 fats are transported into the bloodstream via the lymphatic circulation.

 fermentation produces short-chain fatty acids (SCFAs) and gas.

 Autonomic nerves – sympathetic – fear, pain; parasympathetic – smell, sight
 Ghrelin, a neuropeptide secreted from the stomach, and motilin, a related hormone
secreted from the duodenum, send a “hungry” message to the brain.
 Gastrin – increased acidity- increases gastric motility. Secretin – stimulates
pancreatic juice, inhibits, gastric acid.
 Major functions of CCK are to (1) stimulate the pancreas to secrete enzymes,
bicarbonate, and water; (2) stimulate gallbladder contraction; (3) increase colonic
and rectal motility; (4) slow gastric emptying; and (5) increase satiety.
 Motilin stimulate gastric emptying and intestinal migrating contractions - Combined
with antibiotic erythromycin to treat delayed gastric emptying. Somatostatin
decreases motility of the stomach and intestine and inhibits or regulates the release
of several gastrointestinal hormones – useful for disorders diarrhoea, short bowel
syndrome, pancreatitis, dumping syndrome, and gastric hypersecretion
 intrinsic factor (a glycoprotein that facilitates vitamin B12 absorption in the ileum) is
produced in stomach
 stomach pH 1 to 4
 the duodenum is approximately 0.5 m long, the jejunum is 2 to 3 m, and the ileum is
3 to 4 m.
 passive transport without energy and without any transport protein, with transport
protein facilitated diffusion.
 Active transport require energy and transport protein
 Reduced abundance or
 changes in the relative proportions of these beneficial bacteria, a state called
dysbiosis
 several nutrients are formed by bacterial synthesis, such as vitamin K, vitamin B12,
thiamin, and riboflavin.
 99% protin, 95% to 97% of ingested fat is absorbed,
 The absorption of zinc is impaired with disproportionately increased amounts of
magnesium, calcium, and iron.
 large amounts of iron or zinc may decrease the absorption of copper
 the presence of copper may lower iron and molybdenum absorption.
 Cobalt and iron compete and inhibits one other absorption
 Allostasis -This is a condition of metabolic stability with adjustments for
environmental influences and stresses through physiologic changes
 pro-inflammatory molecules - adipokines and cytokines
 “smoldering disease” – prolonged inflammation for longtime without noticeable
symptoms, finally comeup with tissue damage.
 inflammatory biomarkers, such as high-sensitivity C-reactive protein (CRP-hs)
(plasma), sedimentation rate, interleukin-6 (IL-6), and TNF-alpha - diseases well
characterized by these markers include heart disease, diabetes, autoimmune
diseases, and possibly cancer and Alzheimer’s disease
 Visceral adipose tissue (VAT) - endocrine functions - secretion of inflammatory
adipokines, such as resistin, leptin, and adiponectin, and tumor necrosis-factor-
alpha (TNF-alpha)—all contributing to the systemic total inflammatory load.
 “brown out” or “black out.”- problem with mitochondria (power plant)- problem
with ATP production – identified by coenzyme Q10 and alpha lipoic acid. (fatigue –
symptom of mitochondrial dysfunction to check macronutrient intake)
 study regarding diseases that are related to disturbances in the gut environment and
the immune system is called enteroimmunology.
 too sluggish and congested internal environment, facilitating the development of
chronic diseases such as cancer, cardiovascular disease, and infectious diseases
 Dietary factors helping to maintain healthy fluid viscosity are hydration, vitamin E
with significant gamma-tocopherol, polyunsaturated fatty acids (PUFAs),
monounsaturated fats (MUFAs), and avoidance of any chronic subclinical infections
and foods or substances that may act as antigens
 Common biomarkers of increased body fluid viscosity are blood fibrinogen with
platelets, and urinalysis measurements of specific gravity and the presence of
“cloudiness” or mucus.
 vitamin D, vitamin C, and methylation nutrients such as folate, B12, B6, and B2,
which act as co-nutrients in inflammation and immune-control mechanisms
 critical nutrient-partner balances are omega-6 and omega-3 fatty acids, vitamin D
and vitamin A, magnesium and calcium, and folate, B6, B2, and B12.
 Prostaglandins contribute to the regulation of vascular tone, platelet function, and
fertility.
 Omega 3 EPA eicosanoid - suppress arachidonic acid biosynthesis, an omega-6 fatty
acid (which increases inflammation when taken in excess)
 Omega 3 EPA and DHA -critical component - eye and brain - modulation of metabolic
inflammation.
 GLA not only attenuates intracellular inflammation by converting to DGLA but also
reduces inflammation in the extracellular matrix present in diabetic nephropathy
 AA should be balance with omega 3 intake if not excess AA can contribute to
increase inflammation and increase carcinogen cells
 GLA-rich plant oils from evening primrose, black currant, and borage
 CYP450(cytochrome P450) enzymes are expressed primarily in the liver, but they
also occur in the small intestine, kidneys, lungs, and placenta helps to remove toxins
 Vit D sources - fatty fish, fish eggs or caviar, organ meats, egg yolk, and mushrooms
 Mg – inhibition of inflammation – Mg nutrient partner Ca and Zn
 Zn nutrient partner Cu.
 In a nutrition-focused physical exam, white spots under the nails loss of appetite,
anorexia nervosa, loss of normal taste sensation, alopecia, hyperkeratinization of
skin, dermatitis, and reproductive abnormalities can indicate possible zinc
deficiencies.
 Methylation - Folate, B6, B2 and B12
 Flavonoids and anti- oxidant nutrients - protection against free radical and reactive
oxygen species
 Ascorbate interacts with the vitamin E complex to provide protection to water- and
lipid-soluble surfaces in membranes. glutathione, another water-soluble anti-
oxidant that is synthesized in all cells and which supports the central role of
ascorbate and vitamin E; lipoic acid with its water and lipid molecular components
and sometimes considered the “universal antioxidant”; and coenzyme Q-10 that
functions in protecting lipid structures, especially in cardiac muscle and
mitochondrial membranes.
 Ca 99% in bones and teeth only 1 % in ECF. Half of this is combined with albumin.
The Ca level will decrease in albumin(hypoalbuminemia)
 serum total calcium is about 8.5 to 10.5 mg/dl, whereas normal levels for ionized
calcium are 4.5 to 5.5 mEq/L.
 functions - regulates nerve transmission, muscle contraction, bone metabolism, and
blood pressure regulation and is necessary for blood clotting.
 Calcium is regulated by parathyroid hormone (PTH), calcitonin, vitamin D, and
phosphorus.
 20% to 60% of dietary calcium is absorbed- ileum site of absorption – passive
transport – excretion kidney – less due to protein bound – 100 to 200 mg. RDA –
1000 to 1300mg. upper limit – 2500 – 3000mg
 NA normal range of 135 to 145 mEq/L. About 90% to 95% of normal body sodium
loss is through the urine; the rest is lost in feces and sweat
 Sodium balance is regulated in part by aldosterone, a mineralocorticoid secreted by
the adrenal cortex
 Mg – normal level -.6 to 2.5 mEq/L. half of the body’s magnesium is located in bone,
whereas another 45% resides in soft tissue; only 1% of the body’s magnesium
content is in the extracellular fluids.
 Na RDA - upper limit of 2.3 g of sodium per day (or 5.8 g sodium chloride per day)
 Approximately 30-50% of magnesium ingested from the diet is absorbed (within the
jejunum and ileum though passive and active transport mechanisms)
 the kidneys increase potassium excretion in light of hypomagnesemia so it should be
corrected immediately
 Mg RDA – 310-420mg
 Ph – normal level 2.4 and 4.6 mg/dl. RDA – 700mg. upper limit of 3500 to 4000 mg
 Normal serum K - 3.5 to 5 mEq/L. Potassium-rich food sources include fruits,
vegetables, fresh meat, and dairy products. RDA - 4700 mg
 tetracycline or ciprofloxacin should be warned not to combine the drug with milk,
yogurt, or supplements containing divalent cations, calcium, iron, magnesium, zinc,
or vitamin-minerals containing any of these cations.
 probiotic contains the yeast Saccharomyces boulardii. It should not be used in any
patient with a central line for intravenous therapy, including those on dialysis.
 TJC requires that nutrition screening be completed within 24 hours of admission
 Sentinel events are unanticipated events that involve death, serious physical or
psychologic injury, or the risk thereof.
 Problem-oriented medical records (POMR), subjective, objective, assessment, plan
(SOAP), assessment, diagnosis, interventions, monitoring,
 evaluation (ADIME), electronic medical record (EMR), EHR, and personal health
record(PHR)
 U.S. Departments of Agriculture (USDA) and Department of Health and Human
Services (DHHS)
 Information about the diet and nutritional status of Americans and the relationship
between diet and health is collected primarily by the CDC via its NCHS and National
Health and Nutrition Examination Survey (NHANES).
 Natural medicine approaches known as Holistic medicine.
 chiropractic medicine for back pain, acupuncture for pain relief, select dietary
supplementation for conditions such as macular degeneration, depression, and
diarrhea
 nasogatric - short-term (no more than 3 to 4 weeks) - intolerance to gastric feeding-
Abdominal distention and discomfort, Vomiting, Persistent diarrhea. Risk - aspiration
pneumonia
 Gastrostomy or Jejunostomy - more than 3 to 4 weeks,
 The amount of protein in available commercial enteral formulas varies from 6% to
25% of total kilocalories – protein mostly from derived from casein, whey, or soy
protein isolate.
 Elemental formulas contain di- and tripeptides and amino acids, which are absorbed
more easily. Specialized formulas (for hepatic or renal failure or in cases of multiple,
severe allergies) may include crystalline amino acids.
 Specific amino acids may be added to some enteral formulas. Branched chain amino
acids are used in formulas for patients with severe hepatic disease, and arginine has
been added to formulas marketed for critically ill patients.
 CHO 30 to 85% calories. Hydrolyzed formulas contain carbohydrate from cornstarch
or maltodextrin.
 Fructooligosaccharides (FOS), which are prebiotics, have been added to enteral
formulas, often in combination with source of dietary fiber
 FOS in individuals with irritable bowel syndrome (IBS) may worsen symptoms
 Lipid 1.5 to 55% calories. corn, sunflower, safflower, or canola oil provides between
15% and 30% of the total kilocalories. limited fats are in the form of MCT.
 MCTs do not require bile salts or pancreatic lipase for digestion and are absorbed
directly into the portal circulation.
 Formulas intended for patients with renal or hepatic failure are intentionally low in
vitamins A, D, and E, sodium, and potassium.
 1 ml of water per kilocalorie consumed, or 30 to 35 ml/kg of usual body weight.
 Standard (1 kcal/ml) formulas contain approximately 85% water by volume;
concentrated (2 kcal/ml) formulas contain only approximately 70% water by volume.
 Formula expiry - 4-hour hang time for a product in an open system and 24 to 48
hours for products in closed system
 bolus enteral feedings for stable patient – 5 to 20 mins, 500mlper time, 3 to 4 time
per day. Intolerable reduce feed per time and increase frequency
 intermittent - daily feeding schedule is four to six feedings, each administered over
20 to 60 minutes. Formula administration is initiated at 100 to 150 ml per feeding
and increased incrementally as tolerated.
 Cyclic feeding – daily feeding schedule is 90 to 125 ml per hour of formula
administered over 18 to 20 hours
 Patients with a feeding tube tip in the small intestine should be fed only by
continuous or cyclic infusion
 Aspiration, a common concern for patients receiving EN, diarrhoea, constipation,
 PPN - up to 800 to 900 mOsm/kg of solvent can be infused
 peripherally inserted central catheter (PICC) may be used for short- or moderate-
term infusion
 PN solution amino acid - 3% to 20%. Protein - 15% to 20% of total energy intake
 Carbohydrates - dextrose monohydrate(3.4 calories per gram) - 5% to 70%
 carbohydrate administration should not exceed 5 to 6 mg/kg/min in critically ill
patients. Protein 15 to 20%, fat 20 to 30% remaining CHO as dextrose Excessive
administration can lead to hyperglycemia, hepatic abnormalities, or increased
ventilatory drive
 lipid - aqueous suspensions of soybean oil with egg yolk phospholipid as the
emulsifier.
 10% of calories per day from soybean – 2 to 4% of linoleic acid DV. Should not
exceed 2g /kg. 1 to 1.5 are common. TG should be monitored.
 1% - 1.1kcal/ml, 20% - 2kcal/ml. 20-30% provide 1g fat/kg.
 home parenteral nutrition - Alternative forms of lipids - Lipid sources other than
soybean or safflower oil including coconut, olive, and fish oil are used. 80% olive oil
+20% soyabean oil – 2kcal/ml.
 soybean oil, medium-chain triglycerides, olive oil, and fish oil (SMOF lipid) – safe and
efficacious than std soyabean oil emulsion.
 Monitoring of manganese and chromium status is recommended for PN patients
 Iron, as it is not compatible with lipids, given separately.
 PN should be started below needed and then increased to need on 2 or 3 days,
some may do this with dextrose infusion of 100 to 200mg and then reach max need
on 2 or 3 days. In case of need to stop PN, the rate should be reduced gradually to
stop. Sudden stop may cause hypoglycemia.
 Continuous infusion 24 hrs for critically ill hosp patients, cyclic infusion 12 to 16hrs
for life long patients (homePN)
 transition from PN to EN, introduce a minimal amount of enteral feeding at a low
rate of 30 to 40 ml/hr to establish gastrointestinal tolerance. If tolerated PN can be
reduced gradually and EN rate increase by 25 to 30 ml every 8 to 24 hrs. if 75%
tolerated PN can be discontinued. Formula will be low in lipids and lactose free
 PN to oral, feed should be liquid and diet low in fat, low in fiber, easily digestible and
lactose free.
 EN to oral – co tenuous feed to 12 hrs to 8hrs during night then to liquid, diet if not
compatible both EN and oral
 Oral supplements – 250kcal/8oz or 240ml, 8 to 14g protein, 350-500 to 540kcal
 Oral supplements that contain hydrolyzed protein and free amino acid are
developed for patients with renal, liver, malabsorptive diseases
 Developmental disability onset 22 years
 Cerebral Palsy - disorder of muscle control or coordination resulting from
injury to the brain
 Down’s Syndrome (Genetic Disorder) - Results from an extra chromosome 21
- Gum disease; in
 Prader-Willi Syndrome (Genetic Disorder) - A disorder characterized by
uncontrollable eating habits, inability to distinguish hunger from appetite
 Autism - developmental disorder; diagnostic criteria include communication
problems, ritualistic behaviors, and inappropriate social interactions
 Spina Bifida (Myelomeningocele) - midline defect of the skin, spinal column,
and spinal cord;
 Thyroid - Down’s syndrome, glucose tolerance test Prader-Willi syndrome
 Feeding problems - neuromotor dysfunction, obstructive lesions such as
strictures, and psychosocial factors, oral-motor difficulties, dysphagia,
positioning problems, conflict in parent-child relationships, sensory issues,
and tactile resistance from previous intubation
 Nutritional consequences - inadequate weight gain, poor growth in length,
lowered immunity, anemia, vitamin and mineral deficiencies, dental caries,
and psychosocial problems.
 Excessive or inadequate weights; inadequate dietary intake; excessive or
inadequate fluid intake; altered gastrointestinal problems such as
constipation, vomiting, and diarrhea; intake of foods that are unsafe because
of contamination or food allergies; food-medication interactions; chewing and
swallowing difficulties; and problems with self-feeding
 Dental problems - low sucrose intake
 albumin have been found to be low, evaluation of thyroid function at birth
and thereafter annually
 zinc, copper, and selenium are normal
 resting energy expenditure (REE) of the child with DS is lower -10% lower
than the dietary reference intake (DRI) for energy. After age of 5 energy
calculations are based on height and weight
 Fiber requirement after age 3, is 5 to 6 g per year of age per day. For adults
the recommendation is for 25 to 30 g of dietary fiber daily
 Prader-Willi syndrome (PWS) absence of chromosomal material.
developmental delays, poor muscle tone, short stature, small hands and feet,
incomplete sexual development, and unique facial features. Insatiable
appetite leading to obesity is the classic feature of PWS
 genetic material deleted from chromosome 15 received from the father,
 a child receives both chromosome 15s from the mother called maternal
uniparental disomy
 Growth hormone deficiency, insulin like growth factor deficiency, low IGF
binding protein, low insulin levels
 DNA methylation analysis for early detection
 Growth hormone therapy proved successful with increase in height
 Also, deficiency in the hypothalamic-pituitary-gonadal axis, causing delayed
and incomplete sexual development.
 The cause of the uncontrollable appetite is suspected to involve the
hypothalamus and altered levels of satiety hormones and peptides such as
ghrelin
 decreased lean body mass and increased body fat, even in infancy.
 They have only 53%of the REE of normal obese individual
 They not having interest in physical activity because of low muscle tone
 Tests to be added on addition is fasting blood glucose tests or glucose
tolerance tests
 Many infants have gastroesophageal reflux, requiring medication or
thickening of their formula.
 25% protein, 50% carbohydrate, and 25% fat
 They need 50% to 75% of the energy needs of unaffected children.
 In school age growth hormone therapy for their child helps, but it doesn’t
seem to change the child’s lack of satiety. Appetite-suppressing medications
have been used but are largely unsuccessful.
 In adulthood a very low 6 to 8 kcal per centimeter of height may be
required.
 Spina Bifida generally occurs between 26 to 30 days of gestation higher the
lesion, the greater is the paralysis.
 The national recommendation is 400 mcg/day for all women of childbearing
age proven successful in prevention of spina bifidia
 The lesion van be surgically removed after birth within 24 hours, but the
nerve damage is permanent, resulting in the varying degrees of paralysis of
the lower limbs including UTI and bladder control
 seizures also occurs in 20% individual treated with medications if fail
ketogenic diet
 Due to latex allergy avoid certain foods such as bananas, kiwi, and avocados.
Mild reactions can occur from apples, carrots, celery, tomatoes, papaya, and
melons
 Arm span can be used directly as a height measure (arm span * 1) if there is
no leg muscle mass loss, as in a sacral lesion. Arm span * 0.95 can be used to
determine height if there is partial leg muscle loss, and arm span * 0.90 is
used for a height measurement when there is complete leg muscle loss
 Biochemical measures mainly iron status tests, measurements of vitamin C
and zinc levels
 Energy needs are lower for the child with spina bifida - 7 cal/cm of height for
weight loss and 9 to 11 cal/cm of height to maintain weight.
 Adequate fluid for UTI. Cranberry juice can be offered.
 Cerebral palsy (CP) disorders of motor control or coordination resulting
from injury to the brain
 Biochemical tests vitamin D, calcium, carnitine, and vitamin K levels is
recommended. Bone mineral density
 Gastroesophageal reflux frequently is seen. If aspiration tube feeding
required if needed gastrostomy
 Autism - Autism spectrum disorders (ASD)
 Asperger syndrome - ASD but have normal to high cognitive level
 Causative factors - a nutritionally deficient diet, immune system problems,
oxidative stress, and pesticide exposure, elevated serotonin levels and
disturbances in gamma-amino butyric acid (GABA) receptors, glutamate
transmitters, and cholinergic activity
 Child with autism may need additional omega-3 or EFAs
 gluten and casein as the suspected sources - improved with restriction of
gluten casein soy diet.
 Head circumference has been found to be larger than that of the non-ASD
individual. Biochemical - aminoacid, allergy, thyroid
 mineral and vitamin therapy and elimination diets such as a gluten-free,
casein-free diet; allergy diets; supplementation with essential fatty acids
(EFAs) and megavitamins.
 Sulforaphane - a phytochemical in broccoli seed -shows improvement
 ADHD causes not well understood but use of acetaminophen during
pregnancy was contributing factor
 lack of EFAs is a possible cause of hyperactivity in children also zin and mg
supplement
 Cleft Lip and Palate - Lip and palate development occur between 5 and 12
weeks of gestation
 Causes - genetics and environmental factors include maternal folic acid
deficiency, smoking, alcohol use, anticonvulsant use, and some maternal
illnesses
 Surgery - clept lip 2 to 3 months. Cleft palete - 9 months
 Normal calorie but feeding way expressing milk ang giving with specially
designed bottles
 Fetal alcohol spectrum disorders (FASD) facial stigmata, damaged
neurons, and brain structures, which can result in psychologic or behavioral
problems and other physical problems.
 intellectual disabilities and problems with behavior and learning, particularly
with math, memory, attention, judgment, and poor impulse control. Chil
 Normal calorie and nutrient need but the need increases if failure to thrive
 Controversial research - eliminating sugar for ADHD, blue gre0en algae for
DS, B6 and Mg for autism, also folic acid and antioxidnats for DS.
 Genetic metabolic disorders (autosomal-recessive) - absence or
reduced activity of a specific enzyme or cofactor
 assessment should include blood gas measurements, electrolyte values,
glucose and ammonia tests, and a urine test for ketones.
 Phenylketonuria (PKU) - phenylalanine (Phe) is not metabolized to tyrosine
(Tyr) because of a deficiency or inactivity of phenylalanine hydroxylase
 Diagnostic criteria for PKU include an elevated blood concentration of Phe
and an elevated (i.e., greater than 3) Phe:Tyr ratio.
 Treatment with sapropterin (a synthetic form of BH4) is used. enzyme
substitution with phenylalanine ammonia lyase (PAL) to degrade Phe, or gene
therapy to restore PAH activity
 Blood phenyl alanine range 2 to 6 mg/dl or 120 to 360 mol/L
 Food dairy is effective method
 Increased phe in blood may be due to increased phe foods or tissue
catabolism. Preventing tissue catabolism by maintaining intake of the
formula/medical food as much as possible is essential.
 The diet restriction should be followed throughout the life and careful during
pregnancy to maintain blood phe level within 1 – 5 mg/dl.
 Maple syrup urine disease (MSUD), or branched-chain ketoaciduria –
deficiency of alpha-ketoacid dehydrogenase complex – impaired metabolism
of branched-chain amino acids (BCAAs) leucine, isoleucine, and valine
 Failure to treat this condition leads to acidosis, neurologic deterioration,
seizures, and coma, proceeding eventually to death. Initial phase needs
peritoneal dialysis and hydration
 plasma leucine greater than 10 mg/dl (760 mol/L) often are associated with
alpha-ketoacidemia and neurologic symptoms.
 Therapeutic liver transplantation has been proposed as an option in MSUD
 BCCAs (if leucine level is low in blood), essential AAs and mineral for normal
growth and maintenance. Some require additional supplementation with l-
valine or l-isoleucine to maintain biochemical balance
 Acute infections represent life-threatening medical emergencies in this group
of children. Infection can increase the blood leucine level, if so BCCAs
removed from diet and IV therapy can be started
 organic acid disorders - Propionic acidemia - propionyl–coenzyme A (CoA)
carboxylase in the pathway of propionyl-CoA to methylmalonyl-CoA.
 methylmalonic acidemia or aciduria - At least five separate enzyme
deficiencies - methylmalonyl-CoA mutase apoenzyme. Diagnosis -
methylmalonic acid in blood and urine. Also, hypoglycemia, ketonuria, and
elevation of plasma ammonia and lactate levels.
 Ketone utilization disorders - mitochondrial 2-methylacetoacetyl-CoA
thiolase deficiency - disorders of isoleucine and ketone body metabolism.
 Some patients with propionic acidemia may respond to biotin. Liver damage
and cardiomyopathy. Liver transplant may be helpful
 methylmalonic acidemia – vitamin B12.
 ketone use disorders, the treatment is dietary protein restriction (usually 1.5
g/kg of body weight per day); supplementation with l-carnitine
 normal nutrition to prevent catabolism and hydration to removal of metabolic
wastes. High protein, infection, constipation can make relapse. For relapse
treatment should be immediate because come or death can occur fast.
 Protein 1 – 1.5g/kg can be beneficial for infants. Formula should be diluted to
reduce protein content. Specialized formulas that limit threonine and
isoleucine and omit methionine and valine are used.
 urea cycle disorders (USDs) result in an accumulation of ammonia in the
blood
 elevated ammonia - vomiting and lethargy, seizures, coma, and ultimately
death
 Neurologic damage – hyperammonemia
 Ornithine transcarbamylase (OTC) deficiency, Citrullinemia, Argininosuccinic
aciduria (ASA), Carbamyl-phosphate synthetase (CPS) deficiency
 managed by discontinuing protein intake, intravenous fluids and glucose -
correct dehydration and provide energy.
 If hyperammonemia is severe, peritoneal dialysis, hemodialysis, or exchange
transfusion may be required. Intravenous sodium benzoate reducing the
hyperammonemia.
 protein at 1 to 1.5 g/kg for long term 1-2g/kg. L- arginine supplement. Even
protein restricted other nutrients should be provided adequately to maintain
normal growth and maintenance.
 Hereditary fructose intolerance - liver enzyme aldolase B deficiency.
Initial symptoms include nausea, bloating, and vomiting. Untreated, liver and
kidney damage can occur, along with growth restriction. Fructose restriction
 Galactosemia - galactose-1-phosphate - symptoms are vomiting, diarrhea,
lethargy, failure to thrive, jaundice, hepatomegaly, and cataracts. Not
treated, death frequently occurs. Galactose restricted diet.
 Glycogen storage diseases - symptoms are poor physical growth,
hypoglycemia, hepatomegaly, and abnormal cholesterol and triglycerides.
glucose1-6-phosphatase deficiency (type 1) - Unable to metabolise glycogen
to glucose and also gluconeogenesis resulted in severe hypoglycemia.
 Amylo-1, 6-glucosidase deficiency (type 2) – unable glygenolysis but
gluconeogenesis possible to maintain blood glucose level – symptoms less
sevre – hepatomegaly, hypoglycemia
 Renal dysfunction also a problem but cant be fully treated through medical
therapy but liver transplant may be helpful
 MNT - prevent hypoglycemia by providing a constant supply of exogenous
glucose. Administration of raw cornstarch and a high–complex carbohydrate,
low-fat dietary pattern
 Oral corn syrup if not tolerated glucose continuous drip feeding during night
to prevent hypoglycemia
 Corn syrup administration at interval of 4 – 6 hrs (1.6 – 2.5g/kg). iron
supplement needed as corn starch interfere with iron absorption
 fatty acid oxidation disorders - medium-chain acylCoA dehydrogenase
(MCAD) deficiency and long-chain 3-hydroxyacyl-CoA dehydrogenase
(LCHAD) deficiency
 hypoglycemia without urine ketones, lethargy, seizures, and coma. abnormal
liver function, reduced or absent ketones in the urine, and often secondary
carnitine deficiency
 adequate energy intake and are high in carbohydrates. A low-fat diet is
advocated because fats are not effectively metabolized. Consumption of not
more than 30% of energy as fat. Most children may require additional
carbohydrate before bed, based on individual ability to maintain blood
glucose levels throughout the night.
 Food allergy – allergen triggers immune response – allergen is a food
protein or glycoprotein.
 Food intolerance – same as allergy but doesn’t involve immune response
 Atopy – immune production of IgE antibodies in response to allergen –
confirmed by positive skin prick test - food allergy, atopic dermatitis
(eczema), atopic conjunctivitis, atopic rhinitis, asthma, and symptoms in all
organ systems, with the most severe being life-threatening anaphylaxis
 foreign molecules in the digestive tract recognized as “foreign but safe,”- oral
tolerance.
 Esophagus - 25 cm in adults. assessment of patients with GI disorders clinical
examination and evaluation of anthropometrics, biochemical markers, and
the patient’s nutrition history- typical dietary intake, changes in appetite,
food allergies and intolerances, mastication and swallowing ability, and GI
symptoms such as nausea, vomiting, diarrhea, constipation, and the use of
dietary supplements, weight loss at least 5% in 1 month; at least 10% in 6
months
 Esophagitis (inflammation of the esophagus) and intestinal metaplasia
(Barrett’s esophagus) which causes nocturnal GERD
 The lower esophageal sphincter (LES), the crural diaphragm, and the
anatomic flap valve – make up esogastric junction
 Hiatal hernia – epigastric pain, in stage 3 severe chest pain,
 Chest pain may be a symptom of GERD
 Barrett’s esophagus (BE) normal squamous epithelium of the esophagus
is replaced by an abnormal columnar-lined epithelium known as specialized
intestinal metaplasia – cause unknown. Condition named esophageal
adenocarcinoma. Estrogen protective for this in female
 MNT affeine, alcohol, tobacco, and stress avoidance, weight reduction for
obesity, bed elevation 6 -7 inch, loose fitting garments, peppermint and
spearmint avoid (lower the LES pressure), fermented alcoholic beverage,
carbonated beverage, avoid triggering foods
 Head and neck cancer – dysphagia, odynophagia (painful swallowing –
malnourished during diagnosis- cause loang term alcohol and tobacco use –
surgery, chemo, radiation contribute to malnourishment
 After surgery (gastric pullup) - gastrostomy /jejunostomy tube feeding
progressing to oral feeding (clear liquid, full liquid, semi solid, soft, bland,
normal diet) – some may have dumping syndrome
 Gastric parietal cells produce 1.5 to 2l of acid with pH ranging 1 to 2
 Prostaglandins protect GI tract by stimulating mucus secretion and
bicarbonate production
 Dyspepsia (indigestion)-causes GERD, peptic ulcer disease,
gastritis,gallbladder disease or other identifiable pathologic conditions.
Symptoms – epigastric pain, burning, pressure, or fullness in the epigastric
area, or that they cannot finish a normal-sized meal (early satiety)
postprandial nausea, belching, and abdominal bloating
 MNT - consuming smaller meals with a reduction in dietary fat.
 Gastritis - inflammation of the stomach. Chronic gastritis nausea, vomiting,
malaise, anorexia, hemorrhage, and epigastric pain - result in atrophy and
loss of stomach parietal cells, with a loss of HCL secretion (achlorhydria) and
intrinsic factor, resulting in pernicious anemia
 Helicobacter pylori is a gram-negative bacteria – cause of ulcer (peptic and
gastric) - antibiotic treatment is favored when it is diagnosed.
 Non-Helicobacter pylori Gastritis - Aspirin and non-steroidal
antiinflammatory drugs (NSAIDs) prevent prostaglandin synthesis –
medicines -Antibiotics and proton pump inhibitors
 gastric ulcer - atrophy of acid- and pepsin-producing cells vs duodenal
ulcer increased acid secretion throughout the entire day accompanied with
decreased bicarbonate secretion
