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22 Cards in this Set
- Front
- Back
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What are the differentials for PE (SOB) |
Respiratory: Pneumothorax, pleural effusion, pneumonia, APO, asthma, excacerbation of COPD Cardiovascular: AMI, aortic dissection, pericarditis, CHF, cardiac tamponade MSK: costochondritis, rib fracture Psych: anxiety |
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What are the risk factors to developing a PE |
Virchow's triad Hypercoaguability: surgery, post partum, infection, cancer, dehydration, oestrogen only OCP, fat Endothelial damage: Surgery, trauma/fracture Haemodynamic changes: stasis, turbulence, immobility
Others: increasing age, hyperoestrogenic states, fat, previous history of VTE, poorly anti coagulated |
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What would guide your investigation for PE |
Investigate based on the pretest probability of PE using Well's criteria - high probability of >6 would do CTPA, if not D-dimer assay
Signs of DVT - 3 PE likely diagnosis - 3 Previous hx of DVT/emboli - 1.5 Hr > 100 - 1.5 Recent immobility - 1.5 Haemoptysis - 1 Malignancy - 1
0-2: low, 2-6: moderate, >6: high |
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What diagnostic tests would you perform and what would you find if you suspected a PE? |
Diagnostic - CTPA (gold standard) looking for filling defects - D-Dimer for low suspicion on well's criteria, as has good negative predictive value (high sensitivity) but low specificity especially in inflammation, post op, prothrombotic states (surrogate marker for fibrin degradation products) - V/Q scan if hypersensitive to contrast, shows perfusion defect, reduction of segmental perfusion and NORMAL PERFUSION - Pulmonary angiography if V/Q equivocal - Doppler U/S
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What other tests would you perform to substantiate your diagnosis of PE or to exclude your differentials |
- ECG: sinus tachy, RBBB, right axis deviation, S1Q3T3 - CXR: rule out pneumonia, penumothorax, pleural effusion. PE specific findings: atelectasis, hemidiaphragm elevation, hampton's hump (increased opacity of infarct), fleischer's sign (prominent central pulmonary artery), westermark's sign (oligaemia in PE distribution) - ABG - T1RF, hyperventilation - TTE - LV/RV function - BNP - heart failure - Thrombophilia screen - FBC - EUC |
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How would you treat this patient with PE? |
Depending on haemodynamic compromise
Without: oxygen, morphine, anticoagulation (heparin/LMWH + warfarin)
With haemodynamic compromise (SPB<90) suggesting massive PE - thrombolysis with tPA, morphine, HF O2, anticoagulation with (UFH + warfarin) |
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How would you monitor anticoagulation? |
UF Heparin: aPTT (60-90s), platelets (HIT), bleeding signs and symptoms
LMWH: no monitoring
Warfarin: PT (1.5x control), INR 2-3 for PE, 2.5-3.5 for mechanical heart valves |
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How do you calculate INR? |
INR = (Patient's PT / normal sample's PT)^ ISI (international sensitivity index) |
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What is the mechanism of warfarin and what are its side effects |
Mechanism: vitamin K reductase inhibitor to inhibit synthesis of vitamin K dependent clotting factors II, VII, IX and X and to inhibit synthesis of antithrombotic factors protein C and protein S
Side effects: inter cranial bleeds, skin necrosis, teratogen, dietary and drug restrictions
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How does skin necrosis occur in warfarin |
Protein C has a a shorter t1/2 than other factors -> coagulation factor imbalance when anticoagulation is initiated -> initial hyper coagulable state -> clots form and interrupt blood supply to skin -> skin necrosis -> gangrene |
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What are the interactions of other drugs with warfarin |
Warfarin is metabolised by the cytochrome P450 pathway
P450 inhibitors decrease wafarin metabolism so INR INCREASES (QAAM): quinolones, antiarrhythmics, azoles, macrolides
P450 inducer increase warfarin metabolism so INR decreases: antiepileptics, StJW, rifampicin) |
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How is endogenous vitamin K produced and how is this relevant to antibiotic therapy with warfarin treatment? |
Vitamin K is produced by enteric gut flora, hence antibiotic treatment against enteric bacteria may cause a decrease in vitamin K, leading to increased INR |
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How do you reverse warfarin? |
Quick: prothrombinex (factor II replacement) and FFP
Slow: vitamin K (6-12 hours) |
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How would you monitor INR |
Dietary restrictions, keep a log book, no alcohol, take tablets same time everyday |
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What are some anticoagulants you know? |
Heparin Warfarin Dabigatran Direct Xa inhibitors (danaparoid, apixiban, rivaroxiban, fondaparinux) |
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What is the mechanism of action for UFH, how is this different to LMWH |
Potentiates antithrombin III to inactivate factor IIa (thrombin) and factor Xa to prevent conversion of fibrinogen to fibrin
LMWH have much greater effects on Xa than on IIa
Heparin has an effect on the intrinsic cascade |
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What are the common side effects of heparin treatment |
Common: bleeding, hyperkalaemia, skin necrosis at injection site, renal failure (LMWH)
Severe: HIT (platelet count less than 50% of normal, or absolute <150x10^9) |
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How does HIT occur and how do you manage it |
Development of antibodies to heparin bound platelet factor 4 (PF4)
Management: cease heparin immediately, initiate other non-heparin based (Direct Xa inhibitor i.e. danaparoid) |
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What are restrictions of use for LMWH in renal failure, how is this different with heparin? |
Use reduced dose 50% of LMWH in renal failure, check EUCs regularly,
Heparin is safe to use in renal failure |
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How do you reverse heparin and LMWH? |
LMWH IS NOT REVERSIBLE
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How do you administer heparin and LMWH treatment? |
Heparin: IV/SC LMWH: SC only |
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Why do you need to have bridging heparin treatment? |
Cover with heparin until INR >2 on warfarin because of initial prothrombotic state when warfarin is initiated due to the inhibition of endogenous antithrombotic protein C |
