Dvt
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1) Deep vein thrombosis (DVT) can be caused by Virchow's triad of factors that increase the likelihood of blood clots: damage to vessel walls, slowed blood flow, and increased coagulability. 2) DVT presents as either phlebothrombosis, a clot in a healthy vein, or thrombophlebitis, a clot after vein inflammation. Complications include pulmonary embolism and infection. 3) Diagnosis involves tests like Doppler ultrasound, CT scans, and blood tests. Treatment focuses on prevention with stockings and blood thinners, or surgery to remove clots.
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My YouTube channel: " https://bit.ly/drabbasnaseem " Don't forget to Subscribe, Follow, Like, and Share :)
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Phlebothrombosis refers to thrombosis occurring in deep leg veins without vein wall inflammation, while thrombophlebitis involves thrombosis with inflammatory reaction. Virchow identified three factors predisposing to phlebothrombosis - slowed blood flow, vessel wall changes, and blood changes. Those at higher risk include those with congestive heart failure, recent surgery or immobility, obesity, varicose veins, or contraceptive pill use. Thrombophlebitis can result from trauma, infections, cancers, tropical diseases, or conditions causing vein wall irritation. Clinical manifestations of phlebothrombosis include leg swelling and pain, while thrombophlebitis presents as a reddened, warm
Circulatory disturbances
The document discusses circulatory disturbances, specifically hyperaemia, congestion, and thrombosis. It defines hyperaemia as an increase in blood flow to a tissue, which can be active via artery/arteriole dilation or passive via vein/venule engorgement. Congestion is passive hyperaemia. Thrombosis is the formation of a blood clot within a vessel and can be pale, red, or mixed depending on location and flow. Key causes of thrombosis are endothelial injury, abnormal blood flow, and hypercoagulability. Chronic venous congestion can cause organ damage over time due to increased pressure.
Thrombosis, embolism and infarction
Thrombosis is the formation of a blood clot within a blood vessel or cavity of the heart. Virchow identified three main factors that contribute to thrombosis: endothelial injury, changes in blood flow, and hypercoagulability. Thrombi can propagate or embolize, becoming lodged in another vessel and resulting in infarction of downstream tissue. Infarctions appear pale/white in solid organs and red/hemorrhagic in lungs/other tissues. Over time, infarcted tissue progresses from coagulative necrosis to phagocytosis and scar formation.
Deep vein thrombosis
Deep vein thrombosis is a blood clot that forms in the deep veins, usually in the legs. It can cause complications like pulmonary embolism. Risk factors include age over 60, obesity, immobility, surgery, and inherited or acquired hypercoagulable states. Diagnosis is made using ultrasound, CT, or MRI imaging to detect clots. Treatment involves blood thinners like heparin and warfarin to prevent clot growth and reduce risk of embolism. Prophylaxis with compression stockings or blood thinners is important for high risk patients like those having surgery.
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Hemodynamics disorders
1. The document discusses various hemodynamic disorders including edema, hyperemia, congestion, hemorrhage, thrombosis, embolism, infarction, and shock.
2. Edema results from fluid movement into tissues and can affect subcutaneous tissues, lungs, and brain. Congestion is the passive filling of tissues with blood due to impaired outflow.
3. Thrombosis is the formation of clots within vessels, which can then embolize and travel to other sites (embolism), potentially causing ischemic tissue damage or infarction if blood flow is not restored.
4. Shock represents a failure of circulation to maintain adequate tissue perfusion and oxygenation.
Circulatory disturbances
This document discusses circulatory disturbances and disturbances of blood and body fluids. It covers topics such as hyperaemia and congestion, thrombosis, and venous thrombosis.
Hyperaemia is an increase in blood flow due to vessel dilation, while congestion is passive hyperaemia due to blood engorgement in veins. Thrombosis is the formation of a blood clot within a vessel. It can be caused by endothelial injury, abnormal blood flow, and hypercoagulability. Venous thrombosis commonly occurs in the lower limbs and is due to stasis, hypercoagulability, and endothelial damage. Migratory thrombophlebitis is associated with disseminated cancers. Capillary thrombosis
Venous thromboembolism for Pharm.D
Venous thromboembolism (VTE), Deep vein thrombosis (DVT), Pulmonary embolism (PE), virchow's traid, pathophysiology of venous thromboembolism, clinical presentation of DVT, clinical presentation of PE, treatment of venous thromboembolism, patient care (PHARMACOTHERAPEUTICS-3)
Venous thrombosis
This document discusses venous thrombosis (VT), including its definition, risk factors, diagnosis, and treatment. VT occurs when a blood clot forms in one of the veins, which can lead to complications like pulmonary embolism. Risk factors include patient factors like age, obesity, and pregnancy, as well as diseases and surgeries. Diagnosis involves tests like duplex ultrasound of the veins and CT scanning. Treatment includes blood thinners like low molecular weight heparin and warfarin. Prevention involves risk assessment and use of compression stockings or blood thinners for high-risk patients undergoing surgery.
Pulmonary embolism 1-
Pulmonary embolism (PE) is a blockage in the pulmonary arteries usually caused by blood clots from deep vein thrombosis. Risk factors include age over 40, immobility, surgery, and cancer. Symptoms are nonspecific like dyspnea, chest pain, and cough. Diagnosis is made through CT pulmonary angiography, echocardiogram, D-dimer test, V/Q scan, and chest X-ray. Treatment involves oxygen, heparin, and warfarin for at least 6 months to prevent further clots and complications like cor pulmonale, recurrent PE, or chronic pulmonary hypertension.
HYPERAEMIA & CONGESTION
This document discusses chronic venous congestion (CVC) and its effects on various organs. It describes how CVC results in localized blood volume increase within dilated vessels. It then summarizes the gross and microscopic findings of CVC in the lungs, liver, spleen, and kidneys. The lungs show brown induration and thickened alveolar septa. The liver has a nutmeg appearance and centrilobular necrosis. The spleen exhibits congestion and fibrosis. The kidneys demonstrate mild degenerative changes. Hemorrhage and its causes, effects based on amount/speed of blood loss are also outlined.
2 hyperemia-congestion
This document discusses hyperemia and congestion, two vascular events that involve an increased volume of blood in a particular tissue. Hyperemia is an active process of arteriolar dilation that increases blood volume on the arterial side, while congestion is a passive process caused by impaired venous outflow that increases blood volume on the venous side. Both lead to increased hydrostatic pressure and edema. Examples of congestion discussed include nutmeg liver seen in right-sided heart failure and pulmonary edema seen in left-sided heart failure. Microscopic findings of congestion in the liver include centrilobular necrosis and hemorrhage, while the lungs show engorged capillaries, edema, and hemorrhage.
Phlebography
1) The document provides an overview of venography procedures including patient preparation, indications, contraindications, and technique.
2) Key steps in patient preparation include reviewing prior imaging, restricting oral intake, evaluating renal function, and obtaining consent.
3) Indications for lower extremity venography include evaluating deep vein thrombosis, varicose veins, venous malformations, and tumor involvement.
4) Potential pitfalls include underfilling veins, air injection, and valve turbulence which can create false positives, while complications can include contrast reactions, embolism, and local hematoma or infection at the puncture site.
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Dvt
- 1. DVT Prepared by: Dr. Dounia Mammar Kebbab
- 2. Predisposing factors: Virchow's triad 1. Change in vessel wall with damage of endothelial lining. 2. Venous stasis ( velocity) 3. Hypercoagulability of blood ( viscosity)
- 4. Pathology Thrombosis in a healthy vein phlebothrombosis Calf venous sinuses Red thrombosis ( RBCs + fibrin) PE Phlebothrombosis:
- 5. Thrombosis after inflammation of the vein thrombophlebitis Ileofemoral veins (endothelial damage) White thrombus ( Platelets+ fibrin + WBCs) Non adherent Jelly like propagated thrombus Red tail PE Thrombophlebitis:
- 7. Sequelae: Locally: • Organization of thrombus by fibrous tissue. • Recanalization. • Calcification phlebolith. • Infection abscess.
- 8. Distally: • Oedema and 2ry V.V Proximally: • Aseptic embolism (Phlebothrombosis) pulmonary embolism • Septic embolism (thrombophlebitis) pyaemia and lung abscess
- 9. C/P: Silent cases to classic pictures 1. Asymptomatic group: Unexplained fever and TC. Later: pulmonary embolism or post phlebitis limb may manifest. 2. Symptomatic group: classic triad: Pain: muscle exercise. Tenderness: Homan’s sign. Swellin:
- 11. Complications: Phlegmasia cerulea dolens Phlegmasia alba dolens
- 13. Pulmonary embolism Late cpc: 2ry V.V CVI.
- 14. Investigations Doppler U/S Dupplex U/S Ascending venography Enhanced helical CT I 125 fibrinogen uptake Plethysmography Venous manometry laboratory
- 15. DDx: Swollen paiful calf: 1. Contusion of calf muscle. 2. Calf hematoma. 3. Ruptured plantaris tendon. 4. Reuptured packer’s cyst. Swollen lower limb.
- 16. TTT Prophylaxis = prevention of postoperative DVT Graduated elastic stocking Intermittent pneumatic compression
- 17. Curative TTT: 1.Bed rest with leg elevation and elastic stocking. 2.Anticoagulant therapy : Heparin, warfarin. 3.Fibrinolytic therapy. 4.Surgical TTT: Venous thrombectomy. IVC interruption.
- 18. Merci!