Structure

14.1 Introduction
Gastrointestinal Diseases and Disorders
14.2.1 Diarrhoea
14.2.2 Constipation
14.2.3 Oesophagitis
14.2.4 Gastro Oesophageal Reflux Disease (GERD)
14.2.5 Dyspepsia
14.2.6 Gastritis
14.2.7 Diverticular Disease
14.2.8 Peptic Ulcer
14.2.9 Malabsorption Syndrome '
14.2.9.1 Ccliac Diseasc
14.2.9.2 Stcatorrhoea
14.2.9.3 Lactose Intolerance
14.2.9.4 Inflammatory Bowel Disease (IBD)

14.3 Let Us Sum Up

14.4 Glossary
14.5 Answers to Check Your Progress Exercises

In our previous units, we dealt wit11 major metabolic disorders. In this unit, we shall
study about the diseases and disorders of the gastrointestinal (GI) tract. Have you
ever suffered from abnormal sylnptoms of the gastrointestinal tract? The symptoms
could be as simple as nausea, anorexia, weakness to more severe ones like abdominal
pain, abdominal gas and flatulence, delayed gastric cmplying, diarrhoea or very severe
ones such as the dumping syndrome, malabsorption syndromes arid many others that
we will learn about in this unit. In order to prevent the developmelit 01these disorders,
the gut must remain healthy so that the GI tract functions can be carried out normally
or else the site and the extent of the disease process can affect the nutrient absorption
and cause malnutrition. In this unit, we will touch upon the common gastrointestinal
disorders and diseases to highlight the causes, important signs and symptoms and the
dietary management of the problems.
Objectives
After studying this unit, you will be able to:
o explain the disease conditions, causes, complications of the disorders of the
gastrointestinal tract,
e discuss the effect of diseases on normal functioning of the gastrointestinal tract,
e describe the modification of the regular or normal diet to suit these disease
conditions, and
e enumerate the principles of nutritional management in different disorders and
diseases of the gastrointestinal tract.
Clinical Therapeutic
Nutrition 14.2 GASTROINTESTINfiDISEASES M D
DISOmERS
Before discussing the many gastrointestinal problems, it is useful to understand the
basic physiology of the gastrointestinal tract. Figure 14.1 illustrates the different parts
of the gastrointestinal tract. You would recall from your Applied Physiology Course
($EN-001),Unit 6 that the gastrointestinalsystem performs the following four important
functions. It helps to:
- store food,
- mix the food with enzymes produced in different parts of the gastrointestinal
tract to break the complex foods to simpler forms of food (digestion),
- propel the food mixture through mouth, oesophagus, stomach, duodenum, small
and large intestines to the anus, and
- absorb the various nutrients into the blood especially from small intestine and
outer parts.

Figure 14.1: Various parts of the GI tract iI

Looking at the functions, you canunderstand that any disorder or diseases of a parlicular
part can effect the storage, propulsion, digestion and result in nutrient deficiencies.
We shall discuss the same in this unit and will begin with diarrhoea - one of the most
common and fatal GI tract problems.

14.2.1 Diarrhoea
What is diarrhoea? Diarrhoea is characterized by the fiequent evacuation of liquid
stools, usually exceeding 300 ml, accompanied by an excessive loss of fluids I
and electrolytes, especially sodium and potassium. It occurs when there is
I
I
excessively rapid transit of intestinal contents through the small intestine, decreased.
enzymatic digestion of foods, decreased absorption of fluids and nutrients or increased 1!
14

secretion of fluids into the GI tract. It is important to note here that diarrhoea is a
!
symptom and not a disease.
I
An episode of diarrhoea can be acute (recent origin) or chronic (extended duration I

and repeated episodes) in nature. You may recall reading in the Food Microbiology I

I
ans Safety Course about microbial infections and toxins, which are a major cause of I
diarrhoea among individuals. However, there are several other causes of diarrhoea I

such as metal poisoning, deficiency of enzymes, side effects of drugs, structural1 I

functional abnormalities in the organs etc. Table 14.1 highlights the causes for acute
and chronic diarrhoea. ~
 Table 14.1: Causes of diarrhoea Nutritional Management
aof Gastrointestinal
Disenses nnd Disorders
Acute Diarrhoea Chronic Diarrhoea
Heavy metal poisoning e.g lead, Malabsorption, lesions of anatomic,
mercury, arsenic. mucosal or enzylnatic origin.
Viral infection (rotavirus)
Bacterial toxin (Salmonella, related to Metabolic disease such as diabetic
food poisoning), Bacterial infection neuropathy, Addison's Disease.
(E. Coli; Slzigella)
Drugs (Ncomycin, colichine, antibiotics, Carcinoina of small intestine and colon.
antacids, chemotherapy, digoxin, sorbitol) I

Psychogenic factors Cirrhosis of livcr

Protozoa infection (giardia, lamblia, Allergy and food sensitivity
entamoeba histolytica)

It must be evident from the table above that acute diarrhoea generally occurs in
association with infections, poisons and drugs. Chronic diarrhoea on the other hand
are the result of long-term diseases such as malabsorption syndromes, deficiency of
GI secretions, chronic deficiencies/allergies elc. Some common forms of chronic
diarrhoea which you may come across while managing other disease conditions include:
o Osmotic diarrhoea: This kind of diarrhoea is caused by the presence of
osmotically active substances in the intestinal tract, which in turn, favour the
drawing of large volumes of water in the gut e.g. diarrhoea associaled with
lactose intolerance (sugar lactose is not digcsted duc to lack of enzyme laclase
in the intestine), dumping syndrome (multiple symptoms rclatcd to removal of
part of stomach).
e Secretory diarrltoea: It is a rcsull o f active sccreiion OF electrolytes and watcr
by the intestinal cpitlieliunl caused by bacterial anci viral infections. Thesc, in
turn, lead to the productioil o l cxotoxins and increased intestinal hormone
secretion.
e~ Exudative diarrhoea: It is associatcci with the illucosal damage leading to out
pouring of mucus, blood and plasma proteiils with il net accumulation of water
and electrolytes in the gut.
s Limited mucosal contuct diarrltoea: It results from situations of inadequate
mixing of chyme (semi-liquid Inass of L'ood passing through intestine) and
inadequate exposure of chyme to intestinal epithelium because of destruction
and decreased mucosa due to surgical proccdurc. This type of diarrhoea is
usually complicated by steatorrhoea (increased amount of fat in feces).
Now, let us have a look at the consequences of diai~hoeawith the help of flow chart
given in Figure 14.2.
Consequences of Diarrhoea
All of us must have suffered from diarrhoea atleast once in our liletirnc. I-low do you
feel thereafter? Well moslo1 us must have experienced weakness, dizziness, dryness
of mouth and anorexia. Oyr skin also becomes dry and loose. During diarrhoea the
stools are loose and have a high water content - an indicator that water is being lost
in higher than normal amounts. The stools also conlain a high amount ol: electrolytes
due to enhanced peristaltic movements i.e. increased movements of tlie stoniach and
inteslines. This results in the deficiency of water and electrolytes in the body Which is
referred to as dehydration. Dehydration results in reduction in the extracellular blood
Clinical Therapeutic volume and hence a reduction in the total blood volume which is often referred to as
Nutrition '
hypovolemia. Low blood volume is associated with hypotension and a low cardiac .
output. In response to hypotension, the heart tries to compensate by increasing the
number of cardiac cycles per minute which is indicated by a high pulse rate. You will
often find that during diarrhoea the patients have low blood pressure but usually a
higher than normal pulse rate. As the severity of dehydration increases, despite
enhanced cardiat? cycles, adequate amount of blood and nutrients do not reach all
body parts/organs. The patient is therefore cold to touch at the extremities. Another
complication that may arise if severe dehydration does not receive prompt medical
care is ischemic damage to the tissues of various organs due to reduced supply of
oxygen and nutrients. Of most significance is damage to the kidneys and brain. Reduced
blood volume results in reduced glomelvlar filtration rate and hence a low urine output.
This in turn can'result in accumulation of toxic waste products in the blood which can
be measured by the level of blood urea nitrogen levels. Other associated changes can
be observed in the form of azotemia - abnormal high level of urea and creatinine a ~ d
metabolic acidosis which develop during acute renal failure. Acute renal failure is
particularly observed during severe diarrhoea coupled with delayed or absence of
adequate fluid management. Another consequence, which we were discussing, involved
changes in the nervous system. They can be as mild as dizziness due to less supply of
oxygen, glucose and other nutrients to the braill cells or as severe as resulting in coma
due to excessive accumulation of nitrogenous waste products and other toxic lnctabolites
in the blood. It would thus be evident that maintenance of adequate blood voluine is
imperative to prevent dehydration and its consequences some of whicl~call be life
threatening. A basic oulline of the consequences of diarrhoea has been indicated in
the Figure 14.2.

Loss of water and electrolytes (causes dehydration)

I
J.
Drop in the extracellular fluid volunle
I

Increase in pulse rate

I

Drop it1 blood pressure

\1
Supply of blood to extremities reduced
I
Cold extremities
. J.
Compromised blood supply to vital organs like brain and kidney
J
Impaired consciousness and decreased urine output
I

Disturbed acid base balance

Depletion of base reserves

I
J.
Acidosis

COMA I

\ , j
Figure 14.2: Consequences of diarrhoea
By now, you must have understood the seriousness of diarrhoea and can understand Nutritional Management
of Gastrointestinal
that it is the highest cause of illness and death especially in children. Diseases and Disorders

We will now continue our discussion to learn about the treatment and management of
diarrhoea.
Treatment and nzanagement of diarrhoea
You must have realized by now that diarrhoea should not be neglected and must
receive proinpt medical care to minimize the frequency of morbidity and morlalities.
In light of the complications discussed above, let us now examine what should be the
objectives in the management of this disease.
Objectives
The major objectives in the management of diarrhoea include:
1. Fluid and electrolyte replacement
2. Removal of cause (especially if infection)
3. Nutrition concerns (chronic diarrhoea) '

Pro~nptreplacement of fluids and clectrolytes is of most significance to prevent

morbidities and mortality associated with dehydration. This is follawcd by removal of
cause which is a medical aspect and sllall 1101 be discussed in detail here. Removal of
cause may require antibiotics, gaslric leavngc or opcralive procedures to name a
few. We will now discuss the management of diarrhoea in detail.
The first step should be to determine the status of dehydration. We have already
talked about the mild, inoderate and severe dehydration. In mild to moderate cases
fluid, electrolyte and acid base homeostasis should be preserved. Nutritional status
should be restored and anti-microbial agents should be given. Associated problcms
like persistent vomiting, abdominitl distension and convulsioils should be managed.
The therapy for diarrhoea thus consists of:
1. Determilling h e status of dehydration
2. Fluid management
@ Oral Rehydration Therapy (ORT ) - home madc/commercial Oral
Rehydration Salts (ORS)
cs Emergency treatment and drug ~nanngement
3. ' Nutritional mailagerneilt
Now, let us understand these points.
1. Determining the status of del?yrlratio?zhas been explained to you earlier. The
child in a severe dehydration state must be hospitalized,
2. Fluid management: The key to diarrhoea management is the early replacement
of fluid lost in the stools through intravenous or oral route. While severe cases
need administration of dextrose and elcctroIyte solutions intravenously; mild to
moderate cases can be managed at home. The patient can be easily managed
by giving any fluid at home e.g. coconut water, buttermilk, salted rice kanji,
lemon sugar salt beverage or weak tea. This is con~monlyreferred to as the
Oral rehydration therapy (ORT), Let us read more about ORT.
a Oral Rehydration Therapy (ORT) refers to providing fluids and/or oral
rehydration salt solutions to the patient. An oral rehydration solution can easily
be prepared at home by taking a teaspoon of salt, 3 tablespoon of sugar wit11 or
without lemon juice mixed in a liter of potable water. Oral Rehydration Salt
formulations as suggested by WHO are freely available comncrcially in small
packets.
Clinicnl Therapeutic Composition of Oral Rehydration Salt (WHO Standard Formulation)
Nutrition
1. Sodium Chloride (common salt) = 3.5 g
2. Glucose = 20 g

3. Trisodium Citrate = 2.9 g or sodium bicarbonate = 2.5 g

4. Potassium chloride = 1.5 g.

5. Dissolved in a litre of potable water.

This solution provides (g per litre of water):

1. Glucose (g1100 ml) = 2 (provides energy)

2. Sodium (mEq/L) = 90 (favours rehydartion)

3. Potassium (mEq/L) = 20 (prevents acidosis)

4. Chloride ( mEq/L) = 80 (favours rehydration)

5. Bicarbonale (mEq/L) = 30 (builds base reserves)

6. Osmolality (mOsmfL) = 330 (maintains osmotic balance and favours early

rehy dration).

s Emergency treatment and drug treatment: Severe dehydration is fatal and

requires intravenous fluids and hence hospitalization. You have read about causes
of diarrhoea and know that several types of protozoas, viruses and bacterias
cause diarrhoea. Many toxins are produced by some varieties of bacilli, which
are harmful for the nlucosal lining and hence drug therapy is required.

Next, we shall discuss about thedietary management of diarrhoea.

3. Nutritional management

The conservative concept of treatment for diarrhoea was not in favour of feeding
adequate amount of hod. However, with the identificationof varied underlying causes
and not so positive outcomes of the starvation therapy, it has become evident that
adequate nutritional care is pertinent to ensure enhanced recovery and proper
rehabilitation. Dietary management of diarrhoea has changed completely over the
years and it is now advocated th3t the patient should be prescribed a diet most suitable
for the underlying etiology of diarrhoea. Today we know that the nutrient requirements
and or the quality (consistency) of diet may not necessarily be the same for all forms
of diarrhoea. While the demand for fluids and electrolytes are particularly high during
an acute episode; that of all macro-and micronutrients increases during chronic
diarrhoeas. In our subsequent section, we shall discuss in detail the nutrient requirements
during diarrhoea.

Dieta1.y Recomnzendations during Diarrhoea

The diet should take into account the normal RDI and various adjustments made to
the quantity and quality of the foods to be given. The following information will help
you to understand these concepts.

Energy: During the acute phase of diarrhoea, the caloric intake can be increased
gradually as per the tolerance of the patient. An increment of 200-300 Kcal is a
feasible target. Patients suffering from diarrhoea should never be starved as even in
acute diarrhoea digestive enzymes are functional and almost 60% digestion can take
place. Resting the gut can be most damaging as it can bring about structural changes
in thc gut membrane, which call predispose an individual to associated complications,
Recent studies indicate that children who are fed with appropriate type and amounts Nutritional Manngement
of GnstrointestinnI
of food through the acute phase of diarrhoea show absorption of substailtial amounts Di~eosesand Disorders
of nutrients, and are therefore at lesser risk to nutritional deficiency. These children
show better weight gain, have shorter duration of diarrhoea1 episode and a quicker
recovery. Calories can be provided through easily digestible carbohydrates. Excess
sugar may be avoided to prevent fermentative effect, which may aggravate the
diarrhoea.
Protein: Requirements are increased only in chronic diarrhoea because of associated
tissue depletion. An additional 10 g of protein may be recommended above the normal
requirements. Milk a source of good quality protein is restricted as it is a high residue
food or if it is anticipated that diarrhoea may have developed due to relative deficiency
of lactase in the gastrointestinal tract. Milk in the fermented form like curds is better
tolerated, as it is easy to digest and helps in maintaining the gut health. Other cooked
and diluted milk products like a light porridge; paneer etc can also be tolerated in
small amounts. Apart from these, easily assimilated protein-rich foods like minced
meat, egg, skimmed milk and its preparations can be given,

Fats: Total amount of fat may be restricted as its digestion and absorption is
compromised. In order to increase on the calorie density of the diet, emulisified fats
or those, which are rich in medium chain triglycerides, may be added in restricted
amounts. Fats like butler, ghee and cream are easily digested. Fried food must be
avoided. Invisible form of fat i.e. fat present inherently in the food (egg yolk, whole
milk, paneer, curd, flesh food etc.) is tolerated more as compared to visible Iorm
of fat.
Carbo!zydrates: Adequate amount of carbohydrates i.e 60-65% of the total energy
should be given to the patient. Easily assimilated carbohydrates i.e. principally starches
should be preferred. Glucose, sugar, honey, jaggery, potato, yam, colocasia, rice, sago,
semolina, refined flour, pastas can be incorporated lo prepare dishes such as khichdi,
vegetable/pulse puree, fruit juices, souffli, shakes, custard and kanji. The fibre content
of the diet should be kept minimum and insoluble fibre should particularly be avoided.
Table 14.2 and 14.3 give the low fibre and low residue foods. Alow-residue/low fiber
diet limits the amount of food waste that has to move through the large intestine.
These diets may help control diarrhoea and abdominal cramping and make eating
more enjoyable.

Information provided in Box 14.1 relates to the concept of residue read it carefully.

Box 14.1 Residue in Foods

Residue is defined medically as the solid contents that have reached the lower
intestine. A low residue diet is composed of foods, which are easily digested and
readily absorbed, resulting in a minimuin of residue in the i~ltestiilaltract. Thus,
a low-residue diet contains limited amounts of undigested or only partially digested
ingredients. Foods, which are high in residue, are those, which are high in
roughage, or fiber. The main source of residue is fiber in foods like whoIe-grain
breads and cereals, seeds and nuts, dried fruits, and the stalks and skins of fruits
and vegetables. Milk should be consumed in moderation.

a Fibre: InsolubIe fibre in the form of skins, seeds and structural plant materials
should be strictly avoided to minimize on the irritation of the GI tract. Soluble
fibre in the form of stewed fruits and vegetables like apple juice, stew, guava
nectar and pomegranate juice help in binding the stool and favour good environment
in the gut. Fruits like papaya and banana have an astringent property and are
beneficial.
CLinical Therapeutic Table 14.2: Low fibre foods
Nutrition
Milk products Paneer, curds, toned milk

Cereals Refined cereals: rice, white bread, noodles, maida, suji

Pulses Dehusked pulses - b .

Vegetables Potato, bottle gourd, tomato (without skin or seeds),

spinach
-
Fruits Papaya, banana and fruit juices
1

Table 14.3: Low residue foods

Cereals Rice, refined cereals such as maida, suji, white bread
sweet biscuit, cornflour

Vegetables Tender, well-cooked, pureed low fibre vegetables

Fruits Fruit juices or pureed fruits

-
Meat and its products Chicken and fish

Pasta plain macaroni, noodles, sphagetti etc.

Sweets White sugar, brown sugar, honey, clear jelly

Vitamins nncl wriilerals: Loss of vitamins is related to the degree of rnucosal damage
in chronic diarrhoea, which in turn impair absorption and synlhesis of various essential
substances in the body. The vitamins of importa~lceare B complex vilamins especially
folic acid, vitamin B,, and vitamin C. Fat soluble vitamins (A, D, E and K) can be lost ,
if fat is not digested and lost in stools. Minerals which are of importance iilclude iron
especially if there is an associated bleeding. Sodium and potassium may need to be
replaced. Potassium supplementation [nay favour bowel motility and build up appetite,
Fluids: Intake should be liberal to minimize the risk of dehydration. Remember wc
read about fluid management in this section before. Preference must be given to
diluted drinks as concentrated ones may favour osmotic diarrhoea.
Lastly, a few simple tips which sbould be given to the patient.
s Boiling, steaming, baking, pressure cooking should be encouraged
e Consume small and light meals frequenlly instead 013 big meals a day to replenish
the lost nutrients.
e Have plenty of fluids like lemon juice, fruit juices, vegetable soups, watery dals,
lassi, coconut water etc. to make up for the losses of fluids.
Have fruits like b.anai~laand apple as they are rich in potassium which helps'to
maintain fluid balance.
e Try to restrict the consumption of milk and dairy products, as they are difficult to
digest,
e Avoid fried foods.
0 Avoid raw vegetables like salads.
While the above mentioned principles are applicable for patients of all age groups and
gender, we shall discuss some important aspects of management among infants and
young childreil whicl~are the most vulnerable segments especially with respect to
developing complicatioas. It has also been observed that myths regarding breast Nutritional ~ a n a b e m c n t
of Gastrointestinal
feeding and food consumption are rampant due to ignorance. Efficient and aggressive Discnscs and Disorders
counseling of the parentslcarelakers is equally important for preventing dehydration
and malnutrition which may affect the growth and development of the child in the
long run especially in cases of chronic diarrhoea. Let us now move on to the
management of diarrhoea in children - which is one of the leading causative factors
of infant deaths in our couatry.
Dietary Management of Clzildren with Diarrhoea
Diarrhoeas are more common in children and malnutrition often leads to the elicitation
of this symptom as u~ldernourishedare more prone. Poverty, ignorance, poor sanitation
are often the underlying risk factors. The magnitude of the incidence of diarrhoea in
India is majorly observed in children. It has been estimated that almost 250 million
episodes of diarrhoea annually are observed in children below 5 years and nearly 1.5
million children die of diarrhoea annually. Thus, managing diarrhoea in children is of
great concern. The guidelines for the same are as follows:
1. The first objective is to rehydrate the child. Thus using ORS would be the ideal
modality. The WHO-ORS standard preparation is useful but recent studies have
suggested that the osmolarily of the solution should be reduced from 311mmol/
Iitre to 200-250 mrnol/litre by reducing the concentration of glucose. Sodium has
a beneficial effect on the stool output and duration especially in non-cholera
diarrhoea. This can be achieved by diluting the ORS salt in 1.5 litres instead or
the usual 1 litre for ii~fantsunder age 2 months.
2. Breast feeding should be continued in young inlants during diarrhoea. This helps
in decreasing the number and volume of stools and the duration of diarrhoea.
Starving the child during diarrhoea may deteriorate the nutritional status.
3. Children 4-6 months of age or oldcr should reccive energy rich mixture of soft
weaning foods in addition to breast milk. The energy rich mixture can be a mix
of cereal, pulse, roots, green leafy vegetables, and fats like ghee, butter that are
easy to digest. The caloric density of the feeds can be increascd by using amylase
rich flour (ARF), i.e the flour obtained from germinated grain which is rich in
amylase and call be prepared as a soft and Lhin porridge without taking away
its llulritional value. Fermeilted foods like dhokla, bread, idli, dosa may bc included
in the diet.
4. Foods to be avoided include: spicy and oily foods, confectionary, mithai and
chocolates, as well as, uncooked fruits and vegetables.
5. Supplementation with B-complex vitamills especially folic acid, vitamin B,, and
minerals like zinc help in normalizing the intestine.
6. The criteria for monitoring the state of hydration and nutritional status are: good
urine output, appearance of the eyes, skin, buccal mucosa and weight gain.
7. Consult the doctor, if required.

REMEMBER THE GOLDEN RULE: FEED IN DIARRHOEA, DON'T

STARVE THE CHILD.
THERE ARE MORE LIVES LOST DUE TO STARVATION T H A N
FEEDING.
1 e INFANT: CONTINLTE BREAST FEEDING I
e OLDER CEILDREN; MAKE NECESSARY MODIFICATIONS
IN THE NORMAL DAILY DIET. GIVE FREQUENT LIQUIDS
ORIAND LOW RESIDUE SOFT DIGESTIVE FEEDINGS. GIVE
BLAND A N D LOW FIBRE DIETS.
We shall next proceed over to discuss about another common disorder of 'the gastro-
intestinal tract viz., constipation.
 Ii
Clinicnl Therapeutic 14.2.2 Constipation
Nutrition
Constipation is irregular, infrequent or difficult passage of faeces. It is the most common
physiological disorder of the alimentary tract. It is characterized by inconlplete
evacuation of hard, dried stools. It occurs commonly in children, adolescents, adults
on low fibre diets, patients confined to bed, in invalids and in elderly persons. It is a
condition in which:
a fewer than 3 stools per week are passed while a person is eating a high residue
diet,
a more than 3 days go by without the passage of a stool, and .

stools passed in one day amounting to less than 35 grams.

There are three main types of constipation. These are:
1. Ato~zicconstipation : This type is most common, often it is called the "lazy
.bowel". There is a loss of muscle tone causing weak peristalsis, the causes are:

a) lack of fluids, rouhage and potassium

b) vitamin B Complex deficiency

c) irregular defeaction habit and poor personel hygiene.

d) excessive purgation or use of enema.

e) sedentary lifestyle or lack df exercise

1. Spastic constipation: It results from excessive tone of the colonic muscle.
.-
2. Obstructive constipation:It occurs usually due to obstructio~lin the colon, cancer,
or any other obstruction due lo inflammation or narrowing of the lumen.
Let us see what are the causes and symptoms of constipation.
Etiology
The most common causes of constipation are poor elimination habits, a lack of fibre in
the diet, insufficient fluid intake, lack of exercise and a loss of lone in the intestinal
musculature. Apart from these, chronic overuse of laxatives, nervous strain and worry
are also some common causes. The causes can be classified under two heads -
systemic and gastroirltestinal -as highlighted in Table 14.4.
Table 14.4: General causes of constipation
Systemic Gastrointestinal
Side effects of medications Celiac disease
Metabolic or eildocrinal abnormalities such Duodenal ulcer
as hypotl~yroidism
( Lack of exercise ( Gastric cancer
---
I
1 Ignoring the urge to defecate I Cystic fibrosis
-- -. -- --

1 Vascular disease of the large bowel 1

-- -

( Diseases of the large bowel

-- -- -.
.

I Diet low in fibre .. ( Irritable bowel syndrome -1

Pregnancy Anal fissures & haemorrhoids
Laxative abuse
Synzptonzs
Have you ever sulfered from constipation? Do you recall the symptoms associated
with the problem? Yes, the symptoms were specific to having a bloated stomach,
stomach painslcramps, inability to evacuate, a feeling of fullness in the lower abdomen,
 Nutritional Management
lethargy, irritability, a sensation of dullness or even moderate pain in the head. These of Gastrointestinnl
are the symptoms of constipation. Diseases and Disorders

Let us now move on to the major complications involved in this disorder. If constipation
is suffered frequently, the problem worsens due to a,viciouscycle of events, as depicted
in the Figure 14.3. --

Efficiency of the bowel

1 Old hardened faeces

n
is reduced accumulate in the bowel

Time taken to pass Diameter of the bowel is

faeces is increased effectively reduced

Figure 14.3: Cu~nplicntionsin constipation

Apart from this, the list of olher complications for constipation have been mentioned
in Table 14.5.
Table 14.5: Complications associated with constipation
Haemorrhoids (swollen blood vessels around Diarrhoea
the anus)
Anal fissure (a tear in the anal region) Faecal iricontinence (inability to
control bowel movement)
Rectal bleeding (protruding rcctum Rectal prolapse
through thc anus)
Rectal hernia Faecal impactio~i(hard stools in
the bowel)
Uterine hernia Uterine prolapse (downward
displacement)

What can be done to prevent constipation? Can dietary management help relieve the
problem? Let us find out.
Management of Constipation
You must have realized by now that proper dietary and lifestyle management can
help in maintaining the normal bowel movements to a great extent. Medical
.interventions are required only when constipation arises because of some structural1
functional change in the gastroi~~testinal
tract. In our subsequent discussions, we will
deal with the dietary management of conslipation. Let us first identify the objectives
of the patient care process.
Dietary and Life Style management Goals
The dietary and life style management goals include:
To develop regularity of habits in evacuation
o To follow a regular meal pattern
m ~onsun;ea high fibre diet
 !
1
Clinical Therapeutic e Take adequate amounts of fluids
N~~trition
e Increase physical activity
Based on these objectives, the dietary management of constipation is highlighted next.
Dietary Management of Constipation
Management of constipation lies in developing regularity of habit through a bowel-
training programme and by establishing good healthy habits such as regular meals and
elimination timings, adequate fibre and fluid intake, and sufficient exercise.
The mainstay of the treatment of constipation is however dietary in nature wit11 a lot
of emphasis on dietary fibre and fluid intake. So let us get to know about dietary
fibre - its sources and potential benefits.
Dietary fibre is defined as plant polysaccharide resistant to hydrolysis by the digestive
enzymes in the human intestinal tract. It includes:
o Structural polysaccl~arides(insolublefibre) of the plant cell wall such as cellulose,
hemicelluloses, no11 carbohydrate material, lignin etc.
o Non-structural polysaccharides (soluble fibre) such as pectins, gums and
mucilages.
What are the sources of dietaly fibre in our diet?
The sources of dietary fibre include whole grain cereals, legumes, whole pulses, leafy
vegetables, vegetables like peas, beans, ladies finger, fruits like guava, apple, citrus
fruits, nuts, oilseeds like flaxseeds, methi seeds etc. Remember we read about the
sources of soluble and insoluble fibre in Unit 11 earlier. You may wish to go back and
recapitulate.
Do you know what the recomn~endationsfor fibre are? Well, the crude fibre intake
should be 14 g/1000 Kcal. For adult woman 25 glday and for adult man 38 gtday is
desirable.
Increase in fibre intake may lead to symptoms sucll as flalulence and abdominal .
distention. This can be relieved through use of inputs like sprouting, Ierinentation,
proper distribution of high fibre foods through out the day and adequate fluids. Bran
and powdered supplements may be of help in individuals who do not eat sufficient
amounts of fibrous foods.
What nbozlt the fluid and otlzer nutrient intake during constipatio~z?
The fluid intake should be at least 2 litres daily.This includes fluid as foods and beverage
besides water. The intake of lemon juice, citrus fruit juices, coconi~twater, vegetable
soups, watery dal, lassi and watermelon juice may have an added benefit of adding
vital nutrients like potassium which improve the muscle toile.
As for the other nutrients i.e. calories, proteins, carbohydrates and fat the
requirelnelits would be the same as the RDA for a particular age, sex, occupation of
the individual, weight status etc.
The nutritional management should aim at:
o developi~~g
regularity of habits of evacuation
e following a regular and balanced meal pattern
e consuming a high fibre and adequate fluid diet, and 1
e increase in pllysical activity and exercise
The requirements of various nutrients are not altered in constipation. It is essentially a
I
normal balanced diet (normal RDA's) with modification in fibre and fluid intake. The
intake of fibre should be increased. High fibre foods should be given freely. Some of Nutritional Management
of Gastrointestinal
the foods which can be given freelylavoided have been mentioned in Table 14.6 and Diseascs and Disorders
14.7 respectively.
Table 14.6: Foods to be given freely in constipation
I
Cereals Whole-wheat, maize, millets.
Pulses Whole-pulses such as rajma, chole, wl~olegreen gram etc.
Vegetables Green leafy vegetables, knoll Idol, lotus stem, peas, beans
Fruits Guavas, pomegranate, apples with skin, chickoos, cherries, pear,
peaches and plums.

Table 14.7: Foods to be avoided/ restricted during constipation

Refined foods: pasta, refined cereals like maida, suji, baked products, pizza, patties,
biscuits etc.
Deep fried foods
Pureed fruits and vegetables, banana, mango etc.

When changes. in diet and activity patterns do not ilnprove constipation, further
evaluation is warranted and the need for drugs prescribed by the physician may be
necessary.
Now let us gear ourselves to some check your progress exercise, before we move
any further.
Check Your Progress Exercise 1
1. Make a list of 10 foods low in dietary film and 5 foods low in residue.
.......................................................................................................................
.......................................................................................................................
.......................................................................................................................
2. Suggest ways how you call improve thc dietary fillre ii~lalteof an elderly
man 65 years of age. Justify your selection.
.......................................................................................................................
................... .......................
.......................................................................................................................
3. List five food preparations which call be used in the rehydration of acute
diarrhoea. What is the relationship between salt, sugar and water in ORS?
.......................................................................................................................
.......................................................................................................................
.......................................................................................................................
4. Suggest a feeding schedule for a child recovering from acute diarrhoea and
justify your selection.
.......................................................................................................................
.......................................................................................................................
.......................................................................................................................
Clinical Thernpeutic In the section discussed abovej we learnt about the etiology and management of two
Nutrition distinct disorders of the bowel viz., diarrhoea and constipation. We sball continue our
discussion on certain other common disorders of the gastrointestinal tract such as
oesophagitis and gastrocsophaus reflux disease.
How many of us get the symptoms of heartburn, acidity and bloating often? Do we
know as to why it happens? It is important to leain about these symptoms in view of
their wide prevalence among the general masses, as well as, among patients. Let us
examine and find out the details of the associated condition.

14.2.3 Oesophagitis
We already know that oesophagus is a muscular tube 25 cm in length and basically
helps in transporting the Iood from the mouth to stomach, As the bolus of food is
moved voluntarily from the mouth to the pharynx, the upper oesophageal sphincter
relaxes, the food enters oesopltagus and subsequently the lower oesophageal sphincter
(LES) relaxes to receive the food bolus. With the help of peristaltic waves, the bolus
of food is moved into the stomach.Refer to Unit 6, section 6.6 in the Applied Physiology
Course for more details on this aspect.
Oesophagitis occurs in the lower oesophagus as a result of the irritating effect of
acidic gastric reflux on the oesophageal mucosa. It can an acutelchronic inflammation
of the oesophageal wall. It is associaled with the conlmon syinptom of heartburn
(burning epigastric substernal pain). Other symptoms are regurgitation and dysphagia
(difficulty in swallowing).Difficulty in swallowing occurs due to pain associaled with
inflammation of the tissues of the oesophagus. Regurgitation of the acidic gastric
contents can be cause or result of oesophagitis. Let us learn about the two types of
oesophagitis conditions:
1. ' Acute Owoplzagitis- It is characterized by substernal pain on swallowing. It is
due to prolonged intubation, extensive burns, excessive vomiting, ingestion of a :
toxiii/chetnical or due to diphtheria.
2. Chroriic or Reflux Oesophngitis - It is characterized by intermittent
heartburn, pain on taking hot or cold foods, spicy or acid foods. This is a result of
recurrent gastroesophageal reflux due to hiatus hernia, reduced lower
oesoplsageal sphincter (LES) pressure, increased abdominal pressure (obesity,
pregnancy, hiatus) increased abdominal adiposity and recurrent vomiting.
The severity of the oesophagitis resulting from oesophageal reflux is determined by '
the content of gastric reflux mucosal resistance, clearing rate of oesophagus and rate
of gastric emptying. Content of gastric reflux may include partly digested food, pepsin,
acid and possibly bile and at times pancreaticenzymes. It is probably this combination,
which causes mucosal damage, Symptoms develop when reflux becomes frequent
and mucosa of oesophagus becomes sensitive to the reflux contents.
I

Competency of LES (Lower Oesophageal Sphincter) is important. The pressure of

this sphincter is controlled by many factors, one of which is hormonal. LES decreases
during pregnancy, in women on oral contraceptive and late stage of ineiistrual cycle.
Other factors may include overweight, hiatus hernia, tight clothing, H. pylori bacteria,
aid excessive use of drugs like aspirin and anti-inflammatory drugs.
Certain foods like fatty meals, chocolate, coffee, alcohol, spicy food, citrus juices
I
lower the sphincter pressure (also hormone mediated).
I

The causes include tissue erosion by hydrocliloric acid (EIC1) and pepsin, with symptoms
of subslcrnal burning, cramping, pressure sensation or severe pain. These symptoms
are related to:
e anincompetent gastroesophageal sphincter,
e frequency and duration of the acid reflux, and
o inability of the oesophagus to produce normal peristaltic waves to prevent Nutrition01 Management
of Gastrointestinal
prolonged contact of the oesophageal mucosa with the acid pepsin. Disenses and Disorders I

Tlle patients usually present the following symptoms:

Symptoms
The symptoms of oesophagitis include heartburn or pyrosis, iron-deficiency anaemia
due to chronic tissue bleeding, aspiration, which may cause cough, dyspnea or
pnenmonitis. The complications involved in the disorder are stenosis and oesophageal
ulcer. Significant gastritis in the herniated portion of the stomach may cause occult
(hidden or minute amounts) bleeding and anaemia.
Before we move on to the dietary factors, let us have a look at the following case.
Meeta is a 49-year-old female working in a MNC. From past few days, she had been
complaining of persistent abdominal pain, diarrhoea and weight loss. Her medical
examination revealed the acute condition of oesophagitis. What dietary advice would
you give to her so that her symptoms arc relieved and she gains back her normal body
weight? Let us read and' find out.
Nutrition Management Goals
The objectives of nutritional care include the following:
1. Prevention of irritation of the inflamed oesophageal mucosa (in the acute phase).
2. Prevention of oesophageal reflux
3. To decrease the acidity of the gastric juice.
It is evident from these objectives that there is no significant change in the nutrient
requirements of the patient. We however need to make several qualitative changes in
the diet and feeding pattenl. Let us take an overview on these aspects now.
Dietary Manage~nant
Providing adequate nutrition support may require emphasis of different aspects during
acute and chronic oesophagitis. ' .
In acute phase, the dietary factors to be kept in mind are:
e ,Liquiddiet; small and frequent meals.
Less abrasion to the oesophagus thus avoiding orange juice and other citrus and
tomalo products because of their acidity.
e Spices like chili powder, black pepper to be avoided.
While in chl.onic plzase, following factors must be considered as well:
e Efforts must be taken to increase 1,ES pressure. Mcalslfoods high in protein
increase sphincter pressure and reduce the likelihood of reflux and heartburn.
Avoiding foods that are known to cause heartburn and decrease LES pressure
like chocolate, alcohol, caffeine containing beverages, coffee, cold drink, Eatty
foods ind increased fat intake.
~ i m i n gof the meals is very important especially before the afternoon nap and
evening. The patients should consume nothing except water 3 hours before
lying down. This in turn ensures an almost empty stomach with less likelihood of
reflux on lying down. I

Avoid lying down, bending or straining immediately after eating.

Reduce weight so that abdominal pressure is decreased.
 Ciinicnl Therapeutic e Avoid tight fitting clothes.
.. Nutrition
. .
e Avoid smoking as nicotine decreases.LES pressure.
Other effects of smoking on the GI !&act includes: I
,
1. A decrease in pykoric sphincter pressure which may predispose an individual to
duodenal ulcer.
2. An alteration in the nature of gastric contents- inhibition of bicarbonate secretion,
decreased duodenal pH, acid secretory response to gastrin is increased.
3. Impairs the ability of drugs to lower overnight acid secreti0.n (cemetidine).
4. Impairs healing of wounds - favours ulceration of wounds leading to haemorrhage
necessitating surgery.
Let us now understand one of the most commonly observed conditions associated
with chronic oesop'hagitis i.e. gastroesophageal reflux disease (GERD).

14.2.4 Gastro Oesophageal Reflux Disease (GERD)

GERD refers to the regurgitation of acidic stomach contents illto the oesophagus. It
results in a spectrum of clinical manifestations, the most common being heartburn
and acid regurgitation. The pathologic reflux can result in a wide variety of clinical
presentations. GERD is typically chronic, and while it is generally non-progressive,
some cases are associated with the development of complications of increasing severity
and significance. Reflux occurs when the pressure inside thc stomach is higher than
that maintained by the muscles found where the stomach and oesophagus meet. This
can happen for a number of reasons, outlined in the etiology below.
Etiology
GERD may develop due to any of the following reasons:
e decreased muscle tone or abnormal relaxation of the LES,
e reduced stomach motility, allowing food to remain too long in the stomach (gastric
stasis), where
r hiatus hernia.
Episodes of reflux are triggered or worsened by a variety of factors. Sympton~snlay
be aggravated by chocolate, caffeine, alcohol and spicy foods, which stimulate acid
secretion or by fatty foods, which delay stomach emptying. Gravity works against
normal digestion and can promote reflux when the patient bends over or lies horizontally.
In addition, pregnancy or constipation may worsen GERD by increasing intra-abdominal
pressure. Secondary causes of GERD include reflux caused by acid hypersecretory
states, connective tissue disorders (scleroderma), gastric outlet obstruction as caused
by ulceration and stricture, and delayed gastric emptying due to conditions such as
gastric stasis, neuromuscular disease, idiopathic gastroparesis, pyloric dysfunction,
duodenal dysmotility, or duodenogastroesophageal bile reflux.
Most patients with complicated GERD have a hiatps hernia, which, by displacing the
'
LES segment of the distal oesophagus, both reduces LES pressure and impairs acid
clearance. We will learn about hiatus hernia latter in this section.
Let us move on to the study the signs and symptoms of GERD.
Symptoms
Most commonly, people with GERD complain of heartburn, a painful or
uncomfortable feeling in the chest, which may radiate to the back. often the
patient will recognize a pattern of symptoms related to timing, food or body position.
Heartburn may be mistaken for angina pectoris, which is pain in the chest related
to heart disease;a careful history and physical examination should distinguish between Nutritional Management
of Gastrointestinal
the two (although it is certainly possible for a patient to have both). ~ ~ m ~ are t o m ~ Diseases and Disorders
most often present after meals, especially after eating certain foods, and at night,
while lying in bed, and may be relieved temporarily by antacids or milk.
In addition to heartburn, difficult or painful swallowing, a sour taste in the mouth, and
Frequent belching are common. Less typical Ieatures include chronic cough,
hoarseness, sore throat and a sensation of fullness. Important extra-oesophageal
symptoms include laryngitis, pharyngitis, chronic sinusitis, dental erosions, asthma,
and chronic cough. These symptoms can occur as a result of gastric acid reflux into
the throat and vocal cords or down into the lungs. Acid reflux due to GERD can also
erode teeth.
Some of the common complicatioils which have .been observed among patients with
GERD are being discussed below.
Complications
Apart from the symptoms, which you have just read abovc, there are a few extra
oesophageal manifestations of GERD. Tliese include nausea and vomitiilg and erosive
changes in dental enamel. Occasionally, patients present with occult upper
gastrointestinal bleeding or with iron deficiency anaemia.
The main complicatioils include:
0 oesophagitis (inflammation of the oesophagus),
e bleeding, oesophageal erosions and ulcerations (frequent reflux of acid illto the
oesophagus), stricture (narrowing) of the intestines.
o Barrett's oesophagus (replacement of ulcerated squamous epithelium by a
metaplastic intestinal-type epitheliuin), and
o adenocarcinoma of the oesophagus. Refl~lx-inducedinjury to oesophageal tissue
can result in tissi!e destruction and the development of oesoplrageal erosions or
ulcerations.
Several long/short term complicatioils nlay arise due to GERD which may in turn
increase the frequency or severity of this disease. One of the complications of clinical
relevance is hiatus hernia. Box 14.2 presents a review on hernia.
It must be clear froin our discussioils on the etiology, symptoins and coinplicatioris on
GERD that the nutrient requirements during this condition do not vary much from that
of the RDI for a normal individual. However, as in case of oesophagitis, dietary
management particularly with respect to meal pattern is of greater significance. Let
us brief ourselves on some important aspects.
Nutritional Management and other Factors
As mentioned above the nutrient requirements remain the same as per the RDI for
most patients. It would be important to note here that if GERD has dcveloped due to
obesity, it is essential to prescribe a weight reduction diet for the patient. Nutrient
requirements may also change during certain complications such as blecding thereby
necessitating an increased intake of dietary proteins, iron, B-group vitamins and vitamin
C. Dietary pattern on the other hand needs to be altered for all patients.
Meals are the major aggravating factor of GERD symptoms, since they stimulate
the production of gastric acid available for reflux into the oesophagus. Meals eaten
within 2 to 3 bours of bedtime (which increase acid availability at night time), or
with alcohol, can predispose patients to nocturnal reflux. Dietary fat iin the duodenum
also appears to be a strong reflux trigger, in part by impairing gastric emptying. Also,
it is inappropriate to advise to reduce the fat content of their meals, as least ,with
regard to GERD symptom relief.
343
Clinical Therapeutic
Nutrition
Specific foods that have been identified as potentially aggravating factors in certain
I
r
patients include raw onions, chocolate, caffeine, peppermint, citrus juices, alcoholic
beverages, tomato products and spicy foods. Peppermint and chocolate are thought
to lower LES tone, facilitating reflux. Citrus juice, tomato juice and probably pepper 1
can irritate damaged oesophageal mucosa. Cola drinks, coffee, tea and beer can
have an acidic pH, lowering LESP to precipitate symptoms. Potential oesophageal
1i
irritants should be restricted. 1
i'

Obesity is thought to be another potential predisposing factor to gastroesophageal 1

I

reflux or GERD. Maintenance of ideal weight for age may help in reducing the ,
symptoms. !

Pregnancy is the most common condition predisposing to GERD and is generally

associated with symptomatic GERD (typically heartburn) rather than oesophagitis.
In most cases, symptoms occur for the first time during the pregnancy and subside
soon after delivery. Recurrence is also a possibility with subsequent pregnancies.
A hiatus hernia is frequently fouild among patients with GERD. You will read about
it next. Viewed as part of a GERD continuum, a hiatal hernia is another factor disrupting
the integrity of the gastroesophageal sphinctel; resulting in incrcased oesophageal
acid exposure. Smoking has been found to be related to an increased number of
'reflux events in association with deep inspiration and coughing.

I Box 14.2 1 Hiatus Hernia I

Several longlshort term complications may arise due to GERD which may in turn
increase the frequency or severity of this disease. One of the complications of
clinical relevarice is Hiatus Hernia. What is Hiatus Hernia and why does it occur?
Well, hiatus hernia refers to out pouching of a part of the stomach through several
openings of the diaphragm; the most common one being the hiatus. It occurs wheri
a portion of the upper part of the stomach at this entry point of-the oesophagus
l

protrudes through the hiatus alongside the lower portion of the oesophagus. This is
a major complication of GERD. Depending on ihe extent of herniation and placement
of stomach, it could be of two types:
1, Para Oesophageal Hernia (oesophagus is in ~lormalportion)
2. Oesophageal Hiatus Hernia (elevated oesophagus)
Food may be easily captured in the herniated area of the stomach and mixed with
acid and pepsin. Then it is regurgitated back up to the lower portion of the
oesophagus. Gastritis can occur in the herniated portion of the stomach and may
cause occult bleeding (blood loss small to be detected under microscope) and
anaemia. The problem is found in stocky built overweight middle-aged persons,
pregnant women and sometimes in persons having chronic constipation that weakens
the hiatus.
Next, we shall discuss the symptoms of hiatus hernia.
Symptoms
In most patients, no symptoms are seen. When symptoms do occur, they are:
1. discomfort after heavy meal,
2. difficulty in breathing while lying down and bending over,
3. sensation of heartburn and food sticking,
4. chronic reflux of acid ihto the oesophagus, causing injury and bleeding.
5. anaemia, or low RBC count can result, and
6. belching and hiccups
 Nutritional Mi~nogement
The dietary considerations for this condition are the same as in oesophagitis. The of Gastrointestinal
patient should be recommended to: Diseases and Disorders

e eat smaller meals

e reduce weight
e avoid lying down immediately after meals
e use antacids to relieve burning sensation
e large or sliding hernia may require surgical treatment

In this section, we learnt about oesophagitis and gastroesophgeal reflux disease. We

also read about hiatus hernia, which is a common complication and, at times a cause
of GERD. Given herewith are a few questions as part of the check your progress
exercise which will help you in quick recapitulation.
x
Check Your Progress Exercise 2
1. List a few common symptoms of oesophagitis.Write two lines about nutritional
management of chronic oesophagitis.
........................................................................................................................
........................................................................................................................
................
...............................).........*..............................................................
2. Give the causes that lead to the development of GERD. Also highlight the
points that you would keep in mind while counseling such patients.
........................................................................................................................
........................................................................................................................
..............................................................................................
.........................
3. Name the most common complications of GERD. List any five foods that
must be avoided during this disease.
......................................................*..............~..................................................
........................................................................................................................
...................:......................+.......................................................................*....

In this section we shall learn about some more diseases of the gastrointestinal tract.
Some of them would be as common as dyspepsia and gastritis which we all must have
suffered from at some point of time in our lives. Another disease which we shall
discuss thereafter is diverticulosis which is relatively less common as compared to
dyspepsia and gastritis.
14.2.5 Dyspepsia
Dyspepsia is the most frequent disorder which we all experience some time or the
other. Dyspepsia is the term given to a group of gastrointestilzal symptoms associated
with the taking of food e.g., nausea, heartburn, epigastric pain, discoinfort and
distension. It is commonly known as indigestion.
Dyspepsia may be:
I. Functional
2. Organic .

In functional there is no structural change in any part of the alimentary canal. The
symptoms may be psy'~hological and emotional in origin or due to intolerance gf a
GI -
NI .
particular food or faulty food habits. Adisease or a disorder of the digestive tract or a
Clinical Therapelltic
Nutrition cllronic disease of the kidney or even of the heart generally causes the second type
i.e, organic dyspepsia. Let us read about some of the common symptoms associated
with dyspepsia.

The symptoms are heartburn, upper abdominal discomfort (often food-related)

indigestion, bloating, fullness, nausea and anorexia. Such symptoms can also be seen
in gastroesophageal reflux, peptic ulcer disease and cancer of the stomach or pancreas
and gallstones disease. With other organs associated, many other sympto~nscan be
lloted besides a stomach upset. These are bloating (fullness of stomach), burping,
epigastric pain, gastroiiltestinal bleeding etc.
However, why does dyspepsia occur? Let us find out.
Etiology
The main etiological factor of dyspepsia is the failure of proper digestion and abso~tioll
of food in the alimentary tract and the consequences thereof. Often, dyspepsia is
caused by a stomach ulcer or acid reilux disease. If an individual has acid reflux
disease, stomach acid backs up into tlie oesophagus. This causes paill in tlle chest,
Some medicines like anti-inflammatory medicines can cause dyspepsia. Rarely,
dyspepsia is caused by stomach cancer, so you should take this problcni seriously.
Sometimes no cause of dyspepsia can be found.
Let us move on to some complications of chronic dyspepsia.

Some common complications of dyspepsia are listed below:

e Wright loss: Since eating most oftell provokes the symptoms, paticnts restrict
their food. Restriction of food and skipping of meals often causes weight loss.
Specific foods are also associated will1 synlptoins e.g. fats, vegetables, milk
restriction which can result in calciunl and energy deficiency.
e Alteredsocial l@: Most commonly, funclio~raldiscases interfere with the patie~lts'
comfort and daily activities leading lo alteration in social liEe.
We will now move over to thc dietary management of dyspepsia.
Dietary Managentent
Keeping in mirid tlie etiology, syniptoms and complications of rlyspepsia it must be
clear that treatment and management of [his disorder does not require any major I
!
changes in the nutrient intake. All we need to take care is avoidance of a high fat diet ;
Modifications in the meal pattern and elimination of certain foods may liowever prove
to be beneficial in most of the cases.
Usually, the blarid diets are prescribed in such conditions. For excessive belching
reduce the foods that are gaseous (whole pulses like rajmah, channa). Soakinglsprouting I

whole pulses may lielp in making tlie fibre softer aad hence reduce the symptoms of
belching. Vegetables likc radish, turnip, cauliflower, broccoli, beans and peas should
be avoided.
'
Intolerance to lactose (thc sugar in milk) often is blamed for dyspepsia. Si~icedyspepsia
and lactose intolerance both are common, the two conditions may coexist. In this .
situation, restricting lactose will improve tlxe symptoms of lactose intolerance, but will
not affect the symptoms of dyspepsia. If lactose is determined to bc responsible for I
some or all of the symptoms, elimination of lactose-containing foods is appropriate,
! t

The i~eslylsrylernodi/catio~sin terms of work scliedules,eating bebaviour like consuming i

meals when extremely tired, quitting alcohol and s~nokingwould lielp lo alleviate the !
symptoms of dyspepsia. The patient may be counseled with the following handy lips: . 1
i

L
 e If yoy smoke, stop smoking. Nutritional Mnnagement
of Gastrointestinal
If some foods bother your stomach, try to avoid eatingethem. Diseases and Disorders
, e
e . Gulping of food should be avoided, slow eating should be encouraged;
0 Eat food at least 2 hours before lying down.
0 Try to reduce stress.
o If you have acid reflux, don't eat right before bedtime. Raising the head of your
bed could help.
e Follow the advice of your doctor for taking antacids and anti-inflammatory
drugs.
We will discuss another common disorder of the gastrointestinal tract that is commonly
referred to as acidity by the general masses but actually means hyperacidity or gastritis.
Gastritis may be as mild to get managed by tllc help of a acid neutralizer to as severe
to result in the development of ulcers. Let us Iearn about this disorder in detail,
14.2.6 Gastritis
Gastritis is an influmrnatory lesiolz of the gastric nzucosa, (the inner lining of the
stomach).
The problem is seen in two forms:
a) Acute gastritis
b) Chronic gastritis
Let us review them.
A . Acute Gastritis
It is a sudden inflammatioii of tlie liniiig of the stomach. It occurs mainly due to
overeating, ovenlse of alcohol, tobacco, chronic or excessive dose of aspirin, anti-
inflarnrnat~r~"dn~~s, increased production of bile acids, trauma, surgery, shock, fever,
jaundice, renal failure, bums, radiation therapy, H. Pylori infeclion etc. The synlptoms
o f the disorder are nausea, vomiting, malaise, anorexia, headache, hemorrhage and
pain in the upper abdomen, dark stools, hiccups, tachycardia, rapid pulse and low
blood pressure. Its complication involves severe blood loss, with blood suddenly ffowing
into the region known as liypercmia, inflammatioil and even exudation. In severe
cases there may be erosion of localized areas and even bleeding. The major symptoms
are mentioned below.
Symptoms
Anorexia, epigastric discomfort, heatburn and severe vomiting, pain in upper abdomen,
headache and even bleeding.
L e t us now explore the causalive factors of acute gastritis.

Etiology
Some most frequently associated risk factors for gastritis include: .
r Faulty dietary habits like overeating and taking highly seasoned foods.
Bacterial toxins (Salmonella, Staphylococcus), metabolic toxins (uremia) and
Helicobacter pylori infection.
0 Excessive use of alcohol, drugs (aspirin, anti-inflammatory).
e ' Exposure of gastric rnucosa to irradiation.
o Increased production of bile salts.
- e Burns and renal failure.
 I
Clinical Therapeutic We will now learn about another form of gastritis i.e., chronic gastritis.
Nutrition
B. Chronic Gastritis
It precedes development of organic gastric lesion, or tissue damage. Recurrent
inflammation leads to changes in enzyme activity of gastric mucosal cells. Complete
atrophy results in lack of absorption of vitamin B,, (Pernicious anaemia). The chronic
gastritis is clinically more important than the acute gastritis.
Gastroscopic observation shows 3 types of chronic gastritis:
1. Superficial gastritis: gastric mucosa is red, oedematous, covered with adherent
mucous, mucous haemorrhage and small erosions are frequently seen.
2. Atrophic gastritis: the mucous lining becomes thinner, gray or grayish green
haemorrhage mucosa irregularly distributed.
3. Hypertrophicgastritis: presents a dull spongy nodular appearance of the rnucosa,
the edges are irregular thickened with nodular haemol-rhages or superficial
haemorrhages.
Symptoms
These include anorexia, chronic fatigue, and feeling of fullness, belching, vague
epigastric pain, nausea and vomiting and passage of black tarry stools.
Etiology
They are same as acute. Generally acute gastritis if well treated gets healed in 3-4
days, however if untreated can progress to chronic gastritis.
We will now discuss about the dietary management of gastritis.
Dietary Management
Prompt medical care is successful in the management of an acute attack of gastritis
only if it is accompanied by efficient and judicious nutritional care. During an acute
attack, meeting the nutrient requirements is not of prime importance. Depending on
the seriousness of the patient thc food maybe with held for 24-48 hours. Fluids maybe
given intravenously if needed. Liquid foods are given as per patients tolerance level.
The amount of food and number of feedings are adjusted according to the patients
tolerance, until a full regular diet is achieved. Always follow a progressive diet i.e,
liquid to semi solid to solid as when the symptoms improve. The diet should contain
less fat and must be bland. Many nutritional deficiencies occur in this disorder especialiy
during chronic gastritis e.g. vitamin B,, , iron, and other vitamin deficiencies.
The nutritional treatment must follow general principles of soft diet. The diet should be
adequate in.calories and nutrients. There must be small feedings at regular intervals.
Avoid gastric irritants and highly seasoned foods (onion garlic, chilli, caffeine, cola and
alcohol). Excess water or other liquids with meals may cause distention.
The dietary guidelines are enumerated herewith:
Energy: Give adequate calories through frequent feedings or else proteins would be
utilized for energy of repair work.
Proteirzs: Give adequate proteins (lglkg body weight) through skimmed milk, egg,
steamed fish, chicken, minced meat etc.
Carbohydrates: Simple easy to digest carbohydrates should be included in soft well
cooked form. Thus, semolina, rice, maida, sago, arrowroot etc. may be included whereas
whole cereals and millets should particularly be avoided if gastritis has caused damage
to the mucosa.
Fiber: Eating a diet high in fibre reduces the risk of developing the ulcers and also
speeds up the healing process. However, ca at fibre rich foads
(soluble fibre) are always included in a soft cooked form. Raw foods, seeds etc Nutritional Management
o f Gastrointestinal
should be completely avoided in the diet. While soluble fibre is safer for the patient as Diseases nnd Disorders
compared to insoluble fibre (husk/bran of cereals and pulses, peels of fruits and
vegetables).
Vitamin B,,: Supplementation with vitamin B,, helps to treat pernicious anaemia and
H. pylori infection. Its sources include fish, dairy products, organ meats, eggs, beef
and pork.
Vitamin A: A combination of vitamin A (found in many green and orange coloured
fruits and vegetables) and antacids is helpful in healing ulcers.
Vitamin C: A high dose of vitamin C treatment is effective in treating H. pylori
infection. ,
It has been observed that diets high in soluble fibre, carotenoids, and antioxidants
reduce the risk of developing gastritis.
Abrief list of foods to be avoided is given below in Table 14.8.
Table 14.8: Foods/substances to be avoided

Coffee - with and without caffeine Alcohol

Tobacco/Smoking Carbonated beverages
Fruit juices with citric acid Iligh fat foods
Mint and vinegar Milk
Spices Pepper, onion and garlic

So far we have discussed about dyspepsia and gastritis in this section. Next, we shall
discuss about yet another disorder of the gastrointestinal tract viz., diverticulosis.
14.2.7 Diverticular Disease
A common disorder of the large bowel, diverticulosis, is an early stage of the disease.
It can be identified in 15% of the people over the age of 50 years. It is a conditiorz of
abnormal pouches in portions of the colon (small mucosal sacs called diverticula
protrude through the intestinal wall). It has a history of co~zstipation,which results in
an increased intracolonic pressure, straining to pass hard Iaeces and rupturing of the
bowel wall at weak points to form small pockets, which are called diverticuli.
Inflammation and bacterial overgrowth in diverticuli may result in diarrhoea. When
the pouches become inflamed (often as a result of bacterial infection), symptoms
such as cramping pains, fever, and nausea can result. Such an infection, called as
diverticulitis,is potentially life threatening and requires immediate medical intervention
due to complications like ulceration or perforation or profuse bleeding.
Let us now discuss about the symptoms of diverticulosis.
Symptoms
Depending on the site of diverticula the symbtoms may appear. It occurs most often
in sigmoid colon and frequency increases with age. It is more common in the western
world where the fibre intake is significantly lower. Often diverticula (pouches) cause
no symptoms, except the person may experience some irregularities in bowel habits.
When there is an active infection, there may also be fever, chills, nausea, and vomiting,
changes in bowel habits, rectal bleeding and constipation.
We will now understand the causes of this disease.
Etiology
The causes of diverticular disease are not certain, but several factors may contribute
to changes in the wall of the colon. These include:
Clinical Therapeutic @ aging,
Nutrition
4 the movement of waste through the colon,
e changes in intestinal pressure,
e a low-fiber diet, and
e anatomic defects.
The many complications of the disease include the'following conditions:
e A perforation (hole) in the intestine leading to peritonitis, sepsis, and even shock
e An abscess (gocket of pus)
o Fistulas, which may also lead to sepsis
o Blacked intestine
e Rectal bleeding
It must be clear to you that diverticulosis occurs to a great extent due to faulty dietary
habits and that several complications listed above may necessilate a surgical procedure.
It is thus in~portantto provide good nutritiol~alcare to the patient. We will now highlight
some important aspects of the dietary management.
Dietary Mar~agemeltl
Most of the diseases which we have discussed so far do not fequirc any major changes
in the nutrient intake. The patients generally benefit from a high fibre diet. Hence, a
greater amount of bulk or fiber in the diet will promotc soft, bulky stools that pass
more swiftly and are defecated more easily. Also, the intra lurninal pressure generated
in the lower colon would be less and the fewer diverticuli will be formed. An increased
intake of fluid must be emphasized. A decreased intake of fat in the die1 may be
suggested.
For mild symptoms, a clear liquid diet is recommended. More serious cases may
require bospitalizatio~l,intravenous feeding to rest the bowel, and intravenousantibiotics.
Eating a high-fiber diet and taking psyllium supplement are beneficial. Maintain overall
nutrition. Some important aspects, which need to be taken care of, include:
1. High-fiber Diet:Population based studies suggest that eating a high-fibcr diet
helps prevent diverticular disease and otlter gastrointestinal disorders. A review of
such studies reports that vegetarians are less likely to have diverticular disease, most
likely because they tend to eat more fiber. Lower intake of protcin such as red meat
and tnilkproducts can reduce the risk of diverticulosis. Fibre supplcnlenls could improve
I
constipation. One can give 1-2 tablespoons of wheat bran daily or isabgol. Also,
remember that an amount of 15-20 g/day of crude fibre and 30-60 g/day of dietary
fibre should be given.
I

2. Glutamine:W i l e specific nutrients that may have an impact on diverticuladisease

have not been studied as thoroughly as the high-fiber diet, glutamine supplements are !
beneficial as they strengthen and protect the colon wall. 1I I

3. Omega-3 Essentiat Fatty Acids: Omega-3 essential fatty acids found in flax and /
cold-water fish help fight inflammation. For a condition such as diverticulitis,itma~ j
be wise to eat a diet. rich in omega-3 fatty acids. This, type of diet may also help
I
1
prevent colon cancer.
4. Lifestyle modifications: Obesity may be associated with illcreased severity of
diverticular disease. Hence, maintaining ideal weight for age is beneficial from ail
health aspects. Physical activity like jogging and running are beneficial. fixe~cj
rc.(luces the symptoms of this disorder.
 The prevention strategy for the disease involves the following: Nutritional Management
of Gastrointestinal
a - Eat a high-fiber diet (more than 15 glday of crude fiber). This helps the stools to Diseases and Disorders
, . move smoothly through the intestines maintaining proper pressure in the colon.
Fibre shoulbbe included when the inflammation subsides.
e If diverticula are present, avoid foods such as seeds that may block the opening
of a diverticulum and lead to inflammation and infection.
e Exercise regularly to decrease the occurrence of symptoms.
The management goals discussed above are basic to prevention of diverticulitis.
However, diet therapy during diverticulitis may be limited to clear liquids progressiilg
to full liquids to normal diet. Increase the fibre only when the inflammation subsides.
So please note during a bout of diverticulitis the patient should be given a low fibre
soft bland diet. Severe diverticulitis is treated by surgical methods. In such situations
patient should be prepared for an elective surgery. You may recapitulate about dietary
management pre and post operatively by reading the section on surgery in Unit 5 of
this manual.
We now need to attempt the check your progress exercise 3 given herewith' to
recapitulate what we have learnt so far.

Check Your Progress Exercise 3

1. Differentiate between the following:
a) Acute and chronic gastritis
..........................................................................................................
...........................................................................................................
............................................................................................................
b) ~iverticulosisand Diverticulitis
...........................................................................................................
...........................................................................................................
I
.........................................
,'

2. Discuss the dietary principles involved in the management of dyspepsia.

, .
...................I.............................*...................................................................

.....................................................................................................................
3. Discuss the diet therapy for the treatment of diverticulosis.

..............................,..........,,...,....,....,......,.....................+.~~...........................
So far we have learnt about a wide spectrum of diseases of the gastrointestinal tract
which if .managed efficiently do not resuit in the development of any serious
consequences. In this section we shall discuss about another comrnoil disorder of the
GI tract viz, peptic ulcer. Let us understand it in a Iittle more detail. 351
Clinienl Therapeutic 14.2.8 Peptic Ulcer
Nutrition
Peptic ulcers are one of the more serious forms of gastrointestinal disorders of the
gastrointestinal tract particularly the stomach. The prevalence of ulcers has been
increasing over the past few years owing to massive changes in the dietary habits and
life style practices. We shall learn about these factors in detail in a short while from
,low. However, let us first understand about ulcers.

The term peptic ulcer is used to describe any localized erosion or disintegratioll of
tile mucosal lining that comes in contact with gastricjuice. Mostly, the oesophagus,
stomach and duodenum lining is affected and cause stomach and duodenal ulcers
(peptic ulcers). The disintegration of tissues can also result in necrosis (death of cells/
tissues). The mucosa of the stomach and the duodenum is normally protected from
proteolytic action of gastric juice by the mucosal barrier. Thus, the areas affected in
peptic ulcer (due to erosion) can be:
1. lower part of the oesophagus.
2, slomach (lesser curvature - antrurn, where the food stays for a longer time),
3. first portion of the duodenum which is also called duodenal bulb.

We read a little while ago about the relation of dietary errors and lifestyle practices
wit]) respect to the development of ulcers. In the subsecluent Lexl we shall learn about
the causative factors for the ulcers.

Etiology

Peptic ulcer results when the neural and hormonal abilormality disrupts the factors
that normally maintain rnucosal integrity and permit proteolylic and acidic erosion of
the lnucosal tissue.

Let us learn about the factors, which damage or protect the mucosa. These are
summarized in Table 14.9.
Table 14.9: Factors affecting mucosa
d

Destructive Factors Defensive Factors

Hydrochloric acid Epithelial cells barrier

Pepsin (Proleolytic enzyme) Mucous

Psychological factors (slress Gastric blood flow

and anxiety)

Gastric irritants (alcohol, caffeine, Regillation of ticid sccrction

excess tea, meat extracts and spices)

Nicotine and Tobacco Ability of the body to I.egcner:lte

the cclls
Anti inflammatory drugs1 Analgesics
1

Duodenal ulcers occur in a 3 crn space between the duodcnal bulb in an area '

immediately below the pylorus where the gastric juices are not ncutrrrlized. It can be
attributed to a number of factors:
0 H,pylori infection is strongly implicated which has a damaging effect on the
rnucosal defense thereby increasing the vulnerability to ulceration,
e Increased number of parietal cells or acid secretion.
e Increased gastric emptying rates. t I
 e Reduced ability of the duodenum to hand.le an acid load Nutritional Management
of Gastrointestinal
0 Stress (physical and mental) Diseases and Disorders

0 Excessive use of non steroidal anti inflammatory drugs (NSAID) and

corticosteroids.
Gastric ulcers occur in the lesser curvature of the antrum of stomach. A gastric
ulcer appears to be caused by reflux of bile and factors that disrupt tlie mucosal
barrier permitting the hydrogen ions to diffuse into the mucosal tissue where they
cause damage. The damage causes cell destruction and subsequent ulceration (due
to defect in pyloric sphincter). NSAID dramatically increase the risk of ulcers and is
related to tlie systemic inhibition of prostaglandin production. Thus results in impaired
defense against acidity by the gastric mucosa. Another pathogenetic factor is H.
pylori infection and the resulting impaired mucosal defense. Let us have a look at the
pathogenetic factors in the development of peptic ulcer disease as given in Table
14.10.
Table 14.10: Pathogenic factors
Gastric Ulcer Duodenal Ulcer
Seen at the back of the stomach Appears within 3 cms of the pyloris
Abnormal pyloric function Increased acid secretory capacity
Duodeiiogastric reflux Increased basal acid secretion
Defective gastric mucosal defenses Increased parietal cell mass and sensitivity
Decreased mucosal blood flow, Prolonged meal secretory response
Prostaglandin production,
Bicarbonate production, Gel layer
Abnormal gastric emptying
Abi~ormalduodenal mucosal defenses
Decreased bicarbonate secretion

Peptic ulcers if not managed properly can result in serious consequences which can
even be life threatening. The complications involved in this disease are:

Gastrointestinal bleeding
Intestinal perforation
Peritonitis (inflammation of the lining of abdominal cavity)
Anaemia
Intestinal narrowing and obstruction
e Shock

Following symptoms present a pectic ulcer picture

Symptoms
Increased gastric tone and painful hunger contraction when stomach is empty. Hunger
contraction 1-3 hours after meals is the main complaint. Pain is often described as
dull, piercing, burning and gnawing and is usually relieved by taking food. Frequent
vomiting sometimes with blood leads to loss of weight and anaemia.
'.Ulcers develop gradually, over a period of several months to several years. Majority
of the patients are undernourished and have depleted reserves of several nutrients.
Pain associated with coilsumption of food, vomiting and anaemia due to haemorrhages/
Clinical Therapeutic bleeding resul t in reduced food intake partially due to anorexia. This is a major reason
Nutrition
for weight loss. Maintenance of an optimum nutritional status to promote healing and
proper rehabilitation is therefore the prime objective of the dietician. We shall now
discuss sonie of the important treatment and management aspects in detail.
Medical and ~tttritionalManagement
To provide physiological rest and support tissue healing, treatment should be based
on providing rest to the affected area. Judicious use of drug therapy and dietary
modifications are the key to tlie mailagcinent of pectic ulcers. Recent development of
new drugs like Cimetidine and Ranitidine (Hz blockers) have revolutionized the dietary
regimes used earlier such as the Sippy's diet, He~zhnrtzand Meden Gratcht diet
which were based on milk and contained inadequate protein and protective foods
leading to nutritional deficiencies. Today the new drugs mentioned above are better
than earlicr drugs. Use of these drugs allow a liberal approach for food choices and
the patient is able to restore good nutritional status. It is well known now that a good
dietary regime and nutritional status can help in reducing the impact of tlie disease on
tile overall health and well being of the patient.
Thus, the objectives of the nutritional care process should include the following points:
1. Restoration of good nutritional slatus with dietary modifications and counseling.
2. Alleviate the symptoms.
3. Neutralize acids.
4. Reduce acid secretion.
5. Preservation of epithelial resistiince to the destructive action of gastric juice.
Let us now move on to understand the dietary approach. We shall begin with the
nutrient requirements of the patients. However before we talk about the key nutrient
intake let us brief ourselves on the energy intake.
Energy: The energy intake should be such as to help tlie patient in achieving and
maintaining an ideal body weight. An adequate energy intake is a must to prevent
subsequent weight Ioss and spare the proteins for healing of ulcers. You can calculate
the energy requirements on the basis of patients height, activity arid gender as has
been discussed earlier in Unit 10 on Weight Mmagement.
We shall now understand about the requirement for other nutrients.
Proteks: Ulcer is a form of wound which if not healed on time call get perforated and
bleed. Adequate protein intake ensures synthesis of new tissues essential for healing.
Normal milk protein is valued for their buffering aclion but it is supposed to provide
temporary relief because the products of protein digestion (amino acid and polypeptides)
reach tlie antrum and they stirnulate the secretion of gastrin and gastric acid, Milk
neutralizes gastric acidity only for 20 and 60 minutes after its ingestion and the pH
reverts back to the basal levels. Current stt~diesindicate that a diet with high milk
content^has an adverse effect on the healing rate of ulcer because of high calcium
content. This, in turn, may arso stimulate excess acid production. Thus, the use of milk
should be limited and used for symptomatic relief for a short duration only. Restricte'd
intake of milk gives relief for a short period as it contains the prostaglandin PGE2-a
protective agent against stress induced ulcers.
Proteins from cottage cheese, egg, chickcn and fish in adequate amounts is beneficial
for regeneration of cells. Protein supplemenls may be used and the protein content
can be increased by 10-15 g /day above the RDA.
Fats: These delay the gastric emptying. The products of fat digestioii in tlie small
intestine stimulate entrogastrone, which inhibits gastric juice secretion. Recently paly-
unsaturated fatty acids such as linoleic and eicosapentanoic acid have been found to
be effective against duodenal ulcer by inhibiting in vitro growth of H. Pylroi. Around Nl~tritional
of Gastrointestinal
Management
25-30 g of visible fat may be incorporated in the daily dietaries. Fats should preferably Diseases and Disorders
be emulsified for easier digestion. Fried foods must be avoided as they cause digestive ,
problems.
Q
Carbohydrates:These should provide around 55 to 65% of the daily intak . Emphasis
- J
should be laid on the consumption of 60th simple and complex carbohy rates but in
+oft well cobked form. Soluble fibre is more beneficial as cornparka (0 inso?uble fibre
in view of its physical attributes. The presence of fibre in the diet is advocated because
it delays gastric emptying time and hence prevents the mucosal damage by acidic
gastric juice.
Other important factors which need to be considered have been discussed below:
pH of food: It has.a little therapeutic importance except for patients with lesions in
the mouth or oesophagus. Most f o d s are considerably less acidic than the normal
gastric pH of 1.G. The pH of both orange juice and grapefruit is 3.2 to 3.6. Thus on
the basis of their immediate acidity, acidic fruit juices should be acceptable compoilents
of the diet for the patients with ulcers. Fruits, in general, are related to an alkaline ash
diet. If they are not well tolerated by some individuals, avoid them.
Foods that damage GI ntucosa: A number of spices, herbs and other condiments
have been found to have little or po irritating effccl on the majority of persons with
ulcers. The sight, smell and taste of most food nonnally initiates the cephalic phase of
gastric secretion but no significant change in gastric pH was noted wit11 any particular
items except in case of alcohol, caffeine, black pepper and meat extracts.
Alcohol: Alcohol is known to cause damage to intestinal mucosa independent of
gastric acid content. TIlus high amounts are not advised.
,
Cigarette smoking: Smoking of cigarette causes an adverse effect because of the
presence of nicotine which causes pyloric incompetence, increased reflux of duode11aI
juice into the stomach, increased gastric acid secretion by favouring gastrin secretion,
decrease pancreatic biocarbonate synthesis. Stopping smoking is highly recommended
for peptic ulcer patients.
Food texture: Recent studies indicate that strict omission of fibre is of no help on a
peptic ulcer patient. The recurrence of peptic ulcer was observed to be much lower in
individualson high soluble fibre diet. This has also been attributed to increased salivation
due to increased chewing which has shown to have a buffering effect.
Gas formers: Omitting a number of foods routinely because of their repulation of
being gas formers has also been questioned. Clinical observations have show11 that
tolerancefor avariety of standard foods is higl~lyindividual. Puilses, soyabean, cabbage, .
cauliflower, onions, peas, apple, watermelon are some of the foods identified.
Current approach of liberal managenlent in peptic ulcer medical nutrition therapy
postulates: It is the individual patient who is the f'ucus of treatment tlzz~streat the
patient as a whole and not merely treat the hole. Remember the latesl drug therapy
is essential.
The basic principles involved ark:
The individual must be treal'ed as such and for that careful initial history - daily
living sitpation, attitudes; food reactions, tolerances milst be kept in mind. This
would serve as a basis for fdrmul&ing the nutritional programmg.
The activity of the patient's ulcer will influence the dietary management. During
period of active ulceration more acute modified treatment may be needed to
control acidity and initiate healing. However when pain disappears feedings are
liberalized according to the individual's tolerance levels and desires using a variety
of foods.
355
Clinicnl Therapeutic
Nutrition
Let us move on to the different stages involved in feeding the patient. 1
Stage I : It is characterized by haematemesis (vomiting of blood which may be derived
from mouth, stomach, oesophagus or duodenum or melena (passage of black tarry
stools indicative of GI bleeding). Initially, for bleeding ulcer, if the patient is extremely
nauseated or vomiting, he must be kept on NBM (nil by mouth). This is followed by an
hourly feeding to begin with. Milk and cream 100 ghour (especially in stages of acute
pain) followed by small feedings of easily digestible foods like soft cooked eggs,
custards, refined flour products, cottage chkese, low fibre vegetables like gourds,
clear soup with no seasoning and herbs, soft over ripe fruit whips and light desserts.
The diets must be fed orally, and of liquid I semi liquid I soft consistency, which is easy
to digest.
Stage II : The characteristics of this stage involves -
a marked recovery from pain.
a G meal pattern followed
e light, bland, low fibre diet
e mechanical/thermal, chemical irritation of gastric mucosa to be avoided
a late night feeding avoided, as the end products of digestion may cause the epigastric
pain.
Stage111: In this stage, following characteristics are involved -
e number of feeds reduced to 3-4, as recent studies show no benefit in terms of
gastric acid secretion
a discharged from hospital
e increased amount / feed
Stage N : This stage involves -
a liberalizing the diet depending on the patient's individual tolerance and schedule.
a ensuring optimum intake of calorie, protein, fats, vitamins and minerals.
relaxed atmosphere on eating.
e lifestyle change (stress, alcohol, caffeine, smoking )
Remember to recommend:
1. More than three regular meals to be eaten daily.
2. Eat small meals to avoid stomach distention.
3. Avoid drinking excess of coffee and alcohol.
4. Cut down on or quit smoking cigarettes
5. Avoid using large amount of aspirin, Non Steroidal Anti Inflammatory Drugs
(NSAIDs) and other drugs known to damage the stomach lining.
6. Avoid foods or drinks that cause discomfort. Reduce spices especially black and
red pepper. Increase n-3 and n-6 fatty acid consumption.
7. Eat meals in as relaxed atmosphere as much as possible.
8. Take antacids 1 and 3 hours after meals and before bedtime respectively.
9. Take adequate rest, relaxation and sleep.
10. Take the necessary drugs advised by your doctor, for neutralizing the acid, reducing
acid secretion or preservation of the epithelial tissue or an antibiotic combination
for eradication of the H.pylori infection.
This section dealt wit11 one of the most serious forms of gastrointestinal disorder Nutritional Management
of Gastrointestinal
wherein diet plays an important role ui the causation, treatment, as well as, management Diseases and Disorders
of the disease. We hope that you will benefit from the discussion above. Before we
proceed further try to attempt the check your progress exercise 4.

Check Your Progress Exercise 4

1. What is the difference between gastric and duodenal ulcer?
......................................................................................................................
......................................................................................................................
.....................1..1.....................................................*..............+..........................
2. What is the recent highlight in the etiology of peptic ulcer?
......................................................................................................................
......................................................................................................................
......................................................................................................................
3. Why is the current management approach of peptic ulcer called liberalized?
.......................................................................................................................
......................................I...................*...............*...........................................

......................................................................................................................
We have learnt about a host of diseases in the previous sections. In our last section on
GI disorders we will brief ourselves on certain common malabsorption syndromes
viz., celiac disease, steatorrhoea,lactose intolerance and inflammatory bowel disease.
Some of these disorders are diseases in itself while others are symptoms of another
underlying disease. We shall begin our section with an overview on rnalabsorption
syndromes.
14.2.9 Malabsorption Syndrome
Did you know that a major part of tl~eabsorption of nutrients takes place in the small
intestine and the set of enzymes involved in this process are called disaccharidases.
In some conditions either genetically, or due to some intestii~aldamage tliere appears
to be a deficiency of some of these enzymes, which in turn, leads to the malabsorption
of some of the nutrients precipitating symptoms of diarrhoea, distention and abdominal
discomfort and steatorrhoea (fat in stools).
These conditions are together referred to as Malabsorption Sytzdromes. The term
'malabsorption syndrome', as you have learnt earlier also, is used to describe deficient
absorption to a variable degree of a number of substances such as fats, proteins,
carbohydrates, vitamins, minerals and water.
Before we understand about this syndrome, let us look at the following case study.
Anuradha, a teenager, presents to the physician's office wit11 a two-year history of
intermittent diarrhoea. Her reports reveal a past history of anaemia, anorexia and
minor abdominal pain. Her weight has been the same for 2 years now. Her mother
has attributed this to her having n "rough time in school". Her mother also questions
whether the symptoms could be related to a recent move from their home. She has
not yet reached menarche, A diet history suggests a normal diet with adequate iron
intake. Can you guess what she suffers from and what could be the causative factors
leading to such a condition?
Well, you have guessed it right. She suffers from 'Malabsorption syndrome'. Let us
proceed further and get to know more about it. We shall begin with the etiology.
Clinical Therapeutic Etiology
Nutrition
The causes cited for malabsorption can be associated with a number of diseases.
Many of these diseases you may not know presently but they will unfold as you read
further. These are tabulated in Table 14.11.

Table 14.11: Principal causes of malabsorption

- -

Anatomical or Surgical : Surgical resection, Fistula, Gastric surgery, Blind loop

and stricture and Diverticulosis
Enzyme deficiencies : Pancreatic disease, Biliary obstruction and
Disaccharidase deficiency
Mucosal defects : Celiac disease, Tropical Sprue, Crohn's disease and
Radiation
Systemic causes : Scleroderma, Diabetes, Lymphoma, Thyroid disease and
Severe skin disorders
Drugs : Cholestyrainine, Antibiotics, excess laxatives
Infections : Giardia and parasitic infestation, tuberculosis and
bacterial overgrowth.

Malabsorption ciln thus occur due to a host of reasons. However, what are the
symptoms that would have an impact on the nutrition and health status of thc patient
and hence his dietary intake. Let us read and find out next.
Symptorris
The most common symptoms are weakness, lassitude and marked weight loss.
Steatorrhoea (excess fat in stools), anaemia and chronic ill health. Diarrlloea is the
most cornmoll GI tract disturbance along with flatulence, mild abdominal pain, amrexia,
nausea and vomiting. Nutritional deficiency comnlonly occurs and may manifest itself
as glossitis, tetany, bone pain and paraesthesia and convulsions. The objective evidence
of these are scenas smooth tongue, oedema, dry skin, bleeding, pigmentation, dermatitis,
peripheral neuropathy and proximal muscle atrophy.
Let us now discuss a few important conditions grouped collectively under the tcrril of
malabsorption syndrome. These are:
Celiac disease
0 Tropical spnle
o Steatorrhoea
o Lactose intolerance
o Infla~nmatorybowel syndrome,
o Ulcerative colitis
e Shoa bowel syildrome
We shall brief ourselves on some of these disorders. Let us begin with celiac disease,

14.2.9.1 Celiac Disease I

Gluten-sensitive enteropathy or, as it is more commonly called, celiac clisease, is an

autoirninune inflammatory disease of the small intestine. It is precipitated by the
ingestion of gluten, a component of wheat protein-gliadin, in genetically susceptible
persons. A defect in the enzyme system that.splits this protein fraction along with
atrophy of jejunal mucosa may be the specific cause for celiac disease. It usually ' .
develops within the first three years of life.
 .Nutritional Management
of Gastrointestinal
Disenses and Disorders
Child with celiac's disease fails to thrive, losses appetite and has apotbelly. Stools are
large, pale and offensive due to the presence of fat in the form of fatty acids. Pu~aemia
is present with symptoms of paleness, fatigue, tachycardia (fast pulse). The microscopic
section of the villi show flattening of the villi. When gluten-free foods are given there
is a dramatic recovery in the symptoms and the reversal of villi to normal growth.
Celiac disease has also been noted to be associated with numerous neurologicdisorders,
includiilg epilepsy, cerebral calcifications, and peripheral neuropathy. The list of
symptoms as mentioned in various sources for celiac disease includes:
@ Dige,~tivesynzptoms - diarrhoea, abdominal pain, abdominal bloating, pale stool,
foul-smelling stool, loose stool, flatulence.
Behavioural symptoms - there are also several other symptoms such as
irritability - especially in children, depression and behaviour changes in adults.
0 Inadequate nutrition symptoms - because celiac causes malabsorption, the
body does not get enough nutrients, leading to symptoms such as weight loss,
delayed growth, failure to thrive (infants), missed rnei~strualperiods, anaemia
and fatigue. Anaemia is the most common laboratory n~anifestationof celiac
disease. Iron is absorbed in the proximal small intestine, where celiac
manifestations are most prominent; hence, iron malabsorption is common. Less
commonly, vitamin B,, deficiency, folale de.ficiency, or both inay be present.
@ Gas formation, bone pain, joint pain, seizures and inuscle cramps.
0 Non-specific symptoms - some people get mild but unclear sy~nptomssuch as,
tingling sensation, numbness (due to damage of nerves in the legs), painful skin
rash, tooth discolouration and enamel loss.
Some important complications are enumerated herewith:
Complications
Patients with severe form of celiac's disease for long period are at risk for several
complicationsmainly due to nutrient absorption problems leading to malnutrition. These
complicationsare highlighted in Table 14.12:
Table 14.12: Complications due to Celiac's disease
Congenital defects - in babies born to celiac mothers Miscarriage
Osteoporosis (weak and brittle bones)
Lymphoma (can develop in the intestine) Stunted growth in children
Seizures or convulsions Anaemia
Dietary management of celiac disease is of crucial significance as it is related not
only to the frequency and severity of morbidities but also mortality of the patient,
usually a child. Wewill brief oqrselves on the dietary management next. Based on the
cause, symptoms and complications the major objectives of dietary management iilclude
the following:
e Providing a nutritionally adequate diet
, e Strict restriction of gluten foods
e Vitamin and mineral supplen~entation
In the sibsequent text we will learn about the dietary management of celiac disease.
Dietary Recommendations
The only dietary treatment for celiac disease is to follow a gluten-free diet. For most +

such a diet improves symptoms, heals intestinal damage, and prevents further damage.
Clinical Therapeutic Improvements begin within days of starting the diet, intestines are healed within 3-6
Nutrition
months for children but in adults it could take upto 2 years. The gluten-free diet is a
lifetime requirement. Eating any gluten, no matter how small an amount, can damage
the intestine. A small percentage of people with celiac disease do not improve on the
gluten-free diet because the inlestines are severely damaged. Such patients must be
evaluated for any complications. In such cases there is need for intravenous nutrition
supplements.
m a t is a gluten-free diet? Let us read and find out. The Gluten-Free Diet, as we
have learnt earlier also, is a diet that contains no gluterz. Foods like wheat) rye,
barley, and possibly oats must be avoided. The gluten-free diet is complicated. It
requires a completely new approach to eating that affects a person's entire life. Products
like bread biscuits, breakfast cereals, poories, paranthas, chapathis, macaroni, noodles
and other pasta preparations have to be totally eliminated. Eating out can be a challenge
as the person with celiac disease learns to scrutinize the menu for foods with gluten
and question the waiter or chef about possible hidden sources of gluten. What are
these hidden sources? Well, these hidden sources include additives, preservatives,
and stabilizers found in processed food, medicines, and mouthwashes. Despite tliesc
restrictions, people with celiac disease can eat a well-balanced diet with a variety of
foods.
Table 1.4.13gives an idea of the gluten sources to be avoided by the subject, the food
that can be taken are from tlie non-gluten sources.
Table 14.13: Gluten and Non-gluten sources
Gluten Sources Non-gluten Sources
Beverages: cereal beverages, . Coffee, tea, chocolate drinks (pure
ovaltine, beer and ale cocoa) wine
Milk beverages that contain malt Whole, toned, skim milk and buttermilk
Meat and rneat products: Pure meats, lish, poultry, eggs, cottage
Breaded meats commercially available cheese, peanut butter
Fats and oils: Buttcr fats and oils
Commercial gravies, white sauce
and cream sauces
Cereal and cereal products: Rice, potato flour and soya flour,
Bread, wheat, oals, rye, malt, pastry pure corn, popcorn.
flour (maida), bran, barley, wafers,
pasta.
Vegetables: All fresh vegetables, canned and pured.
Breaded vegetables with any of the
sauces, white sauces etc.
Fruits: All fresh fruits
Any fillings e.g. pies etc.
Snacks: Milk base sweets (pure) without addition
Pastries, patties, pizzas, samosas, of ally cereal products.
mathris etc.
Let us have a look at few of the tips whicli patients can follow and enjoy their meab
and at the same time, avoid any possible nutritioilal deficiency.
e Iron deficiency should be treated with supplemental iron.
e Osteoporosis should be treated with calcium and vitamin D supplements.
e Depending on individual factors, patients with gluten-sensitive enteropathy may
need to take a multivitamin supplement along with iron, calcium, magnesium,
zinc, selenium, vitamin D, or other nutrients,
 e Check for commercial gluten-free products, including breads, cookies, chips, Nutritional M~nagement
of Gastrointestinal
and breakfast cereals that may be available in India. Disenscs and Disorders

e Meats, vegetables, fruit, and most dairy products are free of gluten.

Another common malabsorption syndrome listed in the section 14.8 seatorrhoea

which is discussed below.

1 '14.2.9.2 Steatorrhoea
Steatorrhoea is a symptom of the disorders of fat metabolism and malabsorptioll
syndrome and can be defined as n condition of foul-smelling bulky faces. It is
suspected when the patient passes large, "greasy", and foul-smelling stools. Both
digestive and absorptive disorders can cause steatorrhoea. Digestive disorders
affect the production and release of the enzyme lipase from the pancreds, or bile
from the liver, which are substances that aid digestion of fats. Absorptive disorders
disturb the absoiptive and enzyme functions of the intestine. Any condition that causes
malabsorption or maldigestion is also associated, with increased faecal fat
(steatorrhoea). As an example, children with cystic fibrosis (hereditary disease) have
mucous plugs that block the pancreatic ducts. l'he absence or significant decrease of
the pancreatic enzymes; amylase, lipase, trypsin, and chymotrypsin limits fat, proteiil
and carbohydrate digestion, resulting in steatorrhoea due to fat malabsorption.

A predominant feature is delayed and defective absorption of fat, which results in

bulky stools containing large quantities of fat (known as steatorrhoea). The severity
of steatorrhoea depends on the qualltity of frtt in the diet. Besides the absorptioil of
water, electrolytes, vitamins and minerals is also impaired. These defects are due to
flattening of the villi in the jejunum (a part of the small intestine). Remission and
relapses are common if proper medical and dietary care is not provided. The rnajor
reasons attributable to steatorrhoea have been enumerated below.

I The list of possible underlying causes of steatorrhoea includes:

e Malabsorption

1
(
e
e
~alabiorptianof fats in small intestine

Pancreatitis

( e Celiac disease

The list of symptoms includes:

a Bulky, pale, loose, greasy and foul smelling stools.
e Anorexia, feeling of fullness, pain i11 abdomen.

The major points that we must remember while planning diets for patients suffering
from steatorrhoea are highlighted below for a quick reference.
Nutritional Management

The nutritional.management of steatorrhoea should focus on the following:

e Plenty of rest and relaxation and avoid stress

a Correction of water ba1i1nc.c
 Clinical Therapeutic a Correction of electrolyte problems (Na,K, Ca)
. Nutrition
e Vitamin supplementation (A, D, E and K)
o Inclusion of low fat, carbohydrates and fibre diet
a High to moderate protein intake
o Give digestive enzyme supplements (if required)
The nutrient requirements do not change considerably and other principles of dietary
management remain more or less the same as for chronic diarrhoea.
Next, we will discuss about lactose intolerance - a form of food allergy which has a
widespread prevalence.
14.2.9.3 Lactose Intolerance
We commonly hear from people of all age groups, particularly children and elderly
to be complaining of abdominal discomfort after consumiilg milk. Some individuals
are able to tolerate a small quantity while others are unable to tolerate eve11 a
small amount. Well, this could be due to lactose intolerance. But what is lactose
intolerance?
Lactose intolerance relates to insufficiency of the disaccharidase enzyme 'l~lctu,s~'
which is found in the greatest quantity in-the outer membrane of the mucosal cclI of
the jejunum. The degree of lactase deficiency inay vary in individuals. Lack of lactase
does not break down the disaccharide sugar - lactose present in milk, to gIucosc aild
galactose, it passes unchanged into the large intestii~eswhere it gets converted to '
lactic acid by the bacteria, which subsequei~tlycause diarrhoea and other symptoms
of discomfort, distension and abdominal pain. The problem is gene related and often
seen in infants and young children commonly, but may also be present in adults, Major
causative factors are being discussed below.
Etiology
The etiological factors contributing to lactosc intolerance include:
e Genetic factor
a Reduction in jejunal lactase activity due to infections in the gut.
o Any structural damage to the jejunal mucosa in diseasc conditiol~slike celiac,
tropical sprue, colitis in which the jejunal vili are structurally damaged.
e Surgical causes '.inwhich large part of jejunum is removed.
As discbssed above, the patients usually experience the symptoms as highlighted
next:
Symptoms I

Common symptoms linked to lactose intolerance include: 1

1. Anorexia and nausea.
2. Intestinal distension
3. Abdominal cramps
4. Gas and flatulence
I
5. Severe diarrhoea '

6. Under-nutrition and loss of weight. !

,
The dietary treatment is based upon the determination of lactase activity as the treatment j
depends on the level of activity of lactase enzyme. Let us see how. I
 Nutritional Management Nutritional Manigement
o f Gastrointestinsl
Disenses and Disorders
Diagnostic tests are available that can give information about the level and activity of
the lactase enzyme. Depending on the level of activity (very low level, moderate
level) the dietary treatment could be planned. Let us see how.
o Very low level of lactase activity: at very low level of lactase activity all milk
products must be eliminated, substitutes of milk like soya milk, groundnut milk
and their preparations could be given. Enzyme such as Lactaid and Maxilact are
available in the market. Addition of these in the milk or milk products could
digest 90% of lactose in milk and thus minimize the symptoms of lactose
intolerance.
e Moderate level of Lactase activity : Intake of milk is restricted depending on
the tolerance. Fermented and cooked form of milk should be preferred as it is
better tolerated. Fermentation converts a major part of lactose to lactic acid and
in cooked product lactose gets bound and the conce~ltrationreduces. It is better
tolerated in the form of buttermilk, curds, custards, porridges and cottage cheese
or when mixed with cereals, cocoa etc. These allow gradual lactose breakdown
. and decrease the symptoms of lactose intolerance. Curds are better tolerated
possibly due to microbial culture that facilitates lactose digestion in the intestine.
Small amoulit of milk can be taken with the meal.'
Some important points to remember are highlighted next:
Remember
0 Identify the level of lactase activities (diagtiostic tests).
e Depending on the enzyme activity eliminate milk and milk products.
0 Substitute milk and milk products by giving soya sources like -tofu, soymilk, soy
curd and groundnut milk.
e Give a well balanced diet. r

e If moderate lactase activity is present small amounts of lactose (within individuals

tolerance level) can be given several times a day.
Small amounts of milk in moderate lactose activity can be tolerated if taken with
other foods e.g. after a meal or a snack.
Curds is better tolerated than milk.
e Low lactose foods if available commercially like ice cream, cottage cheese, try
them.
@ Lactose enzymes are available these can be added in the milk.
* Deficiency of lactose and calcium could be supplemented by giving other foods.
The last malabsorption syndrome which will be discussed is the inflammatory bowel
disease which is a broad term that refers to a number of disorders of the bowel.
14.2.9.4 Inflammatory Bowel Disease (IBD)
Inflammatory bowel disease is a general term used to refer to chronic inflammatory
condition of the intestine. It is applied to three conditions having similar symptoms but
different underlying clinical problem. It includes:
1. Ulcerative colitis
2. Cxohn's disease
3. Short bowel syndrome
Clinical Therapeutic When the inflammation is in rectum with extension into the colon without affecting
Nutrition
the right colon or small intestine, the disease is called ulcerutive colitis. When an
inflammatory process involves one or more lengthy segments of the.smal1 or large
intestine with inflammation from the mucosa to serosa, the disease is called Crojzn's
disease.

What is the difference between ulcerative colitis and Crohn's disease? The differences
between the two include:

I) Anatomic distribution of the inflammatory process: Crohn's disease can occur in

any part of the GI tract - the small intestines the colon and even the colorectal
region. However, in ulcerative colitis, the inflamination is confined to left colon
and rectum.

2) In Crohn's disease, inflammatory process affects the entire thickness of the wall
of the small intesti~leleading to strictures that can cause obstructio~~s
or formation
of fistulas. In ulcerative colitis the inflammatory process is in mucosa and sub
lnucosal tissues of the intestine and lasts for a few weeks.
I-Iaving looked at the difference between ulcerative colitis and Crohn's disease, let us
next review the etiology of these diseases.
Etiology
These diseases are referred to as idiopatliic (cause unknown) and though the possible
mechanism suggested includes genetic factors, immune mechanism, bclcterial or viral
agents, sugar (excess) and low fibre intake has also been implicated especially in
Crohn's disease.
The symptoms, complications of inflammatory bowel disease are summarized next.

Inflan~rnatc~ry
bowel diseases are associated with:
o Abdominal cramping, diarrhoea
Steatorrhoea
o Obstruction caused due to bulky foods, and

What are the causes for n~alnutritionin these disease conditions? Let us find out.
~ a l l s e sof Malnutrilion in I~zflammatoryBowel Disease
The causes of malnutrition include:
e Decreased oral intake, which can be disease induced due to abdominal pain,
diarrhoea, nausea, anorexia.
Malabsorption due to decreased absorptive surface (destruction of villi), bile salt
deficiency, bacterial overgrowth and use of drugs.
e Increased secretion and nutrient losses due to GI blood losses, electrolyte, trace
mineral losses.
Increased requirements due to inflammation, fever, increased intestinal cell
tunlover, haemolysis.
a Drugs interference related to corticosteroids, (interferes in calcium absorption
and protein metabolism), sulfasalazine (interferes in folate absorption),
Cl~olestyramine(interferes in fat soluble vitamin absorption).
e Deficiency of folate, vitamins A, C, D, low serum levels of zinc, copper and iron Nutritional Management
of Gnstrointestinal
are observed in patients. Diseases and Disorders

So then, what can be done to manage these conditions? The next section focuses on
the nutritional management of inflammatory bowel diseases.
Nutritional Management: Irzfla~nmatoryBowel Disease
Adequacy of nutritional needs and minimizing stress on the inflamed or narrowed
segment of the bowel are the main principles of nutrition management.
To decrease eating associated symptoms and decreased bowel activity during healing,
patients hospitalized for IBD (Inflammatory Bowel Disease) are placed on a "bowel
rest" programme, which involves reduction in oral intake, clear liquids and low residue
foods. This is normally done to achieve the following:
1. Decrease the absorptive work of the bowel and provide rest.
2. Minimize mechanical trauma caused by the passage of food.
3. Decreased diet associated secretio~~s
(acid, enzymes) that may aggravate
inflammation.
The diet should be liberal in protein and calories and should be sufficiei~tto maintain or
restore weight/support growth of children and adolescents. Supplementation with
multivitamin preparations (1-5 times above RDA) in necessary as this condition
precipitates deficiency of many nutrients, decreases absorptioil and increases
requirements.
Overemphasis on fibre may be avoided in patients with strictures as it may lead to
blockage.
Streatorrhoea is more common in Crohn's disease due to ileal resection. This may
favour calcium-fatty acid complex formation and increased excretion. It may be
accompanied by magnesium (Mg) and zinc (Zn) losses. Steatorrhoea also favours
increased absorption of oxalates. In addition, this state is marked with an increased
binding of fatty acid to calcium and thus more oxalate is free in solution for colonic
absorption. Fatty acid also increases the permeability of oxalate tbrough colonic
mucosa. Thus, a reduction in fat invdke coupled with calcium, magnesium and zinc
supplementation is suggested.
To help you understand the inflammatory bowel diseases better, we have a detail
discussioil on two of these diseases namely ulcerative colitis and small bowel
syndrome. We begin with ulcerative colitis.
A. Ulcerative Colitis
Let us understand clearly about ulcerative colitis by reading the following case.
Varun, a 48-year-old male, had a very successful career in a computer company. His
company was his life. He put in long hours when he was working on an important
contract and seldom even took a Sunday off. He was delighted when a deal came
together, and he celebrated his success at his favourilc Chinese restaurant. When he
worked 10-12 hours at a stretch, he just ordered his favorite Chinese food, which
frequently gave him bouts of diarrhoea. But the latest episode was really bad. EIe felt
nauseated and had cramps for 2 nights and developed a fever. On the second night,
he noticed blood in the stools and he resolved to call the doctor. What do you think he
might be suffering from? Well, this is the case of Ulcerative Colitis. What is it? Let us
find out.
Ulcerative Colitis is a diffuse inflammatory and ulcerativedisease of unknown etiology
involving the mucosa and sub-mucosa of the large intestine. It occurs at any age but
predominates in young adults. Onset is insidious in the majority of cases.
Next, we will understand the etiology of ulcerative colitis.
I
Clinical Therapeutic Etiology
Nutrition
No single etiologic factor has been identified although genetic auto-immune factors
are thought to be involved. Although exacerbations are more likely during the collditions
of mental conflict and emotional stress. Allergy to certain foods especially milk may
be a factor in precipitating the disease.
What are the disease symptoms? Let us find out.
Symptoms
As discussed in the case study above, the common symptoms are:
'
1. Mild abdominaI discomfort, an urgent need to defecate several times a day.

2. Diarrhoea accompailied by rectal bleeding.

3. Weight loss, dehydration, fever, anaemia and general debility.
4. Edematous and hypereni?c mucosa seen in early stages.
5. In more severe disease, necrosis and frank ulceration of the mucosa occurs.
So how to manage this chronic condition? The dietary management is described next.
Dietary Ma?tagerne?it ,

Proper dietary management is important for maintainiilg a good nutritional status of

the patient. Long-teim management is generally required as the disease develops
gradually and it takes a long time to cure this disorder. We will now learn in detail the
important aspects of dietary management. t

The dietary management and nutrient recom~nendationsneed individual attention

depending on the extent of disease and problems of malnutrition exhibited, There is a
wide range of tolerance for various foods observed from one patient to another. Let
us first identify the calorie needs of the patient.
Energy: The calorie requirements must be increased to:
1) restore weight status and maintain ideal weight.
2) compensate for the elevated BMR.
3) support growth especially if the age group is adolescents. A caloric intake of 40-
50 Kcal/kg IBW/day is recommended.
Proteins:Patients with ulcerative colitis lose about 4-8 g fecal N2 as compared to the
normal excretion of 2 g. In severe ulcerative colitis, 20 g NZ(equivalent to 125 g of
protein) may be lost daily. The serum albumin is low. Proteins are necessary for tissue
synthesis, tissue healing and to compensate for the increased losses in stools. Thus,
liberal amounts of high quality protein i.e. 1.5 g / IBW are needed to make up for the
losses. Emphasis should be on tender meats, fish, poultry and eggs for those patients
who are allergic to milk.
Fats: Usual foods, which contain fats (invisible or inherent fal), are permitted but not
fried foods, as they are not easily digested due to liver dysfunction. Thus fats rich in
medium chain triglycerides should be consumed as stealorrhoea is predominant in
ulcerative colitis. Total fat intake can be kept close to 55-60 g with visible fat intake
less than 25-30 &day.
Carbohydrates: They form the easily absorbable source of energy. Bulk-producing
I
vegetables are restricted so as to allow better intake of nourishing foods. Sugars and
slarches can make the increased caloric intake.
Fibre : Eliminating roughage seems to have a better effect on preventing relapses of
the disease. A low residue diet may be given during an acute attack to prevent severe
 bleeding during diarrhoea. Thereafter some degree of fibre restriction is generally Nutritional Management
of Gastrointestinal
needed as many ulcerative colitis patients do not tolerate raw vegetables. It may Diseases and Disorders
cause further damage to the alieady inflamed mucosa. The forms, in which vegetables
are given, can be changed. All kinds of irritant and spicy foods should be strictly
avoided. Raw vegetables, spicy and irritant foods may be avoided.
Vitamins: Commercial multivitamin preparation should be administered orally
especially the ones needed for the healing process and the utilizatioil of calories and
proteins.
Minerals: Mineral losses may be marked and unless replaced may contribute to a
fatal outcome. A patient with moderately advanced ulcerative colitis passes a large
volume over 400 ml of faeces per day a i ~ dthus may lose considerable amount of
sodium (G g NaCl/litre of stool). Thus oral sodium intake is increased by added salt,
sprinkling additional salt in foods. Potassium loss can be estimated as 30 mEq / 2.2 g
of potassium chloride / litre. Usually high excretion of potassium even 167 mEq / day
may sometimes be encountered. Manilcstations of potassium deficiency such as
weakness, hypotonia; abdominal distension and even electrocardiographic changes
may occur. Oral administration of potassium salts as potassium citrate lnily be helpful.
Elimination of milk from the diet inay call upon calcjum supplementatiol~to the
extent of 400-800 rng/day. Protein to Calcium ratio is to be maintained for optinlum
utilization. Iron by the oral route is usually not well tolerated. Daily about 30 mg of
elemental iron is given. 1f anaemia is marked, then blood translusions may be given.
Fluids : A liberal intake of fluid should be given to prevent dehydration. The passage
of at least 1200 ml of urine indicates that a patient is well hydrated.
We will now discuss about another iilflarnmatory bowel disease i.e shorl bowel
syndrome.
B. Short Bowel Syndrome (SBS)
Short bowel syndrome is a group of prol~lemsc~fectingpeople wlzo have Izud Iaav
or more of their small intestine removed. The massive resectiot~of the intestine
decreases the transit time of the faeces. Besides any damage to the small intestine,
especially that of the jejunum affects the nutrient uptake and absorption.
Etiology
The etiological factors involved in this disease are:
1 Anaemia
I Osteoporosis

II Stone formation
Decreased susceptibility to infection
0 Dehydration
The common symptoms elicited by this disease have been mentioned below.
Symptoms
Diarrhoea is the main symptom of short bowel syndrome. Other symptoms include:
Anorexia
Steatorrhoea
Heart bum and cramping
, , (I-. .
Bloating and abdominal pala

'i
Clinicnl Therapeutic Extreme fatigue
Nutrition
e Weight loss
a Fluid retention
c Anaemia and osteomalacia

. Many people with short bowel syndrome are malnourished because their remaining
small intestine is unable to absorb enough water, vitamins, and other nutrients from
food. They may also become dehydrated, which can be life threatening. Problems
associated wit11 dehydration and malnutrition include weakness, fatigue, depression,
weight loss, bacterial infections, and food sensitivities.
Complications
Complications of short bowel syndrome are generally related to malnutrition. What
are the coinplications of malnutrition? Aperson with short bowel syndrome i~likely to
be deficient in a range of important nutrients such as calcium, folate, iron, magnesium,
vitamin Biz and zinc.

Let us read and find out the details of dietary management.

Dietary Management
It must be evident from the syinptoms listed above that the disease results in reduced
food intake, impaired absorption and hence weight loss. The patient generally has
depleted reserves for several nutrients. The Nutritional management Ronls should
therefore include the following objectives: ,

e Relieve the symptoms

e Correct nutritional deficiencies,

e Control inflammation and relieve pain.

The dietary considerations should be aimed to give sufficient carories. Special feeding
methods such as enteral and parenteral feedfng may have to be incorporated. The
following points should be kept in mind:

e A high calorie and low residue diet that also supplies the vitamins, minerals and
other nutrients is necessary. The food should be bland.

e The food sliould be divided into several small meals of protein and complex
carbohydrates. Aminimuin of concentrated sweets, fruit juices should be included.

e Nutritional supplements and dietary restrictions are used in treating SBS. The
vitamin and mineral supplements may have to be several times greater than the
standard recommended daily allowances in order to maintain adequate tissue
functionitlg.
a Special feeding to b,e given when essential (enteral and parenteral feeding). Oral
feedings are started using a basic soft diet, which can be digested without much
work required in the bowel. The complexity of the diet is gradually increased
over time, allowing the remaining digestive system to adapt. Finally, patients are
weaned entirely off the enteral feeding and receive nutrition completely from
oral intake of regular foods. If parenteral feeding is must, it could be given but
enteral feeding should be preferred.

Dietary management is supported with drug therapy. Frequently used medications

include anti-inflammatories, immunosuppressants, antibiotics, corticosteroids and
antidiarrhoeals.
 Nutritional Management
, In this section, we learnt about a spectrum of malabsorption syndromes. You may of Gastrointestinal
have noticed that the dietary management of these disorders is quite varied. Attempt Dise:tses and [)isorders
the questions given in check your progress exercise 5 to recapitulate your concepts.
-
Check Your Progress ]Exercise 5
I. Desribe the term lactose intolerance.
......................................................................................................................
......................................................................................................................
......................................................................................................................
2. Write five lines about celiac diseasc? Give five foods containing glutcn.
......................................................................................................................
......................................................................................................................
......................................................................................................................
3. Differentiate between Crohn's disease and Ul.cerative colitis.
......................................................................................................................
............................................................................................
......................................................................................................................
4. A patient suffering from inflammatory bowel disease is at high risk to
malnutrition. Why?
......................................................................................................................
......................................................................................................................
......................................................................................................................

LET US SUM UP
In this unit, we learnt about a host of disorders associated with a part or entire of thc
gastrointestinal tract. The important and the most frequent occurring GI tract disorders
such as constipation, diarrhoea, oesophagitis, GERD, hernia, ulcers, dyspepsis, gastritis,
various malabsorption syndromes, inflammatory bowel diseases were dealt in Lhis
unit. We first reviewed our knowledge on gastrointestinal diseases in general their
etiology, symptoms and complications followed by nutritional management tuld goals,
dietary modifications and foods to be avoided, restricted and those to be given freely.

Next, we studied about these disorders separately in a greater detail, discussing their
etiology, symptoms, associated complications and clinical manifestations.The nutritional
aspects of these disorders and their corresponding dietary management have also
been emphasized.

114.4 GLOSSARY
Acidosis : Increase in concentration of acidic substances in the
blood.

Crohn's disease : a chronic inflammatory disease of unknown etiology

involving small and large intestines that results in
diarrhoea, strictures, fistula and malabsorptian. 369
Clinical Therapeutic Fistula : an abnormal passage between two internal organs or
Nutrition from an internal organ to the surface of the body.

Welicobacter pylori : a type of bacteria that can chronically infect the

slomach, thought lo be the primary contributor to the
development of gaslritis, peptic ulcers and even gastric
cancers.

Wypokalernia : a condition with low serum potassium levels

characterized by poor muscle tone, impaired gut
motility and electrocardiographic changes.

Myponatremia : a decrease in serum sodium level in the blood

,con~monlyfound in dehydration.
: black tarry stools indicalive oE gastrointestinal
bleeding.
Prebiotics : non-digcstible fc~odproducts thal stirnulute Lhe growth
of symbiotic bacterial spccies already prcsent in the
colon.

Probiotics : lnicrobial foods or supplcmeilts Lhat call he i~sedto

change or reestablish the inlestinal flora and improve
the health of the host.
Prostaglandins : one of the several potent hormone-like compountls
made from PUFA which have diverse cl'fecls, both
harmful and useful.
Regurgitation : is the co~ltrolledflow of slomach contents back into
the oesophagus and mouth.
Residue : the fecal contents, includii~gbacteria, Gl secretiurls
and foods no1 digested and absorbed.
Short Bowel Syndrome : a malabsorption syndromc resulting from major
resections of the small bowel characterized by
diarrhoea, steatorrhoca and malnutrition.

ANSWERS TO CHECK YOUR PROGRESS

EXERCISES
Check Your Progress Exercise 1
1. Dietary fibre rich foods - wliole grain cereals, legu~nes,whole pulses, lcnfy
vegetables, pear, guava, oilseeds, methi seeds, peas, b w ~ ~ladies
s , finger, lvti~s
stem. Low residue foods. Refers to volume of inaterials remai~iingafter 1l1e
digestive processes. Food high in dietary fibre are considered to bc high residue +

foods. However, low fibre foods need not neccessrily be low residue food e.g,
milk is low fibre but a high residue food.
2. Use of methods like sprouting, fermentation etc.; salads and raw fruit may be
given in grated form to be able to chew easily, whole pulses and leprnes may
be sbaked overnight to improve their digestibility, soya flour or whole
Bengal gram flour may be added to wheal flour, bran and powdered supplements
of fibre may also be given to individuals who do not eat sufficient amounts of
fibrous foods.

3. Coconut water, dal water, kanji, barley watel; vegetable slock/soup can help ,
promote rehydration. The basic concept behind combining salt, sugar and water I
I
t

A
 Nutritiunnl Mnnngcment
is to prepare a solution of specific osmolarity that would favour water absorption, of G:~strointcstinal
thus leading to rehydration. Disenses nnd Disorders

4. Feed the child with WHO-ORS standard preparation/honle based rehydration

solutions, continue breast feeding young infants, whilc providing energy rich
mixturc of weaning foods for older children. This would help in preventing
dehydration and prevent further malnourishment of the child.
Check Your Progress Exercise 2
1. I-Ieartburn or burnirlg epigastric substernal pain, regurgitation and dpsphagia art.
the common ~ ~ & ~ t o The m s objectives
. of nutritional care ore to: prcverrt irritation
of the inflammed oesophageal mucosa in thc: acutc phase; prevent oesoptiagcal
rellux; and decrease thc irritating capacity or a-itlity of rhe gastric juice.
2. Decreased mllscle ton(*or ahnormal rcl;ixiltio~~ of thc LES; reduced stomach
motility or hiatus hcrnia due to advancing :age, pregnancy, ohesity or sick effects
of certain drugs can rcslilt in the development of GERI). Patients shuuld bc
cou~~seled regarding: restricting smokin~;~lcohol intake, avoiding lying tlowll
bending aftcr eating meals, kccpinp the Iicild and r~eckraised slightly whilc lying
down, and avoiding astringent or highly flavoured foods.
3. Hiatus Herniit is thc most cornmou citl~seof C7ERD. Avoid ilny Gvc of the
following: carbonated beverages, citrus l't.uits and jllices. tomato pl*oducts,spicy
.
foods, coffce, pepper, alcohol, garlic, onion, chocolate, cream sauccs, gravies,
margarine, butter and oil.
Check Your Progress Exercise 3
1. a) Acute gastritis results due to over eating, overuse of alcohol, tobitcco, excess
dose of aspirin, anti-inflammatory drugs, increased bile acids, trauma,
surgery, shock, jaundice, renal failure, burns, infection while chronic gastritis
precedes development of an urga~licgastric lesion, a cnnccr or a ulcer. It
may be caused by bacterial infections and impuircd n~ucosaldefense
" mechanisms,

b) Diverticulosis is the herniation of the mucosa through the muscular Jayers

of coloilic walls while diverticulitis is an infla~nmationof thc diverticuli.
2. The li$estylc modifications in terms of work schedules, eating behilviour like
consuming meals when extremely tired, preventing episodes or GERD, avoiding
abdominal discomfort and drug use, quitting alcohol and smoking would help to
alleviate the synlpton~sof dyspepsia.
3. The diet therapy for a patient suffering from diverticulitis may be limited Lo clear
liquids progressing to full liquids and then to low residue and Iibre soft to llorlnal
diet. With improvement, in inflammation, an increasc in fibre intake is
recommended.
Check Your Progress Exercise 4
1. Gastric and duodenal ulcers are two forms of peptic ulcers. Duodenal ulccrs
generally occur in the duodenal cap i.e., just above the point of entry or illkatine
pancreatic juice. Gastric ulcer on the other hand refer to locillized erosion of the
lesser curvature of the antrum of stomach.
2. Etiological factors in peptic ulcer involves the following:
0 Destructive factors (HCL, pepsin, psychological, factors, gastric irritants,
nicotin and tobacco and anti-inflammatory clrugs.
Defensive factors (epithelial cells barrier mucous, gistric blood flow,
regulation of acid secretion, ability of the body to regenerate the cells.
Clinical Therrpeulic 3. The conventional approach involved restrictions of almost all foods except milk
Nutrition and cream (Sippy's diet). The liberal approach involves giving a variety of foods
other than those which may increase damage to the ulcerated area. Since it is
the ilidividual patient who is the focus of treatment, it becomes important to treat
the patient completely according to his tolerances and desires. ,

Check Your Progress Exercise 5

1. Lactose intolerancerefers to inability of the body to digest and assimilate lactose.
It occurs as a consequence of lactase deficiency, the degree of which may vary
from hypolactasia to lactase persistence.
2. Celiac disease is an autoimmune inflammatory disease of the small intestine and
is precipitated by the ingestion of gluten, a component of wheat protein while
tropical sprue is a malabsorptioii symdromc of unknown causes that is prevalent
in the tropics and sub-tropics.
Five foods containing gluten include: wlzeat, refined flour (maida) rye, barley,
arid possibly oats and many processed foods.

3. a) Crohn's disease can occur in any part of the GI tract whereas in Ulccrativc
Colitis, the inflammation is confined to colon and rectum.

b) In Crohn's disease, the inflammatory changes become chronic and can

involve any part of GI tract. Inflammatory process follows transmural pattern
i.e., affecting the entire thickness of the wall of the small intestine. This
leads to strictures resulting in a partial or conlpletc obstruction or formation
of fistulas. Ulcerative Colitis relates to acute inflammation oi'colon lasting
for a few weeks and is limited to mucosal and sub rnucosal tissues layers of
the intestinc.
4. The patient is at risk of malnutrition due to:
Decreased food intake due to associated abdominal discomfort.
0 Malabsorption due to decreased absorptivc surface, bile salt deficiency,
bacterial overgrowth and use of drugs.
a Increased secretio~~and nutrient losses due to GI blood losses, electrolyte,
trace mineral losses.
0 Increased requirements due to inflammation, fever, increased intestinal cell
turnover, Izaemolysis.
e Drugs interference related to corticosteroids, sulfasalazine, cholestyramine
I
Deficiency of folate, vitamin4 vitamin C, vitamin D, low serum zinc, copper
and iron are observed.