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Emily: Pharm 2 > Quiz 5: Hematology > Flashcards

Quiz 5: Hematology Flashcards

1
Q

What are the three elements that are largely responsible for maintaining the circulation as a closed hemodynamic system referred to as hemostasis:

A
  • Coagulation
  • fibrinolysis
  • Wound healing
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2
Q

What are the three main points that make up Virchow’s Triad:

A
  • Hypercoagulable State
  • Vascular Wall injury
  • Circulatory Stasis
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3
Q

Virchow’s Triad of hypercoagulable state consist of:

A
  • Malignancy
  • Pregnancy and peri-partum period
  • Oestrogen Therapy
  • Truama or surgery of lower extremity hip abdomen or pelvis
  • Inflamation bowel disease
  • Nephrotic Syndrome
  • Sepsis
  • Thrombophilia
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4
Q

Virchow’s Triad of Vascular wall injury consist of:

A
  • Trauma or surgery
  • Venepuncture
  • Chemical irritation
  • Heart valve disease or replacement
  • Atherosclerosis
  • Indwelling catheters
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5
Q

Virchow’s Triad of circulatory stasis consist of:

A
  • Atrial fibrillation
  • Left ventricular dysfunction
  • Immobility or paralysis
  • Venous insufficiency or varicose veins
  • Venous ovstruction from rumour, obesity or pregnancy
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6
Q

(Extrinsic Pathway) Damage outside (extrinsic to) blood vessels triggers the release of _______ from damaged tissue cells.

A

Thromboplastin (Factor III)

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7
Q

(Extrinsic Pathway) Thromboplastin activates factor ___. Thromboplasten when complexed on the surface of the platelet with ______ (factor IV) and ________ (IIIa) activates factor _ to __.

A
  • VII
  • calcium
  • thromboplastin
  • X
  • Xa
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8
Q

(Intrinsic Pathway) Trauma to the blood itself or exposure of the blood to collagen in a traumatized blood vessel wall activates factor __.

A

XII

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9
Q

(Intrinsic Pathway) XIIa activates factor __ and __ activates factor __.

A
  • XI
  • XI
  • IX
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10
Q

(Intrinsic Pathway) IXa when complexed on the platelet surface with activated factor __:Ca and Ca++ activates factor _.

A
  • VIII

- X

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11
Q

(Common Pathway) Activated factor X when complexed on the platelet surface with activated factor _ and _______ (factor __) on the platelet surface, converts ________ (Factor II) to _______ (IIa).

A
  • V
  • calcium
  • IV
  • prothrombin
  • thrombin
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12
Q

The therapies such as ASA, Plavix, Ticlid, and possible NSAID are TESTED by _____ ______ and the SYSTEM tested is ______ and _________.

A
  • bleeding time
  • Platelets
  • Capillaries
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13
Q

The therapy such as Warfarin are TESTED by _____ and the system tested is the _______ and ______.

A
  • PT
  • Extrinsic
  • Common
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14
Q

The therapy such as Haparin are TESTED by APTT and the system tested is the _____ and _____.

A
  • Intrinsic

- Common

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15
Q

The therapy such as Heparin are
TESTED by TT and the SYSTEM
tested is ____________ to ______.

A
  • fibrinogen

- fibrin

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16
Q

How does heparin work on the INTRISIC pathway?

A

-NEUTRALIZES
thrombin
Factor Xa

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17
Q

What is the source of heparin?

A
  • Porcine intestinal

- Bovine Lung

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18
Q

What is the mechanism of action for heparin:

A

-Heparin increases the rate of the thrombinantithrombin III reaction serving as a catalytic template to which both the AT III and protease bind.

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19
Q

By how much does Heparin increase thethrombinantithrombin II reaction:

A

1000

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20
Q

What does Heparin do to the PTT and TT:

A

Prolongs the time

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21
Q

T/F: Heparin acts both on bound and unbound factors.

A

FALSE (Heparin acts only on UNBOUND factors)

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22
Q

What is so interesting about the half life of heparin?

A

-APPROXIMATELY as the dose double the half life of heparin exponentially increases

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23
Q

Does heparin cross the placenta?

A

NO

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24
Q

What does abnormal LFTs due to heparin toxicity increase?

A
  • transaminases
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25
Q

Heparin toxicity has ________ risk of osteoporosis and spontaneous vertebral fractures.

A

-infrequent

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26
Q

When will HIT most likely be seen in a patient receiving treatment.

A

-1 to 2 WEEKS

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27
Q

In heparin toxicity arterial thrombosis with platelet-fibrin clots are referred to as:

A

White clots(HITTS)

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28
Q

What is the antidote to heparin?

A

-Protamine

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29
Q

What is the mechanism of action of protamine?

A

-protamine complexes with strongly acidic and anionic heparin to form a STABLE SALT

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30
Q

How are the complexes formed by heparin and protamine removed?

A

-Reticuloendothelial system

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31
Q

Are LMWH as susceptible to protamine antagonism?

A

NO (Protamine will approximately neutralize 65%)

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32
Q

What will occur when protamine is given rapidly?

A
  • Acute histamine related:
  • hypotension
  • bradycardia
  • pulmonary hypertension
  • Transient flushing
  • Dyspnea
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33
Q

What will hypersensitivity of protamine cause:

A
  • Uticaria
  • angioedema
  • acute pulmonary hypertension
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34
Q

What type of reaction is it called when protamine causes a lysosomal enzymes from neutrophils with prostaglandins and thromboxane genertation:

A

-Anaphylactoid reaction

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35
Q

NOT SURE ON THIS ONE:You may be more ypersensitive to protamine if:

A
  • Hypersensitive to fish
  • Previous protamine reversal of heparin
  • Protamine containing insulin (NPH)
  • Prvious vasectomy
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36
Q

What would be the pretreatment of a sensitivity reaction to protamine?

A
  • Corticosteroid

- Antihistamine

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37
Q

What would happen if protamine is given alone or in excess of heparin?

A

-result in bleeding theoretically because it has anticoagulatn and antiplatelet effects.

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38
Q

What is the mechanism of action for LMWH:

A
  • Inhibition of factor Xa by antithrombin

- (some factor IIa inhibition)

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39
Q

T/F: PTT and PT relatively insensitive with LMWH therapy.

A

TRUE

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40
Q

What co-morbidity would you want to decrease the dose of LMWH?

A

-Chronic renal insufficiency

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41
Q

Fondaparinux (Arixtra) mechanism of action is:

A

-SYNTHETIC indirect specific inhibitor of FACTOR Xa
-MEDIATED
ATIII

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42
Q

Fondaparinux (Arixtra) has no effect on:

A
  • factor IIa

- platelet function

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43
Q

T/F: Fondaparinux (Arixtra) is associated with H.I.T.

A

FALSE

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44
Q

Argatroban is used for the prevention and treatement of thrombosis in patient with ___ or _____.

A
  • HIT

- HITTS

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45
Q

T/F: Argatroban reversal agent is protamine.

A

FALSE (Argatroban has no reversal agent)

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46
Q

What are direct thrombin inhibitors use for:

A

People whom are intolerant of heparin

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47
Q

(Direct Throbin Inhibitors) Hirudin analogs is the plypeptide that is responsible for the anticoagulant properties of the _____ of the medicinal ______.

A
  • saliva

- leeches

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48
Q

(Direct Thrombin Inhibitors) Hirudin analogs bind _____ to the active catalytic and substrate recognition sites of both _______ and ______ Thrombin (Factor __).

A
  • irreversibly
  • circulating
  • clot bound
  • IIa
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49
Q

Hirudin analogs are excreted by the:

50
Q

What are the hirudin analogs:

A
  • Bivalirudin (Angiomax)

- Lepirudin (refludin)

51
Q

What protein are natural anticoagulant:

52
Q

What is the mechanism of action of Warfarin:

A

-has an INDIRECT anticoagulant that alter sysnthesis of factor II, VII, IX, and X by interfering with the action of vita. K.

53
Q

How long does the anticoagulant such as vita. K1 take to act from a warfarin toxicity:

54
Q

T/F: What route of administration of vita. K is unacceptable?

55
Q

What would be done if a reversible antidote is needed right away for warfarin toxicity?

A

-FFP of 10-20 ml/kg

56
Q

Y/N: Is it safe to administer warfarin to a pregnant mother.

57
Q

________ (tPA) binds to fibrin and plasminogen and converts bound plasminogen to plasmin.

58
Q

_________ has no intinisic enzymatic activity, but forms a stable 1:1 complex with plasminogen causing conformational changes that expose the active site that cleaves free plasminogen to plasmin.

A

-Streptokinase

59
Q

____________ is a two chain serine protease isolated from human kidney cells that converts plasminogen to plasmin.

60
Q

What does streptokinase require prior to a normal dose for an adult and why?

A
  • Loading dose
  • Loading dose is needed to overcome plasma antibodies that inactivate the protein due to a prior streptococcal infection.
61
Q

How long could fibrinolytic activity last for after discontinuation of drug?

A

-7 to 24 hours

62
Q

What labs would be monitored for patient on fibrinolytic therapy?

A
  • fibrinogen concentration
  • thrombin times
  • PTT
63
Q

(Hemostatics) Epsilon aminocaproic acid or AMICAR is a synthetic ____________________ acid.

A

.-monoaminocarboxylic

64
Q

(Hemostatic) What does amicar inhibit:

A
  • fibrinolysis

- indirect inhibitor of plasmin’s anti-platelet effects

65
Q

(Hemostatic) What would rapid IV infusion of amicar cause:

A
  • hypotension
  • bradycardia
  • Arrhythmias
66
Q

This drug would be used in completion of surgery after stopping oozing in patient with cirrhosis.

67
Q

(Hemostatic) Novoseven RT is the coagulation factor of:

A

-VIIa (recombinant)

68
Q

(Hemostatic) On whom would you use Novoseven on:

A
  • Hemophilia A or B

- Patient with congenital factor VII defiency

69
Q

(Hemostatic) Novoseven works on the EXTRINSIC pathway how:

A

-rFVIIa binds to platelets receptors and then activates factor X and generates thrombin and fibrin

70
Q

What are some off label uses for Novoseven:

A
  • Warfarin induced bleeding which FFP or vita. K did not work
  • spontaneous intracranial hemorrhage
  • massive bleeding
  • uncrrectable by surgery
  • Bleeding requiring >6units PRBC in 12 hours
  • No Hx of DVT, PE, arterial thrombosis (MI or CVA)
71
Q

What are the most significant complications of Novoseven:

A
  • myocardial ischemia

- Cerebral ischemia

72
Q

(Oral Agents that are blood thinners) Dabigatran (Pradaxa) works as an oral direct _____ inhibitor.

A

thrombin (IIa)

73
Q

(Oral Agents that are blood thinners) Apixaban (Eliquis) works as an oral direct factor __ inhibitor.

74
Q

(Oral Agents that are blood thinners) Rivaroxaban (Xarelto) work as a oral factor __ inhibitor.

75
Q

What makes the vonWillebrand’s factor (VIII;vWF)

A

Endothelial Cells

76
Q

What does vonWillebrand factor do?

A

-Promotes adhesions to damaged vascular walls

77
Q

What is the most common inherited coagulation defect?

A

-vonWillebrand’s Disease

78
Q

Thromboxane -A2 and ADP promote platelet:

A

Aggregation

79
Q

Fibrinogen (factor I) ataches to the receptors linking the _______ to each other.

80
Q

What does aspirin do to the platelet:

A

-it inhibits the cyclo-oxygenase as nonfunctional for the life of the platelet

81
Q

NSAIDS ______ of thromboxan A2 production by platelets is only temporary by about ______ hours.

A
  • depression

- 24 to 48

82
Q

(Platelet Aggregation Inhibitors) What drugs are thienopyridine ADP-receptor antagonists:

A
  • clopidogrel (Plavix)
  • Ticlopidyne (ticlide)
  • Prasugrel (effient)
  • Ticagrelor (Brilinta)
83
Q

T/F: Ticagrelor (Brilinta) is reversible.

84
Q

(Platelet aggreation Inhibitors) What drugs are platelet glycoprotein (GP IIb/IIIa) receptor Inhibitors:

A
  • Abciximab (ReoPro)
  • Eptifibatide (Integrilin)
  • Tirofiban (Aggrastat)
85
Q

How long will it take for platelet aggregation and bleeding time return to baseline values:

86
Q

How long must you wait before going to surgery if you are on Plavix:

87
Q

What will methylprednisilone 20 mg IV do to people using ticlopidine (Ticlid):

A

-normalize prolonged bleeding time in ~ 2 hours

88
Q

How long must you wait before going to surgery if on Ticlopidine (Ticlid):

A
  • 10 to 14 days
89
Q

What is the difference of Prasugrel (effient) compared to Plavix:

A

-Effient does not have the resistence of plavix

90
Q

Ticagrelor (Brilinta) is a CYP3A4 Substrate.

91
Q

How long must you wait before going to surgery if on ticagrelor (Brilinta).

92
Q

What lab would you use to measure the percentage of platelet inhibition.

93
Q

What P2Y12 would it be considered safe to proceed with surgery:

94
Q

(Platelet Aggregation Inhibitors) What are some platelet glycoprotein GP IIB/IIIa) receptor Inhibitors:

A
  • Abciximab (Reopro)
  • Eptifibatide (Integrelin)
  • Tirofiban (Aggrastat)
95
Q

(Platelet Aggregation Inhibitors) ______ (______): Fab fragment of a monoclonal antibody that binds selectively to GP IIb/IIIa receptors and dissociates slowly from it.

A

Abciximab (Reopro)

96
Q

(Platelet Aggregation Inhibitors) ______ (_____): Synthetic cyclic heptapeptide rapidly reversible.

A

Eptifibatide (Integrelin)

97
Q

(Platelet Aggregation Inhibitors) _______ (_______): synthetic nonpeptide tyrosine derivative, rapidly reersible.

A

Tirofiban (Aggrastat)

98
Q

(Platelet Aggregation Inhibitors) What are the uses of platelet glycoprotein (GP IIb/IIIa) receptor inhibitors.

A
  • Acute ischemic complication of percutaneous coronary intervention (PCI)
  • Unstable angina and non-Q wave MI
99
Q

(Platelet Aggregation Inhibitors) Adverse effect are:

A
  • Bleeding (Not associated with bleeding issues after CABG
  • Thrombocytopenia
  • N/V
  • Hypotension
  • Anaphylaxis
100
Q

Desmopressin is a synthetic analogue of ___.

A

-Anti diuretic hormone

101
Q

Desmopressin causes endothelial cells to release:

A
  • vonWillebrand factor
  • tissue type plasminogen activator
  • Prostaglandins
102
Q

Desmopressin uses are:

A 
-Treatment
DI
Uremia
Chronic liver diseases
types of hemophilia
minamize blood loss
-
103
Q

What are the side effects of desmopressin:

A
  • hypotension OR hypertension
  • Hyponatramia
  • Nausea
104
Q

How early should a catheter insertion take place before the first heparin is administered if no coagulopathy exists.

105
Q

How early could a neuraxial catheter be removed after last dose of heparin AFTER evaluating the patient’s coagulation status?

A

2 to 4 hours

106
Q

T/F: ASA and NSAIDs does not appear to be associated with an increased risk of epidural hematoma.

A

TRUE (It is false if ASA and/or NSAIDS are used with another anti-coagulate.)

107
Q

How long would you wait for a neuraxial blockade is on clopidogrel (plavix):

108
Q

How long would you wait for a neuraxial blockade is on Ticlopidyne:

109
Q

How long would you wait for a neuraxial blockade is on Abciximab:

A

24-48 hours

110
Q

How long would you wait for a neuraxial blockade is on Eptifibatide and tirofiban:

A

4 to 8 hours

111
Q

What labs measure coumadin:

112
Q

What labs measure heparin:

113
Q

When can a neuraxial catheter be removed when a person is on coumadin:

114
Q

How much time should be allotted before placing a neuraxial blockade on a low and high LMWH.

A

LOW =12

High = 24

115
Q

How much time should be alotted before administering a LMWH after removal of a neuraxial catheter:

A

2 to 4 hours

116
Q

What is Dextran good for:

A
  • Expansion of intravascular volume

- prevention of thromboembolism by decrease of blood viscosity

117
Q

What antibody is present in most adults that would be a concern when using dextran:

118
Q

If a rouleaux formation occurs when using dextran what may it do:

A

-make subsequent cross matching of blood difficult.

119
Q

Xigris (Drotrecogin alpha) is a recombinant human activated protein C.

A

TRUE (It was pulled from the market due to elevated mortality rates in patients.

120
Q

Cyclooxygenase is the rate limiting enzyme in the conversion of ______ acid to ________ a2.

A
  • arachidonic

- thromboxane

Emily: Pharm 2 (11 decks)

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