Hypercoagulability and Hypertension Quiz
50 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

Which of the following is NOT a condition that increases a person's risk of developing hypercoagulability?

  • Immobility
  • Diabetes (correct)
  • Prosthetic Valves
  • Pregnancy

    • Which of these genetic mutations can lead to increased risk of hypercoagulability?

  • Factor V Leiden mutation (correct)
  • Thalassemia
  • Cystic fibrosis
  • BRCA1 mutation

    • Which of the following is a risk factor for developing hypercoagulability that is primarily related to lifestyle?

  • Smoking (correct)
  • Surgery
  • Tissue injury
  • Cancer

    • Which of the following is a risk factor for hypercoagulability that is commonly encountered during pregnancy?

    <p>Atrial fibrillation (B)</p> Signup and view all the answers

    Which of the following are potential consequences of hypercoagulability?

    <p>All of the above (D)</p> Signup and view all the answers

    Which of the following conditions is associated with an increased risk of hypercoagulability and is often considered a risk factor during pregnancy?

    <p>Anti-phospholipid Antibody Syndrome (C)</p> Signup and view all the answers

    Which of the following is NOT typically a cause of hypercoagulability?

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

    Which of the following describes a potential mechanism for hypercoagulability?

    <p>Increased production of clotting factors (A), Decreased production of anti-clotting factors (B)</p> Signup and view all the answers

    What is the primary factor that controls peripheral resistance?

    <p>Arterioles (B)</p> Signup and view all the answers

    What are the two main components that contribute to cardiac output?

    <p>Heart rate and stroke volume (B)</p> Signup and view all the answers

    Which of the following is NOT a contributing factor to essential hypertension?

    <p>Renal disease (C)</p> Signup and view all the answers

    What are the primary factors influencing stroke volume?

    <p>Filling pressure and myocardial contractility (D)</p> Signup and view all the answers

    What is a common characteristic found in the pathology of Giant Cell arteritis?

    <p>Inflammation with giant cells and internal elastic membrane fragmentation (B)</p> Signup and view all the answers

    What is the typical age range for an individual to be diagnosed with Giant Cell arteritis?

    <p>Over 50 to 60 years old (C)</p> Signup and view all the answers

    What is the primary characteristic that defines Kawasaki disease?

    <p>Fever for 5 days + 4 specific symptoms (C)</p> Signup and view all the answers

    Which of the following conditions is characterized by fibrinoid necrosis of the arterial wall?

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

    Which of the following can be a consequence of untreated hypertension?

    <p>All of the above (D)</p> Signup and view all the answers

    What is the condition characterized by rapid progression if left untreated, leading to high blood pressure exceeding 200/120 mm Hg?

    <p>Malignant hypertension (C)</p> Signup and view all the answers

    Which condition is associated with platelet activation and leads to a prothrombotic state?

    <p>Heparin Induced Thrombocytopenia (HIT) (C)</p> Signup and view all the answers

    What is the inheritance pattern of Factor V Leiden?

    <p>Autosomal dominant with incomplete penetrance (A)</p> Signup and view all the answers

    Which of the following conditions can occur due to severe sepsis or shock?

    <p>Disseminated Intravascular Coagulation (DIC) (A)</p> Signup and view all the answers

    What indicates a decreased perfusion of tissues in shock?

    <p>Decreased cardiac output or decreased blood volume (D)</p> Signup and view all the answers

    What percentage of children is at risk to inherit Factor V Leiden from a carrier parent?

    <p>50% (B)</p> Signup and view all the answers

    What is the inheritance pattern of Familial Hypercholesterolemia?

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

    What is the typical outcome without aggressive treatment for homozygous patients?

    <p>They usually die by age 30. (A)</p> Signup and view all the answers

    Which method is used to filter LDL from the blood in patients with Familial Hypercholesterolemia?

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

    What still may be insufficient in lowering LDL cholesterol despite a low-fat diet?

    <p>Rigorous adherence to a low-fat diet (C)</p> Signup and view all the answers

    What is the chance of an affected heterozygous parent passing the mutant LDLR allele to their child?

    <p>50% (A)</p> Signup and view all the answers

    Which type of aneurysm involves a wall that bulges circumferentially?

    <p>True fusiform aneurysm (A)</p> Signup and view all the answers

    What is a common clinical consequence of an abdominal aortic aneurysm (AAA)?

    <p>Compression of adjacent structures (A)</p> Signup and view all the answers

    What characterizes aortic dissection?

    <p>Sudden onset of excruciating pain (A)</p> Signup and view all the answers

    Marfan syndrome is primarily caused by a mutation in which gene?

    <p>FBN1 (A)</p> Signup and view all the answers

    What is the most common cause of death in aortic dissection?

    <p>Rupture into pericardial, pleural, or peritoneal spaces (C)</p> Signup and view all the answers

    Primary hypertension is characterized as being:

    <p>Idiopathic (C)</p> Signup and view all the answers

    What factors contribute to stroke volume?

    <p>Filling pressure and myocardial contractility (C)</p> Signup and view all the answers

    Which characteristic is associated with individuals diagnosed with Marfan syndrome?

    <p>Tall and thin body structure (A)</p> Signup and view all the answers

    What is edema primarily caused by?

    <p>Fluid accumulation in tissues (D)</p> Signup and view all the answers

    Which of the following is NOT a cause of edema related to venous return?

    <p>Protein-losing glomerulopathies (B)</p> Signup and view all the answers

    Which condition is associated with too much arterial blood?

    <p>Hyperemia (B)</p> Signup and view all the answers

    What role does aldosterone play in fluid balance?

    <p>Increases sodium reabsorption (C)</p> Signup and view all the answers

    What physiological process primarily helps to clean up excess fluid in the body?

    <p>Lymphatics (B)</p> Signup and view all the answers

    Which of the following conditions leads to sodium retention?

    <p>Renal hypoperfusion (B)</p> Signup and view all the answers

    In which of the following scenarios would a patient likely experience edema due to oncotic pressure?

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

    What is the primary effect of angiotensin II in the body?

    <p>Stimulates aldosterone release (C)</p> Signup and view all the answers

    What can cause lymphatic obstruction leading to edema?

    <p>Inflammatory diseases (C)</p> Signup and view all the answers

    Which factor can lead to pulmonary edema?

    <p>Congestive heart failure (A)</p> Signup and view all the answers

    Which of the following is a correct pathway for fluid retention triggered by low renal perfusion?

    <p>Angiotensin I → Angiotensin II → Increased aldosterone (D)</p> Signup and view all the answers

    What role does the myocardial release of natriuretic peptides play?

    <p>Inhibits sodium reabsorption (A)</p> Signup and view all the answers

    What appearance might congested tissues take on due to deoxygenated blood?

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

    In which condition might a person experience edema due to sodium retention?

    <p>Renal artery stenosis (B)</p> Signup and view all the answers

    Study Notes

    Pathogen 4.1 Vessels - Objectives

    • Illustrate fluid distribution between intravascular and extravascular compartments, applying normal circulation.
    • Differentiate oncotic and hydrostatic causes of edema with clinical examples.
    • Analyze renal pathology's role in disrupting fluid balance.
    • Discuss heart pathology related to fluid balance.
    • Analyze hemorrhage with clinical examples.
    • Illustrate normal hemostasis, describing the roles of endothelial cells, platelets, and coagulation proteins, and addressing pathologic and medicinal implications.
    • Discuss thrombus and embolus formation.
    • Analyze hypercoagulability and its causes.
    • Illustrate infarction and its pathogenesis.
    • Illustrate shock and its pathogenesis.
    • Differentiate major mechanical illnesses of vascular disease, including congenital causes.
    • Illustrate arteriosclerosis.
    • Illustrate aneurysm types and formation.
    • Debate familial hypercholesterolemia's major features, inheritance, etiology, incidence, pathogenesis, and phenotype.
    • Analyze essential and secondary hypertension and its pathogenesis.
    • Distinguish aortic dissection types and their clinical consequences.
    • Inventory the pathogenesis types of vasculitis and vascular tumor.

    Fluid Balance

    • Two opposing forces in fluid balance are hydrostatic pressure and oncotic pressure.
    • Hydrostatic pressure tends to "win" but only a little.
    • Lymphatics remove excess fluid.

    Terms

    • Edema: Fluid accumulation in tissues due to net water movement into extravascular spaces.
    • May include swollen feet or pulmonary edema.
    • Hyperemia: Too much arterial blood in a tissue.
    • Congestion: Excess venous blood in a tissue.
    • Hemostasis: Blood clotting process.
    • Thrombosis: Formation of a blood clot.
    • Embolism: A detached blood clot or other material traveling in the bloodstream.
    • Infarction: Tissue death due to ischemia (lack of blood supply).
    • Cyanotic appearance is associated with congested tissue due to low oxygen levels in the blood.
    • Effusion: Extravascular fluid accumulation in tissues.

    Causes of Edema

    • Venous return problems (e.g., congestive heart failure, constrictive pericarditis, ascites).
    • Venous obstruction (e.g., thrombosis, external pressure).
    • Lower extremity inactivity (dependency).
    • Protein-losing glomerulopathies (e.g., nephrotic syndrome).
    • Liver cirrhosis (decreased albumin).
    • Malnutrition (low protein intake).
    • Protein-losing gastroenteropathy.
    • Lymphatic obstruction (e.g., inflammatory diseases, neoplasms).
    • Increase in sodium intake or decreased kidney function.

    Renin, Angiotensin, Aldosterone

    • Renin is secreted by hypoperfused kidneys to increase renal blood supply.
    • Renin activates angiotensinogen to angiotensin I.
    • Lungs convert angiotensin I to angiotensin II.
    • Angiotensin II stimulates aldosterone release from adrenal cortex.
    • Angiotensin II constricts blood vessels and increases blood pressure.
    • Aldosterone increases sodium and water reabsorption, increasing blood volume and blood pressure.

    BP Regulation: Kidneys, Adrenals, and Heart

    • Kidneys regulate salt concentration and release of renin-angiotensin-aldosterone.
    • Myocardium releases natriuretic peptides, inhibiting sodium reabsorption for volume control.

    One Thing Leads to Another (Heart and Kidney Failure)

    • Heart failure can decrease blood flow to kidneys.
    • Renal failure can lead to fluid accumulation in the heart.
    • Oncotic force, influenced by albumin, impacts fluid balance in the system.

    Hemorrhage Terms

    • Hemorrhage: Blood extravasation.
    • Hematoma: Blood collection.
    • Petechiae/Purpura: Small hemorrhages into skin, mucous membranes.
    • Ecchymoses: Bruises (larger hemorrhages).
    • RBC degradation produces hemosiderin (iron-containing pigment), leading to discoloration.

    Clinical Tie-ins for Hemorrhage

    • Massive hemorrhage leads to hypovolemic shock and death.
    • Hematoma compression can cause tissue damage or compartment syndrome.
    • Intracerebral hemorrhage can cause stroke, potentially fatal.
    • Chronic hemorrhage can cause iron deficiency anemia.

    Hemorrhages

    • Petechial and intracerebral hemorrhages as examples of hemorrhage findings.

    Hemostasis Review

    • Blood clotting or hemostasis involves a series of steps-vasoconstriction, primary and secondary hemostasis, clot stabilization and clot dissolution
    • Arteriolar vasoconstriction reduces blood flow at injury site.
    • Platelet activation and aggregation form a primary hemostatic plug.
    • Secondary hemostasis involves fibrin clot formation by clotting cascade.
    • Clot stabilization prevents further bleeding and growth of the clot.
    • Clot resorption dissolves the clot.

    Clinical Point (Clotting Testing)

    • "Fibrin-split products" or D-dimer are measurable breakdown products of fibrinogen.
    • D-dimer testing signals prior clotting activity.

    Clotting Pathway

    • PT/INR measures extrinsic pathway.
    • PTT measures intrinsic pathway.
    • Feedback loops amplify clotting cascades.

    Clotting Inhibition

    • Heparin-like molecules activate antithrombin, preventing fibrinogen conversion into fibrin, thus inhibiting clotting.
    • Endothelial cells are usually anticoagulant but become procoagulant temporarily after injury.
    • Thrombomodulin and protein C are anticoagulant factors that regulate the clotting cascade to maintain hemostasis.
    • t-PA is an endothelium-derived factor that activates plasmin, breaking down fibrin, causing clot resorption.
    • Other endothelial products like prostacyclin, nitric oxide, and adenosine diphosphatase modulate platelet aggregation and inhibit clotting.

    Medicinal Clotting Inhibition

    • Warfarin inhibits vitamin K-dependent clotting factors.
    • Heparin activates antithrombin—blocking thrombin activity by activating antithrombin.
    • Xa inhibitors—novel oral anticoagulants—directly inhibit clotting factor Xa.
    • Aspirin prevents platelet aggregation.
    • P2Y12 inhibitors inhibit platelet aggregation.

    Clinical Point

    • Heparin can be used to bridge warfarin treatment due to some effects on anticoagulant protein production.

    Clinical Points (Disorders)

    • Pathologies like Factor V Leiden mutation, antithrombin III deficiency, Protein C and S deficiency, and Von Willebrand's disease can predispose individuals to clotting issues.
    • Medical interventions to reduce the associated high risks include anticoagulants and antiplatelet therapies, if needed, along with clot lysis (with tPA).

    Virchow's Triad

    • Endothelial injury
    • Abnormal blood flow
    • Hypercoagulability
    • Common factors leading to thrombosis

    Hypercoagulability

    • Various factors can cause hypercoagulability, such as genetic mutations (e.g., Factor V Leiden), acquired conditions (e.g., cancer, surgery, tissue injury, atrial fibrillation, oral contraceptives), and certain medical conditions (e.g., autoimmune diseases, pregnancy).

    Thrombi and Emboli

    • Morphology
    • Arterial and cardiac thrombi (e.g., those in the aorta or heart chambers, often due to endothelial injury or turbulent flow).
    • Venous thrombi (e.g., due to stasis)
    • Thrombi growth can be towards the heart or with blood flow.
    • Portion of thrombi may break off and become emboli.

    Embolism

    • An embolus is transported to a distant location by the blood and can cause various clinical consequences.

    Embolism (Other Types)

    • Fat emboli-from fractures.
    • Amniotic fluid embolus-rare but serious obstetric complication.
    • Air embolism - from surgical procedures.

    Infarct

    • An infarct is a localized area of ischemic necrosis.
    • Factors influencing outcome include vascular anatomy, occlusion rate, and tissue vulnerability to hypoxia.
    • Different infarcts produce different gross and microscopic findings.

    Infarct (Types)

    • White infarcts often arise from arterial occlusion and exhibit an anemic appearance.
    • Red infarcts usually arise from venous occlusion and tend to be hemorrhagic.

    Factor V Leiden

    • Autosomal dominant genetic disorder, exacerbated by environmental factors.
    • Affects clotting cascade and increases risk for deep-vein thrombosis (DVT) and pulmonary embolism (PE).

    Two Clinically Important Conditions

    • Heparin-induced thrombocytopenia (HIT)
    • Disseminated intravascular coagulation (DIC)

    Shock

    • Shock arises from decreased cardiac output or reduced circulating blood volume, leading to insufficient tissue perfusion.
    • Initial cellular injury is usually reversible.
    • Conditions leading to shock can be various, such as cardiac failure, hypovolemia, and systemic infections.

    Septic Shock and Hypotension

    • Endothelial activation, cytokine release, and vascular leakage occur in response to microorganisms leading to hypotension.

    Septic Shock Hypercoagulation

    • Cytokines favor coagulation by increasing tissue factor production and inhibiting fibrinolysis.
    • Vascular leakage reduces the removal of activated coagulation factors.

    Septic Shock and Metabolic Derangement

    • Cytokines upregulate stress hormones leading to gluconeogenesis.
    • Cytokines also suppress insulin release and cause insulin resistance.
    • This causes hyperglycemia, which adversely affects neutrophil function, and also causes a metabolic acidosis due to lactate levels, as well as a decrease in blood pH.

    Septic Shock and Organ Dysfunction

    • Systemic hypotension, interstitial edema, and vascular thrombosis decrease tissue oxygenation and nutrient delivery, damaging various organs and reducing cardiac output.
    • ARDS (acute respiratory distress syndrome) can occur due to increased vascular permeability.

    Stages of Shock

    • Nonprogressive (compensatory).
    • Progressive (worsening tissue hypoperfusion).
    • Irreversible (cellular and tissue damage that prevents recovery).

    Clinical Manifestations of Shock

    • Symptoms and signs can vary based on the specific type and etiology of shock, including things from hypotension, weak pulse, dyspnea, cold skin, and even warm skin if secondary to inflammation.

    Normal Blood Vessels

    • Arteries have thicker walls with more smooth muscle cells.
    • Veins are compressible and have valves.
    • Vessels exhibit layers-Intima, Media, Adventitia and some layers are separated by elastic laminae.

    Main Forms of Vascular Disease

    • Clogged pipes (e.g., atherosclerosis).
    • Weakened pipes (e.g., aneurysms).
    • Pipes with structural deficits (e.g., congenital anomalies).

    Congenital Anomalies of Vasculature

    • Berry aneurysms, arteriovenous fistulas, and fibromuscular dysplasia are congenital vascular anomalies.

    Arteriosclerosis

    • A generic term meaning arterial wall thickening and loss of elasticity, often developing in various patterns (hyaline, hyperplastic, Mönckeberg's).

    Atherosclerosis

    • A form of arteriosclerosis characterized by atherosclerotic plaques.
    • Plaques are composed of lipid cores, necrotic debris, and fibrous caps.
    • Plaques can cause narrowing and rupture within the vessels.
    • Locations of atherosclerotic plaques often include the cerebral and coronary arteries as well as the aorta

    Atherosclerosis → Aneurysm

    • Plaque formation and rupture in arteries can lead to aneurysm formation.

    Types of Aneurysms

    • True aneurysms (saccular and fusiform), have intact vessel walls.
    • False aneurysms (pseudoaneurysms) have damaged vessel walls with blood collection outside the vessel wall.

    Aortic Aneurysm (AAA)

    • AAA often occurs due to atherosclerosis and has risks for obstruction, structure compression, and rupture into peritoneal cavities.

    Aortic Dissection

    • Dissection involves blood splitting apart the vessel wall layers.
    • Factors like high blood pressure increase the risk.
    • Can be fatal if it ruptures into pericardial, pleural, or peritoneal cavities.

    Marfan Syndrome

    • Marfan syndrome caused by fibrillin mutation, impacting the skeletal and cardiovascular systems.

    Cardiovascular Effects of Marfan Syndrome

    • Weakened connective tissues around the aorta can lead to aortic dilation and other cardiovascular issues.

    Hypertension

    • Primary hypertension often has idiopathic origins.
    • Secondary hypertension has various underlying causes.
    • Classification is categorized by blood pressure levels

    BP Regulation

    • Blood pressure depends on cardiac output and peripheral vascular resistance.
    • Cardiac output depends on heart rate and stroke volume.
    • Stroke volume is impacted by filling pressure and myocardial contractility.
    • Vascular resistance regulated by neural and humoral factors, including vasoconstrictors and vasodilators, and self-regulation (autoregulation).

    Vasculitis and Vascular Tumors

    • Vasculitis encompasses various conditions marked by inflammation of blood vessels.
    • A number of vascular tumors are recognized, with some benign, some intermediate, and some rare highly malignant conditions.

    Key examples of vasculitis:

    • Giant cell arteritis
    • Polyarteritis nodosa
    • Kawasaki disease
    • Thrombangitis obliterans (Buerger disease)
    • Raynaud phenomenon

    Hemangioma

    • Hemangiomas are benign vascular tumors marked by increased numbers of blood vessels.

    Kaposi Sarcoma

    • Kaposi sarcoma is a vascular tumor often associated with AIDS, but can develop in other immunocompromised individuals.

    Angiosarcoma

    • Angiosarcoma describes a malignant vascular tumor with potential for metastasis.

    Familial Hypercholesterolemia

    • FH is an inherited disorder of elevated blood cholesterol levels
    • Caused by mutations impacting the LDL receptor function, leading to increased plasma LDL.
    • Early diagnosis and treatment (with lifestyle changes and medications) are essential to reduce the risk of cardiovascular disease.
    • This condition, through its effects, also potentially impacts the development of atherosclerosis.

    FH (Familial Hypercholesterolemia): Management

    • Aggressive LDL management required.

    FH (Familial Hypercholesterolemia): Inheritance

    • Condition is often inherited as an autosomal dominant disorder, meaning one copy of the mutated gene is sufficient to increase cholesterol levels.

    Studying That Suits You

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

    Quiz Team

    Related Documents

    Pathogen 4.1 Vessels PDF

    Description

    Test your knowledge on the conditions, genetic factors, and lifestyle risks associated with hypercoagulability and essential hypertension. This quiz will cover a range of topics including risk factors during pregnancy and potential consequences of these conditions. Challenge yourself and see how well you understand these significant health issues!

    More Like This

    Use Quizgecko on...
    Browser
    Open
    Browser
    Browser