Archive for May, 2008

Marine Poisoning & its management

Scombriod poisoning

Scombriod fish (mackerel like) include bluefin and yellowfin tuna, albacore, needle fish, skipjack, bonito etc. non scombroid fishes can also contain scombrotoxin. Poisoning with scombrotoxin is called pseudoallergic fish poisoning.

Under inadequate refrigeration/preservation these fishes undergo baterial decomposition and formation of amino acid L- histidine to histamine, histamine phosphate, and hydrochloride. Histamine level of 20 to 50 mgs/100 gm of fish has been noted. But it may be as high as 400 mg/100 gm. The toxin is heat stable and not destroyed by cooking or heating. Affected fish is of typical taste, but it may be without any specific taste or odor. Distribution of poison may not be same, this explain why some people do not get sick after eating same fish.

Symptoms develop within 15 minutes to one hour. Itching, urticaria, flushing which is sharply demarketed, nausea, vomiting, diarrhea, abdominal cramps, epigastric pain, headache, difficulty in swallowing, thirst, burning of mouth, dizziness, high pulse rate, feeling of warmth without increase in core temperature. These symptoms may resolve without any treatment within a day.

Treatment include antihitaminics and symptomatic treatment.

Paralytic Shellfish Poisoning

Paralytic Shellfish poisoning is induced by ingestion of aquacultured filterfeeding organisms like oysters, clams, starfish, mussels, scallops, and sand crabs etc. The toxin they have is accumulated by feeding the planktons where they live. The toxin is water soluble and heat stable. It can also kill large numbers of marine life. Commonest toxin is saxitoxin.

Symptoms appear within few minutes of ingestion of the toxin. It includes loss of sensation of tongue, lips, gums, which may progress rapidly to neck and extremities. Other symptoms include lightheadedness, incoordination, disequilibrium, incoherence, weakness, thirst, salivation, difficulty in swallowing, diarrhea, vomiting, abdominal pain, headache, loss of vision etc.

Treatment is supportive and based on symptoms.

Ciguatera poisoning

Ciguatera poisoning is the commonest non bacterial food poisoning associated with fish in USA, most of the cases occurs in Florida and Hawaii. Poisoning involves tropical and subtropical coral reef fish. Poisoning involve five different types of toxins. These toxins are heat, cold, drying, and gastric acid resistant. These five toxins are colorless, tasteless, and odorless.

Symptoms occur within 15 to 30 minutes of ingestion. They include abdominal pain, diarrhea, vomiting, chills, itching, numbness of throat and tongue, sensation of ‘carbonation’ during swallowing, tremor, fatigue, and headache.

Treatment is symptomatic and supportive. Activated charcoal (100 gm) in sorbitol is useful if given within three hours of ingestion of the toxin. Sedatives can be given if patient is apprehensive. Adequate hydration should be given if there is dehydration.

Snake Bite & its Management

There are thousands of different species of snakes in the world. But very few of them are poisonous. More than 50,000 people die each year due to poisonous snake bite. This may be only the tip, because many go without reporting. Venomous snakes are divided into the following categories Viperidae (old world vipers, asian pit vipers etc), Elapidae (cobras, coral snakes and Australian venomous snakes), Hydrophiidae (all sea snakes), Atractaspididae (burrowing asps), and Colubridae.

It is very difficult to differentiate venomous from non venomous snakes. Fang marks are of no diagnostic value. Symptoms of snake bite include fear of impending death, nervousness, local swelling, redness of the site, sharp pain. More than 20% (75% of sea snakes) of the bite are ‘dry’ type which means either no venom or insufficient venom to cause serous problem or death.

First Aid Measures: If the bite of the snake is in limb it should be immobilized and firm pressure bandaging of the bite area and few inches above the bite site should be tied. These measures significantly delay the spread of the venom. Patients are generally apprehensive and nervous and they should be reassured and sedated if necessary.

Treatment of snake bite:

1) The site of the bite should be cleansed properly and left strictly alone. Nothing should be done with the bite site, otherwise chances of infection increases. Tetanus prophylaxis should be done with tetanus toxoid. If there is necrosis of skin, it should be sloughed off and skin grafting if required.

2) If required sedatives can be administered. General measures like intravenous fluids should be given.

3) Anti venoms should be given only if there is clear evidence of systemic poisoning. But some authorities prefer to give anti venom within four hours if diagnosis of snake bite is confirmed, to avoid necrosis. Anti venom is available for some common snakes only depending on the country, within country also different regions have different types of snakes so also anti venom. If snake is not common in an area anti venom for that particular snake may not be available. If it is available than it should be made sure that it is clear and has no opacities. Depending on the severity 20 to 100 ml is diluted in two units of normal saline and given by slow infusion. Adrenalin (1:1,000 solutions) should be kept ready in case anaphylactic shock (dangerous allergic reaction) develops. Giving anti venom at the earliest is very important because once the venom is lodged it is very difficult to dislodge the venom from the site.

Scorpion Stings

Scorpions are arachnids that feed on arthropods, lizards, which they grab with crablike claws and inject paralyzing venom from stinger which is present at the tip of the tail. There are about one thousand different species of scorpions, out of which only the bark scorpion in USA produces venom which can be lethal to humans. Scorpion sting cause about 5,000 deaths every year worldwide. They feed at night and remain hidden at day time. They like cool places and can enter houses and hide in shoes, cloths, bedding or may enter sink in search of water. Scorpions stings humans only when disturbed.

Scorpion sting can cause sharp local pain, which is followed by swelling of the area, burning sensation, itching etc. Allergic reaction may develop. If condition is severe there will be restlessness, blurring of vision, salivation, lacrimation, running nose, speech difficulty. Muscle cramp, drop in blood pressure, seizure, nausea, vomiting can occur. Symptoms become severe in 5 hours and subside in a day or two.

Offending scorpion should be tried to identify. Treatment of scorpion sting consists of local application of ice pack, cleaning of the bite site, tetanus prophylaxis with toxoid. Painkillers like brufen, diclofenac and antihistaminics like cetirizine, fexofenadine can be given for symptomatic relief. Patient should be advised to be calm and reassurance is given. Specific antivenin if available should be administered in serious cases. But antivenin should be reserved for selected cases only because it can cause potentially dangerous side effects. A C. sculpturatus antivenin is available but not yet approved by FDA. It is available in Arizona State University for use in Arizona only, mainly for research purpose.

Spider Bite: Recluse Spider Bite

There are more than 30,000 recognized spider species in the world. But only about 100 defend themselves aggressively and have fangs long enough to penetrate human skin and can cause harm to humans. Bites of the most spiders are painful but do not cause any harm. The venom that spiders use to hunt their prey can cause necrosis of skin and systemic toxicity. Bites of spiders like brown recluse spiders, widow spiders and very few other species can be life threatening. Specific treatment for spider bite like widow and brown recluse spiders is available, so offending spider should be tried to identify. In many cases it is seen that injury is by something else but spiders are attributed as the offender.

The scientific name of the recluse spider is Loxosceles recluse. Recluse spiders are found southern and Midwestern USA. They are about 0.7 to 1.5 cm in body length and 2 to 4 cm in leg span. Recluse spiders are brown in color and they have violin shaped spot on their surface. Recluse spiders do not spin web. They are not aggressive toward humans and bite only when they are provoked or threatened, or pressed against skin. They invade homes particularly during fall and hide in undisturbed dark places like closets, in furniture, store rooms, garage, and folds of cloths. That’s why bites are common while dressing and the common sites are arms, neck and abdomen. In wild they hide under rocks and logs and in animal burrows and caves. They emerge at night to hunt insects and other spiders.

The venom of recluse spider is clear and viscous and it contain an esterase, alkaline phosphatase, protease and other enzymes which produces hemolysis (breakdown of blood cells) and tissue necrosis (death of tissue). Sphingomyelinase B is the most potent enzyme which causes vascular thrombosis and tissue necrosis. At the beginning the bite is painless, but after few hours the site of the bite becomes painful and itching. The bite site becomes hard and it is surrounded by a pale zone (due to lack of blood and oxygen) and a zone of redness. Maximum cases the lesion resolve spontaneously without any treatment in a few days. But if it is not resolved within 2 to 3 days, the red surrounding spreads, the central pale becomes hemorrhagic and dies. This part sloughs off and a big ulcer forms which, may be sometimes as big as one foot in diameter. It eventually becomes a big depressed scar. Healing of the scar may take up to 3 to 6 months. If subcutaneous fat is involved it may take 3 years to heal properly. Complications of recluse spider bite include secondary infection and injury to nerves. Nausea, vomiting, weakness, fever, chills, headache, rash, painful muscles, arthralgia may develop after the bite. Very rarely renal failure, hemolytic anemia may cause death.

Treatment of Recluse Spider bite:

Initial treatment includes local cleansing of bite site, icepack, dressing and elevation and immobilization of limb if the bite site is limb. Treatment with painkillers, antihistaminics, antibiotics and tetanus prophylaxis is given. If lesion is becoming necrotic dapsone, a leukocyte inhibitor is given within 2 to 3 days, which prevent progression of the lesion. Dapsone (used in treatment of leprosy) is given at the dose of 50 to 100 mgs twice a day orally. Glucose 6 phosphate dehydogenese deficiency should be ruled out before giving dapsone. Loxosceles specific antivenom is not approved in USA. Cleaning of wound and removal of dead tissues should be done. Immediate surgical removal of wound is very useful in serious cases. Finally skin grafting is required in most cases. Patient should be observed for the development of renal failure, hemolysis and other systemic complications.

Preventive measures like wearing full sleeve heavy shirts, full trousers (not half pant or bermuda’s), and hand gloves should be kept in mind while working outdoor and in dark areas indoor in the localities where widow spiders are commonly found.

Spider Bite: Widow Spider Bite

There are more than 30,000 recognized spider species in the world. But only about 100 defend themselves aggressively and have fangs long enough to penetrate human skin and can cause harm to humans. Bites of the most spiders are painful but do not cause any harm. The venom that spiders use to hunt their prey can cause necrosis of skin and systemic toxicity. Bites of spiders like brown recluse spiders, widow spiders and very few other species can be life threatening. Specific treatment for spider bite like widow and brown recluse spiders is available, so offending spider should be tried to identify. In many cases it is seen that injury is by something else but spiders are attributed as the offender.

Widow Spider Bite:

The scientific name of widow spider is Latrodectus mactans. The bite of the female widow spider is dangerous and notorious due to its potent neurotoxin. The black widow spider is found in all of USA except Alaska. It is more common in Southeastern parts of USA. It is about 5 cm in length with a body of one cm. It is shiny black in color and has a red hourglass marking in the abdomen. The red widow and the brown widow are other dangerous types of widow spiders.

Bites are most common during summer and early autumn when their web is disturbed or when they are trapped or provoked. They spin their webs in logs, plants, rock piles, under stones or in dark areas like garages or outhouses. Buttocks are the site of bite if the person sits on a spider. It goes unnoticed at first or may be thought as a sharp pinprick. If examined properly two small red marks will be seen and there will be swelling around the marks. ? latrotoxin which is the most active component of the venom is yellowish and oily in color and may not cause any problem or it may be cause serious toxicity by binding irreversibly to nerves and cause release and depletion of acetylcholine, norepinephrine and other neurotransmitters. In less than half hour painful cramps spread from bite site to large muscles of trunk and limbs. Symptoms like salivation, vomiting, high blood pressure, diaphoresis, breathing difficulties, high pulse rate, weakness, headache, anxiety, urinary retention, hyperreflexia, fasciculation, uterine contraction and premature labor can occur. Peritonitis may develop, which is suggested by rigidity of abdominal muscles and excruciating pain. But there may not be any pain on pressure to abdomen. In very weak and frail person, elderly and young person it may cause renal failure, respiratory arrest, cardiac arrest, brain hemorrhage and death. Excruciating pain may last for several weeks or it may subside in a day.

Treatment of Widow Spider Bite:

At first cleaning of the bite site with plain water, ice packing, and tetanus prophylaxis should be given. If there is high blood pressure it requires specific antihypertensive therapy because it can not be controlled symptomatically. Specific equine antivenin is available but due to its high risk of anaphylaxis and serum sickness it should be reserved for serious cases only. The equine antivenin is administered intravenously relieve pain rapidly. One or two vials are usually sufficient.

Preventive measures like wearing full sleeve heavy shirts, full trousers (not half pant or bermuda’s), and hand gloves should be kept in mind while working outdoor and in dark areas indoor in the localities where widow spiders are commonly found.

Obsessive Compulsive Disorder (OCD)

Obsessive compulsive disorder (OCD) is characterized by obsessive thoughts and compulsive behaviors that hamper day to day activity. Most common forms of OCDs are fear of contamination by germs or dirt, so patients keep washing hands very frequently and having to check and recheck such actions as whether a door is locked or not. The degree by which individuals get affected varies, but all cases of OCD generally take up more than1 hour per day and are undertaken to relieve the anxiety triggered by the core fear. Doctors treating patients of OCD must ask specific questions regarding recurrent thoughts and behaviors, because patients often conceal their symptoms due to embarrassment by the content of their thought and their actions. Physicians must enquire about specific clues like, chafed and reddened hands or patchy hair loss which are due to repetitive hair pulling. Symptoms like depression, anxiety, eating disorders, and tics (eating of earth) are common. Some of the OCD are of benign nature, which does not cause any problem. But some are very much embarrassing and time consuming and harmful in the long run. Some patients are obsessive with counting numbers.

Kleptomania is a dangerous form of OCD, in these patients there is an uncontrollable urge to steal any valuable or non-valuable article whenever the patient finds an opportunity to steal. These kleptomania patients are in need of urgent behavioral and psychiatric treatment.

Onset of OCD is usually gradual, beginning in early adulthood. Childhood OCD is not uncommon. Prevalence of OCD is about 2-3% throughout the world. This disorder usually takes waxing and waning course but certain cases steady deterioration of psychosocial functioning takes place.

Twin studies suggest a genetic predisposition. OCD is more common in males and in the first born children. The OCD is thought to involve the orbital frontal cortex, caudate nucleus, and globus pallidus. The caudate nucleus is involved in acquisition and maintenance of habit and skill learning. Interventions that are successful in reducing obsessive compulsive behaviors decrease the metabolic activities of caudate nucleus.

Treatment of OCD: if OCD is consuming time more than one hour per day it should be treated medically and by behavior therapy. Chlomipramine, fluoxetine, and fluvoxemine are approved for treatment of OCD by USFDA. Chlomipramine is a tricyclic antidepressant which has many side effects. Fluoxetine and fluvoxemine, are equally effective like chlomipramine with lesser side effects, that’s why these two are the preferred drugs for treatment of OCD. Fluoxetine is given at the dose of 40-60 mgs per day in divided doses and fluvoxemine is given 100-300 mgs per day. Only about 50% patients show improvement with medication alone. When therapeutic improvement is achieved long term maintenance is indicated. If pharmacotherapy is combined with behavior therapy than the result is much more encouraging than either of the treatment modalities alone.

For the individuals, particularly with time consuming compulsions behavior therapy gives as good a result as that given by medication. The techniques of behavior therapy include gradual increase in exposure to the stressful situations, maintenance of a diary to clarify the stress factors, and homework assignments which substitute new activities for compulsive behaviors. If patient is gradually exposed to increasing degree of the stressful situation, slowly patient develops tolerance to the stressful situation and it becomes normal over a period of time.

All You Should Know about Parkinsonism & Parkinson ’s Disease (PD)

Parkinson’s disease (PD) is the one of the commonest form of neurodegenerative disorders characterized by accumulation of presynaptic protein ?-synuclein and a variable degree of Parkinsonism. Parkinsonism is characterized by tremor at rest, rigidity, and bradykinesia (slowness of movements). Parkinsonism may also have symptoms like, shuffling gait and flexed posture. All forms of Parkinsonism are the result of reduction of dopaminergic transmission within the basal ganglion. 25% of all PD are genetically predisposed. Remaining 75% are idiopathic and sporadic. In United States alone more than one million patients of PD are present. Peak age at onset is 60 years (range from 35 to 85 years).

Parkinsonism is of two types; primary and secondary Parkinsonism. Primary Parkinsonism is due to familial, idiopathic, due to other neurodegenerative disorders like Alzheimer’s disease, Shy Drager syndrome etc. Genetically mediated primary Parkinsonism include Wilson’s Disease (hepatolenticular degeneration), Chediak Higashi disease, Fragile X syndrome, Huntington’s disease, Prion disease etc. Secondary Parkinsonism is due to repeated trauma (dementia pugilistica), infectious and post infectious diseases like neurosyphillis, postenchephalitic PD, hypoparathyroidism, non Wilsonian degeneration, drugs like, neuroleptics, antipsychotics, anti emetics, ? methyldopa, lithium, fluoxetine etc. Toxins like cyanide, manganese, methyl alcohol, carbon monoxide, carbon disulphide can cause secondary Parkinsonism.

Risk factors include a positive family history, male gender, head injury, exposure to pesticide, consumption of well water, and rural living. Incidence is high if there is combination of environmental factors and genetical predisposition. Factors which reduce incidence of PD include, drinking coffee, use of painkillers, estrogen replacement in postmenopausal women, and smoking.

Diagnosis of PD can be made confidently if at least two of the three cardinal signs are present, which are tremor at rest, rigidity, and bradykinesia. Tremor is present in 85% of patient with true PD, so diagnosis is difficult when tremor is absent and other two signs are present. Gradual onset of symptoms and if it is unilateral is also supportive in diagnosis. The most disturbing feature of PD is bradykinesia (slowness of movements) which interfere in day to day activities like walking, dressing, turning in bed, getting up from bed and rising from chair. Handwriting becomes bad or illegible. Speech becomes soft. Tremor starts in periphery first, like tremors of fingers of one hand and spread to the other next, than it spreads to the legs. Later on tremor appear on lips, tongue and jaw, but the head is spared.

Rigidity is uniform resistance to passive movements in a joint throughout the full range of motion, which gives characteristic “plastic” quality. There may be also “cogwheel” sensation, which is due to regular interruption of resistance during passive movement. Gait disturbance with shuffling short steps and a tendency to turn en block is an important sign of PD. Festinating gait is a classical sign of PD, which is due to combination of flexed posture and loss of postural reflexes, which causes the patient to ‘catch up’ with the body’s center of gravity. Other signs of PD include depression, anxiety, sleep disturbance, loss of smell (anosmia), sensory abnormality and pain, change in mood and behavior. Depression is present in almost half of the patients. Daytime drowsiness and frequent napping are common problems.

Studies of monozygotic and dizygotic twins have proved some of the PD as genetically predisposed. Four genes have been clearly linked to familial form of PD, and a number of genes can possibly cause PD. Among these PARK1 and PARK5 lead to an autosomal form of PD and PARK 2 and PARK 7 lead to autosomal recessive form of PD. Other genes which are thought to be a causative factor in development of PD include PARK 3, 4, 6, 9, 10 etc.

In PD dopaminergic cells die due to genetic weakness, environmental factors, protosomal dysfunction, and oxidative stress by free radicals. Pathological examination of brain reveals mild atrophy (shrinkage) with loss of melanin pigment of midbrain. Microscopically, there is degeneration of dopaminergic cells with the presence of Lewy Bodies (LB) in the remaining nerve cells or neurons. Lewy Bodies have high concentration of ?-synucleinand is the hallmark of the diagnosis of PD.

Treatment of Parkinson’s disease: The goal of treatment of PD is maintenance of quality of life and avoids complications of drug therapy. In the early course of illness almost all symptoms of PD like rest tremor, rigidity, bradykinesia, and abnormal posture respond well to symptomatic treatment. Other symptoms like soft speech respond poorly. To prevent secondary disability regular physical activity programme is required, so regular physical activity is encouraged. Patient of PD should be mentally very strong to prevent worsening of the condition. Recent studies show that regular physical activity can promote neuroprotection against neurotoxins.

As soon as PD starts interfering with quality of life symptomatic drug therapy should be started. The ideal drug for treatment depends on the age of the patient, and cognitive status of the patient. Studies show that if therapy is initiated early, it reduces side effects in later part of the disease. Treatment can be started with levodopa or carbidopa. Initial dose is 25 to 100 mgs per day in three divided doses. Food increase bioavailability of the drug and it should be taken after food. The tablets should not be split, because it reduces controlled release property. The dose of levodopa/carbodopa should be adjusted according to the response. Other dopamine agonists can be combined with levodopa or carbidopa if monotherapy is not giving desired response. They include, non ergot alkaloids ropinirol, pramipexole, and ergot alkaloids pergolide, bromocriptine etc. Treatment of PD has to continue lifelong.

Treatment of Parkinsonism is also symptomatic like Parkinson’s disease. These two conditions are closely related to each other.

Truth about Alzheimer’s disease

Alzheimer’s disease (AD) is the most common cause of dementia in western countries. AD is caused to lack of acetylecholine in brain. Approximately 10% above 70 years have significant memory loss and at least more than half of this is due to Alzheimer’s disease. AD most commonly presents as subtle loss of memory and it is followed by slowly progressive memory loss, and that has a course of several years (8-10 years). AD can occur at any time during adult life. Cost of treatment in USA is nearly $ 75,000 per year, which is a staggering sum of money, which also extracts a heavy emotional toll on family and friends and caregivers. Patho physiology of AD is diffuse atrophy of cerebral cortex and secondary enlargement of ventricular system. Neuritic plaques containing A? amyloids are seen in microscopy, and also accumulation of A? amyloids in the arterial walls of cerebral blood vessels. Four susceptible genes have been identified to cause AD.

Clinical symptoms of AD follow a characteristic pattern, which starts with simple memory loss, impairment of language comprehension and visual deficit. Around 20% of AD patients presents with problem of word comprehension, organizational problems and difficulty in finding places. In early stage of AD memory loss may go unrecognized or may present as simple forgetfulness. Mild Cognitive Impairment (MCI) is the term used when memory loss causes day to day activity disturbance. Slowly MCI starts to disturb daily activities like keeping tracks of finances, daily activities in job, driving automobile, shopping and housekeeping. Some of the patients are not aware of their difficulty which is called anosognosia. Change in environment may be puzzling. Patient may get lost during routine walk, or while driving automobile patient may loose direction. In the middle stage of AD patient is unable to work at his job, he is confused, easily lost and need supervision. Sometimes patient may surprisingly retain superficial conversation, social grace, and routine behaviors. Language is impaired, at first naming then comprehension, and then fluency is lost. Apraxia (inability to use objects correctly) develops, aphasia (loss of power of expression by speech, writing, or sign, or comprehending spoken or written language), visual deficit, interfere with dressing, eating, solving simple puzzles develops. Patient may be unable to do simple calculations and tell time. In late stage some patients remain ambulatory but may wander aimlessly. There is loss of judgment and reasoning. Delusion which may include theft, infidelity, and difficulty in identification is seen. 10% develop Capgras syndrome (believing that the caregiver is an imposter). Sleep pattern is lost; somnambulism (walking during sleep) is a big problem for the patient and family members. Patients become mute, bedridden and incontinence of urine develops. Help is required for simple tasks like, dressing, eating, and toilet function. Sudden brief contraction of some muscles or whole body may occur spontaneously, in response to physical or auditory stimulus. Generalized seizure may develop and cause sudden death. Duration of disease is usually 8-10 years but may range from 1-25 years.

Diagnosis of Alzheimer’s disease is mainly clinical symptoms. In early stages of AD other causes of dementia should be excluded. EEG shows non specific changes. Genotyping of blood is done to find out susceptible genes. CT or MRI is not specific. As AD progresses diffuse atrophy of cortex is seen in MRI. Several genes have been identified which play important role in pathophysiology of AD. The first to be identified was APP gene on chromosome 21. Point mutation of APP gene produces autosomal dominant AD. Adults with trisomy 21 (Down’s syndrome) who survive beyond 40 years of age develop progressive dementia which is accompanied by typical symptoms of AD, which proves its relationship with APP gene. Investigation of large number of families with AD for many generation found that two other genes other than APP gene are responsible. They are Presenilin-1 (PS-2) and Presenilin-2 (PS-1). PS-1 is on chromosome 14 and PS-2 is on chromosome 1. PS-1 encodes a protein called S182, mutation of which can cause early onset of AD, onset much before age 60. PS-2 gene encodes a protein called STM2. PS-1 and PS-2 are homologous. Mutation with PS-1 causes early onset AD with mean age of development at 45 years. This type of AD is rapidly progressive with mean duration of 6-7 years.

Most important risk factor is old age, and positive family history. Frequency of AD increases every decade. In western countries AD is about 30% in people above 80 years of age. Due to longer lifespan females are more prone to develop AD. In one study it was found that the capacity to express complex written language and understand in adulthood correlates with a decrease in the risk of developing AD in later years. Pathology is found in temporal cortex and hippocampus. Most important microscopic finding is neuritic plaques. These plaques accumulate during normal aging but in AD they are present in excess. These plaques contain A? amyloids , proteoglycon ? , antitrypsin and other proteins. A? amyloid is a protein of 39 to 42 amino acids. Accumulation of A? amyloid in cerebral cortex is called amyloid angiopathy, which lead to cerebral hemorrhage and reduction of acetyl choline results from degeneration of cholinergic neurons. There is also reduction of norepinephrine in brain stem.

Alzheimer’s disease can not be cured. Drugs are not effective. Focus should be on symptomatic treatment of patient and building a rapport with family members and caretakers. Cholinesterase inhibitor drugs should be used judiciously. Donepezil, rivastigmine, and galantamine are approved by US FDA (food & drug administration) for use in AD. They inhibit cholinesterase thereby increasing levels of acetylecholine in brain. They improve functioning of patients. Donepezil has less liver toxicity than other drugs and also it is cheap, so it is more commonly used than other drugs. It is given at the dose of 5-10 mgs once daily. In patients, with mild AD, antioxidants selegeline, and vitamin E also helpful. The dose of vitamin E 1000 IU twice daily. A control trial study with Ginkgo biloba found to improve symptoms of AD. The latest strategy of treatment of AD is to develop a vaccine against A? amyloid, which has shown excellent results in mouse models but gave rise to life threatening meningoencephalitis in human volunteers. In mouse models this vaccine could clear amyloid deposits and improve cognitive function. This vaccine develop antibody against A? amyloid, which cross Blood Brain Barrier (BBB). Scientists are trying to find out a solution to this problem with the vaccine. Several retrospective studies have found that statins (HmgCOA reductase inhibitors) and NSAIDs (non steroidal anti-inflammatory drugs) may protect against dementia. Mild to moderate depression common in early stage of AD responds to routine antidepressants. Selective serotonin reuptake inhibitors (SSRI) are also used. Finally it is the sympathetic approach to the patient and his family and friends which goes a long way in the management of Alzheimer’s disease.

A Food Guide during Pregnancy from Conception to Delivery

Your baby is what you eat. Your diet before, during and after pregnancy is the most important determinant factor of your health as well as the health of your baby. Research shows that maternal nutrition not only affects the health of the baby but his susceptibility to disease during adult life. Healthy eating should be a way of life, especially when you are nurturing another life within you.

Pre conceptual Care: Overweight females find it difficult to conceive.If you are planning a baby, and you are overweight, reduce weight first. Begin on a healthy note with healthy eating. Plan your diet for reducing weight and also for maintaining proper nutrition. Cut down on your intake of anti-nutrients such as caffeine, deep-friend foods, cigarettes, alcohol and also painkillers. This ensures healthy conception.

Research shows fifty essential nutrients are needed for proper growth and development of the foetus, of which folic acid is of prime importance. Lack of folic acid causes neural tube defects such as Spina Bifida and other congenital deformities of neural tube. It is a birth defect in which the spinal cord does not develop fully.

Folic acid is extremely crucial for foetal brain development in the first few weeks of pregnancy. Most women do not know they have conceived till they fail to menstruate. That is why; it is of utmost importance that all women of childbearing age consume more than one food which is rich in folic acid.

GOOD SOURCES OF FOLIC ACID:

1. black eye beans chickpeas.

2. peanuts, sprouting beans.

pumpkin, carrot, spinach, greenleafy vegetables.

3. broccoli, letuce.

Positive pregnancy:

If you gain excess weight during your pregnancy, it is less likely that you will revert to your orginal size. Normal weight gain is within the range of 10-13 kg.Excess weight gain can lead to complications like hypertension, preeclampsia , caesarean sections, and extra large baby. Extra large babies can have lots of problems, like diabetes, obesity in later life, and associated problems of obesity. It also means extra weight to burn off after the baby is born.

The amount of fat cells your baby will have is determined in the foetal stage, so your diet must not be too rich in fat. Nevertheless, some fat gain is vital for pregnancy. Compensate with nutrient rich foods and healthy fats found in nuts and oily fish.

Trying to lose weight during pregnancy can be dangerous. Underweight mothers suffer from infections and may give birth to “small for date” babies. Eating for two may be a myth but your calorie demands naturally increase with pregnancy.An average weight person needs only 300 more calories than normal to maintain pregnancy. However, some women reduce their activity, which means normal calorie intake is fine.

If your BMI is more than 25 at the time of conception body weight increase during pregnancy should be little less than normal person. If BMI is less than 18.5 during conception weight gain during pregnancy should be about 15 kgs.

Morning sickness:

Most of the organs of the baby are formed during the first trimester (first 3 months of pregnancy), so during this period, optimum nutrition is extremely important. Yet at this time many women experience continual sickness (nausea & vomiting) and do not feel like eating.

Tips to alleviate nausea and vomiting:

1. Eat anything you like to eat.

2. Eat small quantity of food frequently. Avoid large meals, greasy of spicy foods.

3. Get out of bed slowly, avoiding sudden movements.

4. Eat some dry bread, biscuits of cereal in the morning.

5. Try foods and drinks that have ginger, as it sometimes relieves nausea.

6. Cold foods are better tolerated than hot foods since they are less aromatic.

7. Do not lie down immediately after eating.

8. Do not fast or remain hungry.

Ensure that your diet provides you with enough energy and nutrients for the baby to grow and for your body to deal with the changes taking place.

Post-partum:

The burning question after pregnancy is, “Will I ever get my figure back?”Desperation to fit into your favourite outfit mounts every day. Avoid the temptation to go on a fad diet.

There is no need for any special food after childbirth. You will burn fat with increased physical activity and cutting down on sugary and oily foods. Breastfeeding helps to shed excess weight by burning more calories and mobilizing fat for the production of milk. It stimulates the uterus to contract to its pre-birth size.Eat a healthy, balanced diet and exercise to get back a lean, firm body gradually.Walking is one of the best fat burning exercises for post partum women. Pelvic floor and abdominal exercises are also beneficial.

Now you have a baby, it’s a big responsibility. One of the greatest challenges is to provide proper nourishment and inculcate healthy eating habits in today’s snack culture. But in the long run, this is the greatest contribution you can make to your child’s development.

Scientific Fact About Foods & Nutrition

Nutrition is the science of food and its relationship to health. The subject of food & nutrition is very extensive. Through centuries, food has been recognized as important for human beings in health and disease. The history of man has been to large extent struggle to obtain food. Great advances have been made during last 50 years in knowledge of nutrition and in the practical application of that knowledge. Specific nutritional diseases have been identified and technologies developed to control them, for example protein energy malnutrition, endemic goiter, nutritional anemia, and nutritional blindness.

Foods can be classified into five categories 1) Proteins 2) Fats 3) Carbohydrates 4) Vitamins 5) minerals.

Proteins:

Proteins are the building blocks of human body. The word protein means, “Of first importance”. Indeed they are of the greatest importance in human nutrition. Proteins are complex nitrogenous compounds. They contain carbon, hydrogen, oxygen, nitrogen, and sulphur in varying amount. Proteins differ from carbohydrates and fats in that they contain nitrogen; this is usually 16 % of protein. Proteins constitute about 20% of body weight.

Proteins are made up of smaller units, called amino acids. Some 24 amino acids are required by human body, of which 9 are called “essential” because the body can not synthesize them in amounts what is needed by the body, and therefore they must be obtained from dietary sources. They are: leucine, isoleucine, lysine, metheonine, phenylalanine, threonine, valine, tryptophan, and histidine. Non essential amino acids (which are synthesized in the body) include asparagenic acids, serine, glutamic acid, praline and glycine, arginine. Both essential and non essential amino acids are required for synthesis of proteins. New tissues can not be formed unless all essential amino acids (EAA) are present in the diet. A protein is said to be “biologically complete” if it contain all the EAA’s. if it is lacking in one or more EAA’s it is “biologically incomplete”. From nutritional point of view animal proteins are rated superior to vegetable proteins. Milk and egg proteins are most suitable for humans. If one is a pure vegetarian than he should combine two or more vegetable proteins to overcome deficiencies of EAA’s.

Functions of proteins: proteins give 4 kcal of energy per gram. Proteins are required for body building, repair and maintenance of body tissues, synthesis of substances like, antibodies, plasma proteins, hemoglobin, enzymes, and coagulation factors. Proteins are required for immune mechanism of body.

Sources of proteins: Animal sources include, milk, meat, egg, fish, cheese etc. Vegetable sources include pulses, cereals, nuts, oil-seed cakes etc.

Protein requirement is expressed in terms of body weight. Protein requirement of humans is 1 gram/kg/day.

Fats:

Fats are solid at 200C, they are called “oils” if they are liquid at that temperature. They can be classified into simple lipids, compound lipids, and derived lipids.

Most of the body fat (99%) in adipose tissue is in the form of simple lipid. Adipose tissue constitute 10-15 % of body weight, if it is more than that it is obesity. Fatty acids can be divided into saturated and unsaturated. Some of the fatty acids can not be synthesized in the body, they have to be obtained from dietary sources and are called “essential fatty acids” (EFA). Saturated fatty acids increase amount of cholesterol and unsaturated fatty acids reduce cholesterol.

Sources of fat:

1) Animal fats- major sources are butter, milk, cheese, eggs, fats of meat and fish. Animal fats except cod liver oil and fish oils are mostly saturated fats and increase cholesterol. That’s why animal fats should be consumed less.

2) Vegetable fats- plants store fat in there seeds, e.g. ground nut, mustard, coconut, sesame, sunflower. They contain large amount of unsaturated fat and reduce cholesterol. There percentage should be higher in food compare to animal fat.

3) Other sources- small quantities of fat (invisible fat) are found in most foods like, cereals, pulses, vegetables.

Fats are high energy foods; they provide 9 kcal of energy per gram. WHO expert committee on Prevention of Coronary Heart Diseases has recommended only 20-30% of total dietary intake of calories. At least 50% should be vegetable fat. But in developed countries it is more than 30-40%.

Carbohydrates:

The third major component of food is carbohydrate, which is the main source of energy, providing 4 kcal of energy per gram. They are essential for synthesis of certain non essential amino acids. Carbohydrate reserve of human body is about 500 grams.

There are three main sources of carbohydrates viz. starches, sugars and cellulose. Starch is basic to human diet. It is found in abundance in cereals, roots and tubers. Sugars comprise monosaccharide (glucose, fructose galactose) and disaccharides (sucrose, lactose). Cellulose is the indigestible part of carbohydrate which do not contribute calorie. They contribute to dietary fiber. Dietary fibers are mainly non starch polysaccharides physiologically important. They are found in fruits, vegetables, and grains. Fiber has many functions. It absorbs water and this increase the bulk of the stool, which prevents constipation, by encouraging bowel movement.

Dietary fiber should be more than 40 grams per day. A well balanced diet provides that much of roughage. Excess fiber also decreases absorption of micronutrients. Fiber may also bind to vitamins and minerals like, zinc, iron, and reduce their bioavailability.

Vitamins:

Vitamins are divided into two groups (a) fat soluble vitamins viz. vitamins A, D, E, and K and (b) water soluble vitamins viz. vitamins B- Complex group and C. each vitamins has specific function to perform and deficiency of any particular vitamin may lead to specific deficiency disease. Minimum requirement of the vitamins has been determined.

Vitamin A: daily requirement is 600 micrograms (mcg) for adults, 350 mcg for infants, and 950 mcg for lactating mothers, and children of 1-6 years need 400 mcg.

Sources of vitamin A include liver, egg, meat fish, milk, green leafy vegetables (darker the leaf, more the vitamin content), yellow fruits and vegetables like papaya, mango, pumpkin, tomato etc. Human body can store vitamin in body mainly in liver, which is sufficient for 6-9 months. Deficiency of vitamin A can cause many symptoms like, night blindness, conjunctival xerosis, Bitot’s spot, corneal xerosis, keratomalacia.

Vitamin D: Daily requirement of vitamin D are 2.5 mcg for adults, 5 mcg for infant and children, and 10 mcg in pregnancy and lactation.

Vitamin D is unique because it is derived from sunlight; it is synthesized by the body by the action of UV (ultra violet) rays of sunlight, which is stored in the skin. Sources of vitamin D are only animal origin. Liver, egg yolk butter, cheese is rich in vitamin D.

Deficiency of vitamin D causes Rickets and osteomalacia.

Vitamin E: vitamin E does not have serious deficiency syndrome. Sources of vitamin E are vegetable oil, sunflower seeds, egg, butter etc. vitamin E is very important in maintaining skin texture.

Vitamin K: it occurs in two forms vit K1 and vit K2. Sources include fresh dark green leafy vegetables, cow’s milk, and liver. Vitamin K2 is synthesized by the intestinal bacteria, which usually provide adequate supply of vitamin in man. It stimulates certain coagulation factors and deficiency of vitamin K can cause bleeding disorders. The daily requirement of vitamin K is 0.03 mg/kg.

B-complex group of vitamin include thiamin (B1), riboflavin(B2), niacin, pyridoxine(B6), pantothenic acid, folic acid, vitamin B12.

Thiamin is water soluble vitamin. Its daily requirement is 0.5 mg per 1000 kcal energy intake. Important sources are whole grain cereals, wheat, gram, yeast, pulses, groundnut, meat, fish, egg, vegetables. Being water soluble thiamin is readily lost on boiling and washing. It is also lost on prolonged storage. Deficiency of thiamin causes beriberi and Wernick’s encephalopathy. Beriberi is three types’ dry beriberi, wet beriberi, and infantile beriberi. Because of improved socio-economic status throughout the world beriberi is very rare nowadays.

Daily requirement of riboflavin is 0.6 mg per 1000 kcal of energy intake. Its sources are milk, egg yolk, liver, kidney, and green leafy vegetables. Germination increase riboflavin content of cereals. Deficiency causes angular stomatitis (ulceration and infection of angle of mouth), glossitis.

Niacin is essential for metabolism of carbohydrate, fat and protein. It is also essential for normal functioning of skin, intestine and nervous system. Daily requirement is 6.6 mg per 1000 kcal energy intake. Sources include liver, kidney, poultry, fish, legumes, and groundnut. Deficiency of niacin causes Pellagra. Symptoms of pellagra include diarrhea, dermatitis, dementia (forgetfulness). This condition is rare these days.

Pyridoxine deficiency is rare because our daily diet generally contain enough of it. Its daily requirement is 2 mg/day for adults and 2.5 mg/day for pregnancy and lactation. Sources include egg, milk, liver, meat, grain cereals, legumes, vegetables.

Sources of folic acid include green leafy vegetables, meat, liver, dairy products, egg, milk, fruits and cereals. Daily requirement is 100 mcg (micrograms) for adults, 400 mcg for pregnancy, and 150 mcg for lactation. Severe deficiency during pregnancy can cause congenital malformation. It can also cause infertility or even sterility. Body store of folic acid is small 5-10 mg, so folic acid deficiency develops very fast.

Vitamin B12 is available only in animal sources. So, pure vegetarians can develop B12 deficiency. B12 is required for formation of hemoglobin. B12 cooperate with folic acid in the synthesis of DNA. Sources include egg, milk, fish, meat, and kidney. It is also synthesized by bacteria in colon. Daily requirement is 1 mcg/day for adults and 1.5 mcg for pregnancy and lactation.

Vitamin C: vitamin C (ascorbic acid) is water soluble. It is the most heat sensitive of all vitamins. Vitamin C is antioxidant, and play important role in tissue oxidation. It is needed for formation of collagen, which provide supporting matrix to blood vessels, connective tissues, bones and cartilage. That’s why in vitamin C deficiency bones fracture easily and bleeding occurs, as seen in scurvy, a vitamin C deficiency disease. Main dietary sources are fresh fruits and green vegetables. Liver is rich source. Indian gooseberry is the richest source of vitamin C. daily requirement is about 60 mg/day.

Minerals:

Minerals which are required by the body are calcium, sodium, potassium, phosphorus, magnesium. Trace elements like zinc, copper, cobalt, chromium, selenium, molybdenum, nickel, tin, silicon, vanadium, manganese, iron, fluorine, are also required.

Calcium is required for the maintenance and development of bones. Daily requirement is about half gram. Deficiency may cause softening of bones. Sources include milk and milk products, cheese, egg, fish, meat. Cereals and vegetables also contain good amount of calcium.

Iron is very important trace element. The main function of iron is oxygen transport and cell respiration. Daily requirement of iron is 30 mgs. Women require more iron due to loss of iron in menstruation. Other minerals and trace elements are also very important in daily functioning of body.

It is required for synthesis of hemoglobin. Iron deficiency causes anemia. Iron is also required for brain development and its function, regulation of body temperature