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Comprehensive vocabulary flashcards covering fluid distribution, diagnostics, edema, hyperemia, hemorrhage, thrombosis, embolism, infarction, and the stages of shock as presented in Lecture 6.
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Intracellular fluid (ICF)
The compartment of fluid located inside cells, accounting for 2/3 of the Total Body Water (TBW).
Extracellular fluid (ECF)
The compartment of fluid located outside cells, accounting for 1/3 of the Total Body Water (TBW).
Interstitial fluid
A subdivision of the extracellular fluid that makes up 3/4 of its total volume.
Plasma fluid
A subdivision of the extracellular fluid that makes up 1/4 of its total volume, separated from the interstitium by the capillary endothelium.
Serum albumin
A laboratory measurement used to evaluate oncotic pressure in patients with fluid disorders.
BNP (Brain Natriuretic Peptide)
A marker used to assess heart failure-related edema.
PT/INR and aPTT
Tests used to evaluate coagulation pathways, monitor anticoagulants, and diagnose bleeding disorders.
D-dimer
A laboratory value that is elevated during clot formation and breakdown.
Troponin and CK-MB
Cardiac biomarkers that indicate the occurrence of a myocardial infarction.
Lactate
A substance that becomes elevated in the blood during hypoperfusion and shock.
Anasarca
A clinical form of severe, generalized edema.
Hydroperitoneum (ascites)
The accumulation of fluid in the peritoneal cavity.
Active hyperemia
The dilation of arterioles often caused by blushing, exercise, or inflammation.
Passive hyperemia (congestion)
Fluid accumulation caused by venous backpressure, often associated with hydrostatic edema and cyanosis.
Heart failure cells
Macrophage cells containing hemosiderin granules, typically found in the lungs during chronic passive congestion.
Petechia, ecchymosis, and purpura
Specific forms of skin hemorrhage characterized by bleeding into the skin.
Hemoptysis
Respiratory-related hemorrhage involving the coughing up of blood.
Hematemesis
The vomiting of blood, often associated with upper gastrointestinal bleeding.
Hematochezia
The passage of fresh blood through the anus.
Melena
The passage of black, tarry stools containing digested blood.
Metrorrhagia
Abnormal uterine bleeding between regular menstrual periods.
Menorrhagia
Abnormally heavy or prolonged menstrual bleeding.
Exsanguination
The process of massive blood loss that can lead to hypovolemic shock and death.
Mural thrombi
Thrombi that occur on the walls of the heart chambers, often overlying a myocardial infarct.
Organization and Recanalization
The processing of a thrombus where it either becomes incorporated into the vessel wall or reestablishes blood flow.
Saddle embolus
A large venous thromboembolus that straddles the bifurcation of the pulmonary artery, often leading to sudden death.
Gaseous emboli
Emboli caused by air injection or associated with caisson disease.
White (pale) infarct
A type of infarction typically occurring in solid organs where blood supply is obstructed.
Red (hemorrhagic) infarct
A type of infarction characterized by bleeding into the necrotic area, often in loose tissues or organs with dual blood supply.
Cardiogenic shock
Shock resulting from the pump failure of the heart.
Hypovolemic shock
Shock resulting from the loss of significant fluid or blood from the circulation.
Hypotensive shock
Shock resulting from the loss of peripheral vascular tone.
Compensated shock
The early stage of shock characterized by tachycardia, vasoconstriction of arterioles, and reduced urine production.
Decompensated reversible shock
A stage of shock featuring hypotension, shortness of breath, oliguria, and acidosis.
Irreversible shock
The final stage of shock involving circulatory collapse, loss of vital functions, and marked hypoperfusion of vital organs.
Intracellular fluid (ICF)
The compartment of fluid located inside cells, accounting for 2/3 of the Total Body Water (TBW).
Extracellular fluid (ECF)
The compartment of fluid located outside cells, accounting for 1/3 of the Total Body Water (TBW).
Interstitial fluid
A subdivision of the extracellular fluid that makes up 3/4 of its total volume.
Plasma fluid
A subdivision of the extracellular fluid that makes up 1/4 of its total volume, separated from the interstitium by the capillary endothelium.
Basic aspects of normal circulation
Normal circulation involves the movement of blood through the heart, arteries, veins, and capillaries, effectively distributing oxygen and nutrients to tissues while removing waste products.
Edema
Edema is the abnormal accumulation of fluid in the interstitial spaces of tissues, leading to swelling.
Example 1: Anasarca
A clinical form of severe, generalized edema.
Example 2: Hydroperitoneum (ascites)
The accumulation of fluid in the peritoneal cavity.
Example 3: Active hyperemia
The dilation of arterioles often caused by blushing, exercise, or inflammation.
Example 4: Passive hyperemia (congestion)
Fluid accumulation caused by venous backpressure, often associated with hydrostatic edema and cyanosis.
Example 5: Heart failure cells
Macrophage cells containing hemosiderin granules, typically found in the lungs during chronic passive congestion.
Pathogenesis of Edema – Increased Intravascular Hydrostatic Pressure
This mechanism involves a rise in blood volume or pressure within the blood vessels, often caused by conditions such as heart failure or renal failure. The increased hydrostatic pressure encourages fluid movement from the bloodstream into the surrounding tissues, resulting in edema.
Pathogenesis of Edema – Reduction in Colloid Osmotic Pressure of Plasma
Edema can also occur when there is a decrease in plasma proteins, particularly albumin, which are essential for maintaining fluid within the blood vessels. This reduction can arise from liver disease, nephrotic syndrome, or malnutrition, ultimately causing fluid to leak into the interstitial spaces and leading to swelling.
Pathogenesis of Edema – Increased Retrograde Pressure in Veins and Lymphatic Vessels
This refers to heightened pressure in the venous system, often due to obstructions or compression of veins, resulting in fluid retention. Additionally, impaired lymphatic drainage can contribute to fluid stagnation and edema. Conditions like deep vein thrombosis (DVT) or chronic venous insufficiency often worsen this situation.
Active Hyperemia
Active hyperemia refers to the increased blood flow to a tissue due to the dilation of arterioles, often triggered by physiological responses such as exercise, blushing, or inflammation. This process leads to enhanced delivery of oxygen and nutrients to the affected area, facilitating tissue function and repair.
Example of Active Hyperemia
An example of active hyperemia occurs during physical exercise, where muscle tissues require increased blood flow to meet metabolic demands.
Congestion
Congestion, also known as passive hyperemia, is characterized by the accumulation of blood in a particular area due to impaired venous drainage. This can result from conditions such as heart failure or venous obstruction, leading to increased hydrostatic pressure and potentially causing tissue swelling.
Example of Congestion
An example of congestion is seen in chronic heart failure, where the heart's reduced ability to pump blood effectively leads to venous backlog and pulmonary congestion.
Hemorrhage
Hemorrhage refers to the escape of blood from the circulatory system, which can occur due to various factors such as injury, disease, or vascular abnormalities. This process can lead to significant blood loss and may result in shock or other complications depending on the volume and site of bleeding.
Example of Hemorrhage - Hemoptysis
Hemoptysis is a specific form of hemorrhage characterized by the coughing up of blood, often associated with conditions such as lung infections or pulmonary embolism.
Example of Hemorrhage - Hematemesis
Hematemesis refers to the vomiting of blood, which is commonly linked to gastrointestinal bleeding resulting from ulcers, varices, or malignancies.
Example of Hemorrhage - Hematochezia
Hematochezia is the passage of fresh blood through the anus, frequently indicating lower gastrointestinal bleeding as seen in conditions like diverticulosis or colorectal cancer.
Endothelial Injury
Endothelial injury refers to the damage to the endothelial layer of blood vessels, which is critical in the development of thrombus.
Prothrombotic State
Injured endothelium leads to a prothrombotic state, increasing the likelihood of blood clot formation.
Platelet Adhesion and Activation
Endothelial injury promotes increased platelet adhesion and activation, essential steps in the thrombogenesis process.
Exposure of Collagen and Tissue Factor
Damage to the endothelium exposes underlying collagen and tissue factor, which are vital for initiating the coagulation cascade.
Coagulation Cascade
The coagulation cascade is activated upon endothelial injury, leading to the formation of a thrombus (blood clot).
Inflammation and Thrombogenesis
Endothelial injury can induce local inflammation, further promoting thrombus formation and increasing the risk of serious complications such as myocardial infarction or stroke.
Hypercoagulability
Hypercoagulability is a condition characterized by an increased tendency of the blood to clot, leading to a higher risk of thrombosis.
Causes of Hypercoagulability
Hypercoagulability can arise from various factors, including genetic mutations (such as Factor V Leiden), underlying medical conditions (like cancer or autoimmune disorders), and certain lifestyle factors (such as obesity or smoking).
Mechanisms of Thrombosis in Hypercoagulability
In hypercoagulability, there is an imbalance between pro-coagulant factors and anticoagulant mechanisms, resulting in excessive clot formation which can obstruct blood flow in vessels.
Clinical Consequences of Hypercoagulability
The clinical consequences of hypercoagulability include deep vein thrombosis (DVT), pulmonary embolism, and other thrombotic events that may lead to organ damage or failure.
Diagnosis of Hypercoagulability
Diagnosis of hypercoagulability often involves blood tests to assess clotting factors and to identify any genetic predispositions or underlying conditions contributing to the enhanced clotting risk.
Morphology of Thrombi
Thrombi can exhibit various morphological characteristics depending on their composition and the circumstances of their formation. They typically consist of a mixture of platelets, fibrin, red blood cells, and sometimes leukocytes.
Mural Thrombi
Mural thrombi are thrombi that occur on the walls of heart chambers or blood vessels, often overlying areas of myocardial infarction or damage. They may not completely occlude the vessel but can disrupt blood flow and lead to complications.
Occlusive Thrombi
Occlusive thrombi completely block the lumen of a vessel, preventing blood flow. This can lead to ischemia and necrosis of tissues supplied by the affected vessel, posing serious health risks.
Thrombophlebitis
Thrombophlebitis refers to the inflammation of a vein associated with thrombosis, commonly resulting in pain, swelling, redness, and warmth over the affected area. It often occurs in superficial veins and can be associated with prolonged immobility or injury.
Fate of Thrombi
The fate of thrombi includes several processes, primarily organization, recanalization, and embolization, which influence their outcomes in the vascular system and overall health.
Organization of Thrombi
Organization refers to the process where a thrombus becomes integrated into the vessel wall, typically involving the gradual replacement of the clot with granulation tissue, leading to reformation of the vascular structure over time.
Recanalization
Recanalization is the phenomenon where a thrombus forms channels that restore blood flow within the obstructed vessel. This process often occurs following organization, allowing for partial or complete restoration of circulation in the affected area.
Embolization
Embolization occurs when a thrombus dislodges from its original site and travels through the bloodstream, potentially causing blockage in distant vessels. This can lead to serious complications such as pulmonary embolism or ischemic stroke, depending on the location of the embolus.
Clinical Consequences of Venous Thrombi
Venous thrombi, typically forming in the deep veins, can lead to significant complications such as deep vein thrombosis (DVT), which may cause pain, swelling, and the risk of pulmonary embolism if the clot dislodges and travels to the lungs.
Clinical Consequences of Arterial Thrombi
Arterial thrombi can result in severe events such as myocardial infarction or ischemic stroke by obstructing blood flow in coronary or cerebral arteries, respectively, leading to tissue necrosis and serious health risks.
Emboli
Emboli are particles or substances that travel through the bloodstream and can obstruct blood vessels, leading to various clinical complications.
Example 1: Pulmonary Emboli
Pulmonary emboli are blood clots that travel to the lungs, often originating from deep veins, and can cause sudden respiratory distress and decreased oxygenation.
Example 2: Arterial Emboli
Arterial emboli can travel to the arteries supplying vital organs, potentially leading to ischemic strokes or myocardial infarctions by obstructing blood flow.
Example 3: Fat Emboli
Fat emboli occur when fat globules enter the bloodstream, often following fractures or surgical procedures, and can cause respiratory distress and neurological symptoms.
Example 4: Air Emboli
Air emboli arise when air enters the bloodstream, which can happen during medical procedures, causing blockages that may lead to serious complications like stroke or cardiac arrest.
Example 5: Septic Emboli
Septic emboli are infected particles that can travel through the bloodstream, often resulting from endocarditis, leading to further infections and complications in distant organs.
Infarction
Infarction refers to a localized area of tissue necrosis that occurs due to inadequate blood supply to that specific area.
Causes of Infarction
Infarction commonly arises from the obstruction of blood flow, which can be caused by thrombus formation, embolism, or significant arterial narrowing (stenosis).
Mechanism of Infarction
The mechanism behind infarction involves the disruption of blood flow leading to reduced oxygen and nutrient delivery, thereby causing cellular injury and eventual tissue death.
Consequences of Infarction
The consequences of infarction vary depending on the affected organ and the extent of tissue damage; they can result in functional impairment, complications, and may be life-threatening, such as in myocardial or cerebral infarction.
Shock
Shock is a critical condition that occurs when the body's organs and tissues do not receive sufficient blood flow, leading to inadequate oxygen and nutrient supply.
Causes of Shock
Shock can result from various factors, including cardiogenic (pump failure), hypovolemic (loss of blood volume), and distributive (loss of vascular tone) causes. Each type leads to decreased blood flow and perfusion to vital organs.
Mechanism of Shock
The pathogenesis of shock involves a complex interplay of decreased cardiac output or systemic vascular resistance, which results in reduced perfusion pressure, compromised cellular metabolism, and ultimately organ dysfunction or failure.
Consequences of Shock
The consequences of shock can range from reversible organ dysfunction to irreversible damage, manifesting as reduced ability to respond to stress, increased risk of multiple organ failure, and potentially death if not promptly recognized and treated.