Pathology Test 2

Front 1

what is the storage temperature for RBC's?

Back 1

1-6 C

Front 2

What are the indications for giving red blood cells?

Back 2

Anemia with compromised status
Hb<7 in uncomplicated
Hb<9 cardiorespiratory disease
Hb<15 in prematurity with CR compromise
NOT for volume expansion in a bleeding patient!

Front 3

Blood Type A

Back 3

Antibodies: Anti-B
Compatible: A, O

Front 4

Blood Type B

Back 4

Antibodies: Anti-A
Compatible: B,O

Front 5

Blood Type AB

Back 5

Antibodies: none (universal recipient)
Compatible: AB, A, B, O

Front 6

Blood Type O

Back 6

Antibodies: Anti-A, Anti-B
Compatible: O

Front 7

what is the advantage of using single donor platelets (apheresis) instead of pooled?

Back 7

Decreases the risk of:
infectious disease transmission
immunization with platelet antigens

Front 8

What is the storage temp of platelets?

Back 8

20-24 degrees C

Front 9

How are pooled platelets collected?

Back 9

They are obtained from centrifugation of the whole blood units after the unit has been collected. This exposes the recipient to 6-8 different people.

Front 10

How are apheresis platelets collected?

Back 10

They are collected, centrifuged with a small amount of plasma, then the rest of the blood is returned to the donor.

Front 11

How is optimal platelet function maintained during storage?

Back 11

agitation

Front 12

What are the indications for platelets?

Back 12

Quantitative deficiency: bleeding with low platelets, prevent bleeding with low platelets

Qualitative deficiency: congenital platelet dysfunction, aspirin, NSAIDS, abciximab, uremia

Front 13

What are the numerical cut offs to give platelets to prevent bleeding with low platelet count?

Back 13

<10 K/microliter: no risk factors
<50 k/microliter: before an invasive procedure

Front 14

How does uremia effect platelets?

Back 14

Platelets are reversibly inactivated when BUN is greater than 55. Platelets given to these patients will lead to minimal benefit.

Front 15

Is compatibility with donor platelets essential?

Back 15

no

Front 16

What conditions usually have a poor response to giving platelets?

Back 16

hepatosplenomegaly, large body habitus, presence of anti-platelet or anti-HLA Ab, immune thrombocytopenic purprura, sepsis, DIC

Front 17

What is the storage temperature for granulocytes?

Back 17

20-24 degrees C

Front 18

What else may be packaged with granulocytes?

Back 18

may be contaminated with lymphocytes, platelets, and RBC

Front 19

What are the indications for granulocytes?

Back 19

Bacterial, fungal infections unresponsive to antibiotics AND
1) neutropenia or
2) hereditary neutrophil function defect

Front 20

When are granulocytes collected?

Back 20

only when needed for a specific patient, since their shelf life is so short

Front 21

Do granulocytes have to be blood type compatible?

Back 21

Yes

Front 22

How long do you give granulocytes?

Back 22

until the infection resloves or WBC recover *hard to give enough to recover WBC

Front 23

How can you optimize the amount of granulocytes collected from a donor?

Back 23

Give them prednisone or G-CSF to increase granulocytes prior to collection

Front 24

What is the storage temp for fresh frozen plasma? and for post thawing?

Back 24

1 year= 18 C
24 hrs= 1-6 C after thawing

Front 25

how soon must you freeze fresh frozen plasma?

Back 25

within 8 hours of collection

Front 26

What factors are lost if fresh frozen plasma is held over 24 hours as a liquid?

Back 26

FV and FVIII

Front 27

What are the indications for giving plasma?

Back 27

1) multiple coag factor deficiency (INR>1.8) AND bleeding or procedure planned
2) congenital single factor deficiency

Front 28

Is plasma used for volume expansion?

Back 28

NO

Front 29

Should plasma be blood type compatible?

Back 29

advisable, but not necessary

Front 30

How are platelets given?

Back 30

as a bolus (coag factors have such a short half life that you need this)

Front 31

Is it easy to correct high or low INR's by giving plasma?

Back 31

It is easy to decrease a high INR, but a low INR is hard to normalize because the pt can't tolerate the volume given.

Front 32

What does cryoprecipitate contain?

Back 32

F XIII, fibrinogen, VWF+F VIII (all high molecular weight besides VIII, but it precipitates with VWF on centrifuging

Front 33

How do you prepare cyroprecipitate

Back 33

Thaw plasma at 1-6 C, centrifuge, retain precipitate. Redissolve proteins at 37, and then re-freeze

Front 34

What are the indications for cryoprecipitate?

Back 34

Fibriogen deficiency (qualitative or quantitative), congenital deficiency of FXIII

Front 35

Do you need to be blood type matched to give cryoprecipitate?

Back 35

no

Front 36

What blood products is leukocyte reduction used on?

Back 36

RBC, platelets (NOT granulocytes, this would stop the point of the product)

Front 37

What does leukocyte reduction do?

Back 37

decreases risk of CMV (virus lives in WBC), Ab formation against WBC Ag, febrile reaction to transfusion, cytokines secreted by WBC into unit before transfusion

Front 38

What blood products may be put under irradiation?

Back 38

RBC, Granulocytes, platetes

Front 39

What does irradiation do?

Back 39

prevents transfusion associated GVHD by stoping lymphocyte proliferation

Front 40

Which components of blood can be washed?

Back 40

RBC, platelets (controversial)
NOT granulocytes

Front 41

What does washing do?

Back 41

1) decreases risk of anaphylaxis by removing antibodies from cellular compoents
2) removes excess K+ (necessary for rapid transfusion of infants)

Front 42

What does washing do to the shelf life?

Back 42

decreases it to 24 hours because of possible bacterial contamination during the process

Front 43

When is freezing of RBC done?

Back 43

To freeze rare blood types lacking Ag for patients that require them. May be stored for up to 10 years. (plasma and cryoprecipitate are routinely frozen)

Front 44

Erythropoeitin

Back 44

hematopoeitic growth factor given to limit chronic RBC transfusions

Front 45

G-CSF

Back 45

hemtopoeitic growth factor given to avoid prolonged neutropenia and risk of granulocyte transfusion

Front 46

Recombinant F VIIa

Back 46

activator of extrinsic/common coagulation pathway

Front 47

Desmopressin

Back 47

Releases vWf from the endotheilium

Front 48

FVIII, FIX concentrates

Back 48

specific factor replacements for congenital and acquired anemias

Front 49

Fibrin glues

Back 49

topical formation of fibrin on oozing surface

Front 50

Sprotinin, Tranexamic acid, e-aminocaproic acid

Back 50

limit fibrinolysis

Front 51

Crystalloid

Back 51

Volume expander: saline, hypertonic saline
*Pulls fluid from inside cells (short term)
Distributed: intravascular and extravascular

Front 52

Colloid

Back 52

Volume expander: albumin, dextran, hydroxyethyl starch
*Pull fluid from the interstital space (long acting)
distribute: in intravascular space only

Front 53

How could autologous blood cause a problem?

Back 53

1) clerical error: wrong person gets the blood
2) bacterial infection of blood leads to sepsis

Front 54

What are contraindications for autologous transfusion?

Back 54

infection, malignancy, hemoglobinopathies, pharmacologic agents in the surgical field

Front 55

what is the first treatment of suspected transfusion reaction?

Back 55

STOP THE TRANSFUSION

Front 56

Acute hemolytic transfusion reaction

Back 56

preformed AB (AB, kell) in patient's plasma cause an intravascular lysis of transfused RBC

Front 57

What is the lab evidence of hemolytic anemia?

Back 57

hemoglobinema (free Hb from lysed)
persistant anemia
high LDH (lysed cells), high bilirubin
LOW haptoglobin, spherocytes, postivie direct antiglobulin test (DAT)

Front 58

what causes a febrile transfusion reaction?

Back 58

realease of inflammatory mediators from WBC, PGE2 production, hypothalamus increases body temp.
Prevent: leukocyte reduction

Front 59

What causes an allergic reaction to transfusion?

Back 59

Patient Ab to plasma proteins, rarely IgA (severe reactions seen in IgA deficient pts)
HIVES, dyspnea, shock
PREVENTION: antihistamine, washed RBC, product from IgA negative donor (rare)

Front 60

Transfusion associated circulatory overload

Back 60

cause: too much volume too rapidly ( high risk patients have renal or cardiac problems)
presentation: dyspnea, hypertension, pulmonary edema, elevated BNP
Prevention: transfuse more slowly, add a diuretic

Front 61

TRALI: transfusion associate noncardiogenic pulmonary edema

Back 61

Cause: donor anti-HLA or anti leukocyte Ab reacts with patient WBC
Risk: highest with plasma, platelets
presentation: hypoxia within 6 hrs
Prevention: minimize collection from mulitparous females, eliminate donors that caused this reaction

Front 62

how do you differentiate TRALI from PE

Back 62

BNP is not elevated

Front 63

what bacterial commonly contaminate RBC?

Back 63

gram negative rods that grow well at 4 C which is in the storage range of RBC

Front 64

Which bacteria commonly contaminate platelets?

Back 64

gram positve skin contaminants that grow at 25 C, the range for storage of platelets

Front 65

Are platlets or RBC screened for bacterial contamination?

Back 65

RBC NO
Platelets YES

Front 66

Metabolic transfusion reactions

Back 66

cause: rapid infusion of citrate causes a drop in calcium, aged RBC causes rise in potassium
presents: decreased Ca, increased K, tingling in extremities
Prevention: slow transfusion rate, give calcium gluconate (IV), wash RBC

Front 67

Delayed hemolytic transfusion reaction

Back 67

Cause: primary or memory Ab response to RBC Ag results in extravascular hemolysis of transfused RBC.
Presentation: malaise

Front 68

What are the lab values for hemolytic transfusion reaction?

Back 68

1) drop in Hb days to weeks after transfusion
2) positive DAT coombs
3) increased direct bilirubin (DIRECT differentiates it from acute)

Front 69

Posttransfusion purpura

Back 69

cause: patient Ab to platelet Ag that crossreact wtih autologous platelets
Presentation: bleeding, bruising, profound thrombocytopenia)
Treatment: IVIG to prevent splenic clearance of platelets
NO PROPHYLACTIC IS AVAILABLE (no further transfusions)

Front 70

Iron overload

Back 70

cause: chronic RBC transfusions without blood loss
Presentation: high ferritin, eventual hemosiderosis in heart, liver, and pancreas
Treatment: RBC exchange rather than transfusion, chelation therapy to rid body of iron

Front 71

What viruses are blood screened for?

Back 71

HCV, HIV, HBV, HTLV, west nile virus
bacterial: syphilis, t. cruzi, malaria, crutzfeld-jakob, gonorrhea, babesiosis

Front 72

What is melena? where is the bleed?

Back 72

tarry stools, from an upper GI bleed

Front 73

What is hematochezia? where is the bleed?

Back 73

bloody stools (bright red), from a lower GI bleed

Front 74

Metrorrhagia

Back 74

increased bleeding between cycles

Front 75

Menorrhagia

Back 75

increased menstrual blood flow during the normal period cycle

Front 76

Where are the coagulation proteins made?

Back 76

hepatocytes

Front 77

Here is von Willebrand factor made?

Back 77

in the endothelial cells and megakaryocytes

Front 78

Where is tissue plasminogen activator synthesized?

Back 78

endothelial cells

Front 79

What factors are blocked by anti-thrombin?

Back 79

9a, 10a, 11a
enhanced by heparin!

Front 80

What factor is blocked by tissue-factor pathway inhibitor?

Back 80

TF-FVIIa complex

Front 81

What is the triad of predisposition to thrombi?

Back 81

1) abnormal vessels-endothelial damage (trauma, vasculitis, atherosclerosis)
2) abnormal flow-turbulence, stasis
3) abnormalities of blood: hypercoaguability

Front 82

How can you acquire hypercoagulable states?

Back 82

post-op state (increased thromboplastin), bed rest, pregnancy, oral contraceptives, myeloproliferative disorders, cancer

Front 83

Anti-phospholipid antibody syndrome

Back 83

development of antibodies against plasma proteins with affinity for anionic phospholipids; most commonly beta-2 gylcoprotein 1
Associated with: venous/arterial thrombosis, recurrent fetal loss, thrombocytopenia

Front 84

How would the bleeding test look in a person with antiphospholipid antibody syndrome

Back 84

The PTT will be prolonged

Front 85

How does antiphospholipid syndrome produce thrombosis

Back 85

1) platelet activation
2) inhibition of prostacyclin
3) interference with protein C
4) fetal loss due to antibody mediated inhibition of tPA activity needed for throphoblastic inhibition of the uterus.

Front 86

Factor V Leiden

Back 86

high prevalence, low risk
Factor V can't be cleaved by protein C. Thrombophilia is a mild risk

Front 87

Prothrombin gene mutation

Back 87

increased prothrombin levels (gene mutation) MUST do PCR for diagnosis

Front 88

Protein C deficiency, protein S deficiency

Back 88

low prevalence, high risk

Front 89

Antithrombin deficiency

Back 89

Rare, but HIGH risk

Front 90

Arterial Thrombi

Back 90

White, friable, usually superimposed on a atherosclerotic lesion. Common in: coronary, cerebral, femoral aa.

Front 91

Venous Thrombi

Back 91

occulsive, red coagulative or stasis thrombi because they contain more RBC's. Usually in the LE

Front 92

Mural Thrombi

Back 92

attached to a wall (heart or aorta) may have lines of Zahn (platlets or fibrin) mixed with red cells.

Front 93

Lines of Zahn

Back 93

imply thrombosis at site of blood flow.
made of patelets and fibrin and RBC

Front 94

Propagation of thrombus

Back 94

thrombus may extend, leading to obstruction

Front 95

embolization of thrombus

Back 95

dislodge and travel to another site

Front 96

dissolution of thrombus

Back 96

removal by fibrinolysis

Front 97

organization and recanalization of thrombus

Back 97

ingrowth of endothelial cells, smooth muscle, and fibroblasts, vascular flow may be re-established

Front 98

What pathways does the PT measure?

Back 98

Extrinsic and Common

Front 99

What factors can a deficiency of prolong the PT?

Back 99

Extrinsic and common: VII,X, X, prothrombin, and fibrinogen

Front 100

What is the PT used to monitor?

Back 100

warfarin therapy, evaluate liver disease, vitamin K deficiency

Front 101

What is the ISI?

Back 101

The international sensitivity index, which tells you the sensitivity of thromboplastin that the lab is using.

Front 102

What is normal INR? INR for people on anticoag

Back 102

normal: 1
anticoag: 2-3

Front 103

What do you add to citrated plasma in the PT test?

Back 103

thromboplastin (tissue factor) and calcium

Front 104

What do you add to citrated plasma for the PTT test?

Back 104

phospholipid, calcium

Front 105

What is the normal value for PT? PTT?

Back 105

PT: 9-12 seconds
PTT: 23-30 seconds

Front 106

What pathways does the PTT measure? What factors?

Back 106

Intrinsic and common
Factors: ALL besides VII or XIII

Front 107

What five conditions cause an elevated PTT?

Back 107

1) heparin
2)Factor deficiency associated with bleeding (factors 8 or 9)
3) Factor deficiency with no clinical problems (factor 12)
4) Specific factor inhibitor (Factor 8 hemophilia)
5) Antiphospholipid antibody

Front 108

Mixing Study

Back 108

Test for inhibitory (ANTIBODY)
sample mixed with normal plasma. If it is able to be corrected, it is a factor deficiency, if it remains prolonged, an antibody is at work.

Front 109

Fibrinogen
Nl value:
What would cause decreased values?

Back 109

nl value: 180-350 mg/dL
Decreased in: liver disease and DIC, congenital deficiency

Front 110

D-Dimer

Back 110

Tests for: DVT, PE
tests for excessive generation of products of digestion of cross-linked fibrin by plasmin

Front 111

PFA-100
long closure with col/epi
normal closure wtih col/ADP

Back 111

Usually caused by Drugs (aspirin, NSAIDS)

Front 112

PFA-100
prolonged closure with BOTH col/epi and col/ADP

Back 112

usually caused by qualitative platelet disorder or von willebrand disease, anemia, and thrombocytopenia

Front 113

For bleeding disorders caused by vessel wall abnormalities, what do the coagulation screening tests show?

Back 113

They are usually normal

Front 114

What type of bleeding do platelet abnormalities generally cause?

Back 114

mucocutaneous bleeding (rather than hematomas)

Front 115

Where are platelets made? What is their life span?

Back 115

Made in megakaryocytes in the bone marrow. Live for 7-10 days

Front 116

What constitues Thrombocytopenia

Back 116

Patients with less than 100,000/ microliter

Front 117

What are causes of thrombocytopenia?

Back 117

Decreased platelet production, ineffective platelet production, splenic sequestration, increased peripheral destruction of platelets (non-immune or immune)

Front 118

Acute ITP (immune thrombocytopenic purpura)

Back 118

young children, SEVERE thrombocytopenia, associated with viral infection, usually self-limitied, treat with steroids, IVIG, Rh immune globulin

Front 119

Chronic ITP (immune thrombocytopenic purpura)

Back 119

Adults (women) associated with other AI, not as severe thrombocytopenia, remission and relapses, treat with steroids, splenectomy

Front 120

What is the pentad of sx for TTP (thrombotic thrombocytopenic purpura)

Back 120

thrombocytopenia, microangiopathic hemolytic anemia, neurologic sx, fever, renal insufficiency

Front 121

What factor is deficient in TTP?

Back 121

ADAMTS13 protease that cleaves ultra large von willebrand factors: they aggregate and lead to deposition of thrombi, shearing of RBC (shistocytes)

Front 122

What is the treatment of TTP?

Back 122

plasmapheresis

Front 123

The platelet reaction is a series of what four events?

Back 123

1) adhesion
2) aggregation
3) release reaction
4) clot formation and retraction

Front 124

Bernard Soulier syndrome

Back 124

platelet disorder
deficiency of GPIb receptor: can't aggregate with fibrinogen

Front 125

Glanzmann's Thrombasthenia

Back 125

platelet disorder
deficiency of platelet GP II/IIa: can't aggregate with fibriogen

Front 126

Storage pool disease

Back 126

platelet disorder
defective or absent dense granules: can't release contents to activate

Front 127

How does penicillin effect platelets?

Back 127

coats the surface of platelets, producing variably severe receptor blockade at high doses.

Front 128

Sensitivity

Back 128

defined as the percentage of patients having the disease who have a positive result.

Front 129

Specificity

Back 129

defined as the percentage of patients free of the disease who have a negative result

Front 130

predictive value

Back 130

the percentage of patients correctly classified as having or lacking disease based on the results of diagnostic test.