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113 Cards in this Set
- Front
- Back
what % of PE pts dies w/in the 1st hr
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8-10%
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what is a PE
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abrupt blocking of a pulmonary artery or one of its branches by a thrombus or foreign material
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large thrombi lodge where and cause what?
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lodge at the bifurcation of the main pulmonary artery or the lobar branches and cause hemodynamic compromise
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where are smaller thrombi found
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continue traveling distally, occluding a smaller vessel in the lung periphery
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what is more likely to produce pleuritic chest pain by initiating an inflammatory response adjacent to the parietal pleura
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PE: smaller thrombi
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what is the pattern of most PE
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they are multiple, and the lower lobes are involved more commonly than the upper lobes
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how should beta 3 agonist be used in asthma pts?
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never as sole agents only as supplemental agents
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when follwing an astham pt. what should be monitored to gauge how well the asthma is being treated
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eosinophil count/ how pt. tells you he/she is doing
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what are some other types of emboli
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amniotic fluid/fat emboli
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is PE a dz?
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no it is a complication of DVT
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what is the natural Hx. of venous thrombosis
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Virchow triad of factors that lead to the pathogenesis of venous thrombosis:
1. Venous stasis, 2. Injury to the intima, 3. Changes in the coagulation properties of the blood. |
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what is virchow's triad
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factors that lead to the pathogenesis of venous thrombosis:
1. Venous stasis, 2. Injury to the intima, 3. Changes in the coagulation properties of the blood. |
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thrombosis usually originates as what
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as a platelet nidus (point/focus/loci) in the region of venous valves located in the veins of the lower extremities
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what is a nidus
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point/focus/loci
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how does a PE develop
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originates as a platelet nidus (point/focus/loci) in the region of venous valves located in the veins of the lower extremities. Further growth occurs by accretion of platelets and fibrin and progression to red fibrin thrombus, which may either break off and embolize or result in total occlusion of the vein
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what are the common causes of PE
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venous stasis, Polycythemia, dehydration, immobility, compression of a vein by a tumor, Hypercoagulable states, Immobilization
Surgery and trauma Pregnancy, malignancy |
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what is polycythemia and what are the most common causes
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increased RBC; smoking and hypoxemia
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what is the frequency of PE
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60-80% of patients with DVT, even though more than half the patients are asymptomatic.
300,000-650,000 a yr is US |
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what is the pattern of PE among sexes
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women increased risk
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who is at increased risk for PE
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pregnant women, women, during post partum period, older pts.,
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when is PE commonly missed
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in hospitalized elderly pts.
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what is the pattern found in symptoms of PE
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they are nonspecific and high index of suspicion is required
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what is the Tx of a pt. who has overdosed on warfarin
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if a small amount vitamin K; otherwise fresh frozen plasma
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what is the most frequent symptom of a PE
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dyspnea
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what are the symptoms of PE
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dyspnea, chest pain, hemoptysis, cough, sweats, anxiety/hypertension
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what type of chest pain is seen in a pt. with PE
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pleuritic
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what is the most frequent sign of a PE
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tachycardia
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If pt has had B clot and later has hair loss (alopecia) check them for what
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lupus
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what are the signs of PE
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tachycardia, wheezing/reduced breathing sounds, neck vein distention, crackles, loud pulmonic second sound, pulm. outflow murmors (not common), pleuritic friction rub w/ peripheral pulm. infarct, DVT
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what is a surrogate marker in the presence of signs and symptoms of pulmonary embolus
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DVT
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what are the D dx of PE
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Myocardial infarction
Pericarditis Pneumonia Pneumothorax Chest wall pain Congestive heart failure Pleuritis |
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what are the labs done for a PE
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ABG, D-dimer
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what is seen on the ABG of a PE pt
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hypoxemia, hypocapnia, and respiratory alkalosis
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what is seen on the d dimer of a PE pt
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elevated (>500ng/mL) in 97% of patients
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what imaging studies should be done for PE pts
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Chest radiograph
Spiral CT scanning (helical CT scan), Ventilation-perfusion (V/Q) scanning of the lungs, Doppler ultrasonography, Pulmonary angiography |
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what test for PE is most frequently used in the past few years
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spiral CT scan (helical CT)
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a normal lung scan (VQ) rules out what
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PE
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what is the best form of heparin
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low molecular weight heparin
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what is the criterion standard for the diagnosis of PE
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pulmonary angiography
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what should you check when giving heparin
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PTT- make sure you don't over coagulate
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what is the cut off sign
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Darker area of Reduced Perfusion (Westermark's sign)- PE
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if the pulmonary angiograms show lobulated defects in the dye column filling the pulmonary arteries what has been proven
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PE
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Diagnostic difficulty of PE is a reason for what
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immediate referral to specialist
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what is considered to be the gold standard diagnostic test for PE
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pulmonary angiography
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what is used to determine whether pulmonary angiography is necessary
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integrated diagnostic approach (combining clinical symptoms with noninvasive testing)
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what is the immediate Tx of a pt. suspected to have a DVT or PE
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Immediate full anticoagulation
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initial anticoagulation in a PE/DVT pt is done with what
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IV heparin
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never start warfarin until when
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after the pt has been on heparin for a few hours
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after the pt. (PE) has been started on heparin what else should be done
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should be started simultaneously on oral anticoagulation with Coumadin (warfarin)
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when should the heparin Tx of a PE pt. be discontinued
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After a therapeutic dose of warfarin is established, heparin is discontinued and warfarin therapy is maintained
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what has the highest level of vit. K in a vegetable
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guacamole (avacodo)
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what rapidly dissolves the obstructing pulmonary thrombus and the source of the thrombus in the pelvic or deep leg veins
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thrombolytic therapy
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what is the mainstay of therapy and 1st drug of choice for PE
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heparin
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what prevents conversion of fibrinogen to fibrin
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heparin
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what does heparin prevent
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conversion of fibrinogen to fibrin
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will heparin dissolve an existing clot
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no, but it does prevent clot propagation and embolization
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how is heparin given
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IV or infussion intermittent IV
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what will grapefruit juice do with a drug
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increase activity of what ever drug it is given with (binds with it)/prolongs action of drug
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The efficacy of heparin depends on what
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achieving therapeutic levels of the drug within the first 48h of therapy. The aPTT should be 1.5–2.5X control
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how many times can striptokinase be given
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once b/c of anaphylatic reactions
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what are the side effects of heparin
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Hemorrhage, thrombocytopenia, new thrombus formation (white-clot syndrome)
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what are the Coumadin (warfarin) vitamin K–(antagonist) dependent factors
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factors II, IIV, IX, X
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what is the drug of choice for chronic Tx of PE
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coumadin
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what does the full effect of coumadin
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requires up to 5 days of treatment
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what might coumadin initially cause
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hypercoagulable state, necessitating concurrent therapy with heparin during initiation of therapy
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what is the oral dose of coumadin
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5mg daily for 2-4 days, then adjust dose. Usual maintenance dose is 2-10mg/day
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INR (international normalized ratio) is maintained how in treating with coumadin
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therapuetic range: 2-3
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what are the side effects of coumadin
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first few days of warfarin therapy produce a hypercoagulable state
Numerous drug Interactions |
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what has effects similar to those of heparin
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Enoxaparin sodium (Lovenox) and dalteparin sodium low molecular weight heparins (LMWHs)
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Enoxaparin sodium (Lovenox) and dalteparin sodium low molecular weight heparins (LMWHs) are different from heparin how
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they have improved bioavailability, have
longer half-life, and may be associated with fewer bleeding complications. They also require less monitoring than is required with conventional heparin |
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true or false: LMWHs are as effective as heparin in preventing venous thromboembolism
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true
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what is the dose of LMWH's
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Subcutaneously: twice daily (BID)
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what Is a recommended therapy for the acute treatment of deep vein thrombosis (DVT)
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LMWH's
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what are Streptokinase and urokinase
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thrombolytic agents that rapidly dissolve the obstructing pulmonary thrombus and the source of the thrombus in the pelvic or deep leg veins
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what drugs rapidly dissolve the obstructing pulmonary thrombus and the source of the thrombus in the pelvic or deep leg veins.They also decrease the likelihood of recurrence
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streptokinase and urokinase
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true or false: Thrombolytic therapy is not generally recommended for the routine treatment of pulmonary embolism because it is contraindicated in many patients
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true
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what are tissue plasminogen activators
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Alteplase and reteplase
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true or false: There is some evidence that tissue plasminogen activators have a better safety profile and efficacy than other thrombolytics.
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true
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Pulmonary embolectomy is indicated in patients with what
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massive pulmonary emboli, but it is only performed when thrombolysis is contraindicated and in patients with refractory shock and hypotension
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what is the chronic Tx plan for PE
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6 mo of anticoagulation (reduces rate of recurrence to half of the recurrence rate observed when only 6 wk of anticoagulation is given).
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when is long term anticoagulation indicated
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for patients with an irreversible underlying risk factor and recurrent DVT or recurrent PE
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what is one of the most common risk factors for PE
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Hx of immobilization
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when is prophylaxis for DVT indicated
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in bedridden pts
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women at risk for thromboebolism taking oral contraceptives should be advised what
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to consider other forms of contraception
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what contributes to coexisting complication dzs for PE
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tobacco use
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when is routine thromboprophylaxis used in prevention therapy
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in high risk pts scheduled for surgical procedures (particularly major orthopedic surgery)- PE
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what is increase in blood pressure in the pulmonary artery, pulmonary y vein, or pulmonary capillaries. i.e. the pulmonary vasculature
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pulmonary hypertension
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what is pulmonary hypertension
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increase in blood pressure in the pulmonary artery, pulmonary y vein, or pulmonary capillaries. i.e. the pulmonary vasculature
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what leads to Shortness of breath, dizziness, fainting, and other symptoms, all of which are exacerbated by exertion
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pulmonary hypertension
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what does pulmonary hypertension lead to
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Shortness of breath, dizziness, fainting, and other symptoms, all of which are exacerbated by exertion
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what are the 5 types of pulm. hypertension
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Arterial,
Venous, Hypoxic, Thromboembolic or Miscellaneous / idiopathic |
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Arterial,
Venous, Hypoxic, Thromboembolic or Miscellaneous / idiopathic are 5 types of what |
pulm. hypertension
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Whatever the initial cause, pulmonary arterial hypertension (WHO Group I) involves what
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vasoconstriction
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vasoconstriction results in what
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obstruction to flow through pulm. vasculature
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what happens as a result of obstruction to flow through the vasculature
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vascular fibrosis that leads to further flow restriction
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increased workload of the hear leads to what
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hypertrophy of the right ventricle eventually leading to right heart failure
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what is cor pulmonale
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right heart failure
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what happens during right heart failure
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1. decreased pulm. flow= left heart received less B
2. decreased LH oxygen 3. decreased systemic oxygenation=increased demand on heart, HR, contractility |
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WHO I refers to what
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arterial hypertension
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WHO II refers to what
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pulmonary venous hypertension
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who III refers to what
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hypoxic pulm. hypertension
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compare PAH and PVH
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PVH: no obstructive B flow in the lungs, due to left heart failure PAH: obstructive B flow to lungs, causes right heart failure
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the result of PVH is what
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pulmonary edema and pleural effusion caused by obstruction/back pressure on venous flow through the heart
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PVH is due to what
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left heart failure resulting in obstruction and back pressure on venous flow through the heart
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what causes hypoxic pulm. hypertension
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low levels of oxygen cause vasoconstriction of pulm. arteries leading to HPH
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what is the result of HPH
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similar patho as pulm. artery hypertension
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what does the WHO IV group refer to
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chronic thromboembolic pulm. hypertension
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what caused thromboembolic pulm. hypertension
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B vessels are blocked/narrowed w/ B clots= thromboembolic pulm. hypertension
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what does thromboembolic pulm. hypertension cause
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similar patho to pulm. arterial hypertension
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what is in the WHO 1973 classification
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1.Primary PH
A. Arterial plexiform, B. Veno-occlusive and C. Thromboembolic forms 2. Secondary PH |
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what addressed the causes of secondary pH
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WHO 1998
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WHO 1998 addressed what
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causes of secondary pH
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what modified the WHO classification based on new understandings of dz: risk factor descriptions, the classification of congenital systemic to shunts were revised
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3rd world symposium on pulmonary arterial hypertension 2003 (venice)
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