Term
| how should we consider PE and DVT? |
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Definition
| as one disease entity: venous thromboembolism |
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Term
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Definition
| endogenous or exogenous material that travels to the lungs and into pulmonary circulation. most commonly (95%) of the time, *PEs are due to DVTs. less frequently *emboli form from the axillary/subclavian system (esp those w/central vein catheters) or fat emboli, tumor cells, air bubbles, and talc |
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Term
| how common are venous thromboembolisms (VTEs)? how many go undiagnosed? |
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Definition
| venous thromboembolisms are very common, and 50% go undiagnosed. if untreated, 1 mo mortality is 30%, but if treated, 1 mo mortality is 8%. 95% of PE arise from the proximal deep veins of the lower extremities |
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Term
| what do venous thromboembolisms usually arise from? |
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Definition
| stasis, hypercoagulability and endothelial injury (*virchow's triad - exam question*). prolonged immobilization (sx, medical illness, bed res >5 days) and acquired hypercoagulable states (secondary to malignancy, estrogen use, nephrotic syndrome, pregnancy), cigarette smoking and in situ thrombi (sickle cell) can all lead to these states. |
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Term
| what are risk factors for venous thromboembolisms? |
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Definition
| pts older than 40, obesity, trauma, and inherited thrombophili disorders: deficiency in protein C/S, antithrombin II, *factor V leiden polymorphism (system becomes insensitive to protein C, a coagulant)*, prothrombin, gene mutation 20210A, hyperhomocysteinemia, polycythemia vera, paroxysmal nocturnal hemoglobinuria, APA, SLE/lupus anticoagulant |
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Term
| how would a PE affect the lungs in terms of minute ventilation and pO2? what does the impact of the PE depend on? |
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Definition
| with an acute PE, there is an *increase in minute ventilation - leading to the development of *tachypnea (breathing faster to get rid of CO2) and *hypoxemia. obstruction of the blood flow creates alveolar dead space creates alveolar dead space, resulting in regions of *V/Q mismatch = hypoxemia. the impact of the PE depends on the *extent of the reduction of cross sectional area of the pulm vasculature as well as *cardiopulmonary reserve (which someone w/COPD would have less of) |
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Term
| at what point will a significant increase in pulmonary artery pressure occur? cardiopulmonary collapse? |
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Definition
| when emboli occlude *25-30% of the vascular bed. hypoxemia causes vasoconstriction which further increases the pulm artery pressure. when obstruction of the pulmonary circulation reaches *75%, RV systolic pressures may have to reach 50 mm Hg to overcome pulmonary pressures - which can often lead to RV failure and cardiopulmonary collapse |
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Term
| what is seen in terms of pathophysiology with venous thromboembolism? where are common locations of lethal emboli? how does a pulmonary infarction occur? |
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Definition
| generally the *lower lobes are involved bilaterally. the emboli have *blunt, nontapering ends and may fold over on themselves. often massive emboli that result in death are found in the *RV outflow tract (saddle emboli), PA bifurcation or the main pulm artery. a pulmonary infarction consists of intraalveolar hemorrhage, necrosis of the alveolar walls - usually in the periphery (however, due to dual blood supply from the pulm and bronchial arteries, this is usually only seen in pts with a low cardiopulmonary reserve) |
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Term
| what are the most common symptoms in pts presenting with a PE? |
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Definition
| *dyspnea*, pleuritic pain, cough, leg swelling/pain, hemoptysis (infarction), wheezing, angina-like pain (these are in order of appearance) |
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Term
| what are the most common signs in pts presenting with a PE? |
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Definition
| *tachypnea*, rales, tachycardia, s4, increased P2, fever, homan's sign (flex knee/dorsiflex the foot = pain in back of calf), RV lift. (these are in order of appearance) |
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Term
| what is in the ddx for DVTs? |
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Definition
| baker's cyst (located in bursa behind knee), hematoma, venous insufficiency, lymphedema, sarcoma, myositis/cellultis, abcess, arterial aneurysm |
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Term
| what is in the ddx for a PE? |
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Definition
| dissecting aortic aneurysm, pneumonia, acute bronchitis, bronchogenic carcinoma, pericardial/pleural disease, heart failure, costochondritis, MI, asthma/COPD, and pneumothorax |
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Term
| what are well's criteria for clinical prediction of venous thromboembolisms? |
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Definition
| clinical suspicion of DVT (physical evidence): 3 pts, alternative dx less likely than PE: 3 pts, tachycardia: 1.5 pts, immobilization or sx in prior 4 wks: 1.5 pts, previous DVT/PE: 1.5 pts, hemoptysis: 1 pt, malignancy: 1 pt. -> a score >4 means clinical probability is likely (imaging studied should be performed), if suspicion is lower - test for D-dimer to r/o DVT |
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Term
| what are common positive lab findings for a venous thromboembolism that would likely be tested on many pts? |
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Definition
| blood gas: respiratory alkalosis, hypoxemia, widened A-a gradient (more specific), wackers triad (increased LDH, increased bilirubin, normal SGOT - less imporant these days but possible exam question), and a positive D-dimer |
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Term
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Definition
| a cross-linked degredation product that is elevated during acute illness or venous thromboembolism. the test is specific, but not sensitive, however *in the setting of a low VTE clinical probability and negative D-dimer, almost all PE can be r/o. *in the setting of high clinical suspicion, D-dimer does not have a high enough negative predictive value to r/o PE, and imaging studies are necessary |
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Term
| what are EKG findings consistent with VTE? |
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Definition
| ST segment and T wave changes, axis deviation, sinus tachycardia (*most common), new onset of an atrial fibrillation/flutter, and massive emboli can show changes consistent w/cor pulmonale: S1Q3T3, RBBB or RAD. EKGs are mainly useful in r/o other pathologies such as an MI |
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Term
| what is seen on echocardiographs with venous thromboembolisms? |
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Definition
| *free floating clot/thrombus in the right heart, RA dilatation, RV dilation/hypokinesis, tricuspid regurgitation (due to RA dilatation), pulm HTN, and mcconnell's sign (*RV free wall hypokinesis w/preserved motion of the RV apex* - might need to know). sensitivity w/echocardiograms is 30-50% and can ID pts w/PE who have a poor prognosis. |
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Term
| what are imaging studies ordered to dx VTE? |
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Definition
| CXR, spiral CT (usually first ordered), ultrasound (second ordered), V/Q scanning (final test), *pulmonary arteriography (final test - gold standard - know for test)*, MRI/MRA |
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Term
| what is a compression ultrasound? |
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Definition
| this is done in conjunction w/thoracic imaging when a spiral CT cannot be performed (dye allergy/renal failure) and can indirectly confirm a DVT. the "compression" part refers to whether the vein is compressible, and if it is not = higher likelihood of DVT. however, venography is the gold standard for DVT dx (it is however invasive and requires dye) |
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Term
| what is seen most commonly on a CXR |
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Definition
| atelectasis or infiltrate, though it may still appear normal on a pt w/a VTE - however, CXRs need to be done in pts with SOB to r/o other causes like CHF, pneumonia, pneumothorax etc. |
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Term
| what is the westermark sign? |
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Definition
| a dilatation of the pulmonary vessels proximal to an embolism along with collapse of the distal vessels (distal oligemia) - this is seen on a CXR and is suggestive of a PE |
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Term
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Definition
| a late finding of pulmonary infarction. it is a triangular or rounded pleural-based infiltrate w/the apex pointed toward the hilum |
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Term
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Definition
| a CT w/contrast for dx of acute and chronic PE with a sensitivity of 80-90% and a specificity of 90%+. often the legs are imaged as well, which does not require the administration of more contrast (this increases sensitivity for the VTE) |
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Term
| where is the spiral CT most sensitive in detecting pulmonary emboli? |
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Definition
| the spiral CT is most sensitive in detecting pulmonary emboli in the main, lobar, and segmental pulmonary emboli. it is less sensitive in detecting subsegmental emboli |
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Term
| what advantages does the spiral CT have over the V/Q and pulmonary arteriography? |
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Definition
| the spiral CT is rapid and the CT can define other conditions (lymphadenopathy, emphysema, tumors, pleural disease, pericardial disease, and dissecting aortic aneurysms). its main disadvantage is the need for contrast - which is problematic for renal pts |
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Term
| when would a V/Q scan be ordered? how does a V/Q scan work? |
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Definition
| V/Q scans are used often when pts can't handle the contrast from a spiral CT (used to be the best test). they require administration of radioactive material via *inhaled and *IV routes and subsequent uptake of each. |
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Term
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Definition
| normal, non-diagnostic (very-low, low, intermediate probability) and high probability (w/high clinical suspicion and high probability V/Q scans, the positive predictive value is 96%) |
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Term
| what is the gold standard for VTE detection? |
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Definition
| pulmonary arteriography, which requires the placement of a pulmonary catheter and infusion of IV contrast (therefore, less invasive tests are preferred initially). these are best suited for pts in whom PT must be diagnosed or excluded, but are used less frequently since the advent of CT |
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Term
| can an MRI/MR angiogram be used similarly to pulmonary angiography? |
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Definition
| yes, an MRI/MR angiogram is very good for visualization of blood flow and almost similar to an angiogram (not universal) |
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Term
| what are treatments for VTE? |
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Definition
| anticoagulation, vena cava interruption, thrombolytic therapy and surgical management |
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Term
| how is anticoagulation for PE/DVT pts managed? |
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Definition
| initial management of PE/DVTs begins w/administration of anticoagulation at the time of dx (unless contraindicated, and usually therapy is started empirically if the clinical index of suspicion is high during work up). parenteral anticoagulation is started first w/SC LMWH or IV SQ UFH. warfarin PO is added to the parenteral anticoagulation and pts are generally maintained on warfarin until their INR is therapeutic (2-3). parenteral anticoagulation should be continued for 4-5 days and until an INR of 2-3 for 2 consecutive days is achieved w/warfarin therapy |
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Term
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Definition
| they catalyze the inactivation of thrombin and factor X by antithrombin, and antithrombin III is required as a cofactor (intrinsic pathway) |
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Term
| what is the difference between LMWH (low molecular weight heparin) and UFH (unfractionated heparin)? contraindications? |
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Definition
| LMWH (*enoxaparin) has a similar efficacy, superior safety, superior bioavailabilty, 1-2x daily dosing, no lab monitoring, SQ administration, possible home therapy, and a lower incidence of HIT. LMWH is contraindicated in pts w/creatinine clearance <10 and it is first-line therapy for pregnant women (warfarin = teratogenic). UFH can be advantageous b/c it has a short half life and it is completely reversible w/protamine sulfate (good if pt has a sx procedure the next day). |
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Term
| how does warfarin work in tx of VTEs? why is parenteral therapy of another anticoagulant necessary initially? how long is tx for? |
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Definition
| warfarin is an oral anticoagulant which decreases active vit K (extrinsic pathway), which leads to a decrease in vit K dependent clotting factors (II, VII, IX, X, proteins C+S). it has good oral absorption that takes 4-5 days to take effect. pts may develop an increase in *hypercoagulability in the first few days (b/c proteins C+S are depleted first), and is therefore used aling w/paraenteral therapy initially. it is usually used for 3-6 mos+ in the setting of a recurrent VTE. it can interact w/other drugs |
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Term
| what are the complications of anticoagulation? |
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Definition
| bleeding, HIT (venous/arterial thrombosis due to platelet and thrombin activation by heparin-dependent IgG antibodies working on platelet Fc receptors) - tx:argatroban/lepirudin |
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Term
| what is vena cava interruption? |
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Definition
| this is a filter placed in the vena cava that is used when a pt cannot be anticoagulated in the setting of a proven DVT or PE due to : contraindications to anticoagulation, recurrent embolism w/adequate therapy and bleeding complications during anticoagulation. if these are in for a long time, you can get chronic lower extremity edema. |
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Term
| how is thrombolytic therapy used in tx of VTEs? ADRs? |
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Definition
| tissue-type plasminogen activator (t-PA), streptokinase, and urokinase *activate plasminogen to form plasmin which results in fibrinolysis. this is typically used in the setting of an *acute PE, when there is hemodynamic instability w/hypotension. this is also used when an echo shows *RV dysfunction w/o hypotenstion or a *massive embolism on radiography w/o clear hemodynamic instability and hypoxemia. ADR: intracranial hemorrage |
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Term
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Definition
| pulmonary embolectomy is indicated for massive acute PE w/hemodynamic instability refractory to lytic therapy or contraindication to lytic therapy. mortality is very high (50%). *pulmonary thromboendarterectomy can be done for unresolved chronic PE w/pulmonary HTN |
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Term
| what are important actions to take in prevention of VTE? |
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Definition
| assessment of risk factors, prophylaxis (mechanical or anticoagulation) |
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