IMMUNE DISORDERS

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IMMUNE DISORDERS

• EXAGGERATED RESPONSE TO SECOND OR SUBSEQUENT
• EXPOSURE TO ANTIGEN WHICH RESULTS IN TISSUE
  DAMAGE
• IMMEDIATE (SECONDS TO MINUTES) OR DELAYED (1-2
  DAYS)
• HUMORAL ANTIBODY REACTIONS OR CMI REACTIONS
• TYPE I ANAPHYLAXIS, ALLERGY
• INITIAL EXPOSURE IgE SYNTHESIS, BINDS TO
• RECEPTORS ON BASOPHILS, EOSINOPHILS, MAST CELLS
  
• MAST CELLS WHITE BLOOD CELLS TISSUE
  LOCALIZED-
• PRODUCES VASOACTIVE MOLECULES ( HISTAMINE)
• STORED IN VACUOLES NEAR MEMBRANE,
• HAVE RECEPTORS FOR IgE
• IgE BINDING SENSITIZES THESE CELLS TO THE
  ANTIGEN WHICH STIMULATED THE IgE SYNTHESIS

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• ANAPHYLAXIS
• SECOND OR LATER ANTIGEN EXPOSURE ANTIGEN BINDS
  SPECIFIC ANTIBODY IgE ON MAST CELLS, BASOPHILS,
  EOSINOPHIL
• TRIGGERS DEGRANULATION - RELEASE OF HISTAMINE,
  VASOACTIVE MOLECULES, PROTEASES
• SMOOTH MUSCLE CONTRACTION, VASODILATION,
  INCREASED VASCULAR PERMEABILITY, MUCUS SECRECTION
  ANAPHYLAXIS
• LOCALIZED ATOPIC (OUT OF PLACE)
• UPPER RESPIRATORY TRACT SENSITIZED MAST
  CELLS IN MUCOUS MEMBRANES
• POLLEN SPORES, DANDER, HOUSE MITES
• ITCHING, WATERY EYES, CONGESTION, SNEEZING,
  COUGHING
• ANTI-HISTAMINE

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Figure 31.2 HUMAN BLOOD CELLS
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Figure 32.26 TYPE I HYPERSENSITIVITY (ALLERGIC
RESPONSE)
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Figure 32.27 IN VIVO SKIN TESTING
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• LOWER RESPIRATORY TRACT - SAME ALLERGENS
• AIR SACS ALVEOLI DISTENDED, FLUID, MUCUS,
  ASTHMA
• ANTIGENS ENTER DIGESTIVE SYSTEM HIVES RED
  SKIN
• GASTROENTERITIS
• SYSTEMIC GENERALIZED RESPONSE, WHOLE BODY
• RESPIRATORY IMPAIRMENT (SMOOTH MUSCLE
  CONTRACTION IN BRONCHIOLES)
• DROP IN BLOOD PRESSURE ARTERIOLES EXPAND,
  MORE PERMEABLE, RAPID FLOW INTO TISSUE SPACES
• REDUCED VENOUS BLOOD RETURN, ASPHYXIATION,
  SHOCK
• RAPID, SEVERE, CAN BE FATAL
• DRUGS (PENICILLIN) INSECT VENOM (BEE)
  PEANUTS, ANTI- SERA (TETANUS)

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TYPE II HYPERSENSITIVITY CYTOTOXIC
REACTIONS

• ANTIGEN-ANTIBODY REACTION DAMAGES (LYSES,
  KILLS)HOST CELLS,
• RESULTS IN INJURY
• IgG, IgM REACT WITH HOST CELL SURFACES, TISSUES
• BLOOD TRANSFUSIONS WITH MISMATCHED BLOOD
  ERYTHROBLASTOSIS FETALIS

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ABO BLOOD GROUPS

• RBC TYPE ANTIGENS ON RBC ANTIBODIES IN BLOOD
• A A ANTI B
• B B ANTI A
• AB A AND B NONE
• O NONE ANTI A AND ANTI B
• ANTIGENS PRODUCED POSSIBLE FROM GENE
  GENOTYPES
• A IA IA IA OR IA i
• B IB IB IB OR IB i
• NONE I i i
• A AND B IA IB

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Figure 32.29a IMMUNOHEMATOLOGY
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Figure 32.29b IMMUNOHEMATOLOGY
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Figure 32.29c IMMUNOHEMATOLOGY
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TRANSFUSION REACTIONS

• RECIPIENT BLOOD CONTAINS ANTIBODIES RECEIVES
  BLOOD WITH RBCs COATED WITH ANTIGENS
• INCOMING RBC HEMAGGLUTINATE, LYSE,
• CHILLS, FEVER, PROSTRATION, SHOCK, DEATH
• PREVENT BY BLOOD TYPING AND CROSS MATCHING BLOODS
• TYPING
• UNKNOWN BLOOD PLUS KNOWN ANTI A gt CLUMP MEANS A
  TYPE
• ANTI B gt B
  TYPE
• CLUMPING WITH BOTH ANTI A AND ANTI B gt
  AB TYPE
• NEITHER A NOR B
  O TYPE

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CROSS MATCHING BLOODS

• MAJOR
• RECIPIENT SERUM PLUS DONOR RBC gt IF
  AGGLUTINATION OCCURS THE DONOR RBC WOULD BE
  COATED BY RECIPIENT ANTIBODIES CIRCULATING IN
  BLOOD gt CYTOTOXIC
• MINOR
• RECIPIENT RBC PLUS DONOR SERUM gt IF
  AGGLUTINATION OCCURS THIS BLOOD SHOULD NOT BE
  USED, BUT THIS IS NOT SO IMPORTANT AS THE MAJOR
  CROSS MATCH INCOMING SERUM (CONTAINING SOLUBLE
  ANTIBODIES) WILL BE DILUTED IN RECIPIENTS BLOOD,
  REDUCING THE SEVERITY OF THE PROBLEM
• UNIVERSAL DONOR - TYPE O PERSON - THE ANTI A
  AND ANTI B ANTIBODIES WILL BE DILUTED IN
  RECIPIENT BLOOD CAN BE USED FOR TYPE A, B, AB
  AND O RECIPIENTS
• UNIVERAL RECIPIENT - TYPE AB PERSON NO
  ANTIBODIES TO REACT WITH INCOMING A, B, OR O CELLS

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HEMOLHYTIC DISEASE OF NEWBORN

• ERYTHROBLASTOSIS FETALIS
• Rh ANTIGENS ON SOME RBC
• RHESUS MONKEY RBC gt RABBITS gt ANTISERUM
  AGGLUTINATED MONKEY RBC, BUT ALSO AGGLUTINATED
  RBC OF SOME (BUT NOT ALL) HUMANS?
• SOME PEOPLE PRODUCE THE SAME ANTIGEN ON THEIR RBC
  AS DO RHESUS MONKEYS RH INDIVIDUAL 85
• RH- INDIVIDUALS NO SUCH ANTIGEN AND NO ANTI Rh
  ANTIBODIES
• Rh- MOTHER, Rh FATHER (Rh IS DOMINANT)
• FIRST PREGNANCY WITH Rh FETUS, SMALL
  HEMORRHAGES, BABY RBCs ENTER MOTHERS BLOOD, SHE
  SYNTHESIZES ANTI Rh ANTIBODIES - NO PROBLEM

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• SECOND OR LATER PREGNANCY WITH Rh BABY
• MOTHERS ANTI-Rh ANTIBODIES CROSS PLACENTA
• REACT WITH BABYS RBC, LYSE, LACK OF OXYGEN
  HEMOGLOBIN RELEASE
• HEMOGLOBIN gt DEGRADED TO BILIRUBIN (TOXIC)
• BABY IN UTERUS OXYGEN FROM MOTHER, MOTHERS
  LIVER PROCESSES EXCESS BILIRUBIN
• BIRTH LACK OF OXYGEN, BILIRUBIN IS NOT
  PROCESSED IN INFANT LIVER, BRAIN DAMAGE
• MANAGEMENT MONITOR MOTHERS ANTI Rh ANTIBODY
  LEVEL DURING PREGNANCY FOR TITER INCREASE
• FLUORESCENT LIGHT TO HELP BILIRUBIN
  BREAKDOWN
• MONITOR BILIRUBIN LEVEL DANGEROUS LEVEL
  BLOOD EXCHANGE, Rh- BLOOD, 10 ML IN /
  10 ML 0UT

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Figure 32.30a Rh FACTOR INCOMPATIBILITY CAN
RESULT IN RBC LYSIS
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Figure 32.30b Rh FACTOR INCOMPATIBILITY CAN
RESULT IN RBC LYSIS
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• PREVENTION
• GIVE EXPECTANT MOTHER ANTI-Rh ANTIBODY
• PREVENTS Rh RBC (BABY) FROM STIMULATING
  ANTIBODY SYNTHESIS BY MOTHER
• RhoGam
• SEVERE CASES -
• BILIRUBIN LEVEL AMNIOTIC FLUID - AMNIOCENTESIS
• INFUSION IN UTERO
• Rh- RBC INJECTED INTO FETUS ABDOMEN gt LIVER,
  SPLEEN,
• FUNCTION FOR NEWBORN

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TYPE III IMMUNE COMPLEXES DAMAGE HOST

• TOO SMALL AG-AB COMPLEXES ESCAPE PHAGOCYTOSIS
• CIRCULATING COMPLEXES LODGE IN TISSUES
  INFLAMMATION
• PHAGOCYTES ARRIVE, CANNOT ENGULF THE SMALL
  COMPLEXES, IN FRUSTRATION, RELEASE DIGESTIVE
  ENZYMES INTO TISSUES, FURTHER INJURY
• ACUTE POST-STREPTOCOCCAL GLOMERULONEPHRITIS
• INFLAMMATION OF THE GLOMERULI BASEMENT
  MEMBRANE OF KIDNEY (BLOOD FILTRATION)
• ARTHRITIS - JOINTS
• SKIN SYSTEMIC LUPUS ERYTHEMATOSUS

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Figure 32.31 TYPE III HYPERSENSITIVITY
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TYPE IV DELAYED CMI REACTION

• SPECIFIC TH AND CTL CELLS - 24-48 HRS CELLS
  MIGRATE TO ANTIGEN (ON SECOND OR SUBSEQUENT
  EXPOSURE)
• FIRST EXPOSURE ANTIGEN STIMULATES IMMUNE
  RESPONSE
• SECOND EXPOSURE ANTIGEN FRAGMENTS PRESENTED ON
  CELL SURFACES TH AND CTLs ATTRACTED, DAMAGE
  CELLS, CYTOKINES INCREASE VASCULAR PERMEABILITY,
  ATTRACT OTHE LEUCOCYTES, EXACERBATE INFLAMMATION
• TUBERCULIN SKIN TEST FOR TB (TUBERCULIN M.
  TUBERCULOSIS PROTEIN AND ONE OF ITS ANTIGENS)
• UN-INFECTED PERSON TUBERCULIN INJECTION NO
  REACTION
• INFECTION STIMULATES CMI
• TUBERCULIN INJECTION SKIN INFLAMMATION
• EVIDENCE OF INFECTION

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Figure 32.33 CONTACT DERMATITIS
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Figure 32.34 CONTACT DERMATITIS FROM POISON OAK
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Figure 32.32b TYPE IV (OR DELAYED-TYPE)
HYPERSENSITIVITY
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AUTOIMMUNE DISEASES

• SELF-REACTIVE T AND B CELLS DAMAGE HOST
• RHEUMATOID ARTHRITIS, TYPE I DIABETES
• TRANSPLANTATION REJECTION
• HOST VERSUS GRAFT
• FOREIGN MHC I OR II COMPLEXES ACT AS ANTIGENS,
  STIMULATE CMI IMMUNITY, HOST ATTACKS THE NEW
  TISSUE/ORGAN
• GRAFT VERSUS HOST
• IMMUNOCOMPETENT CELLS IN TRANSPANTED TISSUE
  ATTACK HOST CELLS
• BONE MARROW TRANSPLANTS, HOST IS OFTEN
• IMMUNOSUPPRESSED, CANNOT DEFEND ITSELF

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Figure 32.5 THE MEMBRANE-BOUND CLASS I AND CLASS
II MAJOR HISTOCOMPATIBILITY MOLECULES