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Medical Diagnosis > Lecture 10 (labs)-Exam 5 > Flashcards

Lecture 10 (labs)-Exam 5 Flashcards

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USMLE® Step 1 flashcards
1
Q

Human ABO blood group

  • Who has been credited for the discovery of ABO blood group system?
  • The ABO blood group antigens are encoded by what? What will the off spring recieve?
A

Karl Landsteiner has been credited for the discovery of ABO blood group system in 1900

The ABO blood group antigens are encoded by one genetic locus, which has three alternatives (allelic) forms, A, B, and O
* Off spring receives one of the three alleles from each parent, giving rise to 6 possible genotypes and 4 possible blood types (phenotypes)

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2
Q

Human ABO blood group:
* The system demonstrates both what?

A

Multiple alleles
* 3 alleles of the I gene (IA, IB, and i)

Codominance
* IA and IB are dominant to i but codominant to each other

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3
Q
A
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4
Q

One technique to determine
relatedness is what?

A

blood typing

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5
Q

ABO blood group has three alleles of one gene?
* Individual genotypes will show what?

A
  • IA is dominant to i.
  • IB is dominant to i.
  • IA and IB are co-dominant.
  • Individual genotypes will show two of these alleles.
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6
Q

What are multiple alleles?

A

more than two alleles of a gene are possible

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7
Q

What are all the possible phenotypes and what makes them different? (4)

A
  • Type A has sugar A on the surface of blood cells.
  • Type B has sugar B on the surface of blood cells.
  • Type O has no sugars on the surface of blood cells.
  • Type AB has sugar A and sugar B on the surface of blood cells.
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8
Q

Which blood type is the most common and least common?

A

0 +
AB -

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9
Q

What can be the problem with blood typing?

A
  • If you have certain sugars on your blood cell: A, B, AB – then you have antibodies to opposite sugars.
  • Antibodies cause reactions to blood cells if incompatible
  • RH+/-
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10
Q

Fill in

A
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11
Q

AB antibodies:
* What subtype?
* Present where?

A

Anti-A and Anti-B antibodies
* IgM subtype
* Present in the plasma

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12
Q

Abo antibodies

  • The discovery of ABO blood group occurred when?
  • Once understood the ABO blood type was used by who and why?
A
  • The discovery of ABO blood group occurred 100 years ago – before that blood was assumed to be all the same
  • Once understood the ABO blood type was used by lawyers in paternity suits, police in forensic science and anthropologists
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13
Q
  • The ABO blood group antigens remains the prime importance in what type of medicine? Why?
  • Despite their obvious clinical importance, the physiological functions of ABO blood group antigens remains what?
A
  • The ABO blood group antigens remains the prime importance in transfusion medicine
    * Most common cause of death from blood transfusion is a clerical error in which an incompatible type of ABO blood was transfused
  • despite their obvious clinical importance, the physiological functions of ABO blood group antigens remain a mystery. People with the common blood type O express neither the A nor B antigen, and they are perfectly healthy.
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14
Q

Numerous associations have been made between particular ABO phenotypes and an increased susceptibility to disease.
* What are two examples?

A
  • the ABO phenotype has been linked with stomach ulcers (more common in group O individuals) and gastric cancer (more common in group A individuals).
  • individuals with blood type O tend to have lower levels of the von Willebrand Factor (vWF), which is a protein involved in blood clotting.
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15
Q

ABO antibodies
* ABO antibodies in the serum are formed how? When are they produced?

A

ABO antibodies in the serum are formed naturally. Their production is stimulated when the immune system encounters the “missing” ABO blood group antigens in foods or in micro-organisms. This happens at an early age because sugars that are identical to, or very similar to, the ABO blood group antigens are found throughout nature

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16
Q
  • The ABO locus has three main alleleic forms, what are they?
  • The A allele encodes what? What deoes it produce?
  • The B allele encodes what? WHat does it create?
A
  • The ABO locus has three main alleleic forms: A, B, and O.
  • The A allele encodes a glycosyltransferase that produces the A antigen (N-acetylgalactosamine is its immunodominant sugar)
  • The B allele encodes a glycosyltransferase that creates the B antigen (D-galactose is its immunodominant sugar).
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17
Q

The O allele encodes an enzyme with what? What is not produced

A

The O allele encodes an enzyme with no function, and therefore neither A or B antigen is produced, leaving the underlying precursor (the H antigen) unchanged

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18
Q

ABO expression

  • Although the ABO blood group antigens are regarded as what? They are actually expressed on what?
  • Each human RBC expresses about how many group antigens?
  • What happens to the other blood cells?
  • In individuals who are “secretors”, a soluble form of the ABO blood group antigens is found where?
A
  • Although the ABO blood group antigens are regarded as RBC antigens, they are actually expressed on a wide variety of human tissues and are present on most epithelial and endothelial cells.
  • Each human RBC expresses about 2 million ABO blood group antigens.
  • Other blood cells, such as T cells, B cells, and platelets, have ABO blood group antigens that have been adsorbed from the plasma.
  • In individuals who are “secretors”, a soluble form of the ABO blood group antigens is found in saliva and in all bodily fluids except for the cerebrospinal fluid.
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19
Q

ABO expression

A number of illnesses may alter a person’s what?
* Patients can “acquire” the B antigen during what? What does this release?
* What does happen to patients during this time?

A

A number of illnesses may alter a person’s ABO phenotype.
* Patients can “acquire” the B antigen during a necrotizing infection during which bacteria release an enzyme into the circulation that converts the A1 antigen into a B-like antigen.
* During this time, patients should not receive blood products that contain the B antigen because their sera will still contain anti-B. Once the underlying infection is treated, the patients’ blood groups return to normal.

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20
Q

ABO expresion

Illness can also cause patients to “lose” what?
* Any disease that increases the body’s demand for RBCs may weaken the expression of what? (give example)
* In addition, ABO blood group antigens can be altered by what?

A

Illness can also cause patients to “lose” ABO blood group antigens
* Any disease that increases the body’s demand for RBCs may weaken the expression of ABO blood group antigens, e.g., thalassemia.
* In addition, ABO blood group antigens can be altered by hematological cancers that can modify the sugar chains that bear the ABO blood group antigens, lending to the use of the A and B antigens as tumor markers for acute leukemia, myeloproliferative disorders, and myelodysplasia.

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21
Q

Pretransfusion testing

What are the three types of serologic testing?

A
  • Type and screen
  • Antibody screening
  • Crossmatching in the lab
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22
Q

Pretransfusion testing ⭐️

  • For patients with negative antibody screening and no history of transfusion or pregnancy in the previous three months, samples can be collected when?
  • However, if the patient has been transfused or pregnant in the prior three months, or if this history is uncertain, a pre-transfusion sample is valid for how long?
  • For most hospitalized patients, a fresh sample must be taken when?
A
  • For patients with negative antibody screening and no history of transfusion or pregnancy in the previous three months, samples can be collected up to one month before surgery.
  • However, if the patient has been transfused or pregnant in the prior three months, or if this history is uncertain, a pre-transfusion sample is valid for only three days.
  • For most hospitalized patients, a fresh sample must be taken every three days
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23
Q

Type and Screen/antibody screening

What is the type and screen? What does it use to test?

A

The type and screen is a test designed to detect clinically significant antibodies to blood group antigens using an Indirect antiglobulin test (IAT). The recipient serum or plasma is incubated with a panel of red cells; usually, 2,3 or 4 (un-pooled) cells with a known blood group antigen profile.

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24
Q

The type and screen:
* If it the screening is positive, the next step is what? What is the method?
* The specificity of the antibody is determined based on what?
* Additional testing strategies may be required, namely the use of what?

A
  • If the screening is positive, the next step is to identify the specificity of the antibody and for which an extended panel of un-pooled reagent red blood cells is used (11-20 cell panel). The method includes testing samples against a sufficient number of reagent red cells that lack or express a particular blood group antigen.
  • The specificity of the antibody is determined based on the reactivity pattern of the antibody against the cell panel. Then probability calculation is performed, allowing a minimum requirement of the p-value of 0.05 to zero down on the antibody/antibodies.
  • Additional testing strategies may be required, namely the use of enhancement media (albumin, polyethylene glycol, low ionic strength solution, or chemical/enzyme treatment of the panel cells to aid identification.
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25
Q

What is the direct and indirect antiglobulin test?

A

direct-detects antibodies on surface of RBC - add pts RBCs to combs reagent
indirect- detects antibodies in the serum- add pts plasma to rbcs then reagent

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26
Q

Fill in

A
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27
Q

Blood transfusions risk transmitting infectious microorganisms
* The most common ones are what?
* These number vary based on what?

A
  • The most common ones - in descending order are cytomegalovirus, or CMV, which can occur once every 100 transfusions, hepatitis B, which occurs about once every 200,000 transfusions, and hepatitis C and HIV, both of which occurs about once every 2 million transfusions.
  • These numbers vary quite a bit depending on the healthcare setting because the way blood is screened differs around the world.
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28
Q
  • The patient experiences risk of exposure based on what?
  • What is an example? (RBC, FFP and adult cryopreicpitate)
A

The patient experiences risk of exposure based on the amount of donors the product has come from

Example: Each unit of red cells exposes the patient to one donor per red cell unit transfused
* FFP to approximately 4 to 6 donors per adult dose (of 4 to 6 units FFP)
* Adult cryoprecipitate dose of 10 units (in 2 pools of 5 units each in the UK) results in a donor exposure of 10 donors per adult dose.

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29
Q

What happens with a mismatch?

If a recipient who has blood group O is transfused with non-group O RBCs, what will happen?

A

If a recipient who has blood group O is transfused with non-group O RBCs, the naturally occurring anti-A and anti-B in the recipient’s serum binds to their corresponding antigens on the transfused RBCs. These antibodies fix complement and cause rapid intravascular hemolysis, triggering an acute hemolytic transfusion reaction that can cause disseminated intravascular coagulation, shock, acute renal failure, and death.

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30
Q

Reactions typically occur due to what?
* Naturally occurring antibodies such as what? (2)
* Antibodies made in response to what? These are responsible for what?
* Antibodies present in the blood donor can also cause what?

A

Reactions typically occur due to mismatch or incompatibility of transfused product and the recipient
* Naturally occurring antibodies such as Anti-a and anti-b in the recipient
* Antibodies made in response to foreign antigens (alloantibodies). These are responsible for many reactions including mild allergic, febrile non-hemolytic, acute hemolytic, and anaphylactic
* Antibodies present in the blood donor can also cause reactions and are thought to be involved in transfusion-associated lung injury (TRALI)

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31
Q

Transfusion reactions

  • Range in what?
  • If the response happens during the transfusion it is termed what ?
  • If the response happens days to weeks later it is termed what?
  • Most common signs and symptoms include what?
  • Most symptoms resolve with what?
A
  • Range in severity from minor to life-threatening
  • If the response happens during the transfusion it is termed “Acute transfusion reactions”
  • If the response happens days to weeks later it is termed “Delayed transfusion reaction”
  • Most common signs and symptoms include fever, chills, urticaria, and itching
  • Most symptoms resolve with little or no treatment, but respiratory distress, high fever, hypotension, and hemoglobinuria indicate a more serious reaction
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32
Q

Transfusion reactions

All cases of suspected reactions should prompt what?

A

Immediate discontinuation of transfusion

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33
Q

What are the types of transfusion reaction?

A
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34
Q

Acute Transfusion Reactions

Acute hemolytic transfusion reactions
* Result in what?
* Immune-mediated reactions are often a result of what?
* Non-immune reactions are possible, and occur when red blood cells are what?

A
  • Can result in intravascular or extravascular hemolysis, depending on the specific etiology (cause).
  • Immune-mediated reactions are often a result of recipient antibodies present to blood donor antigens.
  • Non-immune reactions are possible, and occur when red blood cells are damaged
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35
Q

Acute Transfusion Reactions

Febrile non-hemolytic
* Generally thought to be caused by what?
* What can be done to combat this?

A

Generallythought to be caused by cytokines released from blood donor leukocytes (white blood cells). – can wash WBC’s to reduce this - leukoreduction

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36
Q

Acute Transfusion Reactions

What is sepsis caused by?

A

Septic:Caused by bacteria or bacterial byproducts (such as endotoxin) which may contaminate blood.

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37
Q

Acute Transfusion Reactions

  • What is a mild allergy?
  • What is anaphylactic?
A
  • Mildallergic:Attributed to hypersensitivity to a foreign protein in the donor product.
  • Anaphylactic: A more severe reaction. Sometimes this can occur in a patient with IgA deficiency who makes alloantibodies against IgA and then receives blood products containing IgA.
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38
Q

Acute Transfusion Reactions

  • Anaphylactic transfusion reactions are rare but potentially fatal and develop more commonly in patients withwhat? How does this occur?
  • How do you avoid this in the future?
A
  • Anaphylactic transfusion reactions are rare but potentially fatal and develop more commonly in patients withIgA deficiency.
  • These patients have no IgA and thus form anti-IgA IgG and IgE antibodies that bind to the IgA in the donor’s plasma and induce an anaphylaxis reaction.
  • To avoid such life threatening reactions, patients with known IgA deficiency usually wear a medical alert bracelet/necklace indicating their status.
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39
Q

Acute transfusion reactions

Transfusion-associated circulatory overload (TACO):
* Occurs when?
* What is potential complication of transfusion?
* Higher or low mortality rate?

A

Occurs when the volume of the transfused component causes hypervolemia (volume overload).
* all blood products are packed in fluid, and therefore, a potential complication of transfusions is fluid overload
* Higher mortality rate than TRALI due to effect on CV system

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40
Q

Acute transfusion reactions

Transfusion-related acute lung injury (TRALI):
* Acute lung injury is due to what?
* TRALI can start when?

A
  • Acute lung injury is due to antibodies in the donor product (human leukocyte antigen or human neutrophil antigen) reacting with antigens in the recipient.
  • TRALI can start within minutes to 6 hours after blood transfusion
41
Q

What is the underlaying mechanism of TRALI (two hit model)?

A
  • The first “hit” occurs before the transfusion process, when any stressor like sepsis, shock, or trauma, causes neutrophils in the blood to be recruited and sequestered in the pulmonary capillaries. These stressors also cause the neutrophils to be primed, meaning they’re prepared to start an inflammatory response when there’s another stressor or a second “hit”.
  • In TRALI, the second “hit” is the transfusion itself, where antibodies in the donor’s blood activate the primed neutrophils, giving them the signal to start an inflammatory response in the lungs. Neutrophils then respond by releasing inflammatory mediators like cytokines, proteases, oxidases and reactive oxygen species. This in turn will increase pulmonary capillary permeability, leading to fluid accumulation in the lungs’ interstitium. As a result, individuals develop noncardiogenic pulmonary edema, which is when the fluid accumulation is not due to cardiac causes like heart failure
42
Q

CXR findings - TRALI
* _ Infiltrates?
* Appearance?
* Heart size?
* Vascular structure?

A
  • Bilateral Infiltrates: TRALI often presents with bilateral diffuse pulmonary infiltrates on chest X-ray. These infiltrates typically manifest as patchy or confluent opacities throughout both lungs.
  • Ground-Glass Appearance: The infiltrates in TRALI may have a ground-glass appearance, meaning they appear hazy or cloudy, resembling ground glass.
  • Normal Heart Size: Unlike TACO, where heart enlargement may be evident due to fluid overload, TRALI typically does not show cardiomegaly on chest X-ray.
  • Normal Vascular Structures: TRALI usually does not involve prominent vascular congestion or redistribution seen in conditions like cardiogenic pulmonary edema.
43
Q

Delayed Transfusion Reactions

Delayed hemolytic transfusion reaction
* Typically caused by what?

A

Typically caused by an anamnestic response to a foreign antigen that the patient was previously exposed to (generallyby prior transfusion or pregnancy).

44
Q

Delayed Transfusion Reactions

Transfusion-associated graft-versus-host disease:
* Results from what?

A

Results from engraftment of donor lymphocytes (commonly found in cellular blood products) into an immunocompromised recipient’s bone marrow. The donor lymphocytes recognize the patient as foreign and react against the recipient’s body. The patient’s immune system is unable to clear the foreign lymphocytes. This is rare but often fatal.

45
Q

Rh
* Complex or simple?
* Named after what?
* Important?
* Rh status is routinely determined in who?
* Rh incompatibility in who?

A
46
Q

Rh
* An individual is either what? What type of blood can each one recieve? ⭐️

A

An individual is either Rh-positive, meaning they have the antigen on their red blood cells, or Rh-negative, meaning it is absent.
* People who are Rh-positive canreceiveboth Rh-negative and Rh-positive blood.
* Individualswith Rh-negative blood should only receiveRh-negative bloodto prevent hemolytic transfusion reactions.

47
Q

Rh + and - can what in terms of dominant and recessive?

A
  • Rh+ = presence of Rh protein (dominant)
  • Rh- = absence of the Rh protein (recessive)
48
Q

Rh
* Creates IgG antibodies that require prior exposure through what?
* How many donors are negative?

A
  • Creates IgG antibodies that require prior exposure through transfusion or pregnancy
  • 15% of North American donors are negative
49
Q

What happens in Rh incompatibility?

A

InRh incompatibility, maternal anti-D IgG antibodiesform after maternal exposure to fetal Rh positive blood during birth or pregnancy-related complications. The initial pregnancy is not affected; however, subsequent pregnancies are at risk offetal hemolysisand, in severe cases, intrauterine hydrops fetalis, secondary to the passage ofmaternal anti-D IgG across the placenta.

50
Q

Hemolytic disease of the newborn (HDN)
* Caused by what two reasons?

A
  • By ABO antibodies in infants of blood group A or B who are born to group O mothers.
  • Can also happen with incompatibility of Rh+/Rh-
51
Q

Hemolytic disease of the newborn (HDN)
* By ABO antibodies in infants of blood group A or B who are born to group O mothers.
* This is because why?
* Whereas the anti-A and anti-B found where?
* Although uncommon, cases of HDN have been reported in infants born to mothers with blood group

A
  • This is because the anti-A and anti-B formed in group O individuals tend to be of the IgG type (and therefore can cross the placenta),
  • Whereas the anti-A and anti-B found in the serum of group B and A individuals, respectively, tends to be of the IgM type.
  • Although uncommon, cases of HDN have been reported in infants born to mothers with blood group A2 and blood group B.
52
Q

Hemolytic disease of the newborn
* HDN tends to be relatively mild in nature mainly because why?
* Any degree of hemolysis can be what?

A
  • HDN tends to be relatively mild in nature mainly because fetal RBCs don’t express adult levels of A and B antigens. However, the strength of fetal ABO blood group antigens can vary
  • Any degree of hemolysis can be detrimental.
53
Q

Hemolytic disease of the newborn
* After birth the baby may have the following:

A
  • Severe hyperbilirubinemia and jaundice – the babies liver can’t handle the large amount of bilirubin
  • Kernicterus – most severe form of hyperbilirubinemia – build up of bilirubin in the baby’s brain
54
Q

Hemolytic disease of the newborn
* Rh negative mothers that have not been sensitized, receive what? What does this do and when do they get it?
* If the baby is Rh positive, the mother gets what?

A

Rh negative mothers that have not been sensitized, receive injection called Rh immunoglobin (Rhogam) which will stop Rh antibodies from reacting to the babies Rh positive cells – received around 28 weeks of pregnancy
* If the baby is Rh positive, the mother gets a second dose within 72 hours after giving birth

55
Q

In situations where Rh D negative units are unavailable, Rh D positive units may be given to who?
* What is this based on?

A

In situations where Rh D negative units are unavailable, Rh D positive units may be given to men and women over reproductive age after they have been determined to lack anti-D antibodies. This practice is known as “Rh compatibility” or “Rh-matched transfusion” and is based on the understanding that individuals who lack Rh D antigens on their red blood cells (Rh D negative) will not develop antibodies against Rh D antigens upon exposure to Rh D positive blood if they have not previously been sensitized.

56
Q
  • Rh D Incompatibility?
A
  • Rh D Incompatibility: Rh D incompatibility occurs when an Rh D negative individual is exposed to Rh D positive blood, leading to the potential development of anti-D antibodies. This can occur during pregnancy, blood transfusions, or other forms of blood exposure.
57
Q

What is the sensitization risk of Rh transfusion?

A

Sensitization Risk: Sensitization to Rh D antigens is most concerning for women of childbearing age, as anti-D antibodies can cross the placenta during pregnancy and lead to hemolytic disease of the newborn (HDN) in Rh D positive fetuses of Rh D negative mothers. However, the risk of sensitization decreases significantly after menopause or surgical sterilization in women, and it is negligible in men.

58
Q

What is the pre-transfusion testing of Rh transfusion?

A

Pre-transfusion Testing: Before administering Rh D positive blood to an Rh D negative individual, pre-transfusion testing is performed to determine if the recipient has pre-existing anti-D antibodies. If no antibodies are detected, the risk of sensitization is considered minimal, especially in men and women over reproductive age.

59
Q

Transfusing blood products
* Blood products are transfused through what?
* What needs to happen to the line?
* What needs to happen before administering blood?
* Each unit should be transfused within when?

A
  • Blood products are transfused through IV tubing with filters
  • The line is primed first to help keep clots from forming in the IV line
  • 2 providers verify blood products before administering and patients must be monitored for possible reactions
  • Each unit should be transfused within 2-4 hours
60
Q

Whole blood
* Current indications for whole blood transfusion are what?
* What is the most widespread system of whole blood transfusion?
* Sometimes where?
* May lead to what?

A
  • Current indications for whole blood transfusion are generally very few
  • The US military buddy transfusion system is the most widespread system of whole blood transfusion
  • Sometimes in the trauma bay at civilian settings
  • May lead to complications such as volume overload
61
Q

Packed red blood cells (PRBC)
* RBC’s that have had most of what removed? What does it contain?
* Recommended to transfuse how much at a time? How much will increase?
* When do you transfuse a patient?

A
62
Q

Platelets
* in the middle of the last century, blood was collected in what?
* Introduced plastic bags which revolutionized blood storage – also found to be what?

A
  • in the middle of the last century, blood was collected in glass bottles, which depleted platelets in storage
  • Introduced plastic bags which revolutionized blood storage – also found to be gas permeable, which is essential for storing functional platelets
63
Q

Platelets:
* Platelets are a scarce resource, partly because of their short shelf life of what? Stored how?
* Platelet concentrations can be prepared from what?

A
  • Platelets are a scarce resource, partly because of their short shelf life of 5 days. Stored at room temperature – increases some infectious risk
  • Platelet concentrations can be prepared from whole blood or by apheresis
64
Q

Platelets
* Recommended dosing for an adult is what?
* What is the volume amount?
* Each unit of RDP will raise platelet count how much?

A
  • Recommended dosing for an adult is 6 units of pooled random donor platelets or one apheresis unit
  • Volume is 350-400mL
  • Each unit of RDP will raise platelet count 5-10k – standard 6 pack will therefore raise count by 30-60k
65
Q

Platelets
* Platelet transfusion is mainly indicated to treat or prevent what?
* Platelet transfusion threshold in bleeding patients (3)?

A

Platelet transfusion is mainly indicated to treat or prevent bleeding in patients with thrombocytopenia or platelet function disorder

Platelet transfusion threshold in bleeding patients
* < 50,000 in severe bleeding, including Dic
* <30,000 when bleeding, not life threatening, or considered not severe
* <100,000 for bleeding in multiple trauma patients or patients with intracranial bleeding

66
Q

Prophylactic platelet transfusion
* What are the levels/situations for transfusion

A
  • To prevent spontaneous bleeding – transfuse at less than 10,000
  • Before neurosurgery <100,000
  • Before major surgery <50,000
67
Q

Platelets
* Contraindication to platelet transfusion (2)

A
  • Thrombotic thrombocytopenia purpura (TTP) – due to the increased risk of thrombosis
  • HIT (heparin induced thrombocytopenia) is another condition where platelet transfusion may increase the risk of thrombosis – would only transfuse for pre-procedure or surgery
68
Q

Fresh frozen plasma (FFP)
* Indicated for what?
* What does it reverse?
* May not be tolerated in patients with what?

A
  • Indicated for the deficiency of coagulation factors with abnormal coagulation tests in the presence of active bleeding
  • For the reversal of warfarin in the presence of active bleeding
  • May not be tolerated in patients with liver disease as patients may not tolerate the infusion volumes necessary to achieve adequate hemostatic levels of coagulation factors
69
Q

Fresh frozen plasma (FFP)
* What is it?
* What does it contain?
* Standard dose will raise what?
* Each dose has how much fuild?

A
  • Fresh frozen plasma is the fluid portion of a unit of whole blood frozen in a designated time frame, usually within 8 hours
  • Contains all coagulation factors except platelets-> Fibrinogen, albumin , protein C, protein s, antithrombin, tissue factor pathway inhibitor
  • Standard dose will raise factor levels by approximately 20%
  • Each unit contains approximately 250mL of fluid
70
Q

Fresh frozen plasma (FFP)
* How is it stored?
* Must be administered when after thawing? When does it not be used?

A
  • Is stored at -30 Celsius and must be thawed in a water bath at 30-37 Celsius over 20-30min in a FDA cleared device
  • Must be administered immediately after thawing, can be stored again at 1-6 degree Celsius for up to 5 days
    * Should not be used if left at room temperature for more than 4 hours
71
Q

Fresh frozen plasma (FFP)
* What should happen if not used within 24 hours? Why?
* Comes in units, use a weight based dosing of what?
* Each unit of FFP contains how much?

A

If not used within 24 hours, should be discarded
* Once thawed the activity of clotting factors, particularly factor V and factor VIII decline gradually

Comes in units, use a weight based dosing of 10-20 mL/kg of recipient weight
* Each unit of FFP contains approximately 200-250mL

72
Q

70 kg patient, how much FFP do you give?

A

would require 700mL – divided by 250mL = 2.8 units

typical dosing 4-6 units

73
Q

Fresh frozen plasma (FFP)
* May need to be re-administered after what? Why?

A

May need to be re-administered after 6-8 hours if there is ongoing bleeding due to the short half-life of factor VII (2-6 hours)

74
Q

For the reversal of heparin, what should be used?

A

direct thrombin inhibitors, direct factor Xa inhibitors

75
Q

Cryoprecipitate
* Composed of what?
* How long can it stay frozen?
* After thawing it should be infused when?

A
  • Composed of fibrinogen, von Willebrand factor, and factors 8 and 13
  • Kept frozen for up to 36 months
  • After thawing it should be infused as soon as possible though it can be stored at ambient temperature for up to 4 hours
76
Q

Cryoprecipitate
* One unit, is how much fluid?
* How is generally transfused? What is increased and by how much?
* Cryoprecipitate delivers a high dose of what? What does it decrease the risk of?

A
  • One unit of Cryo is15-20 mLin volume and contains 150-250 mg of fibrinogen. Cryo is generally transfused in pools of 10 units, which should increase an adult recipient’s fibrinogen level by 50-100 mg/dL
  • Cryoprecipitate delivers a high dose of fibrinogen in a small fluid volume, compared with therapeutic doses of FFP, so cryoprecipitate may be considered as initial treatment when fibrinogen replacement in a small volume is desirable for example to minimize the risk of TACO
77
Q
A
78
Q
A
79
Q

ABG
* A blood gas can be performed on blood obtained from where?
* An ABG is specifically arterial blood. Provides information on what?
* Obtained through what? What do you need to do before blood draw?

A

A blood gas can be performed on blood obtained from anywhere in the circulatory system (artery, vein, capillary)

An ABG is specifically arterial blood
* Provides information on oxygenation and ventilation status, as well as acid-base balance

Obtained through arterial puncture, usually the radial artery
* Must complete a modified Allens test prior to draw

80
Q

ABG
* Must record what?
* Sample should be what?

A
  • Must record what amount of oxygen the patient is on at time of test
  • Sample should be placed on ice and analyzed as soon as possible
81
Q

What is the allen test?

A
82
Q
A
83
Q

Abg’s
* Your lungs and your kidneys do much of the work to keep what normal?
* Oxygen saturation (O2Sat) measures what?
* Partial pressure of oxygen (PaO2) measures what?

A
  • Your lungs and your kidneys do much of the work to keep your acid-base balance normal.
  • Oxygen saturation (O2Sat).This measures how much oxygen your red blood cells are carrying
  • Partial pressure of oxygen (PaO2).This measures the pressure of oxygen that’s dissolved in your blood. It helps show how well oxygen moves from your lungs to your bloodstream.
84
Q

Abg’s
* Partial pressure of carbon dioxide (PaCO2) measures what?
* Acid-base balance (pH level) measures what?
* Bicarbonate (HCO3)- is calculated by what?

A
  • Partial pressure of carbon dioxide (PaCO2).This measures the amount of carbon dioxide in your blood. It also shows how easily carbon dioxide can move out of your body.
  • Acid-base balance (pH level).This measures the acidity of your blood. Too much acid is called acidosis. Too much base (alkaline) is called alkalosis. These conditions are symptoms of other problems that upset the acid-base balance in your body.
  • Bicarbonate (HCO3)- is calculated using the measured values of pH and PaCO2 to determine the amount of the basic compound made from CO2
85
Q

What is metabolic acidosis, alkalosis?
What is repiratory acidosis and alkalosis?

A
  • Metabolic acidosis – pH<7.35, respiratory CO2 normal, bicarb low (<24mEq/L), split into anion and non anion gap
  • Metabolic alkalosis – pH >7.45, respiratory CO2 normal, bicarb level high
  • Respiratory acidosis – pH <7.35, CO2 elevated >45, elevated HCO3 (bicarb)
  • Respiratory alkalosis – pH >7.45, respiratory CO2 <35
86
Q

Respiratory acidosis is a state in which there is usually a failure of what? What does this cause?

A

Respiratory acidosis is a state in which there is usually a failure of ventilation and an accumulation of carbon dioxide. The primary disturbance of elevated arterial PCO2 is the decreased ratio of arterial bicarbonate to arterial PCO2, which leads to a lowering of the pH. In the presence of alveolar hypoventilation, 2 featurescommonly are seen are respiratory acidosis and hypercapnia.To compensatefor the disturbance in the balance between carbon dioxide and bicarbonate (HCO3-), the kidneys begin to excrete more acid in the forms of hydrogen and ammonium and reabsorb more base in the form of bicarbonate

87
Q

What is an example of resp alkalosis?

A

Example: hyperventilation (blowing off CO2) due to fever, pain, or anxiety

88
Q

What is romanski method of anaysis?

A
89
Q

ABG: pH = 7.39, PaCO2= 51 mm Hg, PaO2= 59 mm Hg, HCO3= 30 mEq/L and SaO2= 90%, on room air.
* How would you use romanski method of analysis on this?

A
  • pH is in the normal range, so use 7.40 as a cutoff point, in which case it is < 7.40, and acidosis is present.
  • The elevated PaCO2indicates respiratory acidosis, and the elevated HCO3indicates a metabolic alkalosis.
  • The value consistent with the pH is PaCO2. Therefore, this is a primary respiratory acidosis. The acid-base that is inconsistent with the pH is the elevated HCO3, indicating a metabolic alkalosis, so there is compensation signifying a non-acute primary disorder because it takes days for metabolic compensation to be effective.
  • Last, the decreased PaO2indicates an abnormality with oxygenation. However, a history and physical will help delineate the severity and urgency of required interventions, if any
90
Q

ABG: pH = 7.45, PaCO2= 32 mm Hg, PaO2= 138 mm Hg, HCO3= 23 mEq/L, the base deficit = 1 mEq/L, and SaO2is 92%, on room air.
* ROMANSKI METHOD OF ANALYSIS?

A
  • pH is in the normal range. Using 7.40 as a cutoff point, it is >7.40, so alkalemia is present.
  • The decreased PaCO2indicates a respiratory alkalosis, and the HCO3is normal but on the low end of normal.
  • The value consistent with the pH is PaCO2. Therefore, this is a primary respiratory alkalosis. The HCO3is in the normal range and, thus, not inconsistent with the pH, so there is a lack of compensation.
  • Last, the PaO2is within the normal range, so there is no abnormality in oxygenation.
91
Q
A
92
Q

What is the anion gap used for? What is the mnemonic?

A
93
Q

Non-gap metabolic acidosis is primarily due to what?

A
94
Q
  • What is Venous oxygenation saturation (SVO2) ?
  • When oxygen supply is insufficient to meet the metabolic demands of the tissues, what will happen?
  • SVO2 dependent on what?
  • Venous blood in the pulmonary artery represents what? what is that called?
A
95
Q

Venous oxygenation saturation (SVO2)
* how is it measured?

A

Measured using a pulmonary artery catheter

96
Q

Venous oxygen saturation
* How is it used diagnostic?

A

As a diagnostic, derangement in venous oxygen saturation can ascertain the underlying etiology. The oxygenconsumption by the tissues by the whole body (VO2) is usually independent of oxygen delivery (DO2). This is because a decrease in DO2 is compensated by an increase in VO2, thereby preventing tissue hypoxia. However, whena’critical’ DO2 is reached, and no further oxygen can be extracted, tissue hypoxia and lactic acidosis sets in.These changes are reflected in venous oximetry andmustbe interpreted correctly in conjunction with other hemodynamic parameters (CO, arterial oxygen content).

97
Q

Mixed venous
* how does this play a role with cardiovascular response?

A

The cardiovascular response to an increase in oxygenrequirement and VO2is an increase in arterial oxygen content or an increase in CO. When these compensatory mechanisms fail to occur, and DO2 drops, a decrease in SvO2is seen. SvO2 also drops if the compensatory mechanisms are insufficient to meet the metabolic demands of the tissues.SvO2 can drop toas low as 30-50% before tissue oxygen extraction is exhausted, and there is an onset of anaerobic metabolism

98
Q

⭐️ ⭐️⭐️⭐️⭐️⭐️⭐️⭐️⭐️⭐️⭐️

Mixed venous results
* What is normal?
* What is compensatory?
* What is exhaustion of extraction?
* What is severe lactic acidsosis?
* What is cell death?

A

Medical Diagnosis (16 decks)

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