Brainscape's Knowledge GenomeTM

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


See full index

Life Support > DVT and Coagulation > Flashcards

DVT and Coagulation Flashcards

1
Q

What is haemostasis?

A

How the body prevents blood loss when a blood vessel is injured/broken

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

What are the 3 stages of haemostasis?

A

PRIMARY HAEMOSTASIS
Vasoconstriction (immediate)
Platelet adhesion (within seconds)
Platelet aggregation and contraction (within minutes)

SECONDARY HAEMOSTASIS
Activation of coagulation factors (within seconds)
Formation of fibrin (within minutes)

FIBRINOLYSIS
Activation of fibrinolysis (within minutes)
Lysis of the plug (within hours)

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

In haemostasis how does the smooth muscle prevent blood leaking out due to tissue damage?

A

VASCULAR SPASM: SM cells contract

Endothelin is released by damage cells that binds to the smooth muscle cells causing contraction.

Direct injury to smooth muscle causes it to contract - myogenic mechanism.

Nociceptor activation by inflammation from tissue damage that causes pain response which leads to contraction of smooth muscle cells.

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

In haemostasis, how does platelet plug formation occur?

A

Damage to endothelial cells causes secretion of Von Wilderbrand factor (vWF).

Damaged endothelial cells can no longer inhibit platelet aggregation.

Platelets bind to vWF.

Platelets release granules, recruiting other platelets and forming the plug.

Granules also bind to smooth muscle causing contraction and vasoconstriction.

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

Why does the platelet plug need secondary haemostasis?

A

Unstable, needs to be stabilised

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How is the platelet plug stabilised?

A

Fibrin forms a mesh over it

Thrombin activated via coagulation cascade which converts fibrinogen to fibirn

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

What clotting tests are there?

A

aPTT – Playing Table Tennis
Intrinsic (inside) pathway

PT – Playing Tennis
Extrinsic (outside) pathway

TT – Same letters
Common pathway

Mixing studies
Performed after finding error in aPTT or PT to determine cause

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

What is PT

A

PT (playing tennis)

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

What is aPTT

A

aPTT (playing table tennis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is TT

A

TT [thrombin time]: fibrinogen to fibrin time. Increased when def in fibrinogen i.e in liver failure

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

What happens in mixing studies

A

Mixing studies: if prolonged PT or PTT. Look to see if there is a deficiency in clotting factor or an inhibitor of factor activity. 50:50 plasma from patient and normal plasma.

If clotting normalises = factor deficiency (normal blood adds the missing factor). If does not normalise, there may be a clotting inhibitor in the patients blood, i.e antiphospholipid antibodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

In haemostasis, what happens in fibrinolysis?

A

Fibrinolysis is how the body limits clots and completes repair.

Tissue plasminogen activator (tPA) on endothelial cells converts plasminogen to plasmin.

Plasmin degrades the fibrin clot.

Fibrin mesh degrades to FDPs (fibrin degradation products) and d-dimer.

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

What factor is vital for coagulation, without which you can’t form clots?

A

Factor 7

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

DiSCo 1972

A

Factors S, C 10, 9, 7 & 2 require Vit K

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

What tests measure intrinsic and extrinsic pathways?

A

aPTT measures the intrinsic pathway – Playing table tennis (intrinsic indoors)

PT measures extrinsic pathway – Playing tennis (extrinsic outdoors)

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

What is another name for factor 3

A

Tissue factor (released from damaged endothelium)

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

Why does clotting occur in a test tube?

A

Factor 12 reacts with the rough chraged wall of the glass

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

Which coagulation pathway is slow?

A

Intrinsic (5 mins)

Extrinsic is fast (30s)

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

Embolus

A

An unattached mass that travels through the bloodstream and is capable of creating blockages

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

Embolism

A

An embolism is the lodigning of an embolus, a blockage-causing piece of material, inside a blood vessel

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

Thrombus

A

Blood clot, final product of the blood coagulation step in haemostasis

A thrombus is aggregated platelets and red blood cells that form a plug, and a mesh of cross-linked fibrin protein.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Thrombosis

A

Formation of blood clot inside a blood vessel obstructing the flow of blood through the circulatory system

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

Venus Thromboembolism (VTE)

A

A combined term for the linked conditions DVT (deep vein thrombosis) and PE (pulmonary embolism)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the types of emboli?

A 
Fat
Air
Thrombus
Bacteria
Amniotic fluid
Tumour

FATBAT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What happens to a thrombus if it doesn’t resolve?

A

Normally it lyses away and disappears

Or can propogate (grow down blood vessel) and cause damage later
Break off as an embolism
Sucked isnide blood vessel (organisation)
Holes punched through it so blood flows through it (recanulisation)

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

What causes thrombosis?

A

Virchow’s triad:

VESSEL INJURY
damage from smoking

VENOUS STASIS
atrial fibrillation, valvular heart disease, prolonged immobility

HYPERCOAGULABILITY
Pregnancy, medications, cancer, inherited thrombophilias

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

Thrombosis risk factors: continuing or intrinsic risk factors

A 
A history of DVT. 
Cancer (known or undiagnosed).
Age over 60 years.
Being overweight or obese.
Male sex.
Heart failure.
Acquired or familial thrombophilia.
Inflammatory disorders (for example, vasculitis, inflammatory bowel disease). 
Varicose veins.
Smoking.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Thrombosis risk factors: that temporarily increase likelihood of DVT

A

Significant immobility.
Significant trauma or direct trauma to a vein (for example, intravenous catheter).
Hormone treatment (for example hormone replacement therapy).
Pregnancy and the postpartum period.
Oral contraceptives (COCP only) & HRT
Dehydration.
Chemotherapy.
Recent trauma, major surgery or hospitalisation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Thrombosis genetic risk factors

A

Factor V Leiden
Protein C or S deficiency
Prothrombin gene G20210A mutation
Antiphospholipid syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Factor V Leiden

A

Coagulation factor 5 mutates and is not inhibited by protein C or S

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Protein C or S Deficiency

A

Proteins that are involved in fibrinolysis – inactivating factor 5 & 8

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Prothrombin gene G20210A mutation

A

Increased prothrombin production

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

Antiphospholipid syndrome

A

Increases risk of VTE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Deep vein thrombosis: definition and diagnostic factors

A

Definition:
Deep vein thrombosis (DVT) is the development of a blood clot within a vein deep to the muscular tissue planes. DVT most commonly affects the legs, but can also affect the arms, and other sites in the body.

Diagnostic factors:
DVTs commonly cause asymmetrical leg swelling, unilateral leg pain, dilation or distension of superficial veins, and red or discoloured skin, but can also be asymptomatic.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

If suspected DVT use…

A

Well’s score

If they score 2 or more, DVT is likely.
1 or less, DVT is unlikely.

DVT Likely: Duplex US within 4 hours (gold standard)
(if not available then start on anticoagulation)

DVT Unlikely: D-dimer within 4 hours
(if not available then start on anticoagulation)

2 points or more = DVT likely: organise duplex ultrasound within 4 hrs. If there is a delay, give anticoagulation until the scan is performed
1 point or less = DVT unlikely: organise D-dimer -> if D-dimer is positive, arrange duplex ultrasound

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

Pulmonary embolism

A

PE is a life threatening condition caused by the obstruction of one or more pulmonary arteries by solid, liquid, or gaseous masses, leading to respiratory dysfunction.

In most cases, the embolism is caused by blood thrombi, which arise from DVT and embolize to the lungs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Suspect PE in a person with…

A

Dyspnoea (SOB) shortness of breath
Tachypnoea
Pleuritic chest pain (pain on inspiration and expiration)
Features of DVT (unilateral leg pain and swelling)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Additional symptoms of PE

A

Cough and haemoptysis
Dizziness and syncope (due to right ventricular failure in severe cases)
Retrosternal chest pain (due to right ventricular ischaemia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Clinical signs of PE

A 
Tachycardia (>100bpm)
Hypoxia
Pyrexia
Elevated JVP
Gallop rhythm (extra heart sound)
Pleural rib
Hypotension and cardiogenic shock (rare)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What respiratory issues can occur in PE?

A

V/Q Mismatch and PE Obstruction

V/Q MISMATCH
Dead space ventilation: reduced perfusion but normal ventilation -> high V/Q (no blood present)
Severity of V/Q mismatch depends on the number, size and location of the embolus
Reduced perfusion  reduced O2 exchange

PE OBSTRUCTION
Infarction and inflammation of lungs and pleura
Pleuritic chest pain and haemoptysis
Cytokines released  bronchoconstriction  decrease in inspired O2

41
Q

What is the result of reduced perfusion and cytokine release in the lungs?

A

Reduced O2 exchange due to reduced perfusion
Bronchoconstriction due to cytokine release leading to decrease in inspired O2

BOTH -> hypoxaemia (decreased PaO2) = type 1 resp failure

  • > hyperventilation
  • > hypocapnia (respiratory alkalosis)
42
Q

How does an embolism in PE lead to compensatory tachycardia?

A 
Embolism in pulmonary arteries 
↓
Increased pulmonary vascular pressure
↓
Backflow of blood to the right side of the heart
↓
Pulmonary hypertension
↓
Right ventricular hypertrophy  Right sided heart failure
↓ 
Decreased SV  decreased CO  decreased BP
↓
Compensatory tachycardia
Whatever happens on RHS affects LHS 
Decreased CO from left ventricle detected by baroreceptors
↓
Stimulates sympathetic response
↓
Tachycardia and vasoconstriction
43
Q

What are the possible ABG changes in PE?

A

TYPE 1 HYPOXIC RESP FAILURE

pO2 < 8kPa (increased alveolar-arterial gradient (> 10kPa difference)
pCO2 < 6.5kPa (respiratory alkalosis)

44
Q

What are the possible ECG changes in PE?

A

SINUS TACHYCARDIA

McGinn-White sign
Right heart strain pattern- complete or incomplete right bundle branch block (RBBB), right axis deviation or T-wave inversion

45
Q

What would the points in a two-level PE Well’s score indicate?

A

5 points or more = PE likely: organise immediate CTPA. If there is a delay, give anticoagulation until the scan is performed

4 points or less = PE unlikely: organise D-dimer -> if D-dimer is positive, arrange immediate CTPA and give anticoagulation until scan is performed

3 points = an alt diagnosis is less likely than PE

If patient has renal impairment or contrast allergy: V/Q scan

46
Q

What investigations would you do for a suspected PE?

A

CT pulmonary angiography (CTPA)
Chest x ray (CXR)
Radionucleotide imaging (V/Q scan)

47
Q

CT pulmonary angiography for PE

A

Radio-dense contrast delivered via IV allowing visualisation of arterial and venous blood vessels

48
Q

CXR for PE

A

Usually normal – used to rule out other pathology, e.g. pneumonia
Pleural effusion
Atelectasis (collapse of small area of lung tissue)
Can see Fleischner sign (enlarged pulmonary artery), Hampton hump (peripheral wedge of airspace opacity and implies lung infarction) or Westermark sign.

49
Q

Radionucleotide imaging (V/A scan) for PE

A

Scintigraphic examination of the lung using gamma radioisotopes.

Ventilation scan: Radio-isotope aerosols are inhaled by the patient  small enough to reach distal tracheobronchial tree

Perfusion scan: Tc-99m MAA is given intravenously  small enough to become lodged in arterioles of lungs.

50
Q

What are the MoA, contraindications and side effects of warfarin?

A

MoA:
Inhibits production of vitamin K dependent coagulation factors (II, VII, IX and X and proteins C and S) by inhibiting epoxide reductase, the enzyme responsible for restoring vitamin K to its reduced form, which is needed for the synthesis of clotting factors
diSCo 1972

Contraindications:
Pregnancy
Liver disease
Caution when taking CYP inhibitors/inducers as they may increase or decrease warfarin metabolism
Certain antibiotics kill gut flora that synthesise vitamin K (increases warfarin’s effect

Side effects:
Haemorrhage
Many patients not sufficiently anticoagulated
Must be co-prescribed heparin for bridging during hypercoagulable phase* of treatment
Needs regular monitoring (aim for INR of 2.5).

51
Q

What are the MoA, contraindications and side effects of Low molecular weight heparin (LMWH)?

A

Dalteparin
Enoxparin

MoA: Direct factor Xa inhibitor

Contrainidications:
Safe for pregnancy!
Severe hypertension
Recent surgery/trauma

Side effects:
Heparin induced thrombocytopaenia at S/C injection site (less common than UFH)

52
Q

What are the MoA, contraindications and side effects of unfractionated heparin (UFH)?

A

MoA:
Inhibits factors Iia and Xa

Contraindications:
Severe hypertension
Recent surgery/trauma

Side effects:
Heparin Induced thrombocytopaenia (HIT) at S/C injection site (more common than LMWH)
Requires monitoring (aim for PTT of 1.5-2.5)

53
Q

Warfarin induced clotting

A

As well as blocking vitamin K recycling, warfarin also inhibits proteins C and S (anticoagulants).
The half life of protein C is shorter than the clotting factors that it inhibits so protein C levels decrease more quickly than clotting factors.
For the first 2 days the patient can be pro-coagulant.

54
Q

DOACs (Direct oral anticoagulant)

A

Don’t Ruin All Evils

Dabigatran (thrombin inhibitor, factor 2)
RivaroXaban
ApiXaban
EdoXaban

^ R, A and E all factor 10a inhibitors

55
Q

Contraindications of DOACs

A

Active bleeding
Significant risk of major bleeding
Prosthetic heart valve

BUT GOOD THING: Less monitoring due to little or no food/drug interactions

56
Q

Why are anticoagulants like warfarin, heparin and DOACs not good for removing the clot?

A

They are preventative, prevent the clot from occuring whereas antiplatelets and thrombolytics act to breakdown the clot while its there

57
Q

PE management if patient is haemodynamically stable

A
  1. Oxygen therapy if hypoxic
  2. Paracetamol if in pain
  3. DOAC’s (rivaroXaban or apiXaban) REMEMBER

Offer LMWH if breastfeeding, pregnant or has active cancer.

Continue anticoagulation for at least 3 months.

If PE was provoked: consider stopping treatment after 3 months
If PE was unprovoked: consider continuing treatment after 3 months

58
Q

PE management if patient is haemodynamically unstable (massive PE – BP <90 systolic or drop >40mmHg in 15mins

A
  1. Continuous UFH infusion (unfactionated heparin)
  2. Thrombolysis (alteplase or streptokinase)
    Surgical thombectomy in those with failed fibrinolysis or patients with a free-floating thrombus in the right atrium or ventricle
59
Q

Types of hypoxia

A

An inadequate level of tissue oxygenation for cellular (aerobic) metabolism

  1. Hypoxic Hypoxia
  2. Hypoxemic Hypoxia
  3. Circulatory Hypoxia
  4. Histotoxic Hypoxia
60
Q

Hypoxic hypoxia

A

Lung problems – low PaO2

  • High altitude (low oxygen in air)
  • Airway obstruction (any cause)
  • Hypoventilation (any cause)

VQ Mismatches:

  • Alveolar pathology
  • Diffusion defects
  • Vascular defects
61
Q

Hypoxaemic hypoxia

A

(anaemic hypoxia)

Blood problems - PaO2 normal

  • Low Hb content
  • Abnormal Hb (e.g. sickle cell)
  • Other stuff bound to Hb (e.g. Kai!)
62
Q

Circulatory hypoxia

A

Circulation problems

  • Shock
  • Blockage
  • Cardiac failure
63
Q

Histotoxic hypoxia

A

Cells can not use the perfectly good oxygen that’s been delivered.

  • Sepsis
  • Drugs
  • Cyanide
64
Q

What contraceptive most increases risk of thrombosis?

A

COCP (bc oestrogen)

65
Q

What is the first line treatment for someone diagnosed with a PE?

A

DOACs (DRAE)

66
Q

A prolonged prothrombin time indicates a fault in which pathway?

A

Extrinsic and common

67
Q

Why would a PE cause hypoxic hypoxia?

A

V/Q mismatch, blood circulation is fine but not getting oxygenated

68
Q

What are anticoagulants?

A

Reduce the ability of the haemostatic system to respond to activation signals. They do not in fact thin the blood

These drugs will not dissolve clots that already have formed, but it will stop an existing clot from becoming worse and prevent future clots

69
Q

Why do we need anticoagulants for:

a) Stroke prevention
b) Venous Thromboembolic disease (VTE)
c) Arterial Thrombotic disease ?

A 
Stroke prevention 70%
•Atrial fibrillation
•Valvular heart disease
•Mechanical heart valves
•Cardiomyopathy
•Intracardiac thrombus

Venous Thromboembolic disease (VTE) 20%
•Treatment
•Prophylaxis

Arterial Thrombotic disease 10%
•Acute coronary syndrome (ACS)
•Myocardial infarction (MI)
•Failed arterial grafts
•Haemodialysis access
70
Q

What factor do most anticoagulants target nowadays?

A

Xa

71
Q

What anticoagulants inhibit Xa?

A

Rivaroxaban
Fondaparinux- INDIRECT
Apixaban

72
Q

What anticoagulants act on thrombin?

A

Dabigatran

Argatroban

73
Q

UFH vs LMWH

A

Unfractionated (UFH)

  • Standard UFH, derived from pig intestine or bovine lung tissue
  • Heterogeneous mixture of polysaccharide chains of varying length

Low molecular weight (LMWH)
-Derived from chemical or enzymatic degradation of UFH into fragments approximately one-third the size of heparin

74
Q

What does heparin target?

A

Antithrombin

75
Q

Why does size of heparin molecule matter?

A

Has pentasaccharide sequence.
Binds directly to antithrombin and inhbits thrombin production
Sequence important in potentiating inhbition of active factor Xa
But need longer molecule to wrap around thrombin and do this so unfractionated can inhibit Xa AND thombin but LMWH mainly inhibits Xa (stopping conversion of prothrombin to thrombin)

76
Q

Why still use unfractionated heparin?

A

Reticuloendothelial clearance- cleared by spleen and liver so used in patients with renal impairment, whereas LMWH cleared by kidneys (so wouldn’t be good for patients w renal issues)

Half life 1.5 hours- in IV infusion so if patient going to theatre, very easy to stop and start IV heparin

77
Q

What are the cons of using unfractionated heparin?

A

APTR monitoring- activated partial thromboplastin time ratio, need to monitor activity and dose

Reversal agent protamine- too much of which can be procoagulant, but in small doses can inhibit unfractionated heparin

78
Q

What setting is best for UFH?

A

Short term, clinical setting as it’s a very controllable coagulant esp patients w renal impairment

79
Q

How is UFH monitored?

A

Activated Partial Thromboplastin Time Ratio – APTTR

–therapeutic range varies with different reagents
•1.5 - 3.5 at SGH
•check local range

–baseline level prolonged by
•antiphospholipid antibodies
•combined Rx with warfarin or thrombolytics
•congenital factor deficiencies

–baseline level shortened by
•high Vlll

80
Q

What are the benefits of using LMWH?

A

Renally cleared
Can just give once daily unlike UFH
Half life 12 hours, peak activity 3-4hours
No monitoring required
used for pregnant women and beastfeeding women
HOWEVER No reversal agent
Anti Xa monitoring performed under certain circumstances

81
Q

Heparin side effects

A

Bleeding: stop heparin and give protamine sulphate 1mg/100units

Heparin induced thrombocytopenia (HIT): minor platelet drop at 5 days, transient, no treatment required
BUT HIT with thrombosis (HITT): stop heparin immediately + use danaparoid or hirudin

Osteoporosis: dose and duration related

82
Q

Warfarin mechanism of action

A

Targets production of vitamin K dependant clotting factors (7, 9, 10 and 2)
Affects production of anticoagulants Protein S and C
Blocks recycling of vitamin K- so vit K cannot carboxylase proteins aka activate them, so these clotting factors do not work

83
Q

Why can patients be procoagulant in the first few days of starting warfarin?

A

Becauase protein C has a short half life compared to other clotting factors, and so will drop and make patient pro-thrombotic. So must wait for other working clotting factors to come out of system which can take 2-3 days

84
Q

Pharmacokinetics and dynamics of warfarin

A 
Good bioavailability-rapidly absorbed
Half life 36 - 42 hours
97% albumin bound in plasma
Eliminated by liver
Cytochrome p450 system metabolise it
85
Q

Warfarin drug interactions

A

–impair absorption of vitamin K: increase anticoagulant effect

–compete for plasma protein binding sites: increase anticoagulant effect

–are hepatotoxic: increase anticoagulant effect

–induce hepatic enzymes: reduce anticoagulant effect

–have antiplatelet activity: cause increased bleeding

86
Q

Consequences of warfarin pharmacology

A

Heparin must be used for initiation of warfarin in patients with thrombosis due to fall in protein C activity
Dose of warfarin required varies widely between individuals

Individual warfarin dose is sensitive to:
– diet (Fat and Vitamin K intake)
– other drugs (+/-)
– ethnicity ( VKORC1 polymorphisms)
– age

Warfarin needs monitoring

87
Q

What test is used to monitor warfarin vs heparin?

A

PT prothrombin time to monitor warfarin

APTT to monitor heparin

88
Q

What does INR measure?

A

Time it takes to form a clot in prothrombin assay, normally 2.5 if it takes longer then overcoagulated

89
Q

Warfarin side effects

A

Skin necrosis
Protein C deficiency
give heparin firsr for VTE Rx
Bleeding

Crosses placenta, coumarin embryopathy 6-12 weeks, doses above 5mg SO NEVER USED IN PREGNANCY

Increased fetal loss: intracerebral haemorrhage, antepartum haemorrhage

90
Q

Warfarin risk factors

A

Age over 70
INR above 4.9
first 3/12 of Rx
comorbid disease

91
Q

Treatment of bleeding

A

Major bleed
–life or limb threatening
–fully reverse anticoagulation immediately: vit K konakion 5 -10mg iv

Prothrombin complex concentrate PCC
–20 – 30 u/kg

Fresh frozen plasma FFP–15ml/kg

Omit anticoagulation till bleeding controlled Beriplex® / Octaplex

92
Q

Direct thrombin inhibitors, examples and what they act on

A

Hirudin: binds to exosite 1 and active site on thrombin

Melagatran and Dabigatran: bind to active site on thrombin

93
Q

Rivaroxaban

A 
Direct inhibitor of Xa
Oral agent
Once daily dosing
Rapid onset of action
Half life4-9 hours
Monitoring not usually necessary
Renal excretion
Few food or drug interactions
GI side effects
94
Q

NOACs pros

A

Oral anticoagulant
Rapid onset/offset of action –No need for bridging
Short half life –Easy to control anticoagulant effect
Little or no food-drug interactions
Limited drug-drug interactions
Predictable anticoagulant effect –No need routine monitoring

95
Q

DOACs in obese patients

A

Standard dose for BMI<40 <120kg
Suggest not used with BMI>40 >120kg

If used suggest drug specific peak and trough levels
Guidance on frequency of monitoring not given

96
Q

Describe the intrinsic, extrinsic and common pathways

A
97
Q

What ion is needed in activation stages of coagulation?

A

Calcium

98
Q

What vitamin is required by factors 2,7,9 and 10?

A

Vitamin K

Life Support (5 decks)

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