Changes

''Kanthasya-shosah'' (dryness of mouth also known as xerostomia) occurs due to diminish salivary gland secretion.  

''Kanthasya-shosah'' (dryness of mouth also known as xerostomia) occurs due to diminish salivary gland secretion.  

Primary cause being fluid loss through diarrhea secondarily it may be association of Sjogrens syndrome with autoimmune disease like primary biliary cirrhosis ~ a secondary Sjogrens syndrome. In this syndrome involvement of other exocrine glands occur leading to diminished secretion of exocrine glands of the gastrointestinal tract, leading to esophageal mucosal atrophy, atrophic gastritis and subclinical pancreatitis.   

Primary cause being fluid loss through diarrhea secondarily it may be association of Sjogren's syndrome with autoimmune disease like primary biliary cirrhosis ~ a secondary Sjogrens syndrome. In this syndrome involvement of other exocrine glands occur leading to diminished secretion of exocrine glands of the gastrointestinal tract, leading to esophageal mucosal atrophy, atrophic gastritis and subclinical pancreatitis.   

Increased appetite (''Kshudha'') is seen because of a negative feedback due to malabsorption or it may be understood under ''rasasheshajeerna''.  

Increased appetite (''Kshudha'') is seen because of a negative feedback due to malabsorption or it may be understood under ''rasasheshajeerna''.  

Antigenic nature of endogenous factors can be understood when helpful bacteria and ''ushna, teekshna guna'' of ''kapha'' trigger inflammatory response leading to autoimmune pathogenesis.

Antigenic nature of endogenous factors can be understood when helpful bacteria and ''ushna, teekshna guna'' of ''kapha'' trigger inflammatory response leading to autoimmune pathogenesis.

In case of hypersecretion of gastrin in gastrinoma [Zollingers – Ellison Syndrome] stimulate the parietal cells of the stomach to secrete acid to their maximal capacity and increase the parietal cell mass three to six fold. The acid output may be so great that it reaches the upper small intestine reducing the luminal pH to 2 or less.

In case of hypersecretion of gastrin in gastrinoma (Zollingers – Ellison Syndrome) stimulate the parietal cells of the stomach to secrete acid to their maximal capacity and increase the parietal cell mass three to six fold. The acid output may be so great that it reaches the upper small intestine reducing the luminal pH to 2 or less.

Pancreatic lipase is inactivated and bile acids are precipitated. It results in diarrhea and steatorrhea. Subtotal villous atrophy occurs due to hyper-secretion which may cause malabsorption. Excessive gastrointestinal secretions cause derangement in fluid and electrolyte transport across the entero-colonic mucosa leading to diarrhea. They are characterized clinically by watery, large volume fecal outputs that are typically painless and persist with fasting because there is no malabsorbed solute; stool osmolalirity is accounted for normal endogenous electrolytes with no fecal osmotic gap.

Pancreatic lipase is inactivated and bile acids are precipitated. It results in diarrhea and steatorrhea. Subtotal villous atrophy occurs due to hyper-secretion which may cause malabsorption. Excessive gastrointestinal secretions cause derangement in fluid and electrolyte transport across the entero-colonic mucosa leading to diarrhea. They are characterized clinically by watery, large volume fecal outputs that are typically painless and persist with fasting because there is no malabsorbed solute; stool osmolalirity is accounted for normal endogenous electrolytes with no fecal osmotic gap.

Bile acids are not present in the diet but are synthesized in the liver by a series of enzymatic steps that also include cholesterol catabolism. Bile acids are either primary or secondary. Primary bile acids are synthesized in the liver from cholesterol and secondary bile acids are synthesized from primary bile acids in the intestine by colonic bacterial enzymes. Bile acids are primarily absorbed by active, sodium dependent process that is located exclusively in the ileum; secondly bile acids can also be absorbed to a lesser extent by non carrier mediated transport processes in the jejunum, ileum and colon. Conjugated bile acids that enter the colon are de-conjugated by colonic bacterial enzyme to unconjugated bile acids and are rapidly absorbed. Colonic bacterial enzymes also dehydroxylate bile acids to secondary bile acids, thus if exogenous factors like diet as discussed above disturb the colonic bacterial growth than bile acids are not absorbed. A decrease in the amount of bile acids returning to the liver from the intestine is associated with an increase in bile acids synthesis/cholesterol catabolism, which helps keep bile acid pool size relatively constant. Defects in any of the steps of the enterohepatic circulation of bile acids can result in decrease in duodenal concentration of conjugated bile acids as a result steatorrhea. Thus steatorrhea can be caused by abnormalities in bile acid synthesis and excretion, their physical state in the intestinal lumen and reabsorption. The bile gives the yellowish nature to the stools  (Verse 66).

Bile acids are not present in the diet but are synthesized in the liver by a series of enzymatic steps that also include cholesterol catabolism. Bile acids are either primary or secondary. Primary bile acids are synthesized in the liver from cholesterol and secondary bile acids are synthesized from primary bile acids in the intestine by colonic bacterial enzymes. Bile acids are primarily absorbed by active, sodium dependent process that is located exclusively in the ileum; secondly bile acids can also be absorbed to a lesser extent by non carrier mediated transport processes in the jejunum, ileum and colon. Conjugated bile acids that enter the colon are de-conjugated by colonic bacterial enzyme to unconjugated bile acids and are rapidly absorbed. Colonic bacterial enzymes also dehydroxylate bile acids to secondary bile acids, thus if exogenous factors like diet as discussed above disturb the colonic bacterial growth than bile acids are not absorbed. A decrease in the amount of bile acids returning to the liver from the intestine is associated with an increase in bile acids synthesis/cholesterol catabolism, which helps keep bile acid pool size relatively constant. Defects in any of the steps of the enterohepatic circulation of bile acids can result in decrease in duodenal concentration of conjugated bile acids as a result steatorrhea. Thus steatorrhea can be caused by abnormalities in bile acid synthesis and excretion, their physical state in the intestinal lumen and reabsorption. The bile gives the yellowish nature to the stools  (Verse 66).

Guru, snigdha and sītā  ahara is dominated by prithvi and jala mahābhuta, these qualities help in reducing the impact of agni mahābhuta thus causing jatharāgni māndyatā resulting in indigestion leading to formation ama. Such ama is responsible for doṣha prakopa.(Madhukoshatika Ma. Ni. Jwara adhyaya/2)  

''Guru, snigdha'' and ''seeta ahara'' is dominated by ''prithvi'' and ''jala mahabhuta'', these qualities help in reducing the impact of ''agni mahabhuta'' thus causing ''jatharagni mandyata'' resulting in indigestion leading to formation ''ama''. Such ''ama'' is responsible for ''dosha prakopa''.(Madhukoshatika Ma. Ni. Jwara adhyaya/2)  

Klinna(moist), guru, piṣṭānna(malt), abhiṣyandi(which increases secretions) ahāra and adhyāśana(over eating) are source for extra calories. Fast foods are defined as any food that contributes little or no nutrient values to the diet, but instead provides excess calories and fat. Common foods include salted snack foods, gum, sweet desserts, fried fast foods, carbonated beverages and candy.

''Klinna''(moist), ''guru, pishtanna''(malt), ''abhishyandi''(which increases secretions) ''ahara''(food) and ''adhyashana''(over eating) are source for extra calories. Fast foods are defined as any food that contributes little or no nutrient values to the diet, but instead provides excess calories and fat. Common foods include salted snack foods, gum, sweet desserts, fried fast foods, carbonated beverages and candy.

Diets rich in trans-fatty acids like deep fried fast food, cake mixes, chips and packed cookies, all have inclusion in guru, piṣṭānna, vishtambi(causing obstruction) ahara. People consuming snigdha ahāra (fatty food) and have sedentary lifestule with very little energy expenditure, and most fat is stored. The above 2 concepts explain why agnimāndya and ajīrṇa have been mentioned after taking heavy food. Excessive heavy food (guru ahara) slows down emptying of stomach (samāna vāta karma is hampered) and enzymes are not secreted into lumen (pitta action hampered) causing agnimāndya. Substances of sīta vīrya causes constriction reducing the secretion (stambhana) of gastrointestinal juices thus hampering lipase activity therefore leading to steatorrhea.  

Diets rich in trans-fatty acids like deep fried fast food, cake mixes, chips and packed cookies, all have inclusion in ''guru, pishtanna, vishtambi''(causing obstruction) ''ahara''. People consuming ''snigdha ahara'' (fatty food) and have sedentary lifestyle with very little energy expenditure, and most fat is stored. The above two concepts explain why ''agnimandya'' and ''ajeerna'' have been mentioned after taking heavy food. Excessive heavy food (''guru ahara'') slows down emptying of stomach (''samana vata karma'' is hampered) and enzymes are not secreted into lumen (''pitta'' action hampered) causing ''agnimandya''.

 

Substances of ''seeta veerya'' causes constriction reducing the secretion (''stambhana'') of gastrointestinal juices thus hampering lipase activity therefore leading to steatorrhea.  

Further heavy meals increase the transit time causing functional stasis which may cause bacterial overgrowth syndrome. Sleeping just after meals may also lead to functional stasis (further study required). Peristalses are also reduced with heavy meals and sleeping after meals causes bacterial overgrowth. Bacteria deconjugate conjugated bile acids and as a result intraduodenal concentration of bile acids will be reduced resulting in steatorrhoea and macrocytic anemia. Bacterial overgrowth also occurs with stasis from a blind loop, small bowel diverticulum or dysmotility.   

Further heavy meals increase the transit time causing functional stasis which may cause bacterial overgrowth syndrome. Sleeping just after meals may also lead to functional stasis (further study required). Peristalses are also reduced with heavy meals and sleeping after meals causes bacterial overgrowth. Bacteria deconjugate conjugated bile acids and as a result intraduodenal concentration of bile acids will be reduced resulting in steatorrhoea and macrocytic anemia. Bacterial overgrowth also occurs with stasis from a blind loop, small bowel diverticulum or dysmotility.   

Postmucosal lymphatic obstruction- The pathophysiology of this condition which is due to the rare congenital intestinal lymphangectasia or due to acquired lymphatic obstruction secondary to trauma, tumour or infections, leads to the unique constellation of fat malabsorption with enteric loss of protein (often causing edema) and lymphocytopenia. Carbohydrates and amino acid absorption are preserved  (Verse 67).

Postmucosal lymphatic obstruction- The pathophysiology of this condition which is due to the rare congenital intestinal lymphangectasia or due to acquired lymphatic obstruction secondary to trauma, tumor or infections, leads to the unique constellation of fat malabsorption with enteric loss of protein (often causing edema) and lymphocytopenia. Carbohydrates and amino acid absorption are preserved  (Verse 67).

Nausea and vomiting are both caused by stimulation at one of the four sites: the gastrointestinal tract, the vestibular system, the chemoreceptor trigger zone and the cerebral cortex. Nausea and vomiting occurs due to disturbed gastric motility caused by heavy meal and delayed gastric emptying. The same is the cause for heavy abdomen and eructation with foul smell and sweet taste.  As the food stays for long time in gastrointestinal tract blood flow increases centrally and reduces the enthusiasm and decrease in libido. The sluggish activity of gastrointestinal tract causes symptoms such as absence of movement in the abdomen (udaraṁ stimitaṁ guru). The heavy abdomen puts pressure on the diaphragm causing symptoms of heaviness in chest (hr̥dayaṁ manyatē styānam).

 

Nausea and vomiting are both caused by stimulation at one of the four sites: the gastrointestinal tract, the vestibular system, the chemoreceptor trigger zone and the cerebral cortex. Nausea and vomiting occurs due to disturbed gastric motility caused by heavy meal and delayed gastric emptying. The same is the cause for heavy abdomen and eructation with foul smell and sweet taste.  As the food stays for long time in gastrointestinal tract blood flow increases centrally and reduces the enthusiasm and decrease in libido. The sluggish activity of gastrointestinal tract causes symptoms such as absence of movement in the abdomen (''udaram stimitam guru''). The heavy abdomen puts pressure on the diaphragm causing symptoms of heaviness in chest (''hridayam manyate styanam'').

Bacterial overgrowth due to undigested guru, klinna, snigdha and abhiṣyandi ahāra causes increased mucoid secretion, thus formed stool is not observed instead bhinnāmaślēṣma-saṁsr̥ṣṭa varcā(loose stools with ama and kapha) is seen; which is also cause for heaviness of stools (guru-varcaḥ-pravartanam) Due to diet pattern and sedentary lifestyle there is accumulation of fat (obesity) but due to decrease protein absorption and malabsorption of essential elements patient feels weakness and laziness without weight loss (Verse 68-70).

Bacterial overgrowth due to undigested ''guru, klinna, snigdha'' and ''abhishyandi ahara'' causes increased mucoid secretion, thus formed stool is not observed instead ''bhinnamashleshma-samsrishta varcha''(loose stools with ''ama'' and ''kapha'') is seen; which is also cause for heaviness of stools (''guru-varchah-pravartanam'') Due to diet pattern and sedentary lifestyle there is accumulation of fat (obesity) but due to decrease protein absorption and malabsorption of essential elements patient feels weakness and laziness without weight loss (Verse 68-70).

Normalcy of vāta pitta and kapha keeps the agni in balanced condition, it means that a specific pH is maintained (pitta); secretion, transportation and villi movement are normal (vāta) and mucosal bed secretes normal mucus and is healthy (kapha), thus maintains samāgni or a normal digestive process (Verse 71).

Normalcy of ''vata pitta'' and ''kapha'' keeps the ''agni'' in balanced condition, it means that a specific pH is maintained (''pitta''); secretion, transportation and villi movement are normal (''vata'') and mucosal bed secretes normal mucus and is healthy (''kapha''), thus maintains ''samagni'' or a normal digestive process (Verse 71).

Protein losing enteropathy is increased protein loss into the gastrointestinal tract which is classified into three groups.

Protein losing enteropathy is increased protein loss into the gastrointestinal tract which is classified into three groups.

   

   

a) Mucosal ulceration; there is protein loss by exudation across damaged mucosa e.g. Ulcerative colitis, peptic ulcer, gastro intestinal carcinoma. In such cases dominance of pitta doṣha needs to be considered.

a) Mucosal ulceration; there is protein loss by exudation across damaged mucosa e.g. Ulcerative colitis, peptic ulcer, gastro intestinal carcinoma. In such cases dominance of ''pitta dosha'' needs to be considered.

b) Non ulcerated mucosa but evidence of mucosal damage; Protein loss primarily represents loss across epithelia with altered permeability e.g. celiac sprue and menetrier’s disease in small intestine and stomach respectively, vāta doṣha and/or kapha doṣha dominancy should be considered.

b) Non ulcerated mucosa but evidence of mucosal damage; Protein loss primarily represents loss across epithelia with altered permeability e.g. celiac sprue and menetrier’s disease in small intestine and stomach respectively, ''vata dosha'' and/or ''kapha dosha'' dominance should be considered.

c) Lymphatic dysfunction, represents either primary lymphatic disease or secondary to partial lymphatic obstruction that may occur as a result of enlarged lymph nodes or cardiac disease. Patient with increased protein loss into gastrointestinal tract due to lymphatic obstruction often have steatorrhea and diarrhea. The steatorrhea is a result of altered lymphatic flow as lipid containing chylomicrons exit from intestinal epithelial cells via intestinal lymphatic’s which may be compared with flow of ahar rasa and/ or presence of vata and kapha.

c) Lymphatic dysfunction, represents either primary lymphatic disease or secondary to partial lymphatic obstruction that may occur as a result of enlarged lymph nodes or cardiac disease. Patient with increased protein loss into gastrointestinal tract due to lymphatic obstruction often have steatorrhea and diarrhea. The steatorrhea is a result of altered lymphatic flow as lipid containing chylomicrons exit from intestinal epithelial cells via intestinal lymphatic’s which may be compared with flow of ahar rasa and/ or presence of ''vata'' and ''kapha''.

Genetic factors (bija dushti) almost all patients with celiac sprue express the HLA-DQ2 allele. Environmental factor, gliadin a component of gluten that is present in wheat, barley and rye contributes to the disease.  Immunologic component (prayatna, bala and urja of vāta, kapha and pitta respectively), serum antibodies – IgA antigliadin, IgA antiendomyasial and IgA antibodies and IgG antibodies are present. In addition, gliadin peptides may interact with gliadin specific T cells that may either mediate tissue injury or induce the release of one or more cytokines that cause tissue injury  (Verse 72).

Genetic factors (bija dushti) almost all patients with celiac sprue express the HLA-DQ2 allele. Environmental factor, gliadin a component of gluten that is present in wheat, barley and rye contributes to the disease.  Immunologic component (prayatna, bala and urja of vāta, kapha and pitta respectively), serum antibodies – IgA antigliadin, IgA antiendomyasial and IgA antibodies and IgG antibodies are present. In addition, gliadin peptides may interact with gliadin specific T cells that may either mediate tissue injury or induce the release of one or more cytokines that cause tissue injury  (Verse 72).