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Immunology > ABO/Rh - Multiple Myeloma > Flashcards

ABO/Rh - Multiple Myeloma Flashcards

1
Q

Composition of Blood

A

Formed elements (red cells, white cells, platelets)

Plasma ( albumin, antibodies, complement, clotting factors, acute-phase proteins), etc

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2
Q

Serum

A

Activate the clotting factors and pull out the clot = let with serum

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3
Q

Blood Group Antigens

A

millions on each RBC of all different types

  • terminal carbohydrate moieties on large glycoproteins and glycolipids on cell membrane
  • core glycogen + terminal sugar
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4
Q

Where are the major RBC antigens?

A

RBC, endothelial cells, platelets, and other cells

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5
Q

Where is the Type A/B glycosyltransferase moiety in the genome?

A

Chromosome 9

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6
Q

How does the glycosyltransferase moiety determine blood type?

A

Adds terminal sugars to a core carbohydrate + H

A allele: adds terminal N-acetylgalactosamine

B allele: adds terminal galactose

O allele: no activity (only H antigen)

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7
Q

Who has the H antigen on their cells?

A

almost everyone :)

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8
Q

What are the potential genotypes of type A?

A

AA or AO

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9
Q

What type of T antibodies are made against the A and B sugar moieties?

A

Mostly IgM (some IgG)

T-independent (no helper T cells needed)

Thus, T-independent Abs are usually of IgM subtype (do not usually class switch)

Preformed Natural Abs

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10
Q

Why are the natural Abs against A and B made?

A

Produced against glycolipid antigens expressed by intestinal microbes

These glycolipids cross-react with our A and B antigens

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11
Q

What is the classification of the reaction if transfuse against wrong blood type?

Is it cytotoxic?

A

Type II Hypersensitivity Reaction

Severe - yes, it is cytotoxic

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12
Q

What is the molecular presentation of Bombay-O?

A

No h –> H conversion

Therefore can never go on to add type A and B antigens

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13
Q

What Abs and Antigens are present on Bombay-O cells?

How do they appear on routine typing?

Who can they receive blood from?

A

Lack both A and B antigens. SO LOOK LIKE “O”

Antibodies: anti-A, anti-B, AND anti-H

***CAUTION: will react to blood of bc of anti-H, thus can only get transfusion from other Bombay-O

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14
Q

Whole blood Transfusions

rules

A

Contains Abs as well as antigen, therefore donor/recipient needs to be IDENTICAL

Emergencies: O,Rh- RBC can be used as universal donor

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15
Q

What type of transfusion can a type A person have?

A

Note: antigen on red cells = A; Ab in plasma: anti-B

Compatible donor plasma lacks anti-A = A and AB

Compatible donor red cells lack B antigen = A and O

Thus only whole blood donor = A

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16
Q

Erythrocyte Transfusion

A

Packed RBC: donor red cells must lack antigens which bind to recipient abs

A (has anti-B), so donor cells must lack B = compatible donors A and O

B (same as A but invert A/B)

AB can get from A, B, AB, and O

O can only get from O

17
Q

Plasma transfusion

A

donor cells must lack Abs which bind to recipients red cells

A: donor plasma must lack anti-A, so compatible donors are A and AB

AB: donors must lack Anti-A and Anti-B (so compatible=AB)

O: compatible with A, B, AB, O

18
Q

What happens in a transfusion rxn (mechanism)?

A

1) IgM coat RBCs and activate compliment –> complement lysis (IgM with many antigens on RBC)

2) Intravascular lysis (can lead to jaundice) –>
macrophages in liver & spleen phagocytose Ab and complement coated RBC

19
Q

What are the effects of complement lysis (result of transfusion)?

A
  • Hb liberated in amts toxic to the kidney
  • Cytokines released in large qtys

-DIC (disseminated intravascular coagulation) possible: lots of clotting factor released –> localized clotting in circulation; cut off blood supply to organs;
bc clotting factor used up –> bleed out even with DIC

20
Q

Rh factor

A
  • Surface Protein (so major Ab are IgG)
  • nonglycosylated
  • CAN cross placenta
  • do not activate complement well

Fxn: opsonize RBCs and facilitate phagocytosis in the spleen

21
Q

Which can cross the placenta: IgG or IgM?

A

IgG

22
Q

Rh Incompatibility Disease

A

Medically important in fetus (esp second fetus: 1) Rh- moms sensitized by Rh+ fetus, 2) subsequent Rh+ babies: hemolysis by maternal Abs that cross placenta)

Rh- mom with a Rh+ fetus. Mom makes Abs agains Rh that attack fetus blood

23
Q

What is the treatment for Rh Incompatibility Disease?

A
  • Type the parents
  • Anti-Rh_0_D Abs ruding 3rd trimester w/in 72 hrs of 1st birth

RHOGAM IMMUNE GLOBULIN:
destroy fetal RBCs before initiate immune response
-Ab fb repress own synthesis (Ab-mediated immune response)
-Cytokines interrupt antigen specific B cells, turning into plasma cells
-ABO incompatibility can have a partial protective effet

24
Q

Anti ABO vs Anti Rh:

Anti ABO

A 
abundant Ag,
IgM (T independent); 
Activate complement well;
Destroy RBC in blood stream;
Intravascular hemolysis
25
Q

Anti ABO vs Anti Rh:

Anti ABO

A 
Sparse Ag; 
IgG (protein);
Does NOT activate complement well; 
Ab coated RBC destroyed by macrophage in liver and spleen;
extravascular hemolysis
26
Q

IgM structure

A

Penta (5 Abs together)

27
Q

Agglutination of RBC

A

Can hold onto several RBCs at once to form a lattice structure (IgM)

used for typing blood A/B/O)

28
Q

Can IgG be used to type blood?

A

No, too small to form lattice

Recall IgG is related to Rh factor (protein)

29
Q

Direct Coomb’s (DAT) Test

A

detects (directly) cell-bound Abs

Against human constant region (Fc) –> can get agglutination of even IgGs

30
Q

Indirect Coomb’s (IDAT) Test

A

Detects anti-red-cell IgG in plasma

(Ie: testing mother’s serum to check babies)

if not agglutination, means you don’t have the antigen/RBCs

31
Q

Multiple Myeloma

A
  • malignancy of Ab-producing plasma cells
  • 1 type of Ab usually not directed toward any type of specific Antigen
  • “multiple” bc by time detected, multiple foci of tumor cells are present.
  • “myeloma” bc tumors form in the bone marrow, that is where most normal plasma cells reside
32
Q

What are key characteristics of multiple myleoma

A

“coin lesions” - wearing away of bone

  • most commonly lymphoid malignancy
  • 20,000 new cases/year in US
  • median age: 70
33
Q

What does the NORMAL Serum Electrophoresis look like?

A

Anode (L) to cathode (R)

Albumin: tall, thin
alpha1;
alpha 2; 
beta;
gamma: long and thin (that's where most of the Abs lie = in the gamma band)
34
Q

Monoclonal Gammopathies (general details)

A
  • plasma cell tumors
  • monoclonal - begin with a single cell
  • all cells of tumor secrete Ab of same isotope
  • the secreted Ab: paraprotein, M protein

“Monoclonal Gammopathies”: bc “gamma globulins lie there”

35
Q

Monoclonal Gammopathies (what are the various types?)

A

MM: many clumps of tumor cells in bone marrow –> erodes bone via stimulation of osteoclasts; secretes IgG (60%) or IgA (25%) or IgE (rarely)

Waldenstorm’s macroglobulinemia: less mature B cell, secretes IgM; viscous blood; less bone marrow involement

Heavy-chain disease: only heavy chain secreted from B cells

Light-chain disease: only light chain secreted secreted from B cells

Light chains in urine are Bence-Jones Proteins (due to MM)

36
Q

What does the Multiple Myleoma Serum Electrophoresis look like?

A

Increased gamma protein!

Anode (L) to cathode (R)

Albumin: tall, thin
alpha1;
alpha 2; 
beta;
gamma: thin and ELEVATED (M  (for myeloma) spike)

NB: serum electrophoresis does not show which isotype is elevated –> need further testing (myeloma electrophoresis)

37
Q

What is the mech for immunosuppression in Multiple myleoma pts?

A

Pumping out tons of one type of Ab that normal Abs are repressed (get more bacterial/viral infections)

38
Q

How do you determine which isotype is elevated in Multiple Myleoma pts?

A

Immunofixation:

  • separate proteins on cellulose acetate strips;
  • flood a strip with Abs to a specific human isotype (eg: sheep Ab specific for human alpha chains, binds only IgA)
  • if Ab binds to plasma protein on strip, a ppt forms

In Multiple Myleoma , a single type of light chain and single type of heavy chain should be elevated

Immunology (8 decks)

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