Secondary Hemostasis Quiz

Podcast

Play an AI-generated podcast conversation about this lesson

Questions and Answers

What is the primary role of tissue factor in secondary hemostasis?

To recruit red blood cells

To stimulate the coagulation cascade (correct)

To promote platelet adhesion

To inhibit platelet activation

Which cell type is responsible for synthesizing tissue factor?

Platelets

Endothelial cells (correct)

Red blood cells

Fibroblasts

When is tissue factor typically released?

At the site of vessel injury (correct)

During normal circulation

Only during inflammatory responses

When blood pressure is elevated

What is the end result of the coagulation cascade stimulated by tissue factor?

Formation of a meshwork of insoluble fibrin clot Signup and view all the answers

Which process occurs as a first response to vascular injury?

Primary hemostasis Signup and view all the answers

What is the primary function of antithrombin III in the human body?

To inhibit the activity of thrombin and other coagulation factors Signup and view all the answers

Which cofactor is primarily inactivated by Protein C?

Factor Va Signup and view all the answers

How is antithrombin activated in the body?

Through interaction with heparin-like molecules Signup and view all the answers

What vitamin is essential for the function of Protein C and S?

Vitamin K Signup and view all the answers

What characterizes heart failure cells in the context of pulmonary circulation?

They are filled with hemosiderin pigment from RBC breakdown. Signup and view all the answers

What happens when antithrombin inhibits thrombin activity?

Blood clot formation is reduced Signup and view all the answers

What is a key feature of acute hepatic congestion?

Increased blood flow in the central veins and sinusoids. Signup and view all the answers

Which statement best describes the condition of peripheral hepatocytes in acute hepatic congestion?

They may suffer from fatty change due to lesser hypoxia. Signup and view all the answers

Which statement is accurate regarding the composition of heart failure cells?

They are primarily composed of hemosiderin-laden macrophages. Signup and view all the answers

What happens to the central veins and sinusoids during acute hepatic congestion?

They become distended with blood. Signup and view all the answers

What is the primary function of GpIIb-IIIa on the platelet surface?

Binding to fibrinogen Signup and view all the answers

Which component acts as a bridge to connect platelets during aggregation?

Fibrinogen Signup and view all the answers

What triggers the activation of GpIIb-IIIa on platelets?

ADP stimulation Signup and view all the answers

Which process is primarily facilitated by the aggregation of platelets?

Primary hemostasis Signup and view all the answers

What role does thrombin play in the coagulation cascade?

Forms fibrin clots Signup and view all the answers

Which glycoprotein facilitates the binding of platelets to von Willebrand factor (VWF)?

GpIb Signup and view all the answers

What is a consequence of irreversible platelet aggregation?

Formation of stable blood clots Signup and view all the answers

Which factor is responsible for the recruitment of additional platelets during hemostasis?

Adenosine diphosphate (ADP) Signup and view all the answers

What initiates the intrinsic pathway of the coagulation cascade?

Hageman factor Signup and view all the answers

Which of the following is NOT a function of thrombin in the coagulation process?

Activating tissue factor Signup and view all the answers

Which pathway of the coagulation cascade is activated by tissue factor?

Extrinsic pathway Signup and view all the answers

What is the primary result of the coagulation cascade?

Formation of thrombin Signup and view all the answers

Which of the following factors is specifically noted as part of the common pathway?

Factor 5 Signup and view all the answers

How is the clotting process regulated at the site of injury?

Through joint action of both intrinsic and extrinsic pathways Signup and view all the answers

Which condition is specifically associated with von Willebrand factor deficiency?

Brenard-souiler syndrome Signup and view all the answers

Which of the following statements about the coagulation cascade is incorrect?

The extrinsic pathway is initiated by Hageman factor. Signup and view all the answers

What condition significantly increases the risk of thrombus formation?

Atrial fibrillation Signup and view all the answers

Which of the following is a primary cause of hypercoagulability?

Factor V mutations Signup and view all the answers

What anatomical condition is often associated with atrial fibrillation and thrombus formation?

Dilated left atrium Signup and view all the answers

What deficiency can lead to hypercoagulability?

Antithrombin III deficiency Signup and view all the answers

What consequence arises from stasis of blood flow in the atrium?

Thrombus formation Signup and view all the answers

Which proteins are often deficient in individuals predisposed to thrombus formation?

Protein C and S Signup and view all the answers

Which of the following describes an abnormality of the heart that might lead to thrombus formation?

Severe mitral stenosis Signup and view all the answers

Which of the following secondary causes does NOT typically contribute to hypercoagulability?

Aging Signup and view all the answers

What is one potential complication of thrombosis in the atrium?

Pulmonary embolism Signup and view all the answers

Which genetic condition is a known contributor to hypercoagulability?

Factor V mutations Signup and view all the answers

Study Notes

Hemodynamic Disorders

Hemodynamic disorders involve thrombosis and shock.
60% of body weight is water.
2/3 of the water is intracellular.
1/3 is extracellular, mostly as interstitial fluid.
5% of extracellular fluid is in the vascular compartment.
Edema is increased fluid in the interstitial tissue spaces.
Fluid collections in body cavities are named according to location (e.g., hydrothorax, hydropericardium, hydroperitoneum).
Anasarca is severe, generalized edema with profound subcutaneous tissue swelling.
The balance between vascular hydrostatic pressure and plasma colloid osmotic pressure drives fluid movement between vascular and interstitial spaces.
Normally, fluid outflow from arteriolar ends is balanced by inflow at venular ends.
A small amount of fluid remains in the interstitium due to slightly higher hydrostatic pressure.
This excess fluid is drained by the lymphatic system.
Normal hydrostatic pressure is 32 mm Hg at the arteriolar end of a capillary bed and 12 mm Hg at the venous end.
The mean colloid osmotic pressure of tissue is approximately 25 mmHg.
In inflammation, arteriolar pressure increases to 50 mmHg due to dilation, and venous pressure increases to approximately 30 mmHg.
Osmotic pressure averages 20 mmHg due to protein leakage across the venules.
The net result is excess extravasated fluid.

Sodium Retention

Excessive sodium intake with renal insufficiency increases sodium reabsorption.
Renal hypoperfusion and increased renin-angiotensin-aldosterone secretion cause increased tubular sodium absorption.

Inflammation

Acute inflammation and chronic inflammation can cause edema.
Angiogenesis can also cause edema.

Reduced Plasma Osmotic Pressure

Protein-losing glomerulopathies (nephrotic syndrome), liver cirrhosis, malnutrition, and protein-losing gastroenteropathy can reduce plasma osmotic pressure.
This reduction results in edema.
Lymphatic obstruction can cause edema, which occurs due to inflammatory, neoplastic, postsurgical, or postirradiation etiologies.

Hyperemia and Congestion

Hyperemia is an active process of increased blood flow caused by arteriolar dilation.
Tissues appear redder due to increased oxygenated blood flow.
Congestion is a passive process of impaired venous return.
Tissues appear bluish/cyanotic due to increased deoxygenated blood.
Chronic passive congestion of the liver can cause pooling of poorly oxygenated blood, hypoxia, parenchymal cell death, capillary rupture, and foci of hemorrhage.
Red blood cell fragments are phagocytosed, leading to the formation of hemosiderin-laden macrophages.
Chronic congestion can cause fibrosis.

Hemorrhage

Hemorrhage means bleeding.
It can occur due to clotting disorders or trauma.
Capillary bleeding can occur from congestion, tissue injury, or inflammation.
Hematoma is the collection of blood within a tissue.

Significance of Bleeding

Bleeding significance depends on volume and location.
Small amounts of bleeding may be fatal if in the cranial cavity.

Petechiae

Small (1-2mm) hemorrhages on the skin or mucous membranes.
These are caused by increased intravascular pressure, low platelet counts, defective platelet function, or clotting factor deficiency.

Ecchymosis

Subcutaneous hematomas (bruises) that are larger (1-2cm).
The red-blue hemoglobin in the clot is broken down to bilirubin and then to hemosiderin.
Changes in color reflect these conversions (starting red-blue and progressively changing to greenish, then yellow, and finally golden-brown).

Hematoma

Blood collection within tissues.
Large hematomas can be fatal.
Bruises are a type of insignificant hematoma.

Larger Blood Accumulations

Hemothorax: blood in the pleural cavity
Hemopericardium: blood in the pericardial cavity
Hemarthrosis: blood in joint spaces
Hemoperitoneum: blood in peritoneal cavity.

Thrombosis/Hemostasis

Hemostasis: the process of maintaining blood in fluid state within vessels.
Thrombosis: the pathological formation of a blood clot within intact vessels.

Normal Hemostasis (Sequence)

Vasoconstriction: immediate response after injury, reducing blood flow to the damaged area. It's triggered by endothelin release from endothelial cells.
Primary hemostasis: platelets stick to the damaged area (adhesion) and change shape to become "sticky" (shape change). Platelets release granules (secretion) containing factors that attract more platelets (and other components), and platelets aggregate. This forms the primary hemostatic plug—it's reversible.
Secondary hemostasis: a cascade of enzymatic reactions, converting inactive plasma proteins into active proteins that activates thrombin.
Thrombin converts fibrinogen to fibrin—insoluble fibrin meshwork forms stable clot.

Antithrombotic Counter Regulation

Tissue Plasminogen Activator (tPA) is activated to limit clot expansion following formation of permanent clot.
tPA converts plasminogen to plasmin—plasmin breaks down fibrin.
This process prevents further clot formation.

Fate of thrombus

Propagation: More fibrin and platelets accumulate on the clot.
Embolization: The clot breaks off and travels through the circulation, potentially lodging in another area, causing embolism.
Dissolution: The clot dissolves.
Organization and canalization: The clot is reorganized and remodeled into healthy vessel tissue.

Venous Thrombosis (Phlebothrombosis)

Most venous thrombi occur in the deep veins, especially in the lower extremities.
Superficial thrombi occur in the saphenous system, especially in varicose veins.
Deep thrombi, especially those above the knee, are more serious.
They are often asymptomatic in 50% of cases.

Pulmonary Thromboembolism

Often arise from deep vein thrombi (DVTs) in the lower extremities.
Emboli travel to the right side of the heart and into the pulmonary arteries.
Saddle emboli can block the main pulmonary artery.
Smaller emboli may lodge in the smaller branches.

Systemic Thromboembolism

These emboli travel through the arterial circulation.
In 80% of cases, the source is mural thrombi in the cardiac walls.
Atherosclerotic plaques in the aorta or aortic aneurysms can also be sources.
Paradoxical emboli can travel through abnormal openings between atria or ventricles.

Fat Embolism

Fat emboli arise from fractures of long bones, releasing fat from bone marrow following sinusoid rupture.
Symptoms appear three days post-injury, including respiratory distress, neurological symptoms, thrombocytopenia, petechiae, and anemia.

Air Embolism

Air emboli result from surgical procedures, scuba diving, or underwater work.
Nitrogen, dissolved in the blood at high pressure, forms bubbles during ascent.
These bubbles can cause focal ischemia in the brain, heart, or bones and respiratory distress.

Caisson Disease

Chronic form of decompression sickness.
Results from persistent gas emboli in bones, causing ischemic necrosis primarily in the heads of femur, tibia, and humerus.

Amniotic Fluid Embolism

Occurs during or shortly after labor.
Amniotic fluid enters the circulation, damaging lungs.
Symptoms include sudden respiratory distress, hypotension, seizures, and coma.

Infarction

Area of ischemic necrosis due to arterial occlusion.
Obstruction to venous drainage can also cause infarction.
Types include myocardial, pulmonary, and bowel infarction.
Infarcts can be red (hemorrhagic) or white (ischemic), depending on blood flow.

Rare Causes of Infarction

Vasospasm (e.g., Prinzmetal angina)
Vessel compression (tumors)
Vessel twisting (testis or intestinal torsion)
Vessel entrapment (strangulated hernia)

Types of Infarcts

Red infarcts are hemorrhagic, occurring in tissues with a dual blood supply or venous obstruction.
White infarcts are not hemorrhagic, occurring in organs with a single arterial blood supply, and no reperfusion.

Factors Affecting Infarct Development

Impaired blood supply
Tissue's susceptibility to hypoxia
Oxygen content of blood
Rate of occlusion development (slow occlusion allows collateral blood supply),

Shock

Systemic hypoperfusion due to reduced cardiac output or blood volume.
Cardiogenic shock: failure of the cardiac pump due to myocardial damage.
Hypovolemic shock: inadequate blood volume due to bleeding, vomiting, diarrhea, or burns.
Neurogenic shock: loss of vasomotor tone from spinal cord injury or trauma.
Septic shock: overwhelming bacterial infection that causes widespread inflammation.
Stages of shock: initial (nonprogressive), progressive, and irreversible.

Studying That Suits You

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

Description

Test your knowledge on the role of tissue factor in secondary hemostasis and its various functions. This quiz covers key concepts related to coagulation, antithrombin III, and the effects of vascular injury. Challenge yourself with questions about the coagulation cascade and its components.