13 Cardiovascular System – Blood Vessels and Blood

Common Diseases and Disorders of Blood Vessels and/or Blood

Arteriosclerosis

Arteriosclerosis is normally defined as the more generalized loss of compliance, “hardening of the arteries,” whereas atherosclerosis is a more specific term for the build-up of plaque in the walls of the vessel and is a specific type of arteriosclerosis.

When arteriosclerosis causes vessel compliance to be reduced, pressure and resistance within the vessel increase. This is a leading cause of hypertension and coronary heart disease, as it causes the heart to work harder to overcome this resistance. Any artery in the body can be affected by these pathological conditions, and individuals who have pathologies like coronary artery disease, may also be at risk for other vascular injuries, like strokes or peripheral arterial disease.

Atherosclerosis is a type of arteriosclerosis in which plaques form when circulating triglycerides, cholesterol and other substances seep between the damaged endothelial lining cells and become trapped within the artery wall, resulting in narrowed arteries and impaired blood flow (see Figure 13.16) (Betts, et al., 2013).

Sometimes a plaque can rupture, causing microscopic tears in the artery wall that allow blood to leak into the tissue on the other side. When this happens, platelets rush to the site to clot the blood. This clot can further obstruct the artery and—if it occurs in a coronary or cerebral artery—cause a sudden heart attack or stroke. Alternatively, plaque can break off and travel through the bloodstream as an embolus until it blocks a more distant, smaller artery.

Peripheral arterial disease (PAD, also called peripheral vascular disease, PVD), occurs when atherosclerosis affects arteries in the legs. A major risk factor for both arteriosclerosis and atherosclerosis is advanced age, as the conditions tend to progress over time. There is also a distinct genetic component, and pre-existing hypertension and/or diabetes also greatly increase the risk. However, obesity, poor nutrition, lack of physical activity, and tobacco use all are major risk factors.

Treatment of atherosclerosis includes lifestyle changes, such as weight loss, smoking cessation, regular exercise, and adoption of a diet low in sodium and saturated fats. Medications to reduce cholesterol and blood pressure may be prescribed. For blocked coronary arteries, angioplasty or coronary artery bypass graft (CABG) surgery may be warranted. In an carotid endarterectomy, plaque is surgically removed from the walls of a the carotid artery, which is the main source of oxygenated blood for the brain (Betts, et al., 2013).

Edema and Varicose Veins

Despite the presence of valves and the contributions of other anatomical and physiological adaptations that assist in moving blood through veins, over the course of a day, some blood will inevitably pool, especially in the lower limbs, due to the pull of gravity. Any blood that accumulates in a vein will increase the pressure within it, which can then be reflected back into the smaller veins, venules, and eventually even the capillaries. This increased pressure in the capillaries will push of fluids out of the capillaries and into the interstitial fluid, causing a condition called edema.

Most people experience a daily accumulation of tissue fluid, especially if they spend much of their work life on their feet (like most health professionals). However, clinical edema goes beyond normal swelling and requires medical treatment. Edema has many potential causes, including hypertension and heart failure, severe protein deficiency, renal failure, and many others. In order to treat edema, which is a sign rather than a discrete disorder, the underlying cause must be diagnosed and alleviated.

Edema may be accompanied by varicose veins, especially in the superficial veins of the legs (see Figure 13.17). This disorder arises when defective valves allow blood to accumulate within the veins, causing them to distend, twist, and become visible on the surface of the skin. Varicose veins may occur in both sexes, but are more common in women and are often related to pregnancy. More than simple cosmetic blemishes, varicose veins are often painful and sometimes itchy or throbbing. Without treatment, they tend to grow worse over time. The use of support hose, as well as elevating the feet and legs whenever possible, may be helpful in alleviating this condition (Betts, et al., 2013).

Hypertension

Hypertension is defined as chronic and persistent blood pressure measurements of 140/90 mm Hg or above. Pressures between 120/80 and 140/90 mm Hg are defined as prehypertension. Hypertension is typically a silent disorder and patients may fail to recognize the seriousness of their condition and fail to follow their treatment plan, putting them at risk for a heart attack or stroke. Hypertension may also lead to an aneurysm, peripheral arterial disease, chronic kidney disease, or heart failure (Betts, et al., 2013).

Hemorrhage

Erythrocyte Disorders

Changes in the levels of RBCs can have significant effects on the body’s ability to effectively deliver oxygen to the tissues (Betts, et al., 2013).

Anemia

The size, shape, and number of erythrocytes, and the number of hemoglobin molecules can have a major impact on a person’s health. When the number of RBCs or hemoglobin is deficient, the general condition is called anemia. There are more than 400 types of anemia.

Anemia can be broken down into three major groups: those caused by blood loss, those caused by faulty or decreased RBC production, and those caused by excessive destruction of RBCs. In addition to these causes, various disease processes also can lead to anemias. These include chronic kidney diseases often associated with a decreased production of EPO, hypothyroidism, some forms of cancer, lupus, and rheumatoid arthritis(Betts, et al., 2013).

Blood Loss Anemias:

Causes:

• Bleeding from wounds or other lesions, including ulcers, hemorrhoids, inflammation of the stomach (gastritis), and some cancers of the gastrointestinal tract
  • The excessive use of aspirin or other nonsteroidal anti-inflammatory drugs such as ibuprofen can trigger ulceration and gastritis
• Excessive menstruation and loss of blood during childbirth.

Anemias Caused by Faulty or Decreased RBC Production:

• Sickle cell anemia

• • A genetic disorder involving the production of an abnormal type of hemoglobin which delivers less oxygen to tissues and causes erythrocytes to assume a sickle (or crescent) shape.
• Iron deficiency anemia
  • The most common type of anemia and results when the amount of available iron is insufficient to allow production of sufficient heme.
• Vitamin deficiency anemia (Generally insufficient vitamin B12 and folate).
• Megaloblastic anemia involves a deficiency of vitamin B12 and/or folate, often due to inadequate dietary intake.
• Pernicious anemia is caused by poor absorption of vitamin B12 and is often seen in patients with Crohn disease, surgical removal of the intestines or stomach (common in some weight loss surgeries), intestinal parasites, and AIDS[/pb_glossary.
• Aplastic anemia is the condition in which myeloid stem cells are defective or replaced by cancer cells, resulting in insufficient quantities of RBCs being produced. This condition by be inherited, or it may be triggered by radiation, medication, chemotherapy, or infection.
• Thalassemia is an inherited condition typically occurring in individuals from the Middle East, the Mediterranean, African, and Southeast Asia, in which maturation of the RBCs does not proceed normally. The most severe form is called Cooley’s anemia (Betts, et al., 2013).

Polycythemia is an elevated RBC count and is detected in a patient’s elevated [pb_glossary id="1613"]hematocrit. It can occur transiently in a person who is dehydrated; when water intake is inadequate or water losses are excessive, the plasma volume falls. As a result, the hematocrit rises. A mild form of polycythemia is chronic but normal in people living at high altitudes. Some elite athletes train at high elevations specifically to induce this phenomenon. Finally, a type of bone marrow disease called polycythemia vera causes an excessive production of immature erythrocytes. Polycythemia vera can dangerously elevate the viscosity of blood, raising blood pressure and making it more difficult for the heart to pump blood throughout the body. It is a relatively rare disease that occurs more often in men than women, and is more likely to be present in elderly patients those over 60 years of age (Betts, et al., 2013).

Platelet Disorders/Clotting Disorders

Thrombocytosis

Thrombocytosis is a condition in which there are too many platelets. This may trigger thrombosis, a potentially fatal disorder. A thrombus (plural = thrombi) is an aggregation of platelets, erythrocytes, and even WBCs typically trapped within a mass of fibrin strands. While the formation of a clot is a normal step in hemostasis, thrombi can form within an intact or only slightly damaged blood vessel, adhering to the vessel wall and decreasing or obstructing the flow of blood. (Betts, et al., 2013).

Thrombophilia

Thrombophilia, also called hypercoagulation, is a condition in which there is a tendency to form thrombosis. This may be an inherited disorder or may be caused by other conditions including lupus, immune reactions to heparin, polycythemia vera, thrombocytosis, sickle cell disease, pregnancy, and even obesity.

When a portion of a thrombus breaks free from the vessel wall and enters the circulation, it is referred to as an embolus. An embolus that is carried through the bloodstream can be large enough to block a vessel critical to a major organ. When it becomes trapped, an embolus is called an embolism. In the heart, brain, or lungs, an embolism may accordingly cause a heart attack, a stroke, or a pulmonary embolism (Betts, et al., 2013).

Thrombocytopenia

Thrombocytopenia is a condition in which there is an insufficient number of platelets, possibly leading to ineffective blood clotting and excessive bleeding (Betts, et al., 2013).

Hemophilia

Hemophilia is a group of related genetic disorders in which certain plasma clotting factors are lacking or inadequate or nonfunctional. Patients with hemophilia bleed from even minor internal and external wounds, and leak blood into joint spaces after exercise and into urine and stool. Regular infusions of clotting factors isolated from healthy donors can help prevent bleeding in hemophiliac patients. At some point, genetic therapy will become a viable option (Betts, et al., 2013).

Leukocyte Disorders

Leukopenia

Leukopenia is a condition in which too few leukocytes are produced. If this condition is pronounced, the individual may be unable to ward off disease (Betts, et al., 2013).

Leukocytosis

Leukocytosis is excessive leukocyte proliferation. Although leukocyte counts are high, the cells themselves are often nonfunctional, leaving the individual at increased risk for disease (Betts, et al., 2013).

Leukemia

Leukemia is a cancer involving an abundance of leukocytes. It may involve only one specific type of leukocyte from either the myeloid line (myelocytic leukemia) or the lymphoid line (lymphocytic leukemia). In chronic leukemia, mature leukocytes accumulate and fail to die. In acute leukemia, there is an overproduction of young, immature leukocytes. In both conditions the cells do not function properly (Betts, et al., 2013).

Lymphoma

Lymphoma is a form of cancer in which masses of malignant T and/or B lymphocytes collect in lymph nodes, the spleen, the liver, and other tissues. As in leukemia, the malignant leukocytes do not function properly, and the patient is vulnerable to infection. Some forms of lymphoma tend to progress slowly and respond well to treatment. Others tend to progress quickly and require aggressive treatment, without which they are rapidly fatal (Betts, et al., 2013).

Other Conditions Related to Abnormal Leukocyte Counts

Bone Marrow Biopsy/Bone Marrow Transplant

Sometimes, a healthcare provider will order a bone marrow biopsy, a diagnostic test of a sample of red bone marrow, or a bone marrow transplant, a treatment in which a donor’s healthy bone marrow—and its stem cells—replaces the faulty bone marrow of a patient. These tests and procedures are often used to assist in the diagnosis and treatment of various severe forms of anemia, such as thalassemia major and sickle cell anemia, as well as some types of cancer, specifically leukemia.

In the past, bone marrow sampling or transplant was very painful, as the procedure involved inserting a large-bore needle into the region near the iliac crest of the pelvic bones. Now, direct sampling of bone marrow can often be avoided as stem cells can be isolated in just a few hours from a sample of a patient’s blood. The isolated stem cells are then grown in culture using the appropriate hemopoietic growth factors, and analyzed or sometimes frozen for later use.

For an individual requiring a transplant, a matching donor is essential to prevent the immune system from destroying the donor cells—a phenomenon known as tissue rejection. To treat patients with bone marrow transplants, it is first necessary to destroy the patient’s own diseased marrow through radiation and/or chemotherapy. Donor bone marrow stem cells are then infused into the recipient's bloodstream, so that they can establish themselves in the recipient’s bone marrow (Betts, et al., 2013).

Common Cardiovascular System - Blood, Abbreviations

Many terms and phrases related to the cardiovascular system - blood are abbreviated. Learn these common abbreviations by expanding the list below.

References

Canadian Medical Association. (2018, August). Hematology profile. CMA Specialty Profiles. https://www.cma.ca/sites/default/files/2019-01/hematology-e.pdf

Canadian Society for Medical Laboratory Science. (n.d.). Who are lab professionals. https://www.csmls.org/Medical-Laboratory-Professionals/About/Who-are-Lab-Professionals.aspx

Canadian Society for Vascular Surgery. (2020). Patients: What is vascular surgery? https://canadianvascular.ca/Patients

[CrashCourse]. (2015, July 20). Blood vessels, part 1 - form and function: Crash course A&P #27 [Video]. YouTube. https://youtu.be/v43ej5lCeBo

Sonography Canada. (2020). Credentials. https://sonographycanada.ca/certification/credentials

Image Descriptions

Figure 13.1 image description: The left panel shows the structure of a skeletal muscle vein pump when the muscle is relaxed, and the right panel shows the structure of a skeletal muscle vein pump when the muscle is contracted.[Return to Figure 13.1].

Figure 13.2 image description: The top left panel of this figure shows the ultrastructure of an artery (labels read from top: tunica externa, tunica media, tunica intima, smooth muscle, internal esastic membrane, vasa vasorum, external elastic membrane, nervi vasorum, endothelium, elastic fiber), and the top right panel shows the ultrastructure of a vein (labels read from top: tunica exerna, tunica media, tunica intima, vasa vasorum, smooth muscle, endothelium). The bottom panel shows a micrograph with the cross sections of an artery and a vein. [Return to Figure 13.2].

Figure 13.3 image description: The major arteries in the human body. Labels read (from top, clockwise) right common carotid, left common carotid, axillary, pulmonary trunk, descending aorta, diaphragm, renal, superior mesenteric, gonadal, inferior mesenteric, common iliac, internal iliac, deep femoral, femoral, descending genicular, doraslis pedis, plantar arch, fibular, anterior tibial, posterial tibial, popliteal, palmer arches, exernal iliac, ulnar, radial, brachial, celiac trunk, ascending aorta, aortic arch, brachiocephalic trunk, right subclavian, vertebral. [Return to Figure 13.3].

Figure 13.4 image description: The major veins in the human body. Labels read (from top, clockwise) internal jugular, brachiocephalic, superior vena cava, intercostal, inferior vena cava, gonadal, lumbar, right and left common iliac, external iliac, internal iliac, deep femoral, femoral, posterior tibial, anterior tibial, dorsal venous arch, plantar venous arch, fibular, small saphenous, popliteal, great saphenous, digital, palmar venous arches, ulnar, median antebrachial, medial cubital, hepatic, basilic, brachial, cephalic, axillary, subclavian, externa jugular. [Return to Figure 13.4].

Figure 13.5 image description: This diagram shows how oxygenated and deoxygenated blood flow through the major organs in the body. Pulmonary circulation involves the lungs, pulmonary artery and vein, vena cava, and aorta. Systemic circulation involves the upper body, hepatic vein, renal vein, aorta, liver, hepatic artery, hepatic portal vein, stomach, intestines, renal artery, kidneys, and lower body. [Return to Figure 13.5].

Figure 13.6 image description: The pulse points as shown on a woman's body. Labels read (from top) temporal artery, facial artery, common carotid artery, brachial artery, radial artery, femoral artery, popliteal artery, posterior tibial artery, dorsalis pedis artery. [Return to Figure 13.6].

Figure 13.7 image description: This figure shows three test tubes with a red and yellow liquid in them. The left panel shows normal blood, the center panel shows anemic blood and the right panel shows polycythemic blood. Labels indicate plasma (water, proteins, nutrients, hormones etc.), buffy coat (white blood cells, platelets), and hematocrit (red blood cells). [Return to Figure 13.7].

Figure 13.8 image description: This flowchart shows the pathways in which a multipotent hemotopoietic stem cell differentiates into the different cell types found in blood. From the top (multipotent hematopoietic stem cell can divide and some cells remain stem cells, while the remaining cell goes down one of two paths depending on the chemical signals received: myleoid stem cell or lymphoid stem cell. A myeloid stem cell then can become either a megakaryoblast (which then turns into a magakaryocyte, then becomes platelets), or it can become a proerythroblas (which then becomes a reticulocyte, then becoming an erythrocite), or it can become a myeloblast (which then becomes either a basophil, neutrophil, eosinophil), or it can become a monoblast (which then it becomes a monocyte). If the cell becomes a lymphoid stem cell, it then becomes a lymphoblas, which then becomes either a natural killer cell or a small lymphocyte ( either T or B lymphocyte). [Return to Figure 13.8].

Figure 13.11 image description: This figure shows how leukocytes respond to chemical signals from injured cells. The top panel shows chemical signals sent out by the injured cells (text labels read: 1) Leukocytes in the blood respond to chemical attractants released by pathogens and chemical signals from nearby injured cells). The middle panel shows leukocytes migrating to the injured cells (text labels read: 2)the leukocytes squeeze between the capillary wall as they follow the chemical signlas to where they are most concentrated (positive chemotaxis)). The bottom panel shows macrophages phagocytosing the pathogens (text label reads: 3) Within the damaged tissue, monocytes differentiate into macrophages that pgagocytize the pathogens.The eosinophils and neutrophils release chemicals that break apart pathogens. They are also capable of phagocytosis.). [Return to Figure 13.11].

Figure 13.12 image description: This figure details the steps in the clotting of blood. Each step is shown along with a detailed text box describing the steps on the left. On the right, a signaling pathway shows the different chemical signals involved in the clotting process. The steps described: 1. Injury: a blood vessel is severed. Blood and blood components (e.g. erythrocytes, white blood cells, etc.) are leaking out of the breaks. 2. Vascular spasm: the smooth muscle in the vessel wall contracts near the injury point reducing blood loss. 3. Platelet plug formation: platelets are activated by chemicals released from the injury site and by contact with underlying collagen. The platelets become spiked and stick to each other and the wound site. Initial platelets are activated by chemicals released from the injured cells and by contact with broken collagen. Bound platelets release chemicals that activate and attract other platelets. platelets move toward source of chemical signals and bind. Platelet plug grows in size. 4. Coagulation. In coagulation, fibrinogen is converted to fibrin (see part b), which forms a mesh that traps more platelets and erythrocytes, producing a clot. Part B Fibryn synthesis cascade: Intrinsic pathway (damaged vessel wall), Extrinsic pathway (trauma to extravascular cells), final common pathway (cross-linked fibrin clot). [Return to Figure 13.12].

Figure 13.14 image description: This figure shows an umbilical artery and vein passing through the placenta on the top left. The top right panel shows the first exposure to Rh+ antibodies in the mother. The bottom right panel shows the response when the second exposure in the form of another fetus takes place. Textboxes detail the steps in each process: First exposure birth of first Rh+ infant: 1. During birth, Rh+ fetal erythrocytes leak into maternal blood after breakage of the embryonic chorion, which normally isolates the fetal and maternal blood. 2) Maternal B cells are activated by the Rh antigen and produce large amounts of anti-Rh antibodies. Second exposure: Rh+ fetus: 3) Rh antibody titer in mother's blood is elevated after first exposure. 4) Rh antibodies are small enough to cross the embryonic chorion and attach the fetal erythrocites. [Return to Figure 13.14].

Figure 13.16 image description: The left panel (a) shows the cross-section of a normal and a narrowed artery. A normal artery has no plaque along the artery walls which means there is normal blood flow. In a narrow artery, plague forms on the arterial walls causing abnormal blood flow. The right panel (b) shows a micrograph of an artery with plaque in it. [Return to Figure 13.16].

Figure 13.18 image description: This photograph shows red blood cells of a person suffering from sickle cell anemia. Instead of being discoid shaped like healthy blood cells, sickle red blood cells are shaped like a sickle. [Return to Figure 13.18].

Unless otherwise indicated, this chapter contains material adapted from Anatomy and Physiology (on OpenStax), by Betts, et al. and is used under a a CC BY 4.0 international license. Download and access this book for free at https://openstax.org/books/anatomy-and-physiology/pages/1-introduction.