Pathology of Infarcts and Edema

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Questions and Answers

What is the most common location for an infarct, and what are the two primary mechanisms that cause it?

Arteries; thrombosis and embolisation

An infarct resulting from venous occlusion, such as ovarian torsion or in the lung, is likely to be classified as what color?

Red (hemorrhagic)

In most tissues, what type of necrosis is characteristic of infarction, and what is the exception?

Ischemic coagulative necrosis; liquefactive necrosis in the brain

A patient has a myocardial infarction due to a failure of the heart's pumping mechanism. What type of shock is the patient most likely experiencing?

Cardiogenic shock Signup and view all the answers

Name three primary factors that affect the development of an infarct in the tissues.

Vascular supply anatomy, rate of occlusion, tissue vulnerability to ischemia Signup and view all the answers

What is the key difference in the mechanism between hyperaemia and congestion?

Hyperaemia is an active process with increased blood inflow due to arteriolar dilation, while congestion is a passive process due to impaired venous outflow. Signup and view all the answers

Name three specific body cavities where fluid can accumulate in cases of edema.

Hydrothorax, Hydropericardium, and Hydroperitoneum (Ascites). Signup and view all the answers

What term describes a massive, generalized edema?

Anasarca. Signup and view all the answers

What are the two opposing forces that maintain homeostasis in the vasculature and what type of pressure are they?

Vascular hydrostatic pressure and plasma colloid osmotic pressure. Signup and view all the answers

Besides inflammation, what is one cause of increased vascular permeability, which results in edema?

Increased vascular permeability can be a result of other factors than inflammation, such as the content does not mention it Signup and view all the answers

How does congestive heart failure contribute to generalized edema?

Congestive heart failure leads to increased central venous pressure and decreased renal perfusion, causing generalized edema. Signup and view all the answers

What plasma protein is primarily responsible for maintaining colloid osmotic pressure?

Albumin. Signup and view all the answers

Provide an example of a condition or situation that would lead to local edema due to impaired venous return.

Deep vein thrombosis (DVT). Signup and view all the answers

What type of thrombi commonly form in heart chambers or the aorta?

Mural thrombi Signup and view all the answers

Besides propagation, embolization, and dissolution, what is another potential outcome for a thrombus?

Organization and recanalization Signup and view all the answers

What is the primary initiating factor in the formation of arterial or cardiac thrombi?

Endothelial injury Signup and view all the answers

What is the material called that travels in the blood, and can be solid, liquid or gaseous?

Embolus Signup and view all the answers

What is the main source of systemic emboli according to the text?

Cardiac mural thrombi Signup and view all the answers

A deep vein thrombosis is most likely to result in what kind of emboli?

Pulmonary emboli Signup and view all the answers

What specific type of injury can cause fat emboli?

Long bone fracture or soft tissue crush injury Signup and view all the answers

Besides bypass surgery, give an example of a situation where air embolism can occur?

Decompression sickness (scuba diving) Signup and view all the answers

What term describes the condition where tissue dies due to a blocked blood supply?

Infarction Signup and view all the answers

Venous thrombi are typically formed in areas characterized by what?

Stasis Signup and view all the answers

What are two primary pathological conditions that can lead to a decrease in colloid osmotic pressure?

Reduced albumin synthesis and increased albumin loss. Signup and view all the answers

Lymphedema, often resulting from lymphatic obstruction, is typically localized. List one common cause of lymphatic obstruction.

Inflammation, complication of therapy, or neoplastic obstruction. Signup and view all the answers

Describe the microscopic appearance of edema.

Clearing and separation of extracellular matrix elements. Signup and view all the answers

Define 'hemorrhage' in the context of blood vessels.

Extravasation of blood from vessels. Signup and view all the answers

Name three types of small hemorrhages, differentiated by size.

Petechiae, purpura, and ecchymoses. Signup and view all the answers

What two factors influence the clinical significance of a hemorrhage?

Volume and rate of blood loss and site of hemorrhage. Signup and view all the answers

Contrast normal hemostasis with pathological hemostasis also known as thrombosis

Normal hemostasis maintains blood in a fluid state within normal vessels and forms a localized plug at the site of injury, while thrombosis is the formation of a blood clot within intact vessels. Signup and view all the answers

What are the four main steps of hemostasis?

Vasoconstriction, primary hemostasis, secondary hemostasis, and antithrombotic mechanisms (fibrinolysis). Signup and view all the answers

In the context of hemostasis, describe the dual role of endothelial cells

Endothelial cells possess both antithrombotic and prothrombotic properties. Signup and view all the answers

What role does tissue factor play in the coagulation cascade?

Tissue factor initiates the coagulation cascade. Signup and view all the answers

Study Notes

Impaired Blood Flow and Other Bodily Fluids

Lecture objectives include describing haemodynamic disorders, thromboembolism, and shock.

Introduction

Normal condition: plasma proteins remain in blood vessels, minimal water and electrolyte movement into tissues.
Pathologic condition: protein may leak out of blood vessels, altering the balance of fluid between blood vessels and tissues.
This imbalance occurs due to factors such as altered endothelial function, increased vascular pressure, or reduced plasma protein content.

Hyperaemia and Congestion

Hyperaemia: active process, increased arteriolar dilation and blood inflow, occurs at inflammation sites or during skeletal muscle exercise (red).
Congestion: passive process, impaired venous blood outflow from a tissue (blue).

Oedema

Edema: fluid accumulating in interstitial spaces; can be protein-poor (transudate) or protein-rich (exudate).
Fluid may accumulate in body cavities (hydrothorax, hydropericardium, hydroperitoneum/ascites).
Massive generalized edema is called anasarca.

Causes of Oedema

Increased hydrostatic pressure (impaired venous return, local venous pressure, generalized venous pressure; e.g., DVT, congestive heart failure, increased arteriolar dilation).
Reduced plasma osmotic pressure (reduced albumin synthesis, e.g., cirrhosis, malnutrition, increased albumin loss, e.g., nephrotic syndrome).
Lymphatic obstruction (inflammation, neoplasia).
Sodium and water retention (renal failure).
Increased vascular permeability (inflammation).

Increased Hydrostatic Pressure

Impaired venous return: reduced blood flow back to the heart.
Local venous pressure: a blockage in a vein, e.g., deep vein thrombosis (DVT), causing edema.
Generalized venous pressure: whole-body edema, e.g., congestive heart failure.
Increased arteriolar dilation: widening of the small arteries.

Congestive Heart Failure

Reduced cardiac output leads to increased venous pressure, causing fluid to leak into tissues.
Symptoms include edema and difficulty breathing.
Imbalance of heart function.

Reduced Plasma Osmotic Pressure

Albumin is crucial for maintaining colloid osmotic pressure.
Reduced albumin synthesis reduces the pressure that draws fluid into blood vessels from surrounding tissues.
Impaired liver function or malnutrition can lead to low albumin levels.
Loss of albumin in urine (e.g., nephrotic syndrome) results in fluid leaking out of blood vessels into tissues.

Lymphatic Obstruction

Impaired lymphatic drainage causes lymphedema.
Localized edema due to inflammation, therapy complications, or neoplastic obstructions.
Examples include parasitic infection affecting inguinal lymphatics, radiation to axillary lymphatics in breast cancer patients, or breast cancer.

Morphology of Oedema

Gross inspection: organ enlargement noticeable.
Microscopic examination: extracellular matrix elements separate and clear.

Haemorrhage

Hemorrhage: blood leaking from blood vessels.
In haemorrhagic diatheses, trauma, atherosclerosis and thrombocytopenia can cause extravasation of blood.
Causes such as colonic mucosa hemorrhages, intracerebral hemorrhage and other conditions.

Haemostasis and Thrombosis

Normal haemostasis: maintaining blood in a fluid, clot-free state within vessels.
Rapid localized haemostatic plug formation occurs at injury sites.
Pathologic haemostasis: thrombus formation within intact blood vessels.

Haemostasis

Vasoconstriction: Reduces blood flow.
Primary hemostasis: Platelet aggregation forms a plug.
Secondary hemostasis: More stable plug formed from RBCs and leukocytes.
Antithrombotic: Fibrinolysis degrades thrombi.

Roles of Endothelium

Central regulator of hemostasis.
Antithrombotic properties (inhibiting platelet aggregation, coagulation factors, and activating fibrinolysis).
Prothrombotic properties (activating platelets and clotting factors).
Antifibrinolytic effect.

Roles of Platelets

Platelet adhesion: Platelets adhere to the damaged blood vessels.
Platelet activation: Activated platelets release granules containing factors for aggregation and plug formation.
Platelet aggregation: Platelets aggregate to form a plug.

Roles of Coagulation Cascade

Tissue factor initiates the cascade.
Thrombin converts fibrinogen into fibrin, forming a hemostatic plug.

Thrombosis

Endothelial injury, abnormal blood flow, or hypercoagulability causes thrombosis.
Common causes like abnormal blood vessel flow, blood clots and conditions such as deep vein thrombosis.

Morphology

Arterial or cardiac thrombi: arise in arteries or the heart due to endothelial injury.
Venous thrombi: frequently form at stasis sites, e.g., deep vein thrombosis (DVT).
Mural thrombi: within heart chambers or aorta.
Vegetations: thrombi in heart valves.

Fate of Thrombus

Propagation: Thrombus grows larger.
Embolization: Thrombus breaks free and travels to other sites.
Dissolution: Thrombus dissolves.
Organization & recanalization: Thrombus becomes incorporated into surrounding tissue; vessels may reform.

Clinical Correlation

Arterial thrombosis: results in myocardial infarction or stroke.
Venous thrombosis: predisposes to pulmonary embolism.

Embolism

An embolus is an intravascular solid, liquid, or gaseous mass carried from one location to another within the blood stream.
Thromboembolism is the most common form.
Embolism can lead to systemic infarction and/or pulmonary circulation problems such as hypoxia or right-sided heart failure.

Two Types of Emboli

Pulmonary embolus: travels via venous system, typically from deep vein thrombosis, causing pulmonary blockage and right heart failure.
Systemic embolus: arises from cardiac mural or valvular thrombi or from atherosclerotic plaques.

Fat, Amniotic Fluid, and Air Emboli

Fat embolism: soft-tissue injury or long bone fractures release fat particles that travel through the circulation.
Amniotic fluid embolism: amniotic fluid enters the maternal circulation during labor, causing immediate respiratory distress or circulatory collapse.
Air embolism: gas bubbles in the blood stream cause blockage of blood vessels, typically occurring during bypass surgery or scuba diving accidents.

Infarction

An infarct is an area of ischemic tissue death caused by reduced blood flow.
Common causes are blood clots (thromboses) or travelling blood clots (emboli).
Affected tissue, which may require surgical intervention.

Morphology of Infarcts

Classified by colour: red (haemorrhagic) or white (anaemic), primarily related to the type of blood supply interruption.
Presence or absence of infection: septic infarcts are infected, bland infarcts are not.

Morphology-Histology of Infarcts

Ischemic coagulative necrosis is common in most tissues.
Brain infarcts exhibit liquefactive necrosis.
Septic infarctions convert into abscesses.

Factors that Influence Infarct Development

Anatomy of vascular supply.
Rate of occlusion (rapid blockage leads to more severe effects).
Tissue vulnerability to ischaemia (some tissues are more susceptible).
Hypoxemia (reduced oxygen levels further harm tissues).

Shock

Shock: final common pathway for several potentially lethal events.
Examples include exsanguination (blood loss), extensive trauma, myocardial infarction, pulmonary embolism, and sepsis.

Three Major Types of Shock

Cardiogenic shock: heart is unable to pump effectively.
Hypovolemic shock: a reduced blood volume.
Septic shock: body's response to infection.

Multiple Organ Failure

Multiple-organ dysfunction syndrome: failure of multiple organs due to shock and other severe events.
Resulting in reduced blood pressure.

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Description

This quiz explores the mechanisms and characteristics associated with infarcts and edema. Examine the common locations for infarcts, types of necrosis, factors influencing tissue infarction, and various causes of increased vascular permeability. Test your understanding of these critical pathological processes.