS BECOME PLASMA CELLS AND THEIR Ab INTERACT WITH COMPLEMENT AND ADCC
  83. MHC IN GRAFT REJECTION
    CLASS I (ABC) TARGETS FOR CTLs

    CLASS II (DP,DQ,DR) TARGETS FOR CD4+

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