Patho Exam 4
Describe the normal forward flow of blood through the heart beginning from where blood
enters through the superior vena cava and inferior vena cava. In your discussion,
identify all valves and all chambers until blood leaves the heart through the aorta.
correct answers -superior vena cava
- right atria
-the AV valve ( tricuspid valve )
-right ventricle.
-pulmonary trunk -pulmonary semilunar valve.
-right or left pulmonary artery
-the lungs (oxygenized)
-return to the heart via the left and right pulmonary veins
-left atrium.
-left atrioventricular valve ( bicuspid valve/ mitral valve)
-the left ventricle.
- aortic semilunar valve
-aorta
Once oxygenated blood is in the aorta it can be distributed to the rest of the body.
Describe what the term "tissue perfusion" specifically refers to. correct answers Tissue
perfusion refers to the having an adequate volume of blood and amount pressure
through the arteries to drive blood through branches of arterioles and capillaries.
Perfusion alone refers to blood flowing through capillaries.
describe the five various stages that link that evolution of an atherosclerotic plaque to
myocardial infarction (a heart attack): correct answers step 1- Birth of Plaque
- excess LDL accumulates in artery wall and undergo chemical alteration which
stimulates endothelial cells to display adhesin molecules which latch onto monocytes
and T cells in the blood. Endothelial cells secrete chemokines which lure snared cells
into intima.
6.3b step 2-Monocytes mature into macrophages. T cells and macrophages produce
inflammatory mediators including cytokines, and factors that promote cell division.
Macrophages display " scavenger receptors which help them digest modified LDLs.
6.3c step 3- Macrophages feast on LDLs becoming filled with fatty droplets called foam
cells. T cells constitute the fatty streak, the earliest form of atherosclerotic plaque.
, 6.3d step 4- Plaque progression- Inflammatory molecules can promote further growth of
the plaque and formation of a fibrous cap over the lipid core. Cap develops when the
molecules induce smooth muscle cells of the media to migrate to the top of the intima,
multiply and produce a tough, fibrous matrix that glues cells together. Cap adds to the
size of plaque but also walls it off safely from the blood.
6.3e step 5- Plaque rupture- Inflammatory substances secreted by foam cells can
dangerously weaken the cap by digesting matrix molecules and damaging smooth
muscle cells, which then fail to repair the cap. Meanwhile, foam cells may display tissue
factor, a potent clot promoter. If the weakened plaque ruptures, tissue factor will interact
with clot-promoting elements in the blood, causing a thrombus, or clot to form. If the clot
is big enough, it will halt blood flow to the heart producing a heart attack-the death of
cardiac tissue.
Steps 1-3 are earliest stages of atherosclerotic lesion.
Describe how atherosclerosis affects the normal anatomy and physiology of a coronary
artery to eventually cause an increased workload on the heart. correct answers
Atherosclerosis affects the normal anatomy and physiology of the coronary artery by
increasing the resistance of blood flow through tissues meaning the workload of the
heart has to increase to over the resistance.
Differentiate between non-modifiable risk factors and modifiable risk factors for the
development of atherosclerosis. correct answers Non-modifiable risk factors are risk
factors that we can not do anything to intervene to change such as age, gender, family
history, and race. Modifiable factors are factors which he have the ability to change
such as Low-density lipoproteins, high-density lipoproteins, hypertension, cigarette
smoking, and C Reactive Protein ( CRP).
Describe how the levels of the biomarkers C-reactive protein and cholesterol serve as
serve as an index for the relative risk of a future heart attack. In your discussion, clearly
indicate the significance of low levels and high levels of both biomarkers. correct
answers C Reactive Protein is an acute phase reactive protein produced by the liver in
response to cytokines generated during inflammation. In response to injury, some
cytokines stimulate liver to increase level of C reactive protein in the plasma. C reactive
protein will be elevated during injury, after period of injury, healing, and inflammation
subsides C reactive protein levels will decrease. With atherosclerosis, C reactive protein
levels can remain chronically elevated, and serve as a biomarker for arteriosclerosis or
risk factor for coronary artery disease in addition to cholesterol levels.
People with low cholesterol are least likely to have a future coronary event. People with
high cholesterol were more likely to have a coronary event.
People with low cholesterol but still had a heart attack were noted to have high C
reactive protein levels. People with high C reactive protein were likely to have a high
risk of developing a coronary event independent of cholesterol levels.
Describe the normal forward flow of blood through the heart beginning from where blood
enters through the superior vena cava and inferior vena cava. In your discussion,
identify all valves and all chambers until blood leaves the heart through the aorta.
correct answers -superior vena cava
- right atria
-the AV valve ( tricuspid valve )
-right ventricle.
-pulmonary trunk -pulmonary semilunar valve.
-right or left pulmonary artery
-the lungs (oxygenized)
-return to the heart via the left and right pulmonary veins
-left atrium.
-left atrioventricular valve ( bicuspid valve/ mitral valve)
-the left ventricle.
- aortic semilunar valve
-aorta
Once oxygenated blood is in the aorta it can be distributed to the rest of the body.
Describe what the term "tissue perfusion" specifically refers to. correct answers Tissue
perfusion refers to the having an adequate volume of blood and amount pressure
through the arteries to drive blood through branches of arterioles and capillaries.
Perfusion alone refers to blood flowing through capillaries.
describe the five various stages that link that evolution of an atherosclerotic plaque to
myocardial infarction (a heart attack): correct answers step 1- Birth of Plaque
- excess LDL accumulates in artery wall and undergo chemical alteration which
stimulates endothelial cells to display adhesin molecules which latch onto monocytes
and T cells in the blood. Endothelial cells secrete chemokines which lure snared cells
into intima.
6.3b step 2-Monocytes mature into macrophages. T cells and macrophages produce
inflammatory mediators including cytokines, and factors that promote cell division.
Macrophages display " scavenger receptors which help them digest modified LDLs.
6.3c step 3- Macrophages feast on LDLs becoming filled with fatty droplets called foam
cells. T cells constitute the fatty streak, the earliest form of atherosclerotic plaque.
, 6.3d step 4- Plaque progression- Inflammatory molecules can promote further growth of
the plaque and formation of a fibrous cap over the lipid core. Cap develops when the
molecules induce smooth muscle cells of the media to migrate to the top of the intima,
multiply and produce a tough, fibrous matrix that glues cells together. Cap adds to the
size of plaque but also walls it off safely from the blood.
6.3e step 5- Plaque rupture- Inflammatory substances secreted by foam cells can
dangerously weaken the cap by digesting matrix molecules and damaging smooth
muscle cells, which then fail to repair the cap. Meanwhile, foam cells may display tissue
factor, a potent clot promoter. If the weakened plaque ruptures, tissue factor will interact
with clot-promoting elements in the blood, causing a thrombus, or clot to form. If the clot
is big enough, it will halt blood flow to the heart producing a heart attack-the death of
cardiac tissue.
Steps 1-3 are earliest stages of atherosclerotic lesion.
Describe how atherosclerosis affects the normal anatomy and physiology of a coronary
artery to eventually cause an increased workload on the heart. correct answers
Atherosclerosis affects the normal anatomy and physiology of the coronary artery by
increasing the resistance of blood flow through tissues meaning the workload of the
heart has to increase to over the resistance.
Differentiate between non-modifiable risk factors and modifiable risk factors for the
development of atherosclerosis. correct answers Non-modifiable risk factors are risk
factors that we can not do anything to intervene to change such as age, gender, family
history, and race. Modifiable factors are factors which he have the ability to change
such as Low-density lipoproteins, high-density lipoproteins, hypertension, cigarette
smoking, and C Reactive Protein ( CRP).
Describe how the levels of the biomarkers C-reactive protein and cholesterol serve as
serve as an index for the relative risk of a future heart attack. In your discussion, clearly
indicate the significance of low levels and high levels of both biomarkers. correct
answers C Reactive Protein is an acute phase reactive protein produced by the liver in
response to cytokines generated during inflammation. In response to injury, some
cytokines stimulate liver to increase level of C reactive protein in the plasma. C reactive
protein will be elevated during injury, after period of injury, healing, and inflammation
subsides C reactive protein levels will decrease. With atherosclerosis, C reactive protein
levels can remain chronically elevated, and serve as a biomarker for arteriosclerosis or
risk factor for coronary artery disease in addition to cholesterol levels.
People with low cholesterol are least likely to have a future coronary event. People with
high cholesterol were more likely to have a coronary event.
People with low cholesterol but still had a heart attack were noted to have high C
reactive protein levels. People with high C reactive protein were likely to have a high
risk of developing a coronary event independent of cholesterol levels.
