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Immunology-Serology and Blood Banking

HISTORY

YEAR PERSONS INVOLVED RESEARCH/EVENT

1492 First blood transfusion recorded in history

1500 Chinese Variolation; Insufflation

- material was dried into a powder and

inhaled by non-immune person

1700 Cross-immunity (exposure to cowpox and

immunity to small pox)

1880 Louis Pasteur Attenuation*, rabies vaccine

- bacteria/viruses are weakened

1888 Phagocytosis

1901 Serum antitoxins

1903 Almoth Wright Opsonizaton

1908 Immunity

- coined the term complement

1919 Explained the complement

1930 Human blood group antigens

The Specificity of Serologic Reactions

1943 Loutit and Mollison Acid-citrate dextrose (ACD)

1957 Citrate-phosphate-dextrose (CPD)

1972 Antibody structure

1977 Radioimmunoassay

1980 George Snell, Jean

Dausset, Baruj

Beneceraf

MHC

1984 T-cell receptor gene

1987 Antibody diversity

1991 Edward Donall

Thomas, Joseph

Murray

Transplantation

Cellular immunity to TB

Paul Ehrlich Side Chain Theory

Anaphylaxis

Immunoregulation

Monoclonal antibody (Hybridoma

technology)

Precipitins

Frank Macfarlane

Burnet

Clonal Selection theory

Gel test

IMMUNITY

☻ ___________ – study of how a host’s body discriminate between self and

foreign antigens and thereby eliminating these foreign substances.

☻ __________ – state of being resistant to infections

☻ __________ – lack of immune response to self-antigens

Innate/Natural/

Nonspecific

Adaptive/Acquired/ Specific

CELLULAR Antigen-presenting cells (eg.

Dendritic cells)

Phagocytes, eosinophils,

basophils, mast cells

NK cells

T-cells (T-cytotoxic and T-

helper)

B-cells and plasma cells

HUMORAL Lysozymes, Lactoferrin

Acute phase reactants

Complement, Properdin

Pepsin, stomach acidity

Cytokines (TNF, INF, beta-lysin

Antibodies

Cytokines

RESPONSE Rapid but short (less potent) Slow but longer (more potent)

MEMORY NO YES (because of memory cells)

SPECIFICITY General Specific antigens

OTHERS *with anatomical barriers – skin (pH 6.5), mucus membranes, normal flora, tears,

cilia, saliva

INNATE IMMUNITY ______________ – process of engulfment of substances to be discriminated; done by

cells called phagocytes

(1) ________ → (2) ________ → (3) ___________ → (4) ________ → (5) ____________

____________ – process in which blood cells pass through the intact walls of

blood cells migrating to the site of injury


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TWO FORMS OF PHAGOCYTOSIS

1. Direct Phagocytosis

2. Indirect Phagocytosis

☻ Mediated by opsonins – antibodies (IgG/IgM), CRP, complement

breakdown products

☻ _____ – most potent opsonin

_______________ – cumulative mechanism (vascular and cellular) in respose to an

injury or invasion by an infectious agent

(1) Vascular Response → (2) Cellular Response → (3) Resolution and Repair

CARDINAL SIGNS:

☻ ______ – redness

☻ ______ – heat

☻ ______ – swelling

☻ ______ – pain

☻ Functio Laesa – loss of function

_________________________ – serum proteins that significantly increase during course

of an inflammation

APR FUNCTION INCREASE RESPONSE TIME (hrs)

Opsonization 1000x 4-6

Cholesterol removal 1000x 24

Ceruloplasmin Binds copper 2x 48-72

Complement C3 Opsonization, lysis 2x 48-72

Alpha1-antitrypsin Protease inhibitor 2-5x 24

Fibrinogen Clot formation 2-5x 24

Haptoglobin Binds hemoglobin 2-10x 24

________________ – proteins that are normally present in serum that has its functions

during inflammation.

FUNCTIONS:

☻ For opsonization (C3b – most potent)

☻ For cell lysis (C5-C9 or MAC)

☻ Clearance of immune complexes

COMPLEMENT

Protein Function Disease (if deficient)

C1q, r or s C1q – binds Fc portion of IgG or IgM Lupuslike syndrome

Recurrent infections C1r – activation of C1s

C1s – cleaves C4 and C2

C4 Part of C3 convertase (C4b2a) Lupuslike syndrome

Pathogen/Microbe

Associated

Molecular Pattern

(PAMPs/MAMPs)

Primitive pattern

recognition

receptors (PPRR)

Acute infections:

PMNs

Chronic infections:

Monocytes

CLASSICAL AND LECTIN PATHWAY ALTERNATIVE PATHWAY


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C2

(most

common def.)

Binds to C4b to form C3 convertase

of classical pathway

Lupuslike syndrome

Recurrent infections

Atherosclerosis

Pivotal point Severe recurrent

infections

Glomerulonephritis

Part of Membrane Attack Complex Neisseria infections

C8 – starts pore formation

C9 – eventual cell lysis No known disease

Binds C3b to form C3 convertase

Cleaves factor B

Stabilizes C3bBb complex (C3

convertase of alternative complex)

Neisseria infections

Similar to C1q; binds to mannose Pneumococcal diseases

Sepsis

Neisseria infections

MASP-1 Similar to C1r

MASP-2 Similar to C1s Pneumococcal diseases

REGULATORY PORTEINS

Dissociates C1r and C1s from C1q

thus inhibiting it

Hereditary angioedema

Factor I Cleaves C3b and C4b Recurrent pyogenic

infections Cofactor of Factor I; inactivates C3b

C4-binding

protein

Cofactor of Factor I; inactivates C4b

Prevents the attachment of C5b67

to cell membrane

Accelerates dissociation of both C3

convertases

Paroxysmal Nocturnal

Hemoglobinuria

MIRL

ADAPTIVE IMMUNITY LYMPHOID ORGANS

PRIMARY

☻ _________

✓ Atrophies as one ages

✓ Located in the thorax

✓ Site of T-cell maturation

☻ _________

✓ Equivalent to Bursa of Fabricius in birds

✓ Site of hematopoiesis

✓ Site of B cell maturation

SECONDARY

☻ _______ – largest secondary lymphoid organ

☻ Tonsils

☻ Lymphoid tissues

☻ Peyer’s patches

☻ Appendix

☻ Mucosa-Associated Lymphoid Tissue (MALT)

LYMPHOCYTES

T CELL B CELL

Cell-mediated immunity Humoral-mediated immunity

Matures in thymus Matures in bone marrow

60-80% 20-30%

CD4+ – T helper cells

CD8+ – T cytotoxic cells

T-regulatory cells

Naive B cell

Activated B cell

Plasma cell

Rosette formation identification

CD2 – receptor for sheep RBCs

Identification by surface

immunoglobulins (IgM and IgD)

Lymphokines (products) Antibodies (products)

CD2, CD3, CD4, CD8 antigens CD19, CD20, CD21, CD40 and MHC

Class II antigens

Located in the paracortex of lymph

nodes

Located in the cortex of lymph nodes

Mitogens:

Concanavalin A

Phytohemagglutinin

Pokeweed mitogen

Mitogens:

LPS

Pokeweed mitogen


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FORMS OF ACQUIRED IMMUNITY

1. WHAT DID YOU ACQUIRE?

☻ If antigen → Active

☻ If antibody → Passive

2. HOW DID YOU ACQUIRE?

☻ Naturally

☻ Artificially

ACTIVE PASSIVE

NATURAL Natural exposure to ANTIGEN Natural exposure to ANTIBODIES

Ex. Recovery from infections Ex. Colostrum, Transplacental

ARTIFICIAL ANTIGEN was injected ANTIBODIES were injected

Ex. Toxoids, Vaccinations Ex. RhIg, anti-rabies, Hepatitis B

Immune globulin, anti-tetanus

CYTOKINES – proteins that regulates immune system

AUTOCRINE PARACRINE

v

ENDOCRINE

ANTIGENS ☻ “antibody generators”

☻ Otherwise known as ____________

☻ Substances that may or may not elicit an immune response

FORMS:

✓ _____________ (autoantigen) – host’s OWN antigen (self-antigens)

✓ ____________ – from DIFFERENT individual of the SAME species

✓ _______________ (Heteroantigen) – from DIFFERENT species

✓ ____________ – antigens that induces an immune response thus

production of antibodies persists. The antibodies produced are specific

for these antigens

✓ ____________ – antigens that reacts with antibodies it did not induce

thus cross reaction exists.

✓ __________– antigens capable of eliciting an immune response

✓ __________– non-immunogenic by itself but can be immunogenic when

coupled with a high molecular weight substance (carrier)

☻ _________ – antigenic determinant

FACTORS AFFECTING IMMUNOGENICITY

1. Foreigness

2. Molecular size

✓ < 1kDa → non-immunogenic

✓ >1kDa but 100kDa → highly immunogenic

3. Chemical composition and complexity

Protein → Polysaccharides → Lipids &Nucleic acids (most immunogenic → least)

4. Route, dosage and timing

✓ Most effective: intraperitoneal and intravenous

5. ___________

✓ Substances that enhances the immunogenicity of an antigen

✓ Included in preparation of antigens in vaccines

✓ Ex. Freund’s complete adjuvant, Freund’s incomplete adjuvant,

Aluminum potassium sulfate and Bacterial lipopolysaccharides

“ALL immunogens are antigens but NOT ALL antigens are

immunogens”

Nearby cell

Circulation

PLEIOTROPY – single chemokine

with different actions

REDUNDANCY – different cytokines

activate same pathways

SYNERGY – acting in networks

produing effects that complement

& enhances each other


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ANTIBODIES ✓ Otherwise known as _____________, ____________ or _______________ (because

of their electrophoretic migration)

✓ _________ – antibody determinant; binding sites

✓ May be present on the surface of B-cells or secreted by plasma cells

✓ Produced in response to immunogenic stimulation

✓ Sediment rate is expressed using ____________

✓ Can be naturally occurring or immunogenic; cold reactive or warm reactive

STRUCTURE

FUNCTION

☻ Binds extracelullar antigens that later initiates phagocytosis or complement

activation

☻ Neutralizes virus (before entry to host cells) or toxins.

MUST KNOW

☻ Location of hinge region – between CH1 and CH2

☻ Complement binding site – CH2 (IgG) and CH3 (IgM)

ISOTYPES

1. IgG

☻ Monomeric

☻ Produced during the secondary immune response

☻ Four subclasses

✓ _____ – most efficient

✓ _____ – can’t cross placenta

✓ _____ – best for complement fixation (3>1>2)

✓ _____ – short hinge; poor mediator of complement fixation

2. IgA

☻ Monomeric (IgA1 = serum) or dimeric (IgA2 = secretions)

☻ Found primarily in mucosal secretions

☻ Neutralizing antibody

☻ Aggregated form can activate alternative pathway

☻ ___________ – IgA and secretory components released to the opposite

surface of cell

3. IgM

☻ Monomeric (on surface of B-cells) or pentameric

☻ Produced during primary immune response (!Mauna)

☻ Largest and heaviest

☻ Best in agglutination!

☻ Free-state = star-like

☻ Combined = Crab-like

☻ Can be dissociated using dithiothreitol (DTT) and 2-mercaptoethanol

(2-ME)

4. IgD

☻ Present on surface of B-cells

☻ First identified in a patient with Multiple Myeloma

5. IgE

☻ “Reaginic antibody”

☻ Heat labile @ ________

☻ Responsible for allergies, helminthic infections and anaphylactic

reactions

☻ Plasma cells in lungs and skin secrete IgE

☻ 2 Fab, 1 Fc

☻ Heavy chain – 5 isotypes (γ, α, μ,

Δ, Ε); has 4-5 domains

☻ Light chain – κ (chromosome 2), λ

(chromosome 22); has 2 domains

✓ Κ : λ ratio = 2:1

☻ Joining chain: only found in IgM

and secretory IgA

☻ Variable region: located in amino

terminal end

☻ Constant region: located in the

carboxy terminal end

☻ PAPAIN cleaves Ab directly in the

hinge region = 2 Fab and 1 Fc

fragments

☻ PEPSIN cleaves Ab below the

hinge region = 1 Fc’ + F(ab)2


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BIOLOGIC PROPERTIES OF ANTIBODIES

IgG IgM IgA IgD IgE

Molecular weight 150,000 900,000 160,000 180,000 190,000

Sedimentation

Coefficient

7S 19S 7S 7S 8S

Heavy Chain

Subclasses

4 0 2 0 0

Percent of total Ig 70-75 10 10-15


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Immune

mediator

IgE IgG and IgM IgG and IgM T cells

Mechanism Release of

mediators

Cytolysis Deposition of

antigen-

antibody

complexes

Release of

lymphokines

Efffector cells Basophils,

mast cells

RBCs, WBCs

and platelets

Host tissue

cells

T cells

Macrophages

Complement

involvement

No Yes Yes No

Examples Anaphylaxis

Atopy

Hives

Asthma

HTR

AIHA

HDN

Goodpasture’s

syndrome

Arthus

reaction

SLE

RA

Serum sickness

TB

Sarcoid

Wegener’s

granulomatosis

Contact

dermatitis

AUTOIMMUNE DISEASES

Disease Autoantibody

Adrenocortical cells

Erythrocyte membrane proteins

Chronic active hepatitis Anti-smooth muscle antibody

Diabetes mellitus Pancreatic islet cells, insulin, glutamic acid

decarboxylase

Goodpasture syndrome Anti-glomerular basement membrane

Thyroid-stimulating hormone receptors

Anti-microsomal antibody, anti-thyroglobulin

Multiple sclerosis Anti-myelin sheath

Anti-acetylcholine receptor

Anti-parietal cell, Anti-intrinsic factor

Primary biliary cirrhosis Anti-mitochondrial

Myocardium

Rheumatoid arthritis Rheumatoid factor, Anti-CCP, Anti-DNP

Anti-dsDNA, anti-Smith

Anti-neutrophilic cytoplasmic

Anti-centromere

Idiopathic or immune

thrombocytopenic purpura

Anti-platelet

IMMUNODEFICIENCIES

Most common

Most severe (absence of T and B cells) –

“bubble boy”

Absence of B cells and all immunoglobulins

Triad: eczema, thrombocytopenia,

immunodeficiency

Uncoordinated muscle movements (ataxia)

& dilatation of blood vessels (telangiectasia);

decreased levels of IgG2, IgA and IgE

Recurrent bacterial infection & sinusitis;

selective IgG deficiency may occur

Markedly increased IgM but decreased

levels of other antibodies

Defective adhesion protein (CD18) on

surface of phagocytes

Absence of thymus gland and T cells Adapted from Immunology and Serology and Blood Banking Notes of Mr. Errol E. Coderes RMT, IMLT, MLS (ASCPi)CM

TUMOR MARKERS

Small cell carcinoma

Hepatocellular and testicular cancer

Bence-Jones Protein Multiple Myeloma

Ovarian cancer

Breast cancer

Gastric, colonic and pancreatic

adenocarcinoma

Familial medullary thyroid carcinoma

Breast, lung, colorectal and stomach cancer

Lung and breast cancer (also bladder cancer)

HCG Choriocarcinoma, testicular cancer

Urinary bladder cancer

Prostatic specific antigen (PSA) Prostate cancer Adapted from Immunology and Serology and Blood Banking Notes of Mr. Errol E. Coderes RMT, IMLT, MLS (ASCPi)CM

SEROLOGY


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AGGLUTINATION METHODS a. ________________ – antigens are found on the surface of particle

b. ________________ – soluble antigens are attached to carrier particles (eg.

Latex, beads or charcoal). Antibody (if present) then attaches to the

particulate antigen.

c. ________________ – antigens are found on the surface of red cells

d. ________________ – antibody is the one attached to a carrier particle, thus if

an antigen is present = agglutination. (eg. CRP)

e. ________________ – the carrier attached to antibody is bacteria (usually S.

aureus)

f. ________________– positive result = lack of agglutination

g. ________________ – detects non-agglutinating antibody by means of coupling

with a second antibody

Precipitation methods

Radial

Immunodiffusion (RID)

“Fak Me, James RID”

Antibody is incorporated into the gel medium; antigen is

placed on the well, diffuses and reacts with an antibody;

diameter of precipitation is measured

• __________ Kinetic method

Measurement is done before

equivalence point

Time: 18hrs

d = log antigen conc

• __________ Endpoint method

Antigen is allowed to diffuse

complemetely before measurement

is made

Time: 24 hrs (IgG) & 50-72 hrs (IgM)

Antibody is incorporated into the gel medium; antigen is

then added, diffuses and reacts with the antibody thus

producing a precipitin band

Ouchterlony double

diffusion

Both antigen and antibody diffuses into the medium

☻ ______________ = serological identity

☻ ______________ = partial identity

☻ ______________ = non-identity

Antigen in serum is electrophoresed to separate protein

fractions. Antiserum is then added to the trough; change

in shape = abnormality

For detection of Bence-Jones protein

Radial immunodiffusion + electrophoresis = rocket band

Height is directly proportional to antigen concentration

Immunofixation

electrophoresis

Differ to immunoelectrophoresis in which the antiserum is

layered on the medium

Measures light scattered by immune complexes Adapted from Immunology and Serology and Blood Banking Notes of Mr. Errol E. Coderes RMT, IMLT, MLS (ASCPi)CM

LABELED IMMUNOASSAYS TERMS

a. Competitive – both labeled and unlabeled antigen are added

simultaneously thus competing for binding sites of antibody (inversely

proportional)

b. Noncompetitive – an excess antibody binding site is present so that all patient

analyte can be bound and measured (directly proportional)

c. _____________ – no washing (separation) step.

d. _____________ – with washing step.

EXAMPLES OF LABELED IMMUNOASSAYS

a. Enzyme immunoassays

✓ Competitive or noncompetitive (eg. ELISA, both direct and indirect)

✓ Most common: ___________________

b. Chemiluminescence

✓ Competitive or sandwich

✓ Isoluminol or acridium esters

c. Fluorescent immunoassay

✓ Homogenous

✓ FITC, TRITC

d. Radioimunnoassay

✓ Most sensitive

✓ Most specific

✓ Competitive

✓ RIST (total IgE) & RAST (allergen specific IgE)

✓ Most common: 125I


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SEROLOGIC TESTS OF INFECTIOUS DISEASES Certain strains of Proteus vulgaris share antigens with Rickettsial

species.

☻ P. vulgaris – OX-2 & OX-19

☻ P. mirabilis – OX-K

Organism Disease

R. prowazekii Epidemic typhus, Brill’s disease

R. ricketsii RMSF

R. tsutsugamushi Scrub typhus

R. akari Rickettsial pox

R. mooseri (R. typhi) Murine typhus

For detection of antibodies in typhoid fever

No agglutination

25% agglutination

50% agglutination

75% agglutination

100% agglutination

Tests for Syphilis Syphilis

☻ STD

☻ T. pallidum is not detected in blood products that have

been stored for more than 48 hrs @ 4°C

Syphilis

Pinta

Rabbit syphilis

Bejel or nonvenereal endemic

syphilis

Yaws

Nontreponemal Determines presence of reagin (antibody against cardiolipin -

antigen)

Based on flocculation

VDRL

☻ Principle: quantitative or qualitative slide flocculation

☻ Serum (complment) inactivaetion is required

✓ Serum is heated @56°C for 30 mins (to be used

within 4hrs)

✓ If >4 hrs = reinaactivation @56°C fir 10 mins is

required

☻ Antigen:

✓ 0.03% Cardiolipin (for reactivity)

✓ 0.9% cholesterol (to increase antigen size)

✓ 0.21% lecithin (for standard reactivity)

☻ Amount of antigen suspension:

✓ Quantitative – 100 drops

✓ Qualitative – 60 drops

☻ Centrifuged @ 180rpm for 4 mins → read microscopically

RPR

☻ Antigen similar to VDRL with addition of

✓ Charcoal (for visibility – macroscopic reading)

✓ EDTA

✓ Thimerosal (preservative)

✓ Choline chloride (stabilizes antigen & inactivates

complement)

☻ Amount – 60 drops

☻ Centrifuged @ 100rpm for 8 mins → read

macroscopically

Treponemal Detects treponemal antibodies

Treponema Immobilization (TPI) Test

☻ Reference test

☻ Interpretation

✓ Positive - > 50% of treponemes are immobilized

✓ Negative -


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☻ Elevated

✓ > 240 Todd units (adult)

✓ > 320 Todd units (child)

✓ > 200 IU/mL (ASO Slide test)

Appears earlier in a streptococcal infection

Streptozyme

test

Slide agglutination screening test

Screening test for presence or absence of heterophil antibodies

– uses sheep RBCs (infectious mononucleosis, serum sickness,

forssman antigen)

Differentiation of heterophile antibodies

✓ IM = adsorbed only by beef erythrocytes

✓ Forssman = adsorbed only by

✓ Serum sickness adsorbed by both beef erythrocytes and

GPK

Rapid test for heterophil antibodies that uses horse RBCs

HIV Screening tests

☻ ELISA (standard)

☻ Agglutination tests

☻ Dot-blot tests

☻ Immunochromatography

Confirmatory

☻ Western blot (atleast 2

of the ff – p24, gp41

or gp120/160)

☻ Indirect

immunofluorescent

☻ Nucleic acid

amplification test

AIDS CD4 T-cell count ( 6.2

> 5.5 x 1010

20-24°C, 5 days with constant

agitation

Pooled: 4hrs

pH: > 6.2

> 3.0 x 1011

20-24°C, 5 days with constant

agitation

Should be prepared within:

6 hrs after collection for ACD

8 hrs = CPD, CP2D, CPDA-1

-18°C – 1 yr

-65°C – 7 yrs

CRYOPRECIPITATE FVIII:C = 80 IU

Fibrinogen of atleast 150

mg/unit

Frozen: -18°C, ___yr

Thawed: 20-24°C, ___hrs

Pooled: 20-24°C, ____hrs

> 1.0 x 1010 PMNs/unit 20-24°C, 24 hrs (without

agitation)

80% RBC recovery


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6.2)

In SDP, WBS = __ > ____ > ____

(most common to least common

blood type)

☻ Antigens are detectable 5-6

weeks in utero

☻ Full expression of antigens – 2 to

4 yrs of age

☻ Antibodies are naturally

occurring

☻ Begins to rise at 3-6 mos and

peaks bet 5-10 yrs

GENE PRODUCT IMMUNODOMINANT

SUGAR

PHENOTYPE

H L-fucosyltransferase O

A N-acetylgalactosaminyltransferase A

B D-galactosyltranferase B

A&B N-acetylgalactosaminyltransferase

D-galactosyltranferase

AB

☻ Bombay phenotype

✓ Nonsecretor, H-deficient

✓ Produces anti-A, anti-B, anti-

A,B and anti-H

✓ Positive with “O” cell

☻ Parabombay

✓ Secretor but still H-deficient

__ > __ > __ > ___ > __ > ___

(greatest to least amt of H

substance)

TYPES OF DISCREPRANCY

I Weakly reacting or missing

antibodies

☻ Causes

✓ Newborn

✓ Elderly patients

✓ Leukemia

✓ Immunodeficiencies

II Weakly reacting or missing

antigens

☻ Causes


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✓ Acquired B phenomenon

(resolution: deacetylation)

✓ Subgroups of A and or B

III Protein or Plasma Abnormality ☻ Causes

✓ Multiple myeloma

✓ Waldenstrom’s

macroglobulinemia

✓ Plasma cell dyscrasias

✓ Plasma expanders (PVP and

Dextran)

✓ Wharton’s jelly

IV Miscellaneous ☻ Causes

✓ Polyagglutination

✓ Cold reactive antibodies

✓ Unexpected ABO

isoagglutinins

Grading Agglutination Reactions (Harmening 5th Ed)

No agglutination or hemolysis

Tiny agglutinates, turbid background

Small agglutinates, turbid background

Medium-sized agglutinates, clear background

Several large agglutinates, clear background

One solid agglutinate

002 MNS M antigen N antigen

1st position Serine Leucine

5th position Glycine Glutamic acid

S antigen s antigen

29th position Methionine Threonine

☻ Anti-M – reacts better at pH ____

☻ Anti-N – found in patients dialyzed

or in equipment sterilized with

formaldehyde

003 P ☻ _______ - neutralized by hydatid cyst

fluid

☻ _______ (Donath-Landsteiner

antibody) – assoc with PCH;

biphasic antibody – binds to P(+)

cells at lower temp. and hemolyzes

cells @ 37°C

☻ Anti-PP1Pk – formerly anti-Tja

004 Rh __ > __ > __ > __ > __

(most to least immunogenic)

☻ e – associated with warm

autoimmune hemolytic anemia

(WAIHA)

☻ antibodies are not naturally

occurring, instead are immune

antibodies

☻ cause of most severe HDN

✓ father – Rh (+)

✓ mother – Rh (-)

✓ child – Rh (+)

✓ production of anti-D

WEAK D EXPRESSIONS

1. Antigen is weaker than expected

2. When C is in trans position with D

Ex. Dce/dCe

3. Anitbodies produced are directed to

the missing parts

In transfusion:

✓ Recipient: D –

✓ Donor: D+

4. ☻ Lacks all Rh antigens

☻ Stomatocytosis

005 Lutheran ☻ Named after a donor named

Lutteran (misinterpretation)

☻ Anti-Lua – discovered in serum of a

patient with diffused lupus

erythematosus; more common

antibody

006 Kell ☻ K is strongly immunogenic (2nd to D)


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☻ Kell antigens are synthesized on

their precursor, Kx

☻ McLeod phenotype – absence of

Kx antigen (acanthocytosis)

☻ CGD – absence of Kx antigen in

WBCs

007 Lewis ☻ Only blood group synthesized by

the RBC membrane

Le (a-b-) → Le (a+b-) → Le (a+b+)

→ Le (a-b+)

(birth → post-delivery → >10 days

→ adults)

☻ Decreased expression of antigens

in pregnancy

☻ ______ has receptors for H. pylori

008 Duffy ☻ Anti-Fya – most common Ab in the

system

☻ ________ – common in blacks;

resistant to P. vivax infection

009 Kidd ☻ NOTORIOUOS ANTIBODY

☻ Assoc with delayed HTR

☻ Jk (a-b-) – resistant to 2M urea; cell

lysis in about 30 mins

☻ Antibodies reactivity are

enhinaced by adding 4 drops of

serum instead of 2.

☻ __________ – causes formation of

autoanti-Jk

010 Diego ☻ Marker of Mongolian ancestry

☻ Antigens are located on anion

exchange molecule 1 (AE-1)

011 Cartwright ☻ Antigens are located on RBC

acetylcholinesterase

012 Xg ☻ Sex-linked

☻ Xga expression: 89% (females) and

66% in males

013 Scianna ☻ Prevalence of Sc2 is higher in

Mennonite population

014 Dombrock

015 Colton ☻ Antigens are found on channel-

forming integral protein or

______________

016 Landsteiner-Weiner ☻ Agglutinates Rh+ and Rh- cells

except Rhnull cells

017 Chido-Rodgers ☻ High Titer, Low Avidity (HTLA)

☻ Associated with HLA

018 H ☻ Anti-H lectin = _______________

019 Kx ☻ Precursor of kell antigens

020 Gerbich ☻ Lecah phenotype (elliptocytosis)

021 Cromer ☻ Located on decay accelerating

factor (DAF)

022 Knops ☻ Antigens are located on

complement receptor 1 (CR1) or

CD35

023 Indian ☻ Antigens are located on CD___

027 I ☻ Product of I gene – N-

acetylglucosaminyl transferase

☻ I = adult red cells

☻ i – newborn or cord cells

☻ _________ = Mycoplasma

pneumonia (cold AIHA)

☻ __________ = infectious

mononucleosis

BLOOD DONATION

1. registration ☻ collection of patient information

☻ date of last donation

✓ 2 days or more – after plasmapheresis, plateletpheresis or

leukapheresis

✓ 4 weeks – after infrequent plasmapheresis

✓ 8 weeks – between whole blood donations

✓ 16 weeks – after 2-unit red cell collection


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2. Health history interview DEFERRALS

Permanent Tegison medication – for severe psoriasis

Persons with HIV

Men engaged in sex with other men since 1977

Indefinite History of Chaga’s disease and Babesiosis

Lived > 3 months in UK from 1980-1996

Lived > 5 years in Europe from 1980 to present

Family history of CJD

Temporary 2 days for platelet donors Aspirin ingestion

Received attenuated vaccines for

Measles (Rubeola), Mumps, Polio (oral),

Typhoid and Yellow Fever

28 days Conclusion of pregnancy

After taking last dose of Accutane or

proscar (for benign protatic

hyperplasia)

Received live attenuated vaccine for

German measles (Rubella) or Chicken

pox (Varicella-zoster)

Avodart (teratogenic drug)

1 year History of syphilis or gonorrhoeae or

treatment

Travel to malaria endemic area

Tattoos or permanent makeup

Recently undergone surgery

Incarceration for >72 hrs

Sexual contact with an individual at

high risk for HIV

History of malaria

Lived in malaria endemic country for 5

consecutive years

Soriatane (treatment for severe

psoriasis)

3. Physical exam

GENERAL REQUIREMENTS FOR DONATION

CRITERIA ACCEPTABLE LIMIT

GENERAL APPEARANCE In good health

HEMOGLOBIN Autologous: > 11.0 g/dL or 110 g/L

Allogeneic: > 12.5 g/dL or 125 g/L

HEMATOCRIT Autologous: _____

Allogeneic: ______

BLOOD PRESSURE Systolic: _____________

Diastolic: ____________

TEMPERATURE _____°C or ____°F

No drinking of coffee or hot beverages

while waiting to donate

PULSE Between ____ and ____ bpm

Athletic donor will have a pulse 100lb (45kg) Adapted from Immunology and Serology and Blood Banking Intensive Review Notes of University of the Immaculate

Conception – Medical Laboratory Science Program

Must remember: blood collection procedure ☻ Patient identification is a MUST

☻ Blood is extracted at the antecubital fossa

☻ Tourniquet of blood pressure cuff: ____________

☻ Needle gauge: ________________

☻ During collection, instruct patient to open and close hand every

_____________

☻ Mixing of blood: 1-2 times/min or 45 seconds

☻ Donation time for a unit of whole blood: 8-12 mins, if >15 mins = platelets, FFP

and cryoprecitated AHF can’t be prepared

☻ Blood should be processed within ______________


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Testing

Compatibility TESTING ☻ Aka serologic crossmatch test

☻ Test to detect unexpected antibodies

☻ Ensures to produce a blood product safe for transfusion

______________________

☻ Tests for alloantibodies in patient’s plasma against donor cells

☻ Donor’s cell + Patient’s plasma

_______________________

☻ Tests for alloantibodies in donor’s plasma against patient’s cells

_______________________

☻ aka enhancement media (increases reactivity of IgG antibodies)

☻ Low ionic saline solution

✓ Action: decreases zeta potential

✓ 10-15 mins incubation time

☻ Polyethylene glycol (PEG)

✓ Action: removes water

☻ 22% albumin

✓ Action: zeta potential is decreased through buffering

Antihuman globulin test PRINCIPLE:

OR

_______________ ☻ Detection of sensitization of red cells in vivo

☻ Examples: AIHA, HDN, HTR

_______________ ☻ Detection of sensitization of red cells in vitro

☻ Sensitization occurred during incubation period

☻ Examples: Weak D testing, AHG-phase compatibility testing, antibody screen

and identification

TRANSFUSION

REACTION

INFORMATION PREVENTION/TREATMENT

1°C increase in temperature

Cause: Anti-leukocyte antibodies

(patient)

Leukoreduced RBCs

ALLERGIC Cause: donor plasma with foreign

proteins

Washed RBCs

Patient has IgA deficiency w/ anti-

IgA antibodies

Patient is afebrile (no fever)

Washed RBCs

IgA-deficient donor

(rare)

Patient has normal IgA with anti-IgA

antibodies

Patient is afebrile

Washed RBCs

IgA-deficient donor

(rare)

MONOCLONAL ANTIBODIES POLYCLONAL ANTIBODIES

AH

G (from immunized animal)

Human IG


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Signs & symptoms resemble

respiratory distress

Cause: Anti-leukocyte antibodies

(donor)

Leukoreduced RBCs

Cause: T lymphocyte proliferation

(donor)

Irradiated RBCs

PTP Cause: anti-platelet antibodies

(HPA-1a negative platelets)

Corticosteroid

Exchange transfusion

IV immunoglobulins

Cause: rapid infusion of large vol. of

blood products (administration of

blood w/o equivalent blood loss)

Iatrogenic

Therapeutic

phlebotomy

IV diuretics

Oxygen therapy

BACTERIAL

CONTAMINATION

Cause: endotoxin production by

psycrophilic bacteria (Y.

enterocolitica)

Sterile technique

Visual inspection of unit

Cause: small bore needle, warming

blood above 50°C, freezing blood

without cryoprotective agent,

citrate toxicity

At risk: transfusion-dependent

patients (aplastic anemia,

thalassemia)

Iron-chelating agent

(deferroxamine)

Transfusion of neocytes Adapted from Immunology and Serology and Blood Banking Notes of Mr. Errol E. Coderes RMT, IMLT, MLS (ASCPi)CM

REFERENCES

Clinical Immunology and Serology: A Laboratory Perspective by Christne Dorresteyn

Stevens

Essentials of Immunology and Serology by Jacqueline Stanley

Modern Blood Banking and Transfusion Practices by Denise Harmening

Fundamentals of Immunohematology by Mary Louise Turgeon

Immunology-Serology and Blood Banking by Rodolfo Rabor

Immunology and Serology and Blood Banking Notes of Mr. Errol E. Coderes RMT, IMLT,

MLS (ASCPi)CM

Blood Banking Checkpoint notes of Ms. Judea Marie Policarpio, RMT

Intensive Review Notes of University of the Immaculate Conception – Medical

Laboratory Science Program

property of medtech review notes do not distribute€¦ · classical and lectin pathway complement...

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