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Due to Pt.'s history of smoking, COPD, along with his sedentary lifestyle, we would expect that the pathogenic response to coagulation necrosis is due to the narrowing, thinning of membrane & obstruction of blood vessels. From a morphological standpoint, proteolysis & phagocytosis is prevented. This can result in a clinical presentation of damage to tissues supplied to these structures, particularly in the lungs and respiratory tract in addition to a greater risk of organ dysfunction including calcific valvular disease and atherosclerosis. Furthermore, research has examined potential links between HPV-18 and end stage kidney disease (ESKD). However, whether is due to a kidney infarct or not is still unclear.

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If we understand the risk of hypoxic hypoxia w/ association with COPD would decrease O2 in vital areas, in particular to the brain, We have learned that any or little timed episodes of no oxygen in the brain can lead to liquefaction necrosis. These would include a diet plan for  anti-inflammatory including leafy greens, cherries, fatty nuts. This would allow for reduced fatty acid oxidation. We can also encourage the patient to eat a diet rich with antioxidants and to work with their provider for COPD management such as bronchodilators.

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The risk for heart muscle hypertrophy increases with hypertension. Hypertension is caused by hypoxia and metabolic waste buildup as the body reacts to try to return to homeostasis. Hypertrophy is caused by the adaptations of the cell (increased organelles and protein structures) in an attempt to keep up with the increased workload, sedentary lifestyle, COPD, and Type II D all may contribute to increased blood pressure. We can focus our clinical recommendations on reducing oxygen stress, increasing blood flow, and eventually lowering BP exercise, diet, breathing.

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1.

a.     Etiology: smoking

b.     Pathogenesis: chronic physical and chemical irritation

c.     Morphological change: signal transduction to change gene expression which replaces normal columnar epithelium with squamous cells

d.     Tissue: respiratory tract

2.     COPD could also be linked to metaplasia due to airway restriction. Stenosis or narrowing of the respiratory tract could increase the rate of physical and chemical irritation from the smoke.

3.     The long-term effects of chronic irritation on the respiratory tract cells can increase the risk of irreversible dysplasia leading to cancer. Chronic physical irritants would also increase inflammation. We would recommend that the patient stop smoking as soon as possible and treat pain with an anti-inflammatory.

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If there is a perceived risk for abnormal epithelial growths such as genital warts and cervical cancer, a form of hyperplasia, increased with accelerated S phase transcription and synthesis and replication of DNA with HPV-18, then we can create a well-informed management plan that includes specific ways to regulate mitosis progression and cell division to prevent malignant progression to neoplasia. An ideal treatment would include slowing down mitosis/preventing S phase transcription and treating symptoms to avoid uncontrollable cancerous growth. If cancer occurs, treatment would change to radiation or drug therapy in order to prevent growth from metastisizing.

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If we understand that the risk for a weakened immune system, a form of extrinsic apoptosis, increases when cytotoxic lymphocytes induce apoptosis causing cell shrinkage and death then I can create a well-informed patient management plan that includes specific ways to boost the patient’s immune system to fight infection. From this knowledge, I may recommend antioxidants to boost their immune response, lower ROS, get all current vaccines & shots and explain to the patient how a healthy diet and cutting back on smoking can help heal the damage in their body.

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I understand that the risk of dystrophic calcification is increased by smoking and COPD causing saponification in our patient. This allows me to create a specific patient management plan that will combat the calcification, by recommending a decrease in smoking and an increase in aerobic exercise. There also may be metastatic calcification caused by sedentary lifestyle increasing bone resorption resulting in hypercalcemia.

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We understand that a result of the combination of all pathologies present in our patient, intrinsic apoptosis can occur. With knowledge of the risk of cytochrome c release resulting in activation of caspase-9, a consequence of intrinsic apoptosis, we can accurately give a suggestion to the patient to improve their conditions. By creating a diet plan with our patient as well as an exercise plan, we can decrease the mitochondrial membrane permeability and therefore decrease caspase-9 activity. With this knowledge we can recommend our patient to increase Omega-3 and decrease fatty carbohydrate intake to help decrease the rate of intrinsic apoptosis. Further, with our knowledge that outward symptoms of mitochondrial membrane permeability and cytochrome c release are not easily diagnosed, by educating our patient on the benefits of changing their exercise and diet we can help improve the patient’s quality of life in the long-term.

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Etiology- HPV

Pathogenesis- Viral infection causes an increase in immunoglobulin production, stimulating immune system to fight virus

Morphologic/molecular change- Russell bodies found in the plasma cells as rough endoplasmic reticulum is engorged due to high production of immunoglobulin

Tissue linked to presentation- Liver

Etiology- Diabetes

Pathogenesis- rapid increase in protein accumulation causes aggregation

Morphologic/molecular change- Russell bodies and resorption droplets in proximal tubules of kidneys

Tissue linked to presentation- Amyloidosis

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Type II diabetes increases the risk for gangrenous necrosis through the depletion of ATP, the shift to anerobic metabolism, and an accumulation of ROS. All of this would then lead to ischemia of peripheral cells leading to things like diabetic foot, which would be a multi-tissue layer necrosis. Wet gangrene, common in diabetic foot, may be accompanied with liquidfactive necrosis. Additionally, the sedentary lifestyle of the patient could be contributing to the ischemia. Diet changes or supplements that include anti-oxidants as well as a more active lifestyle could benefit this patient.