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IMPORTANCE OF BALANCED DIET AND LIVE DAMAGE BY COCAINE AND CIRRHOSIS

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IMPORTANCE OF BALANCED DIET AND LIVE DAMAGE BY COCAINE AND CIRRHOSIS

 

TASK 1

P.O BOX _____ (postal code)

(City and State),

(Date)

 

Mrs. Smith,

P.O BOX 123,

London Road,

Anywhere AA11 2BB.

 

Dear Mrs.Smith,

RE: HEALTH ISSUES.

I am a health practitioner and am writing to respond on how to improve and deal with the medical issues that you are dealing with. The health issues can be resolved with the taking of a balanced diet and slight improvement and change in your lifestyle, especially some long-term diseases. A diet that supplies all the nutrients that are required for good health is a balanced diet. The diet should have in the right quantities protein foods, energy foods also called the carbohydrates and lipids/fats, protective foods should also be included they comprise the vegetables and fruits that supply the body with vitamins (James, 1991, p. 5). Another important nutrient that completes the balanced diet is water.

Proteins are required for good health, their building blocks are amino acids. Amino acids include essential that have to be taken up in diet as the body can’t manufacture them while the non-essential can be manufactured by the body. Some foods have all essential amino acids and are called complete proteins, they include meats and products of animal-like soy milk, eggs, cheese, milk and yogurt (Intellectual Reserve, 2010, p. 2). Plant proteins contain amino acids but not all the essential and thus they can be combined so as to get all of them on a diet. Proteins are important in the diet for the provision of components that are needed for reproduction of genes and cells, they are involved in the carrying out messages from the genes. They make the major part of the muscles and are important information of enzymes and hormones that are important in carrying out several body activities. Proteins are also very important in the repair of body and in the fighting of disease as they form antibodies.

Carbohydrates are the main source of energy for the body (Intellectual Reserve, 2010, p. 3). The energy produced when the carbohydrates are oxidized is used by the brain, muscles and in other body functions. The brain main source of energy is carbohydrates thus carbohydrate intake should not miss in the diet. Carbohydrates also make structures of the body like the connective tissues and cartilage. They combine with other nutrients like the proteins and fats and are useful in the immune system functioning and nervous system working. Some carbohydrates that are not digested in the digestive system form the fiber part and are important in the prevention of constipation as they increase the bulk of the food allowing it to move in the intestines.

Lipid consists of fats and lipids. These are important as they take part in the formation of structural components of the cell like the cell membrane (Intellectual Reserve, 2010, p. 4). They also are important for insulation purposes in the body by reducing heat loss from the body and for the protection of the major organs from mechanical damage by acting as shock absorbers. They are also a source of energy. Intake of excess fats such as cholesterol, Trans-fats and saturated fats are not good for the body as they end up being deposited in the blood vessels and increase the risk of cardiovascular incidents (James, 1991, p. 6). These fats can be replaced by polyunsaturated fats or monounsaturated fats.

Minerals are also very important for the body to be healthy. They are two types, the macro minerals, and the micro minerals. The macro minerals are required in large amounts while the micro minerals are required in small amounts. The macrominerals include calcium that is very important in making the bones strong, for contraction and relaxation of muscles and prevention of muscle cramping. Its sources include canned salmon, soy milk, yogurt, and cheese. Other macro minerals are magnesium and phosphorus. Phosphorus is important in the strengthening of bones while magnesium ensures the muscles function control and nerve functioning in addition to improving the immune system (Intellectual Reserve, 2010, p. 5). Microminerals include iron, iodine, copper, selenium, fluorine, and zinc. Lack of enough iron in the body may result in fatigue.

Vitamins are also part of the balanced diet but they are required in small amounts. Vitamin D is required for the absorption of calcium in the body thus its deficiency may result in weak bones as they do not get enough calcium for mineralization (Intellectual Reserve, 2010, p. 6). Exposure to the sun leads to the formation of vitamin D in the skin.

Water is also very important, it’s a medium for enzymatic and chemical reactions. Food digestion depends in presence of water, energy production in the brain is also affected by water levels and low intake of water also contributes to constipation (Popkin, et al., 2010, p. 6).

Taking of vitamin and mineral supplements will reduce the feeling of tight muscles and numbness in the leg. They will also boost the immune system reducing the occurrence of colds. Reduced intake of cholesterol and other saturated fats will lower cholesterol levels preventing heart palpitations. Taking enough carbohydrates will provide enough energy for the body to use. Increased exercise will also lower the levels of cholesterol in the body lowering fat deposition.

I hope the importance of each nutrient outlined above will help you understand the need for balancing the diet and ensuring you eat healthy meals.

Yours Sincerely,

(Signature)

(Name)

 

Diet plan for Mrs. Smith.

MealsProteinsCarbohydratesFatsVitaminsMinerals
Breakfast

Whole grain cereal 2 servings,

 

 

 

 

 

 

 

 

 

 

 

Reduced fat milk 250 ml

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

8.2 g

Repair of worn out tissues

60g

Energy

 

 

 

 

 

 

 

 

 

 

 

 

 

 

12g

Energy

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

2.4g

Energy

Vitamin B 1( Its important in maintaining the proper working of the nervous system and  cardiovascular working, it improves one’s appetite, boosts body immunity and makes one have a mood that is positive (Adams, 2018)

 

 

 

 

 

Vitamin A good for vision, immune system and reproduction (National Institute of Health., 2013), Vitamin D absorption of calcium (Intellectual Reserve, 2010, p. 6). Vitamin B-6 maintains a healthy metabolism, nerve function, skin health and eye health (Axe, 2015),

Iron, copper zinc and magnesium. Iron is important in   the formation of hemoglobin, magnesium is important for normal muscle and nerve functioning  (Intellectual Reserve, 2010, p. 5)

 

 

 

Calcium, magnesium, and iron. calcium is important in  the formation strong bones and for contraction and relaxation of muscles (Intellectual Reserve, 2010, p. 6)

Lunch

Grilled salmon

 

 

 

 

 

Small serving whole grain

 

Fresh fruit salad I serving

 

14g

Repair of worm out tissues

 

 

 

 

 

 

 

 

1.27g

 

 

 

 

 

 

 

 

30 g

Energy

 

 

 

25g

4g

Energy

 

 

 

 

 

 

 

 

 

 

 

1.63g

 

 

 

 

 

 

 

 

 

 

 

 

 

Vitamin A, Vitamin C is used in the formation of collagen, a number of neurotransmitters and L-  carnitine and has antioxidant activities (Nordqvist, 2017)

Calcium, potassium is important in the transmission of impulses, it’s an electrolyte (Intellectual Reserve, 2010, p. 6)

 

 

 

 

Calcium

Snack

1 medium size Apple

 

Reduced fat yogurt

0.5g

 

 

 

10.2g

25g

Fiber 4.4 g

Sugar 19g

 

4g

0.3g

 

 

 

0.4g

Vitamin C, B-6 and A

 

 

 

Vitamin B6

Sodium, Potassium, magnesium

 

 

Calcium, magnesium, and iron

Dinner

Lean steak 1 oz, steamed vegetables 2 servings

4.0g

 

 

 

 

 

 

 

 

 

 

26g with fiber 6 g

8.2g

 

 

 

 

6g

 

 

 

 

 

Vitamin A and C

Sodium, calcium and iron

 

 

Sodium, calcium, and iron

 

Disorder Causes of disorder and compare each one to the other(similarities and differences)Diagnosis Treatment options and comparisonsPrognosis if left untreated
OsteoporosisChronic systemic and medical diseases like HIV/AIDS, metabolic and endocrine disorders like Cushing syndrome and hyperthyroidism, medications like anticonvulsants and nutrition like deficiency of vitamin D (Sweet, et al., 2009, p. 195).It’s done radiographically or clinically. Central DEXA scan with T-score 2.5 and below. The scan could be for the hip, neck or lumbar spine (Sweet, et al., 2009, p. 194)Nonpharmacological

Prevention of situation that would lead to one falling, taking calcium supplements and vitamin D supplements.

Pharmacological treatments include taking bisphosphonates orally, raloxifene, calcitonin, teriparatide, hormone therapy that involves intake of estrogen (Sweet, et al., 2009, p. 197).

If left untreated the density of the bones reduces to the extent that one becomes very prone to fractures occurring.
TetanyLow levels of ionized calcium, deficiency of vitamin D, recurrent vomiting, acute pancreatitis, hypomagnesia, anxiety hyperventilation (Santra & Barman, 2017, p. 46)Low levels of serum calcium, use hyperventilation test and Trousseau’s sign (O’Donovan, 1948, p. 900).Calcium supplements are taken orally and vitamin D.

Giving calcium gluconate (Coper & Gittoes, 2008, p. 1301)

Tremors muscle twitches, spasms, and cramps (Santra & Barman, 2017, p. 45)
Rickets Inadequate exposure to sunlight, inadequate vitamin D, calcium and phosphorus dietary intake

Mutations in the receptor for vitamin D

Mutation in the phosphate-regulating gene (Nield, et al., 2006, p. 621).

The physical and dental examination involves palpitations done on the skeletal system.

Levels of calcium alkaline phosphatase, urea nitrogen, creatinine, parathyroid hormone, phosphorus calcidiol in serum. Calcium and phosphorous levels in urine (Nield, et al., 2006, p. 622)

Supplements of vitamin D (Craviari, et al., 2008, p. 116)

Supplements of calcium and phosphorus.

Surgical correction may be required for bones that are severely deformed (Nield, et al., 2006, p. 624).

When not treated children will delay to develop and have abnormalities of the bones (Nield, et al., 2006, p. 619)

 

 

 

 

 

 

 

References

Adams, J., 2018. 11 Impressive benefits of vitamin B 1( Thiamine). [Online]
Available at: https://www.naturalfoodseries.com/11-benefits-vitamin-b1-thiamine/
[Accessed 7 June 2018].

Axe, J., 2015. Vitamin B6: Deficiency, sources and health benefits. [Online]
Available at: https://www.google.com/search?biw=1366&bih=662&ei=W1MZW6riNoq4Ud3wr7AI&q=importance+of+vitamin+b+6&oq=importance+of+vitamin+b+6&gs_l=psy-ab.3…1187057.1187742.0.1188812.2.2.0.0.0.0.0.0..0.0….0…1c.1.64.psy-ab..2.0.0….0.fA5eTps31j8
[Accessed 7 June 2018].

Coper, M. S. & Gittoes, N. J. L., 2008. Diagnosis and management of hypocalcaemia. BMJ, Volume 336, pp. 1298-1302.

Craviari, T. et al., 2008. Rickets: An overview and future directions, with special reference to Bangladesh. Journal of health population nutrition, 26(1), pp. 112-121.

Intellectual Reserve, 2010. Nutrition and diet. Salt Lake City: The Church of Jesus Christ of Latter-day Saints.

James, P. W. T., 1991. New concepts of a balanced diet., s.l.: WHO.

National Institute of Health., 2013. Vitamin A. [Online]
Available at: https://ods.od.nih.gov/factsheets/VitaminA-Consumer/
[Accessed 7 June 2018].

Nield, L. S., Mahajan, P., Joshi, A. & Kamat, D., 2006. Rickets: Not a disease of the past. American Family Physician, 74(4), pp. 619-626.

Nordqvist, J., 2017. Vitamin C: Why it is important?. [Online]
Available at: https://www.medicalnewstoday.com/articles/219352.php
[Accessed 7 June 2018].

O’Donovan, D. K., 1948. The diagnosis of latent tetany with observations on the effect of calciferol. British Medical Journal, 2(4585), pp. 900-902.

Popkin, B. M., D’Anci, K. E. & Rosenberg, I. H., 2010. Water, Hydration, and Health.. Nutrition Review, 68(8), pp. 439-458.

Santra, G. & Barman, H., 2017. Etiological spectrum of tetany in a teaching institution of western part of west Bengal-A cross-sectional study. Journal of Current Research in Scientific Medicine, 3(1), pp. 45-50.

Sweet, M. G., Sweet, J. M., Jeremiah, M. P. & Galazka, S. S., 2009. Diagnosis and treatment of osteoporosis. American Family Physician, 79(3), pp. 193-202.

 

TASK 2

COCAINE AND CIRRHOSIS IN LIVER DAMAGE.

Introduction

Cirrhosis refers to the chronic injury of the liver as a result of the histological development of nodules that are regenerative that are surrounded by bands that are fibrous (Schuppan & Afdhal, 2008, p. 838). It occurs due to different factors that include drug abuse, drinking alcohol and hepatitis virus infection (Ueki, et al., 1999, p. 226).  Addition refers to a behavior that can result in pleasure and be able to provide a means of one escaping internal discomfort. According to Goodman (1990, p. 1403), it results in an individual laking the power to control the behavior and keeps continuing with it even if it has bad effects. Cocaine addition refers to the continued abuse of cocaine by an individual.

Effects of cirrhosis and cocaine on the liver.

Cirrhosis can also be described as an advanced fibrosis. Fibrosis occurs when injured tissues are replaced by scars that are collagenous. In the liver, fibrosis is as a result of the normal process for healing wounds being perpetuated leading to connective tissues being produced and deposited, that is fibrogenesis (Schuppan & Afdhal, 2008, p. 838). Cirrhosis destroys hepatic vasculature, interfering with the exchange that occurs between the hepatocytes and the hepatic sinusoids. Hepatocytes are liver cells and carry out most of the functions of the liver. Individuals with cirrhosis have their Disse full of scar tissues, the fenestrations of the endothelial cells are lost.  Patients with cirrhosis have their liver function impaired, there is an increase in intrahepatic resistance and they may develop hepatocellular carcinoma. It is also associated with abnormalities that affect the circulatory system that results in water and salt being retained and the cardiac output increases.

One of the leading causes of liver cirrhosis is increases consumption of alcoholic drinks (Johannes & Berg, 2013, p. 85).  The metabolites of alcohol together with alcohol itself are able to damage the hepatocytes and the parenchymal cells of the liver. Alcohol and the products formed from its metabolism results in the production of excess free radical molecules. The major radicals produced are the reactive oxygen species(ROS) these radicals are capable of carrying out modifications in the key pathways of the cells that are involved in signal transduction (Szabo, 2010, p. 87). These ROS can modify the glucose and lipid metabolism, they can modulate proteins and DNA. When their levels are not reduced it results in the cell being in oxidative stress.

Alcohol can also allow endotoxins of gram-negative bacteria from the small intestines into the bloodstream by increasing the small intestines permeability. When this happens, the body activates immune cells of the liver, these are the Kupffer cells that remove foreign proteins and bacteria from the blood (Szabo, 2010, p. 87). The Kupffer cells produce cytokines that are inflammatory and when in excess they promote the progression of the liver disease. The Kupffer cells also are a source of ROS in the liver and may lead to activated of macrophages. When the production of cytokines in the liver is persistent it results in inflammation that leads to cirrhosis. The cytokines produced such as the TNF-alpha is important in the regulation of apoptosis of liver cells that are damaged, but it also involved in the damaging of the liver tissues.

Hepatocytes are important in the carrying out of homeostatic functions of the liver. Alcohol activation of the Kupffer cells leads to the production of TNF-alpha the ends up in the binding on hepatocyte receptors and induces cell death. Also, the oxidative stress damages the hepatocytes, as a result, activates cell death pathways (Szabo, 2010, p. 90). The TNF-alpha also reduce oxidation of fatty acids in the liver, the lipids increase and end up accumulating in the hepatocytes, this is steatosis. This proceeds to scaring and fibrosis. Hepatic fibrosis is meant to repair the damage but eventually results in collagen being deposited in excess, with time it leads to the reduction in the number of hepatocytes that are functioning (Szabo, 2010, p. 92). Thus at this point liver functioning is greatly reduced and thus removal of toxic substances from the body is reduced too.

Cocaine is formed in the Coca plant leaves. It has been used for centuries with individuals by chewing the leaves but it will take a much great deal of chewing of the leaves for any toxic events to result (Karch, 1999, p. 393). Its toxicity has increased over the years as a result of improvement in the methods that are used in refining and also methods are being used in administration, like snorting and injection of a more pure form of cocaine that has undergone refining. Its addictiveness is related to how much of it gets into the bloodstream and the amount that eventually enters the brain cells.

Once cocaine is in the brain, it affects the limbic system of the brain by causing an increase in dopamine which is a neurotransmitter making the receiving cells to be overactivated (Nestler, 2005, p. 4). Cocaine produces pleasure and euphoria, control loss and responses that are compulsive to cues that are drug-related. This is possible because the limbic system has dopamine-responsive cells that control emotions and are also linked to memories.

Cocaine exists in two main form, cocaine hydrochloride that is a powder and cocaine the base commonly known as crack. Crack is smokable as it is heat stable and once smoked results in a large amount of the drug in the lungs, the other form is snorted (Antai-Otong, 2006, p. 216). The effects of cocaine differ depending on the method used for administration, the method that delivers high amounts into the bloodstream faster have more intense effects. Thus the smoked crack has higher effects than that that is snorted. Using of cocaine has several medical complications apart from the effects pleasure and euphoria.

When cocaine enters the body, it undergoes metabolism where it is converted into its metabolites. In urine a small amount is eliminated unchanged that is between 1-5 %, the remaining about 75-90% can be eliminated as either benzoylecgonine combined or as an ester of ecgonine methyl (Jatlow, 1988, p. 106). In cocaine metabolism, the hepatic mixed function oxidases are involved in its metabolism but have a very limited functional role. In the hepatocytes, cocaine undergoes N-demethylation in the microsomes and ends up producing norcocaine. This pathway may end up forming intermediate metabolites that are hepatotoxic-reactive.

The relationship of liver toxicity to cocaine metabolism doesn’t have much evidence in humans, but it has been shown in rats that that end up having lobular necrosis. The toxicity of cocaine to liver cells is correlated with the oxidation of cocaine in the microsomes. A metabolite of cocaine from this oxidation that is active is found to be responsible for hepatic necrosis (Mallat & Dhumeaux, 1991, p. 275). The metabolite norcocaine was also found to be more potent in the starting of hepatotoxicity and the pathway is seen to require the assistance od cytochrome p-450.

The N-methylated cocaine has also been shown to undergo further oxidation that results in the formation of N-hydoxynorcocaine that has been shown to be one of the metabolites responsible for hepatotoxicity in the liver cells (Toenns, et al., 2003, p. 375). In individuals that have HIV and in use of cocaine, it has been shown that they have a higher rate of liver disease progression compared to those that are not on cocaine use (Campa, et al., 2016, p. 27). This progression and increased mortality are due to the increase of oxidative stress in the cells, mediated by cytochrome P-450 dependent N –oxidative pathways. They end up causing damage to the cells due to oxidation which causes injury to the liver cells. Liver fibrosis results as the liver try to repair the injury that results from the oxidative stress of the cytochrome P-450 oxidative pathways, leading to deposition of scar tissues in the process. According to Ansari, et al. (2017, p. 1182), cocaine undergoes metabolism and the products result in an increase in lipid peroxidation, impaired sequestration of calcium and free radical activity.

Cocaine can cause both chronic and acute liver damage which presents with clinical manifestations that may include an elevated level of liver enzymes, acute rhabdomyolysis and liver failure in some patients with hepatitis. In hepatocytes that survive have shown that its toxicity to liver cells leads to periportal and midzonal necrosis in addition to steatosis. Hepatotoxicity in liver cells is due to cocaine is dependent on N-oxidative metabolites of cocaine (Graziani, et al., 2016, p. 5).

Conclusion

Cirrhosis is one of the diseases that cause death in increased numbers of individuals involved in substance abuse. And one of the most common drugs that are abused is cocaine that causes very many deaths annually. Cocaine toxicity in the liver develops just like alcoholic toxicity. The hepatocytes function to remove toxins from the body, but due to the oxidative metabolites of cocaine, the cells end up undergoing stress that results in the damage of the cells as a  result liver fibrosis begins.

 

 

 

 

 

References

Ansari, M. et al., 2017. A case of reversible drug-induced liver failure. Clinical case reports, 5(7), pp. 1181-1183.

Antai-Otong, D., 2006. Medical complications of cocaine addiction: Clinical implications for nursing practice.. Journal of Addictions Nursing, Volume 17, pp. 215-225.

Campa, A. et al., 2016. Cocaine use and liver disease are associated with al -cause mortality in the Miami adult studies in HIV(MASH) Cohort. Journal of drug abuse, 2(4), p. 27.

Goodman, A., 1990. Addiction: definition and implications. Addiction, 85(11), pp. 1403-1408.

Graziani, M. et al., 2016. Cardiovascular and hepatic toxicity of cocaine: Potential beneficial effects of modulators of oxidative stress.. Oxidative medicine and cellular longevity, pp. 1-14.

Jatlow, P., 1988. Cocaine: Analysis, pharmacokinetics and metabolic disposition. The Yale Journal of Biology and Medicine, Volume 61, pp. 105-113.

Johannes, W. & Berg, T., 2013. The Etiology, Diagnosis, and Prevention of liver cirrhosis. Part 1 of a series on liver cirrhosis. Deutsches Arzteblatt International, 110(6), pp. 85-91.

Karch, S. B., 1999. Cocaine: history, use, abuse. Journal of the royal society of medicine, Volume 92, pp. 393-398.

Mallat, A. & Dhumeaux, D., 1991. Cocaine and the liver. Journal of Hepatology, 12(3), pp. 275-278.

Nestler, E. J., 2005. The Neurobiology of cocaine addiction. Science & Practical Perspectives, 3(1), pp. 4-10.

Schuppan, D. & Afdhal, N. H., 2008. Liver Cirrhosis. The Lancet, 371(9615), pp. 838-851.

Schuppan, D. & Afdhal, N. H., 2008. Liver Cirrhosis. Lancet, 371(9615), pp. 838-851.

Szabo, G., 2010. Focus on: Alcohol and the liver. Alcohol Research and Health, 33(1-2), pp. 87-96.

Toenns, S. W., Thiel, M., Walther, M. & Kauert, G. F., 2003. Studies on metabolic pathways of cocaine and its metabolites using microsome preparations from rat organs. Chemical Research Toxicology, 16(3), pp. 375-381.

Ueki, T. et al., 1999. Hepatocyte growth factor gene therapy of liver cirrhosis in rats. Nature Medicine, Volume 5, pp. 226-230.

 

 

 

 

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