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TOPIC: Thrombosis & SHOCK PREPARED BY: DR.RATHER ALI MOHMADSEMEY STATE MEDICAL UNIVERSITY

PLAN OF LECTUREINTRODUCTIONTYPES MECHANISM OF THROMBOSISPATHOGENESISCAUSESSHOCK TYPES PATHOGENESISCONCLUSION

Thrombosisis the process of a blood clot, also known as a thrombus, forming in a blood vessel. This clot can block or obstruct blood flow in the affected area, as well as cause serious complications if the clot moves to a crucial part of the circulatory system, such as the brain or the lungs.

It is normal for the body to produce clotting factors like platelets and fibrin when a blood vessel is injured, to prevent an excessive loss of blood from the body. If this effect is over productive it can obstruct the flow of blood and form an embolus that moves around the blood stream

Thrombosis Types

Thrombosis can be broadly classified as either: venous thrombosis or arterial thrombosis, according to where the thrombus presents in the body.

Venous thrombosis occurs in the veins and is categorized further according to where it occurs including:

Deep vein thrombosisPortal vein thrombosisRenal vein thrombosisJugular vein thrombosisBudd-Chiari SyndromePaget-Schoetter diseaseCerebral venous sinus thrombosis

Renal vein thrombosisThe renal vein can also be obstructed by a thrombus, which can result in reduced kidney drainage. This type is known as renal vein thrombosis and is common in patients with nephrotic syndrome.

Jugular Vein ThrombosisThrombosis of the jugular vein is an extremely rare type of venous thrombosis that usually occurs as a result of intravenous drug use but is also associated with infection and malignancy. Individuals affected by this type may develop serious complications such as systemic sepsis, pulmonary embolism and papilledema.

Budd-Chiari SyndromeThis type of venous thrombosis involves the obstruction of the hepatic vein and the outflow of blood from the liver. It is uncommon but may be recognized by symptoms of abdominal pain, ascites and hepatomegaly.

Paget-Schroetter DiseaseAlso known as effort thrombosis, this refers to thrombosis occurring in an upper extremity vein, such as the axillary or subclavian vein. It usually affects physically active people and presents most often immediately after or during high-intensity exercise.

Cerebral Venous Sinus ThrombosisThis is a rare type of stroke, caused by a thrombus in the venous channels of the brain. It is characterized by headache, abnormal vision and symptoms of stroke, such as difficulty speaking and moving the facial and arm muscles. The majority of people make a full recovery, but adequate treatment as for a stroke is required to promote healthy recovery.

Thrombotic StrokeThis is a type of arterial thrombosis that involves a blockage in the cerebral artery that is responsible for supply blood and oxygen to the brain. Thrombotic stroke usually presents more gradually than other types of stroke, such as hemorrhagic, due to the gradual build up of the thrombus and the growing obstruction

Venous ThrombosisDeep vein thrombosis(DVT) commonly involves the formation of a blood clot in the femoral vein of the leg and is the most common type of thrombosis to cause serious complications. If the thrombus breaks off to form an embolism it moves with the blood towards the lungs and commonly causes pulmonary embolismTypical signs of deep vein thrombosis are pain, swelling and redness in the legs. If these are noted and DVT is suspected, assessment and management should be conducted as soon as possible to reduce the possibility of pulmonary embolism.

Portal vein thrombosisThis type of thrombosis occurs in the hepatic portal vein and can cause portal hypertension and affect the blood supply to the liver. In most cases, it results from other abnormalities in the body, such as pancreatitis, cirrhosis, diverticulitis or cholangiocarcinoma.

Arterial thrombosis, also known as atherothrombosis due to its association with atheroma rupture, occurs in the arteries. The blood stasis caused by atrial fibrillation may also cause this type of thrombosis.

Causes

There are three main causes of thrombosis: hypercoagulability, injury to the endothelial cells of the blood vessel wall and abnormal flow of the blood.Hypercoagulability, also known as thrombophilia, refers higher levels of coagulation factors in the blood that increase susceptibility to thrombosis. This is usually as a result of genetics or disorders of the immune system.Injury to the epithelial cells on the wall of blood vessels after trauma, surgery or and infection can also precipitate coagulation and possible thrombosis.

Mechanism of thrombosis

Platelets adhere to endothelium forming a projecting mass

Liberation of thromboplastins from platelet aggregate leads to initiate coagulation cascade

Blood clot formation occurs

Thrombotic and antithrombotic mechanisms Thrombotic ThromboplastinFactor VPAFvWF

Anti-thromboticThrombomodulinAnti thrombin IIIAlpha 2 macroglobulintPANormally these two groups are finely balanced to prevent thrombus formation. Damage to endothelium however will favour thrombosis.Most significant in arterial thrombosis

Endothelial cells lossAtheromatous plaques: ulcerationDamage by surgeryArteritisIndwelling vascular cathetersInfusion of sclerosing chemicalsHydrodynamic forcesProlong hypertensionTurbulanceToxins and immune mediated damageBacterial toxinsCigarette smokeImmune mediatd: transplant rejection, immune complex diseaseRadiation

Complications

A common complication of thrombosis is hypoxia, due to the obstruction of the artery of vein. When the majority of the blood vessel is blocked, the oxygen supply to the body is reduced and results in increased production of lactic acid.

Prevention and Treatment

As stasis of the blood is associated with increased risk of thrombosis, it is important that movements are made regularly, particularly if susceptible individuals are likely to be sedentary for long periods of time, such as in bed or on an airplane.For people at high risk of venous thromboembolism, heparin can be administered to reduce risk of pulmonary embolism, although this is associated with higher susceptibility to bleeding due to the reduced efficacy of the clotting factors. Therefore, heparin offers greater use in the treatment, rather than prevention of thrombosis.

A more coherent method to prevent the formation of deep vein thrombosis is the use of compression stockings, which mechanically support the vein to inhibit the formation of blood clots. This is particularly beneficial as there are few side effects.Anticoagulants may increase the risk of major bleeding slightly, but has been found to offer a benefit in both the prevention and treatment of thrombosis

SHOCKis a life-threateningmedicalcondition of low bloodperfusionto tissues resulting in cellular injury and inadequate tissue function.The typical signs of shock arelow blood pressure,rapid heart rate, signs of poor end-organperfusion(i.e.: low urine output, confusion, or loss of consciousness), and weak pulses.

Signs and symptoms

The presentation of shock is variable with some people having only minimal symptoms such as confusion and weakness.While the general signs for all types of shock arelow blood pressure, decreased urine output, and confusion, these may not always be present.While a fast heart rate is common, those on-blockers, those who are athletic and in 30% of cases those with shock due to intra abdominal bleeding may have a normal or slow heart rate.

TYPES of SHOCKCARDIOGENIC: (Acute, Chronic Heart Failure)HYPOVOLEMIC: (Hemorrhage or Leakage)SEPTIC: (ENDOTOXIC shock, #1 killer in ICU)

NEUROGENIC: (loss of vascular tone)ANAPHYLACTIC: (IgE mediated systemic vasodilation and increased vascular permeability)

CARDIOGENIC shockMIVENTRICULAR RUPTUREARRHYTHMIACARDIAC TAMPONADEPULMONARY EMBOLISM (acute RIGHT heart failure or cor pulmonale)

HYPOVOLEMIC shockHEMORRHAGE, Vasc. compartmentH2OVOMITING, Vasc. compartmentH2ODIARRHEA, Vasc. compartmentH2OBURNS, Vasc. compartmentH2O

SEPTIC shockOVERWHELMING INFECTIONENDOTOXINS, i.e., LPS (Usually Gm-)Gm+FUNGALSUPERANTIGENS, (Superantigens are polyclonal T-lymphocyte activators that induce systemic inflammatory cytokine cascades similar to those occurring downstream in septic shock, toxic shock antigents by staph are the prime example.)

CLINICAL STAGES of shockNON-PROGRESSIVEPROGRESSIVEIRREVERSIBLE

CLINICAL STAGES of shockNON-PROGRESSIVEPROGRESSIVEIRREVERSIBLE

NON-PROGRESSIVECOMPENSATORY MECHANISMSCATECHOLAMINESVITAL ORGANS PERFUSED

PROGRESSIVEHYPOPERFUSIONEARLY VITAL ORGAN FAILUREOLIGURIAACIDOSIS

IRREVERSIBLEHEMODYNAMIC CORRECTIONS of no use