Haemodynamic Disorders for 400L Medical Students

Haemodynamic Disorders

• The presentation was given to 400L medical students at Alex Ekwueme Federal University.
• The presenter was Dr. Emmanuel Kunle Abudu, a professor and consultant pathologist.
• The presentation covered haemodynamic disorders, including edema, hyperaemia, hemorrhage, haemostasis, thrombosis, ischemia, infarction, embolism, and shock.

Course Objectives

• Define the terms "Oedema", "hyperaemia", and "haemorrhage".
• Explain the processes of Oedema, hyperaemia, and hemorrhage.
• Define the terms "haemostasis" and "thrombosis".
• Explain how the processes of haemostasis and thrombosis occur.
• Define the terms "ischemia", "infarction", "embolism", and "shock".
• Explain how the processes of ischemia, infarction, embolism, and shock occur.
• Describe the histological changes in Oedema, hyperaemia, hemorrhage, haemostasis, thrombosis, ischemia, infarction, embolism, and shock.
• Describe different types of shock and their aetiology.
• List clinical examples of shock.

Goals and Objectives

• Define thrombosis, embolism, infarct, coagulative necrosis, edema, shock, hyperemia, congestion, hemorrhage, hematoma, and petechiae.
• Identify thrombosis (venous and arterial), embolism, infarction, congestion, edema, and tissue changes related to shock.
• Understand the pathophysiology of normal haemostasis, normal vessel wall constituents, and how they interact with circulating blood
• Understand hypercoaguable states (including primary and secondary).
• Understand the potential fates of thrombi, including embolism (thromboemboli, paradoxical emboli, fat emboli, amniotic fluid emboli, and foreign body emboli).
• Distinguish the pathophysiology between red and pale infarcts.
• Understand the pathophysiology of hemorrhagic shock, cardiogenic shock, septic shock, and anaphylactic shock.

Normal Haemostasis

• Normal haemostasis maintains blood in a fluid state and creates a local haemostatic plug at sites of vascular injury.
• This depends on the integrity of small blood vessels, adequate numbers of platelets, normal amounts of coagulation factors and inhibitors, and adequate amounts of calcium ions in the blood.
• Endothelial cells are antithrombotic and have antiplatelet, anticoagulant, and fibrinolytic properties.
• They also secrete tissue factor for platelet adhesion and aggregation.
• Platelets play a central role, adhering, secreting granule products, aggregating, and forming the primary haemostatic plug.
• The coagulation cascade involving tissue factor and platelet phospholipids results in fibrin polymerization, "cementing" the platelets into a definitive secondary haemostatic plug.
• Counter-regulatory mechanisms (e.g., t-PA, thrombomodulin) limit the hemostatic process to the site of injury.

Haemostasis and Platelets

• Platelets are cytoplasmic fragments of megakaryocytes.
• After vascular injury, platelets adhere, secrete granules products and aggregate to form the primary plug.

Haemostasis and Thrombosis

• Haemostasis depends on well-regulated processes.
• Platelets and the coagulation cascade are involved
• Endothelial cells have antithrombotic and prothrombotic activities.
• Antithrombotic properties include endothelial prostacyclin (PGI2), nitric oxide, heparin-like molecules, and thrombomodulin.
• Prothrombotic properties include endothelial injury exposing collagen, activation by cytokines.
• Thrombosis is formed when there is an intravascular solid or semi-solid build up of blood constituents.

Virchow's Triad on Thrombosis

• Endothelial damage
• alterations in normal blood flow (stasis and turbulence)
• hypercoagulability

Fate of a Thrombus

• Propagation (accumulation of platelets and fibrin leading to vessel obstruction),
• Embolization (thrombi dislodge, travel to other vasculature site),
• Dissolution (removal by fibrinolysis)
• Organization & Recanalization (inflammation and fibrosis, reestablishment of vascular flow).

Thrombosis - Morphology of

Post-mortem vs Ante-mortem thrombi

• Appearance features
• Consistency
• Attachment to blood vessel wall
• Shape characteristics
• Presence/absence of lines of Zahn

Thrombosis- Morphology contd

• Thrombi can develop in various sites of the cardiovascular system.
• Arterial thrombi usually arise at sites of turbulence or endothelial injury, often occlusive.
• Venous thrombi are usually found at areas of stasis, frequently associated with red blood cells.
• Mural, thrombotic occlusion in heart chambers/aortic lumen are known as mural thrombi.

Fat and Marrow Embolism

• Microscopic fat globules (with or without associated haematopoietic) in the circulation.
• Mechanism is via rupture of marrow vascular sinusoids or venules.
• Occurs frequently in individuals with severe skeletal injuries.
• Symptoms may include pulmonary insufficiency, neurological abnormalities, anaemia, thrombocytopenia, petechial rash.

Air Embolism

• Gas bubbles in the circulation can coalesce forming frothy masses, obstructing vascular flow and causing distal ischemic injury. Common causes include coronary bypass surgery, neurosurgery and Obstetrical procedures.
• Symptoms can be sudden decrease in blood pressure, leading to potential heart failure & lung problems due to the gas.

Amniotic Fluid Embolism

• Amniotic fluid embolism is a serious complication of pregnancy.
• It occurs when amniotic fluid enters maternal circulation.
• Common symptoms include sudden dyspnea, cyanosis, shock, and neurological impairment.

Infarction

• Area of ischemic necrosis caused by arterial or venous obstruction.
• Commonly found in Myocardial, cerebral, pulmonary and extremities.
• 99% cases due to thrombotic events, less commonly due to local vasospasm, extrinsic compression, torsion, volvulus, and oedema.

Infarct- Classification

• Histologically: Ischemic coagulative necrosis, liquefactive necrosis, scar tissues.
• Morphologically: Red (hemorrhagic) or White (anemic) infarcts based on their color and extent of hemorrhage and microbial infection.

Red Infarcts vs White Infarcts

• Red: Venous occlusions, loose tissues, dual circulations, low venous outflow.
• White: Arterial occlusions, solid organs, limited haemorrhage.

Morphology of Infarcts

• Infarcts tend to be wedge-shaped, with the occluded vessel at the apex.
• The margins are initially poorly defined, later become better defined due to inflammation.
• The central area exhibits the dominant feature for either coagulative or liquefactive necrosis.

Infarction - Factors Influencing Development

• Nature of the vascular supply
• Rate of development of occlusion, blood oxygen, tissue vulnerability to hypoxia.

Compensatory Shock Stage/ Progressive/ Irreversible Stages

• Compensatory stage: Body tries to compensate for low blood volume/pressure- with symptoms like HR/Respiration increase.
• Progressive: Unfavorable symptoms worsen, such as oliguria, low blood pressure, increased heart rate. Organ failure begins.
• Irreversible: Despite treatment, organs fail leading to death. Characterized by myocardial depression, and massive capillary dilatation.

Shock (General Overview)

• A state where tissue perfusion is insufficient to meet metabolic needs.
• Types of shock: Cardiogenic, hypovolemic, neurogenic, anaphylactic, and septic.
• Compensatory mechanisms initially maintain vital functions.
• Severe shock progresses to organ failure, potentially leading to death.

Disseminated Intravascular Coagulation (DIC)

• A complex pathophysiological process where abnormal blood clotting occurs throughout the body, leading to widespread clots in small blood vessels.

Etiology and Pathogenesis of DIC

• Excessive activation of coagulation, leading to consumption of clotting factors.
• Can be secondary to many conditions, including obstetric complications, cancers (especially acute promyelocytic leukemia), and major trauma.

Some definitions

• SVR: systemic vascular resistance
• CO: cardiac output (heart rate * stroke volume)
• SV: stroke volume
• BP: blood pressure

Morphology of DIC

• Thrombi in many tissues (brain, heart, lung, kidneys, adrenals, spleen and liver).
• Clinically, acute DIC presents with bleeding diathesis whereas chronic DIC presents with thrombotic complications.

This quiz covers key concepts related to haemodynamic disorders, including definitions and processes of oedema, hyperaemia, hemorrhage, haemostasis, thrombosis, ischemia, infarction, embolism, and shock. Designed for 400L medical students, it evaluates understanding of histological changes and clinical examples associated with these conditions.