case studies

Question 1

1. What are the therapeutic advantages of an autologous stem cell transplant on Charlie’s bone marrow and immune system?
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Answer 1

1. Stem cells are self-renewing and are able to continually proliferate.
2. Removing these healthy cells before intensive chemotherapy or radiation therapy allows them to regenerate and repair damaged bone marrow once they are returned to the body.
3. Using an autologous transplant maintains histocompatibility with the host.

Question 2

2. Before harvesting stem cells, a cytokine growth factor is administered to the patient. What is the benefit of this procedure?
   2

Answer 2

1. The cytokine growth factor promotes the proliferation of stem cells and their migration from bone marrow.
2. This provides more cells for rescue before the surgery and for later transplantation.

Question 3

3. Non-Hodgkin lymphoma is a disease involving B and T lymphocytes. What aspects of the immune response are these cells responsible for?
   2

Answer 3

1. B lymphocytes are responsible for humoral-mediated immunity, and
2. T lymphocytes are responsible for cell-mediated immunity.

Question 4

4. When considering erythrocytes, how is the body able to meet hematopoietic demand in conditions such as hemolytic anemia or blood loss?
   3

Answer 4

1. Erythropoietin (EPO) is the cytokine responsible for triggering erythrocyte production.
2. With persistent hemolysis or blood loss, there is resubstitution of red bone marrow for yellow.
3. The spleen and liver can also participate in RBC production.

Question 5

1. Explain, using your knowledge of hypercoagulability, why the trip to Australia contributed to Leona’s DVT? Why was Leona already at risk for thrombus development?
   4

Answer 5

1. immobile.
2. Stasis leads to an accumulation of activated clotting factors and platelets.
3. Immobility also decreases chemical interactions with coagulation inhibitors. The end result is an increased risk for thrombus formation.
4. In Leona’s situation, her weight and smoking habit were additional risk factors for the condition.

Question 6

2. How does Leona’s atherosclerosis affect platelet function? Conversely, what is the effect of increased platelet activity on the development of atherosclerosis?
   2 and 1

Answer 6

1. Atherosclerosis disturbs the flow of blood and damages vessel endothelium causing an increase in platelet adherence.
2. There is also an increased sensitivity by platelets to factors that cause adhesiveness and aggregation.

1.Adhering platelets release growth factors that enhance smooth muscle proliferation in the vessel wall.

Question 7

3. How do atherosclerosis and immobility promote changes in blood coagulation?
   2

Answer 7

1. Both conditions increase coagulability. Atherosclerosis increases platelet function by encouraging aggregation and adherence.
2. Immobility, in contrast, contributes to hypercoagulability by increasing procoagulation factors.

Question 8

4. When Leona was in hospital, she received heparin therapy. Explain why this course of action was taken to treat her DVT. Why was she not given heparin tablets to take back to the hotel with her?
   2

Answer 8

1. Heparin effectively encourages the inactivation of clotting factors, thereby inhibiting fibrin formation.
2. Heparin cannot be absorbed through the gastrointestinal system and can only be administered by injection or IV infusion.

Question 9

1. From what you know of Henry’s history, what type of anemia do you suspect he has? How would Henry’s red blood cells appear on a peripheral blood smear?
   2????

Answer 9

1. Henry has anemia of deficient red blood cell production as a result of his chronic renal failure. The chronic renal failure causes a reduction in erythropoietin production. Furthermore, increased serum levels of nitrogen and uremic toxins interfere with erythropoietin activity and red blood cell survival.
2. On a smear, the red blood cells would appear normocytic and normochromic.

Question 10

2. What is the physiological basis that would explain why Henry’s anemia would cause him to have the symptoms he is experiencing?
   2

Answer 10

1. decrease in circulating erythrocytes and oxygen-carrying capacity of the blood. As a result, tissue hypoxia ensues and creates the symptoms of weakness, fatigue, and dyspnea.
2. Central nervous system hypoxia leads to headaches and dizziness. In the elderly individual, cognitive impairment and depression are also indications of hypoxic change in the central nervous system.

Question 11

3. Predict the cellular adaptations erythrocytes undergo when chronic hypoxia is present. How would this be evident on an oxygen–hemoglobin dissociation curve?
   3

Answer 11

1.There is an increased production of 2,3-DPG by erythrocytes in an attempt to lower hemoglobin affinity with oxygen.
2,The result is that oxygen is more readily released by red blood cells at areas where it is needed most.
3.This is evidenced by a shift to the right on the oxygen–hemoglobin dissociation curve.

Question 12

1. What are the key cellular differences between non-Hodgkin lymphoma and Hodgkin lymphoma?

Answer 12

1. In non-Hodgkin disease, there is a malignant transformation of either B or T lymphocytes.
2. The key feature of Hodgkin disease is the presence of the Reed-Sternberg cell—a cell not found in non-Hodgkin disease.

Question 13

2. The early manifestations of non-Hodgkin lymphoma and Hodgkin lymphoma in lymphatic tissue appear differently. In terms of lymphatic presentation, how would these two diseases appear clinically?
   2.

Answer 13

1. Non-Hodgkin disease is multicentric in nature and often presents with painless, generalized lymphadenopathy with nonnodal concentration, or with several nodes involved.
2. Hodgkin disease begins as a single enlarged node or within a local group. Typically HL begins in nodes above the diaphragm in the younger population. In elderly individuals, it may initially present in nodes below the diaphragm.

Question 14

3. What are the pharmacologic properties of rituximab, and what is its mechanism of action on malignant cells?

Answer 14

1. Rituximab is a pharmaceutic monoclonal antibody (MOA).
2. It acts by recognizing and binding to the CD20 antigen found on the majority of B-cell lymphomas.
3. After binding, the toxic effect of the MOA destroys the malignant cell.

Question 15

4. Outline the structure of lymph node parenchyma including the areas where B and T lymphocytes reside. Where did Max’s lymphoma arise?
   ?????

Answer 15

The parenchyma consists of a cortex, paracortex, and medulla. In the cortex, B cells are found in the primary follicles and secondary follicles. Within the secondary follicles are immunologically active germinal centers. B cells also surround the germinal centers in regions called mantle zones. T cells are also present in lymph nodes and are concentrated in the in the deeper region of the cortex known as the paracortex.
Max’s follicular lymphoma involved the centroblasts and centrocytes in the germinal centers of the lymph nodes.

Question 16

1. Prolonged bed rest decreases plasma levels and vasomotor tone, which can both lead to orthostatic hypotension. How do changes in vascular resistance and radius affect blood flow? Assuming Bertha is otherwise healthy, how does her heart activity change in an attempt to compensate for the orthostatic hypotension she experienced?
   3

Answer 16

1. According to the law of Laplace, the greater the pressure change between two ends of a vessel, the greater the blood flow. A weaker pressure differential decreases blood flow.
2. A very small change in vessel radius has a powerful effect on the movement of blood, and the relationship is inversely proportional: a decrease in vessel radius increases blood flow, and an increased radius decreases flow.
3. Because blood flow is determined by PVR and CO, Bertha’s heart rate (and therefore CO) would increase to compensate for the hypotension she experienced when she stood up.

Question 17

2. Considering the venous circulation, how is blood from the lower extremities returned to the heart?
   4

Answer 17

1. Venous circulation is maintained by a variety of mechanisms.
   2.Valves exist in the veins of the lower extremities to resist retrograde flow and pooling.
   3.Skeletal muscle lies in close proximity to veins and helps to move venous blood.
   4.
   Finally, low intrathoracic and intra-abdominal pressures assist to “pull” venous blood from the lower extremities to the heart.

Question 18

3. Why did Bertha’s capillary fluid pressure (or hydrostatic pressure) change when she moved from a lying to standing position?
   2

Answer 18

1. Capillary fluid pressure (or hydrostatic pressure) is influenced by gravity and is increased by the weight of blood in the vascular column during standing.
2. When recumbent, blood vessels lie at the level of the heart, and hydrostatic pressure is therefore low.

Question 19

1. What are Deborah’s known risk factors for coronary heart disease?

Answer 19

Deborah’s risk factors for coronary heart disease are age (over 55 years old), being overweight, smoking, family history of heart disease, and low serum HDL and high serum LDL levels.

Question 20

2. Deborah’s doctor referred her to a dietician for strict dietary therapy, hoping the intervention would raise her HDL and lower her LDL and cholesterol levels. Why is diet modification necessary to control and moderate the lipids indicated?
   4.

Answer 20

1. An excessive caloric intake lowers HDL levels.
2. Elevated serum cholesterol levels are affected not only by dietary intake of cholesterol but also by a diet high in saturated fats.
3. Hypercholesterolemia results in increased VLDL and LDL levels in the blood.
4. Trans fat is emerging as the most potent atherogenic lipid, and limiting dietary levels of this fat is important in managing the at-risk patient.

Question 21

3. Deborah’s doctor also gave her pamphlets describing strategies to stop smoking and a list of exercise ideas she might want to try. How is smoking thought to contribute to atherosclerotic plaque formation? Why would exercise have a positive effect on Deborah’s lipid profile?
   3 and 2

Answer 21

1. Smoking is thought to contribute to oxidative processes in the lumen of vessels and consequent damage to the endothelium.
2. Furthermore, smoking is thought to magnify endothelial dysfunction when it is already present in predisposed individuals.
3. Finally, smoking decreases circulating levels of HDL. 1.Unlike smoking, exercise increases serum HDL levels. High levels of HDL are inversely related to the development of atherosclerosis and coronary artery disease. they clear cholesterol from atheromatous plaques and move them to the liver for excretion from the body.
4. It is believed they also inhibit the cellular uptake of LDL.

Question 22

4. Atherosclerosis is thought to be an inflammatory disorder. What is the role of macrophages in the formation of atherosclerotic plaques? What is the significance of elevated serum hs-CRP levels in at-risk individuals?2

Answer 22

1. Monocytes migrate to the subendothelial space in blood vessels and become macrophages. Once activated, macrophages release free radicals to oxidize LDL. Oxidized LDL subsequently destroys endothelial tissue. Macrophages also ingest oxidized LDL and form foam cells, a feature common to all atherosclerotic changes. Finally, macrophages promote the proliferation of smooth muscle cells and the deposition of the extracellular matrix at the lesion site.
2. Elevated levels of hs-CRP (a protein involved in the acute-phase inflammatory response) indicate systemic inflammation. It is now considered a major risk factor marker for cardiovascular disease.

Question 23

1. The ECG taken by the paramedics showed Jack was experiencing premature ventricular contractions. In general terms, how do PVCs appear on an ECG? What factors contributed to the onset of PVCs in Jack’s situation?
   4

Answer 23

1.Premature ventricular contractions present with normal beats interspersed by distorted QRS complexes. The PVCs in Jack’s situation may have been triggered by the increased
2.physical activity that generated an increased sympathetic response and heart rate.
3The coffee might have acted as an additional sympathetic stimulant.
4.Finally, his history of previous cardiac events can be a predisposing factor to arrhythmia.

Question 24

Describe the physiologic events in PVC. How is cardiac output disrupted with the presence of PVCs?
4

Answer 24

1. A premature ventricular contraction begins with an electrical event by a ventricular ectopic pacemaker. 2.Because of the ectopic beat, the ventricles are unable to complete repolarization before the next SA impulse. 3.The result is a delay, or compensatory pause, in ventricular systole.
2. PVCs cause a decrease in diastolic filling and therefore a reduction in cardiac output.

Question 25

3. Because of Jack’s history, his PVCs leave him at risk for events such as ventricular tachycardia or ventricular fibrillation. Compare and contrast these two arrhythmias. Why are they particularly dangerous? 3 ND 1 and 3

Answer 25

1. Ventricular tachycardia originates within the conduction system and/or the muscles of the ventricular wall. 2. It involves abnormal QRS complexes on the electrocardiograph and a heart rate falling within 70 to 250 beats/minute. 3. It may be sustained or may spontaneously rectify itself. 1. Ventricular fibrillation creates a series of sine-wave patterns on the electrocardiograph and involves a “quivering” of the ventricular walls instead of contraction. 1Ventricular tachycardia is clinically significant because it inhibits the proper function of the atrial pacemaker and 2.decreases the diastolic filling time. 3. With ventricular fibrillation, cardiac output and pulses are nonexistent.

Question 26

1. Why is Milo presenting with pallor, diaphoresis, and restlessness? 3

Answer 26

1.Hypovolemia creates a sympathetic response in the body in an attempt to maintain homeostasis in the presence of fluid los.. 2, Increased sympathetic activity stimulates sweat gland activity and generates restlessness. 3.The sympathetic response also causes vasoconstriction of the dermal vasculature. In concert with a decline in red blood cells, the skin and mucous membranes appear pale as a result.

Question 27

2. In spite of his blood loss, Milo’s blood pressure was only slightly affected when the paramedics first found him. Describe how cardiovascular compensatory mechanisms serve to maintain homeostasis as long as possible in the early stages of shock. How does ADH contribute to compensation? 3 and 2

Answer 27

1. The heart, under sympathetic influence, beats faster and with greater contractility as a means to maintain homeostasis in the presence of fluid loss. 2. Arteriolar constriction occurs to ensure systemic resistance, while venous constriction ensures venous return to the heart. 3. An added benefit of venous constriction is the movement of blood that has been stored in the capacitance portion of the circulation. 1. Fluid loss also stimulates the release of ADH from the posterior pituitary. ADH stimulates thirst centers in the hypothalamus and assists in the generation of peripheral vasoconstriction. 2. It also has a strong effect on the kidneys and stimulates water resorption by renal tubules.

Question 28

3. What are the disadvantages of prolonged vasoconstriction in hypovolemic shock?

Answer 28

Prolonged vasoconstriction, however, limits tissue perfusion and oxygenation. Tissue cells revert to anaerobic metabolism, which over time leads to lactic acid production and cellular damage.

Question 29

4. If Milo’s respirations were to become progressively deeper and more rapid, what physiological changes in the body would that indicate? 2

Answer 29

1. metabolic acidosis, a result of the shift from aerobic to anaerobic cellular respiration. 2. A decrease in the oxygen-carrying capacity of the blood (due to volume loss) is an additional factor for the alteration in ventilation.