NHS And Community Care Act

NHS And Community Care Act Community care essentially aims to provide individuals in need with social, medical and health support in their own homes, as far as possible, rather than in residential establishments or in long-stay institutions. The enactment of the NHS and Community Care Act in 1990 marked a watershed in the evolution of community care practice in the UK (Means, et al, 2002, p 71). Implemented after years of discussion on the social and financial viability of maintaining people in institutions and homes, the NHS and Community Care Act, initiated by Margaret Thatcher, showcased her desire to radically change the practice and delivery of social and health care in the UK (Means, et al, 2002, p 71). The years following the passing of the Act have witnessed significant developments in the practice and delivery of social work in the country. This short essay attempts to investigate the basic reasons for the enactment of the NHS and the Community Care Act, its basic ideology and thrust, and its impact on the social work sector of the country. The essay also studies the developments in social care that have occurred in the years following the act, with particular focus on direct payments for people with learning disabilities, social care provisions for carers and the contemporary emphasis on personalisation. NHS and Community Care Act 1990 Whilst the initiation of the policy of community care in the UK is by and large attributed to Margaret Thatchers conservative government, the concept of community care, even at that time, was not exactly new (Borzaga Defourny, 2001, p 43). The need for community care existed from the beginning of the 1950s. It aimed to provide a better and more cost effective way to help individuals with mental health concerns and physical disabilities by removing them from impersonal, old, and often harsh institutional environments, and taking care of them in their home environments (Borzaga Defourny, 2001, p 43). Although various governments, since the 1950s, supported the need to introduce community care and tried to bring in appropriate changes, lack of concrete action on the issue resulted in constant increase of the number of people in residential establishments and large institutions during the 1960s, 70s and 80s (Borzaga Defourny, 2001, p 43). With numerous negative stories coming out in the media on the difficult conditions in such establishments, Sir Roy Griffiths was invited by Margaret Thatcher to investigate the issue of community care for the residents of such establishments and make appropriate recommendations (Harris, 2002, p 11). The Griffiths, (1988), Report named Community Care: Agenda for Action, followed by the publication of a White Paper Caring for People: Community Care in the Next Decade and Beyond in 1989 led to the enactment of the NHS and Community Care Act 1990 (Cass, 2007, p 241). Apart from being a strong attempt to improve the lives of people in long term institutions and residential establishments, the law was also an outcome of the conservative governments desire to bring market reforms into the public sector and stimulate the private sector to enter the social services, as well as its conviction that competitive markets would be better able to provide more economic services than a bureaucratised public sector (Harris, 2009, p 3). With social services being among the highest revenue spending departments at the local authority level and domiciliary and residential services for older people consuming the bulk of social service funds, community care for older people presented an obvious area for introduction and implementation of market principles (Harris, 2009, p 3). The act split the role of local and health authorities by altering their internal structures, so that local authority departments were required to ascertain the needs of individuals and thereafter purchase required services from providers (Lewis, et al, 1994, p 28). Health organisations, in order to become providers of such services, became NHS trusts that competed with each other. The act also required local social service and health authorities to jointly agree to community care plans for the local implementation of individual care plans for long term and vulnerable psychiatric patients (Lewis, et al, 1994, p 28). The act has however come in for varying degrees of criticism from service users, observers and experts, with some observers claiming the altered care conditions to be unresponsive, inefficient and offering little choice or equity (Malin, et al, 2002, p 17). Other experts, who were not so pessimistic, stated that whilst the system was based upon an excellent idea, it was little better in practice than the previous systems of bureaucratic resource allocation and received little commitment from social services; the lead community care agency (Malin, et al, 2002, p 17). The commitment of local authorities was diluted by the service legacies of the past and vested professional interest, even as social services and health services workers were unable to work well together (Malin, et al, 2002, p 17). Little collaboration took place between social and health services and the impact of the reforms was undermined by chronic government underfunding. The voluntary sector became the main benefici ary of this thrust for the development of a mixed economy of care (Malin, et al, 2002, p 17). Developments after the Enactment of the NHS and Community Care Act The assumption of government by the labour party in 1997 resulted in the progressive adoption of numerous forward looking policies in various areas of social care. The publication of a white paper in 1998 reinforced the governments commitment to promotion of community based care and peoples independence (Means, et al, 2002, p 79). The paper focused on assisting people to achieve and maintain independence through prevention and rehabilitation strategies, with specific grants being introduced to facilitate their implementation. The Health Act of 1999 removed obstacles to the joint working of health and social services departments through provisions for pooling of budgets and merging of services (Means, et al, 2002, p 79). The formulation of the NHS plan aimed to improve partnership between health and social care, the development of intermediate care and the construction of capacity for care through cash for change grants for development of capacity across social and health care systems (Means, et al, 2002, p 79). Direct Payments for Individuals with Learning Disabilities The Community Care (Direct Payments) Act 1996, which came into operation in April 1997, marked a radical change in the provision of community care for people with disabilities, including those with learning difficulties (Tucker, et al, 2008, p 210). It was illegal, prior to the implementation of the act, for local authorities to support people with disabilities by making cash payments in lieu of providing community care services. Policymakers however realised that many local authorities were successfully supporting independent living schemes, centres for independent living and personal assistance schemes (Tucker, et al, 2008, p 210). Such schemes handled community care payments for disabled people and provided them with help to organise assistance or support. The Community Care (Direct Payments) Act built on this situation, allowing direct payments to be made to replace care services, which otherwise would be given by social service departments (Tucker, et al, 2008, p 210). Direct payments provide flexibility in the way services are provided to eligible people. The giving of money, in lieu of social care services, helps people to achieve greater control and choice over their lives and enables them to decide on the time and mode of delivery of services (Tucker, et al, 2008, p 210). Direct payments can not only be used for services to satisfy the needs of children or their families but also enables carers to purchase the services they need to sustain them in their roles. Research conducted in 1997 in the utilisation of direct payments by people with learning difficulties revealed that whilst utilisation of direct payments by people with learning disabilities was increasing, such utilisation was low among women and individuals from minority or black ethnic groups (Tucker, et al, 2008, p 210). Research also revealed the presence of wide differences in the interpretation of the capacity of persons for consenting to direct payments by local authorities. Whils t some local authorities felt that direct payments could be sanctioned to all persons with learning difficulties who were able, with assistance, to successfully control and use direct payments, other authorities did not heed the fact that such people could indeed be assisted to communicate decisions and consequently assumed their inability to consent to direct payments. Such interpretations, it was felt, could debar many people in need from obtaining the facility for direct payments (Tucker, et al, 2008, p 211). Assistance for Carers Recent years have seen a number of social care initiatives for easing the condition of carers. Carers are people who provide assistance and support, without payment, to family members or friends, who are unable to manage without such assistance, on account of illness, frailty or disability (Government Equalities Office, 2010, p 1). Carers can include adults who care for other adults, parents who care for disabled or ill children, or young people who care for other family members. The governments social care policies for carers include supporting people with caring responsibilities for (a) identifying themselves at early stages, (b) recognising the worth of their contribution, and (c) involving them from the beginning in designing and planning individual care (Government Equalities Office, 2010, p 1). Such policies aim to enable carers to (a) satisfy their educational needs and employment potential, and (b) provide personalised support, both for carers and the people they support, to enjoy family and community life and remain physically and mentally well. Whilst the NHS and community care Act 1990 looked at carers as valued resources because of their ability to provide support, it did not refer to their rights; relying instead on rhetoric to deliver the message of their value to society (Government Equalities Office, 2010, p 2). Succeeding years have however witnessed greater focus on the needs of carers and to progressive introduction of suitable laws and appropriate policies. The passing of the Carers (Recognition and Services) Act 1995 drew attention to the needs of carers. This was followed by the passing of the Carers and Disabled Children Act 2000 and the Carers (Equal Opportunities) Act 2004 (Government Equalities Office, 2010, p 2). These acts entitle carers for (a) assess ment of their needs, (b) services in their own right and support in accessing education training, employment and leisure opportunities. The proposed equality bill introduces four new opportunities for carers. It (a) requires public authorities to give due consideration to socio-economic disadvantages, whilst exercising strategic planning functions, (b) takes account of associative discrimination with regard to disabled people, (c) provides for prevention of indirect discrimination, and (d) calls upon public bodies to ensure that their policies are designed to eliminate harassment and discrimination and further equality of opportunity (Government Equalities Office, 2010, p 2). Personalisation The concept of personalisation in social care, whilst discussed for some years, was formally inducted into social care practice in the UK with the publication of Putting People First in 2007. The concordat outlined the concept of a personalised adult social care system, where individuals will have extensive control and choice over the services received by them. The government committed that social services would progressively be tailored to meet the preferences of citizens, with person centred planning along with self directed support becoming mainstream activities, assisted by personal budgets for maximising control and choice (Aldred, 2008, p 31). Whilst personal budgets and direct payments form an important aspect of personalisation, the idea concerns fitting services to the needs of people, focusing on outcomes, and recognising the worth of the opinions of service users assessing their own needs, planning their service, and producing their outcomes (Aldred, 2008, p 31). Conclusions and the Way Forward This essay investigates the reasons behind the enactment of the NHS and the Community Care Act and studies the developments in social care that have occurred in the years following the act, especially in areas of direct payments for people with learning disabilities, social care for carers and personalisation. It is obvious from the results of the study that social care in the UK has experienced significant change and metamorphosis since the enactment of the 1990 act. Whilst significant progress has been made a consensus s growing that the British social care system is facing a crisis because of drivers like increasing demographic pressures, alterations in family and social structures, rising public expectations, increasing desire for greater choice and control, and eligibility for services (Glasby, et al, 2010, p 11). The need to move people out of local accommodation because of rising rents exemplifies the challenges faced by the social care system. With the financial system becoming more challenging, the social care system will have to find ways of improving efficiencies without diluting the quality of care (Glasby, et al, 2010, p 11). The next round of social reforms, whilst attempting to achieve better delivery efficiencies will have to renew its commitment to satisfying social expectations and basic human rights, reducing costs, preventing future needs, helping people to regain independence, freeing individuals to contribute, and supporting carers to care and contribute to society (Glasby, et al, 2010, p 11).

Shc 23 – Introduction to Equality

Introduction to Equality and Inclusion in Health, Social Care or Children’s and Young People’s Settings 1. 1The term ‘Diversity’ means the state or fact of being diverse; different or unlike. Within equality and inclusion it is the difference between individuals and groups including: culture, nationality, ability, ethnic origin, gender, age, religion, beliefs, sexual orientation and social class. The term ‘Equality’ means the state or quality of being equal; correspondence in-quantity, degree, value, rank, or ability.It means that everyone is offered the same choices and opportunities, everyone is treated with respect and each individuals needs are catered for. The term ‘Inclusion’ means the act of including. Inclusion values diversity meaning that no-one is left out, and places individuals at the centre of planning and support. The term ‘Discrimination’ means the treatment or consideration of, or making a distinction in favor of or against, a person or thing based on the group, class, or category to which that person or thing belongs rather than on individual merit eg racial and religious intolerance and discrimination. . 2There are two main types of discrimination; direct and indirect. Direct discrimination may occur in the workplace in the form of institutional discrimination, whereby people may not think I am as good at working with children and young people because I am a man. Discrimination by individuals including bullying, labelling, prejudice and stereotyping is also direct discrimination because it is usually specifically targeted. This can have a negative effect in the workplace as it can lead to lack of opportunities for certain members of the group.Indirect discrimination can take place by accident. It can come as a result of lack of knowledge and understanding. If I cannot effectively communicate with someone because I don’t know anything about them, that could lead to inadve rtent and unintentional exclusion. 1. 3 Equality and inclusion are the opposite of discrimination. Therefore, practices which support equality and inclusion can only serve to extinguish discrimination. If everybody is treated equally with the same rights and respect for each other regardless of race, age and ability, then discrimination cannot take place.This can be achieved by making all areas accessible to people of all abilities, and by reducing barriers within communication. Together they make the promotion of participation easier. 2. 1Within my role as a trainee practitioner, I have to abide by the following codes of practice and legislation: Human Rights Act 1998 Disability Discrimination Act 1995 Disability Discrimination Act 2005 Special Educational Needs and Disability Act 2001 Race Relations (Amendment) Act 2000 The Equality Act 2010 Equality and Human Rights Commission 2. In our setting, children and adults alike are all treated equally. Religious beliefs, cultures and va lues are all taken into account. An example of this would be our snack table, all dietary requirements – some health reasons and some religious reasons are catered for. As such, nothing is ever served which go against peoples beliefs. Appropriate language is always used when addressing both children and adults, using clear communication. Regardless of age, ethnic origin or religious belief; confidentiality is always maintained unless it someone is in immediate danger. 2. Discrimination can be challenged in different ways, but in order for it to stop, we must also encourage change. If someone feels that they are being discriminated against, then they should follow the correct complaints procedures – note their concerns with a supervisor, manager or SENCO. If I see children discriminating against one another, I can challenge the children and resolve the issue but report the incident to my manager. Staff training on the issue of discrimination is valuable as it means we a re all following the same procedures to curb the behaviour, and makes us reassess our own beliefs and attitudes we might hold.Policy review on the subject is also a fantastic way to challenge discrimination as it can lead to more effective techniques to solve the problem being developed. 3. 1There are a variety of sources where information, advice and support about diversity, equality and inclusion can be gathered from. Advice and information can be gained from Sector Skills Councils such as Skills for Care and Children’s Workforce and Development Council, Professional organisations such as Nursing ans Midwifery Council and Teacher Development Agency; and Third party organisations.It can also be found on government websites which give up to date legislation and codes of practice. 3. 2Access to information, advice and support about diversity, equality and inclusion should be gained when carrying out inter-agency works, or liaising with community leaders and organisations. It c an also be used in order to gain feedback on the work you are already carrying out. This can help you see if you are meeting all standards expected and can also help you progress to the next level because it aids professional development.

Discuss Merle Hodge’S Crick Crack Monkey As a Novel Essay

Merle Hodge born in 1944, in Trinidad is the daughter of an immigration officer. After studying at the Bishop Anstey’s high school of Trinidad, she obtained the Trinidad and Tobago Girls Island Scholarship in 1962 which led her to the university college of London. She obtained a degree in French and later in 1967 a Master Philosophy degree. Merle Hodge traveled a lot in Eastern and Western Europe and when she returned to Trinidad she started teaching French in junior schools. Later she obtained a post of lecturer at the University of the West Indies. In 1979, she started to work for the bishop regime and she was appointed director of the development of curriculum. In 1983, she left Grenada because the bishop was assassinated and she is now working for the Women and Development Studies at the University of the West Indies in Trinidad. She wrote the novel Crick Crack Monkey in 1970 where she deals with the theme of childhood in the West Indies. The main protagonist called Tee lives with Tantie who is a working class woman. She later goes to live with her aunt Beatrice and she faces a new and different world from that of her Caribbean world: â€Å"Hodge’s story is presented through the eyes of a black, lower class girl of Trinidad in the 1950s.† The whole story is one presented from one point of view: Tee’s. She is left alone by her father who goes abroad after the death of her mother and she has to live with her lower class Tantie where she learns about being independent. Later in the story her aunt Beatrice takes her and she then has to adapt herself to the ‘white’ world. She faces a lot of cultural and identity conflict as she does not really know where she belongs or what culture is wrong or right. â€Å"However, looking at the story of â€Å"crick crack monkey† through the eyes of a young white girl, rather than a young black girl, the reader might see the injustice and the ethnic discrimination that a black person must endure. She would not be accustomed to being called a â€Å"little black nincompoop† (Hodge 457), and she would most likely not have to suffer a physical beating with a ruler (Hodge 456)† Tee becomes the narrator and Hodge guides the reader through an â€Å"intensely personal study of the effects of the colonial imposition of various social and cultural values on the Trinidadian female.† Tee narrates the diverse problems in her life in such a way that it is often complicated to split up â€Å"the voice of the child, experiencing, from the voice of the woman, reminiscing; in this manner, Hodge broadens the scope of the text considerably.† It has often been seen that the British have used various techniques to influence the viewpoints of the Caribbean people. â€Å"The people’s self awareness, religion, language, and culture has coped with the influx of British ideals and in coping, the people have changed to appease the islands’ highly influential British population.† Crick Crack Monkey is made to be a novel dealing with the conflict of cultures that Tee has to accept. We first meet Tee when her mother dies and she is portrayed as being surrounded by people. She experiences ‘crowd-scenes’ where she has all her family and friends around her to give her support. At Tantie’s house, she had Tantie’s loud presence and when she was absent she had the presence of other children. This in a way is made to reflect the Caribbean culture where every one is warm and caring and where the people like to stay together and entertain social relationships: â€Å"As Yakini Kemp notes, â€Å"she [Tee] is moving progressively toward the development of a positive self-image while she resides with Tantie† (24). Tee is made to be independent and having a voice for herself in the Trinidadian society. She has a confident personality which has been molded by the culture in which she was living. These episodes where Tee is made to be surrounded by the people of Trinidad are made to contrast with the isolation and the loneliness which Tee is made to feel at her Aunt Beatrice’s place: â€Å"these scenes set up a contrast to the loneliness the narrator-protagonists will experience once removed from their original environment and placed into a Western or Western-aspiring one. What Marjorie Thorpe has said about Crick Crack Monkey thus can also be said for Bedford’s novel: â€Å"Throughout the novel Hodge contrasts the warmth and congeniality of Tantie’s household with the loneliness and isolation which Tee experiences at Aunt Beatrice’s† (36) In Crick Crack Monkey Hodge makes the isolation felt by Tee become associated with cultural alienation. She had always been said to belong to an extended family culture where she feels part of the family but the western culture makes her feel out of place and she thus feels alienated from both cultures at a certain point. This alienation process is depicted through the fact that Tee has to move from an Antillean culture to a supposedly European culture: â€Å"In this novel Merle Hodge presents the process of alienation by depicting Tee’s transition from a typical Antillean tradition to that of a pseudo-European culture.† Tee is made to balance herself between the culture of Tantie who gives her â€Å"the promise of staying on with the original culture of the Caribbean islands† and between Aunt Beatrice who gives her a prospect of another culture: â€Å"Aunt Beatrice offers the lure of abroad – a culture that Tee slowly becomes familiar with but does not b elong to.† It is seen that, while Tantie and Aunt Beatrice represent different perceptions of cultures which were present in the island, Ma, Tee’s Grandma, represents another culture. She is the one who tells the children â€Å"‘nancy† stories and she is near to the Tee’s African roots. Tee visiting her grandmother makes her realize that: â€Å"Ma’s sayings often began on a note of familiarity only to rise into an impressive incomprehensibility, or vice versa, as in ‘Them that walketh in the paths of corruption will live to ketch dey arse†. The three women in Tee’s life makes her realize that each one belongs to a class and a culture which is seemingly different from each other and Tee is unable to even understand the culture of her Grandmother so she becomes alienated from the African culture in a way. She is left with Tantee’s culture and with Aunt Beatrice’s culture where both culture makes her in a way lose her own identity . In Merle Hodge’s Crick Crack Monkey, Tee’s education is responsible for her internalization of the European or the western culture. It is found in the novel that even before Tee is made to go and live with her Anglicized Aunt Beatrice she has to learn about their culture where things which she has learned in her Caribbean culture does not exist â€Å"Books transported you always into the familiar solidity of chimneys and apple trees, the enviable normality of real Girls and Boys who went a-sleighing and built snowmen, ate potatoes, not rice, went about in socks and shoes from morning until night and called things by their proper names, never saying â€Å"washicong† for plimsoll or â€Å"crapaud† when they meant a frog. Books transported you always into reality and Rightness, which were to be found Abroad. (61)† It has often been seen that the colonial education was part of massive artillery to colonize the mind of the people and that this helped to consolidate the colonialists power and culture. It is said that the ‘whole educational apparatus was geared towards cultural domination by consent’ and that in a way it completely destroyed the culture and the cultural education of the colonized people. They were in fact alienated from their own culture through the colonized education and they were made to create an environment where they would desire the Eurocentric culture. This is in a way what happens to Tee who is made to feel alienated from her own culture by the colonial education she is given. Tee’s education thus in a sense puts her in an unbearable state: â€Å"since her own world does not have the same cultural referents as the one she is taught to regard as â€Å"correct,† she is forever trying to â€Å"catch up,† always seeing herself in terms of a world which can never be her own because it is always elsewhere.† She is always lacking in her acceptance of this culture: â€Å"her whole socialization process comes to affirm that however many of the cultural standards prescribed by the educational system, her teachers, or Aunt Beatrice she adopts, she always falls short — and so do her teachers and Aunt Beatrice, who are similarly caught in a cycle of self-denial and self-hatred.† Tantie representing the Caribbean culture warns Tee not to get carried by the colonialist instructions and this warning comes in time when Hodge introduces the teacher, Mr. Hinds who â€Å"is bent on living an English reality in the face of the facts of the Caribbean because he holds Englishness as the highest value in his life, and so it is not surprising that â€Å"[e]everyone knew that Mr. Hinds had been up to England† because he is eager to let everyone know about it. His devotion to the metropolis assumes a worshipful attitude illustrated by his â€Å"daily endeavor to bring the boys to a state of reverence† towards a â€Å"large framed portrait of Churchill† (24).† He makes the colonial education, the center of his teachings and what he teaches the students does not even include the Caribbean reality that the children are living. He tries to instill the English culture in the students: â€Å"from apples to Christmas to snow and the haystacks the children learn about in their school primers — who do not have any lived knowledge of England, thus attempting to erase Caribbeanness in them as it has been erased in him.† There is one passage which addresses the issue of language, identity and of culture. Mr. Hinds being irritated with his students says, â€Å"‘Here I stand, trying to teach you to read and write the English language, trying to teach confounded piccaninnies to read and write. . . . I who have marched to glory side by side with His Majesty’s bravest men — I don’t have to stand here and busy myself with . . . little black nincompoops† (29). This in a way reflects the culture which is often adopted by the western world where people think that the way you speak is a representation of yourself proposed by Ashcroft. The students are made to reject their local language to adopt the language of the colonizer and the†use of the language highlights cultural specificity† when the vernacular language is inserted in the novel. The very rendering of the vernacular in written English gives it equal status to â€Å"mainstream† English and linguistically symbolizes an act of resistance and a cultural alternative – Creole culture — that, in the plot of the novel, is marked by a relative wholeness when juxtaposed to Mr. Hinds’ and Aunt Beatrice’s self-alienation, which is expressed in the above passage through Mr. Hinds’ concern with having his students learn â€Å"proper† English. According to Frantz Fanon: â€Å"Every colonized people — in other words, every people in whose soul an inferiority complex has been created by the death and burial of its local cultural originality — finds itself face to face with the language of the civilizing nation; that is, with the culture of the mother country. The colonized is elevated above his jungle status in proportion to his adoption of the mother country’s cultural standards. He becomes whiter as he renounces his blackness, his jungle. (18)† Mr. Hinds is the representation of the colonized man who tries to act white. He creates walls between himself and the children where he is in a way rejecting his own blackness and is trying to make them accept the culture of the colonized through language: â€Å"attempting to make them like himself, with language as a primary standard of culture, he also tries to prove his own cultural â€Å"redeemability,† the possibility of becoming English.† Tantie represents the Caribbean culture and thus she tries to preserve it in Tee. It seems that the culture in which Tee is living is mixed with the European culture and there are many agents of ‘westernization’ which are present in the society. Mr. Hinds seems only to be a puppet who has been employed to prepare Tee for her awaiting life at the household of Aunt Beatrice: â€Å"it is for good reason that Tantie warns Tee of such indoctrination in the vernacular, since the vernacular is the only cultural basis for Tantie (and potentially for Tee) from which to launch a defense.† The novel shows that the children have to go to Aunt Beatrice’s place in order to obtain the proper education and Tantie has to let the children live with Aunt Beatrice. In a way she knows that the colonial education and system is all that matters to succeed in the world. It seems that Aunt Beatrice’s westernized house is the only ‘proper’ place for the children to stay because it contains all the cultural values of the Europeans. At her arrival there it is immediately shown how the world of aunt Beatrice is different when Tee’s and Todan are made fun of because of their clothes and color: â€Å"Not only color and features are under scrutiny concerning their similarities and dissimilarities to European beauty standards, but so are clothes, as Tee finds out when her cousins inspect her wardrobe soon after her (second) arrival: â€Å". . . We are shown how with the phenomenon of â€Å"double consciousness,† Du Bois’ term: â€Å"While Du Bois speaks of African Americans looking at themselves through the eyes of racist whites, Tee looks at herself through the eyes of her cousins, who have so thoroughly imbibed a British colonialist world view that nothing appears to exist resembling even remnants of a Caribbean identity.† makes Tee feel aware of her color and of her clothes as compared to her colonized cousins. When Tee had gone to Aunt Beatrice’s place the first time, she used to beat up her cousins and later on when she goes there again she is in a way crippled by her education and through her indoctrination of the standards of the European culture. The first time she had Tantie’s culture fully present in her, she had all her Caribbeaness in her and had not been made aware that she has to judge herself by the standards of others and that the European culture was the scale along which she should judge herself and her achievements: â€Å"Tee has already been indoctrinated into standards of â€Å"Reality and Rightness† and she recognizes her cousins as being closer to the Anglophile standards instilled in her, quelling the resistance against their denigration that was still available to her when she drew her world view and strength from Tantie’s cultural orb.† In this new world which is different from the world of Tantie, all that represents the African culture is denigrated and shown to be insignificant. Aunt Beatrice in every way makes Tee feels that the white world and culture is supreme and the clothes she had brought is seen as ‘niggery’ and everything connected with Europeans is adorned and there is the example of the photograph of the ‘white ancestress: â€Å"Such veneration of â€Å"white blood† illustrates that Aunt Beatrice does not merely admire and strive to emulate English culture, but that her Anglophilia is ultimately rooted in racist and Darwinist beliefs in the superiority of bloodlines and â€Å"races.† Thus, in her eyes, African ancestry in and of itself is a liability, not merely African culturally acquired styles and behaviors. This explains her manic attempt to erase everything in herself, in her daughters, and in Tee, reminiscent of such ancestry†. She is in a way trying to ali enate the Caribbean culture in Tee just as Mr. Hinds had tried to do. Tee is made to feel alienated from the world she used to know. In this new world she is made to feel powerless and she feels that she cannot cope when she has to speak or when she dresses as she cannot and is not fully accepted in this Europeanized world of her cousins: â€Å"As Ketu Katrak has said, â€Å"Beatrice cultivates bourgeois values that despise blackness in every form — skin color, speech patterns, food† (66), and this is a legacy from which Tee cannot escape†. She does not belong to the culture of Tantie anymore and nor does she belong to the culture of the Aunt Beatrice ad she only feels torn between the two. This is shown when she cannot accept the food brought to her by Tantie and: â€Å"The final scene demonstrates that Tee now lives between the worlds, not belonging to either. Unable ever to be accepted fully into Aunt Beatrice’s household and Englishness, she is also alien to Tantie’s world.† Ketu Katrak says that â€Å"Colonized people’s mental colonization through English language education, British values, and culture result in states of exclusion and alienation. Such alienations are experienced in conditions of mental exile within one’s own culture to which, given one’s education, one un-belongs.† (62) Tee has received an education and a western culture which is very much unlike the culture of Tantie and which in a way makes her feel the dullness of her Caribbean culture and of Tantie’s world. Tee feels alienated and marginalized since the time she has started to learn the European culture and she did not feel this before in Tantie’s household. Tee’s alienation leads her to hopelessness and feelings that she is unworthy of living: â€Å"(Thorpe 37): â€Å"I wanted to shrink, to disappear. . . . I felt that the very sight of me was an affront to common decency. I wished that my body could shrivel up and fall away, that I could step out new and acceptable† (97). Though she does not actually contemplate killing herself, her self-hatred and eagerness to assimilate are the cultural equivalent of suicide.† Tee is found without a culture and ‘Aunt Beatrice’s self-negating and self-hating cultural influence’ on her seems to destroy her identity. Tee is unable to live in both culture and the novel: â€Å"thus ends on an ironic note: to save Tee, who is unable to return to the Caribbeanness she has known in Tantie’s household through having become socialized in the worship of Englishness, Tantie sends her to the ultimate source of this cultural negation: to the metropolis, to England† â€Å"Hodge goes to great pains to portray the cultural bankruptcy of playing monkey to the Great White Ancestor. In this important respect, the narrative, which in the fiction a mature Tee relates, places considerable vaule on the vulnerable African oral culture that so easily succumbs to the power of the written†. Crick Crack Monkey ending gives us a hope for Tee who goes to London and â€Å"The goal of the novel, it seems, is not to idealize a lost African past but to reveal the cultural sovereignty of Trinidad.† BIBLIOGRAPHY: Web sites: * BILL CLEMENTE: The A, B, C’s of Alienation and Re-Integration : Merle Hodge’S Crick Crack Monkey * httpClemente.htm * httpcrick crack monkey study guide.htm * The Two Worlds of the Child: A study of the novels of three West Indian writers; Jamaica Kincaid, Merle Hodge, and George Lamming * httpJamaica Kincaid, Merle Hodge, George Lamming.htm * Two Postcolonial Childhoods:Merle Hodge’s Crick Crack, Monkey and Simi Bedford’s Yoruba Girl Dan * http Jouvert 6_1 – 2 Martin Japtok, Two Postcolonial Childhoods Merle Hodge’s Crick Crack, Monkey and Simi Bedford’s Yoruba Girl Dancing.htm * http merle.htm books: * HODGE ,MERLE. Crick Crack, Monkey. Andre Deutsch, 1970; London: Heinemann, 1981; Paris: Karthala, 1982 (trans. Alice Asselos-Cherdieu). Lectures: * Lectures by Mrs. MAHADAWO on Island Literatures.

Patient information and presenting complaints - Free Essay Example

Sample details Pages: 25 Words: 7495 Downloads: 1 Date added: 2017/06/26 Category Health Essay Type Essay any type Did you like this example? 1.0 CASE SUMMARY 1.1 Patient information and presenting complaints SAR, a 54-year-old female with weight of 54kg and height of 160cm was referred to the hospital by her GP due to shortness of breath which was not relieved by taking inhaler, minimum cough with yellowish sputum, abdominal pain and mild diarrhoea. Her shortness of breath had been on and off for the past 1 week and the condition was deteriorating on the day of admission. 1.2 Relevant history SAR is a non-smoker and a non-alcoholic housewife. She has had bronchial asthma since childhood. Her siblings and children were found to have family history of bronchial asthma as well. The patient has been taking inhaled salbutamol 200 µg 1 puff when required as reliever and inhaled budesonide 200 µg 2puffs bd as preventer for umpteen years. Besides that, SAR also has medical history of hypertension, diabetes mellitus and ischaemic heart disease (IHD) for 10 years. She has no relevant family history for these illnesses. For the past few years, SAR has been taking rosuvastatin 20mg at night, fenofibrate 160mg OD and ezetimibe 10mg OD for dyslipidaemia, gliclazide 60mg BD and rosiglitazone 4mg OD for diabetes mellitus, losartan 50mg OD for hypertension, ticlopidine hydrochloride 250mg OD for prophylaxis against major ischaemic events and famotidine 20mg OD to prevent gastrointestinal ulceration due to the use of anti-platelet agent. Don’t waste time! Our writers will create an original "Patient information and presenting complaints" essay for you Create order 1.3 Clinical data On examination upon admission, SARs blood pressure and pulse rate were recorded as 111/80 mmHg and 111bpm respectively. Her respiratory rate was normal (16 breaths/min). Her SpO2 measurement was 98% and it showed decreased high flow mask. Her DXT blood glucose test revealed that her random blood glucose level was abnormally high (21.6mmol/L). From the doctors systemic enquiry, SARs ankles were slightly swollen and her respiratory system showed prolonged minimal bibasal crept and rhonchi. Also, SARs chest X-ray showed shadowing in the lower zone of her right lung. The renal function tests gave results of high urea and elevated creatinine levels of 16.3mmol/L and 270 µmol/L respectively. Creatinine clearance derived from Cockcroft and Gault formula is 17ml/min which indicates that the patient has severe renal impairment. The liver function tests revealed a mild decrease in albumin concentration and an increase in the plasma globulin. On the other hand, the haematological tests show ed low red blood cell count (3.41012/L), low haemoglobin count (9.4g/dL), high platelet count (410109/L), high white blood cell count (17.1109/L), high neutrophil count (16.4109/L) and low lymphocyte count (0.5109/L), whereas cardiac marker tests showed abnormally high counts in creatine kinase (156IU/L) and lactate dehydrogenase (627IU/L). 1.4 Diagnosis and Management Plan Based on the patients symptoms, medical history, physical examinations, and laboratory tests, SAR was diagnosed with chronic heart failure (CHF), acute exacerbation of bronchial asthma (AEBA) secondary to pneumonia and uncontrolled diabetes mellitus. Her doctor developed therapeutic plans which included anti-asthmatic drugs and antibiotics, and ordered further investigations such as SpO2 and PEFR. Besides that, her doctor also added diuretic to her ACEI therapy and restrict her fluid intake to not more than 800cc/day. Her uncontrolled diabetes mellitus was under monitoring of DXT blood glucose test 4 hourly and she was referred to dietician for diabetic diet counselling. 1.5 Ward medication Throughout the 3days in hospital, Sarah was being prescribed with medications as listed below: Drug route Dose frequency Start date Stop date Indication/ Comments T. Gliclazide (Diamicron ® MR) 60mg bd Day 1 Diabetes mellitus T.Rosiglitazone 4mg od Day 1 Diabetes mellitus T.Rosuvastatin 20mg nocte Day 1 Dyslipidaemia T.Fenofibrate 160mg od Day 1 Dyslipidaemia T.Ezetimibe 10mg od Day 1 Dyslipidaemia T.Lovastatin 20mg nocte Day 1 Dyslipidaemia T.Ticlopidine HCL 250mg od Day 1 Prophylaxis against ischaemic T.Losartan 50mg od Day 1 CHF T.Famotidine 20mg od Day 1 Prevent GI upset Neb ipratroupium bromide 500 µg, salbutamol 5mg, normal saline 2:1:2 qqh Day 1 Day 3 AEBA IV Hydrocortisone 100mg stat Day 1 Day 1 AEBA Neb Salbutamol 1 puff prn Day 1 AEBA/chronic asthma MDI Budesonide 200mcg 2 puffs bd Day 1 AEBA/chronic asthma T. Azitromycin 500mg od Day 1 Day 3 Pneumonia IV Ceftriaxone 2g stat Day 1 Day 1 Pneumonia IV Furosemide 40mg bd Day 1 Day 2 CHF S/C Actrapid 5? , 10? Day 1 Day 2 Diabetes mellitus T. Prednisolone 30mg od Day 2 AEBA MDI Beclomethasone 200mcg 2puffs tds Day 2 Chronic asthma T.Cefuroxime 250mg bd Day 2 Pneumonia T. Furosemide 40mg od Day 2 CHF S/C Mixtard 30/10? Day 3 Diabetes mellitus 1.6 Clinical Progress and Pharmaceutical Care Issues On the first day of admission, the patients past medication history was confirmed by appropriate patient interview and her family members were being advised to bring SARs home medication to ensure that the appropriate medications were continued and prescribed. From the interview, dust was found to be the chief precipitating factor. The patient was on appropriate drugs (nebulised ipratropium bromide 0.5mg and nebulised salbutamol 5mg in normal saline 4 hourly, IV hydrocortisone 100mg stat) for acute management of severe asthma as according to guidelines and eventually her SOB was relieved.2-3 However, she was prescribed with oral prednisolone at dose as low as 30mg od for acute asthma, it should be suggested to increase prednisolone dose to 40-50mg daily as according to evidence-based guidelines to achieve maximal effects.2-3 Another pharmaceutical care issue is regarding the patients poor inhaler technique. Thus, the pharmacist educated and assessed SAR on her inhaler technique sin ce day 1. Appropriate antibiotics indicated for pneumonia which included IV ceftriaxone 2g stat and oral azitromycin 500mg od were initiated upon admission. Oral cefuroxime 250mg bd was added to the drug regimen on day 2 after stopping IV ceftriaxone 2g on the first day. Therefore, signs of recovery and WBC count were monitored regularly and completion of antibiotic course was ensured. In addition to that, vaccinations against pneumococcal infection and influenza should be strongly recommended in this asthmatic patient.2-3,5-8 Co-administration of high dose IV furosemide (40mg bd) and corticosteroids can increase the risk of hypokalaemia, therefore SAR should be started on potassium chloride 600mg bd which is an appropriate dose for renal insufficiency patient to avoid the potential risk.1 Besides that, potassium level of SAR should also be closely monitored during the administration of potassium chloride. The doctor added lovastatin 20mg at night to her existing triple the rapy of dyslipidaemia (rosuvastatin, ezetimibe, fenofibrate). Rosuvastatin should be avoided if patients creatinine clearance is less than 30ml/min.1 Due to its same mechanism of action as lovastatin and its contraindication in patient with severe renal impairment, rosuvastatin should be withdrawn from the drug regimen. Practically, a comprehensive lipid profile of SAR should be established and monitored in order to choose the best combination of lipid lowering agents to improve the individual components of lipid profile. Combination therapy of ezetimibe and lovastatin is considered more appropriate as concurrent use of fenofibrate and statin may potentiate myopathy. Therefore, fenofibrate and rosuvastatin should not be continued. Liver function should be monitored to avoid the risk of hepatotoxicity. SAR was diagnosed with uncontrolled diabetes mellitus which means her blood glucose level was not adequately controlled with concurrent therapy of gliclazide and rosiglitazone. Her random blood glucose level was fluctuating throughout day 1 (24.9mmol/L, 14.2mmol/L, 7.3mmol/L and 14.7mmol/L). Targets for blood glucose levels should be ideally maintained between 4 and 7mmol/L pre-meal and 9mmol/L post-meal provided there is no significant hypoglycaemia, and HbA1c of ?7% is a more practical target compared to HbA1c of 6.5%.1,4 SAR was started on insulin injections to lower and control her blood glucose level during hospital admission. Type 2 diabetes mellitus management guideline recommends the addition of insulin to the two oral hypoglycaemic agents after the dual oral therapy fails.4 However, rosiglitazone is contraindicated in patient with CHF and not recommended in patient with history of IHD; therefore the use of rosiglitazone should be reviewed.1,5-6 The most appropriate action is to withdraw rosiglitazone from the drug regimen and close monitoring of patients random blood glucose and glycosylated haemoglobin (HbA1c) should be carried out to confirm the eff ectiveness of the combination therapy (gliclazide and insulin) in controlling the blood glucose level. Although metformin is the first line treatment of Type 2 diabetes mellitus, it is contraindicated in Type 2 diabetic patients undergoing treatment with CHF and there is increased risk of lactic acidosis in severe renal impairment patient, therefore addition of metformin should be avoided in this case.1,4 During the hospital admission, SAR was educated on the proper technique of insulin injection. In this case, the decreased plasma levels of haemoglobin and red blood cells in the heart failure patient were most likely exacerbated by the administration of rosiglitazone.1 If the anaemia problem is not improved upon the withdrawal of rosiglitazone, erythropoietin and iron therapy can be considered.9 On day 2, SAR was feeling much more comfortable and had not complaint of SOB. However, SARs maintenance management of asthma was found to be not conformed to the asthma guidelines.2-3 Sh e was prescribed with unacceptable high dose of corticosteroids (MDI beclomethasone 200 µg 2 puffs tds) in addition to her current steroid regimen (MDI budesonide 200 µg 2 puffs bd and oral prednisolone 30mg od). SAR was at potential high risk of experiencing considerable side effects such as diabetes, oesteoporosis, Cushing syndrome with moon face, striae, acne, abdominal distension and other profound effects on musculoskeletal, neuropsychiatric and ophthalmic systems as a result of overdosage of corticosteroids.1 Oropharyngeal side effects such as candidiasis are also more common at high dose of inhaled steroids, but can be minimized if the patient rinse the mouth with water after inhalation. It should be recommended to add the long acting beta agonist (LABA) to the inhaled corticosteroids (ICS) treatment instead of initiating SAR on high dose steroid (2000 µg). Combination inhaler of formoterol and budesonide (Symbicort 200/6 Turbohaler ® 2 puffs bd) should be given and c ontrol of asthma need to be continuing assessed.2-3 If LABA is proved to be not effective, addition of 4th agent (leukotriene receptor antagonist, theophylline or oral beta agonist) can be considered.2 When SAR showed recovery of leg swelling, furosemide was given orally instead of intravenously with reduced frequency and total daily dose. On day 3, SAR was arranged to be discharged. The pharmacist should review the appropriateness of discharged medication by checking discharged prescriptions against ward medication chart and ensure all information relevant to primary care referrals are included. In addition to that, the pharmacist should also reiterate and reinforce the importance of patient compliance and follow-up reviews, counsel on indications, doses and possible adverse effects of each discharged medication, and rechecked SARs inhaler and insulin injection techniques prior discharged. Asthma education includes advice to avoid trigger factors, including caution with NSAIDs a nd avoidance of dust exposure. Greater attention should be paid to inhaler technique as poor technique leading to failure of treatment. SAR should be educated on the use of peak flow meters and advised to monitor and record her own PEFR at home. A written personalised asthma action plans should be designed for SAR prior discharged. Diabetic counselling should emphasize on proper insulin injection techniques and healthy lifestyle modifications. SAR needs to be made aware of the signs of hypoglycaemia and hyperglycaemia and how to response to them. Polypharmacy may adversely affect compliance with prescribed drug therapy, therefore SAR should be taught not to mix up her medicines by using daily pill box and her family member should also be advised to supervise her on medicine taking. 2.0 PHARMACOLOGICAL BASIS OF DRUG THERAPY 2.1 Disease background 2.1.1 Asthma Asthma is a common chronic inflammatory condition of the lung airways affecting 5-10% of the population and appears to be on the increase.5 It is especially prevalent in children, but also has a high incidence in more elderly patient. Asthma mortality is approximately 1500 per annum in the UK and costs in the region of  £2000 million per year in health and other costs.2-3,6 Symptoms of asthma are recurrent episodes of dyspnoea, chest tightness, cough and wheeze (particularly at night or early in the morning) caused by reversible airway obstruction. Three factors contribute to airway narrowing: bronchoconstriction triggered by airway hyperresponsiveness to a wide range of stimuli; mucosal swelling/inflammation caused by mast cell, activated T lymphocytes, macrophages, eosinophils degranulation resulting in the release of inflammatory mediators; smooth muscle hypertrophy, excessive mucus production and airway plugging.7 There is no single satisfactory diagnostic test for all asthma tic patients. The useful tests for airway function abnormalities include the force expiratory volume (FEV1), force vital capacity (FVC) and peak expiratory flow rate (PEFR). The diagnosis is based on demonstration of a greater than 15% improvement in FEV1 or PEFR following the inhalation of a bronchodilator.2,3,6 Repeated pre and post-bronchodilator readings taken at various times of the day is necessary. The FEV1 is usually expressed as the percentage of total volume of air exhaled and is reported as the FEV1/FVC ratio. The ratio is a useful and highly reproducible measure of lungs capabilities. Normal individuals can exhale at least 75% of their total capacity in 1 second. A decrease in FEV1/FVC indicates airway obstruction. 2.1.2 Community-acquired pneumonia Pneumonia is defined as inflammation of the alveoli as opposed to the bronchi and of infective origin. It presents as an acute illness clinically characterized by the presence of cough, purulent sputum, breathlessness, fever and pleuritic chest pains together with physical signs or radiological changes compatible with consolidation of the lung, a pathological process in which the alveoli are filled with bacteria, white blood cells and inflammatory exudates. The incidence of community acquired pneumonia (CAP) reported annum in UK is 5-11 per 1000 adult population, with mortality rate varies between 5.7% and 14% (patients hospitalised with CAP).8 Streptococcus pneumonia is the commonest cause, followed by Haemophilus influenzae and Mycoplasma penumoniae.7 2.1.3 Congestive cardiac failure Congestive cardiac failure occurs when the heart fails to pump an adequate cardiac output to meet the metabolic demands of the body. It is a common condition with poor prognosis (82% of patients dying within 6 years of diagnosis) and affects quality of life in the form of breathlessness, fatigue and oedema.6,7 The common underlying causes of cardiac failure are coronary artery disease and hypertension. Defects in left ventricular filling and/or emptying causes inadequate perfusion, venous congestion and disturbed water and electrolyte balance. In chronic cardiac failure, the maladaptive body compensatory mechanism secondary physiological effects contribute to the progressive nature of the disease.6 2.1.4 Diabetes mellitus Diabetes mellitus is a heterogenous group of disorders characterised by chronic hyperglycaemia due to relative insulin deficiency and/or resistance. It can be classified as either Type 1 or Type 2. In Type 1, there is an inability to produce insulin and is generally associated with early age onset. Decreased insulin production and/or reduced insulin sensitivity, maturity onset and strong correlation with obesity are characteristics of Type 2 diabetes. Diabetes affects 1.4 million people in the UK, over 75% of them have Type 2 diabetes.6 It is usually irreversible and if not adequately managed, its late complications can result in reduced life expectancy and considerable uptake of health resources. 2.2 Drug pharmacology 2.2.1 Treatment for asthma 2.2.1.1Beta-adrenoceptor agonists (e.g. salbutamol, terbutaline) These short-acting selective ?2 agonists (SABA) are the first line agents in the management of asthma and are also known as relievers. The selective ?2 agonists act on ?2 aderenoceptors on the bronchial smooth muscle to increase cyclic adenosine monophosphate (cAMP) leading to rapid bronchodilation and reversal of the bronchospasm associated with the early phase of asthmatic attack.5 Such treatment is very effective in relieving symptoms but does little for the underlying inflammatory nature of the disease. ?2 agonists should be initiated ‘when required as prolonged use may lead to receptor down regulation renders them less effective.5-6 Compared to SABA, long-acting beta-adrenoceptor agonists (e.g. salmeterol, formoterol) have slower rate of onset and their intrinsic lipophilic properties render them to be retained near the receptor for a prolonged period (12hours), which means that they cause prolonged bronchodilation. 2.2.1.2 Muscarinic receptor antagonists (e.g. ipratropium) Ipratropium blocks parasympathetic-mediated bronchoconstriction by competitively inhibiting muscarinic M3 receptors in bronchial smooth muscle.1,5-6 It has slower onset of action than ?2 agonists but last longer. 2.2.1.3 Inhaled corticosteroids (ICS; e.g. beclomethasone, budesonide) and oral prednisolone These agents are used to prevent asthmatic attacks by reducing airway inflmmation. They exert their anti-inflammatory actions via activation of intracellular receptors, leading to altered gene transcription. This results in decreased cytokine production and the synthesis of lipocortin leading to phospholipase A2 inhibition, and the inhibition of leukotriene and prostaglandins.5 Candidiasis occurs as common side effects with inhalation and systemic steroid effects such as adrenal suppression and osteoporosis, occur with high dose inhalation or oral dosing. 2.2.2 Treatment for pneumonia Antiobiotic treatment is appropriate with amoxicillin being used as first choice agent for mild, community-acquired infections. Depending on response and the strain of bacteria, other antibiotic agents can be used. Two groups of antibiotics which were given to the patient in this case scenario will be discussed here. 2.2.2.1 Cephalosporins (e.g. cefuroxime, ceftriaxone) Both ceftriaxone and cefuroxime are broad spectrum bactericidal antibiotics belong to cephalosporins group. They inhibit the synthesis of bacterial cell wall by binding to specific penicillin-binding proteins and ultimately leading to cell lysis. Second generation cefuroxime is beta-lactamase resistant and active against Gram-negative bacteria such as Haemophilus influenzae and Klebsiella pneumoniae. Being third generation cephalosporin, ceftriaxone display high beta–lactamase resistance and enhanced activity against Gram-negative pathogens (including Pseudomonas Aeruginosa), but it has relatively poor activity against Gram-positive organisms and anaerobes.1,5-6 2.2.2.2 Maclolides (e.g. azithromycin, erythromycin, clarithromycin) Maclolides prevent protein synthesis by inhibiting the translocation movement of the bacterial ribosome along the mRNA, resulting in bacteriostatic actions. Azithromycin has slightly less activity than erythromycin against Gram-positive organisms but possesses enhanced activity against Gram-negative bacteria including Haemophilus influenza. 2.2.3 Treatment for chronic cardiac failure 2.2.3.1 Loop diuretics (e.g. furosemide) Diuretics are the mainstay of the management of heart failure and provide rapid symptomatic relief of pulmonary and peripheral oedemia.5,6,9 Loop diuretics are indicated in majority of symptomatic patients and they work by inhibiting Na+/K+/2Cl- transporter in the ascending limb of the loop of Henle, inhibiting the establishment of a hyperosmotic interstitium and thus reducing the production of concentrated urine in kidney, leading to profuse dieresis.5-6 2.2.3.2 Angiotensin II receptor antagonists (e.g. losartan, candesartan, valsartan) These agents block the action of angiotensin II at the AT1 receptor, which will also reduce the stimulation of aldosterone release. Therefore AT1 receptor antagonists can be used as an alternative in patients suffering from a cough secondary to ACE inhibitors. 2.2.4 Treatment for Type II diabetes mellitus 2.2.4.1 Sulphonylureas (e.g. Gliclazide, glibenclamide, glipizide) The sulphonylureas have two main actions: increase basal and stimulated insulin secretion and reduce peripheral resistance to insulin action. They bind to receptors associated with voltage dependent KATP channels on the surface of pancreatic beta cell, causing channel closure which facilitates calcium entry into the cell and leads to insulin release. Sulphonylureas are considered in Type II diabetes patients who are intolerant to metformin, not contraindicated and not overweight. 2.2.4.2 Thiazolidinediones (e.g. rosiglitazone, pioglitazone) These new agents are ‘insulin sensitisers which act as nuclear peroxisome proliferator-activated receptor-gamma (PPAR-?) agonist. They work by enhancing insulin action and promoting glucose utilization in peripheral tissue, and so reduce insulin resistance. Thiazolidinediones is known to be associated with oedema and increased cardiovascular risks, therefore these agents should be avoided in patients with heart failure.1,4,6 3.0 EVIDENCE FORTREATMENT OF CONDITIONS 3.1 Asthma 3.1.1 Evidence for the use of oral prednisolone and IV hydrocortisone in the management of AEBA There are mounting evidences suggesting that systemic corticosteroids effectively influence the airway oedema and mucus plugging associated with acute asthma by suppressing the components of inflammation, including the release of adhesion molecules, airway permeability and production of cytokines.10-12 A randomised trial involving 88 patients (aged 15-70years) with AEBA reported the significant efficacy of oral prednisolone (40mg daily for 7 days) in improving FEV1 and FVC at values of 68 ±45.3% and 53.4 ±46.5% respectively (P=0.04) in prednisolone-treated group.13 A Cochrane meta-analysis involving six trials recruiting 374 acute asthmatic exacerbation patients determined the early use of systemic corticosteroids significantly reduced the number of relapses to additional care, hospitalisation and use of short-acting ?2-agonist without increasing side effects, regardless of the routes of administration studied (oral/intramuscular/intravenous) and choice of agents.14 3.1.2 Evidence for the use of inhaled ipratropium bromide in the management of AEBA A double-blind, randomised controlled trials recruiting 180 patients with AEBA admitted to emergency department showed that ipratropium had beneficial effects in improving pulmonary function, with a 20.5% increment in PEF (p=0.02) and a 48.1% greater improvements in FEV1 (p=0.0001) compared to those given ?2-agonists alone. Ipratropium also demonstrated a 49% reduction in the risk of hospital admission.15 A more recent meta-analysis incorporating thirty-two double-blind, randomised controlled trials including 3611 patients with moderate to severe exacerbations of asthma also showed the benefits of combination treatment of nebuliser ?2-agonists and anti-muscarinic in reducing hospital admissions (relative risk 0.68,p=0.002) and in producing a significant increase in lung function parameters in AEBA patients (standard mean difference -0.36, p=0.00001).16 Another pooled analysis of three multicenter, double-blind, randomised controlled studies also showed that combination therapy of i pratropium bromide and salbutamol for the treatment of AEBA had decreased risk of the need for additional treatment (relative risk=0.92), asthma exacerbation (relative risk=0.84) and hospitalisation (relative risk=0.80).17 3.1.3 Evidence for addition of LABA to ICS in the management of asthma Symbicort Maintenance and Reliever Therapy (SMART) studies demonstrated the combined use of formoterol/budesonide contributes to a greater reduction in risks of exacerbations, improved lungs performance and better control of asthma than high dose of ICS with SABA.18-22 These studies also reported the advantage of this approach in terms of patient compliance as it allows the use of single inhaler for both rescue and controller therapy, and reductions in healthcare costs.18-22 A large double-blind, randomised trial reported that there was a significant 21-39% reduction of severe exacerbations in asthmatic patients treated with SMART therapy compared with high dose budesonide plus SABA.23 A meta-analysis involving 30 trials with 9509 patients showed that the use of combination inhaler (formoterol/beclomethasone 400mcg) resulted in greater improvement in FEV1, in the use of rescue SABA and in the symptom-free days compared to a higher dose of ICS (800-1000mcg/day).24 Another double-bli nd randomised trial investigating the effect of combination budesonide and formoterol as reliever therapy for 3394 patients who were assigned budesonide plus formoterol for maintenance therapy showed that the time to first severe exacerbation was significantly longer in as needed budesonide/formoterol group compared to as needed terbutaline group (p=0.0051). The other finding of the study is the significant lower rate of severe exacerbation for as needed budesonide/formoterol versus as needed terbutaline group (0.19 vs 0.37, p0.0001).25 Chung et al. (2009) reported that addition of LABA may potentiate the anti-inflammatory properties of ICS as addition of formoterol to budesonide resulted in 63% reduction in severe exacerbation rates.26 Other findings of the study are local and systemic side effects of ICS become more frequent when used alone at doses above 800mcg/day, and the increased efficacy of combination with formoterol was achieved with lower dose of budesonide than was requi red in the budesonide group..26 3.2 Community-acquired pneumonia 3.2.1 Evidence use of combination therapy of second and/or third generation cephalosporins and macrolide in the management of pneumonia A multicenter, randomised trial investigated the efficacy of IV ceftriaxone 2g for 1 day followed by oral cefuroxime 500mg bd in the adult pneumonia treatment. The sequential therapy in combination with a macrolide achieved 90% of clinical success, 85% of overall bacteriologic clearance with 100% eradication of S.pneumoniae after 5-7days of treatment.27 An open label, prospective study involving 603 patients demonstrated that adding azithromycin (500mg od for 3days) to IV ceftriaxone 1g/day in the treatment of community-acquired pneumonia resulted in shorter hospital stay (7.3days vs 9.4days) and a significant lower mortality rate (3.7% vs 7.3%) than adding clarithromycin.28 Lack of randomisation and no blinding of evaluators may become the major limitations of this study; however the effectiveness of macrolide in addition to cephalosporins empirical therapy in treating pneumonia is unquestionable. 3.3 Chronic heart failure 3.3.1 Evidence use of loop diuretic in the management of chronic heart failure (CHF) A meta-analysis of 18 randomised controlled trials concluded that diuretics significantly lowered the mortality rate (odds ratio (OR) 0.25, P=0.03) and reduced hospital admissions for worsening heart failure (OR 0.31, P=0.001) in patients with CHF compared to placebo.29 Compared to active control, diuretics significantly improved exercise capacity in CHF patients. (OR 0.37, P=0.007).29 A recent review reappraisaled the role of loop diuretics as first line treatment for CHF concluded that existing evidence of association of loop diuretics with rapid symptomatic relief and decreased mortality supporting the essential role of diuretics in the management of CHF.30 3.3.2 Evidence use of angiotensin II receptor antagonists in the management of CHF The Losartan Heart Failure Survival Study ELITE II, a double-blind, randomised controlled trial involved 3152 patients with NYHA class II-IV heart failure and ejection fraction ?40% reported that there were no significant differences between losartan and enalapril groups in all cause mortality (11.7 vs 10.4% mean mortality rate). However, losartan-treated group showed a lower discontinuation rate due to side effects (9 ·7 vs 14 ·7%, p 0.001), including cough (0.3 vs 2.7%). These results suggested that losartan has similar benefit in improving survival in CHF as enalapril and is significantly better tolerated.31 A randomised trial involved 5010 patients with NYHA class II, III, or IV demonstrated that valsartan significantly reduced the combined end point of mortality and morbidity by 13.2% (P=0.009) and lowered the incidence of hospitalisation (13.8% vs 18.2%, P0.001)) compared to placebo. Significant improvements in signs and symptoms, NYHA class, ejection fraction and qualit y of life were also observed in valsartan-treated group (P0.01).32 3.4 Type II diabetes mellitus 3.4.1 Evidence for continuing sulphoynylureas when initiating insulin therapy in Type II diabetes mellitus A multicenter and randomized controlled trial demonstrated that combination therapy resulted in significantly lower HbA1c levels (p0.001) as compared to insulin monotherapy. There were no significant difference in the hypoglycaemic event rate between the insulin combination and monotherapy (0.36 vs 0.48).33 Kabadi et al. (2003) supported the efficacies of various sulphonylureas in achieving desirable glycaemic control in combination with insulin. Weight gain, number of hypoglycaemic events and daily insulin requirement were significantly lowered (p0.01) for patients treated with both sulphonylureas and insulin as compared to insulin-treated group.34 3.4.2 Evidence against the use of rosiglitazone in diabetic patients with CHF Thiazolinediones are associated with risks of weight gain, fluid retention, peripheral oedema and plasma volume expansion (lead to increased risk of anemia and new or worsening CHF).35-37 A double-blind randomised trial demonstrated that rosiglitazone significantly increased incidence of oedema (25.5% vs 8.8% placebo,P=0.005) and use of CHF medication (32.7% vs 17.5% placebo, P=0.037) in Type II diabetic patients with CHF. 38 Cobitz et al. (2008) evaluated the potential associations of CHF and myocardial ischaemia events in Type II diabetic patients enrolled in clinical trials with rosiglitazones. Higher odds ratio for CHF incidence was obtained when rosiglitazone is combined with insulin or sulphonylurea: rosiglitazone monotherapy versus placebo (OR 0.25), sulfonylurea plus rosiglitazone versus sulfonylurea monotherapy (OR 0.95) insulin plus rosiglitazone versus insulin monotherapy (OR 1.63).39 More myocardial ischemia incidences were reported with rosiglitazone (2.00%) versus con trol (1.53%).39 Nissen et al. (2007) also reported a significant increased risk of myocardiac infarction (OR 1.43, P=0.03) and a borderline significance of increased mortality from cardiovascular causes (OR 1.64, P=0.06) in the rositaglizone group compared to control group.40 The European Medicines Agency (EMEA) and Medicines and Healthcare products Regulatory Agency (MHRA) have issued advice that the use of rosiglitazone in patients with IHD or peripheral arterial disease is not recommended and it is contraindicated in patient with CHF and acute coronary syndrome.4,41 3.4.3 Evidence for combination therapy of statin and ezetimibe or fibrate in treating complication of diabetes mellitus Patients with Type II diabetes mellitus commonly have raised plasma concentrations of low-density lipoprotein cholesterol (LDL-C) or triglycerides, or low plasma concentrations of high-density lipoprotein cholesterol (HDL-C) associated with higher cardiovascular risks. A multicenter, double-blind randomised trial consisting of 1229 Type II diabetic patients demonstrated the efficacy and safety of combination treatment of ezetimibe and simvastatin in providing additional lipid-modifying benefits compared to atorvastatin monotherapy.42 Ezetimibe/simvastatin group showed a significant greater reduction in LDL-C (-53.6% vs -38.3%), superiority in attaining LDL-C levels 70mg/dL (p0.001) and significantly better improvement for total cholesterol, HDL-C and non HDL-C (p?0.001) compared with atovarstatin group. Incidence of clinical adverse effects such as gastrointestinal and hepatocellular-related rashes or allergic reactions and laboratory adverse effects including elevation of creatine kinase and hepatic transaminases were similar in both treatment arms.42 In the simvastatin plus fenofibrate for combined hyperlipidaemia (SAFARI) trial, greater significant changes in triglycerides (-43.0% vs -20.1% with simvastatin alone), LDL-C (-31.2 vs -25.8%) and HDL-C (+18.6% vs +9.7%) were observed in Type II diabetic patients with mixed dyslipidaemia receiving fenofibrate and simvastatin (160/20mg daily) treatment. No drug-related clinical myopathy and liver function severe abnormalities were reported over a 18-week study period.43 The main concern associated with the combination therapy of statin and fibrates is the potential risk of myopathy and rhabdomyolysis, and the interaction is substantial with gemfibrozil.44-45 To date, there is inadequate evidence to conclude that combination treatment of fenofibrate and statin increased the risk of myopathy.46-49 3.4.4 Evidence use of ticlopidine hydrochloride for prevention of macrovascular and microvascular complications of diabetes mellitus A three-year double-blind, randomised-controlled trial involved 435 patients conducted by the Ticlopidine Microangiopathy of Diabetes study (TIMAD) investigators reported that ticlopidine significantly reduced the annual microaneurysm progression by 85% (p=0.03) and showed a preponderance to develop fewer new vessels (p=0.03) in the insulin-treated diabetic patients compared to placebo group. Significant reduction of overall retinopathy progression was also observed in the ticlopidine group (P=0.04).50 Ticlopidine-induced neutropenia (severe in one patient) with no clinical implications, rash or diarrhoea were reported during the treatment period.50 In another study with similar design, Early Treatment Diabetic Retinopathy Study (ETDRS) investigators demonstrated that aspirin had no effect on retinopathy progression in diabetic individuals.51 Due to its association with life-threatening neutropenia or thrombocytopenia, ticlopidine has been limited to patients who are aspirin-intole rant, or who have failed aspirin therapy.52-54 A meta-analysis included 10 trials with 26865 high vascular risk patients investigated the effectiveness of ADP receptor antagonists (ticlopidine and clopidogrel) versus aspirin in preventing serious vascular events in high vascular risk patients. The main outcomes of the trials are ADP receptor antagonists produced a similar significant reduction in the stroke and other serious vascular events compared to aspirin (11.6% vs 12.5%), ADP receptor antagonists significantly reduced gastrointestinal side effects and ticlopidine significantly increased the risk of neutropenia than aspirin.55 The meta-analysis postulated the fact that clopidogrel has a more favourable side effects profile than ticlopidine, therefore it is the thienopyridines of choice.55 4.0 CRITICAL APPRAISAL OF THE EVIDENCE BASED TREATMENTS CONCLUSION The therapeutic management of SARs AEBA is appropriate and SARs response to the treatment is good. Adding nebulised ipratropium bromide to nebulised salbutamol is important to improve the patients pulmonary function and to reduce hospital stay as both agents act rapidly to relieve bronchospasm. Initiation of IV hydrocortisone and short course of oral prednisolone is an essential treatment for AEBA as evidences support that the use of systemic corticosteroids significantly improves lungs performance, reduces relapse rate, hospitalisation and use of short-acting ?2-agonist following the outbreak of acute exacerbation. However, the dose of oral prednisolone should be adjusted to 40-50mg as according to guidelines to achieve the maximal benefits in relieving acute asthma. There are mounting evidences for the benefits of adding LABA to ICS instead of increasing the steroid dose when low dose ICS fail to control asthma symptoms adequately. Combined budesonide/formoterol inhaler has signi ficance in reducing severe exacerbation rates and in improving patient compliance. Patient compliance is of particular concern in this case as SAR with other co-morbid diseases requires polypharmacy. Therefore, Symbicort ® inhaler (combined budesonide/formoterol) should be given to SAR during hospital stay and as discharged medication replacing high dose ICS for the maintenance management of her asthma. The doctors action to start the empirical therapy of cephalosporins (ceftriazxone and cefuroxime) and macrolide (azithromycin) for management of pneumonia in SAR is appropriate as evidenced in clinical trials. These broad spectrum antibiotics have high bacteriological efficacy against the common pathogens implicated in community-acquired pneumonia. SAR was also on appropriate drugs for the management of chronic heart failure. Both furosemide and losartan have significant values in lowering the mortality rate and incidence of hospitalisation, in improving signs and symptoms and q uality of life of heart failure patients. Combination therapy of sulphonylureas and insulin is relatively safe and sufficient to control the blood glucose level of SAR as there are evidences of better glycaemic control and lesser or no differences in hypoglyaemic events as compared to insulin monotherapy. There is a preponderance of the evidences refuting the use of rosiglitazone in the diabetic patients with CHF as rosiglitazone has side effects profile (in particular peripheral oedema and associated cardiovascular risk) unfavorable to CHF patients. Therefore rosiglitazone should be withdrawn from SARs drug regimen. There are no studies concluded the superiority of ezetimibe and statin over fenofibrate and statin and both combinations are proved to have greater effects than monotherapy for secondary prevention of coronary heart disease in diabetic patients. However, the concurrent use of statin and fenofibrate may potentiate myopathy due to pharmacodynamic interaction. Moreov er, SAR had shown to have increased level of creatine kinase. Therefore, ezetimibe and statin should be the preferred combination as both agents do not have clinical interaction and optimal lipid lowering may best be achieved by inhibiting both synthesis and absorption pathways of cholesterol. The use of ticlopidine for the prevention of complications of diabetes mellitus is justified in this case as aspirin is contraindicated in asthmatic patient and ticlopidine has similar effects as aspirin for prevention of coronary and other vascular events. However, ticlopidine is associated with bone marrow toxicity. Therefore, careful haematological monitoring is required for SAR although she has been started on this drug for one year. In conclusion, the therapeutic managements of SARs presenting conditions are considered appropriate although some modifications need to be made to ensure that maximal benefits can be achieved without causing much clinical adverse effects. 5.0 PATIENT MEDICATION PROFILE PATIENT DETAILS Name SAR Consultant Not available General Practitioner Not available Address Not available Gender Female Weight 54kg Height 160cm Community Pharmacist Not available Date of Birth (Age) 54 Known Sensitivities NIL Social History Patient is a housewife. Patients siblings and children are suffering from bronchial asthma. No hx of alcohol drinking and smoking. PATIENT HOSPITAL STAY Presenting complaint in primary care / reason for admission Admission date Day 1 -Patient experienced SOBx3/7(not relieved by taking inhaler), worsening on the admission day. Discharge Date Day 3 -Minimum cough with yellowish sputum, abdominal pain, diarrhoea, fever -No vomiting, no chest pain RELEVANT MEDICAL HISTORY RELEVANT DRUG HISTORY Date Problem Description Date Medication Comments Since childhood Bronchial asthma Before admission T. Rosuvastatin 20mg nocte Dyslipidaemia 3-4 years ago Hypertension Diabetes mellitus Ischaemic heart disease Before admission T. Ticlopidine hydrochloride 250mg OD (Ticlid) Prophylaxis against major ischaemic events Before admission T. Losartan 50mg OD Hypertension Before admission T. Gliclazide 60mg BD (Diamicron ® MR) Diabetes mellitus Before admission T. Fenofibrate 160mg OD Dyslipidaemia Before admission T. Ezetimibe 10mg OD (Ezetrol) Dyslipidaemia Before admission T. Rosiglitazone 4mg OD (Avandia) Diabetes mellitus Before admission T. Famotidine 20mg OD Prevent GI ulceration Since childhood MDI Salbutamol 200 µg 1puff prn Asthma Since childhood MDI budesonide 200 µg 2puffs bd Asthma Clinical/ Laboratory tests Date Results Plasma potassium (3.5-5.1mmol/L) Day 1 Day 2 5.1 5.0 Urea (1.7-8.5mmol/L) Day 1 Day 2 16.3 24 Creatinine (60-130 µmol/L) Day 1 Day 2 270 298 CrCL calculated (78-120ml/min) Day 1 17ml/min(severe renal impairment) Glucose random (11.1mmol/L) Day 1 18.8 Alb (35-50g/L) Day 1 34 Globulin (25-39g/L) Day 1 45 A/G ratio (0.9-1.8) Day 1 0.8 Hb (13.5-18g/dl) Day 1 Day 2 9.4 10.0 RBC (4-5.2)x1012/L Day 1 Day 2 3.4 3.6 Plat (150-400)x109/L Day 1 Day 2 410 400 WCC (4-11) x109/L Day 1 Day 2 17.1 10.8 Neutro (40-74)% Day 1 Day 2 96 86 Lymphocytes (19-48)% Day 1 Day 2 3 8 Monocytes (3.4-9)% Day 1 Day 2 1 6 CK (26-140)IU/L Day 1 156 LDH (240-480)IU/L Day 1 627 SpO2 Day 1 98%, pCO2 (4.8-5.8) kPa Day 1 4.3 pO2 (11.3-13.3) kPa Day 1 9.9 Pulse rate Day 1 111bpm Lung sound Day 1 Rhonchous PEFR Day 2 Day 3 200-220ml/min 250ml/min Chest x-ray Day 1 Shadowing in right lower zone Blood glucose readings (mmol/L) Time Date 0800 1200 1720 1100 Day 1 24.9 14.2 7.3 14.7 Day 2 15.8 12.4 19.7 16.2 Day 3 12.6 4.2 CLINCIAL MANAGEMENT Diagnosis Pharmaceutical Need Acute exacerbation bronchial asthma Neb salbutamol 5mg+ neb ipratropium bromide 500 µg+normal saline 4hourly, IV hydrocortisone 100mg stat,oral prednisolone 30mg od, MDI budesonide 200 µg 2puffs bd, Underlying pneumonia Antibiotics Chronic cardiac failure IV furosemide 40mg bd, Strict I/O chart(restrict fluid intake 800cc/day), low salt intake, KIV to start S/C Clexane if trop-T +ve Uncontrolled diabetes mellitus Insulin, Oral hypoglycaemics Ward medication Drug route Dose frequency Start date Stop date Indication/ Comments T. Gliclazide (Diamicron ® MR) 60mg bd Day 1 Diabetes mellitus T.Rosiglitazone 4mg od Day 1 Diabetes mellitus T.Rosuvastatin 20mg nocte Day 1 Dyslipidaemia T.Fenofibrate 160mg od Day 1 Dyslipidaemia T.Ezetimibe 10mg od Day 1 Dyslipidaemia T.Lovastatin 20mg nocte Day 1 Dyslipidaemia T.Ticlopidine HCL 250mg od Day 1 Prophylaxis against ischaemic T.Losartan 50mg od Day 1 CHF T.Famotidine 20mg od Day 1 Prevent GI ulceration Neb ipratropium bromide 500 µg, salbutamol 5mg normal saline 2:1:2 qqh Day 1 Day 3 AEBA IV Hydrocortisone 100mg stat Day 1 Day 1 AEBA Neb Salbutamol 200 µg prn 1 puff prn Day 1 AEBA/chronic asthma MDI budesonide 200 µg 2 puffd bd Day 1 AEBA/chronic asthma T. Azitromycin 500mg od Day 1 Day 3 Pneumonia IV Ceftriaxone 2g stat Day 1 Day 2 Pneumonia IV Furosemide 40mg bd Day 1 Day 2 CHF S/C Atrapid 5? , 10? Day 1 Day 2 Diabetes mellitus T. Prednisolone 30mg od Day 2 AEBA MDI beclomethasone 200 µg 2puffs tds Day 2 Chronic asthma T.Cefuroxime 250mg bd Day 2 Pneumonia T. Furosemide 40mg od Day 2 CHF S/C Mixtard 30/10? Day 3 Diabetes mellitus Discharged medication Drug route Dose frequency Indication/ Comments T. Gliclazide (Diamicron ® MR) 60mg bd Diabetes mellitus T.Rosiglitazone 4mg od Diabetes mellitus T.Rosuvastatin 20mg nocte Dyslipidaemia T.Fenofibrate 160mg od Dyslipidaemia T.Ezetimibe 10mg od Dyslipidaemia T.Lovastatin 20mg nocte Dyslipidaemia T.Ticlopidine HCL 250mg od Prophylaxis against ischaemic T.Losartan 50mg od CHF T.Famotidine 20mg od (6/52) Prevent GI ulceration Neb Salbutamol 200 µg 1 puff prn Chronic asthma MDI budesonide 200 µg 2 puffs bd Chronic asthma T. Prednisolone 30mg od (5/7) AEBA MDI Beclomethasone 200 µg 2 puffs tds Chronic asthma T.Cefuroxime 250mg bd (5/7) Pneumonia T. Furosemide 40mg od CHF S/C Mixtard 30/10? Diabetes mellitus PHARMACEUTICAL CARE PLAN Date Care Issues/ Desired outputs Actions Outputs Day 1 Confirm past medication history Ensure appropriate pre-admission medication continued and prescribed correctly. -Co-administration of rosuvastatin (pre-admission drug) and lovastatin (newly prescribed) together with other lipid-lowering agents are inappropriate. Confirm with patient that medicines given are correct. Ask patients family member to bring her old medication at home in order to confirm her medical history. Rosuvastatin should not be continued. (avoid in patients with CrCl ?30ml/min). Dose of fenofibrate should be reduced to 67mg od in patient with CrCl?20ml/min. (BNF) -Patients family members brought her medication at home and past medical history was confirmed. -Rosuvastatin and high dose fenofibrate were still given to patient. Day 1 Appropriate management of AEBA Any one of: -PEF 33-50% best or predicted -RR? 25/min -HR?110/min -inability to complete sentences in one breath -According to NICE/GINA guidelines, drugs for AEBA management include -Oxygen, nebulised beta2 agnonist, nebulised ipratropium bromide, IV hydrocortisone, oral prenisolone, inhaled corticosteroids Drugs indicated for AEBA were given. Oral prednisolone should be adjusted to dose of 40-50mg od for at least 5 days (BTS/GINA) Ensure close monitoring of PEFRs before and after bronchodilator treatment. Advise patient to avoid trigger factor (dust) Suggest self- monitoring of PEFR at home (PEF record keeping) -Dose of oral prednisolone was still not adjusted. -PEFR improved. Day 2 Management of chronic asthma -High dose steroids (MDI budesonide 200 µg 2puffs bd+ MDI beclomethasone 200 µg 2 puffs tds) -Local S/E: Oral candidiasis -Systemic S.E: Adrenal suppression, Cushings syndrome, precipitation of diabetes, oesteoporosis LABA should be added to ICS instead of increasing the dose of steroids. (BTS/GINA) Symbicort ® should be prescribed. Not done Day 1-Day 3 Poor compliance with monitoring and treatment (poor inhaler technique) To prevent subsequent attack: -Check inhaler technique -Education on the correct use of the newly-prescribed inhaler device. -Any observed deficiencies should be corrected before discharged. -Effective counselling of asthma management Simple written instructions reminders of when to use medication were given. The pharmacist checked SARs inhaler technique and SAR was educated to use MDI and nebuliser correctly during hospital stay. The pharmacist counselled SAR on the importance of adherence to drug regimen. Advised SAR to avoid trigger factor (dust) Should also be suggested to self- monitored PEFR at home (PEF record keeping) Counselled. Day 1 Appropriate management of pneumonia -IV Ceftriaxone 2g stat -Oral azithromycin 500mg od (3/7) -Oral cefuroxime 250mg bd (5/7) Monitored signs of recovery and WBC count. Repat CXR and look for progression/complications Replaced IV to tablet form when patient showed recovery of pneumonia. (BTS) Ensure completion of antibiotic course. Vaccinations against pneumococcal infection and influenza should be recommended. (BTS) -Patient showed signs of recovery. -On day 2, oral cefuroxime was given replacing IV ceftriaxone. -Patient was told to complete the course of antibiotic at home upon discharged. -Not done. Day 1 Appropriate management of CHF Furosemide was given to alleviate pulmonary oedema and ankle swelling. Restricted intake of fluid (800cc/day) Furosemide should be given orally with reduced frequency and total daily dose when the patient showed recovery of ankle swelling. Monitored plasma K+ level, renal function bp. Losartan 50mg od was continued. -Lungs were clear, no crepitation. -Swelling of ankle resolved. -Input/output restricted. -On day 2, IV furosemide 40mg bd was replaced by oral furosemide 40mg od. Plasma K+ decreased a bit on day 2 (5.0mmol/L), bp was under controlled. Day 2 Avoidance of hypokalaemia -High dose steroids + salbutamol+ furosemide increase the risk of hypokalaemia. Potassium chloride 600mg bd (appropriate dose for severe renal impairment pt) Close monitoring of plasma K+ level. -Not given. Day 1 Appropriate management of uncontrolled DM -Addition of insulin to the two oral hypoglycaemic agents after the dual oral therapy fails (Targets for blood glucose 4-7mmol/L pre-meal, 9mmol/L post-meal, target HbA1c ?6.5%, practically 7%) Mixture of short intermediate acting insulin was given. Close monitoring of blood glucose and HbA1c levels. Monitored signs of hypoglycaemia. Educated on proper insulin injection techniques -Blood glucose level was under control. No signs of hypoglycaemia. -Measurement of HbA1c was not taken. -Patient and her family members successfully demonstrated the use of insulin injection. Day 1 Safe use of rosiglitazone evidences refuting the use of rosiglitazone in the diabetic patients with CHF as rosiglitazone is associated with oedema, plasma volume expansion and increased cardiovascular risks. -Not recommended in patients with IHD or peripheral arterial disease, contraindicated with CHF and ACS. (EMEA,BTS) Rosiglitazone should be withdrawn. -Rosiglitazone was still given to patient. Day 1 Anaemia Hb (13.5-18)g/dL-9.4 RBC (4-5.2)X1012/L -3.4 -Anaemia is common in patients with moderate to severe HF. -Most likely exacerbated by administration of rosiglitazone. Withdraw rosiglitazone Monitor Hb and RBC If the anaemia problem is not improved, erythropoeitin and iron therapy can be considered. Not done. Day 1 Primary and secondary prevention of cardiovascular events and complications of DM Polypharmacy in the use of lipid-lowering agents. -Rosuvastain, lovastatin, ezetimibe,fenofibrate Rosuvastatin lovastatin act via the same mechanism of action. Dual therapy of statin and fenofibrate potentiate the risk of myopathy (pharmacodynamic interactions) Avoid rosuvastatin if CrCl?30ml/min Reduce dose of fenofibrate to 67mg od if CrCl?20ml/min Rosuvastatin and fenofibrate should not be given. (CrCl: 17m/min) Lipid profile should be done. LFTs should be carried out to avoid the risk of hepatotoxicity. Should advise patient to report promptly unexplained muscle pain, tenderness or weakness. -Four lipid lowering agents were still continued in the patient. -Lipid profile was not done. -No abnormalities of liver function. Day 1 Safe use of ticlopidine hydrochloride. -Similar efficacy as aspirin in reducing cononary and other vascular risk -Limited to patients who are aspirin-intolerant/ who have failed aspirin therapy. -Associated with bone marrow liver toxicity. Close monitoring of haematological LFTs should be done. Should be told how to recognise signs of blood disorder or jaundice. If adverse effects occur, clopidogrel can be considered (more favourable side effect profile). No signs of neutropenia, thrombocytopenia and liver abnormalities. Day 3 Patient for discharge Ensure appropriate medication prescribed and the patient is counselled appropriately prior discharged. Check discharged prescriptions against ward medication chart. Review the appropriateness of discharged medication. Ensure all information relevant to primary care included. Reinforced the importance of patient compliance and follow-up reviews. Counselled patient on the indications and possible side effects of those prescribed medications. Advised patient on healthy lifestyles: Regular exercise Adherence to balance diet which is high in oily fish, fruit, vegetables and fibre; low in calories, sugar, salt saturated fat. -Review of appropriateness of discharged medication was not done by the pharmacist. -Follow-up appointment was made and the patient was told. -Patient was given diabetic diet counselling prior discharged. Day 3 Self management education and personalised asthma action plans -Being able to monitor symptoms, PEF measurements, drug usage and knowing how to deal with fluctuations in severity of asthma according to written guidance. Should be offered self-management education that focuses on individual needs. (mentioned earlier) Should be given written personalised action plans. -No personalised asthma action plans was given.