THROMBOSIS ..pptx

Pathophysiology on thrombosis

1. RAPHEAL CHIMBOLA

2. INTRODUCTION THROMBOSIS : Thrombosis is the process of formation of solid mass in circulation from the constituents of flowing blood; the mass itself is called a thrombus .. THROMBUS : Is An aggregation of blood factors primarily platelets and fibrin with entrapment of cellular elements, frequently causing vascular obstruction at the point of its formation. THROMBUS

3. An Embolism is sudden blockage of venous or arterial circulation by any material that can lodge in blood vessel and obstruct its lumen ” Almost all emboli represent some part of dislodged thrombus – thromboembolism Embolus : Detached intravascular solid, liquid or gaseous mass that is carried by the blood to a site distant from its point of origin

4. CLASSIFICATION Thrombosis can be classified based on the following: According to Location Venous Thrombi Arterial Thrombi Cardiac Thrombi Lymphatic Thrombi According location within the blood vessel Lateral thrombus

5. Occluding thrombus Saddle thrombus Canalized thrombus According to ineffective agent Septic thrombosis Parasitic thrombosis Aseptic thrombosis According to colour Pale or white thrombus Red thrombus Mixed thrombus Laminated thrombus

6. ARTERIAL THROMBI Formed from endothelial injury due to turbulence of blood flow .The turbulence makes the cells to come into contact with the endothelial and will damage endothelial as a result atrial thrombi will develop. It is formed rapidly flowing blood of the arteries and heart .

7. Site of arterial thrombi Coronary arteries (A rch of the aort a) coronary_thrombosis Cerebral arteries(cycle of Willis )

8. Femoral arteries Gross Grey- white,friable lines Microscopy   More prominent with alternating pale platelets ad Fibrin disposal alternating with darker RBC’s rich area Composition Consists of fibrin meshwork of platelets , fibrin, red cells degenerating leukocytes Feature of an arterial thrombi

9. Venous Thrombi This is a thrombi caused by stasis of blood flow .meaning there will be no blood flow but only stagnation of the blood with cells.so these cells come I contact with the endothelial cells. when this happens cells like WCB’s that come in contact with the endothelial cells, will damage the endothelial cells by the toxins ad antimicrobial substances that they produce. Similarly when platelets come in contact with the endothelial cells they get activated ad granulate and this interns activate other platelets ad slowly form the platelets aggregation. It is formed in slow flowing blood

10. Sites of venous thrombi Commo-veins of lower extremities Other sites are veins of upper extremities such as periprostatic plexus or ovarian plexus Gross Red blue with fibrin strands Microscopy Lies of zahn with more abundant red cells Composition More enmeshed RCB’S hence also called as red thrombi or stasis thrombi Both venous ad Arterial grow in the direction or propagate towards the heart but a arterial thrombi grow I reverse direction of flow of blood while a venous thrombi grow I direction of blood flow .

11. CARDIAC THROMBI   Formed in any chamber of the heart and on the valve cusps Common in atrial appendages, especially in right atrium Also on -vegetation on mitral and aortic valves They are usually mural (o - occlusive) All -valve thrombus -large round thrombus obstructing mitral valve Agonal thrombi - composed mainly of fibrin and are formed shorty before death in either or both Ventricle

12. L ymphatic thrombus: The formation of lymphatic thrombosis are supported by the release of thromboplastin substances from the injured lymphatic endothelium and the chronic obstruction of lymph flow in the presence of a hypercoagulable milieu. According location within the blood vessel Lateral thrombus - one side of blood vessel Occluding thrombus - Entire circumference of blood vessel

13. Saddle thrombus - At a bifurcation of the blood vessel Canalized thrombus- New blood channels through the clot According to ineffective agent Septic thrombosis- Contains bacteria

14. A Caudal vena cava septic thrombus attached to the wall of the vein Parasitic thrombus- Contains parasites

15. Thrombus caused by a human schistosoma mansoni expresses extracellular tegumental calpains that cleave the blood clotting protein fibronectin Aseptic thrombosis- Non bacteria or parasite Non-bacterial thrombotic endocarditis (NBTE), also called marantic endocarditis. Sterile vegetations consisting of platelets and fibrin characteristically deposit along the line of closure of the valve leaflet. There is no inflammation, infection, or destruction of the underlying valve tissue .

16. According to colour Pale or white thrombus - I rapid blood flow only platelets Red thrombus- slow blood flow ,fibrin attach to platelets Red-thrombus-mainly-composed-of-erythrocytes-and-fibrin and White-thrombus

17. Mixed thrombus- The primary part of propagating thrombus and is red white striped Mixed-thrombus in the lumen of the vessel Hematoxylin-eosin-stain-40 Laminated thrombus- A flattened or matted appearance of thrombus that is non-mobile and tends to imply a more chronic nature and lower potential for embolization

18. ETIOLOGY Using Virchow ‘s triad there are three etiological factors that cause thrombosis and these are;

19. ENDOTHELIAL INJURY This include; Trauma Bacteria-toxin by erysipelothrix,streptococcus,staphylococcus Vieus -such as Hog cholera virus (thrombosis in spleen) Parasite-this include stronglus vularis in anterior mesenteric artery of horse Tumours invading endothelium ABNORMAL BLOOD FLOW When blood flows slow down ,platelet being the outer most in the blood stream ,fall out to the periphery and stick to endothelium by virtue of their adhesive property. Cause of slow blood flow –stasis and turbulence Chronic venous congestion Aged and debilitated animals Varicose vein • Congestive heart failure  

20. HYPERCOAGULABILITY Increased in number of platelets Decrease in levels of antithrombin III, protein c and fibrinolysin Increase in the level of fibrinogen, prothrombin ,factor VII a, VIIIa’Xa

21. PATHOGENESIS Plateles expose phospholipid complex — activates intrinsic coagulation pathway Tissue factor from injured endothelium — activates extrinsic coagulation pathway ADP — reversible primary hemostatic plug ADP, thrombin, TXA2 — irreversible secondary plug Fibrin deposition around platelets Platelets secretes ADP and thromboxane A2

22. MANIFESTAION Thrombosis symptoms depend on the size of the clot, its location (where it forms or gets stuck) and the complications it causes HEART (heart attack) Chest pain or discomfort (angina). Trouble breathing. Dizziness or passing out ARTERY IN LEG AND ARM Skin that looks paler than other areas. Skin that feels cool to the touch. Weakness and inability to move the affected body part. Numbness or tingling (pins and needles), possibly with pain. Blisters, wounds or sores.

23. VEIN IN ARMS OR LEG Skin that looks redder or darker than other areas. Pain, especially around the affected area. Swelling from fluid buildup. Skin that feels warm to the touch BRAIN OR NECK[transient ischemic attack (TIA) or stroke] Weakness or trouble controlling muscles on one side of your body. Slurred or garbled speech. Confusion, agitation or otherwise unusual behavior changes BELLY (mesenteric ischemia) Severe stomach or abdominal pain, especially after eating. Bloating, nausea and vomiting. Diarrhea, which may contain blood. Fever. LUNGS (pulmonary embolism) Sharp pain in your chest and surrounding areas (jaw, neck, shoulder, back or arm). Pain when you breathe in. Sudden trouble breathing when active or at rest. Brain or neck [transient ischemic  

24. DIAGNOSIS The specific diagnostic approach may vary depending on the suspected location of the clot (e.g., deep vein thrombosis, pulmonary embolism, arterial thrombosis) and the individual patient's presentation. Some common methods used in the diagnosis of thrombosis: Medical history and physical examination : The healthcare provider will assess the patient's symptoms, medical history, and risk factors for thrombosis. Symptoms may include pain, swelling, warmth, or discoloration in the affected area. Risk factors can include a personal or family history of thrombosis, recent surgery, immobilization, use of hormonal contraceptives, and underlying medical conditions . Imaging tests : Ultrasound: Doppler ultrasound is commonly used to diagnose deep vein thrombosis (DVT). It uses sound waves to visualize blood flow in the veins and can identify the presence of a clot. Computed tomography (CT) scan: CT scans may be performed to detect pulmonary embolism (PE) or arterial thrombosis. Contrast material may be used to enhance visualization of the blood vessels. Magnetic resonance imaging (MRI): MRI scans can provide detailed images of blood vessels and are sometimes used to evaluate thrombosis in certain situations

25. D-dimer test: D-dimer is a blood test that measures the presence of a protein fragment produced when a blood clot dissolves. Elevated levels of D-dimer can suggest the presence of a clot, but it is not specific to thrombosis and can also be elevated in other conditions. Venography: In some cases, venography may be performed, where a contrast dye is injected into the veins, and X-rays are taken to visualize blood flow and detect clots.  

26. Blood coagulation studies: Laboratory tests, such as prothrombin time (PT), activated partial thromboplastin time ( aPTT ), and international normalized ratio (INR), may be ordered to assess the blood's clotting ability and rule out underlying clotting disorders

27. MANAGEMENT Anticoagulation Warfarin  and  vitamin K antagonists   are  anticoagulants  that can be taken orally to reduce thromboembolic occurrence they stop clots from growing while stopping the formation of new ones and give the enough time to naturally break them down . Where a more effective response is required, heparin can be given (by injection) concomitantly Thrombolysis Thrombolysis   is the pharmacological destruction of blood clots by administering  thrombolytic drugs   including  recombinant tissue plasminogen activator , which enhances the normal destruction of blood clots by the body's enzymes, blood clots contain plasmi n which is usually off and is activated by a substance know as activator which activates the plasmin n causes it to tear down formed blood clots Surgery Arterial thrombosis may require surgery if it causes  acute limb ischemia Endovascular treatment Mechanical clot retrieval and catheter-guided thrombolysis are used in certain situations

28. Antiplatelet agents Arterial thrombosis is platelet-rich, and inhibition of platelet aggregation with  antiplatelet drugs   such as  aspirin  may reduce the risk of recurrence or progression.

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