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Lecture week III COPY > Anti-coagulants > Flashcards

Anti-coagulants Flashcards

1
Q

Steps in coagulation (simple)

A
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2
Q

Diseases possibly caused by thrombus

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3
Q

Inherited risks for thrombogenesis

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4
Q

Acquired risks for thrombogenesis

A
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5
Q

What’s Factor V Leiden disease

A

Factor V Leiden:

  • the most common inherited risk factor for thrombogenesis among UK’s females (and among European ethnicity)
  • mutation in factor V gene (that helps blood to clot)
  • increase in blood coagulability (hyper-coagulability)
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6
Q

Pathophysiology in Factor V Leiden disease

A
  • Mutation -> protein C (which normally inhibits factor V) is not able to bind to it -> hypercoagubility
  • It is AD, with incomplete penetrance (not everyone with the mutation will be symptomatic)
  • Result: Recurrent venous thromboses
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7
Q

Diagnosis of Factor V Leiden disease

A

Caucasian patient below age 45 with thrombotic event

  • lab tests (aPTT - time it takes for blood to clot is decreased)
  • genetic testing for a mutation (PCR)
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8
Q

Management of Factor V Leiden disease

A

Management:

  • no cure -> prevention of thrombotic events
  • lifelong treatment with anti-coagulants

e. g. Warfarin and Heparin (during periods of increased risks for VT e.g. major surgery)
* cannot be prescribed an oestrogen containing pill

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9
Q

Why D-dimer is usually done?

A

D- dimers are done rather for patients who we do not suspect to have a clot -> to exclude it definitely

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10
Q

Ix in DVT

A
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11
Q

PE Investigations

A
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12
Q

Wells score

  • components
  • meaning
A
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13
Q

Pathway for treatment of PE without shock

A
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14
Q

What risk score and components are used to assess for anti-coagulant need

A

CHA2DS2

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15
Q

Possible anti-coagulation drugs for people with score 2 or more on CHA2DS2

A

People with score 2 or above should be offered anti-coagulation with:

  • apixaban
  • dabigatran etexilate
  • rivaroxaban
  • Vitamin K antagonist

* Aspirin monotherapy should not be offered in these patients solely for stroke prevention

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16
Q

What score assesses the risk of major bleeds for a patient on anti-coagulant?

A
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17
Q

Ix and diagnostic findings of PE and DVT

A
  • chest X ray can show lung infract (sometimes)
  • sometimes typical ECG changes
  • Doppler scan -> if we compress on the veins and it collapses means that there is a clot (as normally it should not collapse)
  • V/Q scans (mismatch between perfusion and ventilation)
  • CT Pulmonary Angiogram - preferred by doctors as: able to pick up other abnormalities and also visualise the location of a clot
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18
Q

Examples (3) of ADP antagonist drugs

A
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19
Q

Example of COX inhibitor (1)

A
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20
Q

Example of Phosphodiesterase inhibitor

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21
Q

Examples (3) of GP IIb/IIIa inhibitors

A
22
Q

Mechanism of action of Aspirin

A

Aspirin:

  • inhibition of COX1 (in small dose)
  • inhibition of COX2 (high dose) - analgesia effect (so e.g. headache we need higher dose of

aspirin)

Aspirin permanently blocks enzymes that convert arachidonic acid -> thromboxane (prothrombotic inductors released by platelets)

*as there is high turnover of platelets in the body (everyday 10% is new ones) -> need to carry on with aspirin

23
Q

Examples (4) of ADP antagonists

+ simple MoA

A
  1. Ticlopidine
  2. Clopidogrel
  3. Prasugrel
  4. Ticagrelor

MoA: inhibition of ADP induced platelet aggregation

24
Q

Common use of ADP antagonists

A
  • They are used for patients with cardiovascular disease, as part of dual-anti-platelet therapy (blocking two pathways leading to platelet activation)

​

  • Clopidogrel and Ticagrelor are the most commonly used
25
Q

(2) anti - platelets used in treatment of acute MI

A

In acute MI (e.g. A&E) :

- Aspirin

- Ticagrelor (preferred as rapid onset)

26
Q

Potential side effects of Ticlopidine and Prasugrel

A

Both ADP antagonists - not usually used in acute MI Rx due to SEs:

  • Ticlopidine is not used that much anymore due to neutropenia in 2.4% of patients
  • Prasugrel also not used as increased risk of TIA in elderly patients
27
Q
A
28
Q

What is Warfarin potentiated by?

A

Potentiated by:

  • antibiotics
  • fluconazole
  • cimetidine

they inhibit p450 (therefore less metabolism of other drugs)

29
Q

What is Warfarin antagonized by?

A

Antagonised by:

  • anti-TB drugs
  • anti- epileptics

they will induce p450 (so more metabolism of other drugs)

30
Q

Therapies used in Warfarin overdose

A
  • vitamin K
  • prothrombin complex concentrate
  • FFP
31
Q

What Warfarin is mostly metabolized by?

A

is mostly metabolised by liver (so choice for patients with CKD)

32
Q

Warfarin MoA

A
33
Q

Risks (2) associated with Warfarin therapy

A

Risks with Warfarin:

  • bleeding
  • lots of patients may not be complaint with treatments - may receive sub-therapeutic level of treatment
34
Q

What a dose of Warfarin will depend on?

A

Dose of warfarin will depend on:

Age, BMI, gender, nutritional status, concomitant medications, compliance, comorbid disease

35
Q

Side effects of Warfarin

A
  • haemorrhage
  • skin necrosis
  • teratogenicity (contraindicated with pregnancy -> give Heparin through pregnancy instead)
  • leukopaenia
  • overdose - reversed FFP or prothrombin complex concentrate (Octaplex) or IV vitamin K
36
Q

Heparin MoA

A

Mechanism of action:

  • Binds and enhances antithrombin III
  • Inhibits clotting factors IXa, Xa, XIa and thrombibn
37
Q

Unfractionated vs LMWH Heparin use

A

Options of heparin:

A. Unfractioned - IV route, it acts in short time (30 minutes onset of action with half time 4 hours) - used for acute thrombotic events

*blood tests are checked regularly to monitor treatment’s effectiveness

B. Low molecular weight Heparin - used more commonly due to its half time (12 hours), once again due to sub-cutaneous injection

38
Q

Heparin side effects

A

Side effects:

  • bleeding
  • thrombocytopaenia
  • osteoporosis
  • hair loss
39
Q

Drug used to reverse heparin effects

A

Protamine

40
Q

Use of GP IIb/IIIa inhibitors

A

are usually used only via IV route, on the patients going for angioplasty or any other vascular surgery (sue use in cardio-thoracic surgery)

41
Q

MoA of GP IIb/IIIa inhibitors

A
42
Q

DOACs MoA

A

Mechanism of action:

  • Dabigatran blocks factor II
  • Other drugs from NOAC class block conversion of factor X - Xa (so prothrombin)
43
Q

Advantages of DOAC use

A
  • no need to monitor levels
  • partially metabolized by the liver, partially by kidney

*however much more expensive than Warfarin

44
Q

Dabigatran use and advantages

A
45
Q

‘…xaban’ use and advantage

A

DOACs

46
Q

Half-life, class and use of fondaparinux

A

Fondaparinux

  • belongs to Heparins
  • long half-life (17 h)
  • efficacy comparable to unfractioned and LMWH for treating DVT and PE
  • more cost effective than LMWH
47
Q

Fondaparinux MoA

A

binds to antithrombin -> enhances its activity towards factor Xa

*no activity against thrombin or platelets

48
Q

Fibrinolytics

  • use
  • MoA
  • SE
A

Fibrinolytics used only on stroke unit

SE: acute bleeding

49
Q

Names (4) of thrombolytic drugs

A
50
Q

Use and MoA of thrombolytics

A
51
Q

SE and contraindications of thrombolytics

A

Lecture week III COPY (11 decks)

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