Thrombosis: Pathophysiology, Fate, Clinical Effect, Treatment And MCQs for NEET, GPAT, CSIR NET JRF

Thrombosis: Pathophysiology, Fate, Clinical Effect, Treatment And MCQs for NEET, GPAT, CSIR NET JRF

INTRODUCTION :-

“Thrombosis is a process of formation of solid mass in circulation from the constituent of flowing blood, the mass itself is called as thrombus.”

1.] Thrombosis is characterized by events that essentially involve activation of platelets, the process of clotting involves only the conversion of soluble fibrinogen to an fibrin which is polymerized and is insoluble.

2.] Haematoma is the extra vascular accumulation of blood e.g. into the tissues.

3.] Haemostatic plugs are the blood clots formed in the healthy individuals at the site of bleeding.

HARMFUL EFFECTS CAUSED BY THROMBI :-

A.] ISCHEMIC INJURY : Thrombi may decrease or stop the blood supply to part of an organ or tissue and cause ischemia which may be subsequently result in infarction.

B.] THROMBOEMBOLISM : Thrombus or its part may get dislodged and be carried along in the bloodstream as embolus to lodge in a distant vessel.

PATHOPHYSIOLOGY :-

  • Since the protective haemostatic plug formed as a result of normal homeostasis is an example of thrombosis.
  • Human beings posses inbuilt system by which the blood remains in fluid state normally and guards against the hazards of thrombosis and hemorrhage.
  • Injury to the blood vessel initiates haemostatic repair mechanism or thrombogenesis.
  • A scientist named as Virchow describe three primary events which predispose to thrombus formation also called Virchow’s triad : Endothelial injury, Altered blood flow, Hypercoagulability of blood. To these added the activation processes that follow these primary events : Activation of platelets and clotting system.

FATE OF THROMBUS :-

The outcome of thrombi are as follow :-

1.] PROPAGATION : The thrombus may propagate and eventually cause obstruction of some critical vessels.

2.] EMBOLIZATION : Thrombi may dislodge to distal sites in the vascular tree.

3.] DISSOLUTION : They may be removed by fibrinolytic activity.

4.] ORGANIZATION AND RECANALIZATION : Thrombi may induce inflammation and fibrosis – termed organization and may eventually become recanalization.

CLINICAL EFFECT :-

Clinical effects depends upon not only the site but also on rapidity of formation and nature of thrombi.

  • Cardiac thrombi : Large thrombi in heart that may cause sudden death.
  • Arterial thrombi : These cause ischemia necrosis of the deprived part which may lead to gangrene.
  • Capillary thrombi : Microthrombi in microcirculation may give rise to DIC ( disseminated intravascular coagulation )
  • Venous thrombi (Phelbothrombosis) : These may cause following effects : Thromboembolism, Edema of area drained, Skin ulcers, Painful white legs and Poor wound healing, etc.

Treatment

The treatment for thrombosis depends on whether it is in a vein or an artery, the impact on the person, and the risk of complications from treatment.

Anticoagulation

Warfarin and vitamin K antagonist are anticoagulants that can be taken orally to reduce thrombolembolic occurrence. Where a more effective response is required, heparin can be given (by injection) concomitantly. As a side effect of any anticoagulant, the risk of bleeding is increased, so the international normalized ratio of blood is monitored. Self-monitoring and self-management are safe options for competent patients, though their practice varies. In Germany, about 20% of patients were self-managed while only 1% of U.S. patients did home self-testing (according to one 2012 study). Other medications such as direct thrombin inhibitors and direct Xa inhibitors are increasingly being used instead of warfarin.

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. This carries an increased risk of bleeding so is generally only used for specific situations (such as severe stroke or a massive pulmonary embolism)

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.

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.

Targeting ischemia/reperfusion injury

With reperfusion comes ischemia/reperfusion (IR) injury (IRI), which paradoxically causes cell death in reperfused tissue and contributes significantly to post-reperfusion mortality and morbidity. For example, in a feline model of intestinal ischemia, four hours of ischemia resulted in less injury than three hours of ischemia followed by one hour of reperfusion. In ST-elevation myocardial infarction (STEMI), IRI contributes up to 50% of final infarct size despite timely primary percutaneous coronary intervention. This is a key reason for the continued high mortality and morbidity in these conditions, despite endovascular reperfusion treatments and continuous efforts to improve timeliness and access to these treatments. Hence, protective therapies are required to attenuate IRI alongside reperfusion in acute ischemic conditions to improve clinical outcomes. Therapeutic strategies that have potential to improve clinical outcomes in reperfused STEMI patients include remote ischemic condition (RIC), exenatide, and metoprolol. These have emerged amongst a multitude of cardioprotective interventions investigated with largely neutral clinical data. Of these, RIC has the most robust clinical evidence, especially in the context of STEMI, but also emerging for other indications such as acute ischemic stroke and aneurysmal subarachnoid hemorrhage.

MULTIPLE CHOICE QUESTIONS [MCQs] :-

1.] Line of Zahn are found in ?

a. Thrombus

b. Infarct tissue

c. Postmortem clot

d. All of the above

2.] Which of the following inherited disorders produces arterial thrombosis ?

a. Factor V Leiden mutation

b. Antithrombin deficiency

c. Homocysteinemia

d. Protein S deficiency

3.] Deep vein thrombosis (DVT) occurs in the ?

a. Chest

b. Abdomen

c. Leg

d. Feet

4.] You are at risk for developing DVT or pulmonary embolism if you ?

a. You are obese

b. Have had recent surgery

c. Smoke

d. Any of the above

5.] Sign and symptoms of DVT can include ?

a. Redness, warmth, tenderness and swelling

b. Shortness of breath, chest pain, coughing blood

c. Muscle spasm, vertigo, ringing ears

d. All of the above

6.] Arterial thrombosis is seen in ?

a. Homocysteinemia

b. Anti – Phospholipid syndrome

c. Protein S deficiency

d. Protein C deficiency

7.] Virchow’s  triad include all except ?

a. Injury to vein

b. Venous thrombosis

c. Venous stasis

d. Hypercoagulability of blood

8.] Antiphospholipid syndrome is associated with all except ?

a. Recurrent abortion

b. Venous thrombosis

c. Pancytopenia

d. Antibody to lupus

9.] Predisposing factor for venous thrombosis ?

a. AT lll deficiency

b. Protein S deficiency

c. Protein C deficiency

d. Disfibrinogenemia

e. All of the above

10.] Which of the following is the single most powerful risk marker for development of VTE ?

a. Surgical procedure

b. Malignancy

c. Obesity

d. Prior history of DVT

 

SOLUTIONS :-

1.] (a) Thrombus

2.] (c) Homocysteinemia

3.] (c) Leg

4.] (d)

5.] (a) Redness, warmth, tenderness and swelling

6.] (a) Homocysteinemia

7.] (b) Venous thrombosis

8.] (c) Pancytopenia

9.] (e)

10.] (d) Prior history of DVT

 

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REFERENCES :-

1.] Textbook Of Pathology By Harsh Mohan; 7th edition; Page no. 99 – 105.

2.] Robbin’s Basic Pathology; 5th edition; Page no. 105 – 110.

 

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