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Chronic Disease List (CDL)

Every medical aid scheme must at lease have 25 chronic disease list (CDL) that they cover from formularies. There are 270 conditions that if not given treatment can end up in death these are called PMB (prescribe minimum benefit).

Here follows a list of the 25 chronic disease list (CDL) that must be covered by all medical aid schemes. 

Addison’s disease
Addison’s disease (also chronic adrenal insufficiency, hypocortisolism, and hypoadrenalism) is a rare, chronic endocrine disorder in which the adrenal glands do not produce sufficient steroid hormones (glucocorticoids and often mineralocorticoids). It is characterised by a number of relatively nonspecific symptoms, such as abdominal pain and weakness, but under certain circumstances, these may progress to Addisonian crisis, a severe illness which may include very low blood pressure and coma.
The condition arises from problems with the adrenal gland itself, a state referred to as “primary adrenal insufficiency”, and can be caused by damage by the body’s own immune system, certain infections or various rarer causes. Addison’s disease is also known as chronic primary adrenocortical insufficiency, to distinguish it from acute primary adrenocortical insufficiency, most often caused by Waterhouse-Friderichsen syndrome. Addison’s disease should also be distinguished from secondary and tertiary adrenal insufficiency, which are caused by deficiency of ACTH (produced by the pituitary gland or also known as the master gland) and CRH (produced by the hypothalamus), respectively. Despite this distinction, Addisonian crises can happen in all forms of adrenal insufficiency.
Addison’s disease and other form of hypoadrenalism are generally diagnosed via blood tests and medical imaging.[1] Treatment involves replacing the absent hormones (oral hydrocortisone and fludrocortisone).[2] Lifelong, continuous treatment with steroid replacement therapy is required, with regular follow-up treatment and monitoring for other health problems.[1]

Asthma (from the Greek άσθμα, ásthma, “panting”) is the common chronic inflammatory disease of the airways characterized by variable and recurring symptoms, reversible airflow obstruction, and bronchospasm.[1] Symptoms include wheezing, coughing, chest tightness, and shortness of breath.[2] Asthma is clinically classified according to the frequency of symptoms, forced expiratory volume in 1 second (FEV1), and peak expiratory flow rate.[3] Asthma may also be classified as atopic (extrinsic) or non-atopic (intrinsic).[4]
It is thought to be caused by a combination of genetic and environmental factors.[5] Treatment of acute symptoms is usually with an inhaled short-acting beta-2 agonist (such as salbutamol).[6] Symptoms can be prevented by avoiding triggers, such as allergens[7] and irritants, and by inhaling corticosteroids.[8] Leukotriene antagonists are less effective than corticosteroids and thus less preferred.[9]
Its diagnosis is usually made based on the pattern of symptoms and/or response to therapy over time.[10] The prevalence of asthma has increased significantly since the 1970s. As of 2010, 300 million people were affected worldwide.[11] In 2009 asthma caused 250,000 deaths globally.[12] Despite this, with proper control of asthma with step down therapy, prognosis is generally good.[13]

Bronchiectasis is a disease state defined by localized, irreversible dilation of part of the bronchial tree caused by destruction of the muscle and elastic tissue. It is classified as an obstructive lung disease, along with emphysema, bronchitis, asthma, and cystic fibrosis. Involved bronchi are dilated, inflamed, and easily collapsible, resulting in airflow obstruction and impaired clearance of secretions. Bronchiectasis is associated with a wide range of disorders, but it usually results from bacterial infections, such as infections caused by the Staphylococcus or Klebsiella species, or Bordetella pertussis

Cardiac Failure Definition
Cardiac failure definition is quite different in medical terms than what we the laymen have idea about it. Cardiac failure is that state of the heart where some problems impair its function to pump blood in sufficient amount and supply it to the whole body. Very often heart failure goes undiagnosed because there is no clearly stated and universally accepted one definition of it which results in challenges in a definitive diagnosis. The cases coming to the doctors all round the world dominate one fact that signifying one cause is very difficult due to differences in populace, problems in diagnosis and changes that can be ascribed to the age. Yet there are broadly two divisions of causes behind heart failure. First one being chronic heart failure and its main causes are Ischaemic heart disease where sufficient blood is not supplied to the heart muscles, chain smoking, high blood pressure, diabetes, obesity, dilated cardiomyopathy, infected heart muscles or viral myocarditis, cardiomyopathy caused by HIV, drugs of chemotherapy, arrhythmias etc. Chronic heart failure treatment depends upon the cause behind the disorder. Second cause is acute decompensated heart failure.

Heart failure
Heart failure (HF), often called congestive heart failure (CHF) or congestive cardiac failure (CCF), is an inability of the heart to provide sufficient pump action to distribute blood flow to meet the needs of the body.[1][2][3] Heart failure can cause a number of symptoms including shortness of breath, leg swelling, and exercise intolerance. The condition is diagnosed with echocardiography and blood tests. Treatment commonly consists of lifestyle measures such as smoking cessation, light exercise including breathing protocols, decreased salt intake and other dietary changes) and medications. Sometimes it is treated with implanted devices (pacemakers or ventricular assist devices) and occasionally a heart transplant.
Common causes of heart failure include myocardial infarction and other forms of ischemic heart disease, hypertension, valvular heart disease, and cardiomyopathy.[4] The term “heart failure” is sometimes incorrectly used to describe other cardiac-related illnesses, such as myocardial infarction (heart attack) or cardiac arrest, which can cause heart failure but are not equivalent to heart failure.
Heart failure is a common, costly, disabling, and potentially deadly condition.[4] In developed countries, around 2% of adults suffer from heart failure, but in those over the age of 65, this increases to 6–10%.[4][5]

Cardiomyopathy (literally “heart muscle disease”) is the measurable deterioration of the function of the myocardium (the heart muscle) for any reason, usually leading to heart failure; common symptoms are dyspnea (breathlessness) and peripheral edema (swelling of the legs). People with cardiomyopathy are often at risk of dangerous forms of irregular heart beat and sudden cardiac death.[1] The most common form of cardiomyopathy is dilated cardiomyopathy.[2][3]

Chronic obstructive pulmonary disease
Chronic obstructive pulmonary disease (COPD), also known as chronic obstructive lung disease (COLD), chronic obstructive airway disease (COAD), chronic airflow limitation (CAL) and chronic obstructive respiratory disease (CORD), is the occurrence of chronic bronchitis or emphysema, a pair of commonly co-existing diseases of the lungs in which the airways become narrowed.[1] This leads to a limitation of the flow of air to and from the lungs, causing shortness of breath (dyspnea). In clinical practice, COPD is defined by its characteristically low airflow on lung function tests.[2] In contrast to asthma, this limitation is poorly reversible and usually gets progressively worse over time. In England, an estimated 842,100 of 50 million people have a diagnosis of COPD.[3]
COPD is caused by noxious particles or gas, most commonly from tobacco smoking, which triggers an abnormal inflammatory response in the lung.[4]
The diagnosis of COPD requires lung function tests. Important management strategies are smoking cessation, vaccinations, rehabilitation, and drug therapy (often using inhalers). Some patients go on to require long-term oxygen therapy or lung transplantation.[4]
Worldwide, COPD ranked as the sixth leading cause of death in 1990. It is projected to be the fourth leading cause of death worldwide by 2030 due to an increase in smoking rates and demographic changes in many countries.[5] COPD is the third leading cause of death in the U.S. and the economic burden of COPD in the U.S. in 2007 was $42.6 billion in health care costs and lost productivity.[6][7]

Chronic kidney disease
Chronic kidney disease (CKD), also known as chronic renal disease, is a progressive loss in renal function over a period of months or years. The symptoms of worsening kidney function are unspecific, and might include feeling generally unwell and experiencing a reduced appetite. Often, chronic kidney disease is diagnosed as a result of screening of people known to be at risk of kidney problems, such as those with high blood pressure or diabetes and those with a blood relative with chronic kidney disease. Chronic kidney disease may also be identified when it leads to one of its recognized complications, such as cardiovascular disease, anemia or pericarditis.[1]
Chronic kidney disease is identified by a blood test for creatinine. Higher levels of creatinine indicate a lower glomerular filtration rate and as a result a decreased capability of the kidneys to excrete waste products. Creatinine levels may be normal in the early stages of CKD, and the condition is discovered if urinalysis (testing of a urine sample) shows that the kidney is allowing the loss of protein or red blood cells into the urine. To fully investigate the underlying cause of kidney damage, various forms of medical imaging, blood tests and often renal biopsy (removing a small sample of kidney tissue) are employed to find out if there is a reversible cause for the kidney malfunction.[1] Recent professional guidelines classify the severity of chronic kidney disease in five stages, with stage 1 being the mildest and usually causing few symptoms and stage 5 being a severe illness with poor life expectancy if untreated. Stage 5 CKD is also called established chronic kidney disease and is synonymous with the now outdated terms end-stage renal disease (ESRD), chronic kidney failure (CKF) or chronic renal failure (CRF).[1]
There is no specific treatment unequivocally shown to slow the worsening of chronic kidney disease. If there is an underlying cause to CKD, such as vasculitis, this may be treated directly to slow the damage. In more advanced stages, treatments may be required for anemia and bone disease. Severe CKD requires renal replacement therapy, which may involve a form of dialysis, but ideally constitutes a kidney transplant.[1]

Coronary artery disease
Coronary artery disease (CAD; also atherosclerotic heart disease) is the result of the accumulation of atheromatous plaques [this plaque is made up of fat, cholestrol etc.] within the walls of the coronary arteries[1] that supply the myocardium (the muscle of the heart) with oxygen and nutrients,the filling up of the plaque in the lumen(free space in the artery for the flow of nutrients, oxygen etc.) of artery causes narrowing of lumen of the artery by decreasing its diameter. It is sometimes also called coronary heart disease (CHD).
CAD is the leading cause of death worldwide.[2][3] While the symptoms and signs of coronary artery disease are noted in the advanced state of disease, most individuals with coronary artery disease show no evidence of disease for decades as the disease progresses before the first onset of symptoms, often a “sudden” heart attack, finally arises. After decades of progression, some of these atheromatous plaques may rupture and (along with the activation of the blood clotting system) start limiting blood flow to the heart muscle. The disease is the most common cause of sudden death,[4] and is also the most common reason for death of men and women over 20 years of age.[5] According to present trends in the United States, half of healthy 40-year-old males will develop CAD in the future, and one in three healthy 40-year-old women.[6] According to the Guinness Book of Records, Northern Ireland is the country with the most occurrences of CAD. By contrast, the Maasai of Africa have almost no heart disease.
As the degree of coronary artery disease progresses, there may be near-complete obstruction of the lumen of the coronary artery, severely restricting the flow of oxygen-carrying blood to the myocardium. Individuals with this degree of coronary artery disease typically have suffered from one or more myocardial infarctions (heart attacks), and may have signs and symptoms of chronic coronary ischemia, including symptoms of angina at rest and flash pulmonary edema.
A distinction should be made between myocardial ischemia and myocardial infarction. Ischemia means that the amount of blood supplied to the tissue is inadequate to supply the needs of the tissue. When the myocardium becomes ischemic, it does not function optimally. When large areas of the myocardium becomes ischemic, there can be impairment in the relaxation and contraction of the myocardium. If the blood flow to the tissue is improved, myocardial ischemia can be reversed. Infarction means that the tissue has undergone irreversible death due to lack of sufficient oxygen-rich blood.
An individual may develop a rupture of an atheromatous plaque at any stage of the spectrum of coronary artery disease. The acute rupture of a plaque may lead to an acute myocardial infarction (heart attack)

Crohn’s disease
Crohn’s disease, also known as regional enteritis, is a type of inflammatory bowel disease that may affect any part of the gastrointestinal tract from mouth to anus, causing a wide variety of symptoms. It primarily causes abdominal pain, diarrhea (which may be bloody if inflammation is at its worst), vomiting (can be continuous), or weight loss,[1][2][3] but may also cause complications outside the gastrointestinal tract such as skin rashes, arthritis, inflammation of the eye, tiredness, and lack of concentration.[1] Crohn’s disease is caused by interactions between environmental, immunological and bacterial factors in genetically susceptible individuals.[4][5][6] This results in a chronic inflammatory disorder, in which the body’s immune system attacks the gastrointestinal tract possibly directed at microbial antigens.[5][7] Crohn’s disease has traditionally been described as an autoimmune disease, but recent investigators have described it as an immune deficiency state.[8][9][10][11]
There is a genetic association with Crohn’s disease, primarily with variations of the NOD2 gene and its protein, which senses bacterial cell walls. Siblings of affected individuals are at higher risk.[12] Males and females are equally affected. Smokers are two times more likely to develop Crohn’s disease than nonsmokers.[13] Crohn’s disease affects between 400,000 and 600,000 people in North America.[14] Prevalence estimates for Northern Europe have ranged from 27–48 per 100,000.[15] Crohn’s disease tends to present initially in the teens and twenties, with another peak incidence in the fifties to seventies, although the disease can occur at any age.[1][16] There is no known pharmaceutical or surgical cure for Crohn’s disease.[17] Treatment options are restricted to controlling symptoms, maintaining remission, and preventing relapse. The disease was named after gastroenterologist Burrill Bernard Crohn, who, in 1932, together with two other colleagues at Mount Sinai Hospital in New York, described a series of patients with inflammation of the terminal ileum, the area most commonly affected by the illness.[18]

Diabetes insipidus
Diabetes insipidus (DI) is a condition characterized by excessive thirst and excretion of large amounts of severely diluted urine, with reduction of fluid intake having no effect on the concentration of the urine. There are several different types of DI, each with a different cause. The most common type in humans is central DI, caused by a deficiency of arginine vasopressin (AVP), also known as antidiuretic hormone (ADH). The second common type of DI is nephrogenic diabetes insipidus, which is caused by an insensitivity of the kidneys to ADH. It can also be an iatrogenic artifact of drug use.
Although they have a common name, diabetes mellitus and diabetes insipidus are two entirely separate conditions with unrelated mechanisms. Both cause large amounts of urine to be produced (polyuria), and the term “diabetes” is derived from the Greek name for this symptom. However, diabetes insipidus is either a problem with the production of antidiuretic hormone (cranial diabetes insipidus) or kidney’s response to antidiuretic hormone (nephrogenic diabetes insipidus), whereas diabetes mellitus causes polyuria via a process called osmotic diuresis, due to the high blood sugar leaking into the urine and taking excess water along with it.
The incidence of diabetes insipidus in the general population is three in 100,000.[

Diabetes mellitus
Diabetes mellitus, or simply diabetes, is a group of metabolic diseases in which a person has high blood sugar, either because the body does not produce enough insulin, or because cells do not respond to the insulin that is produced.[2] This high blood sugar produces the classical symptoms of polyuria (frequent urination), polydipsia (increased thirst) and polyphagia (increased hunger).
There are three main types of diabetes mellitus (DM). Type 1 DM results from the body’s failure to produce insulin, and presently requires the person to inject insulin or wear an insulin pump. This form was previously referred to as “insulin-dependent diabetes mellitus” (IDDM) or “juvenile diabetes”. Type 2 DM results from insulin resistance, a condition in which cells fail to use insulin properly, sometimes combined with an absolute insulin deficiency. This form was previously referred to as non insulin-dependent diabetes mellitus (NIDDM) or “adult-onset diabetes”. The third main form, gestational diabetes occurs when pregnant women without a previous diagnosis of diabetes develop a high blood glucose level. It may precede development of type 2 DM.
Other forms of diabetes mellitus include 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.
All forms of diabetes have been treatable since insulin became available in 1921, and type 2 diabetes may be controlled with medications. Both types 1 and 2 are chronic conditions that cannot be cured. Pancreas transplants have been tried with limited success in type 1 DM; gastric bypass surgery has been successful in many with morbid obesity and type 2 DM. Gestational diabetes usually resolves after delivery. Diabetes without proper treatments can cause many complications. Acute complications include hypoglycemia, diabetic ketoacidosis, or nonketotic hyperosmolar coma. Serious long-term complications include cardiovascular disease, chronic renal failure, and diabetic retinopathy (retinal damage). Adequate treatment of diabetes is thus important, as well as blood pressure control and lifestyle factors such as smoking cessation and maintaining a healthy body weight.
Globally, as of 2012, an estimated 346 million people have type 2 diabetes[3].

Cardiac dysrhythmia
Cardiac dysrhythmia (also known as arrhythmia and irregular heartbeat) is any of a large and heterogeneous group of conditions in which there is abnormal electrical activity in the heart. The heartbeat may be too fast or too slow, and may be regular or irregular. A heart beat that is too fast is called tachycardia and a heart beat that is too slow is called bradycardia.
Some arrhythmias are life-threatening medical emergencies that can result in cardiac arrest. In fact, cardiac arrythmias are one of the most common causes of death when travelling to a hospital. Others cause symptoms such as an abnormal awareness of heart beat (palpitations), and may be merely uncomfortable. These palpitations have also been known to be caused by atrial/ventricular fibrillation, wire faults, and other technical or mechanical issues in cardiac pacemakers/defibrillators. Still others may not be associated with any symptoms at all, but may predispose the patient to potentially life threatening stroke or embolism.
The term sinus arrhythmia refers to a normal phenomenon of mild acceleration and slowing of the heart rate that occurs with breathing in and out. It is usually quite pronounced in children, and steadily decreases with age. This can also be present during meditation breathing exercises that involve deep inhaling and breath holding patterns. Proarrhythmia is a new or more frequent occurrence of pre-existing arrhythmias, paradoxically precipitated by antiarrhythmic therapy, which means it is a side effect associated with the administration of some existing antiarrhythmic drugs, as well as drugs for other indications. In other words, it is a tendency of antiarrhythmic drugs to facilitate emergence of new arrhythmias. Some arrhythmias are very minor and can be regarded as normal variants. In fact, most people will on occasion feel their heart skip a beat, or give an occasional extra strong beat; neither of these is usually a cause for alarm.[1]

Epilepsy (from Ancient Greek ἐπιληψία), is a common and diverse set of chronic neurological disorders characterized by seizures.[1] Some definitions of epilepsy require that seizures be recurrent and unprovoked,[1][2][3] but others require only a single seizure combined with brain alterations which increase the chance of future seizures.[4]
Epileptic seizures result from abnormal, excessive or hypersynchronous neuronal activity in the brain.[4] About 50 million people worldwide have epilepsy, and nearly 90% of epilepsy occurs in developing countries.[2] Epilepsy becomes more common as people age.[5][6] Onset of new cases occurs most frequently in infants and the elderly.[7] As a consequence of brain surgery, epileptic seizures may occur in recovering patients.
Epilepsy is usually controlled, but not cured, with medication. However, over 30% of people with epilepsy do not have seizure control even with the best available medications. Surgery may be considered in difficult cases.[8][9] Not all epilepsy syndromes are lifelong – some forms are confined to particular stages of childhood. Epilepsy should not be understood as a single disorder, but rather as syndromic with vastly divergent symptoms, all involving episodic abnormal electrical activity in the brain and numerous seizures.

Glaucoma is an eye disease in which the optic nerve is damaged in a characteristic pattern. This can permanently damage vision in the affected eye(s) and lead to blindness if left untreated. It is normally associated with increased fluid pressure in the eye (aqueous humour).[1] The term ‘ocular hypertension’ is used for people with consistently raised intraocular pressure (IOP) without any associated optic nerve damage. Conversely, the term ‘normal tension’ or ‘low tension’ glaucoma is used for those with optic nerve damage and associated visual field loss, but normal or low IOP.
The nerve damage involves loss of retinal ganglion cells in a characteristic pattern. The many different subtypes of glaucoma can all be considered to be a type of optic neuropathy. Raised intraocular pressure (above 21 mmHg or 2.8 kPa) is the most important and only modifiable risk factor for glaucoma. However, some may have high eye pressure for years and never develop damage, while others can develop nerve damage at a relatively low pressure. Untreated glaucoma can lead to permanent damage of the optic nerve and resultant visual field loss, which over time can progress to blindness.
Glaucoma can be roughly divided into two main categories, “open-angle” and “closed-angle” (or “angle closure”) glaucoma. The angle refers to the area between the iris and cornea, through which fluid must flow to escape via the trabecular meshwork. Closed-angle glaucoma can appear suddenly and is often painful; visual loss can progress quickly, but the discomfort often leads patients to seek medical attention before permanent damage occurs. Open-angle, chronic glaucoma tends to progress at a slower rate and patients may not notice they have lost vision until the disease has progressed significantly.
Glaucoma has been called the “silent thief of sight” because the loss of vision often occurs gradually over a long period of time, and symptoms only occur when the disease is quite advanced. Once lost, vision cannot normally be recovered, so treatment is aimed at preventing further loss. Worldwide, glaucoma is the second-leading cause of blindness after cataracts.[2] It is also the leading cause of blindness among African Americans.[3] Glaucoma affects one in 200 people aged 50 and younger, and one in 10 over the age of eighty. If the condition is detected early enough, it is possible to arrest the development or slow the progression with medical and surgical means.
The word “glaucoma” comes from the Greek γλαύκωμα, “opacity of the crystalline lens”. (Cataracts and glaucoma were not distinguished until circa 1705).[4]

Haemophilia ( /hiːməˈfɪliə/; also spelled hemophilia in North America, from the Greek haima αἷμα ‘blood’ and philia φιλία ‘love'[1]) is a group of hereditary genetic disorders that impair the body’s ability to control blood clotting or coagulation, which is used to stop bleeding when a blood vessel is broken. Haemophilia A (clotting factor VIII deficiency) is the most common form of the disorder, present in about 1 in 5,000–10,000 male births.[2] Haemophilia B (factor IX deficiency) occurs in around 1 in about 20,000–34,000 male births.
Like most recessive sex-linked, X chromosome disorders, haemophilia is more likely to occur in males than females. This is because females have two X chromosomes while males have only one, so the defective gene is guaranteed to manifest in any male who carries it. Because females have two X chromosomes and haemophilia is rare, the chance of a female having two defective copies of the gene is very remote, so females are almost exclusively asymptomatic carriers of the disorder. Female carriers can inherit the defective gene from either their mother or father, or it may be a new mutation. Although it is not impossible for a female to have haemophilia, it is unusual: a female with haemophilia A or B would have to be the daughter of both a male haemophiliac and a female carrier, while the non-sex-linked haemophilia C due to coagulant factor XI deficiency, which can affect either sex, is more common in Jews of Ashkenazi (east European) descent[3] but rare in other population groups.
Haemophilia lowers blood plasma clotting factor levels of the coagulation factors needed for a normal clotting process. Thus when a blood vessel is injured, a temporary scab does form, but the missing coagulation factors prevent fibrin formation, which is necessary to maintain the blood clot. A haemophiliac does not bleed more intensely than a person without it, but can bleed for a much longer time. In severe haemophiliacs even a minor injury can result in blood loss lasting days or weeks, or even never healing completely. In areas such as the brain or inside joints, this can be fatal or permanently debilitating.

Hyperlipidemia, hyperlipoproteinemia, or hyperlipidaemia (British English) involves abnormally elevated levels of any or all lipids and/or lipoproteins in the blood.[1] It is the most common form of dyslipidemia (which also includes any decreased lipid levels).
Lipids (fat-soluble molecules) are transported in a protein capsule. The size of that capsule, or lipoprotein, determines its density. The lipoprotein density and type of apolipoproteins it contains determines the fate of the particle and its influence on metabolism.
Hyperlipidemias are divided in primary and secondary subtypes. Primary hyperlipidemia is usually due to genetic causes (such as a mutation in a receptor protein), while secondary hyperlipidemia arises due to other underlying causes such as diabetes. Lipid and lipoprotein abnormalities are common in the general population, and are regarded as a modifiable risk factor for cardiovascular disease due to their influence on atherosclerosis. In addition, some forms may predispose to acute pancreatitis.

Hypertension (HTN) or high blood pressure, sometimes called arterial hypertension, is a chronic medical condition in which the blood pressure in the arteries is elevated. This requires the heart to work harder than normal to circulate blood through the blood vessels. Blood pressure involves two measurements, systolic and diastolic, which depend on whether the heart muscle is contracting (systole) or relaxed between beats (diastole). Normal blood pressure at rest is within the range of 100-140mmHg systolic (top reading) and 60-90mmHg diastolic (bottom reading). High blood pressure is said to be present if it is persistently at or above 140/90 mmHg.
Hypertension is classified as either primary (essential) hypertension or secondary hypertension; about 90–95% of cases are categorized as “primary hypertension” which means high blood pressure with no obvious underlying medical cause.[1] The remaining 5–10% of cases (secondary hypertension) are caused by other conditions that affect the kidneys, arteries, heart or endocrine system.
Hypertension is a major risk factor for stroke, myocardial infarction (heart attacks), heart failure, aneurysms of the arteries (e.g. aortic aneurysm), peripheral arterial disease and is a cause of chronic kidney disease. Even moderate elevation of arterial blood pressure is associated with a shortened life expectancy. Dietary and lifestyle changes can improve blood pressure control and decrease the risk of associated health complications, although drug treatment is often necessary in people for whom lifestyle changes prove ineffective or insufficient.

Hypothyroidism /ˌhaɪpɵˈθaɪərɔɪdɪzəm/ is a condition in which the thyroid gland does not make enough thyroid hormone.
Iodine deficiency is often cited as the most common cause of hypothyroidism worldwide but it can be caused by many other factors. It can result from a lack of a thyroid gland or from iodine-131 treatment, and can also be associated with increased stress. Severe hypothyroidism in infants can result in cretinism.
A 2011 study concluded that about 8% of women over 50 and men over 65 in the UK suffer from an under-active thyroid and that as many as 100,000 of these people could benefit from treatment they are currently not receiving.[1]

Multiple sclerosis
Multiple sclerosis (MS), also known as “disseminated sclerosis” or “encephalomyelitis disseminata”, is an inflammatory disease in which the fatty myelin sheaths around the axons of the brain and spinal cord are damaged, leading to demyelination and scarring as well as a broad spectrum of signs and symptoms.[1] Disease onset usually occurs in young adults, and it is more common in women.[1] It has a prevalence that ranges between 2 and 150 per 100,000.[2] MS was first described in 1868 by Jean-Martin Charcot.[3]
MS affects the ability of nerve cells in the brain and spinal cord to communicate with each other effectively. Nerve cells communicate by sending electrical signals called action potentials down long fibers called axons, which are contained within an insulating substance called myelin. In MS, the body’s own immune system attacks and damages the myelin. When myelin is lost, the axons can no longer effectively conduct signals.[4] The name multiple sclerosis refers to scars (scleroses—better known as plaques or lesions) particularly in the white matter of the brain and spinal cord, which is mainly composed of myelin.[3] Although much is known about the mechanisms involved in the disease process, the cause remains unknown. Theories include genetics or infections. Different environmental risk factors have also been found.[4][5]
Almost any neurological symptom can appear with the disease, and often progresses to physical and cognitive disability.[4] MS takes several forms, with new symptoms occurring either in discrete attacks (relapsing forms) or slowly accumulating over time (progressive forms).[6] Between attacks, symptoms may go away completely, but permanent neurological problems often occur, especially as the disease advances.[6]
There is no known cure for multiple sclerosis. Treatments attempt to return function after an attack, prevent new attacks, and prevent disability.[4] MS medications can have adverse effects or be poorly tolerated, and many people pursue alternative treatments, despite the lack of supporting scientific study. The prognosis is difficult to predict; it depends on the subtype of the disease, the individual’s disease characteristics, the initial symptoms and the degree of disability the person experiences as time advances.[7] Life expectancy of people with MS is 5 to 10 years lower than that of the unaffected population.[1]

Parkinson’s disease
Parkinson’s disease (also known as Parkinson disease, Parkinson’s, idiopathic parkinsonism, primary parkinsonism, PD, or paralysis agitans) is a degenerative disorder of the central nervous system. The motor symptoms of Parkinson’s disease result from the death of dopamine-generating cells in the substantia nigra, a region of the midbrain; the cause of this cell death is unknown. Early in the course of the disease, the most obvious symptoms are movement-related; these include shaking, rigidity, slowness of movement and difficulty with walking and gait. Later, cognitive and behavioural problems may arise, with dementia commonly occurring in the advanced stages of the disease. Other symptoms include sensory, sleep and emotional problems. PD is more common in the elderly, with most cases occurring after the age of 50.
The main motor symptoms are collectively called parkinsonism, or a “parkinsonian syndrome”. Parkinson’s disease is often defined as a parkinsonian syndrome that is idiopathic (having no known cause), although some atypical cases have a genetic origin. Many risk and protective factors have been investigated: the clearest evidence is for an increased risk of PD in people exposed to certain pesticides and a reduced risk in tobacco smokers. The pathology of the disease is characterized by the accumulation of a protein called alpha-synuclein into inclusions called Lewy bodies in neurons, and from insufficient formation and activity of dopamine produced in certain neurons within parts of the midbrain. Lewy bodies are the pathological hallmark of the idiopathic disorder, and the distribution of the Lewy bodies throughout the Parkinsonian brain varies from one individual to another. The anatomical distribution of the Lewy bodies is often directly related to the expression and degree of the clinical symptoms of each individual. Diagnosis of typical cases is mainly based on symptoms, with tests such as neuroimaging being used for confirmation.
Modern treatments are effective at managing the early motor symptoms of the disease, mainly through the use of levodopa and dopamine agonists. As the disease progresses and dopaminergic neurons continue to be lost, these drugs eventually become ineffective at treating the symptoms and at the same time produce a complication called dyskinesia, marked by involuntary writhing movements. Diet and some forms of rehabilitation have shown some effectiveness at alleviating symptoms. Surgery and deep brain stimulation have been used to reduce motor symptoms as a last resort in severe cases where drugs are ineffective. Research directions include investigations into new animal models of the disease and of the potential usefulness of gene therapy, stem cell transplants and neuroprotective agents. Medications to treat non-movement-related symptoms of PD, such as sleep disturbances and emotional problems, also exist.
The disease is named after the English doctor James Parkinson, who published the first detailed description in An Essay on the Shaking Palsy in 1817. Several major organizations promote research and improvement of quality of life of those with the disease and their families. Public awareness campaigns include Parkinson’s disease day (on the birthday of James Parkinson, April 11) and the use of a red tulip as the symbol of the disease. People with parkinsonism who have enhanced the public’s awareness include Michael J. Fox and Muhammad Ali.

Rheumatoid arthritis
Rheumatoid arthritis (RA) is a chronic, systemic inflammatory disorder that may affect many tissues and organs, but principally attacks flexible (synovial) joints. The process involves an inflammatory response of the capsule around the joints (synovium) secondary to swelling (hyperplasia) of synovial cells, excess synovial fluid, and the development of fibrous tissue (pannus) in the synovium. The pathology of the disease process often leads to the destruction of articular cartilage and ankylosis (fusion) of the joints. Rheumatoid arthritis can also produce diffuse inflammation in the lungs, membrane around the heart (pericardium), the membranes of the lung (pleura), and white of the eye (sclera), and also nodular lesions, most common in subcutaneous tissue. Although the cause of rheumatoid arthritis is unknown, autoimmunity plays a pivotal role in both its chronicity and progression, and RA is considered a systemic autoimmune disease.
About 1% of the world’s population is afflicted by rheumatoid arthritis, women three times more often than men. Onset is most frequent between the ages of 40 and 50, but people of any age can be affected. In addition, individuals with the HLA-DR1 or HLA-DR4 serotypes have an increased risk for developing the disorder. It can be a disabling and painful condition, which can lead to substantial loss of functioning and mobility if not adequately treated. It is a clinical diagnosis made on the basis of symptoms, physical exam, radiographs (X-rays) and labs, although the American College of Rheumatology (ACR) and the European League Against Rheumatism (EULAR) publish classification criteria for the purpose of research. Diagnosis and long-term management are typically performed by a rheumatologist, an expert in joint, muscle and bone diseases.[1]
Various treatments are available. Non-pharmacological treatment includes physical therapy, orthoses, occupational therapy and nutritional therapy but these do not stop the progression of joint destruction. Analgesia (painkillers) and anti-inflammatory drugs, including steroids, are used to suppress the symptoms, while disease-modifying antirheumatic drugs (DMARDs) are required to inhibit or halt the underlying immune process and prevent long-term damage. In recent times, the newer group of biologics has increased treatment options.[1] Clinical trials have shown that consumption of fish oil reduces the number of swollen joints for people with rheumatoid arthritis[2] provides a beneficial anti-inflammatory effect, and provides a protective effect for occlusive cardiovascular disease, for which people with RA are at risk.[3]
The name is based on the term “rheumatic fever”, an illness which includes joint pain and is derived from the Greek word ῥεύμα-rheuma (nom.), ῥεύματος-rheumatos (gen.) (“flow, current”). The suffix -oid (“resembling”) gives the translation as joint inflammation that resembles rheumatic fever. The first recognized description of rheumatoid arthritis was made in 1800 by Dr. Augustin Jacob Landré-Beauvais (1772–1840) of Paris.[4]

Schizophrenia (/ˌskɪtsɵˈfrɛniə/ or /ˌskɪtsɵˈfriːniə/) is a mental disorder characterized by a breakdown of thought processes and by poor emotional responsiveness.[1] It most commonly manifests itself as auditory hallucinations, paranoid or bizarre delusions, or disorganized speech and thinking, and it is accompanied by significant social or occupational dysfunction. The onset of symptoms typically occurs in young adulthood, with a global lifetime prevalence of about 0.3–0.7%.[2] Diagnosis is based on observed behavior and the patient’s reported experiences.
Genetics, early environment, neurobiology, and psychological and social processes appear to be important contributory factors; some recreational and prescription drugs appear to cause or worsen symptoms. Current research is focused on the role of neurobiology, although no single isolated organic cause has been found. The many possible combinations of symptoms have triggered debate about whether the diagnosis represents a single disorder or a number of discrete syndromes. Despite the etymology of the term from the Greek roots skhizein (σχίζειν, “to split”) and phrēn, phren- (φρήν, φρεν-; “mind”), schizophrenia does not imply a “split personality”, or “multiple personality disorder” (which is known these days as dissociative identity disorder)—a condition with which it is often confused in public perception.[3] Rather, the term means a “splitting of mental functions”, because of the symptomatic presentation of the illness.
The mainstay of treatment is antipsychotic medication, which primarily suppresses dopamine (and sometimes serotonin) receptor activity. Psychotherapy and vocational and social rehabilitation are also important in treatment. In more serious cases—where there is risk to self and others—involuntary hospitalization may be necessary, although hospital stays are now shorter and less frequent than they once were.[4]
The disorder is thought mainly to affect cognition, but it also usually contributes to chronic problems with behavior and emotion. People with schizophrenia are likely to have additional (comorbid) conditions, including major depression and anxiety disorders; the lifetime occurrence of substance abuse is almost 50%.[5] Social problems, such as long-term unemployment, poverty and homelessness, are common. The average life expectancy of people with the disorder is 12 to 15 years less than those without, the result of increased physical health problems and a higher suicide rate (about

Systemic lupus erythematosus
Systemic lupus erythematosus ( i/sɪˈstɛmɪk ˈluːpəs ˌɛrɪθiːməˈtoʊsəs/), often abbreviated to SLE or lupus, is a systemic autoimmune disease (or autoimmune connective tissue disease) that can affect any part of the body. As occurs in other autoimmune diseases, the immune system attacks the body’s cells and tissue, resulting in inflammation and tissue damage.[1] It is a Type III hypersensitivity reaction caused by antibody-immune complex formation.
SLE most often harms the heart, joints, skin, lungs, blood vessels, liver, kidneys, and nervous system. The course of the disease is unpredictable, with periods of illness (called flares) alternating with remissions. The disease occurs nine times more often in women than in men, especially in women in child-bearing years ages 15 to 35, and is also more common in those of non-European descent.[2][3][4]
SLE is treatable using immunosuppression, mainly with cyclophosphamide, corticosteroids and other immunosuppressants; there is currently no cure. SLE can be fatal, although with recent medical advances, fatalities are becoming increasingly rare. Survival for people with SLE in the United States, Canada, and Europe has risen to approximately 95% at five years, 90% at 10 years, and 78% at 20 years,[4] and now approaches that of matched controls without lupus.
Childhood systemic lupus erythematosus generally presents between the ages of 3 and 15, with girls outnumbering boys 4:1, and typical skin manifestations being butterfly eruption on the face and photosensitivity.[1]

Ulcerative colitis
Ulcerative colitis (Colitis ulcerosa, UC) is a form of inflammatory bowel disease (IBD). Ulcerative colitis is a form of colitis, a disease of the colon (large intestine), that includes characteristic ulcers, or open sores. The main symptom of active disease is usually constant diarrhea mixed with blood, of gradual onset. The gradual loss of blood from the gastrointestinal tract often leads to patients becoming anaemic which guidelines suggest routinely monitoring for. Treatment of anaemia can be either from oral iron, but in many cases parenteral iron is required[1].
IBD is often confused with irritable bowel syndrome (IBS), a troublesome, but much less serious, condition.
Ulcerative colitis has similarities to Crohn’s disease, another form of IBD. Ulcerative colitis is an intermittent disease, with periods of exacerbated symptoms, and periods that are relatively symptom-free. Although the symptoms of ulcerative colitis can sometimes diminish on their own, the disease usually requires treatment to go into remission. Ulcerative colitis occurs in 35–100 people for every 100,000 in the United States,[2] or less than 0.1% of the population.
The disease is more prevalent in northern countries of the world, as well as in northern areas of individual countries or other regions. Rates tend to be higher in more affluent countries,which may indicate the increased prevelance is due to increased rates of diagnosis. Although ulcerative colitis has no known cause, there is a presumed genetic component to susceptibility. The disease may be triggered in a susceptible person by environmental factors. Although dietary modification may reduce the discomfort of a person with the disease, ulcerative colitis is not thought to be caused by dietary factors.
Ulcerative colitis is treated as an autoimmune disease. Treatment is with anti-inflammatory drugs, immunosuppression, and biological therapy targeting specific components of the immune response. Colectomy (partial or total removal of the large bowel through surgery) is occasionally necessary, but is not a cure for the disease.