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93 Cards in this Set

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Assessing bleeding with history
negative experience (against congenital bleeding) more important than positive
Significance of petechiae in assessment of bleeding
suggest a platelet problem
Significance of ecchymoses in assessing bleeding
large bruises - suggest a disorder of clotting factors
Significance of bleeding into joints in assessment of bleeding
suggests a disorder of clotting factors or (less commonly) von Willebrand’s disease
Significance of purpura in assessment of bleeding
small bruises – non-specific
Significance of palpable purpura in assessment of bleeding
vasculitis (not a hematologic problem)
the pathway from __ to __ is measured by the PTT, partial thromboplastin time
XII to fibrin
the pathway from __ to __ is measured by the PT, the prothrombin time
VII to fibrin
what percent below normal of clotting factors will give abnormal PT or PTT
below 30% of normal

This is clinically useful since levels above 30% don’t give clinical bleeding.
The PTT measures which pathway (intrinsic, extrinsic)?
intrinsic
The PT measures which pathway (intrinsic, extrinsic)?
extrinsic
The PTT is abnormal in deficiencies of which clotting factors?
XII
XI
IX
VIII
X
II (prothrombin)
V
fibrinogen
When PTT is markedly abnormal, i.e >100 s, consider what artifactual cause
line may have been flushed with heparin
The PT will be abnormal in deficiencies of which clotting factors?
VII
X
V
II (prothrombin)
fibrinogen.
Which clotting factors are tested by both PT and PTT?
X
V
II (prothrombin)
fibrinogen.
Which clotting factors are tested exclusively by PT (and not PTT)?
XII
XI
IX
VIII
Which clotting factors are tested exclusively by PTT (and not PT)?
VII
In a high power field of a blood smear, each platelet represents how many per cu mm?

How many per field is normal?
20,000/ cu mm

7-22 is normal
Which tests measure quantitative platelet problems?

Which are for qualitative?
Platelet count

PFA100 and Bleeding time
Name the tests which are used to evaluate a bleeding disorder
PT, PTT, platelet count, +/- PFA 100/bleeding time
Which clotting factor is deficient in hemophilia A?
factor VIII
Which clotting factor is deficient in hemophilia B
factor IX (christmas disease)
clinical picture of factor XIII deficiency
associated with forming a clot and then having delayed bleeding.

XIII converts loose fibrin to tight fibrin.
how to calculate clotting factor replacement amount
plasma volume (40ml/kg)
desired level
and half life
Sources of factor VIII
Cryoprecipitate
Mono VIII--extracted with monoclonal antibody
Human recombinant VIII--$$
Name the 6 acquired disorders of clotting factors
1 Liver disease
2 Vitamin K deficiency
3 Coumadin ingestion
4 Dilution
5 DIC
6 Circulating anticoagulant
When to suspect that liver disease may be cause of bleeding problem
suspect this if clinical liver disease, or if albumin is low
Which clotting factors are vitamin K dependent
II, VII, IX, and X
how does coumadin work?
anticoagulant, which blocks synthesis of Vitamin K
Lab diagnosis of DIC
more specific:
Elevated FSP’s (fibrin split products)

Not specific:
PT>15, Platelets <150,000, Fibrinogen<150 mg/dl
Screening test for circulating anticoagulants
1) Perform a 1:1 mix of normal plasma and the test plasma

2) In a deficiency, the mix will have a level of 50% (1+0)/2=1/2 and the PT or PTT will be normal since 50% levels give normal tests.

3) In an inhibitor, (1+0)/2 gives a level near zero because the inhibitor will neutralize the normal factor.

Note: The samples must be incubated at 37 degrees for 1-2 hours since the reaction of inhibitor and clotting factor is NOT instantaneous (antigen/antibody).
which bleeding test is most affected by heparin in the line?
PTT >PT
Definitive way to tell if thrombocytopenia is due to decreased production or increased destruction
bone marrow exam
significance of peripheral blood smear when evaluating if thrombocytopenia is due to dec production or inc destruction
if peripheral destruction: increased platelet production, therefore large platelets (young)

large platelets evidence against marrow failure
diagnosis suggested by isolated thrombocytopenia (other cells normal)
peripheral destruction of platelets via anti-platelet antibody

immune thrombocytopenia
Differential diagnosis of thrombocytopenia, 3 big classes of thrombocytopenia
1 decreased production
2 sequestration
3 increased destruction
Conditions which cause thrombocytopenia via decreased production of platelets
1 aplastic anemia
2 leukemia
3 myelodysplasia

****Other counts, in addition to platelets, will be abnormal

Diagnosis will be made by marrow exam
Conditions which cause thrombocytopenia via sequestration of platelets (expected lab values?)
Sequestration – hypersplenism (usually mild thrombocytopenia – 50,000-100,000)

Expect hematocrit near 30 in women, near 35 in men

WBC often in 2500 to 3500 range
Conditions which cause thrombocytopenia via increased destruction of platelets
1) ITP –immunogenic thrombocytopenic purpura can be idiopathic drug related (HEPARIN, quinidine) of due to SLE or lupus

2) Post –transfusion purpura

3) Disseminated Intravascular Coagulation – (PT,PTT also abnormal)

4) TTP – thrombotic thrombocytopenic purpura
why are platelet disorders considered as von Willebrand's deficiency vs everything else?
intrinsic disorders treated with platelet transfusion

only one type of extrinsic disorder, von willebrand's
von willebrand's disease inheritance
autosomal dominant
von willebrand's vs hemophilia biochemistry
hemophilia--100% level of VIII. VIII activity is reduced.

VWD--decreased number of molecules
ristocetin cofactor
test of platelet function, clumps normal platelets, but not in vWD
Lab diagnosis of von Willebrand's disease
Bleeding time – prolonged

VIII activity decreased, VIII antigen (vW antigen) proportionately decreased

Ristocetin cofactor – low

Ristocetin aggregation decreased
Koate-HP
a “semi-pure” pooled lyophilized concentrate has vW activity, and is used at Vanderbilt to treat vWD.
Humate-P
a lyophilized anti-hemophiliac product which has von Willebrand factor activity. Not used in hemophilia where it has been replaced by monoclonal or recombinant products, it is used in von Willebrand’s disease.
DDAVP
arginine vasopressin – causes the release of vW factor from endothelial cells.

Though prolonged use can cause refractoriness, it can be used in mild vW patients to get them through an acute event without ANY risk of viral transmission.
how does heparin work?
blocks the activity of thrombin on firbrinogen
heparin affects which bleeding tests?
both the PT and PTT, but mostly PTT
synthesis of what clotting factors impaired by coumadin?
II,VII,IX,and X
--vitamin K dependent
which test used to monitor coumadin?
INR of PT is used to monitor coumadin anticoagulation

--affects PT and PTT
why does coumadin necrosis occur?
before the levels of factors II, VII, IX, and X fall, the levels of protein C and protein S fall, and a result, patients are temporarily hypercoagulable.
ITP
TTP
DIC
Basic mechanism
Antibody mediated immune destruction of platelets

Endothelial damage leads to fibrin thrombi getting deposited in small vessels. Red cells become fragmented, platelets stick to thrombi

Intravascular activation of thrombin leads to consumption of clotting factors and platelets putting patient at risk of bleeding
ITP
TTP
DIC
Laboratory features
Isolated thrombocytopenia, i.e. low platelets but normal WBC and hematocrit though the hematocrit may be a little low from hemorrhage

Microangiopathic hemolytic anemia with thrombocytopenia

Decreased platelets
Prolonged PT
Prolonged PTT
Specific Test:
Increased fibrin degradation products or D-dimer
ITP
TTP
DIC
Clinical association
Patient appears well
May occur after viral illness

Seriously ill patient
May occur after viral illness

A complication of serious illness such as shock, sepsis, or severe complication of pregnancy
ITP
TTP
DIC

Red cells
Normal, or anemia due to hemorrhage

Microangiopathic anemia with schistocytes

DIC will cause anemia if hemorrhage occurs.
Microangiopathic changes are none to minimal
ITP
TTP
DIC

WBC
Normal unless corticosteroid therapy raises the WBC

Elevated as a reflection of serious illness

Elevated as a reflection of serious illness
ITP
TTP
DIC

Platelets
Low
Low
Low
CLASSIFICATION OF VON WILLEBRAND’S: TYPE 1
PARTIAL QUANTITATIVE DEFICIENCY OF VWF
CLASSIFICATION OF VON WILLEBRAND’S: TYPE 2
QUALITATIVE DEFICIENCY OF VWF
CLASSIFICATION OF VON WILLEBRAND’S: TYPE 2A
Qualitative variants with decreased platelet dependent function associated with the absence of high molecular multimers
CLASSIFICATION OF VON WILLEBRAND’S: TYPE 2B
Qualittaive variants with increased affinity for GP Ib
CLASSIFICATION OF VON WILLEBRAND’S: TYPE 2M
Qualittaive variants with decreased platelet dependent function NOT associated with absence of high affinity multimers
CLASSIFICATION OF VON WILLEBRAND’S: TYPE 2N
Qualitative variants with decreased affinity for Factor VIII
CLASSIFICATION OF VON WILLEBRAND’S: TYPE 3
Near complete quantitative deficiency of VWF
Platelet Aggregometry
test in which platelet rich plasma is placed in a cuvette, the test reagent (ADP, epinephrine, collagen, ristocetin) is added, and transmission of light as a function of time is determined

$$$$
PFA-100
platelet rich plasma is pulled through a membrane that has been impregnated with ADP or epinephrine

The time for the aperature to close is determined
INTERPRETING THE PFA-100 TEST FOR PLATELET FUNCTION:

C/ADP & C/EPI BOTH NORMAL
Normal result.

Essentially rules out von Willebrand’s and platelet function defects
INTERPRETING THE PFA-100 TEST FOR PLATELET FUNCTION:

C/ADP & C/EPI BOTH ABNORMAL
Suggests severe von Willebrand’s or a severe platelet function defect

Can also be seen when the hematocrit is very low

Can be seen with drugs that affect platelet function including aspirin

Can be seen with severe thrombocytopenia
INTERPRETING THE PFA-100 TEST FOR PLATELET FUNCTION:

C/EPI ABNORMAL BUT C/ADP NORMAL
Mild von Willebrand’s or mild platelet function defect

Mild thrombocytopenia

Drug effect such as aspirin

Anemia

Could follow up with platelet function studies and tests for vonWillebrand’s disease
INTERPRETING THE PFA-100 TEST FOR PLATELET FUNCTION:
Because the C/EPI is the more sensitive test, this result is very very uncommon
what type immunoglobulin against mistyped blood
IgM
haptoglobin
Plasma glycoprotein that binds to oxyhemoglobin that is free in plasma and the complex is then removed in the liver.
www.nutritionperspectives.com/Other/siteGlossary.cfm

Haptoglobins are proteins in the blood that bind free iron, preventing bacteria from using the iron to grow.
en.wikipedia.org/wiki/Haptoglobin
Approach to febrile transfusion reaction:
1. STOP the transfusion

2. Work up for a possible mismatch

3. Give antipyretics

4. Continue the transfusion (Blood is a precious resource, do not waste it.)
4 possible Causes of a positive direct Coombs test
Autoantibody in immune hemolytic anemia

Alloantibody, if patient was transfused, might have an antibody on the cells due to mismatch (major or minor).

In infant, can reflect maternal antibody to paternally inherited antigen on neonate’s RBC’s.

Non-specific adherence of immunoglobulin to RBC
components of a direct coombs test
Patient’s RBCs and antiglobulin

A positive test means globulin, presumably immunoglobulin and/or complement on the cells.
Antibody screen (Indirect Coombs test)
Patient’s serum plus two red cells that are Type O and that are chosen so that all clinically significant antigens are included between the two. Add anti-IgG.

If the cells aggulutinate (when the direct Coombs is negative) that means that an alloantibody is present. To identify the antibody, a panel of cells must be tested. This test is important in determining pre-transfusion antibody
Type and Screen
Determine ABO and Rh type of the patient

Do an antibody screen.

Run the patient’s serum against two screening Type O red cells to see if any antibodies exist.

If screen cells are positive, run a panel of cells to identify.
Approaches to ordering blood: 2
1. Type and screen: ABO type, Rh type, antibody screen with identification of antibody.

2. Type and cross: Type and screen. Also cross match for number of units ordered. The crossmatch involves incubating the patient’s serum with specific units and adding antiglobulin sera looking for agglutination.
Bllod Options in critical situations (The Emergency Room), 4
1. Type and crossmatch STAT (30-45 minutes)

2. Type and screen, immediate release. If screen is negative, skip the crossmatch.

3. ABO compatible without a screen (takes 10 minutes)

4. Type O blood. Available for immediate release. Risk is missing alloantibodies. Only packed cells should be used to avoid transfusing anti-A and anti-B. Would generally give O negative to females of childbearing age and O positive to others. May be lifesaving in case of exsanguinating hemorrhage.
Fresh frozen plasma components
Contains all clotting factors.
Cryoprecipitate components
Contains VIII, von Willebrand’s factor (VWF), fibrinogen, and XIII.

Also useful for unknown reasons in the platelet dysfunction of uremia.

***may contain anti-A or anti-B
Prothrombin complex concentrate components
Contains II, VII, IX, and X

**contraindicated in liver disease
PLATELET TRANSFUSIONS--usefullness
raise count 10k

useful to control bleeding in thrombocytopenic patients when the low platelets are due to decreased production

***if due to increased destruction (ITP) won't help much

disorders of platelet function (except vWB)

prophylaxis against counts <10k
FRESH FROZEN PLASMA
usefullness
FFP should be used ONLY to increase the level of clotting factors in the face of a demonstrated deficiency

given to bleeders on coumadin

helps patients w/ TTP
Recipient Blood type O
compatible RBC's?
O
Recipient Blood type O
compatible Plasma?
AB, A, B, O
Recipient Blood Type A
Compatible RBC's?
A, O
Recipient Blood type B
Compatible RBC's?
B, O
Recipient Blood Type A
Compatible Plasma?
A, AB
Recipient Blood type B
Compatible Plasma?
B, AB
Recipient Blood type AB
Compatible RBC's?
AB, A, B, O
Recipient Blood type AB
Compatible Plasma?
AB