Are Freuds Theories Of The Oral And Anal Personalities Like essays

Are Freud's Theories Of The Oral And Anal Personalities Like essays This question immediately raises the problem, "how are we to determine which parts of Freudian theory are 'good'?" Freud may well have argued that the evidence he documented from his psychotherapy sessions was sufficient, whilst behaviourists would demand that the various aspects of a theory could only be recognised as 'good' after being exposed to the full rigours of the scientific method. I personally don't feel that one can hope to design a repeatable experiment that will decisively illustrate the existence of, for example, the Oedipus complex. On the other hand I feel that we cannot simply accept a theory that has been moulded to fit a certain experimenters observations, coloured as they must be by their own personality, prejudices, and society. Therefore in this essay I will examine the empirical evidence from studies conducted on these most controversial of Freud's theories, and where that evidence appears on balance to give support to that particular theory, I will accept it a s 'good'. As I said earlier some will regard this measure of worth as too lax to be of any use, whilst others will object to the application of science to the process of personality development, a process that is infinitely complex and unique, and so beyond science. Freud's theories of the oral and anal personality are centred around the idea that the infant is able to experience sexual sensations, and that the basis for these sensations changes during early development. If an infant is over or under stimulated during one of these stages fixation will occur, and certain personality traits will develop. The oral personality, according to Kline (1984) consists of two not entirely opposed constellations of traits, the optimistic oral, associated with late weaning, and the pessimistic oral, associated with early weaning. As both situations cause fixation at the oral stage, many traits are common to both types. Goldman-Eisler (1951) conducted a study, th...

HP essays

HP essays Hewlett-Packard Company (HP) provides IT products and solutions covering infrastructure, personal computing and access devices, imaging and printing. HP trades on the New York Stock Exchange (NYSE) and trades under the symbol HPQ. HP recorded revenues of $73.1 billion during fiscal year ended October 2003, an increase of 29.1% over fiscal 2002. The increase is mainly due to the acquisition of Compaq. This is considered to be the largest merger integration in the history of our industry (Fiorina, 2003 HP Annual Report) The Balance Sheet analysis will consist of three parts. I will first analyze HPs liabilities, followed by equity, and finally, assets will be discussed. Current Liabilities and Long Term Debt Hps Current liabilities have increased over a three year period. Mainly, this is due the Compaq merger. Taking a closer look at how current liabilities are disclosed we can see that this increase is due mainly on an increase in Accounts payable and Other Accrued liabilities. As we can see from the following exhibit we can see a decreased in other current liability accounts. Current liabilities: 2003 2002 Change Notes payable and short-term borrowings 1,080 1,793 Decrease Accounts payable 9,285 7,012 Increase Employee compensation and benefits 1,755 2,012 Increase Taxes on earnings 1,599 1,529 Increase Deferred revenue 3,657 3,260 Increase Accrued restructuring 709 1,309 Decrease Other accrued liabilities 8,545 7,395 Increase Total current liabilities 26,630 24,310 Increase Employee compensations have been reduced by $247 million. This is because HP historically used stock options and other forms of equity-related compensation as key components of their total rewards employee compensation program in order to align employees interests with the interests of the stockholders, encourag ...

Genetic Health information Critical thinking questions Assignment - 1

Genetic Health information Critical thinking questions - Assignment Example 4). The genetic code found in our DNA, has many potential insights for individual resistances and susceptibilities to diseases. The HGP is quite distinct from other biomedical research because it has been defined by a series of very quantifiable and concrete goals. For example, it has been used to construct physical and genetic maps. These maps have been used as vital research tools and have proved to be invaluable in determining more than 100 genes involved in diseases such as achondroplasia, breast cancer, colon cancer, and Huntington disease. HGP has simplified the human genetic code as well as animals and plants in a four-letter alphabet. These chemical constituents of each DNA molecule are A (adenine), C (cytosine), G (guanine) and T (thymine). The project has been able to explain that there are 23 pairs of chromosomes in each human cell, and each contains millions of these nucleotides. Through the project, it has been proved that there are 3 billion nucleotides. Studies on these chromosomes have been used clinically to explain to expectant mothers if they are going to give birth to a baby boy or girl. HGP has led to improved techniques of genetic screening for various diseases before birth. A genetic library has been created. This library contains genetic information of relatively homogeneous regions in human DNA. Therefore, individuals do not have considerable variability at this locus. If it is found out that a genetic disease is produced from a specific allele or mutation being present, screening can be done to identify who the individuals are. It is now possible to determine the chances that a child might inherit genetic disorders associated with parents by analyzing the parental gamete DNA. This has allowed genetic disorders to be corrected before birth. Research is also being carried on rapid selection and insertion of DNA into human individuals; these may soon lead to reproduction

Homeless Veterans Essay Example | Topics and Well Written Essays - 1000 words

Homeless Veterans - Essay Example To save the veteran homelessness, everybody has to join hands. Being in the army is no easy job, and everybody of us knows the implications of such a dangerous profession. Dealing with stressful situations on the battle field and experiencing one of the worst kinds of human slaughter, the thought of war brings with it grisly images for the veterans even when they have returned home. Almost every one of the army men faces extreme depression and Post Traumatic Stress Disorder (PTSD) once their numbness begins to lift. For some war veterans it has even taken a decade before the effects of the war have emerged plunging them into complete darkness. This is helped by little or no support from the government which even though has made independent organizations such as the U.S. Department of the Veteran Affairs (VA) but no real improvements can be observed on ground. This fact is further supported by the figures given by the U.S. Department of Housing and Urban Development that on a single n ight in the United States at least 62,619 war veterans are homeless and living on streets or in shelters (National Coalition for Homeless Veterans). Another 1.4 million veterans are suspected on the verge of homelessness due to various reasons. Is that how we return our services to people who had once served us? If the issue of fixing homelessness for war veterans is not treated as a grave emergency, things can be safely assumed as getting out of control. Though the VA argues on successfully providing shelter, medication and other services to the war veterans, which is even true to some extent, but the number of veterans still homeless indicates huge loopholes. Once the US troops in Afghanistan start returning home, will they as well be welcomed by similar homelessness? Taken the fact that the VA could not get the 62,619 war veterans off the road, little hope can we have for the 63,000 troops. The matter to address veteran homelessness is also barred by political circumstances. Some of the confidential Pentagon reports have suggested that the United States has no intention of evacuating all of its troops from Afghanistan as soon as 2014; it intends to stay much longer. However, even if we expect a fourth section of soldiers from our army, they easily exceed the number that is already homeless. Thus solutions covering a much wider ground are needed to not just home the existing war veterans but any of the future ones as well. To reduce veteran homelessness an array of measures will have to be taken. An organization or two supported by another few cannot alone fight the consequences of such a grave matter. Veterans do not just need shelter but immense psychological and physical support, taken their horrendous experiences at the battlefield. Most of these men have faced extremely unpleasant situations – after all a war has nothing pleasant to it – and as a result they are at a very high risk of developing psychological disorders. Though people argue that families should be responsible for the health of the veterans once they return, they fail to recognize the fact that many of these ex-soldiers have severed ties with their families after the long time-period spent abroad. We have clear evidences of wives leaving their veteran husbands for other guys since their husbands could not provide for them. As veterans find it difficult to acquire jobs after their services in the army,

Treatment for Digoxin Overdose

Treatment for Digoxin Overdose B. Trimble Digoxin Overdose Digoxin is derived from the leaves of a digitalis plant (foxglove). Some plants have chemicals that can cause symptoms similar to digoxin if eaten, such as lily of the valley and oleander. Digoxin is a substrate of P-glycoprotein. Drugs that induce or inhibit P-glycoprotein in the intestines or the kidneys have the potential to alter digoxin pharmacokinetics (Katzung, Mastes, Trevor, 2012). Digoxin increases the strength of heart contractions by inhibiting the activity of the enzyme ATPase. ATPase controls the movement of calcium, sodium, and potassium into the heart muscle. ATPase increases the amount of calcium in heart muscle, which increases the force of contractions. Digoxin slows the electrical conduction between the atrium and ventricles of the heart and slows ventricular contractions. Digoxin is eliminated through the kidneys and should be reduced in dosage in patients with kidney dysfunction (Katzung, Mastes, Trevor, 2012). Medications such as verapamil, quinidine, Amiodarone, indomethacin, spironolactone, Alprazolam and itraconazole can increase drug levels and the risk of toxicity of digoxin. Furosemide and other diuretics that reduce blood potassium or magnesium levels may predispose patients to drug induced abnormal heart rhythms. Saquinvard and ritonavir increase the amount of digoxin in the body and may cause toxicity (PubMed, 2013). Assessment of the severity of toxicity and etiology (accidental, unintentional, or deliberate overdose) altered drug metabolism due to decreased renal function or interaction with other drugs is necessary. Consideration of factors that influence treatment include age, medical history, chronicity of digoxin intoxication, severity of heart disease, and/or renal insufficiency and ECG changes (Katzung, Mastes, Trevor, 2012). Symptoms of digoxin toxicity include anorexia, nausea, vomiting, diarrhea, visual changes, cardiac arrhythmias (1st degree, 2nd degree â€Å"Wenckebach†, or 3rd degree heart block), atrial tachycardia with AV block, AV dissociation, accelerated junctional, unifocal or multifocal premature ventricular contractions, ventricular tachycardia, and ventricular fibrillation (Patel, 2011). Toxicity is usually associated with levels greater than 2 mg/ml. Low body weight, advanced age, impaired renal function, hyperkalemia, hyper-calcemia, or hypo-magnesium may cause d igoxin toxicity. Other symptoms may include decreased consciousness, decreased urine output, difficulty breathing, and overall swelling (Brunton, Chabner, Knollman, 2011). Treatment will consist of emergency protocol if outside the hospital; this includes calling emergency medical services and CPR. Once the patient is in medical care, the treatment will depend upon the severity of symptoms and levels of digoxin in the body. Laboratory testing will include serum electrolytes, digoxin levels, and thyroid function tests. The patient will be placed on continuous cardiac monitoring with a 12 lead ECG obtained (Brunton, Chabner, Knollman, 2011). The primary focus is to correct electrolyte levels; if hypokalemic administer potassium to reach a level of 4.0 to 5.5 mmol/L. Activated charcoal will be administered either orally or per nasogastric tube in order to bind undigested digoxin. If bradycardic and symptomatic, atropine may be given intravenously. Peak cardiac effects of digoxin occur 3 to 6 hours after ingestion. Gastrointestinal symptoms precede cardiac manifestation. Neurological symptoms like fatigue and malaise are common. Visual disturbances occur with aberration in color vision, mostly yellow-green. Activated charcoal binds to the digoxin and prevents recirculation to the enterohepatic circulation. Cholestyramine may be used for chronic toxicity in patients with renal insufficiency. Continuous hemodynamic monitoring includes the ECG and 12 lead EKG (Brunton, Chabner, Knollman, 2011). Prompt measurement of electrolyte levels (potassium, calcium, digoxin, BUN, creatinine, and CMP). Sodium bicarbonate may be administered to correct metabolic acidosis along with glucose and insulin to enhance potassium uptake by the cells (Brunton, Chabner, Knollman, 2011). Magnesium may serve as a temporary antiarrthymic until digifab is available. Hypomagnesium increases myocardial digoxin uptake and decreases cellular sodium/potassium ATPase activity. Digibind (digifab or digoxin immune Fab) is an immunoglobulin fragment that binds with digoxin. In acute intentional overdose digibind (40 mg reconstituted with 4 ml sterile water) is administ ered 4 to 6 vials as a loading dose over 30 minutes as an emergent IV bolus. The bolus is followed by 0.5 mg/minute for 8 hours and then 0.1 mg/ minute for 6 hours (Patel, 2011). For patients with chronic toxicity that are dependent on digoxin, the initial dose is twice the bolus. This avoids complete reversal of clinical effects of digoxin. Response is typically within 20 to 30 minutes after infusion, elimination half- life is around 16 hours. Digoxin levels are unreliable for one to two weeks after therapy. Complications in long-term digoxin users, who receive digibind treatment administration are that it may precipitate worsening of heart failure as reversing the beneficial inotropic agent of digoxin causes hypokalemia and atrial arrhythmias with rapid ventricular response (Katzung, Mastes, Trevor, 2012). Hypokalemia has occurred in patients treated with standard therapy as well as with Fab fragments. Clinically adverse phenomena have occurs in patients with immunotherapy. Other untoward effects of Fab include anaphylaxis and serum sickness, this is because it is a sheep protein, but this is uncommon. Recrudescence of digoxin toxicity is possible within 7 to 14 days because Fab is eliminated more rapidly than digoxin released from tissue binary sites. Plasmapheresis may be performed or the agent reinstituted in such cases (Patel, 2011). If hemodynamically stable, bradycardia and supraventricular arrhythmias may be treated with observation and supportive measures. Ensuring hydration to optimize renal clearance, administering gastrointestinal binding agents may be used. For patients with rate related ischemia or neurological unstable digiFab is the treatment of choice (PubMed, 2013). In unstable premature ventricular contractions, lidocaine may be effective. In ventricular tachycardia the best response is to digiFab, but phenytoin and lidocaine are useful if Fab is ineffective or unavailable (Brunton, Chabner, Knollman, 2011). They depress the enhanced ventricular automaticity without significant slowing of AV conduction. Phenytoin may reverse digoxin induced prolongation of AV nodal conduction. Phenytoin has been shown to dissociate the inotropic and dysrhythmia actions of digoxin, suppressing digoxin tachycardia without diminishing the contractile affect and can terminate SVT induced by digoxin. Doses for lidocaine are 100 mg bolus with an infusion of 1 to 4 mg/minute. Phenytoin dosage is 100 mg every 5 to 10 minutes up to a loading dose of 15 mg/kg. Magnesium sulfate dosage is 2 gram over 5 minutes followed by an infusion of 1 to 2 g/hour, with magnesium levels drawn every one to two hours. Atropine may be given for bradycardia to improve sinus and AV node conduction by inhibiting vagal activity (Brunton, Chabner, Knollman, 2011). Phenytoin may reverse digoxin induced prolongation of the action potential in myocardial cells and may suspend tachycardia, prolongs effective refractory period, and depresses spontaneous depolarization in ventricular tissue. Lidocaine is a class IB antiarrthymic that increases the electrical stimulation threshold of the ventricles, suppressing the automaticity of conduction through the tissue. It combines with sodium channels and inhibits recovery after repolarization, resulting in decreased myocardial excitability and conduction velocity (Brunton, Chabner, Knol lman, 2011). Magnesium sulfate possesses properties that slow the rate of sinoatrial node impulse formation and prolong conduction times (Brunton, Chabner, Knollman, 2011). Prevention of unintentional overdose (accidental overdose, interaction with other medications, or the altered metabolism due to renal insufficiency) is mostly through patient education. Instructing the patient in the correct dosage of the medication; that blood tests will be necessary to ensure appropriate dosage; suggesting daily recording of heart rate and blood pressure. Advise the patient that many drugs interact with digoxin, and to inform the physician and pharmacist of all medications, including over the counter and herbal medications, and if started on a new prescription. Advising the patient to report any sign/symptoms associated with digoxin toxicity. Review signs and symptoms of toxicity with the patient. If the overdose were intentional, the patient would need the same consults as any other patient undergoing treatment (cardiologist, nephrologist, medical toxicologist, regional poison control center) as well as psychiatric consult. Follow up appointments with the patient to monitor drug and electrolyte levels. Reference Brunton, L., Chabner, B., Knollman, B. (2011). Goodman Gilmans:The Pharmacological Basis of Therapeutics (12 ed.). McGraw-Hill. Katzung, B., Mastes, S., Trevor, A. (2012). Basic Clinical Pharmacology (12 ed.). McGraw-Hill. Patel, V. (2011). Digitalis toxicity. Retrieved from Medscape: http://www.emedicine.medscape.com/article/154336-overview PubMed. (2013, Janurary). Digitalis toxicity. Retrieved from PubMed.gov: http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001218

The Birth Of An American Super Essay -- essays research papers fc

The Birth of an American Super Hero Heroes have been an important part of American history. They gave adults and especially young children something to strive for and believe in. Some heroes are real and some are imaginary. Real heroes can be presidents, soldiers, or even a parent. The imaginary hero's can be from books, comic books, or movies. One of the most popular hero's of our time is an imaginary hero created for the pages of comic books. The creation of this hero we all know as Superman took hard work, creativity, determination, and plenty of luck. Jerry Siegel and Joe Shuster were the two Jewish-American teenage boys who created Superman. Jerry Siegel was the writer and Joe Shuster was the artist. Siegel and Shuster met at the age of sixteen while working on their high school newspaper. They made a number of attempts creating the Superman character. The first attempt utilized a bald middle aged man with advanced mental abilities. The next attempt was closer to the Superman we now know. He was younger and had hair but was not an alien with super powers. 'The ultimate version of Superman was born one night in 1934, when Siegel found new ideas coming so fast that he couldn't sleep'; (Daniels 21). Seigel and Shuster collaborated on these ideas and created comic strips created for the Sunday comics. Seigel's new Superman came from a planet called Krypton. 'This was the first benevolent alien created'; (Daniels 21). He wore tights for a futuristic appearance and the cape...

Using Animals in Disease Research

Using Animals in Disease Research People all over the world have different opinions on whether animal testing is an ethical way to research drugs and treatments or not. Almost every medical advancement has involved using of animals including discovery of penicillin, organ transplantation, vaccines etc. Scientists should use animals in disease research because nowadays it is the only right way to develop drugs, treatments and cures for diseases and to be sure that new products are safe to use.The first reason why animals should be used in lab testing is that it is the best way to do the research not on human beings but on something that is very similar to humans by chemistry, cell structure and organization. Only drug testing on animals will shows maximally closest result to what will happen in the human's body. Perhaps we weren't be able to cure even very common diseases in present-day medicine without using animals in researches. The second reason why scientists should use animals i n their researches is that animal’s rights are still protected and they don't feel pain during the testing.According to Foundation for Biomedical Research, the Public Health Service Act, Federal laws, and Animal Welfare act controls the removal of pain. All animals used in procedures always relieved from pain by anesthesia. A well-treated animal provide more reliable scientific results, which is the goal of all researchers. The last reason why using animals in research is necessary is that human beings are more important than animals. Animals quickly reproduce itself and they have short life cycle that help scientists to study effects of the drugs on several generations. Also animals can be donors of organs for humans.The society knows many facts in a last few years about transplanting of animal`s organs into human body. The opponents of using animals in disease research might say that scientists could discover drugs using alternative methods such as computer models. However, scientists should see the drug action in all system of living organism to be sure how it works. Using animals in lab testing and researches is necessary because alternative methods are currently not as reliable. Testing drugs and treatments on animals will someday help scientists find the cure for diseases like Alzheimer, AIDS, and cancer.