1. IMMUNE DISORDERS – EXAGGERATED RESPONSES; DAMAGE HOST
TYPE I – ANAPHYLAXIX, ALLERGY
LOCALIZED, SYSTEMIC
TYPE II- CYTOTOXIC REACTIONS
ABO BLOOD GROUPS TRANSFUSION REACTION
HEMOLYTIC DISEASE – NEWBORN
TYPE III- IMMUNE COMPLEXES
TYPE IV- DELAYED - CMI
POISON IVY, CONTACT DERMATITIS
AUTOIMMUNE DISEASES
TRANSPLANT REJECTION –
HOST VS GRAFT, GRAFT VS HOST

2. IMMUNE DISORDERS TYPE I – ANAPHYLAXIS, ALLERGY
EXAGGERATED RESPONSE TO SECOND OR SUBSEQUENT
EXPOSURE TO ANTIGEN WHICH RESULTS IN TISSUE DAMAGE
IMMEDIATE (SECONDS TO MINUTES) – HUMORAL ANTIBODIES
DELAYED (1-2 DAYS) – 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-
PRODUCE 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

3. TYPE I – ANAPHYLAXIS - CONTINUED
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

4. TYPE I ANAPHYLAXIS - CONTINUED LOCALIZED – ATOPIC (OUT OF PLACE)
UPPER RESPIRATORY TRACT –
SENSITIZED MAST CELLS IN MUCOUS MEMBRANES
CAUSES: POLLEN SPORES, DANDER, HOUSE MITES
SYMPTOMS: ITCHING, WATERY EYES, CONGESTION,
SNEEZING, COUGHING
TREATMENT: ANTI-HISTAMINE
2. LOWER RESPIRATORY TRACT - SAME ALLERGENS
AIR SACS – ALVEOLI – DISTENDED, FLUID, MUCUS, ASTHMA
3. DIGESTIVE SYSTEM – HIVES RED SKIN
GASTROENTERITIS

5. HUMAN
BLOOD
CELL
DEVELOPMENT

6. TYPE I HYPERSENSITIVITY
(ALLERGIC RESPONSE) 6

7. SKIN TESTING FOR
CAUSE OF
HYPERSENSITIVITY

8. TYPE I - ANAPHYLAXIS -CONTINUED
SYSTEMIC – GENERALIZED RESPONSE, WHOLE BODY
RESPIRATORY IMPAIRMENT
(SMOOTH MUSCLE CONTRACTION IN BRONCHIOLES)
DROP IN BLOOD PRESSURE – ARTERIOLES EXPAND,
BECOME MORE PERMEABLE,
RAPID FLOW INTO TISSUE SPACES
REDUCED VENOUS BLOOD RETURN,
ASPHYXIATION, SHOCK
RAPID, SEVERE, CAN BE FATAL
CAUSES: DRUGS (E.G., PENICILLIN); INSECT VENOM (BEE);
PEANUTS, ANTI-SERA (E.G., TETANUS ANTSERUM)

9. TYPE II HYPERSENSITIVITY CYTOTOXIC REACTIONS
ANTIGEN-ANTIBODY REACTION DAMAGES (LYSES, KILLS)
CELLS, RESULTS IN INJURY
IgG, OR IgM REACT WITH CELL SURFACES, TISSUES
FOREIGN IgG (INCOMING) REACT WITH HOST CELLS
HOST IgG REACTS WITH FOREIGN CELLS (INCOMING)
BLOOD TRANSFUSIONS WITH MISMATCHED BLOOD;
ERYTHROBLASTOSIS FETALIS – HEMOLYTIC DISEASE OF
NEW BORN

10. ABO BLOOD GROUPS PRODUCED RBC TYPE ANTIGENS ON RBC FROM GENE: A A IA
B B IB AB A AND B IA & IB
O NONE I
POSSIBLE GROUP GENOTYPES
A IA IA OR IA i
B IB IB OR IB i
A B IA IB
O i i

11. ABO ANTIGENS & ANTIBODIES
RBC TYPE ANTIGENS ON RBC ANTIBODIES IN BLOOD
A A ANTI B
B B ANTI A
AB A AND B NEITHER
O NONE ANTI A AND ANTI B

12. IMMUNOHEMATOLOGY

13. COMPLEMENT
ACTIVATED-
HEMOLYSIS
IMMUNOHEMATOLOGY

14. IMMUNOHEMATOLOGY

15. TRANSFUSION REACTIONS
RECIPIENT BLOOD CONTAINS ANTIBODIES (NATURAL); E.G., ANTI-B
RECEIVES BLOOD WITH RBCs COATED WITH, E.G., ANTIGEN B
INCOMING RBC HEMAGGLUTINATE, LYSE,
CHILLS, FEVER, PROSTRATION, SHOCK, DEATH
PREVENT BY BLOOD TYPING AND CROSS MATCHING BLOODS
TYPING
UNKNOWN BLOOD PLUS KNOWN ANTI A > CLUMP MEANS A TYPE
ANTI B > B TYPE
CLUMPING WITH BOTH ANTI A AND ANTI B > AB TYPE
CLUMPING NEITHER A NOR B O TYPE

16. CROSS MATCHING BLOODS MAJOR
RECIPIENT SERUM PLUS DONOR RBC > IF AGGLUTINATION OCCURS THE DONOR RBC WOULD BE COATED BY RECIPIENT ANTIBODIES CIRCULATING IN BLOOD > CYTOTOXIC
MINOR
RECIPIENT RBC PLUS DONOR SERUM > 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 RECIPIENT’S 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
UNIVERSAL RECIPIENT - TYPE AB PERSON – NO ANTIBODIES TO REACT WITH INCOMING A, B, OR O CELLS

17. HEMOLYTIC DISEASE OF NEWBORN
ERYTHROBLASTOSIS FETALIS
Rh+ ANTIGENS ON SOME RBC
RHESUS MONKEY RBC > RABBITS > 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

18. HEMOLYTIC DISEASE OF NEWBORN
Rh- MOTHER, Rh+ FATHER (Rh+ IS DOMINANT)
FIRST OR LATER PREGNANCY WITH Rh+ FETUS,
SMALL HEMORRHAGES,
BABY RBCs ENTER MOTHER’S BLOOD,
SHE SYNTHESIZES ANTI Rh ANTIBODIES - NO PROBLEM
SECOND OR LATER PREGNANCY WITH Rh+ BABY
MOTHER’S ANTI-Rh ANTIBODIES CROSS PLACENTA
REACT WITH BABY’S RBC, LYSE, LACK OF OXYGEN
HEMOGLOBIN RELEASED
> DEGRADED TO BILIRUBIN (TOXIC)
IN UTERUS – OXYGEN FROM MOTHER, MOTHER’S LIVER
PROCESSES EXCESS BILIRUBIN
BIRTH – LACK OF OXYGEN, BILIRUBIN IS NOT PROCESSED
IN INFANT LIVER, BRAIN DAMAGE

19. HEMOLYTIC DISEASE OF NEWBORN
MANAGEMENT
MONITOR MOTHER’S ANTI Rh ANTIBODY LEVEL DURING PREGNANCY TO CHECK FOR TITER INCREASE
FLUORESCENT LIGHT TO HELP BILIRUBIN BREAKDOWN
MONITOR BILIRUBIN LEVEL – DANGEROUS LEVEL – BLOOD EXCHANGE, Rh- BLOOD, 10 ML IN / 10 ML 0UT
SEVERE CASES - DETERMINE BILIRUBIN LEVEL AMNIOTIC FLUID - AMNIOCENTESIS
INFUSION IN UTERO
Rh- RBC INJECTED INTO FETUS ABDOMEN > LIVER, SPLEEN,
FUNCTION FOR NEWBORN

20. Rh FACTOR INCOMPATIBILITY CAN RESULT IN RBC LYSIS

21. Rh FACTOR INCOMPATIBILITY CAN RESULT IN RBC LYSIS

22. HEMOLYTIC DISEASE OF NEW BORN
PREVENTION
GIVE EXPECTANT MOTHER ANTI-Rh ANTIBODY
PREVENTS Rh+ RBC (BABY) FROM STIMULATING
ANTI Rh ANTIBODY SYNTHESIS BY MOTHER
RhoGam IgG FROM HUMANS; KNOWN TO CONTAIN
ANTI-Rh ANTIBODIES
REDUCES RISK FROM ~15% (UNTREATED)
TO <0.1%

23. TYPE III – IMMUNE COMPLEXES DAMAGE HOST
SMALL AG-AB COMPLEXES ESCAPE PHAGOCYTOSIS
CIRCULATING COMPLEXES LODGE IN TISSUES –
INFLAMMATION; PHAGOCYTES ARRIVE,
CANNOT ENGULF THE SMALL COMPLEXES,
RELEASE DIGESTIVE ENZYMES INTO TISSUES, FURTHER INJURY
ACUTE POST-STREPTOCOCCAL GLOMERULONEPHRITIS
INFLAMMATION OF THE GLOMERULI – BASEMENT MEMBRANE OF KIDNEY (BLOOD FILTRATION)
ARTHRITIS - JOINT INFLAMMATION – ONE OF >100 CONDITIONS
CALLED ARHTRITIS
SYSTEMIC LUPUS ERYTHEMATOSUS – ARTHRITIS, VASCULITIS,
GLOMERULONEPHRITIS

24. TYPE III
HYPERSENSITIVITY

25. TYPE IV – DELAYED CMI REACTION
SPECIFIC TH AND CTL CELLS HRS CELLS MIGRATE TO
ANTIGEN (ON SECOND OR SUBSEQUENT EXPOSURE), DAMAGE HOST
FIRST EXPOSURE – ANTIGEN STIMULATES CMI RESPONSE
SECOND EXPOSURE –
ANTIGEN FRAGMENTS PRESENTED ON CELL SURFACES;
T HELPER AND CTLs ATTRACTED, DAMAGE CELLS,
CYTOKINES INCREASE VASCULAR PERMEABILITY,
ATTRACT OTHE LEUCOCYTES, EXACERBATE INFLAMMATION

26. TYPE IV – DELAYED CMI REACTION
TUBERCULIN SKIN TEST FOR TB –
(TUBERCULIN = M. TUBERCULOSIS PROTEIN
AND ONE OF ITS ANTIGENS)
PEOPLE INFECTED BY M. TUBERCULOSIS OR GIVEN BCG VACCINE:
FORM CMI TO BCG (AND TUBERCLIN)
INJECT TUBERCULIN INTO SKIN:
UN-INFECTED PERSON –– NO REACTION
ANYONE PREVIOUSLY INFECTED
OR VACCINATED WITH BCG
INFLAMMATION AROUND SITE OF INJECTION
EVIDENCE OF PREVIOUS OR ACTIVE INFECTION

27. CONTACT DERMATITIS – E.G. POISON IVY

28. CONTACT DERMATITIS FROM POISON OAK

29. TYPE IV (OR DELAYED-TYPE) HYPERSENSITIVITY

30. AUTOIMMUNE DISEASES SELF-REACTIVE T AND B CELLS DAMAGE HOST
HYPERSENSITIVITY TO ONE’S OWN SELF
RHEUMATIC FEVER – ANTIODIES TO S. PYOGENES PILI EPITOPE
CROSS REACT WITH HEART TISSUE –
TYPE II HYPERSENSITIVIY
TYPE I DIABETES – CYTOTOXIC T CELLS FORM AFTER INFECTION BY SOME VIRUS (?) & ATTACK AND DESTROY INSULIN-
PRODUCING ISLET CELLS OF PANCREAS
TYPE IV HYPERSENSITIVITY
MULTIPLE SCLEROSIS - CMI ATTACKS MYELIN, DEMYELINATES
AXONS, LOSS OF NERVE INSULATION AND FUNCTION