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.

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