Hemodynamics and Edema Disorders Quiz
48 Questions
0 Views

Choose a study mode

Play Quiz
Study Flashcards
Spaced Repetition
Chat to Lesson

Podcast

Play an AI-generated podcast conversation about this lesson

Questions and Answers

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?

  • 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?

  • 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?

<p>A solid, permanent plug preventing hemorrhage (A)</p> Signup and view all the answers

Which factor is activated by the binding of tissue factor in hemostasis?

<p>Factor VII (A)</p> Signup and view all the answers

During hemostasis, what occurs after thrombin generation?

<p>Cleavage of fibrinogen into insoluble fibrin (B)</p> Signup and view all the answers

What is the final step in the process of hemostasis?

<p>Resorption of the clot (D)</p> Signup and view all the answers

What is the purpose of the fibrin meshwork in hemostasis?

<p>Stabilizes the platelet plug and prevents hemorrhage (C)</p> Signup and view all the answers

What condition is described by a tear in the placental membranes or rupture of uterine veins?

<p>Acute pulmonary hypertension (B)</p> Signup and view all the answers

What is a characteristic finding in autopsy and microscopic examination associated with acute pulmonary complications?

<p>Fetal hair, mucin, and squames (B)</p> Signup and view all the answers

What type of infarction occurs in tissues with dual circulations?

<p>Red infarction (D)</p> Signup and view all the answers

Which factor does NOT influence the development of an infarct?

<p>Nutritional status (A)</p> Signup and view all the answers

Which statement is true about red infarction?

<p>It can occur due to venous occlusions. (A)</p> Signup and view all the answers

What condition is characterized by low blood oxygen content, influencing tissue vulnerability to hypoxia?

<p>Hypoxemia (D)</p> Signup and view all the answers

Which type of organ typically experiences white infarcts?

<p>Solid organs with end-arterial circulation (A)</p> Signup and view all the answers

What occurs if blood flow is restored at a site of previous arterial occlusion?

<p>Reestablishment of circulation (C)</p> Signup and view all the answers

What is the primary purpose of normal hemostasis?

<p>To form a blood clot to prevent or limit bleeding (A)</p> Signup and view all the answers

What initiates the formation of the platelet plug during hemostasis?

<p>Exposing subendothelial von Willebrand factor and collagen (C)</p> Signup and view all the answers

Which mechanism primarily facilitates arteriolar vasoconstriction at the site of vascular injury?

<p>Neurogenic reflex mechanism (A)</p> Signup and view all the answers

What role does endothelin play in hemostasis?

<p>It enhances the transient effect of vasoconstriction (C)</p> Signup and view all the answers

What occurs rapidly after platelet activation during hemostasis?

<p>Release of secretory granules (A)</p> Signup and view all the answers

How does platelet activation affect the shape of the platelets?

<p>Platelets undergo a dramatic shape change (A)</p> Signup and view all the answers

Which factor is exposed due to the disruption of the endothelium during hemostasis?

<p>Von Willebrand factor (A)</p> Signup and view all the answers

What is the effect of the transient vasoconstriction response?

<p>To reduce blood flow to limit bleeding (D)</p> Signup and view all the answers

What does the prothrombin time (PT) assay primarily assess?

<p>Function of proteins in the extrinsic pathway (D)</p> Signup and view all the answers

Which factors are part of the intrinsic pathway assessed by the partial thromboplastin time (PTT) assay?

<p>Factors XII, XI, IX, VIII (C)</p> Signup and view all the answers

What is considered the most important anticoagulant factor in the coagulation cascade?

<p>Thrombin (D)</p> Signup and view all the answers

Which activity is NOT performed by thrombin?

<p>Directly dissolving existing clots (A)</p> Signup and view all the answers

How does the body prevent unwanted coagulation beyond the vascular injury site?

<p>By limiting enzymatic activation to the site of injury (D)</p> Signup and view all the answers

What role does thrombomodulin play in coagulation?

<p>Binds and converts thrombin to an anticoagulant (A)</p> Signup and view all the answers

Which of the following is a known factor that limits coagulation?

<p>Activation of fibrinolytic pathways (C)</p> Signup and view all the answers

Which factors are common to both PT and PTT assays?

<p>Factors V and X (D)</p> Signup and view all the answers

What role do heparin-like molecules play in coagulation?

<p>They augment the activity of antithrombin III. (A)</p> Signup and view all the answers

What is a key function of nitric oxide (NO) released by endothelial cells?

<p>To inhibit platelet activation. (A)</p> Signup and view all the answers

Which factor is responsible for maintaining the anticoagulant properties of normal endothelial cells?

<p>Prostacyclin (PGI2). (C)</p> Signup and view all the answers

What happens to the endothelium in response to injury or pro-inflammatory factors?

<p>It loses many of its antithrombotic properties. (A)</p> Signup and view all the answers

Which of the following is NOT a factor expressed by normal endothelial cells?

<p>Tissue factor. (B)</p> Signup and view all the answers

What is the main purpose of the fibrinolytic pathway activated by the endothelium?

<p>To dissolve clots. (B)</p> Signup and view all the answers

Which molecule is key for inhibiting thrombin and thereby reducing procoagulation?

<p>Thrombomodulin. (A)</p> Signup and view all the answers

What determines the balance between clot formation and dissolution?

<p>The balance between procoagulant and anticoagulant factors. (C)</p> Signup and view all the answers

What is the primary effect of endothelial injury on thrombus formation?

<p>Promotes platelet activation (A)</p> Signup and view all the answers

How does turbulence contribute to arterial thrombosis?

<p>By causing endothelial injury and dysfunction (C)</p> Signup and view all the answers

What does hypercoagulability refer to?

<p>An abnormally high tendency of the blood to clot (D)</p> Signup and view all the answers

Which condition is a significant contributor to the development of venous thrombi?

<p>Stasis (A)</p> Signup and view all the answers

What is one of the components of Virchow's triad that relates to thrombus development?

<p>Endothelial injury (A)</p> Signup and view all the answers

What role does stasis play in thrombus formation?

<p>Contributes to the development of venous thrombi (C)</p> Signup and view all the answers

Which alteration is NOT a prothrombotic change associated with endothelial injury?

<p>Inhibition of coagulation factors (A)</p> Signup and view all the answers

What typically results from the interaction of turbulence and stasis in the blood flow?

<p>Formation of local pockets of stasis (C)</p> Signup and view all the answers

Flashcards

Infarction

An area of tissue death caused by a lack of blood supply, usually due to an obstructed artery or vein.

Red Infarction

An infarction characterized by red discoloration due to the presence of blood in the necrotic area.

White Infarct

An infarction characterized by pale discoloration due to the absence of blood in the necrotic area.

Recanalization

The process of re-establishing blood flow to a previously blocked area.

Signup and view all the flashcards

Collateral Circulation

The presence of an alternative blood supply that can compensate for a blocked artery or vein.

Signup and view all the flashcards

Tissue Vulnerability to Hypoxia

The ability of a tissue to tolerate a lack of oxygen.

Signup and view all the flashcards

Hypoxemia

A low level of oxygen in the blood.

Signup and view all the flashcards

Rate of Occlusion

The rate at which a blood vessel is blocked.

Signup and view all the flashcards

Hemostasis

The process of stopping bleeding, involving platelets, clotting factors, and the endothelium.

Signup and view all the flashcards

Arteriolar Vasoconstriction

The narrowing of an arteriole, reducing blood flow to the injured area. It's the first step in hemostasis.

Signup and view all the flashcards

Neurogenic Vasoconstriction

A reflex action that triggers the narrowing of arterioles in the injured area

Signup and view all the flashcards

Platelet Plug Formation

The process of forming a platelet plug at the site of injury within the endothelium.

Signup and view all the flashcards

von Willebrand factor (vWF)

A protein found in the sub-endothelial lining, that triggers platelet activation. This happens when the endothelium is damaged.

Signup and view all the flashcards

Platelet Activation

Shape change of the platelet, as well as the release of secretory granules. This is a crucial step in platelet plug formation.

Signup and view all the flashcards

Platelet Recruitment

The process of recruiting additional platelets to the site of injury by the release of secretory granules.

Signup and view all the flashcards

Primary Hemostasis

The combination of vasoconstriction and platelet aggregation, which temporarily slows blood flow and seals the injury

Signup and view all the flashcards

Initiation of Coagulation

Exposure of collagen and tissue factor in the damaged blood vessel triggers the activation of clotting factors, initiating the coagulation cascade.

Signup and view all the flashcards

Coagulation Cascade

The cascade of enzymatic reactions involving clotting factors leads to the formation of thrombin, a key enzyme in the coagulation process.

Signup and view all the flashcards

Fibrin Formation

Thrombin acts on fibrinogen, converting it to fibrin, a protein that forms the meshwork of the clot.

Signup and view all the flashcards

Platelet Adhesion and Aggregation

Platelets adhere to the exposed collagen and activate, releasing factors that promote further platelet aggregation.

Signup and view all the flashcards

Clot Formation

The fibrin meshwork traps platelets and red blood cells, forming a stable plug to prevent further hemorrhage.

Signup and view all the flashcards

Clot Resorption

Over time, enzymes dissolve the clot, breaking down fibrin and restoring blood flow.

Signup and view all the flashcards

Clot Stabilization

The process involves the strengthening and stabilization of the clot, ensuring its long-term integrity.

Signup and view all the flashcards

Endothelium

The lining of blood vessels that plays a crucial role in regulating blood clotting.

Signup and view all the flashcards

Prostacyclin (PGI2)

A substance released by the endothelium that inhibits platelet activation and aggregation, helping to prevent unwanted clot formation.

Signup and view all the flashcards

Nitric Oxide (NO)

A signaling molecule released by the endothelium that relaxes blood vessels, reducing blood pressure and promoting blood flow.

Signup and view all the flashcards

Adenosine Diphosphatase

An enzyme expressed by the endothelium that breaks down adenosine diphosphate (ADP), a substance that promotes platelet aggregation.

Signup and view all the flashcards

Thrombomodulin

A protein expressed by the endothelium that binds to thrombin, a key coagulation factor, and prevents it from promoting clot formation.

Signup and view all the flashcards

Endothelial Protein C Receptor

A molecule expressed by the endothelium that acts as a cofactor for protein C, an anticoagulant factor, which inactivates clotting factors Va and VIIIa.

Signup and view all the flashcards

Antithrombin III

A natural anticoagulant that inhibits the coagulation cascade, preventing excessive clotting.

Signup and view all the flashcards

Tissue Plasminogen Activator (t-PA)

A key component of the fibrinolytic pathway that breaks down fibrin clots, allowing for the dissolution of clots.

Signup and view all the flashcards

Prothrombin Time (PT)

A laboratory test that measures the time it takes for blood to clot, evaluating the function of the extrinsic pathway of the coagulation cascade.

Signup and view all the flashcards

Partial Thromboplastin Time (PTT)

A laboratory test that measures the time it takes for blood to clot, evaluating the function of the intrinsic pathway of the coagulation cascade.

Signup and view all the flashcards

Tissue Factor

A substance, usually released from damaged tissues, that initiates the coagulation cascade.

Signup and view all the flashcards

Thrombin

A powerful enzyme that plays a central role in coagulation, converting fibrinogen to fibrin and activating platelets.

Signup and view all the flashcards

Fibrinolysis

A process that breaks down blood clots, dissolving fibrin and restoring normal blood flow.

Signup and view all the flashcards

Plasmin

An enzyme involved in fibrinolysis, activated by tissue plasminogen activator (t-PA) and fibrin.

Signup and view all the flashcards

Endothelium's role in blood clotting

The lining of blood vessels that normally prevents blood clotting but can become activated to promote clotting when injured, usually due to damage from physical trauma.

Signup and view all the flashcards

Endothelium's dual role in clotting

Anticoagulant properties are normally present in the endothelium to help regulate blood flow and prevent unwanted clot formation. However, when damaged or activated, the endothelium switches to procoagulant properties to promote clot formation and stop bleeding.

Signup and view all the flashcards

How turbulence can affect clotting

Turbulence in blood flow can contribute to the formation of clots in arteries and the heart by causing endothelial injury or dysfunction. This disruption of normal blood flow creates conditions that promote clot formation.

Signup and view all the flashcards

How blood stasis can affect clotting

Stasis, or the slowing down of blood flow, plays a major role in the development of venous clots. It allows clotting factors to accumulate and increases the chance of clot formation.

Signup and view all the flashcards

What is hypercoagulability?

Hypercoagulability refers to the blood's increased tendency to clot. This can be due to various factors that alter the coagulation system, including the presence of certain proteins in the blood that favor clotting.

Signup and view all the flashcards

What is the Virchow Triad?

The Virchow triad is a classic description of three factors that contribute to thrombus formation: endothelial injury, blood flow abnormalities (turbulence or stasis), and hypercoagulability. The presence of these factors increases the risk of clotting.

Signup and view all the flashcards

What happens to a clot after it forms?

After a clot forms, it can undergo various changes including growing, breaking off, or dissolving. The fate of the clot depends on several factors, including the location of the clot and the body's response to it.

Signup and view all the flashcards

How prothrombotic changes in the endothelium increase clot risk

Prothrombotic changes in the endothelium, such as the release of procoagulant factors, contribute to the formation of clots by creating a more conducive environment for clotting. These changes can occur due to injury or activation of the endothelium.

Signup and view all the flashcards

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.

Studying That Suits You

Use AI to generate personalized quizzes and flashcards to suit your learning preferences.

Quiz Team

Related Documents

Hemodynamics PDF

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!

More Like This

Use Quizgecko on...
Browser
Browser