Metabolic Disorders Essay

Metabolic Disorders Essay

Metabolic Disorders Essay

Week 10: Question for Discussion

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Chapter 19 – Diseases Affecting Vision and Hearing.

Chapter 20 – Metabolic Disorders.

Questions:

1. Choose and explain one of the eye diseases / disorders discuss in you textbook. (GLAUCOMA)

2. Discuss its possible treatments.

Guidelines: The answer should be based on the knowledge obtained from reading the book, no just your opinion. If there are 3 questions in the discussion, you must answer all of them. Your grade will be an average of all answers.Metabolic Disorders Essay

Grading Criteria: Student mentions the eye disease / disorder (30%). Student explains the disease / disorder in detail (35%). Student discusses possible treatments (35%).

Metabolic syndrome is a condition that comprises several disorders like obesity, glucose intolerance, insulin resistance, dyslipidemias, hypotension and cardiovascular disease. Metabolic syndrome is largely associated with mental illnesses. Schizophrenics have been the main targets when assessing for this condition due to their likelihood of living unhealthy lifestyles (one of the risk factors). Use of certain antipsychotic medications could also predispose the individual to metabolic disorders. It is therefore thought that metabolic syndrome is an interaction of socioeconomic status, lifestyle, genetic factors and use of neuroleptics (Ganguli et al., 2011). This paper therefore talks about metabolic disorders in people with severe mental illnesses, health trends of schizophrenics and pathophysiology of the conditions.

Population of Interest
Antipsychotics vary in the ability to induce weight gain with some having greater propensity than others. Patients on neuroleptics have been found to have more abdominal fat deposition than normal members of the society. Such increase in weight could then result into other conditions such as diabetes, hypotension and other cardiovascular conditions. However, some conditions like type-2 diabetes may be brought about by the illness itself. For instance, it has been found that unaffected relatives of schizophrenics record high rates of the illness. This is a clear indicator of genetic relationships between these conditions (Thakore et al. 2005). [“Write my essay for me Metabolic Disorders Essay

Health Trends in People with Schizophrenia
Mortality rates in people with schizophrenia have been on the rise despite improvements in the healthcare. It is estimated that mortality rates in schizophrenia patients is 2-3 times higher than for the general population. Natural deaths and cardiovascular diseases were the main cause of these mortalities. Suicide and unspecified violence also contributed. All these were attributed to the unhealthy lifestyles adopted by these patients due to the illness (Osby et al., 2000).

Epidemiology
There has been varying information on the epidemiologic information about metabolic disorders in patients with severe mental disorders. Prevalence rates for schizophrenic patients under medication ranges from 11 % to 69 % while that for patients not taking medications being 4 % to 26 %. Generally metabolic disorders are more prevalent in schizophrenic patients than as observed in the general population. Increase in age also increases the prevalence of metabolic disorders. However, there is no association between the prevalence and demographic and clinical variables (Malhotra et al., 2013).Metabolic Disorders Essay

Current trends
Antipsychotic treatment is crucial in reducing mortalities resulting from schizophrenia. It has been observed that, though mortalities resulting from schizophrenia are high, there are reduced cases of mortality with antipsychotic treatment rather than with no treatment. Atypical antipsychotics also do not increase cardiovascular mortality and morbidity as is the case with conventional (Bushe et al., 2010).
Despite improvements achieved through the use of atypical antipsychotics in schizophrenia

patients, weight gain, high serum prolactin among other side effects has been noted. Insulin insensitivity and type-2 diabetes have also been largely associated with the use of atypical antipsychotics. It has however been noted that patients that use atypical antipsychotics have lower risks of developing metabolic disorders than those using conventional antipsychotics (Ollendorf et al., 2004).

Studies show that metabolic disorders are likely to develop in young people suffering from schizophrenia and on antipsychotics treatment. Higher prevalence for metabolic disorders is seen from ages 15-25 years and continues to increase with age. This striking finding also correlates with that in the normal population since increased prevalence for metabolic disorders is also observed in the general population (De Hert et al., 2006).Metabolic Disorders Essay

Population health considerations
Schizophrenic patients experience high rates of mortality and morbidity as compared to the general population. These patients have a shorter lifespan by approximately 20 years than people not suffering from the disease. This is mainly due to suicide, cancer and cardiovascular diseases resulting from metabolic disorders. It therefore becomes the responsibility of clinicians to be keen and single out any risks for cardiovascular diseases like abdominal obesity and hypertension. Combination of these two or more such risks further predisposes the individual to cardiovascular diseases.[Need an essay writing service? Find help here.]

Lifestyle psychiatrics should have vast knowledge on the metabolic risks associated with treatments for schizophrenics before initiating any treatment. Establishing a risk profile based on the genetic, lifestyle and medical factors is very crucial for before initializing treatment procedures for these patients. Low risk strategies such as encouraging healthy lifestyles, frequent checkup and monitoring weight, glucose and lipid levels is highly recommended after every treatment (Van Gal et al. 2006).Metabolic Disorders Essay

Pathophysiology and Mechanisms of Metabolic Disorders and Schizophrenia
Adverse effects of antipsychotic medications are largely associated with metabolic disorder syndrome. It has also been found that some of the metabolic disorders like insulin intolerance and diabetes appear at early stages of the disease when even no medication has been started. Despite the fact that all the risk factors for metabolic disorders are known, it is difficult to control them all.

The etiology and pathophysiology of it is not well understood with majority of the hypotheses revolving around lifestyle and dietary habits, antipsychotic drug adverse effects and alterations of hypothalamic pituitary-adrenal axis. Unhealthy dietary habits facilitate obesity which increases the risk for developing cardiovascular diseases; antipsychotic drugs interfere with lipid and carbohydrate metabolism resulting into obesity and diabetes while interference with the hypothalamic pituitary-adrenal axis causing obesity of the trunk.Metabolic Disorders Essay

Pathophysiological Consequences
Metabolic disorder syndrome precipitates cardiovascular diseases through various mechanisms. To start with, reduced insulin sensitivity and high blood sugar levels increase the chance for diabetes. More so this leads to type-2 diabetes which further increases the chances for cardiovascular diseases like hypertension. Obesity on the other hand leads to increased lipid levels and could cause arteriosclerosis that may lead to fatal heart diseases like hypertension or heart attack.

Role of Advance Practice Nurse
The increased prevalence of metabolic syndrome is worrisome for medical providers in general and more so for providers who treat at-risk populations such as persons with SMI. The treatment of SMI appears to be primarily treated with pharmacological treatments. The advanced practice nurse (APN) must be adept pharmacotherapeutics with an expert understanding of the medications prescribed to treat the illnesses in this population. The APN must be proficient in interventions to manage metabolic syndrome. Interventions to include lifestyle modifications and use of metabolic agents and switching medications as needed. Lastly, the APN is well-qualified to lead research into these phenomena and add to the current knowledge base (Mwebe et al. 2016).Metabolic Disorders Essay

Diabetes mellitus is a condition in which the body is unable to control blood glucose levels adequately, resulting in high blood glucose levels (hyperglycaemia). Symptoms include frequent urination due to the osmotic effect of excess glucose in the urine, thirst due to loss of fluids and weight loss. Possible long-term complications of diabetes if blood glucose has been poorly controlled include cardiovascular disease (such as atherosclerosis and stroke) and damage to nerves, the kidney and eyes, which can potentially lead to blindness. Diabetes is a major health problem with an estimated 425 million people affected worldwide, and these numbers are predicted to rise. The rise in numbers is associated with an increase in obesity in the population and treating the complications is a major healthcare cost. In the U.K., some estimates predict the cost could reach 17% of the NHS budget.

Most people will be familiar with the classification of diabetes into the two main forms, Type 1 and Type 2; however, it is increasingly clear that there are in fact several different types of diabetes, some of which overlap to some extent. Recent research analysing nearly 15000 diabetics showed they could be clustered into five distinct groups based on specific biomarkers1 of the condition, which is significant because this better classification system may lead to improved treatment strategies in the future. Type 1 diabetes is an autoimmune disease in which cells of the body’s immune system cause destruction of insulin secreting β-cells in the pancreas, leading to a deficiency of insulin production. There are typically antibodies against key pancreatic proteins involved in insulin storage and secretion. It is a relatively rare form of the disease affecting 5–10% of diabetics, which is usually diagnosed in childhood and is not associated with excess body weight. Type 2 diabetes is the more common form of the disease, affecting 90–95% of diabetics, and is characterised by a loss of ability to respond to insulin (i.e. there is insulin resistance, also termed as insulin insensitivity).Metabolic Disorders Essay  At diagnosis, individuals are typically over 30 years old, overweight, have high blood pressure and an unhealthy lipid profile (referred to as the metabolic syndrome). Established disease is associated with hypersecretion of insulin, but this is still inadequate to restore normal blood glucose levels, and the condition may progress towards insulin deficiency. The causes of diabetes are thought to be a combination of genetic and environmental factors, and it is recognised that being overweight is a strong risk factor for developing Type 2 diabetes.

Insulin action
In healthy individuals, blood glucose levels range between 3.5 and 5.5 mmol/l before meals. This range is maintained by the actions of hormones (primarily insulin and glucagon, but also adrenaline, cortisol and growth hormone) which control the production and uptake of glucose, levels of glycogen (the stored form of glucose), and fat and protein metabolism, as required following meals, during fasting and exercise. Both insulin and glucagon are polypeptides produced by the pancreas (β-cells – insulin; α-cells – glucagon).Metabolic Disorders Essay

Insulin is secreted in response to an increase in blood glucose levels and its overall effect is to store chemical energy by enhancing the uptake and storage of glucose, amino acids and fats; consequently reducing blood glucose levels, via actions on liver, muscle and adipose tissue (specifically adipocytes – fat cells). Glucagon, on the other hand, via a complex interplay with other hormones and the nervous system increases blood glucose by stimulating the breakdown of glycogen, fat and protein. When blood glucose is high, after a meal for example, insulin acts on the liver to decrease glucose synthesis (gluconeogenesis), increase glucose utilisation (glycolysis) and increases glycogen synthesis (glycogenesis). When the storage capacity for glycogen is reached, insulin increases synthesis of fatty acids (lipogenesis), via acetyl CoA as an intermediate, which is then exported for triglyceride synthesis in adipocytes. In muscle, insulin stimulates uptake of glucose, by recruiting the glucose uptake transporter type 4 (GLUT-4), and enhances glycogen synthesis and glycolysis. In adipose tissue, there is facilitated uptake of glucose which is metabolised to glycerol and subsequently used together with fatty acids to synthesise triglycerides. Insulin also inhibits pathways involved in lipolysis. In addition, insulin increases amino acid uptake and protein synthesis in muscle and is considered an anabolic hormone (i.e. one that builds up organs and tissues).Metabolic Disorders Essay

At the biochemical level, insulin produces its effects by binding to the insulin receptor – a cell surface glycoprotein composed of two extracellular α subunits and two β subunits that span the membrane (Figure 1). The receptor has tyrosine kinase activity (i.e. enzyme activity that catalyses the transfer of a phosphate group from ATP to a tyrosine amino acid within a protein, also known as tyrosine phosphorylation). Binding of insulin to the receptor initially causes tyrosine phosphorylation of the receptor itself, and then phosphorylation of intracellular proteins termed as insulin receptor substrate (IRS)-1 and IRS-2, followed by a complex series of intracellular signalling events involving many other kinases that lead to the physiological changes in carbohydrate, fat and protein metabolism discussed above via changes in gene expression and the activity of metabolic enzymes. The effects of insulin on glucose uptake are mediated via the glucose transporter GLUT-4, which is stored in intracellular vesicles in an inactive state, and insulin stimulates the movement of these vesicles to the plasma membrane where GLUT-4 becomes inserted into the membrane forming a pore that allows glucose uptake into the cell (Figure 1).Metabolic Disorders Essay

Figure 1
Abbreviation: P, phosphorylation on tyrosine.
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Insulin signalling in an adipocyte
Abbreviation: P, phosphorylation on tyrosine.

Disease complications and ketoacidosis
Many of the longer term complications of diabetes involve effects on both large arteries (macrovascular) and small arteries and capillaries (microvascular). High blood glucose leads to proteins and lipids becoming modified in a non-enzymatic process by exposure to sugars, forming advanced glycation end products that have been implicated in the disease process. Oxidative stress and damage to the vascular endothelium lining blood vessels is also involved. One of the diagnostic tests for diabetes involves measuring levels of glycated haemoglobin (HbA1c) from red blood cells. This is a valuable test because it gives an assessment of the average plasma glucose concentration over months, because of the 120 days lifespan of a red blood cell, and it also gives an indication of how effective treatment has been.Metabolic Disorders Essay

An acute serious life-threatening condition associated with untreated Type 1 diabetes is diabetic ketoacidosis. It develops in the absence of insulin, during which there is increased glucose production by the liver but because of the absence of insulin cells in the periphery, such as muscle cells, are unable to take-up the glucose and use it. The consequent high blood glucose levels results in the kidneys filtering and removing it from the body in urine. This is associated with osmotic diuresis (loss of fluids and electrolytes) and dehydration. As an alternative energy source, triglycerides (fats) from adipose tissue are broken down to free fatty acids and taken up by the liver. Here they are converted into acetyl CoA which is the precursor for formation of ketones (acetoacetate, β-hydroxy-butyrate and acetone) within mitochondria. These are referred to as ketone bodies and released into the blood and are detectable in the breath giving a distinctive smell similar to that of acetone or pear drops. Release of ketones into the blood causes a drop in pH (acidosis) and the body tries to compensate by hyperventilating. If untreated, these events can lead to coma and death.

Treatment
For treatment of Type 1 diabetes, insulin is essential. Human insulin is now produced by recombinant DNA technology, rather than via extraction from the pancreases of animals. Diet and exercise are key to treatment of Type 2 diabetes and this can be combined with drug treatment.

Cardiovascular disease – atherosclerosis Metabolic Disorders Essay
Introduction
Atherosclerosis, also known as hardening of the arteries, is a chronic arterial disease that develops over many decades and is a major cause of deaths worldwide. A raised patch or plaque, develops in the arterial wall that is rich in fat, cholesterol and calcium, and over time this hardens and narrows the artery depriving the region supplied by the blood vessel of oxygen (ischaemia). Rupture of the plaque causes blood cell fragments called platelets to stick to the surface of the injury, leading to thrombosis (formation of a blood clot) which can result in a total blockage of the affected artery. If a coronary artery is affected, a myocardial infarction (heart attack) may result or if a cerebral artery supplying the brain is affected ischaemic stroke may result. Multiple risk factors have been identified for development of atherosclerosis. Some of these are modifiable, such as an unhealthy blood lipid profile, high blood pressure, Type 2 diabetes, smoking, obesity, stress and physical inactivity. Other factors such as age, gender, race and a family history of heart disease cannot be changed. The biochemistry of lipid metabolism and process of atherosclerosis are discussed below.Metabolic Disorders Essay

Cholesterol metabolism and lipoproteins
Cholesterol and fatty acids are two common types of lipids, defined as water-insoluble molecules in cells, that are soluble in organic solvents (Figure 2). Both molecules have important biological functions. Cholesterol is an important component of cell membranes where it modulates fluidity, and a precursor of vitamin D and steroid hormones produced by the adrenal gland, testes and ovaries. It is also used as a starting point for the synthesis of bile acids in the liver, which are secreted into the intestine where they solubilise fats and aid in the absorption of fat-soluble vitamins (A, D, E and K). Fatty acids are precursors of membrane phospholipids and glycolipids, and are fuel molecules that are stored as triglycerides (esters of glycerol and three fatty acids) (Figure 2).

Figure 2
(A) Structures of cholesterol and cholesterol ester. In cholesterol ester, the R group is a fatty acid as shown in (D). (B) Hydrolysis of triglyceride to glycerol and fatty acids by a lipase. There are several different lipases (e.g. lipoprotein lipase of endothelial cells and hormone-sensitive lipase in adipocytes). (C) Key steps in the multistep synthetic pathway of cholesterol. HMG CoA, 3-hydroxy-3-methylglutaryl-CoA. HMG CoA reductase is the rate-limiting step. (D) Fatty acids are carbon chains (most commonly 12–22 carbons) with a methyl group at one end and a carboxyl group at the other. Saturated fatty acids are ‘filled’ (saturated) with hydrogen and have no double bonds. Monounsaturated fatty acids (MUFAs) have one carbon–carbon double bond which can occur in different positions. These MUFAs may have a double bond with hydrogens in the cis configuration (i.e. hydrogens at either side of the double bond are orientated in the same direction) or the trans configuration (i.e. hydrogens are orientated in different orientations). The cis configuration introduces a kink in the molecular shape of the carbon chain altering physical properties. Polyunsaturated fatty acids (PUFAs) have more than one double bond. The letter n or Greek symbol ω, is used to indicate the position of the bond closest to the methyl end. For example, n−6 PUFAs are characterised by the presence of at least two double bonds with the first between the sixth and seventh carbon from the methyl end.Metabolic Disorders Essay
VIEW LARGEDOWNLOAD SLIDE
Structure and metabolic pathways for some common lipids
(A) Structures of cholesterol and cholesterol ester. In cholesterol ester, the R group is a fatty acid as shown in (D). (B) Hydrolysis of triglyceride to glycerol and fatty acids by a lipase. There are several different lipases (e.g. lipoprotein lipase of endothelial cells and hormone-sensitive lipase in adipocytes). (C) Key steps in the multistep synthetic pathway of cholesterol. HMG CoA, 3-hydroxy-3-methylglutaryl-CoA. HMG CoA reductase is the rate-limiting step. (D) Fatty acids are carbon chains (most commonly 12–22 carbons) with a methyl group at one end and a carboxyl group at the other. Saturated fatty acids are ‘filled’ (saturated) with hydrogen and have no double bonds. Monounsaturated fatty acids (MUFAs) have one carbon–carbon double bond which can occur in different positions. These MUFAs may have a double bond with hydrogens in the cis configuration (i.e. hydrogens at either side of the double bond are orientated in the same direction) or the trans configuration (i.e. hydrogens are orientated in different orientations). The cis configuration introduces a kink in the molecular shape of the carbon chain altering physical properties. Polyunsaturated fatty acids (PUFAs) have more than one double bond. The letter n or Greek symbol ω, is used to indicate the position of the bond closest to the methyl end. For example, n−6 PUFAs are characterised by the presence of at least two double bonds with the first between the sixth and seventh carbon from the methyl end.Metabolic Disorders Essay

Since lipids are insoluble in water, they are transported in the plasma as protein–lipid complexes (lipoproteins), which are divided into different types (chylomicrons, very low-density lipoproteins (VLDL), low-density lipoproteins (LDL), high-density lipoproteins (HDL)) based on their size, lipid composition and the type of protein they contain. The proteins embedded in the lipoproteins have a stabilising function and are recognised by specific receptors in the liver and peripheral tissues. In the exogenous pathway, dietary fat in the small intestine is dispersed into small droplets by bile acids and broken down into fatty acids and glycerol. Once in the enterocyte (cell lining the small intestine), the fatty acids are synthesised into triglycerides again, and packaged into lipoproteins called chylomicrons together with a small amount of absorbed cholesterol, which has been converted into its ester form. Each chylomicron contains several different apoproteins (apoB-48, apoA-I, apoA-II) and acquires apoC-II and apoE. The chylomicrons pass via the lymphatic system and blood capillaries to muscle and adipose tissue. Here the enzyme lipoprotein lipase, on the surface of endothelial cells, breaks down most of the triglycerides into glycerol and fatty acids. These molecules are taken up by the peripheral tissues and either used as an energy source or stored. The remnant chylomicrons which are depleted in triglycerides but still contain the bulk of their cholesterol ester pass to the liver and, following binding of apoE to the LDL receptor on hepatocytes, the entire particle undergoes endocytosis, resulting in cholesterol being taken up by the liver. From here the cholesterol may be stored, converted into bile acids, secreted directly in bile or may enter the endogenous pathway.Metabolic Disorders Essay

In the endogenous pathway, the liver produces VLDL particles with newly synthesised triglyceride and a small amount of cholesterol ester. These particles deliver glycerol and fatty acids to peripheral tissues, as described above for chylomicrons. Removal of the triglyceride fraction from the particles, while retaining the cholesterol component, results in their conversion into intermediate density particles and ultimately LDL particles, laden with cholesterol ester. These LDL particles are the main carrier of cholesterol to cells for incorporation into membranes and steroid synthesis, but also play a key role in development of atherosclerosis by depositing lipid in the wall of blood vessels. The surface of the LDL particle contains apoB-100 which is a ligand (i.e. binds) for the LDL receptor located on pits on the surface of the hepatocyte. Apo-B-100 binding to the LDL receptor results in internalisation of the particle and its removal from plasma. The cholesterol content of the liver cells in turn regulates the levels of LDL receptors and other key genes involved in cholesterol and fatty acid metabolism in order to maintain a balance. The genes that are regulated include the enzyme HMG CoA reductase which is the rate-limiting enzyme in the multistep cholesterol synthesis pathway (Figure 2). The levels of LDL receptor are also regulated by the secreted proprotein convertase subtilisin/kexin type 9 (PCSK9) which binds to the receptor and enhances its degradation in lysosomes. Cholesterol can return to plasma from tissues in HDL particles. HDL particles take up cholesterol, converting it into its ester form in the process, and from here it is transported away from the periphery to the liver. This may occur indirectly via transfer to VLDL particles or directly by a process involving the scavenger receptor B1 in hepatocytes which selectively takes up HDL cholesterol.Metabolic Disorders Essay

Disease process
Atherosclerosis involves damage to, or dysfunction of, the endothelial cells that form the inner lining of blood vessels, resulting in entry of LDL particles into the vessel wall (Figure 3). Lipids and proteins of the LDL particle undergo oxidation by reactive oxygen species (e.g. superoxide, O2−), generated via oxidative stress, to form oxidised LDL (oxLDL). OxLDL molecules participate in atherosclerotic plaque formation in several ways. They activate endothelial cells, promoting movement of monocytes and T cells into the vessel wall. Also the oxLDL is taken up by macrophages via ‘scavenger’ receptors resulting in conversion of the macrophages into lipid-rich foam cells. Accumulation of these cells give rise to the appearance of ‘fatty streaks’ within the endothelium. Various pro-inflammatory mediators are produced during this process which stimulate smooth muscle cell proliferation, and migration of these cells into the subendothelial layer. Matrix proteins such as collagen are deposited in large quantities by the smooth muscle cells leading to formation of a dense fibrous cap overlying the lipid-rich core. The plaque may partially block the lumen of the blood vessel or eventually rupture leading to formation of a thrombus as blood platelets adhere to the exposed subendothelial collagen. Metabolic Disorders Essay

 

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