Clin Lab Med Transfusion (Exam 3)

Front 1

how does TPA work?

Back 1

clears fibrin.

Front 2

how to reverse TPA? pros and cons of each?

Back 2

Tighten BP control, goal SBP 90-140 with nicardipine infusion.

Check STAT fibrinogen and platelets.

Give Amicar.

If the fibrinogen is low

Front 3

I gave too much vit k or kcentra. Now what???

Back 3

give cryoprecipitate.

Front 4

dx that.

huge lymph nodes.

high sed rate.

thrombocytopenia.

what test would you use to verify?

Back 4

monospot to verify mono.

Remember no physical contact for 6 weeks

Front 5

how are large lymphocytes reported by the lab?

Back 5

atypical.

Front 6

MM is a tumor of what?

Back 6

plasma cells

Front 7

universal donor?

Back 7

o negative

Front 8

universal recipient?

Back 8

AB positive

Front 9

RH negative patients can get blood from?

Back 9

only RH negative

Front 10

RH positive patient can receive blood from?

Back 10

RH pos or RH neg.

Front 11

3 L's of white blood cells?

Back 11

left shift.

leukemoid reactions.

leukemia.

Front 12

Left shift of white blood cells is what?

Back 12

increased numbers of immaure forms of WBC's like bands.

Front 13

what can happen leukemoid reaction

Back 13

may be myelocytic or monocytic. Both of those are blast cells leading to myeloid or lymphoid cells. basically it is a normal immune response.

Front 14

what happens in leukemia?

Back 14

lack of WBC's which leads to frequent infecton.

Front 15

leukemia vs leukemoid reactions WBC?

Back 15

leukemia has >100,000 WBC's.

leukemoid reactions has <50,000 WBC

Front 16

leukemia vs leukemoid reactions neutrophils?

Back 16

leukemia has neutrophils has myeloid cells earlier than bands.

leukemoid reactions has mature neutrophils with <10% bands.

Front 17

leukemia vs leukemoid reactions basophils and eosinophils???

Back 17

leukemia has basophilia, Eosinophilia and monocytosis.

Leukemoid reactions have no basophils, no eosinophils, no monocytes.

Front 18

leukemia vs leukemoid reactions platelet count?

Back 18

leukemia has abnormal platelets and there are >1 million platelets.

Leukemoid reactions usually have small platelets and rarely have >600,000

Front 19

leukemia vs leukemoid reactions RBC appearance?

Back 19

leukemia have nucleated RBC's with abnormal forms like tear drop.

leukemoid reactions have normal RBC's with no nucleated RBC's.

Front 20

punched out lesions on radiograph indicate?

Back 20

MM

Front 21

what do you need to consider when giving blood?

Back 21

blood transfusion invite infection because blood love free iron.

It can also lead to TRALI which is transfusion related acute lung injury.

Front 22

when do you transfuse blood?

Back 22

normal patients when 7/21 on hemoglobin/hematocrit ratio.

when MI patient give blood at 8/24.

When there is an orthopedic procedure they will want a higher HGB/HCT ratio because it helps bones heal.

Front 23

what does 2-3 DPG do?

Back 23

helps cleave off O2 from hemoglobin

Front 24

what kind of cells contain 2-3 DPG?

Back 24

young RBC's. Old RBC's don't have as much.

Front 25

what happens to someones antibodies as they receive more and more blood transfusions?

Back 25

They develope more antibodies which can attack incoming blood.

Front 26

indirect coombs test is for what?

Back 26

The direct Coombs test is used to test for autoimmune hemolytic anemia. The direct Coombs test is used to detect antibodies or complement proteins that are bound to the surface of red blood cells. Bound.

The indirect Coombs test is used in prenatal testing of pregnant women and in testing blood prior to a blood transfusion. It detects antibodies against RBCs that are present unbound in the patient's serum. Unbound

Front 27

how long are type and crossmatch good in the hospital?

Back 27

3 days

Front 28

type and screen includes what?

Back 28

ABO & Rh type of recipient RBC's and an indirect coombs test.

Front 29

normal coombs tests looks like what?

Back 29

there is no clumping or aggranulation in the samples.

Front 30

what are type and screen blood samples collected in?

Back 30

plain red tube (no gel in tube)

Front 31

Since many blood units are ordered that are never transfused, T & S does what to the number of crossmatches required.

Back 31

decreases the amount of type and screens performed.

Front 32

type and cross match occur when?

Back 32

usually follows a type and screen when the order to transfuse is given.

Front 33

what does a type and cross match include

Back 33

ABO, Rh, and special type indirect coombs tests with recipients and donors RBC's.

Front 34

what non-blood products need to be crossmatched?

Back 34

none

Front 35

what causes dilutional coagulopathy?

Back 35

giving only PRBC's. It creates a high viscosity environment leading to hypercoagulability.

Front 36

If I lose 1 liter of fluid how much crystalloid fluid do I need to replace it?

Back 36

3 liters. It takes 3 times as much fluid to correct for blood loss.

Front 37

why does it take so much fluid to replace blood?

Back 37

the body switched from aerobic to anaerobic which yields less ATP.

The sodium in the reaction go into the cell which takes water with it so there is fluid going into the peripheral tissue and cells.

Front 38

80 kg male pt with 450 mL of blood loss. How much crystalloid fluid do I give to resuscitate his volume?

Back 38

450*3=1350mL

Front 39

how much fluid is lost in abdominal surgery?

Back 39

1 liter per hour.

Front 40

patient in surgery for 3 hours and lost 2 liters of blood. Patient made 600mL of fluid during procedure. Anesthesia gave 3 units if PRBC's and 2 L of crystalloid fluid. He is now hypotensive. How do you fix it???

Back 40

figure out how much he lost all together.

3000 from surg.

2000 mL from blood loss.

600 mL of urine lost.

anesthesia gave 3 units of PRBC's and 2 liters of NS.

2000*3=6000 mL NS needed to fix blood loss.

600mL urine loss.

6600 loss altogether.

Front 41

shelf life of blood is?

Back 41

40-42 days

Front 42

can hypocalcemia lead to abnormal coagulation?

Back 42

yes

Front 43

transfusion non-immune reaction includes what?

Back 43

BCDH

Bleeding

Circulatory overload

disease transmission and infection.

hypothermia and miscellaneous issues,.

Front 44

transfusion immune reactions

Back 44

FAAG

febrile nonhemolytic reaction.

acute hemolytic reaction.

allergic/hypersensitivity reaction.

Graft vs host disease.

Front 45

pt on pressors but not able to wean. Pt's HgB/HCT is 7.6/21. what now?

Back 45

give transfusion to bring up HgB/HCT to help wean.

Front 46

what is the most reliable finding in cardiac disease

Back 46

dyspnea

Front 47

transfusion non-immune reaction in circulatory overload. what causes it?

Back 47

usually occurs from rapid infusion of blood especially in elderly, infants and patients with cardiac or renal compromise.

Front 48

transfusion non-immune reaction in bleeding . what causes it?

Back 48

massive transfusion without factor or platelet replacement. enzymatic reactions don’t occur that need to so you bleed more even when getting blood products

Front 49

transfusion non-immune reaction in hypothermia. what causes it?

Back 49

Its cold. If it doesn't get thawed or warmed, it makes you cold. easy enough.

Front 50

transfusion non-immune reaction in electrolyte imbalances. what electrolytes would be effected and how?

why?

Back 50

hypocalemia and hyperkalemia.

citrate from blood absorbs free calcium and RBCs destruction releases potassium.

Front 51

symptoms from acute hemolytic reaction from transfusion

Back 51

fever/chills, back pain, flushing, dyspnea, tachycardia, pain at IV site, n/v, hypotension, rash, hematuria, ATN or acute tubular necrosis and shock

Front 52

how to tx acute hemolytic reaction from transfusion?

Back 52

stop transfusion. IV fluids, cardiac and respiratory support as needed.

Front 53

Patient had an acute hemolytic reaction to blood transfusion. Now what?

Back 53

send blood back to Blood bank. get new specimens for type and cross match. Get LDH, bilirubin, coag studies, haptoglobin, BUN, creatinine, and urine samples. Get direct and indirect coombs.

Front 54

what is the worst reaction that can occur in blood transfusion?

Back 54

acute hemolytic reaction

Front 55

how does acute hemolytic reaction occur?

Back 55

mislabeling blood or clerical error.

Front 56

why are duffy, kidd and kell antibodies important?

Back 56

They can be used to ID antibodies on blood to make sure there won't be blood transfusion reactions.

Front 57

what percentage of eligible donors donate blood?

Back 57

5%

Front 58

why is there more of a need for blood?

Back 58

–Aging population

–Elective surgeries (e.g., hip & knee replacements)

–New treatments for heart disease & cancer: prolonging life

Front 59

QALY for west nile virus?

what is the recommended threshold?

Back 59

WNV = $500,000.

recommended = $50,000

Front 60

hysterical and hyster have the same root becaue of why?

Back 60

they use to beleive that uteruses would travel throughout the body and make women hysterical.

Front 61

who drank blood to cure epilepsy and restore spirits after long campaigns.

Back 61

romans

Front 62

life of flesh in the blood

Back 62

leviticus

Front 63

blood contain the soul says who?

Back 63

chinese

Front 64

who discovered circulation

Back 64

william harvey in 1628

Front 65

blood was contained in arteries discovery was made by who

Back 65

galen who was a roman physician in 1642

Front 66

first animal to animal transfusion

Back 66

1666 richard lower

Front 67

first human transfusion

Back 67

1667 jean baptiste. Lamb blood to 15 year old boy. Boy dies and transfusin banned for 150 years.

Front 68

•First documented transfusion w/human blood, treated postpartum hemorrhage

Back 68

1818.

james blundell (OBGYN)

Front 69

ABO blood group created

Back 69

1900 Karl Landsteiner and students

Front 70

•Compatibility testing

Back 70

1907 Reuben Ottenberg

Front 71

what event precipitated the Development of anticoagulants- citrate

Back 71

2 events.

WWI/ WWII Rous/ Turner; Loutit/ Mollison-

Front 72

Soviets set up blood banks with cadaver blood when

Back 72

1930's

Front 73

First US blood bank- where?

who?

Back 73

Chicago Cook County Hospital by Fantus.

*Some claim that first US blood bank was MayoClinic

Front 74

Head of British WWII plasma program ?

Back 74

1940 Charles Drew-

Front 75

•Selective component transfusion includes 4 parts?

Back 75

1.Give only necessary component

2.Limit fluid volume

3.Concentrated component: higher dose

4. Can get more product from each donor

Front 76

what percentage of the population is Rh positive?

Back 76

80% Rh positive

Front 77

What needs to happen for an Rh neg person to have a blood transfusion reaction?

Back 77

they need to be sensitized and then re exposed.

Front 78

3 classifications of HDN?

Back 78

–Rh Hemolytic Disease: Rh incompatibility due to anti-D alone or accompanied by other Rh antibodies – anti-C, -c, -E or –e.

–ABO Hemolytic Disease

–“Other”:unexpected immune antibodies other than anti-D such as Lewis, Duffy, Kidd, Kell

Front 79

most common form of severe HDN?

Back 79

Anti-D is the commonest form of severe HDN.

Front 80

third most common form of severe HDN ?

Back 80

Anti-c.

It can range from a mild to severe disease

Front 81

•Anti-e-and Anti-C -. Are they rare or common?

Back 81

Rare

Front 82

•Antibody combinations (ieanti-c & anti-E antibodies occurring together) - is it severe, mild or moderate?

Back 82

severe

Front 83

Rh hemolytic disease is what

Back 83

•Mother is Rh- & fetus Rh+.

•Mother develops Abs against RBC Rh Ag after being exposed to Rh+ RBCs from maternal fetal hemorrhage, ectopic pregnancy, abortion, amniocentesis, prior blood transfusion with Rh positive RBC's and placental trauma.

1st child usually not affected.

Front 84

Erythroblastosis Fetalis is what what does it lead to?

Back 84

•Most severe form of hemolytic disease of newborn leading to massive hemolysis.

•Leads to severe anemia & compensatory enlargement of the liver & spleen. Liver begins to make tons of albumin causing massive edema called hydrops fetalis.

fulminant profound hemolytic anemia,

Front 85

kernicterus

Back 85

Kernicterus is a bilirubin induced brain dysfunction from hemolysis like that in Erythroblastosis Fetalis.

It is a very rare type of brain damage that occurs in a newborn with severe jaundice.

It happens when bilirubin, builds up to very high levels and spreads into the brain tissues.

Front 86

what kind blood cultures from a bowel perf

Back 86

polymicrobial from enteric gram negative and enteric and anaerobic.

Front 87

CXR looks like pulmonary edema with a normal sized heart

Back 87

ARDS

Front 88

is ARDS a sequalla of being septic

Back 88

O2 not normal

Pa O2 100 but you are breathing 80%

100/.8=125

Front 89

hydrops fetalis is what?

Back 89

fluid accumulation in at least 2 body compartments. (ascites, pleural effusion, facial edema and so on).

It is caused by anemia which induces a high-output heart failure. The heart failure result sin fluid accumulation.

The fetus is at significant risk for intrauterine fetal demise.

Front 90

rhogam prophylaxis is for what?

Back 90

mother who is Rh neg and has Rh pos baby. Get Rh immunoglobulin that neutralizes the Rh antigen to prevent fetal hemolytic problems in subsequent pregnancies.

Passive immunization with rhogam prevents active Antibody response by mother.

Dose is 300 mcg at 28 weeks and second dose within 72 hours of delivery.

Front 91

ARDS is a result of what

Back 91

type 2 cell inflammation leading to alveolar collapse which leads to fibrosis and damage to lungs.

Front 92

what happens when you double the space betwen the alveoli and the capillary beds?

Back 92

half the gas exchange

Front 93

gray dusky colored patient with tachycardia with rapid onset with pulmonary edma sounds and CXR, but normal sized heart?

Back 93

ARDS

Front 94

70 year old with pruritus and worsening headache with hepatosplenomegaly.

Trop >50.

HgB=7.2

BNP 1600.

what do these numbers say to you

Back 94

trop = AMI.

HGB = anemic

BNP says heart failure.

Front 95

plethoric?

Back 95

red in the face. Flushed.

Front 96

normal BNP level

Back 96

less than 100

Front 97

how do split untis work

Back 97

give 1/2 unit over 4 hours. Infusing blood over 4 hours is detrmental to the blood. If you spit the unit a ful unit can be given over 8 hours.

Front 98

PA O2 FI I2 ratio formula

Back 98

PA O2 / percent O2 delivered.

So 100% PA O2 / .21 = 500 which is normal

Front 99

normal value for PAO2/FIO2

Back 99

500

Front 100

ARDS level of PAO2/FIO2

Back 100

<200

Front 101

acute lung injury level of PAO2/FIO2

Back 101

<300

Front 102

9 month old with dark red urine, lethargy, pale, ecteric, febrile, ecteric, spleenomegally, hepatomegally.

blood smears look like little helmets, fragments, bytes seen.

haptoglobin <5.

G6PD enzyme is >8

Back 102

G6PD deficiency anemia

Front 103

normal haptoglobin level

Back 103

41 to 165

Front 104

most common enzyme deficiency in men?

Back 104

G6PD deficiency in infacny

Front 105

G6PD deficency seen in what groups of people?

Back 105

AA, mediterian (italian, greek, sephardic jews)

Front 106

can g6PD be protective?

Back 106

yes. In normal amounts it protects the RBC's from harmful biproducts that cause hemolysis.

Front 107

favism is what?

Back 107

when fava beans cause a G6PD deficiency.

Front 108

how much blood is used by cadiothoracic surgeon?

Back 108

20%

Front 109

why do component therapy

Back 109

get more than one thing our of each blood donor.

limit fluid volume given to patients.

Concentrate components to give higher dose at less volume.

Front 110

hyofibringenemia tx

Back 110

cryoprecipitate

Front 111

when does hemlytic disease occur in pregnant females?

Back 111

1st few days after delivery. when the fetal bood cells are released into the maternal circulation. Antibodies take a number of weeks to develeop.

Front 112

When could a mother who is RH negative mother have a hemolytic reaction on her first pregnancy?

Back 112

Mother is RH neg and has an exposure to RH pos blood like through transfusion.

Front 113

If mom is RH neg and had RH pos baby, what hapens to 2nd baby?

Back 113

RH pos baby can incite anti D antibodies which hemlize baby RH pos cells,

Front 114

what causes the edema with erythoblastosis fetalis?

Back 114

baby get hepatopmegally and spleenomegally from massive hemolysis which injured the liver causing a decrease in albumin production. This leads to edema known as hydrops fetalis.

causes high output HF which leads to intrauterine fetal demise.

Front 115

survival of hydrops fetalis

Back 115

10%

Front 116

fluid overload from transfusion tx?

Back 116

loop diuretic

Front 117

hypothermia can result in excess bleeding. Why?

Back 117

qualitative pleteet problem leading to bleeding

Front 118

what is dilutional coagulopathy and how does it happen

Back 118

it happens because you give the patient a lot of one prodcut, but not the clotting factors to go with it, you create an enviroment in which there is less coag factors per liter, therefor diluted.

Front 119

hypoperfusion leads to aerobic to anaerobic leading to less ATP leading to acidosis, leading to catecholamine dysfunction

Back 119

hypoperfusion leads to aerobic to anaerobic leading to less ATP leading to acidosis, leading to catecholamine dysfunction

Front 120

what happens when you have citrate degredation in the body

Back 120

citrate binds calcium. When the calcium is free you become alkalinic. More alkalotic you get the more the oxyhemaglobin dissociatino curve up and to the left.

Front 121

every few units of blood with citrate will cause hypo calcemia. How to counteract that?

Back 121

every few units give calcium gluconate.

Front 122

hypocalcemia causes

Back 122

tetany, hypotensive, needed in vessels and myocardia activity.

Front 123

when the space between the alveoli and the capillary increases what hapens to your PaO2/FiO2 ratio?

Back 123

down

Front 124

if you give multipe units of blood and the patient develops ciiculatory overload symptoms what should you think?

Back 124

heart failure.

It is a few units think TRALI.

Front 125

which transfusion reaction is potentially fatal

Back 125

hemolytic reaction

Front 126

delayed reaction from blood transfusion is usually caused from what?

Back 126

duffy, kidd and kell antibodies.

Front 127

ABO reaction occurs when during transfusion?

Back 127

during the first few cc's of blood. Stop the transfusion. tachycardia, fever, rash, hematouria and pain.

Front 128

how to prevent acute tubular necrosis with transfusion reaction when not hypotensive?

Back 128

fluids and 10 mg loop diuretics like lasix to flush out kidneys.

Front 129

more common transfusion reactions are what?

Back 129

immune reactions

Front 130

febrile episode during or just after transfusion is most commonly associated with what and what is this kind of reaction called?

Back 130

antibodies against tthe HLA on the donor leukocytes. It is called a febrile non-hemolytic reaction.

These don't happen as often because of leukocyte reduced PRBC's units.

especially important in cancer patients and immunosuppressed.

Front 131

why are leukocyte reduced PRBC's so important?

Back 131

because if you don't the survelince of the cancer patient can be reduced which makes more cancer cells go undetected in the cancer patient. There is only so many immune cells and if they are fighting the leukocytes from blood transfusino, then the cancer cells are more likely to live on and exacerbate the cancer.

Front 132

how often do immne reactions cause hemodynanic instability

Back 132

rarely

Front 133

how to tx patient who has had or is now having a fever during a transfusion with known reaction from the previous transfusion?

Back 133

tylenol

Front 134

mild reaction with blood transfusion tx?

Back 134

benadryl and continue transfsion

Front 135

with TRALI what are the lungs full of

Back 135

inflammation, not fluid.

Front 136

TRALI tx

Back 136

92% with o2 and if you can't maintian that than intubate and ventilate them

Front 137

how does graft vs host disease work?

Back 137

immunocompentent donor cells attack tissues of immunocomprimised host.

Front 138

graft vs host ds s&s

Back 138

severe skin changesdiarrhea, liver dysfunction

Front 139

how to tx graft vs host disease

Back 139

topical steroids, oral prednisone., cyclosporin and other immunosuppresants.

Front 140

how to avoid graft vs host disease in transfusion

Back 140

radiate the blood prior to transfusion

Front 141

how much is considered massive transfusion

Back 141

8 to 10 units in mythical 70 kg person

Front 142

hypothermia can occur how quickly with blood transfusion

Back 142

after 3 untis

Front 143

thrombocytopenia patients needs what?

Back 143

platelets

Front 144

bleeding with increased INR with increased pt and PTT tx???

Back 144

FFP

Front 145

low fibrinogen level tx

Back 145

cyroprecititate

Front 146

DIC tx with significant blood loss tx

Back 146

packed cells.

Front 147

K centra is important in the reversal of what?

Back 147

warfarin.

Front 148

patient treated with warfarin and comes in with ear infection. tx?

Back 148

if abx then alter warfarin levels accrodingly

Front 149

why do abx affect warfarin effectiveness

Back 149

gut flora breaks down warfarin. The less gut flora the less warfarin gets broekn down so it work more effectively.

Front 150

someone comes in and they are bleeding and/or they need surgery or an invasive procedure and their on warfarin at therapeutic levels what do you need to consider?

Back 150

small INR increase isn't imporant, but it also depends on the surgery.

Neurosurgery working on the spine want the INR needs to be less than 1.4.

INR less than 1.5 is perfectly fine to take for an invasive procedure.

Front 151

if the patient has a mild increase in INR how can we reverse it?

Back 151

FFP and vit k and K centra.

Front 152

Do WBCs & PLTs have to be crossmatched?

Back 152

WBC's and platelets have ABO Antigens which means they need to be ABO compatible, not necessarily crossmatched.