SUMMARY of CLINICAL NUTRITION TOPICS
Outline:
1. Nutrition for Cardiovascular Diseases
2. Nutrition for Chronic Liver and Gallbladder Diseases
3. Nutrition for Upper and Lower GI Diseases
4. Nutrition for Renal Diseases
MAJOR FACTORS
 Hypertension
 Cigarette smoking
 BMI > or = to 30 kg/m2
 Physical inactivity
 Dyslipidemia
 DM
 Microalbuminuria or Estimated GFR <
60 ml/min
 > 55 yo for males, > 65 yo for females
 Family history of premature CVD
DISEASE
Hypertension
Identifiable causes: sleep apnea, drug-
induced or drug-related, Chronic Kidney
Disease, Primary aldosteronism, Chronic
steroid therapy and Cushing Syndrome,
Pheochromocytoma, Coarctation of the
Aorta, Thyroid/Parathyroid dse.,
Renovascular Dse.
Acute MI
Congestive Heart Failure
NUTRITION FOR CARDIOVASCULAR DISEASES
OBJECTIVES
 Energy
- mild degree of weight loss even for the cardiac patients of normal weight (eg. 1,000 to 1,500 calorie diet= suitable for an obese patient in bed)
 Sodium restriction
- Indicated when there is retention of fluid and sodium (eg. restriction of 500 mg in CHF)
- Once edema has disappeared, a moderately-restricted sodium diet (of about 1000 mg) is likely to be satisfactory.
 Fluid
- Not required so long as the sodium is restricted- because water is retained only when there is sufficient sodium to maintain physiologic concentrations
 Foods
- Small amounts in 5 or 6 meals is preferred
- Liquid or soft, easily digested foods that require little chewing should be used when decomposition occurs.
- Avoid abdominal distention by omitting cabbage, onions, legumes, turnips, melons, and sweet potatoes in meals.
- Prevent constipation by use of prune juice (aside from the usual fruits, vegetables and adequate fluid intake)
RECOMMENDATIONS
Treatment:
Goals: BP goal is 130/80 in patients with HPN (and DM or Renal disease)
Dietary Management:
1. Calories: decreased to 10% body weight
2. Protein: adequate enough to maintain nitrogen equilibrium
3. Carbohydrates: decreased
4. Fat: decreased to 25% of energy requirement
5. Sodium: according to the degree of HPN
6. Fruits and Vegetables: increased
a. During hospitalization:
i. First 24 hours: NPO, with parenteral dextrose solutions
ii. 2nd and 3rd day: low-fat liquid diets that supply 500-800 kcal, and 1000-1500 ml of liquid in small frequent feedings
iii. No caffeine
iv. Beyond 3 days: 1000-2000 kcal in 5-6 small feedings (especially in patients who are dyspneic or has angina), less than 30% of calories of total
fat, less than 10% saturated fat, 300 mg or less of cholesterol, 2000 mg or less Sodium, fluid restriction. Avoid gas-producing foods.
b. During rehabilitative phase:
i. Based on weight status and blood lipid levels
a. Almost the same as post MI, but more NA and fluid restriction is needed in CHF.
b. Usual Na restriction= 500 mg per day
 SODIUM RESTRICTED DIETS
 No salt used at the table= mild, moderate,
strict
 No salt in cooking= both in Moderate and
Strict
 Normal: 3000 mg to 6000 mg of Na
daily
 Mild Na restriction: 2400 mg/ 1 tsp crude
rock salt per day, may use some salt in
cooking, no salty foods permitted. (Usually
used as a maintenance diet in Cardiac and
Renal diseases)
 Moderate Na restriction: 1,200 mg or ½
tsp crude rock salt per day, no salt in
cooking
 Strict Na restriction: 600 mg or ¼ tsp
crude rock salt per day.
GENERAL POPULATION
1. A healthy eating pattern that includes foods
from each of the major food groups
a. Fruits and vegetables
i. Fruits and vegetables- 5 or more
servings per day, especially those that
are dark green, deep orange or
yellow). Whole fruits rather than juice
are recommended- to ensure an
adequate fiber intake
ii. Grain products, including whole grains.
Choose 6 or more servings per day
1. Foods high in starches
(polysaccharides; eg. bread, pasta,
cereal potatoes) are recommended
over sugar (mono- and
disaccharides).
2. Sources of whole grains and well-
fortified and enriched starches (such
as cereals) should be major sources
of calories in the diet. Grains,
vegetables, fruits, legumes and nuts
are good sources of fiber.
3. Soluble fibers (B-glucan and Pectin)-
can reduce total and LDL cholesterol
levels more than what is achieved by
a diet low in saturated fat and
cholesterol
4. Dietary fiber may promote satiety,
therefore helps to control calorie
intake and BW.
2. A healthy body weight
a. Relative caloric restriction sufficient to
produce weight reductions between 5%
to 10% can reduce the risk factors for
heart disease and stroke
b. < or = 30% of total calories as fat to
predict a weight loss of 1 to 2 lbs per
week (minus 5000 to 1000 kcal/day)
DIETARY GUIDELINES
SPECIAL POPULATION
1. Older individuals
2. Children- diets low in saturated fat can
support adequate growth and development
in children. But care must be taken to
ensure that such diets are consistent with
nutritional needs for normal growth and
development
3. Individuals with specific medical conditions:
a. High LDL cholesterol: those requiring
lipid-lowering drugs, adjunctive dietary
management is indicated as a means of
potentially reducing the dosage
and/number or drugs required to reach
targets.
b. CHF: Na and water restriction
c. Kidney disease: Protein and salt
restriction, and increase in total calories
in those with progressive RF. In contrast,
dialysis patients are urged to eat a higher
amount of protein to avoid loss of muscle
mass.
ANCILLARY LIFESTYLE AND DIETARY
ISSUES
1. Smoking: complete elimination
2. Alcohol use: (recommendation already
stated)
3. Diets with extremes of macronutrient
intake:
a. High unsaturated fat
diets:(recommendation already
stated)
b. Very low fat diets are not
recommended for the general
population because
i. Weight loss is not sustained
ii. It may lead to nutritional
inadequacies for essential FA
iii. It is often associated with the use
of processed low-fat foods that are
calorie dense
iv. It can amplify low HDL cholesterol,
high triglyceride and high insulin
levels in individuals with certain
metabolic disorders.
c. High protein diets:
i. Protein foods from animal sources
are generally higher in fat,
saturated fat and cholesterol.
ii. An average of 15% total energy
OR 50-100 g per day should be
adequate to meet most needs
 c. Choose foods low in added sugars
d. Limit intake of refined CHO and sugars.
This may raise triglycerides and reduce
HDL cholesterol
e. Physical activity- general target is to
expend a total of 100 to 200 kcal.
3. Desirable blood cholesterol and lipoprotein
profile
a. LDL cholesterol
i. Saturated FA, trans-unsaturated FA,
and to a lesser extent, cholesterol-
are major food components that raise
LDL.
ii. Polyunsaturated FA,
monounsaturated FA, and to a lesser
extent, soluble fiber and soy protein.-
decrease LDL. including sustained
weight reduction.
b. HDL cholesterol
i. Reduction may be more evident with
diets high in sugars than in diets in
which CHO is derived from unprocessed
grains.
c. Triglycerides
i. Because of the reciprocal metabolic
relations between plasma HDL
cholesterol and triglyceride levels,
factors such as excess BW, low
physical activity and high intake of
sugar and refined carbohydrates are
associated with relative increases in
triglycerides.
ii. In individuals with severe
hypertriglyceridemia assoc. with
chylomicronemia, restriction of
dietary fat is also indicated and an
increased intake of omega-3 FA
may be beneficial.
d. Saturated FA- the principal determinant
of LDL cholesterol
 i. Reductions in those with average
LDL levels: Intake of <10% of
energy is recommended. Limit
intake of full-fat dairy products, fatty
meats and tropical oils.
ii. Reductions in those with elevated
LDL cholesterol levels or CV
disease: < 7%.
e. Trans-fatty acids- can increase LDL and
reduce HDL cholesterol
i. Found in foods containing partially
hydrogenated vegetable oils (like
cookies, crackers and other baked
goods,commercially prepared fried
foods, and some margarines), fried
foods in restaurants and fast food
chains. Limit intake at an average of
2 to 3 % or total energy.
f. Cholesterol-rich foods that are relatively
low in saturated FA content (egg yolks,
and to a lesser extent, shellfish) have
smaller effects on LDL cholesterol
levels. For all individuals: <300 mg/d on
average is recommended. For
individuals with high LDL levels, DM,
and/or CVD: <200 mg/day, requiring
restriction of all dietary sources of
cholesterol.
g. Substitute grains and unsaturated FA
from fish, vegetables, legumes and nuts
i. Oat products, psyllium, pectin and
guar gum (soluble fibers)- can reduce
LDL in hypercholesterolemic
individuals. For every gram increase
in soluble fiber from these sources,
LDL cholesterol would decrease by
2.2 mg/dl.
ii. Foods high in omega-3
polyunsaturated FA, especially EPA
and DHA, confer cardioprotective
effects than can be ascribed to
improvements in blood lipoprotein
profiles.
 Iii. A-linolenic acid reduces risk of MI
and fatal ischemic heart disease; anti-
inflammatory and autoimmune
diseases; found in salmon, flaxseed
and flaxseed oil, , canola oil, soybean
oil, and nuts. At least 2 servings of
fish per week is recommended.
4. Maintain a normal BP.
a. Limit salt intake to 6 g/day
b. Average systolic and diastolic BP
reduction per kg of weight loss was
1.6/1.1 mmHg
c. Limit alcohol intake to no more than 2
drinks per day (men) and 1 drink per day
(women)
d. fruits , vegetables and low fat dairy
products and reduced fat that can reduce
systolic and diastolic BP by 3.5 and 2.1
mmHg respectively in nonhypertensive
individuals:
i. Fruits and vegetables- 5-9 servings
per day; low-fat dairy products- 2-4
servings per day
ii. Includes whole grains, poultry, fish
and nuts, reduced in fat, red meat,
sweets and sugar-containing
beverages, rich in potassium,
magnesium and calcium.
iii. Increase potassium intake
decreases risk of stroke.
iv. Foods > supplements for increasing
mineral intake.

*** See tables for classification and management of BP (p. 78), lifestyle modification to manage HPN (78-79), and Food selection guide for MI and CHF (p. 80-81)
*** See AHA 2006 diet and lifestyle goals for CVD risk, and AHA 2006 Diet and lifestyle recommendations for CVD (p. 82)
*** Cardiovascular benefits of fish (particularly fatty fish) consumption of at least 2 fish servings per week.
*** Substitute grains and unsaturated fatty acids from vegetables, fish, legumes and nuts
 NUTRITION FOR CHRONIC LIVER AND GALLBLADDER DISEASES
INTRODUCTION
 Malnutrition is an increasingly recognized complication of chronic liver disease.
 Etiology of malnutrition
o Poor oral intake
 Food with sodium, protein, and fluids can discourage adequate oral intake. In addition,
weakness, fatigue, and low-grade encephalopathy can contribute to decrease oral
intake.
o Malabsoprtion
 Possible mechanisms:
 Reduction in bile-salt pool, leading to fat malabsorption
 Bacterial overgrowth resulting from impaired small-bowel motility
 Presence of portal hypertension  malabsorption and gastrointestinal protein loss
 Medications: Neomycin (used in the treatment of hepatic encephalopathy)
*neomycin is a bactericidal aminoglycoside
o Increased energy expenditure
 Hypermetabolism (extrahepatic manifestation of liver disease)
 Infection
 Ascites: removal of ascitic fluid decrease energy expenditure
 Reduction in activity-related energy expenditure
 Portal hypertension: successful treatment of portal hypertension with transjugular
intrahepatic portosystemic shunt replacement  reduction in hypermetabolic state
 Malnourished patients with cirrhosis have a higher rate of complications (hepatic
encephalopathy, infection, variceal bleeding, and refractory ascites) and mortality rate.
 Malnutrition is an independent predictor of mortality in patients with cirrhosis.
 Malnutrition has significant implications for liver transplantation
o Patients with poor nutritional status before transplantation have increased complications
(infection and variceal bleeding) and higher mortality/decrease survival rate postoperatively
o Malnourished patients require more blood intraoperatively, remain on ventilator support
longer postoperatively, have increased length of hospital stay, and have higher incidence of
graft failure.
 Therefore, screening all patients with chronic liver disease for nutritional abnormalities
can identify those at risk of developing preventable complications, and the initiation of
nutritional therapy can reduce the risk of such complications, and improve the overall
mortality rate.
NUTRITIONAL ASSESSMENT
 There are several factors that complicate the evaluation of nutritional status in patients with
cirrhosis
o Weight – not a reliable indicator of malnutrition due to the possible presence of ascites and
edema which will increase the measured weight, whereas lean body mass might be reduced
o Laboratory tests are less reliable – ex. albumin and prealbumin could be low because of low
levels of synthesis and not poor nutritional status
 Common used method is anthropometry
o Include triceps skin-fold thickness and midarm circumference, which assess fat storage and
skeletal muscle mass, respectively
o Limitations: poor interobserver reproducibility and overstimulation of the values due to third-
spacing of fluid (fluid moves into the interstitial or “third” space)
 Subjective global assessment (SGA)
o Combines multiple elements of nutritional assessment to classify the severity of malnutrition
o Components are:
 Weight loss during the previous 6 months
 Changes in dietary intake
 Gastrointestinal symptoms
 Functional capacity
 Metabolic demands
 Signs of muscle wasting
 Presence of presacral or pedal edema
o Useful in predicting outcome following liver transplantation
 Hand-grip strength and respiratory-muscle strength: assesses muscle function; more useful if
taken serially
o Hand-grip strength – highly sensitive and might overestimate the prevalence of malnutrition;
good predictor of complications (ascites, hepatic encephalopathy, spontaneous bacterial
peritonitis, and hepatorenal syndrome) in advanced liver disease; decreased hand-grip
strength before transplantation is associated with longer stays in the ICU and more
postoperative infections
 Depletion of body cell mass (BCM)
o Decrease BCM before tansplantation  threefold increase in post-transplant mortality rates
o Isotope dilution, measurement of whole-body potassium, and in vivo neutron activation
analysis: most accurate but costly and labor intensive  less practical for routine nutritional
screening
o Bioelectrical impedance: more readily available tool for estimating BCM but accuracy can be
affected by fluid retention in patients with cirrhosis
 Evaluation of status of energy metabolism
o Indirect calorimetry, used to estimate REE. It measures the consumption of oxygen and
production of carbon dioxide which enables the calculation of the nonprotein respiratory
quotient, defined as the ratio of energy produced by carbohydrate metabolism to energy
generated by fat oxidation, which confirms whether patient has an altered pattern of fuel
consumption
 PREVALENCE OF PCM IN CHRONIC LIVER DISEASE
 Protein-calorie malnutrition (PCM) is a condition of body wasting related to dietary deficiency of
calories and protein, found in 65-90% of patients with advanced liver disease and in 100% of
candidates for liver transplantation
 Malnutrition in NOT typically a complication of acute liver injury, but manifests with progression
to liver failure
TREATMENT
 Goal: improve PCM and correct nutrient deficiencies
 Consumption of frequent small meals and a late evening snack to reduce protein breakdown
 Oral intake should be encouraged but if patient is unable to maintain adequate intake of orally,
nasogastric tube should be inserted for enteral feeding
 Based on studies, enteral feeding improved nitrogen balance and fewer viral infections after
transplantation
 Parenteral nutrition is less desirable and reserved ONLY for patients in whom enteral feeding
cannot be achieved
o Parenteral feeding superior to enteral in cases of portosystemic shunting, since enteral might
worsen hyperammonemia
 Supplementation with branched-chain amino acid (BCAA) is best administered at night where it is
used for protein synthesis

NUTRITION FOR CHRONIC LIVER DISEASES

DISEASE TREATMENT (Goal: improve PCM and correct nutrient deficiencies) NOTES
Advanced liver  Dietary restrictions: sodium, protein, and fluids – can discourage adequate  65-90% of patients have protein-calorie malnutrition (PCM)
disease oral intake  Have altered sense of taste – might be related to vitamin A and/or zinc deficiency
 Consume four to five small meals per day, as well as a late evening snack  Vitamin A def.  night blindness
 For vit. A def.: supplementation of 25,000 units/day for 4-12 weeks o Resolves within 2 weeks of liver transplantation
o Toxicity: elevated transaminase levels  cirrhosis (25,000IU/day for 6  Persistent problem with dark adaptation, despite adequate vit A supplementation  concomitant
years), chronic hepatitis, or portal hypertension zinc def.
o Toxicity can persist for up to 1 year after discontinuation  Experienced early satiety – can result from an increased serum concentration of leptin
 Malabsorption
o Reduction in bile-salt pool, leading to fat malabsorption
o Bacterial overgrowth resulting from impaired small-bowel motility
 Common complication is infection
 Have altered pattern of fuel consumption, more rapid transition from the use of carbohydrates to
the use of fat stores as a substrate for metabolism – increased use of lipids (also seen in
starvation)
Chronic liver  Calcium 1g/day  Develop micronutrient deficiencies – more insidious presentation than the overt cachexia in
disease  Vitamin D3 800IU/day patients with PCM
 Malabsorption, decreased UV light exposure, or inadequate dietary inatake  Vitamin D
deficiency
 Calcium deficiency  osteomalacia, or osteoporosis
Liver cirrhosis  Enteral feeding improved serum albumin and child-turcotte-pugh scores, and  Often experience early satiety – related to mechanical compression from massive ascites
decreased in-hospital mortality rates  Studies suggested that patients are hypermetabolic when measurements of resting energy
 From the European Society for Clinical Nutrition and Metabolism: expenditure (REE) are corrected for lean body mass; however there are other studies that
o Compensated cirrhosis: consume 25-35kcal/kg body weight per day of suggested that up to 30% of patients with cirrhosis are hypometabolic
non-protein energy and 1-1.2g/kg body weight per day of protein or amino  Research showed that, after an overnight fast, 58% of the energy used by patients derived from
acids fat oxidation (in control participants, 55% of the energy derived from carbohydrates)
o Complicated cirrhosis associated with malnutrition: consume 35-40kcal/kg  Zinc deficiency
body weight per day of non-protein energy and 1.5g/kg body weight per
day or protein intake
  Oral supplementation with branched-chain amino acid (BCAA) for 2 years
improved survival, serum albumin concentration, and quality of life in
patients with decompensated cirrhosis
Alcoholic liver  Alcoholic cirrhosis: studies found that patients receiving a daily supplement  Impaired hepatic 25-hydroxulation of vitamin D seen in alcoholic cirrhosis
disease of 1,000kcal and 34g protein (casein-based enteral nutrition product) had
better outcomes
 Aggressive nutritional intervention with enteral feeding  accelerated
improvement
 25-hydroxyvitamin D supplementation, 25-50mg/day
Hepatic  Enteral feeding  improvement and rapid decrease in bilirubin levels  Zinc deficiency
encephalopathy  From the European Society for Clinical Nutrition and Metabolism:
o Stage I or II: 0.5-1.5g/kg body weight per day of protein intake
o Stage III or IV: 0.5g/kg body weight/day of protein intake
 2003 review concluded that supplementation with branched-chain amino
acid (BCAA) enterally improved chronic encephalopathy
 Zinc supplementation 600mg/day for 3 months  improve mental
functioning
Cholestatic  Patients are subject to calorie depletion
liver disease  Associated with deficiency in fat-soluble vitamins (fat malabsorption)
Noncholestatic  Patients are subject to protein depletion
liver disease

NUTRITION FOR GALLBLADDER DISEASES

DISEASE
INTRODUCTION
 Gallstones are the most common
gastrointestinal disorders (western
populations)
 80% contain cholesterol (cholesterol
monohydrate crystals), 20% pigment
stones (calcium bilirubinate)
 Cholesterol-containing gallstones:
cholesterol stones (90-100% cholesterol)
and mixed stones (50-90% cholesterol)
 Cholelithiasis or gallstone formation
results from combination of several factors
o Supersaturation of bile with
cholesterol: can result from excessive
concentration of cholesterol in bile, a
deficiency of bile salts and
phospholipids, or combination
o Accelerated nucleation of cholesterol
monohydrate in bile
o Bile stasis
o Delayed gallbladder emptying due to
impaired gallbladder motility:
MEDICAL MANAGEMENT
 Cholecystectomy
o Cause resolution of symptoms
o 10-15% postcholecystectomy
syndrome, which is characterized by
a continuation of symptoms thathad
been attributed to gallbladder
disease or the development of new
gastrointestinal symptoms
 Oral administration of naturally
occurring bile acid (ursodeoxycholic
acid or chenodeoxycholic acid)
o Promote gradual dissolution of
radiolucent gallstones over a period
of 6 months to 2 years
o Recurrences are seen in up to 50% of
patients after treatment is
discontinued
 Patients with asymptomatic gallstones
do not require treatment with drugs or
surgery
NUTRITIONAL MANAGEMENT
 Identification and avoidance of allergenic
foods appears to be viable alternative to
cholecystectomy
o Food allergies can be identified by
elimination diet followed by individual
food challenges
 Supplementation with 11.3g per day of
fish oil (high in polyunsaturated fatty
acids) decreased the cholesterol
saturation of bile by 25%
 People at risk of developing gallstones
should avoid excessive intake of refined
sugar
 Supplementation with 10-50g per day or
more of wheat bran for 4-6 weeks
decreased the cholesterol saturation
o Bran work primarily in the colon,
decreasing the formation of
deoxycholic acid by intestinal
bacteria and increasing the
synthesis of chenodeoxycholic acid
NOTES
 Obesity is associated with an increased risk of gallstones
 Excessively rapid weight loss (more than three pounds per
week) may promote development of gallstones or increase
the risk of silent gallstones become symptomatic
o Increase in the ratio of cholesterol to bile salts and to
bile stasis  decerase in gallbladder contractions
 “Allergic cholecystitis” – characterized by edema,
hyperemia, increased mucus secretion, and eosinophilic
infiltration
 Food allergy or intolerance might cause delayed
gallbladder emptying
 In observational studies, higher intake of saturated fat or
trans fatty acids were associated with an increased
incidence of gallstones; in contrast, higher intake of
polyunsaturated or monosaturated fatty acids was
associated with decrease risk
 Higher intake of refined sugars (sucrose and fructose) is
associated with a higher frequency of gallstones
 Consumption of a vegetarian diet, and particularly
vegetable protein, may decrase the risk of developing
gallstones
 hypomotility may occur during
pregnancy, with the use of oral
contraceptives, after surgery or burns,
and in patients with diabetes
 Most gallstones are asymptomatic but
some may experience biliary colic (sudden
and severe right upper quadrant pain,
often accompanied by nausea and
vomiting, occurring postprandially and
lasting one to four hours)
 Acute or chronic cholecystitis may occur
with gallstones
Complications: infection, perforation,
gangrene
o Deoxycholic acid appears to  Higher intake of fiber was associated with a lower
increase the lithogenicity of bile, prevalence of gallstones
while chenodeoxycholic acid o Pectin and guar appear to reduce cholesterol levels
decreases lithogenicity  promote by 10-15%
dissolution of gallstones  In animal studies, administration of caffeine in drinking
 Recommend high-fiber diet water at a concentration of 1mg/mL prevented the
o Fiber and other substances bind development of gallstones induced by feeding a high-
cholesterol stimulating the liver to cholesterol diet
increase production of bile acids, o Caffeine appeared to stimulate bile flow
thereby increasing cholesterol  Iron deficiency play a role in the pathogenesis of gallstine
solubility formation
 Recommend 500-2,000mg per day of  Phospholipids increase the solubility of biliary cholesterol
vitamin C supplement for patients at risk
of gallstones
o Vitamin C is a cofactor for 7a-
hydroxylase, the rate limiting step in
the conversion of cholesterol to bile
acids, that promotes the conversion
of cholesterol tobile salts 
decreasing lithogenicity of bile
 Supplementation with lecithin (high
concentrations of phospholipids) has the
potential to decrease the lithogenicity of
bile by increasing biliary phospholipid
concentrations
o But no strong evidence to support
the use of lecithin to prevent or treat
gallbladder disease

INTRODUCTION
Functions of the GI system:
- extracts nutrients and energy-yielding
molecules from foods
- digests the molecules to smaller subunits for
absorption
- transport food components
- excretes indigestible food wastes
The GI system is able to perform such
functions by means of various digestive
organs, enzymes, regulatory neurochemical
and hormonal substances and other tissues. It
is exposed to mechanical, thermal and
microbial damage and is protected by its
anatomic location, gastric acidity and immune
system.
NUTRITION FOR UPPER AND LOWER GI DISEASES
MALNUTRITION FIBER
 Refers to deficiencies, excesses or imbalances in a person’s intake of energy and/or  Different kinds of fiber (different kinds of effects):
nutrients. cellulose, hemicelluloses, pectin, mucilages, gums,
 Can cause abnormalities in the mucous membranes (mouth, tongue and digestive tract) algal polysaccharides, lignin
 Most severe in younger children  Action of fiber in the GI System:
 Starvation and protein energy malnutrition - ↑flow of saliva
→ inability to absorb or digest food and decreased pancreatic function - ↑mass of intestinal bacteria
→ depressed immune functions - improve feeling of satiety
 Nutrient deficiencies → ulceration, hemorrhage, or loss of resistance to microorganisms - ↓transit time of stools
 Malnutrition → atrophy of GI mucosa → microvilli flatten → lose absorptive surface and - delay digestion and absorption
↓production and secretion of enzymes → food passes undigested and unabsorbed in - bind intestinal bile acids
colon → bacteria in colon induce gas production and influx of water → diarrhea and - ↑stool weights and frequency of elimination
↑damage to GI tract  Animal studies: ↑length of intestine and causes
 Recovery of reduced microvilli occurs slowly, if at all greater proliferation of mucosal cells
 Adverse effects (very rare): intestinal obstruction d/t
 Management:
gel-forming fiber; interference in absorption of Ca, Mg,
- enteral or TPN is employed d/t diarrhea
Zn, Mn and Fe; inflammation of bowel mucosa;
- prevent: dehydration, edema, vitamin and mineral deficiencies
- Prevent excessive accumulation of fat colonic volvulus

DISEASE MEDICAL MANAGEMENT DIETARY MANAGEMENT NOTES/REMARKS

Celiac  Strict removal of gluten from the diet  Aka Non-tropical Sprue or Gluten-induced enteropathy
Disease  Immunologic reaction to gluten fraction of proteins from
wheat, rye or oats
 Ingest gluten→lining of SI atrophies → malnutrition, growth
stunting and anemia
Diarrhea  Electrolytes: ORS (Oresol in the Ph)- most appropriate  Liberal Fluid Intake: prevent dehydration esp in  Most common manifestation of malfunctioning instinal tract
single formulation for worldwide use the very young and the very old  Classification based on ORIGIN: Osmotic (malabsorption
 Loss of electrolytes (Na and K)→profound  NPO for 12-24 hours to rest GIT and steatorrhea) vs. Secretory (change in electrolyte
weakness, anorexia, vomiting, listlessness  PO feeding asap. Return to normal food should be transport) vs. Inflammatory (enterocyte damage)
 Potassium loss: K is important for GIT muscle tone gradual.: Simple foods (broth, gruel, dry toast, tea)  Classification based on ETIOLOGY: Functional (overeating,
 ORS active ingredients/ 1L: → low fiber, high calorie diet (dry skim milk wrong foods, fermentation d/t incomplete digestion,
20.0g Glucose, anhydrous powder + beverages or deserts; glucose/lactose + putrefaction, nervous irritability, endocrine disturbance, sprue,
3.5g NaCl beverage) → Fruit and veg juices → creamed veg pellagra) vs. Organic (poisons, bacterial or protozoan
2.5g NaHCO3 soup → whole cooked foods invasion, viral hepatitis, chronic ulcerative colitis, regional
1.5g KCl 1.5g  Emulsified fats as tolerated (butter or cream) ileitis, lactose intolerance)
27.5g in total  Pectin included in diet for children, high value in
 ORS alternative: tx for diarrhea. (Scraped raw apple, banana powder
¼ tsp rock salt or applesauce in thin rice gruel or veg broth)
1 tbsp sugar  Lactobacillus is a safe and effective tx for
1 glass boiled water or tea children w acute infectious diarrhea (Yogurt: L.
 IV fluid resuscitation if loss is critical bulgaricus, S. thermophiles, L. acidophilus)
Constipation
Reflux
Esophagitis
Gastritis Acute Gastritis
 No specific therapy except for H.pylori
 Fluid and electrolytes PRN esp if px is vomiting,
intravenously
 D/c drugs known to cause gastritis (NSAIDS and alcohol)
 Get rid of offending substance via induced vomiting
and/or lavage, irrigation of the color or use of laxatives
Chronic Gastritis
 Antacid therapy- mainstay
 Treatment is targeted to primary disease
 H.pylori: Multidrug therapy of Clarithromycin, amoxicillin,
metronidazole, tetracyclin, furazolidine
 ↑intake of wheat bran & insoluble fiber: prevent
constipation and relieve its symptoms
 Atonic Constipation:
- Develop regular BM: Bowel Training Progra
- Est good habits: regular meals, high fiber,
adequate fluids and exercise
- HIGH FIBER MEALS > Fiber supplements
 Phytonutrients- protective against chronic
disease
- Fluid Intake: 3-4L/day from food and beverages
Spastic Constipation:
- Low Fiber Diet- to not irritate the mucous
membrane of the intestinal tract
- Smooth, non-irritating foods: milk, eggs,
refined bread, cereals, butter, oil, finely ground
meat, fish, poultry, and simple deserts
- Large amt of fat- for calorie and lubricating
effect
- Vitamin Supplements- esp if restricted diet is
prolonged
 Avoid alcohol, dietary fat, coffee (decaf or not),
spices, tomato and orange juices: they reduce
sphincter pressure
Nutritional Tips:
 Flavonoids to inhibit growth of H. pylori (apples,
celery, cranberries, onion, garlic and tea)
 Antioxidant food (blueberries, cherries)
 B Vitamins and Calcium (almonds, beans, whole
grain, dark leafy greens, and sea vegetables)
 AVOID refined foods (white breads, pastas, sugar)
 ↓red meats and ↑lean meats, cold water fish, tofu
and beans
 Use healthy oils (olive oil and vegetable oil)
 Avoid coffee, alcohol and carbonated beverages
 Drink 6-8 glasses of water per day
 Exercise 30mins/day 5 days/week
 Identify and eliminate food allergies
 Probiotics may help suppress H.pylori infection
and reduce side effects of antibiotics
Acute Gastritis
 NPO for 24-48hrs to rest the bowel
 Low Fiber liquid foods given as tolerated
 Milk, toast, cereal and cream soup given at
intervals of one hour
 Defined as ≤ 3 BM/week
 Can be caused by DM, hypothyroidism, uremia, neurogenic
bowel disorders, and GIT structural abnormalities
 Most constipation cannot be attributed to underlying diseases
 Widely presumed cause: dietary intake patterns = ↓ fiber
and fluid intake
 Atonic Constipation “Lazy Bowel”: loss of rectal sensibility,
rectum is full of feces, urge to defecate is lacking, older
people, pbese, post-op, pregnant and fevers. May be d/t
↓diet, irregular meals, ↓fluid and fiber and failure to est reg
time for defecation
 Spastic Constipation “Irritable Constipation Syndrome” is
caused by overstimulation of intestinal nerve ending →
irregular contraction of the bowel → uncoordinated sigmoidal
mobility and loss of rectal sensibility → abd pain, belching,
heartburn, flatulence, palpitation and nervousness
 Inflammation of the lower esophagus caused by backflow of
stomach acids when the LES does not contract properly
Acute Gastritis
 Inflammation of the gastric mucosa, sudden and violent in
onset, stomach discomfort
 Attacks follow overeating, eating too fast, eating when tired,
emotionally upset, eating foods specifically sensitive to the
individual, alcohol, tobacco, highly seasoned foods, spoiled
foods with staph, drugs containing salicylates and ammonium
chloride
Chronic Gastritis
 Chief manifestation: pain- mild sometimes but severe and
cutting at intervals
 Erosions ulcerations, changes in blood vessels and
destruction of surface cells via endoscopy for diagnosis
  Avoid stimulating broths and highly seasoned
foods
 ↑ number of feeding and amount of food as
tolerated until full regular diet
Chronic Gastritis
 Soft diet with adequate calories and nutrition
 Avoid highly seasoned foods
 Restrict liquids to a bare minimum bc excess
causes discomfort
 Small frequent feedings chewed in small
interspersed
Peptic Ulcer Objectives:  Small frequent meals: varied and balanced diets
Disease  Relief of pain taken slowly in 4-5 small meals/day
(gastric or  Healing of the ulcer  Limited in coffee, alcohol and other food that
duodenal)  Reduction of tendency for recurrence cause discomfort
 Avoid late evening snacks that stimulate nocturnal
Neutralization of acids and reduction of acid secretion: acid
 Antacids- neutralize excessive acidity  Avoid cigarette smoking: accentuates symptoms
 Antispasmodics- inhibit motility and relieve pain and slows healing
 Anticholinergics- inhibit acid secretion like H2  Avoid aspirin: may cause mucosal hemorrhages
receptor antagonist (Cimetidine)  Adequate calorie to maintain DBW
 Proton Pump Inhibitors  High Protein: to promote healing, buffer the
 Metronidazole + Broad-spec antibx for H.pylori acids, replace nitrogen loss form ulcer
 Adequate CHO: energy and spare protein
 High Fat(unsaturated): to inhibit gastric secretion
and motility via cholecystokinin
 Restrict fiber: to reduce motility
 Avoid gas-former foods (cooked cabbage, beans,
milk, onions, fried foods, spiced and orange juice);
individual tolerance is still a factor
 Eat in a pleasant envt w/ a calm and happy frame
of mind
 Rest before and after each meal
Diverticular  Fiber supplements for uncomplicated diverticular  Fiber diet (bran) have reported beneficial effects
Disease disease on pain and constipation and intraluminal pressure
 Local erosions from ↑gastric acid and pepsin, from ↓mucosal
resistance to these substances, defect in control or secretion
and motility or in synthesis of prostaglandins that either inhibit
gastric acid secretion or promote bicarbonate secretion.
 Eroded lesion in the gastric mucosa or duodenal mucosa;
male > female, Type A personalities (naturally tense,
hardworking, workaholic); Acidic env’t is the principal cause
Duodenal Ulcer
 More common than gastric ulcer
 Occur within 3cm of pylorus where acidity is high
 Pathogenesis:
-↑capacity to secrete acid in response to gastrin d/t ↑
number of parietal cells
-↑sensitivity to gastrin
-↑secretion of gastrin
-↓ability to inhibit gastrin
-↑nocturnal gastric acid secretion
-Rapid entry of acidified chime in the duodenum
Gastric Ulcer
 Found at the antrum
 Pathogenesis:
-Pre-ulcer condition: gastritis of inflamm of the antrum
or pyloric gland occur with gastric ulcer
-Gross mucosal damage: chronic backward diffusion
of H ions after disruption of normal gastric mucosal
barrier
-Disturbance in antroduodenal motility → bile acids
from duodenum reflux to stomach → gastritis →
damaged mucosa is susceptible to peptic ulceration
 Diverticula: caused by, acc to research, ↑colonic
intraluminal pressure needed to eliminate small hard stools
from low fiber diet
  Diverticulosis: when diverticula form in the colon and cause
pain in left lower abdomen without fever; do not produce
muscle thickening, changes in intraluminal pressure or
noticeable symptoms
 Diveticulitis: infected diverticula → constipation and
diarrhea, flatulence, abd pain, fever and mucus and blood in
stools
Inflammatory  Low-residue diets  Unknown etiology
Bowel  Caloric supplements  May become severely malnourished
Disease  Elemental enteral or TPN formulas with  Ulcerative Colitis: characterized by rectal bleeding,
complete bowel rest diarrhea, abd cramping, abd pain, loss of appetite, weight
 Avoid potential food allergens: carrageenan loss
thickeners, cow milk  Crohn’s Disease: chronic inflammation anywhere throughout
 Avoid low-fiber diets the length of the GIT, may induce similar symptoms as in
fistulas and narrowing of the bowel
Irritable  Dietary fiber: to improve constipation  Pain, abdominal distention and alteration of bowel habits d/t
Bowel inappropriate rxn of intestinal wall to stress, motility
Syndrome disturbances, diet or food hypersensitivity reactions
Lactose  Modification of milk and milk products by adding  Insufficiency of lactase
Intolerance lactase or use of fermented products (cheese,  Is not an inevitable consequence of lactase deficiency
yogurt) because many lactase-deficient individuals can consume
moderate amounts of lactose-containing foods
Appendicitis  Associated with less-developed regions and low-fiber diet
 NUTRITION FOR RENAL DISEASES
INTRODUCTION DISEASED KIDNEYS
Early stages of Chronic Renal Disease: moderate modification on dietary intake  Impaired excretion of waste products of CHON metabolism, excess electrolytes, and fluids.
1. Products of CHON breakdown These accumulate in tissues and blood UREMIA: final common pathway of Chronic
2. Regulate blood levels of electrolytes and maintain fluid balance progressive kidney disease.
3. Produce rennin and erythropoietin which affects blood pressure and stimulates
production of red blood cells, respectively.
3 MAJOR FUNCTIONS OF THE KIDNEYS DIETARY MODIFICATION GOALS
1. Excrete waste products of CHON breakdown 1. Maintain or improve nutritional status
2. Regulate blood levels of electrolytes and maintain fluid balance 2. Minimize uremic toxicity
3. Produce rennin and erythropoietin which affects blood pressure 3. Retard progression of renal failure
and stimulates production of RBCs, respectively. 4. Promote patient's well-being

COMPONENTS AMOUNT SOURCE NOTES

PROTEIN (CHON) Creatinine clearance Daily protein intake High biologic value CHON:  2/3 must be of high quality (meaning from milk and meat) and distributed
30-20 ml/min 0.60 g/kg -Egg whites (best source) evenly for adequate amino acids (AAs)
19-5 ml/min 0.45 g/kg -Meat, fish milk, egg whites (good  Low biologic value CHON: must be regulated
5 ml/min 0.30 g/kg source)
Children Not less than 1-1.3 g/kg Low biologic value CHON:
-Rice
Loss CHON in urine must be replaced equally -High CHON vegetables
SODIUM (Na) Edema and HPN 60-90 mEq 1380-2070 mg  Table salt  Hypernatremia high blood pressure and edema + weight gain
Extreme edema 60 mEq 1380 mg  Hyponatremia low blood pressure, depletion of ECF volume, rapid
weight loss, excretory capacity deterioration
POTASSIUM (K) Not more than 70 mEq 2370 mg / day  Fruits – good source  K accumulates in renal diseases, hence K restriction is recommended
 Beverages (ie coffee)-  S/s: headache and vomiting, bradycardia, and cardiac arrest
significant amts
PHOSPHORUS (P)  45-65 mEq 700-1000 mg/day  Meat and milk products  Phosphate accumulates in renal diseases
and CALCIUM  May not be low enough to control serum phosphorus;  Ca levels decrease in renal diseases
(Ca) use of phosphate binders ie aluminum hydroxide  Low Ca increase PTH secretioncalcium withdrawal from bones 
(renders phosphate unabsorbable in the intestine) to bone abnormalities
control hyperphosphatemia
 Ca supplements: best for increased calcium needs
FLUIDS 500-600 ml more than the 24 hour urine output- for  Fluids aren’t excreted and conserved efficiently in renal diseases
insensible daily water loss  S/s: edema (swelling of hands and feet) + weight gain, HPN, shortness of
breath
 Total fluid content of diet= drinking water + beverages + water content of
foods and water from food oxidation
CALORIES  At lest 35 kcal/kg/day  Must be adequate to prevent CHON breakdown, to prevent CHON from
 Children: 60-80 kcal/kg (not less than 80% of being used as energy source, and to maintain constant body weight
recommended allowance for age)  Inadequate intake may aggravate uremia
 To prevent growth retardation  CHO and FAT must be adequate to compensate for CHON restriction
 Patient’s must understand overuse of candies, sugar, fats, and oils
MINERALS Excesses and deficiencies are expected
 RENAL DISEASES
CHRONIC RENAL
INSUFFICIENCY (CRI)
Diet modifications p. 139
CHRONIC RENAL FAILURE
(CRF)
Diet Modifications p. 140
ACUTE RENAL FAILURE
(ARF)
Diet Modifications p. 142
POST-KIDNEY
TRANSPLANTATION
Diet Modifications p. 142-143
NEPHROTIC SYNDROME
(NS) p. 144
NOTE:
ECF: Extracellular Fluid
TGs: Triglycerides
***See pages indicated for each Renal Disease and pages 131-138 for renal computations. Based kasi sa samplex, nandiyan yung mga lumabas na questions for RENAL.
NOTES
 Also PRE-DIALYSIS DIET
 Diet composition:
-Restricted in CHON and Phosphorus
-Na, K, fluid, and calories are
restricted based on individual needs
-Deficient in Ca, Fe, B12, and Zn
-Low CHON diet: deficient in
B1(thiamine), B2(riboflavin), B3(niacine)
Diet Composition:
 Controlled CHON, K, Na, P, and fluids
 Fat, Cholesterol, TGs, and fiber are
modified based on individual needs
Diet Composition:
 Controlled CHON, Na, K, P, and fluids
(same with CRF)
 To meet increased Ca and P
demands: 3-4 glasses of milk/day or
 Ca and P supplements (Calcium
phosphate) if milk is note tolerated
Diet Composition:
- Controlled CHON and Na
INDICATIONS
W/o dialysis, more of
prevention
CRF patients with
hemodialysis or peritoneal
dialysis
ARF with or without dialysis
treatment
CRF who have undergone
renal transplantation
NS patients w/o dialysis
GOALS DIET PRESCRIPTION
1.Reduce workload by reducing urea, uric acid, State calorie, CHON, and
creatinine, and, electrolytes (esp. phosphates) electrolytes levels
2.Prevent acceleration of damage from excessive CHON
intake
3. Prevent calcification due to renal dystrophy
4. Prevent renal osteodystrophy
5. Promote well-being and postpone need for dialysis
1.Meet nutritional requirement
2.Minimize uremic complications
3.Maintain acceptable blood chemistries, BP, and fluid
status (in the setting of renal impairment)
4.Promote well-being
1. Reduce accumulation of uremic toxins State calorie, CHON, and
2.Control electrolyte abnormalities electrolyte levels (same with
3.Correct fluid retention CRI)
4. Maintain Nutritional Status
1. Provide adequate calories and CHON to counteract Normal diets may be
the catabolic effect of surgery followed if there are no
2. Manage nutritional side effects of immune- complications
suppressive drugs
1.Minimize edema and proteinuria State energy, CHON, and
2.Control HPN Na levels
3.Slow down progression of Renal disease
4.Prevent muscle catabolism and CHON malnutrition
5. Supply adequate energy
“May mga pagkaing hindi nauubos.”
YUMMY, FOREVER