Max is a 60-year-old living in Iowa. For the 27 years, he has ...

[Mr.Thesaxman]

Max is a 60-year-old living in Iowa. For the 27 years, he has been working in the agricultural industry, particularly in the management of corn production.
 
  Recently he began to feel weak during work and tired easily. During the night he woke up sweating, and he often felt unusually warm during the day. Max was also surprised that, in spite of eating regularly, his weight was declining and his work pants were now too large for him. Upon physical examination, his physician noted his inguinal lymph nodes were swollen although Max said they were not sore. Subsequent laboratory tests confirmed follicular, non-Hodgkin lymphoma. Chemotherapy in conjunction with rituximab was immediately initiated.
 
  What are the key cellular differences between non-Hodgkin lymphoma and Hodgkin lymphoma?
 
  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?
 
  What are the pharmacologic properties of rituximab, and what is its mechanism of action on malignant cells?
 
  Outline the structure of lymph node parenchyma including the areas where B and T lymphocytes reside. Where did Max's lymphoma arise?

Question 2

Deborah is 56 years old, smokes half a pack of cigarettes a day, and is overweight. Her friend wants her to come to a local women's fitness class she attends to once a week.
 
  She knows Deborah's dad had died an acute myocardial infarction when he was 56, and she fears, seeing Deborah's lifestyle, the same fate awaits her friend. What she did not know was that Deborah had also been to her doctor for her annual physical where she was told her LDLs were 180 mg/dL, HDLs were 36 mg/dL, and cholesterol was 239 mg/dL.
 
  What are Deborah's known risk factors for coronary heart disease?
 
  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?
 
  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?
 
  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?

[nothere]

Answer to Question 1

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

Non-Hodgkin disease is multicentric in nature and often presents with painless, generalized lymphadenopathy with nonnodal concentration, or with several nodes involved. 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.

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

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.

Answer to Question 2

being overweight, smoking, family history of heart disease, and low serum HDL and high serum LDL levels.

An excessive caloric intake lowers HDL levels. Elevated serum cholesterol levels are affected not only by dietary intake of cholesterol but also by a diet high in saturated fats. Hypercholesterolemi a results in increased VLDL and LDL levels in the blood. 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.

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

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.
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.

[Mr.Thesaxman]

Excellent

[mcarey591]

TYSM