Diabetes Final

Good practices for treating Diabetes Mellitus in a developing country
Based on a thesis submitted in partial fulfillment of the Universitys requirements for the Master of
International Medicine Health Crisis Management

by GEORGIOS PAPADAKIS, MD, MSc
Authors
THEOFILOS ROSENBERG, MD, PhD, Associate Professor of Surgery ELENI KAKALOU, MD, MSc Internal Medicine specialist GEORGIOS PAPADAKIS, MD, MSc, resident in Endocrinology
The University of Athens in Collaboration with the NGO Mdecins du Monde Greece
AUGUST 2010
2010 Athens, Medical School, University of Athens, Greece

PAGE EDITING: vangelia Stamatellou
estamatellou@yahoo.gr
Contents
Abstract .............................................................................................................................. 5 Intoduction ...................................................................................................................... 7 1. Objectives .................................................................................................................... 9
Monitoring and Evaluation .............................................................................................. 11
2. Methods of therapeutic approach .......................................................... 15

2.1 The profile of the Therapist ...................................................................................... 15 2.2 Barriers to the process of therapeutic work .............................................................. 16 2.3 Approaches and Methods for patient empowerment and improved adherence .... 17
3. Features of the disease .................................................................................. 19

3.1. Pathophysiology of diabetes mellitus ...................................................................... 19 3.2. Types of diabetes ...................................................................................................... 21 3.3. Chronic complications of Diabetes Mellitus ............................................................ 25 Diabetic neuropathy ................................................................................................ 26 Diabetic nephropathy .............................................................................................. 27 Diabetic retinopathy ................................................................................................ 27 Gastrointestinal /genitourinary dysfunction ............................................................ 28 Infections .................................................................................................................. 28 3.4. Diagnosis of Diabetes Mellitus ................................................................................ 29
4. Treatment of diabetes
.................................................................................... 35 4.1. The role of the patient .............................................................................................. 35 4.2. DM and Travel .......................................................................................................... 36 4.3. Diabetic Ketoacidosis, Hyperosmolar Coma ............................................................ 36 4.4. Hypoclycemia ............................................................................................................ 40
CONTENTS
GOOD PRACTICES FOR TREATING DIABETES MELLITUS IN A DEVELOPING COUNTRY
4.5. Antihypertensive Therapy ........................................................................................ 44 4.6. Antidiabetic agents .................................................................................................. 47 4.7. Insulin Therapy .......................................................................................................... 52 General information about insulin .......................................................................... 52 Insulin pens ................................................................................................................ 54 Needles-Syringes ...................................................................................................... 55 Choosing the right insulin ........................................................................................ 56 Insulin dosage ............................................................................................................ 57 Blood Glucose Meters .............................................................................................. 58 4.8. Common practices in the treatment with insulin .................................................... 59 4.9. Lipohypertrophy ........................................................................................................ 60 4.10. Storage of insulin .................................................................................................... 60 4.11. Diabetic Foot .......................................................................................................... 61 4.12. Diabetes and physical activity ................................................................................ 62 4.13. Dietary intervention ................................................................................................ 63 4.14. Diabetes and Obesity .............................................................................................. 66 4.15. Fasting and Diabetes .............................................................................................. 67 4.16. Diabetes and lack of food ...................................................................................... 68
5. Diabetes in patients of special categories
...................................... 71 5.1. Diabetes in children and adolescents ...................................................................... 71 5.2. Diabetes in pregnancy and gestational diabetes .................................................... 73 5.3. Diabetes and surgical procedures ............................................................................ 76 5.4. Diabetes and the elderly patients ............................................................................ 77
Discussion and conslusions ................................................................................ 79 Literature

........................................................................................................................ 81
Abstract
IABETES MELLITUS (D.M.) is a chronic disease with a worldwide impact in both the developed as well as the developing world. In poor countries where hygiene problems overwhelm populations and guide the priorities of local Health systems, diabetes mellitus may not be well treated and this can result in worsening the patients condition. A good number of factors may contribute to it since the patients themselves are quite unaware of their health condition. The Health System on the other hand might prove unable to cope due to lack of health professionals as well as lack of medicines, health materials and supplies. This text attempts to provide basic and concise knowledge on the disease taking into account the realities of everyday life in resource poor settings. It aims also at describing a proposed care delivery model designed for a rural area of a developing country. The model is based on a concept of an outpatient clinic established at district hospital level .Cultural differences, specific problems related to peoples daily lives, their socioeconomical status and educational background must be taken into account in order to set up an effective care delivery model. Methods of attracting patients and raising awareness in the community, have to be developed as integral parts of care for DM. Moreover, a treatment algorithm based on simple steps is presented in order to be used by local health workers such as Clinical Officers and nurses. Special references to needed interventions such as nutrition and physical activity of patients are presented. Specific issues concerning groups such as children, the elderly and pregnancy are also included. Although, the golden standard of care as practiced in resource abundant environments is presented, adapted clinical care pathways more appropriate for resource poor settings are emphasised. By no means does this text aims at substituting neither National guidelines nor more detailed Medical textbooks. For anyone wishing to get more in depth and accurate information on any subject, Medical textbooks on Internal Medicine or DM are recommended. This text aims at concentrating basic background clinical knowledge and perspectives on clinical care of DM in a resource poor setting in a short, easy to use introductory reference for starting to address DM care. Any feedback remarks from readers will be much appreciated by the authors.
Corresponding address for comments: ekakalou@yahoo.gr
ABSTRACT
Introduction
HE RAPIDLY INCREASING incidence of D.M. poses a threat to health systems so much in developed as in a developing countries being faced with a new challenge (2009a). Incidenence of D.M. is increasing at a higher rate in developing countries in recent years (Gersh et al., 2010). At the beginning of the 20th century diabetes was quite rare in Africa but urbanisation and change of lifestyle brought about a rise in the disease and its complications. More than 70% of diabetic sufferers live in countries of average to low income. It is estimated that in 15 years, from 1995 to 2010, the number of people suffering from diabetes in Africa has almost doubled. In 2025 there will be approximately 18,4 million diabetics in Africa with the potential to reach 3,5% of the population. An even higher increase will be noted in developing countries up to 2030 (69% rise in adult with D.M.) (Shaw et al., 2010). It is estimated that 285 million of people suffer from D.M. or 6.4% of adult population worldwide. According to WHO, 76% of the diabetics will be found in developing countries by 2030. The life expectancy of a person diagnosed with D.M. (diabetes type 1) may be 1 year in some African countries where the disease remains uncontrolled (WDF, 2010). Treatment of D.M. varies from country to country in Africa but Health Systems in overall are focused on more serious problems resulting in undertreatment. Chronic diseases tend to be neglected in the developing world where illnesses such as hypertension or diabetes are not a priority (Unwin et al., 1999). Health-care systems in Africa are traditionally geared to the management of acute illnesses and infectious diseases, such as tuberculosis, malaria and gastroenteritis. The HIV-AIDS epidemic has further strained the available but inadequate resources. Even though the HIV-AIDS epidemic is unfolding in sub-Saharan Africa, it is clear that the relative importance of non-communicable diseases will rise, driven by an ageing population, increasing urbanisation and other risk factors, such as tobacco smoking, obesity and physical inactivity. At the same time, successes at treating HIV/AIDS in resource poor settings in recent years brought about by a combination of reduced prices through competition by generic drugs, mobilisation of local communities, international support and funding as well as novel approaches to chronic disease management, have opened a way for other chronic diseases to appear manageable in even the most deprived of communities. Piloting efforts in this area, emerges as a top priority ethical obligation of medical, academic and corporate world.
INTRODUCTION
chapter 1
Our initial goal is to establish quality and comprehensive care for D.M. in rural Tanzania (Ifakara St Francis Hospital). DM care will first be integrated in the services of St Francis Hospital. At a later stage it will be decentralized to at least four points of care in the District, along with development of a referral system. Involvement of patients, their families and the community will be crucial at all stages of design, implementation and scaling up care for DM. Support groups, trained peer educators and expert patients will play a pivotal role in the effort to introduce quality care of DM in Ifakara District. A secondary goal is to record and analyze epidemiological data on prevelance, incidence, immunological-genetic background, complications, morbidity, mortality and all other relevant indexes for DM in a rural African setting. These data will allow the project to set and evaluate impact indicators. Such estimations are impossible for the beginning of the project as very little is yet known for DM in that setting and the country in general. The information that will be produced will permit us to properly evaluate our intervention as the project evolves and scales-up DM care within Ifakara District. Research projects to be developed should be able to directly produce positive impact for patients lifes, answering to the needs of poor rural communities. Research should never be prioritised over patients care. This kind of information is also relevant to any other effort aiming at introducing DM care within the health system in Tanzania. Cost-effectiveness of
A PROPOSED MODEL OF COMPREHENSIVE DM CARE IN A RURAL RESOURCE POOR SETTING
A proposed model of comprehensive DM care in a rural resource poor setting
various interventions has to be estimated, in order to develop a model of care relevant to the needs of the target population. Our ultimate ambition however is for DM to join the agenda of priorities of the Ministry of Health. Contributing to this, by sharing lessons learnt and possible successes of the model established in Ifakara for DM care, is of major importance for multiplying synergies and impact of our limited in time and space intervention. The result of this work may in future be used to strengthen the discussion on the treatment of diabetes. Sharing successes, failures and capacity built at Ifakara Health Structures and local community with other actors at National and International level 1 could be a very positive contribution of the project. Certain actors such as IDF (International Diabetes Federation) or even associations such as the TDA (Tanzanian Diabetes Association) are of paramount importance and much has to be gained by seeking both to learn from them but also to share any experience on possible successes and failures.
General Objective
Reducing the morbidity and mortality of D.M. in a rural community (Ifakara, Tanzania).
Specific objectives
1. Design, implementation and evaluation of a comprehensive prevention and holistic care package for DM
Introducing availablility of basic diagnostic, treatment and follow-up means for

offering free access to clinical care for DM patients (oral antidiabetics, insulin, glucometres and other diagnostics and consumables) Ensuring availability of staff for DM care on a daily basis at outpatient level Linking of hospital services to DM clinic Decentralization of services to at least four points of care within the district and establishment of a rigorous referral system Ensuring uninterrupted logistic supply lines (medicines, diagnostics, consumables etc)
2. Record the epidemiological profile of DM in the rural setting of Ifakara, Tanzania and assess cost effectiveness of various interventions
Assessment surveys of prevalence, incidence, mortality and morbidity rates
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1. Beran et al., 2005.
Clinical cohort data analysis (complication rates, deaths) Cost-effectiveness analysis of interventions introduced by the project
3. Ensure quality care within a model, appropriate for piloting approaches for introducing DM care in resource poor settings
Development and evaluation of a simplified medical algorithm for managing DM,

relevant to the needs and particularities of a rural community in Sub-Saharan Africa
Staff training Education of patients and families Raising awareness and involvement of community in the care of DM
4. Raising awareness, interest and commitment of the health system at local, National and International level
Financial restrictions
Access to adequate and quality health services affordable and accessible to patients must be established. Quality treatment has to be offered and applied in a way that it becomes effective at the lowest possible cost (Abbas and Archibald, 2007).
Monitoring and Evaluation

We aim to assess prevalence and incidence of D.M. along with the complications in Ifakara region and compare the rates with those of previous studies (McLarty et al., 1989) (Ahren and Corrigan, 1984). Measuring quality of care and coverage is extremely important for assessing the projects success and for respecting patient and community rights. A rigorous follow up of implementation, program outputs, transparency and good management practices is essential for both ethical as well as accountability reasons. Thus, the following sets of indicators are proposed for monitoring and evaluation of the project:
A. Process indicators:
Number of new patients enrolled at the program on monthly basis % of patients under follow up at 3, 6, 12, 18 and 24 months after initial diagnosis and
program enrolment
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% of patients missing >1 appointment per year 2 % of patients on treatment with insulin % of patients receiving treatment for hypertention % of patients receiving treatment for hyperlipidemia % of patients following introductory training in disease management and lifestyle modifications (offered at a weekly basis, initially in the hospital and later at community level) Number of patients recruited in the program Number of patients on insulin treatment Number of staff trained Number of peer educators and expert patients trained % of trained peer educators and expert patients still active in the program one year after their initial training and involvement in the program Number of patients diagnosed following referral from general uptake of health structure Number of meetings with health actors at National level (on a six month basis)
B. Output indicators

% of patients achieving Gluc<110-130 mg/dl or HbA1C < 7-8% 3 % of patients with BP values < 140/80 % of patients with BMIs <25 kg/m2 % of patients with values: LDL <130 mg / dl, HDL> 40 mg / dl for men and> 50 mg / dl for women Triglycerides <150 mg/dl. % of lost to follow up patients at 1 year % of limp amputations for patients under treatment and follow up % of deaths due to DM emergency or treatment complications (diabetic ketoacidosis or hyperosmolar non ketosis coma or hypoglycaemia)
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2. Kalyango et al., 2008 and Kengne et al., 2009. 3. Specific values for Gluc, HbA1C, BP, BMI, Lipids to be decided based on recording such values for first 1-3 months of program rolling out. Based on the fact that we are operating in a resource poor setting, less rigorous targets of such values could be set for measuring program outputs. This is a point necessitating further debate.
C. Means of collection
Specifically designed patient data base
RISK STRATIFICATION OF COMPLICATIONS IN RELATION TO DIFFERENT VALUES OF GLUCOSE, BP AND LIPIDS
In more detail, the targets for glucose and lipids regulation are shown below Tables A and B: . Goals of blood glucose levels to reduce the risk of DM complications:
Low risk High risk for macrovascular complications >6 Low risk for microvascular complications >7
HbA1C (%b) (normal = 4-6%) Fasting plasma glucose before meal (mg/dl) Glucose of self-control postprandial (mg/dl)
<6
<110
>110
>125
<135
>135
>160
B. Lipids goals for reducing the risk of complications:

Risk High LDL-Chol. (mg/dl) >130 HDL-Chol. (mg/dl) <35 (men) <45 (women) 35-45 (men) 45-55 (women) >45 (men) >55 (women) Triglycerides (mg/dl) >200
Middle
100 - 129
150 - 200
Low
<100
<150
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chapter 2
Methods of therapeutic approach

2.1. The profile of the Therapist
The clinical therapist in charge plays the most important role in the D.M. treatment team. He/she will have to instruct the patients on how to regulate their D.M. and guide them with their choices in order to enable them to adjust with the disease in their daily lives. The therapist may be a health worker but not necessarily a medical doctor. He/she could be a health carer with the basic knowledge of D.M. and should be able to properly guide the patients (Gill et al., 2008). Preferably the therapist has to be close to the local community (Culica et al., 2008). Finally, control of DM can be guided by experienced patients themselves (trained expert patients) who can provide important advice and guidance to other patients who will get for the very first time an organized medical treatment. (Seung et al., 2008). The therapist must assist patients in making the necessary adjustments concerning diet, physical activity, adherence to treatment and other behavioural issues so as to be able to master themselves control of this chronic disease. Other members of staff, fellow patients (expert patients and peer educators) and the entire community should play an integral part in assisting the clinical care team to support patients. Skills necessary for clinical therapists:
He/she must have basic knowledge of epidemiology, pathophysiology, diagnosis,

complications, treatment and prevention of D.M.
He/she must be skilled in techniques such as giving injections, checking sugar levels
and providing foot care.
He/she should demonstrate good communication skills
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METHODS OF THERAPEUTIC APPROACH
He/she should be surrounded by a team of people who could undertake a part of

treatment. But in poor resources countries the options and possibilities of ensuring availability of a multidisciplinary team (nutritionist, psychologist, paediatrician, surgeon, eye expert, nephrologist, health promotion expert ) could be limited .For this the therapist should be prepared to undertake multiple roles within the program.
2.2. Barriers to the process of therapeutic work

During clinical care the therapist may be met with limitations in his attempt to introduce his patients to an ideal behaviour concerning D.M. The obstacles may be physical disabilities which hinder communication or even psychological problems since it is extremely difficult for some patients to accept confinements entailed by the disease (Neuhann et al., 2002). It is not uncommon for patients to undergo through several stages until they finally accept their condition, therefore the therapist will be asked to cope with the patients denial, anger and depression, before acceptance which usually finally occurs. People with diabetes are very likely to develop depression which is associated with a higher mortality rate. Depression affects negatively a persons ability to manage his/her diabetes and follow the appropriate diabetes care. Moreover, diabetes-related stress is common, particularly the fear of hypoglycaemia and long-term complications Many patients fear the financial side of their disease (Khuwaja et al., 2010). Not everybody can buy medication and insulin nor can they adopt a special diet. Also D.M. as a disease requires frequent visits to the doctor and transfers to the hospitals (Mbanya and Mbanya, 2003). In some countries as in Tanzania for instance, there is legislation for free medication but that has never been put to practice (Shiraishi et al., 2006). In the private sector the prices of the medicines remain very high while in public hospitals serious shortages often exist (Justin-Temu et al., 2009), (Beran, June 2004). Finally there is always the concern whether a patient would be able to continue with his work or his normal life. Additionally, lack of family and social support along with the social stigma can act as obstacles in the therapists efforts. And yet there are always different cultures and attidutes among people suffering from the disease (Belue et al., 2009). Illiteracy proves to be an additional obstacle in the teaching process. Each educational approach must aim at the individual profile of the patient so as to meet needs and particular circumstances of individual patients (Smide et al., 1999). The therapist might also encounter distorted views, prejudice and misconceptions. He/she should thus obtain a good understanding of what is considered true or appropriate by the community. In some communities in Africa for instance, obesity is regarded as a sign of health and prosperity. That might negatively affect the dietary interventions of the therapist. In other
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places there are myths and beliefs concerning the disease and there are populations who regard it as a result of magic. In many cases herbs and magic are preferred to medicines. Misunderstandings still occur as far as the pathogenesis of the disease is concerned. Some believe that it is a result of poisoning or of excessive sugar consumption. Thus, honey they believe, should be consumed rather than sugar. In other traditions the consumption of bitter tree leaves is believed to help lower blood glucose. Traditional healers are the ones to bring upon cure by use of alternative therapies which are more preferable to conventional medicine for most people (2004) (Famuyiwa, 1993). It is also a common belief that the disease is contagious, confined to white populations, the elderly and the rich. Some practices again could be dangerous such as, for instance, to walk barefoot inorder to reduce the temperature of burning foot. Some beliefs are also quite harmful such as the one arguing that diabetics cannot be operated on since the wounds are expected never to heal. In some populations those myths and beliefs are solid into the conscious mind of people and very hard to overcome (Rai and Kishore, 2009). To sum up, the therapist will be faced with the ethical, social and financial aspects of the disease (Bal, 2000).
2.3. Approaches and Methods for patient empowerment and improved adherence
Teaching approaches can apply in groups or individually.
There can be lectures on D.M. where many people can participate. The disadvantage though is the passive participation and low turn-out. Another approach might be through group discussions where participants and therapists can openly exchange ideas and experiences. Although this approach can prove quite flexible, it might not be well focused and become influenced by the interpersonal relations of the participants. Teaching should also include demonstration of some techniques such as giving insulin injections, measuring glucose or foot care. Finally activities, role play and discussions should be included in teamwork (International Diabetes Federation (IDF), 2008). Instructing in groups can be applied to a wider number of people not only to patients but to relatives as well. The teaching project can be realised with the collaboration and liaison of local organisations or institutions if these exist and there will have to be separate sessions concerning diet, foot care, physical activities,
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METHODS OF THERAPEUTIC APPROACH
When in groups, various methods can be used
insulin storage and changes in lifestyle. It will all be within the frame of the basic health care package offered (Beaglehole et al., 2008).
Apart from team work, the therapist will have to meet his patients in private.
This will allow to individualise the programme and allow the patient to learn in his own pace. Restrictions occur when the therapist has a little time in his hands and a large number of patients to deal with. For this reason, nurses must be gradually trained so as to implement routine clinical care and follow up tasks and only the more complicated cases will be reported to doctors. Various approaches to task-shifting have to be developed, so as to better use scare resources (eg. MDs)
Peer to peer education is of utmost importance.

The term refers to the mutual knowledge shared among the diabetics. Usually the patient chosen is a gifted member of the community with good communication skills and it is his responsibility to lead the other patients to the clinic to seek help. Experience exchange among patients is vital. Problems concerning their health in their daily routine are discussed. This encourages passing on knowledge and experience among the patients which is sometimes more effective that the theoretical lectures of the health professionals to whom the illness is not a personal experience (2007) (Wientjens, 2008). Brochures, posters and fliers in local language can be used to enhance learning. Different leaflets giving information about diet, ways of insulin administration or foot care must be distributed so that the patient can refer to them easily. Finally information technology and interactive boards can also be used as efficient ways of teaching. However, something like that in a resource poor environment with high illiteracy rates might sound irrelevant. However, theatre, dance and role playing exercises can be easily introduced in many cultures in the developing world with the active participation and involvement of local communities.
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chapter 3
Features of the disease

3.1. Pathophysiology of diabetes mellitus
Diabetes is a chronic disease characterized by hyperglycaemia due to lack of insulin, resistance to insulin action or combination of both. Diabetes mellitus comprises a group of common metabolic disorders that share the phenotype of hyperglycemia. The knowledge on the effect of beta-cells in the pancreas, the relationship between glucose, insulin and contra-reacting hormones in glucose homeostasis is important so as to understand the pathophysiology of the disease. Chronic hyperglycemia leads to many complications affecting the whole body. The body receives energy from food. Carbohydrates, proteins and fats are the main nutrients. As food gets chemically degraded by enzymes, glucose molecules, amino acids, fatty acids and glycerol are being produced. These are absorbed by the walls of the intestine organ and transported into the bloodstream. The elevated glucose levels stimulate the pancreas to secrete insulin which enables body cells to absorb glucose and turn it into energy. Insulin acts on the liver so that glucose is stored as glycogen which remains as an inactive form of glucose. It also inhibits gluconeogenesis, which is the conversion of non-carbohydrates into glucose. It facilitates the transport of glucose through cell membranes with insulin receptors, such as skeletal cells or heart cells and adipose tissue. Insulin also acts on the metabolism of proteins supporting the transport of amino acids into the cells, thereby enhancing protein synthesis particularly in muscle tissue. In relation to the metabolism of fats, insulin stimulates adipose cells to synthesize and store fat while reducing release of fatty acids from the adipose tissue. By all these ways, insulin reduces the concentration of glucose in plasma.
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FEATURES OF THE RISEASE
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A number of hormones are secreted responding to low plasma glucose. Glycogen is converted into glucose (glycogenolysis) and fats and amino acids are converted into glucose (gluconeogenesis), thus increasing blood glucose. The hormone that mainly compensates the action of insulin is glucagon which is produced by the alpha cells of the pancreas. Glucagon converts glycogen into glucose, and non-carbohydrates such as amino acids into glucose (gluconeogenesis). It also stimulates the degradation of fats into fatty acids and glycerol (lipolysis). As insulin levels decrease between meals or during the night, the secretion of glucagon is activated. When the levels of glucose are rising glycogen is not produced. Growth hormone, cortisone and adrenaline can increase the levels of blood glucose through alternative biochemical pathways. When insulin is absent glucose levels increase and so glucose is not stored in the form of glycogen. The use of glucose by muscle and adipose tissue is reduced and the lack of glucose in the cells results in the production of energy from the degradation of fats and proteins. This leads to the production of ketoacids which result in ketoacidosis a condition which can be life threatening. The secretion of insulin from beta cells of the pancreas is biphasic. The first rapid phase lasts 5-10 minutes and then a prolonged second stage lasts as long as the duration of the stimulus. The half-life of circulating insulin is 4-5 minutes and when insulin is bound to receptors it is longer. The -cells respond to hyperglycaemia in glucose concentration from 5 mmol/lt to about 9 mmol/lt. Above these prices hyperglycemia has negative effects on beta cells. Type 1 diabetes mellitus (T1DM) is characterised by loss of insulin producing beta cells of the Langerhans islets in the pancreas leading to insulin deficiency. This type of diabetes can be further classified as immune-mediated or idiopathic. Viruses and other environmental factors may lead to the production of autoantibodies (GAD, IA-2, ICA antibodies). Patients with permanent insulin deficiency tend to develop ketoacidosis. Idiopathic type by which there is no obvious mechanism of autoimmune reaction is frequent in Africa and Asia. Another type of diabetes can also occur in Africa where patients may periodically develop ketoacidosis. T1DM is less common among black Africans in Sub-Saharan Africa compared to people from other tribes in this region. The average age of the Africans is 23 years, which is a much older age compared to whites. This fact is related to prolonged breastfeeding which is more common in Africa. Moreover, the frequency of GAD antibodies and IA-2 antibodies were found to be significantly rarer in black adults, something that shows that non-autoimmune T1DM is the most common type (Lutale et al., 2007). Type 2 diabetes mellitus (T2DM) is characterised by insulin resistance which may be combined with relatively reduced insulin secretion. The defective responsiveness of body tissues to insulin is believed to involve the insulin receptor. Genetic background, environmental factors, rich in fats diet and reduced physical activity are also related to the development of the disease. There is also strong correlation with obesity of central type and with resistance to insulin. T2DM is caused due to delayed and eventually reduced production
of insulin by beta cells of the pancreas and increased insulin resistance of cells with insulin receptors (Osei et al., 2003). The failure of beta cells may be due to a defect in insulin secretion which leads to high postprandial plasma glucose levels. Other abnormalities may be associated with high levels of inactive forms of insulin release and gradual but steady damage of beta cells. Insulin resistance is associated with dysfunction of insulin receptors. This leads to reduced sensitivity of cells to insulin action and as a result reduced absorption of glucose into cells, while glucose levels in blood stream remain high. As a consequence of elevated glucose, beta cells are stimulated to secrete more insulin. Eventually, the beta cells lose gradually their ability to secrete more insulin to overcome the resistance of peripheral targets and thus hyperglycemia and clinical symptoms worsen.
3.2. Types of diabetes

A most recent classification of diabetes divided the two types of D.M. into insulin and non insulin dependent according to the pathogenesis of the disease. The term type 1 diabetes has replaced several former terms, including childhood-onset diabetes, juvenile diabetes, and insulin-dependent diabetes mellitus (IDDM). Similarly, the term type 2 diabetes is used instead of several former terms, including adult-onset diabetes, obesity-related diabetes, and non-insulin-dependent diabetes mellitus (NIDDM).Another type is the gestational diabetes. The main characteristic of T1DM is its early development due to destruction of beta cells of the pancreas. Most of the patients are diagnosed before the age of 35 years and the onset of the disease may be acute or less acute, depending on the reduction rate of beta-cells of the pancreas. The majority of T1DM is of immune-mediated nature, with beta cell loss being a T-cell mediated autoimmune process. There is also a category of autoimmune destruction of cells in adults at a slower pace (LADA-latent autoimmune diabetes in adults). Usually people with T1DM are of normal or reduced body weight. No preventive measure is known against T1DM, which causes approximately 10% of diabetes mellitus cases. At the beginning of the disease people affected are mostly healthy and of normal weight, while sensitivity and responsiveness to insulin are usually normal. T1DM was traditionally found under the term juvenile diabetes because it represents a majority of diabetes cases in children but it can affect both children and adults. In children and young people the first sign of T1DM may be the diabetic ketoacidosis or a coma. People with T1DM depend on insulin for survival in order to prevent dehydration, ketoacidosis and generalized catabolism. The classic symptoms of hyperglycaemia may roughly translate to polyuria (frequent urination), nocturnal enuresis, polydipsia (increased thirst) and polyphagia (increased hunger), weight loss, headaches, fatigue, and blurry vision disorders (Roche et al., 2005). There may
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22
also be numbness at hands, legs and feet and recurring infections. Symptoms may develop rapidly (weeks or months) in T1DM while in T2DM they usually develop much more slowly and may be subtle or absent. The production of ketoacids is associated with symptoms such as abdominal pain, nausea and vomiting. Under conditions of intense stress and infection the body tends to develop more severe hyperglycemia. Usually, in the diagnosis of T1DM no chronic complications are present. In many countries the mortality can be high and patients may die undiagnosed. Many patients may develop the disease at the beginning of puberty. However in a 10% DM occurs after the age of 65. There are variations depending on origin. Worldwide it is estimated that 5% of the population has T1DM with increasing trends for the future. In Africa the rate is about 2.5% of the total population, estimated by 2025 to raise up to 2.8%. DM is less common in indigenous Africans living in sub-Saharan region. Men seem to have a greater prevalence of the disease compared with women (IDF, 2005). Regarding T2DM, it develops mostly in people older than 40 years, but it can also be found in younger patients. T2DM is the most common type. There is no absolute dependence on insulin for survival. Usually, T2DM is treated with diet, exercise and antidiabetic tablets. After a few years T2DM, may not be controlled by oral drugs and consequently insulin has to be used to achieve good metabolic control. We can categorize patients with T2DM, depending on whether they are obese or not. In Western societies the obese amounted to 80% of the population. In Southern Africa the rate of obesity in T2DM patients is between 20-30%. Nevertheless, there is a genetic component to the expression of disease (Mengesha and Abdulkadir, 1997). T2DM often remains undiagnosed for many years because hyperglycaemia develops gradually. Although T2DM can be considered characteristic of Western lifestyle, it appears to be emerging as an epidemic over the developing world. Only half of the patients may experience the classic symptoms of the disease. The disease can be diagnosed accidentally during a routine check in only a third of cases. Repeated infections may herald the onset of the disease. Finally, it can be diagnosed late, when long-term complications of the disease such as sores on the foot, gangrene, myocardial infarction, peripheral vascular disease and renal disease have already developed. The likelihood of ketoacidosis is not high and certainly much lower compared to T1DM. Diabetic nephropathy in Africa entails a poor prognosis because of lack of treatment means and lack of dialysis units (Rolfe, 1988). The same applies for retinopathy or myocardial ischaemic disease. Average age of onset for T2DM is around 55-60 years. The ratio of men/women is 3/2. The percentage of diabetics is larger in urban areas than in rural areas (Alemu et al., 2009). Diets rich in fats and low in carbohydrates and fibres, high stress levels and the limitation of physical activity are all related to T2DM development. There is also a genetic background. T2DM was not common in younger age groups, but lately it affects younger people too. Childhood obesity is also related to DM, later in life. T2DM is often combined with hypercholesterolemia and hypertriglyceridemia (Mengesha, 2006).
Besides, the metabolic syndrome or syndrome X is quite common in Africa (Longo-Mbenza et al., 2010) (Makuyana et al., 2004). For the diagnosis the following must be present:
central type obesity waist circumference> 102 cm for men and> 88 cm for women or
BMI> 30 kg/m2 plus two of the following criteria:
triglycerides> 150 mg / dl, HDL cholesterol <40 mg / dl for men and <50 mg / dl for
women
blood pressure values BP> 130/85 mmHg fasting plasma glucose> 100mg/dl
These criteria have not been adjusted for indigenous Africans (Gaillard et al., 2009). The table below highlights the main differences between T1DM and T2DM:
Features Onset T1DM Acute T2DM Slow, it develops gradually. Patients may remain undiagnosed for too long >40-45 years old Patient might be asymptomatic for too long Normal or overweight
Age Symptoms
Usually <30-35 years old Yes, severe or less severe
Weight
Thin person, usually big loss of weight before diagnosis Lack of insulin which is necessary for survival
Insulin secretion
Reduction of -cells, low secretion and/or abnormality of insulin receptors in the peripheral tissue, insulin resistance Common, because of late diagnosis Yes FEATURES OF THE RISEASE More rare than T1DM No Stronger correlation Yes Lifestyle, antidiabetics, insulin Mostly macrovascular and later in course of disease microvascular as well
Complications at the time of diagnosis Insulin resistance Ketoacidosis Autoantibodies
Rare
No Yes, usually sets the diagnosis anti-GAD, ICA, 1A-2
Genetic background-susceptibility May be present Syndrome X Therapeutic choices Complications No Insulin Mostly microvascular
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Finally, there is also another category, gestational diabetes (GDM) which first appears during pregnancy. Gestational diabetes can occur at any stage during pregnancy. It usually occurs during the second or third trimester of pregnancy. Typically the rate is estimated between 1-3% in expectant mothers. Women entering pregnancy with pre-existing diabetes are also included in this group. Gestational diabetes is associated with increased rate of perinatal complications. Risks to the baby include macrosomia (high birth weigh), increasing the risk for children of diabetic mothers to become themselves diabetic in later life. Early diagnosis is essential to avoid complications (Iqbal et al., 2009). Age (over 35 years) and obesity are factors to be taken into account for higher risk of gestational diabetes (Hossein-Nezhad et al., 2007). Finally, diabetes may be the result of pancreatic disease in any case where there may be inflammation (pancreatitis), trauma, infection, cancer and post-pancreatectomy. Furthermore, chronic pancreatitis, cystic fibrosis and hemochromatosis destroy beta cells of the pancreas, leading to decreased insulin secretion. Additionally, diabetes may occur as a result of endocrine disorders involving other hormones or as a result of drugs, chemicals and toxins. Congenital diabetes, which is due to genetic defects of insulin secretion, cystic fibrosis-related diabetes, steroid diabetes induced by high doses of glucocorticoids, and several forms of monogenic diabetes are other forms included in D.M disorders. The table below shows etiological classification of D.M.
T1DM (-cell destruction, usually leading to absolute insulin deficiency) (a. Immune mediated, b. Idiopathic) T2DM (may range from predominantly insulin resistance with relative insulin deficiency to a predominantly insulin secretory defect with insulin resistance) Other specific types of diabetes mellitus:
Genetic defects of -cell function Genetic defects in insulin action Diseases of the exocrine pancreas-pancreatitis, pancreatectomy, neoplasia, cystic fibrosis,
hemochromatosis, fibrocalculous pancreatopathy

Endocrinopathies acromegaly, Cushings syndrome, glucagonoma, pheochromocytoma,
hyperthyroidism, somatostatinoma, aldosteronoma

Drug- or chemical-induced Vacor, pentamidine, nicotinic acid, glucocorticoids, thyroid
hormone, diazoxide, -adrenergic agonists, thiazides, phenytoin, -interferon, protease inhibitors, clozapine, beta blockers Infections- congenital rubella, cytomegalovirus, coxsackie Uncommon forms of immune-mediated diabetes Other genetic syndromes sometimes associated with diabetes Downs syndrome, Klinefelters syndrome, Turners syndrome, Wolframs syndrome, Friedreichs ataxia, Huntingtons chorea, Laurence-Moon-Biedl syndrome, myotonic dystrophy, porphyria, Prader-Willi syndrome
Gestational diabetes mellitus (GDM)
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3.3. Chronic complications of Diabetes Mellitus

Diabetes mellitus indicates a condition where various organs fail over the years. People with diabetes should be regularly checked for signs of complications. These chronic complications include damage caused to various organs and systems:
Eyes (eg diabetic retinopathy) Nervous system (eg diabetic neuropathy) Heart and blood vessels (eg diabetic microangiopathy) Kidneys (eg, diabetic nephropathy).
If complications are not diagnosed early and treated properly, they can lead to vision loss, amputations, kidney failure or premature heart disease. The risk of chronic complications increases by the duration of hyperglycemia and they usually become apparent in the second decade of disease. Diabetes can also cause complications during pregnancy. Complications occur in both types of diabetes, irrespectively whether the patient receives insulin or antidiabetic drugs. There are two main categories of complications:
Diabetic microvascular disease:

It affects capillary blood vessels and damage presents as diabetic eye disease (retinopathy, nonproliferative/proliferative, macular edema), neuropathy (sensory, motor mono/polyneuropathy and autonomic neuropathy) and nephropathy.
DIABETIC MACROVASCULAR DISEASE:
It is characterized by early appearance of severe atherosclerosis and it is associated with increased incidence of coronary heart disease (acute myocardial infarction, stroke, cerebrovascular disease and peripheral arterial disease). Other complications include:
MANAGEMENT OF COMPLICATIONS:
Basic diabetes management skills are necessary. These may include good blood glucose control, treatment of hypertension, control of increased cholesterol levels and generally good medical care in order to prevent or delay complications. Good adjustment and long-term regulation of glucose should slow down the process of the disease. As a precaution, people
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Gastrointestinal (diarrhea, gastroparesis due to autonomic neuropathy) Genitourinary (uropathy / sexual dysfunction) Infectious Dermatologic (skin ulceration, protracted wound healing) Glaucoma Cataract
with diabetes should undergo periodic special examinations regularly to detect early damage caused by diabetes in order to prevent the worst (eg regular eye examination for diabetic retinopathy, etc.). In a resource poor setting environment, periodic screening for possible complications could be performed avoiding use of sophisticated means that are not available
Diabetic neuropathy
Approximately 50% of patients with long-standing T1 and T2DM may suffer from diabetic neuropathy. Diabetic microvascular injuries involving small blood vessels that supply nerves (vasa nervorum) in addition to macrovascular conditions can accumulate contributing to development of diabetic neuropathy. Common conditions related to and/or associated with diabetic neuropathy include 3rd nerve palsy, mononeuropathy, mononeuropathy multiplex, diabetic amyotrophy, (a painful polyneuropathy), autonomic neuropathy and thoracoabdominal neuropathy. All peripheral nerves can be affected by diabetic neuropathy. In autonomic nerves, pain fibers and motor neurons can be damaged. Since all organs and systems are innervated they can be seriously affected by diabetic neuropathy. Several distinct syndromes -based on organ systems- can appear in the form of autonomic and/or sensorimotor neuropathy. Symptoms usually unfold gradually and they vary depending on the nerve(s) affected including symptoms other than those listed. Symptoms may include:
Numbness and tingling of extremities Fasciculation (muscle contractions) Diarrhea Dysesthesia (decrease or loss of sensation to a body part) Impotence Difficulty swallowing Erectile dysfunction Urinary incontinence (loss of bladder control) Dizziness Muscle weakness Facial, mouth and eyelid drooping Vision changes Anorgasmia Speech impairment Burning or electric pain
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Diabetic nephropathy
Angiopathy of capillaries in the kidney glomeruli causes Diabetic Nephropathy Characterised by nephrotic syndrome and diffuse glomerulosclerosis. Kidney failure may be caused by glomerulosclerosis and it results in fluid filtration deficits and other various disorders of kidney function. Edema can be caused by hypertension and fluid retention in the body with a reduced plasma oncotic pressure, along with other complications such as proteinuria, and arteriosclerosis of the renal artery. At its onset, diabetic nephropathy shows little symptoms, since they develop gradually in late stages. They may be due to renal failure or a result of excretion of high amounts of protein in the urine. Symptoms may include:
edema: swelling, usually around the eyes in the morning; later, general body edema
may result, such as in the legs foamy appearance or excessive frothing of the urine (caused by the proteinuria) unintentional weight gain (from fluid accumulation) nausea and vomiting anorexia (poor appetite) malaise (general ill feeling) fatigue headache frequent hiccups generalized itching
The first abnormality that can be detected by a special lab test is microalbuminuria. Mostly the diagnosis is suspected when proteinuria occurs in a routine urinalysis of a person with diabetes. As kidney damage progresses and blood glucose is poorly controlled there are signs of glucose in the urine, plus increase in serum creatinine and blood urea levels. Diabetic nephropathy continues its destructive course, especially when complications of chronic kidney failure occur earlier and progress more rapidly. Even transplantation or dialysis do not seem to work so effectively in diabetes patients.
Diabetic retinopathy
Diabetic retinopathy is ocular manifestation of systematic disease. It is caused by complications of diabetes mellitus and it can lead to blindness. Diabetic retinopathy can affect the 80% of all patients with diabetes for 10 years or more. No early warning signs may herald diabetic retinopathy. However, a person with macular edema, who is likely to have blurred vision, does not have any warning signs even though macular edema causes vision loss quite rapidly.
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In part proliferate diabetic retinopathy consists of new blood vessels which form in the eye and they can bleed and blur vision. This may not be too severe the first time it happens. Just a few specks of blood or spots are left in a persons visual field and most probably they will clear away a few hours later.
Gastrointestinal/ genitourinary dysfunction

Motility and function of gastrointestinal and genitourinary systems may be affected by T1 and T2DM. Gastroparesis (delayed gastric empting) and either constipation or diarrhea (altered small and large bowel motility) are the most prominent gastrointestinal symptoms. Symptoms of vomiting, early satiety, anorexia, nausea and abdominal bloating may be present with gastroparesis. Genitourinary dysfunction including erectile dysfunction, female sexual dysfunction and cystopathy can be caused by autonomic neuropathy.
Infections
Frequent and severe infections are a common phenomenon within the diabetic population. Incompletely defined abnormalities in cell-mediated immunity and phagocyte function associated with hyperglycemia as well as diminished vascularization are some of the reasons. Colonization and growth of various organisms (Candida and other fungal species) are favored by hyperglycemia. While many common infections are more frequent and severe in diabetic patients, there are also several rare infections detected almost exclusively in the diabetic population. Some examples of this latter category may be emphysimatous infections of the gall bladder and urinary tract, rhinocerebral mucormycosis, and malignant or invasive otitis externa. Invasive otitis externa usually secondary to P. aeruginosa infection of the soft tissue surrounding the external auditory canal- may first begin with pain and discharge before it rapidly leads to osteomyelitis and meningitis. Other more common infections within the diabetic population are pneumonia, urinary tract infections, and skin and soft tissue infections. It is a fact though that the organisms which cause pulmponary infections are very alike those found in the nondiabetic populations. Pathogens considered more frequent among diabetic patients are: Gram (-) negative organisms Staphylococcus aureus Mycobacterium tuberculosis Several commonly observed yeast species such as Candida parapsilosis, glabrata Bacterial agents like Escerichia coli, resulting from urinary tract infections (either lower or pyelonephritis).
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Emphysematous pyelonephritis and emphysematous cystitis are also complications of urinary tract infections. Patients with diabetic cystopathy are often faced with bacteriuria, superficial candidal infections and vulvovaginitis. These patients also appear to have an increased rate of colonisation by S. aureus at skin folds. A common denominator among these patients is poor glycemic control.
3.4. Diagnosis of Diabetes Mellitus

Diagnosis of diabetes is usually based on clinical suspicion when certain symptoms are present. Along with late diagnosis, long-term health problems have already been established and this is the main reason why early diagnosis is important (Ambady and Chamukuttan, 2008). All risk factors related to the disease should be taken into consideration by the therapist and the health professionals working in the local clinic. Thus diagnosis of new diabetic patients even of those unaware of their disease-can be reached. Risk factors for DM are:
Family history of diabetes (i.e., parent or sibling with type 2 diabetes) Previously identified impaired fasting glyceamia or impaired glucose tolerance History of gestational DM or delivery of baby >4 kg (>9 lb) Habitual physical inactivity Obesity (Body Mass Index > 25 kg/m2) Hypertension (blood pressure >140/90 mmHg) HDL cholesterol level < 35 mg/dL (0.90 mmol/L) and/or a triglyceride level >250 mg/dL (2.82 mmol/L) Polycystic ovary syndrome or acanthosis nigracans Race/ethnicity History of vascular disease Laboratory tests of blood glucose or/and the glucose tolerance test confirm the diagnosis. Usually a fasting blood glucose level >126 mg / dl is diagnostic, unless an infection or any other health problem co-exist which cause temporal rise in blood sugar. Random plasma glucose measurement level should be >200mg/dl (Krein et al., 2009). A single measurement is not sufficient to rely on therefore it must be repeated. The second test can be done after consultation on an empty stomach. An additional glucose tolerance test can be made for further confirmation. If the results are inconclusive then further periodical tests are suggested till a certain diagnosis is reached. Glycated haemoglobin (glycosylated hemoglobin, hemoglobin A1c, HbA1c, A1C, or Hb1c, sometimes also HbA1c) is a form of haemoglobin used primarily to identify the average plasma glucose concentration over prolonged periods of time. It is formed in a non-enzymatic
29
pathway by haemoglobins normal exposure to high plasma levels of glucose. High levels of HbA1c have been associated with cardiovascular disease, nephropathy, and retinopathy. Monitoring the HbA1c in type-1 diabetic patients may improve treatment. Glycosylated haemoglobin test (HbA1c), which represents the average blood glucose for a period of weeks (8-12 weeks) can be used but it is not always available as a method, it is expensive and the biochemical instruments require special storage conditions (Wikblad et al., 1998). A kit to measure HbA1c is also available (Rector et al., 2001). In an environment of limited resources such kits could be donated by sponsors so that glycosylated haemoglobin test can be integrated in diabetes diagnosis and care. Approximate correlation between HbA1c values and eAG (estimated Average Glucose) measurements is given below:
HbA1c (%) GOOD PRACTICES FOR TREATING DIABETES MELLITUS IN A DEVELOPING COUNTRY 5 6 7 8 9 10 11 12
eAG (estimated Average Glucose) (mmol/L) 5.4 (4.26.7) 7.0 (5.58.5) 8.6 (6.810.3) 10.2 (8.112.1) 11.8 (9.413.9) 13.4 (10.715.7) 14.9 (12.017.5) 16.5 (13.319.3) (mg/dL) 97 (76120) 126 (100152) 154 (123185) 183 (147217) 212 (170249) 240 (193282) 269 (217314) 298 (240347)
The glucose tolerance test is a more complicated test especially for a poor resources environment, but it can assist to ascertain diagnosis. The patient doesnt eat anything for 814 hours. After the first blood sample the person receives per os glucose (75 gr for adults and 1.75 g / kg for children). Two hours later the plasma glucose is rechecked. Glu >126 mg/dl before glucose intake and 200mg/dl after glucose intake sets the diagnosis. Fasting glucose=110-126mg/dl and glucose level after 2h=140-199mg/dl represent a state of poor glucose tolerance. These glucose levels indicate that there is a high chance of development of diabetes in the future. Glucosuria testing with a urine stick might also be helpful to set the diagnosis. However, it is not the main test because of its low sensitivity and specificity. It can be preferred, however, if no alternative tests can be conducted (van der Sande et al., 1999). A combination of screening method that uses multiple tests would certainly reach higher sensitivity and specificity for the diagnosis of diabetes (WHO, 2003), but in an environment of limited resources this case stands little chance.
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TO SUM UP, THE CRITERIA FOR THE DIAGNOSIS OF DIABETES ARE:

q
Symptoms of diabetes with random plasma glucose level> 200 mg / dl. The random test means that the sample of blood is taken at any time of the day, regardless of the time of the latest meal. Fasting plasma glucose >126 mg / dl. That means that there is no caloric intake for at least eight hours. 2-hour plasma glucose after receiving 75 gr glucose >200 mg / dl.
CRITERIA FOR DIAGNOSING DISORDERS OF GLUCOSE HOMEOSTASIS ARE:
Impaired fasting glyceamia (IFG): fasting plasma glucose from venous blood sample = 110-125 mg / dl. Impaired glucose tolerance (IGT): 2-hour plasma glucose from venous blood sample = 140-199 mg / dl. If at a random monitoring test glucose> 100 mg / dl, we check fasting plasma glucose (FPG). If FPG > 125 mg / dl in two different measurements _ T2DM If FPG > 110 mg / dl _ Glucose tolerance test (OGTT-75gr) If FPG > 90 mg / dl _ Annual testing, take into account other cardiovascular risk factors Conducting OGTT 75gr and measuring plasma glucose after 2 hours If Glucose after 2 hour > 200 mg / dl in two different measurements _ T2DM If Glucose after 2 hour 140-199 mg / dl _ Impaired glucose tolerance If Glucose after 2 hour <140 mg / dl and FPG> 110 mg / dl _ Impaired fasting glycaemia
q q q
q q q
The following algorithm (page 36) shows how we can figure out whether the patient is diabetic or if he has IFG or IGT as early stages of diabetes:
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Random plasma glucose > 100 mg/dl person with risk factors (hypertension, hypercholesterolemia, obesity, a first grade relative with DM, history gestational diabetes or birth of a child weighting over 4 kg, age over 45 years) or presence of classic symptoms
Check fasting plasma glucose (FPG) twice
< 100 mg/dl? No DM
>125 mg/dl? DM
110-125 mg/dl. Perform OGGT 75 gr GOOD PRACTICES FOR TREATING DIABETES MELLITUS IN A DEVELOPING COUNTRY
Initial fasting plasma glucose. Give 75g of anhydrous glucose. Repeat plasma glucose in 2 hours. If FPG < 100 mg/dl and Glu after 2h < 140 mg/dl it is normal. Otherwise:
Glu 2 h < 140 mg/dl and FPG > 100 mg/dl? IFG (Impaired Fasting Glycaemia)
Glu 2 h = 140-199 mg/dl & FPG = 100 mg/dl-125 mg/dl IGT (Impaired Gluocose Tolerance)
Glu 2 h > 200 mg/dl and FPG > 125 ? DM
Annual fasting plasma glucose
Annual OGGT 75 gr
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If the number of diabetic patients grows rapidly there will not be any chance for multiple diagnostic testing and so we will use the following simplified algorithm:
Person with risk factors (hypertension, hypercholesterolemia, obesity, family history of diabetes, history of gestational diabetes and born of overweight child, age over 45 years) or presence of classic symptoms
Determine plasma glucose. Is it over 126 mg / dl?
Yes: Determine in two other measurements. Is it still above 126 mg/dl?
No: Is it above 110 mg/dl or are there any other risk factors present?
Possible diagnosis of DM
Yes: Check regularly, give lifestyle advices
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chapter 4
Treatment of diabetes
4.1. The role of the patient
The patient develops a personal attitude towards his illness determined by social, psychological and financial factors (Hurwitz, 2006). The disease can cause problems both in the patients life and his familys since there are hindrances often related to lack of family and peer support, prejudice, impoverishment, depression, ageing, impaired vision and last but not least lack of motive and distortion of the right information. Diabetes is a chronic disease which demands constant patient adherence to treatment, vital for the patients understanding and motivation. The patient must be taught in a simple language adapted to meet his needs. He/she must also learn how to change his eating habits, include physical activity in his daily routine, examine his feet and receive medication following instructions. It is important that patient records be kept. The patient must check his blood sugar or or high levels of hyperglycemia during pregnancy, stressful periods, or other illness, a multiple administration of injections is recommended. Glucometers and sugar tapes must be recommended according to availability. It can also be possible to check ketones in the urine when glucose is inadequate to cover body energy needs. Thus, alternative sources are recruited from lipids and proteins. Ketones check is essential in cases where blood sugar cannot be regulated, insulin injections have been neglected or when the patient is under stress. Clinical and lab examination is also highly recommended where possible. Eye and
TREATMENT OF DIABETES
his urine on indicated times of a day before meals or 2 hours later. In cases of irregulation
35
neurological examination, cardio screening, urea and creatinine must be checked annually, so as to diagnose levels of kidney failure and/or harm on feet. The patient must understand that he must reach set targets such as BMI <25 kg/m2, plasma glucose (Glu) <110 mg / dl, HbA1C <7%, blood pressure (BP) <130-140/80 mmHg, and normal cholesterol levels (LDL <100-130 mg / dl, HDL> 40 mg / dl for men and> 50 mg / dl for women and total cholesterol <230 mg / dl) and triglycerides (<150 mg / dl). Lipid examination is desirable but not affordable in a poor resource setting environment in most cases. It is important to understand that the patient should visit a doctor at scheduled meetings and is not to neglect the state of his health. At each visit, the doctor will check the weight, the blood pressure, the glucose level, the veins of the feet and their pulse, as well as urine for ketones.
4.2. DM and Travel

People with diabetes need special preparation and planning when travelling. In Africa, many factors such as the transportation means or the infrastructure make journeys quite difficult for the diabetic traveller especially when long distances have to be covered so as to meet with his therapist or family and for business related reasons . Travelling patients must follow specific instructions for additional food, water, sweets, while sugar must be available especially for the ones who are under insulin treatment and they have to carry their medication. It is recommended that they be accompanied by a person with basic knowledge of the disease. Proper foot wear -customised if possible- must be worn to prevent the walking traveller from injuries. The sedentary traveller must move periodically. In the Western world distinctive bracelets stating the disease are worn to indicate the condition to responding health workers in case of coma. During the journey insulin must be kept in cool temperatures away from direct sunlight. If ice is used, it must be well wrapped in cloth and plastic bags so that insulin is not in direct contact with it. It is also wise to keep insulin wrapped in plastic bags. When the patient reaches his destination he must either keep his insulin in a refrigerator or in the coolest part of the room.
4.3. Diabetic Ketoacidosis, Hyperosmolar Coma

Diabetic ketoacidosis (DKA) and non-ketonic hyperglycemic hyperosmolar coma are the most serious acute metabolic complications of diabetes mellitus. Diabetic ketoacidosis occurs more frequently in patients with T1DM, but it can also occur in patients with T2DM. Hyperglycemic
36
hyperosmolar coma occurs mainly in patients with T2DM aged over 50 years. In both complications frequent trigger factors can be illness (eg, infections, cardiovascular disease, etc.), omission of insulin injection, new-onset diabetes etc. DKA most frequently occurs in those who have already had diabetes but also in those diagnosed for the first time. A particular underlying problem usually leads to the DKA episode. Concurrent conditions such as inadequate insulin administration, myocardial infarction, stroke, pregnancy or the use of drugs may be some of the underlying problems. Recurrent episodes of DKA in young patients may be due to eating disorders or insufficient use of insulin. Young patients are particularly concerned about weight gain, thus prone to reduce insulin dosing. The presence of large amounts of ketones in blood and urine as well as marked metabolic acidosis distinguish diabetic ketoacidosis from other diabetic emergencies. A more common state in T2DM is the Hyperosmolar Hyperglycemic State (HHS or HONK) which features increased plasma osmolarity (above 320 mOsm/kg) due to profound dehydration and concentration of the blood. The phenomenon of mild acidosis and ketonemia which can also occur in this state is not so extensive as in DKA. In spite of the fact that osmolarity may also be increased in DKA there is a degree of overlap between DKA and HHS which makes it possible for the case to be classified into either DKA or HHS. Ketoacidosis does not always result from diabetes since alcohol excess and starvation- in which case glucose level is normal or low- can also lead to the condition. In diabetic patients, other reasons such as poisoning with ethylene glycol or paraldehyde can lead to metabolic acidosis. A rare side affect of lactic acidosis must be mentioned for T2 diabetics who take metformin. The annual incidence of diabetic ketoacidosis is 4.6 to 8 cases per 1000 diabetic patients, while the annual incidence of hyperglycemic hyperosmolar non-ketonic coma is less than 1 case per 1000 diabetic patients. The mortality of patients with diabetic ketoacidosis is less than 5%, while the mortality of patients with hyperglycemia hyperosmolar non-ketonic coma remains high (15%) (Sotiropoulos, 2008). The main disorders in both metabolic complications are lack of insulin and increased levels of contra-acting hormones (glucagon, catecholamines, cortisol, growth hormone). Diabetic ketoacidosis is characterized by hyperglycemia (> 300 mg / dL), reduced levels of bicarbonates (<15 mEq / L) and acidosis (pH <7,30) as well as ketonaimia and ketonouria. The non-ketonic hyperglycemic hyperosmolar coma is characterized by significant hyperglycemia (>600 mg / dL), high plasma osmolarity >320 mOsm/kgH2O, severe dehydration (9L) as a result of osmotic diuresis, bicarbonate >15 mEq / L, absence or middle ketonaimia and disorders of consciousness. The treatment of both disorders is based on fluid replacement, insulin restorage, the correction of metabolic acidosis (in diabetic ketoacidosis) and electrolyte disturbances. It is based also on the treatment of trigerring factors and the related complications such as hypoglycemia, low potassium restorage, cerebral edema, acute pulmonary edema, adult
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respiratory distress syndrome or vascular thrombosis. Through proper education of the patient, and effective communication with the therapist - especially during the acute phase of the disease- many cases of diabetic ketoacidosis and hyperglycemic hyperosmolar nonketonic coma can be prevented. The aim is, however, that all patients learn how to prevent diabetic ketoacidosis. An infection may disturb glucose metabolism and result in a hyperglycemic crisis. Bad psychological disposition or even an injury can have the same outcome. Other hormones such as glucagon, growth hormone, epinephrine and cortisone are released. All these hormones acting in combination result to insulin tolerance leading to hepatic glucose production and reduced use of circulating blood glucose (Fasanmade et al., 2008). Under these circumstances ketonaimia and ketonouria are likely to occur. Gradually diabetic ketoacidosis, related to significant mortality without appropriate treatment (Mbugua et al., 2005) may appear. Attacks of DKA can be prevented in known diabetics to an extent by adherence to sick day rules. These are clear-cut instructions to patients how to treat themselves when unwell. The patient must never firstly omit insulin doses and secondly be dehydrated. Also, any possible disease should be treated promptly and more intensive laboratory testing should be performed Availability of such testing or the need for patients to bear the related costs could have a negative impact on mortality in poor resources settings. If lab support is limited or even inexistent, the use of validated clinical algorithms based on research data, could raise the effectiveness of treatment. Additional insulin may be given and, if necessary, admission to hospital is required before the diabetic coma takes place (Otieno et al., 2005). Long distances and associated travel costs could present a major obstacle in poor communities. Innovative approaches have to be developed (eg funds for bearing travel costs for patients or community involvement along with project funding for referral system costs). The hydration is important and fluids should be given that contain sodium and potassium to replace electrolytes. Fluids can also contain sugar to ensure the intake of carbohydrates. Losing weight can be a warning sign of dehydration for someone who is going to develop diabetic ketoacidosis. In such case, the control should be regular and glucose must be checked every four hours as well as ketones in the urine. The patient must rest and supplementary insulin should be provided. Furthermore, a 10-20% of normal dose can be given so that the level of glucose remains below 240 mg / dl as shown in the following table (page 43). Signs which are alarming and raise the suspicion for admission to hospital may be signs of dehydration such as dry mouth and dry lips, sunken eyes and weight loss, multiple episodes of vomiting, abdominal pain, hyperventilation, nausea and drowsiness. Deep breathing (emitting acetone smell) known as Kussmaul breathing and altered states of consciousness make good signs for hospital admission. Also reason for admission may be a blood glucose value> 240 mg / dl and ketonouria for over 12 hours.
Level of glucose in mg/dl Below 80 mg/dl
Ketones detectable in urine, not just a trace Yes or No
Quantity of supplementary insulin
skip the usual insulin and reduce insulin analogues by 20%. Check after 3-4 hours No supplementary insulin. Check after 3-4 hours 10% of addition supplementary dose of insulin, check after 3-4 hours, repeat dose if no improvement 20% of addition supplementary dose of insulin, check after 3-4 hours, repeat dose if no improvement 20% of addition supplementary dose of insulin, check after 3-4 hours, repeat dose if no improvement
80-240 mg/dl 240-400 mg/dl
Yes or No No
240-400 mg/dl
Yes
>400 mg/dl
Yes or No
Therapeutic algorithms in the hospital now for any kind of coma as follows:
Treatment algorithm for hyperosmolar coma (Stoner, 2005)
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Treatment algorithm of diabetic ketoacidosis (Kitabchi and Wall, 1999)
4.4 Hypoclycemia
Hypoglycemia is the lack of glucose in the blood occurring when insulin levels are high therefore allowing glucose to rapidly enter the blood cells. Respectively, when glucose levels fall to extremely low levels, loss of consciousness or even permanent brain damage may be established leading to hypoglycaemic coma. Hypoglycemia may also occur as a complication of treatment with either insulin or oral medication of diabetes mellitus. Although hypoglycemia is not common in non-diabetic persons it can occur at any age and be related to many causes. Common causes are excessive insulin produced in the body, inborn errors, medications and poisons, alcohol, hormone deficiencies, prolonged starvation, alterations of metabolism associated with infection, and organ failure. Children may also experience it since they are engaged in more physical activity and they tend to neglect the dietary requirements of their disease.
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Throughout a 24 hour period blood plasma glucose levels are generally maintained between 4-8 mmol/L (72 and 144 mg/dL). Although 3.3 or 3.9 mmol/L (60 or 70 mg/dL) is commonly cited as the lower limit of normal glucose, symptoms of hypoglycemia usually do not occur until 2.8 to 3.0 mmol/L. Hypoglycemic coma can be installed quickly and is characterized by normal or rapid breathing, pale and sticky skin, profuse sweating, dizziness and headache, rapid pulse, impaired level of consciousness that can take any form of aggression, lethargy, changed behaviour and hunger. In more severe cases there are seizures, fainting, coma, or weakness in one side of the body. The manifestations of hypoglycaemia are listed below:
ADRENERGIC MANIFESTATIONS
Palpitations, tachycardia Shakiness, anxiety, nervousness, Sweating, feeling of warmth (although sweat glands have muscarinic receptors, thus
adrenergic manifestations is not entirely accurate) Dilated pupils (mydriasis) Pallor, coldness, clamminess Feeling of numbness pins and needles (parasthaesia)
GLUCAGON MANIFESTATIONS
Headache Hunger, borborygmus Nausea, vomiting, abdominal discomfort

NEUROGLYCOPENIC MANIFESTATIONS
Abnormal mental status, impaired judgment Personality change, emotional change Paresthesias, headache Irritability, belligerence, combativeness, rage Nonspecific dysphoric feeling, anxiety, moodiness, depression, crying Ataxia, incoordination, sometimes mistaken for drunkenness Fatigue, weakness, apathy, lethargy, daydreaming, sleep Amnesia, confusion, delirium, dizziness Staring, glassy look, blurred vision, double vision Difficulty speaking, slurred speech Automatic behavior, also known as automatism Stupor, coma, abnormal breathing Focal or general motor deficit, paralysis, hemiparesis Generalized or focal seizures
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Newborns can experience hypoglycemia demonstrating several symptoms such as: irritability, jitters, myoclonic jerks, cyanosis, respiratory distress, apneic episodes, sweating, hypothermia, somnolence, hypotonia, refusal to feed, and seizures or spells. Hypoglycemia can resemble asphyxia, hypocalcemia, sepsis, or heart failure. In spite of neuroglycopenic impairment there is reduction of noticeable symptoms in both young and old patients when the brain habituates to low glucose levels. This phenomenon is termed hypoglycemia unawareness and it proves to be a significant clinical problem when improved glycemic control is attempted especially in insulin-dependent diabetic patients. In each case where the patient does not feel well and enters a hypoglycemic coma, he should be given sugar by mouth, or a sugary juice. Alternatively the patient can take honey. Overtreatment should very carefully be avoided as far as this is possible because the blood glucose can usually be raised to normal within minutes with 15-20 grams of carbohydrate. This can be taken as food or drink and it is contained in approximately 100-120 ml of orange, grape or apple juice, or in one slice of bread and in about one serving of most starchy foods. If hypoglycemic coma is established and the patient is unconscious with impaired ability to swallow, he should be given intravenous dextrose serum (in particular, a serum 50% dextrose 50 ml intravenously). (Infants are given 2cc/kg Dextrose 10%, Children Dextrose 25%, and Adults Dextrose 50%). If no response there must be given a second dose. If the patient feels better and becomes conscious and the glucose is above 70 mg/dl, he should be rechecked regularly. We continue to provide dextrose serum 10% with a rate of one litre at 6 hours. If a vein route for intravenous serum proves difficult to find or no skilled personnel is available then a glucagon injection in the form of prepared syringe can be used. Glucagon is a hormone that rapidly counters the metabolic effects of insulin in the liver, causing release of glucose and glycogenolysis into the blood. It can raise the glucose by 30-100 mg/dl within minutes in any form of hypoglycemia caused by insulin excess (including all types of diabetic hypoglycemia). It requires no fridge storing and is readily available in the event of hypoglycemia (Vermeulen et al., 2003). 1gr is given intramuscularly which takes 10-15 minutes to reach maximum levels in blood. Common side-effects include headache and nausea. It is recommended that patients with a recent hypoglycaemia episode or patients with previous admission in hospital -for the same reasons- are provided with a prefilled syringe of glucagon. Both patients and relatives must be trained how to use the kit for preventive reasons. If the patient shows no signs of improvement after 30 minutes when all the steps have been made then we should search for other potential causes of coma. Typically, the treatment algorithm of hypoglycemia is as follows:
Recognize HYPOGLYCEMIA SYMPTOMS (Adrenergic = Shakiness, anxiety, nervousness, tremor, palpitations, tachycardia, sweating, feeling of warmth, pallor, coldness, clamminess, dilated pupils, Hunger, Neuroglycopenic = abnormal mentation, impaired judgment, moodiness, depression, irritability, personality change, labile emotions, fatigue, weakness, lethargy, slurred speech, confusion, staring, blurred or double vision.)
Assess if MILD/MODERATE (Blood Glucose 41-70 mg/dl) or SEVERE HYPOGLYCEMIA (Blood Glucose 41-70mg/dl with mental status changes, OR, Blood Glucose 40mg)
Treat for hypoglycemia
Moderate Hypoglycemia: Give a fruit juice or honey or gel/tab of glucose per os
Severe Hypoglycemia: If the patient can swallow, we can provide treatment per os, as in the treatment of moderate hypoglycaemia. Is it possible for intravenous fluids (Is the patient inside hospital)?
Redefine the blood glucose after 15-20 min. If Glu<70 mg/dl give extra juice or honey until Glu> 70 mg/dl.
YES: Give a single serum 50% dextrose 50 ml. Check in 15-20 minutes and if the Glu level has not risen give a second dose of serum dextrose 10% at a rate of one liter at 6 hours.
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Repeat after 45 minutes. If still Glu <70 mg/dl extra medical attention is necessary. Otherwise be sure that the patient will receive a satisfying quantity of regular meals for the rest of the day.
NO: Give glucagon injection 1gr. intramuscularly. Check Glu level in 15-20 minutes. If the patient remains unconscious attempt to secure intravenous route and contact a health professional.
4.5. Antihypertensive Therapy

High blood pressure or hypertension may develop in patients suffering from D.M. for several years and so hypertension may coexist with D.M. (Mugusi et al., 1995). The combination of D.M. treatment and that of hypertension can prove quite effective. The objectives of therapeutical levels of BP in people with diabetes are:
Adults: <130 / 80 mmHg Adolescents: <90th percentile for age Systolic blood pressure<160 mmHg. If the objective is achieved, and BP is well regulated then a further reduction in the levels of 140 mmHg should be pursued. Typically, the effectiveness of antihypertensive drugs used in a diabetic patient is as follows (Konzem et al., 2002): Angiotensin converting enzyme A inhibitors (ACE inhibitors): Beneficial effects have been displayed in patients diagnosed with either myocardial ischemia, congestive heart failure or diabetic nephropathy. These drugs have been proven first line therapy for patients with hypertension and diabetes (Gandhi and Isley, 2007). Deterioration of renal function is slowed down (Papadakis, 2001). Patients with D.M. and hypertension tend to increase insulin sensitivity while reducing cardiovascular events as well as the risk of stroke and coronary heart disease. Diuretics: The thiazide diuretics have been shown to benefit patients with diabetes and high blood pressure. They reduce cerebrovascular and cardiovascular events in non-insulindependent diabetic patients who also have high blood pressure. They can be used in combination with ACE inhibitors. Preferably hydrochlorothiazide is used at a dose of 12,5 mg daily to 25 mg daily. Thiazide diuretics are not very effective in patients with renal insufficiency. In these patients loop diuretics are preferred. Calcium channel blockers (CCBS): They represent alternative options in the treatment of hypertension in patients with diabetes, especially the dihydropyridines (eg amlodipine, nifedipine). The calcium channel blockers alone or in combination with another antihypertensive agent were associated with reduced cardiovascular risk mainly due to reduction of high blood pressure. In many patients it is required to add one ACE inhibitor or another antihypertensive agent so as to achieve the desired levels of blood pressure. The combination of an ACE inhibitor and one dihydropyridines calcium channel blocker has shown to reduce proteinuria. Angiotensin II receptors blockers: They are highly recommended especially after side effects are present of the ACE inhibitors. Treatment with losartan has positive effects not only
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on the kidneys but also on reducing blood pressure in diabetic patients with nephropathy. Similarly irbesartan reduces microalbuminuria levels even more than amlodipine. Beta-adrenergic blockers: Traditionally, the use of beta blockers in patients with diabetes has been constrained due to adverse metabolic effects and the masking of the hypoglycaemic symptoms. Atenolol is correlated with greater weight gain compared with captopril but when compared in relation to hypoglycemic episodes, there is no difference. Yet, there is no corresponding reduction in risk of cardiovascular complications. Alternatively, Carvedilol (bblocker and peripheral a-blocking activity) causes fewer changes in lipid and glucose levels compared to traditional beta-blocked but can cause dizziness and hypotension (due to its a-blocking action). Thus, dosage increases should be achieved at a slower rate.. Beta-blockers seem to have a positive effect on atherosclerosis (heart disease). Alpha-adrenergic blockers: They are not considered first line drugs for the treatment of hypertension in patients with diabetes. These drugs can be combined with other antihypertensives for the treatment of poorly controlled hypertension but special should be given to avoid hypotension. Combination therapy: Most patients with coexisting hypertension and diabetes require more than one antihypertensive tablets to achieve adequate control of blood pressure. The combination of ACE inhibitors and CCBs is associated with reduction of cardiovascular events and reduction of proteinuria. Extra caution should be given when CCBs which do not belong to the dihydropyridines are combined with -adrenergic blockers, due to possible negative inotropic action on myocardium. The combination of beta-blocker and ACE has also been associated with additional effects on blood pressure when administered to patients with heart rate below 83 beats per minute. The combination therapy may have proved more effective but there is a risk of mistakes involved on behalf of the patient who might fail to maintain the appropriate combined treatment (Etuk et al., 2008). Treatment algorithm of hypertension in diabetic patients:
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ACE inhibitor /thiazide diuretic. If serum creatinine level is >1,8 mg per dL (159 mol per L), use long acting loop diuretic
BP still not at goal levels (130/80 mmHg): Add long acting CCB, titrate or moderate dosage, if BP goal is achieved, convert to fixed dose combination using an ACE inhibitor and a CCB or an ACE inhibitor and a diuretic
BP still not at goal levels (130/80 mmHg)
Baseline pulse rate >84 beats per minute. Add betaadrenergic blocking agents or alpha- and betaadrenergic blocking agents
Baseline pulse rate <84 beats per minute. Add another subgroup of CCB (i.e. amplodipine-like agent if verapamil or diltiazem is already being used, or the converse)
BP still not at goal levels (130/80 mmHg)
Add night long acting alpha- adrenergic blocking agent, titrate dosages to moderate dosages, or refer patient to a hypertension experienced specialist
Many times the cost of drugs will determine our final choice (Salako, 1993). Generally, in the private sector the value of drugs is higher. Hydrochlorothiazide is relatively inexpensive and can be used more often (Twagirumukiza et al., 2010). Apart from the widespread use of diuretics ACE-inhibitors are also of wide use (Olanrewaju et al., 2010). In any case it should be recommended to the patients to avoid consumption of salt and salty foods in general.
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4.6 Antidiabetic agents

In T2DM there are several alternatives in relation to the release and efficacy of insulin in the tissue region. Treatment with antidiabetic tablets along with exercise and nutrition is likely to achieve a good control of glucose metabolism and of complications of the disease. Medication can rely on a single drug or on a combination of several drugs. When monotherapy does not achieve therapeutic goal a second drug must be used, that belongs to another category. The choice must be made according to some characteristics, such as lifestyle of the patient, the level of glycemic control, access to medicines, and financial costs. Monotherapy is usually the first choice, but as the disease develops we may add supplementary medications. Sulphonylureas and metformin are used more. If the person is overweight (BMI> 25 kg/m2) metformin from the category of biguanides is the first choice. Alternatively we can use theiazolidinediones. Specifically, sulphonylureas are drugs that stimulate insulin secretion through the stimulation of beta cells in the pancreas. If the number of beta cells is significantly reduced then the action of insulin is also reduced respectively. Sulphonylureas are chosen for T2DM when diet alone is not enough. As for side effects, sulphonylureas can lead to low blood sugar and hypoglycemia in cases of insufficient food intake. There are also signs of increased appetite and weight gain. Long-acting sulphonylureas should be avoided in elderly patients because of the risk of hypoglycemia. Short-acting sulphonylureas, or glitazones may be used instead. They must be avoided in T1DM, cases during pregnancy and in liver or kidney disorders. Metformin is preferred in overweight people and it can be combined with a sulphonylurea. It should be prescribed with caution in the elderly people over 75 years of age. It is also contraindicated in patients with impaired renal function and high levels of plasma creatinine. It is also contraindicated in the case of liver and severe heart or lung diseases as well as in pregnancy. Metformin is considered as the only widely used oral drug that does not cause weight gain amongst the commonly used oral diabetic drugs. Theiazolidinediones (pioglikazone, rosiglitazone) are a new class of drugs that act similarly by reducing insulin resistance and increasing insulin action on glucose and lipid metabolism. They also reduce the hepatic glycogenesis and they increase glycogen synthesis in muscle tissue as well as lipogenesis. However, they are associated with weight gain and have are contraindicated in pregnancy, and hepatic or cardiac dysfunction. Meglitinides are related to insulin secretion (repaglinide and nateglinide). These are called short-acting secretagogues and their major role is to help the pancreas to produce insulin. These drugs should only be taken before a meal and they help to control postprandial hyperglycemia. Repaglinide is preferred in cases of renal failure, but it can cause hypoglycemia. The increased cost versus metformin and sulphonylurea is prohibitive for use in communities or health systems where financial resources are limited. Finally, inhibitors of alpha-glucosidase are another category of drugs that inhibit the
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absorption of glucose. Alpha-glucosidase inhibitors are diabetes pills which are not technically hypoglycemic agents since they lack in a direct effect on insulin secretion or sensitivity. These agents act by slowing down the digestion of starch in the small intestine in a way that glucose from the starch enters the bloodstream more slowly so a much more effective result is achieved even though impaired insulin response or sensitivity is present. Acarbose which belongs to this class, inhibits the breakdown of polysaccharides to oligosaccharides and thus reduces the postprandial increase of blood sugar. Alternatively, the newer drugs used to treat T2DM is the GLP-1 analogue (Glucagon-like peptide-1) or similar to the glucagon peptide-1 (liragloutide). GLP-1 analogues are administered with a daily injection and reduce the weight of patients. They can slow down the pace of disease progression and they can be combined with antidiabetic tablets and insulin, while they do not cause hypoglycaemia. Increased cost makes them unavailable in most settings. The following table shows the characteristics of some antidiabetic agents with their brand names in Tanzania, as determined by Tanzania Food and Drug Authority (TFDA):
Name of drug
Starting dose
Max. dose
Major side effects
Contraindications
SULPHONYLUREAS Glibenclamide (GlibenclamideNovartis) Gliclazide (Diabetron GlaxoSmithKline Egypt) Glipizide (Glynase USV Limited Korea) Glimepiride (Amaryl- Aventis) Chlorpropamide (Diabinese Pfizer NV Belgium) Tolazomide (not available in Tanzania) Acetoexamide (not available in Tanzania) Tolbutamide 2,5 mg 20 mg Hypoglycemia, weight gain, skin rashes Pregnancy, use with caution in liver and renal disease
40 mg
320 mg
5 mg
40 mg
1 mg
8 mg
100 mg
500mg
500 mg
2500 mg
250 mg 500 mg
1500 mg 2500 mg
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Name of drug
Starting dose
Max. dose
Major side effects
Contraindications
BIGUANIDES Metformin (Rolab MetforminNovartis), (Metformin Alpharma Limited UK) 500 mg 2250 mg Abdominal pain, nausea, loose bowel motions, lactic acidosis Renal, heart and liver failure pregnancy
THIAZOLIDINE DIONES Rosiglitazone (not available in Tanzania) 4 mg 8 mg Liver impairment, fluid retention, weight gain, dilutional anaemia Renal, heart and liver failure, pregnancy
Pioglitazone (Diavista- Dr. Reddys Laboratories Limited, India)
15 mg
45 mg
MEGLITINIDES Nateglinide (not available in Tanzania) Repaglinide (Novonorm-Novo Nordisk, Denmark) 180 mg 360 mg Hypoglycaemia, weight gain, dyspepsia Heart and liver failure, pregnancy
0,5 mg
16 mg
ALPHA-GLUCOSIDASE INHIBITORS Acarbose (GlucobayBayer, Germany) Meglitole (not available in Tanzania 25 mg 300 mg Dyspepsia, loose bowel motions None
25 mg
300 mg
Out of all those drugs, metformin and sulphonylureas are appropriate for use in poor resource settings due to cost issues. Generally, the algorithm for treatment of diabetes has to be based on the availability of drugs, their cost and cost-benefit criteria. Metformin and sulfonylurea are relatively cheap drugs and can be integrated into the treatment algorithm of a DM clinic in rural African communities. Attention has to be paid to avoid any drug which is substandard or counterfeit (Chauve, 2008).
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Patients will receive treatment in relation to some constraints such as: 1. Initially and based on glucose levels, patients will be advised to make lifestyle changes, start exercising, and avoid smoking and alcohol consumption. Although alcohol use is widely popular in most poverty hit communities, obedity, lack of exercise and smoking are less common in such communities. However, urbanization is rapidly changing daily habits at a fast rate among many deprived communities. 2. If after this period euglucemia levels are not achieved, regular check-ups to ensure that the patient has succeeded in maintaining good glucose metabolism are needed. If glycemic goal is not achieved, sulphonylureas treatment has to start for patients with normal weight and metformin is given for obese patients, as monotherapy. We start with a low dose and we can increase dosages after the first month of treatment. Metformin is given as tablets of 500 mg every day and we can double the dose. If necessary, it can be given at a dose of 850 mg twice daily or even three times daily. Sulphonylureas are adequate for non-obese patients and chlopropramide and tolbutamide are the most common ones which are given per os once daily with breakfast. If it is necessary we can increase the dosing to two tablets daily. The above mentioned sulphonylureas are more easily to be found in Tanzania (Justin-Temu et al., 2009). 3. If after three months we achieve metabolic goal we check the patient regularly to make sure that he maintains this. Otherwise we add another hypoglycaemic agent, first at a low dose and we can increase it after 3 months (combined oral therapy). 4. If after three months we havent reached euglycemia levels, we add intermediate-acting insulin. ( Liraglutide could be used istead but cost is prohibitive). 5. If after three months euglycemia is not achieved, we choose a combination of multiple insulin injections.
In general, treatment phases of diabetes are as follows (International Diabetes Federation (IDF):
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Medication nonadherence highly prevails among patients with chronic conditions. Diabetic patients, for instance, have to face at least two comorbidities and they often require multiple medications. Therefore, one of the reasons for nonadherence is the cost of medication. Medication nonadherence is associated with public health issues and higher health care costs. This makes it important for health care professionals to detect cost related nonadherence since it can lead to strategies to assist patients especially in poor resource environments.. Strategies to reduce non adherence are pill-splitting, and the use of generic drugs. Free access to treatment is the strategy to achieve the greatest impact on the health of the population
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MEDICATION NONADHERENCE:
Therefore reductions in diabetes morbidity and mortality along with significant cost savings to the health care system, can be reached through appropriate and relevant interventions so that nonadherence can improve.
4.7. Insulin Therapy

Insulin is the main treatment for patients with T1DM and for many patients with T2DM. In T1DM there is a lack of beta cells of the pancreas which produce insulin for survival. About Insulin: A healthy normal weight person produces between 18-40 units of insulin every day. Half of it is produced between meals or at night (basal insulin) and the other half is excreted during meals (bolus insulin). This occurs in two phases:
a. During the first phase the secretion of insulin is rapid and it lasts 15-20 minutes. In 2DM this phase is absent or incomplete. b. During the second phase, insulin secretion lasts longer while glucose is released into the bloodstream, for instance during a meal. In T2DM this phase is delayed or incomplete, leading to hyperglycemia.
General information about insulin

Insulin is mostly available in injectable form. This makes it one of the few medicines that cannot be taken in the form of a pill at the present time. Insulin, like many other proteins introduced into the gastrointestinal tract, is reduced to fragments (even single amino acid components) whereupon all insulin activity is lost. Although there has been some research into ways to protect insulin from the digestive tract (so that it can be administered in a pill) this remains entirely at an experimental stage so far. Insulin is either of animal origin or biosynthetic insulin by genetic engineering. The most recently introduced forms of insulin are insulin analogues. Usual forms available are of 40 IU / ml and 100 IU / ml vials. There are three types of insulin: Regular fast acting insulin Insulin isophane (medium acting) Premixed insulin (30% regular /70% isophane) Abnsulin analogues: insulin molecules are attracted to each other and exist as bilateral or six-parts in the solution. For insulin to be absorbed, six parts must break down to monomers. This process can take up to 30 minutes. Insulin analogues are not present in the body, but are produced by a molecular change in
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an amino acid. This change makes them act differently according to the initiation and duration of action of insulin. Insulin analogues help overcome the obstacles of soluble (regular) insulin. Soluble insulin slows the degradation of six parts to two and one part delays the onset of action when injected subcutaneously. Thus, soluble insulin must be injected up to about 30 minutes before lunch, allowing the monomers of insulin to rise in the circulation before glucose levels rise. This time limitation makes it sometimes difficult for the patients to keep the 30 minutes time gap between injection and lunch. They cannot eat before 30 minutes pass. As a result, maximum postprandial insulin level is delayed, as insulin concentrations have risen slowly after subcutaneous injection. This may also introduce higher risk of hypoglycemia, as long as insulin levels may increase before the rise of glucose, or remain at high levels after the postprandial hyperglycemia has passed. In this way there is no simulation of the endogenous insulin secretion. On the other hand, insulin analogues act quickly and do not require this time gap of 30 minutes between time of injection and lunch. They mimic endogenous insulin secretion, allowing a better control of postprandial and 24hour glucose levels. They also increase the risk for hypoglycemia. For all these reasons they allow more flexibility in patients lifestyle but their cost is a lot higher. Analogues are mostly used as: Short acting (bolus), Long-acting (basal 17-24 hrs of action) The premixed analogue. Insulin analogues are more expensive and rather difficult to use in a poor resource settings environment. Regular short acting is human soluble insulin. When it enters the body, it works in the same way as natural insulin and increases overall ability for the body to uptake glucose. Soluble insulin is fast-acting (usually between 30 minutes and an hour) and lasts for approximately eight hours depending on dose. Soluble insulin is usually used before a meal, and controls postprandial blood glucose levels. Regular insulin can sometimes be combined with other types of insulin (longer-lasting) to provide overall control through the day. With all insulin types it is worth bearing in mind that the stricter control exercised over diabetes, the less likely it is to develop into serious complications. Intermediate-acting insulin helps to control blood glucose throughout the day. Premixed Insulin in mixtures of 10/90, 20/80, 30/70, 40/60 and 50/50 mixtures of short acting regular and intermediate acting preloaded pens and also in penfill cartridges and vials. All of these medicines are based around human biphasic isophane insulin. Mixtard is based around soluble insulin and isophane insulin. Pre-mixed insulin such as this acts both rapidly (soluble) and at an intermediate level. The following table shows the main characteristics of the most commonly used insulins:
Insulin pens
An insulin pen is used to inject insulin for the treatment of diabetes. It is composed of an insulin cartridge (integrated or bought separately) and a dial to measure the dose, and is used with disposable Pen needles to deliver the dose. Insulin pens are currently available on the market as insulin delivery system apart from conventional syringes. When the patient learns how to handle the pens properly there is no other financial cost compared with that of vials and syringes (Baser et al., 2010). They can be particularly useful to patients with blurred vision.
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The fact that pens can be used by the trained patient in an easy way and the fact that they can be kept out of the refrigerator (even after opening) are among the main advantages. The use of insulin pens can increase the cost of treatment for many patients in an environment of limited resources and it is difficult to implement it in a diabetes clinic of a developing country. The vial-syringe system is cheaper and can have wider application in such a program.
Needles-Syringes
The needles used with pens are described by two numbers. The first referred in mm refers to the length of the needle. The second expressed in G refers to the thickness of the needle (the higher the number, the thinner the needle). Eg. 6mm (31G) and 80mm (30G). These needles are used with pens. When the patient uses vials and syringes instead of pens and needles he/she can reuse syringes in order to reduce costs and avoid buying large supplies of syringes. This is very important in a poor resource settings environment. Some useful tips we the therapist should give to the patients when reusing syringes are:
Keep the needle clean by keeping it capped when you are not using it. Never let the needle touch anything but clean skin and the top of the insulin bottle. Never let anyone use a syringe you have already used, and do not use anyone elses
syringe. Cleaning it with alcohol removes the coating that helps the needle slide into the skin easily. An important part of good injection technique is to inject at the proper depth. Insulin should be injected in the subcutaneous fat the layer of fat just below the skin- is highly recommended by most professionals. If the injection goes too deep, the insulin could go into muscle, where it is absorbed faster but it might not last long enough and it is much more painful. The onset and duration of action of insulin is also affected when the injection is not deep enough and the insulin goes into the skin. Most people pinch up a fold of skin and insert the needle at a 90 angle to the skin fold. To pinch the skin properly, the patient should follow the steps below:
Squeeze a couple of inches of skin between the thumb and two fingers, pulling the
skin and fat away from the underlying muscle. (If a 5 millimeter mini-pen needle is used to inject, the patient doesnt have to pinch up the skin when injecting at a 90 angle, with this shorter needle, there is no to fear of injecting into muscle.) Insert the needle. Hold the pinch so the needle does not go into the muscle. Push the plunger (or button if a pen is used instead) to inject the insulin.
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Release the grip on the skin fold. Remove the needle from the skin.
Note that not everyone injects at a 90 angle. If the body has less fat, it might be necessary to inject at less than a 45 angle, to avoid injecting into a muscle.
Choosing the right insulin

There are several problems with insulin as a clinical treatment for diabetes:
Selecting the right dose and timing. Mode of administration. Selecting an appropriate insulin preparation (typically on speed of onset and duration
of action grounds).
Adjusting dosage and timing to fit exercise undertaken. Adjusting dosage and timing to fit food intake timing, amounts, and types. Adjusting dosage, type, and timing to fit other conditions, for instance the increased
stress of illness.
Variability in absorption into the bloodstream via subcutaneous delivery It is dangerous in case of mistake (most especially too much insulin). It is not highly recommended that patients inject whenever they eat carbohydrate or
show a high blood reading. The choice of the appropriate type of insulin depends on the patients lifestyle. If the person requires maximum flexibility in his daily activity, it is recommended that he inject insulin four times daily (basal and bolus). This allows the patient to match the insulin injections to his lifestyle. Alternatively, he can apply a figure of two insulin injections daily from premixed insulin. Some features that should be taken into account before choosing the appropriate types of insulin administration have to do with the patients eating habits. The quantity and quality of the meals as well as the dietary preferences of the patient must also be considered. Other important factors are the level of physical activity, age, or certain disabilities. Patients unwilling to undergo multiple injections or reluctant to cooperate should also attract our attention. The level of perception and adaptability as well as the level of health support in the region should also be considered before we start someone on insulin injections. The proper insulin regimen should imitate as much as possible the endogenous insulin secretion characterized by a basal secretion which suppresses the hepatic glucose production, and an increased secretion in response to meals. The most rapidly absorbed and fast acting analogues of insulin reduce the risk of postprandial hypoglycemia. The basic levels of insulin can be achieved with intermediate-acting insulin injection at bedtime with or without reduced morning doses. Long-acting insulin given once a day can produce the same result. A number of dosing regimens can be applied for each patient.
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Insulin dosage
A. In the multiple injection regimen we combine bolus and basal insulin. The starting dose for T1DM is 0,6 IU / kg of total body weight per day and for T2DM 0.2 IU / kg of total body weight per day. 60% of the total daily dose should be administered as a short dose insulin (bolus) (ins. Actrapid) before meals for example, 20% before breakfast, 20% before lunch and 20% before dinner. The remaining 40% should be used as an intermediate-acting insulin (basal) before bedtime (eg at 22:00 hours).
B. The double regimen is simpler and it uses premixed insulin (eg 30/70). The initial dose is for T1DM is 0,6 IU / kg of body weight per day, and for T2DM 0.2 IU / kg of body weight per day. The two thirds of the total dose should be given before breakfast and the remaining one third before the evening (Ministry of Health, 2009).
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C. For people with T2DM bolus insulin can be administered in combination with antidiabetic tablets. In cases of shortage of glycemic control, exclusive insulin analogues can be used instead. a. Additional treatment: Basal insulin in combination with antidiabetic tablets. The dose of antidiabetic drugs is increased gradually and basal insulin is added (long acting) at 10:00 a.m. at a dose equivalent to 0,2 IU / kg of body weight. b. Replacement therapy: If no glycemic control is successfully reached with antidiabetic tablets, a double insulin regimen is introduced . The total daily dose is 0.2 IU / kg of body weight and it is used 2/3 in the morning and the rest 1/3 in the evening. It consists of premixed insulin analogues. Attention must be paid when we increase or decrease the dose of insulin. We should not exceed more than 2-4 IU above or below the previous total dose. Moreover, we should do not change insulin regiments more than once per week. Only if there are ketones present, can we adjust doses more rapidly. There are also several factors that influence insulin absorption, as shown in the table below. Variability of insulin absorption is perhaps the greatest obstacle to replicating physiologic insulin secretion.
Factor Site of injection
Effects Abdominal injection (particularly if above the umbilicus) results in the quickest absorption, arm injection results in quicker absorption than thigh or hip injection Intramuscular injections are absorbed more rapidly than subcutaneous injections Exercising a muscle group before injecting insulin into that area increases the rate of insulin absorption. Local application of heat or massage after an insulin injection increases the rate of insulin absorption
Depth of injection
Exercise
Heat application or massage
In developed countries pumps for insulin secretion can be used. Their implementation requires good health system support which is unlikely to find in a poor settings environment.
Blood Glucose Meters

A glucose meter (or glucometer) is a medical device for determining the approximate concentration of glucose in the blood. It is a key element of home blood glucose monitoring
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by people with diabetes mellitus or hypoglycemia. A small drop of blood, obtained by pricking the skin with a lancet, is placed on a disposable test strip that the meter reads and uses to calculate the blood glucose level. The meter then displays the level in mg/dl or mmol/l. It would be desirable for patients injecting insulin to have a device for measuring blood sugar at home. Unfortunately, many of them cannot afford to buy one together with the strips. When resources are limited projects should prioritize patients more prone to benefit from a more tight control and able to do this as well as to families with diabetic children. (Cho et al., 2006). Patients or relatives to be given such a device should be taught how to use it properly.
4.8. Common practices in the treatment with insulin

Rebound hyperglycemia: A state of hypoglycemia, symptomatic or asymptomatic, which stimulates the secretion of insulin antagonistic hormones. In a normal person increased pancreatic insulin secretion will neutralize the action of these hormones. In a person with insulin deficiency these hormones can cause hyperglycemia, which is a phenomenon known as Somogyi. As a result elevated blood glucose levels can be observed during the morning wake-up. The Dawn phenomenon: Dawn effect is defined as an increase in the blood sugar in the morning and is typically invoked in the context of diabetes. It is different from chronic Somogyi rebound in that Dawn effect is not associated with nocturnal hypoglycemia. In a person without diabetes during sleep insulin levels are low, especially at 3 am. Insulin levels gradually increase by dawn in order to counteract the rising levels of cortisone and growth hormone. For insulin-dependent diabetic patients the insulin pattern should preferably be similar, ie low insulin dose at 3 am and high at 6am. The increase in insulin requirements is called the Dawn phenomenon, and thus we try to provide the evening dose of basal insulin as late as possible in the evening, for example at 22:00. The later the insulin injection is given, the later is the peaking time of insulin. As a result for a person who wakes up with morning hyperglycemia his levels of blood glucose should be checked during the night around 02.00-03.00 hrs in the morning. If glucose is low, the person experiences hypoglycemia followed by rebound hyperglycemic reaction. In this case, we need to reduce the evening dose of insulin and to add a snack at 22:00. If glucose is normal or high, the person may develop the Dawn phenomenon and in this case we must add insulin at 22:00 or choose a basal insulin with a more delayed peak.
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4.9. Lipohypertrophy
The injection sites which are mostly used are the abdomen, the thigh, and the buttock. The arm can also be used, although it is difficult to access. The rate of absorption is fastest on the abdomen and slowest on the unexercised thigh. The thigh should be avoided when exercise follows, as this will increase the rate of absorption of the insulin. One area should be used for an injection at a particular time of day, e.g. the abdomen is the site for the morning injection, and the thigh is the site for the evening injection. Lipohypertrophy is a medical term that refers to a lump under the skin caused by accumulation of extra fat at the site of many subcutaneous injections of insulin. It may be unsightly, mildly painful, and may change the timing or completeness of insulin action. It is a common, minor, chronic complication of diabetes mellitus. In the site of injection hypertrophy of adipose tissue can be observed. It is characterized by appearance of large, elevated, spongy masses of fatty fibrous tissue (lumps) at the injection
site. Easily accessible sites, such as the thighs, are most commonly affected. The injection in these areas is relatively painless, so the patient usually continues to inject insulin at the same site. The absorption of insulin is also reduced in these areas. The necrosis of the skin can occur if injections are done into the skin rather than subcutaneously. In any such a case we should advise the patient to change the site of injection.
4.10. Storage of insulin

Insulin should be stored in a refrigerator at 4-8 C. Human insulin is stable for 30 months from the date of manufacture in these temperatures and the insulin analogues for 24 months. Insulin should be stored in a separate section at the bottom of the refrigerator, away from the ice and not at the door where the temperatures are not stable. Insulin should never be freezed. On rare occasions which this happens and insulin has to be defrosted, the crystal structures will most probably be destroyed, so it is best to be discarded. We should always check the expiring date and examine the bottle closely to make sure the insulin looks normal before we draw the insulin into the syringe. Shortly used insulin does not need to be stored in the refrigerator. If there is no refrigerator or no electricity available, insulin may be stored in a cool place or in special containers, away from sunlight (Allen, 1982) (Gill et al., 2002). A cold injection would also hurt more. At 25 C insulin is stable for 6 weeks and at 37 C for 4 weeks. It should however be kept away from the sun. Analogues remain stable for four weeks at temperatures of 30 C and lower. We should shake the vial gentle before use and avoid the intense shaking that can damage the molecular structures.
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Insulin pens should be stored in the refrigerator before opening and after opening they can be left outside the refrigerator, but in temperatures below 30 C.
4.11. Diabetic Foot

Diabetic foot is an umbrella term for foot problems in patients with diabetes mellitus. Due to arterial abnormalities and diabetic neuropathy, as well as a tendency to delayed wound healing, infection or gangrene of the foot is relatively common. Ten to fifteen percent of diabetic patients develop foot ulcers at some point in their lives and foot related problems are responsible for up to 50% of diabetes related hospital admissions. Micro and macro ischemia as well as diabetic neuropathy are the two main risk factors that cause diabetic foot ulcer. Due to several metabolic and neurovascular factors, diabetic patients often suffer from diabetic neuropathy. Peripheral neuropathy a type of neuropathy- causes loss of pain or feeling in the toes, feet, legs and arms due to distal nerve damage and low blood flow. On numb areas of the feet and legs (such as metatarso-phalangeal joints and the heel region) pressure or injuries may go unnoticed, that may also happen with blisters and sores which eventually become portal of entry for bacteria and infection. Diabetes can reduce both the movement and the sensation in the foot. This can cause loss of sensitivity, touch and temperature. The diabetic foot in conditions of reduced care may have high mortality (GulamAbbas et al., 2002). The patients foot should be examined for any sores, redness, blisters, cellulite, injuries, necrotic tissue, discoloration, reduced peripheral pulse at the legs. The injuries to the foot of patients in developing countries need preventive treatment, otherwise it is difficult to deal with them (Unwin, 2008). We also need to protect feet from rodent bites and stings which can deteriorate the state of the foot (Abbas et al., 2005). Early detection of foot at risk and appropriate treatment reduced the risk of amputations in a program in Tanzania from 9% to 6,5% (WDF, 2008). The costs for the treatment of diabetic foot is proportionately high compared to the total cost of treating diabetes. (Karel Bakker, 2009) Patients are recommended not to walk barefoot (Jayasinghe et al., 2007). They should also wear socks that are not too tight and avoid contact with cold or hot objects. They must examine their toes regularly and they must dry the feet after washing them. Moreover, they must cut nails straight and pay attention to the skin, and if there are wounds they should be covered with gauze and elastic bandage. Multidisciplinary assessment by diabetes specialists and surgeon is requires for foot ulcers in diabetes. Foot ulcers are usually treated with appropriate bandages, antibiotics (against staphylococcus, streptococcus and anaerobe strains), debridement and arterial revascularisation. Flucloxacillin from 500 mg to 1000 mg, amoxicillin of 1g and metronidazole to tackle the putrid smelling bacteria are also used in treatments.
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Projects should aim to increase the level of knowledge about the risks of damage on the foot. Patients and health professionals should be taught all the good practices to reduce the risk of diabetic foot (Matwa et al., 2003). It should also provide appropriate care for patients who have already undergone amputation, as the reinfection rate is often high in patients from Africa (Viswanathan et al., 2010). Finally, in many populations of tropical regions there are observed hands injuries similar to those of the diabetic foot, due to microangiopathy. This complication is considerably rarer than the well-known diabetic foot, but may be more likely to meet in Africa (TDHS, 2002).
4.12. Diabetes and physical activity

Physical activity is an important factor in the treatment of diabetes type 1 and 2. The aim is that all patients learn the benefits of physical activity, and potential risks of intense physical exercise. We must also take into consideration all the physical problems that make it difficult for some patients to exercise, and in each case we must give special recommendations. It seems that the urban population exercises less than the rural population (Kuga et al., 2002). Exercise increases insulin sensitivity and peripheral glucose utilization and improves blood glucose control. In addition, it improves cardiovascular function, it reduces high blood pressure and lipids level that frequently coexist with diabetes, while reducing hepatic glucose release. Exercise also helps the patient to control body weight and gain a feeling of well being. Improvement of muscle strength, increase of bone density and energy level, release of tension and anxiety, while enhancing work capacity are only some of the benefits the patient enjoys after exercising. The risk of intense physical activity on the other hand, is that patients may develop hypoglycemia, mainly the patients on insulin. Also, strenuous physical exercise should be avoided because it can have a bad influence on cardiovascular system, particularly in elderly diabetics. The exercise which is usually recommended is aerobics, a relaxed pace, especially walking or light running, with adequate protection of the feet in order not to be injured. So as to control blood sugar, the patient should try to exercise at the same time for the same duration at least 3 times a week for approximately 30-45 minutes. As far as insulin injection is concerned, insulin must be reduced or avoided if the patient has an intense physical activity. An obstacle for people with diabetes can be the presence of another illness, physical disability, eg polio, blindness, also problems related to the legs such as neuropathy or joints problems. Other possible barriers may be lack of space, time, safety or motivation. Exercise is not recommended when blood sugar level is over 300 mg/dl and if the patient feels sick, short of breath, is experiencing any tingling, pain or numbness in the legs. Diabetics should
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also refrain from exercising when ketones appear in their urine and when the medication is peaking. The concept of physical activity may also vary from region to region. Sure there are populations in the developing country that have adopted a more urbanized way of life which is characterized by obesity and reduced physical activity. But when a person suffering from diabetes is involved in a job which requires strenuous physical activity, many hours of work, or a long way commuting on foot, then the dose of insulin must be adjusted accordingly in order to avoid possible hypoglycemia episodes. In such cases it is essential that special footwear for protection (eg custom made shoes that follow the shape of the feet ) and some food rich in carbohydrates are available. If the patient intends to exercise after he has eaten, a snack high in carbohydrates is much more preferable than a proper meal. Of course, if the patient does heavy aerobic exercise or strenuous work, it is wise to eat a bit more. If the patient hasnt eaten for over an hour or if blood sugar is less than 100 to 120 mg/dl, he should have an apple or glass of milk before working out. In all cases the patient should have a snack with him. Insulin dependent patients should work out after eating and not before. Testing blood sugar before, during and after exercising could be ideal but unfortunately this is not always possible especially in poor resource settings environment.
4.13. Dietary intervention

A change in dietary habits of the patient is an important factor of the treatment of diabetes. The diet should be tailored according to age, needs, religion, cultural characteristics and lifestyle of the patient. The objective of dietary changes is that the patient receives all the necessary calories and nutrient elements which ensure growth and health. The patient should also maintain or achieve the appropriate weight with proper nutrition. In addition euglycemia levels should be reached according to their metabolic needs, physical activity and medication of the patient. In any case, the patient should learn the importance of nutrition in regulating the disease, although health professionals sometimes lack in this knowledge (Abioye-Kuteyi et al., 2005). It is essential that clinical nutritionists are involved in DM care. The diet for diabetes should be applied according to concept of a healthy diet. The diabetic patient can eat a variety of dishes. As a general rule fatty food and sugar should be reduced. Moreover the patient should eat 2-4 fruits daily and avoid sugary juices. Sugar could be replaced by sweeteners. Proposed diets should be tailored to the particular eating habits and food availability at local level. The patients eating habits, time and frequency of main and smaller meals should also be taken into account. Possible allergies must also be considered. The patient must be checked
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for signs of malnutrition, excessive food surplus and alcohol. Each case requires specific diet arrangements according to age, gender, socioeconomic status, ethnicity and occupation. The patients level of perception as well as his willingness to change his dietary habits play an important role. The recommended diet must also depend on the type of diabetes, the prescribed treatment, the level of physical activity, the body mass index, waist circumference and blood pressure. If biochemical control is possible, the lipid profile, liver enzymes, urea and electrolytes must also be checked. After considering all these aspects the therapist can discuss the appropriate changes to be made with the patient. The therapist must keep a follow-up even after his first session with the patient so as to ensure that the patient follows the recommendations. Sometimes further diet changes and adjustments are also required. Specific groups such as pregnant women and patients with renal problems must be checked more regularly. It is common practice within the African culture for the family to gather and eat together from the same dish. The therapist here must emphasize the need for the diabetic member of the family to follow his own specific diet. The understanding of the family can help especially if they all decide to adopt the same healthy eating habits as the patient. This can provide a way out when there is no possibility of cooking separate dishes for the diabetic member of the family. The basic elements of nutrition are discussed below: Carbohydrates are essential for all people with diabetes. In Africa, many diets are rich in carbohydrates and they contribute best for glycemic control. Foods consumed in large quantities are hard porridge, bread, rice, beef, milk, oranges and sunflower oil. The main beverage is water, tea and milk (Hoffmeister et al., 2005). It is recommended that approximately 60% of all calories come from carbohydrates. They are found mainly in cereals, grains, dairy, fruits and vegetables. Fresh fruits are preferred to juice as they contain fibres. Sugar increases blood glucose levels faster compared to starch, and therefore it is suggested that sugar be replaced by other sources of carbohydrates. Sugar is preferred during exercising or when the patient enters a phase of hypoglycemia. The quantity of insulin dosage should also be regulated depending on the level of carbohydrates on the diet. Furthermore, fibres intake is crucial. The glycemic index (GI) is a measure of the effects of carbohydrates on blood sugar levels. Carbohydrates that break down quickly during digestion and release glucose rapidly into the bloodstream have a high GI, carbohydrates that break down more slowly, releasing glucose more gradually into the bloodstream, have a low GI. GI values can be interpreted intuitively as percentages on an absolute scale and are commonly interpreted as follows:
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Classification Low GI
Examples most fruits and vegetables (except potatoes and watermelon), whole-grain breads, pasta, legumes/pulses, milk, yogurt, products extremely low in carbohydrates (some cheeses, nuts), fructose whole wheat products, sweet potato, table sugar corn flakes, baked potatoes, watermelon, white bread, extruded breakfast cereals, most white rices, straight glucose
Medium GI High GI
A lower glycemic index suggests slower rates of digestion and absorption of the foods carbohydrates and may also indicate greater extraction from the liver and periphery of the products of carbohydrate digestion. A lower glycemic response usually corresponds to a lower insulin demand but not always, and may improve long-term blood glucose control and blood lipids. A low-GI food will release glucose more slowly and steadily. A high-GI food causes a more rapid rise in blood glucose levels and is suitable for energy recovery after endurance exercise or for a person experiencing hypoglycemia. Proteins are found mainly in foods of animal origin. The influence of proteins in blood sugar depends on the availability of insulin. In well-regulated diabetes proteins do not increase blood sugar levels, but in T2DM proteins are likely to stimulate the secretion of insulin. Proteins require insulin for metabolism. Approximately 15-20% of calories should come from protein (about 0,8 gr / kg body weight). However, a diet high in protein and low in carbohydrates is not recommended because it is usually accompanied by large quantities of saturated fats. The fats are found mainly in foods of animal origin and cooking oils. They should not exceed 30% of total calories. Fat provides more calories per gram (total 9 kcal / gr). They are distinguished to good and bad fats depending on their effect on cholesterol metabolism. Saturated fats, the bad ones, raise cholesterol levels in blood. They are found mainly in red this category. They are in solid form at room temperature with the exception of coconut and palm fats. Unsaturated or good fats are divided into monounsaturated and polyunsaturated. If saturated fats are replaced in the diet of the patient that will help to lower cholesterol. It is in liquid phase at room temperature. Source of polyunsaturated fats are sunflower, corn, soybeans and fish fats. Monounsaturated fat source are olive oil, nuts (peanuts and nuts) and avocados. A diet high in monounsaturated consumption reduces the risk of cardiovascular disease, whereas polyunsaturated and omega-6 fats reduce triglyceride levels. Finally, trans
meat. The fats from coconuts and palms fruits which are often found in Africa belong to
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fats, found mainly on butter products and fried foods, increase LDL cholesterol and should be avoided. Imported foods rich in conservatives and trans fats are found in Africa, especially in urban settings and their use should be highly discouraged. Preferring dairy products low in fats and removing the visible fat from meat and the skin from chicken make the basic rules for reducing fats in food. Baking food should be preferred instead of frying. Also vegetable oils rich in polyunsaturated and monounsaturated should be consumed, as well as fish. Vegetables should preferably be cooked without butter. To simplify the type and quantity of food recommended for DM we could use the food pyramid. The body needs more cereals, rice, bread and other carbohydrates which are on the basis of the pyramid and less sweets and fats which are on the top of the pyramid. So every day the body needs 6 to 11 parts of starchy foods or bread. This is about a slice of bread, half cup of cooked rice or grains. The body also needs 3-5 parts of vegetables (each part is a cup of raw vegetables), 2-4 parts of fruit (each part is a cup of fruit or half cup of fresh juice without sugar), 2-3 parts of milk products (each part
corresponds to a cup of milk or cup of yogurt), also 2-3 parts of meat (a part corresponding to 57-85gr meat, two eggs and two pieces of cheese) and the total fat should be limited to a spoon of margarine. Important is the willingness of the patient to choose the right foods for him and avoid foods of low nutritional value (Macmullan, December 2009). Moderation is advised with regards to consuming alcohol and the use of some drugs. Alcohol inhibits the glycogenesis in the liver and some drugs inhibit hunger symptoms. This, together with impaired judgment, memory and concentration caused by some drugs can lead to hypoglycemia.
4.14. Diabetes and Obesity

A large number of people with T2DM living in the developing countries are obese (Delpeuch and Maire, 1997), particularly in urban areas (Aspray et al., 2000). Obesity is also no longer a condition that just affects older people, although the likelihood does increase with age, and increasing numbers of young people have been diagnosed with obesity. Obesity is associated with poor prognosis of the disease and its complications. The reduction in body weight has a positive effect on the disease. Obesity is a major factor of the metabolic syndrome. The waist circumference is also a sign of obesity, which we should take into account. We should set realistic targets for reducing weight in an overweight patient, and in order to achieve this we should change the diet and increase the physical activity level. Generally,
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it is difficult for patients to lose weight and maintain the ideal body mass index. Also, in many cases obesity is accepted by a large proportion of the population as it is considered a sign of prosperity or beauty. In such cases it is not easy to convince them to reduce their body weight.
4.15. Fasting and Diabetes

Many people fast for religious or cultural reasons. According to estimates coming from religious leaders and sociologists the Christian and Muslim communities in Tanzania are approximately equal in size, each accounting for 30 to 40 percent of the population, with the remainder consisting of practitioners of other faiths, indigenous religions, and atheists. The culture of each nation carries the values, beliefs about what is good and bad, and suggests ways of behavior. It is important to take into account these cultural characteristics to understand better the daily lives of these people. According to this many diabetics follow their religious beliefs and fast in contrast to the advice and knowledge of the therapist. Therefore we should be careful to adjust treatment to a man who fasts. In such cases the general principle is to recommend to the patients to avoid fasting if it is not absolutely necessary. If they want to follow hard diets, they should not exclude water in any case. There are certain groups of people and circumstances where you may be exempt from fasting. For example:
children (under the age of puberty) the elderly the sick those with learning difficulties those who are travelling pregnant, breastfeeding and menstruating women anyone who would be putting their health at serious risk by fasting, eg people who treat their diabetes with insulin or have diabetic complications (damage to eyes, kidney or the nerves in your hand and feet).
Religion leaders should allow patients to be exempted from fasting. If the person takes insulin or hypoglycaemic drugs, special administration is required to match the reduced calorie intake and to avoid episodes of hypoglycemia. In these patients we should check more regularly blood glucose levels. The complete exclusion of food is not recommended for anyone with diabetes. The necessary hydration of the patient is necessary even during the fasting period. Strenuous physical activity during the period of fasting should be avoided. In cases
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of hypoglycemia or persisting infections the patient should be advised to stop fasting. The same thing is also necessary for patients with renal or heart problems. Muslims fast for one month during Ramadan. From sunrise until sunset they do not eat any kind of food or even water, nor do they smoke or drink. They only eat between sunset and sunrise. Patients who are treated with antidiabetic tablets and diet may fast. The usual dietary advice should also be followed during this period. Patients who take metformin, and alphaglucocidase can continue taking their usual doses, the usual hours. Patients prescribed with chlopropramide (of the sylphonylureas family) should replace it with a shorter acting antidiabetic agent. If they take a second or third generation sulphonylureas (glibenclamide, gliklazide, glipidine) they should take them before the fast ending and not before dawn. If the patient is receiving tolbutamide, he may take both the morning and the afternoon dose, but the lower dose should be taken before dawn. Patients with T2DM who receive insulin injections once daily at bedtime hour they may continue as before. If they take two doses daily, a short and an intermediate acting insulin, the hours should be changed and the patient should receive the usual evening dose of short acting insulin before meals by dawn. Also before dinner the patient should receive the usual dose of the intermediate acting insulin that he used to take before fasting in the morning. It is also useful to measure blood glucose regularly to adjust insulin dosages. Patients with T1DM can receive a long acting insulin by 70% and the rest 30% of short acting. The total dose of insulin before fasting can be reduced up to 85%. The double dose before and after sunset is another alternative (Kassem et al., 2005) Fasting in many religions, especially Christianity can have various forms. Thus, the absolute fasting requires complete abstention from food and water, as during Easter, for instance. It is recommended that this does not last more than three days and it is absolutely not recommended to patients receiving insulin. In some forms of fasting the person abstains from meat, but he can drink water and follow a vegetarian diet. In these forms of diet the patient should receive all the calories and nutrients. If this happens there is no special treatment adjustments needed. The patients can continue to take metformin tablets with meals as well as sulphonylureas and insulin before meals.
4.16. Diabetes and lack of food

Often the therapist will encounter people with low body mass index. This may be due either to malnutrition or it may be the result of T1DM (Lester, 1993). Malnutrition is not related to future development of D.M. in an undernourished person (Swai et al., 1992). In many developing countries due to poverty, wars, or poor crops, patients with diabetes may not have access to food. The body then tries to save energy. The fat stores are consumed
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first and then the proteins and the muscle tissues follow. Primarily the body places an emphasis on providing the brain and the heart with the appropriate energy. The risk of ketoacidosis is high, and this occurs especially to patients with T1DM. In such cases, the therapist has a limited potential to act. The doses of insulin to patients who are malnourished are reduced drastically. Dietary restrictions are not valid anymore and the person is recommended to eat all kinds of food that he finds available. When some meals are found only small doses of short-acting insulin may be given. Hydration of the patient is also essential.
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chapter 5
Diabetes in patients of special categories

5.1. Diabetes in children and adolescents
Throughout the world, incidences of diabetes are on the rise, and consequently so is diabetes amongst children. Most children are affected by T1DM in childhood. However, the number of children and young adults affected by T2DM is also beginning to rise. Life expectancy for a child with T1DM in Africa may be just one year. This is due to incapability of the health system to detect and treat the disease, the limited resources available and the heavy cost of children already diagnosed the glycemic control reached by the applied treatment is not always satisfactory (Majaliwa et al., 2007). Children and adolescents require special treatment specifically during the periods of their growth and development. The program aims to help children and their families to regulate diabetes and achieve a normal development and maturity. Also while emergency complications such as ketoacidosis and hypoglycemia need to be avoided, the knowledge of the community in relation to the risk of diabetes in children should be increased (Bassili et al., 2001). To meet all these needs we should check the environment of the child or adolescent, his stage of development, the family and social support received. The program followed at school and the level of physical activity should be taken into account as well. Sometimes the family regards the child with diabetes as cursed or bewitched. Therefore the child faces the family rejection as well (Bucci, 2008). There is often a family history of children with diabetes and the autoimmune nature of
DIABETES IN PATIENTS OF SPECIAL CATEGORIES
treatment of a child with diabetes for a poor family (Elrayah et al., 2005). In addition, for
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diabetes is confirmed, often with the presence of specific autoantibodies (Fakhfakh et al., 2008). The typical appearance of diabetes in children may include polydipsia, polyuria (often with a recurrence of nocturnal enuresis), tachypnea (typical deep breathing Kussmaul), fatigue and weight loss. Amongst children, specific symptoms may include stomach aches, headaches and behavioral problems. Recurrent tummy pains and an unexplainable history of illness should be treated as possible heralds of diabetes. The delay in diagnosis leads to vomiting, abdominal pain, dehydration, ketoacidosis, drowsiness and coma. Diabetic ketoacidosis has a mortality rate of 10%. The patient emits sweet breathing smell typical of ketones emittance which makes a clinical sign for the diagnosis of ketoacidosis. In addition, fever occurrence suggests coexisting infections and abdominal tenderness can mimic surgical abdomen problems. You should check for the presence of glucose in urine in all children with polydipsia or urinary symptoms. The glucose tolerance test has little value in diabetic children who suffer mostly from T1DM and so it is important to measure blood sugar. The admission to hospital is required in case of diabetic ketoacidosis or dehydration. Insulin is administered subcutaneously or intravenous if there is an intravenous route. When ketonouria is treated, insulin is administered subcutaneously once again. The method of insulin injection should be completely understood by the childs environment. Children who are diagnosed for the first time with diabetes require insulin dose 0.5 to 1 IU / Kg / day. Usually after a few weeks or days the insulin requirements are reduced and sometimes stopped. This period is called honeymoon period. The therapist should be very observant to adjust the dose and avoid possible hypoglycemia episodes. Because type 1 typically means that the vast majority of islet cells have been destroyed and insufficient or zero insulin can be produced, the only certain method of treating diabetes in children is insulin treatment. As a general rule the pre-adolescent dosage is 0,5-0,8 IU / kg / day, adolescent dose 0.8 IU / kg / day and the dose for adults 0.6 IU / kg / day. Insulin can be administered twice daily in a typical treatment regimen, or three times daily in an intensive regimen that offers flexibility on meals and physical activity. The triple regimen may be better applied to older children, with special care to avoid hypoglycemia. Insulin should always be adjusted according to measured blood glucose levels and in relation to physical activities especially when children are concerned. At the same time, we must teach the childs environment to recognize signs of hypoglycemia and ketoacidosis. Such warning signs may be irritability, abnormal behavior or constant complaints of hunger. Children themselves should be trained to avoid hypoglycemia and if possible they should carry a snack rich in glucose, in case they need it. The children also can make more frequent laboratory testing. For example, we can check their urines for ketones with a urine stick, and we need more frequent tests of blood glucose. Ideal levels of fasting glucose are <110 mg / dl, postprandial <150 mg/dl and glycated hemoglobin (HbA1c) 7-9% in children under 5 years, while for older children 7 to 8%.
We should also check the development of the child and if there are any abnormalities we should proceed to intervention as soon as possible. Exercise is also important for a child with diabetes. Nevertheless, children need to understand the impact that the exercise may have on their blood glucose. So, if they undergo a strenuous physical activity they should consume food rich in carbohydrates before exercising. The diet they follow needs to cover all the essential nutrients so as to achieve a healthy development. We nevertheless follow the general instructions concerning dietary interventions and we suggest 4-6 meals every day to avoid hypoglycemia. The family is also an important factor when we treat a child with diabetes. Sometimes parents may be absent or unable to care for their child. These children are in need of special care. Parents or other members of the family must be aware that children with diabetes have diet restrictions and that their activity levels need to be closely monitored. Initially, and throughout the lifetime of the disease, diabetes can be a serious strain. We always try to find someone from the childs environment to work closely with the therapist. Finally, therapists must be prepared in cases that children change their behavioral or sleep pattern, react unpredictably, mainly where their diet is concerned and suffer from infections or viral diseases more frequently. Children are also a more vulnerable group with a smaller body site available for insulin injections.
5.2. Diabetes in pregnancy and gestational diabetes

Gestational diabetes mellitus (GDM) bears resemblance to T2DM in several respects, involving a combination of relatively inadequate insulin secretion and responsiveness. It occurs in about 2%5% of all pregnancies and may improve or disappear after delivery. Gestational diabetes is fully treatable but requires careful medical supervision throughout pregnancy. About 20%50% of affected women develop T2DM later in life. During the perinatal period, women with pre-existing diabetes and women with gestational diabetes have special needs. The overall medical checkup that should be done in these women includes medical and gynecological history, especially the history of a large sized baby. Blood pressure should be below 130/80 mmHg. This can be regulated medically. Also, women with diabetes may suffer from complications in the eyes, which can be verified by ophthalmologic examination. In such cases a caesarean section is recommended in order to avoid bleeding of the vessels in the retina. Additionally, women who have T2DM and treated with anti-diabetic tablets may not be regulated only by them and must take additional insulin. If they are already treated with insulin, hypoglycemic episodes are more likely to occur during the first trimester of pregnancy, whereas during the second and third trimester, the dose of
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insulin will increase due to the contra-acting hormones of pregnancy that resist to the action of insulin. The test for gestational diabetes should be performed on women who have a greater chance to develop it. Women over 35 are at increased risk, as well as those with a history of delivering an overweight baby over 4 kgr, women with a family history of diabetes revealing a first degree relative with T2DM, those who had a history of pregnancies that had many complications. Classical risk factors are a previous diagnosis of gestational diabetes or prediabetes, impaired glucose tolerance, or impaired fasting glycaemia. The ethnic background is quite important since those with higher risk factors are found amongst African-Americans, Afro-Caribbeans, Native Americans, Hispanics, Pacific Islanders, and people originating from South Asia. Additionally, being overweight, obese or severely obese increases the risk by a factor 2.1, 3.6 and 8.6, respectively and finally another risk factor is the previous poor obstetric history. Smokers run a double risk of GDM according to statistics. Although relevant evidence remains controversial, the polycystic ovarian syndrome is considered as a risk factor. More controversial potential risk factors are also studied. There is a wide advocation of all women being screened because the 40-60% of women with GDM have no demonstrable risk factor. Typically women with gestational diabetes exhibit no symptoms (another reason for universal screening), but some women may demonstrate increased thirst, increased urination, fatigue, nausea and vomiting, bladder infection, yeast infections and blurred vision. The medical examination includes oral glucose test and the measurement of blood glucose. A general monitoring of pregnant women by measuring blood glucose may cost less than having to deal with the complications of gestational diabetes in a whole community (Larijani et al., 2003). If blood glucose is not regulated during pregnancy there is an increased risk of early birth, polyhydramnion, hypertension, fetal death or still-born, rapid development renal failure, damage to the cornea of the eye, vaginal and urinary infections. All children born by diabetic mothers are more likely to be large sized and they can easily develop hypoglycemia in the first 72 hours of life, hyperbilirubinemia, polycythemia, hypokalemia, hypomagnesemia and respiratory distress syndrome. There are also related risks of trauma at birth, delayed growth and prematurity along with birth defects and fetal death in case of diabetic ketoacidosis of mother (Coetzee, 2009). In normal circumstances the fetus is dependent on its mother for glucose which passes through the placenta. Glucose and ketones are passed with filtration through the placenta from the mother to the fetus. Insulin is not permeable through the placenta. In a normal pregnancy there is an increase of basic and postprandial insulin secretion. The need for insulin is lower in the first three months, but as the pregnancy progresses and the hormones of pregnancy cause significant insulin resistance, the demand for insulin increases accordingly. In women with diabetes the embryo receives excessive amounts of glucose, less amino acids and more fatty acids due to hyperglycemia. Under these metabolic changes it is likely
that abnormality may develop. Especially during the third trimester the fetus is at increased risk of developing disorders of the central nervous system and behavioral disorders later as a child. Maternal hyperglycemia may also result in large sized babies. Through the mothers placenta glucose can pass while insulin cannot. From the tenth week of pregnancy the fetal pancreas starts working and producing insulin when it detects high levels of glucose. If the mother is hyperglycemic, glucose also is given to the fetus as well as an additional stimulus to the pancreas receptors and so fat tissue is developed additionally to the muscle tissue. Problems can be caused during delivery and if the baby is too large it is recommended to proceed to a caesarean section. Hypoglycemia also after birth is the result of the interrupted supply of glucose from the umbilical cord. The enhanced beta-cells of fetal pancreas still produce extra insulin, thus decreasing immediately after birth the levels of glucose. That is why it is recommended that the baby be fed soon after birth. The respiratory distress syndrome also develops when the surfactant agent is produced at a reduced quantity while there is excess insulin in the circulation of the fetus. To avoid this, blood glucose levels should be at normal level before birth. The desired blood glucose level is 60-90 mg/dl for fasting glucose, 60-104 mg/dl before meals, 101-140 mg/dl one hour after meals, 90-121 mg/dl, two hours after meals and during sleep, and between 2:00 to 6:00 a.m. desired blood glucose is 60-121 mg/dl. If the price of sugar is above 140 mg/dl there is an increased risk for problems in the fetus or the mother. A morning urine test for ketones is also necessary since insufficient calorie intake or poor meals can result in the catabolism of fat. In such a case a meal before bedtime must be added and the patient should not be left hungry for more than 10 hours. Women with T2DM who fail to achieve regulation of blood sugar should take insulin. For a woman who takes for the very first time insulin, the dose should be calculated at 0.5 IU/kg/24h. Preferably mixed insulin may be used. Moreover, 30% of the dose should be shortacting and 70% long-acting insulin. The best site for injection is around the belly because the absorption is faster there. As the pregnancy progresses the injections should not be done in the thighs since the vascular circulation is affected over there because of pressure from the uterus. The dose of insulin is 0,5 IU/kg/24h the fifth month, 0,6 IU/kg/24h the sixth month, 0,7 IU/kg/24h the seventh month, 0,8 IU/kg/24h the 8th and 0,9 IU/kg/24h the ninth month. If a woman with T1DM was used to injecting insulin before her pregnancy, doses should be adjusted upwards accordingly. It is desirable that the expectant mother has the appropriate supplies and learns to control her own blood glucose levels. The best time to check the patients glucose is by testing both fasting and one hour postprandial glucose. At birth, the level of blood glucose can be reduced. That is why we should check blood glucose every hour and give dextrose intravenous fluids if hypoglycemia occurs. The chance of developing T2DM is two times higher. After birth tight control is necessary. In women with T1DM the dose of insulin is gradually reduced so as to reach the same levels as before
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pregnancy. Gestational diabetes generally resolves after delivery. A high rate of recurrence is involved in a second pregnancy within one year of the previous one. During lactation, glucose is reduced at the mothers. The woman should stop taking any anti-diabetic tablets as their substances are absorbed by milk and can cause hypoglycemia to the baby.
5.3. Diabetes and surgical procedures

Operational patients often suffer from diabetes. A surgery may affect the normal blood glucose levels and so we should rearrange meals and treatment. Surgical stress stimulates the secretion of various hormones and inhibits the secretion of insulin. These changes enhance the catabolism and can quickly cause hyperglycemia and ketosis. Hypoglycemia can occur especially in patients who fast before surgery. There is an increased risk for hypoglycemia in patients under anaesthesia. Additionally, patients with diabetes have more postoperative complications such as myocardial injuries and contaminated sections infarcts. Often deterioration of renal function takes place, particularly if diabetic nephropathy existed before the surgery. Diabetics are also characterized by poor and/or slow wound healing, weak skin and tissue at site of surgery. The approach of D.M. treatment at home differs greatly to that in hospital. One good example is the use of regular insulin given intravenously, rather than other types available. Most professionals would avoid administering oral medication or long acting types of insulin. Regular insulin works within a short time allowing the surgeons and staff to have a much better idea of the glucose level. This allows them to treat elevated levels, or low levels immediately. In some cases, blood glucose testing will be done as frequently as every two hours, with medication coverage provided as needed. After surgery, the need for high quality nutrition and tight glycemic control is still present. Nutrition will provide the building blocks for healing and a normal glucose level will promote a faster recovery. Tight control of glucose levels could potentially save days or even weeks of the recovery period when compared to recovery times with elevated blood glucose. Once the surgery is over and the patient is into the recovery phase, it is necessary to aggressively check for signs of infection in the healing wound, in addition to the normal checks (such as checking the feet for problems).
76
5.4. Diabetes and the elderly patients

As people get older ability to confront and deal with everyday problems is reduced. Life expectancy in the developing world might be lower compared to the developed countries but gradually African countries seem to have an increased number of elderly (Nordberg, 1997). Treating and diagnosing diabetes amongst the elderly requires a flexible and unique approach. Older people may have other coexisting problems that must be taken into account before trying to treat DM (Kesavadev et al., 2003). Elderly people are often more frail and susceptible to illness. Some of the most common problems are hearing problems, poor vision, physical disabilities, impaired memory, coexisting medical diseases, especially hypertension, reduction of cardiac and renal function, extensive use of multiple medications, lack of social and family support, depression, dental problems and malnutrition. Many elderly diabetic patients are pre-disposed to hypoglycemia A good number of physiological changes take place as our bodies grow and adapt to new conditions. The expected classic symptoms may not be exhibited in elderly people at risk of developing the disease or with already developed D.M. Age-related changes can mean that some symptoms will be masked, or harder to spot. In any case we have tailor-made program for every elderly patient in order to treat D.M. properly.
77
Discussion and conclusions

W
E WILL REGULARLY TRY TO ASSESS and evaluate whether the objectives of the clinic are reached. So, our first objective is to increase the number of patients visiting the diabetes clinic. It is also very important to detect new diagnosed patients with D.M. who were unaware about their medical condition. Moreover, it is important to determine how widespread the disease is in the region, as well as how to achieve better clinical results with the least possible means and with limited personnel and laboratory tests. Finally, taking into account all the cultural characteristics of the population our ultimate goal to raise health seeking behavior among the community will be assessed. The personal data of each patient will remain anonymous and confidential in any case. The patients will not be obliged to come to the clinic and they will not be given any motives rather than that of the therapeutical benefit of their medical condition. Medical treatment is the primary goal over any other objectives such as possible research conclusions or even financial efficacy of the clinic. We will act respectfully towards the cultural and religious features of the patients in their background. According to this, the therapist will adapt to the particular profile of patients rather than patients to the cultural characteristics of the therapist. We will also be discreet when dealing with the patients and we have to make sure that treatment in the diabetes clinic is not associated with any kind of stigma and discrimination between community members. In addition, there will be no discrimination in choosing the patients, but there will be an increased awareness about vulnerable groups such as pregnant women and children. Our objectives will be evaluated on a monthly basis so that amendments can be made. In any case we will try to come up with innovative proposals, suggestions, and ideas for further investigation or action. The effectiveness of our intervention in quality terms is a priority. We will examine if it introduces the correct behaviours to local health institutions and organizations of diabetics (Beran et al., 2006). The ultimate aim of this project is to contribute to the effort for a new global strategy for diabetes appropriate for the developing world. New strategies should place diabetes on the agenda of global health systems. Global donors must be convinced that millions of people around the world are in immediate need of education and access to D.M. treatment. Above all, it is vital to understand that poverty and underdevelopment are the main obstacles to
79
DISCUSSION AND CONCLUSIONS
proceed to the establishment of good care practices, reducing morbidity and mortality due to chronic diseases on top of the battle against infectious diseases and public health interventions. Therefore the main aim of the project is to establish a DM care clinic aiming at an innovative program that apart from a valuable service to the local community, will also contribute to better understanding the problem of DM in poor rural communities. Medicine is the art of assisting people to survive with dignity in good health. Every effort has to be made to offer good quality and accessible health services to poor people by strengthening health systems all over the world.
80
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Diabetes Final

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Good practices for treating Diabetes Mellitus in a developing country

International Medicine Health Crisis Management

2010 Athens, Medical School, University of Athens, Greece

2. Methods of therapeutic approach .......................................................... 15

3. Features of the disease .................................................................................. 19

GOOD PRACTICES FOR TREATING DIABETES MELLITUS IN A DEVELOPING COUNTRY

5. Diabetes in patients of special categories

Discussion and conslusions ................................................................................ 79 Literature

Corresponding address for comments: ekakalou@yahoo.gr

A PROPOSED MODEL OF COMPREHENSIVE DM CARE IN A RURAL RESOURCE POOR SETTING

A proposed model of comprehensive DM care in a rural resource poor setting

GOOD PRACTICES FOR TREATING DIABETES MELLITUS IN A DEVELOPING COUNTRY

Introducing availablility of basic diagnostic, treatment and follow-up means for

Assessment surveys of prevalence, incidence, mortality and morbidity rates

1. Beran et al., 2005.

Development and evaluation of a simplified medical algorithm for managing DM,

Monitoring and Evaluation

B. Lipids goals for reducing the risk of complications:

A PROPOSED MODEL OF COMPREHENSIVE DM CARE IN A RURAL RESOURCE POOR SETTING

Methods of therapeutic approach

He/she must have basic knowledge of epidemiology, pathophysiology, diagnosis,

He/she should demonstrate good communication skills

METHODS OF THERAPEUTIC APPROACH

He/she should be surrounded by a team of people who could undertake a part of

2.2. Barriers to the process of therapeutic work

GOOD PRACTICES FOR TREATING DIABETES MELLITUS IN A DEVELOPING COUNTRY

METHODS OF THERAPEUTIC APPROACH

When in groups, various methods can be used

GOOD PRACTICES FOR TREATING DIABETES MELLITUS IN A DEVELOPING COUNTRY

Peer to peer education is of utmost importance.

Features of the disease

FEATURES OF THE RISEASE

GOOD PRACTICES FOR TREATING DIABETES MELLITUS IN A DEVELOPING COUNTRY

3.2. Types of diabetes

FEATURES OF THE RISEASE

GOOD PRACTICES FOR TREATING DIABETES MELLITUS IN A DEVELOPING COUNTRY

Usually <30-35 years old Yes, severe or less severe

Complications at the time of diagnosis Insulin resistance Ketoacidosis Autoantibodies

No Yes, usually sets the diagnosis anti-GAD, ICA, 1A-2

GOOD PRACTICES FOR TREATING DIABETES MELLITUS IN A DEVELOPING COUNTRY

hemochromatosis, fibrocalculous pancreatopathy

hyperthyroidism, somatostatinoma, aldosteronoma

3.3. Chronic complications of Diabetes Mellitus

Diabetic microvascular disease:

FEATURES OF THE RISEASE

GOOD PRACTICES FOR TREATING DIABETES MELLITUS IN A DEVELOPING COUNTRY

Gastrointestinal/ genitourinary dysfunction

3.4. Diagnosis of Diabetes Mellitus

FEATURES OF THE RISEASE

TO SUM UP, THE CRITERIA FOR THE DIAGNOSIS OF DIABETES ARE:

FEATURES OF THE RISEASE

Check fasting plasma glucose (FPG) twice

< 100 mg/dl? No DM

Glu 2 h > 200 mg/dl and FPG > 125 ? DM

Annual fasting plasma glucose

Determine plasma glucose. Is it over 126 mg / dl?

Yes: Determine in two other measurements. Is it still above 126 mg/dl?

Yes: Check regularly, give lifestyle advices

FEATURES OF THE RISEASE

4.2. DM and Travel

4.3. Diabetic Ketoacidosis, Hyperosmolar Coma

GOOD PRACTICES FOR TREATING DIABETES MELLITUS IN A DEVELOPING COUNTRY

Level of glucose in mg/dl Below 80 mg/dl