TREATMENT OF ACUTE INFECTIOUS DIARRHEAL DISEASES
Treatment options for patients with acute infectious diarrhea include supportive care (hydration, anti-motility agents) and antimicrobial agents (empiric and agent specific). In all cases, the physician should encourage aggressive oral hydration to prevent dehydration and recognize the need for intravenous fluid replacement. Oral rehydration solutions are available over the counter, or home remedies may be used. Patients should consume glucose-containing electrolyte solutions and avoid hyperosmolar fluids, which can exacerbate symptoms and fluid loss. Milk and lactose-containing products and caffeine can exacerbate diarrhea and should be avoided.Antidiarrheal agents such as opiates (loperamide), which slow intestinal transit time, and adsorbent agents (Kaopectate) may provide symptomatic relief. Use of agents that decrease intestinal transit time Hi infectious diarrhea is controversial, but concerns about the slow clearance of pathogens have not been supported. Bismuth subsalicylate has direct antidiarrheal and antibacterial effects and is generally safe.The use of empiric antibiotics is appropriate while awaiting bacteriologic identification in patients in whom inflammatory diarrhea is likely and are slow to improve, in returning travelers, when diarrhea persists for more than 2 weeks, and when Giardia is suspected. Because many bacterial causes of diarrhea vary in clinical course and degree of morbidity, a decision to treat should be influenced greatly by the patients’ comorbidities, immune state, and clinical appearance, calling for clinical judgment on the part of the physician after a complete history and physical evaluation. In general, the vast majority of cases of infectious diarrhea do not require antimicrobial therapy because there is no effective agent for the organism or because the illness is mild and self-limited (or both). Patients who are improving and have mild illness need no chemotherapeutic intervention. Severe illness, dysentery, persistent symptoms, or immunosuppression mandate an attempt to identify an enteropathogen to provide specific and appropriate treatment. Particular attention should be given to resistance patterns within the community, and antibiotics should be chosen accordingly. Finally, knowledge of the potential for antibiotics to increase complication rates (HUS in EHEC) and prolong shedding and infectivity (Salmonella) is essential when debating the pros and cons of antimicrobial therapy.*75/348/5*
ALLERGIES, CANDIDA AND ASTHMA: IMMUNOLOGY
Resistance to systemic candidiasis depends on cell-mediated immunity, which can be assessed quite easily with a multitest (CMI). Cellular immunity is not the only determinant of infective capacity, however. The ability of the immune system to form antibodies also appears to be crucial to the survival of animals infected with Candida albicans.
Antibodies are seldom, if ever, formed by non-infected people but are often present in cases of candidiasis. When they are not, the diagnostician is clearly given a warning that something is amiss. Immunoglobulins E (IgE) are often raised against Candida in infected people. The diagnosis of candidiasis should not rest on any one single finding, however, because each one can give some false positive and false negative results. Some Candida antibodies tests have an accuracy rate of around 90 per cent. Failure to mount an antibodies defence during a Candida infection is a sign of underlying immunological/biochemical or other problem that should be thoroughly investigated.
Manifestation of visceral (digestive) candidiasis can be subtle and the blood culture is often negative; however, nearly all serological tests have detected antibodies against antigens from yeast organisms.
Allergy Tests
The IgE, radio allergo absorbent test (RAST), skin scratch, end pointing, intradermal and/or sublingual provocation tests will all indicate if someone is allergic to Candida, a variety of associated moulds and fungi. It will also help to differentiate between air-borne moulds and food-borne mould and fungi allergies. These tests are essential for all asthmatics!
I never cease to be amazed at the number of asthma sufferers who have never had an allergy test or, if they have, were not offered either environmental advice or allergy desensitising treatment. This can take various forms, including sublingual allergy drops, homeopathic remedies or neutralising injections.
There is a reasonable correlation between an elevated IgE count and allergies in general as well as Candida in particular. Another advantage of these tests is that if the patient has overt signs and symptoms of candidiasis (tinea; vaginal, oral or skin thrush; monilia and so on) and the tests are negative, this immediately alerts the diagnostician that there could be a problem with the patient’s ability to mount an immunological defence against the organism. As with the Candida antibodies blood test, these tests are often very useful when they are negative.
Cell-mediated Immunity Test (CMI)
This test includes Candida in a number of challenges applied simultaneously to the skin. It is an excellent test, not only for Candida, but to ascertain if it is this particular aspect of one’s immunity that is at fault. Of course it also ferrets out those patients with very poor immune responses (anergy). These are the ones who are more likely to suffer with chronic Candida infections and allergies as well as CFS, asthma and other health problems.
*63\145\2*
SPINAL CORD INJURY: HOW WILL MY INJURY BE TREATED?
In the ER and during the early days in the hospital, maintaining life is the first priority, so the emphasis is on appropriate life-support systems. The medical team ensures that the injured person has adequate respiration (airflow in and out of the lungs), ensures that the heart is functioning adequately, and checks for other serious or life-threatening injuries (such as traumatic brain injury) that sometimes accompany damage to the spinal cord.
An x-ray and MRI (magnetic resonance imaging) scan are done as soon as possible after arrival in the ER. The x-ray reveals any signs of injury to the vertebral column. The MRI scan shows the structural damage to the spinal cord and surrounding tissues, which is important for planning treatment. In MRI, powerful magnets apply a magnetic field to the body while you lie perfectly still in a large machine. Specialized detectors pick up changes in the field, and this information is fed into a sophisticated computer. The computer then reconstructs detailed three-dimensional images of the spinal cord and related structures.
A careful neurological examination, also done in the ER, is essential to determine how the spinal cord is functioning and to establish the neurological level and severity of the injury. While the level of vertebral (bone) injury is revealed with imaging studies (x-rays and scans), the level of the spinal cord injury depends on the function of the spinal cord, which can be determined only by a thorough neurological examination performed by doctors. During this examination, the doctors check for sensation, strength, muscle tone, and reflexes in all four limbs and the trunk.
Many patients require spinal surgery within the first few days after a spinal cord injury. Surgery is usually performed to relieve compression of the spinal cord or to provide internal stabilization of the vertebral column. The spinal cord can be decompressed by removing pieces of bone or other materials that are pressing against it. When the vertebral column is unstable, a bone graft (also called a spinal fusion) may be performed. In this procedure, small pieces of bone are taken from the pelvis and implanted in the neck to give extra support to the spine. These pieces eventually fuse with the bones of the spine, but the vertebrae must be held absolutely still while the bones and ligaments are healing, a process that can take months. Metal plates, screws, or rods are attached during surgery to hold the vertebral bones in place. Braces may be necessary to provide external support. Although these procedures improve the chances for recovery, decompressing the spinal cord and stabilizing the bones of the spine do not ensure any improvement in strength or sensation below the level of injury.
The specifics of early treatment for spinal cord injury depend on the level and type of damage to the vertebral column and spinal cord.
*7/156/5*
In: Healthy bones Osteoporosis Rheumatic
DIETS FOR LIVER DISEASES
Cirrhosis
Studies have shown that there is a direct relationship between calorie intake and mortality in patients with cirrhosis.
Mendenhall’s analysis:
Calorie intake Mortality at 6 mouthy
< 1000 kcal/day 90%
1000-2000 kcal/day 50%
> 2000 kcal/day 20%
It shows that mortality decreases with high calorie diet. Malnutrition is common in cirrhosis and severity of liver diseases is correlated with severity of malnutrition, therefore, it is very essential to feed these patients.
Possible causes of malnutrition:
(a) Poor intake of food is due to anorexia/nausea, ascites causing abdominal fullness, gastroparesis, zinc deficiency;
(b) metabolic inability of liver to cope up with energy requirements which causes muscle breakdown, increase lipolysis, abnormal glucose metabolism.
Essential dietary principles
• Calories/day: 1.2-1.4 times resting energy expenditure (REE)
• Proteins/day: 1.2-1.5 g/kg of ideal body weight (IBW)
• Fats/day: 20-40% of non-protein calories
• Carbohydrates/day: Rest of the calories.
Calories are to be divided into 6-7 small meals including a late evening meal.
• Encephalopathy grade III-IV= 0.5-1.2 kg/IBW
BCAA enriched solution is to be given.
Animal proteins are more encephalopathic, so they should be avoided and replaced with BCAA rich protein.
According to WHO criteria 60-80% of patients with cirrhosis have impaired glucose tolerance and 15-37% has overt diabetes, hence it is recommended to provide:
• 55-60% of energy as complex carbohydrates with low glycemic index (GI), foods rich in soluble fibres.
• Sodium intake to be restricted in ascites.
• Sodium 2-2.5 g/day is permitted.
Fatty liver
Fatty liver is known as the disease of the decade, it may or may not be associated with obesity. Weight management with low-fat diet rich in polyunsaturated and monounsaturated fatty acids is recommended.
Non-alcoholic steatohepatitis (NASH)
It represents a spectrum of conditions. Is generally associated with obesity, diabetes and hypertension. Dietary treatment is based on the associated illness. Occurs in patients who do not consume alcohol in harmful amount; management involves weight maintenance with low-fat diabetic diet and salt restriction for hypertension. Saturated fats are to be replaced with polyunsaturated or monounsaturated fats in limited quantity.
In brief to monitor patients with liver disease follow the following regime:
(i) Assess nutritional status. If moderate to severe malnutrition assess REE.
(ii) Encourage oral intake.
(iii) Count calories for 2-3 days, if inadequate enteral nutrition is to be started. Continuous feed for at least 20 hr/day is beneficial.
(iv) If encephalopathy sets in, change to vegetable proteins and use branched chain amino acids (leucine, valine, isoleucine).
Liver transplantation
Better outcome is seen in patients with a good pre-transplant nutritional status especially so in the survival rate. So all transplant patients should be well-fed in terms of calories and proteins.
*4/356/5*
HOW WE DIAGNOSE A SEIZURE AND DECIDE WHAT IT WILL MEAN FOR YOUR CHILD
A seizure, as we have seen, is a sudden alteration in behavior or in motor function caused by an electrical discharge from the brain.
It should be very easy to diagnose a seizure since it is simply a sudden change in behavior or motor function. But sometimes it’s not that simple; people have sudden changes in behavior all the time. Sometimes children faint, daydream, or fall down. How do you tell if those events were seizures? The only way to diagnose a seizure is to take a very careful history of the event that has occurred.
That’s why doctors ask all those questions. What was the child doing when it happened? What was the first thing that was noticed? What happened next? What was the child doing during the episode? The doctor may ask you to demonstrate what you saw (if you saw it). Was the child trembling, making rapid movements of the arms or legs, or were the child’s arms or legs jerking rhythmically? What was the child like afterward? Was she tired? Was there a headache? Did the child wet herself during the spell? While none of these findings is specific for a seizure, the pattern may make the physician more or less suspicious that the episode was a seizure.
There is no diagnostic test for a seizure or for epilepsy. The diagnosis rests solely on the physician’s interpretation of the history of the episode which occurred.
Since physicians rarely have the opportunity to see the seizure events for themselves, they must depend on the observation of parents or other
witnesses to the episode. Most of these observers have never seen a true seizure and are upset and panicked by what they have seen. When they relay the information through third parties, the story can grow more lurid or lose important details. Frequently events occur at school or when the child is with friends. The person who actually saw the “seizure” will give more useful responses if he or she is calmly questioned about exactly what happened to your child. This is one of the reasons why you are such an important member of the team. The physician can’t make a diagnosis without good information. You may need to talk to teachers, friends, or even other children who saw what happened.
Let us give you an example of how difficult it may be to determine whether a particular episode was a seizure and how we think about the episode’s importance for the child’s future.
*16\208\8*
COPING WITH SIDE-EFFECTS OF DIET THERAPY FOR CANCER: NAUSEA
Nausea, with or without vomiting, is a common side-effect of surgery, chemotherapy, radiation therapy and biological therapy. The disease itself, or other conditions unrelated to your cancer or treatment, may also cause nausea.
Whatever the cause, nausea can keep the patient from getting enough food and needed nutrients. Some ideas that may be helpful are given here. The patient should:
1. Ask the doctor about medicine to help control nausea and vomiting. These drugs are called antiemetics.
2. Try these foods:
- Toast and crackers
- Curd
- Sherbet
- Sponge cake
- Oatmeal
- Skinned chicken (baked or boiled, not fried)
- Fruits and vegetables that are soft or bland, such as stewed apples, bananas
- Clear liquids, sipped slowly
- Ice chips.
3. Avoid these foods:
- Fatty, greasy or fried
- Very sweet, such as candy, cookies or cake
- Spicy or hot
- With strong odours.
4. Eat small amounts often and slowly.
5. Avoid eating in a room that is stuffy, too warm or has cooking odours that might disagree with the patient.
6. Drink fewer liquids with meals. Drinking liquids can cause a full, bloated feeling.
7. Drink or sip liquids throughout the day, except at mealtimes. Using a straw may help.
8. Drink beverages cool or chilled; try freezing.
9. Eat food cold or at room temperature; hot food may add to nausea.
10. Do not forcibly eat favourite foods when feeling nauseated. This may cause a permanent dislike of those foods.
11. Rest after meals, because activity may slow digestion. It is best to rest sitting up for about an hour after meals.
12. Try eating dry toast or crackers before getting up if nausea is a problem in the morning.
13. Wear loose-fitting clothes.
14. Avoid eating for 1 to 2 hours before treatment if nausea occurs during radiation therapy or chemotherapy.
15. Try to keep track of when nausea occurs and what causes it (specific foods, events, surroundings). If possible, make appropriate changes in diet or schedule. Share the information with doctor or nurse.
*10/356/5*
RHEUMATOID ARTHRITIS AND MUSCULOSKELETAL SYSTEM: JOINT SPACE AND FLUID, SYNOVIUM
What is the joint space?
The space between the bones is called a joint space. Fluid made by the cells lining the joint fills the joint space, or the joint can be filled with cartilage. When this fluid becomes inflammatory, the synovial cells assume an amorphous shape. This is called a “pannus.” The pannus can actually eat away at the bone of the joint. It is like a benign tumor in many ways. In the arthritic diseases, the joint space is the site of most inflammation.
What is joint fluid?
Joint fluid is a lubricant for the cells lining the joint and bathes both them and the cartilage cells. This fluid is rich in nutrients and contains some very important lubricants, which stop friction in the joint space. Normal joint fluid is usually very clear and has a slight yellow tinge. The fluid will also “gel” upon standing and is rather thick or viscous.
What is the synovium?
A capsule surrounds the joint space. The inner lining of this capsule is called the synovium, or the synovial membrane. It is usually three cells thick and overlaps on itself.
What do synovial cells do?
The synovial cells act as the major chemical and structural support cells for the joint. They also make up a small immune system within the joint. Some of the cells that make up the synovial membrane can eat germs, some make enzymes within the joint, and some are involved in the synthesis of the synovial fluid that bathes the joint.
Why is the synovium important in RA?
As rheumatoid arthritis progressively worsens, the synovial cells increase in number, and the lining itself gets very thick. The germ-eating synovial cells, in particular, increase. Usually these cells make up about only 20 percent of the synovial cells, but when rheumatoid arthritis is present, these cells increase to encompass 50 to 80 percent of the total synovial cells. The resulting mass is called a pannus. There is also an influx of T cells and the В cells to the area, indicating that there is a severe infection or that there is “cellular confusion” and really no identifiable foreign substance. The latter theory is probably the case, since there seems to be an overwhelming response to an unknown insult that triggers this disease process.
*9/141/5*
MEMORIES THAT DO NOT FADE: GENERIC MEMORIES AND PATTERNS
Enter generic memories, or “memories for patterns.” Every new exposure to the same or similar thing in the environment—or, for that matter, to the same or similar information conveyed through language or by some other means—will breathe new life into the reverberating loop supporting the formation of memory about it, and will increase the memory’s chance of making it into long-term storage. To use our billboard analogy, suppose you are walking home mumbling a useful telephone number you had noticed a few minutes ago. If you encounter another billboard with the same number along the way, the chances of your remembering it by the time you get home will be greatly enhanced.
The process is a bit Darwinian, as different memories compete for coveted but limited space in long-term storage. The more frequently encountered information usually wins, whereas the infrequently used information is likely to go by the wayside, into the dustbin of memory wannabes that never make it. One would think that the selection of memories for long-term storage should be determined by their importance, but we already know that there is no homunculus sitting inside the brain directing neural traffic. Even had there been one, he would have had a hard time predicting which information would prove to be important in the long run and which would not, since “importance” is mostly a prospective notion. Frequency of use becomes a surrogate “actuarial” marker of importance, since particularly pertinent information is likely to be invoked more frequently, and likewise frequently needed information is by definition important.
Nonetheless, importance may exert its influence on the formation of memories more directly as well. If in light of prior experience or genetically determined hard-wiring certain information is instantly recognized as “very important,” then a brain structure called the amygdala becomes part of the memory-forming reverberating circuitry. This vastly facilitates and expedites the formation of a robust memory and gives it preferential treatment in the memory race. The Darwinian nature of many biological processes, including brain processes, has become increasingly apparent to neuroscientists over the last few decades, this being reflected in Gerald Edelman’s memorable phrase “neural Darwinism.” It seems that memory formation is no exception.
Different experiences activate different neuronal networks in the brain, and no two such networks are ever completely alike. But the closer and more similar the experiences are, the greater the overlap between the networks. The common core among the neuronal networks evoked by similar but not necessarily completely identical impressions ends up being activated particularly frequently and stands the best chance of quickly entering long-term storage.
This propensity of the shared properties of similar but not identical situations to be learned quickly is reflected in one of the most fundamental features of the learning process well known to psychologists: the phenomenon of overgeneralization. At early learning stages, both humans and animals tend to relate to similar but not identical situations as if they were indeed identical. The common aspects of the situations are learned much faster than the distinguishing aspects.
The shared network, found on the overlap of specific networks, will be the mental representation not of any single thing or event, but rather of the shared properties of a whole class of similar things or events. We have just traced the formation of a generic memory in the brain! Such generic memories are memories for patterns. The more generic a pattern is and the vaster the set of experiences on whose overlap it emerged, the more robust and invulnerable to the effects of brain damage it is. This means that abstract representations are generally better able to withstand the effects of brain decay than concrete representations corresponding to unique things.
A typical pattern possesses a very interesting property. It contains information not only about the things you have already encountered, but also the information about things you may encounter in the future. This is so because a pattern captures the shared properties and features of every member of a whole class of things or events—all tomatoes, all chairs, all snowstorms, all political crises, all differential equations of a certain kind, all stock market crashes. Therefore, the pattern will help you deal with any member of the class that you may encounter in the future, by immediately informing you of all the essential properties of class members. The notion of generic memory or pattern can refer to the shared properties of entities of any kind, whether they are physical objects, social events, or verbal statements.
Now we understand why of all memories, generic memories or patterns are the most stable, the least vulnerable to any kind of neurological assault on the brain. This becomes particularly clear if one looks at the effects of retrograde amnesia. If different kinds of memories are affected differently in retrograde amnesia, then one could assume that these different kinds of memory are characterized by different degrees of robustness, due to the variability in the frequency of their use or the richness of their associations. Just what kind of memories suffer in retrograde amnesia, and what kind of memories are spared, has been the subject of inquiry and debate among neuropsychologists and neurologists for some time. In the course of this inquiry, some of the most important assertions of cognitive neuroscience have been made.
The first assertion involves the distinction between procedural and declarative memory. First introduced by Larry Squire and his associates, this distinction highlights the difference between “the knowledge how and the knowledge that” Procedural memory is the memory for skills. Riding a bicycle, playing tennis, and knowing how to tie a tie are all examples of procedural memory. By contrast, declarative memory is the memory for facts. Knowledge that there are seven days in a week, that Paris is the capital of France, or that World War II ended in 1945 are all examples of declarative memory. Like many distinctions in neuropsychology, the distinction between procedural and declarative memory is not absolutely cut-and-dried. How would you classify, for instance, the knowledge of chess or checkers moves? Is this truly knowledge, or are these, strictly speaking, skills? Despite this gray area, the distinction has been of great heuristic value to brain research. It has been commonly said that, with some exceptions, declarative memory usually suffers in retrograde amnesia, while procedural memory is usually spared.
Another influential distinction, first introduced by Endel Tulving, has been made between episodic and semantic memory. As we will see, this distinction further divides declarative memory into two more specific categories. Episodic memories are stored together with the memories of the context in which they were acquired. This may be the case both with momentous events or facts and with the most trivial ones. The knowledge that John E Kennedy was assassinated in Dallas or the meaning of 9/11 is embedded in the minds of most people as the memories of personal circumstances surrounding these events. To put it simply, most people who lived through these events remember vividly where they were and what they were doing when the news reached them. The same is true for more mundane life events, like buying your first car or going on your first job interview: Not only are you likely to remember the make of the car or the name of the prospective employer, but also you will have actual memories of going through the motions.
By contrast, semantic memories are stored independently of the context in which they were acquired. Most people know that Rome is the capital of Italy, that Einstein was a great scientist, that there are seven days in a week, or that metal objects don’t float in water, but they have no idea when and under what circumstances they had first learned these facts.
The episodic-semantic distinction has also been among the most influential in cognitive neuroscience and has been used in delineating the scope of retrograde amnesia. It has been commonly assumed that in retrograde amnesia episodic memory suffers and semantic memory is spared. But as it turns out, neither the procedural-declarative distinction nor the episodic-semantic distinction truly captures the fate of different types of memory in brain disease. It is not uncommon in biomedical research that established theories and opinions are challenged and eventually overturned by unusual clinical cases, which cannot be explained by these theories. My associates and I encountered such a case a number of years ago, and it changed our understanding of both the severity of retrograde amnesia and its scope. It is time to examine the memory problems of a fallen horseman.
*25\302\2*
THROAT INFECTIONS: ACUTE TONSILLITIS
The infection of throat and tonsils often first manifests itself with a chill, pain in the head and body, loss of appetite, and fever. The temperature may go up to 103° or 104° F. The tongue is usually coated, and the lymph glands at the back and side of the neck will be swollen. Swallowing is painful and even talking may be difficult. When you look at the throat it will appear red, swollen, and often covered with whitish-yellow spots. The symptoms in the throat last three or four days.
Many people seem to have throats that are easily infected, with trouble every time they are exposed to cold, fatigue, or sudden changes in climate. The streptococci are usually the infecting agent, and, since they are practically always present in the nose and throat of people, the explanation seems to be that they grow and multiply every time the resistance is lowered. In epidemics, streptococci from infected food or milk or from the hands of food-handlers are spread about, and attack those who cannot resist. If children have repeated sore throats with infected tonsils, the tonsils may be removed during an intervening period when inflammation is absent.
An abscess in the tissues around the tonsils is called quinsy. The doctor relieves the pain and swelling by puncturing the abscess and getting the accumulated pus out.
All streptococcal infections of the throat should be taken seriously because of the great danger of secondary rheumatic fever, arthritis, middle ear infection, or other complications. The sulfonamide drugs and penicillin, also aureomycin and terramycin, act powerfully against streptococci, and already the total number of severe and complicated cases has been greatly reduced.
*21/318/5*
SURGERY, DERMATOLOGIC TREATMENT, AND OTHER NONPSYCHIATRIC MEDICAL TREATMENT FOR BDD: DO THESE TREATMENTS WORK? OUR RESEARCHES’ ANSWER
In an important 2001 survey of 265 members of the American Society for Aesthetic Plastic Surgery (ASAPS), 84% of the surgeons who responded said they had operated on a patient who they thought was appropriate for surgery, only to realize after the operation that the patient had BDD. Eighty-two percent of these surgeons thought the patient had a poor outcome with surgery: 43% said the patient was more preoccupied with the perceived defect than before surgery, and 39% said the patient was now preoccupied with a different perceived defects Eighty-four percent had refused to operate on people with BDD.
It’s interesting that only 30% of the surgeons who responded to the survey thought that people with BDD should never have cosmetic surgery. This may reflect the fact that some people don’t tell the surgeon about their unhappiness with the surgical outcome. Others do worry less about the perceived defect after surgery, but the problem is that most don’t experience improvement of BDD overall (for example, their concern may shift to another body area); often, the surgeon isn’t aware of this.
In my experience, most people with BDD are not litigious, physically aggressive, or violent, but 40% of the ASAPS survey respondents said that a patient with BDD had threatened them. Twenty-nine percent of the surgeons said they were threatened legally, 2% physically, and 10% both legally and physically. Certainly, this is a terribly unfortunate outcome for the surgeon and BDD sufferer alike, and it’s yet another reason to avoid surgery.
Recent surgery studies from Sweden and Finland may be relevant to BDD. These studies found that women who have cosmetic breast augmentation surgery are more likely to commit suicide (about three times more likely) than women from the general population. An American study also showed an increased risk of suicide in women opting for breast augmentation. One wonders how many of these women had BDD, and whether BDD might have contributed to at least some of the suicides.
*351\204\8*
In: Anti Depressants-Sleeping Aid