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CVR > Clotting Disorders > Flashcards

Clotting Disorders Flashcards

1
Q

Name the key laboratory tests for haemostasis

A

Platelet count: 150-400 x 10^9/L

Activated Partial Thromboplastin Time APTT

Prothrombin Time PT

INR- international normalised ratio

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2
Q

APTT

A

APTT Activated Partial Thromboplastin Time: 35-45 seconds

  • measures the activity of coagulation factors in the intrinsic system/ amplification phase
  • time to clot formation after addition of a surface activator (kaolin activates FXII), phospholipids and Ca2+ to plasma
  • bleeding time measuring the efficacy of unfractionated heparin
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3
Q

PT

A

Prothrombin Time: 10-20 seconds

  • measures activity of vitamin K dependent clotting factors in the extrinsic system
  • time to clot formation following addition of thromboplastin (fibrinogen & Ca2+)
  • bleeding time informing the INR
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4
Q

INR

A

INR- international normalised ratio: 1

  • ratio of PT in patient to PT in reference sample
  • shows how effective warfarin therapy is
  • high INR means blood clots more slowly
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5
Q

What are anticoagulants indicated for?

A
  • Treatment and prevention of Venous thromboembolism: PE & DVT
  • Stroke prevention in AF patients
  • Prophylaxis of thromboembolism in patients
  • Mechanical heart valves
  • Antiphospholipid syndrome
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6
Q

DVT

A

Deep vein thrombosis occurs when a clot forms in the deep vein in the body, usually the leg.

Red, swollen, warm to touch
50% of VTE patients are asymptomatic- only diagnosed once they have PE

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7
Q

PE

A

Pulmonary embolism (PE) is a blockage of an artery in the lungs by a substance that has moved from elsewhere in the body through the bloodstream (embolism). When the clot from the leg breaks off and travels to the right side of the heart.

Depending on size of clot, it can block the vasculature to the lungs.

Large clots can cause a massive PE whilst small clots can cause subsegmental small PE.

Shortness of breath, chest pain particularly upon breathing in, and coughing up blood.

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8
Q

What is the most serious clinical presentation of VTE?

A

PE

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9
Q

How is PE treated?

A

1) Thrombolysis: alteplase, streptokinase
(dissolution of clot induced artificially by infusion of an enzyme)

2) Pulmonary embolectomy
(surgical removal of clot)

Are only indicated if life threatening, massive PE…

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10
Q

Are anticoagulants used in DVT and PE?

A

Yes for DVT

In a massive PE, anticoagulants will not breakdown the clot and will only prevent further extension and new formation.

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11
Q

What is the impact of VTE on quality of life?

A 
Substantial negative impact
Symptomatic DVT
- worse perceptions of their health
- lower levels of physical functioning
- post-thromotic syndrome

PE

  • persisting breathlessness
  • emotional complaints and distress
  • limitation of activies
  • loss of control
  • life changing event
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12
Q

Risk factors for VTE

A
  • Age
  • CHF- peripheral oedema, pulmonary congestion, increased venous pressure
  • IBS- irritable bowel syndrome
    increases FVII and decreases antithrombin
  • Obesity- >30 (weak risk factor)
  • Malignancy
    tumour cells secrete procoagulants
    activation of factors V, VII, IX, X
  • Pregnancy
  • Previous VTE
  • Surgery
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13
Q

VTE thromboprophylaxis

A

Reduces morbidity, mortality and is cost effective

  • Graduated elastic compression stockings
  • UF
  • H: 5000 units s/c BD

LMWH: dalteparin 2500-5000 units s/c OD
enoxaparin 20mg- 40mg s/c OD

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14
Q

Mechanical thrombopropylaxis

A

Static: anti-embolism stockings

  • classic compression stockings
  • pressure applied helps blood flow back to the heart during periods of immobility

Dynamic : intermittent pneumatic compression

  • cuff sitting around the legs attached to a pump
  • pump inflates and deflates periodically mimicking walking motion and how veins would be decompressed by the muscles
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15
Q

C/I for enoxaparin

A
  • active bleeding
  • bleeding disorders
  • muscle Creatine > 150micromoles/L or <30ml/min
  • thrombocytopenia
  • previous HIT or allergic to enoxaparin
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16
Q

C/I of TEDs/SCDs

A
  • severe peripheral vascular disease
  • leg oedema
  • severe dermatitis
  • recent skin graft
  • peripheral neuropathy
  • leg deformity
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17
Q

Heart valves

A
  • Heart valves are usually replaced because of damage or disease
  • e.g. mitral regurgitation or aortic stenosis
  • two types of valves: prosthetic, or tissue
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18
Q

Two most common valve positions that are replaced?

A

Aortic and mitral valve in left side of heart

mitral valve is more at risk of thromboembolism than aortic

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19
Q

Examples of prosthetic and tissue valves

A

Prosthetic: caged ball, Bileaflet and tilting disk valve

Tissue: porcine valve, bovine pericardial valve

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20
Q

Prosthetic valve

A
  • durable- last 20-30 years
  • thrombogenic- used by patients requiring lifelong anticoagulant therapy
  • preferred in younger patients >10-15 years life expectancy (don’t want to constantly open up chest to replace the valve)
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21
Q

Tissue valve

A
  • limited life: 10-30% of grafts fail within 10-15 years
  • low thrombogenicity- used by patients not on anticoagulants
  • preferred in older patients
  • preferred in those who cannot or will not take anticoagulant therapy
22
Q

Valve thrombosis

A

Thrombosis formed on surface of valve.

Mechanics of valve affected.

Clot is able to embolise off and cause strokes.

23
Q

When is the risk of thromboembolism increased?

A

In prosthetic mechanical valves

In particular caged ball valves at the mitral position.

Therefore intensity of anticoagulation is dictated according to type of valve and position.

24
Q

Stroke in AF patients

A

AF is most common encountered arrhythmia

Those with AF have a 6 fold increased risk of stroke and a 2 fold increased risk of death

AF affects blood flow within chambers- clots develop which travel out of the heart

  • first they travle is the vasculature of the brain
  • can embolise down into the peripheries of hands and feet

Stroke in AF patients compared to those without AF
- greater mortality, morbidity, hospital stays and disability

25
Q

Treatment to prevent stroke in AF patients

A

Anticoagulant therapy is used as prophylactic treatment

  • warfarin (INR= 2-3 lifelong)
  • dose adjusted warfarin reduces risk of stroke by 60%
26
Q

Why is antiplatelet therapy not recommended?

A

Antiplatelet therapy is inert

Aspiring does reduce risk but anticoagulants are preferred

27
Q

CHA2DS2VASC

A 
Congestive heart failure 1 
Hypertension 1
Age > 75 years 2
Diabetes 1
Stroke, TIA, TE 2
Vascular disease (previous STEMI, PAD or aortic plaque) 1
Age 65-74 years 1 
Sex category: F 1

Estimates risk of stroke in patients with AF

28
Q

Anticoagulants

A

Heparins

  • unfractionated heparin
  • low molecular weight heparins- enoxaparin, dalteparin

Vitamin K antagonists
- warfarin

Direct Oral Anticoagulants

  • rivaroxaban
  • apixaban
  • edoxaban
  • dabigtaran
29
Q

Heparins

A

Mixture of mucopolysaccharides derived from mast cells that activate antithrombin

Antithrombin inhibits factors X, IX and XI

Must bind to both thrombin and antithrombin for inhibition of thrombin

Must bind to antithrombin of FX

30
Q

UFH

A

3000-30000 Mw of parent compound

12000-15000 avg molecular weight

anti Xa: anti II activity 1:1

Monitoring is required via APTT

High protein binding

Short elimination half life

Causes thrombocytopenia in some patients

31
Q

LMWH

A

1000-10000 mW
4000- 5000 lower Mwt.

anti Xa: anti IIa 4:1
more specific to Xa than thrombin as only binds to antithrombin

No monitoring required as LMWH have a predictable PK required

Low protein binding

Longer elimination half life

Predictable dose responses

Thrombocyopenia is rare

Given subcu

First line drugs for thromboprophylaxis

32
Q

Adverse effects of LMWH and UF

A
  • Bleeding- protamien sulphate is an antidose (more effective for UFH than LMWH)
  • Osteoporosis
  • Heparin induced thrombocytopenia
  • Hyperkalaemia
33
Q

Type 1 HIT

A

Mild thrombocytopenia

100-130 x 10^9/ L
from days 1-4 of therapy
direct interaction of platelets with heparin
resolves on its own- just monitor FBC

34
Q

Type 2 HIT

A

platelets drops from 5-14 days from initiation of therapy

platelet count drops below 100 or 50% drop in initial platelet count

can be fatal

measure baseline platelet count, then from day 5, do a weekly count

35
Q

Protocol for UFH infusion

A

loading dose: 5000 units I/V over 5 min

initial infusion IV infusion rate: 25000 units heparin in 50mL saline and start at rate of 2.8mL/hr (1400 units/hr)

Check APTTr after 6 hours and then adjust according to results

Targert APTTr 1.5-2.5

36
Q

Properties of warfarin

A
  • completely absorbed from GI tract
  • 99% albumin bound
  • INR used to measure effects
  • inhibits vit K reductase and thus y- carboxylation of prothrombin and factors VII, XI and X in liver
  • only effective in vivo
  • slow onset 1-2 days
    provides effective support for 5 days
37
Q

How is warfarin metabolised?

A

By CYP450 system

mainly metabolised by CYP1A2, CYP2C9

38
Q

What medicines do warfarin interat with?

A

amiodarone- higher INR
carbmazepine- lower INR
erythromycin- high INR
alcohol- high or low?

39
Q

Dosing considerations of warfarin?

A
  • age- <65 yrs- less warfarin given to younger patients
  • disease states- liver disease- lower dose
  • interacting drugs
  • weight- larger patients require a higher dose
  • life style
    diet
40
Q

Adverse effects of warfarin

bants

A

Bleeding due to pharmacological action

Alopecia

Nausea, diarrhoea, vomiting

Teratogenic

Skin necrosis- small vessel thrombosis in thighs and abdominal walls, breasts

41
Q

Target INR ranges for AF, PE , DVT, MI, recurrent DVT, DVT/PE whilst on warfarin, mechanical prosthetic valve

A

AF, PE, DVT, MI recurrent DVT/PE: 2-3

DVT/ PE whilst on warfarin: 3-4

mechanical prosthetic valve: 2-3, 2.5-3.5, 3-4

42
Q

What is used as an antidoe when INR is raised or suffers a bleed?

A

vitamin K

  • used to reverse effect
  • 0.5mg to 10mg IV or orally
  • takes 3-6 hours to have an effect
  • if patient to remain on warfarin , give low dose as vit K will mess up INR control
  • if patient to stop, then give high dose
43
Q

DOAC’s

A

direct oral anticoagulants

apixaban, rivaroxaban, edoxaban are direct Xa inhibitors

dabigatran is a thrombin inhibitor and inhibits FIIa

44
Q

Can DOAC’S reduce stroke in AF patients and be used in VTE?

A

Yes

45
Q

PK properties of apixaban, rivaroxaban, edoxaban, dabiagatran

A

A- 27%
R- 35%
E- 50%
D- 80%

46
Q

Interactions with DOAC’s

A

Inhibitors of P-GP
- amiodarone, quinidine, verapamil, rifampicin, st John’s wort, carbamazepine, phenytoin

Inhibitors of P-GP and CYP3A4
- azole- antimycotics: ketoconazole, itraconzaole voriconzaole, posaconazole HIV protease inhibitors

47
Q

Issues with prescribing DOAC’s

A
  • no monitoring
  • how to deal with in overdose
  • lack of regular contact with a/c clinic tocheck for adherence and tolerance
  • replaces drugs where clinicians have over 50 years of experience
48
Q

Why is there little concern that no antidotesexist for direct Xa inhibitors?

A

esp dabigatrin
no antidote for direct Xa inhibitors

reduced concern due to short elimination half-life
terminating treatment leads to quick clearance from body relative to warfarin

49
Q

Name some potential future antidotes

A

andexanet alpha- antidote for direct Xa inhibitors

ciraparantag

50
Q

Can you used DOAC’s in mechanical valves

A

no

RE-ALIGN study showed dabigatran patients developed stroke/ thrombosis more significantly than warfarin patients

51
Q

Risk of bleeding with DOAC’s

A

2-3% risk of major bleeding with all anticoagulants

risk of intracranial haemorrhage is <1% with warfarin
50% rduction on this with DOAC’s

first month or so is critical as its when bleeding is most likely to occur

CVR (12 decks)

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