Title: Hemodynamic Disorders, Thromboembolism, and Shock
Author: Mark A. Lerman, D.M.D.
Affiliation: Associate Professor and Division Director of Oral Pathology, Tufts University School of Dental Medicine
Date: May 10, 2019
Key concepts include:
Hyperemia and congestion
Edema
Hemorrhage
Hemostasis and thrombosis
Embolism
Infarction
Shock
Key Points:
Intact vessels maintain wall integrity.
Physiologic ranges for intravascular pressure and osmolarity are crucial.
No pressure in capillary beds during normal circulation.
Normal Hydrostatic Pressure:
Approx. 32 mm Hg at arterial end, 12 mm Hg at venous end.
Transudate:
Forms due to increased hydrostatic or decreased osmotic pressure.
Exudate:
Forms during inflammation due to increased vascular permeability.
Transudate:
Low protein content, results from hydrostatic pressure increase.
Exudate:
Protein-rich, results from increased osmotic pressure.
Reiterates key concepts of circulatory issues listed previously.
Definition: Increase in blood volume within tissue.
Process: Active, results from arteriolar dilation and increased capillary flow.
Appearance: Red coloration due to oxygenated blood engorgement.
Definition: Passive process due to impaired outflow.
Causes: Obstructed venous return (e.g., CHF).
Symptoms: Blue-red coloration (cyanosis), potential hypoxia and cell death.
Acute Changes: Blood-engorged vessels, edema.
Chronic Changes: Fibrotic septae, macrophages in alveoli.
Causes: Left heart failure, mitral stenosis.
Histopathology: Congestion leading to "heart failure" cells (hemosiderin-laden macrophages).
Liver and Lower Extremities: Right heart failure causes visible changes in liver.
Appearance: Dilated congested central veins, nutmeg liver appearance.
List of circulatory issues restated.
Definition: Accumulation of interstitial fluid within tissues.
Causes: Imbalance in hydrostatic and osmotic pressures.
Anasarca: Generalized edema.
Hydrothorax: Fluid in pleural cavity.
Hydropericardium: Fluid in pericardial cavity leading to cardiac tamponade.
Hydroperitoneum (ascites): Fluid in peritoneal cavity.
Diagrams indicating locations of edema (lungs, liver, stomach, etc.).
Factors include:
Vascular permeability
Increased hydrostatic pressure
Decreased osmotic pressure
Impaired lymphatic drainage
Sodium retention
Detailing causes of: increased hydrostatic pressure, hypoproteinemia, lymphatic obstruction, sodium retention, etc.
Vascular permeability changes related to allergic responses, acute inflammation, and burns.
Generalized vs. localized increases in pressure due to various underlying conditions (e.g., CHF, DVT).
Overview of factors contributing to edema, including heart failure and nephrotic syndrome.
Conditions leading to decreased albumin levels include nephrotic syndrome, cirrhosis, malnutrition.
Emphasizes the impact of various health conditions on edema formation.
Effects of localized obstruction on lymphatic drainage.
Details on lymphedema from localization.
Impacts of sodium retention leading to increased hydrostatic pressure and reduced osmotic pressure.
Subcutaneous Edema: Indicators of heart or kidney disease.
Pulmonary Edema: Linked to left heart failure or lung infections.
Brain Edema: Life-threatening.
Final restatement of key circulatory dysregulation concepts.
Blood escapes from the vasculature due to vessel damage.
Distinctions between hematomas, petechiae, purpura, and ecchymoses; potential accumulation in various anatomical spaces.
No content.
Acknowledgement of Dr. Michael Kahn.
No content.
No content.
No content.
Further elaboration on the context of hemorrhage.
Definition: Severe bleeding leading to death, often due to trauma or vessel rupture (e.g., aortic aneurysm).
Factors include volume of blood lost, rate of bleeding, and site of damage; implications of external bleeding.
Review of previously discussed circulatory disturbances.
Concepts of hemostasis involving vascular wall, platelets, and coagulation cascade.
Endothelial cells' role in inhibiting or promoting thrombosis.
Factors favoring or inhibiting thrombosis outlined; involvement of various proteins and mediators.
Description of platelet function post-endothelial injury, leading to clotting processes.
Sequential activation leading to clot formation; significance of tissue factor.
Distinction between intrinsic and extrinsic pathways in coagulation.
Description of a thrombus as a solid mass comprising platelets, fibrin, and erythrocytes.
Overview of primary abnormalities leading to thrombosis (Virchow’s triad).
Table listing genetic and acquired hypercoagulable states leading to thrombosis.
Description of different sites where thrombi may develop: arterial and venous.
Potential outcomes include dissolution or organization and their implications on blood flow.
Characteristics of venous thrombi and their pathological implications.
Thrombi that form in heart and aorta; appearance and relevance in terms of damaged muscle.
Description of vegetations due to infective endocarditis and related conditions.
Various forms of vegetations based on causative agents.
Potential outcomes re-emphasized including propagation, embolization, and dissolution.
Conditions contributing to the excessive growth of thrombi.
Definition and process of thrombus parts dislodging and causing blockages.
Factors affecting the degradation and shrinkage of thrombi.
Process whereby thrombi may be integrated into vessel walls and form new paths.
Illustration of the process involved in thrombus organization.
Resulting conditions after thrombus dissolution and the formation of granulation tissue.
Brief overview of previously mentioned circulatory disorders.
Description of emboli and their most common forms.
An illustration highlighting thrombus locations in deep leg veins and their potential complications.
Outcomes based on the origin and path of thromboemboli (e.g., pulmonary complications).
Statistics, causes, and significance of pulmonary embolism in the USA.
Primary locations where emboli may lodge within the pulmonary vascular system.
Description of causes and symptoms associated with fat embolism syndrome.
Characteristics of tumor cells entering circulation.
Causes and effects of air emboli on the body.
Examples of unusual emboli related to medical practices and vascular conditions.
Overview of complications arising from amniotic fluid entering circulation.
Various uncommon emboli not covered by previous sections.
Summary of the circulatory regulation issues.
Definition of infarct and the implications of ischemic necrosis.
Differentiation between types of infarcts based on color and infection presence.
Characteristics and conditions leading to hemorrhagic infarcts.
Characteristics and occurrence areas of ischemic infarcts.
Histopathologic outcomes and types of necrosis resulting from infarction.
Brief mention and implications of renal infarctions.
Overview of factors impacting the likelihood and extent of infarction.
Recap of key issues within circulatory dysfunctions.
Defining shock and its serious implications on health.
Symptoms and physiological changes characteristic of shock.
Different types of shock outlined along with symptoms.
Detailed breakdown of cardiogenic, hypovolemic, and septic shock.
Conditions leading to fluid loss and related shock.
Overview of factors leading to septic shock and its prevalence.
Summary table outlining different shock types with examples and mechanisms.
Description of shock progression stages.
Clinical manifestations associated with the various types of shock.
Factors affecting outcomes and survival rates in different types of shock.
Final summary of circulatory discussion points.
Closing Note: Thank you.