Case Study Of Unstable Angina

Case Study Of Unstable Angina The patient in context is a 61 year old male, Mr. X, admitted to hospital in the late evening for a case of unstable angina. Presenting complaints include left-sided chest pain which was less severe than that of his previous admission and localized pain during rest. Absent symptoms are profuse sweating as well as nausea and vomiting, orthopnea and paroxysmal nocturnal dypsnoea, cough and fever. Patients past medical history includes diabetes mellitus and hypertension diagnosed 6 years ago, ischaemic heart disease (IHD) since 3 years ago, for which the last hospital admission was 11 months ago. In the previous admission for IHD, Mr. X also suffered from pneumonia and ventricular failure, his electrocardiogram (ECG) indicated right bundle branch block, his serum troponin I levels were 0.3 ng/mL (normal levels 0-0.1 ng/mL), and his creatinine levels were 5.0 mg/dL (normal for males 0.2-0.6 mg/dL). Mr. X is also afflicted with chronic kidney disease, for which his baseline creatinine dur ing his last admission was 208 ÃŽÂ ¼mol//L. Mr. X has retired from the military and is living with his wife, who monitors his medications and compliance. He used to be a chronic smoker but has stopped smoking 15 years ago. His previous medication history is as below: Drug and Form Strength Frequency Furosemide tabs 40 mg BD Omeprazole tabs 20 mg PRN Amlodipine tabs 10 mg OD Simvastatin tabs 20 mg ON Perindopril tabs 4 mg OD Table 1: Table showing past medications of Mr. X. Mr. X takes no non-prescription medications and has no known drug allergies. On examination he appears to be alert and comfortable on his nasal cannula for delivery of oxygen 3L/min. His blood pressure is 134/81 mmHg, pulse rate is 76 bpm, body temperature 37oC, SpO2 of 99%, abdomen feels soft and non-tender, and no pedal oedema was observed. A blood glucose strip test reveals that Mr. Xs glucose levels were 10.3 mmol/L. Emergency ECG shows right bundle branch block and no ischaemic changes. The tentative diagnosis was unstable angina and further tests were scheduled, including a full blood count (FBC), renal profile (RP), liver function test (LFT), troponin and creatinine (CKMB) investigations, as well as a urine full examination and microscopy (UFEME). The immediate plan was to give Mr. X subcutaneous enoxaparin 60 mg stat and twice daily thereafter, aspirin 75 mg tablets once daily, lovastatin 20 mg tablets once daily, sublingual glyceryl trinitrate when required, and to continue the 3L/min oxygen cannula. Clinical Progress Day 1 Morning Patient was well, free from chest pain, tolerating orally and suffering from no nausea or vomiting. He had minimal shortness of breath (SOB). Troponin I levels were at 0.15 ng/mL and ECG showed no acute or evolving changes. Fasting plasma glucose was at 4.8 mmol/L (within normal range). Secondary dehydration was observed using the skin pinch test, so patient was started on intravenous normal saline drip (3 x 500 mL bag per 24 hours). Patient was found to be anaemic due to pre-existing chronic renal failure. Evening Patient reported mild chest pain and SOB. His troponin I levels were 0.15 ng/mL and other vitals were normal. His creatinine levels were 423 ÃŽÂ ¼mol/L. Day 2 Patient felt comfortable and his vitals were normal. His creatinine levels decreased to 345 ÃŽÂ ¼mol/L. Day 3 Patients condition was well, no chest pain was reported but he was still experiencing some SOB in the morning, which subsided in the afternoon. Patient was put on continuous peritoneal dialysis in the late morning. Patients vitals were normal, and he was taken off enoxaparin in the evening. Day 4 Patient complained of chest pain in the morning, with minimal SOB. His vitals were normal. Subcutaneous enoxaparin 60 mg was given and the IV saline was continued. Lab Findings Urine Biochemical Analysis (Day 1) Investigation values Normal values Protein ++100 mg/dL Glucose negative negative Blood negative Leucocytes +-10 WBC/ÃŽÂ ¼L Ketone negative negative Bile negative negative Urobillinogen normal Specific gravity 1.025 1.003 1.040 pH 5.5 4.6 8.0 Nitrite negative negative Table 2: Results of urine biochemical analysis on Day 1 Lipid Panel Fasting Serum Lipid Plasma total cholesterol / mmol/L 4.5 Desirable Borderline 5.17-6.19 High risk >6.20 Plasma triglyceride / mmol/L 1.27 à ¢Ã¢â‚¬  Ã¢â‚¬Å" Desirable Borderline 1.7-5.64 High risk >5.65 Plasma LDL-cholesterol / mmol/L 2.91 à ¢Ã¢â‚¬  Ã¢â‚¬Å" Desirable Borderline 3.36-4.12 High risk >4.13 Plasma HDL-cholesterol / mmol/L 1.01 à ¢Ã¢â‚¬  Ã¢â‚¬Å" Desirable >1.03 High risk Total cholesterol / HDL-cholesterol 4.5 Desirable Borderline 3.8-5.8 High risk >5.9 Table 3: Results of lipid panel (fasting serum lipid levels). Renal Profile Electrolytes Measured levels on Day 1-1.14am Measured levels on Day 1-12.54am Measured levels on Day 2-10.47am Normal range Urea / mmol/L 22.8 22.4 21.1 2.8-7.2 Sodium / mmol/L 129 128 129 136-146 Potassium / mmol/L 5.3 4.8 4.7 3.5-5.1 Chloride / mmol/L 98 94 101 98-107 Creatinine / ÃŽÂ ¼mol/L 423 398 345 58-96 Table 4: Renal profile of Mr. X showing levels of electrolytes and creatinine. Plasma troponin I 0.15 ng/mL Liver Function Test Measured level Normal range Plasma total protein 81 g/L 66-83 g/L Plasma albumin 34 g/L 35-52 g/L Plasma globulin 47g/L 25-44 g/L A/G ratio 0.7 0.9-1.8 Plasma alkaline phosphatase 119 u/L 30-120 u/L Plasma aspartate transaminase 19 u/L Plasma alanine transaminase 43 u/L à ¢Ã¢â‚¬  Ã¢â‚¬Ëœ Plasma total bilirubin 6 ÃŽÂ ¼mol/L 5-21 ÃŽÂ ¼mol/L ESR 47mm/hour à ¢Ã¢â‚¬  Ã¢â‚¬Ëœ 0-20 mm/hour Table 5: Results of liver function test showing protein and liver enzyme levels in plasma. Full Blood Count (FBC) (Beckman Coulter) Cell type Measured level Normal range WBC 9.9109/L 4-10109/L RBC 3.341012/L 3.8-4.81012/L Haemoglobin 95g/L 120-150g/L Haematocrit 0.273L/L 0.36-0.46L/L Mean cell volume 81.8fl. 83-101fl. Mean cell haemoglobin 28.4pg. 27-32pg MCH concentration 347g/L 315-345g/L Platelets 353109/L 150-400109/L RDW 19.4% Neutrophils 3.3 2-7 x109/L Lymphocytes 1.74 1-3 x109/L Monocytes 0.55 0.2-1.0 x109/L Eosinophils 0.21 0.02-0.5 x109/L Basophils 0.03 0.02-0.1 x109/L Table 6: Full blood count of Mr. X. Vital Stats Chart Date Time Blood Pressure/ mmHg Temperature / oC Pulse Rate/ bpm SpO2/ % Blood Glucose levels/ mmol/L Day 0 11.05 pm 140/80 37 91 100 13.9 11.30 pm 137/84 37 80 100 Day 1 8.30 am 130/80 37 70 4.8 (fasting) 3.55 pm 130/70 37 90 10.30 pm 108/64 37 81 Day 2 8.20 am 119/69 37 78 4.50 pm 130/90 37 82 9.6 9.45 pm 140/90 37 80 6.7 Day 3 8.50 am 114/77 37 72 98 6.6 Table 7: Records of vital stats of Mr. X from Day 0 3. Disease Overview Pharmacological Basis of Drug Therapy Acute coronary syndrome (ACS) is a broad term used to classify a continuum of symptoms and events stemming from acute ischaemic episodes affecting the cardiac muscle.1 This includes unstable angina, non-ST segment elevation myocardial infarction (NTEMI), and ST segment elevation infarction. It is usually characterised by chest pain which increases in its severity at rest or with physical exertion. The ischaemic events usually arise from the development of unstable atheromatous plaques,2 which explains the fact that stable angina (due to a stable coronary atheromatous plaque) is not included under this umbrella term. Rupture, ulceration or fissures of the atherosclerotic plaque often leads to formation of a thrombus, causing occlusion of coronary arteries and inadequate blood flow and, subsequently, inadequate supply of oxygen and nutrients to the cardiac muscle. This can be precipitated by acute stress factors on the sclerotic cap usually consisting of fibrous material, which is caus ed by local blood flow disturbances or vasospasms3. Unstable angina usually occurs without cardiac muscle damage while myocardial infarction (MI) may occur with or without myocardium damage. The thrombus formed in unstable angina is labile and obstruction is transient, and not a full-on occlusion as would occur in MI.4 Unstable angina occurs at rest and is almost indistinguishable from a non-ST segment elevated myocardial infarction except in the severity of cardiac muscle ischaemia. Theoretical definitions of unstable angina would include changes in usual patterns of stable angina after a stable pain-free period, or severe acute anginal pain causing almost total incapacity5, though it is difficult to define it exactly as the term is often used by medical professionals to describe a range of different conditions intermediate between stable angina and MI. The primary clinical symptoms of unstable angina are: sudden occurrence of chest pain that persists for more than 20 minutes which may be felt in other areas such as the jaw, arm, shoulder, neck or back; without cause (as opposed to stable angina which stems from physical exercise); shortness of breath, rapid pulse rate, and sometimes a rapid drop in blood pressure. Patients suffering from an ACS have a high risk of MI and possible even death; immediate hospitalization is often required1 and treatment is of a more urgent nature compared to that of stable angina. It has been suggested by the National Health Service (NHS) Hospital Episode Statistics in 1998 that 1000 out of every million per population is affected with unstable angina, or 10 acute hospital admissions per week.6 On a more recent note, NHS has reported in 2009 that angina affects between 10-15% of women and 10-20% of men aged 65 and above in England.7 Due to the close relationship between unstable angina and coronary events, it is worth noting that the highest averaged rates of cardiovascular events were observed in Glasgow and Belfast (UK), North Karelia and Kuopio (Finland), Newcastle (Australia), and Warsaw (Poland).8 Diagnosis of an unstable angina episode, or any ACS in that matter, is based on several aspects9. Physical symptoms include anginal pain at rest that lasts for 20 minutes or more; new onset angina severely limiting ability of physical activity; or changes in existing angina intensity, frequency or length of attack. One or more of these symptoms are an urgent indication that the patient is suffering from an ACS attack. Upon admission to hospital, ECG and blood tests should be performed to confirm the type of ACS in order to initiate treatment. In unstable angina, the ST segment is not elevated and levels of cardiac enzymes are normal (especially troponin T and I). If the onset of symptoms is unclear as to indicate ACS, a measurement of serum troponin concentration should be carried out 12 hours from presentation to establish the diagnosis.10 Treatment of unstable angina and NSTEMI are similar in terms of pharmacological management; indeed they are at presentation indistinguishable exc ept in terms of the severity and extent of cardiac muscle ischaemia, in which the ischaemia is less severe in unstable angina and less troponin T and I are released into the bloodstream. Antiplatelet agents. Aspirin and clopidogrel are the immediate emergency drugs used in the ambulance, both being antiplatelet drugs. Aspirin is an irreversible inhibitor of arachidonate cyclooxygenase (COX) enzyme, in which covalent acetylation of the serine moiety in a hydrophobic channel in the enzyme11 reduces synthesis of thromboxane A2 in platelets and prostaglandins in the endothelium. This prevents platelet aggregation and further enlargement of the thrombus formed in the coronary artery. Clopidogrel is an inhibitor of the ADP-dependent activation of the GPIIb/IIIa receptor and prevents the formation of fibrinogen bridges between glycoprotein IIb/IIIa receptors on the surfaces of platelets11, subsequently preventing platelet activation. Glycoprotein IIB/IIIA receptor antagonists, eg, abxicimab, have the advantage of inhibiting all pathways in the platelet activation process by inhibiting the glycoprotein IIB/IIIA receptor. Anticoagulants. Unfractionated heparin is an activator of antithrombin III, which inhibits the action of thrombin and serine proteases. The heparin also binds to thrombin; the combined effect of this and the heparin-antithrombin complex formed inhibits thrombin, which decreases the conversion of fibrinogen to fibrin and reduces platelet aggregation. In contrast, low molecular weight heparins (LMWH) have molecular sizes that are too small to bind to thrombin but still bind to antithrombin III, which inactivates all serine proteases including Factors XIIa, IXa, and Xa11, preventing the coagulation process. Direct thrombin inhibitors such as hirudin and bivalirudin inhibit thrombin reversibly. These agents can bind to free and bound thrombin, thus have the ability to prevent and dissolve preformed clots. Synthetic pentasaccharides (fondaparinux) is a selective indirect inhibitor of Factor Xa. It binds to antithrombin III reversibly, catalyzing the inactivation of Factor Xa12 and inhibit ing the coagulation cascade. Beta blockers. All beta blockers bind to beta-adrenoceptors, competitively antagonizing the action of catecholamines. These drugs block the beta-1 adrenoceptors at the heart, achieving a decreased heart rate and force of cardiac contractions, as well as lowering blood pressure. Atenolol is relatively specific for cardiac beta-1 adrenoceptors and exerts fewer side effects associated with beta-2 adrenoceptor blockade, for example bronchospasm in asthmatics. Nitrates. Organic nitrates mimic the actions of endogenous nitric oxide to relax vascular smooth muscle by increasing the synthesis of cGMP, leading to the dephosphorylation of myosin light chains.11 Vasodilatation of coronary arteries causes increased coronary blood flow and coupled with its effects of decreasing arterial pressure and also cardiac output, the myocardial oxygen consumption is largely reduced. Statins. Also termed HMG-CoA reductase inhibitors, these medicines inhibit the rate-limiting enzyme in the synthesis of cholesterol, in which this enzyme converts HMG-CoA to mevalonic acid. ACE inhibitors are diuretics acting on the rennin-angiotensin system which inhibit the angiotensin-converting enzyme (ACE) and block the production of angiotensin II from angiotensin I. This reduces vascular resistance, increases tissue perfusion, and reduces cardiac afterload. Angiotensin II receptor inhibitors also act on the same system as the ACE inhibitors, except that they block the angiotensin II receptors directly instead of inhibiting their formation. The outcome is the same as above. Evidence for Treatment of the Condition Antiplatelet Agents The SIGN guidelines advocate that aspirin and clopidogrel be given to patients with ECG ischaemic changes or increased levels of cardiac markers; and aspirin is advocated for all patients suffering from ACS. A meta-analysis of 287 randomised trials proves the protective effect of aspirin on patients with unstable angina, halving the rate of cardiovascular events, including death, non-fatal MI and strokes, or also termed the first primary outcome; while in those with an acute MI, it reduces the rate of coronary events by almost a third13. Long-term use of aspirin for these patients was also shown to be a beneficial antiplatelet therapy. According to the same study, reduction of serious vascular events by clopidogrel was 10% compared to aspirin. The combined use of clopidogrel and aspirin as compared with a placebo and aspirin showed significantly higher success rates in reducing occurrences of first primary outcomes (9.3% compared to 11.4%, P On the flipside, although short term studies have shown that antiplatelet medications are effective for patients with renal failure in the prevention of serious vascular events13, the risks of bleeding is increased by renal disease15, posing a possible contraindication for antiplatelets to Mr. X. A clinical study found that treatment for NSTEMI ACS in patients with chronic renal disease (mild to moderate stages) was less aggressive than those with normal renal function, despite the risk that these patients with renal disease would experience greater adverse outcomes from insufficient treatment for ACS compared to the other patient group16. However the available information on adverse effects of antiplatelets on patients with varying degrees of renal disease is limited and it would appear that this would result in the reluctance of medical professionals in using this class of drugs for patients with chronic renal disease as well as ACS. It can be inferred that Mr. X would gain the maximum benefits if his medications were changed to aspirin 300 mg and clopidogrel 300 mg stat and aspirin 75 mg and clopidogrel 75 mg thereafter, in which the patient should be closely monitored for signs of bleeding. Heparins LMWHs A 2003 review of 7 studies involving 11,092 patients with non-ST elevation ACS found that low molecular weight heparins (LMWH) were more effective than unfractionated heparins in reducing MI events, requirement for revascularization procedures, and thrombocytopenia17. No difference in the mortality, recurrent angina, major and minor bleeds were observed in the two types of drugs. A meta-analysis of 12 randomised trials with 17,157 patients involved found that patients who have had a non-ST elevation ACS who were put on aspirin experienced no significant difference in benefits in efficacy (preventing MI or death) or safety (major and minor bleeding complications) when they were put on unfractionated heparin or LMWH17, implicating no difference in the thrombolytic effect in both classes of drugs. These results are partially similar to those of the first review. Another meta-analysis of 2 phase-3 trials comparing enoxaparin and unfractionated heparin, on the other hand, showed a signifi cant (20%) difference in reducing death or severe cardiac ischaemic events18. From an economic point of view, authors of yet another meta-analysis on the subject stated that the cost of LMWH is 3-5 times higher than unfractionated heparin19. From these data it can be concluded that LMWHs does indeed have additional positive treatment outcomes compared to unfractionated heparins22; it does not show significantly decreased side effects (bleeding). Enoxaparin has, though, an increased bleeding effect on patients with renal disease as reported by an investigation of 106 patients, in which total bleeding complications occurred in 22% of normal patients and 51% of patients with impaired renal function (p It is still the drug of choice for patients present with non-ST elevated ACS, and this is applicable to Mr. X with unstable angina. Beta-Blockers Beta-blockers were not prescribed for Mr. X. The SIGN guidelines states that beta-blockers should be the drug of choice for first line treatment of anginal pain in patients with non-ST elevated ACS. A meta-analysis of 5 trials consisting of 4700 patients in all showed a 13% reduction in anginal pain with the use of beta blockers (initially IV then oral for a week) in patients with non-ST elevated, MI-characterised chest pain23. It was stated in the clinical progress Mr. X had chest pain on Day 1 and 4, thus the addition of a beta blocker to his medications would be useful in alleviating his pain. Despite the popular belief that beta-blockers are contraindicated in patients with diabetes mellitus, it is possible to treat these patients using beta-blockers as long as good glycaemic control is achieved and the patient is monitored regularly24. This would further support its use in Mr. X; furthermore, several studies have shown that diabetic patients derive a significant benefit from the use of beta-blockers after an MI, in which diabetic patients had a significantly lower mortality 1 year post-discharge25, total mortality after 3 years, and deaths from cardiac events26. A multicentre randomized trial, the HINT trial, on patients with unstable angina found that metoprolol, a relatively cardioselective beta blocker, reduced occurrence of myocardial ischaemia or progress to MI within 48 hours, indicating that metoprolol has a short term beneficial effect on patients not already taking beta blockers prior to the unstable angina episode27. It has been suggested that beta-blockers be the first line treatment for unstable angina and if patients remain unstable, a calcium channel blocker should be added28. Statins The beneficial effects of statins in reducing mortality and cardiovascular events have been proven by a meta-analysis of large, randomized controlled trials (n=90,056) where coronary artery disease was present or absent29. The positive results were also proven spanning a large range of serum cholesterol levels. Investigations comparing the use of intensive versus moderate doses of statins in the early stages and post-ACS showed positive results: a meta-analysis of 4 large trials (n=27,548) shows a 16% reduction in cardiovascular deaths or MI, as well as a 16% reduction in cardiovascular deaths or coronary events30. This view is shared by another meta-analysis of the same subject of 13 randomised controlled trials which found a decrease in mortality and coronary events after 4 months of treatment31. These data support the use of statins by Mr. X. Nitrates Nitrates have been widely used in relieving pain from unstable angina, despite its lack of clinical evidence in supporting its role in improving survival and reducing the rate of MI and cardiovascular events32. ISIS-433 and GISSI-334 reports no significant difference of the use of glyceryl trinitrate post-MI in reducing the overall mortality; however this may be explained by the fact that more than 50% of patients in the controlled group are also on other forms of nitrate therapy, such as intravenous glyceryl trinitrate. Despite this, nitrates will still be of use for reducing the pain in post-MI patients and those with unstable angina. The BNF advises against the use of nitrates in patients with serious anaemia (Hb Glycaemic control Mr. Xs plasma glucose levels were elevated on the day he was admitted to hospital (13.9 mmol/L). Diabetes mellitus has been proven to be a strong independent risk marker for coronary heart disease: patients with poorly controlled diabetes at hospital admission have a worse outlook on prognosis and future development of cardiovascular events35. The DIGAMI investigation reports that the use of intensive insulin therapy increased long-term prognosis (P=0.011) of patients presenting with hyperglycemia (>11mmol/L) at admission compared with those on standard antidiabetic therapy36. These data support the use of insulin to control the blood glucose levels of Mr. X which were highly increased upon admission. This is also supported by the SIGN guidelines which advocate immediate control of blood glucose is carried out for MI patients with glucose levels of more than 11.0 mmol/L for at least 24 hours. ACE Inhibitors The SIGN guidelines recommend that patients with unstable angina should be given ACE inhibitors as long-term therapy. In patients at high risk of cardiovascular events, ACE inhibitors (ramipril was investigated in a report37) have been proven to reduce overall mortality, MI, and stroke, particularly in patients with diabetes mellitus. Perindopril was found to reduce cardiovascular risk (relative risk reduction =20%, P=0.0003) in a population with stable coronary heart disease in absence of heart failure38 in a double-blinded, randomized multicentre trial involving 13,655 patients. A meta-analysis of the 2 above trials and a third one (PEACE) showed a reduction in overall mortality, cardiovascular death, non-fatal myocardial infarction, stroke, heart failure, and coronary artery bypass surgery by ACE inhibitors39. This demonstrates the benefits of ACE inhibitors in patients with atherosclerosis: as patients who had an ACS event would have a higher rate of cardiovascular events, the po sitive outcomes of ACE inhibitors can perhaps be extrapolated to this population in order to decrease coronary events and improve prognosis. However, the BNF advises caution and close clinical monitoring if ACE inhibitors are to be used in patients with hyponatremia ( Oxygen therapy On admission, Mr. Xs SpO2 was 99% and remained high throughout his stay in the hospital. The use of oxygen therapy is significantly beneficial only in hypoxic patients (with SpO2 Anaemia and Unstable Angina Anaemia can disturb the balance between myocardial oxygen supply and demand: a decrease in the number of red blood cells can lead to a reduction in the supply of oxygen to the myocardium. Thus correction of the causative factor would be sensible in the treatment of unstable angina for the patient in context. Mr. X was given a combination of ferrous fumarate, vitamin B complex, and folic acid for treatment of his anaemia. From the data in Table 6, it can be seen that Mr. X has low haemoglobin concentrations (95 g/L) and a low mean cell volume (81.8 fl.). To confirm that Mr. X is indeed suffering from iron-deficiency anaemia (as suggested by his treatment medication), three parameters must be established namely the plasma iron, the plasma ferritin, and total iron binding capacity. However, as very few conditions can cause abnormalities in the mean cell volume, and a decreased value is due to iron-deficiency anaemia or thalassemia42, it is safe to assume that Mr. Xs anaemic condition is due to an insufficiency of iron. Iron supplements are given to correct the iron status of the patient, in which the ferrous form given orally is found to be cheap, safe and effective in the majority of patients with iron-deficiency anaemia2. Vitamin B complex and folic acid are only indicated in patients with the respective deficiencies2; there is little evidence that they would be of any significant benefit in patients with iron-deficiency anaemia. Summary Based on the evidence given, Mr. Xs aspirin dose should be changed to 300 mg stat and 75 mg thereafter, and clopidogrel should be added into his medication profile in the same doses. These changes ensure that Mr. X is obtaining sufficient antiplatelet effects from his medications to prevent another attack of unstable angina or even a myocardial infarction. Present drugs that were given for his condition that are suitable and supported by evidences include enoxaparin, lovastatin, insulin, and GTN: these can be safely continued without problems. A beta-blocker (metoprolol tablets) may be given additionally in doses of 50-100 mg as evidences described above have shown that they can be safely used in diabetic patients contrary to popular belief; an ACE inhibitor (perindopril as previously used by Mr. X) may be initiated coupled with regular electrolyte

Comparison of Chicken Feed Effects on Development

Comparison of Chicken Feed Effects on Development All six significant domesticated agricultural animals today chicken, cow, goat, horse, pig and sheep had been domesticated in Eurasia by 5000 BP. (Thompson, 2002) The earliest evidence of domestication of chickens relies on interpretation of archaeological discoveries of bones and artefacts. (Crawford, 2003) Archaeological discoveries in China indicate that chickens had been domesticated by 5400 B.C. (Crawford, 2003) People of Cishan Culture (Neolithic Yellow River culture in northern China) had chickens then, but it is not known whether these birds made much contribution to modern domestic fowl. (Crawford, 2003) The jungle fowl (G. gallus), has without a doubt been a major contributor to domestic fowl (Crawford, 2003). The chicken (Gallus, gallus or Gallus domesticus) is generally considered to have evolved from the jungle fowl (G. gallus). (Kennth Kriemhild, 2000) The jungle fowl (G. gallus) ranges throughout the area between eastern India and Java. (Kennth Kriemhild, 2000) There are four key steps to domesticating poultry which were that in early stages of domestication poultry had to forage on their own. (Crawford, 2003) They had to be able to reproduce in captivity (Crawford 2003) the ability to imprint was important in initial taming. (Crawford 2003) and the species had to have a social order that allowed the keeping of large numbers of individuals. (Crawford, 2003) The main role of chickens now is to produce eggs and meet for the market. In 2004/2005 the gross value of production in Australia for the chicken meat and egg industries was estimated at approximately $1.3 billion. (Department of Primary Industries, 2008) Poultry meat is now the most consumed meat in Australia. . (Department of Primary Industries, 2008) Although chickens are strongly associated with egg production, they also have very different associations. (Kennth Kriemhild, 2000) In much of Southeast and East Asia they have been bred both for fighting and as a decoration. (Kennth Kriemhild, 2000) There are four different types of poultry enterprises: broilers (production of chicken for meat), layers (birds producing table eggs), rearing farms (production of point of lay pullets) and breeder farms. (Department of Primary Industries, 2008) The layout of the shed and type of housing differs between the types of poultry operation. (Department of Primary Industries, 2008) The aims of this experiment are to monitor and assess the development of chickens on different feeds using a feed conversion ratio, and to observe and describe their physical and behavioural development over time. On appointed days chickens were to be fed and given water on a daily basis. Excess foods were weighed and recorded so ratios could be calculated and obtained. Chickens were weighed on a weekly basis, on Wednesdays, so that the calculation of growth rate could be put monitored and observed. Along with this observations were made of chickens on various days, if not everyday for behavioural studying purposes. It was hypothesised that chickens fed on broiler feed would have a greater weight gain than chickens fed on layer feed over the 5 week period. METHODS The chickens were obtained from a poultry farm known officially as Wagners Poultry Enterprises. The chickens given were White Leghorn cross New Hampshire at the age of one or two days old. The chickens were divided into groups of six and student groups of approximately sixteen students were assigned to one group of chickens each. Chickens were placed in pens and in turn students were assigned to the pens where the chickens were kept through out the five week duration. The chickens pens located at La Trobe Universitys Agricultural Reserved housed a total of twelve chicken pens. The type of feed given to the chickens was decided by the group number the pen was given. Groups assigned to even number pens were to feed their chickens broiler feed, brand named Brastoc Turkey and Meat Chicken Starter, and odd numbered pens were to feed their chickens layer feed, Barastoc Pullet Starter. The pens were isolated, self-contained and about 1 x 1 x 2 m in size. The floor of the pens was concrete which was covered in black lining and contained a sawdust base. The top of the pen had a plastic mesh over it to prevent escape. The chickens were provided with heat lamps, feeders and water dispensers all attached to a chain and hooked to a pole above the mesh. The feeders and water dispensers along with the heat lamps were adjusted in accordance with the chickens age. Observations were carried out as much as possible, sometimes even twice in the one day, but generally all days except Tuesday was observed in accordance with the students university timetable and their availability. The duration of the observations under went intervals of fifteen minutes, where all aspects of behaviour and development were documented. Observations were done under the least amount of outside influence as possible, in respect to this only two students were allowed in the shed where the chicken pens were being kept and students were encouraged to keep noise to a minimum. As the weeks went on chickens behaviour that was recorded included those such as grooming, resting, drinking, interacting, alarming, ambulatory and aggressive. Above all the behavioural and developing attributes the hierarchy if any of chicken formation was also documented. All observations were recorded and documented into a plain exercise book by each student of the group, with clear indication of whom the observations were done by. Chickens were feed every second day, Monday, Wednesday and Friday, with enough food given on each day to last the chickens for days not fed and on Fridays for the weekend. Initially a total of 240g were placed in the feed dispensers to accommodate the 20g required for each individual chicken and to compensate for the day the chickens would not be fed. The amount given to the chickens on feeding days was adjusted to accommodate for their growth further along in the project. Along with accommodating for the size of chickens the amount of feed to be given to chickens in further weeks was also based upon amount of feed offered and refused, all of which was weighed and kept a record of. Food was weighed on an electric scale in a container provided. The amount of food given and refused was always recorded on a sheet given to us indicating the date and feed given and refused. The sheet was stored along with our observation book, hooked onto a nail on the outside of the allocated chicken pen. Chickens were checked on a daily basis and were given fresh water daily if needed, except for weekends, providing the chickens with fresh drinking water. Replenishment of water was recorded alongside on the same sheet of paper where the feed record was being kept. Table 1. A timetable showing jobs carried out each day over the 5 week period Monday Feed, water check and observations Tuesday Water and chicken check Wednesday Feeding, weighing, water check and observations Thursday Observation, chicken and water check Friday Food, water and observation RESULTS Table 2. Composition of feeds Composition:Â  Crude Protein (minimum) (%) Layer feed:Â  19.5 Broiler feed:Â  22 Composition:Â  Crude Fat (minimum) (%) Layer feed:Â  2.5 Broiler feed:Â  2.5 Composition:Â  Crude Fibre (minimum) (%) Layer feed:Â  6 Broiler feed:Â  5 Composition:Â  Salt (maximum added) (%) Layer feed:Â  0.3 Broiler feed:Â  0.3 Composition:Â  Copper (added) (mg/kg) Layer feed:Â  0.8 Broiler feed:Â  8 Composition:Â  Selenium (added) (mg/kg) Layer feed:Â  0.1 Broiler feed:Â  0.3 Composition:Â  Calcium (minimum) (%) Layer feed:Â  1 Broiler feed:Â  1 Table 2. Shows that layer and broiler feed had the same amount of crude fat, salt and calcium. Broiler feed has more crude protein, copper and selenium than layer feed, whereas Layer feed has more crude fibre than broiler feed. DISCUSSION The results support the hypothesis that chickens fed on broiler feed would have a greater weight gain than chickens fed on layer feed over the 5 week period, as table 3 and figure. 1 show that chickens fed broiler feed had a higher average weight gain then chickens fed on layer feed. The aims of this experiment to monitor and assess the development of chickens were carried out over the five weeks and observations were made describing their physical and behavioural development over time. The experiment was carried out on chickens with different feeds and a feed conversion ratio was calculated. We also provided the chickens with clean drinking water, sufficient food amounts of food according to their age and feed refusal and a suitable environment in which they could grow and develop certain behaviours. The broiler chickens had a higher growth rate, as shown by table 3 and fig. 1. By the end of the 5 weeks, the broiler chickens reached a live-weight of 467 ÂÂ ± 58 where as chickens who consumed the layer feed for the duration of the experiment reached a live-weight of 429 ÂÂ ± 61. The difference between the growth rates of the broiler and layer chickens is closely related to live-weight. Through out the process, beginning in week one, chickens being fed broiler as opposed to layer maintained a higher growth ratio and remained heavier that the chickens being fed the layer product. In respect to this broiler chickens are capable of higher growth rates and greater weight gain than layer chickens. In the poultry industry, broiler chickens are selected for their carcass processing characteristics and meat density, whereas layer chickens are genetically bred to achieve smaller body weights than those of the broilers (Department of Primary Industries, 2009). Another factor of the growth and weight gain in chickens could also be the composition of the feeds. As seen in table 2 the broiler feed contained 2.5% more crude protein, 7.2 mg/kg more copper and 0.2 mg/kg more selenium than the layer feed. All these factors couldve influenced the growth in chickens and could be why chickens fed broiler feed would gain more live-weight as well as maintain a higher growth ratio. The increase in growth rate found within broiler chickens has been found to be linked to an increase in the deposit of fats and the use of energy. (Geraert et al 2006) All ingredients fond within the chickens feed contributes some part to their growth and weight gain. Coppers influence on health and growth within a chicken is present as the antimicrobial properties found within Cooper help to improve an animals performance such as; increase growth in poultry, improved growth rate, feed intake and feed efficiency (Forbes Shariamatdari 1993). Crude protein also influences the diet energy of a chicken when they are still young (Hayashi et al 2000) as well as their metabolic ability. (Hayashi et al 2000) From the experiment as show in table 4, it shown that broiler chickens have a slightly better feed conversion ratio of 1.5 ÂÂ ± 0.129 g but also maintain a higher feed intake 3889 ÂÂ ± 534 g than that of layer chickens, whose feed conversion ratio is similar to that of the broiler chickens at 1.52 ÂÂ ± 0.051 g and less of a feed intake at 3549 ÂÂ ± 247 g. Calcium levels also differ between that of the layer and broiler feeds. Layer feed has 0.5% more calcium than broiler feed. Calcium ratio plays a vital role in the quality of an egg produced, (Department of Primary Industries) As the chickens grew and developed more, so too did their behavioural characteristics. To begin with the chicks were hardly active at all being under the heated lamp majority of the time, however after a fortnight the chickens activity level was significantly higher, showing signs of flapping wings and a lot more running around within the pen. This behaviour of flapping of the wings is a mechanism known as break used by chickens. (Rogers 2006) Within the second week it was observed that chickens were preening one another, this type of behaviour was commenced whilst the chickens were flocked together in a group always near a wall. Preening aids in the removal of lice and is done using the beak (Gush 2006). As the chickens progressed with age in the 4th week a lot of the time was spent sitting perched up above the food and water dispensers. This type of behaviour is normal and is to be expected after four weeks of age. (Rogers 2006) Through out the five week period and supported by table 6 interactions was the most common behaviour during the experiment. Among these interactions were behaviours such as pecking and scratching, which were major contributors to the interaction database. The behavioural interaction of pecking and scratching are present during all ages of a chicken (Rogers 2006) and are the major ways in which chickens interact and assimilate with their surroundings. (Gush 2006) Through out the 5 week period no formal hierarchical establishment appeared to be present. However there was the mild sign of aggression where chickens would kick at each other within the third week but this type of behaviour was rare and unseen after later dates. A hierarchy within chickens is not formed up until about the sixth week or onwards within domestic chickens (Rogers 2006) and thus no aggressive behaviour was present either as aggression is derived from the sequence of the hierarchy. (Rogers 2006) It was found that roosters were among the chickens which were handed out to us. Roosters in general like male and female humans tend to be heavier than that of their female counter. The inclusion of roosters within the results could be erroneous to the over all weight gain results. This experiment could be improved by regulating the gender of the two strains of chickens being introduced to the artificial environment thus giving more accurate and reliable end results and will nullify the problem of genetic variability.

Ednas Struggle for Power in Chopins The Awakening Essay examples --

Edna's Struggle for Power in Chopin's The Awakening Kate Chopin's The Awakening tells the story of Edna Pontellier, a young wife and mother living in the upper crust of New Orleans in the 1890s. It depicts her journey as her standing shifts from one of entrapment to one of empowerment. As the story begins, Edna is blessed with wealth and the pleasure of an affluent lifestyle. She is a woman of leisure, excepting only in social obligations. This endowment, however, is hindered greatly by her gender. Being a woman, she is completely at the mercy of her husband. He provides for her a lifestyle she could not obtain on her own and fixes her place in society. This vulnerability stops Edna from being truly empowered. To gain independence as a woman, and as a person, Edna must relinquish the stability and comfort she finds in the relationship with her husband. Mr. and Mrs. Pontellier's marriage comprises a series of power plays and responds well to Marxist and Feminist Theory. Leonce Pontellier looks "†¦at his wife as one who looks at a valuable piece of property†¦". He views her as an accessory that completes the ideal life for him. Edna, however, begins to desire autonomy and independence from Leonce, so true to the feminist point of view. In Chapter III Mr. Pontellier enters their room in Grand Isle late one night, waking Edna. He is full of self-importance as he talks to her while he begins to ready himself for bed. Since she has just been awakened, Edna does not respond with the enthusiasm Mr. Pontellier deems acceptable. "He thought it very discouraging that his wife †¦ evinced so little interest in things which concerned him, and valued so little his conversation." (12) To assert his dominance, Leonce demands that E... ...cision does not spawn from her relationship with her husband, she cannot yield the independence she has won and return to him. In order to fulfill her quest, she must continue on her search for independence. "The voice of the sea is seductive, never ceasing, whispering, clamoring and murmuring, inviting the soul to wander in the abysses of solitude." She submerges herself in the ocean and in the solitude she has longed for throughout the novel. Only in her death is Leonce completely powerless. She has taken control of her destiny. Edna Pontellier as a literary character is shocking for her time. She achieves true empowerment, a status not often experienced by women in the Victorian Era. She rebels against her husband and the social norms that he represents. True to the time, such a conflict could not resolve in her favor without sorrow, but ultimately Edna triumphs.

Charles dikenson biography :: essays research papers fc

Charles Dickens Biography   Ã‚  Ã‚  Ã‚  Ã‚  Charles Dickens was one of the most popular writers of all time. Dickens was very observant of life, and had a great understanding of humanity.   Ã‚  Ã‚  Ã‚  Ã‚  Charles John Huffam Dickens was born in Portsmouth, England, on February 7, 1812. When he was two years old he and his family moved to London. Dickens father, John Dickens, was a poor clerk who worked for the navy, and he also spent time in prison for debt. When John was not in prison he lacked the money to adequately support his family. When Charles was twelve he worked in a London factory. That job was so miserable that the misery of the experience stayed with him his whole life. Dickens became a newspaper reporter in the late 1820’s. He specialized in covering debates in Parliament and also wrote feature articles. This helped him develop his skill portraying his character’s speech realistically. His first book was â€Å"Sketches by Boz† in 1836; it consisted of articles he wrote for monthly magazine. The book that got him famous was â€Å"The Posthumous Papers of the Pickwick Club. This book describes the adventures and misadventures of a group of people in an English countryside. Dickens founded and edited two highly successful magazines. Those magazines were â€Å"Household Words† and â€Å"All Year Round†. Dickens was always in the news, and was honored, and recognized everywhere he went. In 1836 Dickens married Catherine Hogarth. Catherine had a sister named Mary, who died in 1837. Dickens grieved so much over her death that some people believe that he loved her more then he loved Catherine. Catherine was a good wife but she wasn’t a very intelligent woman. She an Dickens had ten children, and separated in 1858. Dickens had a vast amount of physical and mental energy. He had so much energy that he could record all of his activities and make it interesting to read. Dickens had a life other than writing. He spent much of his free time with his friends from the worlds of art and literature. He also enjoyed drama. He went to the theater as often as he could. When he was rich and famous, he produc ed and acted in amateur theatrical productions. Dickens was also a giving person. When he was not socializing or in the theater, he was giving to various charities. These charities included giving money toward build schools for the poor school children and loans that enabled the poor to move to Australia.

Jewish Art :: essays research papers

Jewish Art On many occasions art has the power to tell a story or even express how someone feels. The speaker on Jewish art was very interesting. She translates many Jewish stories and commandments while portraying it through art. Very few people can accomplish this but I thought she did a pretty good job of it. Her pieces once explained told great stories of Jewish history. One thing that I found very iteresting was her idea of adding new riuals to the jewish religion through her art. I'm glad that I have always liked art because it helped me to understand her feelings towards it. The speaker showed a lot of enthusiasm and love for her art. She seemed to be very care-free and almost worry free. I though she was very cool and really did a good job of expressing her feelings toward her art. One important aspect of her art was that for her seeing her pieces come out of a fire was a reward in itself. She was not in it for the mmoney or material rewards. I think a lot of times people are only in it for material reward and it gets in the way of great art. It seems to me that this helped her to become such a good artist   Ã‚  Ã‚  Ã‚  Ã‚  Her focus was mainly on very well known Jewish objects. Some of these include Menorahs, Sadaka boxes, and Mezuzahs. These where very evident part of her slide show. All of them were very obscure and odd looking but each told a storyf which only she knew. At first glance they were not so great but after her explanation they became beautiful.   Ã‚  Ã‚  Ã‚  Ã‚  Her idea of creating new rituals for our religion through art really striked me. I found her ideas to be very interesting because it was som   Ã‚  Ã‚  Ã‚  Ã‚  I think that many times Judaism is expressed through art because there are so many beliefs on what it means to be a Jew. Many people cant explain how they fell in words so , in this case, a more fun and interesting way was used. Even though many religious people don't agree with this way of expression I feel that it is obviously better than nothing.   Ã‚  Ã‚  Ã‚  Ã‚  It was evident that the Holocaust Had a major influence on her works. She said that she liked the fact that even after her pieces were burned they

William Shakespeare: Greatest Poet & Playwright

England's greatest poet and playwright was born in Stratford, the son of a tradesman and Alderman of Stratford, John Shakespeare in 1564. William, the eldest son, and third child of eight, was baptized on the 26th April 1564. He received his early education at Stratford Grammar School, but little is known of his life up to his eighteenth year. His Grammar School curriculum would have provided a formidable linguistic, and to some extent literary education. It is noted that he did not like grammar but did have a love for dramatics. Shakespeare attended King†s New School in Stratford which was one of the best grammar schools. Shakespeare read many books. He used some of these books as sources for his plays. One of his most prominent sources of literature was the book The Union of the Two Noble and Illustre families of Lancaster and York written by Hall. Shakespeare used this book to help inscribe his plays about many kings including three plays about Henry VI and a play written about Richard III. Also he wrote Othello on the basis of Hecatommithi and Twelfth Night on the basis of His Farewell to Military Profession. More than fifty percent of Shakespeare†s plays were influenced from various groups of topics. Other things that influenced Shakespeare†s plays were his life experiences. As a young boy dramatic events that occurred led to his writing of Hamlet. The drowning of a girl named Katherine he knew was also a source of his playwriting. History affected his writing as well. One of Shakespeare†s most heralded plays was based on the life and demise of Julius Caesar. He gathered information about Caesar, and with his literary brilliance wrote about Caesar and his story in a unique perspective. Also the life of Marc Antony was very influential in one of Shakespeare†s great plays, as well as the bible and other chronicles. Many of these influences were brought upon by his education, which taught his a lot about history and its figures. Many reasons can be given for Shakespeare's enormous appeal. His fame basically is from his great understanding of human nature. He was able to find universal human qualities and put them in a dramatic situation creating characters that are timeless. Yet he had the ability to create characters that are highly individual human beings. Their struggles in life are universal. Sometimes they are successful and sometimes their lives are full of pain, suffering, and failure. In addition to his understanding and realistic view of human nature, Shakespeare had a vast knowledge of a variety of subjects. These subjects include music, law, Bible, stage, art, politics, history, hunting, and sports. Shakespeare had a tremendous influence on culture and literature throughout the world. He contributed greatly to the development of the English language. Many words and phrases from Shakespeare's plays and poems have become part of our speech. Shakespeare's plays and poems have become a required part of education in the United States. Therefore, his ideas on subjects such as romantic love, heroism, comedy, and tragedy have helped shape the attitudes of millions of people. His description of historical figures and events has influenced our thinking more than what has been written in history books. The world has admired and respected many great writers, but only Shakespeare has generated such enormous continuing interest.

Week 1 Knowledge Check

Knowledge Check Week 1The material presented below is not meant to be a comprehensive list of all you need to know in the content area. Rather it is a starting point for building your knowledge and skills. Additional study materials are recommended in each area below to help you master the material. Personalized Study Guide Results: Score: 12 / 12 Concepts Mastery Questions Pricing Decisions 100% Market Systems 100% Market Equilibrium 100% Concept: Pricing Decisions Mastery 100% Questions 1 . Revenue increases when †¢ A. roducer surplus increases Correct : Producer surplus is the difference between the minimum price the producer is willing to receive and what they actually receive. The surplus is their profit, and the larger the surplus, the greater their profit on the good. When it decreases, the producer receives a price closer to the minimum acceptable. The consumer surplus measures what the consumer is willing to pay and that price’s difference from the market price. The closer to the market price, the higher the consumer surplus, as consumers are spending ess than they are willing to, and the less spent, the lower the revenue will be for the good. Materials †¢ Producer Surplus 2 . An increase in the price of an inelastic goods †¢ C. increases revenues Correct : Inelastic goods are necessities that consumers continue to purchase even when the price increases. This increases the revenue, as more is paid for each good. The percentage change in price increases faster than the change in quantity, which may remain constant. When more is paid for a good or a service, revenue increases. Materials †¢ Price Elasticity and the Total-Revenue Curve Inelastic Demand 3 . Price elasticity of Demand increases whe †¢ C. people become more price sensitive over time Correct : Price elasticity of demand measures the percentage change in quantity demanded divided by the percentage change in price. Price elasticity is either inelastic or elastic. As the price elasticity of demand coefficient rises, price elasticity becomes more elastic. A low price elasticity coefficient relates to an item that has very few substitutes, which causes people to be less sensitive to a change in price, such as in gasoline or medicine (inelastic demand, Ed