Scrap reserch duty ppt

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Scrap reserch duty ppt

  1. 1. What are Leopolds maneuvers?Leopolds maneuvers are four specific steps in palpating the uterusthrough the abdomen in order to determine the lie and presentation ofthe fetus. In summary the steps are :Step 1. The top of the uterus (fundus) is felt (palpated) to establishwhich end of the fetus (fetal pole) is in the upper part of the uterus. Ifeither the head or breech (buttocks) of the fetus are in the fundus thenthe fetus is in vertical lie. Otherwise the fetus is most likely intransverse lie.Step 2. Firm pressure is applied to the sides of the abdomen toestablish the location of the spine and extremities (small parts).Step 3. Using the thumb and fingers of one hand the lower abdomen isgrasped just above the pubic symphysis to establish if the presentingpart is engaged. If not engaged a movable body part will be felt. Thepresenting part is the part of the fetus that is felt to be in closestproximity to the birth canal.Step 4. Facing the maternal feet the tips of the fingers of each hand areused to apply deep pressure in the direction of the axis of the pelvicoutlet. If the head presents, one hand is arrested sooner than the otherby a rounded body (the cephalic prominence) while the other handdescends deeply into the pelvis. If the cephalic prominence is on thesame side as the small parts, then the fetus is in vertex presentation. Ifthe cephalic prominence is on the same side as the back , then the headis extended and the fetus is in face presentation.******Labels: Maternal and ChildLeopolds maneuver- are a systematic method of observation and palpation to determine
  2. 2. fetal position, presentation, lie and attitude which helps in predictingcourse of labor. - woman who emptied her bladder should lie in supine position withher knees flexed slightly so abdomen is relaxed.- Warm hands to avoid contraction of abdominal muscles.- gentle but firm touchKeen observation of abdomen should give data about 1. longest diameter in appearance 2. location of apparent fetal movementThe four Leopolds maneuver are:1. First Maneuver- to determine presenting part at the fundus- head is more firm, hard and round that moves independently of thebody
  3. 3. - Breech is less well defined that moves only in conjunction with thebody2. Second Maneuver- to determine fetal back- one hand: will feel smooth, hard resistant surface (the back)- the opposite side, a number of angular nodulation (knees and elbowsof fetus)3. Third Maneuver- to determine position and mobilityof presenting part by grasping thelower portion of the abdomen (just above the symphysis pubis).- if the presenting part moves upward so the examiners hand can bepressed together, then presenting part is not engaged4. Fourth Maneuver- to determine fetal descent- fingers are pressed in both side of the uterus approximately 2 inchesabove the inguinal ligaments, then press upward and inward.- the fingers of the hand that do not meet obstruction palpates the fetalneck, as the fingers of the other hand meet an obstruction above theligaments palpates the fetal brow.- Good attitude if brow correspond to the side (2nd maneuver) thatcontained the elbows and knees.- Poor attitude if examining fingers will meet an obstruction on thesame side as fetal back (hyperextended head).- also palpates infants anteroposterior position. If brow is very easilypalpated, fetus is at posterior position (occiput pointing towards
  4. 4. womans back).Leopolds maneuversFrom Wikipedia, the free encyclopediaJump to: navigation, searchLeopolds ManeuversIn obstetrics, Leopolds Maneuvers are a common and systematic wayto determine the position of a fetus inside the womans uterus; theyare named after the gynecologist Christian Gerhard Leopold. They arealso used to estimate term fetal weight.[1]The maneuvers consist of four distinct actions, each helping todetermine the position of the fetus. The maneuvers are importantbecause they help determine the position and presentation of thefetus, which in conjunction with correct assessment of the shape of the
  5. 5. maternalpelvis can indicate whether the delivery is going to becomplicated, or whether a Cesarean section is necessary.The examiners skill and practice in performing the maneuvers are theprimary factor in whether the fetal lie is correctly ascertained, and sothe maneuvers are not truly diagnostic. Actual position can only bedetermined by ultrasound performed by a competent technician orphysician.Performing the maneuversLeopolds Maneuvers are difficult to perform on obesewomen andwomen who have polyhydramnios. The palpation can sometimes beuncomfortable for the woman if care is not taken to ensure she isrelaxed and adequately positioned. To aid in this, the health careprovider should first ensure that the woman has recently emptied herbladder. If she has not, she may need to have a straight urinarycatheter inserted to empty it if she is unable to micturate herself. Thewoman should lie on her back with her shoulders raised slightly on apillow and her knees drawn up a little. Her abdomen should beuncovered, and most women appreciate it if the individual performingthe maneuver warms their hands prior to palpation.First maneuver: Fundal GripWhile facing the woman, palpate the womans upper abdomen withboth hands. A professional can often determine the size, consistency,shape, and mobility of the form that is felt. The fetal head is hard, firm,round, and moves independently of the trunk while the buttocks feelsofter, are symmetric, and the shoulders and limbs have small bonyprocesses; unlike the head, they move with the trunk.
  6. 6. Second maneuver: Umbilical GripAfter the upper abdomen has been palpated and the form that is foundis identified, the individual performing the maneuver attempts todetermine the location of the fetal back. Still facing the woman, thehealth care provider palpates the abdomen with gentle but also deeppressure using the palm of the hands. First the right hand remainssteady on one side of the abdomen while the left hand explores theright side of the womans uterus. This is then repeated using theopposite side and hands. The fetal back will feel firm and smooth whilefetal extremities (arms, legs, etc.) should feel like small irregularitiesand protrusions. The fetal back, once determined, should connect withthe form found in the upper abdomen and also a mass in the maternalinlet, lower abdomen.Third maneuver: Pawlicks GripIn the third maneuver the health care provider attempts to determinewhat fetal part is lying above the inlet, or lower abdomen.[2] Theindividual performing the maneuver first grasps the lower portion ofthe abdomen just above the pubic symphysis with the thumb andfingers of the right hand. This maneuver should yield the oppositeinformation and validate the findings of the first maneuver. If thewoman enters labor, this is the part which will most likely come first ina vaginal birth. If it is the head and is not actively engaged in thebirthing process, it may be gently pushed back and forth. The PawlicksGrip, although still used by some obstetricians, is not recommended asit is more uncomfortable for the woman. Instead, a two-handedapproach is favored by placing the fingers of both hands laterally oneither side of the presenting part.
  7. 7. Fourth maneuver: Pelvic GripThe last maneuver requires that the health care provider face thewomans feet, as he or she will attempt to locate the fetus brow. Thefingers of both hands are moved gently down the sides of the uterustoward the pubis. The side where there is resistance to the descent ofthe fingers toward the pubis is greatest is where the brow is located. Ifthe head of the fetus is well-flexed, it should be on the opposite sidefrom the fetal back. If the fetal head is extended though, the occiput isinstead felt and is located on the same side as the back.CautionsLeopolds maneuvers are intended to be performed by health careprofessionals, as they have received the training and instruction in howto perform them. That said, as long as care taken not to roughly orexcessively disturb the fetus, there is no real reason it cannot beperformed at home as an informational exercise. It is important to notethat all findings are not truly diagnostic, and as such ultrasound isrequired to conclusively determine the fetal position.When to do a bed bathIf the person youre caring for is sedentary or on bed rest, the bestapproach to bathing may be a bed bath. It sounds simple enough -- you
  8. 8. basically wipe her clean with a wet cloth. But in reality, giving a goodbed bath is a bit tricky.Giving a bed bath requires you to wash the persons front, sides, andback, not to mention crevasses and folds -- while shes lying down.Depending on her condition, merely touching or moving her body maycause discomfort. If she weighs a lot, it can be strenuous for you. Not tomention the challenge of keeping the mattress dry.Dont worry! People have been giving bed baths for centuries: Theyre astandard of hospital and home healthcare. All this practice hasproduced practical techniques that make giving a bed bath much easier.Beginning the bed bathBy Kate Rauch, Caring.com senior editorBefore you begin a bed bath, make sure you have a huge pile of clean,dry bath towels and clean, dry washcloths, at least a dozen of each.Also, there should be a table or shelf within easy reach to hold a watercontainer and supplies. A wheeled cart -- such as a basic TV or kitchencart -- is ideal. Finally, adjust the room temperature so its toasty warm. Lay thick bath towels under the person from head to toe. These are to absorb water, protecting the bedding and mattress. You might want to also use a waterproof sheet under the cloth sheet to ensure that the mattress stays dry. Undress her but keep her under a blanket or large towel. This covering stays on during the whole bath for both warmth and privacy. Fill two large bowls with warm water, one for washing and one for rinsing. Put the bowls within easy reach. Stand at her shoulder. Youll be washing down one side of her body, section by section, lifting the cover away only as much as
  9. 9. necessary. It helps to tilt her up on the side a little, facing awayfrom you, so you can reach underneath her body. Start with hershoulder, then her arm and hand, including the fingers. Move tothe side of her torso and hips, then wash her thigh, lower leg,foot, and toes.The washing itself is straightforward: Soap then rinse, using adifferent washcloth for each. Rinse sufficiently to get all the soapoff. (Soap residue is drying to the skin, and elderly skin is prone todryness.) Refill the water bowls as needed. Make sure thetemperature of the water stays warm to the touch. Whenwashing, stroke in the direction of the heart, toward the torso, tohelp blood circulation.After a section is rinsed, pat it dry with a towel and lay the coverdown as quickly as you can for warmth.After youve finished one side of the body, start at the othershoulder and work down. Afterward, move to the head and neck.This is a great time to shampoo, which is easiest with a soft plasticbed bath shampoo bowl, sold at hospital or medical supply stores.The shampoo bowl can be placed right on the mattress, and allyou need to do is lift or edge your family members head into it.(Dont leave her unattended for even a few seconds when a bowlof water is near her head.) If you dont have a shampoo bowl, laydry towels under her head and do the best you can with yourbowls of water, soaping and rinsing. Consider using babyshampoo, which rinses out easily.Save the privates for last. Do these quickly, lifting the cover onlyas much as necessary to soap and rinse. With a man, youll needto wash under his testicles. With a woman, wash the labia; theresno need for a deep cleaning. To reach the rear, tilt the personsbody to the side as much as you need to or can. Or you can bendher knees and reach under from the front.When youre done, the persons entire body should remaincovered with the blanket or towel. If its damp, exchange it for a
  10. 10. dry one. You may need to add another layer. Slowly pull the wettowels from under her body.Take a deep breath and relax before dressing her. Giving a bedbath is a bona fide workout, and youve earned a break.Alternative bed bath techniques: through-the-towel, the chairbath, and moreBy Kate Rauch, Caring.com senior editorIn addition to the standard bed bath described above, there arevariations on the theme. You may very well discover your ownuseful adaptations as you gain experience.One alternative method of giving a bed bath is to wash and rinsethrough a towel, never touching the persons skin. Using awashcloth, you soap and rinse through the layer of towel, whichacts as a sort of second skin. This is one way around modestyconcerns, which can be extremely uncomfortable for you and her.This technique for giving a bed bath minimizes the need to rub orstroke. Instead, you pat or gently massage the wet towel thatcovers a section of her body. When youre done with that section,take off the wet towel and quickly replace it with a dry one or ablanket to avoid a post-bathing chill.Another twist on giving a bed bath: Keep several washcloths inlarge plastic zip-close bags of warm water, one clean and theother soapy, and take them out as needed. This eliminates theneed to rinse washcloths in bowls of water. As soon as awashcloth gets dirty, stop using it and get a clean one from thebag. Check the bags regularly to make sure the water remainswarm.Then theres the chair bath. If the person youre caring for feelscomfortable sitting up in a chair, this may be the best position forbathing. The routine is pretty much the same as for a bed bath.Of course, youll need to protect the chair from water. Vinyl-covered chairs can work, or you can get creative with plasticgarbage bags or a tarp.
  11. 11. Tips for giving a bed bath to overweight or sensitive peopleBy Kate Rauch, Caring.com senior editorIf the person youre bathing is resistant to a bath or particularlysensitive to water, try using no-rinse soaps and shampoos. Yourub them in and towel them off -- the dirt comes off in thetoweling. No-rinse bathing products can be a huge help, but theydo leave a residue, so youll need to rinse with water every nowand then.Giving a good bed bath requires a lot of movement on your part --lifting, holding, and tilting the persons body. If shes overweightor heavy, a bath may be a two-person job. The same is true ifshes easily irritated or feels pain when touched."You may need other people to help, like a relative or homehealth aide," says Jennifer Serafin, a registered nurse and geriatricnurse practitioner at the Jewish Home for the Aged in SanFrancisco.You can hire a home heath worker to assist you, enlist relatives orfriends, or try a combination of the two. Hiring a professional for aone-time crash course on giving a bed bath could also beextremely helpful.You wont need to give a full-body bed bath daily. Ask the medicalteam, but in most cases a full bath once or twice a week should besufficient.Its recommended that you clean the private areas and under anyskin folds daily. Youll need to wash under the testicles, breasts,armpits, and tummy rolls, which are more of an issue withoverweight people.Once-a-day washing can be done efficiently with a wipe or dampwashcloth. If the person in your care uses the toilet, take thisopportunity for a quick cleaning.
  12. 12. Definition of Last menstrual periodLast menstrual period: By convention, pregnancies are dated in weeksstarting from the first day of a womans last menstrual period (LMP). Ifher menstrual periods are regular and ovulation occurs on day 14 of hercycle, conception takes place about 2 weeks after her LMP. A woman istherefore considered to be 6 weeks pregnant 2 weeks after her firstmissed period.A womans obstetric date is different from the embryologic date (theage of the embryo). The obstetric date is about 2 weeks longer than theembryologic date.Pregnancy Due DateHow Pregnancy Due Date is CalculatedFrom conception vs last menstrual periodThe average duration of pregnancy is 38 weeks (266 days) fromconception. Predicting the pregnancy due date based on conception isthe most accurate way to calculate ones due date, but usually the dateof conception is not known. Therefore, the due date is generallycalculated from the first day of the last menstrual period (LMP). In thiscase, 2 weeks are added to the calculation giving a total of 40 weeks(280 days). This is based on the assumption that ovulation/conceptionoccurs on cycle day 14 in the "average" 28 day menstrual cycle.From ovulationCalculating the due date from LMP is subject to error since ovulationvaries in its timing from the onset of menstruation among differentwomen and from cycle to cycle. Many of Dr. Bergers tubal reversal
  13. 13. patients know their date of ovulation from using an ovulation predictorkit (OPK) or keeping a basal body temperature (BBT) chart. Calculatingthe pregnancy due date from ovulation is more accurate than from thelast menstrual period.Last Menstrual Period DatingHow to Calculate Pregnancy Due DateThe first day of the last menstrual period is used to initially determinethe age of a pregnancy.Pregnancy is a time of joyful waiting and excitement. Expectant parentswant to know when to expect their new little bundle of joy so they canprepare mentally and physically for childbirth and prepare a safe homefor the baby. Obstetricians want to know the due date so they canmonitor fetal growth, which can be an indicator of problems with thepregnancy. The last menstrual period is used to determine theapproximate age of the pregnancy. Ultrasound is often used to confirmthe due date and to monitor growth.Last Menstrual Period (LMP)The age of a pregnancy is determined by the first day of the lastmenstrual period. Gestational age includes the weeks of menstruation,follicular development, and ovulation, which is when conception
  14. 14. occurs. For this reason, gestational age can also be referred to asmenstrual age. It should be about two weeks longer than the fetal age,which is the actual age of the fetus.The following is an example of last menstrual period dating and how itcompares to fetal age:Last menstrual period: January 1On February 12 (six weeks after the last menstrual period), thefollowing would be true:Gestational age / Menstrual age: 6 weeksFetal age: 4 weeksGestational age is commonly used while fetal age is not.Menstrual Cycle Variations and Pregnancy Due DateThe pregnancy due date can be easy to calculate because pregnancycalculators are widely available on the Internet. Many of these arecombined with ovulation calculators. For many women, however, thesecalculators are not accurate.Most women do not have a 28-day menstrual cycle. Some have periodsevery three weeks while others may have them as far apart as fiveweeks. Ovulation occurs at different times for these women. Generally,those with shorter menstrual cycles will be given a gestational age thatis farther along than their LMP suggests, and those with longermenstrual cycles will be given a gestational age that is earlier than theirLMP suggests. This is because ovulation occurs at different times forthose with shorter and longer cycles. Some women have menstrual
  15. 15. cycles that vary in length, so an ultrasound may be necessary forcalculating the pregnancy due date.UltrasoundWhen the first day of the last menstrual period is unknown, or thelengths of the menstrual cycles are varied, ultrasound will most likelybe used to determine the age of the pregnancy. First trimesterultrasound is done to acquire a crown-rump length. The ultrasoundmachine determines the due date and gestational age based upon thecrown-rump length. Second trimester ultrasound is used to acquiremeasurements of the head, abdomen, and femur bone to determine anapproximate due date, gestational age, and weight. This methodbecomes less accurate as the pregnancy progresses.****Naegeles ruleFrom Wikipedia, the free encyclopediaJump to: navigation, searchNaegeles Rule is a standard way of calculating the due date for apregnancy. The rule estimates the expected date of delivery (EDD) byadding one year, subtracting three months, and adding seven days tothe first day of a womans last menstrual period (LMP). The result isapproximately 280 days (40 weeks) from the LMP.History
  16. 16. Naegeles Rule is named after Franz Karl Naegele (1778–1851), theGerman obstetrician who devised the rule. Naegele was born July 12,1778, in Düsseldorf, Germany. In 1806 Naegele became ordinaryprofessor and director of the lying-in hospital in Heidelberg. His"Lehrbuch der Geburtshilfe," published in 1830 for midwives, enjoyed asuccessful 14 editions.The rule estimates the expected date of delivery (EDD) (also called EDC,for estimated date of confinement) from the first day of the womansLMP by adding 1 year, subtracting three months and adding seven daysto that date. The result is approximately 280 days (40 weeks) from theLMP.Example:LMP = 8 May 2009 +1 year = 8 May 2010 -3 months = 8 February 2010 +7 days = 15 February 2010280 days past LMP is found by checking the day of the week of the LMPand adjusting the calculated date to land on the same day of the week.Using the example above, 8 May 2009 is a Tuesday. The calculated date(15 February) is a Friday; adjusting to the closest Tuesday produces 12February, which is exactly 280 days past 8 May. The calculation methoddoes not always result in a 280 days because not all calendar monthsare the same length, it does not account for leap years.Parikhs Formula is a calculation method that considers considers cycleduration. Naegeles Rule assumes an average cycle length of 28 days,which is not true for everyone. EDD is calculated using Parikhs Formulaby adding 9 months to LMP, subtracting 21 days, then adding durationof previous cycles.[1]
  17. 17. In modern practice, calculators, reference cards, or sliding wheelcalculators are used to add 280 days to LMP.AccuracyLMP may not be the best date to use as the basis of a due datecalculation, but it remains popular because few women know exactlywhat day they ovulate or conceive a pregnancy, and because noalgorithm can predict the exact day that spontaneous labor will occurno matter what considerations are taken into account.Average gestation of 40 weeksNaegeles Rule presents 280 days after LMP as an estimate for theaverage onset of spontaneous labor. A number of studies have beenpublished in recent years to support continued use of this number:A standard deviation diagram. When applied to human gestationlength, the curves center is at 280 days (40 weeks) past LMP. The darkblue area shows births within 13 days of the EDD 281 days, with a standard deviation of 13 days, was the result of a population-based study of 427,581 singleton births in Sweden.[2]
  18. 18. 281 days for first-time mothers and 280 days for all others were the medians found by a 1995 American study of 1,970 spontaneous births. Standard deviation was between 7–9 days.[3][4] 282 days was recommended for cases where LMP is the only known factor in a study of 17,450 patients combining LMP and ultrasound measurement techniques.[5] A median of 288 days (274 days from the date of ovulation) for first time mothers and 283 days (269 days from the date of ovulation) for mothers with at least one previous pregnancy was found by a 1990 study of white, private-care patients with uncomplicated pregnancies and spontaneous labor. The authors suggest that excluding pregnancies involving complications (that often lead to pre-term deliveries) accounts for the longer time periods.[6]Given the fact that these gestation lengths are only estimates of anaverage, it is helpful to consider gestation time as a range of datesrather than a single "due date". The median found by Naegeles Rule ismerely a guideline for the day at which half of all births occur earlier,and half of all births occur later. Births rarely occur on a due date, butthey are clustered around due dates.[7]For instance, a standard deviation of 13 days means that 90% of babieswill be born within three weeks of their EDD, and 21% will be bornwithin 3 days of it. Only 4% of births will occur on the EDD, but this issimilar to most other days around the EDD, in fact each day within aweek of the EDD has a 3-4% probability of being the day that birth willoccur. However, any given day two weeks away from the EDD has a lessthan 2% chance of being the day that birth will occur.
  19. 19. Ultrasound confirmation of gestational ageSince the 1970s ultrasound scans have allowed measurement of thesize of developing embryos directly and so allow for an estimation ofgestation age. Ultrasound dating is most accurate if undertaken in thefirst trimester (first 12 weeks of pregnancy) with a 95% error margin of6 days. Scans performed in the second trimester have an error marginof 8 days and those in the third trimester a margin of 2 weeks.Most obstetric departments in Australia, Canada, United Kingdom, andUnited States use a combination of LMP and ultrasound basedestimates for the EDD using either 10-day or 7-day rules, so that if LMPdates and ultrasonographic dates are in agreement within 7 (or 10)days, then the LMP dates are accepted.The Estimated Date of Confinement (EDC) is a term describing theestimated delivery date for a pregnantwoman.[1] Normal pregnancieslast between 37 and 42 weeks.[2]It is a calculated date (i.e., an estimation), determined by countingforward 280 days (40 weeks) from the first day of the womans lastmenstrual period.[3]Origins of the TermThe term confinement is a traditional term referring to the period ofpregnancy whereby a woman would be confined to bed (in an effort toreduce risk of premature delivery). Except in threatened pregnancies(for example, in pre-eclampsia), this is no longer a part of antenatalcare.es·ti·mat·ed date of confinement ( s t -m t d)n. Abbr. EDC
  20. 20. The date at which an infant is expected to be born, calculated from thedate of the last menstrual period. Also called due date.es·ti·mat·ed date of confinement ( s t -m t d)n. Abbr. EDCThe date at which an infant is expected to be born, calculated from thedate of the last menstrual period. Also called due date.The American Heritage® Medical Dictionary Copyright © 2007, 2004 byHoughton Mifflin Company.Published by Houghton Mifflin Company. Allrights reserved.Patient discussion about estimated date of confinement.Q. How many women actually give birth on their EDD (expecteddelivery date)? I am pregnant and my EDD is January 22nd. I waswondering what are the chances I will give birth on that day exactly?A. If its your first pregnancy, you probably will give birth after yourEDD, as first pregnancies tend to be longer. Your EDD is after a full 40weeks of pregnancy. It is most common to give birth between 38- 42weeks of pregnancy.????????Q. How many women actually give birth on their EDD (expecteddelivery date)?I am pregnant and my EDD is January 22nd. I was wondering what arethe chances I will give birth on that day exactly?A1 If its your first pregnancy, you probably will give birth after your EDD, as first pregnancies tend to be longer. Your EDD is after a full 40 weeks of pregnancy. It is most common to give birth between 38- 42 weeks of pregnancy.
  21. 21. A2 Most people are used to being assigned a EDD. Your expected delivery date (EDD) is 40 weeks from the first day of your last menstrual period (LMP). If you birth on your EDD, your baby is actually only 38 weeks old - thats because your menstrual period and ovulation are counted as the first 2 weeks of pregnancy. Its important to remember that your due date is only an estimate - most babies are born between 38 and 42 weeks and only a small percentage of women actually birth on their due date. http://www.naturalattachment.com/BirthMonth.html Hope this helps.A3 Your EDD is 40 weeks from the first day of your last menstrual period (LMP). If you deliver on your EDD, your baby is actually only about 38 weeks old — thats because your egg didnt become fertilized until about 2 weeks after the start of your last menstrual period. Its important to remember that your due date is only an estimate — most babies are born between 38 and 42 weeks from the first day of their mom’s LMP and only a small percentage of women actually deliver on their due date.Diabetes mellitus type 2Diabetes mellitus type 2 – formerly non-insulin-dependent diabetesmellitus (NIDDM) or adult-onset diabetes – is a metabolic disorder thatis characterized by high blood glucose in the context of insulinresistance and relative insulin deficiency.[2] This is in contrast todiabetes mellitus type 1 in which there is an absolute insulin deficiencydue to destruction of islet cells in the pancreas.[3] The classic symptomsare excess thirst, frequent urination, and constant hunger. Type 2diabetes makes up about 90% of cases of diabetes with the other 10%
  22. 22. due primarily to diabetes mellitus type 1 and gestational diabetes.Obesity is thought to be the primary cause of type 2 diabetes in peoplewho are genetically predisposed to the disease.Type 2 diabetes is initially managed by increasing exercise and dietarymodification. If blood glucose levels are not adequately lowered bythese measures, medications such as metformin or insulin may beneeded. In those on insulin there is typically the requirement toroutinely check blood sugar levels.Rates of diabetes have increased markedly over the last 50 years inparallel with obesity. As of 2010 there are approximately 285 millionpeople with the disease compared to around 30 million in 1985. Long-term complications from high blood sugar can include heart disease,strokes, diabetic retinopathy where eyesight is affected, kidney failurewhich may require dialysis, and poor circulation of limbs leading toamputations. The acute complication of ketoacidosis, a feature of type1 diabetes, is uncommon.[4] However, nonketotic hyperosmolar comamay occur.Signs and symptomsOverview of the most significant symptoms of diabetes.
  23. 23. The classic symptoms of diabetes are polyuria (frequent urination),polydipsia (increased thirst), polyphagia (increased hunger), and weightloss.[5] Other symptoms that are commonly present at diagnosisinclude: a history of blurred vision, itchiness, peripheral neuropathy,recurrent vaginal infections, and fatigue. Many people however haveno symptoms during the first few years and are diagnosed on routinetesting. People with type 2 diabetes mellitus may rarely present withnonketotic hyperosmolar coma (a condition of very high blood sugarassociated with a decreased level of consciousness and low bloodpressure).[3]ComplicationsMain article: Complications of diabetes mellitusType 2 diabetes is typically a chronic disease, associated with a ten yearshorter life expectancy.[6] This is partly due to a number ofcomplications with which it is associated including: two to four timesthe risk of cardiovascular disease, including ischemic heart disease andstroke, a 20 fold increase in lower limb amputations, and increasedrates of hospitalizations.[6] In the developed world, and increasinglyelsewhere, type 2 diabetes is the largest cause of non-traumaticblindness and kidney failure.[7] It has also been associated with anincreased risk of cognitive dysfunction and dementia through diseaseprocesses such as Alzheimers disease and vascular dementia.[8] Othercomplications include: acanthosisnigricans, sexual dysfunction, andfrequent infections.[5]CauseThe development of type 2 diabetes is caused by a combination oflifestyle and genetic factors.[7][9] While some are under personal controlsuch as diet and obesity others such as increasing age, female gender,and genetics are not.[6] A lack of sleep has been linked to type 2diabetes.[10] This is believed to act through its effect on
  24. 24. metabolism.[10]The nutritional status of a mother during fetaldevelopment may also play a role with one proposed mechanism beingthat of altered DNA methylation.[11]LifestyleMain article: Lifestyle causes of diabetes mellitus type 2A number of lifestyle factors are known to be important to thedevelopment of type 2 diabetes including: obesity (defined by a bodymass index of greater than thirty), lack of physical activity, poor diet,stress, and urbanization.[6] Excess body fat is associated with 30% ofcases in those of Chinese and Japanese descent, 60-80% of cases inthose of European and African descent, and 100% of Pima Indians andPacific Islanders.[3] Those who are not obese often have a high waist–hip ratio.[3] Dietary factors also influence the risk of developing type 2diabetes. Consumption of sugar sweetened drinks in excess isassociated with an increased risk.[12][13] The type of fats in the diet arealso important, with saturated fats and trans fatty acids increasing therisk and polyunsaturated and monounsaturated fat decreasing therisk.[9] Eating lots of white rice appears to also play a role in increasingrisk.[14]GeneticsMain article: Genetic causes of diabetes mellitus type 2Most cases of diabetes involve many genes with each being a smallcontributor to an increased probability of becoming a type 2 diabetic.[6]If one identical twin has diabetes the chance of the other developingdiabetes within their lifetime is greater than 90% while the rate fornon-identical siblings is 25-50%.[3] As of 2011, more than 36 genes havebeen found that contribute to the risk of type 2 diabetes.[15] All of thesegenes together still only account for 10% of the total heritablecomponent of the disease. The TCF7L2allele for example increases the
  25. 25. risk of developing diabetes by 1.5 times and is the greatest risk of thecommon genetic variants. Most of the genes link to diabetes areinvolved in beta cell functions.[3]There are a number of rare cases of diabetes that arise due to anabnormality in a single gene (known as monogenic forms of diabetes or"other specific types of diabetes").[3][6] These include maturity onsetdiabetes of the young (MODY), Donohue syndrome, and Rabson-Mendenhall syndrome, among others.[6] Maturity onset diabetes of theyoung constitute 1–5 % of all cases of diabetes in young people.[16]Medical conditionsThere are a number of medications and other health problems that canpredispose to diabetes.[17] Some of the medications include:glucocorticoids, thiazides, beta blockers, atypical antipsychotics,[18] andstatins.[19] Those who have previously had gestational diabetes are at ahigher risk of developing type 2 diabetes.[5] Other health problems thatare associated include: acromegaly, Cushings syndrome,hyperthyroidism, pheochromocytoma, and certain cancers such asglucagonomas.[17]Testosterone deficiency is also associated with type 2diabetes.[20][21]PathophysiologyType 2 diabetes is due to insufficient insulin production from beta cellsin the setting of insulin resistance.[3] Insulin resistance, which is theinability of cells to respond adequately to normal levels of insulin,occurs primarily within the muscles, liver and fat tissue.[22] In the liver,insulin normally suppresses glucose release. However in the setting ofinsulin resistance, the liver inappropriately releases glucose into theblood.[6] The proportion of insulin resistance verses beta celldysfunction differs among individuals with some having primarilyinsulin resistance and only a minor defect in insulin secretion and
  26. 26. others with slight insulin resistance and primarily a lack of insulinsecretion.[3]Other potentially important mechanisms associated with type 2diabetes and insulin resistance include: increased breakdown of lipidswithin fat cells, resistance to and lack of incretin, high glucagon levels inthe blood, increased retention of salt and water by the kidneys, andinappropriate regulation of metabolism by the central nervoussystem.[6] However not all people with insulin resistance developdiabetes, since an impairment of insulin secretion by pancreatic betacells is also required.[3]Diagnosis Diabetes diagnostic criteria[23][24] edit 2 hour Condition Fasting glucose HbA1c glucose mmol/l(mg/dl) mmol/l(mg/dl) % Normal <7.8 (<140) <6.1 (<110) <6.0 Impaired fasting ≥ 6.1(≥110) 6.0- <7.8 (<140) glycaemia &<7.0(<126) 6.4 Impaired glucose 6.0- ≥7.8 (≥140) <7.0 (<126) tolerance 6.4 Diabetes mellitus ≥11.1 (≥200) ≥7.0 (≥126) ≥6.5The World Health Organization definition of diabetes (both type 1 andtype 2) is for a single raised glucose reading with symptoms, otherwiseraised values on two occasions, of either:[25]
  27. 27. fasting plasma glucose ≥ 7.0 mmol/l (126 mg/dl) or with a glucose tolerance test, two hours after the oral dose a plasma glucose ≥ 11.1 mmol/l (200 mg/dl)A random blood sugar of greater than 11.1 mmol/l (200 mg/dL) inassociation with typical symptoms[5] or a glycated hemoglobin (HbA1c)of greater than 6.5% is another method of diagnosing diabetes.[6] In2009 an International Expert Committee that included representativesof the American Diabetes Association (ADA), the International DiabetesFederation (IDF), and the European Association for the Study ofDiabetes (EASD) recommended that a threshold of ≥6.5% HbA1c shouldbe used to diagnose diabetes. This recommendation was adopted bythe American Diabetes Association in 2010.[26] Positive tests should berepeated unless the person presents with typical symptoms and bloodsugars >11.1 mmol/l (>200 mg/dl).[27]Threshold for diagnosis of diabetes are based on the relationshipbetween results of glucose tolerance tests, fasting glucose or HbA1c andcomplications such as retinal problems.[6] A fasting or random bloodsugar is preferred over the glucose tolerance test as they are moreconvenient for people.[6] HbA1c has the advantages that fasting is notrequired and results are more stable, but has the disadvantage that thetest is more costly than measurement of blood glucose.[28] It isestimated that 20% of people with diabetes in the United States do notrealize that they have the disease.[6] Diabetes mellitus type 2 ischaracterized by high blood glucose in the context of insulin resistanceand relative insulin deficiency.[2] This is in contrast to diabetes mellitustype 1 in which there is an absolute insulin deficiency due todestruction of islet cells in the pancreas and gestational diabetesmellitus that is a new onset of high blood sugars in associated withpregnancy.[3] Type 1 and type 2 diabetes can typically be distinguished
  28. 28. based on the presenting circumstances.[27] If the diagnosis is in doubtantibody testing may be useful to confirm type 1 diabetes and C-peptide levels may be useful to confirm type 2 diabetes.[29]ScreeningNo major organization recommends universal screening for diabetes asthere is no evidence that such a program would improve outcomes.[30]Screening is recommended by the United States Preventive ServicesTask Force in adults without symptoms whose blood pressure is greaterthan 135/80 mmHg.[31] For those whose blood pressure is less, theevidence is insufficient to recommend for or against screening.[31] TheWorld Health Organization recommends only testing those groups athigh risk.[30] High risk groups in the United States include: those over45 years old, those with a first degree relative with diabetes, someethnic groups including Hispanics, African-Americans, and Native-Americans, a history of gestational diabetes, polycystic ovary syndrome,excess weight, and conditions associated with metabolic syndrome.[5]PreventionMain article: Prevention of diabetes mellitus type 2Onset of type 2 diabetes can be delayed or prevented through propernutrition and regular exercise.[32][33] Intensive lifestyle measures mayreduce the risk by over half.[7] The benefit of exercise occurs regardlessof the persons initial weight or subsequent weight loss.[34] Evidence forthe benefit of dietary changes alone, however, is limited,[35] with someevidence for a diet high in green leafy vegetables[36] and some forlimiting the intake of sugary drinks.[12] In those with impaired glucosetolerance, diet and exercise either alone or in combination withmetformin or acarbose may decrease the risk of developingdiabetes.[7][37] Lifestyle interventions are more effective thanmetformin.[7]
  29. 29. ManagementFurther information: Diabetes managementManagement of type 2 diabetes focuses on lifestyle interventions,lowering other cardiovascular risk factors, and maintaining bloodglucose levels in the normal range.[7] Self-monitoring of blood glucosefor people with newly diagnosed type 2 diabetes was recommended bythe National Health Services in 2008,[38] however the benefit of selfmonitoring in those not using multi-dose insulin is questionable.[7][39]Managing other cardiovascular risk factors including:hypertension, highcholesterol, and microalbuminuria, improves a persons lifeexpectancy.[7] Intensive blood sugar lowering (HbA1C<6%) as opposedto standard blood sugar lowering (HbA1C of 7-7.9%) does not appear tochange mortality.[40][41] The goal of treatment is typically an HbA1C ofless than 7% or a fasting glucose of less than 6.7 mmol/L (120 mg/dL)however these goals may be changed after professional clinicalconsultation, taking into account particular risks of hypoglycemia andlife expectancy.[5] It is recommended that all people with type 2diabetes get regular ophthalmology examination.[3]LifestyleA proper diet and exercise are the foundations of diabetic care[5] with agreater amount of exercise yielding better results.[42]Aerobic exerciseleads to a decrease in HbA1C and improved insulinsensitivity.[42]Resistance training is also useful and the combination ofboth types of exercise may be most effective.[42] A diabetic diet thatpromotes weight loss is important.[43] While the best diet type toachieve this is controversial[43] a low glycemic index diet has been foundto improve blood sugar control.[44] Culturally appropriate educationmay help people with Type 2 diabetes control their blood sugar levels,for up to six months at least.[45] If changes in lifestyle, in those with mild
  30. 30. diabetes, has not resulted in improved blood sugars within six weeksmedications should then be considered.[5]MedicationsMetformin 500mg tabletsThere are several classes of anti-diabetic medications available.Metformin is generally recommended as a first line treatment as thereis some evidence that it decreases mortality.[7] A second oral agent ofanother class may be used if metformin is not sufficient.[46] Otherclasses of medications include: sulfonylureas,nonsulfonylureasecretagogues, alpha glucosidase inhibitors,thiazolidinediones, glucagon-like peptide-1 analog, and dipeptidylpeptidase-4 inhibitors.[7][47] Metformin should not be used in those withsevere kidney or liver problems.[5] Injections of insulin may either beadded to oral medication or used alone.[7]Most people do not initially need insulin.[3] When it is used, a long-acting formulation is typically added at night, with oral medicationsbeing continued.[5][7] Doses are then increased to effect (blood sugarlevels being well controlled).[7] When nightly insulin is insufficient twicedaily insulin may achieve better control.[5] The long acting insulins,glargine and detemir, do not appear much better than neutral
  31. 31. protamine Hagedorn(NPH) insulin but have a significantly greater costmaking them, as of 2010, not cost effective.[48] In those who arepregnant insulin is generally the treatment of choice.[5]SurgeryWeight loss surgery in those who are obese appears to be an effectivemeasure to treat diabetes.[49] Many are able to maintain normal bloodsugar levels with little or no medications following surgery[50] and longterm mortality is decreased.[51] There however is some short termmortality risk of less than 1% from the surgery.[52] The body mass indexcutoffs for when surgery is appropriate are not yet clear.[51]EpidemiologyPrevalence of diabetes worldwide in 2000 (per 1000 inhabitants).World average was 2.8%. no data 45–52.5 ≤ 7.5 52.5–60 7.5–15 60–67.5 15–22.5 67.5–75 22.5–30 75–82.5 30–37.5 ≥ 82.5
  32. 32. 37.5–45Globally as of 2010 it was estimated that there were 285 million peoplewith type 2 diabetes making up about 90% of diabetes cases.[6] This isequivalent to about 6% of the worlds adult population.[53] Diabetes iscommon both in the developed and the developing world.[6] Howeverremains uncommon in the underdeveloped world.[3] Women seem tobe at a greater risk as do certain ethnic groups,[6][54] such as SouthAsians, Pacific Islanders, Latinos, and Native Americans.[5] This may bedue to enhanced sensitivity to a Western lifestyle in certain ethnicgroups.[55] Traditionally considered a disease of adults, type 2 diabetesis increasingly diagnosed in children in parallel with rising obesityrates.[6] Type 2 diabetes is now diagnosed as frequently as type 1diabetes in teenagers in the United States.[3]Rates of diabetes in 1985 were estimated at 30 million, increasing to135 million in 1995 and 217 million in 2005.[56] This increase is believedto be primarily due to the global population aging, a decrease inexercise, and increasing rates of obesity.[56] The five countries with thegreatest number of people with diabetes as of 2000 are India having31.7 million, China 20.8 million, the United States 17.7 million,Indonesia 8.4 million, and Japan 6.8 million.[57] It is recognized as aglobal epidemic by the World Health Organization.[58]HistoryMain article: History of diabetesDiabetes is one of the first diseases described[59] with an Egyptianmanuscript from c. 1500 BCE mentioning "too great emptying of theurine."[60] The first described cases are believed to be of type 1diabetes.[60] Indian physicians around the same time identified thedisease and classified it as madhumeha or honey urine noting that the
  33. 33. urine would attract ants.[60] The term "diabetes" or "to pass through"was first used in 230 BCE by the Greek Appollonius Of Memphis.[60] Thedisease was rare during the time of the Roman empire with Galencommenting that he had only seen two cases during his career.[60] Type1 and type 2 diabetes were identified as separate conditions for thefirst time by the Indian physicians Sushruta and Charaka in 400-500 ADwith type 1 associated with youth and type 2 with being overweight.[60]The term "mellitus" or "from honey" was added by the Briton JohnRolle in the late 1700s to separate the condition from diabetes insipiduswhich is also associated with frequent urination.[60] Effective treatmentwas not developed until the early part of the 20th century when theCanadians Frederick Banting and Charles Best developed insulin in 1921and 1922.[60] This was followed by the development of the long actingNPH insulin in the 1940s.[60]BackgroundType 2 diabetes mellitus consists of an array of dysfunctionscharacterized by hyperglycemia and resulting from the combination ofresistance to insulin action, inadequate insulin secretion, and excessiveor inappropriate glucagon secretion. Poorly controlled type 2 diabetesis associated with an array of microvascular, macrovascular, andneuropathic complications.Microvascular complications of diabetes include retinal, renal, andpossibly neuropathic disease. Macrovascular complications includecoronary artery and peripheral vascular disease. Diabetic neuropathyaffects autonomic and peripheral nerves. (See Pathophysiology andPresentation.)Unlike patients with type 1 diabetes mellitus, patients with type 2 arenot absolutely dependent on insulin for life. This distinction was thebasis for the older terms for types 1 and 2, insulin dependent and non–insulin dependent diabetes.
  34. 34. However, many patients with type 2 diabetes are ultimately treatedwith insulin. Because they retain the ability to secrete someendogenous insulin, they are considered to require insulin but not todepend on insulin. Nevertheless, given the potential for confusion dueto classification based on treatment rather than etiology, the olderterms have been abandoned.[1] Another older term for type 2 diabetesmellitus was adult-onset diabetes. Currently, because of the epidemicof obesity and inactivity in children, type 2 diabetes mellitus isoccurring at younger and younger ages. Although type 2 diabetesmellitus typically affects individuals older than 40 years, it has beendiagnosed in children as young as 2 years of age who have a familyhistory of diabetes. In many communities, type 2 diabetes nowoutnumbers type 1 among children with newly diagnosed diabetes.(See Epidemiology.)Diabetes mellitus is a chronic disease that requires long-term medicalattention to limit the development of its devastating complications andto manage them when they do occur. It is a disproportionatelyexpensive disease; in the United States in 2007, the direct medical costsof diabetes were $116 billion, and the total costs were $174 billion;people with diabetes had average medical expenditures 2.3 times thoseof people without diabetes. The emergency department utilization rateby people with diabetes is twice that of the unaffected population.[2, 3]This article focuses on the diagnosis and treatment of type 2 diabetesand its acute and chronic complications, other than those directlyassociated with hypoglycemia and severe metabolic disturbances, suchas hyperosmolar hyperglycemic state (HHS) and diabetic ketoacidosis(DKA). For more information on those topics, see HyperosmolarHyperglycemic State and Diabetic Ketoacidosis.Pathophysiology
  35. 35. Type 2 diabetes is characterized by a combination of peripheral insulinresistance and inadequate insulin secretion by pancreatic beta cells.Insulin resistance, which has been attributed to elevated levels of freefatty acids and proinflammatory cytokines in plasma, leads todecreased glucose transport into muscle cells, elevated hepatic glucoseproduction, and increased breakdown of fat.A role for excess glucagon cannot be underestimated; indeed, type 2diabetes is an islet paracrinopathy in which the reciprocal relationshipbetween the glucagon-secreting alpha cell and the insulin-secretingbeta cell is lost, leading to hyperglucagonemia and hence theconsequent hyperglycemia.[2]For type 2 diabetes mellitus to occur, both insulin resistance andinadequate insulin secretion must exist. For example, all overweightindividuals have insulin resistance, but diabetes develops only in thosewho cannot increase insulin secretion sufficiently to compensate fortheir insulin resistance. Their insulin concentrations may be high, yetinappropriately low for the level of glycemia.A simplified scheme for the pathophysiology of abnormal glucosemetabolism in type 2 diabetes mellitus is depicted in the image below. Simplified scheme for the pathophysiology oftype 2 diabetes mellitus.With prolonged diabetes, atrophy of the pancreas may occur. A studyby Philippe et al used computed tomography (CT) scan findings,glucagon stimulation test results, and fecal elastase-1 measurements to
  36. 36. confirm reduced pancreatic volume in individuals with a median 15-year history of diabetes mellitus (range, 5-26 years).[4] This may alsoexplain the associated exocrine deficiency seen in prolonged diabetes.Beta-cell dysfunctionBeta-cell dysfunction is a major factor across the spectrum ofprediabetes to diabetes. A study of obese adolescents by Bacha et alconfirms what is increasingly being stressed in adults as well: Beta-celldysfunction develops early in the pathologic process and does notnecessarily follow the stage of insulin resistance.[5] Singular focus oninsulin resistance as the "be all and end all" is gradually shifting, andhopefully better treatment options that address the beta-cell pathologywill emerge for early therapy.Insulin resistanceIn the progression from normal to abnormal glucose tolerance,postprandial blood glucose levels increase first. Eventually, fastinghyperglycemia develops as suppression of hepatic gluconeogenesisfails.During the induction of insulin resistance (such as occurs with a high-calorie diet, steroid administration, or physical inactivity), increasedglucagon levels and increased glucose-dependent insulinotropicpolypeptide (GIP) levels accompany glucose intolerance. However, thepostprandial glucagonlike peptide-1 (GLP-1) response is unaltered.[6]Genomic factorsGenome-wide association studies of single-nucleotide polymorphisms(SNPs) have identified a number of genetic variants that are associatedwith beta-cell function and insulin resistance. Some of these SNPsappear to increase the risk for type 2 diabetes. Over 40 independent
  37. 37. loci demonstrating an association with an increased risk for type 2diabetes have been shown.[7] A subset of the most potent are sharedbelow[8] : Decreased beta-cell responsiveness, leading to impaired insulin processing and decreased insulin secretion (TCF7L2) Lowered early glucose-stimulated insulin release (MTNR1B, FADS1, DGKB, GCK) Altered metabolism of unsaturated fatty acids (FSADS1) Dysregulation of fat metabolism (PPARG) Inhibition of serum glucose release (KCNJ11)[9] Increased adiposity and insulin resistance (FTO and IGF2BP2)[10, 11] Control of the development of pancreatic structures, including beta-islet cells (HHEX)[12] Transport of zinc into the beta-islet cells, which influences the production and secretion of insulin (SLC30A8)[12] Survival and function of beta-islet cells (WFS1)[13]Susceptibility to type 2 diabetes may also be affected by geneticvariants involving incretin hormones, which are released fromendocrine cells in the gut and stimulate insulin secretion in response todigestion of food. For example, reduced beta-cell function has beenassociated with a variant in the gene that codes for the receptor ofgastric inhibitory polypeptide (GIPR).[14]The high mobility group A1 (HMGA1) protein is a key regulator of theinsulin receptor gene (INSR).[15] Functional variants of the HMGA1 geneare associated with an increased risk of diabetes.Amino acid metabolismAmino acid metabolism may play a key role early in the development oftype 2 diabetes. Wang et al reported that the risk of future diabeteswas at least 4-fold higher in normoglycemic individuals with high fasting
  38. 38. plasma concentrations of 3 amino acids (isoleucine, phenylalanine, andtyrosine). Concentrations of these amino acids were elevated up to 12years prior to the onset of diabetes.[16] In this study, amino acids,amines, and other polar metabolites were profiled using liquidchromatography tandem mass spectrometry.Diabetes complicationsAlthough the pathophysiology of the disease differs between the typesof diabetes, most of the complications, including microvascular,macrovascular, and neuropathic, are similar regardless of the type ofdiabetes. Hyperglycemia appears to be the determinant ofmicrovascular and metabolic complications. Macrovascular disease maybe less related to glycemia.Telomere attrition may be a marker associated with presence and thenumber of diabetic complications. Whether it is a cause or aconsequence of diabetes remains to be seen.[17]Cardiovascular riskCardiovascular risk in people with diabetes is related in part to insulinresistance, with the following concomitant lipid abnormalities: Elevated levels of small, dense low-density lipoprotein (LDL) cholesterol particles Low levels of high-density lipoprotein (HDL) cholesterol Elevated levels of triglyceride-rich remnant lipoproteinsThrombotic abnormalities (ie, elevated type-1 plasminogen activatorinhibitor [PAI-1], elevated fibrinogen) and hypertension are alsoinvolved. Other conventional atherosclerotic risk factors (eg, familyhistory, smoking, elevated LDL cholesterol) also affect cardiovascularrisk.
  39. 39. Insulin resistance is associated with increased lipid accumulation in liverand smooth muscle, but not with increased myocardial lipidaccumulation.[18] Persistent lipid abnormalities remain in patients withdiabetes despite the use of lipid-modifying drugs, although evidencesupports the benefits of these drugs. Statin dose up-titration and theaddition of other lipid-modifying agents are needed.[19]Increased cardiovascular risk appears to begin prior to the developmentof frank hyperglycemia, presumably because of the effects of insulinresistance. Stern in 1996[20] and Haffner and DAgostino in 1999[21]developed the "ticking clock" hypothesis of complications, assertingthat the clock starts ticking for microvascular risk at the onset ofhyperglycemia, while the clock starts ticking for macrovascular risk atsome antecedent point, presumably with the onset of insulinresistance.The question of when diabetes becomes a cardiovascular riskequivalent has not yet been settled. Debate has moved beyondautomatically considering diabetes a cardiovascular risk equivalent.Perhaps it would be prudent to assume the equivalency with diabetesthat is more than 5-10 years in duration.Secondary diabetesVarious other types of diabetes, previously called secondary diabetes,are caused by other illnesses or medications. Depending on the primaryprocess involved (eg, destruction of pancreatic beta cells ordevelopment of peripheral insulin resistance), these types of diabetesbehave similarly to type 1 or type 2 diabetes.The most common causes of secondary diabetes are as follows:
  40. 40. Diseases of the pancreas that destroy the pancreatic beta cells (eg, hemochromatosis, pancreatitis, cystic fibrosis, pancreatic cancer) Hormonal syndromes that interfere with insulin secretion (eg, pheochromocytoma) Hormonal syndromes that cause peripheral insulin resistance (eg, acromegaly, Cushing syndrome, pheochromocytoma) Drugs (eg, phenytoin, glucocorticoids, estrogens)Gestational diabetesGestational diabetes mellitus is defined as any degree of glucoseintolerance with onset or first recognition during pregnancy.Gestational diabetes mellitus is a complication of approximately 4% ofall pregnancies in the United States. A steady decline in insulinsensitivity as gestation progresses is a normal feature of pregnancy;gestational diabetes mellitus results when maternal insulin secretioncannot increase sufficiently to counteract the decrease in insulinsensitivity. (For more information, see Diabetes Mellitus andPregnancy.)tiologyThe etiology of type 2 diabetes mellitus appears to involve complexinteractions between environmental and genetic factors. Presumably,the disease develops when a diabetogenic lifestyle (ie, excessive caloricintake, inadequate caloric expenditure, obesity) is superimposed on asusceptible genotype.The body mass index (BMI) at which excess weight increases risk fordiabetes varies with different racial groups. For example, comparedwith persons of European ancestry, persons of Asian ancestry are atincreased risk for diabetes at lower levels of overweight.[22]
  41. 41. Hypertension and prehypertension are associated with a greater risk ofdeveloping diabetes in whites than in African Americans.[23]In addition, an in utero environment resulting in low birth weight maypredispose some individuals to develop type 2 diabetes mellitus.[24, 25]Infant weight velocity has a small, indirect effect on adult insulinresistance, and this is primarily mediated through its effect on BMI andwaist circumference.[26]About 90% of patients who develop type 2 diabetes mellitus are obese.However, a large, population-based, prospective study has shown thatan energy-dense diet may be a risk factor for the development ofdiabetes that is independent of baseline obesity.[27]Some studies suggest that environmental pollutants may play a role inthe development and progression of type 2 diabetes mellitus.[28] Astructured and planned platform is needed to fully explore thediabetes-inducing potential of environmental pollutants.Secondary diabetes may occur in patients taking glucocorticoids orwhen patients have conditions that antagonize the actions of insulin(eg, Cushing syndrome, acromegaly, pheochromocytoma).Major risk factorsThe major risk factors for type 2 diabetes mellitus are the following: Age greater than 45 years (though, as noted above, type 2 diabetes mellitus is occurring with increasing frequency in young individuals) Weight greater than 120% of desirable body weight Family history of type 2 diabetes in a first-degree relative (eg, parent or sibling) Hispanic, Native American, African American, Asian American, or Pacific Islander descent
  42. 42. History of previous impaired glucose tolerance (IGT) or impaired fasting glucose (IFG) Hypertension (>140/90 mm Hg) or dyslipidemia (HDL cholesterol level < 40 mg/dL or triglyceride level >150 mg/dL) History of gestational diabetes mellitus or of delivering a baby with a birth weight of over 9 lb Polycystic ovarian syndrome (which results in insulin resistance)Genetic influencesThe genetics of type 2 diabetes are complex and not completelyunderstood. Evidence supports the involvement of multiple genes inpancreatic beta-cell failure and insulin resistance.Genome-wide association studies have identified dozens of commongenetic variants associated with increased risk for type 2 diabetes.[8] Ofthe variants thus far discovered, the one with the strongest effect onsusceptibility is the transcription factor 7–like 2 (TCF7L2) gene. (Formore information, see Type 2 Diabetes and TCF7L2.)Identified genetic variants account for only about 10% of the heritablecomponent of most type 2 diabetes.[8] An international researchconsortium found that use of a 40-SNP genetic risk score improves theability to make an approximate 8-year risk prediction for diabetesbeyond that which is achievable when only common clinical diabetesrisk factors are used. Moreover, the predictive ability is better inyounger persons (in whom early preventive strategies could delaydiabetes onset) than in those older than 50 years.[29]Some forms of diabetes have a clear association with genetic defects.The syndrome historically known as maturity onset diabetes of youth(MODY), which is now understood to be a variety of defects in beta-cellfunction, accounts for 2-5% of individuals with type 2 diabetes who
  43. 43. present at a young age and have mild disease. The trait is autosomaldominant and can be screened for through commercial laboratories.To date, 11 MODY subtypes have been identified, involving mutationsin the following genes[30, 31] : HNF-4-alpha Glucokinase gene HNF-1-alpha IPF-1 HNF-1-beta NEUROD1 KLF11[32] CEL[33] PAX4[34] INS BLK[35]Most of the MODY subtypes are associated with diabetes only;however, MODY type 5 is known to be associated with renal cysts,[36]and MODY type 8 is associated with exocrine pancreatic dysfunction.[33]A number of variants in mitochondrial deoxyribonucleic acid (DNA)have been proposed as an etiologic factor for a small percentage ofpatients with type 2 diabetes. Two specific point mutations and somedeletions and duplications in the mitochondrial genome can cause type2 diabetes and sensorineural hearing loss.[37]Diabetes can also be a finding in more severe mitochondrial disorderssuch as Kearns-Sayre syndrome and mitochondrialencephalomyopathy, lactic acidosis, and strokelike episode (MELAS).Mitochondrial forms of diabetes mellitus should be considered whendiabetes occurs in conjunction with hearing loss, myopathy, seizuredisorder, strokelike episodes, retinitis pigmentosa, external
  44. 44. ophthalmoplegia, or cataracts. These findings are of particularsignificance if there is evidence of maternal inheritance.DepressionAccumulating evidence suggests that depression is a significant riskfactor for developing type 2 diabetes. Pan et al found that the relativerisk was 1.17 in women with depressed mood and 1.25 in women usingantidepressants.[38] Antidepressant use may be a marker of moresevere, chronic, or recurrent depression, or antidepressant use itselfmay increase diabetes risk, possibly by altering glucose homeostasis orpromoting weight gain.In turn, type 2 diabetes has been identified as a risk factor for thedevelopment of depression. Depressive symptoms and majordepressive disorder are twice as prevalent in patients with type 2diabetes as in the general population.[39]SchizophreniaSchizophrenia has been linked to the risk for type 2 diabetes.Dysfunctional signaling involving protein kinase B (Akt) is a possiblemechanism for schizophrenia; moreover, acquired Akt defects areassociated with impaired regulation of blood glucose and diabetes,which is overrepresented in first-episode, medication-naive patientswith schizophrenia.[40] In addition, second-generation antipsychotics areassociated with greater risk for type-2 diabetes.Epidemiology
  45. 45. Occurrence in the United StatesA 2011 Centers for Disease Control and Prevention (CDC) reportestimated that nearly 26 million Americans have diabetes.[3]Additionally, an estimated 79 million Americans have prediabetes.Diabetes affects 8.3% of Americans of all ages, 11.3% of adults aged 20years and older, and 25% of persons age 65 and older, according to theNational Diabetes Fact Sheet for 2011.[3] About 27% of those withdiabetes—7 million Americans—do not know that they have thedisease. About 215,000 people younger than 20 years had diabetes(type 1 or type 2) in the United States in 2010.[3]Prediabetes affects 35% of adults aged 20 years and older. Prediabetes,as defined by the American Diabetes Association, is that state in whichblood glucose levels are higher than normal but not high enough to bediagnosed as diabetes. It is presumed that most persons withprediabetes will subsequently progress to diabetes. The CDC estimatedthat in 2010, 79 million Americans aged 20 years or older hadprediabetes—35% of US adults aged 20 years or older and 50% of thoseaged 65 years or older.A study by Ludwig et al found that neighborhoods with high levels ofpoverty are associated with increases in the incidence of extremeobesity and diabetes. Although the mechanisms behind this associationis unclear, further investigation is warranted.[41]International occurrenceType 2 diabetes mellitus is less common in non-Western countrieswhere the diet contains fewer calories and daily caloric expenditure ishigher. However, as people in these countries adopt Western lifestyles,weight gain and type 2 diabetes mellitus are becoming virtuallyepidemic.
  46. 46. Rates of diabetes are increasing worldwide. The International DiabetesFederation predicts that the number of people living with diabetes willto rise from 366 million in 2011 to 552 million by 2030.[42] In the UnitedStates, the prevalence of diagnosed diabetes has more than doubled inthe last 3 decades, largely because of the increase in obesity.The top 10 countries in number of people with diabetes are currentlyIndia, China, the United States, Indonesia, Japan, Pakistan, Russia,Brazil, Italy, and Bangladesh. The greatest percentage increase in ratesof diabetes will occur in Africa over the next 20 years. Unfortunately, atleast 80% of people in Africa with diabetes are undiagnosed, and manyin their 30s to 60s will die from diabetes there.Race-related demographicsThe prevalence of type 2 diabetes mellitus varies widely among variousracial and ethnic groups. The image below shows data for variouspopulations. Type 2 diabetes mellitus is more prevalent amongHispanics, Native Americans, African Americans, and Asians/PacificIslanders than in non-Hispanic whites. Indeed, the disease is becomingvirtually pandemic in some groups of Native Americans and Hispanicpeople. The risk of retinopathy and nephropathy appears to be greaterin blacks, Native Americans, and Hispanics. Prevalence of type 2 diabetes mellitus in variousracial and ethnic groups in the United States (2007-2009 data).In a study by Selvin et al, differences between blacks and whites werenoted in many glycemic markers and not just the hemoglobin A1c(HbA1c) level.[43] This suggests real differences in glycemia, rather than
  47. 47. in the hemoglobin glycation process or erythrocyte turnover, betweenblacks and whites.Age-related demographicsType 2 diabetes mellitus occurs most commonly in adults aged 40 yearsor older, and the prevalence of the disease increases with advancingage. Indeed, the aging of the population is one reason that type 2diabetes mellitus is becoming increasingly common. Virtually all casesof diabetes mellitus in older individuals are type 2.In addition, however, the incidence of type 2 diabetes is increasingmore rapidly in adolescents and young adults than in other age groups.The disease is being recognized increasingly in younger persons,particularly in highly susceptible racial and ethnic groups and the obese.In some areas, more type 2 than type 1 diabetes mellitus is beingdiagnosed in prepubertal children, teenagers, and young adults. Theprevalence of diabetes mellitus by age is shown in the image below. Prevalence of diabetes mellitus type 2 by age inthe United States (2007 estimates).PrognosisThe prognosis in patients with diabetes mellitus is strongly influencedby the degree of control of their disease. Chronic hyperglycemia isassociated with an increased risk of microvascular complications, asshown in the Diabetes Control and Complications Trial (DCCT) inindividuals with type 1 diabetes[44, 45] and the United KingdomProspective Diabetes Study (UKPDS) in people with type 2 diabetes.[46]
  48. 48. Prognosis in intensive therapyIn the UKPDS, more than 5000 patients with type 2 diabetes werefollowed up for up to 15 years. Those in the intensely treated group hada significantly lower rate of progression of microvascular complicationsthan did patients receiving standard care. Rates of macrovasculardisease were not altered except in the metformin-monotherapy arm inobese individuals, in which the risk of myocardial infarction wassignificantly decreased.In the 10-year follow-up to the UKPDS, patients in the previouslyintensively treated group demonstrated a continued reduction inmicrovascular and all-cause mortality, as well as in cardiovascularevents, despite early loss of differences in glycated hemoglobin levelsbetween the intensive-therapy and conventional-therapy groups.[47]The total follow-up was 20 years, half while in the study and half afterthe study ended.Other, shorter studies, such as Action in Diabetes and Vascular Disease:Preterax and Diamicron Modified Release Controlled Evaluation(ADVANCE) and the Veterans Affairs Diabetes Trial (VADT), showed noimprovement in cardiovascular disease and death with tight control(lower targets than in the UKPDS).[48, 49, 50]In the Action to Control Cardiovascular Risk in Diabetes (ACCORD)study, increased mortality was noted among the poorly-controlledpatients in the intensive glycemic arm; indeed there was a 66% increasein mortality for each 1% increase in HbA1c; the best outcome occurredamong patients who achieved the target of an HbA1c of less than 6%.The excess mortality between the intensive and conventional glycemicarms occurred for A1c above 7%.Differences between the patient populations in these studies and theUKPDS may account for some of the differences in outcome. The
  49. 49. patients in these 3 studies had established diabetes and had a priorcardiovascular disease event or were at high risk for a cardiovasculardisease event, whereas patients in the UKPDS study were younger, withnew-onset diabetes and low rates of cardiovascular disease.Early, intensive, multifactorial (blood pressure, cholesterol)management in patients with type 2 diabetes mellitus was associatedwith a small, nonsignificant reduction in the incidence of cardiovasculardisease events and death in a multinational European study.[51] The3057 patients in this study had diabetes detected by screening andwere randomized to receive either standard diabetes care or intensivemanagement of hyperglycemia (target HbA1c < 7.0%), blood pressure,and cholesterol levels.The benefits of intensive intervention were demonstrated in the Steno-2 study in Denmark, which included 160 patients with type 2 diabetesand persistent microalbuminuria; the mean treatment period was 7.8years, followed by an observational period for a mean of 5.5 years.Intensive therapy was associated with a lower risk of cardiovascularevents, death from cardiovascular causes, progression to end-stagerenal disease, and need for retinal photocoagulation.[52]A British study indicated that the HbA1c level achieved 3 months afterthe initial diagnosis of type 2 diabetes mellitus predicts subsequentmortality. In other words, according to the report, aggressive loweringof glucose after diagnosis bodes well for long-term survival. (Intensifieddiabetes control must be introduced gradually in newly diagnosedpatients.)[53]Another study, a review of randomized clinical trials, showed thatintensive glycemic control reduces the risk of microvascularcomplications, but at the expense of increased risk of hypoglycemia.All-cause mortality and cardiovascular mortality in the study did notdiffer significantly with intensive versus conventional glycemic control;
  50. 50. however, trials conducted in usual-care settings showed a reduction inthe risk of nonfatal myocardial infarction.[54]Overall, these studies suggest that tight glycemic control (HbA1c < 7%or lower) is valuable for microvascular and macrovascular disease riskreduction in patients with recent-onset disease, no knowncardiovascular diseases, and a longer life expectancy. In patients withknown cardiovascular disease, a longer duration of diabetes (15 ormore years), and a shorter life expectancy, however, tighter glycemiccontrol is not as beneficial, particularly with regard to cardiovasculardisease risk. Episodes of severe hypoglycemia may be particularlyharmful in older individuals with poorer glycemic control and existingcardiovascular disease.Vascular disease considerationsOne prospective study with a long follow-up challenges the concept ofcoronary disease risk equivalency between nondiabetic patients with afirst myocardial infarction and patients with type 2 diabetes butwithout any cardiovascular disease. The study found that patients withtype 2 diabetes had lower long-term cardiovascular risk compared withpatients with first myocardial infarction. Other studies have similarlyquestioned this risk equivalency.[55]Patients with diabetes have a lifelong challenge to achieve andmaintain blood glucose levels as close to the reference range aspossible. With appropriate glycemic control, the risk of microvascularand neuropathic complications is decreased markedly. In addition, ifhypertension and hyperlipidemia are treated aggressively, the risk ofmacrovascular complications decreases as well.These benefits are weighed against the risk of hypoglycemia and theshort-term costs of providing high-quality preventive care. Studies haveshown cost savings due to a reduction in acute diabetes-related
  51. 51. complications within 1-3 years after starting effective preventive care.Some studies suggest that broad-based focus on treatment (eg,glycemia, nutrition, exercise, lipids, hypertension, smoking cessation) ismuch more likely to reduce the burden of excess microvascular andmacrovascular events.Yamasaki et al found that abnormal results on single-photon CTmyocardial perfusion imaging in asymptomatic patients with type 2diabetes indicated a higher risk for cardiovascular events (13%),including cardiac death. Smoking and low glomerular filtration ratewere significant contributing factors.[56] However, an earlier studyquestioned the merit of routine screening with adenosine-stressradionuclide myocardial perfusion imaging (MPI) in otherwiseasymptomatic type 2 diabetic patients (the Detection of Ischemia inAsymptomatic Diabetics [DIAD] study).[57]Diabetes-associated mortality and morbidityIn 2009, diabetes mellitus was the seventh leading cause of death in theUnited States.[58] In addition, diabetes is a contributing cause of death inmany cases, and it is probably underreported as a cause of death.Overall, the death rate among people with diabetes is about twice thatof people of similar age but without diabetes.[3]Diabetes mellitus causes morbidity and mortality because of its role inthe development of cardiovascular, renal, neuropathic, and retinaldisease. These complications, particularly cardiovascular disease(approximately 50-75% of medical expenditures), are the major sourcesof expenses for patients with diabetes mellitus.The American Diabetes Association estimated that in 2007, directmedical costs due to diabetes in the United States were $116 billion,with another $58 billion in indirect costs (eg, disability, work loss,premature mortality). Approximately 1 in 5 health care dollars in the
  52. 52. United States was spent caring for someone with diagnosed diabetes,while 1 in 10 health care dollars was attributed to diabetes.[59]Diabetic retinopathyDiabetes mellitus is the major cause of blindness in adults aged 20-74years in the United States; diabetic retinopathy accounts for 12,000-24,000 newly blind persons every year.[60] The National Eye Instituteestimates that laser surgery and appropriate follow-up care can reducethe risk of blindness from diabetic retinopathy by 90%.[60]End-stage renal diseaseDiabetes mellitus, and particularly type 2 diabetes mellitus, is theleading contributor to end-stage renal disease (ESRD) in the UnitedStates.[60] According to the Centers for Disease Control and Prevention,diabetes accounts for 44% of new cases of ESRD.[3] In 2008, 48,374people with diabetes in the United States and Puerto Rico began renalreplacement therapy, and 202,290 people with diabetes were ondialysis or had received a kidney transplant.[60]Neuropathy and vasculopathyDiabetes mellitus is the leading cause of nontraumatic lower limbamputations in the United States, with a 15- to 40-fold increase in riskover that of the nondiabetic population. In 2006, about 65,700nontraumatic lower limb amputations were performed related toneuropathy and vasculopathy.[60]Cardiovascular diseaseThe risk for coronary heart disease (CHD) is 2-4 times greater inpatients with diabetes than in individuals without diabetes.Cardiovascular disease is the major source of mortality in patients withtype 2 diabetes mellitus. Approximately two thirds of people with
  53. 53. diabetes die of heart disease or stroke. Men with diabetes face a 2-foldincreased risk for CHD, and women have a 3- to 4-fold increased risk.Although type 2 diabetes mellitus, both early onset (< 60 y) and lateonset (>60 y), is associated with an increased risk of major CHD andmortality, only the early onset type (duration >10 y) appears to be aCHD risk equivalent.[61]In patients with type 2 diabetes mellitus, a fasting glucose level of morethan 100 mg/dL significantly contributes to the risk of cardiovasculardisease and death, independent of other known risk factors.[62] This isbased on a review of 97 prospective studies involving 820,900 patients.Adolescents with obesity and obesity-related type 2 diabetes mellitusdemonstrate a decrease in diastolic dysfunction.[63] This suggests thatthey may be at increased risk of progressing to early heart failurecompared with adolescents who are either lean or obese but do nothave type 2 diabetes mellitus.CancerA 2010 Consensus Report from a panel of experts chosen jointly by theAmerican Diabetes Association and the American Cancer Societysuggested that people with type 2 diabetes are at an increased risk formany types of cancer.[64] Patients with diabetes have a higher risk forbladder cancer.[65] Age, male gender, neuropathy, and urinary tractinfections were associated with this risk.Pregnancy outcomeUntreated gestational diabetes mellitus can lead to fetal macrosomia,hypoglycemia, hypocalcemia, and hyperbilirubinemia. In addition,mothers with gestational diabetes mellitus have increased rates ofcesarean delivery and chronic hypertension.
  54. 54. Despite advanced age, multiparity, obesity, and social disadvantage,patients with type 2 diabetes were found to have better glycemiccontrol, fewer large-for-gestational-age infants, fewer pretermdeliveries, and fewer neonatal care admissions compared with patientswith type 1 diabetes. This suggests that better tools are needed toimprove glycemic control in patients with type 1 diabetes.[66] (For moreinformation, see Diabetes Mellitus and Pregnancy.)Patient EducationNo longer is it satisfactory to provide patients who have diabetes withbrief instructions and a few pamphlets and expect them to managetheir disease adequately. Instead, education of these patients should bean active and concerted effort involving the physician, nutritionist,diabetes educator, and other health professionals. Moreover, diabeteseducation needs to be a lifetime exercise; believing that it can beaccomplished in 1 or 2 encounters is misguided.A randomized, controlled trial found that for patients with poorlycontrolled diabetes, individual attention and education is superior togroup education.[67] Nonphysician health professionals are usually muchmore proficient at diabetes education and have much more time forthis very important activity.A systematic review suggested that patients with type 2 diabetes whohave a baseline HbA1c of greater than 8% may achieve better glycemiccontrol when given individual education rather than usual care. Outsidethat subgroup, however, the report found no significant differencebetween usual care and individual education. In addition, comparisonof individual education with group education showed equal impact onHbA1c at 12-18 months.[68]
  55. 55. Patient education is an immensely complex topic, however. The clinicalimpression of most experts in the field is that there is merit in theprovision of careful diabetes education at all stages of the disease.ParasitismFrom Wikipedia, the free encyclopediaJump to: navigation, search"Parasite" redirects here. For other uses, see Parasite (disambiguation).Brood parasitism is a form of parasitismParasitism is a type of non mutual relationship between organisms ofdifferent species where one organism, the parasite, benefits at theexpense of the other, the host. Traditionally parasite referred toorganisms with lifestages that needed more than one host (e.g.Taeniasolium). These are now called macroparasites (typically protozoaand helminths). The word parasite now also refers to microparasites,which are typically smaller, such as viruses and bacteria, and can bedirectly transmitted between hosts of the same species [1]. Examples ofparasites include the plants mistletoe and cuscuta, and organisms suchas leeches.
  56. 56. Unlike predators, parasites are generally much smaller than their host;both are special cases of consumer-resource interactions.[2] Parasitesshow a high degree of specialization, and reproduce at a faster ratethan their hosts. Classic examples of parasitism include interactionsbetween vertebrate hosts and diverse animals such as tapeworms,flukes, the Plasmodium species, and fleas.Parasitism is differentiated from the parasitoid relationship, though notsharply, by the fact that parasitoids generally kill or sterilise their hosts.Parasitoidism occurs in much the same variety of organisms thatparasitism does.The harm and benefit in parasitic interactions concern the biologicalfitness of the organisms involved. Parasites reduce host fitness in manyways, ranging from general or specialized pathology, such as parasiticcastration and impairment of secondary sex characteristics, to themodification of host behaviour. Parasites increase their fitness byexploiting hosts for resources necessary for the parasites survival, e.g.food, water, heat, habitat, and genetic dispersion.Although the concept of parasitism applies unambiguously to manycases in nature, it is best considered part of a continuum of types ofinteractions between species, rather than an exclusive category.Particular interactions between species may satisfy some but not allparts of the definition. In many cases, it is difficult to demonstrate thatthe host is harmed. In others, there may be no apparent specializationon the part of the parasite, or the interaction between the organismsmay be short-lived.Contents 1Etymology 2Types 3Host defenses
  57. 57. 4Evolutionary aspects o 4.1Co-speciation 5Ecology o 5.1Quantitative ecology o 5.2Diversity ecology 6Adaptation o 6.1Transmission o 6.2Roles in ecosystems 7Effects on host behavior 8Value 9See also 10References 11Further reading 12External linksEtymologyFirst used in English 1539, the word parasite comes from the MedievalFrenchparasite, from the Latinparasitus, the latinisation of theGreekπαράςιτοσ (parasitos), "one who eats at the table of another"[3]and that from παρά (para), "beside, by"[4] + ςῖ τοσ (sitos), "wheat".[5]Coined in English in 1611, the word parasitism comes from the Greekπαρά (para) + ςιτιςμόσ (sitismos) "feeding, fattening".[6]TypesParasites are classified based on their interactions with their hosts andon their life cycles.Parasites that live on the surface of the host are called ectoparasites(e.g. some mites). Those that live inside the host are calledendoparasites (including all parasitic worms). Endoparasites can exist inone of two forms: intercellular parasites (inhabiting spaces in the
  58. 58. host’s body) or intracellular parasites (inhabiting cells in the host’sbody). Intracellular parasites, such as protozoa, bacteria or viruses,tend to rely on a third organism, which is generally known as the carrieror vector.[citation needed] The vector does the job of transmitting them tothe host. An example of this interaction is the transmission of malaria,caused by a protozoan of the genus Plasmodium, to humans by the biteof an anopheline mosquito. Those parasites living in an intermediateposition, being half-ectoparasites and half-endoparasites, aresometimes called mesoparasite.An epiparasite is one that feeds on another parasite. This relationship isalso sometimes referred to as hyperparasitism, exemplified by aprotozoan (the hyperparasite) living in the digestive tract of a flea livingon a dog.Social parasites take advantage of interactions between members ofsocial organisms such as ants or termites. In kleptoparasitism, parasitesappropriate food gathered by the host. An example is the broodparasitism practiced by many species of cuckoo and cowbird, which donot build nests of their own but rather deposit their eggs in nests ofother species and abandon them there. The host behaves as a"babysitter" as they raise the young as their own. If the host removesthe cuckoos eggs, some cuckoos will return and attack the nest tocompel host birds to remain subject to this parasitism.[7] The cowbird’sparasitism does not necessarily harm its host’s brood; however, thecuckoo may remove one or more host eggs to avoid detection, andfurthermore the young cuckoo may heave the host’s eggs and nestlingsout of the nest.Parasitism can take the form of isolated cheating or exploitation amongmore generalized mutualistic interactions. For example, broad classesof plants and fungi exchange carbon and nutrients in commonmutualistic mycorrhizal relationships; however, some plant species
  59. 59. known as myco-heterotrophs "cheat" by taking carbon from a fungusrather than donating it.Parasitoids are organisms whose larval development occurs inside oron the surface of another organism, resulting in the death of the host.[8]This means that the interaction between the parasitoid and the host isfundamentally different from that of a true parasite and shares some ofthe characteristics of predation.An adelpho-parasite is a parasite in which the host species is closelyrelated to the parasite, often being a member of the same family orgenus. An example of this is the citrus blackfly parasitoid,Encarsiaperplexa, unmated females of which may lay haploid eggs inthe fully developed larvae of their own species. These result in theproduction of male offspring.[9] The marine worm Bonelliaviridis has asimilar reproductive strategy, although the larvae are planktonic.[10]Host defenses This section requires expansion.Hosts respond to parasitisms in many ways ranging from themorphological to the behavioural. In some cases, plants produce toxinsto deter parasitic fungi and bacteria.[citation needed]Vertebrate animalshave developed complex immune systems, which can target parasitesthrough contact with bodily fluids.[citation needed] Animals are also knownto resort to behavioral defenses, examples of which are the avoidanceby sheep of open pastures during spring, when roundworm eggsaccumulated over the previous year hatch en masse;[citation needed] andthe ingestion of alcohol by infected fruit flies as self medication againstblood-borne parasites.[11] In humans, parasite immunity is developedprominently by Immunoglobulin E antibodies.
  60. 60. Evolutionary aspectsBiotrophic parasitism is a common mode of life that has arisenindependently many times in the course of evolution. Depending on thedefinition used, as many as half of all animals have at least one parasiticphase in their life cycles,[12] and it is also frequent in plants and fungi.Moreover, almost all free-living animals are host to one or moreparasites taxa.[12]Restoration of a Tyrannosaurus with parasite infections. A 2009 studyshowed that holes in the skulls of several specimens might have beencaused by Trichomonas-like parasites[13]Parasites evolve in response to the defense mechanisms of their hosts.As a result of host defenses, some parasites evolve adaptations that arespecific to a particular host taxon, specializing to the point where theyinfect only a single species. Such narrow host specificity can be costlyover evolutionary time, however, if the host species becomes extinct.Therefore many parasites can infect a variety of more or less closelyrelated host species, with different success rates.Host defenses also evolve in response to attacks by parasites.Theoretically, parasites may have an advantage in this evolutionaryarms race because of their more rapid generation time. Hosts
  61. 61. reproduce less quickly than parasites, and therefore have fewerchances to adapt than their parasites do over a given span of time.In some cases, a parasite species may coevolve with its host taxa. Long-term coevolution sometimes leads to a relatively stable relationshiptending to commensalism or mutualism, as, all else being equal, it is inthe evolutionary interest of the parasite that its host thrives. A parasitemay evolve to become less harmful for its host or a host may evolve tocope with the unavoidable presence of a parasite-- to the point that theparasites absence causes the host harm. For example, althoughanimals infected with parasitic worms are often clearly harmed, andtherefore parasitized, such infections may also reduce the prevalenceand effects of autoimmune disorders in animal hosts, includinghumans.[14]Competition between parasites tends to favor faster reproducing andtherefor more virulent parasites. Parasites whose life cycle involves thedeath of the host, to exit the present host and sometimes to enter thenext, evolve to be more virulent or even alter the behavior or otherproperties of the host to make it more vulnerable to predators.Parasites that reproduce largely to the offspring of the previous hosttend to become less virulent or mutualist, so that its hosts reproducemore effectively.[1]The presumption of a shared evolutionary history between parasitesand hosts can sometimes elucidate how host taxa are related. Forinstance, there has been dispute about whether flamingos are moreclosely related to the storks and their allies, or to ducks, geese and theirrelatives. The fact that flamingos share parasites with ducks and geeseis evidence these groups may be more closely related to each otherthan either is to storks.Parasitism is part of one explanation for the evolution of secondary sexcharacteristics seen in breeding males throughout the animal world,
  62. 62. such as the plumage of male peacocks and manes of male lions.According to this theory, female hosts select males for breeding basedon such characteristics because they indicate resistance to parasitesand other disease.Co-speciationIn rare cases, a parasite may even undergo co-speciation with its host.One particularly remarkable example of co-speciation exists betweenthe simian foamy virus (SFV) and its primate hosts. In one study, thephylogenies of SFV polymerase and the mitochondrial cytochromeoxidase subunit II from African and Asian primates were compared.[15]Surprisingly, the phylogenetic trees were very congruent in branchingorder and divergence times. Thus, the simian foamy viruses may haveco-speciated with Old World primates for at least 30 million years.EcologyQuantitative ecologyA single parasite species usually has an aggregated distribution acrosshost individuals, which means that most hosts harbor few parasites,while a few hosts carry the vast majority of parasite individuals. Thisposes considerable problems for students of parasite ecology: the useof parametric statistics should be avoided.[citation needed]Log-transformation of data before the application of parametric test, or theuse of non-parametric statistics is recommended by several authors.However, this can give rise to further problems.[16] Therefore, modernday quantitative parasitology is based on more advanced biostatisticalmethods.
  63. 63. Diversity ecologyHosts represent discrete habitat patches that can be occupied byparasites. A hierarchical set of terminology has come into use todescribe parasite assemblages at different host scales.Infrapopulation All the parasites of one species in a single individual host.Metapopulation All the parasites of one species in a host population.Infracommunity All the parasites of all species in a single individual host.Component community All the parasites of all species in a host population.Compound community All the parasites of all species in all host species in an ecosystem.The diversity ecology of parasites differs markedly from that of free-living organisms. For free-living organisms, diversity ecology featuresmany strong conceptual frameworks including Robert MacArthur and E.O. Wilsons theory of island biogeography, Jared Diamonds assemblyrules and, more recently, null models such as Stephen Hubbells unifiedneutral theory of biodiversity and biogeography. Frameworks are notso well-developed for parasites and in many ways they do not fit thefree-living models. For example, island biogeography is predicated onfixed spatial relationships between habitat patches ("sinks"), usuallywith reference to a mainland ("source"). Parasites inhabit hosts, which

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