Hemodynamics and Edema Disorders Quiz

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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?

A solid, permanent plug preventing hemorrhage Signup and view all the answers

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

Factor VII Signup and view all the answers

During hemostasis, what occurs after thrombin generation?

Cleavage of fibrinogen into insoluble fibrin Signup and view all the answers

What is the final step in the process of hemostasis?

Resorption of the clot Signup and view all the answers

What is the purpose of the fibrin meshwork in hemostasis?

Stabilizes the platelet plug and prevents hemorrhage Signup and view all the answers

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

Acute pulmonary hypertension Signup and view all the answers

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

Fetal hair, mucin, and squames Signup and view all the answers

What type of infarction occurs in tissues with dual circulations?

Red infarction Signup and view all the answers

Which factor does NOT influence the development of an infarct?

Nutritional status Signup and view all the answers

Which statement is true about red infarction?

It can occur due to venous occlusions. Signup and view all the answers

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

Hypoxemia Signup and view all the answers

Which type of organ typically experiences white infarcts?

Solid organs with end-arterial circulation Signup and view all the answers

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

Reestablishment of circulation Signup and view all the answers

What is the primary purpose of normal hemostasis?

To form a blood clot to prevent or limit bleeding Signup and view all the answers

What initiates the formation of the platelet plug during hemostasis?

Exposing subendothelial von Willebrand factor and collagen Signup and view all the answers

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

Neurogenic reflex mechanism Signup and view all the answers

What role does endothelin play in hemostasis?

It enhances the transient effect of vasoconstriction Signup and view all the answers

What occurs rapidly after platelet activation during hemostasis?

Release of secretory granules Signup and view all the answers

How does platelet activation affect the shape of the platelets?

Platelets undergo a dramatic shape change Signup and view all the answers

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

Von Willebrand factor Signup and view all the answers

What is the effect of the transient vasoconstriction response?

To reduce blood flow to limit bleeding Signup and view all the answers

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

Function of proteins in the extrinsic pathway Signup and view all the answers

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

Factors XII, XI, IX, VIII Signup and view all the answers

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

Thrombin Signup and view all the answers

Which activity is NOT performed by thrombin?

Directly dissolving existing clots Signup and view all the answers

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

By limiting enzymatic activation to the site of injury Signup and view all the answers

What role does thrombomodulin play in coagulation?

Binds and converts thrombin to an anticoagulant Signup and view all the answers

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

Activation of fibrinolytic pathways Signup and view all the answers

Which factors are common to both PT and PTT assays?

Factors V and X Signup and view all the answers

What role do heparin-like molecules play in coagulation?

They augment the activity of antithrombin III. Signup and view all the answers

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

To inhibit platelet activation. Signup and view all the answers

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

Prostacyclin (PGI2). Signup and view all the answers

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

It loses many of its antithrombotic properties. Signup and view all the answers

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

Tissue factor. Signup and view all the answers

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

To dissolve clots. Signup and view all the answers

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

Thrombomodulin. Signup and view all the answers

What determines the balance between clot formation and dissolution?

The balance between procoagulant and anticoagulant factors. Signup and view all the answers

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

Promotes platelet activation Signup and view all the answers

How does turbulence contribute to arterial thrombosis?

By causing endothelial injury and dysfunction Signup and view all the answers

What does hypercoagulability refer to?

An abnormally high tendency of the blood to clot Signup and view all the answers

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

Stasis Signup and view all the answers

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

Endothelial injury Signup and view all the answers

What role does stasis play in thrombus formation?

Contributes to the development of venous thrombi Signup and view all the answers

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

Inhibition of coagulation factors Signup and view all the answers

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

Formation of local pockets of stasis Signup and view all the answers

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!