Friday, October 21, 2011

pumpkin-ing

pumpkin roasting, pumpkin pureeing, pumpkin ice cream...and so much more! :)
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gunkpumpkin ice creampumpkin ice creampumpkin ice creampumpkin seedspumpkin ice cream
pumpkin ice creampumpkin skinspumpkin pureepumpkin roastingpumpkin roastingpumpkin roasting
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Monday, October 17, 2011

pumpkin roasting

pumpkin roasting by meredith lynn hunt
    The picture above reminds me of diorama projects from elementary school. i know we used shoe boxes instead of a freshly split open pumpkin, but for some reason this pumpkin looks perfect for having little paper fish floating side it with twine and elmers glue.
    About two hours after this picture was taken, this pumpkin essentially turned into the texture of baby food. It was used to make pumpkin ice cream. And will be used to make pumpkin pie, pumpkin bread, and something else pumpkin that I can't think of right now.
Happy October!

Monday, October 10, 2011

Margarita Monday

a lynchburg church by meredith lynn hunt

This is my fourth time watching You've Got Mail with Meg Ryan and Tom Hanks in the past three days. I bought the movie a few days ago for four dollars. And for some reason I keep watching it.

Today my dog never left my side. We woke up together, had tea together, went back to bed together, woke up again together, had lunch together, went on a walk together, bought pumpkins together, did homework together, and now we are watching You've Got Mail together while drinking Margaritas.

*The picture above is of a church/castle I saw in Lynchburg, VA last week while I was visiting.

Wednesday, September 28, 2011

Some friends

Escot Farms Weekend by meredith lynn hunt

Today was endless listening day.
I'm going to the East Coast on Sunday.
I'm stoaked.

Thursday, September 22, 2011

Nursing Program

Untitled by meredith lynn hunt
I decided that if I don't get into an Nursing Program in the next year and a half, I'm getting my sheep farm. My farm will be by a beautiful river, so I can go fishing or swimming sometimes. Sheep Farm will include: sheep, goats, chickens, a brown cow, alpacas, french angora rabbits, a bee hive, a puppy, a kitten, a little pig (to eat the kitchen garbage), a huge vegetable and flower garden, and a few fruit trees.You can come visit if you want and I'll give you homemade yarn and homegrown food. So I guess just it's not a sheep farm, but merely a farm with sheep.. but the sheep on my farm will be top notch. With loads of crimp per inch in all their fiber (more crimp means softer wool). I guess you don't just start a farm..you need money. So I guess I'll need to win the lottery first or something. So I guess I'll need to buy a lottery ticket or something.

On second thought, maybe there's too much going on on my future sheep farm..I should probably cut back on some things/animals to make it a little less daunting on myself.

Saturday, September 17, 2011

ME? Published?

This photo of mine up above might be published in a Portland Guide! I'm so excited! So excited that I'll share a paper I just wrote about HIV/AIDS! Whoo..




HIV/AIDS: Pathophysiology,
Clinical Manifestations, Nursing Interventions, and
Implications for Nursing Practice
Meredith L. Hunt




Abstract
This paper explores the how’s and why’s of human immune deficiency virus (HIV) and acquired immunodeficiency syndrome (AIDS) from research conducted through the textbook written by Huether and McCance. The symptoms and clinical manifestations of HIV/AIDS are discussed along with the treatments that should be administered for the infected individual. This paper incorporates the importance of a nurse and what the job and responsibility of a nurse might be in the time of treating an individual with an immunity deficiency. The paper ends with not only different treatments of HIV/AIDS a nurse could administer to the patient, but also the preventative care that could be given to individuals that do not have the disease.





HIV/AIDS: Pathophysiology, Clinical Manifestations, Nursing Interventions, and Implications for Nursing Practice
         Acquired immunodeficiency syndrome (AIDS) is a disease that occurs after the immune system is suppressed by HIV, or human immune deficiency (Heuther, S., E., & McCance, K., L., 2008). The human immune deficiency virus gets a hold of the helper T cells. This disrupts the growth and development of both the cytotoxic T cells and the plasma cells. Since HIV is suppressing the human's immunal defenses against itself, ultimately pathogens and opportunistic mircoorganisms are left to develop AIDS. HIV is a member of a family of viruses, which carry genetic information in the form of RNA instead of DNA (Heuther, S., E., & McCance, K., L., 2008). What happens to the genetic material from a retrovirus is that a RNA strand is converted into a DNA strand and put into the infected cell’s genetic material to remain dormant until the cell is activated (Heuther, S., E., & McCance, K., L., 2008). There is a possibility that the cell could remain dormant for years and that the HIV particles will not shed from the infected cell for the amount of time the cell remains dormant. When the cell is activated, then new virions form, the cell dies, and dead cell then sheds the HIV particles. The most common surface receptor on HIV is the envelope protein gp120, this envelope protein binds to the molecule CD4 on the surface of helper T cells (Heuther, S., E., & McCance, K., L., 2008). The decrease in CD4+ cells causes a decrease in response to a wide array of infectious pathogens and malignant tumors (Heuther, S., E., & McCance, K., L., 2008).
         The clinical manifestations of HIV can be unclear. The HIV infected person could have antibodies present for fighting off the HIV, or the infected person could also not have antibodies present. The infected person could be asymptomatic in early stages of HIV (Heuther, S., E., & McCance, K., L., 2008). A person’s infected cells could be dormant for over a year without showing any symptoms of infection from sexual transmission infection, however, the virus may be still be growing. The actions of antibodies are different from an infection through blood products versus an infection through sexual transmission. The current accepted definition of AIDS relies on both laboratory tests and clinical symptoms (Heuther, S., E., & McCance, K., L., 2008). The early stages of HIV disease the symptoms are mild, for example: night sweats, swollen lymph glands, diarrhea, and/or fatigue (Heuther, S., E., & McCance, K., L., 2008). If antibodies are present in the laboratory results, the clinical symptoms and lab results are both used to diagnose the individual with AIDS. The acknowledgment of a decrease in CD4+ T cells numbers is a big indicator of a case of AIDS (Heuther, S., E., & McCance, K., L., 2008).
         The treatment for HIV infection is a combination of drugs, called highly active antiretroviral therapy (HAART) (Heuther, S., E., & McCance, K., L., 2008). This drug has inhibitors of reverse transcriptase and of the viral protease (Heuther, S., E., & McCance, K., L., 2008). HAART has been effective saving many lives from AIDS-related diseases (Heuther, S., E., & McCance, K., L., 2008). Also, along with HAART being an effective drug against HIV, vaccine development is good to prevent initial infection. While caring for patients with immune deficiencies, ordinary ways of immunization may not be the best way help the individual. The evaluation of an individual having reoccurring and uncontrolled infections generally means the diagnosis of HIV. Important information on the specific immune deficiency can be gathered by taking note of certain characteristics of the individual, including the presence of any associated anomalies, age, gender, the types of infections (bacterial, viral, or fungal, and the specific microorganisms involved), family history, and risk factors associated with secondary immune deficiencies (Heuther, S., E., & McCance, K., L., 2008). The different tests available to evaluate specific immune deficiencies can test the complete blood count or test for the antibody production. Perhaps all that is needed for the immune system to begin functioning fully again is a replacement of whatever component is missing. For example, B cell deficiencies call for an administration of gamma globulins, or another example, a replacement of stem cells can treat lymphoid cell development deficiencies (Heuther, S., E., & McCance, K., L., 2008).
         Seeing all the choices of treatment for HIV/AIDS and immunity deficiencies, nurses have from a variety to choose which treatment would be the most effective for the infected individual. Whether it is drug like HAART, or it is a replacement therapy like administrating gamma globulins, nurses are able to treat their patients with effective treatment that have a great chance of overcoming this detrimental disease of immunity deficiency. Perhaps a great preventative treatment would be educating people who do not yet have the immunity deficiency disease. To educate people about safe sex, about sanitation, and about the risks of what could happen to them if they were to get HIV would be beneficial for an unaware individual. Many of the higher risks of HIV transmission are associated with sexual practices with no condom usage, so another common practice for nurses along with safe sex education would be to encourage sexually active people to use condoms while having sex.




Reference
Huether, S.E., Mccane, K.I. (2008). Understanding Pathophysiology (4th edition, pp. 198-205). St Louis, MI: Mosby Inc.

Degenerative Disorders of the Spine

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Spinal CordSpinal Cord
 (Photos of a Human Spinal Cord)


Degenerative Disorders of the Spine

          People in their 30’s or older are more subject to Degenerative disk disease (DDD), due to aging. Inheriting a variation gene for the cartilage intermediate layer protein (CILP) may increase a person’s chances for lumbar disk disease. As biochemical and biomechanical changes occur, disease begins. The different pathologic problems that have been found in Degenerative disk disease are: disk protrusion, spondylolysis, subluxation (spondylolisthesis), degeneration of vertebrae, and spinal stenosis (Heuther, S., E., & McCance, K., L., 2008).
          Spondylolysis is the developmental defect of the spine involving the lamina or neural arch of the vertebra (Heuther, S., E., & McCance, K., L., 2008). The lumbar section of the spine is mostly affected in between the superior and inferior articular facets. Heredity is a major factor because spondylolysis is associated with an incrased incidence of other congenital spinal defects. The symptoms that occur are pain in the lower back and in the lower limb (Heuther, S., E., & McCance, K., L., 2008).
         Spondylolisthesis happens when a vertebra slides forward in relation to he vertebra below and may include a fracture of the pars interarticularis, which happens at the L5-S1 (Heuther, S., E., & McCance, K., L., 2008). The amount of slip the vertebra does is graded from 1 to 4, based on less slip to more slip. Grades 1 and 2 are mostly just managed symptomactically and nonsurgically. Grades 3 and 4 require decompression, stabilization, and sometimes both (Heuther, S., E., & McCance, K., L., 2008).
         Spinal stenosis is a narrowing of the spinal canal that causes pressure on the spinal nerves or cord and can be congenital or acquired (more common) and associated with trauma or arthritis (Heuther, S., E., & McCance, K., L., 2008). The lumbar and cervical spine are the most affected areas in spinal stenosis. Acquired conditions can be: bulging disk, facet hypertrophy, or a thick ossified posterior longitudinal ligament. Symptoms include: pain, numbness, and tingling in the legs. For people with chroninc symptoms and those who don’t respond to medical management, surgical decompression is in order.
         Lower back pain affects the area between the lower rib cage and gluteal muscles and often radiates into the thighs (Heuther, S., E., & McCance, K., L., 2008). Most cases there is no exact diagnosis but the things that can be involved in causing the pain are: tumors, disk prolaps, bursitis, synovitis, rising venous and tissue pressure, abnormal bone pressures, problems with spinal mobility, inflammation caused by infection, bony factures, or ligamentous sprains to pain referred from viscera or the posterior peritoneum (Heuther, S., E., & McCance, K., L., 2008). Some of the most common causes of low back pain is lumbar disk herniation, degenerative disk disease, spondylolysis, spondylolisthesis, and spinal stenosis. The treatment for low back pain can be diagnosed based on physical exampination, electromyelograhy, CT with or without myelography, MRI, nerve conduction studies, diskography, and epidurography (Heuther, S., E., & McCance, K., L., 2008). Most people’s conditions improve wit bed rest, analgesic medications, exercise, physical therapy, and education (Heuther, S., E., & McCance, K., L., 2008). Also anti-inflammatory and muscle relaxant medications can be given to relieve pain from lower back. Aerobic exercises are also an effective treatment.
        Herniated intervertebral disk is a protrusion of part of the nucleus pulposus through a tear in the posterior rim of the annulus fibrous (the fibrous capsule enclosing the genlatinour center of a disk) (Heuther, S., E., & McCance, K., L., 2008). The rupture of an intervertebral disk is usually caused by trauma, degenerative disk disease, or both (Heuther, S., E., & McCance, K., L., 2008). In a herniated disk, the ligament and posterior capsule of the disk are usually torn, allowing the gelatinous material (the nucleus pulposus) to extrude and compress the nerve root (Heuther, S., E., & McCance, K., L., 2008). Large amounts of extruded nucleus pulposus or complete disk herniation may compress the spinal cord (Heuther, S., E., & McCance, K., L., 2008). The location and size of the herniation into the spinal canal, together with the amount of space in the canal, determine the clinical manifestations associated with the injury. A herniated disk in the lumbosacral area is associated with pain that radiates along the sciatic nerve course over the buttock and into the calf or ankle. Pain happens with straining, for example: coughing and sneezing, and usually on straight leg raising. The diagnosis of a herniated intervertebral disk is made throught the history and physical examination, spinal x-ray films, electromyelography, CT scan, MRI, myelography, discography, and nerve conduction studies (Heuther, S., E., & McCance, K., L., 2008). Different therapies are available. The approach without surgery involves: no traction, bed rest, heat and ice to the affected areas, and an effective anti-inflammatory analgesic regimen. The surgical approach is used if there is severe compression (weakness or decreased deep tedon, bladder, or bowel reflexes) or if the non-surgical attempts are unsuccessful (Heuther, S., E., & McCance, K., L., 2008).

Reference

Huether, S.E., Mccane, K.I. (2008). Understanding Pathophysiology (4th edition). St Louis, MI: Mosby Inc.

Sunday, September 11, 2011

Mistakes

You live and learn, but do you have to live it to learn it? No, otherwise we'd all be cocaine addicts, or recovering cocaine addicts.

Thursday, September 8, 2011

funny dog

couldn't make it one more foot apparently.. by water your plants
a photo by water your plants on Flickr.
Woke up to my dog sleeping on the pillows that were on the floor next to my bed. I thought it was funny. I think I remember her barking to have me pick her up and put her on my bed, but I didn't want to move so I guess this was the next best thing.

Saturday, September 3, 2011

http://smittenkitchen.com/

by the way, look at this blog. i love how dark and blue all the pictures are. good night.

You try to help and they end up helping you

Today I moved back to where I grew up. It's now where I recognize nothing but the street signs and no one but the barista. I'm doing online classes so I literally could just stay at home and never leave the house for the next seven months. My parents do the grocery shopping and there is a big, red exercise ball in the living room that I can use to preserve my muscles while I study. I'm tired. This is a picture of me having fun after the last four hours of watching my professor lecture to me online (taken about 10 minutes ago). I'm so tired I'm going to bed.

The title of this post was a story I was going to tell, but I'm too tired to tell it now.

Tuesday, August 30, 2011

This is me

This is me going to sleep too late.
And waking up too early.

Please let me wake up on time so I'm not late for work

6:30 in the morning

I still don't get why Humboldt needs sushi at 6:30 AM on Tuesdays.
I certainly don't.

Thursday, August 25, 2011

The Genetic Basis of Cancer

the banjo i sold by water your plants

Cancer is caused by mutations in Genes. Cancer is mostly a disease for the aging due to an increased number of genetic mutations over time. When clonal proliferation occurs, a single cell with a mutation has an increase growth rate as well as a decreased death rate. With a faster accumulation of this specific mutated cell, it could become an early stage of a tumor. With more and more of the mutated cell, a normal to fully malignant cancer can develop.

There are different types of Gene Mutations in Cancer such as: alteration of progrowth and antigrowth signals, angiogenesis, and telomeres and immortality. For a cancer cell to become fully malignant the cell must be able to grow without needing external growth signals. Some cells stimulate their own growth with autocrine stimulation and some cancers increase their growth factor receptors. Many cancers have an activating mutation in their ras, or their intracellular signaling protein. This 'mutant ras' stimulates growth even when growth factors are lacking. The antigrowth signal must be inactivated in cancer as well as being able to grow without growth factors. Advanced cancers must overcome apoptosis by disabling the self-destructing mechanism. To maintain an advanced cancer or grow a small cancer, angiogenesis is needed. Angiogenesis is the development of blood vessels in order to deliver oxygen and nutrients. Telomeres and immortality is another component to gene mutation in cancer. Cancer cells somehow activate telomerase to restore and maintain there telomeres, protect their chromosomes, and sometimes develop the ability to divide repeatedly.

Oncogenes are mutant genes that in their normal non-mutant state direct synthesis of proteins that positively (accelerate) regulate proliferation. Tumor-suppressor genes encode proteins that are in their normal state negatively (put the brakes on) regulate proliferation. Mutations that create oncogenes are: point mutations, chromosome translocations, and chromosome amplification. A point mutation is the alteration of one or a few nucleotide base pairs. Chromosome translocations can activate oncogenes by either causing an excess and inappropriate production of a proliferation factor or by leading to production of novel proteins with growth-promoting properties. Chromosome amplification is the result of duplicating a small piece of a chromosome over and over again so that there are way too many copies.

When tumor suppressor genes, such as retinoblastoma (Rb) genes are inactivated, cell division is no longer inhibited and the cell can divide and can continue without any disruption. Point mutation can inactivate Rb on a cell's chromosome. When this happens the tumor suppressor will continue to be inactivated in newly made cells. The loss of heterozygosity is the loss of a chromosome region in a tumor and this unmasks mutations in recessive tumor suppressor genes. Gene silencing doesn't require mutations or changes in the DNA sequence, it is an important way to inactivate tumor suppressor gene expression in cancers. When taking mutations into account, the ways the genetic information can be compromised are: during each round of DNA synthesis, during each mitosis when chromosomes are segregated to daughter cells, and when external mutagens alter or disrupt DNA. When chromosome instability is ongoing in certain recessive traits malignant cells are increased due to the acceleration of the loss of tumor suppressor genes and the overexpression of oncogenes. Cancers that are inherited are due to the mutated cell being in the germ line, mutated somatic cells are not inherited. With the characterization of cancer-causing genes and other genetic factors, we can identify and help treat in earlier stages rather in the later stages.

By Meredith Hunt


Works Cited:
Huether, S. , McCance, K. , Brashers, V. , & Rote, N. (2008). Understanding pathophysiology. (4 ed., pp. 228-235). St. Louis: Mosby Elsevier.