C1D4: edema

Edema and Effusions Overview

• Perturbed cardiovascular, renal, or liver function can cause fluid accumulation in tissues (edema) or body cavities (effusions).
• Edema is fluid buildup in interstitial tissues.
• Effusions are fluid accumulations within body cavities.

Pathophysiologic Mechanisms of Edema

• Increased hydrostatic pressure can result from impaired venous return, congestive heart failure, constrictive pericarditis, ascites, venous obstruction, or lower extremity inactivity.
• Arteriolar dilation, caused by heart failure or neural humoral dysregulation, leads to edema.
• Lymphatic obstruction, which may be inflammatory, neoplastic, post-surgical, or post-irradiation, disrupts fluid drainage.
• Sodium retention, due to excessive salt intake with renal insufficiency or increased tubular reabsorption, contributes to edema.
• Acute or chronic inflammation increases vascular permeability and disrupts lymphatic flow
• Growth of new blood vessels can contribute to edema formation

Reduced Plasma Osmotic Pressure (Hypoproteinemia)

• Conditions such as protein-losing enteropathy, liver cirrhosis, malnutrition, and protein-losing gastroenteropathy can result in edema by reducing plasma osmotic pressure.

Morphology of Edema

• Subcutaneous edema, common in lower extremities, manifests as pitting edema.
• Peri-orbital edema is swelling around the eyes.
• Myxedema, associated with hypothyroidism, causes edema in the face, legs, and tongue, presenting with a waxy appearance.
• Pulmonary edema presents as pink fluid in alveolar spaces, leading to frothy, blood-tinged sputum (hemoptysis).
• Brain edema disrupts brain function.

Heart Failure Cells

• Macrophages ingest red blood cells in long-standing pulmonary edema, resulting in hemosiderin-laden macrophages called "heart failure cells".
• Hemosiderin (iron) in macrophages indicates prior bleeding or chronic congestion.

Hyperemia and Congestion

Hyperemia

• Hyperemia is an active process where increased blood flow occurs due to arteriolar dilation It's usually in response to increased metabolic activity.

Congestion

• Congestion is a passive process where blood pools in tissue as a result of reduced venous outflow.

Pulmonary Congestion

• Pulmonary congestion leads to hemosiderin-laden macrophages in alveolar spaces
• Occurs due to left-sided heart failure that causes blood to back up into the lungs.

Liver Congestion

• Liver Congestion is classified as a "Nutmeg liver" because of its appearance
• Chronic passive congestion of the liver occurs because of impaired venous return.

Hemostasis

Purpose of Hemostasis

• Prevents or limits bleeding
• Facilitates repair of vascular injury.

Steps of Hemostasis

• Arterial constriction reduces blood flow
• Primary hemostasis involves platelet plug formation
• Secondary hemostasis involves fibrin deposition
• Clot stabilization with reabsorption

Initiating Hemostasis

• Endothelial cell injury exposes basement membrane and causes platelet adhesion

Platelet Activation

• Platelets are activated by adenosine diphosphate (ADP), thromboxane A2, and collagen
• Platelets release granules and recruit more platelets.

Promoting Coagulation

• Activation of thrombin promotes fibrin deposition and cements platelet plugs
• Coagulation is normally restricted to the site of vascular injury.

Thrombosis

Platelet Defects

• Platelet defects result in purpura, causes bleeding under the skin and inhibits platelet activation.

Coagulation Factor Defects

• Coagulation factor defects cause bleeding into joints

Thrombosis

• Thrombosis is clot formation in blood vessels

Fat Embolism

• A fat or bone marrow embolism is common with long bone fractures.

Shock Definitions

• Shock is a circulatory failure that impairs tissue perfusion, leading to cellular hypoxia.

Cardiogenic Shock

• Etiology: Myocardial infarction, ventricular rupture, arrhythmia, cardiac tamponade, pulmonary embolism
• Mechanism: Failure of myocardium to pump blood

Hypovolemic shock

• Etiology: Fluid loss due to hemorrhage, burns, and diarrhea, causing inadequate tissue perfusion.

Septic Shock

• Etiology: Overwhelming microbial infection
• Mechanism: Systemic inflammatory response, vasodilation, pooling of blood and Disseminated Intravascular Coagulation.

Distributive Shock

• Includes anaphylactic shock, neurogenic shock, endocrine shock
• Due to infectious or non-infectious causes

Anaphylactic Shock

• Severe hypersensitivity reaction

Neurogenic shock

• Disrupts autonomic pathways

Endocrine Shock

• Is due to adrenal failure

Cardiogenic Shocks

• Result from mechanical obstructions or impaired blood flow.

Septic Shock Pathogenesis

• Microorganisms trigger inflammatory cells, leading to a cytokine cascade

Stages of Shock

• Initial stage involves compensatory mechanisms
• Progressive stage has reduced tissue perfusion
• Irreversible stage can cause cell death and eventually death

Morphology of Shock

• Can result in fibrin thrombi in the kidneys
• And Adrenocortical lipid cell depletion
• And also diffuse alveolar damage

Clinical Features include Shock

• Hypotension, rapid pulse, clammy skin
• As well as cardiac
• And pulmonary changes
• And worsening renal function

Overview of Hemostasis

Role of Platelets

• Are cytoplasmic fragments of megakaryocytes containing granules

Function of the Platelets

• Participate in clotting

Role of Endothelial Cells

• Prevent unnecessary clotting through anticoagulant functions

Mechanism of Hemostasis

• Platelet adhesion, occurs activation and aggregation

Platelet Adhesion

• Platelets bind to von Willebrand factor (vWF) via Glycoprotein Ib (GpIb) receptor.

Platelet Aggregation

• Platelets are stick together using Glycoprotein IIb/IIIa (GpIIb/IIIa) receptors

Thrombosis and Embolism

Causes of Thrombosis

• Caused by the Virchow Triad
• Which includes is endothelial cell injury
• And abnormal blood flow
• And hypercoagulable states.

Endothelial Cell Injury

• Is primarily caused by high pressure

Abnormal Blood Flow

• Laminar flow
• Can cause turbulent blood flow

High Homocysteine

• Can lead to B12 vitamin deficiency

Red Infracts

• Has interconnections within blood supply