Podcast
Questions and Answers
What initiates the hemostasis process following vascular injury?
What initiates the hemostasis process following vascular injury?
- Exposure of tissue factor (correct)
- Cascading reactions of thrombin
- Formation of fibrin
- Activation of platelets
What is the role of thrombin in hemostasis?
What is the role of thrombin in hemostasis?
- Inhibiting platelet activation
- Degrading existing fibrin meshwork
- Cleaving fibrinogen into fibrin (correct)
- Reducing blood viscosity
How does platelet aggregation occur at the site of injury?
How does platelet aggregation occur at the site of injury?
- By the direct attachment of platelets to damaged endothelial cells
- Through the action of fibrin degradation products
- As a response to tissue factor alone
- When thrombin activates platelets (correct)
What is formed as a result of polymerization of fibrin during hemostasis?
What is formed as a result of polymerization of fibrin during hemostasis?
Which factor is activated by the binding of tissue factor in hemostasis?
Which factor is activated by the binding of tissue factor in hemostasis?
During hemostasis, what occurs after thrombin generation?
During hemostasis, what occurs after thrombin generation?
What is the final step in the process of hemostasis?
What is the final step in the process of hemostasis?
What is the purpose of the fibrin meshwork in hemostasis?
What is the purpose of the fibrin meshwork in hemostasis?
What condition is described by a tear in the placental membranes or rupture of uterine veins?
What condition is described by a tear in the placental membranes or rupture of uterine veins?
What is a characteristic finding in autopsy and microscopic examination associated with acute pulmonary complications?
What is a characteristic finding in autopsy and microscopic examination associated with acute pulmonary complications?
What type of infarction occurs in tissues with dual circulations?
What type of infarction occurs in tissues with dual circulations?
Which factor does NOT influence the development of an infarct?
Which factor does NOT influence the development of an infarct?
Which statement is true about red infarction?
Which statement is true about red infarction?
What condition is characterized by low blood oxygen content, influencing tissue vulnerability to hypoxia?
What condition is characterized by low blood oxygen content, influencing tissue vulnerability to hypoxia?
Which type of organ typically experiences white infarcts?
Which type of organ typically experiences white infarcts?
What occurs if blood flow is restored at a site of previous arterial occlusion?
What occurs if blood flow is restored at a site of previous arterial occlusion?
What is the primary purpose of normal hemostasis?
What is the primary purpose of normal hemostasis?
What initiates the formation of the platelet plug during hemostasis?
What initiates the formation of the platelet plug during hemostasis?
Which mechanism primarily facilitates arteriolar vasoconstriction at the site of vascular injury?
Which mechanism primarily facilitates arteriolar vasoconstriction at the site of vascular injury?
What role does endothelin play in hemostasis?
What role does endothelin play in hemostasis?
What occurs rapidly after platelet activation during hemostasis?
What occurs rapidly after platelet activation during hemostasis?
How does platelet activation affect the shape of the platelets?
How does platelet activation affect the shape of the platelets?
Which factor is exposed due to the disruption of the endothelium during hemostasis?
Which factor is exposed due to the disruption of the endothelium during hemostasis?
What is the effect of the transient vasoconstriction response?
What is the effect of the transient vasoconstriction response?
What does the prothrombin time (PT) assay primarily assess?
What does the prothrombin time (PT) assay primarily assess?
Which factors are part of the intrinsic pathway assessed by the partial thromboplastin time (PTT) assay?
Which factors are part of the intrinsic pathway assessed by the partial thromboplastin time (PTT) assay?
What is considered the most important anticoagulant factor in the coagulation cascade?
What is considered the most important anticoagulant factor in the coagulation cascade?
Which activity is NOT performed by thrombin?
Which activity is NOT performed by thrombin?
How does the body prevent unwanted coagulation beyond the vascular injury site?
How does the body prevent unwanted coagulation beyond the vascular injury site?
What role does thrombomodulin play in coagulation?
What role does thrombomodulin play in coagulation?
Which of the following is a known factor that limits coagulation?
Which of the following is a known factor that limits coagulation?
Which factors are common to both PT and PTT assays?
Which factors are common to both PT and PTT assays?
What role do heparin-like molecules play in coagulation?
What role do heparin-like molecules play in coagulation?
What is a key function of nitric oxide (NO) released by endothelial cells?
What is a key function of nitric oxide (NO) released by endothelial cells?
Which factor is responsible for maintaining the anticoagulant properties of normal endothelial cells?
Which factor is responsible for maintaining the anticoagulant properties of normal endothelial cells?
What happens to the endothelium in response to injury or pro-inflammatory factors?
What happens to the endothelium in response to injury or pro-inflammatory factors?
Which of the following is NOT a factor expressed by normal endothelial cells?
Which of the following is NOT a factor expressed by normal endothelial cells?
What is the main purpose of the fibrinolytic pathway activated by the endothelium?
What is the main purpose of the fibrinolytic pathway activated by the endothelium?
Which molecule is key for inhibiting thrombin and thereby reducing procoagulation?
Which molecule is key for inhibiting thrombin and thereby reducing procoagulation?
What determines the balance between clot formation and dissolution?
What determines the balance between clot formation and dissolution?
What is the primary effect of endothelial injury on thrombus formation?
What is the primary effect of endothelial injury on thrombus formation?
How does turbulence contribute to arterial thrombosis?
How does turbulence contribute to arterial thrombosis?
What does hypercoagulability refer to?
What does hypercoagulability refer to?
Which condition is a significant contributor to the development of venous thrombi?
Which condition is a significant contributor to the development of venous thrombi?
What is one of the components of Virchow's triad that relates to thrombus development?
What is one of the components of Virchow's triad that relates to thrombus development?
What role does stasis play in thrombus formation?
What role does stasis play in thrombus formation?
Which alteration is NOT a prothrombotic change associated with endothelial injury?
Which alteration is NOT a prothrombotic change associated with endothelial injury?
What typically results from the interaction of turbulence and stasis in the blood flow?
What typically results from the interaction of turbulence and stasis in the blood flow?
Flashcards
Infarction
Infarction
An area of tissue death caused by a lack of blood supply, usually due to an obstructed artery or vein.
Red Infarction
Red Infarction
An infarction characterized by red discoloration due to the presence of blood in the necrotic area.
White Infarct
White Infarct
An infarction characterized by pale discoloration due to the absence of blood in the necrotic area.
Recanalization
Recanalization
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Collateral Circulation
Collateral Circulation
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Tissue Vulnerability to Hypoxia
Tissue Vulnerability to Hypoxia
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Hypoxemia
Hypoxemia
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Rate of Occlusion
Rate of Occlusion
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Hemostasis
Hemostasis
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Arteriolar Vasoconstriction
Arteriolar Vasoconstriction
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Neurogenic Vasoconstriction
Neurogenic Vasoconstriction
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Platelet Plug Formation
Platelet Plug Formation
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von Willebrand factor (vWF)
von Willebrand factor (vWF)
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Platelet Activation
Platelet Activation
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Platelet Recruitment
Platelet Recruitment
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Primary Hemostasis
Primary Hemostasis
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Initiation of Coagulation
Initiation of Coagulation
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Coagulation Cascade
Coagulation Cascade
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Fibrin Formation
Fibrin Formation
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Platelet Adhesion and Aggregation
Platelet Adhesion and Aggregation
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Clot Formation
Clot Formation
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Clot Resorption
Clot Resorption
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Clot Stabilization
Clot Stabilization
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Endothelium
Endothelium
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Prostacyclin (PGI2)
Prostacyclin (PGI2)
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Nitric Oxide (NO)
Nitric Oxide (NO)
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Adenosine Diphosphatase
Adenosine Diphosphatase
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Thrombomodulin
Thrombomodulin
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Endothelial Protein C Receptor
Endothelial Protein C Receptor
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Antithrombin III
Antithrombin III
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Tissue Plasminogen Activator (t-PA)
Tissue Plasminogen Activator (t-PA)
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Prothrombin Time (PT)
Prothrombin Time (PT)
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Partial Thromboplastin Time (PTT)
Partial Thromboplastin Time (PTT)
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Tissue Factor
Tissue Factor
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Thrombin
Thrombin
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Fibrinolysis
Fibrinolysis
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Plasmin
Plasmin
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Endothelium's role in blood clotting
Endothelium's role in blood clotting
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Endothelium's dual role in clotting
Endothelium's dual role in clotting
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How turbulence can affect clotting
How turbulence can affect clotting
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How blood stasis can affect clotting
How blood stasis can affect clotting
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What is hypercoagulability?
What is hypercoagulability?
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What is the Virchow Triad?
What is the Virchow Triad?
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What happens to a clot after it forms?
What happens to a clot after it forms?
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How prothrombotic changes in the endothelium increase clot risk
How prothrombotic changes in the endothelium increase clot risk
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Study Notes
Hemodynamic Disorders, Thromboembolic Disease, and Shock
- Presented by Dr. Yayi Dwina Billianti Susanto, MS, SPPA, Subsp.U.R.L(K), Subsp.Kv.R.M.(K)
- Part of a PPDS PA FKUI semester 1 & S2 Biomedik course
- Date: 15 August 2024
Edema and Effusions
- Disorders affecting cardiovascular, renal, or hepatic function often lead to fluid accumulation in tissues (edema) or body cavities (effusions).
- Elevated hydrostatic pressure or reduced colloid osmotic pressure force fluid out of vessels.
- Fluid accumulation exceeds lymphatic drainage leading to edema in tissues and effusion in nearby body cavities.
Pathophysiologic Categories of Edema
- Increased Hydrostatic Pressure: Caused by impaired venous return (congestive heart failure), obstruction, or external pressure.
- Reduced Plasma Osmotic Pressure (Hypoproteinemia): Reduced protein levels (e.g., kidney disease, malnutrition, liver cirrhosis).
- Lymphatic Obstruction: Blocked lymphatic drainage leads to fluid buildup.
- Sodium Retention: Excessive salt intake or renal dysfunction can cause sodium retention, increasing blood volume and edema.
- Inflammation: Acute or chronic inflammation can cause edema.
Heart Failure, Renal Failure, Malnutrition, Hepatic Failure, and Nephrotic Syndrome
- These conditions can lead to systemic edema.
- Examples include activation of the renin-angiotensin system, sodium and water retention, and reduced plasma albumin.
- Resulting in generalized edema and increased blood volume
Microscopy of Edema
- Microscopically, edema involves clearing and separation of the extracellular matrix (ECM) and subtle cell swelling.
- Pulmonary edema displays a frothy, blood-tinged fluid mixture of air and extravasated red blood cells.
- Transudative effusions have a protein-poor, translucent, straw-colored appearance.
- Lymphatic blockage (chylous effusion) yields a milky fluid.
- Exudative effusions appear protein-rich and are often cloudy due to white cell presence.
Clinical Features of Edema
- Subcutaneous edema: signals underlying cardiac or renal disease and can impair wound healing.
- Pulmonary edema can impede gas exchange, creating favorable conditions for bacterial infection, and is common with left ventricular failure, renal failure, acute respiratory distress syndrome, and pulmonary inflammation.
- Peritoneal effusions (ascites) from portal hypertension are susceptible to bacterial infection.
- Brain edema: severe cases might cause herniation and/or brain stem vascular compromise, leading to potentially fatal consequences.
Hyperemia and Congestion
- Hyperemia: An active process involving increased blood flow (e.g., inflammation, exercise) causes the affected tissue to turn red (erythema).
- Congestion: A passive process caused by reduced venous outflow (e.g., heart failure) leading to a cyanotic (blue-red) color in the affected areas. Can lead to tissue injury and hemorrhagic foci (small areas of bleeding).
Embolism
- An embolus is a detached intravascular mass (solid, liquid, or gaseous) carried by blood to a distant site, leading to tissue dysfunction/infarction.
- Most common is thromboembolism (dislodged thrombus).
- Emboli include fat droplets, nitrogen bubbles, atherosclerotic debris, tumor fragments, bone marrow, or foreign bodies.
- They travel through the bloodstream until they encounter vessels too small, causing occlusion.
Pulmonary Embolism (PE)
- Pulmonary emboli arise from deep vein thrombosis (DVT) and travel to the pulmonary vasculature.
- Size determines the obstruction location (main artery, bifurcation, or branching arteries).
- Massive PE can lead to sudden death, acute right heart failure, and/or cardiovascular collapse.
- While frequently causing hemorrhage, pulmonary infarction is less common due to dual blood supply of the lung (pulmonary and bronchial arteries).
Systemic Thromboembolism
- Systemic emboli (80%) originate from intracardiac mural thrombi (associated with left ventricular wall infarcts or left atrial enlargement).
- Also arise from aortic aneurysms, atherosclerotic plaques, valvular vegetations, or venous thrombi (paradoxical).
- Most lodge in the lower extremities (75%), brain (10%), or other sites, leading to tissue infarction dependent on the collateral blood supply.
Fat Embolism
- Resulting from rupture of vascular sinusoids following trauma (fractures, burns, soft tissue trauma) or releasing fat globules into the bloodstream.
- Fat globules travel to the lung, causing pulmonary insufficiency; neurological symptoms (e.g., irritability, coma), anemia, and thrombocytopenia.
Air Embolism
- Gas bubbles coalescing to form frothy masses within circulation, obstructing blood vessels.
- Leads to distal ischemic injury or central nervous system events possibly causing mental impairment or sudden onset coma.
Decompression Sickness
- Occurs when air breathed at high pressure is released too rapidly.
- Dissolved nitrogen in the blood and tissues comes out of solution.
- Bends, chokes, and staggering are common symptoms.
Amniotic Fluid Embolism
- Amniotic fluid and its components enter the uterine veins, embolizing to the pulmonary circulation.
- Characterized by: dyspnea, cyanosis, shock, and neurological impairment (headache to seizures and coma).
- A significant cause of maternal mortality.
Infarction
- An area of ischemic necrosis resulting from either arterial or venous occlusion.
- Red infarcts, often seen in venous occlusions, exhibit loose, spongy textures with a dual blood supply.
- White infarcts, commonly seen in arterial occlusions, tend to be solid with limited blood seepage.
Factors Influencing Infarct Development
- Anatomy of the vascular supply (alternative blood flow).
- Rate of occlusion.
- Tissue vulnerability to hypoxia.
Normal Hemostasis
- A vital process involving platelets, clotting factors, and endothelium.
- Occurs at the site of vascular injury and forms a blood clot to stop bleeding.
General Sequence of Hemostasis
- Includes vasoconstriction, primary hemostasis (platelet plug formation), secondary hemostasis (fibrin deposition), and clot stabilization/resorption.
- These stages are triggered by tissue injury and dependent on endothelial cells' antithrombotic/procoagulant properties.
Platelets
- Disc-shaped, anucleate cell fragments from megakaryocytes in the bone marrow.
- Crucial for primary hemostasis (platelet plug formation) via adhesion and aggregation.
- Function also relies on glycoprotein receptors, cytoskeleton, and cytoplasmic granules.
Platelet Adhesion and Aggregation
- Platelets adhere to exposed subendothelial collagen and von Willebrand Factor.
- ADP induces conformational changes in platelets leading to aggregation. Deficiencies in proteins associated with these processes (e.g., Glanzmann thrombasthenia) cause bleeding disorders.
Coagulation Cascade
- A series of enzymatic reactions resulting in an insoluble fibrin clot.
- Part of secondary hemostasis.
- Key proteins are involved in triggering and mediating the clotting process.
Clotting in Laboratory vs In Vivo
- Assays like PT and PTT evaluate extrinsic and intrinsic pathways, respectively.
- In vivo, tissue damage exposes tissue factor in the extrinsic pathway; intrinsic pathway begins with damaged endothelium.
Coagulation Cascade (cont.)
- Critical initiator: tissue factor
- Most important anticoagulant: thrombin
- Functions include fibrinogen to fibrin conversion, platelet activation, pro-inflammatory actions conducive to tissue repair, and anticoagulant effects preventing clot extension.
Factors Limiting Coagulation
- Mechanisms like thrombomodulin on endothelial cells and inhibitors for coagulation factors restrict clot formation primarily to the site of injury,
- Limiting enzymatic activation to phospholipid surfaces, circulating inhibitors, and fibrinolytic pathways, primarily at the site of injury.
Endothelium
- Endothelial cells play a crucial role in controlling blood clotting.
- Their anticoagulant properties maintain a balance between procoagulant and anticoagulant factors, regulating clot formation, propagation, or dissolution.
Disseminated Intravascular Coagulation (DIC)
- A pathological process, not a disease in itself.
- Characterized by widespread thrombosis and subsequent consumption of clotting factors and platelets.
- Triggered by various underlying conditions (Sepsis, Trauma, Cancer, Complications in pregnancy).
- Causes include widespread tissue damage, triggering a flood of tissue factor and initiating coagulation.
- Conditions which cause DIC often release substantial procoagulant factors into the bloodstream, leading to widespread microvascular thrombosis .
Consequences of DIC
- DIC leads to tissue ischemia, ultimately damaging multiple organs.
- Consuming platelets and clotting factors simultaneously results in both excessive clotting (thrombosis) and excessive bleeding (hemorrhaging)
- The microvascular thrombosis leads to ischemia(insufficient blood flow) and organ failure. Excessive bleeding occurs because of low clotting factor levels resulting from the consumption of these factors.
Stages of Shock
- Initial non-progressive stage: Neuro-hormonal and haemostatic mechanisms to maintain cardiac output and blood pressure.
- Progressive irreversible stage: Tissue/cellular/metabolic derangement leading to acidosis and not correctable through hemodynamic intervention.
Clinical Presentation of Shock
- Symptoms include altered mental status, pallor, increased sweating, cold/clammy skin , rapid and weak thready pulse and respiration-tachypnia, low blood pressure, temperature abnormalities or lack thereof, and reduced urine output.
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Description
Test your knowledge on hemodynamic disorders, thromboembolic diseases, and shock, as discussed in the Biomedik course. This quiz covers essential concepts related to edema and effusions, including their pathophysiologic categories. Get ready to deepen your understanding of fluid dynamics in the human body!