Pathogen 4.1 Vessels and Fluid Balance

Pathogen 4.1 Vessels

• Objectives include illustrating fluid distribution between intravascular and extravascular compartments, analyzing the role of renal pathology in fluid balance, and analyzing hemorrhage and hemostasis.

• Objectives also include analyzing hypercoagulability, infarction, shock, and various mechanical illnesses of vascular disease, as well as different forms of aneurysm. A discussion of familial hypercholesterolemia, hypertension, types of aortic dissections, and vasculitis and vascular tumor are also part of the objectives.

Fluid Balance

• Fluid balance involves two opposing forces: hydrostatic pressure and oncotic pressure.

• Hydrostatic pressure "wins" but only slightly, with lymphatics clearing the excess fluid.

Causes of Edema

• Causes of edema include venous return issues (e.g., heart failure, constrictive pericarditis), venous obstruction/compression, thrombosis, external pressure, and lower extremity inactivity.

• Oncotic pressure factors include protein-losing glomerulopathies, liver cirrhosis, malnutrition, and protein-losing gastroenteropathy, and lymphatic obstruction.

• Sodium retention (excess salt, impaired kidney function) and inflammatory responses are also contributing factors.

Terms

• Edema describes fluid accumulation in tissues due to net water movement into extravascular spaces.

• Hyperemia refers to excessive arterial blood flow.

• Congestion signifies excessive venous blood flow.

• Hemostasis is the process of blood clotting.

• Thrombosis involves formation of a bad clot.

• Embolism describes a moved clot.

• Infarction results in cell death due to ischemia.

• Effusion involves extravascular fluid collection in tissues.

Renin, Angiotensin, Aldosterone

• Renin triggers a pathway to increase renal blood supply.

• Renin activates angiotensinogen to angiotensin I, then to angiotensin II in the lungs by ACE, which constricts vessels and releases aldosterone.

• Aldosterone increases sodium reabsorption, leading to water retention and higher blood pressure.

BP Regulation

• Blood pressure is determined by cardiac output and peripheral vascular resistance, with cardiac output influenced by heart rate and stroke volume.

• Stroke volume depends on filling pressure (blood volume) and myocardial contractility, affected by alpha and beta adrenergic inputs.

Clinical Points IO:6

• A sign of clotting is the presence of fibrin-split products in the blood, including measurable D-dimer. This is a clinical test to assess clotting.

Blood Vessels

• Arteries have thicker walls with significant smooth muscle, while veins are compressible and have valves.

Normal Blood Vessels

• Blood vessels are structured in 3 concentric layers (intima, media, adventitia), separated by internal and external elastic laminae.

The Main Forms of Vascular Disease

• Vascular diseases can be grouped into clogging, weakening, or being born with diseased pipes. This includes congenital anomalies, hypertension, arteriosclerosis, atherosclerosis, aneurysms and dissections, vasculitis, and tumors.

Congenital Anomalies of Vasculature IO:11

• Berry aneurysms are small, focal dilations in cerebral vessels, often in the circle of Willis, which can be fatal if ruptured.

• Arteriovenous fistulas are abnormal connections between arteries and veins that bypass capillaries, potentially causing abnormal blood shunting.

• Fibromuscular dysplasia is irregular thickening of the medium-large artery walls, due to medial and intimal hyperplasia that results in luminal stenosis. This is common in young women.

Arteriosclerosis

• Arteriosclerosis is a generic term describing hardening of the arteries, involving arterial wall thickening and loss of elasticity. Three types are discussed:
• Arteriosclerosis, which affects small vessels with hyaline and hyperplastic changes
• Mönckeberg medial calcific sclerosis, which is primarily calcium deposits in artery muscle and
• Fibromuscular Intimal Hyperplasia, a medial and intimal lesion.

Atherosclerosis IO:12

• Atherosclerosis is characterized by atheromas, which can impinge on the arterial lumen and rupture, resulting in occlusion.

• Atheromas consist of friable lipid cores (cholesterol and debris) with a fibrous cap.

• Atherosclerosis can affect all arteries, including cerebral, coronary, and aortic arteries, which can lead to stroke, MI, and aneurysm rupture, respectively.

Atherosclerosis → aneurysm IO:12

• Atherosclerosis can lead to aneurysm formation by creating a soft lipid core covered by a fibrous cap, which eventually protrudes into the arterial lumen, resulting in stenosis, weakening, plaque rupture, thrombus formation, and vessel wall expansion.

Types of Aneurysms IO:13

• Aneurysms come in various types including true saccular (locally bulged), and fusiform (circumferentially widened). False aneurysms result from a ruptured vessel, collecting extravascular blood. Vessel dissection is also included, where blood separates the vessel layers.

AAA IO:13

• Abdominal aortic aneurysms (AAAs) can obstruct branch vessels causing issues like compression of adjacent structures, creating an abdominal mass. Rupture into the peritoneal cavity is frequently fatal.

Aortic Dissection IO:16

• Aortic dissection involves a separation of the blood vessel layers due to blood penetrating the layers of the arterial wall; such as the tunica intima and media. Hypertension is a major risk factor.

Marfan Syndrome IO:11

• Marfan syndrome, is an autosomal dominant genetic disorder affecting the skeletal system, cardiovascular system, and eyes. Loss of function in the fibrillin gene causes weakness in connective tissue.

Cardiovascular Effects of Marfan Syndrome IO:11

• The weakening of connective tissue around the base of the aorta is a significant cardiovascular effect of Marfan syndrome.

Hypertension IO:15

• Primary hypertension is idiopathic; above 140/90 mmHg.

• Secondary hypertension is caused by other conditions.

• Major sequelae of hypertension include cardiac hypertrophy, heart failure, and stroke (CVA).

Vasculitis and Vascular Tumor 10:17

• Vasculitis is inflammation of blood vessels, with major types like giant cell (temporal) arteritis, polyarteritis nodosa, Kawasaki disease, and thromboangiitis obliterans.

• Vascular tumors like hemangioma (benign), lymphangioma (benign), angiosarcoma (malignant), glomus tumor (benign), and hemangiopericytoma (malignant) can originate from blood vessels or lymphatics.

• Some examples of vascular tumors are include hemangioma, Kaposi sarcoma, and angiosarcoma.

Thrombi and Emboli

• Thrombi are blood clots in blood vessels. They can arise in arteries or veins. Arterial thrombi frequently arise from injury or turbulence, while venous thrombi tend to occur due to stasis.

• Emboli are detached thrombi, and propagate throughout the body in varying degrees. Pulmonary thromboemboli often originate from deep vein thrombosis in the legs while others can originate from cardiac sources like left ventricle wall infarcts or mitral valve defects, or aortic aneurysms.

Embolism IO:7

• Embolism is the detachment of a solid, liquid or gaseous matter from a source (like a clot) and its propagation through the circulatory system and lodgement in a distant blood vessel. This includes pulmonary thromboemboli and systemic thromboemboli. Other types include fat, amniotic fluid, and air emboli.

Infarct IO:9

• An infarct is an area of ischemic necrosis in tissue caused by occlusion of the vascular supply. Infarcts can result from thrombi or emboli. Two forms are white (arterial occlusion) or red (venous occlusion) infarcts, based on the presence of hemorrhgaic areas.

Factors that affect infarct outcome

• Outcome depends on vascular supply anatomy (alternate paths), rate of occlusion (abrupt/gradual), adequate collateral blood vessel growth, and vulnerability of tissue to hypoxia depending on the anatomical location.

Factor V Leiden IO:7

• Factor V Leiden is a genetic disorder with incomplete penetrance. It accelerates clotting and is exacerbated by other factors

Two clinically important conditions

• Heparin-induced thrombocytopenia (HIT) - autoantibodies bind to heparin-platelet complexes leading to platelet activation, aggregation and consumption, and endothelial injury.

• Disseminated intravascular coagulation (DIC) - widespread vascular clotting and subsequent fibrinolysis, in disease states like sepsis, shock, and advanced malignancy, which leads to bleeding due to the widespread fibrinolysis.

Shock

• Shock occurs when decreased cardiac output or reduced circulating blood volume deprive tissues of adequate perfusion leading to cellular injury and becoming hypoxic. Types of shock include cardiogenic (pump failure), hypovolemic (not enough volume), and septic (due to overwhelming microbes/inflammation and widespread vasodilation).

Stages of Shock

• Non-progressive, progressive, and irreversible stages are discussed based on compensatory mechanisms breakdown, progressive hypoperfusion, eventually resulting in irreversible tissue damage.

Clinical manifestations of shock

• Signs of shock include hypotension, weak pulse, tachypnea, cool clammy skin in varying degrees depending on the underlying cause.

Normal Blood Vessels

• Blood Vessels (arteries and veins) have varying thicknesses and other characteristics; with arteries having thicker walls of different organization including inner (intima), outer (adventitia), and middle (media) layers and having significant smooth muscle cells. Veins have thinner walls and valves.

Hypertension IO:15

• Hypertension is elevated blood pressure; it is characterized by high systolic and diastolic readings (above 140/90 or above 150/90 in individuals 60 and older) and can lead to many health issues. There are primary (idiopathic) and secondary types.

Vascular Tumors

• Vascular tumors can originate from blood vessels and lymphatics and contain endothelial or connective tissue cells with hemangioma (benign), lymphangioma (benign), angiosarcoma (malignant), glomus tumor (benign), and hemangiopericytoma (malignant) as examples.