Hemodynamic Disorders 2019 Lerman handout
Page 1: Title and Author
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
Page 2: Overview of Circulatory Dysregulation
Key concepts include:
Hyperemia and congestion
Edema
Hemorrhage
Hemostasis and thrombosis
Embolism
Infarction
Shock
Page 3: Normal Circulation
Key Points:
Intact vessels maintain wall integrity.
Physiologic ranges for intravascular pressure and osmolarity are crucial.
No pressure in capillary beds during normal circulation.
Page 4: Normal vs. Abnormal Pressures
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.
Page 5: Differences between Transudate and Exudate
Transudate:
Low protein content, results from hydrostatic pressure increase.
Exudate:
Protein-rich, results from increased osmotic pressure.
Page 6: Overview of Circulatory Dysregulation
Reiterates key concepts of circulatory issues listed previously.
Page 7: Hyperemia
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.
Page 8: Congestion
Definition: Passive process due to impaired outflow.
Causes: Obstructed venous return (e.g., CHF).
Symptoms: Blue-red coloration (cyanosis), potential hypoxia and cell death.
Page 9: Congestion in Lungs
Acute Changes: Blood-engorged vessels, edema.
Chronic Changes: Fibrotic septae, macrophages in alveoli.
Page 10: Chronic Passive Congestion
Causes: Left heart failure, mitral stenosis.
Histopathology: Congestion leading to "heart failure" cells (hemosiderin-laden macrophages).
Page 11: Effects of Congestion
Liver and Lower Extremities: Right heart failure causes visible changes in liver.
Appearance: Dilated congested central veins, nutmeg liver appearance.
Page 12: Reiteration of Circulatory Dysregulation
List of circulatory issues restated.
Page 13: Edema
Definition: Accumulation of interstitial fluid within tissues.
Causes: Imbalance in hydrostatic and osmotic pressures.
Page 14: Edema Terminology
Anasarca: Generalized edema.
Hydrothorax: Fluid in pleural cavity.
Hydropericardium: Fluid in pericardial cavity leading to cardiac tamponade.
Hydroperitoneum (ascites): Fluid in peritoneal cavity.
Page 15: Various Types of Fluid Accumulation
Diagrams indicating locations of edema (lungs, liver, stomach, etc.).
Page 16: Causes of Edema
Factors include:
Vascular permeability
Increased hydrostatic pressure
Decreased osmotic pressure
Impaired lymphatic drainage
Sodium retention
Page 17: Pathophysiologic Causes of Edema
Detailing causes of: increased hydrostatic pressure, hypoproteinemia, lymphatic obstruction, sodium retention, etc.
Page 18: Altered Vascular Permeability
Vascular permeability changes related to allergic responses, acute inflammation, and burns.
Page 19: Hydrostatic Pressure and Edema
Generalized vs. localized increases in pressure due to various underlying conditions (e.g., CHF, DVT).
Page 20: Pathways Leading to Edema
Overview of factors contributing to edema, including heart failure and nephrotic syndrome.
Page 21: Decreased Osmotic Pressure
Conditions leading to decreased albumin levels include nephrotic syndrome, cirrhosis, malnutrition.
Page 22: Reiteration of Edema Pathways
Emphasizes the impact of various health conditions on edema formation.
Page 23: Lymphatic Obstruction
Effects of localized obstruction on lymphatic drainage.
Page 24: Repeat of Lymphatic Obstruction Section
Details on lymphedema from localization.
Page 25: Sodium Retention and Edema
Impacts of sodium retention leading to increased hydrostatic pressure and reduced osmotic pressure.
Page 26: Patterns of Edema
Subcutaneous Edema: Indicators of heart or kidney disease.
Pulmonary Edema: Linked to left heart failure or lung infections.
Brain Edema: Life-threatening.
Page 27: Summary of Circulatory Dysregulation
Final restatement of key circulatory dysregulation concepts.
Page 28: Hemorrhage Definition
Blood escapes from the vasculature due to vessel damage.
Page 29: Hemorrhage Patterns
Distinctions between hematomas, petechiae, purpura, and ecchymoses; potential accumulation in various anatomical spaces.
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Page 31: Courtesy Credit
Acknowledgement of Dr. Michael Kahn.
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Page 35: Hemorrhage Revisited
Further elaboration on the context of hemorrhage.
Page 36: Massive Exsanguination
Definition: Severe bleeding leading to death, often due to trauma or vessel rupture (e.g., aortic aneurysm).
Page 37: Clinical Significance of Hemorrhage
Factors include volume of blood lost, rate of bleeding, and site of damage; implications of external bleeding.
Page 38: Recap of Circulatory Dysregulation
Review of previously discussed circulatory disturbances.
Page 39: Hemostasis and Thrombosis Overview
Concepts of hemostasis involving vascular wall, platelets, and coagulation cascade.
Page 40: Vascular Wall and Clotting
Endothelial cells' role in inhibiting or promoting thrombosis.
Page 41: Mechanisms of Thrombosis
Factors favoring or inhibiting thrombosis outlined; involvement of various proteins and mediators.
Page 42: Platelet Activation
Description of platelet function post-endothelial injury, leading to clotting processes.
Page 43: Coagulation Cascade Overview
Sequential activation leading to clot formation; significance of tissue factor.
Page 44: Paths of Coagulation
Distinction between intrinsic and extrinsic pathways in coagulation.
Page 45: Structure of Thrombus
Description of a thrombus as a solid mass comprising platelets, fibrin, and erythrocytes.
Page 46: Causes of Thrombosis
Overview of primary abnormalities leading to thrombosis (Virchow’s triad).
Page 47: Hypercoagulable States
Table listing genetic and acquired hypercoagulable states leading to thrombosis.
Page 48: Locations of Thrombi
Description of different sites where thrombi may develop: arterial and venous.
Page 49: Outcomes of Thrombi
Potential outcomes include dissolution or organization and their implications on blood flow.
Page 50: Phlebothrombosis Features
Characteristics of venous thrombi and their pathological implications.
Page 51: Mural Thrombus Formation
Thrombi that form in heart and aorta; appearance and relevance in terms of damaged muscle.
Page 52: Heart Valve Thrombi
Description of vegetations due to infective endocarditis and related conditions.
Page 53: Summary of Valvular Thrombi
Various forms of vegetations based on causative agents.
Page 54: Outcomes of Thrombi
Potential outcomes re-emphasized including propagation, embolization, and dissolution.
Page 55: Propagation of Thrombus
Conditions contributing to the excessive growth of thrombi.
Page 56: Embolization
Definition and process of thrombus parts dislodging and causing blockages.
Page 57: Dissolution of Thrombus
Factors affecting the degradation and shrinkage of thrombi.
Page 58: Organization and Recanalization
Process whereby thrombi may be integrated into vessel walls and form new paths.
Page 59: Visual Representation of Recanalization
Illustration of the process involved in thrombus organization.
Page 60: Recanalization of Thrombus
Resulting conditions after thrombus dissolution and the formation of granulation tissue.
Page 61: Recap of Circulatory Dysregulation
Brief overview of previously mentioned circulatory disorders.
Page 62: Definition of Embolus
Description of emboli and their most common forms.
Page 63: Deep Vein Thrombosis
An illustration highlighting thrombus locations in deep leg veins and their potential complications.
Page 64: Thromboembolus Outcomes
Outcomes based on the origin and path of thromboemboli (e.g., pulmonary complications).
Page 65: Pulmonary Embolism
Statistics, causes, and significance of pulmonary embolism in the USA.
Page 66: Arrest Locations of Pulmonary Embolism
Primary locations where emboli may lodge within the pulmonary vascular system.
Page 67: Fat Embolism
Description of causes and symptoms associated with fat embolism syndrome.
Page 68: Malignant Tumor Emboli
Characteristics of tumor cells entering circulation.
Page 69: Air Emboli
Causes and effects of air emboli on the body.
Page 70: Foreign Material Emboli
Examples of unusual emboli related to medical practices and vascular conditions.
Page 71: Amniotic Fluid Emboli
Overview of complications arising from amniotic fluid entering circulation.
Page 72: Other Types of Emboli
Various uncommon emboli not covered by previous sections.
Page 73: Overview of Circulatory Dysregulation
Summary of the circulatory regulation issues.
Page 74: Infarction Overview
Definition of infarct and the implications of ischemic necrosis.
Page 75: Types of Infarcts
Differentiation between types of infarcts based on color and infection presence.
Page 76: Red Infarcts
Characteristics and conditions leading to hemorrhagic infarcts.
Page 77: White Infarcts
Characteristics and occurrence areas of ischemic infarcts.
Page 78: Pathological Findings in Infarction
Histopathologic outcomes and types of necrosis resulting from infarction.
Page 79: Renal Infarction
Brief mention and implications of renal infarctions.
Page 80: Factors Influencing Infarction Development
Overview of factors impacting the likelihood and extent of infarction.
Page 81: Summary of Circulatory Dysregulation
Recap of key issues within circulatory dysfunctions.
Page 82: Definition and Overview of Shock
Defining shock and its serious implications on health.
Page 83: Characteristics of Shock
Symptoms and physiological changes characteristic of shock.
Page 84: Categories and Symptoms of Shock
Different types of shock outlined along with symptoms.
Page 85: Types of Shock Explained
Detailed breakdown of cardiogenic, hypovolemic, and septic shock.
Page 86: Causes of Hypovolemic Shock
Conditions leading to fluid loss and related shock.
Page 87: Septic Shock Causes
Overview of factors leading to septic shock and its prevalence.
Page 88: Table of Major Shock Types
Summary table outlining different shock types with examples and mechanisms.
Page 89: Stages of Shock
Description of shock progression stages.
Page 90: Manifestations of Shock
Clinical manifestations associated with the various types of shock.
Page 91: Clinical Course of Shock
Factors affecting outcomes and survival rates in different types of shock.
Page 92: Recap of Circulatory Dysregulation
Final summary of circulatory discussion points.
Page 93: Acknowledgment
Closing Note: Thank you.