Hypercoagulability Quiz

Pathogen 4.1 Vessels

• Vessels are categorized by their function and morphology
• Objectives of this section include illustrating fluid distribution, distinguishing causes of edema, analyzing the role of renal pathology in fluid balance, and analyzing hemorrhage.
• The role of endothelial cells, platelets, and the coagulation proteins in hemostasis is analyzed.
• Pathogenesis of thrombus, embolus, hypercoagulability, infarction, and shock will be examined.
• Different forms of aneurysm, arteriosclerosis, and vascular disease will be discussed.
• The major phenotypic features, inheritance, etiology, incidence, pathogenesis, and clinical course of familial hypercholesterolemia will be dissected.
• Essential and secondary hypertension and related pathogenesis will be distinguished.
• Types of aortic dissection and their consequences are investigated.
• Pathogenesis of vasculitis and vascular tumors is discussed.

Fluid Balance

• Fluid balance is governed by two opposing forces: hydrostatic pressure and oncotic pressure.
• Hydrostatic pressure "wins" but only a little bit.
• Lymphatics manage the extra fluid.
• Causes of edema include venous return issues, oncotic pressure (problems with protein), lymphatic obstruction, and sodium retention (too much salt, kidney issues).
• Edema is the accumulation of fluid in tissues, which may include swollen feet or pulmonary edema.
• Hyperemia, congestion, hemostasis, thrombosis, embolism, and infarction are defined with associated clinical examples.

Hemostasis

• Hemostasis is the process of blood clotting.
• Arteriolar vasoconstriction, platelet plug formation (primary hemostasis), and fibrin clot formation (secondary hemostasis) are primary components.
• Clot stabilization and resorption are described, including the roles of tissue plasminogen activator (t-PA) and plasmin.
• Key tests to assess clotting disorders are presented.
• Heparin acts as an anticoagulant by activating antithrombin.

Renin, Angiotensin, Aldosterone

• The renin-angiotensin-aldosterone system (RAAS) is a hormonal pathway that regulates blood pressure.
• Blood pressure, distal tubular sodium, renin, angiotensinogen, angiotensin I, angiotensin II, and aldosterone secretion cause vasoconstriction, increased blood pressure, and increased cardiac output.
• Feedback mechanisms within the system help maintain homeostasis.
• ACE (angiotensin-converting enzyme) converts angiotensin I to angiotensin II in the lungs.
• Angiotensin II constricts blood vessels, increases blood pressure, and stimulates the release of aldosterone from the adrenal cortex.

BP Regulation

• Blood pressure regulation involves the coordinated actions of kidneys, adrenals, and the heart.
• Kidneys maintain salt and regulate the renin-angiotensin-aldosterone system.
• Myocardium releases natriuretic peptides to inhibit sodium reabsorption when volume expansion is detected.
• Blood pressure regulation maintains homeostasis.

Thrombi and Emboli

• Thrombi are blood clots formed inside a blood vessel.
• Emboli are detached blood clots that travel through the circulatory system.
• Formation and morphology of arterial/cardiac and venous thrombi is discussed.
• Embolism, thromboembolism, and different types of emboli (pulmonary, systemic) are detailed.

Infarct

• An infarct is an area of tissue death caused by ischemia (lack of blood flow).
• Different types of infarcts (white and red) as well as factors impacting outcome are presented.
• Common locations where infarcts develop are discussed.

Hypercoagulability

• Factors like Factor V Leiden mutations, antithrombin III deficiency, Protein C and S deficiency, immobility, cancer, surgery, etc. increase risk of clotting.
• Other factors like tissue injury, prosthetic valves, anti-phospholipid antibody syndrome, smoking, atrial fibrillation, pregnancy, and oral contraceptives increase clotting risk.

Shock

• Definition of shock is presented; either decreased cardiac output or decreased circulating blood volume.
• Types of shock (cardiogenic, hypovolemic, septic) are categorized and associated clinical examples are listed.
• The associated mechanisms and clinical presentations for different types of shock are described.

Vasculature

• Normal vessel structure, including layers (intima, media, and adventitia) and separate layers (internal/external elastic lamina).

Vascular Disease

• Clogging the pipe (e.g., atherosclerosis).
• Weakening the pipe (e.g., aneurysms).
• Born with bad pipes (e.g., congenital anomalies like Marfan syndrome).

Aortic Dissection

• Dissection includes blood splitting the layers of the arterial wall causing massive hemorrhage.

Atherosclerosis

• Atherosclerosis involves friable lipid cores with necrotic debris covered by a fibrous cap.
• Rupture of the fibrous cap leads to thrombus formation, vessel-wall expansion, aneurysm, and potential rupture.

Hypertension

• Types of hypertension are differentiated between primary (essential) and secondary hypertension.
• Blood pressure classifications are shown.
• Important sequelae (e.g., cardiac hypertrophy, heart failure, CVA) are described.

Vasculitis and Vascular Tumors

• Types, presentations, and pathogeneses of different vasculitides are outlined.
• Classification and examples of vascular tumors are provided, including hemangioma, Kaposi sarcoma, and angiosarcoma.

Familial Hypercholesterolemia

• Lipoproteins, including LDL and HDL, are categorized.
• Disease etiology, incidence, pathogenenesis, phenotype, and natural history and management are detailed.