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Chapter 14 Sections D Integration of Cardiovascular Function.
What is total peripheral resistance? Which type of vessel is mostly responsible?
How is it possible for TPR to remain constant even though blood flow through some organs in increased
by arteriolar dilation?
Which homeostatic mechanisms operate to regulate blood pressure over seconds to hours? over the long
term?
Where are baroreceptors located and what stimulates them?
What happens to sympathetic activity and parasympathetic outflow when the baroreceptors are activated
by an increase in the stretch of the vessel wall?
What happens to sympathetic activity and parasympathetic outflow when the baroreceptors experience a
decrease in the stretch of the vessel wall?
Which hormones are secreted in response to a decrease in mean arterial pressure?
List the events that follow a reduction of blood pressure as with hemorrhage. How is cardiac output and
total peripheral resistance affected?
How does hemorrhage affect: peripheral veins, venous pressure, venous return, end diastolic volume,
arteriolar diameter, hematocrit, blood viscosity, plasma volumecardiac contractility, and heart rate?
How are blood pressure and blood volume related? How is it that a change in one leads to a change in
the other?
How are the kidneys involved in regulating blood pressure?
Describe how plasma volume can be increased in response to hemorrhage based on changes in Starling
forces.
Chapter 14 Section E Cardiovascular patterns in health and disease
What stimulates the secretion of erythropoietin from the kidneys and what is the action of this hormone?
During moderate exercise, indicate whether each of the following parameters increases, decreases, or
does not change:
skeletal muscle blood flow
mean arterial pressure
total peripheral resistance
cardiac output
stroke volume
heart rate
end diastolic ventricular volume
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Other than hemorrhage, how else can a person become hypotensive by hypovolemia?
Explain the physiology of fainting due to emotional responses.
Explain the physiology of fainting due to prolonged standing.
Explain why a person’s feet tend to swell in the upright posture.
Explain why a person might feel faint when quickly rising from a lying to a standing position.
Define shock. What are the causes of hypovolemic shock, low-resistance shock, and cardiogenic shock?
What factors boost venous return during moderate exercise?
Describe how feedforward is involved at the onset of exercise.
How do baroreceptors get “reset” during exercise? What is the result of this resetting?
During very strenuous exercise such as resistance training, how is blood flow to skeletal muscles
altered?
How does the physiology of a well-trained athlete differ from otherwise healthy but sedentary
individuals with respect to:
Stroke volume
End diastolic ventricular volume
Heart rate
Maximal Cardiac output
Capillary density in skeletal muscles
How is blood flow increased to skeletal muscles during exercise? How does blood flow to the brain,
heart, skin, kidneys, and gastrointestinal tract change during exercise?
Is the set point for mean arterial pressure altered during exercise?
How is it that isometric contractions lead to fatigue earlier than isotonic exercise?
How is TPR affected by isometric exercise?
What values of blood pressure constitute the lower limit for hypertension?
What is the cause of primary (essential) hypertension?
What change occurs in the left ventricle that is indicative of hypertension?
How do the following drugs accomplish the desired results when used to treat hypertension: diuretics,
beta blockers, ACE inhibitors, sympathetic antagonists.
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How are ventricular contractility and compliance affected with diastolic dysfunction and systolic
dysfunction?
Explain the mechanism whereby fluids are retained in persons with heart failure?
How does failure of the left ventricle lead to pulmonary edema?
What are the actions of these drug treatments for heart failure: diuretics, cardiac inotropic drugs like
digitalis, and vasodilators like ACE-inhibitors?
Define ischemia.
Define angina pectoris.
What is a myocardial infarction?
What does an atherosclerotic artery look like?
How does nitroglycerin work?
What is an embolus?
Chapter 14 Section F: Blood and Hemostasis
What are the three types of plasma proteins? Which are most abundant?
What is serum?
What is the average hemoglobin concentration in blood?
What is the shape and approximate diameter of erythrocytes? What is the significance of the shape?
Where are erythrocytes produced? What is their typical lifespan? What happens when they “die?”
What is the function of ferritin? of transferrin?
What is the source, target, and action of erythropoietin? What stimulates the secretion of this hormone?
Explain the role of folic acid, vitamin B12 and intrinsic factor in erythropoiesis.
Define anemia.
What is the abnormality in persons with sickle cell anemia? What causes the cells to assume a sickle
shape and how does this interfere with blood flow?
What is polycythemia and how does this affect blood viscosity and blood flow?
How are the leukocytes visibly distinguishable based on cytoplasmic staining and nuclear shape?
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Which the most abundant leukocyte? the least abundant?
What is the other name for platelets? Describe a platelet and the cell that generates platelets.
What are the two types of stem cells that give rise to all cell types of the blood? What determines how
many of each cell type will be produced?
What is hemostatsis? hematoma?
What is the location and function of von Willebrand factor?
What happens to platelets once they bind vWF? Is this a form of positive feedback?
What is the source and action of thromboxane A2?
What prevents a platelet plug from spreading beyond the site of vessel damage?
What is the difference between platelet aggregations and blood clotting?
What triggers blood coagulation?
What is the advantage of an enzymatic cascade such as that of blood clotting?
What are the functions of thrombin? How is thrombin formed?
What is the difference in the intrinsic and extrinsic pathways for blood clotting?
For the purposes of this course, it will not be necessary to know the names and numbers of the clotting
factors as shown in Figure 12-76 and Table 12-14 on page 460-461. Rather, it is important to
understand the general scheme of the clotting pathways and the roles of thrombin, fibrinogen, and
vitamin K.
How does blood clotting normally begin? At what point does the intrinsic pathway become involved?
Coagulation is a positive feedback mechanism. How is blood coagulation restricted to the site of vessel
damage? Is thrombin involved? Other substances? Endothelial cells?
The dissolution of a blood clot in a very important step in the resolution of damage to the vasculature.
How is plasminogen involved?
How does aspirin suppress blood clotting?
Within three hours of a myocardial infarction, what drug(s) can be given and what effect does this drug
have on clotting?