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SEE NCE Boards CoreConcepts > Hematology - Anesthesia Review > Flashcards

Hematology - Anesthesia Review Flashcards

1
Q

The extrinsic pathway is initiated by the release of a group of proteins known as _________when tissues are damaged?

A

Tissue Factor when tissues are damaged.

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2
Q

Tissue Factor forms a complex with and

A

Factor VII, and in an enzymatic reaction requiring calcium, catalyzes the activation of Factor X.

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3
Q

Proaccelerin is the other name for factor

A

Factor V

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4
Q

Exposure of the blood to collagen can initiate the

A

intrinsic pathway.

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5
Q

Fibrinogen is another name for

A

factor I.

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6
Q

Sickle cell and hematocrit

A

Sickle cell and hematocrit results in the destruction of red blood cells which lowers the hematocrit

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7
Q

Labs that are elevated in acute DIC

A 
PT
PTT
Thromboplastin time
D-dimer
Fibrin degradation products
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8
Q

The circulating levels of what components will be increased by DDAVP administration in a patient with von Willebrand disease? 2 answers

A

Von Willebrand disease

Factor VIII

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9
Q

Medications that are considered safe for use in patients with porphyria.

A

Nitrous oxide, neostigmine, morphine, fentanyl, succinylcholine, pancuronium, and propofo

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10
Q

Medications that are NOT considered safe and should all be avoided for patients with Porphyria?

A

Ketorolac
thiopental
thiamylal
etomidate, pentazocine, methohexital, and nifedipine s

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11
Q

Factor X deficiency is _______deficiency

A

Stuart-Prower

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12
Q

Aspirin and other NSAIDs on platelet

A

acetylate and inactivate platelet cyclooxygenase.

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13
Q

Aspirin inactivates cyclooxygenase for

A

the life of the platelet

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14
Q

Unlike ASA, NSAIDs inactivate them how and how long does it last?

A

Reversibly, and the effect lasts only about 24 hours.

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15
Q

In the extrinsic coagulation pathway, disruption of the endothelium leads to exposure of tissue factor which binds to

A

factor VII

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16
Q

Tissue Factor forms a complex with Factor VII, and in an enzymatic reaction requiring

A

calcium, catalyzes the activation of Factor X.

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17
Q

Porphyria is a disorder of

A

Heme

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18
Q

Why are Heme pigments essential?

A

are essential elements in the construction of hemoglobin, myoglobin, and the cytochrome

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19
Q

Many pharmacologic agents (especially those that induce the cytochrome p450 system) can precipitate a porphyric crisis such as

A 
BarbSulfaPhenyEtha
Barbiturates
Sulfonylureas
Sulfonamides
Estrogens, phenytoin, tolbutamide, and ethanol.
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20
Q

The underlying cause of organ failure due to disseminated intravascular coagulation is

A

organ ischemia due to thrombosis

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21
Q

What is the second most common cause of hospitalization in sickle cell patients and accounts for 25% of all sickle cell related deaths.

A

Acute chest syndrome

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22
Q

How is acute chest syndrome diagnosed?

A

It is diagnosed by the development of new infiltrates on chest film and may be caused by atelectasis, pulmonary microembolic episodes, or pulmonary infection.

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23
Q

Acute chest syndrome is a potential complication of sickle cell disease. When it develops, it is typically ___days following surgery and

A

2-3

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24
Q

Treatment of acute chest syndrome

A

Aggressive hydration
oxygenation, transfusions to treat anemia
antibiotics to treat pulmonary infection, and occasionally nitric oxide may be used to treat pulmonary hypertension.

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25
Q

Which form of hemoglobin is most commonly found in the normal, adult bloodstream?

A

hemoglobin A

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26
Q

Hemoglobin C is implicated in a type of

A

hemolytic anemia,

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27
Q

2 agents would be appropriate to administer in the treatment of a patient with von Willebrand disease?

A

Cryoprecipitate AND Desmopressin

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28
Q

What is the dose of desmopressin?

A

0.3mcg/kg

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29
Q

Desmopressin given for mild to moderate hemophilia will increase what factors

A

increase plasma levels of factor VIII and vWF

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30
Q

Cryoprecipitate vs FFP which one is preferred for hemophilia A?

A

Cryoprecipitate preferred because it is hard to increase the factors level with FFP alone.

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31
Q

3 treatments for hemophiliac patients : Other than desmopressin

A

Cryoprecipitate
Tranexamic acid
Epsilon aminocaproic acid.

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32
Q

Synthetic Arginine analog of Vasopressin

A

Desmopressin

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33
Q

Cryoprecipitate is made how?

A

Collected off the top of FFPs at it being thawed

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34
Q

In the intrinsic pathway, what is the component required to convert factor XII to factor XI?

A

Prekallikrein

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35
Q

Romponents like High Molecular Weight Kininogen required to activate

A

Factor XI.

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36
Q

Commonly given medication to avoid porphyria crisis

A

Ketorolac

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37
Q

Both hemophilia A and hemophilia B exhibit a

A

prolonged PTT and a normal PT.

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38
Q

The primary function of von Willebrand factor is

A

To promote platelet aggregation and adhesion to collagen

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39
Q

Potential side effect of DDAVP administration in the treatment of von Willebrand disease?

A

HoTN

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40
Q

What treatment regimens are effective in ameliorating the symptoms of von Willebrand disease? (select two)

A

Desmopressin and concentrated von Willebrand Factor are both effective in treating the symptoms of von Willebrand disease.

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41
Q

Factor IX-PCC is used in the treatment of

A

Hemophilia B

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42
Q

Major surgery –> how to replace vWF

A

achieve 100% vWF preoperatively and maintain trough levels of 50% until adequate wound healin

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43
Q

In treating type 1 vWD which agent is preferred?

A

Desmopressin because it produces a complete partial response in more than 90% of patients

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44
Q

In treating type 2 and type 3 vWD which agent is preferred?

A

Type 2 and type 3 require vWF concentrate administration.

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45
Q

Heparin-Induced Thrombocytopenia (HIT) Type I and Type II

A

type I non immune mediated, onset 1-4 days

type II immune mediated (immunoglobulin G) 5-14 days

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46
Q

Blood component therapy for HIT

1. Indications: active bleeding or high risk for bleeding

A
  1. Fresh frozen plasma
  2. Platelets
  3. In some cases, consider cryoprecipitate, antithrombin III
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47
Q

Most events of acute stent thrombosis occur within the

A

first 30 days after stent placement

48
Q

Absolute contraindication to neuraxia

A

Thrombolytics

49
Q

When is there no contraindication for heparin SC dosing for neuraxial.

A

No contraindication with twice-daily dosing and total daily dose < 10,000 units

50
Q

Upper endoscopy and colonoscopy with or without biopsy –> Warfarin stop?

A

NO NEED for interruption in therapy

51
Q

• Endoscopic retrograde cholangiopancreatography (ERCP) without sphincterotomy Warfarin stop ?

A

NO NEED for interruption in therapy

52
Q

Do not need to stop warfarin for these procedures?

A

Prosthetics

Cataracts

53
Q

Elective noncardiac surgery should be delayed______after bare metal stent and _______after DES

A

30 days after bare metal stent (BMS) implantation and optimally 6 months after drug eluting stent (DES) implantation

54
Q

Discontinue ticlopidine _____days prior to neuraxial

A

14 days

55
Q

Discontinue clopidogrel ____Days prior to neuraxial

A

7 days

56
Q

Discontinue GP IIB/IIIa inhibitors _______prior to neuraxial.

A

8–48 hours in advance

57
Q

A powerful vasodilator, also interferes with platelet formation and aggregation is ______

A

prostacyclin

58
Q

Anatomy of a platelet

A

Platelets contain alpha (α) granules that store proteins (e.g., vWF, fibrinogen, fibronectin, platelet factor 4, and platelet growth factor) and dense granules that store nonproteins (e.g., serotonin, ADP, adenosine triphosphate [ATP], histamine, and epinephrine).

59
Q

Converts to plasmin

A

Plasminogen

60
Q

3 Vasoconstrictors of vessesl

A

Thromboxane A2
ADP
Serotonin

61
Q

3 Vasodilators of vessels

A

Nitric oxide

Prostacyclin

62
Q

Vessel Injury contracts after injury leading to

A

a tamponade, decreasing blood flow. This contraction is a result of autonomic nervous system reflexes and the expression of thromboxane- A2 and ADP. The area adjacent to the injury vasodilates and distributes blood to the surrounding organs and tissues

63
Q

After injury to the vessel , contraction leads to what

A

Contraction is followed by three separate stages in the formation of a primary plug: adhesion, activation, and aggregation.

64
Q

Factor not produced by the liver

A

III

65
Q

Substance synthesized vascular wall and extravascular cell membranes; released from traumatized cells

A

vonWillebrand

66
Q

Bleeding time Normal

A

3-7 minutes

67
Q

Normal ACT

A

80-150

68
Q

Normal PT

A

12-14 sec

69
Q

Normal PTT`

A

25-33

70
Q

Extrinsic (Warfarin vs Heparin)

A

Heparin

71
Q

Intrinsic (Warfarin vs Heparin)

A

Warfarin

72
Q

A normal platelet count is

A

150,000 to 300,000/mm3.2

73
Q

Adhesion is associated with

A

Vonwillebrand

74
Q

Activiation and aggregation associated with

A

ADP and thromboxane A2

75
Q

When are PRBCs transfused? are

A

transfused to improve tissue oxygenation

76
Q

The major reasons for transfusion therapy in the operating room are to

A

replace volume and coagulation factors and improve oxygen-carrying capacity.

77
Q

The recommended dose for platelet replacement is

A

one plateletpheresis pack per each 10 kg of patient weight

78
Q

Protamine sulfate dosing

A

1 mg neutralizes 100 units of heparin

79
Q

1 unit of platelet is ______ml

A

250 mL

80
Q

1 unit of plate increases the platelet count by

A

30,000–60,000/mm3

81
Q

FFP unit = _____ml

A

200-250 ml

82
Q

Hypofibrinogenemia, massive hemorrhage –> what is used

A

Cryoprecipitate.

83
Q

Hemophilia, massive hemorrhage

A

Factor VII

84
Q

1 unit single- donor apheresis platelets comes from how many platelet concentrates?

A

Four to five platelet concentrates,

85
Q

Laboratory analysis will reveal the need for FFP by a

A

PT and aPTT prolonged more than 1.5 times normal.

86
Q

Cryoprecipitate is then refrozen and thawed on use. It is rich in.

A

fibrinogen
Factors VIII
Factor XIII
Fibronectin

87
Q

The recommended dose of factor VII for hemophilia is

A

90 to 120 mcg/kg

88
Q

Cryoprecipitate Infusion Guidelines

A

1) When a test of fibrinogen activity indicates a fibrinolysis
(2) When the fibrinogen concentration is less than 80 to 100 mg/dL IN THE PRESENCE OF EXTENSIVE BLEEDING
(3) As an adjunct in massively transfused patients when fibrinogen concentrations cannot be measure in a timely fashion;
(4) For patients with congenital fibrinogen deficiencies.

89
Q

Transfusion of cryoprecipitate is rarely indi- cated if fibrinogen concentration is

A

greater than 150 mg/dL in non- pregnant patients.

90
Q

A sickle cell crisis may be triggered by

A

hypoxemia, hypothermia, infection, dehydration, venous stasis, and acidosis.

91
Q

P2Y12 ADP Receptor Inhibitors: name 3

A

ticlopidine, clopidogrel, prasugrel

92
Q

Platelet Glycoprotein IIb/IIIa Receptor Blockers: Name 3

A

abciximab, tirofiban, eptifibatide

93
Q

Heparin half life

A

1.5 hours

94
Q

Warfarin half life

A

2-4 days

95
Q

Abciximab half life

A

30 minutes

96
Q

ASA half life

A

20 minutes

97
Q

NSAIDs half life

A

2-10 hours

98
Q

COX-1 receptor inhibition by is responsible for the gastric irritation,

A

NSAIDs

99
Q

COX-1 receptor inhibition by NSAIDS is responsible for the

A

Gastric irritation

Decrease in renal blood flow, and platelet inhibition associated with nonselective NSAIDs.

100
Q

The removal of multiple units of blood from the patient right before surgery and replacement of the removed blood volume with crystalloid is referred to as

A

Acute normovolemic hemodilution

101
Q

Preoperative autologous donation is most effective when it is

A

combined with erythropoietin therapy

102
Q

Which of the following are disadvantages to storing blood? (select two)

A

Adenosine triphosphate levels decrease in stored blood

. 2, 3 DPG levels decrease in stored blood

103
Q

Which of the following are disadvantages to storing blood? (select two)

A

Adenosine triphosphate levels decrease in stored blood

2, 3 DPG and ATP levels decrease in stored blood

104
Q

The potassium present in the plasma in

A

packed red blood cells stored for 21 days can reach levels as high as 35 mEq/L.

105
Q

COX-1 receptors in the body

A

distributed throughout the body

106
Q

Which COX inhibition results in inhibition of thromboxane A2?

A

COX-1 receptor. By doing so, it disrupts thromboxane A2’s ability to promote platelet aggregation.

107
Q

COX-2 receptors are present in the

A

kidneys and central nervous system and can be synthesized in response to inflammatory processes.

108
Q

What are the effects of COX-2 receptor inhibition?

A

reduce prostacyclin release from the vascular epithelium and can result in increased platelet aggregation.

109
Q

The ability of coagulation factors to function correctly decreases

A

10 percent with every 1 degree Celsius drop in body temperature. Rapid transfusions of cold blood products can increase the likelihood of further bleeding.

110
Q

Which infectious disease has the highest risk of transmission via blood transfusion?

A

CMV

111
Q

Acute hemolytic transfusion reaction is an _____ mediated reaction.

A

IgM

112
Q

Phosphodiesterase inhibitors increase the level of cyclic AMP which is an

A

inhibitor of platelet aggregation.

113
Q

What sign is consistent with an acute hemolytic transfusion reaction?

A

Hematuria

114
Q

Transfusion-Associated Cardiovascular Overload (TACO) refers to the development of

A

pulmonary edema due to blood product administration. It is not immune-related or due to an alteration in the permeability of pulmonary capillary membranes and is responsive to diuretics and reduction of afterload.

115
Q

During preoperative assessment, a patient reveals a prolonged PT due to vitamin K deficiency. How long does it take for intravenous vitamin K to improve the PT?

A

6-8 hours

116
Q

Vitamin K oral administration exhibits the highest bioavailability, it can take up to ___hours to see effects.

A

24 hours to exhibit significant clinical effects.

SEE NCE Boards CoreConcepts (44 decks)

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