Ln Anemia/coag D/o

Front 1

Anemia definition

Back 1

A reduction in total red cell mass

Front 2

RCM

Back 2

Red cell mass

Front 3

What is the predominant protein component of blood?

Back 3

Hemoglobin

Front 4

Typically, hemoglobin helps carry which three gases?

Back 4

1) Oxygen

2) CO2

3) NO

Front 5

Hemoglobin is a direct or indirect measurement of RCM?

Back 5

Indirect.

Front 6

Three scenarios when hemoglobin or hematocrit misrepresent RCM:

Back 6

1) Acute blood loss (H/H will overestimate RCM)

2) Pregnancy

3) Severe dehydration

Front 7

A mature RBC will circulate in the blood for _____.

Back 7

100-120 days

Front 8

True or False?

"Relative" anemia has a normal total RCM.

Back 8

It does have a normal RCM.

Front 9

What are the three classes of absolute anemia?

Back 9

1) Hemorrhage related

2) Hypoproliferative

3) Hyperproliferative

Front 10

All classes of anemia are classified as either:

Back 10

Primary or Secondary.

Front 11

Hypoproliferative anemia definition:

Back 11

Due to impaired RBC production, absolute reticulocyte count less than 75k/microliter.

Front 12

Hyperproliferative anemia definition:

Back 12

AKA hemolytic anemia. These are due to premature destruction of RBC's with an absolute reticulocyte count of greater than 100k/microliter.

Front 13

_______ reflexes help to mediate the immediate response to acute blood loss, whereas _______ receptors do not play a significant role.

Back 13

Baroreceptors and chemoreceptors

Front 14

What happens to HR and minute ventilation during hemorrhage?

Back 14

They both increase.

Front 15

How does hyperventilation increase cardiac output?

Back 15

It increases right heart filling.

Front 16

Which two physiologic effects increase O2 saturation of arterial hemoglobin via the Bohr effect?

Back 16

Increased pH and decreased PaCo2

Front 17

After hemmhorrage, a significantly lower hemoglobin concentration is measurable within _______.

Back 17

2 minutes after an acute loss of 40% blood volume (because of water redistribution).

Front 18

How do increased levels of 2,3 DPG affect hemoglobin?

Back 18

They decrease O2 uptake in pulmonary capillaries but increase tissue oxygen delivery.

Front 19

How are 2,3 DPG levels affected in transfused blood?

Back 19

They are lower.

Front 20

Increased erythropoetin and increased circulating reticulocyte count can be detected how long after hemorrhage?

Back 20

2 days.

Front 21

Blood hemoglobin concentration increases how long after blood loss?

Back 21

7 days.

Front 22

Chronic anemia is associated with three physiological compensatory traits.

Back 22

1) Expansion of plasma volume.

2) Hyperventilation

3) Increased cardiac output

Front 23

Chronically anemic patients who are anesthetized should transfuse erythrocytes when?

Back 23

As soon as they see an EKG change.

Front 24

What is the major risk of rapid transfusion in compensated chronic anemia patients?

Back 24

CHF

Front 25

Crystalloid solutions are comprised of molecules with a molecular weight below ________.

Back 25

30 kDa

Front 26

Human albumin is unique among colloids because it does not cause ________.

Back 26

Coagulopathy and renal failure.

Front 27

Data shows that albumin treated patients with this injury had a higher mortality rate than if they were treated with sodium chloride.

Back 27

Traumatic brain injury.

Front 28

Dextrans decrease _________.

Back 28

Platelet adhesion and blood viscosity.

Front 29

Good rule of thumb for transfusing red blood cells, you see these signs together:

Back 29

Tachycardia with hypotension with acidemia, WITH NO APPARENT CAUSE.

(The planets must align)

Front 30

True or False?

Transfused RBC's are an Independent risk factor for hospital duration, mortality, and organ dysfunction.

Back 30

True.

Front 31

What is the second highest cause of adverse transfusion effects?

Back 31

Human error. AKA mistransfusion.

Front 32

What is the downside of irradiation of blood?

Back 32

Dose-dependent recurrence of tumor.

Front 33

Leading cause of transfusion related mortality?

Back 33

TRALI

Front 34

TRALI occurs within what timeframe?

Back 34

4 hours of transfusion.

Front 35

Paradoxically, the severity of TRALI is _________.

Back 35

Not permanent.

Front 36

The majority of TRALI patients return to baseline pulmonary function within _________, and have total resolution at ________.

Back 36

2 days, 4 days.

Front 37

How does blood transfusion affect electrolytes?

Back 37

Hyperkalemia

Hypoglycemia

Hypocalcemia

Front 38

Hypocalcemia from blood transfusion is caused by what?

Back 38

Citrate

Front 39

Acute normovolemic hemodilution definition:

Back 39

Removal of predetermined quantity of blood while intravascular volume is replaced.

Front 40

Acute normovolemic hemodilution can remove ______.

Back 40

Up to 50% of RCM.

Front 41

Autologous blood has what shape?

Back 41

A normal bioconcave disk.

Front 42

Allogenic blood loses its shape after how many days?

Back 42

14 days.

Front 43

Contraindications to RBC salvage techniques:

Back 43

1) Infection at operative site

2) Use of microfiber collagens

3) Enteric perforation

Front 44

Risks of coagulopathy from cellsaver are minimal in blood loss less than ______.

Back 44

three liters

Front 45

It is recommended to use cellsaver if _________.

Back 45

If blood loss is greater than 1 liter or 20% of blood volume.

Front 46

Tranexamic acid is used to ________.

Back 46

Inhibit fibrinolysis, inhibit conversion of plasminogen to plasmin.

Front 47

Terrible side effect of tranexamic acid:

Back 47

Increased incidence of perioperative seizure in cardiac patients.

Front 48

In early infancy, what percent of circulating hemoglobin is hemoglobin F?

Back 48

97%

Front 49

Sickle cell hemoglobin is a mutation of which hemoglobin?

Back 49

hemoglobin A on a beta-globin chain

Front 50

In homozygotes for sickle cell, what percent of the hemoglobin is shitty?

Back 50

80-95%

Front 51

Carriers of sickle cell trait have what percent of hemoglobin S?

Back 51

40%

Front 52

Red blood cells of patients with sickle cell disease have a life span of what?

Back 52

10-20 days

Front 53

In a patient with sickle cell disease, what conditions must be avoided which could cause a vaso-occlusive crisis?

Back 53

Hypoxia

Hypothermia

Dehydration

Acidosis

Front 54

Does general anesthesia cause sickle cell crisis?

Back 54

No.

Front 55

How do you optimize sickle cell before surgery?

Back 55

You use blood transfusions to reduce percent of hemoglobin S to 30-40%.

Front 56

Periop mortality in sickle cell disease is most commonly caused by ________.

Back 56

Infection related to immunodepression secondary to splenic infarct.

Front 57

Hemophilia A is a deficiency of ________.

Back 57

factor VIII

Front 58

What kind of genetic trait is hemophilia A?

Back 58

X-linked recessive.

Front 59

Normally, factor VIII activity ranges from ______.

Back 59

50-150%

Front 60

Mild hemophilia A is present in patients with factor VIII level ______.

Back 60

>5%

Front 61

Moderate hemophilia A is present in patient's who have ______.

Back 61

1-5%

Front 62

Hemophilia A factor VIII level percentages are easy because:

Back 62

factor VIII units/ml = percentage/100

Front 63

What is the hallmark of severe hemophilia?

Back 63

Spontaneous Hemarthroses.

Front 64

Can Hemarthroses destroy the joint permanently in hemophiliacs?

Back 64

Yes.

Front 65

What is the typical threshold for spontaneous bleeding events in hemophilia type A?

Back 65

Hemophiliacs with 1-5% factor VIII activity, do not have spontaneous bleeding typically.

Front 66

The most common cause of death in a hemophiliac is ______.

Back 66

Intracranial and intracerebral bleeding.

Front 67

Besides intracranial/intracerebral bleeding, where is spontaneous bleeding common in severe hemophiliacs?

Back 67

GI, joints, mouth.

Front 68

Tell me about pseudo tumors.

Back 68

In severe anemics, frequent hemorrhagic episodes can produce an enlarged pseudo tumor which can invade tissues and destroy them.

Front 69

True or False?

All hemophiliacs have a prolonged aPTT?

Back 69

True.

Front 70

What bleeding tests are typically normal in hemophiliacs?

Back 70

PT, thrombin time, bleeding time, platelet count, and platelet function are normal.

Front 71

What is the goal of factor VIII administration in hemophilia A patients?

Back 71

Factor VIII activity at approximately 3%.

Front 72

What is the treatment goal for acute, life-threatening bleeding attacks in hemophilia A patient's?

Back 72

Factor VIII activity at 50-100% of normal in acute episodes.

Front 73

What must factor VIII levels be restored to in a hemophilia A patient receiving neuraxial anesthesia?

Back 73

100%

Front 74

What must be used for hemophilia A patients who have acquired resistance to factor VIII treatment?

Back 74

Recombinant activated Factor VII.

Front 75

What is factor IX deficiency?

Back 75

Hemophilia B.

Front 76

What drugs should not be given to hemophiliacs?

Back 76

NSAIDs.

Front 77

What is a sign that you have given too much NSAID to a hemophiliac?

Back 77

Profound hematuria.

Front 78

How is hemophilia B transmitted genetically?

Back 78

X-linked recessive trait.

Front 79

How are mild, moderate, and severe forms of hemophilia B defined?

Back 79

Exactly the same as hemophilia A.

(Percentages of normal/100 = units/ml)

Front 80

What happens when you mix hemophilia B plasma with equal parts of plasma from normal individuals?

Back 80

The patient's aPTT will correct to normal time.

Front 81

What develops in hemophilia A and B patients that complicates treatment?

Back 81

Antibodies to factors VIII and IX.

Front 82

How do you treat antibody-resistant hemophilia B?

Back 82

Recombinant activated factor VII.

Front 83

What is the name of recombinant activated factor VII?

Back 83

NovoSeven.

Front 84

What kind of genetic inheritance is von Willebrand's disease?

Back 84

Autosomal dominant.

Front 85

What are the two major roles vWF in the hemostatic process?

Back 85

1) vWF acts as a bridge between platelets and collagen in disrupted endothelium.

2) vWF creates a protective shield for factor VIII, protecting it from destruction in the blood.

Front 86

VWD manifests as:

Back 86

bleeding from mucous membranes, both internal and external.

Front 87

VWD patients should never get _______.

Back 87

NSAIDs.

Front 88

VWD is diagnosed with:

Back 88

1) bleeding times

2) quantities, activity level, and antibodies for vWF as well as levels of factor VIII.

Front 89

The treatment goal for both the periop period and bleeding crises in vWD is _______.

Back 89

vWF at 50-100% of normal.

Front 90

Which drug increases activity levels of vWF and factor VIII?

Back 90

DDAVP

Front 91

What happens to vWF levels in pregnancy?

Back 91

Increase 2-3 fold in second and third trimesters.

Front 92

Does DDAVP serve any purpose in active labor?

Back 92

Yes. If the mother is responsive to the therapy previous.

Front 93

If a mother is not responsive to DDAVP and is in labor with vWD, give her _______.

Back 93

vWF concentrate

Front 94

What are the contact factors?

Back 94

Factor XII, HMW kininogen, preKallikrein.

Front 95

What is special about contact factor deficiency?

Back 95

Causes no bleeding and needs no treatment.

Front 96

What is a sign of contact factor deficiency?

Back 96

Prologned aPTT.

Front 97

Factor XIII is important for?

Back 97

Stabilizing fibrin clots with bonds between fibrin.

Front 98

Most hemorrhage in factor XIII deficiency is _____.

Back 98

triggered by trauma

Front 99

What is the treatment for factor XIII deficiency?

Back 99

Cryoprecipitate and FFP. Factor XIII concentrate is only available in Europe.

Front 100

Normal hemostasis occurs when factor XIII levels are _____.

Back 100

>5%

Front 101

What is the dosage of FFP for factor XIII deficiency?

Back 101

2-3ml/kg.

Front 102

What is afibrinogenemia?

Back 102

Patients with no detectible serum fibrinogen.

Front 103

Signs of afibrinogenemia?

Back 103

Prolonged PT, TT, aPTT.

Front 104

Preop fibrinogen levels must be restored to what in afibrinogenemia?

Back 104

50-100mg/dl.

Front 105

What do you give afibrinogenemia patients?

Back 105

5-10 units of cryo.

Front 106

A single unit of cryo contains how much fibrinogen?

Back 106

250-300mg.

Front 107

What is the formula for calculating dose of fibrinogen concentrate?

Back 107

dose (mg/kg) = [target level (mg/dl) - measured level]/1.7

Front 108

What is the treatment for symptomatic dysfibrinogenemia?

Back 108

Same as afibrinogenemia.

Front 109

Thrombotic variants of dysfibrinogenemia are treated with _______.

Back 109

heparin and oral anticoagulants

Front 110

What is needed to convert fibrinogen to fibrin?

Back 110

Thrombin.

Front 111

Factor IIa AKA ______.

Back 111

thrombin

Front 112

Dysprothrombinemia shows prolonged:

Back 112

PT and aPTT.

Front 113

When does an anticoagulant's half-life not predict the duration of its effect?

Back 113

When its mechanism is irreversible.

Front 114

Aspirin inhibits platelets:

A) reversibly

B) irreversibly

Back 114

Irreversibly.

Front 115

Antithrombotic agents have how many subcategories of drugs?

Back 115

Five:

1) UFH

2) LMWH

3) Activated factor X inhibitor

4) Direct thrombin inhibitor

5) Coumarins

Front 116

UFH is extracted from _________.

Back 116

pig gut or cow lung

Front 117

UFH exerts its effect by ________________________.

Back 117

complexes with antithrombin, making it 1,000 times more powerful at inhibiting prothrombin and factor X

Front 118

UFH prolongs what values?

Back 118

ACT and aPTT.

Front 119

True or False?

Some individuals exhibit insensitivity to heparin.

Back 119

True.

Front 120

Protamine is given in what ratio to UFH?

Back 120

0.7-1.3mg/100 units

Front 121

Protamine is given slowly to prevent?

Back 121

Hypotension and pulmonary hypertension.

Front 122

What drug was developed to create an antithrombotic agent that does not require anticoagulant monitoring (exception with renal insufficiency)?

Back 122

LMWH

Front 123

How long must you wait before elective surgery or neuraxial anesthesia with high doses of LMWH?

Back 123

24 hours.

Front 124

How many half-lives must pass to make any drug virtually non-existent?

Back 124

Five half-lives.

Front 125

LMWH, when bound with antithrombin, exerts its effect on ________.

Back 125

Factor X

Front 126

How long should a patient wait before surgery or spinal anesthesia when given fondaparinux?

Back 126

Four days.

Front 127

What kind of drug is fondaparinux?

Back 127

Activated factor X inhibitor.

Front 128

What's bigger? Arixtra or LMWH?

Back 128

Arixtra.

Front 129

What is the mechanism of Arixtra?

Back 129

Binds with antithrombin and attacks Factor X with 300x the power.

Front 130

Direct thrombin inhibitors, like dabagatran, do what?

Back 130

They prevent thrombin from converting fibrinogen to fibrin.

Front 131

What drug should be given when you can't give heparin because you don't want to cause thrombocytopenia?

Back 131

Argatroban.

Front 132

What is the antidote for direct thrombin inhibitor related bleeding?

Back 132

There is none.

Front 133

How many days must a patient wait to have neuraxial blockade when they are on dabagatran?

Back 133

Five days.

Front 134

Coumarins inhibit which factors?

Back 134

Vitamin K dependent. (II, VII, IX, X and C&S)

Front 135

What are the best two tests to assess vitamin K dependent factors?

Back 135

PT/INR

Front 136

What is the only Coumarin approved by the FDA?

Back 136

Coumadin/warfarin.

Front 137

How long must you stop warfarin before having neuraxial blockade?

Back 137

5 days or an INR of 1.4 or less.

Front 138

Acute reversal of warfarin:

Back 138

FFP or prothrombin administration.

Front 139

What kind of drug is an NSAID?

Back 139

Antiplatelet.

Front 140

Aspirin exerts its effect by ____________.

Back 140

irreversibly inhibiting COX from forming thromboxane A2 from arachadonic acid.

Front 141

NSAIDs are metabolized by ___________.

Back 141

the liver

Front 142

Ibuprofen, ketorolac and naproxen inhibit COX _________.

Back 142

reversibly

Front 143

What must be given to acutely reverse aspirin?

Back 143

Platelets.

Front 144

If a patient is on NSAIDs, how long do they have to wait to get neuraxial anesthesia?

Back 144

They don't.

Front 145

What kind of drug is abciximab?

Back 145

Glycoprotein 2b 3a receptor inhibitor.

Front 146

How long must you wait to do neuraxial blockade when they're on abciximab?

Back 146

1-2 days.

Front 147

How long must you wait for neuraxial block when patient is on eptifibatide?

Back 147

4-8 hours.

Front 148

Clopidogrel is what type of anticoagulant?

Back 148

ADP antagonist.

Front 149

How long must you wait to do neuraxial when patient is on clopidogrel?

Back 149

7 days

Front 150

How long must you wait to do neuraxial when patient is on ticlodipine.

Back 150

14 days.

Front 151

Antithrombin is produced by _______.

Back 151

the liver

Front 152

Antithrombin neutralizes ___________.

Back 152

thrombin and factors IX-XIIa

Front 153

Protein C is produced by ________.

Back 153

the liver

Front 154

Protein C is dependent on vitamin __.

Back 154

K

Front 155

Protein C's purpose:

Back 155

Inhibition of factor Va and VIIIa.

Front 156

Factor V Leiden AKA __________.

Back 156

activated protein C resistance

Front 157

Factor V Leidin is a:

A) Prothrombotic

B) Thrombolytic

Back 157

A) Prothrombotic

Front 158

Heparin induced thrombocytopenia:

Back 158

Type 1: Non-immune-mediated platelet activation

Type 2: Immune-mediated platelet activation

Front 159

Immune-mediated means involvement of _____.

Back 159

IgG

Front 160

What diagnoses HIT type 2?

Back 160

50% decrease in platelet count after heparin administration.

Front 161

True or False?

Profound bleeding, profound thrombosis, OR BOTH, can occur in DIC.

Back 161

True.

Front 162

How do you cure DIC?

Back 162

By figuring out which of the million causes is responsible, and fixing it.

Front 163

Periop goals for DIC:

Back 163

Platelet concentration between 25-50k/microliter, and a fibrinogen level greater than 50mg/dl, and avoidance of anticoagulants.

Front 164

What is thalassemia?

Back 164

Disorder with deficiency of hemoglobin alpha or beta chains.

Front 165

Homozygous thalassemia people have:

Back 165

severe anemia and require chronic blood transfusion.

Front 166

Thalassemic patients have messed up ________.

Back 166

Everything in their blood is ruined. Everything.

Front 167

What is nephrotic syndrome?

Back 167

Profound hypoalbuminemia from peeing out proteins.

Front 168

True or False?

Nephrotic syndrome is a prothrombotic state.

Back 168

True.

Front 169

Second most common cause of death in cancer:

Back 169

Thrombosis.

Front 170

Thrombotic thrombocytopenia purpura:

Back 170

Platelet aggregation leading to microvascular occlusion.

Front 171

Treatment of TTP:

Back 171

glucocorticoids and FFP.