The kidneys usually function well after spinal cord injury. However, voluntary control of the bladder is usually lost. The bladder can become overfilled, resulting in high bladder pressures, and backing-up of urine into the upper urinary tract can lead to serious complications, including kidney failure. At one time, kidney failure was a common cause of death in people with spinal cord injury, but it is now a rare complication. Modern techniques for bladder management, especially intermittent catheterization, have revolutionized the care of individuals with spinal cord injury. Some major problems with bladder care do persist, however.
Some individuals with spinal cord injury cannot retain urine in their bladder and they urinate involuntarily, even when taking medications designed to suppress bladder contraction. Scientists are working to develop better methods of preventing this involuntary bladder contraction. Some people have an incompetent or “leaky” urethral sphincter, which allows urine to leak from the bladder at inconvenient times-Urologists can sometimes inject artificial material directly into the sphincter to tighten it. Urologists and biomechanical engineers are working to develop an implantable artificial urethral sphincter, but we don’t yet know whether these efforts will be successful.
For people who retain urine in the bladder and are unable to urinate, scientists are now developing methods for computerized electrical control of the bladder. In one system, an electrical stimulator produces contraction of the bladder’s muscles, causing it to empty. This research is still at an early stage but may someday lead to an implantable, artificial system for overall bladder control. The device would keep track of the volume of urine in the bladder, signal when the bladder is full, then stimulate the bladder to empty when so instructed. For some people, electrical stimulation of the bladder may need to be combined with an artificial sphincter system to achieve full bladder control.

1. Is there a history of problem drinking in your family?
5   No
4 One close relative
3 More than one close relative
2 I used to have a drinking problem
1 I currently have a drinking problem
2. On the average, how many cigarettes a day do you smoke?
5 None, and I never have
4 None now, but I used to smoke regularly
3 Less than half a pack
2 About a pack a day
1   More than a pack a day
3. How many times in the past year have you been hospitalized?
5   Not at all
4 Once, for a minor problem or childbirth
3   More than once, but only minor problems, no surgery
2 Once for major illness or surgery
1 More than once for major illness or surgery
4. Does your family have a history of cancer, or other immune-suppressive disorders?
5 No history
3 One immediate family member
2 More than one immediate family member
1 I myself have had such disorders
5. How many prescription medicines are you now taking?
5   None
4 One or two
3 Three or four
2 Five or six
1 More than six
6. Do you use illicit drugs?
5 No
4 Not now, but I used to
3 Yes, but infrequently
2 Yes, regularly
1 I am/have been a problem drug user
7. How often do you eat cured or processed meats? (i.e., bacon, sausage, luncheon meats)
5 Never
4 Very infrequently
3 At least once a week
2 Several times a week
1 At least once a day
8. When you shop, do you read food labels for additives?
5 Yes, and I avoid foods with a lot of additives
4 Sometimes, but I don’t always bother
2 Very rarely
1   I don’t really care at all
9. Based on your recent health, do you expect to get sick in the next six months?
5   Definitely not
4 Probably not
3 Maybe one minor cold or flu
2 Probably more than one minor illness 1   I am sick right now
10. Are you taking antibiotics for any medical problem?
5 No
4 Not now, but within the last year
3 Off and on
1 Yes
11. Do you have allergy problems?
5 Never
4 I used to, but no longer
3 Mild, seasonal problems only
2 Mild year-round problems
1 Allergies are a real problem for me
12. How do you describe your health?
5 Excellent, as always
4 Better than before, and still improving
3 Usually good
2 Not as good as it used to be
1 Poor, or getting worse
13. How regular are your bowel movements?
5 Very regular
4 Usually regular
3 Bouts with diarrhea
2 Not very regular
1   Often constipated
14. Which best describes your attitudes about health?
5 The way I live effects my health. I make it a point to treat my body well.
4 Though usually in good health, I’m destined to be sick occasionally.
3 My health is about average, and there’s not much I can do about it.
2 In 20 years, I will be much less healthy than I am now.
1 I worry a lot about my health.
15. Overall, your diet is:
5   Excellent
4 Better than average
3 About average
2 Could be better 1   Poor

Pseudotumor cerebri literally defined means a false tumor of the brain. Although less than an ideal name for a medical problem, the disorder represents a condition in which there occurs an increase of pressure inside the skull. What distinguishes this condition from many other disorders that cause an increase of pressure, such as a brain tumor, is the absence of any identifiable abnormality of the brain tissue. A person affected with pseudotumor cerebri, more recently called “benign intracranial hypertension,” will experience headache as the major symptom of the condition. If the disorder is allowed to worsen for a prolonged period of time, a reduction of vision and ultimate blindness can occur.
The headache associated with pseudotumor cerebri is usually of a nonspecific nature. It is constant and not terribly intense. Pain in the forehead region, behind the eyes, and over the top of the head is common. Interestingly, most but not all persons affected by this disorder are overweight women.
The cause of pseudotumor cerebri remains obscure. In some cases, it has been associated with the use of birth-control pills and other hormone substances (such as cortisone), the taking of a urinary antibiotic called naladixic acid, being pregnant, being obese, or having anemia or low calcium in the blood. Other glandular problems have also been associated with the disorder. In children, pseudotumor cerebri has been observed when tetracycline or too much or too little vitamin A is ingested.
Most cases of pseudotumor cerebri occur without identifiable cause and, as mentioned, the patients are often overweight women. The diagnosis is established by observing swelling of the optic nerves by looking into the eyes with an ophthalmoscope. The increase in pressure is confirmed by performing a lumbar puncture, after tests to rule out a brain tumor and other various conditions have been performed. If the diagnosis is made early in the course of the illness and before visual damage occurs, pseudotumor cerebri can be easily treated by reducing the pressure inside the skull with the use of special medications. In most instances, pseudotumor cerebri does not pose any serious threat to life or health, unless, of course, it is allowed to worsen over months and years.

Gautam had just finished his University Exams. The results looked far away. He gave himself up to reading different books by various authors God knows whether it was the influence of some reading or something else, but Gautam suddenly seemed to have lost interest in everything – no more reading, no more visits to friends or outings, no interest in eating – Most of the time he lay dosing or sleeping and the few hours that he was awake, he sat alone on a bench in a park looking away doing nothing, only musing. His parents were worried. The clinical tests showed ‘All clear’.
For us it was a clear case of Clematis negative state and Clematis remedy brought Gautam once more ‘to earth’. Inattentiveness of Clematis is different from that of Chestnut Bud.
CLEMATIS patient has always a pre-occupied mind -a mind full of fantasis, dreams of rosy future, and occupied with building castles in the air. There is, in effect, no place in his mind to think of the present.
CHEST- NUTBUD patient lives very much in the present. He does not have a pre-occupied mind. Only he does not pay attention to things in which he is not interested, and therefore does not observe properly and makes the same mistakes again and again.

Until very recently, the party line was that from the perspective of bone density, Caucasians and Asians get the short end of the stick compared to African-American, Hispanic and Polynesian people. I was taught that thanks to gene pool differences, and a greater tendency to have small frames, white and Asian people have a significantly higher risk of losing too much bone mass, developing arthritis and suffering fractures. But I recently learned from Dr. Juanita Archer, a metabolic bone specialist at Howard University, that the most recent studies indicate that African-Americans have the same risk as Caucasians. Historically, black people were presumed not to be much at risk for osteoporosis and so by and large weren’t screened for it until there was already a fracture. When doctors challenged the assumptions they’d been working under, and started looking for low bone density in black women at random, they found it was prevalent in them, too. We don’t have the data yet, but I’m guessing that when we begin to look at other ethnic groups, we’ll discover the same risks.
Your grandmother probably gave you many wonderful things both tangible and intangible, but if she had osteoporosis, good bones isn’t one of them. One of the primary warnings you will have that you are at higher risk of low bone density is a history of osteoporosis in your family. If your mother, father, sibling, or grandparent suffered from it (or lost height; or had a dowager’s hump or a hunchback; or got frequent fractures or fractures from minor trauma), you’ll need to pay particular attention to your own plan to avoid a similar fate.

Various physiological changes occur in response to the increased demand of energy, required during exercise. These include:
i) Enhanced cardiac output to meet the increased oxygen demand of the organs.
ii) Augmented respiration to help higher oxygen (02) inflow and CO? elimination from the lungs.
iii) Redistribution of blood flow and raised capillary perfusion pressure.
Major metabolic fuel used by muscles are:
i) Glucose & Free fatty acids: Which are released into circulation by liver and adipose tissue.
ii) Aminoacids: These are not important but contribute less than 10% of total energy supply.
iii) Ketorfe bodies: These can be used only during low glucose availability.
Energy utilization during exercise is mediated and influenced by Insulin and Counter regulating hormones.
A decrease in plasma insulin and presence of glucagon appears to be necessary for early increase in the hepatic productions of glucose during exercise, and during prolonged exercise, increase in plasma glucagon and catecholamines appear to play a key role.
Intracellular Fuel Sources : Fat & Carbohydrate present in the muscles
Extracellular Fuel Source : Site – Liver -Glycogenolysis -Glucose
Lipolysis : Site – Adipose Tissue Fat – Free Fatty Acid
Neoglucogenesis : Site – Liver – Glucose
- 90% comes for oxidation of FFA
Usual work
- Oxidation of glucose & FFA
During short burst of exercise
- Muscle glycogenosis followed by
hepatic glycogenolysis.
If exercise continued
- Hepatic-gluconeogenesis.
If exercise is beyond 30 Minutes
- ERA. generated by adipose tissue
Post-exercise phase
- Restoration of glycogen in muscle
& liver, which is insulin dependent.

To describe the cardiovascular system let’s use a model that most everyone is familiar with – plumbing. While this analogy may be overly simplistic, your cardiovascular system is essentially a network consisting of a pump and multiple pipes. Your heart is the pump, your blood vessels a complex set of pipes and your blood the fluid coursing through the system.
What a pump your heart is! About the size of a fist, this muscular organ contracts and relaxes from 50 to 200 times per minute without rest. At an average heart rate of 70 beats per minute, the human heart beats 4,200 times an hour, 100,800 times a day, 37 million times a year, and an amazing 3 billion times over an 85-year lifetime. The heart pump is divided into two halves, right and left, separated by a muscular wall called the septum. Each half has two chambers, the upper atrium and the lower ventricle. Blood flows into the right atrium and then, through a valve, into the right ventricle. When the right ventricle is full, another valve opens and the heart contracts, or pumps. This sends the blood from the right ventricle to the lungs, where it picks up oxygen. Oxygenated blood returning from the lungs enters the left atrium, then the left ventricle. When the valve between these two chambers closes, the heart contracts again and pumps blood into the arteries, the network of “pipes” that delivers oxygenated blood to your body.

The ‘accommodating patient will usually have some views on the way her treatment should be managed but will generally allow the doctor to make the final decisions.
She has a high awareness of treatments for her condition but much of it is usually from anecdotal evidence and not always reliable. It is important for her that the doctor be informed of her lifestyle and relationships, and thrives on the doctor inquiring after them at appointments. Her level of confidence, or anxiety, is quite apparent as she readily shares her feelings, and will seek out support groups to help her through treatment. She will be able to share all the minute details of her treatment, especially its side effects with her family and friends. She often uses diet and yoga as support therapies. Building rapport is generally a priority as she is dependent on the medical team’s ability to save her life.
The ‘accepting patient will usually have very few views on how her treatment should be managed, as she places complete trust in her doctor to make all the decisions. She usually has a low level of awareness of the treatment and places complete faith in her doctor selecting the most appropriate regime. She is often unable to repeat to family and friends the details of her condition, treatment or conversations with the doctor. Her carer will often have to communicate with the doctor to clarify treatment details. The complex medical terms of her illness do not really interest her, and she is satisfied to use generic terms. She may fuss that the doctor is overworked and is being kept from his/her private life. A low-level user, if any, of complementary therapies, the building of rapport is important, but not critical, as she is highly dependent and accepting of the doctor as ‘God’.
Most doctors try and present with an appropriate positive ‘bedside’ manner, but we often overlook the fact that they too are human. Whilst cancer specialists are highly trained, with specialized skills and knowledge, they are not demigods! They are, however, very keen to support you back to good health in the best possible way and with the least trauma. Cure is always their aim, or prolongation of life. It is important for them that you feel as good as you can. Sometimes however, the tumour is so aggressive that not even their expert knowledge, skills and medicines can save every life. Therefore the relationship you have with your doctor and health team in making the best choices about your treatment is vital in this process.

Medical Causes of DIMS
The many medical conditions that may lead to disturbed sleep. Briefly, then, let me reiterate that such problems as chronic pain, arthritis, hyperthyroidism, heartburn, or breathing conditions such as cough or COPD can cause DIMS. Sometimes the drugs used to treat these conditions can disrupt sleep, either because they stimulate the system, as do beta-adrenergic agonists or steroids, or because they have a rebound effect when the medication wears off. More rarely hypothyroidism or some abnormal tissue growths may affect the central respiratory drive.
Childhood DIMS
Another category of DIMS encompasses those sleep problems that begin during childhood or before puberty and persist into adulthood. While largely similar to the psychophysiological DIMS I described earlier, these childhood-onset disorders lack discernible conditioning factors, arising instead out of early emotional turmoil or psychiatric disturbance. One distinguishing factor of these sleep problems is that they remain relatively constant over time, regardless of the emotional arousal experienced by the individual. Such sleep disorders are notoriously resistant to treatment, because they may stem from malfunctions of the central nervous system that have existed since birth.

Prosthetic joint infections are very common in the first 2 years after implantation of the prosthesis. Reported postoperative incidence is around 6.5 per 1000 within in the first year and 3.2 per 1000 in the second year. Risk factors for infection are the same as those previously mentioned for septic arthritis of a native joint but also include prior joint surgery and perioperative wound complications. Infectious organisms can be introduced directly into the wound or via airborne contamination during the procedure itself. Infection can also occur in the setting of postoperative bacteremia through hematogenous spread. Clinical presentation can vary from acute infectious arthritis to chronic pain due to prosthesis failure. Patients often complain of limited range of motion in the affected joint.
The most common organisms implicated in prosthetic joint infections are coagulase-negative staphylococci (25% of patients), followed by S. aureus, gram-negative bacilli, streptococci, anaerobes, and Enterococcus species. Polymicrobial infection is also commonly seen. These organisms can be isolated through culture of preoperative synovial fluid aspirate or intraoperative tissue. Additional diagnostic studies include erythrocyte sedimentation rate, complete blood cell count, C-reactive protein, and imaging through the use of plain radiographs, bone scan, MRI, or CT.
The choice of antibiotics is based on culture results. Vancomycin is the drug of choice for coagulase-negative staphylococcal infections, whereas nafcillin or cefazolin can be used to treat joint infections caused by S. aureus. Patients with gram-negative bacilli isolated on culture should be given a beta-lactam such as piperacillin, which can be combined with gentamicin.1
Eradication of infection can be achieved in the majority of patients through removal of the prosthesis combined with 4 to 6 weeks of intravenous antibiotic therapy directed at the appropriate pathogen. While re-implantation of a new prosthesis can be performed during the initial extraction, improved outcomes have been demonstrated with a two-stage procedure in which re-implantation follows the completion of a 6-week antibiotic course.
Chronic antibiotic suppression is used in select patients for whom prosthesis removal is not performed. Lifelong oral antibiotics can be given with some success to compliant patients in whom surgical removal is contraindicated. For these patients, one must demonstrate that the prosthesis is not loose and that the causative organism is of low virulence and is sensitive to oral antibiotics. This form of therapy may place patients at risk for developing antimicrobial resistance as well as extension of the infection beyond the joint space.

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