Cardiovascular And Hemopoetic Pathophysiology

Front 1

. Identify a major physiologic manifestation of anemia.

Back 1

Reduced oxygen carrying capacity

Front 2

2. Describe the neurological pathology in individuals with vitamin B12 deficiency anemia who present with paresthesia.

Back 2

Myelin degeneration occurs, causing a loss of nerve fibers in the spinal cord, causing the numbness, gait disturbances, extreme weakness, spasticity, and reflex abnormalities.

Front 3

Identify the classification of anemia based on the RBC size and color for pernicious anemia.

Back 3

Macrocytic-Normochromic anemia

Front 4

4. Predict the response manifested by the respiratory system as compensation to anemia.

Back 4

Hyperventilation: increased depth of breathing (dypnea)

Front 5

5. Identify the cellular component that is most vulnerable to folate and vitamin B12 deficiency.

Back 5

DNA Synthesis

Front 6

6. Identify the type of anemia that arises as a result of defective secretion of intrinsic factor by special cells in the stomach.

Back 6

Macrocytic-Normochromic anemia: Pernicious anemia

Front 7

7. Identify the anemia that presents with erythrocytes that are small, pale (microcytic, hypochromic).

Back 7

Sideroblastic anemia (and Iron defiecency anemia is a part of the group)

Front 8

8. Diagnose the type of anemia in a patient who presents with fatigue, weakness, dyspnea, and with his conjunctiva and palms being, his nails appear brittle, thin, and concave, and he has developed sores at the corners of his mouth.

Back 8

Microcytic-Hypochromic Anemia: Iron Deficiency anemia

Front 9

9. Identify the most common cause of iron deficiency anemia.

Back 9

Pregnancy & Chronic blood loss ie female reproductive years in both developed and developing countries

Front 10

10. Describe the Schilling test and its purpose.

Back 10

Used for testing of Pernicious Anemia by determining cobalamin absorption for B12 deficiency. It’s performed by administering radio-active cobalamin and measuring its excretion in urine, low urinary excretion is significant for PA revealing HCl absence.

Front 11

11. Diagnose the type of anemia in a patient with mild to moderate splenomegaly and hepatomegaly, bronze skin, and cardiac dysrhythmias.

Back 11

Sideroblastic Anemias

Front 12

12. Explain the reason why pancytopenia develops in patients with aplastic anemia.

Back 12

Aplastic anemia may alter stem cell population so it cant proliferate or differentiate, causing thrombocytopenia in cardiovascular and respiratory, hemorrhage in issues causing leucopenia and infection. This could lead to reduction in all blood cellular components.

Front 13

13. Diagnose the type of anemia that is associated with an erythrocyte life span of less than 120 days, ineffective bone marrow response to erythropoietin, and altered iron metabolism.

Back 13

Normocytic-Normochromic: Anemia of Chronic Inflammation

Front 14

14. Describe a major clinical consequence of polycythemia vera.

Back 14

Excessive proliferation of erythrocyte precursors in bone marrow resulting directly from increased blood volume and thickness. May spontaneously convert to acute myelogenous leukemia. IT MAY RESULT TO DVT, PULMONARY EMBOLISM (PE) AND HEART ATTACK AND STROKE

Front 15

15. Identify the most likely anemia that would be a suitable candidate for bone marrow transplantation.

Back 15

Aplastic anemia

Front 16

Describe the characteristic of warm antibody hemolytic anemia

Back 16

Mediated by IgG antibodies specific for erythrocyte antigen; associated with allergic looking red spots or splenomegaly

Front 17

17. Predict the stage when jaundice would occur in patients with hemolytic anemias.

Back 17

Accumulation of end products of red cell destruction (hemolysis). Blood is producing too much bilerubin and liver is unable to metabolize it.

Front 18

18. Identify the hormone or chemical mediator that is most likely responsible for the hypertrophy of the myocardium due to chronic hypertension.

Back 18

Angiotensin II & catecholamine

Front 19

19. Describe the linkage between atherosclerosis and aneurysms.

Back 19

Atherosclerosis is the most common cause of arterial aneurysms because plaque formation erodes the vessel wall and contributes to inflammation and release of proteinases that can further weaken the vessel.

Front 20

Predict the usual source of pulmonary emboli.

Back 20

Pulmonary emboli originate on the venous side (mostly from deep veins of the thigh) of the systemic circulation or in the right heart.

Front 21

Describe the changes in veins that lead to create varicose veins.

Back 21

Vein has pooled blood (accumulation in parts of venous system), producing distended, tortuous, and palpable vessels. Increase hydrostatic pressure leaks and causes interstitial edema

Front 22

22. Describe the pathologic processes in the coronary arteries that lead to myocardial infarction.

Back 22

CELLULAR INJURY>CELLULAR DEATH>STRUCTURAL AND FUNCTIONAL CHANGES>REPAIR


Cellular injury occurs with ischemia for about 20 mins before cellular death takes place. After 30-60sec of hypoxia, the electrocardiographic changes show. Coronaries get clogged up and pressure volume is involved in left ventricle, pulmonary venous congestion ensues; if right ventricle is ischemic, increases in systemic venous pressures occur. Structural and functional changes of cardiac tissues are results of myocardial infarction. Myocyte necrosis

Front 23

23. Identify the risk factors that are responsible for a 2-3 fold increase in the coronary artery disease.

Back 23

Hypertension, hypercholesterolemia, cigarette smoking
Nonmodifiable: advanced age, male gender or women after menopause, and family history
Modifiable: dyslipidemia, hypertension, cigarette smoking, diabetes and insulin resistance, obesity, sedentary lifestyle and atherogenic diet

Front 24

24. Identify the serum lipoprotein that is protective or preventive for the development of atherosclerosis.

Back 24

High HDL or Low LDL

Front 25

Identify the lab test that is an indirect measure of atherosclerotic plaque.

Back 25

C-reactive Protein

Front 26

26. Diagnose myocardial infarctions based on the elevated levels of laboratory indices such as troponin, creatine kinase and lactic dehydrogenase, i.e., how do the levels of these change in the blood.

Back 26

These indices determine MI and its severity. Acute myocardial infarction has occurred if abnormally high levels are found in the blood drawn. Other health conditions may also increase these lab indices.

Front 27

Identify the clinical manifestations of acute pericarditis.

Back 27

Caused by viruses or is idiopathic. Also can be caused by myocardial infarction, uremia, cardiac surgery, some medications, and autoimmune disorders. Indicators or signs include low-grade intermittent fever, dyspnea/tachypnea (a frequent complaint and may be severe with myocarditis, pericarditis, and tamponade), cough, and dysphagia. In tuberculous pericarditis, fever, night sweats, and weight loss were commonly noted (80%)

Front 28

Identify the clinical manifestations of aortic stenosis.

Back 28

signs include Decresed stroke volume, reduced systolic blood pressure, and narrowed pulse pressure. Heart rate is often slow, and pulses are faint.
Now most common valvular abnormality, affecting nearly 2% audlts 65+ yrs old. 3 common causes: congenital bicuspid valve, degeneration with aging and inflammatory damage caused by rheumatic heart disease. Degeneration of aortic valve with aging is associated w/ lipoprotein deposition in the tissue with chronic inflammation and leaflet calcification. Orifice of aortic semilunar valve narrows, causing diminished blood flow from left ventricle into aorta. Outflow obstruction increases pressure within left ventricle as it tries to eject blood through narrow opening.

Front 29

29. Identify the common cause of infective endocarditis.

Back 29

Bacteria including S. aureus, S. epidermis, and group A ß-hemolytic streptococci.

Front 30

Relate primary pulmonary hypertension to the resultant heart failure.

Back 30

Pulmonary hypertension is a rare lung disorder in which the arteries that carry blood from the heart to the lungs become narrowed, making it difficult for blood to flow through the vessels. As a result, the blood pressure in these arteries -- called pulmonary arteries -- rises far above normal levels. This abnormally high pressure strains the right ventricle of the heart, causing it to expand in size. Overworked and enlarged, the right ventricle gradually becomes weaker and loses its ability to pump enough blood to the lungs. This could lead to the development of right heart failure.

Front 31

Differentiate atherosclerosis from arteriosclerosis.

Back 31

Atherosclerosis is the most common form of arteriosclerosis. Arteriosclerosis is characterized by soft deposits of intra-arterial fat and fibrin in the vessel walls that harden over time.

Front 32

32. Correctly predict the prognosis or outcome of aortic aneurysm.

Back 32

An aneurysm that impairs flow to an extremity causes symptoms of ischemia
The outlook for an untreated abdominal aortic aneurysm depends on its size. An abdominal aortic aneurysm larger than 7 centimeters in diameter has a 75% chance of rupturing within 5 years. At 6 centimeters, the risk of rupture is 35% over 5 years. Between 5.0 and 5.9 centimeters, the rupture risk is about 25% over 5 years. The risk of rupture is much lower for aneurysms smaller than 5 centimeters (2 inches).

Front 33

33. Describe the complications of myocardial infarctions.

Back 33

The number and severity of post-infarction complications depend on the location and extent of necrosis, the individual’s physiologic condition before the infarction and the avalibility of swift therapeudic intervention. Risk factor for sudden death are: ischemia, left ventricular dysfunction, and electrical instability.

Front 34

34. Correctly predict which type of heart failure is best tolerated by the body, chronic or acute.

Back 34

Chronic.

Front 35

35. Describe the pathologic alteration that occurs in the left ventricle leading to left heart failure.

Back 35

Atrium cant empty out (more blood coming in) no contraction, decrease blood flow to ventricle and failure

Front 36

36. Describe the response of the pulmonary system to left heart failure.

Back 36

Overexert itself (like cumming to the point of empty)
There is a systolic and diastolic heart failure.

Front 37

37. Correctly predict the effect of left ventricular failure on the systemic blood circulation.

Back 37

Inadequate perfusion, low blood pressure

Front 38

38. Describe the pathological alterations that happen to the left atrium as a result of left ventricular failure.

Back 38

Hypertrophy of atrium

Front 39

39. Describe the pathological process in the coronary arteries that leads to myocardial ischemia.

Back 39

Insufficient blood flow to heart and supply myocardial cells. Causes coronary atherosclerosis

Front 40

40. Predict the general clinical manifestations of chronic right heart failure.

Back 40

Can result from left heart failure when increase in left ventricular filling pressure is reflected back into the pulmonary circulation. As pressure in pulmonary circulation rises, resistance to right ventricular emptying increases, being poorly prepared to compensate the afterload causing dilation and failure. Pressure will rise in systemic venous circulation resulting in peripheral edema and hepatosplenomegaly. Myocardial infarction, cardiomyopathies, and pulmonic valvular disease interfere with right ventricular contractility and can lead to right heart failure. Usually right heart failure comes after left heart failure. COPD

Front 41

41. Describe the linkage between myocardial ischemia and chest pain.

Back 41

Reversible myocardial ischemia chronic coronary obstruction results in recurrent predictable chest pain aka stable angina. Angina is caused by myocardial ischemia, the discomfort is due to the developed infarctions from ischemia.

Front 42

42. Differentiate stable angina from unstable angina.

Back 42

Stable Angina is a condition in which ischemic attacks occur at predictable frequencies and duration following activities increase myocardial oxygen demands, such as exercise and stress. Unstable Angina is a condition in which unprovoked ischemic attacks occur at unpredictable frequencies and may increase in severity, causing chest pain that is not relieved by rest.

Front 43

43. Predict the clinical outcome of sudden cessation of coronary blood flow to cardiac muscle.

Back 43

Cardiac arrest

Front 44

44. Describe the short-term pathologic processes (12-24 hours after) in the myocardium following an acute myocardial infarction.

Back 44

Prolonged ischemia causes irreversible damage to the heart muscle. Myocardial remodeling occurs after myocardial inflammation and necrosis. End with scar

Front 45

Identify the complications of ventricular infarctions.

Back 45

Pulmonary congestion, reduced myocardial contractility , abnormal heart jizz

Front 46

46. Identify the congenital heart defects that occur in trisomy 13, trisomy 18, and Down syndrome.

Back 46

Trisomy 13: Ventricular Septal Defect, Patent Ductus Arteriosus, Dextrocardia
Trisomy 18: Ventricular Septal Defect, Patent Ductus Arteriosus, Pulmonary Stenosis
Down Syndrome: Endocardial Cushion Defect, Ventricular Septal Defect

Front 47

47. Identify the two possible locations for coarctation of the aorta.

Back 47

ductus arteriosus, resulting in increased blood pressure proximal to head and upper extremities (defect) and decreased blood pressure distal to torso and lower extremities (obstruction)

Front 48

48. Describe the most likely clinical feature of patent ductus arteriosus?

Back 48

Infants may be aymptomatic or show signs of pulmonary overcirculation, such as dyspnea, fatigue, and poor feeding. Characteristic machinery-like murmur for aortic flow in to lower pressure pulmonary circulation produces low diastolic blood pressure, widened pulse pressure, and bounding pulses.

Front 49

50. Identify the elevated chemical compound in the blood that is used as a diagnostic marker of essential hypertension in children.

Back 49

aldosterone

Front 50

49. Identify the cardiac chamber from which aorta arises in children with transposition of the great vessels.

Back 50

The positions of the pulmonary artery and the aorta are reversed. The aorta is connected to the right ventricle, so most of the blood returning to the heart from the body is pumped back out without first going to the lungs. The pulmonary artery is connected to the left ventricle, so most of the blood returning from the lungs goes back to the lungs again.