Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

True Learn-Advanced > Heme > Flashcards

Heme Flashcards

1
Q

When patients have VW dz, why would you choose cryo over FFP in hemorrhage setting?

A

Because cryo can be used to infuse VWF without the large volume.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What all is in cryo?

A

Factor 8, VWF, Factor 13, and fibrinogen.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is VWF? If it’s messed up, what other things are messed up? Inheritance pattern.

A

plasma protein that helps platelets adhere to site of injury and stabilizes clotting factor 8. If VWF is messed up, so will platelet adhesion and factor 8. Inheritance: autosomal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Types of VWD and their severity

A

Type 1, type 2 (2 parts), and type 3.

Type 1: partial decrease (quantitative), Type 2: qualitative defect, Type 3: total depletion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

3 strategies to treat VWD

A

1: DDAVP-it increases endogenous concentrations.
2: increase it from an exogenous source of actual DDAVP.
3: Homeostasis and wound healing and given FFP and cryo. KIM FFP you’d have to give so much volume.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Multiple myeloma causes what main symptoms? and infection?

A

bone pain, osteolytic destruction, hypercalcemia, anemia, immunosuppression leading to recurrent infections-d/t overproduction of ineffective monoclonal antibodies, renal failure and neurologic symptoms.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

At the minimum, a sickle cell patient needs to have: ___. Optimum Hct: ____. KIM that it may take a while for their blood to be typed and crossed due to antibodies from previous transfusions, so you will want to have that ready if necessary.

A

a CBC. Hct should be between 30-40%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

In addition to dehydration, what else should SC patient avoid?

A

Avoid hypotension, hypothermia, hypoxemia, hypovolemia and acidosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

SvO2 vs ScvO2: What’s the difference, and which number is higher?

A

ScvO2 is measured in the right atrium, and gets most contribution from SVC. SvO2: true mixed venous saturation measuring blood fro mupper and lower extremities. ScVO2 is typically 5-10% higher than SvO2 due to highly deoxygenated blood from coronary sinus that isn’t being accounted for in ScvO2 measurement.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the 4T’s of HIT? Normal scoring?

A

Thrombocytopenia, Timing of reduced platelet count, Thrombosis, Exclusion of oTher causes. Score of 0-3= low probability, 6-8= high probability. Test on 5/20 for chart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Max effect of DDAVP?

A

seen within 30 minutes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What do you give a pt with Type 1 VWF who will be having a minor surgery? Major surgery?

A

Minor surgery: DDAvP

Major surgery: vWf concentrate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Desmopressin is similar to what hormone and therefore can cause what?

A

similar to ADH and can cause hyponatremia and water retention.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How to treat type 1 vWf:

A

Type 1: ddavp
Type 2: trial of DDAVP-avoid if type 2B, factor concentrate
Type 3: Virus inactivated, vWF containing factor FVII concentrate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Leukopenia is NOT involved in any type of transfusion reaction EXCEPT: ___. What exactly is TRALI? When would you see it? What poses the highest risk?

A

TRALI. This happens because agglutination of leukocytes in recipient’s pulmonary microcirculation.
TRALI: non-cardiogenic pulmonary edema during or after a blood transfusion-ALI/ARDS within 6 hours of blood product administration. Plasma or whole blood from female donors has the highest risk.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Hallmark of TRALI: __. Gold standard for diagnosing? Can’t diagnose if: ___. Treatment:

A

increased permeability of the pulmonary microvasculature with resultant edema. this means hypoxemia, pulmonary infiltrates, hypotension. No gold standard in Diagnosis, and if there is an alternative risk factor for ALI or ARDS, a formal diagnosis of TRALI can’t be made. Treatment: supportive.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

For which blood transfusion reaction is the direct Coombs test helpful?

A

Hemolytic transfusion reaction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Cryo has lots of:

A

fibrinogen, vWF, and factors 8 and 13.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Which laboratory test is used to monitor the AC response to enoxaparin? What exactly is enoxaparin? Why can it be better than Heparin? What do you have to watch out for?

A

Factor Xa activity. It’s a LMWH. Dosing is more simple than UFH and they are therefore good for outpatient use, it also has a more predictable level of AC. BUT-watch out for the kidneys.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How does heparin work? How is it monitored?

A

It binds to and enhances the effects of AT3, and inactivates other clotting factors-making it unpredictable. It is monitored using PTT.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How does enoxaparin work?

A

It also binds and enhances effects of AT3, BUT it preferentially inhibits factor Xa.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Does platelet count represent the therapuetic effect of enoxaparin?

A

No, but it should be checked due to risk of HIT.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How can you treat AT3 deficiency?

A

By giving AT3 and/or FFP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

So, you did a spinal and now you have an awake patient with acute blood loss. What metabolic derrangements are you going to see?

A

Metabolic acidosis with a compensatory respiratory alkalosis. Inadequate organ perfusion cancause the acidosis. An awake and alert patient will compensate by hyperventilating=respiratory alkalosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How long does it take for the body to renally compensate for an acidosis?

A

About 24 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

When a patient is losing blood, how much can it hold out before having hypotension?

A

At 25% it can just increase heart rate and increase catecholamines, but at 40%, you start seeing clinical signs of shock including hypotension.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What brings about attacks in acute intermittent porphyria (AIP)

A

Alcohol is an inducer of the P450 system which leads to an increase in ALA (aminolevulinic acid) concentration. This increase in ALA concentration can precipitate an attack. Barbiturates and high dose benzodiazepines are also contraindicated in AIP for their induction of the P450 system as well.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is AIP?

A

Acute intermittent porphyria (AIP) is the most common form of porphyria. AIP is an autosomal dominant condition that results from an error in porphobilinogen deaminase, an enzyme involved in heme synthesis. Symptoms of AIP are often vague and include abdominal pain, diarrhea or constipation, and neurological complaints. Attacks are often precipitated by conditions that increase aminolevulinic acid (ALA).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Glucocorticoids like dexamethasone-can you use them in AIP?

A

NO.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Dextrose and AIP?
What do you need to avoid temp wise when it comes to AIP?
Sux and AIP-

A

Dextrose is considered safe for use in AIP and is used to suppress ALA synthase. Glucose causes negative feedback and inhibits ALA synthase. Glucose administration, hydration, and avoidance of hypothermia are very important when treating patients with porphyria.
Sux is okay in patients with AiP.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Teardrop shape and TEG: what does this shape mean?

A

Clinically, a “teardrop” shape is used more often to support a diagnosis of increased fibrinolysis than are specific numerical values or measurements.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

TEG: R time-what does it measure? Normal range?

A

Reaction time (R) is from time zero to initial clot formation, defined as a width (amplitude) of 2 mm. Normal range is 1-3 minutes.

33
Q

TEG: Coagulation time K, what conclusion can you draw from it?

A

Coagulation time (K) measures speed of clot formation and strengthening. It is equal to the time from amplitude of 2 mm to 20 mm and relies on fibrinogen. Note that some TEG images show varying lengths for K, but it is always measured to 20 mm amplitude

34
Q

TEG: MA-what does it mean? what about its width?

A

Maximum amplitude (MA), measures the strength of the fully formed clot. It is the maximal width of the TEG. This reflects clot strength as determined by platelet number and function (primarily) as well as fibrin cross-linking. Normal is 50-60 mm

35
Q

What is the alpha angle? what does it rely on?

A

Alpha-angle is the speed of clot formation, and is represented by the angle between baseline and a line tangential to the TEG at 2 mm amplitude. Like the K value, this relies on fibrinogen. Normal alpha angle is 45-55 degrees

36
Q

What would tell you you have decreased fibrin or deficient fibrin formation?

A

Prolonged K values suggest deficiencies of thrombin formation or generation of fibrin from fibrinogen/inadequate fibrinogen. A decrease of the alpha angle has similar implication to a prolongation of K. Measures of clot lysis consistent w/ dramatically narrowing amplitudes and short, tapering rates of fibrinolysis (teardrop configuration) suggest abnormal fibrinolysis. Treatment is with antifibrinolytics.

37
Q

When would you have short R values

A

hypercoaguable state or aggressive factor replacement

38
Q

New vs old TEG machines and how they deal with hypothermia

A

Hypothermia can cause coagulopathy by interfering with both platelets and coagulation factors. When the blood of a cold and coagulopathic patient is placed in the TEG cuvette, which is normally heated to 37 degrees Celsius, a (near) normal trace may be obtained. Newer TEG devices are temperature-adjustable to help avoid this issue.

39
Q

What does cryo have in it?

A

Cryoprecipitate contains von Willebrand factor (vWF), fibrinogen, fibronectin, factor VIII (8), and factor XIII (13)

40
Q

Photo of indications for cryo

A

okay

41
Q

Why would you have prolonged R values? How do you treat it?

A

Prolonged R values result from coagulation factor abnormalities, factor deficiencies, or heparin administration. Treatment consists of giving fresh frozen plasma (FFP)

42
Q

MA value decreased; give:

A

platelets

43
Q

K value prolonged; give:

A

cryoprecipitate

44
Q

R value prolonged; give:

A

FFP

45
Q

Teardrop formation give:

A

anti-fibrinolytics Some examples of antifibrinolytic drugs are aprotinin, tranexamic acid (TXA), epsilon-aminocaproic acid and aminomethylbenzoic acid.

46
Q

Factor VII becomes deficient in the setting of liver disease because it

A

It has a very short half-life (approximately 6 hours). This deficiency serves to prolong the PT.

47
Q

How does cystic fibrosis result in a prolonged PT?

A

Factor VII requires vitamin K for synthesis. Vitamin K deficiency, therefore, can lead to prolonged PT values. Dietary deficiency of vitamin K is generally rare, though it can result from prolonged NPO status, such as patients dependent on total parenteral nutrition, or those with severe malabsorption syndromes. Patients with cystic fibrosis may develop bile obstruction or pancreatic insufficiency. Vitamin K is a fat-soluble vitamin and either of these conditions can result in deficiency due to malabsorption.
Eye roll emoji

48
Q

Lupus prolongs which measurement (PT or PTT)? Is it real?

A

The presence of lupus anticoagulant prolongs activated partial thromboplastin time (aPTT), but not prothrombin time (PT). The phospholipid used as an activator for the aPTT measurement binds with the lupus anticoagulant and results in a prolonged aPTT. It is important to realize this is a laboratory finding. Patients with lupus anticoagulant are actually prothrombotic

49
Q

Prolonged PT may result from liver disease, cystic fibrosis, and warfarin treatment. Lupus anticoagulant results in prolonged aPTT alone. Prolonged PT and aPTT may result from DIC.

A

Thanks

50
Q

Define heparin resistance

A

Heparin resistance is defined as an activated clotting time (ACT) of < 480 seconds after 500 U/kg of IV heparin has been administered or an ACT < 400 seconds at any time during the course of cardiopulmonary bypass (CPB) and heparin administration

51
Q

How does heparin work?

A

Heparin functions by binding to the anticoagulant antithrombin III (AT3) and greatly enhancing its effects. Antithrombin III inactivates multiple coagulation factors including factors IIa (thrombin), VII, IX, X, XI, and XII. Hereditary or acquired AT3 deficiencies can result in heparin resistance such that normal doses of heparin fail to provide adequate anticoagulation

52
Q

Initial therapy for heparin resistance:

A

Initial therapy for heparin resistance is additional heparin, titrated to the required anticoagulant effects (usually measured by ACT). However, this may take substantial time and is not always effective. Other options for refractory or emergent situations include the administration of fresh-frozen plasma (FFP), AT3 concentrate, or recombinant AT3.

53
Q

Risk factors for the development of heparin resistance

A

Risk factors for the development of heparin resistance include: AT3 levels < 60% of normal, platelet count ≥ 300,000/mm^3, preoperative heparin therapy, use of low molecular weight heparin, and age ≥ 65 years. Treatment includes supplemental heparin, AT3, or FFP administration.

54
Q

Morbidly obese ppl have increased risks of DVT-why?

A

Morbidly obese patients have an increased risk of deep vein thrombosis due to higher circulating pro-coagulation factors.

55
Q

What is bivalrudin? MOA? and used for what? Contraindicated in what?

A

Bivalirudin is a direct thrombin inhibitor that may be used in patients with heparin-induced thrombocytopenia (HIT) that has evidence-based support for use in patients undergoing angioplasty and cardiac surgery with cardiopulmonary bypass.
Contraindicated in renal failure
Typical CPB dosing is a 1 mg/kg bolus followed by a 2.5 mg/kg/hr infusion.

56
Q

What is argatroban? can you use it with CPB? Do people do it anyway? contraindicated in who?

A

Argatroban (t1/2 39-51 min), a direct thrombin inhibitor. It is not approved for use with CPB, and is relatively contraindicated in liver failure. However, it is sometimes used for CPB despite being off-label because it is approved for HIT in the non-CPB setting.

57
Q

Explain Type I HIT

A

Heparin-induced thrombocytopenia occurs in two forms, both resulting from exposure to unfractionated or low molecular weight heparin. Type I HIT usually occurs within 2-5 days of heparin administration. It is characterized by mild thrombocytopenia and the absence of thrombosis. It is generally not considered clinically significant. The mechanism behind Type I thrombocytopenia is heparin binding to platelets at GPIb receptors causing the release of ADP, which results in platelet aggregation.

58
Q

Explain Type II HIT:

A

Type II HIT occurs 5-9 days after heparin administration; therefore, a patient may no longer be on heparin at the time of presentation. There are also uncommon cases of rapid onset HIT Type II, which can occur within hours of previously exposed patients (but for examination purposes, go with what occurs commonly). The thrombocytopenia in Type II HIT is more severe, with platelet counts < 100k or a fall of >30-50% from baseline values over several days. The mechanism is via IgG-, IgA-, and IgM-mediated antibodies towards heparin and platelet factor 4 (PF4) complexes, which results in platelet activation and clot formation. About 20% of patients with Type II thrombocytopenia will develop thrombosis due to massive thrombin generation (HIT with thrombosis or HITT); the mortality rate in this population is high. If heparin is used for anticoagulation during cardiac surgery in a patient with positive antibodies, the risk of mortality and/or MI may increase at least twofold.

59
Q

Gold standard for diagnosis of HIT

vs other tests:

A

Heparin-induced serotonin release assay (SRA). This is considered the GOLD STANDARD for diagnosis.Enzyme-linked immunosorbent assay (ELISA) specific for heparin and PF4 complexes. Although these patients may have a positive test they do not always go on to develop thrombosis.
3) Heparin-induced platelet activation assay. The table below may serve as a primer for serologically diagnosing HIT type II:

60
Q

Direct thrombin inhibitors should be considered for cardiopulmonary bypass (CPB), but it is important to remember

A

It is important to remember that there are no reversal agents for these anticoagulants.

61
Q

What is hirudin?

A

Hirudin (t1/2 40 min) is a direct thrombin inhibitor derived from the medicinal leech Hirudo medicinalis. Anticoagulation is followed with the ecarin clotting time (ECT). Ecarin is a prothrombin activator, generally not available clinically, which is derived from viper venom. Lepirudin is a recombinant form of hirudin with essentially identical properties.

62
Q

Direct thrombin inhibitors include

A

hirudin, lepirudin, bivalirudin, argatroban, and ximelagatran.

63
Q

What should you administer during massive transfusion protocol to prevent dilutional coagulopathy

A

Fresh frozen plasma administration should occur during massive transfusion to reduce the risk of dilutional coagulopathy

64
Q

Hemophilia A-Pt vs PTT-which one is prolonged? which one is normal?

A

Hemophilia A is an X-linked inherited deficiency of factor VIII, however as many as one-third may occur without any known family history of the disease. aPTT in these patients is prolonged and PT is normal.

65
Q

________ is classically the first line agent for treatment of Hemophilia A patients with minor bleeding or who are planning to undergo minor surgical procedures.
In the event of active bleeding, what would you choose and why?

A

Desmopressin
In the event of active bleeding, cryoprecipitate is typically the product of choice as it contains high concentrations of factor VIII and fibrinogen.

66
Q

VIIa acts through the _____ pathway, VIII is a part of the _____ pathway, and IIa is _______.

A

VIIa acts through the extrinsic pathway, VIII is a part of the intrinsic pathway, and IIa is downstream of the union of the two pathways.

67
Q

Sooo…if someone has Hemophilia A, but has antibodies against factor 8, what can you do? FFP? Recombinant factor 8?

A

No to FFP because it also has factor 8 and the antibodies will fight it. No to recombinant because antibodies will fight it too.

You can give recombinant factor VIIa, or recombinant factor IIa, or you can do PCCs

68
Q

How does anemia affect coagulation?

A

Although the exact cellular mechanisms have not been completely elucidated, anemia exerts effects on the coagulation cascade. Anemia is associated with a delay in the initiation of the coagulation cascade, a stronger clot, and a clot with superior viscoelastic properties.

69
Q

Transfusion of RBCs is associated with what as far as clot quality?

A

Transfusion of red blood cells is associated with impaired clot quality, with even worse effects on the initial fibrin build-up and clot quality by fresh red cells.

70
Q

Bleeding disorder chart photo

A

Okay

71
Q

If a patient has antibodies to factor 9, then what can you treat it with?

A

In patients with hemophilia B and factor IX inhibition, treatment with recombinant factor VIIa is preferred as there is less of a risk of anaphylactoid reactions when compared with PCCs.

72
Q

Initially in patients with anemia, how does the body compensate? Then what?

A

Initially, the body will compensate for anemia and the decreased arterial oxygen concentration by shifting the oxygen-hemoglobin dissociation curve to the right, allowing more off-loading of oxygen to the tissues. This is followed by redistribution of blood from the skin and kidneys to the ‘critical’ organs (e.g. brain and myocardium)

73
Q

What is Factor V Leiden? What is protein C? What’s most common? Do they get arterial thrombosis?

A

REsistance to Protein C. APC is a natural anticoagulant that works by cleaving and inactivating factors V and VIII. Factor V is a pro-coagulant clotting factor that increases the production of thrombin, which is the enzyme responsible for forming fibrinogen from fibrin. In patients with factor V Leiden, a point mutation in the gene for factor V abolishes the cleavage site of APC, making it resistant to inactivation. The inability to inactivate factor V ultimately leads to increased thrombin and therefore fibrinogen production, leading to a hypercoagulable state. Factor V Leiden is the most common inherited thrombophilia in Caucasians and the most common inherited hypercoagulable state.
Arterial thrombosis in patients with only factor V Leiden is very rare.

74
Q

Treatment of Factor V Leiden:

Is there ever an instance where a patient would need lifelong treatment?

A

The initial management of venous thrombosis in patients with factor V Leiden is the same as the management for the general population. Anticoagulation with either unfractionated heparin or low molecular weight heparin should be started immediately, followed by treatment with warfarin or a direct factor Xa inhibitor. This should be continued for a minimum of 3-6 months. The INR goal for those treated with warfarin is 2-3; the same as the general population.

Lifelong treatment if: (INR goal still 2-3)
Two or more spontaneous thromboses
- One spontaneous thrombosis if the patient has factor V Leiden plus another prothrombotic mutation
- One spontaneous life threatening thrombosis (e.g. near fatal PE)
- One spontaneous thrombosis at an unusual site (e.g. cerebral or mesenteric vein)

75
Q

Citrate binds to what???

A

Citrate is found in blood storage preservatives where it acts as an anticoagulant. Once transfused, large amounts of citrate reversibly bind (chelate) ionized calcium which may lead to hypocalcemia in the setting of rapid transfusion and liver dysfunction. This leads to hypotension, narrow pulse pressure, increased LVEDP, prolonged QT interval, narrowed QRS, and flattened T waves.

76
Q

What does CPDA? And what does each letter stand for?

A

CPDA-1 anticoagulant allows PRBC and whole blood storage for up to 35 days

          - Citrate is the anticoagulant (binds calcium necessary for clot formation) 
          - Phosphate is incorporated for cellular function and ATP production 
          - Dextrose is the nutrition source for glycolysis 
          - Adenine is incorporated for ATP production
77
Q

When would you use fructosamine?

A

Fructosamine testing in diabetes measures a shorter time interval compared with hemoglobin A1c and is typically used for patients who have reduced red cell lifespans (e.g. hemolytic anemia, sickle-cell disease). A HgA1c level of ≥ 6.5% is diagnostic for diabetes mellitus.

78
Q

Does glucose bind irreversibly to RBC?

A

Yes

True Learn-Advanced (16 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions