Rabies

HISTORY
Rabies is a viral disease that causes acute encephalitis in warm-blooded animals.[1] The disease is
zoonotic, meaning it can be transmitted to humans from another species (such as dogs), commonly by a bite from an infected animal. For a human, rabies is almost invariably fatal if postexposure prophylaxis is not administered prior to the onset of severe symptoms. The rabies virus infects the central nervous system, ultimately causing disease in the brain and death. The rabies virus travels to the brain by following the peripheral nerves. The incubation period of the disease is usually a few months in humans, depending on the distance the virus must travel to reach the central nervous system.[2] Once the rabies virus reaches the central nervous system and symptoms begin to show, the infection is virtually untreatable and usually fatal within days. Early-stage symptoms of rabies are malaise, headache and fever, progressing to acute pain, violent movements, uncontrolled excitement, depression, and hydrophobia.[1] Finally, the patient may experience periods of mania and lethargy, eventually leading to coma. The primary cause of death is usually respiratory insufficiency.[2] Rabies causes about 55,000 human deaths annually worldwide.[3] 95% of human deaths due to rabies occur in Asia and Africa.[4] Roughly 97% of human rabies cases result from dog bites.[5] In the United States, animal control and vaccination programs have effectively eliminated domestic dogs as reservoirs of rabies.[6] In several countries, including Australia, Japan, and Singapore, rabies carried by terrestrial animals has been eliminated entirely.[7] While classical rabies has been eradicated in the United Kingdom, bats infected with a related virus have been found in the country on rare occasions.[8]

SIGNS/SYMPTOMS
The period between infection and the first flu-like symptoms is typically 2 to 12 weeks, but incubation periods as short as four days and longer than six years have been documented, depending on the location and severity of the inoculating wound and the amount of virus introduced. Soon after, the symptoms may expand to slight or partial paralysis, anxiety, insomnia, confusion, agitation, abnormal behavior, paranoia, terror, and hallucinations, progressing to delirium.[2][9] Saliva production is greatly increased, and attempts to drink, or even the intention or suggestion of drinking may cause excruciatingly painful spasms of the muscles in the throat and larynx. Hydrophobia (fear of water), the historic name for the disease, refers to the dread of swallowing fluids these patients exhibit.[10][clarification needed] Death almost invariably results 2 to 10 days after first symptoms. Once symptoms have presented, survival is rare, even with the administration of proper and intensive care.[11] In 2005, Jeanna Giese, the first patient treated with the Milwaukee protocol,[12] became the first person ever recorded to have survived rabies without receiving successful post-exposure prophylaxis. An intention-to-treat analysis has since found this protocol has a survival rate of about 8%.

PREVENTION
All human cases of rabies were fatal until a vaccine was developed in 1885 by Louis Pasteur and mile Roux. Their original vaccine was harvested from infected rabbits, from which the virus in the nerve tissue was weakened by allowing it to dry for five to 10 days.[42] Similar nerve tissue-derived vaccines are still used in some countries, as they are much cheaper than modern cell culture vaccines.[43]

The human diploid cell rabies vaccine was started in 1967; a new and less expensive purified chicken embryo cell vaccine and purified vero cell rabies vaccine are now available.[37] A recombinant vaccine called V-RG has been successfully used in Belgium, France, Germany, and the United States to prevent outbreaks of rabies in undomesticated animals.[44] Currently, immunization prior to exposure has been used in both human and nonhuman populations, where, as in many jurisdictions, domesticated animals are required to be vaccinated In the United States, since the widespread vaccination of domestic dogs and cats and the development of effective human vaccines and immunoglobulin treatments, the number of recorded human deaths from rabies has dropped from 100 or more annually in the early 20th century to one to two per year, mostly caused by bat bites, which may go unnoted by the victim and hence untreated.[6] The Missouri Department of Health and Senior Services Communicable Disease Surveillance 2007 Annual Report states the following can help reduce the risk of contracting rabies:[46] Vaccinating dogs, cats, rabbits, and ferrets against rabies Keeping pets under supervision Not handling wild animals or strays Contacting an animal control officer upon observing a wild animal or a stray, especially if the animal is acting strangely If bitten by an animal, washing the wound with soap and water for 10 to 15 minutes and contacting a healthcare provider to determine if post-exposure prophylaxis is required September 28 is World Rabies Day, which promotes the information, prevention, and elimination of the disease

Sexually transmitted disease

HISTORY
The first well-recorded European outbreak of what is now known as syphilis occurred in 1494 when it broke out among French troops besieging Naples.[56] From this centre, the disease swept across Europe, killing more than five million people.[57] As Jared Diamond describes it, "[W]hen syphilis was first definitely recorded in Europe in 1495, its pustules often covered the body from the head to the knees, caused flesh to fall from people's faces, and led to death within a few months," rendering it far more fatal than it is today. Diamond concludes,"[B]y 1546, the disease had evolved into the disease with the symptoms so well known to us today."[58] Prior to the invention of modern medicines, sexually transmitted diseases were generally incurable, and treatment was limited to treating the symptoms of the disease. The first voluntary hospital for venereal diseases was founded in 1746 at London Lock Hospital.[59] Treatment was not always voluntary: in the second half of the 19th century, the Contagious Diseases Act was used to arrest suspected prostitutes. In 1924, a number states concluded the Brussels Agreement, whereby states agreed to provide free or low-cost medical treatment at ports for merchant seamen with venereal diseases. The first effective treatment for a sexually transmitted disease was salvarsan, a treatment for syphilis. With the discovery of antibiotics, a large number of sexually transmitted diseases became easily curable, and this, combined with effective public health campaigns against STDs, led to a public perception during the 1960s and 1970s that they have ceased to be a serious medical threat. During this period, the importance of contact tracing in treating STIs was recognized. By tracing the sexual partners of infected individuals, testing them for infection, treating the infected and tracing their contacts in turn, STI clinics could be very effective at suppressing infections in the general population. In the 1980s, first genital herpes and then AIDS emerged into the public consciousness as sexually transmitted diseases that could not be cured by modern medicine. AIDS in particular has a long asymptomatic periodduring which time HIV (the human immunodeficiency virus, which causes AIDS) can replicate and the disease can be transmitted to othersfollowed by a symptomatic period, which leads rapidly to death unless treated. HIV/AIDS entered the United States in about 1969 likely through a single infected immigrant from Haiti.[60] Recognition that AIDS threatened a global pandemic led to public information campaigns and the development of treatments that allow AIDS to be managed by suppressing the replication of HIV for as long as possible. Contact tracing continues to be an important measure, even when diseases are incurable, as it helps to contain infection.

SIGNS/SYMPTOMS
Most STDs affect both men and women, but in many cases the health problems they cause can be more severe for women. If a pregnant woman has an STD, it can cause serious health problems for the baby. If you have an STD caused by bacteria or parasites, your health care provider can treat it with antibiotics or other medicines. If you have an STD caused by a virus, there is no cure. Sometimes medicines can keep the disease under control. Correct usage of latex condoms greatly reduces, but does not completely eliminate, the risk of catching or spreading STDs.

PREVENTION
Prevention is key in addressing incurable STIs, such as HIV and herpes. Sexual health clinics promote the use of condoms and provide outreach for at-risk communities. The most effective way to prevent sexual transmission of STIs is to avoid contact of body parts or fluids which can lead to transfer with an infected partner. Not all sexual activities involve contact: cybersex, phonesex or masturbation from a distance are methods of avoiding contact. Proper use of condoms reduces contact and risk. Although a condom is effective in limiting exposure, some disease transmission may occur even with a condom.[38] Both partners should get tested for STIs before initiating sexual contact, or before resuming contact if a partner engaged in contact with someone else. Many infections are not detectable immediately after exposure, so enough time must be allowed between possible exposures and testing for the tests to be accurate. Certain STIs, particularly certain persistent viruses like HPV, may be impossible to detect with current medical procedures. Many diseases that establish permanent infections can so occupy the immune system that other diseases become more easily transmitted. The innate immune system led by defensins against HIV can prevent transmission of HIV when viral counts are very low, but if busy with other viruses or overwhelmed, HIV can establish itself. Certain viral STI's also greatly increase the risk of death for HIV infected patients.

Tuberculosis

HISTORY
Tuberculosis has been present in humans since antiquity at the latest The earliest unambiguous detection of M. tuberculosis involves evidence of the disease in the remains of bison dated to approximately 17,000 years ago. However, whether tuberculosis originated in bovines, then was transferred to humans, or whether it diverged from a common ancestor, is currently unclear A comparison of the genes of M. tuberculosis complex (MTBC) in humans to MTBC in animals suggests humans did not acquire MTBC from animals during animal domestication, as was previously believed. Both strains of the tuberculosis bacteria share a common ancestor, which could have infected humans as early as the Neolithic Revolution.] Skeletal remains show prehistoric humans (4000 BC) had TB, and researchers have found tubercular decay in the spines of Egyptian mummies dating from 30002400 BC. Phthisis is a Greek word for consumption, an old term for pulmonary tuberculosis; around 460 BC, Hippocrates identified phthisis as the most widespread disease of the times. It was said to involve fever and the coughing up of blood, which was almost always fatal. Genetic studies suggest TB was present in the Americas from about the year 100 AD Before the Industrial Revolution, folklore often associated tuberculosis with vampires. When one member of a family died from it, the other infected members would lose their health slowly. People believed this was caused by the original person with TB draining the life from the other family members

SIGNS/SYMPTOMS
Tuberculosis may infect any part of the body, but most commonly occurs in the lungs (known as pulmonary tuberculosis). Extrapulmonary TB occurs when tuberculosis develops outside of the lungs, although extrapulmonary TB may coexist with pulmonary TB as well. General signs and symptoms include fever, chills, night sweats, loss of appetite, weight loss, and fatigue. Significant finger clubbing may also occur.

PREVENTION
Tuberculosis prevention and control efforts primarily rely on the vaccination of infants and the detection and appropriate treatment of active cases. The World Health Organization has achieved some success with improved treatment regimens, and a small decrease in case numbers.

Pertussis
HISTORY
B. pertussis was isolated in pure culture in 1906 by Jules Bordet and Octave Gengou, who also developed the first serology and vaccine. Efforts to develop an inactivated whole-cell pertussis vaccine began soon after B. pertussis was grown in pure culture in 1906. In the 1920s, Dr. Louis W. Sauer developed a vaccine for whooping cough at Evanston Hospital (Evanston, IL). In 1925, the Danish physician Thorvald Madsen was the first to test a whole-cell pertussis vaccine on a wide scale.[41] He used the vaccine to control outbreaks in the Faroe Islands in the North Sea. In 1942, the American scientist Pearl Kendrick combined the whole-cell pertussis vaccine with diphtheria and tetanus toxoids to generate the first DTP combination vaccine. To minimize the frequent side effects caused by the pertussis component of the vaccine, the Japanese scientist Yuji Sato developed an acellular pertussis vaccine consisting of purified haemagglutinins (HAs: filamentous strep throat and leucocytosispromoting-factor HA), which are secreted by B. pertussis into the culture medium. Sato's acellular pertussis vaccine was used in Japan since 1981.[42] Later versions of the acellular pertussis vaccine used in other countries consisted of additional defined components of B. pertussis and were often part of the DTaP combination vaccine. The complete B. pertussis genome of 4,086,186 base pairs was sequenced in 2004

SIGNS/SYMPTOMS
The classic symptoms of pertussis are a paroxysmal cough, inspiratory whoop, and fainting and/or vomiting after coughing.[5] The cough from pertussis has been documented to cause subconjunctival hemorrhages, rib fractures, urinary incontinence, hernias, post-cough fainting, and vertebral artery dissection.[5] Violent coughing can cause the pleura to rupture, leading to a pneumothorax. If there is vomiting after a coughing spell or an inspiratory whooping sound on coughing, the likelihood almost doubles that the illness is pertussis. On the other hand, the absence of a paroxysmal cough or posttussive emesis makes it almost half as likely.[5] The incubation period is typically seven to ten days with a range of four to 21 days and rarely may be as long as 42 days,[6] after which there are usually mild respiratory symptoms, mild coughing, sneezing, or runny nose. This is known as the catarrhal stage. After one to two weeks, the coughing classically develops into uncontrollable fits, each with five to ten forceful coughs, followed by a high-pitched "whoop" sound in younger children, or a gasping sound in older children, as the patient struggles to breathe in afterwards (paroxysmal stage). Fits can occur on their own or can be triggered by yawning, stretching, laughing, eating or yelling; they usually occur in groups, with multiple episodes every hour around the clock. This stage usually lasts two to eight weeks, or sometimes longer. A gradual transition then occurs to the convalescent stage, which usually lasts one to two weeks. This stage is marked by a decrease in paroxysms of coughing, both in frequency and severity, and a cessation of vomiting. A tendency to produce the "whooping" sound after coughing may remain for a considerable period after the disease itself has cleared up.

PREVENTION
The primary method of prevention for pertussis is vaccination. There is insufficient evidence to determine the effectiveness of antibiotics in those who have been exposed but are without symptoms.[8] Prophylactic antibiotics, however, are still frequently used in those who have been exposed and are at high risk of severe disease (such as infants)

Methicillin-resistant Staphylococcus aureus

HISTORY
In 1959 methicillin was licensed in England to treat penicillin-resistant S. aureus infections. Just as bacterial evolution had allowed microbes to develop resistance to penicillin, strains of S. aureus evolved to become resistant to methicillin. In 1961 the first known MRSA isolates were reported in a British study, and between 1961-1967 there were infrequent hospital outbreaks in Western Europe and Australia.[109] The first United States hospital outbreak of MRSA occurred at the Boston City Hospital in 1968. Between 1968-mid-1990s the percent of S. aureus infections that were caused by MRSA increased steadily, and MRSA became recognized as an endemic pathogen. In 1974 2% of hospital-acquired S. aureus infections could be attributed to MRSA.[110] The rate had increased to 22% by 1995, and by 1997 the percent of hospital S. aureus infections attributable to MRSA had reached 50%. The first report of CA-MRSA occurred in 1981, and in 1982 there was a large outbreak of CA-MRSA among intravenous drug users in Detroit, Michigan.[109] Additional outbreaks of CA-MRSA were reported through the 1980s and 1990s, including outbreaks among Australian Aboriginal populations that had never been exposed to hospitals. In the mid-1990s there were scattered reports of CA-MRSA outbreaks among US children. While HA-MRSA rates stabilized between 19982008, CA-MRSA rates continued to rise. A report released by the University of Chicago Children's Hospital comparing two time periods (19931995 and 19951997) found a 25-fold increase in the rate of hospitalizations due to MRSA among children in the United States.[111] In 1999 the University of Chicago reported the first deaths from invasive MRSA among otherwise healthy children in the United States.[109] By 2004 MRSA accounted for 64% of hospital-acquired S. aureus infections in the United States. The Office for National Statistics reported 1,629 MRSA-related deaths in England and Wales during 2005, indicating a MRSA-related mortality rate half the rate of that in the United States for 2005, even though the figures from the British source were explained to be high because of "improved levels of reporting, possibly brought about by the continued high public profile of the disease"[112] during the time of the 2005 United Kingdom General Election. MRSA is thought to have caused 1,652 deaths in 2006 in UK up from 51 in 1993.[113] It has been argued that the observed increased mortality among MRSA-infected patients may be the result of the increased underlying morbidity of these patients. Several studies, however, including one by Blot and colleagues, that have adjusted for underlying disease still found MRSA bacteremia to have a higher attributable mortality than methicillin-susceptible S. aureus (MSSA) bacteremia.[114] A population-based study of the incidence of MRSA infections in San Francisco during 200405 demonstrated that nearly 1 in 300 residents suffered from such an infection in the course of a year and that greater than 85% of these infections occurred outside of the healthcare setting.[115] A 2004 study showed that patients in the United States with S. aureus infection had, on average, three times the length of hospital stay (14.3 vs. 4.5 days), incurred three times the total cost ($48,824 vs $14,141), and experienced five times the risk of in-hospital death (11.2% vs 2.3%) than patients without this infection

SIGNS/SYMPTOMS
S. aureus most commonly colonizes the anterior nares (the nostrils). The rest of the respiratory tract, open wounds, intravenous catheters, and the urinary tract are also potential sites for infection. Healthy individuals may carry MRSA asymptomatically for periods ranging from a few weeks to many years. Patients with compromised immune systems are at a significantly greater risk of symptomatic secondary infection. In most patients, MRSA can be detected by swabbing the nostrils and isolating the bacteria found inside. Combined with extra sanitary measures for those in contact with infected patients, screening patients

admitted to hospitals has been found to be effective in minimizing the spread of MRSA in hospitals in the United States,[1] Denmark, Finland, and the Netherlands.[2] MRSA may progress substantially within 2448 hours of initial topical symptoms. After 72 hours, MRSA can take hold in human tissues and eventually become resistant to treatment. The initial presentation of MRSA is small red bumps that resemble pimples, spider bites, or boils; they may be accompanied by fever and, occasionally, rashes. Within a few days, the bumps become larger and more painful; they eventually open into deep, pus-filled boils.[3] About 75 percent of community-associated (CA-) MRSA infections are localized to skin and soft tissue and usually can be treated effectively.[4] But some CAMRSA strains display enhanced virulence, spreading more rapidly and causing illness much more severe than traditional healthcare-associated (HA-) MRSA infections, and they can affect vital organs and lead to widespread infection (sepsis), toxic shock syndrome, and necrotizing ("flesh-eating") pneumonia. This is thought to be due to toxins carried by CA-MRSA strains, such as PVL and PSM, though PVL was recently found not to be a factor in a study by the National Institute of Allergy and Infectious Diseases (NIAID) at the National Institutes of Health. (NIH) It is not known why some healthy people develop CAMRSA skin infections that are treatable while others infected with the same strain develop severe infections or die.[5] People are very commonly colonized with CA-MRSA and are completely asymptomatic. The most common manifestations of CA-MRSA are simple skin infections, such as impetigo, boils, abscesses, folliculitis, and cellulitis. Rarer, but more serious manifestations can occur, such as necrotizing fasciitis and pyomyositis (most commonly found in the tropics), necrotizing pneumonia, infective endocarditis (which affects the valves of the heart), and bone and joint infections.[6] CA-MRSA often results in abscess formation that requires incision and drainage. Before the spread of MRSA into the community, abscesses were not considered contagious, because it was assumed that infection required violation of skin integrity and the introduction of staphylococci from normal skin colonization. However, newly emerging CA-MRSA is transmissible (similar, but with very important differences) from HospitalAssociated MRSA. CA-MRSA is less likely than other forms of MRSA to cause cellulitis.

PREVENTION
Patient screening upon hospital admission, with nasal cultures, prevents the cohabitation of MRSA carriers with non-carriers, and exposure to infected surfaces. The test used (whether a rapid molecular method or traditional culture) is not as important as the implementation of active screening.[52] In the United States and Canada, the Centers for Disease Control and Prevention issued guidelines on October 19, 2006, citing the need for additional research, but declined to recommend such screening.[53][54] In some UK hospitals screening for MRSA is performed in every patient[55] and all NHS surgical patients, except for minor surgeries, are previously checked for MRSA.[56] There is no community screening in the UK; however, screening of individuals is offered by some private companies.[57] In a US cohort of 1300 healthy children, 2.4% carried MRSA in their nose

Headache
HISTORY
The first recorded classification system that resembles the modern ones was published by Thomas Willis, in De Cephalalgia in 1672. In 1787 Christian Baur generally divided headaches into idiopathic (primary headaches) and symptomatic (secondary ones), and defined 84 categories.[8]

SIGNS/SYMPTOMS
There are over 200 types of headaches, and the causes range from harmless to life-threatening. The description of the headache, together with findings on neurological examination, determines the need for any further investigations and the most appropriate treatment.[9]

PREVENTION
can suffer from the same types of headaches as adults do although their symptoms may vary. Some kinds of headaches include tension headaches, migraines, chronic daily headaches, cluster headache and sinus headaches.[25][unreliable source?] Dental braces and orthodontic headgear (due to the constant pressure placed on the jaw area) are also known for causing occasional to frequent headaches in adolescents. It is actually common for headaches to start in childhood or adolescence, for instance, 20% of adults who suffer headaches report that their headaches started before age 10 while 50% report they started before age 20. The incidence of headaches in children and adolescents is very common. One study reported that 56% of boys and 74% of girls between 12 and 17 indicated having experienced a form of headache within the past month.[26] The causes of headaches in children include either one factor or a combination of factors. Some of the most common factors include genetic predisposition, especially in the case of migraine; head trauma, produced by accidental falls; illness and infection, for example in the presence of ear or sinus infection as well as colds and flu; environmental factors, which include weather changes; emotional factors, such as stress, anxiety, and depression; foods and beverages, caffeine or food additives; change in sleep or routine pattern; loud noises. Also, excess physical activity or sun may be a trigger specifically of migraine.[27]

alzheimer's disease,
HISTORY
The ancient Greek and Roman philosophers and physicians associated old age with increasing dementia.[1] It was not until 1901 that German psychiatrist Alois Alzheimer identified the first case of what became known as Alzheimer's disease in a fifty-year-old woman he called Auguste D. He followed her case until she died in 1906, when he first reported publicly on it.[197] During the next five years, eleven similar cases were reported in the medical literature, some of them already using the term Alzheimer's disease.[1] The disease was first described as a distinctive disease by Emil Kraepelin after suppressing some of the clinical (delusions and hallucinations) and pathological features (arteriosclerotic changes) contained in the original report of Auguste D.[198] He included Alzheimer's disease, also named presenile dementia by Kraepelin, as a subtype of senile dementia in the eighth edition of his Textbook of Psychiatry, published on July 15, 1910.[199] For most of the 20th century, the diagnosis of Alzheimer's disease was reserved for individuals between the ages of 45 and 65 who developed symptoms of dementia. The terminology changed after 1977 when a conference on AD concluded that the clinical and pathological manifestations of presenile and senile dementia were almost identical, although the authors also added that this did not rule out the possibility that they had different causes.[200] This eventually led to the diagnosis of Alzheimer's disease independently of age.[201] The term senile dementia of the Alzheimer type (SDAT) was used for a time to describe the condition in those over 65, with classical Alzheimer's disease being used for those younger. Eventually, the term Alzheimer's disease was formally adopted in medical nomenclature to describe individuals of all ages with a characteristic common symptom pattern, disease course, and neuropathology.[202]

SIGNS/SYMPTOMS
The cause for most Alzheimer's cases is still mostly unknown except for 1% to 5% of cases where genetic differences have been identified.[34] Several competing hypotheses exist trying to explain the cause of the disease:

PREVENTION
At present, there is no definitive evidence to support that any particular measure is effective in preventing AD.[111] Global studies of measures to prevent or delay the onset of AD have often produced inconsistent results. However, epidemiological studies have proposed relationships between certain modifiable factors, such as diet, cardiovascular risk, pharmaceutical products, or intellectual activities among others, and a population's likelihood of developing AD. Only further research, including clinical trials, will reveal whether these factors can help to prevent AD.[112] Although cardiovascular risk factors, such as hypercholesterolaemia, hypertension, diabetes, and smoking, are associated with a higher risk of onset and course of AD,[113][114] statins, which are cholesterol lowering drugs, have not been effective in preventing or improving the course of the disease

Cancer
HISTORY
Cancer has existed for all of human history.[157] The earliest written record regarding cancer is from 3000 BC in the Egyptian Edwin Smith Papyrus and describes cancer of the breast.[157] Hippocrates (ca. 460 BC ca. 370 BC) described several kinds of cancer, referring to them with the Greek word karkinos (crab or crayfish).[157] This name comes from the appearance of the cut surface of a solid malignant tumour, with "the veins stretched on all sides as the animal the crab has its feet, whence it derives its name".[158] Galen stated that "cancer of the breast is so called because of the fancied resemblance to a crab given by the lateral prolongations of the tumor and the adjacent distended veins".[159]:738 Celsus (ca. 25 BC 50 AD) translated karkinos into the Latin cancer, also meaning crab and recommended surgery as treatment.[157] Galen (2nd century AD) disagreed with the use of surgery and recommended purgatives instead.[157] These recommendations largely stood for 1000 years.[157] In the 15th, 16th and 17th centuries, it became acceptable for doctors to dissect bodies to discover the cause of death.[160] The German professor Wilhelm Fabry believed that breast cancer was caused by a milk clot in a mammary duct. The Dutch professor Francois de la Boe Sylvius, a follower of Descartes, believed that all disease was the outcome of chemical processes, and that acidic lymph fluid was the cause of cancer. His contemporary Nicolaes Tulp believed that cancer was a poison that slowly spreads, and concluded that it was contagious

SIGNS/SYMPTOMS
General symptoms occur due to distant effects of the cancer that are not related to direct or metastatic spread. These may include: unintentional weight loss, fever, being excessively tired, and changes to the skin.[12] Hodgkin disease, leukemias, and cancers of the liver or kidney can cause a persistent fever of unknown origin.[11] Specific constellations of systemic symptoms, termed paraneoplastic phenomena, may occur with some cancers. Examples include the appearance of myasthenia gravis in thymoma and clubbing in lung cancer.[11]

PREVENTION
Cancer prevention is defined as active measures to decrease the risk of cancer.[95] The vast majority of cancer cases are due to environmental risk factors, and many, but not all, of these environmental factors are controllable lifestyle choices. Thus, cancer is considered a largely preventable disease.[96] Greater than 30% of cancer deaths could be prevented by avoiding risk factors including: tobacco, overweight / obesity, an insufficient diet, physical inactivity, alcohol, sexually transmitted infections, and air pollution.[97] Not all environmental causes are controllable, such as naturally occurring background radiation, and other cases of cancer are caused through hereditary genetic disorders, and thus it is not possible to prevent all cases of cancer.

arthritis

HISTORY
While evidence of primary ankle (kaki) osteoarthritis has been discovered in dinosaurs, the first known traces of human arthritis date back as far as 4500 BC. In early reports, arthritis was frequently referred to as the most common ailment of prehistoric peoples.[25] It was noted in skeletal remains of Native Americans found in Tennessee and parts of what is now Olathe, Kansas. Evidence of arthritis has been found throughout history, from tzi, a mummy (circa 3000 BC) found along the border of modern Italy and Austria, to the Egyptian mummies circa 2590 BC[26] In 1715 William Musgrave published the second edition of his most important medical work De arthritide symptomatica which concerned arthritis and its effects.[27] Blood tests and X-rays of the affected joints often are performed to make the diagnosis. Screening blood tests are indicated if certain arthritides are suspected. These might include: rheumatoid factor, antinuclear factor (ANF), extractable nuclear antigen, and specific antibodies.

SIGNS/SYMPTOMS
Regardless of the type of arthritis, the common symptoms for all arthritis disorders include varied levels of pain, swelling, joint stiffness, and sometimes a constant ache around the joint(s). Arthritic disorders like lupus and rheumatoid can also affect other organs in the body with a variety of symptoms.[7] Inability to use the hand or walk Malaise and a feeling of tiredness Weight loss Poor sleep Muscle aches and pains Tenderness Difficulty moving the joint It is common in advanced arthritis for significant secondary changes to occur. For example, in someone who has limited their physical activity: Muscle weakness Loss of flexibility Decreased aerobic fitness These changes can also impact on life and social roles, such as community involvement.

PREVENTION
The burden of arthritis conditions can be reduced through intervention at various points along the disease continuum including prevention, early diagnosis, prompt initiation of treatment and ongoing management. Although some chronic disease risk factors (for example, family history, age or sex) are not able to be modified and so cannot be incorporated into prevention strategies, they can help to identify people or groups at high risk of developing a disease, enabling a targeted approach.

Anemia
HISTORY
Anemia also spelled is a decrease in number of red blood cells (RBCs) or less than the normal quantity of hemoglobin in the blood.[1][2] Anemia may also be diagnosed where there is decreased oxygen-binding ability of each hemoglobin molecule due to deformity or lack in numerical development as in some other types of hemoglobin deficiency. The name is derived from Ancient Greek: anaimia, meaning lack of blood, from - an-, "not" + haima, "blood". Because hemoglobin (found inside RBCs) normally carries oxygen from the lungs to the capillaries, anemia leads to hypoxia (lack of oxygen) in organs. Since all human cells depend on oxygen for survival, varying degrees of anemia can have a wide range of clinical consequences.Anemia is the most common disorder of the blood. The several kinds of anemia are produced by a variety of underlying causes. It can be classified in a variety of ways, based on the morphology of RBCs, underlying etiologic mechanisms, and discernible clinical spectra, to mention a few. The three main classes include excessive blood loss (acutely such as a hemorrhage or chronically through low-volume loss), excessive blood cell destruction (hemolysis) or deficient red blood cell production (ineffective hematopoiesis).Of the two major approaches to diagnosis, the "kinetic" approach involves evaluating production, destruction and loss,[3] and the "morphologic" approach groups anemia by red blood cell size. The morphologic approach uses a quickly available and low-cost lab test as its starting point (the MCV), although this test can lack sensitivity and specificity in many diseases.[4] On the other hand, focusing early on the question of production may allow the clinician to expose cases more rapidly where multiple causes of anemia coexist.

SIGNS/SYMPTOMS
Anemia goes undetected in many people, and symptoms can be minor or vague. The signs and symptoms can be related to the underlying cause or the anemia itself. Most commonly, people with anemia report feelings of weakness, or fatigue, general malaise, and sometimes poor concentration. They may also report dyspnea (shortness of breath) on exertion. In very severe anemia, the body may compensate for the lack of oxygen-carrying capability of the blood by increasing cardiac output. The patient may have symptoms related to this, such as palpitations, angina (if pre-existing heart disease is present), intermittent claudication of the legs, and symptoms of heart failure.On examination, the signs exhibited may include pallor (pale skin, mucosal linings, conjunctiva and nail beds), but this is not a reliable sign. There may be signs of specific causes of anemia, e.g., koilonychia (in iron deficiency), jaundice (when anemia results from abnormal break down of red blood cells in hemolytic anemia), bone deformities (found in thalassemia major) or leg ulcers (seen in sicklecell disease).In severe anemia, there may be signs of a hyperdynamic circulation: tachycardia (a fast heart rate), bounding pulse, flow murmurs, and cardiac ventricular hypertrophy (enlargement). There may be signs of heart failure.Pica, the consumption of non-food items such as ice, but also paper, wax, or grass, and even hair or dirt, may be a symptom of iron deficiency, although it occurs often in those who have normal levels of hemoglobin.Chronic anemia may result in behavioral disturbances in children

as a direct result of impaired neurological development in infants, and reduced scholastic performance in children of school age. Restless legs syndrome is more common in those with iron-deficiency anemia.

PREVENTION
Many types of anemia can't be prevented. However, you can help avoid iron deficiency anemia and vitamin deficiency anemias by choosing a diet that includes a variety of vitamins and nutrients, including: Iron. Iron-rich foods include beef and other meats, beans, lentils, iron-fortified cereals, dark green leafy vegetables, and dried fruit. Folate. This nutrient, and its synthetic form folic acid, can be found in citrus fruits and juices, bananas, dark green leafy vegetables, legumes and fortified breads, cereals, and pasta. Vitamin B-12. This vitamin is found naturally in meat and dairy products. It's also added to some cereals and soy products, such as soy milk. Vitamin C. Foods containing vitamin C such as citrus fruits, melons and berries help increase iron absorption. Consider genetic counseling if you have a family history of anemia If you have a family history of an inherited anemia, such as sickle cell anemia or thalassemia, talk to your doctor and possibly a genetic counselor about your risk and what risks you may pass on to your children.

influenza
HISTORY
The word Influenza comes from the Italian language meaning "influence" and refers to the cause of the disease; initially, this ascribed illness to unfavorable astrological influences.[166] Changes in medical thought led to its modification to influenza del freddo, meaning "influence of the cold". The word influenza was first used in English to refer to the disease we know today in 1703 by J. Hugger of the University of Edinburgh in his thesis De Catarrho epidemio, vel Influenza, prout in India occidentali sese ostendit.[167] Archaic terms for influenza include epidemic catarrh, grippe (from the French, first used by Molyneaux in 1694 [168]), sweating sickness, and Spanish fever (particularly for the 1918 flu pandemic strain).[169]

SIGNS/SYMPTOMS
Symptoms of influenza can start quite suddenly one to two days after infection. Usually the first symptoms are chills or a chilly sensation, but fever is also common early in the infection, with body temperatures ranging from 38 to 39 C (approximately 100 to 103 F).[23] Many people are so ill that they are confined to bed for several days, with aches and pains throughout their bodies, which are worse in their backs and legs.[1] Symptoms of influenza may include: Fever and extreme coldness (chills shivering, shaking (rigor)) Cough Nasal congestion Runny nose Body aches, especially joints and throat Fatigue Headache Irritated, watering eyes Reddened eyes, skin (especially face), mouth, throat and nose Petechial rash[24] In children, gastrointestinal symptoms such as diarrhea and abdominal pain

PREVENTION
The influenza vaccine is recommended by the World Health Organization and United States Centers for Disease Control and Prevention for high-risk groups, such as children, the elderly, health care workers, and people who have chronic illnesses such as asthma, diabetes, heart disease, or are immunocompromised among others.[89][90] In healthy adults it is modestly effective in decreasing the amount of influenza-like symptoms in a population.[91] Evidence is supportive of a decreased rate of influenza in children over the age of two.[92] In those with chronic obstructive pulmonary disease vaccination reduces exacerbations,[93] it is not clear if it reduces asthma exacerbations.[94] Whether immunizing

health care workers effects patient outcomes is controversial with some reviews finding insufficient evidence[95][96] and others finding tentative evidence.[97][98] Evidence supports a lower rate of influenza-like illness in many groups who are immunocompromised such as those with: HIV/AIDS, cancer, and post organ transplant.[99] In those at high risk immunization may reduce the risk of heart disease.[100] Due to the high mutation rate of the virus, a particular influenza vaccine usually confers protection for no more than a few years. Every year, the World Health Organization predicts which strains of the virus are most likely to be circulating in the next year (see Historical annual reformulations of the influenza vaccine), allowing pharmaceutical companies to develop vaccines that will provide the best immunity against these strains.[101] The vaccine is reformulated each season for a few specific flu strains but does not include all the strains active in the world during that season. It takes about six months for the manufacturers to formulate and produce the millions of doses required to deal with the seasonal epidemics; occasionally, a new or overlooked strain becomes prominent during that time.[102] It is also possible to get infected just before vaccination and get sick with the strain that the vaccine is supposed to prevent, as the vaccine takes about two weeks to become effective.[103] Vaccines can cause the immune system to react as if the body were actually being infected, and general infection symptoms (many cold and flu symptoms are just general infection symptoms) can appear, though these symptoms are usually not as severe or long-lasting as influenza. The most dangerous adverse effect is a severe allergic reaction to either the virus material itself or residues from the hen eggs used to grow the influenza; however, these reactions are extremely rare.

FLU

RABBIES

HEADACHE

ARTHRITS

CANCER

ALZHERIMER

ANEMIA

PERtusis and mrsa

ALBUM IN MAPEH-III

NAME: JANESSA MAY CAPULONG

SECTION: III- RIZAL TEACHER: MRS.COLOYAN

PART I COMMUNICABLE DISEASE

PART II NON COMMUNICABLE DISEASE