This is where residents can post their seminars and classes for NU. The actual class description will be posted in the schedule but I thought splitting the two up with make it clearer for our students.
Gaia
This is where residents can post their seminars and classes for NU. The actual class description will be posted in the schedule but I thought splitting the two up with make it clearer for our students.
Gaia
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I chose this subject on behalf of my granddaughter Reahna.She was born premature and her eyes were not fully developed lacking retinas and lenses.She is a testimony as to how far a person can go when those around do not limit them.We have always let her do everything on her own and even gave her a bike this past Christmas(helmet and training wheels of course as with all kids)and she really loves to ride it.We assist by giving her oral direction and she does well.She hates it when we try to hold her ahnd or lead her and she has to do everything herself.You have seen her photo on my profile and if you were not told she was totally blind even if you were with her.She is now learning sigh language so she can talk to her friends that are deaf and mute.She signs in their hand and they do likewise with her.There are no limits unless we put them there.
Blindness
Have you ever put on a blindfold and pretended that you couldn’t see? You probably bumped into things and got confused about which way you were going. But if you had to, you could get adjusted and learn to live without your sight. Lots of people have done just that. They have found ways to learn, play, and work, even though they have trouble seeing or can’t see at all.
How Seeing Happens
Your eyes and your brain work together to see. The eye is made up of many different parts like the cornea, iris, lens, and retina. These parts all work together to focus on light and images. Your eyes then use special nerves to send what you see to your brain, so your brain can process and recognize what you’re seeing. In eyes that work correctly, this process happens almost instantly.
When this doesn’t work the way it should, a person may be visually impaired, or blind. The problem may affect one eye or both eyes. When you think of being blind, you might imagine total darkness. But some people who are blind can still see a little light or shadows. They just can’t see things clearly. People who have some sight, but still need a lot of help, are sometimes called “legally blind.”
What Causes Blindness?
Vision problems can develop before a baby is born. Sometimes, parts of the eyes don’t form the way they should. A kid’s eyes might look fine, but the brain has trouble processing the information they send. The optic nerve sends pictures to the brain, so if the nerve doesn’t form correctly, the baby’s brain won’t receive the messages needed for sight. Blindness can be genetic (say: juh-neh-tik) or inherited (say: in-her-ut-ed), which means that this problem gets passed down to a kid from parents through genes.
Blindness also can be caused by an accident, if something hurts the eye. That’s why it’s so important to protect your eyes when you play certain sports, such as hockey.
Some illnesses, such as diabetes, can damage a person’s vision over time. Other eye diseases, such as cataracts (say: kah-tuh-rakts), can cause vision problems or blindness, but they usually affect older people.
What Does the Doctor Do?
If a kid has serious trouble with vision, he or she might see an ophthalmologist (say: ahf-thuh-mah-luh-jist), a doctor who specializes in eye problems. Even babies might see an ophthalmologist if their parents think they might be having trouble seeing.
At the doctor visit, the doctor will talk with the parents and the kid (if the kid is old enough to describe what’s going on). A doctor might use an eye chart to find out how well the kid can see. You’ve probably seen these charts that contain letters of different sizes. It’s a way of testing how well a person can see. Someone with really good vision would be able to read certain letters from 20 feet (6 meters) away.
Eyesight this good is called 20/20 vision, although some people can see even better than that. The numbers change depending on how clearly a person can see. The larger or closer something needs to be in order for it to be seen, the worse a person’s vision is.
Many times, glasses or contact lenses are all that’s needed to help kids see better. But if glasses and contact lenses can’t make the person’s vision any better – and the person needs to get really close to something to see it – he or she may be considered blind. For instance, someone with good vision might be able to see an object from 200 feet (61 meters) away, but someone is considered blind if he or she needs to be 20 feet (6 meters) away to see the same object.
Babies and little kids won’t be able to use the eye chart, but doctors can check their vision by doing special vision tests or something as simple as putting a toy in front of the child to see if he or she can focus on it.
The ophthalmologist also will examine the kid’s eyes using special medication and lighting that allows him or her to see into the eyeballs. The ophthalmologist will look at each part of the eye to check for problems, such as a cataract (cloudiness of the eye’s lens). Once the doctor knows what’s causing the vision problem, he or she can begin planning how to treat it.
In some cases, an operation can help improve a kid’s vision. For example, if a kid has a cataract, doctors may do surgery to remove it.
Is Learning Different?
If a baby is blind, he or she can still learn and develop normally. But the baby’s parents will need the help of specialists who know how to help blind children. It’s often a great idea for the child to attend special learning programs designed just for little kids who have trouble seeing. These programs would make the most of the senses that the kid does have, such as touch, hearing, smell, and taste.
Touch comes in handy when a child is older and wants to read books. Kids who are visually impaired can learn to read by using a special system called braille. Braille is a way of expressing letters, words, and thoughts. To read braille, a person feels a series of little bumps that are associated with letters in the alphabet. For instance, “A” is represented as one bump. Computer programs and other devices that can “see” turn the words on a page into braille.
Hearing is another important sense if a kid has vision problems. Some devices can read out loud what’s written on a page. With special equipment, a visually impaired kid can read almost anything. These kinds of technologies can be helpful in learning. Kids who are blind might attend a special school, or they might attend regular classes, aided by special devices and specialists.
Hot Dog!
Kids who have vision problems will get help from their parents, doctors, and teachers. When they are older, some of them may get a hand – or should we say a paw? – from a guide dog. These helper dogs are trained to be a blind person’s eyes. That means the dog learns to be very alert to surroundings so he or she can be a good guide for the person.
Not only are these dogs great friends, they give blind people independence, so they can accomplish what they want to accomplish.
Many blind people have gone on to do amazing things in many different fields, including music, the arts, and even sports. Serious vision problems didn’t stop runner Marla Runyan. She was the first legally blind person to ever qualify for the Olympics!
Comment by mskitte — January 7, 2008 @ 10:06 pm |
Mskittie, what a truly amazing story and information you have taught us here today. When I got the message to moderate your article, there was an add above the email for Amazon ~ a book on Macular Degeneration.By the way, I don’t believe in coincidence. I believe that the world unfolds as it should and thank you for unfolding this vital information.
And how wonderful for your granddaughter to have been born into such a family! I have met many people who have been hindered more by their family than their condition could ever do. And what a huge spirit Reahna has to learn sign language to talk with her friends. Please give her a great hug for me!
And early intervention is so important as well. My astigmatism is much worse for having not been taken to the Dr ~ despite years of warnings from my teachers to my mother. (long story another time). I’ll be picking up my new glasses ~ bifocals ack! ~ this week and can’t wait.
But in many ways, I think that Reahna sees the world much clearer than many do.
Gaia ….. who really needs to get crackin’ on her Chakra course!
Comment by nottingtonuniversity — January 8, 2008 @ 12:05 am |
Comment by nottingtonuniversity — January 8, 2008 @ 2:17 am |
Gaia,I thank you for your comment.I was not sure how to post it.I learn by trial and error.Jump in feet first and if you sink get out and try something else.I look forward to the rest of your seminar.It sounds very interesting and may be of help for all of us.I will be looking for these future seminars with anticipation.As for bifocals,have them,hate them.lol
Comment by mskitte — January 8, 2008 @ 3:42 pm |
[...] by nottingtonuniversity — January 8, 2008 @ 2:17 am |Edit [...]
Pingback by The Seven Chakras « Nottington University — January 8, 2008 @ 5:19 pm |
Brain Aneurysm
This subject is also close to home.My sister had a stroke (last weeks topic)due to a Brain Aneurysm.She had been going to the doctors for over a year with severe headaches and was
misdiagnosed.She was told it was stress and treated for stress.There was no testing done to see if there could have been another cause.She became pregnant at 43 years of age and the added pressure caused the Brain Aneurysm to rupture in her 4th month which caused her to have the stroke.It was a chain reaction,Since she was pregnant she was not able to get the medications nor the therapy she needed and this caused here other complications and a slower process of recovery.The baby is fine and 2 1/2 years old.She is very smart and has no effects of the events her mother went through during the prenatal portion of her life.I hope that the knowledge of the symptoms,causes and treatments will help the residents here in Nottington.
Mskittie
An aneurysm is an abnormal widening or ballooning of a portion of a blood vessel. A cerebral aneurysm refers to a blood vessel within your brain that weakens over time and undergoes such widening. This usually occurs at the junctions of the large arteries at the base of your brain, in an area called the Circle of Willis.
As the blood vessel weakens, it begins to bulge out like a balloon. Often, as an aneurysm develops, it forms a neck with an associated dome, or balloonlike structure. The larger the balloon becomes, the greater the risk it may burst. You would then bleed into your brain.
Autopsy studies have revealed that 3-6% of adults in the United States have aneurysms inside their brains. Fortunately, many of these aneurysms are small and not at risk to break. The rates of aneurysms found by accident when other studies are performed suggest that 8-10 million Americans have brain aneurysms. About 20-30% of people with an aneurysm will have more than 1. Each year, for every 100 people with an aneurysm, roughly 1 of them will suffer a rupture or break—a condition known as subarachnoid hemorrhage.
Currently no one can predict which aneurysms will rupture. Data suggest that aneurysms that rupture tend to be larger than 10 mm (0.4 in). About 25,000-30,000 cases of ruptured aneurysms occur in the US each year. About 40% of the people who suffer bleeding from an aneurysm die within the first month. Approximately another one third have residual major nervous system problems but survive.
Many are left with long-term memory problems. They may have difficulty in the following: thinking, perception, and performing simple daily activities.
People who have survived a rupture of a brain aneurysm are twice as likely as the general population to develop another aneurysm. If a second aneurysm occurs, these people are 6 times more likely to have another ruptured aneurysm and bleeding in their brain.
Brain Aneurysm Causes
Aneurysms in the brain are considered to be acquired problems. They are not present at birth. Rather, they develop over a lifetime.
Other evidence indicates that genetic factors make some people more likely to develop brain aneurysms. The exact pattern of inheritance is not clear.
* According to several studies, up to 20% of people with bleeding from an aneurysm have a first- or second-degree relative with a brain aneurysm.
* These relatives are at higher risk for bleeding in the brain.
* In most families with brain aneurysms, the condition affects only 2-3 members of the extended family, and the method of inheritance is not apparent.
Associated conditions – A number of conditions are associated with brain aneurysms, as follows:
* Polycystic kidney disease – A genetic disorder characterized by the growth of numerous cysts in the kidneys
* Ehlers-Danlos syndrome – A group of inherited connective tissue disorders characterized by extreme flexibility of joints, easily stretched skin and easily damaged tissue
* Marfan syndrome – An inherited disorder of connective tissue, the glue and the scaffolding of your body, which leads to tissue with less strength and that can rupture easier
* Neurofibromatosis – A group of 8 genetic disorders of the nervous system that primarily affect the development and growth of nerve cell tissues (These disorders cause tumors to grow on nerves and produce other abnormalities such as skin changes and bone deformities.)
Environmental factors: Significant evidence suggests that environmental factors make some people more likely to develop brain aneurysms.
* Brain aneurysms are very rare in children.
* The likelihood of having an aneurysm increases throughout life.
* Tobacco
o Cigarette smoking is the only factor that has been consistently demonstrated to increase the risk of ruptured aneurysm.
o Sustaining a rupture of a brain aneurysm is about 10 times more likely in a smoker than in a nonsmoker.
o The more cigarettes smoked, the higher the risk.
* High blood pressure
o Several studies have shown an increased risk for the development and rupture of brain aneurysms in people with high blood pressure.
o Most experts believe that high blood pressure remains a risk factor but not to the extent that cigarette smoking is a risk.
* High cholesterol
o The effect of high cholesterol remains unclear.
o Three studies have looked at high cholesterol as a risk factor for aneurysm and rupture. Two studies showed no association and one study showed a relationship.
* Alcohol consumption
o A moderate to high level of alcohol use is considered a risk factor for the rupture of a brain aneurysm.
o It is unclear if alcohol use increases the risk of developing an aneurysm.
o Binge drinking appears to dramatically increase the risk of subarachnoid hemorrhage from a ruptured aneurysm.
Brain Aneurysm Symptoms
The initial symptom of a brain aneurysm may be a sudden, severe, catastrophic headache.
Most people will not be aware that they have an aneurysm in the brain until the aneurysm ruptures, causing the severe headache. For the majority of people, symptoms do not come directly from the aneurysm, but rather from the following:
* Symptoms of a ruptured aneurysm
o Severe headache
+ If you have a history of headaches, such as migraine or tension headaches, you may experience a headache uniquely different from your normal pattern.
+ You should consider any severe headache different from your customary headache as suspicious for a ruptured aneurysm. You may experience the worst headache of your life, which may also be a sign of a stroke.
+ Up to 50% of people with a ruptured aneurysm will suffer a warning (prodromal) headache several days or even weeks before the rupture. The average is about 2 weeks.
+ This warning headache is thought to be due to minor blood leakage, without rupture of the aneurysm, and is commonly referred to as a “sentinel headache.”
o Neck stiffness
o Nausea
o Vomiting
o Sensitivity to light
* These symptoms may be followed rapidly by an alteration in mental status ranging from confusion to coma.
* Seizures occur in about 25% of people with a ruptured aneurysm.
* Some people will have symptoms of an enlarging, unruptured aneurysm.
o A dilated pupil in 1 eye
o Visual field defects: This refers to the inability to see objects that are in the direction you are looking. For instance, if you are looking directly at a large screen TV, you may not be able to see the whole screen at once. There may be a “hole” in the center or off to the sides that you simply cannot see while looking straight ahead.
o Inability to move 1 eye in all directions
o Pain above or behind the eye
o Pain in the temple, in the back of the skull, or the neck, depending on the location of the aneurysm
When to Seek Medical Care
Call your doctor at once. Evaluation for a suspected rupture of a brain aneurysm must be performed immediately, most appropriately in a hospital’s emergency department.
* If you have any questions about whether or not there is cause for concern, call your doctor for advice. The doctor most likely will advise you to seek care in a hospital’s emergency department.
* If you are a close relative of someone with a known aneurysm, or ruptured aneurysm, inform your doctor. Your doctor will want to be aware of such information. You should realize, though, that you seldom need to be screened for an aneurysm unless you are having symptoms.
A ruptured aneurysm is a life-threatening event. Any headache that is severe and comes on suddenly should prompt immediate evaluation by a doctor, particularly if the headache is associated with any of the following:
* Seizure
* Vomiting
* Alteration in consciousness
* Neurological defects such as inability to speak, to move an extremity, walk, severe dizziness, changes in your vision
* This evaluation most appropriately occurs in the emergency department.
* Rupture of an aneurysm frequently occurs at times of stress or physical exertion. Any severe headache, with or without the symptoms described here, should be investigated immediately.
* People who experience migraine headaches with an established headache pattern should seek evaluation for any headache that is severe, comes on suddenly, and is different from their usual headache pattern. This might include the following:
o A much more intense headache
o A headache of maximum intensity at the onset
o A headache without forewarning, among other symptoms
* Family members, particularly siblings, of people with known aneurysms or a history of ruptured aneurysm are at higher risk for rupture and should seek care promptly for any of these symptoms:
o Unusual headache
o Head pain
o Eye pain
o Visual disturbances
* Anyone who has survived a ruptured aneurysm should be especially concerned and seek care immediately for any new or suspicious headache.
Exams and Tests
If the doctor suspects a ruptured aneurysm, you will have a complete physical exam, with particular attention to the neurologic exam.
* The doctor will be very concerned about your level of consciousness and the presence or absence of localized nerve problems.
* The doctor will seek a quick focused history from you, or from family members if you are unable to give information.
* The doctor quickly will try to determine the likelihood that you have a ruptured aneurysm as opposed to other causes of headache or alterations of consciousness.
* Your physical examination and the history of the event will guide further diagnostic testing.
* Any time you become unstable, such as changes in blood pressure, decreasing level of alertness, or difficulty breathing, the doctor may perform life-saving maneuvers. Such maneuvers might include placing a tube down your throat to protect your airway and provide adequate breathing.
* If you have no symptoms, the doctor may include in your workup many of the following tests, although the tests may be performed on an outpatient basis.
o A CT scan of your brain: A CT scan will detect acute bleeding from a ruptured aneurysm about 90% of the time.
+ Aside from the bleeding, CT scans are able to detect some complications of a ruptured aneurysm such as swelling of the brain.
+ A plain CT scan is not a good test to use to detect aneurysms that have not ruptured.
o A lumbar puncture (spinal tap): If the CT scan shows no evidence of bleeding in your brain, the doctor may perform a lumbar puncture.
+ This procedure involves placing a needle into your spinal canal in the low back, below the level at which the spinal cord ends.
+ The doctor will collect spinal fluid and send it to the lab to look for the presence of blood.
+ If blood is present, particularly if the spinal fluid is yellow, you have bleeding in the brain and the workup proceeds further.
o Cerebral angiography: The doctor likely will perform this test next.
+ The doctor places a catheter into your groin while you are under local anesthesia. It is threaded up toward your brain and then injects an x-ray contrast dye into your arteries.
+ The doctor will take several x-rays to be reviewed by neurosurgeon and a radiologist.
+ These x-rays help the neurosurgeon locate the aneurysm and determine how to manage it.
+ They also will show the presence of other aneurysms.
o Magnetic resonance angiography: Like an MRI, this test is very useful for detecting unruptured aneurysms and for screening high-risk patients.
+ It is noninvasive and virtually risk-free.
+ Doctors consider the test inadequate for planning surgery.
o Helical CT angiography: This test is a recent addition to the diagnostic possibilities.
+ It does involve administering x-ray contrast dye and is not risk-free.
+ It has the potential to aid in surgical planning in that it demonstrates the relation of the aneurysm to bony structures of the skull base.
Brain Aneurysm Treatment
Self-Care at Home
A suspected rupture of a brain aneurysm is a true medical emergency. No specific treatment can be given at home.
Medical Treatment
* Ruptured brain aneurysm
o Doctors locate the aneurysm with cerebral angiography and then surgically clip it.
o
o Doctors generally perform the clipping within 72 hours because an aneurysm has a 30% risk of rebleeding. This risk peaks at 7 days and carries with it a 60% risk of poor outcome or death.
o For people with severe symptoms such as a coma, doctors often delay surgery and instead use other options.
o Options include interventional radiologic procedures such as placing a coil inside the blood vessel during the cerebral angiography. You can think of the coil as a clip placed within the aneurysm, rather than on the outside.
o Either the surgical clip or placing a coil effectively removes the aneurysm from your blood circulation system and eliminates the risk of rebleeding.
o Clipping also allows the doctor to more aggressively manage the associated spasm of your arteries that is likely to follow.
o Virtually all people with a brain aneurysm will receive nimodipine (Nimotop), a calcium channel blocker that helps prevent the blood vessel spasm that regularly accompanies ruptured aneurysms.
+ Additional methods of treating vessel spasm include inducing high blood pressure with fluids and medications in an effort to increase blood flow through areas of spasm and narrowing.
+ Doctors will use a special ultrasound exam, a transcranial Doppler ultrasound, to assess the degree of spasm and help guide treatment.
o Additional treatments that may be required depend on the severity of your symptoms and information obtained by diagnostic studies. These may include the following:
+ A drainage device may be placed through your skull to allow drainage of fluid and decrease pressure within your brain.
+ Antiseizure medications may prevent seizures that frequently accompany ruptured aneurysms.
+ Glucocorticoids, anti-inflammatory steroids, occasionally used to help control swelling in the brain, remain controversial because no proven benefit has been shown.
+ Antifibrinolytic agents may be used to stabilize the clot within an aneurysm in people who cannot undergo a clipping procedure. Increasing numbers of people develop delayed strokes, so doctors now use antifibrinolytic agents infrequently.
* Unruptured brain aneurysm
o The best treatment would be to prevent rupture of an aneurysm once it is discovered.
o Larger aneurysms are more likely to bleed than smaller ones.
o Currently there is no reliable method of determining which aneurysms will rupture. For this reason doctors offer a variety of opinions on how to treat an intact aneurysm once it is discovered.
o Treatment most likely will be a surgical clipping procedure or placement of a coil in the aneurysm similar to those in a ruptured aneurysm.
Next Steps
Follow-up
* After you have been diagnosed with a cerebral aneurysm, your doctor will advise you to modify any risk factors you may have.
o This may mean quitting the use of alcohol and tobacco.
o Your doctor likely will follow your blood pressure closely.
o Your doctor may add medications to help control your blood pressure.
* Your doctor probably will recommend that you have regular physical examinations to monitor for symptoms of an enlarging aneurysm.
o The doctor will be particularly interested in changes in your vision, headache patterns, and examination of your eyes.
o An examination of your nerve functions likely will be performed.
Prevention
* At this time doctors do not recommend screening family members for aneurysms that show no symptoms.
o If you have 1 close family member who has had a rupture of an aneurysm, your lifetime risk of a ruptured aneurysm is about 1% at age 50 years and 2% at age 70 years.
o The risk of surgery to repair an aneurysm that exists but has no symptoms is 2-5%, which is clearly greater than the risk of hemorrhage into the brain for such people.
* Screening is recommended for families who show no symptoms but who have 2 members with a ruptured aneurysm.
o Siblings over age 30 years are at particularly high risk and should be screened.
o Current recommendations are that family members have an MRI angiography or helical CT angiography every 5 years.
* The major modifiable risk factors for rupture of an aneurysm are the following. You can influence 2 of these directly. In cooperation with your doctor, you nearly always can control your blood pressure as well.
o Do not smoke cigarettes.
o Control high blood pressure.
o Avoid binge drinking.
o Additionally, the use of amphetamines (speed), cocaine, and even most medications for the common cold can all dramatically increase blood pressure and increase the risk of rupture in people with brain aneurysms.
Outlook
Most aneurysms show no symptoms until they rupture. The single most important predictor of the outcome of the subarachnoid hemorrhage is your physical condition when you arrive at the hospital.
* Once an aneurysm has ruptured, recovery depends on the degree of bleeding and associated problems.
o Rebleeding
o Increased pressure within your brain
o Subsequent artery spasms and narrowing of the arteries of your brain
* Doctors direct treatment at the time your rupture is diagnosed toward preventing these complications.
* Once you are diagnosed with an unruptured aneurysm the main question is what to do about it.
o Most experts agree that for aneurysms smaller than 10 mm (0.4 in), if you have no history of bleeding into your brain, the risks of surgery outweigh the potential benefits.
+ Factors that would favor surgery are high blood pressure that is poorly controlled and symptoms related to compression of nerve tissue by the aneurysm.
+ Factors weighing against surgery include location of the aneurysm in a surgically difficult area and co-existing illnesses that would increase your risk of surgery.
o A promising treatment for brain aneurysms involves placing a metallic coil inside the aneurysm. The coil causes a clot to form inside, and the clot blocks the aneurysm from your circulation system.
+ This markedly decreases the chance of rupture.
+ The risks of the procedure are much lower than for surgery, but the long-term outcomes are not yet known.
+ Current experience indicates that this technique works best for smaller aneurysms. It may, in fact, cause an increased risk of rupture when used in very large aneurysms.
Comment by mskitte — January 22, 2008 @ 6:30 am |
DIABETES
The term diabetes, without qualification, usually refers to diabetes mellitus, which is associated with excessive sweet urine (known as “glycosuria”) but there are several rarer conditions also named diabetes. The most common of these is diabetes insipidus in which the urine is not sweet (insipidus meaning “without taste” in Latin); it can be caused by either kidney (nephrogenic DI) or pituitary gland (central DI) damage. The principal two idiopathic forms of diabetes mellitus are known as types 1 and 2. The term “type 1 diabetes” has universally replaced several former terms, including childhood-onset diabetes, juvenile diabetes, and insulin-dependent diabetes (IDDM). Likewise, the term “type 2 diabetes” has replaced several former terms, including adult-onset diabetes, obesity-related diabetes, and non-insulin-dependent diabetes (NIDDM). Beyond these two types, there is no agreed-upon standard nomenclature. Various sources have defined “type 3 diabetes” as, among others, gestational diabetes, insulin-resistant type 1 diabetes (or “double diabetes”), type 2 diabetes which has progressed to require injected insulin, and latent autoimmune diabetes of adults (or LADA or “type 1.5″ diabetes.) There is also maturity onset diabetes of the young (MODY) which is a group of several single gene disorders with strong family histories that present as type 2 diabetes before 30 years of age.
Type 1 diabetes mellitus
Type 1 diabetes mellitus is characterized by loss of the insulin-producing beta cells of the islets of Langerhans in the pancreas, leading to a deficiency of insulin. The main cause of this beta cell loss is a T-cell mediated autoimmune attack. There is no known preventative measure that can be taken against type 1 diabetes, which comprises up to 10% of diabetes mellitus cases in North America and Europe (though this varies by geographical location). Most affected people are otherwise healthy and of a healthy weight when onset occurs. Sensitivity and responsiveness to insulin are usually normal, especially in the early stages. Type 1 diabetes can affect children or adults but was traditionally termed “juvenile diabetes” because it represents a majority of cases of diabetes affecting children.
The principal treatment of type 1 diabetes, even from the earliest stages, is replacement of insulin combined with careful monitoring of blood glucose levels using blood testing monitors. Without insulin, diabetic ketoacidosis can develop and may result in coma or death. Emphasis is also placed on lifestyle adjustments (diet and exercise) though these can do absolutely nothing to reverse the loss. Apart from the common subcutaneous injections, it is also possible to deliver insulin by a pump, which allows continuous infusion of insulin 24 hours a day at preset levels, and the ability to program doses (a bolus) of insulin as needed at meal times. An inhaled form of insulin, Exubera, was approved by the FDA in January 2006, although Pfizer discontinued Exubera in October 2007.
Type 1 treatment must be continued indefinitely. Treatment does not significantly impair normal activities, if sufficient patient training, awareness, appropriate care, discipline in testing and dosing of insulin is taken. However, treatment is burdensome for patients, chronic and insulin is replaced in a non-physiological manner, and is therefore is far from ideal. The average glucose level for the type 1 patient should be as close to normal (80–120 mg/dl, 4–6 mmol/l) as is safely possible. Some physicians suggest up to 140–150 mg/dl (7-7.5 mmol/l) for those having trouble with lower values, such as frequent hypoglycemic events. Values above 200 mg/dl (10 mmol/l) is sometimes accompanied by discomfort and frequent urination leading to dehydration. Values above 300 mg/dl (15 mmol/l) usually require treatment and may lead to ketoacidosis, although is not immediately life-threatening. However, low levels of blood glucose, called hypoglycemia, may lead to seizures or episodes of unconsciousness and absolutely must be treated immediately.
Type 2 Diabetes Mellitus
Type 2 diabetes mellitus is due to insulin resistance or reduced insulin sensitivity, combined with reduced insulin secretion. The defective responsiveness of body tissues to insulin almost certainly involves the insulin receptor in cell membranes. In the early stage the predominant abnormality is reduced insulin sensitivity, characterized by elevated levels of insulin in the blood. At this stage hyperglycemia can be reversed by a variety of measures and medications that improve insulin sensitivity or reduce glucose production by the liver. As the disease progresses the impairment of insulin secretion worsens, and therapeutic replacement of insulin often becomes necessary.
There are numerous theories as to the exact cause and mechanism in type 2 diabetes. Central obesity (fat concentrated around the waist in relation to abdominal organs, but not subcutaneous fat) is known to predispose individuals for insulin resistance. Abdominal fat is especially active hormonally, secreting a group of hormones called adipokines that may possibly impair glucose tolerance. Obesity is found in approximately 55% of patients diagnosed with type 2 diabetes. Other factors include aging (about 20% of elderly patients in North America have diabetes) and family history (type 2 is much more common in those with close relatives who have had it). In the last decade, type 2 diabetes has increasingly begun to affect children and adolescents, likely in connection with the increased prevalence of childhood obesity seen in recent decades in some places.
Type 2 diabetes may go unnoticed for years because visible symptoms are typically mild, non-existent or sporadic, and usually there are no ketoacidotic episodes. However, severe long-term complications can result from unnoticed type 2 diabetes, including renal failure due to diabetic nephropathy, vascular disease (including coronary artery disease), vision damage due to diabetic retinopathy, loss of sensation or pain due to diabetic neuropathy, and liver damage from non-alcoholic steatohepatitis.
Type 2 diabetes is usually first treated by increasing physical activity, decreasing carbohydrate intake, and losing weight. These can restore insulin sensitivity even when the weight loss is modest, for example around 5 kg (10 to 15 lb), most especially when it is in abdominal fat deposits. It is sometimes possible to achieve long-term, satisfactory glucose control with these measures alone. However, the underlying tendency to insulin resistance is not lost, and so attention to diet, exercise, and weight loss must continue. The usual next step, if necessary, is treatment with oral antidiabetic drugs. Insulin production is initially only moderately impaired in type 2 diabetes, so oral medication (often used in various combinations) can be used to improve insulin production (e.g., sulfonylureas), to regulate inappropriate release of glucose by the liver and attenuate insulin resistance to some extent (e.g., metformin), and to substantially attenuate insulin resistance (e.g., thiazolidinediones). According to one study, overweight patients treated with metformin compared with diet alone, had relative risk reductions of 32% for any diabetes endpoint, 42% for diabetes related death and 36% for all cause mortality and stroke.Oral medication may eventually fail due to further impairment of beta cell insulin secretion. At this point, insulin therapy is necessary to maintain normal or near normal glucose levels.
Gestational diabetes
Gestational diabetes mellitus (GDM) resembles type 2 diabetes in several respects, involving a combination of relatively inadequate insulin secretion and responsiveness. It occurs in about 2%–5% of all pregnancies and may improve or disappear after delivery. Gestational diabetes is fully treatable but requires careful medical supervision throughout the pregnancy. About 20%–50% of affected women develop type 2 diabetes later in life.
Even though it may be transient, untreated gestational diabetes can damage the health of the fetus or mother. Risks to the baby include macrosomia (high birth weight), congenital cardiac and central nervous system anomalies, and skeletal muscle malformations. Increased fetal insulin may inhibit fetal surfactant production and cause respiratory distress syndrome. Hyperbilirubinemia may result from red blood cell destruction. In severe cases, perinatal death may occur, most commonly as a result of poor placental profusion due to vascular impairment. Induction may be indicated with decreased placental function. A cesarean section may be performed if there is marked fetal distress or an increased risk of injury associated with macrosomia, such as shoulder dystocia.
Other types
There are several rare causes of diabetes mellitus that do not fit into type 1, type 2, or gestational diabetes; attempts to classify them remain controversial. Some cases of diabetes are caused by the body’s tissue receptors not responding to insulin (even when insulin levels are normal, which is what separates it from type 2 diabetes); this form is very uncommon. Genetic mutations (autosomal or mitochondrial) can lead to defects in beta cell function. Abnormal insulin action may also been genetically determined in some cases. Any disease that causes extensive damage to the pancreas may lead to diabetes (for example, chronic pancreatitis and cystic fibrosis). Diseases associated with excessive secretion of insulin-antagonistic hormones can cause diabetes (which is typically resolved once the hormone excess is removed). Many drugs impair insulin secretion and some toxins damage pancreatic beta cells. The ICD-10 (1992) diagnostic entity, malnutrition-related diabetes mellitus (MRDM or MMDM, ICD-10 code E12), was deprecated by the World Health Organization when the current taxonomy was introduced in 1999.
Signs and symptoms
The classical triad of diabetes symptoms is polyuria, polydipsia and polyphagia, which are, respectively, frequent urination; increased thirst and consequent increased fluid intake; and increased appetite. Symptoms may develop quite rapidly (weeks or months) in type 1 diabetes, particularly in children. However, in type 2 diabetes the symptoms develop much more slowly and may be subtle or completely absent. Type 1 diabetes may also cause a rapid yet significant weight loss (despite normal or even increased eating) and irreducible fatigue. All of these symptoms except weight loss can also manifest in type 2 diabetes in patients whose diabetes is poorly controlled.
When the glucose concentration in the blood is raised beyond the renal threshold, reabsorption of glucose in the proximal renal tubuli is incomplete, and part of the glucose remains in the urine(glycosuria). This increases the osmotic pressure of the urine and inhibits the reabsorption of water by the kidney, resulting in increased urine production (polyuria) and increased fluid loss. Lost blood volume will be replaced osmotically from water held in body cells, causing dehydration and increased thirst.
Prolonged high blood glucose causes glucose absorption, which leads to changes in the shape of the lenses of the eyes, resulting in vision changes. Blurred vision is a common complaint leading to a diabetes diagnosis; type 1 should always be suspected in cases of rapid vision change whereas type 2 is generally more gradual, but should still be suspected.
Patients (usually with type 1 diabetes) may also present with diabetic ketoacidosis (DKA), an extreme state of metabolic dysregulation characterized by the smell of acetone on the patient’s breath; a rapid, deep breathing known as Kussmaul breathing; polyuria; nausea; vomiting and abdominal pain; and any of many altered states of consciousness or arousal (such as hostility and mania or, equally, confusion and lethargy). In severe DKA, coma may follow, progressing to death. Diabetic ketoacidosis is a medical emergency and requires hospital admission.
A rarer but equally severe possibility is hyperosmolar nonketotic state, which is more common in type 2 diabetes and is mainly the result of dehydration due to loss of body water. Often, the patient has been drinking extreme amounts of sugar-containing drinks, leading to a vicious circle in regard to the water loss.
Genetics
Both type 1 and type 2 diabetes are at least partly inherited. Type 1 diabetes appears to be triggered by some (mainly viral) infections, or in a less common group, by stress or environmental exposure (such as exposure to certain chemicals or drugs). There is a genetic element in individual susceptibility to some of these triggers which has been traced to particular HLA genotypes (i.e., the genetic “self” identifiers relied upon by the immune system). However, even in those who have inherited the susceptibility, type 1 diabetes mellitus seems to require an environmental trigger. A small proportion of people with type 1 diabetes carry a mutated gene that causes maturity onset diabetes of the young (MODY).
There is a stronger inheritance pattern for type 2 diabetes. Those with first-degree relatives with type 2 have a much higher risk of developing type 2, increasing with the number of those relatives. Concordance among monozygotic twins is close to 100%, and about 25% of those with the disease have a family history of diabetes. Candidate genes include KCNJ11 (potassium inwardly rectifying channel, subfamily J, member 11), which encodes the islet ATP-sensitive potassium channel Kir6.2, and TCF7L2 (transcription factor 7–like 2), which regulates proglucagon gene expression and thus the production of glucagon-like peptide-1. Moreover, obesity (which is an independent risk factor for type 2 diabetes) is strongly inherited.
Various hereditary conditions may feature diabetes, for example myotonic dystrophy and Friedreich’s ataxia. Wolfram’s syndrome is an autosomal recessive neurodegenerative disorder that first becomes evident in childhood. It consists of diabetes insipidus, diabetes mellitus, optic atrophy, and deafness, hence the acronym DIDMOAD.
Pathophysiology
Mechanism of insulin release in normal pancreatic beta cells. Insulin production is more or less constant within the beta cells, irrespective of blood glucose levels. It is stored within vacuoles pending release, via exocytosis, which is triggered by increased blood glucose levels.
Mechanism of insulin release in normal pancreatic beta cells. Insulin production is more or less constant within the beta cells, irrespective of blood glucose levels. It is stored within vacuoles pending release, via exocytosis, which is triggered by increased blood glucose levels.
Insulin is the principal hormone that regulates uptake of glucose from the blood into most cells (primarily muscle and fat cells, but not central nervous system cells). Therefore deficiency of insulin or the insensitivity of its receptors plays a central role in all forms of diabetes mellitus.
Much of the carbohydrate in food is converted within a few hours to the monosaccharide glucose, the principal carbohydrate found in blood and used by the body as fuel. Some carbohydrates are not so converted. Notable examples include fruit sugar (fructose), usable as cellular fuel but it is not converted to glucose, and which therefore does not participate in the insulin/glucose metabolic regulatory mechanism. Additionally, the carbohydrate cellulose (though it is actually many glucose molecules in long chains) is not converted to glucose, as humans and many animals have no digestive pathway capable of breaking up cellulose.
Insulin is released into the blood by beta cells (β-cells), found in the Islets of Langerhans in the pancreas, in response to rising levels of blood glucose after eating. Insulin is used by about two-thirds of the body’s cells to absorb glucose from the blood for use as fuel, for conversion to other needed molecules, or for storage. Insulin is also the principal control signal for conversion of glucose to glycogen for internal storage in liver and muscle cells. Lowered glucose levels result both in the reduced release of insulin from the beta cells and in the reverse conversion of glycogen to glucose when glucose levels fall. This is mainly controlled by the hormone glucagon which acts in an opposite manner to insulin. Glucose thus recovered by the liver re-enters the bloodstream; muscle cells lack the necessary export mechanism.
Higher insulin levels increase some anabolic (“building up”) processes such as cell growth and duplication, protein synthesis, and fat storage. Insulin (or its lack) is the principal signal in converting many of the bidirectional processes of metabolism from a catabolic to an anabolic direction, and vice versa. In particular, a low insulin level is the trigger for entering or leaving ketosis (the fat burning metabolic phase).
If the amount of insulin available is insufficient, if cells respond poorly to the effects of insulin (insulin insensitivity or resistance), or if the insulin itself is defective, then glucose will not be absorbed properly by those body cells that require it nor will it be stored appropriately in the liver and muscles. The net effect is persistent high levels of blood glucose, poor protein synthesis, and other metabolic derangements, such as acidosis.
Diagnosis
The diagnosis of type 1 diabetes, and many cases of type 2, is usually prompted by recent-onset symptoms of excessive urination (polyuria) and excessive thirst (polydipsia), often accompanied by weight loss. These symptoms typically worsen over days to weeks; about a quarter of people with new type 1 diabetes have developed some degree of diabetic ketoacidosis by the time the diabetes is recognized. The diagnosis of other types of diabetes is usually made in other ways. These include ordinary health screening; detection of hyperglycemia during other medical investigations; and secondary symptoms such as vision changes or unexplainable fatigue. Diabetes is often detected when a person suffers a problem that is frequently caused by diabetes, such as a heart attack, stroke, neuropathy, poor wound healing or a foot ulcer, certain eye problems, certain fungal infections, or delivering a baby with macrosomia or hypoglycemia.
Diabetes mellitus is characterized by recurrent or persistent hyperglycemia, and is diagnosed by demonstrating any one of the following:
* fasting plasma glucose level at or above 126 mg/dL (7.0 mmol/l).
* plasma glucose at or above 200 mg/dL (11.1 mmol/l) two hours after a 75 g oral glucose load as in a glucose tolerance test.
* random plasma glucose at or above 200 mg/dL (11.1 mmol/l).
A positive result, in the absence of clinical symptoms of diabetes, should be confirmed by another of the above-listed methods on a different day. Most physicians prefer to measure a fasting glucose level because of the ease of measurement and the considerable time commitment of formal glucose tolerance testing, which takes two hours to complete. According to the current definition, two fasting glucose measurements above 126 mg/dL (7.0 mmol/l) is considered diagnostic for diabetes mellitus.
Patients with fasting glucose levels between 100 and 125 mg/dL (6.1 and 7.0 mmol/l) are considered to have impaired fasting glycemia. Patients with plasma glucose at or above 140 mg/dL or 7.8 mmol/l two hours after a 75 g oral glucose load are considered to have impaired glucose tolerance. Of these two pre-diabetic states, the latter in particular is a major risk factor for progression to full-blown diabetes mellitus as well as cardiovascular disease.
While not used for diagnosis, an elevated level of glucose irreversibly bound to hemoglobin (termed glycosylated hemoglobin or HbA1c) of 6.0% or higher (the 2003 revised U.S. standard) is considered abnormal by most labs; HbA1c is primarily used as a treatment-tracking test reflecting average blood glucose levels over the preceding 90 days (approximately). However, some physicians may order this test at the time of diagnosis to track changes over time. The current recommended goal for HbA1c in patients with diabetes is <7.0%, which is considered good glycemic control, although some guidelines are stricter (<6.5%). People with diabetes who have HbA1c levels within this range have a significantly lower incidence of complications from diabetes, including retinopathy and diabetic nephropathy.
Screening
Diabetes screening is recommended for many people at various stages of life, and for those with any of several risk factors. The screening test varies according to circumstances and local policy, and may be a random blood glucose test, a fasting blood glucose test, a blood glucose test two hours after 75 g of glucose, or an even more formal glucose tolerance test. Many healthcare providers recommend universal screening for adults at age 40 or 50, and often periodically thereafter. Earlier screening is typically recommended for those with risk factors such as obesity, family history of diabetes, high-risk ethnicity (Mestizo/Hispanic, Native American, Afro-Caribbean, Pacific Island, and South Asian ancestry).
Many medical conditions are associated with diabetes and warrant screening. A partial list includes: high blood pressure, elevated cholesterol levels, coronary artery disease, past gestational diabetes, polycystic ovary syndrome, chronic pancreatitis, fatty liver, hemochromatosis, cystic fibrosis, several mitochondrial neuropathies and myopathies, myotonic dystrophy, Friedreich’s ataxia, some of the inherited forms of neonatal hyperinsulinism. The risk of diabetes is higher with chronic use of several medications, including high-dose glucocorticoids, some chemotherapy agents (especially L-asparaginase), as well as some of the antipsychotics and mood stabilizers (especially phenothiazines and some atypical antipsychotics).
Prevention
Type 1 diabetes risk is known to depend upon a genetic predisposition based on HLA types (particularly types DR3 and DR4), an unknown environmental trigger (suspected to be an infection, although none has proven definitive in all cases), and an uncontrolled autoimmune response that attacks the insulin producing beta cells. Some research has suggested that breastfeeding decreased the risk; [19][20] various other nutritional risk factors are being studied, but no firm evidence has been found. Giving children 2000 IU of Vitamin D during their first year of life is associated with reduced risk of type 1 diabetes.
Type 2 diabetes risk can be reduced in many cases by making changes in diet and increasing physical activity.The American Diabetes Association (ADA) recommends maintaining a healthy weight, getting at least 2½ hours of exercise per week (a brisk sustained walk appears sufficient), having a modest fat intake, and eating a good amount of fiber and whole grains. The ADA does not recommend alcohol consumption as a preventative, but it is interesting to note that moderate alcohol intake may reduce the risk (though heavy consumption clearly increases damage to body systems significantly). There is inadequate evidence that eating foods of low glycemic index is clinically helpful.
Some studies have shown delayed progression to diabetes in predisposed patients through prophylactic use of metformin, rosiglitazone, or valsartan. In patients on hydroxychloroquine for rheumatoid arthritis, incidence of diabetes was reduced by 77% Breastfeeding might also be associated with the prevention of type 2 of the disease in mothers.
It is possible that adequate copper could help prevent insulin dependant diabetes since it does so for ATZ poisoned mice and copper in drinking water has somewhat of a protective affect . It could be that copper produces its effects through super oxidase dismutase (SOD) because metaloporpherin based superoxide dismutase can prevent or delay the onset of the autoimmune cascade in diabetes, using mice. However, there are sufficient differences in human and animal models to indicate this is only a theory at the present time.
Children with antibodies treated with vitamin B-3 (niacin) had less than half the onset of diabetes incidence in a 7-year time span as the general population and even lower incidence relative to those with antibodies as above, but no vitamin B-3
Treatment and management
Diabetes mellitus is currently a chronic disease, without a cure, and medical emphasis must necessarily be on managing/avoiding possible short-term as well as long-term diabetes-related problems. There is an exceptionally important role for patient education, dietetic support, sensible exercise, self glucose monitoring, with the goal of keeping both short-term blood glucose levels, and long term levels as well, within acceptable bounds. Careful control is needed to reduce the risk of long term complications. This is theoretically achievable with combinations of diet, exercise and weight loss (type 2), various oral diabetic drugs (type 2 only), and insulin use (type 1 and increasingly for type 2 not responding to oral medications). In addition, given the associated higher risks of cardiovascular disease, lifestyle modifications should be undertaken to control blood pressure and cholesterol by exercising more, smoking cessation, consuming an appropriate diet, wearing diabetic socks, and if necessary, taking any of several drugs to reduce pressure. Many Type 1 treatments include the combination use of regular or NPH insulin, and/or synthetic insulin analogs such as Humalog, Novolog or Apidra; the combination of Lantus/Levemir and Humalog, Novolog or Apidra. Another Type 1 treatment option is the use of the insulin pump with the some of most popular pump brands being: Cozmo, Animas, Medtronic Minimed, and Omnipod.
In countries using a general practitioner system, such as the United Kingdom, care may take place mainly outside hospitals, with hospital-based specialist care used only in case of complications, difficult blood sugar control, or research projects. In other circumstances, general practitioners and specialists share care of a patient in a team approach. Optometrists, podiatrists/chiropodists, dietitians, physiotherapists, clinical nurse specialists (eg, Certified Diabetes Educators and DSNs (Diabetic Specialist Nurse)), or nurse practitioners may jointly provide multidisciplinary expertise. In countries where patients must provide their own health care, the impact of out-of-pocket costs of diabetic care can be high. In addition to the medications and supplies needed, patients are often advised to receive regular consultation from a physician (e.g., at least every three to six months).
Cure
Cures for type 1 diabetes
There is no practical cure now for type 1 diabetes. The fact that type 1 diabetes is due to the failure of one of the cell types of a single organ with a relatively simple function (i.e. the failure of the islets of Langerhans) has led to the study of several possible schemes to cure this form diabetes mostly by replacing the pancreas or just the beta cells. Only those type 1 diabetics who have received either a pancreas or a kidney-pancreas transplant (when they have developed diabetic nephropathy) and become insulin-independent may now be considered “cured” from their diabetes. A simultaneous pancreas-kidney transplant is a promising solution, showing similar or improved survival rates over a kidney transplant alone. Still, they generally remain on long-term immunosuppressive drugs and there is a possibility that the immune system will mount a host versus graft response against the transplanted organ.
Transplants of exogenous beta cells have been performed experimentally in both mice and humans, but this measure is not yet practical in regular clinical practice. Thus far, like any such transplant, it has provoked an immune reaction and long-term immunosuppressive drugs will be needed to protect the transplanted tissue. An alternative technique has been proposed to place transplanted beta cells in a semi-permeable container, isolating and protecting them from the immune system. Stem cell research has also been suggested as a potential avenue for a cure since it may permit regrowth of Islet cells which are genetically part of the treated individual, thus perhaps eliminating the need for immuno-suppressants.A 2007 trial of 15 newly diagnosed patients with type 1 diabetes treated with stem cells raised from their own bone marrow after immune suppression showed that the majority did not require any insulin treatment for prolonged periods of time.
Microscopic or nanotechnological approaches are under investigation as well, in one proposed case with implanted stores of insulin metered out by a rapid response valve sensitive to blood glucose levels. At least two approaches have been demonstrated in vitro. These are, in some sense, closed-loop insulin pumps.
Cures for type 2 diabetes
Type 2 diabetes can be cured by one type of gastric bypass surgery in 80-100% of severely obese patients. The effect is not due to weight loss because it usually occurs within days of surgery, which is before significant weight loss occurs. The pattern of secretion of gastrointestinal hormones is changed by the bypass and removal of the duodenum and proximal jejunum, which together form the upper (proximal) part of the small intestine. One hypothesis is that the proximal small intestine is dysfunctional in type 2 diabetes; its removal eliminates the source of an unknown hormone that contributes to insulin resistance. This surgery has been widely performed on morbidly obese patients and has the benefit of reducing the death rate from all causes by up to 40%. A small number of normal to moderately obese patients with type 2 diabetes have successfully undergone similar operations.
Prognosis
Patient education, understanding, and participation is vital since the complications of diabetes are far less common and less severe in people who have well-controlled blood sugar levels. Wider health issues accelerate the deleterious effects of diabetes. These include smoking, elevated cholesterol levels, obesity, high blood pressure, and lack of regular exercise. According to a study, women with high blood pressure have a threefold risk of developing diabetes.
Anecdotal evidence suggests that some of those with type 2 diabetes who exercise regularly, lose weight, and eat healthy diets may be able to keep some of disease or some of the effects of the disease in ‘remission.’ Certainly these tips can help prevent people predisposed to type 2 diabetes and those at pre-diabetic stages from actually developing the disorder as it helps restore insulin sensitivity. However patients should talk to their doctors about this for real expectations before undertaking it (esp. to avoid hypoglycemia or other complications); few people actually seem to go into total ‘remission,’ but some may find they need less of their insulin medications since the body tends to have lower insulin requirements during and shortly following exercise. Regardless of whether it works that way or not for an individual, there are certainly other benefits to this healthy lifestyle for both diabetics and nondiabetics.
The way diabetes is managed changes with age. Insulin production decreases due to age-related impairment of pancreatic beta cells. Additionally, insulin resistance increases due to the loss of lean tissue and the accumulation of fat, particularly intra-abdominal fat, and the decreased tissue sensitivity to insulin. Glucose tolerance progressively declines with age, leading to a high prevalence of type 2 diabetes and postchallenge hyperglycemia in the older population.Age-related glucose intolerance in humans is often accompanied by insulin resistance, but circulating insulin levels are similar to those of younger people. Treatment goals for older patients with diabetes vary with the individual, and take into account health status, as well as life expectancy, level of dependence, and willingness to adhere to a treatment regimen.
Acute complications
Diabetic ketoacidosis
Diabetic ketoacidosis (DKA) is an acute and dangerous complication that is always a medical emergency. Lack of insulin causes the liver to turn fat into ketone bodies, a fuel mainly used by the brain. Elevated levels of ketone bodies in the blood decrease the blood’s pH, leading to most of the symptoms of DKA. On presentation at hospital, the patient in DKA is typically dehydrated and is breathing rapidly and deeply. Abdominal pain is common and may be severe. The level of consciousness is typically normal until late in the process, when lethargy may progress to coma. Ketoacidosis can become severe enough to cause hypotension, shock, and death. Analysis of the urine reveals significant levels of ketone bodies present (which spill over from the blood when the kidneys filter blood). Prompt proper treatment usually results in full recovery, though death can result from inadequate or delayed treatment, or from complications. Ketoacidosis is much more common in type 1 diabetes than type 2.
Nonketotic hyperosmolar coma
The hyperosmolar nonketotic state (HNS) is an acute complication with many symptoms in common with DKA, but an entirely different cause and different treatment. In a person with very high blood glucose levels (usually considered to be above 300 mg/dl (16 mmol/l)), water is drawn out of cells into the blood by osmosis and the kidneys dump glucose into the urine. This results in loss of water and an increase in blood osmolality. If fluid is not replaced (by mouth or intravenously), the osmotic effect of high glucose levels combined with the loss of water will eventually lead to dehydration. The body’s cells become progressively dehydrated as water is taken from them and excreted. Electrolyte imbalances are also common and dangerous. As with DKA, urgent medical treatment is necessary, especially volume replacement. Lethargy may ultimately progress to a coma, which is more common in type 2 diabetes than type 1.
Hypoglycemia
Hypoglycemia, or abnormally low blood glucose, is a complication of several diabetes treatments. It may develop if the glucose intake does not cover the treatment. The patient may become agitated, sweaty, and have many symptoms of sympathetic activation of the autonomic nervous system resulting in feelings similar to dread and immobilized panic. Consciousness can be altered or even lost in extreme cases, leading to coma, seizures, or even brain damage and death. In patients with diabetes, this may be caused by several factors, such as too much or incorrectly timed insulin, too much or incorrectly timed exercise (exercise decreases insulin requirements) or not enough food (specifically glucose-producing carbohydrates), but this is an over-simplification.
It is more accurate to note that iatogenic (caused by medical treatment) hypoglycemia is typically the result of the interplay of absolute (or relative) insulin excess and compromised glucose counterregulation in type 1 and advanced type 2 diabetes. Decrements in insulin, increments in glucagon, and, absent the latter, increments in epinephrine stand high in the hierarchy of redundant glucose counterregulatory factors that normally prevent or rapidly correct hypoglycemia. In insulin-deficient diabetes (exogenous) insulin levels do not decrease as glucose levels fall, and the combination of deficient glucagon and epinephrine responses causes defective glucose counterregulation.
Furthermore, reduced sympathoadrenal responses can cause hypoglycemia unawareness. The concept of hypoglycemia-associated autonomic failure (HAAF) in diabetes posits that recent incidents of hypoglycemia causes both defective glucose counterregulation and hypoglycemia unawareness. By shifting glycemic thresholds for the sympathoadrenal (including epinephrine) and the resulting neurogenic responses to lower plasma glucose concentrations, antecedent hypoglycemia leads to a vicious cycle of recurrent hypoglycemia and further impairment of glucose counterregulation. In many cases (but not all), short-term avoidance of hypoglycemia reverses hypoglycemia unawareness in most affected patients, although this is easier in theory than it is in practice.
In most cases, hypoglycemia is treated with sugary drinks or food. In severe cases, an injection of glucagon (a hormone with the opposite effects of insulin) or an intravenous infusion of dextrose is used for treatment, but usually only if the person is unconscious. In hospitals, intravenous dextrose is often used.
[edit] Chronic complications
Vascular disease
Chronic elevation of blood glucose level leads to damage of blood vessels (angiopathy). The endothelial cells lining the blood vessels take in more glucose than normal, since they don’t depend on insulin. They then form more surface glycoproteins than normal, and cause the basement membrane to grow thicker and weaker. In diabetes, the resulting problems are grouped under “microvascular disease” (due to damage to small blood vessels) and “macrovascular disease” (due to damage to the arteries).
Image of fundus showing scatter laser surgery for diabetic retinopathy
Image of fundus showing scatter laser surgery for diabetic retinopathy
The damage to small blood vessels leads to a microangiopathy, which can cause one or more of the following:
* Diabetic retinopathy, growth of friable and poor-quality new blood vessels in the retina as well as macular edema (swelling of the macula), which can lead to severe vision loss or blindness. Retinal damage (from microangiopathy) makes it the most common cause of blindness among non-elderly adults in the US.
* Diabetic neuropathy, abnormal and decreased sensation, usually in a ‘glove and stocking’ distribution starting with the feet but potentially in other nerves, later often fingers and hands. When combined with damaged blood vessels this can lead to diabetic foot (see below). Other forms of diabetic neuropathy may present as mononeuritis or autonomic neuropathy. Diabetic amyotrophy is muscle weakness due to neuropathy.
* Diabetic nephropathy, damage to the kidney which can lead to chronic renal failure, eventually requiring dialysis. Diabetes mellitus is the most common cause of adult kidney failure worldwide in the developed world.
Macrovascular disease leads to cardiovascular disease, to which accelerated atherosclerosis is a contributor:
* Coronary artery disease, leading to angina or myocardial infarction (“heart attack”)
* Stroke (mainly the ischemic type)
* Peripheral vascular disease, which contributes to intermittent claudication (exertion-related leg and foot pain) as well as diabetic foot.
* Diabetic myonecrosis (‘muscle wasting’)
Diabetic foot, often due to a combination of neuropathy and arterial disease, may cause skin ulcer and infection and, in serious cases, necrosis and gangrene. It is why diabetics are prone to leg and foot infections and why it takes longer for them to heal from leg and foot wounds. It is the most common cause of adult amputation, usually of toes and or feet, in the developed world.
Carotid artery stenosis does not occur more often in diabetes, and there appears to be a lower prevalence of abdominal aortic aneurysm. However, diabetes does cause higher morbidity, mortality and operative risks with these conditions.[49]
Epidemiology
In 2000, according to the World Health Organization, at least 171 million people worldwide suffer from diabetes. Its incidence is increasing rapidly, and it is estimated that by the year 2030, this number will double. Diabetes mellitus occurs throughout the world, but is more common (especially type 2) in the more developed countries. The greatest increase in prevalence is, however, expected to occur in Asia and Africa, where most patients will likely be found by 2030. The increase in incidence of diabetes in developing countries follows the trend of urbanization and lifestyle changes, perhaps most importantly a “Western-style” diet. This has suggested an environmental (i.e., dietary) effect, but there is little understanding of the mechanism(s) at present, though there is much speculation, some of it most compellingly presented.
Diabetes is in the top 10, and perhaps the top 5, of the most significant diseases in the developed world, and is gaining in significance there and elsewhere (see big killers).
For at least 20 years, diabetes rates in North America have been increasing substantially. In 2005 there were about 20.8 million people with diabetes in the United States alone. According to the American Diabetes Association, there are about 6.2 million people undiagnosed and about 41 million people that would be considered prediabetic. However, the criteria for diagnosing diabetes in the USA means that it is more readily diagnosed than in some other countries. The Centers for Disease Control has termed the change an epidemic. The National Diabetes Information Clearinghouse estimates that diabetes costs $132 billion in the United States alone every year. About 5%–10% of diabetes cases in North America are type 1, with the rest being type 2. The fraction of type 1 in other parts of the world differs; this is likely due to both differences in the rate of type 1 and differences in the rate of other types, most prominently type 2. Most of this difference is not currently understood. The American Diabetes Association point out the 2003 assessment of the National Center for Chronic Disease Prevention and Health Promotion (Centers for Disease Control and Prevention) that 1 in 3 Americans born after 2000 will develop diabetes in their lifetime.
According to the American Diabetes Association, approximately 18.3% (8.6 million) of Americans age 60 and older have diabetes. Diabetes mellitus prevalence increases with age, and the numbers of older persons with diabetes are expected to grow as the elderly population increases in number. The National Health and Nutrition Examination Survey (NHANES III) demonstrated that, in the population over 65 years old, 18% to 20% have diabetes, with 40% having either diabetes or its precursor form of impaired glucose tolerance.
History
The term diabetes (Greek: διαβήτης, diabētēs) was coined by Aretaeus of Cappadocia. It was derived from the Greek verb διαβαίνειν, diabaínein, itself formed from the prefix dia-, “across, apart,” and the verb bainein, “to walk, stand.” The verb diabeinein meant “to stride, walk, or stand with legs asunder”; hence, its derivative diabētēs meant “one that straddles,” or specifically “a compass, siphon.” The sense “siphon” gave rise to the use of diabētēs as the name for a disease involving the discharge of excessive amounts of urine. Diabetes is first recorded in English, in the form diabete, in a medical text written around 1425. In 1675, Thomas Willis added the word mellitus, from the Latin meaning “honey”, a reference to the sweet taste of the urine. This sweet taste had been noticed in urine by the ancient Greeks, Chinese, Egyptians, and Indians. In 1776, Matthew Dobson confirmed that the sweet taste was because of an excess of a kind of sugar in the urine and blood of people with diabetes.
The ancient Indians tested for diabetes by observing whether ants were attracted to a person’s urine, and called the ailment “sweet urine disease” (Madhumeha). The Korean, Chinese, and Japanese words for diabetes are based on the same ideographs (糖尿病) which mean “sugar urine disease”.
Although diabetes has been recognized since antiquity, and treatments of various efficacy have been known in various regions since the Middle Ages, and in legend for much longer, pathogenesis of diabetes has only been understood experimentally since about 1900 The discovery of a role for the pancreas in diabetes is generally ascribed to Joseph von Mering and Oskar Minkowski, who in 1889 found that dogs whose pancreas was removed developed all the signs and symptoms of diabetes and died shortly afterwards. In 1910, Sir Edward Albert Sharpey-Schafer suggested that people with diabetes were deficient in a single chemical that was normally produced by the pancreas—he proposed calling this substance insulin, from the Latin insula, meaning island, in reference to the insulin-producing islets of Langerhans in the pancreas.
The endocrine role of the pancreas in metabolism, and indeed the existence of insulin, was not further clarified until 1921, when Sir Frederick Grant Banting and Charles Herbert Best repeated the work of Von Mering and Minkowski, and went further to demonstrate they could reverse induced diabetes in dogs by giving them an extract from the pancreatic islets of Langerhans of healthy dogs. Banting, Best, and colleagues (especially the chemist Collip) went on to purify the hormone insulin from bovine pancreases at the University of Toronto. This led to the availability of an effective treatment—insulin injections—and the first patient was treated in 1922. For this, Banting and laboratory director MacLeod received the Nobel Prize in Physiology or Medicine in 1923; both shared their Prize money with others in the team who were not recognized, in particular Best and Collip. Banting and Best made the patent available without charge and did not attempt to control commercial production. Insulin production and therapy rapidly spread around the world, largely as a result of this decision.
The distinction between what is now known as type 1 diabetes and type 2 diabetes was first clearly made by Sir Harold Percival (Harry) Himsworth, and published in January 1936.
Despite the availability of treatment, diabetes has remained a major cause of death. For instance, statistics reveal that the cause-specific mortality rate during 1927 amounted to about 47.7 per 100,000 population in Malta.
Other landmark discoveries include:
* identification of the first of the sulfonylureas in 1942
* reintroduction of the use of biguanides for Type 2 diabetes in the late 1950s. The initial phenformin was withdrawn worldwide (in the U.S. in 1977) due to its potential for sometimes fatal lactic acidosis and metformin was first marketed in France in 1979, but not until 1994 in the US.
* the determination of the amino acid sequence of insulin (by Sir Frederick Sanger, for which he received a Nobel Prize)
* the radioimmunoassay for insulin, as discovered by Rosalyn Yalow and Solomon Berson (gaining Yalow the 1977 Nobel Prize in Physiology or Medicine)[59]
* the three-dimensional structure of insulin (PDB 2INS)
* Dr Gerald Reaven’s identification of the constellation of symptoms now called metabolic syndrome in 1988
* demonstration that intensive glycemic control in type 1 diabetes reduces chronic side effects more as glucose levels approach ‘normal’ in a large longitudinal study,[60] and also in type 2 diabetics in other large studies
* identification of the first thiazolidinedione as an effective insulin sensitizer during the 1990s
Social issues
The 1989 Declaration of St Vincent was the result of international efforts to improve the care accorded to those with diabetes. Doing so is important both in terms of quality of life and life expectancy but also economically – expenses to diabetes have been shown to be a major drain on health- and productivity-related resources for healthcare systems and governments.
Several countries established more and less successful national diabetes programmes to improve treatment of the disease.
A study shows that diabetic patients with neuropathic symptoms such as numbness or tingling in feet or hands are twice more likely to be unemployed than those without the symptoms.
Comment by mskittie — January 29, 2008 @ 4:19 pm |
Caregiving Tips for the Bedridden
Tips for caring for the bedridden: If you have a loved one who is bedridden it’s inconvenient to say the least. For the patient it can be somewhat daunting to always call upon another when in need of something that is only slightly out of reach. Whether your loved one is bedridden temporarily or for a long while there are some things you can do to make life easier for him and yourself. Most care-givers are aware of things like bed pans to help the bedridden but there are many more handy items to help.
Keeping things at a distance easily reached by the bedridden person will help quite a bit. Use the headboard to place things within reach or pull up a night stand or table. It helps to set up a two-way monitor that works like a walkie-talkie, or simply use a bell for calling help. Try to find a bell with a clip or attach your own clip to the bell so the patient can clip it on the sheet when not in use.
They make a “reacher” which is found at department stores to help grab things which are placed too far away from the bed. The “grabber” is a small pole with a pincer-type apparatus at one end and a squeezable handle at the other. When squeezed the pincer closes and can allow the patient to pick up objects that are smallish and not too heavy. When the handle is released the pincer opens to allow the removal of the object.
Sliding tables will make life easier as well. If you have enough room use several of them, each holding different items, to slide up to and away from the bed. Keep the tables within reach and have each table contain specific items. One table can hold phone, phone book, pad, pen and reading glasses. Another table can hold puzzles or games. Still another can hold hand wipes, a pitcher of water and snacks. The patient can then slide preferred table up to the bed and slide it back when finished. These tables are designed to be adjustable to many different levels and positions for eating, reading and writing. They slide easily on most floors. Find them at department stores or order from magazines.
Make or purchase a set of bed pockets. They slide between the mattress and box springs of the bed and hang over the side, with pockets to store needy items. They’re easy to make: cut a piece of fabric about a third of the length of the bed and from the floor to a foot or so under the mattress. Cut another piece to go from the bottom of the large piece, about a third of the way up. Sew straight down in several places to form pockets for holding remote, glasses, puzzle books, tissue and medications. Make something similar to lay on sliding tables, with the pockets hanging over 3 edges. The table can now hold much more than before.
Keep hand sanitizing lotion nearby, along with wet-wipes. New wipes are now made for quick body washing purposes, making it easy for the patient to do quick wash-ups on his own. Be sure and have a small trash can located nearby. Use a small plastic tub and squirt bottle or pitcher and glass, on a sliding table, for teeth brushing. Use a small mirror with clamps to attach to the table.
There are lots of things besides games and puzzles that the patient can do when bored. Starting a scrapbook is one idea. Use a duffle bag or another organizer to store the scrapbook items next to the bed. The patient can then lift the bag onto a sliding table when ready to work. Duffels are good for other storage purposes while the patient is bedridden. They come in many sizes, can be stacked upon one another and easily reached from the side of the bed. Pack one with cd player, cd’s, books and journals. For kids, fill a duffel with his or her favorite toys and games.
Consider moving the stereo, VCR and DVD player over to one side of the bed for easy access. Tv’s can be hung on a wall with an inexpensive kit found in most department stores. Be sure to find a stud in the wall to hang the tv safely.
Washing hair is a chore when you’re the care-giver but is easier when you use a stainless steel or plastic tub. Lay the patient’s head, on a folded towel, on the edge of the portable tub. Set water, shampoo and towels on a sliding table for convenience. Squirt bottles make washing short hair very quick and prevent water from splashing everywhere. Pitchers of water help with long hair. It’s best to feel two or three rather than trying to refill each time.
One last thing: if you’re the care-giver remember to take time off for yourself to recoup. Taking care of someone who is bedridden is hard work. You need time to relax and have a break. Talk to friends and neighbors to see if you can find a temporary replacement for a couple of hours per day to take some time for you.
Comment by mskittie — February 11, 2008 @ 2:08 am |
wont let me post
Comment by mskittie — March 24, 2008 @ 1:35 pm |
The Anxious Child
All children experience anxiety. Anxiety in children is expected and normal at specific times in development. For example, from approximately age 8 months through the preschool years, healthy youngsters may show intense distress (anxiety) at times of separation from their parents or other persons with whom they are close. Young children may have short-lived fears, (such as fear of the dark, storms, animals, or strangers). Anxious children are often overly tense or uptight. Some may seek a lot of reassurance, and their worries may interfere with activities. Parents should not discount a child’s fears. Because anxious children may also be quiet, compliant and eager to please, their difficulties may be missed. Parents should be alert to the signs of severe anxiety so they can intervene early to prevent complications. There are different types of anxiety in children.
Symptoms of separation anxiety include:
* constant thoughts and intense fears about the safety of parents and caretakers
* refusing to go to school
* frequent stomachaches and other physical complaints
* extreme worries about sleeping away from home
* being overly clingy
* panic or tantrums at times of separation from parents
* trouble sleeping or nightmares
Symptoms of phobia include:
* extreme fear about a specific thing or situation (ex. dogs, insects, or needles)
* the fears cause significant distress and interfere with usual activities
Symptoms of social anxiety include:
* fears of meeting or talking to people
* avoidance of social situations
* few friends outside the family
Other symptoms of anxious children include:
* many worries about things before they happen
* constant worries or concerns about family, school, friends, or activities
* repetitive, unwanted thoughts (obsessions) or actions (compulsions)
* fears of embarrassment or making mistakes
* low self esteem and lack of self-confidence
Severe anxiety problems in children can be treated. Early treatment can prevent future difficulties, such as loss of friendships, failure to reach social and academic potential, and feelings of low self-esteem. Treatments may include a combination of the following: individual psychotherapy, family therapy, medications, behavioral treatments, and consultation to the school.
If anxieties become severe and begin to interfere with the child’s usual activities, (for example separating from parents, attending school and making friends) parents should consider seeking an evaluation from a qualified mental health professional or a child and adolescent psychiatrist.
Comment by mskittie — June 13, 2008 @ 2:07 am |
Excellent information again MsKittie. Your contribution to NU is appreciated and it enriches us all.
gaia
Comment by nottingtonuniversity — June 13, 2008 @ 3:11 am |
hi what an amazing story Kathern gosh like Gaia said she probably sees the world better than we do, and is full of life and that is so good to hear it makes us think twice about our life, that we should’nt complain about silly little things like colds or anything that their are people out there with serious health problems how to hear how they can cope with it so well is wonderful this story kathern makes us appreciate our family even more well not that we do already
thanks for sharing all this information Kathern it makes us think twice about our little pity things
love
joanne
Comment by joanne1960 — June 13, 2008 @ 1:25 pm |