Brainscape's Knowledge GenomeTM

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


See full index

ACP Hematology > L29 Bleeding disorders - Thrombosis and Anticoagulant therapy (I) > Flashcards

L29 Bleeding disorders - Thrombosis and Anticoagulant therapy (I) Flashcards

1
Q

List the 4 stages of hemostasis in response to vessel injury.

A
  1. Vasoconstriction to reduce blood flow
  2. Primary hemostasis: platelet plug formation
    - von Willebrand factor binds damaged vessel and platelets
  3. Secondary hematosis: activation of the coagulation cascade
  4. Tertiary hemostasis:
    - Cross-linking of fibrin strands
    - Clot maturation and wound healing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

In primary hemostasis, platelets adhere to __________ and __________.

A

exposed collagen and von Willebrand factor

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

Von Willebrand factors

  • anchors _________ to subendothelium
  • bridge between _________
  • carrier of factor _______
A

Platelets;
platelets;
VIII

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

List all the Vitamin K dependent factors.

A

Factor II, VII, IX, X

2,7,9,10

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

Factor VII is involved in the ________ system that binds to ________ to become VIIa.

A 
extrinsic system (tissue damage);
tissue factor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is tertiary hemostasis?

A

Stabilization of platelet plug by fibrin

- fibrin is added to the platelet mass and by platelet-induced clot reaction/ compaction

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

Venous thrombosis VS arterial thrombosis:

Venous thrombosis is heavily dependent on excessive __________ formation from soluble coagulation factors.
_______ is the key to effective treatment and prevention.

A

Thrombin;

Anti-coagulation

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

Venous thrombosis VS arterial thrombosis:
Arterial thrombosis is dominated by _________________________________.
_________ is the mainstay of treatment and prevention.

A

Platelets interacting with damaged endothelium;

Anti-platelets

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

List the 6 steps of artertial thrombosis.

A
  1. Atherosclerosis of the arterial wall
  2. Plaque rupture and endothelial injury
  3. Exposure of subendothelial collagen and tissue factor
  4. Platelet aggregation and adhesion
  5. Thrombus formation
  6. Systemic emboli
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q 
Which of the above is not a risk factor for arterial thrombosis (atherosclerosis)? 
A. Positive family Hx
B. Male
C. Smoker
D. HT, HL, DM
E. Gout
F. Polycythemia 
G. Hypohomocysteinemia 
H. Low serum folate, VitB12, B6
A

G

  • Should be Hyperhomocysteinemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Name components of Virchow’s triad.

A
  1. (circulatory) Stasis
  2. Endothelial injury
  3. Hypercoagulability
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Name 6 common causes of a hypercoagulable state.

A
  1. Malignancy
  2. Pregnancy and peripartum period
  3. Estrogen therapy (increase plasma level of F2,7,8,9)
  4. Inflammatory bowel disease
  5. Sepsis
  6. Thrombophilia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Name 4 common causes for circulatory stasis.

A
  1. Left ventricular dysfunction
  2. Immobility of paralysis
  3. Venous insufficiency
  4. Venous obstruction from tumor, obesity or pregnancy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Name the 3 MC hereditary causes for hypercoaguability.

A
  1. Protein C deficiency
  2. Protein S deficiency
  3. Antithrombin III deficiency
  4. Factor V Leiden

Others

  • Prothrombin G20210A variant
  • Elevated factor 8,9,11 levels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are protein C and S?

A

Naturally occurring anticoagulants (to prevent excessive clotting)

MOA:
- Protein C > activated protein C + protein S cofactor > inhibit factor 8,5a, inhibitor of tissue of plasminogen activator
> enhanced thrombolysis

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

Which of the following concerning protein S and C deficiency are correct?
A. It is an autosomal dominant disease
B. Both are vitamin K dependent proteins
C. Most patients will be symptomatically presented with a VTE
D. Warfarin will reduce protein S and C
E. It causes recurrent VTE in younger patients

A

All except C

  • Many patients are asymptomatic, will never have a VTE

E: Features: spontaneous and often recurrent VTE in young patients

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

Anti-thrombin III MOA?

A

Inhibits factor 11a, 9a, 10a and thrombin

> thus antithrombin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Which of the following concerning Anti-thrombin III deficiency are correct?
A. It is an autosomal dominant disease
B. Recurrent venous thrombosis starting in early adult life
C. Arterial thrombosis also occur occasionally
D. It is clinically less severe than protein C/S deficiency
E. Pregnant patients are given more anti-coagulant as treatment compared to other patients.

A

D is wrong

- more severe!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Factor V leiden gene mutation causes?

A

Activated protein C resistance

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

Which of the following about antiphospholipid syndrome is correct?

A. it is the occurrence of thrombosis/ recurrent miscarriage a/w persistent antiphospholipid antibody (e.g. lupus anticoagulant, anticardiolipin antibodies)

B. Primary antiphospholipid syndrome means it is idiopathic

C. Secondary antiphospholipid syndrome means it is a/w with other autoimmune diseases such as connective tissue disorders like SLE

D. Lymphoproliferative disease is one of the causes

E. Post-viral infections is one of the causes

A

All of the above

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Which of the following about antiphospholipid syndrome is incorrect?

A. It is associated with arterial thrombosis only
B. Thrombocytopenia may be present
C. Oral anticoagulation is used, e.g. warfarin with a higher INR required
D. Low dose heparin and aspirin is used to manage recurrent miscarriages

A

A

  • both arterial thrombosis and venous thrombosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Patient presented with Dyspnea, tachypnea, tachycardia, cyanosis (hypoxia), and hypotension.
Pulmonary embolism or DVT?
What are other S/S concerning this diagnosis?

A

Pulmonary embolism

  • Haemoptysis
  • Syncope
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

List 4 S/S in a patient with DVT.

A
  1. Limb swelling (calf/limb)
  2. Pain
  3. Tenderness
  4. Erythema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How to diagnosis Deep vein thrombosis? (3)

A
  1. Doppler ultrasound of veins in legs/other sites
    - non-invasive, good in the diagnosis of proximal venous thrombosis (above the knee), operator dependent
  2. Venogram
  3. Plasma D-dimer level
    - raised when there is fresh venous thrombosis
    - not specific for DVT, usually used with a clinical scoring system to rule out DVT
    - need to combine with imaging test to confirm the diagnosis
25
Q

Why Plasma D-dimer is not specific for DVT?

A

It is raised also in infection, pregnancy, malignancy

26
Q

How to diagnose pulmonary embolism?

Which is the most commonly used?

A
  1. Chest X-ray
    - usually normal, show pulmonary infarction/ pleural effusion
    a. Ventilation/Perfusion (V/Q) scan - detects areas of the lung being ventilated but not perfused
    b. ***CT pulmonary angiogram - spiral CT scan to detect filling defects in pulmonary arteries
  2. Pulmonary angiography
    - invasive, may be complicated by contrast reaction, arrhythmia
  3. Magnetic resonance pulmonary angiogram
    - new and accurate but expensive
27
Q

What screening tests to be done for thrombophilia?

Name the test and describe what to be tested.

A

MUST

  1. CBC and blood film
    - detect raised Hb level, platelet count, evidence of myeloproliferative neoplasms
  2. Prothrombin time (PT) and activated partial thromboplastin time (APTT)

Others

  1. Protein C, S and antithrombin III level
  2. Lupus anticoagulant, anti-cardiolipin antibodies…
28
Q

Which of the following are correct for thrombophilia testing?
A. It should be tested at the time of VTE event
B. It should not be tested when the patient is receiving anticoagulant therapy
C. It should not be tested if VTE is provoked by strong risk factors (e.g. major trauma, immobility, major illness)
D. Consider testing in patients whom VTE occurs in young age a/w weak provoking factors/ strong family history
E. Goals of testing are identified to aid decision making regarding future VTE prophylaxis

A

All except A
- test at completion of anticoagulation therapy for provoked VTE, for unprovoked: test after treatment for an acute event

29
Q

3 phases of VTE

  1. Acute
  2. Prevention
  3. Extended use

Standard treatment for the acute phase? (3)

A
  1. initial UFH (unfractioned heparin)
  2. LMWH (low molecular weight heparin)
  3. fondaparinux (anticoagulation with LMWH)
    for > 5 days
30
Q

3 phases of VTE

  1. Acute
  2. Prevention
  3. Extended use

Standard treatment for the prevention phase?
INR be kept within?
For how long?

A

Early maintenance VKA (vitamin K antagonist) = warfarin
INR 2-3
> 3 months

Similar for extended use phase, but long-term secondary prevention VKA

31
Q

Name 2 novel oral anticoagulants that requires LMWH > switching.

A
  1. Dabigatran (direct thrombin inhibitor)

2. Edoxaban (Factor Xa inhibitor)

32
Q

Name 2 novel oral anticoagulants that are used in single-drug approach.

A
  1. Rivaroxaban (Factor Xa inhibitor)

2. Apixaban (Factor Xa inhibitor)

33
Q

Patients should receive at least __________(duration) of anticoagulant to treat the acute event of DVT/PE.

Subsequent actions?

A

3 months

>

  • then a decision should be made to either stop treatment/continue it indefinitely
  • with the option of subsequently stopping treatment if the patient’s risk of bleeding becomes excessive or the patient decline treatment
34
Q

Factors associated with a higher risk of recurrence?

A
  • Second/subsequent idiopathic event
  • Positive D-dimer after withdrawing D-dimer (for a month)
  • antithrombin III deficiency
  • antiphospholipid syndrome
  • male, old
    …
35
Q

Which of the following are factors a/w high risk of bleeding thus favor stopping anticoagulation?

A. Age >75
B. History of non-cardioembolic stroke
C. Chronic renal/hepatic failure
D. Concomitant antiplatelet therapy 
E. Poor compliance with anticoagulant therapy/monitor
A

All of the above

Also Previous GI bleeding

36
Q

Anticoagulant therapy is widely used in the treatment and prophylaxis of venous thromboembolic disease such as ?

A
  • Deep vein thrombosis (DVT)
  • PE
  • thromboembolic prophylaxis in patients with AF
  • Prophylaxis in patients with thrombophilia state
37
Q

Anticoagulants can either be parenteral/oral.

List the drugs for both.

A

Parenteral = non-oral

  • Unfractionated heparin (UFH)
  • LMWH

Oral

  1. VKA - warfarin
  2. Direct thrombin inhibitor - Dabigatran
  3. Factor Xa inhibitors - Rivaroxaban/Apixaban/Edoxaban
38
Q

MOA for UFH and LMWH respectively? (differences)

A

UFH (IV)

  • inhibits Factor 9a, 11a, 10a, thrombin
  • impairs platelet function

LMWH (SC)

  • greater ability to inhibit factor Xa than to inhibit thrombin
  • less interaction with platelet function
39
Q

What to monitor if UFH and LMWH are administered respectively? Their bioavailability?

A

UFH

  • APTT
  • 50%

LMWH

  • Xa assay (rarely needed)
  • 100%
40
Q

Advantage of LMWH over UFH? (2)

A
  1. Lower frequency of HIT (heparin-induced thrombocytopenia)

2. Less frequent osteoporosis

41
Q

Why are heparin the drug of choice in pregnant women if needed?

A

It does not cross the placenta

42
Q

Other than treatment/prophylaxis of DVT and PE, heparin can also be used for the treatment of?

A

ACS

also prevent thromboembolism in patients with AF
- in DIC if the clinical problem is mainly thrombosis

43
Q

Which of the following about heparin administration and monitoring is incorrect? *UFH

A. UFH can be given in continuous intravenous infusion with a loading bolus of 5000 units followed by 600-1000 units/hour continuous infusion

B. Dosage of UFH is determined by checking the APTT

C. APTT aim for after UFH given is between 1.5-2.5

D. IV infusion is preferred when heparin is given as prophylaxis against venous thrombosis

A

D

- intermittent SC injection is preferred!

44
Q

Which of the following about heparin administration and monitoring is incorrect?

A. LMWH is usually given by SC injection once daily as prophylaxis/ 1-2 daily as a treatment
B. Dosage is calculated based on APTT
C. Monitoring is not usually needed but can be done with Anti-FXa assay
D. Replace UFH for therapy and prophylaxis of thromboembolism and treatment of unstable angina
E. can be used as home therapy

A

B

- based on body weight!

45
Q

When bleeding occured as a complication of heparin therapy, what to do? (3)

A
  1. Stop treatment
  2. Protamine may be used to neutralize heparin but itself is also an anticoagulant
  3. Less frequent with LMWH (no interaction with platelet, easier dose adjustment)
46
Q

Other than bleeding, other complications of heparin therapy?

A
  1. HIT (Heparin-induced thrombocytopenia)
  2. Osteoporosis
    - long term (> 2 months) heparin therapy, especially in pregnancy
47
Q

___________ works by blocking the gamma-carboxylation of glutamic acid residues of vitamin K dependent clotting factors (2,7,9,10) > reduce their biological activity.

A

Warfarin

48
Q

Which of the following about warfarin is incorrect?
A. Monitored by the international normalized ratio (INR) from day 3 onward and titrate maintenance dose
B. Biological effects can be immediately achieved after administered
C. usually start a loading dose of warfarin 5mg daily for 2 days in the Chinese population
D. Target INR for warfarin use is 2.5 (2.0-3.0)
E. Target of INR is higher if there is recurrent VTE whilst anticoagulated

A

B

take a few days after initiation of treatment to achieve biological effects

D: narrow therapeutic window (stroke VS intracranial bleeding)

49
Q

The most common side effect of warfarin and the most important contraindication?

A

Hemorrhage
(Others: hypersensitivity reaction, skin necrosis, liver dysfunction, jaundice)

Warfarin is teratogenic can cross the placenta.
Heparin is preferred!

50
Q

What drugs would interact with warfarin (vitamin K antagonist)?

A

Drugs that affect the

  1. Albumin binding of oral anticoagulant
  2. Metabolism and excretion of oral anticoagulant
  3. Absorption of vitamin K (competes with warfarin for vitamin K)

also with herbs

51
Q

Other than drugs, list 3 factors affecting control of VKA therapy?

A
  1. Intaking and absorption of vitamin K
    - dietary intake of vitamin K food esp green leave vegetables (should take constant amount of leaves
    - malabsorption/ abx therapy (gut flora produces Vit K > INR fluctuate)
  2. Liver disease
    - decreased synthesis of vitamin K factors
  3. Patients taking anti-platelet agents e.g. NSAIDS and aspirin are more likely to bleed
52
Q

Management for warfarin overdose? (4)

A
  1. Stop warfarin
  2. Vitamin K1 - low dose (e.g. 1mg) orally to rapidly reduce INR to the therapeutic range within 24 hours
  3. Prothrombin complex concentrates (Factors 2,7,9,10)
  4. Plasma transfusion
53
Q

Pathway:
Factor X > Xa > II > IIa
IIa is needed to change fibrinogen to fibrin

Name 4 New oral anticoagulants and state where is their acting targets respectively.

A
  1. Apixaban
  2. Rivaroxaban
  3. Edoxaban
    > inhibit factor Xa
  4. Dabigatran
    > inhibits IIa (inhibits thrombin formation)
54
Q

What is the difference between warfarin and new OAC (oral anticoagulants) in terms of

  1. Onset
  2. Half-life
  3. Dosing
A
  1. Onset
    - warfarin: slow
    - New OACs: rapid
  2. Half-life
    - Warfarin: long
    - New OACs: short
  3. Dosing
    - Warfarin: Variable
    - New OACs: fixed
55
Q

What is the difference between warfarin and new OAC (oral anticoagulants) in terms of

  1. Monitoring
  2. Food/drug interactions
  3. Antidote
A
  1. Monitoring
    - required in warfarin only
  2. Food/drug interactions
    - many interactions with warfarin, very few with new OACs
  3. Antidote
    - no antidote for new OACs
    - antidote for warfarin available
56
Q

Dabigatran relies heavily on ___________ for excretion.

A

Renal function - 80% of drug requires renal excretion

also have low protein binding and it is dialyzable

57
Q

Patients with bleeding on NOAC therapy can be classified into mild, moderate-severe, and life-threatening bleeding.
What to do with mild bleeding?

A
  • Delay next dose or interrupt treatment as appropriate
58
Q

Patients with bleeding on NOAC therapy can be classified into mild, moderate-severe, and life-threatening bleeding.
What to do with moderate-severe bleeding? (4)

A
  1. Stop drug and give fluid replacement and hemodynamic support
  2. Blood product transfusion
  3. Mechanical compression at site of bleeding
  4. Surgical intervention (e.g. angiogram)
59
Q

What can be given if there is dabigatran-caused life-threatening bleeding?

A

Idarucizumab’

also consider PCC (prothrombin complex concentrate)/activated PCC/ recombinant FVII for FXa inhibitors

ACP Hematology (16 decks)

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