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Applied Biochemistry > Coagulation: Surgical Prospective > Flashcards

Coagulation: Surgical Prospective Flashcards

1
Q

normal mechanism of hemostasis (3)

A

vascular phase
platelet phase
coagulation phase

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2
Q

what results when a blood vessel is damaged?

A

vasoconstriction

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3
Q

construction of the injured blood vessel is to diminish

A

blood flow

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4
Q

what occurs during the platelet phase? (3)

A

formation of a loose and temporary platelet aggregate at the site of injury
platelets bind to collagen
after the activation, platelets change their shape and in the presence of fibrinogen, aggregate to form the hemostatic primary platelet plug

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5
Q

through two separate pathways, the intrinsic and extrinsic, the conversion of — to — is complete

A

fibrinogen to fibrin

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6
Q

fibrin tightly binds to platelets to form a

A

clot

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7
Q

what forms during the coagulation phase?

A

formation of a fibrin mesh that tightly binds to the platelet aggregate, which gives rise t o amore stable hemostatic plug (clot)

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8
Q

clot dissolution

A

partial or complete dissolution of the hemostatic plug by plasma

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9
Q

factors affected normal hemostasis mechanism are dependent upon (5)

A 
vessel wall integrity 
adequate numbers of platelets 
proper functioning platelets 
adequate levels of clotting factors 
proper function of fibrinolytic pathway
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10
Q

common tests performed to evaluate hemostasis (3)

A

Platelet Count (Complete Blood Count)
Bleeding Time
Coagulation Profile

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11
Q

PT

A

prothrombin time

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12
Q

APTT

A

activated partial thromboplastin time

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13
Q

INR

A

international normalized ratio

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14
Q

platelet function tests

A

Accurate measurement of platelet function is important for identifying patients with platelet dysfunction

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15
Q

platelet function tests may be recommended for those who

A

bruise easily, have excessive bleeding, or take medications after a stroke or heart attack that can alter platelet function; to detect resistance to aspirin or clopidogrel and before certain surgeries

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16
Q

clotting factor assays (2-12) measures

A

the levels or functional activity of one or more coagulation factors

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17
Q

normal platelet count

A

150,000-400,000 cells/mm3

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18
Q

thrombocytopenia (normal bleeding time)

A

100,000-140,000

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19
Q

mild thrombocytopenia (mild prolonged bleeding time)

A

50,000-100,000

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20
Q

severe thrombocytopenia (bleeding after minor trauma)

A

<50,000

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21
Q

spontaneous bleeding

A

<20,000

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22
Q

bleeding time is how long a

A

precise nick takes to stop bleeding

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23
Q

what does bleeding time provide an assessment of?

A

platelet function

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24
Q

normal bleeding time

A

2-9 minutes

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25
Q

platelet dysfunction bleeding time

A

9-15 minutes (prolonger thrombocytopenia)

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26
Q

what does PT time measure?

A

effectiveness of the extrinsic pathway

tests the rate of conversion of 7 tp 7a (extrinsic pathway)

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27
Q

normal PT time range

A

12-13 s

11-13.5 is also an accepted normal range

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28
Q

common causes of prolonger PT Time include (3)

A

Warfarin use
Vitamin K deficiency from malnutrition, biliary obstruction, malabsorption syndromes, or use of antibiotics
Liver disease, due to diminished synthesis of clotting factors

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29
Q

what does aPTT measure

A

effectiveness of the intrinsic and common pathway (measures intrinsic clotting of blood, congenital clotting disorders)

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30
Q

is aPTT or PTT more sensitive

A

aPTT is considered a more sensitive version and is used to monitor the patients response to heparin therapy

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31
Q

normal APTT

A

30-40 sec

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32
Q

aPTT more than 70 sex signifies

A

spontaneous bleeding

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33
Q

congenital deficiencies of intrinsic system clotting factors such as (6)

A

factors VIII, IX, XI, and XII, including hemophilia A and Hemophilia B

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34
Q

von willebrand disease is the most common

A

inherited bleeding disorder, affecting platelet function owning to decreased von willebrand factor activity

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35
Q

liver cirrhosis

A

the liver makes most of the clotting factors, including those that are vitamin k dependent ones
diseases of the liver may result in an inadequate quantity of clotting factors, prolonging the aPTT

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36
Q

vitamin k deficiency

A

the synthesis of some clotting factors requires vitamin K, so vitamin K deficiency results in an inadequate quantity of intrinsic system and common pathways clotting factors, as a result the aPTT is prolonger

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37
Q

heparin therapy inhibits the

A

intrinsic pathway at several points (prothrombin 2), prolonging the aPTT

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38
Q

Coumadin therapy inhibits the function of (3)

A

factors 1, 9, 10, prolongering aPTT

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39
Q

common causes of prolonger aPTT (6)

A 
congenital deficiencies of intrinsic system clotting factors
von willebrand disease
liver cirrhosis 
vitamin k deficiency 
heparin therapy 
Coumadin therapy
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40
Q

INR formula

A

(patient PT/mean normal PT)^ISI

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41
Q

PT=

A

patient prothrombin time

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42
Q

MNPT=

A

the mean normal prothrombin time

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43
Q

ISI=

A

the international sensitivity index determined for each batch of thomboplastic reagents by manufactures

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44
Q

INR

A

“Modified” PT test, where the sample is “standardized” by using an ISI value (International Sensitivity Index) for the tissue factor used in each test. The ISI is usually between 1.0 and 2.0.

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45
Q

normal INR range

A

0.8-1.2

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46
Q

normal therapeutic levels of coagulation

A

2-3.5

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47
Q

the INR target range is 2.5-3 in which circumstances? (5)

A 
Atrial Fibrillation
Ischemic Stroke, Transient Ischemic attack (TIA) , or systemic embolism
Mitral Stenosis
Planned Cardioversion
After open Heart surgery
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48
Q

bleeding disorders are a group of conditions involving the

A

body’s clotting process

49
Q

such disorders can lead to

A

heavy and prolonger bleeding after injury

50
Q

bleeding disorders may be either (2)

A

congenital or acquired

51
Q

the acquired bleeding disorders are more common than

A

congenital bleeding disorders

52
Q

Hemophilias A and B and Von Willebrand’s disease constitute over –% of all congenital bleeding disorders

A

90

53
Q

congenital bleeding disorders (2)

A

hemophilia A and B

54
Q

hemophilia A

A

clotting factor 8 deficiency

55
Q

hemophilia B

A

clotting factor 9 deficiency (Christmas disease)

56
Q

the decreased levels of factor 8 and 9 affect the normal coagulation cascade and thus the

A

fibrin clot formation in impaired in these patients

57
Q

prevalence of hemophilia A

A

1 in 10,000

58
Q

prevalence of hemophilia B

A

1 in 50,000

59
Q

hemophilia can be inherited in a sex linked recessive manner, but –% of all patients have no family history

A

25%

60
Q

does hemophilia affect more males or females?

A

males (1 in 10,000)

females (1 in 100,000,000)

61
Q

why is it more prevalent in males?

A

critical blood clotting gene is carried on the X chromosome

62
Q

late bleeding following surgery or injury, nhemarthrosis and hematoma formation are

A

classic sequelae of these coagulopathies

63
Q

an elevated APTT is seen when

A

factor 8 or 9 levels fall below 30-50% of normal

64
Q

levels of hemophilia (3)

A

mild
moderate
severe

65
Q

People with mild hemophilia (6% to 49% factor level) usually have problems with bleeding only after serious (3)

A

injury, trauma, or surgery

66
Q

in many cases, mild hemophilia is not discovered until an injury or surgery or tooth extraction results in

A

unusual bleeding

67
Q

the first of mild hemophilia episode may not occur until

A

adulthood

68
Q

People with moderate hemophilia, about –% of the hemophilia population, tend to have bleeding episodes after injuries

A

15

69
Q

people with moderate hemophilia may also experience occasional bleeding episodes without obvious cause. These are called

A

“spontaneous bleeding episodes”

70
Q

severe hemophilia constitutes –% of the hemophilia population

A

60%

71
Q

people with severe hemophilia have bleeding following an injury and may have frequent

A

spontaneous bleeding episodes, often into the joints and muscles

72
Q

preoperative therapy involves giving

A

cryoprecipitate and factor 8 concentrates (hemophilia A) and factor 9 concentrates (hemophilia B)

73
Q

cytoprecipitate is prepared from plasma and contains (4)

A

fibrinogen
von willebrand factor
factor 8
fibronectin

74
Q

cryoprecipate is the only adequate fibrinogen concentrate available for

A

intravenous use

75
Q

additional treatment considerations include the use of splints to retain the venous blood clots in their socket and the avoidance of block local anesthetic unless factors are at least

A

50% of normal

76
Q

the use of vasopressin analogue demopressin is valuable in cases of mild disease as they cause a three to four fold increase in the

A

factor 8 coagulant activity

77
Q

teeth can be extracted under the cover of (2)

A

epsilon-aminocaproic acid or tranexamic acid (both inhibit fibrinolysis)

78
Q

von willebrands disease

A

a bleeding disorder I which a protein called von villebrand factor is missing or does not work well in the body blood system

79
Q

consequently, defective von willebrand factor interaction between platelets and the vessel wall impairs

A

primary hemostasis

80
Q

3 major types of VQD

A

type 1
type 2
type 3

81
Q

type 1 VWD

A

A shortage of von Willebrandfactor (mild). (Between 70% to 80% of all cases)

82
Q

Most common form or VWD?

A

type 1

83
Q

type 2 VWD

A

A flawed von Willebrandfactor (usually mild)(Subclassifiedas Type-2A and Type -2B).

Type 2 VWD is less common than Type 1. It represents 20-25% of allcases.

84
Q

type 3 VWD

A

A complete lack of von Willebrandfactor (more severe). Type 3 VWD is very rare. It affects about 1 in 500,000 people

85
Q

in patients with VWD, injuries and surgery can lead to

A

serve bleeding

86
Q

what should prompt the dentist to consider VWD? (3)

A

an elevated bleeding time, normal platelet count, and no history of asrpij or NSAID use

87
Q

blood tests are available to measure (3)

A

bleeding time
von willebrand factor activity levels
won villibrand factor antigen

88
Q

what can show a defect in a patient with VW factor

A

genetic testing

89
Q

preoperative therapy is usually decided after consultation with a hematologist and varies according to

A

severity of the disease

90
Q

factor 8 cryoprecipitate and desmopressin are often given with

A

aminocaproic acid preoperatively and then again postoperatively after a period of 3 to 5 days

91
Q

desmopressin helps to increase the production of

A

VW factor

92
Q

demopressin is contraindicated in

A

type 2B patients

93
Q

tranexamic acid an also be used intreat of aminocaproic acid as an

A

inhibitor of fibrinolysis

94
Q

the normal platelet count is usually about

A

150,000 to 400,000 per microliter

95
Q

thrombocytopenia (decreased platelet count) elevates the

A

bleeding time

96
Q

the cause of thrombocytopenia is either (2)

A

decreased platelet production or increase platelet destruction

97
Q

the common causes of increased destruction include (3)

A

idiopathic thrombocytopenia purapura (ATP)
drug included ITP (quinidine)
transfusion related purapuras

98
Q

decreased production occurs secondary to

A

myelosuppresion due to antieoplastic agents as well as radiation treatment

99
Q

in a patient with platelets in the range of 50,000-100,000, minor surgery like single tooth extraction nd biopsies are usually

A

tolerated without the need for platelet transfusion

100
Q

following tooth extractions, use of local hemostatic measure measures is useful as it

A

stabilizes the blood clot

101
Q

local measures of hemostatic agents (2)

A

suturing the wound

pressure with oral packs

102
Q

in patients with platelet count below 50,0000, appropriate hematologist consultation should be taken and pre-operative transfusion with platelets or fresh frozen plasma given to a patient before performing

A

any type of oral surgical procedure

103
Q

acquired bleeding disorders are most often drug induced but can also be (2)

A

secondary to alcohol (alcoholics have thrombocytopenia secondary to hyperplenism)
virus induced liver disease (as the liver produces all coagulation factors except factor 8 and possibly factor 13, a history of serious liver disease can cause a possible coagulopathy)

104
Q

vitamin k deficiency from broad spectrum antibiotic use or malabsorption syndromes may also induce a

A

coagulopathy

105
Q

acquired platelet function defect

A

idiopathic thrombocytopenia purpura

106
Q

acquired bleeding disorders (4)

A

drug induced
vitamin k deficiency
acquired platelet function defect
multiple myeloma

107
Q

acquired bleeding disorders (6)

A

patient taking oral anticoagulants (Coumadin, “Pradaxa” dibigatran, “Xarelto” - tivaroxaban)
patients taking anti platelet like placid, clopidogrel, SAIDS
patients with leukemia
patients on chemotherapy
HIV patients with low platelets count
kidney failure

108
Q

it is important to achieve proper hemostasis in all patients during oral surgical procedures, so as to prevent

A

excessive intra-operative and post-operative blood loss

109
Q

for successful peri-operative hematological management of patients with bleeding disorders and those on blood thinners, we need to achieve the following (6)

A

Medical Consultation (If necessary)
Assessment of Laboratory Test results
Referral to Oral and Maxillofacial Surgeon
Withdrawal of anticoagulant /Antiplatelet treatment prior to surgery (Do’s and Don’ts)
Role of Bridging Therapy
Local Measures used to control bleeding (Gelfoam, Surgicel, Tranexamic Acid, Suturing, Pressure Packs)

110
Q

the management of patients receiving anti platelet and anticoagulant therapy is a fundamental skill of the dentist that requires

A

continual re-education as new medication become available for anticoagulation

111
Q

patients on oral anticoagulant/antiplatelet treatment are currently not recommended to

A

discontinues their medication prior to minor oral surgery procedures as this increases their risk of developing a thromboembolic episode

112
Q

in these patients, we currently recommended using local measures to

A

control bleeding after surgery

113
Q

however, if patient’s need major oral surgery procedures, then appropriate medical consultation with physician is sought and the anticoagulant/antiplatelet medication is withheld from patient a few day/days prior to surgery. in this situation, patients on Coumadin are

A

put on a bridging treatment with heparin prior to surgery

114
Q

it is important to understand the fact that the decision to withhold the anti platelet/anticoagulant medication can only be made by

A

the physician and not the treating dentist

115
Q

local measures: hemostatic agents (2)

A

suturing he wound

pressure with oral packs

116
Q

usual dose of local measures to irrigate the wound with tranexamic acid 5%

A

5-10 mL up to 4x daily, it does not need to be further diluted

117
Q

the mouthwash should be rinsed around inside the mouth thoroughly for two minutes and then

A

spat out

118
Q

after you have used this mouthwash, do not

A

eat or drink for one hour

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