Renal colic, the excruciating pain caused by a stone passing down the urinary tract is well known in all countries. The pain stops when the stone is passed naturally or removed by a surgeon. A patient may never have another attack or attacks may recur at irregular & sometimes long intervals. Most stones remain in the kidney where they often produce no symptom & are therefore known as SILENT STONES.
CHEMISTRY OF RENAL CALCULI:
Renal calculi are composed of different types of crystals however mostly renal stones are composed of Calcium Oxalate, Calcium Phosphate, Uric acid, Cystine & Magnesium Ammonium Phosphate crystals.
TYPES OF STONES:
1) CALCIUM STONES : Most of the stones are generally composed of Calcium Oxalate & Calcium Phosphate crystals but Calcium Oxalate stones are more common than Calcium Phosphate stones .The factors that promote the precipitation of Calcium Oxalate & Calcium Phosphate crystals in the urine are as follows ,
a) Hypercalciuria: Hypercalciuria is defied as a daily urinary excretion of calcium above 300 mg in men & 250 mg in women .Hypercalciuria is further classified as Idiopathic & Secondary Hypercalciuria. In Idiopathic hypercalciuria due to unknown reason there is increased intestinal absorption of calcium also there is decreased renal calcium reabsorption & there is increased bone resorption.
Hyperparathyroidism, Sarcoidosis, excessive production of vitamin D, immobilization, medullary sponge kidneys & excessive consumption of Calcium are some of the factors that are responsible for Secondary Hypercalciuria. Hypercalciuria is associated with an increased incidence of stone formation.
b) Hyperoxaluria: Refers to excess of Oxalate in urine .The greater part of the oxalate excreted in the urine is of endogenous origin & often comes from tissue metabolism of Glycine .Excessive intake of Vitamin C also causes hyperoxaluria .The commonest cause of hyperoxaluria is gastrointestinal malabsorption of dietary oxalates. Fatty acid malabsorption leads to calcium binding in the gut to produce calcium soaps of the fatty acids. This leaves the oxalate free & unbound to be absorbed. Enteric hyperoxaluria is exaggerated by a diet low in calcium.
C) Absence of stone forming inhibitors in urine: Substances which inhibit crystal growth are also present in urine. These include citrate, pyrophosphate, nephrocalin, glycosoaminoglycans. Absence of these inhibitors promotes stone formation.
2) URIC ACID STONES : About a quarter of patients with uric acid stones have hyperuricosuria with or without hyperuricemia & in most cases excessive dietary intake of Purine rich foods like liver , kidney sardines , brains etc causes hyperuricosuria . Uric acid is end product of Purine metabolism. Increased level of uric acid in urine causes decrease in pH of urine as a result urine becomes more acidic resulting in uric acid precipitation. Uric acid stones are also associated with acid/base metabolism disorders where the urine is excessively acidic.
3) CYSTINE STONES: Cystinuria is due to an inborn error of metabolism .The renal tubules fail to reabsorb the amino acids Cystine, Lysine, Arginine & Ornithine. These pass in large amounts in urine, where Cystine the least soluble amino acid tends to precipitate out & form stones.
4) STRUVITE STONES (Magnesium Ammonium Phosphate): Also known as infectious stones & Triple phosphate stones are formed due to bacteria Proteus mirabilis (but also Klebsiella, Serratia, and Providencia species) which split urea to ammonia with the help of urease as a result of which urine pH becomes alkaline & leading to stone formation.
5 ) XANTHINE STONES : Are composed of Xanthine
These stones are extremely uncommon and usually occur as a result of a rare genetic disorder.
DIETARY MANAGEMENT:
Depends upon the type of stone & conditions that are responsible for stone formation.
1) Calcium Oxalate Stones :
Particular emphasis should be directed at the calcium & oxalate content of the diet as an excess of both these nutrients has been associated with the formation of stones. If the stones formation is due to hypercalciuria than a diet low in calcium should be taken also a high fiber diet should be encouraged to reduce calcium absorption. Antacids containing calcium should be avoided .Protein & Sodium intake should not be in excess as both increases urinary excretion of calcium.
If the stone formation is due to hyperoxalicuria than a diet high in calcium should be encouraged as calcium will form insoluble complexes with oxalic acid in gut & it will be excreted out of the body in the stools .Also foods rich in Oxalic acid should be avoided
OXALIC ACID CONTENT OF SOME FOODS
1) CEREAL – BAJRA -21mgs/100 gms
2) PULSE - HORSE GRAM – 417mgs / 100 gms
3) LEAFY VEGETABLES –AMARANTH -772 mgs / 100 gms
- SPINACH – 658 mgs / 100 gms
- RHUBARB –is also rich source of Oxalic acid
4) OTHER VEGETABLES - DRUMSTICKS -101mgs /100 gms
5) NUTS – ALMOND – 407 mgs / 100 gms
6) FRUITS – AMLA – 296 mgs /100 gms
Excessive intake of Vitamin C should be avoided as Vitamin C is metabolized & oxalic acid is formed. Fat mal absorption should be treated in order to prevent formation fatty acid & calcium soaps in intestine. Excessive intake of proteins & sodium should be prevented as both increases urinary excretion of calcium & in turn promotes calcium binding with oxalic acid in urine. The intake of water should be increased around 3000 ml of fluid should be taken daily. Stone inhibitors like citrates should be taken to prevent stone formation in urine.
2) Uric acid stones:
Excessive intake of purine rich foods like liver, brain, Sardine etc should be avoided. Also water consumption should be increased & alcohol intake should be restricted. Generally an ALKALINE ASH DIET is recommended since it will help in reducing the acidity of urine by increasing the pH of urine.
An Alkaline Ash Diet consists mainly of fruits , vegetables & milk with little meat , fish , eggs , cheese & cereals , that when catabolized leaves an alkaline residue to be excreted by urine .Alkaline Ash diet includes mostly all vegetables .Among fruits lemon , lime , watermelon , grape fruit , tomato , Avocado etc.
3) Struvite stones :
In case of Struvite stones water should be taken in excess also antibacterial medicines should be taken to destroy bacteria in urine & an ACID ASH DIET is recommended.
An Acid Ash Diet is a diet which mainly comprises of meat, fish, eggs & cereals & consist of no or minimal amounts of fruits, vegetables & milk & it gives acid residue to be excreted in urine when catabolized in the body . Acid Ash diet will make the urine acidic & there by prevent stones formation
Friday, February 13, 2009
Wednesday, February 4, 2009
CORTICOSTEROIDS & ADRENAL DIABETES
The Adrenal Glands are composed of two distinct parts, the adrenal medulla & the adrenal cortex. The Adrenal medulla secretes two hormones EPINEPHRINE & NOREPINEPHRINE in response to sympathetic stimulation. The Adrenal cortex secretes an entirely different group of hormones called CORTICOSTEROIDS .There are two types of Corticosteroids 1) MINERALOCORTICOIDS & 2) GLUCOCORTICOIDS .Both , Glucocorticoids & Mineralocorticoids are steroid compounds
MINERALOCORTICOIDS: The Mineralocorticoids have gained this name because they especially affect electrolytes of the extra cellular fluids (SODIUM & POTASSIUM) .Below are names of some important mineralocorticoids
1) Aldosterone: It is very potent & accounts for 95% or more of Mineralocorticoid activity .It is secreted by ZONA GLOMERULOSA which is the outer most layer of Adrenal cortex.
2) Desoxycorticosterone: Is 1/15th as potent as Aldosterone & secreted in very small quantities.
3) Corticosterone : Has very slight activity
4) 9alpha –Flurocortisol: It is synthetic & has slightly more potent than Aldosterone.
5) Cortisol: Has very slight mineralocorticoid activity.
6) Cortisone: Is synthetic & has very slight activity.
GLUCOCORTICOIDS: The Glucocoricoids have gained their name because they exhibit an important effect in increasing blood Glucose concentration. They also affect Protein & fat metabolism. Below are names of some important glucocorticoids
1) Cortisol: Very potent & accounts for about 95% of all
Glucocorticoid activity .It is secreted by The ZONA FASCICULATA which is the middle layer of Adrenal cortex & the deepest layer – ZONA RETICULARIS.
2) Corticosterone: About 4 % of total glucocorticoid activity but much less potent than Cortisol.
3) Cortisone: Synthetic but as potent as Cortisol.
4) Prednisone: Synthetic but 4 times as potent as Cortisol.
5) Methylprednisone: Synthetic but 5 times as potent as Cortisol.
6) Dexamethasone: Synthetic but 30 times as potent as Cortisol.
**** It is clear from the above list that some of these hormones have both Glucocorticoid & Mineralocorticoid activities.
The level of Cortisol needs to be just right. Too much or too little can cause problems. The amount of Cortisol which is made in the adrenal glands is controlled by another hormone called Adreno-cortico-trophic hormone, or ACTH for short (and sometimes just called Corticotrophin). ACTH is made in the pituitary gland.
The pituitary gland lies just below the brain. It makes several hormones, including ACTH. The amount of ACTH made by the pituitary gland is largely controlled by another hormone called Corticotrophin releasing hormone (CRH). CRH is made in a small part of the brain called the hypothalamus, which is just above the pituitary gland. CRH 'stimulates' certain cells in the pituitary to make ACTH.
ACTH passes into the bloodstream, is carried to the adrenal glands, and 'stimulates' the adrenal gland to make Cortisol. If the level of ACTH increases in the bloodstream, the adrenals make more cortisol.But, Cortisol has a negative 'feedback' effect on the pituitary gland. As the level of Cortisol in the bloodstream rises above a certain level, it 'turns down' the amount of ACTH made by the pituitary. This means the adrenal is then stimulated less, and less Cortisol is made. So, the level of Cortisol is kept within a certain range - just enough as is needed by the body.
MAJOR FUNCTION OF GLUCOCORTICOIDS :
By far the best known metabolic effect of Cortisol & other glucocorticoids on metabolism is their ability to stimulate Gluconeogenesis ( a metabolic process in which glucose is formed from non-carbohydrate carbon substrates such as lactate , glycerol , and glucogenic amino acids by the liver ) . Cortisol often increases the rate of gluconeogenisis as much as six to ten folds. Cortisol causes gluconeogenesis by increasing all the enzymes in the liver cell which are required to convert amino acids to glucose. Also Cortisol causes mobilization of amino acids from the extra hepatic tissues ( mainly muscles ) .As a result more amino acids become available in the plasma to enter into the gluconeogenisis process of the liver & thereby to promote the formation of glucose .Not only this Cortisol causes a moderate decrease in the rate of glucose utilization by the cells every where in the body .
ADRENAL DIABETES:
Excessive production of Cortisol leads to ADRENAL DIABETES Adrenal Diabetes has many similarities with Pancreatic Diabetes. In Adrenal Diabetes the blood Glucose concentration is 50 % or more above normal levels. Administration of Insulin lowers the blood glucose concentration only to a moderate amount .Therefore it said that Adrenal Diabetes is moderately sensitive to Insulin.
CAUSES OF EXCESSIVE PRODUCTION OF CORTISOL:
1) Non Cancerous tumor of Pituitary Gland (Pituitary Adenoma). In this condition the Pituitary gland produces more ACTH (CORTICOTROPHIN) which stimulates the Adrenal gland to produce more Cortisol & the abnormal cells in the adenoma are not 'turned down' by feedback from the high levels of cortisol.
2) Non Cancerous or malignant tumor of Adrenal gland causes excessive production of Cortisol.
3) Hyperplasia of Adrenal gland also leads to more production of Cortisol.
4) Some malignant & non cancerous tumors in other parts of body sometimes cause excessive production of Cortisol by producing ectopic ACTH. ACTH is a hormone which stimulates the Adrenal glands to produce Cortisol. Normally ACTH is produced by Pituitary gland. However some rare tumors like that of Lung cancer produce ectopic ACTH which stimulates the Adrenals to produce Cortisol
5) Excessive intake of Alcohol also increases Cortisol levels.
6) Depression is also responsible for higher production of Cortisol.
TREATMENT:
Depends upon the cause of excessive production of Cortisol. If it is due to excessive intake of Alcohol than avoidance of alcohol will cure Adrenal diabetes. If it is due to tumor of Pituitary or Adrenal gland or other part of body than removal of tumor will cure the Diabetes.
MINERALOCORTICOIDS: The Mineralocorticoids have gained this name because they especially affect electrolytes of the extra cellular fluids (SODIUM & POTASSIUM) .Below are names of some important mineralocorticoids
1) Aldosterone: It is very potent & accounts for 95% or more of Mineralocorticoid activity .It is secreted by ZONA GLOMERULOSA which is the outer most layer of Adrenal cortex.
2) Desoxycorticosterone: Is 1/15th as potent as Aldosterone & secreted in very small quantities.
3) Corticosterone : Has very slight activity
4) 9alpha –Flurocortisol: It is synthetic & has slightly more potent than Aldosterone.
5) Cortisol: Has very slight mineralocorticoid activity.
6) Cortisone: Is synthetic & has very slight activity.
GLUCOCORTICOIDS: The Glucocoricoids have gained their name because they exhibit an important effect in increasing blood Glucose concentration. They also affect Protein & fat metabolism. Below are names of some important glucocorticoids
1) Cortisol: Very potent & accounts for about 95% of all
Glucocorticoid activity .It is secreted by The ZONA FASCICULATA which is the middle layer of Adrenal cortex & the deepest layer – ZONA RETICULARIS.
2) Corticosterone: About 4 % of total glucocorticoid activity but much less potent than Cortisol.
3) Cortisone: Synthetic but as potent as Cortisol.
4) Prednisone: Synthetic but 4 times as potent as Cortisol.
5) Methylprednisone: Synthetic but 5 times as potent as Cortisol.
6) Dexamethasone: Synthetic but 30 times as potent as Cortisol.
**** It is clear from the above list that some of these hormones have both Glucocorticoid & Mineralocorticoid activities.
The level of Cortisol needs to be just right. Too much or too little can cause problems. The amount of Cortisol which is made in the adrenal glands is controlled by another hormone called Adreno-cortico-trophic hormone, or ACTH for short (and sometimes just called Corticotrophin). ACTH is made in the pituitary gland.
The pituitary gland lies just below the brain. It makes several hormones, including ACTH. The amount of ACTH made by the pituitary gland is largely controlled by another hormone called Corticotrophin releasing hormone (CRH). CRH is made in a small part of the brain called the hypothalamus, which is just above the pituitary gland. CRH 'stimulates' certain cells in the pituitary to make ACTH.
ACTH passes into the bloodstream, is carried to the adrenal glands, and 'stimulates' the adrenal gland to make Cortisol. If the level of ACTH increases in the bloodstream, the adrenals make more cortisol.But, Cortisol has a negative 'feedback' effect on the pituitary gland. As the level of Cortisol in the bloodstream rises above a certain level, it 'turns down' the amount of ACTH made by the pituitary. This means the adrenal is then stimulated less, and less Cortisol is made. So, the level of Cortisol is kept within a certain range - just enough as is needed by the body.
MAJOR FUNCTION OF GLUCOCORTICOIDS :
By far the best known metabolic effect of Cortisol & other glucocorticoids on metabolism is their ability to stimulate Gluconeogenesis ( a metabolic process in which glucose is formed from non-carbohydrate carbon substrates such as lactate , glycerol , and glucogenic amino acids by the liver ) . Cortisol often increases the rate of gluconeogenisis as much as six to ten folds. Cortisol causes gluconeogenesis by increasing all the enzymes in the liver cell which are required to convert amino acids to glucose. Also Cortisol causes mobilization of amino acids from the extra hepatic tissues ( mainly muscles ) .As a result more amino acids become available in the plasma to enter into the gluconeogenisis process of the liver & thereby to promote the formation of glucose .Not only this Cortisol causes a moderate decrease in the rate of glucose utilization by the cells every where in the body .
ADRENAL DIABETES:
Excessive production of Cortisol leads to ADRENAL DIABETES Adrenal Diabetes has many similarities with Pancreatic Diabetes. In Adrenal Diabetes the blood Glucose concentration is 50 % or more above normal levels. Administration of Insulin lowers the blood glucose concentration only to a moderate amount .Therefore it said that Adrenal Diabetes is moderately sensitive to Insulin.
CAUSES OF EXCESSIVE PRODUCTION OF CORTISOL:
1) Non Cancerous tumor of Pituitary Gland (Pituitary Adenoma). In this condition the Pituitary gland produces more ACTH (CORTICOTROPHIN) which stimulates the Adrenal gland to produce more Cortisol & the abnormal cells in the adenoma are not 'turned down' by feedback from the high levels of cortisol.
2) Non Cancerous or malignant tumor of Adrenal gland causes excessive production of Cortisol.
3) Hyperplasia of Adrenal gland also leads to more production of Cortisol.
4) Some malignant & non cancerous tumors in other parts of body sometimes cause excessive production of Cortisol by producing ectopic ACTH. ACTH is a hormone which stimulates the Adrenal glands to produce Cortisol. Normally ACTH is produced by Pituitary gland. However some rare tumors like that of Lung cancer produce ectopic ACTH which stimulates the Adrenals to produce Cortisol
5) Excessive intake of Alcohol also increases Cortisol levels.
6) Depression is also responsible for higher production of Cortisol.
TREATMENT:
Depends upon the cause of excessive production of Cortisol. If it is due to excessive intake of Alcohol than avoidance of alcohol will cure Adrenal diabetes. If it is due to tumor of Pituitary or Adrenal gland or other part of body than removal of tumor will cure the Diabetes.
Wednesday, January 14, 2009
PERNICIOUS ANEMIA & IT'S NON MEDICO TREATMENT
Pernicious anemia is a macrocytic (larger than normal RBC) and megaloblastic (immature, abnormal RBC progenitors in the bone marrow) anemia. Pernicious anemia is caused by a deficiency of vitamin B12 (Cobalamin). Generally, vitamin B12 deficiency occurs due to lack of Intrinsic Factor –IF. Intrinsic Factor is a glycoprotein in the gastric juice that is necessary for the absorption of dietary Vitamin B12. It is very rare that B12 deficiency occurs due to lack of dietary intake because of it is wide spread occurrence in all animal foods and synthesis by intestinal flora.
Intrinsic Factor is secreted by parietal cells of gastric glands. It helps in the absorption of B12 by binding it tightly. In the bound state the B12 is protected from digestion by the gastrointestinal enzymes. In the bound state the Intrinsic Factor binds to specific receptor sites on the brush border membranes of the mucosal cells in the Ileum. Finally B12 is transported in to the blood by the process of pinocytosis carrying the Intrinsic factor and the vitamin B12 together through the membrane.
Once B12 has been absorbed from the gastrointestinal tract it is stored in large quantities in the liver & then released slowly as needed to the bone marrow and other tissues of the body .The total amount of vitamin B12 required each day to maintain normal red cells maturation is about 5 micrograms and the normal store in the liver and other body tissues is about 1000 times this amount . Therefore as many as 4 to 5 years of defective B12 absorption are required to cause Pernicious anemia.
Deficiency of vitamin B12 can result in a deficiency of Folic Acid by causing the entrapment of Folate as 5-methyltetrahydrofolate. The methyl group of 5-methyltetrahydrofolate is transferred to Cobalamin (B12) to form Methyl Cobalamine and the folate is returned to the folate pool to further take part in one carbon transfer reactions . In case of deficiency of B12 folate remain trapped with the methyl group it’s further functioning is impaired.
Due to B12 & folic acid inter related roles in the protein synthesis a deficiency of either B12 or Folic Acid will result in megaloblastic anemia. However in B12 deficiency there is an impairment of microbicidal activity of leukocytes .The function of leukocytes is not impaired in Folic acid deficiency. Also due to B12 deficiency gastrointestinal tract, peripheral & nervous system are also affected .Numbness & tingling in the hands & feet, poor muscular coordination, poor memory & hallucinations are some symptoms of B12 deficiency. If the deficiency continues long enough, the nervous system damage may be irreversible even with treatment.
Nutritional Care in Pernicious Anemia:
A high protein diet (1.5 Gm/Kg of body weight) is desirable. Green leafy vegetables should be included in diet. In non vegetarian food items, liver is the richest source of vitamin B12 so it should be included in diet. Beef and pork, eggs, milk and milk products are good sources of vitamin B12, although the cholesterol content should be considered.
Intrinsic Factor is secreted by parietal cells of gastric glands. It helps in the absorption of B12 by binding it tightly. In the bound state the B12 is protected from digestion by the gastrointestinal enzymes. In the bound state the Intrinsic Factor binds to specific receptor sites on the brush border membranes of the mucosal cells in the Ileum. Finally B12 is transported in to the blood by the process of pinocytosis carrying the Intrinsic factor and the vitamin B12 together through the membrane.
Once B12 has been absorbed from the gastrointestinal tract it is stored in large quantities in the liver & then released slowly as needed to the bone marrow and other tissues of the body .The total amount of vitamin B12 required each day to maintain normal red cells maturation is about 5 micrograms and the normal store in the liver and other body tissues is about 1000 times this amount . Therefore as many as 4 to 5 years of defective B12 absorption are required to cause Pernicious anemia.
Deficiency of vitamin B12 can result in a deficiency of Folic Acid by causing the entrapment of Folate as 5-methyltetrahydrofolate. The methyl group of 5-methyltetrahydrofolate is transferred to Cobalamin (B12) to form Methyl Cobalamine and the folate is returned to the folate pool to further take part in one carbon transfer reactions . In case of deficiency of B12 folate remain trapped with the methyl group it’s further functioning is impaired.
Due to B12 & folic acid inter related roles in the protein synthesis a deficiency of either B12 or Folic Acid will result in megaloblastic anemia. However in B12 deficiency there is an impairment of microbicidal activity of leukocytes .The function of leukocytes is not impaired in Folic acid deficiency. Also due to B12 deficiency gastrointestinal tract, peripheral & nervous system are also affected .Numbness & tingling in the hands & feet, poor muscular coordination, poor memory & hallucinations are some symptoms of B12 deficiency. If the deficiency continues long enough, the nervous system damage may be irreversible even with treatment.
Nutritional Care in Pernicious Anemia:
A high protein diet (1.5 Gm/Kg of body weight) is desirable. Green leafy vegetables should be included in diet. In non vegetarian food items, liver is the richest source of vitamin B12 so it should be included in diet. Beef and pork, eggs, milk and milk products are good sources of vitamin B12, although the cholesterol content should be considered.
Monday, December 8, 2008
LIVER CIRRHOSIS & IT'S NUTRITIONAL CARE
Cirrhosis is the final stage of liver injury and degeneration. It occurs in 15 % of heavy drinkers. Other causes of liver cirrhosis are drug or chemical poisoning, hepatitis B virus, cystic fibrosis, etc. Cirrhosis is characterized by liver necrosis meaning the normal liver tissue is gradually destroyed and replaced by inactive fibrous connective tissue (scar tissue).
NUTRITIONAL MANAGEMENT:
Energy Requirements: Due to extreme weight loss in cirrhosis, energy requirements are increased. A diet with 25-35 Kcal/Kg IBW (Ideal Body Weight) per day is recommended. Small and frequent meals should be given.
Carbohydrate Requirements: The carbohydrate content of the diet should be high in order to provide sufficient calories so that protein is not utilized for energy. Also, the liver may store glycogen. Liver function improves when an adequate store of glycogen is present in hepatocytes (liver cells). Simple carbohydrates should be given, i.e., sugars, fruits juices, Sago, Arrowroot products, etc. About 65-70 % of total calories should be provided by carbohydrates.
Protein Requirements: A liberal protein intake is essential for the repair of hepatic cells. The serum albumin which is exclusively synthesized by the liver cells falls down in cirrhosis as a result of which there is water retention. So, in order to maintain serum levels of albumin, it is necessary to take protein. In case of absence of Hepatic Coma (a condition in which ammonia levels increases leading to brain tissue damage), 1.2 -1.5 gms per kg present body weight can be given. Both animal and plant protein can be given. Vegetable and dairy proteins are better tolerated because of their lower content of Aromatic Amino Acids (Methionine and Glutamine) and higher content of Branched chain Amino Acids (Valine, Leucine, and Isoleucine). If protein requirements cannot be met by diet alone, then protein supplements can also be given. However, if cirrhosis progresses to Hepatic Coma, then protein has to be totally restricted.
Fat Requirements: Cirrhosis is marked by impaired fat metabolism and absorption. Triglycerides which contain Medium Chain Fatty Acids (8-10 CARBON FATTY ACIDS) like Ghee, Butter, etc. can be given. These triglycerides do not require bile for their digestion and absorption. This will help to prevent steatorrhea (fatty stools). As the condition improves, large chain triglycerides can be given to avoid deficiency of essential fatty acids.
Vitamin Requirements: All of the vitamin should be supplied in abundance to fortify the liver against stress and to repair the damage. Since the liver is involved in the synthesis of active forms of any B-complex vitamin and due to lack of proper function, it is advisable to give B-complex vitamin supplements. In the presence of steatorrhea, water soluble forms of vitamin A, D, E, and K should be given. In severe cirrhosis with problems of vitamin storage, metabolism, and transport intramuscular injections of Vitamin A, D, E, and K may be necessary.
Mineral Requirements: Iron intake should be increased to prevent anemia because the liver is unable to store iron in the form of Ferritin. Iron supplements can be given. However, simultaneous increase of vitamin C is also required. Calcium intake should also be increased. Iron intake can be increased by following measures:
* Increase the intake of Green leafy vegetables like Spinach, Mint, Methi, Amaranth etc.
* Also, increase the intake of vitamin C. So, consume lots of fresh fruits like Guava, Sweet Lime, Oranges, Aavla, etc.
* Consume raw freshly sprouted pulses. It can be consumed with salads too.
* Consume Ragi (Nachni), soya bean flours. They can be mixed with wheat flour and chapatis can be made out of it.
* Consume Rice flakes (Poha) as they are good source of iron.
* Use jaggery instead of sugar, as jaggery is a good source of iron.
* Soak 2-3 dates in water at night and then in the morning, consume it with milk or with water.
Sodium and Potassium Requirements: Sodium restriction is prescribed if edema (fluid retention in body) is present. Sodium is restricted to 2 gm per day. At the same time, potassium intake is increased. Some potassium-rich foods are coconut water, water obtained after boiling Moong Dal, Amla, Guava, Sapota, Papaya, Sweet lime, Peaches, Phalsa, Plums, and Gourd vegetables like Lauki, Karela, Turai, etc.
In order to make food palatable even with less salt one should make use of pepper powder, lemon juice, etc. Also, avoid food items like Jam, Canned fruits, Sauces, Pickles, Papads, Salted biscuits, Salted dry fruits, Cheese, Butter, Potato chips, and fruits like Lichi, Pineapple. Due to restriction of salt, the food becomes less palatable and therefore the patient becomes irritable. However, we can make food palatable if we follow the following tips:
* Make the food look attractive, so garnish well. Can use coriander leaves, tomato slices, onions, etc. Use Ratanjot for natural red color. Ratanjot is a herb which gives bright red color. Make vagaar with Ratanjot, it will give bright red color to food. Can add Ratanjot in Dal, sabzi, pulav, etc.
* Always serve food hot. When food is consumed hot, one does not feel that there is less salt in food. So, serve soups, dal, sabzi hot and ask the patient to consume it hot only.
* Squeeze lemon juice from top just before serving food. This will curb the need of salt in food.
* Add jeera powder and/or black pepper and/or mango powder to food. This will make food tasty even with less salt.
* Serve food in attractive vessels.
Fluid Requirement: In case of edema, fluid restriction is necessary. Total fluid intake equals to urinary output + 500 ml per day .
Alcohol Intake: Alcohol intake should be completely restricted. Even a single drop can be deadly.
NUTRITIONAL MANAGEMENT:
Energy Requirements: Due to extreme weight loss in cirrhosis, energy requirements are increased. A diet with 25-35 Kcal/Kg IBW (Ideal Body Weight) per day is recommended. Small and frequent meals should be given.
Carbohydrate Requirements: The carbohydrate content of the diet should be high in order to provide sufficient calories so that protein is not utilized for energy. Also, the liver may store glycogen. Liver function improves when an adequate store of glycogen is present in hepatocytes (liver cells). Simple carbohydrates should be given, i.e., sugars, fruits juices, Sago, Arrowroot products, etc. About 65-70 % of total calories should be provided by carbohydrates.
Protein Requirements: A liberal protein intake is essential for the repair of hepatic cells. The serum albumin which is exclusively synthesized by the liver cells falls down in cirrhosis as a result of which there is water retention. So, in order to maintain serum levels of albumin, it is necessary to take protein. In case of absence of Hepatic Coma (a condition in which ammonia levels increases leading to brain tissue damage), 1.2 -1.5 gms per kg present body weight can be given. Both animal and plant protein can be given. Vegetable and dairy proteins are better tolerated because of their lower content of Aromatic Amino Acids (Methionine and Glutamine) and higher content of Branched chain Amino Acids (Valine, Leucine, and Isoleucine). If protein requirements cannot be met by diet alone, then protein supplements can also be given. However, if cirrhosis progresses to Hepatic Coma, then protein has to be totally restricted.
Fat Requirements: Cirrhosis is marked by impaired fat metabolism and absorption. Triglycerides which contain Medium Chain Fatty Acids (8-10 CARBON FATTY ACIDS) like Ghee, Butter, etc. can be given. These triglycerides do not require bile for their digestion and absorption. This will help to prevent steatorrhea (fatty stools). As the condition improves, large chain triglycerides can be given to avoid deficiency of essential fatty acids.
Vitamin Requirements: All of the vitamin should be supplied in abundance to fortify the liver against stress and to repair the damage. Since the liver is involved in the synthesis of active forms of any B-complex vitamin and due to lack of proper function, it is advisable to give B-complex vitamin supplements. In the presence of steatorrhea, water soluble forms of vitamin A, D, E, and K should be given. In severe cirrhosis with problems of vitamin storage, metabolism, and transport intramuscular injections of Vitamin A, D, E, and K may be necessary.
Mineral Requirements: Iron intake should be increased to prevent anemia because the liver is unable to store iron in the form of Ferritin. Iron supplements can be given. However, simultaneous increase of vitamin C is also required. Calcium intake should also be increased. Iron intake can be increased by following measures:
* Increase the intake of Green leafy vegetables like Spinach, Mint, Methi, Amaranth etc.
* Also, increase the intake of vitamin C. So, consume lots of fresh fruits like Guava, Sweet Lime, Oranges, Aavla, etc.
* Consume raw freshly sprouted pulses. It can be consumed with salads too.
* Consume Ragi (Nachni), soya bean flours. They can be mixed with wheat flour and chapatis can be made out of it.
* Consume Rice flakes (Poha) as they are good source of iron.
* Use jaggery instead of sugar, as jaggery is a good source of iron.
* Soak 2-3 dates in water at night and then in the morning, consume it with milk or with water.
Sodium and Potassium Requirements: Sodium restriction is prescribed if edema (fluid retention in body) is present. Sodium is restricted to 2 gm per day. At the same time, potassium intake is increased. Some potassium-rich foods are coconut water, water obtained after boiling Moong Dal, Amla, Guava, Sapota, Papaya, Sweet lime, Peaches, Phalsa, Plums, and Gourd vegetables like Lauki, Karela, Turai, etc.
In order to make food palatable even with less salt one should make use of pepper powder, lemon juice, etc. Also, avoid food items like Jam, Canned fruits, Sauces, Pickles, Papads, Salted biscuits, Salted dry fruits, Cheese, Butter, Potato chips, and fruits like Lichi, Pineapple. Due to restriction of salt, the food becomes less palatable and therefore the patient becomes irritable. However, we can make food palatable if we follow the following tips:
* Make the food look attractive, so garnish well. Can use coriander leaves, tomato slices, onions, etc. Use Ratanjot for natural red color. Ratanjot is a herb which gives bright red color. Make vagaar with Ratanjot, it will give bright red color to food. Can add Ratanjot in Dal, sabzi, pulav, etc.
* Always serve food hot. When food is consumed hot, one does not feel that there is less salt in food. So, serve soups, dal, sabzi hot and ask the patient to consume it hot only.
* Squeeze lemon juice from top just before serving food. This will curb the need of salt in food.
* Add jeera powder and/or black pepper and/or mango powder to food. This will make food tasty even with less salt.
* Serve food in attractive vessels.
Fluid Requirement: In case of edema, fluid restriction is necessary. Total fluid intake equals to urinary output + 500 ml per day .
Alcohol Intake: Alcohol intake should be completely restricted. Even a single drop can be deadly.
Friday, November 28, 2008
TIPS FOR INCREASING NUTRITIVE VALUE OF FOOD
1) Always consume fresh fruits & vegetables only .
2) First wash & than cut the vegetables or fruits , never wash the food item after cutting .
4) Always cut vegetables in to larger pieces to avoid more nutrient loss during cooking . This is because lesser the surface area exposed to heat lesser will be the nutrient loss .
6) When cooking vegetables in Kadai always cover it with lid .
8) Never discard the water obtained after boiling vegetables as that water is rich in nutrients ( USE THAT WATER TO PREPARE DAL OR KNEED DOUGH )
10) If vegetables are to be boiled than first boil the water & than immerse the vegetable in order to reduce the exposure time of nutrients to heat & there by reduce the nutrient destruction by heat .
Sunday, November 23, 2008
LATHYRISM
Lathyrism is a disease caused by excessive consumption of KESARI DAL . LATHYRISM gets it name from the scientific name of kesari dal which is LATHYRUS SATIVUS .Kesari dal is consumed in excess in many parts of Madhya Pradesh , Bihar & Uttar Pradesh . It is staple food in the above mentioned areas because it grows easily with minimum effort & it is comparatively cheaper than other pulses.
Excessive consumption of Kesari dal causes crippling paralysis of both the lower limbs( lathyrism ) mainly in boys & men of the age group 5-45 yers. It has been estimated that if 40 % or more of the diet consists of Kesari dal LATHYRISM manifest itself in 2-4 months . The disease starts with stiffness of the knee joint & legs with pain around the knee & ankle joints . In about 10-30 days after the onset of the symptoms paralysis of lower limbs set in
According to scientists B.O.A.A. a toxic amino acid present in the pulse is responsible for LATHYRISM . This amino acid is not found in other pulses . Till date there is no cure for Lathyrism however lathyrism can be prevented by undertaking following measures.
1) CONSUMING KESARI DAL ONLY AFTER STEEPING FOR 2-3 IN HOT WATER OR PARBOILING & DRAINING AWAY TE WATER. IN PARBOILING THE DAL IS SOAKED IN 70o C WATER FOR 3-4 HOURS & THAN STEAMING IT FOR 3-5 MINUTES . THE WATER IS THAN DISCARDED . BY THIS PROCEDURE B.O.A.A IS REMOVED .
2) NOT CONSUMING THE DAL IN LARGE QUANTITIES AT ANY TIME.
Excessive consumption of Kesari dal causes crippling paralysis of both the lower limbs( lathyrism ) mainly in boys & men of the age group 5-45 yers. It has been estimated that if 40 % or more of the diet consists of Kesari dal LATHYRISM manifest itself in 2-4 months . The disease starts with stiffness of the knee joint & legs with pain around the knee & ankle joints . In about 10-30 days after the onset of the symptoms paralysis of lower limbs set in
According to scientists B.O.A.A. a toxic amino acid present in the pulse is responsible for LATHYRISM . This amino acid is not found in other pulses . Till date there is no cure for Lathyrism however lathyrism can be prevented by undertaking following measures.
1) CONSUMING KESARI DAL ONLY AFTER STEEPING FOR 2-3 IN HOT WATER OR PARBOILING & DRAINING AWAY TE WATER. IN PARBOILING THE DAL IS SOAKED IN 70o C WATER FOR 3-4 HOURS & THAN STEAMING IT FOR 3-5 MINUTES . THE WATER IS THAN DISCARDED . BY THIS PROCEDURE B.O.A.A IS REMOVED .
2) NOT CONSUMING THE DAL IN LARGE QUANTITIES AT ANY TIME.
GINGIVITIS
Gingivitis means inflammation of the gums. It is a manifested as change in color, enlargement, bleeding, puffiness, ulceration.
CAUSES FOR GINGIVITIS:
1)The most common cause is the accumulation of TARTAR (Calculus) is the scaly yellowish or brownish hard chalk like substance that forms at the gum margins around the teeth. This tartar irritates & pushes the gums away from the teeth & causes gingivitis. Tartar contains calcium, magnesium, bacteria & fungus. As a result there is bad smell in mouth. .Hence Tartar should be removed often by the procedure called SCALING by the dentist.
2) Poor oral hygiene is also responsible for gingivitis. Owing to improper or inadequate brushing the teeth, gums become soft & lose their resistance to infection.
3) Those who have the habit of breathing through the mouth keep the lips apart when the air strikes on the gums. The dryness & the absence of the toning effect of Saliva give rise to chronic gingivitis.
4) Pregnancy alters the hormonal balance of women & their gums are prone to enlargement & bleeding which is aggravated by the presence of tartar.
5) A number of skin diseases & general diseases including Syphilis & TB manifest themselves in the inflammation of the gums.
6) Anti –Epileptic drugs causes enlargement of the gingival.
7) Leukemia reflects itself prominently in the mouth. Sometimes the bleeding, enlarged gingival is the first evidence of cancer.
8) Vitamin C deficiency predisposes to reddened, bleeding, enlarged & spongy gums.
NON MEDICAL TREATMENT:
1) Proper oral hygiene.
2) Consume lot of fresh fruits & vegetable especially Vitamin C rich fruits like Guava , plum , peaches , oranges , Aavla , sprouted cereals & grains .
3) Drink plenty of water & do not breathe through mouth.
CAUSES FOR GINGIVITIS:
1)The most common cause is the accumulation of TARTAR (Calculus) is the scaly yellowish or brownish hard chalk like substance that forms at the gum margins around the teeth. This tartar irritates & pushes the gums away from the teeth & causes gingivitis. Tartar contains calcium, magnesium, bacteria & fungus. As a result there is bad smell in mouth. .Hence Tartar should be removed often by the procedure called SCALING by the dentist.
2) Poor oral hygiene is also responsible for gingivitis. Owing to improper or inadequate brushing the teeth, gums become soft & lose their resistance to infection.
3) Those who have the habit of breathing through the mouth keep the lips apart when the air strikes on the gums. The dryness & the absence of the toning effect of Saliva give rise to chronic gingivitis.
4) Pregnancy alters the hormonal balance of women & their gums are prone to enlargement & bleeding which is aggravated by the presence of tartar.
5) A number of skin diseases & general diseases including Syphilis & TB manifest themselves in the inflammation of the gums.
6) Anti –Epileptic drugs causes enlargement of the gingival.
7) Leukemia reflects itself prominently in the mouth. Sometimes the bleeding, enlarged gingival is the first evidence of cancer.
8) Vitamin C deficiency predisposes to reddened, bleeding, enlarged & spongy gums.
NON MEDICAL TREATMENT:
1) Proper oral hygiene.
2) Consume lot of fresh fruits & vegetable especially Vitamin C rich fruits like Guava , plum , peaches , oranges , Aavla , sprouted cereals & grains .
3) Drink plenty of water & do not breathe through mouth.
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