General Pathology Lecture 4.1 PDF
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Uploaded by CuteVignette2993
AAST Alamein
Dr. Kareem Eldin Mohammed Ahmed
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This document is a lecture on general pathology, specifically focusing on the topic of shock and thrombosis. It provides details on different types of shock, their mechanisms, clinical presentations, and pathophysiology. A concise summary of the lecture notes.
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# General Pathology Lecture 4.1 Dr. Kareem Eldin Mohammed Ahmed ## Shock Shock is a life-threatening clinical syndrome of cardiovascular collapse characterized an acute reduction of effective circulating blood volume (hypotension) and an inadequate perfusion of cells and tissues (hypoperfusion)....
# General Pathology Lecture 4.1 Dr. Kareem Eldin Mohammed Ahmed ## Shock Shock is a life-threatening clinical syndrome of cardiovascular collapse characterized an acute reduction of effective circulating blood volume (hypotension) and an inadequate perfusion of cells and tissues (hypoperfusion). If uncompensated, these mechanisms may lead to impaired cellular metabolism and death. By definition "true (or secondary) shock" is a circulatory imbalance between oxygen supply and oxygen requirements at the cellular level. **Clinically,** patients of primary shock suffer from the attack lasting for a few seconds or minutes and develop brief unconsciousness, weakness, sinking sensation, pale and clammy limbs, weak and rapid pulse, and low blood pressure. Although in a given clinical case, two or more factors may be involved in causation of true shock, classification of shock syndrome divides it into: ### Hypovolemic shock: This form of shock results from inadequate circulatory blood volume by various etiologic factors that may be either from the loss of red cell mass and plasma due to hemorrhage, or from the loss of plasma volume alone. therefore, also called as **hemorrhagic shock**. The major effects in this are due to decreased cardiac output and low intracardiac pressure. The severity of clinical features depends upon degree of blood volume lost. Major clinical features are increased heart rate (tachycardia), low blood pressure (hypotension), low urinary output (oliguria to anuria) and alteration in mental state (agitated to confused to lethargic). ### Cardiogenic shock: Acute circulatory failure with sudden fall in cardiac output from acute diseases of the heart without actual reduction of blood volume (normovolaemia) results in cardiogenic shock. Cardiogenic shock results from a severe left ventricular dysfunction from various causes such as acute myocardial infarction. ### Septic (Toxemic) shock: Severe bacterial infections or septicemia induce septic shock. It may be the result of Gram-negative septicemia (endotoxic shock) which is more common, or less often from Gram-positive septicemia (exotoxic shock). Septic shock results most often from Gram-negative bacteria entering the body from genitourinary tract, alimentary tract, respiratory tract or skin, and less often from Gram-positive bacteria. In septic shock, there is immune system activation and severe systemic inflammatory response to infection. ## PATHOGENESIS The following diagram illustrates a possible pathophysiological process that leads to shock: | | | | ---------------------------------- | ----------------------------------------------------- | | **Effective circulating blood volume** | ↓Venous return to heart | | | ↓ Cardiac output | | | ↓ Blood flow | | | ↓ Supply of oxygen | | | **Anoxia** | | | **Inflammatory mediators** | | | **SHOCK** | ## Stages of Shock Shock is divided into 3 stages: initial reversible stage (**compensated shock**), progressive decompensated shock and finally, the stage of **irreversible decompensated shock**. ## Morphological Changes in Shock Shock causes morphologic changes in different organ systems, notably in the brain (hypoxic encephalopathy), heart (hemorrhage and necrosis), lungs (ARDS), kidneys (tubular necrosis), adrenals (hemorrhage and necrosis), liver (focal necrosis), gut (hemorrhagic gastroenteropathy) and other organs. **Clinically,** shock is characterized by low blood pressure, low body temperature, feeble pulse, shallow respiration, pale face and cold clammy skin. ## 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. **Hematoma** is the extravascular accumulation of blood e.g. into the tissues. Hemostatic plugs are the blood clots formed in healthy individuals at the site of bleeding e.g. in injury to the blood vessel. In other words, hemostatic plug at the cut end of a blood vessel may be considered the simplest form of thrombosis. Hemostatic plugs are useful as they stop escape of blood and plasma, whereas thrombi developing in the unruptured cardiovascular system. **Thrombus** may be life-threatening by causing one of the following harmful effects: 1. **Ischaemic injury:** Thrombi may decrease or stop the blood supply to part of an organ or tissue and cause ischaemia which may subsequently result in infarction. 2. **Thromboembolism:** Thrombus or its part may get dislodged and be carried along in the bloodstream as embolus to lodge in a distant vessel. The following diagram illustrates different components of thrombus: | | | | ---------------------------------------- | ------------------------------------------------------------- | | **Endothelium** | **Red blood cells** | | **Platelets** | **Subendothelial collagen** | | **Leucocytes** | **Fibrin strands** | | **Arterial wall, lines of Zahn, residual lumen, thrombus** | A graphic representation of a cross-section of an artery. | **Figure:** Thrombus in an artery. The thrombus is adherent to the arterial wall and is seen occluding most of the lumen. It shows lines of Zahn composed of granular-looking platelets and fibrin meshwork with entangled red cells and leucocytes. ## The Fate of Thrombus **Resolution:** Thrombus activates the fibrinolytic system with consequent release of plasmin which may dissolve the thrombus completely resulting in resolution. Usually, lysis is complete in small venous thrombi while large thrombi may not be dissolved. **Organization:** If the thrombus is not removed, it starts getting organized. **Propagation:** The thrombus may enlarge in size due to more and more deposition from the constituents of flowing blood. **Thromboembolism:** The thrombi in early stage and infected thrombi are quite friable and may get detached from the vessel wall. These are released in part or completely in blood-stream as emboli which produce ill-effects at the site of their lodgment. # Thank You