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Biochem Winter 2012 > Blood Groups Anticoaglulation 2 > Flashcards

Blood Groups Anticoaglulation 2 Flashcards

0
Q

How much time do you have to administer drugs in MI? in Stroke?

A

MI- within 12 hours

Stroke- within 3

problem with brain hemmorrhage

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1
Q

What are 2 activators of Fibrinolysis?

A

clot busters sucha s tPA and urokinase

treat arterial thrombosis by dissolving fibrin clots and loosening up hemostatis plug

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2
Q

What is Deep Vein Thrombosis (DVT) and Pulmoanry Emoblisms

A

rich in FIBRIN

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3
Q

what is a pulmonary embolism?

A

when deep vein thrombus breaks away from site of formation and travels through the blodo to lung wher eit lodges to block blood flow in a pulmonary artery

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4
Q

What factors does Warfarin inhibit and how?

A

It is a Vitamin K antagonist that slows down FIBRIN formation by indirectly inhibiting the carboyxlation of Glu residues in Factor 2, 7a (extrinsic tenase), 9 (intrinsic tenase), 10 (prothrombinase).

Also inhibits Gla modification in Protein C and Portein S

acts in liver to inhibit reductase that recycles Vit K

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5
Q

What have drug companies made to alleviate drawbacks of warfarin side effects

A

orally active inhibitors of thrombin and factor xa

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6
Q

what does Rivaroxaban do?

A

Inhibits Factor Xa

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7
Q

What does Dabigatran do?

A

Inhibits Thrombin

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8
Q

What is the normal platelet count?

A

200,000-400,000 / uL

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9
Q

What platlet count until bleeding disorders observed

A

What platelet conc until count is less than 100,000/ uL

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10
Q

What is platelet count when severe?

A

below 50,000 uL

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11
Q

APTT

A

activated by addition of Partial Thrombopalstin: PL, aCa ions

Excluding factor VII

APTT is prolonged for deficiencies in factors invovled in either the INTRINSIC OR COMMON pathways (HMWK, PK ,fibrinogen, prothrombin as well as factors V, VIII, IX, X, XI and XII)

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12
Q

PT

A

activated by addition of COMPLETE THROMBOPLASTIN (tissue fator) and calciu faoctors

PT is proleonged for deficiencies of facators in the EXTRINSIC OR COMMON PATHWAYS (Factor VII, V, X as well as prothrombina nd fibrinogen)

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13
Q

TT

A

activated by addition of thrombin

prolonged with diminshed expression and/or funtion of FIBRIN

this is the only assay that testst eh activit of a single component in coagualtion

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14
Q

BT

A

defined as time between inflcition of a small, standard cut and the moment when bleeding stops
thsi is extremely difficult to standardize and not often performed

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15
Q

What is the H antigen?

A

It is the precursor for A and B antigens

Everybody has antigen H except for Bombay phenotype

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16
Q

Which phenotype doesnt have the H antigen?

A

Bombay phenotype

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17
Q

What are the antigens of blood groups?

A

Glycoproteins and Glycolipids

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18
Q

Where are the antigens located? (3)

A

1 RBC cell membranes

  1. most tissues, except CT , CNS, and some epithelia
  2. Glycoproteins in blody fluids in 80% of the population (“secretors”)
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19
Q

The termianl sugar that distinguishes the A form teh B antigen is added to the H antigen ,

A

whcih serves as a substrate to produce these antigens

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20
Q

What is the precursor substance

A

THe H antigen is converted the PRECURSOR substrate to produce these antigens

21
Q

What converts the H antigen from precursor substrate to A or B antigen?

A

Oneof two fucosyltransferases encoded by related alleles: H locus (FUT1) and Se locus (FUT2)

Only a difference in four amino acids

22
Q

What is the difference between FUT1 and FUT2

A

differ mainly in where they are expresd and thus have activity

23
Q

What does FUT1 encode for?

A

alpha 1,2-fucosyltransferase that addes fucose to teh terminal galactose of ht precursor substance to produce the H antigen on proteins and lipids in teh membrane of RBC and vascular endothelium

24
Q

What does FUT2 encode for?

A

alpha 1,2 fucosyltransferase that is expresed in secretory glands (sucha s salivary glands, GI tract, and respritaory tract)

25
Q

Enzymatic a tibity requires at least one copy of ???

A

the dominant Se allele to produce H antigetn in bodily secretions

26
Q

What are indivuals taht produce H antigen secretions?

A

SECRETRS and have eithe rhe Se/se or teh Se/Se genotype

80% o the populatiosn has this secretor phenotype

20% remaining are non-secretors b/c htey ave the inactive allele (se/se gentype)

27
Q

What are the genotypes of both secretor and non–secretor populations

A

H/H or H/h genotype and thus express H antigen in teh membrane of RBC

28
Q

What is the difference between seretor and non-secretor?

A

Both have glycoproteins in their seretions

Diff is that non-secretor lacks the A, B, and/or H antigenic specificaiton on their secreted glycoproteins

29
Q

How is the H antigen made?

A

by transferrng fucose onto the precursor substance type 1 or type 2. A precursor glycoprotein or glycolipid (both which are present in every indivual) is acted upon by the product (enzyme) of the H locus (FUT1) or Se locus (FUT2), to yield H antigen

30
Q

How are ABH genotypes defined?

A

by the expression of the enzymes that catalyze attachment of specific monosaccharide moieties.

31
Q

Wat are the ABO antibody specifieicties directed at?

A

not the pirmer gene porducts (enzymes); rather directed towards seocndary gene products (the oligosaccharadies)

32
Q

Int eh case of glyolipids, teh oligosacchardie chain taht carries the A, B, and/or H antigenic specificity is attached to????

A

the primary hydroxyl gorup of SPHINGOSINE

33
Q

What do indiividuals iwth A allele express? what does it recognize

A

A transferase (alpah 1,3, -N-acetyl-galactosyltransferase) which adds galactose to H antigen

A transferase recognizes and transfers N-acetylgalactosamine

34
Q

What do indivduals with B allele express? What does it recognize

A

B transferase (also known as alpha 1,3-galagctosyltransferase, which adds galactose to H antigen

Recognizes and transfers galactose

35
Q

What do individual with O allele express?

A

protein with a point deletion that causes a translational frameshift

resultant protein is almost entirely DIFFFERNT and possesses no enzymatic activity

36
Q

What antigens does OO genotype have?

A

H antigen but neither the A nor B antigen

37
Q

which individuals have anti-H antibodies?

A

Bombay phenotype

38
Q

What genotype do indivduals with Bombay Phenotype have?

A

rare h/h se/se gentoype and thus unable to convert the precursor substanve into H antigen

With no H antigen, no A or B antigens are produced eitehr.

Anti H , anti A and anti B Ab that will agglutinate transfusions from blood types A, B, AB , or O

39
Q

What is the Rh antigen?

A

protein

40
Q

When do Rh antibodies occur in humans?

A

only after immuniation with RBC of non-self genotype

until exposure of Rh-negative person to D antigen in Rh-positive person

blood transfusions or Rh-negative women during pregnancy after exposure to Rh-pos fetal blood

41
Q

What two genes does Rh antigen arise form?

A

RhD and RhCE, each with 10 exons

42
Q

What does RhD protein express?

A

D antigen

43
Q

What does RhCcEe protein express?

A

2 antigens
either C or c antigen and
eitehr E or e antigen

CE locus is very close to D locus and two loci are inherited together

44
Q

What is the Rh null mutation?

A

both D adn CcEe proteins are absent

peopel eithe rlack DCE genes or have an abnormal regulator gene, which controls expression of DCE genes.

THeir RBCs are OSMOTICALLY FRAGILE and often misshapen, suggesting that Rh D/Rh CE proteins are improtant for RBC structure

45
Q

When does HDN occur?

A

when mother produces antibodies vs RBC antigens of the fetus arising from some blood type incompatibilieies. Maternal Ab attack teh fetal RBCs causign them to hae a shortened life span resulting in acquired hymlytic anemia.

46
Q

What causes HDN? 3

A
  1. Rh incompatibility where mother is Rh neg and fetus is Rh pos
  2. ABO incompat where mother has type O blood, which tends to produce IgG Ab that CAN cross placenta and the fetus has type A or B blood which ten to IgM that cannot cross placenta (mild effect)
  3. Incompatibility invovling other blood groops such as Kell or Duffy
47
Q

Can IgG cross placental membrane/ Can IgM?

A

IgG (type O) can cross! IgM (Type A or B) cannot cross

48
Q

When does Rh-neg maother produce anti-Rh IgG Ab?

A

after she has had at least one incompatible prgnancy (IgM Ab produced first and dont corssplacenta)

during 2nd Rh-incompatible pregnancy, small amts of fetal blood normally cross placental barrier and enter maternal blood stream, stimulating IgG Ab against Rh antigen–> cross placenta to cause hemolysis of fetal RBC–> Fetus anemic and rsponse by releaseing a tone of erythroblasts (nucleated immature RBCs) into its bloods tream

Erythroblastosis Fetalis in newborn –> bilirubin –> jaundance

hyperbilirubinemia needst o be treated to prevent depostion of unconjugated bilirubin in brain (kernicterus) whcih can cause certebral damage or death

49
Q

What is the treatment to prevent HDN?

A

block productino of Rh Ab.

During prenancy or after Rh-neg woman gives birth to Rh pos baby, given anti-Rh immune globuluin to prevent prodcutino of antbidoes against Rh antigen

Biochem Winter 2012 (10 decks)

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