Brainscape's Knowledge GenomeTM

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


See full index

PHARM > hemostatsis and thrombosis > Flashcards

hemostatsis and thrombosis Flashcards

1
Q

Hemostasis
caused by:

A
  • “the arrest of blood loss from damaged blood vessels”
  • Essential to life
  • Caused by:
  • Platelet adhesion and activation
  • Fibrin formation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Thrombosis

A
  • “pathological formation of a ‘hemostatic plug’ within the vasculature in the absence of bleeding”
  • Hemostasis in the wrong place
  • Virchow’s triad
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Virchow’s triad

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

White Thrombus

A
  • Arterial clot
  • Primarily platelets and some fibrin mesh
  • Associated with atherosclerosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Red Thrombus

A
  • Venous clot
  • Mostly fibrin and small amount of platelets
  • Higher risk of embolus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Coagulation Cascade

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

Antithrombin III

A

Prevents coagulation
by lysing
Factor Xa and Thrombin

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

Thrombin (Factor IIa) also causes?

A

also causes platelet activation

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

Intrinsic Pathway:
* All components present in?
* Starts when blood comes in contact with? or?
* Monitored by?

A
  • All components present in the blood
  • Starts when blood comes in contact with foreign object or damaged endothelium
  • Monitored by Activated Partial Thromboplastin time (aPTT)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Extrinsic Pathway

A
  • Some components come from outside blood
  • Tissue factor
  • Starts when tissue damage releases tissue factor
  • Monitored by Prothrombin time (PT) and INR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Vitamin K

A
  • Fat soluble vitamin with little stored in the body
  • Most vitamin K obtained from diet or produced by bacteria in the gut
  • Vitamin K is a cofactor in the formation of several clotting factors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

vitamin K dependent factors

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

Platelets Role in Thrombus Formation

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

Platelet Activation and Aggregation diagramm

A

pathways

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

Fibrinolysis

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

Anticoagulant Medication classes

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

Warfarin
Mechanism of Action**

A
  • Acts only in vivo
  • Inhibits vitamin K epoxide reductase component 1
    (VKORC1)
  • The VKORC1 gene is polymorphic resulting in different affinities for warfarin
  • Genetic testing is available for this polymorphism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Warfarin Pharmacokinetics
* Rapidly absorbed after?
* Highly bound to?
* metab where? implication?
* Onset of action?
* Half-life?
* Requires what to be achieved?
* Vitamin K dependent clotting factors?
* Effects of dose change requires?

A
  • Rapidly absorbed after oral administration
  • Highly bound to plasma proteins (i.e. albumin)
  • Hepatically metabolized (CYP 450 2C9 and 3A4)
  • Polymorphism of CYP 450 2C9
  • Onset of action 5-7 days
  • Half-life is ~ 40 hours
  • Requires new steady-state of clotting factors to be achieved
  • Vitamin K dependent clotting factors: II, VII, IX, X, protein C, protein S
  • Effects of dose change require 2-3 days to presen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Warfarin Effect of coagulation parameters

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

Warfarin
Adverse Drug Reactions

A
  • Bleeding (can be life threatening), GI bleeding most common
  • Rash
  • Skin necrosis
  • Taste disturbance
  • “Purple toe” syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Drugs that change hepatic metabolism of warfarin

A
  • Inhibition = more effect of warfarin = elevated INR
  • Induction = less effect of warfarin = decreased INR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Drugs that displace warfarin from protein binding sites

A
  • More free drug = more effect of warfarin = elevated INR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Drugs that change vitamin K levels effect on warfarin

A
  • Broad spectrum antibiotics reduce GI flora = less vitamin K and more effect of warfarin = elevated INR
  • Intake of vitamin K decreases effect of warfarin = decreased INR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Drugs that increase risk of bleeding w warfarin

A
  • ASA and NSAIDS inhibit platelet function = increased risk of bleeding
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Warfarin moa

A

Inhibit vitamin K epoxide reductase
component 1 (VKORC1)

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

warfarin adrs

A

bleeding, taste disturbances, skin necrosis

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

warfarin therpeutic index

A

narrow

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

warfarin interactions
* Increased effect with?
* Decreased effects with?

A
  • Increased effect with NSAIDs, antibiotics, acetaminophen?
  • Decreased effects with barbiturates
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Warfarin (Vitamin K Antagonist)
Dental Implications

A
  • Most procedures can be done without holding
  • For dental procedure that may result in excessive bleeding consult prescribing physician to adjust dose or hold if possible
  • Consider local hemostasis measures to prevent
    excessive bleeding
  • Check INR level prior to performing a dental surgical
    procedure
  • Antibiotic use after dental procedure may increase risk of bleeding
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Heparin
Mechanism of Action

A
  • Inhibits coagulation in vivo and in vitro
  • Activation of antithrombin III
  • Increases antithrombin III affinity for Factor Xa and Thrombin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Heparin
Pharmacokinetics
* Not absorbed from?
* Administered?
* onset?
* Half-life?

A
  • Not absorbed from the gastrointestinal (GI) tract
  • Administered intravenously (IV) or subcutaneously (SQ)
  • Fast onset: immediate after IV, 60 minutes after SQ
  • Half-life is ~ 40-90 minutes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

heparin effects on coagulation parameters:

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Heparin
Adverse Drug Reactions

A
  • Bleeding (can be life threatening), Protamine can reverse effects (binds heparin)
  • Thrombosis
  • Heparin associated thrombocytopenia (HAT)
  • Heparin induced thrombocytopenia (HIT)
  • Osteoporosis- with long-term treatment, mechanism unclear
  • Aldosterone inhibition= hyperkalemia
  • Hypersensitivity reaction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Heparin moa

A
  • MOA: Activation of antithrombin III leading to
    inhibition of thrombin and factor Xa
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

heparin adrs

A

bleeding, thrombosis, osteoporosis, hyperkalemia, hypersensitivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

heparin interactions/dental

A
  • Drug-Drug interactions: none of significance to dentistry
  • Dental implications: none beyond bleeding
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Low Molecular Weight Heparin (LMWH)
Mechanism of Action

A
  • Inhibits coagulation in vivo and in vitro
  • Smaller portion of the heparin molecule
  • Not large enough to interact with thrombin
  • Activation of antithrombin III
  • Increases antithrombin III affinity for Factor Xa but NOT thrombin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Low Molecular Weight Heparin (LMWH)
Pharmacokinetics
* Not absorbed from?
* Administered how?
* onset/response?
* Cleared by?
* Half-life?

A
  • Not absorbed from the GI tract
  • Administered subcutaneously (SQ)
  • Fast onset and predictable response
  • Cleared by the kidneys
  • Half-life is 4.5-7 hours
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Low Molecular Weight Heparin (LMWH effects on coag perameters

A

LMWH do NOT require monitoring of coagulation parameters

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

enoxaparin moa

A

Activation of antithrombin III leading to
inhibition factor Xa but NOT thrombin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

enoxaparin adrs

A

bleeding, thrombosis, osteoporosis, hyperkalemia,
hypersensitivity
* Lower incidence of HIT than unfractionated heparin

42
Q

enoxaparin interactions

A

Increased risk of bleeding with NSAIDs and Aspirin

43
Q

Low Molecular Weight Heparin (LMWH)
Example: enoxaparin- Dental Implications

A
  • Determine why patient is taking medication
  • Delay procedure until treatment complete
  • Do not discontinue therapy
  • Consider local hemostasis measures to prevent
    excessive bleeding
44
Q

Direct Thrombin Inhibitors Mechanism of Action

A
  • Derived for the saliva of medicinal leeches
  • Binds to the fibrin-binding sites of thrombin preventing the conversion of fibrinogen to fibrin
45
Q

Direct Thrombin Inhibitors
* Intravenous agents:
* Oral agent:

A
  • Intravenous agents: Argatroban and Bivalirudin
  • Oral agent: Dabigatran (pro-drug)
46
Q

Direct Thrombin Inhibitors effect on coag perameters

A

Dabigatran does not require monitoring of coagulation tests
* Argatroban and bivalirudin may be monitored by aPTT depending in indication

47
Q

Argatroban and INR

A

Argatroban has a
drug-lab interaction
resulting in a falsely
elevated INR

48
Q

Dabigatran moa

A

Binds to thrombin preventing conversion of fibrinogen to fibrin

49
Q

Dabigatran adrs

A

bleeding (reversal agent available- idarucizumab), Reversal costs ~$5,000

dyspepsia/gastritis- due to formulation

50
Q

Dabigatran interactions

A

ncreased risk of bleeding with NSAIDs and Aspirin

51
Q

Dabigatran dental

A
  • High risk of bleeding
  • High risk of thrombosis if stopped (short half-life)
52
Q

Factor Xa inhibitors
Mechanism of Action

A
  • Binds to factor Xa and prevent
    the conversion of prothrombin
    to thrombin
53
Q

Factor Xa Inhibitors
* Parenteral agent:
* Oral agents:

A
  • Parenteral agent: Fondaparinux (SQ)
  • Oral agents: Apixaban, Edoxaban, Rivaroxaban
54
Q

factor Xa inhibitors effect on coag perameters

A
55
Q

factor Xa inhibitors monitoring

A
  • Factor Xa inhibitors have an inconsistent effect on coagulation tests
  • Factor Xa inhibitors do NOT require routine monitoring- do require renal dosing
56
Q

Apixaban moa

A

Binds to factor Xa and prevents conversion of prothrombin to
thrombin

57
Q

apixaban adrs

A

bleeding (reversal agent available- andexanet alfa)
Reversal costs between $25,000-$30,000

58
Q

Apixaban interactions

A

Increased risk of bleeding with NSAIDs and Aspirin

59
Q

apixaban dental

A
  • High risk of bleeding
  • High risk of thrombosis if stopped (short half-life)
60
Q

NOACs
Non-Vitamin K Oral Anticoagulants

A
  • Overarching term referring to:
  • Apixaban
  • Dabigatran
  • Edoxaban
  • Rivaroxaban
    • Also called DOACs= Direct-acting Oral Anticoagulants
61
Q

Generally NOACs are recommended in?

A

Generally NOACs are recommended in guidelines over
warfarin for prevention of stroke and systemic embolism AF and DVT/PE treatment due to ease of use

62
Q

Antiplatelet Medications types

A

Epoprostenol- this medication is addressed in the vascular section

63
Q

Aspirin
Mechanism of Action
* Inhibits?
* Prevents?
* Low dose?
* length of effect?

A
  • Inhibits cyclo-oxygenase 1 (COX 1)
  • Prevents formation of prostaglandin which is subsequently converted to thromboxane A2
  • Low dose ASA (81mg) inhibits > 95% of platelet TXA2 formation
  • Platelets can not make new COX-1, ASA effects last for life of platelet 7- 10 days
64
Q

Aspirin Adverse Reactions
More Common:
Less common:

A

More Common:
* Bleeding- gastrointestinal
* Gastrointestinal distress
* Rash

Less common
* Angioedema
* Tinnitus
* Respiratory distress

65
Q

Aspirin moa

A

Inhibition of COX-1 preventing the formation of TXA2

66
Q

aspirin adrs

A

bleeding, rash, GI distress, angioedema, tinnitus, respiratory distress

67
Q

aspirin interactions

A
  • Increased risk of bleeding with NSAIDs and other anticoagulants
  • May lower the effectiveness of anti-hypertensive agents
68
Q

Aspirin
Dental Implications

A
  • Determine why ASA is being taken- most procedures can be done without holding ASA
  • Increased risk of bleeding
  • Consider local hemostasis measures to prevent excessive bleeding
69
Q

P2Y12 inhibitors
Mechanism of Action

A
70
Q

Clopidogrel pharmacokenetics

A

*CYP 2C19 polymorphisms effect the efficacy of clopidogrel

71
Q

prasugrel pharmacokenetics

A
72
Q

Ticagrelor pharmacokenetics

A
73
Q

Cangrelor pharmacokenetics

A
74
Q

P2Y12 inhibitors
Adverse Drug Reactions

A
  • Bleeding, Less occurrence than aspirin when used as monotherapy and Increased occurrence when combined with aspirin (DAPT)
  • Skin rash (~ 10%)
  • Thrombocytopenia (rare)
75
Q
  • ADRs unique to ticagrelor:
A
  • Dyspnea- due to off-target adenosine effects
  • Elevated serum creatinine- unknown mechanism usually clinically insignifican
76
Q

P2Y12 inhibitors Drug-Drug interactions
* Mainly due to?
* Prodrugs?
* Proton Pump Inhibitor?
* Ticagrelor?
* All P2Y12 inhibitors interact with?

A
  • Mainly due to CYP 450 inhibition: Ticagrelor 3A4, Clopidogrel & Prasugrel 2C19
  • Prodrugs (Clopidogrel & Prasugrel) require activation by CYP 450 therefore have less activity resulting in increased risk of thrombotic event
  • Proton Pump Inhibitor resulting in a significant drug-drug interaction
  • Ticagrelor active upon administered therefore inhibition results in increased levels and activity leading to increased risk of bleeding
  • All P2Y12 inhibitors interact with other medications that increase risk of bleeding (i.e. anticoagulants, NSAIDs, etc..
77
Q

ticagrelor moa

A

Inhibition of ADP binding to the P2Y12 receptor

78
Q

ticagrelor adrs

A

bleeding, rash, dyspnea, elevated serum creatinine

79
Q

ticagrelor interactions

A
  • Increased risk of bleeding with NSAIDs, aspirin, and other anticoagulants
  • CYP 3A4 inhibitors (i.e. macrolide antibiotics and azoles) may increase effect
80
Q

P2Y12 inhibitors
Example: ticagrelor- Dental Implications

A
  • Plan for increased bleeding
  • Consider local hemostasis measures to prevent
    excessive bleeding
  • Do not stop/hold without consulting prescribing
    physician
  • Do not alter aspirin dose prescribed
  • Ticagrelor specific- potential shortness of breath
81
Q

Glycoprotein IIb/IIIa inhibitors
Mechanism of Action

A
  • Bind to GP IIa/IIIb receptor preventing platelet aggregation
  • Only available intravenously
  • Eptifibatide and tirofiban: small molecules
82
Q

Eptifibatide moa

A

Bind to GP IIa/IIIb receptor preventing platelet aggregation

83
Q

Eptifibatide adrs

A

bleeding (highest of all antiplatelet agents), thrombocytopenia

84
Q

Eptifibatide interactions/ dental

A
  • none of significance to dentistry
  • other drugs that increase bleeding
  • Dental Implications: none
85
Q

PAR-1 antagonist (Vorapaxar)
Mechanism of Action

A
  • Antagonist of the protease activated receptor-1 inhibiting thrombin receptor agonist peptide (TRAP)- induced platelet aggregation
  • Does NOT effect the conversion of fibrinogen to
    fibrin by thrombin
86
Q

Vorapaxar moa

A

Antagonist of the protease activated receptor-1 inhibiting thrombin receptor agonist peptide (TRAP)- induced platelet aggregation

87
Q

Vorapaxar adr

A

bleeding (~25%

88
Q

Vorapaxar interactions/dental

A
  • Drug-Drug interactions: Other drugs that increase bleeding (i.e. aspirin, NSAIDs, anticoagulants)
  • Dental Implications: High bleeding risk medication
89
Q

hold or nor hold these meds in dentistry?

A

“There is general agreement that in most cases, treatment regimens with older anticoagulants (e.g., warfarin) and antiplatelet agents (e.g., clopidogrel,
ticlopidine, prasugrel, ticagrelor, and/or aspirin) should NOT be altered before dental procedures. The risks of stopping or reducing these medication regimens
(i.e., thromboembolism, stroke, MI) far outweigh the consequences of prolonged bleeding, which can be controlled with local measures.”

“On the basis of limited evidence, general consensus appears to be that in most patients who are receiving the newer target-specific oral anticoagulants (i.e.,
dabigatran, rivaroxaban, apixaban, or edoxaban) and undergoing dental interventions (in conjunction with usual local measures to control bleeding), NO
CHANGE to the anticoagulant regimen is required.”

90
Q

In patients with comorbid medical conditions that can increase the risk of prolonged bleeding after dental treatment or who are receiving other therapy that can increase bleeding risk, dental practitioners may wish to?

A

In patients with comorbid medical conditions that can increase the risk of prolonged bleeding after dental treatment or who are receiving other therapy that can increase bleeding risk, dental practitioners may wish to consult the patient’s physician to determine whether care can safely be delivered in a primary care office. Any suggested modification to the medication regimen
prior to dental surgery should be done in consultation and on advice of the patient’s physician

91
Q

Fibrinolytic and Antifibrinolytic medication types

A
92
Q

Plasminogen activators
Mechanism of Action

A

Binds to tissue bound fibrin and plasminogen
converting plasminogen to plasmin (fibrin specific)

Recombinant form of tissue plasminogen activator (TPA)

93
Q

Tenecteplase moa

A

Binds to tissue bound fibrin and plasminogen converting plasminogen to plasmin

94
Q

Tenecteplase adrs

A

bleeding from virtually any site

95
Q

Tenecteplase interactions/dental

A
  • Drug-Drug interactions:
  • None of significance to dentistry
  • Other drugs that increase bleeding (i.e. heparin, aspirin, and clopidogrel)
  • Dental Implications: none
96
Q

Hemostatic Agents
Mechanism of Action

A

Competitive inhibition of plasminogen activation by binding to plasminogen

At higher concentrations non-competitive inhibition of plasmin

97
Q

Tranexamic acid moa

A

Competitive inhibition of plasminogen activation by binding to plasminogen; at higher concentrations non-competitive inhibition of plasmin

98
Q

Tranexamic acid adrs

A

IV- hypotension and giddiness;
PO- headache, abdominal pain, and nasal/sinus symptoms

99
Q

Tranexamic acid interactions

A
  • Reduces the effectiveness of anticoagulants
  • Increased risk of thrombosis
100
Q

Tranexamic acid- Dental Implications

A
  • Used as an antifibrinolytic mouthwash following
    dental surgery to prevent hemorrhage in patients taking oral anticoagulants.
  • Topical administration should have limited systemic effects. If systemic administration considered consult with physician prescribing anticoagulant

PHARM (15 decks)

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