Module 4 - Disorders of the Cardiovascular System

Question 1

What is the function of blood

Answer 1

The function of blood is to transport gases, nutrients, wastes, and hormones. It helps to regulate temperature, pH, and fluid volume.

Question 2

What are the three stages of hemostasis

Answer 2

Hemostasis is divided into vascular constriction, formation of the platelet plug, and blood coagulation in order to stop the flow of blood.

Question 3

What is Vitamin K needed to synthesize

Answer 3

Vitamin K is needed to synthesize protein coagulation factors II, IX, and X, prothrombin, and protein C. A deficiency of vitamin K or liver failure will result in abnormal bleeding as prothrombin will not be made.

Question 4

What are the intrinsic and extrinsic pathways

Answer 4

The intrinsic and extrinsic pathways both form prothrombin activator. The intrinsic pathway begins with activation of factor XII and can cause clotting in 1 to 6 minutes, considered the slower process. The extrinsic pathway can cause clotting in 15 seconds and begins with the release of tissue thromboplastin from the subendothelial cells. Both pathways converge to activate factor X, the conversion of prothrombin to thrombin. Thrombin then converts fibrinogen to fibrin, the material needed to stabilize a clot. Both methods are needed for successful hemostasis.

Question 5

What are the natural and drug therapy anticoagulants

Answer 5

Antithrombin III, protein C, protein S, warfarin, heparin, Dabigatran, Rivaroxaban, Apixaban

Question 6

What is peripheral vascular resistance

Answer 6

Peripheral vascular resistance is the collective resistance of all the vessels in the peripheral circulation. Resistance is the opposition to flow caused by friction between the moving blood and the stationary vessel wall.

Question 7

Hemodynamics or blood flow is affected by what factors?

Answer 7

Pressure, resistance, flow, radius, blood viscosity, compliance, wall tension

Question 8

What is cardiac output

Answer 8

Cardiac output is the volume of blood the heart pumps per minute. It can be calculated by multiplying the heart rate by the stroke volume, which is the blood pumped out by the ventricle with each beat.

Question 9

What is preload

Answer 9

Preload is the end-diastolic pressure when the ventricle has been filled and represents the volume work of the heart. It’s called preload because it is the work on the heart before the contraction begins. It is mainly the result of venous return of blood to the heart and the stretch of the cardiac muscle fibers. In short, it is the volume of blood in the ventricles the heart has to eject.

Question 10

What is afterload

Answer 10

Afterload is the pressure the heart must generate to move blood into the aorta.

Question 11

What is cardiac contractility

Answer 11

Cardiac contractility is the ability of the heart to change its force of contraction without changing its resting (diastolic) length. This is strongly influenced by the number of calcium ions available to participate int he contractile process. Contractility increases cardiac output independent of preload or afterload.

Question 12

What is an inotrope?

Answer 12

An inotropic influence is one that increases the strength of the muscular contraction. An inotrope is an effect that increases or decreases the contractile force. Positive inotropic effects (increasing contractile force) include the sympathetic nervous system, afterload, catecholamines, heart rate, drugs, intracellular calcium levels. Negative inotropic effects (decrease contractile force) include the parasympathetic nervous system, heart failure, hypoxia, and drugs.

Question 13

What is mean arterial pressure

Answer 13

Mean arterial pressure is the average pressure in the arterial pressure in the arterial system during a cardiac cycle and is a good indicator of tissue perfusion. The mean arterial pressure is the product of the cardiac output (SVHR) and the peripheral vascular resistance (MPA = COPVR)

Question 14

Explain the renin-angiotensin-aldosterone system

Answer 14

In the RAAS, kidneys secrete renin, which gets converted eventually into angiotensin II, that forms ADH and aldosterone to reabsorb sodium and water. It increases fluid retention and vasoconstriction. This worsens both pre and afterload. RAAS plays a vital role in blood pressure regulation. If there are changes in extracellular fluid, extracellular sodium levels, a drop in blood pressure, or increased sympathetic activity, the kidney will release renin. In the bloodstream, renin converts angiotensinogen into angiotensin I. Angiotensin I is converted to angiotensin II in the lungs by ACE (angiotensin-converting enzyme). Angiotensin II is a vasoconstrictor, mainly of the arterioles. Arteriole constriction will increase the PVR, regulating blood pressure for a short period of time. Aldosterone will increase salt and water retention by the kidney contributing to the long-term regulation of blood pressure.

Question 15

Explain hypercoagulability

Answer 15

Hypercoagulability is the accelerated activity of the clotting system. There are conditions that create increased platelet activity and conditions that cause increased activity of the coagulation pathways. Arterial thrombi are often a result of conditions characterized by an increase in platelet numbers or restricted blood flow with platelet adhesion. Venous thrombi are associated with conditions, genetic in nature or acquired, that decrease the amount of anticoagulation factors or produce a stasis of blood, which in turn increases the number of pro-coagulation factors.

Question 16

What is thrombocytosis

Answer 16

Thrombocytosis is defined as a platelet count greater than 450,000/microL. The overall platelet count is regulated by a negative feedback loop. If the platelet count falls below normal limits, hormonal thrombopoietin levels will rise to increase the number of platelets, and when the count reaches normal limits, thrombopoietin levels will decrease. Primary thrombocytosis is due to a disorder of the hematopoietic stem cells within the bone marrow resulting in abnormally high levels of thrombopoietin, which leads to an overproduction of platelets. Secondary thrombocytosis is is also an abnormal thrombopoietin production which overproduces platelet production, but is due to a disease state (tissue damage from surgery, infection, cancer, and chronic inflammatory conditions).

Question 17

What are the most common causes of inherited disorders of hypercoagulability

Answer 17

Inherited disorders of hypercoagulability are most commonly caused by a mutation of the factor V gene or prothrombin gene. The mutant factor V cannot be inactivated by protein C which helps to regulate anticoagulation. As a result, a factor V mutation will lead to an increased risk fro developing deep vein thrombosis.

Question 18

What are acquired or secondary factors of hypercoagulability that lead to venous stasis

Answer 18

Prolonged bed rest and immobility, myocardial infarction, cancer, hyperestrogenic states, oral contraceptives, smoking, and obesity

Question 19

What is thrombocytopenia

Answer 19

The term to describe a reduction in platelet number, of less than 150,000/µL which increases the risk of bleeding

Question 20

Describe hemophilia A

Answer 20

Hemophilia A is a recessive genetic disorder that causes an insufficient production in factor VIII which promotes clotting and adhesion of platelets to the vessel wall, bleeding in the soft tissues, GI tract, and joints. Trauma prevention is very important, Factor VIII replacement therapy is the current treatment.

Question 21

Describe Disseminated intravascular coagulation (DIC)

Answer 21

Disseminated intravascular coagulation (DIC) is characterized by widespread coagulation and bleeding. DIC begins with the activation of the extrinsic or intrinsic coagulation cascade, the result of unregulated generation of thrombin, resulting in systemic formation of fibrin. All the major anticoagulant levels are decreased. Microthrombi are formed causing vessel occlusion and tissue ischemia. As all availability coagulation proteins and platelets are being used to form clots, severe hemorrhage ensues. Treatment is focused on managing the primary disease, replacing clotting components, and preventing further activation of clotting mechanisms.

Question 22

How can anemias be classified according to size and color

Answer 22

Anemias can be normochromic (normal color) or hypochromic (decreased color). Red cells can also vary in size: normocytic (normal size), microcytic (small cells), and macrocytic (large cells).

Question 23

Describe sickle cell disease

Answer 23

Sickle cell disease is a genetic disorder characterized by chronic hemolytic anemia, pain, and organ failure caused by abnormal hemoglobin S. Sickle cell disease is a single mutation in the hemoglobin molecule. In conditions of decreased oxygen levels, the cell becomes sickled as the abnormal hemoglobin sticks together. With proper oxygenation, the cells may return to normal shape; with, the cell will remain permanently sickled. This may lead to hemolysis or occlusion. Clinical presentation can include leg ulcers, damage to many organs, acute chest syndrome, asplenia. Diagnosis is confirmed by screening at birth, hemoglobin electrophoresis. Treatment is focused on preventing sickling episodes like infections, cold exposure, severe physical exertion, acidosis, and dehydration.

Question 24

Describe Iron deficiency anemia

Answer 24

Iron Deficiency Anemia is the loss of iron through bleeding or increased demands. Iron is a component of heme and decreased levels lead to impaired oxygen delivery. Clinical presentation includes fatigue, dyspnea, angina, and tachycardia, pica. IDA presents with low hemoglobin and hematocrit, decreased iron stores, low serum iron and ferritin levels. Prevention is key - eating a diet rich in iron containing foods, taking iron fortified vitamins, and treating any underlying chronic blood loss.

Question 25

Describe Thalassemia

Answer 25

Thalassemia is a genetic disease with defective hemoglobin synthesis and hemolysis. It is a hypochromic, microcytic anemia due to decreased synthesis of the affected chain coupled with continued production and accumulation of the unaffected globin chain. People with Thalassemia major must undergo blood transfusions in life or risk severe growth retardation. The ineffective hematopoiesis and hemolysis leads to increased erythropoietin secretion and hyperplasia in the bone marrow which impairs bone growth and leads to osteoporosis or osteopenia.

Question 26

Describe Vitamin B12 Deficiency Anemia

Answer 26

Vitamin B12 Deficiency Anemia is caused by impaired DNA synthesis that results in enlarged red blood cells. B12 is necessary for DNA synthesis and development of the cel nuclei. The clinical presentation includes moderate to severe anemia and mild jaundice. The the MCV is elevated due to large cells and the MCHC is normal. There can be neurologic changes as well caused by meylin breakdown. Diagnosed by low B12 serum level. Treatment includes lifelong intramuscular injections or high oral doses.

Question 27

Describe folic acid deficicency

Answer 27

Folic Acid Deficiency is similar to B12 deficiency, as it is required for DNA synthesis and red blood cell maturation. Most common causes are malnutrition. Supplementation should support people with this condition.

Question 28

What is neutropenia and what are people who have it at risk for

Answer 28

Neutropenia is the abnormal decrease in the circulating neutrophils, thus weakening the immune system. It is the result of decreased production, increased destruction, or relocation to tissue from the bloodstream. For some it is congenital, for others it can be caused by lupus, rheumatoid arthritis, HIV, and hematologic cancers.

Question 29

What are the five types of lipoproteins?

Answer 29

Chylomicrons, very-low-density lipoprotein (VLDL), intermediate-density lipoprotein (IDL), low-density lipoprotein (LDL), and high-density lipoprotein (HDL).

Question 30

Which is the good and which is the bad cholesterol

Answer 30

HDL is good, LDL is bad cholesterol.

Question 31

Where does lipoprotein synthesis take place

Answer 31

Lipoprotein synthesis takes place in the liver and the small intestine.

Question 32

What are xanthomas

Answer 32

Cholesterol deposits along the skin and tendons in extremely elevated hyperlipidemia

Question 33

Describe hyperlipidemia

Answer 33

Hyperlipidemia is the the excess of lipids in the blood. Nutrition, genetics, medications, comorbid conditions, and metabolic disease can all raise blood lipid levels. Treatment focuses on dietary and therapeutic lifestyle changes like increasing physical activity, weight reduction, and smoking cessation. If those don’t work, hyperlipidemia drugs can work.

Question 34

What is atherosclerosis and what is it a major risk factor of

Answer 34

Hardening of the arteries, hyperlipidemia

Question 35

Describe atheroslcerosis pathology and clinical presentation

Answer 35

The etiology is the “response to injury theory” in which injury of a blood vessel (due to inflammation, immune mechanisms, high cholesterol, hypertension, smoking) results in macrophages scavenging the excess cholesterol. They oxidize the LDL and become foam cells which decrease cholesterol from circulation but will release factors that will injure the endothelial cells and the blood vessel. Foam cells will keep collecting and form a lesion on the blood vessel wall, the macrophages will secrete growth factors that secrete cell proliferation. The macrophages will die and leave behind their necrotic debris and then we start to accumulate lipids and this will generate our plaque. The lesion will be covered by smooth muscle, extracellular matrix, and will inhibit flow and increase blood pressure and resistance. If the lesion ruptures, it can cause hemorrhage or a thrombosis. This can present as angina, impotence, wounds that wont heal.

Question 36

What causes coronary artery disease (CAD)

Answer 36

Atherosclerosis

Question 37

What can CAD cause

Answer 37

CAD leads to myocardial ischemia and angina, myocardial infarction (heart attack), cardiac arrhythmias, conduction defects, heart failure, and sudden death

Question 38

What are the major risk factors of CAD

Answer 38

Cigarette smoking, elevated blood pressure, elevated serum total and low-density lipoprotein (LDL) cholesterol, low serum high-density lipoprotein (HDL) cholesterol, diabetes, advancing age, abdominal obesity, and physical inactivity.

Question 39

Describe the different methods used to assess coronary blood flow and myocardial perfusion

Answer 39

Electrocardiography - records electrical potential differences during the cardiac cycle. It is most frequently used cardiovascular procedure that can diagnose and identify ventricular conduction defects, arrhythmias, electrolyte imbalances, drug effects, and genetically mediated electrical or structural abnormalities.

Exercise stress test - observes cardiac function under stress (running on a treadmill). Used for adults with suspected ischemic heart disease, but also physiologic response preoperatively, post MI or revascularization, or the severity of arrhythmias.

Echocardiography - best method to check for structure and function of the heart.

Doppler Ultrasonographic imaging

Cardiac MRI and CT

Cardiac Catheterization - a catheter is inserted into the great vessels and chambers of the heart to inject radiographic contrast.

Angiography

Question 40

Describe the disease states in acute coronary syndrom

Answer 40

Acute coronary syndrome (ACS) represents a range of acute ischemic heart diseases ranging from unstable angina to myocardial infarction. It results from disruption of an atherosclerotic plaque.

Question 41

What are the two different ways heart failure can be defined

Answer 41

Heart failure can be described in terms of systolic dysfunction (the ejection of blood during systole is impaired) or diastolic dysfunction (impaired filling capability of the heart during diastole).

Question 42

Describe heart failure pathology, clinical presentation, diagnosis, and treatment

Answer 42

Clinical manifestations of heart failure include shortness of breath, fatigue, weakness, fluid retention. Diagnosis depends on history, physical exam, lab studies, electrocardiography, etc. Treatment is aimed at stabilizing and correcting the cause of the cardiac dysfunction to receive symptoms, improve quality of life, and reduce risk factors. Diuretics, ACE inhibitors or angiotensin II receptor blockers, beta blockers, digoxin, and vasodilators can be used.

Question 43

Describe the different types of cardiomyopathies

Answer 43

Cardiomyopathy is a disease of the heart muscle that causes it to be enlarged, thick, or rigid. Hypertrophic cardiomyopathy is the thickening of the heart wall, especially in the left ventricle. It makes the chamber smaller which causes an abnormal ventricular filling and decreased stroke volume. Dilated cardiomyopathy causes the left ventricle to be enlarged and cannot contract properly to conduct the blood. Restrictive myopathy causes the heart to lose elasticity so it does not expand well to fill with blood.

Question 44

Describe the different types of arrhythmias

Answer 44

Cardiac arrhythmias are electrical impulses in the cardiac conduction system that fail to coordinate causing the heart rate to increase, decrease, or have an irregular rhythm. There are Tachyarrhythmias in which the heart rate is above 100 beats/min which decreases the fill time of the heart and decreases the CO. Bradyarrhthmias slow the heart rate to less than 60 beats/min and can decrease profusion of our organs.

Question 45

What are the current stages of hypertension

Answer 45

Currently, normal blood pressure is defined as less than 120/80. Elevated blood pressure is < 130/80; hypertension stage 1 is < 140/90; and hypertension stage 2 is > 140/90.

Question 46

Describe hypertension pathology, clinical presentation, diagnosis, and treatment

Answer 46

There are both non-modifiable risk factors (age, family history, gender, race) and modifiable (salt, excessive calorie, alcohol intake). Hypertension can promote and accelerate plaque formation and rupture, it is also a risk factor for CAD, peripheral artery disease, stroke, and heart failure. Prolonged elevation of blood pressure places an increased workload on the left ventricle as it increases the pressure the heart must pump against as it ejects blood into the systemic circulation. Over time, the left ventricle hypertrophies as it compensates for the increased pressure. Left ventricular hypertrophy is a major risk factor for heart disease and even death. Hypertension is diagnosed with repeated blood pressure measurement. Treatment is usually lifestyle changes as well as medication like diuretics, ACE inhibitors, calcium channel receptor blockers.

Question 47

What is cardiogenic shock

Answer 47

Cardiogenic Shock is occurs when the heart fails to pump blood sufficiently to meet the body’s needs.

Question 48

What causes cardiogenic shock

Answer 48

The most common cause is extensive damage to the left ventricle from a myocardial infarction where there is decreased stroke volume and cardiac output which causes low oxygen and perfusion. Myocardial infarction, myocardial contusion, sustained arrhythmias, or cardiac surgery