What are 3 signs and symptoms of leukemia? What causes these symptoms?
- Bleeding, anemia, infection (signs)
- Decreased WBC, RBC, platelets (symptoms)
- Aplastic anemia results, inability to fight infection (lack of leukocytes) and inability to coagulate may also be a cause
Ethan reports to his doctor that he has been having difficulty breathing. His lung funciton tests come back with a decreased FEV1, increased TLC, and an increased RV. What is his likely problem? What else could you measure to diagnose this problem to further confirm your diagnosis?
Ethan is likely having an obstructive disorder. Air could be trapped in his lungs leading to the increased RV and TLC. Further testing would likely reveal a decreased FVC as well. A decrease in the FEV/FVC would also be noted. He could have emphysema, which would mean he’d struggle to breath normally that could lead to an inability to eat normally, thus causing weight loss.
While working at a respiratory rehab center you are treating two friends with obstructive disorders. Robert has emphysema and Ned has chronic bronchitis. Which one of these would be expected to be a blue bloater, and which would be a pink puffer. Why? What would be the expected ventilation/perfusion ration (V/Q) with each condition?
Robert has emphysema, and is the pink puffer because of active expiration. V/Q would be equal due to equal loss in alveoli and surrounding capillaries. The body is able to compensate by overventilation.
Ned has chronic bronchitis and is the blue bloater because of the hypertension that results. V/Q is mismatched because air is trapped in lungs and overventilation doesn’t work as compensation due to hypersecretion of mucus and impaired cilia function.
What are the responses of the cardiovascular, respiratory, and renal systems to anemia? What triggers this change in their function?
The cardiovascular response to anemia tries to raise O2 in the blood by vasoconstriction, tachycardia, and shunting blood away from the skin, which cause palor and increasing flow to the brain. The respiratory system responds by tachypnea to increase PO2 in tissues. The renal system increases RAS to increase perfusion and erythropoietin synthesis to increase oxygen transport by the blood. This is trigger by hypoxia and increased sympathetic stimulation.
Shortly after a routine pernatal checkup, Neko’s ob-gyn ordered a set of tests of the fetal heart. The doctor told her she suspects that the fetus likely has transposition of the great arteries. The doctor was too busy to explain this problem to Neko. Describe normal flow through the heart and how flow through the heart would change with this condition. Is this a cyanotic or non cyanotic congenital defect in the infant? Would it also be cyanotic in the fetus? Why or why not?
Normal flow: inf/sup vena cava –> RA –> bicuspid valve –> RV —> pulmonary semilunar valve –> pulmonary arteries -> lungs –> pulmonary veins –> LA –> mitral valve –> LV –> Aortic semilunar valve –> arterties to systemic circulation
With transposition of the great arteries, the pulmonary arteries and systemic arteries are affected. Two circulations are formed. The right side of the heart forms its own circulation while the left does the same. This is cyanotic in the infant because the oxygenated blood never circulates systemically. The fetus doesn’t depend on their lungs due to the foramen ovale and umbilical supply with the mother. This is however an issue at birth.
Buster had a myocardial infarction from shoveling snow. What type of angina was he experiencing? After he was diagnosed with atherosclerosis he is wondering if there is anything he can do different to decrease his risk of another myocardial infarction. What are two risk factors for atherosclerosis that he could change to decrease the risk?
Buster was experiencing a stable angina.
- Hyperlipidemia: needs to decrease fat intake (especially cholesterol)
- Obesity and sedentary lifestyle: needs to increase physical activity
Is aortic semilunar stenosis a systolic or diastolic dysfunction? What would be the effect on cardiac output? Which chambers of the heart would be affected form this aortic semilunar stenosis and how would they be affected?
Aortic semilunar stenosis is a systolic dysfunction that decreases cardiac output. The left ventricle pressure is increased due to the decreased stroke volume due to the difficulty vacating the ventricle. The heart rate is increased by the body in an attempt to help, however, this only increases the work on the heart, increases pressure and decreases Q even more, eventually leading to ventricular hypertrophy.
Is aortic semilunar valve regurgitation a systolic or diastolic function? What would be the effect on cardiac output? Which chamber of the heart would be affected from this aortic valve regurgitation and how would it be affected?
Aortic semilunar valve regurgitation is a diastolic dysfunction. This would cause a decrease in cardiac output. The left ventricle would try and eject more blood by increasing SV/HR to correct for the decrease in Q. This would increase workload on the LV and would eventually lead to left ventricle hypertrophy.
A few weeks after having a myocardial infarction in the left anterior descending coronary artery, Jim is back in the hospital with dyspnea and an elevated heart rate. Catheter measures show high pressure in the pulmonary veins. He also has ascites and swollen ankles. Describe or diagram the events leading from his myocardial infarction that would cause the pulmonary edema, ascites, and swollen ankles. Is this right and/or left sided heart failure? How would this heart failure on one side contribute to heart failure on the other?
LV dysfunction –> Increased LV pressure/vol –> Increased LA pressure/vol –> increased pulmonary venous pressure –> pulmonary edema
This starts as left sided heart failure and leads to right sided heart failure by:
Pulmonary edema –> Increased pulmonary arteriole pressure –> Increased RV pressure/vol –> Increased RA pressure/vol –> peripheral edema
This eventually results in systemic, or peripheral, edema that causes swollen ankles and can also lead to third space accumulation of fluid or ascites
A few weeks after having a myocardial infarction in the right circumflex coronary artery, Jim is back in the hospital with edema and an elevated heart rate. X rays shows hepatomegaly. Describe or diagram the events leading from his myocardial infarction that would cause the hepatomegaly and edema. Is this right and/or left sided heart failure? How would this heart failure on side contribute to heart failure on the other side.
The myocardial infarction in the RCA leads to the development of right sided heart failure. The dysfunction of the RV caused abnormal volume, pressure and filling of the RV and also similar results in the RA. This backup of fluid then resulted in peripheral edema due to the increase pressure in the periphery. The hepatomegaly was a result of third space accumulation, or ascites, of the fluid.
Right sided heart failure:
Decreased pulmonary flow –> Decreased LA filling –> decreased LV pressure/vol –> decreased blood flow to the body.
Puts more work on the left side of the heart, which can lead to left sided heart failure
Compare and contrast disseminated intravascular coagulation and thrombic thrombocytopenic purpura (TTP). Why are these conditions difficult to treat?
DIC: Spontaneous bleeding and excessive clot formation occur simultaneously, while there is an overactivation of the clotting cascade
TTP: Overactivation of VWF, thus leading to thrombocytopenia and microvascular thrombi formation; dependent on VWF
Difficult to treat because a coagulant would solve the bleeding problem, but increase clot formation. An anti-coagulant would solve the clot problem, but worsen the bleeding, so a careful mixture of the two treatments must be used.
What are the general signs and symptoms of shock? What would be the body’s response to a decrease in cardiac output from cardiogenic shock? Why might this contribute to further decrease in cardiac output?
Shock generally results in a decreased blood pressure. In cardiogenic shock, the body increases HR in attempt to maintain cardiac output. This results in an increased work load on the heart which may lead to further dysfunctions or arrhythmias, decreasing output even further.
Describe the development of atherosclerotic plaque
Endothelial injury –> Cytokines release –> Macrophages oxidize LDL –> Foam cells penetrate intima –> Fatty streak –> fibrous plaque
Ethan presents to his physician with dyspnea and tachycardia. What are two diseases outside of the cardiovascular system that could produce these? What additional sighs and symptoms would be assessed to distinguish these diseases?
Chronic bronchitis and emphysema are two diseases that result in dyspnea and tachycardia. Chronic bronchitis symptoms include sputum production, and pulmonary hypertension. The mucus produced obstructs the path of breathing and a decreased FEV and FVC. Emphysema is characterized by a decrease in elastic recoil due to floppy alveoli after alveolar and capillary death. Difficulty eating and talking, along with weight loss are other factors associated with emphysema. A decreased FEV1 and FVC is observed in these as well. A difference can be distinguished via a pink puffer/blue bloater comparison and the fact that overventilation would be effective in emphysema and not chronic bronchitis. Also, edema and weight loss could be compared.
What are three risk factors for coronary artery disease?
Smoking, diabetes, hyperlipidemia
What are the effects of thrombocytopenic purpura? Why is this condition difficult to treat?
TTP is caused by an excessive amount of VWF causing an accumulation of platelets in small arteries. This results in clotting, but also bleeding at the same time. It is hard to treat because attempts to break up the clots will lead to additional bleeding, and attempting to stop the bleeding will lead to excessive clot formation
Why are people with chronic bronchitis cyanotic and those with emphysema are not? Explain in terms of the ventilation-perfusion ratio.
People with chronic bronchitis are cyanotic because they are unable to compensate a mis-matched ventilation/perfusion ratio with increased respiratory rate. Emphysema patients have a matched ventilation perfusion ratio because of an equal loss of function in alveoli and vessels
A child is brought to the ER after scraping his knee on the playground and having continuous bleeding from the site for six hours. The platelet count is normal, and the prothrombin time (PT) and partial thromboplastin time (PTT) came back normal. What else might account for the bleeding disorder?
PTT and PT measure how fast the blood clots and looks at clotting disorders. Since these are normal, one would thin it is from a lack of platelet numbers, but that was normal as well. The excessive bleeding could be caused from Von Willibrand’s Factor. Dysfunction in this factor leads to improper adhesion of the platelets to the damaged endothelium.
